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Minutes of an International Weekly Meeting held by HCFI Dr KK Aggarwal Research Fund

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Dr Veena Aggarwal, Consultant Womens’ Health, CMD and Editor-in-Chief, IJCP Group & Medtalks Trustee, Dr KK’s Heart Care Foundation of India    19 March 2023

Topic: Acute mesenteric ischemia

 

Speaker: Dr Aviral Roy, Consultant Critical Care & Internal Medicine, Medica Superspecialty Hospital, Kolkata

 

March 4, 2023, Saturday

9.30-10.30am

 

  • Acute mesenteric ischemia (AMI) is typically defined as a group of diseases, which is characterized by an interruption of the blood supply to varying portions of the small intestine leading to ischemia. There are multiple pathophysiologic processes, which have a common end point of bowel necrosis.
  • Despite advances in surgical techniques and imaging modalities, the mortality is still 50-70% depending on the etiology of the disease.
  • AMI is a highly under reported undiagnosed disease. This is unfortunate as time is of the essence here.
  • The superior mesenteric artery (SMA) supplies around 70% of the entire length of the gut. The middle colic artery is the first large branch of the SMA and this is the area where the SMA narrows and where most of the emboli lodge. Any block here will lead to infarction of the ileum, parts of distal jejunum, entire ascending colon and half of the transverse colon.
  • Occlusion of the superior mesenteric vein or portal vein can also lead to AMI.
  • The causes can be arterial or venous. Among arterial, it can be occlusive due to emboli (50%) or thrombosis (15-25%). Thrombotic can be acute (de novo) or acute on chronic. Nonocclusive mesenteric ischemia (NOMI) is usually associated with slow flow states e.g., aortic surgery, cardiogenic shock, abdominal compartment syndrome. 
  • Risk factors for acute mesenteric arterial thrombosis include diffuse atherosclerotic disease, postprandial pain. For acute mesenteric arterial embolism, the risk factors are atrial fibrillation (Afib), recent MI, endocarditis, history of embolic disease, left ventricular aneurysm. NOMI is usually picked up late and risk factors include cardiac failure, multiorgan dysfunction and vasopressors. Mesenteric vein thrombosis occurs in hypercoagulable states, history of VTE, portal HT, estrogen use, thrombophilia.
  • The classical presentation of acute mesenteric ischemia is acute onset of severe abdominal pain, nausea, vomiting and diarrhea. If gut infarction occurs, there is bloody diarrhea. Commonly cardiac in origin (Afib, endocarditis, intraventricular clots). The survival rate ranges from 30-50%.
  • Thrombotic disease most commonly occurs just distal to the origin of the SMA. It is associated with long-standing postprandial pain, nausea, vomiting and chronic intestinal insufficiency. These patients have acute on chronic syndrome and have poor weight gain and are malnourished as every time they take food, they have severe abdominal pain. It usually causes infarction of the entire gut due to the loss of the entire artery. Origin is atherosclerotic disease and risk factors are same as for peripheral vascular disease (PVD) and coronary artery disease (CAD). Because the loss of gut is so extensive, the survival rate is 10-30%.
  • NOMI is usually seen in the elderly and critically ill patients. A high degree of suspicion is important. There is severe mesenteric atherosclerosis with an acute hemodynamic compromise. Such patients are often intubated or sedated. There is unexplained worsening in their clinical condition or a failure to thrive or follow their anticipated recovery course.
  • Mesenteric venous thrombosis usually presents as bilateral non-specific lower quadrant pain. Occasionally postprandial and some patients may have heme-occult stool positive. Blood ascites, third spacing in abdomen worsens the underlying disease worsening ischemia. Hypercoagulability work up is indicated. 
  • Abdominal x-ray has limited utility in diagnosis unless there is perforated gut. It is not the investigation of choice for AMI.
  • Increased lactate and LDH are very sensitive indicators. There are no lab values, which are specific indicators of bowel ischemia or infarction.
  • White cell count is greater than 15,000 in majority of patients.
  • Abdominal pain out of proportion to clinical findings must be taken as acute mesenteric ischemia unless proved otherwise.
  • Unexplained raised lactate in a hemodynamically stable patient of abdominal pain should raise a suspicion of gut ischemia.
  • Treatment includes fluid resuscitation, antibiotics, surgery/endovascular embolectomy or thrombectomy, heparin or LMWH. Discussion with the patient/family is important as this condition may require multiple interventions.
  • Once the diagnosis of AMI is made, fluid resuscitation should begin immediately to enhance visceral perfusion. Electrolyte abnormalities should be corrected.
  • Broad-spectrum antibiotics should be administered immediately.
  • Anticoagulation with IV unfractionated heparin should be started unless contraindicated.
  • If signs of overt peritonitis, prompt laparotomy is indicated.
  • When NOMI is suspected, the focus of treatment is not the gut but the underlying cause and to restore mesenteric perfusion. But if infarcted gut, it should be resected promptly.
  • If there is massive gut necrosis, this requires careful evaluation for underlying comorbid conditions and advanced directives in order to judge whether comfort carries the best treatment.
  • Damage control surgery is an important adjunct for patients who require intestinal resection due to the necessity to reassess bowel viability and in patients with refractory sepsis. Planned re-laparotomy is an essential part of management of AMI.
  • Mesenteric vein thrombosis can often be treated with a continuous infusion of unfractionated heparin.
  • This diagnosis should always be kept in mind, however rare it might be. It must be diagnosed in the OPD or ER and not in the ICU. ICU is the place for diagnosing NOMI.
  • Index of suspicion must be very high.
  • Doing a CT scan without contrast is of no help.
  • Point of care ABG is helpful in diagnosis as along with electrolytes, it also gives lactic acid.
  • In cases of unexplained high lactic acid with abdominal pain and anion gap metabolic acidosis, while the first diagnosis is sepsis, also think of AMI.
  • Risk factors are same as that for cardiovascular diseases.
  • A patient of mesenteric angina presents as an outpatient on regular check up with complaints of abdominal pain after eating, nausea, vomiting. The patient is very lean with history of weight loss.
  • Plain abdominal x-ray is an excellent investigation for volvulus. The bent inner tube sign on abdominal x-ray is a finding in cases of sigmoid volvulus.
  • If the volvulus ties of its blood supply, prompt laparotomy is required to undo the volvulus.
  • A study from an Intestinal Stroke Center has identified predictive factors for intestinal necrosis in acute mesenteric ischemia: organ failure, serum lactate >2 mmol/L and bowel loop dilation on CT scan. The ITIN rate increased from 3% with zero risk factors to 89% if two risk factors were present.

 

Participants

 

Member National Medical Associations

 

Dr Yeh Woei Chong, Singapore, Chair of Council CMAAO

Dr Alvin Yee-Shing Chan, Hong Kong, Treasurer, CMAAO

Dr Ravi Naidu, Malaysia

Dr Akhtar Hussain, South Africa

Prof Ashraf Nizami, Pakistan

 

Invitees

 

Dr Monica Vasudev

Dr EC Ng

Dr Hamid Manzoor

Dr AS Chaudhary 

Dr S Sharma, Editor IJCP Group

 

Moderator

 

Mr Saurabh Aggarwal

 

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