The initial history and physical examination, emergency procedures, and evaluations used to determine extent of injury, need for resuscitation, and need for surgical intervention all occur outside the operating room and at times before an anesthesia provider has been alerted. However, critical initial issues impacting anesthetic management of trauma patients include adequacy of airway and vascular access, ability of the patient to tolerate anesthesia, prevention of hypothermia, access to robust blood bank supplies, and avoidance of crystalloids and vasopressors until hemorrhage is controlled. Therefore, anesthesiologist participation in the earliest assessment of potentially severely injured trauma patients in the emergency room should be encouraged.
Anesthetic Induction & Maintenance
Severely injured, conscious, and oriented trauma patients arriving for emergency surgery should have an abbreviated interview and examination, including emphasis on consent for blood transfusions and advice that intraoperative awareness may occur during emergency surgery. As always, such discussions should be documented in the patient’s record.
The operating room should be as warm as practical. Intravenous fluid warmers and rapid infusion devices should be prepared and ready for use. As previously noted, all patients arriving for trauma surgery should be presumed to have full stomachs with increased risk for aspiration of gastric contents, and the presence of a C-collar for cervical spine stabilization may increase intubation difficulty. Alternative airway devices (eg, fiberoptic bronchoscope, videolaryngoscope) and robust suction equipment must be immediately available and ready for use.
Intravenous access is usually established in the prehospital setting or emergency department. If the existing peripheral intravenous lines are of sufficient caliber and quality for infusing blood under pressure (eg, from a rapid infusion device), a central line may not be necessary for the initial surgical intervention. However, patients may arrive in the operating room so profoundly hypotensive and hypovolemic that peripheral intravenous line placement may be impossible. In these circumstances, a subclavian catheter or intraosseous device should be inserted and blood-based resuscitation initiated. The subclavian vein is often preferred for central venous access for profoundly hypotensive patients due to its position between the clavicle and first rib, which tends to stent the subclavian vein open even in profound hypovolemia. An intraosseous device placed with the use of a small bone drill in the proximal tibia or humerus provides direct access to venous complexes through the bone marrow. Use of interosseous access requires that the bone proximal and distal to the insertion site be intact, otherwise extravasation of infused fluids will occur due to the fluid taking the path of least resistance (the fracture site). Intraosseous infusions require pressure, not gravity, for infusions to overcome the resistance to flow originating in the bone marrow. Finally, the ubiquitous availability of point-of-care ultrasound devices in anesthesia practice may allow safe placement of large-bore or central venous catheters in jugular veins using ultrasound guidance, even in the presence of profound hypovolemia.
Major blood loss and hemodynamic instability create a dangerous situation for the conscious trauma patient and a challenging decision for the anesthesia provider planning the induction of general anesthesia. Trauma patients with severe injuries may experience profound hypotension following even modest doses (0.25–0.5 mg/kg intravenously) of propofol. Etomidate preserves sympathetic tone, which makes it a modestly safer choice than propofol. Ketamine is also a reasonable choice, particularly if given in 10-mg intravenous boluses until the patient becomes unresponsive. Scopolamine, 0.4 mg intravenously, should be considered as an amnestic agent for the profoundly hemodynamically unstable but conscious patient at high risk for hemodynamic collapse on induction of anesthesia arriving in the operating room for emergency surgery. What is most important is not the particular intravenous anesthetic induction agent chosen, but the recognition that the hemodynamically unstable trauma patient will tolerate significantly less medication for induction and maintenance of anesthesia than in normal circumstances.
Fluid management in major trauma resuscitations emphasizes blood products rather than crystalloid fluids, as previously noted. An MTP should be requested and followed, with the blood immediately available upon the arrival of the patient to the operating room. All fluids should be warmed, except for platelets. When blood products are rapidly infused, ionized calcium quickly declines and must be replaced. Vasopressors should not be used, if possible, until the source of bleeding is controlled. Studies suggest that raising the blood pressure with vasopressors during hemorrhage disrupts fresh clots, resulting in more bleeding.
An arterial line is helpful but not mandatory in the initial resuscitation of the trauma victim. Even with the assistance of ultrasonography, cannulating an artery in the presence of profound hypotension may prove difficult. Attempts at placing invasive monitors can continue as the patient is prepared for incision, to include gowning and gloving the person attempting arterial line placement on the surgical side of the drape, if necessary. Although arterial line placement may be a challenge, surgical incision cannot be delayed. Surgical control of bleeding and DCR are the top priorities in trauma resuscitation, not arterial line placement. Patients in this degree of hemodynamic compromise can be presumed to have TIC and be in need of massive transfusion. Attempts for arterial line placement can resume, and are more likely to be successful, as blood pressure improves from operative hemostasis and resuscitative transfusion.
If a trauma patient requires emergent laparotomy for intraabdominal hemorrhage, the trauma surgeon will perform an abbreviated procedure termed damage control surgery (DCS). This surgical intervention is intended to stop hemorrhage and limit gastrointestinal contamination of the abdominal compartment. After making a midline incision, the surgeon quickly searches for sources of bleeding through a quadrant-by-quadrant examination. Definitive repair of complex injuries is not part of DCS. Identification and control of injured blood vessels and solid organs, as well as inspection of injuries in areas relatively inaccessible to midline approaches but potentially addressed by interventional radiology techniques (eg, deep liver lacerations, retroperitoneal hemorrhage), occurs during DCS. Hollow viscus injuries are addressed with resection, stapling, or both. Leaving the intestines disconnected until the patient is more stable reduces intraabdominal contamination and operating time.
Communication among the entire trauma team is essential during DCS. The surgeon must know if the patient is becoming unstable, hypothermic, or coagulopathic. The anesthesia team must speak up when there is a need to pause the surgical procedure to allow resuscitation. Pausing surgery results in the surgeon compressing or packing an area of bleeding during times of profound hypotension until transfusion restores acceptable systolic blood pressure (80–90 mm Hg). If this interruption of surgery is unsuccessful in improving blood pressure, the surgeon can directly compress the aorta. This intervention provides the surgeon direct feedback as to the effectiveness of transfusion—a soft aorta suggests profound hypovolemia, whereas the return of a firm, pulsatile aorta suggests a more acceptable circulating blood volume. A brief episode of bradycardia/asystole may accompany direct aortic compression. When transfusions are ineffective maintaining perfusion, the operation should be interrupted, the bleeding areas packed, and a decision should be made between the surgeon and anesthesia team as to whether the patient can be transferred to the interventional radiology suite to treat bleeding from surgically-inaccessible sites or to the intensive care unit where rewarming, correction of coagulopathy and hemodynamic stabilization may occur.
A key component of DCS is planned re-operation once the patient is more stable. At a later time, bowel continuity can be restored or a colostomy can be performed. The abdominal fascia is often not definitively closed after DCS. The wound may be covered with an occlusive dressing over a wound vacuum sponge. Bowel edema in the setting of a closed abdomen following massive transfusion risks abdominal compartment syndrome, respiratory compromise, and multisystem organ failure.
The interventional radiology suite is increasingly utilized as part of the DCS sequence. Interventional radiology techniques can reach essentially any bleeding vessel and deposit coils or foam that may control hemorrhage, most notably in liver, kidney, and retroperitoneal injuries. Hemorrhage from pelvic ring fractures or major thoracic or abdominal vascular injuries are also potentially controlled by such intravascular interventions. In addition, patients are often taken to interventional radiology following DCS to assess blood flow and hemostasis in organs either injured by the initial trauma or potentially compromised as part of the DCS.
Any trauma patient with an altered level of consciousness must be considered to have a traumatic brain injury (TBI) until proven otherwise (see Chapter 27). Presence or suspicion of TBI mandates attention to maintaining cerebral perfusion pressure and oxygenation during all aspects of care. The most reliable clinical assessment tool in determining the significance of TBI in a nonsedated, nonparalyzed patient is the Glasgow Coma Scale (GCS; see Table 27–2). A declining motor score is suggestive of progressing neurological deterioration, prompting urgent neurological evaluation and possible surgical intervention. Although trauma patients frequently have head injuries, few head injuries require emergent neurosurgical intervention. TBIs are categorized as either primary or secondary. Primary brain injuries are directly related to trauma. Four categories of primary brain injury are seen: (1) subdural hematoma; (2) epidural hematoma; (3) intraparenchymal hemorrhage; and (4) nonfocal, diffuse neuronal injury disrupting axons of the central nervous system. These injuries potentially compromise cerebral blood flow and elevate intracranial pressure (ICP). Death occurring soon after significant head trauma is usually the result of primary brain injury.
Acute subdural hematoma is the most common brain injury warranting emergency neurosurgical intervention and is associated with the highest mortality. Small bridging veins between the skull and brain are disrupted in deceleration or blunt force injuries, resulting in blood accumulation and compression of brain tissue. The accumulation of blood raises ICP and compromises cerebral blood flow. Morbidity and mortality are related to the size of the hematoma and magnitude of the midline shift of intracranial contents. Midline shifts of intracranial contents may exceed the size of the hematoma, suggesting a significant contribution of cerebral edema or underlying intracerebral hemorrhage.
Epidural hematoma occurs when the middle cerebral artery or other cranial vessels are disrupted, often in association with skull fracture. This injury accounts for less than 10% of neurosurgical trauma emergencies and has a better prognosis than acute subdural hematoma. The patient with an epidural hematoma may initially be conscious, followed by progressive unresponsiveness and coma. Emergent surgical decompression is indicated when supratentorial lesions occupy more than 30 mL volume and infratentorial lesions occupy more than 10 mL volume (brainstem compression may occur at much lower hematoma volumes). A small epidural hematoma may not require immediate evacuation if the patient is neurologically intact, if close observation and repeated neurological examinations are possible, and if neurosurgical resources are immediately available should emergent decompression become necessary.
Intraparenchymal injuries are caused by rapid deceleration of the brain within the skull, usually involving the tips of the frontal and temporal lobes, and represent nearly 20% of neurosurgical emergencies following trauma. Such injuries tend to be associated with significant edema, necrosis, and infarcts in areas surrounding the damaged tissue. Intraparenchymal injury may coexist with a subdural hematoma. There is no consensus regarding the surgical interventions that should be performed for intraparenchymal hemorrhage, but surgical decompression may be necessary to reduce dangerously sustained elevated ICP.
Diffuse neuronal injury results from rapid deceleration or movement of brain tissue of sufficient force to disrupt neurons and axons, and is more common in children than in adults. The extent of injury may not be obvious in the period immediately following injury, but will become apparent with serial magnetic resonance imaging. The greater the extent of the diffuse neuronal injury following trauma, the higher the mortality and disability severity. Surgical intervention is not indicated for these injuries unless a decompressive craniectomy is required for relief of refractory elevated ICP.
Secondary brain injuries are considered potentially preventable injuries. Systemic hypotension (systolic blood pressures <90 mm Hg), hypoxia (PaO2 <60 mm Hg), hypercapnia (PaCO2 >50 mm Hg), and hyperthermia (temperature >38.0°C) have a negative impact on morbidity and mortality following head injuries, likely because of their contributions to increasing cerebral edema and ICP. Hypotension and hypoxemia are recognized as major contributors to poor neurological recovery from severe TBI. Hypoxemia is the single most important parameter correlating with poor neurological outcome following head trauma and should be corrected at the earliest possible opportunity. Hypotension (mean arterial blood pressure <60 mm Hg) should also be treated aggressively with fluids, vasopressors, or both, in the presence of isolated head injury.
Management of severe head trauma in the presence of other severe injuries and hemorrhage creates a difficult resuscitation dilemma. Simultaneous emergency neurosurgery and damage control laparotomy is nearly impossible to perform, and in most circumstances, control of life-threatening hemorrhage takes precedence over neurosurgical intervention. Attempts to increase cerebral perfusion pressure in the presence of life-threatening hemorrhage will exacerbate bleeding. Once non-neurosurgical hemorrhage is controlled, attention can be directed toward the neurosurgical emergency, specifically toward restoring cerebral perfusion pressure. The prolonged period of cerebral hypoperfusion in this situation is associated with significant, negative neurological outcome. At this time, no preventative interventions have been proven helpful in preserving neurological function in such a clinical scenario.
Management Considerations for Acute Traumatic Brain Injury
In the absence of an intracranial clot requiring surgical evacuation, medical interventions are the primary means of treating elevated ICP following head trauma. Normal cerebral perfusion pressure (CPP), the difference between mean arterial pressure (MAP) and ICP, is approximately 80 to 100 mm Hg (MAP – ICP = CPP; see Chapter 26). ICP monitoring is not required for conscious and alert patients. In addition, patients who are intentionally anticoagulated or who have bleeding diathesis in response to trauma should not have ICP monitoring. However, an ICP monitor should be placed when serial neurological examinations and additional clinical assessments reveal impairment, or when there is an increased risk for elevated ICP (Table 39–1). Interventions for reducing ICP are indicated when readings are higher than 20 to 25 mm Hg. Multiple studies have evaluated interventions aimed at improving CPP and managing ICP without finding obvious outcome benefits for any treatment scheme. Current Brain Trauma Foundation guidelines recommend maintaining CPP between 50 and 70 mm Hg and ICP at less than 20 mm Hg for patients with severe head injury.
TABLE 39–1Indications for intracranial ICP monitoring.1,2 ||Download (.pdf) TABLE 39–1 Indications for intracranial ICP monitoring.1,2
Severe head injury (defined as GCS score ≤8 after cardiopulmonary resuscitation) plus
(a) Abnormal admitting head CT scan or
(b) Normal CT scan plus ≥2 of: age >40 y, systolic blood pressure >90 mm Hg, decerebrate or decorticate position
|Sedated patients; patient in induced coma after severe TBI |
|Multisystem injury with altered level of consciousness |
|Patient receiving treatment that increases risk of increased ICP, eg, high-volume intravenous fluids |
|Postoperatively after removal or intracranial mass |
|Abnormal values in noninvasive ICP monitoring, increased dynamics of simulated values, or abnormal shapes in transcranial Doppler blood flow velocity waveform (increased pulsatility) with exclusion of arterial hypotension and hypocapnia |
Cerebral blood flow (CBF) is directly related to arterial carbon dioxide concentration. As arterial carbon dioxide levels decrease, cerebral vasoconstriction occurs, reducing CBF and ICP. Conversely, as arterial carbon dioxide levels rise, cerebral vasodilation occurs, increasing CBF and ICP. Changes in arterial carbon dioxide levels exert a prompt CBF and ICP response, making hyperventilation an effective therapeutic intervention in cases of elevated ICP associated with TBI. However, hyperventilation in the presence of systemic hypotension, particularly in the hemodynamically unstable, hemorrhaging trauma patient, increases risk of neurological ischemia and should be avoided until normotension is restored.
Osmotic diuretic therapy is another commonly used and widely accepted intervention for reducing elevated ICP. Intravenous mannitol doses of 0.25 to 1.0 g/kg body weight are effective in drawing extravascular fluid from brain tissue into the vascular system, decreasing brain edema and ICP. Because this intervention also induces brisk diuresis, plasma osmolality and serum electrolytes must be monitored.
Barbiturate coma is an intervention to reduce cerebral metabolic rate, cerebral blood flow, and cerebral oxygen demand in order to reduce elevated ICP and suppress the metabolic rate of ischemic cells until cerebral perfusion improves. Hypotension is commonly associated with this therapy, which limits its use in hemodynamically unstable patients. Vasopressors may be used to maintain CPP between 50 and 70 mm Hg in such cases. The dose of pentobarbital (preferable to thiopental) is based upon electroencephalographic (EEG) evidence of burst suppression, the EEG threshold for maximally reduced cerebral metabolic rate for oxygen and glucose.
Crystalloid is preferable for fluid therapy in the presence of isolated TBI. Although the use of colloid might seem advantageous in preventing brain edema, in a recent study albumin-based resuscitation following TBI nearly doubled mortality. TBI is often associated with blood–brain barrier disruption, and albumin administration in this situation may result in greater brain tissue edema and higher ICP, contributing to higher morbidity and mortality.
The normal spine structure comprises three columns: anterior, middle, and posterior. The anterior column includes the anterior two-thirds of the vertebral body and the anterior longitudinal ligament. The middle column includes the posterior third of the vertebral body, the posterior longitudinal ligament, and the posterior component of the annulus fibrosus. The posterior column includes the laminae and facets, the spinous processes, and the interspinous ligaments. Spine instability results when two or more of the three columns are disrupted.
The trauma patient with a relevant mechanism of injury (typically blunt force involving acceleration–deceleration) must be approached with a high degree of suspicion for spinal cord injury unless it has been ruled out with imaging studies. A lateral radiograph of the cervical spine demonstrating the entire cervical spine to the top of the T1 vertebrae will detect 85% to 90% of significant cervical spine abnormalities. Cervical spine radiographs must be examined for structure and alignment of vertebral bodies, narrowing or widening of interspinous spaces and the central canal, alignment along the anterior and posterior ligament lines, and appearance of the spinolaminar line and posterior spinous processes of C2 through C7. The presence of one spinal fracture is associated with a 10% to 15% incidence of a second spinal fracture.
Thoracolumbar injuries most commonly involve the T11 through L3 vertebrae as a result of flexion forces. The presence of one thoracolumbar spinal injury is associated with a 40% chance of a second fracture caudal to the first, likely due to the force required to fracture the lower spine. Bilateral calcaneus fractures also warrant a thorough thoracolumbar spine evaluation due to the increased incidence of associated spinal fracture associated with this injury pattern.
Cervical spine injuries occurring above C2 are associated with apnea and death. (C3–C5 roots form the phrenic nerve). High spinal injuries are often accompanied by neurogenic shock due to the loss of sympathetic tone. Neurogenic shock may masquerade as hemorrhagic shock in the presence of major trauma because the source of bleeding may be presumed hemorrhagic, rather than neurological, in origin. The presence of profound bradycardia 24 to 48 h after a high thoracic spinal cord lesion likely represents compromise of the cardioaccelerator function found in the T1–T4 region.
The principal therapeutic objectives following spinal cord injury are to prevent exacerbation of primary structural disruption and to minimize risk of extending neurological injury from hypotension-related hypoperfusion of ischemic areas of the spinal cord. In patients with complete spinal cord transection, very few interventions will influence recovery. Patients with incomplete spinal cord lesions require careful management of hemodynamic parameters (eg, avoiding hypotension) and surgical stabilization of the spine to prevent extension of existing injury and exacerbation of existing neurological deficits.
Surgical decompression and stabilization of spinal fractures is indicated when a vertebral body loses more than 50% of its normal height or the spinal canal is narrowed by more than 30% of its normal diameter. Methylprednisolone is often administered for spinal cord injury in this situation. The antiinflammatory properties of this steroid potentially reduce spinal cord edema within the tight confines of a compromised spinal canal. Despite outcome studies from animal models of traumatic spinal cord injury demonstrating benefit from early surgical intervention, steroid therapy, or both, current human studies have failed to demonstrate benefit from either intervention. The presence of a decompressible lesion in the area of an incomplete spinal cord transection is not an indication for early operative intervention unless other, more life-threatening, conditions are present.
Maintaining supranormal mean arterial blood pressure to help ensure adequate spinal cord perfusion in areas of otherwise reduced blood flow due to cord compression or vascular compromise is likely to be of more benefit than steroid administration. Hypotension must be avoided during induction of anesthesia, throughout operative decompression and stabilization of the spine injury, and extending into the postoperative phase.
The elderly are at greater risk for spinal cord injury due to decreased mobility and flexibility, greater incidence of spondylosis and osteophytes, and decreased space within the spinal canal to accommodate spinal cord edema following trauma. The incidence of spinal injury from falls in the elderly is rapidly approaching that of spinal cord injury from motor vehicle accidents in younger patients. Mortality following spinal cord injury in the elderly, particularly those over the age of 75 years, is greater than that in younger patients with similar injury.
The unique injury pattern of penetrating spinal cord injury warrants separate consideration. Unlike blunt spinal trauma, penetrating trauma of the spinal cord due to bullets and shrapnel is unlikely to cause an unstable spine. As a result, C-collar or long-board immobilization may not be indicated in an isolated penetrating spinal cord injury. The C-collar placement in the presence of a cervical spine penetrating injury may actually hinder observation of soft tissue swelling, tracheal deviation, or other anatomic indications of imminent airway compromise. Unlike, blunt trauma, penetrating injuries of the spinal cord induce damage at the moment of injury without risk of subsequent exacerbation of the injury. Like other spinal cord injuries, however, maintenance of spinal cord perfusion using supranormal mean arterial pressure is indicated until spinal cord function can be more thoroughly evaluated.
Burns represent a unique but common traumatic injury that is second only to motor vehicle accidents as the leading source of accidental death. Temperature and duration of heat contact determine the extent of burn injury. Children, because of their high body surface area to body mass ratio, and the elderly, whose thinner skin allows deeper burns from similar thermal insult, are both at greater risk for major burn injury. The pathophysiological and hemodynamic responses to burn injuries are unique and warrant specialized burn care that can be optimally provided only at burn treatment centers, particularly when more than 20% of a patient’s total body surface area (TBSA) is involved in second- or third-degree burns. A basic understanding of burn pathophysiology and of resuscitation requirements, especially early initiation of therapies such as oxygen administration and aggressive fluid resuscitation, will improve patient survival.
Burns are classified as first, second, or third degree. First-degree burns are injuries that do not penetrate the epidermis (eg, sunburns and superficial thermal injuries). Fluid replacement for these burns is not indicated, and the area of first-degree burns should not be included in calculating fluid replacement when more extensive or significant burns are also present. Second-degree burns are partial-thickness injuries (superficial or deep) that penetrate the epidermis, extend into the dermis for some depth, and are associated with blistering. Fluid replacement therapy is indicated for patients with second-degree burns when more than 20% of the TBSA is involved. Skin grafting also may be necessary in some cases of second-degree burns, depending upon wound size and location. Third-degree burns are those in which the thermal injury penetrates the full thickness of the dermis. Nerves, blood vessels, lymphatic channels, and other deep structures may have been destroyed, creating a severe, but insensate, wound, although healthy tissue surrounding the third-degree burn will be very painful. Debridement and skin grafting are almost always required for recovery from third-degree burns.
Major burns (a second- or third-degree burn involving ≥20% TBSA) induce a unique hemodynamic response. Cardiac output declines by up to 50% within 30 min of the injury in response to a burn-induced massive vasoconstriction, inducing a state of normovolemic hypoperfusion (burn shock). Survival depends on restoration of circulating volume and infusion of crystalloid fluids according to recommended protocols (see below). This intense hemodynamic response may be poorly tolerated by patients with significant underlying medical conditions. If adequate intravenous fluid therapy is provided, cardiac function returns to normal within 48 h of injury, then typically progresses to a hyperdynamic physiology as the metabolic challenge of healing begins. Plasma volume and urine output are reduced early on, after major burn injuries.
In contrast to fluid management of blunt and penetrating trauma, where crystalloid fluids are discouraged, burn fluid resuscitation emphasizes the use of balanced crystalloid fluids (see Chapter 51) in preference to albumin, hydroxylethyl starch, normal or hypertonic saline, or blood. Following burn injuries, acute kidney failure is more common when hypertonic saline is used during initial fluid resuscitation, death is more likely when blood is administered, and outcomes are unchanged when albumin (rather than crystalloid) is used in resuscitation.
Fluid resuscitation is continuous over the first 24 h following burn injury. Two formulas are commonly used in guiding burn injury fluid resuscitation; the Parkland and the modified Brooke. Both require an understanding of the Rule of Nines (Figure 39–6) to calculate resuscitation fluid volumes. The adult Parkland protocol recommends 4 mL/kg/% burned TBSA to be given in the first 24 h, with half the volume given in the first 8 h and the remaining volume over the following 16 h. The adult modified Brooke protocol recommends 2 mL/kg/% burned TBSA, with half the calculated volume beginning in the first 8 h and the remainder over the following 16 h. Both formulas use urine output as a reliable indicator of fluid resuscitation adequacy, targeting adult urine production of 0.5 to 1.0 mL/kg/h as indicators of adequate circulating volume. If adult urine output exceeds 1.0 mL/kg/h, the infusions are slowed. In both protocols, an amount equal to half the volume administered in the first 24 h is infused in the second 24-h period following injury. The goal of maintaining adult urine output at 0.5 to 1.0 mL/kg/h continues throughout the initial phase of resuscitation.
The Rule of Nines, utilized to estimate burned surface area as a percentage of total body surface area (TBSA). (Reproduced with permission from American College of Surgeons. ATLS: Advanced Trauma Life Support for Doctors (Student Course Manual). 9th ed. Chicago, IL: ACS; 2012.)
When pediatric burn patients are encountered, the fluid resuscitation protocols are the same as for adults. Children weighing less than 30 kg should receive 5% dextrose in their intravenous fluids and the target urine output is 1.0 mL/kg/h. The target urine output for infants younger than 1 year of age is 1 to 2 mL/kg/h.
Burn Management Considerations
The Parkland and modified Brooke protocols both use urine output as an indicator for adequate fluid resuscitation. However, circumstances may arise in which the volume of fluid administered exceeds the original volume goal. For example, initial fluid resuscitation volumes may be miscalculated if first-degree burns are mistakenly incorporated into the TBSA value. Prolonged use of sedation may result in hypotension, prompting administration of additional fluids rather than vasoconstrictors. The phenomenon of fluid creep occurs when intravenous fluid therapy volumes are increased beyond intended calculations in response to hemodynamic changes related to issues other than circulating volumes. Fluid creep is also associated with abdominal compartment syndrome and pulmonary complications, often leading to resuscitation-related morbidity.
B. Abdominal Compartment Syndrome
Abdominal compartment syndrome (ACS) is a risk for pediatric and adult patients with circumferential abdominal burns and patients receiving intravenous fluid volumes greater than 6 mL/kg/% burned TBSA. Intraabdominal pressure can be determined by measuring intraluminal bladder pressure using a Foley catheter connected to a pressure transducer. The transducer is connected to a three-way stopcock at the point where the Foley catheter connects to the drainage tube. After the transducer is zeroed at the pelvic brim, 20 mL of fluid is instilled into the bladder. Intraabdominal pressure readings are taken 60 s after infusing fluid into the bladder, which allows the bladder to relax. Intraabdominal pressures exceeding 20 mm Hg warrant abdominal cavity decompression. However, an abdominal surgical procedure places the burn patient at increased risk for intraabdominal Pseudomonas infection, particularly if the laparotomy incision is near burned tissue. Early and frequent assessment of intraabdominal pressure and consideration of potential etiologies of hypotension in the burn patient other than hypovolemia are important preventative measures for ACS.
C. Pulmonary Complications
Excessive fluid resuscitation volumes are associated with an increased incidence of pneumonia. Patients with severe burns frequently have pulmonary injury related to the burn. Decreased tracheal ciliary activity, the presence of resuscitation-induced pulmonary edema, reduced immunocompetence, and tracheal intubation predispose burn patients to pneumonia. ACS can have an adverse impact on pulmonary function. Intravenous fluid administration volumes must be monitored closely and documented to be consistent with American Burn Association recommendations (ie, the Parkland or modified Brooke protocol). Fluid administration that exceeds recommendations warrants careful review of the rationale.
D. Carbon Monoxide and Cyanide Poisoning
The differential diagnosis for altered mental status following burn injury and smoke inhalation includes carbon monoxide and cyanide poisoning (see Chapter 57). Endotracheal intubation and mechanical ventilation with high inspired oxygen concentration are indicated in this situation. Carbon monoxide binds hemoglobin with an affinity approximately 250 times that of oxygen. The resultant carboxyhemoglobin (HbCO) leaves less hemoglobin available for binding oxygen and shifts the O2–Hb dissociation curve to the left, both causing impaired delivery of oxygen to tissues. Pulse oximetry provides a falsely elevated indication of oxygen saturation in the setting of carbon monoxide exposure because of its inability to distinguish oxygenated hemoglobin (HbO2) from HbCO. Arterial or venous blood gas analysis can directly measure HbCO. Clinically significant carbon monoxide poisoning is seen when HbCO levels exceed 10% (those who regularly smoke tobacco have HbCO levels of up to 10%). If HbCO exceeds 20%, intubation and mechanical ventilation is indicated in order to improve local tissue oxygenation and accelerate carbon monoxide elimination. Death from carbon monoxide occurs when HbCO levels exceed 60%. Hyperbaric oxygen therapy is indicated for carbon monoxide poisonings from any etiology. Multiple hyperbaric oxygen sessions are required to reduce the long-term consequences of carbon monoxide poisoning.
Anesthetic Considerations for Burn Therapy
A primary characteristic of all burn patients is an inability to regulate temperature. The resuscitation environment must be maintained near body temperature through the use of radiant warming, forced air warming devices, and fluid warming devices. All burn care environments must be maintained near 40°C.
Assessment of the burn patient begins with inspection of the airway. Although the face may be burned (singed facial hair, nasal vibrissae), facial burns are not an indication for tracheal intubation. The need for urgent airway management, mechanical ventilation, and oxygen therapy is indicated by hoarse voice, dyspnea, tachypnea, or altered level of consciousness. Arterial blood gas determination should be obtained early in the treatment process for assessment of HbCO level. Mechanical ventilation should be adjusted to achieve adequate oxygen saturation (based upon measured oxygen levels rather than pulse oximetry) at the lowest tidal volumes.
Tracheal intubation in the early period following burn injury (up to the first 48 h) can be facilitated with succinylcholine for muscle relaxation. In patients with significant burns (>20% TBSA), injury and disruption of neuromuscular end plates occurs, followed by upregulation of acetylcholine receptors. Beyond 48 h after significant burn injury, succinylcholine can produce lethal hyperkalemia. This risk for succinylcholine-induced hyperkalemia persists for up to 2 years following burn injury.
Analgesia for burn patients is challenging. Considerations and concerns regarding opioid tolerance and psychosocial complications of burn therapy are commonplace. Multimodal approaches are often advantageous. Regional analgesia may provide benefit, although in the early post-burn period this technique may mask the symptoms of compartment syndrome or other clinically significant signs and symptoms related to the primary burn injury.