Evaluation of Patients with Polyuria

Muhammad Faizi , Nur Rochmah

Clinical Lecturer of Pediatric Endocrine Div isio n
Sc hool of Medicine Airlang ga University – Dr. So eto mo Ho spital Surabaya.

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Introduction
Polyuria
▪ Adult → > 3 L/day.
▪ Children → > 2 L/m2 or > 4 mL/kg/hour.
▪ ≠ Nocturia ≠ Enuresis.
▪ Incidence / prevalence ??
Osmolality:
▪ The ratio of solute content per liter of water (mOsm/L, or
mOsm/kg)
Osmolality= 2 x [serum Na (mEq/L)] + [serum glucose (mg/dL)/18] + [blood urea nitrogen (mg/dL)/2.8]

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Fluid & Electrolytes homeostasis
4 Endocrine subsystem control over fluid &
electrolytes homeostasis:
▪ Renin-angiotensin-aldosterone axis.
▪ Neurohypophyseal ADH arginine-vasopressin (AVP)
▪ Thirst.
▪ Atrial natriuretic peptide.

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Fluid & Electrolytes homeostasis

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Fluid & Electrolytes homeostasis
Normal blood osmolality ranges between 280 and 290 mOsm/kg H2O

Osmotic thresholds for vasopressin and thirst

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Fluid & Electrolytes homeostasis

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Fluid & Electrolytes homeostasis

Regulation of vasopressin secretion and serum osmolality

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Type of diuresis
Solute (osmotic) diuresis.
▪ Glucosuria.
▪ Urea diuresis.
▪ Sodium diuresis.
▪ Mannitol therapy
Water diuresis.
▪ Central DI.
▪ Nephrogenic DI.
▪ Primary Polydipsia.

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Etiology
Disorders Presentation
Central DI • Autosomal dominant, usually presents < 6yo
• Autosomal recessive, usually presents in infancy
Nephrogenic DI • Variable age presentation
• Congenital NDI can present in the 1st week of life
T1DM • Can present at any age
• Peak between age 5-7
T2DM • Usual presentation is in adolescents.
• Rise in the number of younger children presenting
with T2DM

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Age specific presentation of polyuria
Infants • Forceful sucking
• Soaked nappies
Young children • Primary enuresis
• Toilet training difficulties
Older children • High urinary output
• Nocturia
• Tiredness due disrupted sleep

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Diagnosis
What causes polyuria in children?
▪ Intake of excessive volumes of fluid.
o Polydipsia.
o Over administration of iv fluids.
▪ Hyperglycemia.
▪ Diuretic treatment.
▪ Nocturnal polyuria.
o Enuresis.
▪ Electrolyte imbalances.
▪ Diabetes insipidus.

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History
▪ Can the polyuria or polydipsia be quantified?
o How much does your child drink per day?
o How many times does your child urinate per day?
o How much would they urinate each time?
▪ What type of fluid does your child consume? (habitual polydipsia)
▪ How long have these symptoms been present?
▪ Does it interfere with normal activity?
▪ Are there other associated symptoms such as polyphagia, vomiting
or altered mental status?
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History
▪ Does your child wake at night to drink or can they sleep through the
night?
▪ Does your child urinate at night (nocturia)?
o If so do they drink after nocturnal awakening? (true polydipsia)
o How many dry nights a week do they have?
▪ Does your child urinate without control or warning (enuresis)?
▪ Has there been any weight loss?
▪ Are they still feeding?
▪ Has there been any change in vision?
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History
▪ Have they experienced any head trauma?
▪ Does the history, growth charts or physical examination suggest
other endocrine pathology, neoplasm, recent infection or new
medications?
▪ Is there a family history of DM, hyperthyroidism, renal disease or
any other chronic medical condition?
▪ Is there a psychological reason behind this?
▪ A detailed birth history →in early onset polydipsia/polyuria?

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History
Medication associated with nephrogenic diabetes
insipidus.
▪ Demeclocycline.
▪ Rifampicin.
▪ Lithium.
▪ Amphotericin B.
▪ Foscarnet.

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Physical examination
Red flags
▪ Dehydration.
▪ Visual field loss.
▪ Headache.
▪ Irritability and restlessness.
▪ Altered responsiveness.
▪ Lethargy.
▪ Recurrent vomiting.
▪ Tachycardia and tachypnea.
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Physical examination
Routine
▪ Vital signs.
▪ Anthropometry.
▪ Plotting.
▪ Neurological examination.
▪ Dysmorphism.

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Physical examination
Clinical signs of dehydration
Mild (<5%)
• Dry mucous membranes.
• Reduced skin turgor.
• Tachycardia.
• Pale, despite normal perfusion.
Moderate (5%–10%)
• Weight loss.
• Sunken eyes (±fontanels).
• Tearless.
• Altered vital signs (tachycardia, tachypnoea, ±hypotension).
Severe (>10%)
• Anuric.
• Hypotensive.
• Mottled skin.
• Comatose.
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Lab examination
Baseline investigation
▪ Paired serum and urine osmolality.
▪ Serum and urinary glucose.
▪ Urinary ketones.
▪ Blood urea nitrogen.
▪ Sodium.
▪ Potassium.
▪ Calcium.
▪ Cortisol.
▪ Thyroid function test.
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Lab examination
Case specific investigation
Diabetes insipidus o Paired serum/urine osmolality
o Water deprivation test
o DDAVP test
o Visual field testing
o Cranial MRI
Primary polydipsia o Discuss behavioral management,
provide advice and reassurance.

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Differential diagnosis
Psychogenic o Compulsive water drinking
Infection o UTI
o Encephalitis (CDI)
o Meningitis (CDI)
Metabolic o Hypercalcemia
o Other electrolyte disturbances
Endocrine o Diabetes Mellitus
o Cushings
o Adrenal insufficiency
o RTA type 4
o CAH
Infiltrative/autoimmune o Langerhans cell histiocytosis
o Sarcoidosis

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Differential diagnosis
Neoplastic o Cranipharyngioma
o Germinoma
o Pituitary adenoma
Renal o Polycystic Kidney disease
o Sickle Cell Nephropaty
o RTA (Bartter or Gitelman syndrome)
Congenital (CDI) o SOD
o Kabuki syndrome
o Familial
Iatrogenic o Transient polyuria/polydipsia
o Diuretics i.e. Mannitol
o Medications
Neurological o Head trauma
o Neurosurgery
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Management
The primary aim of treatment → to reduce the rate of polyuria and/or
polydipsia to achieve adequate growth and development of the child.

CDI o Replace AVP with synthetic analogue

o Titrate dose following specialist endocrinology advice
NDI o Maintain fluid input
o Treat underlying factors
o Management is complex → specialist nephrology
o HCT
Diabetes Mellitus o DKA → follow the protocol
o Without DKA → Subcutaneous insulin → refer to local policy

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 Algorithm

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Thank you!

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