By Joshua O. Benditt, et al. American College of Chest Physicians

ISBN-10: 0916609766

ISBN-13: 9780916609764

ISBN-10: 380559366X

ISBN-13: 9783805593663

Directly from the ACCP severe Care drugs Board evaluation 2009 direction, this article covers each subject in a concise, easy-to-use structure. Use as a self-study source to organize for the severe care drugs subspecialty board exam.

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23 Responsible for about 80% of overwhelming infections in asplenic patients, S pneumoniae should be given a particularly high index of suspicion because the clinical entity of post-splenectomy pneumococcal sepsis may initially present as only a flu-like illness with fever and myalgias. 24 Within the course of a few hours, untreated patients may develop a fulminant course that includes disseminated intravascular coagulation, purpura fulminans, symmetrical peripheral gangrene, shock, and ultimately 20 death.

7 mg/kg/d) plus flucytosine (100 mg/kg/d in patients who were tolerant of this agent), followed by therapy with fluconazole (400 mg/d orally for 8 weeks) is safe and effective and should be considered the treatment of choice. The authors noted that high intracranial pressures have been associated with catastrophic neurologic deterioration and death in the absence of hydrocephalus. Of the patients in this study, 13 of 14 early deaths and 40% of deaths during weeks 3 through 10 were associated with elevated intracranial pressure.

These lead to proteolytic cleavage of C3 to generate C3b, and this mechanism can lead to immediate opsonization. In addition to its opsonizing ability and its initiation of the membrane attack complex of complement, C3b can be joined by factors B and D to form a C3 convertase, which is highly labile. When bound by properdin, the C3 convertase is stabilized and can then cleave more C3 to generate more C3b, with a resultant amplification of the alternative complement pathway. 22 There are four clinically relevant situations within the category of defective humoral immunity: (1) disorders of immunoglobulin production; (2) asplenia or hyposplenic states; (3) hypocomplementemia; and (4) impaired neutralization of toxins.

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ACCP Critical Care Medicine Board Review, 20th Edition by Joshua O. Benditt, et al. American College of Chest Physicians

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