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: • Traumatic amputation of foot or leg, due to standing on a buried ‘point detonating’ mine. Mine fragments, grass, soil, parts of shoe and foot are blown upwards with substantial proximal tissue damage and contamination. • More random distribution of penetrating injuries caused by fragment mine triggered near victim by a tripwire. • Severe upper limb and facial injuries due to handling of a mine.

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:

• buried mines detonate and disrupt the foot and lower leg, blasting debris from the mine, the ground, footwear and device fragments up fascial planes towards the knee

• above ground mines, initiated by trip or command wires or electronic sensors, produce a preformed fragment load leading to secondary injury, with a high incidence of ocular damage

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.