Endocrine

Question 1

Review of anatomy of the thyroid?

Answer 1

• Two lobes joined by an isthmus; affixed to anterior and lateral trachea
  
  • isthmus below cricoid cartilage
• Pair of parathyroid glands are on posterior aspect of each lobe
  
  • difficult to preserve parathyroid during thyroidectomy
• RLN and external motor branch of the SLN are in close proximity
• Histology:
  
  • numerous follicles filled with proteinaceous colloid
  • thyroglobulin: iodinated glycoprotein; substrate for thyroid hormone synthesis
  • parafollicular C cells that produce calcitonin
    
    • ​increase bone calcium, decreases serum Ca and decreases phosphorus levels
    • Calcitonin opposes PTH
• innervated by adrenergic and cholinergic nervous systems
• 2 pairs vessels consitute major arterial blood supply (sometimes pt can haveartery in front of cricothyroid membrane causing massive hemorrhage during cric):
  
  • ​superior thyroid artery, arising from external carotid artery
  • inferior thyroid artery

Question 2

Innervation of thyroid?

Answer 2

• Adrenergic and cholinergic innervation to the thyroid
• Vagus X orginates in medulla oblongata and ramifies into superior and inferior vagal ganglia in the neck
• 1st major branch is pharyngeal plexus of the vagus
• next branch is reccurent laryngeal nerve
  
  • innervated the intrinsic muscles of larynx
    
    • responsible for phonation and glottis opening
• inferior to this, it “wanders” (hence name vagus) into the thoracic and abdominal viscera, innervating them with autonomic motor and sensory nerve fibers

Question 3

Physiology of thyroid gland?? What is the HPA axis for the thyroid? Hormones prodcued?

Critical component in thyroid hormones?

Answer 3

• Hypothalamic-pituitary axis
  
  • hypothalamus synthesizes thyrotropin-releasing hormone (TRH), which regulates thyroid stimulating hormone (TSH) secretion by the anterior pituitary gland
    
    • Factors that decrease TSH are
      
      • glucocorticoids
      • somatostatin
      • dopamine
  • TSH stimulates the synthesis and secretion of triiodothyronine (T3) and thyroxine (T4) by the thyroid gland
    
    • thyroid gland can store 2-3 months supply of thyroid hormones in thyroglobulin pool
  • T3 and T4 provide a negative feedback loop through their suppression of TRH
• The T4:T3 ratio of secreted hormones from the thyroid is ~10:1 (sources vary; several say 20% is T3)
  
  • T4 is produced entirely by the thyroid gland
  • 80% of T3 is produced by conversion of T4 to T3 (primarily by the liver)
• T3 has a short half-life (~1 day) and is the primary biologically active form of thyroid hormone
• Iodine is a critical component of thyroid hormones
  
  • A high serum iodine concentration will transiently suppress the release of thyroid hormones (Wolf-Chaikoff effect)
• Thyroid hormones influence growtha nd maturation of tissue, enchance tissue function, stimulate protein synthesis and carb and lipid metabolism
  
  • ​thyroid hormone increases myocardial contractility directly<<– how T3 can have exaggerated hemodynamic effects in hyperthyroidism
  • decreases** **SVR** via **direct** **vasodilation
  • increases** intravascular **volume

Question 4

Lab evaluation of thyroid function?

Answer 4

• TSH assay: best test of thyroid hormone action at the cellular level
• Small changes in TSH reflect large changes in TSH secretion (don’t need to memorize exact numbers thyroid hormones, but know what it means when TSH low vs high)
  
  • TSH level below 0.03 milliunits/L with elevated T3 and T4 is diagnostic of overt hyperthyroidism
  • TSH level of 5.0–10 milliunits/L (mod high) with normal levels of T3 and FT4 is diagnostic of subclinical hypothyroidism
  • TSH level higher than 20 milliunits/L (may be as high as 200 or even 400 milliunits/L) with reduced levels of T3 and T4 is diagnostic of overt hypothyroidism

Question 5

Preop thryoid lab screening?

Answer 5

• Thyroid function assays
  
  • TSH
  • Total T3 and T4 assays measure free (biologically active) and protein-bound (biologically inactive) hormone concentrations
• Levels not always reflective of risk: ‘‘euthyroid sick syndrome’’; subclinical hypothyroidism (abnormal TSH levels with normal levels of free T3 and free T4); alterations in protein binding; and administration of medications such as dopamine, amiodarone, and glucocorticoids—> suppress thyroid
• Little evidence to support routine screening of asymptomatic patients

Question 6

Common causes of hypothyroidism?

Answer 6

• Common disease affecting 0.5- 1% of US population (females>males)

95%: primary hypothyroidism-low thyroid hormone levels with normal or increased TSH

Causes:

• Chronic autoimmune thyroiditis (Hashimoto thyroiditis)<— main cause!
• Radioactive iodine or surgery
• Other iatrogenic causes including drug induced: lithium, amiodarone, iron, cholestyramine, immune checkpoint inhibitors (new cancer tx’s- melanoma, etc)
• Euthyroid sick syndrome in critically ill patients
  
  • stress/surgery induced
  • had enough TSH production to get normal T3/T4 but not enough under additional stress
  • Can be stress/ surgery induced; no tx necessary
• Dietary iodine deficiency is more common in developing nations
• Cretinism is a devastating consequence of congenital hypothyroidism

Question 7

Symptoms of hypothyroidism?

Severe symptoms?

TREATMENT?

Answer 7

• Insidious onset (means that it’s a slow onset and progressive)
  
  • ​**no overt symptoms
• Sx:
  
  • lethargy, fatigue, depression, headaches, dulled intellect, slow speech
  • anorexia
  • hoarse voice,
  • cold intolerance
  • large tongue, periorbital, peripheral edema, dry skin, brittle hair, coarse facial features
  • SIADH, hyponatremia
  • GI dysfunction–> slow, adynamic ileus may occur
• Severe cases:
  
  • heart rate, myocardial contractility, and cardiac output decrease (decreased SV and HR)
    
    • baroreceptor** function can also be **impaired
    • hypercholesterolemia** and **hypertriglyceridemia**–> **CAD
  • ECG changes (flattened T, low amplitude P & QRS, ventricular arrhythmias), pericardial effusions, increased peripheral vascular resistance, blood volume reduced–> pale, cool skin
  • muscle weakness results in hypoventilation and an impaired response to hypoxia and hypercapnia

TREATMENT:

• Levothyroxine (T4) is mainstay treatment
  
  • ~1 week half-life
  • If needed, IV dosing is at ½ oral dose

Question 8

How are thyroid hormons altereed with anesthetics?

Beta receptor function in hypothyroid patient?

How does the thyroid pt respond to hypercarbia and hypoxemia?

Adh secretion?

Answer 8

• Effect of general anesthetics on thyroid hormones: T3 levels decrease and remain low for at least 24 hours
• Plasma catecholamine levels are generally WNL
• beta-adrenergic receptor function is depressed
  
  • Imbalance of alpha/ beta activity with alpha predominating
    
    • Result is depressed cardiac function (inotropy and chronotropy) and increased SVR
• Depressed responses to hypercarbia and hypoxemia
• ADH secretion and/or decreased GFR lead to hyponatremia and fluid retention- intravascular space is contracted due to alpha dominance and patient may still have intravascular volume deficit

Question 9

Physiologic implications of hypothyroidism under anesthesia?

Airway, sedation, GI concerns??

Maintenance of anesthesia?

Answer 9

• Mild to moderate hypothyroidism do not have significant increase in perioperative risk
• Risk/ problems increase with severe hypothyroidism
• Caution with preoperative sedation: increased sensitivity to BZD and narcotics
• Potential airway issues: swollen oral cavity, edematous vocal cords, or goiter
• Delayed gastric emptying increases aspiration risk
• Maintenance: Controlled ventilation is recommended as these patients are at risk for hypoventilation
• Actively warm: propensity for hypothermia

Question 10

Anesthesia concerns with hypothyroid pt relating to fluid replacement?

VA administration?

Intraoperative hypotension treatment?

Answer 10

• Intraoperative fluid replacement
  
  • Consider dextrose containing solution; prone to hypoglycemia
  • Prone to hyponatremia: impaired ability of the renal tubules to excrete free water
• Increased sensitivity to anesthetics though MAC largely unchanged
  
  • Especially sensitive to myocardial depressant effects of volatile anesthetics
• Intraoperative hypotension: ephedrine, dopamine, or epinephrine
  
  • Pure α-adrenergic agonist (phenylephrine) not recommended <<- because already have alpha dominance since beta receptor function depressed
  • Refractory hypotension: supplemental steroid administration

Question 11

What are some common intraoperative complications in hypothryoid patient?

Answer 11

• Common intraoperative problems:
  
  • anemia (25%–50% of patients)
  • platelet dysfunction
  • impaired coagulation factors (especially factor VIII),
  • hyponatremia
  • hypoglycemia
• Monitor for worsening hypothyroidism postoperatively
  
  • Sx: delirium, prolonged ileus, infection without fever, and myxedema coma
• Close attention to airway patency in the postoperative period
  
  • reports of airway obstruction in hypothyroid patients

Question 12

Complications of SEVERE hypothyroidism and anesthesia?

Answer 12

• Severe hypothyroidism: depressed mental status, pericardial effusion, and heart failure in need of urgent/ emergency surgery<<<- not going to take severe hypothyroid pt to elective sx, only emergent
  
  • IV dosing of thyroid supplementation will be needed
    
    • IV l-thyroxine takes 10–12 days to yield a peak basal metabolic rate
    • IV triiodothyronine is effective in 6 hours, Peak basal metabolic rate seen in 36–72 hours
• Consider likelihood of adrenal insufficiency
  
  • Thyroid replacement can precipitate adrenal crisis
  • Administer glucocorticoids concurrently
• Consider phosphodiesterase inhibitors (milrinone) to treat impaired contractility
  
  • MOA independent of β receptors

Question 13

What is myxedema coma? Symptoms?

Answer 13

• Rare, most of often occurs post-op- precipitated by infection, trauma, cold exposure, sedatives, analgesics and various emds
• Sx:
  
  • delirium or unconsciousness
  • hypoventilation
  • hypothermia (80% of patients)
  • bradycardia
  • hypotension
  • severe dilutional hyponatremia
• High mortality (>50%)
• Initial IV bolus of levothyroxine 200 to 500 mcg should be given followed by 50 to 100 mcg/day
• Do not aggressively warm the patient
  
  • ​if you rewarm too quickly, drop SVR , already have poor cardiac function–> code
• Aggressive volume resuscitation with dextrose and normal saline should be instituted
• IV glucocorticoids also be given
• Resolution of symptoms, if properly treated, should be seen within 24 hours.
  
  • HR, BP, T improve 24 hours after admin IV thyroxine/tiiodothyronine
  • Euthyroid state in 3-5 days

Question 14

Severe goiter airway management?

Answer 14

• Swelling of the thyroid gland
  
  • compensatory hypertrophy/ hyperplasia from a reduction in thyroid hormone output
• Evaluate CT neck pre-op
• Minimal to no sedation pre-op
• Awake intubation with FOB with armored tube with fiberoptic bronch
  
  • Pre-op red flag: dyspnea in the upright or supine position (high risk of airway obstruction with GA)
  • Can decompensate with loss of spontaneous ventilation
• Potential underlying tracheomalacia and a collapsible airway
  
  • FOB following resection to evaluate for tracheomalacia
  • Very cautious with extubation; rigid bronchoscope available -need full airway reflexes on wake up
• Substernal extension of mass may lead to airway collapse, CV compromise & SVC syndrome
  
  • CPB may need to be on standby<– need perfusionist anytime substernal extension is suspected/known
  • ECHO in upright and supine position can indicate the degree of cardiac compression
• best is to get local and perhaps shrink tumor preop

Question 15

Causes, sx hyperthyroidism?

Answer 15

• Most common cause: Graves disease (toxic diffuse goiter)
  
  • autoimmune disorder with stimulation of the TSH receptor by autoreactive TSH receptor antibodies
  • other common causes: toxic multinodular goiter; toxic adenoma
• Sx:
  
  • tachycardia
  • atrial fibrillation/palpitations
  • fever,
  • tremor
  • goiter
  • ophthalmopathy- at risk for eye injury intraop
  • gi sx: n/v/ diarrhea
• Subclinical hyperthyroidism may have no sx’s and is occ. seen in elderly
• T3 and T4 have direct inotropic and chronotropic effects on the heart
• Thyroid hormones have a direct effect on vascular smooth muscle decreasing SVR and MAP
  
  • Activates R-A-A-S enhancing sodium reabsorption and increasing circulating blood volume
  • increases cardiac output by 50% to 300%
    
    • ​worry about clinical effects in pt who has CAD concurrently

Question 16

Hyperthyroidism med treatment?

Answer 16

• 1st line treatment: antithyroid drugs, either methimazole or propylthiouracil (PTU).
  
  • PTU also inhibits the peripheral conversion of T4 to T3
  • 6–8 weeks for effective treatment
• Iodide in high concentrations inhibits release of hormones: immediate action but short-lived; reserved for impending surgery or thyroid storm (Wolff-Chakoff effect)
• β-Adrenergic antagonists relieve adrenergic signs and symptoms
  
  • Propranolol also inhibits peripheral conversion of T4 to T3
• Hyperthyroidism during pregnancy: tx w/ low dosages of antithyroid drugs
  
  • Drugs do cross the placenta and can cause fetal hypothyroidism
  • Iodine therapy can cause fetal goiter and hypothyroidism
  • Thyroid storm occurring in pregnancy is managed in the same way as in nonpregnant patients

Question 17

Additional hyperthyroid treatments/sx?

Answer 17

• Ablative therapy with radioactive iodine 131 or surgery recommended if medical management fails
  
  • Also recommended in toxic multinodular goiter or a toxic adenoma
  • Remission rate is 80%–98%
  • 40%–70% of treated patients become hypothyroid within 10 years
• Surgery: prompt control of disease
  
  • Subtotal thyroidectomy corrects thyrotoxicosis in >95% of patients
    
    • will then need exogenous thyroid hormone

Question 18

What is thyroid storm? sx? tx?

Answer 18

• High mortality (10-75%); Stoelting says 20%
• Most common perioperative cause: infection/ sepsis
  
  • Usually occurs post-op after emergency surgery in inadequately treated hyperthyroid patient (either intraop or 48 hours p surgery)
  • the most common cause in periop period is infection (sepsis) get Blood ctx, treat infection ASAP
• Non-specific sx: fever (up to 106 F), tachycardia, anxiety/ delirium
  
  • Ddx: MH, NMS, Pheochromocytoma
• Tx:
  
  • PTU
  • β-blockers (goal HR <90)
    
    • May see AF with RVR: tx β-blockers
  • antipyretics
    
    • tylenol preferred
    • asa can increase concentration of free T3/T4 by reducing thyroid hormone binding to thyroglobulins
  • active cooling measures
  • correct dehydration with volume resuscitation with dextrose supplementation
    
    • Will deplete glycogen stores very quickly with increased metabolism
  • steroids (to decrease peripheral T4 -> T3 conversion)
• • Recovery is usually ~1 week

Question 19

Preop thyroid airway considerations?

Answer 19

• Assess the airway of patients with a goiter- large goiter can weigh several hundred grams (normal thyroid only 20-25 grams) and can obstruct the airway
  
  • Evaluate chest x-ray or CT chest pre-op; see previous slide
• Toxic multinodular goiter : may present with extreme thyroid enlargement
  
  • Sx: dysphagia, globus sensation, and possibly inspiratory stridor from tracheal compression
  • Mass may extend into the thoracic inlet behind the sternum
  • Severe cases: SVC obstruction syndrome may also be present
    
    • CPB on standby
    • risk for CV compression when supine–> code on induction

Question 20

When might we delay an elective case in patient with hyperthyroidism?

How do we handle hyperthyroidism in emergency cases?

Answer 20

• Elective cases may be delayed to allow time for euthyroid state
  
  • May take up to 6-8 weeks for medical management to be optimized
• Emergency cases:
  
  1. IV β-blocker
  2. ipodate- Oral cholecystographic agent that also affects thyroid hormone. inhibits peripheral T4—> T3 conversion and thyroidal hormone release
  3. PTU
     
     • No IV preparation of PTU- give via NG or rectally
  4. Glucocorticoids (dexamethasone 2 mg IV every 6 hours)
     
     • decrease hormone release
     • reduce the peripheral conversion of T4 to T3

Question 21

Goals of anesthesia in hyperthyroidism?

Answer 21

• Pre-op: goal is euthyroid
  
  • HR <85 bpm; pre-op beta-blockers prn
  • Morning dose of anti-thyroid medicine and beta blocker should be taken
• Protect eyes: exophthalmos increases risk of injury
• No proven increased requirement for anesthetics
  
  • No specific volatile agent preferred; N2O is fine as well
  • Adequate depth extremely important to decrease SNS activation
  • SNS stimulants are to be avoided:
    
    • ketamine, pancuronium, atropine, ephedrine, epinephrine
  • Regional anesthesia may be preferred if possible
  • Opioids are safe
  • Reduced requirements for NDMR; titrate carefully; may have co-ex myasthenia gravis
• Hemodynamic monitoring during the procedure is paramount
• Phenylephrine over ephedrine​ (unlike hypothyroid- hypothryoid give epi/ephedrine over phenyl; hyperthyroid- give phenyl over ephedrine)
  
  • Avoid LA with Epi
  • Careful with admin of ephedrine, epi, NE and dopamine—> give in low doses to prevent exaggerated response!

Question 22

Thyroidectomy anesthesia?

Answer 22

• Pre-op and maintenance considerations per previous slides
• Supine; arms tucked (working IV’s; neo gtt prn)
• Airway considerations in goiter
• Potential for RLN injury
  
  • Consideration for IONM (intraoperative nerve monitoring) (see next slide)

Question 23

What is IONM with EMG?

Answer 23

• Intraoperative nerve monitoring with Electromyography
• Monitor recurrent laryngeal nerve function intraoperatively
  
  • EMG stimulating the vocalis muscle to determine RLN integrity; SLN may also be monitored (less frequent)
  • Surgeon must still visually identify and carefully dissect
• Goal: allow adequate depth of anesthesia while accomplishing neuromonitoring
  
  • The monitoring tech/ audiologist will likely communicate with you
• TIVA plus a short acting narcotic are effective for all IONM procedures
  
  • Also acceptable to use volatile anesthetics and N2O
• Avoid: NMB’s and local anesthetics
  
  • May intubate with Sch; some intubate with rocuronium but ensure full recovery before IONM starts

Question 24

What is NIM tube?

Answer 24

• how we monitor recurrent laryngeal nerve intraop
• Typically placed under direct visualization (most prefer VL); audiologist, surgeon, or NM tech will likely want to see placement
• Goal is to have exposed electrodes in contact with the patient’s vocal cords in order to generate an accurate electromyogram
• 7.0 Women; 8.0 for Men
  
  • Slightly larger tube than needed improves electrode contact
  • LTA is not recommended by manufacturer however some still use
• Anticipate neck extension following intubation and allow adequate depth to prevent coughing and movement of electrodes
  
  • tube can make pt cough and can move electrode and throw off nerve monitoring
  • need adequate depth of anesthesia to prevent coughing, because can’t use NMB!

Question 25

Thyroidectomy emergence?

Answer 25

• Awake extubation
  
  • Ensure adequate ventilation
• Very smooth emergence- must prevent coughing/ bucking–> hematoma
• Thyrotoxicosis does not resolve immediately (T4 7-8 day ½ life)
  
  • Anticipate use of beta-blockers in post-operative period

Question 26

Postop managmenet of thyroidectomy/

Answer 26

• 13% Morbidity following thyroid surgery
• RLN (recurrent) injury
  
  • Unilateral: hoarseness but no airway obstruction
  • Bilateral: airway obstruction; difficulty coughing and clearing secretions; may need trach
    
    • _​_assess patency on emergence–> if acute airway obstruction on emergenc–> b RLN injury and need to be reintubated
• SLN (superior) injury: weakening of voice; inability to create high tones (won’t affect ventialtion)
• Post-op hematoma with airway compromise
• Hypoparathyroidism- from inadvertant removal of parathryoids or injury to blood supply
  
  • Hypocalcemia occurs in the first 24–48 hours postoperatively
  • Sx:
    
    • Anxiety
    • circumoral numbness
    • tingling of the fingertips
    • muscle cramping, and positive Chvostek and Trousseau signs
  • Stridor; laryngospasm possible
  • Emergency tx:
    
    • IV calcium gluconate (1 g, 10 mL of a 10% solution) or
    • calcium chloride (1 g, 10 mL of a 10% solution)

Question 27

Role of parathyroid hormone?

Answer 27

• Parathyroid hormone (PTH) regulates the extracellular calcium concentration through its actions on the bone, kidney, and intestine
• Extracellular calcium concentration is the major determinant of PTH secretion
• Single adenoma is most common cause of hyperparathyroidism

Question 28

What is hypoparathyroidism? Symptoms?

Answer 28

• Patients may develop hypoparathyroidism and hypocalcemia after thyroidectomy or removal of a parathyroid adenoma
• Ionized serum and urine calcium should be monitored
• Symptoms:
  
  • fatigue
  • depression
  • neuronal irritability
  • skeletal muscle spasms
  • tetany
  • +/-seizures
• Severe hypocalcemia:
  
  • prolonged QT interval and risk of Torsades des Pointes
  • impaired cardiac contractility and vascular tone;
  • decreased response to β-agonists
• Acute hypocalcemia: stridor, laryngeal spasm— even 24-48 hours later!
• Rare to see coagulopathy

Question 29

Hypocalcemia treatment?

Answer 29

• Tx: electrolyte replacement
  
  • Hypomagnesemia is managed with oral or IV magnesium.
  • Hyperphosphatemia is treated with phosphate-binding resins and possibly dialysis
• Severe symptomatic hypocalcemia :
  
  • 10–20 mL of 10% calcium gluconate or
  • 3–5 mL of 10% calcium chloride followed by a continuous infusion of calcium (1–2 mg/kg/h).
• Avoid respiratory alkalosis<— increases Ca binding, further decreasing Ca levels in blood.
• Be careful with citrate containing blood products–also binds Ca

Question 30

What is hyperparathyroidism? Cuases? comorbidities in pt?

Answer 30

• Primary hyperparathyroidism, a common cause of hypercalcemia, is most often associated with parathyroid adenomas
• Others: hyperplasia, malignancy (rare)
• Secondary hyperparathyroidism is common in ESRD
  
  • because elevated phosphate (can’t clear), low Ca, causing PTH to be secreted in excess
• Co-morbidities: htn, history of congestive heart failure, thromboembolic disease, stroke, or diabetes common
• hypercalcemia enhances digitalis toxicity

Question 31

Hypercalcemia and hyperparathyroidism?

Answer 31

• Symptoms:
  
  • May be asymptomatic (>50%)
  • Renal (kidney stones) and skeletal manifestations (bone demineralization, pathologic fractures)
    
    • Increased PTH causes increase in serum calcium, which is pulled from bones causing bone resorption
  • CNS (confusion, depression),
  • Neuromuscular (skeletal muscle weakness)
  • GI (anorexia, nausea, vomiting, constipation, peptic ulcer disease)
• Symptoms are more common at calcium levels above 11.5–12 mg/dL
• Leading causes of hypercalcemia- hyperparathyroidism and malignancy (up to 20% of all cancer patients; especially common with breast cancer)

Question 32

Hypercalcemia tx in hyperparathyroidism?

Answer 32

• Mild hypercalcemia (<12 mg/dL): hydration
• Moderate to severe hypercalcemia (13–15 mg/dL): IV NS infusion & furosemide (to promote a Na/Ca diuresis)
• Phosphate is also given to treat hypophosphatemia
• Other tx: Bisphosphonates (pamidronate, zolendronate), calcitonin, glucocorticoids, phosphates, mithramycin, plicamycin, and dialysis

Question 33

Parathyroidectomy?

Answer 33

• Surgical excision of the abnormal parathyroid tissue: treatment for adenoma
• Many place art-line for frequent lab draws (PTH)
• NMB: unpredictable secondary to hypercalcemia
  
  • antagonize effets of non-depolarizing muscle relaxants, making patients more resistanct to blockade
• Careful positioning is necessary to avoid bone injuries
• Postoperative complications are similar to thyroid surgery: RLN injury, hematoma, hypocalcemia
• Serum calcium drops within 24 hours postoperatively
  
  • Acute hypocalcemia: all normal parathyroid tissue damaged; give CaCl
• Hypophosphatemia and hypomagnesemia may also occur postoperatively

Question 34

Parathyroidectomy in ESRD?

Answer 34

• Hyperparathyroidism in renal failure is multi-factorial
• Parathyroidectomy: Improves renal osteodystrophy if medical management fails
  
  • Medical mgmt: low-phosphate diet, phosphate binders, adequate intake of calcium and vitamin D, and a high-Ca++, low-aluminum dialysis bath, calcimimetics
  • Calcimimetics (Cinacalcet) have made surgery less common- mimics Calcium at the PTH receptor
  • Surgery improves bone density, fracture risk, calcinosis, hemoglobin levels, and long-term survival

Question 35

Pituitary tumors? Most common? effects seen? less common pituitary tumors?

Answer 35

• Most common: non-secreting adenomas and prolactin secreting micro-adenomas
• Non-secreting adenomas tend to manifest with mass effects (headache, visual disturbance, hypopituitarism)
  
  • typically larger at the time of diagnosis
• prolactin-secreting microadenomas
  
  • usually women who present with secondary amenorrhea or galactorrhea
• hypopituitary presentation: dysfunction of the normal gland caused by compression by the tumor mass
• less common pituitary tumors:
  
  • growth hormone–secreting lesions: acromegaly
  • adrenocorticotropic hormone (ACTH)-secreting tumors: Cushing disease
  • very rare thyroid-stimulating hormone–secreting lesion: hyperthyroidism

Question 36

Preop consideations for pituitary tumor? for hyposecreting, hypersecreting?

Answer 36

• Endocrine status– is this a secreting tumor?
• Visual disturbances– document!
• Hyposecretion:
  
  • Decreased ACTH- Potential for hypoadrenal state: risk of Addisonian crisis due to stress of surgery
  • Hypocortisolism- Evaluate Na+: associated hyponatremia
• Hypersecretion:
  
  • ACTH secreting- Cushing’s disease: htn, diabetes, central obesity
  • GH secreting- Acromegaly and airway concerns

Question 37

Anesthesia consideraitons for trans-sphenoidal pituitary anesthesia?

Answer 37

• Very similar to an ENT/ sinus case
• Lumbar drain sometimes placed
• Bed often 180 degrees with arms tucked (IV x 2); HOB elevated (ensure adequate CPP); verify all connections (especially circuit)
• Airway: Oral RAE taped to left corner of mouth
• Blood loss modest unless cavernous sinus entered–> massive blood loss!!
• Anesthetic choice depends on if ICP elevated
• A-line
  
  • lots of local with epi used
• CO2 management- surgeon preference; do not routinely hyperventilate
  
  • hyperventilation may help pituitary to “Sag” for surgeon so they can visualize it better
• CSF leak post-op: high risk meningitis–> patch
• Emergence: throat pack out?; no bucking or coughing, SMOOTH wake up
  
  • throat pack helps catch draining blood
  • neuro assessment immediately in OR

Question 38

Acromegaly? Cuase? s/s? treatment?

Answer 38

• Acromegaly: excessive secretion of growth hormone
• Primary Cause: Adenoma in anterior pituitary
• Signs and Symptoms:
  
  • Mass effect:
    
    • ​Headache; papilledema
    • increased intracranial pressure
    • visual disturbances if optic chiasm compressed
  • Peripheral neuropathy from trapping of nerves by skeletal, connective, and soft tissue overgrowth
  • Glucose intolerance & perhaps DM (growth hormone has impact on CHO metabolism)
  • Increased risk of hypertension, ischemic heart disease, osteoarthritis, and osteoporosis
  • Increased lung volumes; ventilation/perfusion mismatching may be present
  • Thick and oily skin
  • Skeletal muscle weakness; fatigue
• Primary Treatment: Transsphenoidal surgical excision of pituitary adenomas

Question 39

Biggest concerns for anesthesia in acromegaly patient?

Answer 39

Anticipate a challenging airway!

• Distorted facial anatomy may make masking difficult
• Enlargement of the tongue and epiglottis predisposes to upper airway obstruction
• Tongue interferes with visualization during DL
• Overgrowth of the mandible (longer blade needed since longer distance)
  
  • have larger blade available!
• Glottic opening may be narrowed because of enlargement of the vocal cords
• Voice changes/ hoarseness may indicate RLN stretching or involvement of cricoarytenoid joints
• Potential for subglottic narrowing (have smaller size tubes than predicted for actual size)
• Nasal turbinate enlargement- may be unable to pass NPA or nasal ETT

Have multiple blade sizes and ETT sizes!!!

• Evaluate pre-op for dyspnea, hoarseness, or stridor as warnings for vocal cord involvement
• Monitor blood glucose closely (glucose intolerance)
• Use NDMR with caution and guided by nerve stimulator (pre-existing skeletal muscle weakness)
• Regional anesthesia technically difficult or unreliable due to musculoskeletal changes
• Very careful with radial arterial line- ½ of patients do not have adequate collateral ulnar arterial flow
• Thickened skin can make IV starts very difficult

Question 40

What is DI? Neurogenic DI? Nephrogenic? Diagnosis?

Answer 40

• ADH: increases permeability of cells lining the distal tubule and medullary collecting ducts of the kidney to promote water absorption
• Neurogenic DI: Decreased synthesis and release of vasopressin
  
  • Result of insult to pituitary from trauma, infiltrating lesions, or surgery
  • Will respond to DDAVP [1-deamino-8-d-arginine-vasopressin]
• Nephrogenic DI: Insensitivity of renal tubules to vasopressin
  
  • No response to DDAVP
• Dx: Polyuria with a rising serum osmolality
  
  • Low urine specific gravity
  • 24-hour urine collection for diagnosis (>50ml/kg UOP and Urine <300mOsm/L)

Question 41

Symptoms of DI? Treatment?

Answer 41

• Sx: Hypernatremia and hypovolemia
  
  • Polydipsia- high output of poorly concentrated urine;
  • altered mental status/seizures, fatigue
  • weakness
  • hemodynamic instability
• Desmopressin (DDAVP) is the treatment for neurogenic DI
  
  • During surgery an IV infusion of 100–200 m U/h along with an isotonic crystalloid is given
  • Frequent monitoring of serum Na and plasma osmolality
• Plan for fluid replacement: hourly maintenance fluids plus 2/3 of the previous hour’s urine output
• Anesthesia: closely monitor urine output; follow serum Na and plasma osmolality hourly
• If plasma osmolality exceeds 290 mOsm/L: use hypotonic fluid should be used for resuscitation and increase the vasopressin infusion (goal plasma osmolality is 290)
• Recall: vasopressin causes vasoconstriction of arteriolar beds
  
  • Increased risk myocardial ischemia

DI after pituitary sx usually appears within 24 hours and may last a few days to 6 months

Treatment nephrogenic DI include- chlorpropamide, clofibrate, and thiazide diuretic<– not much anesthesia implications

Question 42

What is SIADH? Causes? symptoms?

Answer 42

• Excess secretion of antidiuretic hormone
• Hyponatremia (Na < 135 mEq/L) is dilutional secondary to resorption of water by renal tubules
• Primary causes: ectopic production of vasopressin
  
  • Small cell lung carcinoma (50% develop SIADH) and carcinoid tumors
• Other causes:
  
  • other types of lung cancer, tumors of the CNS, head and neck, GI tract, GU tract, and ovary (all are also due to ectopic vasopressin)
  • CNS trauma & infections
  • Medications (chlorpropamide, clofibrate, thiazides, antineoplastic agents)
  • Hypothyroidism
  • Major surgery
• Most patients are asymptomatic
  
  • Sx: nausea, weakness, lethargy, confusion, depressed mental status, and seizures (primarliy neuro)

Question 43

SIADH diagnosis/ treatment?

Answer 43

• Rapidity of onset and degree of hyponatremia determine severity
  
  • Slowly developing (weeks to months) much better tolerated
• Dx:
  
  • ​hyponatremia <130 mEq/L
  • serum Osm <270 mOsm/L
  • normal or increased urine Na excretion (>20 mEq/L),
  • inappropriately normal or increased urine osmolality (hypertonic relative to plasma)
• SIADH is corrected gradually with oral fluid restriction and medication
• Severe hyponatremia (Na < 115 mEq/L) may require 3% hypertonic saline or normal saline plus furosemide
  
  • The rate of sodium correction should be slow (0.5 mEq/L/h) until Na concentration is 125 mEq/L, then proceed more slowly to prevent central pontine myelinolysis & permanent CNS damage

Question 44

Anesthesia concerns with SIADH?

Answer 44

• Careful fluid and electrolyte monitoring and replacement- may need CVP
• Fluid resuscitation is usually with NS
• Frequent measures of urine osmolality, plasma osmolality, and serum Na+ are necessary intraoperatively
• Anticipate low urine output
• May see delayed emergence or confusion @ emergence