Effect of Chest Physiotherapy On The Prevention of Ventilator-Associated Pneumonia and Mortality

World Journal of Pharmaceutical Research
Yadu et al. World Journal of Pharmaceutical Research

SJIF Impact Factor 8.084
Volume 12, Issue 9, 1585-1599. Research Article ISSN 2277– 7105
EFFECT OF CHEST PHYSIOTHERAPY ON THE PREVENTION OF

VENTILATOR-ASSOCIATED PNEUMONIA AND MORTALITY
Dr. Arti Yadu M.D.*, Dr. Pankaj Kumar Omar M.D, Dr. Pitamber Patel and
Dr. Sushmita Ghosh
Associate Professor DKS Hospital, Raipur.
ABSTRACT
Article Received on
24 March 2023, Background: Even after a lot of progress that has been achieved in the
Revised on 14 April 2023, recent years in the diagnosis, prevention and treatment of ventilator-
Accepted on 04 May 2023
associated pneumonia (VAP), it still continues to create complication
DOI: 10.20959/wjpr20239-27919
during the course of treatment in a significant proportion of patients
who are mechanically ventilated. Objective: Study was designed to
*Corresponding Author
Dr. Arti Yadu M.D. evaluate the effect of multimodality chest physiotherapy in intubated
Associate Professor DKS mechanically ventilated patients undergoing treatment in the intensive
Hospital, Raipur. care units (ICUs) for the prevention of VAP and overall mortality.
Patients and Methods: A total of 90 adult intubated and mechanically
ventilated patients were included in this study. Manual hyperinflation (MH) and suctioning
were administered to patients in the control group (n = 51), and positioning and chest wall
vibrations in addition to MH plus suctioning (multimodality chest physiotherapy) were
administered to patients in the study group (n = 39) till they were extubated. Both the groups
were subjected to treatment twice a day. Standard care in the form of routine nursing care,
pharmacological therapy, inhalation therapy, as advised by the concerned physician/surgeon
was strictly implemented throughout the intervention period. Results: Data were analyzed
using SPSS window version 9.0. The Clinical Pulmonary infection Score (CPIS) Score and
VAP showed significant decrease at the end of extubation Although, overall mortality was
not different in both the groups. Conclusions: It was observed in this study that twice-daily
multimodality chest physiotherapy was associated with a significant decrease in the CPIS
Scores and development of VAP. There was no significant reduction in the mortality rates
This suggested benefit of physiotherapy in prevention of VAP requires confirmation with a
larger randomized controlled trial.
www.wjpr.net │ Vol 12, Issue 9, 2023. │ ISO 9001:2015 Certified Journal │ 1585
KEYWORDS: Clinical Pulmonary infection Score, multimodality chest physiotherapy,

ventilator-associated pneumonia.
INTRODUCTION
Ventilator-associated pneumonia (VAP) is commonly.[1,2], bacterial in nature, and develops at
least 48 hours after intubation and mechanical ventilation.[3] A recent review[4] reported that
the prevalence of VAP ranged from 9% to 68%, with associated mortality rates ranging from
33% to 71%. Partially this variation may be explained by the existence of widely differing
diagnostic criteria for VAP[3,5], confounded further by the non-specific nature of radiographic
pulmonary infiltrates, which may be caused by pneumonia (≈30%), pulmonary edema
(≈30%), acute lung injury (≈15%), and atelectasis (≈15%), with up to another 10% remaining
of unknown cause.[2] Clinical criteria can provide adequate sensitivity for VAP when
compared to other methods, but invasive testing such as bronchoscopy may be required to
improve test specificity.[5,6,7] Risk factors have been associated with VAP, include the
presence of COPD, airway intubation, reduced GCS,re-intubations, mechanical ventilation
greater than 7 days, use of positive end-expiratory pressure, and supine positioning.[1,8,9,10]
Airway intubation and mechanical ventilation reduces the normal clearance of airway
secretions, increasing the risk of developing VAP.[1] There is some evidence that aggressive
preventative measures may reduce the high rates of morbidity associated with VAP in the
critically ill patients.[11] Chest physiotherapy including gravity-assisted drainage, chest wall
percussion, chest wall vibrations, and manual lung hyperinflation (bagging) are commonly
used intensive care procedures.[12] There is supportive evidence that various combinations of
chest physiotherapy assist in the re expansion of atelectatic lungs.[13,14,15,16,17] and confer
short-term improvement in total lung-thorax compliance[13,18] and expiratory flow rates.[19]
However, there is no clear evidence that chest physiotherapy aimed at enhancing secretion
clearance assists in the prevention or treatment of VAP.[20] The present study prospectively
investigated the effect of chest physiotherapy (aimed at enhancing airway secretion
clearance) in intubated and mechanically ventilated patients, compared to control patients not
receiving this form of therapy, on the prevalence of VAP. Secondary outcomes of interest
were the effect of physiotherapy on the duration of mechanical ventilation and admission to
the intensive care unit (ICU), and on 28-day mortality.
MATERIALS AND METHODS

The study was undertaken in a tertiary care referral hospital over a period of one year. All
adult patients who had undergone mechanical ventilation for >48 hrs referred by the
concerned physician, surgeon, or the intensivist were recruited into the study. Study was
approved by hospital ethical committee and did not require written consent.
All those patients who suffered from acute respiratory distress syndrome, acute pulmonary
edema, untreated pneumothorax, those requiring high-respiratory support with FiO2 > 0.70,
acute myocardial infarction, cardiac arrhythmias, hypovolemia, hemodialysis, intubation <48
h, community-acquired pneumonia, unstable cardiovascular or neurological function or injury
preventing positioning for chest physiotherapy, open heart surgeries, admission with
tracheostomy, and HIV positive patients were excluded from the study.
Baseline data including age, gender, admission diagnosis, ventilatory mode, radiological
features suggesting pneumonia, Glasgow Coma Score, and CPIS Score (Table A) of all
patients were noted. Patients were randomly allocated to one of the two groups, i.e.the control
group or the study group by envelope method.
Table A: Clinical pulmonary infection score (CPIS).

Parameter CPIS Range CPIS Scorea
36.5–38.4 0
Temperature (°C) 38.5–39.0 1
<36.0 or >39.0 2
4.0–11 0
White blood cells ( 109/l) 11–17 1
>17 2
± 0
+ 1
Secretions
++ 2
>240orARDS 0
PaO2/FiO2(mmHg)
240noARDS 2
Clear 0
Chestradiographinfiltrates Patchy 1
Localised 2
As a study protocol manual hyperinflation (MH) and suctioning were administered to the
patients in the control group while patients in the study group received positioning and chest
wall vibrations in addition to MH plus suctioning. Standard careas advised by the concerned
physician, surgeon, or the intensivist was strictly implemented throughout the intervention.
All patients in both groups were treated with chest physiotherapy twice a day (9.30 a.m. and
3.30 p.m.) till they were weaned off from the ventilator [Table 5] and were followed up for
the global outcome in terms of recovery, death, total length of stay on ventilation, discharge
against medical advice, or any other complications.
Manual hyperinflation
In order to ensure a uniform and correct technique, MH was employed by the principal
investigator to all the patients. A 2.0-L reusable manual resuscitator (Hudson RCI-non
disposable and autoclavable (silicone) was used to deliver the MH breaths. The MH
procedure was carried out daily at the rate of 8–13 breaths/min for a period of 20 min at each
session twice a day (9.30 a.m. and 3.30 p.m.). After MH, immediately chest vibrations were
also employed.
Chest vibrations
Chest vibration[6] defined as the manual application of a fine oscillatory movement combined
with compression to the patient‟s chest wall which helps to loosen and mobilize the
secretions was given prior to suctioning. This technique was repeated thrice in each of the
three zones, i.e., upper zone, middle zone, and lower zone of the chest.
Suctioning
Duration of endotracheal suctioning[7] was limited to 15 s. The suctioning session involved
instillation of 1 mL of normal saline in the tracheal tube, followed by suctioning once every
minute for 4 min. During suctioning, the specimen from the lower respiratory tract was
collected in a sterile container after instillation of 1mL of normal saline for culture and
sensitivity testing.
Positioning
At the end of the treatment session, i.e., after suctioning, the head end was arranged to be
positioned at an angle of elevation in the range of 30-45° (as measured by a protractor) and
this positioning was maintained for minimum of 30 min for improving the ventilation in all
patients.[8] The change of positioning from lying supine to lateral orientations by turning the
patients wasmanually done by nursing staff once in every 2 hrs. The control group did not
receive chest physiotherapy treatment whilst in the ICU, however sham treatment was
provided by physiotherapists. This consisted predominantly of cardiopulmonary assessment
and occasional musculoskeletal physiotherapy. In addition, patient re-positioning side-to-side
and airway suctioning could be provided by ICU nursing staff without limit as required by
the patient‟s condition. The data to determine the clinical pulmonary infection score (CPIS)
(Pugin et al.[23], as modified by A „Court et al.[24], see Table 1) was prospectively obtained
daily by the chief investigator (GN) from five commonly used clinical parameters, namely
body temperature, leukocyte count, volume, and character of tracheal secretions, lowest
PaO2/FiO2 ratio, and chest radiographic changes. All physiotherapy, medical, and nursing
staff involved in the study did not have knowledge of the daily CPIS score, as it was not
calculated until completion of trial patient recruitment. For the purposes of this study, VAP
was defined as being present when, on the same calendar day, both the clinical diagnosis
(yes) and total CPIS score both indicated the presence of pneumonia. VAP was defined as
early onset when it occurred < =5 days and late onset when >5 days after ICU admission.
Other patient outcome measures included the median duration of mechanical ventilation, the
median length of stay in the ICU (ICU survivors only), and the mortality in ICU and at 28
days. Other data recorded included demographic information, details of admission diagnosis,
and medical or surgical procedures, comorbid factors including as appropriate a pre-operative
American Society of Anesthesiologists Score (ASA)[25] as appropriate, drug therapy and
smoking history. The APACHE II score[26] was calculated in the first 24 h after admission to
the ICU. Sub-group analyses were undertaken as suggested by of the main outcome variable
VAP and severity of disease indices. Early enteral nutrition was encouraged. Other medical
care provided as clinically appropriate during the ICU stay included antibiotic therapy and
therapeutic fiberoptic bronchoscopy (sputum removal for atelectasis).
Weaning from mechanical ventilation was commenced when a patient‟s condition was
medically stabilized and when a PaO2 >60 mmHg on FiO2 < 0.5 could be maintained, with a
RR <25/ min, T <38C and heart rate <130/ min maintained. Extubation was performed when
the patient had been weaned successfully to a low level of mechanical ventilatory support
(continuous positive airway pressure of 5 cmH2O and pressure support of 10 cmH2O)
combined with the presence of adequate cough and gag reflexes with minimal airway
secretions.
Statistical analysis
Data were analyzed using SPSS window version 9.0. Demographic data were analyzed using
Chi-Square test.Mann–Whitney U-tests were used to analyze the number of days the patients
spent under ventilation, and thenumber of days of the patient‟s stay in the ICU. Students
paired and unpaired „t‟-tests were used to compare the results between and within the groups,
respectively.
RESULTS
During the 12-months study period, a total of 267 intubated and mechanically ventilated
patients were admitted to the ICU, of whom a total of 177 patients were subsequently
excluded as ineligible. Major reasons for exclusion were intubation less than 48h,
community-acquiredpneumonia, and unstable cardiovascular or neurological function or
injury preventing positioning for chest physiotherapy. Other reasons for exclusion were
recent open heart surgery, admission with a tracheostomy, an immunocompromised status,
pneumonectomy or lost data. A further 16 patients were removed subsequently due to death
less than 48 h after admission to the ICU or a diagnosis of terminal illness on ICU admission.
Overall, 90 patients fulfilled all the entry criteria, with 39 patients allocated to the
intervention group and 51 patients allocated to the control group based systematically upon
the date of ICU admission.
The two trial groups were well matched for age, sex, admission APACHE II, and Glasgow
Coma Scores and PaO2/FiO2; however, in the surgical patient subgroup the ASA score was
significantly higher in those who received control treatment (Table 2). There were no
significant differences in several patient characteristics known to be risk factors for VAP.
During the ICU stay there were no differences in the frequency of cardiac arrest or in the use
of intravenous narcotics and sedatives, paralytic agents or intracranial pressure monitoring
and/or drainage (Table 2). Almost all patients developed radiological signs of acute lung
collapse and/or consolidation (approximately 95 %,), however the median duration of
atelectasis was 3 days, and there were no differences between the groups (Table 3). Likewise,
a trend towards a lower use of tracheostomy in the intervention group was present but this
difference also was not statistically significant (Table 3).
Table 2 Patient demographics and management. (SD standard deviation, APACHE II acute
physiology and chronic health evaluation score, ASA American Society of Anaesthetists
preoperative score for surgical subgroup, GCS Glasgow Coma Score, COAD chronic
obstructive air- ways disease, Sedatives/Narco- tics/Paralysis (pharmacological) continuous
intravenous administration of relevant drugs at any time during ICU stay, ICP/VD number and
percentage of patients with intracranial pressure monitoring and/or extra ventriculardrainage
during ICU stay)
Data Control (n=51) Intervention (n=39) P

Age, mean(SD),years
65.1(14.6) 65.0(14.3) 0.99
Male/female
33/18 18/21 0.07
APACHE II score, mean(SD)
18.8(5.4) 20.7(6.9) 0.26
ASA, median(range)
Admission GCS, mean(SD)
4(3–5)(n=21) 4(3–4) (n=11) 0.04a
9.2(5.2) 8.6(4.9) 0.74
Admission PaO2/FiO2, mean(SD)mmHg
325(122) 359(146) 0.35
COAD,n(%)
17(30.6) 9(25.6) 0.77
Smoking,n(%)
18(31.4) 8(19) 0.37
Cardiomyopathy,n(%)
4(8.3%) 4(4.2%) 0.64
Cardiac arrest,n(%)
7(13.9%) 5(12.5%) 1.00
Steroids,n(%)
7(13.9%) 3(8.3%) 0.69
Sedatives & narcotics,n(%)
47(94.4%) 32(83.3%) 0.21
Paralysis (pharmacological),n(%)
5(11.1%) 4(12.5%) 1.00
ICP/VD,n(%)
17(30.6%) 8(20.8%) 0.55
a Mann Whitney U-test
Table 3: Outcome data.

Data Control (n=51) Intervention (n=39) P
Tracheostomy, n (%) 18 (51) 9 (39) 0.19
Bronchoscopy, n (%) 3 (8) 1 (4) 0.64
ICU Antibiotic use, n (%) 49 (97) 34 (87) 0.29
Lung collapse/consolidation, n (%) 47 (94) 37 (96) 1.00
Duration lung collapse, median (range), days 3.0 (0–20) 3.0 (0–19) 0.46
CPIS, mean (SD)a 4.4 (1.5) 3.6 (0.8) 0.01
b
VAP, n (%) 14 (39) 2 (8) 0.01
VAP<=5days(n) 11 3
>5 days (n) 7 0
Ventilation duration, median (range), days 5.2 (2.2–20) 4.4 (2–31) 0.39
ICU duration, median (range), daysc 5.8 (2.6–25) 5.6 (2–35) 0.89
ICU mortality, n/n (%) 4/51 (8) 9/39 (25) 0.14
28-day mortality, n/n (%) 12/51 (24) 10/39 (28) 0.28
a Clinical pulmonary infection score. The mean serial CPIS score was the average daily CPIS
for each patient across their entire ICU stay
b Odds ratio (OR)=0.14, 95% confidence interval (CI)=0.03–0.56
c Survivors of ICU only (control group n=51, intervention group n=39)
Table 4: Patients with and without VAP.

Data No VAP (n=51) VAP (n=39) P
Age mean (SD), years 65.6 (15.2) 63.6 (12.0) 0.61
APACHE II, mean (SD) 20.5 (6.2) 16.9 (4.8) 0.02
GCS, mean (SD) 8.2 (4.9) 10.9 (5.3) 0.09
Ventilation duration, median
3.8 (2–31) 6.9 (2–20) 0.02
(range), days
Tracheostomy, n (%) 14 (32) 10 (62) 0.04
Antibiotic use, n (%) 40 (91) 16 (100) 0.57
Table 5: Predictors of VAP. Overall logistic regression model Hosmer-Lemeshow

goodness-of-fit statistic=5.53, df=7, P=0.60. (OR odds ratio, CI confidence interval,
adjusted by logistic regression for all other variables in this table).
P OR (95% CI)
Parameter Adjusted
Univariate Adjusted
Group (intervention vs control)a 0.02 0.02 0.16 (0.03–0.94)
Tracheostomy (no vs yes) 0.04 0.13 0.22 (0.03–1.58)
APACHE Iib 0.02 0.16 0.90 (0.77–1.05)
Ventilation durationc 0.02 0.76 1.03 (0.86–1.23)
GCSd 0.09 0.28 1.10 (0.92–1.32)
a Univariate OR=0.14, 95% CI 0.030.56
b APACHE II with OR reflecting a 1 unit increment in the score
c Mean number of days receiving mechanical ventilation
d Glasgow coma score with OR reflecting a 1 unit increment in the score
In contrast, the mean CPIS was significantly higher in the control group as was the rate of
VAP (Table 3). The control group received mechanical ventilation for a median of 0.8 days
longer than the intervention group, but this difference was not statistically significant and
there was no difference in the median length of stay in ICU survivors (Table 3). Although
there was no significant difference in 28-day mortality, an adverse trend in ICU mortality in
the intervention group was noted (Table 3). Most of these deaths in ICU were as a result of
withdrawal of active medical care (5/6, 84%) as compared to the control group (1/3, 33%).
Overall, the development of VAP was associated with significant increases in median
duration of mechanical ventilation (6.9 days versus 3.8 days), frequency of tracheostomy
placement, and unexpectedly, somewhat lower admission APACHE II scores (Table 4).
Subgroup analyses performed by dichotomizing the study patients based upon the overall
median APACHE II score of 19.5, showed that in those patients with higher APACHE II
scores (control n=17, intervention n=13) there was a lower frequency of VAP in the
intervention group (n=0) compared with the control group (n=5) (P=0.05). In patients
ventilated for longer than the overall median of 4.65 days (control n=20, intervention n=10),
there was a statistically significant (P=0.02) reduction in the frequency of VAP in the
intervention group (n=1) compared with the control group (n=11). Variables with univariate
P values <0.1, were included in a stepwise logistic regression with backward elimination to
determine those parameters independently associated with development of VAP (Table 5).
This multivariate analysis demonstrated that the provision of chest physiotherapy remained
independently associated with a reduced frequency of VAP following adjustment for several
factors including the presence of a tracheostomy, the severity of illness (APACHE II score),
the GCS, and the duration of mechanical ventilation.
DISCUSSION
CPIS Score, the main outcome variable, was statistically significant at the end of
extubation/successful outcome or discharge in both the groups. This study revealed that
mortality rate was not different in both the groups. Successful weaning was observed more
successfully in the study group. Mean reduction in the CPIS Scores between both the groups
was highly significant (P =0.01) as compared to the baseline CPIS. Score reduction was
higher in study group (3.4 ± 4.4) as compared to that in the control group (1.9 ± 2.9) (P <
0.01).
Ventilator-associated pneumonia is defined as parenchymal lung infection occurring more

than 48 hrs after initiation of mechanical ventilation. Unexpectedly in this investigation,
increased occurrence of VAP showed a univariate association with lower admission
APACHE II scores, although this relationship did not persist after adjustment for other
clinically relevant parameters. The non-randomized allocation of therapy and relatively small
size of the present study may in part explain this finding. In addition, a recent surveillance
investigation[34] failed to identify admission APACHE II score as a predictor of VAP. The
segregation of patients with VAP into groups categorizing them as early- and late-onset has
been shown to be of paramount importance. Early-onset pneumonia, i.e., VAP ≤ 5 days
commonly results from aspiration of endogenous community-acquired pathogens such as
Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilusinfluenzaewith
endotracheal intubation and impaired consciousness being the associated main risk factors.
Late-onset pneumonia, i.e., VAP ≥ 5 days followed by aspiration of oropharyngeal or gastric
secretions containing potentially drug-resistant nosocomial pathogens, is associated with an
attributable excess mortality. The immediate administration of treatment is crucial in VAP,
and inappropriate treatment is associated with an increased risk of death due to pneumonia[29]
In addition to antimicrobial treatment, several risk factors for VAP can be minimized by
simple and inexpensive preventive strategies. Chest physiotherapy is one such common
preventive strategy. where chest physiotherapists routinely treat most of the ICU patients
with various chest physiotherapy techniques such as MH, suctioning, patient positioning,
chest vibrations, chest percussions, various coughing techniques in combination or
individually to prevent pulmonary complications like VAP and atelectasis in the ICUs.[30]
However, a recent review[31], based upon findings in surgical patients has suggested that
chest physiotherapy is of no benefit for the prevention of VAP. Our findings in contrast
suggest that the use of combined chest physiotherapy may be useful in selected ICU patients
for the prevention of VAP. A reduction in VAP may have resulted from increased secretion
clearance (as a result of increased expiratory flow rates[19] associated with chest wall
vibrations and head down positioning and improved re-expansion of collapsed or atelectatic
lungs.Jessica et al.[32] have demonstrated that MH in conjunction with suctioning has
demonstrated beneficial changes in respiratory mechanics in patients receiving mechanical
ventilation with VAP, although they did not study the effects of MH plus suction on the
prevention and treatment of VAP. Effective suctioning is an essential aspect of airway
management and has an important role to play in the prevention of VAP, especially early-
onset VAP.[33] Effectiveness of vibrations has been evaluated in various studies.[34,35] Eales et
al. investigating 37 patients receiving mechanical ventilation after cardiac surgery found that
arterial blood gas analyses (ABG) values and lung compliance did not significantly change
during the treatment course with MH and suction with or without the vibrations. However,
effect of vibrations in prevention of VAP needs to be established.[36] One of the simplest and
the least expensive measures in preventing VAP is maintaining the patient‟s head end of the
bed in an elevated position. Increasing the angle of the head end of the bed is effective
because it decreases the risk of aspiration of infected gastric contents and secretions from the
upper aerodigestive tract. Hess has proposed various procedures such as use of rotational
beds, prone position, and semi-recumbent position as procedures to prevent VAP.[37] The use
of semi-recumbent positioning has also been addressed in evidence-based guidelines.[38] In
the absence of medical contraindications, elevation of the head end of the bed of patients at
an angle of 30–45° may help in decreasing the risk of VAP.[39] Ntoumenopouloset al.[40]
studied the effects of multimodality chest physiotherapy (gravity-assisted drainage or
positioning, chest vibrations, and suctioning), in 60 patients receiving mechanical ventilation
and concluded that chest physiotherapy in the ventilated patients was independently
associated with a reduction in VAP. Some clinical studies have concluded that chest
physiotherapy does not hasten the resolution of pneumonia.[41] However, there has been a
lack of systematic review or meta-analysis of chest physiotherapy for pneumonia, and no
study has been published yet.[40] Other non-pharmacological attempts to reduce VAP have
included the use of heat and moisture exchangers and reduced changes of ventilator
circuits.[3,4,11,30] Most of the cases of VAP in our study (69% of cases) were of early onset (=5
DAYS) making them likely to be a result of aspiration, impaired airway secretion clearance
as a complication of airway intubation, or community-acquired pneumonia. The investigation

by Akça et al.[34] also identified a similar time course, with early onset VAP comprising 67%
of cases in a group of medical, surgical, and trauma patients intubated and ventilated for at
least 48 hrs. The small size of the current study and the non-randomized allocation of therapy
also may have contributed to the absence of a survival benefit with chest physiotherapy in
this study. However, most of the ICU deaths, especially in the chest physiotherapy group,
were due to poor patient prognosis and withdrawal of active medical care. Notably there were
no significant differences in the 28-day mortality rate between treatment groups (Table 3). A
number of factors limit the general applicability of our study‟s findings regarding the efficacy
of chest physiotherapy in mechanically ventilated patients. First, the non-randomised
systematic allocation of our trial patients on the basis of date of admission to the ICU may
have introduced bias. A second limitation of the current study was the use of clinical instead
of invasive bronchoscopic criteria for the diagnosis of VAP, which may have increased the
frequency of the diagnosis of VAP above the true rate; however, this effect would have
influenced both treatment groups similarly. Thirdly, a recent investigation by Fabregas et
al.[6], using as reference the presence of both histological pneumonia and positive lung
cultures immediately after death, demonstrated that the CPIS as originally devised[23] was not
any more accurate (sensitivity 77%, specificity 42%) at diagnosing VAP than conventional
clinical criteria. Nevertheless, the CPIS scoring system may remain a useful screening tool to
assess the likelihood of pneumonia and as such has been shown to be useful to direct
antibiotic therapy.[36] Fourth, the large number of patients excluded from this investigation
(mainly due to insufficient duration of ventilation and pre-existing pneumonia) reduced the
sample size and limited the generalizability of our conclusion to those patients intubated and
ventilated for at least 48 hrs.
In conclusion, this study of intubated and mechanically ventilated critically ill patients found
that twice daily chest physiotherapy was independently associated with a reduction in the
occurrence of VAP. Further study in the form of a larger randomized controlled trial of this
clinical intervention in patients at risk of VAP is warranted to confirm these findings and to
establish which of the combination of physiotherapy techniques holds most therapeutic
potential in the prevention of VAP.
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Effect of Chest Physiotherapy On The Prevention of Ventilator-Associated Pneumonia and Mortality

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Effect of Chest Physiotherapy On The Prevention of Ventilator-Associated Pneumonia and Mortality

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World Journal of Pharmaceutical Research

Yadu et al. World Journal of Pharmaceutical Research

Volume 12, Issue 9, 1585-1599. Research Article ISSN 2277– 7105

EFFECT OF CHEST PHYSIOTHERAPY ON THE PREVENTION OF

Associate Professor DKS Hospital, Raipur.

KEYWORDS: Clinical Pulmonary infection Score, multimodality chest physiotherapy,

MATERIALS AND METHODS

Table A: Clinical pulmonary infection score (CPIS).

Data Control (n=51) Intervention (n=39) P

Table 3: Outcome data.

Table 4: Patients with and without VAP.

Table 5: Predictors of VAP. Overall logistic regression model Hosmer-Lemeshow

Ventilator-associated pneumonia is defined as parenchymal lung infection occurring more

as a complication of airway intubation, or community-acquired pneumonia. The investigation

15. Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G. Re-expansion of

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