Diabetic Ketoacidosis Ver2

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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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