Localized Encephalitis, Brain Abscess and Subdural Empyema 1945-1950"

LOCALIZED ENCEPHALITIS, BRAIN ABSCESS AND SUBDURAL EMPYEMA 1945-1950"

E. H. BOTTERELL, M.D., AND C. G. DRAKE, M.D. Department of Surgery, University of Toronto, and the Neurosurgical Division of the Toronto General Hospital, Toronto, Ontario (Received for publication February 13, 195~)

REVOLUTIONARY change in the treatment of intracranial sepsis occurred during the second World War, when suppurating brain wounds were radically debrided by suction and closed without drainage. With the benefit first of the sulphonamides and later of penicillin primary healing occurred in a high percentage of cases. 2,21 This principle of primary closure of infected brain wounds was established by neurosurgeons at a time when delayed primary closure of war wounds of the extremities was mandatory. McKenzie, 16 in 1946, presented to the Toronto Academy of Medicine a study of 105 cases of brain abscess, treated over a period of ~0 years at the

TABLE 1 Classification of intracranial sepsis 38 cases

1. Nonsuppurative localized encephalitis 5

g. Brain abscess o3 (a) Nonencapsulated 5 (b) Encapsulated lS

3. Acute diffuse subdural empyema 10 (a) *With brain abscess -~ (b) Without brain abscess 6

* Included in consideration of acute brain abscess, nonencapsulated--III (a).

Toronto General Hospital, with an overall mortality rate of 53.6 per cent. This trying experience was shared by all engaged in neurosurgery during the era before the use of antibiotics. This paper presents an account of the methods and results of surgical treatment, supported by the antibiotics and sulphonamides, of a series of 38 consecutive cases of intracranial infection, during the 6-year period 1945 to 1950. On clinical and pathological evidence these cases were classified in three main groups (Table 1).

* Read before the Royal College of Surgeons of Canada at Montreal, December 1950. 348 ENCEPHALITIS, BRAIN ABSCESS AND SUBDURAL EMPYEMA 349 I. DIAGNOSIS AND LOCALIZATION, IN GENERAL Awareness of a potential primary focus of infection alerts the physician to the signs of increased intracranial pressure, such as headaches, drowsi- ness, vomiting and papilloedema, and to evidence of local disturbance of brain function--aphasia, hemiparesis, etc. It must again be emphasized that low-grade fever, a near normal white blood count and bradycardia are generally the common accompaniments of a brain abscess. In recent years, valuable assistance has been obtained from the use of the electro-encephalogram in the recognition and localization of brain infection. X-rays of the skull may demonstrate gas in a brain abscess or displacement of a calcified pineal gland. A burr hole is made over the suspected site and the lesion is sought for with a brain needle. The resistance of the wall of an encapsulated abscess allows its ready differentiation from the soft, necrotic, nonencapsulated abscess. Occasionally accurate localization of an abscess is difficult. Cerebral angiography or ventriculography is then carried out. II. ACUTE LOCALIZED NONSUPPURATIVE ENCEPHALITIS Dandy 6 believed that "a hematogenous brain abscess passes through precisely the same stages of development that obtain for a furuncle." It is submitted that the inflammatory process following the spread of infection into the brain, regardless of its origin, runs a course similar to infection in other tissues. The inflammatory response begins with vascular congestion, oedema and cellular infiltration, resulting in a poorly localized nonsuppurative encephalitis. Before antibiotics and sulphonamides this process usually went on to suppuration, with the formation of a brain abscess, although in a few of these cases the process did resolve. McKenzie15 in 19~9 described three such cases under the heading of "Brain Abscess Sus- pect." Case 1 in our series illustrates the problem as it occurs today: Case 1. A.C., a female, aged 50, was in good health until 4 weeks before admission when she visited her physician, complaining of nasal discharge. Ten days before admission a throbbing pain developed in the left ear, unassociated with any discharge. A week later general malaise developed, with headache, and on the day of admission she had four generalized convulsions. Following these her husband noticed that she was having difficulty with her speech. A lumbar puncture had been done; the CSF contained 160 cells/c.mm., chiefly polymorphonuclear leucocytes. The patient had received penicillin intramuscularly at home. She was admitted to the Toronto General Hospital as an emergency. The patient was drowsy, with a temperature of 100 ~ and a pulse rate of 70. She was dysphasic and had a right lower facial weakness. No field defect could be demonstrated. Early papilloedema was present in the left eye. The WBC was 13,500/c.mm. An EEG showed high voltage slow waves from the left hemisphere, with phase reversals localizing the disturbance in the "central region near the fissures of Sylvius and Rolando on the left side." X-rays revealed clouding of the left mastoid antrum, as well as clouding of the left ethmoid and frontal sinuses.