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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report seven elderly patients with COPD who developed serious infectious complications during prolonged treatment with high doses of corticosteroids. Infections included invasive pulmonary aspergillosis, Herpes simplex stomatitis and esophagitis, cytomegalovirus pneumonia, bacterial sepsis, fungemia and meningitis due to Cryptococcus neoformans. Each of the three patients who developed invasive aspergillus pneumonia died. The efficacy of prolonged therapy with high doses of corticosteroids in patients with COPD is not proven. These cases illustrate the potential for serious infections in patients with COPD treated with corticosteroids.
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PMID:Serious infectious complications of corticosteroid therapy for COPD. 272 Dec 49

A physician's assessment of the probable outcome of an episode of respiratory failure should be based on a combination of survival data from large studies and specific knowledge about the individual case in question. Clearly, mortality rates in cases of ARF are influenced by a number of factors. In general, only a minority of patients with ARF complicating COPD require mechanical ventilation. In these cases, mortality often is related to the nature of the precipitating illness and the severity of the patient's underlying chronic respiratory disease. The long-term prognosis in patients with COPD who survive an episode of ARF is related primarily to the severity of the patient's underlying disease. Acute mortality is higher in patients with ARDS than in patients with ARF complicating COPD. Although a significant number of ARDS patients die of their underlying illness, mortality in others more commonly appears to be related to sepsis and multiple organ failure rather than end-stage respiratory disease. Pulmonary function in survivors of ARDS is quite variable, and may be related to the severity of the acute episode. ARF has a particularly poor prognosis when associated with certain underlying illnesses such as hematologic malignancy.
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PMID:Outcome from respiratory failure. 811 29

Among 182 episodes with ARF (PaCO2 > 50 torr) in 400 episodes of COPD patients who were admitted to Chulalongkorn Hospital during the period 1982 to 1986, despite conservative treatment, 66 developed severe acute respiratory failure requiring assisted ventilation. Patients with a history of chronic cough, pneumonia as a precipitating factor and more severe ARF on admission, as indicated by palpitation, headache, cyanosis, alteration of consciousness, cor-pulmonale and decompensated acidosis (pH < 7.30), were likely to require mechanical ventilation. Indications for mechanical ventilation were carbon dioxide narcosis (43 episodes), severe hypoxemia despite on a high FIO2 (one episode), various combination parameters of respiratory muscle fatigue, cardiovascular instability (22 episodes). The major complications of mechanical ventilation were pneumonia, sepsis, pneumothorax, UGI bleeding of 16, 8, 5 and 9 episodes, respectively. The average duration of assisted ventilation and hospitalization were 15.8 and 19.02 days, respectively. The mortality rate was 50 per cent in the mechanical ventilation group compared with 9.8 per cent in the non-mechanical ventilation group. Increased mortality rate was found in those with pneumonia as the precipitating factor (68.4 vs 14.3%, respectively, in comparing the two groups). Complications of mechanical ventilation, which included pneumonia, sepsis, fluid overload, hyponatremia and persistent acidosis, were high-risk factors for the non-surviving group.
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PMID:Mechanical and non-mechanical ventilation of respiratory failure in chronic obstructive pulmonary disease. 822 88

In a 3-month period (January to March, 1992), patients with rectal temperature below 35 degrees C detected by an electrical rectal thermometer (Diatek, Inc, San Diego, CA) were enrolled. In addition to treatment of the underlying diseases, the patients were rewarmed with either a heating lamp (core temperature > 32 degrees C) or warm fluid intravenous infusion and/or gastric lavage (core temperature < 32 degrees C). Patients' vital signs, serum potassium, pH, initial temperature, mean weather temperature, underlying disease and outcome were recorded and compared between survivors and non-survivors. We collected 23 cases with mean age of 71.6 years and mean core temperature, 33.32 degrees C (29.4-34.9 degrees C). The diagnosis included hypoglycemia in 7 cases, sepsis in 3 cases, active TB in 2 cases, HHNK in 1 case, DKA in 1 case, UGI bleeding in 1 case, parkinsonism in 1 case, intracerebral hemorrhage in 1 case, urinary tract infection in 1 case, brain tumor post operation in 1 case, arrhythmia in 1 case, senile dementia in 1 case, COPD in 1 case and lung CA in 1 case. 12 (52%) cases died during admission. No significant difference in clinical parameters was noted between survivors and non-survivors. In conclusion, although in subtropic area, the hypothermic patients in our country cannot be overlooked. As patients are usually elder and have other diseases, the prognosis is correlated with the severity of the underlying disease. Alert, intensive care, prevention and treatment of the complications that arouse, and careful rewarming are necessary for management of such patients.
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PMID:[Hypothermia in the patients of emergency department]. 828 89

Some conditions that predispose to ventilatory failure increase the work of breathing (chronic obstructive pulmonary disease [COPD], obesity, kyphoscoliosis), whereas others cause severe respiratory muscle weakness. Specific reasons for muscle weakness include critical illness (electrolyte imbalance, acidemia, shock, sepsis), chronic illness (poor nutrition, cachexia), and neuromuscular diseases. Inspiratory muscle weakness from mechanical disadvantage to the diaphragm is characteristic of asthma and COPD. The increased work of breathing combined with muscle weakness increases the pressure needed to inspire a breath and decreases maximal inspiratory pressure. When this pressure exceeds 0.4, dyspnea and inspiratory muscle fatigue ensue. One way to lower this pressure and avert fatigue is to lower the tidal volume. Ventilatory drive is high, not low, in ventilatory failure. Concomitant shortening of inspiration and breath duration cause the small tidal volume and increased respiratory rate. Gas exchange is compromised by ventilation/perfusion imbalance, and the ratio of dead space to tidal volume is also increased by rapid, shallow breathing. Reduction in tidal volume minimizes dyspnea, but the small tidal volume is inadequate for gas exchange. Acute treatment of respiratory muscle failure involves respiratory muscle rest through mechanical ventilation and removal of noxious influences (infection, metabolic disarray), whereas chronic treatment involves rebuilding the contractile apparatus by nutritional repletion and training.
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PMID:Respiratory muscles and ventilatory failure: 1993 perspective. 850 1

Bronchial rupture is a rare but severe complication of intubation with a double-lumen tube. Cardinal symptoms are mediastinal and subcutaneous emphysema as well as pneumothorax. Larger injuries result in an air leak and the endtidal carbon dioxide decreases. The gas exchange may worsen drastically when mucosal prolapse or bronchial haemorrhagia lead to bronchial occlusion. Mediastinitis or sepsis can be the sequel of the opened mediastinum. If bronchial injury is suspected probably fibreoptic bronchoscopy is indicated. We report on a case of bronchial rupture due to overinflation of the endobronchial cuff or movement of the inflated cuff when repositioning the patient. The conservative therapy was successful in spite of the fact that surgical intervention is recommended in the literature following bronchial rupture. To avoid tracheobronchial injuries an adequate tubus size must be selected. The more flexible polyvinylchloride (PVC) tubes without a carinal hook should be preferred to the Carlens tube. An atraumatic intubation is promoted by leaving the stylet inside after the tip of the tube has passed the vocal cords. To identify the minimum occlusive pressure of the endobronchial cuff for lung isolation different methods are described and should be used. The cuff has to be deflated when the patient is repositioned and when one-lung-ventilation is not required. Tumours of the tracheobronchial tree and weakness of the bronchial wall caused by steroid hormone therapy or COPD may increase the risk of tracheobronchial laceration.
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PMID:[Diagnosis, procedures and conservative therapy of a bronchial rupture after intubation with double-lumen tube]. 1007 58

Severe CAP is a life-threatening condition defined by the presence of respiratory failure or symptoms of severe sepsis or septic shock. It accounts for approximately 10% of hospitalized patients with CAP. The majority of patients with severe pneumonia have underlying comorbid illnesses, with COPD, alcoholism, chronic heart disease, and diabetes mellitus being the most frequent. S. pneumoniae, Legionella spp, GNEB (especially K. pneumoniae), H. influenzae, S. aureus/spp, Mycoplasma pneumoniae, respiratory viruses (especially influenza viruses), and P. aeruginosa represent the most important causative organisms of severe CAP. Rapid initiation of appropriate antimicrobial treatment is crucial for a favorable outcome. Initial antimicrobial treatment should be based on an epidemiological (empiric) approach. Microbial investigation may be helpful in the individual case but is probably more useful to define local antimicrobial policies based on local epidemiologic and susceptibility patterns. Mortality rates range from 21% to 54%. The most important prognostic factors include general health state of the patient, appropriateness of initial antimicrobial treatment, and the existence of bacteremia, as well as factors reflecting severe respiratory failure, severe sepsis, septic hypotension or shock, and the extent of infiltrates in chest radiograph. Initial antimicrobial treatment should consist of a second (or third) generation cephalosporin and erythromycin. Modifications of this basic regimen should be considered in the presence of distinct comorbid conditions and risk factors for distinct pathogens. Promising new approaches of nonantimicrobial treatment, including noninvasive ventilation, treatment of hypoxemia, and immunomodulation, are under investigation.
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PMID:Severe community-acquired pneumonia. 1051 5

Acute exacerbation of chronic bronchitis (AECB) is a very common condition, which presents with deteriorating sputum production and dyspnoea in a patient with pre-existing COPD or chronic bronchitis. As these symptoms are relatively non-specific and also the presenting feature of a wide range of other conditions, the physician should carefully consider the differential diagnosis before deciding on whether or not a patient indeed has AECB. The differential diagnosis can be summarised as pneumonia, pneumothorax, cardiac failure/cor pulmonale, bronchiectasis, asthma, tuberculosis, sinusitis and other forms of upper respiratory tract sepsis, diffuse panbronchiolitis, lung cancer, gastro-oesophageal reflux, the presence of a foreign body in the airway, melioidosis, and lung abscess. This article aims to discuss these conditions, with brief presentation of clinical cases, in the evaluation of differential diagnosis of AECB.
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PMID:Solutions for difficult diagnostic cases of acute exacerbations of chronic bronchitis. 1158 3

Nitric oxide (*NO) and its by-products modulate many physiological functions of skeletal muscle including blood flow, metabolism, glucose uptake, and contractile function. However, growing evidence suggests that an overproduction of nitric oxide contributes to muscle wasting in a number of pathologies including chronic heart failure, sepsis, COPD, muscular dystrophy, and extreme disuse. Limited data point to the potential of inhibition various enzymes by reactive nitrogen species (RNS), including (.)NO and its downstream products such as peroxynitrite, primarily in purified systems. We hypothesized that exposure of skeletal muscle to RNS donors would reduce or downregulate activities of the crucial antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX). Diaphragm muscle fiber bundles were extracted from 4-month-old Fischer-344 rats and, in a series of experiments, exposed to either (a) 0 (control), 1, or 5 mM diethylamine NONOate (DEANO: *NO donor); (b) 0, 100, 500 microM, or 1 mM sodium nitroprusside (SNP: *NO donor); (c) 0 or 2 mM S-nitroso-acetylpenicillamine (SNAP: *NO donor); or (d) 0 or 500 microM SIN-1 (peroxynitrite donor) for 60 min. DEANO resulted in a 50% reduction in CAT, GPX, and a dose-dependent inhibition of Cu, Zn-SOD. SNP resulted in significantly lower activities for total SOD, Mn-SOD isoform, Cu, Zn-SOD isoform, CAT, and GPX in a dose-dependent fashion. Two millimolar SNAP and 500 microM SIN-1 also resulted in a large and significant inhibition of total SOD and CAT. These data indicate that reactive nitrogen species impair antioxidant enzyme function in an RNS donor-specific and dose-dependent manner and are consistent with the hypothesis that excess RNS production contributes to skeletal muscle oxidative stress and muscle dysfunction.
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PMID:Specificity of antioxidant enzyme inhibition in skeletal muscle to reactive nitrogen species donors. 1207 89

Only few data concerning weaning by nasal positive pressure ventilation (NPPV) are available, and successful weaning by using NPPV in patients with acute respiratory distress syndrome (ARDS) and severe complications has not yet been described. Two cases with ARDS and both preexisting thoracopulmonary disease (infundibulum abnormality and suspected COPD) and associated complications (recurrent sepsis, acute renal failure, need for lobectomy, severe malnutrition) could not be weaned by invasive ventilatory techniques. Both patients presented with rapid shallow breathing and PaCO(2) values >60 mm Hg during intermittent trials of spontaneous breathing, although the primary pathology and associated complications had been resolved. Patients were successfully adapted on NPPV in a stepwise approach after 93 days and 67 days of invasive ventilation. In one patient withdrawal from NPPV was possible after 2 months. In the other patient the duration of daily ventilation could be significantly reduced from 18 to 6 h/day after 9 months on NPPV. Therefore, patients with ARDS who cannot be weaned by invasive ventilatory strategies might be removed successfully from invasive mechanical ventilation by using NPPV even when there are preexisting thoracopulmonary disease and major complications during invasive ventilation.
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PMID:Weaning from mechanical ventilation by long-term nasal positive pressure ventilation in two patients with acute respiratory distress syndrome associated with pneumococcal sepsis. 1223 58


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