Priorities in the ICU Care of the Adult Trauma Patient

Philip S. Barie

Soumitra R. Eachempati

I. Goals of Care

Fundamental goals of intensive care unit (ICU) management of the critically injured patient include early restoration and maintenance of tissue oxygenation, diagnosis and treatment of occult injuries, and prevention and treatment of infection and organ dysfunction.
Most early deaths from trauma occur from traumatic brain injury (TBI), exsanguination, or refractory shock, and are largely not preventable. Late deaths from multiple organ dysfunction syndrome (MODS) may be minimized by effective resuscitation, prevention or prompt recognition and treatment of hospital-acquired infection, identification and treatment of all injuries, and avoidance of error. Errors of surgical technique and critical care management may contribute to one-half of preventable trauma deaths.
Optimal trauma care in the ICU is provided by a multi-professional team of physicians, nurses, pharmacists, therapists, and others. An ICU environment where communication, patient safety, and infection control are innate to the culture creates conditions for the optimal care of the patient.

II. ICU Admission Criteria.

The decision to admit the trauma patient to an ICU depends on the patient’s age, injury severity, co-morbid conditions, and availability of both ICU beds and intermediate-level care (“step-down”) beds (Table 34-1).

III. Phases of ICU Care

Early phase (<24 hours). Primary concerns include shock, respiratory failure, intracranial hypertension, and the identification of occult injuries; diagnosis and treatment occur simultaneously.

Repetition of the primary survey. Repetition of the evaluation of the trauma patient is essential, beginning with the primary survey and followed by repeated secondary surveys.

Airway. The airway should be secured and positioned appropriately.
Breathing. Minute ventilation (V_E) must be adequate. The inspired oxygen concentration (FiO₂) must be adequate to maintain arterial oxygen saturation (SaO₂) above 90%.
Circulation. Intravenous access must be adequate for the administration of fluids, blood, and blood products sufficient to support the circulation, gas exchange, and hemostasis. If adequate peripheral venous access is unobtainable, insert a central venous catheter. If the circulation cannot be monitored adequately by heart rate, blood pressure, and urine output, assess acid–base status and consider non-invasive (e.g., esophageal Doppler probe, thoracic impedance or bioreactance, or echocardiography) or invasive hemodynamic monitoring.

Disability. The Glasgow Coma Scale (GCS) score is compared with initial observations for signs of neurologic deterioration or improvement. All limbs are re-inspected for deformity, abnormal or absent movement, abnormal sensation (if possible), and signs of vascular insufficiency. The level of sedation is assessed, and short-acting sedatives are given by titration to a validated sedation scale (e.g., Ramsay) to protect the patient from self-harm.

Table 34-1 Injuries and Post-injury Problems that Require ICU Admission

Injuries

– Multi-system trauma
– Severe TBI (GCS ≥8)
- Lesser TBIs of anticoagulated patients (e.g., aspirin, warfarin)
– Cervical spinal cord injury
– Severe pulmonary contusion, flail chest
– Facial or neck trauma with threatened airway
– Repaired major vascular injuries
– Pelvic fracture with retroperitoneal hemorrhage or bony instability
– Blunt cardiac trauma with dysrhythmia or hypotension
– Crush injuries
– Severe burns (>20% TBSA, facial burns)
– Smoke inhalation
– Isolated high-grade solid organ injuries (grade III–V liver or spleen)

Problems

– Respiratory failure requiring mechanical ventilation
– Ongoing shock or hemodynamic instability
– Massive blood or fluid resuscitation
– Base deficit (>5)
– Hypothermia
– Seizures
– Pregnancy

Post-traumatic Injuries or Problems Suitable for Intermediate Care Monitoring^a

– Isolated liver or spleen injuries (especially grade I–II)
– Uncomplicated blunt anterior chest trauma
– Isolated multiple rib fractures or pulmonary contusion with adequate oxygenation and ventilation
– Isolated thoracic spinal cord injury with stable hemodynamics
– Lesser TBI (GCS 9–14)
– Minor injuries with risk of alcohol withdrawal syndrome
– Isolated vascular injuries to the extremities

^aPatients ≥65 years of age with co-morbidity or any hemodynamic instability should be considered for ICU admission.
ICU, intensive care unit; TBI, traumatic brain injury; GCS, Glasgow Coma Scale score; TBSA, total body surface area.

Environmental. Core body temperature is determined and hypothermia (T <35°C) is treated or prevented.

Repetition of the secondary survey. Examination of laboratory and radiologic data are reviewed to identify missed injuries, most often of the spinal column or spinal cord, bone or ligament injuries of the extremities, and injuries of the thoracic aorta, heart, or diaphragm. Seek abdominal compartment syndrome by urinary bladder pressure measurement in the appropriate clinical context.

Intermediate phase (24 to 72 hours). From 24 to 72 hours post-injury, all injuries should have been identified, but resuscitation may be ongoing. Management of respiratory failure and intracranial hypertension following TBI may be particularly active during the first 72 hours.
Late phase (>72 hours). Approximately one-half of critically injured patients remain in the ICU for more than 72 hours. Priorities are defined by injury severity, the prevention of complications, and management of complications that do arise. Prolonged ICU care carries risks of physical de-conditioning, hospital-acquired infection (Chapter 14), pressure ulcers, and organ dysfunction.
Recovery phase. In this phase (regardless of timing), patients are liberated from life support and prepared for the transition to lower levels of care and eventual hospital discharge. At this time, disabilities may become apparent, and physical therapy, assessment of long-term rehabilitation needs and potential and psychological support of patient and family are crucial. Approximately 4% of injured patients remain in the ICU for more than 28 days, but the chance of survival to hospital discharge is still >50%.

IV. Resuscitation and Initial Management

To maximize chances for survival, treatment priorities must focus on resuscitation from shock (defined as O₂ delivery [DO₂]) inadequate to meet O₂ demand (O₂ consumption [VO₂]), including appropriate fluid resuscitation and rapid, definitive hemostasis. Inadequate oxygenation results in anaerobic metabolism and tissue acidosis. The depth and duration of shock leads to a cumulative oxygen “debt” that may not be “repayable” if profound or delayed. Traditional markers of “successful” resuscitation include normalization of blood pressure, heart rate, and urine output. However, occult, ongoing hypoperfusion and lactic acidosis (i.e., compensated shock) may persist despite normalization of vital signs. Prolonged hypoperfusion (and subsequent oxidant stress from re-perfusion) are associated with organ dysfunction and death.

Endpoints of resuscitation. When the traditional parameters remain abnormal (i.e., uncompensated shock), the need for additional resuscitation is clear. However, even after normalization, up to 85% of critically injured patients have evidence of hypoperfusion, whether metabolic acidosis, a persistent base deficit, or an elevated serum lactate concentration. Rapid recognition and reversal of this state are crucial to minimize the risk of organ dysfunction or death. Evidence-based guidelines for determining endpoints of resuscitation are provided in Table 34-2.
Hemostasis in resuscitation. Resuscitation from hemorrhagic shock is impossible without hemostasis. Withholding of fluid resuscitation may lead to exsanguination, whereas aggressive fluid resuscitation may raise blood pressure excessively or dilute clotting factors, leading to increased bleeding. Permissive hypotension may be beneficial until hemorrhage control occurs.

Classification of shock (Chapter 5)

Hypovolemic shock. Hypovolemia is the usual cause of hypotension or occult hypoperfusion in the early post-injury period, and may be caused by incomplete resuscitation, ongoing third-space fluid losses, or active hemorrhage. Failure to respond to volume replacement should stimulate a search for ongoing hemorrhage (the most likely cause) or other causes of shock.
Obstructive shock is a possible cause (e.g., cardiac tamponade, tension pneumothorax, abdominal compartment syndrome [ACS; abdominal hypertension from packing or over-resuscitation leading to decreased venous return], ventilation with high levels of positive end-expiratory pressure [PEEP], or rarely tension pneumopericardium) that should be sought.
Cardiogenic shock. Cardiogenic shock after trauma is usually caused by blunt myocardial injury, but the possibility of myocardial ischemia/infarction must be considered among older trauma patients. Blunt myocardial injury is excluded by an entirely normal electrocardiogram (ECG); with a normal ECG, cardiac enzyme determination is superfluous. Right ventricular function can be impaired by blunt myocardial injury, and is sensitive to volume repletion, followed by inotropic support if cardiac output is still inadequate. Cardiac valve injury is uncommon in patients surviving severe chest trauma, but may require immediate surgical repair. Suspect underlying valvular heart disease (e.g., aortic stenosis, mitral insufficiency) in older trauma patients with cardiogenic shock.

Neurogenic shock. Neurogenic shock can occur with spinal cord injury (or rarely with brain death). Affected spinal cord injury patients are usually paraplegic or quadriplegic. Autonomic dysfunction (loss of sympathetic tone) leads to vasodilation, a form of distributive shock (defined in the next paragraph). Once euvolemia is ensured with volume replacement, the treatment is primarily with a vasoconstrictor (e.g., phenylephrine). Hemodynamic instability may be prolonged, and vasopressor therapy may be required for days to weeks.

Table 34-2 Guide lines for Endpoints of Resuscitation by the Eastern Association for the Surgery of Trauma

Recommendations Regarding Stratification of Physiologic Derangement
Level 1
1. Standard hemodynamic parameters do not quantify adequately the degree of physiologic derangement in trauma patients. The initial base deficit or lactate concentration can be used to stratify patients with regard to the need for ongoing fluid resuscitation, including red blood cell concentrates and other blood products, and the risks of organ dysfunction and death.
2. The ability of a patient to attain supranormal O₂ delivery parameters correlates with an improved chance for survival.
Level 2
1. The time to normalization of base deficit and lactate concentration is predictive of survival.
2. Persistently high or worsening base deficit may be an early indicator of complications (e.g., ongoing hemorrhage, abdominal compartment syndrome).
3. The predictive value of the base deficit may be limited by ethanol intoxication or a hyperchloremic metabolic acidosis, as well as administration of NaHCO₃.
Level 3
1. Right ventricular end diastolic volume index (RVEDVI) measurement may be a better indicator of adequate volume resuscitation (preload) than CVP or pulmonary artery occlusion pressure (PAOP).
2. Measurements of tissue (subcutaneous or muscle) O₂ or CO₂ concentration may identify patients who require additional resuscitation and are at risk for organ dysfunction and death.
3. Serum HCO₃ concentration may be substituted for base deficit.
Recommendations Regarding Improved Patient Outcomes
Level 1
1. There are insufficient data to formulate a Level 1 recommendation.
Level 2
1. The optimal algorithms for fluid resuscitation, blood product replacement, and the use of inotropes or vasopressors have not been determined.

(From Tisherman SA, Barie PS, Bokhari F, et al. Clinical practice guideline: Endpoints of resuscitation. J Trauma 2004;57:898–912.)

Distributive shock. Distributive shock is caused prototypically by sepsis and may develop late after injury. However, severely injured patients can demonstrate early a hyperdynamic state, similar to systemic inflammatory response syndrome (SIRS). A hyperdynamic circulation (cardiac index [CI] >3 L/min/m²), hypotension, and low systemic vascular resistance (SVR <900 dyne/s/cm⁵) are characteristic.

V. Monitoring and Data Interpretation

Additional monitoring is necessary to optimize DO₂ when clinical uncertainty exists, or when refractory hemodynamic instability or other factors confound the clinical assessment of the response to therapy. Remember that such instability is due most commonly to ongoing blood loss.

Blood testing. Blood sampling is essential for monitoring, but can be excessive. Blood removed for testing can exceed 70 mL/day.
- Non-invasive hemodynamic monitoring, adoption of guidelines for diagnostic evaluation, and point-of-care (POC) testing can reduce blood testing while providing optimal patient care.
- Glucose monitoring is the most prevalent example of POC testing, considering that targeted glycemic therapy to avoid excessive hyperglycemia reduces the risk of nosocomial infection, organ dysfunction, and death following trauma.
Blood gas monitoring. Blood gas analyzers measure directly the partial pressures of oxygen (pO₂) and carbon dioxide (pCO₂), and blood pH. SaO₂ is calculated from the pO₂, assuming a normal P₅₀ (SaO₂ is 50% at a pO₂ of 26.6 mm Hg), and normal hemoglobin structure. Some analyzers incorporate co-oximetry to measure hemoglobin concentration directly. Bicarbonate and base excess are calculated from the pH and pCO₂.
Electrocardiography. ECG is standard; avoidance of tachycardia, especially in older patients, reduces morbidity. Tachycardia may be due to hypovolemia, hemorrhage, inadequate analgesia, or other causes. Tachycardia is inherently dangerous because of the risk of myocardial ischemia; however, routine ECG monitoring (four limb leads) is insensitive for detection of acute ST–T wave changes, which portends ischemia. A 12-lead ECG should be performed on patients suspected of myocardial ischemia, electrolyte abnormalities, blunt cardiac injury, or pericardial pathology.
- Perioperative mortality is decreased when beta-adrenergic blockade is started preoperatively before major elective general surgery in older patients, and recent data suggest the same to be true for elderly trauma and burns patients. Even if beta-blockade cannot be started before an emergency operation (e.g., uncorrected hypovolemia), it should be started as soon as possible thereafter, provided underlying hypovolemia, pain, or sepsis are controlled.
Pulse oximetry. Pulse oximetry is reasonably accurate over the range of SaO₂ between 70% and 100%, but less accurate below 70%. Pulsatile blood flow is essential for accurate pulse oximetry; reliable data can be obtained from the finger, earlobe, or forehead.
- Hypothermia, hypotension, hypovolemia, peripheral vascular disease, vasopressor therapy, ambient light, or motion artifact may cause inaccuracy.
- An elevated carboxyhemoglobin concentration will elevate S_pO₂ falsely because reflected light is absorbed at the same wavelength as oxyhemoglobin.

Temperature. The most reliable temperature measurement is core temperature obtained by an esophageal probe or pulmonary artery catheter (PAC) thermistor. Hypothermia may contribute to metabolic acidosis, vasoconstriction, myocardial dysfunction, arrhythmias, electrolyte imbalances, altered pharmacokinetics and drug metabolism, platelet dysfunction, and an increased risk of surgical site infection. Hypothermia may develop from exposure in the field, from disease (e.g., sepsis, hypothalamic injury), or under anesthesia. Induced, controlled hypothermia is an adjunct to several heart, brain, and spinal procedures and after cardiac arrest, but it is not beneficial after TBI or multi-system trauma.

Fever. Fever (temperature exceeding the hypothalamic “set point”) or hyperthermia (a reset hypothalamic set point) will increase heart rate, O₂ consumption, and insensible fluid loss. Postoperative fever is not invariably dangerous. Fever has salutary effects on host defenses, and in non -neurologically injured patients should not be suppressed unless the patient has symptomatic myocardial ischemia or other serious manifestations.
- One-half of episodes of postoperative fever are of non-infectious origin (Table 34-3); in the first 48 hours after surgery, the only consequential infectious causes of fever (other than an infection that prompted surgical intervention for source control) are surgical site infections caused by streptococci or clostridial organisms.
- Physical examination including inspection of ALL wounds is mandatory, but laboratory evaluation of fever is usually not helpful until after the third postoperative day. Thereafter, the differential diagnosis of postoperative fever is extensive (Tables 34-3 and 34-4).
- Suppress elevated temperature in TBI patients to <38°C when possible; this may improve outcomes.

Hypothermia. Anticipate hypothermia in injured patients with exposure or shock, massive volume resuscitation, or prolonged surgery (Chapter 42). Patients who undergo damage control operations (see Chapter 6) are admitted to the ICU from a truncated operative procedure for secondary resuscitation, normalization of body temperature, and correction of coagulopathy. The crucial temperature of injured patients that influences mortality profoundly appears to
be approximately 32°C, but substantial cardiac and hematologic morbidity is possible whenever the core body temperature is <35°C.

Table 34-3 Non-i nfectious Causes of Fever in the ICU

Acute respiratory distress syndrome (ARDS)
Adrenal insufficiency
Atelectasis
Blood transfusion
Cardiac arrest
Gastrointestinal hemorrhage
Ischemia/infarction
Hemorrhage/hematoma-parenchymal
Brain
Lung
Retroperitoneum
Soft tissue
Solid organ (liver, spleen)
Hyperthyroidism
Multiple trauma
Venous thromboembolic disease

The major complications of hypothermia are platelet dysfunction (decreased adhesion due to inhibited thromboxane synthesis), impaired cardiac function (increased afterload due to systemic vasoconstriction), and dysrhythmias (altered myocardial sensitivity to endogenous catecholamines). Clotting
factor function, which is temperature-dependent, is reduced during hypothermia.

Table 34-4 Infec tious Causes of Fever in the ICU

Blood stream infection
   Bacteremia
   Central line–associated blood stream infection
   Fungemia
Peritonitis/intra-abdominal abscess
   Anastomotic or suture line dehiscence
   Abscess of solid organ (e.g., liver, spleen)
   Biliary tract
      Acalculous cholecystitis
      Cholangitis
Pneumonia
   Empyema
Retroperitoneum
   Iliopsoas abscess
   Infected pancreatic necrosis
Sinusitis
Skin/soft tissue
   Hematoma
   Suppurative phlebitis
   Surgical site infection
   Traumatic wound infection
Urinary tract
   Cystitis
   Perinephric abscess
   Pyelonephritis

Methods used for re-warming (Chapter 42) depend on the severity of hypothermia, ongoing hemorrhage and coagulopathy, hemodynamic stability, and availability of equipment and technical support. It is easier to keep a patient warm than to re-warm, as most methods are inefficient at transferring heat.

Capnography. Capnography measures the CO₂ concentration in expired gas, most reliably in ventilated patients. The peak CO₂ concentration occurs at end-exhalation (end-tidal CO₂ [ETCO₂]), at which time ETCO₂ approximates closely the alveolar gas concentration.

Capnography can confirm successful airway intubation and monitor resuscitation and weaning from mechanical ventilation. Used with pulse oximetry, many patients can be liberated from mechanical ventilation without reliance on arterial blood gases or invasive hemodynamic monitoring.

Capnography can provide other valuable information. An ETCO₂–PaCO₂ gradient >13 mm Hg after resuscitation is associated with increased trauma-related mortality. Gradually decreasing ETCO₂ is associated with hypovolemia, whereas a sudden decrease or even disappearance of ETCO₂ is observed with a low cardiac output (Q) state, disconnection from the ventilator, or pulmonary thromboembolism (Table 34-5). A gradual increase of ETCO₂ occurs with hypoventilation; the converse is also true.

Table 34-5 Chang es in End-Tidal CO₂ (ETCO₂)

Increased ETCO₂
Decreased alveolar ventilation
   Reduced respiratory rate
   Reduced tidal volume
   Increased equipment dead space
Increased CO₂ production
   Fever
   Hypercatabolism
   Excess carbohydrate intake
Increased inspired CO₂ concentration
   CO₂ absorber exhausted
   Increased CO₂ in inspired gas
   Re-breathing of expired gas
Decreased ETCO₂
Increased alveolar ventilation
   Increased respiratory rate
   Increased tidal volume
Decreased CO₂ production
   Hypothermia
   Hypocatabolic state
Increased alveolar dead space
   Decreased cardiac output
   Pulmonary embolism (clot, air, fat)
   High positive end-expiratory pressure (PEEP)
Sampling error
   Air in sample line (no or diminished signal)
   Water in sample line (no or diminished signal)
   Inadequate tidal volume (no or diminished signal)
   Disconnection of monitor from tubing (no signal)
   Airway not in trachea (e.g., esophageal intubation) (no signal)

Near-infrared spectroscopy. Near-infrared spectroscopy (NIRS) is a non-invasive method to measure tissue pO₂ in close to real time. Analysis of the reflected light produces a measurement of tissue oxygenation (StO₂) in the skeletal muscle microcirculation. Skeletal muscle StO₂ correlates with DO₂I, base deficit, and serum lactate concentration in experimental and clinical hemorrhagic shock. Detection is most accurate for StO₂ >70%.
- In a multi-center trial, an StO₂ >75% maintained during the first hour of monitoring indicated adequate tissue perfusion, with affected patients having an 88% MODS-free rate of survival. In contrast, StO₂ <75% in the first hour was manifested by 78% of patients who eventually developed MODS and 91% of those who died.
Non-invasive cardiac output determination
- Thoracic bioimpedance. Thoracic bioimpedance derives information from electrodes placed on the anterior chest and neck to estimate Q by determining the left ventricular systolic time interval from time 1/m∼ derivative bioimpedance signals. The main drawback of thoracic bioimpedance is sensitivity to any alteration of electrode contact or positioning on the patient.
- Esophageal Doppler monitor. The esophageal Doppler monitor (EDM) device is a soft, 6 mm catheter that is placed non-invasively into the esophagus. A flow probe at the tip allows continuous monitoring of Q and stroke volume. The primary disadvantage of the EDM is that the waveform may be damped or lost entirely with only a slight positional change, rendering inaccurate readings.

VI. Invasive Monitoring

Arterial catheterization. Arterial blood pressure measurement is the simplest, most reproducible hemodynamic monitor. Although automated blood pressure cuffs are in common use in operating rooms and are suitable for periodic blood pressure measurement in stable patients, low or fluctuating blood pressure may mandate continuous monitoring via an indwelling catheter. Invasive blood pressure monitoring is indicated for prolonged operations (>4 hours), prolonged mechanical ventilation (>24 to 48 hours), unstable hemodynamics, vasopressor therapy, substantial blood loss, frequent blood sampling, or when precise blood pressure control is needed (e. g., TBI patients with low CPP, aortic dissection).
- Insertion technique. Special-purpose thin-walled catheters maintain fidelity of the waveform and minimize luminal obstruction. The radial artery at the wrist is the most common site. Patency of the collateral circulation to the hand should be confirmed before cannulation at the wrist to minimize the possibility of catastrophic tissue loss.
  - In neonates, the umbilical artery may be catheterized; intestinal ischemia is a rare complication. The axillary artery is relatively free of plaque, well collateralized at the shoulder, and easy to cannulate percutaneously.
  - A risk with axillary catheterization is cerebral embolization when flushing the line. The superficial femoral artery is not preferred because of higher risks of distal embolization and infection. The dorsalis pedis artery is accessible, but should be avoided with peripheral vascular disease, hemodynamic instability, or lower extremity trauma. The brachial artery should be strictly avoided because collateral circulation at the elbow is poor; the risk of hand or forearm ischemia from thrombosis is high.
  - Peripheral vasoconstriction during vasopressor therapy may dampen the arterial waveform. A longer catheter placed at a more central location (e.g., axillary, femoral) may restore the fidelity of the tracing. Nosocomial infection of arterial catheters is unusual if basic tenets of infection control are honored and femoral artery catheterization is avoided.
Central venous pressure monitoring. The central venous pressure (CVP) is a function of circulating blood volume, venous tone, and right ventricular function. The CVP measures right ventricular filling pressure as an estimate of intravascular volume status; aside from extreme values (<6 mm Hg or >15 mm Hg), the absolute CVP is less helpful than the trend of CVP response to volume. Strict adherence to
asepsis, full barrier precautions, and adherence to the principles of infection control are crucial to avoid central line–associated blood stream infection.
- Insertion technique. Central venous access can be obtained using the basilic, femoral, external jugular, internal jugular, or subclavian veins.
  - In the ICU, the internal jugular site is popular because of ease of accessibility, a high success rate of cannulation, and relatively few complications.
  - The subclavian site is the most technically demanding, having the highest rate of pneumothorax (1.5% to 3.0%), but the lowest infection rate.
  - The femoral vein site is least preferred in the ICU because of the highest complication rate, despite the relative ease of catheter placement. The risks of arterial puncture (9% to 15%), infection, and venous thromboembolism (VTE) are highest for femoral vein catheterization.
  - Overall complications are comparable for internal jugular and subclavian vein cannulation (6% to 12%), and higher for femoral vein cannulation (13% to 19%).
- Full barrier precautions are mandatory. The operator dons cap, mask, eye protection, and a sterile gown and gloves before preparing the patient’s skin (2% chlorhexidine gluconate is associated with fewer infections than 10% povidone-iodine) and draping the patient completely with a full-bed drape.
Pulmonary artery catheterization. Data from PACs are used mainly to determine Q and preload, which is most commonly estimated by the PA occlusion pressure (PAOP). Other parameters calculated from Q include SVR and pulmonary vascular resistance (PVR), and right and left ventricular stroke work (RVSW, LVSW).
- Data interpretation. Normally, PAOP approximates left atrial pressure, which in turn approximates left ventricular end-diastolic pressure (LVEDP), a reflection of left ventricular end-diastolic volume (LVEDV). The LVEDV represents preload, which is the actual target parameter.
  - Many factors cause PAOP to reflect LVEDV inaccurately, including mitral stenosis, high levels of PEEP (>10 cm H₂O), and changes in left ventricular compliance (e.g., myocardial infarction, pericardial effusion, or increased afterload). Inaccurate readings may result from balloon overinflation, catheter malposition, alveolar pressure exceeding pulmonary venous pressure (PEEP ventilation), or pulmonary hypertension (which may make PAOP measurement difficult, if not hazardous). Elevated PAOP occurs in left-sided heart failure. Decreased PAOP occurs with hypovolemia or decreased preload.
  - Mixed venous oxygen saturation (S_mvO₂) may be measured, although superior vena cava S_vO₂ via a CVP catheter may provide data of comparable utility. Causes of low S_mvO₂ include anemia, pulmonary disease, carboxyhemoglobinemia, low Q, and increased VO₂. The SaO₂: (SaO₂ − S_mvO₂) ratio determines the adequacy of DO₂. Ideally, the P_mvO₂ should be 35 to 40 mm Hg, with an S_mvO₂ of about 70%. Values of P_mvO₂ <30 mm Hg are critically low.
- Clinical use
  - Evidence is lacking that PAC use decreases morbidity or mortality. Some retrospective data even suggest that PAC use is associated with increased mortality.
  - Ventilation of patients with acute respiratory distress syndrome (ARDS) on high levels of PEEP has been monitored commonly via PAC. The application of PEEP can decrease venous return markedly, and therefore Q, in a short time period; maintenance of Q is important to maintain ventilation –perfusion (V/Q) matching. However, the ARDS net investigators demonstrated no difference in outcome of patients with acute lung injury (ALI)/ARDS when managed by PAC or CVP. PACs may still be useful in select circumstances, such as cardiomyopathy, shock of various etiologies, oliguric acute kidney injury, or an unpredicted poor response to fluid therapy. Critically ill patients who require inotropic agents despite large-volume fluid resuscitation may also benefit from monitoring by PAC.
- Complications. Complications common to PACs include infection (2% to 5%), hemo- or pneumothorax (2% to 5%), migration (5% to 10%), arrhythmia (10% to 15%), and hemorrhage (0.2%). Less frequent complications include catheter knotting, pulmonary infarction, cardiac or PA perforation, valvular injury, and endocarditis. A devastating complication is PA rupture, which occurs in fewer than 0.1% of cases, during insertion or during routine determination of PAOP, and is often fatal. Distal migration of the PAC within the PA increases the risk of rupture dramatically, and argues for routine daily bedside chest radiography for all patients with an indwelling PAC.
Intracranial pressure (ICP) monitoring. Monitoring of ICP is common monitoring in patients with severe TBI (GCS ≤ 8). In TBI, these devices facilitate “optimized” CPP above 60 mm Hg, although no outcome himan show a benefit for ICP monitoring in patients with TBI.
- The intra-ventricular or “ventriculostomy” catheter can also drain cerebrospinal fluid (CSF) and thereby decrease elevated ICP. However, ventriculostomy is the most invasive method of ICP monitoring, and poses the highest infection risk (∼8%). Despite the high risk of infection with ventriculostomy, neither prolonged antibiotic prophylaxis nor regular replacement of the catheter at 5- to 7-day intervals reduces the risk.

VII. Missed Injuries

However diligent the assessment in the ED, it is inevitable that some injuries will not be identified until the patient is in the ICU. An altered sensorium and the inability to make a complaint referable to the injury is a common reason, as is prior exigency of managing another life-threatening injury. Extremity fractures and dislocations are the most commonly missed injuries. The most serious missed injuries involve the spinal column, major cardiovascular structures, or hollow viscus.
Missed injuries are discovered by vigilance in the ICU, at a time when stabilization and treatment can still result in a good outcome. For patients with multiple severe injuries, repetition of the secondary survey upon ICU admission and serially thereafter is a prudent and relatively high-yield strategy.

VIII. Prophylaxis

Cardiovascular. Beta-adrenergic blockade, begun preoperatively and continued for approximately 7 days thereafter, reduces the risk of perioperative myocardial infarction and death among elderly patients undergoing major non-cardiac surgery and in trauma patients. However, tachycardia is an important vital sign in the evaluation of the injured patient, particularly with respect to the presence of hypovolemia or pain. Blunting the heart rate response could be deleterious if recognition of such underlying conditions is impaired. Administration of beta-blockers to patients with severe TBI reduces mortality from injury by 50% to 70%, and can decrease catabolism in children with burns.

Stress-related gastric mucosal hemorrhage

Ischemia-reperfusion injury of the stomach is associated with disruption of the mucus blanket, back-diffusion of hydrogen ions, reduced buffering capacity, and ultimately gastric mucosal injury. Gastric mucosal injury may be exacerbated by lack of the trophic stimulus associated with enteral feeding. Mucosal injury has many manifestations, ranging from asymptomatic to overt upper gastrointestinal hemorrhage. The incidence has been reduced markedly by chemoprophylaxis and early nutritional support, to approximately 4% among critically ill patients. Patients at highest risk are those who receive mechanical ventilation for >48 hours, or who are coagulopathic. Trauma patients at increased risk include those with TBI or burns.

Agents for prophylactic use include H₂-histamine receptor antagonists, proton-pump inhibitors, and (rarely) sucralfate. Antacids are not recommended due to cumbersome administration and increased risk of pulmonary aspiration. H₂-antagonists appear to have a lower incidence of overt bleeding (but not
occult bleeding) than sucralfate. No class I data support the use of proton-pump inhibitors for prophylaxis, despite widespread use.

Table 34-6 Risk Factors for Venous Thromboembolism after Trauma: Analysis of 1,602 Episodes from the National Trauma Data Bank

Parameter	Odds ratio	95% confidence interval
Univariate Analysis
Age > 39 y	2.29	2.07–2.55
Pelvis fracture	2.93	2.01–4.27
Lower extremity fracture	3.16	2.85–3.51
Spinal cord injury with paralysis	3.39	2.41–4.77
TBI	2.59	2.31–2.90
Mechanical ventilation >3 d	10.62	9.32–12.11
Injury to major vein	7.93	5.83–10.78
Blood pressure <90 mm Hg on admission	1.95	1.62–2.34
Major surgical procedure	4.32	3.91–4.77
Multi-variable Analysis
Age >39 y	2.01	1.74–2.32
Lower extremity fracture	1.92	1.64–2.26
TBI	1.24	1.05–1.46
Mechanical ventilation >3 d	8.08	6.86–9.52
Injury to major vein	3.56	2.22–5.72
Major surgical procedure	1.53	1.30–1.80
(From Knudson MM, Morabito D, Paiment GD, et al. Use of low molecular weight heparin in preventing thromboembolism in trauma patients. J Trauma 1996;41:446–459.)