Hypertonic saline has many potential advantages in that it can resuscitate with low volume by pulling water into the vascular space and thus avoids excess water during resuscitation. This concept has advantages especially in the military field environment. Hypertonic saline is also thought to be an immune modulator that potentially decreases inflammation associated with resuscitation injury.⁴² However, a multicenter prospective trial in trauma patients with hemorrhagic shock was halted before completion as the outcome was similar between the groups. Overall there was no survival disadvantage in the hypertonic saline arm of the study except in a small subset of patients who did not require blood transfusion. This subset of patients had higher mortality if given hypertonic saline in the field. There was also a subset that required ICU treatment that showed higher survival and decreased multiple organ failure when hypertonic saline was given.⁴³ Since 7.5% hypertonic saline is not commercially available, an alternative is to use 5% hypertonic saline. Those who use 5% hypertonic saline administer it as a one-time bolus in the initial phase of resuscitation. This approach may be beneficial in patients with TBI. The safety of using 5% hypertonic saline has been shown in two studies.^44,45 A caveat of using hypertonic saline is that it causes hyperchloremic acidosis, but clinical significance has not yet been demonstrated. Because of the capability of increasing intravascular volume, the ideal time and place for hypertonic saline use may be in the field, especially in the military setting.⁴⁶

Hyperfibrinolysis associated with traumatic coagulopathy may decrease levels of fibrinogen. High plasma:pRBC ratios adequately replenish the fibrinogen pool required for adequate hemostasis and thus the use of cryoprecipitate rich in fibrinogen as an adjunct to DCR is rational.⁸ The use of cryoprecipitate has additional advantages as it provides particles that act as a low-volume colloid resuscitation and draw water into the vascular system, and is an adjunct in resuscitation. Tranexamic acid is an antifibrinolytic agent found to be safe and effective in reducing the risk of bleeding if used within 3 hours of injury.⁴⁷ The military Tactical Combat Casualty Care Committee has recommended its use in the military setting. Several other novel strategies have also been used as an adjunct in DCR including the use of activated recombinant factor VII (rFVIIa). rFVIIa activates factor Xa at the site of tissue injury by complexing with tissue factor on the surface of platelets. Use of rFVIIa has shown to effectively reduce blood loss and mortality in massive trauma patients; its use is limited by high costs.^48,49 Prothrombin complex concentrate (PCC) is another cost-effective option that reverses coagulopathy in traumatic injury.⁵⁰

The discussion of DCR should also include damage control laparotomy. After injury, when a trauma patient requires laparotomy, some patients may require abbreviated laparotomy in order to better resuscitate the patient so that the prolonged initial surgery does not harm the patient. Although damage control laparotomy has been widely accepted as the standard of care for trauma patients, it was adopted without rigorous proof of concept. One hallmark study suggested that damage control laparotomy is of benefit in trauma patients with numerous major visceral injuries that also have vascular injury; this study also showed that damage control laparotomy in patients without major injuries was associated with worse outcome.⁵¹ Definitive laparotomy may have survival benefit with decrease in morbidities known to accompany damage control laparotomy such as open abdomens and enterocutaneous fistulas. Because of the decreased number of surgeries and morbidities, the cost benefits were significant.^52,53

ENDPOINTS OF RESUSCITATION

The ultimate goal of resuscitation is to ensure adequate oxygen delivery to tissues. Prolonged tissue hypoxia is associated with multiorgan dysfunction syndrome, risk of infection, and increased mortality.

Advanced Trauma Life Support guidelines define the correction of vital signs like blood pressure and heart rate as markers of adequate resuscitation. However, up to 82% of severely injured patients with normalized vital signs have ongoing occult ischemia that is associated with adverse outcomes.⁵⁴ While normalization of vital signs may describe the current perfusion status, they do not assess oxygen debt, defined as ongoing oxygen deficits that have accumulated during the period of shock. Oxygen debt is known to be associated with increased mortality.^55,56 Arterial lactate and base deficit may serve as indicators for severity of shock and may help to stratify patients. Trends in serum lactate levels indicate adequacy of resuscitation.

Invasive monitoring with central venous pressure (CVP) and pulmonary artery catheter (PAC) have been extensively used to guide resuscitation. CVP and pulmonary capillary wedge pressure monitoring provide information regarding the intravascular volume, but concurrent factors like mechanical ventilation and changes in ventricular compliance from myocardial dysfunction limit their efficacy in accurately guiding resuscitation.⁵⁷ Moreover, PAC use in critically ill trauma patients has not been shown to improve outcomes.⁵⁸

ScVO₂ and SVO₂ measure central venous oxygen saturation from the upper body and mixed venous oxygen saturation from both the upper and lower body, respectively. Inadequate oxygen supply from ongoing shock or increased oxygen demand leads to an increased tissue extraction of oxygen, which is reflected as a decrease in the values of ScVO₂ and SVO₂. SVO₂ of less than 65% even in the presence of normal vital signs indicates blood loss and need for transfusion to optimize oxygen supply and demand.⁵⁹ Therefore, ScVO₂ and SVO₂ provide a real-time picture of tissue perfusion and are able to detect very subtle changes in oxygen delivery. The ideal marker for resuscitation may be to determine blood volume, but there is currently no simple way to determine ideal circulating blood volume.

ABDOMINAL COMPARTMENT SYNDROME

4 Abdominal compartment syndrome is an undesired consequence of elevated intra-abdominal pressure and a cause of morbidity and mortality.⁶⁰ The incidence of abdominal compartment syndrome is decreasing with recent evolution in resuscitation strategy, suggesting a possible iatrogenic etiology.⁶¹ Intra-abdominal hypertension is defined as a pressure of greater than or equal to 12 mm Hg. Intra-abdominal hypertension is graded based on increasing intra-abdominal pressure (Table 32-2). Abdominal compartment syndrome is defined as a sustained intra-abdominal pressure greater than 20 mm Hg (with or without an abdominal perfusion pressure of less than 60 mm Hg) with new organ dysfunction or failure.⁶² Experimental data indicate that hepatic arterial, portal venous, and hepatic microcirculatory blood flow are markedly reduced when intra-abdominal pressure is increased.^62,63 Typically, abdominal compartment syndrome is observed after severe abdominal trauma with intra-abdominal hemorrhage, severe liver and kidney injuries, and in both operatively and nonoperatively managed settings (primary abdominal compartment syndrome).^64–66 Excessive large-volume resuscitation, even in the absence of any direct abdominal trauma, can also lead to abdominal compartment syndrome (secondary abdominal compartment syndrome).^67–69 Recurrent or tertiary abdominal compartment syndrome refers to a condition following a previously treated primary or secondary abdominal compartment syndrome.⁶² Risk factors for development of abdominal compartment syndrome include diminished abdominal wall compliance, increased intraluminal and intra-abdominal content, crystalloid resuscitation/leak, and other risk factors such as age, shock, high BMI, coagulopathy, and mechanical ventilation.^70–80 Abdominal compartment syndrome can even occasionally occur in patients with an open abdomen. The diagnosis often begins with findings of a tense and distended abdomen in the presence of high end-inspiratory airway pressures and other signs of organ dysfunction (i.e., oliguria, rising serum creatinine). Additional clinical signs consistent with abdominal compartment syndrome are a reduced cardiac output, elevated systemic vascular resistance, and elevated pulmonary capillary wedge pressure with simultaneous low or normal calculated estimates of end-diastolic volume. The standard for monitoring intra-abdominal pressure is bladder pressure measurement via intravesical technique. Bladder pressure is measured in end-expiration with the patient supine, by distending the bladder with 25 mL of sterile saline.^81,82

Surgical decompression of the abdomen is an option for established abdominal compartment syndrome with associated organ dysfunction and persistent shock with no absolute thresholds for urine output and airway pressure.⁸³ Protocols on fluid resuscitation are recommended to avoid a sustained increase in intra-abdominal pressure.⁸⁴ In addition to decompressive laparotomy for abdominal compartment syndrome, numerous medical and minimally invasive therapies have been proposed such as sedation and analgesia for anxiety relief and brief trials of neuromuscular blockade as temporizing measures. Body positioning and colonic/nasogastric decompression are also suggested noninvasive treatment options.^85–87 Patients with abdominal compartment syndrome may have ascites and drainage of fluid with various catheters can be tried before performing decompressive laparotomy as a less invasive alternative. A common factor among all cases of abdominal compartment syndrome seems to be the use of aggressive crystalloid resuscitation causing resuscitation injury. Use of excessive crystalloid resuscitation is discouraged in DCR and studies show decreased rates of abdominal compartment syndrome in association with decreased rates of crystalloid resuscitation.⁶¹ Attempts to achieve “supranormal” endpoints (cardiac index of >4 L/min/m² or oxygen delivery index of >600 mL/min/m²), while theoretically desirable, have not been shown to be effective as this often requires excessive resuscitation volumes that contribute to abdominal compartment syndrome.⁸⁸ As resuscitation has changed with DCR, the incidence of abdominal compartment syndrome has been decreasing. In the trauma setting, abdominal compartment syndrome has been disappearing rapidly but in the general surgery setting, it is more common. Sepsis as a source of inflammation can create abdominal compartment syndrome even when resuscitation injury is minimized. Source control of the bacterial contamination is the best treatment for abdominal compartment syndrome. End organ failure with microcirculatory disruption and endothelial leak is another source of the syndrome.

TRAUMATIC BRAIN INJURY

5 TBI remains one of the leading causes of injury-related deaths. Initial management of TBI includes hyperosmolar resuscitation, intracerebral pressure (ICP) monitoring, and prevention of hypoxia and hypotension.

Secondary Brain Injury

Injury prevention and better safety are the mainstays for primary brain injury. After the initial insult, the main goal is to prevent or minimize secondary brain injury. Secondary brain injury can be influenced by a cascade of inflammatory responses, occurring as a consequence of the primary injury. Secondary brain injury is also exacerbated by potentially preventable factors such as hypotension, hyperthermia, seizure activity, hyperglycemia, and hypoxemia.

Hypotension at any point (even brief time periods) is associated with a doubling of mortality in patients with severe TBI.^89,90 Although hyperventilation temporarily reduces intracranial pressure and may help to prevent herniation, evidence suggests that excessive hyperventilation may be harmful for patients with TBI. Therefore, brief hyperventilation is only recommended in order to reduce ICP temporarily until surgical decompression can be performed.

Imaging in Traumatic Brain Injury

Computed tomography (CT) scanning remains an essential tool in the initial evaluation and postinjury management of TBI. Patients with mild and moderate TBI who are examinable and not on any anticoagulant medications can be monitored by clinical examination without the need for routine serial CT scans of the head.^91–93 With technologic improvements made to the CT scanners around the world, the incidence of TBI has been increasing. Small insignificant intracranial radiologic findings are the main reason for the increase in the diagnosis of TBI. With increased awareness of mild TBI and with the increased attention to mild TBI with posttraumatic stress disorder, CT scans of the head are being ordered more often and routinely. In trauma, the single most common reason for obtaining a CT scan of the head has been loss of consciousness. Thus increased screening for TBI and improved technology identifying small clinically insignificant intracranial injuries has resulted in the increase of incidence of TBI. TBI is a clinical diagnosis and not just a radiographic diagnosis. There are patients with TBI with normal CT scans of the head who have cognitive deficits as well as posttraumatic stress disorder and there are many with radiographic TBI that do not have clinical deficits. Therefore, significant deterioration in neurologic examination should be considered in the decision for whether repeat head CT scan or consultation of a neurosurgeon is needed. CT scans and neurosurgical consultations are valuable resources with costs to the health care system as well as to the patient. The use of routine repeat head CT and neurosurgical consultations should be restricted to patients on prehospital antiplatelet and anticoagulants, and those with depressed skull fractures. A Brain Injury Guideline has been developed which helps guide when the resources should be used (Table 32-3).^94–96

Progression of lesions on repeat head CT can promptly identify patients who require more invasive neurosurgical interventions and medical therapies. Routine repeat head CT is still recommended for those patients with GCS less than 8 and for those who do not have a reliable clinical examination such as patients that are under general anesthesia or patients that are in the ICU under sedation.

Coagulopathy in TBI

A decreased platelet count (less than 100,000/μL) and/or impaired platelet function after TBI is associated with progression of intracranial hemorrhage, need for neurosurgical intervention, and mortality.^97–99 Admission INR greater than 1.5 also predicts progression of intracranial hemorrhage. The treatment of coagulopathy after TBI is multipronged due to the complexity of the problem. Therapeutic strategies should focus on the treatment of the primary cause and controlling the progression of intracranial bleeding. fresh frozen plasma, platelets, recombinant factor VII, and PCC can be used in various combinations to improve outcomes.^100,101

Antiplatelet and Anticoagulation Therapy in TBI

6 Antiplatelet medications, anticoagulants, and nonsteroidal anti-inflammatory drugs are among the most frequently encountered medications in TBI patients, especially the elderly. Existing evidence shows an increased risk of progression of intracranial bleeding in patients on high-dose aspirin and clopidogrel, whereas low-dose aspirin and ibuprofen do not cause progression on CT or neurologic examination.^102–104 A platelet count of less than 135,000/μL in patients on antiplatelet therapy is predictive of both radiographic and clinical worsening.¹⁰⁵ Reversal of the effect of anticoagulants and antiplatelets is suggested to improve the outcomes.

Use of newer oral anticoagulants like direct thrombin inhibitors and factor Xa inhibitors is increasing. Despite their safety advantage over coumadin, concerns for progression of intracranial bleed and adverse outcomes exist in TBI patients.^106,107 No specific reversal agents are yet available for newer oral anticoagulants. Oral charcoal administration, hemodialysis, PCC, and rFVIIa have shown some efficacy in the reversal of these agents.^108–113

Seizure Prophylaxis after TBI

Posttraumatic seizures increase the cerebral metabolic rate, ICP, and may cause secondary brain injury. Seizures after TBI are associated with worse outcome. It is not known if poor outcomes are due to underlying injury which is associated with posttraumatic seizures or if posttraumatic seizures exacerbate injury. Studies have shown that prophylactic therapy with phenytoin during the first 7 days after injury is effective in reducing the number of early posttraumatic seizures.¹¹⁴ Long-term use of prophylactic anticonvulsants has not been shown to be of benefit. Anticonvulsant prophylaxis is not indicated for late onset posttraumatic seizures (after 7 days). Because phenytoin is cumbersome to use, as it requires frequent drug-level monitoring and can lead to neurodepressive side effects, the use of levetiracetam has become common. However, recent studies have shown that the seizure rate after TBI is very low and the use of levetiracetam has not equated to reduced seizures.¹¹⁵

Penetrating Brain Injury

Gunshot wounds to the brain are the most lethal of all firearm injuries. Aggressive postinjury resuscitation is associated with significant improvement in both survival and organ donor eligibility.^116,117 Early aggressive management includes blood products, hyperosmolar therapy, vasopressors, and/ or PCC. Early aggressive T4 (levothyroxine) therapy and correction of coagulopathy increases the organ donation rate in nonsurvivable patients.^116,118

NUTRITIONAL AND METABOLIC SUPPORT

Stay updated, free articles. Join our Telegram channel

Join