Dr. Vaman Khadilkar*
Pediatric Endocrinologist, Pune .*

Endocrine emergencies in a child often manifest in an occult manner and resemble more commonly seen acute conditions such as sepsis or CNS infection or renal failure. A high index of suspicion is necessary to recognize an endocrine emergency. Once suspected, appropriate tests can be arranged to reach the diagnosis. In this chapter an overview of when to suspect an endocrine emergency, which tests to order and how to manage the child in ICU is discussed. Longterm diagnosis, management and outcome of specific condition is not discussed as it is beyond the scope of this text.

When to suspect Pediatric Endocrine problem in ICU setting?
A high index of suspicion is necessary to diagnose endocrine problem in a sick child admitted to PICU. It is possible to overlook a probable endocrine pathology when all the attention is diverted to the management of other problems such as sepsis or shock.

Pointers to the Diagnosis of Endocrine Disease are:
Laboratory Indicators:

  • Electrolyte imbalance
    • Hyponatremia associated with hyperkalemia
    • Hypernatremia
    • Hypocalcemia associated with hyperphosphatemia
    • Hypercalcemia
  • Glucose imbalance
    • Hypoglycemia
    • Hyperglycemia
    • Ketone bodies in the urine and serum
  • Acid-base disturbance
    • Metabolic acidosis with hyponatremia, hyperkalemia
    • Hypoglycemia with metabolic acidosis
    • Alkalosis with hypocalcemia

Clinical Indicators:
  1. Short stature
  2. Inappropriate tall stature
  3. Obesity
  4. Hypertension
  5. Goiter
  6. Genital abnormalities
  7. Hyper-pigmentation or hypopigmented patches
  8. Acanthosis nigricans
  9. Midline craniofacial defects
  10. Polyuria despite dehydration
  11. Urine output well over 2-3 liters per day

Some Selected Endocrine Emergencies:

Diabetic Ketoacidosis(i,ii):

Diabetes in childhood in increasingly reported from the western world and also from India. As many as 50% of children with diabetes present with DKA as their first presentation. Diabetic ketoacidosis needs early recognition and prompt management in an ICU setup to prevent morbidity and mortality. When diagnosed early and treated in a systematic manner DKA has a good prognosis. Pathophysiology: There is relative or absolute insulin deficiency and elevated levels of stress hormones with increased serum osmolarity due to hyperglycemia and ketosis. Acidosis shifts the oxygen dissociation curve to the left leading to tissue hypoxia and shock. Osmotic diuresis leads to dehydration and sodium and potassium is lost in the urine. Hypoinsulinemia leads to ketosis and lactic acidosis. Some degree of cerebral oedema is always present due to hyperosmolarity, acidosis and electrolyte imbalance.

Management: The principles of management of DKA in a child are prompt recognition of the problem, adequate but cautious fluid replacement, provision of insulin, treatment of associated infections, careful monitoring of glucose, electrolytes, vitals and blood gases in an intensive care unit and prevention of complications in particular cerebral edema. During the management of DKA, first priority is to replenish fluids. The initial fluid should be an isotonic solution like normal saline. Subsequent fluid can be normal or half normal dextrose saline or ringer lactate solution. It is important not to infuse hypotonic fluid as it increases the chance of cerebral edema. The speed of fluid replenishment is a critical factor in determining cerebral edema and hence overzealous fluid replacement in too short a time is best avoided. Insulin infusion is the gold standard of insulin delivery. Subcutaneous insulin should be avoided because acidosis leads to cutaneous vasoconstriction and insulin does not get absorbed in a reliable manner from subcutaneous sites. Studies have shown that there is not much benefit of giving intravenous bolus of insulin at the beginning of therapy either. Since insulin deficiency is the primary pathology in type 1 diabetes and particularly in DKA, it is best not to titrate insulin infusion with the blood glucose level but to titrate the amount of glucose that is infused so that adequate amount of insulin and substrate (glucose) is provided to the child. It is also necessary to saturate insulin-binding sites on the tubing by running about 50 ml of insulin infusion through the tubing before starting the infusate. It is important not to stop insulin infusion early based on the glucose value alone. It must ideally be continued for about 12-24 hours after acidosis has resolved and ketone bodies have disappeared. If the blood glucose continues to fall, glucose concentration of the infusate can be increased from 5% to 10% mixed with half normal saline instead of normal saline so that osmolality of the infusate is maintained. With adequate insulin and glucose, lactate gets converted into bicarbonate in liver thus resolving acidosis. Measurement of ketone bodies in the urine can be tricky. Keto Diastix, which are routinely used for measurement of ketones in the urine do not measure beta-hydroxybutyrate but are sensitive to acetone and acetoacetic acid. In the initial phase of DKA as there is more beta-hydroxybutyrate in the urine, the test may be weakly positive and as the patient improves and more of acetone and acetoacetic acid starts coming out in the urine the test becomes strongly positive giving a false impression of deterioration of the patient's condition. There is no role for routine use of bicarbonate in DKA. Metabolic acidosis, which is often profound, should not be treated with bicarbonate as it usually settles down with adequate fluid and insulin therapy. When fluid and insulin are provided ketones and lactic acid are metabolized to bicarbonate thus correcting the acidosis. Bicarbonate on the other hand worsens cerebral acidosis, leads to hypernatremia and hypokalemia and this leads to poor oxygen delivery to the tissues due to shift of the oxygen dissociation curve. Cerebral edema is the most dangerous complication of DKA and is often precipitated by overzealous fluid replacement. Therefore slow rehydration over 36 hours is recommended. Isotonic and not hypotonic fluids should be used for rehydration. Other complications include electrolyte imbalances and hypoglycemia, these can be prevented by careful monitoring.


Total fluids replaced is a combination of maintenance + deficit + ongoing losses.

Maintenance: 1500 ml/m2/day at all ages

Deficit: 5-10% generally 10% is assumed as the clinical signs of dehydration are less pronounced.

Ongoing losses: Urine output + loss in the vomitus and gastric aspirate

Type: Calculate the total fluid for a period of 36 hours. Initial fluid should be normal saline or ringer lactate. In the first 1-2 hrs the fluid is given at a rate of 10-20 mls per kg to stabilize the circulation. When the blood sugar drops to 200 mg%, add 5% dextrose to the fluid so that risk of hypoglycemia is reduced. Total fluid replacement should be divided as 1/3 in the first 6 hours, next third in the next 12 hours and next third in the next 18 hours (Total 36 hours)


Potassium:Total body potassium is always depleted. Potassium replacement should be started after the initial hour (after the rapid fluid correction is over). It can be started even earlier if the initial potassium is lower than 3 mmol/l. In places where urgent electrolytes are not available, Electrocardiogram should be used to monitor T wave abnormalities. Amount of potassium administration should be 20-30 mmol/l of fluids infused. Ideally potassium should be replaced as half phosphate and half chloride, but this is a problem in India as phosphate containing infusate is not available.

Only when the serum pH <7.0, there is symptomatic hyperkalemia and poor myocardial contractility and insulin resistance, bicarbonate may be used with caution only as slow infusate and never as bolus. WHEN GIVEN IT SHOULD BE GIVEN AS A SLOW IV INFUSION OVER A PERIOD OF 2-4 HOURS and NEVER AS BOLUS Half correction is recommended.

Insulin therapy: Infusion is made as 50 units of short or ultrashort acting insulin (e.g. regular insulin or Lispro) in 500 ml of normal saline and initial 50-60 ml is run off through the tubing to saturate binding sites. Infusion is then given through an infusion pump. INSULIN INFUSION MUST BE CONTINUED UNTIL ACIDOSIS RESOLVES and NOT when sugars are controlled. Half hour before the infusion is discontinued subcutaneous regular insulin is given in a dose of 0.25 iu/kg. The dose of insulin infusion is 0.1 unit/kg/hr.

Monitoring Schedule:
Initial investigations: Glucose, electrolytes, blood gas, creatinine, serum osmolarity, blood count and culture. Subsequent schedule: Glucose: 1-2 hourly Electrolytes: 1-2 hourly, ABG: At 2,4,6,12 and 24 hours Consciousness: (Using a scale like Glasgow coma) should be monitored 2 hourly.

Complications of fluid and electrolyte therapy:
Brain edema

How to suspect brain edema?
Deterioration in the level of consciousness in a child who was improving, bradycardia and other signs of raised ICT and convulsions point to the possibility of brain edema.

Prevention of brain edema:
Slow rehydration over 36-48 hours
Use of isotonic solutions for rehydration
Avoid hypotonic or hypertonic solutions (such as bicarbonate bolus)
Early detection by vigilance

Treatment of Developing Brain Edema:
Manitol 20% i.v. in a dose of 0.5 to 1 gm/kg may be repeated every 15 minutes if necessary
Reduce rate of fluid input
Nurse the child in bed-up position
Assisted ventilation


Hypoglycemia is a common problem encountered in PICU and NICU. Hypoglycemia is diagnosed when blood glucose drops to below 40 mg/dl (2.2 mmol/l) in a neonate and to 50 mg/dl (2.7 mmol/l) thereafter. Hypoglycemia is not a diagnosis by itself but is a manifestation of a variety of metabolic and endocrine disorders. It can be symptomatic or asymptomatic. The serum or plasma level of blood glucose tends to be 12-15 percent higher than the whole blood glucose. Contrary to the general belief, asymptomatic hypoglycemia is as dangerous as symptomatic variety and should be investigated and treated with the same seriousness as the symptomatic form.

Etiology can broadly be divided into those caused by substrate deficiency such as malnutrition, malabsorption, poor hepatic stores etc, decreased production or release of glucose such as defects of the counter-regulatory hormone secretion and hereditary metabolic defects and finally excessive utilization such as hyperinsulinemia.

Clinical Features:
Clinical features of hypoglycemia are usually non-specific especially in the neonatal period. In neonate these include lethargy, jitteriness, apnea, cyanosis, respiratory distress, poor feeding, hypothermia, myoclonic jerks or convulsions. In older children adrenergic hormone release in response to hypoglycemia dominate the symptoms in the form of sweating, tremors, hunger, pallor, tachycardia and shakiness followed by symptoms of neuroglycopenia in the form of sleepiness, lethargy, visual difficulty, ataxia, behavioral abnormalities and frank convulsions or unconsciousness. In cases where hypoglycemia is prolonged and severe, permanent brain damage results.

The most important investigation for the etiological diagnosis is the collection of 'critical sample'. Blood sample taken during the episode of hypoglycemia is the critical sample. The next immediate urine sample should also be analyzed. Following tests should be done on urine and blood.

Blood tests:
  • Glucose
  • Acetone
  • Cortisol
  • Growth hormone
  • Insulin
  • Free fatty acids
  • Lactate and Pyruvate

Urine tests:
  • Ketone bodies
  • Reducing substance
  • Amino acids and organic acids

Approach to Diagnosis of Hypoglycemia:
Broadly speaking, hypoglycemia can be divided into 2 categories: Ketotic and Non-Ketotic depending upon the presence or absence of ketones in the serum and or urine. Non-Ketotic hypoglycemia is usually caused by either hyperinsulinism or by oxidation defects such as carnitine deficiency. Ketotic hypoglycemia can be due to many more causes. Presence of hepatomegaly in Ketotic hypoglycemia suggests glycogen storage disease (such as glucose 6 phosphatase deficiency) and other metabolic defects and specific enzyme assays are necessary for the diagnosis. In Ketotic hypoglycemia, without hepatomegaly endocrine deficiencies such as growth hormone deficiency, adrenal failure and hypothyroidism should be suspected.

Immediate management consists of intravenous bolus of 10% dextrose in a dose of 2-2.5ml per kg slowly after collecting the 'critical sample'. Blood glucose is checked after 5 minutes and if there is no improvement in the blood glucose concentration, another bolus of 10% dextrose in given. The concentration of dextrose should not exceed 10%. Twenty five (25%) dextrose SHOULD NOT BE USED. Hypertonic solutions like this can cause permanent brain damage and must be avoided.

The bolus is then followed by intravenous infusion of dextrose that will give a glucose concentration of 4-8 mg/kg/minute. In cases of refractory hypoglycemia, Hydrocortisone can be used in a dose of 5 mg/kg/24 hours in 8 hourly divided doses. Intramuscular growth hormone in a dose of 1 mg (3 IU) can be used in unresponsive cases.

If and if the critical sample has not been useful in making the diagnosis, a hypoglycemia provocation by starvation under controlled environment can be undertaken by admitting the child to special endocrine units.

Hypocalcemia, like hypoglycemia is more common in neonatal period and infancy although it can occur at any time of life. The symptoms of hypocalcemia are caused by disturbance in neuromuscular excitability due to reduction in the extracellular calcium pool.

Hypocalcemia in the neonatal period:
Hypocalcemia which is common in the neonatal period is mainly seen two forms: early and late. Early neonatal hypocalcemia is typically seen in sick, low birth weight and preterm neonates usually before 72 hours of life. It is caused by transient inability of the parathyroid glands to respond to dropping calcium. Other causes such as transfusion of blood containing high phosphate also contribute to this variety of hypocalcemia.
Hypocalcemia beyond the neonatal period: This is usually seen after first 2 weeks of life in apparently healthy newborn and is associated with hyperphosphatemia. This is caused by transient relative hypoparathyroidism.

Total and ionic Calcium, serum protein
In places where ionic calcium is unavailable, serum proteins are very important to get a correct idea about the true calcium. The correction used for 1 gm of albumin is 0.8 mg of calcium. Eg if albumin is less by 1 gm, add 0.8 mg to the measured calcium value.
Phosphorus and alkaline phosphatase
Parathyroid hormone
Vitamin D level (25 OH D3 is usually sufficient)
Wrist and chest x rays are useful for the diagnosis of rickets, Hyperparathyroidism, renal osteodystrophy etc.

In crisis, 1-2 ml/kg of 10% cal gluconate is given by intravenous infusion over 5 min under cardiac monitoring. This is then followed by i.v. calcium infusion in a dose of 50-75 mg/kg/day of elemental calcium. The dose is reduced to ½ after 24 hrs. Oral calcium can be given in the dose of 100 to 200 mg per kg day in the newborn. Oral calcium and phosphate should preferably be given in a proportion of 2:1 for better absorption.

In neonates and children with transient or permanent hypoparathyroidism, 1-25 (OH2) vitamin D3 may be necessary to improve the calcium levels rapidly. In cases of resistant hypocalcemia, after the sample is collected for calcium, phosphorus, alkaline phosphatase, PTH and Vitamin D, 1-25 (OH2) vitamin D3 may be given in a dose of 0.25 to 4 mcg in 3-4 divided doses orally. There is however no role of 1-25 (OH2) vitamin D3 in routine management of hypocalcemia. Typically in hypoparathyroid patients, the hypocalcemia is very severe, phosphate is significantly elevated and hypocalcemia is resistant to routine management of calcium infusion and regular vitamin D3 supplements.

Addisonian Crisis:
Adrenal failure is usually gradual but manifests acutely due a precipitating cause such as infection, stress or trauma. Irrespective of the etiology of adrenal crisis, the manifestations of acute adrenal failure are similar.

Clinical Features:
After an initial period of failure to thrive, patient may suddenly present with vomiting, lethargy, anorexia, and dehydration. Circulatory collapse may be fatal. The patient suddenly becomes cyanotic, the skin is cold, and the pulse is weak and rapid. The blood pressure falls, and respirations are rapid and labored. In the absence of immediate and intensive therapy, the course can be fatal. The presenting manifestations may be those of hypoglycemia, particularly in the neonate with congenital adrenal hyperplasia. Patients with adrenocortical insufficiency are deficient in gluconeogenic substrates; the hypoglycemia may therefore be associated with ketosis and confused with ketotic hypoglycemia.

Clinical signs such as hyperpigmentation or hypopigmented patches, ambiguous genitalia, asthenic appearance, muscular hypertrophy (in X linked 21p deletions), midline craniofacial defects and achalasia, alacrimia (in case of Triple A syndrome) should increase the suspicion of adrenal insufficiency in an acutely ill child.

Laboratory: Typically the Sodium is low and potassium is high. Neonates can tolerated a very high level of potassium and levels up to 9-10 mmol/l can also be tolerated for a short period of time. Hypoglycemia and metabolic acidosis are common accompaniments. In an older child, X ray of the chest may show a small heart suggesting hypovolemia. Plain X ray of the abdomen may show calcified adrenals in case of adrenal hemorrhage. CT scan and MRI may be helpful. Measuring cortisol, ACTH, 17 hydroxyprogesterone, Aldosterone and renin levels during crisis are useful in making the definitive diagnosis.

Management: Injection hydrocortisone in a dose of 5 mg per kg in 6 hourly doses should be given after collecting the blood for endocrine assays. Even in children with salt wasting crisis this dose of hydrocortisone will prevent salt loss due to its mineralocorticoid action in high dose. Patient can be maintained later on a dose of 12-15 mg/m²/day of hydrocortisone and 100 mcg per m² of fludrocortisone (Both available in India by Samarth Pharma ltd). After the patient is out of ICU a detailed investigation into the etiology of adrenal pathology should be undertaken.

Thyroid storm (iv):
Thyroid storm is rare in children. It is an acute, potentially life-threatening syndrome of thyroid hormone excess which is often precipitated by stress such as infection or surgery. This represents decompensated state of hyperthyroidism that results from increased serum levels of free thyroid hormone however free thyroid hormone levels cannot differentiate between thyroid storm and hyperthyroidism. There is hypercatabolic and hyperdynamic state characterized by vasodilatation, increased cardiac output, heart failure, arrhythmia, diarrhoea, nausea, vomiting, abdominal pain, hyperthermia and CNS disturbances.

Differential diagnosis of this condition includes sepsis, malignant hyperthermia, pheochromocytoma, cocaine intoxication and pancreatitis. Laboratory evaluation shows grossly suppressed TSH (Third or fourth generation assay is necessary), elevated total and free thyroid hormones, hyperglycemia, increased alkaline phosphatase, increased liver transaminase and leukocytosis.

Early diagnosis with high index of suspicion is necessary as mortality can be high in this condition. Aggressive supportive care and treatment of underlying precipitating cause is necessary. Treatment consists of controlling temperature with acetaminophen, fluids and cooling the body. Salicylates are avoided as they displace thyroid hormone from binding proteins. Propylthiouracil (PTU) in the dose of 5-10 mg per kg per day is the medication of choice. Lugol's iodine which gives total iodine of 135 mg/ml is used in a dose of 0.1 to 0.3 ml (10-40 mg) three times daily diluted with water or milk. It should be given 2 hours after PTU to avoid worsening of symptoms. Beta-blockers such as propranolol are important to control adrenergic symptoms. Corticosteroids such as hydrocortisone and dexamethasone are useful as they prevent the conversion of T4 to T3 and may also prevent adrenal crisis in a patient with co-existing undiagnosed hypoadrenalism.

Pheochromocytoma (v ):
Hypertensive crisis in PICU can be caused by Pheochromocytoma. The treatment consists of removal of the tumour and exquisite blood control is mandatory before opertion can be undertaken. Hypertension should be controlled pre-operative with á adrenergic blockers such as phenoxybenzamine in a dose of 0.5 - 1 mg/kg/12 hours or Prazosin in a dose of 0.1-0.4 mg/kg/day in 6 hourly divided doses. Sodium nitroprusside can also be used as infusion at a rate of 1 mcg/kg/min. â blockers such as propranolol may be used to control tachycardia and arrhythmia after á blockade is established. Use of beta-blockers without prior use of alpha blockers can lead to severe hypertension. Alpha blockers are used 2 weeks prior to surgery to minimize the risk of hypertensive crisis that may occur during intubation, induction of anesthesia and tumour handling. Hypovolemia should be corrected with volume expanders post-operatively and by replacing fluid losses.

Blood pressure should be monitored closely during surgery and hypertension should be treated with sodium nitroprusside or phentolamine. Tachycardia and arrhythmia is controlled by use of beta-blockers. If both adrenal glands are removed, hydrocortisone should be used. Blood pressure may not return to normal until 2-3 days of surgery. Hypoglycemia should be prevented by close glucose monitoring.

Peri-operative management of Diabetes Insipidus (vi,vii,viii,ix):
Brain tumour surgery especially in the area of pituitary and hypothalamus can lead to diabetes insipidus in the peri-operative and post-operative period. The commonest tumour in pediatric practice that is associated with this complication is craniopharyngioma.

As cortisol has a permissive role on water clearance, DI often manifests only after adequate cortisol replacement is done. DI can be a temporary phenomenon; hence administration of DDAVP post-operatively should be monitored with extreme caution for the fear of water intoxication. DI usually manifests within 6-12 hours of surgery, lasts for 1-2 days and then recovers for 1-2 days only to return in the majority of patients in 3-5 days. The transient recovery is due to lysis and release of Anti-diuretic hormone (ADH) stored in neuronal cells containing ADH. This triphasic response needs effective management by meticulous assessment of fluid input and output and regular monitoring of electrolytes. In the immediate post-operative period, hourly urine output should not exceed 100-150 ml/m². The urine output can be controlled by using DDAVP. In some patients due to injury to the hypothalamus, a permanent state of adipsic DI leading to chronic hypernatremia and hyperosmolality may develop, which is difficult to manage. As the patient has no thirst, a fixed schedule of replacement and a flexible schedule for DDAVP varying according to the environmental temperature in needed.

Syndrome of Inappropriate ADH:
In children who are acutely unwell with conditions such as pneumonia or meningitis, syndrome of inappropriate ADH is observed. This leads to excessive water reabsorption for the distal convoluted tubule leading to hyponatremia, hypocalcemia and swelling. Water intoxication is seen clinically as edema, altered sensorium and even convulsions. In contrast to adrenal failure, here the sodium is low but the potassium is not high. The urine output is inappropriately low for the clinically edematous child. Diagnosis is made by combined assessment of urinary and serum osmolarity. Serum osmolarity is usually below 265 mmol/l and the urine osmolarity is high at the same time, usually above 800 mmol/l.

SIADH is treated by fluid restriction to about two third of the maintenance amount and other supportive care. If brain oedema is severe and fluid overload is very significant frusemide can be used. Hypertonic saline can be used to correct hyponatremia. When used it should be used over 2-3 hours as infusion.

Cerebral salt wasting (x):

In acute and rarely chronic brain injury, an increase in urinary sodium excretion is seen with increased urinary volume. The urinary loss of sodium is often>100 meq/l. It could be because of increased secretion of atrial natriuretic peptide. It differs from SIADH by increased urinary volume, dehydration and increased urinary loss of sodium. ADH levels are low in cerebral salt wasting while they are high in SIADH.

Management consists of volume by volume replacement of fluids with normal saline and if needed 3% saline. Oral supplementation of sodium chloride will be needed. Some researchers have successfully used mineralocorticoids to treat this condition although it may not always be effective.
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