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DIABETIC KETOACIDOSIS PROTOCOL

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DIABETIC KETOACIDOSIS

Apr 07, 2019

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DIABETIC KETOACIDOSIS. Andrew J. Bauer Pediatric Endocrinology WRAMC. GOALS. REVIEW TYPE 1 DIABETES AND METABOLISM AS THEY RELATES TO DKA. CLINICAL DIAGNOSIS and MISLEADING LABS TREATMENT and CONTROVERSIES TREATMENT GUIDELINES. Type 1 DM.

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• cerebral edematotal fluids
• dec glucose utilization lipolysis
• related deaths
• am j emer med
• impaired insulin secretion
• cerebral edemaother

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DIABETIC KETOACIDOSIS Andrew J. Bauer Pediatric Endocrinology WRAMC

GOALS • REVIEW TYPE 1 DIABETES AND METABOLISM AS THEY RELATES TO DKA • CLINICAL DIAGNOSIS and MISLEADING LABS • TREATMENT and CONTROVERSIES • TREATMENT GUIDELINES

Type 1 DM • Autoimmune destruction of the pancreatic islet cell • Hallmark = lymphocytic infiltration of islets • Progresses over years • Leads to insulin deficiency • Later may be associated with glucagon deficiency as well

Progression to Type 1 DM Autoimmune destruction Honeymoon 100% Islet loss “Diabetes threshold”

Typical Presentation • Polyuria, polydypsia, weight loss • Vomiting • Rapid-deep respiration • CNS depression – coma • Precipitating event

“Typical” Setting….. • 9 yo boy presents to clinic with CC “ 6 day history of stomach pain and diarrhea.” “Vomiting started 2 days ago and has persisted.” • (+) weight loss • PE: HR 140, RR 28, T97.8 Weight: 27 Kg • Tachy mucous membranes • Abd - soft, (+)BS, mild left CVA tenderness • DX: viral gastroenteritis with mild dehydration • Returned to ER 24 hours later • PE: cachectic, quiet, tired, cooperative, (+) ketotic breath

Background • 15-30% of new diabetics present in DKA • < 4 yrs of age = 40% with DKA @ diagnosis • Most common cause of death in diabetics less than 20 years of age • 70% of related deaths in diabetics less than 10 yrs of age • Mortality: 5-15% (1-2% at MEDCEN) • Preventable

Diagnostic Criteria • Blood glucose > 250 mg/dl • pH < 7.35 • HCO3 < 20 mEq/L • Anion Gap > 12 • ketonemia

Etiology • Results from inadequate insulin • Accidental or intentional omission • Inappropriate intervention when stressed

Etiology  DKA violates rules of common sense • Increased insulin requirement despite decreased food intake • Marked urine output in setting of dehydration • Catabolic state in setting of hyperglycemia and hyperlipidemia

PathophysiologyCounter-Regulatory Hormones • Insulin Deficiency is the Primary defect • Stress hormones accelerate and exaggerate the rate and magnitude of metabolic decompensation • Pathophysiology Hormone • Impaired insulin secretion Epi • Anti-insulin action Epi, cortisol, GH • Promoting catabolism All • Dec glucose utilization Epi, cortisol, GH

Islets of Langerhans b-cell destruction Insulin Deficiency Decreased Glucose Utilization & Increased Production Epi,Cortisol GH Stress Muscle Glucagon Amino Acids Adipo- cytes Increased Protein Catabolism Liver Increased Ketogenesis Gluconeogenesis, Glycogenolysis FattyAcids IncreasedLipolysis Threshold 180 mg/dl Polyuria Volume Depletion Ketonuria Hyperglycemia Ketoacidosis HyperTG

Pathophysiology Glucagon Epinephrine Cortisol Growth Hormone Insulin

Pathophysiology Glucagon Epinephrine Cortisol Growth Hormone Insulin Dec Glucose Utilization Lipolysis

Decreased Utilization  post-prandial and Stress-Induced hyperglycemia DKA - Early • Relative Insulin Deficiency  Glycogenolysis & gluconeogenesis restrained Peripheral glucose uptake Elevates blood glucose

Pathophysiology Glucagon Epinephrine Cortisol Growth Hormone Insulin Gluconeogenesis Glycogenolysis Lipolysis Ketogenesis

DKA - Late Increased Production & Decreased Utilization  Fasting hyperglycemia • Insulin Deficiency Glycogenolysis Gluconeogenesis Hepatic glucose output Peripheral glucose uptake Elevates blood glucose Lipolysis Release FFA -> liver VLDL & ketones Ketonemia and hyperTG Acidosis & Diuresis

DKAInitial Evaluation • Hx and PE - • Duration of onset • Level of dehydration • Evidence of infection • Labs - STAT • Electrolytes • Venous blood gas • Serum Osmolality • U/a Osmolality = 2 x (Na + K) + Glucose/18 + BUN/3

700 24.4 518 16.8 47.5 9 yo lab Evaluation • 148| 109| 32 5.6 | <5 | 1.4 • Blood Gas - pH 7.0 5/1.020 Glu >1000, (+) Ketones

Misleading Labs • Sodium • Potassium • Ketones • WBC

Misleading LabsSodium • Na+ depressed 1.6 mEq/L per 100 mg% glucose • Corrected Na+ = measured Na + 1.6 meq/L x (glucose-100)/100)) • Example: • Na+ = 123 meq/L and Glucose = 1,250 mg/dl • 1,250 – 100 = 1,150 / 100 = 11.5 x 1.6 = 18 meq/L • Corrected Na+ = 123 + 18 = 141 meq/L

Misleading LabsSodium • Triglycerides also artificially lower Na Lipid Lipid Serum Na Na Na Na Na Na Na Na Na Na Na Gluc Na Na Gluc

Misleading LabsPotassium • Acidosis leads to flux of K+ out of cells as H+ enters cells to buffer • Dehydration and volume depletion • Aldosterone  Na reabsorption and K+ wasting  Serum K+ usually normal or high, but total body K+ is low

DKA- Risks of TherapyHypokalemia/Hyperkalemia • With insulin therapy • K+ moves into cells (1 meq/L / 0.1 unit pH ) • Even with K+ you must • Give large doses (40 meq/L) K+ • Monitor K+ levels and EKG • High K - tall peaked T, long PR, wide QRS • Low K - depressed ST, diphasic T, Prom U-wave • Cardiac dysrythmia

Misleading LabsKetones • In the absence of insulin, FFA go to the liver, and into mitochondria via carnitine • ß-oxidation excess acetylCoA Nitroprusside reaction • Acetyl-CoA condenses to acetoacetate • Insulin prevents utilization of acetoacetate • so levels and shunt to ß-hydroxybutyrate and acetone

Misleading LabsScreening for Ketonemia • Urine Dip stick vs. anion gap/serum bicarb SensitivitySpecificity DKA 99 % 69 %  Diabetic with minor signs and symptoms and negative urine ketone dip stick is unlikely to have acidosis = high negative predictive value for excluding DKA Am J Emer Med 34: 1999

Misleading LabsWBC count • N = 247 DKA admissions over 6 years • Mean WBC = 17,519/mm3 (+/- 9,582) • 69% without infection • 17.8% presumed viral infection • 12.9% bacterial infection - more common in children < 3 years of age All need to be evaluated and re-evaluated if persistent acidosis Am J Emer Med 19: 270-3, 2001

Let’s start treatment…..

Controversies and Risks of Therapy • Fluids - composition, bolus amount and total fluids/day • Use of Bicarbonate • Phosphate replacement Cerebral Edema

DKA – ControversyCerebral Edema - Truths ? Acute • Idiogenic osmoles in CNS accumulate fluid • Cerebral edema – present in 100% of patients prior to therapy • Treatment exacerbates cerebral edema • Vigorous fluid administration • Hypotonic fluids • Bicarbonate Late Sequelae

DKA – Cerebral Edema Actualities • Etiology is not known • Occurs exclusively in pediatric patients • Mortality Rate = 21% • Morbidity Rate = 27% (permanent neurologic sequelae)  Difficulty is relatively rare occurrence (1-3 %) with subsequent small numbers of patients in retrospective or prospective studies

DKA – Cerebral Edema Actualities • NEJM - Jan 2001 • N = 6977 DKA patients from 10 centers over 15 years • 61 developed cerebral edema (0.9%) • Pediatrics - Sep 2001 • N = 520 DKA patients over 5 1/2 years • 2 developed cerebral edema

DKA – Cerebral EdemaTotal Fluids • > 4 L/m2/day, or > 50 ml/kg in first 4 hrs α hyponatremia α herniation • May occur in patients that receive less • Of 52 patients with neurologic complications 21 had either a rise of serum Na or fall less than 4 mmol/L J Peds 113:10-14, 1988 Attention to fluid rate and tonicity is essential, but may not be sufficient to predict subset that will develop neurologic complications JCEM 85:509-513, 2000

Prior to therapy; longer duration symptoms before diagnosis DKA – Cerebral EdemaVariable Time of Onset # of Children with Neurologic Deterioration NEJM 344:264-69, 2001 Hours after Initiation of Therapy

DKA – Cerebral EdemaOther • Hypoxemia • Children’s brains have higher oxygen requirement, 5.1 mL/100g vs. 3.3 mL/100g • Hypophosphatemia with resultant decreased 2,3-DPG decreases O2 delivery to brain cells • Mannitol - earliest effects are related to decreased viscosity, not to shift of fluid from extravascular space Neurosurg 21: 147-156, 1987 JCEM 85: 509-13, 2000

DKA – Cerebral Edema Signs and Symptoms 1. Sudden and persistent drop in heart rate - not bradychardia - not assoc with HTN - not related to hydration status 2. Change in sensorium 7. Fall in serum 3. Headache Na, or failure 4. Emesis to rise 5. Incontinence 6. Unexplained tachypnea JCEM 85:509-513, 2000

DKA – Cerebral Edema Evaluation • CT may be non-diagnostic at time of symptoms • 9 of 30 - no edema, 6 read as normal • 5 of 9 - 2.5 to 8 hours after onset of coma, read as normal Cerebral Edema is a clinical diagnosis. Need to treat BEFORE imaging. JCEM 85:509-513, 2000

DKA – Risks of TherapyBicarbonate Administration • Administration to acidotic patient generates rapid rise in CO2 • CO2 enters CNS rapidly • HCO3- is delayed by blood-brain barrier • Increased CNS CO2 exacerbates cerebral acidosis CO2 + H2O H2CO3 H+ + HCO3- • May also reduce partial pressure of O2 in CSF  vasoconstriction  brain hypoxia/ischemia

DKA – Risks of TherapyBicarbonate Administration • Multi-center study from 10 pediatric centers, USA and Melbourne, Australia over 15 yr period • 6977 DKA hospitalizations: 61 cases cerebral edema (0.9%) • Presentation: PaCO2BUNGlucoseBicarb Cerebral Edema 11.3 27 758 23/61 (32%) Controls 15.1 21 700 43/174 (23%) •  fluid, insulin, or sodium administration, nor rate of fall in glucose was associated NEJM 344:264-269, 2001

**** **** **** **** **** **** **** **** DKA – Risks of TherapyBicarbonate Administration • Variations in treatment exacerbate an on-going pathologic process • Brain ischemia is major underline etiology • Hyperglycemia increases extent of neurologic damage • Extreme dehydration, hypocapnia • Concept of idiogenic osmotically active substances not supported (no relationship to change in glucose, rate of fluid or Na administration)  Risk related to duration and severity of DKA NEJM 344:264-269, 2001

DKA- Controversy Phosphate Theoretical • Essential phosphate deficit • W/treatment serum phosphate and 2,3-DPG fall • Shift oxyhemoglobin curve reducing O2 deliver Practical • No evidence of direct benefit, but less Cl- • Give ½ K+ replacement as K-phos x 8 hours • Limit to 2 mEq/kg/day to avoid hypocalcemia Endo Met Clin 29:Dec 2000

Elements of Therapy

Elements of Therapy • Fluids – treat shock, then sufficient to reverse dehydration and replace ongoing losses (will correct hyperglycemia) • Insulin – sufficient to suppress ketosis, reverse acidosis, promote glucose uptake and utilization (will stop ketosis) • Electrolytes – replace profound Na+ and K+ losses

Typical Therapy - Fluids • 10% dehydration is standard estimate (use weight if known) • Bolus: treat shock, usual 20-30cc/kg given 10cc/kg at a time • Replace deficit over 48-72 hours • ie. 10 % in 20 Kg pt = 2000ml over 48hrs = maintenance + 42cc/hr x 48 hours

Typical Therapy - Fluids • Use ½ NS to NS • Average = 2 x maintenance • 4:2:1 cc/kg/hr or 100:50:20 cc/kg/day • ie. 25 kg patient • (4 x 10) + (2 x 10) + (1 x 5) = 65 cc/hr • (100 x 10) + (50 x 10) + (20 x 5)/24 hours = 66.7 cc/hr

DKA – Risks of TherapyInsulin 100% Biological effect 0.1 units/kg/hr Current therapy uses continuous insulin drip  Drop glucose 50-100 mg/dl/hr 100 uU/ml Insulin Level

Typical Therapy - Insulin • 0.1 unit/kg/hr continuous drip (regular) • Flush tubing with 50 ml • 250 units regular in 250 cc NS (1.0 units/ml) = 0.1 u/kg/hr = 0.1 ml/kg/hr

Typical TherapyGlucose - 2 Bag Method • Goal - decrease blood glucose by 50-100 mg/dl/hr • Must continue insulin therapy to correct acidosis • Order D10 NS to bedside • when serum glucose < 300: add D5NS ( = 1/2 D10NS + maintenance bag) • when serum glucose < 200: Change to D10NS

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