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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
classification
Classification
  • 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
slide8

Osmotic Diuresis

Decreased renal blood flow and glomerular perfusion

Dehydration

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
pathophysiology
Pathophysiology
  • 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
pathophysiology1
Pathophysiology
  • Hyperglycemia  heightened inflammatory state  exacerbating glucose dysregulation
  • Osmotic diuresis  dehydration  decreased GFR  further glucose elevation
pathophysiology2
Pathophysiology
  • 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
pathophysiology3
Pathophysiology
  • 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
treatment
Treatment
  • 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
complications
Complications
  • Cardiac arrest
  • Refractory arrhythmias
  • Pulmonary thromboemboli
  • Circulatory collapse
  • Refractory shock
  • Acute renal failure
  • Rhabdomyolysis
  • Neurologic deficits
  • Electrolyte disturbances
  • Multisystem organ failure
treatment1
Treatment
  • Adult mortality: 15%
  • Pediatric prevalence of HHS is unknown
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