Asphyxiation: a review Claire Richards and Daniel N Wallis Trauma 2005;7:37-45 Intern 蔡巧榆.

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Presentation transcript:

Asphyxiation: a review Claire Richards and Daniel N Wallis Trauma 2005;7:37-45 Intern 蔡巧榆

Traumatic asphyxia

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 hospital and clinic patients in a 30-month period, of whom had been involed in major accidents.(1930) Dwek reported only one case out of a total of 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.

Thanks for your attention!

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.