Transportation Injuries

Injuries and fatalities occur on all forms of transportation but numerically road traffic
accidents account for the great majority worldwide. In developed countries, they are the most
common cause of death below the age of 50 years, and in young men this trend is even more
marked. The pattern of injury, fatal and otherwise, varies considerably depending upon
wheter the victim is a vehicle occupant, a motorcyclist, a pedal cyclist a pedesrtrian.

The dynamic of vehicular injury

A number of elementary physical facts help to explain the complex pattern of traffic injuries,
especially those sustained by the occupans of vehicle.

- Tissue injury is caused by a change of rate of movement. A constant speed, however

rapid, has no effect whatsoever as is evident from space travel or the rotation of the
earth. It is the change of rate that is traumatic – that is, acceleration of deceleration.
- Change of rate is conveniently measured in ‘gravities’ or ‘G forces’. The amount that
a human body can tolerate depends greatly on the direction in which the force acts.
Decelaration of the order of 300 G can be sustained without injury and even 2000 G
can be survived for a short time, if it acts at right angles to the long axis of the body.
The frontal bone may resist 800 G without fracture and the mandible 400 G, as can
the thoracic cage.
- During acceleration of deceleration the tissue damage produced will depend upon the
force applied per unit area, just a sharp knife penetrates more easily than a blunt one
used with the same force. If a car driver is brought to rest from 80 km/hour by striking
10 cm2 of his head on the windscreen frame, the damage will be vastly more severe
than if the same decelarative force was spread over 500 cm2 of a safety belt.
- Between 60 and 80 per cent of vehicular crashes (either into a fixed structure or into
another vehicle) are frontal, causing violent decelaration. Another 6 per cent are rear
impacts, which accelerate the vehicle and its occupants. Of the remainder, about half
are sideswipes and the rest ‘roll-overs’.
- In the common frontal impact, there is never instant arrest of vehicle, even when it
runs into a massive, immovable structure. The vehicle itself deforms distance and
time, albeit small. In fact, much of the manufactures design research now goes into
making deliberate provision for the crumpling or ‘concertinaing’ of the front and rear
of the car, leaving a central rigid cell that comprises the passenger compartment. The
object is to extend the stopping distance and time, so that the G value acting on the
occupants is reduced.
- The value of the G forces can be calculated from the formula: G = C(V2)/D, where V
is velocity in km/hour, D is the stopping distance in metres after impact, and C is a
constant 0.0039. (If V is in mph and D is in feet, C becomes 0.034.). For example, if a
car travelling at 80 km/hour runs into a stone wall that it penetrates for 25 cm, plus 50
cm crumpling of the front of the car, the deceleration would amount to about 33 G. if
an occupant was rigidly belted into his seat (a practical impossibility), he would also
suffer the same deceleration, which would be survivable. If however, he was
unrestrained, he would continue forwards momentarily at 80 km/hour and suffer
massive G forces, the magnitude of which would depend on his deformation stopping
distance (a few centimetres of tissue compression) when he struck the internal car
structures in front of him.
FIGURE 9.1. Major points of injury to an unrestrained driver of a vehicle in deceleration
impact

Pattern of injury of vehicle occupants

The type of of vehicle (other than motorcycles) in theory makes little difference to the
mechanism of injury, but most statistical surveys divide them into cars and light vans under
1.5 tonnes, on the one hand and heavier vehicles, such as trucks and buses, on the other,
though the latter have different features more akin to passenger aircraft.
Heavy goods vehicles naturally suffer less than cars and light vans in crashes because
of their far greater mass and strength, and also due to their height far greater mass and
strength, and also due to their height above the ground. Structural damage from impact with
other smaller vehicles is less and often suistaned below the level of the driver. Given smaller
deceleration forces, however, the cab occupants are vulnerable to the same injury patterns.
Light vans are virtually identical to cars with respect to the front-seat occupants. In
fact they may be more at risk, as modern vans tend to be flat-fronted and thus have little or no
‘crumple’ potential to increase the stopping time. Concentrating on cars, the most common
vehicular casualty, the pattern of injury varies according to the position of occupant.

FIGURE 9.2 Facial lacerations from a shattered windscreen in an unrestrained driver. The
toughened glass breaks into small fragments, which produce the characteristics ‘sparrow-
foot’ marks. The laceration on the forehead was made bye the windscreen rim.

The Driver

Numerous investigations have been made by road research organizations and car
manufactures using dummies and actual corpses, together with sophisticated recording
equipment and high-speed cinematography. These have established a detailed picture of the
secuence of events in automobile crashes. When the most common event – frontal impact
occurs, the unresrtrained driver first slides forwards so that his legs strike the fascia/parcel-
shelf area, and his abdomen or lower chest contacts the lower edge of the steering wheel. The
body then flexes across the steering wheel and begins to rise. The heavy head goes forwards,
and there is flexion of the cervical and thoracic spines. The upward and forward component
causes the head to strike the windscreen, the upper windscreen rim or the side pillar. The
windscreen is often perforated by the head or face, and the whole body may be ejected
through the broken glass, to land on the bonnet or even on the roadway ahead.
Another factor causing injury is the intrusion of structural parts into the passenger
compartment. Though modern cars are designed to maintain a rigid central passenger
compartment, if the impact is gross, the engine or front-wheel assembly may be forced back
into the seating area, intruding upon the driver. Similarly, the roof or front corner pillar (the
so-called ‘A’-frame) may cave in on top of the driver.
One effect of column, engine, or gearbox intrusion may be to force the floor up and
backwards against the driver’s feet and legs. The control pedals also take part of intrusion,
and, in the usual desperate braking and declutching. The steeting column was formerly a
more dangerous item for intrusion, being forced back to ‘stab’ or crush the driver’s chest or
abdomen. Modern design has reduced this danger by making the column telescopic, hinged
or otherwise collapsible, but injuries still occur – sometimes from the wheel itself breaking
and penetrating the chest. Additionally, the door may burst open and the driver, if
unrestrained, ejected sideways onto the road, especially in a crash that has a roll-over
component.
FIGURE 9.3. Ring fracture around the foramen magnum caused by an impact on the crown
of the head in a car driver, who lost the control of his vehicle and crashed into ………..

In rear impact, the driver is violently accelerated and, if no rigid head restraint is fitted
to the seat, severe hyperextension of the neck occurs, often the followed by the sequence
vehicle or other obstruction in front, causing the popular, if inaccurate name of ‘whiplash’.
In side impacts, the injuries depend upon the amount of intrusion of the driver’s door
and side panels. Restraint devices can offer no protection, though modern vehicles usually
have strengthened side-impact bars built within the doors.
This range of the traumatic events can produce the following lesions in drivers not
wearing seatbelts or protected by airbags:
- Impact against the fascia can cause abrasions, lacerations and fractures anywhere
from foot to femur. The leg can also be injured by violent contact with the fascia or
dashboard and the hip joint may be dislocated posteriorly. Not uncommonly the pelvis
is fractured, often at one or both sacroiliac joints. In mant’s (1978) series of 100
driver fatalities there were 22 pelvic injuries and 31 of the lower limb.
- Impact of the abdomen and chest against the steering wheel may cause severe internal
injuries, usually rupture of the liver (50 per cent) and, less often, spleen (36 per cent).
There may be bruising of the skin surface, but this is often absent even in the presence
of severe internal injuries. Laceration of the skin is rare unless the steering wheel
snaps and penetrates the trunk. Other steering-wheel lesions include bruising of the
lungs, fractured ribs and sternum, cardiac contusion and haemothorax or
pneumothorax or both. Almost 70 per cent of Mant’s series had broken ribs.

FIGURE 9.4 When vehicle structures impinge on the occupants even belt restraints offer
little protection. The engine, front suspension, roof and ‘A’ frame are frequent intruders.

FIGURE 9.5 Bruising, laceration and bilateral leg fractures of a car driver in a frontal
impact.

- Upper limb injuries are less common but may occur from transmitted force through
gripping the steering wheel or from impact against the windscreen, pillars, intrusive
roof, bonnet or ground when held up in a reflex protective position. Only 19 per cent
of Mant’s series had arm injuries.
- The most obvious injuries are often those to the face and head as result of projection
against and ejection through, the windscreen. The unrestrained driver rises and flexed
forwards so that his forehead and skull are likely to contact the upper rim of the
windscreen, leading to lacerations. The face frequently suffers multiple cuts from
contact with the shattered safety glass. In most European vehicles the glass is of the
toughened, not laminated, variety and, when broken, it shatters into small cubes with
relatively blunt edges. These still cause superficial lacerations, often in short ‘V-
shaped’ or ‘sparrow-foot’ patterns. In themselves they are not a danger to life, but
indicate an impact sufficient to hurl the driver on or through the glass. Damage to the
eyes is common.

FIGURE 9.6 Facial Injuries in a car driver unrestrained by a seatbelt. Following a

decelaration impact his face struck the windscreen, causing the typical small cuts from
broken safety glass and lacerations of the temple from striking the windscreen rim or ‘A’
frame.
 - The impact against thr windscreen rim or corner pillar – or after ejection – can cause
any type or degree of head injury, including scalp laceration, fractured skull,
intracranial haemorrhage or brain damage. In Mant’s series there were 42 skull
fractures in 100 drivers. This was less than in the front-seat passengers, a figure at
variance with Eckert’s (1959) series of 300 in the USA, where drivers suffered twice
as many head injuries as the passenger, though it is not stated how many accidents
were to vehicles occupied only by the driver.
- Hyperflexion of the cervical spine when the head swings can cause fractures or
dislocation. There is often a double component in that the hyperflexion of
decelaration is followed by a rebound hyperextension when the head strikes an
obstruction in front. Rear impacts also cause the double ‘whisplash’ effect, as already
mentioned.
One injury that is frequently overlooked at autopsy is the atlanto-occipital
dislocation, which Mant found in a third of his series. Other fractures can occur
anywhere in the cervical spine, often at about C5-6. Seatbelt restraint cannot prevent
cervical spine damage though a rigid head restraint can reduce injuries resulting from
hyperextension. The thoracic spine is less often damage, but in unrestrained drivers
the same ‘whisplash’ effect can fracture or dislocate the upper dorsal spine, often
around T5-6-7.

FIGURE 9.7 Mixed injuries in a restrained car driver from head on collision. Death was
caused by ruptured aorta.

- A more common thoracic injury associated with deceleration is the ruptured aorta. It
may be associated with a severe whiplash effect on the thoracic spine, as the aorta is
tethered to the anterior surface of the vertebrae where the distal arch joins the straight
descending segment. Probably the most common reason for aortic rupture, however,
is the ‘pendulum’ effect of the heart within the relatively pliable thoracic contents.
When the thorax is violently decelerated, the heavy cardiac mass attempts to keep
moving ahead and may literally pull itself off its basal mountings, the most rigid part
of which is the aorta. Separation takes place at the point where the aorta is attached to
spine at the termination of the arch.
The appearance of the aortic rupture is often of a clean-cut circular break,
almost
as sharp as if it had been transected with a scalpel. Sometimes there are addiotional
transverse intimal tears adjacent to the main rupture, the so-called ‘ladder tears’, as
they can resemble the rungs of a ladder. These may be present when no actual rupture
has occurred and may be found as an incidental finding at autopsy. Sometimes they
are deep enough to allow a local dissection of blood to seep into the intima, when
death has not been virtually instaneous. Rarely, a major dissection may lead to
delayed death some hours or even days later. Ruptured aorta is a common lesion in
traffic accidents – in a two-car crash, the author (BK) has seen three transected aortas
among the four fatalities.
The frequency of such tears in common enough for a warning always to be
offered to the autopsy prosector not to use undue force on the neck and thoracic
structures when removing the organ pluck from the body. Rough handling during this
stage can produce artefactual ladder tears in the aorta.
FIGURE 9.8 Ruptured aorta in which car occupant, unrestrained by seatbelt, suffered severe
deceleration. Aorta has torn in the usual place, the distal arch where the curve of the vessel
meets the thoracic spine.

- Other chest injuries can be caused by impact with the steering wheel, ejection through
the windscreen or impact with the road. There may be bruising or laceration on the
chest from steering wheel, though padding, collapsible columns, less fragile wheels,
airbags and seatbelts have reduced the incidence of this formerly common lesion.
Beneath the skin, sternal and rib fractures are common, though fatal visceral injuries
can occur without rib fractures in young people because their ribs are more pliable.
- The heart may be damaged even in the absence of external marks of thoracic cage
fractures. Bruising of the epicardium and underlying myocardium is not uncommon
and the posterior surface may be damaged from impact against the spine. In high-
speed impacts, the heart may bae completely avulsed from its base and be found lying
loose in the chest. Less severe degrees of damage may lacerate the ventricles or atria,
and cause gross haemorraghes. Coronary artery thrombosis has been described
following contusion over a coronary artery. Penetrating injuries from sternum, ribs or
external objects may lacerate the heart directly. Subendocardial haemorrhage the left
side of the interventricular septum and opposing papillary muscles are not a sign of
impact, but and index of catastrophic hypotension. They are also seen in head injuries;
they can occur within the space of few beats, as the author (BK) has seen the
prominent lesions in an avulsed heart after a military aircraft crash.
- The lungs are frequently injured, either from stabbing by fractured ribs penetrating
the pleura or from blunt impact. The latter often leads to a line of bruising down the
posterior part of the lung where it lies in the paravertebral gutter. There may be air
bullae or blood blisters under the pleura overlying in bruised areas and pneumothorax
or haemothorax may result. The interior of the lung may be pulped even in the
presence of an intact visceral pleura, from transmitted force or massive variations in
intrathoracic pressure during the impact. The lung often shows areas of bleeding
under the pleura, which may be from direct contusion, from aspiration of blood from
other damaged areas of lung or from blood sucked down the air passages from injuries
in the nose or mouth.

FIGURE 9.9 Penetration of the wrist and chest by wooden component of a bus seat. The
victim drove his car at speed into a bus and part of the resulting debris penetrated his left
ventricle.

- The major abdominal injury is ruptured liver, which may be damaged in any part. A
common lesions is central tearing of the upper surface, which may extend is often
seen in the form of shallow, sometimes multiple, parallel tears can occur with the
formation of a subcapsular haematoma, which can rupture later. The spleen also
shows shallow tears in some accidents, often around the hilum; in rare cases, it may
be avulsed from the pedicle. The mesentery and omentum often show bruising and,
rarely, there is laceration and fenestration sufficient to cause a lethal haemorrhage.
- Ejection injuries are common, and lethal in both driver and passengers. This is
particularly likely to happen in roll-overs accidents. Must research has been pursued
by manufactures to develop anti burst door locks, which have improved safety. Where
there has been considerable distortion of the vehicle frame, however, nothing can
prevent the doors from opening or even being torn off. It has been shown my Moore
and Tourin’s study (1954) at Cornell that ejection injuries followed steering-column
 lesions as the second most frequent type of trauma and, if a victim was ejected, there
was a fivefold greater chance of dying than if he was retained in the vehicle. Moore
and Tourin found that when doors burst open a third of the car occupants were
ejected.
Almost any kind of injury, usually multiple, may be sustained after ejection,
either from contact with the road surface or (in a significant proportion) from being
struck by other vehicles, especially on motorways.

FIGURE 9.10 Large subcapsular haemorrhage of the liver in a driver who struck the rim of
the steering wheel during severe deceleration. Such subcapsular lesion can remain intact for
hours or even days, then rupture into the abdominal cavity.