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DKA and HHS
This document discusses diabetic ketoacidosis (DKA), providing information on its pathophysiology, classification, precipitating factors, signs and symptoms, laboratory investigations, management, and goals of treatment. It classifies DKA as mild, moderate or severe based on plasma glucose, arterial pH, serum bicarbonate, urine ketones, and anion gap. The key aspects of management include fluid resuscitation to restore intravascular volume, insulin therapy to reduce glucose and ketone levels, and potassium supplementation to correct deficiencies. Bicarbonate supplementation is only recommended if the pH is less than 6.9.
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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
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- 3. A&E(VINAYAKA) IntroductionIntroduction • Acute lifethreatening 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
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- 5. A&E(VINAYAKA) ClassificationClassification Mild DKA Moderate DKA Severe DKA Plasmaglucose > 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
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- 7. A&E(VINAYAKA) • Facilitate uptake ofglucose & 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 isthe primary defect in patients with DKA Muscle Hepatocyte Adipose Glucose Amino Acids Glucose-P Glycogen Pyruvate, CO2 Glucose Free fatty acidsKetoacids Normal Insulin Activity
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- 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
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- 13. A&E(VINAYAKA) • Insulin Deficiency Glycogenolysis Gluconeogenesis Hepaticglucose output Lipolysis: Release FFA -> liver VLDL & ketones Ketonemia and hyper TG Acidosis , Hyperglycemia & Osmotic diuresis DKA - LateDKA - Late Increased Production & Decreased Utilization Fasting hyperglycemia
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- 15. A&E(VINAYAKA) Islets of Langerhans β-cell destructionInsulin 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 ofDKAPrecipitating 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 DKADrugsPrecipitate DKA • Diuretics • Lithium • Beta Blockers • Mannitol • Chlorpromazine • Cimetidine • Glucocorticoids • Neuroleptics • Phenytoin • Didanosine • Calcium-channel blockers • Pentamidine
- 19. A&E(VINAYAKA) Clinical featuresClinical features Hyperglycemia Osmoticdiuresis 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 DKASignsof 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 Xray • ECG • USG Abdomen • CT Head • Lumbar Puncture
- 26. A&E(VINAYAKA) Corrected SodiumCorrected Sodium MeasuredNa + 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
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- 31. A&E(VINAYAKA) Goals of TreatmentGoalsof Treatment • Volume Repletion • Reversal of metabolic consequences of insulin insufficiency • Correction of acid-base & electrolyte imbalances • Recognition & Treatment of precipitating causes • Avoidance of complications
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- 33. A&E(VINAYAKA) Approach to therapyApproachto 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 indiabeticFluid 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
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- 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 •CVPguided 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 Mechanismof 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 toS.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 toS.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 KReplacementGoal 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 SerumPotassium < 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 useof 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 IfPH 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 recoveryfrom ketosis • Elevation of lactic levels • Precipitation of cerebral edema / Pulmonary edema • Thrombophlebitis • Require Central venous cannulation
- 54. A&E(VINAYAKA) HypophosphatemiaHypophosphatemia • Most severe24-48 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 parathyroidhormone 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 assessmentof vital signs • Level of consciousness • Hourly urine output • Serum glucose Q1H • Serum Potassium Q2H • Regular assessment of anion gap
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- 59. A&E(VINAYAKA) DKA in PediatricsDKAin Pediatrics
- 60. A&E(VINAYAKA) Criteria for diagnosisCriteriafor 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
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- 65. A&E(VINAYAKA) Correction of acidosisCorrectionof 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 bicarbonateIndicationfor 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 ofDKAMajor 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 CerebralEdemaReasons 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
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- 72. A&E(VINAYAKA) IntroductionIntroduction • A metabolicemergency 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. HHSDKAVs. 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 • Pneumoniaand 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 • Occursonly in type 2 DM • Could be initial presentation of the diabetic state • Elderly • Obtundation to coma
- 79. A&E(VINAYAKA) Clinical features • Severedehydration 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 varietyof 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 • ExcludeUTI • Proteinuria • Plasma ketone • Plasma electrolyte • Renal function test( Creatinine &BUN) • CBC • Creatine kinase
- 86. A&E(VINAYAKA) Imaging studiesImaging studies Chestradiograph • Exclude pnuemonia • Cardiomegaly CT scan of the head • Exclude haemorrhagic stroke, subdural haematoma • Look for cerebral edema
- 87. A&E(VINAYAKA) ManagementManagement Treatment Goals: • Correctionof hypovolemia • Identify and treating underlying cause • Correcting electrolyte abnormalities • Gradual correction of hyperglycemia and osmolarity • Frequent monitoring
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