Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitrofurantoin is a widely prescribed antibiotic used for the treatment of urinary tract infections. In some patients it can produce an acute pulmonary reaction ranging from mild dyspnea to noncardiogenic pulmonary edema. Symptoms include fever, dyspnea, chills, cough, and chest pain. Physical examination generally reveals an acutely ill, extremely apprehensive patient in varying degrees of respiratory distress. Fever is usually present and there is an increase in heart rate and respiratory rate. Cyanosis, rales, and a maculopapular rash are common findings. Laboratory studies typically demonstrate a leukocytosis with eosinophilia, varying degrees of hypoxia and hypocapnia, and a mild to moderate elevation of the erythrocyte sedimentation rate. The chest x-ray study may be normal but more often demonstrates bilateral lower lobe interstitial infiltrates frequently accompanied by pleural effusions. Treatment in the majority of cases requires only stopping the drug, but steroids, bronchodilators, or antihistamines may be used in selected cases. Once the diagnosis is made and the drug withdrawn, prognosis for full recovery is excellent.
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PMID:Acute pulmonary toxicity to nitrofurantoin. 270 84

The aims of this study were to compare the clinical features of patients with pulmonary embolism (PE) and patients in whom the initial suspected diagnosis was not confirmed by the complementary studies and to determine the possible clinical differences among patients with PE according to age. A retrospective review of the charts of a group of patients with PE (n, 96) and another without PE (n, 96) was carried out. The patients with PE over 65 years of age (n, 64) were compared with those under 66 years of age (n, 32). The variables related to PE were absence of known heart disease, duration of symptoms </=2 days, pleuritic chest pain, absence of cough, pCO(2) <4.8 kPa (36 mmHg), and normal chest X-ray. The variables associated with the existence of PE in patients over 65 years of age, when contrasted with younger patients, were female sex, absence of pleuritic chest pain, abnormal chest X-ray, hypoxemia (pO(2) < 8.7 kPa (65 mmHg) and absence of S1Q3T3 pattern in ECG.The duration of symptoms and the presence of hypocapnia, pleuritic chest pain, and normal chest X-ray may lead to the suspicion of PE. Pleuritic pain and S1Q3T3 pattern are less commonly found in old patients with PE.
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PMID:Influence of age on clinical presentation of acute pulmonary embolism. 1086 63

BACKGROUND: The aim of this retrospective study was to determine the clinical, laboratory, and radiological features of all adult patients with varicella-zoster virus pneumonia (VZVP) treated in our departments during the last 5 years. Important therapeutic and evolutionary features are also reported. METHODS: Fourteen patients (11 males and 3 females, mean age OF 36.4 and 34.3 years, respectively), diagnosed as suffering from VZVP, were included in this study. The antecedents of previous contact with patients with varicella, smoking, pregnancy, and underlying diseases were evaluated. In all cases, the diagnosis of pneumonia was established by clinical and radiological criteria in the course of varicella infection. RESULTS: All but one patient had had previous contact with a varicella patient. Eleven of them (78.57%) were smokers. None of the patients was immunocompromised. All patients had the characteristic rash of the disease, fever, and cough. Only six (43%) had bilateral sparse rales on auscultation. Arterial blood gas analysis at the onset of VZVP revealed hypoxemia in seven patients (50%) and hypocapnia in six (43%). Mean PaO(2) was 55 mmHg (range of 42-68 mmHg) and mean PaCO(2) was 34 mmHg (range of 27-36 mmHg). Chest radiographs showed ill-defined nodular or reticular densities of various sizes scattered throughout both lung fields. A CT scan of the chest, performed in seven patients (50%), confirmed the radiological findings and marked out patchy ground-glass attenuation in three patients and coalescence of lesions in two others. After diagnosis, all patients were immediately started on acyclovir 5-10 mg/kg every 8 h. Five patients (36%) were admitted to the ICU due to acute hypoxemic respiratory failure. Two patients received noninvasive positive pressure ventilation via a facemask and the other three patients with a clinical diagnosis of ARDS were intubated and ventilated mechanically. The duration of patient hospitalization was 16+/-10 days. One patient (8%) died in the ICU on the third day after admission due to multiple organ dysfunction (MOF). All of the other patients recovered completely without any sequelae. CONCLUSIONS: Adult patients with severe VZVP must be admitted and treated in the ICU. The use of intravenous acyclovir may be lifesaving, preventing progressive respiratory failure and reducing the high mortality rate of the disease.
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PMID:Varicella-zoster virus pneumonia in adults: report of 14 cases and review of the literature. 1552 70

The report presents a definition and causes of syncope in children. Syncope differs from other states with loss of consciousness by causes leading to decreased perfusion and resultant transient cerebral dysfunction with decreased muscle tone. The most common causes of syncope noted in almost 15% of children are neurocardiogenic. This group includes vasovagal, carotid sinus reflexive, situational (coughing, dysphagia, micturation and defecation disturbances) and post-exercise syncope. Another group is represented by orthostatic syncope that may be triggered by primary and secondary dis-autonomy, decreased blood volume (hemorrhage, diarrhea, Addison's disease), some medications and substances of abuse (alcohol). An important group, accounting for 2%-6% of all cases, are cardiogenic syncope, caused mainly by congenital/acquired obstructive cardiac sub- and valvar heart defects, various cardiomyopathies, some heart tumors (e.g. myxoma), exudative pericarditis, pulmonary embolus and hypertension, congenital and acquired coronary anomalies, various significant brady-tachyarrhythmias (sick sinus syndrome, supra- and ventricular tachycardias, congenital and acquired atrio-ventricular blocks). Subclavian steal syndrome as the cause of syncope is exceptional in children. Syncope does not include loss of consciousness due to neurological and metabolic (hypoglycemia) causes, hypoxia, hyperventilation with hypocapnia or CO intoxication. Differential diagnosis should also include pseudo-syncope (hysteria). Preliminary diagnostic management should include a detailed medical history, including family history, on the frequency and circumstances of syncope, sudden deaths, a physical exam with orthostatic assessment of peripheral blood pressure and standard ECG (heart rate, intraventricular and atrioventricular conduction defects, cardiac hypertrophy, arrhythmias, L-QT, changes in ST-T). Further specialist tests depend on preliminary findings.
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PMID:[Syncope in children and adolescents]. 1843 21

In the absence of other explanations, exercise-induced dyspnea is often labeled as a manifestation of asthma. The aim of this study was to use exercise provocation in cold air among patients with exercise-induced dyspnea, but without any bronchoconstriction, in order to study induced symptoms and different physiological parameters and to measure the possible influence of exercise in cold air on capsaicin cough sensitivity. Eleven patients with exercise-induced dyspnea but no asthma, along with 11 healthy controls, performed a capsaicin inhalation provocation on two occasions. One of these provocations was preceded by an exercise provocation in a cold chamber. Number of coughs, airway symptoms, spirometry, respiratory rate, pulse rate, end-tidal CO(2), and PSaO(2) were registered. During exercise, the patients coughed more than the controls and also had more airway symptoms. After exercise provocation, spirometry values remained unchanged, but capsaicin cough sensitivity was increased and end-tidal CO(2) decreased among the patients, both in comparison to the controls and in comparison to the patients themselves prior to exercise. Exercise-induced dyspnea may be associated with hypocapnia from hyperventilation and increased capsaicin cough sensitivity. The diagnosis of exercise-induced asthma should be questioned when the patient has no signs of bronchoconstriction.
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PMID:Dyspnea from exercise in cold air is not always asthma. 1895 Dec 64

We describe the case of a 61-year-old male patient, in which the search for the cause of chronic respiratory failure, severe pulmonary hypertension and secondary erythrocytosis resulted in a diagnosis of combined pulmonary fibrosis and emphysema (CPFE). This is a unique, recently characterised syndrome with upper-lobe emphysema and pulmonary fibrosis of the lower lungs. The cause is unknown, but one of the main risk factor remains smoking. The patient was a heavy smoker (over 40 pack-years). He complained of dyspnoea on exertion and cough. Physical examination revealed basal crackles and cyanosis. The patient had severe reduction in diffusing capacity, out of proportion to his lung volumes (DLCO 27% of predicted value, FEV1 2.95 l (100%), FVC 4.41 l (118%), FEV1/FVC (66%). The blood gas showed hypoxemia (pO2 37 mm Hg), hypocapnia and respiratory alkalosis. Diagnosis was based on chest computer tomography, which revealed upper lobe emphysema and lower lobe ground glass changes and honeycombing. Severe pulmonary hypertension (SPAP 80 mm Hg) was confirmed by echocardiography and right cardiac catherisation. The patient received long-term oxygen therapy, inhaled corticosteroid and Ca-blocker.
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PMID:[Combined pulmonary fibrosis and emphysema - case report and literature review]. 1946 58

Amyopathic dermatomyositis (ADM) is a clinical subtype of dermatomyositis, characterized by the absence of motor weakness and the presence of normal muscle enzyme levels. ADM is sometimes accompanied by neoplasm or interstitial pneumonia that shows a rapid progressive course both of them are associated with a poor prognosis. A 56-year-old woman with no medical history was referred to the department of medicine because of arthralgia with a remarkable weight loss. She also complained of rapidly progressive dyspnea, cough and photosensitivity. Physical examination on admission showed scaly erythema on the dorsum of the hands (Gottron sign) and periorbital edema with a purplish appearance (heliotropic rash), arthritis, but no muscle weakness. Auscultation of the chest identified audible fine crackles on the lower aspects of both lungs. Results of laboratory findings on admission revealed a lymphopenia. The serum creatine kinase and serum lactate dehydrogenase concentration were normal. IRM muscle and electromyography were normal. Antinuclear antibody was positive 1:80 and anti-Jo-1 antibody and other autoantibodies to specific antigens were all negative. High resolution computed tomographic chest scans also revealed diffuse ground-glass opacities in both lungs with basilar predominance. Arterial blood gas analysis revealed hypoxia and hypocapnia. LBA was not performed because of the deterioration of respiratory symptoms. There was no neoplasm associated. The diagnosis of ADM complicated with ADM rapidly progressive interstitial pneumonia was made. Despite of IV methylprednisolone pulse therapy (1g*day-1 for 3 days) and cyclophosphamide, she died by respiratory failure.
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PMID:[Interstitial pneumonia complicating amyopathic dermatomyositis: a case report]. 1999 56

Bronchial asthma is a chronic inflammatory disorder of the airways in which many cells play a role, in particular mast cells, eosinophils, neutrophils, T-lymphocytes and epithelial cells. In susceptible individuals this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and/or in the early morning. These symptoms are usually associated with variable and extensive limitations of airflow in the bronchi reversible spontaneously or by treatment. It has been shown that restrain of the effectors of stress response participate in the pathogenesis of bronchial asthma. Anger that is not expressed and frustrations may activate the limbic stress pathway. Thus, the released neurotransmitters followed by excitation thus causing psychogenic (mental or emotional) stress. It is also known that emotional stress may be responsible for the exacerbation of asthma. Namely, pronounced emotions cause hyperventilation and hypocapnia inducing bronchospasm. Certain psychological personality features are related to adaptive or inadequate body response to numerous life events. Thus, until the beginning of the last century, bronchial asthma was referred to as asthma nervosa, because clinicians clearly observed the psychological profile of patients with predominant fear of asphyxia and recurrent attacks of paroxysmal dyspnoea. Besides, increased sensitivity, repression of aggressive feelings and expressive empathy have been identified as the most frequent psychological characteristics of asthmatic patients. However, scientists are still far from a full understanding of bronchial asthma pathogenesis. The contribution of psychic factors has become meaningful in the understanding of the development of bronchial asthma. Having in mind that in the majority of patients asthma is a lifelong condition, there is a hope that further investigations of bronchial asthma psychogenesis will improve prevention and treatment of this disease.
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PMID:[The role of psychic factors in the pathogenesis of bronchial asthma]. 2162 67

A 51 year old woman was admitted for night dyspneic attacks and fainting. When hospitalised the patient reported in the previous 10 days dry cough, edema and pain (left leg). The woman's medical history did not show any risk factors for vein thromboembolism, d-dimer dosage appeared increased and arterial blood gas showed hypoxemia and hypocapnia. ECG and chest X-Rays were within normal limits; a chest CT diagnosed pulmonary embolism that was treated with thrombolytic therapy. Venous lower extremity ultrasound detected ilio-femoral and popliteal venous thrombosis and an abdominal CT showed a swollen and fibromatous uterus, obstructing the left iliac vein system. Thrombolytic therapy was effective to for pulmonary embolism and to begin recanalization of the iliac, femoral, and popliteal veins. The patients was sent home in good clinical conditions, with anticoagulant therapy; later the uterine fibroma was treated with hysterectomy.
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PMID:Deep vein thrombosis and pulmonary embolism in a patient affected by uterine fibroids: clinical case. 2324 42

Clinically evident high-altitude pulmonary edema (HAPE) is characterized by severe cyanosis, dyspnea, cough, and difficulty with physical exertion. This usually occurs within 1-2 days of ascent often with the additional stresses of any exercise and hypoventilation of sleep. The earliest events in evolving HAPE progress through clinically silent and then minimally recognized problems. The most important of these events involves an exaggerated elevation of pulmonary artery (PA) pressure in response to the ambient hypoxia. Hypoxic pulmonary vasoconstriction (HPV) is a rapid response with several phases. The first phase in both resistance arterioles and venules occurs within 5-10 min. This is followed by a second phase that further raises PA pressure by another 100% over the next 2-8 h. Combined with vasoconstriction and likely an unevenness in the regional strength of HPV, pressures in some microvascular regions with lesser arterial constriction rise to a level that initiates greater filtration of fluid into the interstitium. As pressures continue to rise local lymphatic clearance rates are exceeded and interstitial fluid begins to accumulate. Beyond elevation of transmural pressure gradients there is a dynamic noninjurious relaxation of microvascular and epithelial cell-cell contacts and an increase in transcellular vesicular transport which accelerate leakage. At some point with further pressure elevation, damage occurs with breaks of the barrier and bleeding into the alveolar space, a late-stage situation termed capillary stress failure. Earlier before there is fluid accumulation, alveolar hypoxia and hyperventilation-induced hypocapnia reduce the capacity of the alveolar epithelium to reabsorb sodium and water back into the interstitial space. More modest ascent which slows the rate of rise in PA pressure and allows for adaptive remodeling of the microvasculature, drugs which lower PA pressure, and those that can enhance fluid reabsorption will all forestall the deleterious early rise of microvascular pressures and diminished active alveolar fluid reabsorption that precede and underlie the development of HAPE.
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PMID:Early hours in the development of high-altitude pulmonary edema: time course and mechanisms. 3221 12


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