Central Nervous System Infections
Pratibha D. Singhi
Sunit C. Singhi
KEY POINTS
Bacterial Meningitis
Meningitis is inflammation of the meninges that presents acutely when bacterial or viral and subacutely when mycobacterial or fungal.
Bacterial meningitis is a serious bacterial infection that is often missed clinically, and cerebrospinal fluid (CSF) should be obtained when suspected.
CSF in bacterial meningitis has elevated polymorphonuclear neutrophils, low glucose, and high protein.
Bacterial meningitis must be treated emergently with a broad-spectrum antibiotic.
The top three causes of bacterial meningitis include Haemophilus influenzae, Neisseria meningitidis, and Streptococcus pneumoniae; the incidence of Hib and pneumococcal meningitis has decreased dramatically in countries with universal immunizations against these organisms but not in other countries.Aseptic Meningitis
Aseptic meningitis has high polymorphonuclear leukocytes (PMNs) initially and then high lymphocyte counts.
Aseptic meningitis is mainly caused by viruses but is also caused by tuberculosis (TB) and other agents.Encephalitis and Myelitis
Encephalitis is inflammation of brain parenchyma, and myelitis is the inflammation of the spinal cord.
Most agents that cause meningitis may spread to the brain and spinal cord.
Arboviruses are the most common cause of epidemic encephalitis.
Herpes simplex is the most common cause of sporadic encephalitis.
Herpes simplex encephalitis (HSE) must be treated promptly with acyclovir.
Japanese encephalitis (JE) can be prevented with vaccination.
Acute disseminated encephalomyelitis (ADEM) is a postinfectious autoimmune reaction treated with high-dose steroids.Brain and Spinal Cord Abscess
Lumbar puncture is often contraindicated when a brain abscess is suspected.
Antimicrobial therapy with drainage is often necessary in treating central nervous system (CNS) abscesses.Cerebrospinal Fluid Shunt Infection
Most shunt infections are due to Staphylococcus spp.— Staphylococcus epidermidis and Staphylococcus aureus.
Antibiotics, shunt removal, and external drainage are often required for appropriate management of shunt infections.Fungal Infections
Fungal CNS infections often have an insidious onset.
Most fungal CNS infections are due to hematogenous spread from the lung.
Mucormycosis occurs via direct spread from sinuses.
Amphotericin B remains an appropriate initial empiric antimicrobial for most suspected fungal infections of CNS.
Newer and effective antifungal agents are now available.Parasitic Infections
Most parasitic infections of the CNS are subacute, but some can be acute and severe.
The most important etiologic clue to parasitic infection is living in or visiting an endemic area.Infections of the central nervous system (CNS) are among the most devastating infectious diseases, causing death and disability worldwide. They often present as serious medical emergencies, and institution of early, appropriate intensive care is of utmost importance in reducing mortality and morbidity. This chapter is structured to familiarize the intensivist with common CNS infections, to help generate differential diagnoses, and to develop an appropriate treatment plan. It does not attempt to cover all possible infections that may affect the CNS.
A discussion on meningitis—bacterial, aseptic, and tubercular—is followed by sections on encephalitis and myelitis, with special emphasis on herpes, Japanese encephalitis (JE),
and acute disseminated encephalomyelitis (ADEM). A section on brain abscess and epidural abscess, with emphasis on aspects relevant to the intensivist, is also included.
and acute disseminated encephalomyelitis (ADEM). A section on brain abscess and epidural abscess, with emphasis on aspects relevant to the intensivist, is also included.
ANATOMY AND PHYSIOLOGY
As important aspects of CNS anatomy and physiology are discussed in Chapter 55, specific implications of anatomic and/or physiologic issues will be identified in this chapter as they pertain to the specific infections under discussion.
PATHOGENESIS
To cause CNS infections, pathogens must gain access either to the subarachnoid space to cause meningitis or to the brain and spinal cord parenchyma to cause encephalitis, myelitis, or a CNS abscess. Most infections spread to the CNS through the bloodstream; however, different pathogens go to different anatomic locations. The organisms that typically cause bacterial meningitis rarely cause brain abscess, and those found in brain abscesses rarely cause meningitis. At times, the CNS may be infected by direct spread of organisms from an infective focus adjacent to the brain (otitis media, sinusitis, dental abscess) or from a cerebrospinal fluid (CSF) shunt or skull fracture.
CLINICAL PRESENTATION
The main features of CNS infections are fever, headache, and altered sensorium. Focal neurologic signs may also be seen. However, these symptoms and signs are nonspecific and can be seen in noninfectious CNS syndromes as well. Hence, a comprehensive evaluation is necessary to narrow the differential diagnosis. Epidemiologic risk factors for CNS infections and physical examination may provide etiologic clues. Broadly, a child with CNS infections may present with any of the following syndromes.
Acute Meningitis Syndrome
Acute meningitis syndrome presents as acute onset over a few hours to a few days of fever, headache, vomiting, photophobia, neck stiffness, and altered sensorium. An acute upper respiratory tract infection may precede the onset of meningitis 
by a few days. Examples of CNS infections that present with an acute meningitis syndrome include bacterial and viral meningitis.
by a few days. Examples of CNS infections that present with an acute meningitis syndrome include bacterial and viral meningitis.Subacute or Chronic Meningitis Syndrome
Onset is usually gradual, often without any evident predisposing condition. Fever is often present but tends to be lower than in acute meningitis. Progression is slower over a few weeks. Examples of CNS infections that present with a subacute or chronic meningitis syndrome include tuberculous and fungal meningitis.
Acute Encephalitis Syndrome
Acute encephalitis may be diffuse or focal. In diffuse encephalitis, alteration of sensorium is predominant and occurs earlier in the course of disease than in acute meningitis. Seizures are seen more frequently than with meningitis and often during the initial phase of disease. Focal encephalitis reflects tropism of some viruses for specific locations in the CNS, such as temporal lobe infection by herpes simplex virus (HSV).
Encephalopathy with Systemic Infection
Many systemic infections involve the CNS, and CNS symptoms may be the presenting feature in some cases. For example, shigellosis, typhoid fever, malaria, rickettsial diseases, and infective endocarditis may directly involve the CNS or present as septic encephalopathy. It is therefore important to consider systemic infection as a possible underlying cause in children with encephalopathy.
Postinfectious Syndromes
ADEM, transverse myelitis, optic neuritis, and multiple sclerosis (MS) are disorders of demyelination of the CNS (collectively referred to as idiopathic inflammatory diseases of the CNS) that may present global or focal neurologic deficits days to weeks after recovery from an infectious illness, suggesting an autoimmune phenomenon triggered by infection or vaccine.
DIAGNOSIS
A general diagnostic approach to a patient with suspected CNS infection must include a thorough history and physical. Chronicity of signs and symptoms will help to categorize the illness according to one of the just-mentioned syndromes. Significant history, such as ill contacts, trauma, surgery, travel, insect bites, contact with animals, and sexual activity, may help to determine etiology. Premorbid or comorbid conditions, such as prior viral illness, immunodeficiency, presence of CSF shunt, associated diarrhea, respiratory illness, sinusitis, rash, arthritis, and other associated signs and symptoms, are important. Laboratory tests may include general assessment with complete blood count, chemistry panel, C-reactive protein (CRP), liver function tests (LFTs), urine analysis, and other testing to assess systemic illness. Specific testing of blood, including blood culture, thick and thin blood smears, polymerase chain reaction (PCR), antigen testing, and serology, may be indicated. General assessment of the CNS, including CSF opening pressure, white blood cell (WBC) and red blood cell (RBC) counts, protein, and glucose, is most often indicated; the usual CSF characteristics of meningitis are listed in Table 91.1. Specialized studies on CSF, including Gram stain with aerobic and anaerobic bacterial culture, fungal stain and fungal culture, and acid-fast bacilli stain and mycobacterial culture, should be considered. CSF inspection for parasites, viral culture, PCR, antigen testing, and serology may also be indicated. Neuroimaging, electroencephalogram (EEG), and other studies may add to the diagnosis. Drainage of abscesses and obtaining CNS tissue for histopathology are occasionally required.
MANAGEMENT
As with any other serious illness, management starts with the primary survey to ensure immediate attention to the basic airway, breathing, and circulation (ABCs) of life support before looking for an etiologic diagnosis. A secondary survey, with particular attention to the neurologic examination, meningeal signs, and assessment of the severity of coma, if present, is then undertaken. The physical examination in a child with meningitis is mainly geared toward excluding focal neurologic pathology, determining whether the child has clinically significant elevation of intracranial pressure (ICP), finding any
source of infection elsewhere in the body (e.g., sinusitis, otitis, pneumonia), and identifying any other etiologic clues, such as rashes or skin lesions.
source of infection elsewhere in the body (e.g., sinusitis, otitis, pneumonia), and identifying any other etiologic clues, such as rashes or skin lesions.
TABLE 91.1 CEREBROSPINAL FLUID CHARACTERISTICS IN MENINGITIS | ||||||||||||||||||||||||
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Children with a Glasgow Coma Scale (GCS) score of <8, pharyngeal hypotonia, poor gag reflex, and loss of swallowing reflex require intubation and supplemental oxygen. Appropriate techniques should be used to minimize potential increases in ICP associated with endotracheal intubation (see Chapter 24). Clinical signs and laboratory data that warrant admission of a child with meningitis to the PICU are listed in Table 91.2. Antimicrobial therapy must be administered promptly and, due to limited penetration into the CSF, at high doses. Details of antimicrobial therapy are discussed in later sections in which specific etiologies of CNS infection are described.
Any evidence of shock, such as poor perfusion, hypovolemia, and/or hypotension, requires aggressive treatment with normal saline boluses and inotropes, if necessary, to maintain normal blood pressure. Shock in CNS infection may be septic, neurogenic, hypovolemic, or a combination of these.
With increasing severity of illness and raised ICP, the cerebral blood flow (CBF) decreases, especially in the subcortical white matter. The level of impairment of consciousness correlates well with decreased cerebral perfusion, and mortality and sequelae are inversely related to the cerebral perfusion pressure (CPP) and CBF. ICP, therefore, must be maintained within a narrow range in children with meningitis. Although ICP monitoring is not routinely recommended, it may be considered in those children with CNS infection who have clinical signs of moderate-to-severe increase in ICP. The approach to control of ICP in patients with CNS infection follows the same algorithm as in other etiologies of intracranial hypertension.
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Seizures are controlled with IV benzodiazepines, generally diazepam or lorazepam. Approximately half of the patients with seizures progress to refractory status epilepticus (SE). SE associated with intracranial infections is more difficult to treat and has a poor outcome (1). The overall approach to the treatment of SE is discussed in Chapter 63.
Alterations in fluid and electrolyte homeostasis are often seen with CNS infection and may be life-threatening if not corrected in a timely fashion. Accurate recording of fluid intake and output and close monitoring of electrolytes are essential. Fever, diminished intake, and vomiting may lead to significant dehydration and hypovolemia. Capillary leak secondary to sepsis can further add to hypovolemia. Diabetes insipidus (DI) may rapidly lead to hypovolemia and hypernatremia due to urinary free water loss. The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) may lead to free water retention, hypoosmolality, and hyponatremia. These conditions must be recognized early to ensure appropriate management.
Fluid restriction to two-thirds of normal maintenance has historically been practiced with the hope that it reduces cerebral edema, presumably aggravated by the SIADH. However, it has been contended that a raised antidiuretic hormone level is an appropriate response to fluid deficit as it returns to normal on fluid administration. A prospective randomized trial of fluid restriction versus maintenance fluids with a clinical outcome (2) showed that restriction of fluids does not improve the outcome in children with meningitis. The increased fluid volume and mild systemic hypertension in children with meningitis may represent a compensatory mechanism to overcome raised ICP and to maintain adequate CBF and perfusion. Restriction of fluids and, thereby, extracellular volume may adversely affect cerebral perfusion and may worsen the outcome. Empiric fluid restriction in children with CNS infection is therefore not justified. A meta-analysis of fluid therapy trials found evidence to support the use of IV maintenance fluids in preference to restricted fluids in the first 48 hours in settings with high mortality rates and in which patients present late, but it found insufficient evidence to guide practice when children present early and mortality rates are lower (3). Fluid therapy should be aimed at maintaining normovolemia and normal blood pressure, thereby maintaining adequate cerebral perfusion. Careful monitoring of hydration status, intravascular volume, electrolytes, and osmolality should guide fluid management.
Hyponatremia should be identified early and corrected slowly over 36-48 hours with normal saline or, occasionally, with 3% saline, after calculating the sodium deficit. It is
important to prevent and/or treat hyponatremic seizures. Children with meningitis are also prone to develop hypokalemia due to gastrointestinal losses, hemodilution, osmotherapy, diuretic therapy, and associated septicemia.
important to prevent and/or treat hyponatremic seizures. Children with meningitis are also prone to develop hypokalemia due to gastrointestinal losses, hemodilution, osmotherapy, diuretic therapy, and associated septicemia.
BACTERIAL MENINGITIS
Etiology
Worldwide, three major meningeal pathogens (Haemophilus influenzae, Neisseria meningitidis, and Streptococcus pneumoniae) account for the majority of cases, but the proportion caused by each organism is somewhat variable by region and age.
Haemophilus spp. are small, gram-negative, pleomorphic coccobacilli that are either encapsulated or unencapsulated. Encapsulated strains are classified into six types, designated a through f. Nearly all invasive H. influenzae infections are caused by serotype b (Hib). Hib strains have been further classified according to their outer membrane proteins (OMPs), which are useful for epidemiologic studies. Presently, almost all invasive disease worldwide is caused by nine clones of Hib, although nontypeable H. influenzae may rarely cause meningitis.
Neisseria spp. are non-spore-forming, nonmotile, kidneyshaped, gram-negative cocci that often appear in pairs (diplococci). Meningococci are classified by serogroups, which have important epidemiologic and prevention-related implications. Although 13 serogroups are recognized, most meningococcal disease is caused by organisms in serogroups A, B, C, Y, and W135. The virulence of meningococci is determined by their capsular polysaccharide, pili, immunoglobulin (Ig) A protease, lipopolysaccharide (endotoxin), OMPs, and outer membrane vesicles. All isolates from invasive infections are encapsulated (serogroup positive), whereas 20%-90% of those isolated from carriers are unencapsulated (nontypeable).
Pneumococci are non-spore-forming, nonmotile, small, gram-positive streptococci that are generally seen in pairs or chains. They are classified into serotypes on the basis of antigenic differences among capsular polysaccharides, which are essential for pneumococcal virulence. Approximately 90 pneumococcal serotypes have been characterized; however, only some of these cause invasive pneumococcal infections. Capsular types 1, 4, 6, 9, 14, 18, 19, and 23 cause ˜85% of serious infections in children, a pattern different from that observed in adults. The serotypes that cause meningitis have a strong correlation with those that cause pneumonia and bacteremia.
Gram-negative bacilli can also be implicated in meningitis. Most cases of neonatal meningitis and sepsis due to gramnegative bacilli are caused by Escherichia coli strains that bear the K1 capsular polysaccharide antigen, a marker of neurovirulence. In addition to the K1 capsule, many other potential virulence factors for meningitis have been documented. Gramnegative bacterial meningitis in children beyond the neonatal period is generally nosocomial or may be associated with other conditions, such as gut infections, head trauma, neurosurgical procedures, and immunodeficiency. Other Enterobacteriaceae can cause meningitis, including Klebsiella, Salmonella, Enterobacter, and Pseudomonas spp.
Group B streptococci are the most common cause of invasive neonatal disease in many countries. They are classified into six main serotypes; type III is responsible for most cases of neonatal meningitis. A decrease in the incidence of neonatal invasive group B streptococcal disease has been seen in developed countries, secondary to treatment of pregnant women with vaginal colonization at the time of delivery.
Listeria monocytogenes is a gram-positive, non-sporeforming, catalase-positive, aerobic rod. An important cause of neonatal meningitis, its source is generally the genital tract infection of the mother. However, nosocomial infection may also occur, particularly in low-birth-weight babies in longterm intensive care.
Staphylococci are gram-positive organisms that are generally seen in pairs or clusters. Staphylococcus aureus is a virulent organism that is coagulase positive and causes pneumonia, sepsis, endocarditis, osteomyelitis, and meningitis. It is generally seen in malnourished children with staphylococcal skin lesions, dermal sinuses, or CSF shunts. Secondary meningitis may also be seen in children with head trauma, neurosurgical procedures, or sinusitis.
Anaerobic meningitis may occur in certain conditions, such as rupture of brain abscess; chronic otitis, mastoiditis, or sinusitis; head trauma; neurosurgical procedures; congenital dural defects; gastrointestinal disease; suppurative pharyngitis; CSF shunts; and immunosuppression. Bacteroides fragilis, Fusobacterium spp., and Clostridium spp. are anaerobic pathogens that may cause meningitis.
Epidemiology
Hib remains the leading cause of bacterial meningitis in countries where Hib vaccine has not been introduced, particularly in children <5 years of age, with an estimated incidence rate of 31 cases per 100,000 (4). Approximately 80% of cases develop in unvaccinated children <2 years of age, and nearly all cases occur in children <5 years. Meningitis caused by Hib in the first 2 months of life is rare, presumably because of placental transfer of protective maternal bactericidal antibodies. Natural immunity develops after 3 years of age, and concentrations of polyribosylribitol phosphate antibodies reach adult values by 7 years of age (5). The two main factors that determine risk for disease are nasopharyngeal carriage and the concentration of circulating anticapsular antibody. High-risk factors for invasive Hib infection include sickle cell anemia, asplenia, CSF fistulas, and chronic pulmonary infections. If children >6 years have Hib meningitis, such underlying conditions as otitis media, sinusitis, CSF leaks, and immunodeficiency states, including splenectomy, should be excluded.
Meningococcal meningitis occurs primarily in children and young adults. A wide geographic variation exists between the serotypes of meningococci that are endemic and those that cause epidemics. In developed countries, most cases are due to serogroups B and C. However, serogroup A is responsible for large-scale epidemics in many developing countries, including Africa, India, Nepal, and Saudi Arabia. Age-specific incidence of meningococcal infection is inversely proportional to the presence of serum bactericidal antibodies against serogroups A, B, and C. More than 50% of infants possess bactericidal antibody at birth as a result of transplacental transfer; hence, meningococcal meningitis is rarely seen in the first 3 months of life. An intact complement system is also an important host defense against invasive meningococcal disease. Recurrent or chronic neisserial infections have been associated with rare isolated deficiencies of late complement components (C5, C6, C7, or C8, and perhaps C9) due to the role of complement in opsonophagocytosis. Deficiency or dysfunction of properdin, which is a stabilizing factor of C3 convertase in the alternate complement pathway, also predisposes to meningococcal infections. The time from nasopharyngeal acquisition to bloodstream invasion is short (usually 10 days). The incubation period may also be short, because “secondary” cases commonly occur within 1-4 days of the index case.
Pneumococcal meningitis occurs in all age groups, but maximum incidence rates are seen at the extremes of age with an estimated incidence rate of 17 cases per 100,000 population in children <5 years of age (6). The common predisposing
factors include pneumonia, otitis media, sinusitis, CSF fistulas or leaks, head injury, sickle cell disease, and thalassemia major.
factors include pneumonia, otitis media, sinusitis, CSF fistulas or leaks, head injury, sickle cell disease, and thalassemia major.
Enterobacteriaceae, group B streptococci, and Listeria cause meningitis predominantly in neonates. Enterobacteriaceae are normal gut flora, 25% of women are colonized with group B streptococci in the developed world, and may infect or colonize the female gastrointestinal tract, predominantly in the developing world. Aspiration of contaminated secretions, pneumonia, and hematogenous seeding of the meninges result in early-onset meningitis incidence of ˜10 per 100,000 (7).
Vaccines against Hib, S. pneumoniae, and N. meningitidis have decreased the disease burden by 99%, 94%, and 90%, respectively, in countries where vaccines are available. Due to the lack of vaccine availability worldwide, the global disease burden has been reduced by a mere 2%.
Pathogenesis
The development of childhood bacterial meningitis typically progresses through phases that include nasopharyngeal colonization and vascular invasion, meningeal invasion and multiplication in the subarachnoid space, induction and progression of inflammation in the subarachnoid space with associated pathophysiologic alterations, and damage to the CNS.
Nasopharyngeal Colonization and Vascular Invasion
Most organisms that cause bacterial meningitis are transmitted by the respiratory route. They colonize the nasopharyngeal mucosa by adherence to the mucosal epithelium and evasion of mucosal host defense mechanisms. Adherence is mediated through adhesins on the bacterial surface that help surface binding to epithelial cell receptors and differs in various organisms. In N. meningitidis, adherence depends on the binding of fimbriae on the bacterial cell wall, whereas in S. pneumoniae, it depends mainly on the cell wall components. Host secretory IgA antibodies inhibit adherence and penetration of pathogens. The organisms secrete highly specific endopeptidases that cleave the heavy chains of secretory IgA and impair specific mucosal immunity, allowing the organisms to colonize.
Infection of the nasopharyngeal cells causes injury to the ciliated epithelial cells of the respiratory tract, resulting in loss of protective ciliary activity. Bacteria penetrate the mucosal barrier through either transepithelial or paraepithelial means. A number of bacterial factors help the process of invasion, including pili and lipo-oligosaccharides on the outer membranes of N. meningitidis and H. influenzae and the binding of S. pneumoniae to the polymeric immunoglobulin receptors on the mucosa. Pneumolysin and hyaluronidase of the pneumococci also facilitate mucosal invasion.
To survive in the bloodstream, the pathogens must overcome the host defense systems of circulating antibodies, complement-mediated bacterial killing, and neutrophil phagocytosis. The bacterial polysaccharide capsule operates against these mechanisms. In the absence of specific anticapsular antibodies, nonspecific activation of the alternative complement pathway is the main host defense against encapsulated bacteria. Persons with impaired alternative complement pathways and asplenia are at particular risk for overwhelming sepsis and meningitis by these encapsulated bacteria.
Meningeal Invasion
The blood-brain barrier (BBB) normally protects against meningeal invasion. Penetration of BBB occurs via microbial interactions with host receptors and depends on various neurotropic and virulence factors, including capsule characteristics, fimbriae, surface proteins of bacteria, and, perhaps, a critical magnitude of bacteremia.
After penetrating the meninges, the bacteria multiply freely in the CSF, which has diminished host defense mechanisms. The bacterial capsular polysaccharides have high antiphagocytic properties, and the CSF has a very low concentration of specific antibody. The bacteria thus multiply rapidly and spread over the entire surface of the brain and spinal cord along penetrating vessels.
Inflammation of the Subarachnoid Space
The multiplication and autolysis of bacteria in the CSF lead to the release of bacterial components, including fragments of cell wall and lipopolysaccharide that trigger a strong inflammatory response in the subarachnoid space by inducing the production and release of inflammatory cytokines and chemokines. These cytokines can be produced by many brain cells, including astrocytes, glia, endothelial cells, ependymal cells, and macrophages. Early-response cytokines include IL-1β, IL-6, and tumor necrosis factor (TNF), which then trigger a cascade of inflammatory mediators, including other interleukins, chemokines, platelet-activating factor, matrix metalloproteinases, nitric oxide (NO), and free oxygen radicals. The increase in cytokines enhances permeability of the BBB and recruits leukocytes from the blood into CSF, leading to CSF pleocytosis. These mediators also affect CBF and cerebral metabolism and contribute to the development of cerebral edema and neurologic sequelae.
Pathophysiology
Disruption of the Blood-Brain Barrier and Changes in Cerebral Blood Flow
Loss of autoregulation leads to changes in CBF, which increases in the early phase and decreases in the later phase of meningitis. The increase in CBF in early meningitis is secondary to the vasodilatory effect of NO. Later, the CBF progressively declines, most likely as a result of vasospasm. Loss of autoregulation also makes cerebral perfusion dependent on the systemic blood pressure, and the cerebral perfusion pressure drops when blood pressure drops.
In addition to the global cerebral hypoperfusion, focal hypoperfusion can occur due to vasculitis of large and small arteries crossing the inflamed subarachnoid space, which can cause ischemic damage that leads to permanent neurologic sequelae. Occlusion or severe stenosis of the intracranial internal carotid artery or of the middle and anterior cerebral arteries or involvement of the large vessels at the base of the brain can lead to stroke and result in paresis.
Neuropathology
Bacterial meningitis includes inflammation of the subarachnoid space, inflammatory involvement of the cerebral blood vessels, and parenchymal brain damage. Histologic examination reveals loss of neurons, generally focal, particularly in patients who have a late mortality. Cerebral edema in bacterial meningitis may be vasogenic, cytotoxic, or interstitial. Vasogenic cerebral edema occurs as a result of increased BBB permeability, which leads to extravasation of large molecules and serum into the brain parenchyma. Cytotoxic edema occurs because of an increase in intracellular water that is secondary to alterations of the cell membrane permeability and loss of cellular homeostasis, with influx of potassium and calcium into the cell. Interstitial edema occurs due to an increase in CSF volume, which may occur due to increased CSF production
secondary to increased blood flow in the choroid plexus. Associated decrease resorption of the CSF may also occur because of increased outflow resistance across the arachnoid villi of the sagittal sinus. Interstitial edema is probably the main cause of obstructive hydrocephalus in meningitis. Severe brain edema can cause herniation of brain tissue and compression of the brainstem due to increased ICP
secondary to increased blood flow in the choroid plexus. Associated decrease resorption of the CSF may also occur because of increased outflow resistance across the arachnoid villi of the sagittal sinus. Interstitial edema is probably the main cause of obstructive hydrocephalus in meningitis. Severe brain edema can cause herniation of brain tissue and compression of the brainstem due to increased ICP
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