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Diagnosis of diabetic ketoacidosis (DKA)
Dr. Abdullah Alshaya Consultant Pediatric Endocrinologist
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DKA Hyperglycemia: Blood glucose level greater than 200 mg/ dL.
2. Ketonemia: Ketones demonstrable in serum 3. Acidosis: pH less than 7.35 and HCO3 less than 15 mEq/ L. 4. Glucosuria and Ketonuria 5. The clinical manifestations of diabetes
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Diagnosis and Assessment
Think of DKA in a known diabetic child or any child who presents with either of or a combination of the following Classical symptoms of diabetes Acute abdomen Dehydration Acidotic breathing Disturbed level of consciousness
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Important Relevant Points
1st. History Precipitating factors including insulin omission accuracy of dose, stressful conditions including infections, trauma or home conflict. History of recent weight and weight loss.
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2nd. Examinations Signs and complications of fluid, electrolyte and acid base imbalance including shock, hypotension with acidosis, and CNS status. Establish degree of dehydration (mild, moderate and severe). Look for signs of hidden infection and trauma. Obtain accurate weight before starting treatment if possible.
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Classification of diabetic ketoacidosis (DKA)
Normal Mild Moderate Severe CO2 (mEq per L, venous)* 20-28 16-20 10-15 <10 pH (venous)* <7.15 Clinical No change Oriented, alert but fatigued Kussmaul respirations; oriented but sleepy; arousable Kussmaul or depressed respirations; sleepy to depressed sensorium to coma
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Classification of diabetic ketoacidosis (DKA)
Co2 and pH measurement are method dependent; normal ranges may vary. Severe hypernatremia (corrected Na>150 mEq/L) would also be classified as severe DKA (2011)
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Management of Ketoacidosis
The immediate aim of therapy are expansion of the intravascular volume, correction of deficits in fluid electrolytes and acid-base status and initiation of insulin therapy.
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Principles of Management
Treatment of shock Correction of dehydration and replacement of losses with provision of maintenance Correction of electrolyte deficit Correction of hyperglycemia Correction of acidosis Treatment of precipitating factors including sepsis Observation for and treatment of cerebral oedema Prevention of further attacks
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Fluid and Electrolyte Therapy
It is designed to restore most electrolyte deficits, to reverse the acidosis, and to rehydrate the moderately ill child in about 24 hr. A standard water deficit (85 mL/kg) is assumed. This amount, when added to maintenance, yields about 4 L/m² for children of all sizes. The maximum volume: it is prudent to anticipate clinical cerebral edema in all children treated for DKA by limiting the rate of fluid administration to 4.0 L/m²/24hr or less.
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LAB Blood for: glucose urea, creatinine electrolytes gases osmolality,
CBC + diff, (culture: if indicated) 9. Urine: urinalysis + culture (for glucose + ketone)
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Fluid and Electrolyte Therapy
This protocol corrects a deficit of 85 mL/kg (8.5% dehydration) for all patients in the first 24 hr. Children with milder DKA recover in hr (and need less total IV fluid before switching to oral intake), whereas those with more severe DKA require hr with this protocol.
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Diabetic Ketoacidosis (DKA) Treatment Protocol
Time Therapy Comments 1st hour 10-20 mL/ kg IV bolus 0.9% NaCI or lactated ringer Insulin drip at U/kg/hr Quick volume expansion; may be repeated. NPO. Monitor I/O, neurologic status. Use flow sheet. Have mannitol at beside; 1 g/kg IV push for cerebral edema. 2nd hour until DKA resolution 0.45% NaCI; plus continue Insulin drip 20 mEq/ L potassium phospate and 20 mEq/L potassium acetate 5% glucose if blood sugar <250mg/ dL 85mL/kg + maintenance- bolus IV rate= hr If K<3 mEq/L, give 0.5 to 1.0 mEq/ kg as oral K solution OR increase IV K to 80 mEq/L Variable Oral intake with subcutaneous insulin No emesis, CO2 ≥16 mEq/ L; normal electrolytes
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Admission, hr 8, 16,24, then daily
Parameter Recommended Recommended items 1. Clinical features Neulogic check Vital signs weight Every min Admission, hr 8, 16,24, then daily b. Na, K, CI, osmolarity c. Glucose d. BUN e. Urinary ketones f. ECG 2. Fluid Balance Intake (PO, IV) Output (urine and stool) 3. Chemical analysis Arterial blood gases (ABGs) (pH, HCO3) Admission, hr 2, 6, 10, 24 g. Serum Ca 4. Blood culture 5. Urinalysis (bacteria, WBCs) Admission hr 2,6,10,24 Hourly for 24 hrs. Admission, hr 6, 24 Admission hr 6, 10, 24 Admission hr 2, 6 OR Continous if K is <3.5 mEq/L or >7 mEq/L When phosphate is used Admission Admission
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Fluids If patient is shocked give 10 ml/kg of normal saline as quickly as possible ( minutes). Repeat these doses till circulation is restored in the emergency room If not shocked or once circulation is restored, start IV fluids as mentioned below.
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Fluid Replacement Fluid repair should extend over 48 hours to achieve a slower correction of serum hyperosmolality to prevent cerebral oedema. Therefore deficit should be given over 48 hours Maintenance needed for 24 hours
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Deficit The usual deficit in most DKA patients ranges from 5-10% however this should be assessed clinically Age < 2 years Mild 5% Moderate 5-10% Severe 10-15% > 2 years 3% 6% 9%
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Rate of Infusion Add 24 hours maintenance + ½ calculated deficit and divide by 24 to obtain the hourly rate, (or add 48 hours maintenance plus calculated deficit and divide this total by 48 to get the hourly rate)
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Fluid used Use normal saline when blood glucose reaches 13 mmol/L change to 5% dextrose with 0.45 normal saline (or normal saline in older children and adolescents)
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Infusion rate: 0. 1 unit/kg/hour i. e
Infusion rate: 0.1 unit/kg/hour i.e. 0.1 ml/kg/hour of the above-mentioned preparation. Aiming to reduce blood glucose at rate of mmol/hr. Continue this insulin infusion till acidosis is cleared i.e. either pH > 7.3, HCO3 > 15 mmol or normal anion gap (16-18) Note: Discontinuation of insulin infusion is not dictated by blood sugar level, but by clearance of acidosis.
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Sodium Osmotic flux of water into extracellular space reduces serum sodium concentration Actual sodium: 1.6mEq/L per 100mg/dL rise in glucose over 100 Hypertriglyceridemia low sodium pseudohyponatremia
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Potassium Level varies depending on urinary loss and severity of acidosis Potassium moves extracellularly in exchange for hydrogen ions typical hyperkalemia on presentaion Total body stores are depleted due to urinary loss
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Potassium Commenced when the child starts to pass urine or if he is already passing urine and or K is below 5 mmol/L) Add 40 mmol/L of potassium chloride Monitor by EKG, clinically & biochemically If serum potassium is > 6 mmol/L withhold potassium temporarily.
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Management Bicarbonate is almost never administered
Bicarb administration leads to increased cerebral acidosis: HCO3- + H+ dissociated to CO2 and H2O Bicarbonate passes the BBB slowly CO2 diffuses freely exacerbating cerebral acidosis & depression Indications for bicarbonate use: only in severe acidosis leading to cardiorespiratory compromise
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Bicarbonate Dose: Wt Kg X 0.3 X 22 - HCO3 level (or base deficit) divided by 2 Infuse over 4-6 hours
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Phosphorous We don’t use it as a routine. Consider using it in comatose patients or if phosphate level < 0.5 mmol/L. Give the dose as potassium phosphate and half as potassium chloride. Monitor calcium levels every 4-6 hours as patient might develop hypocalcemia. Always check serum calcium level before phosphate is infused.
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Monitoring Blood glucose with a meter hourly during insulin infusion (at least hourly for 1st 4-6 hours then 2 hourly if needed) then every 6 hours thereafter. Blood gases, blood glucose, urea and electrolytes and blood for ketone using optium meter 4-6 hourly
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Vital signs (EKG monitor) and neuro observation (initially hourly till stable then 4-6 hours). Also watch for headache, vomiting or behavior change. Flow sheet to record: blood work up, intake and output, doses of insulin, and urinalysis for glucose ketone. Adequate urine output =>1.5 ml/Kg/hr.
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Problem Solving During Monitoring
After resuscitation, the typical aim of rate of blood glucose fall is mmol/hour When blood glucose falls to < 15 mmol/L change fluids to 5% dextrose with 0.45 saline (or normal saline in older children and adolescents) to maintain blood glucose in the desired range of mmol/L If blood glucose rises again above 15 mmol/L increase the insulin infusion by 25%
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If blood glucose falls below 8 mmol/L or falls too rapidly increase the concentration of glucose to 10% (or more) The insulin infusion rate should only be decreased if blood glucose levels remains below the target range despite glucose supplementation Don’t stop insulin infusion or decrease below 0.05 unit/kg/hr particularly if the patient is still acidotic
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Management of Ketoacidosis
Neurologic check: Sensorium, change of consciousness, headache, bradycardia, apnea, pupillary changes, papilledema, posturing, and seizures
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Problems and Complications
Cerebral Oedema Warning signs and symptoms Headache and slowing of heart rate (not necessarily bradycardia) Vomiting Change in neurological status (restlessness, irritability increased drowsiness, incontinence) or specific neurological signs (e.g. cranial nerve palsies)
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risk factors Younger age New onset Longer duration of symptoms
Lower PCO2 Severe acidosis Increase in BUN Use of bicarbonate Large volumes of rehydration fluids Failure of correction of Na with treatment Bicarb has been linked to increasing the risk of cerebral edema: case controlled study it was found early administration of insulin and high volumes of fluid were important predictors of cerebral edema, not bicarb therapy
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Rising blood pressure, decreased O2 saturation
Rising blood pressure, decreased O2 saturation. More dramatic changes such as convulsions, papilloedema and respiratory arrest are late . signs and are associated with extremely poor prognosis action. Exclude hypoglycemia Give immediate mannitol 1 gm/kg over 20 minutes (i.e. 5 ml kg of 20% solution) (3% saline can be used if no mannitol available.
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Have rehydration infusion rate until situation is improved
Nurse child head elevated Move to PICU (or even earlier if possible) Call you senior assisted ventilation may required
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Consider continuation of mannitol at 0
Consider continuation of mannitol at 0.25 gm/kg/hr to prevent rebound increase in ICP or repeat bolus every 4-6 hours Cranial imaging should only be considered after child is stabilized as other intracranial events as thrombosis, hemorrhage and infarcts may occur. Note: a normal CT doesn’t exclude cerebral oedema. It is a clinical diagnosis.
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Definition Phase 1 Phase II Phase III Phase IV Phase V Emergency Room Till acidosis is cleared (normal anion gap) PH > 7.3 or HC03 > 18 or blood ketone <1.5 pmol/L From clearing of acidosis to: pt. starting to drink and eat When patient is able to drink and eat (24-72 hours) Long-term Investigation Dextrostix B.G. U. E. A. B. G. Urinalysis Culture if indicated CBC Infection Screen B glucose 1-2 hourly Blood & or urine ketones U. E. 4-6 hourly Blood Gases Urine for glucose + ketone 6 hourly Blood Glucose 6 hourly before meals U/E hourly Urine Blood Glucose (meter) 6 hourly U/E once/day Urine 6 hourly Blood Glucose x 4 Urine x 4 Fluids Electrolytes Normal Saline ml/kg if shocked Repeat till shock is over Start IV fluids Normal Saline Change to 5% D + '/2 NS if B- sugar 13 mmol/L (250 mg.dl) K+, P04 + HCO3 (if indicated) 5% D + Zi NS (or normal saline) Oral fluids + food K+ gradually stop I.V. Reduce I.V. fluids Gradually and stop Stop I.V. Insulin I.V. Regular insulin 0.1 unit/kg per hour 0.1 U/kg/hour I.V. f dose to 0.15 — 0.2 units/kg if no improvement in 2-4 hours Low dose infusion (0.05 u/kg or S/C regular or usual dose) May start NPH S/C + Regular S/C Stop I.V. 1-2 days S/C Diet + Oral NPO Try oral fluids after 4 hours After vomiting stops Try oral fluids/food Food Diabetic diet Others History Examination Coma care Stomach suction Reassure Charts -> ECG RI Infection PICU Vital signs Neuro Observation Parents Education
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Thank you!!!
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