The Mechanism Signs And Treatment Biology Essay

Published: Last Edited:

This essay has been submitted by a student. This is not an example of the work written by our professional essay writers.

Explosions can produce a wide variety of injuries from typical blunt and penetrating injuries to unique injuries to organ systems caused by pressure changes in the surrounding environment. Injuries caused by explosions can classified as being either primary, secondary, tertiary or quaternary blast injuries. Primary blast injuries result from the shock wave created by the explosion which interacts with body tissue, depositing energy result in organ damage. Secondary injuries result from the propulsion of objects from the blast which can cause penetrating injuries and blunt trauma. Tertiary injuries occur when an explosion has significant energy to propel the human body into the air and strike it against obstacles. Lastly, quaternary injuries consist of miscellaneous explosion associated injuries such as burns, toxic substance exposure, asphyxia and psychological damage. Another class of explosion injury has recently been suggested after it was reported that victims in an Israeli bombing exhibited a hyper inflammatory response to the blast. However, I will solely be investigating the mechanism of primary blast injuries, the organs frequently involved and management of the associated injuries.

Physics of Primary Blast Injury

An explosion produces a predictable change in surrounding gas pressure over time. The change in gas pressure plotted against time produces a characteristic curve known as the Friedlander curve (see picture) which consists of two phases. In the first phase of an explosion, the detonation of an explosive causes the surrounding gas to expand which displaces the surrounding medium. This gives rise to a positive increase in pressure that decays over distance and time. Thus, the initial phase is known as the positive pressure phase and the positive pressure peak is known as the blast overpressure. In the second phase of an explosion, low pressure develops due to the vacuum created by the displaced air during the positive pressure phase. This phase is known as the negative pressure phase of the blast. Following the negative pressure phase, the gas pressures eventually normalise.

Primary blast injuries occur in response to a blast wave which is generated during the positive pressure phase of the blast. Both the speed at which the blast wave travels and the magnitude of the blast overpressure determines the likelihood of a primary blast injury and its severity. These factors can be augmented under different circumstances.

For instance, the medium in which an explosion occurs can affect the speed of the blast wave. Air is a compressible medium, thus a blast wave travelling through air will expend energy compressing the air. On the other hand, water is a non-compressible medium. Therefore, a blast wave travelling in water will dissipate its energy much slower and travel much further compared to the same explosion occurring in the air. In fact, the blast wave created from the same sized explosion will travel three times further in water than in air. As the blast wave travels further and its energy dissipates more slowly, there is a greater potential for primary blast injury.

Distance from an explosion is another variable factor which determines the magnitude of blast overpressure to which an individual is exposed to. The overpressure of a blast wave decays in a manner inversely to the cube of the distance from the explosion. Thus, if the distance from a blast is doubled, the peak overpressure will be one-eighth of the original value.

Blasts within a confined space are more likely to give rise to primary blast injuries compared to open air blasts. This is due to the blast wave reflecting off solid surfaces which augments the blast overpressure and increases the duration of the primary pressure phase. Confined space explosions have been shown to increase mean injury severity scores, primary blast injury and overall mortality compared to that of open space explosions.

Pathophysiology of primary blast injury

Primary blast injuries are caused by three explosive forces which are spallation, implosion and inertia. Spallation is the displacement and fragmentation of denser medium into a less dense medium. Implosion is the displacement and fragmentation of a less dense medium into a denser medium. Lastly, inertia is sheer stress created by the blast wave travelling through tissues of different densities at different velocities.

Since air is easily compressible by pressure, primary blast injuries occur at their highest frequencies at sites with an air-tissue interface. Particularly susceptible organ systems are the pulmonary system, the gastrointestinal system and the auditory system due to their high air content.

Auditory system primary blast injuries

Auditory injuries are the most frequent primary blast injuries and they occur at the lowest blast overpressure (35kPa) compared to other primary blast injuries. The most common auditory injury is rupturing of the tympanic membrane and symptom of which include hearing loss, tinnitus, pain and dizziness. To confirm is the tympanic membrane is ruptured, otoscopy can be used. The initial treatment of a ruptured tympanic membrane is supportive but operative care may be required later depending on the extent of the injury. Usually small ruptures heal spontaneously. However, ruptures involving more than 5% of the membrane surface may require surgery.

It has been postulated that an intact tympanic membrane suggests little exposure to blast overpressure thus removing the need to further assess for primary blast injuries. However, risk of tympanic rupture not only depends on the magnitude of the blast overpressure but also depends on additional factors such as the head position relative to the blast direction, the presence of cerumen, presence of ear protection and prior injury or infection. Thus lack of tympanic rupture does not strictly rule out the presence of another primary blast injury.

Pulmonary system primary blast injuries

Due to the large air-tissue surface area, the pulmonary system is highly susceptible to primary blast injury. An over pressure of around 100kPa is required to cause a primary blast lung injury known as 'blast lung' and it is the most common fatal blast injury. Initially in a pulmonary blast lung injury, the spalling and implosion forces of the blast wave cause immediate rupture of the alveolar capillaries, which leads to the formation of haemorrhagic foci. Haemorrhagic congestion tends to form on the lung parenchyma behind the intercostal spaces as the ribs protect against the full force of the blast wave. Simultaneously, the compressive forces of the wave drive extravascular fluid into the alveolar space leading to oedema and alveolar haemorrhage. 12 to 24 hours after the initial injury, progressive vascular leak and inflammatory changes develop. Traumatic interstitial emphysema can also develop due to air being driven into the interstitial space by implosion forces.

Other primary blast injuries that can occur include pneumothoraces, haemothoraces and pneumomediatinum due to pleural tear. Sheering forces can give rise to bronchopulmonary fistulas due to disruption of the bronchovascular tree. Arterial air embolisms can develop in pulmonary primary blast injury which can lead to stroke, myocardial infarction, intestinal ischemia or death whereas microscopic embolisms can lead to mental confusion, mental status changes, vision disturbance or vague complaints of pain and weakness.

Patients with blast lung injury tend to show symptoms of dyspnoea, cough, and hypoxia which result from impaired gas exchange, vascular shunting and ventilation mismatching. However, some affected individuals do not show these symptoms as the development of the lung injury may be delayed. If a patient who has been exposed to a high blast overpressure presents with any pulmonary complaints or evidence of any other primary blast injuries, a chest x-ray should be conducted. If blast lung is present, the chest x-ray should show bilateral infiltrates in a butterfly pattern. Though, as mentioned before, the lung injury may be delayed, which would give rise to a normal chest x-ray. Thus, patients who show a normal chest x-ray but still show pulmonary symptoms should be observed for 6-8 hours before discharge. If symptoms are substantial or persistant, a chest CT should be conducted as chest x-rays can miss pulmonary complications.

When managing a patient with blast lung, care must be taken as therapies for different injuries conflict. Extreme care must be given when administrating intravenous fluids as excessive fluid administration can worsen pulmonary oedema. Fluid resuscitation can be carefully monitored with the use of invasive monitoring (e.g. use of a pulmonary artery catheter).

Furthermore care must be taken when optimising the patient's physiological respiratory status with non invasive ventilation techniques as positive pressure ventilation can increase the risk of developing an air embolism. Signs of an air embolism include air in the retinal arteries, tongue blanching, or livedo reticularis. If an air embolism is expected, the patient should be placed in a left deubitus, head down, and feet up position to try to trap air in the apex of the left ventricle and prevent it from spreading.

If pneumothoraces or haemothoraces are present, prompt chest drainage is required to minimise the need for positive pressure ventilation. Prophylactic chest tube thoracostomy should be considered in severe blast lung injuries.

A primary blast injury to the thorax can also cause a cardiovascular response giving rise to bradycardia, prolonged hypotension and apnoea followed by rapid shallow breathing. This is an autonomic reflex and the bradycardia and apnoea are both mediated by a vagal reflex. The immediate cardiovascular response to the blast wave is a decrease in heart rate, stroke volume and cardiac index which occurs in seconds. The normal reflex increase in systemic vascular resistance does not occur, which causes blood pressure to fall. Recent findings have suggested that primary blast injury causes a rapid release of nitric oxide from the pulmonary circulation which could lead to systemic vasodilation and thus decreased total peripheral resistance resulting in the drop in blood pressure. Recovery usually occurs within 15 minutes to 3 hours.

Gastrointestinal system primary blast injuries

Again, due to its high air content, the gastrointestinal system is susceptible to primary blast injury. The colon and ileocaecal region are the structures at the greatest risk of perforation. Implosion and shearing forces cause the intestinal structural layers to separate. Intramural oedema and hemorrhage and microthromboses develop which compromise intestinal perfusion and increase the risk of delayed perforation. Also, interruption of mesenteric blood supply by shearing forces or arterial air embolism can cause intestinal ischemia.

Symptoms of gastrointestinal primary blast injury include abdominal pain, nausea and vomiting, peritonitis consistent with hollow visceral perforation and bloody diarrhoea and testicular pain. Those with minimal initial symptoms may progress to peritonitis days after the initial injury. Individuals who are exposed to an underwater blast may develop more severe abdominal injuries since blast wave travel further and are more powerful in a liquid medium. They may exhibit temporary paralysis, the urgent desire to defaecate and the passage of diarrhoea is usual. Patients may experience sudden severe bilateral testicular pain that may persist for many days. Colicky abdominal pain that persists for many days or weeks is a hallmark finding as is mild pyrexia of unknown origin for the first 3-4 days.

Clinical examinations reveals a spectrum of findings from peritonitis, absent bowel sounds and shock, suggestive of visceral perforation, to more common finding of moderate generalized abdominal tenderness.

The key to diagnosis of gastrointestinal tract injuries remains repeated clinical examinations. Abdominal sonography should be used to identify intraperitoneal fluid and can assist in operative decision making. However, a negative examination does not rule out the possibility of an abdominal primary blast injury. Patients who are hemodynammically stable with abdominal pain should have an abdominal CT to check for solid injuries and perforation. However, a CT scan lacks sensitivity to exclude intestinal contusions and mesenteric injury definitively. Thus, symptomatic patients must be observed for 6-8 hours and then re-examined. Additional investigations include use of diagnostic peritoneal lavage. A peritoneal lavage is useful for diagnosis of immediate blunt intestinal rupture but not intestinal contusion which leads to delayed bowel perforation. A peritoneal lavage allows assessment of the lavage fluid-blood with low grade solid organ trauma is an indication for a potentially non-operative approach, whereas enteric contents mandate intervention. Signs of peritonitis and free intraperitoneal air on imaging mandate intervention in a patient who is fit enough. Patients needing surgical intervention should be assessed for blast lung injury with a chest radiograph as positive pressure ventilation is needed in surgery which can give rise to air embolisms in patients with lung injuries. Also, the use of anesthesia in an laparotomy can have disasterous consequences in a patient with severe pulmonary blast injury.

Patients who develop haemorrhagic shock from the intestinal primary blast injury should get intravenous fluids for volume resuscitation until emergency surgery can be performed. However, as mentioned before, aggressive volume resuscitation can worsen pulmonary blast injuries.

Permissive hypotension (systolic pressures between 80mmHg and 90mmHg) might improve outcomes in people with concomitant blast injureies. However, patients who also have traumatic brain injury should have their blood pressure normalised to minimise cerebral hypoperfusion.

Other primary blast injuries

This includes pulmonary contusion, systemic air embolism and free radical associated injuries such as thrombosis, lipoxygenation and DIC. ARDS may be a result of direct lung injury or of shock from other body injuries.

Possible future treatment

Novel pharmacological means of attenuating the development of blast lung have shown condiserable promise. Initial demonstration that resolution of the inflammatory component of blast lung coincided with engagement of antioxidant and anti-inflammatory mechanisms led to studies using these mechanisms as targets for therapy. Activation of haemoxygenase-1 using haemin was resported to increase survival in rats with blast lung, possibly via and anti-inflammatory mechanism, while administration of the antioxidant N-acetylcysteine amide was found to attenuate the development of blast lung and the associated pulmonary inflammatory response.

Three explosive forces cause primary blast injury, which are spallation, implosion and inertia. Spallation takes place when a pressure wave passes from a dense medium to a less dense medium, resulting in displacement and fragmentation of the dense medium into the less dense medium. Implosion forces take place when gaseous contents within tissues are suddenly compressed by the blast overpressure. As the positive pressure phase passes, the gas re-expands and releases a large amount of kinetic energy. Inertia, or shearing forces, are similar in their pathophysiological effect to deceleration forces. In response to peak ovepressure, tissues of varying densities move at different speeds, and thus as the overpressure passes through an organ, structural components of the different densities can be tethered and damaged by these sheering forces.

Implosion results from displacement of the less dense into the denser medium. Inertia is defined as the sheer stress created by the blast wave travelling through tissues of different densities at different velocities

Injury occurs as a result of propagation of the blast wave across the chest wall rather than along the airway. Spalling and implosion at the level of the alveoli result in nurmersous clinical sequelae: subcutaneous emphysema, pneumothorax, pulmonary interstitial emphysema, air embolism, alveolar haemorrhage, penumopericardium, penumomediastinum, and pneumoperitoneum.

PBI may lead to bowel perforation, haemorrhage, mesenteric shear injuries, solid organ lacerations, and testicular rupture.

Nasogastric drainage of the gastrointestinal tract is useful, particularly in those requiring respiratory support.

It is important to determine the patient's location relative to the centre of the blast. An explosion that occurs in an enclosed space or in water tends to cause more serious injury

Examine lungs for evidence of pulmonary contusion and pneumothorax. Assume that a patient's wheezing is associated with a blast injury from pulmonary contusion. Other causes of wheezing may include inhalation of irritant gases or dust, pulmonary edema from myocardial contusion, and ARDS.

Many experts recommend obtaining a chest radiograph in the presence of isolated tympanic membrane rupture since this may indicate exposure to significant overpressure. However, a patient with isolated TM perforation but no other immediately identified injuries, does not automatically require an extended period of observation. Also, intact TMs do not imply the absence of serious injury, especially if the patient was wearing some type of ear infection

Blast lung is the most common fatal primary blast injury. This includes pulmonary contusion, systemic air embolism and free radical associated injuries such as thrombosis, lipoxygenation and DIC. ARDS may be a result of direct lung injury or of shock from other body injuries.

Thoracic PBI may result in pericardial tamponade even in the absence of penetrating trauma.

Intestinal barotraumas is more common with underwater rather than air blast injuries.

Ossicle fracture or dislocation may occur with high-energy explosions

PBI of the brain may be associated with impaired cerebral vasculat function including compensatory mechanisms for traumatic brain injury. ROS are likely contributors

Because pulmonary contusion tends to evolve over several hours, a period of observation radiography may be necessary if indicated

On a cellular level, shock waves produce an inflammatory response. Interleukion 8 is released, causing mobilization of polymorphonuclear leuckocytes into the systemic circulation. The release of proinflammatory cytokines induces the expression of the CD11b receptor complex on the PMN surface, leading to adnhesion at the site of injury. Select free-radical scavengers and inhibitors of inflammatory pathways are promising in phase I animal trials. In addition, blast injury to the lungs causes levels of inducible nitric oxygen synthase to increases in the brain causing brain injury. The iNOS inhibitor aminoguanidine appears to be effective when administered to mice either before or 1 hour after the blast, but human data is lacking.

PPVand positive end expiratory pressures should be avoided whenever possible in the setting of pulmonary blast injury due to risk of alveolar rupture and subsequent formation of air emboli. However, mechanical ventilation often cannot be avoided.

As symtoms of pulmonary contusion and intestinal hematoma may take 12-48 hours to develop, instruct all discharged patients to return for reevaluation if they develop breathing problems, increasing abdominal pain or vomiting.