Hypocalcemia
Cramps, carpopedal
(hypoparathyroidism)
spasms,
paresthesias,
lethargy, apathy,
convulsions,
hypotension
Diabetes insipidus

Plasma calcium,
phosphate, alkaline
phosphatase

10% calcium
gluconate 1
mL/kg IV over
15 min

Polyuria, polydipsia, Paired plasma and urine Central : IV fluids
dehydration,
osmolality and
at two-thirds
irritability, fever,
sodium
maintenance rate
drowsiness, coma
plus replete
deficit over 48
hrs; vasopressin
1–10 mU/kg/hr

IV
Nephrogenic : IV
fluids at urine
output plus
replete deficit
over 48 hrs
Syndrome of
Anorexia, headache, Paired plasma and urine Seizures : 3%
inappropriate
nausea, vomiting,
osmolality and
saline at 1–3
antidiuretic hormone
irritability,
sodium
mL/kg IV;
secretion
seizures, coma
furosemide 1
mg/kg IV stat;
benzodiazepines
Otherwise : fluid
restriction
Thyroid storm
Goiter,
Free T4 , Total T3, TSH Propranolol 10
exophthalmos,
μg/kg IV over
high fever,
15 min; Lugol

tachycardia,
iodine 9–15
congestive cardiac
drops/day
failure, delirium,
orally;
stupor
methimazole
20–30 mg q6–
12h (initially);
tepid sponging
Neonatal thyrotoxicosis Goiter, failure to
Free T4 , Total T3, TSH Propranolol 1
gain weight,
mg/kg tid orally;
irritability,
potassium
tachycardia,
iodide two drops
congestive cardiac
bid orally;
failure
methimazole


Congenital
hypothyroidism

Hypopituitarism


Asymptomatic:
Free T4 , TSH
hypothermia,
hypoactivity, poor
feeding,
constipation,
prolonged
jaundice, large
posterior fontanel
See features listed
for adrenal
insufficiency and
hypoglycemia

0.5–0.7
mg/kg/day
divided tid
orally
L -thyroxine 10–15
μg/kg/day orally

IV, intravenous; IM, intramuscular; ACTH, adrenocorticotropic hormone; TSH, thyroid-stimulating hormone; tid, three times
daily; bid, twice per day.

DIABETIC KETOACIDOSIS
Goals of Treatment
To identify patients with DKA and initiate treatment per algorithm.
To recognize patients with cerebral edema (1%) and intervene with appropriate treatment.
CLINICAL PEARLS AND PITFALLS
Clinically significant cerebral edema is the most serious immediate risk to the child,

occurring in 1% of cases, and it remains so during the first 24 hours of therapy,
despite the more apparent issues of hypovolemia and acidosis.
The treatment for symptomatic cerebral edema is mannitol and/or 3% hypertonic
saline.
Avoid bicarbonate administration.

Current Evidence
Insulin deficiency initially leads to hyperglycemia that, once above the renal threshold of 180
mg/dL, leads to polyuria due to an osmotic diuresis. Without vigorous oral repletion at home,
the child quickly becomes hypovolemic, prompting a stress response and elevations of the
counterregulatory hormones glucagon, cortisol, growth hormone, and catecholamines. These
hormonal changes produce significant insulin resistance and stimulate glycogenolysis and
gluconeogenesis that worsens the hyperglycemia, hypovolemia, and stress response. In this
insulin-deficient state, adipose tissue is broken down in large quantities into free fatty acids,
subsequently converted into ketoacids in the liver. Ketoacids readily dissociate in the blood to
produce free hydrogen ions, and metabolic acidosis ensues. This reaction is partially


compensated for by a respiratory alkalosis (hyperventilation), with a resultant lowering of PCO
−
2 and plasma bicarbonate (HCO3 ).
Intracellular potassium is depleted because of transcellular shifts of this ion brought about
by the exchange of potassium with excess free hydrogen ions and extracellular dehydration.
Protein catabolism secondary to insulin deficiency causes a negative nitrogen balance and
results in additional efflux of potassium from cells. The potassium is then lost in the urine
during the osmotic diuresis. Volume depletion causes secondary hyperaldosteronism, which
further promotes urinary potassium excretion. Thus, total body depletion of potassium occurs,
although the plasma potassium concentration may not reflect the loss at the time of
presentation.


Clinical Considerations
Clinical Recognition
In cases of new-onset diabetes, the child usually has a history of polyuria and polydipsia for a
few days or weeks before the acute decompensation. Significant weight loss often occurs
despite a vigorous appetite. Vomiting is common once the child has ketoacidosis; these further
losses plus the inability to compensate for polyuria contribute to the hypovolemia.
In children known to have diabetes, the prodrome may be less than 24 hours and
precipitated by an intercurrent illness, inappropriate sick day management, or omission of
insulin doses.
Triage
On physical examination, particular attention should be paid to the degree of dehydration,
including skin turgor and dryness of mucous membranes. Urine output is not a reliable sign of
hydration status. In severe cases, the child may exhibit signs of compensated shock, including
a thready pulse and cold extremities, and rarely, as uncompensated shock with hypotension.
The smell of ketones on the breath and the presence of hyperpneic (Kussmaul) respirations
reflect the ketoacidosis. The patient’s consciousness level, which may range from full alertness
to deep coma, should be noted.
Initial Assessment/H&P
Patients may complain of nausea, vomiting, and abdominal pain, and the parents may have
noticed increasing listlessness. Less than 1% of children are in coma at the time of hospital
admission, although a higher percentage has an altered state of consciousness. The history and
physical examination usually suggest the diagnosis; however, particularly in the patient with
new-onset diabetes, presenting clinical features can be misdiagnosed, especially in the infant
or young child. For example, abdominal pain may be misinterpreted as appendicitis;
hyperpnea may be mistaken as a sign of pneumonia or asthma; and polyuria may be
incorrectly diagnosed as a urinary tract infection. Enuresis, polydipsia, and irritability are
sometimes wrongly categorized as behavioral problems. The child may have exquisite
abdominal tenderness with guarding and rigidity, which can mimic an acute abdomen. The
ears, throat, chest, and urine should be examined because infection is often a precipitating
factor. Careful attention should be paid to the skin examination because there have been

several case reports of fasciitis co-presenting with DKA. The presence of hyperpigmentation


(acanthosis nigricans) on the posterior neck is a sign of long-standing insulin resistance and
should alert the clinician to the possibility of non–insulin-dependent diabetes.
Management/Diagnostic Testing
Diagnostic laboratory findings include plasma glucose greater than 200 mg/dL (commonly 400
to 800 mg/dL) and elevated serum ketones (commonly above 5 mmol/L), the presence of
glucose and ketones in the urine, and acidosis (venous pH less than 7.3 and serum bicarbonate
less than 15 mEq/L). Additionally, high or normal plasma potassium, and slightly elevated
blood urea nitrogen are common. Occasionally, DKA can occur with normoglycemia when
persistent vomiting and decreased intake of carbohydrates are accompanied by continued
administration of insulin or when patients have kept themselves particularly well hydrated
with non–glucose-containing fluids. The measured serum sodium is usually low or in the low
to normal range. In the setting of hyperglycemia, the measured sodium will be lowered; a
commonly used estimate for correction is a decrease of 2 mEq/L Na for every 100 mg/dL
elevation in glucose above normal. Leukocytosis with a left shift may be noted but does not
necessarily signify an underlying infection. Hyperglycemia in the absence of acidosis should
cause the clinician to consider additional possibilities (see Hyperglycemia section).
For the severely dehydrated child, initial treatment is directed toward expansion of
intravascular volume and administration of insulin. Subsequent treatment is directed at the
normalization of the remaining abnormal biochemical parameters. Medical intervention carries
significant risks of hypokalemia and cerebral edema ( Tables 89.2 and 89.3 ).
Fluid and Electrolyte Replacement
Fluid replacement should be instituted promptly. In the first 1 to 2 hours, if hypovolemia is
apparent, 10 mL/kg isotonic (0.9%) crystalloid (either normal saline or lactated Ringer’s)
should be infused intravenously to establish an adequate intravascular volume and improve
tissue perfusion. Normal saline is generally preferred for initial resuscitation given that DKA
patients already have a degree of lactic acidosis, however, lactated Ringer’s has the benefit of a
reduced chloride load. A small head-to-head trial showed no significant differences between

the two fluids. Repeat bolus if the pulse rate and capillary refill rate do not improve, but rarely
is more than 20 mL/kg required in the first hour. The goal of this initial rehydration therapy is
not euvolemia but adequate perfusion of end organs, often best judged by monitoring
mentation, capillary refill, and heart rate.