الفهرس 
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Abstract
Fluid and electrolyte disturbances are commonly seen in children after acute central nervous system (CNS) injury. Cerebral salt wasting syndrome, inappropriate secretion of antidiuretic hormone and central diabetes insipidus are frequently observed disorders after acute CNS insults (Loh et al., 2000 - Ferry et al., 2001- Taplin el al., 2006).
This study aimed to assess water and sodium homeostasis in critically ill children who were subjected to acute central nervous system insults such as: CNS infections (Encephalitis- meningitis and brain abscess)- Hypoxic ischemic insults - Intracranial haemorrhage and Status epilepticus.The study included 31 critically ill children ranging from 1 month to 6 years old with mean age 1.69 ± 2.07 years who were subjected to acute central nervous system insults.Thirteen (41.9%) of the studied cases did not have any changes in their serum sodium levels after acute central nervous system insult, whereas 8 patients (25.8%) have become hyponatremic, 3 patients)9.7%(of them were diagnosed as cerebral salt wasting syndrome, while 5 patients (16.1%) were hyponatremic due to other causes mainly SIADH. Ten patients (32.3%) have become hypernatremic after acute central nervous systm insult, 6 of them (19.4%) were due to confirmed central diabetes insipidus, while the other 4 patients (12.9%) had unconfirmed central diabetes insipidusRegarding water balance disturbances, all our studied patients with acute central nervous system insult were found to be polyuric with urinary output > 3 cc/kg/hour (n=31, 100%).
The mean urinary sodium level was measured in the three studied groups at day 1 and day 5 after acuteCNS insult being highest in hyponatremic patients. This may be explained by the salt losing effects of cerebral salt wasting syndrome as well as sodium loss in SIADH. Negative sodium balance was found mainly in hyponatremic group especially in patients diagnosed as CSWS. This was explained by Taplin et al. (2006) who stated that the key feature of CSWS is negative sodium balance, giving rise to features of increased urine output and extracellular volume contraction. ADH also was measured in all patients at day 1 and day 5 after CNS insults, we found that mean serum ADH was high (above normal level) in the majority of patients in the three study groups.This is explained by Loh and Verbalis (2008)
who stated that the secretion of Antidiuretic Hormone (ADH) is stimulated by osmotic and nonosmotic factors, with changes in plasma osmolality serving as the primary stimulus for ADH release. In general, each 1 mmol/kg H2O increase in plasma osmolality causes an increase in plasma ADH levels from 0.4 picogram (pg)/mL to 0.8 pg/mL.Patients with confirmed CDI in our study were diagnosed at 2
nd
or 3
rd
day after CNS insult.They received Minirin (synthetic Arginine Vasopressin or Desmopressin-Acetate) astreatment and all of them responded by decreased urine output and hypernatremia. Patients with CSWS were diagnosed within the 3
day
rd
to 6
thfrom CNS insult. This was confirmed by Lin et al. (2009) who stated that the time from admission to the onset of cerebral salt wasting syndrome ranged from 2 to 20 days (mean, 6.7 ± 4.2 days). These patients were treated with hypertonic saline solutions which was sufficient in 2 of the 3 cases. In the 3
case, fludrocortisone was started but the course was not continued due to correction of hyponatremia eventually and for fear of more salt retention which may be caused by fludrocortisone. The rest of hyponatremic patients in our study were mostly due to SIADH (Syndrome of inappropriate secretion of ADH). the diagnosis of SIADH is based on the presence of a low serum level of sodium, and the absence of peripheral edema or dehydration with no evidence of adrenal, thyroid, or renal dysfunction (Palmer, 2003). The presence of signs of volume depletion (for example, hypotension, decreased skin turgor, or low central venous pressure) with salt wasting distinguishes CSW from SIADH (Harrigan, 2001). The mainstays of therapy for SIADH include water restriction and NaCl administration (Clark et al., 2008). We concluded that definite diagnosis of water and sodium disturbances is important for accurately distinguishing these disease entities from one another, since treatment strategies are different for each entity (Laredo et al., 2001).