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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To date, pulmonary oedema in breath hold divers has only been reported after dives below 50 meters, hypoxaemic syncope being the most common risk. We recently observed a 35-year-old well-trained breath hold diver who was unable to achieve deep inspiration during a high-level competition. After two hours of repeated dives to a depth of 25 meters for approximately 2-minute periods with intermittent recovery the patient developed cough and haemoptysis. The chest X-ray revealed lung images suggestive of intra-alveolar haemorrhage. The patient had taken 1 g of aspirin per os for three days prior to diving. Symptoms subsided spontaneously in 48 hours and one month later all haematology tests were normal except for minimal alteration of platelet aggregation. Pulmonary oedema in breath hold divers is usually attributed to blood shift to the pulmonary circulation related to the lowered intra-thoracic pressure. In our case, oedema was secondary to intra-alveolar haemorrhage favoured by aspirin which should be avoided before breath hold diving.
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PMID:[Intra-alveolar hemorrhage. An uncommon accident in a breath holding diver]. 756 35

The clinical and laboratory features in 62 patients with acute pulmonary embolism were analized. There were 26 males, and 36 females with mean age of 63 +/- 11 (range 37 to 90). The clinical symptoms include: dyspnea (92%), chest pain and/or chest tightness (65%), cough (50%), wheezing (29%), leg swelling (32%), hemoptysis (24%), syncope (18%), leg pain (10%). Clinical signs include: tachypnea (respiratory rate > or = 20 per minute) (79%), tachycardia (37%), deep vein thrombosis (29%), cyanosis (8%), fever (> 38.5 degrees C) (2%). The possible predisposing factors include: immobilization (18%), surgery (5%), deep vein thrombosis, ever(5%), malignancy (5%), pulmonary embolism, ever (3%). Arterial blood gas analysis (while patients breathed room air) revealed mean PH of 7.46 +/- 0.06, mean PO2 of 64.5 +/- 12.1 mmHg, mean PCO2 of 35.3 +/- 4.6 mmHg, mean Alveolar-arterial O2 difference of 36.5 +/- 16.6 mmHg. The electrocardiographic changes include; nonspecific ST-T change (61%), sinus tachycardia (20%), S1Q2T3 pattern (15%), atrial fibrillation (16%), incomplete right bundle branch block (10%), complete right bundle branch block (8%), atrial premature contraction (7%), paroxysmal supraventricular tachycardia (2%). The chest x-ray findings include: cardiomegaly (48%), regional hypovascularity (31%), atelectasis (5%), pleural effusion (5%), wedge-shaped infiltrate (3%), elevated diaphragm (6%). Venous plethysmography was performed in 49 of 62 patients. Of these 49 patients, 28 patients revealed positive finding. Of these 28 patients with positive finding, 18 patients had clinical evidence of deep venous thrombosis. The in-hospital mortality rate was 10% (6/62).
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PMID:[Pulmonary embolism: clinical and laboratory features in 62 patients]. 904 62

Thrombocytosis in post-splenectomy patients with hereditary spherocytosis (HS) is usually not attended by an increased risk of thrombosis. Review of the literature revealed HS in association with pulmonary thrombosis, portal vein thrombosis, and cerebral infarction in two brothers, TTP in an asplenic patient and a patient with corpora cavernosum thrombosis causing segmental priapism. We report a case of a 30-year-old white male with HS who presented with hemoptysis 29 years after splenectomy. Work-up revealed a hypercoagulable state with thrombocytosis and recurrent pulmonary emboli resulting in severe pulmonary hypertension, cor pulmonale, atrial flutter, and syncope.
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PMID:Hereditary spherocytosis, thrombocytosis, and chronic pulmonary emboli: a case report and review of the literature. 942 23

A retrospective study of adults with Eisenmenger syndrome assessed at a tertiary referral center was performed to identify clinical characteristics and establish prognostic determinants. Mortality and cause of death are reported with baseline clinical data correlated with mortality to identify predictors of death. Clinical events during follow-up, including heart failure, atrial arrhythmia, hemoptysis, and syncope were also reviewed. A total of 109 adults with Eisenmenger syndrome (mean +/- SD age 29 +/- 11 years, 43% men) were followed for a median of 6.3 years. Sixty-six patients (61%) had simple cardiac anatomy (13 atrial septal defect, 43 ventricular septal defect, 10 patent ductus arteriosus). The remainder (43 patients) had complex cardiac anatomy (including atrioventricular septal defect, truncus arteriosus, univentricular heart, and transposition of the great arteries). There were 33 deaths and 9 transplantations during follow-up. Median survival was 53 years. Multivariate Cox regression analysis identified age at presentation (hazard ratio [HR] 0.90), supraventricular arrhythmia (HR 3.44), precordial electrocardiogram voltage (HR 1.61/mV increase), and poor New York Heart Association functional class (HR 2.60) as independent predictors of mortality. There is a large variation in the life expectancy for adults with Eisenmenger syndrome. Baseline characteristics associated with increased mortality include younger age at presentation (associated with complex anatomy), functional class, supraventricular arrhythmia, and an electrocardiogram index for right ventricular hypertrophy.
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PMID:Determinants of survival and length of survival in adults with Eisenmenger syndrome. 1049 38

PRESENTING FEATURES: A 53-year-old man who had human immunodeficiency virus (HIV) presented to the Johns Hopkins Hospital with a 3-month history of increasing dysphagia, cough, dyspnea, chest pain, and an episode of syncope. His past medical history was notable for oral and presumptive esophageal candidiasis that was treated with fluconazole 6 months prior to presentation. Three months prior to presentation, he discontinued his medications, and his symptoms of dysphagia recurred. During that time he developed intermittent fevers and chills, progressively worsening dyspnea on exertion, and a cough productive of white sputum. He also reported a 40-lb weight loss over the past 3 months. On the day prior to presentation, he had chest pain and shortness of breath followed by weakness, dizziness, and a brief syncopal episode. He denied orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, jaundice, hemoptysis, hematemesis, melena, hematochezia, or diarrhea. There was no history of alcohol use, and he stopped smoking tobacco approximately 1 month previously. He smoked cocaine but denied injection drug use. The patient had never been on antiretroviral therapy and had never had his CD4 count or viral load measured. On physical examination, the patient was a thin, cachectic man who appeared older than his stated age. His vital signs were notable for blood pressure of 102/69 mm Hg, resting tachycardia of 102 beats per minute, resting oxygen saturation of 92% on room air, normal resting respiratory rate, and a temperature of 38.1 degrees C. His oropharynx was clear, with no signs of thrush or mucosal ulcers. His pulmonary examination was notable for diminished breath sounds in the lower lung fields bilaterally. Cardiac, abdominal, and neurologic examinations were normal. His skin was intact, with no visible petechiae, rashes, nodules, or ulcers. Laboratory studies showed a total white blood cell count of 3.2 x 10(3)/microL, with a total lymphocyte count of 330/microL, hematocrit of 30.2%, a serum sodium level of 129 mEq/L, and a serum lactate dehydrogenase level of 219 IU/L. The patient had an absolute CD4 count of 8 cells/mm3 and a HIV viral load of 86,457 copies/mL. His arterial blood gas on room air had a pH of 7.51, a PCO2 of 33 mm Hg, and a PO2 of 55 mm Hg. Electrocardiogram and serial serum cardiac enzymes were normal. A chest radiograph showed bilateral upper lobe patchy infiltrates with left upper lobe consolidation. Computed tomographic (CT) scan of the chest with contrast showed bilateral ground glass infiltrates with focal consolidation (Figure 1) and no evidence of pulmonary embolism. Induced sputum was negative for Pneumocystis carinii, fungi, or acid-fast bacilli. A bronchoalveolar lavage was performed. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. Diagnosis: P. carinii pneumonia and primary pulmonary sporotrichosis. 1533 85

Chronic thromboembolic pulmonary hypertension (CTEPH), a disease associated with considerable morbidity and mortality, is the consequence of unresolved thromboembolic occlusion in pulmonary vasculature. CTEPH was considered a rare disease occurring in 0.1-0.5% of patients with pulmonary emboli who survive. Recently, a much higher incidence was reported and some risk factors such as a previous pulmonary embolism (PE), an idiopathic form of PE and the severity of perfusion defect at the time of diagnosis have been identified. Exertional dyspnea is the main symptom at the beginning of the disease while later on patients may suffer from syncope related to low cardiac output or hemoptysis as a consequence of high pulmonary artery pressure. In suspected patients, a confirmation of pulmonary arterial hypertension should be ascertained at transthoracic echocardiography. Then the obstructive nature of the disease may be revealed by ventilation-perfusion lung scan but is better described at pulmonary angiography. Computed tomography scan may be useful to rule out confounding disorders. To prevent recurrences, long-term oral anticoagulants to maintain an INR between 2.5 and 3.5 (target 3.0) are indicated. Treatment of severe CTEPH is essentially surgical (thromboendarterectomy). This procedure may be difficult when distal branches of pulmonary vascular tree are involved. In selected cases, alternative therapies may be the arterial pulmonary vessel angioplasty and lung transplantation.
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PMID:From acute pulmonary embolism to chronic thromboembolic pulmonary hypertension. 1627 Apr 75

The coughing paroxysms of patients with cystic fibrosis may occasion neurological symptoms. Although cough syncope is well-known, and is associated with headache and paralysis, a migrainous mechanism has not been reported. We reviewed the medical records, autonomic testing results, and responses to treatment in two cystic fibrosis patients with similar presentations of cough-induced impairment of consciousness followed by headache and paralysis. A 24-year-old woman and an unrelated 38-year-old man, both with cystic fibrosis, developed post-tussive neurologic deficits. Both patients reported infrequent dramatic spells, always preceded by major hemoptysis, and associated with left-sided paralysis, transient blindness, nausea, and severe pulsating headaches. Autonomic testing demonstrated only postural tachycardia and a near-vasodepressor episode in the woman, and mild, generalized sympathetic dysfunction in the man. Treatment for presumptive migraine with aura with verapamil nearly eradicated symptoms in both patients. Discontinuation of verapamil in the woman was associated with symptom recurrence and a stroke, with significant persistent residual left hemiparesis. In conclusion, cough-induced neurologic deficits were previously reported with cystic fibrosis, without clear understanding of the mechanism of impairment of consciousness. Based on the hemiparesis, nausea, and throbbing headache, which repeatedly followed the events in both patients, and based on the response to verapamil, we hypothesize a migrainous mechanism in both of our patients. The pathophysiology that links the hemoptysis to the spells deserves further investigation.
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PMID:Cough-induced hemiplegic migraine with impaired consciousness in cystic fibrosis. 1637 53

Medical observations are reported from an eight-day world championship breath-hold diving competition involving 57 participants. The deepest dive was to 75 metres, and the longest breath-hold time exceeded 9 minutes. There were 35 diving-related adverse events witnessed or reported, including transient loss of motor control due to hypoxia, syncope during ascent, hemoptysis, and pulmonary edema. All events occurred in healthy individuals, and resolved without apparent sequelae. There was no relationship between symptoms and depth. The medical implications of these adverse events are discussed. Despite the inherent risks of the sport, established organizational procedures for competitive breath-hold diving maintain a high degree of safety.
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PMID:Adverse events in competitive breath-hold diving. 1660 57

Cyst hydatid disease (CHD) can be localized in every organ and frequently seen in Turkey. Twenty weeks pregnant woman was admitted with hemoptysis and dyspnea. Chest X-ray revealed bilateral homogeneous dansities. We planned to end pregnancy or follow until term, as diagnosis of CHD. The patient refused delivery. Eleven months later she was admitted with haemoptysis and syncope. Chest X-ray showed cavitary lesion, pleural effusion, pneumothorax in right lung and another cavitary lesion in left. Tube thoracostomy performed with the diagnosis of perforated cyst hydatid (CH) and the patient operated. CH may enlarge in pregnancy. Cyst rupture can cause anaphylactic shock and hemoptysis. Pregnancy and CHD occur occasionally together and there is no consensus about treatment.
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PMID:[Pregnancy and hydatid cyst]. 1833 Jul 62

A large proportion of patients with congenital heart disease (CHD), in particular those with relevant systemic-to-pulmonary shunts, will develop pulmonary arterial hypertension (PAH) if left untreated. Persistent exposure of the pulmonary vasculature to increased blood flow, as well as increased pressure, may result in pulmonary obstructive arteriopathy, which leads to increased pulmonary vascular resistance that, if it approaches or exceeds systemic resistance, will result in shunt reversal. Eisenmenger's syndrome, the most advanced form of PAH associated with CHD, is defined as CHD with an initial large systemic-to-pulmonary shunt that induces severe pulmonary vascular disease and PAH, with resultant reversal of the shunt and central cyanosis. The histopathological and pathobiological changes seen in patients with PAH associated with congenital systemic-to-pulmonary shunts, such as endothelial dysfunction of the pulmonary vasculature, are considered similar to those observed in idiopathic or other associated forms of PAH. A pathological and pathophysiological classification of CHD with systemic-to-pulmonary shunt leading to PAH has been developed that includes specific characteristics, such as the type, dimensions and direction of the shunt, extracardiac abnormalities and repair status. A clinically oriented classification has also been proposed. The prevalence of PAH associated with congenital systemic-to-pulmonary shunts in Western countries has been estimated to range between 1.6 and 12.5 cases per million adults, with 25-50% of this population affected by Eisenmenger's syndrome. Clinically, Eisenmenger's syndrome presents with multiple organ involvement, with progressive deterioration of function over time. The signs and symptoms of Eisenmenger's syndrome in the advanced stages include central cyanosis, dyspnoea, fatigue, haemoptysis, syncope and right-sided heart failure. Survival of patients with Eisenmenger's syndrome is clearly less than that of the general population, but appears to be better than that of patients with idiopathic PAH in a comparable functional class. The treatment strategy for patients with PAH associated with congenital systemic-to-pulmonary shunts and, in particular, those with Eisenmenger's syndrome is based mainly on clinical experience rather than being evidence based. General measures include recommendations for physical activity, pregnancy, infections, air travel, exposure to high altitudes and elective surgery, and that psychological assistance be provided as necessary. Phlebotomies are required only when hyperviscosity of the blood is evident, usually when the haematocrit is >65%. The use of supplemental oxygen therapy is controversial and it should be used only in patients in whom it produces a consistent increase in arterial oxygen saturation. Oral anticoagulant treatment with warfarin can be initiated in patients with pulmonary artery thrombosis and absent, or only mild, haemoptysis. The following three classes of drugs targeting the correction of abnormalities in endothelial dysfunction have been approved recently for the treatment of PAH: (i) prostanoids; (ii) endothelin receptor antagonists; and (iii) phosphodiesterase-5 inhibitors. The efficacy and safety of these compounds have been confirmed in uncontrolled studies in patients with PAH associated with corrected and uncorrected congenital systemic-to-pulmonary shunts, as well as in patients with Eisenmenger's syndrome. One randomized controlled trial reported favourable short- and long-term outcomes of treatment with the orally active dual endothelin receptor antagonist bosentan in patients with Eisenmenger's syndrome. Lung transplantation with repair of the cardiac defect or combined heart-lung transplantation are options for Eisenmenger's syndrome patients with a poor prognosis. A treatment algorithm based on the one used in the treatment of PAH patients is proposed for patients with PAH associated with corrected and uncorrected congenital systemic-to-pulmonary shunts and Eisenmenger's syndrome.
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PMID:Management of pulmonary arterial hypertension associated with congenital systemic-to-pulmonary shunts and Eisenmenger's syndrome. 1848 98


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