Balanced Resuscitation

Historically, early trauma resuscitation involved large volumes of crystalloid and the last decade has welcomed a new concept in early trauma resuscitation. This change in approach to the resuscitation of the injured patient stresses a balanced resuscitation, using high ratios of red blood cells (RBCs), plasma, and platelets that come close to that of whole blood as early as possible in the care of trauma patients. Whole blood itself has increasingly become available and applied in both the prehospital and hospital setting. The Pragmatic Randomized Optimal Platelet and Plasma Ratios (PROPPR) Trial demonstrated that a 1:1:1 ratio of units of plasma to platelets to RBCs is not only safe but effective. Although not resulting in a mortality benefit at 24 hours and 30 days, a 1:1:1 ratio compared with a 1:1:2 ratio resulted in more patients achieving hemostasis and fewer deaths resulting from exsanguination in the first 24 hours.

Overaggressive crystalloid resuscitation accentuates coagulopathy through dilution of blood components, adds to acidosis through pH alteration, and exacerbates hypothermia via installation of large volumes of cold solution. In order to combat this, balanced resuscitation limits the use of crystalloid in the early resuscitation of the critically injured patient. In fact, the American College of Surgeons Committee on Trauma has recently changed the ATLS approach to limit initial crystalloid infusion from 2 L down to 1 L before adding blood products.

Another mainstay of balanced resuscitation is the concept of permissive hypotension. This allows an adequate but not normal blood pressure in order to preserve vital organ function as well as prevent further hemodilution and disruption of established clot in the patient with ongoing hemorrhage. The literature is mixed but a recent meta-analysis shows that permissive hypotension may not only show a reduction in blood loss and blood product utilization but also a survival advantage.

Many centers have established massive transfusion protocols that permit hospital blood banks to release rapidly standard quantities of uncrossmatched type O-negative red blood cells, plasma, platelets and, increasingly, low titer O-negative whole blood at regular intervals until hemorrhage is controlled. Despite being a strain on hospital blood banks, such protocols appear to be justified by studies showing decreased mortality as low as 15%, decreased overall component usage, and avoidance of overuse. Scoring systems, such as the Assessment of Blood Consumption (ABC) score, designed to predict need for massive transfusion, may help guide activation of such protocols. Trade-offs include risks of transfusion reaction, transmission of blood-borne diseases, and infectious and immune complications.

Hyperfibrinolysis has been recognized as a contributor to ongoing coagulopathy. Although normally striking a balance with thrombosis, increased fibrinolysis in some trauma patients leads to clot breakdown while hemorrhage is still ongoing. Tranexamic acid (TXA) has long been used to stem bleeding in elective surgery. Within the last decade, the use of TXA has been increasingly studied in trauma patients. Although it remains controversial, there is evidence to support its early use in the bleeding trauma patient. The Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage-2 (CRASH-2) trial showed a small but significant reduction in mortality and death secondary to bleeding with TXA. Thrombotic events were not different between the treatment and placebo groups. Late administration (> 3 hours after injury) of TXA showed an increase in mortality.

Choice of ICU Resuscitation Fluid

The fluid of choice for resuscitation after hemorrhage control in critically ill and injured patients is still controversial. Crystalloid solutions are less expensive but are theoretically less effective for maintaining intravascular volume. Although colloid solutions are more expensive, they theoretically remain longer in the intravascular space relative to crystalloid, and thus smaller volumes are required for infusion. Studies have not consistently shown one to be superior to the other for ICU resuscitation. The largest prospective randomized trial to address this issue is the Saline versus Albumin Fluid Evaluation (SAFE) trial, which compared normal saline with 4% albumin for resuscitation in ICU patients. This trial showed no mortality benefit of albumin over saline in a large cohort of ICU patients at 28 days. However, there was a lower amount of total fluid utilized in the albumin group in the first 4 days, a decrease in heart rate, and an increase in central venous pressure, although no change in mean arterial pressure. Post hoc subgroup analysis suggested that trauma patients in the albumin group may have fared worse than those in the saline resuscitation group; nonetheless this was inconclusive because this group also had a higher rate of death from traumatic brain injury.

Although the issue of crystalloid versus colloid has not been settled definitively, it is clear that overresuscitation can occur with any fluid and lead to a variety of complications, both immediate and delayed. Thus the choice of resuscitation fluid is probably less important than the timing and volume of resuscitation.

Transfusion Triggers

Anemia is common in the postinjury period, especially in those injured patients admitted to the ICU. Transfusion of blood products solely based on laboratory values should be approached cautiously. When other factors are controlled for, blood transfusion correlates with organ dysfunction, mortality, and ICU length of stay. Studies in trauma patients have suggested that blood transfusion is an independent predictor of worsened outcomes in patients with solid organ injuries. Large controlled trials in critically ill patients have suggested that restrictive blood transfusion practices (e.g., a hemoglobin transfusion trigger of 7 g/dL) are equal or superior in mortality to more liberal transfusion practices (e.g., a transfusion trigger of 10 g/dL). A smaller body of literature suggests the same is true in the injured population. Post hoc analysis of the Transfusion Requirements in Critical Care (TRICC) trial confirmed the safety of restrictive transfusion practices in trauma patients. Both protocols are similar in terms of mortality and incidence of multiple organ dysfunction. A postinjury practice management guideline is safe and cost effective. Although the transfusion trigger for patients with active cardiac ischemia and patients with head injury is not known, it is likely that most other injured patients with hemorrhage control will not benefit from liberal transfusion strategies. The concept of transfusion threshold should be applied very carefully in the trauma population: any threshold for transfusion presupposes control of hemorrhage. Stated more bluntly, transfusion thresholds do not apply to patients who are still bleeding.

Endpoints of Resuscitation

Clinical judgment is an essential component of multisystem trauma resuscitation. Not all endpoints are applicable to all patients, and a global perspective of the patient’s status is tantamount to the attention to minute details. Endpoints can be classified as clinical, laboratory, or monitoring.

The initial assessment of the trauma patient begins with evaluating and treating the ABCs, and the ongoing care should ensure that the ABCs remain intact. Changes in hemodynamics or oxygenation should prompt reassessment of airway, breathing, and circulation, especially confirming proper position and function of endotracheal tube, chest tubes, catheters, monitors, and surgical drains. In the early postinjury period, hypotension should be assumed to be caused by hemorrhage until proven otherwise.

Traditional clinical indicators such as blood pressure, heart rate, urine output, distal perfusion, and mentation should be used as a starting point for assessing resuscitation. Abnormalities of these basic signs should prompt thorough physical examination and close monitoring of interventions (blood component therapy, fluid challenges, analgesia, sedation). Several caveats relevant to the injured patient should be mentioned: tachycardia is nonspecific and may represent hypovolemia, pain, agitation, presence of illicit substances, or myocardial injury. On the other hand, tachycardia may be absent or blunted in patients who were receiving beta-blocker therapy before the injury. Regarding blood pressure, essential hypertension is widely prevalent, and a “normal” blood pressure may in fact represent relative hypotension and hypovolemia. Finally, mental status may be altered by hypoperfusion, brain injury, the presence of illicit substances, or baseline chronic encephalopathic diseases such as dementia.

Laboratory studies are useful for assessing endpoints of resuscitation. Postinjury acidosis, as manifested by persistently elevated lactic acid or by base deficit (or persistently low serum bicarbonate), suggests occult hypoperfusion or devitalized tissue. Although the initial value (i.e., immediately on arrival to the trauma center) has correlation to outcome, the trend over hours is more useful for assessing treatments and predicting mortality. Persistent acidosis is a grave sign. Failure to normalize serum lactic acid level by 24 hours after injury is associated with worse outcome in injured patients. Similarly, persistent base deficit correlates with worse outcomes.

Viscoelastic tests such as thromboelastography (TEG) and rotational thromboelastometry (ROTEM) can also guide blood component therapy and may be superior to conventional coagulation tests such as PT/INR and PTT for guiding the correction of coagulopathy. ProTime (PT) and activated partial thromboplastin time (aPTT) are usually performed at 37°C. Thus in the normothermic patient, abnormalities of PT and aPTT indicate clotting factor deficiency. However, in the hypothermic patient, these studies fail to assess the qualitative deficiency of coagulation and thus underestimate coagulopathy. TEG may demonstrate coagulopathy with improved fidelity irrespective of body temperature. TEG measures the dynamics of clot development, stabilization/strength, and dissolution. A prolonged R-time may indicate the need for plasma transfusion. An increased K-time or decrease in alpha angle may denote hypofibrinogenemia. A low maximum amplitude reveals low platelet function. LY-30 or lysis of clot at 30 minutes is increased with hyperfibrinolysis and treatment with TXA may be indicated. Component therapy may be directed toward these coagulopathic findings as stated earlier.

Trauma patients who suffer deterioration of these indicators should be presumed to have ongoing or uncontrolled hemorrhage in the thorax, abdomen, retroperitoneum, and extremities. After physical examination, chest radiograph and focused abdominal sonography for trauma (FAST) may help triage the chest and abdominal cavities by diagnosing or excluding recurrent hemothorax or new hemoperitoneum. Hemorrhage in the thorax, abdomen, or extremities that is brisk enough to result in hypotension or acidosis often requires control in the operating room. However, hemorrhage from hepatic lacerations, pelvic fractures, or retroperitoneal injury may be difficult to control in the operating room and instead may require interventional radiology with angiography for diagnosis and embolization for treatment.

Despite the vast cumulative experience with central venous pressure (CVP) monitoring, the amount of objective data available to guide clinicians in deciding which injured patients to monitor are limited. CVP monitoring is probably indicated for patients who have hemorrhage control but have not responded appropriately to initial volume resuscitation or for patients with chronic cardiac and pulmonary disease and low physiologic reserve. The endpoints are similar to those of postsurgical patients. When CVP is unavailable, bedside ultrasonography may be used to assess inferior vena cava diameter, respiratory variability and collapsibility, which can be a surrogate for right atrial pressures and volume status.

The pulmonary artery (PA) catheter remains controversial in trauma patients. Although PA catheterization is theoretically attractive and commonly used, retrospective and prospective studies of critically ill patients have not consistently demonstrated that it has a mortality benefit compared with central venous monitoring. Furthermore, these studies typically have relatively small numbers of injured patients, making results more difficult to apply to the trauma patient. It is likely that the benefit of the PA catheter is not in its presence or absence, but in how the clinician uses the data that are available. Ultimately, the usefulness of the PA catheter may lie in optimizing ventricular preload and overall cardiac efficiency and in preventing over -resuscitation.

Many methods of assessing regional visceral perfusion have been proposed as adjuncts to clinical examination, laboratory studies, and central monitoring. Gastric tonometry demonstrates good correlation with other indices of global perfusion, but it has not found widespread clinical acceptance. Sublingual capnometry may also prove to be a useful, noninvasive marker of perfusion. Esophageal Doppler and surface ultrasound techniques have been investigated as noninvasive means of assessing cardiac output and preload, respectively. Further studies will clarify their roles in achieving adequate resuscitation of the injured patient.

Damage Control

Borrowing from United States Navy vernacular, “damage control” has become widely used in the care of the severely injured patient. The paradigm involves rapid control of exsanguinating hemorrhage and gastrointestinal contamination, followed by resuscitation in the surgical ICU, then a return to the operating room for thorough identification and definitive treatment of injuries when the patient has stabilized. Sometimes, multiple cycles between surgical ICU and the operating room are necessary, depending on the extent of injury and physiologic stability. Some patients have insufficient fascia in the abdominal domain after prolonged periods of damage control and require skin graft closure of the abdomen. Originally described for abdominal injuries, damage control concepts have been extended to the thorax, extremities, neck, and even the cranium.

Successful implementation of damage control requires the coordinated efforts of the trauma surgeon, anesthesiologist, and surgical intensivist. When the source of bleeding and contamination is suspected to be within the abdomen, the surgical team begins with laparotomy and quickly packs all quadrants of the abdominal cavity. Meanwhile, the anesthesiology team begins aggressive resuscitation of the patient with blood and blood products. The surgical team systematically explores the abdominal cavity. The goal of the initial operation is rapid control of life-threatening hemorrhage and massive gastrointestinal contamination. Injuries to major arteries are shunted; injuries to smaller arteries and most veins (except suprarenal inferior vena cava) are ligated; gastrointestinal injuries are quickly closed primarily or resected with staplers without reestablishing continuity; liver injuries are packed; splenic and renal injuries are treated by splenectomy or nephrectomy, respectively. The abdominal fascia is not closed. Rather, temporary abdominal closure is performed, for which many methods have been described. Patients with hepatic or pelvic injuries identified at the initial operation may require diagnostic arteriography and embolization immediately postoperatively. Among patients with hepatic injuries, the therapeutic yield of interventional radiology is high.

Surgery is followed by an ICU phase of damage control. With hemorrhage and gastrointestinal contamination controlled by the trauma team, the intensivist team is charged with attaining physiologic “capture” of the patient. The goal of this period is to prevent or reverse the lethal triad of hypothermia, coagulopathy, and acidosis ( Fig 36.1 ).

Lethal triad of hypothermia, coagulopathy, and acidosis.

Several measures are available to prevent and treat hypothermia. Straightforward measures decrease heat loss and allow rewarming, albeit slowly, by increasing the temperature of the room and using blankets, warming lights, and forced-air warming blankets. An intravenous fluid warmer should be used. The ventilator circuit should have warmed air. Warming pads, placed against the torso and extremities, are highly effective for rewarming. Warmed fluid is circulated through tubes in the pads. Although abdominal cavity lavage with warmed fluid is described, it is unclear whether the rate of rewarming is better than other, less invasive methods. The most rapid and invasive method of rewarming is venovenous bypass, but its primary disadvantage is the requirement for full systemic heparinization.

Acidosis is primarily caused by hypoperfusion and hypothermia and should therefore correct when normothermia and circulating volume are restored. Acidosis per se should not be treated with bicarbonate solutions except to treat myocardial irritability (i.e., pH < 7.2). Coagulopathy is multifactorial, resulting from blood loss, consumption and dilution of platelets and clotting factors, accelerated fibrinolysis, impaired function of blood components, hypothermia, and hypocalcemia. As discussed previously, treatment alongside rewarming and correction of acidosis continues with blood product therapy until laboratory values of coagulation tests or viscoelastic tests are corrected and/or clinically significant hemorrhage is resolved.

Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA)

REBOA is a technique that can be used during the initial treatment of the trauma patient in hemorrhagic shock to control truncal bleeding rapidly and temporarily for noncompressible locations such as the abdomen and pelvis. Another source of noncompressive hemorrhage is junctional hemorrhage or hemorrhage at the junction of an extremity with the torso of the body that is not amenable to tourniquet application. REBOA should not be used in the exsanguinating patient with penetrating thoracic injury because this may hasten thoracic cavity bleeding and should otherwise be controlled with open surgical techniques. In placing a REBOA, the femoral artery is used to introduce the balloon to the lumen of the aorta. A percutaneous approach, when possible, is preferred; however, an open, surgical cut-down may be required. Once thoracic cavity bleeding has been excluded by ultrasound, plain film, or tube thoracostomy, the intraaortic balloon is deployed just proximal to the diaphragmatic hiatus in zone 1 of the aorta ( Fig 36.2 ). For major pelvic or junctional hemorrhage, the balloon is inflated at the level of the aortic bifurcation in zone 3. This temporary control allows a more definitive approach to major vascular injuries.

Aortic zones: Zone I extends from the origin of the left subclavian artery to the celiac artery; Zone II extends from the celiac artery to the most caudal renal artery; and Zone III extends from the most caudal renal artery to the aortic bifurcation. Resuscitative endovascular balloon occlusion of the aorta (REBOA) deployment is limited to Zones I and III.

(From Bogert JN, Davis KM, Kopelman TR, Vail S, Pieri P, Matthews MR. Resuscitative endovascular balloon occlusion of the aorta with a low profile, wire free device: A game changer? Trauma Case Rep 2017; 7: 11–14.)

Proponents of REBOA regard this technique as less invasive than resuscitative thoracotomy and aortic cross clamping in the chest. A retrospective study ( n = 31) at a busy level 1 trauma center showed that balloon inflation correlated with increased blood pressure and temporary hemorrhage control in most patients. However, there have been no randomized trials comparing REBOA with other methods of hemorrhage control. Furthermore, REBOA has been associated with vascular complications necessitating additional procedures.

Intraabdominal Hypertension and the Abdominal Compartment Syndrome

Intraabdominal hypertension (IAH) and the abdominal compartment syndrome (ACS) are well-recognized complications of critically ill trauma patients. Injury, hemorrhage, ischemia, reperfusion, and resuscitation all contribute to these complications. IAH exists when the pressure in the abdomen is elevated without evidence of organ dysfunction. ACS exists when abdominal hypertension causes organ dysfunction or failure. IAH may be signaled by a rising central venous pressure (CVP), high peak airway pressures or difficulty generating tidal volume, oliguria or worsening renal function, or by worsening or new onset of lactic acidosis.

Risk factors for increased intraabdominal pressure (IAP) include major abdominal surgery or trauma, major burns, prone positioning, ileus or intestinal obstruction, acute pancreatitis, decompensated cirrhosis with large volume ascites, hemoperitoneum, intraabdominal infections, large volume crystalloid infusions, and blood transfusion of greater than 10 units.

The World Society on Abdominal Compartment Syndrome (WSACS) published consensus definitions and clinical practice guidelines in 2013. They defined resting IAP at 5–7 mmHg in critically ill adults. IAH was defined as a sustained pressure greater than 12 mmHg and was divided into four grades of increasing pressures (Grade I, IAP 12–15 mmHg; Grade II, IAP 16–20 mmHg; Grade III, IAP 21–25 mmHg; Grade IV, IAP > 25 mmHg). ACS is defined as primary when associated with injury or disease in the abdominopelvic region and frequently requires early surgical or interventional radiologic intervention. Secondary ACS develops as a result of conditions that do not originate from the abdominopelvic region such as ascites secondary to volume overload. Recurrent ACS refers to the condition in which IAH or ACS redevelops following previous surgical or medical treatment of primary or secondary IAH or ACS.

In order to estimate IAP, the bladder pressure is typically used as a surrogate. The bladder is filled with 25 mL sterile saline and the bladder catheter tubing is clamped. The patient should be supine and paralyzed to mitigate external contributors to bladder pressure. The transducer is located at the midaxillary line. The pressure of the system is then transduced.

Noninvasive measures to treat IAH include improvement of abdominal wall compliance by way of sedation, analgesia, and neuromuscular blockade; nasogastric and rectal decompression with evacuation of intraluminal contents; drainage of abdominal fluid by paracentesis; judicious use of fluids, diuretics, and/or dialysis to correct volume overload; optimize ventilation to avoid increased intrathoracic pressures.

Once ACS has been identified, immediate measures to treat the underlying etiology must ensue. If primary ACS is the cause, laparotomy and temporary abdominal closure are required to reduce IAP and to restore perfusion. After decompressive laparotomy, the abdominal fascia is left open and a temporary abdominal closure is fashioned to cover the viscera without exerting tension on the closure. Even so, recurrent ACS in the open abdomen has been described. Even when treated, ACS is associated with increased morbidity and mortality. There is growing appreciation for the iatrogenic component of IAH and ACS, highlighting the importance of reaching—but not exceeding—resuscitation endpoints.

Other Compartment Syndromes

Both blunt and penetrating mechanisms put tissue at risk of compartment syndromes. Extremities—not only calves but also thighs, buttocks, and upper extremities—should be examined carefully for increases in tenseness. Extremities with increased tenseness should be immediately evaluated by a surgeon. The presence of a distal pulse that can be detected by Doppler ultrasonography or palpated does not rule out compartment syndrome. New onset of pain should alert the physician, but pain is often already present and its absence does not rule out compartment syndrome. Other neurologic findings, such as motor or sensory deficits, should prompt immediate surgical evaluation. Invasive monitoring of compartment pressures may help establish the diagnosis, but normal pressures may lead to a false sense of security. In general, it is safer to act on a strong clinical suspicion than to allow compartment syndrome to go untreated. Wide fasciotomies should be performed immediately if compartment syndrome is diagnosed or clinically suspected.

Management of Patients with Brain Injury

Resuscitation of brain-injured patients deserves special mention. Although clinical signs and laboratory studies are useful for global perfusion, head-injured patients with severe head injury (Glasgow Coma score [GCS] ≤ 8) benefit from more direct assessment of brain perfusion. Outcome after head injury is markedly dependent on cerebral perfusion. Hypotension and hypoxemia are to be avoided at all costs. Even one brief episode of hypotension (systolic blood pressure [BP] < 90 mmHg) or hypoxemia (PaO ₂ ≤ 60 mmHg) is detrimental to long-term outcome after head injury. The clinically relevant index of brain perfusion is cerebral perfusion pressure (CPP), defined as the difference between mean arterial pressure (MAP) and intracranial pressure (ICP). Retrospective studies suggest that failure to maintain CPP above 60 mmHg is associated with worse outcome. ICP monitors can guide medical therapies (e.g., fluids and/or pressors to increase CPP; osmotic diuretic to decrease ICP). Maintaining ICP consistently at less than 20 mmHg probably improved outcome after brain injury. The Brain Trauma Foundation recommends ICP monitoring in the following situations:

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  Severe head injury (defined as GCS 3 to 8) with abnormal computed tomography (CT) of the head at admission (e.g., CT demonstrates hematoma, contusion, edema, or compressed basal cisterns).

  
  
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  Severe head injury with normal CT of the head at admission and two or more of the following at admission: age greater than 40 years, unilateral or bilateral motor posturing, systolic BP less than 90 mmHg.

  
  
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  At the physician’s discretion among conscious patients with traumatic mass lesions.

Furthermore, the ICP transducer may have a ventriculostomy catheter to allow drainage of cerebrospinal fluid (CSF) and thereby decrease the ICP. CPP is increased by increasing MAP (volume resuscitation, then vasopressor if necessary) and/or by decreasing ICP (by an osmotic diuretic agent such as mannitol or by drainage of CSF). The ideal transfusion trigger for brain-injured patients is not known. The traditional trigger is 10 g/dL, but this has recently been challenged. Until more definitive studies are completed, it is prudent to be more liberal in RBC transfusion when caring for brain-injured patients. Hypertonic saline is a safe and effective component of brain trauma resuscitation and should be considered after colloid resuscitation. Deliberate hyperventilation is indicated for acute control of ICP, but it has no benefit as a sustained ICU therapy, because the ICP control by hyperventilation is based on decreased cerebral blood flow.

Cerebral cortical oxygenation is being investigated as an adjunct to ICP monitoring. These devices alert the clinician to occult brain tissue hypoxia (partial pressure of oxygen [PO ₂ ] < 15 to 20 mmHg)—that is, ischemic brain tissue despite adequate CPP. Further studies will clarify its role in brain resuscitation.

In addition to these resuscitation measures, the Brain Trauma Foundation has promulgated guidelines for the management of severe TBI and early posttraumatic seizures (PTS) prophylaxis. Although no recommendations have been made for decreasing the incidence of late PTS, level IIa recommendations suggest that phenytoin be used to decrease the incidence of early PTS (within 7 days of injury) when the overall benefit is felt to outweigh the complications associated with such treatment. However, early PTS have not been associated with worse outcomes. At the time the guidelines were published, there was insufficient evidence to recommend levetiracetam over phenytoin regarding efficacy in preventing early posttraumatic seizures and toxicity.

Venous Thromboembolism (VTE)

Injured patients are at higher risk of deep venous thrombosis (DVT) and pulmonary embolism (PE) than either uninjured patients or other groups of hospitalized patients. Meta-analysis reveals an overall DVT rate of 11.8% and a PE rate of 1.5% among all injured patients.

Despite the frequency of thromboembolic complications, there is significant controversy and variability in current practice. Most trauma centers have developed standardized approaches to prophylaxis for venous thromboembolic events. Early mobilization is a simple prophylactic measure. However, many patients are limited by their injuries or mental status. Sequential compressive devices should be considered in all patients without precluding wounds, fractures, splints, and external fixators. Patients with risks factors for VTE and no contraindications should be given chemical prophylaxis.

High risk patients are those anticipated to be hospitalized > 24 hours and have one or more of the following risk factors:

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  Anticipated immobilization > 2 days

  
  
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  Previous history of DVT, PE, or hypercoagulable disease

  
  
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  Head injury with GCS < 8 or unable to respond to commands

  
  
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  Pelvic fracture

  
  
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  Long bone fracture

  
  
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  Spinal fracture

  
  
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  Lower extremity venous injuries

  
  
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  Cancer

  
  
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  Obesity

  
  
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  Multiple rib fractures

Many single-center studies have demonstrated efficacy of one or more of the three most common prophylaxis measures—mechanical prophylaxis with sequential compression devices (SCD), low-dose unfractionated subcutaneous heparin (SQH), and subcutaneous low-molecular-weight heparin (LMWH). When subjected to meta-analysis, none of the measures was statistically more effective than no prophylaxis at all, but this meta-analysis was insufficiently powered to exclude a true benefit of any of the therapies. Among SCD, SQH, and LMWH, LMWH is probably the best choice for DVT prophylaxis in injured patients who are not at excessive risk for bleeding. A study from the University of Michigan used data from the Michigan Trauma Quality Improvement Project (MTQIP) database to conduct a comparative effectiveness study evaluating UFH versus LMWH for the in-hospital outcomes of VTE, PE, DVT, and mortality. They found that trauma patients who received LMWH as their first dose of VTE prophylaxis had a significantly reduced risk of VTE, PE, DVT, and mortality when compared with UFH. LMWH may be more effective than SQH in prevention of DVT with no increased risk for bleeding complications. Contraindications to LMWH include renal insufficiency or renal failure or the presence of an epidural analgesia catheter. In these situations, unfractionated heparin and intermittent compression devices are acceptable alternatives.

For patients at high risk of thromboembolic events who cannot undergo anticoagulation or tolerate additional bleeding (e.g., patients with intracranial hemorrhage, pelvic hematoma, ocular injury with hemorrhage, or injury to liver, spleen, or kidney), prophylactic placement of an inferior vena cava (IVC) filter is controversial. The Eastern Association for the Surgery of Trauma (EAST) guidelines recommend consideration of IVC filter placement but the American College of Chest Physicians (ACCP) recommend against the primary use of IVC filters for VTE prophylaxis and recommend SCDs and starting chemical prophylaxis when the contraindication resolves. The long-term sequelae of IVC filters are not known. A variety of removable IVC filters exist and they may be considered in patients who are deemed candidates for filter placement.

Stress Ulcer Prophylaxis

Injured patients have an increased risk of stress ulcers and prophylaxis is indicated for patients with high risk. Incidence of gastrointestinal bleeding ranges from 1.5% to 8.5% in intensive care unit patients but may be as high as 15% among patients who do not receive stress ulcer prophylaxis. Mortality is significantly higher in ICU patients who develop clinically apparent upper GI bleeding, 49% versus 9%. Risk factors include coagulopathy defined as a platelet count < 50,000 per m ³ , an International Normalized Ratio (INR) > 1.5, or a partial thromboplastin time (PTT) > 2 times the control value, mechanical ventilation for longer than 48 hours, traumatic brain injury, spinal cord injury, burns > 30%, or a history of upper gastrointestinal bleeding. A variety of treatment options exist (sucralfate, histamine-2 receptor antagonists [H ₂ RAs], and proton-pump inhibitors [PPIs]). In the largest meta-analysis of 18 studies, PPI use prevented more upper GI bleeding events than H ₂ RAs without any impact on the rate of pneumonia. Among mechanically ventilated patients, sucralfate and H ₂ RAs are effective for prevention of bleeding, with H ₂ RAs possibly slightly more effective. Some studies suggest that sucralfate is associated with a lower rate of nosocomial pneumonia, but others have been unable to show a difference. Large randomized controlled trials are warranted to elucidate the benefit of one regimen over another and the relationship of stress ulcer prophylaxis and infectious complications.

Nutrition Support

Nutrition support is of utmost importance in the injured patient once acute hemodynamic issues have been addressed. Injured patients are often in a catabolic state and have higher nutritional requirements than in the preinjury state. Both enteral nutrition and parenteral nutrition have roles in postinjury care. The enteral route is preferred. The Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition published guidelines for the assessment and provision of nutrition support in critically ill patients. They recommend determining nutritional risk for ICU patients and starting enteral nutrition when possible and as early as 24 to 48 hours after admission. This should start in the hemodynamically stable patient and be used with caution in patients on vasoactive medications. Among critically ill patients, especially those with abdominal injury, enteral nutrition is associated with a lower rate of septic complications (pneumonia, intraabdominal abscess, line sepsis) than the parenteral route. About half of all patients cannot tolerate goal enteral nutrition at 1 week postinjury. Parenteral nutrition should be considered in patients who do not achieve at least 50% of goal enteral nutrition by postinjury day 7.

Enteral nutrition can be delivered by the intragastric or postpyloric route. Neither route has been proven superior in trauma patients in terms of mortality; however, the postpyloric route may reduce the risk of aspiration and pneumonia. Because intragastric feeding is typically simpler, it should be the first choice. Postpyloric feeds should be considered for patients at high risk of aspiration, especially patients with head injury, in whom gastroparesis is common. Gastric residual volumes were traditionally used to assess tolerance but have since been disproven and are associated with a decrease in calorie delivery. Other ways to assess tolerance include abdominal distension, pain, nausea, emesis, diarrhea, constipation > 3 days, and/or a large gastric bubble seen on plain film of the abdomen. Enteral formulas with various supplements (e.g., arginine, glutamine, fish oils) have been studied in critical care populations, including trauma patients, but no specific enteral formulation has demonstrated consistently superior outcomes. Based on systematic review, guidelines have not formally recommended enhanced enteral nutrition formulas but simply suggest considering them. Rather, it appears that simply avoiding starvation is the key to reducing septic morbidity in the critically ill.

Glycemic Control

Hyperglycemia in trauma patients is associated with increased infectious complications and mortality. Injured patients with a serum glucose level greater than 200 mg/dL have consistently demonstrated worsened outcomes: increased ICU length of stay (and thus increased hospital length of stay), longer duration of mechanical ventilation, higher rates of infection, and higher mortality. However, the optimal target range for glycemic control has been debated over the past two decades—in particular, whether lower glycemic targets are associated with improved outcomes. The largest trial to date concerning glycemic control was the multicenter Normoglycemia in Intensive Care Evaluation Survival Using Glucose Algorithm Regulation (NICE-SUGAR) trial, which randomly assigned 6104 medical and surgical ICU patients to either intensive insulin therapy (target blood glucose level of 81–108 mg/dL [4.5–6 mmol/L]) or conventional glucose control (target blood glucose of < 180 mg/dL [< 10 mmol/L]). The intensive insulin group had a higher mortality and higher incidence of severe hypoglycemia. However, a subgroup analysis suggested a possible trend toward improved outcomes with intensive insulin in trauma patients. Nonetheless, a blood glucose target of 140 to 180 mg/dL (7.7–10 mmol/L) rather than a more stringent target of 80 to 110 mg/dL (4.4–6.1 mmol/L) or a more liberal target (e.g., 180–200 mg/dL [10–11.1 mmol/L]) is currently recommended for ICU surgical patients.

Infectious Complications

Trauma patients often have gastric contents present at the time of injury, placing them at higher risk of aspiration pneumonitis and aspiration pneumonia, either from inability to protect the airway or from rapid-sequence intubation. “Ventilator bundles,” designed to reduce the risk of ventilator-associated pneumonia (VAP), are commonplace in the ICU. Within limits of the patient’s injuries and treatments, mechanically ventilated trauma patients should receive all such therapies to decrease the incidence of VAP. Intubated trauma patients should have the head of the bed at 45 degrees after thoracic and lumbar spine clearance. Until then, or if spine injury is present, the patient should be placed in reverse Trendelenburg position.

The incidence of catheter-related blood stream infections is higher in trauma patients. This may reflect the less than ideal conditions in which they are placed. These lines should be removed or replaced with peripheral access as soon as possible. Likewise, catheter-associated urinary tract infections can be mitigated with early removal of bladder catheters.

There is no role for routine antibiotic administration in most patients. In patients requiring a laparotomy, a single preoperative dose given within 1 hour of incision is appropriate. If hollow viscus injury is identified and repaired in a timely fashion, there is evidence for limiting postoperative antibiotics to 24 hours postoperatively. Longer courses of antibiotics do not decrease rates of infection and abscess formation. Antibiotic prophylaxis may be justified in some open fractures.

Analgesia

Pain management in the trauma patient is similar to that of the postoperative patient. Critically injured patients require careful assessment of their pain. Whenever possible, opioid based medications should be limited or avoided and a nonopioid multimodal pain medication regimen should be followed. The American Society of Anesthesiologists Acute Pain Task Force Guidelines recommend the use of a multimodal pain management therapy plan, neuraxial/regional blockade with local anesthetics, and an around-the-clock regimen of cyclooxygenase (COX) inhibitors, nonsteroidal antiinflammatory drugs (NSAIDs), or acetaminophen.

Numerous studies have documented a strong relationship between rib fractures and either respiratory complications or mortality. Although rib fractures are debilitating for all patients, older adult patients with rib fractures are particularly susceptible. Some studies have suggested that epidural analgesia is superior to patient-controlled analgesia in patients with rib fractures, but others have found no benefit. Operative fixation of multiple rib fractures and flail chest is gaining acceptance and may enhance pulmonary mechanics and decrease complications such as pneumonia and death. Clinical trials are lacking and more research is warranted in this field.