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Crack Cocaine, Myocardial Infarction, and Troponin I Levels at the Time of Cesarean Delivery

Livingston, Jeffrey C. MD*; Mabie, Bill C. MD*; Ramanathan, Jaya MD

doi: 10.1097/00000539-200010000-00026
OBSTETRIC ANESTHESIA: CASE REPORT
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Implications During the peripartum period, cocaine-abusing women are highly susceptible to myocardial infarction. This report describes a case of myocardial infarction diagnosed by increased troponin I levels in a pregnant patient with a history of recent crack cocaine use and severe preeclampsia.

Departments of *Obstetrics and Gynecology and †Anesthesiology, University of Tennessee-Memphis, Memphis, Tennessee

June 5, 2000.

Address correspondence to Jaya Ramanathan, MD, Department of Anesthesiology, 877 Jefferson Ave., Sixth floor Chandler, Suite Room 631, Memphis, TN 38103.

The incidence of cocaine-induced myocardial infarction (MI) in pregnancy is unknown; however, it does occur. During the peripartum period, cocaine-abusing women are susceptible to MI caused by the effects of cocaine on a heart that is already being stressed by the physiologic and hemodynamic changes associated with pregnancy, labor, and delivery (1). The diagnosis of MI in these women is often difficult to make because the hemodynamic changes of pregnancy may mimic MI, and routine diagnostic tests may be unreliable (2). We describe a case of MI diagnosed by increased troponin I levels in a pregnant patient with a history of recent crack cocaine use and severe preeclampsia.

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Case History

The patient was a 36-yr-old, 68-kg woman who presented at 29 wk of gestation with no previous prenatal care, complaining of headache. Her two previous pregnancies, complicated by severe preeclampsia, culminated in cesarean deliveries (CS). Her anesthetic history revealed uneventful epidural and general anesthetics for her previous surgeries. She admitted to daily cocaine and ethanol use.

At admission, arterial blood pressure (BP) was 210–221/148–151 mm Hg, heart rate (HR) was 98–101 bpm, and temperature was 37.5°C. She had generalized edema and exaggerated deep tendon reflexes. Examinations of her cardiovascular and respiratory systems were unremarkable. Her urine output was >30 mL/h. Pertinent laboratory findings included 4+ proteinuria, hematocrit 29.2%, and cocaine positive urine toxicology. Serum electrolytes were sodium 134 mmol/L, potassium 4.2 mmol/L, chloride 106 mmol/L, glucose 84 mg/dL, and blood urea nitrogen 19 mg/dL. Serum creatinine 1.7 mg/dL and uric acid 8.6 mg/dL were increased. Coagulation indices were platelet count 169,000/μL, prothrombin time 10.3 s, activated partial thromboplastin time 26.9 s, international normalized ratio 0.87, and fi-brinogen 438 mg/dL. Total protein (4.8 g/dL), albumin (1.3 g/dL), and albumin- globulin ratio (0.4) were low. All hepatic enzymes were increased; alkaline phosphatase 252 U/L, serum glutamic oxaloacetic transaminase 69 U/L, and lactic dehydrogenase 454 U/L. Electrocardiogram (EKG) demonstrated left ventricular hypertrophy, nonspecific S-T and T wave abnormalities, and poor R wave progression on leads V1-4. A diagnosis of severe preeclampsia was made, and because of the severity of her symptoms, she was admitted to the obstetric intensive care unit for monitoring and treatment.

Two peripheral IV lines and a radial arterial line were inserted. IV magnesium sulfate 6 g was given as a bolus followed by an infusion at 2 g/h. BP was poorly controlled with IV hydralazine but decreased to 170–176/108–110 mm Hg after the administration of IV nicardipine 2.5 mg/h. pHa was 7.5, Paco2 32 mm Hg, Pao2 95 mm Hg, and base excess −2.0 mEq/L. After 18 h of observation, the fetal heart rate (FHR) became “nonreassuring,” and the patient was taken to the operating room for a semiurgent CS.

On arrival in the operating room, her BP was 170–176/108–110 mm Hg, and HR was 94–98 bpm. The EKG, radial arterial pressures, O2 saturation, and end-tidal CO2 were monitored continuously. After an infusion of 1000 mL of lactated Ringer’s solution, an epidural catheter was inserted at the L3-4 interspace, and 18 mL of 2% lidocaine with fentanyl 2 μg/mL was injected in 4- to 5-mL increments. Sensory level of T4 was established within 10 min. BP decreased gradually from 170/110 to 128 - 134/74–82 mm Hg. HR remained stable at 84–86 bpm. Surgery began, and 6–7 min after skin incision (approximately 30 min after the induction), the patient complained of severe chest pain, followed, after several minutes, by a decrease in BP to 100/56 mm Hg. EKG showed regular sinus rhythm with a rate of 90 bpm. The sensory level remained at T4-5. Fentanyl 50 μg and midazolam 1 mg were administered IV with relief of symptoms. After a 500-mL fluid bolus and 10 mg of IV ephedrine, BP was restored to 126–130/74–80 mm Hg, at which time the HR was 98–104 bpm. Both BP and HR remained stable for the remainder of the surgery, which lasted for 45 min. The estimated blood loss was 1000 mL. At the completion of surgery, an epidural infusion of fentanyl was begun for postoperative pain control. Two hours after delivery, the patient experienced an episode of severe chest pain, with a decrease in BP from 124/74 to105/60 mm Hg and an increase in HR from 78 to 100–110 bpm. Auscultation revealed rales at lung bases. Her 12-lead EKG failed to show any changes from admission. Chest radiograph revealed bilateral basilar effusions. CK MB level was < 0.4 EU/L (normal 0–3.3 EU/L), and troponin I level was 2.9 EU/L (normal 0–0.7 EU/L). Eight and 16 h later, troponin levels were still increased at 3.4 and 2.7 EU/L, respectively. A subsequent EKG revealed S-T segment depression in leads I, II, V4-6 (non-Q wave anterolateral ischemia). EKG changes persisted for 4 days postpartum. Echocardiogram revealed left ventricular hypertrophy, an ejection fraction of 40%–45%, and diastolic dysfunction. A technetium dipyridamole scan performed 5 days later revealed ischemia in the lateral and distal anterior regions of the myocardium with a prominent inferior apical scar. Her proteinuria resolved, and all enzyme levels normalized within 2 days after delivery. She was discharged home on hospital Day 15 with cardiology clinic follow-up. Discharge medications included atenolol 150 mg, hydrochlorothiazide 25 mg, benezapril 40 mg, and prazosin 1 mg daily. Unfortunately, a cardiac catheterization was not performed, as the patient failed to keep her follow-up appointment.

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Discussion

MI occurs in 1 in 10,000 pregnancies, usually during the third trimester or peripartum (2,3). Risk factors include advanced maternal age, cigarette smoking, cocaine use, underlying congenital or acquired cardiac disease, and atherosclerosis (2,3). Maternal mortality remains at approximately 30% (2,3). Animal studies demonstrate that cocaine produces dose and time related cardiovascular alterations (4). Physiologic and hemodynamic changes in pregnancy may predispose pregnant cocaine users to myocardial ischemia (5). In addition, cocaine abuse may lead to premature atherosclerosis, and pregnant women are more susceptible to the toxic effects of cocaine because of both increased sensitivity and altered metabolism (5). Cocaine-related MI may ensue as a result of coronary artery spasm, thrombus, or a combination of these (6). EKG changes after cocaine use include P-R, QRS, and Q-T interval prolongation, increased voltage ST-T segment, and pathologic Q wave (7,8). The diagnosis of MI in parturients is difficult, as biochemical markers such as creatinine kinase (CK) and its muscle-brain isoenzyme (CK-MB) are often increased because of uterine and placental production (9,10). Until troponin I levels became available, biochemical screening for MI had limited use during the peripartum period.

The anesthetic management in such a case is difficult. General anesthesia and tracheal intubation can cause a severe hypertensive response in cocaine-abusing patients (5). Neuraxial anesthesia may lead to severe hypotension which may not respond to ephedrine (5), and might thus require the use of neosynephrine, which might be problematic in a preeclamptic patient with a history of recent cocaine use. We chose epidural anesthesia for several reasons. In our patient, hypertension was difficult to control, and we anticipated severe hypertension in response to tracheal intubation. The coagulation indices were within acceptable limits, and there was no evidence of placental abruption. The presence of a nonreassuring FHR pattern added an extra complexity to this case but, in our opinion, did not preclude the use of regional anesthesia. Regarding our choice of local anesthetics, neither the slow onset of block associated with 0.5% bupivacaine nor the rapid onset and hypotension with 3% 2 chloroprocaine would be optimal in a patient undergoing a semiurgent CS for nonreassuring FHR. With 2% lidocaine plus fentanyl, a T4 level was established within 10 min and thus provided the speed necessary to allow for an expeditious delivery, but without a precipitous decrease in BP.

It is unclear when our patient sustained the MI. It may have been preoperatively as a result of cocaine or preeclampsia- induced vasospasm. However, there were no symptoms or signs of MI while the patient was being monitored in the intensive care unit before CS. Intraoperatively, with the cephalad spread of sensory block to T4 level, BP decreased gradually over 10–15 minutes, and there were no significant HR changes. Both BP and HR were stable before the episode of chest pain. The single episode of hypotension occurred only after the onset of chest pain, approximately 30 minutes after the establishment of a T4 block. If this patient did sustain an MI intraoperatively, we believe that it was not related to her epidural anesthetic. Although transient S-T segment changes consistent with MI can occur in 25%–60% of normal pregnancies during CS under regional anesthesia (11,12), no intraoperative EKG changes indicative of ischemia were present in our patient. It is quite possible that the MI occurred at the time of severe chest pain in the postpartum period, at which time the patient developed pulmonary edema. The lack of typical EKG changes at that time can be explained by the absence of a transmural infarction. Later on, EKG changes indicative of anterolateral ischemia were clearly evident, and these persisted for several days. It can be argued that the echocardiographic evidence of diastolic dysfunction may have been caused by the chronic increase of sympathetic tone from cocaine use. However, evidence of systolic dysfunction (ejection fraction of 40%–45%) was also present, suggesting myocardial ischemia.

Among all the biochemical markers, troponin I, a cardiac-specific protein, is superior in detecting perioperative MI (13). The cardiac troponins are more specific than CK-MB for myocardial injury (14). After myocardial injury, cardiac troponins increase within four hours and remain increased for several days (14,15) When used together, increased troponin levels and echocardiography are powerful predictors of adverse cardiac events in patients with anginal pain (15). Additionally, troponin I has a high specificity for MI, even in the presence of recent cocaine use, whereas CK-MB levels appear to be less specific than troponin in such patients (16). Maternal troponin I levels are not increased in peripartum women (17), whereas, CK and CK-MB are produced by the uterus and placenta (9,10). Other enzymes, such as serum glutamic oxaloacetic transaminase and lactic dehydrogenase, may be significantly increased in severe preeclampsia, especially in those with partial or complete hemolysis, elevated liver enzymes, and low platelet count syndrome (18) and are not useful markers for the diagnosis of adverse cardiac events in the peripartum period.

In summary, we describe a parturient with a history of recent cocaine use who developed a MI after CS for severe preeclampsia. As the routine diagnostic tests for MI are unreliable in pregnancy, troponin I levels may be superior for the diagnosis of MI in these patients.

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References

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