Pediatric Trauma

5.2. What Types of Injuries are Associated with Blast Trauma?

Primary Injury

Primary injury is the result of the excessive pressure generated by the blast wave. It affects all air or fluid filled cavities (lungs, ears, gastrointestinal tract). It may cause air embolism resulting in a stroke or in acute abdominal or spinal cord injury.

Secondary Injury

Secondary injuries are caused by pieces of flying debris that act as projectiles, resulting in penetrating or blunt injuries. About 10% of these are eye injuries.

Tertiary Injury

Tertiary injuries occur when the body is thrown by the blast wind and may include fractures, brain injuries, traumatic amputations and other injuries.

Quaternary Injuries

Quaternary trauma injuries include all other blast trauma injuries such as burns, crush injuries, respiratory (dust/ toxins) injuries, and others.

Blast Lung Injuries

Blast lung is the most common primary blast injury among victims of explosions. It may appear up to 48 hours after the explosion. The acceleration/deceleration process may tear the lung parenchyma off the stationary vascular tree, causing hemorrhage and air emboli. Lung injury may also be induced by smoke inhalation; symptoms include dyspnea, cough, hemoptysis, chest pain, and hypoxia. The initial triad of apnea, bradycardia, and hypotension may occur. Pulmonary injuries that may occur vary from petechiae to pulmonary hemorrhage.

In general, primary blast injury of the lung is manifested as pulmonary contusion. The development of respiratory symptoms and hypoxia may occur in either a fulminant pattern or gradually over the first 48 hours.

Other potential injuries include bronchopleural fistula or arterial air embolism that may be associated with low vascular pressures after hemorrhage or high airway pressures during resuscitation with positive pressure ventilation. Arterial air embolism to the brain or heart may be the most common cause of immediate death from primary blast injury or of death at the moment when positive pressure ventilation is initiated.

Initially, treat all children who have potential pulmonary primary blast injury with 100% oxygen.

Casualties who present with asymmetrically decreased air entry and evidence of shock call for an immediate attempt at needle thoracentesis to decompress a potential tension pneumothorax.

This life-threatening condition may be caused by any combination of primary, secondary, tertiary, or miscellaneous blast injuries.

Acute respiratory distress syndrome (ARDS) may develop within 24 to 48 hours of injury.

Head Injuries

Blast fatalities associated with head injuries are basically related to subarachnoid and subdural hemorrhages. Among survivors, significant traumatic brain injuries are usually easily identified. Remember, however, that mild traumatic brain injuries are common and may be overlooked. Other injuries may also serve to distract the medical provider, making the diagnosis of subtle neurologic findings more difficult. Take into consideration subtle signs and symptoms of potential mild traumatic brain injury, such as memory problems, headaches, fainting, uneven gait, blurred vision, irritability, and confusion.

Abdominal Injuries

Primary intestinal blast injury is uncommon and depends on exposure to a very high air pressure. Injuries may include intestinal petechiae, hemorrhages, large intramural hematomas, intestinal laceration, or bowel perforation. The colon, where gas accumulates, is the most common site of injury. Ruptures may occur acutely or several days later due to stretching, ischemia, and subsequent weakening of the bowel wall. A tension pneumoperitoneum may also occur. Mesenteric, retroperitoneal, or scrotal hemorrhages are other potential injuries.

Eye Injuries

Up to 10% of all blast survivors have eye injuries. Perforations from high velocity projectiles present as penetrating trauma. Assess patients for altered vision, eye pain, foreign body sensation, decreased visual acuity, hyphema, or lacerations.

Ear Injuries

Blast injuries to the ear can be easily overlooked. Tympanic membrane perforation is the most common injury; however, injuries to the ossicular chain occur in 33% of cases of ear trauma. Inner-ear sensoroneural hearing loss may also occur. Blast related eardrum perforation may have local consequences, including infection, tinnitus, temporary or permanent hearing loss, and vertigo. Such patients need follow-up by otorhinolaryngologist.

Other Injuries

Other injuries associated with blast trauma include compartment syndrome, rhabdomyolysis, acute renal failure, severe burns, and inhalation of toxins. If the explosion occurred in an enclosed space or was accompanied by fire, tests for carboxyhemoglobin and electrolytes, as well as assessment of acid/base status should be performed. Elevated lactate levels are seen in cyanide toxicity.

Crush Injuries

Building collapse is a common disaster, particularly in earthquake situations. The collapse of a multistory building may cause crush injury in up to 40% of the extricated survivors. Crush injury should be suspected in any individual who has either had compression of parts of his/her body or has lain immobile on a hard surface for hours. In the Kobe, japan earthquake of 1995, among the 372 patients with crush syndrome, the mortality rate was about twice that of other trauma patients. It is important to note that the crush injury patients with associated injuries such as abdominal injury or extremity fracture had increased mortality rates (50% and 17.2%, respectively). Little information exists on children with crush injuries, but it appears that children have more recoverable renal function than adults. According to epidemiologic studies following the 1999 earthquake in Marmara, Turkey, infants seemed relatively immune to severe acute renal failure. Up to 20% of the cases of musculoskeletal trauma in Turkey occurred in people <18 years of age with the following injury patterns: ankle (30%), thigh (28.6%), head (23.8%), and forearm (7%). Many of these had crush syndrome in addition to their extremity injuries. Surgical amputations and multiple fasciotomies were performed on 12.6% of this pediatric population. Acute renal insufficiency occurred in 27% of these children; however, only 19% of earthquake victims needed dialysis, compared to 93% of adult victims that required hemodialysis (Sarisozen et Durak, 2003). Modern disaster plans need to anticipate high incidence of crush injury and be proactive in providing intravenous fluids in the critical hours following extrication, and even prior to extrication when possible.

Even short periods of entrapment can cause muscle compression injuries that may result in a crush syndrome, also known as traumatic rhabdomyolysis (Box 10). Crush syndrome is a severe systemic manifestation of trauma and ischemia involving soft tissues, mainly skeletal muscle, due to prolonged severe crushing. It leads to increased permeability of the cell membrane to sodium, water, and extracellular calcium and to the release of potassium, enzymes, and myoglobin from within cells. Cells begin to swell and intracellular calcium increase, thus disrupting cellular functioning and mitochondrial respiration, which all leads to myocytic death and can lead to compartment syndrome. Ischemic renal dysfunction secondary to hypotension and diminished renal perfusion results in acute tubular necrosis and uremia (Better OS et al, 2003; Ashkenazi et al, 2005).

Gonzalez D. Crush syndrome. Critical Care Medicine 2005;33-1

Crush syndrome/traumatic rhabdomyolysis results from muscle reperfusion with subsequent secondary systemic effects. The destruction of muscle tissue and the influx of myoglobin, potassium, and phosphorus into the circulation results in the classic picture of traumatic rhabdomyolysis. The syndrome is characterized by hypovolemic shock and hyperkalemia. It is crucial to initiate volume expansion as soon as possible. Crush syndrome can result in several potential medical conditions that can be associated with significant morbidity or mortality (Box 11).

Patients have classically been described as presenting with muscle weakness, malaise, and fever and commonly have other injuries such as pelvic and limb fractures, as well as abdominal injuries. The real danger lies in the cardiovascular effects resulting from electrolyte imbalance and renal failure. Look for the physical presence of skin trauma or local signs of compression (erythema, ecchymosis, abrasion, etc.) on the muscle mass. The absence of a pulse or a weak pulse to the distal limbs may be an indicator of muscle swelling or compromised circulation. Continued assessment may demonstrate a pale, cool, tense, edematous and diaphoretic limb with progressive loss of sensation, movement, and vascular circulation. Perform a lab evaluation for urine myoglobin, serum creatine phosphokinase, and serum electrolytes whenever possible. If nothing else an EKG should be done to look for STsegment changes resulting from hyperkalemia.

Key aspects to therapy are volume expansion through intravenous fluid resuscitation, ensuring alkalinized diuresis, and early detection of metabolic abnormalities. Initiate normal saline 20 mL/kg bolus at the scene of disaster, before or after extrication. Actually, normal saline or LR should be used with the addition of Nabicarb. Once the patient is hemodynamically stable, switch intravenous fluids to 50% normal saline with 40 mEq sodium bicarbonate for urine alkalinization with a goal infusion of 20ml/kg/hour in adults and children with a goal urine output of at least 2 cc/kg/hour (Ashkenazi et al, 2005). A urine pH between 6 and 7 has been identified as a reasonable goal (Better, 1990). The addition of bicarbonate avoids precipitation of toxic myoglobin metabolites in nephrons, improves acidosis, and facilitates a drop in serum K levels (Levinsky, Harrison’s Principals of Internal Medicine).

Diuresis can be forced with the use of either furosemide or mannitol. Furosemide is believed to help by causing renal vasodilatation, decreased renal oxygen demands, and increased renal intratubular flow. Mannitol works as an osmotic diuretic and volume expander. The goal of diuresis is to increase the elimination of myoglobin by the kidney and prevent deposition which leads to renal failure. It has been suggested that if rehydration fluids are not successful in achieving diuresis within 4 hours, then mannitol should be administered. The maximal daily dose of mannitol is 2 g/kg/day (not to exceed 200 g). Mannitol should not be used in patients with heart failure or established anuric renal failure. Administer analgesics, such as opiates or ketamine. If diuresis can not be achieved with lasix and manitol, given adequate hydration, then preparation for dyalisis is needed.

One of the leading causes of death from crush injuries is severe hyperkalemia (serum potassium >7.0 mEq/L). Hyperkalemia generates electrocardiographic (ECG) disturbances, such as peaked Twaves, loss of P-waves, and widening of the QRS complex, which if not treated can progress to the deadly torsades de points. Treat symptomatic hyperkalemia or hyperkalemia with ECG disturbances with calcium chloride 10% (0.2 mL/kg IV) or calcium gluconate 10% (0.5-1 mL/kg IV) to stabilize the cardiac membrane. Of note, intravenous calcium may be ineffective as a treatment for hyperkalemia if given to a patient with hyperphosphatemia.

Additional treatment measures include mobilization of potassium into the intra-cellular space by plasma alkalinization (sodium bicarbonate 1 mEq/kg IV) or glucose administration (0.5-1 g/kg, 25% dextrose in water) plus insulin (0. 1 units/kg IV); albuterol aerosol; or kayexalate (sodium polystyrene sulfonate) 1 mg/kg orally or by rectal route. In extreme cases, hemodialysis may be needed (Cronan and Norman, 2000; Gaffar, 2003).

Hypocalcemia is defined as a calcium concentration <9 mg/dL. Clinical presentation includes weakness, paresthesias, and irritability, with ECG findings of prolonged QT interval, bradycardia and arrythmias. Treatment focuses on calcium administration, with continued ECG monitoring and calcium serum level determinations.

Intensive care support often is required for crush syndrome complications. Patients with anuria or oliguria are likely to require hemofiltration or dialysis. Aggressive treatment is necessary to decrease mortality and morbidity. Treatment during the acute phase of the rhabdomyolysis is aimed at maintaining adequate circulating volume and sufficient diuresis to prevent renal, cardiac, and pulmonary complications.

It is possible that crushed victims can progress to compartment syndrome, a situation that occurs when there is an increased pressure in a muscle compartment. This can lead to ischemia with eventual muscle necrosis and nerve damage (palsies). The anterior compartment of the lower leg is the most commonly affected; as there are four susceptible compartments in this commonly injured location. In severe trauma the compartment integrity may actually be disrupted, preventing high intra-compartment pressures from being reached. Clinicians should look for increasing and severe pain, especially pain associated with passive extension of the compartment.

The compartment syndrome examination is geared toward the classic description of the "five Ps":

1. Pain out of proportion for the injury or pain to passive movement of the fingers or toes
2. Pallor of the extremity
3. Paralysis
4. Paresthesias
5. No pulse or reduced pulse

Confirmation of elevated pressures may be obtained by direct measurement of the compartment. Definitive treatment in the presence of a compartment syndrome is surgical release of the compartment connective tissue, i.e., fasciotomy.

Always consider compartment syndrome when the diagnosis of crush syndrome is suspected.

The development of a compartment syndrome in crush injury is due to the uptake of fluid into damaged muscle tissue that forcedly remains within a restricted compartment. Once compartment pressure exceeds capillary perfusion pressure at about 30 to 40 mm Hg, the tissue inside the compartment becomes ischemic and compartment syndrome develops. Although the traditional treatment of the compartment syndrome is fasciotomy, some evidence indicates that initial treatment with mannitol can also decompress a compartment syndrome, avoiding the need for surgery (Better, 1999).