A legal complaint was received from an attorney alleging that a 59 year old male received an injection of Flu shield on an unspecified date in December 2001. It is alleged that the plaintiff developed Guillain Barre syndrome. According to the medical records, the pt presented to an emergency room on 12/26/01, with a two day history of bilateral facial weakness, difficulty closing his eyes, slurred speech secondary to mouth and labial weakness, difficulty drinking and eating "food and liquids falls out of mouth," and decreased ability to stand from a sitting positing. The pt denied double vision, headaches, loss of consciousness, seizures, or any other symptoms. He had recently been diagnosed with sinusitis and had started a course of Levaquin seven days prior to admission. Upon admission to the ER, the pt's physical examination revealed a body temp of 96.4 deg F; blood pressure 150/94; pulse 100 and respirations 28. The pt had sacrral and bilateral 1-2+ pedal edema of the lower extremities, as well as, lower extremity weakness. He was alert and oriented to person, place and time. A CT scan of the head was performed; the results were normal except for mild ethmoid inflammation. There was no evidence of intracranial hemorrhages or masses. A complete blood count was performed: the results are as follows: WBC 8.5; Hgb 15.0; Hct 39.9; platelets 282. An erythrocyte sed rate was 56. Blood chemistries were performed: the results are as follows: glucose 117; BUN .5; creatinine .9; sodium 127; potassium 4.3; chloride 98; and carbon dioxide 24. A lumbar puncture was performed: the results are as follows: the cerebrospinal fluid was clear; total protein 275 and there were no WBC's. The physician indicated that the pt's cranial nerve palsies could be indicative of Lyme meningitis versus Guillain Barre syndrome. Due to the "increased total protein in the CSF" without WBC, the physician's clinical impression was acute Guillain Barre Miller Fisher Varient. The pt's negative inspiratory force was 60. The physician recommended that the pt be admitted to ICU and treatment should include IVIG versus plasmaphoresis. On that same day, the pt was transferred via helicopter to another facility for admission and evaluation. Upon admission to that facility, the pt's physical examination revealed a body temp was 36.9 deg C; blood pressure 142/81; and respirations 20. The pt was alert, awake, and pleasant though dysarthic speech was noted as well as bilateral facial droop. The lungs were clear. Heart was regular rate and rhythm. Abdomen was soft, nontender, nondistended, with good bowel sounds. There was trace edema in both extremities. On neurological examination, the strength in the upper extremities was 5/5 bilaterally, lower extremities was 4+/5. Deep tendon reflexes in the upper extremities were 1+ symetrically and were absent in the lower extremities. The bilateral Babinski reflexes were downgoing. The pt's sensation was intact but decreased to pinprick, percussion and vibratory sense. Finger-to-toe was intact bilaterally and gait was somewhat wide-based. An unspecified MRI was performed; the results were as follows: degenerative disc disease at L2, 3-4, 4-5, and 5-6. An MRI of the head was performed; the results are as follows: there were a few, nonenhancing, subcentimeter foci of FLAIR and T2 prolongation involving bilateral periventricular white matter. There was no mass or mass effects. The brain morphology appeared unremarkable. There was no pathological enhancement or evidence of acute or hyperacute ischemia. Incidental note was made of mutifocal various amounts of T2 hyperintesity involving bilateral ethmoid air cells. There was no evidence for hemorrhage or hemorrhage products. An MRA revealed no evidence of stenosis, aneurysm, or focal ectasia. There was probable air fluid in the right sphenoid sinus and probable multifocal ethmoid sinus disease. On 1/7/02, the results of the Lyme test on the CSF fluid showed the following: Gram stain showed rare white blood cells and the body fluid culture revealed no definite organisms and rare white blood cells. A diagnosis of Guillain Barre syndrome was made. The pt was plasmapheresed five times over the course of the hospitalization. He was examined by an opthalmoligist for diplopia, the cause of which was concluded to be Guillain Barre syndrome. The pt was examined by a nephrologist for his history of nephrotic syndrome. A renal biopsy was performed; the results revealed membraneous glomerulonephritis. The pt's hospital course was unremarkable and he steadily "recovered" some of his motor function. His facial droop was markedly reduced but still noticeable bilaterally and his speech was much less dysrthric. On 1/10/02, the pt was considered "stabilized" and discharged from the hospital. Discharge medications included pre-admission medications plus Lipitor, Lacri-Lube, Zestril, Senakot, Peri-Colace and Vicodin. The pt was scheduled as an outpatient for speech therapy, nephrology and an EMG. The legal complaint alleges that as a result of the lips; permanent impaired vision; permanent inability to control his mouth causing biting of lips and cheeks; permanent inability to control muscles while eating and drinking; and permanent depression and anxiety.