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