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Diabetic Ketoacidosis

is an acute, major, life-threatening

complication of diabetes

mainly occurs in patients with type 1 diabetes

is a state of absolute or relative insulin

deficiency aggravated by ensuing

hyperglycemia, dehydration, and acidosis-

producing derangements in intermediary

metabolism

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Diabetic Ketoacidosis

defined clinically as an acute state of severeuncontrolled diabetes associated withketoacidosis that requires emergency treatment

with insulin and intravenous fluids Biochemically, as an increase in the serum

concentration of ketones greater than 5 mEq/L, ablood glucose level greater than 250 mg/dL, and

a blood pH less than 7.3. Ketonemia andketonuria are characteristic, as is a serumbicarbonate level of 18 mEq/L or less

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Precipitating factors include

medications and drugs that affect carbohydratemetabolism such as corticosteroids, thiazides,loop diuretics, sympathomimetics, anti-hypertensives, anti-histamines, tricyclic

antidepressants, alcohol, cocaine and ecstasy Often DKA develops because of an acute illness

or infection such as pneumonia or urinary tractinfection

Pregnancy, gastroenteritis, trauma, burns,surgery, sepsis, pancreatitis, stroke and silentmyocardial infarction

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Risk Factors Include

Age; preschoool children are most at risk

Stress due to co-existing illness or infection

Inadequate insulin use or poor management of

blood glucose during periods of illnesses are alsorisk factors In children, the most common cause of DKA is poor

compliance with insulin and/or diet.

In adolescents, eating disroders may contribute inup to 20% of recurrent DKA cases

There is no predilection for sex in DKA

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4 main characteristics of DKA

1. Hyperglycemia

2. Ketosis and acidosis

3. Dehydration4. Electrolyte imbalance

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Pathophysiology

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Clinical Presentation

Feeling unwell for a short period, often less than 24 hours

Polydipsia and increased thirst

Polyuria/ nocturia

Polyphagia

Weight lossNausea and vomiting, vomitus can have coffee-ground colour

due to haemorrhagic gastritis

Abdominal pain, due to dehydration and acidosis

WeaknessNeurologic signs: restlessness, agitation, lethargy and

drowsiness, coma. Increased osmolality is the main factorthat contributes to altered mental status

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Clinical Presentation

Deep and rapid breathing, known as Kussmaul breathing,may have acetone odour on breath.

Signs of dehydration due to fluid loss through polyuria,

vomiting and breathing: reduced skin turgor, drymucous membranes

Signs of hypovolaemia: tachycardia, hypotension, posturalhypotension due to fluid loss over 3 litres

Mild hypothermia due to acidosis-induced peripheralvasodilation, warm dry skin.

Fevers are rare despite infection. Severe hypothermia is apoor prognostic sign.

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Diagnostics

Complete blood countLeukocytosis issuggested to be associated with ketosis.Leukocytosis of 10,000-20,000 attributed to

dehydration or stress. 30,000+ suggests aninfection

Blood gas analysisThis is done through VBG.This is done to assess pH and bicarbonate status.

Elevated anion gapComputed as [(Na+K)(Cl+HCO3)]. Mild >10 mM, moderate >12 mM, severe>16 mM

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Diagnostics

BUN and CreatinineMay reveal the presence

of renal failure

Serum electrolytesK is particularly

important. Hyperkalemia may relfect

extracellular shift of K due to insulin deficiency

and acidosis. Later hypokalemia may reflect

depletion of K.

Urinalysisto detect ketonuria and glucosuria

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Management

1. Oxygenation/ ventilation1. 1stpriority, maintain airway and breathing.

2. If patients GCS

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Management

1. Electrolyte replacement1. Giving insulin can cause hypokalemia as glucose is

transported into cells with K.

2. If K < 3.3 mM, replace with KCl at 10 mM/hr until serum K

> 4.4 mM. Place patient on a cardiac monitor whileinfusing to detect arrhythmias.

3. No need to correct Na abnormalities

2. Insulin therapy1. Give insulin only when patient has been hydrated

2. Give bolus of 0.1 U/kg then IV drip of 0.1 U/kg/hr3. Do not reduce glucose by > 4mM/hr or this may cause

cerebral edema

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