You are not logged in.

**dinoiii** · 06-29-2007, 06:31 PM

For the Love of Science & Medicine Part II: Another PH case

For those new to the forum, this is how this works. I present a real case we see in IM/endocrine clinic, but stop short of saying what I chose to do for the patient and/or how mangement went. Instead I am giving you guys about a week to take a crack at it. For now, it is for fun...in the future, I hope to offer free product, etc... to the person(s) that get it correct. Think about it. Do some research if you have to and come back answering the questions I list at the bottom.

Have some fun. You can too see what it is like to be a clinician.

This was a great case and I so wanted to share it with you. Feel free to ask questions.

___________________________________________

CASE

TB is a 32 yr old man with no significant past medical history presents with a four-day history of generalized fatigue and malaise. He noticed these symptoms one day when he was at work and it got to the point that his co-workers were telling him "he looked like death." His boss finally sent him home against his desires.

He does note a slight right upper quadrant pain and some Left-sided chest pain that does NOT radiate (namely down left arm) and provides him with no diaphoresis (drenching sweat episodes).

He also notes transient periods of dizziness with head ache and diplopia (double vision). He denies myalgias (muscle aches) and/or arthralgia (joint aches).

He notes no allergies, but does imply that he uses some dietary supplements. On further quesitoning, his supplement use includes a 2-year STRAIGHT concurrent use of methyldienelone + MOHN in doses of 60mg A PIECE and you're worried about 10 or 20 mg of Superdrol - GEESH! His dose didn't necessarily surprise me as I have seen people with up to 120 mg of M1T alone.

He denies fever, chills, nausea, vomitting, diarrhea, constipation, blurred vision, heamaturia (blood in urine), hematochezia (blood in stool), clay-colored stool or melena (dark stool).

On physical exam, he is noted to have icteric sclera (yellow whites of his eyes), minor tenderness to palpation to RUQ of abdomen, negative Murphy's sign (pain on expiration of RUQ with concurrent compression). The remainder of his physical exam is unremarkable.

Lab Tests reveal a CPK (creatine kinase) of 8 times the normal limit. Liver function tests were surprisingly normal! His indirect bilirubin was up a tad.
Fasting Lipid Panel and CBC (complete blood count) were both NORMAL.
_________________________________________

QUESTIONS

(1) What additional labs would you want to investigate and why?

(2) What is the differential diagnosis?

(3) How would you treat this man?

**dinoiii** · 06-29-2007, 06:33 PM

QUESTIONS

(1) What additional labs would you want to investigate and why?

- 200 was the labs “upper limit” of CPK – therefore, 1600 U/L was the number I was referencing above. It would still be imperative to get an isoenzyme panel. The isoenzyme panel revealed (BB- 0%, MB – 0%, MM – 100%, therefore “NORMAL” – denoting the CPK was likely musculoskeletal in nature). The one necessity would be to check if he was spilling myoglobin in the urine – so I had to get it sent out frozen. While his CPK was NOT as high as someone with the “prototyical” Rhabdomyolysis – it was necessity to check this status – especially considering the generalized fatigue + malaise. And renal falure has been noted in patients with CPKs as "low" as 5 times normal (we were at 8) which he obviously had surpassed. While waiting on the urine, a CXR would be done to consider his chest pain. This came back negative. It was followed with a Abdominal CT scan which too came back negative. Arteriography revealed multiple masses on BOTH the liver AND spleen (the largest liver mass 2 x 8 cm, the largest splenic mass to show was 0.8 x 1.2 cm). In the meantime, Ur Myoglobin came back at 54 ug / L (Normal = < 28)! A serum calcium level was later drawn, which proved to be low. NO evidence of clinical symptomatology (i.e. - Chvostek’s sign, etc...).

(2) What is the differential diagnosis?

The spilling of myoglobin put Rhabdomyolysis at the top of the list in the differential for the CPK level. Of course, it would have been difficult to distinguish between pretty intense exercise and the Rhabdo had there not been a urine myoglobin. Alternatively, he notes NO intramuscular injections or recent surgeries or seizures – making these items less likely in the differential – but again, it was the Ur myoglobin that cinched this diagnosis. An initial challenge because as it may be evident of pink to red urine, this is NOT always the case and WAS NOT here either.

But what about the multiple masses on arteriography studies?

This placed peliosis hepatis at the top of the differential. A wedged hepatic venography would later confirm the diagnosis.

[author's note: for description of peliosis hepatis, please see PCT: A Clinician's View Part II - Post-Cycle Supplements for elaboration under section entitled "neoplasms" - brief summary: blood-filled cysts seen with long term oral use of AAS]

(3) How would you treat this man?

Rhabdo:

A) Fluids: Crystalloid infusion was given to maintain a high urine output (> 3 - 4 mLs/hr).
B) Sodium Bicarbonate: We opted for urine alkalinization which has been proposed for the prevention of myoglobin nephrotoxicity, but its effectiveness has not been demonstrated conclusively. I sort of erred on the side of caution here. [author’s note: this is not protocol]
C) Continued monitoring for peripheral neuropathy – patient NEVER exhibited signs/symptoms.

Hypocalcemia (low calcium): This would essentially be watched clinically. It is not atypical of rhabdo cases and usually resolves spontaneously as the rhabdomyolytic condition is treated. As rhabdo resolved – sure enough…with it went the hypOcalcemia.

Liver / Splenic masses: Will have to monitor them over the course of a series of follow ups. Due to peliosis hepatis, it would be impossible to take any kind of aspirate (due to risk of hemorrhage) nor was it entirely necessary at this time. Because LFTs were normal, it would be hard to gauge when the next appropriate wedge venogram should be performed, but we did it at 4 months based on literature in diagnostics from the journal Radiology. Wedged venography performed at that time revealed morphologic improvement. Complete clinical resolution of RUQ and LUQ pain was also seen at 4 months. We would likely repeat at 8 months in follow-up series. Continued stability of LFTs would be imperative. The 8 month follow-up is February. Will keep you posted.