Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five patients with neurogenic pulmonary edema (NPE) were reported. The edemas were caused by head injuries in four patients and by a craniotomy in the fifth. The onset of NPE was either acute (3 hours after injury) or was slow to develop (4 days later). Clinical symptoms included the sudden onset of coughing, tachypnea, tachycardia, and pink bubbly sputum. Moreover, the patients also suffered cyanosis, confusion, or respiratory failure. The distribution of the resulting pulmonary edema was diffuse in 4 cases and localized within a single lobe of the lung in 1 case. Treatment of the NPE included reducing intracranial pressure (glycerol), diuresis (furosemide and mannitol), narcotics (morphine, phenobarbital), and blocking the peripheral effect of sympathetic reflex activity (hydralazine, sodium nitroprusside). Mechanical ventilation support (CPU-1) in combination with controlled hyperventilation may also be necessary. The inability to correct hypoxemia without toxic levels of oxygen necessitates the use of PEEP (positive end-expiratory pressure, +5-10 cmH2O). Resolution of symptoms was noted 24 to 48 hours after treatment in 4 patients. Early diagnosis and intensive care of the pulmonary edema may have a significant bearing on the recovery of lung functions. Unfortunately, 4 of the patients failed to survive because of central nervous system failure. We therefore want to emphasize that NPE can cause secondary deterioration of neurological functions. In conclusion, when dealing with respiratory distress patients with CNS injuries, the possibility of additional damage from a NPE must be taken into consideration.
Gaoxiong Yi Xue Ke Xue Za Zhi 1992 Sep
PMID:[Neurogenic pulmonary edema: five cases report]. 129 67

507 cases of lung hamartoma (30 cases reported and 477 reviewed) were analysed. 467 cases of them were of intrapulmonary type, 30 were endobronchial, 8 were multiple and 2 were diffuse. 505 were benign and 2 malignant. The male to female ratio was 1.74:1. The age span was from infant to 67 years with a mean of 41.4 years. 44.3% of the lesions showed no symptoms. The frequently seen symptoms were cough and chest pain. X-ray findings of the intrapulmonary type were characterized by sharply outlined round or oval mass (87.9%), with diameters 3.0 cm (62.1%), lobulation (33.5%), calcification (23.6%). These tumors grew slowly. The average doubling time for 16 cases was 4.2 years. The diagnosis was confirmed in only 18% cases preoperatively. The other cases were misdiagnosed as lung cancer, tuberculoma, metastatic tumors of the lung, etc. The etiological causes, classification, diagnosis, differential diagnosis and treatment of the tumors were discussed.
Zhonghua Wai Ke Za Zhi 1992 Sep
PMID:[Lung hamartoma: a report of 30 cases and review of 477 cases]. 130 31

A study of 4 comparable communities in central & northeastern Bombay (2 each) among randomly matched 349 subjects in 1988-9, along with ambient sulfur dioxide (SO2), Nitrogen dioxide (NO2) & suspended particulate matter (SPM) air monitoring was carried out. The levels in winter were higher particularly for SO2 in Parel (upto 584 micrograms) in Maravali; Deonar showed lower pollution. There were inter-area differences for housing, income, residential history but age-sex differences were small; these were reduced by matching. Clinical respiratory symptoms were higher in Parel & Maravali (cough 12% and 11.2%, dyspnoea 17% & 13.3% respectively). Cardiac problems are commoner in Parel (11.0%). Smoker had cough more often but not dyspnoea. Maravali had a high prevalence for headache and eye irritation (9.5%). Those using kerosene suffered more than those using gas (22.2% as compared to 9.2%) Lung functions (FVC, FEVI) were lowest in Parel for males and in Maravali for females. Expiratory flow rates were lower at Dadar and then at Maravali. Despite lower SO2 pollution, Maravali residents suffered equally as in Parel. This may be due to added effect of diesel exhausts (NO2, SPM) or other unmeasured chemicals.
J Assoc Physicians India 1992 Sep
PMID:Air pollution related respiratory morbidity in central and north-eastern Bombay. 130 13

Superior vena cava syndrome (SVCS) is rare in children. In Veterans General Hospital-Taipei, a total of 364 cases of SVC syndrome were diagnosed in the past 12 years. Of them only seven cases were younger than 18 years of age, ranging from 6 to 17 years, and they were all caused by mediastinal tumor. The underlying malignancy included malignant lymphoma in 4, teratocarcinoma in one and unknown in 2. The most common initial symptom was cough, followed in order of frequency by chest discomfort or neck mass. Dyspnea, orthopnea, swelling of head and neck, and venous engorgement might develop gradually within one to three weeks. Of the reported seven cases, two cases received immediate resuscitation upon arrival but expired in 1-2 hours. The other five cases received treatment with intravenous steroid as well as chemotherapy, and three cases also received committent emergent radiotherapy. Two of them expired 4 months and 2 years after treatment, respectively. Of the two surviving cases, one has received a complete course of chemotherapy and the other is still under regular chemotherapy in our hospital. Both of them are stable till now.
Zhonghua Yi Xue Za Zhi (Taipei) 1992 Sep
PMID:Superior vena cava syndrome in children with malignancy: analysis of seven cases. 133 Feb 48

A retrospective study was carried out by a computerized questionnaire in a sample of 109 sarcoidosis patients (43 men, 66 women) diagnosed between 1977 and 1990 in Pisa. 94% of the patients were resident in Tuscany. The onset of disease was earlier in the men than in the women; in 73% of the patients the symptoms were first noticed between February and July with two incidence peaks; 71% of them had never smoked; 10% of patients were symptom-free and the disease was discovered by chance; the other patients (90%) underwent chest X-ray because of joint symptoms (35%), erythema nodosum (34%), cough (28%), dyspnoea (27%), and fever (24%) which was often associated with other symptoms. Symptoms from the respiratory tract was present in 66 patients (61%); 58% of patients were resident in rural areas; the level of education was limited to primary school in 50% of the patients; as to the prevailing working positions, 27% were clerical workers, 24% manual workers, and 26% housewives.
Sarcoidosis 1992 Sep
PMID:Sarcoidosis in Tuscany. A preliminary report. 134 53

Lung function and clinical evidence of muscle weakness were assessed in 12 ASA I patients who received vecuronium 0.01 mg kg-1 pretreatment as a part of their anaesthetic management, before and 3 min after pretreatment. Most patients demonstrated ptosis and diplopia, while five of the 12 were unable to raise the head for > 4 s and had difficulty in swallowing. Significant reductions occurred in forced vital capacity, forced expiratory volume in 1 s, and maximum mid-expiratory flow rate. Among static lung volumes, functional residual capacity and expiratory reserve volume decreased significantly. However, these changes were not serious enough to cause clinically significant impairment of coughing or a decrease in oxygen saturation in any patient.
Br J Anaesth 1992 Sep
PMID:Lung function after vecuronium pretreatment in young, healthy patients. 135

The upper and lower airways have complimentary roles in the ultimate object of supplying the body with oxygen whilst removing waste products of metabolism. Pathology in one area may trigger a response in another, the physiology of which, in the case of virus-induced asthma exacerbations remains poorly characterized. Viral infection of the upper airways by common cold viruses frequently triggers a response in the lower airways leading to prolonged morbidity, especially in subjects with significant pre-existing airway disease. The induction or amplification of BHR may be an important mechanism whereby asthmatic symptoms are produced although the cellular and tissue events or reflex mechanisms activated by viral illnesses and underlying BHR changes are poorly defined and may be dependent on the type and the severity of infection. Children and asthmatics tend to develop frequent colds setting in motion a sequence of events culminating in airway obstruction and symptoms of wheezing, coughing and chest tightness. This may reflect independent inflammatory changes caused by a simply additive effect of viral damage to the mucosa superimposed upon pre-existing allergic inflammation (Fig. 1). Few if any symptoms will develop in normal subjects with a mild cold whereas significant symptoms may ensue if the cold is severe and induces marked lower airway swelling, secretions and smooth muscle contraction; pathology to which children who have small calibre airways may be particularly susceptible. In asthmatics even a mild cold frequently induces exacerbation of symptoms, while serious life-threatening asthma attacks may occur associated with a severe cold. Some studies have suggested that this effect is not only additive but also synergistic and brought about by release of the mediators already present in increased quantities, the induction of IgE synthesis, or by the potentiation of neural and epithelial damage. The combined effect of both asthma and viruses may thus be amplified and result in a sustained and refractory period of airway obstruction, severe symptoms and unstable asthma. As most hospital admissions for asthma occur over the winter months and soon after the start of the school terms [115], spread of viruses through the community to susceptible individuals may be the single most important cause of sustained exacerbations of asthma. Definition of the pathological and physiological mechanisms involved will lead to better understanding and may thus provide a basis for prevention and the development of effective forms of treatment for virus-induced asthma.
Clin Exp Allergy 1992 Sep
PMID:Viruses as precipitants of asthma symptoms. II. Physiology and mechanisms. 135 15

The effects of alpha 2-adrenoceptor and GABA receptor agonists on citric acid-induced cough and increased tidal volume were investigated in conscious guinea pigs. Inhalation of low doses of B-HT 920 (5-allyl-2-amino 5,6,7,8-tetrahydro-4H-thiazolo[4,5-d]azepine dihydrochloride), and xylazine significantly inhibited citric acid-induced cough and tidal volume increases. Intraperitoneal administration of higher doses of B-HT 920 than those given by aerosol were ineffective. The inhibitory effects of B-HT 920 were antagonised by prior intraperitoneal administration of yohimbine, but not atropine. Inhalation of GABA or baclofen inhibited tidal volume increases, but had no effect on cough. Inhaled alpha 2-adrenoceptor or GABA agonists had no effect on the reduced respiratory rate after citric acid inhalation. It is concluded that alpha 2-adrenoceptor agonists inhibit cough via a mechanism which may not be related to their ability to reduce citric acid-induced tidal volume increases, since GABA and baclofen inhibited tidal volume increases but not cough. We suggest that alpha 2-adrenoceptor agonists may have therapeutic potential in the treatment of cough.
Eur J Pharmacol 1992 Sep 22
PMID:Effects of inhaled alpha 2-adrenoceptor and GABAB receptor agonists on citric acid-induced cough and tidal volume changes in guinea pigs. 135 50

This preliminary study was conducted to identify a facet joint syndrome in low back pain. Ninety maneuvers and symptoms were compared between patients relieved (responders) and those unrelieved (nonresponders) after intraarticular blocks. Fifty-one patients participated in the study; 11 were excluded from evaluation because of unsuccessful injection into the joints as planned. Of the 40 patients included, 20 had four joints anesthetized, 16 had two joints anesthetized, and four had three joints anesthetized. Twenty-two were responders, 17 of whom had more than 90% relief of pain. Only a few variables were more frequent in the responder group: older age, absence of exacerbation by coughing, relief when recumbent, absence of exacerbation by forward flexion and when raising from this flexion, absence of worsening by hyperextension, and extension-rotation. When four of these seven variables were present in the same patient, sensitivity was 81.8% and specificity 77.8%, but this discriminant power must be evaluated in a new population.
Arch Phys Med Rehabil 1992 Sep
PMID:Facet joint block for low back pain: identifying predictors of a good response. 138 21

We studied recovery in 25 adult patients, ASA I, undergoing elective orthopaedic procedures after anaesthesia with 0.65 MAC desflurane (n = 16) or isoflurane (n = 9) with 60% nitrous oxide in oxygen. Early emergence from anaesthesia was assessed in the operating room by measuring time to spontaneous movement, cough, response to painful pinch, tracheal extubation, opening of the eyes and stating correct age, name and body parts. The return of cognitive functions in the late recovery phase was assessed in the post-anaesthesia care unit (PACU) by post-anaesthesia recovery scores (PARS), the Trieger dot test (TDT), and the digit substitution test (DST). In the early recovery phase, time to tracheal extubation, opening eyes, telling correct name, age and body parts occurred significantly faster in the desflurane group than in the isoflurane group (P < 0.05). The mean "triple orientation" time (to name, age, body parts) was 10.9 (SEM 0.9) min for desflurane, compared with 18.6 (2.5) min for isoflurane (P < 0.01). In the late recovery phase, desflurane patients had significantly greater PARS, more correct responses to the DST and fewer error responses to the TDT. Recovery times were not increased by increased duration of desflurane anaesthesia. The desflurane patients showed no delirium, minimal sedation and less shivering during the entire postoperative course. We conclude that desflurane anaesthesia was superior to isoflurane anaesthesia, not only in emergence, but also in the recovery of cognitive functions.
Br J Anaesth 1992 Sep
PMID:Recovery of cognitive functions after anaesthesia with desflurane or isoflurane and nitrous oxide. 138 42


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