Title: Awakening Thirst: Unraveling a Case of Propofol-Induced Central Diabetes Insipidus Amidst Septic Turmoil

Author(s): Kwabena Owusu Ansah, MD; Aekta Gupta, MD; Kathleen Castillo, MD; Erdal Sarac, MD

Email: KOwusuAnsah@mercy.com

Background: Diabetes insipidus (DI) presents a significant challenge in perioperative care, especially when associated with anesthetic agents. This case report explores a rare instance of transient central diabetes insipidus (CDI) following propofol anesthesia in a patient undergoing debridement for septic shock. Discussion encompasses a review of literature on the varying likelihoods of DI induction by different anesthetics, focusing on clinical presentation, management, and resolution of DI post-surgery.

Case Presentation: A 64-year-old female with a history of multiple comorbidities presented with left heel abscess and underwent surgical debridement. She was found to have hypernatremia (Na 150 mmol/L), which was corrected to 145 mmol/L with D5W pre-operatively. Despite initial treatment, sodium levels rose postoperatively to 148 mmol/L with a low urine osmolality (Urine Osmo 170), suggesting an impaired ability to concentrate urine, leading to suspicion of DI. Diagnostic confirmation came with a desmopressin challenge that resulted in a substantial increase in urine osmolality, indicating an initially inadequate endogenous production or release of vasopressin. Her hypernatremia resolved after a few doses of desmopressin, indicating that the DI was likely transient and related to the stress of surgery and general anesthesia with propofol.

Discussion: This case highlights the complex interplay between anesthetics and DI. Dexmedetomidine has been identified in the literature as the anesthetic most frequently linked to DI, with propofol being less commonly implicated. Yet, the presented case emphasizes that propofol can also trigger transient CDI. The potential mechanisms include propofol’s action on the hypothalamus inhibiting arginine vasopressin release. Such a response necessitates careful monitoring of fluid balance and electrolytes in the perioperative setting, especially in patients with extensive comorbidities.

Management and Outcomes: Prompt recognition of the signs of DI, coupled with the appropriate use of desmopressin, can effectively reverse the effects of transient CDI induced by anesthesia. In this case, the timely administration of desmopressin following propofol anesthesia led to the resolution of the patient’s hypernatremia, without any long-term sequelae.

Conclusion: Anesthesiologists must be aware of the potential for propofol and other anesthetics to induce transient DI, especially in patients undergoing surgery for septic shock, who may already have an impaired homeostatic response to fluid and electrolyte management. This case underscores the importance of preoperative assessment of the patient’s risk factors for DI and the need for close postoperative monitoring of fluid and electrolyte balance. It also suggests that despite the less frequent association with DI, propofol should be used with caution, keeping in mind the potential for inducing central DI. The use of desmopressin in cases of suspected DI can be a lifesaving measure, ensuring the swift resolution of the condition and the prevention of further complications.