Endocrine Emergencies Flashcards

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1
Q

endocrine emergencies

A
  • Group of potentially life threatening conditions that are frequently over looked
  • This results in delay in diagnosis and treatment
  • This further contributes to already high mortality rates
  • This discussion will highlight 5 of the most prevalent endocrine emergencies
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2
Q

most prevalent edocrine emergencies

A
  • Thyroid Storm
  • Myxedema Coma - critical hyperthyroidism
  • Diabetic Ketoacidosis
  • Hyperosmolar Hyperglycemic State
  • Adrenal Crisis
  • Hyperosmolar and diabetic ketoacidosis are both types of hyperglycemia
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3
Q

thyroid storm

A
  • Hyperthyroidism or thyrotoxicosis refers to disorders that result from overproduction and release of hormone from the thyroid gland.
  • This refers to any cause of excessive thyroid hormone.
  • Malignant thyrotoxicosis or thyroid storm represents an extreme manifestation with resultant end-organ dysfunction.
  • Grave’s disease (autoimmune hyperthyroidism is the most common cause of this)
  • Thyrotoxicosis = overproduction or release of thyroid hormone. - hyperthy and thyrotox are the more benign types of too much thy
  • End organ disease: this is where we see changes in the heart, etc.
  • Graves disease is also MCC of hyperthyroidism
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4
Q

thyroid storm description

A
  • Malignant or critical thyrotoxicosis or thyroid storm is a life threatening medical emergency in which excessive concentrations of thyroid hormone produce organ dysfunction.
  • It occurs in <10% of the patients hospitalized for hyperthyroidism.
  • If untreated, there is an 80-90% mortality rate.
  • Even with treatment the mortality rated exceeds 20%.
  • Early recognition and management is critical.
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5
Q

thyroid storm incidence

A
  • Occurs in both men and women of any age
  • More common in teenage or young adult woman
  • Maybe initial manifestation of a thyroid condition
  • Often precipitated by surgery, trauma, iodine ingestion or d/c of antithyroid medications
  • Definitely from a thyroid perspective, women are more likely, but men still get them
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6
Q

clinical manifestations of thyroid storm

A
  • Marked hypermetabolism results in multiorgan dysfunction.
    • Thermoregulatory dysfunction: high fever, warm moist skin, diaphoresis
    • Neurologic manifestations: mental status change, seizure, coma, hyperreflexia, lid lag
    • Cardiovascular dysregulation: atrial fibrillation, tachycardia, hypertension, CHF
    • Respiratory distress: dyspnea, tachypnea
    • Gastrointestinal Dysfunction: diarrhea, abdominal pain, nausea vomiting
  • They feel hot and they are hot because they are constantly burning calories
  • HYPERREFLEXIA
  • Lid lag: people have the whites of their eye showing all the way around their iris
  • Not necessarily diarrhea but they have VERY frequent bowel movements
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7
Q

thyroid storm physical

A
  • Eyes: Stare due to upper eyelid retraction and eyelid lag (both due sympathetic over-activity).
    • Grave’s ophthalmopathy (periorbital edema, proptosis) is an autoimmune mediated inflammation and edema of extraocular muscles and intra-orbital connective tissue.
  • Neck: Smooth, diffusely and symmetrical goiter. No palpable nodularity. Typically NTTP, may have bruit over a large vascular gland
  • Cardiac: sinus tachycardia. Heart failure and arrhythmia (atrial fibrillation) more common in adults. High cardiac output produces bounding pulse, widened pulse pressure.
  • Skin: Warm (cutaneous vasodilation) and moist (diaphoresis) Grave’s dermatopathology (bilateral non-pitting edema with associated thickening and induration of the skin) Typically seen over the ankles and feet. Rare in children
  • Neuro: Altered mental status, hand tremor, agitation, psychosis, hyperreflexia
  • Not everyone who has graves has a goiter
  • Diffusely enlarged, smooth and symmetric – this is VERY indicative of Graves
  • Paper test – will help someone tell if they have a hand tremor
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8
Q

differential diagnosis for thyroid storm

A
  • Endocrine: pheochromotcytoma
  • Sepsis
  • CNS infection
  • Anticholinergic or adrenergic intoxication
  • Acute psychiatric illness: Anxiety, panic attack
  • Medication withdrawal: cocaine opiates
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9
Q

biochemical abnormalities of thyroid storm

A
  • TSH <0.01 with elevated Free T4 and T3 (because of increased T4 to T3 conversion the T3 elevation is typically more dramatic)
  • Hypercalcemia (From osteoclast mediated bone remodeling)
  • Elevated Alk phos (caused by bone remodeling)
  • Hyperglycemia (secondary to enhanced glycogenolysis and increased catecholamines)
  • Adrenal insufficiency (especially among Grave’s disease patients should be evaluated prior to the initiation of treatment)
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10
Q

treatment of thyroid storm

A
  • Supportive Care to minimize secondary effects of organ failure
  • Respiratory and hemodynamic support and treatment of hyperthermia
    • Antipyretics can be given but salicylates (eg. Aspirin) should be avoided as they are associated with displacement of thyroid hormone binding with TBG
  • Identify and treat precipitating event if warranted
  • You don’t want to give anything that will increase the amount of free hormone
  • T3 is the more active hormone and T4 is the hormone more abundantly produced
  • We want the conversion of T4 to T3 and block production of T4 and T3
  • Most Critical (Thionamide) Block the release and effects of circulating thyroid hormone and inhibit peripheral conversion of T4 to T3.
    • Propylthiouracil is preferred as it blocks the production and the peripheral conversion
      • Loading dose 600-1000mg and 1200mg/d divided into dose Q4-5 hours
    • Methimazole alternative but does not block T4 to T3 conversion
      • Beta blockers can improve tachycardia and hypertension
  • propranolol IV 1mg Q 10-15min
  • Iodine therapy blocks the release of prestored hormone and decreases iodide transport and oxidation in follicular cells.
  • Lugol solution can be given to stop thyroid hormone release.
    • Thionamide therapy must be instituted first, and these drugs only given at least 1 h later.
    • Lugol solution can be given three to four times to a total of 30–40 drops/day. Initial treatment may start with 8–10 drops. Lugol solution provides 8 mg iodide/drop.
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11
Q

myxedema coma

A
  • Uncommon presentation of Severe hypothyroidism
  • Mortality rates exceeds 60%
  • Better termed critical hypothyroidism as myxedema and coma are not diagnostic criteria or common at presentation
  • Very rare because its easy to test for
  • This would happen in pts in a care facility and the pt has some problem (i.e. stroke or heart attack) and they go to the hospital and the friend brings all the meds but doesn’t think about thyroid meds
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12
Q

myxedema coma incidence

A
  • Occurs most often in patients with long standing, pre existing hypothyroidism
  • Hypothyroidism is 4 times more common in women than men and 80% of these cases occur in women.
  • Almost always age > 60
  • 300 cases reported in literature
  • Most cases are during winter
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13
Q

clinical manifestations of myxedema coma

A
  • Can be precipitated by infections especially pneumonia or cardiac events or cerebral infarction
  • Findings are similar to hypothyroidism but are more profound
    • Hypothermia
    • Hypotension
    • Bradycardia
    • Mental status depression
    • May result in centrally mediated hypoventilation and hypercapnic respiratory failure
    • Myxedema is generalized skin and soft tissue swelling, periorbital edema, ptosis, macroglossia and cool, dry skin.
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14
Q

biochemical abnormalities of myxedema coma

A
  • Clinical diagnosis confirmed with TFTs but do not wait for results to initiate treatment
  • The degree of hypothyroidism does not distinguish hypothyroidism from myxedema coma the distinction is based on clinical findings
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15
Q

treatment of myxedema coma

A
  • Rapid replacement of thyroid hormone
    • IV bolus of 300-500mcg followed by 50-100mcg daily depending on age and weight
    • All patients need to be monitored continuously for hypertension and cardiac ischemia (Most common cause of death in these patients)
  • Treatment of precipitating causes
  • General supportive measures
    • Ventilator support
    • Passive external rewarming
    • Correction of underlying electrolyte abnormalities
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16
Q

diabetic ketoacidosis

A
  • Potentially fatal acute metabolic complications of diabetes mellitus
  • Triad
    • Hyperglycemia
    • Ketonemia
    • Metabolic acidosis
  • Potentially fatal!!
  • This triad is not always correct!
  • Typically associated with Type 1 diabetes
    • Can occur in Type 2 diabetes during periods of infection, trauma or CV emergencies
  • More common in young people and in females
  • Maybe presenting manifestation of diabetes
  • Can be precipitated by many clinical situations
    • Most commonly inadequate dosing of insulin and infection
    • Pancreatitis
    • CV disorder
    • Drug use ( steroids, diuretics, SGLT2s)
  • Results from severe alteration in carbohydrate, protein and lipid metabolism
    • Consequence of severe cell starvation and death due to a relative or absolute insulin deficiency needed to transport glucose into the cells
    • This causes increased gluconeogenesis and glycogenolysis and decreases use of glucose by the muscle, liver and fat
    • Insulin deficiency promotes lipolysis this provides a substrate for ketone bodies
    • Decreased clearance of ketone bodies leads to ketonemia and results in anion gap (metabolic acidosis)
17
Q

incidence of diabetic ketoacidosis

A
  • Typically associated with Type 1 diabetes
    • Can occur in Type 2 diabetes during periods of infection, trauma or CV emergencies
  • More common in young people and in females
  • Maybe presenting manifestation of diabetes
  • Can be precipitated by many clinical situations
    • Most commonly inadequate dosing of insulin and infection
    • Pancreatitis
    • CV disorder
    • Drug use ( steroids, diuretics, SGLT2s)
18
Q

clinical manifestation of diabetic ketoacidosis

A
  • Polyuria, polydipsia, polyphagia and weakness
  • Glucosuria can lead to profound intravascular volume depletion
    • Manifested by dry mucous membranes, flattened neck veins, tachycardia, hypotension and orthostasis
  • Nausea and vomiting occur in 80% of individuals
  • Patients often have a fruity odor to breath due to elevated serum acetone levels
  • Tachypnea is a compensatory response to metabolic acidosis
    • Can develop Kussmaul respirations (rhythmic, gasping. deep respirations with normal or reduced frequency
19
Q

diagnosis of DKA

A
  • This relies on prompt clinical recognition of the features
  • Initial evaluate should focus on identifying metabolic derangements and recognize possible causative factors
  • Hyperosmolarity from both Intravascular volume depletion and hyperglycemia is common
    • Diagnosis is confirmed by identifying serum ketones associated with a widened anion gap, metabolic acidosis. Hyperglycemia is almost always seen but is not required for the diagnosis (think SGLT2)
  • Most patients have elevation in BUN and creatinine reflecting a reduced GFR induced by hypovolemia.
  • Hyponatremia results from osmotic diuresis
  • Initial serum potassium is typically normal or elevated because of the extracellular migration of potassium in response to acidosis.
  • Potassium is generally in deficit and levels will fall during treatment as insulin therapy drives potassium into cells. If serum potassium is not monitored and replaced as needed, life-threatening hypokalemia may develop.
  • One big problem in DKA is recognizing the potassium deficit and treating it properly
20
Q

treatment of DKA

A
  • Focus on normalization of glucose and electrolytes, restore intravascular volume and resolve the metabolic acidosis (closure of the ion gap)
  • Hyperglycemia should be initially treated with a continuous infusion of intravenous insulin
    • Initial IV bolus of regular at 0.1u/kg followed by continuous infusion at rate of 0.1u/kg/hr is standard therapy.
    • Manage drip until anion gap closes
    • Measure glucose hourly if his becomes normal or low in the presence of persistently widening gap IV dextrose should be given and IV insulin dose reduced but not stopped.
    • A rise in insulin causes phosphate to move to the intracellular compartment, thus hypophosphatemia must be watched for with treatment.
  • Electrolyte abnormalities including potassium, magnesium and phosphorus should be expected and replaced
  • Serum electrolytes should be measured and replaced every 2-4 hours initially
  • Initial fluid therapy is directed toward IV volume expansion.
  • Patients with DKA can require up to 6 liters to adequately replace intracellular volume.
  • Caution must be taken during fluid repletion as rapid reduction in plasma osmolality can precipitate cerebral edema.
  • Isotinic saline is the initial resuscitative fluid of choice
  • Rapid infusion is required for patients who are in shock
  • If patient is hemodynamically stable isotonic saline can be given at a rate of 15-20ml/kg/hr for the first several hours.
  • Once serum glucose is below 200-250mg/dl the fluids should be changed to half NS with dextrose given at a rate sufficient to replace the free water loss induced by the osmotic diuresis
  • Normalization of the anion gap should be followed and reflects correction of the ketoacidosis
  • Once the gap normalizes conversion to long acting insulin and short acting insulin can be done with close monitoring because premature d/c can result in reemergence of the anion gap.
21
Q

DKA summary

A
  • This is a commonly encountered life threatening endocrine emergency
  • Aggressive treatment and close monitoring are essential to decrease mortality
  • Mortality from DKA may results from numerous causes including
    • Cerebral edema
    • Intravascular volume depletion
    • Failure to recognize and replace electrolyte abnormalities
22
Q

Hyperosmolar Hyperglycemic State

A
  • Occurs in elderly patients with Type 2 diabetes
  • Similar to DKA except that insulin deficiency is less profound. Less ketosis so abdominal symptoms are less likely and patients less motivated to seek medical care.
  • Impaired thirst mechanism exacerbates tendency towards HHS, these patients are more dehydrated than those with DKA and have higher BUN and creatinine.
23
Q

Symptoms of HHS

A
  • Due to hyperglycemia patients have polyuria, polydipsia, blurred vision and weight loss if prolonged.
  • Weakness, lethargy, malaise and headache.
  • Less nausea, vomiting and abdominal pain. Probably due to lack of ketotic or acidotic state.
  • Focal neurological signs (hemisensory deficits, hemiparesis, aphasia) mimic CVA.
24
Q

Treatment of HHS

A
  • Airway management is the top priority. Patients maybe comatose consider ET intubation
  • Rapid and aggressive intravascular volume replacement is always indicated as the first line of therapy for patients with HHS.
    • Isotonic sodium chloride solution is the fluid of choice for initial treatment because sodium and water must be replaced in these severely dehydrated patients.
  • Although many patients with HHS respond to fluids alone, IV insulin in dosages similar to those used in diabetic ketoacidosis (DKA) can facilitate correction of hyperglycemia.
  • All patients diagnosed with HHS require hospitalization and virtually all require ICU admission
25
Q

Adrenal crisis

A
  • Acute adrenal insufficiency (Adrenal Crisis) is an extreme life-threatening manifestation of adrenal insufficiency.
  • It occurs secondary to interruption of normal or hyper functioning adrenal or pituitary gland or sudden interruption of adrenal replacement therapy
26
Q

Adrenal insufficiency (3 categories)

A
  • Chronic primary adrenal insufficiency (Addison’s)
    • Autoimmune destruction of the adrenal cortex
  • Chronic Secondary adrenal insufficiency
    • Insufficient ACTH: commonly due to exogenous glucocorticoid therapy but could be pituitary insufficiency
  • Adrenal crisis
    • Can occur in patients with adrenal hemorrhage, pituitary apoplexy or secondary to stress or abrupt withdrawal of chronic steroid use or stress in the presence of untreated primary insufficiency
      • Causes could be adrenal hemorrhage due to meningococcus or necrosis or thrombosis pituitary dysfunction from postpartum pituitary necrosis (Sheehan) or macroadenoma that leads to this
27
Q

Adrenal crisis: clinical manifestations

A
  • Hypotension or shock
  • Anorexia
  • Weakness
  • Nausea / vomiting
  • Abdominal pain
  • Lethargy
  • Confusion
  • Coma
  • If someone is in an accident or has a problem, they need their stress dose of hormones immediately! They need to wear medical alert bracelets
28
Q

Adrenal crisis diagnosis

A
  • Immediate therapeutic intervention is required
    • Often have hyponatremia and hyperkalemia
    • Empiric steroids should be given until lab results are available
    • In a patient who is medically unstable, serum cortisol, ACTH, aldosterone and DHEA-S and renin should be drawn before hydrocortisone administration.
      • A high cortisol >20mg/dl can exclude diagnosis
      • A low cortisol of <5 done early in the am or in a state of stress strongly supports the diagnosis
      • A high ACTH is consistent with primary adrenal insufficiency while a low or normal ACTH is consistent with secondary or tertiary adrenal insufficiency
      • Cortrosyn stim test can be confirmed once the patient is stable
29
Q

Cotrosyn Stim test for adrenal insufficiency

A
  • Draw baseline serum cortisol and ACTH levels
  • Inject 250 mcg cosyntropin (ACTH) IV or IM
  • Draw cortisol level at 30 and 60 minutes
  • Rise in cortisol > 18ug/dl within 60 min is a normal result
  • Rise in cortisol <18 ug/dl is an abnormal response
  • An elevated baseline ACTH level suggests primary adrenal failure
30
Q

Adrenal crisis treatment

A
  • Once diagnostic labs have been obtained immediate treatment should begin
    • IV fluids, steroid replacement and reversal of electrolyte abnormalities.
    • Normal saline is IV fluid of choice
    • Stress dose steroid 100mg IV push of h/c followed by 150-300mg/d infusion for 2-3 days
    • Mineralocorticoid fludrocortisone should be administered 0.1mg/d
    • Steroid therapy can be tapered over 1-2 days and then converted to oral maintenance dose
    • Usual replacement hydrocortisone 25-40mg/d divided
  • You need fludricortisone in people with primary adrenal insufficiency
  • We treat everyone with hydrocortisone because it fits more the diurnal pattern
  • The latest the bedtime dose, the better people feel when they wake up in the morning.
  • Sodium – chloride + bicarb = anion gap à this is how you close the gap!!