For a country not traditionally prone to gunshot homicide or bombing, it is not unreasonable to expect critical care trainees to only have vicarious experience of such trauma patterns. It is therefore surprising to find questions about this topic in the CICM Part II exams. Question 2 from the second paper of 2017 placed the exam candidate in a position where they need to manage a guy who accidentally blew himself up in his garage. Why is this man hypotensive, the college asked. The question also asks about the causes and management of hypotension in severe burns, but because explosion is mentioned, it offers a handy excuse to include a chapter on blast injury (even though this meth lab likely underwent a deflagration rather than detonation, and therefore actual blast would likely have been minimal).

As far as published resources go, the "Ballistic injury" chapter from Oh's Manual by Michael C Reade and Peter D (Toby) Thomas groups projectile and blast trauma as allied categories, and is a good starting resource for the time-poor exam candidate. Virtually all that is required to answer Question 2 from the second paper of 2017 can be found in that chapter. If one needs to have a more detailed look for whatever reason, one's morbic curiosity would be well-satisfied by Maria Mayorga's excellent article "The pathology of primary blast overpressure injury" (1997) and "Shrapnel management" by Peyser et al (2006). For management of blast injuries in the ICU, the best resource is probably the article by Lavery et al (2004).

In summary, blast injury can be classified into five major categories:

Primary blast injury 
  • Acutely, vagally mediated bradycardia, hypotension and apnoea
  • Rupture of eardrums
  • Pneumothorax or tension pneumothorax
  • Peritonitis following overpressure rupture of bowel loops
  • Alveolar capillary injury with alveolar haemorrhage
  • Leaky pulmonary capillaries, "blast lung"
  • Lung contusion
  • Gas emboli due to disruption of pulmonary vessels
  • Rupture of the globe of eye
  • Traumatic brain injury (typically mild)
  • Long bone fractures and traumatic amputation
Secondary blast injury
  • High-velocity penetrating shrapnel injury
  • Low-velocity widespread superficial wounds ("battle acne")
Tertiary blast injury
  • Crush injury
  • Damage from falling debris, which could be anything
  • Trauma from being thrown against things, eg. walls, windows
Quarternary injury
  • Burns
  • Toxic gas or smoke inhalation, toxic element exposure. eg. lead poisoning from shrapnel
  • Radiation exposure
  • Asphyxia
  • Infection from retained shrapnel fragments
Quinary injury
  • Systemic inflammatory response and fever
  • Organ system failure due to sequelae of other blast injuries

Primary blast injury

Primary blast injury is the effect of a supersonic pressure wave moving through the body. No mass movement of air occurs- this is a pressure wave in the same sense that the arterial pulse is a pressure wave. This mainly does damage to hollow organs (middle ear, lung, gas-filled loops of bowel).  Few survivors will come to the ICU with primary blast injury effects being the dominant feature.

Prior to the recent American engagements, much of what we knew about blast injury came from man's inhumanity towards man. Between World Wars, cruel animal experiments also added some data. Some of these would have been instant YouTube classics. For instance, in 1939 Sir Joseph Barcroft published on the effects of placing goats within 15 feet of a 500lb bomb. Owing to limitations in contemporary munitions design "lung haemorrhages were the principal autopsy finding"; one might have expected the investigators to be showered with goat fragments had this thing been a modern ordinance. 

The graph below has been misappropriated from the excellent review of primary blast injury by Maria Mayorga (1997). The recordings were taken from a bunker which took a hit from some sort of shoulder-mounted weapon. Graph (b) demonstrates the classical pattern of pressure.

blast pressure wave recordings

The initial spike (well above atmospheric) represents the first encounter with the blast wave. The subsequent depression of pressure is the vacuum liberated by the expanding gases of the explosion. The oscillations in graph (a) represent reflected pressure waves (mainly from the ground in an open-space environment); in an enclosed space these reflected waves will amplify the damage.

Three major forces produce damage from the primary blast wave:

  • Implosion is where the blast wave travels through a gas-filled organ and causes the gas inside that organ to be compressed. As the primary blast wave passes, the compressed gas inside the organ re-expands with force, releasing a large amount of kinetic energy.
  • Spallation is the term used to describe the passage of a pressure wave from a dense medium to a less dense medium; the result is fragmentation of the dense medium at the level of the interface. An excellent example of this is the fountain of water which is seen over an underwater explosion.
  • Shearing trauma occurs when the pressure wave travels through tissues with different density and elasticity characteristics. These tissues can tear away from one another because the pressure wave causes these tissues to move at different velocities.

In summary, the effects of primary blast injury are:

  • Acutely, vagally mediated bradycardia, hypotension and apnoea
  • Rupture of eardrums
  • Pneumothorax or tension pneumothorax
  • Peritonitis following overpressure rupture of bowel loops
  • Alveolar capillary injury with alveolar haemorrhage
  • Leaky pulmonary capillaries, "blast lung"
  • Lung contusion
  • Gas emboli due to disruption of pulmonary vessels
  • Rupture of the globe of eye
  • Traumatic brain injury (typically mild)
  • Long bone fractures and traumatic amputation

Death from primary blast injury

Primary blast injury accounts for a small proportion of the total morbidity from explosions, but for the majority of explosion-related deaths.  This death can be quite sudden. Tunbridge and Wilson (1943) describe the case of "a German officer found dead in the act of moving a chess piece". Most of these people die from massive air embolism and the disruption of the pulmonary circulation by the pressure wave. Shearing of large airways and surrounding vessels occurs, with air being forced into the circulation by the re-expansion of intrathoracic air after its initial compression by the pressure wave.

Immediate cardiovascular response to being hit by a blast wave

The most immediate effects of primary blast injury (apart from instant death by air embolism) are mainly related to the vasovagal consequences of chest compression by the blast wave. Think of it as a massive sudden Valsalva manoeuvre. Bradycardia, hypotension and apnoea are seen immediately after the blast.  Ohnishi et al (2001)  exploded a bunch of rats and found that this effect can be completely abolished by vagotomy. At least in the rat model, this effect wears off within five minutes.

Lung contusions due to primary blast injury

The respiratory tract represents a column of gas, and therefore a conduit for the blast wave. It travels through them until it meets an air/tissue interface, and there it imparts some of its energy. This manifests as lung contusion, histologically featuring edema and alveolar haemorrhage. The distribution of these contusions is peripheral, i.e wherever the lungs abut the ribcage, heart and diaphragm. The airways also have some of their epithelium stripped as the cells are separated from their basal lamina by the blast wave.

Bowel perforation due to primary blast injury

Gas pockets other than the lung will also take a hit from the overpressure wave. Specifically, pockets of gas in the bowel are susceptible. The gut wall may rupture immediately, but the peritonitis and abdominal collections which result from this are typically not seen until some hours or days have passed, and so one might describe them as "delayed" sequelae.

Secondary blast injury

One might summarise this pattern of trauma as "being hit by flying debris". The explosive device has some sort of physical form, which likely consists at minimum of a casing and detonator fuse. Neither of these is going to disintegrate completely during the explosion, and some of these physical components will be launched at high speed at anybody in the vicinity. The velocity of these fragments dissipates more slowly than the primary blast wave, which means that casualties well outside of the "lung contusion and bowel rupture" radius will still end up being severely damaged with multiple penetrating injuries. Munitions designed for terrorist purposes factor this in, and are made with fragmentation in mind (packed as they are with coins, ball bearings or nails). 

Management of any individual shrapnel wound occupies the same spectrum as bullet holes or any other penetrating trauma for that matter. Peyser et al (2006) in their detailed discussion of shrapnel management have brought up several issues to consider:

  • It looks worse than it is. Recent changes in practice among trauma surgeons have yielded improved rates of limb preservation because they have become more conservative twith their early debridement. For instance, muscle which looks dead upon initial inspection ends up looking viable two or three days later. The current recommendations are to only debride tissue which is clearly devitalised, i.e. tissues which are obviously disconnected from their vascular supply.
  • It may get infected.  The penetrating injuries from explosion debris have that magically bacteriophilic combination of being deep and containing devitalised tissue. Contrary to popular belief, being exploded does nothing to sterilise shrapnel. Ergo, infections may develop.
  • Deep shrapnel can stay where it is, unless obviously needing to be removed (eg. becoming in nidus for infection). Needlessly digging around can have adverse consequences and promotes surgical complications. The only situations where you'd remove such fragments would be if they were in a joint space (which would limit function) or if they are somewhere near a vital organ (eg.  near the aorta, where they create a risk of catastrophic erosion). An alternative reason is decontamination; not all shrapnel is biologically inert, eg. one finds that retained lead shot can cause lead toxicity over time (particulalry if it is in the CNS); depleted uranium in particular has multiorgan toxicity which takes years to manifest. 

Tertiary blast injury

This form of blast injury is not very blast-specigic, and can be summarised as "being thrown against things, and having those things collapse on you". The tertiary injuries from a blast are mediated by the outward expansion and mass movement of superheated gases. The force of this mass movement has a tendency to throw people and objects. This is responsible for such things as traumatic limb amputation and head injuries. After being thrown, one may come to rest in a position under a structure which then collapses and buries one in rubble. An unusual consequence of this brave new world filled with IEDs is the routine occurrence of vehicles being exploded from beneath, giving rise to a trauma patters whereby the floor of the vehicle is thrown forcefully against the lower limbs of the occupants.

Quaternary blast injury

Quaternary blast injuries can be loosely defined as "all other explosion-related injuries, illnesses, or diseases not due to primary, secondary, or tertiary mechanisms" (tacmedaustralia.com.au). This includes:

  • Burns
  • Toxic gas or smoke inhalation, toxic element exposure. eg. lead poisoning from shrapnel
  • Radiation exposure
  • Asphyxia
  • Infection from retained shrapnel fragments

"Quinary" blast injury

This fifth pattern of blast injury is not widely recognised, and may belong in the category of apocrypha. It was described by Kluger et al in 2006 as some sort of otherwise unespected inflammatory response, manifested as "hyperpyrexia, sweating, low central venous pressure, and positive fluid balance".  The authors interpreted it as systemic response to the absorption of undecomposed pentaerythritol tetranitrate, a potent explosive material which has seen peak use prior to World War II. As a nitrate it has vasodilator properties, and had at one point been marketed by Pfizer under the trade name "Pentrax".

How is this not quaternary blast injury, all other explosion-related injuries, illnesses, or diseases not due to" etc.? Not since 2006 have we heard about this classification group. The Reade & Thomas chapter for Oh's Manual omits this from their classification.

ICU management of blast injury

Much of the management described here falls into the "generic supportive" category, as there is nothing magical about the ICU management of blast injury which is not common with any other sort of polytrauma. The dominant focus is usually going to be on the acute lung injury due to primary blast effects, which will manifest as pulmonary oedema or ARDS initially, and progress into pulmonary contusions. 

Immediate and pre-hospital management issues:

  • Under warzone conditions, CPR is contraindicated. US army guidelines for the management of battlefield blast casualties recommend against it.
  • Vagal bradycardia following primary blast injury may mask haemorrhagic shock

Early ICU care:

  • A - intubation (airway burns, fractures of tracheal cartilages etc)
  • B - mechanical ventilation with lung-protective strategy (the "blast lung" will behave like ARDS). However, barotrauma is even more likely, and ECMO is not an option. Pizov et al (1999) found that the anticoagulation from ECMO has a tendency to produce fatal pulmonary haemorrhage.
  • C - fluid resuscitation,  consisting mainly of blood products (1:1:1) and following the principles of haemostatic resuscitation
  • D - Analgesia and sedation as standard
  • E - Electrolyte testing needs to consider potential for significant contamination from metallic cations which may interfere with ion-selective electrode function.
  • F - Acute kidney injury from rhabdomyolysis needs to be anticipated with adequate hydration.
  • G - Damage control laparotomy for intra-abdominal injuries should specifically look for bowel perforations
  • H - Blood transfusion should follow massive transfusion protocols and the proportion of products should be proactively chosen to avoid dilutional coagulopathy
  • I - Antibiotics should be given, covering for aerobic gram-positive skin organisms. At minimum tetanus prophylaxis should be given.

References

Michael C Reade and Peter D (Toby) Thomas. "Ballistic injury". In: Oh's Manual, 8th ed. p 861

Wightman, John M., and Sheri L. Gladish. "Explosions and blast injuries." Annals of emergency medicine 37.6 (2001): 664-678.

Wolf, Stephen J., et al. "Blast injuries." The Lancet 374.9687 (2009): 405-415.

Tunbridge, R. E., and J. V. Wilson. "The pathological and clinical findings in blast injury." QJM: An International Journal of Medicine12.3 (1943): 169-184.

Clemedson, Carl-Johan. "Blast injury." Physiological reviews 36.3 (1956): 336-354.

Zuckerman, Solly. "Experimental study of blast injuries to the lungs." The Lancet 236.6104 (1940): 219-224.

Mayorga, Maria A. "The pathology of primary blast overpressure injury." Toxicology 121.1 (1997): 17-28.

Sawdon, Marina, et al. "The effects of primary thoracic blast injury and morphine on the response to haemorrhage in the anaesthetised rat." Experimental physiology 87.6 (2002): 683-689.

Ohnishi, M., et al. "Reflex nature of the cardiorespiratory response to primary thoracic blast injury in the anaesthetised rat.Experimental physiology 86.3 (2001): 357-364.

Peyser, Amos, Amal Khoury, and Meir Liebergall. "Shrapnel management." Journal of the American Academy of Orthopaedic Surgeons 14.10 (2006): S66-S70.

Kluger, Yoram, et al. "The quinary pattern of blast injury." American journal of disaster medicine 2.1 (2006): 21-25.

Hughes, F.N. "New Drugs"Can Med Assoc J. 80 (12): 997–998. 1959.

Lavery, Gavin G., and Ken G. Lowry. "Management of blast injuries and shock lung." Current Opinion in Anesthesiology 17.2 (2004): 151-157.

Pizov, Reuven, et al. "Blast lung injury from an explosion on a civilian bus." CHEST Journal 115.1 (1999): 165-172.