Diabetes Insipidus

Production of arginine vasopressin – by magnocellular neurons in the supraoptic and paraventricular nuclei of the hypothalamus.  Transported to the neurohypophysis via hypothalamo-hypophyseal tract.  Injury to these structures leads to DI.

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Triphasic response in DI:

  1. First phase – DI caused by “stunning” of the magnocellular neurons, no AVP secretion.
  2. Second phase – injured hypothalamic cells degenerate and release their stored AVP
  3. Third phase – if majority of these neurons are destroyed, permanent phase of DI begins

 

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Reference:

Schreckinger, Matthew, Nicholas Szerlip, and Sandeep Mittal. “Diabetes Insipidus Following Resection Of Pituitary Tumors”. Clinical Neurology and Neurosurgery 115.2 (2013): 121-126.

 

 

RANDOM NOTES ON Diabetes insipidus (DI)

Nephrogenic DI – renal insensitivity to vasopressin, acquired or genetic; lithium

Central DI – deficiency in production of ADH

  • Related to extent of excision
  • Usually transient phenomenon after surgery
  • SIADH in second phase – follow serum Na on day 7
  • Symptoms: polyuria, nocturia, polydipsia / thirst

 

Patients with DI, especially if drowsy and unable to maintain adequate fluid intake, can rapidly become dehydrated.


 

ALGORITHM:

Measure Is and Os hourly, sum every 6 hours

Foley catheter

Onset of dilute polyuria UOP >250cc/hr x2  hours

Check other reasons:

  1. diuretics
  2. large resuscitation
  3. mannitol
  4. hyperglycemic
  5. salt wasting

Labs

  1. USG <1.005
  2. UOsm 50-200 (<serum)
  3. Hypernatremia

? rountine serum Na – every 6 hours on day 1, then every 12h until stable, then daily x 1 week

Replace fluids

  1. normal saline to replace previous hour output, switch to 0.45% saline if UO 4-6ml/kg/h, switch to D5W if >6 ml/kg/h
  2. if awake, fluids ad libidum; may be able to maintain fluid balance by drinking to satiety, still DDAVP so patients can sleep comfortably at night

DDAVP (1-desamino-8-D-argnine vasopressin)

  • DDAVP: activates V2R – water reabsorption in kidney; mobilizes water channel aquaporin to luminal membrane of DCT and CD
  • Liquid form – given intranasal; oral tablet form; parenteral form

 

  Tablets Spray Solution for injection
Dose comparison 100 mcg 2.5 mcg N/A
200 mcg 5 mcg Less than 0.5 mcg
400 mcg 10 mcg Less than 1 mcg

 

  • Usual dose 1 ug q12h
  • Empiric – give minimum dose required to control polyuria; goal to control nocturia, partial control of polyuria during the day
  • Water retention à hyponatremia is a potential risk; patient education, serum NaHS

 

ENDOCRINE

Post-op complications: hematomas, epistaxis, HCP, CSF leaks, meningitis

Preop labs with hypopituitarism – stress doses of hormonal replacement; keep on physiological dose until outpatient assessment

Lab tests post-op for evidence of early endocrinological remission

Cushing – no steroids unless necessary; serum cortisol q6h until nadir; if <5 + symptoms, start glucocorticoid therapy and then transition to maintenance doses until outpatient reassessment

Normal cortisol function prior to surgery – no steroids; assess post-o with AM fasting cortisol on POD1 or POD2; new start steroid replacement if cortisol <10 until reassessed outpatient

Acromegaly – POD1 serum GH level predicts early remission; delayed IGF1 level 6 weeks after

Prolactinomas – POD 1 AM prolactin level normalizes with remission

 

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