An 80-year-old male patient is recovering from a 3-vessel CABG he underwent 2 weeks prior when he develops abdominal pain with distension and obstipation. His heart rate is 115 bpm and his laboratory test results are notable for a WBC of 15 and potassium of 2.6. He is on a scheduled narcotic regimen prescribed by pain medicine for chronic back pain and ciprofloxacin for a UTI. He denies any history of melena and states his last screening colonoscopy was 4 months ago, which was normal. An obstructive series is ordered demonstrating the following findings:
What is the next BEST step in the management of this patient?
Correct Answer: B
This patient has imaging findings concerning for a large bowel obstruction that is most likely caused by a sigmoid volvulus as seen by the presence of an inverted U-shaped colon that is distended and extending from the pelvis to the right upper quadrant along with paucity of air in the rectum. Abdominal radiographs can only diagnose sigmoid volvulus in 60% of cases and usually require CT imaging or contrast enema. The most appropriate next step requires CT of the abdomen/pelvis and surgical consultation. CT is useful to rule out other causes of obstruction such as a tumor, impacted stool, or foreign body. The management of sigmoid volvulus requires sigmoidoscopy to evaluate the mucosa, and if no signs of ischemia are present, the next step would be an attempt at endoscopic detorsion with elective sigmoidectomy, as there is a 60% recurrence rate of nonsurgical management. If the mucosa is ischemic the patient would require an emergent sigmoidectomy. The patient’s age and history of recent antibiotic exposure places him at risk of C. difficile colitis and toxic megacolon, and occasionally C. difficile colitis presents with ileus but empiric treatment without a positive stool sample is unlikely to improve the patient’s symptoms. Nasogastric tubes function even in large bowel obstructions independent of a competent ileocecal valve but serial abdominal examinations would lead to perforated sigmoid colon in this patient. The obstructive series shows no significant stool burden, and constipation is unlikely to be driving this process. Intestinal pseudoobstruction (Ogilvie syndrome) is a diagnosis of exclusion and usually involves dilation of the entire colon. It is more common in cardiac surgery patients and supportive care including correction of electrolytes, especially hypokalemia, and avoidance of narcotics are beneficial. Neostigmine can be used for treatment of patients refractory to supportive care. However, neostigmine can cause significant bradycardia (which can be treated with atropine), and thus needs to be administered in a monitored setting. However, a mechanical obstruction must be ruled out before administration of neostigmine, as this can lead to proximal colonic perforation. Further management includes colonic decompression.
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A 60-year-old male with no significant past medical history presents with sigmoid diverticulitis diagnosed by CT scan, which demonstrated microperforation and phlegmon. His vitals on presentation are within normal limits, laboratory test results are only significant for a leukocytosis, and abdominal examination demonstrates mild left lower quadrant abdominal tenderness without rebound or guarding. He is admitted to the hospital, kept NPO, and started on IV ciprofloxacin and metronidazole. On hospital day 4 he is transferred to the ICU with atrial fibrillation with rapid ventricular rate but remains normotensive. He is started on metoprolol with successful rate control. Laboratory test results demonstrate an acute kidney injury. His abdomen is distended and tender diffusely to palpation.
What is the next BEST step in his management?
The patient has complicated diverticulitis as evidenced by microperforation and phlegmon. Patients who are hemodynamically stable are treated with parenteral antibiotics and NPO status. They are assessed daily for improvement in vital signs, abdominal examination, and diet toleration. Most improve within 2 to 3 days. This patient is showing signs of worsening abdominal pain, new onset atrial fibrillation, and end organ damage all concerning for sepsis. Failure to improve should prompt repeat imaging to evaluate for complications of diverticulitis such as abscess, frank perforation, or obstruction. As the patient has an acute kidney injury, contrast would place the patient at increased risk for worsening renal failure although it would surely increase the sensitivity of the CT scan. However, complications of diverticulitis such as frank perforation, free air and large abscesses, and distended bowel and obstruction will likely be evident on noncontrast CT scans. The patient with no past medical history and no recent hospital exposure is likely not at high risk for resistant organisms, such as extended spectrum beta lactamases. Thus, changing antibiotics to meropenem is less likely to improve the patient’s course. The patient has new onset atrial fibrillation, which began a few hours earlier and is responding well to rate control, which is the preferred strategy for initial management over rhythm control. His CHA2DS2 -VASc score is 0 and no valvular disease, lowering his risk for thromboembolism and not likely to require anticoagulation. The patient may require surgery based on the CT scan results; however, intra-abdominal abscesses related to diverticulitis respond well to percutaneous drainage and antibiotics.
A 38-year-old male presents after a bout of hematemesis at home and subsequently vomits another 400 mL of bright red blood in the emergency room. He is tachycardic and hypotensive. Large bore IVs are obtained and he receives 2 units of packed red blood cells. He is intubated for airway protection and admitted to the ICU. On chart review he is found to have a significant alcohol abuse history and several admissions for alcoholic pancreatitis, but his liver function studies and coagulation parameters are within normal limits. A recent MRI of the abdomen and liver biopsy show no evidence of cirrhosis. The patient is started on an IV proton pump inhibitor and IV octreotide. Bedside ultrasound showed no signs of ascites. He subsequently undergoes an EGD that demonstrates oozing gastric varices that were sclerosed with cyanoacrylate, and EUS shows thrombosis of the splenic vein and calcification of the pancreas. He remains hemodynamically stable and is extubated after the procedure. Six hours later he has another large volume hematemesis and becomes hypotensive. He receives an additional 3 units or packed red blood cells and it stabilizes his blood pressure.
What is the next BEST step?
Correct Answer: D
The patient has a history significant for chronic pancreatitis, which carries an 8% risk of splenic vein thrombosis. Splenic vein thrombosis can lead to left-sided (sinistral) portal hypertension. The majority of patients with splenic vein thrombosis have no gastrointestinal bleeding, and splenectomy is no longer considered the ideal treatment in asymptomatic patients. Patients typically have normal liver function tests and no signs of cirrhosis. Management includes EGD for diagnosis and management with banding and sclerotherapy/obliteration. However, in the acutely bleeding patient who has failed endoscopic management, splenectomy is the ideal choice to control gastric variceal bleeding. Nadolol is useful to decrease the portal pressures for chronic management but is not useful in the acutely bleeding patient. TIPS will not decrease the portal pressure within the splenic vein as the obstruction is proximal to the portal vein. The patient has now stabilized after receiving 2 units or pRBCs thus ongoing massive transfusion protocol would not be useful. tPA is currently not indicated for portal vein thrombosis.
A 70-year-old male with a history of diabetes, hypertension, and colon cancer status post a left hemicolectomy 10 years prior is brought to the emergency room from an outside hospital with a contained ruptured abdominal aortic aneurysm (AAA). On arrival he was hypotensive with a heart rate 115 bpm and blood pressure 85/55 mm Hg. He is taken emergently for endovascular aneurysm repair, which was uncomplicated. Postoperatively he is transferred to the surgical intensive care unit and remains stable overnight. Twelve hours later you are called to bedside as the patient is complaining of severe abdominal pain and distension. His vitals are as follows:
Laboratory test results are significant for:
Which is the MOST likely reason for the patients decline?
Colonic ischemia complicates 1% to 3% of elective AAA repairs but up to 10% of ruptured AAA repairs. Physicians must have a high index of suspicion as no laboratory values are pathognomonic for colonic ischemia. Patients commonly develop abdominal pain with fever, elevated lactate, and leukocytosis, while only 30% will have the classic finding of bloody diarrhea. Colonic ischemia can occur in both open and endovascular repairs of AAA. Inferior mesenteric ligation (IMA) in open repairs and coverage of IMA with endovascular repairs likely leads to insufficient blood flow, and prior colon resections likely lead to decreased collaterals between the superior and inferior mesenteric arteries. Atheromatous embolization is also believed to be a culprit in colonic ischemia. Additional risk factors for colonic ischemia include longer operative time, renal insufficiency, and hypotension. Flexible sigmoidoscopy is the diagnostic modality of choice to confirm diagnosis and plan subsequent treatment. Mild forms of colonic ischemia limited to the mucosa may be treated with antibiotics, bowel rest, and serial sigmoidoscopies; however, transmural necrosis requires colectomy and carries a high mortality rate. Retroperitoneal hematoma and endoleak are complications of endovascular surgery and should be kept high on the differential; however, with a stable hemoglobin and signs of colonic ischemia, they are less likely. Ruptured AAAs can result in a large retroperitoneal hematoma before bleeding is controlled and can lead to significant third spacing resulting in abdominal compartment syndrome with signs of hypovolemia or shock; however, this would be unlikely to manifest as fever and leukocytosis.
A 55-year-old female is admitted to the surgical intensive care unit with severe abdominal pain, nausea, vomiting, and diarrhea for the last 3 days. Her vitals at arrival are as follows: heart rate 122 bpm, blood pressure 100/50 mm Hg, temperature 102°F. On examination her abdomen is diffusely tender with voluntary guarding. Laboratory test results are notable for a leukocytosis of 18,000 cells/mL and hypokalemia. A thorough medical history is significant for a recent diagnosis of ulcerative colitis treated with sulfasalazine and a recent urinary tract infection of which she completed a 7-day course of ciprofloxacin. A CT of the abdomen and pelvis is performed, which demonstrates a significantly dilated colon up to 6 cm in diameter and diffuse colonic wall thickening with patent vasculature.
What additional testing is required before full medical management can be initiated.
Correct Answer: C
This patient has findings concerning for toxic megacolon based on the following criteria: radiologic evidence of colonic distension, plus at least three of the following: fever >38°C, heart rate >120 bpm, neutrophilic leukocytosis >10,500 or anemia; plus at least one of the following: dehydration, altered sensorium, electrolyte disturbances, hypotension. In contrast to ulcerative colitis where inflammation is limited to the mucosa, toxic megacolon is characterized by extension of severe of inflammation to the smooth muscle layer, which is thought to lead to the colonic distension. Although toxic megacolon is most commonly recognized as a complication of inflammatory bowel disease (IBD), it can also occur with infectious and ischemic colitides. Toxic megacolon most commonly occurs during the first several months after diagnosis of IBD and not infrequently is the first manifestation of the disease. IBD is also a risk factor for C. difficile colitis and so is her recent antibiotic exposure. Medical treatment for IBD versus C. difficile differs in the choice of antibiotics and the use of corticosteroids. Steroids have not been found to increase the risk of colonic perforation; however, they will significantly suppress the immune systems response to infectious colitides such as cytomegalovirus (CMV), amebic, and bacterial (Shigella, Salmonella, Campylobacter, and C. difficile). This patient has no prior history of immunosuppression, and thus CMV is unlikely and the diagnosis of CMV colitis often requires endoscopic biopsies, which is too risky in toxic megacolon. Barium enemas to rule out distal obstruction are also high risk for perforation and should be avoided if possible.
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