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Pediatric Endocrine Emergencies

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Maria Sy

on 12 November 2014

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Transcript of Pediatric Endocrine Emergencies

Pediatric Endocrine Emergencies
Difficult task, especially in the child with no known underlying condition
Signs and symptoms of these disorders are
varied
and
nonspecific
delayed or missed diagnosis can have serious consequences
cerebral dysfunction leading to coma or death as seen in diabetic ketoacidosis, hypoglycemia, or adrenal insufficiency
Hypoglycemia
Symptoms usually occur when BG falls below 60-70g/dL
Although for children with diabetes, symptoms may occur at higher BG levels
Goal: return BG to normal
Usually not a diagnosis but a manifestation of a variety of metabolic and endocrine disorders.
Adrenal Insufficiency
(Acute Adrenal Crisis)
often precipitated by acute illness, trauma, surgery or exposure to excess heat
vague and nonspecific symptoms
if unrecognized, life-threatening crisis with acute cardiovascular collapse
primary AI
in adults: autoimmune (>80%), tuberculosis
in children: CAH, autoimmune, adrenoleukodystrophy, syndromes [Wolman, Triple A (AI, achalasia, alacrima), Zellweger)], unexplained AI
secondary AI
abrupt discontinuation of glucocorticoid therapy or stress while on suppressive doses
HypoCalcemia
Clinical manifestations:
tetany, neuromuscular irritability with weakness, paresthesias, fatigue, cramping, AMS, seizures, laryngospasms, cardiac arrhythmias
Trousseau sign, Chvostek sign
EKG: prolonged QT interval
Diabetic Ketoacidosis (DKA)
Clinical Suspicion
polydypsia, polyuria, nocturia, enuresis
abdominal pain, nausea, vomiting
presence of hyperglycemia (random BG >200mg/dL)
relative ketosis ("fruity odor")
clinical metabolic acidosis
tachypnea/Kussmaul breathing
dehydrated appearance
Clinical Suspicion
N/V/D, abdominal pain, fatigue, dehydration, hypotension, metabolic acidosis, AMS, shock
symptoms may mimic GI illness or psychiatric disorder
hyperpigmentation of skin & salt craving - only in primary AI
hypoglycemia - most common in children
Labs: hypoglycemia, hyponatremia, hyperkalemia
decreased serum cortisol and aldosterone
elevated ACTH and renin
in CAH, 17-hydroxyprogesterone is elevated
Management
(of Acute Adrenal Crisis)
rapid volume expansion to support blood pressure
sufficient dextrose to support blood glucose
measure cortisol, electrolyte, glucose, ACTH levels, renin, aldosterone
stress dose of glucocorticoids:
hydrocortisone
Recognition and treatment of endocrine/metabolic emergencies in children
Management
Clinical Suspicion
Management
Fluids
Electrolytes
Insulin
Lab values
Fluids
assume 5-10% dehydration
total fluid deficit = 10mL/kg for each 1% dehydration
give 10-20mL/kg bolus NS or LR over 1hr
replace remaining fluid deficit equally over 48hr plus maintenance
Na - fluids should contain one half NS; Na should rise as glucose drops
K
K > 6 = no K initially
K 4-6 = 40mEq/L
K <4 = 60mEq/L
HCO3
rarely/never used
consider in only severe cases of acidosis (pH <7)
may cause paradoxical CNS acidosis
begin with continuous IV drip (0.1U/kg/hr) after first fluid bolus
goal glucose: 80-100
when glucose reaches 250-300 or if glucose decr >100mg/dL/hr, add D5
once pH > 7.30, HCO3 > 16, AG resolved and patient tolerating PO, start SC insulin
discontinue IV drip 1hr after SC dose
check blood glucose Q1H
check VBG and electrolytes (incl Ca and PO4) Q2H until stable, then Q4H
monitor urine for ketones and glucose with each void
Electrolytes
Insulin
Lab values
HyperCalcemia
HypoNatremia
HyperNatremia
HypoKalemia
HyperKalemia
Hyperthyroidism
(Thyrotoxicosis)

References:
Oberlin JM, Rogers WM, Fenton CL. Endocrine emergencies: recognizing signs and symptoms. Pediatr Ann. 2005 Nov;34(11):870-7; quiz 893-4.
Kappy MS1, Bajaj L. Recognition and treatment of endocrine/metabolic emergencies in children: part I. Adv Pediatr. 2002;49:245-72.
Kappy MS1, Bajaj L. Recognition and treatment of endocrine/metabolic emergencies in children: part II. Adv Pediatr. 2003;50:181-214.
The Harriet Lane Handbook: Mobile Medicine Series, 20e Paperback – June 3, 2014 by Johns Hopkins Hospital, Engorn B, Flerlage J.

http://www.luhs.org/depts/emsc/peddka_pdf.pdf


Diagnosis:
Primary
elevated plasma ACTH (>100pg/mL)
low serum cortisol (<10pg/mL)
Stim test (250ug or 15ug/kg for infants <2yo): subnormal peak cortisol level <18ug/dL 60mins after admin
mineralocorticoid def: low aldosterone, high renin
Secondary
low blood cortisol and ACTH
gold standard: insulin-induced hypoglycemia - risk of seizures and severe hypoK
Evaluation:
Give 50mg/m2 of hydrocortisone by IV bolus
rapid estimate:
infant = 25mg
children = 50-100mg
Followed by 50mg/m2/24hr by continuous drip or divided by Q3-4H
Management
of adrenal insufficiency
Glucocorticoid maintenance
Mineralocorticoid maintenance
Stress-dose glucocorticoids
Diagnostic Studies:
Managemement:
total and ionized Ca, PO4, ALP, Mg, total protein, BUN, Cr, 25-OH vit D, PTH
albumin, pH
Acute: consider IV calcium gluconate
Chronic: consider oral supplement
consider Vit D supplementation (400 IU/day)
Clinical manifestations: weakness, irritability, lethargy, seizures, coma, abdominal cramping, anorexia, nausea, vomiting, polyuria, polydipsia, renal calculi, pancreatitis
EKG: shortened QT interval
Management:
treat underlying disease
hydration
increase urine output and Ca excretion
diuresis with furosemide
hemodialysis in refractory cases
steroids - in malignancy, granulomatous disease, vit D toxicity
severe/persistent - calcitonin, bisphosphonate
Hypomagnesemia:
HypoCa cannot be corrected if underlying hypoMg exists.

Clinical manifestations: anorexia, nausea, weakness, malaise, depression, nonspecific psychiatric symptoms, hyperreflexia, carpopedal spasms, clonus, tetany
EKG changes: atrial and ventricular ectopy; torsades de pointes
mild sx:
oral glucose in the form of OJ or dextrose tablets
profound sx:
IV infusion of dextrose
IV glucose bolus of 0.25g/kg
measure BG every 30mins
glucagon at 0.03mg/kg (if excess insulin is suspected; contraindicated if as a result of sulfonylurea meds)
IV glucocorticoid if AI suspected
AM cortisol levels
ACTH stimulation test
to measure ability of the adrenal gland to produce cortisol in response to ACTH
Mineralocorticoid deficiency confirmed with high renin and low aldosterone
Factitious etiologies:
hyperlipidemia
hyperproteinemia
hyperglycemia

Clinical manifestations: predominantly neurological symptoms - nausea, HA, lethargy, seizures, coma
Management: replace losses/restrict fluids, treat underlying cause

Clinical manifestations: predominantly neurological symptoms - lethargy, weakness, AMS, irritability and seizures; also muscle cramps, depressed DTR, respiratory failure

Management: replace free water losses and treat cause
Clinical manifestations: skeletal muscle weakness or paralysis, ileus, cardiac arrhythmias
EKG: delayed depolarization, with flat or absent T waves; in extreme cases, U waves
Management: replace K (rate depends on severity of symptoms)
Clinical manifestations: skeletal muscle weakness, paresthesias
EKG: peaked T waves, loss of P waves with widening of QRS, ST-segment depression with further QRS widening, bradycardia, AV block, ventricular arrhytmias, torsades de pointes, cardiac arrest

Management: stop K-containing infusions, kayexalate, calcium gluconate, insulin, NaHCO3, albuterol
Non-specific
In neonates
: lethargy, jitteriness, apnea, cyanosis, respiratory distress, poor feeding, hypothermia, myoclonic jerks or convulsions
Older children
: sweating, tremors, hunger, pallor, tachycardia, shakiness
Severe
: sleepiness, lethargy, visual difficulty, ataxia, behavioral abnormalities, convulsions or unconsciousness
Stress Dose:
Most common cause of death in children who have type 1 diabetes.
profound insulin-deficient state
characterized by:
blood glucose >200mg/dL
pH <7.30
serum bicarbonate <15
along with evidence of an accumulation of ketoacids in the blood (measurable serum or urine ketones, increased anion gap).
Dehydration, electrolyte loss, and hyperosmolarity contribute to the presentation and potential complications.

Hyperosmolar hyperglycemic state (HHS)
caused by inadequate insulin
defined as:
blood glucose >600mg/dL
pH >7.30
bicarbonate >15
serum osmolarity >320
small amount of ketones maybe present
PREVENTION

Through early recognition and diagnosis of diabetes in a child who has polydipsia and polyuria and through careful attention to the treatment of children who have known diabetes, particularly during illnesses.
Best Treatment of DKA:
Diagnostic Criteria for Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State
Clinical manifestations: hyperactivity, irritability, altered mood, insomnia, heat intolerance, sweating, pruritis, tachycardia, palpitations, weight loss despite increased appetite, diarrhea, oligo/amenorrhea, tremor, hyperreflexia, hair loss
Thyroid storm: acute onset of hyperthermia, tachycardia, restlessness, delirium, coma, death
Tx: propranolol, potassium iodide
long term: methimazole
Neonatal thyrotoxicosis
Presentation: microcephaly, frontal bossing, IUGR, tachycardia, systolic hypertension with widening pulse pressure, irritability, FTT, exophthalmos, goiter, flushing, V/D, jaundice, thrombocytopenia, cardiac failure or arrhythmias
**occurs exclusively in infants born to mothers with Graves - caused by transplacental passage of maternal TSI

treatment: propranolol, methimazole, digoxin for heart failure
usually resolves by 6 months
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