What is the most likely cause of bilateral adrenal hemorrhage in a middle‑aged man with ischemic heart disease (LVEF 35 %) who underwent coronary artery bypass grafting, then developed acute pancreatitis with septic shock, is receiving norepinephrine and postoperative anticoagulation, and has CT evidence of adrenal enlargement with heterogeneous enhancement?

Bilateral Adrenal Hemorrhage Post-CABG: Etiology

In this patient, the bilateral adrenal hemorrhage was most likely caused by the combination of postoperative anticoagulation (heparin during and after CABG), septic shock from acute pancreatitis, and the hemodynamic stress of cardiac surgery itself—a perfect storm of coagulopathy, critical illness, and vascular stress that predisposes the adrenal glands to hemorrhagic infarction. 1, 2, 3

Primary Contributing Factors

Postoperative Anticoagulation

• Heparin therapy during and after CABG is a well-established risk factor for adrenal hemorrhage, as anticoagulant therapy directly increases bleeding risk in highly vascularized organs like the adrenal glands 2, 4, 3
• The FDA label for heparin explicitly warns that "adrenal hemorrhage (with resultant acute adrenal insufficiency)" can occur during anticoagulant therapy with heparin 2
• Postoperative complications (including anticoagulation-related bleeding) account for 41% of all adrenal hemorrhage cases in recent large series 3
• The combination of intraoperative heparin for cardiopulmonary bypass and postoperative anticoagulation creates a prolonged window of hemorrhagic risk 1, 2

Septic Shock from Acute Pancreatitis

• Sepsis is a recognized independent risk factor for adrenal hemorrhage, accounting for 3% of cases, and the CT findings explicitly note "septic shock" as part of the clinical context 3
• Critical illness itself predisposes to adrenal hemorrhage through multiple mechanisms: hypotension, coagulopathy, and increased adrenal metabolic demand 3
• The combination of septic shock with anticoagulation creates a synergistic risk, as sepsis-induced coagulopathy compounds the bleeding tendency from therapeutic anticoagulation 5, 3

Hemodynamic Stress of Cardiac Surgery

• CABG with cardiopulmonary bypass causes complex alterations in coagulation, including reductions in clotting factors, alterations in platelet function, and increases in fibrinolytic products 6
• The postoperative state after cardiac surgery is an established risk factor for bilateral adrenal hemorrhage, with documented cases occurring specifically after CABG 7
• Hemodynamic instability during and after surgery increases adrenal vascular stress, as the adrenal glands have a unique blood supply vulnerable to ischemia and hemorrhage under stress conditions 5, 7

Mechanism of Adrenal Vulnerability

Anatomic and Vascular Factors

• The adrenal glands receive blood from three arterial sources but drain through a single central vein, creating a vascular anatomy prone to venous congestion and hemorrhage under stress 5, 3
• During critical illness and septic shock, increased ACTH stimulation causes adrenal hyperemia and enlargement, further predisposing to hemorrhage 5, 3
• The combination of increased blood flow (from stress response) and impaired coagulation (from anticoagulation and sepsis) creates ideal conditions for hemorrhagic infarction 5, 3

Bilateral vs. Unilateral Presentation

• Bilateral adrenal hemorrhage is rare (7% of all adrenal hemorrhage cases) but is strongly associated with underlying coagulopathy (44% of bilateral cases vs. 3% of unilateral cases) 3
• Patients with bilateral adrenal hemorrhage develop primary adrenal insufficiency in 72% of cases, explaining this patient's persistent vasopressor dependence despite normal 8 AM cortisol (which may have been measured before complete adrenal failure) 3

Clinical Correlation with Vasopressor Dependence

Adrenal Insufficiency Despite "Normal" Cortisol

• The reported "normal" 8 AM cortisol does not exclude acute adrenal insufficiency in the setting of septic shock, where cortisol levels should be markedly elevated 8
• A cortisol level that is "normal" in the context of critical illness and septic shock is functionally inadequate and represents relative adrenal insufficiency 8
• The Surviving Sepsis Campaign recommends adding hydrocortisone 200 mg/day if hemodynamic stability cannot be achieved with adequate fluid resuscitation and vasopressor therapy, which applies directly to this case 8

Persistent Vasopressor Requirement

• The inability to wean norepinephrine despite clinical improvement of pancreatitis and absence of other complaints is a hallmark of adrenal insufficiency 8
• Bilateral adrenal hemorrhage with evolving infarction (as described on CT) causes progressive loss of cortisol production, leading to refractory hypotension 5, 3

Additional Risk Factors in This Case

Acute Pancreatitis

• Pancreatitis itself can cause distributive shock and is recognized as an inflammatory state that contributes to vasopressor requirements 9
• The combination of pancreatitis-induced inflammation and adrenal hemorrhage creates a dual mechanism for persistent hypotension 9, 3

Low Ejection Fraction (LVEF 35%)

• Pre-existing cardiac dysfunction increases the risk of postoperative complications and hemodynamic instability 1
• Patients with reduced LVEF have higher mortality after CABG and are more vulnerable to additional insults like adrenal insufficiency 1

Critical Pitfalls to Avoid

• Never assume a "normal" 8 AM cortisol excludes adrenal insufficiency in septic shock—cortisol should be markedly elevated in critical illness, and a normal value represents inadequate adrenal response 8
• Never delay empiric corticosteroid therapy in patients with bilateral adrenal hemorrhage on imaging who have refractory hypotension, as waiting for confirmatory testing risks cardiovascular collapse 8, 5
• Never attribute persistent vasopressor dependence solely to sepsis when imaging shows bilateral adrenal pathology—this is adrenal insufficiency until proven otherwise 5, 3
• Never discontinue stress-dose corticosteroids prematurely in patients with bilateral adrenal hemorrhage, as recovery of adrenal function may take months or may never occur (72% develop permanent primary adrenal insufficiency) 3