Professional Documents
Culture Documents
DOI 10.1007/s00134-009-1743-6
ORIGINAL
Jason Phua
Yvonne L. E. Ang
Kay Choong See
Amartya Mukhopadhyay
Erlinda A. Santiago
Eleanor G. Dela Pena
Tow Keang Lim
Introduction
Although once thought of as an orphan disease [1], it is now
evident that the prevalence of non-cystic fibrosis (CF)
bronchiectasis remains high [2, 3]. Patients with non-CF
bronchiectasis often die of causes related to bronchiectasis
and acute respiratory failure (ARF) [47]. However, to the
best of our knowledge, there are only two small retrospective reports to date that describe the course of
639
with NIV and IMV, and secondly to identify the predic- Data collection
tors of hospital mortality and the failure of NIV in these
We recorded the following via medical record review
patients.
onto standardised data collection forms: demographics,
the underlying cause and predominant radiological type of
bronchiectasis (cylindrical, cystic or varicose [17]) and
the use of long-term oxygen therapy (LTOT).
Methods and materials
We grouped the causes of ARF into: (1) acute exacPatient population
erbation of bronchiectasis without identified precipitating
factors and (2) specific causes superimposed on bronchiThis study was approved by our university hospitals ectasis. These causes included pneumonia (new chest
institutional review board with a waiver of informed radiograph infiltrate plus fever, leucocytosis or leucopenia
consent. Using admission and discharge records, we [18]), heart failure (pulmonary or peripheral oedema and
included all consecutive adult patients above 21 years of an abnormal echocardiogram [19]), haemoptysis, tuberage with bronchiectasis who were on NIV or IMV for culosis (Mycobacterium tuberculosis in the sputum [20])
ARF in our medical ICU between January 2000 and and lung abscess (cavity on the chest radiograph with an
November 2007. Only the first episode of ventilatory air-fluid level [21]). We recorded any symptoms of
support and ICU stay for each patient was included. The increased sputum production and signs of reduced alertinclusion and exclusion criteria applied to both patients ness, vital signs and arterial blood gas measurements
on NIV and IMV.
before and 1 h after ventilation, ventilator settings during
We defined bronchiectasis based on: (1) symptoms of the first hour, culture results, the Acute Physiology and
chronic sputum production or cough for C1 year before Chronic Health Evaluation (APACHE) II score, if the
the ICU admission and (2) the following computed patients were admitted to the ICU from the emergency
tomography (CT) findings: nontapering bronchus with department or the general ward, and any do-not-intubate
internal diameter C110% compared to the adjacent pul- orders.
monary artery or visible bronchi within 1 cm of the costal
pleural surface or adjacent to the mediastinal pleural
surface [3, 11, 12]. We gave preference to high-resolution Treatment regimes
(HRCT) rather than conventional CT scans. In the
absence of CT scans, bronchiectasis was only defined Our ICU and emergency department have a common
when (1) clinical features were ascertained to be consis- protocol for the initial support of ARF patients. Specific
tent with bronchiectasis by the attending respiratory therapies include nebulised salbutamol and ipratropium
physician and (2) chest radiograph findings were bromide and systemic steroids for wheezing, empiric
ascertained to be consistent with bronchiectasis by a broad-spectrum antibiotics and chest physiotherapy for
respiratory secretions. Patients who failed such conserradiologist.
We defined ARF as either (1) hypoxemic [partial vative measures and had persistent ARF as defined above
pressure of arterial oxygen (PaO2) \60 mmHg on room were put on NIV or IMV.
We recommend the following indications for endoair] or (2) hypercapnic [partial pressure of arterial carbon
dioxide (PaCO2) [50 mmHg] respiratory failure with or tracheal intubation and IMV: respiratory arrest or
without acidemia (pH \ 7.35), plus (3) at least two of pauses, agitation requiring sedation, systolic blood
the following: worsening dyspnea, respiratory rate [25 pressure \70 mmHg and new-onset multiorgan failure
breaths/min, use of the accessory muscles of respiration, involving C2 non-pulmonary organsultimately, clinical
cyanosis and reduced alertness (any state ranging from judgment is applied. Reduced alertness from hypercapnia
drowsiness simulating light sleep to stupor and coma) alone was not a definite indication for intubation [22]. We
start with assist control volume-limited ventilation, tidal
[13].
We excluded patients who were ventilated for reasons volumes of 6 ml/kg predicted body weight, and respiraother than ARF such as non-pulmonary sepsis or airway tory rate and positive end-expiratory pressure (PEEP) set
protection for massive haemoptysis. To ensure no overlap to avoid dynamic hyperinflation. We switch to a pressure
between bronchiectasis and COPD, we excluded all support of 15 cmH2O when the patients improve, while
patients in a COPD registry that our ICU has kept since keeping the respiratory rate \30/min. We utilise heat and
1999 [14, 15]. The diagnosis of COPD was based on the moisture exchangers, inline suctioning for secretions,
Global Initiative for Chronic Obstructive Lung Disease metered dose inhalers for bronchodilator delivery
guidelines [16]. We do not perform routine HRCT scans through the ventilator circuit, and a nursing and respirafor COPD patients and therefore did not include any tory therapist-directed sedation and weaning protocol
COPD patients with non-clinically significant bronchiec- with daily spontaneous awakening and breathing trials
[23].
tasis detected on HRCT scans in this study.
640
Results
Patient characteristics
There were 31 patients in the NIV group and 26 in the
IMV group (Fig. 1). Table 1 shows their baseline characteristics. No differences in demographic data and
underlying causes of bronchiectasis existed between these
groups. Forty-one patients CT scans were available for
review, of which 26 were HRCT scans. The predominant
type of bronchiectasis was cylindrical, cystic and varicose
in 24, 14 and 3 patients, respectively.
Most patients treated with NIV had acute exacerbations
of bronchiectasis without identified precipitating factors,
while most patients treated with IMV had specific triggers
including pneumonia (Table 1). The majority (48 patients)
in both groups had hypercapnic respiratory failure with
acidemia. At baseline, while there were no differences in
vital signs and frequency of reduced alertness, the NIV
group had a greater frequency of increased sputum production, and was less acidemic and hypoxemic than the
IMV group. The APACHE II score was numerically but
not significantly lower in the NIV group.
641
Fig. 1 Inclusion and immediate outcomes of patients. Asterisk represents total of five deaths in the ICU in the NIV group and six deaths
in the ICU in the IMV group. SBT spontaneous breathing trial
642
Table 1 Baseline characteristics of patients treated with noninvasive ventilation versus invasive ventilation
Baseline characteristics
Demographics
Age (years)
Male/female
Underlying cause of bronchiectasis, n (%)
Idiopathic
Pulmonary tuberculosis
Nontuberculous mycobacteria
Gastroesophageal reflux disease
Kartageners syndrome
Childhood pneumonia
Long-term oxygen therapy
Cause of acute respiratory failure, n (%)
Precipitating factors identified
Pneumonia
Haemoptysis
Heart failure
Tuberculosis
Lung abscess
No factors identified
Type of respiratory failurea
Hypoxemic
Hypercapnic
With acidemia
Without acidemia
Symptoms and signs
Increased sputum production
Reduced alertness
Vital signs
Heart rate/min
Mean blood pressure (mmHg)
Respiratory rate/min
Arterial blood gas measurementsa
pH
PaCO2 (mmHg)
PaO2/FiO2 (mmHg)
APACHE II score
Direct intensive care unit admissionb
Do-not-intubate orders
Respiratory cultures, n (%)c
Pseudomonas aeruginosa
Staphylococcus aureus
Klebsiella pneumonia
Moraxella catarrhalis
Acinetobacter baumannii
Pasteurella multocida
Citrobacter diversus
Noninvasive ventilation
(n = 31)
Invasive ventilation
(n = 26)
73.0 12.3
11/20
66.2 13.7
9/17
12 (38.7)
16 (51.6)
1 (3.2)
1 (3.2)
1 (3.2)
0 (0)
5 (16.1)
12 (46.2)
13 (50.0)
0 (0)
0 (0)
0 (0)
1 (3.8)
3 (11.5)
4 (12.9)
2 (6.5)
0 (0)
1 (3.2)
1 (3.2)
0 (0)
27 (87.1)
17 (65.4)
11 (42.3)
4 (15.4)
0 (0)
1 (3.8)
1 (3.8)
9 (34.6)
2 (6.5)
29 (93.5)
28 (90.3)
1 (3.2)
4 (17.4)
19 (82.6)
19 (82.6)
0 (0)
23 (74.2)
14 (45.2)
10 (38.5)
17 (65.4)
0.006
0.13
107.6 22.1
83.9 22.1
28.7 6.9
110.8 21.4
80.9 17.3
25.7 5.1
0.59
1.00
0.07
7.25 0.07
77.8 19.1
249.4 120.4
25.3 5.1
17 (54.8)
11 (35.5)
7.18 0.11
83.7 36.5
173.2 97.3
28.4 7.5
14 (53.8)
0 (0)
0.008
0.45
0.02
0.07
0.94
0.001
0.76
6
5
1
1
1
0
1
5
2
2
0
0
1
0
0.05
0.95
0.56
0.72
\0.001
0.38
(19.4)
(16.1)
(3.2)
(3.2)
(3.2)
(0)
(3.2)
(19.2)
(7.7)
(7.7)
(0)
(0)
(3.8)
(0)
Data expressed as mean standard deviation and number c Semiquantitative cultures of the sputum and tracheal aspirates.
Some patients had more than one positive culture. Aside from
(percentage) unless otherwise specified
Pseudomonas aeruginosa and Staphylococcus aureus, the other
APACHE Acute Physiology and Chronic Health Evaluation
a
Arterial blood gas measurements were unavailable for three organisms were susceptible to beta-lactam antibiotics
patients in the invasive ventilation group
b
Direct admission to the intensive care unit from the emergency
department rather than from the general ward
643
120
7.35
NS
110
Arterial pH
7.30
100
90
7.15
7.10
Before
Before
During
During
100
100
95
90
7.20
NS
80
90
85
80
75
80
70
60
NS
NS
50
70
Before
During
Before
32
300
During
NS
NS
30
7.25
28
26
24
22
20
250
200
150
*
*
18
Before
During
Fig. 2 Vital signs and arterial blood gas measurements before and
1 h into ventilatory support. Dotted lines represent the noninvasive
ventilation (NIV) group, while bold lines represent the invasive
mechanical ventilation (IMV) group. Mean values are shown. Error
bars represent the 95% confidence intervals. *Significant change in
100
Before
During
644
Table 2 Outcomes of patients treated with noninvasive ventilation versus invasive ventilation
Outcome
Noninvasive ventilation
(n = 31)
Invasive ventilation
(n = 26)
24.0 (5.027.0)
4.0 (2.06.0)
9.0 (6.015.0)
5 (16.1)
8 (25.8)
10 (32.3)
12.0 (025.0)
7.5 (4.513.3)
11.5 (8.028.8)
6 (23.1)
7 (26.9)
Not applicable
0.06
0.002
0.054
0.51
0.92
Not applicable
Univariate analysisa
Multivariate analysisb
Survivors (n = 42)
Nonsurvivors (n = 15)
13 (31.0)
29 (69.0)
106.1 21.1
231.9 113.0
25.5 6.1
8 (53.3)
7 (46.7)
117.3 21.9
172.9 118.7
30.0 6.5
OR (95% CI)
0.12
0.11
0.09
0.10
0.02
0.12
0.19
0.04
Data are expressed as number (percentage) and mean standard c Precipitating factors include pneumonia, haemoptysis, heart failure, tuberculosis and lung abscess
deviation unless otherwise specified
OR odds ratio, CI confidence interval, APACHE Acute Physiology d PaO2/FiO2 ratio was unavailable for three patients who did not
have arterial blood gas measurements before invasive mechanical
and Chronic Health Evaluation
a
ventilation
Variables with p values \0.15 on univariate analysis
b
The same variables with p values less than 0.15 on univariate
analysis are included and entered into a logistic regression analysis
Discussion
Our studys key findings are as follows. One-quarter of
our patients with bronchiectasis and ARF died in the
hospital. This mortality was independently predicted by
the APACHE II score. Physicians often reserved NIV for
patients with acute exacerbations without identified precipitating factors and who were less acidemic and
645
Univariate analysisa
Multivariate analysisb
NIV success
(n = 21)
NIV failure
(n = 10)
OR (95% CI)
0 (0)
21 (100.0)
84.0 17.9
292.1 107.4
4 (40.0)
6 (60.0)
64.8 14.9
149.7 88.2
0.007
0.06
0.007
0.002
1.02 (1.001.03)
per mmHg decrease
0.07
0.04
APACHE II score
24.3 4.0
27.3 6.7
0.13
0.22
646
References
1. Barker AF, Bardana EJ Jr (1988)
Bronchiectasis: update of an orphan
disease. Am Rev Respir Dis
137:969978
2. Tsang KW, Tipoe GL (2004)
Bronchiectasis: not an orphan disease
in the East. Int J Tuberc Lung Dis
8:691702
3. ODonnell AE (2008) Bronchiectasis.
Chest 134:815823
4. Loebinger MR, Wells AU, Hansell DM,
Chinyanganya N, Devaraj A, Meister
M, Wilson R (2009) Mortality in
bronchiectasis: a long-term study
assessing the factors influencing
survival. Eur Respir J 34:843849
5. Onen ZP, Gulbay BE, Sen E, Yildiz OA,
Saryal S, Acican T, Karabiyikoglu G
(2007) Analysis of the factors related to
mortality in patients with bronchiectasis.
Respir Med 101:13901397
6. Keistinen T, Saynajakangas O,
Tuuponen T, Kivela SL (1997)
Bronchiectasis: an orphan disease
with a poorly understood prognosis.
Eur Respir J 10:27842787
7. Ellis DA, Thornley PE, Wightman AJ,
Walker M, Chalmers J, Crofton JW
(1981) Present outlook in
bronchiectasis: clinical and social study
and review of factors influencing
prognosis. Thorax 36:659664
8. Dupont M, Gacouin A, Lena H, Lavoue
S, Brinchault G, Delaval P, Thomas R
(2004) Survival of patients with
bronchiectasis after the first ICU stay for
respiratory failure. Chest 125:18151820
9. Alzeer AH, Masood M, Basha SJ,
Shaik SA (2007) Survival of
bronchiectatic patients with respiratory
failure in ICU. BMC Pulm Med 7:17
10. Garpestad E, Brennan J, Hill NS (2007)
Noninvasive ventilation for critical
care. Chest 132:711720
647
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.