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Diabetic Ketoacidosis

Contents
  1. Read book excerpt
  2. Diabetic Ketoacidosis: Introduction
  3. Diabetic Ketoacidosis Misdiagnosis
  4. Diabetic Ketoacidosis Causes
  5. Diabetic Ketoacidosis Treatments
  6. Latest treatments
  7. Clinical trials
  8. Diagnosis of Diabetic Ketoacidosis
  9. Diabetic Ketoacidosis Overview
  10. More book excerpts for Diabetic Ketoacidosis

Diabetic Ketoacidosis: Excerpt from The 5-Minute Pediatric Consult

David R. Langdon, MD

Diabetic Ketoacidosis - BASICS

Diabetic Ketoacidosis - description

  • Severe metabolic derangement that occurs in patients with diabetes mellitus, either type 1 or untreated type 2, secondary to insulin deficiency and stress hormone excess
  • Principal features are dehydration, hyperglycemia, ketosis, and metabolic acidosis.

Diabetic Ketoacidosis - general prevention

  • Timely recognition of new diabetes in children, especially toddlers, with polyuria and polydipsia
  • Anticipatory illness management education to check ketones when feeling ill or glucose is high, to take extra insulin, and to call if ketones persist
  • Parental supervision of insulin injections and early ketone testing can prevent most recurrent diabetic ketoacidosis (DKA). Psychosocial assessment and family counseling may be useful, but is no substitute for parental participation in the diabetes care.
  • Recognition of insulin omission to control weight, and appropriate education or counseling

Diabetic Ketoacidosis - incidence

  • Up to 67% of DKA occurs at diabetes onset; higher percentage in children <4 years and in families with lower socioeconomic status (SES)
  • Annual hospitalization rates for DKA are around 10/100,000 children per year
  • Risk of DKA in established type 1 diabetes is 1–10% per patient per year.
  • DKA accounts for 65% of all hospital admissions in diabetic children <19 years old.
  • DKA accounts for >50% of childhood deaths from diabetes.

Diabetic Ketoacidosis - risk factors

  • Poor metabolic control
  • Previous episodes of DKA
  • Adolescent girls
  • Lower SES

Diabetic Ketoacidosis - pathophysiology

  • DKA results from a combination of insulin deficiency and metabolic stress effects.
  • Insulin deficiency may be absolute (new diabetes or omitted insulin) or relative (insufficient dose to offset illness stress).
  • Metabolic stress involves counter-regulatory hormones glucagon, cortisol, and epinephrine, triggered by acute illness or insulin deficiency.
  • Counter-regulatory hormones amplify glucose production, impair peripheral uptake, and increase proteolysis and lipolysis.
  • Lipolysis and ketosis produce metabolic acidosis. Hyperglycemia produces hyperosmolality, leading to osmotic diuresis, dehydration, and urinary electrolyte loss.
  • Approximate deficits per kilogram of body weight:
    • Water: 100 mL/kg
    • Na: 6–10 mEq/kg, K: 3–5 mEq/kg
    • Cl: 3–5 mEq/kg, PO

    Diabetic Ketoacidosis - etiology

    • Insulin deficiency due to unrecognized development of either type 1 or type 2 diabetes
    • Inappropriate withholding or reduction of insulin during acute illness
    • Overwhelming acute illness
    • Insulin omission due to parental disengagement, eating disorder, psychosocial stress, substance abuse

    Diabetic Ketoacidosis - associated conditions

    Candidal vaginitis or balanitis

    Diabetic Ketoacidosis - DIAGNOSIS

    Diabetic Ketoacidosis - signs & symptoms

    Diabetic Ketoacidosis - history

    • Polyuria, polydipsia from hyperosmolality
    • Nausea, vomiting, and abdominal pain are related to acidosis and electrolyte disturbance.
    • Precipitating event (e.g., intercurrent illness) should be identified if possible.

    Diabetic Ketoacidosis - physical exam

    • Dehydration effects: Tachycardia, dry mucous membranes, sunken eyes, poor skin turgor, poor distal perfusion, hypotension
    • Acetone odor to breath from ketosis
    • Deep Kussmaul hyperventilation is respiratory compensation for metabolic acidosis.
    • Abdominal tenderness due to ketosis, acidosis
    • Altered mental status, obtundation due to hyperosmolality, dehydration
    • Body temperature is typically low.

    Diabetic Ketoacidosis - tests

    Diabetic Ketoacidosis - lab

    • Glucose: >200 mg/dL (typically 400–1,200)
    • Urinalysis: Marked glycosuria and ketonuria
    • Sodium: Initial Na may be low, normal, or high:
      • Serum Na reflects duration and severity of hyperglycemia, duration and degree of dehydration, and degree of hyperlipidemia.
      • Prolonged hyperglycemia depresses Na by about 1.6 mEq/L for every 100 mg/dL of elevation, but Na may rise as dehydration becomes extreme (BUN >30 mg/dL).
      • Disproportionately low initial Na may indicate severe hyperlipidemia or adrenal crisis.
      • Whole body Na is depleted.
    • Potassium: Initial serum levels are usually elevated but may be normal or low. Regardless of initial K, body K is depleted.
    • Total COHCOHCO
    • HCO
    • Phosphate: Initially normal, high, or low
      • Despite initial level, whole-body P is depleted.
    • Arterial blood gas reflects metabolic acidosis, with low pH (<7.3), low pCOCBC: Stress may increase white cell count to 35,000/cu.mm. even without infection.
    • Β-hydroxybutyrate and serum ketones are elevated (typically >5 mmol/L).
    • Hypertriglyceridemia may be high enough to distort electrolyte measurement.
    • Liver enzymes (ALT, AST) may be mildly elevated.
    • Amylase and lipase are often mildly elevated. Plasma osmolality is high, and can be estimated by 2(Na+K) + (BUN/2.6) + (glucose/18).

      • Diabetic Ketoacidosis - differencial diagnosis

      • Gastroenteritis
      • Acute abdomen (pancreatitis, appendicitis)
      • UTI
      • Pneumonia
      • Stress hyperglycemia
      • Salicylate ingestion
      • Inborn error of metabolism
      • Nonketotic hyperosmolar coma
      • Adrenal crisis

      Diabetic Ketoacidosis - TREATMENT

      Diabetic Ketoacidosis - initial stabilization

      • Assess and assure airway and breathing.
      • Restore circulation: Normal saline bolus of 10–20 mL/kg; repeat as needed:
        • Urine output and specific gravity do not reflect hydration because of osmotic diuresis.
        • Avoid giving more fluids than necessary to reverse or prevent shock. Rapid osmolar correction may incur cerebral edema risk.

      Diabetic Ketoacidosis - general measures

      Use of a DKA protocol improves outcomes.

      Diabetic Ketoacidosis - iv fluids

      • Amount and rate of IV fluids:
        • Assume 10% dehydration, 15% in infants.
        • Replace evenly over 24–48 hours.
        • Add maintenance rate to rehydration rate for total IV rate but do not add additional fluid to replace ongoing urine output.
        • Increase rate for inadequate renal or body perfusion. Decrease rate for suspected cerebral edema or pulmonary edema.
      • Composition of IV fluids: Tonicity and Na:
        • Start with normal saline. Change to 1/2 normal when circulation is secure and Na is >130.
        • IV fluids should contain K after the 1st hour, or when anuric renal failure or extreme hyperkalemia is ruled out.
      • Composition of IV fluids: Potassium:
        • Should contain K at 40 mEq/L, often 1/2 KCl and 1/2 K phosphate (never all phosphate)
        • Problems from inadequate or excessive K are rare if K replacement is begun early by gradual infusion without boluses, riders, or high central line concentrations.
      • Composition of IV fluids: Glucose:
        • Add 5% dextrose to IV stock when blood glucose <300 mg/dL.
        • Change to 10% dextrose when glucose <200 mg/dL so that full insulin rate can continue.
      Diabetic Ketoacidosis - insulin

      Insulin: As IV infusion for rapid adjustment

      • 1 U of regular insulin per cc of normal saline
      • Initial bolus unnecessary, but prompt initiation of insulin infusion halts ketoacid production.
      • For most patients, 0.1 U/kg/h will steadily correct hyperglycemia and ketoacidosis without need to adjust rate.
      • Biological effect of IV insulin dissipates in 10–20 minutes if the infusion is interrupted.
      • Ideal rate of glucose decline is <100 mg/dL/h, but fluid bolus may induce faster fall in 1st hours. If it continues to fall rapidly, add dextrose rather than reduce insulin rate.
      • If it is necessary to change IV insulin rate, increase or decrease by 50%.
      Diabetic Ketoacidosis - monitoring
      • Admit high risk patients to pediatric ICU: Infants, hemodynamic or neurologic instability, extreme acidosis (pH <7), dehydration (BUN >40, Na >145), or hyperglycemia (>800)
      • Most complications occur in 1st 24 hours and are reversible if recognized quickly.
      • Check vital signs, urine output, and perfusion adequacy hourly.
      • Check neurologic status and rousability hourly.
      • Check serum glucose hourly.
      • Check basic chemistries q2h in high risk patients, q4h in moderate severity:
        • If initial Na was low, it should rise steadily toward normal during therapy; a fall may indicate impending cerebral edema.
        • Hypernatremia >150 after prolonged normal saline suggests inadequate free water.
        • K may fall during therapy, but if K replacement was started early, it is usually unnecessary to exceed 40 mEq/L in IV.
        • T waves of EKG reflect K status.
        • Total COCheck urine ketones q2h. Ketonuria is usually the last lab abnormality corrected.
      Diabetic Ketoacidosis - transition to-diet-and-sc-insuline
      • Allow oral intake when acidosis is reversed, glucose lowered, and child is alert and not vomiting.
      • Begin SC insulin when child is awake, able to eat, glucose <200, and ketones nearly gone. Because effect of IV insulin is short, do not stop IV insulin until SC injection is given.
      Diabetic Ketoacidosis - bicarbonate

      Degree of acidosis reflects DKA severity and overall risk, but insulin reverses acidosis and few patients need alkali therapy.

      • Bolus bicarbonate use has been associated with a higher risk of cerebral edema.
      • The recommended way to give bicarbonate for extreme acidosis (pH <6.9) is IV infusion of 2 meq/kg over several hours.

      Diabetic Ketoacidosis - FOLLOW UP

      Diabetic Ketoacidosis - disposition

      Diabetic Ketoacidosis - issues for referral

      Refer to a pediatric endocrine service for initial diabetes education or for recurrent DKA.

      Diabetic Ketoacidosis - prognosis

      Mortality of DKA in children is ~0.2–0.3%.

      Diabetic Ketoacidosis - complications

      • Death in childhood DKA results from cerebral edema (57–87%) or cardiovascular collapse.
      • Cerebral edema refers to several forms of acute neurological catastrophe, especially brainstem herniation and stroke:
        • Highest risk patients are youngest, and those with most severe dehydration and acidosis.
        • Cause of brain swelling still unsettled: Hypotheses include water influx as osmolality falls, or excessive blood flow.
        • Commonly occurs 6–18 hours into treatment, often as patient is improving
        • Heralded as headache, change in mental status, focal neurologic signs, rising blood pressure, or unexpected drop of serum Na.
        • From neurologic changes, brain herniation and respiratory arrest may occur rapidly.
        • Treatment of suspected cerebral edema includes slowing of IV fluids, mannitol 0.5–1.0 g/kg by IV infusion over 15 minutes.
        • Obtain CT scan to confirm brain swelling only if patient can be treated during procedure.
        • Prepare to intubate, ventilate if arrest occurs.
      • Cardiovascular collapse and death from shock usually due to delay or interruption of IV fluids, or to inadequate fluid rates:
        • Leads to hypovolemic shock and shock damage to kidneys, other organs
        • Give isotonic IV fluid to restore perfusion.
      • Some complications are largely avoidable:
        • Hypo- and hyperkalemia can cause arrhythmias. Hypo-K often from delayed K replacement. Hyper-K can occur if K boluses given as “catch-up,” or renal failure or rhabdomyolysis.
        • Hypoglycemia can be avoided with frequent glucose checks.
        • Hypocalcemic tetany usually results from excessive phosphate replacement.
        • Hypernatremia reflects prolonged normal saline or bicarbonate, or inadequate water.
      • Other complications, not directly attributable to treatment, can occur in severe cases:
        • Pulmonary edema or adult respiratory distress syndrome (ARDS)
        • Pneumomediastinum from hyperventilation
        • Rhabdomyolysis
        • Thrombosis, especially at central line site
        • Disseminated intravascular coagulation (DIC)
        • Rhinocerebral mucormycosis
        • Gastric atony and dilatation
        • Pancreatitis

      Diabetic Ketoacidosis - bibliography

      1. Dunger DB, Sperling MA, Acerini CL, et al. European Society for Paediatric Endocrinology/Lawson Wilkins Pediatric Endocrine Society consensus statement on diabetic ketoacidosis in children and adolescents. Pediatrics. 2004;113:e133–e140.
      2. Glaser N. Pediatric diabetic ketoacidosis and hyperosmolar state. Pediatr Clin North Am. 2005;52:1611–1635.
      3. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med. 2001;344:264–269.
      4. Green SM, Rothrock SG, Ho JD, et al. Failure of adjuvant bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emerg Med. 1998;31:41–48.

      Diabetic Ketoacidosis - CODES

      Diabetic Ketoacidosis - icd9

      250.1 Diabetes with ketoacidosis

      Diabetic Ketoacidosis - PATIENT TEACHING-MED

      Diabetic Ketoacidosis - prevent

      Ketone testing and illness management

      Diabetic Ketoacidosis - FAQ

      • Q: What are the usual triggers for DKA?
      • A: Mismanagement of minor illness, or omissions of insulin due to lack of parental education or participation.
      • Q: What are the most common management errors that contribute to a poor outcome?
      • A: Failure to recognize early DKA, prolonged telephone management, delayed fluid start, excessive fluid in emergency department, delayed K replacement, bolus bicarbonate use, inadequate fluids for fear of cerebral edema, failure to monitor closely, failure to respond quickly to mental status changes.
      • Q: Does an episode of DKA mean that the usual daily insulin regimen is inadequate?
      • A: No. The usual regimen is best assessed by hemoglobin A1c and hypoglycemia frequency. DKA indicates missed insulin or a failure to respond to an unusual situation.
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      Book Source Details

      • Book Title: The 5-Minute Pediatric Consult
      • Author(s): M. William Schwartz MD; et al.
      • Year of Publication: 2008
      • Copyright Details: The 5-Minute Pediatric Consult, Copyright © 2008 Lippincott Williams & Wilkins.

      More About Diabetic Ketoacidosis

      More Medical Textbooks Online about Diabetic Ketoacidosis

      Review other book chapters online related to Diabetic Ketoacidosis:

      Medical Books Excerpts
      • Diabetes Mellitus
      • "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
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      Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.



      More About This Book:
      Title: The 5-Minute Pediatric Consult
      Authors: M. William Schwartz MD; et al.
      Publisher: Lippincott Williams & Wilkins
      Copyright: 2008
      ISBN: 0-7817-7577-9

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