Book 4, Case 7-UPP and OSA

Question 1

Diagnosis of OSA made how? what is hypopnea? Index of OSA? What anesthetic considerations do you have as far as-coexisting disease, choice of anesthetic, airway mgmt, admin of pain meds, extubation, post op pain control and discharge guidelines?

Answer 1

Sleep study with 5 or more events of apnea (no breathing for 10 seconds)and in conjunction with a decrease in arterial
oxygenation of greater than 4%. The apnea-hypopnea index, consisting of the total
number of apneas and hypopneas ( 50% reduction in airflow for greater than 10
seconds) per hour, is often used to classify the severity of the disease. Therefore, this
obese patient’s apnea-hypopnea index of 280 indicates severe obstructive sleep
apnea/hypopnea syndrome (severe:> 30; moderate: 16-30; mild: 5-15), which raises
the following anesthetic considerations: (1) the presence of coexisting disease (i.e.
hypertension, CAD, cardiac arrhythmias, pulmonary hypertension, right ventricular
failure); (2) the choice of anesthetic (regional is preferable, if possible); (3) airway
management (difficult intubation is experienced in 13-24% of obese patients with
OSAHS), (3) the administration of central nervous system depressants (extreme
sensitivity to these drugs may result in airway obstruction and apnea), ( 4)
maintenance of anesthesia (preferred: hydrophilic and short acting drugs), (5)
extubation (preferred: fully awake, semi-upright position, full reversal of
neuromuscular blockers, intact airway reflexes, and performed in a controlled and
monitored environment), (6) post-operative pain control (preferred: non-steroidal
anti-inflammatory drugs, regional analgesia, and minimal short-acting narcotics); and
(7) appropriate discharge criteria (ASA practice guidelines recommend monitoring
OSA patients for a median of 3 hours longer than non-OSA patients, and for at least 7
hours after the last episode of airway obstruction or hypoxemia. The adequacy of the
patient’s post-operative respiratory function should be evaluated with the patient
breathing room air in a non-stimulating environment).

Question 2

What is the difference between obstructive sleep apnea (OSA), obstructive sleep
hypopnea syndrome (OSH), obesity-hypoventilation Syndrome (OHS), and
Pickwickian syndrome?

Answer 2

OSA is defined as a complete cessation of airflow for more than 10
seconds, occurring five or more times per hour of sleep, despite continued respiratory
effort against a closed glottis, and associated with a > 4% decrease in Sp02. OSH
represents a milder form of the disease, diagnosed when a sleep study demonstrates a50% reduction in airflow for more than 10 seconds, occurring 15 or more times per
hour of sleep, and associated with a > 4% decrease in Sp02. OHS is a condition that
develops secondary to obesity and/or as a long-term consequence of OSA. It is
defined by the constellation of obesity (BMI > 30 kg/m2

), daytime arterial
hypercapnia (PaC02 > 45 mmHg), nocturnal hypoxia, and polycythemia, in the
absence of known causes ofhypoventilation (i.e. pulmonary disease). Pickwickian
syndrome is a severe form of OHS in which chronic hypoventilation leads to
pulmonary hypertension and right ventricular failure.

Question 3

Why would you not want to do a severe OSA patient at an outpatient ASC?

Answer 3

I would not. This patient would not be a good candidate for outpatient
surgery do to the significant risk of postoperative airway obstruction and apnea
associated with performing airway surgery requiring general anesthesia for a patient
with sever obstructive sleep apnea who is likely to require significant post-operative
opioids.
Factors that I would consider when determining whether outpatient care is
appropriate for a patient with OSA include, severity of sleep apnea, anatomical and
physiologic abnormalities, coexisting diseases, nature of the surgery, type of

anesthesia being performed, need for postoperative opioids, adequacy of post-
discharge observation, and the capabilities of the outpatient center.

Question 4

How do you evaluate anyone’s cardiac status?

Answer 4

Given this patient’s history of obesity, sedentary lifestyle, dyspnea on
exertion, uncontrolled hypertension, and OSA, I would consider him to have
significant risk factors for coronary artery disease and congestive heart failure. I
would attempt to illicit further symptoms or cardiac risk factors through a focused
history (i.e. unstable and/or severe angina, previous cardiac testing, decompensated
heart failure, arrhythmias, myocardial infarction, and functional capacity) and
physical exam (i.e. jugular venous distension, hepatomegaly, peripheral edema, and
pulmonary edema). If I were unable to adequately assess his cardiac risk, I would
consider additional testing, such as a chest radiograph, ECG, ABG, PFTs, and/or an
echocardiogram. A stress echocardiogram, in particular, would provide valuable
information regarding myocardial ischemia, systolic function, and diastolic filling.

Question 5

What cardiac abnormalities are you expecting to see in pts with OSA?

Answer 5

Chronic arterial hypoxemia and hypercarbia, and an associated
increase in serum catecholamine levels, leads to: (1) pulmonary hypertension,
secondary to increased sympathetic tone and hypoxic pulmonary vasoconstriction; (2)
nocturnal and diurnal systemic hypertension, secondary to increased sympathetic.tone; (3) cardiac arrhythmias; (4) polycythemia; and (5) increased platelet
aggregability. Pulmonary hypertension eventually leads to right ventricular
hypertrophy and failure ( cor pulmonale ), while untreated systemic hypertension leads
to left ventricular hypertrophy and failure. Cardiac arrhythmias may lead to angina,
myocardial ischemia, and myocardial infarction in these patients who are already at
increased risk of coronary artery disease. Finally, polycythemia and increased
platelet aggregability make these patients more susceptible to thrombotic and embolic
cardiac and cerebrovascular events.

Question 6

How are you evaluating airway of UPPP pts?

Answer 6

I would begin with a history and review of his medical records,
looking for information concerning previous intubations, difficulties encountered
during airway management, and successful intubation techniques. Next, I would
perform a physical exam focusing on his Mallampati score, nasopharyngeal
characteristics, neck circumference, tonsil size, tongue volume, mouth opening,
thyromental distance, cervical range of motion, and any anatomical and physiologic
abnormalities of the airway. , I would
ensure the availability of emergency airway equipment and personnel, regardless of
the planned intubation technique.

Question 7

The patient is extremely anxious and starting to hyperventilate. The nurse
wants to know if she can administer preoperative midazolam. What do you
think?

Answer 7

Recognizing that the administration of even small doses of central
nervous system depressant drugs places this patient with sleep apnea at risk for
airway obstruction, hypoventilation, and/or apnea, my preference would be to avoid
administering any preoperative midazolam. Rather, I would go talk to the patient in
order to identify his concerns, answer any questions, and provide the appropriate
reassurance.

Question 8

I’m thinking A line for OSA pts: why?

Answer 8

Since his history of uncontrolled hypertension, dyspnea on
exertion, and signs of right heart failure on echocardiography (i.e. right ventricular
enlargement, elevated right ventricular systolic pressure) are suggestive of pulmonary
hypertension and right heart failure, I would also place an arterial line, pulmonary
artery catheter, and a 5-lead EKG.

Question 9

Pt with OSA says he doesn’t want an awake fiberoptic: what do you say?

Answer 9

I would tell him that, although his history of successful intubation is
somewhat reassuring, it does not necessarily diminish his risk. I would explain that I
remain concerned because he has experienced significant weight gain and worsening
symptoms of airway obstruction since being successfully intubated 2 years ago.
Given these concerns, I would tell him that an awake intubation without sedation
remains the safest method of securing his airway, and I would reassure him that I
would make every effort to make him comfortable during the procedure.
If he refused to undergo an awake intubation without sedation, or did not tolerate the
procedure, I would cautiously sedate him using dexmedetomidine, with the goal of
maintaining patient cooperation, spontaneous ventilation, and intact airway reflexes.
Other options for sedation would include benzodiazepines and opioid agonists.
Whatever the chosen agent, I would avoid polypharmacy and ensure the presence of
appropriate reversal agents (i.e. flumazenil and/or narcan).

Question 10

UPPP and ETT-which one are you choosing?

Answer 10

In deciding which type of endotracheal tube to use for the case, I
would discuss the planned surgical procedure, patient positioning, and endotracheal
tube preference with the surgeon. Usually, a standard or oral rae polyvinyl chloride

(PVC) endotracheal tube is utilized. However, ifthe surgeon was planning a laser-
assisted uvulopalatopharyngoplasty (LAUPPP), a procedure where laser energy is

used to eliminate pharyngeal tissue, I would consider using a laser resistant
endotracheal tube.

Question 11

Maintenance anesthetic of OSA pts with UPPP

Answer 11

Given this patient’s obesity and severe OSA, the ideal anesthesia
agents for maintenance of anesthesia would be short-acting, without active or toxic
metabolites, lack depressive effects on ventilation, and allow for a rapid return of
airway reflexes. Therefore, I would maintain anesthesia using a balanced technique
including desflurane (insoluble, lowest hepatometabolism of the volatile agents -
0.02%, fastest wake-up and return of airway reflexes), remifentanil (rapid
onset/offset, rapid metabolism by nonspecific esterases, inactive metabolites), and
cisatracurium (Hoffman elimination - morbidly obese patients often demonstrate
liver dysfunction).

Question 12

Assuming the surgeon is planning on using a laser for the procedure, would you
use an oxygen/nitrous oxide mixture?

Answer 12

While the use of nitrous oxide provides some advantages, such as a
short duration of action and a low blood-gas solubility coefficient, I would not use it
in this case due to the patient’s apparent pulmonary hypertension (Enlarged right
ventricle and right ventricular systolic pressure > 40 mmHg). Therefore, rather than
nitrous oxide, I would use air to reduce the Fi02 as much as possible during laser use.In reducing the Fi02, I would be balancing the risk of airway fire against the risk of
hypoxia in this obese patient with increased oxygen demand and signs of right heart
strain/failure.

Question 13

Does the dosing of intravenous anesthetic agents need to be adjusted due to the
patient’s obesity?

Answer 13

The volume of distribution of hydrophilic drugs, on the other
hand, is less affected by increased fat stores. Therefore, these drugs (e.g., NMBAs)
should, theoretically, be dosed based on ideal body weight (IBW).
lipophilic drugs (benzodiazepines, opioids, barbiturates,
etc.) have a larger volume of distribution in obese patients secondary to increased
deposition into body fat, making an initial loading dose based on total body weight
(TBW) reasonable.

Question 14

Suddenly the airway pressure alarm goes off and the bellows do not fill in
between breaths. What do you think is going on?
Low airway pressures and inadequate gas flow to fill the ventilation
bellows is consistent with

Answer 14

anesthesia circuit leak. While the most likely locations
for a significant leak include the circle system, Y-piece, endotracheal tube
connection, or the endotracheal tube cuff, I would also consider the gas flow meters,
C02 absorber, scavenging system, and ventilation bellows.While attempting to locate the leak, I would switch to hand ventilation, increase my
fresh gas flows, and deliver a Fi02of100%. If hand ventilation via the current circuit
proved inadequate, and I was unable to quickly identify the leak, I would attempt to
ventilate the patient using an AMBU bag with 100% oxygen. If ventilation remainedinadequate, I would consider the possibility of a ruptured ETT cuff and prepare for
replacement of the damaged ETT over a tube exchanger.

Question 15

The surgeon reports that he has accidentally cut a hole in the endotracheal tube
and there is a large leak in the oropharynx. What would you do?

Answer 15

I would immediately call for help, increase my fresh gas flows, ensure
the delivery of 100% oxygen, and hand ventilate the patient. If ventilation and
oxygenation proved inadequate despite high gas flows, I would advance the ETT
under fiberoptic visualization until the leak was past the vocal cords. If that failed to
improve oxygenation, I would ask the surgeon to prepare for a possible emergency
tracheostomy, have the operating room personnel prep and drape the patient’s neck,
and attempt to exchange the ETT over an exchange catheter adapted for oxygen
insufflation.

Question 16

After a brief episode of hypoxia, you successfully exchange the ETT over an
exchange catheter. The hypoxia resolves, but the blood pressure is now 66/31
mmHg. What is your differential diagnosis?

Answer 16

The timing of his hypotension, immediately following an episode of
hypoxia, suggests the possibility that the patient is experiencing myocardial ischemia,
myocardial infarction, a cardiac arrhythmia, and/or acute heart failure. Other
potential causes ofhypotension include excessive anesthesia, tension pneumothorax
(central line was placed), and anaphylactic reaction.
In addressing this hypotension, I would quickly evaluate the EKG, arterial blood

pressure, PA pressure, cardiac output, systemic vascular resistance, Sa02, and end-
tidal C02. Depending on my findings, I would discontinue any volatile agent to

attenuate the reduced systemic vascular resistance associated with volatile agents;
place the patient in the trendelenburg position to improve preload (increased venous
return to the heart); start a fluid bolus; and consider administering an inotrope and/or
an appropriate vasoactive drug.

Question 17

Pt hemodynamically unstable with a fib: you giving amiodarone?

Answer 17

This patient with significant hemodynamic instability may not tolerate
the administration of antiarrhythmic drugs, which may lead to bradycardia and
worsening hypotension. However, if it were determined that the benefits of
pharmacologic cardioversion outweighed the risks, I would administer a 150 mg
intravenous bolus of Amiodarone over 10 minutes (preferred drug with significant
heart disease), followed by a 1 mg/minute infusion for 6 hours, and a 0.5 mg/minute
infusion for 18 hours (maximum dose: 2.2 g/24 hours). At the same time, I would
prepare to quickly address any subsequent deterioration in hemodynamics.

So, synchronized cardio version in pts with hemodynamic instability-start with 200 J

Question 18

OSA: After successful extubation the patient is taken to the P ACU. How would you
monitor this patient’s respiratory status post-operatively and when would you
consider it safe to discharge him home?

Answer 18

(1) place him in a non-
supine position throughout the recovery process; (2) provide continuous supplemental

oxygen until he was able to maintain his baseline oxygen saturation while breathing
room air; (3) utilize continuous pulse-oximetry throughout his hospital stay; and (4)
apply continuous CP AP or NIPPY, if he had used either of these modalities
preoperatively. I would not discharge him to an unmonitored setting (e.g. home or
unmonitored hospital bed) until his pain was controlled without narcotics, airway
swelling had decreased, and I no longer considered him to be at risk for postoperative
respiratory depression. I would verify this by ensuring he was able to maintain his
normal baseline oxygen saturation while breathing room air in a quiet environment
(preferably while asleep).

Question 19

30 minutes later you are called stat to the PACU where you find the staff
attempting to mask ventilate your patient. He is hypoxic with a Sa02 of 78%.
What would you do?

Answer 19

I would immediately call for help, the emergency airway cart, and the
ENT surgeon. I would then ensure the patient was in the head-up position (to
improve respiratory mechanics), take over mask ventilation, place an oral or nasal
airway, provide a two handed jaw thrust, and attempt to mask ventilate with 100%
oxygen. If ventilation were still inadequate, I would place an LMA and consider re-
intubation. At the same time, I would continuously monitor the patient for signs of
cardiovascular deterioration.

Question 20

Bag mask ventilation is ineffective, intubation attempts are unsuccessful, and he
has become bradycardic. What would you do?

Answer 20

I would ask the ENT surgeon to proceed with an emergency surgical
airway while I continued to attempt to ventilate the patient. If a surgeon were not
available, I would perform a cricothyroidotomy by placing a needle through the
cricothyroid membrane until air was aspirated, passing a wire through the needle,
making a skin incision next to the wire, and advancing a tracheostomy or
endotracheal tube over the wire. Once the airway was in place, I would confirm
ventilation by auscultation of all lung fields and observation of adequate chest rise
and consistent end-tidal C02

Question 21

After successful tracheostomy and resuscitation, the patient remains mildly
hypoxic with a Sa02of89% while breathing 100% oxygen. What do you think
is going on?

Answer 21

There are several possible explanations for this obese patient’s
continued hypoxia following an emergency surgical airway, such as aspiration of
blood and/or gastric contents during resuscitation, bronchospasm, pulmonary edema
(heart failure or negative pressure pulmonary edema), atelectasis, hypoventilation,
pneumothorax, malpositioned cricothyroidotomy tube, pulmonary embolism, and
acute heart failure. In addressing his hypoxia, I would auscultate the lungs; confirm
proper cricothyroidotomy tube placement and adequate ventilation; evaluate his PA
pressure and cardiac output; and order a CXR. Depending on my findings, I would
administer a bronchodilator, adjust the cricothyroidotomy tube, place a chest tube,
optimize his hemodynamics, and/or adjust ventilator settings.

Question 22

Physical exam reveals diffuse pulmonary crackles and CXR shows generalized
pulmonary edema that was not present preoperatively. What could have caused
this?

Answer 22

Given his OSA, HTN, and recent hypoxic event, his pulmonary edema
most likely represents either negative pressure pulmonary edema or left heart failure.
In the case of upper airway obstruction, sustained ventilatory effort against a closed
glottis could have resulted in high negative intrapleural pressure with subsequent
movement of fluid from the pulmonary capillary bed into the alveoli. On the other
hand, hypoxia-induced ischemia, dysrhythmias, and/or hypertension may have led to
left heart failure with subsequent pulmonary edema. Other potential causes or
contributing factors would include fluid overload, aspiration, and anaphylaxis.

Question 23

Assuming this were negative pressure pulmonary edema, how would you
manage his condition?

Answer 23

Recognizing that the treatment of negative pressure pulmonary edema
(NPPE) is supportive, I would ensure a patent upper airway, provide supplemental
oxygen, and positive pressure ventilation. If his oxygenation did not improve, I
would consider the addition of positive end-expiratory pressure (PEEP) to promote
alveolar expansion. While diuretics are sometimes utilized in the treatment of this
condition, their use is controversial, and I would not administer these drugs unless
hemodynamic data indicated hypervolemia.