|Year : 2006 | Volume
| Issue : 3 | Page : 10-15
Hyponatremia in acute neurological disorders - Is it always due to siadh ?
Indira Jayakumar1, S Ranjit1, C Balasubramaniam2
1 Departments of Pediatric Intensive Care Kanchi Kamakoti Childs Trust Hospital, Nungambakkam, Chennai, India
2 1Pediatric Neurosurgery, Kanchi Kamakoti Childs Trust Hospital, Nungambakkam, Chennai, India
New No. 14 Second Main Road, CIT Colony, Mylapore, Chennai - 600 004,
Source of Support: None, Conflict of Interest: None
Hyponatremia in acute CNS diseases is often attributed to the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH). Other causes may be in operation and may be overlooked. Aims: The objective of the study was to determine the etiology, evaluate treatment modalites and assess the outcome in children with an underlying acute neurologic disease who were hyponatremic. All these children were admitted to the Intensive Care Unit (ICU). Methods and Materials: This is descriptive hospital based retrospective chart review. Clinical indices of hydration, serum and urine sodium and osmolality were used in children to determine the cause of hyponatremia. In such of those who were hyponatremic, the cause of hyponatremia, treatment and outcome were assessed. Management of hyponatremia depended on etiology and severity of symptoms. Symptomatic patients had serum sodium raised by 3-5 mEq/l in order to control symptoms, following which a more gradual correction was carried out. Children with SIADH were fluid restricted while those with hyponatremic dehydration and Cerebral Salt Wasting (CSW) received supplemental saline and fluids. Results: Out of 1371 Pediatric Intensive Care Unit (PICU) admissions over a 30-month period, 385 (28%) had primary CNS disorders and of these, 58 were hyponatremic. The causes were SIADH in 19 (33%), hyponatremic dehydration in 16 (28%), drug-induced hyponatremia in 13 (22%) and CSW in 10 (17%) patients. About 10 of the 58 hyponatremic patients expired. All deaths were due to the severity of the underlying neurological condition. About 3 patients were hyponatremic at the time of death. Conclusion: The etiology of hyponatremia in acute CNS disease is multifactorial, and is not always due to SIADH. Careful evaluation and targeted therapy is required for the optimal management of these children
Keywords: cerebral salt wasting; hyponatremia, syndrome of inappropriate antidiuretic hormone secretion
|How to cite this article:|
Jayakumar I, Ranjit S, Balasubramaniam C. Hyponatremia in acute neurological disorders - Is it always due to siadh ?. J Pediatr Neurosci 2006;1, Suppl S1:10-5
Children presenting with neurological illness form a significant portion of admissions to the critical care unit. Hyponatremia may either be seen at admission or during the course of Intensive Care Unit (ICU) stay. An incidence as high as 25% has been reported in children with head trauma. Hyponatremia in the setting of CNS disease, especially when associated with hypo osmolality, is often attributed to the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH). However the etiology of hyponatremia may be multifactorial - ranging from simple hyponatremic dehydration to lesser-known clinical states like Cerebral Salt Wasting Syndrome. Management of hyponatremia poses a serious challenge. Errors in the diagnosis and management can precipitate the Osmolar Dysequilibrium Syndrome (ODS) and worsen the existing neurological condition.,,,
| » Methods and Materials|| |
This retrospective study was undertaken to
1. To determine the incidence and cause of hyponatremia in children presenting to the Pediatric Intensive Care Unit (PICU) with acute neurological illness.
2. To evaluate the management and outcome of hyponatremia in such children.
In this retrospective study, children aged 1 month to 18 years with an acute onset of neurological disorder admitted to the PICU of the Kanchi Kamakoti Childs Trust Hospital, a tertiary care referral teaching children's hospital, over a 30 month period from January 1997 to August 1999 were prospectively evaluated.
Children with significant neurological symptoms and signs including altered mental status (Glasgow Coma Score £ 10), seizure activity, focal neurological deficits or meningeal signs were identified as having a neurological disorder. Postoperative (craniotomy) neuro-surgical patients were also included.
The study group comprised of children with the above neurological disorders and a serum sodium level equal to or less than 125 mEq/l at the time of admission to the PICU or at any time during the PICU stay. Eunatremic patients with acute neurological disorders formed the control group. We took a cut off level of 125 mEq/l for significant hyponatremia, since most symptoms have been attributed to this level of hyponatremia.
Continuous monitoring of the heart rate, respiratory rate and oxygen saturation was carried out and the blood pressure was measured noninvasively every 15 min unless persistent circulatory compromise was present, in which case continuous invasive arterial blood pressure and central venous pressure monitoring was carried out. The neurological status was evaluated on an hourly basis by assessing the Glasgow Coma Score, pupillary reaction and power of the extremities.
Meticulous charting of the fluid status was carried out, with documentation of the total intake and output of fluid including assessment of insensible losses. Monitoring of the serum biochemical parameters (electrolytes, glucose, renal parameters) was carried out at least once a day or more frequently if the patient was receiving osmotic or loop diuretics or drugs such as vasopressin. Once a patient was detected to have hyponatremia, the serum sodium levels were repeated at least thrice a day if asymptomatic and every 2-4 h if symptomatic and/or receiving corrections with 3% saline. In addition, serum osmolality, urine sodium, osmolality and specific gravity were also measured.
Serum sodium was estimated by the ion-selective electrode method using an automated analyzer. Urinary sodium was estimated by flame photometry. Serum and urine osmolalities were measured by an osmometer that calculates osmolality by measuring change in the freezing point that occurs in a solution with increasing osmolality. The normal range for serum osmolality was considered to be 285-295 mOsm/kg while that for urine osmolality was 50-1400 m Osm/kg. Urine sodium less than 20 mEq/l was taken as low, 20-40 normal, 40-100 high.
Diagnosis of SIADH was made in the presence of hyponatremia, low plasma osmolality, absence of dehydration, normal or decreased urine output, high urine sodium and inappropriately high urine osmolality after having ruled out thyroid, adrenal, renal disease, heart failure and cirrhosis., Hyponatremic dehydration was diagnosed when a low plasma sodium level was accompanied by clinical features of dehydration, low urine sodium and high urine osmolality.
Cerebral Salt Wasting (CSW) was identified by hyponatremia accompanied by dehydration, polyuria, low plasma osmolality, high urinary sodium and normal to increased urine osmolality.,, ,,,,
In all cases, normal renal function was a prerequisite for diagnosis, although transient elevations of the serum urea levels with subsequent normalization was accepted in children with hyponatremic dehydration.
With respect to the underlying neurological disorder, patients were treated in a standard fashion including specific and supportive therapy, which included, where indicated, mechanical ventilation, appropriate antibiotics and measures to control raised intracranial pressure (ICP)., When raised ICP was suspected, 20% mannitol was administered at a dose of 0.25-0.5 g/dose thrice or four times a day provided the child was normally hydrated and hemodynamically stable with a serum osmolality < 320 mOsm/kg. Those patients in whom the ICP was deemed to be refractory received in addition, furosemide at doses of 0.5 mg/kg at 12th hourly intervals. Furosemide was also given as the single diuretic in children with a serum osmolality > 320 mOsm/kg in whom mannitol is contra-indicated.
Maintenance intravenous fluids were not restricted even if raised ICP or central nervous infections were present and intravenous fluids in these circumstances consisted of 5% glucose in normal saline with potassium chloride added at 10-40 mEq/l depending on the patient's serum potassium level. Enteral nutrition was initiated in all children on the second ICU day unless specifically contra-indicated. This was increased to full maintenance as tolerated over a period of 36-48 h. Following correction of hyponatremia, children with CSW receiving enteral nutrition had salt supplement added to the feeds as long as needed.
In the event of shock or hypoperfusion, patients received repeated boluses of normal saline until the circulating volume was restored. Shock persisting despite normovolemia documented by central venous pressure monitoring was an indication for vasoactive agents, the choice of which depended on the degree of hemodynamic instability and echocardiographic evaluation of myocardial function.
The optimal treatment of hypotonic hyponatremia requires balancing the risks of hypotonicity against those of therapy. The presence of symptoms and their severity largely determine the pace of correction.,
Slow correction of hyponatremia was carried out unless patients were symptomatic. Patients who had acute symptomatic hyponatremia were treated with 3% saline infusion in order to raise the serum sodium by 4-6 mEq/l over 1-2 h until symptoms of brain swelling abated. This was followed by intravenous normal saline in order to gradually restore eunatremia at a rate no greater than 10-12 mEq/l/day and minimize the risk of recurrence of hyponatremia.
Maintenance fluids were restricted in patients with SIADH and exogenous vasopressin-induced hyponatremia, while increased volume of maintenance fluids was administered to patients with hyponatremic dehydration, diuretic-induced hyponatremia and CSW.
All data were analyzed using Microsoft Excel 7.0 analysis tool pack version 97. Statistical analysis of significance was performed with chi-square analysis for qualitative variates when n > 30 and students t test for quantitative variables. A P value of less than 0.05 was considered statistically significant.
| » Results|| |
About 1371 children were admitted to the PICU in the study period and of these 385 (28%) were admitted primarily for management of neurological illnesses. Among patients with neurologic illness, 58 (15%) had significant hyponatremia during their PICU stay and 15 were hyponatremic at the time of admission.
The 58 hyponatremic children formed the study group and the remaining 327 patients with eunatremic CNS disorders formed the control group. About 49% of the children with neurologic disorders were below 3 years of age. In comparison, 60% of the hyponatremic group were below 3 years. Male/female ratio was 1.5 : 1 in hyponatremics as compared to 2.3 : 1 in all patients with CNS disorders.
In the 58 hyponatremic patients, the majority (55%) had CNS infections while those with neoplasms formed the next most frequent group [Table - 1].
The cause of hyponatremia in the study group is illustrated in [Figure - 1]. Hyponatremia was attributed to the Syndrome of Inappropriate Secretion Antidiuretic Hormone in 33% (19/58 cases), hyponatremic dehydration in 28% (16/58) drug-induced hyponatremia in 22% (13/58) and in 17% (10/58) CSW was responsible for hyponatremia.
Amongst patients with drug-induced hyponatremia, diuretics (osmotic and loop) were the agents responsible for hyponatremia in 11 patients (19%). Of all 385 patients with acute cerebral insults admitted to the PICU during the study period, 70 patients (18%) received diuretics amongst whom 11 children developed hyponatremia. Mannitol alone was administered in 50 patients, 15 received both mannitol and furosemide while five patients were given only furosemide.
Vasopressin excess was responsible for drug-induced hyponatremia in two additional patients. Eight children with tumours in the suprasellar region received vasopressin to treat Central Diabetes Insipidus (DI) following craniotomy. Evaluation of the endocrine status was carried out prior to surgery in all eight patients and, where required, appropriate replacement therapy had been initiated preoperatively. Two patients developed dilutional hyponatremia secondary to vasopressin excess and resultant fluid retention.
Hyponatremic dehydration due to loss of salt and water from various sites occurred in 16 children. In these patients, the source of loss was gastrointestinal in seven (diarrhea), cerebrospinal fluid loses through ventriculostomy in five, third space loss (meningitis with septic shock and plasma leakage due to capillary leak) in three and renal loss (from pre-existing renal tubulopathy) in one patient.
The mean of the lowest serum sodium values recorded in the eunatremic patients with CNS disorders and the hyponatremic group was 131 mEq/l (SD ± 3.8) and 122 mEq/l (SD ± 2.4), respectively ( P < 0.05).
Symptoms associated with hyponatremia are presented in [Table - 2]. About 55 (95%) of patients were symptomatic, reflecting the acute nature of the hyponatremia. A 43 of 58 patients with hyponatremia had seizures compared to 182 of 327 in the eunatremic group. Seizures were statistically more common in hyponatremic children ( P < 0.005). A 65% had two or more symptoms.
Management of hyponatremia depended on the presence and the cause of symptoms. A 55 symptomatic patients required hypertonic saline in order raise the serum sodium by 4-6 mEq/l to relieve acute symptoms, following which eunatremia was attained in a controlled fashion as described earlier. The 19 children with SIADH were initially managed by fluid restriction (2/3 maintenance) and 18 of these required 3% saline supplements in view of persistent hyponatremia. Serum sodium remained in the hyponatremic range between 121 and 124 mEq/l in two patients with extensive infarcts following acinetobacter meningitis, both of whom died.
Of the 11 children who had diuretic-induced hyponatremia, decreasing or temporarily withholding the dose of the offending agent and administering supplemental fluids achieved eunatremia. In both children with vasopressin-induced hyponatremia, withholding vasopressin and fluid restriction resulted in improvement.
Of the eight postoperative patients with supra-sellar tumours, the tri-phasic response was seen in seven patients. Anticipation of swings in sodium and water balance along with carefully titrated fluid management prevented hyponatremia in five patients. Although one of the five patients had concomitant CSW, the lowest serum sodium was 126 mEq/l, and hence did not qualify for inclusion in the study. Two patients developed symptomatic hyponatremia during the phase of permanent DI, where the dose of vasopressin that was initially appropriate, needed to be revised downwards.
Boluses of normal saline to treat hypoperfusion were administered in 4 of 16 patients with hyponatremic dehydration and hypotension and 3 of 10 patients with CSW. Three patients with hyponatremia secondary to SIADH with underlying CNS infection had fluid refractory shock requiring inotropes (dopamine in two and adrenaline in one). None of the patients with CSW required vasoactive agents, their circulatory status having been normalized with saline boluses followed by one and a half to twice the required amount of maintenance fluids in order to prevent recurrence of hyponatremia and dehydration. Three children with CSW received fludrocortisone in addition to saline administration, in view of persistent or recurrent hyponatremia in two patients and significant neurological symptoms in one child (unresponsive coma) with an extensive sub-arachnoid hemorrhage. The last child expired although the serum sodium had improved from 115 to 124 mEq/l over 28 h of PICU stay.
The osmotic disequilibrium syndrome of central pontine myelinolysis did not occur in any patient. With respect to the outcome, 10 of 58 children (15%) expired. Three children were hyponatremic at the time of death, (SIADH in two and CSW in one) although none of the deaths was attributable to hyponatremia. Of the 10 children who died, seven had a CNS infection as the primary pathology. The cause of death was a rapidly progressive transtentorial herniation; in five children (viral encephalitis in three and pneumococcal meningitis in two) and extensive infarcts in two children (with acinetobacter meningitis). Death occurred due to discontinuation of life-support at parents request in view of poor prognosis for recovery in two patients. One child died following rapid progression to deep unrousable coma secondary to extensive sub-arachnoid bleed. The cause of death in the three hyponatremic patients were related to extensive infarcts in two patients with meningitis, both of who had SIADH. The third hyponatremic patient with CSW died with features of progressive brain death due to aneurysmal sub-arachnoid bleed. The death was not attributed to either hyponatremia or rate of correction in any patient as the serum sodium, although still in the hyponatremic range, had risen in all three cases at a rate of 7-11 mEq/l/24 h. Furthermore, the underlying CNS pathology was not compatible with survival.
| » Discussion|| |
Hyponatremia may be the cause or effect of neurological dysfunction in children and in our study, was caused most often by SIADH followed by hyponatremic dehydration, diuretics and CSW. Establishing the cause of hyponatremia is the key to successful management as treatment may be diametrically opposite in certain situations viz the need for fluid restriction in SIADH and fluid resuscitation in CSW and hyponatremic dehydration.
Hyponatremia is the commonest metabolic disorder in neurologically impaired children admitted to the PICU. Although hyponatremia is defined as serum sodium of 135 mEq/l we took a cut off limit of 125 mEq/l for our study since symptoms have been attributed to levels at or below this value. In our study, hyponatremia was seen in 15% of children with CNS disorders. SIADH was the commonest cause of hyponatremia occurring in a third of the patients followed by hyponatremic dehydration and drug-induced hyponatremia (diuretics and vasopressin). The CSW was seen in ten patients (17%).
The cause of hyponatremia in the setting of neurological disease is often attributed to SIADH. The characteristic features of SIADH are hyponatremia and hypo-osmolar serum with clinical euvolumia, failure of the urine to be appropriately dilute in the presence of hyponatremia, and absence of other hyponatremia producing disease states such as adrenal insufficiency, hypothyrodism or renal disease. However many cases thought to be SIADH may in fact be CSW.,,,, This entity has been poorly understood and not often reported over the years. Though the term CSW was introduced by Peters and colleagues in 1950, it was eclipsed by identification of SIADH which was described in 1957. The CSW is the renal loss of sodium due to intracranial disease leading to hyponatremia, decrease in extra cellular fluid volume and consequent systemic dehydration. Unlike SIADH, these children have hypovolaemia, polyuria, large urinary losses of sodium and the plasma concentration of Atrial Natriuretic Peptide (ANP) is increased suggesting this is caused by over secretion of ANP., A recent review article of CSW has suggested that an overall negative balance of sodium needs to be demonstrated for the diagnosis of this entity. We did not demonstrate a negative sodium balance in any of our ten patients with CSW; rather the diagnosis of CSW was based on criteria described in the standard review articles that were available at the time our study was conducted.,, Identical acute neurological insults may cause either SIADH or CSW. The clinical and biochemical manifestation of both conditions can be virtually identical and the main discriminative feature is the status of extracellular volume: it tends to be expanded in SIADH and low in CSW. Clinical findings helpful to differentiate CSW from SIADH include assessment of hydration status, hemodynamic features suggestive of volume loss, fluid intake and urine output monitoring and measurement of body weight daily.
In patients in whom the diagnosis may be unclear, particularly if the volume status cannot be reliably estimated by physical examination, (malnourished patients, or trauma and postcraniotomy patients with facial edema) objective measurement of the volume status by CVP monitoring may be indicated.,, None of our patients required CVP monitoring in order to establish the etiology of hyponatremia as the diagnosis of CSW was possible owing to the unique constellation of acute onset hyponatremia, polyuria despite dehydration and high urine sodium.
In our study, diuretic-induced hyponatremia has been considered a separate cause of hyponatremia, since the serum sodium may be lowered by more than one mechanism. Osmotic agents such as mannitol, widely used to treat cerebral edema, usually cause urinary free water loss resulting in hypernatremia. However, mannitol can also result in hyponatremia secondary to increased urinary sodium losses., Similarly, loop diuretics such as furosemide are well known to cause hyponatremia due to natriuresis accompanying the diuresis. Hyponatremia may be worsened when diuretic-induced sodium loss is replaced by hypotonic fluids, resulting in a combined depletional and dilutional hyponatremia.
Hypovolemic hyponatremia is common in critically ill patients and can result from fluid and electrolyte loss from the gut (vomiting and/or diarrhea), plasma leakage into the interstitial space owing to capillary leak. This also occurs in disease states in the presence of systemic inflammatory response syndrome (e.g., trauma, surgery, sepsis and septic shock), and where there is excessive CSF losses and in patients with renal tubulopathies (disease or drug-induced). The loss of both water and the predominant extracellular cation (sodium) is common to all these conditions. Providing supplemental sodium alone in these hyponatremic states will seldom be successful in restoration of eunatremia unless the attendant fluid deficits are also vigorously addressed. This may be accomplished most simply by saline supplements.,
Central DI is caused by a deficiency of antidiuretic hormone (ADH), caused by destruction or degeneration the supraoptic and paraventricular nuclei of the hypothalamus. Suprasellar tumours are the commonest causes of DI in childhood. Cerebral insults resulting from head trauma or hypoxic brain injury involving the hypothalamic-pituitary area are also well known causes of transient or even permanent DI.
The destructive lesion, or more often, neurosurgical removal of the hypothalamic-pituitary tumour causes DI. The triple response has been described as occurring in the postoperative phase and it is characterized by initial DI followed, after 4-8 days, by a transient remission or excessive release of ADH lasting 1-14 days and then re-occurrence of - usually - permanent DI.
The DI normally leads to polyuria with excessive urine free water loss that, in patients with an intact thirst sensation, will be compensated by an excessive drinking. Plasma osmolality will be in the normal range if adequate fluid replacement has occured. The laboratory findings of ADH deficiency will be an inappropriate low urine osmolality compared to the high plasma osmolality.
While hypernatremia is usual in patients with DI due to increased free water loss, hyponatremia with DI can be caused by water intoxication secondary to excessive vasopressin replacement, to coexistent CSW and to concurrent untreated or undertreated cortisol deficiency.
When CSW co-exists with DI, the excessive polyuria secondary to natriuresis can easily be mistaken for inadequate control of DI. Increasing vasopressin dose in situations where hyponatremia is caused by concomitant CSW will further exacerbate the hyponatremia. The presence of hyponatremia with elevated urine sodium in urine samples collected while the patient develops polyuria (prior to desmopressin dose) will point towards a coexistence of CSW and DI. If there if only DI the urine will be dilute with no natriuresis.
Maintenance of normal fluid and osmolar balance in children following neurosurgical procedures for suprasellar tumours may be a challenge because of the extreme lability in fluid balance on account of the triphasic response described above. Replacement therapy of vasopressin must be carried out with frequent re-assessment of the dose because of the potentially variable nature of DI.
Symptoms largely depend on the rate and acuity of sodium decline and in our series, 90% of our patients had altered mental status while almost three fourth had seizures reflecting the rapid onset of hyponatremia.
Although there is no clear consensus about the optimal treatment of symptomatic hyponatremia, most would agree that correction should be of a sufficient pace and magnitude to reverse the manifestations of hypotonicity but not be so rapid and large as to place a patient at risk of the development of osmotic demyelination., Cerebral edema and symptoms such as depressed consciousness and seizures can be controlled by rapid but relatively small increases in the serum sodium concentration that average only 3-7 mEq/l., All 55 patients with symptomatic hyponatremia in our study were treated with 3% saline with a view to raise the serum sodium by 4-6 mEq/l with further gradual correction aimed at raising the sodium level by not greater than 10-12 mEq/l per day.
Although ten children died and three were hyponatremic at time of death, the death was not related to the hyponatremia but rather to the severity of the underlying neurologic disease as described earlier.
| » Conclusion|| |
Hyponatremia is not uncommon in critically ill children with neurological disorders. Although traditionally attributed to SIADH, there are several other causes leading to hyponatremia in such children. Some of these conditions mimick SIADH. A careful clinical and biochemical assessment is important for the diagnosis to be established, only then can the proper treatment be instituted.
It is important to remember that the therapy that is useful in one condition may be detrimental in the other. A clear understanding of the underlying cause of hyponatremia is required so that the therapeutic approach does not worsen the existing neurological status.
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[Figure - 1]
[Table - 1], [Table - 2]
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