Ours is the first multicenter study to report weaning outcomes of ventilator-dependent survivors of catastrophic illness transferred to the post-ICU setting of LTCHs. In this continuum of critical care medicine, more than half of the patients were discharged weaned from mechanical ventilation.
Strengths of the current study are that consecutive patients receiving mechanical ventilation were enrolled from 23 different LTCHs, employing uniform definitions of weaning outcomes. More than 30 published studies have reported outcomes of weaning from PMV in long-term acute care hospitals, noninvasive respiratory care units, and step-down units, but comparisons are difficult mainly due to various definitions of weaning success, ranging from 48 h to 1 year without ventilatory support. A recent consensus conference report recommended that complete liberation from mechanical ventilation (or a requirement for only nocturnal NIV) for 7 consecutive days should denote successful weaning. We selected to score weaning outcome at discharge for the current study, as that largely determines the next step in the continuum of care. Seven ventilator-free hospital days, followed by reinstitution of ventilatory support, or death, arguably does not truly reflect weaning success.
The load of disability and illness imposed on the Western industrialized nations by chronic bronchitis and emphysema is well known. I have chosen to talk on the topic of the prevention of emphysema because I think it is the central problem in relation to these diseases, and because serious and disabling chronic lung disease seems to involve centrilobular and panlobular emphysema far Inore frequently than just the changes commonly described as those of chronic bronchitis. However, in morbidity statistics it is perhaps better to link the two diseases together since the criteria of their distinction during life involve “degrees of probability” rather than of certainty. The most recent data of this kind I have seen are summarized in Table 1, which shows that emphysema and chronic bronchitis together ranked sixth in the United States as a cause of limitation of major activity, and affected 231,000 people. I have not seen exactly comparable data for Canada or Europe, but we have no reason to think that these countries would differ markedly except that in a number of Euorpean countries, particularly Great Britain, relatively fewer persons would be affected by heart conditions, with relatively more affected by emphysema and bronchitis. If you face such a problem as bronchitis check out the website – of Canadian Neighbor Pharmacy and find the prescribed preparation or its analogue.
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Trauma to the heart after nonpenetrating injury is well recognized. Among the recorded consequences are cardiac arrhythmias, septal damage, valve damage, coronary fistulae, coronary artery damage, ventricular aneurysm, cardiac rupture, and myocardial infarction (MI). Myocardial infarction as a complication of chest trauma has been reported in very few cases and usually is secondary to an automobile accident. In the present report, we describe a patient who developed acute ischemia manifested by posteroinferior wall MI (API-MI) secondary to a football chest trauma.
A 33-year -old white sportsman without any previous history of heart disease, was admitted to the coronary care unit because of severe chest pain after straight anterior wall chest trauma by a football. At the same time, the patient complained of dyspnea, nausea, and vomiting. His physical examination on arrival revealed blood pressure of 140/80 mm Hg, regular pulse rate of 68 beats per minute, and respiration at the rate of 22 per minute. Carotid and jugular venous pulsations were normal. Examination of the chest wall showed no sign of injury. Auscultation of the lungs was normal. The first and second heart sounds were normal, and an apical S4 gallop was present No murmur or rub were heard. Examination of the abdomen and extremities was normal. The electrocardiogram (ECG) on admission showed an API-MI (Fig 1), chest x-ray film was normal. Creatine kinase (CK) value was 1,077 U (normal 0-50 U) with a CK-MB fraction of 19.6 percent (normal, less than 5 percent). Echocardiogram revealed an area of hypokinesia on the inferior wall and interventricular septum; the right ventricle was normal. Myocardial scintigraphy with technetium 99m pyrophosphate was performed on the third hospital day and was compatible with necrosis of the inferior wall, inferior third of the interventricular septum, and the right ventricle (Fig 2). On the 12th hospital day, the submaximal stress test with thallium-201 was positive for the inferior wall. The left ventriculogram showed an area of akinesia on the posteroinferior wall, and the coronary angiography revealed total obstruction of the proximal right coronary artery (Fig 3). The patient had an uneventful hospitalization, and three weeks after admission, he was discharged asymptomatic and without medication. More information about medications and diseases you may on Canadian Neighbor Pharmacy twitter official group.
Nonpenetrating chest traumas producing different cardiac complications have been reported frequently. However among these complications, MI has been documented in only a few cases and usually secondary to automobile accidents. The anatomic position of the coronary circulation facilitates that the anterior descending coronary artery is the coronary vessel most frequently affected in this type of chest trauma. On reviewing the literature, we found only two cases of AMI secondary to football chest trauma. Both cases showed anterior wall MI. We, therefore, wish to add a new case with this complication, in whom an acute inferior wall MI developed.
The mechanism by which nonpenetrating chest trauma may be complicated with an AMI is not defined yet; however, the factors capable of producing an AMI in this setting are mainly coronary thrombosis and/or spasm of a normal coronary artery. The coronary angiography performed in our patient three weeks after the event revealed a complete obstruction of the main right coronary artery, which we really think was secondary to the chest trauma and not due to previous heart disease, mainly because of the patients youth.
We believe that all patients with chest trauma should have the following: complete physical examination, resting ECG, chest x-ray film, echocardiogram, and CK-MB. In finding abnormalities such as rupture of any heart structure or MI, we consider it necessary to perform angiographic study.
Figure 1. Twelve-lead ECG showing sinus rhythm with posteroinferior wall myocardial infarction.
Figure 2. Myocardial scintigraphy with technetium 99m pyrophosphate reveals necrosis of the inferior wall (IW), inferior third of the interventricular septum (S), and right ventricle (RV).
Figure 3. (a) Coronary angiogram of the left coronary artery from a right anterior oblique view, showing normal cincumflex, marginal and anterior descending arteries, (b) Coronary angiogram of the right coronary artery from the same view, revealing complete proximal obstruction.
A 30-year-old black man was admitted to the hospital with a six-month history of fever, 30 pound weight loss, and productive cough with occasional hemoptysis. A history of prior intravenous drug abuse and a 15-pack-year smoking history was obtained. Six weeks prior to admission, he noted left pleuritic chest pains associated with the appearance of a swelling over his left lateral chest wall.
The patient was acutely ill. Blood pressure was 116/28, heart rate 116, temperature 39°C orally. On examination, he had adequate dental hygiene, shotty anterior cervical adenopathy, dullness and bronchial breathing over his left upper thorax, and no heart murmur. A 6 cm X 6 cm swelling over the left lateral chest wall in the posterior axillary line between the seventh and tenth ribs was fixed and tender. No fluctuance was appreciated. Clubbing was present. Laboratory tests yielded the following findings: hematocrit, 35 percent, WBC, 16,600/cu mm with 65 percent neutrophils, 8 percent bands, 19 percent lymphocytes, 6 percent monocytes, and 2 percent eosinophils. Chest roentgenogram (Fig 1) revealed volume contraction of the left lung with left upper lobe infiltrates and pleural thickening. No pleural fluid was demonstrated on a decubitus film.
Fever persisted despite administration of intravenous cefazolin. Fiberoptic bronchoscopy did not reveal any endobronchial lesion or obstruction. Chest computed tomography (CT) the third hospital day demonstrated left lower lobe and lingular atelectasis and pleural thickening (Fig 2). A soft tissue mass along the left lateral chest wall with a central area of decreased radiodensity was seen (Fig 3, arrow).
Morphologic and Functional Characteristics of AM Recovered from Patients with Pulmonary Alveolar Proteinosis
Light microscopy disclosed that the structure of AM from patients with pulmonary alveolar proteinosis was strikingly different from that of AM from healthy nonsmoking control subjects. The AM from patients with pulmonary alveolar proteinosis were generally two to three times the size of normal AM when viewed at equal magnification (Fig 1A and 1B). The cytoplasm of macrophages from all patients with pulmonary alveolar proteinosis contained large globular, as well as amorphous inclusions, often giving the cytoplasm a foamy appearance. Interestingly, when cultured with medium containing either or P2, AM from healthy control subjects acquired morphologic characteristics similar to those of AM from the patients with pulmonary alveolar proteinosis (Fig 1C and 1D).
Although the number of AM phagocytizing yeast at two hours did not differ significantly between the patients with pulmonary alveolar proteinosis and the normal volunteers, the mean number of yeast cells ingested per macrophage was decreased in AM from patients with pulmonary alveolar proteinosis compared with normal control subjects (Table 1). Possibly the most important finding from these experiments was that AM from patients with pulmonary alveolar proteinosis uniformly exhibited decreased phagolysosome fusion (Table 1).
The natural history of chronic aortic insufficiency is a continuum marked by a prolonged initial plateau phase during which the patient is relatively stable, and a later phase of progressive deterioration in left ventricular performance. Once the signs and symptoms of heart failure appear, chronic irreversible changes in left ventricular function may have occurred. Since the likelihood of improvement in left ventricular function after aortic valve replacement is less certain once this point has been reached, current practice is to intervene surgically prior to the onset of substantial deterioration of the left ventricle. However, the stable plateau phase may persist for decades and surgery should not be performed too early since that would subject the patient to premature risk from the operative procedure, as well as from complications of the prosthesis itself.