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

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diabetes insipidus

Diabetes Insipidus

Cindy A. Fehr

Malaspina University-College

BSN Program

NRSG 335

Fall 2005

renal failure reviewed
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 < 10-20% normal rate  called End Stage Renal Disease  dialysis or transplantation required
renal failure reviewed4
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
diabetes insipidus5
Diabetes Insipidus
  • Definition
    • lack of ADH production or release or use, depending on type of DI
  • Characteristics– regardless of cause, S&S same
    • polyuria (excessive dilute urination) > 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
diabetes insipidus types
Diabetes Insipidus-Types
  • Neurogenic/Central DI
    • d/t insufficient amounts ADH  synthesis, transportation, release
    • hypothalamus doesn’t produce enough ADH or posterior pituitary doesn’t release ADH
    • Most frequently seen
    • Causes – anything that can affect brain’s 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
diabetes insipidus types cont
Diabetes Insipidus-Types cont.
  • Nephrogenic DI
    • inadequate renal response to ADH
    • ADH produced normally but distal tubules & collecting ducts can’t respond to hormone’s signal to reabsorb H2O
    • ADH levels normal or high
    • Collecting ducts don’t  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
diabetes insipidus types cont8
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
patients at risk of di
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 ****
insufficient adh
insufficient ADH

What HappensDuring DI

immediate excretion large volumes dilute urine & urine specific gravity low

Unconscious Patients

 plasma osmolality

Conscious Patients

Thirst mechanism stimulates polydipsia

Fluid ingestion< requirements

Fluid ingestion= or > loss

Fluid ingestion< requirements

Hypernatremia

Dehydration

signs symptoms
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)
diagnostics
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 can’t concentrate urine
treatment options
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 > 9L/day & urine osmolality < 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, won’t  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
treatment options14
Treatment Options
  • Nephrogenic DI
    • Kidneys don’t 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
treatments goals
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