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EDITORIAL DEBATE
Year : 2015  |  Volume : 63  |  Issue : 5  |  Page : 663-664

Craniopharyngiomas: Postoperative assessment of fluid and electrolyte disturbances


Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication6-Oct-2015

Correspondence Address:
Preeti Dabadghao
Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.166577

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How to cite this article:
Dabadghao P. Craniopharyngiomas: Postoperative assessment of fluid and electrolyte disturbances. Neurol India 2015;63:663-4

How to cite this URL:
Dabadghao P. Craniopharyngiomas: Postoperative assessment of fluid and electrolyte disturbances. Neurol India [serial online] 2015 [cited 2019 Oct 23];63:663-4. Available from: http://www.neurologyindia.com/text.asp?2015/63/5/663/166577


Craniopharyngiomas (CP) are the most common sellar or suprasellar tumors in childhood. One-third to three-fourths of CP patients have endocrinal dysfunction, with 17-27% of patients having diabetes insipidus (DI) at presentation.[1],[2] Polyuria and polydipsia are the presenting features but may not be obvious in milder forms of the disorder or may be masked by secondary hypocortisolism.

Surgery for CP involving the hypothalamic–pituitary area is often accompanied by abnormalities in fluids, electrolytes, and osmoregulation due to handling and/or vascular compromise of the neurohypophysis.[1] Conditions like central DI, syndrome of inappropriate antidiuretic hormone (SIADH) secretion, cerebral salt wasting (CSW), and adipsic diabetes can occur or coexist, making clinical management very challenging. With improving surgical technique and expertise, most pituitary surgeries are accomplished without complications, but careful monitoring of fluid intake and output, serum sodium, and osmolality is required for timely management. It is observed that patients with fluid and electrolyte imbalance have a longer hospital stay (median, 19 days) as compared with normonatremic patients (median, 12 days),[3] and also have a higher mortality.[4]

Central DI (CDI) is the most common postoperative complication in CP surgery.[5] The risk factors for the development of DI are younger age, male gender, cerebrospinal fluid leak, and extent of surgery.[6] CDI can be transient, permanent, or triphasic. In the triphasic type, initial CDI phase is followed after 3-5 days with an oliguric phase of SIADH and then followed 7-10 days later by the polyuric phase of permanent DI.[7] Transient DI is evident 24-48 hours after surgery and lasts for the initial 7 days. The initial phase of triphasic DI and transient DI is believed to be due to temporary dysfunction of neurons that produce ADH. The second oliguric SIADH phase is due to uncontrolled secretion of ADH from the damaged neurons or the degenerating posterior pituitary. The final phase of DI is because of ADH depletion due to degeneration of hypothalamic ADH-secreting neurons.

Some patients may develop CSW syndrome, where there is defect in renal conservation of sodium leading to extracellular volume depletion and hyponatremia. It is difficult to differentiate it from SIADH. Owing to the location of CP in the hypothalamic region, patients may develop thirst abnormalities, adipsia, or hypodipsia. Adipsic DI may lead to severe hypernatremia and wide fluctuations in serum osmolality, making management of fluid and electrolytes challenging.

The diagnosis of DI is made on the basis of polyuria (urine output >2.5 ml/kg/hour), plasma osmolality >300 mOsmol/kg, urine osmolality <200 mOsmol/kg, and hypernatremia.[8] Serum sodium should be monitored every 4-6 hours in the early postoperative period (48-72 hours), then 12-hourly for 7-10 days, and daily once the patient is allowed solid food. Strict record of intake–output has to be maintained to document polyuria and decide the fluid replacement. It is difficult to assess DI in the first 24 hours after surgery, as polyuria could be due to the fluid replacement in the intraoperative period. Desmopressin is used along with fluid replacement to decrease the need for infusing large volumes of fluid. “On demand” policy of using desmopressin is advocated, that is, the next dose of desmopressin is given after a breakthrough of the previous dose. This is a good strategy, especially in the first week after surgery, as it prevents water intoxication and hyponatremia if SIADH is developing as a second phase of the triphasic response. Desmopressin is continued if the DI is permanent.

Patients with CDI who have an intact thirst mechanism and a free access to fluids usually do not develop hypernatremia or hyperosmolality. Those who are unable to drink or are adipsic are encouraged to drink a certain amount of fluids to facilitate obligate fluid excretion. In addition, they are given desmopressin and fluid replacement to maintain serum osmolality and sodium within the normal range. This involves daily weighing, monitoring intake–output, and frequent serum sodium measurements. Management of these adipsic patients is extremely difficult, especially in our country in summer months when extrarenal losses are high. These patients can also be given low osmolar oral rehydration fluids to replace their fluid loss.

Fluctuations in serum sodium depend on the type of fluid infused for replacement. Leuenbecher et al., used normal saline as the sole postoperative fluid, which caused an erratic rise in serum sodium in the presence of DI.[9] Mukherjee et al. have reported, in a prospective data analysis of 15 patients, that patients who were infused 0.45% normal saline for replacement had lesser rise in serum sodium from the preoperative value.[10] The occurrence of hypernatremia was higher (100%) in patients who were given normal saline as replacement therapy. Hyponatremia, hyperglycemia, and seizures were seen more in patients who were infused 5% dextrose solution for replacement. They concluded that 0.45% normal saline is the fluid of choice in the postoperative period in craniopharyngioma patients who develop CDI.

In this issue, Pratheesh et al., have evaluated the efficacy of protocol-based management of DI in patients with CP in the postoperative period.[11] Half-normal saline was used as the replacement fluid, and it was shown that there were fewer fluctuations in serum sodium values; the incidence of hypo- or hypernatremia was also lower as compared with historical controls. The study clearly shows the benefits of strict monitoring of serum sodium and intake–output in the early postoperative period and the early use of desmopressin, whenever required. However, the rationale of giving 5% dextrose in patients who have severe DI (urine output >6 ml/kg/hour) is not clear. With this polyuria, the patients will have urinary sodium loss, so infusing 5% dextrose, sodium-free fluid for replacement will increase the chances of hyponatremia. The study has limitations as historical controls were taken. The number of patients in group 1 who had severe DI and were infused 5% dextrose for replacement, and the number of patients among those who developed hyponatremia, will be interesting to determine.

Despite the changing concepts of the extent of surgery (radical excision versus limited excision followed by radiotherapy)[12] in patients with a craniopharyngioma, fluid electrolyte abnormalities will be observed in a significant number of patients, more commonly in those who have had a radical excision, especially in the early postoperative period. There is lack of literature about the type of replacement fluid to be used. More studies involving larger number of patients with a predecided protocol of management are needed to address this issue. Simple measures of frequent monitoring of serum sodium osmolality as well as intake–output measurement can lead to a better management of fluid electrolyte abnormalities in craniopharyngioma patients in the pre- and postoperative period.

 
  References Top

1.
Müller HL. Craniopharyngioma. Endocr Rev 2014;35:513-43.  Back to cited text no. 1
    
2.
Cohen M, Guger S, Hamilton J. Long term sequelae of pediatric craniopharyngioma—literature review and 20 years experience. Front Endocrinol (Lausanne) 2011;2:81.  Back to cited text no. 2
    
3.
Sherlock M, O'Sullivan E, Agha A, Behan LA, Owens D, Finucane F, et al. Incidence and pathophysiology of severe hyponatraemia in neurosurgical patients. Postgrad Med J 2009;85:171-5.  Back to cited text no. 3
    
4.
Erfurth EM, Holmer H, Fjalldal SB. Mortality and morbidity in adult craniopharyngioma. Pituitary 2013;16:46-55.  Back to cited text no. 4
    
5.
Müller HL. Consequences of craniopharyngioma surgery in children. J Clin Endocrinol Metab 2011;96:1981-91.  Back to cited text no. 5
    
6.
Loh JA, Verbalis JG. Diabetes insipidus as a complication after pituitary surgery. Nat Clin Pract Endocrinol Metab 2007;3:489-94.  Back to cited text no. 6
    
7.
Jane JA Jr, Vance ML, Laws ER. Neurogenic diabetes insipidus. Pituitary 2006;9:327-9.  Back to cited text no. 7
    
8.
Edate S, Albanese A. Management of electrolyte and fluid disorders after brain surgery for pituitary/suprasellar tumours. Horm Res Paediatr 2015;83:293-301.  Back to cited text no. 8
    
9.
Lehrnbecher T, Müller-Scholden J, Danhanser-Leistner I, Sörensen N, von Stockhausen HB. Perioperative fluid and electrolyte management in children undergoing surgery for craniopharyngioma. Childs Nerv Syst 1998;14:276-9.  Back to cited text no. 9
    
10.
Mukherjee KK, Dutta P, Singh A, Gupta P, Srinivasan A, Bhagat H, et al. Choice of fluid therapy in patients of craniopharyngioma in the perioperative period: A hospital-based preliminary study. Surg Neurol Int 2014;5:105.  Back to cited text no. 10
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11.
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. 11
  Medknow Journal  
12.
Buchfelder M, Schlaffer SM, Lin F, Kleindienst A. Surgery for craniopharyngioma. Pituitary 2013;16:18-25.  Back to cited text no. 12
    




 

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