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Diabetic Ketoacidosis &

Hyperosmolar HyperglycemicState- Inpatient management

Susan Schayes M.D

Assistant Professor-CT

Family Medicine, Emory University

School of Medicine

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High Impact Diseases

/

Jonas Brothers

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Learning objectives

• Define diagnostic criteria

for diabetic ketoacidosis

• Define diagnostic criteria

for hyperosmolar 

hyperglyemia

• Understand the five keycomponents to the

treatment algorithm

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In 1552 BC

Diabetes 1st Described In Writing

• Earliest known record of diabetes

mentioned on 3rd Dynasty Eqyptian papyrus

by physician Hesy-Ra: mentions polyuriaas 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.

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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 commonlydiagnosed by “water tasters” who drank the

urine of those suspected of having

diabetes, as it was sweet-tasting.

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Early Diabetes Discoveries

• In the 1869, Paul Langerhans, a

German medical student announced

in a dissertation, that the pancreascontains two systems of cells.

•1889 Oskar Minkowski and Josephvon Mering in France, removed the

pancreas from a dog to determine

the effect of an absent pancreas on

digestion

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Fredrick Banting &

Charles Best

• Boss leaves on vacation

May 1921

• Banting and his assistant

Best isolate insulin fromdogs, and give it to

diabetic dogs.

• Boss returns and is

skeptical that insulin

works

• Try extract on

themselves, then on:

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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 poundsand was about to slip into a coma and die. At

first he received Dr, F. Banting’s and Dr. Charles

Best’s 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

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Type 1 vs. type 2 diabetesLambert P, et al. Medicine 2006; 34(2): 47-51

Nolan JJ. Medicine 2006; 34(2): 52-56

Features of type 2 diabetes

• Usually presents in over-30s (butalso seen increasingly inyounger people)

•  Associated with

overweight/obesity• Onset is gradual and diagnosis

often missed (up to 50% of cases)

• Not associated with

ketoacidosis, though ketosis canoccur 

• Immune markers in only 10%

• Family history is often positivewith almost 100% concordancein identical twins

Features of type 1 diabetes

• Onset inchildhood/adolescence

• Lean body habitus

•  Acute onset of osmoticsymptoms

• Ketosis-prone

• High levels of isletautoantibodies

• High prevalence of geneticsusceptibility

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Goals of management• Manage symptoms

• Prevent acute and late complications• Improve quality of life

•  Avoid premature diabetes-associated death

•  An individualized approach

Management

Glycemic

control

BP

Lipids

Patienteducation

Lifestyle

(e.g. diet & exercise)

Foot care

Eye careMicroalbuminuria

& kidneys

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Normal Physiologic Insulin

Sensitivity and β-Cell Function

Produce Euglycemia

Pancreas

Normal Insulin Sensitivity

Liver 

EuglycemiaEuglycemia

Islet β-Cell Degranulation;

Insulin Released in Response to

Elevated Plasma Glucose Muscle Adipose Tissue

Increased Glucose

Transport 

Decreased

Lipolysis

↓ Glucose

Production

↑ Glucose

Uptake

Normal Physiologic 

Plasma Insulin

Decreased Glucose Output 

Normal β-Cell Function

Decreased

Plasma FFA

Decreased

Plasma FFA

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β-Cell Dysfunction and Insulin

Resistance Produce Hyperglycemia in

Type 2 Diabetes

Pancreas

Insulin Resistance

Liver 

HyperglycemiaHyperglycemia

Islet β-Cell Degranulation;

Reduced Insulin Content 

Muscle Adipose Tissue

Decreased Glucose

Transport & Activity 

(expression)

of GLUT4

Increased

Lipolysis

↑Glucose

Production

↓Glucose

Uptake

Reduced 

Plasma Insulin

Increased Glucose Output 

β-Cell Dysfunction

Elevated

Plasma FFA

Elevated

Plasma FFA

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Diabetic Ketoacidosis:

• Key features: hyperglycemia, ketosis, acidosis

• Clinical presentation: polyuria, polydipsia,

polyphagia, weakness, Kussmauls’respirations,

nausea and vomiting

• Can be mistaken for AGE

 

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Diabetic Ketoacidosis

•  

Cause: reduced insulin levels, decreasedglucose use, increased gluconeogenesis

Primarily affects TIDM, but can be T2DM

Precipitating factor: Infection,

Noncompliance,

Other acute event ie MI

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Diabetic Ketoacidosis:

• Treatment involves 5 key components:

• Monitoring

• Fluid resuscitation

• Insulin and dextrose infusion

• Electrolyte repletion

• Treating underlying cause

 

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PATHOGENESIS

OsmoticDiuresis

Renal Hypoperfusion

Impaired Excretion of Ketones & Hydrogen ions

Fluid & ElectrolyteDepletion

Vomitin

g

 AcidosisHyperglycemia

Glycosuria

GlucoseKetones

Ketoacidosis

is a state of 

uncontrolled catabolismassociated with

insulin deficiency.

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CLINICAL FEATURES

•  Polyuria leading to Oliguria

• Dehydration, Thirst

• Hypotension, Tachycardia,

• Peripheral circulatory failure

• Ketosis

• Hyperventilation

• Vomiting

• Abdominal pain (acute abdomen)

• Drowsiness, Coma

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METABOLIC FEATURES

• Hyperglycemia

• Glycosuria

• Non-respiratory Acidosis

• Ketonemia

• Uremia

• Hyperkalemia

• Hypertriglyceridemia

• Hemoconcentration

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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,2005;71:1705-1714

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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,2005;71:1705-1714

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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,2005;71:1705-1714

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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,2005;71:1705-1714

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DKA- Monitoring

 

• ICU

• 2 IV’s, 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

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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

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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 severedehydration with normal saline

• 1l,1l,1l,then 500ml X4 hours, reassess/reassess

 

• Once glucose below 250, switch to

D5W/.45% N saline

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Insulin

• Initially 10 units R Insulin IV,

.15 units/kg

• Insulin drip, most protocols 5-7units per hour, .1 units/kg/hr 

• Patient to ICU

•Stop insulin drip when sugar isless than 250

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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

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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

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Electrolytes- Mg

•  A serum deficit usually exists

of .5-1 mmol per L

• Consider repleting if less than 1.8 mg/dL

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DKA & HONK

Protocols- but use

Common sense whichis not common