Chapter 26 ICU Infections

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SECTION II • Medical and Surgical Crises

Complications Four important complications of acute bacte- rial meningitis are (1) cerebral edema, (2) inap- propriate antidiuretic hormone (ADH) syndrome, (3) obstructive hydrocephalus, and (4) seizures. Because one in three adults with meningitis experi- ences seizures, prophylactic anticonvulsant therapy is a rational adjunct. Signs of increased intracranial pressure (e.g., lethargy, papilledema, cranial nerve palsies, hemiparesis) should prompt emergent eval- uation for cerebral edema or hydrocephalus by CT scanning. Unexplained hyponatremia (usually in conjunction with concentrated urine) should raise concern for syndrome of inappropriate antidiuretic hormone secretion (SIADH). Although rare, high- volume urine output with a rising serum sodium level should prompt consideration of diabetes insip- idus caused by pituitary injury. Craniotomy patients are at particular risk of meningitis caused by Staphylococcus and Gram- negative rods in the early postoperative period. Conversely, the Pneumococcus is responsible for more than 90% of late meningeal infections in patients with persistent posttraumatic CSF leakage. Septic cerebral embolism (e.g., from subacute bac- terial endocarditis) and parameningeal infections (epidural abscess, brain abscess, sinusitis, and otitis media) are often confused with meningitis because they produce similar symptomatology and CSF pleocytosis. Paraspinal tenderness accompanied by radicular pain or weakness should be a clue to epi- dural abscess. S. aureus is the causative organism in more than one half of such cases. Brain abscess most often is a polymicrobial infection caused by Staphylococcus, Streptococcus, and anaerobes. Abscess may develop by exten- sion from the sinuses or ears or by hematogenous seeding (infected dialysis shunts, heart valves) or long-standing purulent lung disease (abscess, bron- chiectasis). Brain abscess rarely is confused with uncomplicated bacterial meningitis because it usu- ally presents with a less toxic picture and with focal neurologic signs. Unless otherwise guided by the dictates of culture and sensitivity results, penicil- lin together with chloramphenicol or metronidazole should comprise the treatment. In selected cases, a third-generation cephalosporin or antistaphylococcal agent may be indicated. Surgical intervention gener- ally is reserved for lesions that compress vital struc- tures, those unresponsive to medical management,

be obtained or is nondiagnostic, a third-generation cephalosporin and vancomycin with or without ampicillin (if Listeria is considered) is the safest alternative. Because the spectrum of causative organisms in the hospitalized patient is so broad, initial therapy for nosocomial infections should include both vancomycin and a third-generation cephalosporin or meropenem. Acid-fast smears and cultures are negative in most patients with tuber- culous meningitis. Therefore, empiric antituber- culous therapy should be considered for patients with subacute and chronic meningitis syndromes, especially if the CSF glucose concentration is low. Although still somewhat controversial, pread- ministration or coadministration of dexamethasone with antibiotics may decrease the risk of long-term neurological deficits in patients with meningitis. This effect has been shown most convincingly for pneumococcal disease. If dexamethasone is given, typical doses are 10 mg IV every 6 hours for 2 to 4 days. Benefits of corticosteroid therapy are unproven if begun hours or days after initiating anti- microbial therapy. Patients with acquired immunodeficiency syn- drome (AIDS) certainly can acquire any form of bacterial meningitis, but a diagnosis of Cryptococcus neoformans, a common cause of meningitis in AIDS, must be pursued. The CSF inflammatory response in patients with untreated AIDS is often minimal; therefore, absence of an impressive pleocytosis should not dissuade one from the diagnosis of men- ingitis, especially if the glucose is low. Although an India ink examination of CSF reveals organisms in only 50% of cases, the CSF cryptococcal antigen is positive in almost 90%. Combining these two tests promptly identifies the disease in most patients. The remainder are diagnosed when cultures return positive. Because cryptococcal infection is so fre- quently a cause of meningitis in patients with AIDS, empiric amphotericin B probably is indi- cated unless CSF examination clearly indicates a bacterial cause. Tuberculous meningitis should also be considered when the patient infected with HIV presents with a syndrome of meningitis but has minimal CSF abnormalities. The higher frequency of brain abscess, toxoplasmosis, and central ner- vous system lymphoma in HIV-infected individuals necessitates a low threshold for head CT or MRI scanning, especially if focal defects are apparent on examination.