DIABETES INSIPIDUS (DI)
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🧀Absence/ ineffectiveness of ADH to concentrate urine
🧀Leads to the passage of a large volume of inappropriately dilute urine with a consequent rise of plasma osmolality (due to disproportionate loss of water over sodium) and progressive dehydration.
DIAGNOSIS
🧀DI is present when the urine output is excessive, the urine osmolality is inappropriately low relative to serum osmolality (which is above normal because of water loss), and the urine specific gravity is less
🧀Polyuria (more than 4 ml/kg/hr in children, more than 6 ml/kg/hr in neonates or, in an adult >250 mL/hour or 4 to 14 L/day) of dilute urine
🧀Dehydration
🧀Hypernatremia
🧀increased serum osmolality (>295 mOsm/kg)
🧀decreased urine osmolality (<300 mOsm/kg)
🧀decreased urine specific gravity (<1.002-1.005)
TREATMENT
Hydration
🧀The amount and content of intravenous fluids are guided by urine volume, serum electrolytes and serum osmolality.
🧀 If fluid is replaced early, it is not necessary to administer free water (D5W). Rather, a hypotonic solution such as 0.45% sodium chloride (NaCl) or lactated Ringer's may be given.
🧀 Insulin and potassium supplementation might be required when dextrose-containing fluids are used, especially if corticosteroids are used concomitantly. Give appropriate potassium supplementation.
Hormonal
🧀 If the urine output is >250-300 mL/hour for 2 hours hormonal treatment is given
🧀 Desmopressin (DDAVP), a synthetic analog of the natural hormone arginine vasopressin, is available as intranasal, oral, or IV forms.
✔️The intranasal preparation of DDAVP delivers a 10 ug dose per spray, and doses of 10-30 ug per day are usually effective.
✔️The IV form (4 ug/mL) is given IV, intramuscularly (IM), or subcutaneously in doses of 0.5–2 ug every 8–12 hours as needed.
✔️Oral tablets (0.1–0.2 mg) in doses of 0.1–1.2 mg/day can also be given to obtain adequate diuresis.
✔️Vasopressin can be given subcutaneously in doses of 4–10 units every 6 hours as needed for urine output exceeding 250 mL.
✔️Alternatively, a continuous infusion can be used, as the half-life of vasopressin given IV is only 20 minutes. A dose of 0.008 – 0.04 units/kg/hour is usually effective
🧀 Once intravascular volume has been restored, persistent hypernatremia may be treated with thiazide diuretics, such as hydrochlorothiazide, 50 to 100 mg/day i.v.
Syndrome of inappropriate antidiuretic hormone secretion (SIADH).
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🧀Various cerebral pathologic processes (mostly head trauma) can cause excessive release of ADH, which leads to the continued renal excretion of sodium (>20 mEq/L), despite hyponatremia and associated hypo osmolality.
🧀 The key findings are urinary sodium loss without corresponding loss of water, leading to a decrease in plasma osmolality in the presence of hypertonic urine.
Urine osmolality is therefore high relative to serum osmolality.
🧀 Blood urea nitrogen (BUN) and serum creatinine are normal and serum uric acid is generally low.
TREATMENT
🧀 The mainstay is fluid restriction to 1,000 mL/24 hours of iso-osmolar solution.
🧀 If hyponatremia is severe (<110 to 115 mEq/L), the administration of hypertonic (3% to 5%) saline and furosemide might be appropriate. Because rapid correction of hyponatremia has been associated with the occurrence of central pontine myelinolysis, restoring serum sodium at a rate of approximately 2 mEq/L/hour is advisable.
Cerebral Salt Wasting Syndrome (CSWS)
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🧀 It is renal loss of sodium due to intracranial disease, leading to hyponatremia and hypovolemia.
🧀 Raised levels of circulating ANP and BNP mediate, increased natriuresis and hyponatremia in acute brain injury
🧀 CSWS is predominantly associated with SAH but has also been described in conjunction with TBI, glioma, and tuberculous or carcinomatous meningitis.
🧀 The key distinction to be made is that patients with CSWS are clinically hypovolemic compared with the euvolemic or slightly hypervolemic status of patients with SIADH. Patients with CSWS may have abnormally elevated BUN greater than creatinine, increased hematocrit, and increased serum uric acid.
DO U KNOW❓
🧀 Hypothyroidism is another important consideration in patients with hyponatremia following pituitary surgery. It may even occur in patients who are partially treated.
🧀 decreased cardiac output (with stimulation of baroreceptors leading to increased ADH release), decreased clearance of ADH, or resetting of the osmostat may all contribute (ref : Postoperative Care Following Pituitary Surgery, Journal of Intensive Care Medicine 20(3); 2005, P:134)
ADDITIONAL EXPLANATION: DI
🧀 In neurologic practice, it is particularly associated with pituitary surgery,Traumatic Brain Injury and anterior communicating artery aneurysmal SAH.Patients who become brain dead often develop severe DI and this is relevant in the management of potential organ donors.
🧀 Diuresis of solute may also be caused by osmotic diuresis secondary to the use of mannitol or hypertonic saline, for control of intracranial pressure, or hyperglycemia.
🧀 DONT DO THIS❗️Excess fluids are sometimes administered intravenously during the perioperative period, which are then excreted appropriately postoperatively. If this large postoperative diuresis is matched with continued intravenous fluid infusions, an incorrect diagnosis of DI may be made based on the resulting hypotonic polyuria. Therefore, if the serum [Na] is not elevated concomitantly with the polyuria, the rate of parenterally administered fluid should be slowed with careful monitoring of the serum [Na] and urine output until a diagnosis of DI can be confirmed by continued hypotonic polyuria in the presence of hypernatremia or hyperosmolality.
ADDITIONAL EXPLANATION: SIADH
🧀 The most common causes in the neurologic group include meningitis/encephalitis, brain tumor, SAH, and TBI.
🧀 Also reported following spinal surgery.
🧀 Drug-related hyponatremia secondary to the antiepileptic drugs carbamazepine and oxcarbamazepine
#anaesthesia ,#neurosurgery , #endocrinology ,#pituitary , #DiabetesInsipidus , #desmopressin , #siadh
REFERENCE:
Endocrinol Metab Clin N Am 37 (2008) 213–234Disorders of Water and Salt Metabolism Associated with Pituitary Disease Jennifer A., Joseph G. Verbalis
Newfield, Philippa; Cottrell, James E., Handbook of Neuroanesthesia, 4th Edition
Disturbances of Sodium in Critically Ill Adult Neurologic Patients A Clinical Review Martin Tisdall, MRCS, Matthew Crocker,Jonathan Watkiss and Martin Smith, (J Neurosurg Anesthesiol 2006;18:57–63)
