Book 3, Case 5-Transphenoidal and Acromegaly

Question 1

With patients who have pituitary tumors, what concerns do you have overall?

Answer 1

potential for endocrinologic conditions like Cushings, panhypopituitarism, acromegaly, hyperthyroidism and diabetes insipidus. Procedure related issues like massive hemorrhage, air embolism, cranial nerve damage

Question 2

Pituitary tumor pt with headache, blurred vision and rhinorrhea-what are you concerned about?

Answer 2

These symptoms are consistent with parasellar extension of the pituitary tumor (at sella-causing headache),compressing the optic chiasm (blurred vision), and inferior
extension of the adenoma (rhinorrhea).

Question 3

How does a prolactinoma present:

Answer 3

amenorrhea, galactorrhea and infertility

Question 4

How does cushing’s present:

Answer 4

truncal obesity, abdominal striae, HTN and hyperglycemia

Question 5

GH tumor presentation:

Answer 5

acromegaly, HTN, insulin resistance, visceromegaly, osteoporosis, skeletal overgrowth

Question 6

Ant pituitary fxn:

Answer 6

synthesis, storage and growth of the 6 tropic hormones; adrenocorticotrophic hormone.
(ACTH), which stimulates the adrenal cortex secretion; 2) prolactin, which stimulates
the secretion of breast milk and inhibits ovulation; 3) human growth hormone,responsible for body growth; 4) thyroid-stimulating hormone (TSH), which stimulates
thyroid secretion and growth; 5) follicle-stimulating hormone (FSH), responsible for
ovarian follicle growth in females and spermatogenesis in males; and 6) luteinizing
hormone, which stimulates ovulation in females and testosterone secretion in males.

Question 7

Post pituitary fxn:

Answer 7

(1) antidiuretic hormone (ADH), which promotes water retention and regulates
plasma osmolarity, and (2) oxytocin, which causes uterine contraction and the
ejection of breast milk.

Question 8

Bromocriptine and Octreotide mechanism:

Answer 8

Bromocriptine is used to treat the excessive excretion of both
prolactin and growth hormone from functional pituitary tumors. It is a synthetic
dopamine-2 receptor agonist that inhibits the secretion of both growth hormone and
prolactin, bringing their levels down sufficiently to improve symptoms in many
patients. Since this patient is also being treated with Octreotide, a drug not often
utilized in the treatment of a functional prolactinoma, I suspect that he is receiving
these medications to treat acromegaly. Octreotide is a somatostatin analogue that
inhibits the release of growth hormone and may actually shrink the size of pituitary
tumors.

Question 9

Dx of acromegaly is made how?

Answer 9

The diagnosis of acromegaly is based on an initial clinical suspicion,
due to the presence of several characteristic manifestations, and confirmed by
biochemical testing.
The characteristic manifestations of acromegaly include skeletal
overgrowth (large body, hands, and feet; prognathism), soft tissue overgrowth (large
lips, tongue, epiglottis, and vocal cords), recurrent laryngeal nerve paralysis
(secondary to stretching caused by overgrowth of surrounding structures), peripheral
neuropathy (secondary to trapping caused by the overgrowth of surrounding tissue),
visceromegaly, glucose intolerance, osteoarthritis, osteoporosis, hyperhidrosis, and
skeletal muscle weakness. Biochemical tests used to confirm the diagnosis include
measurement of serum IGF-I (the most reliable test since it is less variable throughout
the day),

Question 10

What general anesthetic concerns would you have in someone with Acromegaly?

Answer 10

My primary concern in patients with acromegaly is the potential for
difficult airway management. Distorted facial anatomy (difficult mask fit),
enlargement of the tongue and epiglottis (predisposition to upper airway obstruction
& impaired visualization during laryngoscopy), overgrowth of the mandible
(prognathism), a narrowed glottis opening (may require smaller endotracheal tube),
enlarged nasal turbinates (may inhibit nasal passage of an airway), and recurrent
laryngeal nerve paralysis may all compromise airway management.
Other than the airway, my concerns would include an increased incidence of coronary
artery disease and the risks associated with hypertension, cardiomegaly, congestive
heart failure, obstructive sleep apnea (mask ventilation, postoperative apnea, and
inadequate pain control), diabetes mellitus, and peripheral neuropathy (positioning).

Question 11

Would you require an echo prior to starting a case (neuro case in the sitting position?)

Answer 11

Given the increased risk of venous air embolism during intracranial
procedures performed with the head above the level of the heart, I would prefer to
perform a bubble study with precordial echocardiography or transesophageal
echocardiography to rule out a patent foramen ovale, which would place him at risk
for paradoxical embolism to the coronary or cerebral circulations.

Question 12

Any neuro case-just do a ___

Answer 12

Foley!

Question 13

A line in acromegaly pts-where?

Answer 13

possibly femoral since pts withacromegaly have poor collateral blood flow to the hand, increasing the
risk of ischemia with partial or complete obstruction of the radial artery.

Question 14

Visual evoked potentials: when are they used? They are sensitive to what?

Answer 14

Visual evoked potentials (VEPs) are sometimes used to monitor the
integrity of the optic nerves when the surgeon believes they are at significant risk of
surgical trauma during tumor resection. Unfortunately, VEPs are extremely sensitive
to inhalational and intravenous anesthetics, making consistent monitoring very
difficult during general anesthesia. I would use balanced technique withnarcotics and a low concentration of volatile agent to minimize anesthetic
interference with VEP monitoring.

Question 15

Prior to induction, the surgeon injects the nasal mucosa with cocaine and the
patient suddenly loses consciousness. What do you think is going on? What
would you do?

Answer 15

Therefore, I would: (1) apply
cricoid pressure (risk of aspiration with GERD), (2) intubate the patient (to reduce the
risk of aspiration and control ventilation -7 avoiding hypoxia, hypercapnia, and
acidosis is very important in the setting oflocal anesthetic toxicity), (3) ventilate with
100% oxygen, ( 4) check the EKG and blood pressure, (5) call for a lipid emulsion kit,
and ( 6) administer vasoactive, inotropic and antiarrhythmics agents as indicated. If I
suspected local anesthetic toxicity, I would (7) administer a benzodiazepine (to avoid
seizure-induced patient injury and acidosis), (8) administer small doses of
succinylcholine to treat ongoing tonic-clonic movement (to minimize the hypoxia and
acidosis associated with muscle activity,) and (9) provide hemodynamic support as
required. If the signs and symptoms of local anesthetic toxicity appeared to be
rapidly progressing, the patient experienced prolonged seizure activity, or he
developed signs of cardiac toxicity (i.e. bradycardia, heart block, hypotension,
asystole, or ventricular arrhythmia), I would (10) initiate lipid emulsion therapy and
(11) alert the nearest facility with cardiopulmonary bypass capability.

Question 16

Treatment of LAST as per OpenAnesthesia:

What do you avoid in these pts?

Intralipid dosing

Answer 16

Stop local anesthetic
Check for a pulse-
CPR/ACLS if pulseless-SO CHECK A PULSE
Call for help and intralipid

WHILE THAT”S coming, I will intubate the patient and ventilate with 100% O2 to avoid hypoxia and hypercarbia, Check EKG, other vital signs and administer benzos

Once Intralipid arrives:
-TC pacing for bradycardic rhythms
Continue CPR for at least 60 min

Intralipid dosing:
Load 1.5ml/kg

Followed by infusion: 0.25 ml/kg/hr
Avoid Vasopressin, CCBs, Beta blockers and local anesthetics

Question 17

Which tubes do you need on hand during Acromegaly induction:

Answer 17

ensure the presence of emergency airway equipment,

including smaller ETTs in case there is subglottic stenosis. Have FOB in room!

Question 18

Don’t forget! When pt is in sitting position with open skull-and there is sudden hypotension-think of :
And then wdyd?

Answer 18

Venous air embolism!!!! Therefore, I would deliver 100% oxygen, verify proper endotracheal
tube placement, auscultate the chest, verify proper function of the arterial line,
evaluate the EKG, reduce my anesthetic agent, ask the surgeon about bleeding, look
at the surgical field, listen to the precordial Doppler, (or look at TEE) check the end-tidal C02, and look for hemoglobin in the urine.

Question 19

If pt in sitting position and ETCO2 decreases,Does this move venous air embolism to the top
of your list? ANd what would you do to make the intra-op diagnosis?

Answer 19

Since the patient is in the sitting position, venous air embolism (V AE)
is already at the top of my list. However, a decrease in end-tidal C02 is not
diagnostic for V AE. While the increased alveolar dead space and/or reduced cardiac
output that results from significant V AE does lead to a decrease in end-tidal C02, this
same decrease would be seen with any event that significantly reduced cardiac output.other clinical signs of V AE,
such as tachycardia, cardiac arrhythmias, hypoxia, and cyanosis. Therefore, to
determine if this clinical picture were secondary to V AE, I would listen for sporadic
roaring sounds from the precordial Doppler, auscultate the heart for the characteristic
“mill wheel” murmur (best heard through an esophageal stethoscope), attempt to
aspirate air through the central venous catheter, and/or consider transesophageal
echocardiography.

Question 20

So doppler is emitting sporatdic roaring sounds-wdyd? (basically a VAE has been diagnosed)

Answer 20

would
immediately ask the surgeon to flood the field with saline; discontinue nitrous oxide
(probably should be avoided in the first place) and deliver 100% oxygen; attempt to
aspirate entrained air through the central venous catheter (to remove air that may be
interfering with right-sided cardiac output); consider the application of direct jugular
venous compression to increase venous pressure at the surgical site, provide
cardiovascular support with fluid, vasoconstrictors, inotropes, and chest
compressions, as necessary; and treat bronchospasm with th-adrenergic agonists
(reflex bronchospasm may occur with the entry of air into the pulmonary artery)

Question 21

Why would someone use PEEP in VAE, and why should you not?

Answer 21

PEEP has been recommended to increase venous pressure at the surgical site .
However, the application of PEEP may not be optimal for several reasons: 1) the
potential for impaired systemic venous return in a patient with significant
cardiovascular dysfunction; 2) it is less effective than jugular venous compression
in increasing cerebral venous pressure when in the sitting position (where the
head is significantly higher than the heart); and 3) PEEP may reverse the normal
trans-atrial (left> right) pressure gradient, increasing the risk of paradoxical
embolism with an unrecognized patent foramen ovale.

Question 22

Can you turn pt to LLD during VAE?

Answer 22

You can, because it could move air into right atrium where it is more easily aspirated, but it wastes valuable treatment time and is difficult to achieve

Question 23

Plan to extubate pt with acromegaly, obesity, OSA and GERD?

Answer 23

Given these concerns and the fact
that his GERD increases his risk of aspiration during emergence, I would place the
patient in the semi-upright position, provide 100% oxygen, and extubate him only
after he was awake and demonstrating full neuromuscular block reversal (especially
with history of obstructive sleep apnea), adequate ventilation and oxygenation,
hemodynamic stability, and intact airway reflexes. If I were concerned about the
presence of CAD, I would have administered lidocaine prior to extubation to blunt a
potential sympathetic response to extubation .

Question 24

Would your plan for extubation change if the CSF space had been opened intra-
operatively?

Answer 24

Basically, if a pt needs to be awake for extubation, they need to be awake for extubation.

If the CSF space had been entered intraoperatively a smooth
emergence (avoiding coughing) is desirable to prevent the reopening of the CSF leak,
which would increase the risk of subsequent meningitis. Although coughing during
emergence may increase a CSF leak, I would plan to extubate this patient awake to
avoid airway obstruction, laryngospasm, aspiration, and hypoventilation. I would
attempt to prevent coughing by administering intravenous lidocaine just prior to
extubation.

Question 25

Pt has OSA and just had transphenoidal surgery-now they can’t get his sat above 90%-DDx?

Answer 25

**Don’t forget that too much narcotic is a DDx. This is concerning to me because this obese patient with obstructive
sleep apnea is at increased risk of post-operative airway obstruction and apnea,
especially with the use of narcotics for post-operative pain management. Other
potential causes or contributing factors include atelectasis (hypo ventilation of this
obese patient), pulmonary edema (secondary to congestive heart failure and/or air
entering the pulmonary artery during V AE), aspiration (leading to bronchospasm or
atelectasis ), inadequate reversal of neuromuscular blockade, hypo/hyperglycemia
(diabetic patient), electrolyte abnormalities, arrhythmia, myocardial infarction, or
stroke (paradoxical emboli, ischemia).

Question 26

How are you managing signifiant OSA pts post op? For how long would you monitor this pt for airway obstruction or hypoxemia after the last episode of airway obstruction/hypoxemia?

Answer 26

Postoperatively, I would maintain the patient in a seated or lateral
position (avoiding supine positioning) and provide supplemental oxygen until the
patient was able to maintain his baseline oxygen saturation on room air. Additionally, I would apply his home CP AP machine as soon
as possible; administer NSAIDs for analgesia with the goal of avoiding sedatives and
narcotics, if possible; and utilize continuous pulse-oximetry until his oxygen
saturation remained above 90% during sleep.
for at least 7 hours after the last episode of
airway obstruction or hypoxemia while breathing room air in a non-stimulating
environment.

Question 27

On the second postoperative day, the nurse reports over two liters of urine
output in the last hour. What do you think is the cause? (pt had neurosurgery)
What are you going to do?
What tests will you order? Can it develop intraop?

Answer 27

This patient’s postoperative polyuria could be due to central diabetes
insipidus (DI), mobilization of third-spaced fluid, diuretic use, or osmotic diuresis
from hyperglycemia. Therefore, I would review the fluids and medications
administered; rule out hyperglycemia; and further evaluate the patient for DI, a
condition that occurs in as many as 40% of patients following hypophysectomy (tests:
urine specific gravity, serum osmolality, serum/urine electrolytes). DI is
characterized by marked impairment in renal concentrating ability secondary to
decreased ADH secretion, and usually occurs 4-12 hours postoperatively (but may develop intraop

Question 28

When would you suspect DI?

Answer 28

This condition is suspect~d when a patient produces
copious amounts of urine despite rising serum sodium levels (increased serum
osmolality). Confirmed when hyperglycemia is ruled out and urine osmolality increases with the administration of exogenous ADH

Question 29

How can you tx pts wiht DI? (central)

Answer 29

1/2 normal saline

Question 30

4th post op day after transphenoidal surgery, pt gradually develops hypotension refractory to fluid and pressors-DDx? How to tx/

Answer 30

adrenal insufficiency secondary to panhypopituitarism or pituitary
apoplexy, a known complication of surgical hypophysectomy. This diagnosis could
be confirmed by identifying decreased cortisol and ACTH plasma concentrations, and
would require specific hormone replacement therapy, including glucocorticoids,
mineralocorticoids, and thyroid hormone.