Tropical Neurology - part 2 pptx

44 Tropical Neurology 2 kyphus. In active disease, intraoperative traction usually results in partial correction of the deformity. When the deformity exceeds 40˚ it may be wise to first instrument posteriorly, achieve deformity correction and then debride and fuse anteriorly. Pos- terior fixation is, however, not always necessary but if done helps in deformity cor- rection and graft consolidation in the desired position. For high cervical levels, a submandibular approach is used while the classical Southwick Robinson’s approach suffices in other patients. Cervicothoracic junction: Surgical options in this region are transmanubrial anterior decompression, transclavicular anterior decompression, and high costo-transversectomy. The transclavicular approach requires either dislocation or surgical fracturing of the clavicle which is morbid. In addition, access to the spine is always anterolateral and oblique. In comparison, the transmanubrial approach re- quires splitting of only the manubrium (which is easily rejoined and heals without nonunion), saves the thoracic duct from iatrogenic damage and, most importantly, allows direct anterior access to the spinal column for easy grafting and fixation. Management of Lumbosacral Tuberculosis Backache is an important sequelae of the disease and is present in 54% of the cases bearing a direct relation to the number of vertebrae involved and the abnormal lumbo-sacral angles. 7 Any change in Lumbosacral angles to less than 10˚ will usually result in accelerated degeneration and pain. Hence, surgery may be aggressively ad- vocated in cases of acute deformity but no deficit. Role of thoracoscopic surgery: Thoracoscopic surgery is being used for drainage of nonresolving abscesses and for the treatment of spinal tuberculosis with paraplegia; Fig. 2.11. Illustration showing the various approaches used in decompression of tuber- culous spondylirtis. 45 Spinal Tuberculosis 2 although, its efficacy is yet to approach that of open surgery. The main advantage of this technique lies in its minimal invasiveness and decreased morbidity. Management of kyphosis: Radical debridement and fusion is far superior to only debridement in adults and children past their growth sensible age. The changes in deformity in children are similar to those in adults, although some children have a tendency toward spontaneous correction of the deformity. Progression of deformity in these cases is solely due to graft resorption, fracture or dislodgement with second- ary collapse. 8 Management of Paraplegia The general principle of management of paraplegia applies to Pott’s paraplegia as well. Besides antitubercular and surgical therapy, general care of the paraplegic patient is very important such as— Bladder care: if retention—clean, intermittent self-catheterization. Prevention of bedsores: frequent changes in position and water or air mattress. Prevention of deep vein thrombosis: low dose heparin and physiotherapy. Severe spasticity: baclofen, diazepam or tizanidine. Intraspinal Tuberculous Granuloma Intraspinal tuberculous granuloma is usually associated with Pott’s spine although it rarely can occur without vertebral involvement. The spinal tuberculoma may be extradural, intradural extramedullary or intramedullary. Extradural spinal tuberculoma: Most extradural spinal tuberculomas are second- ary to vertebral disease. A number of patients have been reported in which evi- dences of bony tuberculosis could not be detected. These lesions are most likely due to hematogenous spread. The patient may present with paraparesis or quadriparesis depending on the site of the lesion. The granuloma can be visualized on spinal MRI which can be confirmed at surgery. Treatment consists of decompressive laminec- tomy or laminoplasty. The anterior granuloma can be safely left if decompression is otherwise satisfactory. Antitubercular therapy is continued at least for 18 months. Intradural spinal tuberculoma: Intradural extramedullary spinal tuberculoma is rare and presents either as a round or oval hard mass adherent to the inner aspect of the dura and the spinal cord or as a granulomatous mass surrounding the spinal cord. Clinically, patients present with extramedullary compressive myelopathy. Intramedullary spinal tuberculoma: Isolated intramedullary tuberculoma is rare. The lesion is usually a single, hard, circumscribed mass of 7-10 mm in diameter associated with localized arachnoiditis. The majority of these patients have associ- ated pulmonary tuberculosis. Neurological deficit in the form of paraplegia or quad- riplegia develops insidiously. Spinal MRI or contrast CT scan show an enhancing lesion with or without associated perifocal edema. Intramedullary tuberculoma can be easily enucleated under the cover of antitubercular therapy. Tubercular Arachnoiditis Tubercular arachnoiditis or radiculomyelopathy associated with spinal meningi- tis refers to inflammation of the arachnoid alone or all three meninges which may be acute or chronic, mild or severe, or localized or extensive. It is always associated with cellular, vascular and fibrous reaction of varying degrees. Tuberculous spinal arachnoiditis can develop in the following three ways: 1) a tuberculous lesion start- ing primarily in the spinal meninges; 2) secondary extension from basal cranial meningitis or 3) extension from caseous vertebra. 46 Tropical Neurology 2 The primary spinal variety of tuberculous arachnoiditis constitutes 29% of all arachnoiditis. It is believed that spinal arachnoiditis arises as a flare-up lesion of focal parenchymal lesion on the surface of the spinal cord similar to what happens in cranial tubercular meningitis. The meningeal reaction varies depending on the im- mune response of the host. Pathology Gross examination of the spinal cord reveals a thick collar of exudate (Fig. 2.12). The meninges are thick, opaque and lustreless. Discrete and conglomerated tubercles with a caseating center may be seen in the exudate. There is spinal cord atrophy. On histopathological examination four types of changes have been reported with spinal arachnoiditis which include borderzone rarefaction and spongification of the cord, central necrosis, ischemic myelopathy and associated intramedullary tuberculoma. Clinical Features Subacute or chronic, single or multiple level and ascending or transverse radiculomyelopathy comprise the clinical picture of spinal arachnoiditis. The sever- ity and extent of root or cord symptoms depend on the site of maximal involve- ment, such as a cauda equina lesion that presents as radiculopathy and higher lesions as multifocal or single level radiculomyelopathy. No age is exempt from spinal arach- noiditis. In the subacute form, the clinical symptoms develop on an average of two months although maximum severity is seen within 2-5 days following, during which time the course may be stationary. The presentation consists of root pain, paresthe- sia, weakness, wasting and bladder dysfunction. Root pain is lancinating in charac- ter, arising from single or multiple roots, or may be widespread. Tingling numbness follows the root pain. Vibration and joint position sense may be impaired in the lower limbs. Paralysis of the limbs is mostly severe and produces paraplegia or quad- riplegia which is of upper or lower motor neuron type or a mixed variety depending upon the extent of radiculomyelopathy. Retention of urine may be an early or a late feature. The patient may have associated constitutional symptoms such as fever, anorexia and weight loss. Chronic forms of adhesive spinal arachnoiditis progress over months or years and may be indistinguishable from spinal cord compression by a tumor. It may be suspected if the root pain is scattered, persistent and upper motor neuron signs are associated with lower motor neuron signs. Investigation CSF: There is often partial or complete subarachnoid block which may result in a dry tap. The CSF is generally clear or xanthochromic depending on protein level which is usually elevated. There is CSF pleocytosis ranging from a few cells to a few hundred cells. CSF should be examined for AFB. However CSF may be normal in localized or chronic arachnoiditis. An extra CNS source of tuberculosis should also be explored. Myelography: With the availability of water soluble contrast agents, myelography is safe and commonly employed in the diagnosis of spinal arachnoiditis. The myelo- graphic findings in spinal arachnoiditis include: 1. Slow movement of the dye column often with a filling defect and frag- mentation of the column. 2. Total block appears as a ragged edge, or the dye column may extend ob- liquely for two or more vertebral levels. At times there may be a pitch fork 47 Spinal Tuberculosis 2 Fig. 2.12. Dense adhesive arachnoiditis encasing the lumbar spinal cord. The transverse section above shows exudate around the spinal cord (Courtesy Prof. S.K. Shankar). 48 Tropical Neurology 2 appearance or a distinct cut out with a concave edge of the block as seen in spinal tumor. 3. Contrast column with or without block may show multiple small and spotty filling defects, candle guttered appearance over a long length of spinal cord, faggot stick or rat tail in case of cauda equina arachnoiditis and multiple small round clear areas or a large single lesion suggesting cyst formation. In those in whom both cisternal and lumbar myelograms are performed, there may be filling defect extending over many segments which have irregular columns above and below the defect. CT and MRI of spinal cord are preferred techniques because of the facility of the axial section and because they are noninvasive. Spinal cord pathology is clearly seen. CT and MRI show displacement of nerve roots of cauda equina and adherence of roots particularly in clumps on the posterior dorsal sac. Contrast MRI reveals en- hancement of the roots and meninges. The final confirmation of the diagnosis is achieved by biopsy of leptomeninges. A patient with adhesive arachnoiditis should be investigated for infective and noninfective causes of arachnoiditis which are ennumerated in Table 2.4. Treatment The mainstay of the treatment of tubercular spinal arachnoiditis is antitubercu- lar therapy on the same principles as described for tuberculous meningitis. The role of corticosteroids is controversial. Initial oral prednisolone 1 mg/kg body weight is given for one month and tapered over two to three months thereafter. Intrathecal use of hydrocortisone and hyaluronidase have been reported to be useful but have inherent risk of secondary infection. Surgery has a limited role. Surgery should be considered if a large cyst and a localized hard band is found on imaging and its level corresponds with clinical findings. Summary In tuberculosis the spinal cord can be affected in vertebral involvement, tubercu- loma and adhesive arachnoiditis in isolation or various combinations. Spinal tuber- culosis is the commonest form of osteoarticular disease and accounts for 50% of all cases. Vertebral destruction, spinal deformity and paraplegia are the main attributes of the disease. Although paradiscal disease is the commonest type, atypical presenta- tions occur frequently in the form of extensive disease, multifocal infection, epidu- ral granuloma, intradural abscess and posterior element disease. Diagnosis is based on clinical features along with radiological and laboratory evidence of tubercular infection. Despite modern imaging and laboratory techniques, tuberculous destruc- tion at times mimics malignancy and biopsy becomes necessary for cytological and Table 2.4. Causes of spinal adhesive arachnoiditis Infective Tubercular, syphilis, pyogenic, cryptococcus neoformans Noninfective Prolapsed intravertebral disc Trauma Spondylotic radiculomyelopathy Intraspinal tumor, spinal angioma, secondaries Drugs-Penicillin, streptomycin, anaesthetics, myodil Idiopathic 49 Spinal Tuberculosis 2 histopathological diagnosis. In addition to eradication of the disease, prevention and treatment of sequelae like paraplegia and deformity are the main aims of treat- ment. Multi-drug chemotherapy is effective in the treatment of most cases of tuber- culous spondylitis. Surgery is reserved for resistant cases, progressive deformity and severe neurologic deficit. Paraplegia in active disease responds much better to sur- gery than late onset paraplegia. In all cases of paraplegia, surgery must aim at ad- equate neural recovery. In children with significant residual spinal growth, surgery must aim at the preservation of the vertebral endplates. In this regard, a combined anterior and posterior fusion corrects deformity and arrests its progres- sion. The treatment of progressive kyphosis depends on the residual spinal growth, activity of the disease and neurologic status of the patient. In general, deformity correction is safer and easier in active than in healed disease. Implants may be used to correct deformity and stabilize the spine. References 1. Tandon PN, Pathak SN. Tuberculosis of central nervous system. In: Spillaine JD ed. Tropical Neurology. London: Oxford University Press, 1973:37-62. 2. Rajasekaran, S., and Shanmugasundaram, T. K. Prediction of the angle of gibbus deformity in tuberculosis of the spine. J Bone Joint Surg 1987; 69-A:503-509. 3. Kumar KA. Clinical classification of Posterior spinal tuberculosis. Int Orthop 1985; 9:147-152. 4. Lifeso R. Atlanto-axial tuberculosis in adults. J Bone Joint Surg 1987; 69(2):183-187. 5. Ninth Report of the Medical Research Council Working Party on Tuberculosis of the Spine: A 10-Year Assessment of Controlled Trials of Inpatient and Outpatient Tr eatment and of Plaster-of-Paris Jackets for Tuberculosis of the Spine in Children on Standard Chemotherapy. Studies in Masan and Pusan, Korea. J Bone Joint Surg 1985; 67-B (1):103-110. 6. Tuli S. Tuberculosis of the Skeletal System. New Delhi: Jaypee Brothers, 1991:268. 7. Pun WK, Chow SP, Luk KDK, Cheng CL, Hsu LCS, Leong JCY. Tuberculosis of the lumbosacral junction. Long-term follow-up of 26 cases. J Bone Joint Surg 1990; 72-B (4):675-678. 8. Schulitz KP, John CY, Leong et al. Growth changes of solidly fused kyphotic block after surgery for tuberculosis. Spine 1997; 22:1150-1115. CHAPTER 3 Tropical Neurology, edited by U. K. Misra, J. Kalita and R. A. Shakir. ©2003 Landes Bioscience. Pyogenic Infections of the Central Nervous System Kameshwar Prasad, Sumit Singh, Shailesh Gaekwad and Chitra Sarkar Pyogenic infections of the nervous system include acute bacterial meningitis, brain abscess, subdural empyema and epidural abscess. Despite the availability of effective antibiotics, these disorders are still common and are an important cause of morbidity and mortality. In this chapter, various pyogenic infections of the CNS are reviewed with special reference to the tropical countries. Acute Bacterial Meningitis Acute bacterial meningitis (ABM) may be defined as an inflammation of the pia-arachnoid matter and the cerebrospinal fluid (CSF) of the subarachnoid space due to bacterial infection. The subarachnoid space extends through the brain, spinal cord and sheaths of the optic nerves. Any infection of this space involves all the spaces and is invariably associated with some ventriculitis. Epidemiology Bacterial meningitis is widely prevalent throughout the world. The incidence of ABM is difficult to estimate, particularly in the developing countries where a large number of patients remain unreported; however, it is probably more common in developing than in developed countries. H. influenzae type B (Hib) is the most important cause of meningitis in children. The majority of patients with Hib men- ingitis are seen in the months of June to September displaying a bimodal, seasonal variation. 1 Hib meningitis is common in children below five years of age, although it is rare below the age of two months, probably due to transplacental transmission of protective maternal antibodies. The occurrence of Hib meningitis is inversely proportional to the concentration of age-related and type-specific antibodies against the capsular antigens. Susceptibility to Hib meningitis depends upon the presence of H. influenzae in the nasopharynx and the concentration of the type-specific anticapsular antibodies in the host. N. meningitidis is the commonest cause of epi- demic meningitis. 2 It has a worldwide distribution. The Sub-Saharan African region has a ‘meningitis belt’ which extends from 5-15˚ north of the equator and includes Chad, Dahomey, Ghana, Mali, Niger, Nigeria and Sudan. The annual incidence of meningococcal meningitis in this endemic belt is 70/100000 population, the peak incidence being in the months of April and May as opposed to winter and early spring in industrialized nations. The reported cases and deaths due to meningitis in India are summarized in Table 3.1. Acute meningococcal meningitis is usually seen in children and young adults, and only less than 10% cases are above 45 years of age. In the United States, the majority of affected patients is under five years, whereas in the tropics the majority of patients are between five and nine years. 3 Epidemics usually occur due to group A 51 Pyogenic Infections of the Central Nervous System 3 meningococcii every 8-12 year interval in the meningitis belt. This trend of the infection is probably due to the concentration of people who do not have immunity against the disease. For the epidemic to occur there must be enough nonimmune individuals with the concerned pathogen. Once an epidemic occurs, the herd im- munity of the population rises due to an increase in the nasopharyngeal carrier state. With the passage of time, the number of nonimmune individual increases and when a critical mass is reached, an epidemic occurs. An added factor may be a change in the strain of the bacteria with increased virulence. The meningococcal infection spreads through droplets from the nasopharyngeal secretions of the carriers; there- fore, meningococcal meningitis is more common in overcrowded places such as schools and camps. Streptococcus pneumoniae is the commonest cause of meningitis in the adults. Its incidence in the tropical countries is not well known. The average annual incidence of this disease is between 1-2.3/100000 population in the United States with the peak incidence between the months of December and May. 4 Risk factors for pneu- mococcal meningitis are extremes of age, sickle cell disease, post-splenectomy state, lobar pneumonia and acute otitis media. Pneumococci are the commonest cause of recurrent meningitis following CSF leak and meningitis in acquired or primary immunodeficiencies. 5 Etiology The etiology of acute bacterial meningitis depends on the setting in which it occurs. Community and hospital acquired meningitis differ widely in their bacte- riologic spectrum. Community Acquired Meningitis H. influenzae, S. pneumoniae and N. meningitidis together account for about 75% of community acquired meningitis, and the remaining 25% are caused by Gram-negative bacilli or other organisms. There is a striking age-related predisposi- tion for different organisms to cause meningitis. The Gram-negative bacilli and the group B streptococci are the commonest cause of meningitis in neonates, Hib and meningococci in infants and young children, and pneumococci and Gram-negative bacilli in adults. Gram-negative infections are common in infants and children in developing countries. Klebsiella and Salmonella are also more common pathogens in developing countries as opposed to the E. coli in developed countries. 6 Listeria Table 3.1. Reported cases and deaths due to meningitis in India Year Cases Deaths 1987 9080 1596 1988 16834 3304 1989 22263 3511 1990 16757 2984 1991 11995 2290 1992 12305 2009 1994 6496 1035 Source : Health Information India, Govt. of India (DGHS) 1994 52 Tropical Neurology 3 monocytogenes meningitis has been increasingly reported from all over the world and is an important cause of meningitis at the extremes of age. It is more common in alcoholics, immunocompromised individuals and patients with hematological ma- lignancy. Patients with immunodeficiency are also more prone to Gram-negative and pneumococcal meningitis. Hospital Acquired Meningitis Staphylococcus epidermidis is the commonest cause of meningitis associated with ventriculo-peritoneal shunts at all ages. S. aureus usually causes meningitis associated with infective endocarditis and is a common cause of post-shunt menin- gitis, post-traumatic meningitis and infections following neurosurgical procedures. Anaerobic bacteria account for 1% of all cases of meningitis, being under-recog- nized, as the CSF is rarely cultured for anaerobic organisms. Chronic otitis media, mastoiditis and sinusitis are the common predisposing conditions for anaerobic bac- terial meningitis. There is also a marked geographical variation in the pathogens causing meningi- tis. Hib is the most common pathogen in the USA causing more than half of the meningitis. In the UK, the meningococci and the pneumococci are more common than in the USA, but the most common cause is still Hib. In the meningitis belt of sub-Saharan Africa, the meningococcus is the most common pathogen. Pathogenesis The capability of an organism to cause meningitis depends on its “pathogenic potential.” To cause meningitis, the bacteria must enter the host, colonize at a par- ticular site, produce bacteremia and cross the blood brain barrier (BBB) to reach the subarachnoid space where the organism easily proliferates. The infection usually begins by colonization of the pathogen in the nasopharynx. The bacterial factors enhancing the colonization include presence of fimbriae, which play an important role in the adherence of meningococci to the nasopharyngeal mucosa. H. influenzae adhere by their capsules and pneumococci by their lipopolysaccharide capsules. The host prevents the adherence of the bacteria to the epithelium by the local secretion of IgA. Adherence of organisms followed by activation of local immune-mechanisms causes cytotoxicity mediated disruption of the tight junctions of the nasal epithe- lium; loss of cilia and ciliostasis; and finally the penetration of the organisms to the submucosa. Once the bacteria enters the submucosal bloodstream, their polysac- charide capsules provide antiphagocytic activity. The pneumococci activate the al- ternate complement pathway, which facilitates opsonization and subsequent phagocytosis of the bacteria. Patients with defects in the alternative complement pathway are at a greater risk of pneumococcal infections e.g., patients with splenec- tomy and sickle cell disease. The mechanism of invasion of the subarachnoid space (SAS) by the bacteria is still under speculation. The dural venous sinuses, the thin dura over the cribriform plate, the choroid plexus, and the monocytes have all been implicated as the site of invasion by the organisms. The bacteria may also enter the subarachnoid space through the hematogenous route from a parameningeal suppurative focus or through the defects in the dura. The normal CSF has almost undetectable levels of IgM, whereas IgG and IgA are barely detectable. The low level of complement in the CSF accounts for the impaired opsonization and phagocytosis in patients with meningitis. 7 The meninges respond to the bacterial invasion by polymorphonuclear leukocytosis. 53 Pyogenic Infections of the Central Nervous System 3 The mechanism of entry of leukocytes into the SAS traversing the BBB is not known although the role of a C5a complement has been suggested. In the absence of a proper opsonic and bactericidal activity of neutrophils, there is a relentless multipli- cation of the pathogenic organisms in the SAS resulting in inflammation of the subarachnoid space. In meningitis, there is breakdown of the tight junctions of the capillary endothelial cells and an increased pinocytosis across the cells. This is due to the lipopolysaccharide capsules of the bacteria, cytokines and interleukins. The breach of the blood brain barrier produces vasogenic cerebral edema resulting in increased intracranial pressure (ICP) which adds to the cytotoxic and interstitial cerebral edema. The release of toxic substances from the bacteria or neutrophils results in cytotoxic edema and the released cells and/or molecules impair CSF flow leading to intersti- tial cerebral edema. The inflammation of the meninges and the presence of an in- flammatory exudate in the subarachnoid space results in vasculitis of the large blood vessels traversing this space. This causes relative ischemia of the brain. Associated phlebitis of the cerebral veins may result in cortical venous thrombosis or dural sinus thrombosis which leads to focal deficits and seizures. In meningitis, cerebral autoregulation is impaired and cerebral blood flow reduced. Recently, the role of free radicals and reactive oxygen species in the neuronal injury in pyogenic meningi- tis has been suggested. Pathology The response to bacterial invasion of the SAS is more marked over the convexi- ties of the cerebral cortex, imparting a yellowish-green color. The exudate envelops the basal cisterns and extends to the spinal SAS mostly to the posterior surface of the spinal cord. 8 Microscopically, exudate shows neutrophils and bacteria in the early stage (Fig. 3.1). As the opsonic activity of the neutrophils is impaired, live bacteria can be demonstrated in the neutrophils. There is subintimal inflammatory infiltrate comprising neutrophils and lymphocytes in the meningeal arteries which is unique to pyogenic infections of the meninges. The veins also share the inflammatory re- sponse and become distended. Mural inflammation can result in cortical venous thrombosis with resultant cortical infarctions. By the end of the first week in un- treated patients, the neutrophils are removed by macrophages and replaced by lym- phocytes. Subtle changes such as edema of the subependymal and ependymal tissues, sloughing of the ependymal lining and swelling of the astrocytes and glial cells may be visible in the brain parenchyma. As the exudates increase, the SAS is reduced and CSF flow may be compromised. Obstruction of the foramina of Luschka and Magendie results in noncommunicating hydrocephalus. The inflammatory exudate also blocks the arachnoid villi and further impedes CSF absorption, resulting in oozing of CSF in the periventricular white matter leading to interstitial edema. The exudate is very thick in Hib and is mostly localized to the basal cisterns, whereas it is thinner and more extensive on the cerebral convexities in pneumococcal infections. The SAS may be devoid of any inflammatory exudate in acute fulminant meningo- coccemia, whereas, the interstitial edema may be very significant. These pathologi- cal features are usually seen in the untreated cases, and the pathology is markedly altered following antibiotic therapy. Clinical Manifestations Patients with ABM usually present with a classical triad of fever, headache and altered sensorium. Almost all patients have fever and headache, but alteration in [...]... bacterial meningitis Neurology India 1989; 37: 52 5-5 28 Committee on Infectious Diseases, Academy of Pediatrics Treatment of bacterial meningitis Pediatrics 1988; 81:90 4-9 07 Tunkel AR, Wispelwey B, Scheld WM Bacterial meningitis: Recent advances in pathophysiology and treatment Ann Intern Med 1990; 1 12: 61 0-6 23 Tunkel AR, Scheld WM Acute bacterial meningitis Lancet 1995; 346:167 5-1 680 Allan R, Tunkel... children, fluid restriction can cause dehydration, particularly if fever is present A daily requirement of 120 0 ml/m2 is mandatory with 2 0-4 0 meq K+/m2 body surface area Steroids Corticosteroids reduce cytokine-mediated inflammation Dexamethasone is the most studied corticosteroid in this condition and at least 10 clinical trials have been reported Moreover, meta-analyses of the clinical trials suggest that... relative penicillin resistance J Infect Dis 1987; 156:73 2- 7 36 Musher DM Infections caused by Streptococcus pneumoniae: Clinical spectrum, pathogenesis, immunity and treatment Clin Infect Dis J 19 92; 14:80 1-8 09 Appede-GGO, Adeyemi O, Ogyi EO Gram-negative bacillary meningitis in infants and children in developing countries East-Afr Med J 1996; 73(9):58 6-9 1 Kadurgammua JL, Hangstler B, Bray MA, Zak O Incubation... be reserved for multi-resistant cases Pyogenic Infections of the Central Nervous System 61 Table 3.3 Antibiotics dose schedule to be used in pyogenic meningitis Penicillin G Ampicillin Ceftriaxone Cefotaxime Ceftazidime Nafcillin Oxacillin Vancomycin 2 0 -2 4 million U/day intravenously (divided doses every 4 h) 12 g/day intravenously (every 4 h) 2- 4 g/day intravenously (every 12 h) 8 g/day intravenously... Tropical Neurology Table 3 .2 Common pathogens and empiric therapeutic recommendations based on age of patients with bacterial meningitis Age of Patient Common Bacterial Pathogens Empiric Antimicrobial Therapy* 1-4 weeks Streptococcus agalactiae, Escherichia coli, Listeria monocytogenes, Klebsiella pneumoniae, Enterococcus species Ampicillin plus cefotaxime, or ampicillin plus an aminoglycoside 4-1 2. .. management of bacterial meningitis American Family 1997; 56:135 5-1 3 62 Prasad K, Haines T Dexamethasone therapy in acute bacterial meningitis: How strong is the evidence for routine use? J Neurol Neurosurg Psych 1995; 59:3 1-3 7 Beek D van de, Gans J de, McIntyre P, Prasad K Corticosteroids as adjunctive 74 Tropical Neurology 17 18 19 3 20 therapy in acute bacterial meningitis (Cochrane Review) In: The... Editorial Lancet 1999; 354(9179):615–616 Schwartz B, Al-Ruwais A, As’Ashi J et al Comparative efficacy of ceftriaxone and rifampicin in erradicating pharyngeal carriage of group A Neisserria meningitides Lancet 1988; 1: 123 9-1 24 2 Beller AJ, Sahar A, Praiss I Brain abscess Review of 89 cases over 30 years J Neurol Neurosurrg Psychiat 1973; 36:75 7-7 68 Mamelak AN, Obara WG, Flaherty JF, Rosenblun ML Nocardial... should be continued for at least three to four weeks There are no randomized trials to support the choice of any particular antibiotic and the therapy can be tailored, depending upon the source of infection Vancomycin may substitute for penicillin in cases of empyema second- 3 72 3 Tropical Neurology ary to trauma Antiepileptics are to be given for seizures and mannitol and steroids for raised ICP The... negative bacteria, particularly pseudomonas Duration of Therapy The duration of therapy depends on the suspected or isolated organism The patients with meningococcal and Hib meningitis usually recover with seven and ten days therapy, respectively Those with pneumococcus do so in two weeks The Gram-negative organisms need to be treated for three to six weeks It may be noted 3 62 Tropical Neurology that... inflammatory reactions by prostaglandin E2 in experimental meningitis J Infect Dis 1989; 160:71 5-7 19 Escourolle R, Poviner J Pathology of infectious diseases In: Escourolle R, PovierJ, eds Manual of Basic Neuropathology Philadelphia: WB Saunders, 1995 Durand ML, Calderwood SB et al Acute bacterial meningitis in adults: A review of 493 episodes N Engl J Med 1993; 328 :2 1-8 Prasad K, Behari M, Ahuja GK Normocellular . 1596 1988 16834 3304 1989 22 263 3511 1990 16757 29 84 1991 11995 22 90 19 92 123 05 20 09 1994 6496 1035 Source : Health Information India, Govt. of India (DGHS) 1994 52 Tropical Neurology 3 monocytogenes. dehydration, particularly if fever is present. A daily re- quirement of 120 0 ml/m 2 is mandatory with 2 0-4 0 meq K + /m 2 body surface area. Steroids Corticosteroids reduce cytokine-mediated inflammation Brothers, 1991 :26 8. 7. Pun WK, Chow SP, Luk KDK, Cheng CL, Hsu LCS, Leong JCY. Tuberculosis of the lumbosacral junction. Long-term follow-up of 26 cases. J Bone Joint Surg 1990; 7 2- B (4):67 5-6 78. 8.