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Diabetic Ketoacidosis: Follow-up

Author: William H Lamb, MBBS, MD, FRCP(Edin), FRCP, Clinical Lecturer, Department of Child Health, The General Hospital, Bishop Auckland, UK
Contributor Information and Disclosures

Updated: Dec 11, 2008

Follow-up

Further Inpatient Care

  • Children with severe acidosis (ie, pH <7.1) or with altered consciousness should be admitted to a pediatric intensive therapy unit (ITU).
  • Following recovery from diabetic ketoacidosis (DKA), the patient requires SC insulin therapy (see Diabetes Mellitus).
  • In cases in which diabetic ketoacidosis occurs signaling a new diagnosis of diabetes, the process of education and support by the diabetes team should begin when the patient recovers.
  • In cases in which diabetic ketoacidosis occurs in a child with established diabetes, explore the cause of the episode and take steps to prevent a recurrence.

Further Outpatient Care

  • Organize outpatient care through the pediatric diabetes care team.

Inpatient & Outpatient Medications

Transfer

  • Transfer any child with severe diabetic ketoacidosis who has a pH lower than 7.1 or who has altered consciousness to a pediatric ICU.

Deterrence/Prevention

  • Diabetic ketoacidosis in a patient in whom diabetes is newly diagnosed can be prevented only if the general public and primary care physicians know the symptoms and if physicians are alert to the possibility, particularly in young children.36 A urine test for glycosuria is easy to perform.
  • Adequate education and support for patients with established diabetes (and for their families) should prevent diabetic ketoacidosis occurring as a result of illness. Intervention is much more difficult when insulin is withheld deliberately or administered improperly. Identification of children at risk for such behaviors and intervention with social and psychological support may alleviate these problems.37

Complications

  • Cerebral edema is the most important complication of diabetic ketoacidosis. The overall risk of cerebral edema is 0.7-1% occurring in 0.4% of established cases and in 1.2% of newly diagnosed cases. Mortality rates are high, approximately 25-30%, with permanent neurologic deficits in 35% or more of survivors.8,13 The cause of cerebral edema associated with diabetic ketoacidosis is unknown.
  • Two theories explain the pathogenesis of diabetic ketoacidosis–related cerebral edema. The first postulates that brain cells produce idiogenic osmoles to prevent cell shrinkage in a hyperosmolar environment. These osmoles are slow to clear from the cells, and as plasma osmolarity falls during treatment, water is drawn into the brain cells by the resulting osmotic gradient. This accounts for the belief that over-rapid correction of hyperosmolarity is associated with cerebral edema. The second theory proposes an effect on the cell membrane sodium/hydrogen transport system. As diabetic ketoacidosis develops, acidic molecules accumulate in both intracellular and extracellular fluids. With treatment, the concentration of acid falls more rapidly in the extracellular compartment, causing a net influx of sodium and water into the cells as hydrogen ions are exchanged. This may explain why cerebral edema seems to appear with biochemical correction of the acidosis.
  • Presentation 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, are important to avoid death or damage.
  • Clinical signs of developing cerebral edema can be divided into 3 main categories. One diagnostic criteria, two major criteria, or one major and two minor criteria have a sensitivity of 92% and false-positive rate of 4%.38
    • 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)
  • If cerebral edema is suspected and hypoglycemia is excluded, prompt treatment with an osmotic diuretic is indicated followed by a CT scan and referral to a neurosurgeon. Intubation, hyperventilation, and intracranial pressure monitoring reportedly improve outcomes.
  • Although mannitol has been the most commonly used osmotic diuretic, theoretical and experimental reasons for using hypertonic saline (3%) are noted.39
  • Unfortunately, only half of children who develop cerebral edema have obvious signs of deterioration; children may present with respiratory arrest. Young children have a greater risk of respiratory arrest, and the outcome for these children is particularly bad. A recent United Kingdom study reported that every child who presented with respiratory arrest either died or was left with neurologic deficits.

Prognosis

  • Expect full recovery with appropriate management. The degree and quality of monitoring are probably the most important factors determining outcomes.

Patient Education

Miscellaneous

Medicolegal Pitfalls

  • Regularly monitor neurologic status to detect cerebral edema, which must be treated promptly if death or disability is to be avoided.
  • Carefully monitor potassium status to prevent complications from hypokalemia.
  • Hypoglycemia should not occur with adequate monitoring and is less likely if low-dose, continuous insulin infusions are administered together with dextrose when blood glucose levels fall below 200 mg%.
  • Early in the treatment of diabetic ketoacidosis, when blood glucose levels are very elevated, the child can continue to experience massive fluid losses and deteriorate. Strict measurement of fluid balance is essential for optimal treatment.

Special Concerns

  • Diabetic ketoacidosis during pregnancy is associated with a very high risk of fetal loss.
  • 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 (CSII).
 


More on Diabetic Ketoacidosis

Overview: Diabetic Ketoacidosis
Differential Diagnoses & Workup: Diabetic Ketoacidosis
Treatment & Medication: Diabetic Ketoacidosis
Follow-up: Diabetic Ketoacidosis
Multimedia: Diabetic Ketoacidosis
References
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References

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Further Reading

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Keywords

diabetic ketoacidosis, DKA, cerebral edema, DKA, diabetes, diabetes mellitus, insulin deficiency, hyperglycemia, low bicarbonate, acidosis, ketonemia, ketonuria, type 1 diabetes, type 1 diabetes mellitus, insulin-dependent diabetes, IDD, insulin-dependent diabetes mellitus, IDDM, childhood diabetes, childhood diabetes mellitus, childhood-onset diabetes, childhood-onset diabetes mellitus, diabetes in childhood, diabetes mellitus in childhood, juvenile-onset diabetes, juvenile-onset diabetes mellitus, ketosis-prone diabetes, autoimmune diabetes mellitus, brittle diabetes mellitus, maturity-onset diabetes of the young, MODY, chamber-pot dropsy, thirst disease, sugar disease, sugar sickness, hypokalemia, hypoglycemia, hyponatremia, acute respiratory distress syndrome, ARDS, pneumothorax, rhabdomyolysis, acute renal failure

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Contributor Information and Disclosures

Author

William H Lamb, MBBS, MD, FRCP(Edin), FRCP, Clinical Lecturer, Department of Child Health, The General Hospital, Bishop Auckland, UK
William H Lamb, MBBS, MD, FRCP(Edin), FRCP is a member of the following medical societies: British Medical Association, Royal College of Paediatrics and Child Health, and Royal College of Physicians
Disclosure: Medtronic UK Honoraria Speaking and teaching

Medical Editor

G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital
G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

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.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

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, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

 
 
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