The big clue is the ALT > 150. While not highly sensitive, this is highly specific for gallstone pancreatitis. My 3rd year student found the reference to that clue. I had always thought that the alk phos was the most useful test in this situation – so I learned something.

Even without that clue, the symptoms made us highly suspicious of gallstone pancreatitis. This is the most common cause in the US. I believed his no alcohol history, and found no clues on labs that he was not telling the truth.

h/t to David whose first post he spot on.

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He had type II diabetes mellitus, hypertension, coronary artery disease (stent), and a known right kidney mass. His medication list included simvastatin, januvia, aspirin, cilostazol, famotidine, actos, lisinopril, plavix, lasix prn and metformin.

Social history was negative for alcohol, tobacco or illegal drugs.

He was afebrile, BP 139/64, heart rate 101, respirations 18. He had mild epigastric tenderness without guarding or rebound. His stool was heme negative and rectal exam showed no tenderness.

Complete blood count showed a slightly elevated WBC – 11. Liver tests:

His lipase was 1056.

RUQ ultrasound showed no stones on this admission as well as his previous admission. The radiologist did note some gallbladder wall thickening.

Consider the differential diagnosis of acute pancreatitis. How would you evaluate the patient further?

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Here are the labs and question again:

 Direct bilirubin – 5.8

Your job:

construct a differential diagnosis and make your best guess for the correct answer.  We do know the answer.

=========

I will write this answer at the 3rd year medical student level, with apologies to anyone who thinks I have become pedantic.  I do know that many students and residents read this blog and like these cases.

As you can see, I have constructed my grid for liver tests into 3 categories.  The first category represents cellular destruction.  This patient has markedly elevated AST and ALT, therefore, the patient has significant cellular destruction – or hepatitis.  I will discuss that differential soon.

The patient has minimal elevation of alk phos, but a high total bilirubin.  The minimal alk phos could represent obstruction, but my experience suggests that for obstruction to cause cellular destruction, I would see a much higher alk phos.  Most cellular destruction causes local swelling and thus some increase in alk phos.  I suspect the patient does have some intrahepatitic ductal obstruction with swelling, and thus the elevated bilirubin.  Elevated bilirubin occurs commonly with significant acute cellular destruction.

The normal albumin and INR make a diagnosis of cirrhosis unlikely.  Despite the cellular destruction, the liver’s factory functions are still intact.

What could cause such acute cellular destruction?  When I first heard this presentation at morning report I assumed viral hepatitis.  Medications could do this, but I knew that the patient was not taking any medications (even for his seizures.)  Hypotension could do this – shock liver – but the patient had not had any known hypotensive episodes.

So I assumed a viral etiology.  The most likely candidates would be A, B or C.  I have seen EBV and CMV present like this.

Our patient had positive IgM antibodies for hepatitis C, confirming the diagnosis of acute hepatitis C.

Congratulations to Grant for guessing the right answer.

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Here is a puzzle for you to consider.  One of my residents told me that I needed to post more clnical problems.

Patient is  28-year-old white male with new jaundice.  His only significant medical history is a 6-month history of grand mal seizures with a normal head CT.

He has noticed pale stools and dark urine for 3 days.  He complains of epigastric pain.

Social history – previous work as an EMT ambulance worker. Had significant blood exposure 6 months ago (saved the life of a woman who jumped out of window).

His exam was remarkable for jaundice and a slightly enlarged liver.

Lab tests:

Normal CBC, normal basic metabolic panel

 Direct bilirubin – 5.8

Your job:

construct a differential diagnosis and make your best guess for the correct answer.  We do know the answer.

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45 year old woman presents with RUQ pain, fatigue and loss of appetite

 Total protein 4.2

 GGT 308

 RUQ ultrasound showed gallbladder "sludge."

 Questions:

1. Likely diagnosis

As several readers surmised, these labs represent a classic presentation of alcoholic hepatitis.  The patient admitted to significant alcohol consumption. 

She also had classic deficiencies – K, Phos, and Mg.  She had low platelets (around 100k.)

She probably had both alcoholic hepatitis and cirrhosis.  The AST being greater than twice the ALT represents the classic picture of alcohol liver injury.  Generally, patients have AST <300 with alcoholic hepatitis.

The decreased albumin suggests major liver damage.

Patients with alcoholic hepatitis often complain of RUQ pain.

2. Treatment options

She had a very poor prognosis.  One way to determine that is Maddrey’s discriminant function. Her PT was about 18 with a control of 12. 

I would generally use prednisolone 40 mg for 30 days in such patients.  This patient did not receive prednisolone because the physicians caring for her were worried about infection.  The used pentoxifylline (Trental) which some articles have supported as a treatment option.  Unfortunately, after a couple of days she had a major cerebral hemorrhage and died.  The cause of the hemorrhage could have been the elevated PT from the alcoholic liver disease.  The pentoxifylline may have contributed, as it decreases platelet function.

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 Total protein 4.2

 GGT 308

 RUQ ultrasound showed gallbladder "sludge."

 Questions:

1. Likely diagnosis

2. Treatment options

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His liver tests show classic hepatocellular injury.  His normal alkaline phosphatase argues strongly against extrahepatic obstruction.  His normal albumin and INR argue against cirrhosis.

He could have any etiology of acute hepatocellular injury – toxins, shock or viral hepatitis.  The loss of taste for cigarettes is a classic finding in viral hepatitis.  He had acute hepatitis B.

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Provide a differential diagnosis and speculate on the most likely diagnosis.

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I must congratulate the 2 responders, obviously astute diagnosticians.  As they surmised, the liver tests did not support primary liver disease.  The albumin was low but not what we would expect with cirrhosis.  The other liver tests were remarkably normal.

We obtained an echocardiogram which showed severe pulmonary hypertension and pure right sided dilation and heart failure.  I will followup on the pulmonary consultation.  I suspect that the patient has obstructive sleep apnea, and possibly also COPD.

This patient represents a fascinating cognitive issue.  He presented with ascites and anasarca.  The SAAG was consistent with portal hypertension.  Assuming primary liver disease was the natural error.  This presentation requires further thought.  His lab values were not consistent with that clinical assumption, so we reconsidered our assumptions.  This reconsideration allowed us to hone in on the correct explanation.

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Later that evening he becomes hypoxic and is transferred to intensive care.  He is placed on a 50% rebreathing mask.

In reviewing his lab data we find:

His ABG the next morning on 50% O₂

When he was admitted he had a serum bicarbonate of 31.

He has cardiomegaly on chest xray.

Questions:

1. What liver diseases might he have – what is your best guess?

2. What other tests would you order?

3. Why is his pCO₂ so high?

I will provide some answers and a strong hypothesis.

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