Emergency War Surgery NATO Handbook: Part I: Types of Wounds and Injuries: Chapter V: Blast Injuries
United States Department of Defense
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Primary blast injury effects may be only a part of the problem in a casualty suffering from multiple trauma. In the setting of injury associated with a large blast, the basic principles of trauma care still apply, and resuscitation and evaluation should proceed by the usual numbers. The key to recognizing that primary blast injury is present is a history or setting suggestive of a powerful explosion. One should then search for corroborative findings with a careful examination of the tympanic membranes, retinal arteries, chest, and abdomen. Specialized military ordinance such as a fuel air explosive or underwater blast may cause a relatively pure form of primary blast injury. Fuel air explosive ordinance is a particularly powerful air blast designed to clear mine fields by detonating the land mines in place.
The ear and the upper respiratory tract are the structures most sensitive to primary blast injury. Rupture of the tympanic membrane may cause tinnitus, pain, and hearing loss. Physical examination will reveal blood in the external canal and otoscopic evidence of perforation. In severe injury, there can be vestibular damage with disordered equilibrium. Pressure levels high enough to cause serious injury to the lungs or gut almost invariably rupture the eardrums. This may not be the case when ears were protected by ear muffs or ear plugs. Often the tympanic membranes are not ruptured by high-grade underwater explosions if the head is above water and the tympanic membranes are not exposed to the underwater pressure wave. Petechial hemorrhage in the hypopharynx and larynx is also observed at relatively low pressure levels and, like tympanic rupture, its absence speaks against exposure to high levels of blast. Upper airway petechial hemorrhage such as this is unlikely to cause airway compromise or other symptoms.
Arterial air emboli represent an immediate threat to life. Clinical evaluation in the presence of air emboli will reveal evidence of cerebral dysfunction such as altered affect, confusion, disorientation, or focal neurologic signs. When such findings are noted after an explosion, one must first consider a skull fracture or other closed head injury. Direct trauma to the skull from secondary or tertiary blast effects is more likely than air emboli in most settings. It may be possible to directly visualize air bubbles in the retinal vessels or to observe patchy blanching of the tongue. Emboli to the coronary arteries will be evidenced by arrhythmias or ischemic electrocardiograph changes. Emboli to other vascular beds might be expected to give a clinical picture similar to the "bends" or decompression illness.
Primary blast injury of the lung presents a clinical picture similar to that of pulmonary contusion from blunt chest trauma, but without rib fractures or chest wall injury. Chest tightness, pain, and hemoptysis are common complaints. One observes tachypnea, the employment of accessory muscles of respiration, and other signs of respiratory distress. Evidence of pulmonary consolidation may indicate either contusion or a hemothorax. A pneumothorax may present as unilateral hyper-resonance with decreased breath sounds and a contralateral shift of the trachea and mediastinum. A precordial systolic crunch on auscultation indicates extravasation of air into the mediastinum. Roentgenographic examination of the chest is mandatory. A simple, frontal view will be diagnostic in most instances of significant barotrauma. Pneumothorax, hemothorax, pneumomediastinum, pleural blebs, subcutaneous emphysema and pulmonary interstitial emphysema can be confirmed by the chest X-ray. The manifestations of contusion may develop over the course of hours and may have the appearance of a local or diffuse infiltrate. The clinical picture of "blast lung" may develop over 24-48 hours. In a complex trauma setting, it is very difficult to differentiate the respiratory insufficiency of the adult respiratory distress syndrome with its varied etiologies from that due solely to primary blast injury to the lungs. Aside from arterial blood gas determinations, laboratory studies have little to offer early on.
Gastrointestinal injury usually presents a less dramatic clinical picture and its diagnosis may be suppressed by the more life-threatening effects of air emboli or respiratory insufficiency. Signs of peritoneal irritation such as involuntary guarding, rebound tenderness, and absent bowel sounds may indicate visceral rupture. Bright red rectal bleeding has occurred with low sigmoid injury: Contused bowel may necrose and perforate several days after the initial trauma. Abdominal X-rays may reveal tree peritoneal air or air within the lumen of the bowel wall. Although multiple organ injury is the usual case in underwater blast injury, visceral injury may predominate and may represent the sole major injury.
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