COPD is one of the major public health problems around the world and acute exacerbation of COPD is the major cause of significant morbidity and mortality worldwide. Though the prevalence varies in different countries along with the age and sex of an individual, COPD is going to be the fifth leading cause of disability and the third leading cause of death worldwide by 2020. [11] According to the study conducted by Dhimal et al in a different part of Nepal, the Prevalence of COPD was 11.7%. [12]
Respiratory failure is a common and important event, which is frequently associated with severe exacerbations of COPD. [13] The higher mortality rate is associated with the presence of hypercapnia in respiratory failure. [14] Changes in lung mechanics are believed to be the significant determinants of the physiological variations from the norm that describe hypercapnic respiratory failure. A subject would need to expand their ventilation to overcome the wasted ventilation in high ventilation/perfusion ratio units, however, their failure to do so regardless of the respiratory boost that a rising CO2 strain gives has been the subject of a lot of discussions. [15]
In this study, among 112 patients, 47 (41.96%) were male and 65 (58.04%) female. Similar findings were observed in a study done by Ghosh V et al. which had 59.6% female patients in comparison to 40.4% male patients.[16] One reason could be increased exposure to biomass among females, due to involvement in household cooking. In contrast, Dhimal et al, in their study, concluded male predominance among patients with COPD.[12]
The plausible hypothesis regarding increased incidence among females might be a genetic predisposition for smoking-related lung changes in certain families. Silverman et al, in his study of 84 probands, not only observed high prevalence among females (71.4%) but also had an almost double risk of having obstructive lung disease. [17] Studies with an animal had shown the role of Estrogen in the metabolism of tobacco-smoke. In the animal model; estrogen upregulated the cytochrome p-450 enzymes; which plays a role in increasing susceptibility to cigarette smoke-related oxidant injury in the lung parenchyma. [17] Anatomically, Females have smaller lung and airways compared to males, hence, with the same amount of exposure to smoking they are more prone to develop the disease.
Cigarette smoking is a well-established cause for COPD followed by biomass exposure in a country like Nepal and India.[4, 18] Among the study population, 94.6% were smoker whereas the rest were non-smokers. 33.9% (n = 38) patients had a history of both tobacco smoking and biomass exposure of which 33 (86.8%) were female whereas only 5(13.2%) were male. Among 112 patients, 39.3% of patients still had a history of biomass exposure. Among total study patients, all male patients were tobacco smokers whereas only 9.23% of females were non-smokers.
A significant association between SpO2 and FEV1 was found (p < 0.001), unlike other studies where there was no significant correlation between FEV1 % predicted and SpO2 values.[19, 20] FEV1 value was compared with the hospital stay which showed a consistent and important association of decreasing FEV1 (increasing severity of COPD stage) with the prolonged hospital (p-value − 0.004). A similar finding was found in the study done by Sijapati et al.[21]
In this study, as compared to Type 1 respiratory failure, the patients with type 2 respiratory failure had prolonged hospital stay (p < 0.001) (Table 4). This may be because of the intervention needed to washout the CO2 utilizing either Invasive or non-invasive ventilator supports. Other studies also have findings similar to ours. [14, 21, 22] A study done by Nousheen et al observed that hypercapnic patients had a longer hospital stay (mean 9.27 ± 7.57 days), increased requirement for non-invasive mechanical ventilation on admission (n = 45 (78.94%)) and longer mean time to clinical stability (4.39 ± 2.0 days) compared with the other groups.[23] Hypercapnic patients had a longer duration of hospital stay in comparison to normocapnic patients (Table 3 ).
Among 61.6% of our patients receiving steroids, no significant change in the duration of hospital stay was observed (p > 0.05). Scholl et al, in his study done at Colorado Hospital between July 1, 2012, and May 20, 2016, included AECOPD patients (89 in the steroid group and 49 in the non-steroid group). No significant difference was seen in the mean duration of hospital stay (4.7 ± 3.2 versus 4.2 ± 2.1 days, p = 0.27). [24] In contrary to this and our study, Woods et al experienced a significantly shorter length of hospital stay in comparison to placebo (8.5 versus 9.7 days, P = 0.03). (25) The role of steroids in the length of hospital stay has to be studied further.