Intestinal ischemia resident survival guide

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2]

Definition

Intestinal ischemia are a heterogeneous group of diseases characterized by hypoxia of the small bowel and/or colon, which most commonly arises from occlusion, vasospasm, and/or hypoperfusion of the mesenteric vasculature. Intestinal ischemic disorders have been classified into the following three major types.

Clinical subgroups	Definitions
Acute mesenteric ischemia (AMI)	It includes superior mesenteric artery embolism (SMAE) (50%); nonocclusive mesenteric ischemia (NOMI) (20% to 30%); superior mesenteric artery thrombosis (SMAT) (15% to 25%); and superior mesenteric vein (SMV) thrombosis (5%). It is most commonly associated with compromise of the blood flow in the superior mesenteric artery (SMA) distribution affecting all, or portions of, the small bowel and right colon.
Chronic mesenteric ischemia (CMI)	It usually refers to intestinal angina, where the splanchnic circulation is insufficient in meeting the functional demands of the gut, but there is no loss of tissue viability.
Colonic ischemia (CI)	It is the most common vascular disorder of the gut that includes reversible ischemic colopathy, transient ulcerating ischemic colitis, chronic ulcerating ischemic colitis, colonic stricture, colonic gangrene, and fulminant universal ischemic colitis.

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. Intestinal ischemia itself may present or complicate as a life-threatening condition and must be treated as such irrespective of the causes.

Common Causes

• Arterial embolism
• Arterial thrombosis
• Hypercoagulable states
• Non-occlusive ischemia
• Cardiogenic shock
• Vasculitis
• Vasoconstrictors: Cocaine, ergot, vasopressin, or norepinephrine.
• Venous thrombosis

Management

The algorithm is based on the American College of Gastroenterology guidelines for management of intestinal ischemia in adults.

Management of Acute Mesenteric Ischemia

Characterize the symptoms: ❑ Abdominal pain: ❑ Onset (sudden or insidious) ❑ Duration (persistent for more than 2-3 hours) ❑ Location (localized or generalized) ❑ Severity (often out of proportion to findings on physical examination) ❑ Nausea and vomiting ❑ Abdominal distention ❑ Bloody stools ❑ Mental status change Inquire about risk factors for AMI: ❑ Cardiovascular: ❑ Congestive heart failure ❑ Cardiac arrhythmias ❑ Recent myocardial infarction ❑ Valvular heart disease ❑ Previous H/O DVT, PVD, PE, vasculitis ❑ Recent hypovolemia ❑ Recent hypotension ❑ Cardiac surgery and dialysis ❑ Hypercoagulable states: ❑ Protein C deficiency and Protein S deficiency ❑ Antithrombin III deficiency ❑ Activated protein C resistance (APC) ❑ Paroxysmal nocturnal hemoglobinuria ❑ Myeloproliferative disease ❑ Intestinal angina: ❑ Chronic postprandial pain ❑ Aversion to eating ❑ Weight loss ❑ Sepsis, abdominal infections ❑ Blunt abdominal trauma ❑ Pancreatitis, splenectomy, and malignancy in the portal region ❑ Familial history of atheroembolism

Assess volume status: ❑ General condition ❑ Thirst ❑ Pulse ❑ Blood pressure ❑ Eyes ❑ Mucosa Examine the patient: ❑ Abdomen: ❑ Abdominal distension ❑ Occult blood in the stool ❑ Signs of peritoneal inflammation (rebound tenderness and guarding) ❑ Bowel sounds (absent in bowel infarction) ❑ Cardiovascular system (murmur) ❑ Respiratory system ❑ Anorectal (bleeding) ❑ Signs of vasculitis

High clinical suspicion with known risk factors Resuscitate the patient: ❑ NPO ❑ Intravenous fluids ❑ Avoid vasoconstrictors and digitalis ❑ If required, use dobutamine, low-dose dopamine, or milrinone ❑ Correct predisposing or precipitating factors: ❑ Relieving acute congestive heart failure and hypotension ❑ Correction of hypovolemia ❑ Correction of cardiac arrhythmias ❑ Antibiotics for sepsis ❑ Monitor vitals every 1/2 to 1 hour Order tests (urgent): ❑ CBC: Leukocytosis ❑ Serum electrolytes ❑ ESR: Elevated ❑ D dimer: Elevated ❑ Serum lactate: Elevated ❑ Serum amylase ❑ ABG: Metabolic acidosis or metabolic alkalosis ❑ Serum alpha-glutathione S-transferase (alpha-GST): Elevated ❑ Urinary and plasma intestinal fatty acid-binding protein (I-FABP): Elevated ❑ Total serum protein and albumin ❑ Urinalysis ❑ BUN ❑ Creatinine ❑ Serum glucose

Plain abdominal X-ray (urgent)

Other causes ❑ Perforated peptic ulcer Or ❑ Gallbladder disease Or ❑ Pancreatic pathology Or ❑ Intestinal obstruction

History of DVT or familial hypercoagulable state

Treat accordingly

Yes

No

Dynamic CT scan

Peritoneal signs

Mesenteric venous thrombosis

No

Yes

Mesenteric angiography * Hemodynamic stabilization should be achieved prior to arteriography

Laprotomy

Normal findings

No persistent peritoneal findings

Persistent peritoneal findings

Observe

Laprotomy

Mesenteric venous thrombosis

Major arterial occlusion (non-embolic)

Minor arterial occlusion or embolic

Major embolus

Splanchnic vasoconstriction (no occlusion)

Management of Mesentric Venous Thrombosis

Mesentric venous thrombosis

Symptomatic acute mesentric venous thrombosis

Asymptomatic mesentric venous thrombosis ❑ Diagnosis made on a CT scan obtained for reasons other than abdominal pain

No persistent peritoneal findings

Persistent peritoneal findings

❑ No therapy Or ❑ Anticoagulation for 3-6 months

Immediate institution of anticoagulant therapy ❑ Low molecular weight heparin: ❑ 7-10 days ❑ Bolus of 80 U/kg, not to exceed 5000 U ❑ Infusion at 18 U/kg/h until full conversion to oral warfarin ❑ Monitor anticoagulation using activated partial thromboplastin time (aPTT) ❑ Oral warfarin: ❑ 3-6 months or for life in permanent hypercoagulable states ❑ Tailor the dose to maintain INR in the 2-3 range With or without thrombolytic therapy ❑ IV tissue plasminogen activator Or ❑ IV streptokinase Or ❑ IV urokinase

Laprotomy ❑ Initiate heparin preoperatively ❑ Resection for short ischemic segment and non-viable extensive ischemic segment ❑ Consider second-look procedure (re-exploration within 12-24 hours) ❑ Long term parental nutrition after resection ❑ Thrombectomy, heparin and papaverine for viable extensive ischemic segment with main vessel occlusion ❑ Heparin and papaverine for viable extensive ischemic segment with open or reconstituted main ❑ Warfarin prophylaxis

Laprotomy if peritoneal signs develop in due course

Management of Major and Minor Embolus

Major embolus

Minor embolus

No persistent peritoneal findings

Persistent peritoneal findings

No persistent peritoneal findings

Persistent peritoneal findings

Selected cases ❑ Contraindications to surgery ❑ Good perfusion of the vascular bed distal to the embolus after a vasodilator (tolazoline)

Continous papaverine infusion preopratively

Continous papaverine infusion Or Thrombolytic therapy Or Anticoagulants

Continous papaverine infusion

Yes

No

Exploratory laprotomy ❑ Embolectomy ❑ Resection of the infarcted bowel

Observe and repeat angiogram

Laprotomy ❑ Embolectomy ❑ Local resection

Continous papaverine infusion

Surgical embolectomy Or Thrombolytic therapy ❑ Presentation is within 12 hours of the onset of symptoms ❑ Thrombus is partially occluding or ❑ Thrombus is in one of the branches of the SMA or ❑ Thrombus is in the main SMA distal to the origin of the ileocolic artery

Continous papaverine infusion postoperatively

Angiogram normal

Stop the infusion and remove the catheter

Repeat angiogram

Repeat angiogram and possibly a second look operation in 24-48 hours

Observe

Do's

Hemodynamic stabilization should be achieved prior to arteriography.

References

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