Poster Presentation ESA-SRB-ANZBMS 2024 in conjunction with ENSA

Propofol-induced transient arginine vasopressin deficiency (#614)

Huyen Nguyen 1 , Michael D Luppino 2 , Matilda Smale 3 , Rebecca Madigan 4 , Morton G Burt 1 , Mahesh M Umapathysivam 1
  1. Southern Adelaide Diabetes and Endocrine Services , Adelaide
  2. Flinders University, Adelaide
  3. Southern Adelaide Local Health Network, Adelaide
  4. Department of Anaesthetics, Flinders Medical Centre, Adelaide

66b60a080a2f4-Figure+1.jpgCase

A 26-year-old female underwent endoscopic resection of a sinonasal alveolar rhabdomyosarcoma. Anaesthesia was initiated with propofol, remifentanil and rocuronium, and maintained with propofol and sevoflurane. Shortly after induction, the patient developed increased urine output >550 mL/hr, accompanied by rising serum sodium, osmolality and lactate which peaked at 5 hours after induction (Figure 1). The urine was dilute at 160 mosmol/kg. Five hours post-induction, the copeptin level was 0.8 pmol/L with a serum osmolality of 310 mosmol/kg and serum sodium of 154 mmol/L, consistent with AVP-deficiency (AVP-D). 

Five hours and thirty-five minutes post-induction, one microgram of subcutaneous desmopressin was administered, resulting in reduction of urine output (Figure 1). She required a second dose twenty-three hours later.

Twenty-five hours post-induction, at least partial recovery was demonstrated with a copeptin of 4.1 pmol/L, serum osmolality of 285 mosmol/kg and serum sodium 140-143 mmol/L.­ Urine output was monitored for the following seventy-two hours with no further polyuria.

 

Discussion

Anaesthesia-induced AVP dysfunction is rare, but potentially life-threatening. Within the literature, there are two reported case of propofol-induced AVP dysfunction. Kassebaum et al. present a case demonstrating normalisation of urine output, plasma osmolality and plasma sodium following administration of desmopressin(1), supporting an AVP-D driven aetiology. In the case of the patient exposed to both sevoflurane and propofol, switching the anaesthetic agent to propofol caused a dramatic increase in urine output, while switching to sevoflurane resulted in prompt reduction(2). A potential mechanism is offered by murine models, in which propofol inhibited the secretory capacity of supraoptic nuclei cells(3). Case reports of sevoflurane-induced AVP dysfunction have not responded to desmopressin(4,5), suggesting a nephrogenic cause, possibly secondary to a transient decrease in aquaporin-2(6). Given the reported rapid response to discontinuation of causative anaesthetic agents(2,7), it may be a viable management option to switch the anaesthetic agent and monitor.

  1. Kassebaum, N., Hairr, J., Goldsmith, W., Barwise, J., & Pandharipande, P. (2008). Diabetes insipidus associated with propofol anesthesia. J Clin Anesth, 20(6), 466-468. https://doi.org/10.1016/j.jclinane.2008.04.013
  2. Soo, J., Gray, J., & Manecke, G. (2014). Propofol and diabetes insipidus. J Clin Anesth, 26(8), 679-683. https://doi.org/10.1016/j.jclinane.2014.02.012
  3. Inoue, Y., Shibuya, I., Kabashima, N., Noguchi, J., Harayama, N., Ueta, Y., Sata, T., Shigematsu, A., & Yamashita, H. (1999). The mechanism of inhibitory actions of propofol on rat supraoptic neurons. Anesthesiology, 91(1), 167-178. https://doi.org/10.1097/00000542-199907000-00025
  4. Cabibel, R., Gerard, L., Maiter, D., Collin, V., & Hantson, P. (2019). Complete Nephrogenic Diabetes Insipidus After Prolonged Sevoflurane Sedation: A Case Report of 3 Cases. A A Pract, 12(5), 155-159. https://doi.org/10.1213/XAA.0000000000000871
  5. L'Heude, M., Poignant, S., Elaroussi, D., Espitalier, F., Ferrandiere, M., & Laffon, M. (2019). Nephrogenic diabetes insipidus associated with prolonged sedation with sevoflurane in the intensive care unit. Br J Anaesth, 122(5), e73-e75. https://doi.org/10.1016/j.bja.2019.02.009
  6. Morita, K., Otsuka, F., Ogura, T., Takeuchi, M., Mizobuchi, S., Yamauchi, T., Makino, H., & Hirakawa, M. (1999). Sevoflurane anaesthesia causes a transient decrease in aquaporin-2 and impairment of urine concentration. Br J Anaesth, 83(5), 734-739. https://doi.org/10.1093/bja/83.5.734
  7. Schirle, L. (2011). Polyuria with sevoflurane administration: a case report. AANA J, 79(1), 47-50. https://www.ncbi.nlm.nih.gov/pubmed/21473226