Journal of Clinical Anesthesia (2014) 26, 410–413

Case Report

West Nile virus infection and postoperative neurological symptoms: a case report and review of the literature☆ Natalie C. Moreland MD (Instructor)a , Laura B. Hemmer MD (Assistant Professor)a,b,⁎, Antoun Koht MD (Professor)a,b,c a

Department of Anesthesiology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA Department of Neurological Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA c Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA b

Received 18 January 2013; revised 26 February 2014; accepted 27 February 2014

Keywords: West Nile fever encephalitis; West Nile fever meningitis; West Nile virus postoperative complications

Abstract The incidence of West Nile virus, which may cause a range of clinical presentations including subclinical infections, mild febrile illness, meningitis, or encephalitis, has increased over recent years. Rare complications, including optic neuritis, also have been reported. A patient who presented with preoperative asymptomatic West Nile virus developed fever, altered mental status and temporary vision loss after elective multilevel spine fusion surgery. © 2014 Elsevier Inc. All rights reserved.

1. Introduction West Nile virus is a flavivirus transmitted by infected mosquitoes that can cause West Nile fever and encephalitis. The majority of human infections are asymptomatic; however, one in 5 patients develops mild febrile illness and one in 150 patients develops meningitis or encephalitis. Rare neurologic manifestations have been reported, including ataxia, cranial nerve abnormalities, myelitis, seizures, polyradiculitis, and optic neuritis [1]. West Nile virus was first documented to infect humans in 1999 in New York State. Since 1999, the disease has progressed, with over 1,300 deaths and 12,000 ☆ Supported by departmental funding only. ⁎ Correspondence: Laura B. Hemmer, MD, Department of Anesthesiology, Northwestern University Feinberg School of Medicine, 251 East Huron St., F5-704, Chicago, IL 60611, USA. Tel: 312 695–0061. E-mail address: [email protected] (L.B. Hemmer).

http://dx.doi.org/10.1016/j.jclinane.2014.02.005 0952-8180/© 2014 Elsevier Inc. All rights reserved.

cases of meningitis or encephalitis between 1999 and 2010 [2]. As of December 2012, 5,387 cases have been reported to the Centers for Disease Control, and 2,734 (51%) of these cases were classified as neuroinvasive disease such as meningitis or encephalitis. The prevalence of disease from West Nile virus appears to be increasing, as this is the largest number of cases reported within a given year since 2003 [3]. There is a lack of literature about the implications of West Nile virus infection in the perioperative period other than infection acquired via organ transplantation surgery [4,5]. A patient with preoperative asymptomatic West Nile virus infection developed fever, altered mental status, and temporary vision loss after elective multilevel spine fusion surgery.

2. Case report A 46 year old, 79 kg woman with a history of idiopathic kyphoscoliosis, marked positive sagittal imbalance, iatro-

West Nile virus infection & neuro symptoms genic flat-back syndrome, and L5 radiculopathy presented for Stage I of a planned two-stage procedure consisting of removal of L1-L4 segmental instrumentation, placement of new segmental instrumentation from T4-S1, and left L5-S1 foraminotomy. Her past medical and surgical history included anxiety, depression, 45 pack-year smoking history, and multiple previous back fusions complicated by instrumentation failure. Her medications included aripiprazole for depression, varenicline for smoking cessation, pregabalin for chronic pain, cyclobenzaprine, oxycodone, and hydrocodone-acetaminophen. Her preoperative blood pressure (BP) was 148/86 mmHg, heart rate was 72 bpm, and room air oxygen saturation was 97%. Physical examination was remarkable only for decreased strength of the left extensor hallucis longus. Two weeks prior to her scheduled surgery, she underwent autologous blood donation, which tested positive for West Nile virus by polymerase chain reaction (PCR). She underwent repeat testing 5 days before surgery, which was again positive by PCR. The patient denied symptoms typical of West Nile virus infection, including fever, weakness, nausea, vomiting, headaches, or mental status changes at that time or in the weeks prior to surgery. An infectious disease physician recommended proceeding with the surgery because the patient was asymptomatic. Intraoperative monitors included ASA standard monitors, intra-arterial BP, central venous pressure, urine output, somatosensory evoked potentials, transcortical motor evoked potentials, and free running electromyography. General anesthesia was induced with intravenous (IV) fentanyl 200 μg, lidocaine 100 mg, propofol 200 mg, and rocuronium 50 mg. Methadone 40 mg IV was given at surgical incision, and anesthesia was maintained with approximately 0.5 minimum alveolar concentration desflurane, IV propofol infusion 30–60 μg/kg/min, and IV remifentanil infusion 0.06 - 0.12 μg/kg/min. There was no exposure to nitrous oxide. The anesthetic course was uncomplicated, and the patient was hemodynamically stable. The intraoperative vital signs are shown in Table 1. Estimated intraoperative blood loss was 3000 mL; the patient received 4000 mL of crystalloid, 2000 mL of colloid, 5 units of packed red blood cells, two units of

Table 1

Intraoperative data

Vital Sign

Mean (range)

Systolic blood pressure (mmHg) Diastolic blood pressure (mmHg) Mean arterial pressure (mmHg) Heart rate (bpm) Oxygen saturation (%) Central venous pressure (mmHg) Hemoglobin (g/dL)

108 (77–135) ⁎ 61 (42–82) 76 (56–105) 67 (50–81) 100 (98–100) 11 (6–16) 9.2 (7.5-10.0)†

⁎ Baseline blood pressure was 104/60 mmHg; † Duration of low hemoglobin of 7.5 g/dL was one hour.

411 cryoprecipitate, and one unit of platelets. Transfusion was guided by the institution’s protocol for intraoperative management of high-risk spine patients. Total surgical time was 8 hours, 46 minutes. Arterial blood gas, hemoglobin (Hb), platelets, and coagulation profile were drawn every two hours for the first 6 hours and every hour for the remaining hours during the surgery, according to the protocol [6]. The mean Hb value was 9.2 g/dL (range 7.5 - 10.0 g/dL). Lactic acid was normal throughout surgery. At the conclusion of surgery, the patient was transferred intubated and sedated to the intensive care unit. Approximately 7 hours postoperatively, the patient was febrile to 39° C. Blood and urine cultures were negative. Chest radiograph at the time of fever was not concerning for pulmonary infection, showing only patchy bibasilar airspace opacities. Antibiotics were not started and the patient’s fever resolved after approximately 12 hours. The patient’s trachea was extubated approximately 18 hours postoperatively after she was breathing spontaneously and demonstrated a leak around the endotracheal tube. After extubation, the patient was awake, following commands, and able to state her name. About 4 hours later, she developed altered mental status characterized by agitation, fluctuating alertness, and screaming “no, no, no,” for no reason. In addition, shortly after extubation the patient put her glasses on and stated, “I can’t see.” An ophthalmology consult showed a normal examination of the anterior and posterior segments and prompt pupillary response. On postoperative day 2, the patient’s vision returned. The patient underwent Stage II of her surgery 4 days later. The surgical course was significant only for a possible cerebrospinal fluid (CSF) leak, for which an external ventricular drain was placed. Cerebrospinal fluid was positive for West Nile virus IgM antibodies (4.72, reference range positive if N 1.10). Clinically, she had an uncomplicated further postoperative course and was discharged 6 days later.

3. Discussion The cause of the patient’s fever, altered mental status, and temporary vision loss is unclear. Postoperative vision loss is a rare (b 0.2%) but devastating complication of spine surgery, and is most commonly caused by ischemic optic neuropathy, central retinal artery occlusion secondary to external compression of the eye, or cortical blindness [7–12]. Of these causes, posterior ischemic optic neuropathy is the most common, and it presents with painless vision loss, afferent pupillary defect, absence of light perception, or visual field cut [12]. The pathophysiology and cause of this entity remain unknown. In the ASA Postoperative Visual Loss Registry, 96% of patients with postoperative visual loss had estimated blood loss (EBL) greater than 1,000 mL or anesthetic duration greater than 6 hours. Other risk factors may include

412 vascular risk factors such as hypertension, diabetes, coronary artery disease, obesity, tobacco use, and preoperative anemia [12,13]. Although our patient had risk factors including tobacco use, EBL greater than 1,000 mL, and anesthetic duration greater than 6 hours, the normal eye examination of the anterior and posterior segments and lack of afferent pupillary defect made injury to either optic nerve very unlikely [12]. Central retinal occlusion secondary to eye compression was unlikely because the patient was positioned in Mayfield pins. Cortical blindness also was unlikely, as there were no significant periods of hypotension or hypoxemia. Infectious causes of the patient’s fever were negative. Several of the patient's home medications have been associated with vision changes, including aripiprazole, pregabalin, cyclobenzaprine, and varenicline. However, it is unlikely that there was a pharmacologic mechanism responsible for the constellation of symptoms in this patient. West Nile virus may cause vision loss in patients with encephalitis or meningitis. The vision changes typically are temporary and are manifested as chorioretinitis with typical chorioretinal lesions, uveitis, or optic neuritis [14–19]. However, the patient had an entirely normal anterior and posterior segment ophthalmologic examination. While West Nile virus infection has not been reported to cause vision loss without an abnormal examination of the retina, the presence of CSF West Nile virus IgM antibodies supports central nervous system (CNS) infection because IgM antibodies cannot cross the blood–brain barrier. Therefore, West Nile virus infection is a possible cause of the patient’s constellation of symptoms of fever, altered mental status, and temporary vision loss [1]. With a lack of literature about the anesthetic considerations in patients with preoperative West Nile virus infection, and after consultation with an infectious diseases physician, we elected to proceed with the case because the patient was asymptomatic. Inhalational anesthetics, however, may have a depressive effect on the immune system that predisposes subclinical infection to become symptomatic. In fact, mouse experiments published by Katz et al and Ben-Nathan et al have suggested that stressors such as exposure to inhalational anesthetics cause an attenuated experimental West Nile virus strain to become neuro-invasive and lethal in mice. An immunosuppressive effect was suggested by these studies based on the decrease in spleen weight of the exposed mice [20,21]. The authors concluded that the enhanced virulence of the virus was caused by immunosuppression as opposed to a change in the virus itself. This statement is significant because the morbidity and mortality of the West Nile virus infection increase when it invades the CNS [20]. Anesthesiologists may encounter patients presenting preoperatively or postoperatively with symptomatology consistent with West Nile virus infection. Symptoms may include sudden onset of fever, malaise, nausea, vomiting, headache, myalgia, rash, cough, lymphadenopathy, mental status changes, and stiff neck after an incubation period of about 3 to 14 days [1]. Diagnosis is based on clinical

N.C. Moreland et al. suspicion and specific laboratory tests; IgM antibody to West Nile virus in serum collected within 8 to 14 days of symptom onset or IgM antibody to West Nile virus in CSF collected within 8 days of illness onset using the IgM antibodycapture, enzyme-linked immunosorbent assay (MACELISA). The diagnosis should be strongly considered in a patient over age 50 years, who presents with encephalitis or meningitis in early July to mid-November, or at any time of the year in Southern states [22]. There are also data to suggest that patients who are immunocompromised or taking immunosuppressant drugs may be at increased risk for severe disease when infected [4]. There is no definitive therapy for West Nile virus infection and treatment is largely supportive. Intravenous immunoglobulin (IVIG), however, has been used successfully for treatment of severe neuroinvasive West Nile virus infection contracted after liver transplant [5]. Although it is not possible to definitively attribute the patient’s symptoms to West Nile virus, both the presence of IgM antibodies in the CSF and the possibility of aggravation of infection secondary to stress from the perioperative period and volatile anesthetics make West Nile virus a possible etiology, as patients who are over age 50 years and/or immunocompromised are at increased risk for severe disease [5,22]. In some instances, delaying the procedure until antibodies clear, which may take up to 6 months, may be safest [1,23,24]. If there is suspicion that the patient is becoming symptomatic postoperatively, an Infectious Diseases consult should be obtained and prompt administration of IVIG considered [5].

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West Nile virus infection and postoperative neurological symptoms: a case report and review of the literature.

The incidence of West Nile virus, which may cause a range of clinical presentations including subclinical infections, mild febrile illness, meningitis...
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