THE World Health Organization estimates that 2.5 million people worldwide are infected with Taenia solium  (pork tapeworm, a platyhelminth).1,2It is the most prevalent parasitic central nervous system disease and is endemic in Africa, South and Central America, and Southeast Asia, where seroprevalence was estimated to be 4.9–24%.1,2Its occurrence is uncommon in developed countries, but there has been a significant increase in cysticercosis prevalence in United States, especially in areas where there is an increasing immigrant population from endemic areas.3 

Humans are the only definitive host of T. solium , and pigs are the common intermediate host. A human may also become an intermediate host by ano-oral contamination or eating food containing T. solium  eggs. The hatched eggs can penetrate the intestines and then hematogenously spread to somatic muscles, the eyes, and the central nervous system. There, they develop into a cysticercus, a fluid-filled cyst with an invaginated scolex, leading to cysticercosis.3,4The central nervous system is involved in 60–90% of cases. The brain parenchyma is the most commonly affected. However, the ventricular system, subarachnoid space, and basilar cisterns may be involved and lead to obstructive hydrocephalus, intracranial hypertension, seizures, or meningoencephalitis, all of which have significant anesthetic and analgesic implications for treatment of parturients during labor and delivery.3,4Furthermore, diagnosis of neurocysticercosis during pregnancy is often confounded by the fact that many of these associated symptoms, such as headache, nausea/vomiting, visual or other neurologic changes, and seizures, may occur during pregnancy and/or preeclamptic/eclamptic states and they may also be misdiagnosed as post–neuraxial anesthetic complications, such as meningitis or post–dural puncture headaches. A Medline literature search revealed no published case reports and limited information on anesthetic/analgesic management of parturients with symptomatic neurocysticercosis.

A 23-yr-old Hispanic woman, gravida 4, para 2012, at 32 weeks’ gestation presented to the emergency room with the symptom of waking up in the morning with headache and weakness in the right arm and leg. While in the emergency room, she had two episodes of witnessed tonic–clonic seizures. The seizures were treated initially with lorazepam and intravenous magnesium with the presumptive working diagnosis of eclampsia. Although drowsy, she followed commands with no further focal neurologic deficits. She denied any history of seizures, right upper quadrant pain, or visual changes. She was normotensive with no proteinuria. Her liver function and basic metabolic profile test results were normal.

On further evaluation, a noncontrast computed tomographic cranial scan was obtained, which showed evidence of a left parenchymal lesion with significant surrounding cerebral edema consistent with stroke, infection, or tumor. A subsequent magnetic resonance imaging study with and without contrast showed an 8-mm cystic lesion that was thought to be more consistent with either infectious etiology or tumor, such as glioma. Further interrogation of the patient and family revealed a history of living in Mexico on a pig farm, eating undercooked pork and dirt secondary to pica. Together with her clinical history, the diagnosis of neurocysticercosis was made after consultation with neurology, neurosurgery, neuroradiology, and infectious disease. Antihelminthics were not initiated because of possible worsening of symptoms with cyst destruction during pregnancy. Betamethasone was administered for fetal lung maturity, and dexamethasone was administered for controlling cerebral edema. Magnesium was discontinued, and phenytoin was administered, which was subsequently changed to divalproex because of recurrent seizures. Fetal heart tracing was reassuring and the biophysical profile score, a measure of fetal well-being that incorporates a nonstress test and four ultrasound variables (breathing movement, body movement, muscle tone, and amniotic fluid volume), was 8 out of 10. Two days later, the patient again had a witnessed tonic–clonic seizure necessitating an increase in the divalproex dose. The following morning, she also developed new right-sided weakness and a progressive headache. A repeated magnetic resonance imaging study showed no significant interval changes in the cranial scan and no cystic lesions in the spine or spinal cord. Furosemide and mannitol were administered to further decrease cerebral edema. A team discussion about options for delivery included vaginal delivery with passive second stage versus  a cesarean delivery because of cerebral edema and possible associated increased intracranial pressure. With continual reassuring fetal heart tracing, a cesarean delivery was planned the following morning after overnight fasting and stabilization of the patient.

With cricoid pressure applied, general anesthesia was induced for the cesarean delivery using modified rapid sequence technique with thiopental, succinylcholine, and fentanyl to blunt the sympathetic response to laryngoscopy and intubation. The maintenance anesthetic consisted of oxygen, nitrous oxide, isoflurane, and intravenous morphine. A live infant, weighing 2,081 g, was delivered with Apgar scores of 7 and 9 at 1 and 5 min. The neonate was taken to the neonatal intensive care unit, where he required nasal continuous positive airway pressure support for 6 days and eventually did well. The patient remained stable throughout the operative period and was extubated at the end of the case awake and following commands. The patient was transferred to the intensive care unit. Postoperatively, 400 mg oral albendazole twice a day was initiated in addition to ongoing antiseizure prophylaxis with 500 mg divalproex every 6 h and 4 mg dexamethasone every 12 h. On postoperative day 2, the patient experienced another seizure, but no further neurologic changes or seizures ensued, and the focal deficits present before delivery resolved. On postoperative day 4, she was discharged home in stable condition on divalproex, dexamethasone, and albendazole. She reportedly had full resolution of her neurologic symptoms and intracranial lesion after completion of her 30-day course of treatment.

Multiple neurologic disorders may complicate pregnancy, leading to seizure activity or altered mental status.5Preeclampsia and eclampsia occur in 6–8% and 0.04–0.1% of pregnancies in developed countries, respectively. However, signs of severe preeclampsia (increased blood pressure, proteinuria, and edema) may be mild or absent in up to 30% of eclamptic patients.6,7Until the diagnosis is confirmed, all new-onset seizures occurring during pregnancy should be considered eclampsia.5,6However, new onset seizures during pregnancy without increased blood pressure or proteinuria merit a full neurologic investigation to rule out cerebral, parenchymal, or metabolic diseases.

In this patient, computer tomographic and magnetic resonance imaging studies combined with clinical history led to the diagnosis of neurocysticercosis. Initial treatment is control of seizures using antiepileptic drugs. Antiinflammatory agents, although controversial, may also be used because symptoms often are caused by an inflammatory reaction to a ruptured cyst.2,4,8Although safe use of antihelminthics during pregnancy has been reported, these are often withheld until the postpartum period if symptoms are well controlled.9An increase in cerebral edema from an inflammatory reaction to cyst destruction by antihelminthics can exacerbate the neurologic symptoms in 50–80% of patients, usually occurring between days 2 and 5 after initiation.9Our patient showed exacerbation on day 2 of treatment but without further symptoms afterward. Medical or surgical treatment, such as cerebrospinal fluid diversion or cyst removal, is required if seizures are uncontrolled, if intracranial hypertension or encephalitis is present, or if the neurocysticercosis is an extraparenchymal form.8 

The location and size of the cystic lesion may preclude the use of neuraxial anesthesia because cerebral edema and mass effect may be exaggerated. The decrease in colloid oncotic pressure and increase in blood volume and cardiac output during pregnancy can further increase cerebral edema and intracranial pressure.10This patient continued to have seizures, altered mental status, and new neurologic deficits despite treatment with antiepileptics and dexamethasone. Therefore, both furosemide and mannitol were administered to reduce her cerebral edema.

Seizures, altered mental status, cerebral edema, and intracranial hypertension make the administration of neuraxial anesthesia controversial in this patient. Vaginal delivery would have required a passive second stage, which is also controversial because painful uterine contractions can increase intracranial pressure.11In other circumstances, where neurologic symptoms are well controlled or absent, vaginal delivery with epidural analgesia and passive second stage forceps-assisted delivery seems appropriate.12 

With spinal anesthesia being relatively contraindicated and after careful airway evaluation, general anesthesia was the appropriate cesarean delivery anesthetic. The goal of anesthetic induction without further increase of intracranial pressure was achieved using thiopental, opioid, and muscle relaxant together with gentle, quick laryngoscopy and intubation. Were antihypertensives needed, labetalol or esmolol would have been our first choice because they do not cause cerebral vasodilation. The use of succinylcholine is controversial, but the longer onset time of nondepolarizing muscle relaxant for induction may expose the patient to aspiration, hypoventilation, and hypercapnia. Although hyperventilation reduces intracranial pressure, normocapnia was maintained because hypocapnia and alkalosis result in the deleterious umbilical and uterine vasoconstriction with a left shift of the oxyhemoglobin dissociation curve causing fetal acidosis.13 

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