DKA/HHS. Incidence Physiology Diagnosis Predisposing Factors Treatment Incidence Physiology ...
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Transcript of DKA/HHS. Incidence Physiology Diagnosis Predisposing Factors Treatment Incidence Physiology ...
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DKA/HHSDKA/HHS
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DKA/HHSDKA/HHS
Incidence Physiology Diagnosis Predisposing Factors Treatment
Incidence Physiology Diagnosis Predisposing Factors Treatment
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Diabetic KetoacidosisDiabetic Ketoacidosis
115,000 hospitalizations in U.S - 2003
10-30% of admissions with primary diagnosis of Diabetes
Mortality fallen 22% over the past 20 years
115,000 hospitalizations in U.S - 2003
10-30% of admissions with primary diagnosis of Diabetes
Mortality fallen 22% over the past 20 years
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Hyperglycemic Hyperosmolar Syndrome
Hyperglycemic Hyperosmolar Syndrome
Lower incidence compared to DKA 1% of DM related admissions Much high mortality rate
~40% compared to <5% for DKA No significant improvement in recent past
Lower incidence compared to DKA 1% of DM related admissions Much high mortality rate
~40% compared to <5% for DKA No significant improvement in recent past
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DiagnosisDiagnosis
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PathophysiologyPathophysiology
Insulin Deficiency Decreased Glucose utilization Increased Lipolysis Increased Ketoacids
Increased Counterregulatory Hormones Osmotic Diuresis
Dehydration Electrolyte Loss
Potassium
Insulin Deficiency Decreased Glucose utilization Increased Lipolysis Increased Ketoacids
Increased Counterregulatory Hormones Osmotic Diuresis
Dehydration Electrolyte Loss
Potassium
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PathophysiologyPathophysiology
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DKA vs. HHSDKA vs. HHS
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Ketosis Prone T2DMKetosis Prone T2DM
Mostly minorities African Americans and Hispanics
Presents with DKA Require insulin treatment initially Can usually be transitioned quickly to Oral
hypoglycemics as outpatient Due to Glucose toxicity or lipotoxicity to
the Beta-Cells
Mostly minorities African Americans and Hispanics
Presents with DKA Require insulin treatment initially Can usually be transitioned quickly to Oral
hypoglycemics as outpatient Due to Glucose toxicity or lipotoxicity to
the Beta-Cells
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PresentationPresentation
Dehydration polyuria, polydipsia
Weight loss Weakness Abdominal Pain
Correlates with severity of acidosis May be confused with Acute Abdomen
Dehydration polyuria, polydipsia
Weight loss Weakness Abdominal Pain
Correlates with severity of acidosis May be confused with Acute Abdomen
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PresentationPresentation
Mental Status changes Related to osmolality more than hyperglycemia
or acidosis More common in HHS
Signs & Symptoms related to underlying cause Infection, CV disease etc…
Mental Status changes Related to osmolality more than hyperglycemia
or acidosis More common in HHS
Signs & Symptoms related to underlying cause Infection, CV disease etc…
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Which statement is incorrectWhich statement is incorrect
Diabetic patients may have silent cardiac ischemia precipitating DKA even without chest pain.
Infection is the most common precipitating factor for DKA.
Cocaine and other illicit drugs are a common factor in DKA.
Prescription drugs only rarely are a precipitating cause of DKA.
Diabetic patients may have silent cardiac ischemia precipitating DKA even without chest pain.
Infection is the most common precipitating factor for DKA.
Cocaine and other illicit drugs are a common factor in DKA.
Prescription drugs only rarely are a precipitating cause of DKA.
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Predisposing FactorsPredisposing Factors
Acute Illness Infection CVA/MI Acute Pancreatitis Venous Thromboembolism Acute Abdomen Renal Failure Heat Stroke Burns Subdural Hematoma Thyrotoxicosis Cushing’s Syndrome
Acute Illness Infection CVA/MI Acute Pancreatitis Venous Thromboembolism Acute Abdomen Renal Failure Heat Stroke Burns Subdural Hematoma Thyrotoxicosis Cushing’s Syndrome
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Predisposing FactorsPredisposing Factors Drugs
Glucocorticoids Beta-Blockers Anti-Psychotics Thiazide Diuretics Niacin TPN
Previously undiagnosed diabetes Pregnancy
Corticosteroids for lung maturity Terbutiline to prevent pre-term labor
Drugs Glucocorticoids Beta-Blockers Anti-Psychotics Thiazide Diuretics Niacin TPN
Previously undiagnosed diabetes Pregnancy
Corticosteroids for lung maturity Terbutiline to prevent pre-term labor
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EvaluationEvaluation
Metabolic Panel Glucose, Na, K, CL, BUN, SCr Anion Gap, Calculate Osm
Arterial Blood Gas CBC, Cultures ECG, required in all older patients Remainder driven by Hx & Px
Metabolic Panel Glucose, Na, K, CL, BUN, SCr Anion Gap, Calculate Osm
Arterial Blood Gas CBC, Cultures ECG, required in all older patients Remainder driven by Hx & Px
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Anion GapAnion Gap
(Na+) - [(Cl-) + (HCO3)] = 12 +/- 2
Increased ketoacids are the cause for acidosis in DKA
(Na+) - [(Cl-) + (HCO3)] = 12 +/- 2
Increased ketoacids are the cause for acidosis in DKA
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Calculated OsmolalityCalculated Osmolality
2(Na+) + Glu/18 = 285-295
>320 usually associated with Mental status change
2(Na+) + Glu/18 = 285-295
>320 usually associated with Mental status change
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TreatmentTreatment
Fluids Potassium Insulin Acidosis Monitoring and Transition
Fluids Potassium Insulin Acidosis Monitoring and Transition
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FluidsFluids
Most Important Initial Treatment Give Normal Saline, 1-1.5 liter in first hr Can Switch to .45% Saline when patient is
Volume replaced and has normal Na+ Add 5% Dextrose when Glucose is
<250mg/dl.
Most Important Initial Treatment Give Normal Saline, 1-1.5 liter in first hr Can Switch to .45% Saline when patient is
Volume replaced and has normal Na+ Add 5% Dextrose when Glucose is
<250mg/dl.
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Which of these therapies for DKA may worsen hypokalemia?
And Why?
Which of these therapies for DKA may worsen hypokalemia?
And Why?
a) IV Fluid Hydration
b) Insulin
c) Bicarbonate
d) All of the above
a) IV Fluid Hydration
b) Insulin
c) Bicarbonate
d) All of the above
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PotassiumPotassium
K+ is total body deficient May be normal to high at presentation
Acidosis, Insulin deficiency
May start supplementation when K+ is <5.0 K+ 4-5meq/L start with 20mEq/L of fluids K+ 3.3-4mEq/L - 40mEq/L of fluids
K+ is total body deficient May be normal to high at presentation
Acidosis, Insulin deficiency
May start supplementation when K+ is <5.0 K+ 4-5meq/L start with 20mEq/L of fluids K+ 3.3-4mEq/L - 40mEq/L of fluids
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PotassiumPotassium
K+ < 3.3mEq/L - Hold Insulin Insulin will drive K+ into cells acutely High risk of Hypokalemic arrhythmia
Give 10-20mEq/L per hour until >3.3 Continue to add 40mEq/L to fluids after
starting insulin
K+ < 3.3mEq/L - Hold Insulin Insulin will drive K+ into cells acutely High risk of Hypokalemic arrhythmia
Give 10-20mEq/L per hour until >3.3 Continue to add 40mEq/L to fluids after
starting insulin
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InsulinInsulin
Fluids and Potassium first! Insulin in pt that is hypovolemic will produce
hypotension secondary to fluid shifts Insulin drives K+ into the cells causing
hypokalemia
Start with 0.1unit/Kg IV bolus
Fluids and Potassium first! Insulin in pt that is hypovolemic will produce
hypotension secondary to fluid shifts Insulin drives K+ into the cells causing
hypokalemia
Start with 0.1unit/Kg IV bolus
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InsulinInsulin
Start Insulin drip Mild cases may be treated with SC insulin
0.1unit/Kg/Hr as continuous infusion Goal is to lower Glucose 50-70mg/hr Do Not Forget:
Add 5% Dextrose when glucose <250mg/dl Goal to keep Glucose 150-200 with continued
insulin infusion Why?
Start Insulin drip Mild cases may be treated with SC insulin
0.1unit/Kg/Hr as continuous infusion Goal is to lower Glucose 50-70mg/hr Do Not Forget:
Add 5% Dextrose when glucose <250mg/dl Goal to keep Glucose 150-200 with continued
insulin infusion Why?
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What do you follow to prove the ketoacidosis has resolved?
What do you follow to prove the ketoacidosis has resolved?
a) pH on ABG
b) Plasma Glucose
c) Anion Gap
d) Serum Ketones
e) Serum Bicarbonate
a) pH on ABG
b) Plasma Glucose
c) Anion Gap
d) Serum Ketones
e) Serum Bicarbonate
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Close the GapClose the Gap
Insulin necessary to utilize glucose and decrease ketoacids
Recommend continuing insulin infusion until Anion Gap and acidosis resolved
Important to transition to SC insulin and make sure patient is eating before stopping the insulin infusion
Insulin necessary to utilize glucose and decrease ketoacids
Recommend continuing insulin infusion until Anion Gap and acidosis resolved
Important to transition to SC insulin and make sure patient is eating before stopping the insulin infusion
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AcidosisAcidosis
Decrease Ketoacids Fluids increase renal clearance Insulin decreases production
Bicarbonate Consider bicarb only if pH<7.0 -
Life threatening Otherwise no indication
Decrease Ketoacids Fluids increase renal clearance Insulin decreases production
Bicarbonate Consider bicarb only if pH<7.0 -
Life threatening Otherwise no indication
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PhosphatePhosphate
Not an immediate concern Consider treatment if Phos <1.0mg/dl. Change KCl replacement to K-Phos This may help avoid hyperchorlemic
acidosis sometimes associated with aggressive NS fluids
Not an immediate concern Consider treatment if Phos <1.0mg/dl. Change KCl replacement to K-Phos This may help avoid hyperchorlemic
acidosis sometimes associated with aggressive NS fluids
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DKA vs. HHSDKA vs. HHS
Differences in treatment: Fluid deficit is larger in HHS Add 5% Dextrose at 300mg/dl in HHS No acidosis or AG to follow HHS resolved when Glucose is <300mg/dl,
Osmolality <320mEq/L and mental status is clear
Differences in treatment: Fluid deficit is larger in HHS Add 5% Dextrose at 300mg/dl in HHS No acidosis or AG to follow HHS resolved when Glucose is <300mg/dl,
Osmolality <320mEq/L and mental status is clear
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Transition to sc Insulinand Ward!
Transition to sc Insulinand Ward!
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TransitionTransition
Continue Insulin infusion until resolution of ketoacidosis
Start SC insulin at least 1-2 hrs before stopping the infusion
Think Ahead: if planning/hoping to stop infusion - consider starting low dose SC insulin that morning or long acting SC insulin the night before
Continue Insulin infusion until resolution of ketoacidosis
Start SC insulin at least 1-2 hrs before stopping the infusion
Think Ahead: if planning/hoping to stop infusion - consider starting low dose SC insulin that morning or long acting SC insulin the night before
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TransitionTransition
Make sure the patient is eating before stopping the infusion
Transition is where I see most mistakes made causing either return to ICU or prolonged stay
Make sure the patient is eating before stopping the infusion
Transition is where I see most mistakes made causing either return to ICU or prolonged stay
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Insulin DosingInsulin Dosing
Based on underlying cause If Non-compliance - return to previous
dosing that showed good control Underlying medical disease may cause
increased insulin requirements Several protocols available if patient is
newly diagnosed Diabetic Endocrine team is happy to help!
Based on underlying cause If Non-compliance - return to previous
dosing that showed good control Underlying medical disease may cause
increased insulin requirements Several protocols available if patient is
newly diagnosed Diabetic Endocrine team is happy to help!
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Starting InsulinStarting Insulin
Weight based insulin regimen 0.4 – 0.8units/Kg/day
How much depends on insulin resistance Obesity Fam hx of type II DM Concomitant illness
40-50% of total as basal and the rest distributed as short acting insulin with meals
Weight based insulin regimen 0.4 – 0.8units/Kg/day
How much depends on insulin resistance Obesity Fam hx of type II DM Concomitant illness
40-50% of total as basal and the rest distributed as short acting insulin with meals
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Questions?Questions?