Portal Venous Gas

Brief HPI

Young male with no significant medical history presenting with progressively worsening right lower quadrant abdominal pain with marked tenderness to palpation and involuntary guarding.

Imaging

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CT Abdomen/Pelvis with Contrast

Inflammatory changes in the right lower quadrant concerning for ruptured appendicitis with approximately 9 cm abscess.
Gas in the liver likely representing portal venous gas which can be seen in the setting of appendicitis vs less likely secondary to bowel ischemia.

Differentiation between Portal Venous Gas and Pneumobilia

Portal venous gas vs. Pneumobilia

References

  1. Rabou Ahmed A and Frank Gaillard. “Pneumobilia.” Radiopaedia. http://radiopaedia.org/articles/pneumobilia.
  2. Morgan Matt A and Donna D’Souza. “Portal venous gas.” Radiopaedia. http://radiopaedia.org/articles/portal-venous-gas
  3. Sebastià C, Quiroga S, Espin E, Boyé R, Alvarez-Castells A, Armengol M. Portomesenteric vein gas: pathologic mechanisms, CT findings, and prognosis. Radiographics. 2000;20(5):1213–24–discussion1224–6. doi:10.1148/radiographics.20.5.g00se011213.
  4. Sherman SC, Tran H. Pneumobilia: benign or life-threatening. J Emerg Med. 2006;30(2):147-153. doi:10.1016/j.jemermed.2005.05.016.

Lactic Acidosis

HPI:

59F with a reported history of congestive heart failure, presenting with intermittent chest discomfort for three days.

She characterized this discomfort as “heartburn”, describing a mid-epigastric burning sensation radiating up her neck, not associated with exertion, lasting 1-2 hours and resolving with antacids. The patient has poor exercise tolerance at baseline and for the past several years has been able to ambulate only short distances around her home, and states that these symptoms have been worsening in the past week. She denies chest pain on exertion, orthopnea or paroxysmal nocturnal dyspnea. She states that she was diagnosed with congestive heart failure five years ago, but was never prescribed medications.

On further questioning, the patient reports several weeks of mouth and lip pain which has limited oral intake, though no dysphagia to solids or liquids. She otherwise denies fevers/chills, abdominal pain, nausea/vomiting, cough, changes in urinary or bowel habits.

In the emergency department, the patient was noted to have an elevated serum troponin, though ECG showed no changes of acute ischemia/infarction.

PMH:

  • Congestive heart failure

PSH:

  • None

FH:

  • Mother with diabetes
  • Father with MI at age 65

SHx:

  • 4-5 drinks of alcohol/day
  • No tobacco or drug use

Meds:

  • None

Allergies:

NKDA

Physical Exam:

VS: T 37.4 HR 106 RR 18 BP 145/82 O2 100% RA
Gen: Morbidly obese female, lying in bed, in no acute respiratory distress, speaking in complete sentences.
HEENT: Dry, cracked lips, slightly erythematous, otherwise moist mucous membranes, poor dentition. Mild scleral icterus. No cervical lymphadenopathy.
CV: Rapid rate, regular rhythm, normal S1/S2, II/VI systolic ejection murmur at LUSB, no radiation appreciated. No jugular venous distension.
Lungs: Clear to auscultation in posterior lung fields bilaterally, no crackles appreciated.
Chest: Well-circumscribed erythematous patch in folds beneath left breast, no underlying fluctuance, no significant tenderness to palpation. On contralateral breast, some hyperpigmentation but no erythema.
Abdomen: Obese, non-tender, non-distended. Patch of erythema below pannus, mildly tender to palpation.
Ext: Bilateral lower extremities with marked edema and overlying scaly plaques, some slightly ulcerated weeping serous fluid. Peripheral pulses are difficult to palpate, capillary refill difficult to assess.

Labs/Studies:

  • CBC: 11.1/11.1/34.5/212 (MCV 114.2)
  • BMP: 140/4.5/97/20/10/1.14/64
  • Anion Gap: 23
  • LFT: AST: 73, ALT: 26, AP: 300, TB: 4.6, DB: 2.1, Alb: 3.0, INR 1.3
  • BNP: 158
  • Troponin: 1.284
Sinus tachycardia, LVH, secondary repolarization abnormalities

Sinus tachycardia, LVH, secondary repolarization abnormalities

Imaging:

CT Pulmonary Angiography:
No evidence of central pulmonary embolism, thoracic aortic dissection, or thoracic aortic aneurysm. Evaluation of the peripheral vessels is limited due to motion artifact. No focal consolidation or pneumothorax.

CT Abdomen/Pelvis non-contrast:
No evidence of intra-abdominal abscess or definite source of infection. Marked hepatic steatosis.

CT Lower Extremity non-contrast:
Diffuse circumferential subcutaneous edema involving both lower extremities from the level of the mid thighs distally through the feet. There are bilateral subcutaneous calcifications which are likely venous calcifications in the setting of chronic venous stasis disease. There is some overlying skin thickening.

TTE:
There is moderate concentric left ventricular hypertrophy with hyperdynamic LV wall motion. The Ejection Fraction estimate is >70%. Grade I/IV (mild) LV diastolic dysfunction. No hemodynamically significant valve abnormalities.

US Abdomen:
Hepatomegaly, echogenic liver suggesting fatty infiltration. Moderately blunted hepatic vein waveforms suggesting decreased hepatic parenchymal compliance.

Assessment/Plan:

The patient was admitted to the cardiology service for management of NSTEMI and evaluation of undiagnosed CHF. She was started on a heparin continuous infusion. In addition, a CT pulmonary angiogram was obtained to evaluate for pulmonary embolism as an explanation of her progressive dyspnea on exertion. No PE, consolidation or effusion was identified.

Despite the patient’s reported history of congestive heart failure, there was no evidence that her symptoms were a result of an acute exacerbation with only a mildly elevated BNP but no jugular venous distension or evidence of pulmonary edema. The patient’s significant lower extremity edema was more suggestive of chronic venous stasis.

One notable laboratory abnormality that was explored was her elevated anion gap metabolic acidosis. Studies submitted included serum lactate, salicylates, osmolarity, CK, and urinalysis for ketonuria. This evaluation was notable for an elevated serum lactate of 13.2mmol/L and an arterial blood gas that showed adequate respiratory compensation (and no A-a gradient). Given the patient’s modest leukocytosis (with neutrophil predominance), and tachycardia, the concern for sepsis was increased though the source remained unclear. Prominent possibilities included a skin and soft-tissue infection vs. less likely intra-abdominal source though the patient’s physical examination was not suggestive of a process that would produce such a substantial lactic acidosis. Blood cultures were drawn and the patient was started on empiric antibiotics for the suspected sources. In addition, the patient was cautiously volume resuscitated given her reported history of CHF while pending a transthoracic echocardiogram to evaluate cardiac function. Additional imaging including CT abdomen/pelvis and lower extremities was obtained (though without contrast due to the patient’s recent exposure), and no obvious source was identified.

Over the next two days, the patient’s serum lactate downtrended to normal range, as did the serum troponin. A transthoracic echocardiogram showed an LVEF >70% with mild concentric hypertrophy and diastolic dysfunction. Blood and urine cultures were without growth.

Additional issues managed during the hospitalization included elevated serum transaminases (AST > ALT), conjugated hyperbilirubinemia and evidence of decreased hepatic synthetic function with hypoalbuminemia and elevated INR. Given the patient’s history of EtOH use, as well as other corroborating findings including macrocytic anemia, hypomagnesemia, folate and B12 deficiency, this was attributed to alcoholic hepatitis (discriminant function <32). Infectious hepatitis serologies were negative. The patient was started on nutritional supplements. Finally, the patient persistently complained of lip and oral mucosal pain. Examination was without discrete lesions but some mucosal redness was identified. Despite poor dentition, there was no evidence of abscess and HSV/HIV testing was negative. This was thought to be stomatitis caused by her identified nutritional deficiencies.

Differential Diagnosis of Elevated Serum Lactate 1,2

Differential Diagnosis of Elevated Serum Lactate

Algorithm for Evaluation of Acidemia 3,4

Algorithm for Evaluation of Acidemia

Algorithm for Evaluation of Alkalemia 3,4

Algorithm for Evaluation of Alkalemia

References:

  1. Fall, P. J., & Szerlip, H. M. (2005). Lactic acidosis: from sour milk to septic shock. Journal of intensive care medicine, 20(5), 255–271. doi:10.1177/0885066605278644
  2. Luft, F. C. (2001). Lactic acidosis update for critical care clinicians. Journal of the American Society of Nephrology : JASN, 12 Suppl 17, S15–9.
  3. Ingelfinger, J. R., Berend, K., de Vries, A. P. J., & Gans, R. O. B. (2014). Physiological Approach to Assessment of Acid–Base Disturbances. The New England journal of medicine, 371(15), 1434–1445. doi:10.1056/NEJMra1003327
  4. Ingelfinger, J. R., & Seifter, J. L. (2014). Integration of Acid–Base and Electrolyte Disorders. The New England journal of medicine, 371(19), 1821–1831. doi:10.1056/NEJMra1215672

Biliary Duct Dilation

A 45 year-old male presents with progressive jaundice over 1 month, he denies abdominal pain.

Ultrasound

Liver
Common Bile Duct
Gallbladder Wall

CT Abdomen/Pelvis

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  • Markedly dilated intrahepatic biliary ducts, common bile duct and pancreatic duct.
  • Ill-defined fullness in the pancreatic head consistent with pancreatic adenocarcinoma vs. noncalcified obstructing biliary stone.

Differential Diagnosis of Biliary Duct Dilation: 1,2,3

Differential Diagnosis of Biliary Duct Dilation

References:

  1. Kim, H. J., Lee, K. T., Kim, S. H., Lee, J. K., Lim, J. H., Paik, S. W., & Rhee, J. C. (2003). Differential diagnosis of intrahepatic bile duct dilatation without demonstrable mass on ultrasonography or CT: benign versus malignancy. Journal of gastroenterology and hepatology, 18(11), 1287–1292.
  2. Levy, A. D. (2009). Biliary Ducts – Pathology. The Radiology Assistant, 1–4. Retrieved from http://www.radiologyassistant.nl/en/p49e17de25294d/biliary-ducts-pathology.html
  3. Teefey, S. A., Baron, R. L., Schulte, S. J., Patten, R. M., & Molloy, M. H. (1992). Patterns of intrahepatic bile duct dilatation at CT: correlation with obstructive disease processes. Radiology, 182(1), 139–142. doi:10.1148/radiology.182.1.1727277

Ultrasound Gallery

Appendicitis

Appendicitis

Non-compressible tubular structure in the RLQ of a patient with focal abdominal tenderness. >6mm in diameter.

Common Bile Duct

Common Bile Duct

A tubular structure typically anterior to the portal vein without flow. Normally measures <4mm, increases by 1mm per decade after 40yrs.

Cellulitis

Cellulitis

"Cobblestone" appearance of soft tissue suggesting infection/edema.

Fetal Heart Rate

Fetal Heart Rate

Placing the M-Mode marker over the most visibly active portion of the fetal heart allows for measurement of the fetal heart rate.

Free Fluid

Free Fluid

Free fluid in the hepatorenal recess.

Hydronephrosis

Hydronephrosis

Severe hydronephrosis.

Thoracic Aorta Aneurysm

Thoracic Aorta Aneurysm

Subxiphoid view of thoracic aorta, markedly dilated (>3cm) with thrombus.

Pericardial Effusion

Pericardial Effusion

Mild pericardial effusion in a patient with pleuritic chest pain.

Inferior Vena Cava

Inferior Vena Cava

IVC without significant respiratory variation.

B-lines

B-lines

B-lines extending deep from pleura suggestive of interstitial fluid accumulation (pulmonary edema).

"Shred" sign

"Shred" sign

Irregular, "shredded" pleural line suggestive of consolidation.

Pneumothorax

Pneumothorax

Transition point with loss of lung sliding in a patient with a small spontaneous pneumothorax.

Hepatic Abscess

HPI:

42M with 1.5 weeks of fevers. Initially presented to ER 1wk ago and treated for possible otitis media, however follow-up ENT appointment showed no evidence of OM on exam. Fevers persisted and he developed headaches and went to urgent care where a CT head and LP were negative. A mild elevation of serum transaminases was noted and the following CT abdomen/pelvis was obtained. He denied GI symptoms.

Imaging:

Hepatic Abscess - Axial

Hepatic Abscess - Axial

- 7.4 cm cystic lesion in the inferior right lobe of the liver most consistent in appearance with hepatic abscess.
- Multiple calcified gallstones with a 10 mm gallstone in the neck of the gallbladder or possibly in the cystic duct.

Hepatic Abscess - Coronal

Hepatic Abscess - Coronal

- 7.4 cm cystic lesion in the inferior right lobe of the liver most consistent in appearance with hepatic abscess.
- Multiple calcified gallstones with a 10 mm gallstone in the neck of the gallbladder or possibly in the cystic duct.

Assessment & Plan:

# Liver abscess: likely pyogenic s/p CT-guided drainage with 60cc purulent fluid removed. Gram stain showed GNR and WBC’s, culture grew Klebsiella pneumonia. Treated with ceftriaxone 2g IV q24h, metronidazole 500mg PO TID.

Differential Diagnosis of Hepatic Abscess:1

Differential Diagnosis of Hepatic Abscess

References:

  1. Krige J, Beckingham IJ. Liver abscesses and hydatid disease. BMJ. 2001;322(7285):537–540.

Alcoholic Hepatitis

HPI:

43 year-old female with a history of alcohol abuse and alcoholic hepatitis, presenting after referral from breast clinic for abnormal labs (notable for total bilirubin 18.1). The patient was well until two weeks ago when she noted increasing fatigue associated with morning nausea/vomiting (non-bloody) as well as yellowing of skin and eyes. She also reports darkening of urine, but no dysuria, change in volume of urine, or visible blood. She also denies fevers/chills, increased abdominal girth, abdominal pain, changes in bowel habits or bloody/dark stools.

She reports drinking 1 pint of vodka daily for the past 15 years, and perhaps more in the past 3 weeks. Her last drink was in the morning on the day of admission, she denies any history of seizures and reports withdrawal symptoms (tremor, nausea) relieved with more alcohol. She currently denies anxiety/agitation, tactile/visual/auditory hallucinations.

The patient was in breast clinic for evaluation of a painful breast mass which developed after biopsy of a lesion which was ultimately found to be benign. The patient noted the mass was growing in size and becoming more painful over the past month.

PMH:

  • EtOH abuse
  • Alcoholic hepatitis

PSH:

  • None

FH:

  • No family history of breast/gynecologic malignancy.
  • Mother with history of stroke. Father with diabetes.

SHx:

  • Lives alone.
  • Denies current or previous tobacco/drug use. Drinks 1 pint of whiskey daily for the past 15 years.
  • Not currently sexually active, no history of STI.

Meds:

  • None

Allergies:

NKDA

Physical Exam:

VS: T 98.9 HR 104 RR 19 BP 117/67 O2 99% RA
Gen: Well-appearing obese female in no acute distress
HEENT: PERRL, marked scleral icterus, sublingual icterus, MMM, no lesions
CV: Tachycardia, regular rhythm, normal S1/S2, no M/R/G
Lungs: CTAB, no crackles/wheezing
Abd: +BS, soft, non-distended, liver edge palpated 6cm below costal margin, irregular texture slightly tender to palpation, spleen not palpated, no fluid wave or shifting dullness, no rebound/guarding.
Ext: Warm, well-perfused, 2+ pulses (DP/PT), slight yellowing.
Skin: Vascular spiders on anterior chest, left breast with 5x5cm ecchymosis and tender underlying mass, no erythema, warmth, skin dimpling, nipple discharge.
Neuro: AAOx4, CN II-XII intact, no tremor noted, gait normal.

Labs/Studies:

1mo prior to admission:

  • AST/ALT/AP/TB: 444/77/234/2.5

Day 1:

  • AST/ALT/AP/TB: 185/61/184/18.1
  • PT/PTT/INR: 14.7/37.0/1.2

Day 4:

  • AST/ALT/AP/TB: 142/50/153/25.5
  • PT/PTT/INR: 20.1/38.9/1.7

Imaging:

Abdominal US

  1. Markedly echogenic and enlarged liver with a nodular surface of cirrhosis.
  2. Markedly blunted hepatic vein waveforms commonly seen due to decreased hepatic parenchymal compliance although other etiologies causes of obstruction to hepatic venous outflow.
  3. Splenomegaly.

Assessment/Plan:

44F hx EtOH abuse, alcoholic hepatitis, presenting with acute alcoholic hepatitis.
# Alcoholic hepatitis: Rapid onset of jaundice, tender hepatomegaly, and elevation of transaminases (AST > ALTx2) in the setting of chronic alcohol use suggestive of alcoholic hepatitis. Initial Maddrey discriminant hepatic function (mDH) score 37 suggestive of severe disease with high short-term mortality. Initiated trental 400mg p.o. t.i.d.
# EtOH withdrawal: Last drink <24h ago, monitor for signs of withdrawal, treat with Ativan per withdrawal protocol. # Cirrhosis: Newly diagnosed on abdominal ultrasound. Complicated by coagulopathy, and likely portal hypertension given splenomegaly/thrombocytopenia. Plan for outpatient screening EGD and continued GI follow-up. # Breast mass: Likely hematoma 2/2 biopsy associated given increased size associated with progression of coagulopathy/thrombocytopenia. Outpatient ultrasound and follow-up scheduled. # Anemia: Macrocytic, potentially related to vitamin deficiency vs. bone-marrow suppression associated with chronic alcohol use. Start thiamine/folate/multivitamin. # FEN/GI/PPx: Encourage p.o. intake (2g sodium restriction), continue ondansetron p.r.n. nausea/vomiting, obtain nutrition consult.

Hospital Course

Patient’s liver function continued to decline as evidenced by worsening coagulopathy and increased serum bilirubin. mDH had increased to 58 by day four of hospitalization and steroids were added.

Pathophysiology of Alcoholic Hepatitis: 1

Ethanol promotes translocation of bacterial components (lipopolysaccharide) across the intestinal wall, into the portal venous system and liver. These trigger a local and systemic inflammatory response which leads to hepatocellular injury and systemic effects such as fever, anorexia and weight loss.

Evaluation of Alcoholic Hepatitis: 1,2

Clinical features:

  • Rapid onset jaundice
  • Tender hepatomegaly
  • Fever
  • Ascites
  • Proximal muscle loss
  • Encephalopathy

Labs:

  • AST > ALT (x2), generally < 300IU/mL
  • Leukocytosis
  • ↑Total serum bilirubin
  • ↑INR
  • ↑Creatinine associated with poor prognosis

Other studies:

  • Screening for infection: PNA, UTI, SBP
  • Abdominal US to evaluate hepatic abscess, HCC, extrahepatic biliary obstruction

Management of Alcoholic Hepatitis: 1,2

Grading Severity:

  • Maddrey’s discriminant function
  • Glasgow score
  • Lille score (assess response to corticosteroids after 1wk)

Treatment:

  • Immediate and lifetime abstinence from alcohol
  • Trental 400mg p.o. t.i.d.
  • Prednisolone 40mg p.o. daily (controversial, some benefit in subgroup with Maddrey > 32)
  • Ascites: Sodium restriction, diuretics
  • Encephalopathy: Lactulose, rifaximin
  • Hepatorenal syndrome: albumin, vasopressors
  • Nutritional support

Interpretation of Liver Function Tests: 3

Disorder Bilirubin AST/ALT Albumin PT
Hemolysis
Gilbert
↑(indirect)
No bilirubinuria
Acute hepatocellular necrosis ↑ALT > AST
> 500IU

(poor prognosis if elevated)
Chronic liver disease

< 300IU

Alcoholic hepatitis

AST:ALT > 2

Intra- extra-hepatic cholestasis

< 500IU

↑↑

(>4x normal)

Features of Components of Liver Function Tests: 3,4

Features of Components of Liver Function Tests

References:

  1. Lucey, M. R., Mathurin, P., & Morgan, T. R. (2009). Alcoholic hepatitis. The New England journal of medicine, 360(26), 2758–2769. doi:10.1056/NEJMra0805786
  2. Sohail, U., & Satapathy, S. K. (2012). Diagnosis and management of alcoholic hepatitis. Clinics in liver disease, 16(4), 717–736. doi:10.1016/j.cld.2012.08.005
  3. Kaplan MM. Chapter 302. Evaluation of Liver Function. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012.
  4. Johnston, D. E. (1999). Special considerations in interpreting liver function tests. American family physician, 59(8), 2223–2230.

Elevated Hemidiaphragm

CXR - PA
CXR - Lateral

Causes of an Elevated Hemidiaphragm

Causes of an elevated hemidiaphragm

References:

  1. Lavender, JP, Potts DG (1959). Differential diagnosis of elevated right diaphragmatic dome. The British journal of radiology, 32(373), 56–60.
  2. Nason, L. K., Walker, C. M., McNeeley, M. F., Burivong, W., Fligner, C. L., & Godwin, J. D. (2012). Imaging of the diaphragm: anatomy and function. Radiographics : a review publication of the Radiological Society of North America, 32(2), E51–70. doi:10.1148/rg.322115127
  3. Prokesch, R. W., Schima, W., & Herold, C. J. (1999). Transient elevation of the hemidiaphragm. The British journal of radiology, 72(859), 723–724.
  4. Burgener, F., Kormano, M. & Pudas, T. (2008). Differential diagnosis in conventional radiology. Stuttgart New York: Thieme.

Hyperbilirubinemia

Gray's: Pancreas Anatomy

CC:

Yellow eyes

HPI:

51yo AA male with hx DM, HTN, sarcoidosis presents with yellowing of eyes and full-body itching x3wks. This was associated with dark urine and loose, light-brown stools. He denies N/V, abdominal pain, PO intolerance, F/C, recent travel, weight loss. He states that this has not occurred in the past, and he does not have any prior history of post-prandial abdominal pain.

PMH:

  • DM
  • HTN
  • Sarcoidosis

 PSH:

  • None

FH:

  • No GI malignancy

 SHx:

  • No tobacco or drug use, 10 years of 10 drinks/wk stopped 1yr ago

Meds:

  • lisinopril 20mg p.o. daily
  • pioglitazone 15mg p.o. daily
  • sitagliptin 100mg p.o. daily
  • lansoprazole 15mg p.o. daily

Allergies:

  • Vicodin (rash)

Physical Exam:

VS: T 97.9 HR 102 RR 12 BP 128/68 O2 99% RA
Gen: WA, NAD
HEENT: Marked scleral icterus, PERRL, yellowing of posterior oropharynx and floor of mouth, MMM, no cervical lymphadenopathy
CV: RRR, S1/S2 normal, no murmurs
Lungs: CTAB with good air movement
Abd: Obese, +BS, soft, NT/ND, no rebound/guarding, no palpable organomegaly, negative Murphy
GU: No inguinal lymphadenopathy
Ext: Warm, well-perfused, no LE edema, peripheral pulses 2+
Skin: No visible skin lesions
Neuro: AAOx3

Labs:

  • CBC: 16/12.4/35.1/281
  • LFT: AST 281, ALT 302, AP 264, T.bili 22.1, D.bili 16.8

Studies:

  • RUQ US: Biliary sludge, no stones, no GBW thickening, no pericholycystic fluid
  • ERCP: 3cm stricture of distal CBD, biopsies taken

Assessment/Plan:

51AAM w/DM, HTN, sarcoidosis with 3wks painless jaundice. Obstructive pattern along with only modest elevation of liver enzymes suggests the obstruction is likely extrahepatic which was supported by ERCP finding of a distal CBD stricture. Patient has no history of prior instrumentation to cause iatrogenic stricture, and while sarcoidosis is associated with cholestatic complications (portal granulomas), pathology from biopsy showed papillary adenocarcinoma. The patient was scheduled for surgery with a plan for initial laparoscopic survey of the abdomen followed by Whipple if no evidence of widespread disease.

Imaging:

ERCP

ERCP

3cm stricture of distal CBD

MRCP

MRCP

Filling defect in the common bile duct with marked dilatation of the common duct and intrahepatic ducts.
Findings may reflect an intraluminal mass or stone.

CT Abdomen/Pelvis

CT Abdomen/Pelvis

Common bile duct stent present
Expected air in the intrahepatic biliary tree and mild biliary ductal dilatation

Differential Diagnosis of Hyperbilirubinemia: 1, 2

A System for Hyperbilirubinemia

Evaluation of Hyperbilirubinemia: 3

Evaluation of Hyperbilirubinemia

References:

  1. Heathcote, E. J. (2007). Diagnosis and Management of Cholestatic Liver Disease. Clinical Gastroenterology and Hepatology, 5(7), 776–782. doi:10.1016/j.cgh.2007.05.008
  2. Hirschfield, G. M., Heathcote, E. J., & Gershwin, M. E. (2010). Pathogenesis of cholestatic liver disease and therapeutic approaches. Gastroenterology, 139(5), 1481–1496. doi:10.1053/j.gastro.2010.09.004
  3. McGill, J. M., & Kwiatkowski, A. P. (1998). Cholestatic liver diseases in adults. The American Journal of Gastroenterology, 93(5), 684–691. doi:10.1111/j.1572-0241.1998.206_a.x