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Comprehensive information about diving and undersea medicine for the non-medical diver, the non-diving physician and the specialist. |
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Underwater Blast
Injuries
DR. P.G. LANDSBERG MD
Originally published in "Trauma & Emergency Medicine Vol 17 No 2 July 2000
in South Africa.
Thanks to Myrna Schmidt
catschmidt@icon.co.za
INTRODUCTION
The term blast refers to the intense sound wave created by a
detonated
explosive. The detonation energy of an explosion is distributed between
(1) the initial shock wave
(2) the velocity imparted to the water from the pressure of the steep
fronted shock wave
(3) the pulses produced by successive collapses of the bubble
(4) the turbulence & thrusting action of the mass motion
of the surrounding water (Shilling 1).
TERMINOLOGY
Blast injury refers to the bio-physical & patho-physiological
events
& the clinical syndrome & patho- anatomical changes caused by
exposure
of a living body to the shock (blast) wave generated by a detonated
high
explosive. There are 4 types of blast injury & an individual
patient
may be injured by more than one mechanism (Stapsynski 2, Lavonas 7).
(1) Primary blast injury is caused by the shock wave & the effects
are greatest at the gas-liquid interface, thus air containing organs
are
most easily damaged in air & underwater blasts.
(2) Secondary blast injury is caused by displaced debris.
(3) Tertiary blast injury is due to collision with stationary objects.
Both are due to the shock wave accelerating loose objects outward from
an explosion.
(4) Miscellaneous injuries include exposure to dust which may be
radioactive
& thermal burns from the explosion & fires.
Other terms used, particularly for air blast, are blast concussion
& reflex paralysis, blast chest, shell shock, vent du boulet, wind
of shot, ”breath of the cannon ball”(Shilling 1).
Blast injury was first described in 1924. World War II studies in
England
& Germany established the clinical & pathological features of
this
syndrome. Research into the pathophysiology of primary blast injury
continues
using free-radical scavengers & inflammatory inhibitors in animal
experiments
(Lavonas 7). However, blast is not past history, for explosives are
used
in salvage & demolition operations by civilian divers & the
charges
are large enough to cause blast injury & death. Minor explosions
have
caused blast injury & death during underwater electric cutting
&
welding & even in sport diving where a thunderflash was thrown onto
a diver. (Personal communication medico legal inquest May 1999).
Blast injuries were once rare in peacetime, but the world wide spread
of terrorism has made no country immune from the potential of civilian
blast injuries (Stapcynski2,Lavonas 7).
.
BLAST PHYSICS
For an explosion with the same energy & at the same distance an
underwater blast is more dangerous than an air blast. This is because,
in air, the blast dissipates more rapidly & tends to be reflected
at
the body surface; in water the blast wave travels through the body
&
causes internal gas liquid inter-face organ damage (Edmonds 3, Lavonas
7).
An explosion is a very fast chemical reaction, which propagates through
the explosive at 2-9 km/s. The products of the reaction are heat &
combustion gases (CO2).A bubble of gas is formed in the
water.
The pressure in the gas bubble is up to 50 000 ATA & the
temperature
3000 C. The bubble rapidly expands in a sphere, displacing water, which
is incompressible. This rapid expansion generates the first
pressure
wave or primary pulse as the pressure in the gas bubble is transferred
into the water (Edmonds 3).
The initial pressure change of the blast wave is steep, rising to a
peak pressure within milliseconds. The pressure in the bubble falls as
it expands & the gas cools. The fall of pressure at the end
of
the explosion reflects the end of the expansion of the gas & takes
milliseconds. The pressure is then less than the previous ambient
pressure. .Most organ damage is due to the primary shock wave
(Stapcynski
2, see Figure 1).
The momentum of the water which has been displaced by the bubble,
displacement wave -->, enlarges the bubble past it’s equilibrium
volume
& a series of volume swings are initiated. These volume
oscillations
of the gas bubble cause a series of secondary pressure waves, or
secondary
pulses (Edmonds 3).
Near the point of detonation the velocity of the shock wave is great
& is related to the speed with which the explosion
detonates.
There are 2 main types of explosives :-
(1) High explosives (HE) detonate rapidly, the chemical reaction is
triggered by a mechanical shock wave (detonator), that travels at high
speed (20 000 m/s) through the explosive. TNT (Tri Nitro Toluene)
is a HE, 1g releases 1 120 calories of blast energy generating a
pressure of 10x60 Kpa within the initial gas bubble. This rapid
release
of energy & pressure has a shattering power on nearby objects
called
brisance. (2) Gun powder is ordinary explosive releasing energy
slowly
by burning & does not have brisance (Stapcynski 2).
.
At some distance from the detonation, the velocity of the pressure
waves slows to that of sound (1.5km/s) & they are reflected &
absorbed
like sound waves. In air the gas & air surrounding the
explosion are compressed & absorb energy from the explosion.
In water, being incompressible, there is little absorption & the
pressure
wave is transmitted with greater intensity over a longer range.
The
lethal range of an explosion in water is far greater than the same mass
of explosion in air & this increases mortality in underwater
explosions.
The potential damage depends on (1) the size of the charge (2) depth of
detonation (3) distance from the target (Edmonds 3, Lavonas 7).
When a small explosive is detonated in an empty open drum it does not
dent it. When the drum is filled with water the same explosive
will
rupture the drum. A man, unharmed by an air explosion of a hand
grenade
at 5m (out of shrapnel line) would be killed by the same explosion
underwater.
Other reflected waves from an underwater explosion combine with the
primary & secondary waves causing increased damage. If the
seabed
is distant from the detonation this effect is negligible.
The surface of the water will be broken or shredded & thrown up
into a dome. This dissipates a small part of the primary pressure wave
& the rest is reflected back into the water. The slick is a
rapidly
expanding ring of dark water due to advancing pressure waves. The
plume is the last manifestation of an underwater explosion & is the
result of gas breaking the surface.
CHARGE SIZE, DISTANCE & RISK OF INJURY for TNT is given by :-
(Imperial pounds divided by 2.2 convert to metric kilograms)
Pressure (lb/in2) = 13000x charge size (lb)1/3 divided by Distance
from the charge (feet) (3ft=1m)
2000 lb/in2 = 909 kg will cause death
500 lb/in2 = 227 kg will cause serious injury or death.
MECHANISM OF BLAST INJURY IN AIR
IN air the cause of damage is from the shock wave, shrapnel &
objects
drawn into the pressure wave. In water these objects are
retarded.
In air much of the pressure wave is reflected at the body surface
because
this is an interface between media of different densities,any blast
effect
acting through the ear nose & mouth. Intestinal injury rarely
occurs. The threshold for lung damage =100Kpa,15psi(Edmonds 3
Lavonas
7).
MECHANISM OF BLAST INJURY IN WATER
The blast wave passes through the body as it is of similar consistency
to water. Molecules are displaced very little except in gas
spaces capable of compression. Damage is at the gas water interfaces
within
the body. The gas in the gas filled cavities is instantaneously
compressed
as the pressure wave passes & the walls of the spaces are torn or
shredded
as in barotrauma. Damage occurs in the lungs, intestines, sinus
&
ear cavities. In the lungs the damage is not due to pressure
transmitted
via the upper airways (as in air blasts) but as a result of
transmission
of the wave directly through the thoracic wall.
ANIMAL EXPERIMENTS
RESPIRATORY damage: pulmonary haemorrhage at bases, bronchi
& trachea; alveolar & interstitial emphysema;
pneumo-haemothorax.
INTESTINAL damage: subserous & submucosal
haemorrhage;
perforation. No kidney, bladder, liver or gallbladder
damage.
If the thorax & abdomen were immersed, the lungs would be
more
affected .If only the abdomen were immersed the intestines were
most
affected with rectal bleeding.
The above results show the importance of the air-water interface in
damage from an underwater blast. If 3 loops of bowel are
experimentally
occluded, collapsing 1,filling 2 with saline & filling 3 with air,
only the air loop is damaged.
CAUSES OF DEATH : PRIMARY
(1) PULMONARY. Low arterial 02 saturation (PaO2) hypoxaemia.
High arterial CO2 retention (PaCO2) hypercarbia.
Respiratory acidosis.
(2) BRAIN.Petechial haemorrhage & oedema caused by a rapid
increase in the venous pressure, following compression of the thoracic
& abdominal venous reservoirs by the pressure wave. With this
transmission of pressure into the cerebral venous system small blood
vessels
rupture.
(3) AIR EMBOLISM, due to rupture of lung alveoli & compression
of the alveolar gas which enters the pulmonary vein left ventricle
&
cerebro-vascular system with air embolism to the brain.
: SECONDARY
Pulmonary broncho-pneumonia; brain coma; Intestinal perforation
& peritonitis (Edmonds 3, Lavonas 7).
CLINICAL PRESENTATION
Clinical signs & symptoms in primary blast injured patients result
from damage to the lungs, heart, brain, bowel & ear.
LUNGS Massive haemorrhage due to alveolar rupture
is the most prominent feature; dyspnoea, chest pain, haemoptysis,
difficulty in exhaling & cyanosis result. In animals
apnoea
up to 1min or until death occurs. This is due to vagal reflexes
from
the damaged lungs as a protective mechanism to restrict lung activity
to
a minimum to maintain life, sparing the damaged lung tissue, &
preventing
further bleeding. Contraction of the pulmonary capillaries,
increases
pulmonary pressure, decreases pre-load causing cor pulmonale.
HEART Animal experiments demonstrated instantaneous
bradycardia
with the first post detonation normal heart beat occurring only 30sec
later.
Bradycardia is due to vagal reflexes from the damaged lungs.
Circulatory
hypotension is due to decreased cardiac output from blood loss in the
lungs,
cor pulmonale &/or myocardial ischaemia from air emboli in the
coronary
arteries. ECG shows sinus tachycardia, Q waves or ST ischaemia,
due
to secondary effects of coronary artery air emboli.
NERVOUS SYSTEM Brain concussion, headache, delirium
to coma(subdural hematoma) Air embolism to coronary arteries, left
brain
& circle of Willis, will cause death at or soon after the time of
injury.
Systemic air embolism may be difficult to detect clinically. Air
emboli may be seen in the retina & on MRI. Always have
a high index of suspicion. Spinal cord concussion causes a
transient paralysis when the blast is close. Concussion to the
autonomic
nervous system may cause ileus of the bowel.
INTESTINAL Abdominal pain, nausea & vomiting, with
tenesmus occurs with tender, rebound, bright red rectal bleed, silent
disstended abdomen. Early (1-2 days) or late (14 days) bowel
perforations.
The most consistent findings were retroperitoneal & subserosal
haemorrhages.
Mesenteric thrombosis with bowel gangrene, obstruction &
peritonitis
also occur.
EAR Tympanic membrane (™) rupture, indicates high
pressure (40Kpa,6psi) primary shock wave damage which correlates with
more
serious organ damage. At a hyperbaric pressure (100Kpa, 15psi,
2ATA)
the TM will always rupture. Deafness with tinnitis is due to
dislocation
of the ossicles, TM rupture & sensineural hearing loss (Shilling
1,4
Edmonds 3 Lavonas 7).
EMERGENCY TREATMENT
Advanced Trauma Life Support: Initial evaluation, resuscitation
& supportive care as standardized (ATLS 1995, 5).
Supplemental O2 is always given because the damage to the lungs may
not be initially apparent. Pulmonary barotrauma is the most common
fatal
primary blast injury. This includes pulmonary contusion, arterial air
embolism
& free radical associated injuries including thrombosis,
lipoxygenation
& disseminated intravascular coagulation (DIC). Adult
respiratory
distress syndrome (ARDS) may be the result of direct lung injury or
shock
due to other body injuries.
Arterial gas embolism (AGE) resulting from pulmonary barotrauma,
requires
recompression treatment. Hyperbaric oxygen therapy (HBOT) is the
definitive
treatment & the patient should be transferred to a hyperbaric
oxygen
chamber. Air transport by low altitude helicopter is necessary to
prevent expansion of air emboli.Haemo-pneumothorax should be carefully
monitored & chest tubes inserted as necessary.
Airway must be stable & patent Patients without
adequate
spontaneous respiration should have endo-tracheal intubation &
mechanical
ventilation. Mechanical ventilation (PPV & PEEP) carries the
risk of pneumo-thorax, air embolism & decreased cardiac output.
General anesthesia is poorly tolerated during the 24-48 hour period
following blast injury due to the risk of air emboli during surgery.
Observation of all patients, especially with TM rupture, is necessary
as primary blast injuries may evolve over a period of longer than 4
hours.(Stapcynski
2 Edmonds 3 Lavonas 7).
PREVENTION
Avoid diving in areas where explosions are possible. A dry diving
suit gives the most protection. Float on back on surface. If the
diver is near a shallow surface the primary pressure wave may be
prolonged
by reflected waves. Lift the chest & abdomen out of the water, on a
solid support. Face away from explosion (Edmonds 3).
DIVING ACCIDENT INVESTIGATION PANEL
Examination of fatal diving accident reports indicates that future
accidents may be prevented by a panel of experts which examines all
aspects
of the accident & gives a confidential report to the inquest
magistrate
(Landsberg 6).
.
UW BLAST REFERENCES
(1) SHILLING et al (1984):The Physician’s Guide to Diving Medicine;
Blast 421-426.
(2) STAPCYNSKI J S (1982):Blast Injury,An Emerg Med 11:687.
(3) EDMONDS C et al(1984):Diving & Subaquatic Med 3rd Ed Underwater
Explosions: 348.
(4) SHILLING ET AL (1976):The Underwater Handbook:A Guide to Physiology
& Performance for the Engineer.Underwater Blast 637.
(5) ATLS (1995):American College of
Surgeons.
(6) LANDSBERG P G (1976):South African Underwater Diving
Accidents
1969-1976. S Afr Med J 50. 2155.
(7) LAVONAS E , DANZL D (1999): Blast Injuries.
Medline & citation search.
HYPERLINK http://www.emedicine.com/emerg/topic63.htm
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