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This document discusses diabetic ketoacidosis (DKA) and other ketoacidotic syndromes. It defines DKA as an acute, life-threatening complication of diabetes characterized by hyperglycemia, ketoacidosis, and ketonuria. The document outlines the pathophysiology, clinical features, diagnostic testing, management, and complications of DKA. It also briefly discusses other ketoacidotic syndromes and their management.

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Diabetic Ketoacidosis and Ketoacidotic Syndromes Kibrom Tsegay, EMCC R1 Moderator:Dr Filmon, EMCC R2 Advisor:Dr Haimanot, EMCC consultant 8/30/2022 Kibrom Tsegay, EMCC R1 1
OUT LINE Objectives Diabetic Ketoacidosis Epidemiology Pathophysiology Clinical features Diagnostic testing Management Complications Disposition and follow-up Ketoacidotic syndromes 8/30/2022 Kibrom Tsegay, EMCC R1 2
Objectives Understanding the definition and pathophysiology of DKA and other ketoacidotic syndromes Understanding Clinical features and Diagnostic testing in DKA Understand Management of DKA and its complications Understanding the disposition and follow-up of DKA patient Understanding Ketoacidotic syndromes and their management 8/30/2022 Kibrom Tsegay, EMCC R1 3
Diabetic Ketoacidosis Acute, life-threatening complication of diabetes mellitus. Characterized by hyperglycemia, ketoacidosis and ketonuria 8/30/2022 Kibrom Tsegay, EMCC R1 4
Epidemiology Predominant in type 1 diabetes mellitus Increasing in non insulin dependent diabetics Incidence of ~ 10,000 cases/year in US Mortality decreased to <1% (prior to insulin was 100%) Mortality is up to 5%, in patients with significant comorbidity & advanced age 8/30/2022 Kibrom Tsegay, EMCC R1 5
Pathophysiology 8/30/2022 Kibrom Tsegay, EMCC R1 6
Pathophysiology 8/30/2022 Kibrom Tsegay, EMCC R1 7
Pathophysiology Absolute or relative insulin deficiency Increase in counter regulatory hormones Glucagon, cortisol, growth hormone, epinephrine gluconeogenesis, glycogenolysis, Sever hyperglycemia DKA after pancreatectomy ? 8/30/2022 Kibrom Tsegay, EMCC R1 8
Pathophysiology Lipolysis Serum FFA Acetone, hydroxybutyrate,acetoacetic acid Increased ketone production with decreased ketone use leads to ketoacidosis Vomiting ,anion gap metabolic acidosis 8/30/2022 Kibrom Tsegay, EMCC R1 9
Dehydration and electrolyte loss Increased glucose load in kidney leads to increased glucose in urine and osmotic diuresis Osmotic diuresis + poor intake and vomiting, produces profound dehydration and electrolyte imbalance Volume depletion leads to impaired GFR RAAS activation 8/30/2022 Kibrom Tsegay, EMCC R1 10
Causes An acute insult leads to decompensation of a chronic disease Inadequate insulin therapy and infection are the most common precipitants New onset diabetes (particularly in children) Myocardial ischemia or infarction Alcohol or drug related problem 8/30/2022 Kibrom Tsegay, EMCC R1 11
CLINICAL FEATURES Clinical manifestations of DKA are related directly to hyperglycemia, volume depletion, and acidosis. Polyuria and polydipsia are usually the only symptoms until ketonemia and acidosis develop 8/30/2022 Kibrom Tsegay, EMCC R1 12
CLINICAL FEATURES History Polydipsia, polyuria, polyphagia Weakness Weight loss Nausea/Vomiting Abdominal Pain 8/30/2022 Kibrom Tsegay, EMCC R1 13
CLINICAL FEATURES Physical Examination Acetone odor on breath (fruity smell) Kussmauls respirations Tachycardia Hypotension Altered mental status Abdominal tenderness 8/30/2022 Kibrom Tsegay, EMCC R1 14
Diagnosis Traditionally, DKA is divided into mild, moderate, and severe states based on total- body deficits of water and electrolytes. 8/30/2022 Kibrom Tsegay, EMCC R1 15
Diagnosis. Definitive diagnosis is established by laboratory criteria (hyperglycemia, ketosis and acidosis Blood glucose level >250 milligrams/dL Anion gap >10 to 12 mEq/L Bicarbonate level <15 mEq/L and a pH <7.3 with moderate ketonuria or ketonemia Urine ketone >=+2 8/30/2022 Kibrom Tsegay, EMCC R1 16
EUGLYCEMIC DKA glucose <250mg/dl Patients presenting shortly after receiving insulin Type1diabetics who are young and vomiting Patients with impaired gluconeogenesis (alcohol abuse or liver failure) Low caloric intake/starvation Pregnancy SGLT2inhibitors 8/30/2022 Kibrom Tsegay, EMCC R1 17
Diagnostic Testing Essential Diagnostic Tests Serum glucose Typically > 250 mg/dL Euglycemic DKA (< 250 mg/dL) Blood gas Patients will exhibit an anion gap metabolic Electrolytes: hypo/hyper/normokalemia,hyponatremia Arterial or venous blood gas can be used 8/30/2022 Kibrom Tsegay, EMCC R1 18
Urinalysis Glucosuria Ketonuria Electrocardiogram (EKG) Typically will exhibit non-specific changes including sinus tachycardia Can see changes associated with hyperkalemia or hypokalemia 8/30/2022 Kibrom Tsegay, EMCC R1 19
Diagnostic Testingcont. Serum potassium Patients with DKA are total body K+ depleted Osmotic diuresis + vomiting lead to potassium loss Often depleted by 100s of mEq Initial serum K+ can be elevated, normal or low Potassium elevation 2ry to acidemia + hyperglycemia 4-6% of patients will present with hypokalemia Serum K+ correction: subtract 0.6 mEq/L from the laboratory K+ value for every 0.1 decrease in pH 8/30/2022 Kibrom Tsegay, EMCC R1 20
Sodium and Other Electrolytes Osmotic diuresis leads -> excessive renal losses of NaCl Hyperglycemia artificially lowers serum sodium l Correction factor: Add 1.6 mEq Na for every 100 mg/dL the glucose is >100mg/dl Osmotic diuresis -> urinary losses and total-body depletion of phosphorous, calcium, and magnesium Hemoconcentration -> 8/30/2022 Kibrom Tsegay, EMCC R1 21
? If the potassium is reported as 5 mEq/L and the pH is 6.94, the corrected potassium value would be ? IF RBS is 400mg/dl , and measured Na is 130 what is the corrected Na measurenment? 8/30/2022 Kibrom Tsegay, EMCC R1 22
Diagnostic Testingcont. BUN/Cr Patients will often exhibit prerenal acute kidney injury BUN/Cr ratio will be elevated reflecting intravascular volume depletion Serum ketones are typically unnecessary in the Emergency Department Blood cultures and other laboratory tests should be done as clinically indicated 8/30/2022 Kibrom Tsegay, EMCC R1 23
Management Basics: ABCs, IV, Cardiac Monitor and 12-lead EKG Establish at least 2 peripheral IVs as patients typically require multiple medication and infusions Diagnosis should be suspected at triage Begin aggressive fluid therapy before receiving laboratory results Diligently search for the underlying cause 8/30/2022 Kibrom Tsegay, EMCC R1 24
Management The goals of therapy are volume repletion reversal of the metabolic consequences of insulin insufficiency correction of electrolyte and acid-base imbalances recognition and treatment of precipitating causes avoidance of complications 8/30/2022 Kibrom Tsegay, EMCC R1 25
Management VOLUME REPLETION Role Replenish intravascular depletion resulting from osmotic diuresis Correct decreased GFR The average adult patient has a water deficit of 100 mL/ kg (5 to 10 L) sodium deficit of 7 to 10 mEq/kg 8/30/2022 Kibrom Tsegay, EMCC R1 26
Management VOLUME REPLETION ADA: 1000-1500 mL of 0.9% NS during the first hour After the 1st hr: maintain between 250 and 500mL/h Adjust to hemodynamic and electrolyte status ADA:Patients with eu or hypernatremia 0.45%NS UK: 9% NS continued throughout the management Blood glucose <250 mg/dL -> add 5% dextrose Patient in hypovolemic shock ? 8/30/2022 Kibrom Tsegay, EMCC R1 27
Management 9% NaCl (Normal Saline) Large volume infusions can cause hyperchloremic metabolic acidosis (unclear impact on patient) In profoundly acidemic patients, avoidance of NS may be beneficial Lactated Ringers Closer to physiologic solution Does not cause hyperchloremic metabolic acidosis Other options: balanced solutions (i.e. Plasma-Lyte) 8/30/2022 Kibrom Tsegay, EMCC R1 28
Management Electrolyte Disorder Correction Potassium most important lab value in DKA Aggressive repletion frequently necessary Patients often 100s of mEq depleted DKA treatments (i.e. fluids, insulin) will decrease serum potassium level Insulin infusion shifts potassium intracellularly 8/30/2022 Kibrom Tsegay, EMCC R1 29
Management POTASSIUM REPLACEMENT Replace after adequate renal function (urine output) is assessed K+ >5.2 initiate regular insulin & check K+ in 2 hrs K+ >3.3 <5.2 add 20-30 meq of K+ to each L of fluid and continue insulin drip K+ <3.3 hold insulin drip and give K+ @20-30 meq/hr until K+ is >3.3 then initiate insulin drip 8/30/2022 Kibrom Tsegay, EMCC R1 30
Management Bicarbonate for acidosis Hypothetically prevent cardiorespiratory compromise Potential deleterious effects Worsening hypokalemia and intracellular acidosis Inhibition of RBC oxygen release at tissue level Delay in improvement of ketosis If pH <6.9 give 100 mmol NaHCO3 in 400ml of water with 20 meq KCL at 200 ml/hr Repeat q 2 hours until pH >7 + Check K+ q 2 hrs 8/30/2022 Kibrom Tsegay, EMCC R1 31
Management Sodium Typically dilutional hyponatremia Will correct without specific treatment Magnesium Hypokalemia = Hypomagnesaemia Both electrolytes lost during osmotic diuresis Cannot replete intracellular K+ without Mg Serum Mg level may not correlate with total body stores Add 0.35 mEq/kg of Mg in the fluids of the first 3 to 4 hrs 8/30/2022 Kibrom Tsegay, EMCC R1 32
Management Insulin therapy Ultimately, patients will require insulin repletion in order to reverse pathophysiology in DKA and stop ketosis Dont give insulin if K+ is <3.3, replace K+ and fluid deficit first 8/30/2022 Kibrom Tsegay, EMCC R1 33
Management Dose Continuous Regular infusion 0.14 units/kg Bolus 0.1units/kg then 0.1/kg/hr continuous infusion If serum glucose doesnt fall by 50-70mg/dl in the first hour double rate of infusion When serum glucose reaches 200 mg/dl decrease infusion rate by 0.02-0.05 units/kg/hr Continue insulin infusion until ketoacidosis is resolved, blood glucose <200, subcutaneous insulin is begun 8/30/2022 Kibrom Tsegay, EMCC R1 34
Management Transition from IV Insulin After DKA Correction It is important to overlap the IV and SC insulin for 2 to 4 hours to avoid potential relapse to hyperglycemia or DKA New-onset diabetics can be started on a total daily dose of 0.5 to 0.8 unit/kg/dL, previously treated diabetic patients can be restarted on their previous insulin dosage. 8/30/2022 Kibrom Tsegay, EMCC R1 35
Continued Management Continuous Monitoring Vital Signs Urine output Serum glucose, K+, Cl, HCO3 , pH q1 hour until stable Insulin Infusion Continue until anion gap normalizes When serum glucose < 250 mg/dL add D5W/0.45%NS solution to avoid hypoglycemia 8/30/2022 Kibrom Tsegay, EMCC R1 36
COMPLICATIONS 8/30/2022 Kibrom Tsegay, EMCC R1 37
Complications COMPLICATIONS RELATED TO THERAPY Hypokalemia from inadequate K+ replacement Hypoglycemia Alkalosis from overaggressive bicarbonate replacement pulmonary edema from overaggressive hydration Cerebral edema 8/30/2022 Kibrom Tsegay, EMCC R1 38
Complications Cerebral Edema Excess accumulation of intracellular and extracellular fluid in the brain Rare (< 1%) complication but high mortality (> 30%) More common in patients with newly diagnosed diabetes presenting with DKA Cause: it is unclear what causes patients to develop cerebral edema usually develops within 4 to 12 hours but can present up to 24 to 48 hours after starting treatment 8/30/2022 Kibrom Tsegay, EMCC R1 39
Complications Signs + Symptoms potential neurologic deterioration New onset or intensifying headache Decline in level of consciousness, Lethargy Focal neurologic deficits (CN III, IV or VI palsy common) recurrent vomiting, incontinence, irritability, abnormal respirations, delayed rise in serum sodium with treatment, 8/30/2022 Kibrom Tsegay, EMCC R1 40
Complications Management Prompt administration of mannitol help to abort further neurologic deterioration Elevate head of bed to 30 degrees Decrease IV fluid infusion Mannitol: 1 gm/kg over 20 minutes 3% Hypertonic saline: 5-10 ml/kg 8/30/2022 Kibrom Tsegay, EMCC R1 41
Complications Best Practice to Prevent Cerebral Edema Slow reduction of osmolality during treatment Avoid large volumes of hypotonic fluid Drop blood glucose slowly during treatment Do not allow plasma Na+ to fall during treatment Avoid unnecessary bicarbonate during treatment Avoid hypoxia, hypo-K+,PO4, Mg 8/30/2022 Kibrom Tsegay, EMCC R1 42
Complications LATER COMPLICATIONS Metabolic acidosis refractory to routine therapy Unrecognized infection (lactic acidosis) Rarely insulin antibodies Improper preparation or administration of the insulin drip Shock that is unresponsive to aggressive fluid therapy Hyperchloremic nonanion gap metabolic acidosis 8/30/2022 Kibrom Tsegay, EMCC R1 43
Complications Late vascular thrombosis Cerebral vessels appear to be most susceptible Volume depletion, low CO, increased blood viscosity, and underlying atherosclerosis may predispose the elderly to this complication Thrombosis may occur Several hrs or days after institution of therapy After resolution of ketoacidosis No studies support prophylactic anticoagulant use 8/30/2022 Kibrom Tsegay, EMCC R1 44
DISPOSITION AND FOLLOW-UP Experienced nursing staff trained in monitoring and management of DKA Written guidelines for DKA management Access to a laboratory presenting early in the course of their illness who can tolerate oral liquids may be managed safely in the ED or observation unit and discharged after 6 to 12 hours of therapy 8/30/2022 Kibrom Tsegay, EMCC R1 45
8/30/2022 Kibrom Tsegay, EMCC R1 46
SPECIAL POPULATIONS RECURRENT DKA PATIENTS PATIENTS WITH INSULIN PUMPS DKA IN PREGNANCY 8/30/2022 Kibrom Tsegay, EMCC R1 47
DKA IN PREGNANCY fetal mortality rate of approximately 30% Lower maternal fasting glucose relative insulin deficiency increased levels of counter regulatory hormones vomiting and urinary tract infections are increased Maternal hyperglycemia, acidosis, hypokalemia also happen in the fetus 8/30/2022 Kibrom Tsegay, EMCC R1 48
Ketoacidotic Syndromes Several conditions result in excessive production of ketoacids The challenge is to differentiate excessive, uncontrolled ketoacidosis from Physiologic ketonemia States where excessive ketones may be produced Toxin altering normal metabolism 8/30/2022 Kibrom Tsegay, EMCC R1 49
8/30/2022 Kibrom Tsegay, EMCC R1 50
PATHOPHYSIOLOGY Ketones are produced through metabolism of long-chain fatty acids Serum ketones are also used as an energy source for the brain The normal blood ketone level is about 1 milligram/dL 8/30/2022 Kibrom Tsegay, EMCC R1 51
PATHOPHYSIOLOGY Ketone production is typically tightly regulated prevent excessive ketoacid production and metabolic acidosis Ketones are metabolized as rapidly as they are formed low levels of insulin are not found in ketoacidotic syndromes except DKA 8/30/2022 Kibrom Tsegay, EMCC R1 52
PATHOPHYSIOLOGY Pathologic states arise when production exceeds metabolism or consumption, resulting in metabolic acidosis. Acetyl coenzyme A, an energy source that can enter the citric acid cycle for metabolism, is produced in the liver and then converted to the ketones 硫-hydroxybutyrate and acetoacetate. 8/30/2022 Kibrom Tsegay, EMCC R1 53
COMMON KETOACIDOTIC SYNDROMES ALCOHOLIC KETOACIDOSIS Occur in alcoholic patients who enter a period of fasting after a dramatic period of ethanol binging results in metabolic acidosis and dehydration, with variable levels of serum glucose Nausea, vomiting, abdominal pain Elevated ratio of 硫-hydroxybutyrate to acetoacetate(10:1) 8/30/2022 Kibrom Tsegay, EMCC R1 54
STARVATION KETOSIS During periods of fasting (overnight) or increased energy demands (exercise), local ketone production increases As the duration of carbohydrate fasting increases hepatic ketone production and Intracerebral ketone utilization increase 8/30/2022 Kibrom Tsegay, EMCC R1 55
STARVATION KETOSIS Fasts of 14 days are well tolerated in those with Adequate endogenous insulin and no other No coexisting condition that alters the serum hormonal milieu Pregnancy induced 24 to 48 hours of vomiting and inadequate oral intake can lead to ketone production with metabolic acidosis, ketonuria, and dehydration 8/30/2022 Kibrom Tsegay, EMCC R1 56
NUTRITIONAL KETOSIS athletic performance enhancement KETOGENIC DIET weight control and seizures TOXIC INGESTIONS primary result of the toxin acetone, aspirin, isoniazid, isopropanol ,methanol, and propylene glycol INBORN ERRORS OF METABOLISM 8/30/2022 Kibrom Tsegay, EMCC R1 57
TREATMENT Treatment of ketoacidosis is supportive Reestablish intravascular volume Monitor and correct electrolyte abnormalities Administer supplemental dextrose Acidosis should clear within 12 to 24 hours 8/30/2022 Kibrom Tsegay, EMCC R1 58
DISPOSITION AND FOLLOW-UP Adults with an uncomplicated ED course can be discharged home resolution of acidosis the patient is able to tolerate oral fluids When caring for complicated conditions coordinate care with the primary team treating the underlying disorder 8/30/2022 Kibrom Tsegay, EMCC R1 59
Reference ROSENS EMERGENCY MEDICINE:CONCEPTS AND CLINICAL PRACTICE, 8th edition Tintinallis Emergency Medicine A Comprehensive Study Guide, 9th edition Uptodate DKA protocol for Emergency and critical unit of Tikur Anbessa Specialized Hospital ADA/UK guidelines 8/30/2022 Kibrom Tsegay, EMCC R1 60
Thank you 8/30/2022 Kibrom Tsegay, EMCC R1 61

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DKA.pptx

  • 1. Diabetic Ketoacidosis and Ketoacidotic Syndromes Kibrom Tsegay, EMCC R1 Moderator:Dr Filmon, EMCC R2 Advisor:Dr Haimanot, EMCC consultant 8/30/2022 Kibrom Tsegay, EMCC R1 1
  • 2. OUT LINE Objectives Diabetic Ketoacidosis Epidemiology Pathophysiology Clinical features Diagnostic testing Management Complications Disposition and follow-up Ketoacidotic syndromes 8/30/2022 Kibrom Tsegay, EMCC R1 2
  • 3. Objectives Understanding the definition and pathophysiology of DKA and other ketoacidotic syndromes Understanding Clinical features and Diagnostic testing in DKA Understand Management of DKA and its complications Understanding the disposition and follow-up of DKA patient Understanding Ketoacidotic syndromes and their management 8/30/2022 Kibrom Tsegay, EMCC R1 3
  • 4. Diabetic Ketoacidosis Acute, life-threatening complication of diabetes mellitus. Characterized by hyperglycemia, ketoacidosis and ketonuria 8/30/2022 Kibrom Tsegay, EMCC R1 4
  • 5. Epidemiology Predominant in type 1 diabetes mellitus Increasing in non insulin dependent diabetics Incidence of ~ 10,000 cases/year in US Mortality decreased to <1% (prior to insulin was 100%) Mortality is up to 5%, in patients with significant comorbidity & advanced age 8/30/2022 Kibrom Tsegay, EMCC R1 5
  • 8. Pathophysiology Absolute or relative insulin deficiency Increase in counter regulatory hormones Glucagon, cortisol, growth hormone, epinephrine gluconeogenesis, glycogenolysis, Sever hyperglycemia DKA after pancreatectomy ? 8/30/2022 Kibrom Tsegay, EMCC R1 8
  • 9. Pathophysiology Lipolysis Serum FFA Acetone, hydroxybutyrate,acetoacetic acid Increased ketone production with decreased ketone use leads to ketoacidosis Vomiting ,anion gap metabolic acidosis 8/30/2022 Kibrom Tsegay, EMCC R1 9
  • 10. Dehydration and electrolyte loss Increased glucose load in kidney leads to increased glucose in urine and osmotic diuresis Osmotic diuresis + poor intake and vomiting, produces profound dehydration and electrolyte imbalance Volume depletion leads to impaired GFR RAAS activation 8/30/2022 Kibrom Tsegay, EMCC R1 10
  • 11. Causes An acute insult leads to decompensation of a chronic disease Inadequate insulin therapy and infection are the most common precipitants New onset diabetes (particularly in children) Myocardial ischemia or infarction Alcohol or drug related problem 8/30/2022 Kibrom Tsegay, EMCC R1 11
  • 12. CLINICAL FEATURES Clinical manifestations of DKA are related directly to hyperglycemia, volume depletion, and acidosis. Polyuria and polydipsia are usually the only symptoms until ketonemia and acidosis develop 8/30/2022 Kibrom Tsegay, EMCC R1 12
  • 13. CLINICAL FEATURES History Polydipsia, polyuria, polyphagia Weakness Weight loss Nausea/Vomiting Abdominal Pain 8/30/2022 Kibrom Tsegay, EMCC R1 13
  • 14. CLINICAL FEATURES Physical Examination Acetone odor on breath (fruity smell) Kussmauls respirations Tachycardia Hypotension Altered mental status Abdominal tenderness 8/30/2022 Kibrom Tsegay, EMCC R1 14
  • 15. Diagnosis Traditionally, DKA is divided into mild, moderate, and severe states based on total- body deficits of water and electrolytes. 8/30/2022 Kibrom Tsegay, EMCC R1 15
  • 16. Diagnosis. Definitive diagnosis is established by laboratory criteria (hyperglycemia, ketosis and acidosis Blood glucose level >250 milligrams/dL Anion gap >10 to 12 mEq/L Bicarbonate level <15 mEq/L and a pH <7.3 with moderate ketonuria or ketonemia Urine ketone >=+2 8/30/2022 Kibrom Tsegay, EMCC R1 16
  • 17. EUGLYCEMIC DKA glucose <250mg/dl Patients presenting shortly after receiving insulin Type1diabetics who are young and vomiting Patients with impaired gluconeogenesis (alcohol abuse or liver failure) Low caloric intake/starvation Pregnancy SGLT2inhibitors 8/30/2022 Kibrom Tsegay, EMCC R1 17
  • 18. Diagnostic Testing Essential Diagnostic Tests Serum glucose Typically > 250 mg/dL Euglycemic DKA (< 250 mg/dL) Blood gas Patients will exhibit an anion gap metabolic Electrolytes: hypo/hyper/normokalemia,hyponatremia Arterial or venous blood gas can be used 8/30/2022 Kibrom Tsegay, EMCC R1 18
  • 19. Urinalysis Glucosuria Ketonuria Electrocardiogram (EKG) Typically will exhibit non-specific changes including sinus tachycardia Can see changes associated with hyperkalemia or hypokalemia 8/30/2022 Kibrom Tsegay, EMCC R1 19
  • 20. Diagnostic Testingcont. Serum potassium Patients with DKA are total body K+ depleted Osmotic diuresis + vomiting lead to potassium loss Often depleted by 100s of mEq Initial serum K+ can be elevated, normal or low Potassium elevation 2ry to acidemia + hyperglycemia 4-6% of patients will present with hypokalemia Serum K+ correction: subtract 0.6 mEq/L from the laboratory K+ value for every 0.1 decrease in pH 8/30/2022 Kibrom Tsegay, EMCC R1 20
  • 21. Sodium and Other Electrolytes Osmotic diuresis leads -> excessive renal losses of NaCl Hyperglycemia artificially lowers serum sodium l Correction factor: Add 1.6 mEq Na for every 100 mg/dL the glucose is >100mg/dl Osmotic diuresis -> urinary losses and total-body depletion of phosphorous, calcium, and magnesium Hemoconcentration -> 8/30/2022 Kibrom Tsegay, EMCC R1 21
  • 22. ? If the potassium is reported as 5 mEq/L and the pH is 6.94, the corrected potassium value would be ? IF RBS is 400mg/dl , and measured Na is 130 what is the corrected Na measurenment? 8/30/2022 Kibrom Tsegay, EMCC R1 22
  • 23. Diagnostic Testingcont. BUN/Cr Patients will often exhibit prerenal acute kidney injury BUN/Cr ratio will be elevated reflecting intravascular volume depletion Serum ketones are typically unnecessary in the Emergency Department Blood cultures and other laboratory tests should be done as clinically indicated 8/30/2022 Kibrom Tsegay, EMCC R1 23
  • 24. Management Basics: ABCs, IV, Cardiac Monitor and 12-lead EKG Establish at least 2 peripheral IVs as patients typically require multiple medication and infusions Diagnosis should be suspected at triage Begin aggressive fluid therapy before receiving laboratory results Diligently search for the underlying cause 8/30/2022 Kibrom Tsegay, EMCC R1 24
  • 25. Management The goals of therapy are volume repletion reversal of the metabolic consequences of insulin insufficiency correction of electrolyte and acid-base imbalances recognition and treatment of precipitating causes avoidance of complications 8/30/2022 Kibrom Tsegay, EMCC R1 25
  • 26. Management VOLUME REPLETION Role Replenish intravascular depletion resulting from osmotic diuresis Correct decreased GFR The average adult patient has a water deficit of 100 mL/ kg (5 to 10 L) sodium deficit of 7 to 10 mEq/kg 8/30/2022 Kibrom Tsegay, EMCC R1 26
  • 27. Management VOLUME REPLETION ADA: 1000-1500 mL of 0.9% NS during the first hour After the 1st hr: maintain between 250 and 500mL/h Adjust to hemodynamic and electrolyte status ADA:Patients with eu or hypernatremia 0.45%NS UK: 9% NS continued throughout the management Blood glucose <250 mg/dL -> add 5% dextrose Patient in hypovolemic shock ? 8/30/2022 Kibrom Tsegay, EMCC R1 27
  • 28. Management 9% NaCl (Normal Saline) Large volume infusions can cause hyperchloremic metabolic acidosis (unclear impact on patient) In profoundly acidemic patients, avoidance of NS may be beneficial Lactated Ringers Closer to physiologic solution Does not cause hyperchloremic metabolic acidosis Other options: balanced solutions (i.e. Plasma-Lyte) 8/30/2022 Kibrom Tsegay, EMCC R1 28
  • 29. Management Electrolyte Disorder Correction Potassium most important lab value in DKA Aggressive repletion frequently necessary Patients often 100s of mEq depleted DKA treatments (i.e. fluids, insulin) will decrease serum potassium level Insulin infusion shifts potassium intracellularly 8/30/2022 Kibrom Tsegay, EMCC R1 29
  • 30. Management POTASSIUM REPLACEMENT Replace after adequate renal function (urine output) is assessed K+ >5.2 initiate regular insulin & check K+ in 2 hrs K+ >3.3 <5.2 add 20-30 meq of K+ to each L of fluid and continue insulin drip K+ <3.3 hold insulin drip and give K+ @20-30 meq/hr until K+ is >3.3 then initiate insulin drip 8/30/2022 Kibrom Tsegay, EMCC R1 30
  • 31. Management Bicarbonate for acidosis Hypothetically prevent cardiorespiratory compromise Potential deleterious effects Worsening hypokalemia and intracellular acidosis Inhibition of RBC oxygen release at tissue level Delay in improvement of ketosis If pH <6.9 give 100 mmol NaHCO3 in 400ml of water with 20 meq KCL at 200 ml/hr Repeat q 2 hours until pH >7 + Check K+ q 2 hrs 8/30/2022 Kibrom Tsegay, EMCC R1 31
  • 32. Management Sodium Typically dilutional hyponatremia Will correct without specific treatment Magnesium Hypokalemia = Hypomagnesaemia Both electrolytes lost during osmotic diuresis Cannot replete intracellular K+ without Mg Serum Mg level may not correlate with total body stores Add 0.35 mEq/kg of Mg in the fluids of the first 3 to 4 hrs 8/30/2022 Kibrom Tsegay, EMCC R1 32
  • 33. Management Insulin therapy Ultimately, patients will require insulin repletion in order to reverse pathophysiology in DKA and stop ketosis Dont give insulin if K+ is <3.3, replace K+ and fluid deficit first 8/30/2022 Kibrom Tsegay, EMCC R1 33
  • 34. Management Dose Continuous Regular infusion 0.14 units/kg Bolus 0.1units/kg then 0.1/kg/hr continuous infusion If serum glucose doesnt fall by 50-70mg/dl in the first hour double rate of infusion When serum glucose reaches 200 mg/dl decrease infusion rate by 0.02-0.05 units/kg/hr Continue insulin infusion until ketoacidosis is resolved, blood glucose <200, subcutaneous insulin is begun 8/30/2022 Kibrom Tsegay, EMCC R1 34
  • 35. Management Transition from IV Insulin After DKA Correction It is important to overlap the IV and SC insulin for 2 to 4 hours to avoid potential relapse to hyperglycemia or DKA New-onset diabetics can be started on a total daily dose of 0.5 to 0.8 unit/kg/dL, previously treated diabetic patients can be restarted on their previous insulin dosage. 8/30/2022 Kibrom Tsegay, EMCC R1 35
  • 36. Continued Management Continuous Monitoring Vital Signs Urine output Serum glucose, K+, Cl, HCO3 , pH q1 hour until stable Insulin Infusion Continue until anion gap normalizes When serum glucose < 250 mg/dL add D5W/0.45%NS solution to avoid hypoglycemia 8/30/2022 Kibrom Tsegay, EMCC R1 36
  • 38. Complications COMPLICATIONS RELATED TO THERAPY Hypokalemia from inadequate K+ replacement Hypoglycemia Alkalosis from overaggressive bicarbonate replacement pulmonary edema from overaggressive hydration Cerebral edema 8/30/2022 Kibrom Tsegay, EMCC R1 38
  • 39. Complications Cerebral Edema Excess accumulation of intracellular and extracellular fluid in the brain Rare (< 1%) complication but high mortality (> 30%) More common in patients with newly diagnosed diabetes presenting with DKA Cause: it is unclear what causes patients to develop cerebral edema usually develops within 4 to 12 hours but can present up to 24 to 48 hours after starting treatment 8/30/2022 Kibrom Tsegay, EMCC R1 39
  • 40. Complications Signs + Symptoms potential neurologic deterioration New onset or intensifying headache Decline in level of consciousness, Lethargy Focal neurologic deficits (CN III, IV or VI palsy common) recurrent vomiting, incontinence, irritability, abnormal respirations, delayed rise in serum sodium with treatment, 8/30/2022 Kibrom Tsegay, EMCC R1 40
  • 41. Complications Management Prompt administration of mannitol help to abort further neurologic deterioration Elevate head of bed to 30 degrees Decrease IV fluid infusion Mannitol: 1 gm/kg over 20 minutes 3% Hypertonic saline: 5-10 ml/kg 8/30/2022 Kibrom Tsegay, EMCC R1 41
  • 42. Complications Best Practice to Prevent Cerebral Edema Slow reduction of osmolality during treatment Avoid large volumes of hypotonic fluid Drop blood glucose slowly during treatment Do not allow plasma Na+ to fall during treatment Avoid unnecessary bicarbonate during treatment Avoid hypoxia, hypo-K+,PO4, Mg 8/30/2022 Kibrom Tsegay, EMCC R1 42
  • 43. Complications LATER COMPLICATIONS Metabolic acidosis refractory to routine therapy Unrecognized infection (lactic acidosis) Rarely insulin antibodies Improper preparation or administration of the insulin drip Shock that is unresponsive to aggressive fluid therapy Hyperchloremic nonanion gap metabolic acidosis 8/30/2022 Kibrom Tsegay, EMCC R1 43
  • 44. Complications Late vascular thrombosis Cerebral vessels appear to be most susceptible Volume depletion, low CO, increased blood viscosity, and underlying atherosclerosis may predispose the elderly to this complication Thrombosis may occur Several hrs or days after institution of therapy After resolution of ketoacidosis No studies support prophylactic anticoagulant use 8/30/2022 Kibrom Tsegay, EMCC R1 44
  • 45. DISPOSITION AND FOLLOW-UP Experienced nursing staff trained in monitoring and management of DKA Written guidelines for DKA management Access to a laboratory presenting early in the course of their illness who can tolerate oral liquids may be managed safely in the ED or observation unit and discharged after 6 to 12 hours of therapy 8/30/2022 Kibrom Tsegay, EMCC R1 45
  • 47. SPECIAL POPULATIONS RECURRENT DKA PATIENTS PATIENTS WITH INSULIN PUMPS DKA IN PREGNANCY 8/30/2022 Kibrom Tsegay, EMCC R1 47
  • 48. DKA IN PREGNANCY fetal mortality rate of approximately 30% Lower maternal fasting glucose relative insulin deficiency increased levels of counter regulatory hormones vomiting and urinary tract infections are increased Maternal hyperglycemia, acidosis, hypokalemia also happen in the fetus 8/30/2022 Kibrom Tsegay, EMCC R1 48
  • 49. Ketoacidotic Syndromes Several conditions result in excessive production of ketoacids The challenge is to differentiate excessive, uncontrolled ketoacidosis from Physiologic ketonemia States where excessive ketones may be produced Toxin altering normal metabolism 8/30/2022 Kibrom Tsegay, EMCC R1 49
  • 51. PATHOPHYSIOLOGY Ketones are produced through metabolism of long-chain fatty acids Serum ketones are also used as an energy source for the brain The normal blood ketone level is about 1 milligram/dL 8/30/2022 Kibrom Tsegay, EMCC R1 51
  • 52. PATHOPHYSIOLOGY Ketone production is typically tightly regulated prevent excessive ketoacid production and metabolic acidosis Ketones are metabolized as rapidly as they are formed low levels of insulin are not found in ketoacidotic syndromes except DKA 8/30/2022 Kibrom Tsegay, EMCC R1 52
  • 53. PATHOPHYSIOLOGY Pathologic states arise when production exceeds metabolism or consumption, resulting in metabolic acidosis. Acetyl coenzyme A, an energy source that can enter the citric acid cycle for metabolism, is produced in the liver and then converted to the ketones 硫-hydroxybutyrate and acetoacetate. 8/30/2022 Kibrom Tsegay, EMCC R1 53
  • 54. COMMON KETOACIDOTIC SYNDROMES ALCOHOLIC KETOACIDOSIS Occur in alcoholic patients who enter a period of fasting after a dramatic period of ethanol binging results in metabolic acidosis and dehydration, with variable levels of serum glucose Nausea, vomiting, abdominal pain Elevated ratio of 硫-hydroxybutyrate to acetoacetate(10:1) 8/30/2022 Kibrom Tsegay, EMCC R1 54
  • 55. STARVATION KETOSIS During periods of fasting (overnight) or increased energy demands (exercise), local ketone production increases As the duration of carbohydrate fasting increases hepatic ketone production and Intracerebral ketone utilization increase 8/30/2022 Kibrom Tsegay, EMCC R1 55
  • 56. STARVATION KETOSIS Fasts of 14 days are well tolerated in those with Adequate endogenous insulin and no other No coexisting condition that alters the serum hormonal milieu Pregnancy induced 24 to 48 hours of vomiting and inadequate oral intake can lead to ketone production with metabolic acidosis, ketonuria, and dehydration 8/30/2022 Kibrom Tsegay, EMCC R1 56
  • 57. NUTRITIONAL KETOSIS athletic performance enhancement KETOGENIC DIET weight control and seizures TOXIC INGESTIONS primary result of the toxin acetone, aspirin, isoniazid, isopropanol ,methanol, and propylene glycol INBORN ERRORS OF METABOLISM 8/30/2022 Kibrom Tsegay, EMCC R1 57
  • 58. TREATMENT Treatment of ketoacidosis is supportive Reestablish intravascular volume Monitor and correct electrolyte abnormalities Administer supplemental dextrose Acidosis should clear within 12 to 24 hours 8/30/2022 Kibrom Tsegay, EMCC R1 58
  • 59. DISPOSITION AND FOLLOW-UP Adults with an uncomplicated ED course can be discharged home resolution of acidosis the patient is able to tolerate oral fluids When caring for complicated conditions coordinate care with the primary team treating the underlying disorder 8/30/2022 Kibrom Tsegay, EMCC R1 59
  • 60. Reference ROSENS EMERGENCY MEDICINE:CONCEPTS AND CLINICAL PRACTICE, 8th edition Tintinallis Emergency Medicine A Comprehensive Study Guide, 9th edition Uptodate DKA protocol for Emergency and critical unit of Tikur Anbessa Specialized Hospital ADA/UK guidelines 8/30/2022 Kibrom Tsegay, EMCC R1 60
  • 61. Thank you 8/30/2022 Kibrom Tsegay, EMCC R1 61

Editor's Notes

  • #4: Explanation