A 60-year-old previously healthy man was admitted to the emergency department of Shohadaye Tajrish Hospital with a chief complaint of malaise and weakness. A month before his admission he had been treated for left lower extremity radicular pain with oral non-steroidal anti-inflammatory drugs (NSAIDs) and diazepam. The patient had sought medical attention at another center two weeks prior to admission in our ED, with a chief complaint of generalized weakness, fatigue, and anorexia. At the time, a previously unrecognized renal failure was diagnosed and the patient was discharged.
The patient was a mine worker without any history of smoking, alcohol consumption, illicit drug abuse, or unsafe sexual contact. He did not have any history of recent travel, blood transfusion, or animal contact. The patient’s father had been treated for pulmonary tuberculosis. There was no complaint of visual symptoms, cough, dyspnea, fever, night sweats, or bowel habit changes, but a gradual weight loss within the past two to three months was recorded.
During the physical examination he was ill, lethargic, and confused. Initial vital signs were as follows: Blood pressure 95/50 mmHg, heart rate 100 bpm, Respiratory Rate 16 bpm and his body temperature was 37°C. Examination of the head and neck revealed a bitemporal atrophy. His ENT (Ear, Nose, and Throat) exams were normal except for dry mucosa. Clear lung fields and a II/VI systolic murmur in the apex was detected on cardiopulmonary auscultation. The abdomen was soft with normal bowl sounds. No lymphadenopathy was detected throughout the body. The nails were free of clubbing, cyanosis and edema, with normal symmetric pulses. Reduced skin turgor was detected and rehydration therapy was initiated. Initial ECG examination showed sinus tachycardia with normal axis, segments and intervals. The chest X-ray (
Figure 1) showed a bilateral miliary pattern with few patchy consolidations, and a ground glass density in both of lower lobes, more evident in the right lung. The findings are presented in Table 1.
Figure 1. Chest X-Ray With Miliary Pattern
Table 1. Initial Laboratory Examinations
Laboratory Examinations Cell Blood Count WBC 8400 mm 3 (poly 65%, Lymph 30%, Mono 2%, Eos 2%) HB 13.8 g/dL, Hct 40.7%, MCV 80.6 fl, Plt 226000 mm 3 PT 15 s, PTT 25 s, INR 1.15 Biochemistry Analysis ALT 79, AST 58, ALKP 135, LDH 104, CKMB 6, CK 33 (U/L) Na 143 mEq/L, K 5 mEq/L, Ca 8.1 mg/dL Cr 2.2 mg/dL, BUN 87 mg/dL GLU 150 mg/dL ABG pH 7.40, PCO2 39.8 mm Hg, PO2 67.3 mm Hg, HCO3 24.4 mEq/dL, O2 sat 93.3% Urinalysis RBC 20-25, WBC 6-8, blood+ , SG 1016, acetone trace, pH 6, bacteria rare, yeast rare 24-Hour urine collection V 1800 cc, Creatinine 738 mg/L, protein 1008 mg/L, Immunologic: Anti HIV negative PPD negative ESR 40 mm/h, CEA 1.8 ng/mL, AFP 1.9 iu/mL, CA19-9: 18 u/mL, CA125: 10.4u/mL, total PSA 0.6 ng/mL, CRP+ Blood and urine cultures negative
a Abbreviations: ABG, Arterial Blood Gases; ALKP, Alkaline Phosphatase; ALT, Alanine Transaminase; BUN, Blood Urea Nitrogen; CK, Creatinine phosphokinase; CKMB, Creatinine phosphokinase MB component; GLU, Serum Glucose AST, Asparagine Transaminase; HB, Hemoglobin; Hct, Hematocrit; INR, International Normalization Ratio; LDH, Lactate Dehydrogenase; MCV, Mean Corpuscular Volume; PT, Prothrombin Time; PTT, Partial Thromboplastin Time; RBC, Red Blood Cell count; SG, Specific Gravity; WBC, White Blood Cell count.
Echocardiography was done to rule out congestive heart failure and showed moderate mitral regurgitation, moderate tricuspid regurgitation, pulmonary hypertension with a pulmonary artery pressure of 36 mmHg, septal hypertrophy and a left heart ejection fraction of 65−70%.
Whole body scan was performed with the suspicion of undiagnosed myeloma and metastatic foci with an unknown source. It revealed high diffuse activity in axial skeleton, which was suggestive of metabolic bone disease causing low back pain. Electrophoresis of serum proteins also showed normal results.
Based on the results of the urinalysis and the new onset of renal failure, an ultrasonography of the urinary tract was prescribed and the right and left kidney size was 130 and 129 mm respectively, with an increased parenchymal echo. Bilateral hydronephrosis with mild distention of proximal ureters was also detected. A 10-mm stone in the right middle calyx and an 8-mm stone in the left superior calyx detected. Daily BUN and creatinine was checked, which showed decreasing trends in both elements. On the 5th day of admission, the patient developed papular cutaneous lesions on his face and upper limbs, which gradually spread to the other parts of the body whichbecame umbilicated. After a dermatologist consult, skin biopsy was done, and IV acyclovir was administered with a presumptive diagnosis of Kaposi Varricelliform. On the 7th day of admission, the lesions on face and lumbar region became hemorrhagic and a new aphthus ulcer in the oral cavity was detected for which oral nistatin drops were administered.
Thoracic and abdomen pelvic CT−scans showed no pathologic findings. A few small calcified lymph nodes in the mediastinum with a diffuse nodular pattern in both lungs were detected. A blind broncoalveolar lavage (BAL) was carried out which drained a bloody specimen sent for serologic and pathologic evaluations. During the second week of admission, the patient had a limited episode of Upper GI bleeding without coagulopathy. UGI endoscopy showed pangasteroduodenitis and colonoscopy revealed colitis. Biopsy specimens were also obtained. On the 11th day of admission he developed a sudden loss of consciousness with neck rigidity. The patient withdrew from pain and manifested a rightward gaze. He was afebrile and no other focal neurologic deficits were detected. Brain CT scan without contrast revealed subarachnoid hemorrhage at the base of his skull. An attempt to perform lumbar puncture failed to retrieve CSF and repeated attempts were avoided due to the patient’s critical condition. Anti−Tuberculosis medication was added to antibiotics and antiviral treatment to cover viral hemorrhagic fever. He was intubated and mechanical ventilation was initiated.
Despite antibiotic, antiviral and anti−TB regimens the patient’s condition continued to deteriorate. The patients BUN and creatinine levels dropped to 38 mg/dL and 1.4 mg/dL respectively. On the other hand the patient had hypernatremia and hypokalemia that were treated accordingly. Gradual onset of metabolic acidosis was also demonstrated by repeated ABG analysis. Leukocytosis with a WBC of 11800 was detected on the 12th day of admission. One day later, apnea and cardiac arrest occurred and resuscitation was unsuccessful.
Results from skin biopsy, BAL, GI biopsy and post mortem lung and liver necropsy approved the presence of
Cryptococcus neoformans in smears and cultures.