Hepatobiliary Emergencies

Condition	Key MRI Findings	Tips
Choledocholithiasis	T2-hypointense filling defect in bile duct on MRCP. Obstructive: upstream dilatation, abrupt caliber change. Trace entire biliary system on thin MRCP/T2W Choledocholithiasis: T2-dark filling defect (arrow) on MRCP	GB neck and cystic duct are blind spots. Pneumobilia can mimic calculi (nondependent, blooms on GRE). Crossing vessel on coronal MRCP can mimic filling defect — check axial reformats
Gangrenous cholecystitis	Focal GB wall nonenhancement or discontinuity; intramural abscess (rim-enhancing + diffusion-restricting collection); contained perforation Gangrenous cholecystitis: focal wall nonenhancement	Abscess: rim enhancement + central DWI restriction. Hematoma: central DWI restriction but no rim enhancement + T1 hyperintensity
Hemorrhagic cholecystitis	Distended GB with T1-hyperintense and T2-hypointense contents; blooming on T2* GRE; active bleed on subtraction images. No enhancement within hematoma itself T1W: hyperintense blood products	Both hemorrhage and inspissated bile are T1-bright — use GRE blooming to distinguish. Check subtraction images for active extravasation
Bile leak / biloma	T2W MRCP: delineate anatomy. Gadoxetate (Eovist) hepatobiliary phase: extravasation of excreted contrast from duct into collection. Add 60–90 min delayed phase if 20–30 min scan is negative 20 min HBP: leak site identified Delayed: extravasation confirmed	Avoid gadoxetate if bilirubin >3 mg/dL, severe hepatic failure, or competing drugs (methotrexate, tamoxifen, cisplatin)
Hepatic abscess	Rim-enhancing collection + central diffusion restriction; double-target sign; perilesional hyperemia (arterial phase) Hepatic abscess: rim enhancement	Overlaps with cystic metastases — abscess favored by clinical context (fever, leukocytosis, recent biliary intervention). Short-term follow-up if unclear
Hemorrhagic hepatic lesion	Lesion with T1-hyperintense and T2-hypointense blood products; blooming on GRE; nonenhancing hemorrhagic component on subtraction. Look for enhancing viable tumor around hematoma	HCC: check for tumor-in-vein (thrombus enhances like primary tumor). Adenoma: young women, OCP use, peripheral enhancement pattern. Subtraction mandatory when T1 hyperintensity is present

Quick Reference: Peliosis Hepatis vs. Hepatic Abscess

⚠ Critical safety note: Misdiagnosing peliosis hepatis (PH) as abscess and performing percutaneous drainage can cause life-threatening hemorrhage from the blood-filled sinusoidal cavities. When imaging is equivocal, biopsy (transjugular preferred) rather than drainage.

Feature	Peliosis Hepatis	Hepatic Abscess
Clinical	Usually incidental/asymptomatic (70–92%); known associated condition (malignancy, steroids, OCP, immunosuppression, HIV). Normal or mildly elevated LFTs. No fever.	Fever (>90%), RUQ pain, leukocytosis, elevated ALP/bilirubin. Identifiable source (biliary disease, portal pyemia, post-procedural). Blood cultures positive in 33–65%.
Enhancement pattern	Progressive centrifugal (center → out) or centripetal (periphery → in) filling; becomes isodense to liver on delayed phase — reflects slow blood pooling	Persistent rim enhancement with non-enhancing necrotic center; rim does not fill in on delayed phases
DWI/ADC	No restricted diffusion; ADC ≈ 1.5 × 10⁻³ mm²/s (freely mobile blood)	Restricted diffusion; low ADC ≈ 0.9–1.1 × 10⁻³ mm²/s (viscous pus)
T2 signal	Mildly hyperintense (similar to or slightly above liver)	Markedly hyperintense (approaching CSF brightness)
Perilesional changes	No perilesional edema; ill-defined margins blending with parenchyma	Perilesional edema (T2 halo); wedge-shaped perilesional arterial hyperemia; well-defined sharp border
T1W	Hypointense; may have T1-bright foci (subacute blood products)	Hypointense throughout
Internal features	No gas; no septations; may show internal vascular structures	Gas bubbles ± fluid levels; internal septations possible
Margins	Ill-defined, not well-demarcated	Well-defined, sharp borders
Hepatobiliary phase	Hypointense	Hypointense ± perilesional enhancement

MRI showing peliosis hepatis — unenhanced phase with hypodense hepatic lesions — PH — Pre-contrast: hypointense lesions, ill-defined margins

MRI showing peliosis hepatis — early post-contrast with peripheral nodular filling pattern — PH — Early: peripheral nodular fill-in (centripetal)

MRI showing peliosis hepatis — delayed phase becoming isointense to liver parenchyma — PH — Delayed: fills in, approaches liver isointensity

Key Distinguishing Pearl

The combination of no DWI restriction + progressive delayed fill-in + ill-defined margins + asymptomatic patient = peliosis until proven otherwise. The combination of restricted diffusion + persistent rim + perilesional edema + fever/leukocytosis = abscess.

A unique overlap entity: bacillary peliosis (Bartonella henselae in HIV/AIDS) can present with fever and elevated ALP mimicking abscess — but shows the vascular fill-in pattern of PH. Responds to erythromycin or doxycycline.

Management

Abscess suspected: Image-guided aspiration for culture ± drainage
PH suspected: Discontinue offending agent (androgens, steroids, OCP) — lesions often regress. Treat underlying condition.
Equivocal: Transjugular biopsy preferred over percutaneous (lower hemorrhage risk given vascular nature of PH)

Pancreatic Emergencies

Condition	Key MRI Findings	Tips
Acute interstitial edematous pancreatitis	Pancreatic edema (loss of normal T1 hyperintensity) + peripancreatic fluid on T2W + preserved parenchymal enhancement on post-Gd IEP: loss of T1 signal, preserved enhancement, peripancreatic fluid	Normal pancreas is T1-bright (brighter than liver). Loss of T1 signal = edema/inflammation. DWI restriction is sensitive for early pancreatitis. India ink artifact on out-of-phase shows subtle fat stranding
Acute necrotizing pancreatitis	Lack of parenchymal enhancement on post-Gd = necrosis. Hemorrhage: T1 hyperintensity + GRE blooming. Vascular complications: thrombosis (filling defect on bSSFP/post-Gd), pseudoaneurysm Necrotizing pancreatitis: nonenhancing parenchyma = necrosis	Pitfall: Diffuse hemorrhagic necrosis can appear T1-bright, mimicking normal pancreas. Always check post-Gd for absent enhancement and T2W for necrosis
Pancreatic trauma	Full-thickness laceration = T2-hyperintense linear signal disrupting parenchyma. Trace pancreatic duct on T2W axial images (MRCP often limited by surrounding fluid)	Ductal injury (AAST Grade III+) = surgical indication. MRI better than CT for delineating duct integrity. Contusions (Grade I/II) without duct injury → conservative

Bowel & Peritoneal Emergencies

Condition	Key MRI Findings
Appendicitis (pregnancy)	Dilated appendix ≥7 mm, wall thickness >2 mm, periappendiceal fluid/fat stranding on T2W. Appendicolith: T2-hypointense filling defect (confirm on bSSFP). Appendix migrates cranially with gestational age. Sensitivity 94%, specificity 97% Appendicitis: dilated appendix, periappendiceal stranding
Diverticulitis	Colonic wall thickening >3 mm with diverticula; pericolic fat stranding on T2W FS; abscess: rim-enhancing + DWI-restricting collection. MRI sensitivity 86–94%, specificity 88–92%. Better soft-tissue resolution for fistula, oophoritis Diverticulitis: wall thickening, pericolic T2 stranding
Crohn complications	Stricture: wall thickening >3 mm + luminal narrowing >50% + upstream dilatation. Penetrating: sinus tract, fistula, phlegmon, abscess (rim enhancement + DWI restriction). Active inflammation: wall edema + hyperenhancement on T2W FS and post-Gd
Perianal fistula	Small-FOV T2W FSE along anal canal is key. Report: tract type (Parks classification — intersphincteric / transsphincteric / suprasphincteric / extrasphincteric), internal and external openings, branches, abscess. DWI + post-Gd for abscess vs granulation vs fibrosis Perianal fistula: T2W tract, internal opening, sphincter relation
Pneumoperitoneum	Subtle T2-hypointense foci in peritoneal cavity. Air-fluid levels. Susceptibility artifact on bSSFP and T1W GRE sequences. Can be easily missed — look for abnormal extraenteric T2-dark foci Pneumoperitoneum: T2-dark extraenteric foci, GRE susceptibility

Renal & GU Emergencies

Condition	Key MRI Findings
Pyelonephritis	Wedge-shaped T2 hyperintensity with striated nephrogram; wedge-shaped hypoenhancement on post-Gd; wedge-shaped DWI restriction. Abscess: rim-enhancing collection with central DWI restriction Pyelonephritis: wedge-shaped diffusion restriction
Renal infarct	Wedge-shaped nonenhancement with cortical rim sign (preserved capsular vessel enhancement); cortical DWI restriction Renal infarct: wedge-shaped nonenhancement Delayed: cortical rim sign
Urolithiasis (pregnancy)	Hypointense filling defect in dilated ureter — better seen on bSSFP than T2W. Distinguish from physiologic hydroureteronephrosis (gradual tapering at pelvic brim, right > left)
Spontaneous renal hemorrhage (Wünderlich syndrome)	Subcapsular/perirenal T1-hyperintense collection with T2 signal heterogeneity. Subtraction images mandatory to exclude underlying enhancing neoplasm (AML, RCC most common causes)

OB/GYN Emergencies

Condition	Key MRI Findings
Placental abruption	Retroplacental or subchorionic hematoma: T1-hyperintense blood products (T1 better than T2 for hemorrhage detection). T2 can underestimate hemorrhage extent. bSSFP may show subchorionic hematoma better than T2
Ectopic pregnancy	Gestational sac outside endometrial cavity on T2W. Locations: tubal (most common), cornual, cervical, cesarean scar. MRI localizes ectopic precisely when US is indeterminate. Cesarean scar ectopic: sac in lower uterine segment scar, residual myometrium <2 mm = rupture risk
Ovarian torsion (pregnancy)	Enlarged ovary with peripheral follicles and stromal edema on T2W. Pelvic ascites. Compare with contralateral ovary. Whirlpool sign of twisted pedicle Ovarian torsion: enlarged ovary, peripheral follicles, stromal edema
Postpartum hemorrhage — RPOC vs UVA	RPOC: enhancing endometrial tissue (≤ myometrium = moderate; > myometrium = hypervascular). Serial β-hCG decreases. UVA/AVF: serpiginous flow voids, early draining vein on time-resolved MRA. Low-flow UVA: myometrial blush without early draining vein

MRI in pregnancy: Safe at ≤3 T (prefer 1.5 T in 1st trimester). GBCAs are FDA Class C — avoid unless benefit clearly outweighs risk; use lowest dose of macrocyclic Group II GBCA with informed consent. Non-contrast sequences (T2W SSFSE, DWI, bSSFP, T1W) are sufficient for most acute indications. For renal failure (eGFR <15): Group II GBCAs can be used after risk-benefit discussion; space injections ≥7 days apart.

Reference

Panda A, Aswani Y, Heming CAM, et al. On-Call Body MRI: A Primer. RadioGraphics. 2025;45(1).

Acute Body MRI — On-Call Hepatobiliary, Pancreatic, Bowel, Renal, and OB/GYN Emergencies