CRITICAL CARE MANAGEMENT (also see Chapter 74 and Chapter 75 )

Mechanical Ventilation after Trauma

Research has delineated many of the etiologies of acute lung injury and ARDS. Classic risk factors associated with trauma are listed in Table 63-18 .^{[231] [232] [233]} Recent studies have further clarified the role that mechanical ventilation plays in these pathologies. It is now apparent that inappropriate ventilatory strategies can lead to lung injury.^[234] A patient who has suffered a traumatic injury is at increased risk for several reasons.

Physiologic Changes

After injury, the patient is immobilized in the supine position on a long backboard and may remain in this position for several hours during prehospital transport and initial diagnostic workup. Dependent atelectasis is seen early in trauma patients as a result of these positioning restrictions. Sedation and analgesia further exacerbate atelectasis because of cephalad movement of the diaphragm into the thoracic cavity and compression of dorsal/dependent lung regions. General anesthesia exacerbates this problem, and the addition of neuromuscular blockade worsens it further. ^[235] Obesity will compound atelectasis because of marginal baseline functional residual capacity. In patients with rib fractures, "splinting" as a result of pain will lead to atelectasis and subsequent hypoxemia. Pulmonary contusions, if severe, can be life-threatening early in the hospital course, and the disruption in pulmonary integrity may be exacerbated by the need for massive blood and crystalloid replacement, thus adding further insult to the already "leaky" capillaries and parenchyma.

Invasive Mechanical Ventilation

It is now recognized that mechanical ventilation can initiate lung injury. Pathologic analyses from animal studies that induce pulmonary damage to simulate acute lung injury or ARDS cannot be distinguished from the alveolar damage occurring after studies that use mechanical ventilation strategies to induce injury. ^[236] High peak inspiratory pressures and low PEEP settings can lead to inflammatory processes in the lung that disseminate throughout the body and eventually cause MOSF. Acute lung injury results in an alteration in lung micromechanics that leads to uneven distribution of ventilation.^[237] Uneven distribution of ventilation results in a chaotic pattern of pressure and volume changes as the lung inflates and deflates.^[238] Alveolar instability leads to dyssynchronous recruitment followed by derecruitment during cyclic ventilation. The heterogeneity of lung units in acute lung injury results from multiple forces that create a range of opening and closing pressures. The net result is nonuniform distribution of ventilation, which potentiates alveolar stress failure and ultimately affects gas exchange. Overdistention is more likely to occur in healthier, nondependent regions where the bulk of ventilation is delivered. Shear forces develop in dependent lung regions as airspaces are cyclically recruited and derecruited. The early stages of ventilator-associated lung injury develop at commonly used airway pressures (transalveolar pressure >35 cm H₂ O) in animals

TABLE 63-18 -- Risk factors for development of acute respiratory distress syndrome after trauma

Old age

Preexisting physiologic impairment (diabetes, acquired immunodeficiency syndrome, malignancy, etc.)

Direct pulmonary or chest wall injury

Aspiration of blood or stomach contents

Prolonged mechanical ventilation

Severe traumatic brain injury

Spinal cord injury with quadriplegia

Massive transfusion

Hemorrhagic shock

Occult hypoperfusion

Wound or body cavity infection

2486

PEEP should be applied to sustain recruitment of as many alveoli as possible in order to maximize gas exchange and improve the distribution of ventilation. Levels of PEEP required to maintain end-expiratory lung volume and limit shear forces may be substantial (>20 cm H₂ O). Although the exact level of PEEP needed to eliminate cyclic airway closure and eliminate shear forces completely is unknown, recent data suggest that within an acutely injured lung, a spectrum of airway closing and opening pressures exists. Several researchers have published data showing that ventilator management with low tidal volumes (6 to 8 mL/kg), limiting distending pressures (transpulmonary or plateau pressure <35 mm Hg), and setting PEEP above the lower inflection point on the pressure-volume curve may decrease mortality, reduce ICU length of stay, and decrease ventilator days.^{[239] [240] [241]} Recommendations for ventilator management, culled from several randomized, prospective trials, are suggested in Table 63-19 . These recommendations refer to both intraoperative and ICU locations. For patients with respiratory failure who require surgery, if the ventilator settings in the ICU exceed the capability of the OR ventilator, the patient should be taken to the OR on the ICU ventilator and remain on the ICU ventilator for the surgical procedure. Alternatively, the procedure can be performed at the bedside in the ICU.

The combination of traumatic lung injury, fluid resuscitation, and supine positioning results in alveolar damage, alveolar collapse (derecruitment), worsening gas exchange, and declining compliance ( Fig. 63-13 ). A shift of the pressure-volume curve to the right, seen with worsening compliance, requires adjustments of the ventilator to prevent both low-end shear and high-end overdistention. As ARDS develops, less of the lung parenchyma is recruitable, compliance worsens, and the physician is often left with progressively increasing peak airway pressures in an attempt to oxygenate the patient. Newer modalities, such as airway pressure release ventilation (APRV), negate the need for paralysis or deep sedation by allowing spontaneous breathing throughout the respiratory cycle. Spontaneous breathing significantly improves ventilation-perfusion matching, cardiac output, CO₂ clearance, and renal blood flow.^[242]

An investigation comparing two modes of ventilation studied 18 patients with acute lung injury maintained for 24 hours on volume-controlled inverse ratio ventilation and then for 24 hours on APRV.^[243] Eleven of the subjects were multiple trauma patients with lung contusions or ARDS. In addition to confirming previous study findings of a significant decrease in peak inspiratory pressure (P < .01), a further decrease in peak inspiratory pressure was seen after 24 hours (P < .05), probably because of effective recruitment over time. The alveolar-arterial gradient and venous admixture also improved with APRV (P < .01). This study was the first to report a decrease in the use of sedative agents during APRV. Patients treated by inverse ratio ventilation required deep sedation, but those treated by APRV were comfortable with much lower

TABLE 63-19 -- Recommendations for ventilator settings in acutely injured patients

Tidal volumes of 6–8 mL/kg

PEEP higher than the lower inflection point (in the most critically ill, those with massive volume resuscitation, ALI, or ARDS, a minimum of 10–15 cm H2 O is recommended)

Limit peak/plateau pressure to <40/35 cm H2 O (patients with burn injuries, morbid obesity, or massive volume resuscitation may require higher pressure to adequately distend the lung because much of the measured distending pressure is actually needed to lift the restricted chest wall away from the thoracic cavity)

Adjust the I:E ratio and respiratory rate as needed to achieve the above recommendations

Wean FIO2 to obtain a PaO2 of 80–100 (or oxygenation saturation of 93%–97%)

Convert to pressure-controlled inverse-ratio ventilation if necessary or transfer the patient to an ICU ventilator

ALI, acute lung injury; ARDS, acute respiratory distress syndrome; ICU, intensive care unit; I:E ratio, inspiratory-to-expiratory ratio; PEEP, positive end-expiratory pressure.

doses and were not given paralytics. APRV has also been studied in trauma patients with ARDS, again with findings of decreased peak inspiratory pressure and higher airway pressure, without derangements in gas exchange.^[244]

Noninvasive Mechanical Ventilation

NIPPV may be an alternative to endotracheal intubation in certain trauma patients (i.e., those without facial injuries, with a mental status that permits both cooperation and the ability to protect the airway, and with a low risk of aspiration). Either a nasal mask or a facemask may be used. NIPPV is a treatment modality used most commonly in children and in patients with chronic respiratory diseases.

Figure 63-13 Computed tomographic chest scan of a recently injured trauma patient showing profound consolidation of the posterior lung segments.

2487