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  1. Listeria monocytogenes meningitis
    gram-positive bacillus that can cause invasive disease in immunocompromised states, including alcoholism, extremes of age (neonates and those >50 years of age), malignancy, immunosuppression, diabetes mellitus, pregnancy, hepatic failure, chronic kidney disease, iron overload, collagen vascular disorders, use of antitumor necrosis factor-α agents, and HIV infection. The gastrointestinal tract is the usual portal of entry with symptoms typically developing after consumption of contaminated cole slaw, raw vegetables, milk, cheese, processed meats, smoked seafood, and hot dogs, potentially resulting in a febrile gastroenteritis syndrome including diarrhea. The organism can continue to multiply at refrigerator-level temperatures.
  2. Neisseria meningitidis meningitis
    • primarily in children and young adults. This illness is characterized by abrupt onset of flu-like illness including fever, headache, neck stiffness, altered mental status, intense myalgias, and rash. The rash is often petechial, purpuric, or maculopapular. The evolution of this infection can be rapid and fulminant, potentially resulting in septic shock and death. Invasive infections can be established by the growth of these gram-negative diplococci from CSF and blood cultures. Biopsy and culture of skin lesions may also reveal the organism.
    •  This infection most commonly occurs in children and young adults. The Centers for Disease Control and Prevention (CDC) recommends routine immunization with the meningococcal vaccine, which protects against serogroups A, C, Y, and W-135, but not serogroup B, the causative agent in as many as one third of U.S. cases and the recent cause of other cases of meningitis on campus.
    • Early in its course, meningococcal disease may be indistinguishable from other common viral illnesses; however, the rapidity with which the disease worsens (often over hours) and progresses to septic shock differentiates it from these other illnesses. A petechial rash is most common and may coalesce to form purpuric lesions. The diagnosis is established on the basis of clinical presentation and confirmed with blood and cerebrospinal fluid (CSF) cultures.
  3. Streptococcus pneumoniae meningitis
    most common cause of bacterial meningitis in adults. The clinical presentation of pneumococcal meningitis is not specific, but CSF and possibly blood cultures will reveal growth of gram-positive diplococci.
  4. viral meningitis
    CSF findings typically reveal a lymphocytic pleocytosis, a glucose level greater than 45 mg/dL (2.5 mmol/L), protein level less than 200 mg/dL (2000 mg/L), and a negative Gram stain. In the evaluation of patients with acute bacterial or viral meningitis, a CSF protein concentration greater than 220 mg/dL (2200 mg/L), CSF glucose less than 34 mg/dL (1.9 mmol/L), CSF blood-glucose ratio less than 0.2, CSF leukocytes greater than 2000/µL (2000 × 106/L), or CSF neutrophils greater than 1180/µL (1180 × 106/L) are individual predictors of bacterial etiology with a 99% or greater certainty.
  5. Undifferentiated meningitis management - dexamethasone, vanco, ampicillin, ceftriaxone
    • The most likely etiologic agents are Streptococcus pneumoniae,Listeria monocytogenes, Neisseria meningitidis, and aerobic gram-negative bacilli. Pending culture results and results of in vitro susceptibility testing, empiric treatment with antimicrobial therapy consisting of vancomycin, ampicillin, and ceftriaxone for infection caused by penicillin-resistant pneumococci and L. monocytogenes is necessary. Administration of adjunctive dexamethasone should be strongly considered in patients with acute bacterial meningitis because clinical trials have established the benefit of adjunctive dexamethasone on adverse outcomes and death in adults with suspected or proven S. pneumoniae meningitis.
    • Most infectious disease experts would recommend vancomycin plus ceftriaxone for the treatment of penicillin-resistant S. pneumoniae; however, this combination would not adequately treat meningitis caused by L. monocytogenes, which requires the addition of ampicillin. Trimethoprim-sulfamethoxazole does treat Listeria meningitis, but the combination of vancomycin plus trimethoprim-sulfamethoxazole would be potentially inadequate treatment for S. pneumoniae meningitis.
  6. Acute ischemic stroke management
    • This patient should receive intravenous recombinant tissue plasminogen activator (rtPA). He has clinical symptoms and signs and radiologic evidence of an acute left hemispheric stroke. The probable mechanism of stroke is ischemic infarction, given the results of the head CT scan. He was brought to the emergency department within 1 hour of the witnessed onset of stroke symptoms, and his evaluation is completed 1 hour later. He does not appear to have any clinical, radiologic, or laboratory contraindication to receiving the preferred treatment of intravenous rtPA, and he can receive it within the recommended window of 3 hours from stroke onset.Aspirin is indicated for acute ischemic stroke in patients who are not eligible for rtPA. For patients with acute stroke who are eligible for thrombolysis, aspirin should be withheld in the emergency department and for 24 hours after rtPA administration.
    • Elevated blood pressure is common at the time of initial stroke presentation, even among patients without chronic hypertension. Rapid lowering of blood pressure may further impair cerebral blood flow and worsen the ischemic injury. Elevated blood pressure often will resolve spontaneously or improve gradually during the first few days after a stroke. The threshold for acute blood pressure lowering in patients with acute stroke who are eligible for thrombolysis is 185/110 mm Hg. In such a setting, preferred agents include intravenous infusions of labetalol or nicardipine. Because this patient's blood pressure is already below that threshold, there is no indication for intravenous use of labetalol at this time.
    • For uncomplicated ischemic strokes in patients without concurrent acute coronary artery disease or heart failure, consensus exists that antihypertensive medications, such as intravenous labetalol or nicardipine, should be withheld if the systolic blood pressure is less than 220 mm Hg or the diastolic blood pressure is less than 120 mm Hg, unless there are other manifestations of end-organ damage.
  7. Thunderclap headache with normal CT
    • A thunderclap headache is a severe and explosive headache that is maximal in intensity at or within 60 seconds of onset. CT scanning is the first test to be conducted in a patient with thunderclap headache in whom a subarachnoid hemorrhage is suspected; a ruptured intracranial aneurysm is the most serious cause of such headaches. The ability to detect subarachnoid hemorrhage is dependent on the amount of subarachnoid blood, the interval after symptom onset, the resolution of the scanner, and the skills of the radiologist. On the day of the hemorrhage, extravasated blood will be present in more than 95% of patients, but in the following days, this proportion falls sharply. If an initial CT scan of the head reveals nothing, a lumbar puncture should be performed next in patients with this presentation. The finding of xanthochromia or gross hemorrhage is diagnostic for subarachnoid hemorrhage. Subsequent angiography (CT or MRI) can confirm the presence of a ruptured aneurysm in patients with a positive lumbar puncture.
    • In patients with an initial subarachnoid hemorrhage, there is substantial risk of rebleeding (2% per day for the first month). Rebleeding is associated with high mortality. The treatment of subarachnoid hemorrhage involves localizing the aneurysm with cerebral angiography and securing it to prevent subsequent bleeding. Traditionally, surgical clipping within 72 hours of onset has been recommended. Aneurysms also may be treated endovascularly by filling them with metallic coils and promoting localized thrombosis within the aneurysm to obliterate it from the cerebral circulation. Hospital observation as the sole management option for this patient places her at increased risk for rebleeding and death.
  8. Bell's palsy
    • Research strongly suggests it may be the result of herpes simplex virus infection of the facial nerve. Bell palsy is not considered contagious. The seventh cranial nerve innervates all muscles of facial expression (the mimetic muscles). Any cause of a complete facial neuropathy will therefore impair the entire hemiface, including the forehead corrugators typically spared by cerebral lesions. Bell phenomenon describes the reflexive rolling upwards of the globe during eye closure. When a normal patient is asked to close the eyes, forced eyelid opening will reveal this phenomenon, as will the selective paralysis of the orbicularis oculi due to a facial neuropathy. Facial neuropathies will otherwise spare the extraocular muscles that govern globe movement. Because Bell palsy is a diagnosis of exclusion, clinicians need to make every effort to exclude other identifiable causes of facial paralysis, such as Lyme disease, HIV disease, acute and chronic otitis media, cholesteatoma, and multiple sclerosis. Other common causes of acute peripheral facial paralysis will often have findings on history or physical examination that suggest the correct diagnosis.
    • Cerebral infarction, brain hemorrhage, or any structural brain lesion can cause weakness of the lower face but not of the forehead because the bilateral cortical representation of the midline forehead spares the forehead corrugators. Some limb or sensory abnormality is also often, but not universally, observed in the setting of cerebral infarction; no such abnormality was observed in this patient. Therefore, despite her cerebrovascular risk factors of oral contraception and cigarette smoking, this patient is unlikely to have had a cerebral infarction.
  9. GBS
    Patients with Guillain-Barré syndrome typically develop paresthesias distally in the lower extremities that are followed by limb weakness and gait unsteadiness. In addition to sensory loss and limb weakness, deep tendon reflexes are characteristically absent or markedly reduced. The diagnosis is confirmed by electromyography, which usually shows a demyelinating polyradiculoneuropathy. Cerebrospinal fluid (CSF) analysis characteristically shows albuminocytologic dissociation, whereby the spinal fluid cell count is normal but the spinal fluid protein level is elevated. CSF analysis may also yield normal results early in the course of the disease. However, a normal CSF cell count is useful in excluding other infectious conditions, such as polyradiculoneuropathies associated with HIV and cytomegalovirus infection, infection due to West Nile virus, and carcinomatous or lymphomatous nerve root infiltration. By definition, symptoms in patients with Guillain-Barré syndrome peak within 4 weeks of onset. Intravenous immune globulin and plasma exchange are equally efficacious in the treatment of Guillain-Barré syndrome.
  10. Diabetic Neuropathy
    Diabetic neuropathy involves injury to sensory, motor, and autonomic nerves. Loss of sensation in a “stocking-glove” distribution that is associated with paresthesias or painful dysesthesias is the most common presentation of this condition. Loss of sensation in the lower extremities is typical and plays a major part in the development of foot ulcerations, which can lead to limb loss. No direct treatment for diabetic neuropathy exists, other than to improve glycemic control. Pharmacologic therapy, however, may help symptoms. Partial serotonin and norepinephrine reuptake inhibitors (duloxetine), tricyclic antidepressants (amitriptyline), and various antiseizure medications (gabapentin, phenytoin, carbamazepine) are frequently used to treat the pain associated with this condition.
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