Sir,
Postoperative diabetes insipidus is an uncommon presentation after liver transplantation and provides a new set of challenges for the intensivist. We present a case of idiopathic central diabetes insipidus in a 77-year-old male (weight 60 kg), diagnosed with hepatitis B-related chronic liver disease with hepatocellular carcinoma, who underwent living donor-related liver transplantation (LDLT). After a thorough preoperative workup (preoperative renal function tests were normal), the patient was taken up for transplantation, and the surgery was uneventful. Intraoperative urine output was 50 mL/h on an average, but increased to about 150–200 mL/h after reperfusion. The trachea was extubated on postoperative day (POD) 1 and the patient was haemodynamically stable. On POD 1, the urine output increased to around 500 mL/h. Fluid restriction was done and samples were sent for testing of serum electrolytes, urine specific gravity, urine and serum osmolality, and plasma antidiuretic hormone (ADH) levels. The serum electrolytes were in the normal range, urine specific gravity was 1.002, urine osmolality was 170 mOsm/kg, while the serum osmolality was 297 mOsm/kg. The investigation reports pointed towards diabetes insipidus, and on this basis, desmopressin nasal spray was started (2 sprays twice a day), and the fluid restriction was done. The nasal spray pump delivers doses of 0.1 mL (10 mcg) or multiples of 0.1 mL. Another issue that crept up was a decrease in the portal flows on Doppler ultrasound and increasing lactate levels, after about 6 h of fluid restriction. This was a major dilemma as low portal flows could affect the graft liver perfusion and function, and thus, it was decided to replace at least 50% of the urine output in addition to the maintenance fluids, and the portal flow and lactate levels were regularly monitored. On POD 1, the patient had a urine output of 8 mL/kg/h (total of approximately 11 L/day) on an average. A magnetic resonance imaging of the brain was also done to rule out any damage to the hypothalamus or pituitary, and no abnormality was detected. The frequency of desmopressin spray was increased (2 sprays thrice a day) and the urine output slightly decreased to 5 mL/kg/h (totalling around 7 L/day) on POD 2. On POD 2, the urine osmolality and urine specific gravity were again measured and found to be slightly increased from the previous day's levels. The increased urine output remained high till POD 4. On POD 5, the urine output decreased further to about 1–2 mL/kg/h, and desmopressin was discontinued. The urine specific gravity and urine osmolality levels were sent again sent for testing on POD 6, and this time they were in the normal range. The patient was shifted out of ICU on day 8 and was discharged on day 15. The diagnosis of central diabetes insipidus was confirmed by the report of low plasma ADH levels (0.8 pg/mL) (sent on POD 1) received on day 11. Throughout the ICU stay, the electrolyte levels, lactate levels, and portal flows were monitored twice a day. This was of utmost importance as the lactate levels and portal flows were indicative of the graft perfusion and also of the fluid status. Balancing the fluid status to manage adequate graft perfusion on one hand and fluid restriction to decrease the urine output on the other hand play an important role in the management of diabetes insipidus post liver transplant. Matsusaki et al. had reported a case of pituitary apoplexy causing diabetes insipidus in a post liver transplant patient, but in that case, the patient had a second laparotomy also, and diabetes insipidus was diagnosed on day 13.[1] Central diabetes insipidus is a rare presentation after LDLT, but can affect the mortality and morbidity significantly, and thus, it becomes imperative for anaesthesiologists and intensivists in the LDLT settings to consider this uncommon presentation.
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Conflicts of interest
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REFERENCE
- 1.Matsusaki T, Morimatsu H, Matsumi J, Matsuda H, Sato T, Sato K, et al. Pituitary apoplexy precipitating diabetes insipidus after living donor liver transplantation. J Anesth. 2011;25:108–11. doi: 10.1007/s00540-010-1070-7. [DOI] [PubMed] [Google Scholar]