The Case: A 20 year-old male h/o DM was found down and unresponsive after a gas explosion downtown with agonal respirations and extensive burns to anterior trunk, right upper extremity and bilateral lower extremities. Vital signs were BP 150/92 HR 98 RR 10 O2 sat 97% on room air, FSG 235. Patient was intubated in the field and was placed in a cervical collar. On exam, the patient had a GCS 6T, partial thickness burns BSA ~40%, ruptured right TM with blood from external canal.
The initial concern was for blast injuries, intracranial injuries, possible carbon monoxide or cyanide poisoning. CXR and CT chest showed diffuse bilateral ground glass opacities and CT head/cervical spine/abdomen/pelvis showed no acute pathology. Lab work was significant for lactate of 3.5, normal carboxyhemoglobin, and a P/F ratio of 115. PEEP was increased, and he was continued on FiO2 of 100% . The patient received 3L of LR (in addition to 2L NS via EMS). The patient was transferred to a burn center for further management. The ICU course was complicated by an arterial gas embolism that resulted in left sided weakness. The patient was ultimately discharged with mild residual neurologic deficits.
Edwards et. al reviewed over 43 years of reported terrorist bombings, encompassing an excess of 58,000 events. Of these events, 167 had published data that could be included. These events were traditionally classified as either open space or closed space events due to different injury profiles associated with each. Open space events occur outside in the open, whereas closed space events occur in a closed environment, such as a building or vehicle. This review found that 61% were closed-space bombings and 12% were semi-confined-space bombings. There was no difference in mortality from open space vs. closed space blasts, but there was an average of 32 deaths and 180 injuries per incident. Tympanic membrane rupture was found to be significantly more common with closed-space injuries than open-space ones, while the latter had a significantly higher number of limb amputations (1).
Rozenfeld et. al later reviewed 823 patients from 65 explosive events of the Second Intifada and further broke down the taxonomy of bombings into 5 categories: inside buildings, near buildings, inside buses, near buses, and in open space. He found that inside buildings and inside buses had the most severe injuries, while near buses had the least severe. Open-space had the lowest proportion of blast trauma and burns. Near building explosions had a high proportion of primary blast injuries, purportedly due to blast wave reflection from the building itself (2).
Types of Blast Injuries
Primary – direct effect of blast overpressure on tissue; generally, affects organs with an air/tissue interface like the tympanic membrane, lungs, and gastrointestinal tract
Secondary – indirect from projectiles flung by blast wave
Tertiary – high-energy explosives that propel victim into other objects
Quaternary – all other injuries caused by explosions; i.e. carbon monoxide poisoning, burns.
General Evaluation and Management of the Blast Injured Patient
- Treat injuries like you would in any other trauma (ATLS protocol)
- Keep in mind specific primary blast injury patterns:
- Tympanic membrane rupture
- Blast lung injury
- Abdominal blast injury
Tympanic Membrane (TM) Rupture
The TM is usually first organ involved in blast injury due to its sensitivity to blast overpressure. This should be evaluated in all blast-injured patients. Rupture of TM is generally benign but requires ENT follow up for audiometry and possible tympanoplasty (3). The classic teaching is that patients with intact TM’s can be discharged, but this is not supported by evidence (4). The presence of ruptured TM cannot be used to rule in or rule out other blast injuries. In a small review, nearly 50% of blast lung injuries presented with intact TM’s (4). Another study found patients could present with isolated TM rupture without other blast injuries (5). In patient with isolated TM rupture, obtain CXR and observe for emergence of blast injury symptomatology (5). The ideal time for observation is uncertain but 4-6 hours is reasonable. If no other injuries, patients should be discharged with ofloxacin otic drops which may speed recovery (5,6)
Blast Lung Injury
Patients with primary blast lung injury will commonly present with dyspnea, hemoptysis, chest pain, respiratory distress, or cyanosis, similar to a pulmonary contusion (7). The classic chest x-ray finding is bilateral pulmonary infiltrates in a “butterfly” or “bat wing” pattern (8). Patients should be intubated, if necessary and should be evaluated for concurrent pneumothorax or hemothorax. Complications of blast lung injury include bronchopleural fistula and arterial gas embolism (AGE). The risk of AGE is greatest within the first 24 hours and is increased by positive pressure ventilation (7). It can present with coronary, intestinal, or cerebral ischemia, air leak, hypotension, mental status changes, visual disturbances, or death (8). Treatment involves using 100% FiO2, left lateral decubitus positioning with Trendelenburg, and hyperbaric oxygen therapy when clinically stable (7,8).
When it comes to ventilator management in blast lung injury, it is important to remember that these patients can suffer significant complications from barotrauma. Although there have been no randomized control trials to compare ventilator management strategies in these patients, most experts agree that PEEP should be minimized as positive pressure increases the risk of AGE (7). Other lung protective strategies are similar to strategies used in ARDS, like using low tidal volumes, pressure controlled settings, jet ventilation, nitric oxide, high frequency oscillatory ventilation, extracorporeal membrane oxygenation, inverse I:E ratios with zero PEEP, and permissive hypercapnia (7,8,9). Hypercapnea, however, should be avoided in patients with concomitant neurological injury (3,7). The following classification scheme was proposed by Pizov et. al and modified later by Wightman et. al can be used to predict the need for positive pressure ventilation in a patient with lung injury (3). Note that as in ARDS, the P/F ratio plays an important role in categorizing severity.
|CXR Infiltrates||Unilateral||Asymmetric bilateral||Diffuse bilateral|
|PPV requirement||Unlikely||Likely to require conventional methods||Universal, may require unconventional methods|
|PEEP requirement||<5 if needed||5-10 usually||>10 commonly|
Abdominal Blast Injury
Abdominal blast injuries are rare. By some estimates, they will affect less than 1% of survivors (10). The effects of blast overpressure are amplified underwater. These injuries are often subtle and are easily missed, especially in patients who cannot provide a good history and exam. Injuries can include hemorrhage, perforation, hematomas, or intestinal contusion, which can result in delayed “secondary perforation” (7). In rat studies, abdominal blast injuries usually present 3-5 days after the initial blast injury, but have been noted as far as two weeks after (10). Evaluation should include serial abdominal exams and advanced imaging if there is concern for surgical pathology.
Cardiac Blast Injury
There is a relative paucity of data on cardiac blast injury. The pathology and presentation appear similar to blunt cardiac injury (3,7), including dysrhythmias, free wall/septal rupture, tamponade, papillary muscle rupture, valvular injury, or coronary vessel injury. Two studies subjected rats to blast waves to test the effects on the cardiovascular system. One study induced myocardial depression and bradycardia without compensatory vasoconstriction, leading to hypotension (11). The other study noted ECG changes such as PVCs and VF, which may account for some immediate deaths after blast injury (12). Given the types of injuries that patients can suffer, evaluation for blunt cardiac injury should include ultrasound, ECG, and troponin (3).
Quaternary Injuries and Considerations
- Treat similarly to rhabdomyolysis from any other etiology with aggressive fluid administration (7)
- Local burn centers should be consulted. Patients with significant burns will require large volume fluid resuscitation, however, with concomitant blast lung injury, over-resuscitation must be avoided. This can lead to fluid overload and worsening respiratory status. Fluid resuscitation should target end-organ perfusion and adequate urine output.
- Lacerations and wounds from blast injuries tend to be contaminated so prophylactic antibiotics should cover gram positive organisms. Injuries that breach the abdominal cavity should cover gram negative and anaerobic organisms (13)
- Treat with decontamination if necessary
- Do not forget to consider carbon monoxide/cyanide toxicity as with any burn patient and treat these as you would in any other situation
- The TM’s, lungs, and GI tract are at particular risk from explosions
- Intact TM’s do not rule out other blast injuries!
- Employ lung protective strategies with minimal positive pressure for blast lung injury
- Cardiac blast injury should be assessed and managed similarly to blunt cardiac injury
- Due to subtle presentations, most patients will require short observation and reassessment (4-6 hours) for development of symptoms
- Edwards D, McMenemy L, Stapley S, Patel H, Clasper J. 40 years of terrorist bombings – a meta-analysis of the casualty and injury profile. Injury. March 1, 2016;47:646-652.
- Rozenfeld M, Givon A, Shenhar G, Renert L, Peleg K. A new paradigm of injuries from terrorist explosions as a function of explosion setting type. Ann Surg. June 2016;263(6):1228-1234.
- Wilkerson R, Lemon C. Blast Injuries. Trauma Reports [serial online]. May 2016;17(3):1-19.
- Peters P. Primary Blast Injury: An Intact Tympanic Membrane Does Not Indicate the Lack of a Pulmonary Blast Injury. Military Medicine [serial online]. January 2011;176(1):110-114
- Leibovici D, Gofrit ON Shapira SC. Eardrum perforation in explosion survivors: is it a marker of pulmonary blast injury? Ann Emerg Med. 1999;Aug34(2):168-72
- Lou Z, Lou Z, Tang Y, Xiao J. The effect of ofloxacin otic drops on the regeneration of human traumatic tympanic membrane perforations. Clin Otolaryngol. 2015 Oct 14.
- Matthews ZR, Koyfman A. Blast Injuries. The Journal of Emergency Medicine. 2015;49(4):573-587.
- Wolf S, Bebarta V, Bonnett C, Pons P, Cantrill S. Seminar Blast injuries. The Lancet [serial online]. January 1, 2009;374:405-415
- Sasser S, Sattin R, Hunt R, Krohmer J. Blast lung injury. Prehospital Emergency Care [serial online]. April 2006;10(2)165-172.
- Yeh D, Schecter W. Primary blast injuries–an updated concise review. World Journal Of Surgery [serial online]. May 2012;36(5):966-972
- Irwin RJ, Lerner MR, Bealer JF, Brackett DJ, Tuggle DW. Cardiopulmonary physiology of primary blast injury. J Trauma. Oct 1997;43(4):650-5.
- Guy RJ, Watkins PE, Edmondstone WM. Electrocardiographic changes following primary blast injury to the thorax. J R Nav Med Serv. 2000; 86(3):125-33.
- Lavery GG, Lowry KG. Management of blast injuries and shock lung. Curr Opin Anaesthesiol 2004;17:151–7.
Latest posts by edenkim (see all)
- Epinephrine/Terbutaline in Acute Asthma Exacerbation - March 12, 2017
- EM-Critical Care: IT’S NOT A TOOMAH!! Lysis Syndrome and Retroperitoneal Hematoma - January 6, 2017
- Cellulitis – Observe, Admit, or Discharge? - November 28, 2016