1
Q
Review of anatomy of the thyroid?
A
- 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
2
Q
Innervation of thyroid?
A
- 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
- innervated the intrinsic muscles of larynx
- inferior to this, it “wanders” (hence name vagus) into the thoracic and abdominal viscera, innervating them with autonomic motor and sensory nerve fibers
3
Q
Physiology of thyroid gland?? What is the HPA axis for the thyroid? Hormones prodcued?
Critical component in thyroid hormones?
A
- 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
- Factors that decrease TSH are
- 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
- hypothalamus synthesizes thyrotropin-releasing hormone (TRH), which regulates thyroid stimulating hormone (TSH) secretion by the anterior pituitary gland
- 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
4
Q
Lab evaluation of thyroid function?
A
- 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
5
Q
Preop thryoid lab screening?
A
- 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
6
Q
Common causes of hypothyroidism?
A
- 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
7
Q
Symptoms of hypothyroidism?
Severe symptoms?
TREATMENT?
A
- 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
- heart rate, myocardial contractility, and cardiac output decrease (decreased SV and HR)
TREATMENT:
- Levothyroxine (T4) is mainstay treatment
- ~1 week half-life
- If needed, IV dosing is at ½ oral dose
8
Q
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?
A
- 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
- Imbalance of alpha/ beta activity with alpha predominating
- 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
9
Q
Physiologic implications of hypothyroidism under anesthesia?
Airway, sedation, GI concerns??
Maintenance of anesthesia?
A
- 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
10
Q
Anesthesia concerns with hypothyroid pt relating to fluid replacement?
VA administration?
Intraoperative hypotension treatment?
A
- 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
11
Q
What are some common intraoperative complications in hypothryoid patient?
A
- 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
12
Q
Complications of SEVERE hypothyroidism and anesthesia?
A
- 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
- IV dosing of thyroid supplementation will be needed
- 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
13
Q
What is myxedema coma? Symptoms?
A
- 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
14
Q
Severe goiter airway management?
A
- 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
15
Q
Causes, sx hyperthyroidism?
A
- 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
16
Q
Hyperthyroidism med treatment?
A
- 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
17
Q
Additional hyperthyroid treatments/sx?
A
- 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
- Subtotal thyroidectomy corrects thyrotoxicosis in >95% of patients
18
Q
What is thyroid storm? sx? tx?
A
- 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
19
Q
Preop thyroid airway considerations?
A
- 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
20
Q
When might we delay an elective case in patient with hyperthyroidism?
How do we handle hyperthyroidism in emergency cases?
A
- 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:
- IV β-blocker
- ipodate- Oral cholecystographic agent that also affects thyroid hormone. inhibits peripheral T4—> T3 conversion and thyroidal hormone release
- PTU
- No IV preparation of PTU- give via NG or rectally
- Glucocorticoids (dexamethasone 2 mg IV every 6 hours)
- decrease hormone release
- reduce the peripheral conversion of T4 to T3
21
Q
Goals of anesthesia in hyperthyroidism?
A
- 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!
22
Q
Thyroidectomy anesthesia?
A
- 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)
23
Q
What is IONM with EMG?
A
- 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
24
Q
What is NIM tube?
A
- 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!
25
Thyroidectomy emergence?
* 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
26
Postop managmenet of thyroidectomy/
* 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)
27
Role of parathyroid hormone?
* 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*
28
What is hypoparathyroidism? Symptoms?
* 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
29
Hypocalcemia treatment?
* **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*
30
What is hyperparathyroidism? Cuases? comorbidities in pt?
* **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*
31
Hypercalcemia and hyperparathyroidism?
* **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)**
32
Hypercalcemia tx in hyperparathyroidism?
* 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
33
Parathyroidectomy?
* 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 i**s 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**
34
Parathyroidectomy in ESRD?
* 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
35
Pituitary tumors? Most common? effects seen? less common pituitary tumors?
* 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
36
Preop consideations for pituitary tumor? for hyposecreting, hypersecreting?
* 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
37
Anesthesia consideraitons for trans-sphenoidal pituitary anesthesia?
* 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 routinel**y **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*
38
Acromegaly? Cuase? s/s? treatment?
* 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 intoleranc**e & 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
39
Biggest concerns for anesthesia in acromegaly patient?
**_Anticipate a challenging airway!_**
* Distorted facial anatomy may make masking difficult
* **Enlargement of the tongu**e 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 stimulato**r (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**
40
What is DI? Neurogenic DI? Nephrogenic? Diagnosis?
* 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)
41
Symptoms of DI? Treatment?
* 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*
42
What is SIADH? Causes? symptoms?
* 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)
43
SIADH diagnosis/ treatment?
* **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 c**orrected 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 ****_sl_**ow _(0.5 mEq/L/h)_** until Na concentration is **125 mEq/L**, then proceed **more slowly** to prevent **_central pontine myelinolysis & permanent CNS damage_**
44
Anesthesia concerns with SIADH?
* 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
CO-EXIST Test 4!
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