Diabetes Insipidus - 1 Nursing CE

Author: Kristi Hudson RN MSN CCRN

Written: March 19, 2005

Updated: August 31, 2009

Course Objectives

Upon completion of this course, the student will be able to:

·         Differentiate between Neurogenic and Nephrogenic Diabetes Insipidus

·         List 2 causes of Diabetes Insipidus

·         Explain necessary lab findings that assist in the diagnosis DI

·         State the correct dosing for DDAVP

·         Discuss 3 important nursing interventions when caring for a patient with DI

Definition

Diabetes Insipidus is a condition of decreased secretion of Anti-Diuretic Hormone (ADH) from the Posterior Pituitary Gland or the inability of kidneys to synthesize or absorb ADH.

Types of Diabetes Insipidus

Central Neurogenic Diabetes Insipidus– This type of DI is due to destruction of the Posterior Pituitary Gland which results in an absence of Anti-Diuretic Hormone. Central Neurogenic Diabetes Insipidus can further be broken down into four types which include:

• Classical Severe DI – failure to synthesize or release ADH
• Defective Osmoreceptor DI – in which high plasma osmolality fails to trigger the release of ADH
• Reset Osmoreceptor DI – in which the release of ADH only occurs after plasma osmolality is higher then the usual threshold
• Partial DI – in which the amount of ADH that is released is lower then required

Nephrogenic Diabetes Insipidus – Though uncommon, NDI can be acquired through drug toxicity (lithium, gentamycin, amphotericin B or Lasix). It can be differentiated from Central Neurogenic Diabetes Insipidus in that it does not respond when DDAVP is administered.

Causes

Central Neurogenic Diabetes Insipidus may be neurogenic or idiopathic. Specific causes include:

·         Primary Brain Tumor (30%)

·         Head Trauma (17%)

·         Neurosurgery (9%)

·         Metastatic Carcinoma (8%)

·         Intracranial Hemorrhage (6%)

·         Granulomatous Disease (5%)

·         Idiopathic Diabetes Insipidus (25%)

NOTE: The presence of DI is common in brain death especially when hemodynamic and respiratory support is continued in order to implement the organ donor process.

Pathophysiology

ADH is the primary determinant of free water excretion in the body. Its main target is the kidney, where it acts by altering the water permeability of the cortical and medullary collecting tubules. Water is reabsorbed by osmotic equilibration with the hypertonic interstitium and returned to the systemic circulation. The actions of ADH are mediated through at least 2 receptors—V1 mediates vasoconstriction, enhancement of corticotrophin release, and renal prostaglandin synthesis; V2 mediates the antidiuretic response.

Diagnosis

·   Clinical Findings for Diabetes Insipidus include:

·   Polyuria

·   Urine Specific Gravity less than 1.005

·   Plasma osmolality increases--typically to greater than 300 mOsm/kg (normal is 280-295 mOsm/kg)

·   Urine osmolality decreases--typically to less than 200 mOsm/kg (normal, 300-1,000 mOsm/kg)

·   Elevated serum electrolytes are common

·   Signs and Symptoms of dehydration

Medical Treatment

Pharmaceutical therapy for diabetes insipidus includes subcutaneous, nasal, and oral preparations of vasopressin analogues such as:

Desmopressin acetate (DDAVP)

·   DDAVP is a synthetic analogue of the natural pituitary hormone 8-arginine vasopressin (ADH), an antidiuretic hormone affecting renal water conservation

·   DDAVP increases cellular permeability of collecting ducts, resulting in reabsorption of water by kidneys

·   DDAVP has an onset time of 1 hour

·   Dosage for DDAVP must be individualized and is supplied:

o       Parenteral (4 mcg/mL)

o       Nasal (100 mcg/mL rhinal tube)

o       PO (0.1- and 0.2-mg tab) preparations

Ad·         

Adult Doses:

·         0.5 mU (0.0005 unit) per /kg/h IV continuous infusion initially

·         Dilute in 0.9% NaCl or 5% glucose to 0.1-1 U/mL

·         Dosage may be doubled q30min prn; not to exceed 10 mU/kg/h

·         5-10 U IM/SC bid/qid prn; not to exceed 60 U/d

Vasopressin (Pitressin)

·   Vasopressin has vasopressor and antidiuretic hormone (ADH) activity

·   Vasopressin increases water reabsorption at distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout vascular bed of renal tubular epithelium (vasopressor effects)

·   Vasopressin increases vasoconstriction in splanchnic, portal, coronary, cerebral,   peripheral, pulmonary, and intrahepatic vessels

·         Only the aqueous preparation of Vasopressin should be used as it has a short half-life

·         Vasopressin tannate in oil, which has a longer action, should not be used

Adult Doses:

·         0.5 mU (0.0005 unit) per /kg/h IV continuous infusion initially

·         Dilute in 0.9% NaCl or 5% glucose to 0.1-1 U/mL

·         Dosage may be doubled q30min prn; not to exceed 10 mU/kg/h

·         5-10 U IM/SC bid/qid prn; not to exceed 60 U/d

Other Medical Treatment includes:

• Urine Replacement
• Avoid Hyperglycemia
• Avoid Fluid Overload
• Correct Hypernatremia (reduce sodium by 0.5 mmol/L/hour)
• Correct Other Electrolyte Imbalances

Nursing Care and Management

·         Obtain baseline plasma/serum osmolality levels

·         Weigh patient (loss of 2 kg is thought to be significant)

·         Q 1 hour urine output

·         Q 2 hour urine specific gravity

·         Q 1 hour vital signs

·         Monitor for fluid volume overload/deficit

·         Monitor hypotension/hypertension/tachycardia

·         If DDAVP is administered, re-check urine osmolality 1 hour after administration and compare to baseline

·         To differentiate Neurogenic DI from Nephrogenic DI, remember that Nephrogenic DI will not respond to DDAVP

Possible Nursing Diagnosis