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1/10. An unusual complication of tapping a ventriculoperitoneal shunt.

    A case is reported describing a complication of an unsuccessful attempt to aspirate the reservoir of a ventriculoperitoneal shunt system with a suspected shunt infection. This arose due to a misunderstanding of the anatomy of the shunt and resulted in an intracerebral haematoma. The complications of cerebrospinal fluid shunting and the difficulty in the diagnosis thereof are outlined. We discuss the role and method of shunt tapping in diagnosing shunt problems before reviewing the literature describing the rationale. The variation in shunt design is emphasized. Guidelines are then proposed not to dissuade physicians from tapping shunts but to ensure that the procedure is performed safely and in collaboration with neurosurgical units.
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2/10. Bilateral diaphragmatic paralysis and related respiratory complications in a patient with west nile virus infection.

    The case report is presented of a patient with west nile virus infection and ventilator dependent respiratory failure in whom bilateral diaphragmatic paralysis developed. If the prevalence of west nile virus infection continues to rise, recognition of diaphragmatic paralysis and related respiratory complications will become increasingly important to the pulmonary/critical care physician.
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3/10. Fatal pulmonary mycobacterium abscessus infection in a patient using etanercept.

    A case of fatal pulmonary mycobacterium abscessus infection in a 56-year-old man is reported. The patient had a longstanding history of seropositive, nodular rheumatoid arthritis with severe joint manifestations that had been treated with a regimen of prednisone, leflunomide, and etanercept. He presented to our facility with complaint of productive cough, persistent fevers, pleuritic chest discomfort, and dyspnea at rest. The patient was admitted to hospital, placed in isolation, a left-sided chest tube was inserted (left pneumothorax identified), and sputum acid-fast bacteria stains and cultures were obtained. Fluorochrome stains demonstrated numerous acid-fast bacteria, and M. abscessus was recovered from the culture media. He was treated with a regimen of amikacin, cefoxitin, and clarithromycin. He initially responded well, and was discharged home with this regimen. He remained afebrile with decreased cough and sputum production until 15 days after discharge when he was again admitted to hospital, with acute onset dyspnea and right-sided chest discomfort (right pneumothorax identified). He ultimately expired, due to overwhelming pulmonary infection, 20 days after readmission to hospital. autopsy revealed acid fast bacilli in the setting of numerous, bilateral, necrotic, granulomatous, cavitary pulmonary lesions. Based on its mechanism of action, we propose an association between the use of etanercept, a tumor necrosis factor alpha (TNF-alpha) inhibitor, and this case of fatal pulmonary mycobacterial infection. We recommend that physicians exercise cautious clinical judgment when initiating etanercept therapy in persons with underlying lung disease, especially in communities in which mycobacterial organisms are highly prevalent. We also advise physicians to maintain a high level of vigilance for late onset granulomatous infection in persons using etanercept.
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4/10. Postviral bronchial hyperreactivity syndrome: recognizing asthma's great mimic.

    Although there are no prospective studies regarding the frequency of postviral bronchial hyperreactivity syndrome, it is a common complication of upper and lower respiratory tract viral infections. The respiratory symptoms closely resemble those of asthma, but they are present for only 3 weeks to 3 months following the acute infection phase. Defining the mechanisms of this syndrome may provide insight into the pathogenesis of asthma. Postviral bronchial hyperreactivity syndrome is frequently misdiagnosed and inappropriately managed because many physicians are unfamiliar with this illness. Because of its characteristic history, diagnosis is straightforward when the physician knows what to look for, and response to therapy is excellent. This report presents a case history followed by a review of the proposed mechanisms of bronchial hyperreactivity following viral respiratory infections. The clinical features and criteria for diagnosing postviral bronchial hyperreactivity syndrome are also discussed.
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5/10. Respiratory infections may reflect deficiencies in host defense mechanisms.

    Serious respiratory tract infections are rare in the healthy individual and most of the nuisance morbidity that occurs results from nasopharyngeal viral infections that many people get once or twice a year. The economic impact from these upper respiratory tract infections is appreciable, however, in terms of absenteeism from school or work, but unfortunately there is little that can be done to ward them off in a practical way. pneumonia is an infrequent lifetime experience for most non-smoking adults and when it occurs, unusual circumstances may pertain--a particularly virulent microorganism is in circulation, or perhaps one has been exposed to a newly recognized germ, such as has occurred with legionella species in the past 8 years or so. What protects us the great majority of the time is a very effective network of respiratory tract host defenses. These include many mechanical and anatomical barrier mechanisms concentrated in nose and throat; mucociliary clearance, coughing and mucosal immunoglobulins in the conducting airways and in the air-exchange region of the alveolar structures, phagocytes, opsonins, complement, surfactant and many other factors combine to clear infectious agents. The ability to mount an inflammatory response in the alveoli may represent the maximal and ultimate expression of local host defense. In some way these host defenses are combating constantly the influx of micro-organisms, usually inhaled or aspirated into the airways, that try to gain a foothold on the mucosal surface and colonize it. But many general changes in overall health such as debility, poor nutrition, metabolic derangements, bone marrow suppression and perhaps aging promote abnormal microbial colonization and undermine the body's defenses that try to cope with the situation. It is a dynamic struggle. The departure from normal respiratory health may not be obvious immediately to the patient or to the physician and repeated episodes of infection or persisting symptoms of cough, expectoration and sinus or ear infections may develop before serious assessment of the situation is taken and appropriate diagnosis gotten underway. Obvious explanations for respiratory infections may be apparent and, nowadays, side effects from antineoplastic chemotherapy or immunosuppressive therapy for a variety of diseases that create an immunocompromised host are common. In a few subjects, especially young adults who present with a cumulative history of frequent but mild infections in childhood and youth, a subtle deficiency in host defenses may exist and have been partially masked because of attentive pediatric medical care and prompt use of broad spectrum antibiotics.(ABSTRACT TRUNCATED AT 400 WORDS)
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6/10. The cough and the bedsheet.

    Of 33 patients with psychogenic cough tic, 31 were successfully treated using an unusual reinforced suggestion technique. The cough usually follows an incidental upper respiratory tract infection and persists as a loud paroxysmal barking or honking sound for weeks to months. Paroxysms occur all day but cease with sleep. The diagnosis is often delayed for weeks to months while the patient is exposed to an increasing intensity of diagnostic procedures and therapy. Thirty percent of some 20 patients previously reported in the literature had been hospitalized. The reinforced suggestion technique depends upon the physician's convincing the patient that the persistent cough has weakened the chest muscles, which are now unable to contain the cough, and that a bedsheet tightly wrapped around the chest will provide the necessary support to stop the cough within 24 to 48 hours. The typical patient can produce the cough on command, has an ambivalent response to the prospect of care, is unconcerned about his symptoms, submits willingly to the examination and procedures, and is kept out of school for the duration of the cough. Findings on physical examination are normal except for abnormal gag and corneal reflexes. The gag reflex was depressed in six and absent in 20 of the 31 patients. The corneal reflex was depressed in 16 and absent in 5 of the 31 patients. These abnormal responses help to corroborate the psychogenic etiology. Early recognition of the nonorganic nature of this syndrome will reduce parental anxiety, loss of school time, risk of iatrogenic complications, and unnecessary medical and hospital expense.
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7/10. Serious group A beta-hemolytic streptococcal infections complicating varicella.

    STUDY OBJECTIVE: To alert practicing emergency physicians to an important and possibly increasing relationship between life-threatening group A beta-hemolytic streptococcal (GABHS) infections and children recovering from varicella. DESIGN: A case series of six patients managed from January through March 1993. SETTING: A university-affiliated pediatric specialty emergency department. TYPE OF PARTICIPANTS: Six previously healthy immunocompetent children between 1 and 5 years of age seen in our ED over a nine-week period. RESULTS: Six children had onset of varicella two days to two weeks before developing a serious life-threatening GABHS infection. Children presented with clinical symptoms of invasive GABHS infection with bacteremia (one patient); streptococcal toxic shock syndrome with negative blood culture (two), pneumonia with pleural effusion and streptococcal toxic shock syndrome (one), pneumonia with pleural effusion (one), and pyomyositis of the thigh (one). Four of six patients required intensive care admissions and aggressive support of vital signs. All six survived. CONCLUSION: Emergency physicians should be aware of the association between varicella and serious GABHS infections and be prepared to recognize and aggressively manage serious complications should they occur.
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8/10. torsades de pointes induced by erythromycin.

    We describe two patients who develop torsades de pointes in a temporal relationship to the intravenous administration of erythromycin lactobionate in the absence of other drugs or metabolic abnormalities known to cause the arrhythmia. We also review the current literature regarding this topic, including other case histories and the evidence for erythromycin's effect on cardiac tissue. Due to the increasing use of erythromycin in clinical practice, we believe it is important that all physicians be made aware of this potential complication, which was not recognized at our institutions until these patients were seen by one of us (B.G.).
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9/10. delayed diagnosis of acute rheumatic fever in adults: a forgotten cause of febrile polyarthritis.

    Acute rheumatic fever is a nonsuppurative sequela of upper respiratory tract infection with group A streptococci. We describe our recent experience with the diagnosis and management of 3 cases of acute rheumatic fever to highlight the delays that may arise in the diagnosis of this condition. In adults, febrile polyarthritis is the most common presentation of acute rheumatic fever. Increased awareness on the part of the physician is necessary to ensure both prompt and accurate diagnosis of this cause of febrile polyarthritis.
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10/10. Transient diabetes insipidus with elevated serum osmolarity associated with 'benign' febrile illness.

    A 38-year-old physician developed polyuria and hypodipsia four days after the onset of an upper respiratory tract infection. Subsequent investigation showed a concentration defect with dehydration that partially corrected with vasopressin injection (Pitressin) administration compatible with partial central diabetes insipidus (DI). skull roentgenograms, EEG, and lumbar puncture were normal. The polyuria and hypodipsia slowly resolved without treatment. Normal urinary concentration ability was achieved by the 48th day, but a residual elevation in serum osmolarity persisted for one year. review of the literature failed to show previous documentation of transient DI with elevated serum osmolarity from an acute, febrile illness. The mechanism is speculative, but may be related to a subclinical encephalitis. The true frequency of this syndrome and its relationship to the frequent observation of transient polydipsia and polyuria in "benign" febrile illness remains to be determined.
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