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Asphyxiation: a review. Claire Richards and Daniel N Wallis Trauma 2005;7:37-45 Intern 蔡巧榆. Traumatic asphyxia. Incidence and Etiology.
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Asphyxiation: a review Claire Richards and Daniel N Wallis Trauma 2005;7:37-45 Intern 蔡巧榆
Incidence and Etiology • Traumatic asphyxia is a rare condition when considering the numbers of major trauma victims seen in emergency departments, although this may be because many cases are unrecognized or unreported. • Laird and Borman found only seven cased out of 107000 hospital and clinic patients in a 30-month period, of whom 75000 had been involed in major accidents.(1930) • Dwek reported only one case out of a total of 18500 accident victims in an area with heavy military traffic. (1946)
Incidence and Etiology • A heavy load to the thoracoabdominal region, such as being pinned or crushed by a vehicle or piece of heavy machinery is the commonest cause. • In 35 cases of traumatic asphyxia seen over a 5-year period in New Mexico, 14(40%) were due to road traffic accidents where the patient was ejected from the vehicle and then crushed as it rolled over them. • The syndrome has also been described following unsuccessful suicide attempts by hanging, blast injury, asthma attack, diving, epileptic seizures, violent vomiting and difficult obstetric delivery.
Incidence and Etiology • In experiments on guinea pigs and dogs the incidence of death due to traumatic asphyxia is a function of absolute weight and duration of compression. • There is great variation in the amount and duration of application of force required to produce the characteristic featured of this condition, and in some cases to cause death. • Death in cases of prolonged compression is presumably caused by hypoxic cardiac arrest due to complete restriction of respiratory movements.
Clinical features • The skin of the face, neck and upper torso may appear blue-red to blue-black but it blanches. • The discolouration and petechiae are often more pronounced on the eyelids, nose and lips. • These petechiae also usually blanch, and increase in intensity in the first few hours but then fade over days to weeks. • The subconjunctival hemorrhage, which almost always occurs, and is considered to be due to the relative lack of tissue support around this area, fades slowly and disappears.
Clinical features • Exophthalmos occurs in 20% of cases and this also slowly resolves fully. • There may be periorbital edema and ecchymosis. • Other mucous membranes that lack tissue support such as the buccal mucosa, undersurface of the tongue, palate and pharynx commonly show petechiae or ecchymoses. • Epistaxis is often present and hemotympanum has also been described. • Associated injuries include pulmonary, cardiac, neurological, ophthalmic, abdominal and orthopaedic injury.
Clinical features • Pulmonary injuries are those most commonly associated with traumatic asphyxia and are the most serious, including pulmonary contusion, pneumo-and/or hemothorax and lung lacerations. • The most common neurological consequences are transient loss of consciousness and confusion, which may be prolonged but are generally self-limiting. There may also be agitation, disorientation and restlessness.
Clinical features • Abdominal injuries include liver and/or splenic lacerations and gastrointestinal hemorrhage due to blunt abdominal trauma. Diaphragmatic rupture is another complication that has been described. • Transient microscopic hematuria and proteinuria may occur due to increased venous pressure in the kidneys. • Orthopaedic injuries include fracture of the clavicle, long bones, pelvis and vertebrae.
Differential diagnosis • The diagnosis of traumatic asphyxia syndrome is usually evident, based on history and the striking characteristic clinical features. • However, features of SVC obstruction and basilar skull fracture closely resemble the appearances of traumatic asphyxia, in particular the subconjunctival hemorrhages, periorbital ecchymosis, epistaxis and hemotympanum.
Differential diagnosis • However, the history of traumatic injury would rule out SVC obstruction, and skull fractures are very rare in traumatic saphyxia because the force of compression is not applied to the head. • In addition, the venous pressure in the head and neck is normal in traumatic asphyxia after thoracic compression has been relieved, in contrast to patients with SVC obstruction.
Treatment • Management of these patient is supportive, and treatment is aimed at associated injury. • The mainstay of treatment is oxygenation, and elevation of the head of the bed to 30。once the spine has been cleared of injury. • Oxygen has almost no effect, however. On the resolution of the facial discoloration. • Patients should be admitted initially to an ICU for observation.
Treatment • Supportive ventilation may be required of there is significant underlying pulmonary injury, chest wall damage or respiratory depression due to cerebral hypoxia. • If a significant crush injury has been sustained, treatment with fluids, mannitol and bicarbonate must be given as necessary to prevent renal failure secondary to rhabdomyolysis. • Since the probability of associated injury is high, the physical assessment of the patient must be thorough, if other injuries are not to be missed with potentially disastrous consequences.
Prognosis • Long-term follow-up of patients who have survived traumatic asphyxia shows there are no long-term sequelae from the condition itself; morbidity and mortality are from associated injuries. • There are determined by the severity, nature and duration of the compressive force. • The prognosis of those with traumatic asphyxia alone is excellent if the patient survives to reach the emergency department, despite their rather startling appearance. • Approximately 90% of patients without associated injury and surviving one hour after crush injury will recover.