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Traumatic asphyxia
Traumatic Asphyxia Ming-Chung Lee, MD, FICA, Sing-Sieng Wong, MD, Jaw-Ji Chu, MD, Jen-Ping Chang, MD, Pyng-Jing Lin, MD, Ming-Jang Shieh, MD, and Chau-Hsiung Chang, MD Division of Thoracic and Cardiovascular Surgery, Department of Surgery, Chang Gung Memorial Hospital, Taipei, Taiwan, Republic of China
During a 5-year period, we treated 14 cases of traumatic asphyxia. There were 12 male and 2 female patients ranging in age from 2 to 32 years. Most suffered crushing injuries at work or were run over by motor vehicles. Mild to severe cervicofacial cyanosis and petechiae developed in all patients. A fear response was reported by 12 of the patients. Subconjunctival hemorrhage was also found in 12 patients. Nine patients had tachypnea and 7 complained of dyspnea. Most of the patients suffered some associated injuries including 8 head injuries, 7 pulmonary contusions, and 6 cases of blunt abdominal trauma.
Less-associated injuries were rib fractures, brachial and radial nerve injuries, hemothorax, and pneumothorax. The hospital stay ranged from 4 to 28 days (mean, 14 days) and follow-up from 10 to 60 months (mean, 32 months). Treatment for traumatic asphyxia included measurement of arterial blood gases, oxygen supplementation, and intubation with mechanical ventilation. The patients’ recovery conditions were relative to the severity of injury and the associated injuries.
T
department were excluded. There were 12 male and 2 female patients. The ages ranged from 2 to 32 years. Patients were stabilized in the emergency department, including intubation if required, before elucidation of the history. Arterial blood gas measurements, chest roentgenography, and any other indicated studies were then performed. Among our 14 patients, 9 suffered from thoracic, abdominal, or thoracoabdominal crushing injuries at work, 3 were run down by motor vehicles, 1was compressed by a steering wheel, and the final 1 had a crushing force on the right side of the chest. On questioning 12 of our patients reported a fear response just before the crushing. Clinical features of cervicofacial cyanosis and petechiae of the head and neck regions developed in all patients in varying degrees (severe, 4; moderate, 7; mild, 3). Subconjunctival hemorrhage developed in 12 patients. Other commonly noted symptoms were disturbance of consciousness (3), tachypnea (9), and dyspnea (7). Two patients were in shock; 1of them had left diaphragm rupture and the other had multiple long bone fractures. All other patients were hemodynamically stable. Other associated injuries included head injuries in 8 patients, with variable changes in the Glasgow Coma Scale. None had surgical lesions. Six patients had abdominal tenderness with elevation of serum glutamicoxaloacetic transaminase level. Only the patient with the left diaphragmatic rupture with herniation of the stomach and intestine required operation.
he classic syndrome of traumatic asphyxia includes cervicofacial cyanosis, subconjunctival hemorrhage, ecchymosis, and petechiae of the face, usually secondary to blunt trauma (Fig 1). These were first observed by Ollivier [l] in 1837; he termed the syndrome “masque ecchymotique” when noting these characteristic features in a patient trampled to death by crowds in Paris. It was not until 1900 that Perthes [2] made a more extensive review and detailed its pathophysiology and features including mental dullness, hyperpyrexia, hemoptysis, tachypnea, and contusion pneumonia. Since then, there have been a number of series discussing its pathophysiology and mechanisms of injury, but all hypotheses remain controversial. In 1968, Williams and associates [3] suggested the fear response was an important factor in the production of craniofacial petechiae. The fear response is defined as the feeling of impeding doom as the patient realizes he or she is about to be crushed. This is a 4-year review of our experience with and results of cases of traumatic asphyxia.
Material and Methods We retrospectively collected 14 cases of patients who sustained thoracoabdominal compressive injury with clinical features of cervicofacial cyanosis or facial petechiae (Table 1).They were all admitted through our emergency room to our cardiovascular intensive care unit from May 1984 until December 1988. Patients sustaining severe associated injuries who died on arrival in our emergency Accepted for publication Sep 10, 1990. Address reprint requests to Dr Lee, Department of Cardiovascular Surgery, Chang Gung Memorial Hospital, 199, Tun-Hwa North Rd, Taipei, Taiwan, Republic of China. 0 1991 by The
Society of Thoracic Surgeons
(Ann Thorac Surg 2992;52:86-8)
Results The initial arterial blood gas results revealed the lowest oxygen tension levels in the 7 patients who were found to 0003-4975/91/$3.50
Ann Thorac Surg 1991;51:8&8
Fig 1. Prominent features of traumatic asphyxia include cervicofacial cyanosis with multiple petechiae and subconjunctival hemorrhage.
have pulmonary contusions on chest roentgenogram. Four of these patients were intubated for pulmonary care or head injury protection. All other patients were treated with oxygen supplementation alone, and all patients seemed to recover well. The hospital stay varied from 4 to 28 days with a mean of 14 days. The follow-up period ranged from 10 to 60 months with a mean of 32 months. Most patients recovered with no sequelae. The only morbidity was due to associated injuries: 1 patient had subglottic stenosis with a tracheocutaneous fistula after prolonged intubation, and another patient had a radial nerve injury with an incomplete recovery.
Comment In 1866, Tardieu [4] offered the first explanation that “the punctiform ecchymosis of the face, neck and chest are caused by the effort in which resistance to suffocation manifested itself.” Heuter [5] later had two hypotheses: first, a mechanical reflux of blood out of the compressed chest into the valveless veins of the head and neck leading to venular and capillary atony and stasis cyanosis, and second, that contusion of the abdominal sympathetic nerves causes vasodilation of the head and neck region. Bolt [6], in his study, postulated four factors: (1) deep
LEEETAL TRAUMATIC ASPHYXIA
87
inspiration, (2) closure of glottis, (3) thoracoabdominal effort, eg, splinting of thoracic and abdominal musculature, and (4) thoracic or abdominal compression that forces blood into the cervicofacial regions producing venular and capillary stasis. More recently, Reichert and Martin [7] in 1951 in canine experiments found that occlusion of the superior vena cava alone could cause a considerable congestion of the upper extremities and head regions, but they were not able to duplicate the clinical features of traumatic asphyxia. In 1968, Williams and associates [3] concluded that just at the moment of impending disaster, a fear response is practically always present. This fear reflex would lead the patient to take a deep breath, hold it, and brace himself or herself. The closed epiglottis would then enhance greatly the intrathoracic pressure during compression. In 1989, Thompson and co-workers [8] found that valves can only play a limited role in the protection of venous beds against high pressure, but the elevated intraabdominal pressure developed during the fear response followed by an acute abdominal thoracic compression can cause collapse of the inferior vena cava, thereby protecting the lower torso from the venous injury seen in traumatic asphyxia. The striking physical characteristics include multiple punctiform petechiae and bluish discoloration extending over the face, neck, and sometimes the upper part of the chest to the level of nipples anteriorly and approximately to the lower level of trapezius posteriorly. The petechiae practically never reach the elbow laterally. These petechiae usually blanch on pressure and almost always increase in intensity over the first few hours and then gradually fade over days to weeks. Frequently, they are associated with mild to massive subconjunctival hemorrhage, periorbital edema, and ecchymosis. Immediate impairment or loss of vision has also been reported as a result of retinal edema, but may promptly recover within hours or days. Permanent vision loss is very rare. Neurologically, the syndrome initially manifests primarily as agitation, restlessness, and disorientation. Williams and associates [3] suggested these neurological signs may be associated with minor intracranial hemorrhage or cerebral edema. These are usually reversible within 24 hours without any sequelae. In our series, associated injuries were frequently encountered especially involving the brain, thorax, and abdomen. With major pulmonary complications such as severe pulmonary contusion or flail chest, therapy mainly involved respiratory support. In cases of minor chest injury, administration of oxygen therapy by nasal cannula or mask was sufficient. Our experience indicates that patient prognosis depends on the morbidity of associated injuries. The victim may die within minutes due to severe associated injuries, or may need long-term rehabilitation if neurological damage or long bone fractures have been sustained. For those patients with pure traumatic asphyxia syndrome who survive to the emergency room, a full recovery should be expected.
88
Ann Thorac Surg 1991;51:8&3
LEEETAL TRAUMATIC ASPHYXIA
Table 1 , Cases of Traumatic Asphyxia ~~
Patient No.
Age (Y)
Sex
Mechanism
1
32
M
Moderate ME"
BAT
2
24
M
Thoracoabdominal compression Steering-wheel compression
Moderate ME
10
10
M
Mild ME
4
...
24
F
Abdominal compression Chest compression
Multiple ribs fracture, lung contusion, facial laceration BAT
25
...
26
M
Chest compression
Moderate ME
18
...
32
M
Severe ME
13
...
4
M
Thoracoabdominal compression Chest compression
27
Subglottic stenosis
27
M
Chest compression
Moderate ME
16
M
Abdominal compression
Moderate ME
10
2
M
Thoracoabdominal compression
Mild ME
11
18
M
Crush with roller machine
Severe ME, shock
12
4
F
Run down by bus
Mild ME
13
28
M
Run down by bus
Severe ME
14
22
M
Run down by truck
Moderate ME
Left brachial plexus injury Lung contusion with R pneumothorax, R scapular fracture Flail chest BAT, brain edema Head injury, L diaphragm hernia Back 3" burn, brain edema Rib fracture, pulmonary contusion, brain edema Pulmonary contusion, BAT, rib fracture, head injury BAT, R humerus fracture, both femoral fracture Trunk abrasion wound Head injury, trunk abrasion Head injury, pulmonary contusion
Signs and Symptoms
Moderate ME
Severe ME, shock
Associated Injuries
Hospital Stay (d)
Complications
5
...
19 11
...
11
23
R radial nerve palsy
( A m 28
...
12
...
a Moderate ME as in Figure 1; mild ME: petechiae only localized on periorbital and cervical region; severe ME: petechiae become confluent over whole cervicofacial region. 3" = third-degree. ME = masque ecchymotique; BAT = blunt abdominal trauma; AAD = against advice discharge;
References 1. Ollivier d-A. Relation medicale des evenements survenus au Champs-de-Mars le 14 juin, 1837. Ann Hyg 1837;18:485-9. 2. Perthes G. Uber "Druckstawing." Dtsch Chir 1900;55:3%92. 3. Williams JS, Minken SL, Adams JT. Traumatic asphyxia reappraised. Ann Surg 1968;167384-92. 4. Tardieu A. Relation medico-legale de I'accident survenu au pont de la concorde, a Paris, le 15 aout 1866. Pour servir a I'historie de la mort par suffocation. Ann Hyg 1866;2:338.
5. Heuter G. Ueber die Dilatation der Blutgefaesse der Kopfes bei sehweren verletzungen des Unterleibes. Dtsch Chir 1874;4382. 6. Bolt RA. Traumatic asphyxia-report of a case. Cleve Med J 1908;7647-59. 7. Reichert FL, Martin JW. Traumatic asphyxia, experimental and clinical observations with a report of a case with concomitant paraplegia. Ann Surg 1951;134:361-8. 8. Thompson A, Illescas FF, Chiu RC. Why is the lower torso protected in traumatic asphyxia? A new hypothesis. Ann Thorac Surg 1989;47:247-9.
During a 5-year period, we treated 14 cases of traumatic asphyxia. There were 12 male and 2 female patients ranging in age from 2 to 32 years. Most suffered crushing injuries at work or were run over by motor vehicles. Mild to severe cervicofacial cyanosis and petechiae developed in all patients. A fear response was reported by 12 of the patients. Subconjunctival hemorrhage was also found in 12 patients. Nine patients had tachypnea and 7 complained of dyspnea. Most of the patients suffered some associated injuries including 8 head injuries, 7 pulmonary contusions, and 6 cases of blunt abdominal trauma.
Less-associated injuries were rib fractures, brachial and radial nerve injuries, hemothorax, and pneumothorax. The hospital stay ranged from 4 to 28 days (mean, 14 days) and follow-up from 10 to 60 months (mean, 32 months). Treatment for traumatic asphyxia included measurement of arterial blood gases, oxygen supplementation, and intubation with mechanical ventilation. The patients’ recovery conditions were relative to the severity of injury and the associated injuries.
T
department were excluded. There were 12 male and 2 female patients. The ages ranged from 2 to 32 years. Patients were stabilized in the emergency department, including intubation if required, before elucidation of the history. Arterial blood gas measurements, chest roentgenography, and any other indicated studies were then performed. Among our 14 patients, 9 suffered from thoracic, abdominal, or thoracoabdominal crushing injuries at work, 3 were run down by motor vehicles, 1was compressed by a steering wheel, and the final 1 had a crushing force on the right side of the chest. On questioning 12 of our patients reported a fear response just before the crushing. Clinical features of cervicofacial cyanosis and petechiae of the head and neck regions developed in all patients in varying degrees (severe, 4; moderate, 7; mild, 3). Subconjunctival hemorrhage developed in 12 patients. Other commonly noted symptoms were disturbance of consciousness (3), tachypnea (9), and dyspnea (7). Two patients were in shock; 1of them had left diaphragm rupture and the other had multiple long bone fractures. All other patients were hemodynamically stable. Other associated injuries included head injuries in 8 patients, with variable changes in the Glasgow Coma Scale. None had surgical lesions. Six patients had abdominal tenderness with elevation of serum glutamicoxaloacetic transaminase level. Only the patient with the left diaphragmatic rupture with herniation of the stomach and intestine required operation.
he classic syndrome of traumatic asphyxia includes cervicofacial cyanosis, subconjunctival hemorrhage, ecchymosis, and petechiae of the face, usually secondary to blunt trauma (Fig 1). These were first observed by Ollivier [l] in 1837; he termed the syndrome “masque ecchymotique” when noting these characteristic features in a patient trampled to death by crowds in Paris. It was not until 1900 that Perthes [2] made a more extensive review and detailed its pathophysiology and features including mental dullness, hyperpyrexia, hemoptysis, tachypnea, and contusion pneumonia. Since then, there have been a number of series discussing its pathophysiology and mechanisms of injury, but all hypotheses remain controversial. In 1968, Williams and associates [3] suggested the fear response was an important factor in the production of craniofacial petechiae. The fear response is defined as the feeling of impeding doom as the patient realizes he or she is about to be crushed. This is a 4-year review of our experience with and results of cases of traumatic asphyxia.
Material and Methods We retrospectively collected 14 cases of patients who sustained thoracoabdominal compressive injury with clinical features of cervicofacial cyanosis or facial petechiae (Table 1).They were all admitted through our emergency room to our cardiovascular intensive care unit from May 1984 until December 1988. Patients sustaining severe associated injuries who died on arrival in our emergency Accepted for publication Sep 10, 1990. Address reprint requests to Dr Lee, Department of Cardiovascular Surgery, Chang Gung Memorial Hospital, 199, Tun-Hwa North Rd, Taipei, Taiwan, Republic of China. 0 1991 by The
Society of Thoracic Surgeons
(Ann Thorac Surg 2992;52:86-8)
Results The initial arterial blood gas results revealed the lowest oxygen tension levels in the 7 patients who were found to 0003-4975/91/$3.50
Ann Thorac Surg 1991;51:8&8
Fig 1. Prominent features of traumatic asphyxia include cervicofacial cyanosis with multiple petechiae and subconjunctival hemorrhage.
have pulmonary contusions on chest roentgenogram. Four of these patients were intubated for pulmonary care or head injury protection. All other patients were treated with oxygen supplementation alone, and all patients seemed to recover well. The hospital stay varied from 4 to 28 days with a mean of 14 days. The follow-up period ranged from 10 to 60 months with a mean of 32 months. Most patients recovered with no sequelae. The only morbidity was due to associated injuries: 1 patient had subglottic stenosis with a tracheocutaneous fistula after prolonged intubation, and another patient had a radial nerve injury with an incomplete recovery.
Comment In 1866, Tardieu [4] offered the first explanation that “the punctiform ecchymosis of the face, neck and chest are caused by the effort in which resistance to suffocation manifested itself.” Heuter [5] later had two hypotheses: first, a mechanical reflux of blood out of the compressed chest into the valveless veins of the head and neck leading to venular and capillary atony and stasis cyanosis, and second, that contusion of the abdominal sympathetic nerves causes vasodilation of the head and neck region. Bolt [6], in his study, postulated four factors: (1) deep
LEEETAL TRAUMATIC ASPHYXIA
87
inspiration, (2) closure of glottis, (3) thoracoabdominal effort, eg, splinting of thoracic and abdominal musculature, and (4) thoracic or abdominal compression that forces blood into the cervicofacial regions producing venular and capillary stasis. More recently, Reichert and Martin [7] in 1951 in canine experiments found that occlusion of the superior vena cava alone could cause a considerable congestion of the upper extremities and head regions, but they were not able to duplicate the clinical features of traumatic asphyxia. In 1968, Williams and associates [3] concluded that just at the moment of impending disaster, a fear response is practically always present. This fear reflex would lead the patient to take a deep breath, hold it, and brace himself or herself. The closed epiglottis would then enhance greatly the intrathoracic pressure during compression. In 1989, Thompson and co-workers [8] found that valves can only play a limited role in the protection of venous beds against high pressure, but the elevated intraabdominal pressure developed during the fear response followed by an acute abdominal thoracic compression can cause collapse of the inferior vena cava, thereby protecting the lower torso from the venous injury seen in traumatic asphyxia. The striking physical characteristics include multiple punctiform petechiae and bluish discoloration extending over the face, neck, and sometimes the upper part of the chest to the level of nipples anteriorly and approximately to the lower level of trapezius posteriorly. The petechiae practically never reach the elbow laterally. These petechiae usually blanch on pressure and almost always increase in intensity over the first few hours and then gradually fade over days to weeks. Frequently, they are associated with mild to massive subconjunctival hemorrhage, periorbital edema, and ecchymosis. Immediate impairment or loss of vision has also been reported as a result of retinal edema, but may promptly recover within hours or days. Permanent vision loss is very rare. Neurologically, the syndrome initially manifests primarily as agitation, restlessness, and disorientation. Williams and associates [3] suggested these neurological signs may be associated with minor intracranial hemorrhage or cerebral edema. These are usually reversible within 24 hours without any sequelae. In our series, associated injuries were frequently encountered especially involving the brain, thorax, and abdomen. With major pulmonary complications such as severe pulmonary contusion or flail chest, therapy mainly involved respiratory support. In cases of minor chest injury, administration of oxygen therapy by nasal cannula or mask was sufficient. Our experience indicates that patient prognosis depends on the morbidity of associated injuries. The victim may die within minutes due to severe associated injuries, or may need long-term rehabilitation if neurological damage or long bone fractures have been sustained. For those patients with pure traumatic asphyxia syndrome who survive to the emergency room, a full recovery should be expected.
88
Ann Thorac Surg 1991;51:8&3
LEEETAL TRAUMATIC ASPHYXIA
Table 1 , Cases of Traumatic Asphyxia ~~
Patient No.
Age (Y)
Sex
Mechanism
1
32
M
Moderate ME"
BAT
2
24
M
Thoracoabdominal compression Steering-wheel compression
Moderate ME
10
10
M
Mild ME
4
...
24
F
Abdominal compression Chest compression
Multiple ribs fracture, lung contusion, facial laceration BAT
25
...
26
M
Chest compression
Moderate ME
18
...
32
M
Severe ME
13
...
4
M
Thoracoabdominal compression Chest compression
27
Subglottic stenosis
27
M
Chest compression
Moderate ME
16
M
Abdominal compression
Moderate ME
10
2
M
Thoracoabdominal compression
Mild ME
11
18
M
Crush with roller machine
Severe ME, shock
12
4
F
Run down by bus
Mild ME
13
28
M
Run down by bus
Severe ME
14
22
M
Run down by truck
Moderate ME
Left brachial plexus injury Lung contusion with R pneumothorax, R scapular fracture Flail chest BAT, brain edema Head injury, L diaphragm hernia Back 3" burn, brain edema Rib fracture, pulmonary contusion, brain edema Pulmonary contusion, BAT, rib fracture, head injury BAT, R humerus fracture, both femoral fracture Trunk abrasion wound Head injury, trunk abrasion Head injury, pulmonary contusion
Signs and Symptoms
Moderate ME
Severe ME, shock
Associated Injuries
Hospital Stay (d)
Complications
5
...
19 11
...
11
23
R radial nerve palsy
( A m 28
...
12
...
a Moderate ME as in Figure 1; mild ME: petechiae only localized on periorbital and cervical region; severe ME: petechiae become confluent over whole cervicofacial region. 3" = third-degree. ME = masque ecchymotique; BAT = blunt abdominal trauma; AAD = against advice discharge;
References 1. Ollivier d-A. Relation medicale des evenements survenus au Champs-de-Mars le 14 juin, 1837. Ann Hyg 1837;18:485-9. 2. Perthes G. Uber "Druckstawing." Dtsch Chir 1900;55:3%92. 3. Williams JS, Minken SL, Adams JT. Traumatic asphyxia reappraised. Ann Surg 1968;167384-92. 4. Tardieu A. Relation medico-legale de I'accident survenu au pont de la concorde, a Paris, le 15 aout 1866. Pour servir a I'historie de la mort par suffocation. Ann Hyg 1866;2:338.
5. Heuter G. Ueber die Dilatation der Blutgefaesse der Kopfes bei sehweren verletzungen des Unterleibes. Dtsch Chir 1874;4382. 6. Bolt RA. Traumatic asphyxia-report of a case. Cleve Med J 1908;7647-59. 7. Reichert FL, Martin JW. Traumatic asphyxia, experimental and clinical observations with a report of a case with concomitant paraplegia. Ann Surg 1951;134:361-8. 8. Thompson A, Illescas FF, Chiu RC. Why is the lower torso protected in traumatic asphyxia? A new hypothesis. Ann Thorac Surg 1989;47:247-9.