Cns Infections Flashcards

1
Q

Bacterial meningitis is

A

acute purulent infection within the subarachnoid space (SAS). It results in decreased consciousness, seizures, raised intracranial pressure (ICP), and stroke

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2
Q

The organisms most often responsible for community- acquired bacterial meningitis are

A

Streptococcus pneumoniae (~50%), Neisseria meningitidis (~25%), group B streptococci (~15%), and Listeria monocytogenes (~10%).

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3
Q

There are a number of predisposing conditions that increase the risk of pneumococcal meningitis

A

most important of which is pneumococcal pneumonia. Additional risk factors include coexisting acute or chronic pneumococcal sinusitis or otitis media, alcoholism diabetes splenectomy hypogammaglobulinemia, complement deficiency head trauma with basilar skull fracture and CSF rhinorrhea.

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4
Q

The presence of petechial or purpuric skin lesions can provide an important clue to the diagnosis

A

meningococcal infection.

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5
Q

Gram-negative bacilli cause meningitis in individuals with

A

chronic and debilitating diseases such as diabetes, cirrhosis, or alcoholism and in those with chronic urinary tract infections. Gram- negative meningitis can also complicate neurosurgical procedures, particularly craniotomy, and head trauma associated with CSF rhinorrhea or otorrhea.

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6
Q

Meningitis complicating endocarditis may be due to

A

viridans streptococci, S. aureus, Streptococcus bovis, the HACEK group Group B Streptococcus, or

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7
Q

Streptococcus agalactiae, was previously responsible for meningitis predominantly in

A

neonates

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8
Q

L. monocytogenes is an increasingly important cause of meningitis in

A

neonates (<1 month of age) pregnant women individuals >50years immunocompromised Alcoholism

ingesting foods contaminated by Listeria.

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9
Q

…….. are important causes of meningitis that occurs following invasive neurosurgical procedures, particularly shunting procedures for hydrocephalus, or as a complication of the use of intrathecal chemotherapy.

A

S. aureus and coagulase- negative staphylococci are

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10
Q

PATHOPHYSIOLOGY

A

initially colonize the nasopharynx by attaching to nasopharyngeal epithelial cells. Bacteria are transported across epithelial cells in membrane- bound vacuoles to the intravascular space . Bloodborne bacteria can reach the intraventricular choroid plexus, directly infect choroid plexus epithelial cells, and gain access to the cerebrospinal fluid (CSF). Much of the pathophysiology of bacterial meningitis is a direct con- sequence of elevated levels of CSF cytokines and chemokines.
The combination of interstitial, vasogenic, and cytotoxic edema leads to raised ICP and coma. Cerebral herniation usually results from the effects of cerebral edema, either focal or generalized; hydrocephalus and dural sinus or cortical

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11
Q

CLINICAL PRESENTATION

A

Meningitis can present as either an acute fulminant illness over hours subacute infection over days. With triad of symptoms + positive Kermit’s and brdzenesky

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12
Q

The classic triad of meningitis is

A

fever, headache, and nuchal rigidity, but the classic triad may not be present.

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13
Q

A decreased level of consciousness occurs in

A

75%.

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14
Q

Focal seizures in mengigitis patients are usually due

A

focal ischemia, cortical venous thrombosis with hemorrhage, focal edema or associated meningoencephalitis

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15
Q

In meningitis patients Generalized seizure activity and status epilepticus may be due to

A

hyponatremia, cerebral anoxia, or, less commonly, the toxic effects of antimicrobial agents.

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16
Q

Signs of increased ICP include

A

deteriorating or reduced level of consciousness, papilledema, dilated poorly reactive pupils, sixth nerve palsies, decerebrate posturing, and the Cushing reflex (bradycardia, hypertension, and irregular respirations)

17
Q

the need to obtain neuroimaging studies (CT or MRI) prior to lumbar puncture (LP) requires clinical judgment.

A

immunocompetent patient with no known history of recent head trauma, a normal level of consciousness, and no evidence of papilledema or focal neurologic deficits,

18
Q

The classic CSF abnormalities in bacterial meningitis are

A

(1) (PMN) leukocytosis (>100 cells/μL in 90%), (2) decreased glucose concentration (<40 mg/ dL] and/ or CSF/serum glucose ratio of <0.4 in ~60%), (3) increased protein concentration [>45 mg/dL] (4) increased opening pressure (>180 mmH2O in 90%). (5) positive gram statin and culture

19
Q

A CSF/serum glucose ratio <0.4 is highly suggestive of bacterial meningitis but may also be seen in other conditions, including

A

fungal, tuberculous, and carcinomatous meningitis.

20
Q

MRI is preferred over CT because of its superiority in

A

demonstrating areas of cerebral edema and ischemia. diffuse meningeal enhancement is often seen after the administration of gadolinium.

21
Q

DIFFERENTIAL DIAGNOSIS

A

1- HSV encephalitis typically presents with headache, fever, altered consciousness, focal neurologic deficits (e.g., dysphasia, hemiparesis), and focal or generalized seizures. The typical CSF profile with viral CNS infections is a lymphocytic pleocytosis with a normal glucose concentration, in contrast to the PMN pleocytosis and hypoglycorrhachia characteristic of bacterial meningitis. MRI abnormalities (other than meningeal enhancement) are not seen in uncomplicated bacterial meningitis. By contrast, in HSV encephalitis, high signal intensity lesions are seen in the orbitofrontal, anterior, and medial temporal lobes in the majority of patients within 48 h of symptom onset. Some patients with HSV encephalitis htave a distinctive periodic pattern on EEG. 2- Focal subdural and epidural empyema and brain abscess 3- vascular Subarachnoid hemorrhage is generally the major consideration. pituitary apoplexy Cerbral venous thrombosis 4- meningitis associated with inflammatory disorders such as sarcoid, systemic lupus erythematosus (SLE), CNS vasculitis and Behçetʼs syndrome 5- acute dessaminated encephalomyelitis (ADEM) 6- fulminate TB meningitis 6- chemical meningitis

22
Q

Complications of meningococcal sepsis are

A

Meningitis
Rash morbilliform , petichial of purpurin
Shock
Intravascular coagulation
Renal failure
Peripheral gangrene
Arthritis
Pericarditis

23
Q

Bacterial causes of meningitis in diff ages

A

In neonate E. coli and group B street
In preschool age the most hemophylus the lower streptococcus while in the older and adult the vice verse and in both between them the Nigeria and tb

24
Q

The goal is to begin antibiotic therapy within

A

within 60 min of a patientʼs arrival in the emergency room.

25
empirical therapy shoulds include a combination of
dexamethasone, a third or fourth- generation cephalosporin (e.g., ceftriaxone, cefotaxime, or cefepime), and vancomycin, plus acyclovir Ampicillin should be added to the empirical regimen for coverage of L. monocytogenes in individuals <3 months of age those >55 year impaired cell-mediated immunity because of chronic illness organ transplantation pregnancy malignancy immunosuppressive therap Metronidazole is added to the empirical regimen to cover gram- negative anaerobes in patients with otitis, sinusitis, or mastoiditis.
26
In hospital-acquired meningitis, and particularly meningitis following neurosurgical procedures, staphylococci and gram-negative organisms including P. aeruginosa are the most common etiologic organisms. In these patients, empirical therapy should include a combination
vancomycin and ceftazidime or meropenem.
27
ADJUNCTIVE THERAPY
Dexamethasone exerts its beneficial effect by decreasing CSF outflow resistance, and stabilizing the blood-brain barrier. The ratio- nale for giving dexamethasone 20 min before antibiotic therapy .
28
INCREASED INTRACRANIAL PRESSURE
Emergency treatment of increased ICP includes Addmision to ICU elevation of the head to 30– 45° intubation and hyperventilation (Paco2 25– 30 mmHg) And mannitol with ice monitoring device
29
PROGNOSIS
Mortality rate is 3–7% for meningitis caused by H. influenzae, N. men- ingitidis, or group B streptococci; 15% for that due to L. monocytogenes; and 20% for S. pneumoniae.
30
20% for S. pneumoniae. In general, the risk of death( poor prognostic factors) from bacterial meningitis increases with
(1) decreased level of consciousness on admission (2) onset of seizures within 24 h of admission, (3) signs of increased ICP (4) young age (infancy) and age >50 (5) the presence of comorbid conditions including shock and/or the need for mechanical ventilation (6) delay in the initiation of treatment.