Adrenal hemorrhage is bleeding within the adrenal gland, which may develop due to traumatic or non-traumatic causes. Non-traumatic causes include anticoagulant therapy (most common), sepsis (Waterhouse-Friderichsen syndrome — bilateral adrenal hemorrhage in meningococcal sepsis), stress (major surgery, burns), coagulopathy, thrombocytopenia, ICU patient (critical illness), neonatal birth trauma, and pregnancy. May be unilateral or bilateral. Bilateral adrenal hemorrhage can lead to acute adrenal insufficiency (Addisonian crisis) — a life-threatening condition. Imaging findings vary by hemorrhage stage: acute hemorrhage is hyperdense on CT (50-80 HU), subacute stage shows T1 hyperintensity on MRI (methemoglobin), chronic stage develops atrophy and calcification.
Age Range
0-85
Peak Age
-
Gender
Equal
Prevalence
Uncommon
The adrenal gland has one of the highest blood flows relative to body weight — the imbalance between three arterial sources (inferior phrenic, aorta, renal artery branches) and a single venous drainage (central vein) creates susceptibility to venous congestion and hemorrhage. During stress, sepsis, or ACTH stimulation, adrenal blood flow increases and the already fragile medullary sinusoidal vessels may rupture. In anticoagulant-related hemorrhage, uncontrolled growth of small capillary bleeds occurs. In Waterhouse-Friderichsen syndrome, DIC (disseminated intravascular coagulation) triggered by meningococcal endotoxins leads to adrenal microvascular thrombosis and subsequent hemorrhagic necrosis. The pathophysiological basis of imaging findings: The high CT attenuation in acute hemorrhage (50-80 HU) results from hemoglobin protein's high electron density (iron atom Z=26). MRI signal changes depend on hemoglobin's oxidation state: hyperacute (oxyhemoglobin: T1 isointense, T2 mildly hyperintense), acute (deoxyhemoglobin: T1 isointense, T2 hypointense), early subacute (intracellular methemoglobin: T1 hyperintense, T2 hypointense), late subacute (extracellular methemoglobin: T1 hyperintense, T2 hyperintense), chronic (hemosiderin: T1 hypointense, T2 markedly hypointense). This staging reflects changes in the magnetic properties of hemoglobin degradation products.
A hyperdense (50-80 HU), non-enhancing adrenal mass on acute CT, in the context of hemorrhage (trauma, anticoagulant, sepsis), is highly diagnostic for adrenal hemorrhage. Beginning of size decrease within 6-8 weeks on follow-up confirms the diagnosis. Failure to shrink or development of solid enhancing component should suggest hemorrhagic lesion due to underlying tumor and further evaluation should be performed.
Acute adrenal hemorrhage appears as a hyperdense (50-80 HU) mass on non-contrast CT. Density changes with hemorrhage stage: acute (1-3 days): 50-80 HU, subacute (1-4 weeks): gradually decreasing density (30-50 HU), chronic (>4 weeks): low density (10-30 HU) and eventually calcification or atrophy. Adrenal gland contours may be preserved or enlarged. Periadrenal stranding may be seen.
Report Sentence
A hyperdense mass measuring approximately ___ cm at ___ HU in the left/right adrenal gland on non-contrast CT is seen; in the clinical context, consistent with acute adrenal hemorrhage; size follow-up is recommended.
On contrast-enhanced CT, no enhancement is seen within the hematoma — this is the most important differentiating finding from solid tumors (metastasis, pheochromocytoma, ACC). Thin peripheral capsular enhancement may be seen. In the presence of active bleeding, contrast extravasation (active bleeding focus) may be seen — important finding in emergencies.
Report Sentence
On contrast-enhanced CT, no enhancement is seen within the mass, consistent with hematoma; no active contrast extravasation is observed.
The T1 signal of adrenal hemorrhage on MRI depends on the hemorrhage stage. Hyperacute (<24 hours): oxyhemoglobin — T1 isointense. Acute (1-3 days): deoxyhemoglobin — T1 isointense. Early subacute (3-7 days): intracellular methemoglobin — T1 markedly hyperintense (MOST DIAGNOSTIC STAGE). Late subacute (1-4 weeks): extracellular methemoglobin — T1 hyperintense. Chronic (>4 weeks): hemosiderin — T1 hypointense.
Report Sentence
On MRI, the adrenal lesion shows markedly hyperintense signal on T1-weighted images, consistent with subacute hemorrhage (methemoglobin).
T2 signal depends on hemorrhage stage. Acute: deoxyhemoglobin — T2 markedly hypointense ('dark blood'). Early subacute: intracellular methemoglobin — T2 hypointense. Late subacute: extracellular methemoglobin — T2 hyperintense. Chronic: hemosiderin rim — T2 markedly hypointense peripheral rim (characteristic). Blooming artifact on GRE/T2* sequences.
Report Sentence
On T2-weighted images, the lesion shows heterogeneous signal with a peripheral hypointense hemosiderin rim; susceptibility artifact is present on GRE sequences.
On DWI, acute hematoma may show mild-to-moderate diffusion restriction (T2 shine-through effect should be carefully evaluated). Diffusion restriction is not seen in subacute and chronic stages. DWI is not a primary tool for adrenal hemorrhage diagnosis.
Report Sentence
On DWI, mild diffusion restriction consistent with acute phase is seen in the lesion; confirmation with ADC map is recommended.
On FDG PET-CT, organizing hematoma typically shows no significant FDG uptake. Mild inflammatory FDG uptake may be present in the acute phase but usually remains below liver SUV. High FDG uptake should suggest underlying tumor or infection — hemorrhagic tumor (e.g., pheochromocytoma, ACC) should be excluded.
Report Sentence
On FDG PET-CT, no significant FDG uptake is observed in the adrenal lesion, consistent with organizing hematoma.
Criteria
Post-trauma. Right adrenal more common (70-80%, compression with liver). Usually unilateral.
Distinct Features
Detected in 2% of polytrauma CTs. Usually self-resolving. Follow-up CT recommended.
Criteria
Under anticoagulant use (warfarin, heparin, DOAC). Usually unilateral. Associated with supratherapeutic INR.
Distinct Features
Most common non-traumatic cause. INR correction and anticoagulant discontinuation/change needed. Surgical drainage for large hematomas.
Criteria
Bilateral adrenal hemorrhagic necrosis in meningococcal sepsis. DIC-triggered. Acute adrenal insufficiency. Very high mortality.
Distinct Features
Emergency steroid replacement is life-saving. Bilateral adrenal enlargement + sepsis + shock triad is diagnostic. Antibiotics + steroids + ICU.
Distinguishing Feature
Metastasis contains enhancing solid component, grows on follow-up. Hemorrhage does not enhance, shrinks on follow-up.
Distinguishing Feature
Hemorrhagic pheochromocytoma: solid enhancing component + elevated catecholamines. Simple hemorrhage: no solid component, normal catecholamines.
Distinguishing Feature
ACC: solid enhancing component, invasion, large size, functional syndrome. Hemorrhage: no enhancement, no invasion, shrinks on follow-up.
Distinguishing Feature
Pseudocyst results from organized hemorrhage — thick fibrous wall, calcification, chronic appearance. Acute hemorrhage: hyperdense, thin wall, acute clinical context.
Urgency
urgentManagement
conservativeBiopsy
Not NeededFollow-up
6-monthAdrenal hemorrhage management depends on etiology and clinical status. Unilateral hemorrhage is usually managed conservatively — anticoagulant dose adjustment, supportive care. Bilateral hemorrhage + hypotension = emergency cortisol replacement (IV hydrocortisone). In traumatic hemorrhage, accompanying organ injuries are evaluated. CT follow-up at 6-8 weeks is recommended — shrinkage confirms diagnosis. Failure to shrink or development of solid component suggests underlying tumor and requires further evaluation (MRI, biopsy). Biopsy is generally not needed — follow-up is sufficient in the absence of solid component.
Adrenal hemorrhage usually resolves spontaneously. Size decrease should be confirmed with follow-up imaging. Bilateral adrenal hemorrhage can lead to adrenal insufficiency (Waterhouse-Friderichsen).