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Preventing Neurological Complications from Dysnatremias in Children

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Preventing Neurological Complications from Dysnatremias in Children Pediatr Nephrol (2005) 20:1687–1700 DOI 10.1007/s00467-005-1933-6 REVIEW Michael L. Moritz · J. Carlos Ayus Preventing neurological complications from dysnatremias in children Received: 30 November 2004 / Revised: 28 February 2005 / Accepted: 2 March 2005 / Published online: 4 August 2005 IPNA 2005 Abstract Dysnatremias are among the most common ongoing free-water losses or when mild hypernatremia electrolyte abnormalities encountered in hospitalized pa- (Na>145 mE/l) develops. A group at high-risk for neu- tients. In most cases, a dysnatremia results from improper rological damage from hypernatremia in the outpatient fluid management. Dysnatremias can occasionally result setting is that of the breastfed infant. Breastfed infants in death or permanent neurological damage, a tragic must be monitored closely for insufficient lactation and complication that is usually preventable. In this manu- receive lactation support. Judicious use of infant formula script, we discuss the epidemiology, pathogenesis and supplementation may be called for until problems with prevention and treatment of dysnatremias in children. We lactation can be corrected. report on over 50 patients who have suffered death or neurological injury from hospital-acquired hyponatremia. Keywords Hypernatremia · Hyponatremia · Cerebral The main factor contributing to hyponatremic encepha- edema · Myelinolysis · Fluid therapy lopathy in children is the routine use of hypotonic fluids in patients who have an impaired ability to excrete free- water, due to such causes as the postoperative state, Introduction volume depletion and pulmonary and central nervous system diseases. The appropriate use of 0.9% sodium Dysnatremias are a common electrolyte abnormality in chloride in parenteral fluids would likely prevent most children in both the inpatient and outpatient settings. A cases of hospital-acquired hyponatremic encephalopathy. serious complication of dysnatremias is brain injury. We report on 15 prospective studies in over 500 surgical Brain injury is an especially tragic complication because patients that demonstrate that normal saline effectively in most cases it is a result of improper fluid management prevents postoperative hyponatremia, and hypotonic flu- or inappropriate therapy. While there are numerous ids consistently result in a fall in serum sodium. Hy- causes of dysnatremias in children, there are a few set- ponatremic encephalopathy is a medical emergency that tings where the neurological sequelae are most common, should be treated with hypertonic saline, and should never and therefore could be prevented. Our goals are to point be managed with fluid restriction alone. Hospital-ac- out the dangers of dysnatremias [1], outline the most quired hypernatremia occurs in patients who have re- important measures that can be instituted for prevention stricted access to fluids in combination with ongoing free- of dysnatremias [2] and discuss how to recognize and water losses. Hypernatremia could largely be prevented treat symptomatic dysnatremias [3]. by providing adequate free-water to patients who have M. L. Moritz ()) Prevention and treatment Division of Nephrology, Department of Pediatrics, of hyponatremic encephalopathy Children’s Hospital of Pittsburgh, The University of Pittsburgh School of Medicine, Pathogenesis of hyponatremia 3705 Fifth Ave., Pittsburgh, PA, 15213-2538, USA e-mail: [email protected] Hyponatremia, defined as a serum sodium <135 mEq/l, is Tel.: +1-412-6925182 Fax: +1-412-6927443 a common disorder that occurs in both the inpatient and outpatient settings. The body’s primary defense against J. C. Ayus developing hyponatremia is the kidney’s ability to gen- Division of Nephrology, Department of Medicine, erate a dilute urine and excrete free-water. Rarely is ex- University of Texas Health Science Center at San Antonio, cess ingestion of free-water alone the cause of hypona- San Antonio, TX, USA AS - Moritz 306-105-001 1688 Table 1 Disorders in impaired renal water excretion [2]. A major consequence of hyponatremia is the influx of 1. Effective circulating volume depletion water into the intracellular space resulting in cellular a. Gastrointestinal losses: vomiting, diarrhea swelling, which can lead to cerebral edema and enceph- b. Skin losses: cystic fibrosis alopathy. Hyponatremic encephalopathy is a serious c. Renal losses: salt wasting nephropathy, diuretics, complication of hyponatremia that can result in death or cerebral salt wa sting, hypoaldosteronism d. Edemetous states: heart failure, cirrhosis, nephrosis, permanent neurological injury. The true incidence of hypoalbuminemia hyponatremic encephalopathy in hospitalized children is e. Decreased peripheral vascular resistance: sepsis, hypothyroid unknown as large prospective studies have not been done. 2. Thiazide diuretics A critical review of retrospective studies in children re- 3. Renal failure veals that encephalopathy is a common complication of a. Acute b. Chronic hyponatremia in both the inpatient and outpatient setting. 4. Non-hypovolemic states of ADH excess Over 50% of children with a serum sodium <125 mEq/ a. Central nervous system disturbances: l will develop hyponatremic encephalopathy (Table 2). meningitis, encephalitis, brain tumors, head injury Hospital-acquired hyponatremic encephalopathy is most b. Pulmonary disease: pneumonia, asthma, bronchiolitis c. Cancer often seen in association with the syndrome of inappro- d. Medications: cytoxan, vincristine, morphine, SSRIs, priate antidiuretic hormone secretion (SIADH) or in the carbamazepine postoperative period [3, 4, 5]. SIADH is caused by ele- e. Nausea, emesis, pain, stress vated ADH secretion in the absence of an osmotic or f. Postoperative state g. Cortisol deficiency hypovolemic stimulus [6]. SIADH can occur because of a variety of illnesses, but most often occurs because of central nervous system (CNS) disorders, pulmonary dis- orders, malignancies and medications. Hyponatremia tremia, as an adult with normal renal function can typi- from SIADH is particularly dangerous in children with cally excrete over 15 l of free-water per day. It is also rare CNS injury such as encephalitis, as mild hyponatremia to develop hyponatremia from excess urinary sodium (sodium <135 mEq/l) has been associated with neuro- losses in the absence of free-water ingestion. In order for logical deterioration and herniation [7, 8]. A common hyponatremia to develop it typically requires a relative contributing factor in hospitalized children with SIADH excess of free-water in conjunction with an underlying who develop hyponatremic encephalopathy is the ad- condition that impairs the kidney’s ability to excrete free- ministration of hypotonic intravenous fluids. water (Table 1). Renal water handling is primarily under Postoperative hyponatremia is a serious problem in the control of argenine vasopressin (AVP), which is children; the majority of deaths resulting from hypona- produced in the hypothalamus and released from the tremic encephalopathy have been reported in healthy posterior pituitary. AVP release impairs water diuresis by children following routine surgical procedures [3, 4, 9]. increasing the permeability to water in the collecting tu- Postoperative hyponatremia is caused by a combination of bule. There are osmotic, hemodynamic and non-hemo- nonosmotic stumuli for ADH release, such as subclinical dynamic stimuli for AVP release. In most cases of hy- volume depletion, pain, nausea, stress, narcotics edema- ponatremia there is a stimulus for vasopressin production forming conditions and the administration of hypotonic that results in impaired free-water excretion. The body fluids. It is estimated that the mortality directly at- will attempt to preserve the extracellular volume at the tributable to hyponatremic encephalopathy in children expense of the serum sodium; therefore, a hemodynamic with postoperative hyponatremia (sodium <129 mEq/l) is stimulus for AVP production will override any inhibitory 8% [3]. The most important factors resulting in postop- hypoosmolar effect of hyponatremia [1]. There are nu- erative hyponatremic encephalopathy are the failure to merous stimuli for AVP production (Table 1) that occur in recognize the compromised ability of the patient to hospitalized patients that can make virtually any hospi- maintain free-water and the administration of hypotonic talized patient at risk for hyponatremia. fluids. Hyponatremic encephalopathy is also a concern in the outpatient setting [10, 11, 12]. It is primarily attributable Epidemiology of hyponatremic encephalopathy to oral water intoxication in infants. Overall, 10% of children less than 2 years of age presenting to the emer- Moderate hyponatremia, defined as a serum sodium gency department with seizures are found to have hy- <130 mEq/l, occurs in over 1% of hospitalized children ponatremic encephalopathy (sodium <126 mEq/l) [10]. Of Table 2 Incidence of hyponatremic encephalopathy in hospitalized children Author Reference no. Inclusion criteria serum Na (mEq/l) Incidence of hyponatremic encephalopathy (%) Wattad et al. 1992 [2] <125 53 Sarnaik et al. 1991 [5] <125 60 Halberthal et al. 2001 [4] <130 in 48 h 78 AS - Moritz 306-105-002 1689 those children with no other recognized cause of seizures, will have a hemodynamic or non-hemodynamic stimulus the incidence of hyponatremic encephalopathy is 56% for for ADH production (Table 1), resulting in impaired free- children less than 2 years of age and 70% for children less water excretion. The administration
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