UBP 3.1 (Long Form): Obstetrics – Aortic Stenosis Flashcards

Secondary Subject -- Bacterial Endocarditis Prophylaxis / Neuraxial Anesthesia in the Anticoagulated Patient / Atrial Fibrillation / Post-Dural Puncture Headache / Perioperative Steroid Replacement / Multiple Sclerosis / Uterine Atony / Epidural or Spinal Hematoma / Pulmonary Embolism

1
Q

Intra-Operative Management:

After multiple attempts at placement, you unintentionally enter the intrathecal space with the epidural needle.

Would you place an intrathecal catheter for neuraxial anesthesia?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

While the placement of an intrathecal catheter would avoid further instrumentation and potentially reduce the risk of post-dural puncture headache

(leaving the catheter in place for 24 hours following delivery may reduce the incidence of PDPH by reducing the loss of CSF into the epidural space and by inducing an inflammatory response that promotes closure of the puncture site),

I would NOT place and utilize an intrathecal catheter for analgesia because of the increased risk of exacerbating her multiple sclerosis and due to my desire to avoid a rapid sympathectomy in a patient with preeclampsia and severe aortic stenosis.

The fact that many preeclamptic patients are hypovolemic, despite increased systemic vascular resistance, further increases my concern that a rapid sympathectomy could lead to significant hypotension with a subsequent reduction in preload (which would not be well tolerated by someone with severe aortic stenosis).

Instead, I would place an epidural catheter and make the patient aware of the risks, signs and symptoms, and therapeutic options associated with post-dural puncture headache.

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2
Q

Intra-Operative Management:

What are the signs and symptoms of post-dural puncture headache?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

The lost CSF, decreased buoyant support for the brain, and cerebral vasodilation (increased cerebral blood flow to compensate for decreased CSF) that accompanies significant dural puncture, can lead to a PDPH, the signs and symptoms of which include a frontal-occipital headache, decreased pain with recumbent positioning, nausea, vomiting, neck stiffness, back pain, photophobia, diplopia, difficulty in accommodation, tinnitus, and hearing loss.

Rarely, PDPH is associated with seizures (most likely secondary to cerebral vasospasm), abdominal pain, and diarrhea.

Loss of CSF can also lead to cranial nerve stretching with subsequent palsy.

Stretching of the sixth cranial nerve (the cranial nerve that is the most susceptible to traction) impairs eye abduction, and may result in diplopia.

Hearing loss may occur due to reduced CSF pressure and an alteration of hair cell position in the inner ear.

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3
Q

Intra-Operative Management:

You place an epidural catheter, which is working well for labor, but the baby’s heart tones are non-reassuring and the obstetrician wants to perform a cesarean section.

Would you provide any preoperative medications?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

As time permitted, I would give her:

  1. albuterol to optimize her asthmatic condition;
  2. metoclopramide, an H2-blocker, and a nonparticulate antacid to reduce the risk of aspiration pneumonitis;
  3. corticosteroid supplementation (her steroid treatment may have resulted in adrenal suppression), and
  4. consider administering a B-blocker to prevent tachycardia in this patient with severe aortic stenosis.

While the administration of a benzodiazepine would be helpful in preventing anxiety and the resultant tachycardia, placental transfer would potentially cause neonatal hypotonia.

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4
Q

Intra-Operative Management:

Would you provide perioperative steroid supplementation?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

I would provide her with steroid supplementation, since her prior treatment with exogenous steroids may have resulted in suppression of her hypothalamic-pituitary-adrenal (HPA) axis and an inability to produce adequate cortisol under the physiologic stresses experienced during the perioperative period.

Insufficient cortisol production could result in an Addisonian crisis, a life-threatening condition during which patients may experience fever, abdominal pain, dehydration, nausea and vomiting, hypoglycemia, circulatory collapse (this would be even more concerning in the setting of severe aortic stenosis), and depressed mentation.

Perioperative corticosteroid supplementation is controversial because of the questionable necessity of supplementation beyond the patient’s usual steroid dose, and due to the potential deleterious effects of supraphysiologic doses of steroids, such as infection, poor wound healing, fluid retention, electrolyte imbalances, immunosuppression, hypertension, and hyperglycemia.

However, many of these side effects are unproven and/or not clinically significant; and the risk/benefit ratio of administering supraphysiologic doses of steroids is usually considered to be small.

Therefore, assuming this patient was receiving at least the equivalent of 5 mg of prednisone per day (long term suppression of the hypothalamic-pituitary-adrenal axis is unlikely with smaller doses), I would administer 75 mg of intravenous hydrocortisone preoperatively, with a rapid taper to her usual dose in 1-2 days.

  • Clinical Note:*
  • Common Steroid Replacement Regimens
  1. 100 mg of intravenous hydrocortisone preoperatively, followed by 100 mg every 8 hours on the day of surgery.
  2. 25 mg of intravenous hydrocortisone at induction, followed by 100 mg over the next 24 hours.
  3. Minor Surgery: 25 mg of intravenous hydrocortisone preoperatively, the day of surgery. No additional tapered dosing is required.
  4. Moderate Surgery: 50-75 mg of intravenous hydrocortisone preoperatively, on the day of surgery. Tapered dosing: 50 mg intraoperatively, followed by 20 mg every 8 hours on the first day, and returning to the patient’s usual dose on day 2.
  5. Severe Surgery: 100-150 mg of intravenous hydrocortisone preoperatively, on the day of surgery. Tapered dosing: 50 mg intraoperatively, followed by 25-50 mg every 8 hours for 2 days, and returning to the patient’s usual dose on day 3.
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5
Q

Intra-Operative Management:

The baby’s heart tones go down into the 50’s for 4 minutes and the obstetrician makes the cesarean section emergent.

Would you use her neuraxial catheter for the case?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

Given my concerns about difficult airway management in this obese and pregnant patient with a Mallampati score of 3, my preference would be to utilize her epidural catheter to provide anesthesia for the cesarean section.

However, given the patient’s preeclampsia (likely hypovolemia) and the need to avoid a precipitous drop in systemic vascular resistance in the presence of severe aortic stenosis, the establishment of adequate levels of analgesia for cesarean section would likely require significantly more time than would inducing general anesthesia, placing this potentially distressed baby at increased risk.

Therefore, I would optimize the mother’s hemodynamics, ensure adequate left uterine displacement, and provide 100% oxygen, hoping to improve the baby’s condition.

If the heart tones remained down, I would perform a more thorough airway evaluation, weigh the risks of difficult airway management against the risks of delaying delivery of the baby, and make a decision to proceed with either regional or general anesthesia, always keeping in mind that the mother is my primary patient.

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6
Q

Intra-Operative Management:

Is using a higher concentration local anesthetic, as would be required for cesarean section, acceptable in a patient with multiple sclerosis?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

While there is evidence that the use of higher concentrations of local anesthetic for epidural analgesia may increase the risk of exacerbating the symptoms of multiple sclerosis,

this risk may be minimized by the usually short duration of cesarean section, which limits the progressive increase in CSF concentration of local anesthetic.

So, while the use of regional anesthesia for cesarean section in patients with multiple sclerosis is controversial, some practitioners feel that the benefits of utilizing regional anesthesia (avoidance of airway instrumentation, reduced risk of aspiration, superior post-operative analgesia, etc.) outweigh the potential risks.

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7
Q

Intra-Operative Management:

You aspirate blood through the catheter and decide to provide a general anesthetic. You are concerned about her airway, but she refuses an awake intubation.

How will you induce her?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

Given her potentially difficult airway and various comorbidities, I would:

  1. verify the presence of the appropriate lines and monitors;
  2. make sure all premedications had been given, including esmolol to prevent tachycardia during laryngoscopy (esmolol is short acting and B1-selective for asthmatic patient);
  3. ensure the presence of difficult airway equipment, external cardioversion pads (loss of the “atrial kick” is not well tolerated by patients with severe aortic stenosis), and phenylephrine (for treatment of reduced SVR);
  4. place the patient in the sniff position with adequate left uterine displacement (while reverse-trendelenburg position would also facilitate rapid intubation, it may not be tolerated due to decreased cardiac filling);
  5. apply cricoid pressure;
  6. administer a combination of ketamine and low-dose etomidate (risks sympathetic response and tachycardia, but avoids myocardial depression and reduced SVR); and
  7. rapidly secure the airway with an endotracheal tube.

My goals during induction would be to maintain spontaneous ventilation (difficult airway); avoid tachycardia, bradycardia, and/or myocardial depression (aortic stenosis); achieve an adequate depth of anesthesia to avoid bronchospasm (asthma) while maintaining SVR (aortic stenosis); and reduce the risk of aspiration (obesity and pregnancy).

  • Clinical Note:*
  • Succinylcholine would NOT be appropriate in this case due to the potential for difficult airway management and the risk of an exaggerated hyperkalemic response (secondary to upregulation of ACh receptors at the neuromuscular junction with chronic skeletal muscle weakness).
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8
Q

Intra-Operative Management:

You aspirate blood through the catheter and decide to provide a general anesthetic. You are concerned about her airway, but she refuses an awake intubation.

How will you maintain anesthesia?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

Prior to delivery of the baby, I would maintain anesthesia primarily with a volatile agent, administering narcotic only if necessary to prevent tachycardia in this patient with severe aortic stenosis (if possible, narcotics and benzodiazepines should be avoided until the baby is delivered).

Following delivery, I would maintain anesthesia and ensure amnesia by providing a low concentration of volatile agent, a small dose of benzodiazepine, and intravenous narcotics.

If I were concerned about impaired left ventricular function, I would consider avoiding volatile agents and administering higher doses of narcotics (nitrous oxide could also be utilized).

Given her severe aortic stenosis, my goal would be to maintain adequate anesthesia while avoiding myocardial depression, decreased systemic vascular resistance, tachycardia, and dysrhythmias.

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9
Q

Intra-Operative Management:

You notice ST depression on the EKG.

Would you give nitroglycerine?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

Nitroglycerine would NOT be my first choice.

While it could potentially improve coronary blood flow to more ischemic areas of the subendocardium and relieving any coronary artery spasm, it could also lead to significantly reduced preload (nitroglycerine produces significant venodilation in addition to some arterial dilation).

Although a reduction in afterload is often beneficial for patients experiencing myocardial ischemia and/or left ventricular dysfunction, the potential drop in preload secondary to venodilation may not be well tolerated by a patient with severe aortic stenosis.

Moreover, the benefits usually obtained through a reduction in afterload are limited due to the relatively fixed afterload imposed by the stenotic aortic valve.

Therefore, in the presence of systemic hypotension, I may consider the administration of a vasoconstrictor, recognizing that decreases in systemic vascular resistance are more likely to decrease coronary perfusion during diastole than to reduce myocardial oxygen demand.

In a situation where I believed a reduction in afterload would be beneficial (e.g. left ventricular dysfunction), I would consider administering nicardipine, carefully titrated to reduce afterload without significantly affecting ventricular preload (some consider nicardipine to be preferable to SNP or nitroglycerine since it results in less venodilation).

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10
Q

Intra-Operative Management:

The ST depression resolves with treatment and the baby is delivered. Following delivery, the uterus is “boggy” and the patient has lost 1400 mL of blood.

What would you do?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

First, I would verify that the patient was receiving an infusion of Pitocin, keeping in mind that Pitocin can cause peripheral vasodilation with subsequent hypotension and tachycardia, and being prepared to treat these cardiovascular effects aggressively with phenylephrine (tachycardia and hypotension significantly increase the risk of myocardial ischemia in the setting of severe aortic stenosis).

In addition, I would:

  1. apply 100% oxygen and check my monitors to ensure the patient was stable (especially the EKG and blood pressure, given this patient’s severe aortic stenosis);
  2. encourage the obstetrician to continue bimanual compression and uterine massage;
  3. verify adequate IV access and obtain a type and cross-match;
  4. order baseline coagulation studies and a complete blood count;
  5. notify the blood bank of the possible need for blood transfusion; and
  6. observe the surgical field (including the uterus, if externalized) looking for an obvious cause of continued bleeding.

If it appeared that uterine atony was the cause of continued bleeding, I would consider reducing my inhalational agent and increasing the dose of oxytocin.

If these interventions were unsuccessful or inadequate, I would consider administering a rectal dose of misoprostol (Cytotec; a prostaglandin E1 analogue; 800-1000 mcg per rectum).

Finally, if all of these measures were unsuccessful, the surgeon may have to employ an intrauterine balloon (works via tamponade; success rate up to 80%); place uterine compression sutures; ligate the internal iliac, uterine, and ovarian arteries; and/or perform an emergency hysterectomy.

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11
Q

Intra-Operative Management:

The ST depression resolves with treatment and the baby is delivered. Following delivery, the uterus is “boggy” and the patient has lost 1400 mL of blood.

Would you use any other uterotonic agents?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

Only as a last resort.

While methylergonovine (methergine), 15-methyl-prostaglandin F2-alpha (hemabate), and dinoprostone (prostaglandin E2) are often utilized in the treatment of uterine atony, I would be reluctant to administer these drugs to this patient with preeclampsia, asthma, chorioamnionitis, and severe aortic stenosis for the following reasons:

  1. methergine should be avoided, if possible, in preeclamptic patients due to the potential for exacerbated hypertension;
  2. methergine can also cause coronary artery vasoconstriction, which would not be well tolerated by this patient whose myocardial oxygen supply is already compromised, and who has already experienced significant blood loss (resulting in reduced oxygen carrying capacity);
  3. hemabate may cause bronchospasm and is relatively contraindicated in asthmatic patients; and
  4. the decreased systemic vascular resistance and tachycardia often associated with dinoprostone administration would not be well tolerated in the setting of severe aortic stenosis.
  • Clinical Note:*
  • Prostaglandins (i.e. hemabate and dinoprostone) tend to be less effective in patients with chorioamnionitis.
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12
Q

Post-Operative Management:

Five hours after pulling the epidural catheter, the patient is febrile and experiencing back pain and bilateral leg weakness.

What do you think?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

While her symptoms may be secondary to a combination of less serious conditions such as bacteremia from chorioamnionitis (fever), tissue damage with needle instrumentation (back pain), and residual epidural blockade (ongoing bilateral leg weakness), I would be concerned that they were representative of something more significant, such as relapsing multiple sclerosis or epidural/spinal hematoma.

While the exacerbations associated with multiple sclerosis are usually reduced during pregnancy, this patient’s fever (secondary to chorioamnionitis) places her at increased risk for relapse.

Likewise, the peripartum administration of anticoagulants combined with traumatic epidural catheter placement may increase her risk for epidural or spinal hematoma, especially if the plan of care deviated from ASRA recommendations.

Therefore, in order to rule out a more serious condition, I would evaluate the patient for signs and symptoms consistent with epidural/spinal hematoma, such as –

  • back pain or pressure that is severe and unrelenting,
  • tenderness over the spinous or paraspinous area,
  • bowel or bladder dysfunction,
  • progressive weakness (rather than recessive weakness),
  • paresthesias,
  • sensory deficits, and
  • unexplained fever (hers would be explained by her chorioamnionitis).

Likewise, I would look for signs and symptoms consistent with relapsing multiple sclerosis, such as –

  • paresthesias,
  • weakness,
  • sensory deficits,
  • urinary incontinence,
  • bowel retention,
  • visual and gait disturbances,
  • emotional lability, and
  • autonomic dysfunction.

While this patient’s symptoms would also be consistent with epidural/spinal abscess or meningitis, these conditions are less likely to occur so soon after neuraxial placement.

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13
Q

Post-Operative Management:

The patient subsequently develops urinary incontinence.

What will you do?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

Urinary incontinence combined with leg weakness is consistent with a relapse of her multiple sclerosis.

However, given the peripartum administration of anticoagulants, the traumatic epidural placement, and her other symptoms consistent with spinal cord compression secondary to epidural or spinal hematoma (i.e. leg weakness, back pain, and unexplained fever),

I would aggressively attempt to rule out this potentially catastrophic complication.

To this end, I would:

  1. examine the patient for tenderness over the spinous or paraspinous area;
  2. attempt to determine if her weakness was progressive, rather than recessive (recessive weakness would be more consistent with slowly resolving neuraxial blockade);
  3. obtain an MRI of the spine to identify spinal cord compression; and, if this finding was confirmed,
  4. consult a neurosurgeon for possible spinal cord decompression (which should occur within 6-12 hours in order to avoid irreversible spinal cord injury).
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14
Q

Post-Operative Management:

You determine that her urinary incontinence and leg weakness are the result of relapsing multiple sclerosis.

The obstetrician asks you when she can restart her preoperative dose of enoxaparin.

What would you tell him?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

Since this patient is receiving twice-daily dosing of enoxaparin, I would recommend that her first post-operative dose occur at least 24 hours following surgery.

Moreover, I would ensure that the epidural catheter was removed at least 2 hours prior to restarting this anticoagulant, since an indwelling catheter is contraindicated in conjunction with twice-daily dosing of enoxaparin.

I would also make it clear that the decision as to when to restart thromboprophylaxis following surgery and neuraxial instrumentation involves weighing the risks of thromboembolism against the risks of surgical bleeding and epidural/spinal hematoma.

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15
Q

Post-Operative Management:

Prior to restarting the enoxaparin, the patient becomes dyspneic.

What do you think may be the cause?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

Given this pregnant patient’s deep vein thrombosis, severe aortic stenosis, asthma, relapsing multiple sclerosis, preeclampsia, increased risk for aspiration, and recent central line placement,

my differential for her dyspnea would include:

  1. pulmonary thromboembolism (deep vein thrombosis, temporary discontinuation of enoxaparin, pregnancy, preeclampsia, and cesarean section all increase the risk);
  2. heart failure (aortic stenosis, myocardial ischemia, loss of “atrial kick” with dysrhythmia);
  3. myocardial infarction (aortic stenosis places her at increased risk);
  4. bronchospasm (asthma);
  5. tension pneumothorax (recent central line placement);
  6. pulmonary edema (preeclampsia; aortic stenosis);
  7. aspiration (pregnancy); and
  8. multiple sclerotic involvement of the brain stem (can lead to hypoxemia and respiratory failure).
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16
Q

Post-Operative Management:

How is pulmonary thromboembolism diagnosed?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

Many of the manifestations of pulmonary embolism are nonspecific, making a clinical diagnosis very difficult.

Therefore, diagnostic testing is often required in addition to clinical assessment to establish a diagnosis and initiate treatment.

Clinical signs and symptoms of pulmonary thromboembolism include:

  1. dyspnea,
  2. tachypnea,
  3. cough,
  4. hemoptysis,
  5. tachycardia,
  6. fever,
  7. accentuated or split second heart sound,
  8. pleuritic pain,
  9. localized rales,
  10. hypoxemia,
  11. hypocapnea,
  12. thrombophlebitis (unilateral extremity swelling, erythema, and tenderness),
  13. jugular venous distention (pulmonary hypertension can lead to right heart failure and jugular venous distention),
  14. hemodynamic instability,
  15. palpitations,
  16. central venous and pulmonary artery catheter changes, such as normal to low pulmonary artery occlusion pressure (<15 mmHg), increased pulmonary artery pressure, and increased central venous pressure, and
  17. EKG changes, such as new right bundle branch block, ST-T wave changes, peaked P waves, right-axis deviation, T-wave inversion, and supraventricular arrhythmias.

Diagnostic testing options include:

  1. lower extremity venous ultrasonography (for DVT),
  2. Spiral (helical) computed tomography,
  3. ventilation-perfusion scan,
  4. pulmonary angiography (gold standard),
  5. CXR (atelectasis, pleural effusion, elevated hemidiaphragm, segmental infiltrate),
  6. D-dimer assay,
  7. transthoracic echocardiography (right ventricular overload), and
  8. transesophageal echocardiography (acute right atrial and/or ventricular dilation, pulmonary artery hypertension, thrombus in pulmonary arteries).
17
Q

Post-Operative Management:

Assuming this were pulmonary embolism, how would you treat her?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

In treating her pulmonary thromboembolism, I would:

  1. apply 100% oxygen;
  2. administer inotropes and fluids using the CVP and PAC to guide therapy;
  3. provide analgesics as hemodynamically tolerated;
  4. continue monitoring with the arterial line, central venous pressure catheter, and pulmonary artery catheter;
  5. consider administering a pulmonary vasodilator, if she developed pulmonary hypertension (the phosphodiesterase inhibitors, amrinone and milrinone, cause pulmonary arterial vasodilation and improve myocardial contractility);
  6. intubate and initiate mechanical ventilation, if necessary; and
  7. transport the patient to the ICU when stable enough for transport.

While anticoagulation with unfractionated heparin or LMWH would be desirable in order to prevent the formation of new clots and limit the extension of existing clots, it may be advisable to avoid it in this case due to her recent surgery and the subsequent increased risk of bleeding.

Rather, consideration should be given to the placement of a vena-cava filter to prevent the passage of lower extremity emboli into the heart and lungs.

If she were experiencing massive pulmonary embolism with severe hemodynamic depression, severe hypoxemia, and cardiac arrest, or was unresponsive to resuscitative measures, I would employ transesophageal echocardiography and consider pulmonary embolectomy.

Given the high risk of bleeding having undergone recent surgery, I would only administer thrombolytics as a treatment of last resort.

18
Q

Post-Operative Management:

Two days later she is extubated, stable, and complaining of a headache. What do you think?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

The most common type of postpartum headache is a tension headache.

However, given her history of migraines and recent accidental dural puncture with an epidural needle, I would place migraine headache, lactation headache (patients with a history of migraine headaches sometimes experience an intense headache during breast feeding), post-dural puncture headache (PDPH), and pneumocephalus (often sudden in onset following dural puncture using air for loss of resistance; may persist for up to a week) very high on my differential.

However, I would consider the possibility that her headache was related to her preeclampsia (headache is a premonitory sign of eclampsia) or, given her recent chorioamnionitis with fever (suggestive of bacteremia), that it was associated with meningitis.

Moreover, pregnancy may increase the risk of subarachnoid hemorrhage (possibly due to increased blood volume combined with hormonally-induced changes affecting arterial integrity), while dural puncture increases the risk of subdural hematoma (leakage of CSF → decreased ICP → increased stress on cerebral bridging vessels) and cortical vein thrombosis (leakage of CSF → cerebral vasodilation and decreased ICP → predisposition to cerebral thrombosis).

Finally, I would consider other potential causes of postpartum headache, such as – caffeine withdrawal, sinusitis, cerebral ischemia/infarction, and intracranial tumor.

19
Q

Post-Operative Management:

Assuming it is a post-dural puncture headache, how would you treat her?

  • (A 28-year-old, 104 kg, G2P1 female, with premature rupture of membranes at 37 weeks gestation and preeclampsia, is being induced secondary to maternal fever, suspected chorioamnionitis, and fetal tachycardia. She is requesting an epidural for vaginal delivery.*
  • PMH: The patient developed exertional dyspnea 9 months ago secondary to worsening aortic stenosis. She was planning corrective surgery when she discovered she was pregnant. She subsequently refused any procedures, including balloon valvuloplasty, until after the baby was born. Her medical history also includes asthma, migraine headaches, multiple sclerosis, and deep vein thrombosis that developed during this pregnancy.*
  • PSH: No previous surgery*
  • Medications: Digoxin, albuterol, methylprednisolone, antibiotics, and enoxaparin 80 mg BID*
  • Allergies: NKDA*
  • PE: Vital Signs: HR 90; BP = 146/88 mmHg; R = 10; T = 38.8 °C (101.8 °F)*
  • Airway: Mallampati III*
  • Heart: RRR; 3/6 systolic ejection murmur radiating to the apex*
  • Lungs: CTA Bilaterally*
  • Extremities: Edema noted in the lower extremities*
  • ECG: NSR, Left ventricular hypertrophy*
  • Echo: Severe aortic stenosis; mean transvalvular gradient of 50 mmHg; aortic valve area of 0.7 cm2 ; EF = 50%*
  • Lab: Hgb = 12.6 g/dL; Plt = 115,000; Urinary Protein = 400 mg collected over 24 hours)*
A

I would explain that epidural blood patch is the most effective treatment for PDPH and involves the injection of 15-20 mL of her blood into the epidural space at the level of the dural puncture.

However, assuming she was receiving anticoagulants (heparin, LMWH, or warfarin) as part of her treatment for pulmonary embolism, an epidural blood patch would be inappropriate due to the increased risk for epidural or spinal hematoma.

Therefore, I would initiate more conservative treatment options such as hydration (no evidence of therapeutic benefit), caffeine, the placement of an abdominal binder (increases abdominal pressure, possibly leading to an increase in CSF pressure), and pain control.

Moreover, I would reassure her that PDPHs are self-limited and almost always resolve within a week.