dka/hhs. incidence physiology diagnosis predisposing factors treatment incidence physiology ...

DKA/HHSDKA/HHS

DKA/HHSDKA/HHS

Incidence Physiology Diagnosis Predisposing Factors Treatment

Incidence Physiology Diagnosis Predisposing Factors Treatment

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

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

DiagnosisDiagnosis

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

PathophysiologyPathophysiology

DKA vs. HHSDKA vs. HHS

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

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

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…

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.

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

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

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

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

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

TreatmentTreatment

Fluids Potassium Insulin Acidosis Monitoring and Transition

Fluids Potassium Insulin Acidosis Monitoring and Transition

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.

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

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

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

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

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?

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

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

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

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

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

Transition to sc Insulinand Ward!

Transition to sc Insulinand Ward!

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

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

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!

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

Questions?Questions?