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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