Traumatic asphyxia (TA), namely, perthes syndrome, thoracic compression syndrome, superior cava vena compression syndrome, has been rarely reported in literature, but its incidence is likely to be underestimated. 8 It was initially reported by Ollivier d’Angers in an entrapment accident in France, and it was further illustrated by perthes with focus on neurological symptoms.1-2Later, TA was found in car accident, object compression, entrapment or even without a large external force, such as crying, asthma, epilepsy.3
The recognized mechanism of TA was the counterforce between respiration and thorax, and increase of central venous system by thoracic compression and fear response9, leading to superior vena cava (SVC) obstruction with incompetent valves to inhibit flowing back, arterial low perfusion and hypoxia, which could cause facial edema and cyanosis, neurological symptoms, petechiae of upper body and hemorrhage of conjunctiva, retina, ear, nose, oral mucosa, bronchi, etc.3
In our study, all patients showed petechiae on the upper body, especially on face. 25 patients (49.0% CI 34.8%-63.2%) out of 51 presented with facial edema. As for subconjunctival hemorrhage, 29 patients (56.9%, CI 42.8%-70.9%) presented with subconjunctival hemorrhage. It is consistent with previous literature except that subconjunctival hemorrhage was of less percentage10. Compared to other existing literature were subconjunctival hemorrhage was seldomly absent11, we got a much lower occurrence as 56.86%. This is possibly due to observation negligence or lacked medical recording by doctors who were not familiar with TA manifestations. Also, the incidence of facial petechiae was higher than previously reported, the reason for which might be that doctors are more possible to consider diagnosis of TA when encountering such characteristic appearance.
Hemorrhages of nose and ear were common in appearance and auxiliary examinations in this series. There were 7 mastoid hemorrhage and 10 hematocele of paranasal sinuses. Patients also showed nasal hemorrhage in 7, ear hemorrhage in 5, oral mucosa hemorrhage in 2 and hemoptysis in 1. Hemorrhage of mastoid and paranasal sinuses is possibly related to venous stasis and fear response through Eustachian tube and imbalanced pressure between middle ear and thorax with possible barotrauma.12 As both brain and other region of head have veins belonging to SVC, it is reasonable to assume that hemorrhages out of brain could reduce the cerebral impairment as a protective reaction.12
There are differing neurological symptoms as loss of consciousness, confusion, epileptic seizure.13 In our study, 22 children underwent loss of consciousness within minutes or days, 3 children got confusion within days, and 25 remained conscious after injury. 6 patients went through epileptic seizure, 5 vomited, and 11 got incontinence after injury, which may be correlated to both TA itself by circulatory abnormality and companion injuries as head bump. These symptoms revolved within days without surgical intervention except debridement suture. Only a patient with severe hypoxic-ischemic brain injury remained intellectual disability. Both respiratory inhibition and hemodynamic disturbances contribute to cerebral impairment in TA.13-14 However, their respective role is yet to be determined with not striking pathologic changes except congested vessel and petechial perivascular hemorrhage.15
We want to highlight the evidence in viscera impairment of TA. There were autopsy evidence of subepicardial and subpleural petechiae.12 Children got a less rigid thorax with intolerance to compression. Thus, the inner organs could suffer more from the compression with danger in cardiac and pulmonary impairment.16 The potential mechanism of myocardial injury is the compression itself, the anoxia, and the cardiac capillary rupture due to venous hypertension as cardiac petechiae was found in TA victims.12 We found a high percentage as 74.3%, indicating necessity in evaluation and intervention of cardia for TA patients. The mechanism of fear response, including deep inspiration, closure of the glottis, splinting of the thoracic and abdominal musculature, and chest compression, might provide protection to heart with elevated intra-thoracic pressure.17 In addition, we found a percentage of hepatic insufficiency as 53.1% while the role of inferior vena cava (IVC) change in TA has been less focused in literature, even although there are evidence of increased pressure in IVC and visceral changes as “nutmeg” liver or liver petechiae during autopsy.12,18
Also, the evaluation of retina through fundus is necessary. We found an incidence of 20.0% (CI 4.3%-48.1%) from 15 patients in retinal hemorrhage, edema and exudates. Based on the result of 1 patient (Figure 3), the retina was hemorrhagic with edema and exudates around the optic disc in the left eye. Moreover, the optic disc was pushed temporally, thus with optic nerve compression. The low-dosage dexamethasone was used as treatment for 3 days. However, in the 1-month and 1.5-month follow up, the retina still turned atrophy and optic disc was drafted nasally. It is reasonable to assume that the impairment is irreversible and could lead to lifelong amblyopia. Based on that, this evaluation is especially important for children as they are not capable to express feelings clearly and optic impairment could make its influence throughout their life.19
As for other companion injuries, they are the main factors determining the prognosis and pulmonary contusion was the most frequent concomitant injury both in our study and other literature.20 Pulmonary parenchymal injury results from several mechanisms, including direct compression, counter-coup compression, shearing forces and laceration by fractured ribs.21 Interestingly, flail chest has not been found in our study. Accordingly, apart from suffocation, associated injuries are more causal in death instead of TA itself.22
In addition, based on our study, there are 3 spinal injury. Spinal injury deserves more attention as a severe injury correlating intimately with prognosis. Spinal injury was seldom reported with assumed injury mechanism as spinal anoxia and unstable blood flow.23 However, we considered spinal injury as concomitant injury because spinal fracture often accompanies and spinal MRI usually showed spinal edema and abnormal signal from a specific segment, especially from the thorax.
No death occurred in our study, which is consistent with previous literature that TA got a rather good prognosis. This might be due to their thoracic wall elasticity.12 Death of traumatic asphyxia is mostly caused by large compression force, compression overtime, and associated injuries.12 The prognosis of TA depends on the severity of prognostic-related injuries.
Limitations and strengths
As a retrospective study, the medical record might be imperfect because facing the rarely encountered TA by doctors from different departments, some symptoms might be neglected or misjudged. We failed to collect enough data about the forces causing traumatic asphyxia. There lacked accurate description of accident details as mechanism, time and patient’s state after injury. The examinations were not complete for myocardial markers, hepatic function, fundus and urine routine. CT scan was not completed immediately after injury or admission, which not only interferes our analysis with possibly lower positive rates in statistics but also probably inhibit proper and timely treatment for concomitant injury.
Meanwhile, as a large and highly ranked medical center for children, we have collected 51 pediatric cases in TA, which is, from the acknowledgement of authors, of the largest sample ever. We reported also the rare OCT, fundus and thickness map results with comparison between admission and follow-up, thus drawing attention to the importance of retinal evaluation of TA.