Clinical Features and Diagnosis of Diabetic Ketoacidosis in Children

7/27/2019 Clinical Features and Diagnosis of Diabetic Ketoacidosis in Children

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Official reprint from UpToDate

www.uptodate.com 2013 UpToDate

AuthorsGeorge S Jeha, MD

Morey W Haymond, MD

Section EditorJoseph I Wolfsdorf, MB, BCh

Deputy EditorAlison G Hoppin, MD

Clinical features and diagnosis of d iabetic ketoacidosis in chi ldren

Disclosures

All topics are updated as new evidence becomes available and ourpeer review process is complete.

Literature review current through: Sep 2013. | This topic last updated: feb 13, 2013.

INTRODUCTION Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with type

1 diabetes mellitus. DKA can less commonly occur in children with type 2 diabetes mellitus [1,2]. (See "Classification

of diabetes mellitus and genetic diabetic syndromes".)

In recent years, the incidence and prevalence of type 2 diabetes mellitus have increased across all ethnic groups.

This has been coupled with an increasing awareness that children with type 2 diabetes mellitus can present with

ketosis or DKA, particularly in obese African American adolescents [1-6]. (See "Classification of diabetes mellitus

and genetic diabetic syndromes", section on 'DKA in type 2 diabetes' .)

The clinical features and diagnosis of DKA in children will be reviewed here. This discussion is primarily based upon

the large collective experience of children with type 1 diabetes mellitus. There is limited experience in the

assessment and diagnosis of DKA in children with type 2 diabetes mellitus, although the same principles should

apply. The management of diabetes in children, treatment of DKA in children and the epidemiology and

pathogenesis of DKA are discussed separately. (See "Management of type 1 diabetes mellitus in children and

adolescents" and "Treatment and complications of diabetic ketoacidosis in children" and "Epidemiology and

pathogenesis of diabetic ketoacidosis and hyperosmolar hyperglycemic state".)

DEFINITION Consensus statements from the European Society for Paediatric Endocrinology/Lawson Wilkins

Pediatric Endocrine Society (ESPE/LWPES) in 2004, the American Diabetes Association (ADA) in 2006, and the

International Society for Pediatric and Adolescent Diabetes (ISPAD) in 2007 defined the following biochemical

criteria for the diagnosis of DKA [7-10]:

Hyperglycemia, blood glucose of >200 mg/dL (11 mmol/L)

AND

Metabolic acidosis, defined as a venous pH 15 mmol/L, absent to mild ketonemia and

ketonuria, and effective serum osmolality >320 mOsm/L. HHS occurs most commonly in adults with poorly controlled

cal features and diagnosis of diabetic ketoacidosis in children http://www.uptodate.com/contents/clinical-features-and-diagnosis-

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type 2 diabetes, but has also been reported in African-American adolescents with type 2 diabetes [ 11-13].

Recognition of HHS is important because it is reported to be associated with more severe dehydration and difficult to

manage hypotension than typically occurs in DKA. As in DKA, management of HHS requires carefully monitored

fluid and electrolyte management, and it has been suggested that patients may require higher rates of fluid

administration than are typically used in DKA. Management of HHS is discussed in a separate topic review. (See

"Treatment of diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults", section on 'Fluid replacement'.)

EPIDEMIOLOGY DKA is frequently the initial presentation of children with new onset type 1 diabetes mellitus. In

a surveillance study of almost 3000 episodes of DKA in the United Kingdom, 38 percent occurred in patients at thetime of initial diagnosis of diabetes mellitus [14]. In other studies from Europe and North America, the frequency of

DKA as the initial presentation for type 1 diabetes mellitus is approximately 25 percent (range from 15 to 67 percent)

[9,15].

Although population-based studies are lacking, the incidence of DKA as the initial presentation in type 2 diabetes

mellitus varies considerably. In a systematic review, factors associated with increased risk for having DKA at

presentation are younger age (


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emphasize compliance with management recommendations, including adherence to the insulin regimen and the use

of home glucose monitoring.

Type 2 diabetes mellitus Although less common, ketosis and DKA can occur in children with type 2 diabetes

mellitus, particularly in African-American children [1-6]. In a retrospective review of 69 patients (between 9 and 18

years of age) who presented with DKA at a tertiary center, 13 percent had type 2 diabetes mellitus [5]. At

presentation, there was no difference in the serum pH level but patients with type 2 diabetes mellitus compared to

those with type 1 diabetes mellitus had higher blood glucose levels. (See "Classification of diabetes mellitus and

genetic diabetic syndromes", section on 'DKA in type 2 diabetes' .)

PRECIPITATING FACTORS Recurrent episodes of DKA with established type 1 diabetes mellitus are primarily

the result of underlying poor metabolic control and frequently missed insulin injections [23]. Omission of insulin

injections is particularly common among adolescents.

Stress is also an important precipitating factor. Stress increases the secretion of catecholamines, cortisol, and

glucagon, which promote both glucose and ketoacid production. As an example, infection can precede an episode of

DKA [25]. (See "Epidemiology and pathogenesis of diabetic ketoacidosis and hyperosmolar hyperglycemic state".)

In addition, medications such as corticosteroids, atypical antipsychotics, diazoxide, and high dose thiazides, have

precipitated DKA in individuals not previously diagnosed with type 1 diabetes mellitus.

DIAGNOSTIC EVALUATION The clinical diagnosis of diabetes in a previously healthy child requires a high indexof suspicion. Signs and symptoms of DKA are related to the degree of hyperosmolality, volume depletion, and

acidosis.

Signs and symptoms The earliest symptoms are related to hyperglycemia. Older children and adolescents

typically present with polyuria (due to the glucose-induced osmotic diuresis), polydipsia (due to the increased urinary

losses), and fatigue. Other findings include weight loss, nocturia (with or without secondary enuresis), daytime

enuresis, and vaginal or cutaneous moniliasis. Hypovolemia may be severe if the urinary losses are not replaced.

In infants, the diagnosis is more difficult because the patients are not toilet trained and they cannot express thirst. As

a result, polyuria may not be detected and polydipsia is not apparent. However, decreased energy and activity,

irritability, weight loss, and physical signs of dehydration are common findings. In addition, severe Candida diaper

rash or otherwise unexplained metabolic acidosis or hypovolemia should heighten the suspicion for diabetes. (See

"Overview of diaper dermatitis in infants and children".)

A number of other clinical findings may be seen:

Polyphagia usually occurs early in the course of the illness. However, once insulin deficiency becomes more

severe and ketoacidosis develops, appetite is suppressed. Some patients present with anorexia, nausea,

vomiting, and abdominal pain, which at times can mimic appendicitis or gastroenteritis. (See "Acute

appendicitis in children: Clinical manifestations and diagnosis".)

Hyperventilation and deep (Kussmaul) respirations represent the respiratory compensation for metabolic

acidosis. Hyperpnea results from an increase in minute volume (rate x tidal volume) and can be increased by

tidal volume alone without an increase in respiratory rate. As a result, the patient's chest excursion as well as

respiratory rate should be carefully observed. In infants, the hyperpnea may be manifested only by tachypnea.

Patients may also have a fruity breath secondary to exhaled acetone.

Although children with DKA are volume depleted, they are less likely to show the classic signs of hypovolemia

such as dry oral mucous membranes and decreased skin turgor than patients with the same degree of weight

loss from vomiting or diarrhea due to gastroenteritis. This important distinction is a reflection of water loss in

excess of sodium with a glucosuria-induced osmotic diuresis and water loss from hyperventilation. Water is

freely distributed between the extracellular and intracellular fluids. As a result, water loss produces less

extracellular fluid volume depletion than salt and water loss. Water loss also is largely responsible for the


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marked rise in plasma osmolality.

Neurologic findings, ranging from drowsiness, lethargy, and obtundation to coma, are related to the severity of

hyperosmolality and/or to the degree of acidosis [26]. Cerebral edema occurs in 0.5 to 1 percent of cases of

DKA in children, and is the leading cause of mortality. The clinician should be vigilant for early signs of

cerebral edema and should treat promptly if cerebral edema is suspected ( table 2). (See "Cerebral edema in

children with diabetic ketoacidosis".)

Fluid and electroly te deficits Studies estimating water and electrolyte losses in DKA were conducted in the1940s and 1950s. Most included adults, but one was a detailed study of a 10-year-old female [ 27-29]. The data from

the available studies are consistent with the following average losses in severe DKA:

Water 70 (range 30 to 100) mL/kg

Sodium 5 to 13 mEq/kg

Potassium 6 to 7 mEq/kg

It is difficult to assess clinically the degree of dehydration in children presenting with DKA as these children are less

likely to show the classic signs of hypovolemia because of chronic and acute losses of intracellular and extracellular

water as compared with children with more acute causes of dehydration [30]. Children with DKA generally present

with a 5 to 10 percent fluid deficit [4,7]. Initial fluid management is based on the assumption of a 5 to 7 percent deficit

for moderate DKA, and 10 percent dehydration for severe DKA [9]. This recommendation is consistent with theabove studies that assessed fluid and electrolyte losses. However, to minimize risks for cerebral edema and

electrolyte imbalances, hypovolemia should be corrected gradually. The maximal volume of isotonic solution used for

initial treatment is 10 mL/kg, unless the patient is objectively hypotensive. (See 'Signs and symptoms' above.)

Laboratory findings Initial laboratory testing should include serum testing for glucose, electrolytes, creatinine

and urea nitrogen, blood gases, and hematocrit [7,8]. Direct measurement of beta-hydroxybutyrate in the blood

should also be performed if possible; accurate bedside meters for this measurement are available [ 31]. The

diagnosis of DKA is confirmed by the findings of hyperglycemia, a high anion gap acidosis, ketonuria, and

ketonemia. Treatment of these abnormalities is discussed elsewhere. (See "Treatment and complications of diabetic

ketoacidosis in children".)

Serum glucose The serum glucose is, by definition, greater than 200 mg/dL (11 mmol/L) [7,8]. This degree of

hyperglycemia exceeds the renal tubular threshold for glucose reabsorption, resulting in an osmotic diuresis with

polyuria and subsequent volume depletion. Glucosuria also predisposes to candidal infections in diapered children

and adolescent girls.

Acid-base status The second criterion for the diagnosis of DKA is a serum bicarbonate


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in a study of patients with DKA: ketone production averaged 51 mEq/h, while net acid excretion with the

ketoacid anions averaged 15 mEq/h or 30 percent of the acid load [33]. The conversion of acetoacetic acid to

acetone can neutralize another 15 to 25 percent of the acid load [33].

The adequacy of the compensatory respiratory alkalosis

Conventional urine screening tests for ketones are performed with nitroprusside impregnated strips or tablets

(Acetest). Nitroprusside reacts with acetoacetate and acetone but not beta-hydroxybutyrate. In DKA,

beta-hydroxybutyrate makes up 75 percent of the circulating ketones. Thus, clinical testing with nitroprusside mayunderestimate the severity of ketoacidosis and ketonuria. On the other hand, during recovery beta-hydroxybutyrate

is converted to acetoacetate and acetone, which persist for a longer period. As a result, urine testing may give a

false impression of persistent ketoacidosis. Therefore, direct measurement of beta-hydroxybutyrate should be used

whenever possible.

Blood testing for beta-hydroxybutyrate may be available both in the clinical chemistry laboratory, and more

importantly, at points of care such as emergency departments and physician's offices, as well as at home (Precision

Xtra, Abbott Laboratories). The meter measures a current produced during oxidation of beta-hydroxybutyrate to

acetoacetate, and is accurate in children and adults in a variety of clinical settings for plasma beta-hydroxybutyrate

concentrations of up to 5 to 7 mMol/L [34,35].

The Anion Gap (AG) is useful in estimating the severity of ketosis, and the normalization of the anion gap is a directmeasure of the resolution of ketoacidemia. However, the anion gap may also underestimate the degree of acidosis.

The loss of ketoacid anions in the urine (as the sodium and potassium salts of beta-hydroxybutyrate and to a lesser

degree acetoacetate) lowers the anion gap without affecting the plasma bicarbonate concentration or therefore the

degree of acidosis.

When insulin is given to patients with diabetic ketoacidosis, metabolism of the ketoacid anions results in the

regeneration of HCO3- and correction of the metabolic acidosis. For this reason, ketoacid anions have been called

"potential bicarbonate," and their loss in the urine represents the loss of HCO3-. As a result, a normal AG acidosis is

typically seen during the treatment phase of diabetic ketoacidosis due to the urinary loss of these bicarbonate

precursors. (See "Approach to the child with metabolic acidosis", section on 'Overlap'.)

The serum anion gap is calculated from the following formula in units of mEq/L or mmol/L:

Serum anion gap = Serum sodium - (Serum chloride + bicarbonate)

The normal value in children is 122 mmol/L

Serum sodium The serum sodium concentration is affected by hyperglycemia. The magnitude of this effect is

determined by two major factors.

Hyperglycemia will increase the plasma osmolality, resulting in osmotic water movement out of the cells which

lowers the serum sodium by dilution. Theoretical calculations suggest that the serum sodium should be

lowered by 1.6 mEq/L for every 100 mg/dL (5.5 mmol/L) elevation in serum glucose [36]. There is no

experimental verification of this estimate in children. Experimental data in adults suggest that a better overallestimate is a reduction in serum sodium of 2.4 mEq/L for every 100 mg/dL (5.5 mmol/L) elevation of plasma

glucose [37].

The direct effect of hyperglycemia to lower the serum sodium is counteracted to a variable degree by the

glucosuria-induced osmotic diuresis. The diuresis results in water loss in excess of sodium and potassium,

which will tend to raise the serum sodium concentration and plasma osmolality. Inadequate water intake,

which may be a particular problem in hot weather and in infants and young children who cannot

independently access water, prevents partial correction of the hyperosmolality and can even lead to

hypernatremia despite the presence of hyperglycemia. On the other hand, consumption of large volumes of

dilute fluid, since thirst is stimulated by hyperosmolality, can contribute to hyponatremia.


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A third factor that can affect the measured serum sodium concentration represents a laboratory artifact.

Hyperlipidemia can cause pseudohyponatremia by reducing the fraction of plasma that is water. As a result, the

amount of sodium in the specimen is reduced and the measured plasma sodium concentration will be lower, even

though the physiologically important plasma water sodium concentration and plasma osmolality are not affected [38].

Ion-selective electrodes have been used to measure directly the plasma water sodium concentration in this setting,

but they have been shown to have variable accuracy and are not routinely used [38]. (See "Evaluation of the patient

with hyponatremia", section on 'Serum osmolality'.)

Serum potassium The osmotic diuresis and increased ketoacid excretion promote urinary potassium loss,while vomiting and diarrhea, if present, increase gastrointestinal potassium losses. In adults, average potassium

losses during DKA are 3 to 5 mEq/kg; the estimated potassium loss in children has been less well studied but

average losses appear to be 6 to 7 mEq/kg [27].

The potassium losses will tend to produce hypokalemia. However, the combination of insulin deficiency, which

impairs potassium entry into the cells, and hyperosmolality, which pulls water and potassium out of the cells, tends to

raise the serum potassium concentration. Ketoacidosis itself appears to have little effect on transcellular potassium

movement. (See "Potassium balance in acid-base disorders".)

Because of these counteracting effects, the serum potassium at the time of presentation can be normal, increased,

or decreased. Regardless of the initial level, therapy with insulin and fluids will predictably lower the serum

potassium concentration, which needs to be monitored carefully. (See "Treatment and complications of diabeticketoacidosis in children".)

Serum phosphate Children with DKA are typically in negative phosphate balance because of decreased

phosphate intake and phosphaturia caused by the glucosuria-induced osmotic diuresis. Despite the presence of

phosphate depletion, at presentation the serum phosphate concentration is usually normal or even high because

both insulin deficiency and metabolic acidosis cause a shift of phosphate out of the cells [ 39]. This transcellular shift

is reversed and the true state of phosphate balance is unmasked after treatment with insulin. (See "Treatment of

diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults", section on 'Phosphate depletion' .)

Blood urea nitrogen Patients with severe hypovolemia often have elevated blood urea nitrogen

concentrations [40]. This finding at presentation may have predictive value since it is a risk factor for cerebral edema

during therapy [41].

Assessment of severi ty At presentation, the following clinical and laboratory findings may be used to estimate

the severity of DKA:

Acid-base status The venous pH and serum bicarbonate concentration directly reflect the severity of the

acidosis (table 1). The respiratory rate also may be helpful, since the magnitude of the respiratory

compensation is directly related to the severity of the acidosis.

Ketosis The magnitude of the anion gap is another measure of the severity of the ketosis and can be a

helpful estimate of acidosis. A very large anion gap may also reflect decreased renal perfusion, which limits

ketoacid excretion. Measurement of plasma beta-hydroxybutyrate is now widely available and is a direct

method for monitoring the degree of ketoacidemia. (See 'Acid-base status' above.)

Neurologic status Severe neurologic compromise at presentation is a poor prognostic indicator, in part

because such patients are at increased risk for developing cerebral edema during therapy. This was

illustrated in a retrospective multicenter study of 61 children with DKA and cerebral edema; all patients who

either died or survived in a persistent vegetative state presented with Glasgow coma score 7 (score of 6 to 7

includes an abnormal or absent purposeful response to pain) (table 3) [42]. Because of the high morbidity and

mortality of cerebral edema, it is important to recognize and treat at the earliest signs of neurologic

compromise (table 2). The pathophysiology and treatment of cerebral edema in children with DKA is

discussed in detail separately. (See "Cerebral edema in children with diabetic ketoacidosis".)


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Volume status Estimated fluid deficit, (generally 5-10% fluid deficit).

Duration of symptoms A long duration of symptoms, as well as depressed level of consciousness or

compromised circulation, is evidence of severe DKA and should prompt close monitoring for potential

complications of DKA, such as cerebral edema [7,8]. Symptoms of cerebral edema typically occur several

hours after the initiation of treatment for DKA [9]. The presence of such symptoms at presentation indicates a

poor neurologic prognosis.

Based upon the severity of presentation, the clinician can ascertain the appropriate clinical setting in which to treatthe child. As an example, mild DKA without vomiting may be safely managed in an ambulatory setting under close

supervision and with appropriate monitoring by an experienced diabetes team. On the other hand, a patient with

severe DKA should be managed in a pediatric intensive care unit [7,8]. (See "Treatment and complications of

diabetic ketoacidosis in children".)

INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The Basics and

Beyond the Basics. The Basics patient education pieces are written in plain language, at the 5th

to 6th

grade

reading level, and they answer the four or five key questions a patient might have about a given condition. These

articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the

Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the

10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable withsome medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these

topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on

patient info and the keyword(s) of interest.)

Basics topics (see "Patient information: Diabetic ketoacidosis (The Basics)")

SUMMARY AND RECOMMENDATIONS

Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with type 1 diabetes

mellitus. DKA also can occur in children with type 2 diabetes mellitus, particularly in obese African-American

adolescents.

DKA is diagnosed when patients with diabetes mellitus exhibit BOTH hyperglycemia (blood glucose of >200

mg/dL [11 mmol/L]) and metabolic acidosis (venous pH


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acidosis, significant ketonemia, and metabolic acidosis. (See 'Laboratory findings' above.)

The venous pH and serum bicarbonate concentration directly reflect the severity of the acidosis ( table 1).

Neurologic status should also be formally assessed at presentation and periodically during treatment ( table 2),

because cerebral edema is an important cause of morbidity and mortality in patients with DKA. (See

'Assessment of severity' above.)

Hyperosmolar hyperglycemic state (HHS) is a hyperglycemia emergency which is distinguished from classic

DKA by marked hyperosmolality (effective osmolality of >320 mOsm/L) due to severe hyperglycemia (plasma

glucose >600 mg/dL), in the absence of severe metabolic acidosis (serum CO2 >15 mmol/L, absent to small

ketonemia and ketonuria). (See 'Definition' above and "Clinical features and diagnosis of diabetic ketoacidosis

and hyperosmolar hyperglycemic state in adults".)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

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6.

Dunger DB, Sperling MA, Acerini CL, et al. ESPE/LWPES consensus statement on diabetic ketoacidosis inchildren and adolescents. Arch Dis Child 2004; 89:188.

7.

Dunger DB, Sperling MA, Acerini CL, et al. European Society for Paediatric Endocrinology/Lawson Wilkins

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common threat in youth. J Pediatr 2013; 162:330.

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ketoacidosis at diagnosis of diabetes in children and young adults: a systematic review. BMJ 2011; 343:d4092.

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Neu A, Willasch A, Ehehalt S, et al. Ketoacidosis at onset of type 1 diabetes mellitus in children--frequency

and clinical presentation. Pediatr Diabetes 2003; 4:77.

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new onset type 1 diabetes mellitus. Clin Pediatr (Phila) 2003; 42:591.

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diabetes mellitus in children in a North Rhine-Westphalian region, Germany. J Pediatr Endocrinol Metab 2002;

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than 6 years. J Pediatr 2006; 148:366.

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Flood RG, Chiang VW. Rate and prediction of infection in children with diabetic ketoacidosis. Am J Emerg Med

2001; 19:270.

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Edge JA, Roy Y, Bergomi A, et al. Conscious level in children with diabetic ketoacidosis is related to severity of

acidosis and not to blood glucose concentration. Pediatr Diabetes 2006; 7:11.

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acidosis. J Pediatr 1952; 41:688.

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Atchley DW, Loeb RF, Richards DW, et al. ON DIABETIC ACIDOSIS: A Detailed Study of Electrolyte Balances

Following the Withdrawal and Reestablishment of Insulin Therapy. J Clin Invest 1933; 12:297.

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BUTLER AM, TALBOT NB. Metabolic studies in diabetic coma. Trans Assoc Am Physicians 1947; 60:102.29.

Koves IH, Neutze J, Donath S, et al. The accuracy of clinical assessment of dehydration during diabetic

ketoacidosis in childhood. Diabetes Care 2004; 27:2485.

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Bashford J, Acerini CL. How to use near-patient capillary ketone meters. Arch Dis Child Educ Pract Ed 2012;

97:217.

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re-evaluated. Kidney Int 1984; 25:591.

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Diabetes 1981; 30:510.

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ketosis in the acute care setting. Pediatr Diabetes 2004; 5:39.

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blood ketone meter: guidelines for clinical practice. Diabet Med 2001; 18:640.

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Kebler R, McDonald FD, Cadnapaphornchai P. Dynamic changes in serum phosphorus levels in diabetic

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Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis.

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Pediatrics. N Engl J Med 2001; 344:264.

Marcin JP, Glaser N, Barnett P, et al. Factors associated with adverse outcomes in children with diabetic

ketoacidosis-related cerebral edema. J Pediatr 2002; 141:793.

42.

Topic 5809 Version 12.0


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GRAPHICS

Assessment of severity of diabetic ketoacidosis in children

Mild Moderate Severe

Defining features

Venous pH 7.2-7.3 7.1-7.2


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Bedside evaluation of neurological state of children with diabetic

ketoacidosis (DKA)

Major criteria

Altered mentation/fluctuating level of consciousness

Sustained heart rate deceleration (decline of more than 20 beats per minute) not attributable to

improved intravascular volume or sleep state

Age-inappropriate incontinence

Minor criteria

Vomiting

Headache

Lethargy or being not easily aroused from sleep

Diastolic blood pressure >90 mmHg

Age


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Glasgow coma scale and pediatric Glasgow coma scale

SignGlasgow Coma

Scale[1] Pediatric Glasgow Coma Scale

[2] Score

Eye

opening

Spontaneous Spontaneous 4

To command To sound 3

To pain To pain 2

None None 1

Verbal

response

Oriented Age-appropriate vocalization, smile, or orientation

to sound, interacts (coos, babbles), follows

objects

5

Confused, disoriented Cries, irritable 4

Inappropriate words Cries to pain 3

Incomprehensible

sounds

Moans to pain 2

None None 1

Motor

response

Obeys commands Spontaneous movements (obeys verbal

command)

6

Localizes pain Withdraws to touch (localizes pain) 5

Withdraws Withdraws to pain 4

Abnormal flexion to

pain

Abnormal flexion to pain (decorticate posture) 3

Abnormal extension to

pain

Abnormal extension to pain (decerebrate posture) 2

None None 1

Best total score 15

The Glasgow coma scale (GCS) is scored between 3 and 15, 3 being the worst, and 15 the

best. It is composed of three parameters: best eye response (E), best verbal response (V),

and best motor response (M). The components of the GCS should be recorded individually;

for example, E2V3M4 results in a GCS of 9. A score of 13 or higher correlates with mild brain

injury; a score of 9 to 12 correlates with moderate injury; and a score of 8 or less represents

severe brain injury. The pediatric Glasgow coma scale (PGCS) was validated in children 2

years of age or younger.Data from:

Teasdale G and Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet

1974; 2:81.

1.

Holmes JF, Palchak MJ, MacFarlane T, Kuppermann N. Performance of the pediatric Glasgow coma scale

in children with blunt head trauma. Acad Emerg Med 2005; 12:814.

2.


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