Endo 38 Endocrine Emergencies
Calcium: 45% is protein –bound, of that 70% is bound to albumin, other 55% is free
 When you order Ca level know if it is free or total
Alkalosis: ↑ protein binding so ↓ free Ca, hyperventilation  symptomatic hypocalcemia d/t alkalosis
Acidosis: ↓ protein binding so ↑ free Ca
Acid-base status really effects Ca levels
Ionized Ca: best to ask for DIRECT measurement, can calculate level based on albumin level, change serum Ca by
0.8 for each 1 mg/dl change in serum albumin
Hypercalcemic crisis: serum Ca >14 mg/dl associated w/ acute s/s
 S/S: volume depletion, metabolic encephalopathy, cardiac arrhythmias, shortened QT, BBB, bradycardia,
cardiac arrest, N/V, constipation, AMS, coma
 Etiology: Inpatients: usually maliganancy e.g. metastatic lung or breast CA
o Outpatients: Hyperparathyroidism, Granulomatous ds, Hyperthyroidism, meds
 Eval: Total Ca (know acid-base status), Ionized Ca, PTH, 25(OH)D and 1,25(OH)D levels
 Cycle: ↑ urinary Ca loss  nephrogenic diabetes insipidus and volume depletion, ↓ in GFR, then more
severe hypercalcemia d/t ↑ Ca resorption
 Tx: aggressive IV hydration (NS 2-4 L/day), cautious use of loop diuretics after hydration – don’t use
Thiazides! Be sure not to cause dehydration
o Calcitonin: 4-8 IU/kg IM or IV q 12 hrs to inhibit osteoclasts and ↓ reabsorption
o Bisphosphonates: Pamindronate 30-90 mg IV over 24 hrs, impairs osteoclasts
o Glucocorticoids: Hydrocortisone 200-300 mg/24 hrs, if Vit D toxicity, sarcoid, granulomatous ds,
adrenal insufficiency, and some malignancies
o Dialysis if can’t lower Ca
o Note: don’t remember doses
Hypocalcemic Emergencies: d/t hypomagnesemia, hypoparathyroidism, renal ds, liver ds, pancreatitis
 Nervous system manifestations: numbness, paresthesias, seizures
 Chvostek’s (tap facial nerve  twitching) and Trousseau’s (hyperflexion of wrist, extension of metatarsal
jt) signs are abnormal
 Cardiac: arrhythmias, hyper or hypotension, CHF, prolonged QT
 Hypomagnesemia seen in poor diets and homeless, can impair PTH action and release
 Tx: Try to confirm w/ ionized Ca level, ck magnesium level, obtain PTH and Vit D levels, IV Ca infusion
followed by infusion of .3-2.0 mg elemental Ca/kg/hr, replete magnesium, begin oral Ca, replete Vit D if
necessary
o Watch closely for vitamin toxicity
Thyroid Storm: extreme, life-threatening hyperthyroidism, uncommon, mortality rate of 50%
 Typically in known hyperthyroid pt w/ infection, trauma, general anesthesia & surgery, partuition, acute
illness, RAI Rx, iodinated contrast administration
 Can occur spontaneously
 S/S of hyperthyroidism: fever, organ system decompensation, tachycardia, arrhythmias, CHF, N/V,
diarrhea, abd pain, profound wt loss, agitation, tremulousness, psychosis, obtundation
 Dx: ↑ serum T4 or T3 in presence of compatible clinical picture, TSH low/undetectable

Tx: ↓ level of circulating hormone and block catecholamines: beta blockers , prevent synthesis of new
hormones w/ antithyroid PTU, prevent the synthesis and release of stored hormone from the gland
(SSKI)
 Hyperthyroidism and Atrial Fib: high risk for embolization from intermittent a. fib/conversion to normal
rhythm, initiate anticoagulation, do NOT attempt to medically or electrically cardiovert until adequately
anticoagulated and thyroid levels are normal
 Supportive therapy: hydration, fluid and electrolytes, cooling blanket, ID and tx underlying problem,
hydrocortisone or dexamethasone to ↓ T4 to T3 conversion
Myxedema coma: profound reduction of circulating thyroid hormone w/ depression of the resp center,
reduction of cardiac output and cerebral hypoxia, mortality rate 50%
 Symptoms: lethargy, weakness, cold intolerance, and dry skin
 Signs: bradycardia, hypothermia, depressed mental status/coma, delayed DTRs, periorbital edema, dry
yellow skin,
 Setting: thyroid/ pituitary failure, stopping thyroid hormone therapy, prev thyroid irradiation/sx
 Precipitants: CNS depression by narcotics/analgesics, exposure to low temps, acute medical
illness/stress, trauma, surgery
 Objective Findings: Low free T4, low T3, high TSH, sinus bradycardia, low voltage EKG, pericardial or
pleural effusion, hyponatremia, macrocytic anemia, ↑ cholesterol, ↑ cpkd/t muscle damage, ↑
BUN/CR, check cortisol level
 Tx: general support: tx hypothermia, hypotn, hyponatremia, hypoglycemia, CO2 retention w/ resp
support, fluids, give levothyroxine, can give exogenous T3 but is rare
o Further tx: IV hydrocortisone, ventilator if needed, tx hyponatremia w/ fluids, tx hypothermia,
find and tx precip cause
Diabetic Ketoacidosis: Mortality rate of 5-15%, more common in young pts & women
 Incidence of 4.6 per 1000 diabetics
 Cost in US may exceed $1 billion per year
 Pathogenesis: ineffective insulin action or lack of insulin, w/ concomitant elevations of counterregulatory hormones to insulin e.g. epi, cortisol, glucagon, and GH
 Metabolic changes: accumulation of ketone acids, acetoacetate and beta hydroxybutyrate from
augmented lipolysis/ fa oxidation and ↓ ketone utilization, ↑ serum acetone, marked ↑ BS
 Sequence: ↑ lipolysis in adipose tissue  ↑ fatty acid delivery to liver, stimulation of beta oxidative
pathways & augmented ketone prod  inadequate ketone metabolism by muscles
 Ketone acids present in blood ratio 3:1 favoring beta hydroxybutyrate
 Acetoacetic acid is first ketone formed then reduced to betahydroxybutarate
 Acetone is formed by the decarboxylation of acetoacetate
 Acetone may be detected as fruity odor on pts breath
 Acidosis: Direct measurement of beta-hydroxybutyrate is preferred
o Nitroprusside tablets or sticks detect acetoacetate and acetone only
 Clinically: metabolic acidosis d/t hyperketonemia
o Hyperosmolarity d/t hyperglycemia and water loss
o Dehydration d/t osmotic dieresis, vomiting
 Consequences: Osmotic dieresis w/ water and salt losses, vomiting w/ further losses, fluid/electrolyte
imbalances

Precipitating factors: new onset DM usually Type 1, omission or inadequate use of insulin, ↑ insuling
requirements d/t infection, trauma, inflammation, misc event like CVA or MI
 Dx and eval: hyperglycemia BS>250 mg/dl, low bicarb d/t large amts of acids present, ↑ anion gap (Na –
Cl – CO2  >10-15, low arterial pH w/ ketonemia
o Consider eval: cbc, lytes, urinalysis, urine cultures, blood cultures, EKG
 Sx on presentation: N/V, deep labored breathing, depressed mental fx or coma
 PE: dehydrated, fruity odor on breath, hypotensive, tachycardic, may have abd pain
 Volume depletion: ave fluid loss is 3-6 L, aim of therapy is to replace extracellular fluid volume w/o
inducing cerebral edema d/t too rapid ↓ of plasma osmolality
 Tx: aggressive hydration, .45% NS once hypotn resolved/ HR <100, add 5% dextrose once BS <250, base
treatment on pt, not everyone tx the same
 Insulin therapy: lowers serum glucose by ↓ hepatic glucose production, diminishes ketone prod by ↓
lipolysis and glucagon secretion, may augment ketone utilization
o Standard conc: regular insulin 100 units in 100 ml NS via infusion pump
 Insulin: Initial bolus followed by low dose infusion, maintain BS btw 100-200 mg/dl
o SC insulin reserved for mild DKA pts
 Potassium: initially normal or high d/t shift in K from intracellular to extracellular fluid, body K stores
become depleted, can’t replace too fast bc have renal failure and can’t clear it
 Bicarb therapy: reserve for pH < 7.0: oxidation of ketone acids when insulin given  bicarb
o Rapid ↑ may cause ↓ CNS pH and worsening mental status and ↓ K
o Alkalinization shifts theO2 dissociation curve to L, limiting tissue O2 delivery
o Give to pts w/ pH <7.0, ↓ cardiac contractility, vasodilation  impaired tissue perfusion, or pts
w/ life threatening hyperkalemia
 Phosphate: fall in serum phosphate during DKA tx is acute and self limiting, usually no adverse effects
but replacement may be indicated in pts w/ cardiac dysfx, hemolytic anemia, or resp depression, or <1.0
mg/dl
 Monitoring in ICU: hourly glucose, electrolytes every 1-4 hrs, monitor renal fx, PO4, intake/output, EKG
 Other considerations: pregnancy test, magnesium, HbA1C, troponin, urine and blood cultures, amylase,
drug screen, lactic acid, TSH
 If really sick: DVT prophylaxis w/ levenox, heparin, compression stockings, stress ulcer prophylaxis,
home meds
 Complications: Cerebral edema, ARDS, hyperchloremic acidosis, manage underlying problem such as
sepsis, MI, shock, etc.
 When to transition to SC insulin: after acidosis is resolved and anion gap <12 or bicarb > 18, venous pH >
7.3, pt should be able to eat
Nonketotic Hyperosmolar Coma/ Hyperglycemic/ Hyperosmolar nonketotic syndrome (HHNS)
 Pathophysiology: hyperosmolarity from osmotic dieresis
 Precipitating factors: old age, dementia, debilitation, dehydration, new onset DM, acute illnessinfection, CVA, MI, GI bleed, Meds: diuretics, phenytoin, steroids, beta blockers
 Symptoms: polyuria, polydipsia, dizziness, lethargy, weakness
 Signs: orthostasis, tachycardia, cool skin, neuro impairment
 Lab findings: blood glucose > 1000 mg/dl, no ketosis, or minimal as insulin is present, measured or
calculated osmolality above 340 mOsm/L


Hyponatremia: may be pseudohyponatremia d/t hyperglycemia, if Na >120 may be correctable
Tx: NS @ 50-500 cc/hr, insulin therapy drip or SC, K, Mg, PO4 repletion, monitor renal fx, main thing is
hydration and some insulin
 Complications: vascular events, thromboses, stroke, MI, mortality up to 50%
Hypoglycemia: pts taking precose must give lactose to ↑ BS, not glucose bc it won’t be absorbed, if pt unable to
swallow give glucagon IV or SC, or start glucose infusion
Acute Adrenal Insufficiency: usually in undx or tx Addison’s ds pt exposed to stress, infection, trauma, surgery,
dehydration, etc.
Addison’s ds: Adrenal insufficiency caused by autoimmune destruction of adrenal glands, seen in isolation or in
conjunction w hypothyroidism or other autoimmune hormone deficiency
 S/S: weakness, lethargy, wt loss, fever, anorexia, N/V, abd pain, flank pain, tachycardia, orthostatic
hypotn, shock
o Long standing  hyperpigmentation d/t high levels of ACTH, vitiligo, black freckles/scars
 Labs: hyponatremia, hyperkalemia, acidosis, hypoglycemia, lymphocytosis and eosinophilia
o Obtain STAT cortisol and ACTH levels or cortrosyn stimulation test (synthetic ACTH)
 Adrenal atrophy/autoimmune 80%, adrenal infiltration by TB, histo, malignancy, amyloidosis, sepsis, or
hemochromatosis, chronic glucocorticoid use/injections, congenital adrenal hyperplasia, pituitary or
hypothalamic insufficiency
 Bilateral adrenal hemorrhage: sepsis, anticoagulant, post CABG, SLE, burns, toxemia, severe infections,
MI, CHF, thrombocytopenia
 Tx: hydrocortisone bolus followed by infusion, volume repletion,
Pheochromocytoma crisis: tumors derived from chromaffin cells in adrenal medulla or sympatheic ganglia,
release catecholamines into the circulation
 Crisis: dramatic and sustained release of catecholamines often triggered by event
 Do not want to biopsy the mass bc could  catecholamine release
 Presentation: extreme HTN, diaphoresis, tachycardia, HA, mental obtundation, cardiovascular
complications, noncardiogenic pulmonary edema, acute renal failure
 Tx: IV phentolamine, esmolol IV to conrol tachyarrhythmias, prep pt for surgery
 Preop management: long-acting alpha blockers, beta blockers to control tachycardia after alpha block
established, stress doses of steroids, volume repletion
Pituitary Apoplexy: sudden expansion of pituitary d/t hemorrhage or necrosis into a tumor
 60% of tumors are prolactinomas, many are endocrinologically silent, more easy to dx in women
 Sx: loss of pituitary hormone fx, sever HA, opthalmoplegia, subarachnoid irriation, visual impairment,
blindness, ↓ LOC, 3rd, 4th, or 6th cranial nerve palsy
 Tx: Stat CT/MRI, careful monitoring, IV steroids, urgent pituitary evacuation may be needed,