Trauma has been dubbed the forgotten epidemic and the neglected disease of modern society. Trauma annually impacts hundreds of thousands of individuals and costs billions of dollars in direct expenditures and indirect losses. Trauma care has improved over the past 20 years, largely from improvements in trauma systems, assessment, triage, resuscitation, and emergency care.
However, an Institute of Medicine report identified a US crisis in access and distribution to emergency care that may impact trauma system efficiency and effectiveness. Similarly, a predicted deficit in critical care practitioners may similarly degrade the post-emergency department care of the critically injured patient. The American College of Surgeons Committee on Trauma (ACS-COT) and the American Association for the Surgery of Trauma (AAST) acute care surgery initiative is designed to integrate trauma, emergency general surgery, and surgical critical care and to bolster new trainee interest in this field. Its sensitivity for identifying major trauma patients is lower and specificity higher than previously described, particularly among elders. 
Work must still be done to continuously improve trauma care nationally, regionally, and institutionally, and the ACS-COT applies rigorous standards to performance improvement prior to verifying US trauma centers. For this improvement to occur, the ongoing application of the unique principles and practice of intensive care medicine is necessary.
Patient outcomes after major trauma have improved in regions where comprehensive trauma systems have evolved. Crucial components of such a system should include a coordinated approach to both prehospital care and hospital care and to training providers in both areas. Paramedics and medical staff should be provided with a clear and objective framework for assessing patients, establishing and engaging treatment protocols, following triage guidelines, engaging in transportation and communication protocols, and implementing ongoing performance improvement programs. It is essential to recognize that care of the significantly injured patient is critical care in that critical care is a concept, not a location.
The most seriously injured patients must be identified in the field and safely transported to a designated trauma center where appropriate care is immediately available. This is the principle of triage and is subject to both under-triage and over-triage. Clearly, from a patient-centered view, over-triage is preferable, but, from a system perspective, over-triage may be problematic in an overcrowded and oversubscribed emergency department.
Trauma scoring systems describe injury severity and correlate with survival probability. Various systems facilitate the prediction of patient outcomes and the evaluation of aspects of care. The scoring systems vary widely, with some relying on physiologic scores (eg, Glasgow Coma Scale [GCS] score, Revised Trauma Score), and others relying on descriptors of anatomic injury (eg, Abbreviated Injury Score, Injury Severity Score). No universally accepted scoring system has been developed, and each system contains unique limitations. This limitation has resulted in the use of a number of such systems in different centers around the world.
Principles involved in the initial assessment of a patient with major trauma are those outlined by the American College of Surgeons (ACS) in their Advanced Trauma Life Support (ATLS) guidelines or those of the Australasian College of Surgeons in the Early Management of Severe Trauma guidelines. [2, 3] The principles involved consist of (1) preparation and transport; (2) primary survey and resuscitation, including monitoring, urinary and nasogastric tube insertion, and radiography; (3) secondary survey, including special investigations, such as CT scanning or angiography; (4) ongoing reevaluation; and (5) definitive care.
Preparation and Communication
Trauma-receiving hospitals should receive advance communication from emergency medical services care providers about the impending arrival of seriously injured patients. The patient's mechanism of injury, vital signs, field interventions, and overall status should be communicated. This allows for the in-house trauma team to be called and for the emergency department staff to make appropriate preparations.
The trauma team members vary based on world geography but incorporate many similar elements, including representation from emergency medicine, trauma, critical care, with or without anesthesia, nursing, respiratory therapy, blood bank, radiology, social services, and registration. A team leader is identified, and it is the team leader's responsibility to ensure that the resuscitation proceeds in an organized and efficient manner through the diagnostic and therapeutic protocols.  Additional consultants may be engaged in response to specific injuries. In addition to this team, many trauma centers also have a trauma care coordinator (usually a nurse), who follows the patient through his or her hospital course.
On the patient's arrival, a concise transfer of the patient from the paramedics should occur. One person should be talking, while everyone else is listening; this is crucial information for the whole team. In many trauma centers, the team leader is a senior or chief resident in surgery or emergency medicine, with close supervision from appropriate attending staff. Increasingly, mid-level practitioners (eg, physician associates, nurse practitioners) may serve in this role as well.
Most trauma centers use a system of prehospital triage that characterizes patients into those with physiologic derangements and those who have a suggestive mechanism of injury. Those patients with obvious derangements should prompt a full team response, while patients with less injury may be cared for by a modified team complement.
The primary survey aims to identify and treat immediately life-threatening injuries relying on the ABCDE system. This system comprises airway control with stabilization of the cervical spine, breathing (work and efficacy), circulation including the control of external hemorrhage, disability or neurologic status, and exposure or undressing of the patient while also protecting the patient from hypothermia. These elements are explored below.
Airway with control of the cervical spine
Airway assessment should proceed while maintaining the cervical spine in a neutral position. The latter is achieved by using a rigid cervical immobilization collar. Airway clearance maneuvers are extensively described elsewhere and are not reviewed in this article.
When the airway is in jeopardy, or when the GCS score is less than 8, an artificial airway is essential. Airway control is commonly achieved by means of rapid-sequence orotracheal intubation (OETT) performed with in-line stabilization of the cervical spine. Correct placement of the endotracheal tube is confirmed (1) by the aid of an end-tidal carbon dioxide monitoring device, (2) by observation of the tube passing through the vocal cords, and (3) by auscultation of the chest.
Several well-defined options for achieving airway control must be established in the event that OETT placement is not able to be achieved. These options include laryngeal mask airway (LMA), intubating LMA, fiberoptic intubation, percutaneous cricothyroidotomy, and surgical cricothyroidotomy (tracheostomy in children). Tracheal inspection is essential to determine if there is peritracheal crepitus or deviation from the midline indicating potential direct airway injury or intrathoracic pulmonary or major vascular injury.
One must next assess the adequacy of gas exchange. This is most readily accomplished by visual inspection of thoracic cage movement, palpation of the thoracic cage movement, and auscultation of gas entry. One is assessing for inequalities from one side to the other, crepitus, and local movement asymmetry as in paradoxic thoracic cage movement in flail chest. One is also evaluating for signs of impending respiratory failure, such as uncoordinated thoracic cage and abdominal wall movement, accessory muscle use, and stridor.
Inadequate ventilation may result in hypoxemia, hypercarbia, cyanosis, depressed level of consciousness, bradycardia, tachycardia, hypertension, or hypotension. As a general rule, until stability has been assured, administer high-flow oxygen by mask to all patients to abrogate the potential for hypoxemia.
Classic signs of a tension pneumothorax, hemothorax, or combined hemopneumothorax include tracheal deviation, jugular vein distension, hypoxia, tachycardia, and hypotension. Intrathoracic tension physiology is a clinical diagnosis and requires immediate decompression. This is initially commonly accomplished with a 14-gauge catheter-over-needle assembly placed in the second intercostal space (ICS) midclavicular line (MCL). Patients treated in this way should have a tube thoracostomy placed to manage simple pneumothorax and to evacuate thoracic cavity blood when present. Life-threatening hemorrhage identified when placing a tube thoracostomy may be managed with a resuscitative thoracostomy.
Circulation and hemorrhage control
Emergent treatment of patients with exsanguinating hemorrhage or shock can be life-saving. This assessment includes identifying and managing rapid external hemorrhage. This can often be achieved with a simple pressure dressing, but surgical intervention may be required. As more experience is gained with procoagulant dressings (used principally by the military), external hemorrhage control may gain pharmacologic support embedded in dressings.
Shock in trauma patients, defined as inadequate organ perfusion and tissue oxygenation, is most commonly caused by hemorrhage leading to hypovolemia, but many other causes are readily identified, including cardiac tamponade, tension pneumothorax or hemothorax, and spinal cord injury. Signs of shock include tachypnea, tachycardia, decreased pulse pressure, hypotension, pallor, delayed capillary refill, oliguria, and a depressed level of consciousness. In patients with hypovolemia, the neck veins may be flat. A normal mental status generally implies an adequate cerebral perfusion pressure, while diminished mentation may be associated with shock with or without intracranial trauma.
ATLS readily identifies 4 different classes of shock. Class I and II shock generally does not need red cell mass restoration and is well managed with asanguineous fluids for plasma volume expansion. Hypotension and disordered mentation generally indicate at least class III shock and should prompt plasma volume expansion and red cell mass repletion if the hypotension fails to resolve after an initial 2000-cc crystalloid bolus, according to ATLS.
A systematic approach for detecting the source of hypovolemic shock should consider 5 sources of ongoing hemorrhage, as follows: (1) external (eg, from the scalp, skin, or nose), (2) pleural cavities, (3) peritoneal cavity, (4) pelvis/retroperitoneum, and (5) long-bone fracture. Fracture alignment and stabilization is essential in limiting blood loss. Pelvic fractures may be initially stabilized with a pelvic binder or a wrapped sheet secured with a towel clip as a means of reducing pelvic volume to limit hemorrhage.
During the acute resuscitation period, a brief assessment of neurologic status should be performed. This assessment should include the patient's posture (ie, any asymmetry, decerebrate or decorticate posturing), pupil asymmetry, pupillary response to light, and a global assessment of patient responsiveness.
A recommended system is the AVPU method, as follows: A = Patient is awake, alert, and appropriate; V = Patient responds to voice; P = Patient responds to pain; U = Patient is unresponsive.
A complementary assessment using the GCS should be made at this time, during the secondary survey, and at any time that the patient’s mental status appears to change. A more detailed assessment of the patient’s neurologic status is to be made during the secondary survey.
Patients should be completely disrobed during the initial assessment and the subsequent secondary survey. This helps ensure that significant injuries are not missed. At the same time, efforts to prevent significant hypothermia, using a warm ambient room (28-30°C), overhead heating, and warmed IV fluids, should be instituted. The patient's temperature should be measured on arrival at the emergency department, and strenuous efforts should be made to avoid significant hypothermia during resuscitation and therapeutic intervention.
Urinary drainage catheters are commonly placed to assess for genitourinary system hemorrhage and to monitor urine flow. Precautions to avoid urethral injury should be taken for patients with pelvic trauma and for those who have blood at the urethral meatus. Digital rectal examination to identify a high-riding prostate should precede catheter insertion. Abnormal findings from the rectal examination or concern as to the continuity of the urethra should prompt a retrograde urethrocystogram to identify a urethral injury. If identified, a suprapubic catheter should be inserted, and a urologist should be consulted.
Gastric drainage tubes should be orally inserted into all major trauma patients requiring endotracheal intubation. Even in the absence of brain injury, oral gastric tube insertion is preferred to decrease the likelihood of sinusitis from drainage pathway obstruction. Children, in particular, are prone to gastric dilatation, which can significantly impair their respiration and lead to hemodynamic compromise. Immediate decompression may be life-saving. Ongoing monitoring of pulse rate, blood pressure, respiratory rate, oxygen saturation, and temperature is a standard of care in the US.
Initial imaging in the resuscitation room should be limited to a portable anteroposterior (AP) chest radiograph plus an AP pelvic image if the patient was involved in a high-speed motor vehicle collision or a fall from a height. Prior recommendations for lateral cervical radiography have been supplanted by routine pan-cervical imaging with image reformation using CT scanning, especially if the patient will undergo a brain CT scan.
Definitive clearing of the neck is managed in different ways in different institutions, but certain common features are identified. Patients with a clear sensorium and no distracting injuries may be clinically cleared if there is no neck pain on palpation and active flexion/extension/rotation. Patients with a normal CT scan but an abnormal mental status should remain in a rigid cervical immobilization device until they may participate in a physical examination or they undergo early (< 72 h postinjury) MRI to detect the presence of ligamentous injury.
Chest radiographs should be assessed for the position of tubes and lines, the presence of treatable life-threatening conditions, including space-occupying lesions, mediastinal widening, lung parenchymal injuries, and injuries to the thoracic cage or vertebral column.
A high-energy pelvic fracture identified on physical examination or pelvis film may substantially contribute to shock. Persistent hypotension suggests the need for early operative external stabilization, operative extraperitoneal pelvic packing, or angioembolization. Technique selection depends on the facility’s resources and practitioner skill set.
The secondary survey follows in the wake of correction of immediately life-threatening injury and completion of the primary survey. Thus, the secondary survey may not occur until after an emergency operation has been completed. The secondary survey includes a detailed history, complete physical examination, additional radiologic examinations, and special diagnostic studies. Many institutions include the focused assessment with sonography in trauma (FAST) examination as part of the primary survey rather than part of the secondary survey.
The history should include an assessment of the following items, which can be remembered by using the AMPLE acronym: A = Allergies; M = Medications; P = Past medical, surgical, and social history; L = Last meal; and E = Events leading to injury, scene findings, notable interventions, and recordings en route to the hospital.
Head and face and neurology
Palpate the entire cranium and face evaluating for injury and instability. Sutures, staples, or Rainey clips may be helpful in controlling bleeding from large scalp flaps. Palpate for facial crepitus and a mobile middle third of the face as a clue to potential difficulty in airway control. Hemotympanum and the presence of bruising around the eyes (ie, raccoon eyes) and mastoid process (ie, Battle sign) suggest basal skull fracture.
Recheck the pupils, and repeat GCS scoring. Evaluate the cranial nerves, peripheral motor and sensory function, coordination, and reflexes. Identify any neurologic asymmetry. Patients with lateralizing signs and those with an altered level of consciousness (GCS score of < 14) should undergo cranial CT scanning. Patients with traumatic brain injury (TBI) are particularly susceptible to secondary brain injury, in particular from hypoperfusion, hypoxia, hypercarbia, hyperglycemia, hyperthermia, and seizure activity. While primary brain injury and primary brain damage (induced apoptosis after primary brain injury) are beyond the clinician’s control, secondary injury is a preventable complication with careful attention to detail.
Maintaining cervical spine stabilization when removing a rigid cervical immobilization device is imperative. Penetrating injuries of the neck may require angiographic, bronchoscopic, or radiologic examination depending on the level of injury (ie, zone I, II, or III). In particular, zone II injuries that violate the platysma may be readily explored, while those injuries in zone I or III benefit from additional investigation because of the difficulty in identifying and controlling injuries in those zones.
Reexamine the chest. Initiate further investigations as indicated by physical examination findings or radiography results. While aortography was previously identified as the criterion standard investigation to identify aortic transaction, CT angiography has essentially replaced intra-arterial contrast injection. Transesophageal echocardiography using an omniplane probe may be safely used as well but suffers from difficulty with technology access after hours, dependence on user skill set, problematic probe insertion in patients requiring cervical immobilization, and blind spots at the aortic arch.
Inspect, percuss, palpate, and auscultate the abdomen, noting tenderness and examining for fullness, rigidity, guarding, or an obvious bruit (rare). Remember that blood is not always a peritoneal irritant, and hemoperitoneum may occur without obvious external signs.
Inspection of the abdomen may be confounded by distracting injuries and impaired consciousness from TBI, intoxicants, or prescription medications. FAST scans are routine in most emergency departments and serve to establish the presence or absence of fluid in 4 distinct domains: pericardium, right upper quadrant, left upper quadrant, and pelvis. Diagnostic peritoneal lavage is now rarely used. Extended FAST scanning may also interrogate the thoracic cavity for evidence of pneumothorax. The practitioner should be aware that FAST scanning is not organ-based imaging, and FAST scanning should not be used to establish the presence or absence of solid organ injury. Hemodynamically acceptable patients with a positive FAST scan generally undergo CT scanning to establish the source of presumed hemorrhage. Patients with a positive FAST scan who are unstable generally proceed to operative intervention in the emergency department (cardiac tamponade) or the operating room (intraperitoneal hemorrhage).
FAST scanning does not evaluate the retroperitoneum, and a normal FAST scan may coexist with substantial retroperitoneal hemorrhage. Also, a positive FAST scan may indicate ascites instead of blood, especially in those with renal or hepatic impairment.
Inspect, palpate, and move the limbs to determine their anatomic and functional integrity. Pay attention to the adequacy of the peripheral circulation and integrity of the nerve supply. Arterial insufficiency in patients with a displaced fracture or dislocation requires immediate treatment, generally fracture reduction and/or joint relocation. Pulse inequality should be assessed by means of an ankle-brachial index with diagnostic intervention reserved for those with an absolute ABI difference of 0.2 or greater from one side to the other. Liberal use of diagnostic plain radiography is essential in excluding extremity fracture in patients with mixed mechanisms of injury and in those who cannot participate in an examination because of significant TBI, intoxicants, or other causes.
The log roll refers to the slow controlled turning of the patient to each side to assess the dependent part of the supine trauma patient. Care must be taken to avoid secondary injury from an as-yet undiagnosed unstable fracture. This examination concentrates on the back of the head, neck, back, and buttocks, and it includes a rectal examination. The log roll also provides a convenient time to remove the long immobilization board. The board has not been shown to prevent injury in the presence of an unstable vertebral fracture, but it is highly correlated with pressure ulceration in patients who remain on the board for prolonged periods of time (ie, until diagnostic intervention is complete).
This procedure should be carried out by at least 4 people. The first person stabilizes the head and neck, the second and third persons turn the patient, and the fourth person examines the patient’s dorsum and performs the digital rectal examination. At the completion of the examination, and if the patient is not on an x-ray film bearing stretcher, the chest x-ray plate is readily positioned behind the patient. Spine imaging most commonly proceeds as part of the CT scan using reformatted images. This technique has been demonstrated to have equal, and in some studies superior, efficacy to AP and lateral thoraco-lumber spine imaging for fracture identification.
During the secondary survey, the ABCDE system should be used to constantly reevaluate the patient, and an ongoing diagnostic and therapeutic plan should be revised, as indicated, by the patient’s response to intervention and diagnostic test results.
Prolonged Emergency Department Management
The Institute of Medicine identified an emergency department crisis in US health care. Emergency departments are overcrowded and understaffed for the overutilization by those with and without insurance. Additionally, with the decline in subspecialty coverage, critically injured patients are increasingly being transferred to regional resource trauma centers (ie, Level 1 centers). This regionalization further stresses an already stressed emergency medicine system. Exacerbating this problem is the overcrowding of the current intensive care unit (ICU) beds in the trauma facilities. Thus, it is expected that prolonged emergency department length of stay will occur in the oversubscribed trauma facility. An increasing role is therefore anticipated for the emergency medicine practitioner in the prolonged emergency department management of the trauma patient.
The initial management and injury identification detailed above initiates multiple pathways for the trauma patient that may lead to discharge home, transfer to a specialty facility (ie, burn center), hospital admission (general ward, step-down unit [intermediate dependency unit], ICU [high dependency unit]), operating room, or angiography suite. The specific management is beyond the scope of this article, but management of the injured patient is often collaborative because of the nature of the injury complex, as well as manpower limitations.
With the rise of acute care surgery, as promulgated by the American College of Surgeons Committee on Trauma and the American Association for the Surgery of Trauma, the trauma surgeon increasingly covers trauma, surgical critical care, and emergency general surgery. Therefore, the emergency medicine practitioner who is resident in the emergency department needs to assume a larger role in the management of trauma patients who are awaiting a destination bed for ongoing management.
Generation of jointly agreed upon guidelines for management is essential in ensuring smooth, high-quality care for the injured patient. Often, subspecialty input is of significant benefit in guideline generation (ie, management and clearance of the cervical spine). Additionally, several guidelines have been generated by the Eastern Association for the Surgery of Trauma (EAST; www.east.org) that address injured patient management in general as well as with regard to specific injury complexes.
Subsequent Critical Care Considerations
The information presented thus far describes the initial evaluation of the patient sustaining serious injury. The wide multitude of individual injuries precludes describing each on in detail. Instead, the critical care considerations that are important in the subsequent care of the critically injured patient are explored. They are conveniently grouped into the following domains: neurologic injury, acute respiratory failure, organ failure, anemia, coagulopathy, thermal dysregulation, sepsis, unnecessary fluid administration, damage control sequelae, and acid-base imbalance.
Traumatic brain injury (TBI) occurs commonly in the setting of major trauma and significantly contributes to poor outcomes. Despite advances in all aspects of trauma care, severe TBI carries a mortality rate of approximately 30%. Conservative estimates place the incidence of TBI at 200 cases per 100,000 patients.
Outcome prediction is usually straightforward in those with minimal injury as well as in those with severe injury. Prediction is difficult for those with moderate and severe injury but not unsurvivable injury patterns. Survivors of severe and moderately severe head injuries are likely to be left with some degree of disability. These disabilities may vary from subtle changes in behavior, including depression or loss of independence and earning power, to major cognitive, sensory, or motor deficits.
Some patients unfortunately progress to or never awaken from a chronic vegetative state. It is in these patients that end-of-life discussions to establish a goal of therapy are perhaps most useful. Quite often, consultation with an ethics team or a palliative care team is helpful for both the critical care team and the family.
The principles of treatment of a patient with TBI apply equally at the time of initial assessment as they do during ongoing inpatient care. These principles are aimed at preventing secondary brain injury. Secondary brain injuries include but are not limited to hypotension, hypoxemia, hypercarbia, fever, seizure, uncontrolled hyperglycemia leading to cerebral hyperglycosis, acidosis, severe alkalosis, and hyperthermia. Sound prehospital care has a significant impact on patient outcome. This involves adequate oxygenation and ventilation and the maintenance of an adequate cerebral perfusion pressure as measures to avoid secondary brain injury. Primary brain injury occurs at the time of the trauma and is not modifiable by the practitioner.
Secondary brain damage is different from secondary brain injury. Secondary brain damage is the term applied to the apoptosis that is identified in the injured but not irreparably damaged cells after a primary brain injury. Thus, the practitioner is limited at present to avoiding secondary brain injury as the others are not subject to control.
The initial assessment is the same as for any trauma patient. Immediate protection from secondary injury by avoiding hypoxia and hypotension and by preventing hypercarbia improves patient outcome. Early airway control in patients with a clinically significant depressed level of consciousness (GCS score of 8 or acute decreased in GCS score by 2) is essential in supporting outcomes and in avoiding secondary brain injury.
Hospital assessment involves the history of trauma, physical examination, evaluation of posture and pupillary responses, and additional investigations.
The history of trauma is gained from the patient, witnesses at the scene, attending ambulance staff, and knowledge of the mechanism of injury.
The severity of the injury is defined by carefully examining the patient's mental status by using the GCS score, posture, and pupillary responses.
The GCS score quantifies the patient's neurologic status and enables the rapid and uniform communication of the initial assessment of the patient's possible neurologic injury. The GCS score is a familiar descriptor used in the emergency department. It is derived from observation and responses to eye opening, best motor responses, and best verbal responses (see the Table below).
In the absence of confounding factors, such as illicit and prescription drugs and alcohol use, a low GCS score is a strong predictor of a poor prognosis. Of the 3 parameters assessed following injury, the best motor response elicited appears to be the most accurate prognostic indicator. A GCS score of 3-8 indicates a severe head injury, whereas a GCS score of 14-15 is mild. A GCS score of 15 is normal. A GCS score of 8 defines coma.
Table 1. GCS Score (Open Table in a new window)
|Eye Opening (E)|
|To loud voice||3|
|Best Motor Score (M)|
|Verbal Response (V)|
Assess the patient's posture and pupillary response. In patients who are comatose, note any decerebrate or decorticate posture and pupillary responses to light (normal response is constriction).
Operative versus nonoperative treatment in the setting of head trauma
Typical indications for operative intervention are as follows: (1) extra-axial collections with mass effect, (2) significant mass effect from contusion or hemorrhage resulting in a shift of intracranial structures, (3) penetrating head injury with necrotic foreign body tracks, (4) removal of a foreign body if it compromises neurologic function, and (5) significantly depressed (>1 cm) skull fractures.
Nonoperative or medical therapies are aimed at avoiding secondary brain injury. The 2 major management philosophies following TBI are as follows: ICP management versus cerebral perfusion pressure (CPP) management. The ICP management theorists argue that all efforts should be made to keep the ICP at less than 20 mm Hg. The CPP proponents argue that the ICP may be greater than 20 mm Hg if the CPP is greater than 60 mm Hg. CPP can be estimated by subtracting the ICP from the mean arterial pressure (MAP). It is likely that both schools of thought have merit, and the optimal strategy is a combination of both.
Major management techniques used in the ICU are described below.
PO 2 of greater than 100 Torr to avoid cerebral tissue hypoxia
PCO 2 of 35-40 Torr to avoid cerebral hyperemia or excessive vasoconstriction and induction of cerebral ischemia
Maintenance of a neutral cervical spine position to avoid impairment of cerebral venous drainage
Avoidance of jugular venous lines on the ipsilateral side of a brain injury
Drainage of CSF with an external ventricular drainage (EVD) catheter when the ICP is greater than 20 mm Hg
Isovolemic dehydration for patients with cerebral edema and a high ICP
Avoidance of any unnecessary glucose for the first 48 hours after injury
Avoidance of hyposmolarity to prevent increasing cerebral edema
Controversy surrounds nursing patients in the head-of-bed up position, as this may decrease cerebral oxygen delivery.
Mannitol is generally avoided in the patient without cerebral edema because of the risk of hypovolemia from excessive intravascular volume loss. The use of craniectomy is controversial in the management of cerebral edema. Interrogate for intra-abdominal hypertension in the patient with intractably elevated ICP, as there are reports of successful management with abdominal decompression.
ICP can be measured by various routes and devices; however, the criterion standard is considered to be a fluid-coupled ventriculostomy catheter inserted into a lateral ventricle (normal ICP < 15 mm Hg). Other devices may be placed into the brain parenchyma, such as the fiberoptically tipped parenchymal pressure monitoring catheter. Some of these devices are also coupled with a tissue oximeter probe to measure cerebral parenchymal tissue oxygen tension. Their use in enhancing outcome is not yet clear. Moreover, these devices do not afford the ability to remove CSF as part of the treatment for elevations in ICP.
Acute Respiratory Failure
Acutely injured patients often present with hypoxemia, hypercarbia, and an unsupportable work of breathing, leading to urgent or emergent airway control. The causes of acute respiratory failure are multitudinous, but they all require management of both oxygenation and ventilation. Acutely hypovolemic patients may suffer severe hypotension with positive pressure ventilation, and they will need vigorous plasma volume expansion to address hypovolemia.
As patients age, COPD is an increasingly prevalent comorbid disease process. Thus, the clinician must be ready to adjust mechanical ventilation to address the expected abnormalities of gas exchange that characterize different pulmonary conditions of reduced compliance, increased resistance, or restriction. The clinician should decide what minute ventilation (VE) is desired for a given patient, and then the clinician should decide on the respiratory rate based upon the desired tidal volume derived from the patient’s ideal body weight (VE = VT X RR).
Acutely injured patients without acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) do not need to be managed along a specific ventilatory pathway, but all means of mechanical ventilation should ensure that lung injury is not initiated. This means specifying PEEP, flow rate, and waveform, and assessing the resultant peak and plateau pressures for each patient. An initial ABG is ideal to assess whether the targeted minute ventilation was correct with regard to CO2 clearance. Avoid establishing a “one ventilator prescription fits all” method of managing acute respiratory failure (ie, AC 14, VT 700, 100%,+ 5 for all), as ventilator prescription, like fluid prescription, should be individualized to optimize pulmonary dynamics.
Similarly, each clinician should have a well-designed rescue plan for patients who are unable to be adequately oxygenated on their initial ventilator mode once the settings have been optimized. Available options include pressure control ventilation, airway pressure release ventilation, high frequency oscillation ventilation, and prone positioning in conjunction with volume cycled/pressure cycled/APRV modes. No single mode has demonstrated superiority with regard to outcome, but certain modes offer unique advantages versus other modes.
The author prefers APRV, as it is a modified form of CPAP that allows for spontaneous breathing at 2 different pressure levels, affords for reduced sedation, and has been demonstrated to enhance cardiac performance and to abrogate basilar consolidation. The interested reader is referred to established works describing this mode in detail.
The established trauma patient may develop respiratory failure in-house from pulmonary embolism or pulmonary sepsis, and the clinician should be keenly aware of the timing of acute respiratory failure to structure an appropriate differential diagnosis.
The longer a patient is mechanically ventilated, the greater is the likelihood that the patient will develop ventilator associated pneumonia (VAP). VAP reduction bundles have demonstrated efficacy in reducing VAP incidence and include head-of-bed elevation of greater than 30 degrees, oral hygiene measures, spontaneous breathing trials to assess liberation from mechanical ventilation readiness (if not contraindicated), infection control practice adherence, and, promisingly, silver impregnated endotracheal tubes to address biofilm-related promotion of tracheal colonization leading to infection.
Of course, appropriate antibiotic prescription practices that reduce induction pressures for resistant pathogen genesis aid in reducing hospital associated pneumonia (HAP) and health care associated pneumonia (HCAP), as well as VAP. In several studies, the invasive diagnosis of VAP has been demonstrated to be more cost effective than traditional diagnostic criteria (fever, bronchorrhea, leukocytosis, and radiographic infiltrate), principally by establishing confidence in the diagnosis of “no pneumonia” and by eliminating treatment of a diagnosis that is not present. This also curbs selection pressure for resistant pathogen genesis, and most notably influences prevalence rates for MRSA, VRE, and ESBL producing gram-negative rods. Acute respiratory failure is often a prelude to other organ failures in the critically injured patient.
Multisystem Organ Failure
Acute renal injury and acute renal failure
While prior literature was replete with widely varying definitions of renal failure and renal insufficiency, the Acute Dialysis Quality Initiative (ADQI; www.ADQI.net) and the Acute Kidney Injury Network (AKIN) proposed and then validated a new set of specific diagnostic criteria to characterize renal perturbations in a precise fashion.
The criteria are known as the RIFLE criteria (R = Risk, I = Injury, F = Failure, L = Loss, E = End-stage renal disease). Importantly, the RIFLE criteria also correlate rather closely with mortality in hospitalized patients. The most recent ADQI Consensus Conference (ADQI 5) specifically addressed whether fluid therapy created or mitigated the risk for acute kidney injury (AKI).
AKI, like the remainder of the RIFLE definitions, weds a period of oliguria with a measurable but small increase in serum creatinine concentration. Larger increases and more persistent oliguria define acute renal failure. ADQI 5 identified that the most consistent risk factor for AKI is a period of hypoperfusion and that there is some animal data and lesser human data that hyperchloremia plays a role in AKI initiation when plasma volume expansion is used to treat hypovolemia. Other important causes of acute kidney injury and acute renal failure (ARF) and progression along the RIFLE pathway include radiocontrast nephropathy and rhabdomyolysis.
Radiocontrast nephropathy (RCN) appears to be an issue in discrete patient populations. Risk factors include preexisting chronic kidney disease, hypovolemia, hypotension, diabetes, and iodinated contrast exposure dose. Trauma patients receiving multiple diagnostic studies are at particular risk for RCN because of repeated iodinated contrast material exposure; for example, an initial CT scan, a carotid/vertebral CT angiogram, and then perhaps a traditional celiac angiogram for angioembolization, all within a 24-hour period.
Prophylactic regimens have explored plasma volume expansion with a variety of fluids and electrolyte compositions, most recently NaHCO3 based solutions, coupled with N -acetyl cysteine (NAC) plus ascorbic acid. The most robust data support the use of NaHCO3 (D5 W+150 mEq/L NaHCO3) plasma volume expansion prior to and following radiocontrast material administration. It is unclear whether the effect is unique to bicarbonate as an anion, to the simple abrogation of HCMA when present, or to an absolute or relative reduction in chloride concentration. At present, no convincing data support the use of NAC or vitamin C. There is no role for mannitol in RCN prevention, and mannitol may be injurious by inducing dehydration and a hyperosmolar state. No outcome benefit has been identified for prophylactic dialysis for RCN prevention.
Trauma patients are also at risk for rhabdomyolysis following various injuries, most notably a crush injury, and oxygenated reperfusion of a limb with more than 6 hours of warm ischemia time. The current recommendation is vigorous plasma volume expansion to establish urine flows of approximately 1.5 cc/kg body weight (BW) per hour. Patients who received aggressive, early therapy had lesser degrees of renal injury than those receiving lesser amounts of fluid therapy. If a patient is able to achieve the above urine output target, then urinary alkalinization is unnecessary and will not confer an outcome advantage. Patients who cannot reach the target may benefit from alkalinization using NaHCO3.
At present, there is no evidence-based role for mannitol in managing rhabdomyolysis, and there is evidence of potential harm from inducing hyperosmolarity. Avoidance of inducing HCMA is a supportive goal based on experimental data identifying that hyperchloremia can decrease renal blood flow and glomerular filtration rate in an independent fashion.
It is likely that a more precise understanding of AKI/ARF and progression of renal disease will await large-scale studies of the natural history of renal biomarkers in serum (cystatin) and urine (kidney injury marker-1, N -acetyl-b-D glucosaminidase [tubular damage], glutathione transferase-a [proximal tubular damage], and neutrophil gelatinase-associated lipocalin [putative indicator of renal ischemia]).
Similarly, understanding the precise relationship among endothelial glycocalyx integrity and plasma volume expander selection, dose, and timing requires a more in-depth investigation into the molecular underpinnings of that particular system and its behavior in the low oxygen tension environment of the renal medulla.
A common organ to fail besides the lungs and the kidneys is the liver. Hepatic failure is a marker of the patient’s overall status. It is not uncommon to identify hyperbilirubinemia with concomitant sepsis, but acute hepatic failure, identified as hypoproteinemia, coagulopathy, jaundice, and ascites, is a grave sign. The clinician should look for treatable causes of fulminant hepatic failure, including acute portal vein thrombosis, hepatic vein thrombosis, intoxicants, medication reactions, undisclosed cirrhosis, blood transfusion incompatibility, hepatic artery injury, and acute viral hepatitis.
Adrenal insufficiency, absolute or relative, may accompany adrenal hemorrhage after injury, but it appears to do so less frequently than as a result of sepsis.
At present, no consensus exists as to how to diagnose adrenal insufficiency (absolute cortisol level vs stimulation test vs clinical scenario without testing), as to how to treat (glucocorticoid alone vs the addition of mineralocorticoid), or as to how to terminate therapy once it is initiated (abrupt cessation at 7 d vs taper over a total of 10-14 d).
Glycemic control failure
Hyperglycemia may be considered another endocrine system failure in that the native system is unable to meet the demands placed upon it in those without preexisting diabetes. Current data support glycemic control by a continuous infusion of insulin in patients requiring mechanical ventilation as a means of improving sepsis relevant as well as other outcomes. The target range is currently unclear and spans 110-150 mg/dL. Increasing data documents the deleterious effects of hypoglycemia, in particular in those with TBI, when engaging in tight glycemic control (intensive insulin therapy; IIT). It is currently unclear if the benefits ascribed to tight glycemic control are time limited (ie, only realized over the first 2-7 d) or whether benefits accrue over prolonged periods (ie, the ventilated patient spending 3 mo in the ICU).
One retrospective study of 1422 trauma patients examined 3 glucose control regimens (moderate, aggressive, and relaxed) and found that the moderate protocol appeared to provide the best glycemic control with the lowest incidence of hypoglycemia. 
Anemia/bone marrow failure
Injured patients may commonly develop anemia as a result of external losses (eg, scene hemorrhage, intraoperative losses), underproduction, and excessive blood sampling. Hemolysis is a much less common cause of anemia following injury. It is clear that patients who are bleeding should be transfused with packed red blood cells for restoration of red cell mass and with fresh frozen plasma, as required, for coagulopathy correction. The optimal target hemoglobin level has yet to be established. Current evidence documents that a hemoglobin level of 7 g/dL may be safely maintained in the critically ill without untoward effects on mortality or cardiac appropriate outcome variables compared to a hemoglobin level of 9 g/dL.
The reader should note that these studies excluded patients with active myocardial ischemia, but they did include patients with known coronary artery disease. It is clear that red blood cell transfusion is associated with unfavorable immunomodulation, especially with older banked blood, and it has been strongly correlated with an increased risk of infection and ALI. While most of the blood in the United States is leukoreduced, it is not WBC free. The absolute impact of leukoreduction is less clear than one might like but has become established as a standard. All blood transfused in the European Union is leukoreduced by law.
Anemia management with erythropoiesis stimulating agents (ESAs) has drawn intense scrutiny and criticism, polarizing clinicians and patients. The latest trial of ESAs in trauma patients (EPO III) noted a significant improvement in trauma patient survival when treated with erythropoietin. It appeared that the effect was separate and distinct from the hematinic effect of the delivered erythropoietin dose. This suggests another mechanism of action for erythropoietin that merits investigation. Nonetheless, EPO therapy is not inexpensive and has not been universally adopted mainly based on cost analysis.
Patients in the ICU after major trauma are often total body water and salt overloaded. They may or may not have concomitant intravascular volume overload; hypovolemia commonly coexists with total body water and salt excess.
In this set of patients in particular, one finds an increased risk of pressure ulceration. Despite routine turning and repositioning, patients may develop pressure ulceration. None of the pressure ulceration risk scoring systems were developed to address this unique patient population. Rather, the scales were developed for general ward patients and have thus been applied to a patient population in which they were not originally validated. Therefore, it is not uncommon to identify patients with a lower score who nonetheless develops an "unanticipated" ulcer.
Rigid cervical immobilization devices and TLSO braces present another significant risk for pressure ulceration in the trauma patient. Thus, early clearance of the cervical spine, when feasible, is an optimal manner in which to reduce ulceration. Careful attention to TLSO brace fit is essential, as many patients undergo significant body habitus alteration with large changes in total body fluid (acutely) or total body mass (more slowly, especially after a major septic episode).
Coagulopathy and Massive Transfusion
Trauma patients are at risk for coagulopathy via several mechanisms.
First, patients with hemorrhagic shock will lose clotting factors. This loss will be further compounded by plasma volume expansion leading to dilution of clotting factors. Second, hypothermia impairs the enzyme kinetics of the serine based proteases. (Clotting factors are enzymes.) Major efforts are devoted to the maintenance of intraoperative normothermia, and normothermia has been associated with reductions in surgical site infection. Third, acidosis also impairs the enzyme kinetics of those same proteases.
Surgical hemorrhage should be differentiated from microvascular hemorrhage. Surgical bleeding requires a physical repair to correct. Microvascular hemorrhage requires restoration of clotting factors, correction of hypothermia, correction of clotting cofactors (eg, calcium, magnesium, oxygen), abrogation of thrombocytopenia, and correction of acidosis. Microvascular hemorrhage control also commonly requires cavity packing and is further augmented by procoagulants, like recombinant activated factor VII (rfVIIa).
The reader should note that different doses have demonstrated efficacy for different conditions. There is no single agreed upon dose to be used for trauma-associated hemorrhage. Moreover, since rfVIIa has a half-life of approximately 2.5 hours, it is unclear whether patients should be routinely redosed or await a clearly defined need.
Also, the discordance between correction of PT and aPTT and the clinical resolution of hemorrhage is not an infrequent report. Nonetheless, rfVIIa has become an integral part of the massive transfusion protocols at many trauma centers. With massive transfusion, the trauma patient is at risk for alloimmunization, major and minor histocompatibility reaction, hemolysis, and, with transfusion of fresh frozen plasma, transfusion-associated lung injury (TRALI). TRALI requires supportive care and does not respond to steroids or antibiotics.
Sepsis is a ubiquitous condition throughout ICUs worldwide.
Trauma patients are no different than other patients with regard to sepsis management, source control, adherence to sepsis bundles, and outcome, with one exception. In the immediate peri-injury period, and particularly with major solid organ injury (AAST Grade III and greater) or with intraaxial or extraaxial central nervous system injury, the use of activated protein C is problematic. The major limitation of activated protein C is hemorrhage risk. The individual practitioner must weigh the risk of hemorrhage based on the time postinjury compared to the benefit of activated protein C.
Attention should be paid to antibiotic selection in that patients hospitalized for more than 4 days, especially in an ICU, should be covered for nosocomial pathogens according to the local antibiogram instead of community acquired pathogens.
As hospital acquired, health care associated, or ventilator associated pneumonia is a common infection leading to sepsis in trauma patients, one should address the diagnosis using bronchoscopy and bronchoalveolar lavage instead of the traditional 4 criteria (ie, fever, leukocytosis, bronchorrhea, and radiographic infiltrate). An invasive approach has been demonstrated to be more sensitive, more specific, and more accurate leading to confidence in the diagnosis of “no pneumonia” and reductions in total care cost and the incidence of multidrug resistant infection.
The Surviving Sepsis Campaign has made a number of recommendations for best practices in ICUs to avoid and manage sepsis. These recommendations are conveniently grouped into time-sensitive bundles. Importantly, these recommendations address timely antibiotic administration, appropriate cultures, goal-directed fluid administration, glycemic control, head-of-bed elevation, oral hygiene, and regular reassessment of the appropriateness of weaning, as well as the appropriate use of activated protein C. Adherence to the bundles is less than uniform, but adherence is strongly associated with enhanced survival from sepsis.
Plasma Volume Expansion Considerations
Recently, significant attention has been focused on the sequelae of plasma volume expansion. In the wake of the negative press devoted to the pulmonary artery catheter, many companies developed less invasive monitoring techniques that have shifted monitoring attention from a pressure-based system to a flow-based system. Examples include the LiDCO and PICCO systems with routine monitoring of stroke volume. In fact, anesthesia guidelines in the United Kingdom require start and end of case monitoring and recording of stroke volume in operating room cases requiring monitoring. Similar extensions to the ICU or high-dependency unit are anticipated. Accordingly, these techniques allow one to determine the point at which additional plasma volume expansion will not lead to a further increase in cardiac performance (ie, no further volume recruitable cardiac performance).
When plasma volume expansion proceeds, despite no increase in flow-based parameters, edema is a predictable result. In multiple venues (eg, colon, biliary surgery), excess fluid administration has been associated with increased postoperative pain, weight gain, lung injury, ICU and ventilator length of stay, postoperative nausea and vomiting, diplopia, skin bullae, diuretic use, and fluid and electrolyte abnormalities. One study demonstrated a reduced incidence of intraabdominal hypertension when using colloids instead of crystalloid fluids for plasma volume expansion. The reduced intraabdominal hypertension was ascribed to a reduced total fluid need based on the increased efficacy of colloids compared to crystalloids.
Damage Control Surgery Sequelae
In 1993, Rotondo coined the term “damage control” to describe a salvage philosophy for patients suffering from exsanguinating hemorrhage.  This technique uses field recognition of hemorrhagic shock, abbreviated initial laparotomy (hemorrhage control plus contamination control), planned or unplanned re-exploration (relief of abdominal compartment syndrome when necessary; restoration of GI continuity, enteral access, definitive or temporary abdominal wall closure), definitive reconstruction for those with a nondefinitive closure method that was initially used, and ultimate rehabilitation. Using damage control techniques will leave a large number of patients with an open abdomen that requires management. These patients are at risk for enterocutaneous fistula formation, tertiary peritonitis, large volume transperitoneal fluid loss (artificially reduces plasma creatinine by serving as a modified form of peritoneal dialysis), and GI injury during re-exploration.
Moreover, despite having a temporary abdominal wall closure with one of a number of techniques, these patients are at risk for recurrent abdominal compartment syndrome (ACS). ACS is defined by the World Society for Abdominal Compartment Syndrome (www.wsacs.org) as an intra-abdominal pressure of greater than 20 mm Hg with an attributable organ failure. Trauma patients are at risk for primary (usually related to hemorrhage or visceral edema) and secondary abdominal compartment syndrome (usually related to visceral edema or ascites). Decompression is the criterion standard for management. This may be done in the operating room or at the bedside in the ICU. Increasingly, abdominal re-exploration is also performed at the bedside with no acutely identified negative sequelae.
The earlier the patient’s abdomen is closed, the less the ICU length of stay and accrued risk for complications. Previously, patients with open abdomens were routinely heavily sedated and neuromuscularly blocked. Currently, sedation without neuromuscular blockade is the norm and avoids prolonged neuromuscular blockade syndrome and a host of other well-documented complications.
Vacuum-assisted closure (VAC; KCI Corporation) and the Wittmann patch are 2 techniques that are useful to help achieve primary fascial closure. For those who are not able to be closed, either Vicryl mesh (2 thicknesses) with an overlying split-thickness skin graft or skin flaps will achieve a temporary closure that leaves the patient with a planned giant ventral hernia. A waiting period of 6-12 months is generally undertaken prior to reconstruction.
Alternatively, abdominal wall closure with AlloDerm (human acellular dermis; LifeCell Corporation) has been increasingly used as a regenerative matrix. Mixed results were initially achieved because of improper placement techniques and improper tensioning. Currently, underlay techniques and proper tensioning guidelines have helped make this a successful strategy for abdominal wall reconstruction, both acutely and in those with a planned giant ventral hernia. Many other options exist, including permanent meshes and component separation of parts techniques.
Metabolic Acid-Base Imbalance
In the United States, the standard for plasma volume expansion is crystalloid fluids, principally as lactated Ringer’s solution, but 0.9% NSS is also commonly used for part of the resuscitation (especially with packed RBC transfusion).
In the late 1990s, the distinct entity of hyperchloremic metabolic acidosis (HCMA) was identified as a consequence of plasma volume expansion with solutions rich in chloride relative to human plasma. Acute sequelae include the need for increased minute ventilation to buffer the induced acidosis, immune activation, altered intracellular communication, induction of a cytokine storm, RBC swelling, and induced coagulopathy. Increasingly commonly, buffering of HCMA occurs by using a nonchloride maintenance fluid, such as D5 W+75 mEq NaHCO3/L at a body weight calculated maintenance rate. One review noted that there is a discrete and increased mortality associated with HCMA that is different from the mortality rate for lactic acidosis.
Currently, the best available data establish that resolution of lactic acidosis correlates closely with survival. It is also clear that many trauma patients have an elevated lactate level without an explainable acid-base abnormality. These patients have hyperlactatemia, not lactic acidosis. The elevated lactate level is related to increased endogenous catecholamines that increased carbon moiety flux through the glycolytic cascade producing lactate and pyruvate in a normal ratio. No pH changes accrue, but the lactate level is readily measurable. The major error stems from believing that the elevated lactate represents hypoperfusion and providing additional plasma volume expansion. The end result is to increase plasma chloride leading to HCMA as above.
Metabolic alkalosis is uncommon as a presenting acid-base disorder, except in those with comorbid diseases who are managed using loop diuretics that induce metabolic alkalosis (ie, furosemide). In general, alkalosis is a late finding and reflects either deliberate buffering of HCMA or induced alkalosis from diuretic therapy managing the increased total body water and salt that remains from the initial resuscitation. Most alkaloses are chloride responsive and provision of either KCl or salt in enteral feeds. Since the average 70-kg person needs 1-2 mEq Na+ per kilogram of body weight (BW) per day, the average person needs less than the 9 grams of Na+ per day. Each liter of NSS has 9 grams of sodium chloride, and a regular diet has 9 grams of sodium chloride. Thus, one may add salt tablets (3- to 9-g aliquots) to tube feeds to repair metabolic alkalosis.
Avoiding HCMA is a readily achievable goal. Using fluids with physiologic concentrations of chloride for resuscitation eliminates HCMA. However, since LR and NSS have supraphysiologic concentrations of chloride, one must usually compensate for the increased chloride load. In particular, using a "custom" fluid, such as ½ NSS+75 mEq NaHCO3, as resuscitation fluid works well instead of LR or NSS.
Colloid plasma volume expansion also works well since one delivers one third less chloride per cc of plasma volume expansion because of intravascular retention. The reader should note that despite the current but unsubstantiated concern that starch resuscitation in sepsis leads to acute kidney injury or acute renal failure, no such concern exists for hemorrhagic shock.
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- Trauma Systems
- Initial Assessment
- Prolonged Emergency Department Management
- Subsequent Critical Care Considerations
- Neurologic Injury
- Acute Respiratory Failure
- Multisystem Organ Failure
- Coagulopathy and Massive Transfusion
- Plasma Volume Expansion Considerations
- Damage Control Surgery Sequelae
- Metabolic Acid-Base Imbalance
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