Neurosurgery notes/Other specialities/ITU/Endocrine/Hypernatremia/Central Diabetes Insipidus (CDI)

Central Diabetes Insipidus (CDI)

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Hypernatremia

Definition

  • Excretion of large volumes of dilute urine (polyuria) due to vasopressin (ADH) deficiency.
  • Polyuria is characterised by a urine volume in excess of
    • 2 l/m2/24 h or approximately 150 ml/kg/24 h at birth,
    • 100-110 ml/kg/24 h until the age of 2 years
    • 40-50 ml/kg/24 h in an older child or adult.

Numbers

  • Newer conservative surgical treatments like endoscopic transsphenoidal surgery and cyst decompression with or without intracystic treatment have been introduced to reduce morbidities.
    • This has led to less postoperative endocrine complications like permanent CDI, now seen in 50-55% of patients after conservative surgery combined with radiation surgery [14], as compared to 60-90% of patients with aggressive surgery.
  • CDI is a common postoperative complication that occurs in 83% of patients with intrasellar and parasellar tumours

Test

  • Paired plasma and urine osmolality and electrolytes should be tested immediately postoperatively and every 8 h, but changes in plasma sodium of >5 mmol/l will require more frequent testing (every 4 to 6 hours)
  • Water deprivation test
      • Post-Dehydration Serum Osmolality
      Post-Dehydration Urine Osmolality
      Post-DDAVP Urine Osmolality
      Diagnosis
      280-90
      >750
      Do not give DDAVP
      Normal
      >290-300<
      <300
      <300
      Nephrogenic DI
      >290-300<
      <300
      >750
      Cranial DI
      >290-300<
      300-750
      >750
      Partial cranial DI
      <290
      300-750
      300-750
      Partial nephrogenic DI, chronic psychogenic polydipsia
      <290
      300-750
      >750
      Psychogenic polydipsia
    • Technique
      • Serial 2 hourly measurement of serum and urine osmolality (and body weight) over a water deprivation period of 6-8 h
      • If serum osmolality > 290 and urine < 300 by the end it is suggestive of DI and DDAVP is given. If kidneys are functioning normally, DDAVP should cause a rise in urine osmolality to > 750 suggesting a cranial (failure of posterior pituitary vasopressin secretion, as in this case) cause for the DI.
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Diagnostic criteria Post op CDI

  • Textbook criteria
      1. Increased plasma osmolality >300 mosm/kg
      1. Increased urine output >2.5 ml/kg/h for 2 consecutive hours
      1. Urine osmolality <200 mosm/kg
      1. Urine/plasma osmolality ratio <1
          • Urine Specific Gravity (USG) determined by both reagent strip and refractometry has a correlation of approximately 0.75 with urine osmolality
          • This relationship between the specific gravity and osmolality is disturbed when the urine contains an abnormal solute, such as glucose or protein.
          • USG is also affected by temperature, with urine density decreasing (lower USG) with increasing temperature.
  • Working criteria
    • U.O. >250 ml/hr for 1–2 hrs + SG< 1.005 (usually < 1.003) (dilute urine) +/- inc. of serum Na+.

Mechanisms

  • Diabetes insipidus cannot occur in primary adrenal insufficiency (hypocortisolism/hypoaldosteronism) because mineralocorticoid activity is required for kidneys to produce free water
  • Urine output patterns: follows one of three patterns
    • Transient DI: lasts for 12–36 hrs post-op then normalizes
    • “Prolonged” DI: lasts months, or rarely may be permanent
    • “Triphasic response” (least common).
      • 3 stages:
          1. Transient CDI
              • DI (short duration): due to injury to posterior pituitary
              • Partial or complete pituitary stalk section, which damages the connection between the cell bodies of ADH-secreting neurons in the hypothalamus and their nerve terminals in the posterior pituitary gland, which prevents ADH secretion.
              • Within 24 -48 hrs of surgery can last for 5 days
              • Caused by a temporary dysfunction of ADH-producing neurons due to
                • Oedema due to trauma to the connections between the magnocellular cell bodies and the nerve terminals in the posterior pituitary
                • Axonal shock from perturbations in the vascular supply to the pituitary stalk and posterior pituitary
          1. SIADH
              • Normalization or SIADH-like picture:
              • Due to release ofADH from neuron endings form hypothalamus.
              • It is during this phase that there is a risk of severe iatrogenic hyponatremia from overtreatment initiated during the initial DI phase
              • Caused by an uncontrolled release of ADH into the blood stream from the degenerating nerve terminals in the posterior pituitary.
              • Can last for 2- 14 days
                • Partial or limited damage to some axons connected to the posterior pituitary may be associated with isolated second phase SIADH due to the uncontrolled release of accumulated ADH resulting in transient asymptomatic or symptomatic hyponatremia
          1. DI (long-term)
              • Within 2 wks
              • After all of the ADH stored in the posterior pituitary gland has been released, a third phase of diabetes insipidus develops if more than 80-90% of ADH-secreting neuronal cell bodies in the hypothalamus have degenerated.
              • Depletion of ADH due to the degeneration of hypothalamic ADH-secreting neuronal cell bodies
              • A major determinant of whether CDI following transection of the pituitary stalk is permanent or not is related to how close the level of the lesion is to the ADH-secreting neurons' cell bodies in the hypothalamus
notion image
DP: desmopressin
DP: desmopressin

Risk factors

  • Large tumours damaging the ADH-secreting neurons
  • Radical surgical excision with pituitary stalk resection.
    • Endoscopic transsphenoidal surgery and cyst decompression with or without intracystic treatment + Radiotherapy
      • Post op Permanent CDI, 50-55%
        • VS 60-90% of patients with aggressive surgery.
  • Young age
  • Male gender
  • CSF leak
  • Resection of certain types of lesions including
    • Craniopharyngiomas
    • Rathke's cleft cysts
    • ACTH-secreting pituitary adenomas

Differential

  • Intra-operative fluid overload also presents with hypo-osmolar polyuria.
  • Glycosuria and hyperglycaemia, especially if the patient is on dexamethasone.

Management

  • If DI develops
  • Check patient has intact thirst mechanism
    • If intact thirst mechanisms and able to drink
      • Often have a craving for ice-cold water and increased thirst if the thirst mechanism is intact.
      • Patient may not develop hypernatraemia and hyperosmolality.
      • Match UO with oral and IV intake;
    • If not intact thirst mechanism or not able to keep up with fluid loss
      • As long as fluids are replaced, CDI is not life-threatening.
      • Patient need to be encouraged to drink and should be offered drinks regularly.
      • Fluid losses in excess of the maintenance fluid rates minus insensible losses (300 ml/body surface area in m2) should be replaced volume for volume by calculating and matching the fluid balance at least 6 hourly
        • Fluids can be replacement
          • Urinary fluid loss
            • Water given orally or via a nasogastric tube or
            • 0.45% saline intravenously in eunatraemic patients.
          • Non-urinary fluid loss
            • Replaced with 0.9% saline.
        • If UO rate is too high for IV/PO replacement (> 300 ml/hr/4hrs or > 500 cc/hr/2hrs), check urine S.G. and if< 1.005 then give a vasopressin preparation
          • 5U aqueous vasopressin (Pitressin®) IVP/IM/SQq 6 hrs PRN
          • Desmopressin (DDAVP®) injection SQ/IV titrated to UO.
            • Usual adult dose: 0.5–1ml (2–4 mcg) daily in 2 divided doses
            • Desmopressin
              • Given to reduce the total daily fluid intake/output.
              • Adults
                • PRN Desmopressin
                  • Dosage
                    • Initial dose of
                      • 50-100 μg (tablets) orally,
                      • 5-10 μg intranasally or
                      • 30-60 μg sublingually.
                    • Each subsequent dose of DP should be given after the demonstration of
                      • Dilute urine with an osmolality <200 mosm/l OR
                      • A specific gravity <1.005, AND
                      • A urine output of >2.5 ml/kg/h for >2 h.
                  • Treatment causes reduction in urine output, with the effect lasting for 6-18 h, and doses should be titrated according to the daily total urine output.
                  • To minimize the risk of water intoxication and Hyponatremia in resolving transient CDI, DP should be given on an ‘as-required basis' until it is established that the CDI is permanent.
                  • If the route of administration needs to be changed for any other reason, the dosages of the different forms of DP are not directly interchangeable.
                    • Dosage equivalency when changing routes of administration: 1 mcg IV/SC/IM = 10 mcg intranasal = 100-200 mcg oral
                • Regular Desmopressin
                  • Should only be prescribed when CDI is stable and permanent.
                  • The aim of the treatment is to ameliorate polyuria and polydipsia, not to entirely normalise daily fluid intake.
                  • Once a day, breakthrough polyuria before dosing should be encouraged to avoid water intoxication.
                  • If Hyponatremia occurs during Desmopressin therapy, the Desmopressin dose should be withheld until the sodium level normalises.
                    • If Desmopressin is continued or if excreted free water is continued to be replaced, this can lead to cerebral oedema.
          • When nasal packs out,
            • Intranasal DDAVP (100 mcg/ml): range 0.1–0.4 ml (10–40 mcg)
            • Intranasally BID (typically 0.2 ml BID) PRN
          • Clofibrate (Atromid S®) 500mg PO QID (does not always work)
  • Paediatric (intensive care setting)
    • Low dose DP (0.1-0.2 μg s.c./i.m) OR
    • Dilute arginine ADH (0.25-3 mU/kg/h) by a continuous intravenous infusion is often used in the first 24-48 h postoperatively.
      • Arginine ADH has a short half-life (10-20 min), and its therapeutic effects dissipate quickly once the infusion is stopped.
      • Intravenous arginine ADH infusion also increases blood pressure.
    • The continuous infusion needs close monitoring of the fluid balance and electrolytes and frequent titration of the infusion rate to achieve the desired fluid output.
    • Prolonged use of arginine ADH may result in antibody formation and in a shortened duration of action of the drug

Reference