West Nile virus--the eye of the storm: a case study.
Mr. R is a 55-year-old construction worker who had been digging ditches much of the summer. Prior to admission, he was struck in the right thoracic region with a back hoe and thrown 10 feet. Mr. R did not lose consciousness, but did experience back pain. He promptly recovered and returned to work. Two weeks later, Mr. R awoke with tingling in his right shoulder and pain radiating down his back. He began developing progressive numbness, tingling, and weakness in his lower extremities. He presented to a chiropractor, who did not do any manipulation but rather referred him to the hospital. By the time he reached the emergency department (ED), Mr. R had difficulty walking. He also explained to the ED staff that he had recently experienced difficulty swallowing and had a hoarse voice.
Mr. R's medical history was significant for diabetes mellitus with peripheral neuropathy, as well as hypothyroidism, and a possible bleeding disorder. He had quit smoking 5 years previously after an extensive history of smoking for 35 years.
In the ED, Mr. R had diffuse weakness, 4+/5, in his legs and right arm with a C4 sensory level of decreased light touch and pinprick. In addition, he was areflexic, although this may have been secondary to his diabetes mellitus. His vital signs were within normal limits; he was afebrile and his blood pressure was 150/80 mm Hg. At that time, steroids were initiated.
Mr. R was experiencing marked weakness, altered sensation, areflexia, and swallowing difficulties. The differential diagnoses were cervical myelopathy secondary to a hematoma resulting from his recent trauma, a herniated disc or a tumor. Cervical stenosis and diabetic neuropathy could have accounted for his extremity weakness and sensory changes, but not his swallowing difficulties. Another possible diagnosis was Guillian-Barr6 Syndrome.
The initial work-up consisted of laboratory studies, lumbar puncture, and magnetic resonance imaging (MRI) of the head and cervical spine. Mr. R's metabolic panel was within normal limits with the exception of a glucose level of 162 mg/dL. The complete blood count was also within normal limits with the white blood count at 7.4 K/UL. The MRI of his head was normal, and the MRI of his cervical spine demonstrated cervical stenosis with disk protrusion at C5-6 and C6-7. However, this mild stenosis did not account for rapid onset of quadriparesis. In addition, Mr. R had significant weakness above C5, hyporeflexia, and worsening dysphagia, which prompted ongoing investigation. A lumbar puncture was performed. The cerebrospinal fluid (CSF) revealed 6 C/cmn nucleated cells with a normal differential, 18 C/cmn neutrophils, and 54% lymphocytes. The CSF glucose level was elevated at 133 mg/dL, but the protein level was normal. Mr. R's blood and CSF were sent to the state health laboratory for evaluation of West Nile virus (WNV) and St. Louis encephalitis virus.
The next day, Mr. R's respiratory status was compromised with an oxygen saturation of 86% and respiratory rate of 28. He was transferred to the intensive care unit for closer monitoring. The diagnostic work-up continued. A video swallow study showed significant aspiration with the absence of a spontaneous cough. As a result, enteral feedings were started. Also, electromyogram/nerve conduction velocities testing showed severe diffuse sensory motor polyneuropathy, which was predominantly axonal in nature. These studies, combined with Mr. R's clinical presentation of progressing quadriparesis, areflexia, and dysphagia led to a probable diagnosis of Guillian-Barr6 syndrome and plasma exchange was initiated.
Mr. R presented numerous challenges that required the care of an interdisciplinary healthcare team. His marked weakness quickly progressed to quadriplegia, causing a formerly active, healthy man to be dependent on others for all of his care. Four days into his hospitalization, Mr. R's respiratory status deteriorated requiring endotracheal intubation. A bronchoscopy revealed tracheal bronchitis with mucous plugs. His sputum cultures grew hemophilus influenza and appropriate antibiotics were started. During this time, Mr. R's blood pressure dropped requiring vasopressors for support. Mr. R was cognitively intact but was frustrated with his inability to communicate secondary to the endotracheal tube. With the help of speech therapists, Mr. R was instructed to use a communication board to express his thoughts. The nurses were very diligent in their respiratory care, suctioning frequently. A positive airflow bed was used during the acute care hospitalization. This bed allowed Mr. R to be rotated from side-to-side, which assisted in airway perfusion and skin protection. To aid in the healing process, Mr. R's nutritional status was monitored closely. The nutritional support team managed his caloric, protein, and electrolyte intake to ensure that he received adequate nutrition. During this time, his diabetes mellitus was also monitored closely. Due to the stress of the illness and the intravenous steroids, Mr. R's blood sugars were high, and required an insulin drip.
During the eighth day of Mr. R's hospitalization, the West Nile virus assay was confirmed as positive for both serum and CSE The plasma exchange was discontinued after five exchanges and a 7-day course of intravenous immunoglobulin G (IgG) was started.
Physical and occupational therapists worked closely with Mr. R throughout his hospitalization. Passive range-of-motion exercises were performed while in the intensive care unit, allowing gradual progression into a strengthening program. By the end of the second week, Mr. R was able to raise his arms off the bed and wiggle his toes. On the tenth day, due to prolonged ventilatory needs, Mr. R underwent surgery for placement of a tracheostomy and percutaneous gastrostomy tube. Mr. R continued to improve slowly and was transferred to the pulmonary unit on day 18, where he was slowly weaned from the ventilator. Within a month of his admission into the hospital, Mr. R's tracheostomy was removed and he was transferred to an inpatient rehabilitation unit. By day 33, he passed his video swallow study and was allowed to eat. Mr. R continued toward a remarkable recovery, each day growing stronger and more independent. Six weeks after the onset of WNV, Mr. R was discharged to his home with outpatient therapy.
During a telephone interview 4 months after discharge from the rehabilitation unit, Mr. R reported that he was able to ambulate with the assistance of a cane but was unable to climb stairs. In addition, Mr. R revealed that his sensory deficits have persisted. He stated that he did not have any feeling from the middle of his calves through his feet and continued to experience burning sensations in his left face and arm. The nurse discussed safety concerns with Mr. R and reminded him to check the water temperature prior to bathing and to wear warm boots when out in the cold. Mr. R received outpatient warm water therapies two times each week. The resistance of the water allowed Mr. R to regain his lower-extremity strength. Since contracting WNV, Mr. R has been on disability leave from work.
West Nile Virus
West Nile virus (WNV) is a mosquito-borne disease or arbovirus commonly found in Africa, West Asia, and the Middle East (Ben-Nathan et al., 2003). WNV emerged in the United States in the summer of 1999 in New York City. During this outbreak, 62 people presented with meningoencephalitis, and seven people died (Nash et al., 2001). The disease usually occurs in the late summer and fall when there is a plethora of mosquitoes. Birds, especially crows, and horses carry the WNV. Mosquitoes become infected with the WNV when feeding on an infected animal or host. When they bite, the infected mosquitoes spread the virus to humans, horses, and other animals (Petersen & Marfin, 2002). In addition, a small number of cases of people acquiring WNV through blood transfusions, organ transplantation, and breast milk have been reported (Centers for Disease Control [CDC], 2004a; Jeha, et al., 2003).
WNV migrated westward across the United States. In 2000 and 2001, 21 cases and 66 cases, respectively, of the virus were reported to the Centers for Disease Control and Prevention (CDC). WNV continued to increase in prevalence. In 2002, 4,156 cases with 284 deaths from WNV were reported (CDC, 2004b; Petersen & Marfin, 2002). In 2003, the number of WNV cases reported to the CDC were 9,862 with 264 deaths (CDC, 2004c). The majority of WNV cases have occurred in the central United States, which in effect became "the eye of the storm." The number of WNV cases is significantly less this year with 2,151 cases and 68 subsequent deaths [as of October 19, 2004 (CDC, 2004d)].
After being bitten by an infected mosquito, there is an incubation period of 3-14 days before a person develops symptoms (CDC, 2004e; Petersen & Marfin, 2002). Most WNV infections are asymptomatic or produce mild symptoms consisting of fever, malaise, nausea, vomiting, myalgia, headache, backache, and possibly a maculopapular rash (Craven & Roehrig, 2001; Hazell, 2004). Approximately 1 in 150 cases of WNV is severe and may present with high fever, nuchal rigidity, headache, hyporeflexia, and significant neurological deficits including altered mental status, confusion, seizures, visual changes, diffuse muscle weakness to paralysis, and coma (CDC, 2004e; Sejvar et al., 2003). Severe cases are more prominent in young persons, the elderly, and in persons with diabetes mellitus or immunosuppression that increases the susceptibility to the infection (Craven & Roehrig, 2001; Harrison, 2002). The WNV outbreaks that occurred in New York City in 1999, and Israel in 1998, resulted in 10% of people experiencing bilateral flaccid paralysis (Klein, et al., 2002; Nash, 2001) With bilateral flaccid paralysis, WNV attacks the anterior horn cells causing acute flaccid paralysis, resulting in a poliomyelitis-like syndrome (Li et al., 2003; Sejvar et al., 2003).
Infections from WNV should be considered in persons who present with unexplained encephalitis or meningitis during the late summer or fall. Diagnosis of WNV is based on history, clinical presentation, and laboratory tests. State health departments and other major clinical laboratories can perform serum and CSF testing to confirm WNV (Hazell, 2004). The most conclusive laboratory test consists of IgM antibody-capture enzymelinked immunosorbent assay (ELISA) and is sensitive in both serum and CSF (Petersen & Martin, 2002). Polymerase chain reaction (PCR) can also be performed on CSF and is sensitive for detecting WNV (Craven & Roehrig, 2001). Following a lumbar puncture, the CSF shows pleocytosis, with a predominance of lymphocytes, elevated protein, and normal glucose. The MRI of the brain may show enhancement of leptomeninges and periventricular areas, or both, but often is negative (CDC, 2004d; Petersen & Martin, 2002; Sejvar, et al., 2003).
There is no definitive treatment for WNV. Ribavirin and interferon [alpha]2b have been shown to inhibit the virus in laboratory studies; however, further investigation is still necessary (CDC, 2004d; Craven & Roehrig, 2001; Petersen & Martin, 2002). WNV is endemic in Africa, West Asia, and the Middle East with approximately 40% of the population possessing antibodies for WNV. Genetic testing determined that the strain of WNV found in Israel was the same strain of WNV found in New York City in 1999. Animal studies have found that passive transfer of pooled immunoglobulin from Israeli donors contains anti-West Nile virus antibodies that can stop or slow the progression of WNV infection when administered in the early phases of the infection (Ben-Nathan et al., 2003). Medical and nursing management are directed towards supportive care including intravenous fluids, respiratory support, nutrition, and prevention of secondary infections and complications.
Studies have shown that long-term morbidity is significant for those individuals hospitalized with WNV. In the 1999 New York City outbreak, more than half of the persons with WNV had not returned to their prior level of functioning at discharge and only one-third were fully ambulating. Reports have shown neurological sequelae such as fatigue, memory loss, difficulty walking, and depression persisted for more than a year post-infection (Petersen & Marfin, 2002).
No human vaccine is available for the WNV. The most effective way to prevent WNV is to avoid being bitten by a mosquito. Measures include avoiding being outdoors around sunrise and sunset and using an insect repellent that contains approximately 20%-35% N, N-diethyl-3-methylbenzamide (DEET). Light-colored, long-sleeved shirts and pants are more refractory to insects. Other preventive measures include limiting mosquito-breeding grounds by emptying all standing water in areas such as flowerpots, rain gutters, or wheelbarrows. Many local and state agencies have developed programs for mosquito control and prevention by spraying insecticides over large areas to kill larvae and adult mosquitoes. Animals will often acquire WNV before humans become symptomatic; therefore, surveillance studies should monitor for large numbers of unexpected deaths of birds and horses (Harrison, 2002).
WNV is a seasonal epidemic that is rapidly migrating westward across the United States, infecting more individuals each year. Surveillance studies are critical. In 2003, the eye of the WNV storm was in the central United States. Healthcare professionals are advised to be aware of the incidence of WNV in their communities. Recognizing the symptoms of WNV infection such as fever, headache, malaise, nausea, vomiting, and myalgia is imperative. In late summer or fall, WNV infection should be considered in the differential diagnosis of a patient who presents to the ED with flaccid paralysis or tmexplained encephalitis or meningitis. The diagnosis of WNV is based on history, clinical presentation, and laboratory tests.
Unfortunately, there is no cure for WNV. A neuroscience nurse is instrumental in providing supportive care for persons affected by WNV. Symptoms must be treated depending on the presentation, and a nurse must also be alert to preventing complications from aspiration, immobility, and compromised respirations. However, the best treatment for WNV is prevention. Application of insect repellent, protective clothing, and elimination of standing water are preventive measures. It is critical that local and state agencies proactively develop mosquito control programs that include insecticide application early in the season to avoid the eye of the WNV storm.
Ben Nathan. D., Lustig, S., Tam, G., Robinzon, S., Segal, S., & Rager-Zisman, B. (2003). Prophylactic and therapeutic efficacy of human intravenous immunoglobulin in treating West Nile virus infection in mice. Journal of Infectious Diseases, 188(1) 5-12.
Centers for Disease Control (2004a). West Nile virus: What you need to know. Retrieved March 2004, from http://www.cdc.gov/nci dod/dvbid/westnile/wnv_factSheet.htm
Centers for Disease Control (2004b). Questions and answers: Cases of West Nile human disease. Retrieved March 2004, from http://www.cdc.gov/ncidod/dvbid/wesmile/qa/cases.htm
Centers for Disease Control (2004c). Statistics, surveillance, and control: West Nile virus 2003 human cases as of May, 2004. Retrieved October 2004, from http://www.cdc.gov/ncidod/dvbid/westnile/surv&controlCaseCount03.htm
Centers for Disease Control (2004d). Statistics, surveillance, the control: West Nile virus 2003 human cases as of October 19, 2004. Retrieved October 2004 from http://www.edc.gov/ncidod/dubid/westnile/ surv&control casecount03_detailed.htm.
Centers for Disease Control (2004e). Fact sheet: West Nile virus (WNV) infection: Information for clinicians. Retrieved March 2004 from http: //www.cdc.gov/ncidod/dvbid/westnile/resources/fact_sheet_ clinician,htm
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Klein. C., Kimiagar, I., Pollak, L., Gandalman Matron, R., Itzhaki, A., Milo, R. et al. (2002). Neurological features of West Nile virus infection during the 2000 outbreak in regional hospital in Israel. Journal of Neurogical Science. 200, 63-66.
Li, J., Loeb, J.A., Shy, M.E., Shah, A.K., Tselis, A.C., Kupski, W.J., et al. (2003). Asymmetric flaccid paralysis: A neuromuscular presentation of West Nile virus infection. Annuals of Neurology, 53(6), 703-710.
Nash, D., Mostashari. F., Fine, A., Miller, J., O'Leary, D., Murray, K., et al. (2001). The outbreak of West Nile virus infection in the New York City area in 1999. New England Journal of Medicine. 344(24). 1807-1814.
Petersen. L.R., & Martin, A.A. (2002). West Nile virus: A primer for the clinician. Annuals of Internal Medicine. 137(3), 173-179.
Sejvar, J.J., Leis, A.A.. Stokic, D.S., Van Gerpen, J.A., Marfin, A.A., Webb, R., et al. (2003). Acute flaccid paralysis and West Nile virus infections. Emerging Infectious Diseases, 9(7), 788-793.
Questions or comments about this article may be directed to Michelle V. VanDemark, MSN RN CNRN, by phone at 605/333-3205 or by e-mail at email@example.com. She is a neuroscience clinical nurse specialist at Sioux Valley Hospital USD Medical Center, Sioux Falls, SD.
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|Author:||VanDemark, Michelle V.|
|Publication:||Journal of Neuroscience Nursing|
|Date:||Dec 1, 2004|
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