期刊论文详细信息
BMC Research Notes
An unusual case of central diabetes insipidus & hyperglycemic hyperosmolar state following cardiorespiratory arrest
Abdul Jabbar1  Ali Asghar1  Suneel Kumar2  Muhammad Qamar Masood1 
[1] Department of Medicine, Section of Endocrinology, Aga Khan University Hospital, Stadium Road, P.O. Box 3500, Karachi 74800, Pakistan;Department of Medicine, Endocrinology, Sultan Qaboos University Hospital, Muscat, Oman
关键词: Arrest;    Cardiopulmonary;    State;    Hyperglycemic;    Hyperosmolar;    Insipidus;    Diabetes;    Central;   
Others  :  1141886
DOI  :  10.1186/1756-0500-6-325
 received in 2013-04-25, accepted in 2013-08-12,  发布年份 2013
PDF
【 摘 要 】

Background

We are describing an unusual case of severe hyperglycemia and hypernatremia, resistant to treatment.

Case presentation

A thirty year old female with adenocarcinoma of rectum was admitted with increasing lethargy, headache and drowsiness. She deteriorated rapidly and had cardiac arrest, following which she remained comatose. Her initial serum glucose and sodium were normal, but after receiving dexamethasone and mannitol, the serum glucose progressively increased to 54.7 mmol/L and sodium to 175 mmol/L, despite receiving very high dose of intravenous (IV) insulin infusion. She was evaluated for diabetes insipidus because of continued polyuria even after correction of hyperglycemia. Her serum osmolality was 337 mmol/kg, and urine osmolality was 141 mmol/kg which rose to 382 mmol/kg, after receiving 4 mcg of IV Desmopressin.

Conclusion

Our patient developed central diabetes insipidus post cardiac arrest and severe dehydration because of diabetes insipidus. Stress of critical illness, dehydration, dexamethasone and IV dextrose infusion were likely responsible for this degree of severe and resistant to treatment hyperglycemia.

【 授权许可】

   
2013 Masood et al.; licensee BioMed Central Ltd.

【 预 览 】
附件列表
Files Size Format View
20150327163537411.pdf 132KB PDF download
【 参考文献 】
  • [1]Rothschild M, Shenkman L: Diabetes insipidus following cardiorespiratory arrest. JAMA 1977, 238(7):620-621.
  • [2]Arisaka O, Arisaka M, Ikebe A, Niijima S, Shimura N, Hosaka A, Yabuta K: Central diabetes insipidus in hypoxic brain damage. Childs Nerv Syst 1992, 8(2):81-82.
  • [3]Beasley EW 3rd, Phillips LS: Polyuria and refractory hypernatremia after cardiopulmonary arrest. Am J Med 1987, 82(2):347-349.
  • [4]Udoshi MB, Trivedi AD, Desai RC, Lichtenstein E: Diabetes insipidus following cardiorespiratory arrest. J Natl Med Assoc 1981, 73(9):797-800.
  • [5]Sweeney AT, Blake MA, Adelman LS, Habeebulla S, Nachtigall LB, Duff JM, Tully GL 3rd: Pituitary apoplexy precipitating diabetes insipidus. Endocr Pract 2004, 10(2):135-138.
  • [6]Agha A, Thornton E, O’Kelly P, Tormey W, Phillips J, Thompson CJ: Posterior pituitary dysfunction after traumatic brain injury. J Clin Endocrinol Metab 2004, 89(12):5987-5992.
  • [7]Robalo R, Pedroso C, Agapito A, Borges A: Acute Sheehan’s syndrome presenting as central diabetes insipidus. BMJ Case Rep 2012.
  • [8]Atmaca H, Tanriverdi F, Gokce C, Unluhizarci K, Kelestimur F: Posterior pituitary function in Sheehan’s syndrome. Eur J Endocrinol 2007, 156(5):563-567.
  • [9]Kamboj MK, Zhou P, Molofsky WJ, Franklin B, Shah B, David R, Kohn B: Hemorrhagic pituitary apoplexy in an 18 year-old male presenting as non-ketotic hyperglycemic coma (NKHC). J Pediatr Endocrinol Metab 2005, 18(6):611-615.
  文献评价指标  
  下载次数:25次 浏览次数:36次