Case presentation

A 78-year-old male patient presented to the hospital due to pathological findings on a computed tomography (CT) scan performed on an outpatient basis. The imaging findings revealed a space-occupying lesion measuring 4.4 cm in the right lower lobe, with metastatic sites in the liver. His past medical history was unremarkable. Physical examination revealed a palpable liver and diminished breath sounds in the right lower lobe during auscultation. Vital signs showed a blood pressure of 135/86 mmHg and a pulse rate of 68 bpm. The patient underwent a liver biopsy, which confirmed lung adenocarcinoma. During his hospitalization, the patient exhibited elevated levels of direct bilirubin (7.85 mg/dL) and underwent magnetic resonance imaging (MRI) and magnetic resonance cholangiopancreatography (MRCP). MRI and MRCP revealed a metastatic mass in segment IV of the liver, with a diameter of 9.6 cm, causing compressive phenomena on the biliary tree at the confluence of the hepatic ducts with the common hepatic duct, resulting in dilation of the intrahepatic bile ducts (Figures 1-2). The patient underwent percutaneous transhepatic biliary drainage, and bilirubin levels progressively improved. Subsequently, the patient was discharged with instructions for oncological follow-up and management.

Figure 1: Axial contrast-enhanced T1-weighted MRI image demonstrating a large metastatic lesion in hepatic segment IV (red arrow).MRI: magnetic resonance imaging

Figure 2: MRCP demonstrating marked dilatation of the right (blue arrow) and left (green arrow) intrahepatic bile ducts secondary to extrinsic compression at the hepatic duct confluence (red arrow), consistent with malignant hilar biliary obstruction.MRCP: magnetic resonance cholangiopancreatography

After 10 days, the patient presented to the Emergency Department due to general weakness and severe fatigue accompanied by nausea and two episodes of vomiting. On initial examination, vital signs showed a blood pressure of 100/67 mmHg, a pulse rate of 83 bpm, oxygen saturation of 97% (at room air), and a body temperature of 36°C. Physical examination revealed jaundice, a palpable liver with hepatomegaly, poor skin turgor, delayed capillary refill, dry mucous membranes, orthostatic hypotension, and decreased jugular venous pressure. The patient appeared clinically hypovolemic, with no peripheral edema, ascites, or other evidence of third spacing. Laboratory tests revealed hyponatremia (Na: 118 mmol/L) and acute kidney injury (Table 1). The patient did not exhibit any clinical features suggestive of hyponatremic encephalopathy. Additionally, there was no history of diarrhea or diuretic use that could account for the patient's hyponatremia or volume depletion.

Blood Tests | Normal Values | Initial Visit | Second Visit | Discharge
Urea (mg/dL) | 17-43 | 27 | 148 | 17
Creatinine (mg/dL) | 0.66-1.44 | 0.71 | 1.29 | 0.58
K (mmol/L) | 3.5-5.1 | 4.5 | 5.0 | 3.3
Na (mmol/L) | 136-146 | 139 | 118 | 136
Cl (mmol/L) | 101-109 | 103 | 81 | 96
Ca (mg/dL) | 8.6-10.6 | 9.1 | 8.5 | 8.8
Glucose (mg/dL) | 70-99 | 68 | 78 | 93
Total bilirubin (mg/dL) | 0.3-1.2 | 0.65 | 3.80 | 2.10
Direct bilirubin (mg/dL) | <0.2 | 0.15 | 2.10 | 0.97
Aspartate aminotransferase (U/L) | <50 | 83 | 46 | 26
Alanine aminotransferase (U/L) | <50 | 113 | 61 | 18
γ-glutamyl transferase (U/L) | <55 | 372 | 507 | 400
Alkaline phosphatase (U/L) | 30-120 | 393 | 336 | 315
Urine Na (mmol/L) | - | - | 8 | -
Urine creatinine (mg/dL) | - | - | 69 | -
Triglycerides (mg/dL) | <150 | - | 311 | -
Total protein (g/dL) | 6.6-8.3 | - | 5.4 | 5.2
Albumin (g/dL) | 3.5-5.2 | - | 2.4 | 2.7
T3 (ng/mL) | 0.28-1.63 | - | 0.34 | -
T4 (μg/dL) | 5.85-14.16 | - | 8.23 | -
TSH (μIU/mL) | 0.38-5.33 | - | 2.79 | -
White blood cells (K/μL) | 4-11 | 10.72 | 26.38 | 24.20
Neutrophils (K/μL) | 2.5-7.5 | 8.90 | 25.46 | 22.68
Hematocrit (%) | 42-54 | 36.8 | 33.4 | 28.7
Platelets (K/μL) | 150-400 | 459 | 262 | 353
Prothrombin time (sec) | 10-15 | 12.6 | 11.7 | 15.5
INR | 0.85-1.2 | 1.13 | 1.57 | 1.44

The patient was admitted to the Internal Medicine Unit. The acute kidney injury (urea: 148 mg/dL and creatinine: 1.29 mg/dL), with a fractional excretion of sodium (FENa) of 0.1%, was attributed to prerenal causes. Moreover, pseudohyponatremia was excluded based on the normal glucose value and by obtaining a lipid profile and serum protein panel, both of which were within normal limits. His serum osmolality was 265 mOsm/kg, which classified the hyponatremia as hypotonic. Subsequently, because of a low urine sodium concentration (spot urine sodium: 8 mmol/L), hyponatremia was attributed to extrarenal causes. The sodium concentration in bile was 133 mEq/L, and percutaneous drainage of the biliary vessels yielded an average of 680 mL per day. Excluding other causes, percutaneous transhepatic biliary drainage was considered the cause of hyponatremia. The patient received crystalloids, and the next morning, sodium levels were 123 mmol/L. Over the subsequent two days, sodium levels reached 133 mmol/L. Serum sodium was corrected gradually to avoid osmotic demyelination syndrome. Sodium and urea levels were fully restored, and the patient was discharged with a sodium level of 136 mmol/L and a urea level of 17 mg/dL.