The Journal of Emergency Medune. Vol 5 pp 185-189. 1987
Printedin the USA
J. Lee Garvey,
CopyrIght ‘S 1987 PergamonJour~ls Lid
A CASE REPORT
‘Unlverslty of Clnclnnatl College of Medune and tAwstant Professor, Department of Emergency Medlclne, Unlverslty of Clnclnnatl College of Medlclne Reprint address. Alexander Trott. MD, Department of Emergency Medlclne, Unlverslty of Cmclnnatl Hospital, 234 Goodman Street, Clnclnnatl, OH 45267.0769
causative agent of recurrent bacterial meningitis.’ Although there appears to be a great variability in the duration of colonization before invasion, the risk of meningitis seems to be greater in patients who have recently been colonized.h Colonization alone rarely leads to meningitis. Other factors that play a significant role in its development include pneumonia, sinusitis, endocarditis, splenectomy, sickle hemoglobinopathy, immunosuppressive therapy, alcoholism, and recent or old head trauma.h The last, old head trauma, is the most common pathophysiologic factor leading to recurrent meningitis.’ Colonization of the nasopharynx with pathogenic bacteria becomes particularly significant if there is a preexisting bony defect involving the paranasal air passages. The following is a report of a case of recurrent pneumococcal meningitis 6 years after the patient sustained multiple skull fractures in a motor vehicle accident.
U Abstract-Recurrent meningitis is an uncommon clinical problem. It is most likely to result from head trauma. Streptococcus pneumoniue is the most common infecting pathogen. Computed tomographic techniques are required to identify persistent bony defects in the skull that might predispose to this disorder. Because emergency physicians regularly care for victims of head trauma and meningitis, knowledge of this entity can be useful. 0 Keywords - meningitis, recurrent; head injury
Introduction An attack of acute bacterial meningitis is a life-threatening medical emergency. However, it is not often thought of as a disorder that can strike a patient more than once. Emergency physicians are frequently faced with patients in whom the diagnosis of meningitis is suspected. A history of meningitis, especially following head trauma” is a risk factor for later recurrence. The most common pathogens causing bacterial meningitis are those that have colonized the nasopharynx.h Approximately 25% of healthy persons transiently acquire new strains of Streptococcus pneumoniae each year,’ the most common
Case Report A 35year-old woman was brought to the University of Cincinnati Center for Emergency Care following the acute onset of
RECEIVED: 23 May 1986; ACCEPTED: 9 October 185
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seizures and altered mental status. The patient had awakened during the night complaining of a headache. Sometime later she was noted to be shaking in an uncontrolled manner. She was unresponsive during and after this episode. A life squad was called and she was immediately transported to the Center for Emergency Care. The patient had received severe head trauma as a result of an automobile accident in 1976. She had a 6-week hospitalization for a depressed frontal skull fracture, a basilar skull fracture with cerebrospinal fluid otorrhea, and a cervical spine injury. Her course was complicated by purulent meningitis (causative agent unknown), and she was discharged with the sequelae of permanent left-sided hearing loss, anosmia, ageusia, transient amenorrhea, and electrolyte disorders. Four years following the injury, she was evaluated for severe frontal headaches, which ultimately were diagnosed as muscular in origin. Computed tomography (CT) done at that time revealed frontal lobe encephalomalacia consistent with old injury. Scanning technique was not adequate to reveal bony defects. On presentation to the emergency department, the patient’s blood pressure was 120/50 mm Hg; pulse rate, 150 beats per minute; respirations, 16/min; rectal ternperature, 105.8 F. Initial neurologic assessment revealed her to be responsive only to painful stimuli, with a Glasgow coma scale of 5. Nuchal rigidity as well as positive Kernig’s and Brudzinski’s signs were present. An endotracheal tube was inserted and oxygen administered to the patient at a flow of 8 L/min. One ampule (25 g) of 50% dextrose and water and two ampules (0.8 mg) of naloxone were administered by intravenous (IV) push. The patient was placed on a hypothermia blanket and ice packs were applied to the groin and axillae. Initial blood gases after intubation showed a pH of 6.78 with a Paoz of 125 and a Pace? of 46 mm Hg. One ampule (50 mEq) of sodium bicarbonate was
J. Lee Garvey and Alexander Trot!
given IV. Peripheral blood leukocyte count was 32,OOO/pL, with a shift to the left noted on differential. A urine toxicology screen was negative. A lumbar puncture revealed purulent CSF containing 4,000 leukocytes/pL, with a differential of 63% segmented neutrophils and 37% band neutrophils. Microscopic examination of a Gram’s stain preparation of the CSF demonstrated extracellular and intracellular Gram’s positive diplococci. Culture of the CSF later grew S pneumoniae. Blood cultures subsequently demonstrated the presence of the same organism. The patient was admitted to the medical intensive care unit and was begun on penicillin G, 2,000,OOO units every two hours. She progressed to status epilepticus and required a thiopental sodium drip for control. Over the next 24 hours she developed disseminated intravascular coagulation, continued to have profound acidosis, and became progressively hypotensive despite maximal cardiovascular support. No therapeutic intervention altered her fatal course, and she died on the second hospital day. A CT examination done during the hospitalization revealed only bifrontal polar low densities, consistent with her old trauma, without any mass effect. Motion artifact prevented adequate evaluation of the bony calvaria for defects. At postmortem examination, the calvaria showed multiple old fractures of the frontal bone. A prominent remote fracture extending across the right orbital plate and cribriform plate through the left orbital plate was noted. Microscopic examination of a section through the area of previous trauma in the frontal orbital cortex showed reactive gliosis and neutrophil infiltration. It was the opinion of the prosector that, based on the neuropathological findings, direct extension of S pneumoniae from the paranasal sinuses to the cranial vault could have been the cause of meningitis.
Discussion This case demonstrates the grave nature and rapid course of S pneurnoniae meningitis of whatever cause. As a result of the profound nervous system involvement, and despite early, aggressive antibiotic therapy and supportive measures, the deterioration of the patient’s condition could not be prevented. Conditions in which the patient’s defenses are compromised or the pathogens gain direct access to the subarachnoid space are common predisposing factors to recurrent attacks of bacterial meningitis. Recurrent pneumococcal meningitis has been documented in defects in the compliment system,” and in sickle hemoglobinapathy,‘] agammaglobulinemia,li’ splenectomy,” meningocele,‘? congenitalI and acquired skull defects.14 Although old head trauma is the most common predisposing factor for recurrent meningitis,’ the actual incidence is low and difficult to calculate. Following a basilar skull fracture, the initial attack of meningitis, if it is to occur, generally is seen \vithin two weeks of the injury.‘,“ However, cases hale been reported in which the trauma preceded the occurrence of meningitis by as many as 20 years.’ Finally, multiple episodes, up to six, have been reported in a single individual following head trauma.’ The patient presented in this report had esperienced purulent meningitis 6 years earlier during her hospitalization for head injuries. The meningitis resulted in permanent neurologic sequelae, but she survived the episode. Although the patient did not experience persistent rhinorrhea or otorrhea, the defect in the dura and skull bones may have healed in a manner that could allow invasion of microbial pat hogens and result in delayed recurrence of meningitis. Small vascular cuffs of meninges have been reported to heal within the bony fracture defect and are potential portals of entry for microorganisms.” Persistent otorrhea or rhinorrhea is not a
clinical prerequisite for recurrent posttraumatic meningitis. The occurrence of meningitis in the patient with previous head trauma, even years previously, should prompt the search for an anatomic defect in the skull.” Radiographic techniques have been developed to uncover defects as small as 1.5 mm.“,‘” High-resolution scanners, thin-section techniques, and coronal combined with sagittal views all offer an excellent opportunity to reveal offending bony defects.‘- I4 Other techniques for the localiLation of crania1 defects and cerebrospinal fluid leaks include the injection of dyes and radioactive isotopes intrathecally.” In the absence of detected pathways and sources of infection or other predisposing conditions in a patient with a history of head trauma, delayed attacks of meningitis may be assumed to arise via lingering crania1 defects.” An important issue that this case raises is that of prevention of meningitis in patients with skull fracture, particularly basilar skull fractures. The two ma,jor modalities of prevention are antibiotic prophylaxis and immuno-proph),lactic vaccination. Antibiotics have been used routinely o\‘er the years in the setti.ng of skull fracture with cerebrospinal fluid leaks to prevent meningitis.“‘,‘l Evidence in recent years, however, suggests that antibiotic prophylaxis offers no clear adlantage in protecting against posttraumatic meningitis.?,ZZm?4 Because the incidence of recurrent meningitis is low relative to the incidence of skull fractures, and because antibiotic prophylaxis has not been proven to be efficacious, there is little indication for antibiotic prophylaxis following head injury. Pneumococcal vaccines have ILICC~S+ fully given protection against pneumonia, but there is little clinical information concerning their ability to pre\‘ent meningitis. The Immunization Practices Ad\ isor) Committee on pneumococcal poly5accharide vaccine currently recommends
J. Lee Garvey and Alexander Trott
188 that pneumococcal vaccine be administered to patients with known cerebrospinal fluid leaks.25 Skull fracture alone is not specifically mentioned. Since patients with basilar skull fractures are at an increased risk for developing bacterial meningitis, and since the causative organism in more than 85% of episodes of posttraumatic bacterial meningitis is S pneumoniae,15 pneumococcal vaccination may be warranted in such cases. A polyvalent/ polysaccharide vaccine for the prevention of bacterial meningitis caused by Neisse-
ria meningitidis, Spneumoniae, ilus influenzae, Escherichia
group E streptococci is currently under study.2h Vaccines, however, may be unable to prevent all cases of bacterial meningitis after skull fracture, since the pathogens may gain direct access to the CSF, where little immunologic protection exists.27 Ultimately, the most efficacious way to prevent meningitis following head injury is the recognition and surgical repair of any existing cranial defects. Most cases of CSF otorrhea and rhinorrhea resolve
spontaneously and can be managed conservatively without antibiotic prophylaxis or surgical intervention. For CSF leaks that persists beyond 14 days, the risk of meningitis increases greatly and surgical intervention should be strongly considered.5
Summary Although not a common problem, recurrent meningitis is a well-documented entity, A skull fracture, particularly, basilar, is the most common predisposing factor for the occurrence of this disorder. The failure of antibiotics to prevent meningitis and the small likelihood that vaccines will be of any real value in this setting make early recognition and CT evaluation important in patients at risk for recurrence. Emergency physicians, because of the frequency with which they care for head-injured patients, can potentially affect the outcome of this disorder by understanding the problem of recurrent meningitis.
REFERENCES I. Whitecar 2.
JP, Reddin JL, Spink WW: Recurrent pneumococcal meningitis. N Engl J Med 1966; 274:1285-1289. Dgai TF, Meyer FB, Poletti CA: The incidence and prevention of meningitis after basilar skull fracture. Am JEmerg A4ed 1983; 3:295-298. Sengupta RP, Gravan N: Recurrent fulminating meningitis 20 years after head injury. J Neurosurg 1974; 11758-761. Schneider RC, Thompson JM: Chronic and delayed traumatic cerebra-spinal rhinorrhea as a source of recurrent attacks of meningitis. Ann Surg 1957; 145:517-529. Westmore GA, Whittman DE: Cerebrospinal fluid rhinorrhea and its management. Br J Surg 1982; 69:489-492. McGee ZA, Kaiser AB: Acute Meningitis, in Mendell GL, Douglas RG, Bennett JE (eds): Principles and Practices of Infectious Diseases, 2nd ed. New York, John Wiley & Sons, 1985, pp 560-573. Suhs RH, Feldman HA: Pneumococcal types detected in throat cultures from a population of “normal” families. Am J Med Sci 1965; 250:424-429. Swartz MN, Dodge PR: Bacterial meningitis: A
14. 15. 16. 17.
review of selected aspects. N Engl J Med 1865; 272:725-731. Greissmer DA, Winklestein JA, Luddy R: Pneumococcal meningitis in patients with a major sickle hemoglobinopathy. J Pediatr 1978; 92:82-86. Prassad AS, Koza AW: Agammaglobulinemia. Ann Intern Med 1954; 411629-638. Smith CH, Erlandson M, Schulman I, et al: Hazards of severe infections in splenectomized infants and children. Am J Med 1957; 22:390-404. Steele RW, McConnell JR, Jacobs RF, et al: Recurrent bacterial meningitis: coronal thin section cranial computed tomography to delineate anatomic defects. fediafrk 1985; 76:950-953. Von Haacke NP: Recurrent meningitis due to congenital malformation of the middle ear. Br MedJ 1983; 286:1248-1249. Applebaum E: Meningitis following trauma to the head and face. JAMA 1960; 173:1818-1822. Hand WL, Sanford JP: Posttraumatic bacterial meningitis. Ann Intern Med 1970; 72:869-874. Saito H: Late post-traumatic rhinogenic meningitis. Adv Oforhinoluryngol 1983; 31:175-183. Johnson DH, Colman M, Larsson S, et al: Com-
puted tomography in medial maxilla-orbital fractures. d Covrput Assis/ Tomogr 1984; 8:416-419. Guyon J, Brant-Zawadzki M, Seiff S: CT demonstration of optic canal fractures. ilrn J Rad 1984; 148:1031-1034. Johnson DW, Hasso AN, Stewart CE, et al: Temporal bone trauma: high resolution Computed Tomographic evaluation. Radiology 1984; 151:411-415. Sanford JP: Pharmacology and modes of action in relation to clinical anti-microbial therapy. C/in Neurosurg 1967; 14:178-190. Raskind R. Doria A: Cerebrospinal fluid rhinorrhea and otorrhea of traumatic origin. In/ Surg 1966; 46:223-227. Einhorn A. Mirrahi EM: Basilar skull fractures
in children. ,4/n J Di.r Ch//d lY78; 132:1121-1124. Ignelzi RJ, VanderArk CD: Analysis of the treatment of basilar skull fractures with an without antibiotics. JNeurosurg 1975; 43:721-725. Hoff JT, Brewin A, Hoi Sang U: Antibiotics for basilar skull fracture. JNeurosurg 1976; 44:649. CDC-ACIP: Update: Pneumococcal Polycaccharide vaccine usage-United States. .4!tn 1~ fern /Wed 1984; 101:348-350. Beuvry EC: Immunization against bacterial meningitis. J Infect 1981; 3(suppl):71L79. Rahal JJ, Simberkoff MS: Host defense and antimicrobial therapy in adult gram negative bacillary meningitis. .4nn Inrerri .&lea’ 1982; 9614688473.