Bacterial, Fungal, & Parasitic Infections of the Nervous System 1

Question 1

Bacterial meningitis pathogenesis

Answer 1

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.

Question 2

Bacterial meningitis: special entry mechanisms of bacteria

Answer 2

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

Question 3

Bacterial meningitis risk factors

Answer 3

• 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.

Question 4

What is the cause of devastating sequences of meningitis

Answer 4

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

Question 5

Bacterial meningitis major complications

Answer 5

• 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

Question 6

Mechanism of stroke in meningitis

Answer 6

consequence of arteritis as large blood vessels cross through the exudate (εξίδρωμα) at the base of the brain

Question 7

Most common causes of bacterial meningitis in the US

Answer 7

1) S pneumoniae (58%)
2) group B streptococci (18%)
3) Neisseria meningitidis (13.9%)
4) H influenzae type B (6.7%)

Question 8

Common cause of meningitis in immunocompromised patients

Answer 8

Haemophilus influenzae type b
causes meningitis in immunocompromised patients (e.g., postsplenectomy and in chronic lung disease).

The most common though is cryptococcus

Question 9

Bacterial meningitis caused by Neisseria meningitides treatment

Answer 9

Question 10

Bacterial meningitis caused by Streptococcus pneumoniae treatment

Answer 10

Question 11

Bacterial meningitis caused by Haemofilus influenzae type B treatment

Answer 11

Question 12

Bacterial meningitis caused by listeria monocytogenes treatment

Answer 12

Question 13

Bacterial meningitis caused by staphylococcus aureus treatment

Answer 13

Question 14

Bacterial meningitis caused by staphylococcus epidermidis and MRSA treatment

Answer 14

Question 15

Bacterial meningitis caused by pseudomonas aeruginosa treatment

Answer 15

Question 16

Bacterial meningitis caused by group B streptococcus treatment

Answer 16

Question 17

Bacterial meningitis: empiric antibiotic treatment of age-associated pathogens

Answer 17

** 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.)

Question 18

When to administer dexamethasone in bacterial meningitis

Why

How to administer

Undesirable effect

Answer 18

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

Question 19

Should other than antimicrobial treatment be added in bacterial meningitis

Answer 19

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

Question 20

Duration of treatment in bacterial meningitis

Answer 20

Question 21

Bacterial meningitis prevention

Answer 21

• 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.

Question 22

Bacterial meningitis clinical findings

Answer 22

• 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

Question 23

Time course of bacterial meningitis (and difference from other causes)

Answer 23

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.

Question 24

Percentage of patients with classic findings of bacterial meningitis

Answer 24

the classic triad of fever, altered mental status, and nuchal rigidity is present in less than 50% of patients.

Question 25

Bacterial meningitis laboratory findings

Answer 25

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

Question 26

Bacterial meningitis imaging

Answer 26

• 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

Question 27

Major pathogen in bacterial meningitis caused by spread from sinusitis or mastoiditis

Answer 27

S pneumococcus or H influenzae
(more prolonged antibiotic course of treatment required)

Question 28

Potential imaging findings in recurrent meningitis

Answer 28

Thin cuts through the base of the skull may reveal a basilar skull fracture, sinus compromise, or other potential breach of the dura

Question 29

Bacterial meningitis differential diagnosis

Answer 29

• 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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Question 30

Indication to repeat lumbar puncture in bacterial meningitis

Answer 30

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.

Question 31

Trastentorial herniation management

Answer 31

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

Question 32

Electrolyte abnormalities in bacterial meningitis

Answer 32

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.

Question 33

Serious complication of meningococcal meningitis

Answer 33

Waterhouse - Friderichsen

thrombocytopenia
disseminated intravascular coagulation
shock

Question 34

Bacterial meningitis: all cause mortality

Answer 34

10-30% in high-income countries

50% in low-income countries

Question 35

Risk factors for brain abscess

Answer 35

• 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)

Question 36

Is cerebritis and encephalitis the same

Answer 36

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

Question 37

How are the symptoms in brain abscess caused

Answer 37

• seizures
• pressure on nearby structures
• arteritis causing stroke
• from rupture into a ventricle

Question 38

Brain abscess causal organisms

Answer 38

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.

Question 39

Brain abscess prevention

Answer 39

• 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)

Question 40

Brain abscess clinical findings

Answer 40

• 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.

Question 41

Brain abscess laboratory findings

Answer 41

• 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)

Question 42

Brain abscess imaging findings

Answer 42

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

Question 43

Imaging difference between abscess and metastasis or high-grade glioma

Answer 43

• 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

Question 44

Brain abscess differential diagnosis

Answer 44

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

Question 45

Brain abscess treatment

Answer 45

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

Question 46

Brain abscess antibiotics duration comparing to meningitis

Answer 46

brain abscesses require a longer duration of therapy (at least four to eight weeks)

Question 47

Antibiotic treatment in brain abscess according to infection source

Answer 47

Question 48

Brain abscess prognosis

Answer 48

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.

Question 49

Subdural empyema risk factors

Answer 49

complication of:
* frontal or ethmoid sinusitis
* otitis media
* mastoiditis
* meningitis
* osteomyelitis

It can also follow venous sinus thrombosis, skull fracture, penetrating trauma, or craniotomy.

Question 50

Subdural empyema clinical findings

Answer 50

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.

Question 51

Subdural empyema imaging

Answer 51

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.

Question 52

Syndromes associated with skull base infection

Answer 52

Question 53

Antibiotic treatment of epidural abscess

Answer 53

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)

Question 54

Spinal epidural abscess: pathogenesis, risk factors and most common pathogen

Answer 54

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.

Question 55

Spinal epidural abscess: clinical findings

Answer 55

The classic diagnostic triad for SEA consists of:
* fever
* back pain
* neurologic deficits

Question 56

Spinal epidural abscess: when to suspect

Answer 56

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)

Question 57

Spinal epidural abscess: management

Answer 57

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

Question 58

Most frequent dural sinus to become infected and thrombosed

Answer 58

Cavernous sinus

Question 59

Septic cavernous sinus thrombosis: risk factors and most common pathogen

Answer 59

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.

Question 60

Septic cavernous sinus thrombosis: clinical findings and diagnosis

Answer 60

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

Question 61

Septic cavernous sinus thrombosis: management

Answer 61

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

Question 62

Septic cavernous sinus thrombosis: differential diagnosis

Answer 62

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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Question 63

Should anticoagulation be given in septic cavernous sinus thrombosis

Answer 63

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.

Question 64

Septic transverse sinus thrombosis: risk factors and most common pathogen

Answer 64

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

Question 65

Septic transverse sinus thrombosis: symptoms and diagnosis

Answer 65

● 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.

Question 66

Septic transverse sinus thrombosis: management

Answer 66

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.

Question 67

Septic superior sagittal sinus thrombosis: risk factors and causes of high mortality

Answer 67

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

Question 68

Pathophysiology of papilledema in bacterial meningitis

Answer 68

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

Question 69

Indications for CT scan prior to LP

Answer 69

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

Question 70

Findings in CT scan in increased intracranial pressure caused by space-occupying mass (and contraindication for LP)

Answer 70

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)

Question 71

Causes of low CSF glucose

Answer 71

** (star) Etiologies reported to cause severe hypoglycorrhachia, generally defined as cerebrospinal fluid glucose level ≤10 mg/dL