Han Yu Chang

Prediction of Arterial Blood Gas Values from Venous Blood Gas Values in Patients with Acute Respiratory Failure Receiving Mechanical Ventilation

BACKGROUND AND PURPOSE Arterial blood gas (ABG) analysis is useful in evaluation of the clinical condition of critically ill patients; however, arterial puncture or insertion of an arterial catheter may cause many complications. This study evaluated whether pH, partial pressure of carbon dioxide (PCO2) and bicarbonate (HCO3-) values of venous blood gas (VBG) could accurately predict their ABG analogs for patients with acute respiratory failure treated by mechanical ventilation in an intensive care unit (ICU). METHODS Forty six patients who were admitted to the ICU due to acute respiratory failure and treated by mechanical ventilation were included in this study. Blood for VBG analysis was sampled from the cubital or dorsal palmar veins, while ABG was sampled simultaneously from the radial or brachial arteries via an arterial catheter at the other upper extremity. Regression equations and mean percentage-difference equations were derived to predict arterial pH, PCO2, and HCO3- values from their VBG analogs. The equations were validated by evaluating VBG and ABG samples from a separate group of 11 patients. RESULTS A total of 46 paired samples from 46 patients were evaluated. The mean percentage differences between the venous and arterial values divided by venous values for pH, PCO2, and HCO3- were (mean +/- SD): deltapH (%), 0.50 +/- 0.45; deltaPCO2 (%), 17.09 +/- 9.60; and deltaHCO3- (%), 9.72 +/- 7.73; respectively. Regression equations for prediction of pH, PCO2 and HCO3- values were: arterial pH (pHa) = 0.45 + 0.94 x venous pH (pHv) [r = 0.83, p < 0.0001]; partial pressure of arterial CO2 (PaCO2) = 3.06 + 0.76 x partial pressure of venous CO2 (PvCO2) [r = 0.86, p < 0.0001]; and arterial HCO3- (HCO3-a) = 2.34 + 0.82 x venous HCO3- (HCO3-v) [r = 0.91, p < 0.0001]. The predicted ABG values from the mean percentage-difference equations were derived as follows: pHa = pHv x 1.005; PaCO2 = PvCO2 x 0.83; and HCO3-a = HCO3-v x 0.90. Validation of the regression equations and mean percentage-difference equations revealed only a small (clinically insignificant) variation between the actual and predicted ABG values. CONCLUSIONS Venous blood gas can accurately predict the ABG values of pH, PCO2 and HCO3- for patients with acute respiratory failure being treated with mechanical ventilation.

Successful treatment of diffuse lipoid pneumonitis with whole lung lavage.

Diffuse lipoid pneumonitis is rare. Prednisolone can be beneficial, but no other method of treatment has been tried. The first case of diffuse lipoid pneumonitis successfully managed with whole lung lavage is described.

Comparative effects of l-NOARG and l-NAME on basal blood flow and ACh-induced vasodilatation in rat diaphragmatic microcirculation

The effects of Nω‐nitro‐l‐arginine (l‐NOARG) and Nω‐nitro‐l‐arginine methyl ester (l‐NAME) on diaphragmatic microcirculation in male Sprague‐Dawley rats were assessed under basal conditions and after acetylcholine (ACh) stimulation. In addition, l‐arginine (l‐arg) was used with the aim of preventing l‐NOARG and l‐NAME from inhibiting ACh‐induced vasodilatation, in order to explore the possibility that l‐NOARG is not only a nitric oxide (NO) synthase inhibitor but also a muscarinic receptor antagonist. Male Sprague‐Dawley rats were anaesthetized with urethane and mechanically ventilated. The left hemi‐diaphragm of each rat was prepared and microvascular blood flow was recorded during continuous superfusion with bicarbonate‐buffered prewarmed Ringer solution by using laser‐Doppler flowmetry. The drugs were topically applied to the surface of the hemi‐diaphragm. Baseline microvascular blood flow was unaffected after 15 min superfusion with any one of the following agents: l‐NOARG (0.1 mm), l‐NAME (0.1 mm), l‐arg (10 mm). ACh (0.03 mm, 0.1 mm and 0.3 mm) elicited a significant increase of microvascular blood flow (171±16%, 214±55%, and 323±68% of baseline values, respectively), via interaction with the muscarinic receptor, for the vasodilator response was severely inhibited by 15 min superfusion with atropine (0.3 mm). Following 15 min superfusion with either of the l‐arg analogues (0.1 mm), the ACh‐induced vasodilator response was significantly inhibited. Pretreatment with l‐arg (10 mm) for 5 min, followed by co‐administration of l‐arg (10 mm) and l‐NOARG (0.1 mm) for another 15 min significantly prevented the inhibitory effect of l‐NOARG on ACh‐induced vasodilatation. However, a similar pretreatment schedule with l‐arg failed to prevent l‐NAME from exerting its inhibitory effect. Neither of the l‐arg analogues potentiated sodium nitroprusside (10 μm and 30 μm)‐induced vasodilatation. However, adenosine (0.1 mm)‐induced vasodilatation was slightly but significantly attenuated by either l‐NOARG (0.1 mm) or l‐NAME (0.1 mm), an effect which was prevented by l‐arg (10 mm). In conclusion, an increase in endothelium‐dependent blood flow stimulated by ACh may occur in diaphragmatic microcirculation of anaesthetized rats independently of low baseline NO activity. The results also suggest that l‐NAME has muscarinic receptor antagonist action in addition to its ability to inhibit NO synthase. Thus, we suggest that l‐NAME should not be used as a specific NO synthase inhibitor in the rat diaphragm in situations in which there is potential for muscarinic receptors to be stimulated.

A retrospective study of catastrophic invasive fungal infections in patients with systemic lupus erythematosus from southern Taiwan

As very few large scale publications of invasive fungal infection (IFI) have been reported in lupus patients from individual medical centers, a retrospective study was performed from 1988 to 2009 in southern Taiwan. Demographic characteristics, clinical and laboratory data, and mycological examinations were analyzed. Twenty cases with IFI were identified in 2397 patients (0.83% incidence). There were 19 females and one male with an average age of 31.8 ± 12.6. Involved sites included eight disseminated cases, six central nervous system, four lungs, one abdomen and one soft tissue. IFI contributed to a high mortality with 10 deaths (50%), and there were no survivors for the disseminated cases and Candida-infected patients. High activity (Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) > 8) was noted in 50% of IFI episodes. The survival from IFI diagnosis to death was only 7.7 ± 4.2 days, all in a rapid course. No statistical difference was found between survivors and non-survivors when comparing their SLEDAI. Eighty-five percent of IFI episodes under high dosages of corticosteroids therapy and 95% of patients had lupus nephritis. There was an increased risk of IFI in the lupus patients receiving high daily dosage of prednisolone therapy. Critical information from analyses of the present large series could be applied into clinical practices to reduce the morbidity and mortality in such patients.

Fatal acute pulmonary oedema after inhalation of fumes from polytetrafluoroethylene (PTFE)

The cases of three patients with acute pulmonary oedema caused by inhalation of fumes from heated polytetrafluoroethylene (PTFE) in a plastic factory are described. One patient died from profound hypoxaemia and shock shortly after admission, and the other two patients survived after medical treatment. This is the first report of fatal pulmonary oedema in a worker exposed to PTFE heated in a plastic extruding operation. From this observation, it appears that inhalation exposure to pyrolytic products from polytetrafluoroethylene can cause fatal respiratory complications. Special precautions are warranted in this kind of operation to prevent workers from being exposed to these substances.

Mite-Induced Allergic Airway Inflammation in Guinea Pigs

BACKGROUND Mites are the most common aeroallergen in human allergic asthma. However, no animal model of mite-induced allergic airway inflammation has been reported before. In this study, an animal model of mite-induced allergic airway inflammation in guinea pigs was developed. METHODS Firstly, we found that two intraperitoneal injections of 100 micrograms crude mite extract (CME), but not multiple aerosol inhalations of 10 mg/ml CME, can cause sensitization in guinea pigs. The sensitization to mites was confirmed by the measurement of serum antimite antibody titer and the detection of anaphylactic bronchoconstriction after intravenous injection of CME solution. Then, single or multiple aerosol challenges with different concentrations (8, 4 or 1 mg/ml) of CME in these sensitized animals were performed. The total white cell and differential counts in the bronchoalveolar lavage (BAL) fluids were studied at different time intervals after challenge in different animals, and tracheal pathology was performed to detect the allergic airway inflammation. For comparison with the study in animals treated with CME, a BAL study in animals treated with ovalbumin was also performed. RESULTS The inhalation challenge of CME aerosol in sensitized animals caused prolonged eosinophilia in BAL fluid which persisted for at least 7 days after single challenge. Neither inhalation challenge at higher concentrations of CME aerosol nor repeated inhalation challenges increased the degree of eosinophilia in BAL fluid compared to a single challenge. Using the same procedures, we also found that the mite model caused more eosinophilia in BAL fluid than did ovalbumin. CONCLUSION This is the first report of an animal model of mite-induced allergic airway inflammation in guinea pigs which can provide us with a useful model to study airway inflammation of mite-induced asthma in humans.

The involvement of ATP‐sensitive potassium channels in β2‐adrenoceptor agonist‐induced vasodilatation on rat diaphragmatic microcirculation

The effects of glibenclamide (GLB), a blocker of ATP‐sensitive potassium (KATP) channels, on diaphragmatic microcirculation in male Sprague‐Dawley rats were assessed under basal conditions and after β2‐adrenoceptor‐agonist stimulation. In addition, forskolin was used to bypass β‐adrenoceptors and GTP‐binding proteins (G‐protein) to explore the possible mechanism of GLB effects. For comparison, the relationships between KATP channel activity and cyclic GMP‐mediated vasodilator responses to acetylcholine (ACh) and sodium nitroprusside (SNP) were also assessed. Male Sprague‐Dawley rats were anaesthetized with urethane and mechanically ventilated. The left hemi‐diaphragm of each rat was prepared and microvascular blood flow (QLDF) was recorded with laser‐Doppler flowmetry during continuous superfusion with bicarbonate‐buffered, prewarmed Ringer solution. The drugs were topically applied to the surface of the hemi‐diaphragm. Salbutamol (0.32–32 μM), terbutaline (0.32 μM–0.32 μM) and forskolin (0.32–10 μM) each elicited a concentration‐dependent increase in QLDF. Baseline microvascular blood flow was unaffected by a 30 min suffusion of 1 μM GLB (295±51 mV vs 325±62 mV, P=0.738). The vasodilator response elicited by salbutamol (0.32 μM, 1 μM and 3.2 μM), was significantly attenuated by a 30 min superfusion with 1 μM GLB; this salbutamol‐induced vasodilatation was mediated via an interaction with β‐adrenoceptor receptors, as in other experiments it was greatly inhibited by 30‐min superfusion with propranolol (10 μM). Similarly, following 30‐min superfusion with GLB (1 μM), the terbutaline (1 μM, 3.2 μM and 10 μM)‐induced vasodilator response was almost abolished and the vasodilator responses induced by incremental concentrations of forskolin (0.32 μM, 1 μM and 3.2 μM) were also significantly attenuated. Cromakalim (1.5 μM, 3 μM and 3.2 μM) produced an increase of QLDF in a dose‐dependent manner, which was virtually abolished by GLB (1 μM). In contrast, the vasodilator responses induced by acetylcholine (32 μM, 0.1 mM, and 0.32 mM) or sodium nitroprusside (3.2 μM, 10 μM and 20 μM) were independent of GLB (1 μM). In conclusion, KATP channels may be functional, but tonically inactive in the resting diaphragmatic microcirculation and the vasodilator effect of β2‐adrenoceptor agonists may be partly mediated by KATP channels; the activation of KATP channels may involve the accumulation of cyclic AMP in vascular smooth muscle cells.

Using Post-bronchodilator FEV1 is Better Than Pre-bronchodilator FEV1 in Evaluation of COPD Severity

Abstract Background: The current standards for the diagnosis and treatment of patients with COPD clearly rely on the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria based on post-bronchodilator spirometric values. However, clinical evidence for using the post-bronchodilator FEV1 in the severity classification has not been fully investigated. Methods: Patients with COPD were enrolled and followed up prospectively between October 2006 and January 2011. We compared the observed 3-year risk of all causes and respiratory mortality with the risk predicted by the pre- and post-bronchodilator percent predicted FEV1. Other important phenotypes including BMI, MMRC dyspnea scale, ECOG performance status and severe AECOPD (acute exacerbation) were also compared between the two groups. The different severity classifications of COPD, measured according the GOLD guidelines by post- and pre-bronchodilator percent predicted FEV1 were compared for prediction of mortality. Results: There were 35 deaths among the 300 COPD patients (11.7%). Multivariate analysis showed that the post-bronchodilator percent predicted FEV1 was a significant independent predictor of mortality but pre-bronchodilator percent predicted FEV1 was not (p = 0.008 vs 0.126) and it was more strongly correlated with all studied predictors of outcome than the pre-bronchodilator percent predicted FEV1. Kaplan-Meier analysis showed that the discrimination ability to predict mortality from the GOLD criteria using post bronchodilator percent predicted FEV1 (p = 0.009) was better than using pre-bronchodilator percent predicted FEV1 (p = 0.131). Conclusions: The post-bronchodilator percent predicted FEV1 is better than the pre-bronchodilator percent predicted FEV1 in the evaluation of the severity of disease in COPD patients and is more accurate in predicting the risk of death by the GOLD classification.

A retrospective study of pulmonary infarction in patients with systemic lupus erythematosus from southern Taiwan

Since large-scale reports of pulmonary infarction in systemic lupus erythematosus (SLE) are limited, a retrospective study was performed for this manifestation in 773 hospitalized patients in southern Taiwan from 1999 to 2009. Pulmonary infarction was defined as the presence of pulmonary embolism, persistent pulmonary infiltrates, and characteristic clinical symptoms. Demographic, clinical, laboratory, and radiological images data were analyzed. There were 12 patients with pulmonary embolism and 9 of them had antiphospholipid syndrome (APS). Six patients (19 to 53 years, average 38.2 ± 12.6) with 9 episodes of lung infarction were identified. All cases were APS and four episodes had coincidental venous thromboembolism. There were four episodes of bilateral infarction and seven episodes of larger central pulmonary artery embolism. Heparin therapy was routinely prescribed and thrombolytic agents were added in two episodes. Successful recovery was noted in all patients. In conclusion, there was a 0.8% incidence of pulmonary infarction in patients with SLE, all with the risk factor of APS. Differentiation between pulmonary infarction and pneumonia in lupus patients should be made; they have similar chest radiography with lung consolidation but require a different clinical approach in management. Although this report is a retrospective study with relatively small numbers of lupus patients with lung infarcts, our observation might provide beneficial information on the clinical features and radiological presentations during the disease evolution of pulmonary infarction in SLE with APS.

Comparison of global initiative for chronic obstructive pulmonary disease 2013 classification and body mass index, airflow obstruction, dyspnea, and exacerbations index in predicting mortality and exacerbations in elderly adults with chronic obstructive pulmonary disease.

To examine whether the Global Initiative for Chronic Obstructive Pulmonary Disease (GOLD) 2013 revision offers greater predictive ability than the body mass index, airflow obstruction, dyspnea, and exacerbations (BODEx) index in elderly adults with chronic obstructive pulmonary disease (COPD).