Acute abdominal pain out of proportion to exam is a key finding that should prompt suspicion for mesenteric ischemia, a condition that has historically carried very high mortality. Mesenteric ischemia is a group of disorders resulting in decreased blood and oxygen supply to the small intestine that is typically categorized as acute or chronic, with identification of the type of mesenteric ischemia and underlying cause guiding treatment. The last 150 years have seen significant advancements in treatment options, improving the mortality of this condition.
Advancements in medicine
Surgical intervention was first attempted in the late 19th century, with the first accounts of successful surgeries for mesenteric ischemia documented as early as 1895. By the early 20th century, literature on mesenteric vascular ischemia characterizes the diagnosis as having a hopeless prognosis and indicates that treatment is pointless.1 Current literature shows the mortality for acute mesenteric ischemia ranges from 40% to 100%.2-4 Several factors affect mortality including the etiology (for example, venous versus arterial or occlusive versus nonocclusive); the segment of bowel involved; the patient's age; the presence of kidney disease, diabetes, or hypotension; and the occurrence of a delay in identification and treatment.5 Historically, surgical intervention often involved removal of necrotic bowel and a late stage of disease; mortality remained high despite intervention. In 1951, revascularization became a viable means of treatment as the first successful surgical embolectomy to treat a superior mesenteric artery occlusion was performed. By reopening the blood supply at a time early enough in the disease process, it became possible to salvage the bowels and prevent the need for surgery in some cases. Even with these advances in treatment, current mortality is generally considered to exceed 50%.6 These advances in modern medicine changed the approach to managing mesenteric ischemia, expanding treatment options for patients by underlining the need for involvement of a multidisciplinary team (general surgery, vascular surgery, and interventional radiology).6
Overview
Mesenteric ischemia occurs when there is insufficient splanchnic circulation, preventing the small intestine from receiving the blood and oxygen needed to meet their metabolic demands. Three main blood vessels perfuse the intestines and organs such as the stomach, pancreas, spleen, and liver: namely, the celiac artery (CA), superior mesenteric artery (SMA), and the inferior mesenteric artery (IMA). The small intestines receive most of their blood supply from the SMA. The CA supplies the pancreaticoduodenal artery, which provides a collateral blood supply to the small intestines.5 Between the collateral blood supply and several mechanisms that enable the mesenteric circulation to autoregulate blood supply, the small intestine can tolerate up to a 75% reduction in overall blood supply for up to 12 hours.7,8 If there is a complete occlusion, however, there can be permanent ischemic damage within 6 hours.7 This can result in the bowels becoming necrotic. Although mesenteric ischemia accounts for only 0.09%-2% of gastrointestinal diseases evaluated in the ED, it has a high mortality.7-9
Mesenteric ischemia can be divided into acute or chronic, with acute having an occlusive or nonocclusive cause. Acute mesenteric ischemia can result from arterial embolism, arterial thrombosis, venous thrombosis, or nonocclusive disease. Chronic mesenteric ischemia can progress to acute mesenteric ischemia if not identified early, and it is associated with severe atherosclerotic disease most of the time, with a smaller percentage of cases due to vasculitis, radiation, malignancy, or various forms of dissection.7
Mesenteric ischemia remains a high mortality condition despite advancements in treatment, regardless of the underlying cause. Early identification of risk factors, recognition of signs of ischemia on imaging, and treatment are needed to improve patient outcomes. A meta-analysis evaluating over 10,000 patients with acute mesenteric ischemia identified factors that were significantly associated with increased mortality risk, including patient age (odds ratio [OR] 1.17, 95% confidence interval [CI] 1.08-1.27), chronic renal disease presence (OR 2.47, 95% CI 1.37-4.45), arrhythmia presence (OR 1.93, 95% CI 1.38-2.69), hypotension presence (OR 3.44, 95% CI 1.81-6.54), large bowel involvement (OR 2.98, 95% CI 1.44-6.17), small and large bowel involvement (OR 1.86, 95% CI 1.23-2.81), creatinine level (OR 1.67, 95% CI 1.27-2.20), lactate level (OR 1.43, 95% CI 1.26-1.62), and use of inotropes (OR 3.79, 95% CI 1.47-9.77).3 Delay to surgery was found to be significantly associated with increased risk of mortality as well, highlighting the importance of early identification. Vasopressors can cause vasoconstriction and further decrease blood flow to the intestines, making mesenteric ischemia worse.7,10 Factors that were significantly associated with increased chance of survival included anticoagulation and revascularization.5 With high mortality, it is essential that acute care NPs recognize the clinical presentation of mesenteric ischemia, the underlying pathophysiology, and treatment options to improve patient outcomes.
Acute occlusive mesenteric ischemia
Occlusive mesenteric ischemia is a type of acute mesenteric ischemia that is caused by occlusion of intestinal blood supply. Blockages can be caused by acute mesenteric arterial embolism, acute mesenteric arterial thrombosis, and mesenteric venous thrombosis.
Acute mesenteric arterial embolism
Arterial embolism is the most common cause of acute mesenteric ischemia, accounting for about 50% of cases.3 Arterial embolism occurs when an embolus starts in one area and then moves to another location, thereby causing an obstruction in blood flow and potentially leading to occlusive mesenteric ischemia.7 Sources of emboli within the heart include the left atrium, left ventricle, and heart valves. Plaque can also cause emboli. The anatomy of the SMA, with its large diameter and acute angle of origination as it branches off from the aorta, makes it particularly prone to emboli.7
Risk factors. Conditions that increase the risk of emboli formation include arrhythmias such as atrial fibrillation, rheumatic heart disease, cardiomyopathies, cardiac thrombus, mitral valve disease, prosthetic valve, recent myocardial infarction, left ventricular aneurysm, and endocarditis.3,7 Some procedures, such as cardiac catheterization and coronary or cerebral angiography, can also increase the risk of an arterial embolism; assessing for a recent history of these procedures in patients with abdominal pain can assist in early identification of this condition.7
Clinical presentation. Arterial embolism causing mesenteric ischemia usually presents with acute severe abdominal pain that generally occurs within hours.2 Considered a clinical triad, this pain is often seen with bowel emptying in the setting of a known embolic event or high-risk condition for emboli (for example, atrial fibrillation, peripheral emboli, or transient ischemic attack). Abdominal pain out of proportion to exam is a classic feature but is not always present. The most common clinical course is an episode of severe abdominal pain followed by mild improvement that then progresses to peritonitis and worsening pain.5 On physical exam, the patient may have diffuse abdominal tenderness, peritoneal signs, and/or abdominal distension.2
Acute mesenteric arterial thrombosis
Mesenteric arterial thrombosis generally occurs in the setting of atherosclerosis. As plaque builds up, a collateral blood supply develops, allowing blood to reach the end organs even if there is thrombosis or stenosis. When an SMA thrombosis occurs along with stenosis of the CA, the available blood supply can decrease to the point of causing mesenteric ischemia and symptoms severe enough for patients to present to the ED for evaluation.7
Risk factors. Given the pathology of thrombosis, diffuse atherosclerotic disease is a significant risk factor for mesenteric arterial thrombosis. Other risk factors include systemic vasculitis, history of chronic postprandial pain, aortic dissection extending into the SMA, isolated dissection of the SMA, history of progressive weight loss, or aneurysms.3,7
Clinical presentation. The signs of acute occlusive mesenteric ischemia caused by an arterial thrombosis are often less pronounced than symptoms associated with other causes for mesenteric ischemia and can vary greatly among patients.5 On presentation, patients may report a range of symptoms such as vomiting and/or acute severe abdominal pain. Symptoms are determined by the location and extent of the occlusion. Often, both the SMA and CA are involved, and patients commonly have evidence of atherosclerotic disease. The presence of postprandial pain, weight loss, and hesitation to eat ("food fear") prior to the onset of acute abdominal symptoms should raise concern for arterial thrombosis.3,7
Mesenteric venous thrombosis
Mesenteric venous thrombosis can occur either acutely or chronically, with the current published literature estimating a range between 2.9% and 18% of acute mesenteric ischemia cases being caused by venous thrombosis.3,4,6 While advanced age is a risk factor for other causes of acute mesenteric ischemia, mesenteric venous thrombosis is seen more often in younger individuals (those younger than age 50). This is likely due to the existence of those medical conditions that increase the risk of thrombosis-such as a hypercoagulable state or previous thrombosis-or the use of medications that increase risk such as contraceptives.3,7 Patients with a hypercoagulable disorder are up to three times more likely to develop recurrent venous thrombosis, which can lead to a postthrombotic syndrome of the abdomen, where venous collateralization and portal hypertension on imaging can occur. It can also result in recurrent admissions for abdominal pain.11
Mesenteric venous thrombosis does not usually require vascular surgery.3 Instead, this cause of occlusive mesenteric ischemia is typically treated with bowel rest, fluid resuscitation, and systemic anticoagulation.3,11
Risk factors. Risk factors for mesenteric venous thrombosis include thrombophilia, portal hypertension, history of venous thromboembolism, oral contraceptive use, estrogen use, and pancreatitis or other local intra-abdominal processes.3,7 Thrombosis can be idiopathic. Patients with inherited hypercoagulability (for example, as a result of Factor V Leiden or antiphospholipid syndrome) or acquired hypercoagulability (for example, induced by malignancy or oral contraceptives) are at increased risk of venous thrombosis.3
Clinical presentation. With acute venous thrombosis, symptoms-typically abdominal pain-can present suddenly or over days to weeks. Alternatively, patients may experience abdominal distension or cramping, nausea, vomiting, and, occurring in about 10% of cases, GI bleeding.3,7 Presentation of chronic venous thrombosis is usually more consistent with dull abdominal discomfort over weeks to months. Obtaining a good history from the patient or family and performing a thorough physical exam assists greatly with accurately characterizing symptoms and time of onset.7
Nonocclusive mesenteric ischemia
Nonocclusive mesenteric ischemia (NOMI) occurs as a result of hypoperfusion of the intestines due to vasoconstriction of mesenteric arteries in the setting of circulatory failure.1 It is an imbalance of intestinal oxygen delivery and metabolic demand due to decreased perfusion despite patent arteries. A decrease in perfusion pressure of the intestinal vasculature prompts pressure flow autoregulation and increased oxygen extraction.12 Arterial vascular resistance decreases to redistribute blood flow to areas of mucosa with more metabolic activity. Intestinal capillaries are recruited beyond the 20%-25% normally open at rest, improving oxygen extraction. This ability to increase oxygen extraction enables the intestine to sustain a 75% reduction in blood flow for up to 12 hours to prevent ischemic injury.7,8 Autoregulation fails in periods of prolonged significant hypotension, resulting in intestinal hypoxia and ischemic injury.
Risk factors
NOMI is often seen in patients with existing severe illness. It can be seen in patients with severe heart failure or low cardiac output states, atrial fibrillation, hypovolemia, sepsis, multiorgan dysfunction, end-stage renal failure requiring intermittent hemodialysis, liver failure, aortic insufficiency, or major cardiac or aortic surgery and is more common in patients older than 50 years of age.1,3,12,13 Increased intra-abdominal pressure can also impair intestinal perfusion and result in ischemia. Vasoactive medications used in a patient with hypovolemia may precipitate NOMI.3
Enteral nutrition in critically ill patients with shock is controversial. These patients may not tolerate enteral nutrition due to the increase in oxygen demand in intestinal mucosa in the setting of decreased perfusion, and thus, they may develop NOMI.10,12 NOMI has been found to occur more often in critically ill patients requiring high doses of vasopressors and receiving rapid advancement of enteral nutrition.14 The incidence of NOMI in critically ill patients receiving vasopressors is higher with jejunal feeding as compared with gastric feeding.10
Clinical presentation
Clinical presentation of NOMI is often nonspecific; therefore, clinical suspicion is vital to diagnosis.15 No single abdominal exam finding is specific to NOMI.15 Abdominal pain is typically diffuse and intermittent.3 NOMI should be suspected in patients with abdominal distension and shock of unknown etiology. It should also be suspected in patients with recent history of cardiac arrest who develop bacteremia and diarrhea.7 Abdominal pain/tenderness, absent bowel sounds, high nasogastric tube output, leukocytosis, elevated lactate, and metabolic acidosis may also accompany NOMI.10,12 GI bleeding can be present and may be one of the only signs of NOMI in a sedated critically ill patient.3
Vasopressors should be avoided or limited in the setting of mesenteric ischemia if possible. Vasopressin reduces splanchnic blood flow, though it may vary with the clinical situation.12,14 Dopamine and epinephrine also have a negative impact on intestinal blood flow.10 Norepinephrine has fewer negative effects on intestinal blood flow, though this is dose-dependent.10 Dobutamine and milrinone to improve cardiac function have less impact on mesenteric blood flow than other vasopressors.12 Ultimately, intestinal ischemia is associated with higher doses of vasoactive agents or with use of multiple agents.7,12
Testing and diagnosis
Rapid diagnosis is essential in optimizing outcomes. As soon as there is clinical suspicion for an acute abdominal process, diagnostic testing and imaging can help to identify mesenteric ischemia. NPs should order labs including complete blood count (CBC) with differential, comprehensive metabolic panel (CMP), lactate, amylase, D-dimer, and lactate dehydrogenase (LDH). Although there can be variation in lab abnormalities, the most common concerns include neutrophilic leukocytosis, hemoconcentration, anion gap metabolic acidosis, elevated amylase, elevated LDH, and elevated aspartate aminotransferase.6 Lactate also can be elevated and can be a sign of irreversible damage from mesenteric ischemia; otherwise, elevated lactate may be due to intravascular volume depletion or kidney injury. Studies have shown that elevated lactate with mesenteric venous thrombosis in the setting of genetic thrombophilia strongly predicted need for bowel resection.3 Since elevated lactate levels are a late sign of mesenteric ischemia, fluid resuscitation should start immediately upon diagnosis to prevent further injury.
A plain abdominal radiograph is often performed during evaluation of abdominal pain. It can be helpful as a first step in identifying certain conditions such as intraperitoneal free air or bowel perforation, but it is not effective in assessing for mesenteric ischemia. The gold standard is computed tomography angiogram (CTA) of the abdomen and pelvis, which has a sensitivity of 85%-98% and specificity of 91%-100% for diagnosis of mesenteric ischemia. A CTA should be done without oral contrast when assessing for mesenteric ischemia.7 For occlusive processes, the CTA can identify the obstruction. With mesenteric venous thrombosis, a common CTA finding is the "target sign." Visualized during the venous phase of the CTA, the target sign indicates a thrombus in the superior mesenteric vein. It can be accompanied by findings of ascites, bowel wall thickening, splenomegaly, or pneumatosis. The presence of portal or mesenteric venous gas is suggestive of bowel infarction.3,7
As with occlusive mesenteric ischemia, the most effective diagnostic imaging for NOMI is CTA. CTA has the highest sensitivity for NOMI and can help guide treatment.6 CTA might reveal bowel ischemia and intraperitoneal free fluid in NOMI, although the mesenteric vessels remain patent.3 There may also be mucosal thumbprinting, dilated bowel, thickened bowel wall, mucosal hypoperfusion, portal venous gas, ascites, intestinal pneumatosis, or pneumoperitoneum on imaging.12
A 2020 study by Calame et al. comparing computed tomography (CT) scan features of major causes of transmural bowel necrosis found that the prevalence of certain features on CT imaging differed by cause.16 Occlusive acute mesenteric ischemia more often displays an absence of bowel wall enhancement and less mesenteric fat stranding on CT than NOMI, whereas NOMI is more frequently associated with findings of pneumatosis intestinalis and portal venous gas than occlusive acute mesenteric ischemia. The study also revealed that 93% of patients with NOMI and transmural bowel necrosis had at least one of these three signs: bowel loop dilatation (86%), ascites (79%), and portal venous gas (48%).16
Treatment
NPs play a crucial role in assessment, diagnosis, commencement of supportive care, and initiation of appropriate consults. Patients whose clinical presentation is concerning for acute mesenteric ischemia need early initiation of supportive care. Regardless of the specific type, initial treatment should include volume resuscitation with crystalloids to improve perfusion and oxygenation; provision of supplemental oxygen; connection of the nasogastric tube to suction and N.P.O. status for bowel rest; correction of electrolyte abnormalities; and initiation of systemic anticoagulation, unless there are contraindications. Unfractionated heparin is preferred due to its short half-life, ease of monitoring and titration, and reversibility. Broad-spectrum antibiotics should also be administered immediately after diagnosis.7 The regimen should be tailored as appropriate. Duration of antibiotic therapy is dependent on patient-specific factors.
Treatment guide by cause
For suspected acute mesenteric ischemia, regardless of occlusive versus nonocclusive process, NPs should obtain a CTA as previously outlined to confirm diagnosis and attempt to determine cause. NPs should also evaluate for clinical signs of peritonitis upfront. The treatment process should be commenced according to the following guide based on the cause supported by CTA findings and depending on the presence of clinical signs of peritonitis.
Without peritonitis. If there are no clinical signs of peritonitis, proceed according to the guide alongside the appropriate CTA finding below.
1) Arterial embolism: Consult vascular surgery, as endovascular intervention for definitive revascularization (for example, aspiration embolectomy, catheter thrombolysis, or percutaneous transluminal angioplasty) is indicated.3,7 Anticoagulation should be initiated prior to, but should not delay, the procedure. General surgery also may need to be consulted to determine whether a laparotomy is indicated.7
2) Arterial thrombosis: Consult vascular surgery, as endovascular intervention for definitive revascularization (for example, percutaneous transluminal angioplasty with stent, aspiration thrombectomy, thrombolysis, use of antispasmodics [such as papaverine]) is indicated.3,7 Anticoagulation should be initiated prior to, but should not delay, the procedure. General surgery also may need to be consulted to determine whether an open abdominal surgery with bypass or laparotomy is indicated.7
3) Mesenteric venous thrombosis: These patients should undergo nonoperative management. Commence fluid resuscitation. A nasogastric tube should be placed to suction with bowel rest. First-line treatment is systemic anticoagulation with unfractionated heparin or low-molecular-weight heparin. Early initiation of heparin infusion has been associated with positive patient outcomes.11 Plan to transition to oral anticoagulation prior to discharge.3,7,11
4) NOMI: Treatment for NOMI is medical management aimed at correcting the underlying cause, improving perfusion to the bowels, and decreasing arterial spasm.6,7 Volume expansion with fluid resuscitation, optimization of hemodynamic status, use of antibiotics, discontinuation or avoidance of vasopressors, and use of anticoagulation are mainstays of therapy.6 Once CT imaging reveals NOMI, catheter-directed infusion of vasodilatory and antispasmodic agents can be done. Papaverine hydrochloride is an antispasmodic that is injected directly into the SMA and then maintained with a continuous infusion for 24 to 72 hours.6,7 Other options for intra-arterial administration of vasodilators include nitroglycerin, prostaglandin E1, and glucagon. There are no contemporary or comparative studies evaluating different vasodilators, dosages, or regimens, making it impossible to issue precise recommendations in this respect.17 The patient should be monitored in the ICU.7
With peritonitis. If acute mesenteric ischemia (regardless of type) is found on CTA and the patient has clinical signs of peritonitis, emergency laparotomy or laparoscopy is typically needed for resection of necrotic bowel.7 Proceed according to the guide alongside the appropriate CTA finding below.
1) Arterial embolism: Initiate anticoagulation and consult vascular surgery, as endovascular intervention (for example, open embolectomy) is indicated. General surgery also should be consulted to evaluate the need for damage control surgery.7
2) Arterial thrombosis: Initiate anticoagulation and consult vascular surgery, as endovascular intervention (for example, percutaneous transluminal angioplasty with stent) is indicated. General surgery also should be consulted to evaluate the need for damage control surgery.7
3) Venous thrombosis: Initiate anticoagulation and consult general surgery, as surgery (for example, laparotomy with possible need for resection) is indicated.3,7 Consult vascular surgery to evaluate the need for a thrombectomy. After intervention, the patient should be monitored in the ICU. The general surgery team will decide whether a second-look surgery is needed (generally 24 to 48 hours after the initial surgical intervention).
4) NOMI: If there is no evidence of an occlusion, determine and treat the underlying medical cause for NOMI. Consult general surgery to evaluate the patient for the need for a laparotomy. The patient might need an intraoperative angiogram. General surgery will determine whether the patient needs damage control surgery. Treat with vasodilator infusion (for example, prostaglandin E1). Monitor in the ICU.7
Surgical intervention
Surgical intervention for acute mesenteric ischemia can be associated with significant mortality. Operative mortality ranges from 26% to 72%, with a pooled mortality of 47%. Operative morbidity and adverse event rates in survivors range from 39% to 64%.2 For patients with NOMI requiring an exploratory laparotomy to remove necrotic bowel, mortality remains very high at 50%-85%.3,7 Damage control surgery involves a second-look surgery 24 to 48 hours later to evaluate for further ischemia/necrosis and to close the abdomen.
Case study
Patient history
A 78-year-old White female who is a nonsmoker with a past medical history of severe aortic stenosis, atrial fibrillation on anticoagulation, chronic obstructive pulmonary disease, type 2 diabetes mellitus, chronic kidney disease stage 3, and carotid atherosclerosis presents to the ED with severe abdominal pain. Her symptoms started 36 hours ago with nausea, vomiting, and diarrhea before progressing 4 hours later to abdominal pain. Symptoms have worsened over the past 12 hours, with development of marked abdominal distension and intolerable pain, prompting her to present to the ED for evaluation.
Clinical question. As an acute care NP, what testing and initial treatment do you anticipate being performed in the ED?
Clinical presentation
On arrival to the ED, the patient was normotensive without tachycardia and afebrile. She later developed a fever of 102.7 [degrees]F (39.3 [degrees]C). Physical exam was positive for abdominal distension, abdominal tenderness, and signs of peritonitis. Lab test results showed elevated serum lactate of 2.9 mmol/L that soon increased to 6.1 mmol/L, leukocytosis (18.9 x 109/L), elevated C-reactive protein (8.1 mg/dL), and creatinine which was elevated from baseline (2.6 mg/dL from 1.2 mg/dL). Serum lipase (24 U/L) and international normalized ratio (1.0) were normal. Hemoglobin was at patient's baseline (13.1 g/dL).
The patient was started on broad-spectrum antibiotics and crystalloid I.V. fluids for volume resuscitation. She underwent a CTA of the abdomen and pelvis with I.V. contrast, demonstrating thrombus in the mesenteric arteries, extensive portal venous gas throughout the liver, pneumatosis intestinalis, and dilated transverse and ascending colon containing gas and air-fluid levels. The CTA was also notable for severe extensive atherosclerosis.
Clinical questions. Lab collection, initiation of fluid resuscitation and broad-spectrum antibiotics, and a CTA of the abdomen and pelvis have been performed in the ED. As the acute care NP consulted to see the patient, what is your main differential diagnosis? With whom do you want to speak next? Which labs will you be closely monitoring after the CTA?
Surgical intervention
Given the concern for advanced acute mesenteric ischemia and irreversible ischemia, anticoagulation is started, and general surgery is consulted. Extensive conversations are held with the surgical team, patient, and family regarding the gravity of the patient's condition, and the decision is made to proceed with surgery. The patient is taken to the OR emergently for a laparotomy under general anesthesia.
After surgery, the patient is transported to the ICU, intubated and sedated with an open abdomen. As the NP caring for the patient, you meet anesthesia and general surgery at the bedside as the patient arrives. General surgery relays its findings. The cecum was necrotic, and the right colon was dusky. Ischemic demarcation appeared to involve the ileocolic and right colic territories. General surgery performed an ileocecectomy and right colectomy, resecting the terminal ileum and the right colon. The bowel was left in discontinuity and the abdomen was temporarily closed with a negative-pressure wound therapy dressing.
Clinical questions. What questions do you have for general surgery? What postoperative labs do you want to order for the patient?
Postoperative care
Postoperatively, a CMP, CBC, and lactate are obtained. The patient's labs are all normal. The patient becomes hypotensive postoperatively. After taking into consideration that the patient may still be underresuscitated from surgery and could have insensible losses from the open abdomen, you start by ordering crystalloid I.V. fluids before ordering a low-dose vasopressor.
ICU management
In the ICU, the patient will require BP management with I.V. fluids and vasopressors as needed; management of mechanical ventilation; serial labs; and good communication with the general surgery team about her clinical condition, treatment goals, and treatment plans. As an NP caring for this patient, you want to make sure that her family is updated regularly, receiving information in lay terms and demonstrating that they understand the information they are receiving. You also need to establish that the general surgery team, critical care team, and family are all in agreement about the patient's clinical condition and treatment plan. Two days after the initial surgery, the patient no longer requires vasopressors to support her BP.
Second-look surgery
The general surgery team takes the patient back to the OR for a planned second-look procedure. Following the procedure, general surgery informs you that they created an ileocolonic anastomosis and that the bowel is no longer in discontinuity. Biopsy specimens from the resected bowel were sent to the pathology lab, and findings showed necrosis and associated inflammation. The patient returns to the ICU intubated and sedated, and with no further plans for surgery, the critical care team now focuses on medical management.
Clinical question. What medical management do you anticipate for this patient who has undergone surgical treatment for acute mesenteric ischemia?
ICU medical management
While working toward liberation from the ventilator, you place orders for nursing and respiratory therapy to perform a daily spontaneous awakening and breathing trial. As soon as the patient meets extubation criteria, you extubate her. Since the patient is postoperative from an abdominal surgery, you ensure that she has a multimodal pain management plan in place to minimize use of narcotics. After discussion with general surgery on the timing of anticoagulation, you start therapeutic anticoagulation with a continuous infusion of heparin.
Transthoracic echocardiogram is performed and confirms known severe aortic stenosis. Transesophageal echocardiogram is also performed and rules out a left atrial thrombus. Screening for antiphospholipid antibodies (anti-beta 2 glycoprotein I, anticardiolipin antibody, and lupus anticoagulant) is sent, and all are negative. Ongoing discussions with general surgery confirm your suspicion that the patient will not be able to receive enteral nutrition for weeks; you therefore start parenteral nutrition.
Clinical question. What do you anticipate needs to occur prior to discharge?
Prior to discharge
Anticoagulation has been shown to improve patient outcomes and is an essential part of treatment for acute mesenteric ischemia. This patient will need to be transitioned to oral anticoagulation prior to discharge. Primary care follow-up is imperative to manage outpatient anticoagulation and address any modifiable risk factors.
Conclusion
When a patient presents with severe abdominal pain that is out of proportion to the physical exam, acute mesenteric ischemia should be suspected. It is critical for NPs to be aware that, with this condition, delays in diagnosis and treatment increase mortality. Acute mesenteric ischemia may be caused by an occlusive process, as seen with arterial embolus, mesenteric arterial thrombosis, and mesenteric venous thrombosis, or by a nonocclusive process. CTA should be obtained as soon as possible when acute mesenteric ischemia is suspected to confirm the diagnosis and attempt to determine its cause. Treatment should be commenced quickly in accordance with the cause and whether the patient exhibits any clinical signs of peritonitis. The NP is critical throughout this process by making appropriate referrals, coordinating care, and managing the overall treatment course.
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