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Diabetic Ketoacidosis (DKA)
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IntroductionDiabetic ketoacidosis (DKA) is an acute, major,
life-threatening complication of diabetes. DKA is defined:
Clinically as an acute state of severe uncontrolled diabetes that
requires emergency treatment with insulin and intravenous fluids.
Biochemically as an increase in the serum concentration of ketones
greater than 5 mEq/L, a blood glucose level of greater than 250
mg/dL (although it is usually much higher),blood pH of less than
7.2, and a bicarbonate level of 18 mEq/L or less.
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PathophysiologyDKA is characterized by hyperglycemia, acidosis,
and ketonuria.DKA is consequence of absolute or relative insulin
deficiency with increase in counter-regulatory hormones .Insulin
and counter-regulatory hormoneGluconeogenesis and glycogenolysis
Hyperglycemia .Lipolysis Free Fatty Acids Ketogenesis Ketonemia and
ketonuria pH and bicarbonate serum levels Metabolic acidosis
Ketoacidosis.
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Pathophysiology cont.Hyperglycemia Glycosuria Osmotic diuresis
dehydration and tissue hypoperfusion.Hyperglycemia, osmotic
diuresis, serum hyperosmolarity, and metabolic acidosis
concentration disturbance.Osmotic diuresis Potassium Sodium loss in
the urine.
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Causes and Precipitating FactorsThe most common
precipitantsInfections (3050%): pneumonia, urinary tract
infections, sepsis, gastroenteritis Inadequate insulin treatment
(2040%): includes noncompliance, insulin pump failure
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Other precipitants
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Clinical
FeaturesSymptoms:Polydypsia.Polyuria.Hyperglycemia.Nausea,
lethargy, anorexia, weakness.Abdominal pain.Reduced motility of
GI.Vomiting.Signs:Dehydration: Dry skin and mucous .Orthostatic
hypotension. Tachycardia. Reduced JVP.Reduced mental
functionKetosis: Sweet odor Kussmaul breathing
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InvestigationsGlucose level.Serum Ketones.Acid-base status: pH,
Serum bicarbonate.Electrolytes: Na +K+ Mg +2ECGCBC,
WBC.Urinalysis.Cardiac markers, Liver enzymes and Amylase.Chest
X-Ray.Blood and urine culture.
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ManagementAssess:Serum electrolytes, Acid-base status and Renal
function.Replace fluids: 23 L of 0.9% saline over first 13 h (1015
mL/kg per hour) subsequently, 0.45% saline at 150300 mL/hchange to
5% glucose and 0.45% saline at 100200 mL/h when plasma glucose
reaches 250 mg/dL (14 mmol/L).
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Management cont.Administer short acting insulin: IV (0.1
units/kg) or IM (0.3 units/kg), then 0.1 units/kg/hour by
continuous IV infusion; increase 2- to 3-fold if no response by 24
h. If initial serum K+ is < 3.3 mmol/L ,do not administer
insulin until the potassium is corrected to > 3.3 mmol/L.Assess
patient: What precipitated the episode (noncompliance, infection,
trauma, infarction, cocaine)? Initiate appropriate workup for
precipitating event (cultures, CXR, ECG).Measure capillary glucose
every 12 h; measure electrolytes (especially K+, bicarbonate,
phosphate) and anion gap every 4 h for first 24 h.
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Management cont.Monitor vital signs, mental status, fluid intake
and output every 14 h.Replace K+: 10 mEq/h when plasma K+ < 5.5
mEq/L, ECG normal, urine flow and normal creatinine documented;
administer 4080 mEq/h when plasma K+ < 3.5 mEq/L or if
bicarbonate is given.Continue above until patient is stable,
glucose goal is 150250 mg/dL, and acidosis is resolved. Insulin
infusion may be decreased to 0.050.1 units/kg per hour.
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ComplicationsCerebral edemaCardiac dysrhythmiaPulmonary
edemaNonspecific myocardial injury may occur in severe
DKAMicrovascular changes consistent with diabetic retinopathy
