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EDITORIAL DEBATE
Year : 2015  |  Volume : 63  |  Issue : 5  |  Page : 661-662

Management of diabetes insipidus in craniopharyngiomas


Brain and Spine Center, Fortis Hospitals Mumbai, Fortis Hospitals Ltd, Mumbai, Maharashtra, India

Date of Web Publication6-Oct-2015

Correspondence Address:
Deepu Banerji
Brain and Spine Center, Fortis Hospitals Mumbai, Fortis Hospitals Ltd, Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.166576

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How to cite this article:
Banerji D. Management of diabetes insipidus in craniopharyngiomas. Neurol India 2015;63:661-2

How to cite this URL:
Banerji D. Management of diabetes insipidus in craniopharyngiomas. Neurol India [serial online] 2015 [cited 2019 Aug 21];63:661-2. Available from: http://www.neurologyindia.com/text.asp?2015/63/5/661/166576


Central diabetes insipidus (DI) is known to occur preoperatively in 8-35%, and postoperatively in 70-90% of patients with a craniopharyngioma.[1] Usually evident in the first 24 hours after surgery, it may settle down in the next few days to weeks, or may become permanent in a small percentage of patients. The cause of DI in the perioperative period is the deficiency of arginine vasopressin (AVP; also known as antidiuretic hormone [ADH]) production. Extensive damage to magnocellular cells of the hypothalamus (supraoptic and paraventricular nuclei) leads to permanent DI, especially if the pituitary stalk section is in proximity to or directly involves the median eminence.[2] The classical triphasic response starts with a transient DI due to AVP deficiency, followed by the syndrome of inappropriate antidiuretic secretion (SIADH) due to the release of AVP from disintegrating magnocellular cells, finally leading to permanent DI over a few weeks.[3]

Management of DI in the perioperative period is very challenging. It can lead to a significant morbidity and mortality if it remains uncontrolled, especially in children. The management becomes even more difficult if the patient is in an altered sensorium or is adipsic owing to hypothalamic damage (the latter is a condition where the normal thirst mechanisms are absent). This is often compounded by the subsequent development of SIADH (hyponatremia with euvolemia/hypervolemia) or cerebral salt wasting (CSW) syndrome (hyponatremia with hypovolemia). Thus, it is important to have an intensive monitoring of fluid and electrolyte balance for 48-72 hours in the intensive care unit (ICU) setting.

DI is diagnosed when plasma osmolality is >300 mOsm/kg, with the corresponding urine osmolality <300 mOsm/kg, and is accompanied by polyuria (urine volume >4-5 ml/kg/hour for 2 hours consecutively [or 250 ml/hour × 2 hours]).[4] The urine specific gravity of <1.005 is another inexpensive bedside test for the diagnosis and evaluation of DI. Plasma sodium concentration of >145 mEq/L is an important parameter for an early intervention. In an ICU setting, it is important to monitor the urine output hourly and correct fluid balance by replacing fluids in proportionate amounts. Estimation of 8-10 hourly plasma sodium (Na) levels for the first 24-72 hours provides a proper estimation of the type of fluid replacement required and also indicates the need to administer injectable pitressin or nasal/oral deamino-8-d-arginine vasopressin (DDAVP). The type of fluid to be administered is not well defined in the available literature; however, the recent article by Pratheesh et al., provides a good protocol for deciding the type of fluid to be administered based on plasma sodium values and the urine output. They advocate an early use of 0.45% saline when polyuria is in the range of 4-6 ml/kg/hour and the plasma Na concentration is >145 mEq/L, and a switch to 5% dextrose solution if the urine output increases to >6 ml/kg/hour and the serum Na concentration becomes >150 mEq/L.[5] Once the patient is awake with the normal thirst mechanism intact, plain water is given orally or through the Ryle's tube to cover the fluid deficiency. It is important to keep monitoring the urine output and serum Na daily for at least a week, as SIADH or CSW syndrome may set in and may require a different management strategy. SIADH would need fluid restriction and oral salt replacement to avoid fluid overload. CSW syndrome would require fluid replacement with normal saline (to manage the presence of severe hypovolemia and dehydration) along with oral salt. An indirect indication of hypovolemia can be increased albumin, haematocrit or bicarbonate.[2] It is important to ascertain that central corticotrophin–cortisol and thyrotropin axes are intact and are normally functional.

The development of a triphasic or permanent DI has been correlated with prolonged surgery or an attempted gross total resection.[6] Although direct injury to the hypothalamic–pituitary axis is common, vascular injury is also an important etiopathological factor. The upper pituitary stalk and the hypothalamus are supplied by the superior hypophyseal artery, which gets attenuated and distorted by the tumor and is liable to be injured. Usually in craniopharyngiomas, it is displaced posterolaterally.

In the Indian subcontinent, where the majority of patient population is uneducated and lacks basic diagnostic and healthcare facilities, it may be difficult to monitor and manage DI, especially in extremes of weather. In this context, it is important to modify the surgical approach to the patient's socioeconomic profile and habitat, that is, opt for the therapeutic option of subtotal resection and irradiation. Also, in the patients in whom DI is manifested in the postoperative period, the patient or his immediate family members need to be properly counseled regarding the importance of fluid management and the monitoring for early signs of fluid and electrolyte imbalance. It is needless to emphasize that for an optimal outcome in an institutional setting, a comprehensive team comprising a neurosurgeon, an intensivist, an endocrinologist, and a pediatrician is mandatory for the optimum management of these patients.

 
  References Top

1.
Ghirardello S, Hopper N, Albanese A, Maghnie M. Diabetes insipidus in craniopharyngioma: Postoperative management of water and electrolyte disorders. J Pediatr Endocrinol Metab 2006;19 (Suppl 1):413-21.  Back to cited text no. 1
    
2.
Joseph M. Sodium–water disorders in a neuro ICU. In: Banerji D, Apoorva Pauranik A, editors. Progress in Clinical Neurosciences. Vol. 25. Delhi: Byword Books; 2011. p. 3-10.  Back to cited text no. 2
    
3.
Hollinshead WH. The interphase of diabetes insipidus. Mayo Clin Proc 1964;39:92-100.  Back to cited text no. 3
[PUBMED]    
4.
Di Iorgi N, Napoli F, Allegri AE, Olivieri I, Bertelli E, Gallizia A, et al. Diabetes insipidus—diagnosis and management. Horm Res Paediatr 2012;77:69-84.  Back to cited text no. 4
    
5.
Pratheesh R, Swallow DM, Joseph M, Natesan D, Rajaratnam S, Jacob KS, et al. Evaluation of a protocol-based treatment strategy for postoperative diabetes insipidus in craniopharyngioma. Neurol India 2015;63:712-7.  Back to cited text no. 5
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6.
Finken MJ, Zwaveling-Soonawala N, Walenkamp MJ, Vulsma T, van Trotsenburg AS, Rotteveel J. Frequent occurrence of the triphasic response (diabetes insipidus/hyponatremia/diabetes insipidus) after surgery for cranipharyngioma in childhood. Horm Res Paediatr 2011;76:22-6.  Back to cited text no. 6
    




 

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