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Traumatic asphyxia: an indicator of potentially severe injury in trauma
Copyright ELSEVIER
lt~jury Vol. 27, No. 10, pp. 746-749, 1996 0 1997 Elsevier Science Ltd. All rights reserved Printed in Great Britain 0020-1383/96 $15.00 + 0.00
PII: SOO20-1383(96)00113-l
Traumatic asphyxia: an indicator severe injury in trauma J. R. Dunne’,
of potentially
G. Shaked2 and M. Golocovsky”
‘Department of Surgery, National Naval Medical Center, Bethesda, MD, USA and 2Department of Surgery, Washington Hospital Center, Washington DC, USA
Injury, Vol. 27, No. 10, 746-749,1996
of the abdomen and subclavian veins. Ophthalmological examination revealed bilateral subconjunctival haemor-
Introduction
rhages and ocular hypertension. The patient was admitted for observation and discharged on the following day. He was noted to have complete recovery of all clinical signs
Ollivier, in 1837, while doing autopsies of people trampled by crowds in Paris, noted a complex of craniocervical cyanosis, subconjunctival haemorrhage, and cerebral vascular engorgement and coined the term ‘masque ecchymotic”. In 1900, Perthes’ gave a more complete description of this syndrome to include mental dullness, hyperpyrexia, haemoptysis, tachypnoea, and contusion pneumonia2. Since then others have further defined this syndrome, documenting petechiae of the mucous membranes, epistaxis, oesophageal haemorrhage, haematemesis, microscopic haematuria, albuminuria, spinal-cord muscle paralysis, peripheral nerve damage, amnesia and convulsions describing what is now known as ‘traumatic asphyxia”,‘. Traumatic asphyxia is an unusual syndrome caused by a crush-type injury to the chest or upper abdomen and can be an indicator of severe injury. We describe two cases of traumatic asphyxia as well as an updated review of the literature.
Case reports cnse1 A 53-year-old Caucasian man was injured while working on his automobile. The jack apparently slipped, pinning his anterior chest under the vehicle. Extrication time was longer than 1 h, after which the patient was transported to a level 1 trauma centre. On arrival, he was awake and alert with a Glasgow Coma Scale of 15, breathing spontaneously and had a blood pressure of 1701104 mmHg, a heart rate of 74 and a respiratory rate of 12. The patient was complaining of chest pain and bilateral eye pain. A physical examination revealed significant bilateral subconjunctival haemorrhages, cyanosis extending from the nipple line superiorly to include the entire face, and distended neck veins bilaterally (Figure 1). A chest X-ray revealed no evidence of rib fractures or pneumothorax. Cervical spine X-rays were normal as was a computed tomography (CT) scan of the head. A cardiac contusion work-up was also normal as were ultrasound examinations
during follow-up 1 week later. cLL5Y? 2 A 41-year-old
Caucasian man was run over by an industrial
crane and sustaineda crush injury to his anterior abdomen and pelvis. He did not lose consciousness and was awake and alert upon arrival at a level 1 trauma centre. He complained of abdominal, pelvic and left lower-leg pain. His vital signsincluded a blood pressureof 166/87mmHg,
a heart rate of 96, a respiratory rate of 20 and a temperature of 37.O”C. Physical examination revealed cyanosis with bilateral distension of the jugular (Figure
facial veins
2). Bilateral subconjunctival haemorrhages were
noted. The tympanic membranes were intact without evidence of haemotympanum. There was no cyanosis of the chest wall and his lungs were auscultated and found to be clear bilaterally. Cardiac examination was normal. Abdominal examination was significant for a large diffuse ecchymosis/abrasion over the anterior abdominal wall with peritoneal signs (Figure 2). The pelvis was grossly unstable with blood noted at the meatus and there was a deformity of the left thigh with distal pulses present. A chest X-ray showed no evidence of pneumothorax or fractured ribs. Further X-rays revealed an open-book pelvic fracture, a right navicular fracture dislocation and a midshaft left femur fracture. A retrograde urethrogram and cystogram were normal. Transoesophageal echo revealed no abnormalities. An abdominal ultrasound scan revealed no free fluid in the abdomen or the pericardium. The patient was taken to the operating room where an exploratory laparotomy revealed extensive destruction of the anterior abdominal wall without evidence of intraperitoneal injury. His left femur was rodded by orthopedics intra-operatively. The patient’s hospital course was complicated by a left popliteal vein thrombosis which was treated by standard heparinization and an Enterobmfer pneumonia treated with appropriate antibiotics. The patient was transferred to a rehabilitation facility on the 7th hospital day.
Case reDorb
Discussion Traumatic asphyxia is classically considered to be a rare condition. Laird and Borman documented only seven cases from 107000 hospital and clinic patients5 of whom over 75000 were involved in major accidents. Dwek reported only a single case out of 18500 accident victim9. The true incidence of this condition, however, cannot be accurately stated
1. Patient with a, cyanosis extending from the nipple line superiorly, and b, facial cyanosis with distended neck veins all secondary to a crush injury to the chest.
Figure
747
because many cases either go unrecognized and/or unreported. The mechanism of traumatic asphyxia is usually caused by a severe crush injury to the chest or upper abdomen. The most common cause is from road traffic accidents (RTAs). Sklar and Baack’ reported that 14 out of 35 traumatic asphyxia cases over a 5-year period were secondary to RTAs. Most of these injuries resulted from the patient being ejected from the vehicle and then crushed as it rolled over them’. Other causes include patients being trapped under vehicles while working on them, as in our first case, or being crushed by construction vehicles or falling debris as in our second case8. It has occurred once in a deep-sea diver9 and in persons who were unsuccessfully hangedlO. Less pronounced manifestations of traumatic asphyxia have appeared in patients with epileptic seizures, whooping cough, violent vomiting, bronchial asthma or following difficult deliveries6,1’-‘4. The amount of weight has varied anywhere from 18.5 lb/in2 in a deep-sea diver to over 1600 pounds (728 kg) from a construction crane’,‘5. In most instances, the maximal pressure is sustained at the moment of injury. The exact pathophysiology of traumatic asphyxia is not completely understood. It is generally believed that following a severe crush injury to the chest or upper abdomen a positive pressure is transmitted to the mediastinum. This results in blood being forced out of the right atrium and into the valveless innominate and great veins of the head and neck. This back pressure is transmitted to the capillaries of the head and neck, which become engorged with blood and result in minor haemorrhages producing the petechiae often seen l6. Capillary atony and dilation result in stasis of blood. If there is no counterpressure, the blood remains stagnant, desaturates, and produces the characteristic facial colour changes17. It is interesting to note that the characteristic colour changes fail to appear under points of constriction such as collar bands, head bands and suspenders. This is thought to occur secondary to the counterpressure applied to the skin preventing overdistension of these capillaries and veinP. Numerous animal studies have been done to reproduce experimentally this condition. Some characteristic signs have been reproduced by occluding the superior vena cava in dogs” but compression of the chest alone has failed to be effective”. Williams et al.” hypothesized and later proved that airway obstruction after deep inspiration and just before compression would produce a marked and rapid rise in jugular pressure and a reversal of venous flow with capillary stasis or rupture producing the typical ecchymotic rash that characterizes the syndrome. The study showed that in the ‘moment of impending disaster’ individuals reflexively take a deep breath, hold it and brace themselves thereby greatly increasing the intrathoracic pressure before the compressive episode3. The vast majority of signs of traumatic asphyxia are confined to the upper torso. The lower torso is often spared, and it used to be thought that the series of valves in the venous system protected it from injury. Thompson and co-worker? found, however, that valves could only play a limited role in
748
Injury:
International
Journal
of the Care of the Injured
Vol. 27, No. lo,1996
2. Patient with a large abdominal ecchymcsis and profound facial cyanosis secondary to a crush injury to the abdomen.
Figure
the protection of venous beds against the very high pressure induced by the compressive episode. They demonstrated that the elevated intra-abdominal pressure during the fear response, along with the compressive force from the injury, could be enough to collapse the inferior vena cava and thereby protect the lower torso from venous injury. Clinically, the most obvious manifestations are the facial oedema and cyanosis combined with the ecchymotic haemorrhages of the face and upper chest as was seen in both our representative cases. These characteristics usually increase in intensity over the first few hours but then gradually subside over days to weeks. Other manifestations include subconjunctival haemorrhages, periorbital oedema is seen in approxiand ecchymosis 21. Exophthalmos mately 20 per cent of patients and is believed to be the result of haemorrhage, congestion and oedema in the orbit”. Proptosis and diplopia have also been reported and are thought to be due to traumatic displacement of the orbital fat23. Visual loss has also been reported to occur”. Life-threatening injuries to the pulmonary, cardiac and gastrointestinal systems as well as orthopaedic injuries may occur. Associated pulmonary injuries can include pulmonary contusions, flail chest, pneumothorax and lacerations of the lung25. Despite the similar mechanisms of deceleration and thoracic compression, blunt cardiac injuries are rarely reported but have none the less occurred. There have been isolated reports of coronary artery thrombosis, cardiac rupture and myocardial contusion associated with traumatic asphyxiaZfZ7. Liver and splenic lacerations have also been reported to occur with traumatic asphyxia caused by blunt abdominal injuries as has gastrointestinal haemorrhage7. With severe thoracoabdominal compressive forces as seen in traumatic
asphyxia, unstable pelvic fractures can also be a significant contributor to mortality7. Life-threatening central nervous system injuries may also occur. Neurologically, the syndrome initially presents with agitation, restlessness and disorientatior?. Other more severe neurological injuries include loss of consciousness in up to 40 per cent of patients, prolonged confusion, and seizures. The proposed mechanism for the first two includes a combination of cerebral hypoxia, ischaemia, and venous hypertension, which leads to cerebral dysfunctions. These neurological manifestations usually resolve within 24-48 h3. Rarely will intracranial haemorrhages be found even in fatal cases. This is most likely due to the rigid structure of the cranium, which resists the sudden increase in venous pressure, and to the large venous sinuses in the base of the brain which dampen its transmission16. The diagnosis should be evident from the history and physical examination. Superior vena cava syndrome can closely mimic the clinical features of traumatic asphyxia and needs to be excluded. This was the leading diagnosis in both of our patients before the findings of normal venous pressure in the subclavian and jugular veins and normal chest X-rays. Basilar skull fractures may also be confused with traumatic asphyxia. Both conditions may present with subconjunctival haemorrhages, periorbital ecchymosis and epistaxis? It should be emphasized that skull fractures are rare in traumatic asphyxia because the force of compression is usually directed at the chest or upper abdomen and not the skull. Although the clinical presentation is usually straightforward, the possibility of associated severe injuries mandates a diagnostic effort to rule out such injuries. This effort should include a CT scan of the head, duplex ultrasound of the venous system in the
Case reports
neck and upper extremities, echocardiogram and abdominal and pelvic CT scans. The treatment of traumatic asphyxia is generally supportive in nature and should be directed toward the associated injuries such as pulmonary contusions, pneumothoraces, myocardial contusions, intraabdominal injuries, skeletal fractures and neurological injuries. Because the mechanism of injury is a crush-injury related to massive compression, syndrome needs to be ruled out (as was seen in our second case where a large area of the abdominal wall was damaged) and to prevent its sequelae with fluids, mannitol and bicarbonate if needed. Rapid administration of oxygen with effective ventilation is the mainstay of treatment along with elevation of the head of the bed. If the patient survives the crush injury initially, the prognosis is excellent. Approximately 90 per cent of patients surviving after 1 h will recover’“,‘R. In 116 patients with traumatic asphyxia that survived the crush injury, 104 recovered, whereas 12 eventually died from associated injuries and subsequent infections5. These same factors will determine the rapidity and extent of recovery”,29. In conclusion, traumatic asphyxia can be easily diagnosed and treated when present by itself. The challenge occurs when traumatic asphyxia is associated with other injuries. In these situations, successful management depends on aggressive identification and treatment of these associated injuries. The physician needs to first have a heightened awareness of the potential injuries involved. Secondly, these potential injuries need to be ruled out by standard radiographic and laboratory tests as dictated by the physical assessment. These injuries need to be treated to avoid the inherent morbidity and mortality associated with them.
References 1 Ollivier d.-A. Relation medicale des evenements survenus au Champs-de-Mars le 14 juin 1837. Ann d’Hyg 1837;18: 485. 2 PerthesG. Uber Druckstawing. Dtsck Z Ckirurg 1900; 55: 384. 3 Williams JS, Minken SL and Adams JT. Traumatic asphyxia reappraised.Ann Surg 1968;167:384. 4 JonesMJ and JamesEC. The managementof traumatic asphyxia. J Trauma 1976; 16: 235. 5 Laird WR and Borman MC. Traumatic asphyxia. Surg GynecolObstet1930;50: 578. 6 Dwek J. Ecchymotic mask.I Int Co11 Surg 1946;9: 257. 7 Sklar DP and Baack B. Traumatic asphyxia in New Mexico: a five-year experience.Am J Emerg Med 1988; 6: 219. 8 Jongewaard WR, Cogbill TH and Landercasper J. Neurologic consequences of traumatic asphyxia. J Trauma 1992; 32: 28.
9 Green TM. Traumatic asphyxia. Surg Gynecol Obstet 1922;35: 122. 10 Stickney JM and Hagedorn AB. Chest injuries and traumatic asphyxia. Proc Staff Meet Mayo Clin 1944; 19: 207. 11 Fred HL and Chandler FW. Traumatic asphyxia. Am J Med 1960;29: 508. 12 Alexander EG. A case of stasiscyanosis following an epileptic seizure, stimulating traumatic asphyxia. Ann Surg 1909;49: 762. 13 Robertson LB. Traumatic asphyxia with report of six cases.GunMed Assoc J 1914;4: 501. 14 Bolt RA. Traumatic asphyxia, with report of a case.C/ezle Med J 1908;7: 647. 15 Parker FJ. Optic atrophy from traumatic asphyxia, with report of a case.Arch Opktkalmol 1911;40: 159. 16 Ghali GE and Ellis E. Traumatic asphyxia: report of a case.J Oral Maxillofuc Surg 1989;47: 867. 17 Lowe L, Rapini RP and Johnson TM. Traumatic asphyxia. J Am Acad Dermatol 1990;5: 972, 18 B&&in JG.Traumatic asphyxia. Lancet 1941;ii: 333. 19 Reichert FL and Martin JW. Traumatic asphyxia; experimental and clinical observationswith a report of a case with concomitant paraplegia.Ann Surg 1951; 134: 361. 20 Thompson A, Illescas FF and Chiu RC. Why is the lower torso protected in traumatic asphyxia? A new hypothesis.Ann ThoracSurg 1989;47: 247. 21 Lee MC, Wong SSand Chu JJ.Traumatic asphyxia. Ann Tkoruc Surg. 1991;51: 86. 22 Heuer GJ. Traumatic asphyxia; with especialreference to its ocular and visual disturbances.Surg Gynecol Obstet 1923;36: 686. 23 Macnab AJ, Baldwin GA and McCormick AQ. Proptosis and diplopia following traumatic asphyxia. Ann Emerg Med 1987;16: 289. 24 Baldwin GA, Macnab AJ and McCormick AQ. Visual loss following traumatic asphyxia in children. J Trauma 1988;28: 557. 25 Newquist MJ and Sobel RM. Traumatic asphyxia: an indicator of significant pulmonary injury. Am J Emerg Med 1990;8: 221. 26 Schiowitz MF, Litchman J and Rizzo TF. Traumatic asphyxia and blunt cardiac injury: case report and selectedreview. Am J Emerg Med 1991;9: 325. 27 Rosato RM, Shapiro MJ and Keegan MJ. Cardiac injury complicating traumatic asphyxia. J Trauma1991;31: 387. 28 Young HM. Traumatic asphyxia. Can Med Assoc J 1929; 21: 570.
29 Dodds ME. Traumatic asphyxia. Am J Surg 1950;79: 748.
Paper accepted 12 June 1996. reprints should be addressed to: Dr Mario Golocovsky, Department of Trauma Services, Washington Hospital Center, 110 Irving Street NW, Washington DC 200010-2975, USA. Requests for
lt~jury Vol. 27, No. 10, pp. 746-749, 1996 0 1997 Elsevier Science Ltd. All rights reserved Printed in Great Britain 0020-1383/96 $15.00 + 0.00
PII: SOO20-1383(96)00113-l
Traumatic asphyxia: an indicator severe injury in trauma J. R. Dunne’,
of potentially
G. Shaked2 and M. Golocovsky”
‘Department of Surgery, National Naval Medical Center, Bethesda, MD, USA and 2Department of Surgery, Washington Hospital Center, Washington DC, USA
Injury, Vol. 27, No. 10, 746-749,1996
of the abdomen and subclavian veins. Ophthalmological examination revealed bilateral subconjunctival haemor-
Introduction
rhages and ocular hypertension. The patient was admitted for observation and discharged on the following day. He was noted to have complete recovery of all clinical signs
Ollivier, in 1837, while doing autopsies of people trampled by crowds in Paris, noted a complex of craniocervical cyanosis, subconjunctival haemorrhage, and cerebral vascular engorgement and coined the term ‘masque ecchymotic”. In 1900, Perthes’ gave a more complete description of this syndrome to include mental dullness, hyperpyrexia, haemoptysis, tachypnoea, and contusion pneumonia2. Since then others have further defined this syndrome, documenting petechiae of the mucous membranes, epistaxis, oesophageal haemorrhage, haematemesis, microscopic haematuria, albuminuria, spinal-cord muscle paralysis, peripheral nerve damage, amnesia and convulsions describing what is now known as ‘traumatic asphyxia”,‘. Traumatic asphyxia is an unusual syndrome caused by a crush-type injury to the chest or upper abdomen and can be an indicator of severe injury. We describe two cases of traumatic asphyxia as well as an updated review of the literature.
Case reports cnse1 A 53-year-old Caucasian man was injured while working on his automobile. The jack apparently slipped, pinning his anterior chest under the vehicle. Extrication time was longer than 1 h, after which the patient was transported to a level 1 trauma centre. On arrival, he was awake and alert with a Glasgow Coma Scale of 15, breathing spontaneously and had a blood pressure of 1701104 mmHg, a heart rate of 74 and a respiratory rate of 12. The patient was complaining of chest pain and bilateral eye pain. A physical examination revealed significant bilateral subconjunctival haemorrhages, cyanosis extending from the nipple line superiorly to include the entire face, and distended neck veins bilaterally (Figure 1). A chest X-ray revealed no evidence of rib fractures or pneumothorax. Cervical spine X-rays were normal as was a computed tomography (CT) scan of the head. A cardiac contusion work-up was also normal as were ultrasound examinations
during follow-up 1 week later. cLL5Y? 2 A 41-year-old
Caucasian man was run over by an industrial
crane and sustaineda crush injury to his anterior abdomen and pelvis. He did not lose consciousness and was awake and alert upon arrival at a level 1 trauma centre. He complained of abdominal, pelvic and left lower-leg pain. His vital signsincluded a blood pressureof 166/87mmHg,
a heart rate of 96, a respiratory rate of 20 and a temperature of 37.O”C. Physical examination revealed cyanosis with bilateral distension of the jugular (Figure
facial veins
2). Bilateral subconjunctival haemorrhages were
noted. The tympanic membranes were intact without evidence of haemotympanum. There was no cyanosis of the chest wall and his lungs were auscultated and found to be clear bilaterally. Cardiac examination was normal. Abdominal examination was significant for a large diffuse ecchymosis/abrasion over the anterior abdominal wall with peritoneal signs (Figure 2). The pelvis was grossly unstable with blood noted at the meatus and there was a deformity of the left thigh with distal pulses present. A chest X-ray showed no evidence of pneumothorax or fractured ribs. Further X-rays revealed an open-book pelvic fracture, a right navicular fracture dislocation and a midshaft left femur fracture. A retrograde urethrogram and cystogram were normal. Transoesophageal echo revealed no abnormalities. An abdominal ultrasound scan revealed no free fluid in the abdomen or the pericardium. The patient was taken to the operating room where an exploratory laparotomy revealed extensive destruction of the anterior abdominal wall without evidence of intraperitoneal injury. His left femur was rodded by orthopedics intra-operatively. The patient’s hospital course was complicated by a left popliteal vein thrombosis which was treated by standard heparinization and an Enterobmfer pneumonia treated with appropriate antibiotics. The patient was transferred to a rehabilitation facility on the 7th hospital day.
Case reDorb
Discussion Traumatic asphyxia is classically considered to be a rare condition. Laird and Borman documented only seven cases from 107000 hospital and clinic patients5 of whom over 75000 were involved in major accidents. Dwek reported only a single case out of 18500 accident victim9. The true incidence of this condition, however, cannot be accurately stated
1. Patient with a, cyanosis extending from the nipple line superiorly, and b, facial cyanosis with distended neck veins all secondary to a crush injury to the chest.
Figure
747
because many cases either go unrecognized and/or unreported. The mechanism of traumatic asphyxia is usually caused by a severe crush injury to the chest or upper abdomen. The most common cause is from road traffic accidents (RTAs). Sklar and Baack’ reported that 14 out of 35 traumatic asphyxia cases over a 5-year period were secondary to RTAs. Most of these injuries resulted from the patient being ejected from the vehicle and then crushed as it rolled over them’. Other causes include patients being trapped under vehicles while working on them, as in our first case, or being crushed by construction vehicles or falling debris as in our second case8. It has occurred once in a deep-sea diver9 and in persons who were unsuccessfully hangedlO. Less pronounced manifestations of traumatic asphyxia have appeared in patients with epileptic seizures, whooping cough, violent vomiting, bronchial asthma or following difficult deliveries6,1’-‘4. The amount of weight has varied anywhere from 18.5 lb/in2 in a deep-sea diver to over 1600 pounds (728 kg) from a construction crane’,‘5. In most instances, the maximal pressure is sustained at the moment of injury. The exact pathophysiology of traumatic asphyxia is not completely understood. It is generally believed that following a severe crush injury to the chest or upper abdomen a positive pressure is transmitted to the mediastinum. This results in blood being forced out of the right atrium and into the valveless innominate and great veins of the head and neck. This back pressure is transmitted to the capillaries of the head and neck, which become engorged with blood and result in minor haemorrhages producing the petechiae often seen l6. Capillary atony and dilation result in stasis of blood. If there is no counterpressure, the blood remains stagnant, desaturates, and produces the characteristic facial colour changes17. It is interesting to note that the characteristic colour changes fail to appear under points of constriction such as collar bands, head bands and suspenders. This is thought to occur secondary to the counterpressure applied to the skin preventing overdistension of these capillaries and veinP. Numerous animal studies have been done to reproduce experimentally this condition. Some characteristic signs have been reproduced by occluding the superior vena cava in dogs” but compression of the chest alone has failed to be effective”. Williams et al.” hypothesized and later proved that airway obstruction after deep inspiration and just before compression would produce a marked and rapid rise in jugular pressure and a reversal of venous flow with capillary stasis or rupture producing the typical ecchymotic rash that characterizes the syndrome. The study showed that in the ‘moment of impending disaster’ individuals reflexively take a deep breath, hold it and brace themselves thereby greatly increasing the intrathoracic pressure before the compressive episode3. The vast majority of signs of traumatic asphyxia are confined to the upper torso. The lower torso is often spared, and it used to be thought that the series of valves in the venous system protected it from injury. Thompson and co-worker? found, however, that valves could only play a limited role in
748
Injury:
International
Journal
of the Care of the Injured
Vol. 27, No. lo,1996
2. Patient with a large abdominal ecchymcsis and profound facial cyanosis secondary to a crush injury to the abdomen.
Figure
the protection of venous beds against the very high pressure induced by the compressive episode. They demonstrated that the elevated intra-abdominal pressure during the fear response, along with the compressive force from the injury, could be enough to collapse the inferior vena cava and thereby protect the lower torso from venous injury. Clinically, the most obvious manifestations are the facial oedema and cyanosis combined with the ecchymotic haemorrhages of the face and upper chest as was seen in both our representative cases. These characteristics usually increase in intensity over the first few hours but then gradually subside over days to weeks. Other manifestations include subconjunctival haemorrhages, periorbital oedema is seen in approxiand ecchymosis 21. Exophthalmos mately 20 per cent of patients and is believed to be the result of haemorrhage, congestion and oedema in the orbit”. Proptosis and diplopia have also been reported and are thought to be due to traumatic displacement of the orbital fat23. Visual loss has also been reported to occur”. Life-threatening injuries to the pulmonary, cardiac and gastrointestinal systems as well as orthopaedic injuries may occur. Associated pulmonary injuries can include pulmonary contusions, flail chest, pneumothorax and lacerations of the lung25. Despite the similar mechanisms of deceleration and thoracic compression, blunt cardiac injuries are rarely reported but have none the less occurred. There have been isolated reports of coronary artery thrombosis, cardiac rupture and myocardial contusion associated with traumatic asphyxiaZfZ7. Liver and splenic lacerations have also been reported to occur with traumatic asphyxia caused by blunt abdominal injuries as has gastrointestinal haemorrhage7. With severe thoracoabdominal compressive forces as seen in traumatic
asphyxia, unstable pelvic fractures can also be a significant contributor to mortality7. Life-threatening central nervous system injuries may also occur. Neurologically, the syndrome initially presents with agitation, restlessness and disorientatior?. Other more severe neurological injuries include loss of consciousness in up to 40 per cent of patients, prolonged confusion, and seizures. The proposed mechanism for the first two includes a combination of cerebral hypoxia, ischaemia, and venous hypertension, which leads to cerebral dysfunctions. These neurological manifestations usually resolve within 24-48 h3. Rarely will intracranial haemorrhages be found even in fatal cases. This is most likely due to the rigid structure of the cranium, which resists the sudden increase in venous pressure, and to the large venous sinuses in the base of the brain which dampen its transmission16. The diagnosis should be evident from the history and physical examination. Superior vena cava syndrome can closely mimic the clinical features of traumatic asphyxia and needs to be excluded. This was the leading diagnosis in both of our patients before the findings of normal venous pressure in the subclavian and jugular veins and normal chest X-rays. Basilar skull fractures may also be confused with traumatic asphyxia. Both conditions may present with subconjunctival haemorrhages, periorbital ecchymosis and epistaxis? It should be emphasized that skull fractures are rare in traumatic asphyxia because the force of compression is usually directed at the chest or upper abdomen and not the skull. Although the clinical presentation is usually straightforward, the possibility of associated severe injuries mandates a diagnostic effort to rule out such injuries. This effort should include a CT scan of the head, duplex ultrasound of the venous system in the
Case reports
neck and upper extremities, echocardiogram and abdominal and pelvic CT scans. The treatment of traumatic asphyxia is generally supportive in nature and should be directed toward the associated injuries such as pulmonary contusions, pneumothoraces, myocardial contusions, intraabdominal injuries, skeletal fractures and neurological injuries. Because the mechanism of injury is a crush-injury related to massive compression, syndrome needs to be ruled out (as was seen in our second case where a large area of the abdominal wall was damaged) and to prevent its sequelae with fluids, mannitol and bicarbonate if needed. Rapid administration of oxygen with effective ventilation is the mainstay of treatment along with elevation of the head of the bed. If the patient survives the crush injury initially, the prognosis is excellent. Approximately 90 per cent of patients surviving after 1 h will recover’“,‘R. In 116 patients with traumatic asphyxia that survived the crush injury, 104 recovered, whereas 12 eventually died from associated injuries and subsequent infections5. These same factors will determine the rapidity and extent of recovery”,29. In conclusion, traumatic asphyxia can be easily diagnosed and treated when present by itself. The challenge occurs when traumatic asphyxia is associated with other injuries. In these situations, successful management depends on aggressive identification and treatment of these associated injuries. The physician needs to first have a heightened awareness of the potential injuries involved. Secondly, these potential injuries need to be ruled out by standard radiographic and laboratory tests as dictated by the physical assessment. These injuries need to be treated to avoid the inherent morbidity and mortality associated with them.
References 1 Ollivier d.-A. Relation medicale des evenements survenus au Champs-de-Mars le 14 juin 1837. Ann d’Hyg 1837;18: 485. 2 PerthesG. Uber Druckstawing. Dtsck Z Ckirurg 1900; 55: 384. 3 Williams JS, Minken SL and Adams JT. Traumatic asphyxia reappraised.Ann Surg 1968;167:384. 4 JonesMJ and JamesEC. The managementof traumatic asphyxia. J Trauma 1976; 16: 235. 5 Laird WR and Borman MC. Traumatic asphyxia. Surg GynecolObstet1930;50: 578. 6 Dwek J. Ecchymotic mask.I Int Co11 Surg 1946;9: 257. 7 Sklar DP and Baack B. Traumatic asphyxia in New Mexico: a five-year experience.Am J Emerg Med 1988; 6: 219. 8 Jongewaard WR, Cogbill TH and Landercasper J. Neurologic consequences of traumatic asphyxia. J Trauma 1992; 32: 28.
9 Green TM. Traumatic asphyxia. Surg Gynecol Obstet 1922;35: 122. 10 Stickney JM and Hagedorn AB. Chest injuries and traumatic asphyxia. Proc Staff Meet Mayo Clin 1944; 19: 207. 11 Fred HL and Chandler FW. Traumatic asphyxia. Am J Med 1960;29: 508. 12 Alexander EG. A case of stasiscyanosis following an epileptic seizure, stimulating traumatic asphyxia. Ann Surg 1909;49: 762. 13 Robertson LB. Traumatic asphyxia with report of six cases.GunMed Assoc J 1914;4: 501. 14 Bolt RA. Traumatic asphyxia, with report of a case.C/ezle Med J 1908;7: 647. 15 Parker FJ. Optic atrophy from traumatic asphyxia, with report of a case.Arch Opktkalmol 1911;40: 159. 16 Ghali GE and Ellis E. Traumatic asphyxia: report of a case.J Oral Maxillofuc Surg 1989;47: 867. 17 Lowe L, Rapini RP and Johnson TM. Traumatic asphyxia. J Am Acad Dermatol 1990;5: 972, 18 B&&in JG.Traumatic asphyxia. Lancet 1941;ii: 333. 19 Reichert FL and Martin JW. Traumatic asphyxia; experimental and clinical observationswith a report of a case with concomitant paraplegia.Ann Surg 1951; 134: 361. 20 Thompson A, Illescas FF and Chiu RC. Why is the lower torso protected in traumatic asphyxia? A new hypothesis.Ann ThoracSurg 1989;47: 247. 21 Lee MC, Wong SSand Chu JJ.Traumatic asphyxia. Ann Tkoruc Surg. 1991;51: 86. 22 Heuer GJ. Traumatic asphyxia; with especialreference to its ocular and visual disturbances.Surg Gynecol Obstet 1923;36: 686. 23 Macnab AJ, Baldwin GA and McCormick AQ. Proptosis and diplopia following traumatic asphyxia. Ann Emerg Med 1987;16: 289. 24 Baldwin GA, Macnab AJ and McCormick AQ. Visual loss following traumatic asphyxia in children. J Trauma 1988;28: 557. 25 Newquist MJ and Sobel RM. Traumatic asphyxia: an indicator of significant pulmonary injury. Am J Emerg Med 1990;8: 221. 26 Schiowitz MF, Litchman J and Rizzo TF. Traumatic asphyxia and blunt cardiac injury: case report and selectedreview. Am J Emerg Med 1991;9: 325. 27 Rosato RM, Shapiro MJ and Keegan MJ. Cardiac injury complicating traumatic asphyxia. J Trauma1991;31: 387. 28 Young HM. Traumatic asphyxia. Can Med Assoc J 1929; 21: 570.
29 Dodds ME. Traumatic asphyxia. Am J Surg 1950;79: 748.
Paper accepted 12 June 1996. reprints should be addressed to: Dr Mario Golocovsky, Department of Trauma Services, Washington Hospital Center, 110 Irving Street NW, Washington DC 200010-2975, USA. Requests for