For a country not traditionally prone to gunshot homicide or bombing, it is not unreasonable to expect critical care trainees to only have a 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 morbid 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||
|Secondary blast injury||
|Tertiary 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.
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:
In summary, the effects of primary blast injury are:
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.
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.
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. Again, much of this data comes from people in the (mostly) post-World-War-I period experimenting with animals. D.R Hooker (1923) famously went to the Sandy Hook Proving Ground and tied household pets to artillery pieces used for powder-testing. Original notes are available to describe these scenes, offering a glimpse into an almost afffectionate reationhip between cruel experimenter and doomed subject:
The term "lung contusion" was never used to describe the lesions, but clearly that's what they were:
"Cursory post-mortem examination revealed normal viscera except the lungs. These organs showed areas of red hepatization especiallv in the lower lobes, which were practically solidified."
In the modern era, where blast-injured human subjects have become much more ethically acceptable, Mackenzie & Tunnicliffe (2011) reported similar autopsy findings. Between 35% and 45% of blast injury fatalities from the battle of Monte Cassino (1944) and from Northern Ireland (1969-1974) had diffuse lung contusions.
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.
Though the relative homogeneity and fluid cushions of the brain tend to protect it from the all but the worst blacsts, traumatic brain injury can occur from exposure to explosions, and this can range from mild concussion to extensive cerebral oedema and diffuse axonal injury (Hicks et al, 2011). The symptoms of post-concussive syndrome and cerebral oedema have historically been described as "shell shock" or commotio cerebri. The onset of clinical features may be insidious. Frederick Mott, the Pathologist to the London County Counci Asylums, gave an excellent account of this from 1917:
"Although he remarked to another man that he "could not stand it much longer," he did not give way until the following day, twelve hours later, when perhaps six shells came over... Next morning he woke up apparently well, and suddenly died."
Examination of the man's brain, kindly pickled in Kaiserling's fluid and sent back from the front by Lieut.-Colonel T. R. Elliott and Professor Arthur Keith, revealed a brain which was "extremely congested, and on each side of every superficial vessel there was an ecchymosis." Apart from gross damage, histologically it appears that the blast wave produces a widespread activation of microglia in the white and gray matter. Long-lasting neurological sequelae often follow.
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:
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 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:
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.
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:
Early ICU care: