Book 6, Case 1-PET and Airway Flashcards

1
Q

Pt has high BPs and RUQ pain-you worried?

A

right upper quadrant pain may indicate hepatic involvement, a
complication associated with severe preeclampsia and HELLP syndrome. HELLP is as
serious condition that may lead to impaired hepatic function, hepatic hematomas, and even
hepatic rupture with massive blood loss.

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2
Q

When does HELLP usually present?

A

Usually before delivery, but can happen afterwards.

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3
Q

What is HELLP syndrome associated with? Clinical mgmt includes:
What is definitive tx?

A

The syndrome is associated with an
increased risk of preterm delivery, DIC, acute renal failure, ascites, cerebral edema, placental
abruption, pulmonary edema, hepatic bleeding, hepatic failure, retinal detachment, sepsis,
stroke, acute respiratory distress syndrome, and maternal and/or fetal death. Signs and
symptoms consistent with HELLP syndrome include: (1) right upper quadrant or epigastric
pain, (2) hypertension, (3) headache, ( 4) nausea and vomiting, (5) and proteinuria (keep in
mind that hypertension and proteinuria are not always present).
Clinical management includes: (1) providing magnesium for seizure prophylaxis, (2)
administering antihypertensive medications for blood pressure control (i.e. SBP < 160
mmHg; DBP < 105 mmHg), (3) correcting any coagulopathy, and, when time permits, (4)
administering corticosteroids to accelerate fetal lung maturity. Definitive treatment,
however, requires (5) delivery of the baby.

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4
Q

For babies at 24-32 weeks gestational age magnesium sulfate is often administered for

A

neuroprotection (reduced rate of cerebral palsy).

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5
Q

PET/HELLP: benefits/cons of fluid bolus

A

Obvi fluid bolus is worth it,
It is reasonable to provide a judicial fluid bolus prior to
initiating a regional or general anesthetic. Patients with preeclampsia tend to be hypovolemic
with increased SVR, decreased colloid oncotic pressure, and increased vascular permeability.
Decreased colloid oncotic pressure and increased vascular permeability place the patient at
risk for cerebral and pulmonary edema especially with overaggressive fluid administration. However, since preeclampsia is associated with decreased uteroplacental and organ
perfusion, the avoidance ofhypotension is important.

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6
Q

Pts can get Mg for PET, but what else can they get it for?

A

Magnesium is utilized in the treatment of preeclampsia primarily for seizure
prophylaxis. However, there may be some beneficial maternal hemodynamic effects such as
decreased SVR and increased uteroplacental perfusion. Despite a high therapeutic index,
there are some potential complications associated with magnesium toxicity such as muscle
weakness and respiratory and cardiovascular depression. These complications can be
avoided with careful monitoring of the patient for signs of toxicity such as loss of patellar
reflexes, visual changes, muscle weakness, and somnolence.
It also provides neuro protection to baby between 24-32 weeks of age

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7
Q

As you consider regional anesthesia, are you concerned about her coagulation status? Don’t forget to perform _____

A

I am concerned about her coagulation status. While pregnant women tend to
be hypercoagulable, preeclampsia can reduce platelet number and impair platelet function,
increasing the risk for epidural or spinal hematoma. In making a decision to provide regional
anesthesia in this case, I would consider the trend of the platelet number in addition to the
absolute number. I would also perform a history and physical exam focusing on the airway
and signs of coagulopathy such as bleeding at the IV site, mucosal bleeding, and marked or
easy bruising.

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8
Q

You have dosed the epidural with local anesthetic. However, when the surgeon makes
the incision, the patient complains of significant pain. What will you do?

A

Depending on the status of the baby (urgency of C/S) and the location and
severity of the pain, I would consider re-dosing, repositioning, or replacing the catheter; local
infiltration with/without sedation; or general anesthesia. If time allowed, I would attempt to
improve the function of the epidural in order to avoid: (1) replacing a catheter in a
preeclamptic patient with potential coagulopathy (there is an additional risk of vascular
trauma during replacement); (2) providing sedation to a pregnant patient with a potentially
difficult airway and increased risk of aspiration; (3) or inducing general anesthesia for a
patient with an increased risk of difficult airway management and aspiration.

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9
Q

Everything has been tried and the epidural will not work. The baby’s heart tones are
down and the OB says, “We have to cut now!” What will you do?

A

The first step would be to optimize
the mother’s hemodynamics by ensuring adequate uterine displacement and addressing any
hypotension, hypertension, hypoxia (apply 100% oxygen), and/or rapid or irregular heart rate
that might compromise utero-placental perfusion. This may improve her baby’s condition
and buy time to achieve adequate analgesia. If these interventions were unsuccessful, and
local infiltration combined with a small dose of ketamine were insufficient to control herdiscomfort (given her potentially difficult airway, any sedation should be administered with
the goal of maintaining spontaneous respirations), the most conservative option would be to
delay surgery until I could safely secure the airway
In this case, I would: (1) ensure the presence of difficult airway
equipment, (2) prepare for a possible cricothyrotomy or tracheostomy, (3) preoxygenate with
100% oxygen via a tight fitting mask, (4) apply cricoid pressure, (5) place the patient in
slight reverse-trendelenburg (improved respiratory mechanics and intubating conditions
along with reduced risk of passive aspiration), (6) perform an inhalational induction, with
the goal of maintaining spontaneous respiration, and (7) attempt to intubate the patient. If
intubation were unsuccessful after one attempt, I would continue to deliver volatile agent
through the mask and allow the obstetric team to deliver the baby. Following delivery of the
baby, I would ask the surgical team delay closure until I definitively secured the airway (i.e.
fiberoptic bronchoscope, video laryngoscope, intubating LMA, etc.).

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10
Q

Despite some difficulty, you manage to intubate the patient; her blood pressure
increases to 208/104 mmHg. What will you do?

A

First, I would check another blood pressure and, at the same time, verify
proper ETT placement. I would then check my monitors and ventilation settings, and look
for signs of light anesthesia such as tearing, sweating, and movement. If I thought light
anesthesia were the cause rather than hypoxia, hypercarbia, increased ICP (she is
preeclamptic ), drug error, or artifact, I would administer a bolus of propofol and titrate on a
higher concentration of inhalational agent. If the high blood pressure persisted, I would
consider administering labetalol or even sodium nitroprusside if necessary.
Clinical Note:
• It would be important to rule out elevated intracranial hypertension before treating her
blood pressure aggressively. In the setting of intracranial hypertension, it would be more
appropriate to begin with measures to reduce intracranial hypertension.

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11
Q

Why hydralazine in PET?

A

Hydralazine and labetalol are the most commonly used – hydralazine, a vasodilator, is alleged to increase uterine placental flow

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12
Q

After delivery, baby Bis not crying and remains apneic. The mother is stable. You are
asked to help with neonatal resuscitation. What will you do?

A

As long as the mother was stable and if no one else was immediately
available to resuscitate the baby, I would have someone call for help and have the nurse push
the baby’s crib to the head of the operating table where I could assist in resuscitation while at
the same time monitoring the mother’s condition. In this situation, I would keep in mind that
the mother is my primary responsibility and then weigh the risk of taking any actions that would prevent me from taking care of the mom

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13
Q

You giving calcium to babies?

A

Since calcium administration may lead to cerebral calcification and decreased
survival in stressed newborns, I would only administer this drug to treat known magnesium
toxicity. However, recognizing the potential for magnesium toxicity in this case
(preeclamptic mother receiving magnesium sulfate), I would check the neonate’s magnesium
level and treat accordingly. If magnesium toxicity were confirmed, I would administer
calcium (100 mg/kg of calcium gluconate or 30 mg/kg of CaCb).

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14
Q

When and where are you using pulse oximeter probe for the neonate?

A

I would consider utilizing oximetry when I anticipated the need for
resuscitation, when positive pressure ventilation was required for more than a few breaths,
when supplemental oxygen was necessary, or when cyanosis was persistent. I would place
the oximeter on the right upper extremity (finger, wrist, or medial palmar surface) in order to
monitor pre-ductal blood flow, which provides a better assessment of central nervous system
oxygenation. Unfortunately, it often takes 1-2 minutes to place and obtain reliable readings
from the pulse oximeter.

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15
Q

When would you consider intubating the neonate?

A

(2)
bag mask ventilation was ineffective; (3) chest compressions became necessary; (4)
prolonged mechanical ventilation was anticipated; (5) endotracheal administration of drugs
was desired (intravenous or intraosseous administration is preferred); and ( 6) when required
for special resuscitation circumstances, such as congenital diaphragmatic hernia or extremely
low birth weight (<1000 g).

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16
Q

You can’t get IV access in the neonate, but really need it-wyd?

A

If I was unable to obtain intravenous access in a timely manner, I would
attempt to acquire intraosseous access by inserting a 20-guage needle into the proximal tibia
at a caudal angulation (about 1 cm below the tibial tuberosity), recognizing that this
procedure risks tibial fracture and osteomyelitis (the line should be removed in 1-2 hours to
reduce the risk of the latter complication). If I were similarly unable to establish intraosseous
access in a timely manner, I would consider administering epinephrine through the
endotracheal tube. Since there is some evidence that the normal IV dose of 0.01-0.03 mg/kg
is ineffective when administered through the endotracheal tube, I would consider
administering a higher dose up to 0.1 mg/kg diluted in 1-2 cc of normal saline, recognizing
that the safety and efficacy of administering epinephrine through an ETT is not clearly
established.

17
Q

You have successfully resuscitated the baby. Maternal bleeding, however, continues
despite the administration of oxytocin. What will you do?

A

I would make sure the patient is stable, ensure adequate IV access, and give
fluids, blood, and vasoactive agents as necessary. I would also communicate with the
surgeon and observe the surgical fieldIf it appeared that uterine atony was the cause of continued bleeding, I would consider
reducing my inhalational agent, increasing the dose of oxytocin, and/or administering 15-
methyl-prostaglantin F2-alpha (Hemabate). If these interventions did not resolve the
problem, I would consider administering misoprostol (Cytotec; a prostaglandin E1 analogue;
800-1000 μg per rectum) or dinoprostone (prostaglandin E2; 20 mg vaginal or rectal
administration). Given the potential for exacerbation of hypertension following
methylergonovine (Methergine) administration, I would probably avoid giving this
medication to this patient with pregnancy-induced hypertension. Moreover, depending on
severity of the bleeding, I may employ a rapid infusing device or a cell-saver.
If all of these measures were unsuccessful, the surgeon may have to employ an intrauterine
balloon (works via tamponade; success rate up to 80%);

18
Q

How do oxytocin, Methergine, and Hemabate work?

A

Oxytocin, Methergine, and Hemabate cause contraction of myometrial
smooth muscle by increasing intracellular calcium levels. It is important to remember that
Hemabate is associated with bronchospasm and should probably be avoided in asthmatic
patients when possible. Methergine is associated with hypertension, especially when
administered intravenously, and should be given intramuscularly except in the case of life
threatening hemorrhage. Oxytocin can cause hypotension when given as an intravenous
bolus and should be administered in a dilute solution (20 units in 1 liter of fluid).

19
Q

PET pt has seizure in PACU: DDX and what are you going to do?

A

This is most likely an eclamptic seizure resulting from the physiologic
changes that occur with preeclampsia. However, hypoxia, hypotension (hypovolemia,
residual anesthetic, etc.), intracranial hemorrhage (secondary to preeclampsia and/or the
significant intra-operative hypertension following intubation), hypoglycemia (diabetic and
taking insulin), and local anesthetic toxicity (large amounts of local anesthetic most likely
administered when attempting to achieve adequate epidural anesthesia) should be
considered.

Given that securing the airway at the beginning of the case was somewhat
difficult, I would: (1) provide 100% oxygen, (2) administer 3-5 cc’s of propofol (or a small
dose of a benzodiazepine ), (3) have someone get the difficult airway cart and ( 4) call a
surgeon capable of performing a tracheostomy. I would then (5) position the patient in
reverse trendelenburg (to reduce the risk of passive regurgitation and to facilitate intubation),
(6) apply cricoid pressure, and (7) perform laryngoscopy with the goal of maintaining
spontaneous respirations. However, I would recognize that utilizing such a small dose of
propofol for intubation places this patient with a full stomach and eclampsia at increased risk
for aspiration, hypertension, and cerebral hemorrhage (due to light anesthesia). Finally, after
the ETT was secured, I would consider (8) administering midazolam for its anti-seizure and
amnestic effects.

20
Q

If she were breathing spontaneously, would you attempt to intubate her when you had
difficulty doing so at induction?

A

Yes. I think that it is important to secure her airway because her mental
status, which may already be diminished, could deteriorate further with worsening cerebral
pathology, placing her at progressively increasing risk of aspiration, hypoventilation, and apnea. The fact that intubation and/or ventilation may prove difficult makes securing her
airway now, while she is spontaneously breathing, even more important. Her current ability
to breathe spontaneously allows me more time to safely secure her potentially difficult
airway. A “wait and see” strategy could place me in the position of having to emergently
secure her airway with little time for preparation and intubation.

21
Q

Wouldn’t a muscle relaxant stop the seizure?

A

No. While a muscle relaxant would stop the physical appearance of a seizure
and decrease the metabolic consequences of sustained muscle contraction such as
hyperthermia, metabolic acidosis, and hyperkalemia, it would not stop the seizure. And,
more importantly, it would result in apnea in a patient with a potentially difficult airway.
And, as I stated earlier, I believe the risk of inducing apnea is more significant than the risk
of aspiration.

22
Q

PET pt that just seized: The glucose level comes back at 65 mg/dL. Would you treat it?

A

I would carefully treat her hypoglycemia understanding that it is most likely
not the cause of the seizure and recognizing that treatment risks hyperglycemia in this
diabetic patient. Hyperglycemia is of particular concern in this case because it is associated
with worsened neurologic outcome under conditions of neuronal ischemia, as would likely
occur during a seizure.

23
Q

The patient is intubated. Thirty minutes later she desaturates to 90% and there is pink
frothy fluid coming out of the ETT. How will you evaluate and manage this patient?

A

I would make sure the patient’s vital signs are stable, verify ETT positioning,
provide 100% oxygen, and auscultate the chest. This clinical picture is consistent with
pulmonary edema, which could result from preeclampsia, fluid overload, left ventricular
failure, aspiration, negative pulmonary pressure, or a combination of these inciting factors.
Therefore, I would apply high peak airway pressures and PEEP as hemodynamically
tolerated to aid in recruiting atelectatic alveoli and improving gas exchange. Additional
treatment depends on the cause of the pulmonary edema. If I thought the cause was
cardiogenic in origin such as myocardial ischemia, hypotension, or a dysrhythmia, I may
consider using diuretics, inotropic agents, beta-blockers, or afterload reducing agents. If a
non-cardiogenic cause was more likely, I might simply provide diuretic therapy and fluid
restriction.

24
Q

How does PEEP work?

A

PEEP recruits atelectatic, fluid-filled alveoli, decreasing intrapulmonary
shunting and possibly increasing compliance. PEEP does not necessarily move fluid out of
the lungs, but it moves the fluid to areas where gas exchange is not taking place.

25
Q

Rule of thumb for FiO2 and PaO2 relation:

A

(Rule of thumb: Fi02 times 5 = Pa02).

26
Q

After treatment for 5 days, the patient’s condition has improved. The ABG is as
follows: pH= 7.26; PaC02 = 51; Pa02 = 76; HC03 = 25 on a Fi02 of 40%. Would you
extubate her? (Pt had pulmonary edema,)

A

the ABG shows a metabolic and
respiratory acidosis and the Pa02 is only 76 mmHg on 40% oxygen when it should be in the
hundreds (Rule of thumb: Fi02 times 5 = Pa02). This suggests that there remains significant
shunting secondary to pulmonary edema or possibly ARDS, and I would not extubate the
patient at this time.