Ch. 33 Flashcards
Trauma occurs when an external force of energy impacts the body and causes structural or physiologic alterations, or injury. External forces can be radiation, electrical, thermal, chemical, or mechanical forms of energy. Trauma that occurs from high-velocity impact (mechanical energy) is most common. Mechanical energy can produce blunt or penetrating traumatic injuries. Understanding
Blunt Trauma
Penetrating Trauma
Mechanism of injury
is seen most often with MVCs, falls, contact sports, or blunt-force injuries
occurs because of the forces sustained during a rapid change in velocity (deceleration).
As the body stops suddenly, tissues and internal organs continue to move forward. This sudden change in velocity can cause significant external and internal injury. Blunt injury may be difficult to diagnose, as injuries are not always obvious or readily apparent.
Blunt Trauma
those that puncture the body and result in damage to internal structures—occur with stabbings, firearms, or impalement.
Damage is created along the path of penetration.
can be misleading, because the appearance of the external wound may not accurately reflect the extent of internal injury.
Several factors determine the extent of damage sustained as a result of penetrating trauma.
With penetrating stab wounds, factors that determine the extent of injury include the type and length of object used and the angle of insertion.
Penetrating Trauma
Development of the Advanced Trauma Life Support (ATLS) guidelines by the American College of Surgeons has enhanced assessment skills of prehospital care providers, expedited transport of critically injured patients, identified the importance of designated trauma care centers, created evidence-based protocols for injured patients, and focused on injury prevention, all which have affected the timing of death after trauma. At present, with improvements in trauma resuscitation described earlier, most deaths occur in a bimodal distribution
The first peak of trauma deaths occurs within 48 hours after initial injury, and the second peak occurs days to weeks after injury. In the first peak, death often occurs on scene or very soon after admission to the hospital, usually as a result of severe traumatic brain injury (TBI) or hemorrhage. During the second peak, death frequently occurs in the critical care unit as a consequence of complications from the initial injury, such as infection or multiple-organ dysfunction syndrome (MODS).
The golden hour of trauma resuscitation is often viewed as a critical time frame in which the injured patient will die unless definitive care is delivered.
Major advances have been made in the management of patients with traumatic injuries in the prehospital, emergency department, and critical care settings. Nursing management of a patient with traumatic injury begins the moment a call for help is received and continues until the patient’s death or return to the community.
Prehospital Care
Emergency Department
Primary survey
Secondary Survey
Critical Care Phase
End Points in Trauma Resuscitation
Phases of trauma care
immediate identification of life-threatening injuries and transport (ground or air) to the closest appropriate medical facility. Airway maintenance, recognition and control of external bleeding and shock, and immobilization of the patient are essential priorities.
Initiation of a peripheral intravenous (IV) line, splinting of fractures, and pain management are also vital components.
Prehospital Care
assist health care providers with the essential actions necessary for rapid assessment, immediate identification of life-threatening injuries, and initial resuscitation of trauma patients in the emergency department.
guiding principles delineate a systematic approach to initial assessment and care of a trauma patient that includes a rapid primary survey, resuscitation of vital organ systems, a more detailed secondary survey, and initiation of the most appropriate care.
Emergency Department
On arrival of the trauma patient in the emergency department, the primary survey is initiated. The purpose of this initial assessment is to identify and treat any life-threatening injuries that, if left untreated, could potentially cause the patient’s death.
The five steps in the ATLS primary survey are commonly referred to as the ABCDEs of trauma resuscitation
Airway maintenance with cervical spine protection
Breathing and ventilation
Circulation with hemorrhage control
Disability: Neurologic status
Exposure or environmental control
control hemorrhage in a trauma patient without becoming overly preoccupied with other components of the primary survey.
Airway.
Breathing.
Circulation.
Exposure.
Primary survey
assessed for patency and possible airway obstruction. Trauma patients are at risk for ineffective airway clearance, especially in the presence of altered consciousness, effects of drugs and/or alcohol, and maxillofacial or thoracic injuries.
Airway obstruction can be caused by foreign bodies, blood clots, or broken teeth. Airway patency is assessed by inspecting the oropharynx for foreign body obstruction and listening for air movement at the nose and mouth.
Airway placement must incorporate cervical spine immobilization.
The cervical spine must be immobilized at all times in all trauma patients until a cervical spinal cord injury (SCI) has been ruled out.
Airway.
The patient is assessed for signs of visible chest movement. An open, clear airway does not always ensure adequate ventilation and gas exchange. Assessment includes a visual inspection of chest wall integrity and respiratory rate, depth, and symmetry. Auscultation is performed to assess the presence or absence of breath sounds. Decreased or absent breath sounds or alteration in chest wall integrity may necessitate chest tube placement. Supplemental oxygen is administered to some injured patients but may not be required in the spontaneously breathing trauma patient who is awake, alert, talking, and has an oxygen saturation with pulse oximetry (SpO2) greater than 92%.
Endotracheal intubation may be required for patients who have compromised airways caused by mechanical factors, who are unconscious, or who have ventilatory problems.
Breathing.
assess for the presence of a palpable pulse, assess any evidence of external or internal hemorrhage, and, if possible, obtain a baseline measurement of the patient’s vital signs. Rapid evaluation of circulatory status includes assessment of level of consciousness (LOC), skin color, and pulse. The LOC provides data on cerebral perfusion.
Facial color that is ashen or gray and extremities that are pale or slightly mottled may be ominous signs of hypovolemia and shock.
Central pulses (femoral or carotid artery) are assessed bilaterally for rate, regularity, and quality. If a pulse is not present, cardiopulmonary resuscitation (CPR) must be initiated immediately.
Measurement and trending of systolic and diastolic blood pressure, mean arterial pressure (MAP), and SpO2 readings are more important than individual values.
rapid neurologic assessment is performed. During this important step, the patient’s baseline LOC and pupil size and reaction are assessed and documented.
AVPU method can be used to quickly describe the patient’s
A: alert
V: responds to verbal stimuli
P: responds to painful stimuli
U: unresponsive
Circulation.
all of the patient’s clothing is removed to facilitate a thorough examination of all body surfaces for the presence of injury. The patient is turned (logrolled) while full spinal precautions are maintained.
After clothing is removed, the patient must be protected from hypothermia.
This can be accomplished through warm blankets, increasing room temperature, and warm IV fluids.
Exposure.
secondary survey begins when the primary survey is completed, potentially life-threatening injuries have been identified, and resuscitation initiated.
secondary survey is a more detailed, in-depth physical examination of the trauma patient.
nurse ensures the completion of all necessary procedures, such as an electrocardiogram, radiographic studies (chest, cervical spine, thorax, and pelvis), ultrasonography, and insertion of gastric and urinary catheters.
nurse continuously monitors the patient’s vital signs (heart rate, blood pressure, MAP, and SpO2) and response to resuscitation interventions. Emotional support to the patient and family also is imperative.
Patient history is also an important aspect of the secondary survey. The patient’s pertinent past history can be assessed by use of the mnemonic AMPLE:
A: Allergies
M: Medications currently used
P: Past medical illnesses/pregnancy
L: Last meal
E: Events/environment related to the injury
Head injury, shock, or the use of drugs and/or alcohol may preclude obtaining information from the patient. Prehospital care providers (paramedics, emergency medical technicians), family members, or sometimes bystanders can be excellent sources of information.
Hemorrhagic shock in trauma.
Damage control resuscitation.
Permissive hypotension.
Secondary Survey
Hypovolemic shock as a result of hemorrhage is the most common type of shock that occurs in trauma patients. The traditional signs and symptoms of hemorrhagic hypovolemic shock may not appear until approximately 30% to 40% of circulating blood volume is lost. Hemorrhage in trauma must be identified and treated rapidly. Two large-bore (14-gauge to 16-gauge) peripheral IV catheters, the intraosseous device, or central venous catheter is inserted.
Both crystalloid solutions are physiologically isotonic, provide volume to the volume-depleted patient, and are often readily available.
Hemorrhagic shock in trauma.
Is an evidence-based strategy employed in trauma centers worldwide to control and assist in stabilization of the trauma patient in hemorrhagic shock. Components of damage control resuscitation include permissive hypotension, massive transfusion protocols, and damage control surgery.
begins in the field and continues through the emergency department, operating room, and critical care unit.
Damage control resuscitation.
Involves low-volume IV fluid resuscitation. The goal is to maintain the blood pressure low enough to prevent worsening of hemorrhage but high enough to maintain perfusion of vital organs, including the brain. It is not, under any circumstances, to be considered as a substitute for surgical control of bleeding in the hemorrhaging trauma patient.
Individualized assessment of each trauma patient is mandatory. Aggressively infusing IV fluid into a trauma patient may dilute clotting factors, disrupt any clots that have formed, and exacerbate hemorrhage.
Permissive hypotension.
Critically injured trauma patients are frequently admitted to the critical care unit as direct transfers from the emergency department, diagnostic imaging, or operating room.
Information the critical care nurse must obtain from prehospital, emergency department, or operating room personnel can be summarized using the SBAR communication tool: Situation, Background, Assessment, and Recommendations
information is ideally obtained before the patient’s admission to the critical care unit to ensure availability of needed personnel, equipment, and supplies, although this may not always be possible.
Priority nursing care during the critical care phase includes ongoing repeated physical assessments, monitoring laboratory and diagnostic test results, and observing trends in the patient’s response to treatment. The nurse is continually aware that the second peak of the bimodal distribution of trauma deaths occurs most often in the critical care setting as a result of complications including prolonged shock states, acute respiratory distress syndrome (ARDS), sepsis, and MODS. Ongoing nursing assessments are imperative for early detection and treatment of complications.
Oxygen delivery must be optimized to prevent further system damage. The trauma patient is at high risk for impaired oxygenation as a result of various factors
Prevention and treatment of hypoxemia depend on accurate assessment of the adequacy of pulmonary gas exchange (arterial blood gas), oxygen supply (fraction of inspired oxygen), and oxygen consumption (assessment of LOC, tissue perfusion, capillary refill, urinary output).
Acidosis (pH less than 7.2), hypothermia (temperature less than 35 C), and clinical coagulopathy are often present in trauma patients.
The goal of the critical care nurse is to continue resuscitation and assist in correcting hypothermia, coagulopathy, and acidosis.
Critical Care Phase
During resuscitation, all attempts are made to improve cellular oxygenation. Resuscitation is aimed at ensuring adequate perfusion of tissues with fluid, oxygen, and nutrients to support cellular function. No single resuscitation end point is sufficient. Resuscitation end points (variables or parameters) must be viewed across the continuum of trauma resuscitation.
During resuscitation from traumatic hemorrhagic shock, normalization of standard clinical parameters such as blood pressure, heart rate, and urine output is inadequate.
Frequent and thorough assessments of all body systems are the cornerstone of medical and nursing management of critically injured trauma patients in critical care. The critical care nurse is able to detect subtle changes in patient condition and facilitate the implementation of timely therapeutic interventions to prevent complications often associated with trauma.
End Points in Trauma Resuscitation
TBI can be caused by both blunt and penetrating trauma. The leading causes of TBI include MVCs, violence (suicide and firearm injuries), and falls
Pathophysiology
Classification of Skull and Brain Injuries
Neurologic Assessment of Traumatic Brain Injury
Medical Management
Nursing Management
Traumatic brain injuries
Traumatic brain injuries
Maxillofacial injuries
Thoracic injuries
Specific Abdominal Organ Injuries
Musculoskeletal Injuries
Complications of Trauma
Specific Trauma Injuries
It is important that the nurse understand these two distinct phases of TBI, because critical care interventions are often directed at limiting the effects of and reducing morbidity and mortality
Primary injury.
Secondary injury.
Pathophysiology
occurs at the moment of impact as a result of mechanical forces to the head. Primary injuries include those injuries that directly damage the brain parenchyma.
may be mild, with little or no neurologic damage, or severe, with major brain and tissue damage.
The extent of and recovery from injury are often related to whether the primary injury was localized (limited to a specific area) or diffuse (widespread) throughout the brain. Immediately after brain injury, a cascade of neural and vascular processes is activated.
Primary injury.
the biochemical and cellular response to the initial trauma that can exacerbate the primary injury and cause additional damage and impairment in brain recovery.
caused by ischemia, hypotension, hypercapnia, cerebral edema, seizures, or metabolic derangements. Hypoxia and hypotension, the best-known culprits for secondary injury, typically are the result of extracranial trauma.
Cerebral edema.
Hypotension.
Ischemia.
Hypercapnia.
Secondary injury.
as a result of the changes in the cellular environment caused by contusion, loss of autoregulation, and increased permeability of the blood brain barrier.
The combined effects of increasing pressure and decreasing perfusion precipitate a downward spiral of events. The extent of cerebral edema can sometimes be minimized by managing aspects of secondary injury, such as oxygenation, ventilation, and perfusion.
Cerebral edema.
Significant hypotension will not adequately perfuse neural tissue. Hypotension is rarely observed in the patient with TBI on admission to the hospital unless terminal medullary failure has occurred.
With loss of autoregulation, an increase in blood pressure occurs, which results in increased intracranial blood volume and elevates intracranial pressure (ICP).
Hypotension.
Tissue ischemia occurs in areas of poor cerebral perfusion as a result of primary injury, edema, hypotension, or hypoxia.
The cells in ischemic areas become edematous.
Extreme vasodilation of the cerebral vasculature occurs in TBI in an attempt to supply oxygen and nutrients to the cerebral tissue. This sudden increase in blood volume increases intracranial volume and raises ICP.
Ischemia.
Hypercapnia is a powerful vasodilator of cerebral vessels. Most often caused by hypoventilation in an unconscious patient, hypercapnia results in cerebral vasodilation, increased cerebral blood flow (volume), and increased ICP
Hypercapnia.
Injuries of the skull and brain are described by the mechanism of injury, location of injury in the brain, and anatomic changes or losses that occur.
Skull fracture.
Concussion.
Contusion.
Cerebral hematoma.
Penetrating brain injury.
Diffuse axonal injury.
Classification of Skull and Brain Injuries
are common, but they do not by themselves cause neurologic deficits. Skull fractures can be classified as open (dura mater is torn) or closed (dura mater is not torn), or they can be classified as fractures of the vault or fractures of the base.
Assessment findings may include cerebrospinal fluid (CSF) leakage—described as rhinorrhea (from nose) or otorrhea (from ear), Battle sign (ecchymosis overlying the mastoid process behind the ear), “raccoon eyes” (subconjunctival and periorbital ecchymosis), or palsy of the seventh cranial nerve.
The significance of a skull fracture is that it identifies a patient with a higher probability of having or developing an intracranial hematoma.
Bone window views are helpful in identifying bone tumors, and in trauma patients with TBI, a bone window scan provides an enhanced view of cranial abnormalities.
Open skull fractures require surgical intervention to remove bony fragments and close the dura mater. Major complications of basilar skull fractures are cranial nerve injury and CSF leakage.
Skull fracture.
is a brain injury accompanied by a brief loss of neurologic function, in particular, loss of consciousness.
Neurologic dysfunctions include confusion, disorientation, and sometimes a period of anterograde or retrograde amnesia. Other clinical manifestations that occur after concussion are headache, dizziness, nausea, irritability, inability to concentrate, impaired memory, and fatigue.
Concussion.
“bruising” of the brain, is frequently associated with acceleration deceleration injuries, which result in hemorrhage into the superficial parenchyma.
Coup injury affects the cerebral tissue directly under the point of impact.
Contrecoup injury occurs in a line directly opposite the point of impact
Clinical manifestations of a contusion are related to the location of the injury, the degree of contusion, and the presence of associated lesions.
Contusion.
Extravasation of blood creates a space-occupying lesion within the cranial vault that can lead to increased ICP.
Traumatic intracerebral hemorrhage (ICH) directly damages neural tissue and can produce further injury as a result of pressure and displacement of intracranial contents.
Epidural hematoma.
Subdural hematoma.
Acute subdural hematoma.
Subacute subdural hematoma.
Chronic subdural hematoma.
Intracerebral hemorrhage and hematoma.
Cerebral hematoma.
is a collection of blood between the inner skull and the outermost layer of the dura mater
occurs as a result of trauma to the skull and meninges as seen in the CT scan
As the artery bleeds, it pulls the dura mater away from the skull, creating a pouch that expands into the intracranial space.
The classic clinical manifestations of EDH include brief loss of consciousness followed by a period of lucidity. Rapid deterioration in the LOC should be anticipated, because arterial bleeding into the epidural space can occur quickly. The patient may complain of a severe, localized headache and may be sleepy.
A dilated and fixed pupil on the same side as the impact area is a hallmark of EDH.
Treatment of EDH requires urgent surgical intervention to remove the blood and to cauterize the bleeding vessels
Epidural hematoma.
is the accumulation of blood between the dura mater and underlying arachnoid membrane, is most often related to a rupture in the bridging veins between the cerebral cortex and the dura mater
Acceleration deceleration and rotational forces are major causes of SDH, which often is associated with cerebral contusions and ICH.
Subdural hematoma.
are hematomas that occur after a severe blow to the head. The clinical presentation of acute SDH is determined by the severity of injury to the underlying brain tissue at the time of impact and the rate (speed) at which blood accumulates in the subdural space.
presents with a decreased LOC; in other situations, the patient has a lucid period before deterioration.
inequality of pupils or motor movements
Rapid surgical intervention, including craniectomy, craniotomy, or burr hole evacuation, can reduce mortality.
Acute subdural hematoma.
that develop 4 days to 3 weeks after trauma.
Occurs within the meninges in the subdural space.
Diagnosed: alteration in neurologic symptoms and by CT scan expansion of the hematoma occurs at a rate slower than that observed in acute SDH and less than an epidural bleed.
Clinical deterioration of a patient with a subacute SDH is also usually slower than deterioration with an acute SDH, but treatment by surgical intervention, when appropriate, is the same
Subacute subdural hematoma.
when symptoms appear 21 days or more after injury.
Clinical manifestations of chronic SDH are deceptive. The patient may report a variety of symptoms such as lethargy, absent-mindedness, headache, vomiting, stiff neck, and/or photophobia.
They may also show signs of transient ischemic attack, seizures, pupillary changes, or hemiparesis.
surgical intervention is required, evacuation of chronic SDH may be accomplished by craniotomy, burr holes, or catheter drainage.
Chronic subdural hematoma.
