Hyperglycemic Crises Flashcards
Normal Physiological Response to Increased Serum Glucose
Increased serumglucose
Detected by the pancreatic beta cells and insulinwill be released
insulin will
↓glucagonsecretionfrom pancreatic alpha cells
↓gluconeogenesis andglycogenolysis in theliver
↑glucoseuptake by muscle andadipose cells
Hyperglycemia
DKA & HHS
Results from problems relating to insulin (absolute deficiency or insulin resistance):
↓glucose utilization by peripheral tissues (muscle and adipose cells)
↑glycogenolysis and ↑gluconeogenesis by the liver
Leads to:
↑plasma osmolality (high solute – glucose) → draws water out of the cells → outside the cell the sodium concentration is now dilute
hyperglycemia
High serumglucose level (> 180 mg/dL) exceeds renal threshold causing
Glucosuria
Increase inosmotic pressure of the urine leading topolyuria
Loss of water → dehydration → worsens plasma osmolality (hyperosmolality) → potassium shifts out of cells → ↑ extracellularpotassium, ↓ intracellular potassium
Impaired renal function (AKI)
DKA
Epidemiology
More frequently seen in younger patients
Mostly seen inpatients with type 1diabetes
Accounts for ~14% of all hospital admissions for diabetics
Mortality rate of 5% in individuals < 40 years; ↑ mortality with advanced age
HHS
epidemiology
Usually associated with older individuals (≥ 65 years)
Patientswill usually have type 2 diabetes
Accounts for < 1% of all hospital admissions for diabetics
Mortality rate: 10%–20%
HHS & DKA
etiology
Infections(most common)
Inadequate or noncompliance withinsulintreatment
Acute illnesses (stroke,myocardial infarction,pancreatitis, surgery, trauma)
Medications - corticosteroids
Illicit drugs - cocaine
Alcohol
HHS
etiology
Dehydration
Medications – diuretics, beta-blockers
Endocrine disorders: Cushing syndrome
DKA
etiology
new onset diabetes - type 1
DKA
Clin Man
Rapid onset of symptoms (over 24 hours)
Polyuria
Polydipsia
Nausea andvomiting
Diffuse abdominalpain
Weakness
History ofweight loss → common with a new diagnosis oftype 1diabetes
DKA
PE Findings
Physical exam findings:
Vitals:
Tachycardia
Hypotension
Hypothermia
Rapid, deep respirations (Kussmaul respirations) → compensatoryhyperventilation (attempting to blow off carbon dioxide – acid)
Fruity breath → exhaledacetone
DKA and HHS
Evidence of severedehydration
Dry mucous membranes
Sunken eyes
Decreasedskin turgor
Decreasedurine output
HHS
Clin Man
Gradual development of symptoms (over days to weeks)
Polyuria
Polydipsia
Nausea andvomiting
Neurologic changes:
Lethargy
Delirium
Coma(in severe disease)
Seizures
Sensory deficits
Vision changes
HHS
PE Findings
Physical exam findings:
Vitals:
Tachycardia
Hypotension
Hypothermia
Altered mental status, lethargy, or coma
DKA
Dx
Serum glucose: >250 mg/dL
Serum bicarbonate: ↓↓ (< 18 mEq/L)
Anion gap: Yes(the higher the more severe the presentation)
Serum osmolality: Variable
Serum ketones (beta-hydroxybutyrate, acetone): Positive
Urine ketones: Positive
Arterial blood gas: pH < 7.3; ↓ pCO2 (increase resp to reduce CO2 and lessen acidosis)