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
hyperosmolar hyperglycemic state labs
Severe hyperglycemia >500
Plasma osmolarity >320 (very dehydrated)
Relative insulin deficiency (but not enough to cause DKA)
No ketones
hyperosmolar hyperglycemic state management
Fluid + electrolyte replacement
IV insulin, transition to SQ
Treat underlying problem
Thyrotoxicosis definition
excessive amount of circulating thyroid hormone.
not synonymous with hyperthyroidism, includes exogenous
Hyperthyroidism presentation
Fever Palpitations Diarrhea Hypervigilant, agitate Prominent eyes Tremor Hyperreflexia Prominent, tender thyroid Confusion
Hyperthyroidism diagnostics
Low TSH, high FT3, high FT3
EKG→ irregularly irregular rhythm + tachycardia→ Atrial fibrillation with rapid ventricular response +/- rate related ST depression
Pharmacologic management of hyperthyroidism/thryoid storm
Methimazole→ decrease thyroid hormone synthesis→ long half life, low hepatotoxicity, restores euthyroidism more quickly→ preferred for severe hyperthyroidism
PTU→ decrease thyroid hormone synthesis, blocks conversion of T4→ T3→ more effective, preferred for thyroid storm
Thyroid storm vs myxedma croma: mortality
Storm: 10-30%
Coma: 30-40%
Weird things that can trigger thyroid storm
Acute iodine load
Post-partum
How to diagnose thyroid storm
Low TSH, high FT3, high FT3
Diagnostic criteria: severe + life threatening symptoms→ hyperpyrexia, cardiovascular dysfunction, AMS
Supportive care for thyroid storm
ICU admission → ABCs
Cooling measures→ Antipyretic, cooling blankets
Appropriate IV fluid resuscitation, Electrolyte replacement, Nutritional support
Thyroid specific therapy for thyroid storm goals
Prevent thyroid hormone release and decrease peripheral action of circulating thyroid hormone
Reduce heart rate, Support the circulation
Treat the precipitating condition→ same meds as thyrotoxicosis except higher doses more frequently
Adjunctive treatments for thyroid storm which are given simultaneously
Glucocorticoids → hydrocortisone→ reduce T4→ T3 conversion, promote vasomotor stability, +/- treat relative adrenal insufficiency
Bile acid sequestrants→ cholestyramine→ decrease enterohepatic circulation of thyroid hormones
When does a thyroid storm patient need a thryoidectomy?
allergy or contraindication to thioamides or refractory to tx
When does a thyroid storm patient need a thyroidectomy?
allergy or contraindication to thioamides or refractory to tx
Pretibial myxedema
skin manifestations of autoimmune thyroid disease (Grave’s)
Weird things that can precipitate myxedema coma
MI
Cold exposure
Opioids/sedative drugs
Presentation of myxedema coma
Lethargic, weak, sleeping more than usual Slowed speech, delayed response Hypothermia CNS depression/Coma Hypotension Bradycardia Hypoglycemia Hypoventilation Rapid or insidious onset Elderly women at risk Myxedema
Hypothermia
CNS depression/Coma
Hallmarks of myxedema coma
nonpitting edema with abnormal deposits of mucin in skin and other tissues→ puffiness, thickened nose, swollen lips,
myxedema
High index of suspicion for myxedema coma
Hypothyroidism \+ AMS \+ hypothermia \+ hyperventilation \+ hypotension
Myxedema coma labs
Hyporeflexia, muscle strength weakness
Low T3/T4
TSH→ high or low
Usually high. low→ hypothyroidism is secondary to hypothalamic or pituitary dysfunction
EKG→ bradycardia, flattening or inversion of T waves, +/- conduction abnormalities
ABG→ hypoxemia with hypercarbia if hypoventilating
CBC→ normal
CMP→ +/- hypoglycemia, hyponatremia
CT head→ (-) unless trauma was precipitating event
CXR→ normal unless pericardial effusion or pneumonia were precipitating events
Myxedema coma management
ABCs
T4 +/- T3
Glucocorticoids – hydrocortisone→ given until
adrenal insufficiency is ruled out
(both simultaneously common)
IV fluids (isotonic)
Correction of any electrolyte imbalances→ may correct with thyroid hormone alone
Rewarming blankets
Find the precipitating cause and treat
Recovery is slow
T3 for myxedema coma
Controversial more rapid but can cause MI or arrhythmia→ start with lower doses, give with T4
Lack of cortisol is
adrenal insufficiency
life threatening
Primary adrenal insufficiency
Addison’s Disease
Adrenal gland is damaged/not functioning
and it cannot produce glucocorticoids or
mineralocorticoids
Secondary adrenal insufficiency
Defect of the pituitary gland inhibiting proper release of ACTH
1. Occur in conjunction
with other pituitary hormone deficiencies
(panhypopituitarism)
2. Isolated ACTH deficiencies are rare (typically caused by an autoimmune condition)
Tertiarty adrenal insufficiency
Suppression of hypothalamic-pituitary-adrenal function
Abrupt withdrawal of chronic administration of high doses of glucocorticoids (Most common)
Mineralocorticoid secretion→ normal→ depends on the
renin-angiotensin system
Ex: COPD and chronic prednisone use
Acute adrenal crisis
Primary adrenal insufficiency
Acute exacerbation of chronic insufficiency.
Trigger: sepsis, surgical stress
Caused by: adrenal hemorrhage
adrenal infarction, anticoagulation
complications, or congenital abnormalities
Acute adrenal crisis
Fever, Abdominal pain, N/V
Intermittent confusion
Weight loss
Profound hypotension
Waterhouse-Friderichsen Syndrome
Adrenal infarction due to meningococcemia→ fever, AMS, purpura
Diagnosis of acute adrenal crisis is based off of
Mild tachycardia
distinguish from other forms of shock
Unexplained shock + responsive to vasopressor and volume replacement
Management of acute adrenal crisis
ABCs
IV fluids, Correct electrolytes→ monitor closely
Hydrocortisone→ in any patient with any suspicion ASAP
100 mg IV q 6 hrs.
Mineralocorticoid
0.1 mg po qd
(less important in acute stages of disease)
Bacterial etiology suspected (sepsis) → blood cultures and empiric abx
