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

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.

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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

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

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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

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.

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"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.

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Journal reference:

1. 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

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.

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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.

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Journal reference:

1. 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

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

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

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

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

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

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.

1. 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

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

1. 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.
2. Schnitzer PG, Ewigman BG. Child deaths resulting from inflicted injuries: household risk factors and perpetrator characteristics. Pediatrics. 2005;116:e687-93.
3. 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.
4. Billmire M, Myers P. Serious head injury in infants: accident or abuse? Pediatrics. 1985;75:340-2.
5. Hettler J, Greenes DS. Can the initial history predict whether a child with a head injury has been abused? Pediatrics. 2003;111:602-7.
6. Jenny C, Hymel KP, Ritzen A, Reinert SE, Hay TC. Analysis of missed cases of abusive head trauma. JAMA. 1999;281:621-6.
7. Peters ML, Starling SP, Barnes-Eley ML, Heisler KW. The presence of bruising associated with fractures. Arch Pediatr Adolesc Med. 2008;162:877-81.
8. 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.
9. 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.
10. 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.
11. 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.
12. Rubin DM, Christian CW, Bilaniuk LT, Zazyczny KA, Durbin DR. Occult head injury in high-risk abused children. Pediatrics. 2003;111:1382-6.
13. Laskey AL, Holsti M, Runyan DK, Socolar RR. Occult head trauma in young suspected victims of physical abuse. J Pediatr. 2004;144:719-22.
14. 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.
15. 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.
16. Merten DF, Radkowski MA, Leonidas JC. The abused child: a radiological reappraisal. Radiology. 1983;146:377-81.
17. Diagnostic imaging of child abuse. Pediatrics. 2009;123:1430-5.
18. Kleinman PK, Marks SC, Blackbourne B. The metaphyseal lesion in abused infants: a radiologic-histopathologic study. AJR Am J Roentgenol. 1986;146:895-905.
19. 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.
20. 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.
21. 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.
22. 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.
23. US Department of Health and Human Services Administration on Children Youth and Families. Child Maltreatment 2006. Washington, DC: US Government Printing Office; 2008.
24. 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.
25. Makoroff KL, Putnam FW. Outcomes of infants and children with inflicted traumatic brain injury. Dev Med Child Neurol. 2003;45:497-502.
26. 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

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

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

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

1. Hirshberg B, Biran I, Mendel G, Mordechai RK. Hemoptysis: etiology, evaluation, and outcome in a tertiary referral hospital. Chest 1997; 112: 440-444.
2. Weaver LJ, Solliday N, Cugell DW. Selection of patients with hemoptysis for fiberoptic bronchoscopy. Chest 1989; 76: 116-119.
3. 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.
4. Montgomery E, Goldblum JR, Fisher C. Myofibrosarcoma: a clinicopathologic study. Am J Surg Pathol 2001; 25: 219-228.
5. 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

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

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.¹ Therefore, 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