Dr. Megan Fix (Emergency Medicine): A 45-year-old man was transferred on an emergency basis to this hospital from a community health center because of abdominal pain and hypotension.
On the day of admission, while lifting an air conditioner, he suddenly experienced severe abdominal pain, along with weakness and diaphoresis. He went to a community health center, arriving approximately 20 minutes later. He rated the pain as 10 on a scale of 0 to 10 (with 10 representing the most severe pain). He had not vomited. On examination, he was pale, profusely diaphoretic, and in extreme discomfort. His blood pressure was 84/49 mm Hg, and his pulse 100 beats per minute; respirations were 20 breaths per minute and shallow; oxygen saturation was 98% while he was breathing ambient air. His neck was supple, and his chest clear. His abdomen was rigid and diffusely tender, with guarding in all quadrants; the point of greatest tenderness was in the periumbilical area. Blood was drawn for laboratory testing, and a peripheral 20-gauge intravenous line was placed. Crystalloid intravenous solution was infused rapidly, and oxygen was administered at a rate of 2 liters per minute by nasal cannula. Emergency medical services were called to transport the patient to this hospital 15 minutes after his arrival at the health center.
Approximately 3 months before admission, the patient had been admitted to this hospital because of epigastric pain, nausea, and chills that had gradually developed hours after he had been drinking alcohol heavily. On examination at that time, his temperature was 38.3°C, and his abdomen was slightly distended. Testing for human immunodeficiency virus (HIV) antibody and HIV RNA was negative. Other laboratory-test results are shown in Table 1. Computed tomographic (CT) scanning of the abdomen, performed after the administration of contrast material, revealed splenomegaly with prominent mesenteric vasculature, stranding of mesenteric fat, a small amount of ascites, and gallstones without evidence of cholecystitis or pancreatitis. An ultrasonogram of the abdomen showed a diffusely echogenic liver, which was consistent with mild fatty infiltration. The patient's pain resolved; he refused further evaluation and was discharged the next day.
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The patient had undergone a left inguinal herniorrhaphy and surgical repair of a fracture of the right humeral head; he had a tattoo. He had a history of alcohol abuse and, according to relatives, had been drinking excessively in the previous 2 days. He did not smoke or use illicit drugs. He lived alone and was receiving disability compensation because of the shoulder injury. His parents had died in their 60s from myocardial infarctions. He had no allergies. Medications included cyclobenzaprine and ibuprofen.
When the patient arrived in the emergency department (30 minutes after leaving the health center and approximately 60 minutes after the onset of symptoms), his blood pressure was 77/46 mm Hg, and his pulse 118 beats per minute. He appeared to be in severe distress and was incontinent of stool, which was not bloody. His abdomen was tense and tender, without abdominal ecchymosis or palpable masses. Distal pulses were diminished. Laboratory-test results are shown in Table 1. A subclavicular central venous line and another peripheral line were inserted. In addition to crystalloid intravenous solution, uncrossed packed red cells were transfused simultaneously through the second peripheral venous catheter and the central line.
A diagnostic procedure was performed.
Differential Diagnosis and Management
Dr. Sanjeeva P. Kalva: Three months before the current admission, abdominal CT (Figure 1), performed after the administration of oral contrast material, showed mild hepatosplenomegaly and minimal ascites, diffuse fatty infiltration of the liver, and calcified gallstones with no evidence of cholecystitis. Although the CT was not directed toward assessment of the vessels, there was a suspicion of celiac-axis stenosis. Ultrasonography of the abdomen showed minimal ascites and an enlarged, echogenic liver with an irregular surface, suggesting the possibility of chronic liver disease.
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Dr. Nancy Lee Harris (Pathology): The discussants for this case are aware of the diagnosis, and several participated in this patient's care. They will discuss the roles of emergency services, surgery, and interventional radiology in the diagnosis and management of this case and others like it.
Emergency Evaluation and Management
Dr. Andrew T. Reisner: Emergency care begins with assessment of the airway, breathing, and circulation (the ABCs). This patient's airway and respiration were not compromised; however, the circulation was abnormal, with hypotension, diminished pulses, severe abdominal symptoms, and loss of bowel control. There was no time for additional testing, and our provisional diagnosis was circulatory shock, a state of global hypoperfusion that is inadequate for sustained survival.
Differential Diagnosis of Circulatory Shock
The differential diagnosis of shock in this patient with abdominal pain includes hemorrhage, which can result from a perforated viscus, a ruptured abdominal aortic aneurysm, or, in female patients, a ruptured ovarian cyst. Processes that cause hypovolemia because of interstitial fluid sequestration, such as pancreatitis, or that cause relative hypovolemia, such as a sepsis syndrome due to bacterial peritonitis, are unlikely to cause such precipitous decompensation.
Cardiogenic causes should also be considered. In one series of atypical acute coronary syndromes,1 5% of patients presented with abdominal pain. In this case, a primary cardiogenic cause seems unlikely, but a secondary cardiogenic component is possible, since global hypoperfusion impairs cardiac function, and in late-stage hypovolemic shock even restoration of blood volume cannot stop cardiac deterioration.2,3 Moreover, the patient may have preexisting disease, such as valvular disease or, more likely in this case, alcoholic cardiomyopathy that affects his presentation. Finally, vasogenic (distributive) causes, such as sepsis, anaphylaxis, and adrenal insufficiency, could be considered. Low vascular tone is a common late end point for circulatory shock from all causes.4 Cardiovascular compromise can also result from obstruction of the circulation by pulmonary embolism, tension pneumothorax, arterial dissection, air embolism, or compression of the inferior vena cava (often due to a gravid uterus). In this case, such causes appear to be unlikely, though in the first few minutes of any emergent care, historical information can be unreliable, and a broad differential diagnosis is prudent.
Considering the suddenness of the onset of symptoms and the tenderness of the abdomen in this patient, a sudden loss of blood from the circulation was the likely cause of shock. The patient's initial vital signs and the findings on physical examination were consistent with class III hemorrhage (loss of approximately 30 to 40% of blood volume), after already receiving almost a liter of prehospital crystalloid volume. Moreover, the endogenous shift of an additional liter or so of interstitial fluid into the vasculature would be typical after 30 to 60 minutes of hypovolemic hypotension.5,6 Circulatory arrest could occur in this patient in a matter of minutes if bleeding continued or secondary cardiac dysfunction developed.
Management of Hemorrhagic Shock
We immediately administered non–cross-matched packed red cells. As important as the decision to use blood products is the decision about how to administer them. The short length of large-bore peripheral intravenous catheters makes them effective for rapid-volume infusion.7,8 Large-caliber (e.g., 8 or 9 French) introducer catheters inserted into a central vein are another good option; the presence of side ports and long triple-lumen central lines results in a higher resistance to flow than from short, wide-bore catheters.9,10 Use of pressure bags and dilution of the packed red cells to reduce viscosity improve the flow.11 The early need for fresh-frozen plasma, platelets, or both should be anticipated, since uncontrolled coagulopathy is a major cause of potentially preventable early deaths in this setting.12,13 The electrocardiogram and temperature were monitored continually in this patient, and serum electrolyte concentrations were measured frequently; with massive transfusion or abnormal hepatic function, as this patient had, citrate in the red-cell units may cause hypocalcemia. Extracellular potassium levels may become too high (because of red-cell lysis) or too low (when transfused red cells become active).14
Although it is often safer and easier to perform airway intubation in a controlled fashion well in advance of any respiratory failure, we deferred endotracheal intubation because this patient was protecting his airway, and we thought that intubation would be likely to exacerbate his dire circulatory state. Positive-pressure ventilation reduces the pressure gradient for venous return, and many anesthesia-induction agents may exacerbate shock by means of either centrally mediated sympatholysis or direct vasodilatation. In preparation for possible intubation, we did administer supplemental oxygen to maximize alveolar oxygen reserve. We secured a bag-valve mask tightly to the patient's face; this type of mask can provide more oxygen than a nonrebreather mask when used with a high rate of oxygen flow.15,16 However, we allowed the patient to breath spontaneously, without providing positive pressure, to avoid gastric insufflation and the associated risk of aspiration during subsequent intubation. Pressors were also prepared in case his blood pressure fell further.
The optimal systolic blood pressure in patients with uncontrolled hemorrhage is not known. Normal blood pressures may theoretically disrupt recently formed thrombi at the site of bleeding and drive additional hemorrhage. Some animal models suggest a survival benefit with permissive hypotension during uncontrolled hemorrhage.17,18,19 Data on clinical outcomes are mixed, with one study after penetrating trauma20 showing a benefit and another after penetrating and blunt trauma21 showing no benefit with prolonged permissive hypotension (delayed resuscitation). In this case, our target was a systolic blood pressure of 90 mm Hg.
Simultaneously with resuscitation, emergency surgical consultation was requested.
Surgical Evaluation and Management
Identifying the Source of the Hemorrhage
Dr. Marc A. de Moya: In the initial surgical evaluation of a patient such as this, who appears to be in hemorrhagic shock, the source of bleeding is the primary consideration. It is important to remember that control of the hemorrhage is the first priority in patients with hemorrhagic shock. Fluid or blood-component resuscitation is not a substitute for definitive control of the hemorrhage.22
There are five regions into which exsanguination may occur: the intraperitoneal space, the retroperitoneum, the thoracic cavity, the thigh compartments (in the case of femoral fractures), and the exterior of the body. Careful attention to the history of the injury will suggest specific regions. In this case, the history of lifting followed by intense abdominal pain and tenderness narrowed the region of concern to the peritoneal cavity and the retroperitoneal space.
Focused Assessment with Sonography for Trauma
To confirm that the abdomen was the site of bleeding, we performed a focused assessment with sonography for trauma (FAST), a rapid bedside ultrasound examination of the abdomen that allows rapid evaluation of the abdominal cavity for the presence of fluid or blood. The FAST examination is composed of four specific views; the right upper quadrant (or Morison's pouch), the left upper quadrant (or lienorenal recess), the pelvis, and the pericardium. If bleeding into the peritoneal cavity has occurred, there is a high likelihood of positive results on examination. However, FAST is limited by its inability to detect the precise source of the bleeding or to assess the retroperitoneum; its accuracy depends on the skill of the operator, and examinations may be equivocal in obese patients. FAST cannot distinguish blood from other types of fluid in the abdomen.
FAST in this patient (Figure 2) disclosed a large amount of intraperitoneal fluid. However, since the patient had a history of liver disease, the fluid could represent blood or ascites. Fortunately, the electronic medical record contained the results of the earlier CT and ultrasound examinations, which showed minimal ascites. We were able to compare the images of the ultrasound examination from 3 months earlier with the FAST results, and we could conclude that the fluid seen on the latter examination was probably blood. The combination of the patient's symptoms, the physical findings, and the presence of new abdominal fluid led to the conclusion that an emergency laparotomy was necessary. The patient was immediately transferred to the operating room without further testing.
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Exploratory Laparotomy Findings
A midline incision from the xiphoid process to the pubis was performed, and the abdomen was entered. A large amount of blood was found within the peritoneal cavity. A rapid but systematic evaluation of the abdomen revealed a large supramesocolic hematoma filling the lesser sac, as well as free intraperitoneal hemorrhage. The aorta was cross-clamped with a spinal compressor in the supraceliac position for initial proximal control of the bleeding. When the lesser sac was opened, the source of the bleeding was identified along the inferior border of the pancreas. The middle colic artery was identified and traced to the base of the mesocolon; it was not bleeding. A branch, thought to be coming from the inferior pancreaticoduodenal artery, was identified along the inferior border of the pancreas, which contained an aneurysm that had ruptured. Because the base of the aneurysmal artery extended into the pancreas, it was difficult to dissect the distal artery completely. The wall of the aneurysmal vessel was oversewn to stop the bleeding. The bleeding subsided, and the cross-clamp was removed. The bowel appeared to be viable.
The patient was becoming hypothermic and acidotic at the completion of the vascular control, indicating that the lethal triad of hypothermia, acidosis, and coagulopathy was imminent.23 We decided to leave the abdomen open in order to lower the risk of an abdominal compartment syndrome and allow easy access for a second-look operation. The patient was transferred to the surgical intensive care unit for further resuscitation and warming. His vital signs remained stable, and he was returned to the operating room 8 hours later for reinspection. The bowel still appeared viable; there was a small amount of blood oozing from the base of the mesentery. Since we had been unable to fully access the pancreaticoduodenal arcade as it entered the pancreas, a definitive diagnosis was still necessary. To better visualize the arterial anatomy, angiography was performed.
Dr. Marc A. de Moya's Diagnosis
Ruptured pancreaticoduodenal-artery aneurysm.
Pancreaticoduodenal Aneurysms
Dr. Glenn M. LaMuraglia: Aneurysm of the pancreaticoduodenal artery is a very unusual problem. Aneurysms of visceral arteries are rare, and only 2% of them occur in the pancreaticoduodenal artery. There are three major clinical presentations of visceral-artery aneurysms: hemorrhagic collapse from rupture, as in the case under discussion; vague abdominal symptoms, with an aneurysm found on imaging; and an incidental finding in an otherwise asymptomatic person. In contrast to the situation with aneurysms of other arteries, the size of pancreaticoduodenal-artery aneurysms does not appear to be related to the risk of rupture.
Pancreaticoduodenal aneurysms may be either true aneurysms, resulting from a primary abnormality of the vessel wall, or false aneurysms, resulting from injury and erosion of the vessel wall, most commonly after trauma or inflammation.24 In the absence of a history of abdominal surgery or trauma, this patient probably has a true aneurysm. True aneurysms of the pancreaticoduodenal artery are more common in men than in women and are associated with a history of alcohol use or pancreatitis. The mean age at presentation is 40 to 50 years, suggesting that the pathophysiology of these aneurysms is different from that of the atherosclerotic aneurysms that occur in the elderly.25,26 The demographic characteristics of this patient are thus consistent with pancreaticoduodenal-artery aneurysm.
Celiac-Artery Stenosis
A CT scan obtained 3 months before admission showed a suggestion of celiac-artery stenosis in this patient. Pancreaticoduodenal-artery aneurysms, both primary and secondary, are associated with celiac-artery stenosis or occlusion in 60 to 75% of cases.26 Obstruction of the celiac artery is thought to contribute to the formation of aneurysms by causing the development of collaterals to fill the hepatic and splenic arteries, creating a low-resistance vascular bed and resulting in high flow through the pancreaticoduodenal artery (Figure 3).24 This high flow is thought to contribute to the development of an aneurysm. Celiac-artery obstruction is typically caused by pressure from the median arcuate ligament. Incising the arcuate ligament in these instances of performing a bypass from the aorta to the hepatic artery may result in regression of pancreaticoduodenal-artery aneurysms.25
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Management of Pancreaticoduodenal Aneurysm
The connections and collaterals between the pancreaticoduodenal, gastroduodenal, and other visceral arteries are numerous, and the anatomy can be quite variable.27 For these reasons, one of the most important steps in planning treatment, either radiologic or surgical, is to determine which end-organ vessels are involved and what their relationship is to the aneurysm; it can then be decided whether the aneurysm can be safely embolized or the vessel ligated, or whether the aneurysm must be ligated or repaired with a bypass.
The treatment options are revascularization of the celiac artery, surgical repair, or percutaneous embolization of the pancreaticoduodenal artery aneurysm. Revascularization of the celiac artery, which is typically performed as an elective procedure before an acute episode of bleeding has occurred, can be accomplished by incising the arcuate ligament or stenting or bypassing the artery.
The surgical treatment options for the pancreaticoduodenal artery aneurysm include ligation of the aneurysm, with or without a bypass, depending on the anatomy, and repair by suture plication. The artery can be excluded or resected by tying the proximal and distal vessels. Before 1980, the majority of patients with bleeding pancreaticoduodenal-artery aneurysms were either not treated or treated surgically; the mortality was approximately 40%. Since 1980, with better resuscitation methods and the use of catheter embolization, the mortality is as low as 0% in some studies.25,26 In patients with acute bleeding, such as this patient, embolization is the treatment of choice, if it is available; otherwise, surgical intervention should be considered.
In this case, we decided to perform catheter embolization.
Vascular Radiographic Evaluation and Management
Dr. Kalva: An abdominal aortogram was obtained, which showed high-grade stenosis of the celiac axis, with retrograde filling of the common hepatic and splenic arteries through the pancreaticoduodenal arcade and dorsal pancreatic artery. The superior mesenteric artery, portal vein, and renal arteries were normal. A selective superior mesenteric arteriogram (Figure 4A) confirmed the findings seen on the aortogram. In addition, the anterior and posterior inferior pancreaticoduodenal arteries were enlarged, and there were aneurysms in the posterior inferior pancreaticoduodenal artery and dorsal pancreatic artery. The posterior inferior pancreaticoduodenal artery and the dorsal pancreatic artery were selectively catheterized with a microcatheter, and the aneurysms were embolized with 0.018 microcoils. After embolization (Figure 4B), the aneurysms were occluded, and there was persistent filling of the celiac axis through the pancreaticoduodenal arcade.
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Dr. de Moya: Unfortunately, despite the successful treatment of the aneurysms, fulminant liver failure developed, complicated by ventilator-associated Pseudomonas aeruginosa pneumonia, the acute respiratory distress syndrome, and the hepatorenal syndrome, and the patient died about 1 month after admission. Permission for an autopsy was declined. It appeared that the severity of the underlying liver disease impeded recovery from the circulatory compromise that was due to the intraabdominal hemorrhage.
Dr. Reisner: Emergency management in a case like this illustrates the value of the electronic medical record. This patient had been previously treated in our system, and so his medical history was immediately available to us. A mechanism offering universal access to electronic health records would extend this advantage to all patients.28,29 Despite legitimate concerns of privacy advocates, such information is vital to emergency management.
Anatomical Diagnosis
Celiac-artery stenosis and multiple aneurysms of the pancreaticoduodenal arcade, with rupture.
Dr. Reisner reports receiving grant support from Sharp and holding patents related to noninvasive measurement of blood pressure; Dr. LaMuraglia, receiving consulting fees from Light Sciences and grant support from Cook Zenith, Gore, and Medtronic; and Dr. Kalva, receiving consulting fees from Cordis Endovascular and Cordis (a Johnson & Johnson company), and grant support from Cordis Endovascular and Cook. No other potential conflict of interest relevant to this article was reported.
Source Information
From the Divisions of Trauma, Emergency Surgery, and Surgical Critical Care (M.A.M.) and Vascular and Endovascular Surgery (G.M.L.), and the Departments of Emergency Medicine (A.T.R.), and Radiology (S.P.K.), Massachusetts General Hospital; and General Surgical Service (M.A.M., G.M.L.), and the Departments of Medicine (A.T.R.) and Radiology (S.P.K.), Harvard Medical School.
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