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Diabetic Ketoacidosis & Hyperosmolar Hyperglycemic State- Inpatient management

Susan Schayes M.D Assistant Professor-CT Family Medicine, Emory University School of Medicine

High Impact Diseases

Jonas Brothers

Learning objectives
Define diagnostic criteria for diabetic ketoacidosis Define diagnostic criteria for hyperosmolar hyperglyemia Understand the five key components to the treatment algorithm

In 1552 BC Diabetes 1st Described In Writing

Earliest known record of diabetes mentioned on 3rd Dynasty Eqyptian papyrus by physician Hesy-Ra: mentions polyuria as a symptom. 250 BC, Apollonius of Memphis coined the name "diabetes meaning "to go through" or siphon. He understood that the disease drained more fluid than a person could consume.

The Word Diabetes Mellitus First Used

Gradually the Latin word for honey, "mellitus," was added to diabetes because it made the urine sweet.

Up to 11th century diabetes was commonly diagnosed by water tasters who drank the urine of those suspected of having diabetes, as it was sweet-tasting.

Early Diabetes Discoveries

In the 1869, Paul Langerhans, a German medical student announced in a dissertation, that the pancreas contains two systems of cells. 1889 Oskar Minkowski and Joseph von Mering in France, removed the pancreas from a dog to determine the effect of an absent pancreas on digestion

Fredrick Banting & Charles Best

Boss leaves on vacation May 1921 Banting and his assistant Best isolate insulin from dogs, and give it to diabetic dogs. Boss returns and is skeptical that insulin works Try extract on themselves, then on:

Leonard Thompson
The first patient to receive injections of pancreatic extract on January 11, 1922. He was 14. The young Toronto resident had been diabetic since 1919. He weighed only 65 pounds and was about to slip into a coma and die. At first he received Dr, F. Bantings and Dr. Charles Bests extract. Two weeks later he used the purified extract of Dr. J.B. Collip and Thompson's symptoms began to disappear; his blood sugar returned to normal and he was brighter and stronger. Thompson lived another 13 years with the insulin. He died at the age of 27 due to pneumonia, a complication of his diabetes

Type 1 vs. type 2 diabetes

Lambert P, et al. Medicine 2006; 34(2): 47-51 Nolan JJ. Medicine 2006; 34(2): 52-56 Features of type 1 diabetes Onset in childhood/adolescence Lean body habitus Acute onset of osmotic symptoms Ketosis-prone High levels of islet autoantibodies High prevalence of genetic susceptibility Features of type 2 diabetes Usually presents in over-30s (but also seen increasingly in younger people) Associated with overweight/obesity Onset is gradual and diagnosis often missed (up to 50% of cases) Not associated with ketoacidosis, though ketosis can occur Immune markers in only 10% Family history is often positive with almost 100% concordance in identical twins

Manage symptoms Prevent acute and late complications Improve quality of life Avoid premature diabetes-associated death An individualized approach

Goals of management

Glycemic control Lifestyle (e.g. diet & exercise) Microalbuminuria & kidneys

BP Lipids Management Patient education Eye care Foot care

Normal Physiologic Insulin Sensitivity and -Cell Function Produce Euglycemia

Normal -Cell Function Pancreas Liver
Decreased Plasma FFA

Normal Insulin Sensitivity

Decreased Lipolysis

Islet -Cell Degranulation; Insulin Released in Response to Elevated Plasma Glucose Normal Physiologic Plasma Insulin




Decreased Glucose Output

Adipose Tissue

Increased Glucose Transport


-Cell Dysfunction and Insulin Resistance Produce Hyperglycemia in Type 2 Diabetes

-Cell Dysfunction Pancreas Liver
Elevated Plasma FFA

Insulin Resistance

Increased Lipolysis

Islet -Cell Degranulation; Reduced Insulin Content



Increased Glucose Output Reduced Plasma Insulin


Adipose Tissue


Decreased Glucose Transport & Activity (expression) of GLUT4

Diabetic Ketoacidosis:
Key features: hyperglycemia, ketosis, acidosis Clinical presentation: polyuria, polydipsia, polyphagia, weakness, Kussmaulsrespirations, nausea and vomiting Can be mistaken for AGE


Diabetic Ketoacidosis
Cause: reduced insulin levels, decreased glucose use, increased gluconeogenesis Primarily affects TIDM, but can be T2DM Precipitating factor: Infection, Noncompliance, Other acute event ie MI


Diabetic Ketoacidosis:
Treatment involves 5 key components: Monitoring Fluid resuscitation Insulin and dextrose infusion Electrolyte repletion Treating underlying cause


Glucose Hyperglycemia Glycosuria

Ketoacidosis is a state of uncontrolled catabolism Osmotic associated with Diuresis insulin deficiency.

Ketones Acidosis Vomitin g

Fluid & Electrolyte Depletion

Renal Hypoperfusion Impaired Excretion of Ketones & Hydrogen ions

CLINICAL FEATURES Polyuria leading to Oliguria Dehydration, Thirst Hypotension, Tachycardia, Peripheral circulatory failure Ketosis Hyperventilation Vomiting Abdominal pain (acute abdomen) Drowsiness, Coma

METABOLIC FEATURES Hyperglycemia Glycosuria Non-respiratory Acidosis Ketonemia Uremia Hyperkalemia Hypertriglyceridemia Hemoconcentration

Dx Criteria for Mild DKA

Glucose > 250 Arterial pH 7.25-7.30 Serum bicarb 15-18 mEq Urine and Serum ketones B-hydroxybutyrate- high Anion gap >10 Patient is alert
Trachtenbarg David, Diabetic Ketoacidosis, American Family Physician, 19 2005;71:1705-1714

Dx Criteria for Moderate DKA

Glucose > 250 Arterial pH 7.00-7.24 Serum bicarb 10 to <15 mEq Urine and Serum ketones B-hydroxybutyrate- high Anion gap >12 Patient is alert/drowsy
Trachtenbarg David, Diabetic Ketoacidosis, American Family Physician, 20 2005;71:1705-1714

Dx Criteria for Severe DKA

Glucose > 250 Arterial pH <7.00 Serum bicarb <10 mEq Urine and Serum ketones B-hydroxybutyrate- high Anion gap >12 Patient is stupor/coma
Trachtenbarg David, Diabetic Ketoacidosis, American Family Physician, 21 2005;71:1705-1714

Dx Criteria for HHS

Glucose > 600 Arterial pH <7.30 Serum bicarb <15 mEq Urine and Serum ketones- small B-hydroxybutyrate- n or elevated Anion gap-variable Patient is stupor/coma
Trachtenbarg David, Diabetic Ketoacidosis, American Family Physician, 22 2005;71:1705-1714

DKA- Monitoring
ICU 2 IVs, Oxygen, cardiac monitor, continuous vitals, pulse ox Foley to monitor I &O Initially blood work every 1-2 hours If pH is less that 6.9 be frightened

DKA- Monitoring Standard blood work

Glucose, lytes with calculated anion gap, Mag Bun & creatinine, calculate GFR Beta-hydroxybutyrate or serum ketones UA CBC EKG

Infection-cultures,chest xray Cardiac status-cardiac enzymes


DKA- Fluids
Deficits are typically 100 ml per kg Fluid replacement will lower glucose Initial Tx usually fluid, fluid, fluid Initial resuscitation 15-20 ml/kg stat for severe dehydration with normal saline 1l,1l,1l,then 500ml X4 hours, reassess/reassess Once glucose below 250, switch to D5W/.45% N saline


Initially 10 units R Insulin IV, .15 units/kg Insulin drip, most protocols 5-7 units per hour, .1 units/kg/hr Patient to ICU Stop insulin drip when sugar is less than 250


Electrolytes- K
Whole body potassium deficits exist. (3-5 mmol/kg) Acidosis increases K Glucose + Insulin lowers K Start K with K less than 5 mmol and adequate urine output If initial K less than 3.3 mmol replete, and then start insulin when K above 3.3 mmol/L

Electrolytes- K
Commonly under repleted Resident mistakenly uses the replacement of potassium protocol, which vastly under repletes potassium Watch like a hawk!!!! Replace/repete/replace/repete

Electrolytes- Mg
A serum deficit usually exists of .5-1 mmol per L Consider repleting if less than 1.8 mg/dL



Protocols- but use Common sense which is not common