Paediatric Endocrine

Emergencies
 Diabetic ketoacidosis in children and
adolescents
 Hypoglycaemia
 Neonatal hypoglycaemia
 Hypocalcaemia
 Hyperthyroid crisis
 Acute adrenal insufficiency – adrenal crisis
 Hyponatraemia
 Diabetic ketoacidosis (DKA) and
hypoglycaemia in children and adolescents
with diabetes
https://www.ispad.org/ ‎
ISPAD Clinical Practice Consensus Guidelines 2009
Chapter 10, chapter 11
 There is wide geographic variation in the
frecuency of DKA at onset of diabetes, and
correlated with regional incidence of T1DM
 Frequency range from 15 % to 70% in Europe
and North America

 Causes:
Diabetic ketoacidosis results from absolute or
relative deficiency of circulating insulin and
the combined effects of increased levels of
counterregulatory hormones
 Dehydratation
 Rapid, deep (Kussmaul) respiration
 Nausea, vomiting, and abdominal pain mimicing an
acute abdomen
 Progressive obtundation and loss of consciousness
 Increased leucocyte count with left shift
 Non specific elevation of serum amylase
 Fever only when infection is present
 Biochemical criteria for diagnosis of DKA:

 Hyperglycaemia ( blood glucose >11mmol/l)

 Venous pH <7.3 , or bicarbonate <15 mmol/l
 Ketonemia ir ketonuria

The severity of DKA is categorize by the degree of acidosis:

 Mild - venous pH <7.3 , or bicarbonate< 15 mmol/l

 Moderate - pH <7.2, bikarbonate < 10 mmol/l
 Sever - pH <7.1, bikarbonate < 5 mmol/l

ISPAD 2009
 Correct dehydratation
 Correct acidosis and reverse ketosis
 Restore blood glucose to near normal
 Avoid complications of therapy
 Identify and treat any precipitating event
 Inadequate rehydration
 Hypoglycaemia
 Hypokalemia
 Hyperchloremic acidosis
 Cerebral edema
  Cerebral edema ussually develops 4-12 hours
after treatment has started

 Warning signs and symptoms of cerebral

edema:
1. Headache & slowing of heart rate
2. Change in neurological status ( restlessness,
irritability, increase drowsiness, incontinence)
3. Specific neurological signs (e.g. cranial nerve
palsies)
4. Rising blood pressure
5. Decreased O2 saturation
Water and salt deficits must be replaced in 24 – 48 hours
 Rehydration:
 0,9% saline NaCl 10- 20ml/kg in 10-30min. Later 10ml/kg/h over 2
hours.
 The rate of fluid IV and oral should be calculated to rehydrate evenly
over 48 hours.

 Insulin : short or rapid acting 0,1 -0,05unit/kg/hour

 Route of administration I/V
 Glucose concentration decreases > 5mmol/l/h.
 If glucose falls to 14-17 mmol/l, add 5-10 % glucose +0,45 % NaCl
solution.
 Aim to keep blood glucose 8-12mmol/l, insulin infusion 0,05-
0,1unit/kg/hour.
 Pottassium replacement:
◦ Children with DKA suffer total body potassium deficits
◦ If renal function is normal:
◦ Potassium chloride (KCl) 3-5 mmol/kg/24h. Potassium
replacement should continue throught IV fluid therapy

 Bikarbonate:
◦ Bicarbonate is not reccomended
◦ If bicarbonate is necessary (pH<6,9), cautiously give
1-2mmol/kg over 60 min in IUC.
ISPAD 2009
 Hypoglycaemia: blood glucose < 3,9 mmol/l

 Risk factors for hypoglycaemia:

◦ Treatment regim is altered:
◦ More insulin
◦ Less food
◦ More exercise
◦ Alcohol
 Symptoms:

◦ Weakness, tremors, sweating

◦ Drowsiness, speech, behavior disorder

 Treatment:
◦ 5-15g glucose or sugar
◦ 100ml sweet drink (juice, sweet, tea)

◦ If there is no effect - repeat after 10-15min.

 Symptoms: loss of consciousness, seizures

 Urgent treatment:
◦ Glucagon i/m, s/c
◦ 0,5 mg, for age < 12 m
◦ 1,0 mg, for age > 12 m

◦ Dextrose i/v
◦ Dextrose 10-30% at a dose 200 – 500 mg/kg, (dextrose 10% is
100mg/ml )

◦ Improved condition - carbohydrate per os, and or i/v

infusion of glucose, e.g. dextrose 10%, 1.2 - 3.0 ml/kg/h.
 Common first days after birth

 Often transitory

 Non-specific symptoms of hypoglycaemia :

Apathy, apnoe, cyanosis, hypothermia, hypotonia,
irritability, lethargy, tremors, tachipnoe, seizures, asistoly

 Also it may be asymptomatic

 2 hours after birth glycemia drops to
average 2.8 mmol/l

 After 72 hours varies around 4.0 mmol/l

 Praematurity
 Hypoxia
 Sepsis
 Congenital heart defects
 Small-for-gestational age newborns
 Hypothermia
 Diabetic mothers newborns
 Rhesus haemolytic disease
 Beckwith-Wiedemann syndrome
 Macrosomia
 Small external genitalia
The main sings of the BWS:
o Omfalocelė;

o Macroglossia;

o Macrossomia.

It is a large clinical
heterogeneity
o Macrosomia - height
and weight > 97‰

o Hemihyperplasia -
asymmetric growth of
one or more body
areas, organs.

o Macroglossia.

o Neonatal
hypoglycaemia.
o Hernia umbilicalis, diastasis m. recti.
o Visceromegalia
o Germinal tumors of childhood
o (Wilms tumor, hepatoblastoma,
neuroblastoma, rabdomiosarcoma).
o Renal dysplasia, nephromegalia,
nephrocalcinozė.
o Cardiomegalia, congenital heart
disease, cardiomiopatia.
 In asymptomic newborns in the risk group
glycemia should be measured in the
capillary blood:
 2,4,6,8,10,12,18,24,36,48 and 72 hours
after birth
 Normal weight full-term infants:

 First 3 hour<2,0 mmol/l

 3-24 hours<2,3mmol/l
 >24 hours <2,5 mmol/l
(Srinivasan et all.)
 Decrease glucose production

 Increased glucose consumption:

hyperinsulinism

 Decrease glucose production and increase

glucose consumption
 Prematurity :
Ca <1,75 mmol/l or Ca++ <1 mmol/l

 Normal:
Ca <2 mmol/l or Ca++ <1,2 mmol/l
Early neonatal hypocalcaemia:
 First 3-4day after birth

Late neonatal hypocalcaemia:

 Symptomatic hypocalcaemia, which persists in the
treatment of adequate dose of Ca

 If Ca preparations administered at > 72 h of age

 Hypocalcemia, manifesting the second week after birth

Causes:
 Prematurity
 Birth asphyxia
 Intrauterin growth restriction (IUGR)
 Preeclampsia
 Infant of diabetic mother
 Maternal anticonvulsants (phenobarbital etc.)
 Maternal hypercalcaemia
 Iatrogenic (diuretics, blood transfusion, etc.).
 Serum Ca , Ca ++, if:

1. Prematurity < 32 hebd.

2. Born from diabetic mothers
3. Severe perinatal asphyxia (Apgar <4
points in 1 min.)

 Analyzed 24 h and 48h after birth

Asymptomic: accidentally found plasma Ca 

Symptomatic :

 Neuromuscular symptoms (seizures, myoclonus, etc.)

 Cardiac symptoms (tachycardia, heart failure,  QT interval, 

contractility)

 Other (apnea, cyanosis, tachypnea, vomiting, laryngospasm)

Causes:

 Hight phosphate load (cow’s milk feeds, renal failure)

 Hypomagnesaemia

 Vitamin D deficienty in mother and infant

 PTH resistance syndrome

 Hypoparathyroidism (primary, secondary, mother, suffered from

hyperparathyroidism)

 Alkalosis

 Iatrogenic causes (bicarbonate therapy, lipid infusion, diuretics,

GK, alkalosis, phototherapy)
 Ca
 Ca++
 P
 Mg
 Alkaline phospatase
 25-OH vit. D3
 PTH
 I/v bolus of 10 % Ca gluconate 0,1ml/kg

 Dilute with 0,9 % NaCl or 5 % glucose and infuse over 10

min into central line or large cannula in large vein as severe
risk of calcium burns with tissue leak from peripheral site

 Do not co-administer with sodium bicarbonate as this cause

calcium carbonate precipitation

Next steps:
 Ca infusion 1-2 mmol/kg/day via central line

 Magnesium infusion if low

When to suspect it:
 Infant of mother with active or previously thyroidectomized
Grave’s disease

 Neonatal persistent tachycardia and cardiatic compromise

Age group:
 Mostly neonatal, but rare

 Severe thyrotoxicosis in an older child or adolescent is

extremely rare
Precipitating factors:

 Infection
 Trauma
 Surgical intervention;
 Sympathomimetic use;
 Anti-thyroid drug treatment interruption;
 Radioactive iodine therapy.
 Irritabily
 Restlessness
 Voracious feeding
 Weight loss or failure to gain weight
 Temperature >38,5 C°
 Tachycardia (inadequate C°)
 Sings of cardiac failure
 Tachypnoe
 Gastrointestinal disorder (vomiting,
diarrhea)
 Goitre
 Coma
 fT3
 fT4
 TSH
 Thyroid receptor antibody titre
 Monitoring of respiratory and cardiovascular
function

 Normalization of body temperature

 Reduction thyroid hormone effects on peripheral

tissues:
1. Antithyroid drugs(carbimazle 0,25 mg/kg every 8 hours;
propilthiouracil 0,5-1,5mg/kg/ day once),
2. ß-blockade (propranolol 0,25-0,75 mg/kg every 8 hours,
3. Aqueoes iodine oral solution (Lugol’s solution),
4. Steroid treatment may be considered in severe cases
The most common causes:

 Congenital adrenal hyperplasia

 Meningococcal septicaemia
 Haemorrhage into the adrenal glands
 Cessation of glucocorticoid therapy
 Adrenoleucodystrophy
Clinical manifestation:
o Cerebral sclerosis
o Decrease visual acuity, blindnes
o Cognitive loss
o Ataxia
o Dementia,
o Adrenal inssufficiency

o Genetics
o Mutation ALD gene, Xq28chromosome
o ALD protein may be to transport VLCFA-COA synthetase

o VLCFA (very long chain fatty acids) investigate for

all boys with adrenal inssufficiency
 Vomiting without diarrhea
 Drowsiness, fainting
 Signs of shock, hypotension, tachycardia,
 Dehydration
 Glucose (hypoglycaemia)
 Electrolytes (hyponatremia)
 Acidosis
 Cortisol
 Adrenal steroids
 ACTH
 Fluid balance restoration saline and glucose
solutions (0.9 % NaCl 10-20 ml/kg per 20-60
min, after 0.9 % NaCl-5 % glucose solutions 10-15
ml/kg/d.)

 Monitor and correct sodium and potassium

disturbances (Na requirement 10-15mmol/kg/d)

 Hydrocortisone i/v (2 mg/kg i/v bolus),

 Establish hydrocortisone infusion 10mg/kg/ 24h
 Hyponatraemia - serum sodium is below 130
mmol/l

Classification :
1. Hypovolaemic hyponatraemia
2. Euvolaemic hyponatraemia
3. Hypervolaemic hyponatraemia
Renal loss:
 Adrenal insufficiency (MCC deficiency)
 Cerebral salt wasting syndrome
 Tubular defect
Extra renal losses:
 Gastrointestinal tract (vomiting, diarrhea,
pancreatitis, intestinal fistula)
 Skin (burns)
 Lungs
 Syndrome of inappropriate secretion of
antidiuretic hormone (SIADH)
 ACTH – deficiency (glucocorticoid)
 Psychogenic polydipsia
 Hypothyroidism
 Water intoxication
 Nephrotic syndrome
 Cirrhosis
 Heart failure
 Renal failure