Mesenteric ischemia

It is a rare but potentially fatal disease that needs a high degree of clinical suspicion to clinch the diagnosis early. It is seen typically in >60 year age group with underlying conditions that predispose to ischemia like HT, DM, atrial fibrillation, dyslipidemias, smoking, arterial dissection, cocaine abuse etc. Presentation is with severe abdominal pain with nausea, vomiting and bloody diarrhea. Patients may complain of post-prandial abdominal pain (abdominal angina). Depending on the etiology presentation may be acute or chronic. Abdominal pain is out of proportion to the physical exam. Initially, peritoneal signs may be absent. Later on, abdominal distension, guarding, rebound, rigidity and absent bowel sounds will be seen. Fever and shock will occur once sepsis sets in.

Common causes are mesenteric artery embolism, mesenteric artery thrombosis, mesenteric vein thrombosis and non-occlusive ischemia.

Common causes of mesenteric ischemia

Mesenteric artery embolism: Acute, most common, embolus occludes distal SMA, distal small intestine infarcted, seen in AF, mural thrombus in heart, valvular heart disease, cholesterol embolism
Mesenteric artery thrombosis: Chronic, atherosclerotic plaques, proximal SMA, entire small intestine involved

Arterial occlusion. Contrast-enhanced CT image of the abdomen in a 54-year-old female with superior mesenteric arterial thrombosis. a, b: Contrast-enhanced axial CT scan demonstrates a thrombus in the superior mesenteric artery in coronal (a) and axial plane (b) (white arrow)

Mesenteric vein thrombosis: Thrombosis of superior mesenteric vein, hypercoagulable states like Factor V leiden, Protein C deficiency, pancreatitis, diverticulitis, OC pill use, malignancies, post-surgical state, cirrhosis; less severe pain

Venous occlusion. Contrast-enhanced CT image of the abdomen in 49-year-old female with superior mesenteric vein thrombosis. (a) Contrast-enhanced axial CT scan shows a thrombus in the superior mesenteric vein in axial plane (orange arrow); (b) wall thickening of the ascending colon (white arrow). Ascites (*) is also visible

Non-occlusive ischemia: Seen in severe, prolonged hypotension, shock, prolonged vasoconstriction, seen in critically ill patient

Local findings include areas of hemorrhage, necrosis, ulcerations and infarcts. Initially, superficial necrosis is seen in the mucosa, followed by damage to submucosa and muscularis propria. Continued ischemia leads to full thickness infarction. Mucosal damage is followed by bacterial invasion from bowel lumen into the bloodstream causing septicaemia and sepsis. Abdominal X rays are normal early in the disease. In later stages imaging shows distended bowel loops, thickening of the bowel walls, air in the bowel wall or pneumatosis intestinalis (indicates septicaemia and invasion of microbes from the bowel lumen into the wall). Bowel wall edema gives a “halo sign” or “target sign” on CT scan. Mesenteric fat-stranding may be seen. Preferred investigations are CT angiography (CTA) and conventional mesenteric angiography. Conventional angiography allows the delivery of thrombolytics and papaverine locally to lyse the thrombus or embolus. Advantage of CTA is that it is more readily available and helps to rule out other diagnoses as well. MRA can be used as a substitute. Treatment is supportive with fluid resuscitation, antibiotics like ceftriaxone and metronidazole and anticoagulants like heparin, warfarin, antiplatelet therapy, revascularization with embolectomy, angioplasty and surgical intervention with resection of gangrenous bowel. Emergency laparotomy should be done in the presence of peritoneal signs.

Bowel wall thickness and enhancement. a Contrast-enhanced axial CT images show a target sign (larger white arrow) in the small bowel wall due to mesenteric venous occlusion. b The vascular engorgement (*) and oedema of the bowel wall in turn lead to leakage of extravascular fluid into the bowel wall and mesentery. The resultant oedematous bowel may have a “halo” or “target” appearance due to mild mucosal enhancement (straight white arrow), submucosal and muscularis propria nonenhancement (red arrow), and mild serosal/subserosal enhancement (orange arrow). Bowel wall thickness is greatly increased measuring up to 1.5 cm

Whipple disease or non-tropical sprue or intestinal lipodystrophy: It is a chronic, multisystem, malabsorption disorder caused by intestinal infection with the bacteria Tropheryma whipplei. It is seen more commonly in individuals who are HLA B27+. It presents with diarrhea, steatorrhea, abdominal pain, weight loss, joint pain, fatigue, darkening of skin and neurological symptoms such as ataxia, memory loss, confusion, seizures and visual disturbances. Biopsy shows PAS positive macrophages with Gram-positive and non-acid fast bacilli. Treatment is with penicillin G , ceftriaxone or prolonged administration of trimethoprim-sulfamethoxazole. Vitamin and iron supplementation may be needed.

Short bowel syndrome: It is a malabsorptive syndrome that follows resection or functional loss of part of the small bowel that is seen after surgical resection of the small bowel, mesenteric ischemia, Crohn’s disease, malignancies etc. It presents with diarrhea, dehydration, weight loss, anorexia, fatigue, steatorrhea, nutritional deficiencies. Treatment is with total parenteral nutrition, eating small but frequent meals, octreotide and supportive therapy.

Lactose intolerance: It is caused by acquired or genetic deficiency of the small intestinal brush border enzyme lactase. Lactase breaks down lactose to glucose and galactose. Lactase deficiency may be secondary to IBD, abdominal surgery, gastrointestinal infections etc. Undigested lactose in the gut increases the osmotic load causing an osmotic diarrhea. Fermentation of lactose by gut microbes releases gases like hydrogen, carbon dioxide, methane and short chain fatty acids. Clinical features include bloating, abdominal pain, diarrhea and excessive gas after consumption of lactose containing foods like milk and milk products. Some patients may have fatigue, arthralgia and mouth ulcers. Diagnosis is by clinical history, hydrogen breath test (increase in breath hydrogen after lactose consumption) and determining lactase activity from small intestinal biopsy. Treatment is by avoiding lactose in diet, using probiotics and enzyme replacement.

Blind loop syndrome or small intestinal bacterial overgrowth (SIBO): It results from bacterial overgrowth in a segment of the small intestine that is not in continuity with rest of the bowel and forms a “blind loop” as a result of surgeries like gastric bypass, intestinal adhesions, intestinal diverticulosis, Crohn’s disease, scleroderma, radiation enteritis, celiac disease and other conditions like DM that slow the movement of bowel contents. SIBO interferes with absorption and digestion of food and lead to deficiency of vitamins A,D,E,K, B12 with resulting disorders, osteoporosis from decreased calcium absorption and renal stones. Temporary lactose intolerance may occur. SIBO presents with bloating, flatulence, abdominal pain, fatigue, weight loss, diarrhea and constipation. Diagnosis can be confirmed by a breath test or gas chromatography, after ingestion of glucose or lactulose and observing an increase in hydrogen and methane. Endoscopic aspiration of small intestinal fluid followed by bacterial cultures and colony counts can help quantify the bacterial overgrowth. Treatment is withoral antibiotics such as rifaximin and/or neomycin, vitamin supplementation and surgical correction.

Small versus large bowel obstruction

It presents with abdominal pain that is initially colicky and later on becomes continuous; abdominal distension, nausea, vomiting (bilious if obstruction is below opening of bile duct and non-bilious if obstruction is above that), failure to pass flatus and bowel movements (obstipation) , peritoneal signs and fever, shock in bowel perforations. Abdominal examination shows tympanic percussion, high pitched borborygmi in early obstruction and minimal or absent bowel sounds as the obstruction proceeds. Imaging studies including plain X rays and CT scan with contrast are used for diagnosis. Ultrasound and MRI can be used if radiation exposure has to be avoided such as in pregnant women and children. Perforated viscus can be seen as air under the diaphragm on erect or left lateral decubitus films. Conservative management with NPO (nothing per oral), decompression with naso-gastric suction or long intestinal tube and intravenous fluids is done in the absence of evidence of ischemia or perforation. Water-soluble or gastrografin contrast orally can help in two ways - if the contrast takes a long time to reach the colon, then patient can be taken for surgery as it suggests a more severe obstruction; gastrografin is hyperosmolar and draws fluid into the bowel lumen which helps to relieve less severe adhesive obstructions. Underlying condition causing the obstruction should be treated like repairing a hernia or relieving obstruction from a malignant growth by stenting or surgery.

Comparing small bowel (SBO) versus large bowel obstruction (LBO)

Small bowel obstruction (SBO)

Causes: Adhesions (most common), hernias, malignancies, IBD, radiation, gallstone ileus, foreign bodies, bezoars, intussusception, endometriosis
Findings on imaging studies: Dilated small bowel loops; dilated loops more centrally located; absence of air in the colon; valvulae conniventes seen; air-fluid levels

Large bowel obstruction (SBO)

Causes: Colon cancer (most common), volvulus, diverticula, IBD, postanatomotic stenosis, ischemic stenosis
Findings on imaging studies: Dilated loops of colon; dilated loops located peripherally; cecum may be distended; Dilated haustra; air-fluid levels

Necrotizing enterocolitis (NEC)

It is an inflammatory disorder affecting the gastrointestinal tract causing necrosis, bacterial invasion and sepsis. It is seen in premature infants typically 8-10 days after birth. Breastfeeding is protective while antibiotic use, IUGR or very low birth weight, enteral feeding, umbilical catheterization, maternal gestational diabetes etc. are associated with increased risk. Immaturity of the intestinal mucosa and hyper-reactive local immune responses with increased expression of toll-like receptor 4 or TLR4, increased transcription of NF-kB, cytokine cascade with increased IL8 levels and reduced biodiversity of intestinal microbial flora are implicated in the pathogenesis of NEC. Clinical features include temperature instability, abdominal distension and tenderness, vomiting, bloody stools, discoloration of abdominal wall, lethargy, apnea, bradycardia, hypotension. Imaging studies show dilated bowel loops, free air in the abdomen (perforation), portal venous gas and pneumatosis intestinalis (air in the bowel wall). Treatment is with bowel rest, decompression, antibiotics and supportive therapy.

Contrast-enhanced CT image of the abdomen in an 82-year-old male with embolism of the superior mesenteric artery. (a) Contrast-enhanced axial CT shows pronounced intrahepatic portal venous gas (branching hypoattenuating areas) extending into the periphery of the left liver lobe (red arrow). (b) Contrast-enhanced axial CT scan shows dilated and gas-filled loops with an extreme thinning of the bowel wall, a “paper thin wall”, due to transmural small-bowel infarction (orange arrow). Pneumatosis (white arrow) is also seen; fat stranding (*) and gas in mesenteric veins (white arrowhead)