DKA and HHS
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Management of Hyperglycemia emergencies
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DKA and HHS
- 1. A&E(VINAYAKA) Diabetic Ketoacidosis Hyperglycemic Hyperosmolar State Dr. Soumar Dutta PG Trainee Accident and Critical Care Medicine
- 3. A&E(VINAYAKA) IntroductionIntroduction • Acute life threatening complication of DM • DKA predominantly seen in type 1 DM • DKA represents body’s response to cellular starvation due to insulin deficiency & counter regulatory hormone excess
- 5. A&E(VINAYAKA) ClassificationClassification Mild DKA Moderate DKA Severe DKA Plasma glucose > 250 mg/dl > 250 mg/dl > 250 mg/dl Arterial ph 7.25-7.30 7.0-7.24 < 7.0 Serum bicarbonate 15-18 10-<15 < 10 Urine ketones + + + Anion gap >10 >12 >12 Alteration in sensorium alert alert/drowsy stupor/coma
- 7. A&E(VINAYAKA) • Facilitate uptake of glucose & conversion into glycogen • Inhibits glycogenolysis & gluconeogenesis • Increase lipogenesis • Inhibit lipolysis • Uptake of amino acids into muscle cell • Prevents release of amino acids from muscle
- 8. A&E(VINAYAKA) Pathophysiology Insulin Deficiency is the primary defect in patients with DKA Muscle Hepatocyte Adipose Glucose Amino Acids Glucose-P Glycogen Pyruvate, CO2 Glucose Free fatty acidsKetoacids Normal Insulin Activity
- 11. A&E(VINAYAKA) DKA - EarlyDKA - Early • Relative Insulin Deficiency • Glycogenolysis & gluconeogenesis • Peripheral glucose uptake Elevates blood glucose Decreased Utilization post-prandial and Stress-Induced hyperglycemia
- 13. A&E(VINAYAKA) • Insulin Deficiency Glycogenolysis Gluconeogenesis Hepatic glucose output Lipolysis: Release FFA -> liver VLDL & ketones Ketonemia and hyper TG Acidosis , Hyperglycemia & Osmotic diuresis DKA - LateDKA - Late Increased Production & Decreased Utilization Fasting hyperglycemia
- 14. A&E(VINAYAKA)
- 15. A&E(VINAYAKA) Islets of Langerhans β-cell destruction Insulin Deficiency Adipo- cytes Muscle Liver Decreased Glucose Utilization & Increased Production Glucagon Increased Protein Catabolism Increased Ketogenesis Glucoaneogenesis, Glycogenolysis IncreasedLipolysis Hyperglycemia Ketoacidosis HyperTG Polyuria Volume Depletion Ketonuria Amino Acids FattyAcids Stress Epi,Cortisol GH,Glucagon Threshold 180 mg/dl
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- 17. A&E(VINAYAKA) Precipitating factors of DKAPrecipitating factors of DKA • Omission or reduced daily insulin injection • Infection • Pancreatitis • Myocardial Infarction • Mesentric Ischemia • Renal Insufficeincy • CVA • Pulmonary embolism • G I hemorrhage • Heat related illness • Parenteral/enteral alimentation • Rhabdomyolysis • Severe Burns
- 18. A&E(VINAYAKA) Drugs Precipitate DKADrugs Precipitate DKA • Diuretics • Lithium • Beta Blockers • Mannitol • Chlorpromazine • Cimetidine • Glucocorticoids • Neuroleptics • Phenytoin • Didanosine • Calcium-channel blockers • Pentamidine
- 19. A&E(VINAYAKA) Clinical featuresClinical features Hyperglycemia Osmotic diuresis and renal loss of Na, K, PO4, Ca and Mg Hypovolemia,acidosis and hyperventilation
- 20. A&E(VINAYAKA) Clinical featuresClinical features • Increased PGI2 and PGE2peripheral vasodilation ,nausea, vomiting and abdominal pain. • Vomiting maladaptive response to counter acidosis exacerbates the potassium losses
- 21. A&E(VINAYAKA) Signs of DKASigns of DKA • Dehydration • Hyperventilation • Ketotic breath • Tachycardia and hypotension • Disturbed conscious state and shock • Alteration of consciousness correlate better with elevated serum osmolality (>320 mOsm/L) than with severity of metabolic acidosis
- 22. A&E(VINAYAKA) SymptomsSymptoms • Polyuria • Polydipsia • Nausea and vomiting • Abdominal Pain • Breathing difficulty
- 23. A&E(VINAYAKA) Lab InvestigationsLab Investigations • Serum glucose • Serum electrolytes • Complete blood count • Renal function test • Serum & urine ketones • Blood gas analysis
- 24. A&E(VINAYAKA) Lab InvestigationsLab Investigations • Blood cultures • Sputum collection • Urine analysis & Culture • Liver function tests & Coagulation profiile • Cardiac enzymes • Thyroid function tests • Toxicological Screening
- 25. A&E(VINAYAKA) RadiologyRadiology • Chest X ray • ECG • USG Abdomen • CT Head • Lumbar Puncture
- 26. A&E(VINAYAKA) Corrected SodiumCorrected Sodium Measured Na + 1.6 (Glucose-100) 100 •Na+ depressed 1.6 mEq/L per 100 mg% glucose rise above 100 mg/dl.
- 27. A&E(VINAYAKA) Corrected SodiumCorrected Sodium Example: Na+ = 123 meq/L and Glucose = 1,250 mg/dl Measured Na + 1.6 (Glucose-100) 100 = 123 + 1.6 (1250-100) 100 Corrected Na+ = 123 + 18 = 141 meq/L
- 28. A&E(VINAYAKA) Serum OsmolaritySerum Osmolarity 2(Na) + Glucose + BUN 18 2.8
- 30. A&E(VINAYAKA) Management of DKAManagement of DKA
- 31. A&E(VINAYAKA) Goals of TreatmentGoals of Treatment • Volume Repletion • Reversal of metabolic consequences of insulin insufficiency • Correction of acid-base & electrolyte imbalances • Recognition & Treatment of precipitating causes • Avoidance of complications
- 32. A&E(VINAYAKA) Management of DKAManagement of DKA
- 33. A&E(VINAYAKA) Approach to therapyApproach to therapy • Correcting the hyperosmolar state and dehydration is the initial aim of therapy. • Insulin therapy should be undertaken only after the patient is stable hemodynamically. Glucose and H2O H2O lost in urine Loss of ECF, vascular collapse and death
- 34. A&E(VINAYAKA) Fluid ResuscitationFluid Resuscitation • Single most important step • Fluid deficit around 100ml/kg (5-10L) • Helps in Restore I/V volume • Perfuse vital organs • Increase GFR • Decrease serum Glucose & Ketone levels • To restore normal tonicity
- 35. A&E(VINAYAKA) Fluid balance in diabeticFluid balance in diabetic hyperosmolarityhyperosmolarity ECF = 14 L ICF = 28 L H2O ECF ICF H2O Osmotic Diuresis Osmotic Diuresis ECF hyperosmolar from ICF autotransfusion ECF and ICF both hyperosmolar
- 36. A&E(VINAYAKA) Fluid ResuscitationFluid Resuscitation • NS most frequently administered fluid • 1 litre in 30 min • 2 litres in 2 hours • 2 litres in 2-6 hours • 2 litres in 6-12 hours
- 37. A&E(VINAYAKA)
- 38. A&E(VINAYAKA) Fluid ResuscitationFluid Resuscitation • 2–3 L of 0.9% saline over first 1–3 h (10–15 mL/kg per hour) • 0.45% saline at 150–300 mL/h; change to 5% glucose and 0.45% saline at 100–200 mL/h when plasma glucose reaches 250 mg/dl.
- 39. A&E(VINAYAKA) Fluid ResuscitationFluid Resuscitation •CVP guided fluids should be considered for elderly & those with heart disease •Excess fluid may lead to ARDS & cerebral edema
- 40. A&E(VINAYAKA) Insulin therapyInsulin therapy Mechanism of Action: • Inhibit gluconeogenesis, lipolysis, catabolic hormone secretion, production of ketoacids • Promote potassium, glucose & phosphate uptake in tissues
- 41. A&E(VINAYAKA) Insulin therapyInsulin therapy • Ideal way to administer insulin by continuous infusion of small doses of regular insulin 0.1unit/kg/hr once hypokalemia is excluded. • I/M or S/C administration of regular insulin should be avoided as insulin absorption may be erratic in volume depleted & vasocostricted patient
- 42. A&E(VINAYAKA) Insulin therapyInsulin therapy • Goal is to decrease Glucose by 50-75mg/dl/hr.50-75mg/dl/hr. • Infusion should continue until anion gap normalized • S/C insulin should bridge for atleast one hour before discontinuation of I/V insulin • Insulin administration should be W/H if K <3.3 mEq till K is supplemented
- 43. A&E(VINAYAKA) DKA: Switch to S.C. insulinDKA: Switch to S.C. insulin Can consider switch to SC insulin when: • AG normalized • BS < 250 mg/dl • Insulin IV requirements < 2U/h • Patient able to eat • Hemodynamically stable
- 44. A&E(VINAYAKA) DKA: Switch to S.C. insulinDKA: Switch to S.C. insulin • Overlap insulin IV with 1st SC insulin by 2-4h to avoid recurrent ketosis • T2 DM patients with DKA: • Don’t necessarily have to be continued on insulin • Once acute stress resolved, many do well on OHA
- 45. A&E(VINAYAKA) Potassium CorrectionPotassium Correction • K+ defecit: 3-5 mEq/Kg (350 mEq for 70Kg) • Normal to high serum K+ K+ K+ H+ H+ Ketoacidosis Insulin
- 46. A&E(VINAYAKA) Potassium CorrectionPotassium Correction • Deficiency is due to • Decreased insulin levels • Metabolic Acidosis • Osmotic Diuresis • Frequent Vomitting
- 47. A&E(VINAYAKA) Goal of K ReplacementGoal of K Replacement • To maintain a normal extracellular K+ conc during the acute phase of therapy and to replace intra- cellular deficits over a period of days
- 48. A&E(VINAYAKA) K SupplementationK Supplementation Serum Potassium < 3 mEq/L Give 60mEq/l to IVF 3-3.9 mEq/L 40mEq/l to IVF 4-5.4 mEq/L 20 mEq/L to IVF > 5.5 mEq/L No Replacement necessary Verify Normal kidney function & Urine output before treatment
- 49. A&E(VINAYAKA) BicarbonateBicarbonate • Routine use of supplemental bicarbonate in Rx of DKA is not recommended • Can be given if PH Is less than 6.9
- 50. A&E(VINAYAKA) ADA RecommendationADA Recommendation If PH 6.9-7.0 50mEq of NaHCo3+200ml sterile water+10mEq KCl over 1 hour If Ph <6.9 100mEq of NaHCo3+400ml sterile water+10mEq KCl over 2 hours Repeat dose of bicarb every 2 hours till PH>7
- 51. A&E(VINAYAKA) Theoretical AdvantagesTheoretical Advantages • In case of severe acidosis • Improve myocardial contractility • Improve catecholamine tissue response • Decrease work of breathing • In case of Hyperkalemia • Elevate ventricular fibrillation threshold
- 52. A&E(VINAYAKA) DisadvantagesDisadvantages • Severe & worsening hypokalaemia • Paradoxical CNS acidosis • Impair oxyhemoglobin dissociation • Hypertonicity • Sodium overload
- 53. A&E(VINAYAKA) DisadvantagesDisadvantages • Delayed recovery from ketosis • Elevation of lactic levels • Precipitation of cerebral edema / Pulmonary edema • Thrombophlebitis • Require Central venous cannulation
- 54. A&E(VINAYAKA) HypophosphatemiaHypophosphatemia • Most severe 24-48 hours after treatment • Treatment If Levels <1.0 mg/dl • C/F • Hypoxia • Rhabdomyolysis • Hemolysis • Respiratory failure • Cardiac Dysfunction
- 55. A&E(VINAYAKA) HypophosphatemiaHypophosphatemia • IV (K2PO4 ) : 1ml/hr. (4.4 mEq potassium + 93 mg phosphate ) • S/E • Hyperphosphatemia • Hypocalcemia • Hypomagnesemia • Metastatic soft tissue calcification • Hypernatremia • Osmotic diuresis
- 56. A&E(VINAYAKA) HypomagnesemiaHypomagnesemia • Inhibit parathyroid hormone secretion • hypocalcaemia & hyper phosphatemia • Supplementation if Mg <1.2 mg/dl • Can give Oral Magnesium oxide or • Parenteral Magnesium sulphate
- 57. A&E(VINAYAKA) MonitoringMonitoring • Periodical assessment of vital signs • Level of consciousness • Hourly urine output • Serum glucose Q1H • Serum Potassium Q2H • Regular assessment of anion gap
- 59. A&E(VINAYAKA) DKA in PediatricsDKA in Pediatrics
- 60. A&E(VINAYAKA) Criteria for diagnosisCriteria for diagnosis • Hyperglycemia: CBG > 300mg/dl. • Metabolic acidosis: pH < 7.25 – 7.30 HCO3 - < 15 mEq/L • Ketonemia
- 61. A&E(VINAYAKA) Clinical featuresClinical features • Polyuria • Polydipsia • Polyphagia • Abdominal pain • Nausea and vomiting • Rapid weight loss • Fatigue • Confusion • Visual changes
- 62. A&E(VINAYAKA) SignsSigns • Dehydration • Tachycardia • Hypotension • Kussmaul respiration (rapid & deep) • Sweet, fruity odour on the breath • LOC/Coma (look for cerebral edema)
- 63. A&E(VINAYAKA) Treatment goalsTreatment goals • Establish good perfusion status • Reverse the acidosis • Correct electrolyte disturbances • Control hyperglycemia • Ketonemia
- 65. A&E(VINAYAKA) Correction of acidosisCorrection of acidosis Don’t use bicarbonate as • It will increase chances of cerebral edema by 4 times. • can lead to volume overload, hypernatremia, paradoxical cerebral acidosis, accelerated K+ loss Is there any role for bicarbonate in DKA?
- 66. A&E(VINAYAKA) Indication for bicarbonateIndication for bicarbonate • pH < 7.0 • Hemodynamically unstable • Not responding to fluids • Depressed cardiac contractilty • Poor perfusion Dose: 0.5 – 2 mEq/kg over 1-2 hrs Stop correction once pH >7.0
- 67. A&E(VINAYAKA) Major complication of DKAMajor complication of DKA • Cerebral Edema: most dreaded complication • 57-87% of all pediatric DKA-associated deaths • More in < 5yrs Rare in > 20 yrs.
- 68. A&E(VINAYAKA) Reasons for Cerebral EdemaReasons for Cerebral Edema • Over aggressive fluid correction • Failure of Na+ to rise with fall of glucose during treatment • Cerebral ischemia due to severe dehydration and hypocarbia Onset : 6-12 hrs. after onset of therapy
- 69. A&E(VINAYAKA) Clinical featuresClinical features • Severe headache • Seizures • Papilledema • Respiratory arrest • Altered mental status
- 70. A&E(VINAYAKA)
- 72. A&E(VINAYAKA) IntroductionIntroduction • A metabolic emergency that occurs in diabetic patient usually Type 2 Diabetes Mellitus • Characterised by uncontrolled hyperglycemia that induces hyperosmolar state and dehydration without significant ketoacidosis.
- 73. A&E(VINAYAKA) Diagnostic featuresDiagnostic features • Plasma glucose level of 600 mg/dL or greater • Effective serum osmolality of 320 mOsm/kg or greater • Profound dehydration (8-12 L) with elevated serum urea nitrogen (BUN)-to-creatinine ratio
- 74. A&E(VINAYAKA) Diagnostic featuresDiagnostic features • Small ketonuria and absent-to-low ketonemia • Bicarbonate concentration greater than 15 mEq/L • Some alteration in consciousness
- 75. A&E(VINAYAKA) DKA Vs. HHSDKA Vs. HHS DKA HHS Glucose 250-600 >600 Sodium 125-135 135-145 Potassium Normal/inc Normal Bicarbonate <15meq/l Normal/slightly reduced Arterial pH <7.3 >7.3 Anion gap Increased Normal/slightly increased pCO2 20-30 Normal Osmolality 300-320 >320
- 76. A&E(VINAYAKA) CausesCauses • Dehydration • Pneumonia and UTI • Counter-regulotary hormone (e.g cortisol, cathecolamine, glucagon) • Dialysis • TPN • Non-compliance to OHA or insulin therapy Drugs • Diuretics • B-blocker • Histamine(H2) Blocker • Anti-psychotics Clozapine, Olanzapine • Alcohol and cocaine
- 77. A&E(VINAYAKA) PathophysiologyPathophysiology Concomitant illness Circulating insulin & of counter- regulatory hormones renal clearance and peripheral utilization of glucose Hyperglycemia Osmotic diuresis Loss of electrocyte and water Dehydration Hyperosmolarity Intracellular dehydration
- 78. A&E(VINAYAKA) Clinical features • Occurs only in type 2 DM • Could be initial presentation of the diabetic state • Elderly • Obtundation to coma
- 79. A&E(VINAYAKA) Clinical features • Severe dehydration invariable • May have associated lactic acidosis due to hypoxia • Precipitating factors similar to DKA • Mortality rate is high
- 80. A&E(VINAYAKA) SymptomsSymptoms Symptoms of hyperglycemia : Polydipsia Polyuria Lethargic Others : Weight loss Loss of consciousness
- 81. A&E(VINAYAKA) SymptomsSymptoms A wide variety of focal and global neurologic changes may be present : • Drowsiness and lethargy • Delirium • Coma • Focal or generalized seizures • Visual changes or disturbances • Hemiparesis • Sensory deficits
- 82. A&E(VINAYAKA) Physical examinationPhysical examination Dehydrated : dry skin, lips, mucous membrane, loss skin turgor Vital sign : tachycardia (early dehydration), hypotension (later), temperature Systemic examination to ruled out the cause.
- 83. A&E(VINAYAKA) Differential diagnosisDifferential diagnosis • Alcoholic ketoacidosis • Delirium (altered mentation) • Dementia • Overdose • Thyrotoxicosis (tachycardia, fever, dehydration)
- 84. A&E(VINAYAKA) Lab studiesLab studies • Plasma glucose Hyperglycemia: CBG : > 600 mg/dl • ABG PH> 7.3 HCO3>15 mmol/l • Serum osmolality >320 mmol/l
- 85. A&E(VINAYAKA) OthersOthers • Urine-analysis • Exclude UTI • Proteinuria • Plasma ketone • Plasma electrolyte • Renal function test( Creatinine &BUN) • CBC • Creatine kinase
- 86. A&E(VINAYAKA) Imaging studiesImaging studies Chest radiograph • Exclude pnuemonia • Cardiomegaly CT scan of the head • Exclude haemorrhagic stroke, subdural haematoma • Look for cerebral edema
- 87. A&E(VINAYAKA) ManagementManagement Treatment Goals: • Correction of hypovolemia • Identify and treating underlying cause • Correcting electrolyte abnormalities • Gradual correction of hyperglycemia and osmolarity • Frequent monitoring