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In the elderly a simple low energy fall may result in multiple displaced rib fractures and significant disruption of thoracic function arthritis knee exercises nhs buy 100 mg celecoxib with mastercard. Rapid deceleration is the usual force involved in high-speed motor vehicle accidents and falls from a height arthritis in fingers and toes symptoms 200 mg celecoxib with amex. The degree of external trauma may not fully predict the severity of internal injuries and clinical suspicion of cardiac and vascular trauma should be heightened rheumatoid arthritis stages celecoxib 100mg lowest price. Direct impact by a blunt object can cause localised fractures of the ribs rheumatoid arthritis ketogenic diet 100 mg celecoxib amex, sternum or scapula with underlying lung parenchyma injury, cardiac contusion or pneumothorax. Sudden dynamic anterior-posterior compression forces place indirect pressure on the ribs, causing lateral, mid-shaft fractures. Lateral compression forces applied to the shoulder are common causes of sternoclavicular joint dislocation and clavicle fractures. Massive blunt injury to the chest wall may comprise elements of deceleration, direct impact, and dynamic compression to yield multiple adjacent rib fractures. In this setting, a free-floating segment of the chest wall can move paradoxically with respiration causing ineffective ventilation. Continued static compression of the chest by a very heavy object, which prevents respiration, causes marked increases in pres- In pregnancy, more of the abdominal contents are beneath the front margin of the thoracic rib cage Penetrating wounds of the chest (gunshot or stab wound) may cause comminuted fractures of a rib, with bone fragments driven into the lung substance. The most common manifestation of penetrating trauma to the visceral and parietal pleura is disruption of normal negative intrapleural pressure resulting in pneumothorax. Penetrating wounds cause both direct injury to structures encountered by the weapon and indirect injury. The amount of indirect tissue damage remote from the track of a penetrating object depends on the energy transfer from the object to the tissues as it traverses the tissue. High levels of energy transfer can cause damage at a significant distance from the track. Therefore the extent of internal injuries cannot be judged by the appearance of a skin wound. Blunt forces applied to the chest wall cause injury by three mechanisms: 177 sure within veins of the upper thorax. Not only will it result in worsening respiratory acidosis, it may result in traumatic asphyxia. Compression of the chest in entrapped patients, requires urgent removal of the entrapping force before any further steps in the extrication evolution take place. As well as respiratory insufficiency thoracic trauma may cause haemorrhagic shock due to haemothorax and rarely haemomediastinum. Haemothorax is common in both penetrating and non-penetrating injures to the chest. If the haemorrhage is severe, it may cause not only hypovolaemic shock but also dangerously reduced vital capacity by compressing the lung on the involved side. Persistent haemorrhage usually arises from an intercostal or internal thoracic (internal mammary) artery and less frequently from the major hilar vessels. Bleeding from the lung generally stops within a few minutes, although initially it may be profuse. In some cases haemothorax may come from a wound to the heart or from abdominal structures such as the liver or spleen if the diaphragm has been lacerated. In addition, hypovolaemic shock and haemomediastinum can derive from thoracic great vessel injury that may be result of penetrating or blunt trauma. The most common aetiology is from penetrating trauma; however, the descending thoracic aorta, the innominate artery, the pulmonary veins, and the vena cava are all susceptible to deceleration injury and rupture from blunt trauma. Microscopic disruption occurs at any air-tissue interface where energy is dissipated (of which the lungs have 178 plenty). Injuries involving rapid high energy transfer rather than slow crushing are more likely to cause pulmonary contusion. The concussive loss of vessel integrity results in intraparenchymal and alveolar haemorrhage, decreased pulmonary compliance and increased shunt fraction. Pulmonary contusion frequently manifests itself as hypoxaemia and dyspnoea but this may develop over the first 24-48 hours.

Actually there are a few cases- and these are usually instances of pure motor hemiplegia- in which the evolution of a thrombotic stroke is evenly progressive over a period of days arthritis jar opener purchase celecoxib 100 mg on line. In addition to these several modes of evolution of atherothrombotic stroke vitamins for arthritis in back buy celecoxib uk, thrombotic stenosis or occlusion of certain large vessels may lead instead to the generation of embolic fragments (artery-to-artery embolus) arthritis pain and associates cheap celecoxib 200mg without a prescription, thereby precipitating a new stroke in a region distal to the occlusion zoom for arthritis in dogs buy celecoxib 200mg on-line. This is most likely to occur during the period of clinical fluctuation and active thrombus formation. The most common occurrence of artery-to-artery embolism is with carotid artery thrombosis, the embolus passing to branches of the ipsilateral middle or anterior cerebral artery. With atherothrombotic blockage of the vertebral or lower basilar artery, the embolus orig- inates in the occluded vessel but then proceeds to lodge in the posterior cerebral artery or the top of the basilar artery. In most of the cases of this nature that we have observed, there are additional telltale signs of slight pontine strokes (dysarthria, diplopia, see page 702. Arterial thrombosis is not usually accompanied by headache, but lateralized cranial pain occurs in some cases. Usually the pain is located on one side of the head in carotid occlusion, at the back of the head, or simultaneously in forehead and occiput in basilar occlusion, and behind the ipsilateral ear or above the eyebrow in vertebral occlusion. The headache is less severe and more regional than that of intracerebral or subarachnoid hemorrhage, and there is no stiffness of the neck. The mechanism is unclear; presumably it is related to the disease process or distention of the vessel wall, since it may antedate the other manifestations of the stroke by days or even weeks. As mentioned in the introductory section, hypertension is more often present than not in patients with atherothrombotic infarction. The retinal arteries may show uniform or focal narrowing, increase and irregularity of the light reflex, and arteriovenous "nicking," but these findings correlate with hypertension rather than atherosclerosis. The patient is more often elderly but may be in the fourth decade of life or even younger. Laboratory Findings these have been discussed at various points in the preceding pages and need only be recapitulated briefly. In the laboratory investigation of atherothrombotic infarction, one may employ noninvasive techniques. Ultrasonography will reveal with fair accuracy the cervical and intracranial segments of the internal carotid and vertebrobasilar arteries. While the latter reveals hemorrhage immediately after it occurs, softened tissue cannot be seen until several days have elapsed. This method has to a large extent replaced conventional angiography, which is reserved for cases in which the diagnosis is in doubt. A persistent pleocytosis, however, suggests a chronic meningitis (syphilis, tuberculosis, cryptococcosis), granulomatous arteritis, septic embolism, thrombophlebitis, or a nonvascular process as the cause of vascular occlusion. Serum cholesterol, triglycerides, or both are elevated in many cases, but normal values are not helpful. Course and Prognosis When the patient is seen early in the course of cerebral thrombosis, it is difficult to give an accurate prognosis. One must ask where the patient stands in the stroke process at the time of the examination. No rules have yet been formulated that allow one to predict the early course with confidence. Anticoagulation and thrombolytic therapy may alter the course, as discussed further on. In basilar artery occlusion, dizziness and dysphagia may progress in a few days to total paralysis and deep coma. The course of cerebral thrombosis is so often progressive that a cautious attitude on the part of the physician in what first appears to be a mild stroke is justified. As indicated above, progression of the stroke is due most often to increasing stenosis and occlusion of the involved artery by mural thrombus. In some instances, extension of the thrombus along the vessel may block side branches and hinder anastomotic flow. In the basilar artery, thrombus may gradually build up along its entire Figure 34-17.

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