Meningitis: Difference between revisions
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| style="padding: 5px 5px; background: #F5F5F5;" |'''Coagulase-negative staphylococci (especiallyS. epi-dermidis), S. aureus,aerobic gram-negative bacilli(includingP. aeruginosa), Propionibacterium acnes''' | | style="padding: 5px 5px; background: #F5F5F5;" |'''Coagulase-negative staphylococci (especiallyS. epi-dermidis), S. aureus,aerobic gram-negative bacilli(includingP. aeruginosa), Propionibacterium acnes''' | ||
| style="padding: 5px 5px; background: #F5F5F5;" |'''ancomycin plus cefepime, vancomycin plus ceftazi-dime, or vancomycin plus meropenem''' | | style="padding: 5px 5px; background: #F5F5F5;" |'''ancomycin plus cefepime, vancomycin plus ceftazi-dime, or vancomycin plus meropenem''' | ||
===Secondary Prevention=== | ===Secondary Prevention=== |
Revision as of 01:34, 2 December 2020
Resident Survival Guide |
Template:DiseaseDisorder infobox
Meningitis Main Page |
For patient information click here.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Synonyms and keywords: Leptomeningitis, Inflammation of meninges
Overview
The meninges (singular meninx) is the system of membranes which envelop the central nervous system. The meninges consist of three layers: the dura mater, the arachnoid mater, and the pia mater. The primary function of the meninges and of the cerebrospinal fluid is to protect the central nervous system. Meningitis is the inflammation of these protective membranes.
Meningitis may have been described in the Middle Ages, but it was first accurately identified by the Swiss Vieusseux (a scientific-literary association) during an outbreak in Geneva, Switzerland in 1805. In 1661, Thomas Willis first described the inflammation of meninges and an epidemic of meningitis. In the 17th century, Robert Whytt provided a detailed explanation of tuberculous meningitis and its stages. This was further elaborated by John Cheyne in the same century. Meningococcal meningitis was than described by Gaspard Vieusseux, Andre Matthey in Geneva and Elisa North in Massachussetes.
Meningitis may develop in response to a number of causes, including infectious agents (bacteria, viruses, fungi, or other organisms) or non-infectious causes, such as systemic illnesses that may involve CNS (e.g. neoplasms or connective tissue diseases, such as sarcoidosis, systemic lupus erythematosus (SLE), and wegener's) or certain drugs (e.g. nonsteroidal antiinflammatory drugs, intravenous immunoglobulin, intrathecal agents, and trimethoprim-sulfamethoxazole). While some forms of meningitis are mild and resolve spontaneously (e.g. viral meningitis), meningitis is a potentially serious condition owing to the proximity of the inflammation to the brain and spinal cord. The potential for serious neurologic damage or even death necessitates prompt medical attention and evaluation. The common presenting features of meningitis are, fever, neck stiffness and headache. Other symptoms include, photophobia (inability to tolerate bright light), phonophobia (inability to tolerate loud noises), irritability, altered mental status (in small children), and seizure. Physical examination of meningitis may vary in adults and infants. In adults, physical examination findings may include bradycardia, disorientation, papilledema, neck stiffness, positive brudzinski's and kernig's sign. However, petechial rash, bulging fontanelle, neck stiffness, jaundice, and convulsions are physical examination findings in infants. Diagnosis is based on clinical findings and CSF analysis. Treatment options are based on etiology and varies from supportive care and observing the patient (viral meningitis) to antibiotic therapy for bacterial meningitis or chemotherapy and/or irradiation for neoplastic meningitis.[1][2][3][4][5][6][4][7][8]
Causes
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Classification
Meningitis could be classified to two main groups based on etiology:
- Infectious
- Non-infectious
Infectious meningitis
Infectious meningitis may be classified as the following algorithm based on chronicity of symptoms.
Infectious Meningitis | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Viral | Bacterial | Fungal | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Acute | Chronic | Recurrent | Acute | Subacute | Chronic | Recurrent | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Non-infectious meningitis
Systemic illnesses, such as malignancies and connective tissue diseases (e.g. sarcoidosis, SLE, and wegener's) may involve meninges in their course and present as chronic meningitis.
Certain drugs may cause meningeal irritation and resemble as meningitis including:
- Nonsteroidal antiinflammatory drugs (NSAIDs)
- Intravenous immunoglobulin
- Intrathecal agents
- Certain antibiotics (eg, trimethoprim-sulfamethoxazole)
Differential diagnosis
Diseases | Symptoms | Physical Examination | Past medical history | Diagnostic tests | Other Findings | |||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Headache | ↓LOC | Motor weakness | Abnormal sensory | Motor Deficit | Sensory deficit | Speech difficulty | Gait abnormality | Cranial nerves | CT /MRI | CSF Findings | Gold standard test | |||
Meningitis | + | - | - | - | - | + | + | - | - | History of fever and malaise | - | ↑ Leukocytes,
↑ Protein ↓ Glucose |
CSF analysis[28] | Fever, neck |
Encephalitis | + | + | +/- | +/- | - | - | + | +/- | + | History of fever and malaise | + | ↑ Leukocytes, ↓ Glucose | CSF PCR | Fever, seizures, focal neurologic abnormalities |
Brain tumor[29] | + | - | - | - | + | + | + | - | + | Weight loss, fatigue | + | Cancer cells[30] | MRI | Cachexia, gradual progression of symptoms |
Hemorrhagic stroke | + | + | + | + | + | + | + | + | - | Hypertension | + | - | CT scan without contrast[31][32] | Neck stiffness |
Subdural hemorrhage | + | + | + | + | + | - | - | - | + | Trauma, fall | + | Xanthochromia[33] | CT scan without contrast[31][32] | Confusion, dizziness, nausea, vomiting |
Neurosyphilis[34][35] | + | - | + | + | + | + | - | + | - | STIs | + | ↑ Leukocytes and protein | CSF VDRL-specifc
CSF FTA-Ab -sensitive[36] |
Blindness, confusion, depression,
Abnormal gait |
Complex or atypical migraine | + | - | + | + | - | - | + | - | - | Family history of migraine | - | - | Clinical assesment | Presence of aura, nausea, vomiting |
Hypertensive encephalopathy | + | + | - | - | - | - | + | + | - | Hypertension | + | - | Clinical assesment | Delirium, cortical blindness, cerebral edema, seizure |
Wernicke’s encephalopathy | - | + | - | - | - | + | + | + | + | History of alcohal abuse | - | - | Clinical assesment and lab findings | Ophthalmoplegia, confusion |
CNS abscess | + | + | - | - | + | + | + | - | - | History of drug abuse, endocarditis, immunosupression | + | ↑ leukocytes, ↓ glucose and ↑ protien | MRI is more sensitive and specific | High grade fever, fatigue,nausea, vomiting |
Drug toxicity | - | + | - | + | + | + | - | + | - | - | - | - | Drug screen test | Lithium, Sedatives, phenytoin, carbamazepine |
Conversion disorder | + | + | + | + | + | + | + | + | History of emotional stress | - | - | Diagnosis of exclusion | Tremors, blindness, difficulty swallowing | |
Metabolic disturbances (electrolyte imbalance, hypoglycemia) | - | + | + | + | + | + | - | - | + | - | - | Hypoglycemia, hypo and hypernatremia, hypo and hyperkalemia | Depends on the cause | Confusion, seizure, palpitations, sweating, dizziness, hypoglycemia |
Multiple sclerosis exacerbation | - | - | + | + | - | + | + | + | + | History of relapses and remissions | + | ↑ CSF IgG levels
(monoclonal bands) |
Clinical assesment and MRI [37] | Blurry vision, urinary incontinence, fatigue |
Seizure | + | + | - | - | + | + | - | - | + | Previous history of seizures | - | Mass lesion | Clinical assesment and EEG [38] | Confusion, apathy, irritability, |
Diagnosis
Diagnosis of meningitis, is based on clinical presentation in combination with CSF analysis. CSF analysis has major role for diagnosis and rule out other possibilities. The following table summarizes the CSF findings in different types of meningitis.[39][40][41][42][3]
Cerebrospinal fluid level | Normal level | Bacterial meningitis[42] | Viral meningitis (except SARS-CoV-2 meningitis) [42] | SARS-CoV-2 associated meningitis | Fungal meningitis | Tuberculous meningitis[43] | Neoplastic meningitis[39] |
---|---|---|---|---|---|---|---|
Cells/ul | < 5 | >300 | 10-1000 | 10-1000 | 10-500 | 50-500 | >4 |
Cells | Lymphocyte | Leukocyte > Lymphocyte | Lymphocyte > Leukocyte | Lymphocyte > Neutrophil | Lymphocyte > Leukocyte | Lymphocyte > Leukocyte | Lymphocyte > Leukocyte |
Total protein (mg/dl) | 45-60 | Typically 100-500 | Normal or slightly high | Normal or slightly high | High | Typically 100-200 | >50 |
Glucose ratio (CSF/plasma)[40] | > 0.5 | < 0.3 | > 0.6 | > 0.6 | <0.3 | < 0.5 | <0.5 |
Lactate (mmols/l)[41] | < 2.1 | > 2.1 | < 2.1 | NA | >3.2 | > 2.1 | >2.1 |
Others | Intra-cranial pressure (ICP) = 6-12 (cm H2O) | CSF gram stain, CSF culture, CSF bacterial antigen | PCR of HSV-DNA, VZV | RT-PCR for detection of viral RNA i n CSF ( not approved by FDA) | CSF gram stain, CSF india ink | PCR of TB-DNA | CSF tumour markers such as alpha fetoprotein, CEA |
Treatment
Medical Therapy
Empiric therapy for meningitis must be initiated after CSF obtained. The choice of empiric antibiotic therapy is depend on patient age and underlying comorbid disease.
Predisposing factor | Common bacterial pathogen | Antimicrobial therapy |
---|---|---|
1 month | Streptococcus agalactiae, Escherichia coli, Listeriamonocytogenes, Klebsiellaspecie | Ampicillin plus cefotaxime or ampicillin plus anaminoglycoside |
1–23 months | Streptococcus pneumoniae, Neisseria meningitidis,S. agalactiae, Haemophilus influenzae, E. coli | Ampicillin plus cefotaxime or ampicillin plus anaminoglycoside |
2–50 years,150 years | N . meningitidis, S. pneumoniae,S. pneumoniae, N. meningitidis, L. monocytogenes,aerobic gram-negative bacill | Vancomycin plus a third-generation cephalosporin,Vancomycin plus ampicillin plus a third-generationcephalosporina, |
Head traumaBasilar skull fracture | S. pneumoniae, H. influenzae,group Ab-hemolyticstreptococci | Vancomycin plus a third-generation cephalospori |
Penetrating trauma | Staphylococcus aureus,coagulase-negative staphylo-cocci (especiallyStaphylococcus epidermidis),aer-obic gram-negative bacilli (includingPseudomonasaeruginosa) | Vancomycin plus cefepime, vancomycin plus ceftazi-dime, or vancomycin plus meropenem |
Postneurosurgery | Aerobic gram-negative bacilli (includingP. aeruginosa),S . aureus, coagulase-negative staphylococci (es-peciallyS. epidermidis) | ancomycin plus cefepime, vancomycin plus ceftazi-dime, or vancomycin plus meropenem |
CSF shunt | Coagulase-negative staphylococci (especiallyS. epi-dermidis), S. aureus,aerobic gram-negative bacilli(includingP. aeruginosa), Propionibacterium acnes | ancomycin plus cefepime, vancomycin plus ceftazi-dime, or vancomycin plus meropenem
Secondary PreventionThere are no established measures for the secondary prevention of [disease name]. OR Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3]. References
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