Diabetic Ketoacidosis in Children. Overview Review the incidence and pathophysiology of DKA Define...

transcript

Diabetic Ketoacidosis in Children

Overview

Review the incidence and pathophysiology of DKA

Define the role of patient self-monitoring including blood ketones testing and the healthcare professional advice in preventing DKA

Describe current approaches to the clinical diagnosis of DKA, including the role of ketone body levels

List treatment options for DKA

Definition

Hyperglycemia BG > 200 mg/dl (11 mmol/l) (young or partially treated children, pregnant adolescents may

present with “euglycemic ketoacidosis”)

Venous pH <7.3 and/or bicarbonate <15 mmol/L mild DKA pH <7.3 bicarbonate <15 moderate pH <7.2 bicarbonate <10 severe pH <7.1 bicarbonate < 5

Glucosuria and ketonuria/ketonemia (β-HOB)

Incidence of DKA at onset

Wide geographic variation in DKA rates at diabetes onset: 15 -70%

More common in developing countries

DKA rates inversely related to incidence of type 1 diabetes

Risk factors for DKA at onsetAge <12 yrs

No first degree diabetic relative

Lower socioeconomic status

High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs

Poor access to medical care

PATHOPHYSIOLOGY

Diabetes Care 2006 29:1150-1159

Normal statepostprandial

glucose

acetyl CoA

pyruvate

Krebs cycle

oxaloacetate

citrateEnergy

glucose

fatty acids (+ glycerol)

acetyl CoA

lipase

fatty acyl CoA

pyruvate

Krebs cycle

oxaloacetate

citrate

-oxidation

insulin

Energy

fatty acids (+ glycerol)

acetyl CoA

acetoacetate

acetone -OHB

lipase

fatty acyl CoA

Krebs cycle acetoacetyl CoA

-oxidation

HMGCoA synthase

insulin

Energy

Ketosis in DKA- alternative source of energy

glucose fatty acids

acetyl CoA

acetoacetate

acetone -OHB

lipase

fatty acyl CoA

pyruvate

Krebs cycle

oxaloacetate

citrate

acetoacetyl CoA

-oxidation

HMGCoA synthase

insulin

glucagon

Energy

Clinical features

Signs of DKA

Vomiting Increased urinationAbdominal painFruity odor to breathDry mouth and tongueDrowsinessDeep breathingComa

MANAGEMENT OF DKA

EMERGENCY ASSESSMENT

CONFIRM DIAGNOSIS AND ITS CAUSE Vital Signs - including weight Hydration 3 important signs ( 5% dehydration) -prolonged cft -abnormal skin turgor -abnormal resp patternOther signs – dry mucous membranes,sunken eyes,absent

tears,weak pulses & cool extremities (>10% dehydration) -poor pulses,hypotension,oliguria Mental Status (GCS scale)

Biochemical assessmentObtain a blood sample for laboratory

measurementof serum or plasma glucose, electrolytes (includingbicarbonate or total carbon dioxide), blood ureanitrogen, creatinine, osmolality, venous (or arterialin critically ill patient) pH, pCO2, calcium,

phosphorus,and magnesium concentrations (if possible),HbA1c, hemoglobin and hematocrit or completeblood count.

An elevated white blood cell count in response to stress is characteristic of DKA and is not necessarily indicative of infection

• Perform a urinalysis for ketones.• Measurement of blood ß-hydroxybutyrate

concentration, if available, is useful to confirm ketoacidosis

And may be used to monitor the response to treatment• Obtain appropriate specimens for culture (blood,urine, throat), if there is evidence of infection.• If laboratory measurement of serum potassium isdelayed, perform an electrocardiogram (ECG) forbaseline evaluation of potassium status

Initial Laboratory Evaluation

Venous pH BUN Serum Osmolality Phosphorus CalciumAnion Gap

Glucose* Ketones* Sodium Potassium Chloride HCO3

*Always perform in an ill child

SERUM OSMOLALITY:

2[NA+K]+ (GLUCOSE/18) + BUN/2.8

SERUM NA:CORRECTED NA =

MEASURED NA + (1.6)(GLUCOSE - 100)/100

ANION GAP:[NA] – ( [CL]+[HCO 3 ] )

NORMALLY 12+/ -2 MMOL/L

Calculations

Supportive measures

Secure the airway and if there is deterioration inconscious level, empty the stomach by continuousnasogastric suction to prevent pulmonary aspiration.• A peripheral intravenous (IV) catheter should beplaced for convenient and painless repetitive bloodsampling. An arterial catheter may be necessary insome critically ill patients managed in an intensivecare unit.

• A cardiac monitor should be used for continuouselectrocardiographic monitoring to assess T-wavesfor evidence of hyper- or hypokalemia .• Give oxygen to patients with severe circulatoryimpairment or shock.• Give antibiotics to febrile patients after obtainingappropriate cultures of body fluids.• Catheterization of the bladder usually is notnecessary, but if the child is unconscious or unableto void on demand (e.g., infants and very ill youngchildren) the bladder should be catheterized.

Clinical and biochemical monitoring

Monitoringshould include the following:• Hourly (or more frequently as indicated)

vital signs(heart rate, respiratory rate, blood pressure)• Hourly (or more frequently as indicated)

neurological observations (Glasgow coma score) for warning signs and symptoms of cerebral edema

o headache

o inappropriate slowing of heart rateo recurrence of vomitingo change in neurological status (restlessness,

irritability, increased drowsiness, incontinence) or specific neurologic signs (e.g., cranial nerve

palsies, abnormal pupillary responses)o rising blood pressureo decreased oxygen saturation• Amount of administered insulin

Additional calculations that may be informative:

• In DKA the anion gap is typically 20–30 mmol/L; an anion gap >35 mmol/L suggests concomitant lactic acidosis • Effective osmolality = (mOsm/kg) 2x(Na + K) + glucose (mmol/L)

Goals of therapy

• Correct dehydration• Correct acidosis and reverse ketosis• Restore blood glucose to near normal• Avoid complications of therapy• Identify and treat any precipitating event

Principles of Water and Salt Replacement

• For patients who are severely volume depleted

but not in shock, volume expansion (resuscitation)

should begin immediately with 0.9% saline

• In the rare patient with DKA who presents in shock, rapidly restore circulatory volume with isotonic saline (or Ringer’s lactate) in 20 mL/kg boluses

-The volume and rate of administration dependson circulatory status and, where it is clinicallyindicated, the volume administered typically is10 mL/kg/h over 1–2 hours, and may be repeatedif necessary

One litre of lactated Ringer's solution contains:130 mEq of sodium ion = 130 mmol/L109 mEq of chloride ion = 109 mmol/L28 mEq of lactate = 28 mmol/L4 mEq of potassium ion = 4 mmol/L3 mEq of calcium ion = 1.5 mmol/LLactated Ringers has an osmolarity of 273

NS contains 154 mEq/L of Na+ and Cl−. It has a slightly higher degree of osmolarity (i.e. more solute per litre) than blood

Subsequent fluid management (deficit replacement)

Should be with 0.9% saline or Ringer’s acetate for at

least 4–6 hourso Thereafter, deficit replacement should be

with asolution that has a tonicity equal to or greaterthan 0.45% saline with added potassium

chloride,potassium phosphate or potassium acetate

o The rate of fluid (IV and oral) should be calculated

to rehydrate evenly over 48 hours o As the severity of dehydration may be difficultto determine and frequently is under- or

overestimated, infuse fluid each day at a raterarely in excess of 1.5–2 times the usual dailymaintenance requirement based on age,

weight, orbody surface area

Insulin therapyDKA is caused by a decrease in effective circulatinginsulin associated with increases in counter-regulatoryhormones (glucagon, catecholamines, GH, cortisol).

Extensive evidence indicates that ‘low dose’ IV insulin

administration should be the standard of care • Start insulin infusion 1–2 hours after starting fluidreplacement therapy; i.e. after the patient hasreceived initial volume expansion .

• Correction of insulin deficiencyo Dose: 0.1 unit/kg/hour (for example, one

methodis to dilute 50 units regular [soluble] insulin in50 mL normal saline, 1 unit = 1 mL) o Route of administration IV o An IV bolus is unnecessary , may increase the risk of cerebral edema , and should not be

used at the start of therapy

The dose of insulin should usually remain at 0.1unit/kg/hour at least until resolution of DKA (pH>7.30, bicarbonate >15 mmol/L and/or closure ofthe anion gap)

If the patient demonstrates marked sensitivity toinsulin (e.g., some young children with DKA,patients with HHS, and some older children withestablished diabetes), the dose may be decreased to0.05 unit/kg/hour, or less, provided that metabolicacidosis continues to resolve.

During initial volume expansion the plasma glucose

concentration falls steeply. Thereafter,and after commencing insulin therapy, the

plasmaglucose concentration typically decreases at a

rateof 2–5 mmol/L/hour, depending on the timing

andamount of glucose administration

• To prevent an unduly rapid decrease in plasma glucose

concentration and hypoglycemia, 5% glucoseshould be added to the IV fluid (e.g., 5% glucosein 0.45% saline) when the plasma glucose falls toapproximately 14–17 mmol/L (250–300 mg/dL), orsooner if the rate of fall is precipitous o It may be necessary to use 10% or even 12.5%

dextroseto prevent hypoglycemia while continuing toinfuse insulin to correct the metabolic acidosis.

If BG falls very rapidly (>5 mmol/L/h) after initial fluid expansion, consider adding glucose even before plasma glucose has decreased to 17 mmol/L

• If biochemical parameters of DKA (pH, anion gap) do not improve, reassess the patient, review insulin therapy, and consider other possible causes of impaired response to insulin; e.g., infection, errors in insulin preparation

In circumstances where continuous IV administration is not possible, hourly or 2-hourly SC or IM administration of a short- or rapid-acting insulin analog (insulin lispro or insulin aspart) is safe and may be as effective as IV regular insulin infusion, but should not be used in subjects whose peripheral circulation is impaired

o Initial dose SC: 0.3 unit/kg, followed 1 hour later by SC insulin lispro or aspart at 0.1 unit/kg every hour, or 0.15–0.20 units/kg every two hours.

o If blood glucose falls to <14 mmol/L (250 mg/dL) before DKA has resolved, (pH still <7.30), add 5% glucose and continue with insulin as above.

o Aim to keep blood glucose at about 11 mmol/L

(200 mg/dL) until resolution of DKA

IF THE BLOOD GLUCOSE CONCENTRATION FALLS TOO QUICKLY OR TOO LOW BEFORE DKA HAS RESOLVED ,INCREASE THE AMOUNT OF GLUCOSE ADMINISTERED.DO NOT DECREASE THE INSULIN INFUSION

Potassium replacementChildren with DKA suffer total body potassiumdeficits of the order of 3 to 6 mmol/kg The major loss of potassium is from the intracellularpool. Intracellular potassium is depleted because of Hypertonicity(increased plasma osmolality causes solvent drag in which

water and potassium are drawn out of cells) glycogenolysis and proteolysis VomitingOsmotic diuresis.Secondary hyperaldosteronism, which promotes urinary

potassium excretion.

Thus, total body depletion of potassium occurs, but at presentation serum potassium levels may be normal, increased or decreased .

Renal dysfunction, by enhancing hyperglycemia and reducing potassium excretion, contributes to hyperkalemia. Administration of insulin and the correction of acidosis

will drive potassium back into the cells, decreasing serum

levels . The serum potassium concentration may decrease abruptly, predisposing the patient to cardiac arrhythmias.

Replacement therapy is required regardless of theserum potassium concentration • If the patient is hypokalemic, start potassiumreplacement at the time of initial volume expansionand before starting insulin therapy. Otherwise, startreplacing potassium after initial volume expansionand concurrent with starting insulin therapy. If the patient is hyperkalemic, defer potassium replacementtherapy until urine output is documented .• If immediate serum potassium measurements areunavailable, an ECG may help to determine whetherthe child has hyper- or hypokalemia . # Flattening of the T wave, widening of the QT interval, and the appearance of U waves indicating hypokalemia.

#Tall,peaked,symmetrical, T waves and shortening of the QT interval are signs of hyperkalemia.

The starting potassium concentration in the infusate should be 40 mmol/L.

Subsequent potassium replacement therapy should be based on serum potassium measurements

o If potassium is given with the initial rapid volume expansion, a concentration of 20 mmol/L should be used.

• Potassium phosphate may be used together with potassium chloride or acetate; e.g., 20 mmol/L potassium chloride and 20 mmol/L potassium phosphate

or 20 mmol/L potassium phosphate and 20 mmol/L potassium acetate .

• Potassium replacement should continue throughout IV fluid therapy .

• The maximum recommended rate of intravenous

potassium replacement is usually 0.5 mmol/kg/hr .

• If hypokalemia persists despite a maximum rate of

potassium replacement, then the rate of insulin infusion can be reduced.

Phosphate Depletion of intracellular phosphate occurs in

DKA and phosphate is lost as a result of osmotic

diuresis. Insulin, which promotes entry of phosphate

into cells . Clinically significant hypophosphatemia may

occur if intravenous therapy without food intake is prolonged beyond 24 hours .

Administration of phosphate may induce hypocalcemia

Acidosis

Controlled trials have shown no clinical benefitfrom bicarbonate administration

Bicarbonate therapy may cause paradoxical CNS acidosis

Rapid correction of acidosis with bicarbonate causes hypokalemia , and

Failure to account for the sodium being administered and appropriately reducing the NaCl concentration of the fluids can result in increasing osmolality .

Selected patients who may benefit from cautious alkali therapy include:

Patients with severe acidemia (arterial pH <6.9) inwhom decreased cardiac contractility and peripheralvasodilatation can further impair tissue perfusion,

andpatients with life-threatening hyperkalemia • Bicarbonate administration is not recommendedunless the acidosis is profound and likely to affectadversely the action of adrenaline/epinephrine duringresuscitation

• If bicarbonate is considered necessary, cautiously give 1–2 mmol/kg over 60 minutes

Introduction of oral fluids and transition to SC insulin injections

• Oral fluids should be introduced only when substantial clinical improvement has

occurred (mild acidosis/ketosis may still be present)

• When oral fluid is tolerated, IV fluid should be reduced

When ketoacidosis has resolved, oral intake is

tolerated, and the change to SC insulin is planned, the most convenient time to change to SC insulin is just before a mealtime .

To prevent rebound hyperglycemia the first SCinjection should be given 15–30 minutes (with rapid

actinginsulin) or 1–2 hours (with regular insulin)before stopping the insulin infusion to allow sufficienttime for the insulin to be absorbed .With intermediate- or long-acting insulin, the overlapshould be longer and the IV insulin graduallylowered. For example, for patients on a basal-bolusinsulin regimen, the first dose of basal insulin may beadministered in the evening and the insulin infusionis stopped the next morning .

Multiple Insulin Injection Therapy

INSULIN TYPES DURATION OF ACTION

0 3 6 9 12 15 18 21 24

Insulin Preparations

Action Name Onset Duration

Very rapid Lispro / Novo rapid 10-15 min 2-3 hrsRapid Crystalline zinc (CZI) 30-45 min 4-6 hrsIntermediate Neutral Protamine

Hagedorn (NPH) 1-2 hrs 6-12 hrsLente zinc

Long acting Ultralente zinc 6-8 hrs 18 hrsLantus (glargine) 4-8 hrs 24 hrs

Premixed 80% NPH+20%CZI 30-45 min 6-12 hrs70% NPH+30%CZI 30-45 min 6-12 hrs50% NPH+50%CZI 30-45 min 6-12 hrs

Principles of insulin therapyFrequently used regimens♦ Two injections daily of a mixture of short or rapid

and intermediate acting insulins (before breakfastand the main evening meal).♦ Three injections daily using a mixture of shortor rapid and intermediate acting insulins beforebreakfast; rapid or regular insulin alone beforeafternoon snack or the main evening meal;intermediate acting insulin before bed or variationsof this.

Western regimen

6 9 12 3 6 9 12 3

Two doses:The usual dosing commonly used.Initial insulin therapy

6 9 12 3 6 9 12 3

Four doses:Brittle diabetic patient.Pregnant mothers specially type 1.

6 9 12 3 6 9 12 3

Four doses:Brittle diabetic patient.Pregnant mothers specially type 1.Motivated patients.

6 9 12 3 6 9 12 3

Three doses:Used for active patients.Patients taking two main meals.

Western regimen

6 9 12 3 6 9 12 3

Two doses:The usual dosing commonly used.Initial insulin therapy

6 9 12 3 6 9 12 3

Three doses:Used for active patients.Patients taking two main meals.

6 9 12 3 6 9 12 3

Four doses:Brittle diabetic patient.Pregnant mothers specially type 1.

6 9 12 3 6 9 12 3

Four doses:Brittle diabetic patient.Pregnant mothers specially type 1.Motivated patients.

♦ Basal-bolus regimen• of the total daily insulin requirements, 40–60%should be basal insulin, the rest pre-prandialrapid-acting or regular insulin.• injection of regular insulin 20–30 minutes beforeeach main meal (breakfast, lunch and the mainevening meal); intermediate-acting insulin orbasal/long acting analog at bedtime or twice daily(mornings, evenings).

injection of rapid acting insulin analog immediately before (or after) each main meal (breakfast, lunch and main evening meal). Rapid acting analogs may need to be given 15 minutes before the meal to have full effect, especially at breakfast .

• intermediate-acting insulin or basal/long-acting analog at bedtime, probably before breakfast and occasionally at lunchtime or twice daily(mornings, evenings).

Distribution of insulin dose♦ Children on twice daily regimens often require

more(perhaps two-thirds) of their total daily insulin inthe morning and less (perhaps 1/3) in the evening.♦ On this regimen approximately one-third of theinsulin dose may be short-acting insulin andapproximately two thirds may be intermediate

actinginsulin although these ratios change withgreater age and maturity of the young person.

♦ Glargine is often given once a day, but many childrenmay need to be injected twice a day or combined withNPH to provide daytime basal insulin coverage • Glargine can be given before breakfast, beforedinner or at bedtime with equal effect, but nocturnalhypoglycemia occurs significantly less often afterbreakfast injection • When transferring to glargine as basal insulin, thetotal dose of basal insulin needs to be reduced byapproximately 20% to avoid hypoglycemia

Somogyi Phenomenon

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24

Cause: Counter regulatory hormones response to hypoglycemia at med-night.

Increase in hepatic glucose production.

Insulin resistance because of the Counter regulatory hormones.

Treatment: Decrease pre-supper intermediate insulin.

Defer the dose to 9 PM.

Change or start pre-bed snack.

Dawn Phenomenon

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24

Cause: Less insulin at bed time.

More food at bed time.

Not using NPH at night.

Treatment: Use enough dose.

Reduce bed time snack.

Add NPH pre-supper.

Cerebral Edema

Major cause of death in childhood DKA 20% with cerebral edema die 20% with mild to severe neurologic outcomes

At risk: Initial pH < 7.1 Baseline mental status abnormal Newly diagnosed, < 5 years old Rapid rehydration (> 50cc/ kg in first 4 hrs) Hypernatremia/ persistent hyponatremia

Cerebral edema

CE occurs in 0.3%- 1% of all episodes of DKA

Initial 24 hours of treatmentYounger children (< 4 yrs)Delayed diagnosisGreater dehydration and acidosis,

lower pCO2 Insulin given before fluids

Time of onset of Neurological Compromise (hours)

0-2.9 3-5.9 6-8.9 9-11.9 12-14.9 >15

# ofpatients

Muir A, et al, Diab Care. July 2004

Timing of Onset of Cerebral Edema in DKA

Symptoms and signs of cerebral edema

HeadacheDecreased or worsening level of

consciousnessSlowing of the HR Increase in BPSudden onset/return of vomitingWarning signs occur before the onset of

Clinical Factors Associated with Cerebral Edema

Prolonged IllnessSevere acidosis - low PA CO2Severe dehydrationBicarbonate therapyPersistent hyponatremiaExcessive fluid admistration

Etiology of CE

Vasogenic - excessive accumulation of water and solutes in the interstitial space, due to dysfunction of the blood-brain barrier

Cytotoxic - excessive accumulation of water and solutes in the intracellular space, due to dysfunction of cell-volume regulatory mechanisms

Both forms may co-exist

Excessive Free Water

Corrected Na = Na(measured)+1.6 (glucose-100)/100

Calculated sodium is low and falling in many cases of cerebral edema

ADH levels rise 5-50 times in DKA and contribute to increase in free water and hyponatremia

Cerebral Edema

Know what to look for Altered mental status/ severe headache Recurrence of vomiting Changes in pupil size, seizures, bradycardia Clinical worsening despite improving lab values CT/ MRI changes may not be seen in early cerebral

Cerebral Edema Bedside Score

Muir Diab Care 2004 27:1541-46

Caveat – note that patient needs to be significantly affected to meet diagnostic criteria

Treatment of cerebral edema

Mannitol: 1 gram/ kg IV over 30 minutes Elevate the head of the bed Decrease IVF rate and insulin infusion rate Pediatric ICU management Do not delay treatment until radiographic evidence

Diagnosis and prevention of DKAin outpatients

Why do ketones develop?No carbohydrate intake

• fasting• gastroenteritis• Atkins diet, neonates fed high-fat milk

Prolonged exercise, pregnancy

Lack of insulin activity• onset of diabetes (insufficient secretion)• interruption of insulin delivery in established pt

Increase in insulin resistance• infection, illness, surgery, stress

Alcohol, salicylate ingestion, inborn metabolic errors

Treatment of Mild DKA to Prevent Progression: Key: Early Detection

Check blood ketones (-OHB) for a person with diabetes any time:

1) A SMBG is >300 mg/dL (16.7 mmol/L)

2) An illness or infection is present

3) Unusual symptoms are present

4) It is realized a shot/bolus was missed or bad insulin

Old Paradigm: Check urine ketones

New Paradigm: Check blood -OHB

1) Blood -OHB tells you how you are doing at the time of the test. (Urine may have been in bladder for hrs)

2) Urine ketone levels may not accurately reflect the severity of the ketonemia

3) A person may not be able to void

4) Some (teens) give false urine test results

Hand-held deviceAbbott/MediSense

· The results are not real time

· The readings are qualitative: color comparisons indicating

high, medium or low levels

· Short shelf life (typically 90 days on opening a vial)

· Sulfhydryl drugs, including the ACE inhibitor, Captopril,

may cause false-positive results

· High doses of Vitamin C may cause false-negative results

· Method does not detect the major ketone body -hydroxybutyrate

Disadvantages to Urine Ketone Testing

Interpretation of Blood -OHB

-OHB level (mmol/L):

< 0.6 = normal >1.0 = hyperketonemia

0.6-1.0 = take extra insulin + fluids

1.0-1.5 = as above; recheck in 1 hr and, if no improvement, call diabetes provider

1.5-3.0 = call diabetes provider STAT

> 3.0 & sick = KETOACIDOSIS > Go to ED

A D A , J U N E , 2 0 0 7

Use of Blood -hydroxybutyrate Levels at the Bedside

During Treatment of DKA

Is bedside β-OHB monitoring using hand-held device as accurate as reference laboratory method ?

CONCLUSION

Real-time bedside measurement of -OHB is generally as accurate as reference laboratory, especially at levels up to 3.0- 4.0 mmol/L

Is capillary blood β-OHB monitoring superior to testing urine for

ketones ?

Measurement of Ketones

• Urine ketone measurements use a “dip stick” method based on a chemical reaction with acetoacetate. E.g., Chemstrip® from Roche; Clinistix®, Ketostix® , Keto-Diastix® from Bayer)

• Blood ketone testing that specifically measures ß-hydroxybutyrate are available for use in the laboratory (e.g., Sigma®, Cobos® from Roche) and a hand-held meter (Abbott / MediSense)

Blood β-OHB testing is superior to urine ketone testing in detecting ketosis

Sensitivity SpecificityPositive

predictive valueNegative

predictive value

Ketonuria 63% 100% 100% 72%

Capillary blood β-OHB

80% 100% 100% 83%

Guerci B , et al. Diabetes Care 2003

Similar data: Taboulet P et al. Eur J Emerg Med 2004

Gold standard – plasma β-OHB by reference laboratory method

(KONE Delta Automatic Analyzer)

Advantages Blood β-OHB vs.Urine Ketone Testing

• -OHB is a better marker of ketosis than acetoacetate

• -OHB is ‘real-time’ while ketonuria is usually ‘old news’

• Ketonuria doesn’t accurately reflect severity of ketonemia

• A dehydrated person may not be able to void

• Some people are too ill or exhausted to do the urine test

• Some patients (teens) give false urine sample

• Urine ketone strips spoil after opened >6 months

Schade DS, Eaton RP Special Topics in Endo and Metab 1982;4:1-27

-hydroxybutyrate is a better indicator of metabolic status when detecting and treating DKA

β-OHB in diagnosis of DKAin ED

Can bedside β-OHB monitoring shorten duration of

Prisco F, et al. Pediatr Diabetes 2006;

In most newly-diagnosed children with ketosis, capillary ketonemia resolves sooner than ketonuria

In children with DKA, capillary ketonemia resolves on average 11 hours sooner than ketonuria (n=40)

Noyes KJ, et al. Pediatr Diabetes 2007, confirming Vanelli M, et. Al. Diabetes Care 2003

Example of an individual treatment profile

pH >7.3

β-OHB <1.0

pH >7.3

No ketonuria

β-OHB

i.v. insulin U kg/h

CONCLUSIONS

Real-time bedside measurement of -OHB may help to optimize treatment of DKA and shorten the duration of hospitalization

thanks

Diabetic Ketoacidosis in Children. Overview Review the incidence and pathophysiology of DKA Define...

Documents