Emergency Medicine Clinics of North America
Volume 14 Number 3 August 1996
Copyright 1996 W. B. Saunders Company

 


Gastrointestinal Emergencies, Part I

 


VASCULAR ABDOMINAL EMERGENCIES

James S. Walker DO

Daniel J. Dire MD

From the Section of Emergency Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma

 


Address reprint requests to James S. Walker, DO Section of Emergency Medicine University of Oklahoma Health Sciences Center 800 Northeast 13th Street Room EB-319 Oklahoma City, OK 73104

 

The views expressed in this article are those of the authors and do not reflect the official policy or position of the Department of the Navy, the Department of Defense, or the US Government.

 

Vascular abdominal emergencies are an uncommon but significant cause of abdominal pain, back pain, hemorrhagic shock, and death in adults. Vascular disorders in the abdominal cavity incorporate a wide spectrum of pathologic processes from thrombosis to embolism to aneurysms. Prompt diagnosis calls for knowledge of the typical as well as the atypical presentations of the array of these vascular diseases. It is imperative that emergency physicians be proficient in conducting a systematic evaluation in patients who may be asymptomatic, symptomatic, or in hemorrhagic shock. Efficient and timely management requires that the emergency physician has a thorough comprehension of the nuances associated with diagnosis and treatment.

INTRODUCTION

The term acute abdomen is generally applied when abdominal pain is objectively significant in nature, rapid or sudden in onset, and may be accompanied by nausea, vomiting, hematemesis, diarrhea, constipation, melena, hematochezia, urinary symptoms, syncope, hypotension, and hypovolemic shock. The clinician is faced with the burden of determining whether the abdominal pain is visceral, somatic, or referred. Is the source of this acute abdomen inflammatory, infectious, obstruction or perforation of a hollow viscus, urologic, obstetric, gynecologic, vascular, or even metabolic in origin?[21] [24] [31] [50] [57] [78] It is evident that even the most experienced clinician can be challenged by this diagnostic enigma called the acute abdomen. In short, the evaluation of the acute abdomen can be difficult. In many instances, there are no pathognomonic laboratory tests nor are there any pathognomonic radiographic studies (plain films). No diagnostic aid is of more value than a complete, thorough history and physical examination combined with a high index of suspicion.[21] [50] [57] [78] These concepts are especially true when the acute abdomen is secondary to a vascular lesion or pathologic process.

 

The common pathophysiologic mechanism for vascular abdominal emergencies is the interference or interruption of normal blood flow (arterial or venous) to the organs of gastrointestinal (GI) tract and other organs within the abdominal cavity.[24] [31] [57] [78] This disruption of normal blood flow can be mediated by a number of different vascular processes. These include intravascular hyperviscosity, arteriosclerosis, thrombosis, vasculitis, emboli, prolonged hypoperfusion, aneurysms, various forms of vascular ectasia, and GI-vascular fistulas.[24] [31] [57] [78] Regardless of the vascular cause, these disorders have symptoms of abdominal pain, bleeding (GI or intra-abdominal), or both. With such a diverse and nonspecific clinical presentation, it is easy to see why the evaluation of a vascular acute abdomen can be perplexing. Even a short delay in diagnosis, however, can lead to significant morbidity and mortality. It is the intent of this article to heighten the awareness of the emergency physician to the spectrum of vascular abdominal emergencies and to facilitate a timely diagnosis and efficient management. This article does not discuss the management of GI bleeding, per se, because it is a topic in itself and is discussed elsewhere in this issue.

 

To accomplish these goals, it is beneficial to review the vascular anatomy of the abdomen and to identify the risk factors that predispose one to the development of these vascular abdominal emergencies.

REVIEW OF ABDOMINAL VASCULAR ANATOMY

The primary artery supplying the digestive system and other organs within the abdominal cavity is the abdominal aorta. The abdominal aorta enters into the abdomen through the aortic opening of the diaphragm at the level of the 12th thoracic vertebra. It travels behind the peritoneum but anterior to the lumbar vertebrael column to the level of the 4th lumbar vertebra. Here, at L4, the aorta branches into the two common iliac arteries.[67] [68]

 

Text Box: Figure 2. The celiac artery and its three major branches: the splenic, left gastric, and hepatic arteries.
 
The intra-abdominal portions of the digestive tract (stomach, small intestine, and large intestine) are nourished almost entirely by the three major unpaired arterial tracts arising from the ventral aspect of the abdominal aorta. These are the celiac artery, the superior mesenteric artery, and the inferior mesenteric artery. Approximately 30% of the resting cardiac output flow through these three splanchnic arteries. The anatomic condition of these three main arteries and their interrelationships by means of collateral circulation determines the potential for occurrence of acute or chronic vascular ischemia.[67] [68]

Celiac Artery

The celiac artery originates from the aorta at the level between the 12th thoracic vetebrae. The celiac artery is large in diameter, short in length, and almost perpendicular to the aorta. The celiac artery is the artery of the foregut and supplies the GI tract from the lower third of the esophagus down as far as the middle of the second part of the duodenum. The celiac artery almost immediately gives rise to its three major branches: the splenic, left gastric, and hepatic arteries (Fig. 2). The splenic artery feeds the greater curvature of the stomach. The left gastric artery provides the lesser curvature of the stomach, whereas the hepatic artery gives rise to the gastroduodenal artery, the right gastroepiploic, and superior pancreatoduodenal arteries. The hepatic artery nourishes the pancreas and duodenum.[67] [68]

 

It is noteworthy that because of the large size of the celiac artery and its angle of departure from the aorta (90 degrees) that ischemic events (embolic or thrombotic) are extremely rare. Another factor is the extensive network of collateral circulation between the pancreatoduodenal arteries and the superior mesenteric artery protects against an ischemic event.[67] [68]

Superior Mesenteric Artery

The superior mesenteric artery (SMA) arises from the ventral surface of the abdominal aorta just caudal to the celiac artery at the level of the first lumbar vertebra. The SMA is the artery of the midgut and serves the digestive tract from the middle of the second part of the duodenum to the distal third of the transverse colon. The SMA originates from the aorta at approximately a 45-degree angle and then branches into the inferior pancreatoduodenal artery, middle colic artery, right colic artery, ileocolic artery, and jejunal and ileal arteries (Fig. 3). There is a significant potential for collateral flow within the primary and secondary arcades. The arteriae rectae, however, appear to represent end arteries with few anastomotic connections. Anastomotic connections between the middle colic artery and the inferior mesenteric artery are large in number and provide a significant capacity for collateral circulation.

Inferior Mesenteric Artery

Text Box: Figure 3. The superior and inferior mesenteric arteries and their anastomotic connections.
 
The inferior mesenteric artery (IMA) arises from the abdominal aorta at the level of the third lumbar vertebra. This is just cephalad to the bifurcation of the aorta into the common iliac arteries at the level of the fourth lumbar vertebra. The IMA is the artery of the hindgut and accommodates the large intestine from the distal third of the transverse colon to halfway down the anal canal (Fig. 3).

 

 

The IMA branches into the left colic artery and then gives rise to two or three. sigmoid branches and terminates as the superior rectal artery.[67] [68]

 

There are three primary routes of communication or collateral flow between the SMA and the IMA. These are the marginal artery of Drummond, the central anastomotic artery, and the arc of Riolan. In the presence of occlusion of the SMA or the IMA, large collateral flow will occur in the central anastomotic artery or the arc of Riolan to prevent massive intestinal ischemia.[67] [68]

Renal Arteries

The renal arteries are short, paired, lateral branches of the abdominal aorta which have a blood flow rate of 20% to 25% of the resting cardiac output.[67] [68] It is important to note that the renal arteries as well as the abdominal aorta are retroperitoneal. The right renal artery is found at the level of the first lumbar vertebrae, whereas the left renal artery is located a little cephalad to the right renal artery.[67] [68] Reduced blood flow to the kidney will activate the reninangiotensin system and will, in turn, elevate the systemic blood pressure by eliciting vasoconstriction of the arterioles and increased aldosterone secretion. These physiologic changes result in increased blood flow to the kidney and other organs. The vascular lesions to be wary of here are renal artery thrombosis and renal artery aneurysms.

GENERAL ANATOMIC OBSERVATIONS

The stomach and intestines receive their blood supply from the celiac, superior mesenteric, and inferior mesenteric arteries. The collateral blood flow between these three arteries is so great that usually arterial flow can be maintained despite obstruction to one or more major arteries. Another important point is the ability to distinguish between large vessel disease and small vessel disease.[8] Large vessel disease exhibits a tendency toward embolic and thrombotic events that occur at the proximal aspect of the major arterial branches. Small vessels, called arteriae rectae, derived from the terminal branches of the intestinal arcade in the small intestine and from the marginal artery in the colon, penetrate the muscle layer of the gut to form a rich submucosal plexus. In the small intestine, arterioles arise from the submucosal plexus to supply each villus. A central arteriole runs the length of each villus and branches at the tip to form a capillary network, which is drained by venules that parallel the central arteriole. It becomes apparent that small vessel disease is much more sensitive to vasculitis and prolonged hypoperfusional states than is large vessel disease. Also, the potential for collateral flow is much less in small vessel disease than in large vessel disease.

Venous Circulation

In general, veins parallel arteries in the smaller branches and for parts of the main mesenteric trunks. The superior mesenteric vein and splenic vein, however, join to form the portal vein which enters the liver after receiving the coronary vein. The inferior mesenteric vein drains into the splenic vein. Connections between the splanchnic and systemic venous beds become enlarged in the setting of portal hypertension. These areas of collateral flow as a result of portal hypertension become clinically significant as sites of potential thrombosis, for example, hepatic vein thrombosis, portal vein thrombosis, and splenic vein thrombosis. Thrombosis of the inferior vena cava (IVC) is usually secondary to the external compression of the IVC by a retroperitoneal mass (tumor or metastatic lymph nodes).[67] [68] Thrombosis of the IVC usually results in the development of enormous venous collateral flow via the lumbar veins. It is important to note that thrombosis of the IVC presents clinically with bilateral lower extremity edema and not abdominal pain.

 

In conclusion, if the occlusion of a large vessel is insidious in onset, adequate collateral circulation may develop so that the ischemic process may be minimized or even prevented. Occlusion of a vessel over a short period, however, may not allow for the development of collateral circulation and result in ischemic necrosis. Small vessels are relative end-arterioles and have little opportunity for collateral blood flow.

RISK FACTORS

A multitude of anatomic and physiologic conditions can predispose one to interfere or impede normal blood flow to intra-abdominal organs. Anatomic conditions associated with vascular diseases of the bowel include: arteriosclerosis, vasculitis, thrombus, emboli, ectasia, and aneurysms. The most common cause of arterial thrombosis, in general, is ordinary atherosclerotic vascular disease. Emboli (arterial) are secondary to atrial fibrillation, valvular heart disease, bacterial endocarditis, ventricular aneurysms, and acute myocardial infarction. Physiologic conditions associated with vascular occlusion of the bowel include the following: hypercoagulable states, portal hypertension, prolonged hypoperfusion,[24] [31] [57] drugs/medications, cardiac arrhythmias, and inflammatory processes in the bowel.

SIGNS AND SYMPTOMS

Unfortunately, there are very few pathognomonic presentations of vascular abdominal pain. In the majority of situations, the abdominal pain is nonspecific and difficult to localize. The pain displayed by the patient is usually out of proportion to the physical finding by the neutral examining physician. The disregard or inattention to the complaints of severe pain because there were no peritoneal signs, leukocytosis, or other objective findings of an acute abdomen has lured many emergency physicians down the path of humility.[21] [24] [31] [50] [59] [79] Misdiagnosis is a common problem because of the lack of objective findings. More than 50% of the patients with a vascular abdominal emergency will not have a straightforward presentation.[59] A leaking abdominal aortic aneurysm is characterized by severe abdominal pain, often radiating to the groin, flank, or back. This same presentation could be easily mistaken for renal colic. Only when the patient starts to develop hypotension and cardiovascular collapse does it become plain that the problem is an abdominal vascular emergency. To not make the diagnosis until the patient becomes hemodynamically unstable, however, does not speak well for his or her outcome or the physician's diagnostic skills. Mesenteric ischemia is a particularly difficult diagnostic challenge. Classically, the early symptoms are severe, diffuse abdominal pain with minimal physical findings. As the vascular pathologic process continues to evolve, the patient will develop systemic toxicity (look "sick," acidosis, bleeding, and shock). The morbidity and mortality rates are high. Again, a delay in diagnosis can be deleterious to the patient and litigious to the physician.

 

The emergency physician should always enter an abdominal vascular emergency into the differential diagnosis of every acute abdomen that he or she evaluates. Also, the reliance on laboratory tests and routine radiographic studies to establish the diagnosis is filled with pitfalls.

SYSTEMATIC APPROACH TO ABDOMINAL VASCULAR EMERGENCIES

From the preceding discussion, it is apparent that abdominal vascular lesions cover a spectrum of pathophysiologic processes with many different modalities of management. Clinically, because it is almost impossible to identify if the lesion is occurring in the SMA or the IMA distribution or the renal artery versus an aortic aneurysum, it would be best to review these vascular disorders by the following classification system: thrombosis, emboli, and aneurysms.

ABDOMINAL VASCULAR THROMBOSIS

Abdominal vascular thromboses are rare events that may present with acute, subacute, or chronic symptoms. The underlying causes are most commonly atherosclerosis, hyperviscosity, hypercoagulable states, or trauma. Clinical symptoms vary with the anatomic site of occlusion and the ischemic or infarcted organs involved.

Aortic Thrombosis

Aortic thrombosis is relatively rare and has been reported following blunt abdominal trauma and in nontraumatic conditions even in the absence of an abdominal aortic aneurysm.[6] [7] [26] [34] [37] [41] [44] [52]

Patients with subacute or chronic ascending aortic thrombosis may present with the classic Leriche syndrome of intermittent calf, thigh, and hip claudication associated with impotence.[20] Acute aortic thrombosis will classically present with loss of femoral pulses with signs of lower limb ischemia, and with anterior spinal artery syndrome. A proportion of patients will develop sudden hypertension.[84] Rapid total occlusion of the abdominal aorta may be manifested by the sudden onset of pain, pallor, and paralysis. Infarction of the spinal cord in the distribution of the anterior spinal artery results in paraplegia, loss of pain, and thermal sensation, but preservation of position, vibration, and deep pain sensation. If the aortic thrombosis is limited to the infrarenal aorta, the spinal cord is preserved.[46]

 

Conditions associated with aortic thrombosis include trauma, atherosclerosis, antithrombin III deficiency, protein C deficiency, lupus anticoagulant, nephrotic syndrome, spinal metastases, following arterial catheterization, and following heparin-induced thrombocytopenia.[26] [41] Traumatic aortic thrombosis is thought to occur by rapid deceleration and shearing forces that produce intimal tears, dissection, and thrombosis.[34] Resultant complication of aortic thrombosis includes renal failure, renal or bowel infarction, limb loss, and spinal cord infarction.

 

Diagnosis and definitive therapy need to be done rapidly if aortic thrombosis is suspected, because the longer the time delay, the poorer the prognosis for recovery of motor and sensory functions.[37] Acute aortic thrombosis is often fatal with a mortality of 14% to 50%.[7] [26] The treatment of choice for acute aortic thrombosis is emergent surgical aortic reconstruction or a bypass procedure.[41]

Mesenteric Artery Thrombosis

Thrombosis of the superior and inferior mesenteric arteries are caused by atherosclerosis, hypoperfusion states, or hypercoagulable conditions and result in bowel ischemia. These are discussed in the section on mesenteric ischemia and infarctions below.

Renal Artery Thrombosis

Renal artery thrombosis is most commonly caused by a thrombus superimposed on atherosclerotic plaque.[64] [82] It has also been associated with blunt abdominal trauma[12] [18] [38] ; idiopathic nephrotic syndrome, idiopathic thrombocytopenia, polycythemia vera, and thromboangiitis obliterans[82] ; renal transplantation[32] ; intra-aortic catheter placement[2] ; oral contraceptive use[27] ; cyclosporine toxicity[62] ; intravenous (IV) cocaine injection[83] ; postoperative hypercoagulability; and renal angiography[11] ; but it can occur spontaneously.[11] [51] It is most commonly seen in patients 30 to 50 years of age.[11]

 

Traumatic renal artery thrombosis is thought to result from stretching of the arteries during deceleration producing intimal tears, subintimal dissection, and thrombosis.[38] Unilateral injury is more common on the left because of the greater length and mobility of the left renal pedicle.

 

The most frequent symptom of renal artery thrombosis is flank pain, which may be a sudden, sharp unremitting pain located in the flank or upper abdomen.[11] The pain may be associated with fever, leukocytosis, nausea, vomiting, hematuria (in 33% to 50%), proteinuria, and hypertension. Gross hematuria is present in 30% of patients with unilateral thrombosis, microscopic hematuria is present in 43%, and 27%, of patients have no hematuria.[3] The presentation often mimics ureterolithiasis; therefore, thrombotic occlusion of the renal artery should be considered in patients who present with lumbar flank pain and hematuria, in whom the excretory urogram shows severe malfunction of one kidney, and stone disease can be excluded.[73]

 

A high index of suspicion is required to make the diagnosis of renal artery thrombosis. When suspected, the initial diagnostic study is an intravenous pyelogram. Alternatively, in the setting of blunt abdominal trauma, an abdominal CT scan with intravenous contrast may be substituted as it will reveal associated intra-abdominal injuries.[13] [40] If the affected kidney is not visualized, an arteriogram should be rapidly performed to make the definitive diagnosis in order to expedite treatment.[11] Traumatic thrombosis of a segmental branch of the renal artery is being diagnosed with increased frequency by isotope renography, arteriography, or CT.[13]

 

Patients with traumatic renal artery thrombosis are best treated with prompt surgical revascularization with bypass grafting being the procedure of choice.[38] Nontraumatic occlusion may be treated with thrombolytic therapy or prompt surgical revascularization individualized for each patient situation. Long-term complications include renal artery stenosis, hypertension, and in the case of bilateral involvement, renal insufficiency.

Renal Vein Thrombosis

Renal vein thrombosis is more common than renal artery thrombosis. The causes fall into four basic categories: (1) alteration of renal blood flow, which is most common in infants and children; (2) thromboembolic states, either as an extension of lower extremity or pelvic deep venous thrombosis, or as a result of hypercoagulable states (e.g., malignancy, oral contraceptives, congestive heart failure); (3) involvement of the vascular pedicles is seen with retroperitoneal fibrosis, abscess, or lymphoma; and (4) nephropathic conditions and tumors, including renal cell carcinoma, membranous and membranoproliferative glomerulonephritis, amyloidosis, collagen vascular diseases, and diabetic glomerulosclerosis.[29] [36] Renal vein thrombosis is most commonly a consequence of nephrotic syndrome with an average incidence of 9%.[85]

 

The clinical manifestations of renal vein thrombosis vary because thrombosis can occur abruptly or gradually, and completely or incompletely.[74] It most often presents clinically in a subacute fashion. Presenting symptoms include nausea, apathy, weakness, and edema.[29] Less often, it presents with acute sudden flank pain, with or without hypertension and hematuria. In some chronic cases, it is only recognized when impairment of renal function develops.

 

In pediatric patients there are three groups of patients seen with renal venous thrombosis.[56] The first group (9% of patients) are healthy, full-term infants, with no associated illnesses who have thrombosis at birth or they may manifest acutely, often with a febrile illness. The second and most common group (72%) are infants and young children with predisposing conditions who develop thrombosis that are found, or remain undetected only to either spontaneously resolve or to be detected at autopsy. The third group is older children with severe coexisting renal disease (e.g., nephrotic syndrome) who present with acute flank pain, unlike adults who have a chronic, asymptomatic presentation.[56]

 

A number of diagnostic modalities have been evaluated. Excretory urography may show a diminished nephrogram, faint excretion of contrast, enlargement of one or both kidneys, and ureteral notching due to collateral circulation.[29] Contrasted CT scans may demonstrate low attenuation clot in the renal veins, IVC, or both, along with associated enlargement of the renal veins; enlargement of the kidney; thickening of the Gerota fascia; perirenal collateral vessels; and an abnormal renal opacification pattern.[29] Selective renal venography is the most specific diagnostic test that demonstrates a filling defect or defects within the renal vein[42] [85] ; however, because of its invasiveness, it is not recommended as a screening examination in asymptomatic patients with nephrotic syndrome.[80] Digital subtraction venography has been studied as a safe, noninvasive procedure to diagnosis renal vein thrombosis and has been found to be quite efficient.[61] Doppler flow ultrasonography can determine the blood flow through the renal vein and thus assess the functional impact of the thrombus.[74] In pediatric patients, contrast radiography has been replaced by ultrasonography (especially in the newborn), which has an accuracy of 92%.[56]

 

The mainstay of treatment is now conservative with rehydration, correction of electrolyte and acid-base balance, and systemic anticoagulation replacing aggressive surgical thrombectomy.[29] [85] Systemic anticoagulation with heparin followed by warfarin tends to preserve and improve renal function and prevents thrombus spread to the IVC and contralateral renal vein.[74] Thrombolytic therapy with streptokinase and urokinase has been reported to be successful.[10] [60] The degree of renal impairment at the time of diagnosis is the main prognostic factor for improvement of renal function after thrombolytic therapy. Indications for surgical thrombectomy includes failure to control thromboembolic events by medical therapy; contraindications to medical therapy; severe systemic toxicity from renal hemorrhagic infarction; oliguria refractory to medical treatment from bilateral renal vein thrombosis; solitary kidney; and infection resistant to antibiotics.[74]

TABLE 1 -- CLASSIFICATION OF MESENTERIC ISCHEMIA

Occlusive

Nonocclusive

Arterial

Nonocclusive mesenteric ischemia

Acute

Neonatal necrotizing enterocolitis

Chronic

 

Venous

 

Strangulation

 

MESENTERIC ISCHEMIA AND INFARCTION

Mesenteric ischemia is the focal or widespread ischemia of the small or large intestines as a result of a critical decrease in blood and oxygen to the mesentery. Mesenteric infarction implies necrosis of the same. The small bowel, right colon, and proximal transverse colon are often involved because the superior mesenteric artery is the usual blood vessel involved.[63] The classification of mesenteric ischemia is listed in Table 1 .[81] Conditions associated with mesenteric ischemia are shown in Table 2 .[15] [63]

Acute Mesenteric Ischemia

Acute mesenteric ischemia is caused by the sudden occlusion or marked reduction of flow usually in the superior mesenteric artery. The sudden occlusion is the result of embolization (12% to 25% of the cases of mesenteric infarctions) which is usually from the heart, or by spontaneous primary thrombosis (also 12% to 25% of cases) of atherosclerotic arteries. The heart is the most common source of emboli, either from atrial fibrillation or prosthetic valves. Isolated dissection of the superior mesenteric artery has been reported as a cause of mesenteric ischemia with only one reported survivor.[77] Mesenteric vein thrombosis may cause bowel infarction when the venous collaterals are also blocked. Cirrhosis, abdominal infection, and hypercoagulable and low-flow states are the most common predisposing factors for venous thrombosis, which is most frequent in the distribution of the superior mesenteric vein.[15]

TABLE 2 -- CONDITIONS ASSOCIATED WITH MESENTERIC ISCHEMIA

Portal Hypertension

Postoperative Status

Drugs

Miscellaneous

Cirrhosis

Nonpulsatile cardiac bypass

Amitriptyline

Anaphylaxis

Congestive splenomegaly



Cocaine

Bowel obstruction



Other postoperative states

Digitalis

Burns

Trauma

 

Diuretics

Crash dieting

 

Splenectomy

Dextroamphetamine

Idiopathic

Abdominal trauma

 

 

Immunosuppression

Head trauma

Hematologic and Hypercoagulable States





 

 

Ergotomine

Intussusception

Inflammation

 

Estrogen

Kidney transplantation

 

 

Methamphetamine

Lower GI bleeding

Cholangitis

Antithrombin III deficiency

Oral contraceptives

Parasitic infection

Diverticular disease

 

 

Pheochromocytoma

Inflammatory bowel disease

Deep vein thrombosis

Pitressin

Renal disease



Migratory thrombophlebitis

Propranolol

Sepsis

Intra-abdominal abscess

 

Vasopressors

Upper GI bleeding

 

Neoplasms

 

Volvulus

Pelvic abscess

Polycythemia vera

Cardiovascular Disease



Peritonitis

Pregnancy

 

 

 

Protein C or S deficiency

Arrhythmias

 

 

 

Arteritis

 

 

Sickle cell disease

Atherosclerosis

 

 

Thrombocytosis

CHF

 

 

 

CVA

 

 

 

Myocardial infarction

 

 

 

Valvular disease

 

 

Most patients who present with acute mesenteric ischemia are older than 50 years of age and appear to be seriously ill. The patients experience the sudden onset of severe, dull, diffuse, poorly localized, unrelenting abdominal pain with a paucity of physical examination findings. Vomiting is present in 75% of patients and occult or gross blood is found in the gastric contents of 73%.[15] As the disease progresses, large volumes of fluid are lost in the bowel lumen. Diarrhea is common and often is guaiac positive. As ischemia worsens or bowel necrosis occurs, systemic symptoms and abdominal findings become more prominent and may include tachycardia, tachypnea, hypotension, fever, altered mental status, grossly bloody stool, peripheral cyanosis, and mottling. Leakage of bacteria or bacterial toxins into the circulation during mesenteric ischemia leads to the systemic components.[5] Signs of bowel infarction include localized abdominal tenderness, rebound tenderness, and rigidity.[25] The cause of death is usually sepsis and multiorgan failure.[5] The early diagnosis and liberal use of arteriography and vasodilator therapy has reduced the mortality to approximately 50%.[63]

Chronic Mesenteric Ischemia

Chronic mesenteric ischemia (intestinal angina) is almost always a result of atherosclerosis of the proximal visceral arteries with usually all three involved in symptomatic patients. Patients have crampy, postprandial abdominal pain that occurs so predictably after eating that patients may avoid eating to prevent the discomfort, which leads to progressive weight loss. The abdominal pain occurs 15 to 30 minutes after eating and may last up to 1 to 4 hours.[15] Some patients may have less-specific symptoms of nausea, vomiting, diarrhea, or symptoms of malabsorption, thus delaying the diagnosis.[33]

Nonocclusive Mesenteric Ischemia

Nonocclusive mesenteric ischemia is a poorly understood condition marked by progressive intestinal ischemia leading to infarction, sepsis, and death in a high proportion of patients.[81] It most commonly occurs in critically ill elderly patients who have markedly diminished cardiac output, hypovolemia, or who are receiving vasoconstrictive therapy.[15] This type of ischemia is associated with up to 50% of all mesenteric infarctions found at autopsy. The median age of patients is 75 years old. The onset of dull, diffuse, and poorly localized abdominal pain may be insidious and evolve over days to weeks.

Colonic Ischemia

Colonic ischemia is the most common vascular disorder of the intestines.[15] [55] It results from either iatrogenic ligation of the inferior mesenteric artery during abdominal aortic aneurysm surgery or may be spontaneous because of transient low colonic blood flow. Ninety percent of patients are older than 60 years. The most common sites of ischemia are the splenic flexure and descending and sigmoid colon. Patients present with mild, crampy, left-lower quadrant pain, tenderness, and guarding. They may have moderate rectal bleeding or bloody diarrhea.[55]

Diagnostic Studies

There is no specific diagnostic study available in the emergency department (ED) to reliably diagnose or exclude mesenteric ischemia. Because many more common diagnoses may be entertained, a high level of suspicion for mesenteric ischemia should be maintained, especially in patients with a history of arterial emboli, cardiac valvular disease, cardiac arrhythmias, and aortic atherosclerosis.[63] A leukocytosis (12,000 to 15,000 mm3 ) is common, but not specific. Hemoconcentration may be reflected in an elevated hemoglobin and hematocrit. The serum phosphate and amylase levels may be elevated. A metabolic acidosis is often a late finding and has been considered to be indicative of bowel infarction, although one study found it to be an equally common finding in those without infarction at the time of surgery.[17] In a small study of 31 patients, D-lactate was found to be significantly elevated in patients with mesenteric ischemia, other abdominal catastrophes, and bowel obstruction.[48] The negative predictive value of D-lactate was 96%.

 

Plain abdominal and upright chest radiographs should be obtained to exclude other causes of abdominal pain.[15] Signs of bowel wall thickening, pseudotumor "thumbprinting" (caused by submucosal edema or hemorrhage), ground-glass appearance secondary to ascites, intramural air (Fig. 4), gas in the portal system, or free intraperitoneal air indicate advanced stages of ischemia. CT scans, ultrasonography, and MR imaging have not been found to be useful in the emergency diagnosis of bowel ischemia, but may exclude other causes of acute abdominal pain.

Text Box: Figure 4. Left lateral decubitus view of an elderly patient with bowel infarction, demonstrating air/fluid levels and intramural air.

Mesenteric arteriography is the diagnostic procedure of choice and should be obtained early when bowel ischemia is suspected. Arteriography demonstrates the presence of thrombosis, emboli, and mesenteric vasoconstriction as well as the adequacy of collateral circulation. The arteriographic definition of the site and type of vascular occlusion will more accurately guide surgical intervention, and the catheter placement will allow access for selective vasodilator infusion. Patients should undergo intravascular volume resuscitation before arteriography to avoid false-positive findings.[81]

Emergency Management

Surgical consultation should be initiated early in the ED management of all patients in which mesenteric ischemia is suggested. Patients should be made NPO and have vigorous IV fluid resuscitation initiated. Digitalis and vasopressors should be avoided if possible because of their vasoconstrictive effects on mesenteric vessels.[8] Nasogastric tube placement is indicated in patients who are vomiting, have an ileus, have signs of peritonitis, or are in preparation for surgery.[15] Central venous or Swan-Ganz monitoring should be strongly considered in patients who are hypotensive.

 

In the ED, intravenous antibiotics are given to patients with peritonitis, sepsis, radiographic evidence of bowel necrosis or perforation, and in preparation for surgery. Antibiotic choices include cefoxitin 1 g; ceftriaxone 1 to 2 g plus metronidazole 15 mg/kg; or gentamicin 1 to 1.5 mg/kg plus either clindamycin 600 mg or metronidazole 15 mg/kg.[8]

 

Exploratory laparotomy without delay is indicated in patients with evidence of bowel necrosis or perforation. When arteriography demonstrates the presence of mesenteric occlusion, vasodilator therapy may be initiated through the arteriography catheter. Intraarterial papaverine, 30 to 60 mg bolus, followed by a 30 to 60 mg/h continuous infusion is given until resolution of symptoms or surgical intervention.[8] [63]

ABDOMINAL VASCULAR EMBOLI

Arterial emboli to the GI tract most commonly lodge in a bifurcation of the superior mesenteric artery and less commonly in the inferior mesenteric artery. Arterial emboli to the celiac artery are extremely rare. As previously mentioned, possible causes for mesenteric arterial emboli include atrial fibrillation, prosthetic heart valve, valvular heart disease, bacterial endocarditis, left atrial myxoma, myocardial infarction, atherosclerotic plaques from the thoracic aorta or the upper abdominal aorta, or may be caused secondary to angiographic studies. Patients with valvular or atherosclerotic heart disease with mural thrombi in the heart are the most frequent victims.

 

The classic clinical setting is a patient who has recently developed a cardiac arrhythmia and notices the sudden onset of severe epigastric/periumbilical pain. The patient then experiences nausea, vomiting, diarrhea, and positive guaiac stools.

 

Arterial emboli to the superior mesenteric artery account for 40% to 50% of all acute mesenteric ischemia.[8] These emboli are usually emanated from the left atrium or the left ventricle. A good number of the patients with superior mesenteric artery emboli have had peripheral artery emboli in the past. It is reported that 20% of patients with a SMA embolism will have a simultaneous embolus to another artery.[8]

 

Initial management of patients with suspected acute mesenteric ischemia should focus on the resuscitation of the patient and is essentially the same as the treatment outlined for mesenteric ischemia earlier. Urgent attempts to convert any cardiac dysrhythm to a normal sinus rhythm should be withheld.

Abdominal Aortic Emboli

Despite its large lumenal diameter, the abdominal aorta is also subject to arterial emboli. The most common site of embolization of the abdominal aorta is at the level of the fourth lumbar vertebra where the aorta narrows and bifurcates into the right and left common iliac arteries. A large embolus lodged at this site will significantly reduce the blood flow to both legs. A so-called saddle embolus can result in the complete loss of both lower extremities. The absence of bilateral femoral and popliteal pulses along with painful, pale, and cold legs should make the diagnosis a strong possibility. More commonly, the occlusion will be incomplete and only one leg will be affected. The causes for abdominal aortic emboli are the same as for the other abdominal vascular emboli.[67] [68]

ABDOMINAL VASCULAR ANEURYSMS

An aneurysm or "true aneurysm" is described as the aberrant, localized, and irreversible dilatation of an artery of a minimum of 1.5 times its normal diameter.[30] By definition, the true aneurysm wall will be intact and contain all three layers of the artery (intima, media, and adventitia).[28] A false aneurysm (pseudoaneurysm or pulsating hematoma) will have aberrant localized dilatation but will not involve all three layers of the artery.[30] Commonly, the adventitial layer of the pseudoaneurysm will be violated. A traumatic aneurysm refers to a false aneurysm that results from perforation of the arterial wall with formation of a perivascular hematoma. Clinically, peripheral arterial aneurysms behave quite differently than central arterial aneurysms (abdominal aorta and visceral arteries). Peripheral artery aneurysms tend to be predisposed to thrombosis or embolism and not to rupture, whereas central artery aneurysms are inclined to rupture.[30] The rate of growth of the aneurysm is dependent on the causative agent. If the aneurysm is secondary to atherosclerosis, then the growth rate will be quite slow and may take years to attain clinical significance. If the aneurysm is due to trauma or infection, then the growth rate can be very rapid and requires prompt, if not immediate, attention.

Abdominal Aortic Aneurysms

Abdominal aortic aneurysms (AAA) are the most frequently occurring, as well as the most clinically significant of the vascular emergencies found in the abdominal cavity.[23] In fact, rupture of an AAA is reported to be the 13th most common cause of death in the United States and accounted for 15,500 deaths in 1993.[16] [19] [23] Furthermore, the incidence of mortality from ruptured AAA is increasing while the morbidity and mortality of coronary artery disease and cerebrovascular disease is decreasing.[16] [47] Based on these facts, it is apparent that emergency physicians should have a heightened awareness for this disease process and have a game plan or organized approach for a timely diagnosis and efficient management.[59]

 

The following risk factors have been identified for the development of abdominal aortic aneurysms: male sex, age greater than 65 years, hypertension, tobacco smoking, atherosclerotic peripheral vascular disease, chronic obstructive lung disease, Marfan's syndrome, Ehlers-Danlos syndrome, and a first-degree relative with a history of AAA.[23] [28] Moreover, AAA is associated with numerous other disease states. Sepsis, bacterial endocarditis, and even a contiguous spread of infection can result in the formation of mycotic aneurysms of the aorta.[54] In the past, syphilis was a culprit. Historically, atherosclerosis was believed to be the primary cause in the generation of AAAs.[31] Recent studies have shown, however, that patients with advanced atherosclerosis do not develop aneurysms, they develop thrombosis or occlusive disease instead. A comparison of patients with aneurysms and thrombosis reveals many differences, for example, gender predilection, age of onset, and postoperative course.[59] It is now postulated that aortic aneurysm generation is in some way linked to hyperactivity of connective tissue proteases, a lack of inhibition of proteolysis, or a defect in the stability of aortic connective tissue.[59] [75]

 

Most patients with AAAs are asymptomatic. If an AAA is palpated in a patient, it is important to determine if the presenting symptoms correlate to the suspected AAA. If it is established that the patient's complaints are from another source, then ultrasonography (us) of the aorta should be performed within the next 72 hours. If the AAA is less than 4 cm in diameter, then the patient will require follow-up and repeat US every 6 months. If the AAA is 5 cm or greater, the decision to repair depends on a number of factors. The absolute size of the aneurysm, the presence of concurrent medical problems, and the overall lifestyle and life expectancy of the patient are salient considerations.

 

Patients with rapidly expanding or ruptured AAAs will have abdominal, flank, or back pain.[19] [78] Some patients may become syncopal as a result of hemorrhage. Most patients with ruptured AAAs are unaware that they have an aneurysm and will have had no prior symptoms. The straightforward cases of AAA manifested by abdominal or flank pain, hypotension, tachycardia, and a pulsatile abdominal mass are present in only 30% to 50% of the time.[59] All too common, the physical findings in patients with AAA are very deceptive, as well as subtle. The abdominal examination is usually unremarkable. Particular attention should be paid to finding an abdominal bruit. Palpation directed at finding an AAA should focus on the supraumbilical region just to the right of the midline. It is important to mention that an AAA will cross the midline. If it does not cross the midline it is probably just a tortuous aorta. Another distinguishing palpatory characteristic of an AAA is a lateral displacement of the pulse wave.[59] Peritoneal signs may or may not be present depending on the site of rupture and subsequent retroperitoneal hemorrhage. Additional indications of AAA may include diminished pulses in the lower extremities and other signs of peripheral arterial thrombosis or embolization.

 

Ten percent of all patients with ruptured AAA will present with urologic symptoms.[59] Flank pain with radiation to the groin accompanied by hematuria is the clinical presentation for about 9.5% of ruptured AAAs. Needless to say, an emergency physician should have a ruptured AAA high on the differential diagnosis of a patient over the age of 65 years who presents with renal colic. Five percent of all patients with ruptured AAA will present with neurologic symptoms. Syncope is the most common neurologic symptom and is attributed to hypotension as a result of hemorrhage. Spinal cord ischemia, especially at the T10 to T12 region, is the second most common neurologic symptom and is explained by the interruption of blood flow to the greater radicular artery from the abdominal aorta. Lower extremity pain as a result of peripheral emboli is the initial declaration of AAA in 5% of patients. The sudden onset of lower extremity ischemia, particularly of the toes, is secondary to emboli originating from the thrombus in the lumen of the aorta.

 

From the preceding discussion, it becomes clear that the diagnosis of AAA can be challenging as well as elusive. In many respects, it is the "great masquerader" of the elderly. The diagnosis of AAA should be entertained in all geriatric patients with abdominal pain, back pain, renal colic, syncope, hypotension, and leg pain.

 

The initial management of AAA is directed at stabilization of the patient. Depending on the hemodynamic stability of the patient, as well as the manner of presentation will determine the speed of acquiring surgical and radiologic consultations. Patients who are clinically unstable should not be taken to the CT scanner or the arteriography suite, but straight to the operating room. The only diagnostic modality to be considered in this setting is portable US performed at the bedside. Bedside US may not be able to discern a ruptured AAA per se, but it will be able to detect the presence of an AAA and free blood within the peritoneal cavity.[59] In the past, it was advocated for physicians to base their diagnostic concerns of AAA on the interpretation of plain abdominal radiographs (kidney, ureter, bladder); however, the limitations of plain films dictate that they should never be used to exclude the presence of an AAA. The primary role of plain films is to determine the presence of intestinal obstruction or perforation. Patients who are symptomatic and are hemodynamically stable may have either a US, CT scan, MR imaging, or arteriogram performed. US is best used as a screening tool for AAA in stable patients and bedside US is the study of choice for unstable patients. Bowel gas and a number of other structures interfere with imaging to present it from being a definitive study in stable patients. CT scan has the benefits of being able to measure the AAA, determine the full extent of the AAA, and identify other structures in the abdomen which may be responsible for the presenting complaints. Although angiography is helpful in depicting the anatomy of the aorta, it is losing its popularity because it is invasive, costly, fraught with complications, and not entirely reliable. MR imaging is rapidly gaining recognition in assessing AAA because of its enhanced accuracy, resolution, and ability to quantitate blood flow. Regardless, prompt surgical consultation is warranted. The surgeon should be involved in the decision-making process of obtaining a particular radiographic study. A surgeon's requirement for documentation before surgery varies from hospital to hospital. In some hospitals, an arteriogram is necessary for surgery. The emergency physician's primary role is to stabilize the patient and establish a tentative diagnosis as swiftly as possible.

Splenic Artery Aneurysms

Splenic artery aneurysms are the most common form of visceral artery aneurysms and account for 60% of all visceral arterial aneurysms.[71] [72] These are the only known aneurysms to be more frequent in women than in men (4:1).

 

Those at risk for developing such aneurysms have been found to have portal venous hypertension, arterial fibrodysplasia, and pregnancy.[53] [71] [72] [76] It is thought that the increased incidence in pregnancy is caused by the increased splenic arteriovenous shunting associated with the physiologic changes associated with pregnancy.[2] Arterial fibrodysplasia is seen in a number of collagen vascular diseases, namely, polyarteritis nodosa.[71] [72] People with splenic artery aneurysms secondary to portal hypertension and arterial fibrodysplasia are diagnosed between the ages of 50 and 80 years with a mean of 58 years.[71] [72]

 

Most patients with splenic artery aneurysms are asymptomatic.[45] [71] [72] The evolution of symptoms almost always signifies aneurysm growth and rupture. Symptomatic patients tend to present with the insidious onset of vague epigastric or left upper quadrant pain that may or may not radiate to the left subscapular or shoulder area. Physical examination of the abdomen is usually unremarkable.[45] This is because the aneurysm is usually less than 2 cm in diameter. Only in rare circumstances will a bruit be heard in the left upper quadrant or a pulsatile mass be palpated in the left upper quadrant. Less than 5% of the patients will present with the acute onset of epigastric/left upper quadrant pain accompanied by diaphoresis and hypotension. It is reported than only 2% of splenic artery aneurysms result in life-threatening rupture.[71] Of those that do rupture, however, 95% occur in pregnant women. Aneurysm rupture is most common during the third trimester.[2] [43]

 

The differential diagnosis for a gravid female patient with a rupture of the splenic artery aneurysm would include a ruptured ectopic pregnancy (depending on the gestational age), placental abruption, uterine rupture, or even normal labor.[49] Conversely, this diagnosis should be considered in any pregnant patient who presents with acute abdominal pain and fetal compromise. The differential diagnosis for a 60-year-old person with a ruptured splenic artery aneurysm would encompass an acute myocardial infarction, abdominal aortic aneurysm, acute pancreatitis, peptic ulcer disease (with possible perforation), biliary colic, renal colic, or mesenteric ischemia. Erosion of the aneurysm into the stomach can present as an upper GI bleed.[71] [72]

 

Diagnostically, radiographic studies are particularly helpful. In the older patient, a characteristic signet-ring-appearing or eggshell-appearing calcification in the left upper quadrant may be present on the plain films of the abdomen. CT of the abdomen with IV contrast is probably the most practical study to confirm the diagnosis, whereas an angiogram is the golden standard.

 

Treatment of the patient with a ruptured splenic artery aneurysm should be directed toward a fluid resuscitation to include the type and cross-matching of packed red blood cells. It is understood that the patient will be administered oxygen, placed on a cardiac monitor, and have the establishment of at least two large-bore peripheral IV catheters. Symptomatic splenic artery aneurysms require immediate surgical consultation and intervention.

Hepatic Artery Aneurysm

Hepatic artery aneurysms are the second most common visceral artery aneurysms and are responsible for 20% of all visceral artery aneurysms.[72] They usually occur in individuals greater than 60 years of age and are twice as common in men than women. Those at risk for developing such aneurysms have been found to have atherosclerosis, major abdominal trauma, arterial fibrodysplasia (polyarteritis nodosa), and a history of IV drug abuse.[72]

 

Most patients with hepatic artery aneurysms are asymptomatic.[72] The development of symptoms denotes the expansion and pending rupture of the aneurysm. Symptomatic patients exhibit symptoms suggestive of biliary colic, that is, epigastric/right upper quadrant pain radiating to the back. Large hepatic artery aneurysms may mimic symptoms associated with pancreatitis. Physical examination of the abdomen is usually unremarkable. Only on rare occasions will one find an abdominal bruit or palpable pulsatile mass in the right upper quadrant. This is because the aneurysm is small. Interestingly, hepatic artery aneurysms may rupture into common bile duct, peritoneum, or adjacent hollow viscera. Rupture of a hepatic artery aneurysm is related to a 35% mortality rate.[72]

 

Diagnostically, radiographic studies are very helpful. Calcification of the aneurysm is occasionally seen on plain films. Reliable diagnosis, however, requires the use of angiography. Treatment focuses on addressing hemorrhagic shock and stabilizing the patient for surgery. Surgical resection of the aneurysm is recommended in patients who are good operative candidates.

Superior Mesenteric Artery Aneurysms

Superior mesenteric artery aneurysms are the third most common visceral aneurysm and represent 10% of visceral artery aneurysms.[72] They are found in men and women in equal ratios (1:1) and usually occur before the age of 50 years. Those at risk for developing such aneurysms have a history of bacterial endocarditis of IV drug use, atherosclerosis, and abdominal trauma.[72] It is reported that 60% of superior mesenteric artery aneurysms are caused by nonhemolytic streptococcus from left-sided bacterial endocarditis.[72] Some authors call such an aneurysm a mycotic aneurysm. The term mycotic tends to generate some confusion.[35] First it should be clarified that a mycotic aneurysm has no connection with fungal disease. Second, some authors use the term mycotic to describe any and every type of infectious aneurysm. Third, the term mycotic should be used exclusively for infected aneurysms resulting from bacterial endocarditis.[35] [54] [72]

 

Most patients with superior mesenteric artery aneurysms will complain of the insidious onset of epigastric pain which is intermittent and commonly occurs 10 to 30 minutes after eating, gradually increases in severity, reaches a plateau, and then resolves over 1 to 3 hours. The physical examination is remarkable because a pulsatile abdominal mass will be found in half of the patients. The physical findings associated with subacute bacterial endocarditis may be present. Patients with a rupture of the SMA aneurysm will present with syncope, hypotension, and even hypovolemic shock in conjunction with an acute abdomen. Plain films of the abdomen may or may not show a calcified aneurysm. Angiography is necessary to confirm the diagnosis.[54] [72]

 

Treatment should be focused on resuscitating the patient from hemorrhagic shock. A surgeon should be consulted early in the evaluation. The surgical management is formidable because it depends on the shape of the aneurysm, bowel viability, and the overall condition of the patient.

Renal Artery Aneurysms

Renal artery aneurysms (RAA) are the fourth most common visceral artery aneurysms and have a rate of incidence between 0.01% and 1%. RAA tend to be more common in men than women (3:2) and have a mean age of 63 years. The pathogenesis or causes for RAA include atherosclerosis, fibromuscular dysplasia (polyarteritis nodosa), trauma, pregnancy, and congenital causes[9] [58] [66] The location of the aneurysm can be extraparenchymal or intraparenchymal. Extraparenchymal aneurysms occur more frequently than intraparenchymal aneurysms, with atherosclerotic aneurysms located at the first bifurcation of the renal artery being the most common site.[22] Surprisingly, RAA are bilateral in 20% of the cases.[14]

 

Approximately 70% to 90% of patients with RAA have hypertension which is recalcitrant to pharmacologic therapy.[14] A large number have coexistent renal artery stenosis and renal ischemia. RAA alone is seldom seen with hypertension. Measurement of differential renal vein renin will indicate the degree of renal ischemia in the involved kidney.[14]

 

No pathognomonic signs and symptoms are associated with renal artery aneurysms. The most common presentation is hypertension (55% to 75%). Hematuria, whether macroscopic or microscopic, is the second most common sign (30%). Flank pain is only present when there is an impending rupture of the RAA. The most important complication of a RAA is rupture.[22] Risk factors predisposing to rupture include the following: size greater than 1.5 cm in diameter, lack of calcification, pregnancy, and coexistent uncontrollable hypertension.[43] [58] Clinical manifestations of a ruptured RAA include flank, abdominal, or back pain simulating renal colic. Bleeding into the renal pelvis can give rise to renal colic accompanied by gross or macroscopic hematuria.

 

Most RAA are detected incidentally on plain abdominal films and IV pyelograms. US, CT, and arteriograms are also beneficial in identifying RAA. Asymptomatic small (<1.5 cm) RAA, especially those with circumferential calcification, usually do not require immediate treatment.[22] Small asymptomatic RAA in women of child-bearing years, however, should be repaired. The presence of hypertension, enlargement of an RAA, solitary kidney, bilateral kidney involvement, or RAA rupture may be indications for surgical intervention.

CONCLUSION

Although rare in occurrence, abdominal vascular emergencies tend to be rather catastrophic when they transpire. The common underlying theme of abdominal vascular emergencies is the cessation of normal blood to organs within the abdominal cavity. The clinical presentation of these processes will be abdominal pain, bleeding, or both. In many cases, there will be no pathognomonic physical findings, laboratory studies, or readily accessible radiographic studies. There is no substitute for a thorough history and physical combined with a high index of suspicion. Abdominal thrombosis, embolism, and aneurysms comprise the majority of abdominal vascular emergencies.

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