ICU Management of Trauma Patients

Samuel A. Tisherman, MD, FCCM; Deborah M. Stein, MD, MPH, FCCM


Crit Care Med. 2018;46(12):1991-1997. 

In This Article

Specific Injuries

Chest Trauma

Severe chest trauma can cause injuries to the airways, lungs, heart, great vessels, and esophagus. Ultrasound (the extended Focused Assessment by Sonography for Trauma) can rapidly identify immediately life-threatening injuries, whereas CT of the chest can further define these injuries and allow precise interventions.

Pneumo- and hemothoraces are typically managed with tube thoracostomy. Early interventions, such as video-assisted thoracic surgery to drain a retained hemothorax, may reduce long-term morbidity.[68] Rib fractures can result in significant morbidity particularly in older patients. Adequate pain control is imperative to prevent splinting, atelectasis, and pneumonia. Regional analgesia[69] and rib fracture plating may be beneficial.[70]

Pulmonary contusions can cause profound acute respiratory failure. Treatment is largely supportive with traditional mechanical ventilation, although advanced ventilator modes (e.g., APRV) and ECMO may be required in the most severe cases.[17,23,24]

For patients with blunt aortic injury, the management has dramatically changed in recent years. The standard open repair for significant injuries has largely been replaced by endovascular repairs.[71–74] For less significant injuries and for injuries in which repair is delayed due to competing priorities or patient physiology, strict blood pressure and heart rate control are imperative.[74]

Abdominal Trauma

For patients with blunt abdominal trauma, solid organ (liver, spleen, kidney) injuries are most common. Many of these injuries can be successfully managed nonoperatively as long as the patient remains hemodynamically stable. Unexplained hemodynamic instability or physiologic deterioration early after injury in a patient who is being managed nonoperatively should prompt an investigation into whether the patient has "failed" nonoperative management and bled or if the patient has a missed injury. Hollow viscus injuries from blunt trauma may be missed during the initial assessment of the patient because of an altered mental status, distracting injuries, or falsely negative imaging studies. Changes in the patient's abdominal examination or unexplained sepsis should prompt consideration of a hollow viscus injury and need for laparotomy.

Patients with penetrating trauma have traditionally required laparotomies more frequently than patients with blunt injuries. However, nonoperative management of patients with penetrating trauma who are hemodynamically stable with isolated solid organ injury and no peritonitis at the time of admission has also become standard.[75–77]

For trauma patients in extremis who undergo a damage control laparotomy, during which major bleeding is controlled, contamination minimized, and the abdomen packed, the abdominal fascia is left open to prevent abdominal compartment syndrome and allow reexploration once homeostasis has been restored. Ideally, the abdomen is left open for no more than 72 hours.[78] During this time, patients are usually sedated. Neuromuscular blockade is only used if absolutely necessary. Prior to reexploration and attempted closure, minimizing use of crystalloids and judicious fluid removal, either with diuretics or renal replacement therapy, may improve fascial closure rates.[79]

Patients with active hemorrhage and orthopedic injuries may not tolerate early, definitive fixation of fractures. A damage control orthopedics approach, focusing on hemorrhage control, restoration of perfusion, and minimization of contamination, similar to that described above for abdominal trauma, may be appropriate.[80] Definitive repairs can be postponed.


For patients with severe TBI, there is little that can be done to treat the "primary injury" to the brain. Therefore, ICU management of the patient with TBI largely focuses on prevention and mitigation of "secondary insults" such as hypoxia, hypotension, cerebral edema, and ischemia. Patients may present to the ICU either postoperatively after evacuation of a mass lesion (such as a subdural or epidural hematoma), for close neuromonitoring in the setting of severe TBI, or with severe concomitant injuries in the setting of a mild or moderate TBI.

Comatose patients, typically defined as having a Glasgow Coma Scale score of less than 9, should have their airway secured. Rigorous prevention of hypoxia is essential. Maintaining adequate ventilation is also important as hypercarbia can increase intracranial pressure (ICP). Standard management should include adequate analgesia and sedation, initiation of posttraumatic seizure prophylaxis, maintenance of normothermia, initiation of enteral nutrition when possible, stress gastritis prophylaxis, and venous thromboembolism prophylaxis. Frequent neurologic tests including a pupillary examination are important to detect early evidence of worsening that may require neurosurgical intervention.

Intracranial pressure monitoring may decrease early mortality following severe TBI, although some studies have not demonstrated benefit.[81–83] If ICP monitoring is employed, the current recommended threshold for treatment of elevated ICP is 22 mm Hg.[84] Any unexplained elevation in ICP should be evaluated by a neurologic assessment and repeat CT to rule out recurrent or worsening intracranial hemorrhage. Management of elevated ICP is based on the principle of the Monro-Kellie doctrine that the intracranial space has three components: brain tissue, blood, and cerebrospinal fluid (CSF). Tiered treatment is targeted toward reduction in the volume of one of these components.[85] First tier therapies generally include head of bed elevation to improve cerebral venous drainage, short acting sedation and analgesia to allow for reduction in cerebral metabolic rate, and subsequent cerebral blood flow while maintaining ability to perform clinical neurologic assessments and drainage of CSF via an external ventricular drain. Second tier therapies include hyperosmolar therapy with either mannitol or hypertonic saline to reduce cerebral edema, mild hyperventilation inducing reflexive cerebral vasoconstriction, and, in some cases, neuromuscular blockade. Third tier therapies, such as decompressive craniectomy, therapeutic hypothermia, and barbiturate coma, are controversial.[84,86–89]

Maintenance of cerebral perfusion pressure (CPP = MAP – ICP) has become a cornerstone of therapy in patients with TBI. Through autoregulation, the normal cerebral vasculature maintains adequate blood flow across a wide range of systemic pressures. Cerebral autoregulation, however, is often abnormal in patients with severe TBI.[90] With a loss of autoregulation, a rise in systemic pressure can increase ICP, whereas systemic hypotension can cause hypoperfusion and ischemia. The standard target CPP is 60–70 mm Hg depending on the patients' autoregulatory status.[91–93]

Spinal Cord Injury

Spinal cord injury (SCI) is a particularly devastating sequela of trauma. Cervical spinal cord injuries account for over 50% of traumatic spinal cord injuries and are associated with much higher short- and long-term morbidity than injuries affecting the thoracic or lumbar cord.[94] Given that little can be done for the acute primary injury to the spinal cord, the mainstay of treatment of all patients with SCI is largely supportive, focusing on minimizing secondary insults and complications.

Most patients with severe cervical SCI are initially endotracheally intubated. The development of respiratory dysfunction correlates with the level of injury and severity of SCI as measured by the American Spinal Injury Association Impairment Scale.[95] In addition to causing a secondary insult,[89] hypoxemia can cause severe bradycardia and even asystole in patients with high cervical SCI due to unopposed vagal stimulation.[96–99]

The respiratory management of the patient with SCI should include a combination of chest physiotherapy, secretion clearance, bronchodilators, mucolytics, respiratory muscle training, assisted breathing, and assisted coughing devices and techniques.[100] Early aggressive pulmonary care, ventilator "bundles," and dedicated weaning protocols are associated with improved survival, reduced frequency of pulmonary complications (including pneumonia), and decreased need for long-term ventilatory support.[97,100,101] Early tracheostomy in high-risk patients may reduce ICU length of stay and duration of mechanical ventilation,[102] plus improve patient comfort, ease of secretion clearance, ability to perform safer weaning trials, and ability to communicate more effectively. Patients with high cervical SCI (above the C3 level) can also be liberated from mechanical ventilation with technologies such as laparoscopically implanted diaphragm pacing systems.[103]

Neurogenic shock from loss of sympathetic nervous system stimulation at the T6 level or above is a form of distributive shock, which can last for 1–3 weeks.[104] Unopposed parasympathetic activity and vagal stimulation can cause profound bradycardia and atrioventricular nodal block in addition to hypotension. The higher and more complete the injury, the more severe and refractory the neurogenic shock. First-line therapy is fluid resuscitation to maintain euvolemia. Second-line treatment includes vasopressors (particularly norepinephrine), inotropes, or a combination.[98,105]

Aggressive prevention of hypotension may improve neurologic outcome.[106] Current recommendations are to maintain MAP above 85–90 mm Hg for the first 7 days following acute cervical SCI.[98,105] Treatment of bradycardia, for example, β-agonist therapy with enteral albuterol, is typically reserved for symptomatic patients.[107]

Brain Death and Organ Donation

Brain death, defined as the "irreversible cessation of all functions of the entire brain, including the brain stem," is an unfortunate but frequent sequela of severe TBI.[108] Increasing ICP initiates a Cushing reflex characterized by systemic arterial hypertension and bradycardia. Rostral to caudal ischemia of the brain stem occurs, resulting in initial sympathetic stimulation with severe vasoconstriction leading to end-organ dysfunction followed by profound brainstem ischemia and hypothalamic-pituitary failure, resulting in severe hypotension. When ICP exceeds MAP, blood flow to the brain ceases.

The American Academy of Neurology guidelines for determining brain death include the following: 1) Establishment of an irreversible and proximate cause of coma without confounding factors, such as hypothermia, hypotension, drugs, and severe metabolic or electrolyte imbalances. 2) Clinical evaluation demonstrates the absence of all brainstem reflexes and no spontaneous breathing. 3) Ancillary testing, such as electroencephalography, cerebral angiography, nuclear scan, and transcranial Doppler, can be used if portions of the clinical examination cannot be completed. 4) Documentation of the official time of death in the medical record.[109]

Death following TBI is a significant source of organs for donation. The hemodynamic changes that occur surrounding brain death can significantly impact extracerebral organs.[110,111] Other systemic effects of brain death include hypothermia, coagulopathy, and diabetes insipidus. A strategy that includes hemodynamic support, low tidal volume ventilation, aggressive normalization of electrolytes, aggressive treatment of hyperglycemia, and hormonal replacement therapy (vasopressin, corticosteroids, and thyroid hormone) for persistent vasodilatory shock, along with intensivist-led management, can decrease the risk for organ dysfunction.[112–115]