diabeticketoacedosis

8/2/2019 diabeticketoacedosis

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Nursing management of aNursing management of apatientpatient

with diabetic ketoacidosiswith diabetic ketoacidosis


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INTERNATIONALINTERNATIONAL - incidence is not- incidence is notknown but may be higher inknown but may be higher in

developing countries.developing countries.RACERACE - incidence is higher in whites- incidence is higher in whites

because of higher incidence ofbecause of higher incidence of

type1diabetes in this racial group.type1diabetes in this racial group.SEXSEX - common in females than in- common in females than in

males.males.AGEAGE - individuals


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Mortality/MorbidityMortality

/Morbidity

o 2% per episode2% per episode

o before discovery of insulin in 1922 thebefore discovery of insulin in 1922 the

mortality rate was 100%mortality rate was 100%

o best results with patient treated in ICUbest results with patient treated in ICU

during first two days of hospitalization.during first two days of hospitalization.

o

in contrast mortality rate is still high inin contrast mortality rate is still high in

developing countries and among nondeveloping countries and among non

hospitalized patients.hospitalized patients.


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DefinitionDefinition

Diabetic ketoacidosis is defined clinically as anDiabetic ketoacidosis is defined clinically as an

acute state of severe uncontrolled diabetes thatacute state of severe uncontrolled diabetes that

requires emergency treatment with insulin andrequires emergency treatment with insulin and

intravenous fluids.intravenous fluids.

DKA is defined biochemically as an increase in theDKA is defined biochemically as an increase in the

serum concentration of ketones greater thanserum concentration of ketones greater than

5mEq/L, a blood glucose level of greater than5mEq/L, a blood glucose level of greater than

250mg/dl, blood pH of less than 7.2 and a250mg/dl, blood pH of less than 7.2 and a

biocarbonate level of 18mEq/L or less.biocarbonate level of 18mEq/L or less.


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CAUSES OF DKACAUSES OF DKA

PATIENTS WITH TYPE1 DIABETESPATIENTS WITH TYPE1 DIABETES acute insulin deficiencyacute insulin deficiency poor compliance with insulinpoor compliance with insulin psychological stress or lack of educationpsychological stress or lack of education bacterial infectionbacterial infection intercurrent illnessintercurrent illness medical, surigal, or emotional stressmedical, surigal, or emotional stress brittle diabetesbrittle diabetes idiopathicidiopathic anti insulin factorsanti insulin factors Insulin infusion catheter blockageInsulin infusion catheter blockage

mechanical failure of insulin infusion pump.mechanical failure of insulin infusion pump. PATIENTS WITH TYPE2 DIABETESPATIENTS WITH TYPE2 DIABETES

intercurrent illnessintercurrent illness medicationsmedications


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Pathophysiology of DKAPathophysiology of DKA

Absolute/relativeAbsolute/relative

insulin deficiencyinsulin deficiency ++

Increase in counter-Increase in counter-

regulatory hormones.regulatory hormones.

(glucagon,(glucagon,

cortisol,growthcortisol,growthhormone,epinephrine)hormone,epinephrine)

Hormonal imbalanceHormonal imbalance

Enhances gluconeogenesis , glucogenolysis (lipolysis)


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SevereSeverehyperglycaemiahyperglycaemia

Exceeds renalExceeds renal

threshold of glucosethreshold of glucoseabsorption & results inabsorption & results in

significant glycosuria.significant glycosuria. Increases water loss inIncreases water loss in

urin due to osmoticurin due to osmotic

diuresis,diuresis, SevereSevere

dehydration,acidosis.dehydration,acidosis.

Increases serumIncreases serumfattyacids.fattyacids.

hepatic metabolismhepatic metabolism

of fattyacids.of fattyacids.

ketogenesis.ketogenesis.

Results in intermediateResults in intermediateand end metabolites.and end metabolites.(ketones & ketoacids)(ketones & ketoacids)


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AcetoneAcetone

produces ketotic breathproduces ketotic breath

BetahydroxybutyrateBetahydroxybutyrate

Induces nausea &Induces nausea &vomitingvomiting

Increases fluid electrolyteIncreases fluid electrolyteloss.loss.

AcetoacetateAcetoacetate

Progressive rise of bloodProgressive rise of blood

concentration of theseconcentration of theseacidic organic substances.acidic organic substances.

leads toleads to

State of ketonemia.State of ketonemia.


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Natural body buffers can buffer ketonemia in early stage.Natural body buffers can buffer ketonemia in early stage.

Accumulated ketones exceed bodys capacity of extracting them,Accumulated ketones exceed bodys capacity of extracting them,they overflow into urine.they overflow into urine.

i.e, ketonuria.i.e, ketonuria.

If not treated promptly.If not treated promptly.

More accumulation of organic acids leads to frank clinical metabolicMore accumulation of organic acids leads to frank clinical metabolicacidosis.acidosis.

i.e, ketoacidosisi.e, ketoacidosis

Ph HCO3 LEVEL Respiratory compensation of thisPh HCO3 LEVEL Respiratory compensation of thisacidotic condition.acidotic condition.

KUSSMAUL RESPIRATION.KUSSMAUL RESPIRATION.


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Clinical features of DKAClinical features of DKA POLYURIA, POLYDIPSIA, POLYPHAGIA.POLYURIA, POLYDIPSIA, POLYPHAGIA. NAUSEA, VOMITING.NAUSEA, VOMITING.

DIFFUSED ABDOMINAL PAIN.DIFFUSED ABDOMINAL PAIN. GENERALISED WEAKNESS.GENERALISED WEAKNESS. ALTERED SENSORIUM.ALTERED SENSORIUM. FLU LIKE SYMPTOMS.FLU LIKE SYMPTOMS. KETOTIC BREATH.KETOTIC BREATH. HYPERVENTILATION.HYPERVENTILATION. EXTREME WT LOSS.EXTREME WT LOSS. MUSLE WASTING.MUSLE WASTING. ACUTE CHEST PAIN OR PALPITATION .ACUTE CHEST PAIN OR PALPITATION . PAINLESS INFARCTION.PAINLESS INFARCTION. H/O MISSING INSULIN DOSE.H/O MISSING INSULIN DOSE. H/O RAPID WT LOSSIN PTS WHO ARE NEWLY DIAGNOSED TYPE 1H/O RAPID WT LOSSIN PTS WHO ARE NEWLY DIAGNOSED TYPE 1 DIABETES MELLITUS.DIABETES MELLITUS. SIGNS OF DEHYDRATION.SIGNS OF DEHYDRATION. SIGNS OF ACIDOSIS.SIGNS OF ACIDOSIS. SIGNSOF INTERCURRENT ILLNESS.SIGNSOF INTERCURRENT ILLNESS.


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Lab studiesLab studiesComplete blood cell countComplete blood cell count

Blood glucose levels >250mg/dlBlood glucose levels >250mg/dl Sodium decreasesSodium decreases Potassium increasesPotassium increasesHCO3 levels assess degree of acidosisHCO3 levels assess degree of acidosis

ABG levels pH is often


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MANAGEMENT OF DKAMANAGEMENT OF DKA THERAPEUTIC GOALS FOR DKATHERAPEUTIC GOALS FOR DKA:-:-

To improve circulatory volume and tissue perfusion.To improve circulatory volume and tissue perfusion. To reduce blood glucose and serum osmolality towardsTo reduce blood glucose and serum osmolality towards

normal levels with insulin.normal levels with insulin.

To clear ketones from serum and urine at steady rate.To clear ketones from serum and urine at steady rate.

To correct electrolyte imbalance, particularly potassiumTo correct electrolyte imbalance, particularly potassiumloss.loss.

To indentify precipitating factors.To indentify precipitating factors.

To correct acid-base balance.To correct acid-base balance.

To treat concurrent infection.To treat concurrent infection.

To provide immediate hyperglycemic care.To provide immediate hyperglycemic care.

To prevent complications.To prevent complications.


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Correction of fluid loss with iv fluidsCorrection of fluid loss with iv fluids

FLUIDS sodium or by ringer lactate.FLUIDS sodium or by ringer lactate.

administer 1lt over the first 30 minutes.administer 1lt over the first 30 minutes.

administer 1lt over the 2administer 1lt over the 2ndnd hour.hour.

administer 1lt over the following 2hrs.administer 1lt over the following 2hrs.

administer 1lt every 4hrs.administer 1lt every 4hrs.

euvolemic or hypernatremic switch toeuvolemic or hypernatremic switch to

half the isotonic sodium chloride solution.half the isotonic sodium chloride solution.When blood sugar falls less thanWhen blood sugar falls less than

180mg/dl, saline is replaced with 5-10%180mg/dl, saline is replaced with 5-10%

dextrose with half isotonic saline.dextrose with half isotonic saline.


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To correct hyperglycemia with insulinTo correct hyperglycemia with insulinA low dose insulin regime has the advantage of not inducingA low dose insulin regime has the advantage of not inducing

severe hypoglycemia or hypokalemia.severe hypoglycemia or hypokalemia.

Only short acting insulin is used for correction ofOnly short acting insulin is used for correction ofhyperglycemia.hyperglycemia.

Insulin dose 0.1u/kg/hr.Insulin dose 0.1u/kg/hr. 6u/hr until the blood sugar drops to less than 180mg/dl.6u/hr until the blood sugar drops to less than 180mg/dl.

The rate of infusion decreases to 2-3u/hr until the ketoacidoticThe rate of infusion decreases to 2-3u/hr until the ketoacidoticstate abates.state abates.

The optimal rate of glucose decline is 100mg/dl/hr.The optimal rate of glucose decline is 100mg/dl/hr. Do not allow the blood glucose level to fall below 200mg/dlDo not allow the blood glucose level to fall below 200mg/dl

during first 4-5hrs of treatment.during first 4-5hrs of treatment. Hypoglycemia may develop rapidly with correction of acidosis.Hypoglycemia may develop rapidly with correction of acidosis. Rebound hyperglycemia which requires long durationRebound hyperglycemia which requires long duration

treatment.treatment. May induce cerebral oedema.May induce cerebral oedema.


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To correct electrolyte imbalanceTo correct electrolyte imbalance potassiumpotassium

K level >6meq/l do not administer k supplement.K level >6meq/l do not administer k supplement.

K level 4.5 to 5meq/l administer 10meq/l of kcl.K level 4.5 to 5meq/l administer 10meq/l of kcl.

K level 3-4.5meq/l administer 20 meq/l of kcl.K level 3-4.5meq/l administer 20 meq/l of kcl.

Monitor serum k levels hrly, and stop infusion if kMonitor serum k levels hrly, and stop infusion if k

level is >5meq/l.level is >5meq/l.

Continue monitoring serum k levels to preventContinue monitoring serum k levels to prevent

recurrence of hypokalemia.recurrence of hypokalemia. In case of severe hypokalemia do not startIn case of severe hypokalemia do not start

insulin therapy to avoid severe cardiacinsulin therapy to avoid severe cardiac

dysrhythmias.dysrhythmias.


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To correct acid-base balanceTo correct acid-base balance

Sodiumbicarbonate only is infused ifSodiumbicarbonate only is infused ifdecompensated acidosis starts to threatendecompensated acidosis starts to threatenthe pts life. Especially when associatedthe pts life. Especially when associatedwith sepsis or lactic acidosis.with sepsis or lactic acidosis.

If sodiumbicarbonate is indicated 100-If sodiumbicarbonate is indicated 100-150ml of 1.4% conc is infused initially.150ml of 1.4% conc is infused initially.This MAY be repeated every half hour ifThis MAY be repeated every half hour ifnecessary.necessary.

Rapid and early correction of acidosis withRapid and early correction of acidosis withsodiumbicarbonate may worsensodiumbicarbonate may worsenhypokalemia and cause paradoxical cellularhypokalemia and cause paradoxical cellular

acidosis.acidosis.


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To treat concurrent infectionTo treat concurrent infection

In the presence of infection,In the presence of infection,

administer proper antibiotics guided byadminister proper antibiotics guided by

the results of culture and sensitivitythe results of culture and sensitivity

studies.studies.

Starting emperic antibiotics onStarting emperic antibiotics onsuspicion of infection until culturesuspicion of infection until culture

results are available may be advisableresults are available may be advisable..


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Immediate post hyperglycemic careImmediate post hyperglycemic care When DKA has been controlled, s/c insulin can be started.When DKA has been controlled, s/c insulin can be started.

Administer s/c dose of regular insulin 1hr beforeAdminister s/c dose of regular insulin 1hr beforediscontinuing iv insulin.discontinuing iv insulin. In pts who are unable to eat, 5% dextrose in hypotonicIn pts who are unable to eat, 5% dextrose in hypotonic

saline is continued @100-200ml/hr.saline is continued @100-200ml/hr. Monitor blood glucose levels every 4hrly and administerMonitor blood glucose levels every 4hrly and administer

insulin s/c as per sliding scale.insulin s/c as per sliding scale. When pts are able to eat, multidose subcutaneous therapyWhen pts are able to eat, multidose subcutaneous therapy

with both regular (short-acting) & intermediate actingwith both regular (short-acting) & intermediate actinginsulin may be given.insulin may be given.

Newly diagnosed diabetes 0.6-0.7u/kg/day insulin isNewly diagnosed diabetes 0.6-0.7u/kg/day insulin isadequate to achieve metabolic control.adequate to achieve metabolic control.

Known diabetes pts can be given the same dose they hadKnown diabetes pts can be given the same dose they hadbeen receiving.been receiving.


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Complications of DKAComplications of DKAHYPOGLYCEMIA.HYPOGLYCEMIA.HYPOKALEMIA.HYPOKALEMIA. RECURRENT HYPERGLYCEMIA.RECURRENT HYPERGLYCEMIA. CEREBRAL OEDEMA.CEREBRAL OEDEMA.

KETOACIDEMIA.KETOACIDEMIA. FLUID @ ELECTROLYTE DEPLETION.FLUID @ ELECTROLYTE DEPLETION.ASPIRATION.ASPIRATION. PULMONARY OEDEMA.PULMONARY OEDEMA.MYOCARDIAL INFARCTION.MYOCARDIAL INFARCTION.ARDS.ARDS. UNRECOGNISED RENAL TUBULAR NECROSIS.UNRECOGNISED RENAL TUBULAR NECROSIS.

HYPERCHLOREMIC METABOLIC ACIDOSIS.HYPERCHLOREMIC METABOLIC ACIDOSIS.

St t i t t di b tiSt t

i t t di b ti


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Strategies to prevent diabeticStrategies to prevent diabetic

ketoacidosisketoacidosis Diabetic education.Diabetic education. Blood glucose monitoring.Blood glucose monitoring. Sick-day management.Sick-day management. Home monitoring of ketones or beta-Home monitoring of ketones or beta-

hydroxybutyrate.hydroxybutyrate. Supplement short-acting insulins.Supplement short-acting insulins. Easily digestible liquid diets when.Easily digestible liquid diets when. Reducing, rather than eliminating, insulin whenReducing, rather than eliminating, insulin when

patients are not eating.patients are not eating. Guidelines for when patients should seek medicalGuidelines for when patients should seek medical

attention.attention. Case monitoring of high-risk patients.Case monitoring of high-risk patients.

Special education for patients on pump management.Special education for patients on pump management.


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diabeticketoacedosis

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