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Dka and Honk
Dka and Honk
Dka and Honk
Susan Schayes M.D Assistant Professor-CT Family Medicine, Emory University School of Medicine
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
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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.
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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 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
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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
Decreased Lipolysis
Islet -Cell Degranulation; Insulin Released in Response to Elevated Plasma Glucose Normal Physiologic Plasma Insulin
Glucose
Production
Glucose
Uptake
Muscle
Adipose Tissue
Euglycemia
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Insulin Resistance
Increased Lipolysis
Glucose
Production
Glucose
Uptake
Muscle
Adipose Tissue
Hyperglycemia
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Diabetic Ketoacidosis:
Key features: hyperglycemia, ketosis, acidosis Clinical presentation: polyuria, polydipsia, polyphagia, weakness, Kussmaulsrespirations, nausea and vomiting Can be mistaken for AGE
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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
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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
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
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
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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 severe dehydration 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 5-7 units per hour, .1 units/kg/hr Patient to ICU Stop insulin drip when sugar is less 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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