Pediatric emergency medicine trisk 474

accomplished slowly because overly rapid volume correction can cause cerebral edema,
seizures, and death.
If the child is not hypotensive, or once the hypotension and perfusion have been corrected,
free water replacement is done over 48 hours. Calculations of appropriate fluids must include
maintenance requirements, replacement needs, and ongoing urinary losses (see Chapter 22
Dehydration ).
If DI is strongly suspected on the basis of discrepant serum and urine osmolality,
Desmopressin (DDAVP®) (10 μg intranasally or 0.2 to 0.4 mCg/kg subcutaneously) may be a
useful adjunct to IV fluid therapy. If desmopressin is not available or cannot be used for some
reason, other antidiuretic agents are available. Aqueous vasopressin (Pitressin® ) may be
administered as a continuous IV infusion starting at 2.5 mU/kg/hr and slowly (every 15 to 30
minutes) increasing the rate by increments of 2.5 milliunits (maximum 10 mU/kg/hr) to
decrease urine output to less than 2 mL/kg/hr.
Desmopressin and vasopressin act rapidly to promote tubular resorption of free H2 O;
clinically, this response should be apparent as decreased urinary output, when being measured
with a bladder catheter, and should demonstrate increased urine osmolality within 15 minutes
of administration. Once the patient has responded, however, extreme care must be used in
subsequent fluid management because the patient can no longer excrete excess water.
Therefore, baseline IV fluid administration must be restricted to 1 L/m2 of body surface area
per day (or roughly two-thirds maintenance fluids) using a low sodium infusate, such as 5%
dextrose with one-fourth normal saline (0.23%), in addition to the fluid designed to replete the
initial estimated free water deficit over 48 hours.
Failure to respond to either form of ADH suggests the possibility of tubular
unresponsiveness to ADH (nephrogenic DI); however, more commonly, failure to respond
results from improper administration of the medication or use of desmopressin that has lost its
potency. Because of these factors, if cessation of diuresis is not noted within 2 hours of
administration of the first dose, a second dose from a different bottle of desmopressin should
be tried. The use of an ADH agonist generally simplifies management by reducing the quantity
of fluid that must be infused; however, careful monitoring of input and output remains
essential. Children who fail to respond to desmopressin are likely to have nephrogenic DI and
must be managed acutely with fluid therapy alone. Hypercalcemia and renal failure are the

most common causes of nephrogenic DI. Paradoxically, the thiazide diuretics have proven to
be useful in the chronic control of nephrogenic DI.
The child should be closely observed for changes in level of consciousness, pulse rate, and
blood pressure. Fluid input and output should be meticulously monitored. Serum osmolality
and [Na+ ] should be determined every 1 to 2 hours until the rate of their decline can be
determined. Urine osmolality should be measured every 1 to 2 hours to determine the
responsiveness of the renal tubule to DDAVP. Because large volumes of dextrose-containing
fluids are used, the blood glucose should also be followed closely. If the blood glucose exceeds
150 mg/dL, the concentration of dextrose in the infusate should be decreased.
Clinical Indications for Discharge or Admission
Clinically significant electrolyte derangements or the inability to maintain hydration status are
indications for admission in well-appearing child. Children with intact thirst mechanism who


are able to tolerate PO can be discharged with plan for close outpatient follow-up.

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
SECRETION
Goals of Treatment
The goals of treatment in a child with syndrome of inappropriate antidiuretic hormone
(SIADH) are to raise the serum sodium and improve the neurologic status of the patient;
secondarily, causes of SIADH should be identified.
CLINICAL PEARLS AND PITFALLS
Most patients are asymptomatic from SIADH until the serum sodium <125 mEq/L.
SIADH is present in a high proportion of patients with bacterial meningitis (50%),
positive pressure ventilation (20%), and Rocky Mountain spotted fever (70%).
There are numerous relatively benign causes of SIADH, including fever, nausea,
pain, pneumonia, and a wide range of physiologic stressors.
For severe lethargy, seizure, or coma administer 3% saline emergently (3 mL/kg
every 10 to 20 minutes as needed) and consider furosemide with a normal saline

infusion.
For asymptomatic or mildly symptomatic patients, treat with rigorous fluid restriction and
consider a vasopressin receptor antagonist if recurrent.

Current Evidence
Excessive secretion of ADH accompanying normal or low plasma osmolality or [Na+ ] is
inappropriate because it further depresses the plasma osmolality and [Na+ ]. The overall
incidence of the SIADH secretion in childhood is unknown, but it is common in certain
disease states. Normal ADH secretion is stimulated by hypertonicity of the fluid surrounding
the hypothalamic osmoreceptors, volume receptors in the right atrium, and ill-defined nervous
impulses from higher cortical centers. Disorders of the CNS ( Table 89.8 ) may cause
excessive ADH secretion by producing either a local disturbance of the hypothalamic
osmoreceptors or some undetermined nervous stimuli. Many intrathoracic conditions are
associated with SIADH, probably due to the vestigial ability of the lung to produce ADH.
Physical and emotional stress, severe pain, and nausea are also potent stimuli of ADH
secretion. Excessive secretion of ADH leads to water retention by the collecting tubules of the
kidneys, a mechanism mediated by insertion of water channels into the luminal membrane of
the collecting duct and allowing water reabsorption along the medullary concentration
gradient. The retained water expands the intravascular compartment, dilutes all plasma
constituents, and lowers the plasma osmolality.


TABLE 89.8
SOME CAUSES OF SYNDROME OF INAPPROPRIATE ANTIDIURETIC
HORMONE SECRETION IN CHILDREN
Disorders of central nervous system
Infection (meningitis, encephalitis)
Trauma, post-neurosurgery
Hypoxic insults, especially in the perinatal period
Brain tumor

Intraventricular hemorrhage
Guillain–Barré syndrome
Psychosis
Intrathoracic disorders
Infection (tuberculosis, pneumonia, empyema)
Positive pressure ventilation
Asthma
Cystic fibrosis
Pneumothorax
Patent ductus arteriosus ligation
Miscellaneous
Pain (e.g., after abdominal surgery)
Nausea
Severe hypothyroidism
Tumors (e.g., neuroblastoma)
Drug induced
Increased antidiuretic hormone secretion
Vincristine
Cyclophosphamide
Carbamazepine
Adenine arabinoside
Phenothiazines
Morphine
Potentiation of antidiuretic hormone effect
Acetaminophen
Indomethacin

Clinical Considerations
Clinical Recognition

Most patients with SIADH are asymptomatic until the plasma [Na+ ] falls to less than 125
mEq/L. Associated with the low serum sodium, children may be weak, have altered mental
status, or have seizures. Patients may have mild signs of hypervolemia.
Triage
Assess mental status and neurologic examination, treat for precipitating conditions.
Initial Assessment/H&P
Symptoms associated with hyponatremia range from anorexia, headache, nausea, vomiting,
irritability, disorientation, and weakness to seizures and coma, leading potentially to death.
Absence of edema and dehydration are usual and significant clinical findings.
Management/Diagnostic Testing
Laboratory investigations for diagnostic purposes must include concomitant serum and urine
samples ( Table 89.9 ).
Hyponatremia, hypoosmolality (serum), and low blood urea nitrogen will be present. In
contrast, the urinary osmolality and [Na+ ] are inappropriately elevated for the hypotonicity of
the serum. Due to the euvolemic or hypervolemic state, aldosterone is suppressed and urine
potassium will be low. Radioimmunoassay for ADH is available and has been helpful in
defining this syndrome; however, the results of this test are unlikely to be available on an
emergency basis.
The underlying cause of the syndrome should be investigated according to the physician’s
clinical judgment. Severe hyperlipidemia may falsely lower laboratory measurement of [Na+ ],
leading to a factitious hyponatremia. Hyperglycemia and hypoproteinemia, however, lead to
true hyponatremia. Renal salt wasting secondary to adrenal insufficiency should be
accompanied by hyperkalemia and dehydration. Cerebral salt wasting may have laboratory
parameters similar to SIADH but is characterized by hypovolemia and a high urine output as
long as renal perfusion remains intact. The urine osmolality in water intoxication states is
usually low compared with that found in SIADH.
Severely Symptomatic Children
Patients with a persistent seizure attributable to severe hyponatremia and those who are
severely lethargic or comatose need urgent treatment with hypertonic (3%) saline by infusing

small amounts of 3% saline in the range of 3 mL/kg every 10 to 20 minutes until symptoms
remit. One milliliter per kilogram of 3% saline should raise the serum [Na+ ] by
approximately 1 mEq/L. Since the administration of 3% is high-risk therapy, it should only
be given in the quantity needed to extinguish the adverse clinical finding (e.g., altered mental
status, seizure). A single dose of furosemide (1 mg/kg) also can be administered
intravenously. Close monitoring of fluid balance, plasma and urinary sodium, potassium, and
osmolality is essential.
Seizures should be treated concomitantly with a standard emergency anticonvulsant protocol
(see Chapters 72 Seizures and 97 Neurologic Emergencies ). Of note, phenytoin (Dilantin®)
or fosphenytoin (Cerebyx®) intravenously (5 to 10 mg/kg) inhibits ADH release and may be
helpful in the patient with seizures secondary to CNS causes of SIADH.