L9: Endocrine Emergencies Flashcards
“Impaired counter regulatory axis” means
Hypoglycemia caused by lack of glucagon, epi, or cortisol
Major med that can cause hypoglycemia, especially with renal insufficiency
Sulfonylurea
Hypoglycemia=
BG <70/<54
No ketones
Hypoglycemia presentation
Tachycardia Diaphoresis Confusion/AMS Irritable Weak Blurred vision \+/-focal neurological exam (stroke like)
Management of asymptomatic hypoglycemia
Defensive actions→ repeat blood glucose, eat carbs, adjust treatment, don’t drive
Management of symptomatic hypoglycemia
15-20 g oral carbs→ 3-5 glucose tabs/hard candies, ½ cup of juice/soda → raise blood sugar without inducing hypoglycemia
Follow with Long acting carb to prevent recurrence
Management of
severe hypoglycemia with AMS
Swallowing unsafe→ SQ/IM glucagon .5-1.0 mg → regain consciousness within minutes→ N/V
25 g 50% dextrose IV→ followed by more infusion or eating
Management of hypoglycemia due to a sulfonyurea
ADMIT
sulfonylureas have a long half life
____ is the presenting sign of T1DM at diagnosis
DKA
don’t rule this out on a question if the pt has no history of T1DM
DKA labs
Low bicarb/ABG→ metabolic acidosis with anion gap
Ketones→ urine and serum
High blood glucose→ 350-500 (not diagnostic)
BUN/Cr→ elevated
Elevated WBC (stress→ demargination)
Low K+ (usually) → but can be elevated at presentation due to lack of insulin and hyperosmolality→ K+ outside of cells→ resolution of hyperglycemia→ rapid fall in K* → MONITOR
Falsely low Na+
Low chloride
Elevated serum osmolarity
+/- infection on UA/CXR
+/- EKG→ MI, electrolyte abnormalities, arrhythmias
+/- Head CT→ Stroke
Goals of managing DKA, in order of importance
Restore circulatory volume Correct serum osmolarity Clear serum ketones Correct electrolytes & anion gap Treat underlying causes Reduce blood glucose
DKA presentation
Abdominal pain, Vomiting Frequent urination Confusion, Tachycardia Signs of dehydration (turgor, dry, hypotension, shock) Fruity odor on breath Hyperventilation (kussmaul) 3 P’s→ polyuria, polydipsia, polyphagia Weight loss
Managing DKA
.9 NS IV→ 15-20 mL/kg lean body weight/hour
Max 50 mL/kg in first 4 hours
Monitor urine output→ >5-1 ml/kg/hr
Add dextrose when blood glucose drops to 200-250→ reverse ketogenesis
Replete K+, monitor
Replete sodium, phosphate (if severe)
Continuous IV insulin +/- Insulin IV bolus→ continue as long as anion gap is present even if glucose normalizes→ prevents liolysis
Bicarb + DKA (in general)
No bicarb→ reduces hyperventilatory drive→ increased pCO2→ uptake of CO2 by cells→ intracellular cerebral acidosis→ paradoxical fall in cerebral (CSF) pH→ neurological deterioration
Hypernatremia, hypokalemia, residual serum alkalosis
May slow rate of recovery of ketosis→ reversal of acidemia which was slowing organic acid generation
When is bicarb given for DKA
Significant hyperkalemia +/- pH <6.9 (without hyperkalemia)
lifesaving, lower serum potassium by pushing it into cells
How to correct falsely low Na+ in DKA
for every 100 of glucose >100, add 2 mEq/L to Na+
MUDPILES for causes of elevated anion gap metabolic acidosis
Methanol Uraemia→ renal failure Diabetic, alcoholic, or starvation ketoacidosis Paracetamol, propylene glycol, paregoric Inborn errors of metabolism, Iron, Ibuprofen, Isoniazid Lactic acid Ethylene glycol Salicylate (aspirin)
Older nursing home patient
think hyperosmolar hyperglycemic state
hyperosmolar hyperglycemic state pathophys
Hyperglycemia→ glycosuria→ dehydration→ hemoconcentration
hyperosmolar hyperglycemic state presentation
Insidious onset AMS (>DKA) Generalized and focal weakness Polydipsia, polyuria Dehydration
