Blast injury and gunshot wounds: Pathophysiology and principles of management

Chapter 77 Blast injury and gunshot wounds


pathophysiology and principles of management



Widespread terrorist outrages in the recent past have once again served to emphasise that unpredictable events can suddenly deliver numbers of casualties to civilian hospitals, with unfamiliar patterns of injury. An understanding of the pathophysiology of blast injury, and the impact of such events on hospital function, will help medical staff make appropriate management decisions, often under difficult circumstances.14



BLAST INJURY



PHYSICS OF EXPLOSIONS5


An explosion is the almost instantaneous release of stored energy. The energy may come from, for example, pressurised gas, a nuclear reaction or stored chemical energy. Thus specific ‘explosives’ are not necessarily required. Explosives are materials that contain stored chemical energy that may be released rapidly. High-performance explosives release this energy by means of a chemical reaction which propagates through the explosive material faster than the speed of sound; thus the detonation velocity is of the order of 8 km/s compared with the speed of sound in air, 0.33 km/s.5 This produces a supersonic shock front (blast wave) with a rapidly expanding cloud of gaseous reaction products which causes damage to structures and people in the vicinity. In effect, there is an extremely rapid increase in atmospheric pressure, ‘positive overpressure’, the duration of which is dependent on the magnitude of the explosive charge. This dies away exponentially and is followed by a negative pressure phase produced by gases forced away from the centre of the blast leaving a vacuum. Blast winds may subsequently move paradoxically towards the explosion as pressures equalise.


The blast wave carries with it energised environmental debris and device fragments. These are propelled substantial distances. In air, the blast wave intensity dies away rapidly with distance (with an inverse cube relationship) while debris travels further with the capacity to damage and injure at much greater distances. This is reversed in an underwater blast. Water propagates the blast wave effectively but ‘drag’ reduces the range of debris and device fragments.


In addition to the kinetic energy released, heat and light energy are also produced, and can contribute to damage and injury. For a deliberate explosion, such as that produced by a military or terrorist device, the precise characteristics depend upon a number of factors including the size and nature of the container, the environment, and the dispositions of buildings and rooms.




EXPLOSIVE DEVICES (Table 77.1)


Conventional military anti-personnel devices rely on fragment generation to produce ‘secondary’ injuries. The device’s casing is designed to produce fragments, and may contain preformed fragments or notched wire to increase the fragment load. An 81 mm mortar round contains a small quantity (∼1 kg) of high explosive; the blast itself would only be lethal within 2–3 m, but the fragment cloud generated will seriously injure or kill within a radius of around 85 m. Improvised explosive devices (IED), built by terrorists, contain material (e.g. bolts, nails) to increase secondary injury. Larger devices, such as air-delivered free-fall bombs, missiles or artillery shells, contain sufficient explosive to produce secondary injury by throwing bricks, masonry debris and glass substantial distances. In addition, the blast may collapse physical structures such as walls and buildings.


Table 77.1 Types of explosive devices















Conventional munitions: e.g. grenades, aerial bombs, mortar bombs, rockets All types of blast injury may occur, but penetrating injuries from multiple fragments predominate. Primary fragments are derived from the munition; preformed within the shell or from the casing when the munition explodes. Other materials (building debris, vehicle components) energised by the blast form secondary fragments.
Terrorist devices: typically contain a few kilograms of explosive (NB: Recent attacks have been larger, more sophisticated and specifically designed to maximise casualties) Although the reported incidence of primary blast injuries varies from 1 to 76%, serious primary blast injury is uncommon and secondary and tertiary injuries predominate. Mortality is low unless the device is large, explodes in a confined space or there is structural collapse. Less than 50% of those presenting to hospital will require admission.2
Antipersonnel landmines: common in developing countries; indiscriminate in action Patterns of injury:


Enhanced-blast munitions, e.g. fuel-air or thermobaric explosives Designed to injure by primary blast effect rather than by fragmentation. Used in recent conflict situations.

Anti-personnel mines are broadly of two types:





PRIMARY BLAST INJURY


A blast wave passing through an individual behaves like an acoustic wave, giving up energy at interfaces between materials of differing acoustic quality, causing damage. Air-containing organs – the lungs, the gut and the ears – are particularly vulnerable.8,9 Massive pressure pulses, causing body wall distortion, can tear solid organs from their vascular supplies. Recent work suggests that traumatic amputation is caused by shock wave-induced stress concentrations that fracture the long bones which are subsequently removed by flailing and blast wind effects.10 This explains why amputations are generally not through joints.11


Primary blast injury (PBI) is unusual amongst survivors,12 but very common in those killed immediately.13 The blast wave dies away rapidly with distance, but device fragments and energised debris travel and injure at greater distances. If a casualty is close enough to sustain primary injury there will be overwhelming secondary and tertiary damage. The majority of survivors from an explosion will have sustained secondary or tertiary injuries.12 Military and terrorist devices are specifically designed to maximise casualties by the use of fragments.


Primary injury does sometimes occur and an understanding of mechanisms is useful in guiding management of such casualties. Survivors presenting with signs of one PBI (e.g. visceral perforation) must be assumed to have damage to other vulnerable regions and investigated accordingly. Casualties as close to the blast as other overwhelmingly injured fatalities must be investigated carefully for PBI. The absence of eardrum damage does not exclude PBI, as eardrum rupture depends on a number of factors, including critically the orientation of the head to the blast.



THE LUNG


Immediate effects of severe blast exposure may include apnoea and bradycardia.9 The blast wave produces disruption of the alveolar–capillary barrier leading to intra-alveolar haemorrhage that may be massive. This occurs in regions of the chest subjected most directly to the incident blast wave (not by a pressure pulse travelling down the trachea). The wave may ‘echo’ around the pleural cavity, exhibiting interference effects and injuring other regions at points of stress wave concentration. Such regions include the juxtamediastinal tissue and the diaphragmatic recesses. Pulmonary contusions are produced, with associated shunt and reduction in compliance, and pulmonary fat embolism has recently been described.14 The surface of the lung may evolve bullae, which are mechanically weak and may rupture producing pneumothoraces. These may present early or late, perhaps triggered by mechanical ventilation. Damage to hilar structures may be produced by severe and long duration overpressures; pulmonary artery and vein injuries are usually rapidly fatal. A variety of clinical features have been described and these are summarised in Table 77.2. Radiological features are outlined in Table 77.3.


Table 77.2 Clinical features of blast lung



























Symptoms Dyspnoea
Cough – dry to productive with frothy sputum; haemoptysis
Chest pain or discomfort (typically retrosternal)
Signs Cyanosis
Torrential pulmonary haemorrhage
Tachypnoea
Reduced breath sounds, dullness to percussion
Coarse crackles, wheeze
Features of pneumothorax or haemopneumothorax. Subcutaneous emphysema.
Retrosternal crunch (pneumomediastinum)
Retinal artery air emboli

Table 77.3 Radiological evidence of blast lung















Diffuse pulmonary opacities or ‘infiltrates’ (typically these develop within a few hours, become maximal at 24–48 hours and resolve over 7 days)
Pneumothorax/haemopneumothorax
Interstitial (peribronchial) emphysema
Subcutaneous emphysema
Pneumomediastinum
Pneumoperitoneum (usually secondary to perforation of an abdominal viscus, but tension pneumoperitoneum has been ascribed to blast lung)

Investigations obtained may depend on availability and prioritisation if the casualty burden is high. Chest X-ray (CXR), blood gas analysis and pulse oximetry monitoring are useful. CXR will provide data concerning pneumothorax, pneumomediastinum, subcutaneous and interstitial emphysema and subdiaphragmatic air from visceral perforation. The CXR is a poor modality for quantifying extent of contusion, for which computed tomography (CT) is better.15,16 CT may be unavailable or overwhelmed with demand. In the majority of cases CT will not provide management-altering data. The priority is close clinical observation of conventional parameters to identify the drift toward respiratory failure.


The management of significant PBI is similar to that of any other pulmonary contusion with a number of corollaries from the pathology. PBI renders the lungs prone to development of pneumothorax, and importantly, significant air emboli may be created.17 Historically, continuous positive airway pressure (CPAP) and mechanical ventilation were regarded as so hazardous as to be treatments of last resort. This was due to fear of creating or exacerbating air embolism. Modern strategies based around modest gas exchange targets, with limited volume excursion and pressure change, has ameliorated these concerns.18,19 A variety of non-conventional strategies including hyperbaric chambers, inhaled nitric oxide, high frequency jet ventilation and extracorporeal membrane oxygenation (ECMO) have been tried with varying success. The prognosis for pulmonary function in survivors is generally excellent.20



THE ABDOMEN


The hollow viscera are at risk of primary blast injury, particularly in cases of immersion blast. Isolated PBI to the gut is unusual in air blast, and generally occurs in the presence of severe secondary and tertiary injuries. At high overpressures, immediate rupture of the gut wall occurs with bleeding and spillage of intraluminal contents into the peritoneal cavity. More commonly, and at lower overpressures, haemorrhage develops within the intestinal wall, ranging from small petechiae to confluent haematomas. These lesions are characterised by varying degrees of vascular damage and thus some will progress to necrosis of the gut wall and late perforation.21


With large numbers of casualties, surgical triage is difficult. Data derived from a pig model provide some guidance as to those contusions at greater risk of late perforation.22 Bowel contusions > 15 mm diameter and colonic contusions > 20 mm diameter were at higher risk and warranted resection; smaller lesions could be treated conservatively. Circumferential lesions and those on the antimesenteric border were also associated with greater evidence of microvascular damage and perforation risk. Subcapsular haematomas, lacerations of solid organs, testicular rupture and retroperitoneal haematomas have all been described. These result from high blast loads and are likely to present early with abdominal signs and cardiovascular instability. In some patients the indications for exploratory laparotomy are obvious; in others PBI to the abdomen represents a diagnostic challenge, since it may be clinically silent until complications are advanced.


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Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on Blast injury and gunshot wounds: Pathophysiology and principles of management

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