Thanks to Myrna Schmidt
The term blast refers to the intense sound wave created by a
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).
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).
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.
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.
(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.
Pulmonary broncho-pneumonia; brain coma; Intestinal perforation & peritonitis (Edmonds 3, Lavonas 7).
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).
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).
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.