Post-stroke Infections – Diagnosis, Prediction, Prevention and Treatment
the lung as well as in blood. In experimental stroke, these changes in immunity precede the development of bacterial infection in the lung.30–33
Impaired early lymphocyte responses, in particular
reduced interferon gamma (IFN-γ) production by natural killer (NK) and T cells, appear to be an essential stroke-induced defect in the antibacterial defence as prevention of lymphocyte apoptosis by caspase inhibitors,34
adoptive transfer of IFN-γ-producing
lymphocytes (i.e. T and NK cells) or early treatment with recombinant IFN-γ inhibit pneumonia after experimental stroke.30,35 Stroke-induced immunodepression is long-lasting and facilitates the development of severe pneumonia after aspiration of an otherwise harmless small dose of Streptococcus pneumoniae even 14 days after experimental stroke.35
Recent evidence from clinical studies36–41 indicates that down-
regulation of systemic cellular immune responses, including rapid decrease in peripheral blood lymphocyte counts and functional deactivation of monocytes and T-helper type 1 cells, also occurs in stroke patients. Additionally, signs of immunodepression are more prominent in patients who develop infectious complications. Collectively, these clinical data corroborate experimental findings that changes in immune responsiveness after stroke occur before the onset of infectious complications and indicate that the extent of stroke-induced immunodepression correlates with the risk of infectious complication.
Recently, we and others described immune parameters significantly associated with infectious complications after stroke.36,38,42,43
For
example, patients with infection had significantly lower levels of the major histocompatibility class II (MHCII) molecule human leukocyte antigen-DR (HLA-DR) on monocytes at days one, three and eight than non-infected patients. Moreover, reduced monocytic HLA-DR expression at day one was a strong independent predictor of subsequent post-stroke infection.36,41
Thus, immunological or
infection parameters may be helpful predictors of post-stroke pneumonia. The current concept of post-stroke infections is shown in Figure 1.
Urinary Tract Infection
Several parameters are known to increase the risk of UTI after stroke including female sex, age, dependency before stroke, stroke severity (measured by NIHSS), poor cognitive function and catheterisation.22,44 Catheterisation is a well-described risk factor for healthcare- associated UTI. Their inappropriate use may be more common in stroke patients, thereby further increasing the risk of UTI. Usually, catheterisation is a consequence of urinary dysfunction and retention, occurring in 29–58% of stroke patients.45
Urine-storage
disorder due to bladder hyper-reflexia seems to be more common after stroke.46
Risk factors for bladder dysfunction include large infarcts and cortical involvement. In addition, aphasia, cognitive impairment and severe functional impairment are independently associated with bladder dysfunction.47
Only a few studies have focused on the use of Foley catheters in patients with acute stroke; therefore, frequency of use remains unclear. However, clinical characteristics of stroke patients may promote catheter placement. Disturbance of consciousness and dysphasia impaired the ability to communicate the need to urinate. In addition, the high incidence of bladder dysfunction will increase the probability of being catheterised. Immobilisation due
EUROPEAN NEUROLOGICAL REVIEW
However, screening for dysphagia is effective to prevent post- stroke pneumonia. Using a formal dysphagia screening protocol decreases the risk of pneumonia in patients hospitalised for ischaemic stroke by three-fold.50
In order to reduce the risk of
aspiration, dysphagia is usually managed by placement of a nasogastric tube. Percutaneous endoscopic gastrostomy (PEG) is applied to patients who remain unable to swallow in the long term. Although a nasogastric tube is easy to insert, it is uncomfortable and can be easily dislodged, leading to treatment failure and aspiration. PEG placement is an invasive procedure and can be complicated by peritonitis or bowel perforation.51
The Feed Or
Ordinary Diet (FOOD) trials demonstrated that early enteral tube feeding might reduce case fatality compared with no tube feeding for more than seven days after stroke onset. However, the overall increase in survival was associated with an increased proportion of survivors with poor outcome. Compared with nasogastric tube feeding, early PEG tube feeding might be associated with poorer outcome and should be avoided in stroke patients. Furthermore, there were no significant differences between groups in the frequency of pneumonia, suggesting that early tube feeding does not prevent or favour infection rates.52
41 Post-stroke infections
to motor dysfunction will complicate transfer to the toilet and even hamper the use of helpful devices, such as urinals or bedpans. In addition, the above-mentioned immunodepressive state induced by the acute CNS lesion may lead not only to chest infections but also to UTI.
Prevention of Post-stroke Infections Pneumonia
As dysphagia is the most important risk factor for post-stroke pneumonia, several approaches aim at minimising the risk of aspiration. One well-known drawback is the lack of reliable diagnostic screening methods to identify patients at high risk of aspiration. Clinical bedside assessments have been shown to miss up to 40% of those patients who aspirate (‘silent aspiration’).47–49 Videofluoroscopy (VFS) can be considered the gold standard in diagnosing dysphagia with aspirations (silent or not) because of its ability to study the entire process of swallowing.49
Nevertheless,
this examination requires patient co-operation and a sitting posture, so it cannot be proposed for all patients in the early period after stroke.
Clinical sequalae
• immobilisation • altered level of conciousness • dysphagia • catheterisation
Immunodepression
• lymphopenia • lymphocytic dysfunction • monocytic dysfunction • mediated by sympathetic nerve system
Stroke Figure 1: Current Concept of Post-stroke Infections
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64 |
Page 65 |
Page 66 |
Page 67 |
Page 68 |
Page 69 |
Page 70 |
Page 71 |
Page 72 |
Page 73 |
Page 74 |
Page 75 |
Page 76 |
Page 77 |
Page 78 |
Page 79 |
Page 80 |
Page 81 |
Page 82 |
Page 83 |
Page 84 |
Page 85 |
Page 86 |
Page 87 |
Page 88 |
Page 89 |
Page 90 |
Page 91 |
Page 92 |
Page 93 |
Page 94 |
Page 95 |
Page 96 |
Page 97 |
Page 98 |
Page 99 |
Page 100 |
Page 101 |
Page 102 |
Page 103 |
Page 104 |
Page 105 |
Page 106 |
Page 107 |
Page 108 |
Page 109 |
Page 110 |
Page 111 |
Page 112 |
Page 113 |
Page 114 |
Page 115 |
Page 116