Case Report: A 48-Year-Old Woman With Acute Abdomen

Case

A 48-year-old woman presented to the ED with significant periumbilical abdominal pain and left lower extremity pain, which she rated an “8” on a scale of 1 to 10. She stated that the pain worsened with movement and change in position. The claudication in the patient’s left lower extremity began a few weeks prior to presentation, at which time she had received medical attention, including ankle brachial index testing that showed an abnormal value in the left lower extremity. The patient noted that when the abdominal pain began, the pain in her leg became more frequent and of higher intensity, with intermittent numbness. She reported some nausea, paresthesia, and sensory changes to the left lower extremity; however, she denied diarrhea, headache, fever, back pain, urinary symptoms, chest pain, and shortness of breath.

Regarding social history, the patient admitted to smoking half a pack of cigarettes a day and drinking alcohol socially. She denied any significant family history of disease. The patient’s own medical history included colon cancer, claudication, and multiple abdominal surgeries. The patient had been diagnosed with stage II colon cancer 4 years earlier, for which she had undergone a colon resection.

During the physical examination, the patient was diaphoretic, uncomfortable, and in severe distress. Her vital signs were: blood pressure, 146/77 mm Hg; respiratory rate, 18 breaths/minute; heart rate, 129 beats/minute; and temperature within normal limits. Oxygen saturation was 94% on room air.

The abdominal examination revealed a distended abdomen that was severely tender to palpation, with rigidity, guarding, and rebound tenderness. Examination of the lower extremities revealed an absent palpable dorsalis pedis pulse to the left lower extremity, but dorsalis pedis pulse and posterior tibial pulse in the left lower extremity were appreciated by Doppler. The right lower extremity had palpable 2+ dorsalis pedis and posterior tibial pulses.

The patient was immediately started on fentanyl and intravenous (IV) fluids; she was also given IV ondansetron and promethazine for nausea. Her pain was refractory to treatment, and required multiple doses of hydromorphone. Laboratory evaluation revealed leukocytosis with a white blood cell (WBC) count of 15.1 thou/cmm.

Computed tomography angiography (CTA) with runoff was ordered to evaluate lower extremity vasculature and perfusion, as well as abdominal vasculature and intra-abdominal organ pathology. The CTA revealed 99% stenosis in the left iliac artery; multiple areas of stenosis within the abdominal vasculature, including the superior mesenteric artery (SMA) and inferior mesenteric artery (IMA); and a small ventral hernia slightly left of the umbilicus but without evidence of obstruction. The patient remained stable while in the ED, and an emergent vascular surgery consultation was ordered. She was transferred to surgical services.

Mesenteric Ischemia

Mesenteric ischemia is a condition in which the intestine does not receive adequate blood supply, resulting in inflammation and injury. Cases of the disease may be acute or chronic. Acute mesenteric ischemia (AMI) may be occlusive or nonocclusive. Occlusive AMI is most commonly caused by embolic or thrombotic occlusion of one or more mesenteric arteries. Nonocclusive AMI (NMI) is most commonly due to primary splanchnic vasoconstriction.¹ It can also be seen in patients on high-dose vasopressor agents. Chronic mesenteric ischemia indicates continuous intestinal hypoperfusion that is often associated with meals and referred to as postprandial or intestinal angina.

Mesenteric ischemia is associated with poor outcomes, having a mortality rate ranging from 40% to 70%.² It is imperative that diagnosis and treatment commence rapidly to avoid potentially catastrophic complications such as transmural bowel infarction. Although visceral ischemia is rare, occurring in only 2 to 3 per 100,000, the high mortality rate makes prompt and accurate diagnosis essential to decreasing morbidity and mortality.³

Symptoms and Signs

The classical presentation of mesenteric ischemia is sudden onset of abdominal pain out of proportion to physical examination findings; however, peritoneal signs are also not uncommon later in the disease process. The most common presenting symptoms are abdominal pain, nausea, and diarrhea. Laboratory findings associated with mesenteric ischemia include leukocytosis, metabolic acidosis, elevated lactate, and an elevated D-dimer.²

Early recognition is crucial given the significant risk of bowel necrosis. Signs of peritonitis are frequently present late in the disease course; signs such as nausea, vomiting, and constipation are more frequent. Patients may also have complications such as ileus, gastrointestinal bleeding, and pancreatitis, which may mask the diagnosis of AMI.⁴

Prompt diagnosis and treatment are paramount. Acute AMI should especially be considered in patients who are over age 60 years, have a history of atrial fibrillation, claudication, hypercoagulable states or a previous history of atherosclerotic disease, myocardial infarction, and a history of postprandial abdominal pain and weight loss.

Laboratory Evaluation

The most common laboratory abnormalities in AMI are hemoconcentration, leukocytosis, elevated lactic acid, metabolic acidosis, and a high anion gap. Elevated amylase and creatinine phosphokinase are also frequently observed but are not specific for AMI. Hyperphosphatemia and hyperkalemia are frequently late signs and are associated with bowel infarction. Findings on plain abdominal radiographs are nonspecific and should not be utilized in the workups. Barium enemas also have no place in diagnosis, as this may reduce perfusion to the bowel wall and cause perforation.⁵ Leukocytosis and high lactate levels appear to be present in the majority of patients, though these are not specific for acute mesenteric ischemia.⁴

Imaging Studies

In the past, catheter-based angiography was considered the gold standard for diagnosis. However, the more readily available CTA is emerging as the primary imaging modality to diagnose mesenteric ischemia.³ Both CT and contrast angiography play a major role in the diagnosis. In addition to mesenteric ischemia, CT also allows for identification of nonvascular causes of abdominal pain. Contrast angiography has an important role in early diagnosis and is helpful in treatment planning as well as operative interventions.⁴

While CTA is the most frequently used technique in suspected AMI, contrast-enhanced three-dimensional magnetic resonance angiography (MRA) is also widely used. However, the inferior mesenteric artery and other splanchnic vessel periphery are currently better assessed with CTA due to the higher special and temporal resolution of the former. Both CTA and MRA are excellent screening techniques for AMI due to various causes.⁶

Duplex Doppler sonography has also been suggested as a screening tool in patients with suspected mesenteric ischemia, but this modality has multiple limitations, including failure to obtain adequate Doppler signal due to bowel gas or vessel wall calcification. Since significant disease is often common in the SMA and the celiac arteries of asymptomatic elderly patients, this modality should be considered when examining patients with suspected mesenteric ischemia.⁷

Treatment

Endovascular intervention or catheter-directed vasodilator therapy can be started immediately postangiography. The role of endovascular therapy in AMI is controversial. In NMI, a catheter-directed vasodilator infusion continues to be the treatment of choice in patients without peritonitis. Catheter-directed thrombolysis and percutaneous angioplasty have also been investigated in the treatment of AMI.⁴

The goal of surgical care is the removal of necrotic and nonsalvageable bowel and the prevention of further infarction. Stenting of the affected arteries may be utilized. An exploratory laparotomy remains the gold standard for assessment of bowel viability. Multiorgan failure poses a great risk in patients with AMI and mortality remains high.⁴ The most preferred surgical revascularization technique in embolic AMI remains the balloon catheter thromboembolectomy—with or without patch angioplasty of the superior mesenteric artery.

Prevention therapy should be utilized aggressively for AMI; patients with atrial fibrillation should be started on anticoagulants. Elective and timely revascularization may be undertaken in patients with chronic claudication and AMI secondary to atherosclerotic disease. In addition, patients should be advised not to smoke.⁴

Upon diagnosis of AMI, aggressive IV fluid resuscitation with crystalloids should be administered starting with volumes as high as 100 mL/kg to correct any metabolic derangements. A broad-spectrum antibiotic should also be started as early as possible. If no contraindications to anticoagulation exist, therapeutic IV heparin sodium should be administered to maintain an activated partial thromboplastin time at twice the normal value.⁵ The patient in this case was started on IV heparin and broad-spectrum antibiotics. In an optimized hemodynamic status, attempts to reduce acute vasospasm in AMI can be made with an IV glucagon infusion, starting at 1 mcg/kg/minute. The presence of peritoneal signs indicates bowel infarction and mandates an emergency laparotomy.⁵ As noted in the patient’s history, she was not on any anticoagulants on presentation and was a smoker.

Conclusion

The causes of abdominal pain range from benign to life threatening; therefore, it is imperative for clinicians to obtain a thorough history and physical examination of patients presenting with abdominal pain, and to consider a vascular etiology in the differential diagnosis. This case is unique in that the patient had multiple areas of stenosis within the abdomen, including the SMA and IMA, and either an acute or chronic occlusion, and claudication of her left lower extremity. 

Dr Orlik is a resident, department of emergency medicine, Akron General Medical Center, Ohio. Mr Bosman is an undergraduate research fellow, department of emergency medicine, Akron General Medical Center, Ohio. Dr Simon is the emergency medicine research director, department of emergency medicine, Akron General Medical Center, Northeast Ohio Medical University.

Case

A 48-year-old woman presented to the ED with significant periumbilical abdominal pain and left lower extremity pain, which she rated an “8” on a scale of 1 to 10. She stated that the pain worsened with movement and change in position. The claudication in the patient’s left lower extremity began a few weeks prior to presentation, at which time she had received medical attention, including ankle brachial index testing that showed an abnormal value in the left lower extremity. The patient noted that when the abdominal pain began, the pain in her leg became more frequent and of higher intensity, with intermittent numbness. She reported some nausea, paresthesia, and sensory changes to the left lower extremity; however, she denied diarrhea, headache, fever, back pain, urinary symptoms, chest pain, and shortness of breath.

Regarding social history, the patient admitted to smoking half a pack of cigarettes a day and drinking alcohol socially. She denied any significant family history of disease. The patient’s own medical history included colon cancer, claudication, and multiple abdominal surgeries. The patient had been diagnosed with stage II colon cancer 4 years earlier, for which she had undergone a colon resection.

During the physical examination, the patient was diaphoretic, uncomfortable, and in severe distress. Her vital signs were: blood pressure, 146/77 mm Hg; respiratory rate, 18 breaths/minute; heart rate, 129 beats/minute; and temperature within normal limits. Oxygen saturation was 94% on room air.

The abdominal examination revealed a distended abdomen that was severely tender to palpation, with rigidity, guarding, and rebound tenderness. Examination of the lower extremities revealed an absent palpable dorsalis pedis pulse to the left lower extremity, but dorsalis pedis pulse and posterior tibial pulse in the left lower extremity were appreciated by Doppler. The right lower extremity had palpable 2+ dorsalis pedis and posterior tibial pulses.

The patient was immediately started on fentanyl and intravenous (IV) fluids; she was also given IV ondansetron and promethazine for nausea. Her pain was refractory to treatment, and required multiple doses of hydromorphone. Laboratory evaluation revealed leukocytosis with a white blood cell (WBC) count of 15.1 thou/cmm.

Computed tomography angiography (CTA) with runoff was ordered to evaluate lower extremity vasculature and perfusion, as well as abdominal vasculature and intra-abdominal organ pathology. The CTA revealed 99% stenosis in the left iliac artery; multiple areas of stenosis within the abdominal vasculature, including the superior mesenteric artery (SMA) and inferior mesenteric artery (IMA); and a small ventral hernia slightly left of the umbilicus but without evidence of obstruction. The patient remained stable while in the ED, and an emergent vascular surgery consultation was ordered. She was transferred to surgical services.

Mesenteric Ischemia

Mesenteric ischemia is a condition in which the intestine does not receive adequate blood supply, resulting in inflammation and injury. Cases of the disease may be acute or chronic. Acute mesenteric ischemia (AMI) may be occlusive or nonocclusive. Occlusive AMI is most commonly caused by embolic or thrombotic occlusion of one or more mesenteric arteries. Nonocclusive AMI (NMI) is most commonly due to primary splanchnic vasoconstriction.¹ It can also be seen in patients on high-dose vasopressor agents. Chronic mesenteric ischemia indicates continuous intestinal hypoperfusion that is often associated with meals and referred to as postprandial or intestinal angina.

Mesenteric ischemia is associated with poor outcomes, having a mortality rate ranging from 40% to 70%.² It is imperative that diagnosis and treatment commence rapidly to avoid potentially catastrophic complications such as transmural bowel infarction. Although visceral ischemia is rare, occurring in only 2 to 3 per 100,000, the high mortality rate makes prompt and accurate diagnosis essential to decreasing morbidity and mortality.³

Symptoms and Signs

The classical presentation of mesenteric ischemia is sudden onset of abdominal pain out of proportion to physical examination findings; however, peritoneal signs are also not uncommon later in the disease process. The most common presenting symptoms are abdominal pain, nausea, and diarrhea. Laboratory findings associated with mesenteric ischemia include leukocytosis, metabolic acidosis, elevated lactate, and an elevated D-dimer.²

Early recognition is crucial given the significant risk of bowel necrosis. Signs of peritonitis are frequently present late in the disease course; signs such as nausea, vomiting, and constipation are more frequent. Patients may also have complications such as ileus, gastrointestinal bleeding, and pancreatitis, which may mask the diagnosis of AMI.⁴

Prompt diagnosis and treatment are paramount. Acute AMI should especially be considered in patients who are over age 60 years, have a history of atrial fibrillation, claudication, hypercoagulable states or a previous history of atherosclerotic disease, myocardial infarction, and a history of postprandial abdominal pain and weight loss.

Laboratory Evaluation

The most common laboratory abnormalities in AMI are hemoconcentration, leukocytosis, elevated lactic acid, metabolic acidosis, and a high anion gap. Elevated amylase and creatinine phosphokinase are also frequently observed but are not specific for AMI. Hyperphosphatemia and hyperkalemia are frequently late signs and are associated with bowel infarction. Findings on plain abdominal radiographs are nonspecific and should not be utilized in the workups. Barium enemas also have no place in diagnosis, as this may reduce perfusion to the bowel wall and cause perforation.⁵ Leukocytosis and high lactate levels appear to be present in the majority of patients, though these are not specific for acute mesenteric ischemia.⁴

Imaging Studies

In the past, catheter-based angiography was considered the gold standard for diagnosis. However, the more readily available CTA is emerging as the primary imaging modality to diagnose mesenteric ischemia.³ Both CT and contrast angiography play a major role in the diagnosis. In addition to mesenteric ischemia, CT also allows for identification of nonvascular causes of abdominal pain. Contrast angiography has an important role in early diagnosis and is helpful in treatment planning as well as operative interventions.⁴

While CTA is the most frequently used technique in suspected AMI, contrast-enhanced three-dimensional magnetic resonance angiography (MRA) is also widely used. However, the inferior mesenteric artery and other splanchnic vessel periphery are currently better assessed with CTA due to the higher special and temporal resolution of the former. Both CTA and MRA are excellent screening techniques for AMI due to various causes.⁶

Duplex Doppler sonography has also been suggested as a screening tool in patients with suspected mesenteric ischemia, but this modality has multiple limitations, including failure to obtain adequate Doppler signal due to bowel gas or vessel wall calcification. Since significant disease is often common in the SMA and the celiac arteries of asymptomatic elderly patients, this modality should be considered when examining patients with suspected mesenteric ischemia.⁷

Treatment

Endovascular intervention or catheter-directed vasodilator therapy can be started immediately postangiography. The role of endovascular therapy in AMI is controversial. In NMI, a catheter-directed vasodilator infusion continues to be the treatment of choice in patients without peritonitis. Catheter-directed thrombolysis and percutaneous angioplasty have also been investigated in the treatment of AMI.⁴

The goal of surgical care is the removal of necrotic and nonsalvageable bowel and the prevention of further infarction. Stenting of the affected arteries may be utilized. An exploratory laparotomy remains the gold standard for assessment of bowel viability. Multiorgan failure poses a great risk in patients with AMI and mortality remains high.⁴ The most preferred surgical revascularization technique in embolic AMI remains the balloon catheter thromboembolectomy—with or without patch angioplasty of the superior mesenteric artery.

Prevention therapy should be utilized aggressively for AMI; patients with atrial fibrillation should be started on anticoagulants. Elective and timely revascularization may be undertaken in patients with chronic claudication and AMI secondary to atherosclerotic disease. In addition, patients should be advised not to smoke.⁴

Upon diagnosis of AMI, aggressive IV fluid resuscitation with crystalloids should be administered starting with volumes as high as 100 mL/kg to correct any metabolic derangements. A broad-spectrum antibiotic should also be started as early as possible. If no contraindications to anticoagulation exist, therapeutic IV heparin sodium should be administered to maintain an activated partial thromboplastin time at twice the normal value.⁵ The patient in this case was started on IV heparin and broad-spectrum antibiotics. In an optimized hemodynamic status, attempts to reduce acute vasospasm in AMI can be made with an IV glucagon infusion, starting at 1 mcg/kg/minute. The presence of peritoneal signs indicates bowel infarction and mandates an emergency laparotomy.⁵ As noted in the patient’s history, she was not on any anticoagulants on presentation and was a smoker.

Conclusion

The causes of abdominal pain range from benign to life threatening; therefore, it is imperative for clinicians to obtain a thorough history and physical examination of patients presenting with abdominal pain, and to consider a vascular etiology in the differential diagnosis. This case is unique in that the patient had multiple areas of stenosis within the abdomen, including the SMA and IMA, and either an acute or chronic occlusion, and claudication of her left lower extremity. 

Dr Orlik is a resident, department of emergency medicine, Akron General Medical Center, Ohio. Mr Bosman is an undergraduate research fellow, department of emergency medicine, Akron General Medical Center, Ohio. Dr Simon is the emergency medicine research director, department of emergency medicine, Akron General Medical Center, Northeast Ohio Medical University.

Case

A 48-year-old woman presented to the ED with significant periumbilical abdominal pain and left lower extremity pain, which she rated an “8” on a scale of 1 to 10. She stated that the pain worsened with movement and change in position. The claudication in the patient’s left lower extremity began a few weeks prior to presentation, at which time she had received medical attention, including ankle brachial index testing that showed an abnormal value in the left lower extremity. The patient noted that when the abdominal pain began, the pain in her leg became more frequent and of higher intensity, with intermittent numbness. She reported some nausea, paresthesia, and sensory changes to the left lower extremity; however, she denied diarrhea, headache, fever, back pain, urinary symptoms, chest pain, and shortness of breath.

Regarding social history, the patient admitted to smoking half a pack of cigarettes a day and drinking alcohol socially. She denied any significant family history of disease. The patient’s own medical history included colon cancer, claudication, and multiple abdominal surgeries. The patient had been diagnosed with stage II colon cancer 4 years earlier, for which she had undergone a colon resection.

During the physical examination, the patient was diaphoretic, uncomfortable, and in severe distress. Her vital signs were: blood pressure, 146/77 mm Hg; respiratory rate, 18 breaths/minute; heart rate, 129 beats/minute; and temperature within normal limits. Oxygen saturation was 94% on room air.

The abdominal examination revealed a distended abdomen that was severely tender to palpation, with rigidity, guarding, and rebound tenderness. Examination of the lower extremities revealed an absent palpable dorsalis pedis pulse to the left lower extremity, but dorsalis pedis pulse and posterior tibial pulse in the left lower extremity were appreciated by Doppler. The right lower extremity had palpable 2+ dorsalis pedis and posterior tibial pulses.

The patient was immediately started on fentanyl and intravenous (IV) fluids; she was also given IV ondansetron and promethazine for nausea. Her pain was refractory to treatment, and required multiple doses of hydromorphone. Laboratory evaluation revealed leukocytosis with a white blood cell (WBC) count of 15.1 thou/cmm.

Computed tomography angiography (CTA) with runoff was ordered to evaluate lower extremity vasculature and perfusion, as well as abdominal vasculature and intra-abdominal organ pathology. The CTA revealed 99% stenosis in the left iliac artery; multiple areas of stenosis within the abdominal vasculature, including the superior mesenteric artery (SMA) and inferior mesenteric artery (IMA); and a small ventral hernia slightly left of the umbilicus but without evidence of obstruction. The patient remained stable while in the ED, and an emergent vascular surgery consultation was ordered. She was transferred to surgical services.

Mesenteric Ischemia

Mesenteric ischemia is a condition in which the intestine does not receive adequate blood supply, resulting in inflammation and injury. Cases of the disease may be acute or chronic. Acute mesenteric ischemia (AMI) may be occlusive or nonocclusive. Occlusive AMI is most commonly caused by embolic or thrombotic occlusion of one or more mesenteric arteries. Nonocclusive AMI (NMI) is most commonly due to primary splanchnic vasoconstriction.¹ It can also be seen in patients on high-dose vasopressor agents. Chronic mesenteric ischemia indicates continuous intestinal hypoperfusion that is often associated with meals and referred to as postprandial or intestinal angina.

Mesenteric ischemia is associated with poor outcomes, having a mortality rate ranging from 40% to 70%.² It is imperative that diagnosis and treatment commence rapidly to avoid potentially catastrophic complications such as transmural bowel infarction. Although visceral ischemia is rare, occurring in only 2 to 3 per 100,000, the high mortality rate makes prompt and accurate diagnosis essential to decreasing morbidity and mortality.³

Symptoms and Signs

The classical presentation of mesenteric ischemia is sudden onset of abdominal pain out of proportion to physical examination findings; however, peritoneal signs are also not uncommon later in the disease process. The most common presenting symptoms are abdominal pain, nausea, and diarrhea. Laboratory findings associated with mesenteric ischemia include leukocytosis, metabolic acidosis, elevated lactate, and an elevated D-dimer.²

Early recognition is crucial given the significant risk of bowel necrosis. Signs of peritonitis are frequently present late in the disease course; signs such as nausea, vomiting, and constipation are more frequent. Patients may also have complications such as ileus, gastrointestinal bleeding, and pancreatitis, which may mask the diagnosis of AMI.⁴

Prompt diagnosis and treatment are paramount. Acute AMI should especially be considered in patients who are over age 60 years, have a history of atrial fibrillation, claudication, hypercoagulable states or a previous history of atherosclerotic disease, myocardial infarction, and a history of postprandial abdominal pain and weight loss.

Laboratory Evaluation

The most common laboratory abnormalities in AMI are hemoconcentration, leukocytosis, elevated lactic acid, metabolic acidosis, and a high anion gap. Elevated amylase and creatinine phosphokinase are also frequently observed but are not specific for AMI. Hyperphosphatemia and hyperkalemia are frequently late signs and are associated with bowel infarction. Findings on plain abdominal radiographs are nonspecific and should not be utilized in the workups. Barium enemas also have no place in diagnosis, as this may reduce perfusion to the bowel wall and cause perforation.⁵ Leukocytosis and high lactate levels appear to be present in the majority of patients, though these are not specific for acute mesenteric ischemia.⁴

Imaging Studies

In the past, catheter-based angiography was considered the gold standard for diagnosis. However, the more readily available CTA is emerging as the primary imaging modality to diagnose mesenteric ischemia.³ Both CT and contrast angiography play a major role in the diagnosis. In addition to mesenteric ischemia, CT also allows for identification of nonvascular causes of abdominal pain. Contrast angiography has an important role in early diagnosis and is helpful in treatment planning as well as operative interventions.⁴

While CTA is the most frequently used technique in suspected AMI, contrast-enhanced three-dimensional magnetic resonance angiography (MRA) is also widely used. However, the inferior mesenteric artery and other splanchnic vessel periphery are currently better assessed with CTA due to the higher special and temporal resolution of the former. Both CTA and MRA are excellent screening techniques for AMI due to various causes.⁶

Duplex Doppler sonography has also been suggested as a screening tool in patients with suspected mesenteric ischemia, but this modality has multiple limitations, including failure to obtain adequate Doppler signal due to bowel gas or vessel wall calcification. Since significant disease is often common in the SMA and the celiac arteries of asymptomatic elderly patients, this modality should be considered when examining patients with suspected mesenteric ischemia.⁷

Treatment

Endovascular intervention or catheter-directed vasodilator therapy can be started immediately postangiography. The role of endovascular therapy in AMI is controversial. In NMI, a catheter-directed vasodilator infusion continues to be the treatment of choice in patients without peritonitis. Catheter-directed thrombolysis and percutaneous angioplasty have also been investigated in the treatment of AMI.⁴

The goal of surgical care is the removal of necrotic and nonsalvageable bowel and the prevention of further infarction. Stenting of the affected arteries may be utilized. An exploratory laparotomy remains the gold standard for assessment of bowel viability. Multiorgan failure poses a great risk in patients with AMI and mortality remains high.⁴ The most preferred surgical revascularization technique in embolic AMI remains the balloon catheter thromboembolectomy—with or without patch angioplasty of the superior mesenteric artery.

Prevention therapy should be utilized aggressively for AMI; patients with atrial fibrillation should be started on anticoagulants. Elective and timely revascularization may be undertaken in patients with chronic claudication and AMI secondary to atherosclerotic disease. In addition, patients should be advised not to smoke.⁴

Upon diagnosis of AMI, aggressive IV fluid resuscitation with crystalloids should be administered starting with volumes as high as 100 mL/kg to correct any metabolic derangements. A broad-spectrum antibiotic should also be started as early as possible. If no contraindications to anticoagulation exist, therapeutic IV heparin sodium should be administered to maintain an activated partial thromboplastin time at twice the normal value.⁵ The patient in this case was started on IV heparin and broad-spectrum antibiotics. In an optimized hemodynamic status, attempts to reduce acute vasospasm in AMI can be made with an IV glucagon infusion, starting at 1 mcg/kg/minute. The presence of peritoneal signs indicates bowel infarction and mandates an emergency laparotomy.⁵ As noted in the patient’s history, she was not on any anticoagulants on presentation and was a smoker.

Conclusion

The causes of abdominal pain range from benign to life threatening; therefore, it is imperative for clinicians to obtain a thorough history and physical examination of patients presenting with abdominal pain, and to consider a vascular etiology in the differential diagnosis. This case is unique in that the patient had multiple areas of stenosis within the abdomen, including the SMA and IMA, and either an acute or chronic occlusion, and claudication of her left lower extremity. 

Dr Orlik is a resident, department of emergency medicine, Akron General Medical Center, Ohio. Mr Bosman is an undergraduate research fellow, department of emergency medicine, Akron General Medical Center, Ohio. Dr Simon is the emergency medicine research director, department of emergency medicine, Akron General Medical Center, Northeast Ohio Medical University.