Despite the publication of over 2000 studies on damage-control strategy for trauma in peer-reviewed journals, not even 1 provides prospective, randomized, and class-1 evidence supporting the practice.1 Nevertheless, among experienced experts in trauma, the nearly universal opinion is that survival outcomes over the last 30 years have benefitted more from the adoption of the damage-control strategy than from all other improvements in trauma care combined.
Prior to the current era of damage-control strategy, surgeons attempted the definitive operative repair of all injuries in a single, often prolonged procedure. In contrast, the damage-control strategy only temporizes the immediate life-threatening injuries at the first operation, and then addresses lower-acuity injuries later, in multiple, staged procedures. Physiologic stabilization of the severely injured patient in an intensive care unit (ICU) in between, and after the staged surgical procedures is integral to the damage-control strategy. As a consequence, it is imperative that intensivists who manage trauma patients have an overall understanding of the damage-control strategy,2 as well as in-depth knowledge of critical care objectives and pitfalls specific to trauma patients.
Since the late 1980s, the surgical management of the unstable trauma patient has evolved from a thorough and definitive treatment at the first operation to a damage-control strategy. Specifically, damage-control involves an abbreviated laparotomy, surgical control of arterial bleeding, temporary control of enteric spillage, stabilization of long bone fractures, abdominal packing to control venous bleeding, and temporary wound closures to accommodate swelling and to avoid compartment syndrome. This first operation is completed as expeditiously as possible, ideally within an hour, at which time the patient, likely still in shock, and consequently cold, acidotic, and coagulopathic, is brought to the safe harbor of an ICU where resuscitation is continued, coagulopathy is corrected, and physiologic homeostasis restored.
Frequently, with severely injured trauma patients, the initial hypotension is a consequence of uncontrolled bleeding. As described elsewhere, a massive transfusion strategy will have been implemented and continued intraoperatively while surgeons attempt to control the sources of bleeding. The main benefit of massive transfusion protocols is to expedite red cell and blood-product availability to prevent death by exsanguination from uncontrolled surgical bleeding. Although the specific ratios of packed red blood cells (PRBCs) to fresh-frozen plasma (FFP), to platelets are debatable, the objectives of resuscitation, transfusions, and fluid management are not. Oxygen-carrying capacity must be maintained with PRBCs, the coagulation system must be supported with FFP and platelets, and after meeting those 2 objectives, any remaining hypovolemia can be corrected with balanced crystalloid.3 During periods of uncontrolled bleeding, oxygen-carrying capacity and coagulation status can change quickly. The inherent delay in obtaining laboratory measurements means that objective data are already old by the time they arrive back to the provider, and thus during periods of rapid, uncontrolled bleeding, presumptions regarding deficits must be inferred (eg, transfusion of PRBC:FFP:platelets in a 1:1:1 ratio) so as to avoid any episodes of undertreatment. Once rapid exsanguination from surgical bleeding has been controlled, the massive transfusion protocols should be terminated. Further blood and blood-product transfusions should be directed at correction of documented deficits in oxygen-carrying capacity or coagulopathy, not simply at blindly fulfilling preordained ratios.
The degree of anemia and hypovolemia that any individual patient might be able to tolerate during the early phase of resuscitation is variable, and will depend on the patient's cardiac status, presence or absence of vascular disease, and most importantly, presence or absence of a concomitant head injury with elevated intracranial pressure (ICP). If elevated ICP is suspected, then mean arterial pressure (MAP) should be high enough to maintain a cerebral perfusion pressure (CPP) = (MAP – ICP) of 55 mm Hg or more.
No ideal single marker of resuscitation adequacy exists. Each has its pitfall (see also Chapter 73). For example, serum lactate may be elevated in a perfectly resuscitated patient with baseline liver insufficiency. Base deficit values will be acutely elevated from a benign hyperchloremic acidosis if normal saline (or its equivalents) are used for resuscitation, even though intravascular volume and perfusion may be normal. A safer strategy is to initially collect data for as many endpoints of resuscitation as possible, and over the initial few hours, narrow the focus on those with the best signal-to-noise ratio, individualized to each patient.
Endpoints of resuscitation can monitor regional organ-specific function (eg, urine output, ST-segment abnormalities, and mental status) (Table 53–1), or global perfusion (lactate, base deficit) (Table 53–2). Ideally, specifically tailored for each patient, 1 global and 1 local marker of resuscitation will be monitored that together optimize sensitivity and specificity for diagnosing shock and recovery.4
Table 53–1Endpoints of resuscitation—markers of regional perfusion. ||Download (.pdf) Table 53–1Endpoints of resuscitation—markers of regional perfusion.
|Regional Markers ||Notes/Pitfalls |
|Capillary refill ||Unknown baseline for comparison |
|CPK levels ||Too slow for acute changes |
|Echocardiography || |
Requires special operator skills
Absent esophageal or gastric pathology
|Electrocardiogram ||Unknown baseline for comparison |
|Jugular bulb saturation ||Not routinely available |
|Mental status || |
Unavailable during general anesthesia
Unreliable with intoxication
|NIR spectrometry ||Not routinely available |
|Sublingual tonometry ||Not routinely available |
|Troponin levels ||Too slow for acute changes |
|Urine output ||Unreliable with acute or chronic renal failure, SIADH, or neurogenic DI |
Table 53–2Endpoints of resuscitation—markers of global perfusion. ||Download (.pdf) Table 53–2Endpoints of resuscitation—markers of global perfusion.
|Global Markers ||Notes/Pitfalls |
|Anion gap ||May be elevated for reasons other than lactic acidosis |
|Base deficit ||May reflect nonanion gap acidosis |
|Cardiac output || |
Requires pulmonary artery catheter
Abnormal in shock syndromes in addition to hypovolemia
|Core temperature || |
Hypothermia is a marker of late or advanced shock
Fever is the most common transfusion reaction
|Elevated with chronic obstructive pulmonary disease |
|Heart rate ||Unknown beta-adrenergic blocker use |
|Lactate ||Impaired clearance with hepatic dysfunction |
|Mean arterial pressure || |
Generally well compensated until late
|pH ||May reflect respiratory and/or nonanion gap acidosis |
Lower from the following:
Shunt (eg, pulmonary contusion, aspiration)
Hypovolemia-related V/Q mismatch
Hypoxemia from shunt does not generally respond to supplemental oxygen
Hypoxemia from V/Q mismatch easily corrected with supplemental oxygen
|Pulse pressure ||Difficult to interpret if accompanied by bradycardia |
|Respiratory systolic pressure variation ||Difficult to interpret with obesity or with abdominal compartment syndrome |
|Svo2 || |
Requires pulmonary artery catheter
Abnormal in shock syndromes other than hypovolemia
The “lethal triad of death” describes the downward spiral of physiologic homeostasis in a patient with uncontrolled hemorrhage and shock. Obviously, if shock is the initial cause of the patient's lactic acidosis, coagulopathy, and hypothermia, even after visible bleeding has been successfully controlled, then inadequate attention to the correction of coagulopathy and hypothermia will lead to continued deterioration. It is during the second phase of damage control, in the ICU, that coagulation system support and aggressive rewarming occur. Classically, the coagulopathy associated with trauma and massive resuscitation was thought to be simply a consequence of clotting factor and platelet dilution, consumption, and dysfunction. More recently, data have emerged which demonstrate that an acute traumatic coagulopathy can be observed within 30 minutes postinjury, more quickly than can be explained by acidosis, consumption, or dilution, indicating that a more complex process is involved. Ongoing research to elucidate the underlying etiology has focused on catecholamine, and inflammatory mediators, protein C activation, and shedding of glycocalyx. Regardless of the underlying complex initial biochemical pathophysiology, by the time a patient survives the first phase of damage control and is transferred to the ICU, the classic concerns of clotting factor and platelet dilution and hypothermia must be addressed.5
Thromboelastography (TEG) is a real-time measure of whole blood clotting. Results are available within 10 to 45 minutes—too slow to be useful in the acutely exsanguinating patient, however once surgical bleeding has been addressed, it should be considered. TEG data graphically reveal abnormalities in platelet function, intrinsic, extrinsic pathway integrity as well as fibrinogen deficits and thrombolysis. TEG-guided resuscitation, using targeted platelets, FFP, cryoprecipitate, or other directed therapy may be the optimal strategy during this phase, and likely superior to blindly continuing a massive transfusion protocol following predetermined ratios.6
Abdominal Compartment Syndrome
Intra-abdominal hypertension causes symptoms of abdominal compartment syndrome (ACS) when intra-abdominal pressure (IAP) exceeds systemic venous pressure. IAP is traditionally approximated by transducing an indwelling bladder catheter after instillation of saline, which establishes a continuous fluid column from the bladder to the pressure transducer. The transducer is zeroed at the symphysis pubis. Normal IAP is 3 to 10 mm Hg. With mild elevations up to 15 to 20 mm Hg, bowel becomes congested, renal and portal veins may collapse, and urine output may decrease. Provided that the systemic arterial blood pressure and intravascular volume can tolerate it, aggressive diuresis at this stage may be able to break the vicious cycle of increased bowel edema leading to increased venous congestion leading to decreased abdominal organ perfusion, increased edema, and increasing IAP. Because capillary fluid extravasation during the early posttrauma period is largely driven by the inflammatory response to trauma, diuresis usually fails to reverse the progression (Figure 53–1).
Intra-abdominal hypertension and abdominal compartment syndrome management algorithm. (Reproduced with permission from Kirkpatrick AW, Roberts DJ, De Waele J, et al: Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome, Intensive Care Med 2013 Jul;39(7):1190-1206.)
Once IAP rises more than 25 mm Hg, urine output is severely impaired, bowel perfusion is compromised, and airway pressures rises as a consequence of cephalad pressure on the diaphragm. At IAP more than 30 mm Hg, bowel ischemia, renal failure, and hypoxia from severe atelectasis are usually observed. The definitive treatment of ACS is to surgically decompress the abdominal fascia. Often at the initial damage-control operation, even if no intra-abdominal injury is found, ACS is anticipated and the abdominal fascia is left open prophylactically until the inflammatory response subsides and sequestered, third-space fluid is mobilized.7 Intraperitoneal dialysis with a hypertonic glucose solution is a promising intervention to optimize bowel wall perfusion, minimize inflammation, and more rapidly decrease edema.8
Other Early Trauma ICU Concerns
During the second phase of damage control, the focus remains on resuscitation. Gradual physiologic improvement should be observed over the subsequent 24 to 48 hours at which time the patient returns to the operating room for definitive repair of remaining injuries. If a patient's condition continues to deteriorate, serious consideration must be given to a missed vascular injury. Interventional radiology may be utilized to diagnose and possibly embolize arterial bleeding that cannot be accessed surgically. Alternatively, a return to the operating room earlier than planned may be required.
The second phase of damage control in the ICU provides the opportunity to repeat and document a thorough baseline head-to-toe physical examination. Commonly, minor extremity fractures may be missed which can be associated with significant long-term disability, if not treated appropriately. Additionally, any extremity swelling should raise the concern of limb compartment syndrome and monitored with serial creatinine kinase (CK) levels or intramuscular pressure transduction as appropriate. Perioperative prophylactic antibiotics should be given9 and a nutritional plan established.
Any vascular access obtained in the field, or in less-than-sterile conditions, should be removed and replaced if needed. If the patient's cervical spine cannot be cleared, then the extrication collar placed by EMS for cervical immobilization must be replaced with a collar designed for longer-term usage such as a Miami-J or Philadelphia-type collar. Extrication collars are made of thin, hard plastic with minimal padding, designed to be placed in tight quarters and they (as well as backboards) can cause decubitus ulcers within hours.
The patient's family or friends should be updated as to the patient's condition, and also queried regarding the patient's comorbidity, medications, allergies, and social history. Often, details of the patient's history emerge during these conversations which significantly alter the care plan.
Organ-System Supportive Care
Neurologic (See Also Chapters 48 and 50)
Traumatic Brain Injury—Traumatic brain injury (TBI) frequently accompanies major blunt trauma. Managing elevated ICP in the setting of severe bleeding, hypovolemia, and shock is particularly challenging. In the absence of head injury, during resuscitation, the mean arterial blood pressure (MAP) is targeted to be as low as possible so as to minimize additional bleeding while at the same time maintaining organ perfusion. However in the presence of elevated ICP, optimizing CPP becomes the priority.
In order to accurately calculate CPP, arterial blood pressure, central venous pressure, and ICP must be monitored directly. ICP is monitored either via ventriculostomy and intraventricular catheter or by a parenchymal or subarachnoid transducer (see also Chapter 101). Interventions to consider which optimize CPP are head-of-bed elevation, cerebral spinal fluid drainage (if a ventriculostomy is present), judicious diuresis with osmotic agents such as mannitol (used with discretion in the presence of hypovolemia), intravascular hypertonic saline, deep sedation to achieve burst suppression on EEG, and alpha-agonist vasoconstriction. Interventions which have not shown to be of benefit or which may be harmful include hyperventilation, coticosteroids, and hypothermia.
Current recommendations for the ICU management of TBI can be found in the Guidelines for the Management of Severe Traumatic Brain Injury10 which is published and updated by the Brain Trauma Foundation and available on-line.
Spinal Cord Injury and C-Spine Clearance—As soon as possible upon admission to the ICU, a thorough neurologic exam should be repeated. Any paraplegias or hemiplegias should raise the suspicion of spinal cord injury (SCI). Cervical and thoracolumbar vertebral immobilization should be maintained until the patient can cooperate with an appropriate examination, or until radiographic studies can be obtained which demonstrate absence of both bony injury (computed tomography [CT] scan) and soft-tissue ligamentous injury (magnetic resonance imaging). If the patient is known to have a spinal cord transection, any accompanying hypotension, bradycardia, or shock should be treated supportively. Anticipate the need for ongoing respiratory support for cervical spinal cord injuries. Corticosteroids for SCI are no longer recommended.
The prerequisite to the clinical clearance of a suspected or potential cervical SCI requires first the evaluation of any radiographic studies and confirmation of the absence of bony fractures or alignment abnormalities. In order for the cervical spine to be clinically cleared, the patient must be able to (1) focus fully on the exam (no distractions), (2) localize and discriminate mildly noxious stimuli, and (3) move and feel all extremities. A practical method of assessing distraction from any cause is to apply a mildly noxious stimulus to the patient's extremities and query if they feel discomfort. This demonstrates the patient's ability to localize sensation, focus on and cooperate with the examination, and communicate adequately with the care provider.
Coma Prognosis—Prognosis for patients with coma following TBI differs from that following anoxic brain injury. Following anoxic brain injury, if no improvement in the patient's neurologic status is observed after 72 hours, it is unlikely that the patient will have a significant recovery. In contrast, following TBI, treatment of concurrent injuries may delay or obscure early recovery from coma. Once the patient has been stabilized from other injuries, most neurologic recovery from TBI can be observed within 6 months with additional incremental improvements up to an year or more following the injury, especially with aggressive rehabilitation.
Sedation/Analgesia/Amnesia (See Also Chapter 16)—Trauma patients often require analgesia for soft-tissue and bony injuries. Intravenous opioids remain the standard means to control pain, either as a continuous or patient-controlled infusion. Appropriate constipation prophylaxis must be initiated. Alternatively, and especially for thoracic trauma and rib fractures, regional anesthesia, nerve blocks, and epidural catheters are effective. Nonsteroidal agents can be used with caution, especially if ongoing bleeding or renal injury is major concern. With few exceptions, a “wake-up” test, or suspension of sedation should be implemented once daily, and the opportunity taken to reassess neurologic function before restarting sedative/hypnotic agents. Utilization of benzodiazepines for amnesia or sedation is controversial. On the one hand, any recall of uncomfortable, upsetting, or delirium-induced memories has a high correlation with development of posttraumatic stress disorder (PTSD). On the other hand, benzodiazepine use is associated with delirium.
Delirium (See also Chapter 49)—Delirium is frequently observed patients following major trauma. Its etiology is likely multifactorial. Disinhibition can occur from frontal lobe contusions in patients with TBI, systemic inflammatory response or renal failure can cause a metabolic encephalopathy, and given the prevalence of alcohol-related trauma, delirium tremens can occur from ethanol withdrawal. Treatment is largely supportive, with intravenous benzodiazepines for alcohol withdrawal and intravenous haloperidol a typical means of treatment for other causes of delirium in the acute setting. As the inflammatory response subsides, haloperidol can rapidly be tapered off within 2 or 3 days, dystonic reactions and neuroleptic malignant syndrome are rare in this setting. QT-intervals must be monitored closely. Patient recall of delirium episodes is a particularly potent risk factor for PTSD, and an amnestic agent such as a benzodiazepine may be of benefit once delirium has developed. In the absence of head injury, delirium developing in previously healthy trauma patients is temporary, and as they recover from their injuries and inflammation subsides, their mental status also normalizes.
Brain Death Determination—Brain death is the complete and irreversible cessation of all brain and brainstem function. Because cardiopulmonary function may be temporarily suspended and restarted as during cardiopulmonary bypass, even a “cardiac” death is not final until it becomes brain death. The determination of brain death in a patient whose remaining organs can retain function with support enables those organs to be procured for transplantation. The potential for organ transplantation is the only rationale for continuing cardiopulmonary support once brain death has been determined. Occasionally, family members may request continued organ support after death for cultural or religious reasons, and while efforts should be made to accommodate reasonable requests, they should not compromise the care provided to live patients in the ICU.
Specific protocols for the determination of brain death are mandated by individual jurisdictions and adapted at each hospital. In general, the process involves establishing a diagnosis, reviewing radiographs, assessing for potentially reversible causes of coma, conducting a neurologic examination of brain and brainstem function, repeating or confirming the examination, and finally performing an apnea test whereby the arterial carbon dioxide levels are allowed to rise. The apnea test is performed as the final step because increasing CO2 will potentially increase ICP and if the patient was not brain dead, the apnea test could theoretically complete a partial herniation, which is not the intention of the test. See Figure 53–2 for a sample protocol for the determination of brain death in adults.
Algorithm for the determination of brain death. (Reproduced with permission from Marino PL, Sutin KM: The ICU Book, 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2007.)
Pulmonary contusion is a respiratory condition unique to trauma. Contusion can occur directly from blunt injury or indirectly from the blast effect and pressure wave created by a projectile passing through the tissue. The initial chest radiograph may appear normal, however after 4 to 24 hours, the contusions blossom into dense infiltrates. Oxygenation deteriorates as a consequence of shunt, and the degree of hypoxia is proportional to the degree of hypoxic pulmonary vasoconstriction impairment, usually driven by inflammation and thus worse following blunt trauma compared to penetrating. Care is supportive, and an open-lung, protective ventilation strategy should be followed similar to that used to manage acute respiratory distress syndrome (see Chapter 19).
“Flail chest” is a condition whereby 2 or more adjacent ribs are fractured in 2 or more locations following blunt trauma. Historically, mortality was quite high, and thought to be a consequence of compromised respiratory mechanics. Significant effort was directed at stabilizing rib fractures with splints and plates, with minimal outcome benefit. We have come to realize that the true insult in flail chest is the underlying pulmonary contusion, and with adequate epidural analgesia, intubation and supportive ventilator management until the contusions resolve, outcomes have improved.
Occasionally a patient's fall or motor vehicle crash is precipitated by loss of consciousness due to another medical condition such as hypoglycemia, seizure, or pulmonary embolism. Commonly, the syncope is cardiac in origin. Myocardial infarction and arrhythmias must be considered, especially in elderly trauma patients. Cardiac monitoring must continue and evaluation undertaken concurrently with the trauma work-up.
Blunt cardiac injury (BCI) following thoracic trauma is a potentially lethal syndrome. In extreme cases, it can lead to cardiac rupture, valvular dysfunction, or coronary occlusion; however, most cases manifest as impaired ventricular function. Mortality, when it occurs, is typically from malignant arrhythmias. Consequently, when BCI is suspected, the patient must have a baseline electrocardiogram (ECG) and cardiac troponin level.
The Eastern Association for the Surgery of Trauma publishes updated guidelines12 for the management of BCI. Among their most recent recommendations (2012):
If the admission ECG reveals a new abnormality (arrhythmia, ST changes, ischemia, heart block, and unexplained ST changes), the patient should be admitted for continuous ECG monitoring.
For patients with preexisting abnormalities, comparison should be made to a previous ECG to determine need for monitoring.
For patients with a normal ECG and normal troponin level, BCI is ruled out.
Patients with normal ECG results but an elevated troponin level should be admitted to a monitored setting.
For patients with hemodynamic instability or persistent new arrhythmia, an echocardiogram should be obtained.
If no new arrhythmias develop in a hemodynamically stable patient for 24 to 48 hours, then continuous ECG monitoring may be discontinued.
Tachycardia—The most common cardiac abnormality in the trauma patient is sinus tachycardia. The finding is nonspecific in trauma patients, and can be a consequence of hypovolemia, anemia, pain, anxiety, inflammation, fever, or elevated catecholamines. Each patient's ability to tolerate tachycardia must be weighed against the stress placed on the heart. Any evidence of strain or ischemia must prompt an investigation to diagnose and treat the underlying cause. If the tachycardia fails to resolve, or is attributable to elevated catecholamines, central fevers, or dysautonomia, then beta blockers should be considered for sustained heart rates more than 130 bpm so as to avoid tachycardia-induced cardiomyopathy.
Anticoagulation Management (See Also Chapters 20 and 34)—Although the early concern during resuscitation is directed at correcting coagulopathy, within hours to days, trauma patients become hypercoagulable and at significantly increased risk for deep vein thrombosis (DVT), especially if other trauma-related risk factors are present (see Table 53–3).
Table 53–3Trauma-related DVT risk factors. ||Download (.pdf) Table 53–3Trauma-related DVT risk factors.
|Trauma-Related DVT Risk Factors |
|Lower extremity fractures |
|Pelvic fracture |
|Spinal cord injury |
|Traumatic brain injury |
|Vascular injury, embolization, or repair |
DVT prophylaxis should be initiated as soon as appropriate once bleeding is controlled, and the coagulopathy has been corrected. In patients with TBI, pharmacologic DVT prophylaxis with subcutaneous unfractionated or low-molecular weight heparin is safe to begin once the patient's neurologic exam and head CT scans are stable for 24 hours. Although the combination of mechanical DVT prophylaxis with pharmacologic prophylaxis has not been shown to decrease the incidence of DVT compared to each used alone, because of the high likelihood of missed heparin doses and periods of time where sequential compression devices are removed or turned off, many adopt a “belt and suspenders” approach and implement both modalities concurrently.
General surveillance screening with Doppler evaluation for the presence of DVT in trauma patients has not been shown to be cost-effective provided appropriate DVT prophylaxis is maintained. A notable exception would be a patient at high risk for DVT, who is not a candidate for therapeutic anticoagulation in whom placement of an inferior vena cava (IVC) filter would be considered if a DVT were present.
Unfortunately, definitive data do not exist to guide the appropriate usage of IVC filters in trauma patients.13 Although retrievable filters are available, for various reasons the actual retrieval rate remains low. The protective benefit of IVC filter placement for pulmonary thromboembolism is temporary, yet the potential IVC complications of erosion and embolization are long-term. On the other hand, for patients with compromised cardiopulmonary function, even a relatively small pulmonary embolus can be fatal.
Fat Embolism Syndrome—Multiple critical care concerns arise as a consequence of bony and soft-tissue injury to the extremities. Fat embolism syndrome (FES) manifests as pulmonary, neurologic, cardiac, and renal dysfunction following pelvic and long-bone fractures.14 The injurious substances released into systemic circulation are most likely bone marrow constituents rather than purely fat. The diagnosis is one of exclusion and care is supportive. Neither corticosteroids, anticoagulation, nor IVC filter placement are recommended. Because movement of bony fragments is thought to be a contributing factor in the development of FES, the splints, traction, and external fixation devices placed during the first phase of damage control must be assiduously maintained throughout the patient's ICU course.
Crush Injury/Rhabdomyolysis—Mechanical limb compression, prolonged ischemia, blast effect, and vascular insufficiency are all factors which can contribute to delayed myonecrosis. Typically prophylactic fasciotomies are created to prevent limb compartment syndrome. When a limb salvage approach is chosen over early amputation, the intensivist must be aware of the progressive pathophysiology which may follow. Initially the skin and soft tissue of the limb appear normal, however serum CK levels must be monitored closely. If CK levels rise, rhabdomyolysis has begun, and surgical debridement of necrotic tissue (or extension of fasciotomies) must be undertaken before renal failure progresses to multiorgan system failure or worse.15 If the patient's systemic condition continues to deteriorate, amputation may be necessary. The Mangled Extremity Severity Score (MESS)16 can aid in anticipating the success or failure of limb salvage (see Table 53–4).
Table 53–4Mangled extremity severity score. ||Download (.pdf) Table 53–4Mangled extremity severity score.
|Component ||Points |
|Skeletal and Soft-Tissue Injury |
|Low energy (stab, simple fracture, “civilian gunshot wound”) ||1 |
|Medium energy (open or multiplex fractures, dislocation) ||2 |
|High energy (close-range shotgun or “military” gunshot wound, crush injury) ||3 |
|Very high energy (same as above plus gross contamination, soft-tissue avulsion) ||4 |
|Limb Ischemia (score is doubled for ischemia > 6 h) |
|Pulse reduced or absent but perfusion normal ||1 |
|Pulseless, paresthesias, diminished capillary refill ||2 |
|Cool, paralyzed, insensate, numb ||3 |
|Systolic blood pressure (BP) always > 90 mm Hg ||0 |
|Hypotensive transiently ||1 |
|Persistent hypotension ||2 |
|Age (yr) |
|< 30 ||0 |
|30-50 ||1 |
|> 50 ||2 |
|TOTAL || |
Limb salvage success is significantly diminished when the MESS is greater than 7. Intravenous hydration with close monitoring of electrolytes, directed at maintaining renal function is the mainstay of treatment for rhabdomyolysis. Alkalinization of urine and forced diuresis may be considered.
Besides the usual factors associated with renal failure in the critically ill (advanced age, hypertension, vascular disease, diabetes), trauma patients have additional risk factors contributing to a high rate of renal insufficiency and need for renal replacement therapy. For instance, direct renal trauma leading to nephrectomy results in an immediate decrease in glomerular filtration rate by half. Multiple exposures to contrast during the radiographic work-up of injuries, or during interventional vascular procedures is common. Rhabdomyolysis, exposure to aminoglycosides, and sepsis are potential additional insults.
Except for hydration therapy for rhabdomyolysis, the evidence supporting renal protective interventions for contrast-induced nephropathy is inconsistent. The potential outcome benefit demonstrated by intravenous hydration, bicarbonate administration, urine alkalinization, and oral N-acetylcysteine administration results in a lower peak creatinine level compared with placebo. Renal prophylactic therapies have neither been shown to improve survival nor to decrease the need for renal replacement therapy. However, because of the low cost, minimal risk, and potential benefit, renal prophylaxis for intravenous contrast exposure is often implemented.
In many trauma patients, gastrointestinal ileus develops directly as a consequence of bowel injury or indirectly from an elevated stress response or from narcotic exposure. At the same time, metabolic requirements necessary to heal wounds increase demands significantly following trauma. Interestingly, even relatively minor TBI increases metabolic demands well out of proportion to what might be anticipated from the amount of tissue damaged.
A plan for nutritional support must be established as early as possible. Often, if it can be anticipated that a patient will not be able to eat by mouth for a prolonged period, surgical feeding access may be obtained at the first take-back damage-control operation. Although there appears to be no difference in aspiration risk between nasogastric and postpyloric nasoduodenal tube feeding, a tube placed beyond the ligament of Trietz into the jejenum for feeding, with a proximal gastric port for evacuation may offer some benefit (see also Chapter 70).
Damage-control laparotomy with an open abdomen is not itself a contraindication to enteral nutrition.17 Intestinal luminal cells derive a portion of their energy from directly absorbed enteral nutrition, so providing even minimal trophic feeding could be expected to increase bowel perfusion and motility, enhance anastomotic integrity and decrease interstitial edema. In fact, in patients without bowel injury, enteral feeding in the open abdomen is associated with increased fascial closure rates, decreased complication rates, and decreased mortality.
Traditionally, enteral feeding is suspended prior to any planned operative procedure. The severely injured trauma patient may return to the operating room almost daily for various staged repairs in a damage-control strategy. As a consequence, nutritional support can become severely compromised. A more prudent approach is to continue enteral nutrition perioperatively, provided that the airway remains protected with a cuffed endotracheal tube, and the planned surgical procedure does not involve the aerodigestive tract.
Unlike the majority of critically ill patients who are admitted to an ICU after a long-term trajectory of deterioration from a chronic disease or condition, most trauma patients are relatively healthy prior to their injury. Indeed, many have never been hospitalized before. Trauma patients require a tremendous amount of social support and assistance ranging from tracking down family members to arranging for pets to be fed. A skilled and experienced trauma social worker is an invaluable member of the team.
As the trauma patient begins to regain consciousness, they often experience retrograde amnesia even if they did not suffer a head injury. The last thing they remember might be events from the day before they were injured. They may not know what happened, where they are, how they got there, nor realize, for instance, that a loved one perished in the same vehicle crash, or that they have lost a limb. As difficult as those conversations are to have, providing truthful information to the patient is the only way to alleviate their extreme anxiety and fear of not knowing. Anticipating how best to compassionately inform a patient of the events surrounding their trauma enables the care team to enroll the expertise of psychologists, social workers, grief counselors, clergy, family members, or even former trauma patient volunteers who can be available to provide support and answer questions for patients and their families.
As gratifying as it can be to care for severely injured trauma patients and enable them to recover from their physical injuries, neglecting their psychologic well-being can undermine an otherwise successful outcome. Trauma patients are at elevated risk for PTSD, and early screening and treatment can begin during their critical care stay.18 Full-blown PTSD can be incapacitating, but even posttrauma anxiety or depression can lead to substance abuse, alcoholism, and risk-taking that partly explain how trauma can become a chronic, relapsing condition.
Early mobility and ambulation, even in the ICU, has been shown to improve outcomes for specific types of injuries, while at the same time prolonged bedrest and immobility have almost universally been associated with increased ICU complications. Physical and occupational therapy availability for trauma patients in the ICU enhances their recovery and eases the transition to their next phase of care.19