Overview

Definition:
-Hypopituitarism is a rare endocrine disorder characterized by the deficiency of one or more pituitary hormones
-In pediatrics, growth hormone (GH) deficiency leads to impaired growth, while ACTH deficiency results in adrenal insufficiency, a potentially life-threatening condition.
Epidemiology:
-The prevalence of pediatric hypopituitarism is estimated to be around 1 in 3,000 to 1 in 10,000 live births
-GH deficiency is the most common pituitary hormone deficiency, occurring in approximately 1 in 4,000 children
-ACTH deficiency is less common but more acutely dangerous.
Clinical Significance:
-Undiagnosed or inadequately managed hypopituitarism can lead to severe growth failure, metabolic disturbances, and life-threatening adrenal crisis
-Early diagnosis and appropriate hormone replacement are crucial for normal development, growth, and overall well-being, directly impacting patient outcomes and resident preparedness for critical care scenarios.

Clinical Presentation

Symptoms:
-Growth hormone deficiency symptoms: Short stature, significantly below the 3rd percentile
-Slow growth velocity (less than 5 cm/year after age 2-3)
-Proportional short stature is typical
-ACTH deficiency symptoms: In infants, hypoglycemia, poor feeding, vomiting, lethargy, and failure to thrive
-In older children, pallor, fatigue, weight loss, abdominal pain, and recurrent infections
-Signs of adrenal crisis: Hypotension, shock, fever, confusion, or coma.
Signs:
-Growth hormone deficiency signs: Proportional short stature
-Younger appearance than chronological age
-High-pitched voice
-Central obesity may be present
-ACTH deficiency signs: Pale or grayish skin
-Hypotension
-Bradycardia (relative to fever)
-Signs of dehydration
-Evidence of other pituitary hormone deficiencies (e.g., hypothyroidism, hypogonadism).
Diagnostic Criteria:
-Diagnosis is based on clinical suspicion, confirmed by endocrine testing
-Low IGF-1 and IGFBP-3 levels in children with short stature suggest GH deficiency
-Provocative testing (e.g., insulin tolerance test, glucagon stimulation test, arginine-GHRH test) is required to confirm GH deficiency
-ACTH deficiency is diagnosed by low cortisol levels and unresponsiveness to ACTH stimulation testing.

Diagnostic Approach

History Taking:
-Detailed birth history (macrosomia, birth asphyxia, CNS malformations)
-Developmental milestones
-Growth pattern assessment (serial height/weight measurements)
-History of head trauma, CNS infections, radiation, or surgery
-Family history of endocrine disorders or short stature
-Symptoms suggestive of adrenal insufficiency: recurrent vomiting, failure to thrive, recurrent infections, hypoglycemia.
Physical Examination:
-Accurate measurement of height, weight, and head circumference
-Calculation of BMI and plotting on growth charts
-Assessment of growth velocity
-Examination for dysmorphic features suggestive of congenital syndromes
-Palpation for thyromegaly
-Assessment of pubertal development
-Evaluation for signs of dehydration, pallor, or hypotension.
Investigations:
-Initial investigations: Complete blood count (CBC), electrolytes, blood urea nitrogen (BUN), creatinine, calcium, phosphate, glucose
-Thyroid function tests (TSH, free T4)
-Liver function tests
-Insulin-like growth factor-1 (IGF-1) and IGF-binding protein-3 (IGFBP-3) levels
-Provocative testing for GH deficiency (e.g., ITT, glucagon test, GHRH-arginine test), aiming for a peak GH < 10 ng/mL
-ACTH stimulation test (e.g., cosyntropin stimulation test): Measure baseline cortisol and 30/60-minute cortisol after synthetic ACTH 1-24 administration
-A peak cortisol < 18-20 mcg/dL (500-550 nmol/L) confirms adrenal insufficiency
-Pituitary MRI: To identify structural abnormalities (tumors, cysts, congenital malformations) or absence of the pituitary gland.
Differential Diagnosis:
-For short stature: Familial short stature, constitutional delay of growth and puberty, nutritional deficiencies, chronic illnesses (renal, cardiac, GI), skeletal dysplasias, hypothyroidism, Cushing’s syndrome, psychosocial dwarfism
-For ACTH deficiency: Other causes of adrenal insufficiency (e.g., congenital adrenal hyperplasia, autoimmune adrenalitis), severe sepsis, dehydration, hypovolemic shock.

Management

Initial Management:
-For adrenal crisis: Immediate intravenous fluid resuscitation with normal saline, intravenous hydrocortisone (100 mg/m² as bolus, then continuous infusion or repeated boluses), and correction of hypoglycemia with dextrose
-Prompt transfer to ICU if unstable
-Once stabilized, determine the etiology of hypopituitarism
-For GH deficiency: Hormone replacement should only be initiated after other life-threatening deficiencies (especially ACTH) have been addressed.
Medical Management:
-Growth hormone replacement: Recombinant human growth hormone (rhGH) administered subcutaneously, typically once daily
-Dosing is usually 0.025-0.05 mg/kg/day (0.06-0.12 IU/kg/day), adjusted based on growth response and biochemical markers
-Adrenal replacement: Hydrocortisone is the drug of choice for cortisol replacement in children
-Dosing is typically 8-10 mg/m²/day, divided into 2-3 doses, with the largest dose in the morning
-Stress dosing is crucial during illness or injury
-Fludrocortisone may be needed if mineralocorticoid deficiency is present.
Surgical Management:
-Surgical intervention is indicated for pituitary tumors (e.g., craniopharyngioma, adenoma) or other structural lesions causing hypopituitarism
-Transsphenoidal surgery is the preferred approach for most pituitary adenomas
-Craniopharyngiomas may require transfrontal or transsphenoidal approaches
-Surgery aims to remove the tumor and decompress the optic pathways, but may also lead to further pituitary damage
-Radiotherapy may be considered for residual tumor or unresectable lesions.
Supportive Care:
-Regular monitoring of growth parameters, IGF-1 levels, and bone age
-Close monitoring for signs of adrenal insufficiency, especially during illness
-Education of parents and patient regarding stress dosing of hydrocortisone and emergency preparedness
-Nutritional assessment and support
-Psychosocial support for the child and family
-Regular follow-up with pediatric endocrinology team.

Complications

Early Complications:
-Adrenal crisis, which can be fatal if not recognized and treated promptly
-Electrolyte imbalances (hyponatremia, hyperkalemia) due to ACTH deficiency
-Severe hypoglycemia due to ACTH or GH deficiency
-Severe dehydration.
Late Complications:
-Failure to achieve adequate adult height despite GH replacement
-Development of other pituitary hormone deficiencies (hypogonadism, hypothyroidism, diabetes insipidus) over time
-Impaired bone density and increased fracture risk
-Psychological issues related to short stature or chronic illness
-Increased risk of cardiovascular disease in untreated GH deficiency
-Complications related to pituitary surgery or radiotherapy (e.g., visual impairment, new hormone deficiencies, recurrence of tumor).
Prevention Strategies:
-Strict adherence to hormone replacement therapy schedules
-Thorough education of patients and families on stress dosing protocols for hydrocortisone and recognition of adrenal crisis symptoms
-Regular medical follow-ups to monitor growth, hormone levels, and overall health
-Prompt management of intercurrent illnesses
-Screening for other pituitary hormone deficiencies
-Careful surgical planning and post-operative care for pituitary tumors.

Prognosis

Factors Affecting Prognosis:
-The underlying etiology of hypopituitarism
-The extent of pituitary hormone deficiencies
-The age at diagnosis and initiation of treatment
-Adherence to treatment regimens
-The presence and management of complications such as adrenal crisis
-Success of surgical intervention for pituitary tumors.
Outcomes:
-With appropriate GH replacement, children can achieve significant improvements in growth velocity and final adult height, though typically not reaching the mid-parental target height
-Adequate glucocorticoid replacement is life-saving
-Patients with isolated GH deficiency generally have a good prognosis for growth
-Patients with multiple pituitary hormone deficiencies require lifelong hormone replacement and vigilant monitoring
-Prognosis for pituitary tumors depends on the tumor type, size, and extent of resection.
Follow Up:
-Lifelong follow-up with an endocrinologist is essential
-GH replacement therapy is typically continued through adolescence and sometimes into adulthood if GH deficiency persists
-Regular assessments of growth, puberty, bone health, and psychosocial adjustment
-Monitoring for new pituitary hormone deficiencies and the potential recurrence of pituitary tumors
-Education regarding the need for medical alert bracelets and carrying emergency hydrocortisone.

Key Points

Exam Focus:
-Recognize the signs and symptoms of GH and ACTH deficiency in pediatric patients
-Understand the indications and interpretation of provocative endocrine tests for GH and ACTH
-Be proficient in the medical management of adrenal crisis and chronic adrenal insufficiency (stress dosing)
-Grasp the principles of GH replacement therapy (dosing, monitoring)
-Differentiate hypopituitarism from other causes of short stature and adrenal insufficiency.
Clinical Pearls:
-Always rule out ACTH deficiency first in a child with suspected hypopituitarism, as it is a medical emergency
-Infants with unexplained hypoglycemia, vomiting, and poor weight gain should be screened for adrenal insufficiency
-Growth hormone therapy is indicated for confirmed GH deficiency with a growth failure
-it is NOT for short stature of other etiologies without GH deficiency
-Patients on hydrocortisone must be educated about stress dosing: double the dose for mild illness, triple for moderate, and IV hydrocortisone for severe illness/vomiting.
Common Mistakes:
-Initiating GH therapy before ruling out and treating ACTH deficiency
-Underestimating the severity of adrenal crisis or failing to initiate prompt treatment
-Inadequate stress dosing of hydrocortisone during illness
-Relying solely on IGF-1 levels without provocative testing for GH deficiency diagnosis
-Failure to consider structural lesions (tumors) as a cause of hypopituitarism, especially in older children or those with other neurological signs.