Clinical Consequences of Infection in Patients With Acute Stroke

Abstract

Background and Purpose-It is unsettled whether stroke-associated infection (SAI) is an independent prognostic factor, and a recent clinical trial failed to show that antibiotic prophylaxis prevented SAI. Contrarily, this trial suggested that antibiotic prophylaxis impaired clinical recovery. We sought to evaluate the predisposing factors and clinical consequences of SAI to gather additional insight on the need of exploring other antibiotics in acute stroke. Methods-Between March 2001 and April 2002, 229 consecutive patients were admitted into the neurological wards within 24 hours of stroke onset. Demographics, risk factors, National Institutes of Health Stroke Scale (NIHSS) score, vital data, imaging, and laboratory findings were prospectively evaluated. SAI was treated as early as possible. Multivariate regression analyses assessed predisposing factors of SAI and the independent association between SAI and poor stroke outcome at day 7 (Rankin Ͼ2). Results-Sixty (26%) patients developed SAI, most frequently chest infections, and within 3 days of stroke onset. Tube feeding (odds ratio [OR], 3.2; 95% CI, 1.3, 7.8) was the strongest predisposing factor of SAI. Poor outcome at hospital discharge was associated to baseline NIHSS score (OR, 10.0; 95% CI, 1.5, 100) and tube feeding (OR, 16.6; 95% CI, 2.9, 100.0), adjusted for confounders including antibiotic use. SAI was not independently associated to poor outcome (OR, 0.9; 95% CI, 0.9, 1.0). Conclusions-SAI is a marker of the severity of stroke without an independent outcome effect when it is promptly treated.These results support current stroke guidelines that advise prompt treatment of infection and warn against antibiotic prophylaxis. Yet, these recommendations should not prevent the performance of acute stroke trials assessing the value of antibiotics with acknowledged neuroprotective properties. (Stroke. 2006;37:461-465.)

Antigen Presentation After Stroke

“…However, studies aimed at analyzing the prognostic consequences of SAI have often failed to find an independent deleterious effect of infections, suggesting that several confounders could sway [126]. The determinants of SAI are multifactorial and include the severity of neurological deficits, dysphagia that favors bronchoaspiration, and a number of systemic immune changes dubbed as stroke-induced immunodepression syndrome [5].…”

“…For instance, high mobility group box-1 release from the ischemic brain induced the proliferation of bone marrow-derived suppressor cells, inhibiting the adaptive immune responses and resulting in lymphopenia and functional exhaustion of monocytes [74]. In patients with stroke, the best established features of SAI are increased levels of stress hormones and antiinflammatory cytokines like IL-10 [124][125][126][127][128][129][130][131], decreased numbers of circulating lymphocytes [129,131,132], and monocyte deactivation with reduced expression of human leukocyte antigen-antigen D related and reduced capacity to produce inflammatory cytokines [129,131].…”

Prophylactic Antibiotic Therapy for Preventing Poststroke Infection

“…Studies regarding the effects of infection on worsening stroke symptoms have yielded ambiguous results [14]. While several studies could not demonstrate an independent association between infection and worsening of neurological deficit after stroke [15][16][17], the majority of studies showed that infections in hospitalized patients in the acute phase after stroke are associated with a worse functional outcome and increased mortality [6,[18][19][20]. In the largest study, Katzan et al [21] described a 30-day mortality of 27 % after poststroke pneumonia compared with a mortality rate of 4 % in patients without pneumonia.…”

Systemic Infections After Acute Stroke

“…In general, PSIs are found to occur in 25-65% of patients admitted to hospital with acute stroke [15,[17][18][19][20][21][22][23]. In these studies, pneumonia occurs in 4-22% of all stroke patients, and UTIs occur in 3-44% [15,[17][18][19]21,[24][25][26][27][28].…”

“…Many studies have demonstrated that PSI may lead to poor functional outcome [24,29,[48][49][50][51], but this finding is not universal across all studies, and the relationship between PSI and functional outcome remains unclear [20,66]. Owing to the complexity of the pathophysiological process of acute stroke, and the variation in the process of acutestroke care, it is possible that previous studies of functional outcome have not completely adjusted for case-mix and other crucial factors that could have potentially affected the outcome.…”