Diabetes Insipidus following Traumatic Brain Injury

OVERVIEW

• Diabetes insipidus (DI) results from decreased secretion and action of anti-diuretic hormone (ADH)
• ADH is produced in the hypothalamus and transported to the posterior pituitary gland
• ADH is released into the circulation in response to thirst, increased plasma osmolarity and hypotension
• It is a key hormone involved in water regulation and the defence of blood volume

MECHANISMS

In a head injured patient decreased production and secretion of ADH can result from:

1. direct disruption of the hypothalamus or pituitary
2. interruption of the blood supply to these parts of the brain
3. increased ICP or oedema causing herniation of the brain and subsequent compression of the pituitary stalk or gland

Consequences of decreased ADH action

• decreased H2O reabsorption in the collecting ducts of nephron
• decreased Na+ reabsorption
• increased K+ secretion
• decreased GFR from relaxation of mesanglial cells in glomerulus
• contraction of intravascular volume (dehydration and hypovolaemia)
• polyuria
• loss of tone in vascular tree causing hypotension
• decreased aldosterone secretion
  -> decreased Na+ reabsorption, increased K+ loss
• decreased angiotensin II
  -> vasodilation, decreased nordrenaline secretion from post-ganglionic sympathetic neurons, decreased thirst sensation, decreased ADH secretion

DIAGNOSIS

• polyuria
• high serum Na+
• low serum K+
• high plasma osmolality
• high urinary Na+ (inappropriate)
• high K+
• low urine osmolality (inappropriate)
• low plasma ADH level
• worsening of biochemical markers with fluid restriction
• improvement in biochemical markers and polyuria with desmopressin treatment
• MRI to quantify anatomical integrity of hypothalamus and cerebral blood flow may be required to confirm diagnosis

Diabetes Insipidus following Traumatic Brain Injury

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Diabetes Insipidus following Traumatic Brain Injury 2015-05-16T02:00:00-07:00 Rating: 4.5 Diposkan Oleh: Unknown