Acute Bacterial Meningitis

Epidemiology and Risk Factors. There are approximately 25,000 cases of bacterial meningitis in the United States each year, but this disease is much more prevalent in developing countries. Group B streptococci and gram- negative enteric bacilli are the etiological organisms of the majority of cases of bacterial meningitis during the neonatal period in developed countries. In underdeveloped countries, gram-negative bacilli, predominantly Escherichia coli, are the most common pathogens.^ Risk factors that predispose the newborn to bacterial meningitis include maternal infections, particularly of the urinary tract and uterus, obstetrical risk factors, including prolonged rupture of membranes and birth trauma, prematurity, low birth weight (less than 2500 g), congenital anomalies, perinatal hypoxia/ asphyxia, cardiopulmonary resuscitation and monitoring, prolonged ventilatory support, and intravenous lines. [1] After the neonatal period, Streptococcus pneumoniae and Neisseria meningitidis are the most common etiological agents of bacterial meningitis. Haemophilus influenzae type b (Hib) was the leading cause of bacterial meningitis in young children before the widespread use of the Hib conjugate vaccine. The latter has resulted in a marked reduction in the incidence of invasive infections caused by Hib in the United States. N. meningitidis causes meningitis primarily in children and young adults, with the majority of cases occurring in individuals under age 30. Major epidemics are heralded by disease occurring in older age groups. The "meningitis belt" of sub-Saharan Africa refers to areas of Africa in which there are repeated epidemics of serogroup A meningococcal meningitis. [2] Annual outbreaks of meningitis occur in the meningitis belt in late April and early May when the dry desert winds have ceased and temperatures are high throughout the day. The epidemic tends to end with the onset of the rainy season. Transmission of meningococci is facilitated by airborne droplets, and the nasopharynx is the natural reservoir for this organism. During periods of low humidity, an alteration in the nasopharyngeal mucosal barrier predisposes the individual to infection. In addition, crowding, the presence of other respiratory pathogens, poor hygiene, and other poorly defined environmental factors contribute to the development of an epidemic of meningococcal meningitis. [2] Colonization of the nasopharynx in an individual may result in an asymptomatic carrier state or invasive infection.

S. pneumoniae is the most common causative organism of community-acquired bacterial meningitis in the adult. Pneumonia and acute and chronic otitis media are important antecedent events. Chronic disease, specifically alcoholism, sickle cell anemia, diabetes, renal failure, cirrhosis, splenectomy, hypogammaglobulinemia, and organ transplantation are predisposing conditions for pneumococcal bacteremia and meningitis. The pneumococci are a common cause of recurrent meningitis in patients with head trauma and cerebrospinal fluid (CSF) rhinorrhea. In the older adult (50 years of age and older), S. pneumoniae is likely to cause meningitis in association with pneumonia or otitis media, and gram-negative bacilli are the likely organisms to cause meningitis in association with chronic lung disease, sinusitis, a neurosurgical procedure, or a

chronic urinary tract infection. y , [4 The most common gram- negative bacilli causing meningitis in the older adult are E. coli, Klebsiella pneumoniae, H. influenzae, Pseudomonas organisms, Enterobacter species, and Serratia species.y y [6] Listeria monocytogenes is an important causative organism of neonatal meningitis and of meningitis in patients that are diabetic, alcoholic, elderly, or immunosuppressed, especially transplant recipients. [2 Infection with L. monocytogenes may be acquired through the consumption of soft cheeses, raw vegetables, seafood, cole slaw, and undercooked chicken and delicatessen meats. The staphylococci are the etiological organisms of meningitis primarily in the neurosurgical patient. S. aureus and coagulase-negative staphylococci are the predominant organisms causing infections in patients with CSF shunts or subcutaneous Ommaya reservoirs.

Pathogenesis and Pathophysiology. The most common bacteria that cause meningitis, N. meningitidis and S. pneumoniae, initially colonize the nasopharynx by attaching to the nasopharyngeal epithelial cells. The organisms are able to attach to the nasopharyngeal epithelial cells via an interaction between bacterial surface structures, such as the fimbriae of N. meningitidis and host cell surface receptors. The bacteria are then either carried across the cell in membrane-bound vacuoles to the intravascular space or invade the intravascular space by creating separations in the apical tight junctions of columnar epithelial cells. [7] , [8 S. pneumoniae and N. meningitidis are both encapsulated bacteria, and once they gain access to the bloodstream, they are successful in avoiding phagocytosis by neutrophils and classic complement-mediated bactericidal activity because of the presence of the polysaccharide capsule. Bacteria that are able to survive in the circulation enter the CSF from the bloodstream through the choroid plexus of the lateral ventricles and other areas of altered blood-brain barrier permeability. The CSF is an area of impaired host defense because of a lack of sufficient numbers of complement components and immunoglobulins for the opsonization of bacteria. [7] Normal uninfected CSF contains no phagocytic cells, has a low protein concentration, contains no IgM, and has low concentrations of C 3 and C4 .[9] In addition, the fluid medium of the CSF impairs the phagocytosis of bacteria by neutrophils. [9] , y Bacteria multiply rapidly in the subarachnoid space. Both the multiplication of bacteria and the lysis of bacteria by bactericidal antibiotics result in the release of bacterial cell wall components. These induce the formation of the inflammatory cytokines, interleukin-1 (IL-1) and tumor necrosis factor (TNF), by monocytes, macrophages, brain astrocytes, and microglial cells, which leads to altered blood-brain barrier permeability and the recruitment of polymorphonuclear leukocytes. This process results in the formation of a purulent exudate in the subarachnoid space, which is the basis for the neurological complications of bacterial meningitis. The inflammatory cytokines, IL-1 and TNF, that are produced in response to the release of bacterial cell wall components induce the formation of leukocyte adhesion molecules on vascular endothelial cells. The adherence of neutrophils to vascular endothelial cells is a necessary prerequisite for neutrophils to traverse the blood-brain barrier. It is not clear what role, if any, neutrophils play in eradicating the infection in the subarachnoid space. Large numbers of leukocytes in the subarachnoid space contribute to the purulent exudate and obstruct the flow of CSF. Adherence of leukocytes to the cerebral capillary endothelial cells increases the permeability of blood vessels, allowing for the leakage of plasma proteins through open intercellular junctions that lead to vasogenic brain edema. The leukocytes that successfully migrate into the CSF can subsequently be stimulated by the inflammatory cytokines to degranulate and release toxic oxygen metabolites, producing cytotoxic cerebral edema. Interleukin-1 is a chemoattractant for neutrophils. [7] , y Interleukin-1 may also have a role in the altered level of consciousness and the production of fever in bacterial meningitis. It has been demonstrated that IL-1 facilitates slow-wave sleep and produces fever by its effect on the hypothalamus. y , y Other inflammatory cytokines, including interleukin-6 and interleukin- 8, also have a role in the induction of meningeal inflammation, but the role of these cytokines has not been studied as extensively as that of IL-1 and TNF. Platelet activating factor (PAF) also has a prominent role in increasing blood- brain barrier permeability. y

The alteration in blood-brain barrier permeability during bacterial meningitis results in vasogenic cerebral edema, which contributes to increased intracranial pressure. It also allows for the leakage of plasma proteins into the CSF that contribute to the inflammatory exudate in the subarachnoid space. [8] The purulent exudate in the subarachnoid space interferes with the resorptive function of the arachnoid granulations. As resorption is obstructed, CSF dynamics are altered, and there is transependymal movement of fluid from the ventricular system into the brain parenchyma, which contributes to interstitial edema. The purulent exudate in the basal cisterns obstructs CSF outflow through the ventricles, also contributing to interstitial edema.

An increase in intracranial pressure affects cerebral perfusion pressure (CPP), which is defined as the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP) (CPP = MAP-ICP). Cerebral perfusion pressure is also adversely affected by a loss of cerebral autoregulation. Cerebral blood flow is initially increased in bacterial meningitis; however, shortly thereafter cerebral blood flow begins to decrease. Cerebral blood flow is normally protected through cerebrovascular autoregulation. There is dilatation or constriction of cerebral resistance vessels in response to alterations in CPP, as a result of either changes in the MAP or changes in ICP.y The loss of cerebral autoregulation means that cerebral blood flow decreases when systemic blood pressure decreases and increases when systemic blood pressure increases. Because patients with bacteremia and bacterial meningitis are at risk for hypotension, the loss of cerebral autoregulation also puts them at risk for decreased cerebral blood flow. Cerebral blood flow is also affected by narrowing of large arteries at the base of the brain due to encroachment by the purulent exudate in the subarachnoid space. Furthermore, infiltration of the arterial walls by inflammatory cells with secondary intimal thickening, and thrombosis of the major sinuses and thrombophlebitis of the cerebral cortical veins contribute to diminished cerebral blood flow.

Clinical Features and Differential Diagnosis. The classic presentation of bacterial meningitis is headache, fever, stiff neck, and an altered level of consciousness, but

the clinical symptoms and signs may vary depending on the age of the patient and the duration of illness before presentation. The symptoms and signs of bacterial meningitis in the neonate are often subtle and typically nonspecific, and include fever or hypothermia, lethargy, seizures, irritability, bulging fontanel, poor feeding, vomiting, and respiratory distress. Meningitis should always be considered when sepsis is suspected in the neonate. [1] , y In children and adults, the symptoms and signs of bacterial meningitis are fever, headache, vomiting, photophobia, nuchal rigidity, lethargy, confusion, or coma. Meningitis in children typically presents as either a subacute infection that gets progressively worse over several days, following an upper respiratory tract or ear infection or as an acute fulminant illness that develops rapidly in a few hours. The typical rash of meningococcemia is a petechial-purpuric rash that develops on the trunk, lower extremities, mucous membranes, conjunctiva, and occasionally on the palms and soles. A petechial, purpuric, or erythematous maculopapular rash is also seen in enteroviral meningitis, N. gonorrhoeae sepsis, H. influenzae type b and pneumococcal meningitis, Rocky Mountain spotted fever, and S. aureus endocarditis. Children with bacterial meningitis may also be ataxic as a result of labyrinthine dysfunction or vestibular neuronitis. In adults, an upper respiratory tract infection frequently precedes the development of meningeal symptoms, and its presence should be sought in the history. '7 , y Adults typically complain of headache, photophobia, and stiff neck, and they may have a rapid progression from lethargy to stupor and coma. The clinical presentation of meningitis in an older adult consists of fever and confusion, stupor, or coma.

Cranial nerve palsies, and most notably sensorineural hearing loss, are a common complication of bacterial meningitis and may be present early in the course of the illness. A stiff neck is the pathognomonic sign of meningeal irritation, resulting from a purulent exudate or hemorrhage in the subarachnoid space. Nuchal rigidity or meningismus is present when the neck resists passive flexion. Kernig's sign is also a classic sign of meningeal irritation, and as originally described by Kernig, it requires the patient to be in the seated position. Kernig noted that attempts to passively extend the knee while the patient was seated were met with resistance in the presence of meningitis so that a contraction of the extremities was maintained. '17] , '13] Jozef Brudzinski described at least five different meningeal signs. His best known sign, the nape of the neck sign, is elicited with the patient in the supine position and is positive when passive flexion of the neck results in spontaneous flexion of the hips and knees.y , y

Seizures occur in 40 percent of patients with bacterial meningitis typically during the first week of illness. Ihe etiology of seizure activity can be attributed to either one or a combination of the following: (1) fever; (2) cerebrovascular disease consisting of either focal arterial ischemia, infarction or cortical venous thrombosis with hemorrhage; (3) hyponatremia; (4) subdural effusion or empyema producing a mass effect; and (5) antimicrobial agents (e.g., imipenem, penicillin). y Raised ICP is an expected complication of bacterial meningitis and presents as one or a combination of the following clinical signs: (1) an altered level of consciousness; (2) the Cushing reflex--bradycardia, hypertension, and irregular respirations y ; (3) dilated, nonreactive pupil or pupils; (4) unilateral or bilateral cranial nerve six palsies; (5) papilledema; (6) neck stiffness; (7) hiccups; (3) projectile vomiting; and, (9) decerebrate posturing. y Acute ischemic stroke may occur in the course of bacterial meningitis as a result of narrowing of the large arteries at the base of the brain. This may occur from encroachment by a purulent exudate in the subarachnoid space or infiltration of the arterial wall by inflammatory cells (vasculitis). Vasospasm, thrombotic or stenotic occlusion of branches of the middle cerebral artery, and septic venous sinus thrombosis with thrombophlebitis of cortical veins may also occur. '7

Ihe differential diagnosis of this clinical presentation includes viral meningoencephalitis, fungal meningitis, tuberculous meningitis, focal intracranial mass lesions, subarachnoid hemorrhage, Rocky Mountain spotted fever, and neuroleptic malignant syndrome.

Evaluation. Ihe gold standard for the diagnosis of bacterial meningitis is the examination of the CSF. Ihe classic CSF abnormalities in bacterial meningitis are (1) an increased opening pressure; (2) a polymorphonuclear leukocytic pleocytosis; (3) a decreased glucose concentration; and (4) an increased protein concentration. Raised ICP is an expected complication of bacterial meningitis and can theoretically contribute to brain herniation following lumbar puncture. When there are clinical signs of raised ICP and urgent lumbar puncture is indicated, a bolus of mannitol 1 g/kg of body weight can be given intravenously and the lumbar puncture can be performed 20 minutes later. In addition, the patient can be intubated and hyperventilated. Alternatively, lumbar puncture can be deferred and blood cultures obtained until the raised intracranial pressure can be treated. Regardless, the lumbar puncture should be performed with a 22-gauge needle. y When obtaining CSF for analysis it is important to remember that adults have approximately 150 ml of CSF, but infants and children have smaller amounts, in the range of 30 to 60 ml in the neonate and 100 ml in the adolescent. y Ihe volume of CSF in a child 4 to 13 years of age is in the range of 65 to 140 ml, with an average volume of 90 ml. y Approximately 10 to 12 ml of CSF should be withdrawn from an adult, and the withdrawal of 3 to 5 ml is recommended in the neonate and child. y Ihe CSF glucose concentration is low when the value is less than 40 mg/dl or when the CSF/ blood glucose ratio is less than 0.6. When an ampule of 50 ml of 50 percent glucose (D50) has been given enroute to the emergency room, 30 minutes is required for the ampule of D50 to influence the CSF glucose concentration. Ihe CSF white blood cell (WBC) count is usually more than 100 cells/shmm3 and is often more than 1000 WBCs/ mm3 in bacterial meningitis. Although there is typically a predominance of polymorphonuclear leukocytes in the CSF in bacterial meningitis, a predominance of lymphocytes has been reported in cases of acute bacterial meningitis when the CSF WBC concentration was less than 1000/mm3 and in bacterial meningitis due to L. monocytogenes. y , y Ihe initial CSF examination in neonatal bacterial meningitis may have an absence of pleocytosis and normal glucose and protein concentrations. A Gram stain of the CSF should be examined carefully, and a high index of suspicion for meningitis should be maintained in the neonate with fever, seizure activity, irritability, lethargy, and/or

respiratory distress.y , y Oral antimicrobial therapy administered before lumbar puncture will not significantly alter the CSF WBC count or glucose concentration but will decrease the likelihood of identifying the organism on Gram's stain or isolating it in culture. y Ihe latex particle agglutination test for the detection of bacterial antigens of H. influenzae type b, S. pneumoniae, N. meningitidis, group B streptococcus, and E. coli K1 strains in the CSF is very useful in making a rapid diagnosis of bacterial meningitis. It is also helpful in making the diagnosis of bacterial meningitis in patients who were pretreated with antibiotics and in the patient whose Gram's stain and CSF culture are negative. Ihe Limulus amebocyte lysate test is very sensitive in detecting gram-negative bacterial meningitis. It has a 77 to 99 percent sensitivity for the detection of gram-negative endotoxin in the CSF. y A good rule is that the Gram's stain and bacterial culture should be negative in the CSF obtained 24 hours after the initiation of intravenous antimicrobial therapy, if the organism is sensitive to that antibiotic.

Management. Empiric therapy of bacterial meningitis in the neonate should include the combination of ampicillin (50 mg/kg q 6 to 3 hr) and either cefotaxime (50 mg/kg q 3 to 12 hr) or an aminoglycoside, such as gentamicin (2.5 mg/kg q 3 to 12 hr) or amikacin (10 mg/kg q 3 to 12 hr). '1] Empiric therapy of bacterial meningitis in infants 4 to 12 weeks of age requires antimicrobial agents that are active against the likely pathogens of the neonatal age group as well as those that cause infection in infants and children. An appropriate regimen in this age group is ampicillin and either cefotaxime or ceftriaxone (100 mg/kg/d intravenously in divided doses q 12 hr). A third-generation cephalosporin, either cefotaxime (225 mg/kg/d intravenously in divided doses q 6 hr) or ceftriaxone (100 mg/kg/d intravenously in divided doses q 12 hr) plus vancomycin (40 mg/kg/d intravenously in divided doses q 6 hr) is recommended for empiric therapy of bacterial meningitis in the older infant and child. Empirical therapy of bacterial meningitis in adults should include a combination of ceftriaxone (2 g intravenously twice daily) or cefotaxime (3 to 12 g/d intravenously in divided doses q 4 hr) plus vancomycin (500 mg intravenously q 6 hr). In the older adult and in the immunocompromised adult in whom L. monocytogenes may be the etiological organism, ampicillin (12 g/d in divided doses q 4 hr) should be added to this regimen. In patients who have recently undergone a neurosurgical procedure or who are immunocompromised, Pseudomonas aeruginosa may be the etiological agent, and ceftazidime (6 g/d intravenously in divided doses q 3 hr) should be substituted for cefotaxime or ceftriaxone. Once the causative organism has been identified, antimicrobial therapy can be modified based on the recommendations for that specific organism. Recommendations for antimicrobial therapy based on the infecting organism are listed in X┬žbIe 4.2.:1 .

Ihe American Academy of Pediatrics recommends the consideration of dexamethasone for bacterial meningitis in infants and children 2 months of age and older. Ihe recommended dose is 0.6 mg/kg/d in four divided doses (0.15 mg/kg/dose) given intravenously for the first 4 days of antimicrobial therapy. '231 Ihe first dose of dexamethasone should be administered 20 minutes before the first dose of antimicrobial therapy. It is also entirely reasonable to use



Antibiotic and Dose (Intravenous Unless Indicated)

Infants (> 2000 g)



Group B streptococcus

Ampicillin 50 mg/kg every 6 hr plus amikacin 10 mg/kg every 8 hr or gentamicin 2.5 mg/kg every 8 hr

Neisseria meningitidis

Penicillin G 250,000 to 400,000 U/kg/d (divied every 4 hr) plus (at end of therapy) oral rimamfin, older than 1 yr: 10 mg/kg every ] 12 hr for 2 d. Younger than 1 yr: 5 mg/kg every l2 hr for 2 d

Penicillin G 20 to 24 million U/d (divided every 4 hr) plus (at end of theraphy) oral rifampin 600 mg every 12 hr for 2 d

Streptococcus pneumoniae

Cefotaxime 225 mg/kg/d (divided every 6 hr) of ceftriaxone 100 mg/kg/d (in once or twice daily dosing interval) plus vancomycin 40 mg/kg/d (every 6 hr dosing interval)

Cefotaxime 3 to 12 g/d (divided every 4 hr) or ceftriaxone 4 g/d (2 g every 12 hr) + vancomycin 2 g/d (in a 6 hr or 12 hr dosing interval)

Enteric gram-negative bacilli (except Pseudomonas aeruginosa)

Cefotaxime 50 mg/kg every 8 hr plus amikacin or gentamicin

Cefotaxime or cefriaxone (as above)

Cefotaxime or cefriaxone (as above)

Pseudomonas aeruginosa

Ceftazidine 50 mg/kg every 8 hr

Ceftazidine 150 mg/kg/d (every 3 hr dosing interval)

Ceftazidime 6 g/d (every 3 hr dosing interval)

Listeria monocytogenes

Ampicillin 50 mg/kg every 6 hr plus amikacin or gentamicin for 3 to 5 d

Ampicillin 150 to 200 mg/kg/d (every 4 hr dosing interval)

Ampicillin 12 g/d (divided every 4 hr)

Haemophilus influenza tybe b


Cefotaxime or ceftiaxone

Cefotoxime or ceftriaxone

Staphylococcus aureus Methicillin-sensitive

Methicillin 50 mg/kg every 6 hr

Oxacillin 200 to 300 mg/kg/d (divided every 4 hr)

Oxacillin 12 g/d (divided every 4 hr)

Staphylococcus aureus Methicillin-resistant

Vancomycin 15 mg/kg every 8 hr

Vancomycin 40 mg/kg/d (divided every 6 hr)

Vancomycin 2 g/d (divided every 6 hr)

dexamethasone therapy in adults with bacterial meningitis in the same dose as recommended for children. Dexamethasone is beneficial in preventing the neurological complications of bacterial meningitis by decreasing meningeal inflammation. Dexamethasone inhibits the synthesis of the inflammatory cytokines, interleukin-1 and tumor necrosis factor, produced by brain astrocytes and microglial cells in response to bacterial cell wall components in the subarachnoid space. As discussed earlier, the inflammatory cytokines increase the permeability of the blood-brain barrier and recruit polymorphonuclear leukocytes from the bloodstream to the CSF. The result is the production of a purulent exudate in the subarachnoid space. Although the majority of patients in the clinical trials evaluating the efficacy of dexamethasone in bacterial meningitis have been infants and children, the production and the role of the inflammatory cytokines in the neurological complications of this infection are the same in infants, children, and adults. It is therefore reasonable to recommend dexamethasone therapy in adults. In the single clinical trial that evaluated the efficacy of dexamethasone in pneumococcal meningitis in adults, patient mortality was reduced despite the use of an ampicillin dose that is now considered sub- therapeutic. y Dexamethasone appears to be reasonably safe. The third-generation cephalosporins penetrate the CSF extremely well even in the presence of dexamethasone. y , [31] The penetration of vancomycin, however, may be adversely affected by dexamethasone therapy since meningeal inflammation improves the penetration of vancomycin into the CSF. The clinical significance of this is unclear. Consideration should therefore be given to the use of higher doses of vancomycin (60 mg/kg/d in divided doses q 6 hr) or intrathecal vancomycin in cases of highly penicillin- resistant and cephalosporin-resistant pneumococcal meningitis when dexamethasone is used concomitantly with antimicrobial therapy. The use of an H2 antagonist with dexamethasone is recommended to avoid gastrointestinal bleeding.

The majority of children with bacterial meningitis are hyponatremic with serum sodium concentrations less than 135 mEq/L at the time of admission owing to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The time-honored treatment of SIADH was fluid restriction. This practice, however, has recently received renewed attention because of the knowledge that autoregulation of cerebral blood flow is lost in the course of bacterial meningitis. A decrease in the mean systemic arterial pressure is therefore associated with a decrease in the cerebral blood flow. In experimental pneumococcal meningitis, fluid-restricted rabbits had a greater decrease in MAP and cerebral blood flow than did euvolemic rabbits. y The present recommendations are to limit the initial rate of intravenous fluid administration to approximately three quarters of the normal maintenance requirements (or 1000 to 1200 ml/m 2 / 24 hr). The intravenous fluid should be a multielectrolyte solution containing between one quarter and one half normal saline and potassium at 20 to 40 mEq/L in 5 percent dextrose. Once the serum sodium concentration increases above 135 mEq/L, the volume of the fluids administered can be gradually increased. y , y

The development of seizure activity should be anticipated in the patient with bacterial meningitis. Seizure activity occurs in approximately 30 to 40 percent of children with acute bacterial meningitis and in more than 30 percent of adults with pneumococcal meningitis, typically occurring in the first few days of the illness. There is an increased risk of epilepsy following bacterial meningitis especially in those individuals who have seizures in the first few days of infection. y Raised ICP is an expected complication of bacterial meningitis and should be anticipated at the time of the initial lumbar puncture. The ICP should be measured by an ICP monitoring device. The treatment of raised ICP in bacterial meningitis includes one or more of the following: (1) elevation of the head of the bed 30 degrees; (2) hyperventilation to maintain the PaCO2 between 25 to 33 mm Hg; (3) mannitol 1.0 g/kg bolus intravenous injection, then 0.25 to 0.5 g/kg intravenous every 3 to 5 hours to achieve a serum osmolarity of 295 to 320 mOsm/L; (4) dexamethasone 0.15 mg/kg q 6 hr; and (5) pentobarbital coma with a loading dose 5 to 10 mg/kg administered intravenously at a rate of 1 mg/kg/min and a maintenance dose of 1 to 3 mg/kg/hr.y , y Subdural effusions commonly develop in the course of bacterial meningitis in children when the infection in the adjacent subarachnoid space leads to an increase in the permeability of the thin-walled capillaries and veins in the inner layer of the dura. The result is leakage of albumin-rich fluid into the subdural space. This is usually a self-limited process, and as the inflammatory process subsides, fluid formation ceases and the fluid in the subdural space is reabsorbed. y , y , y The indications for aspiration of a subdural fluid collection include the clinical suspicion of infected fluid (prolonged fever), a rapidly enlarging head circumference in a child without hydrocephalus, focal neurological findings, or clinical signs of increased ICP.y

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