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SIADH Diabetes Insipidus

Cerebral Salt Wasting

Disorders of Antidiuretic Hormone (ADH)

Tandy Aye, M.D Assistant Professor, Pediatric Endocrinology

Vasopressin (ADH) is the principal regulator of plasma osmolality.

· 9 amino acid peptide · Synthesized in the paraventricular and supraoptic nuclei of the hypothalamus · Transported to the posterior pituitary by axonal projections · Secreted by the posterior pituitary · Half life in the circulation is 5-10 minutes · Works via the V2 receptor in the kidney

ADH changes water permeability in the apical membranes of the collecting duct cells

From Saul Leif, Dept of Integrative Physiology, University of Colorado

Regulation of vasopressin secretion

· Rate of vasopressin release depends

mainly upon plasma osmolality and intravascular volume.

· Plasma osmolality calculated by:

Osm=(2)(Na) + Glucose/18 + BUN/2.8

· Normal blood osmolality ranges between

280-290 mOsm/kg H20

Plasma Osmolality and Vasopressin Level

· #1 Controlling Factor!!! · Osmoreceptors ­ HIGHLY sensitive · Plasma osmolality of 280mmol/L is the set point for ADH release

Vasopressin responds less to baroreceptors

Baroreceptors located in

left atrium carotid sinus aortic arch

Change in volume of 5-10% needed for action.

Sensation of thirst is also regulated

· Mediated by angiotensin II · May not be same osmosensors · Threshold for thirst is at 293 mOsm/kg · Immediately after water ingestion, before ·

any change in blood osmolality or volume, vasopressin concentrations fall and thirst ceases Related to coldness and volume of ingested fluid.

Sperling, Pediatric Endocrinology 2nd Ed.

When the System Fails!

Failure of water homeostasis can result from inadequacy of either AVP-dependent water conservation or thirst-mediated water acquisition

DI VS. SIADH

Clinical Presentation

The primary symptoms · EXCESSIVE THIRST · POLYDIPSIA · POLYURIA · (NOCTURIA and possible NOCTURNAL ENURESIS)

· · · ·

In infants - often masked and may present as FTT, unexplained fevers, vomiting and constipation. Children are INCONSOLABLE if fluid is withheld

Preference for ice-water, helps their chronic thirst, they avoid high-salt foods IF NO WATER > CNS manifestations

DDx of Polyuria and Polydipsia

· Diabetes Insipidus "tasteless water"

­ Central

· Genetic (autosomal dominant) · Acquired

­ Trauma ­ Congenital ­ Drugs -Neoplasms -Infiltrative -Autoimmune -Infectious

Trauma and Surgery

·

The triphasic phenomenon · Neurosurgery (20%) · Trauma (15%) Accidental head trauma: DI within 24hr · In 50-60% spontaneously resolves · Patients can osmoregulate ­ if water intake via intact thirst mechanism · Water intoxication

·

Tumors and Infiltrative Diseases ·

Pituitary and hypothalamic tumors · Craniopharyngioma - visual disturbances and ant. pituitary deficiency before DI · Germinomas - DI is frequently the first symptom presenting · Gliomas Histiocytosis · accounts for majority of infiltrated diseases causing DI · About 50% present with DI · The DI is permanent in almost all cases, even after medical

therapy

·

Further evaluation

· MRI ­ head

­ Look for the bright spot ­ Thickening of the pituitary stalk ­ Tumor/mass

· Infection:

meningitis/encephalitis

http://3d-brain.ki.se/mri/mri-pictures/pituitary

DDx of Polyuria and Polydipsia

· Diabetes Insipidus

­ Central · Genetic (autosomal dominant) · Acquired

­ Trauma ­ Congenital ­ Drugs -Neoplasms -Infiltrative -Autoimmune -Infectious

­ Nephrogenic · Genetic · Acquired

­ Hypercalcemia ­ Drugs -Hypokalemia -Kidney disease

· Primary Polydipsia · Diabetes Mellitus

Chemical Mediators: What Alters Renal Responsiveness to Vasopressin??

· Increase ADH action

­ ­ ­ ­ Chlorpropamide Carbamazepine Chronic dehydration Non-steroidal anti-inflammatory

· Decrease ADH action

­ ­ ­ ­ ­ ­ ­ ­ ­ alpha-Adrenergic agents Atrial natriuretic peptide PGE2 Hypokalemia Hypercalcemia Protein kinase C Lithium Demeclocycline Ethanol!!!

DI Diagnosis - Simple

·

Paired Morning plasma and urine osmolality with urine specific gravity and serum sodium

­ Hypotonic urine = specific gravity of 1.005 or less and urine osmolality < than 200 mmol/L ­ High serum Osmolality (> than 287 mOsm/L) ­ Hypernatremia (> 150 mEq/L)

­ In psychogenic or other thirst order, then sodium will be low or normal with low serum osmolality. Response to Vasopressin central disease

DI Diagnosis - Complex

GOLD STANDARD is Water Deprivation Test

· Monitor every 30 mins Weight ­ Vital sign ­ Serum Na, OSM ­ Urine NA, OSM, specific gravity, volume/hour

· If serum osm >300, Na <145, urine osm <600, continue. · If urine osm >1000 or >600 and stable stop test Normal. · If serum osm>300 and urine <600 = Diabetes Insipidus. ­ Administer DDAVP · Urine output decrease · Urine osmolality should double within next hour = Central DI · Partial response = Nephrogenic DI

· Monitor every hour plasma vasopressin level

Treatment

· Pts with intact thirst mechanism can be · · · ·

treated with free access to oral fluids but rather inconvenient (also hydroureter) Fluids alone in neonates and infants Fluids alone should be considered postoperatively DDAVP (Replacement of L-arginine w/ D-arginine)

DDAVP Treatment options

Potency IV/SubQ, intranasal, PO (1:10:100)

An option in the PICU

· History of DI · Strong suspicion of DI · Vasopressin Drip

Treatment

· Fluid Management ­ follow

electrolytes/osmolality, I's/O's, daily or BID weight

­ administer fluids at a rate to reduce serum sodium concentration by 0.5 mEq/L/hr ­ Water deficit = 0.6 × BW × ([Na+ ] - 140)/140

· Demyelinating encephalopathy

· Too rapid correction with hypotonic fluid > cerebral edema

SIADH

· Syndrome of Inappropriate Antidiuretic Hormone

(SIADH) Clinically normovolemic patient Without renal or adrenal disease Has low serum sodium and osmolality excretes an inappropriately concentrated urine with high sodium content

Serum Sodium/ Osmolality Urine Sodium/ Osmolality

Clinical Presentation · · ·

Typically arises along with associated pathology Normal or decreased urine output, euvolemia CNS Sx

­ ­ ­ ­ ­ ­ ­ ­ ­ ­ ­ Lethargy Restlessness Confusion Edema (rare) Anorexia N/Vomiting Headache Irritability Seizures Coma Asymptomatic

Etiology of SIADH

INTRATHORACIC

Bronchial carcinoma Mediastinal malignancies Pneumonitis Acute respiratory failure

NERVOUS SYSTEM

Hydrocephalus Trauma Hemorrhage Encephalitis Meningitis Demyelinating disease Other inflammatory causes

DRUGS

ADH amplification (Chlorpropramide) Carbamazepine Chemotherapy Nicotine Phenothiazide Tricyclics

OTHERS

Malignancies,intestinal etc Leukemia

Diagnosis ·

Paired plasma and urine osmolality and sodium; Vasopressin Level

­ ­ ­ ­ Hypertonic urine with urine osmolality > than 200 mmol/L Low serum Osmolality Hyponatremia High Vasopressin Level

·

Fluid Restriction

Cerebral Salt Wasting ­ Possible Hyponatremia with increased

urine output and sodium loss, hypovolemia, decreased vasopressin

Treatment (Standard)

· Correct body water osmolality and restore

cell volume to normal

Raising the ratio of sodium to water in the ECF Diagnostic and therapeutic maneuver - water restriction. Restricted to 600 to 800 mL/m2 daily If SIADH

a 2- to 3-kg weight loss correction of hyponatremia cessation of salt wasting

Treatment (Severe) ·

Severe hyponatremia - 120 to 125 mmol/L and CNS manifestations requires immediate treatment Slow infusion of 3% NaCl 3-5ml/kg with Furosemide therapy to maintain diuresis and excrete dilute urine Long-term correction with fluid restriction for next 48hr Rapid correction > central pontine myelinolysis In chronic SIADH - Very few treatment options available Demeclocycline Fludrocortisone (Florinef)

·

Putting It All Together

DI Serum High Na Serum Osmola High lity Urine Low Na Urine Osmola Low lity Urine Specifi Low c grav SIADH Low Low High High

High

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