Hypoglycemia + DKA

HYPOGLYCEMIA

• Definition: Abnormally low blood glucose level below 70 mg/dL.

• Causes of Hypoglycemia:

  • Excessive administration of insulin or oral hypoglycemic agents.

  • Excessive physical activity.

  • Inadequate food intake.

• Symptoms:

  • Adrenergic Symptoms: Symptoms due to the activation of the sympathetic nervous system, which may include:

  • Tachycardia

  • Sweating

  • Palpitations

  • Central Nervous System Symptoms: Include:

  • Confusion

  • Dizziness

  • Severe Hypoglycemia Symptoms: Can lead to seizures or loss of consciousness.

DKA & HHS

OBJECTIVES

• Describe treatments for Hypoglycemia.

• Differentiate between diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS).

• Identify laboratory markers associated with DKA and HHS.

• Describe treatments for DKA and HHS.

• Discuss potential complications for DKA, HHS, and hypoglycemia.

DIABETES

• Definition: Diabetes is a metabolic disorder characterized by either decreased production of insulin or an inability of the body to respond adequately to insulin.

• Types of Diabetes:

  • Type I Diabetes: Autoimmune dysfunction leading to the pancreas not producing insulin.

  • Type II Diabetes: A progressive disease characterized by insulin resistance.

DIABETIC KETOACIDOSIS (DKA)

Pathophysiology of DKA

• Occurrence: Most commonly occurs in Type 1 Diabetes Mellitus (DM).

• Mechanism:

  • When stressors like infection increase the need for insulin, there may be insufficient insulin produced.

  • The absence of insulin leads to increased lipolysis and the formation of ketone bodies from triglycerides.

  • Step-by-step mechanism:

  • Absolute insulin deficit results in the release of free fatty acids from adipose tissue.

  • Hydrolysis of free fatty acids in the liver leads to ketogenesis (formation of ketone bodies like beta-hydroxybutyrate (BOHB) and acetoacetate (AcAc)).

  • Acetyl CoA is produced and used as energy by cells, which perceive a lack of glucose, triggering hunger (polyphagia).

  • Glucose remains unutilized in the blood, leading to elevated blood glucose levels.

  • This state triggers the increased release of catabolic hormones (glucagon, epinephrine, cortisol, GH) trying to elevate blood glucose for cellular absorption.

  • This results in decreased protein synthesis, increased proteolysis, gluconeogenesis, and glycogenolysis in the liver.

• Consequences:

  • Formation and accumulation of ketone bodies in the blood leading to metabolic acidosis.

  • Osmotic diuresis leading to polyuria and dehydration, causing up to 4-5L of fluid loss.

  • Electrolyte disturbances, particularly potassium depletion due to osmotic diuresis.

  • Neurological effects due to disruption of ion osmosis and reduced perfusion to the brain.

• Clinical Symptoms of DKA:

  • Hyperglycemia.

  • Severe dehydration.

  • Acidosis; may present with Kussmaul respirations (deep, rapid breaths).

  • Fruity odor on breath due to ketone presence.

  • Abdominal pain, weakness, confusion, and potential for coma.

DKA: TREATMENT

• Initial Treatment Goals:

  1. Rehydrate with IV fluids.

  2. Administer insulin to reduce blood glucose.

  3. Monitor and restore electrolyte balance, especially potassium.

  4. Identify and treat the precipitating causes of DKA.

  5. Monitor and address low phosphate after ketosis resolves.

• Insulin Administration: Administer 0.1-0.15 units/kg IV push followed by continuous infusion at 0.1 units/kg/hr.

• Electrolyte Monitoring:

  • Frequent monitoring of glucose, ketones, bicarbonate, and potassium.

• Evaluation of Treatment Effectiveness:

  • Evaluate when ketones are <0.6 mmol/L, pH >7.3, bicarbonate >15 mmol/L, and glucose <200.

DKA vs. HHS

HYPERGLYCEMIC HYPEROSMOLAR STATE (HHS)

• Definition: Hyperosmolar hyperglycemia caused by a lack of sufficient insulin, with minimal or absent ketosis.

• Pathophysiology: Hyperglycemia leads to osmotic diuresis and consequent loss of water and electrolytes, leading to hypernatremia and increased serum osmolality.

• Clinical Features:

  • Blood glucose >600 mg/dL.

  • Profound hypotension and dehydration.

  • Tachycardia and variable neurologic signs due to cerebral dehydration.

HHS: CAUSES

• Underlying Conditions:

  • Infection, stress, or chronic medical conditions like myocardial infarction and sepsis.

• Medications Influencing HHS:

  • Glucocorticoids, thiazide diuretics, phenytoin, beta-blockers, calcium channel blockers.

HHS: TREATMENT

• Solutions:

  • Initiate rehydration.

  • Administer insulin.

  • Monitor fluid balance and electrolyte status.

  • Implement preventative measures to manage risk factors.

PATIENT CARE FOR OLDER CLIENTS

• Important Considerations:

  • Educate about regular medication adherence and maintaining hydration.

  • Recognize changes in mental status as they may indicate complications.

DISCHARGE PLAN

• Patient Education:

  • Identify risk factors contributing to diabetic crises.

  • Notify healthcare provider if:

  • Illness lasts >24 hours.

  • Glucose levels exceed 250 mg/dL.

  • Unable to tolerate food or liquids.

  • Ketones present in urine for over 24 hours.

  • Fever >101.5 °F (38.6 °C) for over 24 hours.

REFERENCES

• Hinkle, J. L., Cheever, K. H., & Overbaugh, K. J. (2022). Brunner & Suddarth’s Textbook of Medical-Surgical Nursing (15th ed.). Wolters Kluwer.

• ATI Nursing Education (2019). RN Adult Medical-Surgical Nursing (11th ed).