Pathogenesis and pathophysiology of bacterial meningitis
The pathogenesis and pathophysiology of bacterial meningitis involve a complex interplay between virulence factors of the pathogens and the host immune response. Much of the damage from this infection is believed to result from cytokines released within the cerebrospinal fluid (CSF) as the host mounts an inflammatory response
●Bacterial meningitis develops when virulence factors of the pathogen overcome host defense mechanisms. For the most common pathogens causing bacterial meningitis in adults, such as Streptococcus pneumoniae andNeisseria meningitidis, meningeal invasion is related to several virulence factors that allow the bacteria to colonize host mucosal epithelium, invade and survive within the bloodstream, cross the blood-brain barrier, and multiply within the CSF.
●In experimental animal models, subcapsular bacterial surface components are most important for the induction of CSF inflammation and blood-brain barrier injury.
●Some studies suggest that the mechanism by which these meningeal pathogens induce an inflammatory response and blood-brain barrier injury is through the in situ generation of inflammatory cytokines (eg, interleukin-1, interleukin-6, and tumor necrosis factor-alpha) and matrix metalloproteinases within the CSF.
●Once inflammation is initiated, a series of injuries occur to the endothelium of the blood-brain barrier (eg, separation of intercellular tight junctions) that result in vasogenic brain edema, loss of cerebrovascular autoregulation, and increased intracranial pressure. This results in localized areas of brain ischemia, cytotoxic injury, and neuronal apoptosis.
●Evidence also suggests that reactive nitrogen intermediates, nitric oxide, peroxynitrite (a powerful oxidative agent), and excitatory amino acids may also play important roles in either the inflammatory process or other pathophysiologic events (including neuronal injury) during bacterial meningitis.
Bacterial meningitis in children older than one month: Clinical features and diagnosis
Streptococcus pneumoniae and Neisseria meningitidis are the most common causes of bacterial meningitis in infants and children older than one month of age.
●Certain host factors may predispose to bacterial meningitis with a particular organism (table 2). Additional risk factors for bacterial meningitis include exposure to someone with meningococcal or Haemophilus influenzaetype b (Hib) meningitis, cochlear implantation device, recent neurosurgical procedure, or anatomic defect (dermal sinus or urinary tract anomaly).
●Most patients with bacterial meningitis present with fever and symptoms and signs of meningeal inflammation (movie 1A-B). However, the clinical manifestations of bacterial meningitis are variable and nonspecific; no single sign is pathognomonic.
●Suspected bacterial meningitis is a medical emergency, and immediate diagnostic steps must be taken to establish the specific cause (algorithm 1).
●The laboratory evaluation of children with suspected meningitis should include a complete blood count with differential and platelet count, two aerobic blood cultures, and serum electrolytes, glucose, blood urea nitrogen, and creatinine. Evaluation of clotting function is especially indicated if petechiae or purpuric lesions are noted.
●A lumbar puncture should be performed on any child in whom, after careful history and physical examination, the diagnosis of meningitis is suspected unless specific contraindications to lumbar puncture are present. Examination of the cerebrospinal fluid (CSF) should include cell count and differential, glucose and protein concentration, Gram stain, and culture.
●If there is a contraindication to or inability to perform a lumbar puncture or if the lumbar puncture is delayed by the need for cranial imaging, blood cultures should be obtained and empiric antibiotics administered as soon as possible.
●Laboratory findings characteristic of bacterial meningitis include CSF pleocytosis with a predominance of neutrophils, elevated CSF protein, decreased CSF glucose, the presence of an organism on CSF Gram stain, and isolation of a pathogenic organism from the CSF and/or blood culture (tble 3).
●Isolation of a bacterial pathogen from the CSF (by culture or other diagnostic techniques) confirms the diagnosis of bacterial meningitis
●In children who were treated with antibiotics before CSF was obtained, increased CSF cell count, elevated CSF protein concentration, and/or decreased CSF glucose concentration usually are sufficient to establish the diagnosis of meningitis; blood cultures and/or rapid diagnostic tests may help to identify the pathogenic organism.
●Empiric therapy for bacterial meningitis (a third-generation cephalosporin and vancomycin) should be initiated immediately after the results of lumbar puncture are received or immediately after the lumbar puncture is performed if the clinical suspicion for bacterial meningitis is high.
Characteristic features of common causes of bacterial meningitis
| Organism | Site of entry | Age range | Predisposing conditions |
| Neisseria meningitidis | Nasopharynx | All ages | Usually none, rarely complement deficiency |
| Streptococcus pneumoniae | Nasopharynx, direct extension across skull fracture, or from contiguous or distant foci of infection | All ages | All conditions that predispose to pneumococcal bacteremia, fracture of cribriform plate, cochlear implants, cerebrospinal fluid otorrhea from basilar skull fracture, defects of the ear ossicle (Mondini defect) |
| Listeria monocytogenes | Gastrointestinal tract, placenta | Older adults and neonates | Defects in cell-mediated immunity (eg, glucocorticoids, transplantation [especially renal transplantation]), pregnancy, liver disease, alcoholism, malignancy |
| Coagulase-negative staphylococci | Foreign body | All ages | Surgery and foreign body, especially ventricular drains |
| Staphylococcus aureus | Bacteremia, foreign body, skin | All ages | Endocarditis, surgery and foreign body, especially ventricular drains; cellulitis, decubitus ulcer |
| Gram-negative bacilli | Various | Older adults and neonates | Advanced medical illness, neurosurgery, ventricular drains, disseminated strongyloidiasis |
| Haemophilus influenzae | Nasopharynx, contiguous spread from local infection | Adults; infants and children if not vaccinated | Diminished humoral immunity |
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Host immune defects predisposing to meningitis
| Host problem | Organism favored | Frequency of defect actually leading to infection |
| Absence of opsonizing antibody | Streptococcus pneumoniae | Common in all age groups |
| Haemophilus influenzae | Common in very young children | |
| Asplenia: surgical or functional | S. pneumoniae | Rare |
| Neisseria meningitidis | Very rare | |
| Complement deficiency | N. meningitidis | Very rare |
| Glucocorticoid excess | Listeria monocytogenes | Rare |
| Cryptococcus neoformans | Rare | |
| HIV infection | C. neoformans | About 5 percent eventually get cryptococcal meningitis |
| S. pneumoniae | Common presenting illness | |
| L. monocytogenes | Rare | |
| Bacteremia/endocarditis | Staphylococcus aureus; various gram-negative rods | Rare |
| Basilar skull fracture | S. pneumoniae; other upper respiratory tract flora | Very rare |
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Etiology of bacterial meningitis in 231 children from 20 pediatric emergency departments, United States 2001-2004
%: percent.
* Citrobacter diversus, Enterobacter cloacae, Klebsiella spp, Pasteurella multocida, Pseudomonas aeruginosa, Salmonella spp.
• Listeria monocytogenes (2 percent); group A streptococcus (2 percent), Moraxella catarrhalis (0.4 percent).
* Citrobacter diversus, Enterobacter cloacae, Klebsiella spp, Pasteurella multocida, Pseudomonas aeruginosa, Salmonella spp.
• Listeria monocytogenes (2 percent); group A streptococcus (2 percent), Moraxella catarrhalis (0.4 percent).
Data from: Nigrovic LE, Kuppermann N, Malley R. Children with bacterial meningitis presenting to the emergency department during the pneumococcal conjugate vaccine era. Acad Emerg Med 2008; 15:522.
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Dermal sinus
Dermal sinus lesions may predispose to meningitis withStaphylococcus aureus, Coagulase-negative staphylococci, and enteric Gram-negative organisms, such as Escherichia coli and Klebsiellaspecies.
Courtesy of Sheldon L Kaplan, MD.
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Management algorithm for infants (≥1 month) and children with suspected bacterial meningitis
STAT: intervention should be performed emergently; CBC: complete blood count; PT: prothrombin time; PTT: partial thromboplastin time; BUN: blood urea nitrogen; CSF: cerebrospinal fluid; CNS: central nervous system.
* Antimicrobial therapy should not be delayed if lumbar puncture cannot be performed or is unsuccessful.
¶ Decisions regarding the administration of dexamethasone should be individualized depending on careful analysis of the risks and benefits as discussed in the text. (See "Treatment and prognosis of acute bacterial meningitis in children").
Δ Empiric antibiotic therapy and dexamethasone (if warranted) should be administered immediately after cerebrospinal fluid is obtained; if dexamethasone is to be administered, it should be given before, or immediately after, the first dose of antimicrobial therapy.
* Antimicrobial therapy should not be delayed if lumbar puncture cannot be performed or is unsuccessful.
¶ Decisions regarding the administration of dexamethasone should be individualized depending on careful analysis of the risks and benefits as discussed in the text. (See "Treatment and prognosis of acute bacterial meningitis in children").
Δ Empiric antibiotic therapy and dexamethasone (if warranted) should be administered immediately after cerebrospinal fluid is obtained; if dexamethasone is to be administered, it should be given before, or immediately after, the first dose of antimicrobial therapy.
Adapted from:
- Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management of bacterial meningitis. Clin Infect Dis 2004; 39:1267.
- Fleisher GR. Infectious disease emergencies. In: Textbook of Pediatric Emergency Medicine, 5th ed, Fleisher GR, Ludwig S, Henretig FM (Eds), Lippincott Williams & Wilkins, Philadelphia 2006. p.792.
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Typical cerebrospinal fluid findings in central nervous system infections*
| Glucose (mg/dL) | Protein (mg/dL) | Total white blood cell count (cells/microL) | |||||
| <10¶ | 10 to 40Δ | 100 to 500◊ | 50 to 300§ | >1000 | 100 to 1000 | 5 to 100 | |
| More common | Bacterial meningitis | Bacterial meningitis | Bacterial meningitis |
Viral meningitis
Nervous system Lyme disease (neuroborreliosis)
Neurosyphilis
TB meningitis¥ | Bacterial meningitis |
Bacterial or viral meningitis
TB meningitis |
Early bacterial meningitis
Viral meningitis
Neurosyphilis
TB meningitis |
| Less common |
TB meningitis
Fungal meningitis |
Neurosyphilis
Some viral infections (such as mumps and LCMV) | Some cases of mumps and LCMV | Encephalitis | Encephalitis | ||
TB: tuberculosis; LCMV: lymphocytic choriomeningitis virus.
* It is important to note that the spectrum of cerebrospinal fluid values in bacterial meningitis is so wide that the absence of one or more of these findings is of little value. Refer to the UpToDate topic reviews on bacterial meningitis for additional details.
¶ <0.6 mmol/L.
Δ 0.6 to 2.2 mmol/L.
◊ 1 to 5 g/L.
§ 0.5 to 3 g/L.
¥ Cerebrospinal fluid protein concentrations may be higher in some patients with tuberculous meningitis; concentrations >500 mg/dL are an indication of blood-brain barrier disruption or increased intracerebral production of immunoglobulins, and extremely high concentrations, in the range of 2 to 6 g/dL, may be found in association with subarachnoid block.
* It is important to note that the spectrum of cerebrospinal fluid values in bacterial meningitis is so wide that the absence of one or more of these findings is of little value. Refer to the UpToDate topic reviews on bacterial meningitis for additional details.
¶ <0.6 mmol/L.
Δ 0.6 to 2.2 mmol/L.
◊ 1 to 5 g/L.
§ 0.5 to 3 g/L.
¥ Cerebrospinal fluid protein concentrations may be higher in some patients with tuberculous meningitis; concentrations >500 mg/dL are an indication of blood-brain barrier disruption or increased intracerebral production of immunoglobulins, and extremely high concentrations, in the range of 2 to 6 g/dL, may be found in association with subarachnoid block.
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Streptococcus pneumoniae in cerebrospinal fluid
S. pneumoniae under high-power magnification (1000x) in cerebrospinal fluid.
Courtesy of Harriet Provine.
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Neisseria meningitidis in cerebrospinal fluid
Gram stain of cerebrospinal fluid (x1000) shows inflammatory cells and kidney-shaped, gram-negative diplococci (arrows). Neisseria meningitidis grew from this specimen.
Courtesy of Harriet Provine.
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Haemophilus influenzae in cerebrospinal fluid
Gram stain of cerebrospinal fluid (x1000) shows inflammatory cells and small, pleomorphic, gram-negative coccobacilli. Haemophilus influenzae grew from this specimen.
Courtesy of Harriet Provine.
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Group B streptococcus in cerebrospinal fluid
Gram stain of cerebrospinal fluid (x1000) shows inflammatory cells and gram-positive coccobacilli. Streptococcus agalactiae (group B streptococcus) grew from this specimen.
Courtesy of Harriet Provine.
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Listeria monocytogenes in cerebrospinal fluid
Gram stain of cerebrospinal fluid (1000x) shows inflammatory cells and small, gram-positive rods and coccobacilli. Culture of this specimen revealed moderate-sized, beta-hemolytic colonies composed of small, motile gram-positive rods, confirmed to be Listeria monocytogenes.
Courtesy of Harriet Provine.
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Howell-Jolly bodies following splenectomy
This peripheral blood smear shows two red blood cells (RBCs) that contain Howell-Jolly bodies (black arrows). Howell-Jolly bodies are remnants of RBC nuclei that are normally removed by the spleen. Thus, they are seen in patients who have undergone splenectomy (as in this case) or who have functional asplenia (eg, from sickle cell disease). Target cells (blue arrows) are another consequence of splenectomy.
Courtesy of Carola von Kapff, SH (ASCP).
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Normal peripheral blood smear
High-power view of a normal peripheral blood smear. Several platelets (arrows) and a normal lymphocyte (arrowhead) can also be seen. The red cells are of relatively uniform size and shape. The diameter of the normal red cell should approximate that of the nucleus of the small lymphocyte; central pallor (dashed arrow) should equal one-third of its diameter.
Bacterial meningitis in children older than one month: Treatment and prognosis
Immediate and supportive care
●Antibiotic therapy should be initiated immediately after the lumbar puncture (LP) is performed if the clinical suspicion for meningitis is high (algorithm 1).
●The pretreatment evaluation of children with suspected bacterial meningitis should include a complete history and physical examination, cerebrospinal fluid (CSF) examination (cell count and differential, glucose, protein, Gram stain and culture), complete blood count (CBC) with differential and platelet count, blood cultures, serum electrolytes, glucose, blood urea nitrogen, creatinine; evaluation of clotting function is indicated if petechiae or purpuric lesions are noted (algorithm 1).
●Immediate management of children with suspected bacterial meningitis includes assessment and stabilization of ventilation and perfusion, and initiation of hemodynamic monitoring and support while obtaining appropriate laboratory studies and establishing venous access. Empiric antibiotic therapy and dexamethasone, if warranted, should be administered as soon as possible after lumbar puncture. Hypoglycemia, acidosis, and coagulopathy should be treated as necessary.
●For children who are neither in shock nor dehydrated, we suggest moderate fluid restriction (1200 mL/m2 per day) until evidence of inappropriate secretion of antidiuretic hormone can be excluded (Grade 2B).
Antibiotic and dexamethasone therapy
●We recommend that the empiric regimen for infants and children older than one month with bacterial meningitis include coverage for antibiotic-resistant Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b (Hib) (Grade 1A).
An appropriate empiric regimen includes vancomycin 60 mg/kg per day IV (maximum dose 4 g/day) in 4 divided doses plus high doses of either cefotaxime 300 mg/kg per day intravenously (IV) (maximum dose 12 g/day) in 3 or 4 divided doses or ceftriaxone 100 mg/kg per day IV (maximum dose 4 g/day) in 1 or 2 divided doses.
An appropriate empiric regimen includes vancomycin 60 mg/kg per day IV (maximum dose 4 g/day) in 4 divided doses plus high doses of either cefotaxime 300 mg/kg per day intravenously (IV) (maximum dose 12 g/day) in 3 or 4 divided doses or ceftriaxone 100 mg/kg per day IV (maximum dose 4 g/day) in 1 or 2 divided doses.
●We recommend the use of dexamethasone for children with Hib meningitis (Grade 1A).
●Decisions regarding the use of dexamethasone in children with pneumococcal meningitis, or in whom bacterial meningitis is suspected but the etiology unknown, must be individualized after careful analysis of the potential risks and benefits. The author of this topic review usually does not administer dexamethasone to children with suspected pneumococcal or meningococcal meningitis. In the same patients, other experts may choose to use dexamethasone.
●We recommend not using dexamethasone if more than one hour has elapsed since the first dose of antimicrobial therapy (Grade 1A).
●The empiric regimen may need to be broadened in infants and children with immune deficiency, recent neurosurgery, penetrating head trauma, and anatomic defects. Patients with these conditions should be managed in consultation with a specialist in pediatric infectious diseases.
●Once the causative agent and its in vitro antimicrobial susceptibility pattern are known, empiric antimicrobial therapy can be altered accordingly
●The duration of antimicrobial therapy depends upon the causative organism and the clinical course.
Response to treatment
●The response to therapy is monitored clinically (eg, fever curve, resolution of symptoms and signs). Repeat examination of the spinal fluid may be necessary in some patients.
●Re-examination of CSF is indicated for patients who have a poor clinical response despite 24 to 36 hours of appropriate antimicrobial therapy. This is particularly true for children with third-generation cephalosporin-resistant pneumococcal meningitis and for children with pneumococcal meningitis who were treated with dexamethasone. In addition, re-examination of the CSF is necessary after two to three days of treatment for Gram-negative bacillary meningitis to determine appropriate duration of therapy.
●Neuroimaging is indicated in infants and children with signs or symptoms of complications and/or recurrent meningitis.
Prognosis and follow-up
●The overall mortality for bacterial meningitis in infants and children is approximately 5 percent in developed countries and 8 percent in developing countries.
●Neurologic sequelae, including deafness, intellectual disability, spasticity and/or paresis, and seizures occur in 15 to 25 percent of survivors.
●Children who have been treated for bacterial meningitis should undergo hearing evaluation at the time of or shortly after discharge. They should also be followed closely for other neurologic sequelae including gross motor and cognitive impairment.
Antibiotic prophylaxis
●Chemoprophylaxis is recommended for certain contacts of patients with meningococcal meningitis and Hib meningitis.
Management algorithm for infants (≥1 month) and children with suspected bacterial meningitis
STAT: intervention should be performed emergently; CBC: complete blood count; PT: prothrombin time; PTT: partial thromboplastin time; BUN: blood urea nitrogen; CSF: cerebrospinal fluid; CNS: central nervous system.
* Antimicrobial therapy should not be delayed if lumbar puncture cannot be performed or is unsuccessful.
¶ Decisions regarding the administration of dexamethasone should be individualized depending on careful analysis of the risks and benefits as discussed in the text. (See "Treatment and prognosis of acute bacterial meningitis in children").
Δ Empiric antibiotic therapy and dexamethasone (if warranted) should be administered immediately after cerebrospinal fluid is obtained; if dexamethasone is to be administered, it should be given before, or immediately after, the first dose of antimicrobial therapy.
* Antimicrobial therapy should not be delayed if lumbar puncture cannot be performed or is unsuccessful.
¶ Decisions regarding the administration of dexamethasone should be individualized depending on careful analysis of the risks and benefits as discussed in the text. (See "Treatment and prognosis of acute bacterial meningitis in children").
Δ Empiric antibiotic therapy and dexamethasone (if warranted) should be administered immediately after cerebrospinal fluid is obtained; if dexamethasone is to be administered, it should be given before, or immediately after, the first dose of antimicrobial therapy.
Adapted from:
- Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management of bacterial meningitis. Clin Infect Dis 2004; 39:1267.
- Fleisher GR. Infectious disease emergencies. In: Textbook of Pediatric Emergency Medicine, 5th ed, Fleisher GR, Ludwig S, Henretig FM (Eds), Lippincott Williams & Wilkins, Philadelphia 2006. p.792.
Graphic 74865 Version 8.0
Dermal sinus
Dermal sinus lesions may predispose to meningitis withStaphylococcus aureus, Coagulase-negative staphylococci, and enteric Gram-negative organisms, such as Escherichia coli and Klebsiellaspecies.
Courtesy of Sheldon L Kaplan, MD.
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Antimicrobial therapy for bacterial meningitis in children caused by Streptococcus pneumoniae based upon susceptibility test results in patients begun on vancomycin and either cefotaxime or ceftriaxone
| Susceptibility test results* | Antibiotic management¶ |
| Susceptible to penicillin |
Discontinue vancomycin
AND
Begin penicillin (and discontinue cephalosporin)
OR
Continue cefotaxime or ceftriaxone aloneΔ
|
Not susceptible to penicillin (intermediate or resistant)
AND
Susceptible to cefotaxime and ceftriaxone
|
Discontinue vancomycin
AND
Continue cefotaxime or ceftriaxone
|
Not susceptible to penicillin (intermediate or resistant)
AND
Not susceptible to cefotaxime or ceftriaxone (intermediate or resistant)
AND
Susceptible to rifampin
|
Continue vancomycin AND
Either cefotaxime OR ceftriaxone
Rifampin may be added in selected circumstances◊
|
* Based upon quantitative susceptibility studies.
¶ See text for doses.
Δ Some physicians may choose this alternative for convenience and cost savings.
◊ Addition of rifampin after 24 to 48 hours of therapy may be warranted if:
¶ See text for doses.
Δ Some physicians may choose this alternative for convenience and cost savings.
◊ Addition of rifampin after 24 to 48 hours of therapy may be warranted if:
- Clinical condition worsens, or
- Gram stain or culture of repeat cerebrospinal fluid (CSF) indicates failure to substantially reduce bacterial number, or
- Cefotaxime or ceftriaxone minimum inhibitory concentration (MIC) of 4 mcg/mL or greater
From: American Academy of Pediatrics. Pneumococcal infections. In: Red Book: 2012 Report of the Committee on Infectious Diseases, 29th ed, Pickering LK (Ed), American Academy of Pediatrics, Elk Grove Village, IL 2012. Used with the permission of the American Academy of Pediatrics. Copyright © 2012. The contents of this table remain unchanged in the Red Book: 2015 Report of the Committee on Infectious Diseases, 30th ed.
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Glasgow Coma Scale and Pediatric Glasgow Coma Scale
| Sign | Glasgow Coma Scale[1] | Pediatric Glasgow Coma Scale[2] | Score |
| Eye opening | Spontaneous | Spontaneous | 4 |
| To command | To sound | 3 | |
| To pain | To pain | 2 | |
| None | None | 1 | |
| Verbal response | Oriented | Age-appropriate vocalization, smile, or orientation to sound, interacts (coos, babbles), follows objects | 5 |
| Confused, disoriented | Cries, irritable | 4 | |
| Inappropriate words | Cries to pain | 3 | |
| Incomprehensible sounds | Moans to pain | 2 | |
| None | None | 1 | |
| Motor response | Obeys commands | Spontaneous movements (obeys verbal command) | 6 |
| Localizes pain | Withdraws to touch (localizes pain) | 5 | |
| Withdraws | Withdraws to pain | 4 | |
| Abnormal flexion to pain | Abnormal flexion to pain (decorticate posture) | 3 | |
| Abnormal extension to pain | Abnormal extension to pain (decerebrate posture) | 2 | |
| None | None | 1 | |
| Best total score | 15 | ||
The Glasgow Coma Scale (GCS) is scored between 3 and 15, 3 being the worst, and 15 the best. It is composed of three parameters: best eye response (E), best verbal response (V), and best motor response (M). The components of the GCS should be recorded individually; for example, E2V3M4 results in a GCS of 9. A score of 13 or higher correlates with mild brain injury; a score of 9 to 12 correlates with moderate injury; and a score of 8 or less represents severe brain injury. The pediatric Glasgow coma scale (PGCS) was validated in children two years of age or younger.
Data from:
- Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974; 2:81.
- Holmes JF, Palchak MJ, MacFarlane T, Kuppermann N. Performance of the pediatric Glasgow coma scale in children with blunt head trauma. Acad Emerg Med 2005; 12:814.
Bacterial meningitis in children: Neurologic complications
Permanent neurologic sequelae occur in up to one-half of children with bacterial meningitis. The most common sequelae include intellectual/behavioral deficits, neurologic deficits (including spasticity and/or paresis and seizures), hearing loss, and intellectual disability
●Clinical features that have been associated with increased risk of neurologic sequelae include prolonged or complicated seizures, low cerebrospinal fluid (CSF) glucose concentration, ≥107 colony forming units/mL of CSF, and focal neurologic deficits.
●Seizures that are prolonged, difficult to control, or begin more than 72 hours after hospitalization are more likely to be associated with neurologic sequelae. Persistent neurologic deficits are the major predictor of late afebrile seizures in children.
●Hemiparesis or quadriparesis resulting from meningitis often improves with time.
●Permanent sensorineural hearing loss occurs in as many as 11 percent of children with bacterial meningitis.
●Survivors of childhood meningitis are at increased risk of developmental, learning, and behavioral difficulties, even if they did not have acute neurologic complications or physical sequelae.
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