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Table 1. Criteria for the diagnosis of diabetes insipidus in the post- growth hormone deficiency via provocative testing, in
operative period which case the measurement of a baseline insulin-like
growth factor-1 level can be helpful. If the patient is re-
(1) Increased plasma osmolality >300 mosm/kg
(2) Increased urine output >2.5 ml/kg/h for 2 consecutive hours ceiving growth hormone therapy, this should be stopped
(3) Urine osmolality <200 mosm/kg prior to surgery, as is recommended in any patient with
(4) Urine/plasma osmolality ratio <1 an acute critical illness [11].
Hypoadrenalism associated with suprasellar tumours
can be secondary or tertiary. This hypoadrenalism is po-
tentially lethal if not recognized and managed appropri-
sults in impaired water excretion despite a normal or in- ately. It has been reported pre-operatively in 50% of pa-
creased plasma volume. tients with pituitary and suprasellar tumours [1] and in
CSW is defined by the development of extracellular about 25–71% of patients with craniopharyngiomas on
volume depletion due to a renal sodium transport abnor- provocative testing (short synacthen or insulin toler-
mality in patients with intracranial disease and appropri- ance test) [4–10]. An appropriately raised early morn-
ate adrenal and thyroid status. ing cortisol (for instance >500 nmol/l in patients not
severely unwell [12]) makes the diagnosis unlikely. Hy-
pocortisolism may cause HN through an increase in
Pre-Operative Overview ADH levels and by impaired free water excretion [13].
Cortisol replacement should be initiated if patients are
In children, craniopharyngioma is the commonest tu- found to be cortisol deficient pre-operatively. Stress
mour involving the mentioned anatomic areas. Other tu- doses of corticosteroids should be used be prescribed to
mours are functioning and non-functioning pituitary cover neurosurgery in these patients as well as in pa-
adenomas, germinomas and non-germinomatous germ tients with a normal adrenal axis. If the patient is receiv-
cell tumours, Langerhans cell histiocytoses, chiasmatic ing treatment with dexamethasone for a neurosurgical
(low-grade) gliomas, suprasellar arachnoid cysts and hy- indication, no additional corticosteroid cover for sur-
pothalamic-pituitary astrocytomas [1]. These tumours gery is required, but postoperative cortisol replacement
present with acute or more insidious compression symp- should be initiated once dexamethasone is weaned and
toms of adjacent neural structures leading to a raised in- continued until there is a formal assessment of the hy-
tracranial pressure with hydrocephalus in 50%, visual pothalamic-pituitary-adrenal axis.
impairment in 38% and endocrine abnormalities in 66– CDI is found in 12% of patients with pituitary and su-
77% of cases [1, 2], with a higher incidence in craniopha- prasellar brain tumours at presentation [1]. In a recent
ryngiomas than in the other tumour types [2–5]. Al- review of children with craniopharyngiomas, 17–27%
though symptoms due to neuroendocrine dysfunction have been reported to have diabetes insipidus [14]. CDI
may not be obvious at presentation [6], clinical features is also the most frequent central nervous system manifes-
of endocrinopathies are frequently found on careful as- tation of Langerhans cell histiocytosis, occurring in 10–
sessment and have often been present for months or 50% of all patients [15, 16], while in intracranial germ cell
years prior to presentation. Establishing the endocrine tumours CDI occurs in 82% of cases [17]. Polyuria and
status of the patient before surgery is essential in manag- polydipsia are the presenting symptoms but may not be
ing peri-operative complications. obvious in mild forms of CDI. If CDI coexists with un-
Growth hormone deficiency is one of the commonest treated adrenal insufficiency, polyuria and polydipsia can
endocrine abnormalities, being present in 50% of chil- be masked due to the free water retention caused by the
dren with suprasellar and pituitary tumours at diagnosis adrenocortical failure. These symptoms may become ap-
[1]. This is higher in children with craniopharyngiomas parent on direct questioning, documentation of a 24-h
where an incidence of 72–95% can be found on provoca- fluid balance or following the initiation of a pharmaco-
tive testing [4–10]. Growth deceleration is one of the logical steroid treatment. In patients with CDI, a normal
commonest findings in children but is often recognized sense of thirst with free access to fluid intake will allow
only retrospectively, as presentation with growth failure normal plasma electrolytes and osmolality. If, however,
is less common [3]. As the need for urgent surgical inter- patients are unable to compensate for urinary losses, for
vention for raised intracranial pressure takes priority at example due to unconsciousness, vomiting or restricted
diagnosis, there is less opportunity to make a diagnosis of fluid access, they will develop increased plasma osmolal-
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Table 2. Pre-operative endocrine assessment and investigations Postoperative Overview
(1) Careful medical history, previous growth pattern and physical Surgery in the hypothalamic-pituitary area is often ac-
examination
(2) Current height, weight, surface area, pubertal staging and companied by disturbances of water, electrolytes and os-
bone age moregulation due to manipulation and vascular altera-
(3) Accurate fluid intake and output record tion of the neurohypophysis. Abnormalities in blood os-
(4) Paired early morning plasma and urine osmolalities molality can be life-threatening if they are not properly
(5) Serum urea, creatinine, electrolytes and glucose
recognized and treated. Fluid intake and output should
(6) Thyroid function (thyroxine and thyrotropin)
(7) Cortisol at 9 a.m. (if patient is not receiving steroids) be recorded very accurately and reviewed every 6–8 h.
(8) Prolactin (to exclude prolactinoma) Insertion of a urinary catheter may be necessary for an
(9) α-Fetoprotein and β-hCG (to exclude secreting germinoma) accurate output record. Extra fluid losses like stools, ce-
(10) Insulin-like growth factor-1 rebrospinal fluid or drain outputs should be accounted
for and replaced. Paired plasma and urine osmolality and
electrolytes should be tested immediately postoperatively
and every 8 h, but changes in plasma sodium of >5 mmol/l
ity (>300 mosm/l) with decreased urine osmolality and a will require more frequent testing (every 4 to 6 hours)
urine/plasma osmolality ratio <1. In the peri-operative [21].
period, formal water deprivation testing is not needed as CDI is a common postoperative complication that oc-
it may not provide any more information towards the di- curs in 83% of patients with intrasellar and parasellar tu-
agnosis of CDI in children with a known pituitary hypo- mours [2], especially in those with large tumours damag-
thalamic endocrine tumour. If time allows, a patient with ing the ADH-secreting neurons and radical surgical exci-
newly diagnosed pre-operative CDI should be treated and sion with pituitary stalk resection. Other factors found to
stabilized before surgery by the use of desmopressin (DP), be associated with an increased risk of developing post-
which is a synthetic analogue of ADH, otherwise fluid operative CDI are a young age, male gender, CSF leak,
losses should be appropriately replaced. and resection of certain types of lesions including cranio-
SIADH has occasionally been described before sur- pharyngiomas, Rathke’s cleft cysts and ACTH-secreting
gery, presenting with HN and seizures responding to flu- pituitary adenomas [22–24].
id restriction [18, 19]. The tumour mass might cause in- Over the last decade, the surgical approach towards
appropriate ADH release by direct mechanical stimula- craniopharyngiomas has been changing. Previously,
tion and/or ischaemic changes on the osmoreceptor/ gross resection of the tumour was the treatment of choice.
ADH-secreting neurons. In recent years, newer conservative surgical treatments
Secondary/tertiary hypothyroidism has been de- like endoscopic transsphenoidal surgery and cyst decom-
scribed in 2.7–42% of patients with craniopharyngio- pression with or without intracystic treatment have been
mas pre-operatively [4–6, 8–10]. Central hypothyroid- introduced to reduce morbidities. This has led to less
ism presents with an inappropriately low thyrotropin postoperative endocrine complications like permanent
level in a setting of low thyroxine or free thyroxine lev- CDI, now seen in 50–55% of patients after conservative
els. It should be treated with thyroxine replacement be- surgery combined with radiation surgery [14], as com-
fore surgery. In moderate to severe hypothyroidism, pared to 60–90% of patients with aggressive surgery.
HN can occur due to reduced cardiac output which can The course of postoperative CDI can be transient, per-
lead to the release of ADH via the carotid sinus barore- manent or triphasic. The triphasic pattern (fig. 1) occurs
ceptors and decreased glomerular filtration with re- in 3.4% of patients who undergo transsphenoid surgery,
duced free water excretion [20]. In naïve patients with and only the first 2 phases occur in 1.1% of patients [22].
both thyrotropin and adrenocorticotropin deficiencies, In the triphasic pattern, the initial phase of CDI is fol-
hydrocortisone replacement should precede the re- lowed by a second oliguric phase of SIADH and then by
placement of thyroxine as the latter increases the meta- a third and final phase of permanent CDI [25, 26].
bolic clearance of glucocorticoids and may lead to adre- Transient CDI becomes evident within 24–48 h of
nal crisis if the initiation of thyroxine precedes that of surgery (fig. 1a). The hypotonic polyuria lasts for 5–7
hydrocortisone. days. This initial phase of the triphasic pattern and tran-
Whenever possible, pre-operative endocrine assess- sient CDI are both thought to be caused by a temporary
ment and investigations (table 2) should be performed. dysfunction of ADH-producing neurons either second-
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Capillary
Cell body
ary to oedema due to trauma to the connections between The third phase of permanent CDI, in which polyuria
the magnocellular cell bodies and the nerve terminals in reappears within 2 weeks, follows depletion of ADH due
the posterior pituitary or to axonal shock from perturba- to the degeneration of hypothalamic ADH-secreting neu-
tions in the vascular supply to the pituitary stalk and pos- ronal cell bodies (fig. 1c). A major determinant of wheth-
terior pituitary. Transient CDI usually resolves when er CDI following transection of the pituitary stalk is per-
ADH-secreting neurons recover their normal function manent or not is related to how close the level of the lesion
[26]. is to the ADH-secreting neurons’ cell bodies in the hypo-
The second phase of SIADH is caused by an uncon- thalamus [28].
trolled release of ADH from either degenerating posterior Figure 2 illustrates the changes in the urine output and
pituitary tissue or from the remaining magnocellular plasma sodium concentrations with the main therapeutic
neurons whose axons have been damaged (fig. 1b). In this interventions during the first 14 postoperative days in a
phase, urine output decreases and urine becomes concen- 10-year-old child with craniopharyngioma who devel-
trated. The duration and severity of this phase is variable oped the triphasic response.
and may last from 2 to 14 days [26]. Severe and long-last- In addition, the patients may develop CSW, which can
ing HN due to SIADH can be a predictor for a future oc- develop as a primary (neuronal insult) or as a secondary
currence of permanent CDI, as both conditions are due response to SIADH. In CSW, there is a defect in the renal
to damage to the ADH-secreting neuronal cell bodies in sodium transport which leads to extracellular volume de-
the hypothalamus. pletion and HN.
Partial or limited damage to some axons connected to Thirst abnormalities, such as adipsia or hypodipsia
the posterior pituitary may be associated with isolated due to osmoreceptor damage, can lead to hypernatraemia
second phase SIADH due to the uncontrolled release of and wide fluctuations in osmolality complicating the
accumulated ADH resulting in transient asymptomatic management of the water and electrolyte balance, as they
or symptomatic HN [27]. usually coexist with CDI and ACTH deficiency.
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7 150
Fig. 2. Triphasic response. This represents the daily urine output In the initial phase of transient diabetes insipidus, DP was used
(measured as ml/kg/h) and the plasma sodium concentration in on an ‘as-required basis’ to reduce the urine output. In the second
the first 14 postoperative days in a 10year-old child with cranio- phase of the SIADH, fluid access was restricted. When the third
pharyngioma who developed a triphasic response. The main ther- phase with permanent diabetes insipidus developed, DP was re-
apeutic interventions are represented at the bottom of the graph. started and given on a regular basis.
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Table 3. Clinical and biochemical differences between SIADH and Depending on the severity and clinical symptoms of HN,
CSW isotonic or hypertonic fluids are given to correct volume
depletion. Sodium can be supplemented by the oral route.
SIADH CSW
CSW may need an aggressive replacement of fluids in the
Body weight increased same or decreased paediatric intensive care unit, with central venous pres-
Plasma volume high low sure monitoring. A strict fluid regime of ‘millilitre for
Evidence of volume no yes millilitre’ replacement should be avoided as a vicious cy-
depletion
Central venous
cle of replacing fluids might result in polyuria. Although
pressure same or increased decreased water and salt supplementation is the primary therapy,
Plasma sodium low low mineralocorticoid administration (fludrocortisone) has
Urine sodium high high been used for the treatment of CSW at doses of 0.025–1
Net sodium loss normal high mg/day [43, 45, 46]. The commonest adverse effects of
Urine output usually low very high
Plasma osmolality low low
fludrocortisone are hypokalaemia, which was observed in
Urine osmolality high high 73% of patients [43, 47], and hypertension [46, 47].
Urine/plasma Once the underlying cause of CSW is corrected, CSW
osmolality ratio >1 >1 is usually a transient condition that resolves within 3–4
Plasma urea low normal/high weeks. Occasionally, it can be long-standing and can last
Serum uric acid low normal
Haematocrit low normal/high for months [48–50]. If the duration of CSW is prolonged,
Plasma renin suppressed normal/high/suppressed conditions such as CNS infection, CSF obstruction and
Plasma aldosterone normal/high suppressed tumour progression should be carefully checked for. If
Plasma ADH high suppressed these conditions are present, they can sustain CSW.
Plasma NP high high
Coexisting CDI and CSW
In patients where CDI and CSW coexist, sodium loss
due to CSW in itself contributes to the polyuria. This poly-
CSW and SIADH both present with similar laboratory uria should not be considered as a sign of poorly con-
findings in acute clinical circumstances: low serum osmo- trolled CDI [50]. Higher DP doses should be avoided as
lality and inappropriately high urine osmolality. There is this increases renal free water reabsorption and aggravates
significant natriuresis (urinary sodium losses >40 mmol/l) HN. Treatment consists of sodium and fluid replacement,
in both conditions. While the urinary sodium excretion titrated against losses, and cautious continuation of DP,
[urinary sodium concentration (mmol/l) × urinary vol- with close monitoring of plasma electrolytes and osmolal-
ume (l/24 h)] is substantially higher than the sodium in- ity. Central venous pressure monitoring may be needed to
take in the CSW syndrome, it generally equals the sodium guide fluid replacement in deteriorating patients.
intake in SIADH. Therefore, the net sodium balance (in-
take minus output) is negative in CSW with polyuria, Hypothalamic ADI
while in SIADH there is a euvolemic or mild extracellular This is a rare, but challenging condition characterised
fluid expansion. The clinical history of polyuria or oliguria by hypotonic polyuria due to ADH deficiency and failure
and clinical signs of hypovolaemia, such as hypotension, to generate the sensation of thirst in response to hyperna-
tachycardia and poor skin turgor, are useful in differenti- traemia and increased plasma osmolality [51]. The sites
ating the 2 conditions [43, 44]. Sometimes, in milder cas- of lesion are the osmoreceptor cells in the circumventric-
es of hypovolaemia and euvolaemia, it is challenging to ular organ of the anterior hypothalamus. Patients with
distinguish CSW from SIADH. Table 3 summarizes the this condition fail to drink fluids due to the lacking thirst
main clinical and biochemical differences between the 2 mechanism, resulting in dehydration with hypernatrae-
conditions. In an intensive care setting, where patients re- mia. They are also at risk of HN if they have coexisting
ceive different types of intravenous fluids, calculating the CDI and excessive fluid is given while they are on DP.
net sodium and water balance as well as the fractional ex- Both hypernatraemia and HN result in similar clinical
cretion of the sodium/free water clearance can be helpful symptoms such as lethargy, weakness, irritability, nausea,
in understanding water and electrolyte imbalances. vomiting, seizures, coma and even death. The manage-
Early appropriate fluid therapy and salt supplementa- ment of the fluid balance in patients with hypothalamic
tion should be initiated to prevent further complications. ADI is therefore very challenging.
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References
1 Taylor M, Coute-Silva A, Adan L, Trivin C, cases with long-term follow-up. Clin Endo- and magnetic resonance imaging in the long-
Sainte-Rose C, Zerah M, Valteau-Couanet D, crinol (Oxf) 2005;62:397–409. term follow-up of childhood Langerhans cell
Doz F, Chalumeau M, Brauner R: Hypotha- 8 Banna M, Hoare RD, Stanley P, Till K: Cra- histiocytosis. J Clin Endocrinol Metab 1998;
lamic-pituitary lesions in pediatric patients: niopharyngioma in children. J Pediatr 1973; 83:3089–3094.
endocrine symptoms often precede neuro- 83:781–785. 17 Jorsal T, Rørth M: Intracranial germ cell tu-
ophthalmic presenting symptoms. J Pediatr 9 Sklar CA: Craniopharyngioma: endocrine ab- mours: a review with special reference to endo-
2012;161:855–863. normalities at presentation. Pediatr Neuro- crine manifestations. Acta Oncol 2012;51:3–9.
2 Matarazzo P, Genitori L, Lala R, Andreo M, surg 1994;21(suppl 1):18–20. 18 Gonzales-Portillo G, Tomita T: The syn-
Grossetti R, de Sanctis C: Endocrine function 10 Paja M, Lucas T, Gracia-Uria J, Salame F, Bar- drome of inappropriate secretion of antidi-
and water metabolism in children and adoles- cela B, Estrada J: Hypothalamic-pituitary dys- uretic hormone: an unusual presentation for
cents with surgically treated intra/parasellar function in patients with craniopharyngioma. childhood craniopharyngioma: report of
tumours. J Pediatr Endocrinol Metab 2004; Clin Endocrinol (Oxf) 1995;42:467–473. three cases. Neurosurgery 1998;42:917–921.
17:1487–1495. 11 Teng Chung T, Hinds CJ: Treatment with GH 19 Lederbogen S, Windeck R, Rauhut F, Benker
3 Larijani B, Bastanhagh MH, Pajouhi M, and IGF-1 in critical illness. Crit Care Clin G: Syndrome of inappropriate ADH secretion
Kargar Shadab F, Vasigh A, Aghakhani S: 2006;22:29–40. in hypophyseal tumours (in German). Med
Presentation and outcome of 93 cases of cra- 12 Van Aken MO, Lamberts SW: Diagnosis and Klin (Munich) 1988;83:307–308.
niopharyngioma. Eur J Cancer 2004; 13: 11– treatment of hypopituitarism: an update. Pi- 20 Hanna FWF, Scanlon MF: Hyponatraemia,
15. tuitary 2005;8:183–191. hypothyroidism, and role of arginine vaso-
4 DeVile CJ, Grant DB, Hayward RD, Stanhope 13 Reynolds RM, Seckl JR: Hyponatraemia for pressin. Lancet 1997;350:755–756.
R: Growth and endocrine sequelae of cranio- the clinical endocrinologist. Clin Endocrinol 21 Spoudeas HA (ed): Paediatric Endocrine Tu-
pharyngioma. Arch Dis Child 1996; 75: 108– (Oxf) 2005;63:366–374. mours. A Multidisciplinary Consensus State-
114. 14 Cohen M, Guger S, Hamilton J: Long term se- ment of Best Practice from a Working Group
5 Halac I, Zimmerman D: Endocrine manifes- quelae of paediatric craniopharyngioma – lit- Convened under the Auspices of the British
tations of craniopharyngioma. Childs Nerv erature review and 20 years of experience. Society for Paediatric Endocrinology and Di-
Syst 2005;21:640–648. Front Endocrinol 2011;2:81. abetes (BSPED) and the United Kingdom
6 De Vries L, Lazar L, Philip M: Craniopharyn- 15 Grois N, Potschger U, Prosch H, Minkov M, Children’s Cancer Study Group (UKCCSG).
gioma: presentation and endocrine sequelae Arico M, Braier J, Henter JI, Janka-Schaub G, Crawley, Novo Nordisk Ltd, 2005, pp 16–46.
in 36 children. J Pediatr Endocrinol Metab Ladisch S, Ritter J, Steiner M, Unger E, Gad- 22 Hensen J, Henig A, Fahlbusch R, Meyer M,
2003;16:703–710. ner H: Risk factors for diabetes insipidus in Boehnert M, Buchfelder M: Prevalence, predic-
7 Karavitaki N, Brufani C, Warner JT, Adams Langerhans cell histiocytosis. Pediatr Blood tors and patterns of postoperative polyuria and
CB, Richards P, Ansorge O, Shine B, Turner Cancer 2006;46:228–233. hyponatraemia in the immediate course after
HE, Wass JA: Craniopharyngiomas in chil- 16 Maghnie M, Bossi G, Klersy C, Cosi G, Geno- transsphenoidal surgery for pituitary adeno-
dren and adults: systematic analysis of 121 vese E, Arico M: Dynamic endocrine testing mas. Clin Endocrinol (Oxf) 1999;50:431–439.
61.129.42.15 - 5/5/2015 4:56:35 AM
DOI: 10.1159/000370065
Downloaded by:
23 Nemergut EC, Zuo Z, Jane JA: Predictors of 34 Baylis PH: The syndrome of inappropriate 47 Mori T, Katayama Y, Kawamata T, Hirayama
diabetes insipidus after transsphenoidal sur- antidiuretic hormone secretion. Int J Bio- T: Improved efficiency of hypervolemic ther-
gery: a review of 881 patients. Neurosurgery chem Cell Biol 2003;35:1495–1499. apy with inhibition of natriuresis by fludro-
2005;103:448–454. 35 Olson BR, Rubino D, Gumowski J, Oldfield cortisone in patients with aneurysmal sub-
24 Pratheesh R, Swallow DM, Rajaratnam S, Ja- EH: Isolated HN after transsphenoidal pitu- arachnoid haemorrhage. J Neurosurg 1999;
cob KS, Chacko G, Joseph M, Chacko AG: In- itary surgery. J Clin Endocrinol Metab 1995; 91:947–952.
cidence, predictors and early post-operative 80:85–91. 48 Jimenez R, Casado-Flores J, Nieto M, Garcia-
course of diabetes insipidus in paediatric cra- 36 Sherlock M, O’Sullivan E, Agha A, Behan LA, Teresa MA: Cerebral salt wasting syndrome
niopharygioma: a comparison with adults. Owens D, Finucane F, Rawluk D, Tormey W, in children with acute central nervous syn-
Childs Nerv Syst 2013;29:941–949 Thompson CJ: Incidence and pathophysiol- drome injury. Pediatr Neurol 2000; 35: 261–
25 Hoorn EJ, Ziestse R: Water balance disorders ogy of severe HN in neurosurgical patients. 263.
after neurosurgery: the triphasic response re- Postgrad Med J 2009;85:171–175. 49 Oruckaptan HH, Ozisik P, Akalan N: Pro-
visited. Nephrol Dial Transplant Plus 2010;3: 37 Liamis G, Milionis HJ, Elisaf M: Endocrine longed cerebral salt wasting syndrome associ-
42–44. disorders: causes of hyponatremia not to ne- ated with the intraventricular dissemination
26 Loh JA, Verbalis JG: Diabetes insipidus as a glect. Ann Med 2010;43:1–9. of brain tumours. Pediatr Neurol 2000; 33:
complication after pituitary surgery. Nat Rev 38 Albanese A, Hindmarsh P, Stanhope R: Man- 16–20.
Endocrinol 2007;3:489–494. agement of hyponatraemia in patients with 50 Lara D, Joyanes B, Llaneza A, Perez O, Llor-
27 Ultmann MC, Hoffman GE, Nelson PB, Rob- acute cerebral insults. Arch Dis Child 2001; ente B, Runkle I: Prolonged coexistent central
inson AG: Transient HN after damage to the 85:246–251. diabetes insipidus and cerebral salt wasting
neurohypophyseal tracts. Neuroendocrinol- 39 Yeates KE, Singer M, Morton AR: Salt and syndrome following neurosurgery. Open J
ogy 1992;56:803–811. water: a simple approach to hyponatremia. Pediatr 2013;3:74–77.
28 Lipsett MB, Maclean JP, West CD, Li MC, Can Med Assoc J 2004;170:365–369. 51 Ball SG, Vaidja B, Baylis PH: Hypothalamic
Pearson OH: An analysis of the polyuria in- 40 Vaidya C, Ho W, Freda BJ: Management of adipsic syndrome: diagnosis and manage-
duced by hypophysectomy in man. J Clin En- hyponatremia: providing treatment and ment. Clin Endocrinol (Oxf) 1997; 47: 405–
docrinol Metab 1956;16:183–195. avoiding harm. Cleve Clin J Med 2010; 77: 409.
29 Imran S, Eva G, Christopher S, Flynn E, 715–726. 52 Smith D, Finucane F, Phillips J, Baylis PH,
Henner D: Is specific gravity a good estimate 41 Maghnie M, Genovese E, Lundin S, Bonetti F, Finucane J, Tormey W, Thompson CJ: Ab-
of urine osmolality? Clin Lab Anal 2010; 24: Arico M: Iatrogenic extrapontine myelinoly- normal regulation of thirst and vasopressin
426–430. sis in central diabetes insipidus: are cyclospo- secretion following surgery for craniopha-
30 Lehrnbecher T, Muller-Scholden J, Danhaus- rine and 1-desamino-8-D arginine vasopres- ryngioma. Clin Endocrinol (Oxf) 2004; 61:
er-Leistner I, Sorensen N, von Stockhausen sin harmful in association? J Clin Endocrinol 273–279.
HB: Perioperative fluid and electrolyte man- Metab 1997;82:1749–1751. 53 Smith D, McKenna K, Moore K, Tormey W,
agement in children undergoing surgery for 42 Segura S, Balaguer M, Cambra FJ, Zambudio Finucane J, Philips J, Baylis P, Thompson CJ:
craniopharyngioma. A 10-year experience in S, Martin JM, Palomeque A: Fluid and elec- Baroregulation of vasopressin release in adip-
a single institution. Childs Nerv Syst 1998;14: trolyte disorders following surgery for brain sic diabetes insipidus. J Clin Endocrinol
276–279. tumours (in Spanish). An Pediatr (Barc) 2007; Metab 2002;87:4564–4568.
31 McDonald JA, Martha PM, Kerrigan J, Clarke 67:225–230. 54 Sinha A, Ball S, Jenkins A, Hale J, Cheetham
WL, Rogol AD, Blizzard RM: Treatment of 43 Momi J, Tang CM, Abcar AC, Kujubu DA, T: Objective assessment of thirst recovery in
the young child with postoperative central di- Sim JJ: Hyponatremia – what is cerebral salt patients with adipsic diabetes insipidus. Pitu-
abetes insipidus. Am J Dis Child 1989; 143: wasting? Perm J 2010;14:62–65. itary 2011;14:307–311.
201–204. 44 Yee AH, Burns JD, Wijdicks EFM: Cerebral 55 Crowley RK, Sherlock M, Agha A, Smith D,
32 Lugo N, Silver P, Nimkoff L, Caronia C, Sagy salt wasting: pathophysiology, diagnosis, and Thompson CJ: Clinical insights into adipsic
M: Diagnosis and management algorithm of treatment. Neurosurg Clin N Am 2010; 21: diabetes insipidus: a large case series. Clin En-
acute onset of central diabetes insipidus in 339–352. docrinol (Oxf) 2007;66:475–482.
critically ill children. J Pediatr Endocrinol 45 Kinik ST, Kandemir N, Baykan A, Akalan N: 56 Bergada I, Aversa L, Heinrich JJ: Peripheral
Metab 1997;10:633–639. Fludrocortisone treatment in a child with se- venous thrombosis in children and adoles-
33 Stoelting RK, Hillier SC: Pharmacology and vere cerebral salt wasting. Pediatr Neurosurg cents with adipsic hypernatremia secondary
Physiology in Anesthetic Practice, ed 4. Phila- 2001;35:216–219. to hypothalamic tumours. Horm Res 2004;61:
delphia, Lippincott Williams & Wilkins, 46 Taplin CE, Cowel CT, Silink M, Ambler GR: 108–110.
2006, p 471. Fludrocortisone therapy in cerebral salt wast-
ing. Pediatrics 2006;118:e1904–e1908.