Diabetic Ketoacidosis(DKA)

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    Diabetic

    Ketoacidosis(DKA)

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    Definition DKA - acidosis accompanied by the accumulation

    of ketone bodies in diabetes patient. (1)

    Consist of the biochemical triad of ketonemia,hyperglycemia, and acidemia. (2)

    Most patients with DKA have autoimmune type 1

    diabetes , however patients with type 2 diabetesare also at risk during catabolic stress of acuteillness. (3)

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    Pathophysiology Absolute or relative insulin deficiency accompanied by

    an increase in counter-regulatory hormones whichenhances hepatic gluconeogenesis , glycogenolysis ,and lipolysis. (3,4)

    Absolute insulin deficiency may occur in certaincondition such as undiagnosed type 1 diabetes andpatient who miss their insulin doses. (5)

    Relative insulin deficiency may occur whenconcentrations of counterregulatory hormonesincrease in response to stress conditions. (5)

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    Gluconeogenesis and glycogenolysis will increase

    the blood glucose level and causinghyperglycemia.(3)

    Lipolysis increase serum fatty acids which will

    undergo oxidation as an alternative energy sourceto produce ketone bodies resulting ketonemia andmetabolic acidosis. (3)

    Fluid depletion can occur due to hyperglycemiainduce osmotic diuresis, vomiting due toketoacidosis and inability to take in fluid due todiminished level of consciousness. (2)

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    Sign and symptoms Dry skin

    Characteristic acetone (ketotic) breath odor

    Nausea, vomiting, or abdominal pain

    Tachypnea

    Hypotension

    Tachycardia

    Hypothermia Polyuria, polydipsia, and nocturia

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    Diagnostic criteria (3)

    DIABETES CARE, VOLUME 32, NUMBER 7, JULY 2009

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    Goals of therapy

    Expansion of the intravascular volume.

    Correction of deficit in fluids, electrolyte & acid

    base status.

    Initiation of intravenous insulin infusiontherapy.

    Assessment and monitoring of therapy.

    Treatment of concurrent infection if present.

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    General management issues1. Fluid administration and deficits the most important initial therapeutic intervention

    to restore circulatory volume, clearance of ketonesand correction of electrolytes imbalance.

    Typical deficits in DKA:

    Water (ml/kg) 100

    Sodium (mmol/kg) 7-10

    Chloride (mmol/kg) 3-5

    Potassium (mmol/kg) 3-5

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    2. Insulin therapy

    Insulin has the effects of suppression ofketogenesis, reduction of blood glucose andcorrection of electrolyte imbalance

    Administration of intravenous insulin infusionat a fixed rate of 0.1 units/kg is recommended

    Priming dose of insulin is not necessaryprovided if the insulin infusion is startedpromptly at a dose of at least 0.1 unit/kg/hr .(Kitabchi 2008)(2)

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    3. Metabolic treatment targets

    The recommended targets areReduction of blood ketone concentration by 0.5

    mmol/L/hr

    Increase in venous bicarbonate by 3 mmol/L/hrReduce capillary blood glucose by 3 mmol/L/hrSerum potassium level should be maintain

    between 4-5 mmol/L

    If these rates are not achieved then the fixed rateof intravenous insulin infusion should beincreased.

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    4. Intravenous glucose concentration

    Administration of intravenous infusion of 10%glucose is necessary in order to avoidhypoglycemia and to allow the continuation of a

    fixed rate IVII to suppress ketogenesis.

    Introduction of 10 % glucose is recommendedwhen the blood glucose falls below 14mmol/L

    IVII should not be discontinued until the patientis eating and drinking normally.

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    Management pathway

    Joint British Diabetes Societies Inpatient Care

    Group. The Management of Diabetic Ketoacidosis

    in Adults (March 2010).

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    1. Immediate management upon

    diagnosis at the first hourAims

    Start IV 0.9% sodium chloride solution

    Start a fixed rate IVII after starting fluid therapyEstablished monitoring regime hourly blood

    glucose, ketone measurement and at least 2 hourlyserum potassium for the 1st 6 hours

    Clinical and biochemical assessment of the patient

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    Actions

    1.Intravenous access and initial investigation ABC, IV fluid replacement, clinical assessment,

    lab investigation, and consider precipitatingcauses and treat appropriately.

    2.Restoration of circulating volume

    SBP below 90 mmHg give 500ml of 0.9% Naclover 10-15 minutes.

    Once SBP above 90 mmHg follow fluidreplacement as in table 1

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    Table 1

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    Fluid replacement (Sarawak handbook 3rd ed)

    1 liter NS in 1 hour

    Then 1 liter in 2 hour Then 1 liter in 4 hour

    Then 1 liter in 6 hour

    Then 1 liter in 8 hour

    Potassium replacement

    More than 5 mmol/L no need add KCl

    4.5 5.0 mmol/L add 1 g KCl each liter 3.5 4.5 mmol/L add 2 g KCl each liter

    3 3.5 mmol/L add 3 g KCl each liter

    Less than 3 add 4 g KCl each liter

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    3. Potassium replacement

    Serum K is often high on admission (although totalbody potassium is low) but falls precipitously upontreatment with insulin.

    To maintain K level at 4-5 mmol/L with 20-40

    mmol/L K.

    4. Starting a fixed rate intravenous insulin infusion

    50 units of insulin made up to 50 ml of NS and

    infused at a fixed rate of 0.1 unit/kg/hr Only give stat dose of insulin if there is a delay in

    setting up a fixed rate of IVII.

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    2. 60 minutes to 6 hours

    Aims

    Clear the ketones from blood and suppressketogenesis

    Achieve a rate of fall of ketones of at least 0.5mmol/L/hr

    Or bicarbonate should rise by 3 mmol/L/hr andblood glucose should fall by 3 mmol/L/hr

    Maintain serum K and avoid hypoglycemia

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    Actions

    1.Reassess patient and monitor vital signs Consider urinary catheterisation isfincontinent oranuric

    Accurate fluid balance chart, minimum urine

    output 0.5ml/kg/hr

    2.Review metabolic parameters

    Assess the resolution of ketoacidosis

    Calculate the rate of change of ketone level fall orglucose or rise in bicarbonate

    Ketone falling at least 0.5mmol/L/hr, bicarbonaterise at least 3 mmol/L/hr or glucose falling at least

    3 mmol/L/hr

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    Increase the rate of intravenous insulin infusion ifthe ketone or glucocose level did not fall orbicarbonate level did not increase as above.

    Continue the IVII until ketones less than 0.3mmol/L, venous pH over 7.3 and/or venousbicarbonate over 18 mmol/L

    If glucose falls below 14 mmol/L, 10% glucoseshould be given at 125ml/hr with 0.9% Naclsolution.

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    6 to 12 hoursAims

    Ensure that clinical and biochemical parameters areimproving

    Continue IV fluid replacement and IVII

    Assess for complications of treatment example fluid

    overload or cerebral edemaAvoid hypoglycemia

    Actions

    1. Reassess and monitor patient vital sign2. Review of biochemical and metabolic

    parameters

    Resolution of DKA is defined as ketones less than

    0.3 mmol/L, and venous pH over 7.3

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    12 to 24 hours

    By 24 hours the ketonemia and acidosis shouldhave resolved.

    Aims

    Ensure all parameters are improving or havenormalised.

    Continue iv fluids if not eating or drinking

    Reassess for complications of treatmentTransfer to subcutaneous insulin if patient eating

    and drinking normally

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    Actions

    1. Reassess and monitor patient vital sign

    2. Review of biochemical and metabolicparameters

    Resolution is defined as ketones < 0.3 mmol/L,venous pH > 7.3

    3. Subcutaneous insulin is started before IVinsulin is discontinued. Ideally givesubcutaneous fast acting insulin and a meal anddiscontinue IV insulin one hour later.

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    Complication of DKA treatment

    Hypokalemia and hyperkalemiaPotentially life threatening

    Risk of acute renal failure associated with severedehydration and therefore recommend that no

    potassium should be given with initial fluid resuscitation

    K will always falls as the DKA is treated with insulin andrecommended that 0.9% Nacl solution with potassium40 mmol/L is given as long K level below 5.5 mmol/Land patient is passing urine.

    Joint British Diabetes Societies Inpatient Care Group.The Mana ement of Diabetic Ketoacidosis in Adults March 2010 .

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    Hypoglycemia

    Blood glucose may fal