UBP 1.3 (Short Form): Obstetrics – Preeclampsia/Eclampsia Flashcards
What do you think is going on with this patient?
(A 29-year-old 5’7” 105 kg G1P0 female presents at 34 weeks gestation to the obstetric floor following emergency transport from a small rural town. You enter the patient’s room to find her somewhat obtunded and uncooperative. The nurse reports that the patient’s husband found his wife unconscious on the kitchen floor. She was then taken by ambulance to her hometown hospital where she received a loading dose of magnesium and 10 mg of Ativan. The referring hospital’s E.R. physician placed a nasal “trumpet” and had her transported to your obstetric service. When family members are asked about additional medical history, they report that the patient has glucose-6-phosphate dehydrogenase deficiency (G6PD) and HIV. Vital Signs: P=83, BP=148/92 mmHg, R=16, T=37 C.)
This clinical history is consistent with an eclamptic seizure and
any seizures occurring in a pregnant patient should be considered eclampsia until proven otherwise.
However, her current condition could also have resulted from –
- medication,
- trauma,
- placental abruption
- (amniotic fluid embolism occurring with placental abruption can cause a seizure),
- encephalitis,
- epilepsy,
- meningitis,
- cerebral tumor,
- cerebral hemorrhage,
- cerebral infarction,
- hyponatremia, or
- hypoglycemia.
A careful history and physical with some basic lab work would likely help to narrow this differential.
What are the diagnostic criteria for preeclampsia?
(A 29-year-old 5’7” 105 kg G1P0 female presents at 34 weeks gestation to the obstetric floor following emergency transport from a small rural town. You enter the patient’s room to find her somewhat obtunded and uncooperative. The nurse reports that the patient’s husband found his wife unconscious on the kitchen floor. She was then taken by ambulance to her hometown hospital where she received a loading dose of magnesium and 10 mg of Ativan. The referring hospital’s E.R. physician placed a nasal “trumpet” and had her transported to your obstetric service. When family members are asked about additional medical history, they report that the patient has glucose-6-phosphate dehydrogenase deficiency (G6PD) and HIV. Vital Signs: P=83, BP=148/92 mmHg, R=16, T=37 C.)
The diagnostic criteria for mild preeclampsia includes:
- two readings of a systolic blood pressure (SBP) >/= 140 mmHg and/or a diastolic blood pressure (DBP) >/= 90 mmHg, taken 6 hours apart
- (this elevated blood pressure may be superimposed on chronic hypertension);
- proteinuria as demonstrated by a urine dipstick >/= 1+ and/or a 24-hour urine level >/= 300 mg
- (a significant increase from baseline levels may be substituted); and
- > 20 weeks gestation.
Preeclampsia is considered severe when one of the following criteria develop in the presence of preeclampsia:
- sustained SBP >/= 160 mmHg or DBP >/= 110 mmHg, while on bed rest and measured 6 hours apart;
- proteinuria >/= 5 grams (5000 mg) in a 24-hour collection and/or >/= 3+ on urine dipstick (some say that this should require 2 urine dipstick readings at least 4 hours apart);
- sudden oliguria ( < 400 mL in 24 hours), especially when associated with an elevated creatinine;
- central nervous system disturbances (i.e. headache and/or vision changes);
- pulmonary edema;
- liver dysfunction;
- epigastric or right upper quadrant pain (occurs secondary to stretching of the hepatic “Glisson’s” capsule);
- thrombocytopenia;
- HELLP
- (which can occur without proteinuria or hypertension); and
- evidence of fetal compromise (i.e., intrauterine growth restriction, oligohydramnios, nonreassuring fetal testing).
More recently the onset of preeclampsia is being used, rather than the “mild” versus “severe” classification, to determine the likely severity of the disease.
The onset of preeclampsia prior to 34 weeks gestation is associated with a more severe form of the disease, whereas the onset >/= 34 weeks is associated with less severe disease.
Other changes to the diagnostic criteria include –
- the elimination of edema as a criterion and
- the de-emphasis in the utilization of proteinuria in making management decisions beyond the initial diagnosis.
What are you going to do?
Are you concerned about her mental status?
(A 29-year-old 5’7” 105 kg G1P0 female presents at 34 weeks gestation to the obstetric floor following emergency transport from a small rural town. You enter the patient’s room to find her somewhat obtunded and uncooperative. The nurse reports that the patient’s husband found his wife unconscious on the kitchen floor. She was then taken by ambulance to her hometown hospital where she received a loading dose of magnesium and 10 mg of Ativan. The referring hospital’s E.R. physician placed a nasal “trumpet” and had her transported to your obstetric service. When family members are asked about additional medical history, they report that the patient has glucose-6-phosphate dehydrogenase deficiency (G6PD) and HIV. Vital Signs: P=83, BP=148/92 mmHg, R=16, T=37 C.)
In caring for this patient, I would:
- quickly assess the mother’s vital signs, oxygen saturation, and EKG tracing;
- ensure adequate oxygenation, uterine displacement, and intravenous access;
- evaluate the baby’s heart tones; and
- perform a quick physical exam focusing on neurologic status (mental status, signs of increased intracranial pressure, etc.), airway, cardiopulmonary function, and signs of coagulopathy.
If I felt that her mental status was significantly impaired, I would:
- secure her airway as soon as possible to reduce the risk of aspiration (mental status, pregnant, recent food ingestion?) and/or inadequate ventilation.
The maintenance of adequate ventilation is even more important in this patient with possible cerebral edema and/or intracranial hemorrhage, where the development of acidosis, hypoxia, and hypercarbia could lead to increasing intracranial pressures.
Progressive increases in ICP could, in turn, lead to further mental deterioration, placing her at ever-increasing risk of aspiration, hypoventilation, apnea, and emergent airway management.
Finally, in the setting of G6PD deficiency, the development of hypoxia and acidosis could precipitate significant hemolysis.
You decide to perform an awake fiberoptic assisted intubation.
Would you use benzocaine for topical analgesia of the airway?
(A 29-year-old 5’7” 105 kg G1P0 female presents at 34 weeks gestation to the obstetric floor following emergency transport from a small rural town. You enter the patient’s room to find her somewhat obtunded and uncooperative. The nurse reports that the patient’s husband found his wife unconscious on the kitchen floor. She was then taken by ambulance to her hometown hospital where she received a loading dose of magnesium and 10 mg of Ativan. The referring hospital’s E.R. physician placed a nasal “trumpet” and had her transported to your obstetric service. When family members are asked about additional medical history, they report that the patient has glucose-6-phosphate dehydrogenase deficiency (G6PD) and HIV. Vital Signs: P=83, BP=148/92 mmHg, R=16, T=37 C.)
While the rapid onset (< 1 minute) and short duration of action (10 minutes) of benzocaine make it a useful drug for achieving airway analgesia, I would not utilize it in this case due to the increased risk for methemoglobinemia, which would potentially confuse the clinical picture during initial airway management.
Benzocaine, like prilocaine (600 mg can lead to clinically significant methemoglobinemia), can cause methemoglobinemia (some sources say the spray should not be utilized for more than one second),
a condition that results in decreased oxygen carrying capacity and impaired oxygen delivery to tissues (oxygen/hemoglobin dissociation curve is shifted to the left).
A pulse-oximeter that compares only two wavelengths of light may provide a false reading because methemoglobin absorbs the same amount of light at both 660 nm and 960 nm (oxyhemoglobin absorbs more light at 960 nm; deoxyhemoglobin absorbs more light at 660 nm), resulting in a 1:1 absorption ratio with a corresponding saturation reading of 85%.
Moreover, even if his methemoglobin levels were not high enough to result in tissue hypoxia (<30% = no tissue hypoxia; 30-50% = signs and symptoms of tissue hypoxia; > 50% can lead to coma and death), a level greater than 10% can lead to a cyanotic appearing patient, despite an adequate measured PaO2.
This discoloration, in conjunction with a falsely reduced pulse oximetry reading, could greatly confuse the clinical picture during the initial stages of airway management.
If your patient developed methemoglobinemia, how would you treat her?
(A 29-year-old 5’7” 105 kg G1P0 female presents at 34 weeks gestation to the obstetric floor following emergency transport from a small rural town. You enter the patient’s room to find her somewhat obtunded and uncooperative. The nurse reports that the patient’s husband found his wife unconscious on the kitchen floor. She was then taken by ambulance to her hometown hospital where she received a loading dose of magnesium and 10 mg of Ativan. The referring hospital’s E.R. physician placed a nasal “trumpet” and had her transported to your obstetric service. When family members are asked about additional medical history, they report that the patient has glucose-6-phosphate dehydrogenase deficiency (G6PD) and HIV. Vital Signs: P=83, BP=148/92 mmHg, R=16, T=37 C.)
If the methemoglobinemia were mild,
- I would simply identify and avoid any additional oxidizing agent, recognizing that tissue hypoxia does not develop until the methemoglobin levels are > 30%.
If, however, the methemoglobinemia were clinically significant,
- I would not only remove the offending agent, but also
- provide 100% oxygen and
- consider an exchange transfusion.
While methylene blue is often utilized to treat significant poisoning (2 mg/kg of a 1% solution in saline over 3-5 minutes; may be repeated after 30 minutes, if necessary), I would NOT administer it to this patient with G6PD deficiency.
Methylene blue not only requires the activity of G6PD to be effective, but may induce hemolysis in patients deficient in G6PD.
You avoid using benzocaine because of your concerns about inducing methemoglobinemia.
What is glucose-6-phosphate dehydrogenase deficiency (G6PD)?
(A 29-year-old 5’7” 105 kg G1P0 female presents at 34 weeks gestation to the obstetric floor following emergency transport from a small rural town. You enter the patient’s room to find her somewhat obtunded and uncooperative. The nurse reports that the patient’s husband found his wife unconscious on the kitchen floor. She was then taken by ambulance to her hometown hospital where she received a loading dose of magnesium and 10 mg of Ativan. The referring hospital’s E.R. physician placed a nasal “trumpet” and had her transported to your obstetric service. When family members are asked about additional medical history, they report that the patient has glucose-6-phosphate dehydrogenase deficiency (G6PD) and HIV. Vital Signs: P=83, BP=148/92 mmHg, R=16, T=37 C.)
G6PD deficiency is ⇒
an enzymatic disorder that inhibits the regeneration of glutathione in red blood cells, making them more susceptible to oxidative damage, with subsequently accelerated clearance from the circulation (the half-life of affected cells is reduced from 120 days to about 60 days).
This X-linked disorder, which is primarily found in African Americans, Africans, Asians, Indians, and Mediterranean populations, can lead to – fatigue, cyanosis, jaundice, anemia, hypotension, lumbar and abdominal pain, hemolysis, hematuria, and renal failure.
Depending on the severity of the disease, affected individuals may experience – chronic hemolytic anemia, intermittent hemolysis, or hemolysis that only develops in the presence of increased oxidants and free radicals (such as those produced by infection or by ingestion of certain medications and foods).
Laboratory findings associated with G6PD deficiency include –
- normocytic anemia,
- increased serum bilirubin levels,
- an increased reticulocyte count, and
- Heinz bodies in the peripheral blood smear.
How would your anesthetic management change for a patient with G6PD deficiency?
(A 29-year-old 5’7” 105 kg G1P0 female presents at 34 weeks gestation to the obstetric floor following emergency transport from a small rural town. You enter the patient’s room to find her somewhat obtunded and uncooperative. The nurse reports that the patient’s husband found his wife unconscious on the kitchen floor. She was then taken by ambulance to her hometown hospital where she received a loading dose of magnesium and 10 mg of Ativan. The referring hospital’s E.R. physician placed a nasal “trumpet” and had her transported to your obstetric service. When family members are asked about additional medical history, they report that the patient has glucose-6-phosphate dehydrogenase deficiency (G6PD) and HIV. Vital Signs: P=83, BP=148/92 mmHg, R=16, T=37 C.)
In managing a patient with G6PD deficiency, I would:
- consider the patient’s disease history
- (i.e. hemolysis, precipitating factors, and renal failure);
- check a hematocrit and reticulocyte count, preoperatively;
- avoid drugs that induce methemoglobinemia
- (i.e. benzocaine, lidocaine, articaine, prilocaine, sodium nitroprusside, and silver nitrate), recognizing that methemoglobin produces a significant volume of potent oxidizing agents;
- avoid specific antibiotics, (i.e. nitrofurantoin, chloramphenicol, co-trimoxazole), chemicals (i.e. methylene blue), and other medications (i.e. high dose aspirin, methyldopa, hydralazine, procainamide, quinidine) that may precipitate hemolysis;
- avoid and/or treat other factors known to potentially precipitate hemolysis, such as –
- hypothermia, acidosis, hypoxia, hyperglycemia, and infection; and
- continue to monitor the patient’s hemoglobin, reticulocyte count, and urine output during the perioperative period.
Clinical Notes:
- While isoflurane, sevoflurane, diazepam, and midazolam have been demonstrated to depress G6PD activity in vitro, there has been no in vitro evidence implicating any anesthetics as hemolytic agents.
- General anesthesia may mask the initial symptoms of hemolysis, making it more difficult to identify the problem, intra-operatively.
- Therefore, it is very important to closely monitor patients with G6PD deficiency, post-operatively, for clinical and laboratory signs of hemolysis.
- Cardiopulmonary bypass has initiated hemolysis in G6PD deficient patients.
- Factors that can precipitate hemolysis include:
- Hypothermia
- Acidosis
- Hypoxia
- Blood products
- Stress
- Hyperglycemia
- Infection
- Food (Fava beans)
- Chemicals (methylene blue and antimalarial drugs)
- Drugs
- Antibiotics (nitrofurantoin, chloramphenicol, co-trimoxazole)
- Other Meds (high dose aspirin, methyldopa, hydralazine, procainamide, quinidine)
On further exam, you are unable to visualize the oropharynx due to a large and swollen tongue, and you are convinced that an awake fiberoptic intubation would prove impossible.
Given these additional findings, would you attempt to intubate her if she were spontaneously breathing?
(A 29-year-old 5’7” 105 kg G1P0 female presents at 34 weeks gestation to the obstetric floor following emergency transport from a small rural town. You enter the patient’s room to find her somewhat obtunded and uncooperative. The nurse reports that the patient’s husband found his wife unconscious on the kitchen floor. She was then taken by ambulance to her hometown hospital where she received a loading dose of magnesium and 10 mg of Ativan. The referring hospital’s E.R. physician placed a nasal “trumpet” and had her transported to your obstetric service. When family members are asked about additional medical history, they report that the patient has glucose-6-phosphate dehydrogenase deficiency (G6PD) and HIV. Vital Signs: P=83, BP=148/92 mmHg, R=16, T=37 C.)
While I could employ a “watch and wait” strategy for this spontaneously breathing patient, I would be very concerned that further deterioration of her mental status could place me in a position of managing her airway emergently (i.e. apnea).
Given the potential difficulty of managing her airway, secondary to her large and swollen tongue, obesity, presumed eclampsia (associated with increased airway edema and friability), and the physiologic changes associated with pregnancy,
I would prefer to proceed with intubation while she was still capable of spontaneous ventilation, rather than take the chance that I would be required to manage her airway under more emergent conditions, when there was insufficient time for proper preparation.
Therefore, I would proceed with ETT placement with the goals of maintaining spontaneous ventilation, avoiding aspiration, and minimizing any factors that could contribute to increasing intracranial pressures or reduced cerebral perfusion, such as hypercarbia, sympathetic stimulation, or hypotension.
With these goals in mind, and assuming an awake fiberoptic intubation were impossible, I would ensure the presence of difficult airway equipment, position the patient in 30º reverse-trendelenburg (in order to decrease the risk of aspiration, facilitate venous drainage from the intracranial compartment, improve the respiratory mechanics of this obese and pregnant patient, and facilitate rapid intubation), be prepared for an emergency tracheostomy, and apply cricoid pressure.
Since my primary goal when inducing this patient with a potentially difficult airway is to maintain spontaneous respirations, I would avoid succinylcholine (despite the risk of aspiration) and perform a slow controlled induction using ketamine, recognizing that ketamine could potentially increase the cerebral blood flow (increased ICP) and/or the regional CMRO2 (total CMRO2 is not increased) of this patient who may have elevated intracranial pressures.
Does the patient need a CT scan of her head prior to cesarean section?
(A 29-year-old 5’7” 105 kg G1P0 female presents at 34 weeks gestation to the obstetric floor following emergency transport from a small rural town. You enter the patient’s room to find her somewhat obtunded and uncooperative. The nurse reports that the patient’s husband found his wife unconscious on the kitchen floor. She was then taken by ambulance to her hometown hospital where she received a loading dose of magnesium and 10 mg of Ativan. The referring hospital’s E.R. physician placed a nasal “trumpet” and had her transported to your obstetric service. When family members are asked about additional medical history, they report that the patient has glucose-6-phosphate dehydrogenase deficiency (G6PD) and HIV. Vital Signs: P=83, BP=148/92 mmHg, R=16, T=37 C.)
If the baby’s heart tones were ok, it may be appropriate to obtain a CT of the mother’s head since, in the presence of an intracranial bleed, the patient may benefit from a neurosurgical consult and treatment prior to undergoing the stresses associated with delivery.
However, obtaining a CT scan would likely involve transporting her to a location remote to the obstetric suite.
Therefore, I would secure her airway and ensure hemodynamic stability prior to transport (the latter is not only important to the mother, but serves to optimizing uteroplacental blood flow).
Moreover, I would be prepared to quickly return to the obstetric suite should the baby’s heart tones go down.
Would you consider administering Flumazenil to see if the Ativan is the cause of her altered mental state before taking the time to send her for CT?
(A 29-year-old 5’7” 105 kg G1P0 female presents at 34 weeks gestation to the obstetric floor following emergency transport from a small rural town. You enter the patient’s room to find her somewhat obtunded and uncooperative. The nurse reports that the patient’s husband found his wife unconscious on the kitchen floor. She was then taken by ambulance to her hometown hospital where she received a loading dose of magnesium and 10 mg of Ativan. The referring hospital’s E.R. physician placed a nasal “trumpet” and had her transported to your obstetric service. When family members are asked about additional medical history, they report that the patient has glucose-6-phosphate dehydrogenase deficiency (G6PD) and HIV. Vital Signs: P=83, BP=148/92 mmHg, R=16, T=37 C.)
Despite the loading dose of magnesium, I would prefer NOT to reverse the Ativan since this may lower her seizure threshold.
While her change in mental status may be the result of the large dose of Ativan she received (the maximum dosage for acute seizure treatment should be 8 mg every 12 hours), it may also represent postictal confusion following an eclamptic seizure.
However, if it became important to rule out Ativan as the cause of her mental state, I would continue the magnesium infusion, administer Flumazenil, and be prepared to treat any resultant seizure with small doses of propofol.
The baby’s heart tones are down.
Would you consider performing the c/s prior to head CT/MRI?
(A 29-year-old 5’7” 105 kg G1P0 female presents at 34 weeks gestation to the obstetric floor following emergency transport from a small rural town. You enter the patient’s room to find her somewhat obtunded and uncooperative. The nurse reports that the patient’s husband found his wife unconscious on the kitchen floor. She was then taken by ambulance to her hometown hospital where she received a loading dose of magnesium and 10 mg of Ativan. The referring hospital’s E.R. physician placed a nasal “trumpet” and had her transported to your obstetric service. When family members are asked about additional medical history, they report that the patient has glucose-6-phosphate dehydrogenase deficiency (G6PD) and HIV. Vital Signs: P=83, BP=148/92 mmHg, R=16, T=37 C.)
If the baby’s heart tones were done, I would –
- ensure adequate blood pressure,
- apply 100% oxygen,
- verify adequate left uterine displacement, and
- proceed with the cesarean section under general anesthesia with plans to take the patient for CT as soon as the case was over.
Due to the potential for elevated ICP, general anesthesia would be provided using a high narcotic neuroprotective technique with the goal of avoiding anything that might increase ICP or compromise cerebral perfusion pressure.
I would then notify the neonatologist that I was administering a large amount of narcotics since these drugs are likely to further depress the already compromised neonate.
