DIABETIC DIABETIC KETOACIDOSISKETOACIDOSIS

Dr.Padmesh. VDr.Padmesh. V

Dept of PediatricsDept of Pediatrics

Dr.SMCSI Medical College,Dr.SMCSI Medical College,

Karakonam, TrivandrumKarakonam, Trivandrum

Dr.Padmesh.V

DKADKA

Diabetic ketoacidosis (DKA) is an acute, major, life-Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes. threatening complication of diabetes.

DKA mainly occurs in patients with type 1 diabetes, DKA mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 but it is not uncommon in some patients with type 2 diabetes. diabetes.

DKA is clinically defined as an acute state of severe DKA is clinically defined as an acute state of severe uncontrolled diabetes that requires emergency uncontrolled diabetes that requires emergency treatment with insulin and intravenous fluids. treatment with insulin and intravenous fluids.

Dr.Padmesh.V

DKA :definitionDKA :definition

A state of A state of absoluteabsolute or or relativerelative insulin insulin deficiency deficiency resulting in resulting in hyperglycemiahyperglycemia and an and an accumulation of accumulation of ketoacidsketoacids in the blood in the blood with subsequent with subsequent metabolic acidosismetabolic acidosis

HyperglycemiaHyperglycemia– Blood glucose >250mgBlood glucose >250mg

%%

AcidosisAcidosis– pH < 7.30pH < 7.30– Bicarb < 20 mmol/LBicarb < 20 mmol/L

KetosisKetosis– Elevated serum or Elevated serum or

urine ketonesurine ketones– Serum ketones Serum ketones

>5mEq/L>5mEq/L

Dr.Padmesh.V

Physiology of carbohydrate metabolismPhysiology of carbohydrate metabolism

Glucose and lipid metabolism are Glucose and lipid metabolism are regulated by the pancreatic hormone regulated by the pancreatic hormone InsulinInsulin, ,

and its and its CCounter-regulatory hormonesounter-regulatory hormones::– GGlucagonlucagon– GGrowth hormonerowth hormone– CCatecholaminesatecholamines– CCortisolortisol

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To develop DKA there must be both To develop DKA there must be both a relative a relative lack of insulinlack of insulin and and a relative a relative overactivity of counter-regulatory hormonesoveractivity of counter-regulatory hormones

InsulinInsulin (anabolic)(anabolic)– Glucose used for Glucose used for

energy substrate or energy substrate or stored as glycogenstored as glycogen

– Protein formationProtein formation– Fats stored as Fats stored as

triglyceridestriglycerides

CCounterregulatory ounterregulatory hormones (hormones (ccatabolic)atabolic)– GlycogenolysisGlycogenolysis– Proteolysis-Proteolysis-

gluconeogenesisgluconeogenesis– Lypolysis-FFA & Lypolysis-FFA &

ketone bodiesketone bodies

PhysiologyPhysiology

Dr.Padmesh.V

Physiology of DKAPhysiology of DKA

Diabetic ketoacidosis is a Diabetic ketoacidosis is a superfasted superfasted statestate in which the body’s tissues are in which the body’s tissues are robbed of their normal energy substrate robbed of their normal energy substrate Glucose,Glucose,

And the body resorts to And the body resorts to catabolism of catabolism of glycogen, protein and fat for energy. glycogen, protein and fat for energy.

Dr.Padmesh.V

Physiology of carbohydrate metabolismPhysiology of carbohydrate metabolism

– Glycogen is broken down to form glucose Glycogen is broken down to form glucose ((glycogenolysisglycogenolysis))

– PProtein is catabolized to rotein is catabolized to aamino acids which are mino acids which are converted to converted to gglucose (lucose (gluconeogenesisgluconeogenesis))

– Fats are broken down to free fatty acids, which Fats are broken down to free fatty acids, which are converted in the liver to glucose or ketoacids are converted in the liver to glucose or ketoacids

((ketogenesisketogenesis))

To develop DKA there must be both To develop DKA there must be both a relative a relative lack of insulinlack of insulin and and a relative a relative overactivity of counter-regulatory hormonesoveractivity of counter-regulatory hormones

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Thus,this type of hormonal imbalance enhancesThus,this type of hormonal imbalance enhances Hepatic Gluconeogenesis, Hepatic Gluconeogenesis, Glycogenolysis, Glycogenolysis,

& &

Lipolysis.Lipolysis.

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Hepatic Gluconeogenesis, Hepatic Gluconeogenesis, Glycogenolysis secondary to insulin deficiency, and Glycogenolysis secondary to insulin deficiency, and

counter-regulatory hormone excess counter-regulatory hormone excess result in severe result in severe hyperglycemia.hyperglycemia.

Lipolysis increases Lipolysis increases serum free fatty acidsserum free fatty acids. .

Hepatic metabolism of free fatty acids as an Hepatic metabolism of free fatty acids as an alternative energy source (ie, ketogenesis) results alternative energy source (ie, ketogenesis) results in in accumulation of acidic metabolitesaccumulation of acidic metabolites (ie, ketones, (ie, ketones, ketoacids). ketoacids).

((Ketones include acetone, acetoacetate & beta hydroxybutyrate)Ketones include acetone, acetoacetate & beta hydroxybutyrate)

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Pathophysiology of DKAPathophysiology of DKA

Severe insulinopenia or lack of effective Severe insulinopenia or lack of effective insulin action results in a physiological insulin action results in a physiological cascade of events in cascade of events in

3 PATHWAYS3 PATHWAYS

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1. 1. Excessive glucose productionExcessive glucose production

+ Reduced glucose utilization+ Reduced glucose utilization

Increased serum glucoseIncreased serum glucose

Osmotic diuresis,with loss of fluids,electrolytesOsmotic diuresis,with loss of fluids,electrolytes

DehydrationDehydration

Activation of Renin-Angiotensin-Aldosterone axisActivation of Renin-Angiotensin-Aldosterone axis

Accelerated Potassium lossAccelerated Potassium loss

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2. 2. Increased Catabolic processesIncreased Catabolic processes

Cellular losses of sodium,potassium,phosphateCellular losses of sodium,potassium,phosphate

3. 3. Increased release of free fatty acids from Increased release of free fatty acids from

peripheral fat storesperipheral fat stores

Substrate for hepatic ketoacid productionSubstrate for hepatic ketoacid production

Ketoacids accumulateKetoacids accumulate

Buffer systems are depletedBuffer systems are depleted

METABOLIC ACIDOSIS occursMETABOLIC ACIDOSIS occurs

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Progressive rise of blood concentration of these acidic organic Progressive rise of blood concentration of these acidic organic substances initially leads to a state of substances initially leads to a state of ketonemia. ketonemia.

Natural body buffers can buffer ketonemia in its early stages. Natural body buffers can buffer ketonemia in its early stages.

When the accumulated ketones exceed the body's capacity of When the accumulated ketones exceed the body's capacity of buffering them, they overflow into urine (ie, buffering them, they overflow into urine (ie, ketonuriaketonuria). ).

If the situation is not treated promptly, more accumulation of If the situation is not treated promptly, more accumulation of organic acids leads to frank clinical metabolic acidosis (ie, organic acids leads to frank clinical metabolic acidosis (ie, ketoacidosisketoacidosis), with a drop in pH and bicarbonate serum levels. ), with a drop in pH and bicarbonate serum levels.

Respiratory compensationRespiratory compensation of this acidotic condition results in of this acidotic condition results in rapid shallow breathing (rapid shallow breathing (Kussmaul respirationsKussmaul respirations).).

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Ketones, in particular Ketones, in particular beta hydroxybutyratebeta hydroxybutyrate, induce nausea , induce nausea and vomiting that consequently aggravate fluid and and vomiting that consequently aggravate fluid and electrolyte loss already existing in DKA.electrolyte loss already existing in DKA.

Acetone Acetone produces the characteristic fruity breath odour of produces the characteristic fruity breath odour of ketotic patients.ketotic patients.

Hyperglycemia usually exceeds the renal threshold of Hyperglycemia usually exceeds the renal threshold of glucose absorption glucose absorption Significant glycosuria Significant glycosuria Osmotic Osmotic diuresis diuresis Water is lost in urine resulting in Severe Water is lost in urine resulting in Severe dehydration, thirst, tissue hypoperfusion, and, possibly,lactic dehydration, thirst, tissue hypoperfusion, and, possibly,lactic acidosis.acidosis.

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Hyperglycemia, osmotic diuresis, serum Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis hyperosmolarity, and metabolic acidosis result in severe electrolyte disturbances. result in severe electrolyte disturbances.

The most characteristic disturbance is total The most characteristic disturbance is total body potassium loss. body potassium loss.

This loss is not mirrored in serum potassium This loss is not mirrored in serum potassium levels, which may be low, within the normal levels, which may be low, within the normal range, or even high. range, or even high.

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PotassiumPotassium

KK++ is largely an intracellular ion. is largely an intracellular ion.

Both lack of insulin (catabolic predominance) and Both lack of insulin (catabolic predominance) and acidosis cause a shift of Kacidosis cause a shift of K++ extracellularly. extracellularly.

High urinary losses of KHigh urinary losses of K++ occur due to this occur due to this compartmental shift ,due to osmotic diuresis & due to compartmental shift ,due to osmotic diuresis & due to kaliuretic effect of hyperaldosteronism.kaliuretic effect of hyperaldosteronism.

Serum KSerum K++ levels are usually normal, even when total levels are usually normal, even when total body Kbody K++ is depleted, because: is depleted, because:– The compartmental shift of KThe compartmental shift of K++ inside to outside the inside to outside the

cellcell– Only extracellular KOnly extracellular K++ is measured is measured

Dr.Padmesh.V

Pathophysiology of Potassium lossPathophysiology of Potassium loss

AcidosisAcidosis

Extracellular accumulation of Hydrogen ionsExtracellular accumulation of Hydrogen ions

Shift of Potassium from the intracellular to the Shift of Potassium from the intracellular to the extracellular space in exchange with hydrogen ions extracellular space in exchange with hydrogen ions

A large part of this shifted extracellular potassium is A large part of this shifted extracellular potassium is lost in urine because of osmotic diuresislost in urine because of osmotic diuresis

HYPOKALEMIA HYPOKALEMIA

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SodiumSodiumInitial serum sodium may be Initial serum sodium may be ‘low’‘low’ for several reasons: for several reasons:– Depletion secondary to urinary losses / vomitingDepletion secondary to urinary losses / vomiting

– Hyperlipidemia displaces sodium in the most Hyperlipidemia displaces sodium in the most frequently used laboratory assay, factitiously lowering frequently used laboratory assay, factitiously lowering sodium values.sodium values.

– Hyperglycemia Hyperglycemia High serum osmolarilty High serum osmolarilty Water driven from Intra to Extracellular space Water driven from Intra to Extracellular space Dilutional hyponatremiaDilutional hyponatremia

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For each 100mg% increase of serum glucose above 100mg%, For each 100mg% increase of serum glucose above 100mg%, there is an expected decrease of about 1.6mEq/L in measured there is an expected decrease of about 1.6mEq/L in measured sodium.sodium.

The ‘true’ serum sodium level can be calculated as:The ‘true’ serum sodium level can be calculated as:

[Na] + Glucose-100 x 1.6[Na] + Glucose-100 x 1.6

100100

The sodium should The sodium should increaseincrease by about 1.6 mmol/L for each 100mg/dL by about 1.6 mmol/L for each 100mg/dL decline in glucose.decline in glucose.

If the corrected value is >150 mmol/L, severe hypernatremic dehydration If the corrected value is >150 mmol/L, severe hypernatremic dehydration may be present and may require slower fluid replacement.may be present and may require slower fluid replacement.

Declining sodium may indicate excessive water accumulation & risk of Declining sodium may indicate excessive water accumulation & risk of cerebral edema.cerebral edema.

Dr.Padmesh.V

With prolonged illness & severe DKA, total With prolonged illness & severe DKA, total body losses can approach:body losses can approach:

- 10-13 mEq/kg of Sodium- 10-13 mEq/kg of Sodium

- 5-6 mEq/kg of Potassium- 5-6 mEq/kg of Potassium

- 4-5 mEq/kg of Phosphate- 4-5 mEq/kg of Phosphate

These losses continue for several hours during therapy These losses continue for several hours during therapy until catabolic state is reversed & diuresis is controlled.until catabolic state is reversed & diuresis is controlled.

Even though Sodium deficit may be repaired within Even though Sodium deficit may be repaired within

24 hours, intracellular Potassium & Phosphate may not 24 hours, intracellular Potassium & Phosphate may not be completely restored for several days.be completely restored for several days.

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The combined effects of The combined effects of

Serum hyperosmolarity, Serum hyperosmolarity,

Dehydration, and Dehydration, and

AcidosisAcidosis

Result in increased osmolarity in brain cells Result in increased osmolarity in brain cells

Clinically manifests as an Clinically manifests as an altered altered

consciousness. consciousness.

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CLINICAL FEATURESCLINICAL FEATURES

Precipitated by intercurrent illness, trauma,Precipitated by intercurrent illness, trauma, infections.infections.

Symptoms:Symptoms: -Nausea / Vomiting-Nausea / Vomiting -Polydipsia / Polyuria / Nocturia-Polydipsia / Polyuria / Nocturia -Abdominal pain-Abdominal pain -Shortness of breath-Shortness of breath -Weakness-Weakness

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Signs:Signs:

- Dehydration- Dehydration

- Hypotension- Hypotension

- Tachycardia- Tachycardia

- Tachypnea / Kussmaul respirations - Tachypnea / Kussmaul respirations

- Acetone odour of breath- Acetone odour of breath

- Abdominal tenderness - Abdominal tenderness

- Lethargy / altered level of - Lethargy / altered level of

consciousness / possibly coma consciousness / possibly coma

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Lab Abnormalities and DiagnosisLab Abnormalities and Diagnosis

Serum glucose is elevated Serum glucose is elevated >250mg/dL >250mg/dL

Serum bicarbonate Serum bicarbonate <20 mmol/L<20 mmol/L

Arterial pH Arterial pH <7.3<7.3, depending on the severity of the , depending on the severity of the acidosis. acidosis.

Anion gap [Anion gap [(Na+K)(Na+K) – – (Cl+HCO3)(Cl+HCO3)] ] >12-16 mEq/L>12-16 mEq/L

Urine analysis: Glucosuria + KetonesUrine analysis: Glucosuria + Ketones

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Laboratory Abnormalities and DiagnosisLaboratory Abnormalities and Diagnosis

Serum amylase - may be due to pancreatitis. Serum amylase - may be due to pancreatitis.

(but if S.lipase is not ,this is likely to be (but if S.lipase is not ,this is likely to be non-specific/salivary)non-specific/salivary)

Serum Creatinine may be falsely elevated due to Serum Creatinine may be falsely elevated due to interference by ketones in the autoanalyzer interference by ketones in the autoanalyzer methodology.methodology.

Blood Urea Nitrogen (BUN) may be elevated.Blood Urea Nitrogen (BUN) may be elevated.

Complete Blood Counts: may reveal possible Complete Blood Counts: may reveal possible

infectious etiology.infectious etiology.

CSF study, CXR to rule out other causesCSF study, CXR to rule out other causes

for the clinical condition.for the clinical condition.

Dr.Padmesh.V

Despite a Despite a total-body potassium deficittotal-body potassium deficit, the serum , the serum potassium at presentation may be mildly potassium at presentation may be mildly elevated, secondary to the acidosis. elevated, secondary to the acidosis.

Total-body stores of sodium, chloride, Total-body stores of sodium, chloride, phosphorous, and magnesium are also reducedphosphorous, and magnesium are also reduced in DKA but are not accurately reflected by their in DKA but are not accurately reflected by their levels in the serum because of dehydration and levels in the serum because of dehydration and hyperglycemia.hyperglycemia.

Elevated blood urea nitrogen (BUN) and serum Elevated blood urea nitrogen (BUN) and serum creatinine levelscreatinine levels reflect intravascular volume reflect intravascular volume depletion.depletion.

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To summarize..To summarize..

Dr.Padmesh.V

In short…In short…

Dr.Padmesh.V

MANAGEMENT MANAGEMENT

OFOF DKADKA

Dr.Padmesh.VAims of management:Aims of management:

Restore normal hemodynamic status.Restore normal hemodynamic status.Restore normal acid-base balance.Restore normal acid-base balance.Correct blood glucose level.Correct blood glucose level.

Restore perfusion by giving Restore perfusion by giving fluidsfluids, which will increase glucose , which will increase glucose use in the periphery, restore GFR, and reverse the use in the periphery, restore GFR, and reverse the progressive acidosis.progressive acidosis.

Stop ketogenesis by giving Stop ketogenesis by giving insulininsulin, which will reverse , which will reverse proteolysis and lipolysis, and stimulate glucose uptake and proteolysis and lipolysis, and stimulate glucose uptake and processing, normalize blood glucose, and reverse acidosis.processing, normalize blood glucose, and reverse acidosis.

Correct electrolyte losses by Correct electrolyte losses by electrolyteelectrolyte supplementation. supplementation.

Avoid the complications of treatment, including Avoid the complications of treatment, including intracerebral complications, hypoglycemia, and intracerebral complications, hypoglycemia, and hypokalemia.hypokalemia.

Dr.Padmesh.VTREATMENT OF DKA TREATMENT OF DKA

(Milwaukee DKA PROTOCOL)(Milwaukee DKA PROTOCOL)

Time Therapy CommentsTime Therapy Comments11stst hour hour 10-20 ml/kg IV bolus NS or RL NPO.10-20 ml/kg IV bolus NS or RL NPO.

Insulin drip at 0.05-0.1 UInsulin drip at 0.05-0.1 U/kg//kg/hr hr Can be repeated. Can be repeated.

22ndnd hour until hour until 0.45% NS 0.45% NS + + Continue insulin dripContinue insulin drip. . If K<3mEq/L, give 0.5-1mEq/KgIf K<3mEq/L, give 0.5-1mEq/Kg

DKA resolution DKA resolution 20 mEq/L Kphos & 20 mEq/L KAc. 20 mEq/L Kphos & 20 mEq/L KAc. as oral K soln or increase IV Kas oral K soln or increase IV K

5% glucose if bl.sugar <250mg/dL 5% glucose if bl.sugar <250mg/dL to 80 mEq/Lto 80 mEq/L

Variable Oral intake + S/C insulin Variable Oral intake + S/C insulin No emesis.Normal No emesis.Normal electrolytes.electrolytes.

CO2 >16mEq/L. pH>7.30CO2 >16mEq/L. pH>7.30

IV rate = IV rate = 85ml/kg85ml/kg + maintenance – bolus + maintenance – bolus

23 hr23 hr

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This protocol This protocol corrects a deficit of 85ml/kg (8.5% dehydration)corrects a deficit of 85ml/kg (8.5% dehydration) for all for all patients in the first 24 hours.patients in the first 24 hours.

Children with mild DKA rehydrate earlier & can be switched to oral Children with mild DKA rehydrate earlier & can be switched to oral intake, whereas those with severe DKA and a greater volume intake, whereas those with severe DKA and a greater volume deficit require 30-36 hours with this protocol.deficit require 30-36 hours with this protocol.

The initial BOLUS given is a sugar freeThe initial BOLUS given is a sugar free ISOTONICISOTONIC solution. The solution. The patient is invariably hypertonic,keeping most of the initial infusion patient is invariably hypertonic,keeping most of the initial infusion in the in the intravascular spaceintravascular space. This ensures quick volume expansion.. This ensures quick volume expansion.

Subsequent fluid is Subsequent fluid is HYPOTONICHYPOTONIC tto repair the free water deficit,to o repair the free water deficit,to allow allow intracellularintracellular rehydration and to allow a more appropriate rehydration and to allow a more appropriate replacement of on-going hypotonic urine losses.replacement of on-going hypotonic urine losses.

IV rate = IV rate = 85ml/kg85ml/kg + maintenance – bolus + maintenance – bolus 23 hr23 hr

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Insulin should be given at the beginning toInsulin should be given at the beginning to -accelerate the movement of glucose into cells-accelerate the movement of glucose into cells -to subdue hepatic glucose production-to subdue hepatic glucose production -to halt movement of fatty acids from periphery to liver-to halt movement of fatty acids from periphery to liver

However,an initial insulin BOLUS does NOT speed However,an initial insulin BOLUS does NOT speed recovery,and may increase the risk of hypoglycemia and recovery,and may increase the risk of hypoglycemia and hypokalemia. Therefore,insulin hypokalemia. Therefore,insulin INFUSION INFUSION is started is started (WITHOUT A BOLUS) at the (WITHOUT A BOLUS) at the rate of 0.1 U/kg/hour.rate of 0.1 U/kg/hour.

Rehydration also lowers glucose levels byRehydration also lowers glucose levels by -improving renal perfusion -improving renal perfusion enhancing renal excretion enhancing renal excretion

Once glucose level goes below 180 mg/dL, osmotic diuresis Once glucose level goes below 180 mg/dL, osmotic diuresis stops and therefore rehydration becomes faster without stops and therefore rehydration becomes faster without further increase in fluid infusion rate.further increase in fluid infusion rate.

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Hyperglycemia is corrected well before the correction of acidosis. Hyperglycemia is corrected well before the correction of acidosis. Therefore,even after normal glucose levels are reached, insulin is Therefore,even after normal glucose levels are reached, insulin is still required to control fatty acid release.still required to control fatty acid release.

Thus insulin infusion can be lowered but NOT STOPPED once Thus insulin infusion can be lowered but NOT STOPPED once hyperglycemia has resolved.hyperglycemia has resolved.

However ,to continue insulin infusion without causing However ,to continue insulin infusion without causing hypoglycemia, GLUCOSE should be added to the solution- hypoglycemia, GLUCOSE should be added to the solution- usually as a 5% solution.usually as a 5% solution.

This glucose is added when serum glucose has decreased to 250 This glucose is added when serum glucose has decreased to 250 mg/dL, so that there is sufficient time to infusion before serum mg/dL, so that there is sufficient time to infusion before serum glucose falls further.glucose falls further.

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Cautious rehydrationCautious rehydration::Important to approach any child with hyperosmotic state Important to approach any child with hyperosmotic state with cautious rehydration.with cautious rehydration.

Effective Serum Osmolality =Effective Serum Osmolality =

{ 2 x [Na uncorrected] + [Glucose] }{ 2 x [Na uncorrected] + [Glucose] }

(This is an accurate index of tonicity of body fluids reflecting the intracellular & (This is an accurate index of tonicity of body fluids reflecting the intracellular & extracellular hydration better than measured plasma osmolality.)extracellular hydration better than measured plasma osmolality.)

This value is usually elevated in the beginning,and should gradually This value is usually elevated in the beginning,and should gradually normalize.normalize.

A rapid decline or a slow decline to a sub-normal range may indicate A rapid decline or a slow decline to a sub-normal range may indicate an excess of free water entering the vascular space,and therefore an excess of free water entering the vascular space,and therefore an increasing risk of developing an increasing risk of developing CEREBRAL EDEMA.CEREBRAL EDEMA.

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Complications of DKAComplications of DKA

Dehydration/shock/ Dehydration/shock/ hypotension hypotension

Hypokalemia – Hypokalemia – hyperkalemiahyperkalemia

Hypoglycemia Hypoglycemia

Aspiration pneumoniaAspiration pneumonia

SepsisSepsis

Acute tubular Acute tubular necrosisnecrosis

Myocardial infarctionMyocardial infarction

StrokeStroke

Cerebral edemaCerebral edema

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Cerebral edemaCerebral edemaClinically apparent cerebral edema occurs in approximately 1% of childhood DKA and is associated with high mortality and neurological morbidity.

The pathogenesis of the cerebral edema is not understood; Some studies have attributed it to cellular swelling as a result of rapid osmolar changes occurring during intravenous infusions.

Several studies, however, have shown no relationship to the volume or sodium content of the infusion nor any association with the rate of change in serum glucose concentration. This suggests that other factors may be important in the pathophysiology of DKA-related cerebral edema.

Clinical signs are variableClinical signs are variable– Gradual deterioration and worsening of conscious level, or Gradual deterioration and worsening of conscious level, or – More commonly a gradual general improvement followed by sudden More commonly a gradual general improvement followed by sudden

neurological deteriorationneurological deterioration

Requires a high index of suspicion.Requires a high index of suspicion.

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Cerebral Edema – Clinical Features:Cerebral Edema – Clinical Features:

Decreased sensoriumDecreased sensorium

Sudden and severe Sudden and severe headacheheadache

IncontinenceIncontinence

Persistent vomitingPersistent vomiting

Disorientation; Disorientation; agitationagitation

OphthalmoplegiaOphthalmoplegia

Pupillary changesPupillary changes

PapilledemaPapilledema

Posturing; SeizurePosturing; Seizure

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Cerebral edema –Treatment :Cerebral edema –Treatment :

Urgent recognition and treatment are Urgent recognition and treatment are essential.essential.

MannitolMannitol

Reduce IV fluid rate to 70% maintenance Reduce IV fluid rate to 70% maintenance

Elevate head end of bed to 45Elevate head end of bed to 45oo

Consider intubation & Controlled Consider intubation & Controlled hyperventilation hyperventilation ((vasoconstrictor effect of hypocarbia)

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PREVENTION IS PREVENTION IS

BETTER THAN CURE!!!BETTER THAN CURE!!!

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