critical endo
Pathophysiology: DKA and HHS
DKA (Diabetic Ketoacidosis)
Mechanism involves:
Activation of hormone-sensitive lipase.
Increased counter-regulatory hormones including cortisol, glucagon, growth hormone, catecholamines.
Leads to hyperglycemia via increased glycogenolysis and gluconeogenesis.
Results in metabolic acidosis and formation of ketone bodies due to elevated free fatty acids (FFAs).
HHS (Hyperglycemic Hyperosmolar State)
Mechanism characterized by:
Insulin resistance and pronounced osmotic diuresis.
Elevated serum osmolality leading to dehydration and increased pro-inflammatory cytokines.
DKA and HHS: Risk Factors
Both conditions arise from physical stress like:
Injury, illness, infection, surgery
Alcohol abuse
New onset diabetes and elevated HbA1C
Noncompliance with insulin therapy
Medication impacts: corticosteroids, antipsychotics, antidepressants
Specific Risk Factors
DKA:
Typical ages 13 to 25, more prevalent in females, previous bouts of DKA.
HHS:
Occurs primarily in those over 65, notably among African American, Native American, Hispanic populations, and those with morbid obesity.
DKA and HHS: Impact on Overall Health
DKA:
Results in metabolic acidosis, muscle weakness, dehydration, electrolyte loss, cardiac arrhythmias, Kussmaul respirations (deep labored breathing), reduced kidney perfusion.
HHS:
Characterized by severe neurological implications, profound dehydration, risk for thromboembolic events, and similar cardiac and renal challenges as seen in DKA.
DKA and HHS: Clinical Presentation
General symptoms include:
Decreased consciousness, nausea, vomiting, abdominal pain, fruity breath (specific to DKA), hyperventilation, hypotension, arrhythmias, blurred vision, polydipsia, weight loss.
DKA and HHS: Lab and Diagnostic Studies
Key laboratory values include:
Serum blood glucose levels: DKA > 250 mg/dL; HHS > 600 mg/dL.
Complete blood count (CBC): monitor white blood cell count (WBC).
Electrolytes assessment: potassium (K), magnesium (Mg), sodium (Na), chloride (Cl), phosphorus (Phos).
Arterial Blood Gases (ABGs): DKA clients will exhibit metabolic acidosis (pH < 7.3 and HCO3 < 15).
Anion gap: DKA > 10 mEq/L indicating acidosis; HHS typically within normal range.
Serum osmolality: HHS > 320 mOsm/kg.
Urine studies: assess for glucose and ketones; in DKA, both are typically present, with osmolality above expected range.
Additional diagnostic tools include chest X-rays and ECGs for dysrhythmia assessment.
DKA and HHS: Treatments and Therapies
General Treatment Goals
RESTORE circulatory volume.
Secure large bore IV access or central line.
Replace half of fluid deficit within the first 12-24 hours via IV isotonic fluid.
Monitor sodium levels, transitioning to hypotonic solutions when appropriate.
Hyperglycemia Management
Avoid rapid decline in blood glucose.
Administration includes:
Initial bolus of IV regular insulin based on weight (0.1 units/kg).
Continuous IV insulin infusion aimed at reducing blood glucose by 50-70 mg/dL/hour, with adjustments as needed.
Once blood glucose is consistently < 200 mg/dL (DKA) or < 300 mg/dL (HHS), decrease IV insulin infusion rate.
Electrolyte Management
Specific Goals for electrolytes:
Maintain potassium at 4.0 to 5.0 mEq/L.
Use IV fluids to correct sodium and supplement magnesium as necessary.