Barnes v. United States

• Decision Date: 29 June 1981
• Docket Number: Civ. A. No. 80-425.
• Citation: 516 F. Supp. 1376
• Parties: Sandra K. BARNES and Robert E. Barnes, Plaintiffs, v. UNITED STATES of America, Defendant.
• Court: U.S. District Court — Eastern District of Pennsylvania

516 F. Supp. 1376

Sandra K. BARNES and Robert E. Barnes, Plaintiffs, v. UNITED STATES of America, Defendant.

Civ. A. No. 80-425.

United States District Court, W. D. Pennsylvania.

June 29, 1981.

James L. Weisman, Weisman, Pass, Swartz & Trimm, Pittsburgh, Pa., Brendan V. Sullivan, Jr., Williams & Connolly, Washington, D. C., for plaintiffs.

Craig R. McKay, Asst. U. S. Atty., Pittsburgh, Pa., for defendant.

FINDINGS OF FACT AND CONCLUSIONS OF LAW

COHILL, District Judge.

I. Background

Plaintiff, Sandra K. Barnes, suffered Guillain-Barre Syndrome as a result of a shot she received during the 1976 United States swine flu inoculation program. She is permanently crippled and confined to a wheelchair.

The defendant, the United States of America, has admitted liability for her injuries. The only issues to be determined in this non-jury case relate to the damages to be awarded.

Robert E. Barnes, Mrs. Barnes' husband, seeks damages for loss of consortium.

The case was brought before the Court pursuant to the National Swine Flu Immunization Program of 1976, 42 U.S.C. § 247b (1976), the Federal Tort Claims Act, 28 U.S.C. § 2671 et seq. (1976), and 28 U.S.C. § 1346(b) (1976).

Pursuant to Fed.R.Civ.P. 52, we make the following Findings of Fact and Conclusions of Law.

II. Findings of Fact

A. Overview

In this case the defendant has conceded that Mrs. Barnes suffered from Guillain-Barre Syndrome caused by receiving a swine flu shot and has admitted liability.

The National Swine Flu Immunization Program of 1976, 42 U.S.C. § 247b (1976), was an attempt by the Federal Government to inoculate the entire adult population of the United States against the threat of a swine flu epidemic. It was the largest immunization program in this country's history, and over forty-five million Americans — or one-third of the adult population — were vaccinated. The initial vaccinations occurred on October 1, 1976; the program was suspended on December 16, 1976.¹ The program, for which $135 million was initially appropriated by Congress, called for using both private and public health care systems to achieve its goal of inoculating the entire adult population by the end of November, 1976. The November deadline was critical since the season of intense flu transmission in the United States is generally considered to be September through March. See The Swine Flu Program: An Unprecedented Venture in Preventive Medicine, Report to Congress by the Comptroller General of the United States, June 27, 1977.

The Swine Flu Act became law on August 12, 1976 and was applicable to all swine flu inoculations administered after September 30, 1976. Important provisions of the Act include the following:

1. The Act creates a cause of action against the United States for any personal injury or wrongful death sustained as a result of the swine flu inoculation, 42 U.S.C. § 247b(k)(2)(A);

2. it makes that cause of action the exclusive remedy, 42 U.S.C. § 247b(k)(3), and it abolishes any cause of action against the vaccine manufacturer; and

3. it makes the procedures of the Federal Tort Claims Act applicable to suits brought pursuant to the Swine Flu Act, 42 U.S.C. § 247b(k).

The program was prompted in part by the medical discovery in early February, 1976 at Fort Dix, New Jersey, of military personnel having a new strain of influenza virus antigenically related to the virus prevalent during the 1918-19 swine flu pandemic. That pandemic was responsible for twenty million deaths worldwide, including 400,000 in the United States alone.² Prior to 1930, the 1918-19 strain was the predominate cause of influenza in the United States. Since 1930, the virus had been limited to transmission among swine only with occasional transmission from swine to human and no secondary person-to-person transmission.³

In addition, the Swine Flu Act was occasioned by the collapse of the commercial liability insurance market, both for vaccine manufacturers and other program participants.⁴ The cases of Davis v. Wyeth Laboratories, Inc., 399 F.2d 121 (9th Cir. 1968), and Reyes v. Wyeth Laboratories, 498 F.2d 1264 (5th Cir.), cert. denied, 419 U.S. 1096, 95 S.Ct. 687, 42 L.Ed.2d 688 (1974), which held a manufacturer of polio vaccine strictly liable in tort, greatly contributed to the insurance problem. For this reason, the Swine Flu Act provided that the exclusive remedy for injury caused by the vaccine would be against the United States. However, since the manufacturers could still insure themselves against negligence liability, they may be liable in a suit by the United States if the United States is found liable on a negligence theory. 42 U.S.C. § 247b(k)(7).

History has demonstrated that no swine flu epidemic occurred during the winter of 1976-77. As can be expected, many people who were inoculated also incurred some type of illness, injury or adverse medical condition in a period relative to the vaccination. Lawsuits such as the instant one, were filed throughout the country for illnesses allegedly resulting from the immunization. In addition, numerous administrative claims have been filed. The critical question presented in these cases is the causal relationship between the immunization from the claimed illness. However, mere temporal relation between the onset of a disease and the vaccination is insufficient to establish legal causation. In the case of Guillain-Barre Syndrome, the government has stipulated that the swine flu vaccine can cause Guillain-Barre Syndrome in some instances, and it has so conceded here.

Guillain-Barre Syndrome is a neurologic disorder, inflammatory in nature, which affects the peripheral, as opposed to the central, nervous system. The syndrome characterizes a set of neurologic symptoms rather than defining a specific organic disorder. The disease was first described in 1859 by Dr. O. Landry, and referred to as "Landry's Paralysis."⁵ It was again described in 1916 by Drs. Guillain, Barre and Stohl.⁶ To date, medical science has not established the syndrome's exact etiology or cause.

Based on the literature we have reviewed, Guillain-Barre Syndrome generally has these characteristics:

1. it is a neurologic disorder which affects the peripheral nervous system and nerve roots;

2. the primary clinical symptoms are symmetrical motor weakness and reflex impairment;

3. sensory impairment is typically negligible;

4. the primary laboratory symptoms are elevated protein levels in the cerebrospinal fluid and decreased nerve conduction rates; and

5. the disease usually peaks within one month of onset followed by recovery without permanent motor malfunction.

The NINCDS⁷ ad hoc committee has advanced criteria for the diagnosis of Guillain-Barre Syndrome. Features required for diagnosis of Guillain-Barre Syndrome within the NINCDS guidelines are progressive motor weakness of more than one limb and areflexia (loss of tendon jerk). Universal areflexia is the rule, although distal areflexia with weakening of the reflexes in the biceps and knees will suffice if other features are consistent.

Various descriptions of Guillain-Barre Syndrome are listed in the medical dictionaries:

The Attorney's Dictionary of Medicine (Schmidt 1978) defines it as

a neurological disorder of unknown cause due to a virus, sensitivity to a virus, or to a perverse immunological reaction of the body to constituents of certain vaccines, resulting in allergic neuritis (inflammation of nerves) and the destruction of myelin (a fatty substance covering some nerve fibers).

The Merck Manual (13th Ed. 1977) states:

Symptoms begin peripherally, often in the digits, and progress centrally. Although numbness, tingling, and other paresthesias are common and there may be mild distal sensory loss, flaccid muscular weakness predominates, with associated muscle tenderness, and diminished tendon reflexes. The weakness often ascends from legs to arms to face. The sphincters usually escape. In severe cases, motor cranial nerves and trunk muscles may be involved and respiration may be impaired. Sympathetic involvement is indicated by hyperhidrosis, edema, a livid skin, and postural hypotension. The respiratory paralysis and autonomic deficits may be life-threatening.

The interval between the prodromal infectious episode and the onset of symptoms is variable; most frequently it is one to three weeks. On occasion the interval between the infection and the onset of Guillain-Barre Syndrome may be less than one week. Typically, those cases are the most acute. It should be pointed out that the infectious illness has usually subsided by the time the neuropathic symptoms surface. Arnason at 1110.

The most significant clinical features of Guillain-Barre Syndrome are progressive bilateral⁸ motor weakness and areflexia. See NINCDS Criteria, supra. The severity of weakness covers a wide spectrum from mild ataxia (failure of muscle coordination) to total paralysis of every motor and cranial nerve. In most instances, the weakness is first noticed in the legs and gradually ascends through the body. Rarely are there solely sensory symptoms in the absence of motor debility. Tendon reflexes are usually abolished in affected areas although a flicker of activity may remain in mild cases. Arnason at 1121-1123.

Other clinical symptoms include facial diplegia, impaired swallowing and chewing, and respiratory difficulties.

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 that usually advances to completion within a period of weeks to a few months.⁹ 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...