Cases reported "Dyspnea"

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1/20. thyroid gland hematoma after blunt cervical trauma.

    Thyroid hematoma is a rare cause of airway obstruction in victims of blunt trauma. The case of a 34-year-old woman who developed orthopnea after a low-energy motor vehicle accident is described. Presenting greater than 24 hours after her accident, the patient noted dysphagia, tracheal deviation, and postural dyspnea. The diagnosis of thyroid gland hematoma was made with a combination of fiberoptic laryngoscopy, cervical computed tomography, and great vessel and carotid angiography. Invasive airway management was not required. The patient underwent a total thyroidectomy and recovered without complications.
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2/20. Persistent left superior vena cava: case report and literature review.

    A persistent left superior vena cava (PLSVC) is the most common thoracic venous anomaly. It is a persistent remnant of a vessel that is present as a counterpart of normal right-sided superior vena cava (SVC) in early embryological development but normally disappears later. Although it can be easily diagnosed by the characteristic chest radiographic appearance of a pulmonary artery catheter (PAC) passed through it after being inserted into the left subclavian or jugular vein, its diagnosis is usually missed by the presence of normal (right) SVC and the passage of the catheter on the right side. Its diagnosis can be confirmed by many noninvasive and invasive tests, or it is incidentally diagnosed at thoracic surgery or autopsy. If it is not associated with other congenital cardiac anomalies, it is usually asymptomatic and hemodynamically insignificant. However, PLSVC has important clinical implications in certain situations. In this article, we describe a patient with bilateral SVC (a normal right SVC and a PLSVC) identified by a PAC in the PLSVC and the pacemaker wires in the right SVC. In addition, we review the literature on prevalence, embryological development, diagnosis, and clinical implications of PLSVC.
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3/20. February 2001: A 74 year old man with a history over 3 months of increasing dyspnea and malaise.

    The February COM: A man of 78 years with idiopathic late-onset cerebellar ataxia developed renal failure in association with a high ESR and positive pANCA. This was complicated by a subclinical spinal subarachnoid hemorrhage which was related to necrotizing inflammation of small leptomeningeal vessels. Renal cortical infarcts were due to similar inflammation in arcuate and interlobular arteries. Spinal subarachnoid hemorrhage is rare and usually due to rupture of an arteriovenous malformation. However, an immunogenic connective tissue disorder should be considered in the differential diagnosis. In this case, the histology and results of an autoantibody screen support a diagnosis of microscopic polyangiitis.
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4/20. Antigen inhalation as a triggering factor in systemic small-sized-vessel vasculitis. Four cases.

    In order to identify small-sized-vessel vasculitis occurring immediately after massive inhalation of particles which could be considered antigenic, we performed a retrospective review of patients who consulted our Department of internal medicine between 1980 and 1998 and were diagnosed as having small-vessel vasculitis that developed immediately after massive exposure to inhaled particles. Four patients, 27 to 55 years old, presented with small-sized-vessel vasculitis (one with Wegener's granulomatosis and three with churg-strauss syndrome) which developed after massive inhalation of particles. Clinical manifestations occurred from a few hours to 10 days after inhalation of diesel fumes, cereal dust, flour or cereal dust and/or pigeon droppings. Three patients remain disease-free 8, 9 and 18 years after discontinuing treatment. One patient remains well after 3 years on low-dose corticosteroids and cyclophosphamide therapy. Our data suggest that primary antigens can cause small-sized-vessel vasculitides. Identifying such etiological factors could improve our understanding of the pathogenesis of systemic vasculitides and prevent relapses due to similar antigenic exposure.
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5/20. Breathless.

    This case presented the scenario of a patient who had severe bronchospasm from an unknown etiology. Further, she had difficulty speaking and denied any past medical history, which made a diagnosis more difficult. Prehospital providers were challenged with determining the differential diagnosis for bronchospasm and hypoxemia. Was the patient experiencing an anaphylactic reaction, acute asthmatic attack or something else? The key here, once again, is conducting a thorough assessment and patient history. Remember, all that wheezes is not asthma; therefore, providers in this case had to determine if the patient was suffering something such as anaphylaxis, asthma, bronchitis, pneumonia or even congestive heart failure (CHF). Typically, anaphylaxis and asthma affect ventilation, not oxygenation, so until the late stages of anaphylaxis or asthma, the patient will have difficulty moving air, but will be oxygenating OK. We understand that many respiratory conditions can cause wheezing, but CHF? Yes: As left ventricular function diminishes and leads to increased pulmonary pressure, serum begins to leak out of the pulmonary vessels and into the interstitial space. As the interstitial pressure increases, it causes narrowing of the bronchioles, and air traveling through the narrowed bronchioles causes the wheezing sound. Fluid may also be leaking out of the pulmonary capillaries and occupying space in the alveolar sacs. When the interstitial pressure is high and the bronchioles continue to narrow, providers may initially hear only the wheezing and not the crackles from the smaller airways. In these conditions, oxygen is not exchanged adequately into the blood, and the patient becomes hypoxemic. Good assessment and patient history will guide the EMS provider to the cause of bronchospasm. For example, does the patient have a history of asthma? If yes, asthma is likely to be the cause. Does the patient have any rash, hives or swelling? If yes, anaphylaxis is likely the cause. Is the patient elderly, and does he/she show pedal edema, JVD, hypoxemia and/or distended neck veins? If yes, CHF may be the cause. [table: see text] There are questions regarding the use of bronchodilators in patients suffering CHF. If a CHF patient is wheezing (bronchospasm), then a beta-2 selective breathing treatment may be appropriate, along with nitrates and diuretics. Oxygenation is the critical problem in CHF, and hypoxemia will continue to worsen cardiac function. Remember, both bronchoconstriction and alveolar sacs filling with fluid will impair oxygenation of the RBCs and ultimately the vital organs. Focused prehospital management of CHF is aggressive in restoring oxygenation. For example, many agencies are now using oxygen, nitrates, ACE inhibitors and CPAP. By better understanding the pathophysiology of respiratory emergencies and their differential diagnosis, we will improve patient outcomes.
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6/20. bone marrow necrosis with dyspnea in a patient with malignant lymphoma and plasma levels of thrombomodulin, tumor necrosis factor-alpha, and D-dimer.

    Non-Hodgkin's lymphoma (peripheral T cell, unspecified, clinical stage IIIEA) was diagnosed in a 54-year-old male. He was treated weekly with chemotherapy consisting of pirarubicin hydrochloride, cyclophosphamide, methotrexate, vincristine sulfate, etoposide, and prednisolone. After 6 weeks of treatment in a state of partial remission, he exhibited sudden dyspnea, chest pain, fever, and drowsiness. The patient had received 100 microg/day of granulocyte colony stimulating factor (G-CSF) for 6 days before the onset. Laboratory data showed an elevated lactate dehydrogenase (LDH) level, leukoerythroblastosis in the peripheral blood, and no decrease in the serum haptoglobin level. There were no findings of acute myocardial infarction or pulmonary thromboembolism. bone marrow specimen showed the characteristic features of necrosis without any signs of the involvement of lymphoma cells. No indications of infections were found. This patient was diagnosed as having bone marrow necrosis (BMN) during the recovery phase of bone marrow with G-CSF treatment after chemotherapy for malignant lymphoma. After conservative therapy, inhalation of oxygen and stopping the administration of G-CSF, all clinical symptoms subsided except that the elevation of LDH continued for 1 month. The plasma level of tumor necrosis factor-alpha (TNF-alpha) was high just after the onset of BMN. The thrombomodulin (TM) level was high just before the onset of BMN and continued to be high for 2 weeks. Cross-linked fibrin degradation products (D-dimer) were also high just after the onset of BMN and continued to be high for 3 weeks after the onset. Although dyspnea is a rare symptom of BMN, it is important to rule out in BMN during the recovery phase of bone marrow with G-CSF treatment after chemotherapy for malignant lymphoma. Activated neutrophils in the small vessels of the lung by G-CSF and microthrombi, suggested by the elevation of D-dimer, may participate in the onset of dyspnea, which is a rare symptom of the onset of BMN.
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7/20. Pulmonary capillary hemangiomatosis associated with primary pulmonary hypertension: report of 2 new cases and review of 35 cases from the literature.

    Pulmonary capillary hemangiomatosis (PCH) is a rare cause of primary pulmonary hypertension characterized by thin-walled microvessels infiltrating the peribronchial and perivascular interstitium, the lung parenchyma, and the pleura. These proliferating microvessels are prone to bleeding, resulting in accumulation of hemosiderin-laden macrophages in alveolar spaces. Here we report 2 cases of PCH with pulmonary hypertension, 1 of them associated with mechanical intravascular hemolysis, a feature previously reported in other hemangiomatous diseases, but not in PCH. Case 2 was diagnosed by pulmonary biopsy; to our knowledge the patient is the second adult to be treated with interferon alpha-2a. review of the literature identified 35 patients with PCH and pulmonary hypertension. The prognosis is poor and median survival was 3 years from the first clinical manifestation. dyspnea and right heart failure are the most common findings of the disease. hemoptysis, pleural effusion, acropachy, and signs of pulmonary capillary hypertension are less common. Chest X-ray or computed tomography scan usually shows evidence of interstitial infiltrates, pulmonary nodules, or pleural effusion. Hemodynamic features include normal wedge pressures. Radiologic and hemodynamic findings are undifferentiated from those of pulmonary veno-occlusive disease but differ from other causes of primary pulmonary hypertension. epoprostenol therapy, considered the treatment of choice in patients with primary pulmonary hypertension, may produce pulmonary edema and is contraindicated in patients with PCH. Regression of lesions was reported in 1 patient treated with interferon therapy and 2 other patients stabilized, including our second patient. PCH was treated successfully by lung transplantation in 5 cases. Early recognition of PCH in patients with suspected primary pulmonary hypertension is possible based on clinical and radiologic characteristics. diagnosis by pulmonary biopsy is essential for allowing appropriate treatment.
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8/20. A case of primary pericardial undifferentiated sarcoma.

    Primary pericardial sarcomas are extremely rare. The authors report a case of a 46-yr-old woman in whom a large mediastinal mass was discovered. The patient presented with cough, dyspnea, and orthopnea. Diagnostic investigations, such as echocardiography, computed tomography, and exploratory thoracotomy provided the evidence of a large mass in the mediastinum, attached by a broad base to the superior portion of the pericardium. A excisional biopsy was performed, and histologic examination of a biopsy specimen showed undifferentiated sarcoma. However, the complete removal of the mass was impossible due to adhesion to the adjacent great vessels. After the completion of the chemotherapy the patient was completely asymptomatic. However, follow-up transesophageal echocardiography showed a residual 3 x 4 cm-sized mass. The patient received the radiotherapy with a total dose of 55 Gy over 6 weeks. At present, there is no evidence of disease progression.
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9/20. hamartoma of the larynx: an unusual cause of upper airway obstruction.

    Hamartomas are rare lesions in the larynx. Both clinical and histopathological findings may be misleading to both the physician and the pathologist in terms of diagnosis. A 51-year-old female with the complaints of nonproductive cough and severe dyspnea lasting for a year was found to have a subglottic, submucosal mass almost totally obstructing the laryngeal lumen. Excisional biopsy was performed under suspensory direct laryngoscopy. Histopathological examination showed numerous, large, distended blood vessels, some of which had prominent thickened walls and mature adipose tissue beneath the surface epithelium. The final diagnosis was hamartoma, but we discussed its validity and other possible identifications in accordance with the literature.
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10/20. Cardiac hydatid cyst rupture as cause of death.

    echinococcosis is a frequent parasitic human infection in sheep-farming areas. It is caused by the larval or the cyst stage of a tapeworm, mainly echinococcus granulosis. humans can be infected by ingesting tapeworm eggs, from which cysts will be developed mostly in the liver and the lung. Cardiac involvement of echinococcosis is rare and its clinical evolution is silent till the complication stage. A young adult died suddenly. The autopsy showed a ruptured hydatid cyst hollowed on the right side of the interventricular septum, protruding in the ventricle. The left pulmonary artery contained white-colored fragments of a membrane, similar to the one found in the right ventricle, associated to small vesicles. All these elements were obstructing this vessel, extending to small pulmonary arterial branches. dissection of the other organs did not show other locations. Microscopic examinations ascertained the diagnosis of echinococcosis. Death was imputed to a right ventricular hydatid cyst rupture with pulmonary artery embolism.
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