Complex-Endocrine Part 3 DKA, HHS

What makes up Diabetic ketoacidosis?

• hyperglycemia

• Ketosis

• metabolic acidosis

What does Insulin do in the body at the cellular level?

• Promotes glycogenesis (not gluconeogenesis)​

• Promotes lipogenesis (not lipolysis)​

• Promotes protein synthesis (not catabolism​

• Inhibits glucagon release​

• Role in appetite regulation

What conditions does Insulin help treat clinically?

• DM I, II, GD​

• DKA & HSS​

• Stress-related hyperglycemia​

• Treat hyperkalemia​

What is Diabetic Ketoacidosis (DKA)?

• Series of metabolic derangements: uncontrolled hyperglycemia, ketonemia, & acidemia​

• Result = abnormal metabolism of carbohydrates, fats, proteins with the production of highly acidic ketones bodies, leads to metabolic acidosis​

• Life threatening complication of diabetes (can lead hypovolemic shock)​

• Typically seen in type I diabetics​

• Most common acute hyperglycemic complication of type 1 diabetes mellitus​

What are the causes of DKA?

Lack of Insulin

• Sepsis​

• Sickness (Stomach virus & Flu) = most common​

• Stress (surgery, any source)​

• Skip insulin: pump failure, can be unknown​

• Other: Undiagnosed DM, medications

No insulin. No sugar in cell. ​

Fuel = ketones. Faster onset. Younger population. ​

Easier fix than HHS

What is the pathophysiology of Diabetic Ketoacidosis?

• Lack of insulin​

• Lack of intracellular glucose, rise in serum BG​

• Gluconeogenesis (noncarbs leads to glucose)​

• Hyperglycemia results​

• Kidneys secrete excess glucose along with water & electrolytes (Na, K) = Osmotic diuresis leads to polyuria​

• Dehydration & electrolyte loss with glucosuria​

• Lipolysis leads to FFA & glycerol leads to FFA converted to ketone bodies = acidic​

• Metabolic acidosis results

What are the clinical manifestations of Hyperglycemia due to DKA?

• Polyuria, polydipsia​

• Marked fatigue, weakness​

• Blurred vision​

• Headache​

• Orthostatic hypotension (if hypovolemic); thready pulse, tachycardia

What are the clinical manifestations of Ketosis/Acidosis due to DKA?

• GI SS (anorexia, N/V/abd pain)​

• Palpitation, chest pain​

• Acetone breath (fruity odor)​

• Hyperventilation (why?)​

• Alert, lethargic, comatose

What is the most serious complication of DKA?

Cerebral edema due to rapid shifts in fluid within the brain, often resulting from the treatment of DKA, rather than the DKA itself

High blood glucose in DKA creates a high osmotic pressure in the blood, drawing water from brain cells. During treatment, rapid reductions in glucose and plasma osmolality can cause a sudden shift of water back into brain cells, leading to swelling

What Assessment and Diagnostic findings are seen w/ DKA?

What DKA management is needed if the pt needs Rehydration?

• Fluid loss: polyuria, hyperventilation, diarrhea, vomiting​

• Goals: maintain tissue perfusion & promotes renal excretion of excess glucose ​

• Treat: IVF (crystalloids) ​

  • initially 0.9% sodium chloride rapid infusion (0.5-1L/h x 2-4h) ​

  • 0.45% NaCl for HTN, hypernatremia, heart failure or after first few hours ​

• Once BG <300mg/dL, change to dextrose 5% in water (D5W)​

• Monitor: Frequent labs, exam, VS, I&O​

• Watch: peds/elderly, renal insufficiency, HF

How would you Restore electrolytes in a pt w/ DKA?

• Potassium replacement asap ​

  • Rehydration may cause hypokalemia​

  • Rehydration causes ↑UO and potassium excretion​

  • Insulin treatment drives potassium into cells​

• Potassium replacement even if normal plasma levels since blood levels ↓ during DKA treatment ​

  • (contraindicated for EKG abnormalities or anuria)​

• Avoid hypokalemia arrhythmias​

• Initially frequent ECGs (q2-4h) & potassium labs

How would you reverse acidosis in a pt w/ DKA?

• DKA acidosis is secondary to lipolysis​

• Treat with INSULIN​

  • MOA = inhibits lipolysis (ceases ketone formation and acid build up)​

• Treatment: slow continuous REGULAR insulin infusion (5 units/h)​

• Monitor: q1h blood glucose (BG)​

• IVF + glucose (D5NS, D50.45%NS) for BG of 250-300mg/dL to prevent hypoglycemia​

• Continue IV insulin until subcutaneous insulin administered; (Goal is serum bicarb or BG level)​

• ↑ rate/conc of dextrose IVF to prevent hypoglycemia prn & until patient eating ​(since BG levels corrected before acidosis)​

• Avoid bicarb infusion to correct severe acidosis since results in sudden drop in potassium

What makes up Hyperglycemic Hyperosmolar Syndrome (HHS)?

• Hyperglycemia

• High Serum Osmolality

• Absence of Acidosis

What is Hyperglycemic Hyperosmolar Syndrome (HHS)?

• Defined: metabolic disorder of type II diabetes secondary to relative insulin deficit caused by illness raising insulin demand​

• Predominantly hyperosmolality & hyperglycemia with minimal to absent ketones​

  • because there is enough insulin present to suppress fat breakdown (lipolysis) and ketogenesis

• Affects sense of awareness (altered sensorium)​

• Defect  lack of effective insulin (insulin resistance)​

• Population: Older pts (50-70 years old); no known diabetic history or have DMII​

• Causes: infection, acute illness (eg stroke), some meds (eg thiazides), treatment (eg dialysis)​

What is the pathophysiology of Hyperglycemic Hyperosmolar Syndrome (HHS)?

• Severe Hyperglycemia

  • Blood glucose levels often exceed 600 mg/dL (33.3 mmol/L).

  • Unlike diabetic ketoacidosis (DKA), there is usually no significant ketosis.

  • The insulin level is low, but sufficient to prevent ketogenesis, which is why there's no acidosis.

• Hyperosmolarity

  • The extremely high glucose draws water out of the cells into the bloodstream.

  • This leads to severe dehydration and increased serum osmolality (>320 mOsm/kg).

• Osmotic Diuresis

  • High glucose spills into the urine (glucosuria), pulling water and electrolytes with it.

  • This causes polyuria, electrolyte imbalances (especially potassium), and further dehydration.

• Altered Mental Status

  • As the brain becomes dehydrated due to hyperosmolarity, neurological symptoms arise:

    • Confusion

    • Lethargy

    • Seizures

    • Coma (in severe cases)

What are the causes of Hyperglycemic Hyperosmolar Syndrome?

infection, acute illness (eg stroke), some meds (eg thiazides), treatment (eg dialysis), stressful events

Some insulin allows sugar in cell. (no ketones).​

Higher BG, more dehydration, slower onset, older population, more symptoms, higher mortality, more severe neuro symptoms. Harder fix.

What are the clinical manifestations of HHS?

• Hypotension ​

• Profound dehydration​

  • Dry mucous membranes​

  • Poor skin turgor​

• Tachycardia​

• Variable neurologic symptoms ​

  • Altered consciousness, seizures, weakness, hallucinations​

• Polyuria, polydipsia, polyphagia

What is some diagnostic criteria differences b/w DKA/HHS?

How do you manage HHS?

• Identify underlying issue​

• Like DKA: fluid replacement, electrolyte correction, insulin (less)​

• IVF: 0.9% NS then hypotonic IVF (Na level and degree of hypovolemia will dictate this)​

• Central venous or hemodynamic pressure monitoring guides IVF​

• Potassium added to IVF if good UO​

• Frequent labs and continuous EKG monitoring​

• Rehydration fixes hyperglycemia​

• Insulin lesser role since no acidosis​

  • Continuous low rate with replacement dextrose IVF (once BG 250-300mg/dL)​

Monitor: volume status, electrolyte imbalances, HF, arrhythmias

What Reassessment is needed for a pt w/ HHS?

• Maintain fluid & electrolyte balance​

• BG hourly​

• Rehydration signs​

  • BP, HR, cap refill, ​

  • Skin color, warm temp​

  • UO (30ml/hr)​

  • Low spec gravity (1.005-1.030)

What IV med is needed for managing HHS?

Potassium

• Telemetry first!​

• Never IV push​

• 10-20mg max/hour on pump​

• Site: central line and slow infusion

What insulin is needed for management of HHS?

• IV insulin, REGULAR only (DKA)​

• Then SQ or insulin pump (HHS)

What should be monitored when managing HHS?

• Fluid overload, hypo/hyperglycemia, hypokalemia, cerebral edema​

• Arrhythmias (K+)

What Education is needed for managing HHS?

DM self-management/care, DKA/HHS prevention, medication consistency, diet, sick day rules

• Can take 3-5 days for resolution of neurologic SS (older population)​

• HHS treatment ongoing after metabolic abnormalities resolved​

• May or may not need insulin & meds after recovery​

• Self-management of BG is the best prevention!​

• Educate!