ubp_set_4_extra_topics_copy_20190502182008

Question 1

If you had been the intensive care physician responsible for this patient with status asthmaticus four days ago, how would you have treated her condition?

(A 12-year-old female presents to the operating suite with acute appendicitis. Her parents inform you that she has severe asthma. They further report that their daughter was hospitalized and treated 4 days ago for status asthmaticus. Her lungs are currently clear to auscultation bilaterally, but she is extremely nauseous. Her current medications include dexamethasone, omalizumab, and salmeterol.)

Answer 1

When treating a patient with this life-threatening condition, I would:

1. provide supplemental oxygen to maintain the oxygen saturation above 90%;
2. administer B2-agonists (i.e. albuterol), corticosteroids (recognizing that it may take 4-6 hours to realize a therapeutic benefit), aminophylline (to induce bronchodilation, stimulate the central respiratory cycle, reduce diaphragmatic muscle fatigue, and relax vascular smooth muscles), empirical broad-spectrum antibiotics, and intravenous fluids (although the benefits of this treatment are limited);
3. order pulmonary function tests and arterial blood gases to monitor the adequacy of oxygenation, ventilation, and the patient’s response to treatment;
4. consider the addition of intravenous magnesium sulfate (for bronchodilatory affects), if the patient’s response to other bronchodilators is inadequate; and
5. consider mechanical ventilation, if the patient begins to show signs of respiratory fatigue and/or inadequate ventilation and oxygenation (PaCO2 > 50 mmHg).

Question 2

When would you intubate a patient with status asthmaticus, and what ventilator strategy would you employ?

(A 12-year-old female presents to the operating suite with acute appendicitis. Her parents inform you that she has severe asthma. They further report that their daughter was hospitalized and treated 4 days ago for status asthmaticus. Her lungs are currently clear to auscultation bilaterally, but she is extremely nauseous. Her current medications include dexamethasone, omalizumab, and salmeterol.)

Answer 2

I would consider intubation and the initiation of mechanical ventilation if the patient began to show signs of respiratory fatigue and/or inadequate ventilation and oxygenation.

Therefore, I would monitor the patient’s response to therapy using pulmonary function tests and arterial blood gases.

If pulmonary function testing showed a FEV₁ or peak expiratory flow rate = 25% of normal, or if arterial blood gases showed a PaCO2 > 50 mmHg, despite aggressive therapy, I would intubate the patient and initiate mechanical ventilation.

My goals during mechanical ventilation are to decrease the work of breathing, maintain adequate oxygenation, and augment alveolar ventilation without causing intrinsic lung injury.

Therefore, I would employ a pressure control mode of ventilation, recognizing that the decelerating flow pattern associated with this mode of ventilation will more efficiently overcome the high resistance of the asthmatic’s airways, minimize the peak pressures required to deliver a given tidal volume, and improve the distribution of ventilation.

Moreover, I would establish a prolonged expiratory phase to allow for complete exhalation and to avoid auto-PEEP (breath stacking), which can result in barotrauma.

When the patient’s FEV₁ or peak expiratory flow rates increased to >/= 50% of normal, I would initiate weaning from mechanical ventilation.

Question 3

Ok. Back to our current situation, with the patient having been discharged from the hospital several days ago and now presenting to the operating suite with acute appendicitis.

How would you assess this patient’s asthmatic condition, pre-operatively?

(A 12-year-old female presents to the operating suite with acute appendicitis. Her parents inform you that she has severe asthma. They further report that their daughter was hospitalized and treated 4 days ago for status asthmaticus. Her lungs are currently clear to auscultation bilaterally, but she is extremely nauseous. Her current medications include dexamethasone, omalizumab, and salmeterol.)

Answer 3

I would first perform a careful history, focusing on the severity and characteristics of her pulmonary disease, along with the effectiveness of her current therapy.

To this end, I would attempt to elicit information concerning the –

• age of onset,
• triggering events,
• allergies,
• recent respiratory infection,
• changes in symptomatology (cough, sputum, wheezing, etc.),
• current medications,
• anesthetic history, and
• her recent hospital course.

Next, I would perform a physical exam to identify any pulmonary wheezing or crepitations and/or the use of accessory muscle of respiration.

Considering the severity of her disease, I would order:

1. pulmonary function tests, before and after bronchodilator therapy, to more accurately assess the severity of obstruction and her response to therapy;
2. arterial blood gases, to evaluate the adequacy of ventilaton/oxygenation and to establish baseline levels (helpful in the event of subsequent respiratory dysfunction); and
3. chest x-rays, to identify or rule out pulmonary infection.

Question 4

How would you prepare her for emergent surgery?

(A 12-year-old female presents to the operating suite with acute appendicitis. Her parents inform you that she has severe asthma. They further report that their daughter was hospitalized and treated 4 days ago for status asthmaticus. Her lungs are currently clear to auscultation bilaterally, but she is extremely nauseous. Her current medications include dexamethasone, omalizumab, and salmeterol.)

Answer 4

My goals in preparing this patient for surgery are to optimize her asthma, control her pain, reduce her anxiety, and minimize the risk of aspiration.

Therefore, I would reassure the patient and family, continue her current medications, and consider chest physiotherapy.

Moreover, I would administer –

• fentanyl, to avoid the pulmonary splinting, decreased ability to cough, and bronchospasm potentially associated with pain (avoid narcotics that release histamine and carefully titrate to avoid respiratory depression);
• diphenhydramine (an H1-receptor blocker), to inhibit histamine-induced bronchoconstriction and reduce the potential for anxiety-induced bronchospasm; a
• stress dose of hydrocortisone (100 mg), given the potential for hypothalamic-pituitary-adrenal suppression with chronic steroid treatment (she is being treated with dexamethasone);
• metoclopramide, to facilitate stomach emptying; and
• ondansetron, to treat her nausea.

Just prior to induction, I would administer –

• a short acting B2-agonist (i.e. albuterol), to minimize the risk of bronchoconstriction during intubation.

Question 5

Would you give atropine, pre-operatively?

(A 12-year-old female presents to the operating suite with acute appendicitis. Her parents inform you that she has severe asthma. They further report that their daughter was hospitalized and treated 4 days ago for status asthmaticus. Her lungs are currently clear to auscultation bilaterally, but she is extremely nauseous. Her current medications include dexamethasone, omalizumab, and salmeterol.)

Answer 5

Anticholinergic medications may be beneficial for asthmatic patients secondary to reduced mucous gland secretions (possibly improving inflammation) and airway hyperreactivity (secondary to reduced vagal tone and inhibition of muscarinic cholinergic receptors).

However, their preoperative administration is controversial, since they could result in increased inspissation (increased viscosity and thickening of airway secretions), potentially leading to airway plugging and the initiation of an asthmatic attack.

Therefore, considering these potential complications, and recognizing that the intramuscular doses of anticholinergic medications typically used for pre-anesthetic medication are unlikely to significantly decrease her airway resistance (they would be sufficient to reduce airway secretions), I would NOT administer this medication pre-operatively.

If I wanted to administer an anticholinergic, preoperatively, to optimize his asthmatic condition, I would consider providing an inhaled medication, such as ipratropium.

Question 6

You are planning general anesthesia for the procedure. How will you induce her?

(A 12-year-old female presents to the operating suite with acute appendicitis. Her parents inform you that she has severe asthma. They further report that their daughter was hospitalized and treated 4 days ago for status asthmaticus. Her lungs are currently clear to auscultation bilaterally, but she is extremely nauseous. Her current medications include dexamethasone, omalizumab, and salmeterol.)

Answer 6

My goals when inducing this severely asthmatic patient with a full stomach and nausea, are to achieve an adequate plane of anesthesia to avoid bronchoconstriction in response to mechanical stimulation while, at the same time, minimizing the risk of aspiration.

Therefore, assuming her airway exam were reassuring, I would:

1. administer a short acting B2-agonist;
2. denitrogenate with 100% oxygen;
3. ensure that she had received metoclopramide and ondansetron to facilitate gastric emptying and treat her nausea, respectively;
4. administer 2 mcg/kg of fentanyl, 2-3 minutes prior to induction, to avoid light anesthesia during laryngoscopy;
5. give 1-2 mg/kg of intravenous lidocaine, 1-2 minutes prior to induction, to prevent reflex-induced bronchoconstriction
   
   • (Topical lidocaine may also be used, but the application may provoke bronchospasm if the depth of anesthesia is insufficient. Since there is significant risk for light anesthesia during a RSI, I would not employ this technique.);
6. apply cricoid pressure; and
7. perform a RSI using ketamine (induces bronchodilation), propofol (produces bronchdilation and a more reliable depth of anesthesia as compared to thiopental), and succinylcholine.
   
   • While succinylcholine could potentially result in significant histamine release (risk for histamine-induced bronchospasm), I believe that its ability to facilitate the rapid placement of an endotracheal tube is important to reduce the risk of aspiration in this patient presenting for emergent surgery (inadequate fasting), an acute abdominal process (delayed gastric emptying), and active nausea.

Question 7

How does shock wave lithotripsy disintegrate renal calculi without causing an unacceptable amount of tissue damage?

(A 64-year-old man with an automatic internal cardiac defibrillator (AICD) and pacemaker is scheduled for extracorporeal shock wave lithotripsy (ESWL) of right renal calculi. Your hospital utilizes a first-generation lithotripter.)

Answer 7

During ESWL, the sudden vaporization of water by an energy source generates a pressure wave that is focused (F2 focal zone) on the urinary stone.

When this generated shock wave encounters a sudden change in impedance, such as occurs at the tissue-stone interface, compressive energy is released causing shear forces on the stone.

Since the acoustic impedance of water and body tissues is similar, the shock wave travels through body tissues without a significant dissipation of energy, causing minimal tissue damage.

However, some signs of tissue injury, such as skin bruising, flank ecchymosis, and hematuria (secondary to endothelial injury to the kidney and ureter), do commonly occur (especially with the more powerful first generation lithotripters).

Moreover, when the shock waves are focused on an air-tissue interface, such as found in the lungs or intestine, the difference in acoustic impedance can lead to a dissipation of energy and significant tissue damage.

Question 8

How would you provide anesthesia for this case?

(A 64-year-old man with an automatic internal cardiac defibrillator (AICD) and pacemaker is scheduled for extracorporeal shock wave lithotripsy (ESWL) of right renal calculi. Your hospital utilizes a first-generation lithotripter.)

Answer 8

While intravenous analgesia and sedation are usually adequate for procedures performed with second and third generation lithotripters, the increased discomfort associated with the more powerful first-generation lithotripters often requires general anesthesia, neuraxial anesthesia, or flank infiltration with/without intercostal blocks.

Therefore, considering the advantages of general anesthesia (when compared to neuraxial anesthesia), such as – rapid onset, reduced diaphragmatic excursion (less stone movement with respiration), and quicker recovery, my preference would be to provide general anesthesia for this procedure.

In choosing this technique, I would recognize that his lack of consciousness increases the risk of – positional injury (due to patient positioning in the bath while unconscious), and complicates patient transport to other locations for adjunctive procedures, such as cystoscopy or stent placement (which are sometimes necessary).

Question 9

Would your anesthetic plan change if the patient had a Mallampati III airway?

(A 64-year-old man with an automatic internal cardiac defibrillator (AICD) and pacemaker is scheduled for extracorporeal shock wave lithotripsy (ESWL) of right renal calculi. Your hospital utilizes a first-generation lithotripter.)

Answer 9

If I were concerned about difficult airway management, I would consider utilizing an epidural or spinal anesthetic for the procedure.
Either one of these choices eliminates the need for airway manipulation and reduces the risk of peripheral nerve injury associated with positioning and transporting an unconscious patient.

The principal disadvantage of epidural anesthesia is a slow onset and recovery,

while the principal disadvantage of spinal anesthesia is the increased incidence of hypotension.

While these techniques are associated with increased diaphragmatic excursion (due to a spontaneously ventilating patient), the subsequent stone movement, in most cases, does not significantly interfere with the procedure (stone movement is usually limited to the F2 focal zone).

Question 10

Could you proceed with flank infiltration and intercostal nerve block placement?

(A 64-year-old man with an automatic internal cardiac defibrillator (AICD) and pacemaker is scheduled for extracorporeal shock wave lithotripsy (ESWL) of right renal calculi. Your hospital utilizes a first-generation lithotripter.)

Answer 10

While this technique is a viable option for the procedure,

I believe that neuraxial anesthesia would more reliably provide adequate analgesia (as compared to flank infiltration combined with intercostal nerve blocks),

thus reducing the potential necessity for additional sedation.

Since one of my principal goals in managing this patient with a potentially difficult airway is to maintain spontaneous ventilation and avoid the necessity for airway manipulation,

I would prefer to proceed with the technique that most reliably avoids the need for supplemental intravenous sedation.

Question 11

What are the risks associated with performing ESWL on a patient with an AICD?

(A 64-year-old man with an automatic internal cardiac defibrillator (AICD) and pacemaker is scheduled for extracorporeal shock wave lithotripsy (ESWL) of right renal calculi. Your hospital utilizes a first-generation lithotripter.)

Answer 11

While the overall risk is low, there is some risk that patients with a cardiac rhythm management device (CRMD),

such as a pacemaker or automatic implantable cardioverter-defibrillator (AICD),

will experience shock wave-induced intraoperative arrhythmias during ESWL (as are those with a history of arrhythmias).

Moreover, lithotripter-induced shock waves can lead to CRMD malfunction, such as – switching to magnet mode, pacing suppression, oversensing of asynchronous shocks, and damage to rate-sensing piezoelectric crystals (affects rate-responsive CRMDs).

However, as long as the CRMD generator is not located in the abdomen (usually located in the pectoral region), ESWL is not contraindicated in patients with these devices.

To minimize the risk of CRMD associated complications, I would:

1. ascertain the indication for placement, the patient’s underlying rhythm and rate, and the degree of pacemaker dependency;
2. determine the type, manufacturer, programmability, and functionality of the device (i.e battery life, lead integrity, the presence of any alert status, and sensing/pacing thresholds);
3. verify the behavior of the device when exposed to a magnet (usually disables tachydysrhythmia detection and therapy);
4. ensure the availability of a programming device, trained pacemaker programmer, and alternative pacing modality in the operating room;
5. make sure that the patient’s CRMD is not in the shock wave path (the focal point of the lithotripter should be kept at least six inches away from the pacemaker);
6. employ continuous telemetry;
7. begin lithotripsy with low energy shock waves followed by gradually increasing energy levels, while closely monitoring pacemaker function;
8. terminate lithotripsy if the patient developed an arrhythmia; and
9. use a magnet only if there were inhibition of the device’s pacemaker function.

I would NOT require preoperative interrogation as long as his device had been checked within the last 6 months

(Recommendation: implantable cardioverter-defibrillators should ideally be checked within last 6 months, and pacemakers within the last 12 months).

Moreover, given the low risk that the acoustic pulse from the lithotripter will interfere with his CRMD, I would NOT require preoperative reprogramming to disable tachyarrhythmia sensing and treatment, or that his device was set to asynchronous mode.

In this case, interrogation would only be necessary if the patient experienced device-related complications.

Question 12

Postoperatively his hemoglobin has dropped from 14 mg/dL to 10.4 mg/dL.

Are you concerned?

What do you think is the cause?

(A 64-year-old man with an automatic internal cardiac defibrillator (AICD) and pacemaker is scheduled for extracorporeal shock wave lithotripsy (ESWL) of right renal calculi. Your hospital utilizes a first-generation lithotripter.)

Answer 12

A drop of 3.6 mg/dL in the hemoglobin concentration is significant, and would elevate my suspicion of intra-abdominal or retroperitoneal hemorrhage.

In evaluating his progressive anemia, I would –

examine the patient’s abdomen,

stabilize his hemodynamics,

look for other sources of bleeding, and

consider radiographs or CT to identify any hematoma formation.

During this evaluation, I would also –

consider other potential causes of his postoperative anemia, such as hemodilution from excessive fluid administration and/or shock wave-induced damage to the gastrointestinal, pulmonary, or urinary systems.

Question 13

Does she need further cardiac evaluation prior to surgery?

(A 34-year-old female with a history of mitral valve prolapse (MVP) is scheduled for shoulder arthroscopy in the sitting position. She is otherwise healthy and taking no medications.)

Answer 13

The presence of asymptomatic mitral valve prolapse uncomplicated by other medical conditions is not a sufficient reason for further cardiac testing.

However, if her MVP were associated with significant mitral regurgitation, syncope, chest pain, or symptoms of congestive heart failure, further testing may be warranted.

Therefore, I would begin by performing a focused history and physical exam to illicit signs and symptoms of congestive heart failure or myocardial ischemia such as angina, orthopnea, dyspnea on exertion, exercise tolerance, peripheral edema, pulmonary rales, S3 gallop, systolic ejection click, or murmur.

If she reported significant symptomatology that was insufficiently evaluated by previous cardiac workup, I would consider pre-operative echocardiographic evaluation.

Cardiac echocardiography would be helpful in identifying any mitral regurgitation and the presence or absence of a patent foramen ovale, with the latter being important due to the increased risk of air embolism when undergoing surgery in the sitting position (in the presence of a patent foramen ovale, an air embolism may pass into the coronary or cerebral circulations).

Question 14

After induction the patient is placed in the sitting position.

Her blood pressure drops to 63/38 and heart rate is 90.

What do you think is the cause?

(A 72-year-old female undergoing CABG is about to go on bypass. The patient was given a standard heparin dose, but the ACT is still low.)

Answer 14

Since normal autonomic responses may be impaired under general anesthesia, her hypotension may simply represent an uncompensated decrease in blood pressure with movement into the head-up position.

However, I would also consider potential contributing factors, such as –

• hypovolemia;
• the systemic vasodilation and myocardial depression associated with excessive anesthesia;
• dysrhythmias (often associated with MVP); and
• the development of acute mitral regurgitation and decreased cardiac output.

The latter may occur because patients with MVP often experience worsening prolapsed and/or mitral regurgitation with increased emptying of the left ventricle.

Therefore, factors such as –

• tachycardia (decreased filling time),
• increased myocardial contractility (sympathetic stimulation and inotrope administration),
• decreased systemic vascular resistance (decreased afterload),
• hypovolemia (reduced filling), and
• assumption of the upright posture (decreased filling)
  
  • may result in –
    
    • acute mitral regurgitation,
    • decreased cardiac output, and
    • hypotension.

Finally, I would consider less likely causes, such as –

• myocardial ischemia,
• tension pneumothorax, and
• pulmonary embolism.

Question 15

How would you treat this patient?

(A 72-year-old female undergoing CABG is about to go on bypass. The patient was given a standard heparin dose, but the ACT is still low.)

Answer 15

I would –

• inform the surgeon,
• return the patient to the supine position,
• evaluate the EKG,
• auscultate the chest for cardiac murmurs and bilateral ventilation,
• ventilate with 100% oxygen,
• give a fluid bolus,
• administer a pure alpha-1-agonist such as phenylephrine (the tachycardia associated with the administration of an indirect vasoconstrictor, such as ephedrine, may worsen mitral valve prolapse and mitral regurgitation), and
• consider reducing my anesthetic.

During treatment, I would avoid agents that would increase cardiac contractility and accentuate mitral regurgitaiton.

If she remained unstable despite these interventions, I would utilize TEE to further evaluate her cardiac condition.

Question 16

What is your differential diagnosis?

(A 34-year-old female health care worker is scheduled for an exploratory laparoscopy for a suspected tubal pregnancy. Her medical history is significant for tobacco abuse, with a 20-year history of smoking. Fifteen minutes into the procedure, her systolic blood pressure drops to 44 mmHg and her peak airway pressures increase to 52 cm H2O.)

Answer 16

Given the timing of her symptoms and the fact that she is undergoing laparoscopic surgery,

my differential would include the following:

1. upward pressure on the diaphragm and a reflex increase in vagal tone with formation of the pneumoperitoneum;
2. mainstem intubation, due to upward movement of the diaphragm during pneumoperitoneum formation;
3. tension pneumothorax, secondary to smoking-associated lung disease;
4. capnothorax, due to movement of insufflated gas into the pleural cavity (potential communication channels between the peritoneal cavity and the pleural sac may open with increased intraperitoneal pressure);
5. CO₂ embolism, with “gas lock” in the vena cava and right atrium and/or paradoxical embolism;
6. anaphylaxis, with associated bronchospasm and cardiovascular collapse;
7. severe bronchospasm (increased risk with tobacco use), with subsequent hypoxia leading to cardiovascular depression; and, if high dose narcotics have been administered,
8. stiff chest syndrome, which could lead to reduced venous return and/or hypoxia with subsequent cardiovascular depression.

Question 17

How does anaphylaxis differ from an anaphylactoid reaction?

(A 34-year-old female health care worker is scheduled for an exploratory laparoscopy for a suspected tubal pregnancy. Her medical history is significant for tobacco abuse, with a 20-year history of smoking. Fifteen minutes into the procedure, her systolic blood pressure drops to 44 mmHg and her peak airway pressures increase to 52 cm H2O.)

Answer 17

Anaphylaxis is a type 1 hypersensitivity reaction that occurs with the second exposure to an antigen that previously evoked the production of antigen-specific IgE antibodies.

Degranulation of mast cells and basophils results in the release of histamine, leukotrienes, prostaglandins, TNF, and various cytokines, with subsequent –

• increased capillary permeability (histamine, leukotrienes),
• peripheral vasodilation (histamine),
• bronchoconstriction (histamine, leukotrienes, prostaglandins),
• negative inotropy (leukotrienes), and
• coronary artery vasoconstriction (leukotrienes).

The initial manifestations of this life-threatening reaction usually occur within 10 minutes of exposure to the inciting antigen.

The clinical presentation of an anaphylactoid reaction is indistinguishable from anaphylaxis, with the primary difference being that –

mast cell and basophil degranulation is triggered by direct interaction with certain allergens, rather than by interaction with antigen-specific IgE antibodies.

Anaphylactoid reactions, therefore, do NOT require prior sensitization and produce anaphylaxis-like symptomatology in a dose-dependent manner.

Classic anaphylaxis, by contrast, does not behave in a dose-dependent manner, since the immune system is primed to recognize even minute amounts of the offending allergen and is able to amplify the reaction via IgE mediation.

Question 18

Assuming she is having a type I hypersensitivity reaction, how would you treat this condition?

(A 34-year-old female health care worker is scheduled for an exploratory laparoscopy for a suspected tubal pregnancy. Her medical history is significant for tobacco abuse, with a 20-year history of smoking. Fifteen minutes into the procedure, her systolic blood pressure drops to 44 mmHg and her peak airway pressures increase to 52 cm H2O.)

Answer 18

In managing this situation, I would – inform the surgeon and call for help;

discontinue all infusions and inhalational agents;

ventilate with 100% oxygen;

start a 1-2 liter fluid bolus (to replace intravascular volume);

infuse intravenous epinephrine (administer subcutaneously when the patient is normotensive);

administer corticosteroids (enhances B-agonist effects of other drugs and inhibits the production of leukotrienes and prostaglandins, but the effects are delayed for 4-6 hours), histamine blockers, an H2-blocker, and an inhaled B2-agonist; and

provide supportive care.

Recognizing that early intervention with intravenous epinephrine plays a critical role in reversing the life-threatening events associated with anaphylaxis, I would – double the dose of epinephrine every 1-2 minutes until a satisfactory systemic blood pressure response was achieved.

If her hypotension proved refractory, I would consider – administering bicarbonate to correct any acidemia

(acidemia attenuates the effects of epinephrine on the heart and systemic vasculature),

starting a vasopressin infusion (often used to treat refractory hypotension associated with high cardiac output), and

evaluating her cardiac function using echocardiography.

Question 19

How does epinephrine help in the treatment of anaphylaxis?

(A 34-year-old female health care worker is scheduled for an exploratory laparoscopy for a suspected tubal pregnancy. Her medical history is significant for tobacco abuse, with a 20-year history of smoking. Fifteen minutes into the procedure, her systolic blood pressure drops to 44 mmHg and her peak airway pressures increase to 52 cm H2O.)

Answer 19

Epinephrine’s alpha-agonist activity leads to vasoconstriction and reversed hypotension,

while the drug’s B-agonist activity relaxes bronchial smooth muscles and increases intracellular cAMP, with the increase in intracellular cAMP serving to restore membrane permeability and decrease the release of vasoactive mediators.

The severity of my patient’s condition would determine the dose and route of administration.

For this patient in complete cardiovascular collapse, I would start with a 100 mcg (range of 100 mcg-1 mg) intravenous dose of epinephrine.

If, however, my patient were hypotensive, but not in complete cardiovascular collapse, I would start with a 10 mcg intravenous dose of epinephrine.

Finally, if my patient were normotensive, I would avoid intravenous epinephrine and administer 0.3-0.5 mg subcutaneously.

In all cases, I would double and repeat epinephrine dosing every 1-2 minutes until I achieved an adequate cardiovascular response.

Question 20

What are the risk factors for latex allergy?

(A 34-year-old female health care worker is scheduled for an exploratory laparoscopy for a suspected tubal pregnancy. Her medical history is significant for tobacco abuse, with a 20-year history of smoking. Fifteen minutes into the procedure, her systolic blood pressure drops to 44 mmHg and her peak airway pressures increase to 52 cm H2O.)

Answer 20

The risk of latex allergy is highest in – children with spina bifida due to repeated latex exposure associated with their increased health care requirements.

Other risk factors include – congenital urinary tract abnormalities, undergoing multiple surgeries or medical procedures, and

working in the health care field or rubber industry.

Finally, patients with an allergy to certain foods containing similar allergens to those found in latex, such as – avocados, bananas, chestnuts, kiwis and passion fruit, may have antibodies that cross-react with latex.

Question 21

Are there any ways healthcare workers can reduce the risk of latex allergy?

(A 34-year-old female health care worker is scheduled for an exploratory laparoscopy for a suspected tubal pregnancy. Her medical history is significant for tobacco abuse, with a 20-year history of smoking. Fifteen minutes into the procedure, her systolic blood pressure drops to 44 mmHg and her peak airway pressures increase to 52 cm H2O.)

Answer 21

The most effective way to prevent health care workers from becoming “latex sensitive” is to reduce work-related exposure

by utilizing non-powdered latex gloves or latex-free gloves.

A healthcare worker who develops a skin rash and/or is suspected of having a latex allergy, should be referred to an allergist for further evaluation.

If a healthcare worker is diagnosed with latex allergy, then strict avoidance of latex is critical to preventing a potential anaphylactic reaction.

Question 22

How would you evaluate his hypertension?

(A 22-year-old male presents for ORIF of the wrist. His blood pressure is 164/92 mmHg.)

Answer 22

In order to further evaluate his hypertension I would:

1. perform a focused history and physical to identify the cause of his hypertension, additional cardiovascular risk factors, and any end-organ damage (i.e. left ventricular hypertrophy or a strain pattern on ECG);
2. review his current therapy;
3. obtain an ECG, electrolyte panel, blood urea nitrogen, and creatinine to further evaluate end-organ damage and identify metabolic derangements resulting from medications used in the treatment of hypertension; and,
4. if the cause of his hypertension were unknown, attempt to identify potential causes of hypertension in a young adult, such as –
   
   • pheochromocytoma,
   • hyperthyroidism,
   • coarctation of the aorta, and
   • illicit drug use (cocaine, amphetamines, steroids, etc.)

Question 23

What is your anesthetic plan?

(A 22-year-old male presents for ORIF of the wrist. His blood pressure is 164/92 mmHg.)

Answer 23

If there were no contraindications, my plan would be to perform an axillary block, which is easy to perform, provides complete anesthesia at the wrist, and has a low complication rate.

As with any regional block, I would discuss the risks with the patient, including the possibility of sedation and conversion to a general anesthetic, should the block be inadequate.

Question 24

How would you perform an axillary block?

(A 22-year-old male presents for ORIF of the wrist. His blood pressure is 164/92 mmHg.)

Answer 24

I would place the patient in the supine position with the arm abducted and the elbow flexed at 90 degrees.

Next, I would prep and drape the axillary area in a sterile fashion, use ultrasound to identify the axillary artery and fascial sheath, insert a 22 gauge short bevel needle into the nerve sheath under ultrasound guidance, aspirate to ensure extravascular needle placement, and inject 15-20cc of local anesthetic.

I would then identify the musculocutaneous nerve within the coracobrachialis muscle and inject 5cc of local anesthetic next to the nerve.

If a tourniquet was required for the surgery, I would perform a subcutaneous field block just distal to the axilla to block the medial brachial cutaneous and intercostobrachial nerves.

Question 25

What are the complications associated with an axillary block?

(A 22-year-old male presents for ORIF of the wrist. His blood pressure is 164/92 mmHg.)

Answer 25

While the axillary approach to a brachial plexus block is associated with a very low complication rate, there are potential complications, including –

• intravascular injection,
• hematoma,
• infection, and
• block failure.

Question 26

Which nerve is most commonly missed?

(A 22-year-old male presents for ORIF of the wrist. His blood pressure is 164/92 mmHg.)

Answer 26

The musculocutaneous nerve, which provides motor innervation to the biceps muscle and sensory innervation to the lateral aspect of the forearm, has already left the sheath at the level of the axilla and, subsequently, is the most commonly missed.

Adequate blockade of the musculocutaneous nerve is achieved by injecting 5cc of local anesthetic into the coracobrachialis muscle.

Question 27

What do you think is the cause?

(A 72-year-old female undergoing CABG is about to go on bypass. The patient was given a standard heparin dose, but the ACT is still low.)

Answer 27

There are several possibilities, including –

• administration of the wrong medication,
• an insufficient dose of heparin,
• infiltration of the IV,
• inaccurate ACT measurement (machine malfunction), and
• heparin resistance.

Heparin resistance can be due to –

• Antithrombin III deficiency, which may result from –
  
  • inherited defects in production,
  • excessive loss (e.g. nephrotic syndrome), or
  • excess consumption (e.g., sepsis, trauma).

If Antithrombin III deficiency was thought to be the problem, then the treatment would be –

• to administer FFP.

Question 28

Why give FFP?

(A 72-year-old female undergoing CABG is about to go on bypass. The patient was given a standard heparin dose, but the ACT is still low.)

Answer 28

If I suspected that the ACT was low due to an insufficient antithrombin III, I would administer FFP to correct this deficiency.

Antithrombin III = is a serine protease that contributes to anticoagulation by irreversibly binding to thrombin and factors X, XI, XII, and XIII.

Heparin exerts its anticoagulant effect by complexing with antithrombin III and enhancing its activity 1000 fold.

Therefore, in the presence of an antithrombin III deficiency, heparin is ineffective in producing adequate anticoagulation.

(Note to self – what about giving Antithrombin III as a treatment???)

Question 29

After coming off bypass, the patient is given protamine for heparin reversal at 1:1 Ratio.

Suddenly the blood pressure drops to 61/28 mmHg and the pulmonary artery (PA) pressure increases.

What do you think might be happening?

(A 72-year-old female undergoing CABG is about to go on bypass. The patient was given a standard heparin dose, but the ACT is still low.)

Answer 29

Protamine-induced histamine release may lead to increased pulmonary vascular resistance and decreased systemic vascular resistance.

On the other hand, the increased pulmonary artery pressure may be the result of a type III protamine reaction.

In this case, protamine-heparin complex-induced release of thromboxane A2 in the pulmonary circuit, leads to increased pulmonary artery pressures with subsequent right heart failure.

Another possible cause of hypotension and increased PA pressure is left ventricular dysfunction.

(REVIEW Protamine-induced Reactions!)

Protamine Rxns (two past exams) 3 types:

1. Type 1 describes hypotension related to rapid drug administration.
   
   • This may be related to histamine release w/ vasodilation leading to mild transient decrease in BP. There is no associated negative inotropy but those w/ poor LV function may be less tolerant to decreased SVR because compensatory responses are less.
2. Type 2 describes anaphylactoid responses.
   
   • Leading to hypotension, decreased SVR, flushing edema and bronchospasm
   • This a true antibody mediated anaphylaxis (IgE) which follows previous exposure to protamine or protamine containing insulin preparations, i.e. NPH.
   • No increased risk in protamine allergic rxn in:
     
     • Vasectomized males
     • Fish allergy
3. Type 3 describes catastrophic pulmonary hypertension
   
   • This may be due to complement activation and thromboxane A2 release causing pulmonary vasoconstriction, pulmonary HTN, and bronchoconstriction.

Best initial tx of severe protamine rxn = epinephrine followed by fluids.

Question 30

What steps can you take to prevent a type III protamine reaction?

(A 72-year-old female undergoing CABG is about to go on bypass. The patient was given a standard heparin dose, but the ACT is still low.)

Answer 30

There is NO reliable way to prevent this type of reaction, but diluting the protamine (e.g., dilute in 50-100 cc and infuse via micro drip) and administering it slowly (e.g. over at least 5-10 minutes) seems a reasonable approach.

Question 31

Would you infuse protamine via pulmonary artery catheter (PAC) or inject the medicine directly in the bypass circuit?

(A 72-year-old female undergoing CABG is about to go on bypass. The patient was given a standard heparin dose, but the ACT is still low.)

Answer 31

I would NOT administer it directly into the PAC since it could cause pulmonary HTN, nor would I administer it directly into the bypass circuit because it may result in clot formation in the bypass machine.

In general, the route of administration, central vs. peripheral, does not seem to make a difference in the likelihood of adverse reactions.
However, there is some evidence that aspirin administered one week prior to CPB may be beneficial.

Question 32

What do you think is going on?

(A 64-year-old man scheduled for total knee arthroplasty receives a femoral and sciatic nerve block pre-operatively to facilitate post-operative pain control. During placement of the blocks, he becomes agitated, develops a tonic-clonic seizure, and loses consciousness.)

Answer 32

While I could consider several potential causes of these symptoms, such as –

• hypoxia,
• acidosis,
• myocardial ischemia,
• alcohol withdrawal, and
• a seizure disorder,
• the timing of the event and the progression of his symptomatology are most consistent with local anesthetic toxicity.

Recognizing that the presentation of local anesthetic toxicity is extremely variable in onset and initial symptomatology, I would consider this possibility in any situation where a patient experienced an altered mental state, neurologic symptoms, or cardiovascular instability following the administration of local anesthetic for regional anesthesia.

Question 33

What are the signs and symptoms associated with local anesthetic toxicity?

(A 64-year-old man scheduled for total knee arthroplasty receives a femoral and sciatic nerve block pre-operatively to facilitate post-operative pain control. During placement of the blocks, he becomes agitated, develops a tonic-clonic seizure, and loses consciousness.)

Answer 33

Initially, the patient developing local anesthetic toxicity may experience nonspecific neurologic symptoms such as –

• metallic taste,
• circumoral paresthesias,
• tongue numbness,
• visual disturbances (i.e. blurred vision and difficulty focusing),
• auditory disturbances (i.e. tinnitus),
• lightheadedness,
• dizziness, and
• a feeling of “impending doom”.

In the classical description, these subjective symptoms are followed by symptoms of central nervous system (CNS) excitation, such as –

• agitation,
• shivering,
• muscle twitching,
• tremors of the face and distal extremities, and
• tonic-clonic seizures (CNS excitation is thought to occur secondary to an initial blockade of inhibitory pathways in the cerebral cortex).

As toxicity increases, the patient experiences CNS depression, with subsequent resolution of seizure activity, respiratory depression, loss of consciousness, coma, and respiratory arrest (as plasma levels of local anesthetic increase, both inhibitory and excitatory CNS pathways are blocked, resulting in CNS depression).

With very high levels of toxicity, the patient may experience hypertension, tachycardia, and ventricular arrhythmias (cardiac excitation) followed by bradycardia, decreased contractility, hypotension, conduction block, and asystole (cardiac depression).

When administering local anesthetics, it is important to keep in mind that patients may progress rapidly to seizure activity and cardiac toxicity without experiencing any of the initial nonspecific neurologic symptoms, as may occur following a direct arterial injection.

Likewise, the onset of symptoms may be significantly delayed, as may be the case following tumescent procedures (delayed for over 15 minutes in some reports).

Clinical Notes:

• Direct arterial injection (especially into the carotid or vertebral arteries) may result in the rapid progression of symptoms because toxic levels of local anesthetic may be delivered to the brain before undergoing significant extraction in the lungs (which would occur following intravenous injection).
• The symptoms of local anesthetic toxicity are delayed with –
  
  • intermittent intravascular injection,
  • lower extremity injection (longer circulation time),
  • low cardiac output states (longer circulation time), and
  • delayed tissue absorption (such as may occur following a tumescent procedure).

Question 34

Are there any advantages to using ropivacaine rather than bupivacaine?

(A 64-year-old man scheduled for total knee arthroplasty receives a femoral and sciatic nerve block pre-operatively to facilitate post-operative pain control. During placement of the blocks, he becomes agitated, develops a tonic-clonic seizure, and loses consciousness.)

Answer 34

Single enantiomer derivatives of bupivacaine, such as ropivacaine and levo-bupivacaine (S stereoisomer) have been developed and utilized in an attempt to achieve lasting regional anesthesia, while avoiding the significant cardiovascular toxicity associated with racemic bupivacaine (S and R stereoisomers).

The reduced cardiotoxicity associated with these single enantiomer drugs may be due to reduced affinity for brain and myocardial tissue.

In the case of ropivacaine, the reduced cardiac depression of its propyl side chain, as compared to the butyl side chain of bupivacaine, may also play a role.

Another potential advantage of ropivacaine is the provision of similar sensory blockade in association with less extensive motor blockade, as compared to an equal dose of bupivacaine.

• Clinical Notes:*
• Cardiac Toxicity: Lidocaine < Ropivacaine < Bupivacaine

Question 35

Does the addition of epinephrine reduce the risk of local anesthetic toxicity?

(A 64-year-old man scheduled for total knee arthroplasty receives a femoral and sciatic nerve block pre-operatively to facilitate post-operative pain control. During placement of the blocks, he becomes agitated, develops a tonic-clonic seizure, and loses consciousness.)

Answer 35

The addition of epinephrine may reduce the risk of local anesthetic toxicity by –

• reducing systemic absorption (secondary to vasoconstriction) and/or
• helping to identify unintended intravascular injection (i.e. an increase in heart rate of 10 beats/minute or an increase in systolic pressure of > 15 mmHg).

However, there is some evidence that this may be accompanied by – an undesirable reduction in the seizure threshold for intravenous local anesthetics (rat studies).

This reduction in the seizure threshold may be due to –

• vasoconstrictor-induced hyperdynamic circulatory changes that lead to increased delivery of local anesthetic to the brain (increased cerebral blood flow),
• disruption of the blood-brain barrier, and
• decreased clearance of local anesthetics (blood flow redistribution away from the liver).

Question 36

How do local anesthetics affect the heart?

(A 64-year-old man scheduled for total knee arthroplasty receives a femoral and sciatic nerve block pre-operatively to facilitate post-operative pain control. During placement of the blocks, he becomes agitated, develops a tonic-clonic seizure, and loses consciousness.)

Answer 36

The inhibition of voltage-gated sodium channels results in the following direct cardiac effects:

1. slowed cardiac conduction (increased PR-interval and widened QRS complex),
2. decreased rate of depolarization (secondary to a reduction in availability of the fast sodium channels that allow the rapid sodium influx required for membrane depolarization),
3. a dose-dependent reduction in cardiac contractility (potentially contributing to hypotension, metabolic acidosis, and reduced clearance of local anesthetic), and
4. depressed spontaneous pacemaker activity in the sinus node (potentially leading to bradycardia and cardiac arrest).

Peripheral vascular effects vary depending on the amount of local anesthetics in the plasma, with – –

1. low concentrations resulting in vasoconstriction and
2. high concentrations causing vasodilation.

Question 37

The patient’s blood pressure is stable, but he continues to experience seizure activity and develops stable monomorphic ventricular tachycardia.

Assuming his condition is the result of local anesthetic toxicity, what will you do?

(A 64-year-old man scheduled for total knee arthroplasty receives a femoral and sciatic nerve block pre-operatively to facilitate post-operative pain control. During placement of the blocks, he becomes agitated, develops a tonic-clonic seizure, and loses consciousness.)

Answer 37

In treating this complication, I would:

1. stop injecting local anesthetic;
2. call for help and a lipid rescue kit;
3. ensure adequate ventilation and oxygenation to correct and/or avoid factors that enhance the systemic toxicity of local anesthetics, such as –
   
   • hypercarbia
     
     • (increased cerebral blood flow, intra-neuronal ion trapping of the drug, and decreased plasma protein binding of local anesthetics),
   • acidosis
     
     • (reduces the seizure threshold and decreases plasma protein binding of local anesthetics), and
   • hypoxemia;
4. administer a benzodiazepine to treat his seizure
   
   • (seizure activity increases metabolism, which may lead to hypoxemia, hypercarbia, and acidosis);
5. administer succinylcholine and intubate the patient if –
   
   • ventilation were inadequate,
   • the risk of aspiration was significant (history of GERD or hiatal hernia), or
   • if tonic-clonic movements persisted despite benzodiazepine administration (while succinylcholine would minimize the metabolic acidosis associated with seizure-induced muscle activity, it would not affect the acidosis that develops secondary to seizure-induced increases in cerebral metabolism;
6. initiate lipid emulsion therapy with a bolus of 1.5 mL/kg of 20% lipid solution (roughly 100 mL in adults) and a continuous infusion at 0.25 mL/kg/minute, with plans to discontinue the infusion only after establishing hemodynamic stability for at least 10 minutes
   
   • (repeat bolus and double infusion rate every 5 minutes as necessary,
   • keeping in mind that the recommended upper limit for initial dosing is 10 mL/kg for 30 minutes);
7. administer adenosine and/or amiodarone for additional treatment of his ventricular dysrhythmia
   
   • (procainamide, lidocaine, B-blockers, calcium channel blockers, and vasopressin should be avoided when treating bupivacaine-induced ventricular arrhythmias);
8. perform immediate synchronized cardioversion if the patient became unstable (assuming he remained in monomorphic VT-polymorphic VT usually requires unsynchronized shock); and
9. consider cardiopulmonary bypass if the patient’s response to these therapies was inadequate (cardiopulmonary bypass may serve as “bridging therapy” until tissue levels of local anesthetic have diminished).

Clinical Notes:

• Resuscitation drugs that deserve special consideration in association with local anesthetic toxicity include:
  
  • Epinephrine – Standard resuscitation doses of epinephrine (1 mg) are not recommended during resuscitation of a patient experiencing local anesthetic toxicity because epinephrine is highly arrhythmogenic and can reduce the efficacy of lipid rescue. Therefore, it is recommended to utilize smaller doses in this setting (< 1 mcg/kg or 10-100 mcg boluses).
  • Vasopressin – Animal studies have associated the use of vasopressin in the treatment of local anesthetic toxicity with poor outcomes and pulmonary hemorrhage. Therefore, practitioners should consider avoiding this drug in this setting.
  • Local Anesthetics – Drugs like procainamide and lidocaine should be avoided in the resuscitation of patients experiencing local anesthetic toxicity since they would exacerbate the primary cause of cardiovascular instability.
  • Calcium Channel Blockers – Calcium channel blockers should be avoided in the treatment of local anesthetic toxicity due to their effects on the cardiovascular system, such as slowed cardiac conduction, negative inotropy, and vasodilation.
  • B-blockers – B-blockers should be avoided in the treatment of local anesthetic toxicity due to the reduced blood flow to the liver (potentially reducing the metabolism of amide local anesthetics), negative inotropic effects, and negative chronotropic effects associated with their use.

Question 38

The nurse runs to get some versed.

In the meantime, you realize you have propofol at the bedside.

Could you just administer propofol to stop his seizure?

(A 64-year-old man scheduled for total knee arthroplasty receives a femoral and sciatic nerve block pre-operatively to facilitate post-operative pain control. During placement of the blocks, he becomes agitated, develops a tonic-clonic seizure, and loses consciousness.)

Answer 38

GIven the potential for cardiovascular instability in this situation,

I would NOT administer propofol.

While propofol and thiopental are acceptable alternatives to quickly stop seizure activity, they should be avoided in the setting of cardiovascular instability because of their direct cardiodepressant effects.

Furthermore, the low lipid content of propofol makes it an inappropriate substitute for lipid emulsion therapy.

Question 39

When is the appropriate time to initiate lipid emulsion therapy?

(A 64-year-old man scheduled for total knee arthroplasty receives a femoral and sciatic nerve block pre-operatively to facilitate post-operative pain control. During placement of the blocks, he becomes agitated, develops a tonic-clonic seizure, and loses consciousness.)

Answer 39

The appropriate time to initiate lipid emulsion therapy is controversial.

Since early treatment may prevent cardiovascular collapse, many practitioners believe that waiting until standard therapy has failed to initiate lipid emulsion therapy is unreasonable.

On the other hand, administering lipids at the first sign of local anesthetic toxicity would result in unnecessary treatment, since only a fraction of patients progress from the initial premonitory symptoms to severe toxicity.

Therefore, I would initiate therapy when the signs and symptoms of local anesthetic toxicity appeared to be rapidly progressing or when a patient experienced prolonged seizure activity or signs of cardiac toxicity (i.e. bradycardia, heart block, hypotension, asystole, or ventricular arrhythmia).

Clinical Note:

• Patients should be monitored for at least 30 minutes following the administration of potentially toxic doses of local anesthetic because toxicity has been reported to present longer than 15 minutes after injection (this recommendation refers to patients who have yet to develop any signs or symptoms of toxicity).
  
  • (More likely to happen in tumescent procedure)
• Patients should be monitored very closely for at least 12 hours following significant local anesthetic toxicity because local anesthetic can continue to redistribute to the circulation from tissue depots, potentially resulting in delayed recurrence of severe toxicity.

Question 40

How would you interpret this fetal heart rate (FHR) pattern?

(A 20-year-old primigravida at 38 weeks gestation presents to the labor and delivery suite with pre-eclampsia and regular contractions. The patient is admitted, and an oxytocin infusion is started to induce delivery. Several hours later, she is noted to have the following fetal heart rate pattern.)

Answer 40

Since distinct decelerations are beginning within 10-30 seconds after the beginning of each uterine contraction, and resolving within 10-30 seconds following the end of each contraction, I would – conclude that this FHR tracing is showing late decelerations.

Moreover, although the baseline heart rate is normal (110-160 bpm), fetal heart rate variability, defined as – fluctuations in the FHR of more than 2 cycles per minute, appears to be minimal (<5 bpm).

While the reduced FHR variability may be secondary to magnesium sulfate-induced central nervous system depression (the patient is most likely receiving magnesium to treat her pre-eclampsia),

this fetal heart rate tracing would be considered non-reassuring and may represent fetal distress.

Question 41

What is considered normal fetal heart rate variability, and

what is the significance of normal and abnormal FHR variability?

(A 20-year-old primigravida at 38 weeks gestation presents to the labor and delivery suite with pre-eclampsia and regular contractions. The patient is admitted, and an oxytocin infusion is started to induce delivery. Several hours later, she is noted to have the following fetal heart rate pattern.)

Answer 41

As I mentioned, baseline variability is defined as fluctuations in the fetal heart rate of more than 2 cycles per minute.

Normal FHR variability is suggestive of a normally functioning autonomic nervous system and fetal well-being (atlhough it is not always predictive of a good outcome).

Absent or persistently minimal FHR variability, on the other hand, appears to be the most significant intrapartum sign of fetal compromise.

Various factors that may cause or contribute to decreased FHR variability include – fetal hypoxia, fetal sleep state, prematurity, fetal neurologic abnormalities, fetal tachycardia, betamethasone administration, congenital abnormalities, and/or the administration of central nervous system depressants such as opioids, barbiturates, magnesium sulfate, and benzodiazepines.

• Clinical Note:*
• Absent Variability = amplitude range undetectable*
• Minimal Variability = < 5 bpm*
• Moderate Variability = 6-25 bpm*
• Marked Variability = > 25 bpm*

Question 42

What are the different types of fetal heart rate decelerations?

(A 20-year-old primigravida at 38 weeks gestation presents to the labor and delivery suite with pre-eclampsia and regular contractions. The patient is admitted, and an oxytocin infusion is started to induce delivery. Several hours later, she is noted to have the following fetal heart rate pattern.)

Answer 42

Depending on the time of onset and offset in relation to maternal contractions, fetal heart rate decelerations can be classified as – early, variable, or late.

Early (type 1) decelerations are uniform FHR decelerations that are usually less than 20 bpm below baseline and coincide with the onset and offset of uterine contractions.

• Early decelerations are most likely related to reflex vagal responses to mild hypoxia or transient increases in intracranial pressure as would occur with uterine compression of the fetal head.

Late (type 2) decelerations are gradual and uniform FHR decelerations whose onset and recovery occur around 10-30 seconds after the onset and recovery of a uterine contraction.

• These decelerations are further classified as either
  
  • reflex late decelerations
    
    • (maternal hypotension → reduced uterine blood flow → fetal hypoxia → increased vagal tone → FHR deceleration) or
  • nonreflex late decelerations
    
    • (fetal hypoxia → myocardial decompensation → increased vagal tone → FHR deceleration).
• Reflex late decelerations are usually associated with maternal hypotension and good FHR variability; while nonreflex late decelerations are associated with uteroplacental insufficiency, intrauterine growth retardation, prolonged hypoxia during pregnancy, and decreased or absent FHR variability.

Variable (type 3) decelerations are non-uniform (shape and duration) decelerations occurring variably in relationship to uterine contractions.

• These decelerations are further classified as – mild, moderate, or severe – based on their degree and duration.
• Variable decelerations are thought to result from increased vagal activity secondary to complete or partial umbilical cord occlusion.
• During the second stage of labor, dural stimulation from compression of the head may lead to increased vagal activity and variable decelerations.
• While mild to moderate variabie decelerations (> 80 bpm) are usually well tolerated, variable decelerations that are persistent, prolonged, and/or severe (< 60 bpm) may lead to fetal decompensation.

Question 43

If this FHR pattern represented late decelerations

how would you treat this patient?

(A 20-year-old primigravida at 38 weeks gestation presents to the labor and delivery suite with pre-eclampsia and regular contractions. The patient is admitted, and an oxytocin infusion is started to induce delivery. Several hours later, she is noted to have the following fetal heart rate pattern.)

Answer 43

Assuming this patient’s FHR pattern represented late decelerations I would:

1. inform the obstetrician, provide supplemental oxygen, ensure adequate uterine displacement (or even turn the patient on her side), discontinue the administration of oxytocin (a tocolytic may be considered in the presence of tonic uterine contractions), begin a fluid bolus, and optimize maternal hemodynamics;
2. perform a careful history and physical focusing on her airway (exam, previous anesthetics, etc.), coagulation status (platelet count and trend; signs of a primary hemostatic defect – easy bruising, bleeding at IV sites, etc.), comorbidities, other complications associated with pre-eclampsia (cerebral edema - change in mental status, pulmonary edema, hypovolemia), and prenatal course;
3. discuss the obstetric plan with the obstetrician; and, assuming there were enough time and no contraindications to regional anesthesia (i.e. coagulopathy),
4. recommend the early initiation of epidural anesthesia in order to avoid the need for general anesthesia (especially if her airway was concerning).