Bacterial, Fungal, & Parasitic Infections of the Nervous System 1 Flashcards
Bacterial meningitis pathogenesis
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 and Neisseria 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.
- They then reproduce, releasing proinflammatory cytokines in the meninges. These cytokines, such as tumor necrosis factor and interleukin-1, break down the blood–brain barrier, leading to edema and cell death.
- Occlusion of the arachnoid granulations by protein and in sinuses by white cells leads to decreased CSF resorption and dilatation of meningeal vessels, which contributes to more cerebral edema.
Bacterial meningitis: special entry mechanisms of bacteria
Special entry mechanisms include:
1) thrombosed veins in the presence of extracranial infection such as otitis or mastoiditis, which allow retrograde transmission of infection
2) After nasal, mastoid, sinus, or cranial surgery, or penetrating head trauma, violation of the dura allows a passageway for bacterial entry of those colonizing the skin or sinuses
3) Staphylococcal bacteria gain access to the CNS after injection of epidural corticosteroids or anesthesia, or through placement of spinal cord or deep brain stimulators, or lumbar or ventricular drains
4) Foreign bodies within the brain such as ventricular drains or shunts, Ommaya reservoirs, and deep brain and corticography electrodes can also become infected after even transient bacteremia
Bacterial meningitis risk factors
- recent cranial or complex spine procedures with penetration of the dura
- chronic sinus or mastoid infection
- endocarditis or bacteremia (dental cleaning, injection drug use)
- very young or advanced age
- presence of HIV/AIDS
- failure to have received vaccinations
- complement pathway deficiency, including treatment with targeted monoclonal antibodies such as eculizumab, makes patients vulnerable to less virulent strains of bacteria.
What is the cause of devastating sequences of meningitis
Although meningitis refers only to inflammation of the lining of the brain, the devastating consequences are the result of:
- inflammation within the adjacent brain
- secondary effects of edema after thrombosed veins and blockage of CSF resorption (these can lead to hydrocephalus or increased intracranial pressure and herniation)
- Abscess and subdural empyema
Bacterial meningitis major complications
- Cerebral edema with depression of consciousness
- Septic shock and disseminated intravascular coagulation
- stroke (15%)
- cognitive impairment (25%)
- deafness (10-20%)
- Abscess and subdural empyema
- Hydrocephalus
- Seizure in the acute phase (most do not develop epilepsy)
- Developmental delay/ intellectual behavior disorder in children
Mechanism of stroke in meningitis
consequence of arteritis as large blood vessels cross through the exudate (εξίδρωμα) at the base of the brain
Most common causes of bacterial meningitis in the US
1) S pneumoniae (58%)
2) group B streptococci (18%)
3) Neisseria meningitidis (13.9%)
4) H influenzae type B (6.7%)
Common cause of meningitis in immunocompromised patients
Haemophilus influenzae type b
causes meningitis in immunocompromised patients (e.g., postsplenectomy and in chronic lung disease).
The most common though is cryptococcus
Bacterial meningitis caused by Neisseria meningitides treatment
Bacterial meningitis caused by Streptococcus pneumoniae treatment
Bacterial meningitis caused by Haemofilus influenzae type B treatment
Bacterial meningitis caused by listeria monocytogenes treatment
Bacterial meningitis caused by staphylococcus aureus treatment
Bacterial meningitis caused by staphylococcus epidermidis and MRSA treatment
Bacterial meningitis caused by pseudomonas aeruginosa treatment
Bacterial meningitis caused by group B streptococcus treatment
Bacterial meningitis: empiric antibiotic treatment of age-associated pathogens
** third-generation cephalosporin = Ceftriaxone or cefotaxime
Vancomycin: As a component of empiric therapy or pathogen-specific therapy (eg, MRSA or penicillin- and cephalosporin-resistant S. pneumoniae)
Ceftriaxone: As a component of empiric therapy (community-acquired infections in immunocompetent patients) or pathogen-specific therapy (eg, Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Cutibacterium acnes, and susceptible gram-negative bacilli
Ampicillin: As a component of empiric therapy (community-acquired infections in immunocompetent patients >50 years of age and immunocompromised patients) or pathogen-directed therapy (eg, Haemophilus influenzae, L. monocytogenes, Neisseria meningitidis, Streptococcus agalactiae, Streptococcus pneumoniae, Enterococcus spp.)
When to administer dexamethasone in bacterial meningitis
Why
How to administer
Undesirable effect
For adults with suspected community-acquired bacterial meningitis due to an unknown organism, administration of dexamethasone in addition to antimicrobial therapy is recommended.
Adjunctive dexamethasone should be given shortly before or at the same time as the first dose of antibiotics, when indicated.
Dexamethasone should be only continued if the CSF Gram stain and/or the CSF or blood cultures reveal S. pneumoniae.
Intravenous administration of glucocorticoids (usually dexamethasone) prior to or at the time of administering antibiotics has been associated with a reduction in the rate of
1) hearing loss
2) other neurologic complications
3) mortality
in patients with meningitis caused by S. pneumoniae
Helps to prevent the inflammatory response triggered by death of the bacteria
Dexamethasone should be continued for four days if the Gram stain reveals organisms consistent with S. pneumoniae or if the cerebrospinal fluid (CSF) or blood culture grows S. pneumoniae.
There is no proven benefit from dexamethasone therapy for adult patients with meningitis due to other pathogens
The recommended intravenous dexamethasone regimen 10mg every six hours for four days
It may induce progression of undiagnosed tubercular infection
Should other than antimicrobial treatment be added in bacterial meningitis
Extremely ill-appearing patients should receive antiviral coverage for herpes encephalitis in addition to antibacterial therapy when the diagnosis of bacterial meningitis is in doubt.
Until another organism is identified (by PCR, culture, or Gram stain) or tuberculosis cultures are negative (which takes 4 weeks), antitubercular therapy is also prudent in patients who appear very sick or are at high risk, such as those with AIDS or other immunosuppressed states
Duration of treatment in bacterial meningitis
Bacterial meningitis prevention
- Vaccination programs against common pathogens such as H influenzae, N meningitidis, S pneumoniae.
- Men who have sex with men should also be vaccinated against N meningitides.
- All patients undergoing splenectomy should be vaccinated against S pneumoniae.
- Patients with a meningeal breach from congenital or acquired structural deficits (trauma, tumor, postneurosurgical procedure) are at particular risk of infection from organisms in the nasopharynx, ears, or paranasal sinuses.
Corrective repair is the best way to avoid recurrent meningitis. - Prophylactic antibiotic treatment before dental work or other surgical procedures is recommended for some patients with mitral valve prolapse (previously suffering from endocarditis), rheumatic heart disease, congenital heart disease, and prosthetic valves.
Bacterial meningitis clinical findings
- Classic symptoms of bacterial meningitis include headache, fever (in 80–95%), and stiff neck with flexion, but not lateral rotation and altered mentation.
- Cognitive dysfunction may progress from confusion and irritability with difficulty concentrating to obtundation and coma.
- Kernig sign (ie, pain or resistance when the examiner attempts to extend the patient’s knee while the hip is flexed) and Brudzinski sign (ie, hip flexion when the examiner bends the patient’s neck forward)
- Signs of increased intracranial pressure include depressed consciousness, vomiting and papilledema on fundoscopic examination.
- Focal signs occur as a consequence of cerebral infarct or transtentorial herniation.
- Fluctuating signs may occur with unwitnessed seizures followed by postictal (“Todd”) deficits.
-
Cranial nerve palsies are the result of inflammation affecting nerves as they traverse the meninges;
trochlear and abducens palsies can also occur as a result of increased intracranial pressure.
Third nerve palsy, with pupillary or extraocular muscle dysfunction (in either sequence), may indicate transtentorial herniation. - eighth nerve damage causing abrupt permanent deafness
- Focal or generalized seizures result from the diffuse microvascular effects of meningeal inflammation, from coexisting abscess or subdural empyema, or more rarely from toxins released systemically by organisms such as Shigella.
- Meningococcal meningitis is accompanied by a petechial rash on the trunk, legs and mucous membranes
Time course of bacterial meningitis (and difference from other causes)
Symptoms develop acutely in bacterial meningitis, allowing differentiation from more subacute or chronic causes such as tubercular or fungal meningitis.
Acute meningitis progresses over hours or a few days.
Symptoms may persist for at least 4 weeks, even with appropriate treatment.
Bacterial meningitis laboratory findings
CSF:
- cloudy appearance
- culture - Gram stain is positive in 70–85% of patients (especially in those with S pneumoniae, N meningitides, and gram-negative bacilli)
Ancillary testing for fungal (cryptococcal) or viral (herpes) infection should be done if CSF is suggestive of nonbacterial infectious source.
- film array
- Opening pressure is elevated (>180 mm H2O in adults)
- Pleocytosis of more than 100–10,000 WBCs/μL is present, usually 80–95% neutrophils, although lymphocytes or monocytes may predominate.
Absence of pleocytosis is associated with poor outcome, and is seen in 5–10% of patients, especially immunocompromised individuals ones.
Rupture of a brain abscess causes extreme pleocytosis.
- Protein concentration is elevated (>50 mg/dL) and is greater than 200 mg/dL in 50% of patients.
- CSF glucose that is less than 30% of simultaneously obtained serum glucose is present in 70% of cases.
- CSF lactate elevation above 35 mg/dL is consistent with bacterial meningitis as opposed to aseptic or viral causes.
Serum:
- Increased inflammatory markers
procalcitonin (>2 ng/mL), C-reactive protein (>40 mg/L) and erythrocyte sedimentation rate (ESR)
plus: Culture of blood, sputum, or fluid from the nasopharynx or sinuses or from any decubitus or wound can provide diagnostic clues
Bacterial meningitis imaging
- hemispheric shift or mass lesions large enough to lead to herniation are discovered in less than 5% of studies.
Contrast-enhanced CT and MRI show:
- meningeal enhancement
- sulcal effacement (beginning with the Sylvian fissures)
- cerebral edema
- and if present any parameningeal infection such as subdural empyema or mastoiditis
Imaging also has a role in diagnosing late complications of meningitis, such as:
* hydrocephalus
* abscess
* stroke
* subdural empyema
Post constrast T2 FLAIR and delayed postcontrast T1 sequences may be helpful additions in detecting subtle cases
Major pathogen in bacterial meningitis caused by spread from sinusitis or mastoiditis
S pneumococcus or H influenzae
(more prolonged antibiotic course of treatment required)
Potential imaging findings in recurrent meningitis
Thin cuts through the base of the skull may reveal a basilar skull fracture, sinus compromise, or other potential breach of the dura
Bacterial meningitis differential diagnosis
- Viral meningitis (tend to be milder, has clear consciousness, no seizures or focal deficits)
- TB meningitis
- Fungal meningitis
- Viral encephalitis (less headache)
- Chemical meningitis
- Sarcoidosis
- Lymphoma
- Carcinoma
- Collagen - vascular disease
- Autoimmune disorders
- Meningitis secondary to systemic medications
- Subarachnoid hemorrhage
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Indication to repeat lumbar puncture in bacterial meningitis
in patients with pneumococcal meningitis a repeat spinal tap after 48 hours is indicated to be sure therapy is correct
Although protein elevation, hypoglycorrhachia, and pleocytosis may remain abnormal at 48 hours, the culture should become negative if a successful choice of antibiotic was initiated.
Trastentorial herniation management
Hyperventilation, mannitol, and drainage of CSF from intraventricular catheters if present.
Fluid management can be difficult; the clinician must balance the need for adequate blood pressure with that of avoiding increased intracranial pressure
Electrolyte abnormalities in bacterial meningitis
Hyponatremia is more common than hypernatremia (20% vs 7% of cases) and may be due to syndrome of inappropriate antidiuretic hormone (SIADH), cerebral salt wasting, or fluid mismanagement.
Serious complication of meningococcal meningitis
Waterhouse - Friderichsen
thrombocytopenia
disseminated intravascular coagulation
shock
Bacterial meningitis: all cause mortality
10-30% in high-income countries
50% in low-income countries
Risk factors for brain abscess
- dental work and hematogenous spread of infected material
- congenital heart defects
- valve infection
- lung arteriovenous fistulas
- contiguous spread following meningitis or infection in nearby structures such as the nasopharynx and sinuses (frontal lobe) or middle ear and mastoid (temporal lobe or cerebellum)
- penetrating head trauma
- open skull fracture
- neurosurgery, especially with placement of a foreign body (ventricular drain, shunt, intracranial pressure monitor)
Is cerebritis and encephalitis the same
Cerebritis is essentially the same as encephalitis except that it is used to denote brain parenchymal inflammation secondary to infection with bacteria or other non-viral pathogens.
In contrast, encephalitis usually is assumed to denote inflammation due to a virus or paraneoplastic/autoimmune process
How are the symptoms in brain abscess caused
- seizures
- pressure on nearby structures
- arteritis causing stroke
- from rupture into a ventricle
Brain abscess causal organisms
Streptococcus 60–70%
Bacteroides 20–30% (Anaerobe)
Enterobacter 25–33%
Staphylococcus 10–15% and
rarely Listeria or Nocardia
Polymicrobial abscesses make up 25% of all cases.
Brain abscess prevention
- changing sterile gloves before placement of drains or intraventricular catheters and their removal at the first sign of bacteremia
- Vaccination in patients in conditions known to predispose to CNS infection, such as
(1) individuals undergoing splenectomy or cochlear implant placement or suffering from sickle cell disease (S pneumoniae) and
(2) young adults living in close quarters (N meningitides)
Brain abscess clinical findings
- Seizures (have a focal signature before generalizing)
- Cortical signs: personality change, aphasia, hemiparesis, hemisensory loss, and visual field defects.
- Infratentorial signs include ataxia, nystagmus, cranial nerve dysfunction, nausea, and vomiting
-
headache in about 75% of patients, fever in
more than 50%, deterioration of mental status in 50%, and papilledema. -
Obtundation or coma may be due to increased
intracranial pressure, often caused by
i) obstructive hydrocephalus
ii) location of the abscess pressing on the brainstem, especially cerebellar abscess
iii) following rupture of an abscess into the ventricles. - Hypothalamic dysfunction may lead to diabetes insipidus or temperature dysregulation, and hyponatremia from SIADH also sometimes occurs.
Brain abscess laboratory findings
- elevation of ESR and mild leukocytosis are present in 50% of patients
- Blood cultures
- culturing of infected sites, such as decubitus ulcer
- Open biopsy can usually be safely performed if the abscess is located near the brain surface. When the abscess is deep, needle aspiration under stereotactic guidance may be necessary
Because many cultures are sterile, PCR with DNA sequencing may prove useful in establishing the presence of an organism
CSF contraindicated (Uptodate)
Brain abscess imaging findings
CT scan:
poorly defined low-density lesion(s) that do not initially enhance with contrast.
After about 2 weeks the enhancing rim forms, representing the beginning of capsule formation
MRI:
T2-weighted or fluid-attenuated inversion recovery (FLAIR) images: hypointense areas of necrosis surrounded by hyperintense signal
Diffusion-weighted imaging (DWI):
high sensitivity and specificity
the abscess is hyperintense, with reduced coefficient compared to lesions that do not contain pus (eg, cystic tumor)
T1+C:
Contrast enhancement with gadolinium outlines the capsule
Venous thrombosis can be seen with magnetic resonance venography
Imaging may also show complications such as infarction or subdural empyema
Imaging difference between abscess and metastasis or high-grade glioma
- rCBV elevated in tumors, reduced in abscesses
(Cerebral blood volume is one of the parameters generated by perfusion techniques (CT perfusion and MR perfusion)) - the cystic component does not show restricted diffusion, unlike abscess!!!
- Tumors do not demonstrate cytosolic amino-acids on MRS
When a lesion demonstrates both ring enhancement and central restricted diffusion the differential is very much narrowed, and although cerebral abscess is by far the most likely diagnosis, cerebral metastases (particularly necrotic adenocarcinoma) should also be included on the differential
Brain abscess differential diagnosis
primary or metastatic neoplasm or lymphoma, the latter especially in immunosuppressed patients
Nonbacterial abscess occurs, especially in diabetic or immunocompromised hosts
Other considerations include
Abscess with early cerebritis and/or early capsule:
1) subacute stroke
2) radiation necrosis
3) resolving hematoma
4) herpes encephalitis
5) neuroinflammatory and demyelinating lesions including acute disseminated encephalomyelitis
Brain abscess treatment
Successful management of a brain abscess usually requires a combination of antibiotics and surgical drainage
1) Antibiotics:
Initial treatment regimens should be based on the presumptive source of the abscess, Gram stain results (if available), and patient-related factors (eg, if the patient is immunocompromised).
If the source is unknown, treatment with vancomycin plus metronidazole (for anaerobic bacteria) plus ceftriaxone or cefotaxime
Expanded gram-negative coverage (eg, cefepime) should be used instead of ceftriaxone or cefotaxime if Pseudomonas is possible
2) Glucocorticoids
For patients who have substantial mass effect on imaging, glucocorticoids in conjunction with antimicrobial therapy are suggested
Dexamethasone is administered at a loading dose 10 mg intravenously (IV) followed by 4 mg every six hours;
the drug should be discontinued once the mass effect as well as the patient’s mental status and neurologic manifestations have improved
3) Surgical drainage
needle aspiration or surgical excision should be performed to identify the causative pathogen prior to the initiation of antibiotic therapy and to reduce the size of the collection
Brain abscess antibiotics duration comparing to meningitis
brain abscesses require a longer duration of therapy (at least four to eight weeks)
Antibiotic treatment in brain abscess according to infection source
Brain abscess prognosis
10% mortality in developed countries
Survivors have up to a 25% incidence of focal deficits and a highly variable rate of epilepsy
Prognosis is worse in patients older than 60 years and in those with multiple lesions, ruptured abscess, or decreased state of consciousness on presentation.
Subdural empyema risk factors
complication of:
* frontal or ethmoid sinusitis
* otitis media
* mastoiditis
* meningitis
* osteomyelitis
It can also follow venous sinus thrombosis, skull fracture, penetrating trauma, or craniotomy.
Subdural empyema clinical findings
Initial extracranial infection (eg. otitis media, sinusitis) is followed in days to weeks by increasing localized pain or headache, recurrent fever, and development of cortical signs
or focal seizures.
Depressed sensorium occurs eventually, along with hemiparesis and cranial nerve deficits, including papilledema.
Development of stroke or brain abscess occurs if the problem is unrecognized for prolonged periods.
Subdural empyema imaging
CT should be performed with contrast, which reveals enhancement of the margins of the low-density collection overlying the cortex
Empyemas are hyperintense in T2/ FLAIR and typically demonstrate striking diffusion restriction on DWI.
Syndromes associated with skull base infection
Antibiotic treatment of epidural abscess
if contiguous infection of the paranasal sinuses, ear, or mastoid is the source: metronidazole plus either ceftriaxone or cefotaxime.
In most other instances: vancomycin plus metronidazole plus either cefotaxime, ceftriaxone, ceftazidime, or cefepime;
(ceftazidime or cefepime should be the cephalosporin selected if Pseudomonas aeruginosa is a possible or likely pathogen)
Spinal epidural abscess: pathogenesis, risk factors and most common pathogen
Bacteria can gain access to the epidural space hematogenously, by direct extension from infected contiguous tissue, or via direct inoculation into the spinal canal.
The most common sources are soft tissue infections and complications of spinal surgery or other invasive procedures, including indwelling epidural catheters.
Staphylococcus aureus accounts for about two-thirds of SEA cases caused by pyogenic bacteria.
Spinal epidural abscess: clinical findings
The classic diagnostic triad for SEA consists of:
* fever
* back pain
* neurologic deficits
Spinal epidural abscess: when to suspect
The diagnosis of SEA should be suspected in febrile patients with spinal pain accompanied by an examination consistent with a radiculopathy or other focal neurologic findings, especially if the pain is worsened by palpation or percussion.
In patients who have only fever and back pain or only new-onset back pain, a low threshold for suspicion of SEA is warranted if risk factors are present (eg, injection drug use, chronic indwelling venous catheter, distant infected foci, older age, or recent spinal manipulation)
Spinal epidural abscess: management
Surgical decompression and drainage, in addition to systemic antibiotic therapy, is the treatment of choice for many patients and should be performed as early as possible.
Surgical intervention is particularly important for those with acute or progressive neurologic deficits, spinal instability, ring-enhancing lesions on MRI, or disease progression on antibiotic therapy
Antibiotics are required and should be started as soon as the diagnosis of SEA is strongly suspected and immediately following the collection of two sets of blood cultures.
In patients with SEA, an empiric regimen of vancomycin and a third- or fourth-generation cephalosporin is suggested
Once culture identifies the infecting organism(s), treatment regimens should be simplified and directed to that pathogen
The usual duration of antimicrobial therapy is four to eight weeks
Most frequent dural sinus to become infected and thrombosed
Cavernous sinus
Septic cavernous sinus thrombosis: risk factors and most common pathogen
The underlying site of infections includes the sphenoid or ethmoid sinuses, facial infections, and dental infections.
Staphylococcus aureus accounts for 70 percent of all infections and is the etiologic pathogen in nearly all cases associated with facial infection or sphenoid sinusitis.
Septic cavernous sinus thrombosis: clinical findings and diagnosis
Headache is the most common early symptom and generally precedes fever and periorbital edema by several days.
Other common clinical manifestations include eye swelling and diplopia.
MRI with gadolinium is the imaging modality of choice
Septic cavernous sinus thrombosis: management
Urgent empiric antibiotic therapy is required.
For most patients, we suggest a regimen that includes vancomycin plus ceftriaxone or cefepime.
Metronidazole should be added if anaerobic coverage is required (eg, suspected dental or sinus infection).
We suggest early anticoagulation (heparin) in patients with UNILATERAL cavernous sinus thrombosis in order to prevent bilateral extension
** Surgical drainage of sphenoid sinus infection that has been documented on imaging should be strongly considered and, if done, should be performed emergently
Septic cavernous sinus thrombosis: differential diagnosis
More common:
* Orbital cellulitis
* Intraorbital abscess
* Intracavernous carotid artery aneurysm or arteriovenous fistula
* Neoplastic or inflammatory infiltration of the cavernous sinus (from meningioma or metastasis, as well as neurosarcoid, IgG4-related disease, idiopathic pachymeningitis or granulomatosis with polyangiitis, and Tolosa-Hunt syndrome)
* Aseptic cavernous sinus thrombosis
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Should anticoagulation be given in septic cavernous sinus thrombosis
We suggest immediate anticoagulation in patients with UNILATERAL cavernous sinus thrombosis in order to prevent bilateral extension.
** For patients with bilateral disease, we do not use anticoagulation.
For patients treated with anticoagulation, we suggest continuous-infusion heparin anticoagulation, adjusting the dose to maintain a partial thromboplastin time ratio of 1.5 to 2.5
The duration of anticoagulation has not been determined.
We continue anticoagulation until the infection as well as the symptoms and signs of cavernous sinus thrombosis (eg, periorbital edema, fever, leukocytosis) have resolved or significantly improved.
Septic transverse sinus thrombosis: risk factors and most common pathogen
Septic sigmoid sinus thrombosis most often occurs as a complication of acute or chronic otitis media.
Infection is often polymicrobial, containing both aerobes and anaerobes, reflecting the bacteriology of chronic otitis media
Septic transverse sinus thrombosis: symptoms and diagnosis
● Along with symptoms of ear infection, patients develop headache along with neurologic signs such as vertigo and fifth and sixth nerve impairment. Some patients develop increased intracranial pressure.
● The diagnosis of septic transverse sinus thrombosis is made by contrast-enhanced MRI. Other essential tests include lumbar puncture and blood cultures.
Septic transverse sinus thrombosis: management
Treatment consists of antibiotic therapy and surgery in most cases; some patients require management of elevated intracranial pressure:
*Urgent empiric antibiotic therapy is required. For most patients, we suggest a regimen that includes metronidazole plus either ceftriaxone or cefepime.
Meropenem is an acceptable alternative.
*In addition, we recommend surgical treatment unless the patient responds rapidly to antibiotic treatment within 12 to 24 hours
*We suggest against anticoagulation in most patients with transverse sinus thrombosis, unless a hypercoagulable state is documented.
However, in patients not responding to antibiotic and surgical treatment, it is reasonable to provide anticoagulation treatment along with monitoring for hemorrhagic complications of anticoagulation
** For patients with increased intracranial pressure, monitoring and interventions are guided by the clinical examination.
Septic superior sagittal sinus thrombosis: risk factors and causes of high mortality
Septic superior sinus thrombosis is a rare complication of bacterial meningitis, bacterial sinusitis, and facial surgery.
- hemorrhagic infarcts with cerebral edema
- hydrocephalus
- transtentorial brainstem herniation
Pathophysiology of papilledema in bacterial meningitis
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
Indications for CT scan prior to LP
A CT scan of the head before LP should be performed in adult patients with suspected bacterial meningitis who have one or more of the following risk factors:
-Immunocompromised state (eg, HIV infection, immunosuppressive therapy, solid organ or hematopoietic stem cell transplantation)
-History of CNS disease (mass lesion, stroke, or focal infection)
-New onset seizure (within one week of presentation)
-Papilledema
-Abnormal level of consciousness
-Focal neurologic deficit
Findings in CT scan in increased intracranial pressure caused by space-occupying mass (and contraindication for LP)
Features include:
* distortion of symmetry and midline structures
* compression of ventricles
* the presence of a visible mass lesion
(CT scan should also be checked for more subtle signs of mass effect or cerebral edema including loss of differentiation between gray and white matter, effacement of sulci or basal cisterns, and ventricular enlargement)
Causes of low CSF glucose
** (star) Etiologies reported to cause severe hypoglycorrhachia, generally defined as cerebrospinal fluid glucose level ≤10 mg/dL
