A 64-year-old Persian man presented with abdominal pain. He was confused and affected by hypersomnia and fatigue. The patient also had retrosternal chest pain, exertional dyspnea, nausea, vomiting, and constipation. He was previously diagnosed with right adrenocortical carcinoma and had undergone right adrenalectomy with regional lymph nodes resection 5 months previously; the histopathology revealed adrenal cortical carcinoma with a score of 6 based on Weiss criteria, and immunohistochemistry was positive for synaptophysin, inhibin, and CKAE1/AE3 (Additional file
1: Fig. S1, Additional file
2: Fig. S2, Additional file
3: Fig. S3). He had a history of hypertension, and amlodipine was his only hypertensive medication. For constipation he had received lactulose, and oxycodone was prescribed for pain relief. The patient was a heavy cigarette smoker and had been using opium for more than 20 years. At admission, the patient had a blood pressure of 120/76 mmHg and a heart rate of 107 bpm. His respiratory rate was 20 breaths per minute. A body temperature of 36.7 °C and SPO
2 of 93% were also recorded. On physical examination, the patient had abdominal distension and mild tenderness at the right upper quadrant. Pitting edema was detected bilaterally in the lower extremities. Other physical examinations were insignificant. Chest pain and dyspnea prompted echocardiography (ECG), which was unremarkable with estimated ejection fraction of 55% and no pericardial effusion. In addition to abdominal pain, nausea, and vomiting, the patient did not have defecation and gas passage for two consecutive days. To evaluate possible gastrointestinal obstruction, consultation with the surgery department and abdominopelvic x-ray were performed. Accordingly, the possibility of obstruction was ruled out. Abdominopelvic computed tomography (CT) revealed multiple and large lesions suggestive of liver metastases. In initial laboratory results, hyperkalemia (potassium 6 mg/dl), hyperuricemia (uric acid 16.4 mg/dl), hyperphosphatemia (phosphorus 6.9 mg/dl), and hypocalcemia (calcium 7.8 mg/dl), with elevated serum creatinine level (creatinine 3.8 mg/dl), were detected. White blood cell count of 26.58 × 10
9/L, C-reactive protein (CRP) of 45 mg/L, and alkaline phosphatase (ALP) of 1144 IU/L were indicative of an inflammatory process (Table
1). In urine analysis, significant amounts of blood and protein were found. Due to these electrolyte disturbances (hyperkalemia, hyperuricemia, and hyperphosphatemia), which fulfilled Cairo–Bishop criteria, tumor lysis syndrome was considered as an etiology of acute kidney injury for this patient, and since he had not ever received chemotherapy or radiotherapy, the patient was diagnosed as having spontaneous tumor lysis syndrome (TLS) and treated accordingly. Hydration with crystalloid intravenous fluids such as normal saline at a rate of 200 ml/hour was started as initial management to expand the intracellular volume and increase renal excretion of uric acid and other metabolites. A loop diuretic was used as add-on therapy to prevent volume overload and to wash out obstructing uric acid crystals. After ensuring a sufficient level of G6PD in the patient, rasburicase was administered to convert uric acid to more soluble and easily excreted compounds. Hyperkalemia, a life-threatening abnormality in TLS, was managed with sodium polystyrene sulfonate as a potassium-lowering agent. Insulin plus hypertonic glucose was also prescribed as a temporizing measure. In addition to massive hydration and hypouricemic agents, we considered restriction of dietary phosphate intake and administration of a phosphate binder such as sevelamer carbonate, to treat hyperphosphatemia. Blood and urine cultures were drawn, and piperacillin–tazobactam was administrated to treat possible sepsis. Due to volume overload signs (i.e., pulmonary congestion and peripheral edema), severe oliguria, and blunted consciousness during hospitalization, the patient underwent renal replacement therapy with hemodialysis on three consecutive days. Despite immediate and intensive care with hydration, treatment with a hypouricemic agent, and renal replacement therapy, the patient ultimately passed away from cardiopulmonary failure.
Table 1
Patient’s laboratory data during hospitalization
Na (mEq/l) | 136 | 139 | 133 | 132 | 131 | 132 | 137 | 137 |
K (mEq/l) | 6.0 | 5.3 | 3.7 | 3.2 | 3.1 | 4.5 | 5.1 | 6.0 |
BS (mg/dl) | 55 | 71 | - | - | 57 | - | 55 | 42 |
Urea (mg/dl) | 189 | 243 | 188 | 196 | 207 | 202 | 207 | 182 |
Cr (mg/dl) | 3.8 | 4.0 | 3.6 | 3.7 | 4.4 | 4.4 | 4.3 | 4.6 |
Ca (mg/dl) | 7.8 | 7.2 | 6.7 | 6.3 | 7.1 | 7.1 | 7.2 | 7.2 |
P (mg/dl) | 6.9 | 8.5 | 7.2 | 7.9 | 8.6 | 5.7 | 8.5 | – |
Mg (mg/dl) | 3.1 | 3.5 | 3.0 | 2.3 | 2.6 | 2.7 | 2.8 | 2.6 |
Uric acid (mg/dl) | 16.4– | 4.0 | 7.1 | 2.5 | 2.0 | 1.2 | – | 2.7 |
CPK (mg/dl) | – | 174 | – | – | – | – | 2.6 | – |
LDH (mg/dl) | – | 8223 | – | – | – | – | – | – |
WBC (count) | 26,580 | – | – | – | 23,500 | 25,960 | – | 20,800 |
Hb (%) | 9.8 | – | – | – | 10.7 | 9.7 | – | 10 |
Platelet (count) | 486,000 | – | – | – | 385,000 | 403,000 | – | 341,000 |
PT (seconds) | 15.3 | – | 17 | – | – | – | – | – |
PTT (seconds) | 32 | – | 37 | – | – | – | – | – |
INR | 1.17 | – | 1.3 | – | – | – | – | – |
AST (mg/dl) | 360 | – | – | – | – | – | – | – |
ALT (mg/dl) | 44 | – | – | – | – | – | – | – |
ALP (mg/dl) | 1144 | – | – | – | – | – | – | – |
Bilirubin total (mg/dl) | 0.8 | – | – | – | – | – | – | – |
CRP (mg/dl) | 45 | – | – | – | – | – | – | – |
Albumin (g/dl) | – | – | 2.6 | – | – | 2.1 | – | – |