Study guide
12.2 Mesenteric Ischemia and Abdominal Compartment Syndrome (01.S.6–7)
ABIM Neurocritical Care Subspecialty Certification Exam
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1 Introduction & Exam Overview
1.1 Current Exam Facts 1.2 Eligibility, Practice Pathway, and the IM Training Route 1.3 Format, Scoring, Pearson VUE, and Score Reports 1.4 How to Use This Independent Study Guide
2 ICU Neurologic Exam, Cerebral Physiology, and CSF
2.1 Neurological Examination in the ICU 2.2 Cerebral Physiology, ICP, CBF, and Autoregulation 2.3 CSF Physiology
3 Core Neuropharmacology
3.1 Osmotic Agents 3.2 Anti-Seizure Drugs 3.3 Anesthetics, Sedatives, Analgesia, and Paralytics 3.4 Antihypertensives, Vasopressors, and Inotropes
4 Reperfusion Drugs, Airway, and Ventilation
4.1 Thrombolytics, Anticoagulants, and Antiplatelets 4.2 Reversal of Anticoagulation After Acute Hemorrhage 4.3 Airway Management and Tracheostomy 4.4 Mechanical Ventilation
5 Hemodynamics and Shock
5.1 Hemodynamic Monitoring 5.2 IABP, Temporary VADs, LVAD, and ECMO 5.3 Diagnosis and Management of Shock
6 Nutrition, Temperature, and ICU Prophylaxis
6.1 Nutrition (01.J) 6.2 Temperature Control (01.K) 6.3 ICU Prophylaxis, Delirium, and Early Mobility (01.L)
7 General Trauma
7.1 Emergency Evaluation of Polytrauma, Chest, and Abdominal Trauma 7.2 Long-Bone Fractures and Fat Embolism 7.3 Burns, Electrical Injury, and Hanging/Strangulation
8 Pulmonary Critical Care
8.1 Pulmonary Physiology and ARDS (01.N.1–2) 8.2 PE, Pneumonia, and Pulmonary Edema (01.N.3, 7–8) 8.3 COPD, Asthma, PAH, and Bronchoscopy Basics (01.N.4–6, 9)
9 Cardiovascular Critical Care
9.1 Cardiovascular Physiology, Stress Cardiomyopathy, ACS, and Valves 9.2 Arrhythmias and Pacing 9.3 Acute Aortic Dissection and Cardiac Ultrasound
10 Renal and Infectious Disease
10.1 AKI, RRT, and Renal Drug Dosing 10.2 Acid-Base and Electrolyte Disorders 10.3 Severe Sepsis, Septic Shock, and Infective Endocarditis 10.4 Antimicrobial Use and Infection in the Immunosuppressed
11 Endocrine and Salt-Water Disorders
11.1 Pituitary Apoplexy, DI, and Panhypopituitarism (01.R.1–4) 11.2 SIADH and Cerebral Salt Wasting (01.R.5–6) 11.3 Thyrotoxicosis, Myxedema, Adrenal Crisis, and Dysglycemia (01.R.7–9)
12 Gastrointestinal Critical Care
12.1 GI Physiology, Acute Abdomen, Bleed, Ileus, and Perforation (01.S.1–5) 12.2 Mesenteric Ischemia and Abdominal Compartment Syndrome (01.S.6–7) 12.3 Fulminant Liver Failure, Cirrhosis Decompensation, and Hepatic Dosing (01.S.8–10)
13 Hematologic Disorders
13.1 Anemia, Transfusion, Thrombocytopenia, Coagulopathy, and DIC (01.T.1–4) 13.2 VTE in the Neuro ICU (01.T.5) 13.3 Chemo/Immune, SCT, CAR-T, Sickle Cell, and TMA (01.T.6–10)
14 Neuroimaging
14.1 CT of Brain and Spine 14.2 MRI and CT/MR Perfusion 14.3 Noninvasive Angiography and Catheter Angiography
15 EEG, EMG, and CSF Analysis
15.1 EEG, Standard and Processed (02.B) 15.2 Basic EMG Interpretation (02.G) 15.3 CSF Analysis (02.H)
16 ICP, TCD, and Multimodality Monitoring
16.1 ICP Monitoring (02.C) 16.2 Transcranial Doppler (02.D) 16.3 Brain-Tissue Oxygen and Multimodality Monitoring (02.E–F)
17 Brain Death and Bedside Procedures
17.1 Brain Death Prerequisites and Clinical Exam (02.I) 17.2 Apnea Testing and Ancillary Studies (02.I) 17.3 Vascular Access, Thoracic Echo, and Lung Ultrasound (02.J–L)
18 Coma, Anoxia, and Intracranial Hypertension
18.1 Coma and Other States of Altered Consciousness (03.A) 18.2 Global Anoxia-Ischemia and Post-Resuscitation Encephalopathy (03.A.1) 18.3 Toxidromes, ICU Delirium, and Hypertensive Encephalopathy (03.A.2–4) 18.4 Intracranial Hypertension as a Disease State (03.B)
19 Acute Ischemic Stroke
19.1 IV Reperfusion Therapy (03.C.3) 19.2 Mechanical Thrombectomy Windows and Imaging Selection (03.C.3) 19.3 Malignant Hemispheric Infarction and Basilar Artery Occlusion (03.C.1–2)
20 Intraparenchymal Hemorrhage
20.1 Intracerebral Hematoma (03.D.1) 20.2 Cerebellar Hematoma (03.D.2) 20.3 Intraventricular Hemorrhage (03.D.3)
21 SAH, CVST, and Spinal Cord Infarction
21.1 Aneurysmal Subarachnoid Hemorrhage (03.E.1) 21.2 Non-Aneurysmal SAH (03.E.2) 21.3 Cerebral Venous Sinus Thrombosis (03.F) 21.4 Spinal Cord Infarction (03.G)
22 Vascular Anomalies and Traumatic Brain Injury
22.1 Unruptured Aneurysm, Cavernoma, AVM, and Dural AVF (03.H) 22.2 Diffuse Axonal Injury and Cerebral Contusions (03.I.1–2) 22.3 Epidural Hematoma, Subdural Hematoma, and Penetrating Injury (03.I.3–4, 7) 22.4 Arterial Dissection and Carotid-Cavernous Fistula (03.I.5–6)
23 Spine, Hydrocephalus, and CNS Infection
23.1 Spinal Cord Injury, Central Cord, and Neurogenic Shock (03.J) 23.2 Unstable Spine Fractures (03.K) 23.3 Hydrocephalus and CSF Diversion (03.L) 23.4 Acute CNS Infections (03.M)
24 Seizures and Neuromuscular Emergencies
24.1 Status Epilepticus and Seizures (03.N) 24.2 Guillain-Barré Syndrome (03.O.1) 24.3 Myasthenic Crisis (03.O.2) 24.4 Motor Neuron Disease, Acute Myopathies, Rhabdomyolysis, and CINM (03.O.3–6)
25 Inflammatory Disease, Neuro-Oncology, and Special Populations
25.1 Fulminant Demyelinating Diseases (03.P) 25.2 Autoimmune Encephalitis and Acute Autonomic Hyperactivity (03.Q–R) 25.3 Neuro-Oncology and Treatment Complications (03.S) 25.4 Pregnancy/Post-Partum, Post-Transplant, and Pediatric Patients (03.T–U)
26 Neurosurgical and Perioperative Complications
26.1 Postoperative Seizures, Hemorrhage, Ischemia, and Hyperperfusion (04.A, C, D, H) 26.2 Infection, CSF Leak, and Pneumocephalus (04.B, E, F) 26.3 Complications of EVD and Lumbar Drain (04.G, I)
27 Ethics, Prognostication, and Organ Donation
27.1 Communication, Decision-Makers, Advance Directives, and DNR (05.A, B, G) 27.2 Uncertainties of Prognostication and the Self-Fulfilling Prophecy (05.C) 27.3 Palliative Care, Withdrawal, Withholding, and Futility (05.D–F) 27.4 Donation After Cardiac Death and Care of the Organ Donor (05.H–I)
12.2 Mesenteric Ischemia and Abdominal Compartment Syndrome (01.S.6–7)
Key Takeaways Explain This Topic AI
CTA with intravenous contrast is the first-line test for suspected acute mesenteric ischemia; a normal lactate does not exclude the diagnosis because lactate rises late.
The four mechanisms — arterial embolus, arterial thrombosis, mesenteric venous thrombosis, and nonocclusive mesenteric ischemia — have different vessels, tempos, and treatments.
World Society of the Abdominal Compartment Syndrome (WSACS) ACS is a sustained intra-abdominal pressure >20 mm Hg with new organ dysfunction; IAH is IAP ≥12 mm Hg.
Measure bladder pressure with a 25 mL saline instill, fully supine, at end-expiration, transducer zeroed at the mid-axillary line; 50–100 mL instills falsely raise the reading.
High intra-abdominal pressure raises intrathoracic pressure, impedes cerebral venous return, increases ICP, and can drop cerebral perfusion pressure; abdominal perfusion pressure is MAP minus IAP.
Last updated: September 2026
Two abdominal catastrophes share a neuro ICU habit of presenting without a helpful examination: acute mesenteric ischemia (AMI) and abdominal compartment syndrome (ACS) . Both raise lactate late. Both can look like “just ileus” or “just ventilator asynchrony.” Both interact with ICP. Independent ExamFinch teaching for this examination follows the mesenteric-ischemia and ACS topics in the ABPN Content Specifications and is not a surgical-society product.
Why the gut infarcts quietly here
Pain out of proportion to physical findings is the classic arterial-embolic phrase. In a sedated SAH or TBI patient there may be no pain report at all . Clues become unexplained lactic acidosis after ICP is controlled, a sudden vasopressor spike, bloody diarrhea, abdominal distention, and feeding failure. By the time the abdomen is rigid, transmural infarction and perforation are already present and mortality is high. The examination item is therefore early CTA , not waiting for a surgical abdomen.
Four mechanisms, four plans
Rough epidemiologic shares in mixed series are arterial embolus ~40–50% , arterial thrombosis ~20–30% , nonocclusive mesenteric ischemia (NOMI) ~20% , and mesenteric venous thrombosis ~5–15% . Those percentages are orientation, not a scoring system. What you must separate is anatomy and treatment.
Arterial embolus usually lodges in the SMA distal to the origin of the middle colic artery . Atrial fibrillation, a ventricular thrombus after myocardial infarction, and endocarditis are the usual sources — all common after stroke or after anticoagulation was stopped for intracranial hemorrhage. Onset is abrupt. Proximal jejunum and the transverse colon may be relatively spared because the embolus sits beyond those branches. The patient may have other emboli (limb, spleen, kidney).
Arterial thrombosis occurs at an atherosclerotic SMA origin . There is often a prodrome of postprandial pain, sitophobia, and weight loss (chronic mesenteric ischemia) then an acute occlusion. Because the ostium is lost, a greater length of midgut is at risk and collaterals from the celiac axis or IMA may already be tenuous. Endovascular stenting or surgical revascularization plus resection of dead bowel is the language of this disease; anticoagulation alone is not.
Mesenteric venous thrombosis (usually superior mesenteric vein) is slower: days of pain in a younger or hypercoagulable patient, or after abdominal surgery, pancreatitis, or cirrhosis with portal hypertension. CTA in the portal venous phase shows the clot. If there is no peritonitis , first-line therapy is anticoagulation (unfractionated heparin in the ICU so it can be stopped for a craniotomy or EVD revision). Operate for dead bowel; second-look laparotomy is common; anticoagulation continues afterward unless a neurosurgical constraint is absolute and then the conversation is about IVC filters and timing, not about ignoring the vein clot.
NOMI is low-flow splanchnic vasoconstriction with patent proximal arteries. The usual patient is already in your unit: cardiogenic shock, hypovolemia, high-dose norepinephrine or vasopressin, cocaine, or ergot. CTA shows bowel ischemia — wall hypoenhancement, pneumatosis, fluid — with open SMA/IMA trunks . Treatment is restore perfusion: volume, inotropes if the problem is cardiac output, and weaning vasoconstrictors . Catheter-directed papaverine or other vasodilators appear in older angiographic algorithms when a catheter is already in the SMA. Laparotomy is for perforation or clearly dead bowel, not for every patent-vessel NOMI.
Type Typical patient Vessel finding First specific therapy
Arterial embolus AF, sudden pain, soft belly SMA cutoff beyond middle colic origin Resuscitate, heparin if the brain allows, embolectomy/endovascular plus resect dead bowel
Arterial thrombosis Atherosclerosis, postprandial prodrome Ostial SMA occlusion Revascularize; resect infarct
Venous thrombosis Hypercoagulable, slower tempo SMV/portal thrombus on venous-phase CTA Anticoagulation if no peritonitis; resect only necrotic bowel
NOMI Shock, high-dose vasopressors Patent origins, ischemic bowel Reverse low flow; vasodilator infusion in selected cases; operate for dead bowel
Lactate is late; CTA is the test
Do not wait for lactate. A normal lactate does not exclude AMI; an elevated lactate does not prove it and may reflect seizure, hypoperfusion, or metformin. Leukocytosis, metabolic acidosis, and phosphate elevation are likewise late. D-dimer is sensitive and hopelessly nonspecific. The first-line imaging study is multiphasic CT angiography of the abdomen and pelvis with intravenous contrast: noncontrast (if looking for bleed or hyperdense thrombus), arterial, and portal venous phases. Oral contrast delays care and can hide mural enhancement. Catheter angiography is now mostly a treatment platform (embolectomy, stent, papaverine) rather than the screening test. Plain films are for free air, not for ruling out ischemia.
If CTA shows occlusion and the abdomen is surgical, the patient goes to the operating room (often with a hybrid endovascular option). Damage-control resection of frankly necrotic bowel, temporary abdominal closure, and a second look at 24–48 hours are standard because bowel of uncertain viability can recover after flow is restored. Do not perform a massive primary anastomosis in a vasopressor-dependent, acidotic patient.
Worked example: a 78-year-old whose anticoagulation was held after lobar ICH develops sudden abdominal pain. The belly is soft. Lactate is 1.4 mmol/L . The wrong answer is reassurance because lactate is normal. The right answer is CTA now , looking for an SMA embolus from atrial fibrillation. If ICH still prohibits full anticoagulation, that is a documented risk–benefit problem after the diagnosis is made — it is not a reason to skip the scan.
Abdominal compartment syndrome
Intra-abdominal pressure (IAP) is the steady pressure in the abdominal cavity. The WSACS 2013 consensus, still the definition set examinations use, is precise:
Normal IAP in a critically ill adult is about 5–7 mm Hg .
Intra-abdominal hypertension (IAH) is a sustained or repeated IAP ≥12 mm Hg .
IAH grades: I 12–15, II 16–20, III 21–25, IV >25 mm Hg.
ACS is a sustained IAP >20 mm Hg (with or without abdominal perfusion pressure <60 mm Hg ) plus new organ dysfunction or failure .
Abdominal perfusion pressure (APP) = mean arterial pressure (MAP) − IAP. Analogous to cerebral perfusion pressure, APP conceptually tracks whether the gut and kidneys are actually perfused. A MAP of 80 mm Hg with an IAP of 24 mm Hg is an APP of 56 mm Hg — not a comfortable number.
Primary ACS starts in the abdominopelvic compartment (hemorrhage, pancreatitis, bowel edema after ischemia, packing). Secondary ACS starts outside it: massive crystalloid resuscitation , burns, sepsis capillary leak, and the neuro ICU pattern of liters of fluid after SAH, TBI, or spinal shock. Recurrent ACS returns after a prior decompression, including after a tight abdominal closure or a binder.
How to measure bladder pressure
The reference intermittent method is transvesical . Instill a maximum of 25 mL of sterile saline into the empty bladder (larger instills — 50 to 100 mL — falsely elevate IAP). Place the patient fully supine , wait until abdominal muscles are quiet (sedate or paralyze if the patient is straining), zero the transducer at the mid-axillary line , and read at end-expiration . Report mm Hg , not cm H2O (1 mm Hg ≈ 1.36 cm H2O). Head-of-bed elevation, a full bladder, and coughing all artifactually raise the number; they do not mean you should skip measurement in a patient who cannot lie flat — document the conditions and trend.
Clinical clues that should trigger a measurement: oliguria not explained by hypovolemia, high peak inspiratory pressures , a tight abdomen, new vasopressor need, and a rising ICP without a new cranial mass. The abdomen is a compartment; treat it like one.
Medical decompression, then the knife
ACS is not an automatic trip to laparotomy if you can drop IAP in minutes, but it is also not a “watch the number overnight” disease once organs are failing. A WSACS-style medical bundle:
Evacuate intraluminal contents — nasogastric tube, rectal tube, treat ileus, consider colonoscopy only if it will actually decompress a mega-colon.
Evacuate extra-luminal contents — paracentesis for tense ascites (common in cirrhosis and in some SAH patients who received volume).
Improve abdominal wall compliance — adequate sedation, neuromuscular blockade if the wall is rigid from fighting the ventilator, reverse Trendelenburg or head-up if ICP allows a compromise, remove constricting binders.
Limit further volume injury — stop reflexive crystalloid, use blood products for hemorrhage, consider hypertonic fluids or continuous renal replacement for overload.
Support perfusion — raise MAP if APP is low, remembering that extra norepinephrine can worsen NOMI.
Decompressive laparotomy if ACS persists with organ failure. Leave the abdomen open with a temporary closure; a tight primary fascia can recreate ACS in an hour.
Worked example: a 52-year-old after aneurysm clipping received 8 L of crystalloid and 4 units of red cells. Peak airway pressure is 38 cm H2O, urine output 10 mL/h, bladder pressure 23 mm Hg , ICP 24 mm Hg , MAP 80 mm Hg . APP = 80 − 23 = 57 mm Hg . CPP = 80 − 24 = 56 mm Hg . The same number that is failing the kidney is failing the brain. NGT, paralysis if fighting, stop the fluid, drain ascites if present — and if those do not drop IAP, open the abdomen . Raising PEEP to “treat” the high airway pressure makes venous return and ICP worse.
Interaction with ICP and CPP
The abdomen and the skull share a venous system. Elevated IAP is transmitted through the diaphragm to intrathoracic pressure , which raises central venous pressure and impedes jugular and vertebral venous outflow . Cerebral venous congestion raises cerebral blood volume and therefore ICP . MAP may fall at the same time because venous return to the heart falls, afterload on the right ventricle rises, and high airway pressures worsen dead space. CPP = MAP − ICP therefore drops from both ends. High PEEP, abdominal binders, Trendelenburg, and ACS are additive. In a monitored TBI patient, a sudden ICP spike with oliguria and a rock-hard abdomen is ACS until measured.
Conversely, decompressive laparotomy in true ACS can lower ICP. That is not a license to open every tense belly; it is the reason a neurointensivist measures bladder pressure instead of stacking osmotic therapy for an ICP crisis that originated below the diaphragm. After a hemicraniectomy the skull is no longer a closed box, but venous obstruction from ACS still harms remaining brain and the opposite hemisphere.
- Pressure relationship Formula or threshold Neuro ICU implication
- CPP MAP − ICP Falls if ACS drops MAP or raises ICP
- APP MAP − IAP Gut/kidney analog; ACS often APP <60 mm Hg
- ACS IAP >20 mm Hg + new organ failure Laparotomy if medical bundle fails
- IAH IAP ≥12 mm Hg Start the medical bundle before organs fail
- Bladder method 25 mL, supine, end-expiration, mid-axillary zero Do not instill 70 mL “to get a waveform”
Exam traps: waiting for lactate before CTA; treating NOMI with SMA embolectomy; treating venous thrombosis with immediate extensive resection and no heparin; diagnosing ACS from a grade-II IAP of 18 mm Hg without organ failure; calling ACS “ruled out” because the abdomen is not rigid in a paralyzed patient; and treating ACS-related high airway pressures with more PEEP while ignoring IAP.