Case 26 - DM Flashcards
Describe pathophysiology of Diabetes mellitus (DM)
- DM = metabolic disease due to defects in insulin secretion (DM1) and/or insulin responsiveness (DM2)
pathophys
- pancreatic Beta cells secrete insulin
- insulin shifts glucose into cells
- stores excess nutrients as glycogen in liver, fat in adipose tissue, protein in muscle (will be broken down into energy during fasting states)
Dx of DM
- hb1ac > 6.5%
- fasting glucose > 126
- 2 hr plasma glucose > 200 during oral glucose tolerance test
- symptomatic and random plasma glucose > 200
What is DM1?
- absolute deficiency of insulin secretion
- autoimmune destruction of pancreatic B cells
- require exogenous insulin for survival
-
DKA
- decrease insulin leads to decrease glucose utilization (glucose cannot shift intracellularly)
- body resorts to increased lipolysis of fat –> fatty acid levels increased and converted to ketoacids.
Review:
autoimmune beta cell destruction
insulin defiency
exogenous insulin required
propensity toward DKA
What is DM2?
- **tissue insulin resistance **
- develops due to increase age, obesity, inactivity
- oral medications early in disease (may require insulin later on)
- propensity towards HHS
what are the autonomic dysfunction affects of DM?
- intraop hypothermia
- impaired peripheral vasoconstrict
- orthostatic hypotension
- HD instability, syncope upon standing, exagerated hypotension on induction
- denevation of vagal control and cardioacelerator controlf of HR
- atropine or BB will have no affect on HR
Are you concerned for a full stomach in a diabetic patient coming for sx?
- chronic hyperglycemia damages gastrointestinal ganglion cells
- delays gastric emptyin, increase risk of aspiration during anesthesia
-
DM pts suspect or known to have gastroparesis –> treat with full stomach precautions, RSI
- consider premed to neutralize acidity of stomach and metoclopramide
are there fluid and electrolyte disturbances you should be concerned about in DM patients?
- volume depletion 2/2 hyperglycemia (polyuria)
-
diabetic nephropathy
- hyperkalemia
- metabolic acidosis (bicarb loss)
- anemia (CKD 2/2 DM nephropathy; dec erythropoietin)
What is the revised cardiac risk index? is DM included?
- Ischemic heart disease
- CHF
- CVA
- DM (insulin dependent)
- SCr > 2
- high risk surgery (intraperitoneal, intrathoracic, suprainguinal vascular sx)
6 pts total
determine risk of major cardiac event (MI, Vfib/cardiac arrest, pulm edema, complete heart block)
- DM is independent risk factor for CAD
what are the anesthesia implications of Metformin use prior to sux
- oral hypoglycemic agent
- decrease hepatic gluconeognesis, improve insulin sensitivity
-
side effect is lactic acidosis
- hold morning of surgery
- resume when renal and HD status normalized
What are the onset, peak, and duration of action for insulin aspart/lispro, and insulin regular
Aspart/lispro
- ultra-rapid acting
- onset 5-15 min
- peak 45-75 min
- duration 2-4 hour
Regular
- rapid acting
- onset 30 min
- peak 2-4 hours
- duration 5-8 hours
considerations
- ambulatory sx - consider aspart as less risk of hypoglycemia if patient goes home due to quick duration of action
What impact does hyperglycemia have on perioperative morbidity and mortality?
periop causes of hyperlycemia
- DM patients who did not take their insulin
-
neuroendocrine stress response
- counterregulatory hormones: glucagon, epi, cortisol –> all inhibit insulin section and increase gluconeogensis
- perioperative steroid administration
M&M
- impair wound healing
- reduce local perfusion
- increased risk of infection (impaired leukocyte function
- increase severity of neurologic insult (brain and spine)
- renal injury (polyuria –> hypovolemia; nephropathy)
A diabetic patient comes for surgery, his blood glucose is 210. What glucose level are you targeting for this patient?
- tight glucose (80-100 mg/dL)
- liberal/conventional (140-180 mg/dL)
- glycemic control reduces mortaility, bacetermia, acute kidney injury, blood transfusion, duration of mech ventilation, ICU stays
Tight vs liberal glucose
- hyperglycemia and increased M&M is strong
- not info evidence to support tight glucose control
- higher incidence of hypoglycemia seen in tight control group
- insulin metabolized by liver and kidney; organ dysfunction can prolong insulin duration of action
- Goal: target BG 140-180 mg/dL; carefully monitor and tx hypoglycemia
Describe DKA
- DM 1
- decrease insulin levels –> reduce glucose utilization –> body turns to lipolysis for source of energy –> increase FFA –> converted to ketone bodies
- dehydration, deep and rapid breathing (kussmaul respiratin), fruity smelling breath, N/V. Confusion and coma
-
Metabolic Acidosis with increase Anion Gap
- AG = Na+ - (HCo3 + Cl)
- AG = representative of the unmeasured ions in plasma or serum. Maintain eletrical neutrality between cation and anions
- AG normal 8-14
Can hyponatremia be false in presence of hyperglycemia or hypertriglyceridemia
For every 100 mg/dL increase in glucose above 200 mg/dL, sodium measured decreases by 1.5 mEq/L.
Example; glucose is 700 mg/dL and measured sodium is 128 meq/L. The actual corrected sodium will be 128 + (1.5 x 5) = 136.
what is HSS (Hyperglycemic hyperosmolar state)?
- DM 2
- result of decrease glucose utilization 2/2 inadequate insulin levels
- however, there is enough insulin to prevent lipolysis (therefore no ketone bodies (DKA))
- confused, coma
- pH > 7.3 (DKA has pH < 7.2)
- high osmolality (>315 mOsm/L)
DKA and HSS Causes
- inadequate insulin therapy and infection
- any stressful event: MI, CVA, PE, etc…
Diabetic patient comes to you with AMS, hypotension, funny smelling breath. He did not take his insulin for the past 3 days. You suspect DKA. What is your initial assessment?
DKA/HHS Assessment
- ABC and mental status - tx accoringly
-
obtain lab work
- glucose, electrolytes, BUN/Cr, ABG, CBC, plasma osmolality, urinalysis, urine ketones
- Calculate Anion Gap
