Approach to Polyuria in Children... Dr.Padmesh

49,668 views 29 slides Dec 01, 2011
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Approach to Polyuria in children


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Approach to polyuria Dr.Padmesh.V

Definition of Polyuria : Urine output > 5 ml/kg/hr Or > 2 L/m2/day Definition of Oliguria : Urine output < 0.5 – 1 ml/kg/hr Or < 300 ml/m2/day

Surface area = Ht ( c m) X Wt ( k g) 3600 ( Daily insensible water loss = 300-400 ml/m2 )

CAUSES OF POLYURIA: 1 . INCREASED FLUID INTAKE 2 . INCREASED URINARY SOLUTE EXCRETION 3 . IMPAIRED URINARY CONCENTRATION

CAUSES OF POLYURIA: 1. INCREASED FLUID INTAKE 1.Iatrogenic 2.Compulsive water drinking (Psychogenic polydipsia ) 2. INCREASED URINARY SOLUTE EXCRETION OSMOTIC DIURESIS: 1.Diabetes mellitus 2.Mannitol treatment SALT LOSS: 1.Adrenal insufficiency 2.Diuretics 3.Cerebral salt wasting 4.Aldosterone resistance 3. IMPAIRED URINARY CONCENTRATION INEFFICIENT ADH ACTION: (DIABETES INSIPIDUS): 1.CENTRAL (NEUROGENIC) DIABETES INSIPIDUS: 2.NEPHROGENIC DIABETES INSIPIDUS: RENAL DISORDERS: 1.Renal Tubular acidosis 2.Bartter Syndrome 3.Gitelman Syndrome

CAUSES OF POLYURIA: 1. INCREASED FLUID INTAKE: Iatrogenic Compulsive water drinking (Psychogenic polydipsia )

CAUSES OF POLYURIA: 2. INCREASED URINARY SOLUTE EXCRETION: OSMOTIC DIURESIS: 1.Diabetes mellitus 2.Mannitol treatment SALT LOSS: 1.Adrenal insufficiency 2.Diuretics 3.Cerebral salt wasting 4.Aldosterone resistance

CAUSES OF POLYURIA: 3. IMPAIRED URINARY CONCENTRATION: INEFFICIENT ADH ACTION: (DIABETES INSIPIDUS): 1.CENTRAL (NEUROGENIC) DIABETES INSIPIDUS: 2.NEPHROGENIC DIABETES INSIPIDUS: RENAL DISORDERS: 1.Renal Tubular acidosis 2.Bartter Syndrome 3.Gitelman Syndrome

CAUSES OF POLYURIA: 3. IMPAIRED URINARY CONCENTRATION: INEFFICIENT ADH ACTION: (DIABETES INSIPIDUS): 1.CENTRAL (NEUROGENIC) DIABETES INSIPIDUS: -Genetic defects: AR, AD, Wolfram DIDMOAD Synd. -Malformations: Septo -optic dysplasia, Holoprosencephaly,Anencephaly . -Neurological insults: Head trauma, Neurosurgery, Infection,Brain death. -Infiltrative disorders: Sarcoidosis , Histiocytosis . -CNS tumors: Craniopharyngioma , Germinoma , Pinealoma

CAUSES OF POLYURIA: 3. IMPAIRED URINARY CONCENTRATION: INEFFICIENT ADH ACTION: (DIABETES INSIPIDUS): 2.NEPHROGENIC DIABETES INSIPIDUS: -Genetic: XL (V2 receptor defect), AR, AD ( Aquaporin defect) -Acquired: Hypokalemia , Hypercalcemia , Obstructive uropathy , Nephrocalcinosis .

APPROACH TO POLYURIA: 1.HISTORY 2.CLINICAL EXAMINATION 3.INVESTIGATIONS

HISTORY: Age of onset: Congenital / Acquired H/O fever: UTI Failure to thrive: DM, Nephrogenic D.I, RTA, CAH, Bartter H/O head trauma,neurosurgery : Central D.I H/O meningitis: Central D.I

HISTORY: contd … H/O weight loss: DM, RTA H/O rash,seborrhea : Histiocytosis H/O muscle weakness: Hypokalemia - RTA, Bartter H/O drug intake: Mannitol , Diuretics, out-dated Tetracyclines .

HISTORY: contd … Symptoms of increased ICT: CNS tumors H/O polyuria , shock in newborn period: CAH H/O constipation,paresthesia : Hypercalcemia H/O psychological problems: Psychogenic polydipsia H/O abdominal cramps, arthralgia , etc: Sickle cell anemia

CLINICAL EXAMINATION: Anthropometry: To r/o Failure to thrive : DM, DI, RTA, CAH Fever: UTI Mental retardation: CNS malformations Neurological deficits: CNS pathologies

CLINICAL EXAMINATION: Genital ambiguity: CAH Mid line defects: Central D.I Features of Rickets: Renal Tubular Acidosis, Renal failure Acidotic breathing: RTA

CLINICAL EXAMINATION: Rash, Seborrhea, ear discharge: Histiocytosis Hyperpigmentation : Adrenal insufficiency Muscle weakness,neck flop: Hypokalemia : RTA, Bartter Also look for signs of dehydration, shock..

INVESTIGATIONS: 24 hour urine output >5ml/kg/hr or >2L/m2/day POLYURIA Further investigations

INVESTIGATIONS: Contd … Urine examination for: WBCs: UTI Sugar: D.M Specific gravity: <1.005 – D.I Urine Osmolality : <300 mOsm /kg- D.I

INVESTIGATIONS: Contd … Urea, Creatinine Serum Electrolytes Calcium Blood gas analysis Blood glucose Plasma Osmolality

INVESTIGATIONS: Contd … High Plasma Osmolality >300 mOsm /kg Low Urine Osmolality <300 mOsm /kg Urine Sp.gravity < 1.005 Serum Sodium > 145 mmol /L Serum Osmolality <270 Urine Osmolality >600 mOsm /kg Urine Sp.gravity >1.010 D.I D.I unlikely

INVESTIGATIONS: Contd … High Plasma Osmolality >300 mOsm /kg Low Urine Osmolality <300 mOsm /kg Urine Sp.gravity < 1.005 Serum Sodium > 145 mmol /L Serum Osmolality <270 Urine Osmolality >600 mOsm /kg Urine Sp.gravity >1.010 D.I D.I unlikely

INVESTIGATIONS: Contd … High Plasma Osmolality < 300 mOsm /kg WATER DEPRIVATION TEST Serum Osmolality > 270

WATER DEPRIVATION TEST -Determines ability of kidneys to concentrate urine. -Useful in the diagnosis of DI. -Requires careful supervision because dehydration and hypernatremia may occur.   

WATER DEPRIVATION TEST : Method: Begin the test after a 24-hr period of adequate hydration & stable weight. Obtain a baseline weight after bladder emptying. Restrict fluids for 7 hours . Measure body weight and urine specific gravity and volume hourly. Check serum Na + and urine and serum osmolality every 2 hr. Terminate the test if weight loss approaches 5%.

WATER DEPRIVATION TEST: Interpretation: Normal individuals & Psychogenic DI: Central or Nephrogenic DI: When water is deprived Will concentrate urine (to 500-1400 mOsm /L) Urine osmolality remains <150-300 mOsm /L Plasma osmolality will be 288-291 mOsm Plasma Osmolality > 300 mOsm Urine specific gravity rises to at least 1.010 Urine Specific gravity remains <1.005 Urine volume decreases significantly No significant reduction of urine volume There will be no appreciable weight loss. Weight loss of up to 5% usually occurs

VASOPRESSIN RESPONSE TEST: To differentiate CENTRAL D.I from NEPHROGENIC D.I Baseline Urine osmolality is recorded Vasopressin injection given Urine Osmolality measured at 1 hr & 4 hrs after injection Increase in urine osmolality >50% increase from baseline <50% increase from baseline CENTRAL D.I NEPHROGENIC D.I

OTHER TESTS: Central D.I: MRI of hypothalamic-pituitary region Nephrogenic D.I: Renal imaging Genetic Studies as required.

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