Chap 360 -- Meningtis, Encephalitis, Brain Abscess, Empyema
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CHAPTER 360: MENINGITIS, ENCEPHALITIS, BRAIN ABSCESS, EMPYEMA •
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Prodrome of fever, headache are benign until altered consciousness, focal neurologic deficits or seizures appear. Approach to the patient: first identify if infection is in the subarachnoid space. Viral: encephalitis Bacterial/ fungal: cerebritis or abscess Nuchal rigidity is the pathognomonic sign of meningeal irritation. Kernigs’ sign Brudzinski’s sign Failure of a patient suspected with viral encephalitis to improve should prompt reevaluation. Bacterial meningitis is an acute purulent infection within the subarachnoid space. Bacterial meningitis may result to decreased consciousness, seizures, raised ICP and stroke. Meningoencephalitis – the parenchyma, meninges ad subarachnoid Bacterial meningitis is the most common form of suppurative CNS infection. S. pneumoniae is the most common cause in adults >20 N. meningitides is common in ages 2-20 with petechial and purpuric lesions. Group B or S. agalactiae predominates in neonates and elderly >50 Listeria predominates in neonates and pregnant women due to organisms in ready to eat foods H. influenzae in unvaccinated children Staph aureus and CN-staph are causes of infection following an invasive neurosurgical procedure Pathophysiology: Bacteria are able to avoid phagocytosis because of a polysaccharide capsule. A critical event in the pathogenesis of bacterial meningitis is the
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inflammatory reaction induced by the invading bacteria. Lysis of bacteria with the subsequent release of cell wall components into the subarachnoid space is the initial step in the induction of the inflammatory response. Cytokine response is followed by an increase in CSF protein concentration and leukocystosis. Much of the pathophysiology of bacterial meningitis is a direct consequence of elevated levels of CSF cytokines and chemokines. TNF and IL1 act synergistically to increase the permeability of the blood brain barrier resulting in vasogenic edema and the leakage of serum proteins into the subarachnoid space. During the very early stages of meningitis there is an increase in cerebral blood flow followed by a decrease in blood flow and loss of cerebrovascular autoregulation. Combination of cytotoxic, vasogenic and interstitial edema lead to increased ICP and coma. Clinical presentation: clinical triad of meningitis: fever, headache and nuchal rigidity. Focal seizures may be due to focal arterial ischemia, infarction, and cortical venous thrombosis with hemorrhage or focal edema. Generalized seizures or status epilepticus may be due to hyponatremia and cerebral anoxia. Raised ICP is an expected complication and is the major cause of obtundation and coma. Signs of increased ICP are: papilledema, dilated poorly reactive pupils, 6th nerve palsies, decerebrate posturing and Cushing’s reflex ( bradycardia, hypotension, irregular respirations) Most disastrous complication is cerebral herniation. Diagnosis: made by examination of CSF Classic CSF abnormalities: leukocystosis (>100 cells), decreased glucose <2.2 mmol/L or serum glucose of <0.4, increased
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protein concentration >0.45 g/L and increased opening pressure >180 mmH2O CSF latex agglutination test has a specificity of 95-100% for S. pneumoniae and N. meningitides, so a + test is virtually diagnostic of bacterial meningitis. Limulus amoebocyte lysate assay is a rapid diagnostic test for the detection of gram – endotoxin in CSF MRI is preferred than Ct because of its superiority in demonstrating areas of cerebral edema and ischemia, Differential diagnosis: findings on CSF studies, neuroimaging and EEG distinguishes HSV encephalitis from bacterial meningitis Viral CSF infections: lymphocytic pleocytosis with a normal glucose Bacterial: PMN pleocytosis and hypoglycorrhachia Subacutely evolving meningitis may on occasion be considered as differentia diagnosis of acute meningitis. Principal causes include M. tuberculosis, C. neoformans, H. capsulatum, C. immitis and T. pallidum Treatment: bacterial meningitis is a medical emergency. Goal is to begin antibiotic therapy within 60 min. Ceftriaxone + vancomycin or Cefotaxime + vancomycin Cefepime has greater activity against Enterobacter and P. aeruginosa Ampicillin to cover Listeria In meningitis following neurosurgical procedures: vancomycin and ceftazidime Ceftazidime is the only cephalosporin with adequate activity against CNS infections with P. aeruginosa. Meropenem is a carbapenem antibiotic that is highly active in vitro against Listeria, P. aeruginosa and penicillin resistant pneumococci. Meningococcal meningitis: Pen G, if resistant Ceftriaxone.
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Chemoprophylaxis with Rifampicin. Rifampicin is CI in pregnant. Pneumococcal meningitis: cephalosporin + vancomycin, MICs > 0.5 ug/mL treat with cefotaxime or ceftriaxone, MICs of >1 ug/mL vancomycin Patients with penicillin and cephalosporin resistant strains of S. pneumoniae who don’t respond to vancomycin may be given intraventricular vancomycin L. monocytogenes meningitis: ampicillin/ gentamicin. In penicillin allergic patients give cotrimoxazole Staphylococcal meningitis: nafcillin, for MRSA use vancomycin Gram – bacillary meningitis: 3rd gen cephalosporins but with P. aeruginosa use ceftazidime Adjunctive therapy: Dexamethasone For increased ICP: elevate head to 30-45 degrees, intubation, hyperventilation and mannitol. Acute Viral Meningitis: fever, headache and meningeal irritation accompanied by arthralgia, malaise and anorexia. Photophobia and pain on moving the eyes. Kernig’s and brudzinski’s sign are absent. Enteroviruses account for 75-90% of aseptic meningitis. Laboratory Diagnosis of CSF: lymphocytic pleocytosis and slightly elevated protein concentration with normal glucose. As a rule, lymphocytic pleocytosis with a low glucose concentration should suggest fungal, listerial or tuberculous meningitis. PCR – diagnostic procedure of choice HSV PCR- for recurrent episodes of aseptic meningitis Oligoclonal bands can also be found in noninfectious neurologic diseases. Enterovirus infection can have exanthema, foot and mouth disease, herpangina, pleurodynia, myopericarditis and hemorrhagic
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conjunctivitis ( stigmata of enterovirus infection) Arbovirus – bird deaths HSV meningitis- HSV2, Mollaret’s meningitis VZV meningitis: chickenpox and shingles, acute cerebral ataxia. EBV infections may also produce aseptic meningitis characterized by atypical lymphocytosis in peripheral blood. HIV meningitis: aseptic meningitis is a common manifestation. Mumps: orchitis, oophoritis, parotitis and pancreatitis, also elevations in serum lipase and amylase LCMV infection: exposure to house mice presenting with leucopenia, thrombocytopenia or abnormal liver function tests. Treatment is symptomatic Hyponatremia may develop due to inappropriate vasopressin secretion (SIADH) Oral acyclovir may be of benefit in meningitis caused by HSV, EBV or VZV Patients with HIV should be given HAART. Vaccination is an effective method Prognosis: prognosis for full recovery from viral meningitis is excellent. Viral encephalitis: involvement of the brain parenchyma Involvement of the spinal cord is encephalomyelitis Nerve root involvement is encephalomyeloradiculitis Confusion, altered level of consciousness, hallucinations, agitations, personality change, behavioral disorders and a frankly psychotic state is seen. Focal findings include: ataxia, aphasia, hemiparesis Temperature dysregulation, diabetes insipidus, SIADH Most common viruses causing sporadic cases are HSV1, VZV and enteroviruses. Epidemics of encephalitis are caused by arboviruses.
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Laboratory: lymphocytic pleocytosis, mildly elevated protein and normal glucose concentration. Hemorrhagic encephalitis is seen in HSV and Colorado tick fever virus. CSF PCR is the primary diagnostic test for CNS infections caused by CMV, EBV, and VZV. Demonstration of WNV IgM antibodies is diagnostic of WNV encephalitis. Focal neurologic findings always point to HSV as the etiologic agent. Brain biopsy was once considered the gold standard. Differential Diagnosis: differentiate from vascular diseases, abscess, empyema, fungal, parasitic, rickettsial, tuberculous infections, tumors, Reye’s syndrome, toxic encephalopathy, subdural hematoma and SLE. Primary amebic meningoencephalitis – Naegleria fowleri Subacute or chronic granulomatous amebic meningoencephalitis – Acanthamoeba and Balamuthia Raccoon exposure Bartonella sp- agents of cat scratch fever which is the most common bacterial infection mimicking viral encephalitis. Involvement of the inferomedial frontotemporal regions of the brain is present in HSV encephalitis. If deep gray matter, basal ganglia and thalamus are affected suspect flaviviruses. Deaths in crows and corvid birds are due to WNV. Treatment: acyclovir is the treatment for HSV. Ganciclovir and foscarnet are used for CMV related CNS infections. Cidofovir if it doesn’t respond to Ganciclovir. Side effects of Ganciclovir: granulocytopenia and thrombocytopenia, retinal detachment. IV Ribavarin for California encephalitis (Lacrosse) virus. Side effect: hemolysis, anemia Subacute Meningitis: typically manifest with unrelenting
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headache, stiff neck, fever and lethargy Common causative agents: M. tuberculosis, C. neoformans, H capsulatum, C. immitis, T. pallidum. The most common pathogen causing fungal encephalitis is C. neoformans. T. pallidum invades the CNS in the early course of the illness, affecting cranial nerves VII & VIII. Culture remains to be the gold standard in the diagnosis of tuberculous meningitis Eosinophils may be seen in C. immitis meningitis. Cryptococcal polysaccharide antigen tests for cryptococcal meningitis is highly sensitive. Diagnosis of syphilic meningitis is made when a reactive treponemal test is associated with lymphocytic pleocytosis. A negative CSF FTA ABS or MHA TP rules out neurosyphilis. Treatment: initial therapy of Rifampicin, isoniazid, pyrazinamide and ethambutol. Dexamethasone if with hydrocephalus. C. neoformans- amp B and flucytosine H. capsulatum- amp B and itraconazole C. immitis- IV amp B The most common complication of fungal meningitis is hydrocephalus. Syphilitic meningitis is treated with aq. Pen G. Chronic Encephalitis: Progressive multifocal leukoencephalopathy is pathologicaly characterized by multifocal areas of demyelination. Astrocytes and oligoendrocytes are enlarged. PCR analysis is diagnostic. No therapy is available Subacute Sclerosing Panencephalitis: measles Treatment: Isoprinosine and interferons Progressive Rubella Panencephalitis: primarily affects males with congenital rubella syndrome.
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No therapy is available. Brain abscess – is a focal suppurative infection within the brain parenchyma typically surrounded by a vascularized capsule. Caused by Toxoplasma, Aspergillus, Nocardia, Mycobacteria and C. neoformans Taenia solium in Latin America Direct spread from a contiguous cranial site of infection such as paranasal sinusitis, otitis media, mastoiditis or dental infection Otogenic abscesses usually in the temporal lobe. Cryptogenic abscesses are due to dental infections. Enterobacteriaceae and P. aeruginosa are important causes of abscesses associated with urinary sepsis. Tetralogy of Fallot Intact brain is resistant to infections; only in the presence of ischemia, hypoxia and infarct will it be able to be penetrated. Early cerebritis – infiltrates Late cerebritis- pus formation 3rd stage: is early capsule formation Late capsule stage characterized with a well formed necrotic center Marked gliosis will cause the sequelae – seizures. Brain abscess presents as a mass. Triad: fever, focal Neurologic deficits and fever Headache is the most common complaint. Hemiparesis seen in frontal lobe lesion Dysphasia is seen in temporal lobe lesion Nystagmus and ataxia are cerebellar lesions. MRI is used for diagnosis. When fever is absent suspect tumors. Treat with 3rd gen cephalosporins, ceftazidime for P. aeruginosa and vancomycin for staphylococci. Non bacterial causes of infectious focal cns lesions: neurocysticercosis is the most
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common parasitic disease of the CNS worldwide T. gondi from cat feces Associated with resolution of the inflammatory response Toxoplasma infection is usually asymptomatic. MRI or CT scans. Parenchymal calcifications and scolex ca be visualized. Albendazole and praziquantel. CNS toxoplasmosis is treated with combination of sulfadiazine + pyrimethamine Folinic acid to prevent megaloblastic anemia Clindamycin + pyrimethamine are an alternative for patients who cannot tolerate sulfadiazine. Subdural empyema – is a rare disorder characterized by a collection of pus between the dura and arachnoid membrane. Sinusitits is the most common predisposing condition and typically involves the frontal sinuses. Young males are more affected. Also may develop as complication of head trauma or neurosurgery Presents with fever and progressively worsening headache Headache is the most common complaint Contralateral hemiparesis and hemiplegia is the most common focal Neurologic deficit. MRI or CT scan. CT may show a crescent shaped hypodensity over one or both hemispheres. SDE is a medical emergency. Burr-hole drainage or craniotomy is the management. 3rd gen cephalosporins and vancomycin and metronidazole. Epidural abscess- is a suppurative infection occurring in the potential space between the inner skull table and dura. Develops as a complication of craniotomy or infectious from an area with osteomyelitis. Staph is usually the etiologic agent. MRI is the procedure of choice. Neurosurgical drainage is indicated.
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3rd gen cephalosporins+nafcillin or vancomycin+ metronidazole Ceftazidime is used for neurosurgical patients. Suppurative Thrombophlebitis- is septic venous thrombosis of cortical veins and sinuses Occur as a complication of bacterial meningitis, SDE, epidural abscess. Superior sagittal sinus is the largest of the venous sinuses. Bacterial meningitis is a common predisposing condition for septic thrombosis of the superior sagittal sinus. Thrombosis of the superior sagittal sinus is often associated with thrombosis of superior cortical veins and small parenchymal hemorrhages. Septic thrombosis of the superior sagittal sinus with headache, fever, nausea, vomiting and confusion and seizures. There maybe a rapid development to stupor or coma. Nuchal rigidity, Kernig’s and Brudzinski’s may be present. Septic cavernous sinus thrombosis presents with fever, headache frontal and retroorbital pain and diplopia. Classic signs are ptosis, proptosis, chemosis and extraocular dysmotility due to deficits of cranial nerves II, IV and VI, hyperesthesia of the 5th nerve and decreased corneal reflex, papilledema. Headache and earache are the most frequent symptoms of transverse sinus thrombosis. it may also present with Gradinego’s syndrome ( facial pain ). Sigmoid sinus and internal jugular vein thrombosis may present with neck pain. Cerebral angiography for definitive diagnosis. Septic venous sinus thrombosis is treated with antibiotics and hydration. Dose adjusted heparin Aseptic venous sinus thrombosis through urokinase therapy, rTPa and IV heparin.
Liz IIIB
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Prodrome of fever, headache are benign until altered consciousness, focal neurologic deficits or seizures appear. Approach to the patient: first identify if infection is in the subarachnoid space. Viral: encephalitis Bacterial/ fungal: cerebritis or abscess Nuchal rigidity is the pathognomonic sign of meningeal irritation. Kernigs’ sign Brudzinski’s sign Failure of a patient suspected with viral encephalitis to improve should prompt reevaluation. Bacterial meningitis is an acute purulent infection within the subarachnoid space. Bacterial meningitis may result to decreased consciousness, seizures, raised ICP and stroke. Meningoencephalitis – the parenchyma, meninges ad subarachnoid Bacterial meningitis is the most common form of suppurative CNS infection. S. pneumoniae is the most common cause in adults >20 N. meningitides is common in ages 2-20 with petechial and purpuric lesions. Group B or S. agalactiae predominates in neonates and elderly >50 Listeria predominates in neonates and pregnant women due to organisms in ready to eat foods H. influenzae in unvaccinated children Staph aureus and CN-staph are causes of infection following an invasive neurosurgical procedure Pathophysiology: Bacteria are able to avoid phagocytosis because of a polysaccharide capsule. A critical event in the pathogenesis of bacterial meningitis is the
•
• •
•
• • •
• •
•
• • •
inflammatory reaction induced by the invading bacteria. Lysis of bacteria with the subsequent release of cell wall components into the subarachnoid space is the initial step in the induction of the inflammatory response. Cytokine response is followed by an increase in CSF protein concentration and leukocystosis. Much of the pathophysiology of bacterial meningitis is a direct consequence of elevated levels of CSF cytokines and chemokines. TNF and IL1 act synergistically to increase the permeability of the blood brain barrier resulting in vasogenic edema and the leakage of serum proteins into the subarachnoid space. During the very early stages of meningitis there is an increase in cerebral blood flow followed by a decrease in blood flow and loss of cerebrovascular autoregulation. Combination of cytotoxic, vasogenic and interstitial edema lead to increased ICP and coma. Clinical presentation: clinical triad of meningitis: fever, headache and nuchal rigidity. Focal seizures may be due to focal arterial ischemia, infarction, and cortical venous thrombosis with hemorrhage or focal edema. Generalized seizures or status epilepticus may be due to hyponatremia and cerebral anoxia. Raised ICP is an expected complication and is the major cause of obtundation and coma. Signs of increased ICP are: papilledema, dilated poorly reactive pupils, 6th nerve palsies, decerebrate posturing and Cushing’s reflex ( bradycardia, hypotension, irregular respirations) Most disastrous complication is cerebral herniation. Diagnosis: made by examination of CSF Classic CSF abnormalities: leukocystosis (>100 cells), decreased glucose <2.2 mmol/L or serum glucose of <0.4, increased
•
•
•
•
• • •
• • • • • • •
•
•
protein concentration >0.45 g/L and increased opening pressure >180 mmH2O CSF latex agglutination test has a specificity of 95-100% for S. pneumoniae and N. meningitides, so a + test is virtually diagnostic of bacterial meningitis. Limulus amoebocyte lysate assay is a rapid diagnostic test for the detection of gram – endotoxin in CSF MRI is preferred than Ct because of its superiority in demonstrating areas of cerebral edema and ischemia, Differential diagnosis: findings on CSF studies, neuroimaging and EEG distinguishes HSV encephalitis from bacterial meningitis Viral CSF infections: lymphocytic pleocytosis with a normal glucose Bacterial: PMN pleocytosis and hypoglycorrhachia Subacutely evolving meningitis may on occasion be considered as differentia diagnosis of acute meningitis. Principal causes include M. tuberculosis, C. neoformans, H. capsulatum, C. immitis and T. pallidum Treatment: bacterial meningitis is a medical emergency. Goal is to begin antibiotic therapy within 60 min. Ceftriaxone + vancomycin or Cefotaxime + vancomycin Cefepime has greater activity against Enterobacter and P. aeruginosa Ampicillin to cover Listeria In meningitis following neurosurgical procedures: vancomycin and ceftazidime Ceftazidime is the only cephalosporin with adequate activity against CNS infections with P. aeruginosa. Meropenem is a carbapenem antibiotic that is highly active in vitro against Listeria, P. aeruginosa and penicillin resistant pneumococci. Meningococcal meningitis: Pen G, if resistant Ceftriaxone.
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Chemoprophylaxis with Rifampicin. Rifampicin is CI in pregnant. Pneumococcal meningitis: cephalosporin + vancomycin, MICs > 0.5 ug/mL treat with cefotaxime or ceftriaxone, MICs of >1 ug/mL vancomycin Patients with penicillin and cephalosporin resistant strains of S. pneumoniae who don’t respond to vancomycin may be given intraventricular vancomycin L. monocytogenes meningitis: ampicillin/ gentamicin. In penicillin allergic patients give cotrimoxazole Staphylococcal meningitis: nafcillin, for MRSA use vancomycin Gram – bacillary meningitis: 3rd gen cephalosporins but with P. aeruginosa use ceftazidime Adjunctive therapy: Dexamethasone For increased ICP: elevate head to 30-45 degrees, intubation, hyperventilation and mannitol. Acute Viral Meningitis: fever, headache and meningeal irritation accompanied by arthralgia, malaise and anorexia. Photophobia and pain on moving the eyes. Kernig’s and brudzinski’s sign are absent. Enteroviruses account for 75-90% of aseptic meningitis. Laboratory Diagnosis of CSF: lymphocytic pleocytosis and slightly elevated protein concentration with normal glucose. As a rule, lymphocytic pleocytosis with a low glucose concentration should suggest fungal, listerial or tuberculous meningitis. PCR – diagnostic procedure of choice HSV PCR- for recurrent episodes of aseptic meningitis Oligoclonal bands can also be found in noninfectious neurologic diseases. Enterovirus infection can have exanthema, foot and mouth disease, herpangina, pleurodynia, myopericarditis and hemorrhagic
• • • •
• •
•
• • • • • • • • • •
• • • •
conjunctivitis ( stigmata of enterovirus infection) Arbovirus – bird deaths HSV meningitis- HSV2, Mollaret’s meningitis VZV meningitis: chickenpox and shingles, acute cerebral ataxia. EBV infections may also produce aseptic meningitis characterized by atypical lymphocytosis in peripheral blood. HIV meningitis: aseptic meningitis is a common manifestation. Mumps: orchitis, oophoritis, parotitis and pancreatitis, also elevations in serum lipase and amylase LCMV infection: exposure to house mice presenting with leucopenia, thrombocytopenia or abnormal liver function tests. Treatment is symptomatic Hyponatremia may develop due to inappropriate vasopressin secretion (SIADH) Oral acyclovir may be of benefit in meningitis caused by HSV, EBV or VZV Patients with HIV should be given HAART. Vaccination is an effective method Prognosis: prognosis for full recovery from viral meningitis is excellent. Viral encephalitis: involvement of the brain parenchyma Involvement of the spinal cord is encephalomyelitis Nerve root involvement is encephalomyeloradiculitis Confusion, altered level of consciousness, hallucinations, agitations, personality change, behavioral disorders and a frankly psychotic state is seen. Focal findings include: ataxia, aphasia, hemiparesis Temperature dysregulation, diabetes insipidus, SIADH Most common viruses causing sporadic cases are HSV1, VZV and enteroviruses. Epidemics of encephalitis are caused by arboviruses.
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Laboratory: lymphocytic pleocytosis, mildly elevated protein and normal glucose concentration. Hemorrhagic encephalitis is seen in HSV and Colorado tick fever virus. CSF PCR is the primary diagnostic test for CNS infections caused by CMV, EBV, and VZV. Demonstration of WNV IgM antibodies is diagnostic of WNV encephalitis. Focal neurologic findings always point to HSV as the etiologic agent. Brain biopsy was once considered the gold standard. Differential Diagnosis: differentiate from vascular diseases, abscess, empyema, fungal, parasitic, rickettsial, tuberculous infections, tumors, Reye’s syndrome, toxic encephalopathy, subdural hematoma and SLE. Primary amebic meningoencephalitis – Naegleria fowleri Subacute or chronic granulomatous amebic meningoencephalitis – Acanthamoeba and Balamuthia Raccoon exposure Bartonella sp- agents of cat scratch fever which is the most common bacterial infection mimicking viral encephalitis. Involvement of the inferomedial frontotemporal regions of the brain is present in HSV encephalitis. If deep gray matter, basal ganglia and thalamus are affected suspect flaviviruses. Deaths in crows and corvid birds are due to WNV. Treatment: acyclovir is the treatment for HSV. Ganciclovir and foscarnet are used for CMV related CNS infections. Cidofovir if it doesn’t respond to Ganciclovir. Side effects of Ganciclovir: granulocytopenia and thrombocytopenia, retinal detachment. IV Ribavarin for California encephalitis (Lacrosse) virus. Side effect: hemolysis, anemia Subacute Meningitis: typically manifest with unrelenting
• • • • • • •
• • • • • • • • •
• • • • • •
headache, stiff neck, fever and lethargy Common causative agents: M. tuberculosis, C. neoformans, H capsulatum, C. immitis, T. pallidum. The most common pathogen causing fungal encephalitis is C. neoformans. T. pallidum invades the CNS in the early course of the illness, affecting cranial nerves VII & VIII. Culture remains to be the gold standard in the diagnosis of tuberculous meningitis Eosinophils may be seen in C. immitis meningitis. Cryptococcal polysaccharide antigen tests for cryptococcal meningitis is highly sensitive. Diagnosis of syphilic meningitis is made when a reactive treponemal test is associated with lymphocytic pleocytosis. A negative CSF FTA ABS or MHA TP rules out neurosyphilis. Treatment: initial therapy of Rifampicin, isoniazid, pyrazinamide and ethambutol. Dexamethasone if with hydrocephalus. C. neoformans- amp B and flucytosine H. capsulatum- amp B and itraconazole C. immitis- IV amp B The most common complication of fungal meningitis is hydrocephalus. Syphilitic meningitis is treated with aq. Pen G. Chronic Encephalitis: Progressive multifocal leukoencephalopathy is pathologicaly characterized by multifocal areas of demyelination. Astrocytes and oligoendrocytes are enlarged. PCR analysis is diagnostic. No therapy is available Subacute Sclerosing Panencephalitis: measles Treatment: Isoprinosine and interferons Progressive Rubella Panencephalitis: primarily affects males with congenital rubella syndrome.
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No therapy is available. Brain abscess – is a focal suppurative infection within the brain parenchyma typically surrounded by a vascularized capsule. Caused by Toxoplasma, Aspergillus, Nocardia, Mycobacteria and C. neoformans Taenia solium in Latin America Direct spread from a contiguous cranial site of infection such as paranasal sinusitis, otitis media, mastoiditis or dental infection Otogenic abscesses usually in the temporal lobe. Cryptogenic abscesses are due to dental infections. Enterobacteriaceae and P. aeruginosa are important causes of abscesses associated with urinary sepsis. Tetralogy of Fallot Intact brain is resistant to infections; only in the presence of ischemia, hypoxia and infarct will it be able to be penetrated. Early cerebritis – infiltrates Late cerebritis- pus formation 3rd stage: is early capsule formation Late capsule stage characterized with a well formed necrotic center Marked gliosis will cause the sequelae – seizures. Brain abscess presents as a mass. Triad: fever, focal Neurologic deficits and fever Headache is the most common complaint. Hemiparesis seen in frontal lobe lesion Dysphasia is seen in temporal lobe lesion Nystagmus and ataxia are cerebellar lesions. MRI is used for diagnosis. When fever is absent suspect tumors. Treat with 3rd gen cephalosporins, ceftazidime for P. aeruginosa and vancomycin for staphylococci. Non bacterial causes of infectious focal cns lesions: neurocysticercosis is the most
• • • • • • • • • •
• • • • • • • • •
• •
• • • •
common parasitic disease of the CNS worldwide T. gondi from cat feces Associated with resolution of the inflammatory response Toxoplasma infection is usually asymptomatic. MRI or CT scans. Parenchymal calcifications and scolex ca be visualized. Albendazole and praziquantel. CNS toxoplasmosis is treated with combination of sulfadiazine + pyrimethamine Folinic acid to prevent megaloblastic anemia Clindamycin + pyrimethamine are an alternative for patients who cannot tolerate sulfadiazine. Subdural empyema – is a rare disorder characterized by a collection of pus between the dura and arachnoid membrane. Sinusitits is the most common predisposing condition and typically involves the frontal sinuses. Young males are more affected. Also may develop as complication of head trauma or neurosurgery Presents with fever and progressively worsening headache Headache is the most common complaint Contralateral hemiparesis and hemiplegia is the most common focal Neurologic deficit. MRI or CT scan. CT may show a crescent shaped hypodensity over one or both hemispheres. SDE is a medical emergency. Burr-hole drainage or craniotomy is the management. 3rd gen cephalosporins and vancomycin and metronidazole. Epidural abscess- is a suppurative infection occurring in the potential space between the inner skull table and dura. Develops as a complication of craniotomy or infectious from an area with osteomyelitis. Staph is usually the etiologic agent. MRI is the procedure of choice. Neurosurgical drainage is indicated.
• • • • • •
•
• • •
•
•
• • • • •
3rd gen cephalosporins+nafcillin or vancomycin+ metronidazole Ceftazidime is used for neurosurgical patients. Suppurative Thrombophlebitis- is septic venous thrombosis of cortical veins and sinuses Occur as a complication of bacterial meningitis, SDE, epidural abscess. Superior sagittal sinus is the largest of the venous sinuses. Bacterial meningitis is a common predisposing condition for septic thrombosis of the superior sagittal sinus. Thrombosis of the superior sagittal sinus is often associated with thrombosis of superior cortical veins and small parenchymal hemorrhages. Septic thrombosis of the superior sagittal sinus with headache, fever, nausea, vomiting and confusion and seizures. There maybe a rapid development to stupor or coma. Nuchal rigidity, Kernig’s and Brudzinski’s may be present. Septic cavernous sinus thrombosis presents with fever, headache frontal and retroorbital pain and diplopia. Classic signs are ptosis, proptosis, chemosis and extraocular dysmotility due to deficits of cranial nerves II, IV and VI, hyperesthesia of the 5th nerve and decreased corneal reflex, papilledema. Headache and earache are the most frequent symptoms of transverse sinus thrombosis. it may also present with Gradinego’s syndrome ( facial pain ). Sigmoid sinus and internal jugular vein thrombosis may present with neck pain. Cerebral angiography for definitive diagnosis. Septic venous sinus thrombosis is treated with antibiotics and hydration. Dose adjusted heparin Aseptic venous sinus thrombosis through urokinase therapy, rTPa and IV heparin.
Liz IIIB
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