Brain Trauma Stroke
Table 3: Clinical Risk Factors for Post-stroke Pneumonia >65 years of age
Stroke severity Dysphagia
Dysarthria/dysphasia Dementia
Sources: Walter et al., 2007,23
Non-lacunar basal ganglia infarction Other infection at stroke onset Mechanical ventilation Male gender Infarct volume
Kwon et al., 2006,25 Sellars et al., 200726 and Minnerup, 2010.69 asymptomatic bacteriuria.59,60 Thus, the general use of antiseptic- coated or condom catheters can not be recommended.
Antimicrobial prophylaxis may reduce the risk of stroke-associated UTI. However, the current urological guidelines strongly discourage prophylactic antibacterial treatment due to the lack of convincing evidence that it prevents bacteriuria and the risk of adverse events and antimicrobial resistance.61
Table 4: Anti-infective Treatment of Post-stroke Pneumonia
Drug Daily Dosage
Without Risk Factors for Higher-level Resistant Bacteria Ampicillin/sulbactam Cefuroxime Ceftriaxone Levofloxacin Moxifloxacin
3x3g
3x1.5g 1x2g
2x500mg 1x400mg
With Risk Factors for Higher-level Resistant Bacteria Ceftazidime
3x2g Combined with gentamicine 5–7mg/kg bodyweight
Treatment of Post-stroke Infections Current guidelines for stroke treatment recommend early diagnosis and antibacterial treatment in cases of suspected infection.62,63 Basically, anti-infective treatment of post-stroke infection follows current treatment guidelines of hospital-acquired (bacterial) pneumonia (HAP) or UTI, respectively. After initiating empirical antibacterial treatment, the isolation of pathogens from relevant species should be the main diagnostic focus. Thereafter, treatment should be adapted to results of resistance testing.
Pneumonia
Post-stroke pneumonia usually occurs within the first three to five days after hospitalisation36,54,55
and thus can be considered as early-
Table 5: Treatment of Symptomatic Urinary Tract Infection
Drug
Trimethoprim/sulfamethoxazole Ampicillin/sublactam Ceftriaxone Ciprofloxacin Levofloxacin
Dosage
2x800/160mg 3x3g 1x2g
2x500mg 2x500mg
Another practical approach to prevent post-stroke pneumonia is anti-infective prophylaxis. In a rodent stroke model, moxifloxacin given immediately or 12 hours after middle cerebral artery occlusion prevented infection and fever, significantly reduced mortality and improved neurological outcome.53
Over the last few years, three
Differences in inclusion criteria, infection criteria, type of intervention and outcome measures may have led to conflicting results. Although a meta-analysis demonstrated that antibacterial prophylaxis reduced the occurrence of post-stroke infection from 38 to 24% (odds ratio [OR] 0.44, 95% confidence interval [CI] 0.23–0.86),56
heterogeneous randomised clinical trials have tested the efficacy of antibiotic prophylaxis in acute stroke to prevent post-stroke infection.36,54,55
the beneficial effect on stroke outcome remains an open matter and has to be evaluated in future trials.
Urinary Tract Infection
As the use of Foley catheters increases the risk of UTI after stroke, the limited use of catheterisation may prevent UTI after stroke. Educational interventions can influence the inappropriate use of Foley catheters57,58 of UTI.58
Importantly, empirical antibacterial treatment should follow local information about antimicrobial resistance. It is strongly recommended to stratify the risk of higher-level resistant bacteria using the following risk factors: inhabitant of healthcare facilities, medical co-morbidity (chronic heart disease, cirrhosis, renal insufficiency) and preceding anti-infective treatment.
Patients with low risk of higher-level resistant bacteria should be treated with antibacterial monotherapy. Aminopenicillin/β-lactamase inhibitors (BI) (e.g. amoxicilline/sulbactam), cephalosporins group II/III (e.g. cefuroxime/ceftriaxone) or fluorochinolones (e.g. moxifloxacin/ levofloxacin) are recommended in these cases.
High-risk patients should be treated with a combination of cephalosporines group IIIb (e.g. ceftazidime) and aminoglycosides (e.g. gentamicine). Three to five days after clinical improvement, the antibacterial treatment should be terminated. In total, the treatment period should not exceed 10 to 14 days (see Table 4).
and thus dramatically reduce the frequency
Antiseptic-coated catheters have also been studied in the prevention of UTI. Only small clinical trials have shown that silver- oxide-coated catheters may reduce asymptomatic bacteriuria. However, these trials did not evaluate the efficacy of silver-oxide- coated catheters in symptomatic UTI.59
Antibiotic-impregnated catheters or condom catheters may reduce the frequency of 42 Urinary Tract Infection
The most common pathogen in UTI remains Escherichia coli (55–80%). In about 5–10% of cases, other Enterobacteriaceae, such as Proteus mirabilis and Klebsiella spp., can be isolated. Occasionally, Staphylococcus saprophyticus are isolated.66–68
Knowledge of the
antimicrobial susceptibility profile of uropathogens causing uncomplicated UTI in the community should guide therapeutic
EUROPEAN NEUROLOGICAL REVIEW
onset HAP. Early-onset HAP is primarily attributed to Gram-negative bacteria, such as Haemophilus influenzae, and Gram-positive bacteria such as methicillin (meticillin)-sensitive Staphylococcus aureus (MSSA) and S. pneumoniae. Late-onset nosocomial pneumonia is usually attributed to higher-level antibiotic-resistant Gram-negative bacteria (e.g. Pseudomonas aeruginosa, Acinetobacter spp.) and Gram-positive bacteria (e.g. methicillin-resistant S. aureus [MRSA]). This classification leads to different strategies for empirical antimicrobial treatment: monotherapy with narrow-spectrum antibiotics for the treatment of early-onset pneumonia but broad- spectrum therapy for Pseudomonas spp. or MRSA with late-onset infection. However, this dichotomised concept is currently under discussion.64,65
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