The opinion of the court was delivered by: CONABOY
Plaintiff Lucy McDonald instituted this action pursuant to the Federal Tort Claims Act, 28 U.S.C. §§ 1346(b), 2671 et seq. (1976), and the National Swine Flu Immunization Program of 1976 (Swine Flu Act), formerly codified at 42 U.S.C. § 247b(j)-(l) (1976),
seeking to recover compensatory damages for injuries allegedly suffered as a result of her inoculation with the swine influenza vaccine.
The case was filed with this Court on September 25, 1980, and subsequently transferred by the Judicial Panel on Multidistrict Litigation to the United States District Court for the District of Columbia for coordinated and consolidated pretrial proceedings pursuant to 28 U.S.C. § 1407 (1968). Following the entry of a Stipulation and Final Pretrial Order, the case was remanded to this Court for further proceedings on November 9, 1981. A non-jury trial was held from December 13 to 29, 1982 and, in accordance with the Court's directive of December 29, 1982, the parties have each filed post-trial submissions.
I. SUMMARY OF CONTENTIONS AND HOLDING
The central issue involved here is the diagnosis of the Plaintiff's neurological disorder. The Plaintiff's primary contention is that she is suffering from Guillain-Barre Syndrome (GBS) caused by the swine flu inoculation she received on November 14, 1976. The Defendant's position is that the Plaintiff's illness is not GBS, but Transverse Myelitis (TM), a disease of the spinal cord, which the Defendant contends has no causal relationship to the swine flu vaccine.
As the medical testimony developed at trial, it was apparent to the Court that there exists in the neurological field two schools of thought on the symptomatology of the GBS disorder. There was general agreement among the medical experts that GBS is primarily a disease of the peripheral nervous system. There was much controversy, however, as to whether this disease can also involve the central nervous system, particularly the spinal cord, and if so, to what extent. The Plaintiff's view is that even the presence of significant spinal cord involvement, albeit it was asserted that there was only a minor degree in this case, would not rule out the diagnosis of GBS; whereas the Defendant's experts were inclined to conclude that where there are demonstrable physical findings signifying more than minimal spinal cord involvement, then the neurological disease process could not properly be termed GBS.
Endeavoring to fulfill the Court's judicial duty to render a precise determination in an area of medical science which the trial testimony has shown to be characterized by inexactness and controversy, we have objectively reviewed the scholarly medical testimony presented, both at trial and by deposition, and the numerous articles of medical literature concerning the Guillain-Barre Syndrome, transverse myelitis, and the swine flu vaccine. After a comprehensive examination and consideration of all these evidentiary sources, the Court finds that the Plaintiff developed GBS as a proximate result of her swine flu inoculation; and is entitled to recover from the Defendant for the damages she has suffered.
The following constitutes the Court's findings of fact and conclusions of law, as required by Rule 52(a) of the Federal Rules of Civil Procedure.
The National Swine Flu Immunization Program of 1976 was an attempt by the federal government to inoculate the entire adult population of the United States against the perceived threat of a swine flu epidemic. From its commencement on October 1, 1976 until its suspension on December 16, 1976, over forty-five million Americans were vaccinated, resulting in the largest immunization program ever in this country's history. See Administration of the National Influenza Immunization Program of 1976, Final Report to Congress by Department of Health, Education and Welfare (1978). The historical genesis of this mass inoculation effort and the legislative response thereto has been exhaustively discussed on numerous occasions by other courts and commentators and need not be repeated here. See Hunt v. United States, 204 U.S. App. D.C. 308, 636 F.2d 580, 589-593 (D.C.Cir.1980); Unthank v. United States, 533 F. Supp. 703, 716-21 (D.Colo. 1982); Bean v. United States, 533 F. Supp. 567, 571-72 (D.Colo.1980); Baynes, Liability for Vaccine Related Injuries: Public Health Considerations and Some Reflections on the Swine Flu Experience, 21 St. Louis L.J. 44, 62-69 (1977).
1) The Act created a cause of action against the United States for any personal injury or wrongful death sustained as a result of the swine flu inoculation resulting from the act or omission of the program participant
upon any theory of liability that would govern in an action against such program participant including negligence, strict liability in tort, and breach of warranty. 42 U.S.C. § 247b(k)(2)(A).
2) The Swine Flu Act made the above cause of action the exclusive remedy and abolished any causes of action against the vaccine manufacturer by individual claimants. 42 U.S.C. § 247b(k)(3).
3) It made the procedures of the Federal Tort Claims Act applicable to suits brought pursuant to the Swine Flu Act. 42 U.S.C. § 247b(k)(4).
On a substantive level, to be entitled to a monetary recovery under the Act, a plaintiff must establish by the fair weight or preponderance of the evidence: (1) the nature of his or her illness; (2) a causal nexus with the swine flu vaccine; (3) a theory of liability against the government or program participant, i.e., strict liability, negligence, or breach of warranty; and (4) damages. However, under the terms of the final pre-trial order entered by the Multidistrict court, Plaintiffs who can establish that they contracted Guillain-Barre Syndrome after receipt of the swine flu vaccine need not establish a theory of liability; only causation and damages must then be proven. See In Re Swine Flu Immunization Products Liability Litigation, Final Pretrial Order paragraph IX, M.D.L. No. 330, Misc. No. 78-0040 (J.P.M.D.L.1979).
As previously noted, Plaintiff's main contention is that she is suffering from GBS caused by the swine flu vaccine. Alternatively, she argues that even if the Court finds her present neurological disorder is transverse myelitis, as the Defendant contends, this disease process is the result of the swine flu vaccine. Furthermore, the Plaintiff posits various theories of liability against the government in support of this alternative argument.
The government's position, as set forth above, is that the Plaintiff is physically disabled not from GBS but rather from a transverse myelitic lesion of the spinal cord which has no causal relationship to the swine flu vaccine.
III. PLAINTIFF'S PERSONAL AND MEDICAL HISTORY
Lucy McDonald, presently 39 years old, was born on May 3, 1943 in Pittston, Pennsylvania. She is a high school graduate and was awarded an academic scholarship to College Misericordia in Dallas, Pennsylvania. Her intention of becoming a teacher was interrupted when she was forced to withdraw after one academic year to care for her parents, who were both in ill health. Her father died in 1962 from heart-related complications and her mother passed away in 1968.
In 1971 the Plaintiff began work in the garment industry in the shipping department of the Lee Manufacturing Company. She soon was promoted to a presser's position (the highest paid in the facility) and was described as an excellent worker and employee. She would have remained in her employment were it not for her illness.
Plaintiff's medical history was unremarkable. She has hypertension, and is insulin dependent since her diagnosis as a diabetic in 1975. Neither of these conditions interfered with her normal life or employment, nor contributed to her present condition.
IV. THE SWINE FLU INOCULATION AND THE ONSET OF PLAINTIFF'S MALADIES
Lucy McDonald received the swine flu vaccination on November 14, 1976 at the Pittston Area High School. Because of her diabetic condition, she was administered the bivalent, rather than the monovalent, vaccine.
Prior to receiving this injection, Lucy was interviewed briefly by non-medical personnel and given a document entitled "Influenza Immunization Consent/Data Form"
to peruse and sign. A section of that document labeled "Possible Side Effects" read:
A small percentage of persons receiving this vaccine may experience one or more of the following symptoms: Redness, warmth and tenderness of the injection site, fever (usually 101 degrees or less), chills, nausea, loss of appetite, muscle aches, joint pains, headache or fatigue. These reactions are usually short-lived, lasting less than 48 hours, but local reactions at the injection site may persist for more than several days. As with any vaccine or medication, the possibility of severe or potentially fatal reactions to flu vaccine must be considered. However, flu vaccine has rarely been associated with severe or fatal reactions.
After a cursory review of this form, the Plaintiff signed it and was then instructed to report to the appropriate line to receive the bivalent vaccine. While waiting in line, she was handed another document entitled "Fight Flu -- Immunize",
which included only the following information concerning possible side effects of the vaccine:
These vaccines have been field tested and shown to produce very few side effects. Some people who receive the vaccine had fever and soreness during the first day or two after vaccination. These tests and past experience with other flu vaccines indicate that anything more severe than this would be highly unlikely.
As indicated, some individuals will develop fever and soreness after vaccination. If you have more severe symptoms or if you have fever which lasts longer than a couple of days after vaccination, please consult your doctor or a health worker wherever you receive medical care.
During the evening of November 14, 1976, Plaintiff experienced the predicted fever along with nausea, headache, diarrhea and a general achy feeling throughout her body. These "flu-like" symptoms subsided in approximately two to three days and she enjoyed her normal good health until mid-December of 1976. On December 14 or 15, 1976, she felt some numbness in her right hand while at work. She relieved this "pins and needles" feeling by running her hand under lukewarm water for several minutes. Approximately one week later, again while at work, she experienced an "achy feeling" in her lower back. She remembers bending over her ironing board in an attempt to stretch her back muscles to alleviate the ache. On or about December 22, 1976, Plaintiff experienced numbness and a "pins and needles" sensation in her right foot which "felt like a sponge" on the sole of her foot. By Christmas day or shortly thereafter, this tingling sensation had progressed to both feet and her legs were beginning to feel "heavy" and weak. This numbness and weakness ascended to her calf and thigh area by December 27, 1976 and it was becoming increasingly difficult for her to perform the normal household tasks of cooking and cleaning. By December 30th, she was having considerable trouble getting out of bed by herself and it was necessary for her husband to assist her with this as well as to help her to the bathroom and into the shower. New Year's Eve, 1976, is the last time the Plaintiff can ever remember standing on her own. Over the course of the next few days her condition worsened and, at the direction of her family physician, she was finally admitted to Wilkes-Barre General Hospital on January 5, 1977.
Lucy McDonald remained a patient at the Wilkes-Barre General Hospital (WBGH) from January 5, 1977 until March 2, 1977. The admission history, elicited by Dr. Norina D'Ioria, Plaintiff's family physician, was as follows:
This is a 33 year old female, diabetic, who was admitted with a two week history of progressive numbness, of the legs. The numbness is described as a pickey, pins and needles feeling, starting in the toes, and working up gradually, and at the present time, is in the mid portion of the thigh. In association with this, in the past few days, there has been difficulty in ambulation and the patient has been getting around with the aid of crutches. She had her swine flu vaccine in November. There is no pain in association with this and she has had no history of back injury.
The few days prior to her admission to WBGH, the Plaintiff had also experienced problems urinating.
During the first three weeks of her stay at WBGH, the Plaintiff underwent numerous diagnostic evaluations, including x-rays, a myelogram, a nerve conduction study, a cystometrogram, and various laboratory tests. The x-rays and myelogram were essentially normal; they indicated no significant abnormalities in the spinal or abdominal structures and no evidence of a space occupying lesion on or near the spinal cord. Nerve conduction studies done on January 8, 1977 by Dr. A. Samii, a neurologist, evidenced prolonged latencies in the left and right peroneal nerve, an absence of motor conduction in the left and right tibial nerve and a dispersion of the evoked responses in the peroneal nerve. The cystometrogram examination undertaken by Dr. Penugonda, a urologist, revealed that the Plaintiff had a "flaccid neurogenic bladder" of the "lower motor neuron" type. A spinal fluid analysis indicated a slightly elevated total protein level and an abnormally high ratio of total protein to IgG (immunoglobulin G) of 22%, the normal being approximately 10%. The day after Plaintiff's admission to WBGH the deep tendon reflexes (DTR's) in her ankles were absent and diminished at her knees. The following day, January 7, 1977, the DTR's at both knees were absent. At this time, the reflexes in the upper extremities were reported as "good" and "equally present."
The disease process which was affecting the Plaintiff's body continued its progressively deteriorating course until its peak sometime in mid-January, 1977 and, upon her transfer to Allied Services for the Handicapped, Inc. (Allied), her major physical deficits were paralysis from the waist down and dysfunction of the bowel and bladder.
She was admitted to Allied on March 2, 1977 and remained there on an in-patient basis until October 28, 1977. While at Allied she was seen on three occasions by a neurologist, Dr. Stanley Rosenblatt. The notes of one of these consultations, on March 3, 1977, indicates that the Plaintiff had no DTR's in her upper or lower extremities. Bladder studies conducted there by various physicians reported a "reflex bladder" with "uninhibited contractions" present and also a "spastic striated muscle." On April 8, 1977, an electromyographic (EMG) study was conducted which revealed the presence of fibrillations and positive sharp waves, a sign of denervation in the peripheral nervous system. The Plaintiff also developed a sacral decubitus ulcer (bedsore) during this time but it gradually healed without the necessity of surgery. The Allied records also reported the presence of a urinary tract infection on two occasions which cleared with antibiotics. Despite some slight improvement in her condition, upon discharge from Allied, Plaintiff's primary deficits of paraplegia and bowel and bladder dysfunction persisted and, in fact, continue until this day.
Subsequent to her discharge from Allied, Plaintiff returned to her family home in Pittston, Pennsylvania with her husband, Francis. From that time until 1982, she received no significant neurological, urological or orthopedic treatment or evaluation for her medical problems. Recently, however, she has since been examined on numerous occasions by the following Plaintiff's medical witnesses: Dr. Charles Poser, three times; Dr. Peter Lichtenfeld, Dr. Robert Rhamy, Dr. H. Penugonda, twice each, and Dr. Albert Janerich, once; and on one occasion by the Defendant's medical witness, Dr. Richard Tenser. The diagnostic significance of these physicians' clinical findings will be discussed infra; however, before doing so, we believe that a brief description of the two disease processes involved in this action, GBS and transverse myelitis, is appropriate.
V. GUILLAIN-BARRE SYNDROME
GBS is a neurologic disorder, inflammatory in nature, which primarily affects the peripheral nervous system.
It has been described as a "subacutely evolving paralytic disease of unestablished etiology." Arnason, Inflammatory Polyradiculoneuropathies, Ch. 56 of Dyck, et al., Peripheral Neuropathy at 1110 (1975). The term GBS describes not a single well-defined organic disorder, but rather a collection or constellation of neurological symptoms and findings; thus, the features which allow a positive diagnosis of GBS should include clinical, laboratory, and electrodiagnostic criteria. Asbury, Diagnostic Considerations in Guillain-Barre Syndrome, 9 Annals of Neurology 1 (Supp.1981). The characteristic pathologic presentation is lymphocytic cellular infiltration of the peripheral nerve and destruction of the myelin, the white, fatty substance which protects, insulates and nourishes the peripheral nerves. The resulting segmental demyelinization impairs the nerves' ability to conduct electrical impulses from the brain which control the reflexes and movement of certain muscles. GBS generally proceeds in a patchy rather than diffuse pathological manner, resulting often times in the partial rather than total denervation of the affected peripheral nerves.
The onset of symptoms is typically subacute. Evolution of the syndrome is complete after two weeks in over fifty percent of the cases; after three weeks in eighty percent; and after four weeks in ninety percent. In other words, the disease peaks within one month of onset in a vast majority of the episodes. A stable period of brief duration precedes the recovery phase. Satisfactory recovery occurs by the end of four to six months in eighty-five percent of the cases, although some patients show permanent deficits of varying severity. Id. at 1121. The criteria also lists certain clinical, laboratory and electrodiagnostic findings as "strongly supportive" of the diagnosis. The two most important clinical signs under this category are progression of the motor weakness and a relatively symmetrical evolutionary disease process. A significant number of GBS patients also show evidence of slowed nerve conduction on electrodiagnostic testing and an increase of cerebrospinal fluid protein on lumbar puncture during the acute phase of the illness. The criteria also lists six features as "casting doubt" on the diagnosis of GBS.
In general, the NINCDS criteria "were by intention somewhat restrictive because they were designed for use by both neurologists and nonneurologists in case identification during field studies of GBS." Asbury, supra at 3. They purposely define only the "core disorder" and, thus, the precise "diagnostic limits of the disorder are still uncertain." Id. at 1.
Transverse myelitis is an internal, inflammatory process which results in the production of a spinal cord lesion. Its evolution is generally acute, but may be subacute, and the presenting symptoms often consist either of diffuse tingling sensations in the lower extremities, a burning sensation in the girdle surrounding the affected spinal cord segment, or severe back pain. Plum and Olson, Myelitis and Myelopathy, Ch. 36 in Clinical Neuropathy at 26 (Baker & Baker ed. 1973). The lesion transects the spinal cord horizontally but is generally limited vertically to one or a few spinal segments. All sensation is lost below the level of the lesion and deep tendon reflexes are nearly always intact but hyperactive. Willson, Neurology at 226 (2d ed. 1955). It is more commonly associated with a sharp sensory level and pain and also with spasticity in the affected extremities and autonomic components, i.e., the bowel, bladder and sphincter. It is generally of unknown etiology but is believed to represent an abnormal autoimmune response to an antigen such as a viral infection or vaccine. Plum and Olson, supra at 24, 26.
VII. EXPERT TESTIMONY REGARDING PLAINTIFF'S ILLNESS AND CAUSATION
Peter Lichtenfeld, M.D., Neurologist and Assistant Professor of Neurology, State University of New York
William H. Jeffreys, M.D., Director of Neurology Services, Geisinger Medical Center
Robert K. Rhamy, M.D., Professor and Chairman of the Department of Urology, Vanderbilt University
Haragopal Penugonda, M.D., Urologist, Wilkes-Barre, Pennsylvania
Albert D. Janerich, M.D., Director of Physical Medicine and Rehabilitation, NPW Medical Center
John J. Shane, M.D., Pathologist, Director of Clinical Laboratories, Allentown & Sacred Heart Hospital Center.
Charles M. Poser, M.D., Professor of Neurology, Boston University
The first doctor testifying for the Plaintiff was Dr. Peter Lichtenfeld, a board-certified clinical neurologist, who has cared for approximately 75 GBS patients as the primary treating physician in his private practice. He was affected himself with GBS in 1967 and, as a result of his own affliction has become very actively interested in the GBS disease process itself, its progression and the variety of symptoms that may appear in different patients stricken with this disease. He testified that he has made a detailed study of some 28 patients with GBS for phenomena that had not been given much attention by other doctors and writers. He described GBS as a syndrome, rather than a disease, with a combination of symptoms characterized by weakness in the extremities . He went on to testify that many patients have involvement not only of the peripheral nerves, but also the nerve roots, the spinal cord and the brain, and indeed, noted that the autonomic nervous system is also often affected by GBS. He has published a paper on this latter phenomenon. See Lichtenfeld, P.: Autonomic Dysfunction in the Guillain-Barre Syndrome, The American Journal of Medicine, Vol. 50, 772-80 (1971).
Dr. Lichtenfeld was somewhat critical of the NINCDS criteria because he believed that there was not enough set forth in the criteria to show how many variables are often found in GBS. He went on to point out that, historically speaking, there was not a great deal of familiarity with GBS prior to the swine flu program in 1976 and that GBS was often alluded to by other names.
He testified that while there is often significant recovery in GBS cases, it is not unusual to find spinal cord involvement and that the amount of recovery varies greatly from case to case. The recovery is usually consonant with the amount of damage done throughout the body as a result of the initial attack on the myelin. He distinguished transverse myelitis from GBS saying that transverse myelitis is usually an attack on a very limited area of the spinal cord and usually does not affect the peripheral nervous system. He stated that GBS, on the other hand, does concern itself with the peripheral nervous system, but that it is not uncommon at all to find some manifestation in the spinal cord or the central nervous system. Indeed, he went on to testify that there is often a resultant effect on the autonomic nervous system, particularly the blood pressure in GBS patients.
Dr. Lichtenfeld did examine the Plaintiff on two occasions in September and December of 1982, and also reviewed the medical records from WBGH and Allied. In his examination, he testified that he found remaining weakness in the Plaintiff's upper extremities and demonstrated the tests he performed on her. He stated that the lack of deep tendon reflexes in the lower extremities of the Plaintiff is indicative of GBS and not indicative of TM, indicating that indeed, in TM, the patient would have deep tendon reflexes which would be hyperactive. He also testified that spinal shock could not explain the loss of these DTR's since there is no evidence of this in the records.
He pointed out that in TM cases the bladder of the patient is usually spastic, whereas in the Plaintiff's case, she has a large, distended flaccid bladder which is more in keeping with the diagnosis of GBS. He testified that the Plaintiff manifests the two basic NINCDS criteria for a diagnosis of GBS, i.e., progressive motor weakness in more than one limb and loss of deep tendon reflexes, and that she has no symptoms which would rule out GBS. Further, he noted that while some of the symptoms that she has might be consistent with other diseases, nonetheless, when taken in connection with her overall clinical picture, they all lead to the inescapable conclusion of GBS.
Dr. Lichtenfeld testified that the electrodiagnostic testing performed on the Plaintiff showed that there was nerve conduction loss and that the condition in her legs got progressively worse. He stated that the results of these tests would be different if the Plaintiff had transverse myelitis, because even though there would be a central nervous system disorder in transverse myelitis, the peripheral nerves would still innervate the muscles which would show on the electrodiagnostic testing.
To the contrary in this case, he said that the electrodiagnostic test of Dr. Janerich's on May 27, 1982 shows that there was denervation in many of the Plaintiff's leg muscles and that an illness that has this phenomenon should not be referred to as TM. He said that all of these electrodiagnostic tests are consistent with GBS, since they refer to an attack on, or a problem with, the nerve roots and the peripheral nerves in the extremities. In explaining that the Plaintiff has a positive Babinski response
in one of her legs, he said this would not rule out GBS because while she ...