Traumatic Asphyxia-Reappraised
JAMES S. WILLIAMS, M.D., STANLEY L. MINKEN, M.D.
JAMES T. ADAMS, M.D.
From the Department of Surgery, University of Rochester Medical Center,
260 Crittenden Boulevard, Rochester, New York 14620
OLLIVIER,14 in 1837, found at autopsy of
persons who had been trampled by crowds
in Paris, craniocervical cyanosis, subcon-
junctival hemorrhage, and cerebral vascu-
lar engorgement. He applied the term
masque ecchymotic. Similar reports subse-
quently appeared in the French and Ger-
man literature," 12, 16, 24 but without expla-
nation. In 1900, Perthes 16 observed mental
dullness, hyperpyrexia, hemoptysis, tachyp-
nea, and contusion pneumonia, and, since
then, petechial hemorrhages of the mucus
membranes, epistaxis, hematemesis, rectal
bleeding, hematoma of the esophagus, albu-
minuria, microscopic hematuria, paraplegia,
peripheral nerve damage, amnesia, and con-
vulsions have been described in what is now
known as traumatic asphyxia.7-11'17, 23, 26
The first explanation for the develop-
ment of the syndrome was offered by Tar-
dieu 25 in 1866, when he stated "the puncti-
form ecchymosis of the face, neck, and
chest are caused by the effort in which re-
sistance to suffocation manifested itself."
Lejars 13 and later Ryerson 21 in 1907, re-
affirmed Tardieu's contention that the pa-
tient plays an active role in the develop-
ment of the syndrome by his panic strug-
gling. They felt that the victim made a
"forcible thoraco-abdominal effort" leading
to a marked increase in the craniocervical
intravascular pressure.
Hueter 12 postulated two mechanisms for
the development of the bluish discoloration
localized to the craniocervical area. The
first was a mechanical reflux of blood out
Submitted for publication September 11, 1967.
384
of the compressed chest into the valveless
veins of the head and neck producing venu-
lar and capillary atony and stasis cyanosis.
The second was that contusion of abdomi-
nal sympathetic nerves produced reflex
vasodilatation in head and neck vessels.
Support for this was offered by Beach and
Cobb 2 who demonstrated small vessel en-
gorgement by skin biopsy. Bolt 3 felt that
four factors were involved in the genesis of
traumatic asphyxia: 1) deep inspiration; 2)
closure of the glottis; 3) thoraco-abdominal
effort (splinting of thoracic and abdominal
musculature); and 4) thoracic or abdomi-
nal compression which forces blood into
the cervico-facial region producing venular
and capillary stasis.
Alexander 1 observed that the clinical
signs of traumatic asphyxia developed in
patients following an epileptic seizure. In
1946, Dwek5 reviewed 170 cases and re-
emphasized that the syndrome could be
produced by vomiting, deep sea diving,
and whooping cough and did occur with-
out chest compression.
Fred and Chandler 6 reviewed 178 cases
from the literature and reported a case of
traumatic asphyxia in 1960. Since then,
Quigley18 reported two cases and Sham-
blin and McGoon 22 added five more. This
brings the total number of reported cases
to 186.
Recent experiments to define the basic
pathophysiology of traumatic asphyxia have
been inconclusive. Reichert and Martin 19
produced acute thoracic compression by
dropping weights on the chest of experi-
mental animals. Two to five minutes of
Volume 167
Number 3
TRAUMATIC ASPHYXIA-REAPPRAISAL 385
TABLE 1. Summary of Fatal Cases
Nature of Injury Physical Findings Pathological Findings
Warn- Conjunc-
Case Age* History ing Death Mask tiva Chest Abdomen Brain

A826 40 Chest crushed when + Immediate + Hemor- Congested Congested Negative

bulldozer rolled rhage lungs liver and
over spleen
A262 50 Chest and abdomen + Immediate + Hemor- Congested Congested Negative
crushed when car rhage lungs and lacer-
slipped from jack ated
spleen
A126 36 Chest crushed when + Immediate + None Acute con- Congested Multiple
car slipped off gestion spleen petechiae
jack of'lungs; and in-
vessels testine
engorged;
medias-
tinal
petechiae
A217 28 Chest and abdomen + Immediate + None Acute con- None None
compressed in an gestion;
underground medias-
cave in tinal
petechiae
AIOO 39 Chest crushed when + Immediate + Hemor- Acute con- None Meninges
tractor he was rhage gestion had
driving fell over of lungs petechiae
on him

Al 16 64 Chest crushed by + 13 hours - Hemor- Acute con- Congested Multiple

2,000 pounds rhage gestion; spleen petechiae
sheet metal; multiple and in-
pinned face down medias- testine
tinal
petechiae
A338 31 Head on collision - Immediate - Hemor- Ruptured None None
after falling rhage aorta
asleep; chest
crushed between
seat and engine
A765 58 Chest and abdomen - Immediate - None Acute con- Lacerated None
compressed when gestion liver and
hit by steel girder of lungs spleen
from rear while
on scaffold

* All were male patients.

such compression produced venous stasis
and capillary dilatation. In other experi-
ments, the superior vena cava was ob-
structed by direct clamping for 10 minutes.
Again, venous stasis and capillary dilata-
tion occurred. They were unable to con-
clude that stasis and dilatation were the
result of venous obstruction alone or were
due to tissue anoxia.
The pathogenesis of the traumatic as-
phyxia syndrome remains obscure. It ap-
pears related to a voluntary or involuntary
abdominal muscular contraction against a
closed glottis after deep inspiration.
386 WILLIAMS, MINKEN AND ADAMS
750 mm
FIG. 1. Experimental preparation. Cuffed endo-
tracheal tube allows control of airway. Hemo-
dynamic parameters measured include carotid ar-
tery and jugular vein flow, brachial and femoral
artery pressures and jugular and inferior vena
caval pressures.
Whether increased venous pressure in the
head and neck is related to functional
obstruction of the superior cava or to retro-
grade ejection of venous blood from the
thoracic cavity is unclear.
The present study was undertaken to
evaluate the possibility of a pre-impact
fear response in patients who develop trau-
matic asphyxia, and to examine experi-
mentally the role of the airway on the
hemodynamic alterations thought to occur.
Case Material
Case histories of four surviving patients
with traumatic asphyxia treated at Strong
Memorial Hospital and eight fatal cases
of thoraco-abdominal crush injuries on
record at the Monroe County Medical Ex-
aminer's Office, Rochester, New York were
reviewed. Analysis included the nature of
the injury, pre-impact warning, presence
Annals of Surgery
March 1968
of cyanosis and petechiae, clinical signs
and symptoms in surviving patients, and
autopsy findings in fatal cases.
Case Reports
Surviving Patients
Case 1. A five-year-old boy was hospitalized
after falling from a moving tractor. An automobile
trailing the tractor squeezed his chest and upper
abdomen against a rear tire for several minutes.
When first seen, he was irritable and responded
poorly to command. Generalized facial edema,
multiple fascial, cervical, and shoulder petechiae,
and subconjunctival hemorrhage were present.
The abdomen was firm and tender to palpation.
Abdominal paracentesis aspirated free blood. Uri-
nalysis showed two plus albumin and three to
five red blood cells per high powered field.
A lacerated liver was found at laparotomy
and treated by segmental resection. Irritability
continued for 12 hours postoperatively but cere-
bration became normal 24 hours after the injury.
Cervico-facial cyanosis cleared in 3 days and re-
covery was complete.
Case 2. A 15-year-old girl slipped off the tail-
gate of a slowly moving jeep as it tipped over on
a side hill pinning her chest to the ground. She
was incarcerated for 2 minutes, during one minute
of which she was unconscious. When seen, she
was drowsy but oriented, and her face was swollen
and cyanotic. Multiple petechiae of the face and
neck were observed. Bilateral subconjunctival
hemorrhages were present. The abdomen was un-
150 4 DOGS
EXHIBITED
cZ:, REVERSED
FLOW
t 100 -
K50~
CONTROL NON OBSTCONTROL NON OBST
OBST OBST.
JUGULAR CAROTID
VEIN ARTERY
FiG. 2. Per cent change in mean blood flow
in the jugular vein and carotid artery without
and with airway obstruction and acute thoracic
compression.
Volume 167
Number 3
TRAUMATIC ASPHYXIA-REAPPRAISAL
TABLE 2. Carotid Artery and Jugular Vein Flow
Control
Mean Range
Carotid artery* 160.6 90-250
Jugular vein* 121.5 50-193
* cc. per minute
remarkable, but the left humerus was fractured
and the arm was lacerated. Neurological examina-
tion was normal, urinalysis revealed positive albu-
min and microscopic hematuria.
The left arm wound was debrided under local
anesthesia and a cast applied. The patient was
drowsy for several hours after admission and her
pupils were unequal but reactive. Twenty-four
hours later her somnolescence cleared and the
pupils were normal. Facial edema and petechiae
cleared in 72 hours, but subconjunctival hemor-
rhages persisted for one week. Recovery was
uneventful.
Case 3. A 41-year-old man stopped his flat-bed
truck abruptly at a red light and a shifting load
of steel pipe jumped the barrier of the trailer
compressing his chest between the back wall of
the cab and the steering wheel. He was incar-
cerated for 10 miinutes and unconscious when
freed.
When first seen he was unreactive and respira-
tions were labored. Pulse and blood pressure were
normal; his face and neck were "swollen and cya-
notic." He had multiple petechiae over both
shoulders. The chest was normal except for mul-
tiple anterior and posterior contusions. Bilateral
ankle clonus and a positive Babinski on the right
were present. Urinalysis revealed three to five red
blood cells per high powered field. Twenty min-
utes after admission he was aphasic and demon-
strated marked cerebral irritability requiring re-
straints. Twenty-four hours after admission, apha-
sia cleared but his speech was slurred. A right
seventh cranial nerve weakness was noted. Ba-
binski reflexes could no longer be elicited. Forty-
eight hours after injury the cervico-facial cyanosis
and petechiae had disappeared and he was read-
ing a newspaper. His facial weakness was still
present when last seen 3 months after the accident.
Case 4. A 19-month-old boy ran into the front
of a moving automobile. When admitted, he was
sleepy but could be aroused. His face was swollen,
cyanotic and multiple petechiae were seen. La-
bored grunting respirations were 50/minute.
There were subconjunctival hemorrhages on the
left and a large abrasion over the right shoulder
387
Non-Obstructed Obstructed
Mean Range Mean Range
145 60-268 22.3 0-50
98.4 43-176 -5.5 -22-11
and right posterior hemithorax. Rales were heard
over the right base. Urinalysis showed one plus
albumin and many red blood cells. Twenty-four
hours after admission the child was no longer ir-
ritable but had an elevated temperature. A right
lower lobe infiltration was found and appropriate
therapy was instituted. Three days after admis-
sion there was no evidence of petechiae or cyano-
sis. The child was discharged 7 days after admis-
sion fully recovered.
Fatal Cases
The case histories and findings of the
fatal cases are summarized in Table 1. All
were severe thoracic or thoraco-abdominal
crushing injuries.
Clinical Results. The postmortem cases
and three of the four survivors were sub-
jected to prolonged compression. Two fatal
cases had no period of preimpact warning
and had no ecchymotic masks. Another
fatal case, in which there was no warning,
was pressed face down and did not have
craniocervical cyanosis. Subconjunctival
hemorrhage was present in three surviving
patients and in five autopsy subjects. Facial
edema was seen only in survivors and
cleared within 12 hours. Cutaneous pe-
techiae and cyanosis were limited to the
head, neck and upper thorax and lasted up
to 72 hours. Microscopic hematuria or al-
buminuria were present in all surviving
patients.
Varying degrees of cerebral dysfunction
were noted in the surviving cases, however,
these symptoms cleared in 48 hours.
Associated injuries in surviving patients
were treated and did not influence the
course of traumatic asphyxia or eventual
recovery.
 388 WN'ILLIAMS, MIIN KEN AN-D ADAMS
Postmicortemn examination of the tlhoracic
x ities shoxwed acute pulinonarx colnges-
tioIi in seven cases anId the abdomllinal x is-
cera shoxved varxying degrees of acuite coIn-
gestioin throughoutt. N europathologic find-
ings were limited to the brain. In one case
there 'were diffuse intracerebral petechial
lhemorrlhages aind meninigeal congestioni
wvas seen in another. The cause of death
xw as listed as acute pulmonary congestion
in six case instances, trainsected thoracic
aorta in one. aindI lacerated brain stem in
one.
Experimental Study
Methods. Twenty-three experiments wvere
performed under sodium pentothal anes-
thesia on seven fasted adult moingrel dogs
weighing betw-eeni 15 and 25 Kg. The air-
wav was controlled by a cuffed endotra-
886 690
c_z
Kz)
K2
K~
K)3
CONTROL NON OBST CONTROL
OBST. OBST
JUGULAR INFERIOR
VEI N VENA CAVA
Fl(;. 3. Per cent chainge in mean venous pres-
sure in the jugular vein and inferior vena cava
without and with airwxay obstruction and acute
thoracic compression.
Annals of Surgery
March 196S
chleal tube. Continuots direct arterial blood
presstres xwrc recordled 1)N- idxw ellir
polycthylncue cannulae in the bracliial anid
fem)oral.arteries. Similarly, venous pres-
suires xere recorded bx cainnulation of a
branclh of the external jugular vein and the
iniferior vena. cava via the femoral vein.
Blood flox7 was measured by noncannilulat-
ing, electromagnetic square wave floxv
probes placed oIn the opposite external
juguilar vein and common carotid artery.
A pneumiiiatic tourrniquet wvas placed arouilnd
the tlhorax to produce acute thoracic com-
pressioni. To simulate the pre-impact fear
response, a girdle wvas w\rapped around the
abdcomen to produce muscular splinting
(Fig. 1). All pressures were recorded
throuiglh transducers oIn a Sanborn direct
writing poly-graph. Flow data was similarlyr
measurecl.
After a control period, two series of ex-
periimenits w7ere carried out on each dog.
The toutrniquet x\ as inflated to 750 mim.
Jig for 30 secoinds durinig each acute phase.
The first series inclu(ded two experiments
in wlhiclh carotid aind jugular blood flowx
wx as m onitored xx ithout airway obstruiction.
In the second series, these flows were re-
corde(d after the lungs xxcre fully inflated
1b anI Amnbu bag anid the airx\-ay occluded
utist priior to compression. Continuous pres-
sure recorclings x7ere obtained througlhout
all acute and recovery periods wxith record-
inlgs made at 30 second intervals for 2 min-
utes and then at 5 minute intervals until
control levels xere regained.
Experimental Results. Acute thoracic
coiimpressioii produced a uiniform series of
clhanlges in the airxvay obstructed and non-
airxva- obstructed groups. Alterations in
jugular venous and carotid arterial blood
flow in both groups are shoxvn in Table 2.
Clhaniges in arterial and venous pressures
ar-e seen in Table 3. The mean jugular ve-
nous floxy xvas 81 of control value xwith
a p)atenit airxx7av, xvhile xvith obstruction
flox fell to 6% of normal anid in fotur dogs
xvas actually reversed to a mean rexversed

Volunme 167
Number 3
TRAUMATIC ASPHYXIA-REAPPRAISAL
flow of 13.6 cc. per minute (Fig. 2). Caro-
tid flow was 90%o of control value without
airway obstruction and 14%o of control
flow when the airway was obstructed
(Fig. 2).
Animals with airway obstruction showed
an average increase in jugular pressure of
886%o of control value during the acute
compressive period (Fig. 3). In one ani-
mal, an increase of 1,500% occurred. The
nonobstructed group showed an increase
to only 145%o of control. Inferior vena caval
pressures showed a similar trend, increas-
ing 690%o of control in the airway ob-
structed group and 300% in the non-
obstructed group (Fig. 3).
Mean brachial artery pressures in-
creased 6%o over control during compres-
sion in the nonobstructed group but de-
creased to 50.3%o with airway occlusion
(Fig. 4). Similarly, femoral artery pres-
sures increased 12% over the control val-
ues in the open airway group and de-
creased to 52%o with obstruction.
A representative pressure and flow trac-
ing in a dog with airway obstruction is
shown in Fig. 5.
Although petechial hemorrhages were
not seen in the skin or mucous membranes
of any animals, conjunctival injection did
occur.
Discussion
The results of the clinical study indicate
that development of traumatic asphyxia is
associated with a fear response in the acci-
dent victim just prior to injury. In this
"moment of impending disaster," the indi-
vidual reflexly takes a deep breath, holds
it, and braces himself. All the surviving
patients in this series and six fatal cases,
by the nature of the accidents, had warn-
ing of impending injury. On the other
hand, in two fatal instances, one fell asleep
at the wheel and the other was struck from
behind, neither had warning and did not
develop the characteristic craniocervical
cyanosis. One fatal case who did have
lr E--
389
150-
K_
112
106
(Z o00o--
50
50-
CONTROL NON OBST. CONTROL NON OBST.
OBST. OBST.
FE MORAL BRACHIAL
ARTERY ARTERY
FIG. 4. Per cent change in mean arterial pres-
sure in the femoral and brachial arteries without
and with airway obstruction and acute thoracic
compression.
warning was violently pressed face down
in the ground and had neither a mask nor
subconjunctival hemorrhage, the face and
chest were subjected to a high counter-
pressure which prevented venular conges-
tion and petechial hemorrhage.20
The increase in intrathoracic pressure
associated with a closed glottis and its
pathophysiologic effect is dependent upon
the force of thoracic or thoraco-abdominal
compression and its duration. The exact
force of compression was 2,000 pounds in
one fatal case. Forces up to 16,000 pounds
have been previously reported.15 The one
surviving patient who was compressed for
10 minutes showed early severe neurologi-
cal derangement, but only a mild seventh
nerve weakness remains. In all but one of
the fatal cases, compression was prolonged.
A great force, applied instantaneously, is
likely to produce pulmonary contusion in
addition to facial cyanosis, as in the five-
year-old boy who was struck by an auto-
mobile. If the compression is prolonged
death may result from suffocation. It is dif-
ficult to say whether or not the pulmonary
congestion seen in the fatal cases was re-
lated to the force of compression or was
 WILLIAMS, MINKEN AND ADAMS
390
TABLE 3. Arterial and Venous Pressure
Control
Vessel Mean Range
Brachial artery* 141 125-155
Femoral artery* 124 120-150
Jugular vein** 4.0 2-5
Inferior vena cava** 5.5 4-10
* mm. Hg.
** mm. H20.
secondary to acute heart failure prior to
death.
Since air cannot escape from the thoracic
cavity during compression in the face of a
closed glottis, the increased pressure is
transmitted centrally to mediastinal veins,
superior and inferior vena cavae, and right
atrium. The blood in these structures is
squeezed from the chest into the valveless
vein of the head, neck, and abdomen. The
cephalad regurgitation of venous blood
was sufficient in nine of twelve cases to
produce characteristic facial discoloration,
subconjunctival hemorrhage and, in sur-
vivors, cerebral dysfunction. In addition,
one fatal case demonstrated meningeal
vascular congestion and another diffuse
petechial brain hemorrhage.
The effects of increased venous pressure
and reversed flow are transmitted to the
intra-peritoneal viscera as well. Evidence
in survivors of transient hematuria, albu-
minuria, or both, and in the fatal cases of
varying degrees of organ congestion may
be explained on the basis of this pressure
increase. The augmented intra-abdominal
venous pressure may be of sufficient mag-
nitude to produce gastrointestinal bleed-
ing.8, 14
Previous investigators have shown that
obstruction of the vena cava above the
azygos vein for 10 minutes will produce
marked venous congestion and petechial
hemorrhage.19 If the rise in jugular pres-
sure is related to functional obstruction of
the superior vena cava alone, then arterial
Annals of Surgery
March 1968
NonObstructed Obstructed
Mean Range Mean Range
150 120-175 71 35-100
150 115-175 70 35-100
5.1 3-10 35.4 17-60
16.4 3-38 37.9 17-70
inflow should be initially unimpaired. Our
experiments in which the airway was
not obstructed during chest compression,
showed carotid artery flow only slightly
reduced and arterial pressure actually in-
creased in some animals. However, with
airway obstruction and compression, caro-
tid artery inflow was drastically reduced
and arterial pressure dropped markedly.
Furthermore, the fact that jugular flow
was reversed in four animals with airway
obstruction during compression is addi-
tional evidence that mechanical venous ob-
struction does not occur in traumatic
asphyxia.
The experimental evidence supports the
clinical hypothesis that airway obstruction
after deep inspiration and just prior to
compression produces a marked and rapid
rise in jugular pressure and a reversal of
venous flow. Chest compression alone has
little influence.
Increased intrathoracic pressure produces
a rise in intra-abdominal venous pressure
as well. Elevation of caval pressure in un-
obstructed animals is most likely related
to impingement on the inferior vena cava
by the overlying liver or diaphragm at the
time of chest compression. In the airway
obstructed animals, however, venous pres-
sure rose considerably above control values
in the face of falling arterial pressure.
Although no petechiae developed in mu-
cous membranes or skin of experimental
animals, vascular engorgement did occur.
Since the total pressure exacted on the
Volume 167 TRAUMATIC ASPHYXIA-REAPPRAISAL
Number 3 391
dogs' thorax was 1,200 pounds (14 pounds
per square inch), sufficient to produce
clinical traumatic asphyxia, it appears that
either the canine capillary is more resistant
to increased pressure or that the animals
coat offers some degree of counterpressure.

Summary
A clinical and experimental appraisal
of traumatic asphyxia has been presented.
Four surviving patients with traumatic
asphyxia and the records of eight fatal
cases of blunt thoraco-abdominal trauma
were analyzed. All patients who developed
the craniocervical cyanosis characteristic of
the syndrome had accidents in which there
was warning of impending trauma. Sur-
viving patients had varying degrees of
transient cerebral dysfunction and hema-
turia or albuminuria. The ecchymotic rash
in these patients cleared within 5 days.
Fatal cases showed varying degrees of pul-
monary and intra-abdominal congestion at
autopsy. One had diffuse intra-cortical pe-
techial hemorrhages and another acute
meningeal congestion.
FIG. 5. Representative pressure and flow trac-
In experiments on dogs acute thoracic ings. With acute chest compression and airway
compression was produced with a pneu- obstruction, brachial artery pressure fell from a
control level of 150 mm. Hg to 35 mm. Hg.
matic tourniquet placed around the chest Upon release of the airway obstruction and with
and inflated to 750 mm. Hg. Airways were continued chest compression, the brachial pressure
rebounded to 200 mm. Hg. A similar pattern was
controlled with cuffed endotracheal tubes seen in the femoral arterial pressure. Jugular ve-
and hemodynamic alterations were re- nous peressure increased rapidly from a control
value of 5 mm. Hg to 35 mm. Hg (600% in-
corded. With chest compression for 30 sec- crease) with compression and airway obstruction
onds and airway obstruction in full inspira- and then fell rapidly to slightly below the control
level when the airway obstruction was relieved.
tion, jugular and inferior vena caval pres- Jugular flow, with the airway obstructed and the
sure was markedly increased above normal chest acutely compressed, decreased from a con-
trol value of 110 ml./minute to a reversed flowv
and jugular flow was rapidly diminished of 17 ml./minute and then rebounded to 400
or actually reversed. Carotid artery flow ml./minute with release of the airway obstruction
while maintaining chest compression.
and brachial and femoral artery pressures
also decreased significantly. When the air- vidual performs a Valsalva maneuver,
way was unobstructed during chest com- which if prolonged, as with a seizure, vom-
pression, pressures and flows were only iting, or accompanied by thoraco-abdomi-
slightly different from controls. nal compression, results in a marked eleva-
On the basis of this clinical and labora- tion of venous pressure and reversal of
tory study, it is evident that airway occlu- venous flow with capillary stasis or rupture
sion plays an integral role in the patho- producing the typical ecchymotic rash that
physiology of traumatic asphyxia. The indi- characterizes the syndrome.
392 WILLIAMS, MINKENWILLIAMS,
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