DKA/HHS

DKA/HHS Incidence Physiology Diagnosis Predisposing Factors Treatment

Diabetic 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

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

Diagnosis Table with diagnostic parameters

DKA Triad Fig. #2.

Pathophysiology Insulin Deficiency Decreased Glucose utilization Increased Lipolysis Increased Ketoacids Increased Counterregulatory Hormones Osmotic Diuresis Dehydration Electrolyte Loss Potassium

Pathophysiology

DKA vs. HHS

Ketosis Prone T2DM Mostly minorities Presents with DKA 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

Presentation Dehydration Weight loss Weakness Abdominal Pain polyuria, polydipsia Weight loss Weakness Abdominal Pain Correlates with severity of acidosis May be confused with Acute Abdomen

Presentation 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 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.

Predisposing Factors Acute Illness Infection CVA/MI Acute Pancreatitis Venous Thromboembolism Acute Abdomen Renal Failure Heat Stroke Burns Subdural Hematoma Thyrotoxicosis Cushing’s Syndrome Find good table of factors

Predisposing Factors Drugs Previously undiagnosed diabetes Pregnancy Glucocorticoids Beta-Blockers Anti-Psychotics Thiazide Diuretics Niacin TPN Previously undiagnosed diabetes Pregnancy Corticosteroids for lung maturity Terbutiline to prevent pre-term labor

Evaluation Metabolic Panel Arterial Blood Gas CBC, Cultures 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 Gap (Na+) - [(Cl-) + (HCO3)] = 12 +/- 2 Increased ketoacids are the cause for acidosis in DKA

Calculated Osmolality 2(Na+) + Glu/18 = 285-295 >320 usually associated with Mental status change

Treatment Fluids Potassium Insulin Acidosis Monitoring and Transition

Fluids 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? IV Fluid Hydration Insulin Bicarbonate All of the above

Potassium 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

Potassium 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

Insulin Fluids and Potassium first! Start with 0.1unit/Kg IV bolus 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

Insulin 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? pH on ABG Plasma Glucose Anion Gap Serum Ketones Serum Bicarbonate

Close 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

Acidosis Decrease Ketoacids Bicarbonate Fluids increase renal clearance Insulin decreases production Bicarbonate Consider bicarb only if pH<7.0 - Life threatening Otherwise no indication

Phosphate 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. 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

Transition to sc Insulin and Ward!

Transition 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

Transition 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 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!

Starting 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

Questions?