CPC #2: Tuesday, October 22, 2002
Hurd Hall, The Johns Hopkins Hospital
12:00 Noon

Chief Complaint:
A 51- year-old man status-post liver transplant with cough and dark urine for one week.

History of Present Illness:
The patient is a 51-year-old African-American man, status-post orthotopic liver transplant in 1998 for hepatitis C that had progressed to end stage liver disease and portal hypertension. He presented in May 2001 to an outside hospital with a one-week history of cough productive of yellow sputum. He denied dyspnea, hemoptysis or chest pain. He also complained of "dark urine" for one week. He denied associated frequency, urgency, or dysuria. He reports low-grade fever (99.8 F) and chills intermittently throughout the week. At the outside hospital, he was diagnosed with Pseudomonas urinary tract infection and was treated with antibiotics (Ciprofloxacin/Zosyn). He was also found to have elevated liver enzymes, hyperbilirubinemia, and increased creatinine. After two days, he was transferred to The Johns Hopkins Hospital.

Review of Systems:
At the time of admission, he had a mild headache, but no visual disturbances. He denies sensory or motor disturbances. There is no abdominal pain, nausea, vomiting, change in bowel habits, bloody stools or change in weight. He denies musculoskeletal pain.

Past Medical History:
End stage liver disease with orthotopic liver transplant (07/98)
Diabetes mellitus.
Chronic hepatitis C infection
Sigmoid colonic polyps with histoplasmosis found on biopsy (08/00)
Nephrolithiasis.

Past Surgical History:
Orthotopic liver transplant (7/98)

Social History:
Single, no children; Lives with parents; Remote history of intravenous drug use and alcohol abuse (quit 1998); Remote history of tobacco use (quit 1999); no recent travel

Family History:
Mother and Father with diabetes mellitus; no history of CNS, cardiac, gastrointestinal, pulmonary or hematologic disease.

Physical Exam on admission:
Vital Signs:T= 38.0 C; BP= 110/75; HR= 105; R=18 (97% on RA)
General: in no apparent distress; well-developed man.
HEENT: sclera and oral mucosa are very icteric; pupils equal and reactive
Neck: supple; no lymphadenopathy; no bruit; no JVD
Cardiovascular: no murmurs, rubs or gallops
Respiratory: lungs are clear bilaterally
Abdomen: abdomen is soft and non-tender; no masses or organomegaly
Neurological: alert and oriented; sensory and motor grossly intact

Laboratory Values on admission:
Sodium 131 mEq/L, Potassium 3.4 mEq/L, Chloride 102 mEq/L, Bicarb 17 mEq/L, BUN 52 mg/dL, Creatinine 2.3 mg/dL, Glucose 377 mg/dL

WBC 5210 cells/mm3, Hgb 9.0 g/dL, Hct 26.1%, platelets 128,000/mm3
Total Bilirubin 16.3 mg/dL, AST 181 U/L, ALT 120 IU/L, Alk phos 207 IU/L

Chest X-ray: no infiltrates, no effusion

Urine: no WBC's, minimal bacteria

Hospital Course:
Hepatic biopsy at that time of admission showed mild to moderate acute rejection superimposed on chronic hepatitis C infection. He was treated with high dose corticosteroids for rejection. Approximately 14 days into his hospital course he developed acute on chronic renal failure and worsening portal hypertension with increasing ascites. Corticosteroids 30 mg/d were continued for presumed rejection. He became progressively coagulopathic and thrombocytopenic. He was started on Vancomycin after methicillin resistant Staphylococcus aureus grew from one of three blood cultures. Paracentesis did not reveal peritonitis. 21 days after admission he developed hypotension and tachycardia and he was transferred to the ICU. Blood cultures were repeatedly negative. Echocardiogram revealed a pericardial effusion requiring pericardiocentesis yielding a sterile exudate. Post-pericardiocentesis the blood pressure improved but he remained tachycardic. His condition continued to deteriorate as he developed cardiac dysrhymias, declining mental status, hypoxemia and pancytopenia. Repeat blood cultures were negative. Chest X-ray demonstrated bilateral upper lobe alveolar infiltrates, focal ill-defined alveolar infiltrates in the right lower lung, and atelectasis in the left lower lobe. Bronchoalveolar lavage revealed no pathogens. Zosyn, Ciprofloxacin, Vancomycin, and Fluconazole were administered empirically. Corticosteroids were being gradually tapered to 10 mg/d. Radiologic studies of the brain performed to evaluated altered mental status showed multiple non-enhancing acute infarctions (see Images 1-5 below). The patient developed multi-system organ failure and refractory hypotension expired one month after admission.

Image #1. Unenhanced CT brain: Focal area of low attenuation left basal ganglia appearing since last exam, no evidence of acute hemorrhage (additional areas of low attenuation seen in both cerebellar hemispheres - not shown). Atrophy.

Image #2. MRI brain, FLAIR sequence: Abnormal increased T2 signal left basal ganglia, left posterior limb internal capsule corresponding to CT abnormality. Additional foci are seen; for example, left occipital lobe in this image. Cerebellar lesions demonstrated corresponding to CT abnormality (not shown).

Image #3. MRI brain, FLAIR sequence: Additional lesion right fronto-parietal region.

Image #4. MRI brain, diffusion-weighted sequence: Increased signal compatible with acute infarct (confirmed by decreased signal as demonstrated by ADC maps, not shown).

Image #5. MRI brain, diffusion-weighted sequence: Additional lesion compatible with acute infarct.

Comment: pre-contrast T1 images demonstrate no evidence of acute hemorrhage, Gadolinium enhanced images demonstrate no evidence of suspicious enhancement, acute infarcts confirmed by ADC maps (not shown).

What is the most likely cause of death?

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