Book 6, Case 4-Non OB surgery in an OB pt

Question 1

Concerns for surgery in an OB pt?

Answer 1

The mother is exposed to increased risk of failed intubation,
pulmonary aspiration, hemorrhage, infection, and thromboembolism. The baby is also
exposed to increased risk, including preterm labor/delivery (especially with abdominal
surgery), teratogenesis (although the highest risk is during organogenesis, which occurs
around the 15th _5oth day post-conception), fetal asphyxia, intrauterine growth restriction,
miscarriage, and neurotoxicity (exposure of the developing brain to general anesthesia may
lead to neurodegeneration, with subsequent long-term neurocognitive deficits). Undergoing
laparoscopic surgery carries specific risks for the obstetric patient, such as damage to the
gravid uterus (this risk is reduced by employing alternative sites for the Varess needle and
trocars), increased risk of miscarriage or preterm labor (because abdominal surgery), and
hypercapnia-induced fetal acidosis (risk reduced by adjusting mechanical ventilation to
maintain normocapnia or by employing gasless laparoscopy).

Question 2

When is the best time to perform semi-elective surgery on a pregnant patient?

Answer 2

Given the increased risk of miscarriage and teratogenesis in the first trimester,
and the increased risk of preterm labor/delivery in the third trimester, the optimal time for
semi-elective surgery during pregnancy is the second trimester.Furthermore, it is preferable
to operate before the 23rd week of pregnancy in order to further minimize the risk of preterm
labor and allow for adequate surgical access within the abdomen.

Question 3

Which anesthetic agents are teratogenic?

Answer 3

While almost any agent can prove teratogenic if the dose is large enough and
given at the right time, human studies have not conclusively shown that any anesthetic agent
results in increased congenital abnormalities. The conclusions of past studies that suggested
possible teratogenic effects associated with nitrous oxide and benzodiazepines have been
questioned, and are not supported by more recent studies and epidemiologic data.

Question 4

Baby is 22 weeks: Would you administer prophylactic glucocorticoids prior to surgery?

Answer 4

I would not administer prophylactic glucocorticoids for the purpose of fetal
lung maturation, since this baby has not yet reached the age of viability (23-24 weeks).
Current recommendations are to administer a single course of corticosteroids when there is a
significant risk of preterm delivery between 24 and 34 weeks gestation. Prophylactic
administration at this gestational age has been demonstrated to significantly reduce theincidence of respiratory distress syndrome, intraventricuiar hemorrhage, and neonatal death
in infants delivered prior to 30 weeks gestation.
I would, however, consider administering dexamethasone to help with the mother’s nausea,
keeping in mind that the administration of a glucocorticoid to a diabetic patient may further
complicate glucose control.

Question 5

Would you administer a prophylactic tocolytic?

Answer 5

I would not administer prophylactic tocolytics because, although surgery
places the pregnant patient at increased risk of preterm delivery (the risk is even higher with
abdominal surgery, as in this case), there is no evidence to support the routine use of
prophylactic tocolytic agents.Unfortunately, monitoring of uterine contractions and early tocolytic therapy has not been
proven to reduce the incidence of preterm delivery.

Question 6

Is aspiration prophylaxis necessary at this gestational age? 22 weeks gestation

Answer 6

most practitioners recommend aspiration
prophylaxis after 18-20 weeks gestation. This patient not only falls within this range, but is
at increased risk due to the emergent nature of the procedure, an increased risk of difficult
intubation (due to the physiologic changes of pregnancy and/or diabetic stiff joint syndrome),
potential gastroparesis (acute abdomen and/or diabetic autonomic neuropathy), concurrent
nausea and vomiting, and the fact that she is undergoing laparoscopic surgery. Therefore, I
would take steps to minimize the risk of pulmonary aspiration, such as administering
metoclopramide, an H2-receptor antagonist, and/or a nonparticulate antacid; performing a
rapid sequence induction with cricoid pressure and the patient in reverse trendelenburg
(improves respiratory mechanics, facilitates rapid intubation, and inhibits passive
regurgitation); emptying the stomach with a nasogastric or orogastric tube; and delaying
extubation until the patient is fully awake.

Question 7

What is diabetic stiff joint syndrome?

Answer 7

Diabetic stiff joint syndrome (a.k.a. diabetic scleroderma), which is due to
glycosylation of proteins and abnormal collagen cross-linking, may develop in patients with
long-standing type I diabetes mellitus. The syndrome can result in limited movement of the
atlanto-occipital, temporomandibular, and cervical spine joints, potentially increasing the
difficulty of direct laryngoscopy and intubation. I would use the “prayer sign” to screen for
this syndrome. If the patient is unable to completely approximate the palmar surfaces of the
phalangeal joints of the hands (prayer sign), this is suggestive of stiff joint syndrome, which
raises concerns of difficult airway management.

Question 8

Her blood sugar comes back at 356 mg/di. What would you do?

Answer 8

Given this patient’s clinical picture, including potential infection, high blood
sugar, abdominal pain, and nausea and vomiting, I would be very concerned that this type I
diabetic has developed diabetic ketoacidosis (DKA) secondary to, or independent of,
appendicitis (abdominal pain, nausea, and vomiting are all symptoms ofDKA as well as
appendicitis).

Therefore, I would notify the surgeon; administer an intravenous bolus of 10
U of insulin; begin fluid replacement with normal saline; check for serum and urinary
ketones; obtain an arterial blood gas, blood urea nitrogen, creatinine, and electrolytes; and
determine the anion gap (DKA results in an increased anion gap acidosis).
If it were determined that the patient was in DKA, I would continue fluid replacement; start
an insulin infusion with the goal ofreducing plasma glucose by 75-100 mg/dL per hour
(more rapid reductions risk cerebral edema); add 5% dextrose to the insulin infusion when
the serum glucose reaches 250 mg/dL (to prevent hypoglycemia and to provide a continuous
energy source); replace potassium, phosphate, and magnesium as necessary; and continue to
closely monitor serum potassium, blood glucose, serum ketones, and the anion gap.

Question 9

Anion gaps can be different at different institutions, so…

Answer 9

Therefore, you should always consult your specific laboratory’s
normal reference range when making clinical decisions.

Question 10

DKA Tx:

Answer 10

Treat with fluids (NS + K @ 10 cc/kg/hr) and insulin (10 U IV push then 0.1 U/kg/hr) followed by dextrose when BG < 250. Mortality rate 5-10%.

HHS: same precipitating events as DKA with the addition of renal failure and/or dehydration. Caused by severe osmotic diuresis and subsequent dehydration/prerenal failure. These patients are not ketoacidotic because they produce insulin and have enough sensitivity to avert mobilization of fatty acids/ketogenesis. Glucose ~ 1000. Treat similarly to DKA (fluids and insulin). Electrolyte abnormalities less severe than in DKA, volume deficits and osmolarity are worse. Mortality 10-15%.

Question 11

You determine that she is in DKA. Would you delay this emergent case?

Answer 11

The decision to delay this case for treatment is a risk/benefit decision that
must be made in consultation with the surgeon. In that discussion, I would point out that
even a short delay to partially resolve metabolic acidosis, hypovolemia, and hypokalemia
may reduce the risk of intraoperative cardiac arrhythmias and hypotension. However, the
decision would have to be made recognizing that delaying the case risks worsening
appendicitis, peritonitis (if not already present), and further metabolic deterioration.

Question 12

Monitors for this DKA pt:

What about SCDs-and why?

Answer 12

(1) an arterial line for frequent blood draws
(e.g. electrolytes, blood sugar), arterial blood gas analysis, and blood pressure management
(DKA, 24 hours of nausea and vomiting, and possible diabetic autonomic neuropathy place
her at risk for hemodynamic instability); (2) a Foley catheter to follow urine output and
decompress the bladder (to improve the surgeon’s view and reduce the risk of perforation
during laparoscopy); (3) transvaginal Doppler ultrasonography for continuous intraoperative
fetal heart rate monitoring (allows for optimization of maternal hemodynamics when the
FHR suggests fetal stress); and
In addition to these monitors, I would place an orogastric or nasogastric tube to empty and
decompress the stomach (reduces the risk of pulmonary aspiration and surgical perforation
during laparoscopy) and pneumatic compression devices on the lower limbs to reduce the
risk of embolism (pregnant patients are hypercoagulable, and creation of the
pneumoperitoneum promotes intraoperative venous stasis).

Question 13

Is there any reason for continuous intraoperative fetal heart rate monitoring if the baby
is not viable? And what will you do if FHR suggests distress?

Answer 13

Yes. Even though an emergent cesarean section is not an option for a
nonviable baby ( <23 weeks), intraoperative monitoring allows for optimization of maternal
hemodynamics when the FHR suggests fetal stress. While intraoperative monitoring is not
always warranted, this patient’s medical condition places her at increased risk for
hemodynamic instability. Should an unexplained change in FHR occur intraoperatively, I
would quickly ensure adequate left uterine displacement, blood pressure, oxygenation, and
volume replacement. I would then verify sinus rhythm; attempt to identify excessive
bleeding or surgical impairment of uterine perfusion; check electrolytes, hemoglobin, and an
ABG; and consider reducing the pneumoperitoneum (intra-abdominal pressures should
optimally be maintained between 8-12 mmHg).

Question 14

The patient is intubated and the surgery proceeds. During creation of the
pneumoperitoneum, her heart rate decreases to 46 bpm and her blood pressure begins
to fall. What will you do?

Answer 14

Since the timing of this event suggests a reflex increase in vagal tone with
creation of the pneumoperitoneum, I would: ( 1) ask the surgeon to discontinue insufflation;
(2) evaluate the ECG (the increased vagal tone can lead to cardiac arrhythmias), (3) check
her blood pressure; (4) administer atropine (while glycopyrrolate is less likely to cross the
placenta, the onset of action is too slow for acute treatment); (5) ensure adequate
oxygenation, ventilation, and left uterine displacement; and ( 6) provide fluids and
vasopressors as indicated. However, recognizing that there are other potential causes of
these hemodynamic changes (i.e. tension pneumothorax, metabolic and/or electrolyte
disturbances, and significant C02 embolism), I would also: (7) verify proper endotracheal
tube placement; (8) auscultate the chest; and (9) check the patient’s blood sugar, electrolytes,
and arterial blood gasses. Following hemodynamic stabilization, I would ensure adequate
intra vascular volume and depth of anesthesia prior to allowing re-insufflation of the abdomen
(preferably at a lower insufflation pressure).

Question 15

Assume you placed a transvaginal Doppler to monitor fetal heart tones. Now, you
check the fetal heart rate tracing and note the absence of variability. What do you
think?

Answer 15

Fetal heart rate variability is important because it serves as a good indicator of
fetal well-being. However, the lack of variability is expected in this case, because fetal heart
rate variability does not develop until the 25th to 2ih week of gestation. If the baby’s
gestational age were more advanced and fetal heart rate variability was present
preoperatively, it would be necessary to distinguish the reduction in variability that occurs
with the administration of atropine (since I used this in the treatment of the mother’s
bradycardia) or induction of general anesthesia (especially when opioids are used) from that
resulting secondary to fetal hypoxia. ill either case, the presence of severe and persistent
bradycardia, tachycardia, or repetitive decelerations on the FHR tracing should prompt
optimization of the mother’s hemodynamics and uteroplacental oxygen delivery (i.e. LUD,
100% oxygen, volume resuscitation, and blood pressure support).

Question 16

The surgeon deflated the pneumoperitoneum at your request and the patient’s blood
pressure stabilized. Upon re-inflation the peak airway pressures increase and her
oxygen saturation begins to drop. What do you think is happening? What will you do?

Answer 16

Recognizing that these findings are consistent with two complications
associated with the creation of a pneurnoperitoneurn, right rnainstern intubation ( cephalad
displacement of the diaphragm and carina during pneurnoperitoneurn inflation can result in
right rnainstern intubation) and pneurnothorax (e.g. capnothorax secondary to movement of
C02 into the thorax via congenital diaphragmatic defects or trauma-induced diaphragmatic
communications), I would: (1) hand ventilate; (2) switch to 100% oxygen; (3) auscultate the
lungs; ( 4) verify proper endotracheal tube positioning (possibly using a fiberoptic
bronchoscope); and (5) check the ECG, blood pressure, and PETC02 (increases with
capnothorax and is usually unchanged with right stern intubation). If the ETT were correctly
positioned and the PETC02 was elevated (most likely capnothorax), I would ask the surgeon
to release the pneurnoperitoneurn and adjust her ventilation to facilitate the normalization of
her C02 levels.

Question 17

The endotracheal tube was in the right mainstem bronchus, and the patient’s airway
pressures return to normal after you correctly position it. Would you proceed with the
case using 100% oxygen?

Answer 17

Given this patient’s DK.A and hernodynarnic instability, I would proceed with
100% oxygen in order to optimize maternal and fetal oxygenation. Using 100% oxygen
instead of a mixture including N20 would have the additional advantage of avoiding an
unfair association of a subsequent congenital abnormality with the use of nitrous oxide
during the case (the use ofN20 could become a medico-legal issue despite the evidence that
there is no increased risk of congenital abnormalities with intraoperative exposure to N20).

Question 18

Would you be worried about intrauterine retrolental fibroplasia or premature closure
of the ductus arteriosus with the use of 100% oxygen?

Answer 18

Due to a large maternal-fetal oxygen tension gradient, fetal oxygen saturation
never exceeds 50-60 rnrnHg, even with very high maternal oxygen saturation.Therefore,increased maternal Pa02 does not increase the risk of intrauterine retrolental fibroplasia or
premature closure of the ductus arteriosus. However, despite this limited increase in fetal
Pa02, the practice of providing 100% oxygen to the mother during times of fetal stress is
justified because even small increases in fetal Pa02 may prove significant in improving fetal
oxygenation due to the steep slope of the fetal oxyhemoglobin dissociation curve near the P5o
of fetal blood (21 mm Hg).

Question 19

The post-op nurse calls you because the patient is nauseous. What are this patient’s
risk factors for post-operative nausea and vomiting?

Answer 19

This patient’s risk factors for post-operative nausea and vomiting include
female gender, laparoscopic surgery, pain (surgical pain and the inflammation from
appendicitis), diabetic ketoacidosis, and the fact that she is a nonsmoker. Other potential
risks would include anxiety, a prolonged surgical procedure, a history of motion sickness,
and the intraoperative administration of volatile agents, nitrous oxide, opioids, and
neostigmine.

Question 20

Tell me what steps could have been taken preoperatively and intraoperatively to reduce
the risk of post-operative nausea and vomiting (PONV) for this patient at high risk? What about dexamethasone? NSAIDS? and droperidol?

Answer 20

Due to the multifactorial etiology of PONV, multimodal strategies have
proven to be the most successful in reducing the incidence in high-risk patients. Therefore, I
could have provided adequate hydration, a scopolamine patch, and a benzodiazepine (should
consider the medico-legal ramifications of giving a pregnant woman a benzodiazepine).
Moreover, the use of total intravenous anesthesia with propofol would have taken advantage
of the antiemetic properties of propofol while avoiding the use of volatile agents and nitrous
oxide (both of which may increase the incidence of PONV). Finally, I could have asked the
surgeon to inject local at the port sites to reduce post-operative narcotic requirements;
administered a serotonergic receptor antagonist (i.e. ondansetron) and/or a neurokinin-1
receptor antagonist (aprepitant) at wound closure;

While nonsteroidal anti-inflammatory drugs (reduce the need for opioid requirements),
dexamethasone, and droperidol are often used to prevent or treat nausea, I would avoid them
in this particular case. The administration ofNSAIDs risks premature closure of the fetal
ductus arteriosus, and should be used with caution in the second half of pregnancy (risk is
greatest after 32 weeks gestation). Droperidol, a dopamine receptor antagonist, is a category
C drug and should only be given in pregnancy when the benefits outweigh the risks. Finally,
giving dexamethasone to this diabetic patient in DK.A may further complicate plasma glucose
control.

Question 21

Pt is preggo: The patient has been suffering from major depression and is scheduled to receive
electroconvulsive therapy (ECT) next week. Would you agree to this procedure? 

And while we’re on it-what are contraindications to ECT?

Answer 21

If pharmacotherapeutic agents were not an option (e.g. patient refusal, drug-
resistant disorder, etc.) and the psychiatrist believed that treatment was necessary, then I

would agree to proceed with ECT. The decision to perform ECT during pregnancy is made
in consultation with the patient’s psychiatrist and obstetrician, and involves weighing the
risks of performing the procedure against the risks associated with an untreated psychiatric
disorder (e.g. suicide, severe malnutrition/dehydration, catatonic state, etc.). While
Performing ECT during pregnancy has been associated with vaginal bleeding, abdominal
pain, uterine contractions, preterm labor, and neonatal cerebral infarction, withholding
treatment could lead to severe malnutrition/dehydration or even suicide.

Contraindications: Conditions that have been listed as contraindications to ECT therapy include: (1)
intracranial mass lesions (2) vascular malformations, (3) recent MI(< 3 months), (4)
recent stroke(< 1 month), (5) increased ICP from any cause, and (6) pheochromocytoma.

Question 22

The psychiatrist and obstetrician determine that ECT is necessary. What are the
physiologic effects of ECT?

Answer 22

The parasympathetic discharge associated with the initial electrical stimulus
results in bradycardia, increased airway secretions, and hypotension (the bradycardia usually
lasts about 10-15 seconds, can be profound, and may progress to asystole ). Within 1 minute,
generalized seizure activity results in sympathetic activation, with subsequent tachycardia,
hypertension, and possible dysrhythmias (the hypertension lasts for 2-10 minutes and may be
significant, sometimes approaching 150% of baseline values). The rapid increase in systemic
blood pressure associated with this sympathetic activation results in increased cerebral blood
flow (up to a seven-fold increase), intracranial pressure, and cerebral oxygen consumption.
Intraocular and intragastric pressures may also increase during the procedure (intraocular
pressure may increase more than two-fold).

Question 23

How would you perform the anesthetic?

Answer 23

In performing this anesthetic, I would: (1) consult an obstetrician; (2) verify
the absence of contractions (tocodynamometry) and check the fetal heart rate immediately
prior to the procedure; (3) optimize her blood sugar; (4) ensure adequate hydration (these
patients are at increased risk for hypotension due to parasympathetically-induced bradycardia
and poor oral intake secondary to depression or psychosis); (5) provide aspiration
prophylaxis (increased risk for aspiration secondary to pregnancy and the increase in
intragastric pressure associated with ECT); (6) administer glycopyrrolate (0.2 mg) 1-2
minutes prior to induction to reduce airway secretions and attenuate the bradycardia that
often occurs within the first few seconds of electrical stimulation (glycopyrrolate is less
likely to cross the placenta than atropine); (7) ensure left uterine displacement (required after
18 weeks gestation); (8) perform a rapid sequence induction with succinylcholine, etomidate,and cricoid pressure (Etomidate produces a longer seizure duration, but may result in
myoclonus, more severe postictal hypertension, and delayed recovery. Other options include
Methohexital and Propofol.); (9) place an ETT; (10) insert a bite guard; (11) moderately
hyperventilate the patient to enhance the quality and duration of seizures; and (12) administer
labetalol with the initiation of generalized seizure to attenuate the hypertension and
tachycardia that often occurs secondary to seizure-induced activation of the sympathetic
system (although esmolol may have a lesser effect on seizure duration, its use in pregnancy is
controversial secondary to an association with fetal bradycardia and maternal hypotension).
Following the procedure, I would (13) extubate the patient when fully awake and (14)
monitor the patient postoperatively for uterine contractions, decreased fetal heart rate, and
vaginal bleeding.

Question 24

Would you perform a rapid sequence induction for ECT in this pt, or could you just mask?

Answer 24

Although this procedure is often performed with mask ventilation, I would
perform a rapid sequence induction in this case due to her increased risk for aspiration
secondary to the increases in intragastric pressure that occur with ECT, her diabetes
(potential diabetic autonomic neuropathy), and the physiologic changes associated with
pregnancy, such as progesterone-induced reductions in lower esophageal sphincter tone,
increased intragastric pressure (secondary to increasing uterine size), delayed gastric
emptying, and the mechanical effects of the gravid uterus on the gastro-esophageal junction.
However, since initial ECT therapy often occurs three times per week (as opposed to
maintenance therapy, which would occur less frequently), I recognize that repeated
intubations place her at increased risk for airway trauma and/or edema. Therefore, I would
make every effort to place the ETT as atraumatically as possible.

Question 25

ECT:Is muscle relaxation necessary?

Answer 25

Muscle relaxation is usually employed to reduce the risk of bone fractures and
joint dislocations that may occur secondary to seizure-induced skeletal muscle contractions.
Small doses of succinylcholine (0.25 mg/kg) are usually sufficient to attenuate these muscle
contractions, while still allowing for the visual confirmation of seizure activity. When larger
doses of succinylcholine (0. 7 5-1.5 mg/kg) or nondepolarizers are utilized, seizure activity
may be confirmed by EEG or the application of a tourniquet to an extremity prior to the
administration of the muscle relaxant (allows for the visualization of tonic/clonic activity the
extremity).

Question 26

ECT: Patient is preggo: you giving toradol?

Answer 26

While ketorolac (15-30 mg IV) is sometimes utilized to reduce ECT-induced
myalgia in younger patients, I would not administer it to this patient due to the risk of
premature closure of the fetal ductus arteriosus with the administration ofNSAIDs in the
second half of pregnancy (she is in her 22”d week of gestation). Since endogenous
prostaglandins play a role in ductus patency in utero, the inhibition of prostaglandin
production by NSAIDs could result in premature closure (the risk increases even further after32 weeks gestation). Therefore, I may utilize acetaminophen or aspirin to reduce her risk of
post-ECT myalgia.)

Question 27

Post ECT:Thirty minutes following the procedure, you find the patient disoriented, unable to
follow commands, blinking rapidly, and constantly moving her feet. What would you
do?

Answer 27

Since the findings of disorientation, an inability to consistently follow
commands, and motor agitation (e.g. increased blinking and excessive foot movement) are
consistent with postictal agitation (PIA), I would administer dexmedetomidine or a small
dose of propofol. While benzodiazepines are often utilized to treat this complication, I would
prefer to avoid them in this patient due to her pregnancy.