Pediatric Diabetic Ketoacidosis Follow-up

  • Author: William H Lamb, MBBS, MD, FRCP(Edin), FRCP, FRCPCH; Chief Editor: Timothy E Corden, MD   more...
 
Updated: Aug 19, 2011
 

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.
Next

Further Outpatient Care

  • Organize outpatient care through the pediatric diabetes care team.
Previous
Next

Inpatient & Outpatient Medications

Previous
Next

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.
Previous
Next

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.[41] 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.[42]

Supporting Media

See the videos below.

Carbs for Kids-Count Them In: The Constant Carbohydrates Diet.
Diabetes Sick Day Rules.
Taking Diabetes Back to School.
Previous
Next

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.[12, 17] The cause of cerebral edema associated with diabetic ketoacidosis is unknown.

Various theories have been produced to 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.

A 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.

A more recent proposal is that cerebral edema develops secondary to cerebral ischaemia caused by hypocapnia, dehydration, and hyperglycemia. This explains why some children present with cerebral edema before treatment and most known factors (eg, severity of hypocapnia, acidosis, dehydration, duration of ketoacidosis). Cerebral imaging studies of children with diabetic ketoacidosis and animal models make this the most compelling theory and offer an opportunity to actively prevent or better treat cerebral edema developing with ketoacidosis.[43]

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%.[44]

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.[45]

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.

Previous
Next

Prognosis

  • Expect full recovery with appropriate management. The degree and quality of monitoring are probably the most important factors determining outcomes.
  • However, even if cerebral edema has not occurred, a risk of long-term intellectual deficit is noted in children who have had an episode of diabetic ketoacidosis.[46]
Previous
Next

Patient Education

Previous
 
Contributor Information and Disclosures
Author

William H Lamb, MBBS, MD, FRCP(Edin), FRCP, FRCPCH  Clinical Lecturer, Department of Child Health, The General Hospital, Bishop Auckland, UK

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

Disclosure: Roche Diabetes Care Honoraria Speaking and teaching

Specialty Editor Board

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.

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.

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 E Cataletto, MD  Director of Children's Sleep Services, Winthrop Sleep Disorders Center, Mineola, NY; Professor of Clinical Pediatrics, State University of New York at Stony Brook, Stony Brook, NY

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.

Additional Contributors

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

References

  1. Wolfsdorf J, Craig ME, Daneman D, et al. Diabetic ketoacidosis. Pediatr Diabetes. Feb 2007;8(1):28-43. [Medline].

  2. Marshall SM, Walker M, Alberti KGMM. Diabetic Ketoacidosis and Hyperglycaemic non-ketotic coma. In: Alberti, Zimmet, Defronzo eds. International Textbook of Diabetes Mellitus. 1997:1215-30.

  3. Fagan MJ, Avner J, Khine H. Initial fluid resuscitation for patients with diabetic ketoacidosis: how dry are they?. Clin Pediatr (Phila). Nov 2008;47(9):851-5. [Medline].

  4. Rewers A, Klingensmith G, Davis C, et al. Presence of diabetic ketoacidosis at diagnosis of diabetes mellitus in youth: the Search for Diabetes in Youth Study. Pediatrics. May 2008;121(5):e1258-66. [Medline].

  5. Smith CP, Firth D, Bennett S, et al. Ketoacidosis occurring in newly diagnosed and established diabetic children. Acta Paediatr. May 1998;87(5):537-41. [Medline].

  6. Rewers A, Chase HP, Mackenzie T, et al. Predictors of acute complications in children with type 1 diabetes. JAMA. May 15 2002;287(19):2511-8. [Medline].

  7. Levy-Marchal C, Patterson CC, Green A. Geographical variation of presentation at diagnosis of type I diabetes in children: the EURODIAB study. European and Dibetes. Diabetologia. Oct 2001;44 Suppl 3:B75-80. [Medline].

  8. Edge JA, Dunger DB. Variations in the management of diabetic ketoacidosis in children. Diabet Med. Dec 1994;11(10):984-6. [Medline].

  9. Neu A, Hofer SE, Karges B, Oeverink R, Rosenbauer J, Holl RW. Ketoacidosis at diabetes onset is still frequent in children and adolescents: a multicenter analysis of 14,664 patients from 106 institutions. Diabetes Care. Sep 2009;32(9):1647-8. [Medline].

  10. Usher-Smith JA, Thompson MJ, Sharp SJ, Walter FM. Factors associated with the presence of diabetic ketoacidosis at diagnosis of diabetes in children and young adults: a systematic review. BMJ. Jul 7 2011;343:d4092. [Medline].

  11. Fritsch M, Rosenbauer J, Schober E, Neu A, Placzek K, Holl RW. Predictors of diabetic ketoacidosis in children and adolescents with type 1 diabetes. Experience from a large multicentre database. Pediatr Diabetes. Jun 2011;12(4 Pt 1):307-12. [Medline].

  12. Edge JA, Ford-Adams ME, Dunger DB, et al. Causes of death in children with insulin dependent diabetes 1990-96. Arch Dis Child. Oct 1999;81(4):318-23. [Medline]. [Full Text].

  13. Neu A, Willasch A, Ehehalt S, et al. Ketoacidosis at onset of type 1 diabetes mellitus in children--frequency and clinical presentation. Pediatr Diabetes. Jun 2003;4(2):77-81. [Medline].

  14. Warner DP, McKinney PA, Law GR, Bodansky HJ. Mortality and diabetes from a population based register in Yorkshire 1978-93. Arch Dis Child. May 1998;78(5):435-8. [Medline]. [Full Text].

  15. Durr JA, Hoffman WH, Sklar AH, et al. Correlates of brain edema in uncontrolled IDDM. Diabetes. May 1992;41(5):627-32. [Medline].

  16. Hale PM, Rezvani I, Braunstein AW, et al. Factors predicting cerebral edema in young children with diabetic ketoacidosis and new onset type I diabetes. Acta Paediatr. Jun 1997;86(6):626-31. [Medline].

  17. Mel JM, Werther GA. Incidence and outcome of diabetic cerebral oedema in childhood: are there predictors?. J Paediatr Child Health. Feb 1995;31(1):17-20. [Medline].

  18. Silver SM, Clark EC, Schroeder BM, Sterns RH. Pathogenesis of cerebral edema after treatment of diabetic ketoacidosis [published erratum appears in Kidney Int 1997 May;51(5):1662]. Kidney Int. Apr 1997;51(4):1237-44. [Medline].

  19. Okuda Y, Adrogue HJ, Field JB, et al. Counterproductive effects of sodium bicarbonate in diabetic ketoacidosis. J Clin Endocrinol Metab. Jan 1996;81(1):314-20. [Medline].

  20. Hoffman WH, Locksmith JP, Burton EM, et al. Interstitial pulmonary edema in children and adolescents with diabetic ketoacidosis. J Diabetes Complications. Nov-Dec 1998;12(6):314-20. [Medline].

  21. Holsclaw DS Jr, Torcato B. Acute pulmonary edema in juvenile diabetic ketoacidosis. Pediatr Pulmonol. Dec 1997;24(6):438-43. [Medline].

  22. Delamater AM, Shaw KH, Applegate EB, et al. Risk for metabolic control problems in minority youth with diabetes. Diabetes Care. May 1999;22(5):700-5. [Medline]. [Full Text].

  23. Cohn BA, Cirillo PM, Wingard DL, et al. Gender differences in hospitalizations for IDDM among adolescents in California, 1991. Implications for prevention. Diabetes Care. Nov 1997;20(11):1677-82. [Medline].

  24. Quinn M, Fleischman A, Rosner B, et al. Characteristics at diagnosis of type 1 diabetes in children younger than 6 years. J Pediatr. Mar 2006;148(3):366-71. [Medline].

  25. 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. Feb 2006;7(1):11-5. [Medline].

  26. Musey VC, Lee JK, Crawford R. Diabetes in urban African-Americans. I. Cessation of insulin therapy is the major precipitating cause of diabetic ketoacidosis. Diabetes Care. Apr 1995;18(4):483-9. [Medline].

  27. Thompson CJ, Cummings F, Chalmers J, Newton RW. Abnormal insulin treatment behaviour: a major cause of ketoacidosis in the young adult. Diabet Med. May 1995;12(5):429-32. [Medline].

  28. Morris AD, Boyle DI, McMahon AD, et al. Adherence to insulin treatment, glycaemic control, and ketoacidosis in insulin-dependent diabetes mellitus. The DARTS/MEMO Collaboration. Diabetes Audit and Research in Tayside Scotland. Medicines Monitoring Unit. Lancet. Nov 22 1997;350(9090):1505-10. [Medline].

  29. Smaldone A, Honig J, Stone PW, et al. Characteristics of California children with single versus multiple diabetic ketoacidosis hospitalizations (1998-2000). Diabetes Care. Aug 2005;28(8):2082-4. [Medline]. [Full Text].

  30. Holstein A, Abel C, Zumwalde I. Recurrent severe diabetic ketoacidosis due to intoxication with synthetic drugs ('Ecstasy' and 'Speed'). Intensivmedizin und Notfallmedizin. 1997;34(1):46-50.

  31. Brandenburg MA, Dire DJ. Comparison of arterial and venous blood gas values in the initial emergency department evaluation of patients with diabetic ketoacidosis. Ann Emerg Med. Apr 1998;31(4):459-65. [Medline].

  32. Wiggam MI, O'Kane MJ, Harper R, et al. Treatment of diabetic ketoacidosis using normalization of blood 3- hydroxybutyrate concentration as the endpoint of emergency management. A randomized controlled study. Diabetes Care. Sep 1997;20(9):1347-52. [Medline].

  33. Noyes KJ, Crofton P, Bath LE, et al. Hydroxybutyrate near-patient testing to evaluate a new end-point for intravenous insulin therapy in the treatment of diabetic ketoacidosis in children. Pediatr Diabetes. Jun 2007;8(3):150-6. [Medline].

  34. Fiordalisi I, Novotny WE, Holbert D, Finberg L, Harris GD. An 18-yr prospective study of pediatric diabetic ketoacidosis: an approach to minimizing the risk of brain herniation during treatment. Pediatr Diabetes. Jun 2007;8(3):142-9. [Medline].

  35. Harris GD, Fiordalisi I. Physiologic management of diabetic ketoacidemia. A 5-year prospective pediatric experience in 231 episodes. Arch Pediatr Adolesc Med. Oct 1994;148(10):1046-52. [Medline].

  36. Puttha R, Cooke D, Subbarayan A, Odeka E, Ariyawansa I, Bone M. Low dose (0.05 units/kg/h) is comparable with standard dose (0.1 units/kg/h) intravenous insulin infusion for the initial treatment of diabetic ketoacidosis in children with type 1 diabetes-an observational study. Pediatr Diabetes. Jul 6 2009;[Medline].

  37. Butkiewicz EK, Leibson CL, O'Brien PC, Palumbo PJ, Rizza RA. Insulin therapy for diabetic ketoacidosis. Bolus insulin injection versus continuous insulin infusion. Diabetes Care. Aug 1995;18(8):1187-90. [Medline].

  38. [Best Evidence] Della Manna T, Steinmetz L, Campos PR, Farhat SC, Schvartsman C, Kuperman H. Subcutaneous use of a fast-acting insulin analog: an alternative treatment for pediatric patients with diabetic ketoacidosis. Diabetes Care. Aug 2005;28(8):1856-61. [Medline].

  39. Green SM, Rothrock SG, Ho JD, et al. Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emerg Med. Jan 1998;31(1):41-8. [Medline].

  40. Hale PJ, Crase J, Nattrass M. Metabolic effects of bicarbonate in the treatment of diabetic ketoacidosis. Br Med J (Clin Res Ed). Oct 20 1984;289(6451):1035-8. [Medline].

  41. Vanelli M, Chiari G, Ghizzoni L, et al. Effectiveness of a prevention program for diabetic ketoacidosis in children. An 8-year study in schools and private practices. Diabetes Care. Jan 1999;22(1):7-9. [Medline]. [Full Text].

  42. [Guideline] Miller SG. Family therapy for recurrent diabetic ketoacidosis: Treatment guidelines. Family Systems Medicine. 1996;14(3):303-14.

  43. Glaser N. Cerebral injury and cerebral edema in children with diabetic ketoacidosis: could cerebral ischemia and reperfusion injury be involved?. Pediatr Diabetes. Dec 2009;10(8):534-41. [Medline].

  44. Muir AB, Quisling RG, Yang MC, Rosenbloom AL. Cerebral edema in childhood diabetic ketoacidosis: natural history, radiographic findings, and early identification. Diabetes Care. Jul 2004;27(7):1541-6. [Medline].

  45. White H, Cook D, Venkatesh B. The use of hypertonic saline for treating intracranial hypertension after traumatic brain injury. Anesth Analg. Jun 2006;102(6):1836-46. [Medline].

  46. Ghetti S, Lee JK, Sims CE, Demaster DM, Glaser NS. Diabetic ketoacidosis and memory dysfunction in children with type 1 diabetes. J Pediatr. Jan 2010;156(1):109-14. [Medline].

 
Previous
Next
 
A graphical representation of the ECG changes of hypokalemia.
A graphical representation of the ECG changes of hyperkalemia (due to overcorrection of potassium loss).
Glasgow Coma Scale, modified for age of verbal response.
Page 1 (of 4), diabetic ketoacidosis (DKA) treatment and results flow chart.
Page 2 (of 4), diabetic ketoacidosis (DKA) treatment and results flow chart.
Page 3 (of 4), diabetic ketoacidosis (DKA) treatment and results chart.
Page 4 (of 4), diabetic ketoacidosis (DKA) treatment and results flow chart.
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%



AppearanceThirsty, alertThirsty lethargicDrowsy, cold
Tissue turgorNormalAbsentAbsent
Mucous membranesMoistDryVery dry
Blood pressureNormalNormal or lowLow for age
PulseNormalRapidRapid and weak
EyesNormalSunkenGrossly sunken
Anterior fontanelleNormalSunkenGrossly sunken
Table 2. Suggested daily maintenance fluid replacement rates.
WeightInfusion rate
0-12.9 kg80 mL/kg/24 h
13-19.9 kg65 mL/kg/24 h
20-34.9 kg55 mL/kg/24 h
35-59.945 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/LCarefully monitored administration of 1 mEq/kg body weight by separate infusion over 1 h
2.5-3.5 mEq/L40 mEq/L
3.5-5 mEq/L20 mEq/L
5-6 mEq/L10 mEq/L (optional)
Over 6 mEq/LStop K+ and repeat level in 2 h
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.