Diabetes Insipidus

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Diabetes Insipidus

• Cindy A. Fehr
• Malaspina University-College
• BSN Program
• NRSG 335
• Fall 2005

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Renal Failure Reviewed

• Acute Renal Failure
• When kidneys fail suddenly
• Function usually returns to normal if renal
  system supported, sometimes require dialysis in
  short-term
• Chronic Renal Failure
• Slow progressive deterioration of kidney
  function
• Usually irreversible when nephrons stop working
• Causes ? diabetes, HTN
• When functioning reaches lt 10-20 normal rate ?
  called End Stage Renal Disease ? dialysis or
  transplantation required

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Renal Failure Reviewed

• ADH
• Produced in hypothalamus stored in posterior
  pituitary
• Causes fluid retention or lack of diuresis
• Also known as vasopressin in large amounts ?
  constricts arterioles
• Released in response to ? circulating volume
  (dehydration, ? plasma osmolality, hypotension,
  hypoxia associated with hypovolemia raises ADH
  release)
• Acts by conserving H2O to ? blood volume BP
  return serum osmolality to normal

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Diabetes Insipidus

• Definition
• lack of ADH production or release or use,
  depending on type of DI
• Characteristics regardless of cause, SS same
• polyuria (excessive dilute urination) gt 2L/day
• Polydipsia
• If left untreated ? changes in LOC, tachycardia,
  tachypnea, hypotension (shock-like symptoms), but
  unlike hypovolemic shock, u/o ?
• Can lead to hypernatremia ? restlessness,
  agitation, ? deep tendon reflexes, seizures
• Prevention
• No specific preventive measure for initial
  disturbance
• Prevention of repeat occurrences by treating,
  preventing cause

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Diabetes Insipidus-Types

• Neurogenic/Central DI
• d/t insufficient amounts ADH ? synthesis,
  transportation, release
• hypothalamus doesnt produce enough ADH or
  posterior pituitary doesnt release ADH
• Most frequently seen
• Causes anything that can affect brains ability
  to release ADH
• Congenital
• CNS disorders tumors (pituitary or brain),
  infections
• Cerebrovascular disease or cerebral trauma
• Well recognized complication of closed head
  injury
• Cerebral surgery near the hypothalamohypophysial
  tract
• pregnancy

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Diabetes Insipidus-Types cont.

• Nephrogenic DI
• inadequate renal response to ADH
• ADH produced normally but distal tubules
  collecting ducts cant respond to hormones
  signal to reabsorb H2O
• ADH levels normal or high
• Collecting ducts dont ? permeability in response
  to ADH
• Causes
• Congenital genetics familial
• Renal obstruction or damage (pyelonephritis,
  polycystic disease, amyloidosis)
• Chronic kidney disease or end organ failure
• Medications (lithium, demeclocycline, anesthetic
  methoxyflurane) that damage renal tubules
  (reversible)
• Severe electrolyte disturbances
• Idiopathic with abrupt onset

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Diabetes Insipidus-Types cont.

• Psychogenic DI
• uncommon
• Causes
• Psychogenic disorders or disorders associated
  with abnormal thirst
• Eg. Water intoxication disorder which is
  associated with schizophrenia

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Patients at Risk of DI

• Head injuries
• Neurosurgery
• Pituitary tumors
• Inflammation or infection of brain tissues
• Those taking medications that inhibit AHD release
  or action on kidneys
• Ethanol
• Glucocorticoids
• Adrenergics
• Phenytoin
• Opiod antagonists
• Lithium

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insufficient ADH
What HappensDuring DI
immediate excretion large volumes dilute urine
urine specific gravity low
? plasma osmolality

• Unconscious Patients

Conscious Patients
Thirst mechanism stimulates polydipsia
Fluid ingestionlt requirements
Fluid ingestion or gt loss
Fluid ingestionlt requirements
Hypernatremia
Dehydration
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Signs Symptoms

• Change in mentation
• Insomnia
• Excessive thirst polydipsia
• Weight loss
• Urinary frequency polyuria 4-18 L/day
• Nocturia
• Skin, mucous membranes cool
• Low urine osmolality low urine specific gravity
• High normal plasma osmolality after 8 hrs H2O
  deprivation (keep in mind plasma osmolality
  always higher than urine)

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Diagnostics

• Correlating clinical presentation with serum
  osmolarity
• Plasma ADH levels
• Water deprivation test
• Dangerous because can cause those with DI, ?
  vascular volume ? circulatory collapse shock
• Without DI ? rapid ? urine volume
• With DI ? no ? urine volume urine osmolality
  100 mOsm/kg
• ADH test
• Differentiates between neurogenic and nephrogenic
  DI
• Challenged with ADH (usually DDAVP intranasally)
  u/o measured before after DDAVP
  administration
• Neurogenic DI ? kidneys respond by concentrating
  urine
• Nephrogenic DI ? kidneys cant concentrate urine

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Treatment Options

• Depends on cause and severity of disorder
• Neurogenic DI
• Based on extent of ADH deficiency, age, endocrine
  and cardiovascular status, lifestyle variables
• If symptomatic ? u/o gt 9L/day urine osmolality
  lt 100 mOsm/kg after dehydration or water
  restriction test
• ADH replacement (synthetic vasopressin analog
  DDAVP desmopressin, either po or intranasally)
• Why intranasally?
• No effect on smooth muscle, wont ? BP, less
  likely to cause arrhythmias
• Must monitor for fluid overload and hyponatremia
• Chlorpropamide (also helps ? thirst)
• Carbamazepine (similar effects to chlorpropamide)
• Indapamide (similar effects to thiazide
  diuretics)
• IM pitressin or Pituitrin (bovine extract with
  oxytocin vasopressin) with less side effects
• Vasopressin IV in emergency situations

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Treatment Options

• Nephrogenic DI
• Kidneys dont respond to ADH
• Do not respond to pharmacologic preparations of
  hormone
• Low salt diet
• May respond partially to thiazide diuretics which
  ? Na excretion by kidneys ? ? GFR ?
  reabsorption of H2O in proximal tubule rather
  than collecting duct (which is under ADH
  influence for H2O reabsorption)
• Incomplete ADH Deficiency
• Can maintain normal or near normal water balance
  when permitted to drink water in response to
  thirst
• Drugs that potentiate action of otherwise
  insufficient amounts endogenous ADH
• Chlorpropramide
• Thiazide diuretics

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Treatments Goals

• Assess, identify and begin treatment early
• Identify underlying cause/disorder treat
• Balance fluid intake with output
• Acute cases ? rapid fluid replacement
• Chronic cases ? slow replacement to prevent
  cerebral edema
• Replacement of ADH (IV, subcutaneous, intranasal)
  with DDAVP (desmopressin acetate) Sometimes need
  to remove pituitary gland
• Medications to stimulate production of ADH ?
  symptoms aggravating process
• Daily weights, accurate in/out, urine specific
  gravity, osmolality
• Age culturally appropriate information