Diabetic Ketoacidosis(DKA)

7/28/2019 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 fall very rapidly as ketoacidosisis corrected and is a common mistake to allow theblood glucose drop to hypoglycemic levels

This may result a rebound ketosis by counter

regulatory hormones.Severe hypoglycemia can associate with cardiac

arrhythmias brain injury and death.

Once blood glucose drops to 14 mmol/L

intravenous glucose 10% should be given to patient



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Cerebral edema

More common in childrenExact cause is unknown but recent studies suggest

that cerebral hypoperfusion with subsequentreperfusion may be the mechanism operating.

Pulmonary edema

Rapid infusion of crystalloids over a short period oftime increase the risk of complication

Elderly and impaired cardiac function patient alsoat the risk of developing pulmonary edema



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Recommendation and discussion

1. Arterial vs venous measurement?

Difference btw arterial and venous pH is 0.02-0.15 units and bicarbonate is 1.88mmol/L

Not really affect the diagnosis or managementof DKA

Venous blood are easily obtained

Measure venous rather than arterialbicarbonate and pH



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2. Colloid vs crystalloid

Many guideline suggest that in hypotensive patientsinitial fluid resuscitation should use colloid.

However hypotension results from a loss ofelectrolyte solution and it is more physiological to

replace with crystalloid fluid.

It is recommended that 0.9% sodium chloridesolution should be the fluid of choice for

resuscitation in all clinical areas as it supports safepractice and is available ready to use.



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0.9% Nacl vs compound sodium



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3. Initiating treatment with a priming dose of

insulin? Is not really necessary if the insulin infusion is

started promptly at a dose of at least 0.1unit/kg/hr

4. Intravenous phosphate?

No evidence of benefit of phosphate replacement

However, in the presence of respiratory andskeletal muscle weakness, phosphatereplacement should be considered.



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5. Intravenous bicarbonate?

Is not indicated Adequate fluid and insulin therapy will resolve

the acidosis

Acidosis is an adaptive response to improve

oxygen delivery to the tissue causing a rightshift to the oxygen dissociation curve .

Excessive bicarbonate may cause a rise in CO2partial pressure in CSF and may lead to a CSFacidosis.

Use of bicarbonate may increase the risk ofcerebral edema in children and young adults



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Thank you


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Diabetic Ketoacidosis(DKA)