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Pediatric Diabetic Ketoacidosis Clinical Presentation

  • Author: William H Lamb, MD, MBBS, FRCP(Edin), FRCP, FRCPCH; Chief Editor: Timothy E Corden, MD  more...
 
Updated: Apr 25, 2014
 

History

When diabetic ketoacidosis occurs as a first presentation of diabetes, symptoms are likely to develop over several days, with progressive dehydration and ketosis. In a small child wearing diapers and with naturally high fluid intake, polyuria and polydipsia are easily missed. When diabetes is developing, the stress and symptoms of another illness may precipitate diabetic ketoacidosis, as well as mask the underlying problem.

Diabetic ketoacidosis can develop very rapidly in a patient with established diabetes, particularly when insulin therapy has been forgotten, deliberately omitted, or disrupted, as with children on continuous subcutaneous insulin infusions or using the newer analogue insulins. Under these circumstances, diabetic ketoacidosis may present with relatively normal blood glucose levels (ie, 250 mg/dL, 15 mmol/L) or less.

Hyperglycemia

Symptoms of hyperglycemia include the following:

  • Polyuria - Increased volume and frequency of urination
  • Polydipsia - Thirst is often extreme, with children waking at night to consume large quantities of any available drink
  • Nocturia and secondary enuresis in a previously continent child
  • Weight loss - May be dramatic due to breakdown of protein and fat stores
  • Muscle pains and cramps

Acidosis and dehydration

Symptoms of acidosis and dehydration include the following:

  • Abdominal pain that may be severe enough to present as a surgical emergency; for children with a failure of continuous subcutaneous insulin infusion, this may be the first presenting sign, along with vomiting
  • Shortness of breath that may be mistaken for primary respiratory distress
  • Confusion and coma in the absence of recognized head injury [1]

Cerebral edema

Presentation of cerebral edema varies; most cases occur 4-12 hours after initiation of treatment. Typically, the child appears to be improving until a sudden deterioration occurs, with increasing coma; fixed, dilated pupils; and, finally, respiratory arrest. Other patients may have a progressively worsening coma. Children may occasionally present with signs of cerebral edema before treatment begins. Regular monitoring of neurologic status to detect early changes, together with prompt corrective treatment, is important to avoid death or damage.

Clinical signs of developing cerebral edema can be divided into 3 main categories. One diagnostic criteria, 2 major criteria, or 1 major and 2 minor criteria have a sensitivity of 92% and false-positive rate of 4%.[34]

Diagnostic criteria

  • Abnormal motor or verbal response to pain
  • Decorticate or decerebrate posture
  • Cranial nerve palsy (especially III, IV, and VI)
  • Abnormal neurogenic breathing pattern (eg, Cheyne-Stokes), apneusis

Major criteria

  • Altered mentation, fluctuating level of consciousness
  • Sustained and inappropriate bradycardia
  • Age-inappropriate incontinence

Minor criteria

  • Vomiting
  • Headache
  • Abnormally drowsy
  • Diastolic hypertension (>90 mm Hg)

Additional symptoms

Patients with diabetic ketoacidosis may also have the following symptoms:

  • Vomiting
  • Signs of intercurrent infection (eg, urinary tract infection, respiratory tract infection)
  • Weakness and nonspecific malaise that may precede other symptoms of hyperglycemia
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Physical Examination

Dehydration may be observed in patients with diabetic ketoacidosis. The degree of dehydration is often reported to be approximately 5-10% but easily can be overestimated (see Table 1, below). One report suggested that children with severe ketoacidosis are rarely more than 8% dehydrated.[5] Clinical signs such as dry mouth, sunken eyes, and decreased skin turgor, are present from about 3% dehydration. Little correlation with hydration status was found in diabetic ketoacidosis patients when using single biochemical or clinical markers.[35]

Table 1. Clinical Assessment of Dehydration (Open Table in a new window)

  Mild (< 3%) Moderate



(3-8%)



Severe (8%) and



Shock (>10%)



Appearance Thirsty, alert Thirsty, lethargic Drowsy, cold
Tissue turgor Normal Absent Absent
Mucous membranes Moist Dry Very dry
Blood pressure Normal Normal or low Low for age
Pulse Normal Rapid Rapid and weak
Eyes Normal Sunken Grossly sunken
Anterior fontanelle Normal Sunken Grossly sunken

Other symptoms can include the following:

  • Blood pressure - Usually normal until terminal stages of illness
  • Tachycardia - May be present
  • Capillary refill - Initially maintained, but a combination of increasing acidosis and dehydration cause poor tissue perfusion
  • Kussmaul breathing or deep sighing respiration - A mark of acidosis; these symptoms may be mistaken for status asthmaticus, pneumonia, and even hysterical hyperventilation
  • Ketone odor - Patient may have a smell of ketones on the breath, although many people cannot detect this smell
  • Impaired consciousness - Occurs in approximately 20% of patients
  • Coma - May be present in 10% of patients
  • Abdominal tenderness - May occur; tenderness is usually nonspecific or epigastric in location; bowel sounds may be reduced or absent in severe cases

Rapid onset of diabetic ketoacidosis that presents with relatively low blood glucose levels, vomiting, and abdominal pain can occur in children using short-acting and long-acting insulin analogues or continuous subcutaneous insulin infusions.

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Contributor Information and Disclosures
Author

William H Lamb, MD, MBBS, FRCP(Edin), FRCP, FRCPCH Consultant Paediatric Diabetologist, The Great North Children's Hospital, The Royal Victoria Infirmary; Honorary Clinical Lecturer, University of Newcastle upon Tyne; Honorary Clinical Lecturer, University of Durham, UK

William H Lamb, MD, MBBS, FRCP(Edin), FRCP, FRCPCH is a member of the following medical societies: British Medical Association, Royal College of Physicians, Royal College of Paediatrics and Child Health, British Society of Paediatric Endocrinology and Diabetes, International Society for Pediatric and Adolescent Diabetes

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Eli Lily and Company.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami, Leonard M Miller School of Medicine; Medical Director, Palliative Care Team, Director, Pediatric Critical Care Transport, Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Manager, FEMA, Urban Search and Rescue, South Florida, Task Force 2; Pediatric Medical Director, Tilli Kids – Pediatric Initiative, Division of Hospice Care Southeast Florida, Inc

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Acknowledgments

The author would like to thank Debbie Matthews and Tim Cheetham for reading the manuscript and for all of their support.

References
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Glasgow Coma Scale, modified for age of verbal response.
A graphical representation of the electrocardiographic changes of hypokalemia.
A graphical representation of the electrocardiographic changes of hyperkalemia (due to overcorrection of potassium loss).
Diabetic ketoacidosis treatment and results chart (page 1 of 4).
Diabetic ketoacidosis treatment and results chart (page 2 of 4).
Diabetic ketoacidosis treatment and results chart (page 3 of 4).
Diabetic ketoacidosis treatment and results chart (page 4 of 4).
Carbs for Kids-Count Them In: The Constant Carbohydrates Diet.
Diabetes Sick Day Rules.
Taking Diabetes Back to School.
Table 1. Clinical Assessment of Dehydration
  Mild (< 3%) Moderate



(3-8%)



Severe (8%) and



Shock (>10%)



Appearance Thirsty, alert Thirsty, lethargic Drowsy, cold
Tissue turgor Normal Absent Absent
Mucous membranes Moist Dry Very dry
Blood pressure Normal Normal or low Low for age
Pulse Normal Rapid Rapid and weak
Eyes Normal Sunken Grossly sunken
Anterior fontanelle Normal Sunken Grossly sunken
Table 2. Suggested Daily Maintenance Fluid Replacement Rates
Weight Infusion rate
0-12.9 kg 80 mL/kg/24 h
13-19.9 kg 65 mL/kg/24 h
20-34.9 kg 55 mL/kg/24 h
35-59.9 kg 45 mL/kg/24 h
Adult (>60 kg) 35 mL/kg/24 h
Table 3. Infusion Rates of Potassium Chloride
Serum/Plasma K+ (mEq/L) Potassium Chloride (KCL) Dose in Infusion Fluids
< 2.5 mEq/L Carefully monitored administration of 1 mEq/kg body weight by separate infusion over 1 h
2.5-3.5 mEq/L 40 mEq/L
3.5-5 mEq/L 20 mEq/L
5-6 mEq/L 10 mEq/L (optional)
Over 6 mEq/L Stop K+ and repeat level in 2 h
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