肺挫伤

肺挫伤是由胸部创伤引起的肺部瘀伤。由于微血管受损，血液和其他液体会积聚在肺组织中。多余的液体会干扰气体交换，可能导致氧气水平不足（缺氧）。与肺裂伤（另一种肺损伤）不同，肺挫伤不涉及肺组织的割伤或撕裂。
肺挫伤通常由钝挫伤直接造成引起，但也可能由爆炸伤或与穿透伤相关的冲击波引起。两次世界大战中大量的爆炸物伤害，使得爆炸导致的肺挫伤受到重视。到了1960年代，一般大众也渐渐注意到肺挫伤－－通常是由交通事故造成的。使用安全带和安全气囊可降低车辆内乘客与驾驶的风险。
肺挫伤的诊断乃基于受伤机转、理学检查和胸部 X 光片。典型的病征和症状包括身体创伤的直接影响（例如胸痛和咳血），以及身体未能获得足够氧气的迹象（例如发绀）。一般而言，支持治疗下肺挫伤可自行恢复，通常只需要补充氧气和密切监测，不过病人可能需要重症监护。但如果呼吸受到严重影响，病人可能需要接受呼吸器治疗。此外，可能需要补充输液以使病人有足够的血管内容积，但输液治疗必须谨慎，因为体液过多会加重肺水肿而可能致命。
肺挫伤的严重程度变化很大。小挫伤可能对健康几乎没有影响，但肺挫伤却也是最常见的致命性胸部创伤（严重胸部伤害病人有 30-75% 发生肺挫伤）。肺挫伤病人的死亡风险约为 14-40%。肺挫伤通常伴有其他损伤；虽然病人经常死于相关伤害，但肺挫伤被认为是四分之一到一半的病人的直接死因。儿童发生肺挫伤的风险较高，因为儿童的骨骼较为柔韧、冲击力容易传递到肺部。肺挫伤的常见并发症是肺炎和急性呼吸窘迫症候群，可能导致长期呼吸功能障碍。
肺部外伤.
肺挫伤和肺裂伤都是对肺组织的损伤。在肺裂伤，肺组织被撕裂或切割，但肺挫伤并无巨观构造遭到破坏。肺裂伤导致伤口处充满血液，造成肺血肿（血液积聚成块，但并未沿著肺组织散布）；肺挫伤则是肺泡（充满空气而负责气体交换的的小囊）出血。当肋膜腔（肺外空间）积聚血液（血胸）、空气（气胸），或两者兼有（气血胸）时，可能会导致肺塌陷。这些情况并不直接伤及肺组织，但可能伴有肺组织的损伤。胸壁损伤（包括肋骨骨折和连枷胸）也不等同于肺损伤，但仍可能伴有肺损伤。在连枷胸，病人的多根肋骨断裂，使得胸壁的某区域与胸壁的其余部分分离并独立移动。
病征与症状.
肺挫伤的临床表现可能并不明显。轻微肺挫伤的病人可能根本没有症状。但肺挫伤经常会出现与肺本身受损或是其它相伴损伤的病征（客观征像）和症状（主观感觉）。由于气体交换受到影响，病征与症状通常与低血氧饱和度有关，例如动脉血气体分析发现血中氧浓度过低，以及发绀（皮肤和粘膜泛蓝）。病人常有呼吸困难，对运动的耐受程度可能会降低。其它征象还有呼吸急促和心率加快。更严重的肺挫伤，以听诊器听诊可能发现呼吸音减弱，或是发现啰音（呼吸时的杂音）。严重肺挫伤病人可能会有水样痰液。病人呼吸可能会有喘鸣音，也可能会有咳嗽；高达一半的病人出现咳血或血痰。病人的心脏输出量可能会减少，低血压也是常见的现象。此外，由于胸壁损伤，肺挫伤附近的胸壁可能会有疼痛，或是在触诊时发现压痛。
但肺挫伤的病征与症状可能会因时间进展而渐渐出现，多达一半的病例最初并无症状。损伤越严重，症状恶化越快。严重肺挫伤可能会在受伤后三、四个小时内迅速出现症状。低血氧症一般通常在受伤后 24-48 小时内逐渐恶化。肺挫伤的病程恶化常常需时数天，但如不及时治疗，可能迅速恶化或死亡。
成因.
肺挫伤通常导因于移动中的胸部撞击到固定物时的激烈减速，是胸部钝挫伤中最常见的损伤，可见于 25-35% 的病例。大约 70% 的病例来自于车祸，最常见的是胸部撞击汽车内部。其它原因还有跌倒、袭击和运动伤害。爆炸伤害也可能导致肺挫伤；最容易受到爆炸伤害的器官是那些内含有气体的器官，例如肺，结果导致严重的肺挫伤、出血或水肿，伴有肺泡和血管损伤。这是爆炸中第一时间并未死亡的人后续的主要死因。爆炸导致的肺挫伤特别之处在于胸壁可能并未受伤，而其它机转所致的肺挫伤常并存其他部位的伤害。
穿透伤也可造成肺挫伤。快速移动的物体穿透肺部所造成的挫伤，发生物体穿过组织路径的周边。压力波将组织推开，暂时形成空腔，虽然组织轻易回到原位，但已受损。伴随于枪伤和刀伤的肺挫伤通常并不是受害者预后的主要决定因素；与钝挫伤相比，穿透性创伤引起的肺损伤范围较小。例外的是霰弹枪伤，可能因为爆炸伤而严重损害大范围的肺组织。
创伤机制.
虽然肺挫伤发生过程中的物理现象仍不明了，但已知当胸壁遭受撞击时向内弯曲时，会压挤肺组织。另外还有三种可能机制：惯性效应、剥落效应和内爆效应。
挫伤通常发生在撞击部位正下方的肺部，但与脑部外伤一样，撞击对面的部位也可能发生对冲挫伤。重击前胸可能导致肺后部的挫伤，因为冲击波穿过胸部至中弯曲的胸壁后部而后能量反射集中于肺后部。当背部受到重击，肺前部可能会出现类似的情形。
转移到肺部的能量主要取决于胸壁的顺应性（柔软度）。儿童的肋骨较有弹性，肋间软骨的骨化程度较低，其胸部较柔韧。受到撞击时，儿童的胸壁弯曲，所吸收的力量较小，而有较多的力传递到其下的器官。 成年人的胸壁骨化程度较高，会吸收更多的力量，而向下传递的力量较少。因此发生肺挫伤的儿童经常并没有肋骨骨折，而老年人则比较容易发生骨折。 一项研究发现，62% 的儿童肺挫伤和 80% 的成人肺挫伤案例伴有骨折。
病理生理学.
肺挫伤导致出血和液体渗入肺组织，肺组织变得僵硬并失去其正常弹性。在受伤后的最初 72 小时内，肺部的水含量增加，较严重的情况下可能导致明显的肺水肿。整体而言，肺挫伤可能随著时间而恶化，导致缺氧。
出血与水肿.
挫伤部位遭撕裂的毛细血管会使体液渗漏到周围的组织里。肺泡和毛细血管之间的膜被撕裂，损伤导致血液和液体渗入肺泡和肺的间质空间（细胞周围的空间）。创伤越严重，水肿、出血和肺泡撕裂就越严重。 肺挫伤的特征是外伤导致肺泡与气道结构和血管分离时，发生了微观尺度的出血。血液最初聚集在间质空间，受伤后一至两个小时出现水肿。发生挫伤的肺，出血区域周边通常会有水肿区域。在正常肺部的气体交换中，二氧化碳以扩散作用通过毛细血管内皮、间质空间和肺泡上皮；氧气则以反向扩散。 堆积的液体干扰气体交换，并可能使得肺泡因水肿与出血而充满蛋白质与塌陷。 损伤面积越大，对呼吸的影响越严重。
肺实质化与塌陷.
肺挫伤可导致部分肺部发生实质化、肺泡塌陷，以及范围不一的肺塌陷。正常情况下充满空气的肺，如因病理变化而被其它物质（例如血液）充满，就会发生实质化。在受伤后的几个小时内，受伤区域的肺泡会变厚并可能发生实质化。肺泡表面活性剂的产量减少，也使肺泡更易发生塌陷与实质化；表面活性剂的失活使得肺泡的表面张力增加。但最初并未受伤的周围组织，表面活性剂的产量也可能减少。
挫伤会导致血液成分进入组织，可能造成肺部发炎，也可能使得部分肺部塌陷。巨噬细胞、中性球细胞、其他发炎细胞与血液成分，可以进入肺组织并释放导致发炎的因子，使得病人更易发生呼吸衰竭。由于发炎，产生过多的粘液，可能会堵塞肺部的某些部分而使其塌陷。即使只有一侧胸部受伤，发炎反应也可能影响另一侧肺部。未受伤的肺组织可能会发生水肿、肺泡隔膜增厚和其他变化。严重的发炎会导致肺部功能障碍，如同急性呼吸窘迫症候群的状况。
通气／灌注不匹配.
正常情况下，通气对灌注比约为一比一，也就是说，进入肺泡的空气量（通气）大约等于肺泡周围毛细血管中的血液量（灌注）。但在肺挫伤时，充满液体的肺泡未能充满空气，通气对灌注比下降，因而血红蛋白未能完全饱和携带氧气，离开肺部的血液并未完全氧合。此外，呼吸器设定未能满足病人需求，或是胸部外伤的其它连带损伤（例如连枷胸），也可能导致肺部通气不足，造成通气／灌注不匹配的情形。随著通气和灌注之间的不匹配增加，血氧饱和度降低。在肺挫伤，可能发生肺低氧性血管收缩，也就是缺乏氧气的肺泡之邻近血管因为氧气浓度降低而收缩（管径变窄）。于是肺部挫伤处的血管阻力增加，流入其中的血液量减少，更多血液流到通气较佳的区域。虽然减少流往通气不良肺泡的血液可以因应通往此区域的血液氧合不佳，但血液的氧含量仍然比正常低。太过严重时，单仅补充氧气并不足以矫正肺泡内积液导致的低血氧；这是许多外伤致死案例的死因。
诊断.
诊断基于理学检查发现、受伤机转病史、放射线影像检查。 实验室检查发现可能也有帮助；例如动脉血气体分析可能会发现，即使给予病人氧气补充，病人血中仍然氧气不足或二氧化碳过多。 但在刚刚发生肺挫伤的病人，血液气体分析的结果数值可能并未异常。
胸部 X 光片.
胸部 X 光片是最常用的诊断方法，可辅助确认基于临床检查所做出的诊断。在 X 光片上实质化的区域会呈现白色。挫伤的分布范围一般并不沿著肺叶或肺段的解剖边界分布。但在X光片上看来，肺挫伤与肺部吸入异物的表现相似，而病人如有血胸或气胸，可能会影响从X光片判读肺挫伤影像。在受伤后 48 小时才在X光片上出现的肺挫伤迹象，有可能其实是吸入异物、肺炎或急性呼吸窘迫症候群所致的类似影像表现。
虽然胸部 X 光片是诊断的重要工具，但其在受伤后初期发现病情的敏感度通常不佳。在三分之一的病例中，在受伤后所照的第一张胸部X光片看不到肺挫伤的迹象。典型的白色区域平均需要 6 小时才能在胸部 X 光片上出现，且在受伤后48小时之内也可能看不出肺挫伤。但当 X 光片显示明显的肺挫伤，暗示胸部遭受到严重创伤，如进行电脑断层扫描，可能会发现未显示于 X 光片上的其他损伤。
电脑断层扫描.
电脑断层扫描用于诊断肺挫伤，敏感性比胸部X光更高，还可以检查是否有伴随的腹部、胸部或其他损伤。研究显示胸部 X 光片在 16.3% 的严重钝挫伤患者中发现肺挫伤，而电脑断层扫描则在 31.2% 的患者中发现肺挫伤。与 X 射线不同，在受伤后，电脑断层扫描后几乎可立即发现挫伤。但电脑断层扫描与一般胸部X光片的影像一样，随著出血和肺组织水肿的恶化，在创伤后的最初 24-48 小时内，挫伤的迹象可能会更加明显。 电脑断层扫描也有助于确定挫伤的范围，可作为患者是否需要机械通气的参考；肺挫伤范围体积越大，病人越可能需要使用机器通气。电脑断层扫描也有助于鉴别挫伤和肺血肿。然而肺挫伤如仅于电脑断层扫描可见，而一般胸部 X 光片上看不出来，其严重程度通常较轻而并不至于影响治疗或预后。
超音波检查.
目前仍不常以超音波在病床或事故现场诊断肺挫伤，仅限于对于以超音波诊断其它问题（如气胸、气道处理、血胸）有经验的单位。但有研究指出其准确性可与电脑断层扫描相当。
预防.
肺挫伤的预防方式与其他胸部创伤相似。使用安全气囊加上安全带，在发生碰撞时可以防止乘员胸部撞击车辆内部，并将碰撞的力量较均匀地分布在整个身体，以提供保护。 然而，极少数情况下，如果安全气囊张开时乘员刚好处于不恰当的位置，反而会导致肺挫伤。汽车安全座椅等儿童约束装置在车祸中可保护儿童。某些运动可使用护具预防胸部和肺部损伤，例如垒球的捕手要穿戴护甲。 至于无法穿戴护具的运动，例如篮球，可训练运动员保护胸部免受冲击。 也可穿戴防护服减轻爆炸中的肺挫伤。尽管由刚性板或其他重型材料制成的传统防弹衣可以抵挡爆炸产生的破片，但并不能防止爆炸的冲击波传递到肺部，也就无法避免肺挫伤。因此针对很可能遭受爆炸伤的人员设计了特殊的防护衣，可以防止冲击波通过胸壁传播到肺部，以保护穿著者免受爆炸性肺损伤。 这类服装将具有高声阻抗（物质密度和物质中波速的乘积）和低声阻抗的材料层交错排列，分散冲击波，避免其传播到组织中。
治疗.
目前没有治疗可以加速肺挫伤的恢复，治疗方针主要是支持性治疗。要小心病人是否有伴随挫伤的其它伤害、避免其它损伤，并以支持性治疗让病人的肺挫伤恢复。因为患者的病情可能会逐渐恶化，需要以脉搏血氧仪监测病人的血氧饱和度，并监测液体输出入平衡与呼吸功能。特别要注意病人是否发生肺炎和急性呼吸窘迫症候群等并发症。治疗目标是预防呼吸衰竭并确保足够的血液氧合。可以给予补充氧气，并可将氧气加温和加湿。如果上述治疗无法改善肺挫伤病人的状况，可以使用体外膜氧合，也就是将血液引入机器，在体外进行氧合并移除二氧化碳后再输回病人体内。
People with signs of inadequate respiration or oxygenation may need to be intubated and mechanically ventilated. Mechanical ventilation aims to reduce pulmonary edema and increase oxygenation. Ventilation can reopen collapsed alveoli, but it is harmful for them to be repeatedly opened, and positive pressure ventilation can also damage the lung by overinflating it. Intubation is normally reserved for when respiratory problems occur, but most significant contusions do require intubation, and it may be done early in anticipation of this need. People with pulmonary contusion who are especially likely to need ventilation include those with prior severe lung disease or kidney problems; the elderly; those with a lowered level of consciousness; those with low blood oxygen or high carbon dioxide levels; and those who will undergo operations with anesthesia. Larger contusions have been correlated with a need for ventilation for longer periods of time.
Pulmonary contusion or its complications such as acute respiratory distress syndrome may cause lungs to lose compliance (stiffen), so higher pressures may be needed to give normal amounts of air and oxygenate the blood adequately. Positive end-expiratory pressure (PEEP), which delivers air at a given pressure at the end of the expiratory cycle, can reduce edema and keep alveoli from collapsing. PEEP is considered necessary with mechanical ventilation; however, if the pressure is too great it can expand the size of the contusion and injure the lung. When the compliance of the injured lung differs significantly from that of the uninjured one, the lungs can be ventilated independently with two ventilators in order to deliver air at different pressures; this helps avoid injury from overinflation while providing adequate ventilation.
Fluid therapy.
The administration of fluid therapy in individuals with pulmonary contusion is controversial. Excessive fluid in the circulatory system (hypervolemia) can worsen hypoxia because it can cause fluid leakage from injured capillaries (pulmonary edema), which are more permeable than normal. However, low blood volume (hypovolemia) resulting from insufficient fluid has an even worse impact, potentially causing hypovolemic shock; for people who have lost large amounts of blood, fluid resuscitation is necessary. A lot of the evidence supporting the idea that fluids should be withheld from people with pulmonary contusion came from animal studies, not clinical trials with humans; human studies have had conflicting findings on whether fluid resuscitation worsens the condition. Current recommendations suggest giving enough fluid to ensure sufficient blood flow but not giving any more fluid than necessary. For people who do require large amounts of intravenous fluid, a catheter may be placed in the pulmonary artery to measure the pressure within it. Measuring pulmonary artery pressure allows the clinician to give enough fluids to prevent shock without exacerbating edema. Diuretics, drugs that increase urine output to reduce excessive fluid in the system, can be used when fluid overload does occur, as long as there is not a significant risk of shock. Furosemide, a diuretic used in the treatment of pulmonary contusion, also relaxes the smooth muscle in the veins of the lungs, thereby decreasing pulmonary venous resistance and reducing the pressure in the pulmonary capillaries.
Supportive care.
Retaining secretions in the airways can worsen hypoxia and lead to infections. Thus, an important part of treatment is pulmonary toilet, the use of suction, deep breathing, coughing, and other methods to remove material such as mucus and blood from the airways. Chest physical therapy makes use of techniques such as breathing exercises, stimulation of coughing, suctioning, percussion, movement, vibration, and drainage to rid the lungs of secretions, increase oxygenation, and expand collapsed parts of the lungs. People with pulmonary contusion, especially those who do not respond well to other treatments, may be positioned with the uninjured lung lower than the injured one to improve oxygenation. Inadequate pulmonary toilet can result in pneumonia. People who do develop infections are given antibiotics. No studies have yet shown a benefit of using antibiotics as a preventative measure before infection occurs, although some doctors do recommend prophylactic antibiotic use even without scientific evidence of its benefit. However, this can cause the development of antibiotic resistant strains of bacteria, so giving antibiotics without a clear need is normally discouraged. For people who are at especially high risk of developing infections, the sputum can be cultured to test for the presence of infection-causing bacteria; when they are present, antibiotics are used.
Pain control is another means to facilitate the elimination of secretions. A chest wall injury can make coughing painful, increasing the likelihood that secretions will accumulate in the airways. Chest injuries also contribute to hypoventilation (inadequate breathing) because the chest wall movement involved in breathing adequately is painful. Insufficient expansion of the chest may lead to atelectasis, further reducing oxygenation of the blood. Analgesics (pain medications) can be given to reduce pain. Injection of anesthetics into nerves in the chest wall, called nerve blockade, is another approach to pain management; this does not depress respiration the way some pain medications can.
Prognosis.
Pulmonary contusion usually resolves itself without causing permanent complications; however it may also have long-term ill effects on respiratory function. Most contusions resolve in five to seven days after the injury. Signs detectable by radiography are usually gone within 10 days after the injury—when they are not, other conditions, such as pneumonia, are the likely cause. Chronic lung disease correlates with the size of the contusion and can interfere with an individual's ability to return to work. Fibrosis of the lungs can occur, resulting in dyspnea (shortness of breath), low blood oxygenation, and reduced functional residual capacity for as long as six years after the injury. As late as four years post-injury, decreased functional residual capacity has been found in most pulmonary contusion patients studied. During the six months after pulmonary contusion, up to 90% of people suffer difficulty breathing. In some cases, dyspnea persists for an indefinite period. Contusion can also permanently reduce the compliance of the lungs.
Complications.
Pulmonary contusion can result in respiratory failure—about half of such cases occur within a few hours of the initial trauma. Other severe complications, including infections and acute respiratory distress syndrome (ARDS) occur in up to half of cases. Elderly people and those who have heart, lung, or kidney disease prior to the injury are more likely to stay longer in hospital and have complications from the injury. Complications occur in 55% of people with heart or lung disease and 13% of those without. Of people with pulmonary contusion alone, 17% develop ARDS, while 78% of people with at least two additional injuries develop the condition. A larger contusion is associated with an increased risk. In one study, 82% of people with 20% or more of the lung volume affected developed ARDS, while only 22% of people with less than 20% did so.
Pneumonia, another potential complication, develops in as many as 20% of people with pulmonary contusion. Contused lungs are less able to remove bacteria than uninjured lungs, predisposing them to infection. Intubation and mechanical ventilation further increase the risk of developing pneumonia; the tube is passed through the nose or mouth into the airways, potentially tracking bacteria from the mouth or sinuses into them. Also, intubation prevents coughing, which would clear bacteria-laden secretions from the airways, and secretions pool near the tube's cuff and allow bacteria to grow. The sooner the endotracheal tube is removed, the lower the risk of pneumonia, but if it is removed too early and has to be put back in, the risk of pneumonia rises. People who are at risk for pulmonary aspiration (e.g. those with lowered level of consciousness due to head injuries) are especially likely to get pneumonia. As with ARDS, the chances of developing pneumonia increase with the size of the contusion. Children and adults have been found to have similar rates of complication with pneumonia and ARDS.
Associated injuries.
A large amount of force is required to cause pulmonary contusion; a person injured with such force is likely to have other types of injuries as well. In fact, pulmonary contusion can be used to gauge the severity of trauma. Up to three quarters of cases are accompanied by other chest injuries, the most common of these being hemothorax and pneumothorax. Flail chest is usually associated with significant pulmonary contusion, and the contusion, rather than the chest wall injury, is often the main cause of respiratory failure in people with these injuries. Other indications of thoracic trauma may be associated, including fracture of the sternum and bruising of the chest wall. Over half of fractures of the scapula are associated with pulmonary contusion. The contusion is frequently found underlying fracture sites. When accompanied by a fracture, it is usually concentrated into a specific location—the contusion is more diffuse when there is no fracture. Pulmonary lacerations may result from the same blunt or penetrating forces that cause contusion. Lacerations can result in pulmonary hematomas; these are reported to develop in 4–11% of pulmonary contusions.
Epidemiology.
Pulmonary contusion is found in 30–75% of severe cases of chest injury, making it the most common serious injury to occur in association with thoracic trauma. Of people who have multiple injuries with an injury severity score of over 15, pulmonary contusion occurs in about 17%. It is difficult to determine the death rate (mortality) because pulmonary contusion rarely occurs by itself. Usually, deaths of people with pulmonary contusion result from other injuries, commonly traumatic brain injury. It is controversial whether pulmonary contusion with flail chest is a major factor in mortality on its own or whether it merely contributes to mortality in people with multiple injuries. The estimated mortality rate of pulmonary contusion ranges from 14–40%, depending on the severity of the contusion itself and on associated injuries. When the contusions are small, they do not normally increase the chance of death or poor outcome for people with blunt chest trauma; however, these chances increase with the size of the contusion. One study found that 35% of people with multiple significant injuries including pulmonary contusion die. In another study, 11% of people with pulmonary contusion alone died, while the number rose to 22% in those with additional injuries. Pulmonary contusion is thought to be the direct cause of death in a quarter to a half of people with multiple injuries (polytrauma) who die. An accompanying flail chest increases the morbidity and mortality to more than twice that of pulmonary contusion alone.
Pulmonary contusion is the most common cause of death among vehicle occupants involved in accidents, and it is thought to contribute significantly in about a quarter of deaths resulting from vehicle collisions. As vehicle use has increased, so has the number of auto accidents, and with it the number of chest injuries. However an increase in the number of airbags installed in modern cars may be decreasing the incidence of pulmonary contusion. Use of child restraint systems has brought the approximate incidence of pulmonary contusion in children in vehicle accidents from 22% to 10%.
Differences in the bodies of children and adults lead to different manifestations of pulmonary contusion and associated injuries; for example, children have less body mass, so the same force is more likely to lead to trauma in multiple body systems. Since their chest walls are more flexible, children are more vulnerable to pulmonary contusion than adults are, and thus suffer from the injury more commonly. Pulmonary contusion has been found in 53% of children with chest injuries requiring hospitalization. Children in forceful impacts suffer twice as many pulmonary contusions as adults with similar injury mechanisms, yet have proportionately fewer rib fractures. The rates of certain types of injury mechanisms differ between children and adults; for example, children are more often hit by cars as pedestrians. Some differences in children's physiology might be advantageous (for example they are less likely to have other medical conditions), and thus they have been predicted to have a better outcome. However, despite these differences, children with pulmonary contusion have similar mortality rates to adults.
History.
In 1761, the Italian anatomist Giovanni Battista Morgagni was first to describe a lung injury that was not accompanied by injury to the chest wall overlying it. Nonetheless, it was the French military surgeon Guillaume Dupuytren who is thought to have coined the term "pulmonary contusion" in the 19th century. It still was not until the early 20th century that pulmonary contusion and its clinical significance began to receive wide recognition. With the use of explosives during World War I came many casualties with no external signs of chest injury but with significant bleeding in the lungs. Studies of World War I injuries by D.R. Hooker showed that pulmonary contusion was an important part of the concussive injury that results from explosions.
Pulmonary contusion received further attention during World War II, when the bombings of Britain caused blast injuries and associated respiratory problems in both soldiers and civilians. Also during this time, studies with animals placed at varying distances from a blast showed that protective gear could prevent lung injuries. These findings suggested that an impact to the outside of the chest wall was responsible for the internal lesions. In 1945, studies identified a phenomenon termed "wet lung", in which the lungs accumulated fluid and were simultaneously less able to remove it. They attributed the respiratory failure often seen in blunt chest trauma in part to excessive fluid resuscitation, and the question of whether and how much to administer fluids has remained controversial ever since.
During the Vietnam War, combat again provided the opportunity for study of pulmonary contusion; research during this conflict played an important role in the development of the modern understanding of its treatment. The condition also began to be more widely recognized in a non-combat context in the 1960s, and symptoms and typical findings with imaging techniques such as X-ray were described. Before the 1960s, it was believed that the respiratory insufficiency seen in flail chest was due to "paradoxical motion" of the flail segment of the chest wall (the flail segment moves in the opposite direction as the chest wall during respiration), so treatment was aimed at managing the chest wall injury, not the pulmonary contusion. For example, positive pressure ventilation was used to stabilize the flail segment from within the chest. It was first proposed in 1965 that this respiratory insufficiency is most often due to injury of the lung rather than to the chest wall, and a group led by J.K. Trinkle confirmed this hypothesis in 1975. Hence the modern treatment prioritizes the management of pulmonary contusion. Animal studies performed in the late 1960s and 1970s shed light on the pathophysiological processes involved in pulmonary contusion. Studies in the 1990s revealed a link between pulmonary contusion and persistent respiratory difficulty for years after the injury in people in whom the injury coexisted with flail chest. In the next decade studies demonstrated that function in contused lungs improves for years after the injury.
External links.
-->