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Diabetes Mellitus. Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta. Goals & Objectives. Understand the action of insulin on the metabolism of carbohydrates, protein & fat Understand the pathophysiology of IDDM & DKA

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diabetes mellitus

Diabetes Mellitus

Pediatric Critical Care Medicine

Emory University

Children’s Healthcare of Atlanta

goals objectives
Goals & Objectives
  • Understand the action of insulin on the metabolism of carbohydrates, protein & fat
  • Understand the pathophysiology of IDDM & DKA
  • Understand the management approach to the patient with DKA
  • Appreciate the complications that occur during treatment
  • Type I (insulin-dependent diabetes mellitus, IDDM)
    • Severe lacking of insulin, dependent on exogenous insulin
    • DKA
    • Onset in childhood
    • ?genetic disposition & is likely auto-immune-mediated
  • Type II (non-insulin-dependent diabetes mellitus, NIDDM)
    • Not insulin dependent, no ketosis
    • Older patient (>40), high incidence of obesity
    • Insulin resistant
    • No genetic disposition
    • Increase incidence due to prevalence of childhood obesity
iddm epidemiology
IDDM: Epidemiology
  • 1.9/1000 among school-age children in the US; 12-15 new cases/100,00
  • Equal male to female
  • African-Americans: occurrence is 20-30% compared to Caucasian-Americans
  • Peaks age 5-7 yrs and adolescence
  • Newly recognized cases: more in autumn & winter
  • Increase incidence in children with congenital rubella syndrome
type i dm
Type I DM
  • 15-70% of children with Type I DM present in DKA at disease onset
  • 1/350 of type I DM will experience DKA by age 18 yo
  • Risk of DKA increased by:
    • Very young children
    • Lower socioeconomic background
    • No family history of Type I DM
  • DKA:
    • Most frequent cause of death in Type I DM
    • One of the most common reasons for admission to PICU
iddm etiology pathophysiology
IDDM: Etiology & Pathophysiology
  • Diminished insulin secretion by destruction of pancreatic islets cells via autoimmune process
  • 80-90% of newly diagnosed cases have anti-islet cell antibodies
  • More prevalent in persons with Addison’s disease, Hashimoto’s thyroiditis, pernicious anemia
type i dm pathophysiology
Type I DM: Pathophysiology
  • Progressive destruction of -cells progressive deficiency of insulin  permanent low-insulin catabolic state
  • Phases:
    • Early: defect in peripheral glucose predominates
    • Late: insulin deficiency becomes more severe

Osmotic Diuresis

Decreased renal blood flow and glomerular perfusion


Stimulates counter regulatory hormone release

Increased lactic acidosis

Accelerated production of glucose and ketoacids

type i dm pathophysiology1
Type I DM: Pathophysiology
  • Hyperglycemia glucosuria (renal threshold 180 g/dL)  osmotic diruresis: polyuria, urinary losses of electrolytes, dehydration, & compensatory polydipsia
  • Hyperglycemia  hyperosmolality: cerebral obtundation
    • {Serum Na+ + K+} x 2 + glucose/18 + BUN/3
  • Counter-regulatory hormones (glucagon, catecholamines, cortisol) are released
    • Increased hepatic glucose production  impairing peripheral uptake of glucose
type i dm dka
Type I DM: DKA
  • Lipid metabolism: increase lipolysis
    • Increased concentration of total lipids, cholesterone, TG, free FA
    • Free FA shunted into ketone body formation; rate of production>peripheral utilization & renal excretion  ketoacids
    • Ketoacidosis  -hydroxybutyrate & acetoacetate  metabolic acidosis
    • Acetone (not contribute to the acidosis)
type i dm dka1
Type I DM: DKA
  • Electrolytes loss
    • Potassium: 3-5 mEq/kg
    • Phosphate: 0.5-1.5 mmol/kg
      • 2,3-diphosphoglycerate: facilitates O2 release from HgB
      • Deficient in DKA, may contribute to formation of lactic acidosis
    • Sodium: 5-10 mEq/kg
dka presenting features
DKA: Presenting Features
  • Polyuria
  • Polydipsia
  • Polyphagia
  • Nocturia
  • Enuresis
  • Abdominal pain
  • Vomiting
  • Profound weight loss
  • Altered mental status
  • weakness
type i dm clinical manifestations
Type I DM: Clinical Manifestations
  • Ketoacidosis is responsible for the initial presentation in up to 25% of children
    • Early manifestations: vomiting, polyuria, dehydration
    • More severe: Kussmaul respirations, acetone odor on the breath
    • Abdominal pain or rigidity may be present & mimic acute abdomen
    • Cerebral obtundation & coma ultimately ensue
  • DKA exists when there is hyperglycemia (>300 mg/dL & usually <1,000 mg/dL); ketonemia, acidosis, glucosuria & ketonuria
dka physical exam
DKA: Physical Exam
  • Tachycardia
  • Dry mucous membrane
  • Delayed capillary refill
  • Poor skin turgor
  • Hypotension
  • Kussmaul breathing
dka physical exam1
DKA: Physical Exam
  • Dehydration
    • Hyperosmolar: translocation of intracellular water to extracellualr comparment
    • A rough estimation of how dehydrated the patient is to facilitate proper rehydration
    • Studies have shown that clinical approximations often are poor
dka laboratory
DKA: Laboratory
  • Blood glucose
  • Urinary/plasma ketones
  • Serum electrolytes
  • BUN/Cr
  • Osmolarity
  • CBC, blood cx (if infection is suspected)
  • Blood gas
dka laboratory findings
DKA: Laboratory Findings
  • Elevated blood glucose (usually <1,000)
  • Low bicarbonate level
  • Anion gap metabolic acidosis
    • Unmeasured ketoacids
    • Urine dipsticks measure acetoacetate: in DKA B-hydroxybutyrate to acetoacetate is 10:1
    • Helpful in determining if there is ketoacids in urine but not sererity of DKA or response to treatment
dka laboratory findings1
DKA: Laboratory Findings
  • Sodium: low
    • Osmotic flux of water into extracellular space reduces serum sodium concentration
    • Actual sodium: 1.6mEq/L per 100mg/dL rise in glucose over 100
    • Hypertriglyceridemia  low sodium  pseudohyponatremia
  • Potassium:
    • Level varies depending on urinary loss and severity of acidosis
    • Potassium moves extracellularly in exchange for hydrogen ions  typical hyperkalemia on presentaion
    • Total body stores are depleted due to urinary loss
dka laboratory findings2
DKA: Laboratory Findings
  • Phosphate
    • Depleted in the setting of DKA
    • Serum level may not accurately represent total body stores
dka management
DKA: Management
  • Goals: correction of
    • Dehydration
    • Acidosis
    • Electrolytes deficits
    • Hyperglycemia
dka management1
DKA: Management
  • Fluids:
    • Avoid impending shock
      • Fluid replacement >4L/m2/24 hrs has been associate with cerebral edema
    • Usually necessary to help expand vascular compartment
      • Fluid deficit should gradually be corrected over 36-48 hrs
    • Rehydration fluids should contain at least 115-135 mEq/L of NaCl
      • Start with NS and switch to ½ NS if neccessary
dka management2
DKA: Management
  • Postassium:
    • Total body depletion will become more prominent with correction of acidosis
    • Continuous EKG monitoring is standard of care
    • 30-40 mEq/L: in either KCl or KPhos
dka management3
DKA: Management
  • Phosphate:
    • Total body depletion will become more prominent with correction of acidosis
    • Hypophosphatemia may cause rhabdomyolysis, hemolysis, impaired oxygen delivery
    • Calcium should be monitored during replacement
dka management4
DKA: Management
  • Insulin should be initiated immediately
    • Insulin drips 0.1 U/kg/hr (NO BOLUS)
    • Gradual correction reducing serum glucose by 50-100 mg/dL/hr
    • Serum glucose often falls after fluid bolus: increase in glomerular filtration with increased renal perfusion
dka management5
DKA: Management
  • Dextrose should be added to IVF when serum glucose <300
    • Blood glucose levels often correct prior to ketoacidosis
    • Should not lower insulin infusion unless: rapid correction of serum glucose or profound hypoglycemia
dka management6
DKA: Management
  • Bicarbonate is almost never administered
    • Bicarb administration leads to increased cerebral acidosis:
    • HCO3- + H+  dissociated to CO2 and H2O
    • Bicarbonate passes the BBB slowly
    • CO2 diffuses freely  exacerbating cerebral acidosis & depression
  • Indications for bicarbonate use: only in severe acidosis leading to cardiorespiratory compromise
dka complication cerebral edema
DKA: Complication, Cerebral Edema
  • Cerebral edema: 0.5-1% of pediatric DKA
    • Mortality rate of 20%
    • Responsible for 50-60% of diabetes deaths in children
    • Permanent neurologic disability rate of 25%
  • Typically develops within the first 24 hrs of treatment
  • Etiology is still unclear
  • Signs & symptoms:
    • Headache
    • Confusion
    • Slurred speech
    • Bradycardia
    • Hypertension
dka complication cerebral edema1
DKA: Complication, Cerebral Edema
  • Theories of cerebral edema
    • Rapid decline in serum osmolality
      • This leads to the recommendation of limiting the rate of fluid administration
    • Edema due to cerebral hypoperfusion or hypoxia
    • Activation of ion transporters in the brain
    • Direct effects of ketoacidosis and/or cytokines on endothelial function
dka cerebral edema risk factors
DKA: Cerebral Edema, risk factors
  • Younger age
  • New onset
  • Longer duration of symptoms
  • Lower PCO2
  • Severe acidosis
  • Increase in BUN
  • Use of bicarbonate
  • Large volumes of rehydration fluids
  • Failure of correction of Na with treatment
dka cerebral edema treatment
DKA: Cerebral Edema, treatment
  • Lower intracranial pressure
    • Mannitol or 3% saline
  • Imaging to rule out other pathologies
  • Hyperventilation & surgical decompression are less successful at preventing neurologic morbidity & mortality
dka complications
DKA: Complications
  • Thrombosis (esp with CVL)
  • Cardiac arrhythmias
  • Pulmonary edema
  • Renal failure
  • Pancreatitis
  • Rhabdomyolysis
  • Infection
    • Aspiration pneumonia
    • Sepsis
    • Mucormycosis
  • Insulin levels are sufficient to suppress lipolysis and ketogenesis
  • Insulin levels are inadequate to promote normal anabolic function & inhibit gluconeogeneis & glycogenolysis
  • Cell deprivation triggers counter-regulatory surge, increasing glucose via enhanced hepatic glucose generation & insulin resistance
  • Hyperglycemia  heightened inflammatory state  exacerbating glucose dysregulation
  • Osmotic diuresis  dehydration  decreased GFR  further glucose elevation
  • Morbidity & mortality associated with acute hyperglycemia
    • Vascular injury
    • Thrombus formation
    • Disrupts the phagocytotic & oxidative burst functions of the immune systemt
    • Disrupts BBB
    • Disrupts metabolism of the CNS worsens the effects of ischemia on brain tissue
  • Dehydration is a major component
  • 15-20% volume depleted
    • 5-10% in DKA
  • Greater electrolyte loss due to massive osmotic diuresis
clinical presentation
Clinical Presentation
  • Similar to DKA
    • Polyuria
    • Polydipsia
    • Weight loss
    • Neurologic impairment
  • Different from DKA
    • Kussmaul breathing
    • Acetone breath
    • Abdominal discomfort, nausea & vomiting are less severe
laboratory findings
Laboratory Findings
  • Glucose: >600 mg/dL
  • HCO3>15
  • Serum osmolarity >320 mOsml/L
  • pH>7.3 without evidence of significant ketosis
    • Level of acidemia is influenced by severity of shock & starvation
  • Lab values consistent with acute renal failure, rhabodmyolysis & pancreatitis
  • Insulin plays a secondary role
    • Hyperglycemia can often be corrected via volume resuscitation
    • Renal perfusion is improved, GF is enhanced
    • Insulin gtt 0.1 U/kg/hr
  • Cardiac arrest
  • Refractory arrhythmias
  • Pulmonary thromboemboli
  • Circulatory collapse
  • Refractory shock
  • Acute renal failure
  • Rhabdomyolysis
  • Neurologic deficits
  • Electrolyte disturbances
  • Multisystem organ failure
  • Adult mortality: 15%
  • Pediatric prevalence of HHS is unknown