Presentation on theme: "POLYURIA Tutorial Dr Amir Babiker MBBS, MRCPCH (UK), CCT (UK), Msc Endocrinology and Diabetes (Queen Mary University, London, UK) Consultant Paediatric."— Presentation transcript:
POLYURIA Tutorial Dr Amir Babiker MBBS, MRCPCH (UK), CCT (UK), Msc Endocrinology and Diabetes (Queen Mary University, London, UK) Consultant Paediatric Endocrinologist, KKUH and Assistant Professor, KSU
Objectives Definition of polyuria Causes of polyuria and Approach Types of diabetes: Assessment and Mmt Emergency management: DKA & hypoglycaemia Clinical Scenarios
Definition Excessive or abnormally large production or passage of urine (usually > 2000 ml/m2/day) or (> 5 ml/kg/hr). Surface area= Ht(cm) X Wt(kg)/3600 Increased production and passage of urine may also be termed diuresis. Frequency is usually an accompanying symptom. Polydipsia (increased thirst)= Cause or effect.
(1)INCRAESED FLUID INTAKE: – Iatrogenic – Compulsive water drinking (Psychogenic polydipsia) (2) INCREASED URINARY SOLUTE EXCRETION – OSMOTIC DIURESIS: 1. Diabetes mellitus (DM) 2. Mannitol treatment – SALT LOSS: 1. Adrenal insufficiency 2. Aldosterone resistance 3. Diuretics 4. Cerebral salt wasting (CSW) or salt diuresis
(3) IMPAIRED URINARY CONCENTRATION: -INEFFICIENT ADH ACTION (DIABETES INSIPIDUS, DI): 1. Central (Neurogenic) DI 2. Nephrogenic DI -RENAL DISORDERS: 1.UTI 2. Renal tubular acidosis (RTA) 3. Bartter and Gitelman Syndromes 4. Renal glucosuria 5. Chronic renal failure
Clinical and biochemical similarities DM and renal glucosuria DI and Psychogenic polydipsia UTI, aldosterone resistance, Bartter and Gitelman syndromes, and RTA Chronic renal failure and adrenal insufficiency
History Age of onset: Congenital/Acquired Fever: UTI Polydipsia: nocturnal, odd behaviour. Salt craving: Adrenal insufficiency, CSW Failure to thrive: DM, Nephrogenic D.I, RTA, CAH, Bartter Hyperphagia or loss of appetite: DM Head trauma, neurosurgery: Central D.I Meningitis: Central D.I Drug intake: Diuretics, Mannitol.
Water Deprivation test DI Posm, Not able to concentrate urine Water deprivation test Psychogenic polydipsia Posm, able to concentrate urine DDAVP response test Central DI Nephrogenic DI Posm >270 and <300 mOsm/kg
Management Central DI responds to DDAVP (IV, oral, Intranasal). NDI: DDAVP is ineffective. Hydrochlorothizide (HCTZ) +/- Amiloride and indomethacin OR ttt of the cause Adequate hydration is important. CWD: Psycological and behavioural treatment
DM Condition2 hour glucoseFasting glucoseHbA 1c mmol/l(mg/dl) % Normal<7.8 (<140)<6.1 (<110)<6.0 Impaired fasting glycaemia <7.8 (<140) ≥ 6.1(≥110) & <7.0(<126) 6.0–6.4 Impaired glucose tolerance ≥7.8 (≥140)<7.0 (<126)6.0–6.4 DM ≥11.1 (≥200)≥7.0 (≥126)≥ 6.5 OR Symptoms of hyperglycaemia and casual plasma glucose ≥ 11.1 mmol/l (200 mg/dl) A positive result, in the absence of unequivocal hyperglycemia, should be confirmed by a repeat of any of the above methods on a different day. Diabetes mellitus is characterized by recurrent or persistent hyperglycaemia, and is diagnosed by demonstrating any one of the following: [ [
Concepts Honeymoon phase or partial remission: weeks to 2 years, due to B cell hyperplasia. Early morning hyperglycaemia: with NPH & Regular (Somogyi & Dawn phenomena) Sick day rules: Check Blood sugar every 2-4 hrs Check ketones Drink plenty of fluids Need extra insulin to clear ketones Never omit insulin Hypoglycaemia may be a problem especially in young children
DKA Children with T1DM who have: Hyperglycaemia (BG >11 mmol/l) pH < 7.3 Bicarbonate < 15 mmol/l With ketonaemia and/ or ketonuria. and who has: Acidotic respiration, dehydration, drowsiness and/or abdominal pain/vomiting
DKA They can die from : Cerebral oedema: This is unpredictable, occurs more frequently in younger children and newly diagnosed diabetes and has a mortality of around 25%. Hypokalaemia: This is preventable with careful monitoring and management Aspiration pneumonia: NGT.
DKA Emergency management 1. Resuscitation 2. Confirm diagnosis 3. Investigations Full Clinical Assessment 1. Assessment of dehydration (weight) 2. Conscious level 3. Physical examination (C oedema, infection, ileus) 4. Role of PICU (Age, LOC, severe acidosis, shock, staff)
DKA Management: Fluids – volume, rate, type, oral fluids Insulin: 0.1 units/kg/hour (0.1ml/kg/hour: Start after 1 hr of IV fluids. Potassium: 40 mmol/l, when the pt PU Bicarbonate: rarely required, PH < 6.9 Phosphate: Not usually required. Continuing management.
Hourly rate = 48 hr maintenance + deficit – resuscitation fluid already given 48 Example : A 20 kg 6 year old boy who is 10% dehydrated, and who has already had 20ml/kg saline, will require 10 (%) x 20 (kg) x 10 = 2000 mls deficit plus 60 ml x 20 kg = 1200 mls maintenance each 24 hours 2 x 1200 mls = 1400 + 2000 = 4400 mls minus 20kg x 20ml = 400 mls resus fluid 4000 mls over 48 hours = 83 mls/hour
DKA Fluids required: Blood Glucose Level Type of Fluid >14 mmol/l Normal saline 4 – 14 mmol/l During 1st 6 hours 5% Dex+ 0.9% saline After 1st 6 hours 5% Dex+ 0.45% saline <4mmol/l 10% Dextrose
DKA Observations to be carried out: Ensure full instructions are available to nursing staff emphasising the need for : strict fluid balance: Input/Output testing for glucose & ketones hourly BP and basic observations hourly capillary blood glucose measurements U&E: after 2 hrs initially, then 4 hrly. twice daily weight.
DKA hourly or more frequent neuro observations initially reporting immediately to the medical staff, even at night, symptoms of headache or any change in either conscious level or behaviour reporting any changes in the ECG trace, especially T wave changes suggesting hyperkalaemia
Cerebral Oedema headache & slowing of heart rate change in neurological status (restlessness, irritability, increased drowsiness, incontinence) specific neurological signs (eg. cranial nerve palsies) rising BP, decreased O2 saturation abnormal posturing More dramatic changes such as convulsions, papilloedema, respiratory arrest are late signs associated with extremely poor prognosis
Cerebral Oedema Management If suspected inform senior staff immediately. The following measures should be taken immediately while arranging transfer to PICU: exclude hypoglycaemia as a possible cause of any behaviour change give Mannitol 1 g/kg stat (= 2.5 ml/kg Mannitol 20% over 20 minutes) OR 3% saline restrict IV fluids to 50 % maintenance and replace deficit over 72 rather than 48 hours the child will need to be moved to PICU (if not there already) once the child is stable, exclude other diagnoses by CT scan a repeated dose of Mannitol should be given after 2 hours if no response document all events (with dates and times) very carefully in medical records
CASE 1 A 14 yr old girl had recurrent severe hypoglycaemias with 2 episodes leading to convulsions and hospital admission. She was diagnosed with T1DM at 9 yrs of age and was treated with BD injections of Novomix 30 at 30 U am and 18 U pm. No recent change in her diet or level of activity and she does not drink alcohol.
Questions and answers What Invx would you consider doing? – HbA1c – CD (TTG) – AAA – TFT If the results of these Invx proved normal, what further explanation could account for her recurrent hypoglycaemias? – Insulin overdose. This adolescent was not coping well with DM management – improved with psychological support
Case 2 An 11-year-old boy presented with an 8-week history of polyuria and polydipsia. He was otherwise well apart from recent headaches. Investigations in clinic demonstrated the following: Serum sodium 142 mmol/L Serum potassium 3.7 mmol/L Serum urea 2.3 mmol/L Serum creatinine 52 mol/L Plasma osmolality 305 mOsm/kg Plasma glucose 6.2 mmol/L Urine sodium 16 mmol/L Urine osmolality 78 mOsm/kg
Questions and answers (1) What further investigation is required to clarify the diagnosis? (2) What additional investigations are then required? (1): Given that this child is spontaneously hyperosmolar, a formal water deprivation test is contraindicated. However, it is not clear whether this child has cranial or nephrogenic DI - Desmopressin response test: His urinary osmolality increased from 75 to 530 mOsm/kg and there was a dramatic reduction in his urine output suggesting that he has cranial diabetes insipidus. (2): Given a diagnosis of CDI and headache: MRI brain and Pituitary function tests.
Summary Polyuria: Definition Causes Approach DI Vs Psychogenic polydipsia DM and its complications