Emergency Doctor-Community

ER Physician Tells You How To Avoid A Lightning Strike And What To Do If One Occurs

2009-08-15T14:42:00.001+07:00

An estimated 200 people die each year in the U.S. after being struck by lightning. An extremely brief but intense hit delivers more than 10 million volts and is fatal in about 30 percent of cases. Recent lightning strikes in Newark resulted in one death and three injuries.

Most survivors have significant complications. Half of people struck by lightning will suffer rupture of the tympanic membrane in the ear. Many go on to develop cataracts.

“Lightning presents a grave risk of death,” warns Shreni Zinzuwadia, M.D., an emergency department physician at UMDNJ-The University Hospital and instructor of surgery at the UMDNJ-New Jersey Medical School. “Cardiac or respiratory arrest may result from being hit by lightning.”

There are other dangers outside of a direct hit, she added, from three additional types of strikes.

A side strike happens when lightning jumps from its initial point of contact to the victim. “For example, if you seek protection under a tree, which is one of the worst places to be during a storm, the lightning can hit the tree then jump to you, a better conductor of electricity since humans are mostly salty water,” she explained. “This kind of strike can kill the tree and the person.”

A contact strike occurs when lightning hits an object the person is holding or wearing, such as a watch or eyeglasses.

The other type of strike - step potential – happens when a current traveling through the ground goes up your leg, travels through you and then goes down the other leg and back into the ground. “That is why Boy Scouts practice standing on one leg during a storm,” she explained. “They are attempting to decrease the likelihood that the current will go through them by having only one foot on the ground.”

Prevention begins by seeking cover at the start of a storm. “Lightning seems to be concentrated at the forefront of a storm,” according to Zinzuwadia, “so there tends to be a greater risk of being hit by lightning at the beginning of a storm.”

According to the Federal Emergency Management Agency (FEMA), part of the U.S. Department of Homeland Security (DHS), individuals who hear thunder roar should go indoors because no place outside is safe when lightning is in the area. Stay indoors until 30 minutes have passed after you hear the last clap of thunder.

Once inside, FEMA advises that people avoid contact with corded phones and electrical equipment or cords; do not wash your hands, take a shower, wash dishes, or do laundry because plumbing and bathroom fixtures can conduct electricity; stay away from windows and doors; stay off porches; and do not lie on concrete floors or lean against concrete walls.

If you are outside during a storm, crouch down and try to touch as little of the ground as you can, Zinzuwadia suggests. “Even if you are hit by the current, the less contact there is between you and the ground, the less likely it is that all of your major organs will be hit,” she says. “It increases your chances of survival.”

What signs might indicate that a person has been struck by lightning? “You may see superficial burns on the skin or clothing may burst into flames or be torn away from the body,” Zinzuwadia said. “A person may fall to the ground.

“People who are hit by lightning commonly die from ventricular fibrillation, asystole (cardiac arrest), or respiratory arrest,” Zinzuwadia added. “Bystanders should immediately check for a pulse and spontaneous breathing.”

Immediately call 911 for help if someone is hit by lightning, Zinzuwadia emphasizes.

If a person is in respiratory arrest – has a pulse but is not breathing - provide rescue breaths until the victim resumes spontaneous breathing.

If the victim goes into cardiac arrest, where the heart just stops due to the impact of the massive electrical current, CPR should be administered, Zinzuwadia said. “Give cardiac compressions and provide respiratory support for them.”

Source : http://www.sciencedaily.com/releases/2009/08/090805193601.htm

Cystic Fibrosis Treatments May Have Unseen Long-term Benefits

2009-07-23T21:04:00.001+07:00

Cystic fibrosis medicines that help to break down mucus in the lungs may carry an unexpected long-term benefit, a study suggests.

The treatments not only help breathing in the short term - they may also make lung infections develop to be less harmful in the long run, research from the University of Edinburgh shows.

Scientists studied how bacteria which infect the lungs of cystic fibrosis patients gather nutrients from their surroundings. The work builds on the knowledge that most bacteria co-operate to scavenge what they need from their environment, but some bacteria do not actively hunt, instead stealing nutrients from neighbouring bacteria.

Scientists found that in a viscous environment, similar to thick mucus, the co-operating type of bacteria is most common. However, in a more liquid environment - similar to mucus having been broken down by medicine - the number of thieving bacteria increases, eventually outnumbering the scavenging type. In this environment, because the thieving bacteria are less adept at obtaining food, the bacterial growth slows down.

The results suggest that liquefying lung mucus would be expected to limit the impact of infection in cystic fibrosis.

Dr Rolf Kuemmerli, formerly a researcher at the University of Edinburgh, who led the study, said: "Treating cystic fibrosis patients with drugs that clear their lungs delivers short-term relief for the patient, but may have long-term health benefits too. We hope that our findings will underline the need for treatments that target mucus in the lungs."

Dr Freya Harrison of the University of Bath, who took part in the study, added: "Bacterial infections develop over time, and understanding how medical treatments affect this could be very important for managing long-term infections such as those found in cystic fibrosis."

Cystic fibrosis is an inherited condition that affects more than 8,000 people in the UK, according to the Cystic Fibrosis Trust. Thick mucus can clog the internal organs, especially the lungs and digestive system, making it hard to breathe and digest food.

The study, carried out by researchers at the Universities of Edinburgh, Oxford and Bath, was published in Proceedings of the Royal Society B. Work was supported by the Royal Society and the Leverhulme Trust.

Source : http://www.sciencedaily.com/releases/2009/07/090716113243.htm

Low Birth Weight Linked To Long-term Respiratory Problems

2009-07-18T11:43:00.001+07:00

Infants who weigh less than five and a half pounds at birth often enter the world with a host of medical complications, including respiratory problems. New research shows that these respiratory problems may persist well beyond their infancy and childhood and into adulthood.

"We report a previously unrecognized excess risk of hospitalization for respiratory illnesses in young adults with a history of low birth weight," wrote lead researcher Eric C. Walter, M.D., of the University of Washington Division of Pulmonary and Critical Care. "Our findings suggest that not only are [low birth weight] survivors at increased risk for long-term respiratory disorders, but that these disorders are clinically significant and associated with increased health care utilization."

The researchers used hospitalization records from the Washington State Comprehensive Hospital Abstract Reporting System's discharge database between January 1, 1998 and December 31, 2007. They selected as potential cases any person who was 18 years old at the time of hospitalization and who was discharged with a respiratory code listed among the top four diagnoses. They then linked these cases to birth weight data listed on birth certificates where possible. Control subjects were randomly selected from birth certificate data.

They found that individuals with very low birth weight (less than 1.5 kg, or 3.3 lbs.) or moderately low birth weight (1.5 to 2.5 kg or 3.3 to 5.5 pounds) had a 83 and 34 percent higher risk of hospitalization for respiratory diagnoses respectively. Those who had a history of very low birth weight had twice the risk of being hospitalized for asthma or respiratory infection and 2.6 times the risk of respiratory failure requiring mechanical ventilation.

After adjusting for covariates, including demographic characteristics and maternal smoking, the significant association between birth weight and risk of hospitalization persisted. Furthermore, while the data could not definitively prove a linear link, researchers did note a trend toward greater risk of respiratory problems with lower birth weights.

"In our study the percentage of respiratory disease attributable to moderately or very low birth weight was estimated to be 1.8 percent. If this were extrapolated to the 1.2 million U.S. hospitalizations for respiratory illnesses per year for ages 18 to 44, low birth weight may account for over 22,000 adult hospitalizations per year, with charges in excess of $225 million per year," said Dr. Walter.

While the study did not distinguish between premature birth and retardation of in utero development as causes of low birth weight, previous research has found that both conditions increase risk of abnormal pulmonary function in adolescence and adulthood.

Dr. Walter notes that maternal smoking is a risk factor for low birth weight, and that children of mothers who smoked are more likely to smoke themselves. The relationship, therefore, is difficult to fully tease apart. "It is unknown if adults with a history of low birth weight are more likely to smoke than adults with a history of normal birth weight," he said. "[In this study] we did not find that maternal smoking confounded the affect of low birth weight on adult respiratory disease, but further research is needed comparing hospitalization and smoking rates between adults with history of low birth weight and normal birth weight to better understand this relationship."

While more research is needed to further clarify the relationship between birth weight and subsequent respiratory problems, these results do strongly suggest a looming public health issue. Since the mid-1980s, the proportion of low- and very low birth weight births in the U.S. has increased by more than 20 percent, and in 2005, there were 330,000 combined low- and very low birth weight births in the U.S.

"Given the data from the present study, it would seem prudent to include such a bleak forecast in long-term planning for the provision of health care services," wrote Anne Greenough, M.D. of King's College, London in an accompanying editorial.

Journal reference:

Walter et al. Low Birth Weight and Respiratory Disease in Adulthood: A Population-based Case-Control Study. American Journal of Respiratory and Critical Care Medicine, 2009; 180 (2): 176 DOI: 10.1164/rccm.200901-0046OC

Source : http://www.sciencedaily.com/releases/2009/07/090707121415.htm

Inflammation Markers Linked More With Fatal Than Nonfatal Cardiovascular Events In Elderly

2009-07-16T21:11:00.001+07:00

A new study shows that for elderly people at risk of cardiovascular disease, the presence of inflammatory markers in the blood can identify that an individual is at a higher risk of a fatal rather than a non-fatal heart attack or stroke.

Inflammation is an immune response to injury. However, inflammation is also thought to play a role in cardiovascular disease. Previous studies have shown an association between high levels of markers of inflammation in the circulation with a greater risk of a cardiovascular event, such as a heart attack or stroke. In this study, Naveed Sattar of the University of Glasgow and colleagues used data from an existing trial known as PROSPER (the Prospective Study of Pravastatin in the Elderly at Risk), which involved participants aged between 70 and 82 who had or were at risk of cardiovascular disease.

They examined if three inflammatory markers—interleukin-6 (IL-6), C-reactive protein (CRP) and fibrinogen—were each more strongly massociated with fatal cardiovascular events than with non-fatal cardiovascular events in the period of over three years in which the patients in the trial were monitored.

Using several statistical models, the researchers found that in this group of elderly patients increased levels of all three inflammatory markers, and in particular IL-6, were more strongly associated with a fatal heart attack or stroke than with a non-fatal heart attack or stroke. They also investigated the predictive value of these inflammatory markers—in other words, whether it was useful to include these markers in tools designed to distinguish between individuals with a high and a low risk of heart attacks, strokes and other cardiovascular events.

They report that adding IL-6 to the established risk factors in predictive tools—including lifestyle factors such as smoking, high blood pressure and high blood cholesterol, all of which greatly increase the risk of cardiovascular disease—could help better identify those individuals at a risk of a fatal stroke or heart attack, but not those at risk of a non-fatal cardiovascular event.

The findings of the study suggest inflammatory markers may be more strongly associated with fatal heart attacks and strokes than non-fatal cardiovascular events. The researchers acknowledge that these findings now need to be confirmed in younger populations and larger studies to demonstrate an outright association and the design of the current study cannot show whether the proposed association is a causal one. Nevertheless, the findings should stimulate further investigation into whether the application of inflammatory markers may help better predict the risk of deaths from cardiovascular disease, and whether novel treatments which dampen inflammation might help prolong life.

Journal reference:

Sattar N, Murray HM, Welsh P, Blauw GJ, Buckley BM, et al. Are Markers of Inflammation More Strongly Associated with Risk for Fatal Than for Nonfatal Vascular Events? PLoS Med, 6(6): e1000099 DOI: 10.1371/journal.pmed.1000099

Source : http://www.sciencedaily.com/releases/2009/06/090622201921.htm

Radiographic Pneumonia Uncommon in Children With Wheezing

2009-07-12T18:34:00.000+07:00

Because radiographic pneumonia in children with wheezing but without fever is uncommon, the routine use of chest radiography in these children should be discouraged, according to the results of a prospective cohort study reported in the July issue of Pediatrics.

"The diagnosis of pneumonia in children with wheezing can be difficult, because the clinical history and auscultatory findings may be difficult to distinguish from those for children without pneumonia," write Bonnie Mathews, MD, from Children's Hospital Boston and Harvard Medical School in Boston, Massachusetts, and colleagues. "Limited data exist regarding predictors of pneumonia among children with wheezing. The goal was to identify factors associated with radiographically confirmed pneumonia among children with wheezing in the emergency department (ED) setting."

The study sample consisted of 526 individuals not older than 21 years who were seen in the ED, who had wheezing on clinical examination, and who underwent chest radiography because of possible pneumonia. Before learning the chest radiograph results, treating physicians obtained a medical history and performed and recorded a physical examination. Two blinded radiologists independently read the chest radiographs.

Among the included patients, median age was 1.9 years (interquartile range, 0.7 - 4.5 years), 47% had a history of wheezing, 36% were hospitalized, and 4.9% (95% confidence interval [CI], 3.3% - 7.3%) had radiographic pneumonia. Children with wheezing who were afebrile, defined as a temperature of less than 38°C, had a very low rate of pneumonia (2.2%; 95% CI, 1.0% - 4.7%).

Factors linked to an increased risk for radiographic pneumonia were a history of fever at home (positive likelihood ratio [LR], 1.39; 95% CI, 1.13 - 1.70), a history of abdominal pain (positive LR, 2.85; 95% CI, 1.08 - 7.54), triage temperature of 38°C or higher (positive LR, 2.03; 95% CI, 1.34 - 3.07), maximal temperature in the ED of 38°C or higher (positive LR, 1.92; 95% CI, 1.48 - 2.49), and triage oxygen saturation of less than 92% (positive LR, 3.06; 95% CI, 1.15 - 8.16).

Limitations of this study include time constraints, preventing enrollment of all eligible children; reliance on blinded radiologist review; and chest radiographs ordered at the discretion of the physicians caring for the patients, which may have introduced selection bias. The findings are not generalizable to all children with wheezing, and the rate of pneumonia may have been overestimated.

"Radiographic pneumonia among children with wheezing is uncommon," the study authors write. "Historical and clinical factors may be used to determine the need for chest radiography for wheezing children. The routine use of chest radiography for children with wheezing but without fever should be discouraged."

Source : http://www.medscape.com/viewarticle/705639?sssdmh=dm1.497700&src=nldne

Nasal Cannula Treatment May Be More Useful Than CPAP for Kids With OSA

2009-07-11T14:26:00.000+07:00

For treatment of obstructive sleep apnea in children, a high-flow open nasal cannula may be as effective as a continuous positive airway pressure (CPAP) mask but less intrusive and easier to tolerate.

At Johns Hopkins Hospital in Baltimore, Maryland, Dr. Brian McGinley and colleagues assessed the effect of warm, humidified air delivered at a rate of 20 L/min via open nasal cannula in 12 obese children (mean age, 10 years) with mild to severe obstructive apnea-hypopnea syndrome.

In the July issue of Pediatrics, the researchers note that while the home treatment with CPAP had been prescribed for these children, adherence was low and most were not being effectively treated.

According to the article, treatment with nasal insufflation reduced patients' inspiratory flow limitation, respiratory rate, and inspiratory duty cycle. Furthermore, oxygen stores improved and the children experienced fewer arousals, which reduced the occurrence of obstructive apnea from a mean of 11 events to 5 events per hour.

Ten of the children had previously undergone CPAP titration, and in eight of these patients "the reduction in the apnea-hypopnea index on treatment with nasal insufflation was comparable to that on CPAP," the authors report

When subanalyses were performed for sleep stages, the mean apnea-hypopnea index fell from 8 to 4 events per hour during non-REM sleep (p<0.01) p="0.01).

This "marked reduction in apneic events during REM sleep" was greater than the researchers had expected on the basis of their earlier studies of this approach in adults. It's possible, they speculate, that nasal insufflation might be increasing pharyngeal pressure to a greater extent in children because the cannula is relatively large compared with the nares.

It's also possible that higher chest wall and lung compliance during REM sleep in the children might have allowed a slight increase in pharyngeal pressure to produce a relatively larger increase in lung volume, leading to improvements in oxygen stores and upper airway patency, or that the treatment stimulated upper airway neuromuscular responses.

Noting that studies in larger and more varied pediatric populations are still necessary, the researchers conclude that "the minimally intrusive nasal interface (of the cannula) may improve adherence to treatment in children and may ultimately prove more effective in managing the long-term morbidity and mortality of sleep apnea."

Pediatrics 2009;124:179-188.

Source : http://www.medscape.com/viewarticle/705388?src=mpnews&spon=34&uac=133298AG

First Maintenance Therapy for Advanced Lung Cancer Approved by the FDA

2009-07-08T23:39:00.000+07:00

The US Food and Drug Administration (FDA) has approved pemetrexed (Alimta, Eli Lily) for the maintenance therapy of advanced or metastatic nonsquamous non–small-cell lung cancer (NSCLC). Pemetrexed is the first drug indicated as a maintenance therapy in this setting.

"This drug represents a new approach in the treatment of advanced non–small-cell lung cancer," said Richard Pazdur, MD, director of the Office of Oncology Drug Products in the FDA's Center for Drug Evaluation and Research, in a press statement. "Typically, patients whose tumors respond to chemotherapy do not receive further treatment after four to six chemotherapy cycles. This study demonstrates an advantage in overall survival in certain patients who received Alimta for maintenance therapy."

In a phase 3 trial recently presented at the American Society of Clinical Oncology (ASCO) meeting, patients received either pemetrexed (n = 441) or placebo (n = 222), along with the best supportive care. Patients had advanced or metastatic (stage 3B or 4) NSCLC (both squamous and nonsquamous subtypes) that had not progressed after 4 cycles of initial platinum-based chemotherapy.

For all patients in the study, the pemetrexed treatment group had an overall survival of 13.4 months, compared with 10.6 months for the placebo group. However, for the nonsquamous subgroup, overall survival was 15.5 months for patients taking pemetrexed and 10.3 months for patients taking placebo. The difference was statistically significant (P = .002).

However, as reported by Medscape Oncology from ASCO, 2 lung-cancer experts attending the meeting questioned the appropriateness of using pemetrexed as a maintenance therapy. Neither was involved with this phase 3 trial.

"I don't think we have the answer as to when it is best to start pemetrexed. Should we start immediately after standard chemotherapy or later on? All you can say is that it improves survival in nonsquamous-cell patients. In my clinic, I will present maintenance therapy as an option," said Julie Brahmer, MD, from the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, in Baltimore, Maryland.

"I endorse the use of pemetrexed as a second-line therapy for advanced non–small-cell lung cancer, but I don't think that all patients need immediate maintenance therapy following first-line treatment," said Nasser H. Hanna, MD, from the department of medicine at Indiana University, in Indianapolis, adding that the trial design did not allow it to definitively establish pemetrexed as a maintenance therapy.

Dr. Hanna explained the phase 3 trial was not designed to indicate whether maintenance therapy was superior to using pemetrexed at time of disease progression.

"Only 19 patients who were on placebo received pemetrexed at time of disease progression because, in part, the drug was not available at all of the centers involved in the study. In short, we know the drug improves survival but not that maintenance therapy is the best way to use it," he said.

A form of chemotherapy, pemetrexed is a folate analog metabolic inhibitor, which means that it disrupts metabolic processes that depend on the B-vitamin folate, a necessary ingredient for cell replication.

In the phase 3 study presented at ASCO, severe adverse effects (grade 3 or 4) were more common in the pemetrexed than in the placebo group, including fatigue (5% vs 0.5%) and low white-blood-cell counts (2.9% vs 0%).

Other reported adverse events included nausea, loss of appetite, tingling or numbness in the hands and feet, and skin rash, according to the FDA statement.

Source : http://www.medscape.com/viewarticle/705354?sssdmh=dm1.496281&src=nldne

Depression Symptoms Linked to Cardiovascular Mortality in Patients With Atrial Fibrillation, Heart Failure

2009-07-07T03:10:00.000+07:00

Elevated depression symptoms are linked to cardiovascular mortality in patients with comorbid atrial fibrillation (AF) and congestive heart failure (CHF) who receive optimal treatment, according to the results of a study reported online in the June 29 issue of Circulation.

"Depression predicts prognosis in many cardiac conditions, including...CHF," write Nancy Frasure-Smith, PhD, from the Montreal Heart Institute and Université de Montréal in Canada, and colleagues from the Atrial Fibrillation and Congestive Heart Failure Investigators (AF-CHF).

"Despite heightened cardiac risk in patients with comorbid...AF and CHF, depression has not been studied in this group. This substudy, from the AF-CHF Trial of rate- versus rhythm-control strategies, investigated whether depression predicts long-term cardiovascular mortality in patients with left ventricular ejection fraction ≤35%, CHF symptoms, and AF history who receive optimal medical care."

Of 974 participants (833 men) who completed a Beck Depression Inventory-II (BDI-II) measuring symptoms of depression, 32.0% had elevated scores (BDI-II ≥ 14). During a mean follow-up of 39 months, the primary outcome of cardiovascular death occurred in 246 patients. Secondary outcomes were presumed arrhythmic deaths (n = 111) and all-cause deaths (n = 302). Cox proportional hazards models were used to adjust for prognostic factors including age, marital status, cause of CHF, creatinine level, left ventricular ejection fraction, paroxysmal AF, previous hospitalization for AF, previous electrical conversion, and baseline medications.

After adjustment, elevated depression score was a significant predictor of cardiovascular mortality (adjusted hazard ratio [HR], 1.57; 95% confidence interval [CI], 1.20 - 2.07; P < .001), arrhythmic death (HR, 1.69; 95% CI, 1.13 - 2.53; P = .01), and all-cause mortality (HR, 1.38; 95% CI, 1.07 - 1.77; P = .01). Mortality risks associated with depression and marital status were additive, with the highest risk in unmarried depressed patients.

"Elevated depression symptoms are related to cardiovascular mortality even after adjustment for other prognostic indicators in patients with comorbid AF and CHF who receive optimized treatment," the study authors write. "Unmarried patients are also at increased risk. Mechanisms and treatment options deserve additional study."

Limitations of this study include lack of generalizability to all patients with CHF and AF, lack of clinician ratings and reliance on self-report of depression symptoms, and only 1 measurement of depressive symptoms. In addition, data were not available on the use of antidepressant medications, and the sample size in most of the participating countries was too small to allow evaluation of country-specific factors.

"The American Heart Association recently recommended depression screening in CAD [coronary artery disease] patients to identify those who might benefit from additional evaluation or treatment, and there is evidence that selective serotonin reuptake inhibitor antidepressant medications are as safe and efficacious in CAD patients as in the nonmedically ill," the study authors conclude. "In the absence of clinical trials specifically addressing these psychosocial risks among CHF patients with AF, we believe that depression and lack of a marital partner should be considered as risk markers identifying patients who may require additional treatment efforts to manage their cardiac conditions and modify other known risks."

Source : http://www.medscape.com/viewarticle/705261?sssdmh=dm1.495575&src=nldne

The Art of Patient Care in Clinical Medicine

2009-07-04T12:00:00.000+07:00

"... the secret of the care of the patient is in caring for the patient."
-Frances Peabody, 1925

There was a time not long ago, when physicians and nurses didn’t have much else to offer patients other than personal attention, comfort, compassion and concern for their ailments. Medical professionals were revered and respected for that and for what little they could do in regard to symptomatic treatment for incurable conditions.

The Twenty-First Century has thrust health care into an era of modernization, precipitated by advances in medical technology and computerization of everything in sight. We have made fantastic strides in the diagnosis and treatment of many serious illnesses. Patients are living longer and more productive lives as a result of these wonderful advances.

However, concomitant with these changes, we have experienced the indisputable depersonalization of patient care. Patients are often treated as diseases or numbers. We often hear medical personnel referring to a patient as “the gallbladder in room 232” or “the COPDer in 476”. We order test after test instead of taking a history because if we don’t “prove” our diagnosis with a test, we may be subjected to a lawsuit later if something goes wrong.

Health care costs have spun out of control. Forty-three million people in the US can no longer afford health insurance. Access to care has deteriorated. Prenatal care and birth rates are suffering. Doctors’ salaries are restricted by insurance companies. Busy primary care physicians have to see 30-40 patients a day to make enough income to pay off their own expenses beginning with a $250,000 debt for medical training.

There is no time to spend 20 minutes with an 80 year-old patient with diabetes, arthritis, heart failure, and hypertension out of control who has just developed shortness of breath recently, and who needs 6 prescriptions rewritten. Other patients in the waiting room are feeling ignored.

These are very difficult challenges. Unfortunately, in the middle of it all, we often lose site of the fact that our patients are people – in many cases, very ill people - who are looking to us for support and guidance as well as medical care. There is an art to providing this support and to personalizing care for each and every patient in the midst of an imperfect environment.

Anyone who works in the health care profession knows there is a right way and a wrong way to approach patient care. They also know this is somewhat different for every patient they encounter due to multiple variables – type of illness, gender, age, background, etc. This is an art that we learn mostly by experience – both by our own personal experience and by observing the experiences of others. How well we assimilate the information from these experiences and how well we use that knowledge determines a very large part of how we interact with patients and how we are perceived as medical professionals.

The key word here is the art of patient care. For the purposes of this site, the reference is not so much on the science of medicine per se, but rather on how medical personnel can interact with patients to improve the healing process, rather than dismantle it.

This is not to say that science is unimportant; but rather that concern for the humanity of the patient should not be so overwhelmed by science as to be nonexistent at the bedside. Indeed, true clinical competence is a blend of knowledgeable application of medical science along with the recognition and understanding of the human condition. The art of this blend, the integration of these two disciplines, and how well it is done, is what determines the quality of patient care that we provide. One without the other is not sufficient.

This can be a science unto itself. One of the influences that this site will hopefully promote is more discussion and ultimately more research on how to practice this art in a more meaningful and fulfilling way for both ourselves and our patients alike. In addition, the more formal exploration and inclusion of these concepts into medical training programs would have a huge effect on the future of medicine in this country.

Some people say you have to be born with this talent. I don’t think so. I do think it comes easier to some than others; but, whatever the genetics and background of the individual, patient care is an art that can be learned and practiced and improved upon, just as drawing or painting a thoughtful picture can be learned and practiced to the point where it can be greatly appreciated by others.

So what kind of doctor or nurse or care partner do you want to be?

What is your approach to patient care?

How do patients perceive your approach to them and your overall competence?

If you long to be one of those caring, well-respected and revered medical professionals that patients (and even other professionals) admire and tell their friends and neighbors about, you’ve found the right place.

Read and study the pages on this site. You will become a much more people-oriented professional, knowledgeable about how to approach all kinds of patients and challenging situations, and who will at the very least be perceived as someone who cares and is concerned about his or her patients.

If you practice what you learn here, you may find yourself actually rediscovering virtues you didn’t know you had. If you already have the nurturing gene, these pages will help you hone that talent into something very special; and your patients will benefit from it in ways you never thought possible.

Source : http://www.art-of-patient-care.com/

AHA Publishes Statement on Integrating Prehospital ECGs Into Care for ACS Patients

2009-07-03T22:51:00.000+07:00

The American Heart Association (AHA) has issued a scientific statement on the use of prehospital electrocardiograms (ECGs) to improve the quality of care delivered to patients with ST-segment-elevation MI (STEMI), published online August 13, 2008 in Circulation [1]. The central challenge, say the authors, will not be in acquiring the ECG, but rather in using and integrating the diagnostic information obtained by emergency medical service (EMS) personnel into existing systems of care.

"First medical contact with a patient is usually with the EMS, and this is the next phase of coordination that we need to reach out to," said lead author Dr Henry Ting (Mayo Clinic, Rochester, MN). "We've coordinated the emergency department, the cath lab, and the cardiology group and have done well with reducing door-to-balloon times, but we've not truly engaged the prehospital phase of care. This is critically important."

The AHA national guidelines, as well as other consensus and scientific statements, recommend the acquisition and use of prehospital ECGs by EMS for the evaluation of patients with suspected acute coronary syndrome. The current recommendation is class 2a with a B level of evidence. Speaking with heartwire , Ting said that the technology is currently available, but that hospitals do not have protocols in place that allow prehospital ECGs to serve any useful purpose.

"For the past 10 years, this equipment has been available to many paramedics, but what is happening is that when they acquire the ECG it's not really utilized," said Ting. "It's acquired, then the patient is brought to the emergency department, and in hospitals without these systems of care, they're told this is a patient with chest pain, and we have an ECG, but then the patient is placed in a critical-care room and receives another ECG. Where's the value in that?"

Not a One-Size-Fits-All Solution

In the scientific statement, the authors review the benefits of using prehospital ECGs and the barriers and challenges to routine use and recommend approaches for using the diagnostic information for improving quality of care. In terms of benefits, Ting said the Mayo Clinic has been incorporating the use of prehospital ECGs for one year, and in doing so, has reduced door-to-balloon times to consistently less than 30 minutes, with 25 minutes being the average.

Ting said there are many ways of interpreting the ECG once it has been obtained. Computer algorithms, paramedic interpretation, and wirelessly transmitting the data to a physician for interpretation are three ways to interpret the data. The diversity of the EMS providers and the differing sizes of cities they cover, as well as wireless coverage available to transmit data, are not likely to lead to a one-size-fits-all solution, he said.

A recent survey found that 90% of EMS systems serving the largest US cities have 12-lead ECG equipment, and there are prehospital ECG programs in Boston, Los Angeles County, and North Carolina, as well as in Ottawa, ON. Paramedics in Boston, for example, are allowed to bypass non–percutaneous coronary intervention (PCI) hospitals and have an emergency-department physician activate the cardiac cath lab. North Carolina, on the other hand, allows paramedics to occasionally divert some STEMI patients to PCI hospitals and activate the cath lab directly (or have it activated by an emergency-department physician). Paramedics in Ottawa can also activate the cath lab directly through a central operator. Los Angeles County paramedics use a computer algorithm to interpret the ECG, and the cath lab is activated by the emergency department based on this diagnosis.

Allowing paramedics to "do something downstream" with the information is critical, said Ting, as is changing when the paramedics perform the ECG. "If you truly want to coordinate things,you want to start the prehospital ECG as early as possible in the examination," he said. "Once you establish that the patient has stable vital signs and doesn't have a cardiac arrhythmia, you probably want to do a prehospital ECG at the scene, as early as possible. If you detect ST elevation, the next steps are very different from treating a patient who has chest pain but no ST elevation."

Implementing prehospital ECGs into existing systems of care has the potential to "change the ball game," said Ting. He noted that the focus should begin to move away from door-to-balloon times toward a measure that provides a gauge of quality and performance that is more patient centered. The national "Door to Balloon: An Alliance for Quality" campaign launched in 2006 has helped improve the timeliness of lifesaving therapy for myocardial infarction (MI) patients at all US hospitals that perform emergency angioplasty, but from a patient perspective, first medical contact to balloon is a more relevant measure of quality of care.

Ting added that too many patients still take themselves to the emergency department or are driven there by friends or family, a decision that affects the course of care because it's impossible to obtain a prehospital ECG and then activate all the necessary hospital teams.

"The public doesn't perceive EMS as transforming care," said Ting. "They view it as transportation with sirens. They think, 'If Uncle Joe can drive me there just as fast, then why do I need to call 911 and create all the hassle in the neighborhood?' But the prehospital ECG can really change the course of treatment, something that can't happen when you drive yourself or have a friend take you."

Dr. Ting has received research grants from the American College of Cardiology and the Mayo Foundation for Medical Education and Research. A complete list of disclosures is available in the original article.

Ting HH, Krumholz HM, Bradley EH et al. Implementation and integration of prehospital ECGs into systems of care for acute coronary syndrome. Circulation. 2008;118:published online before print. DOI:10.1161/circulationaha.108.190402.

Source : http://www.medscape.com/viewarticle/586405

Decreased Alertness in a 10-Month-Old Girl

2009-07-02T13:24:00.004+07:00

A 10-month-old girl is transferred from an outside urgent care center to the emergency department (ED) for dehydration and a change in her level of alertness. According to her mother's boyfriend, she had been crying in her crib before she was noted to throw her arms in the air for approximately 5 minutes and then breathe irregularly. She vomited once and continued to cry inconsolably before she arrived at the urgent care center. An abdominal radiograph was performed at the urgent care center and interpreted as consistent with possible constipation, but it was otherwise unremarkable. She has had multiple episodes of nonbloody, nonbilious emesis on the way to the ED. There is no recent history of diarrhea or change in bowel habits.

The patient was recently diagnosed with an upper respiratory infection and has received several doses of acetaminophen over the last few days. Her symptoms have included tactile fevers, runny nose, and raspy cough. Before this occurrence, her breathing had been normal and without increased effort. She had been feeding well earlier today. She is currently taking no prescription medications and has no reported allergies. Her immunizations are not up-to-date; she only received immunizations at 2 months of age. She lives at home with her mother, her mother's boyfriend, and her 2-year-old brother.

The physical examination is most notable for her general appearance; she appears somnolent, is lying motionless, is not making eye contact or engaging in other social interactions, and is not crying. She vomits several times during the evaluation. Her vital signs include an axillary temperature of 99.1°F (37.3°C), a heart rate of 90 bpm, a blood pressure of 101/56 mm Hg, a respiratory rate of 12 breaths/min, and an oxygen saturation of 100% while breathing room air. Her pupils are equal and 5 mm in diameter; they are measured at 3 mm in response to light. The anterior fontanel is flat. A small, 5-mm, purple ecchymosis overlying the left maxilla is noted. Two lacerations on the inferior mucosal surface of the upper lip are identified that line up with the upper incisors. The lungs are clear to auscultation and the heart sounds are normal. The abdomen feels soft and appears nondistended and nontender. Bowel sounds are present. The stool is guaiac-negative. Capillary refill of the fingernails is less than 2 seconds. The neurologic examination is notable for diffuse hypotonia.

In the ED, she is given a bolus of 200 mL of normal saline with 5% dextrose and continued on maintenance fluid. The initial laboratory results are significant for leukocytosis and anemia, with a white blood cell (WBC) count of 18.4 × 10³/µL (18.4 × 10⁹/L), with 72% neutrophils (0.72), a hemoglobin of 9.7 g/dL (97 g/L), and a hematocrit of 27.1% (0.271). Her serum glucose is normal at 108 mg/dL (5.99 mmol/L), and the electrolytes are likewise within normal limits. An ophthalmologic examination (see Figure 1) and computed tomography (CT) scanning of the head (see Figure 2) are performed. A skeletal survey is ordered as well.

Questions answered correctly will be highlighted.

What is the diagnosis?

Hint: The findings of the retinal examination are very characteristic of this diagnosis.

Meningitis

Abusive head trauma

Cysticercosis

Discussion

The initial CT scan of the head obtained in the ED (see Figure 2) shows bilateral subdural hematomas outlining bilateral cerebral convexities, with hyperdense blood noted in the left frontal lobe. The patient was started on fosphenytoin for seizure prophylaxis. The ophthalmologic examination revealed bilateral retinal hemorrhages extending into the periphery (see Figure 1). Intraretinal hemorrhages of the macula were noted in the left eye, with possible choroidal rupture. On careful questioning, the caretaker repeatedly denied any history of trauma. A skeletal survey was performed that revealed a healing right radial neck fracture. The medical record from the urgent care center was obtained; this included a clinical note dated 4 months prior to patient's presentation to the ED, which described a visit for repeated emesis and irritability. A bruise on the chin was noted on that visit, and the explanation given was a fall inside the patient's crib that occurred 4 days prior to that visit. A report to the Department of Children and Families was found to have been made for missed well-child visits. The level of suspicion for suspected abusive head trauma (AHT) and child abuse was extremely high. It is important for emergency clinicians to be mindful of the diagnosis of AHT, but there are other rare causes that can mimic abuse.

Abusive head injury, sometimes referred to as "shaken baby syndrome,"^[1] is the most common cause of death resulting from child abuse.^[2] The majority of cases occur in infants less than 1 year old.^[3] Head injury among infants in this age group is often the result of abuse and the mechanism of injury, although much debated, is usually thought to be significant forces generated from angular deceleration with or without impact. AHT in this population represents a significant fraction of young children admitted for head injury.^[4] Approximately 30% of children aged 0-3 years admitted to pediatric hospitals for intracranial injury have been found to meet the criteria for abuse.^[5] Many children with AHT also have a clinical history or findings consistent with prior maltreatment. Crying is thought to be a trigger for many cases of AHT and prevention efforts are directed toward caregiver response to colicky babies and crying infants.

The diagnosis of AHT can be difficult to establish; the clinical presentations may be nonspecific, children are often too young to give history, and witnesses and confessions are rare. The reasons for seeking care in children include seizure, breathing difficulty, apnea, and apparent lifelessness. A history of trauma is often lacking. Approximately 30% of children with AHT may be missed on the initial presentation.^[6] Common misdiagnoses include viral gastroenteritis, sepsis, and accidental head injury. A history of injury mechanism incompatible with an infant's developmental stage or degree of force required to inflict severe injury may raise the suspicion for AHT. Common symptoms at presentation are often the result of acute brain injury (ie, lethargy, decreased level of consciousness, vomiting, apnea, hypotonia, and seizures).

The physical examination findings may include evidence of soft tissue injury, particularly swelling or bruising; however, the absence of bruising or other evidence of trauma neither excludes injury nor abuse.^[7] Funduscopic examination should be performed in any child suspected to have abusive head injury, preferably by an ophthalmologist with sufficient pediatric experience to determine the significance of any identified injury.^[8] Retinal hemorrhages are a hallmark finding in abusive head injury, and they are present in a majority of children who carry the diagnosis.^[9] They may be unilateral or bilateral and involve 1 or more layers. Not all retinal hemorrhages are the same with respect to their significance in predicting an abusive mechanism. The most specific pattern of retinal hemorrhages is numerous hemorrhages involving several layers of the retina and extending to the periphery.^[10] No pattern of hemorrhages, however, is pathognomonic for abuse. The mechanism of retinal hemorrhages is unclear, but the leading theory is that they are caused by vitreous traction on the retina during acceleration/deceleration. Lasting visual impairment in those children who survive AHT is common.^[11]

CT scanning is an essential part of the initial workup of suspected head trauma. CT scanning can also be helpful as a screening neuroimaging study in children with suspected abuse. Even without clinical examination findings of brain injury, a significant number of abused infants will have important findings on neuroimaging.^[12,13] Unilateral, bilateral, or parafalcine subdural hemorrhages are the most common radiologic finding in infants with AHT. Subdural hemorrhages of mixed attenuation have previously been considered as evidence for repeated head injury, with hyperdense components of the hemorrhage associated with injury occurring in the past 48-72 hours and hypodense components representing older injury occurring more than 3 weeks prior to the scan. Hyperacute bleeding or the mixing of blood and cerebrospinal fluid (CSF), however, can produce mixed-density lesions from a single injury.^[14] While the presence of subdural hemorrhage lends supporting evidence to the diagnosis of head trauma, inferences about the timing and mechanism of injury cannot be drawn with certainty from a single noncontrast CT scan.^[15] Magnetic resonance imaging (MRI) can be a useful study for demonstrating parenchymal contusion, axonal shearing, extra-axial hemorrhages, and posterior fossa injuries. Diffusion-weighted imaging and apparent diffusion coefficient mapping are particularly useful in identifying acute hypoxic-ischemic injury.

Additional supportive evidence for child abuse is obtained through a skeletal survey. The presence of previously healed fractures in infants is strongly suggestive of chronic abuse.

While the cause of subdural hematoma in association with retinal hemorrhage will most commonly be abusive head injury, a differential diagnosis for these findings must be considered. Coagulopathies have been associated with retinal and intracranial hemorrhage in infants, including hemophilia, vitamin-K deficiency, and disseminated intravascular coagulopathy. Retinal hemorrhages in these disorders are typically confined to the posterior pole, and the nature of the bleeding problem can be detected by laboratory tests. It is recommended to perform a prothrombin time, activated partial-thromboplastin time, and a platelet count as minimum screening tests.

Glutaric aciduria type I, a rare metabolic disease, is associated with developmental delay and subdural hemorrhages. Performing an assay for organic acids in the urine can test for this disease. Other causes of intracerebral hemorrhage include cerebral malaria, intracranial aneurysms, galactosemia, and meningitis. Osteogenesis imperfecta is an uncommon connective tissue disorder that frequently results in fractures. Subdural hemorrhage has rarely been described as a complication of this disease.^[22] Because these disorders can closely mimic abusive head trauma, it is important to maintain a nonaccusatory and open-minded posture during the initial evaluation, as parents are understandably sensitive to the possibility that they are being accused of harming their children. Some helpful statements include "I'm concerned that someone may have harmed your child" and "several diseases can explain this pattern of injury, including trauma. We need to check for other signs of these illnesses to make sure your child is safe."

AHT is likely underdiagnosed and underreported, which contributes to the dismal outcomes for children eventually diagnosed with abuse.^[24] In multiple series, the mortality is approximately 20%.^[11,25] The neurologic outcome is also poor, with many survivors having persistent neurologic and behavioral deficits.^[11,26] Having a high suspicion for abusive head injury is critical in the appropriate setting. Clinicians should have a low threshold for performing CT scans of the head on infants coming in with nonspecific findings that could be explained by head injury, when appropriate. While reporting a reasonable suspicion for abuse is mandatory, it is not the job of the healthcare provider to determine the social or legal management of any case. A child protection team, if available, should be consulted with any concerns of abusive injury.

The patient in this case was admitted to the pediatric intensive care unit (ICU). A repeat CT scan of the head was performed 10 hours after presentation because her somnolence failed to improve. It showed an interval increase in subdural blood located above the tentorium. She was then taken emergently to the operating room (OR) for evacuation of the subdural hematomas and placement of bilateral subdural external drains. The subdural pressure was noted to be markedly elevated. Subdural membranes were noted to separate layers of blood in the left frontal lobe. She was again taken to the OR several days later for removal of the subdural drains. She gradually became more alert and playful. The child protection team was contacted in the ED and suspicion for abuse was reported. Further conversations with the mother revealed a history of physical abuse at the hands of her current boyfriend. The Department of Children and Families (the regional department responsible for addressing issues of child safety and potential abuse) assumed immediate temporary custody of the patient and of her older brother. Testing for conditions that mimic the signs of abuse was completed, and no sign of other medical illnesses was found. The patient was discharged 12 days after admission and has had follow-up visits with neurosurgery and ophthalmology. She is currently living with her second foster family and is noted to have persistent developmental delay. Her retinal findings have improved and her foster parents have not noticed any evidence of visual impairment.

Questions answered correctly will be highlighted.

You suspect that a patient you are examining is being abused. Which of the following injuries, if they were present in the patient you are examining, would be pathognomonic for abusive injury?

Bilateral subdural hemorrhages

Rib fractures

Retinal hemorrhages

Bruising in infants

None of the above

During the course of several days, you evaluate a number of children with injuries as reported by their parents. You obtain a history and perform a physical examination on each child, and radiographs are subsequently performed. Which of the following situations should alert you to a strong possibility of abuse/nonaccidental injury?

A spiral tibia fracture in a 3-year-old boy who fell and twisted his leg while jumping on a couch.

A supracondylar fracture in a 6-year-old who fell from the monkey bars onto an outstretched arm.

A posterior rib fracture in a 13-month-old who fell backwards off a single step.

The mechanism of injury must always be considered when evaluating for whether or not there is any suspicion that any given fracture may have occurred by nonaccidental means. Infants and young toddlers typically cannot generate enough force to result in a fracture unless falling from a height. In this case, a fall from 1 step is not sufficient to result in a rib fracture. Certain types of fractures also should raise concern, such as spiral fractures of long bones. The exception to this is a spiral fracture of the tibia, often referred to as a "toddler fracture" since it is particularly seen amongst toddlers. These children are often rambunctious and, although lacking in coordination, they have the physical capacity to climb, jump, and fall while running, all of which may result in an accident that will generate enough energy to cause this type of fracture.

References

Christian CW, Block R Committee on Child Abuse and Neglect; American Academy of Pediatrics. Abusive head trauma in infants and children. Pediatrics. 2009;123:1409-11.
Schnitzer PG, Ewigman BG. Child deaths resulting from inflicted injuries: household risk factors and perpetrator characteristics. Pediatrics. 2005;116:e687-93.
Duhaime AC, Christian CW, Rorke LB, Zimmerman RA. Nonaccidental head injury in infants--the "shaken-baby syndrome". N Engl J Med. 1998;338:1822-9.
Billmire M, Myers P. Serious head injury in infants: accident or abuse? Pediatrics. 1985;75:340-2.
Hettler J, Greenes DS. Can the initial history predict whether a child with a head injury has been abused? Pediatrics. 2003;111:602-7.
Jenny C, Hymel KP, Ritzen A, Reinert SE, Hay TC. Analysis of missed cases of abusive head trauma. JAMA. 1999;281:621-6.
Peters ML, Starling SP, Barnes-Eley ML, Heisler KW. The presence of bruising associated with fractures. Arch Pediatr Adolesc Med. 2008;162:877-81.
Morad Y, Kim YM, Mian M, Huyer D, Capra L, Levin AV. Nonophthalmologist accuracy in diagnosing retinal hemorrhages in the shaken baby syndrome. J Pediatr. 2003;142:431-4.
Levin AV, Morad Y. Ocular Manifestations of Child Abuse. In: Reece RM, Christian CW, editors. Child Abuse Medical Diagnosis & Management. 3rd ed. American Academy of Pediatrics;2009:211-26.
Adams G, Ainsworth J, Butler L, Bonshek R, Clarke M, Doran R, et al. Update from the ophthalmology child abuse working party: Royal College ophthalmologists. Eye. 2004;18:795-8.
Barlow KM, Thomson E, Johnson D, Minns RA. Late neurologic and cognitive sequelae of inflicted traumatic brain injury in infancy. Pediatrics. 2005;116:e174-85.
Rubin DM, Christian CW, Bilaniuk LT, Zazyczny KA, Durbin DR. Occult head injury in high-risk abused children. Pediatrics. 2003;111:1382-6.
Laskey AL, Holsti M, Runyan DK, Socolar RR. Occult head trauma in young suspected victims of physical abuse. J Pediatr. 2004;144:719-22.
Vinchon M, Noule N, Tchofo PJ, Soto-Ares G, Fourier C, Dhellemmes P. Imaging of head injuries in infants: temporal correlates and forensic implications for the diagnosis of child abuse. J Neurosurg. 2004;101:44-52.
Tung GA, Kumar M, Richardson RC, Jenny C, Brown WD. Comparison of accidental and nonaccidental traumatic head injury in children on noncontrast computed tomography. Pediatrics. 2006;118(2):626-33.
Merten DF, Radkowski MA, Leonidas JC. The abused child: a radiological reappraisal. Radiology. 1983;146:377-81.
Diagnostic imaging of child abuse. Pediatrics. 2009;123:1430-5.
Kleinman PK, Marks SC, Blackbourne B. The metaphyseal lesion in abused infants: a radiologic-histopathologic study. AJR Am J Roentgenol. 1986;146:895-905.
Scherl SA, Miller L, Lively N, Russinoff S, Sullivan CM, Tornetta P, 3rd. Accidental and nonaccidental femur fractures in children. Clin Orthop Relat Res. 2000:96-105.
Strait RT, Siegel RM, Shapiro RA. Humeral fractures without obvious etiologies in children less than 3 years of age: when is it abuse? Pediatrics. 1995;96:667-71.
Islam O, Soboleski D, Symons S, Davidson LK, Ashworth MA, Babyn P. Development and duration of radiographic signs of bone healing in children. AJR Am J Roentgenol. 2000;175:75-8.
Tokoro K, Nakajima F, Yamataki A. Infantile chronic subdural hematoma with local protrusion of the skull in a case of osteogenesis imperfecta. Neurosurgery. 1988;22:595-8.
US Department of Health and Human Services Administration on Children Youth and Families. Child Maltreatment 2006. Washington, DC: US Government Printing Office; 2008.
Theodore AD, Chang JJ, Runyan DK, Hunter WM, Bangdiwala SI, Agans R. Epidemiologic features of the physical and sexual maltreatment of children in the Carolinas. Pediatrics. 2005;115:e331-7.
Makoroff KL, Putnam FW. Outcomes of infants and children with inflicted traumatic brain injury. Dev Med Child Neurol. 2003;45:497-502.
King WJ, MacKay M, Sirnick A. Shaken baby syndrome in Canada: clinical characteristics and outcomes of hospital cases. CMAJ. 2003;168:155-9.

http ://cme.medscape.com/viewarticle/705052

Experts Debate Benefits and Risks of Stimulants for Healthy People

2009-07-02T01:19:00.000+07:00

Two new editorials debate the question of whether healthy people should take stimulants, especially methylphenidate, to enhance cognitive performance.

John Harris, DPhil, from the school of law at the University of Manchester, in the United Kingdom, argues that it is unethical to stop healthy adults from taking methylphenidate to enhance cognitive performance and asserts that chemical cognitive enhancers should be freely available to those who choose to use them.

Anjan Chatterjee, MD, from the Center for Cognitive Neuroscience at the University of Pennsylvania, in Philadelphia, disagrees, maintaining that making methylphenidate freely available to those who want to enhance performance would cause undue medical risk and that these drugs should be reserved for those who suffer from attention-deficit/hyperactivity disorder (ADHD). The risks of methylphenidate include potential for abuse and dependence and risk for sudden death and serious cardiovascular events, he points out.

Their discussion is published online June 18 in BMJ.

Risk for Sudden Death

Methylphenidate was also the subject of a recent case-control study published in the American Journal of Psychiatry that showed an increased risk for sudden death in healthy children and adolescents who take the medication (Gould MS et al. Am J Psychiatry. 2009;AIA:1-10). In response, however, the US Food and Drug Administration (FDA) issued an advisory noting that children with ADHD should not stop stimulants based on this study, because its conclusions were limited by several flaws.

Dr. Harris argues that methylphenidate is safe enough to be used widely in children and adults with ADHD, and its significant advantages for healthy adults include improved executive function, study skills, and the ability to focus. In an interview, he noted that access to methylphenidate could be improved by taking it off prescription or allowing it with a pharmacist consultation.

Methylphenidate's health risks should be dealt with in the same way as are those of cigarettes; while adults who use the drug should be warned of its potential for abuse and cardiac risks, sale should not be prohibited. "We should not police healthy adults," he said. "We can issue them a warning as we do on other dangerous products."

Social Coercion?

Dr. Chatterjee, however, warns of the public-health risks that could occur should methylphenidate be freely available. He notes that the risks for serious cardiovascular events with methylphenidate are likely to be higher in older people with undetected cardiac disease — 1 group that might be likely to use the drug if it were sold over the counter.

He also said that expanding access to methylphenidate would invite subtle societal coercion to use the drug to enhance performance in school or in the workplace. "We live in a very competitive society, where people think that every little bit that gets you ahead is advantageous," he said in an interview. Were methylphenidate freely available, there might be implicit pressures to use the drug to improve school grades or cognitive abilities during long working hours, he writes in his editorial.

Dr. Chatterjee also argues that the use of methylphenidate might pose another risk for society that is rarely considered in debates about the subject. He notes that enhancing focus with methylphenidate might mean sacrificing creativity. "Most models of creativity suggest that you have to have some down time in order to have the leaps of imagination that end up being creative insights; it requires not being focused," he said.

Dr. Harris, however, equated methylphenidate with electric light — a valuable technology that may also have the adverse effect of potential overuse. "With the advent of synthetic sunshine, work and social life could continue into and through the night, creating competitive pressures and incentives for those able or willing to use it to their advantage," he writes in his editorial.

"The solution, however, was not to outlaw synthetic sunshine but to regulate working hours and improve access," he adds. "The same is or will be true of chemical cognitive enhancers."

Source : http://www.medscape.com/viewarticle/705057?sssdmh=dm1.492967&src=nldne

CT-Angiography-Identified Vulnerable Plaque Associated With Higher Risk of ACS

2009-06-30T15:16:00.000+07:00

Vulnerable plaques identified visually by computed-tomography (CT) angiography are more likely to result in a subsequent acute coronary syndrome during follow-up, a new study has shown [1]. Identifying these unstable coronary plaques, which have areas of low attenuation and have undergone positive remodeling, could be used to aggressively treat patients who are at higher risk for future events, according to researchers.

"Our data suggest that once a patient is identified to be at risk of having an adverse event on the basis of traditional clinical, biochemical, and biomarker risk profiles, imaging may help identify those at greater risk of acute coronary events," write lead investigator Dr Sadako Motoyama (Fujita Health University School of Medicine, Toyoake, Japan) and colleagues in the June 30, 2009 issue of the Journal of the American College of Cardiology.

Speaking with heartwire , Dr Renu Virmani (Cardiovascular Pathology Institute, Gaithersburg, MD), one of the study investigators, said the results show for the first time that high-risk, vulnerable lesions, characterized previously in pathologic studies, are able to identify patients with future symptoms, and this moves the field forward by a "big step."

"This is just the beginning, but it is a good beginning," she said. "It is the first study we have showing us that we can actually identify these lesions and that these are the lesions that are going to produce symptoms in patients. Before that, it's all been a theory. We were able to say these are vulnerable plaques, and we should watch and worry about them, but we had no way of showing these were the ones that would go on to produce symptoms."

More Than 1000 Patients Assessed by CTA

To determine whether the characteristics of atherosclerotic lesions were associated with future acute coronary syndromes, the researchers analyzed the lesions based on the presence of positive vessel remodeling and low-attenuation plaques. Virmani explained that these two characteristics, along with a necrotic core, are thought to be associated with subsequent plaque rupture.

Among the 1059 patients who underwent CT angiography, 45 patients had coronary plaques that had undergone positive remodeling and were classified as low attenuation. After more than two years of follow-up, 10 patients, 22.2%, with both characteristics of vulnerable plaque developed an acute coronary syndrome. On the other hand, just one of the 27 patients with only one feature, either low attenuation or positive remodeling, developed symptoms, while only 0.5% of the 820 patients without any features of vulnerable plaque developed an acute coronary syndrome.

In a multivariable regression analysis, the presence of low-attenuation plaque or positive remodeling was associated with a 23-fold increase in the risk of an acute coronary syndrome (hazard ratio 22.8; 95% CI 6.9-75.2; p<0.001).

Virmani told heartwire that it is not always easy to identify low-attenuation plaque and that there are those who doubt whether visualizing these softer plaques can be done reliably, although the technology is improving. On the horizon are better imaging modalities, including 320-detector-row CT scanners that improve resolution, as well as machines that limit the amount of radiation exposure.

Systemic vs Focal Disease

Commenting on the results of the study for heartwire , Dr Steven Nissen (Cleveland Clinic, OH) said he was skeptical of the results and the vulnerable-plaque hypothesis, in general. In a recent editorial in the Journal of the American College of Cardiology: Cardiovascular Imaging, Nissen said that many diagnostic techniques designed to detect vulnerable plaques, including thermography, virtual histology, and optical coherence tomography, among others, have promised much but delivered little [2].

Last week, noted Nissen, a CT-angiography study, reported by heartwire , showed that the technology was unable to reliably identify the functional significance of coronary lesions in patients with stable angina and atypical chest pain. To now suggest that CT angiography can identify plaques at risk for rupture is "asking an awful lot from this technology." Also, he said the investigators did not show that the lesion of the coronary artery identified by CT angiography as vulnerable is responsible for the acute coronary syndrome.

"They don't close the loop," said Nissen. "We don't find out that the site that had positive remodeling and low attenuation is the site where the plaque ruptured. Without that, this becomes much more speculative."

In general, Nissen said that he believes the vulnerable-plaque approach is the wrong approach because atherosclerosis is a systemic disease, and if anything is likely to predict outcomes, it's a systemic, not focal, marker. Virmani, on the other hand, strenuously disagrees, telling heartwire that Nissen is "missing the boat" regarding these high-risk focal lesions because evidence shows that patients with coronary events have a focal thrombus formation.

"If you look at acute-myocardial-infarction patients, it occurs in one vessel, in the proximal areas," said Virmani. "Why? Those are the most prone areas. That's where we need to concentrate. His [Nissen's] idea of concentrating on systemic factors, such as LDL cholesterol, diabetes--yes, absolutely, but those are the patients that then have focal lesions. I don't deny that you need hypercholesterolemia for a patient to have focal lesions, but in the patients that are high risk, they do develop them at focal spots."

Did Anybody See My Stolen Horse?

In an editorial accompanying the published study, Dr Eugene Braunwald (Harvard Medical School, Boston, MA) adopts the middle road, hailing the study by Motoyama and colleagues as a landmark trial, while acknowledging the current limitations in the detection of vulnerable plaque [3].

Braunwald notes that widespread clinical application of CT angiography to characterize coronary lesions at risk for future rupture, which he aptly describes as "locking the barn before the horse is stolen," will require more potent measures for the prevention of plaque rupture than are currently available. Dual antiplatelet therapy, possible stenting, or more potent anti-inflammatory drugs are just some of the possibilities, writes Braunwald.

"Nobody is saying we need to start treating these patients," adds Virmani. "Start treating them systemically, just as Dr Braunwald points out in his editorial. Right now, we don't know how to treat these patients. We might need to think of different therapies. Some patients might need anti-inflammatory drugs, or some might need stents, but we won't know until we learn how these lesions behave prospectively."

Dr Mario Garcia (Mount Sinai School of Medicine, New York) told heartwire that low-attenuation plaques with positive remodeling are features identified as characteristics of thin-cap, lipid-rich plaques in intravascular ultrasound (IVUS) correlative studies. He added that while the present study identifies a novel imaging biomarker as a powerful predictor of future ACS, there remain unanswered questions, particularly whether the predictive accuracy of CT is superior to established serum biomarkers such as high-sensitivity C-reactive protein (CRP) and whether the same predictive utility could be extrapolated to asymptomatic subjects at risk.

In addition, like Braunwald and Nissen, Garcia says trials are needed to determine the optimal treatment strategy to follow--for example, intensive medical therapy vs prophylactic PCI--once these "high-risk features" are identified in a patient.

Source : http://www.medscape.com/viewarticle/705017?sssdmh=dm1.492501&src=nldne

Endobronchial Myofibroblastic Sarcoma Presenting With Hemoptysis

2009-06-25T11:31:00.003+07:00

Abstract

Hemoptysis is an important symptom in clinical practice. The diagnosis of the underlying cause is often difficult, particularly in patients presenting with a normal chest x-ray. We report a case of hemoptysis with a normal chest x-ray due to a rare endobronchial neoplasm: myofibroblastic sarcoma.

Introduction

Hemoptysis, a relatively common and important symptom, is usually initially evaluated by chest x-rays. We report a case of endobronchial myofibroblastic sarcoma as a rare cause of hemoptysis and detected by computed tomography (CT) with normal chest x-ray. To the best of our knowledge, this is the first reported case of this entity.

Case Report

A 26-year-old man presented with a one-month history of cough, hemoptysis, and dyspnea. He was initially treated with antibiotics but there was no improvement. There was a smoking history of 12 packs per year. Neither cardiac diseases, venous thromboembolism, nor occupational lung disorder were reported. Ear, nose, and throat examination showed mucosal hyperemia of the nose, pharynx, and the oropharynx. Plain chest x-ray was interpreted as normal. Computed tomography (CT) scans of the chest showed a well-defined soft tissue mass 15 by 10 mm in the right main bronchus, and localized precarinal small calcified lymph nodes (Fig. 1). Fiberoptic bronchoscopy demonstrated a bronchial tumor with subtotal occlusion of the right main bronchus. Biopsies were taken, and pathologic examination indicated a malign mesenchymal tumor. Sleeve resection of the right main bronchus was performed. Histopathology documented that the tumor was composed of a mixture of a cell-rich fascicular area and a hypocellular area with myxoid matrix. There were six mitotic figures per 10 high-power field. Hemorrhages and necrosis were also evident. Immunohistochemically, the tumor was positive for vimentin, O-13 (cytoplasmic and membranous), and negative for actin, desmin, keratin, S-100, and protein CD34. Given these cellular features, the tumor was interpreted as myofibroblastic sarcoma. The patient was well three months after the operation.

(Enlarge Image)

Figure 1.

Computed tomography scan shows soft tissue mass in the right main bronchus, and precarinal small calcified lymph nodes.

Discussion

Hemoptysis is a relatively common and serious symptom that can be caused by a number of pathologies, the most common causes being neoplasms, chronic bronchitis, and bronchiectasis.^[1] A chest x-ray is usually the first investigation performed. However, 20 to 30% of patients have a normal chest x-ray.^[2] Studies assessing the role of CT and bronchoscopy in the diagnosis of hemoptysis showed that CT should precede bronchoscopy in patients with hemoptysis and normal or nonlocalizing chest x-rays to optimize detection of abnormalities and direct cytologic and microbiologic sampling.^[3]

Myofibroblasts are mesenchymal cells found in granulation tissue and benign neoplasms including fibromatoses and myofibroblastomas. Myofibroblastic sarcomas are uncommon tumors. There are few reports of them in the literature. The tumors are usually found in the breast, bones, pleura, thyroid gland, and the soft tissues including the subcutaneous, submucosal, intramuscular, mesenteric, and scrotal.^[4,5]

Conclusion

Hemoptysis is a common symptom. Diagnostic workup is important since normal chest x-rays may not be decisive in determining the pathology. As reported here, CT may show a rare endobronchial lesion, myofibroblastic sarcoma, as a cause of the hemoptysis, although the chest x-ray is normal.

References

Hirshberg B, Biran I, Mendel G, Mordechai RK. Hemoptysis: etiology, evaluation, and outcome in a tertiary referral hospital. Chest 1997; 112: 440-444.
Weaver LJ, Solliday N, Cugell DW. Selection of patients with hemoptysis for fiberoptic bronchoscopy. Chest 1989; 76: 116-119.
Set PA, Flower CD, Smith IE, Cahn AP, Twentyman OP, Sheerson JM. Hemoptysis: comparative study of the role of CT and fiberoptic bronchoscopy. Radiology 1993; 189: 677-680.
Montgomery E, Goldblum JR, Fisher C. Myofibrosarcoma: a clinicopathologic study. Am J Surg Pathol 2001; 25: 219-228.
Taccagani G, Rovere E, Masullo M, Christensen L, Eyden B. Myofibrosarcoma of the breast: review of the literature on myofibroblastic tumors and criteria for defining myofibroblastic differentiation. Am J Surg Pathol 1997; 21: 489-496.

Source : http://www.medscape.com/viewarticle/472617

FDA Approves Ibuprofen Injection to Treat Pain and Fever

2009-06-20T22:07:00.000+07:00

The US Food and Drug Administration (FDA) yesterday approved an injectable formulation of ibuprofen (Caldolor, Cumberland Pharmaceuticals, Inc) for the treatment of pain and fever. The product will be available for hospital use only.

"Injectable ibuprofen and other nonsteroidal anti-inflammatory drugs (NSAIDs) are promising pain management options," commented Bob Rappaport, MD, in an agency news release. "But until now there were only oral forms of most NSAIDs. An injectable ibuprofen product can provide patients with relief from pain and fever when they cannot take oral products."

Dr. Rappaport is director of the Division of Anesthesia, Analgesia and Rheumatology Drug Products in the FDA's Center for Drug Evaluation and Research.

Adjunctive use of ibuprofen injection may also reduce the need for opiate pain relief. In a clinical trial of 319 women who had undergone abdominal hysterectomy, patients receiving the product were less likely to require morphine on an as-needed basis.

When treating acute pain, the recommended dosing regimen for injectable ibuprofen is 400 to 800 mg administered for 30 minutes every 6 hours. To treat fever, a 400-mg dose should be followed by 400 mg every 4 to 6 hours or 100 to 200 mg every 4 hours as needed.

Adverse events reported most commonly in clinical studies were nausea, flatulence, vomiting, and headache. Hypertension, serious dermatologic reactions, and severe allergic reactions may also occur.

As with other NSAIDs, ibuprofen injection should be used with caution in patients with congestive heart failure, those with kidney impairment, those at risk for blood clots, and patients with a prior history of ulcers or gastrointestinal bleeding. To reduce the risk for adverse events in these patients, the lowest effective dose should be administered for the shortest duration of time.

Source : http://www.medscape.com/viewarticle/704331?src=mpnews&spon=34&uac=133298AG

Acute Coronary Syndromes

2009-06-19T20:10:00.000+07:00

Introduction

Acute coronary syndrome (ACS) refers to the spectrum of clinical presentations ranging from ST-segment elevation myocardial infarction (STEMI) to non–ST-segment elevation myocardial infarction (NSTEMI) to unstable angina (ie, acute coronary syndrome without release of enzymes or biomarkers of myocardial necrosis).

In terms of pathology, acute coronary syndrome is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related artery. However, in some instances, stable coronary artery disease (CAD) may result in acute coronary syndrome in the absence of plaque rupture and thrombosis when physiologic stress (eg, trauma, blood loss, anemia, infection, tachyarrhythmias) increases demands on the heart.

The diagnosis of acute myocardial infarction in this setting requires a finding of the typical rise and fall of biochemical markers of myocardial necrosis in addition to at least 1 of the following: ischemic symptoms, development of pathologic Q waves, ischemic ST-segment changes on ECG or in the setting of a coronary intervention.¹Therefore, presence of appropriate symptoms in temporal relation to rise and fall in cardiac enzymes constitutes acute myocardial infarction even if typical ischemic ECG changes are absent. On the other hand, a minimal rise in troponin levels in a patient with renal failure is insufficient to diagnose acute myocardial infarction if symptoms and/or ECG changes are absent.

The terms transmural and nontransmural (subendocardial) myocardial infarction are no longer used because ECG findings in patients with this condition are not closely correlated with pathologic changes in the myocardium. Therefore, a transmural infarct may occur in the absence of Q waves on ECGs, and many Q-wave myocardial infarctions may be subendocardial, as noted on pathologic examination. Because elevation of the ST segment during acute coronary syndrome is correlated with coronary occlusion and because it affects the choice of therapy (urgent reperfusion therapy), ACS-related myocardial infarction should be designated STEMI or NSTEMI.

This article focuses on non–ST-elevation acute coronary syndrome. Patients with a new or presumed new left bundle-branch block are also excluded from the discussion below because they are regarded as having ST-elevation acute coronary syndrome and treated accordingly.

Key points of discussion include the following:

Increasing public awareness of the typical and atypical presentations of acute coronary syndrome is of utmost importance for optimal and timely treatment. Many patients do not recognize that their symptoms are cardiac in origin, and they delay seeking medical help. Guidelines from the European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA) recommend that patients with established coronary artery disease call emergency medical services if they have chest pain that does not resolve after they take a sublingual nitroglycerin tablet.
An ECG obtained by emergency medical services personnel in the field can be helpful in making an early diagnosis of myocardial ischemia.
Immediate triage and obtaining a 12-lead ECG within a few minutes of the patient's arrival to the emergency department are extremely important in initially determining the patient's risk category.
Further early risk stratification depends on the patient's clinical history, findings on physical examination, repeat ECG results, and results of blood work including markers of myocardial damage.
NSTEMI is distinguished from unstable angina by elevated levels of cardiac enzymes and biomarkers of myocyte necrosis. Differentiation is generally based on 3 sets of biomarkers measured at 6- to 8-hour intervals after the patient's presentation to ED. The current definition of NSTEMI requires a typical clinical syndrome plus elevated troponin (or creatine kinase isoenzyme MB [CK-MB]) levels to >99% of the normal reference (with a coefficient of variation of <10%>

For related information, see eMedicine articles Unstable Angina and Myocardial Infarction.

Pathophysiology

Atherosclerosis is primarily responsible for acute coronary syndrome. Most cases of acute coronary syndrome occur from disruption of a previously nonsevere lesion (an atherosclerotic lesion that was previously hemodynamically insignificant yet vulnerable to rupture). The vulnerable plaque is typified by a large lipid pool, numerous inflammatory cells, and a thin fibrous cap. New modalities, such as optical coherence tomography (OCT), palpography, and virtual histology, are being studied to identify vulnerable plaques.

The major trigger for coronary thrombosis is considered to be plaque rupture caused by the dissolution of the fibrous cap due to the release of metalloproteinases (collagenases) from activated inflammatory cells. This event is followed by platelet activation and aggregation, activation of the coagulation pathway, and vasoconstriction. This process culminates in coronary intraluminal thrombosis and variable degrees of vascular occlusion. Distal embolization may occur. The severity and duration of coronary arterial obstruction, the volume of myocardium affected, the level of demand, and the ability of the rest of the heart to compensate are major determinants of a patient's clinical presentation and outcome.

Demand influences acute coronary syndrome due to increased myocardial oxygen and nutrition requirements (such as exertion, emotional stress, or physiologic stress such as dehydration, blood loss, hypotension, infection, thyrotoxicosis, and surgery). Anemia and hypoxemia can precipitate myocardial ischemia in the absence of severe reduction in coronary artery blood flow. Elevated demand can produce acute coronary syndrome in the presence of a high-grade fixed coronary obstruction. Acute coronary syndrome without elevation in demand requires a new impairment in supply, typically due to thrombosis and/or plaque hemorrhage.

A syndrome consisting of chest pain, ischemic ST-segment and T-wave changes, elevated levels of biomarkers of myocyte injury, and transient left ventricular apical ballooning (takotsubo syndrome) has been shown to occur in the absence of clinical coronary artery disease, after emotional or physical stress. The pathogenesis of this syndrome is not well understood but is thought to relate to a surge of catechol stress hormones and/or high sensitivity to those hormones.

Attention to the underlying pathophysiologic mechanisms of ischemia is important when managing acute coronary syndrome. A simple predictor of demand is rate-pressure product, which can be lowered by beta blockers (eg, metoprolol or atenolol) and pain/stress relievers (eg, morphine), while supply may be improved by oxygen, adequate hematocrit, blood thinners (eg, heparin, IIb/IIIa agents such as abciximab, eptifibatide, tirofiban, or thrombolytics) and/or vasodilators (eg, nitrates, amlodipine). Recently, ranolazine² was released as a new agent that slows fast channel activity in diastole and provides an additional means to treat angina, but it has risk of QT prolongation and its inclusion for acute coronary syndrome treatment did not reduce the risk of major cardiovascular events such as death, heart attack, or recurrent ischemia.

Frequency, Mortality and Morbidity, Sex, Age, and Race

Frequency

In the United States, approximately 1.7 million cases of acute coronary syndrome were diagnosed in 2001. Rates of first-listed admission diagnosis of unstable angina fell 87% from 29.7/10,000 in 1988 to 3.9/10,000 in 2001 for all age and sex groups, and rates of acute coronary syndrome as a primary diagnosis declined 44%.

Internationally, cardiovascular diseases cause 12 million deaths throughout the world each year, according to the third monitoring report of the World Health Organization, 1991-1993. Cardiovascular disease causes almost half of all deaths in the developed world and 25% of deaths in the developing world. By the year 2020, cardiovascular disease will cause an estimated 25 million deaths worldwide, becoming the predominant cause of death in the world, surpassing infectious diseases.

Mortality and morbidity

Cardiovascular disease is the leading cause of death in the United States. Each year, approximately 500,000-700,000 deaths are attributed to coronary artery disease. About 13% of individuals with non–ST-segment elevation myocardial infarction (NSTEMI) acute coronary syndrome and 8% of those with unstable angina who reach the hospital die within 6 months, according to the Global Registry of Acute Coronary Events (GRACE). In the same period, the rate of new stroke is 1.5-3%, and the rate of rehospitalization for a further acute coronary syndrome is 17-20%.

Sex

The incidence of acute coronary syndrome demonstrates a male predominance to approximately 70 years of age, when incidences converge in both sexes.

Women are more likely than men to be older and to have more comorbid conditions at the time of first presentation. Abnormal locations of pain, nausea, vomiting, fatigue, dyspnea, and other atypical presentations are most common in women.

Young women with acute coronary syndrome should be counseled regarding the potential teratogenic effect of statins. Hormonal replacement therapy with estrogen or progesterone) should be stopped in women who present with acute coronary syndrome.

Age

The incidence of acute coronary syndrome increases with age. Older patients with acute coronary syndrome are most likely to present with atypical symptoms. Many elderly patients with acute coronary syndrome do not receive evidence-based therapies. This situation emphasizes the importance of improving quality-of-care programs to reinforce the use of therapies among elderly individuals.³

Race

No racial predilection is observed. Racial disparities in treatment and outcome have been noted.

History, Presentation, Physical Examination, and Causes

History

Factors that predispose individuals to develop acute coronary syndrome include the following:

Age older than 70 years
Male sex
Diabetes mellitus
Known history of coronary artery disease, including myocardial infarction
Family history of premature coronary artery disease
Hypertension
Hyperlipidemia
Tobacco use

Presentation

Patients with acute coronary syndrome may present with a chief symptom of pain or discomfort in the chest or left arm, particularly if it reproduced previously documented angina.

Principal presentations of unstable angina include the following findings:

Rest angina that occurs at rest and that usually lasts >20 minutes
New-onset angina at least as severe as Canadian Cardiovascular Society (CCS) class III (ie, marked limitation of ordinary physical activity)
Increasing (crescendo) angina, ie, previously diagnosed angina that has become distinctly more frequent, longer in duration, or lower in threshold (ie, increased by ≥1 CCS class to at least CCS III severity)
Shortness of breath, which might be an anginal equivalent or a symptom of heart failure.

Patients might also present with atypical symptoms, such as arm, jaw, neck, ear, or epigastric discomfort. When the symptoms are clearly related to exertion or stress or when they are promptly relieved with nitroglycerin, they could be anginal equivalents. Atypical presentations are common and frequently lead to misdiagnoses of abdominal pain, altered mental status, shock, or renal failure, for example.

Physical examination

Physical findings can vary from normal to any of the following:

Hypotension or hypertension
Diaphoresis
Pulmonary edema and other signs of left heart failure
Extracardiac vascular disease
Fourth heart sound (S₄), which may be heard in patients with ischemia or systolic murmur secondary to mitral regurgitation. (This is frequently present, especially in patients with inferior-wall ischemia.)
Other findings (eg, cool, clammy skin and diaphoresis in patients with cardiogenic shock)
Systolic murmur related to dynamic obstruction of the left ventricular outflow tract (This is caused by hyperdynamic motion of the basal left ventricular myocardium and may be heard in patients with an apical infarct.

Causes

The most common cause of acute coronary syndrome is coronary thrombosis on a preexisting plaque. The degree of occlusion determines the patient's subsequent presentation.

Risk factors for coronary artery disease include the following:

Age
Sex
Family history of premature coronary heart disease
Tobacco use
Diabetes mellitus
Hypertension
Dyslipidemia
Obesity, especially the male-pattern truncal form
Peripheral vascular disease
Previous stroke

Other causes of NSTEMI acute coronary syndrome include the following:

Dynamic obstruction (coronary spasm or vasoconstriction)
Cocaine or amphetamine use, which increases myocardial oxygen demand and which may cause coronary vasospasm
Use of certain medications, such as selective serotonin reuptake inhibitors (SSRIs)
Progressive mechanical obstruction
Inflammation⁴ and/or infection
Embolic occlusion of the coronary arteries
Congestive heart failure
Underlying coronary artery disease, which severe anemia or hypoxemia might precipitate
Coronary artery dissection (spontaneous or iatrogenic)
Coronary artery injury during blunt or penetrating chest trauma
Coronary artery anomaly, such as a left anterior descending coronary artery originating from the pulmonary trunk or a left main coronary artery originating from the right coronary sinus of the aortic valve with a course between the great vessels

Differential Diagnoses and Other Problems to Consider

Differential diagnoses

Aortic dissection
Aortic stenosis
Esophageal spasm
Gastroesophageal reflux disease
Myocarditis
Pneumothorax
Pulmonary embolism

Other problems to consider

Acute cholecystitis
Hypertensive emergency
Panic attack
Pericarditis

Laboratory Studies

Electrocardiography

Recording an ECG during an episode of the presenting symptoms is valuable. Transient ST-segment changes (>0.05 mV) that develop during a symptomatic period and that resolve when the symptoms do is strongly predictive of underlying coronary artery disease and has prognostic value. Comparison with previous ECGs is often helpful.

Alternative causes of ST-segment and T-wave changes are left ventricular aneurysm, pericarditis, Prinzmetal angina, early repolarization, Wolff-Parkinson-White syndrome, drug therapy (eg, with tricyclic antidepressants, phenothiazines).

Measurement of cardiac enzyme levels

Measure cardiac enzyme levels at regular intervals, starting on admission and continuing until the peak is reached or until 3 sets of results are negative. Biochemical biomarkers are useful for both diagnosis and prognostication (see Media file 1).

This plot shows changes in cardiac markers over time after the onset of symptoms. Peak A is the early release of myoglobin or creatine kinase isoenzyme MB (CK-MB) after acute myocardial infarction (AMI). Peak B is the cardiac troponin level after infarction. Peak C is the CK-MB level after infarction. Peak D is the cardiac troponin level after unstable angina. Data are plotted on a relative scale, where 1.0 is set at the myocardial-infarction cutoff concentration. Courtesy of Wu et al (1999). ROC = receiver operating characteristic.

Of note, cardiac-specific troponins are not detectable in the blood of healthy individuals; therefore, they provide high specificity for detecting injury to cardiac myocytes. These molecules are also more sensitive than CK-MB for myocardial necrosis and, thus, improve early detection of small myocardial infarctions. Although blood troponin levels increase simultaneously with CK-MB levels (about 6 h after the onset of infarction), they remain elevated for as long as 2 weeks. As the result, troponin values cannot be used to diagnose reinfarction. New methods of detecting troponins in the blood can measure levels as low as 0.1-0.2 ng/mL.

Minor elevations in these molecules can be detected in the blood of patients without acute coronary syndrome in the setting of myocarditis (pericarditis), sepsis, renal failure, acute congestive heart failure, acute pulmonary embolism, or prolonged tachyarrhythmias.

Measurement of CK-MB levels
- CK-MB, the isoenzyme specific to the heart muscle, was the principal biomarker of cardiac injury until troponin supplemented it.
- In the setting of myocardial infarction, plasma CK-MB concentrations typically rise about 4-6 hours after the onset of chest pain. They peak within 12-24 hours and return to baseline levels within 24-48 hours.
- Serial measurements obtained every 6-8 hours (at least 3 times) are warranted until peak values are determined.
- Clinical settings other than acute coronary syndrome, such as trauma, heavy exertion, and skeletal muscle disease (eg, rhabdomyolysis) may elevate CK-MB values.
- The area under the concentration-time curve for CK-MB created with serial measurements of blood enzyme levels provides a reliable estimate of the size of the infarct.
- Determination of subforms of CK-MB (CK-MB2 that is more specific to heart muscle) may improve the sensitivity of this test.
Measurement of troponin levels
- Troponin is part of the contractile apparatus of the myocyte associated with tropomyosin and actin and myosin filaments. Troponin has 3 subunits: TnT, TnI, and TnC. TnI and TnT are normally not detectable in the blood.
- Measurement of troponin level has both diagnostic and prognostic value.
- Positive troponin levels are virtually diagnostic of myocardial infarction in the most recent revisions of the ACC/AHA guidelines, as they are without equal in terms of combined specificity and sensitivity in diagnosing myocardial infarction.
- Elevated troponin levels might help in identifying patients who might greatly benefit from aggressive antiplatelet and other adjunctive therapy.⁵
- Troponin levels are typically measured serially along with CK values.
Measurement of myoglobin levels
- Myoglobin is not cardiac specific, but it may be detected as early as 2 hours after myocardial necrosis starts.
- Myoglobin results should be supplemented with other more specific cardiac biomarkers, such as CK-MB or troponin.
- Myoglobin values have a high negative predictive value when blood is sampled in the first 4-8 hours after onset.

CBC determination

The CBC helps in ruling out anemia as a secondary cause of acute coronary syndrome. Leukocytosis has prognostic value in the setting of acute myocardial infarction.

Basic metabolic panel

Close monitoring of potassium and magnesium levels is important in patients with acute coronary syndrome because low levels may predispose them to ventricular arrhythmias. Routine measurement of serum potassium levels and prompt correction are recommended.

A creatinine level is also needed, particularly if cardiac catheterization is considered. Use of N -acetylcysteine and adequate hydration can help prevent contrast material–induced nephropathy.⁶

New biomarkers

Levels of brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-pro-BNP) are elevated in acute MI and provide predictive information for risk stratification across the spectrum of acute coronary syndrome.^7,8

In the future, a combination of levels of troponin (a biomarker of myocardial necrosis), NT-pro-BNP (an indicator of elevated left ventricular end-diastolic pressure and wall stress), and C-reactive protein (CRP, an estimate of extent of systemic inflammation) may prove useful for predicting the outcome of patients with acute coronary syndrome.

Routine measurement of BNP and CRP levels in patients with acute coronary syndrome is not warranted at this time.

Imaging Studies

Chest radiography

Chest radiography helps in assessing cardiomegaly and pulmonary edema. A chest radiograph may also assist in diagnosing concomitant disease (eg, pneumonia in an elderly patient) as a precipitating cause of acute coronary syndrome.

Echocardiography

An echocardiogram may play an important role in the setting of acute coronary syndrome. Regional wall-motion abnormalities can be identified. Echocardiograms are especially helpful if the diagnosis is questionable.

An echocardiogram can also help in defining the extent of the infarction and assess overall function of the left and right ventricles. In addition, an echocardiogram can help identify complications such as acute mitral regurgitation, left ventricular rupture, and pericardial effusion.

Absence of segmental wall-motion abnormality on echocardiography during active chest discomfort is a highly reliable indicator of a nonischemic origin of symptoms.

Myocardial perfusion imaging

Myocardial perfusion is a valuable method for triaging patients with chest pain in the emergency department. Myocardial perfusion imaging at rest is highly sensitive for detecting acute myocardial infarction, and it can be supplemented with provocative testing after infarction is excluded.

Results of clinical trials can be applied only in centers with proven reliability and experience.

The sensitivity of single photon emission computed tomography (SPECT) is sufficient to detect infarcts of at least 10 g, but MRI with gadolinium enhancement may depict infarcts as small as 1–5 g.

Cardiac angiography

Cardiac catheterization helps in defining the patient's coronary anatomy and the extent of the disease.

Patients with cardiogenic shock, intractable angina despite medication, severe pulmonary congestion, or right ventricular infarction should immediately undergo cardiac catheterization.

For high-risk patients with acute coronary syndrome without persistent ST elevation, angiography with glycoprotein IIb/IIIa inhibition has been recommended.

Most patients benefit from angiography when they have a TIMI risk score of less than 3 points (see Table).

Table

Characteristic	Risk Score
History
Age ≥65 y	1
At least 3 risk factors for coronary heart disease	1
Previous coronary stenosis ≥50%	1
Use of aspirin in previous 7 d	1
Presentation
At least 2 anginal episodes in the previous 24 h	1
ST-segment elevation on admission ECG	1
Elevated levels of serum biomarkers	1
Total score	0-7

Characteristic	Risk Score
History
Age ≥65 y	1
At least 3 risk factors for coronary heart disease	1
Previous coronary stenosis ≥50%	1
Use of aspirin in previous 7 d	1
Presentation
At least 2 anginal episodes in the previous 24 h	1
ST-segment elevation on admission ECG	1
Elevated levels of serum biomarkers	1
Total score	0-7

Note—Event rates significantly increased as the TIMI risk score increased in the test cohort in the TIMI IIB study. Rates were 4.7% for a score of 0/1, 8.3% for 2, 13.2% for 3, 19.9% for 4, 26.2% for 5, and 40.9% for 6/7 (P < .001, χ² test for the trend). The pattern of increasing event rates with increasing TIMI risk score was confirmed in all 3 validation groups (P < .001).

After the diagnosis of acute coronary syndrome is established, risk stratification based on TIMI risk scores and the GRACE risk of death can be useful in making clinical decisions regarding the need for an invasive approach. Patients are at higher risk if the following findings are present:

Clinical instability
Accelerating chest pain in the 48 hours before presentation
Prolonged ischemic chest pain
Clinical evidence of heart failure
Hypotension
Ventricular tachycardia
ECG changes of ischemia
Positive cardiac biomarkers
TIMI risk score of more than 3 points (see the Table above) or a GRACE risk of death more than 4%.

Medical Care and Coronary Interventions

Medical Care

Initial therapy for acute coronary syndrome should focus on stabilizing the patient's condition, relieving ischemic pain, and providing antithrombotic therapy to reduce myocardial damage and prevent further ischemia.
Morphine (or fentanyl) for pain control, oxygen, sublingual and/or intravenous nitroglycerin, soluble aspirin 162-325 mg, and clopidogrel with a 300- to 600-mg loading dose are given as initial treatment.
Humidified oxygen may reduce the risk of nosebleeds in patients with acute coronary syndrome who are receiving antiplatelet and antithrombin therapy.
Do not administer nitrates if the patient is hypotensive (systolic BP <90>
Patients with known hypersensitivity to antiplatelet agents, active internal bleeding, and bleeding disorders should not receive antiplatelet or antithrombotic therapy.
High-risk patients with non–ST-segment elevation myocardial infarction (NSTEMI) acute coronary syndrome should receive aggressive care, including aspirin, clopidogrel, unfractionated or low molecular weight heparin (LMWH), intravenous platelet glycoprotein IIb/IIIa complex blockers (eg, tirofiban, eptifibatide), and a beta-blocker. The goal is early revascularization.
Intermediate–risk patients with NSTEMI acute coronary syndrome should rapidly undergo diagnostic evaluation and further assessment to determine their appropriate risk category.
Low-risk patients with NSTEMI acute coronary syndrome should undergo further follow-up with biomarkers and clinical assessment. Optimal medical therapies include use of standard medical therapies, including beta-blockers, aspirin, and unfractionated heparin or LMWH. The CURE study has shown that clopidogrel would be beneficial even in low-risk patients.¹⁰ If no further pain occurs, and follow-up studies are negative, a stress study should drive further management.
First-line therapy in patients with chest pain regardless of their risk strategy includes a combination of oxygen, aspirin, nitroglycerin, and morphine.
Mehta et al studied 3031 patients with acute coronary syndromes. Early intervention (coronary angiography £ 24 h after randomization; median time 14 h) in acute coronary syndromes did not differ greatly from delayed intervention (coronary angiography >24 h randomization; median time 50 h) in preventing the primary outcome (ie, composite of death, myocardial infarction, or stroke at 6 mo). Early intervention did reduce the rate of the secondary outcome (ie, death, myocardial infarction, or refractory ischemia at 6 mo) and improved the primary outcome in patients who were at highest risk (ie, Global Registry of Acute Coronary Events [GRACE] risk score >140).¹¹

Anti-ischemic therapy

Nitrates¹² do not improve mortality. However, they provide symptomatic relief by means of several mechanisms, including coronary vasodilation, improved collateral blood flow, decrease in preload (venodilation and reduced venous return), and decrease in afterload (arterial vasodilation). Care should be taken to avoid hypotension because this can potentially reduce coronary perfusion pressure (diastolic BP - left ventricular diastolic pressure).

Beta-blockers are indicated in all patients unless they have the following contraindications:

Hypotension
Shock
Severe bradycardia
High-grade atrioventricular block
Severe obstructive pulmonary disease

Beta-blockers reduce oxygen demand and ventricular wall tension. They also decrease mortality and adverse cardiovascular events. These drugs may prevent mechanical complications of myocardial infarction, including rupture of the papillary muscle, left ventricular free wall, and ventricular septum. Beta-blockers meliorate dynamic obstruction of the left ventricular outflow tract in patients with apical infarct and hyperdynamic basal segments.

The most frequently used regimen is intravenous metoprolol 2-5 mg given every 5 minutes (up to 15 mg total) followed by 25-100 mg given orally twice a day.

Beta-blockers should not be used acutely in patients with cardiogenic shock or signs of heart failure on presentation.

Antithrombotic therapy

Aspirin permanently impairs the cyclooxygenase pathway of thromboxane A2 production in platelets and, thus, inhibits platelet function. Aspirin reduces morbidity and mortality and is continued indefinitely.¹³

Clopidogrel (thienopyridine) inhibits adenosine 5'-diphosphate (ADP)–dependent activation of the glycoprotein IIb/IIIa complex, a necessary step for platelet aggregation. This process results in intense inhibition of platelet function, particularly in combination with aspirin. In the Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) trial, thienopyridine reduced the rate of myocardial infarction by 20%.

Clopidogrel is a class I recommendation for patients when early noninterventional approach is planned in therapy for at least 1 month to as long as 9 months.¹⁴ When percutaneous coronary intervention (PCI) is planned, clopidogrel is started and continued for at least 1 month and up to 9 months, if the patient is not at high risk for bleeding.

The optimal dosage for clopidogrel is still being evaluated. Reports show that a loading dose of 600 mg might be more beneficial than 300 mg. Withhold clopidogrel for at least 5 days before elective coronary artery bypass grafting (CABG). Since 12% of patients with non-ST elevation acute coronary syndrome have coronary anatomy that favors CABG, use of clopidogrel is withheld until coronary angiography at some institutions.

The TRITON TIMI 38 trial studied patients with acute coronary syndromes with scheduled percutaneous coronary intervention. Prasugrel therapy was associated with significantly reduced rates of ischemic events, including stent thrombosis, but with an increased risk of major bleeding, including fatal bleeding. Overall mortality did not differ significantly between treatment groups.¹⁵

Ticagrelor is the first reversible oral P2Y receptor antagonist. It provides faster, greater, and more consistent adenosine diphosphate–receptor inhibition than clopidogrel, and is being studied in the PLATO trial.¹⁶

Glycoprotein IIb/IIIa receptor antagonists include abciximab^17,18, eptifibatide¹⁹, and tirofiban²⁰. These drugs inhibit the glycoprotein IIb/IIIa receptor, which is involved in the final common pathway for platelet adhesion and aggregation.

Two trials with tirofiban and 1 trial with eptifibatide have also documented their efficacy in unstable angina/NSTEMI patients, only some of whom underwent interventions. These antagonists are a class I recommendation in patients where catheterization and PCI are planned. Intermediate- and high-risk patients appear to respond favorably to glycoprotein IIb/IIIa inhibitors.²¹ They include patients with ST-segment depression, elevated risk scores, elevated serum troponin levels²², and/or diabetes mellitus.

Use eptifibatide or tirofiban in patients with high-risk features in whom invasive treatment is not planned.

The EARLY ACS trial compared a strategy of early, routine administration of eptifibatide with delayed, provisional administration in patients who had acute coronary syndromes without ST-segment elevation and who were assigned to an invasive strategy. The use of eptifibatide 12 hours or more before angiography was not superior to the provisional use of eptifibatide after angiography, and early use of eptifibatide was associated with an increased risk of non–life-threatening bleeding and need for transfusion.²³

Anticoagulation

Unfractionated heparin was associated with a 33% reduction in the risk of myocardial infarction or death in patients with unstable angina who were treated with aspirin plus heparin compared with aspirin alone.²⁴

LMWHs might be superior to heparin in reducing cardiovascular outcomes with a safety profile similar to that of heparin in patients receiving medical care.

Nine randomized trials have directly compared LMWH with unfractionated heparin. Two trials evaluated dalteparin, another evaluated nadroparin, and 6 evaluated enoxaparin.^25,26 Heterogeneity of trial results has been observed. Trials with dalteparin and nadroparin reported similar rates of death or nonfatal myocardial infarction compared with heparin, whereas 5 of 6 trials of enoxaparin found point estimates for death or nonfatal myocardial infarction that favored enoxaparin over heparin. The benefit of enoxaparin appeared to be driven largely by a reduction in nonfatal myocardial infarction, especially in the cohort of patients who had not received any open-label anticoagulant therapy before randomization.

The role of LMWHs in patients for whom PCI is scheduled is relatively ill defined. However, it is likely to be at least equivalent to that of heparin. It appears reasonable to minimize the risk of excessive anticoagulation during PCI by avoiding crossover of anticoagulants (ie, maintain consistent anticoagulant therapy from the pre-PCI phase throughout the procedure itself). Additional experience with regard to the safety and efficacy of the concomitant administration of LMWHs with GP IIb/IIIa antagonists and fibrinolytic agents is currently being acquired.

Current guidelines for patients with moderate- or high-risk acute coronary syndromes recommend an early invasive approach with concomitant antithrombotic therapy, including aspirin, clopidogrel, and unfractionated or low-molecular-weight heparin. The ACUITY trial evaluated the role of thrombin-specific anticoagulation with bivalirudin in this patient population. In patients with moderate- or high-risk acute coronary syndromes who were undergoing invasive treatment with glycoprotein IIb/IIIa inhibitors, bivalirudin was associated with rates of ischemia and bleeding that were similar to those with heparin. Bivalirudin alone was associated with similar rates of ischemia and significantly lower rates of bleeding.²⁷ Further, glycoprotein IIb/IIIa inhibitors can be initiated at the time of angiography; routine administration 12-24 hours before the procedure carries an increased risk of bleeding and no improvement in outcome.

In summary, for patients in whom an invasive strategy is selected, regimens with established efficacy include enoxaparin and unfractionated heparin (Class I, Level of Evidence: A) and bivalirudin and fondaparinux (Level of Evidence: B). For patients in whom a conservative strategy is selected, regimens using either enoxaparin or UFH (Class I, Level of Evidence: A) or fondaparinux (Level of Evidence: B) have established efficacy. In patients in whom a conservative strategy is selected and who have an increased risk of bleeding, fondaparinux is preferable (Level of Evidence: B).

For unstable angina/NSTEMI patients in whom an initial conservative strategy is selected, fondaparinux is preferable to UFH as anticoagulant therapy unless CABG is planned within 24 hours (Class IIa, Level of Evidence: B).

Thrombolysis

Thrombolysis has no role in NSTEMI acute coronary syndrome.

Coronary Interventions

An early invasive strategy is indicated in unstable angina/NSTEMI patients who have refractory angina or hemodynamic or electrical instability without serious comorbidities or contraindications to such procedures (Class I). An early invasive strategy is also indicated in initially stabilized unstable angina/NSTEMI patients without serious comorbidities or contraindications to such procedures who have an elevated risk for clinical events (Class I). In NSTEMI acute coronary syndrome , early revascularization reduces myocardial infarction and death rates compared with a more selective strategy, particularly in high-risk patients. Use of glycoprotein IIb/IIIa blockers followed by early invasive catheterization is the most logical approach. An early invasive strategy should be considered in patients with large myocardial infarction, hypotension, shock, right ventricular infarction, and refractory chest pain.

Further Patient Care

Consultations

Emergency department personnel should be well aware of the initial evaluation, triaging, and treatment of patients with chest pain (see Media file 2).

Suggested algorithm for triaging patients with chest pain. ACS = acute coronary syndrome; ASA = aspirin; EKG = ECG; MI = myocardial infarction; Rx = treat; STEMI = ST-elevation myocardial infarction. Courtesy of Wu et al (1999).
Internists manage many cases of acute coronary syndrome.
Have a low threshold for consulting cardiologists, particularly if the patient has high-risk acute coronary syndrome and if cardiac catheterization is being considered.

Diet

Patients should receive nothing by mouth (NPO) until their condition is stabilized and treated.
Maintain the patient's NPO status from midnight before cardiac catheterization if it is being considered.
After initial therapy and admission, a dietitian should instruct the patient regarding an appropriate diet, as recommended by the AHA. A low-salt, low-fat, and low-cholesterol diet is generally recommended.

Activity

Limit patients to bed rest to minimize their oxygen consumption until reperfusion and initial therapy are complete. After that, the patient's activity may slowly be increased as tolerated and as the clinical situation allows.
Start cardiac rehabilitation before the patient is discharged.

Further inpatient care

Patients may receive additional care in a telemetry-monitored unit if their condition is stable. Carefully monitor patients for arrhythmia, recurrent ischemia, and other possible complications. If patients have not undergone cardiac catheterization and if they have no complications, an ischemia-driven approach to PCI can be taken.

Further outpatient care

Arrange for follow-up within 2 weeks of the patient's discharge.

Inpatient and outpatient medications

Long-term use of aspirin in patients who have had a myocardial infarction significantly reduces the subsequent risk of death.
Clopidogrel, along with aspirin, should be prescribed for at least 9 months after discharge if the patient has no contraindications. To reduce the risk of bleeding, the dose of aspirin can be reduced to 81 mg.
In 2009, Ho et al reported on clopidogrel use after hospital discharge in a retrospective cohort study of more than 8000 patients with acute coronary syndrome. The authors determined that the use of clopidogrel concomitantly with proton pump inhibitors is associated with an increased risk of adverse outcomes, including death, compared with the use of clopidogrel alone. These results indicate that proton pump inhibitors may reduce the benefits of clopidogrel after acute coronary syndrome.²⁸
If aspirin cannot be tolerated, clopidogrel is the antiplatelet drug of choice.
Beta-blocker therapy has confirmed therapeutic benefits in survivors of acute myocardial infarction. This therapy is most beneficial in patients with the highest risk.
Many trials have shown a clear benefit of lipid-lowering therapy in the primary and secondary prevention of coronary artery disease.²⁹
The National Cholesterol Education Panel has set guidelines for target cholesterol levels. In general, patients who have had a myocardial infarction should achieve a low-density lipoprotein cholesterol (LDL) level less than 100 mg/dL, a high-density lipoprotein cholesterol (HDL) level greater than 40 mg/dL, and a triglyceride level less than 200 mg/dL. High-risk patients should be treated to a target LDL level of less than 70 mg/dL.
In the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) trial, Schwartz et al showed that starting atorvastatin during hospitalization for an acute coronary syndrome, irrespective of lipid levels, reduces the frequency of recurrent ischemic events.³⁰ This treatment significantly reduced the frequency of the combined end point of death, recurrent death, myocardial infarction, or worsening unstable angina requiring hospitalization.
The Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT)–Thrombolysis in Myocardial Infarction (TIMI) 22 trial showed that the use of intensive statin therapy versus standard therapy improved clinical outcomes over 2 years in patients with acute coronary syndrome.

Transfer

Patients with acute coronary syndrome with high-risk features should be transferred to a facility where catheterization is available. Start eptifibatide or tirofiban with other medical therapy, and transfer the patient to a facility where PCI can be performed.

Complications and Prognosis

Complications

Monitor and immediately treat arrhythmias in the first 48 hours. Pay attention to exacerbating factors, such as disturbances in electrolytes (especially potassium and magnesium), hypoxemia, drugs, or acidosis. Correct these factors accordingly.

Recurrent ischemia may be due to incomplete reperfusion. In the setting of PCI, consider stent thrombosis as a possible cause. Whether drug-eluting stents have an increased rate of thrombosis compared with bare metal stents is unclear.

CHF can be due to systolic dysfunction or diastolic dysfunction in the setting of myocardial infarction. Aggressive treatment is indicated to prevent worsening of the situation.

Cardiogenic shock is defined as a systolic BP less than 90 mm Hg in the presence of organ hypoperfusion. This finding is associated with a high mortality rate. Pressor agents, such as dopamine, and inotropic agents, such as dobutamine, may be needed.

Some patients with intractable chest pain or severe hypotension may require the insertion of an intra-aortic balloon pump. The EuroHeart survey showed a nearly 40% reduction in the risk for death in patients with acute coronary syndrome who received support with an intra-aortic balloon pump. This benefit was independent of the status of the ST segment.

Patients presenting with cardiogenic shock should undergo PCI as soon as possible.

Prognosis

Six-month mortality rates in the GRACE registry were 13% for patients with NSTEMI acute coronary syndrome and 8% for those with unstable angina.

Patient Education

The mnemonic ABCDE might be helpful.

A = Aspirin and antianginals
B = Beta-blockers and BP
C = Cholesterol and cigarettes
- Educate all patients who have had a myocardial infarction about the critical role of smoking in the development of coronary artery disease.
- Smoking-cessation classes should be offered to help patients avoid smoking after a myocardial infarction.
- Cigarette smoking is a major risk factor for coronary artery disease. The risk of recurrent coronary events decreases 50% at 1 year after smoking cessation.
- Provide all patients who smoke with guidance, education, and support to avoid smoking.
- Bupropion increases the likelihood of successful smoking cessation.
D = Diet and diabetes
- Diet plays an important role in the development of coronary artery disease.
- Educate patients who have had a myocardial infarction about the role of a low-cholesterol and low-salt diet.
- Educate patients about AHA dietary guidelines regarding a low-fat, low-cholesterol diet.
- A dietitian should see and evaluate all patients who have had a myocardial infarction before they are discharged.
E = Exercise and education
- A cardiac rehabilitation program after discharge might reinforce education and enhance compliance.
- Failure to diagnose a myocardial infarction is the leading cause of litigation against emergency physicians and cardiologists.
- Consider the possibility of atypical presentations in women, elderly patients, and patients with diabetes.
- ECGs should be reviewed promptly.
- Early imaging is useful to assess wall-motion abnormalities in difficult cases with nondiagnostic ECGs, such as those involving a left bundle-branch block.
- Involve a cardiologist when in doubt.

Special Concerns

Elderly patients
- Elderly patients are at increased risk for adverse outcomes.
- Decisions about their care should reflect considerations of their general health, cognitive status, and life expectancy.
- Altered pharmacokinetics and sensitivity to drugs are other issues to be considered.
Women
- Women with acute coronary syndrome should be cared for as men are.
- Like their male counterparts, women with unstable angina and/or NSTEMI should receive aspirin and clopidogrel.
- Indications for testing are similar in men and women.
Patients with diabetes mellitus
- Outcomes are worse in patients with diabetes than in those without diabetes.
- Tight glycemic control should be maintained.
Patients who have undergone CABG
- Medical treatment should follow the same guidelines as those established for patients who have not undergone CABG.
- Have a low threshold for catheterization in patients with acute coronary syndrome who underwent CABG.
Patients with cocaine use
- Give nitroglycerin and oral calcium antagonists for patients with STEMI or depression that accompanies chest discomfort.
- Immediately perform catheterization if ST elevation persists after the administration of nitroglycerin and calcium channel blockers.
Patients with Prinzmetal angina
- Perform angiography in patients with episodic chest pain and ST-segment elevation that resolves with nitroglycerin and/or calcium channel blockers.
- Administer nitrates and calcium channel blockers in patients whose catheterization does not show obstructive coronary artery disease.
Patients with syndrome X
- Offer reassurance, and provide medical therapy with nitrates, beta-blockers, and calcium channel blockers alone or in combination.
- Reduce risk factors.

Multimedia

(Enlarge Image)

Media file 1: This plot shows changes in cardiac markers over time after the onset of symptoms. Peak A is the early release of myoglobin or creatine kinase isoenzyme MB (CK-MB) after acute myocardial infarction (AMI). Peak B is the cardiac troponin level after infarction. Peak C is the CK-MB level after infarction. Peak D is the cardiac troponin level after unstable angina. Data are plotted on a relative scale, where 1.0 is set at the myocardial-infarction cutoff concentration. Courtesy of Wu et al (1999). ROC = receiver operating characteristic.

(Enlarge Image)

Media file 2: Suggested algorithm for triaging patients with chest pain. ACS = acute coronary syndrome; ASA = aspirin; EKG = ECG; MI = myocardial infarction; Rx = treat; STEMI = ST-elevation myocardial infarction. Courtesy of Wu et al (1999).

Keywords

acute coronary syndrome, ACS, myocardial infarction, MI, ST-segment elevation myocardial infarction, STEMI, non–ST-segment elevation myocardial infarction, NSTEMI, coronary artery disease, CAD, unstable angina, UA, transmural MI, nontransmural MI, subendocardial MI, cardiovascular disease, CVD, chronic heart failure, congestive heart failure, CHF, coronary heart disease, CHD.

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Source : http://emedicine.medscape.com/article/164525-overview?src=emed_whatnew_nl_0#EarlyIntervention

Hospital-related incidents; causes and its impact on disaster preparedness and prehospital organisations

2009-06-18T10:26:00.003+07:00

Abstract

Background

Hospital’s capacity and preparedness is one of the important parts of disaster planning.
Hospital-related incidents, a new phenomenon in Swedish healthcare, may lead to ambulance
diversions, increased waiting time at emergency departments and treatment delay along with
deterioration of disaster management and surge capacity. We aimed to identify the causes and
impacts of hospital-related incidents in Region Västra Götaland (western region of Sweden).

Methods

The regional registry at the Prehospital and Disaster Medicine Center was reviewed (2006-
2008). The number of hospital-related incidents and its causes were analyzed.

Result

There were an increasing number of hospital-related incidents mainly caused by emergency
department´s overcrowdings, the lack of beds at ordinary wards and/or intensive care units
and technical problems at the radiology departments. These incidents resulted in ambulance
diversions and reduced the prehospital capacity as well as endangering the patient safety.

Conclusion

Besides emergency department overcrowdings, ambulance diversions, endangering patient’s
safety and increasing risk for in-hospital mortality, hospital-related incidents reduces and
limits the regional preparedness by minimizing the surge capacity. In order to prevent a future
irreversible disaster, this problem should be avoided and addressed properly by further
regional studies.

Background

Region Västra Götaland is the public healthcare provider for the western part of Sweden,
with a population around 1.5 million. This task is achieved through around 150 primary
healthcare centres and 10 emergency hospitals (the largest Sahlgrenska University Hospital in
Gothenburg). PKMC (Prehospital Disaster and Medicine Centre) is a regional unit responsible
for (medical) risk assessment and emergency planning as well as staff training in disaster
management. The center is also associated with Sahlgrenska Academy in disaster research
funded by the National Board of Health and Welfare. PKMC assumes command and control
on a regional (“gold”) level in case of major incidents/disasters [1]. All incidents and
consequent activities caused by them have been registered at the centers registry (PKMC
registry) since 1999 and can be analyzed retrospectively.
The current economical crisis within most healthcare systems has resulted in local, regional
and national plans to reduce economic deficits. Most of these plans aim to increase the
healthcare systems effectiveness by reducing hospital beds and expanding out-patients
departments, which in turn challenges the mode of operation at emergency departments (ED)
[2-3]. During past decades the increasing number of patients at ED’s treatment areas has
resulted in a work overload, making EDs to operate beyond their capacity. Hospital bed
shortage enforces a rapid turnover of patients, increasing the number of patients discharged as
early as possible and endangers patient safety. Together with increasing number of non-urgent
patients these are main factors causing ED-overcrowding [1, 4-5]. To counter with
EDovercrowding escalation, new methods (e.g. triage) have been deployed, which mainly deal
with its infrastructure and internal organization [1, 6]. ED is, however, the hospital´s main
contact point with surrounding world and an important part of disaster preparedness in the
area served by the hospital. An overloaded ED has a great impact on other adjacent activities
e.g. prehospital organization, ambulance transports, elective production (surgery), and
individual patient´s safety [7-9].
During the last years a new category of incidents, “hospital-related incidents”, has appeared in
the PKMC registry. We hypothesized that these incidents are, directly or indirectly, associated
with hospital bed shortage and ED-overcrowding and consume huge regional resources. The
aim of this paper was to identify the causes of these incidents in the Region Västra Götaland
(western region of Sweden) by reviewing the PKMC registry data collected between January
1st, 2006 and December 31st, 2008.

Methods

All incoming data concerning hospital-related incidents in Region Västra Götaland , between
1st of January 2006 and 31st of December 2008, was collected. An incident was defined as an
alert from EMS (emergency medical services) dispatch centre to the regional duty officer on
call (RTiB). The RTiBs have medical background as within emergency care and special
training in management of major incidents. They have a thorough understanding of regional
resources. As a second line senior consultants (RBL) also with special training in major
incident management are available on a 24/7 basis.
Every time a contact is taken between SOS Alarm and the RTiB, data concerning this incident
and the actions that resulted are entered into a web-based registry (Saltwater TM) [10]. These
data were reviewed and analyzed for a 3-year period. The data concerning hospital-related
incidents and their impacts on that hospital´s or adjacent hospital´s ordinary activities were
extracted and evaluated. The causes of subnormal capacity at affected hospitals were then
divided into following groups; hospital bed shortage (no details specified), bed shortage at
intensive care unit, bed shortage at ordinary wards, emergency departments overcrowding and
technical dysfunction at radiology departments

Results

There were an increasing number of hospital-related incidents between 2006-01-01 and 2008-
12-31, leading to ED-overcrowding and ambulance diversions. Four incidents were registered
in 2006, of which one was due to bed shortage at intensive care units, one bed shortage at
ordinary ward and two due to technical dysfunction at a radiology department. In these
occasions ordinary patients were referred to other hospitals directly from ED, while critically
ill patients already admitted or on their way to the ED by ambulances, were transported to
other hospitals. The number of incidents has then steadily increased during 2007 and 2008,
reaching its peak at 61 incidents in 2008, which is fifteen times higher than that in 2006
(Table 1, Figure 1). During the same period, besides 61 healthcare related missions, 1046
other regional (e.g. traffic accidents, sport events), national (e.g. storm, flooding), and
international (e.g. terrorist actions, evacuation of Swedish citizens from war zones), incidents
were also entered into the PKMC registry.
Bed shortage at intensive care units could either be due to high inflow of operated patients or
high admission of critically ill patients (in need of assisted ventilation). The higher rate of
operated patients was directly related to higher number of planned operations and
simultaneous increasing in number of emergency cases. These numbers changed in 2008 to
35% and 65% for bed and respirators shortage, respectively. The lack of hospital beds at
ordinary wards was mainly due to overloaded wards. The impact on individual patients or
patients groups or the number of patients affected could not be assessed by analyzing
available data. These incidents, however, led to a total number of 350 actions undertaken by
the center. The actions undertaken were consultative, informative and supportive. However, if
necessary, the centre intervenes to coordinate and redistribute regional resources by
contacting hospitals, emergency departments, and prehospital organizations. Consequently,
unaffected patients and healthy individuals were advised to visit their general practitioners
healthcare centers or other hospitals. Current ambulance transports were diverted and planned
transports were directed to other hospitals. There was no information about the severity of
diseases in transported patients; however, critically ill patients were transported to the nearest
hospitals. The active time spent for coordinating and resolving these incidents was 21188 min
(354 hrs or 45 working days á 8h). The active reporting and writing time was 487 min.
In order to find out if hospital-related incidents are hospital-dependent, the number of
incidents per hospital was calculated. In 2006, only three hospitals in the Region Västra
Götaland, with various sizes and capacities, were involved. However the number of hospitals
reporting such incidents in the region increased during 2007 and 2008; with the highest
increase in number of incidents in the smaller hospitals. Among hospitals with 24 h
emergency departments, the smallest hospital (hospital D) was the one affected most (Table 2,
Figure 2).

Discussion

The purpose of this work was to analyze the causes of the increasing number of hospitalrelated
incidents in Region Västra Götaland of Sweden and their impacts on the prehospital
and hospital preparedness in case of major incidents. In our study the alert is initiated by the
affected ED requesting the EMS dispatch centre to divert patients transported by ambulance
to other EDs. One limitation to this study is the lack of possibility to measure the impact of
ambulance diversions on individual patients or patients groups. The main cause of hospital related incidents in this report was labeled as ED-overcrowding. There is however no
universal definition for ED-overcrowding, as each hospital might have its own definition.
Disasters seldom occur, but if they strike a fast and effective response from healthcare
services is expected. An increasing number of reports on incidents when emergency hospitals,
for different reasons, cannot operate at their normal capacity are a matter of concern for
patient safety as well as disaster response preparedness [7]. In the available literature hospital
bed shortage and ED downsizing are reported to be some of the causes of ED-overcrowding
leading to impaired responsiveness and ambulance diversions [4, 6, 8-9, 11-12]. In our study,
we could also show that hospital bed shortage and technical dysfunction at radiology
departments, beside the increasing number of patients at EDs are the main reasons for EDovercrowding in our region. Our findings (Table 1, Figure 1) are consistent with those earlier
reported. Like in many other parts of the world, reduction of hospital beds and corresponding
staff in combination with increasing number of out-patients treatments and coordination of
activities between nearly located hospitals, have been some of the solutions to handle the
economical constrain on the healthcare systems [9, 11, 13]. The mean length of hospital stay
(LOS) has been reduced in Sweden, as well as other Scandinavian countries, having the
lowest LOS worldwide [5, 14]. Although these measures all seem to be logical steps taken to improve healthcare effectiveness and reducing the costs, they also, in a negative way, affect
the surge capacity of a hospital. Such capacity in hospitals is necessary for proper
management of extraordinary incidents and is influenced by 3 essential elements; staff,
supplies/equipment, and structure [15-16]. Structure refers to both location for patients and
the organizational infrastructure. A key to a successful major incidents response of a hospital
is an ED that is able to effectively sort (triage) the casualties, continue or start lifesaving
treatment and rapidly transfer patients to facilities for definitive treatment within the hospital.
If this key function is overcrowded already at the onset of a disaster response, the outcome for
the patients will be suboptimal. It is already reported that ED-overcrowding is associated with
both space and staff shortage [4, 7, 17-18].
Hospital bed occupancy of > 90% has been shown to correlate with a blocked access to the
wards, defined as patients waiting in the ED for more than 8 h when the decision has been
made to admit them [4, 19-21]. For severely ill patients this consequently leads to initiation of
extra measures e.g. multiple testing, interventions and administration of drugs during their
prolonged stay in the ED [4, 7, 19-20]. In such situations the ED serves as a holding area for
admitted patients, sometimes remaining for more than 24 h, due to the lack of beds [4]. This
even includes patients in need of beds at the intensive care units. Earlier reports indicate that
the average waiting time for an inpatient acute or critical care bed in the USA EDs has nearly
been doubled (> 6 h) in hospital with consistently overcrowded ED. The results, besides
missed diagnoses, poor outcomes, prolonged pain and suffering for some patients, long
waiting times, patient dissatisfaction, more ambulance diversions, lower physician and staff
productivity and higher levels of frustration among medical staff, are higher hospital costs and
longer LOS [2, 11-13, 21].
In addition many patients in the early time period of their diseases may leave ED due to long
waiting time, without treatment. Curable disease may then become more critical and incurable
when they return [4]. Delay of > 6 h in bringing ED patients in critical condition to intensive
care unit has also shown to increase hospital LOS and result in higher intensive care unit and
hospital mortality [20].
Long-lasting hospital closure are associated with significant but temporary increase in
ambulance diversions to the nearest ED. Fewer EDs and increasing number of patient visits
over time, may also cause ED-overcrowding and consequent ambulance diversions [9, 22].
Ambulance diversion has a huge impact on public health, since it may place the patient at risk
for poor outcome, prolonged pain and suffering. Ambulance diversion results in increasing
transport time between hospitals, delayed treatments and may also increase mortality in
severely injured trauma patients [7, 9, 22]. It also results in significant loss of hospital revenue
due to the throughput delays that prevent the use of existing bed capacity for additional
patient admissions [23]
In conclusion hospital-related incidents are by no means extraordinary incidents, but part of
the ordinary shortcoming of the healthcare system caused, among others, by reduction in
number of hospital beds, downsizing and/or closure of hospitals EDs. Such measures results
in overcrowding of EDs and ambulance diversions. They also endanger patient´s safety and
may increase in-hospital mortality. It counteracts medical preparedness by minimizing the
surge capacity. In the context of disaster preparedness this problem must be further studied
and properly addressed by our political decision makers (24)

References

1. Prehospital and Disaster Medicine. Västra Götalandsregion, Sweden (2009).
[http://www.vgregion.se/sv/Regionkansliet/Prehospitalt-och-Katastrofmedicinskt-
Centrum/In-English/]
2. Richardson DB. Reducing patient time in the emergency department. MJA 2003, 179:
516-7
3. McConnell KJ, Richards CF, Daya M, Bernell SL, Weathers CC, Lowe RA. Effect of
Increased ICU Capacity on Emergency Department Length of Stay and Ambulance
Diversion. Ann Emerg Med 2005, 45: 471-8
4. Cowan R and Trzeciak S. Clinical review: Emergency department overcrowding and
the potential impact on the critically ill. Critical care 2005, 9: 291-5
5. Baer RB, Pasternack JS, Zwemer Jr FL. Recently Discharged Inpatients as a Source of
Emergency Department Overcrowding. Acad Emerg Med 2001, 8: 1091-94
6. Hess EP, Wells GA, Jaffe A, and Stiell IG. A study to derive a clinical decision rule for
triage of emergency department patients with chest pain: design and methodology.
BMC Emerg Med 2008, 8: 3 (1-10)
7. Kaji AH, Koenig KL, Lewis RJ. Current Hospital Disaster Preparedness. JAMA 2007,
298: 2188-90
8. Fatovich DM, Hirsch RL. Entry overload, emergency department overcrowding, and
ambulance bypass. Emerg Med J 2003, 20: 406-9
9. Sun BC, Mohanty SA, Weiss R, Tadeo R, Hasbrouck M, Koenig W, Meyer C, Asch S.
Effects of Hospital Closure and Hospital Characteristics on Emergency Department
Ambulance Diversion, Los Angeles County, 1988 to 2004. Ann Emerg Med 2006, 47:
309-16
10. Saltwater AB, Sweden (2009). [http://www.saltwater.se
11. Estey A, Ness K, Saunders LD, Alibhai A, Bear RA. Understanding the causes of
overcrowding in emergency departments in the Capital Health Region in Alberta: a
focus group study. CJEM 2003, 5: 87-94
12. Fatovich DM, Nagree Y and Sprivulis P. Access block causes emergency department
overcrowding and ambulance diversion in Perth, Western Australia. Emerg Med J
2005, 22: 351-4
13. Baylay MD, Schwartz JS, Shofer FS, Weiner M, Sites FD, Traber KB, Hollander JE. The
financial burden of emergency department congestion and hospital crowding for
chest pain patients awaiting admission. Ann Emerg Med 2005, 45: 110-17
14. OECD Health Data (2008). [http://www.oecd.org/]
15. Barbisch DF, Koenig KL. Understanding surge capacity: essential elements. Acad
Emerg Med 2006, 13: 1098-102
16. Kaji AH, Lewis RJ. Hospital disaster preparedness in Los Angeles County. Acad
Emerg Med 2006, 13: 1198-203
17. Koenig Kl, Cone DC, Burstein JL, Camargo CA Jr. Surging to the right standard of
care. Acad Emerg Med 2006, 13: 195-8
Derlet WR, Richards JR, Kravitz RL. Frequent Overcrowding in U.S. Emergency
Departments. Acad Emerg Med 2001, 8: 151-55
19. Sprivulis PC, Da Silva JA, Jcobs IG, Frazer ARL, and Jelinek GA. The association
between hospital overcrowding and mortality among patients admitted via Western
Australian emergency departments. MJA 2006, 184: 208-12
20. Chalfin DB, Trzeciak S, Likourezos A, Baumann BM, Dellinger RP. Impact of delayed
transfer of critically ill patients from the emergency department to the intensive care
unit. Crit Care Med 2007, 35: 1477-83
21. Trzeciak S and Rivers EP. Emergency department overcrowding in the United States:
an emerging threat to patient safety and public health. Emerg Med J 2003, 20: 402-5
22. Pham JC, Patel R, Millin MG, Kirsch TD, Chanmugam A. The Effects of Ambulance
Diversion: A Comprehensive Review. Acad Emerg Med 2006, 13: 1220-27
23. Falvo T, Grove L, Stachura RS, Zirkin W. The Financial Impact of Ambulance
Diversions and Patient Elopements. Acad Emerg Med 2007, 14: 58-62
24. Cherry RA, Trainer M. The Current Crisis in Emergency Care and the Impact on
Disaster Preparedness. BMC Emerg Med 2008, 8: 7 (1-7)

Source : http://www.sjtrem.com/content/pdf/1757-7241-17-26.pdf

Trauma in Pregnancy

2009-06-15T11:55:00.003+07:00

Incidence

6% to 7%; “at no other time in a woman’s adult life is she more at risk for trauma than the third trimester of pregnancy”

Motor vehicle accidents:
number one cause of trauma during pregnancy; incidence distributed equally throughout pregnancy

Falls:
second most common cause of trauma during pregnancy; most occur during 20 to 30 wk gestation; patients have altered center of gravity, respiratory alkalosis (causing lightheadedness and dizziness), and laxity of pelvic ligaments, predisposing them to falls

Domestic abuse:
third leading cause of trauma during pregnancy; tends to be associated with significant fetal injury because trauma almost always directed toward abdomen and uterus

Trauma:
leading cause of nonobstetric death in women and leading cause of death in women of childbearing age; maternal survival leading predictor of fetal survival

Normal changes during pregnancy

all systems involved; cardiac output increases by almost 40% by 10 wk gestation and remains elevated until term; heart rate increases 10 to 15 beats/min by term (80-95 beats/min normal during pregnancy); systemic vascular resistance decreases; widened pulse pressure (due to larger drop in diastolic than in systolic blood pressure), low blood pressure

Supine hypotensive syndrome:
gravid uterus resting on inferior vena cava decreases venous return, can decrease cardiac output by up to 30%; placing patient in left lateral decubitus position increases blood pressure; if changing patient’s position contraindicated, manually displace uterus to left

Blood volume:
increases by 50% by 28 wk gestation; red blood cell mass increases 18% to 30%, resulting in dilutional physiologic anemia of pregnancy (obtaining previous medical records helpful); hemoglobin and hematocrit (H&H) lowest at 30 to 34 wk; pregnant women can lose 10% to 20% of blood volume acutely without change in vital signs, 33% if blood loss gradual (fetus probably will not survive; increased blood volume needed to feed fetus)

Leukocytosis of pregnancy:
hormonally mediated; average white blood cell count 12,000 to 18,000/mm³(almost all polymorphonuclear leukocytes, making it difficult to assess infection), reaching up to 25,000/mm³during labor

Hypercoagulable state:
prevents or decreases effects of maternal hemorrhage; predisposes patients to thromboembolic disease (highest risk in third trimester and first month postpartum); prothrombin time (PT) and partial thromboplastin time (PTT) shortened; fibrinogen almost doubles (normal reading probably early indicator of disseminated intravascular coagulation [DIC])

Pulmonary changes:
minute ventilation increases up to 40%; normal PCO ₂of woman in third trimester approximately 30 mm Hg (bagging patient to 40 mm Hg will cause fetal and maternal acidosis and fetal distress)

Diaphragm:
abdominal contents pushed cephalad; decreased functional residual capacity; chest tube should be placed 1 to 2 intercostal spaces higher than usual; diaphragm can rise as much as 4 cm; bowel motility and gastric emptying decreased (general relaxation of gut); decreased lower esophageal sphincter pressure (effect of progesterone; causes reflux); increased gastric acid production; empty stomach using nasogastric (NG) tube to decrease risk for aspiration; alkaline phosphatase markedly increased (placental origin); uterus largest intra-abdominal organ by third trimester (not problem in blunt trauma but significant injuries possible with penetrating trauma); due to stretched peritoneum and abdominal muscles, patients often show minimum signs of peritoneal irritation despite as much as liter of blood in abdomen

Genitourinary system:
uterus can increase to 1200 g by third trimester (normally 60-80 g); blood flow increases from 60 mL/min to 600 mL/min (every 10 min, entire circulating blood volume of mother goes through uterus; patient can exsanguinate in approximately 10 min); always admit pregnant patients with pyelonephritis because natural hydroureter and hydronephrosis increase risk of seeding blood stream; glomerular filtration rate increases by 50%, blood urea nitrogen (BUN) and creatinine drop by approximately 50%; in pregnant trauma victim, borderline or high creatinine indicates significant renal injury until proven otherwise

History
last menstrual period (always obtain pregnancy test on every woman of childbearing age in trauma); estimate length of pregnancy; if fetus not viable, direct all resuscitative measures to mother; if fetus viable, must alter treatment; patients with history of cesarean delivery at increased risk for uterine rupture

Physical examination
estimate fundal height (if greater than or equal to 2 finger breadths above umbilicus, fetus probably viable); look for uterine tenderness, uterine contour, and contractions (signs of abruption or uterine rupture); check for fetal heart rate by stethoscope (by 18-20 wk), Doppler imaging (10-14 wk), or transabdominal or transvaginal ultrasonography (6-7 wk); normal fetal heart rate 120 to 160 beats/min (if outside this range, fetal distress until proven otherwise); fetal hemodynamics most sensitive indicator of maternal hemodynamics

Pelvic examination
contraindicated in patients in third trimester with vaginal bleeding; if no contraindications, perform sterile speculum examination looking for perineal and vaginal lacerations and urethral injury; examine vagina for open os, light urethral dilation, crowning; measure pH (alkaline pH suggests ruptured membranes; ferning in fluid sample from posterior fornix more specific for amniotic fluid)

Blood
obtain blood type and screen on all pregnant patients beyond 12 wk gestation; complete blood count (CBC) and H&H low

Kleihauer-Betke test
no longer recommended for all pregnant trauma patients; identifies presence and estimates gross amount of fetal red blood cells in maternal circulation (no relation to severity of injury); obtain only on Rh-negative mothers to quantify how much RhoGAM (Rh_O[D] immune globulin) to give; 300 µg of RhoGAM protects mother from 30 mL of fetal-maternal hemorrhage; Kleihauer-Betke test can help determine whether more RhoGAM needed)

Coagulopathy studies
if mother has significant trauma, draw baseline blood sample to determine whether she is going into DIC (clue to abruption)

Imaging studies
“if the woman was not pregnant and she needed the x-rays, get the x-rays”; “the risk of missing the injury is much, much greater than any risk of radiation exposure to the fetus”; no significant risk of increased teratogenic effect if fetus exposed to <10>15 rads; fetus most vulnerable in weeks 2 to 7; unlikely x-rays cause harm to fetus at >20 wk gestation; shield pelvis and limit number of views if possible (eg, to clear C-spine, use only lateral, anteroposterior, and odontoid views, omit oblique view); routine pelvic films no longer indicated in trauma patients

Ultrasonography:
key to evaluation; determine fetal heart rate (good indicator of how fetus and mother are doing); determine fetal age; only 50% sensitive for detecting abruption

Abdominal ultrasonography:
perform focused assessment with sonography for trauma (FAST) examination; should not have fluid in cul de sac or between liver and peritoneum; if FAST examination positive and patient hemodynamically unstable, send patient to operating room (OR); if FAST positive and patient stable, send patient for computed tomography (CT); if FAST negative, observe or scan again in 30 min

Cranial CT:
be sure to shield fetus

CT of abdomen and pelvis:
causes more radiation exposure; reduce radiation by performing 3-cm cuts instead of 1-cm cuts (some sensitivity lost but not enough to significantly alter interpretation of examination); can see uterine rupture and abruption; not good for detecting fetal injury

Angiography:
performed for therapeutic as well as diagnostic reasons; contrast not contraindicated in pregnancy

Diagnostic peritoneal lavage (DPL):
indicated only when CT and ultrasonography not available; use supraumbilical open approach; does not detect retroperitoneal injuries

Fetal monitoring:
if fetus <23>23 wk, use continuous cardiotocographic monitoring

Cardiotocographic monitoring:
measures fetal heart rate and uterine contractions; best test for abruption (100% sensitive); have low threshold for performing this test (reassures mother); if no uterine contractions in 2 hr, can send patient home safely; if even one contraction, monitor for another 2 hr

Management
administer high-flow 100% O₂(benefits fetus; fetus has O₂-hemoglobin dissociation curve different from that of mother); if fetus >20 wk gestation, place mother in left lateral decubitus position if not contraindicated; if contraindications present, displace uterus to left; no role for military antishock trousers (MAST; inappropriate and may be harmful); cardiac monitor for mother, intermittent monitoring for fetus if <23>23 wk

Fluids:
2 large-bore intravenous (IV) lines (use upper extremities if possible); restoring circulating volume initial goal; Ringer’s lactate preferred over normal saline; give blood transfusion early (fetus will die if physician waits for signs of shock)

NG tube:
empty stomach; pregnant patients at increased risk for aspiration

Vaccinations:
tetanus toxoid and tetanus immune globulin safe in pregnancy; indicated if vaccinations not up-to-date

Medications:
RhoGAM for Rh-negative mothers (give if >12 wk gestation); safe to give penicillin, Timentin (ticarcillin and clavulanate), Augmentin (amoxicillin and potassium clavulanate), cephalosporins, erythromycin, clindamycin, nitrofurantoin; stay away from tetracyclines (can cause teeth and bone problems in fetus, maternal toxicity), fluoroquinolones (can cause cartilage problems and arthropathy in fetus), sulfa agents (in third trimester; cause kernicterus), trimethoprim (folate inhibitor), chloramphenicol; Tylenol (acetaminophen) safe; make sure patient not taking aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs; can cause premature closure of ductus arteriosus); narcotics safe in pregnancy, but avoid codeine in first trimester (associated with increased incidence of cleft palate); can give Demerol (meperidine) or morphine

Abruption
1% to 5% incidence in minor trauma, 20% to 50% in major trauma; second leading cause of death in fetuses (death of mother most common cause); patients classically present with vaginal bleeding and abdominal pain; not all have classic presentation (bleeding may be hidden behind placenta; pain may be minimal or patient may have distracting injuries); consider abruption if mother has hypotension and no apparent sign of blood loss (uterus can hold 2 L of blood), fundal height much higher than expected for dates, or uterus expanding; cardiotocographic monitoring best test; increasing use of D-dimer test to detect early DIC; fetus with <25%>50% separation unlikely to survive unless delivered immediately; obstetric specialist must make decision on what to do with abruptions of 25% to 50%; do not let absence of vaginal bleeding prevent diagnosis of abruption

Uterine rupture
rare (incidence <1%);>

Traumatic cardiac arrest
if fetus <23>23 wk gestation, obtain obstetric consult and consider early resuscitative thoracotomy; do not cross-clamp aorta.

Source : http://emcrit.org/030-064/031-trauma.pregnant.htm

Blast Injury

2009-06-15T11:30:00.002+07:00

Trauma caused by explosions traditionally has been divided into the injury caused by the direct effect of the blast wave (primary injuries); the effects caused by other objects that are accelerated by the explosive wave, (secondary injuries); the effects caused by movement of the victim (tertiary injuries); and miscellaneous effects caused by the explosion or explosives.

High-Order Explosives

High-order explosives are chemical materials that have an extremely high reaction rate. This reaction often is called a detonation. Examples of high-order explosives include nitroglycerin, dynamite, C-4, picric acid, Semtex, ammonium nitrate fuel oil mixture (ANFO), trinitrotoluene (TNT), and pentaeruthrotetranitrate (PETN).

When an HE detonates, it is converted almost instantaneously into a gas at very high pressure and temperature. For example, the major ingredient in Composition C-4 (Cyclotrimethylenetrinitramine or RDX [Royal Demolition eXplosive]) can generate an initial pressure of more than 4 million pounds per square inch (4x10E6 PSI).13 These high pressure gases rapidly expand from the original volume and generate a marked pressure wave—the blast wave that moves outward in all directions. The result is a sudden shattering blow to the immediate surroundings.

HEs further are categorized as primary and secondary high explosives. The primary HE is very sensitive, can be detonated very easily, and generally is used only in primary and electrical detonators. Secondary HEs are less sensitive, require a high energy shock wave to achieve detonation, and generally are safer to handle.

The blast wave refers to an intense rise in pressure—often called over pressure—that is created by the detonation of a high explosive
This increase in pressure can be so abrupt that it can shatter materials—also known as a shock wave. This effect is termed brisance and varies from one HE to another. Because the explosive gases continue to expand outward, the pressure wave rapidly deteriorates into an acoustic wave. Until the wave deteriorates enough to completely engulf the body simultaneously, tissue damage will depend on both the magnitude of the pressure spike and the duration of the force (represented by the area under the curve).

A blast wave that would cause only modest injury in the open can be lethal if the victim is in a confined area or near a reflecting surface such as a solid wall or a building.9 If the pressure wave is near a solid barrier, the pressure exerted at the reflecting surface may be many times that of the incident blast wave.

Low-Order Explosives

LEs are designed to burn and subsequently release energy relatively slowly. These explosives often are called propellants because the most common use is to propel a projectile through a barrel. The principal military uses for LEs are as propellants and in fuses. Typical improvised LEs include pipe bombs, gunpowder, black powder, and petroleum-based bombs such as Molotov cocktails or gasoline tankers. Since LEs do not form shock waves, they do not have the quality of brisance.

Three Possible Mechanisms of Injury of Primary Blast Injury

The first mechanism of injury usually described as the etiology of primary blast injury is the implosion of gas-filled spaces as the high pressure blast wave compresses them.18,19 This theory states that the organs that are most vulnerable to blast injury are those containing air because the air readily is compressed. Hollow organs are compressed and disrupted by the rapid external pressure increase. The resulting force causes shearing of vascular beds, ear damage, pulmonary contusions, pneumothorax, and gastrointestinal (GI) hemorrhage. In some cases, the force of a pressure wave can be significant enough that it forces air into a blood vessel, creating air emboli. There isn’t enough time during the passage of the overpressure phase of the blast wave for gas to transfer from the lungs to the outside world through the trachea.20

The second possible major mechanism of primary blast injury often is termed spalling. This is thought to occur when a blast wave moves from a dense medium such as water to a less dense medium such as air. This often is compared to the effect of striking the outside of a rusty bucket with a hammer and watching the flakes of rust fly off the inside of the bucket. In human tissues, the transfer of reflected blast injury through the dense substrates such as muscle and liver into the less dense material of the GI tract and lungs may cause spalling. Spalling also is believed to occur when the blast wave transits from the rib cage into the lung.

The third possible mechanism of primary blast injury is the inertial effect related to the differences in tissue density and speed of the blast wave through the tissues of different densities. This may be the most important effect of the blast injury and currently is thought to be the major cause of primary blast injuries. The differences in speed of movement result in shearing and tearing forces expressed as a stress wave propagated into the underlying tissues.21,22 The resulting forces exceed the tensile strength of the material and cause shearing of vascular beds, pulmonary contusions, and GI hemorrhages.23

The true mechanism of primary blast injury likely is some combination of these theoretical mechanisms. Of these, the shearing and tearing forces appear to fit best. Primary blast injury is common in the ear, the respiratory tract, and the GI tract.

Ear Damage

Of the three organ systems, the ear is the most easily damaged, but it also is the easiest to protect. The structures of the ear are designed to collect and magnify sounds, so that the tympanic membrane moves with the sounds. Unfortunately, the ear’s structures also collect and magnify pressure waves. At a pressure of about 35 kilopascals (5 PSI), the human eardrum may rupture. With an overpressure of 100 kPa (14 PSI) almost all eardrums rupture. The eardrum most frequently ruptures into the inferior pars tensa. At lesser pressures, the overpressure may cause hemorrhage into the drum without a rupture. With extremely high pressures, the drum may be destroyed and the ossicles dislocated or fractured.

Rupture of the eardrum will cause pain, hearing loss, and may cause tinnitus. Eardrum perforations, hearing loss, and dizziness may interfere with daily activities and may affect the individual’s quality of life.24

Physical examination may reveal blood in the external canal. Examination of the tympanic membrane with an otoscope may show evidence of the perforation.

It often is held as gospel that rupture of the tympanic membrane is a marker for serious gastrointestinal or pulmonary injury. If the patient has ear protection, this may not be the case. Likewise, if the patient is in the water with his head out of the water, the tympanic membranes may not be exposed to an underwater blast wave. Isolated eardrum rupture does not appear to be a good marker of either concealed pulmonary blast injury or poor prognosis.25

Auditory barotrauma is quite common in blast injuries. In the Oklahoma City bombing, the incidence of auditory injury was 35%.1,13 This does not count those patients with partial, temporary hearing loss or those who complained of tinnitus for an extended period of time.24

Pulmonary Damage

The lungs have been considered to be the non-auditory organs most at risk for suffering primary blast injury. Blast lung is a direct consequence of the supersonic pressure wave generated by an HE.26 (See Figure 4.) It is the most common fatal injury caused by the primary blast injury among the initial survivors of the explosion. These lung injuries may not be apparent externally or immediately, but may lead to death if not diagnosed and treated promptly. An overpressure of about 40 PSI causes lung injuries.

Damage to the lungs can include pulmonary contusions with or without a laceration, and/or pulmonary barotrauma such as pneumothorax, pulmonary interstitial emphysema, pneumomediastinum, or subcutaneous emphysema.

It is best to assume that if a patient is wheezing after a blast injury, that the wheezing is due to a pulmonary contusion. Other causes of wheezing may be pulmonary edema from myocardial contusion or infarction, or exacerbation of underlying disorders such as asthma or chronic obstructive pulmonary disease (COPD).

The most common lung injury associated with a blast wave is a pulmonary contusion. This may take the form of micro-hemorrhages with perivascular/peribronchial disruption. It appears to be more common on the side closest to the explosion, but this may be influenced by the geometry of the surrounding area and reflected energy.27-29 The alveolar wall may be torn, causing a blood-filled emphysematous change to the lung. Pulmonary contusions may develop with or without a pulmonary laceration.

Pulmonary contusions impair gas exchange at the alveolar level. The changes seen on microscopic examination closely resemble the pulmonary contusions seen in non-penetrating blunt chest trauma.

Parallel thoracic ecchymoses, once thought to be along the ribs, may be seen with larger blast loads.20,28 These ecchymoses parallel the intercostal spaces. Rib fractures may occur due to blast injury, but are much more likely to be due to secondary or tertiary blast injury mechanisms, at least in survivors.29,30

The patient may have minimal or no symptoms initially. The patient also may complain of chest pain or respiratory distress. Signs of blast lung usually are present at the time of the initial evaluation, but have been reported as late as 48 hours after the explosion occurs.

The overpressure may cause pulmonary barotrauma, including pneumothorax or pneumomediastinum. The patient may develop pulmonary interstitial emphysema, subcutaneous emphysema, and systemic air embolism with larger blast loads.20,22,23 Significant bronchopleural fistulae may lead to air embolism. Air emboli may present in a variety of ways, including shock, myocardial infarction, spinal infarction, or cerebrovascular accident.

Blast lung is characterized clinically by the triad of apnea, bradycardia, and hypotension. The clinician should suspect blast lung in any victim who presents with dyspnea, cough, hemoptysis, or chest pain following blast exposure.

A simple frontal chest x-ray is diagnostic for most cases of pulmonary barotrauma from blast. Blast lung produces a characteristic butterfly pattern on chest x-ray. The pulmonary injuries found may range from scattered isolated petechiae to confluent pulmonary hemorrhages. The radiographic evidence of pulmonary injury usually begins within hours of the explosion and begins to resolve within one week.31

Gastrointestinal Damage

GI injuries may not be apparent externally. They have a great potential to cause death and may be much more difficult to protect against.

GI injuries once were thought to occur with the same frequency as lung injury. A recent large Israeli case series found that abdominal injuries were seen only with massive trauma.32 In this series, all patients were injured from open air explosions. The patient may have a greater risk for GI injury when exposed to an underwater explosion.33

The GI injury of primary blast injury is inconsistent in presentation. It may consist of hemorrhage beneath the visceral peritoneum or may extend into the mesentery, colon, and cecum.27,28 Contused bowel may necrose and perforate several days after the initial trauma. The perforated bowel may be apparent immediately, or may perforate only after a delay of up to 48 hours.34,35

Pneumoperitoneum is a relatively rare complication of GI barotrauma.36 This complication has a wide differential diagnosis ranging from perforated viscus to simple dissection of air through the retroperitoneum.

The colon is the most common site of both hemorrhage and perforation.33 This is thought to be because the colon has the most bowel gas accumulation in the GI tract.

Solid organ laceration and testicular rupture also are seen due to primary blast injury, but are less frequent and often are associated with large blast loads.37 The most common solid organ lesions reported were subcapsular hematomas in the liver, spleen, and kidneys.31 Mesenteric, scrotal, and retroperitoneal hemorrhages have been reported.28

These lesions can lead to the clinical signs of absent bowel sounds, bright red blood per rectum, guarding, and rebound tenderness. The clinical symptoms can include abdominal pain, nausea, vomiting, diarrhea, and tenesmus. Blast injury to the GI tract should be suspected in anyone exposed to an explosion who has abdominal pain, nausea, vomiting, hematemesis, rectal pain, testicular pain, unexplained hypovolemia, or any finding compatible with an acute abdomen.

The clinician should be aware that the abundant high-velocity fragments associated with recent suicide bombs also may cause intra-abdominal injuries. These injuries certainly can include penetrating bowel injuries.38 Initial symptoms of penetration are the same as outlined above.

Brain Injury

Primary blast injury can cause concussion or traumatic brain injury, although this finding is difficult to differentiate from the concussion due to impact with another object. The clinician should be quick to consider computed tomography (CT) or magnetic resonance imaging (MRI) in these patients.

Cardiac Injury

Myocardial contusion may occur with arrhythmia or hypotension.39

Secondary Blast Injury

Secondary blast injury is caused by the bomb fragments and other debris that are propelled by the intense energy release of the explosion. (These fragments often erroneously are referred to as “shrapnel.” Shrapnel is the name for an artillery round containing multiple round lead balls that was designed during World War I by then-Lt. Shrapnel. This round essentially functions as a very large shotgun with several hundred half-inch lead balls.) (See Figures 5-7.) Conventional military explosives may create multiple fragments with initial velocities of up to 2500 m/second (8202 feet/second).40 (In contrast, the very fast moving M-16 round has a muzzle velocity of 2800 feet [853 meters] per second.)41

Glass causes many of the secondary blast injuries (up to 50% of all blast injuries). Victims who are peppered with glass often are difficult to distinguish from victims who are peppered with glass and have penetrating injuries.42

Secondary blast injuries may not be obvious initially. A seemingly small abrasion or wound may mask the entrance wound for a substantial fragment.

Up to 10% of blast survivors have significant eye injuries.43 (See Figure 8.) These injuries may be perforations from high-velocity projectiles. Glass is notorious for causing these ocular injuries. Window fragments often don’t kill, but they can cause blindness and ruptured globes. At the speed that explosively propelled fragments of glass travel, there is no time for the blink reflex to operate. These injuries may occur with minimal initial discomfort and may present days after the event. Symptoms include eye pain and irritation, foreign body sensation, alterations of vision, periorbital swelling, or periocular contusions. Signs can include loss of vision, decreased visual acuity, globe perforation or rupture, lid lacerations, and subconjunctival hemorrhage around the point of entry.

Tertiary Blast Injuries

Tertiary blast injuries are caused when the victim’s body is propelled into another object by the blast winds.20,44 Tertiary effects result from the bulk flow of gas away from the explosion. Blast winds can generate a body acceleration of more than 15 gs. They most often occur when the victim is quite close to the explosion.

This displacement of the victim can take place relatively far from the point of detonation if the victim is positioned in the path gases must take to vent from a structure, such as a doorway, window, or hatch. Likewise, if the patient is in an alley, magnification of the blast wind may occur due to the configuration of the buildings.

The deceleration caused by impact into a rigid structure causes the majority of injuries. A person who is flung into a fortified immovable object with a velocity greater than 26 feet/second (7.92 meters/second) has a mortality rate of about 50%.45 The most common injuries are fractures and closed head injuries. Isolated body parts may be broken, dislocated, or even amputated. Injuries from this mechanism also depend on what the victim hits in the environment and can range from simple contusions to impalement. Victims may tumble along the ground, sustaining abrasions, contusions, and “road rash.”

Miscellaneous Blast Effects (Quaternary Blast Injuries)

This category of injury includes burns from fire or radiation, crush injury associated with structural collapse, poisoning from carbon monoxide or other toxic products of the explosion, and inhalation of dust or chemicals from the explosion.

The unprotected human body can survive a blast with a peak overpressure of 30 PSI (206 kPa), but buildings and other structures collapse with the stress of only a few pounds per square inch. This means that people may survive the effects of the blast only to be injured by collapsing buildings.

The blast may be a vector for chemical and biological warfare agents. The effects of these agents on the body may well overshadow any part of the explosive energy.

Patients who have been exposed to a blast in an enclosed area should have carboxyhemoglobin levels obtained. Inhalation of irritant gases or dusts also may trigger wheezing in these patients.

Immediate Death

Fatal injuries may occur due to blast effects involving the head, chest, and abdomen and often are seen in victims who are close to the detonation.46 Indeed, in some of these victims close to the site of the blast, parts of the victim (or perpetrator) may become missiles that kill or wound other victims.47 Immediate death may occur from massive pulmonary bleeding with rapid suffocation despite good care. The patient may develop a massive air embolism or may sustain a significant brain injury. The patient may suffer a traumatic amputation and exsanguinate before help arrives. Finally, the patient may have a crush injury or impalement injury that causes rapid death before extrication can occur.

The field physician or paramedic should consider a patient dead in the field when:
there is an amputated body part without signs of life;
there are no effective respirations;
there is no palpable pulse; and
there are dilated pupils.
Persons with immediate, severe respiratory insufficiency that is caused by a blast effect have far less chance of survival.

Cardiopulmonary resuscitation (CPR) at the scene never is indicated. There will be too many injured, not enough medical providers, and no significant chance of successful resuscitation in this blunt trauma patient.

Evaluation and Management

Expect that the most severely injured patients will arrive after the less injured. The less injured often skip EMS and proceed directly to the closest hospitals. For a rough prediction of the number of “first wave” of casualties, double the first hour’s casualty count. Remember that a secondary device may be employed that can cause substantial additional casualties, which may include EMS, fire, police, and media.

Most of the injuries seen after a conventional explosive detonates are blunt, penetrating, and thermal trauma that is well known to prehospital providers, emergency physicians, and trauma surgeons.48 Much of this trauma includes soft-tissue, orthopedic, or head injuries.11,49,50 The approach to the casualty with blast-related injury, therefore, is the same as for any other trauma victim.

The first and most important step of management is assessment of life support needs and ensuring that the patient has an adequate airway, appropriate ventilation, and adequate circulation. A thorough physical examination then should be performed. The clinician should look for sentinel signs of potentially significant blast exposure. (See Tables 2 and 3.) Unfortunately, when the health care provider is faced with dramatic injuries such as amputations, fragment injuries, and multiple critically ill patients, it is altogether too easy to miss the subtle signs of blast injury. If the clinician does not consider the possibility of primary blast injury, the patient’s care may be complicated further.

Pulmonary

Blast lung is treated by correcting the effects of barotrauma if any is found. Gas exchange is supported. The provider should be aware that positive pressure ventilation may exacerbate pneumothorax and cause air embolism in the presence of bronchopleural fistula. The patient’s body should be positioned to ensure that the effects of air embolism are minimized.

In victims with mild respiratory distress, supplemental oxygen by nasal cannula is appropriate. Those patients with significant respiratory distress or hemoptysis should have an endotracheal tube placed. This is not without hazard, however.

Positive pressure ventilation markedly increases the possibility of both air embolism and pulmonary barotrauma. The provider should take the least invasive measure that still provides appropriate airway support in these patients.51 Avoid peak end-expiratory pressure (PEEP) and high ventilation pressures.

In one study using thoracic CT scans of patients with pulmonary contusion (not blast injury), patients with less than 18% contusion did not require intubation or ventilation.52 Patients with more than 28% contusion always required ventilation.

Because the combination of positive pressure ventilation and blast lung injury poses such a high risk for tension pneumothorax, some authors suggest bilateral prophylactic chest tubes after intubation. If the patient needs air evacuation, this becomes more desirable. If a patient with a blast lung injury abruptly decompensates, the clinician should presume that the patient has a tension pneumothorax and treat accordingly.

If the patient survives the blast lung and other trauma, there is a good chance that he will regain lung function within a year.53

Hypotension

Hypotension in blast injury victims can be due to several mechanisms:

blood loss due to wounds (otherwise not related to the cardiovascular system);
blood loss due to gastrointestinal hemorrhage;
blood loss due to intra-abdominal solid organ rupture;
hypotension from compression of vessels and heart by pneumothorax;
hypotension due to the cardiovascular effects of an air embolism; and
hypotension due to vagal reflexes.
The patient’s fluid volume should be supported without excessive fluid replacement. Often, blood products or colloid solutions should be used rather than crystalloid. Too much fluid replacement of course can cause increased respiratory distress as either congestive heart failure or acute respiratory distress syndrome.

Gastrointestinal

Blast injury of the GI tract can be managed in much the same way as blunt trauma of the abdomen. If the patient has an obvious penetrating wound of the abdomen, then urgent surgical management is indicated. If the patient is unconscious but hemodynamically stable or is conscious with abdominal complaints and is hemodynamically unstable, then fluid resuscitation should be undertaken. If the patient’s blood pressure stabilizes and remains stable, then a CT scan of the abdomen is appropriate. If the blood pressure does not improve, then urgent surgical management is indicated.

If the patient is conscious with abdominal findings and is hemodynamically stable, then an abdominal CT scan should be obtained. If the patient is stable, then an abdominal CT scan with oral and intravenous contrast is a reasonable screening procedure.

While abdominal CT scan is appropriately specific, it may not be sufficiently sensitive to identify hollow viscus injury.31 If patients who have been scanned continue to have signs of abdominal pathology, then a diagnostic peritoneal lavage is appropriate. If the effluent contains significant red blood cells, bacteria, bile, or fecal matter, then urgent laparotomy is indicated. CT must precede peritoneal lavage or false positive air and fluid will be introduced.

In the context of a mass casualty incident, there should be a low threshold for laparotomy when a hollow viscus injury is suspected. Close observation may not be available because of the number of casualties. Clinical signs and symptoms of early bowel injury, particularly in children, may be so subtle as to be easily missed in the patient with multiple injuries.54

Wound Management

For lacerations and fragment wounds, avoid primary closure and consider the use of delayed primary closure in these wounds. There is about an 80% rate of infection when fragment wounds are sutured. All debris that is flung by the explosion is not radiopaque, and the wise provider carefully should explore injuries and consider CT, ultrasound, or MRI of wounds to evaluate for radiolucent foreign bodies. Update the tetanus status as appropriate.

Air Embolism

Air embolism should be treated as soon as the diagnosis is considered. The first step should be to place the patient on high flow oxygen. Next, the patient should be positioned properly. The usual recommended positioning is the left lateral decubitus position with the head down. If only one lung is injured, the injured lung should be placed in the dependent position (which may override the left side down position described above.) By placing the injured lung down, the alveolar oxygen pressure is lower with a subsequent decreased risk of air entering the lungs. It should be noted that a recent review article about gas embolism opined that a flat position would be more appropriate.55 The review article also discusses use of increased fluids, heparin, and corticosteroids as treatments for gas embolism. This review article does not cite any work about blast injury in its bibliography and does not mention blast lung injury as an etiology of gas embolism. The author feels that there isn’t enough evidence specific to blast lung as an etiology of gas embolism to make a more specific recommendation.

The definitive treatment for air embolism is hyperbaric oxygenation, which often is not available in a timely fashion. Hyperbaric oxygenation will reduce the bubble size (by Boyle’s gas law), increase tissue oxygenation, and increase the solubility of the gas. The United States Navy protocols for gas embolism and decompression sickness would be an appropriate reference.

Disposition

The disposition of these patients depends on the injury sustained by each victim. Those who were close to the center of the explosion should be considered for observation for at least 24 hours.

Source : http://emcrit.org/030-064/030-blastinj.htm

Severe Abdominal Pain in a Young Girl After a Hug

2009-06-13T10:26:00.004+07:00

A 16-year-old girl in Macedonia presents to the local emergency department (ED) with a sudden onset of severe abdominal pain following what she describes as a "bear hug from a friend." The pain began a couple of hours before arrival to the ED. She describes the pain as sharp, constant, most intense in the right upper quadrant, and radiating to her right shoulder. The patient also reports having mild, dull abdominal discomfort and a feeling of progressive abdominal fullness for the past few months, but she has not sought medical attention for these symptoms. She also complains of having a diffuse, itchy rash that seems to have appeared around the same time as the onset of the abdominal discomfort. The patient has no history of food allergy and has not eaten any new foods before this episode. She denies having any fevers, nausea, or abnormal bowel movements. She has not had any changes in her skin coloration. She reports occasional use of acetaminophen in the last 2 weeks for the abdominal discomfort, but she is not otherwise taking any regular medications. She has no chronic medical conditions or past surgical history. She reports no significant family history. There are 2 dogs in her house which she cares for, but no other pets are present.

On physical examination, the patient is in obvious discomfort. Her body temperature is 99.1°F (37.3°C), she has a blood pressure of 110/70 mm Hg, and her pulse is 110 bpm. Her skin is pale and without jaundice, but she does have a diffuse urticarial rash that is most prominent on the trunk and proximal extremities. She appears well-nourished and well-developed. Her chest has symmetrical movements during respiration and clear breath sounds are noted on auscultation. Her heart sounds are normal, with a regular rhythm and no detectable murmurs. A firm mass overlying the liver edge in the right upper quadrant is noted on palpation. The entire upper abdomen is markedly tender and rigid, particularly in the right subcostal region.

The laboratory testing is remarkable for leukocytosis, with a white blood cell (WBC) count of 18.6 × 10³/µL (18.6 × 10⁹/L) and 40% neutrophils (0.40), 22% lymphocytes (0.22), 8% monocytes (0.08), and 21% eosinophils (0.21) (normal ranges: WBC, 4.5-11 × 10³/µL; neutrophils, 40-70%; lymphocytes, 22-44%; monocytes, 4-11%; eosinophils, 0-8%). An elevated total bilirubin level of 1.98 mg/dL (33.8 μmol/L) was also noted (normal range, 0.3-1.0 mg/dL). Her aspartate aminotransferase (AST; also known as serum glutamic oxaloacetic transaminase [SGOT]) is 101 U/L and her alanine aminotransferase (ALT; also known as serum glutamic pyruvic transaminase [SGPT]) is 104.7 U/L. Her hematocrit and platelet counts are normal. An upright radiograph of the abdomen shows a nonspecific bowel gas pattern and no findings of pneumoperitoneum. An ultrasound is performed for a suspicion of possible gallbladder disease; it reveals a large hypoechogenic zone in the liver, with irregular margins and a small amount of free fluid around the liver. A computed tomography (CT) scan of the abdomen is subsequently performed (see Figures 1 and 2).

What is the diagnosis?

Hepatic hydatid cyst rupture

Acute cholecystitis

Cholangitis
Hepatocelular Carsinoma

Discussion

Figure 2.

The CT scan of the abdomen reveals a fluid-filled cystic mass with an irregular margin in the fourth segment of the liver. The mass communicates with the gallbladder and is associated with a small amount of free fluid around the liver and in the peritoneal cavity. These imaging findings in the setting of eosinophilia, an associated allergic reaction, and a history of acutely worsening abdominal pain with sudden pressure applied to the abdomen, are consistent with a ruptured hydatid cyst.

Echinococcosis, otherwise known as hydatid or alveolar cyst disease, is an infection caused by the larval stage of small taeniid-type tapeworms of the Echinococcus species. Human disease is acquired by ingesting viable parasite eggs, usually in food. There are 3 forms of human hydatid disease. Echinococcus granulosus and Echinococcus vogeli produce unilocular cystic lesions, whereas Echinococcus multilocularis produces multilocular alveolar lesions that are locally invasive. E vogeli is uncommon and occasionally found in the South American highlands. E multilocularis is more common than E vogeli, but it is probably not the etiologic organism in this case. It is different from E granulosus in that it remains in a proliferative phase, is always multilocular, and survives in wild canines as the definitive hosts and small rodents as the intermediate hosts.

The adult form of E granulosus (3-5mm long) inhabits the intestines of definitive hosts (which are most commonly dogs, but it can also be found in coyotes or wolves). It has 3 proglottides, including immature, mature, and gravid. The gravid proglottid splits into eggs that can be found in the feces of the definitive host. Intermediate hosts, such as humans, sheep, cattle, and goats, get infected by consuming plants that are contaminated by the feces of affected animals or by direct contact with an affected animal. After humans ingest the eggs, they hatch into embryos in the small intestine. The embryos penetrate the intestinal mucosa, enter the portal circulation, and are carried to the liver.^[3,4] Some are destroyed in the liver while others form into hydatid cysts. A small percentage of the eggs may pass through the liver and form cysts in other parts of the body, including the lungs, central nervous system (CNS), spleen, and pancreas. After the developing embryos localize in a specific organ, they transform and develop into larval echinococcal cysts.^[1] This process is referred to as primary echinococcosis.

The cyst is composed of 2 layers: the endocyst, which is filled with clear fluid, and the pericyst, which is a fibrous capsule that develops as a host response to the growth of the echinococcal cyst.^[3,4] Nutritive substances that contribute to the cyst's growth pass through the pericyst. The pericyst encompasses the endocyst, which is of larval origin.^[2] It is composed of an outer laminated layer, or hyaline membrane, and an inner multipotential germinal layer. Daughter cysts develop from the inner aspect of the germinal layer, as do germinating cystic structures called brood capsules. New larvae, called protoscolices, develop in large numbers within the brood capsule. The cysts typically expand slowly over a period of years, at a rate of approximately 1-3 cm per year.^[4]

In primary echinococcosis, approximately two-thirds of patients experience liver hydatid cysts. In 85% of cases, the cysts are located in the right lobe of the liver.^[2] The second most commonly involved organ is the lungs. Because of the slow rate of growth of the cysts, patients with simple uncomplicated cysts are usually asymptomatic. The cysts are often discovered incidentally on routine imaging studies. In patients with liver echinococcosis, the most common symptoms are mild abdominal pain and an upper abdominal mass . On physical examination, hepatomegaly may be present in addition to a palpable abdominal mass. In about 10% of the patients, an elevated eosinophil count is noted.^[1]

More dramatic findings are present when complications of hydatid cyst disease occur. The most frequent complication in hepatic echinococcosis is intrabiliary rupture, which occurs in approximately 10-15% of patients.^[1] This results in biliary obstruction manifested by jaundice and biliary colic. In some cases, cholangitis or, even more rarely, pancreatitis may ensue. Infection of the cyst may also occur, and it is usually caused by bacteria residing in the biliary system. This may result in fever, leukocytosis, and possible formation of a liver abscess. Patients may be septic and should be treated aggressively with broad-spectrum antibiotics if signs of systemic infection are present.

Rupture of a hydatid cyst into the peritoneal cavity may happen spontaneously or may be caused by trauma, as in this case. Symptoms following the rupture are often dramatic and may include severe abdominal pain, syncope, or fever. Some patients exhibit signs of an allergic reaction, such as pruritus, urticaria, eosinophilia, or even anaphylaxis. Intraperitoneal rupture usually results in secondary implantation of cysts into the peritoneal cavity. Some rare but possible complications of liver echinococcosis include ascites, portal hypertension, Budd-Chiari syndrome, or compression of the vena cava. Rupture of the cyst into the vena cava is a very rare but universally fatal complication. Pulmonary hydatid cysts, when symptomatic, can cause chest pain, chronic cough, or hemoptysis. They may rupture into the bronchial tree and cause expectoration of a cyst fluid. Rupture of the hydatid cyst into the pleural cavity leads to pleuritic chest pain and dyspnea. Although rare, localization of hydatid cysts in the CNS can cause neurologic symptoms related to mass effect, including headache and seizures. Infection of skeletal tissue can cause pathological fractures as a result of invasion of the medullar cavity and slow bone erosion. Cardiac involvement may result in pericarditis or conduction abnormalities.^[4]

Various radiographic and related imaging techniques can be used in detecting and evaluating echinococcal cysts in different parts of the body. Plain radiographs may show pulmonary cysts as round masses with uniform density.^[1] Hydatid cysts will not typically be seen on plain abdominal radiographs unless calcification is present. Ultrasonography is the method of choice in detecting and evaluating hepatic hydatid cysts. It can reveal well-defined cysts with thick or thin walls in otherwise solid organs.^[1] It can also elucidate the density of the fluid inside the cyst. The most pathognomonic finding on ultrasonography is the presence of daughter cysts; however, small cysts under 2 cm in size and peripherally located cysts can be missed by ultrasonography. Hydatid cysts may be unable to be distinguished from simple benign cysts if there are no signs of daughter cysts. CT scanning is no more sensitive or specific than ultrasonography, but it is useful in localization of the cyst and defining its relation to other structures, such as large blood vessels or biliary structures. This is of a great value when the clinician is considering surgery.^[1]

Immunologic diagnosis is highly sophisticated and is used to distinguish simple benign cysts from hydatid cysts, as well as being used for postsurgical monitoring of persistent disease. The most valuable serologic test in the diagnosis of human hydatid disease is immunoelectrophoresis.^[1] It is highly specific but requires high levels of antibodies for sensitivity. It is also the most valuable test for postsurgical monitoring because of its relative rapid reversion to negative when the organism is cleared. Enzyme-linked immunosorbent assay (ELISA) is a valuable test for primary diagnosis, but it is not useful in postsurgical follow-up because it takes years to revert to negative. Latex agglutination or indirect hemaglutination tests may be also be used for diagnosis. The sensitivity of these tests is best for hepatic disease, but it is much less sensitive for detecting lung or other organ disease.

Surgery is the traditional treatment of choice for hydatid cysts; however, a number of cysts are now treated with PAIR (percutaneous aspiration, infusion of scolicidal agents, and reaspiration). PAIR may be a reasonable approach for treating patients with inoperable disease, and it is typically performed while patients are on antihelminthic therapy to decrease the risk of cyst dissemination. Ultrasonographic staging is used to determine the ideal method of treatment. The success of the surgical approach depends on the location and size of the cyst and the potential for injury to surrounding structures. PAIR is contraindicated for superficially located cysts, cysts communicating with the biliary tree, and cysts with multiple internal septal divisions. Surgery is still preferred for complicated cysts under these conditions. Care must be made to remove cysts without contaminating the surrounding tissues, as anaphylaxis and dissemination of infectious protoscolices may result. In cases of intraperitoneal rupture, the peritoneal cavity should be searched for any hydatid elements and very thoroughly lavaged with large quantities of saline.

Albendazole and mebendazole are used for the medical treatment of echinococcosis in patients with contraindications for surgery. Albendazole is the preferred agent because of its greater absorption from the gastrointestinal tract, which results in higher serum levels. Multiple factors can be used to predict the patient response to treatment. These drugs may also be used for perioperative prophylaxis. The use of praziquantel as a prophylactic agent for preventing the implantation of spilled protoscolices is still controversial.

This patient was admitted to the surgery department and surgically treated the same night. The intraoperative findings included intraperitoneal and intrabiliary rupture of a hepatic hydatid cyst. Evacuation of the cyst fluid and its elements as well as sterilization with hypertonic saline solution was performed. Cholecystectomy was performed, and a T-tube was inserted. In the postoperative period, she was treated with albendazole and discharged to home after approximately 2 weeks. She was instructed to continue on the albendazole for a period of 3 months. At a 1 month postoperative follow-up visit, she was doing well and was without complications.

Which of the following statements is NOT true?

Surgery is the treatment of choice for complicated hydatid cysts, such as those communicating with the biliary tree.

Albendazole is used only as a prophylactic agent in cases with ruptured hydatid cysts.

Ultrasonography is the method of choice for detecting liver cysts.

The most valuable test for postsurgical follow-up is immunoelectrophoresis.

Echinococcus granulosus causes unilocular cysts.

Which of the following is the most common complication of liver hydatid cysts?

Intraperitoneal rupture

Anaphylaxis

Liver abscess

Intrabiliary rupture
Acites

Source : http://cme.medscape.com/viewarticle/704048

Alcohol Dependence, Psychosis, and Diabetes: Oh My!

2009-06-13T09:25:00.003+07:00

Introduction

Concurrent addiction and medical illness is common in patients with psychosis, and this combination of conditions complicates treatment. In this case, the patient had simultaneous, acute exacerbations of 3 illnesses.

Case Presentation

A 47-year-old man was brought to hospital by police. A motel manager had reported that the patient, a registered guest, was creating a disturbance by yelling in his room. Upon arrival in the emergency department, the patient said that his parents-in-law were persecuting him. He claimed to have heard them in an adjacent room of the motel threatening to tie him to the bathtub, and he feared that they would take his life. Police reports indicated that he had been taken into custody for psychiatric reasons several months previous to this admission, when neighbors reported a disturbance at his apartment building. On that occasion, police discovered many empty liquor bottles in his residence.

Psychiatric History

The patient had poorly characterized episodes of depression 10-20 years prior to the index admission. Eight years prior to the index admission, he was admitted for paranoid delusions, after which he had intermittent outpatient treatment. He had no subsequent hospitalizations until about 2 years before the present admission, and that hospitalization occurred soon after he lost his job. Since then, he has received, at different times, risperidone oral medication and injectable risperidone microspheres (RISPERDAL® CONSTA®), but his adherence to treatment has been poor. His last appointment at the mental health clinic was 3 months prior to admission.

Medical History

The patient has type 2 diabetes, which was managed with metformin during the previous 18 months. He also has a history of hypertension for which he receives trandolapril. He has kept semiregular appointments with a family physician, and he denies having any drug allergies.

Social History

The patient is of South Asian descent, but he emigrated from Fiji with his family when he was an adolescent. He is divorced and has a daughter with whom he has infrequent contact. He was married for more than 20 years, but available information suggests his wife, also of South Asian origin, left him because of alcohol abuse.

He lives alone in an apartment within walking distance of his mother, who resides in an assisted-living facility. He visits her weekly. His father is deceased.

Before losing his job, he worked for an airline in aviation maintenance. He currently receives unemployment benefits after being laid off when his job was outsourced.

Substance Use

The patient evidently gave an unreliable history, because records from another hospital indicate an admission for delirium tremens 6 months before the index admission. At that time, he experienced paranoia, hallucinations, and confusion, and required intensive-care admission. He apparently declined intervention for his alcoholism.

The patient is evasive about his alcohol use, but he admits that for several months he has been drinking at least 300 mL of vodka daily along with several cans of beer. He denies having significant problems related to alcohol use, and either does not recall or refuses to acknowledge the episode of delirium tremens. He denies the use of tobacco, cannabis, and other drugs.

Mental Status Examination

On examination, the patient was found to be hypervigilant, suspicious, and distractible. He was oriented to person, place, but not fully to date. He spoke rapidly, and his thinking was circumstantial. He believed that his ex-wife's parents were pursuing him, which was why he checked into a motel, and that they have followed him to the hospital. He claimed to have heard them taunting and threatening to attack him. He denied having visual hallucinations as well as suicidal and homicidal ideation. His mood was fearful, and his affect was anxious. His short-term memory was intact, but his judgment and insight were highly impaired.

Physical Examination

On examination, he was afebrile, had a heart rate of 98 beats per minute, and blood pressure of 148/96 mm Hg. His body mass index was 27. The examination was otherwise unremarkable, except for diminished sensation in his distal lower extremities.

Laboratory Tests

On admission, the patient's complete blood cell count was normal, with a RBC mean cell volume (MCV) of 93. The gamma-glutamyl transferase (GGT) level was elevated at 385 U/L. Glucose was 8.3 mmol/L, and hemoglobin A1c was 6.9%. The levels of both potassium and magnesium were low at 3.4 mmol/L and 0.45 mmol/L, respectively. Other electrolytes and markers of renal function were normal. Thyroid-stimulating hormone (TSH) and serum B12 levels were normal. Electrocardiography showed a QTc interval of 474 milliseconds. A computed tomography scan of his head was unremarkable.

Diagnostic Formulation

Axis I	Psychotic disorder not otherwise specified Alcohol dependence
Axis II	No diagnosis
Axis III	Adult-onset diabetes mellitus Hypertension Overweight Mild peripheral neuropathy
Axis IV	Social isolation, unemployment
Axis V	Global assessment of functioning, 25

Hospital Course

Two psychiatrists certified the patient under prevailing law and admitted him involuntarily. He received intravenous therapy to correct electrolyte imbalance, along with thiamine and folate, and he was monitored closely for alcohol withdrawal. Although he required several doses of benzodiazepines, his withdrawal was uncomplicated. He resumed taking his antihypertensive medication.

He continued to hear humiliating and threatening voices and remained anxious. As treatment for these manifestations, he received clonazepam, 1 mg twice daily and risperidone, 1.5 mg daily. The dosage of risperidone was increased to 5 mg daily by hospital day 10. The outpatient treatment team recommended that he receive risperidone microsphere injections because of his history of poor adherence. Despite treatment with metformin at 1000 mg twice daily, his blood glucose remained elevated. An endocrinologist evaluated the patient and determined that insulin was necessary to treat the diabetes, and insulin was started on a sliding scale. Even with insulin, his blood glucose was labile, with readings as high as 17 mmol/L. His psychosis was diminishing, however.

Discussion Questions:

What role does alcohol dependence play in this patient's psychosis?

Would a change in antipsychotic medication be indicated?

Community Feedback

Community CME activities are developed in part from discussions by physicians in Medscape Physician Connect. View the complete discussion in Physician Connect in (physicians only; click here to learn more).

Much of the discussion about this patient, who presented with severe alcoholism and late-onset psychosis, centered on the diagnosis. Participants were divided as to whether the patient has schizophrenia or an alcohol-induced psychosis. As one commentator wrote, "Alcohol probably has a lot to do with the current psychosis" (comment 4). This view was shared by a commentator who suggested alcoholic hallucinosis as a possible diagnosis (comment 19), and another who remarked that people who hear voices during acute alcohol withdrawal frequently go on to have chronic auditory hallucinations (comment 24).

However, several participants favored a diagnosis of schizophrenia, including the participant who said, "I think that this man likely has a primary psychotic disorder, such as paranoid schizophrenia" (comment 7). A few participants suggested that the patient may have a mood disorder. One such commentator said, "With a history of depressive episodes and alcohol dependence, I agree with previous posters that bipolar disorder should be at the top of differentials" (comment 15).

A few participants who favored alcoholic hallucinosis suggested that antipsychotics could be discontinued if the patient remained abstinent. Some recommended treating the addiction aggressively, such as the participant who wrote, "This patient needs a long-term rehab admission" (comment 9). Those who thought the patient has schizophrenia recommended long-term chemotherapy. One such participant said, "I would favor starting him on either Haldol® or Prolixin Decanoate®" (comment 7).

Another thread of discussion focused on the patient's diabetes. A participant suggested that alcohol had suppressed the patient's glucagon secretion, but once removed from the alcohol source, his blood sugar levels would increase (comment 20). Several commentators were concerned about the effect that an antipsychotic would have on glucose control. One commented, "Risperdal® while not the worst offender, can unquestionably destabilize glucose metabolism" (comment 24). Another commentator wrote, "In this case, all second-generation antipsychotics are contraindicated due to their diabetogenic effects, with the possible exception of ziprasidone" (comment 8).

A poll posted with the discussion asking participants whether, in their experience, acute psychosis and acute hyperglycemia are often concurrent presentations. The majority, 59% of participants, said that they do not often occur concurrently, whereas 41% of participants said that they do.

Case Resolution

Establishing the Diagnosis

According to many discussion participants, this patient was experiencing a clear case of alcoholic hallucinosis, which is a psychosis occurring in the context of withdrawal in patients with alcohol dependence. The corresponding Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition diagnosis is alcohol-induced psychotic disorder, which is uncommon, distinct from delirium, and is characterized by menacing auditory hallucinations. The psychosis, which typically occurs in middle-aged men, resolves within several weeks, but chronic cases occur. Chronic hallucinosis has been successfully treated with risperidone.^[1]

Given the illness chronicity, the patient's poor insight, and his previous history of psychosis, the diagnosis of schizophrenia is a consideration. Only a period of abstinence from alcohol and a closely observed discontinuation of antipsychotic medication would allow confirmation of the diagnosis. In the meantime, the diagnosis used was that of psychotic disorder not otherwise specified.

Treatment

The endocrinologist on the case suggested that risperidone could be contributing to the difficulty in controlling the patient's serum glucose. A decision was made by the clinical team to switch the patient to a first-generation antipsychotic that could be administered by depot injection. An examination for abnormal involuntary movements showed no signs of tardive dyskinesia, the presence of which would have argued against the continued use of antipsychotic therapy. The patient was started on fluphenazine, 2.5 mg daily, and his risperidone dosing was gradually discontinued. In the meantime, his insulin requirements were established, and a diabetes nurse specialist instructed him how to self-administer insulin. He expressed confusion about the need for insulin injections, but was adherent to treatment.

On a daily fluphenazine dose of 7.5 mg, his hallucinations largely resolved, but he continued to believe that his former parents-in-law could be a future threat. He received a 50-mg injection of fluphenazine decanoate, which he tolerated well. Although he received instruction about the steps required to manage his psychosis and alcohol dependence, his insight remained poor. He insisted that he could avoid drinking as long as he was not overwhelmed by anxiety, and he was not interested in addiction treatment and in attending self-help groups.

The patient was discharged on a community treatment order to attend mental health clinic appointments and to accept fluphenazine decanoate injections every 2 weeks. He had learned to self-inject both regular insulin, at 10 U twice daily, as well as insulin glargine, at 24 units, once daily in the evening. Follow-up appointments with his family physician and the hospital diabetes clinic were scheduled.

Commentary

Although little is known about alcohol-induced psychosis, comorbidity in patients with chronic psychosis is typical. Patients with schizophrenia and bipolar disorder have a 50% to 60% prevalence of concurrent addiction or substance abuse, and the most commonly used intoxicant is alcohol. Concurrent substance abuse disorders, including alcoholism, reduce adherence to treatment in patients with schizophrenia.^[2]

The prevalence of medical illness is high in patients with psychosis and alcoholism. In a recent study of 80 patients with schizophrenia who received naltrexone for alcohol dependence, 43% had hypertension, and the prevalence of chronic pulmonary disease and coronary disease was higher in the study group than in the general population.^[3] Metabolic syndrome and diabetes are also more common in patients with schizophrenia, even in those patients who are not treated with antipsychotic agents.^[4]

Several second-generation antipsychotic drugs increase the risk for weight gain, elevated serum glucose, and abnormal serum lipids. Guidelines published by a multidisciplinary, expert panel recommend that patients who experience worsening glucose control on one antipsychotic drug can be switched to another for possible improvement in glucose control.^[5] Risperidone may have contributed to this patient's severe hyperglycemia, although causality was not established.

In this patient, the comorbidities reinforced one another, which made clinical management challenging. If untreated, any of them could be debilitating or fatal. Good communication among clinicians and use of all available tools, such as depot injections and a community treatment order, were essential in preparing the patient to resume his life. The prognosis was clouded, however, by a precontemplative attitude toward his addiction.

The patient in this case presented with severe alcoholism and late-onset psychosis and was diagnosed as having which of the following?

Schizophrenia

Alcohol-induced psychosis

Bipolar disorder

Alcohol hallucinosis

Psychotic disorder not otherwise specified

A patient with diabetes who has severe alcoholism and psychosis characterized by hallucinations and paranoia is best treated with which of the following?

Risperidone

Olanzapine

Fluphenazine

A program of addiction treatment

A self-help group

Source : http//cme.medscape.com/viewarticle/703014

An Uncommon Cause of Chest Pain in a Healthy Young Man

2009-06-12T16:04:00.004+07:00

An 18-year-old man with no significant past medical history presents to the emergency department (ED) complaining of a sudden onset of chest pain that awakened him from sleep at 4 AM. The pain is located in the midsubsternal region and radiates to the neck. The patient describes it as a sharp pain; when asked to rate the pain on a scale of increasing severity from 1 to 10, he states that it is an 8. The pain worsens with inspiration and is associated with shortness of breath. The patient denies having any fevers, chills, cough, hemoptysis, nausea, or vomiting. He has not had any recent trauma or surgeries. The patient has an 8 pack-year history of smoking cigarettes. He admits to occasional marijuana use and remote experimentation with inhaled methamphetamines. He denies any alcohol use. He states that he is not currently taking any medications and does not have any known allergies to medications.

On physical examination, he is noted to be a well-developed, well-nourished male in no acute distress. He does not appear to be tachypneic or cyanotic. The vital signs show a temperature of 98.1°F (36.7°C), a blood pressure of 94/58 mm Hg, a heart rate of 67 bpm, a respiratory rate of 20 breaths/min, and an oxygen saturation of 95% while breathing room air. No jugular venous distention is noted, and the patient has a normal respiratory effort. The lungs are clear to auscultation bilaterally, without any wheezes, rales, or rhonchi. The heart examination reveals a regular rate and rhythm, with normal S1 and S2 heart sounds and no murmurs, rubs, or gallops. The abdomen is soft, nontender, and nondistended. His extremities do not exhibit any clubbing, cyanosis, or edema. No subcutaneous crepitus is appreciated on examination of the skin.

The initial laboratory findings show a white blood cell (WBC) count of 11.0 × 10³/μL (11.0 × 10⁹/L; normal range, 3.8-10.9 × 10³/μL), with neutrophils at 73.9% (0.73; normal range, 41.8%-77%), a hemoglobin of 15.1 g/dL (9.37 mmol/L; normal range, 13.6-17.3 g/dL), a hematocrit of 44.0% (0.44; normal range, 39.8-50.7%), and platelets of 263 × 10³/μL (263 × 10⁹/L; normal range, 141-401 × 10³/μL). The basic metabolic panel is normal. A urine toxicology screen is negative. The erythrocyte sedimentation rate (ESR) is 5 mm/hr (normal range, <15>

Questions answered incorrectly will be highlighted.

What is the cause of this man's chest pain?

Hint: Look closely at the heart and surrounding structures.

Pulmonary embolism

Pneumomediastinum

Aortic dissection

Discussion

Figure 2b.

The chest radiograph showed linear and curvilinear radiolucencies in the anterior mediastinum and possibly pericardium suggestive of pneumomediastinum and minimal pneumopericardium. A computed tomography (CT) scan of the chest was subsequently obtained, which confirmed the presence of pneumomediastinum (see Figures 2a and 2b) and pneumopericardium, with air tracking superiorly along the right carotid sheath (not included on the images provided). There was no evidence of pneumothorax, bullous changes, or bronchopleural fistula. The remaining portions of the lungs were normal, with no areas of focal consolidation or pleural effusion. The esophagus and trachea appeared normal. There was no mediastinal or hilar lymphadenopathy. The vascular and bone structures had no abnormalities. A diagnosis of pneumomediastinum and pneumopericardium was established based on the imaging studies, and the patient was admitted to the hospital for observation.

Spontaneous pneumomediastinum is defined as the presence of free air in the mediastinum without any apparent precipitating cause. Secondary pneumomediastinum is caused by certain events, such as trauma, infections in the intrathoracic or oropharyngeal spaces, or disruption of the aerodigestive tract. Spontaneous pneumomediastinum is a rare, usually self-limited disease primarily affecting young men. More than 75% of reported cases occur in males, with a mean age of 20 years. The incidence of spontaneous pneumomediastinum has not been clearly established because the only published reports available are case studies or small case series. Newcomb and Clark reported an incidence of 1 in 29,670 emergency department presentations, whereas the figure observed in the study by Macia et al was 1 in 44,511. Other sources have found the incidence of spontaneous pneumomediastinum to be between 1 in 800 and 1 in 42,000 hospital admissions. The incidence of this disease could be underestimated, given that it frequently goes unrecognized. The clinical presentation of spontaneous pneumomediastinum can often be subtle, and the diagnosis is sometimes missed or delayed.^[1-7]

The most commonly proposed cause of pneumomediastinum is alveolar rupture, which occurs in the presence of elevated intra-alveolar pressure or damage to the alveolar walls. An increased pressure gradient between the intra-alveolar and interstitial spaces leads to air leakage from small alveolar openings and ruptured alveoli into the perivascular spaces, which leads to interstitial emphysema. The pressure gradient then favors dissection of air along the vascular sheaths toward the hilum. Air can then decompress into the subcutaneous tissues and the deep cervical spaces, eventually spreading into the pericardial space and leading to pneumopericardium. Dissection of free air into the pericardial space is a common complication of barotrauma in neonates, but it is quite rare in adults, in whom the apposition of the pericardial layers is very tight.^[1-3,7]

Various conditions can cause elevation of intra-alveolar pressure, including airway obstruction (eg, mucous plugging in an asthmatic or a foreign body), mechanical ventilation, blunt trauma, coughing, emesis, or the Valsalva maneuver (eg, during parturition). Certain conditions that can cause damage to the alveolar walls include pneumonitis, emphysema, lung fibrosis, and adult respiratory distress syndrome (ARDS).^[1-4]

In order to make a diagnosis of spontaneous pneumomediastinum, the clinician must rule out causes of secondary pneumomediastinum. This is particularly vital because alternative causes of pneumomediastinum are potentially life-threatening. It is important to determine if the patient has had recent dental surgery and/or procedures of the upper digestive tract, as well as evaluate for underlying conditions that can lead to pneumomediastinum, such as gas-producing infections in the head, neck, and abdomen, or neoplasms disrupting the mucosal integrity of the esophagus. Esophageal rupture must be ruled out by obtaining an esophagram when indicated. Events or conditions known to precipitate spontaneous pneumomediastinum include vomiting (especially retching), asthma exacerbation, coughing, or physical activity.^[1,3,5,7]

Pneumomediastinum has also been found to be associated with inhalational drug use. Theoretically, this has been thought to be caused by barotrauma from prolonged forceful breath holding. Cocaine and marijuana users perform a Valsalva-type maneuver during deep inhalation of the respective substance (often through a water pipe), leading to an increase in intra-alveolar pressure and subsequent alveolar rupture. There is no evidence of a direct pharmacological effect of illicit drugs on spontaneous pneumomediastinum.^[1-4]

Patients with spontaneous pneumomediastinum most commonly present with complaints of chest pain, dyspnea, and neck pain or discomfort. Chest pain is the most common symptom, and it typically presents as an acute, retrosternal, pleuritic pain that may radiate to the neck, back, or shoulders. Other, less common symptoms include odynophagia, dysphagia, dysphonia, cough, back pain, or abdominal pain. Physical examination may reveal signs of respiratory distress, subcutaneous emphysema, and the Hamman sign, which is pathognomonic for pneumomediastinum. The Hamman sign refers to crunching, crackling, or bubbling sounds that are synchronous with the heart beat on auscultation. This signifies air in the mediastinum. The prevalence of the Hamman sign is highly variable; however, subcutaneous emphysema, mainly at the neck, is a more frequent finding that is seen in 40% to 100% of cases.^[1-5,7]

The differential diagnosis of spontaneous pneumomediastinum is broad and includes musculoskeletal disorders, acute coronary syndrome, pericarditis, pneumothorax, pulmonary embolism, tracheobronchial tree rupture, and Boerhaave syndrome. Tracheobronchial tree rupture and Boerhaave syndrome are potentially life-threatening conditions. Boerhaave syndrome can be ruled out with a contrast-enhanced esophagogram if it is suspected and, if tracheobronchial tree rupture is suspected, it can be ruled out with a bronchoscopy.^[1-3]

The diagnosis of pneumomediastinum is confirmed by obtaining posteroanterior and lateral chest radiographs. Posteroanterior chest radiographs typically reveal radiolucency between the left heart border and the mediastinal pleura. A lateral view should always be obtained because, if only a posteroanterior radiograph is taken, the diagnosis will be missed in up to 50% of cases. When air is limited in quantity, the only sign of pneumomediastinum on plain chest radiography may be a radiolucent band (hyperlucency) in the retrosternal area, which can only be seen in the lateral view. Up to 30% of patients with spontaneous pneumomediastinum present with a normal radiograph; therefore, if the clinical suspicion is high, a CT scan of the chest can be obtained in those cases in which the diagnosis is unclear.^[1-3]

Spontaneous pneumomediastinum is almost always a benign, self-limited condition. The treatment consists of supportive measures, including rest, oxygen, and analgesics. Breathing 100% oxygen helps to enhance reabsorption of the free air by increasing the gradient of nitrogen between the alveoli and the tissues. Antibiotic therapy is not required for spontaneous pneumomediastinum. Patients respond well to supportive treatment and pain typically resolves within 1-2 days. Follow-up chest radiography should be obtained within 12-24 hours. The chest radiograph findings usually return to normal within a week. Significant complications are virtually nonexistent, and most published series have not reported any cases of recurrence.

Figure 3b.

In the case of this patient, he was admitted to the hospital for observation and supportive treatment was initiated with supplemental oxygen and analgesics. The patient had a normal complete evaluation by an ear, nose, and throat (ENT) surgeon. In addition, a CT scan of the neck was obtained and was found to be normal. A repeat CT scan of the chest obtained the day after admission showed no interval progression in the pneumomediastinum and pneumopericardium. The patient's pain and shortness of breath resolved within 24 hours, and the patient was subsequently discharged to home after a 2-day hospital stay. A CT scan of the chest performed 3 days after discharge showed mild improvement in the pneumomediastinum and resolution of the pneumopericardium (see Figures 3a and 3b). At the time of discharge, the patient was instructed to refrain from future drug use and smoking, and to avoid air travel or prolonged stays at high altitudes for 1 month. Physical activity was not restricted except for scuba diving, which he was directed not to do for at least 6 months. These suggestions are based on the theoretical risk for recurrence of spontaneous pneumomediastinum. The actual rate and risk factors for recurrence are not known, so recommendations on avoidance of potential high risk activities must be individualized based on patient factors and known information about the recurrence of pneumothorax.

On chest radiography, what is(are) the optimal view(s) needed to establish a diagnosis of pneumomediastinum?

Lateral view

Posteroanterior view

Posteroanterior and lateral views

Oblique view

Anterolateral views

What is the Hamman sign?

A hypodense line in the mediastinum on posteroanterior chest radiography.

Blueish discoloration on the lips of patients with spontaneous pneumomediastinum resulting from a lack of oxygenation.

A gurgling sound coming from a patient's stomach as a result of air escaping from the mediastinum.

Crunching, crackling, or bubbling sounds that are synchronous with the heart beat on auscultation.
e. None of above

Posteroanterior chest radiographs typically reveal radiolucency between the left heart border and the mediastinal pleura. A lateral view should always be obtained because the diagnosis of pneumomediastinum will be missed in up to 50% of cases if only a posteroanterior radiograph is taken.

Source : http://cme.medscape.com/viewarticle/702661

Congestive Heart Failure and Pulmonary Edema

2009-06-03T12:42:00.003+07:00

Introduction

Background

Congestive heart failure (CHF) is an imbalance in pump function in which the heart fails to adequately maintain the circulation of blood. The most severe manifestation of CHF, pulmonary edema, develops when this imbalance causes an increase in lung fluid secondary to leakage from pulmonary capillaries into the interstitium and alveoli of the lung.

CHF can be categorized as forward or backward ventricular failure. Backward failure is secondary to elevated systemic venous pressure, whereas left ventricular failure is secondary to reduced forward flow into the aorta and systemic circulation. Furthermore, heart failure can be subdivided into systolic and diastolic dysfunction. Systolic dysfunction is characterized by a dilated left ventricle with impaired contractility, whereas diastolic dysfunction occurs in a normal or intact left ventricle with impaired ability to relax and receive as well as eject blood.

Chest radiograph shows signs of congestive heart failure (CHF).

The New York Heart Association's functional classification of CHF is one of the most useful. Class I describes a patient who is not limited with normal physical activity by symptoms. Class II occurs when ordinary physical activity results in fatigue, dyspnea, or other symptoms. Class III is characterized by a marked limitation in normal physical activity. Class IV is defined by symptoms at rest or with any physical activity.

Pathophysiology

Congestive heart failure (CHF) is summarized best as an imbalance in Starling forces or an imbalance in the degree of end-diastolic fiber stretch proportional to the systolic mechanical work expended in an ensuing contraction. This imbalance may be characterized as a malfunction between the mechanisms that keep the interstitium and alveoli dry and the opposing forces that are responsible for fluid transfer to the interstitium.

Maintenance of plasma oncotic pressure (generally about 25 mm Hg) higher than pulmonary capillary pressure (about 7-12 mm Hg), maintenance of connective tissue and cellular barriers relatively impermeable to plasma proteins, and maintenance of an extensive lymphatic system are the mechanisms that keep the interstitium and alveoli dry.

Opposing forces responsible for fluid transfer to the interstitium include pulmonary capillary pressure and plasma oncotic pressure. Under normal circumstances, when fluid is transferred into the lung interstitium with increased lymphatic flow, no increase in interstitial volume occurs. However, when the capacity of lymphatic drainage is exceeded, liquid accumulates in the interstitial spaces surrounding the bronchioles and lung vasculature, thus creating CHF. When increased fluid and pressure cause tracking into the interstitial space around the alveoli and disruption of alveolar membrane junctions, fluid floods the alveoli and leads to pulmonary edema.

Etiologies of pulmonary edema may be placed in the following 6 categories:

Pulmonary edema secondary to altered capillary permeability: Acute respiratory distress syndrome (ARDS), infectious causes, inhaled toxins, circulating exogenous toxins, vasoactive substances, disseminated intravascular coagulopathy (DIC), immunologic processes reactions, uremia, near drowning, and other aspirations
Pulmonary edema secondary to increased pulmonary capillary pressure: Cardiac causes and noncardiac causes, including pulmonary venous thrombosis, stenosis or veno-occlusive disease, and volume overload
Pulmonary edema secondary to decreased oncotic pressure found with hypoalbuminemia
Pulmonary edema secondary to lymphatic insufficiency
Pulmonary edema secondary to large negative pleural pressure with increased end expiratory volume
Pulmonary edema secondary to mixed or unknown mechanisms including high altitude pulmonary edema (HAPE), neurogenic pulmonary edema, heroin or other overdoses, pulmonary embolism, eclampsia, postcardioversion, postanesthetic, postextubation, and post–cardiopulmonary bypass

This article is limited to cardiac causes of pulmonary edema and congestive heart failure (CHF) and its relevant emergency care.

Frequency

United States

More than 3 million people have congestive heart failure (CHF), and more than 400,000 new patients present yearly. The prevalence rate of CHF is 1-2%.

Mortality/Morbidity

Approximately 30-40% of patients with congestive heart failure (CHF) are hospitalized every year. CHF is the leading diagnosis-related group (DRG) among hospitalized patients older than 65 years. The 5-year mortality rate after diagnosis was reported in 1971 as 60% in men and 45% in women. In 1991, data from the Framingham heart study showed the 5-year mortality rate for CHF essentially remaining unchanged, with a median survival of 3.2 years for males and 5.4 years for females. This may be secondary to an aging US population with declining mortality due to other diseases.
The most common cause of death is progressive heart failure, but sudden death may account for up to 45% of all deaths. After auditing data on 4606 patients hospitalized with CHF between 1992-1993, the total in-hospital mortality rate was 19%, with 30% of deaths occurring from noncardiac causes.
Patients with coexisting insulin-dependent diabetes mellitus have a significantly increased mortality rate.

Race

Blacks are 1.5 times more likely to die of CHF than whites are. Nevertheless, black patients appear to have similar or lower in-hospital mortality rates than white patients.

Sex

Prevalence is greater in males than in females in patients aged 40-75 years.
No sex predilection is noted among patients older than 75 years.

Age

Prevalence of CHF increases with increasing age and affects about 10% of the population older than 75 years.

Clinical

History

Anxiety
Dyspnea at rest
Dyspnea upon exertion: This has been found to be the most sensitive symptom reported, yet the specificity for dyspnea is less than 60%.
Orthopnea and paroxysmal nocturnal dyspnea (PND): These symptoms are observed; however, the sensitivity for orthopnea and PND is only 20-30%.
Cough: Cough that produces pink, frothy sputum is highly suggestive of congestive heart failure (CHF).
Edema
Nonspecific symptoms
- Weakness
- Lightheadedness
- Abdominal pain
- Malaise
- Wheezing
- Nausea
Past medical history
- Cardiomyopathy
- Valvular heart disease
- Alcohol use
- Hypertension
- Angina
- Prior myocardial infarction
- Familial heart disease

Physical

Findings such as peripheral edema, jugular venous distention, and tachycardia are highly predictive of congestive heart failure (CHF). Overall specificity of physical examination has been reported at 90%; however, this same study reported a sensitivity of only 10-30%.
Tachypnea, using accessory muscles of respiration, has been observed.
Hypertension may be present.
Pulsus alternans (alternating weak and strong pulse indicative of depressed left ventricle [LV] function) may be observed.
The skin may be diaphoretic or cold, gray, and cyanotic.
Jugular venous distention (JVD) is frequently present.
Wheezing or rales may be heard on lung auscultation.
Apical impulse is frequently laterally displaced.
Cardiac auscultation may reveal aortic or mitral valvular abnormalities (S₃ or S₄).
Lower extremity edema may also be noted, especially in the subacute process.

Causes

Various cardiac diseases cause congestive heart failure (CHF) and pulmonary edema.
The most common cause of heart failure is coronary artery disease, which is secondary to loss of left ventricular muscle, ongoing ischemia, or decreased diastolic ventricular compliance.
Other disease processes include hypertension, valvular heart disease, congenital heart disease, other cardiomyopathies, myocarditis, and infectious endocarditis.
CHF is often precipitated by cardiac ischemia or dysrhythmias, cardiac or extracardiac infection, pulmonary embolus, physical or environmental stresses, changes or noncompliance with medical therapy, dietary indiscretion, or iatrogenic volume overload.
One also must consider systemic processes such as pregnancy and hyperthyroidism as precipitants of CHF.

Differential Diagnoses

Acute Respiratory Distress Syndrome	Pneumonia, Bacterial
Altitude Illness - Pulmonary Syndromes	Pneumonia, Immunocompromised
Anaphylaxis	Pneumonia, Mycoplasma
Anemia, Acute	Pneumonia, Viral
Bronchitis	Pneumothorax, Iatrogenic, Spontaneous and Pneumomediastinum
Chronic Obstructive Pulmonary Disease and Emphysema	Pulmonary Embolism
Dysbarism	Shock, Septic
Hyperventilation Syndrome	Venous Air Embolism
Myopathies
Pericarditis and Cardiac Tamponade
Pneumonia, Aspiration

Workup

Laboratory Studies

Until recently, differentiating asthma and other pulmonary disease has been difficult in the acute setting, particularly because of the poor sensitivities and specificities of most elements of history and physical examination. The standard of care has been shotgun therapy, namely treating patients for both congestive heart failure (CHF) and an acute pulmonary process such as asthma, with both diuretics and beta-agonists.

The Breathing Not Properly Study has suggested that serum levels of beta-natriuretic peptide (BNP) and the BNP precursor, Pro-BNP, can help identify CHF as the origin of acute dyspnea.¹This study found sensitivities of 90% with specificities of 76%. Positive predictive value was 79%, with a negative predictive value of 89%. Mueller et al found a reduction in hospital length of stay of 3 days when BNP levels were used.² This study assumed an average length of stay of 11 days; however, the average length of stay in the United States for CHF exacerbations is approximately 4 days. Also, although the time to initiation of therapy was reduced in this study from 90 to 60 minutes, the general practice in the United States is immediate initiation of shotgun therapy.
In the primary care setting, Wright et al identified 305 patients with heart failure and then reevaluated them with or without the Pro-BNP result.³Diagnostic accuracy improved from 52% to 60% without Pro-BNP and from 49% to 70% with Pro-BNP.
Maisel et al identified in the Breathing Not Properly Study a 20% increase in patients with CHF who presented with dyspnea and a history of asthma or COPD but no prior history of CHF.⁴
Mueller et al found that BNP reduced time to discharge from 12 to 3 days and reduced costs of hospitalization by 15%.²
BNP is available as a point-of-care test, with results available within 15 minutes; however, only Pro-BNP can be concomitantly used with nesiritide.
Serum levels of BNP lower than 100 pg/mL are unlikely to be from CHF. In the Breathing Not Properly Study, a BNP level of 50 pg/mL increased sensitivity from 90% to 97%, although specificity was reduced.¹Levels of 100-500 pg/mL may be CHF. However, other conditions that also elevate right filling pressures (eg, pulmonary embolus, primary pulmonary hypertension, end-stage renal failure, cirrhosis, hormone replacement therapy) may also cause elevated BNP levels in this range. BNP levels more than 500 pg/mL are most consistent with CHF.

Serum laboratory values may reveal prerenal azotemia or elevated alanine aminotransferase (ALT), aspartate aminotransferase (AST), or bilirubin levels, which is suggestive of a congestive hepatopathy. Cardiac enzymes and other serum markers for ischemia or infarction may also be useful.
ABG levels may be of benefit in evaluation of hypoxemia, ventilation/perfusion (V/Q) mismatch, hypercapnia, and acidosis.
Mild azotemia, decreased erythrocyte sedimentation rate(ESR), and proteinuria are observed in early and mild-to-moderate disease.
Increased creatinine levels, hyperbilirubinemia, and dilutional hyponatremia are observed in severe cases.

Imaging Studies

Chest radiography
- Although diagnostic tests are of limited benefit in acute congestive heart failure (CHF), chest radiography is the most useful tool. A recent study showed that 1 out 5 patients admitted to the hospital with CHF lacked signs of congestion on chest radiograph.⁵
- Cardiomegaly may be observed with a cardiothoracic ratio greater than 50%. Pleural effusions may be present bilaterally or if they are unilateral more commonly observed on the right.
- Early CHF may manifest as cephalization of pulmonary vessels, generally reflecting a pulmonary capillary wedge pressure (PCWP) of 12-18 mm Hg. As the interstitial fluid accumulates, more advanced CHF may be demonstrated by Kerley B lines (PCWP is 18-25 mm Hg).
- Pulmonary edema is observed as perihilar infiltrates often in the classic butterfly pattern, reflecting a PCWP of more than 25 mm Hg.
- Several limitations to chest radiography are observed when attempting to diagnose CHF. Classic radiographic progression is often not found, and as much as a 12-hour radiographic lag from onset of symptoms may occur. In addition, radiographic findings frequently persist for several days despite clinical recovery.
Emergency transthoracic echocardiography
- Emergency transthoracic echocardiography (ECHO) may help identify regional wall motion abnormalities as well as globally depressed or myopathic left ventricular function.
- ECHO may help reveal cardiac tamponade, pericardial constriction, and pulmonary embolus.
- ECHO is also useful in revealing valvular heart disease, such as mitral or aortic stenosis or regurgitation.

Other Tests

ECG is a nonspecific tool but may be useful in diagnosing concomitant cardiac ischemia, prior myocardial infarction (MI), cardiac dysrhythmias, chronic hypertension, and other causes of left ventricular hypertrophy.

Procedures

No defined role is recognized for invasive monitoring devices such as central venous placement (CVP) lines. Time-consuming placement of pulmonary artery catheters has not been shown to prolong survival, even in the coronary care unit and, thus far, has not been well studied in the emergency department (ED) setting.
Cardiac catheterization may be necessary for a complete evaluation and assessment of prognosis.

Treatment

Prehospital Care

Prehospital notification by emergency medical services (EMS) personnel should alert ED staff of a patient presenting with signs and symptoms of congestive heart failure (CHF) and pulmonary edema. They should receive online medical advice for patients with high-risk presentations.
Begin treatment with the ABCs. Administer supplemental oxygen, initially 100% nonrebreather facemask.
Use cardiac monitoring and continuous pulse oximetry.
Obtain intravenous access, as well as a prehospital ECG, if available.
Provide nitroglycerin sublingual or spray for active chest pain in the patient without severe hypotension and intravenous furosemide.

Emergency Department Care

Begin ED treatment of a patient presenting with signs and symptoms of congestive heart failure (CHF) and pulmonary edema with the ABCs. Administer supplemental oxygen, initially 100% nonrebreather facemask. Use cardiac monitoring and continuous pulse oximetry. Obtain intravenous access.
To reduce venous return, elevate the head of the bed. Patients may be most comfortable in a sitting position with their legs dangling over the side of the bed, which allows for reduced venous return and decreased preload.
Therapy generally starts with nitrates and diuretics if patients are hemodynamically stable. Many other treatment modalities may play some role in acute management.
If possible, treat the underlying cause as well, if identified. This is particularly necessary for patients with known diastolic dysfunction who respond best to reductions in blood pressure, rather than to diuretics, nitrates, and inotropic agents. Serum BNP levels may be very useful in the setting of undifferentiated dyspnea, or in the future may be useful to gauge therapeutic success.
Eliminate contributing factors when possible.
Restrict fluid and sodium.
Consider other treatment modalities, including nesiritide. Nesiritide may be useful in lieu of nitroglycerin in patients with moderate respiratory distress, particularly if the patient will not tolerate noninvasive ventilation or in the patient who cannot have nitroglycerin by protocol (ie, in an observation unit).
- Data comparing nasal CPAP therapy and facemask ventilation therapy have demonstrated decreased need for intubation rates when these modalities are used.⁶However, in patients with severe CHF treated with CPAP, no significant difference was found in short-term mortality rates and length of hospital stay. Although BiPAP therapy may improve ventilation and vital signs more rapidly then CPAP, a higher incidence of MI associated with BiPAP has been reported. BiPAP and CPAP are contraindicated in the presence of acute facial trauma, the absence of an intact airway, and in patients with an altered mental status or who are uncooperative.
- Alternating tourniquets, formerly a mainstay of therapy, have been used to decrease preload. Their use has been supplanted by newer therapies such as intravenous nitroglycerin and nitroprusside.
- Phlebotomy with removal of 500 mL of blood or via plasmapheresis is another former mainstay of therapy used to decrease preload. Its use has been supplanted by newer therapies such as intravenous nitroglycerin and nitroprusside.

Consultations

Cardiologist
Critical care specialist
Cardiothoracic surgeon, for possible heart valve surgery or transplantation

Medication

The goal of pharmacotherapy is to achieve a PCWP of 15-18 mm Hg and a cardiac index of more than 2.2 L/min/m² while maintaining adequate blood pressure and perfusion to essential organs. These goals may need to be modified for some patients.

Use of diuretics, nitrates, analgesics, and inotropic agents are indicated for the treatment of congestive heart failure (CHF) and pulmonary edema. Calcium channel blockers, such as nifedipine and nondihydropyridines, increase mortality and increase prevalence of recurrent CHF with chronic use. Conflicting evidence currently argues both in favor of and against the use of calcium channel blockers in the acute setting; at this time, limit their acute use to patients with diastolic dysfunction and heart failure, a condition not easily determined in the emergency department.

ACE inhibitors, such as sublingual (SL) captopril or intravenous enalapril, may rapidly reverse hemodynamic instability and symptoms, possibly avoiding an otherwise imminent intubation. Haude et al compared 25 mg of SL captopril with 0.8 mg of sublingual nitroglycerin in 24 patients with class III and class IV CHF and found that captopril induces a more sustained and more pronounced improvement in hemodynamics.⁷Annane et al gave 1 mg of intravenous enalapril to 20 patients presenting with acute class III and class IV CHF over 2 hours and reported rapid hemodynamic improvement with no significant adverse effects on cardiac output or hepatosplanchnic measurements.⁸

Captopril may play a unique role in sustaining patients with renal failure and concomitant acute CHF while awaiting definitive therapy with dialysis. Because the information on this subject is still controversial and is limited to small studies, the routine use of ACE inhibitors cannot be recommended at this time. ACE inhibitors remain a promising area in need of further study.

Beta-blockers, possibly by restoring beta-1 receptor activity or via prevention of catecholamine activity, appear to be cardioprotective in patients with depressed left ventricular function. The US Carvedilol Heart Failure study group demonstrated a two-thirds decrease in mortality in patients taking carvedilol with left ventricular ejection fractions of 35% or less. Beta-blockers, particularly carvedilol, have been shown to improve symptoms in patients with moderate-to-severe heart failure. However, the role of beta-blockers in the acute setting is currently unclear; limit use until hemodynamic studies indicate that further deterioration is not possible.

Because differentiating CHF and asthma exacerbations is often difficult, treating both with the shotgun approach is often used, particularly as both may cause bronchospasm. Aerosolized beta-2 agonists, which are the more selective of beta-agonists, decrease tachycardia, dysrhythmias, and cardiac work while transiently enhancing cardiac function. Terbutaline has been shown to be successful in this setting, as well as albuterol, isoetharine, and bitolterol.

Limit roles of theophylline and aminophylline in the acute setting. They are positive inotropic agents mediated by an increase in catecholamines, and they dilate coronaries and exert mild diuretic effects. Nevertheless, they can exacerbate dysrhythmias (eg, multifocal atrial tachycardia [MAT], ischemia) by increasing cardiac work.

Steroids, intravenous or orally administered, have been shown to worsen preexisting heart failure due to systemic sodium retention and volume expansion, hypokalemia, and occasional hypertension. Inhaled steroids, because of their lack of systemic side effects, may be a reasonable option in this confusing patient presentation; however, given their delayed onset of action, they remain an area in need of further study.

Please see the article on Asthma for dosing schedules.

Diuretics

First-line therapy generally includes a loop diuretic such as furosemide, which inhibits sodium chloride reabsorption in the ascending loop of Henle.

Furosemide (Lasix)

Administer loop diuretics IV because this allows for both superior potency and higher peak concentration despite increased incidence of side effects, particularly ototoxicity.

Dosing

Adult

A reasonable approach for furosemide might be as follows:
10-20 mg IV for patients symptomatic with CHF not already using diuretics
40-80 mg IV for patients already using diuretics
80-120 mg IV for patients whose symptoms are refractory to the initial dose after 1 h of its administration
Higher doses and more rapid redosing may be appropriate for the patient in severe distress

Pediatric

Not established

Metolazone (Mykrox, Zaroxolyn)

Both chlorothiazide and metolazone have been used as adjunctive therapy in patients initially refractory to furosemide. Chlorothiazide, however, at doses of 250-500 mg IV, decreases GFR with CHF and, thus, is less potent and causes a greater loss of potassium. Conversely, metolazone has been demonstrated to be synergistic with loop diuretics in treating refractory patients.

Dosing

Adult

5-10 mg PO before redosing with furosemide

Pediatric

Not established

Nitrates

These agents reduce myocardial oxygen demand by lowering preload and afterload.

In patients with severe hypertension, nitroprusside causes more arterial dilatation than nitroglycerin. Nevertheless, due to thiocyanate toxicity and the coronary steal phenomenon associated with nitroprusside, intravenous nitroglycerin is still the therapy of choice for afterload reduction.

Nitroglycerin (Nitro-Bid, Nitrol, Nitrostat)

SL nitroglycerin and nitrospray are particularly useful in patients who present with acute pulmonary edema with a systolic blood pressure of at least 100 mm Hg.
Similar to SL, nitrospray's onset is 1-3 min with a half-life of 5 min. Applicability of nitrospray may be easier, and storage is up to 4 y. One study reported significant and rapid hemodynamic improvement in 20 patients given nitrospray with pulmonary edema in an ICU setting.
Topical nitrate therapy is reasonable in a patient presenting with class I to II CHF. However, in patients with more severe signs of heart failure or pulmonary edema, IV nitroglycerin is preferred because it is easier to monitor hemodynamics and absorption, particularly in the patients with diaphoresis.
Because of delayed absorption, PO nitrates have little role in the acute presentations of CHF.

Dosing

Adult

Nitrospray: Single spray (0.4 mg) equivalent to a single 1/150 SL; may repeat q3-5min as hemodynamics permit, up to a maximum of 1.2 mg
Ointment: Apply 1-2 inches of nitropaste to chest wall
Injection: Start at 20 mcg/min IV and rate to effect in 5-10 mcg increments q3-5min

Pediatric

Not established

Nitroprusside sodium (Nitropress)

Produces vasodilation and increases inotropic activity of the heart. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate. Easily titratable.

Dosing

Adult

10-15 mcg/min IV and titrate to effective dose range of 30-50 mcg/min and a systolic blood pressure of at least 90 mm Hg

Pediatric

Not established

Analgesics

Intravenous morphine is an excellent adjunct in acute therapy. In addition to being both an anxiolytic and an analgesic, its most important effect is venodilation, which reduces preload. This agent also causes arterial dilatation, which reduces systemic vascular resistance (SVR) and increases cardiac output. Narcan can also reverse the effects of morphine. However, some evidence indicates that morphine use in acute pulmonary edema may increase the intubation rate.

Morphine sulfate (Duramorph, Astramorph, MS Contin)

DOC for narcotic analgesia due to reliable and predictable effects, safety profile, and ease of reversibility with naloxone.
Morphine sulfate administered IV may be dosed in numerous ways and is commonly titrated until desired effect is obtained.

Dosing

Adult

2-5 mg IV and repeated q10-15min unless respiratory rate is <20>

Pediatric

Not established

Inotropic agents

Principal inotropic agents include dopamine, dobutamine, inamrinone (formerly amrinone), milrinone, dopexamine, and digoxin. In patients with hypotension presenting with CHF, dopamine and dobutamine are usually used. Inamrinone or milrinone inhibits phosphodiesterase, resulting in an increase of intracellular cyclic adenosine monophosphate (AMP) and alteration in calcium transport. As a result, they increase cardiac contractility and reduce vascular tone by vasodilatation.

Dopexamine is a new synthetic catecholamine with beta-2 and dopaminergic properties that cause vasodilation and increased inotropism but with tachycardia as well. Dopexamine may ultimately have a role as an emergent inotropic agent; however, dobutamine is probably the current agent of choice.

Digoxin has no role in the emergency management of CHF due to delayed absorption and diminished efficacy at times of increased sympathetic tone. Thus, digoxin has little, if any, benefit in patients who present with atrial fibrillation and rapid ventricular response. Limit use of digoxin to chronic CHF, in which its role has been well established.

These agents augment both coronary and renal blood flow.

Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effects depend on the dose. Lower doses stimulate mainly dopaminergic receptors that produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation is produced by higher doses.
Positive inotropic agent at 2-10 mcg that can lead to tachycardia, ischemia, and dysrhythmias. Doses >10 mcg cause vasoconstriction, which increases afterload.

Dosing

Adult

Depending on the response to initial ED therapy, disposition decisions vary.

With few exceptions, patients presenting with acute symptoms of congestive heart failure (CHF) or pulmonary edema require hospital admission. However, many patients who rapidly respond to early therapy may require only standard hospital ward admission with telemetry monitoring if ischemic etiologies are being considered.
Some criteria for discharge from the ED would include gradual onset of shortness of breath, rapid response to therapy, oxygen saturation greater than 90%, and acute coronary syndromes and MI unlikely as the precipitating event.
Those patients who require intubation or remain with significant respiratory, hemodynamic, and/or cardiovascular compromise often require intensive care unit or critical care unit admission.
If left ventricular function has not been previously well established, perform either multigated nuclear imaging (MUGA) scanning or echocardiography, which enable assessment of valvular function and wall motion abnormalities as well as ejection fraction.
In patients refractory to medical therapy or with evidence of cardiogenic shock, cardiac catheterization, angioplasty, coronary bypass, or intraaortic balloon pump (IABP) may be helpful.

Further Outpatient Care

Center outpatient care around patient education with specific instructions regarding dietary restrictions and compliance with medical therapy.

Inpatient & Outpatient Medications

ACE inhibitors are indicated in patients with ejection fractions of 35% or less.
Digoxin may also be helpful in patients with ejection fractions of 35% or less.
Diuretics, such as furosemide, may be helpful regardless of ejection fraction.
Beta-blockers appear to be cardioprotective in patients with depressed left ventricular function. The US Carvedilol Heart Failure Study Group demonstrated a two-thirds decrease in mortality in patients taking carvedilol with left ventricular ejection fractions of 35%. Beta-blockers are indicated as therapy for patients with diastolic dysfunction or for patients with coronary insufficiency.
Calcium channel blockers, such as nifedipine and nondihydropyridines, increase mortality rates and incidence of recurrent CHF with chronic use in patients with depressed LV function. Amlodipine is the exception to this rule. Calcium channel blockers are useful in patients with diastolic dysfunction and heart failure.

Transfer

Consider transfer for unstable patients being evaluated in a center without access to cardiac catheterization or IABP. These patients may include the following:

Those who are refractory to medical therapy
Those in cardiogenic shock
Those with significant aortic stenosis or other valvular abnormalities possibly requiring surgical intervention or valvuloplasty

Deterrence/Prevention

Emphasize patient education with intense instruction regarding compliance with dietary restrictions and medical therapy.
Emphasize close monitoring of blood pressure, particularly in patients with diastolic dysfunction.
Patient should modify diet as follows:
- Sodium restriction (initially 4 g/d)
- Weight reduction (if appropriate)
- Appropriate fluid restriction
Patient should modify activity as follows:
- During severe stage, bed rest with elevation of head of bed and anti-embolism stockings to help control leg edema
- Gradual increase in activity with walking to help increase strength

Complications

Complications of congestive heart failure (CHF) and pulmonary edema may include the following:

Acute MI
Cardiogenic shock
Arrhythmias (most commonly atrial fibrillation)
Ventricular arrhythmias, such as ventricular tachycardia, often are seen in patients with significantly depressed left ventricular function.
Electrolyte disturbances
Mesenteric insufficiency
Protein enteropathy
Digitalis intoxication

Prognosis

Based on data from 4606 patients hospitalized with congestive heart failure (CHF) between 1992-1993, the total in-hospital mortality rate was 19%, with 30% of deaths occurring from noncardiac causes.⁹However, these patients were noted to have had suboptimal use of proven efficacious therapy, compared with those who survived hospitalizations, particularly among women and the elderly. Thirty-year data from the Framingham heart study demonstrated a median survival of 3.2 years for males and 5.4 years for females.¹⁰
Results of initial treatment are usually good, regardless of cause.
Long-term prognosis varies. Mortality rates range from 10% in patients with mild symptoms to 50% with advanced, progressive symptoms.

Patient Education

Provide instructions to patients discharged home to return to the ED for recurrence or changes in severity of symptoms.
Provide specific instructions to patients discharged regarding dietary restrictions and compliance with medical therapy.
Require patients to promptly follow up with their primary care physician or cardiologist.
Advise patients that printed information is available from the following organizations:
- American Heart Association
  1615 Stemmons Freeway
  Dallas, TX 75207
  (214) 748-7212
- American College of Cardiology
  9111 Old Georgetown Rd
  Bethesda, MD 20814
  (301) 897-5400
For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education article Congestive Heart Failure.

Miscellaneous

Medicolegal Pitfalls

Failure to recognize and initiate early management of a patient who presents with signs and symptoms of congestive heart failure (CHF) and pulmonary edema is a pitfall because therapy must begin with the ABCs, and early treatment should include nitrates and diuretics, if hemodynamics are stable.
Failure to obtain an ECG early is a pitfall because this may be useful in diagnosing dysrhythmias, concomitant cardiac ischemia, or prior MI; early ECG also is helpful in differentiating CHF from other etiologies. Remember, the most common cause of CHF is coronary artery disease.
Failure to consider use of both CPAP and BiPAP early in therapy as a means to decrease need for intubation and improve acute respiratory status is a pitfall.
Failure to consider and evaluate for diseases with similar presentations is also a pitfall.
Failure to educate patients concerning changes or noncompliance with medical therapy and dietary restrictions to help prevent further recurrence is a concern.
Discharging patients who may have had acute MI as a cause of CHF is a pitfall.

Source : http://emedicine.medscape.com/article/757999

Hypertensive Emergencies

2009-06-03T11:40:00.003+07:00

Background

Approximately 50 million people in the United States are affected by hypertension (HTN).^1,2Substantial improvements have been made with regards to improving awareness and treatment of hypertension. However, approximately 30% of adults are still unaware of their hypertension; up to 40% of people with hypertension are not receiving treatment; and, of those treated, up to 67% do not have their blood pressure (BP) controlled to less than 140/90 mm Hg.³

New data have shown an increased lifetime risk of hypertension and have also highlighted the increased risk of cardiovascular complications with BP levels previously considered to be normal. Given this information, the Joint National Committee (JNC-7) has introduced a new classification system for hypertension.³

Prehypertension - Systolic blood pressure (SBP) 120-139 mm Hg or diastolic blood pressure (DBP) 80-89 mm Hg
Stage I hypertension - SBP 140-159 mm Hg or DBP 90-99 mm Hg
Stage II hypertension - SBP >160 mm Hg or DBP >100 mm Hg

Hypertensive emergency

Hypertensive emergencies encompass a spectrum of clinical presentations where uncontrolled BPs lead to progressive or impending end-organ dysfunction (EOD). In these conditions, the BP should be lowered aggressively over minutes to hours.

Acute end-organ damage⁴

Neurological
- Hypertensive encephalopathy
- Cerebral vascular accident/cerebral infarction
- Subarachnoid hemorrhage
- Intracranial hemorrhage
Cardiovascular
- Myocardial ischemia/infarction
- Acute left ventricular dysfunction
- Acute pulmonary edema
- Aortic dissection
Other
- Acute renal failure/insufficiency
- Retinopathy
- Eclampsia
- Microangiopathic hemolytic anemia

With the advent of antihypertensives, the incidence of hypertensive emergencies has declined from 7% to approximately 1% of patients with hypertension.⁵In addition, the 1-year survival rate associated with this condition has increased from only 20% (prior to 1950) to a survival rate of more than 90% with appropriate medical treatment.6

Emergency department considerations

Many patients present to the emergency department (ED) with elevated blood pressures; however, only a small proportion of patients will require emergent treatment.

The primary goal of the emergency physician (EP) is to determine which patients with acute hypertension are exhibiting symptoms of end-organ damage and require immediate intravenous parenteral therapy. In contrast, patients presenting with acutely elevated blood pressures (SBP >200 mm Hg or DBP >120 mm Hg) without symptoms require initiation of medical therapy and close follow-up in the outpatient setting.⁷

Optimal control of hypertensive situations balances the benefits of immediate decreases in BP against the risk of a significant decrease in target organ perfusion. The EP must be capable of the following:

Appropriately evaluating patients with an elevated BP
Correctly classifying the hypertension
Determining the aggressiveness and timing of therapeutic interventions
Making disposition decisions

An important point to remember in the management of the patient with any degree of BP elevation is to "treat the patient and not the number."

Pathophysiology

The pathophysiology of hypertensive emergencies is not well understood. Failure of normal autoregulation and an abrupt rise in systemic vascular resistance (SVR) are typically initial steps in the disease process. Increases in SVR are thought to occur from the release of humoral vasoconstrictors from the wall of a stressed vessel. The increased pressure within the vessel then starts a cycle of endothelial damage, local intravascular activation of the clotting cascade, fibrinoid necrosis of small blood vessels, and the release of more vasoconstrictors. If the process is not stopped, a cycle of further vascular injury, tissue ischemia, and autoregulatory dysfunction ensues.8,9

Single-organ involvement is found in approximately 83% of patients presenting with hypertensive emergencies. Two-organ involvement is found in 14% of patients, and multiorgan involvement (>3 organ systems) is found in approximately 3% of patients presenting with a hypertensive emergency.¹⁰

The most common clinical presentations of hypertensive emergencies are cerebral infarction (24.5%), pulmonary edema (22.5%), hypertensive encephalopathy (16.3%), and congestive heart failure (12%). Less common presentations include intracranial hemorrhage, aortic dissection, and eclampsia.¹⁰

Central nervous system

Cerebral autoregulation is the inherent ability of the cerebral vasculature to maintain a constant cerebral blood flow (CBF) across a wide range of perfusion pressures.

Patients with chronic hypertension can tolerate higher mean arterial pressures (MAP) before they have disruption of their autoregulation system. However, such patients also have increased cerebrovascular resistance and are more prone to cerebral ischemia when flow decreases, especially if blood pressure is decreased into normotensive ranges.

Rapid rises in blood pressure can cause hyperperfusion and increased CBF, which can lead to increased intracranial pressure and cerebral edema.¹¹

Hypertensive encephalopathy is one of the clinical manifestations of cerebral edema and microhemorrhages seen with dysfunction of cerebral autoregulation and is characterized by hypertension, altered mentation, and papilledema.12

Cardiovascular system

Chronic hypertension causes increased arterial stiffness, increased systolic BP, and widened pulse pressures. These factors act to decrease coronary perfusion pressures, increase myocardial oxygen consumption, and lead to left ventricular hypertrophy.¹²During hypertensive emergencies, the left ventricle is unable to compensate for an acute rise in systemic vascular resistance. This leads to left ventricular failure and pulmonary edema or myocardial ischemia.⁴

Renal system

Chronic hypertension causes pathologic changes to the small arteries of the kidney. The arteries develop endothelial dysfunction and impaired vasodilation, which alter renal autoregulation. When the renal autoregulatory system is disrupted, the intraglomerular pressure starts to vary directly with the systemic arterial pressure, thus offering no protection to the kidney during BP fluctuations. During a hypertensive crisis, this can lead to acute renal ischemia.⁴

Frequency

United States

The prevalence of hypertension in the United States from 2003-2004 was approximately 29.3%.¹³Although significant increases have been made in the control of hypertension, the prevalence of the disease has not decreased.

Factors independently associated with hypertension include age older than 40 years, obesity (body mass index >30 kg/m³), and race (non-Hispanic black race).¹³Prevalence of the disease increases with advancing age such that approximately half of people aged 60-69 years and three quarters of people aged 70 years or older are affected by hypertension.³

Hypertensive crises affect less than 1% of hypertensive adults in the United States.14

International

Worldwide, approximately 1 billion people have hypertension, contributing to more than 7.1 million deaths per year.¹⁵

Mortality/Morbidity

Death from both ischemic heart disease and stroke increase progressively as the BP increases. For every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood pressures above 115/75 mm Hg, the mortality rate for both ischemic heart disease and stroke doubles.³

The morbidity and mortality of hypertensive emergencies depend on the extent of EOD on presentation and the degree to which BP is controlled subsequently. With BP control and medication compliance, the 10-year survival rate of patients with hypertensive crises approaches 70%.¹⁶

Race

Hypertension develops at an earlier age, leads to more clinical sequelae, and is more common and severe in African Americans compared with age-matched non-Hispanic whites.¹⁷Hypertensive crises are also more common in African Americans compared with other races.

The prevalence and incidence of hypertension in Mexican Americans are similar to or lower than those in non-Hispanic whites.¹⁸In general, Mexican Americans and Native Americans have lower BP control rates than non-Hispanic whites and African Americans.¹⁹

Sex

The lifetime risk for hypertension is 86-90% in females and 81-83% in men.³

Age

Hypertensive crises are more common among elderly persons.

Clinical

History

The history should focus on the presence of end-organ dysfunction (EOD), the circumstances surrounding the hypertension, and any identifiable etiology. The history and physical examination determine the nature, severity, and management of the hypertensive event.

Medications
- Details of antihypertensive drug therapy and compliance
- Intake of over-the-counter preparations such as sympathomimetic agents
- Use of illicit drugs such as cocaine
Duration and severity of preexisting hypertension
Degree of BP control
Presence of previous EOD, particularly renal and cerebrovascular disease
Date of last menstrual period
Other medical problems (eg, prior hypertension, thyroid disease, Cushing disease, systemic lupus, renal disease)
Assess whether specific symptoms suggesting EOD are present.
- Chest pain - Myocardial ischemia or infarction
- Back pain - Aortic dissection
- Dyspnea - Pulmonary edema, congestive heart failure
- Neurologic symptoms - Seizures, visual disturbances, altered level of consciousness (hypertensive encephalopathy)

Physical

The physical examination should assess whether EOD is present.

Vital signs
- BP should be measured in both the supine position and the standing position (assess volume depletion).
- BP should also be measured in both arms (a significant difference may suggest aortic dissection).
Ear, nose, and throat (ENT): The presence of new retinal hemorrhages, exudates, or papilledema suggests a hypertensive emergency.
Cardiovascular - Evaluate for the presence of heart failure.
- Jugular venous distension
- Crackles
- Peripheral edema
Abdomen - Abdominal masses or bruits
CNS
- Level of consciousness
- Visual fields
- Focal neurologic signs

Causes

The most common hypertensive emergency is a rapid unexplained rise in BP in a patient with chronic essential hypertension. Most patients who develop hypertensive emergencies have a history of inadequate hypertensive treatment or an abrupt discontinuation of their medications.

Other causes
- Renal parenchymal disease - Chronic pyelonephritis, primary glomerulonephritis, tubulointerstitial nephritis (accounts for 80% of all secondary causes)
- Systemic disorders with renal involvement - Systemic lupus erythematosus, systemic sclerosis, vasculitides
- Renovascular disease - Atherosclerotic disease, fibromuscular dysplasia, polyarteritis nodosa
- Endocrine - Pheochromocytoma, Cushing syndrome, primary hyperaldosteronism
- Drugs - Cocaine, amphetamines, cyclosporin, clonidine withdrawal, phencyclidine, diet pills, oral contraceptive pills
- Drug interactions - Monoamine oxidase inhibitors with tricyclic antidepressants, antihistamines, or tyramine-containing food
- CNS - CNS trauma or spinal cord disorders, such as Guillain-Barré syndrome
- Coarctation of the aorta
- Preeclampsia/eclampsia
- Postoperative hypertension

Differential Diagnoses

Workup

Laboratory Studies

The following laboratory studies are indicated for patients with hypertensive emergencies:

Electrolytes, BUN, and creatinine levels to evaluate for renal impairment
CBC and smear to exclude microangiopathic anemia
Urinalysis
- Dipstick urinalysis (UA) to detect hematuria or proteinuria (renal impairment)
- Microscopic UA to detect RBCs or RBC casts (renal impairment)
Optional studies
- Toxicology screen
- Pregnancy test
- Endocrine testing

Imaging Studies

Chest radiography is indicated in patients with chest pain or shortness of breath.
- Cardiac enlargement
- Pulmonary edema
- Widened mediastinum
Head CT and/or brain MRI are indicated in patients with abnormal neurologic examinations or clinical concern for the following:
- Intracranial bleeding
- Cerebral edema
- Cerebral infarction
Chest CT scan, transesophageal echocardiography, or aortic angiography is indicated in cases where aortic dissection is suspected.

Other Tests

Electrocardiography (ECG) to assess for evidence of myocardial ischemia or left ventricular hypertrophy

Treatment

Prehospital Care

Address the manifestations of a hypertensive emergency such as chest pain or heart failure. Reduction of BP may not be indicated in the prehospital setting.
Under most circumstances, attempting to treat hypertension directly in the prehospital setting is unwise. In particular, rapid lowering of BP can critically decrease end-organ perfusion.

Emergency Department Care

Between 3% and 45% of adult ED patients will have at least one increased BP during their stay in the ED.⁷The fundamental principle in determining the necessary ED care of the hypertensive patient is the presence or absence of end-organ dysfunction (EOD).

Initial considerations (if the patient is not in distress)
- Place the patient who is not in distress in a quiet room and reevaluate after an initial interview. Most evidence suggests that two blood pressure measurements are adequate for screening purposes.²⁰
- Consider the context of the elevated BP (eg, severe pain often causes an increase in BP).
Screen for EOD: The patient's history, physical examination, laboratory studies, and diagnostic tests, as outlined in Workup, should be used to determine if EOD exists.
Patients without evidence of EOD may be discharged with follow-up.
The misconception remains that a patient never should be discharged from the ED with an elevated BP. As a result of this belief, patients are given oral medicines, such as nifedipine, in an effort to lower BP rapidly before discharge. This is not indicated and may be dangerous.
Attempts to temporarily lower BP by using these medicines may result in a precipitous and difficult-to-correct drop in BP. Should this occur, end-organ hypoperfusion may result. Furthermore, patients who present with high BP may have had this elevation for some time and may need chronic BP control but may not tolerate rapid return of BP to a "normal" level.
Acute lowering of BP in the narrow window of the ED visit does not improve long-term morbidity and mortality rates. The follow-up recommended for these situations by the Joint National Committee on High Blood Pressure is outlined in Follow-up.
Patients with EOD usually require admission and rapid lowering of BP using intravenous medications. Suggested medication depends on the affected organ system.
Even in cases of hypertensive emergencies, the BP should not be lowered to normal levels.
Rapid reduction in BP below the cerebral, renal, and/or coronary autoregulatory range results in marked reduction in organ blood flow, possibly leading to ischemia and infarction.
In general, the MAP should be lowered by no more than 20% in the first hour of treatment. If the patient remains stable, the BP should then be lowered to 160/100-110 mm Hg in the next 2-6 hours. Please note the exceptions to this general rule listed below.
These BP goals are best achieved by a continuous infusion of a short-acting, titratable, parenteral antihypertensive agent along with constant, intensive patient monitoring.
Rapid BP reduction is indicated in the following circumstances:

Neurological emergencies

Hypertensive encephalopathy
- Preferred medications
  - Labetalol
  - Nicardipine
  - Esmolol
- Medications to avoid
  - Nitroprusside
  - Hydralazine
- Treatment guidelines: Reduce mean arterial pressure (MAP) 25% over 8 hours.²¹
Acute ischemic stroke
- Preferred medications
  - Labetalol
  - Nicardipine
- Treatment guidelines: Withhold antihypertensive medications unless the systolic blood pressure (SBP) is >220 mm Hg or the diastolic blood pressure (DBP) is >120 mm Hg UNLESS patient is receiving IV or IA fibrinolysis, then goal BP: SBP <185>21
Acute intracerebral hemorrhage
- Preferred medications
  - Labetalol
  - Nicardipine
  - Esmolol
- Medications to avoid
  - Nitroprusside
  - Hydralazine
- Treatment guidelines: Treatment based on clinical/radiographic evidence of increased intracranial pressure (ICP). If signs of increased ICP, maintain MAP just below 130 mm Hg (or SBP <180>21
Subarachnoid hemorrhage
- Preferred medications
  - Nicardipine
  - Labetalol
  - Esmolol
- Medications to avoid
  - Nitroprusside
  - Hydralazine
- Treatment guidelines: Maintain SBP <160>21

Cardiovascular emergencies

Aortic dissection
- Preferred medications
  - Labetalol
  - Nicardipine
  - Nitroprusside (with beta-blocker)
  - Esmolol
  - Morphine sulfate
- Medications to avoid
  - Avoid beta-blockers if there is aortic valvular regurgitation or suspected cardiac tamponade.
- Treatment guidelines: Maintain SBP <110>22
Acute coronary syndrome
- Preferred medications
  - Beta-blockers
  - Nitroglycerin
- Treatment guidelines: Treat if SBP >160 mm Hg and/or DBP >100 mm Hg. Reduce BP by 20-30% of baseline. Thrombolytics are contraindicated if BP is >185/100 mm Hg.²³
Acute heart failure
- Preferred medications
  - Nitroglycerin
  - Enalaprilat
- Treatment guidelines: Treatment with vasodilators (in addition to diuretics) for SBP ≥140 mm Hg. IV or sublingual nitroglycerin is the preferred agent.²³

Other disorders

Cocaine toxicity/pheochromocytoma
- Preferred medications
  - Diazepam
  - Phentolamine
  - Nitroglycerin/nitroprusside
- Medications to avoid
  - Beta-adrenergic antagonists prior to phentolamine administration
- Treatment guidelines: Hypertension and tachycardia from cocaine toxicity rarely require specific treatment. Alpha-adrenergic antagonists (phentolamine) are the preferred agents for cocaine-associated acute coronary syndromes.²⁴ Pheochromocytoma treatment guidelines are similar to that of cocaine toxicity. Beta-blockers can be added for BP control only after alpha-blockade.
Preeclampsia/eclampsia
- Preferred medications
  - Hydralazine
  - Labetalol
  - Nifedipine
- Medications to avoid
  - Nitroprusside
  - Angiotensin-converting enzyme inhibitors
  - Esmolol
- Treatment guidelines: In women with eclampsia or preeclampsia, SBP should be <160>3 BP should be maintained below 150/100 mm Hg. Patients with eclampsia or preeclampsia should also be treated with IV magnesium sulfate to avoid seizures.25
Perioperative hypertension
- Preferred medications
  - Nitroprusside
  - Nitroglycerin
  - Esmolol
- Treatment guidelines: Target perioperative BP to within 20% of the patient’s baseline BP, except if there is the potential for life-threatening arterial bleeding. Perioperative beta-blockers are first choice in patients undergoing vascular procedures or in patients with an intermediate or high risk of cardiac complications.²²
Acutely lowering of BP in the ED for clinical situations other than those listed here is controversial and generally should be avoided.

Consultations

Consultations may be indicated for comorbid conditions and their definitive treatment.
Because hypertension is usually a chronic problem, access to a primary care provider and long-term follow-up are essential for all patients.

Medication

Once the diagnosis of a true hypertensive emergency is established and EOD is confirmed, BP should be lowered by up to 20% of the MAP or the DBP should be decreased to 100-110 mm Hg over minutes to hours. More rapid reduction in BP should be avoided since it may worsen end-organ function. See specific guidelines under Treatment.

Beta-adrenergic blockers

These agents are used for hypertensive emergencies, especially with aortic dissection and myocardial infarction. They may be used alone or in combination with sodium nitroprusside. Pure beta-blockers should not be used alone in cases that are the result primarily of alpha stimulation (eg, pheochromocytoma, MAOI-tyramine interaction).

Labetalol (Normodyne)

Alpha-, beta1-, and beta2-blocker, especially useful with aortic dissection. Lowers BP, reduces incidence of myocardial infarctions and death.

Dosing

Adult

20 mg (0.25 mg/kg for an 80-kg patient) IVP over 2 min; may administer 40-80 mg at 10-min intervals, up to 300 mg total dose
Alternatively, IV infusion: Initially, 2 mg/min; titrate to response up to 300 mg total dose, if needed

Pediatric

0.4-1 mg/kg/h IV; maximum dose 3 mg/kg/h

Esmolol (Brevibloc)

Ideal for use in patients at risk for complications from beta-blockers, especially patients with mild to moderately severe LV dysfunction or peripheral vascular disease. Has short half-life of 8 min; thus, easily titratable to desired effect. In addition, therapy may be stopped quickly if necessary.

Dosing

Adult

Loading dose: 250-500 mcg/kg IV infused over 1-3 min
Maintenance infusion: 50 mcg/kg/min IV over 4 min; if adequate effect not observed within 5 min, repeat loading dose and follow with maintenance infusion using increments of 50 mcg/kg/min IV (for 4 min); this regimen may be repeated up to 4 times if necessary
As desired BP approached, skip loading infusion and reduce dose increments in maintenance infusion from 50 mcg/kg/min IV to 25 mcg/kg/min; if necessary, may increase interval between titration steps from 5-10 min

Pediatric

Suggested dose: 100-500 mcg/kg IV over 1 min, then 25-200 mcg/kg/min IV; increase by 25-50 mcg/kg/min IV q5-10min
Maximum dose: 50-250 mcg/kg/min IV

Alpha-adrenergic blockers

At low doses, alpha-adrenergic receptor blockers may be used as monotherapy in treatment of hypertension. At higher doses, they may cause sodium and fluid retention. As a result, concurrent diuretic therapy may be required to maintain the hypotensive effects.

Phentolamine (Regitine)

Alpha1- and alpha2-adrenergic blocking agent, effective for pheochromocytoma and hypercatecholaminergic-induced hypertension.

Dosing

Adult

Clevidipine butyrate (Cleviprex)

Dihydropyridine calcium channel blocker. Rapidly metabolized in blood and tissues and does not accumulate in the body. Administered IV and indicated for rapid and precise blood pressure reduction. Available in a concentration of 0.5 mg/mL as single-use vials (50 mL or 100 mL).

Follow-up

Further Inpatient Care

Patients with a true hypertensive emergency require the careful titration of intravenous medications for good control and a smooth reduction of their BP.
Close monitoring is required; therefore, an intensive care unit is the most suitable place for admission.
Other problems or comorbid conditions need to be addressed appropriately (ie, surgery for aortic dissection).

Further Outpatient Care

Hypertension is a chronic problem. The most important factor in a patient's overall risks of morbidity and mortality is appropriate long-term care.
If a patient presents with a high BP but ED evaluation reveals no evidence of end-organ dysfunction (EOD), the patient does not need immediate treatment in the ED. The patient does require proper follow-up. See recommendations below.
The Joint National Committee on High Blood Pressure has published a series of recommendations for appropriate follow-up, assuming no EOD.^3,7
- Prehypertension (SBP 120-139 mm Hg, DBP 80-89 mm Hg: BP should be rechecked within 1 year.
- Stage I hypertension (SBP 140-159 mm Hg, DBP 90-99 mm Hg): BP should be rechecked within 2 months.
- Stage II hypertension: (SBP >160 mm Hg or DBP >100 mm Hg): BP should be confirmed and the patient should have follow-up within 1 month.
- If BP is >180/110 mm Hg: BP should be confirmed and the patient should have follow-up within 1 week. The EP should consider initiating BP treatment upon discharge from the ED.
- If SBP is >210 mm Hg or DBP >120 mm Hg: Confirm BP, initiate antihypertensive treatment upon discharge from the ED, and arrange close follow-up within 1 week.

Transfer

Transfer requirements are based on the ability of the institution to care for the patient and the patient's associated comorbid conditions.
- A patient with an uncomplicated hypertensive emergency needs an ICU setting.
- Patients with comorbid conditions, such as aortic dissection or subarachnoid hemorrhage, may require transfer to a higher level of care.

Deterrence/Prevention

Good long-term control of hypertension is the best method for prevention of acute hypertensive emergencies.
Patient education and close follow-up care in patients who have had a hypertensive crisis are essential to prevent recurrent hypertensive emergencies.
Proper use of antihypertensive medications is the major tool in avoiding development of hypertensive emergencies.

Complications

Congestive heart failure
Myocardial infarction
Renal failure
Retinopathy
Cerebrovascular accident
Abrupt lowering of BP may result in inadequate cerebral or cardiac blood flow, leading to stroke or myocardial ischemia.

Prognosis

The 1-year mortality rate is 79% for patients with untreated hypertensive emergencies.¹⁸
Five-year survival rate among all patients who present with hypertensive crisis is 74%.²⁶

Patient Education

Patients need continuing education about antihypertensive medications and complications arising from inadequate BP control.
Dangers of uncontrolled hypertension, including associated serious morbidity and death, must be emphasized.
Education and maintenance of BP control are important to help prevent further complications.

Miscellaneous

Medicolegal Pitfalls

Administering long-acting oral/sublingual medications to acutely lower nonurgent elevations in BP
Failure to arrange timely and appropriate follow-up
Failure to recognize the serious complications of severe hypertension

Source : http://emedicine.medscape.com/article/758544-overview?src=emed_whatnew_nl_0

World Health Organization Issues Guidelines on Hand Hygiene in Healthcare

2009-05-23T12:42:00.001+07:00

May 6, 2009 — The World Health Organization (WHO) has issued Guidelines on Hand Hygiene in Health Care, offering a thorough review of evidence on hand hygiene in healthcare and specific recommendations to improve hygiene practices and reduce transmission of pathogenic microorganisms to patients and healthcare workers (HCWs).

The guidelines target hospital administrators and public health officials as well as HCWs, and they are designed to be used in any setting in which healthcare is delivered either to a patient or to a specific group, including all settings where healthcare is permanently or occasionally performed, such as home care by birth attendants. Individual adaptation of the recommendations is encouraged, based on local regulations, settings, needs, and resources.

Hand Hygiene Indications

Indications for hand hygiene are as follows:

• Wash hands with soap and water when visibly dirty, when soiled with blood or other body fluids, or after using the toilet.

• Handwashing with soap and water is preferred when exposure to potential spore-forming pathogens, such as Clostridium difficile, is strongly suspected or proven.

• In all other clinical situations, use an alcohol-based handrub as the preferred means for routine hand antisepsis, if hands are not visibly soiled. Wash hands with soap and water if alcohol-based handrub is not available.

• Hand hygiene is needed before and after touching the patient; before touching an invasive device used for patient care, whether gloves are used; after contact with body fluids or excretions, mucous membranes, nonintact skin, or wound dressings; if moving from a contaminated body site to another body site on the same patient; after touching inanimate surfaces and objects in the immediate vicinity; and after removing gloves.

• Hand hygiene is needed before handling medication or preparing food using an alcohol-based handrub or handwashing with water and either plain or antimicrobial soap.

• Soap and alcohol-based handrub should not be used together.

Hand Hygiene Techniques

Specific recommendations for hand hygiene technique are as follows:

• Rub a palmful of alcohol-based handrub over all hand surfaces until dry.

• When washing hands, wet hands with water and apply enough soap to cover all surfaces; rinse hands with water and dry thoroughly with a single-use towel. Whenever possible, use clean, running water. Avoid hot water, which may increase the risk for dermatitis.

• Use the towel to turn off the tap or faucet, and do not reuse the towel.

• Liquid, bar, leaf, or powdered soap is acceptable; bars should be small and placed in racks that allow drainage.

Surgical Hand Preparation

Specific recommendations for surgical hand preparation are as follows:

• Before beginning surgical hand preparation, remove jewelry. Artificial nails are prohibited.

• Sinks should be designed to reduce the risk for splashes.

• Visibly soiled hands should be washed with plain soap before surgical hand preparation, and a nail cleaner should be used to remove debris from underneath the fingernails, preferably under running water.

• Brushes are not recommended.

• Before donning sterile gloves, surgical hand antisepsis should be performed with a suitable antimicrobial soap or alcohol-based handrub, preferably one that ensures sustained activity. Alcohol-based handrub should be used when quality of water is not assured.

• When using an antimicrobial soap, scrub hands and forearms for the length of time recommended by the maker, usually 2 to 5 minutes.

• When using an alcohol-based surgical handrub, follow the maker's instructions; apply to dry hands only; do not combine with alcohol-based products sequentially; use enough product to keep hands and forearms wet throughout surgical hand preparation; and allow hands and forearms to dry thoroughly before donning sterile gloves.

Selecting Hand Hygiene Agents

Some specific recommendations for selection and handling of hand hygiene agents are as follows:

• Provide effective hand hygiene products with low potential to cause irritation.

• Ask for HCW input regarding skin tolerance, feel, and fragrance of any products being considered.

• Determine any known interaction between products used for cleaning hands, skin care products, and gloves used in the institution.

• Provide appropriate, accessible, well-functioning, clean dispensers at the point of care, and do not add soap or alcohol-based formulations to a partially empty dispenser.

Skin Care Recommendations

Some specific recommendations for skin care are as follows:

• Educate HCWs about hand-care practices designed to reduce the risk for irritant contact dermatitis and other skin damage.

• Provide alternative hand hygiene products for HCWs with confirmed allergies to standard products.

• Provide HCWs with hand lotions or creams to reduce the risk for irritant contact dermatitis.

• Use of antimicrobial soap is not recommended when alcohol-based handrub is available. Soap and alcohol-based handrub should not be used together.

Recommendations for Glove Use

Some specific recommendations for use of gloves are as follows:

• Glove use does not replace the need for hand hygiene.

• Gloves are recommended in situations in which contact with blood or other potentially infectious materials is likely.

• Remove gloves after caring for a patient, and do not reuse.

• Change or remove gloves if moving from a contaminated body site to either another body site within the same patient or the environment.

"In hand hygiene promotion programmes for HCWs, focus specifically on factors currently found to have a significant influence on behaviour, and not solely on the type of hand hygiene products," the guidelines authors write. "The strategy should be multifaceted and multimodal and include education and senior executive support for implementation. Educate HCWs about the type of patient-care activities that can result in hand contamination and about the advantages and disadvantages of various methods used to clean their hands."

Four of the guidelines authors have disclosed various financial relationships with GOJO, Clorox, and GlaxoSmithKline, and other companies and institutions. A complete description of their disclosures is available in the original article. The other guidelines authors have disclosed no relevant financial relationships.

WHO Guidelines on Hand Hygiene in Health Care. May 2009.

Clinical Context

In 2004, WHO convened a group of international experts in infection control to prepare guidelines for hand hygiene in healthcare. In 2002, the Centers for Disease Control and Prevention Guideline for Hand Hygiene in Health-Care Settings was adopted. Following a systematic review of the literature and task force meetings, the Advanced Draft of the WHO Guidelines on Hand Hygiene in Health Care was published in 2006. An Executive Summary of the Advanced Draft of the Guidelines is available separately (http://www.who.int/gpsc/tools/en/). Pilot testing of the advanced draft occurred, with subsequent updating and finalization of the guidelines.

The WHO Guidelines on Hand Hygiene in Health Care includes a review of scientific data, consensus recommendations, process and outcome measurements, proposals for large scale promotion of hand hygiene, patient participation in promotion of hand hygiene, and a review of national and subnational guidelines. The recommendations are expected to be valid until 2011 and will be updated every 2 to 3 years.

Study Highlights

Indications for washing hands with soap and water include visibly dirty hands, hands visibly soiled with body fluids, or after using the toilet.
Handwashing with soap and water is preferred after exposure to potential spore-forming pathogens, including Clostridium difficile outbreaks.
Alcohol-based handrub is preferred in the following situations if hands are not visibly soiled: before and after touching a patient; before handling an invasive device for patient care; after contact with body fluids or excretions, mucous membranes, nonintact skin, or wound dressings; between contact with a contaminated body site to another site on the same patient; after contact with inanimate surfaces and objects; and after removing sterile or nonsterile gloves.
Handwashing with soap and water is recommended when alcohol-based handrub is unavailable.
Alcohol-based handrub or soap and water can be used before handling medication or preparing food.
Concomitant alcohol-based handrub and soap use is not recommended.
Soap and water hand-washing technique includes using a towel to turn off the faucet, thorough drying of hands, and single towel use.
Acceptable forms of soap are liquid, bar, leaf, or powdered.
Bar soap racks should allow drainage to ensure that the soap dries.
Alcohol-based handrub technique includes applying palmful amount of handrub, covering all surfaces, and rubbing hands until dry.
Surgical hand hygiene recommendations include removal of jewelry, no brushes, and use of either antimicrobial soap or alcohol-based handrub according to the maker's recommendations.
Selection of hand hygiene agents should consider input from HCWs, interaction with other products or gloves, risk for contamination, accessibility and proper functioning of dispensers, approval of dispensers for flammable materials, and cost comparisons.
Soap or alcohol-based handrub should not be added to partially empty soap dispensers.
Skin care irritation in HCWs can be avoided by providing educational programs, alternative hand hygiene products for those with allergies or adverse reactions to standard products, and hand moisturizers to reduce irritant contact dermatitis.
Glove use does not replace the need for handrub or handwashing.
Gloves should be used if contact with potentially infectious body fluids, mucous membranes, or nonintact skin is anticipated.
Gloves should be removed or changed after each patient or after contact with a contaminated body site.
Artificial nails or extenders should not be used, and the length of natural nail tips should be less than 0.5 cm.
Educational and motivational programs for HCWs should focus on behavior; be multimodal; include senior executive support; educate about the advantages and disadvantages of various hand hygiene methods; monitor adherence and provide performance feedback; and encourage partnership between patients, families, and HCWs.
Healthcare administrators should provide and monitor safe, continuous water supply; provide alcohol-based handrub at the point of patient care; prioritize compliance; provide leadership, administrative support, and financial resources; ensure training; implement a multidisciplinary, multifaceted, and multimodal program to improve adherence; and adhere to national safety guidelines and local legal requirements.
National governments should prioritize adherence; consider funded, coordinated implementation and monitoring; support strengthening of infection control in healthcare settings; promote community hand hygiene; and encourage use of hand hygiene as a quality indicator in healthcare settings.

Clinical Implications

The WHO guidelines recommend handwashing with soap and water for visibly dirty hands, hands visibly soiled with body fluids, after toilet use, exposure to potential spore-forming pathogens, and if alcohol-based handrub is not available in other situations.
The WHO guidelines recommend alcohol-based handrub before and after touching patients; before handling invasive devices; after contact with body fluids or excretions, mucous membranes, nonintact skin, or wound dressings; between touching contaminated body site and another body site; after contact with inanimate surfaces and objects; and after removing gloves.

Source : http://cme.medscape.com/viewarticle/702403?src=cmenews

Call for Routine Cardiac Screening in Emergency-Department Patients with Cocaine Intoxication, Addiction

2009-05-23T11:38:00.001+07:00

May 21, 2009 (San Francisco, California) — Despite the fact that cocaine abuse accounts for approximately 25% of nonfatal myocardial infarctions (MIs) in young people, most addicted individuals presenting to the psychiatric emergency department are not routinely screened for this potentially lethal complication, new research suggests.

A retrospective study presented here at the American Psychiatric Association 162nd Annual Meeting showed that, of 122 cocaine-addicted patients, only 42% received an electrocardiogram (ECG) upon presentation to the emergency department. However, of these individuals, more than 90% had abnormal ECG results — including significant patterns of peak T waves. Further, 4 patients (8.2%) had ST elevations indicative of significant cardiac ischemia.

Valerie D'Aurora and John Charooonbara

"Many cocaine-addicted patients present to the psychiatric emergency department vs a medical emergency department. So this is potentially the only opportunity to screen for cardiac complications. Yet our research suggests psychiatrists are not being vigilant enough with respect to this," Valerie D'Aurora, from St. George's University School of Medicine, in Grenada, the West Indies, told Medscape Psychiatry.

Baseline ECG Should Be Standard Practice

To determine current management of cocaine-addicted patients presenting to the psychiatric emergency department and examine cardiac risk factors in this patient population, the researchers conducted a chart review of 122 patients with a diagnosis of cocaine dependence.

Of these individuals, 52 (42.6%) received an ECG and 4 (3.3%) had measurement of cardiac bioenzymes, including troponin and creatine kinase (CK)-MB. Among subjects who did receive an ECG, the most common findings were:

Nonspecific ST-T wave changes in 15 (31.2%) patients.
Peaked T waves in 23 (47.9%) patients.
Early afterdepolarizations in 19 (39.6%) patients.
ST elevations in 2 or more contiguous leads in 4 (8.3%) patients. However, the investigators note there were no baseline ECGs available for comparison to determine the acuity of changes.

The researchers also note ECGs were conducted, on average, 2 days after patients presented to the emergency department, with follow-up in only 2 (1.6%) patients. This, in spite of the fact that research shows the greatest risk for MI is 1 hour after cocaine use and is independent of dose, frequency, or routine. They also note that even trace amounts of cocaine in urine indicate the need to implement acute coronary syndrome (ACS) protocol.

"We're lucky if these patients get to the emergency department an hour after use, so they need to get an ECG immediately upon presentation," said Ms. D'Aurora.

Few Patients Assessed for Cardiac Risk Factors

Concomitant alcohol dependence was identified in 40 (32.8%) patients, and 81 (66.4%) individuals were nicotine dependent. In addition, 63 (51.6%) were also dependent on opioids and 26 (21%) on benzodiazepines.

When researchers analyzed data on additional cardiac risk factors, they found that this information, including family history of heart disease, hypertension, obesity, diabetes, and abdominal aortic aneurysm, were documented in only 21.3% of study subjects.

In light of these findings, Ms. D'Aurora and colleagues have developed an algorithm for individuals presenting to the psychiatric emergency department with a high suspicion of cocaine abuse to optimize patient care that includes a baseline ECG within 1 hour of presentation to the emergency department.

"What was really surprising about this study is what is not being done. When these patients have positive ECGs, they are not being referred to cardiologists per the ACS guidelines."

Regardless of whether they present to a medical emergency department or psychiatric emergency, they should be assessed for potential cardiac complications, said Ms. D'Aurora.

"With all of the other things that go on in a psychiatric emergency department, I think the importance of this is probably underrated. But even if it just means taking out your stethoscope and listening to the heart or taking a pulse, cardiac assessment in these patients needs to become part of the standard management in the psychiatric department," she said.

High Index of Suspicion

Asked by Medscape Psychiatry to comment on the study, Mark Willenbring, MD, director of the division of treatment and recovery research at the National Institute on Alcohol Abuse and Alcoholism, said the findings highlight the need to have a higher index of suspicion for cardiac complications in cocaine addiction and intoxication.

"We've known for a long time that this patient group is at particular risk of cardiac complications. This study suggests that there are significant cardiac abnormalities that are being missed in patients who are triaged to a psychiatric service, and I suspect that's quite likely," said Dr. Willenbring.

"That said, I'm not a cardiologist, and so I don't know if providing a routine ECG in all of these patients is necessary or cost-effective, but I do think one should always have a very high index of suspicion and investigate for the possible presence of cardiac abnormalities with a lower threshold in these patients than you would with others," he added.

Source : http://www.medscape.com/viewarticle/703149?sssdmh=dm1.474949&src=nldne

Acute Coronary Syndrome	Hyperthyroidism, Thyroid Storm, and Graves Disease
Aneurysm, Abdominal	Myocardial Infarction
Anxiety	Pregnancy, Eclampsia
Congestive Heart Failure and Pulmonary Edema	Pregnancy, Preeclampsia
Cushing Syndrome	Stroke, Hemorrhagic
Delirium Tremens	Stroke, Ischemic
Dissection, Aortic	Subarachnoid Hemorrhage
Encephalitis	Systemic Lupus Erythematosus
Glomerulonephritis, Acute	Toxicity, Amphetamine
Headache, Cluster	Toxicity, Phencyclidine
Headache, Migraine
Headache, Tension