Chapter 55: Principles of Critical Care

The last few decades have seen great advances in the care of the injured patient from prehospital triage and transport to care in the intensive care unit (ICU). Care in the ICU is designed to reestablish homeostasis and minimize secondary and iatrogenic injury. Excluding early deaths in the operating room, most traumatic hospital deaths will occur in the ICU. More than ever, the outcome of critically injured patients is dependent on a solid understanding of the pathophysiology and evolution of traumatic injuries. Attention to detail is critical and an awareness of the pitfalls is essential if one is to be successful in avoiding preventable morbidity and mortality.

In the last several years, increasing emphasis has been placed on quality of care indicators and physician staffing models for ICUs. A modern surgical ICU in the 21st century provides evidence-based care using algorithms, clinical practice guidelines (CPGs), and checklists; uses cutting-edge technology for physiologic monitoring; and has a robust quality improvement process to continuously evaluate its outcomes and to identify opportunities for improvement.

This chapter focuses on elements of critical care essential to the management of the acutely injured patient, reviews some recent advancements in the monitoring of the critically ill patient, and lists some of the common complications and pitfalls observed in the ICU.

Given the wide variety of clinical expertise and patient populations, several patterns of ICU physician organization have developed. The first is the “closed” unit that relies almost exclusively on a critical care team (or attending intensivist) for primary patient management. Under this scheme, comprehensive management is assumed by the ICU team along with responsibility for all orders and procedures, with other services providing care as consultants on an as-needed basis.

In an alternative model, the “open” unit, there may or may not be a designated ICU director, a separate ICU team, or even an intensivist immediately available to the ICU. Under this system, individual physicians manage and direct intensive care for their respective patients, depending on their institutional privileges. Consultative involvement of a board-certified intensivist is at the discretion of each primary attending physician, and is neither required nor necessarily expected.

Many larger surgical and trauma ICUs have a “semiopen” or collaborative plan of practice whereby the ICU is staffed with intensivists who coordinate care with primary surgeons. While primary surgeons may write orders on their patients, critical care team involvement with each patient is typically either mandatory or expected. There are often specific areas of designated Critical Care autonomy, such as the management of mechanical ventilators, invasive hemodynamic monitoring, pain management, and sedation. In these units, the ultimate responsibility for the patient remains with the primary team, but patient care is a collaborative effort. This semiopen model combines the advantages of critical care expertise for trauma and surgery patients while maintaining primary surgical service responsibility for overall patient management. This arrangement is consistent with Accreditation Council for Graduate Medical Education (ACGME) program requirements for general surgery and neurosurgery training programs as well as guidelines for the optimal care of the injured patient suggested by the American College of Surgeons Committee on Trauma for Level 1 Trauma Centers.¹ There is now a growing body of work examining the relationship between ICU staffing models and patient outcomes. For these purposes, rather than trying to compare various models of care, a distinction has been made between “high-intensity” and “low-intensity” physician staffing models. Loosely translated, a “high-intensity” model involves 24/7 dedicated physician staffing and mandatory ICU team involvement with patient management. This includes all closed units and most semiopen units. The remaining “open” units typically utilize “low-intensity” ICU physician staffing. The principal hypothesis is that dedicated, higher-intensity intensivist staffing for ICU patients will ultimately improve outcomes from a variety of conditions and illnesses. In a meta-analysis of 26 pooled studies, Pronovost et al found a relative risk of 0.71 (95% CI = 0.62–0.82) for hospital mortality and 0.61 (95% CI = 0.5–0.75) for ICU mortality associated with high-intensity ICU staffing for adults and children.² Similar results were found by Nathens et al who specifically examined the effect of high-intensity staffing on outcomes following major trauma.³ Utilizing prospective cohort data from 68 trauma centers, the authors reported a relative risk reduction of 0.78 (95% CI = 0.58–1.04) for ICUs whose patients were either managed (closed unit) or comanaged (semiopen) by board-certified intensivists.

The mortality rate among surgical patients who develop complications, called failure to rescue is also reduced by the presence of intensivists in the ICU. Failure to rescue (FtR) is a quality measure that looks at the hospital mortality rate of surgical patients with complications. Hospitals with intensivists on their rapid response teams or in their ICUs have lower FtR rates.⁴ The presence of surgical intensivists also reduces complications and improves National Surgical Quality Improvement Program (NSQIP) general surgery quality measures.⁵

These and other observations have resulted in the creation of ICU staffing guidelines. In 2000, a group of Fortune 500 companies and large public and private health care purchasers formed the Leapfrog Group for the purpose of identifying and creating incentives for sustained patient safety measures in acute care hospitals. This group has identified standards for physician staffing for the ICU that requires the presence of experienced intensivists providing daytime care and response requirements for off-hours care.⁶

Quality assurance and performance improvement in a surgical ICU are complex processes requiring the ongoing identification of outcome measures or performance indicators, data collection and analysis, and the development of action plans to correct deficiencies and subsequent monitoring of the performance (outcome) measures. The underlying goal of delivering high-quality care also depends on specialization (critical care specialists), provider education and training, good communication and collaborative interaction between specialty and ancillary services. Existing critical care quality assurance programs have used a variety of clinical indicators or “filters” as a measure of the quality of care. These indicators may reflect process measures (eg, percentage of eligible patients receiving deep venous thrombosis prophylaxis in a timely manner), and outcome measures (complication rate [%] for central venous line sepsis). Illness severity indices have been developed for the purpose of predicting outcomes in critically ill patients and are being increasingly used as benchmarking tools, allowing participating units to compare their outcomes with those predicted by the various indices. These performance measurement systems will become increasingly important in allowing managed care organizations to assess program performance. In addition to improved instruments for assessing critical care outcomes, the development and implementation of clinical protocols and CPGs directed at reducing undesirable treatment variability are being linked to ICU performance improvement. Protocols and guidelines, once developed and implemented, can later be analyzed in terms of their clinical efficacy and cost-effectiveness and can be modified further to improve efficiency.

The effectiveness of CPGs has been demonstrated for a variety of problems and conditions including ventilator weaning, pneumonia, nutrition, and sedation.^7,8,9,10 The difficulties that most institutions experience, however, relate more to the implementation of CPGs rather than to their development. Current methods of improving implementation of, and compliance with, CPGs include ongoing education, defined order sets, the assignment of some management responsibilities to specialized teams (eg, nutrition and respiratory therapy), and the use of advanced practice staff (nurse practitioners and physician’s assistants).

More recently, several fields in medicine, motivated by an increased awareness of errors in medical care delivery, have incorporated lessons learned from the aviation industry to clinical practice in an attempt to improve quality and patient safety. A checklist is just one of the tools used in the aviation industry that have been tested in many ICUs to potentially improve safety, quality, and consistency of ICU care.¹¹ Inspired by an article by Vincent¹² where he described a checklist using the mnemonic FASTHUG (feeding, analgesia, sedation, thromboembolic prevention, head of the bed elevation, stress ulcer prophylaxis, and glucose control), we implemented a modified checklist (mFASTrHUGS) by adding mouth care (m), restraints (r), and skin care (s) (Table 55-1). We use the checklist as a template for daily multidisciplinary rounds and the nursing staff uses it at the end of their shift for turnover. Each item on the checklist is reviewed during rounds assessing its implementation and need. If any item has not been implemented for a particular patient, then the team has to identify a contraindication (eg, pharmacologic DVT prophylaxis during the first day following a significant traumatic brain injury), otherwise the measure has to be implemented. mFASTrHUGS is a package implemented to all patients in our surgical ICU.

One of the characteristics of the ICU is the utilization of intensive physiologic monitoring. Monitoring devices can be used to determine if the patient has stable organ function, and to detect anomalies that may indicate impending organ dysfunction. In recent years there has been a dramatic increase in the ability to monitor a wider variety of physiologic parameters. Monitors can be useful in determining if a patient’s trajectory is deviating from the anticipated or optimal course; however, any monitor’s output requires interpretation and integration with the overall clinical picture. Monitoring itself can be associated with serious and lethal complications, including device related complications and errors in interpretation that lead to errors in clinical decision making. The questions that must be addressed with any form of monitoring include “when?” (indication and timing), “what?” or “how much?” (which specific monitoring tools or techniques), and “why?” (an analysis of the associated risks and benefits).

Hemodynamic monitoring is directed at assessing the results of resuscitation and as a guide to reestablishing and maintaining tissue and organ perfusion (see Chapter 56). The restoration of normal arterial blood pressure, central venous pressure (CVP), pulmonary arterial (PA) pressure, and cardiac output (CO) provides some reassurance that there is adequate organ perfusion. This reduces the likelihood of death and serious morbidity due to complications of hemorrhagic shock including post-injury inflammatory response syndrome and multiple organ failure (see Chapter 61). However, the phenomenon of regional circulation and inadequate perfusion of specific organs, particularly the gut, in the presence of normal arterial pressures remains a concern. New types of monitors are becoming available that can monitor CO and intravascular volume status in a relatively noninvasive fashion, and may be able to determine perfusion at the tissue level.¹³

Arterial Pressure Monitoring

Noninvasive blood pressure monitoring is widely available through the use of automated blood pressure cuffs. These devices can be set to perform repetitive blood pressure measurements as frequently as every minute. However, they are usually considered insufficient in patients with significant hypotension due to poor sensitivity at low blood pressures as well as the intermittent nature of the readings. Insertion of an arterial intraluminal catheter or “arterial line” allows instantaneous measurement and continuous display of arterial blood pressure, even at very low blood pressures. Arterial lines have a wide variety of indications (Table 55-2) and are the preferred method of arterial blood pressure management in patients receiving continuous infusions of vasoactive drugs as they allow better drug titration. Arterial lines are typically placed in the radial artery, although they can also be placed in the dorsalis pedis, femoral, or brachial arteries. Infection of arterial lines is less common than that of central venous lines; however, sterile technique should still be utilized to avoid the risk of catheter related blood stream infections. Thrombotic complications can also occur at any arterial line site and may lead to tissue ischemia, including loss of digits. This is particularly common in patients with prolonged hypotension or sepsis or who have been treated with vasopressors. Although Allen tests are frequently performed before the insertion of a radial arterial line, these do not exclude the possibility of this complication.

Minimally invasive continuous arterial pulse waveform analysis devices are available that quantify pulse pressure variability (PPV), and stroke volume variation (SVV) by analyzing the variations in arterial waveform with respiration and the area under the arterial pressure waveform. These devices can also utilize the calculated stroke volume to provide an estimate of CO without need of a PA catheter. Recent meta-analyses found that PPV and SVV of at least 11–13% both had excellent ability to identify critically ill patients who were likely to respond to fluid challenge with an area under the curve (AUC) of 0.94 and 0.84 respectively.^14,15 However, it should be kept in mind the PPV and SVV are most reliable in patients on mechanical ventilation with no spontaneous respirations, and may be less reliable in patients with arrhythmias, spontaneous respirations, as well as those on low tidal volume ventilation.¹⁴

Central Venous Pressure Monitoring

Monitoring CVP is most useful in patients at high risk of over or underresuscitation (see Chapter 56). These include patients with limited cardiac reserve, including the elderly and those with cardiac disease. Patients with traumatic brain injury are another group in whom CVP monitoring is frequently performed to avoid hypotension associated with underresuscitation or overresuscitation resulting in increased cerebral edema. Although guidelines suggest CVP goals between 8 and 12 mm Hg,¹⁶ these end points may be less reliable in patients on positive pressure ventilation, making trends of CVP over time in response to therapy, rather than static measurements more useful in guiding overall resuscitation. The central venous catheter can also be used to obtain a mixed venous blood gas measurement. Since the mixed venous oxygen saturation (MVo₂) is usually slightly lower in the superior vena cava (SVC) as compared with that in the inferior vena cava (IVC) due to the relatively low oxygen consumption (Vo₂) of the kidneys, the blood oxygen saturation obtained from a central venous catheter is usually slightly higher than that obtained from a PA catheter. Central venous catheters that have an oximetric tip can measure the saturation of blood at the tip of the central venous catheter or Scvo₂, allowing continuous measurement of this marker of global perfusion.

Pulmonary Artery Catheters

The Swan-Ganz PA catheter was first introduced in 1970; however, in the mid-1990s there were a number of studies questioning their efficacy and reports of complications including pulmonary infarction and pulmonary artery thrombosis, perforation, bleeding, and pseudoaneurysm. More recent studies have not demonstrated increased major adverse sequelae associated with the PA catheter.¹⁷ However, these studies also failed to demonstrate any significant improvement in outcomes associated with PA catheters. Currently PA catheters are primarily utilized in patients who have known or suspected myocardial dysfunction.

An alternative to invasive PA catheter placement is the FloTrac/Vigileo (Edwards Lifesciences, Irvine CA, USA) system which utilizes arterial waveform analysis to calculate SVV, stroke volume, and CO. Initial studies of this technology were disappointing,¹³ but recent meta-analyses suggests the technology has improved with better concordance with PA catheter and echocardiographic estimates of CO with a percentage of error less than or equal to 30%.¹⁵ However, this optimal concordance only occurs in patients with normal ejection fraction (EF ≥40%) and SVR.^15,18,19 Other minimally invasive devices utilize arterial waveform analysis in conjunction with lithium dilution (LiDCO [Cambridge, UK]), and thermodilution (PiCCO [PULSION medical system, Munich Germany]) to estimate SVV and CO. However, these devices require placement of a central venous catheter, calibration every 8 hours, and are also less accurate among patients with arrhythmias, valvular disease, depressed cardiac function and high or low SVR.¹⁹

Echocardiography

The formal transthoracic echocardiogram (TTE) can be invaluable in assessing the function and structure of the heart as well as the health of its components including valves and chambers. Limited TTE can also detect such conditions as pneumothorax and pleural effusions.^18,20 However, in about 50% of trauma patients it is difficult or impossible to perform a complete TTE due to chest trauma, subcutaneous air, obesity, or surgical dressings. Transesophageal echocardiography (TEE) can overcome many of these limitations and can be used in the detection of such injuries as blunt aortic rupture (see Chapter 26).^13,18,19,20 However, frequent use of TEE in the ICU can be limited due to availability, cleaning requirements, and the skill required by the operator. However, there are now FDA-approved TEE devices using a disposable probe that can be left in the esophagus or stomach for up to 72 hours allowing for repeated exams over time. Studies of this catheter demonstrate excellent image quality and utility in directing therapeutic decision making.^13,19,21

Other Monitoring Modalities

Bioimpedance

Transthoracic impedance, also known as bioimpedance cardiography, uses an electrical current applied to the thorax. Changes in bioimpedance to this current are used to measure heart rate, left ventricular EF, and intrathoracic fluid content and calculate stroke volume, CO, and SVR. However, the technology is limited by patient movement, and arrhythmias; and is inaccurate in pregnancy, obesity, pleural fluid or gas, heart failure, severe valvular disease, and pulmonary edema. A new device is available that utilizes impedance electrodes on the outside surface of an endotracheal tube, Endotracheal Cardiac Output Monitor (ECOM, ConMed, Irvine, CA). This allows impedance measurements without interference from abnormalities or motion of the chest wall. However studies have demonstrated an inability to accurately estimate or trend CO when compared to thermodilution.^13,22

Near-infrared spectroscopy

Near-infrared spectroscopy (NIRS) is a noninvasive technique in which a probe utilizing near-infrared light is applied to the thenar eminence. This allows detection of the tissue oxygen saturation (Sto₂) of the muscle of the thenar eminence. Decreased Sto₂ correlates with increased mortality and organ failure in patients with hemorrhagic shock or sepsis.²³

Transfusions

Blood transfusions are common in the ICU with 30–62% of critically ill patients receiving an average of 2–4 U of packed red blood cells.^24,25 Blood transfusions independent of shock or injury/disease severity are associated with worse outcomes. Increased infection, multiple organ dysfunction, and mortality are directly correlated with the amount of blood transfused.^25,26 Lowering target hemoglobin from 10–12 to 7–9 g/L was associated with improved outcomes in ICU patients in the Transfusion Requirements in Critical Care (TRiCC) study.²⁷ The TRiCC trial results have been reaffirmed by multiple subsequent studies and meta-analyses in various ICU and surgical populations including cardiac disease, respiratory failure, and those on mechanical ventilation. In addition to improved survival these studies also found that restrictive transfusion strategies were associated with reductions in rebleeding, acute coronary syndrome, pulmonary edema, and bacterial infections without adversely affecting functional recovery or length of stay.^28,29 Despite initial support for liberal transfusion among septic patients, subsequent studies have failed to demonstrate any benefit to transfusion triggers above 7 g/L within this population.^27,30 The updated Surviving Sepsis Campaign Guidelines from 2012, support a transfusion trigger of less than 7.0 g/dL with a target hemoglobin concentration of 7–9 g/dL.¹⁶ The appropriate trigger for patients with traumatic brain injury remains unclear. However, recent studies have demonstrated increased mortality with transfusions in traumatic brain injury patients with hemoglobin levels greater than 10 g/dL, no benefit in neurologic outcome, and a significantly increased risk of thromboembolic events and transfusions with a trigger of 10 g/dL when compared to a trigger of 7 g/dL.^31,32

A general approach to transfusion is that patients with hemorrhage need transfusion, while those who are not bleeding infrequently require immediate transfusion. In the trauma bay, operating room, and ICU, red blood cells are often the most available and effective initial resuscitation fluid, and prudence suggests a liberal transfusion strategy until hemorrhage control is achieved.

One source of anemia well within the control of the surgical intensivist is phlebotomy related blood loss. A study in 2012 demonstrated average ICU phlebotomy losses to be 436 mL for all comers and 679 mL for patients with an ICU length of stay of at least 4 days.³³ Studies have also demonstrated small changes in the amount of blood drawn, as little as 3.5 mL/d, can significantly increase risk for blood transfusion.²⁴ Concerted efforts should be made in the ICU to reduce the number of serial labs, eliminate unnecessary studies, and utilize minimal or pediatric tubes for all necessary tests. Additionally, technology such as continuous noninvasive hemoglobin monitors may avoid unnecessary serial blood tests, and have been shown to reduce the percent of patients receiving transfusions as well as the average volume of blood transfused per patient.²⁶

Erythropoiesis-Stimulating Agents

The anemia of critical illness resembles that of chronic inflammatory disease; low circulating erythropoietin levels are found in critical illness and are thought to be one of the causative factors. Although epoetin alfa and darbepoetin alfa have been widely accepted for anemia due to chronic kidney disease, these agents are also attractive for anemia of critical illness as they may restore hemoglobin levels without transfusion. However, the optimal hemoglobin targets and dosing have not been established and clinical trials (EPO-1 and EPO-2) demonstrating improved hemoglobin levels or transfusion reduction used target hemoglobin higher than those suggested by TRiCC.^34,35 Subsequent studies (EPO-3) while demonstrating an increase in hemoglobin with Erythropoiesis-stimulating agent (ESA) failed to find a reduction in transfusions.³⁶ A subset analysis of the trauma patients in the EPO-2 and EPO-3 studies suggested there was approximately a 50% reduction in 29-day mortality with ESAs.³⁷ This survival benefit was redemonstrated in patients with traumatic brain injury.³⁸ However, there is no clear consensus on ESA dosing in trauma patients, and increased adverse outcomes, including micro and macrovascular thromboembolic events and increased mortality have been seen in ESA trials utilizing high dose regimens and higher hemoglobin targets.³⁹ Optimal response to ESAs may not be achieved in the presence of relative iron deficiency, which is common in ICU patients. Concomitant iron administration has been recommended with ESAs, but randomized, clinical studies have not shown improved transfusion rates with enteral iron supplementation.⁴⁰

One of the principal indications for admission to the ICU for trauma patients is the need for frequent neurologic assessments in those with known or suspected traumatic brain injury (see Chapter 19). There are two goals for monitoring traumatic brain injury: first, the avoidance of secondary brain injury by avoidance of hypoxia and hypotension and maintenance of cerebral perfusion; second, the detection of increased intracranial pressure (ICP) due to cerebral edema or expanding intracranial hematomas. Reassessment should be done frequently as even subtle changes may herald increases in ICP or cerebral ischemia.

Intracranial Pressure Monitoring

ICP monitoring with a ventriculostomy catheter or subdural bolt is a common practice in most major centers for patients who have a neurologic exam that is unavailable or unreliable following traumatic brain injury. The Brain Trauma Foundation (BTF) guidelines recommend early and aggressive monitoring of ICP and the calculated cerebral perfusion pressure (CPP), which is the difference between the mean arterial pressure (MAP) and ICP.⁴¹ Monitoring of the ICP and CPP can be used to guide therapy such as vasopressors, sedation, paralysis, hyperosmolar therapy, or cerebrospinal fluid drainage and to provide surveillance for increasing cerebral edema or intracranial hemorrhage. Adherence to BTF guidelines, including compliance with placement of ICP monitors has been associated with improved mortality in patients with traumatic brain injury.^42,43,44

Investigational noninvasive monitoring systems for ICP include transocular ultrasound monitoring of optic nerve sheath diameter (ONSD).⁴⁵ The optic nerve sheath is an extension of the intracranial dura matter and has been shown to become distended with elevated ICP. Continuous transcranial Doppler ultrasound, brain tissue oxygen, and cerebral microdialysis monitoring are other investigational approaches for ICU monitoring of traumatic brain injury that may contribute to decision making and eventually improve outcomes in these patients.⁴⁶

Current guidelines indicate the need for nutritional assessment and monitoring for patients admitted to the ICU (see Chapter 60). Enteral nutrition, which may help preserve gut mucosal barrier function, is the preferred approach. Nutritional assessment should begin with an assessment of the degree of pre-injury malnutrition as well as current requirements. Nutritional monitoring in the ICU is controversial but can include calculation of nitrogen balance, weight, prealbumin, and albumin. The literature to date suggests serial weight measurements and serum albumin predict outcomes such as mortality and length of stay poorly in the critically ill. In comparison, nitrogen balance (goal 2–4 g positive nitrogen balance) and prealbumin more accurately predict outcomes.⁴⁷ Indirect calorimetry (metabolic cart) provides an assessment of caloric requirements and metabolic rate. The device calculates Vo₂ and carbon dioxide production (Vco₂). Standard metabolic carts requiring an integral mechanical ventilator were intended for intermittent use; however, newer devices can be used with standard ventilators with an adapter that can then continuously sample end-tidal oxygen and carbon dioxide. Co₂ and Pco₂ can be used to then determine the respiratory quotient (RQ) and caloric needs can be estimated. The RQ can also be used to determine the prominent nutritional substrate being used, excess carbohydrates leading to RQs of 1.0 or more, with RQs below 0.8 indicating possible excess lipid utilization.

Hyperglycemia with or without insulin resistance appears to be a common phenomenon in critically ill patients. Studies have also shown that hyperglycemia in trauma patients correlates with higher mortality rates.⁴⁸ The van den Berghe trial demonstrated that tight glucose control (at or below 110 mg/dL) with intensive insulin therapy improved mortality and reduced complications such as infection rate, multiorgan failure rate, ventilator days, and morbidity.⁴⁹ However, the intensive insulin regimen initially proposed by Van den Berghe et al is associated with increased hypoglycemia and has failed to show a mortality benefit in subsequent multi-institutional studies such as Glucontrol and Normoglycemia in Intensive Care Evaluation Survival Using Glucose Algorithm Regulation (NICE-SUGAR).^50,51 In the NICE-SUGAR trial, 90-day mortality was actually increased in patients assigned to intensive insulin therapy, as compared with an intermediate target range for blood glucose. Improved glucose control is still a guideline used in most ICUs; however, a moderate protocol (goal glucose level <180 mg/dL) rather than an aggressive one is most likely to result in optimal prevention of hyperglycemia without inducing higher mortality or hypoglycemic events.^16,48

The normal response to physiologic stress is to increase levels of tissue corticosteroids; this is also seen in response to critical illness. Failure to recognize and treat adrenal insufficiency has been associated with increased mortality. Normal corticosteroid response can be impaired in a variety of conditions including sepsis, systemic inflammatory response syndrome (SIRS), and traumatic brain injury. Identification of patients with acute adrenal insufficiency can be difficult; random cortisol sampling (<15 mcg/dL) and corticotropin stimulation tests (15–34 mg/dL) have been used in the past but are not sensitive or specific. Patients with abnormal stimulation tests (increases <9 mg/dL) were felt to require corticosteroid supplementation. While a 2002 study by Annane et al suggested a benefit to low-dose steroids in sepsis, the 2008 multi-institutional CORTICUS trial did not show any 28-day mortality benefit with 300 mg/d of hydrocortisone in patients with septic shock, either overall or in patients who did not have a response to corticotropin.^52,53 However, hydrocortisone did hasten reversal of shock in CORTICUS study patients. Lacking adequately powered positive studies, low-dose steroid therapy (200 mg/d) should be limited to patients with septic shock whose blood pressure is poorly responsive to fluid resuscitation and vasopressor therapy.¹⁶ Corticotropin stimulation has no role in determining steroid use in patients with septic shock.¹⁶ Steroids should be discontinued if the patient does not respond to treatment given the potential risks of infection, hyperglycemia, and critical illness polyneuropathy.

Mortality after trauma in the ICU is often attributed to infection. Infections are thought to contribute to more than 88,000 ICU deaths annually in the United States.⁵⁴ Infectious complications of major injury (see Chapter 18) may be due to the results of the injury itself (eg, open fractures), as a result of complications of treatment (eg, anastomotic leak), or as iatrogenic complications of critical care management (eg, ventilator-associated pneumonia [VAP] and central line infection). Specific monitoring for infections will depend on injury type and severity, types of interventions performed, and the duration of post-injury critical illness. Regulatory authorities have recently mandated surveillance cultures on admission to the ICU for certain health care–associated infections (HAIs) such as nasal swabs for methicillin-resistant Staphylococcus aureus (MRSA). In a study using multiple regression analysis, the most common predictors of infection were central venous catheters, mechanical ventilation, chest tubes, and trauma with open fractures.⁵⁵ Patients at risk for infectious sequelae should be routinely tested by culture and examined for clinical indications such as fever, leukocytosis, change in physical examination, pyuria, and development of purulent sputum or new infiltrate on chest x-ray. HAIs such as central line–associated bloodstream infection (CLABSI) may have standardized definitions in some jurisdictions and regulatory requirements for surveillance. Other HAIs such as VAP may require adoption of a local or institutional standard definition and therapy given the lack of a national consensus. The decision to start presumptive (empirical) antibiotics should be based on risk factors, the expected sequelae of injury, and prior infections. Presumptive treatment should be started, if indicated, stopped at a defined end point for culture-negative patients, and appropriately deescalated when final culture information and sensitivities are available. Importantly, not all critically injured trauma patients with unexplained fevers require antibiotics. Fever in these patients may have a noninfectious origin (Table 55-3) or be due to occult infection that has not been considered, successfully cultured, or has no identifiable signs or symptoms. Fungal sepsis should be considered in patients with prolonged ICU stays, multiple prior antibiotic therapies, and immunosuppression (see Chapter 18).

The need for mechanical ventilation is the most common indication for admission to the ICU. The general principles for intubation and mechanical ventilation are the following:

1. Secure and establish an airway.

2. Decrease the work of breathing (WOB).

3. Improve oxygenation.

4. Improve ventilation (CO₂ gas exchange) and maintain control of Paco₂ especially in acute brain injury.

5. Anticipate worsening respiratory status or airway patency such as the need for large-volume resuscitation, severe neck/thoracic trauma, upper torso/facial burns, and inhalation injury.

Current ventilator technology is diverse and advanced; however, the essential physical principle of mechanical ventilation is pushing oxygen-rich air into the lungs by positive pressure and removal of waste CO₂ by reduced pressure. Ventilator management can change rapidly; therefore, a nucleus of critical care expertise is needed not only to optimize respiratory support but also to interpret acute changes in pulmonary mechanics that can often be a harbinger of systemic pathology.

Monitoring of Gas Exchange

Rapid assessment of arterial oxygen tension (Pao₂) is essential for both evaluating and managing the adequacy of alveolar–arterial oxygen gas exchange. Oxygen (O₂) is driven from the alveolar airspace into the pulmonary capillaries along a diffusion gradient between the respective tissue beds. Calculating the efficiency of pulmonary oxygen exchange can be cumbersome since the equation for the A–a gradient requires alveolar and arterial CO₂ concentrations, shunt fraction, water vapor pressure, and body temperature. A more convenient and simple bedside index of oxygen exchange is the Pao₂/Fio₂ (P/F) ratio that adjusts for a fluctuating Fio₂ and helps in defining lung injury. The use of pulse oximetry to determine arterial oxygen saturation (Sao₂) has replaced continuous arterial blood gas measurements as a real-time, noninvasive method to assess arterial oxygenation. There are limitations to Sao₂ and its nuances are important in interpreting the significance of an absolute Sao₂ percentage. First, because of the kinetics of oxygen–hemoglobin binding, Sao₂ and the oxygen dissociation curve is sigmoidal and not linear. Therefore, small changes in Sao₂ may reflect a much larger drop in Pao₂. Second, under instances of carbon monoxide poisoning or severe circulatory shock, oxygen delivery will be abnormally low despite a near-normal Sao₂.

In addition to oxygenation adequate ventilation, end tidal (Et)CO₂, and resultant arterial CO₂ tension (Pco₂) have important physiologic and clinical implications and must be monitored in mechanically ventilated patients. The immediate detection of CO₂ through qualitative capnography relies on the lower pH of EtCO₂-rich air changing the color of pH-sensitive filter paper in the capnograph. As a rule, a disposable capnograph remains purple if EtCO₂ is less than 0.5% and turns yellow when EtCO₂ is greater than 2.0%.⁵⁶ Normal EtCO₂ is greater than 4%; therefore, capnography turns yellow when the endotracheal tube is positioned in an airway. This device is very sensitive unless the patient is in circulatory arrest and adequate pulmonary perfusion is compromised. The presence of a large volume of acidic gastric contents may give a false impression of successful endotracheal intubation in some cases of esophageal intubation. In these circumstances, initial detection of EtCO₂ decreases rapidly with subsequent tidal volumes. Continuous quantitative capnography analyzes EtCO₂ and, depending on the alveolar–arterial gradient, can give an indication of the arterial Pco₂. In patients without preexisting pulmonary disease, the normal alveolar–arterial gradient is between 1 and 3 mm Hg. Utilizing quantitative capnography can be helpful in brain injury where hyperventilation may curtail rising ICP. However, EtCO₂ measurements are affected by pulmonary dead space fraction and pulmonary perfusion that can be greatly altered in cases of hemorrhagic shock, thoracic trauma, and increased airway resistance. Warner et al performed a prospective study of 180 freshly intubated trauma patients and correlated EtCO₂ measurements with Pco₂ from blood gas analysis.⁵⁷ Using regression analysis, the authors found a direct correlation between EtCO₂ and Pco₂; however, patients ventilated with an EtCO₂ of 35–40 mm Hg were likely to have a Pco₂ greater than 40 mm Hg 80% of the time, and a Pco₂ greater than 50 mm Hg 30% of the time. In severely injured patients, where an increase in pulmonary shunt may exist, the measurement of Pco₂ through blood gas analysis remains the most accurate measure of assessing ventilation.

Causes of hypoventilation can be multifactorial. Increased dead space from pulmonary contusion, acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), pulmonary embolism, and oversedation can be contributing factors causing hypercapnia especially during the weaning phase of mechanical ventilation.

Assessment of Lung Mechanics and Inspiratory/Expiratory Pressure

Assessing pulmonary mechanics can significantly aid in diagnosing and treating a patient’s sudden or progressive pulmonary insufficiency. One of the most important parameters to measure is compliance and the ability to distinguish between static and dynamic compliance. Compliance, the change in volume produced by a change in pressure, is calculated based on measurements taken from the ventilatory circuit itself. In general, a sudden decrease in compliance will mean a concomitant rise in both plateau pressure (PP) and peak inspiratory pressures (PIPs) for a given tidal volume (V_T) as seen in pneumothorax or abdominal compartment syndrome. However, measuring the individual changes of either static or dynamic compliance may indicate a specific pulmonary pathology.

Compliance

In static compliance, the change of volume produced is measured from the inspiratory hold pressures or plateau pressure using the following formula: Compliance_static = V_T/PP – PEEP. Static compliance reflects the alveoli and chest wall, rather than the airways. Cases of decreased static compliance (normal = 50–100 mL/cm H₂O) with normal or elevated PIP generally indicate intra-alveolar pathology such as ARDS, ALI, and pulmonary edema.

Dynamic compliance utilizes the PIP (Compliance_dynamic = V_T /PIP – PEEP) to estimate resistance of the airways. Sudden decreases in dynamic compliance or a measured difference between static and dynamic compliance reflect increased airway resistance during bronchospasm, mucous plugging, kinked endotracheal tube, or foreign body aspiration.

Pressure–Volume Curves

A well-accepted principle in mechanical ventilation is the importance of increasing alveolar recruitment to improve oxygenation. Assessment of the pressure–volume curve in mechanical ventilation has been utilized to determine the mean pressure needed for the inflection point, or P_flex (Fig. 55-1). This point represents the critical pressure needed to open collapsed alveoli and corresponds to the zone of optimal alveolar recruitment. The pressure reading at the inflection point may reflect an optimal PEEP setting. In ARDS, ALI, and pulmonary edema the normal pressure–volume curve is shifted (Fig. 55-1) leading to derecruitment of alveolar units and increasing pulmonary shunt. During these instances, increasing driving pressure and PEEP are often employed to maximize gas exchange.

Ventilatory Capacity

Ventilator capacity encompasses the ability of a patient to generate muscular forces needed to meet the ventilatory work required for physiologic demand. Assessing ventilatory capacity in the mechanically ventilated patient can be an important physiologic indicator of clinical improvement and predict successful extubation, particularly in patients who have been intubated for prolonged periods of time, or have neurologic (spinal cord injury and myasthenia gravis) or mechanical (flail chest and rib fractures) injury affecting the thorax. Forced vital capacity (FVC) and negative inspiratory force (NIF) are the most frequently measured indices of ventilator capacity. A normal vital capacity is between 65 and 75 cm³/kg depending on ideal body weight and sex. The NIF estimates inspiratory muscle strength and a value of –25 to –30 cm H₂O is indicative of adequate inspiratory force to maintain airflow after extubation.⁵⁸

Spontaneous breathing utilizes negative intrathoracic pressure to fill alveoli (Fig. 55-2). In contrast, mechanical ventilation utilizes positive pressure to fill alveoli and negative pressure for exhalation. Positive pressure mechanical ventilation can improve gas exchange by recruiting atelectatic alveoli, increasing functional residual capacity (FRC), and reducing areas of ventilation/perfusion mismatch, thereby decreasing pulmonary shunt fraction. Negative effects of mechanical ventilation vary according to ventilatory mode; however, adverse effects common to all positive pressure modes include barotrauma, ventilator-induced lung injury, and impairment of cardiac output from decreased venous return. It is important to assess the physical mechanics behind each mode of ventilation since correct management of ventilated patients will decrease total ventilation days and improve patient outcomes. In choosing which mode of ventilation is best suited for a particular patient, it is helpful to evaluate the patient’s current oxygenation, ventilation, pulmonary compliance, muscular strength, and mental status.

Mandatory Volume Control Ventilation

Both continuous mandatory ventilation (CMV) and assist-control (AC) mode ventilation are preset volume-cycle modes that deliver a fixed tidal volume at a specific respiratory frequency. The individual names of these modes are commonly referenced interchangeably; however, CMV delivers a set tidal volume exclusive of a patient’s ventilatory effort, whereas AC synchronizes delivery of a set tidal volume to each patient-initiated breath. Consequently, an awake and breathing patient will have episodes of respiratory dysynchrony causing significant discomfort, breath stacking, or barotrauma.⁵⁹ Because of this CMV is rarely used.

In AC, the ventilator recognizes a patient-triggered breath (either flow or pressure mediated) and delivers a synchronous, identical preset tidal volume (Fig. 55-3). Most modern ventilators are “flow triggered”; a continuous flow of gas passes around the breathing system patient inspiration deflects this flow and triggers the ventilator. AC modes also have a set rate to assure ventilation in an apneic, paralyzed, or heavily sedated patient, in these circumstances AC becomes indistinguishable from CMV. In an awake or lightly sedated patient, full synchronous respiratory support will be achieved with each initiated breath, thereby decreasing WOB and assuring adequate ventilation. Awake or agitated patients may trigger several full tidal volume breaths causing high minute ventilation and respiratory alkalosis.

Synchronized Ventilation Modes

Synchronous intermittent mandatory ventilation (SIMV) is similar to AC but allows for spontaneous ventilation in addition to the preset breaths (Fig. 55-4). In contrast to AC ventilation, where every patient-initiated breath receives the full tidal volume, SIMV mode allows for respiratory work between the preset tidal volumes. The degree of ventilatory support can be increased or decreased by adjusting the set rate and amount of pressure support delivered by the ventilator with patient breaths. SIMV can be useful in reducing minute ventilation in patients who are significantly overbreathing during AC ventilation causing respiratory alkalosis.

Excessive airway pressures (>50 cm H₂O) can increase the incidence of barotrauma and lung injury especially in states of decreased pulmonary compliance. Pressure-regulated volume control (PRVC) ventilation modulates the inspiratory flow pattern during a volume-controlled breath, thus reducing PIP. This flow pattern, coined “decelerating inspiratory flow,” is in contrast to pure AC/CMV modes where there is constant inspiratory flow resulting in a continuous rise in airway pressure.

Pressure support ventilation (PSV) originally termed pressure assist, provides a baseline level of inspiratory airway pressure and decreases the WOB by augmenting spontaneous respiration (Fig. 55-5). The patient, therefore, is aided in overcoming the resistance of the ventilatory circuit and has complete control over the rate, and tidal volume. Each PSV breath is supported by a specific flow limited by a preset pressure that is triggered by patient inspiration. Because this mode requires spontaneous breathing, PSV can only be utilized in lightly sedated or awake patients without paralytic therapy or neuromuscular disease. Although PSV can be used as a sole ventilation mode, it is most frequently used during ventilator weaning (see the section “Weaning From Mechanical Ventilation”).

Pressure-Controlled Ventilation

In patients with ALI/ARDS with poor pulmonary compliance, the limitations of volume-cycled ventilation are increasingly recognized. To achieve a specific preset tidal volume, progressively higher airway pressure must be delivered as compliance worsens increasing the likelihood of barotrauma. In contrast to volume control, time-cycled pressure control pressure-controlled ventilation (TCPV) delivers breaths at a fixed flow rate dictated by a preset pressure (driving pressure). Regardless of pulmonary or chest wall elasticity, the PIP is fixed and will not exceed the set driving pressure; however, the delivered tidal volume will vary as a function of compliance. TCPV is useful in patients with ARDS and meets acute respiratory distress syndrome network (ARDSNet)⁶⁰ criteria so long as the set driving pressure and PIPs are set below 30 cm H₂O. Despite the theoretical advantages to using pressure modes of ventilation in patients with poor compliance, the literature to date has failed to identify a statistically significant benefit to mortality or barotrauma with either mode of ventilation.⁶¹

In conventional AC/CMV mode the inspiratory to expiratory ratio is approximately 1:2, thereby minimizing airway pressures and allowing adequate ventilation. In severely hypoxic patients the ratio can be reversed, inverse ratio ventilation (IRV). Typically IRV allows I:E ratios 1.5:1–2:1. In principle, IRV allows maximal recruitment of alveoli by expanding marginal airspaces. When using IRV, it also is important to be cognizant of rising intrinsic PEEP that can lead to barotrauma or a progressive decrease in cardiovascular return effecting cardiac output.

Airway Pressure Release Ventilation

Airway pressure release ventilation (APRV), or bilevel ventilation, is essentially continuous positive airway pressure (CPAP) ventilation with the exception that the pressure setting is generally higher (P_high) for a longer duration (T_high) than typical CPAP and there is a short “release” of high pressure (T_low and P_low) allowing for ventilation and CO₂ exhalation. The long duration of P_high (as long as 6 seconds) is thought to improve alveoli recruitment, FRC, and gas exchange by increasing mean airway pressure without the expense of high PIP’s. APRV’s greatest benefit is the presence of a floating release valve that allows for patients to breathe spontaneously during the prolonged P_high phase. This may provide greater patient comfort and decreases the need for sedatives. Studies have demonstrated overall safety and improvements in oxygenation with APRV but have not shown a mortality benefit compared to other modes of ventilation when lung protective strategies are utilized.^62,63

Adjuvant Therapies in Respiratory Therapy

Treating severe respiratory failure can be a daunting task to the ICU team and difficulty maintaining adequate oxygenation can at times seem futile. In the past several years adjunct therapies, both mechanical and pharmaceutical, have been evolving, although with variable efficacy.

Prone Positioning

Poorly or nonaerated lung units localize in dependent lung zones while in the supine position. Prone positioning improves gas exchange and ventilation/perfusion mismatch by expanding atelectatic portions of the lung akin to the zones of West. Prone positioning also prevents ventilator induced lung injury by prevention of alveolar hyperinflation; more homogeneous distribution of transpulmonary pressure and ventilation; and prevention of atelectotrauma through improved alveolar recruitment compared to supine positioning.⁶⁴ One large randomized controlled study and several large meta-analyses have found a significant survival benefit as well as improved oxygenation with prone positioning in ARDS patients with severe hypoxia.^64,65 However, prone positioning is associated with a significantly higher incidence of complications, most importantly pressure ulcer formation and endotracheal tube dislodgment.⁶⁵

Pharmacologic Agents

The two most common agents used to improve hypoxia in severe ARDS are inhaled nitric oxide (NO) and inhaled epoprostenol. The mechanism of action is likely related to the relaxation of vascular smooth muscle in the lung, thereby improving shunt fraction and optimizing the ventilation/perfusion ratio by selectively vasodilating aerated lung zones.⁶⁶ Clinical trials have shown both agents to transiently improve oxygenation, but neither agent has been shown to improve survival, and NO may increase the risk of renal dysfunction.^66,67 Other pharmacologic therapies for ARDS, including sildenafil, corticosteroids, and exogenous surfactant, have not been shown to be consistently efficacious.

Managing and weaning a patient from mechanical ventilation is highly variable and the duration and success of weaning is dependent on each specific clinical scenario. It is additionally important to separate the principles of weaning from extubation despite the fact that the terminology is used interchangeably. As a set of general principles: (1) weaning should be considered early in the course of a ventilated patient, (2) pressure support weaning or AC mode transitional weaning seem to be the most tolerated, and (3) spontaneous breathing trial is the best diagnostic test to assess progress of weaning.

Several factors influence successful weaning including the type of injury sustained, preexisting medical problems, patient toxicology, and the general state of health. Weaning should be directed toward decreasing WOB and improving ventilatory capacity (Table 55-4).

WOB is a function of the force required to expand the airways, lungs, and chest wall to an appropriate volume in order to meet oxygen and physiologic demands (pressure × volume/time). Excess WOB may be secondary to inappropriate ventilator settings, increased airway resistance, and decreased pulmonary or thoracic wall compliance. Additionally, increased WOB may also reflect higher CO₂ production from sepsis, fever, or overfeeding.

Methods and Protocols for Weaning

The process of weaning can be long and variable and may account for over 40% of total ventilator time.⁶⁸ There remains a lack of uniformity in weaning protocols and there is a paucity of data available to support standardization. Nevertheless, weaning should focus on conditioning and strengthening the muscles of breathing.

The methodology of weaning has evolved in the last three decades from a physician-driven approach to a modern protocol-based approach. Options include a “stepwise” methodology where patients’ ventilatory assistance (pressure support or rate) is decreased in a stepwise manner. However, in the stepwise approach there is no set period of unassisted respiratory exercise, and this approach may prolong mechanical ventilation leading to chronic fatigue and deconditioning.⁶⁸ This method is in contrast to the “sprint” approach (spontaneous breathing trials) where intermittent trials of spontaneous breathing are used once or twice daily and an assessment of WOB and ventilatory capacity is determined accordingly.

In an effort to empirically evaluate optimal weaning techniques, the Spanish Lung Failure Collaborative Group analyzed four weaning methods as important, large (n = 546), multicenter, prospective trial. Patients were randomized into a stepwise progressive mode: (1) IMV where patients had a set mean frequency of 10 breaths/min and decreased, (2) PS where support was initially a mean of 18 cm H₂O and decreased; or into an intermittent spontaneous breathing method, (3) greater than 2/day with PS less than 5 cm H₂O, or (4) once daily T-piece for 2 hours only. Both spontaneous breathing methods had the higher rates of successful weaning than the stepwise methods.⁶⁹ Among the three most popular weaning modes, T-piece wean, PS wean, and IMV wean, current data suggest a trend toward longer duration of ventilation with IMV weaning compared to spontaneous trials; however, it is important to note that little data have shown any link between weaning method and mortality.⁷⁰

Despite the controversy that exists in method of weaning, the benefit of a formal protocol to hasten weaning is clear.⁷¹ Implementing an aggressive weaning protocol should incorporate the Screen, Trial, Exercise, Evaluate, and Report (STEER) Principle. Using this protocol, a team of highly trained respiratory therapists, in conjunction with the ICU team, implement the following daily regimen on each mechanically ventilated patient:

• Screen for weaning contraindications (hypoxia, fevers, hemodynamic instability, high WOB, uncontrollable ICP, and sedation).

• Trial of minimum support breathing (ie, PS <5 cm H₂O).

• Exercise according to set protocol (ie, a 2-hour PS trial, or T-piece trial).

• Evaluate progress.

• Report the results to the ICU team.

These protocols reduce physician practice variability and have been shown in several studies and meta-analyses to reduce ventilator and ICU days and weaning duration.^70,71

Extubation

The weaning process begins shortly after mechanical ventilation is initiated. However, extubation, the final removal of the artificial airway, should not be equated or confused with weaning. In a collective national task force consensus paper,⁷² discontinuation of mechanical ventilation should be considered if the following physiologic parameters are met:

1. Reversal of underlying cause of respiratory failure

2. Adequate oxygenation (P/F ratio >150–200 with PEEP <5–8, Fio₂ <0.4–0.5, and pH >7.25)

3. Hemodynamic stability

4. The capability to initiate a respiratory effort

As in weaning, prediction of successful extubation varies greatly factors most frequently studied include tidal volume, NIF, vital capacity, rapid shallow breathing index (RSBI), and minute ventilation; however, there are no standardized agreed upon criteria.⁷³ The seminal study by Yang and Tobin demonstrated that patients with RSBI greater than 105 breaths/min/L were 95% likely to fail; while those with a RSBI less than 100 breaths/min/L were 80% likely to succeed.⁶⁸ Although these authors have demonstrated the importance of the RSBI, other criteria should be utilized when deciding upon extubation, including ability to protect the airway, secretion control, and sustainability (Table 55-5). Head injury patients can be particularly difficult to manage, since neurologic symptoms can change making criteria for airway and secretion control difficult to evaluate. A GCS of greater than 8 is generally associated with the greatest extubation success. In head injury patients, early tracheostomy may be a consideration to establish definitive airway control (see the section “Tracheostomy”).

Unplanned Extubations

Despite rigorous patient observation and appropriate sedation, unplanned extubations (UE) remain a serious complication with a reported incidence of 0.1–3.6 events per 100 intubation days.⁷⁴ Consequences of UE include aspiration, pneumonia, vocal cord trauma, hypoxia, cardiopulmonary arrest, and death. Risk factors for UE include male gender COPD, agitation, lower sedation, and less experienced nurses. UE require reintubation in 33–58% of cases, with the majority (62–74%) occurring within 1 hour. When required, reintubation increases mortality. Predictors of reintubation include GCS less than 11, age greater than 65, Pao₂/Fio₂ ratio of less than 200, and pneumonia.⁷⁴ Preventing UE requires attention to endotracheal tube security, particularly during transfers, bedside procedures, or prone positioning. Adequate sedation and analgesia are paramount and physical restraints, especially in patients with high sedative tolerance, may be temporarily necessary. Protocols and checklists to prevent UE including nursing and physician education, standardization of procedures, patient surveillance, and identification of high risk patients can reduce the risk of UE by 22–53%.⁷⁴ An emergency protocol should be readied in the event of an UE, reintubation may be difficult and a team of experts with appropriate experience that can provide a surgical airway should be immediately present.

Tracheostomy in a chronically ventilated patient can offer several advantages including improved oral care, improved pulmonary toilet, decreased sedation requirements, decreased oral and vocal cord trauma, decreased airway resistance and dead space, and the ability to more aggressively wean ventilation. However, tracheostomy can be complicated by infection, subcutaneous emphysema, hemorrhage, tracheal stenosis, tracheoinnominate and tracheoesophageal fistula, and tracheomalacia. Because of this significant controversy exists regarding optimal timing for tracheostomy. Definitions of early tracheostomy (ET) and late tracheostomy (LT) vary with ET ranging from 48 hours to 8 days and LT generally being greater than 10 days. The literature to date is heterogeneous, making strong conclusions regarding ET difficult but overall consensus including a large meta-analysis of over 400 patients, suggests a benefit to ET with reduction in duration of ventilation and ICU days, and a possible reduction in pneumonia.⁷⁵ However, no mortality benefit can be found in the majority of studies, including a large randomized controlled trial.⁷⁶ Perhaps the greatest benefit of early tracheostomy may be seen in the traumatic brain injury population, where multiple studies, including a large cohort study of over 2000 patients, have shown ET to decrease ventilation days, ICU days, and pneumonia, although no benefit in mortality was conferred.⁷⁷ Tracheostomy may be performed via open or percutaneous method. The technique used should be based on patient needs and clinician experience as multiple large studies in heterogeneous ICU populations have shown both methods to be safe and effective with a possible morbidity benefit to percutaneous methods over open techniques.^75,78 Percutaneous tracheostomy may also be more easily performed at the bedside than open tracheostomy avoiding the need and cost of transport to the operating room.

Patients suffering traumatic injury may be suffering severe pain and may require directed and effective analgesia. Significant trauma may lead to prolonged critical illness, mechanical ventilation, and long-term sedation. Many trauma patients also have a history of substance abuse and are at risk for acute withdrawal symptoms and may have opiate and benzodiazepine tolerance. Inadequate control of pain, agitation, and delirium (PAD) can lead to patient suffering, additional complications, and unnecessarily prolonged intubation, mechanical ventilation, and ICU stay. The need for adequate analgesia and sedation must be balanced against the risks of oversedation. Oversedation may result in hemodynamic instability, increased length of stay and costs, increased respiratory complications including VAP, and possibly long-term decreases in cognitive function. Oversedation may also increase the risks of delirium and possibly post-traumatic stress disorder (PTSD). Delirium is related to increased length of hospital stay, increased health care costs, and higher mortality. ICU care may lead to pain and discomfort due to catheters, drains, endotracheal tubes, and performance of routine nursing care such as airway suctioning, physical therapy dressing changes, and an enforced mobilization. Consensus CPGs exist for management of PAD.⁷⁹ Most academic ICUs have adopted algorithms for assessment and management of PAD. An example of an ICU patient assessment and management PAD algorithm is shown in Fig. 55-6.

Choice of Parenteral Opioid for Analgesia

Pain is almost universal in trauma patients; it has been described as an unpleasant sensory or emotional experience that is associated with tissue damage or described in terms of tissue damage. Many patients later recall unrelieved pain when interviewed about their ICU stays. It is a standard of practice to regularly and frequently assess pain; this is readily accomplished by the use of validated pain scores. The Joint Commission has labeled the pain score “the fifth vital sign.” The Behavioral Pain Scale (BPS) and the Critical-Care Pain Observation Tool (CPOT) are the most valid and reliable behavioral pain scales for monitoring pain in medical, postoperative, or trauma (except for brain injury) adult ICU patients who are unable to self-report and in whom motor function is intact and behaviors are observable.^80,81 Parenteral opioids have a long history of efficacy and safety for pain and ICU patient. Since bioavailability and efficacy is variable in this patient population, the intravenous route is to be used whenever possible. Intramuscular and subcutaneous roots should be avoided due to irregular absorption and highly variable serum levels. Patient-controlled analgesia (PCA) may be of great utility in patients able to use it due to the self-control and immediate administration of agent given to the patient. Recent guidelines have recommended preferred parenteral likely agents in the treatment of pain and adult ICU patient. Table 55-6 lists characteristics of the preferred agents in the SCCM guideline: morphine, fentanyl, and hydromorphone (Dilaudid).⁷⁹

Morphine remains the most commonly used opioid analgesic in the ICU setting due to clinicians’ familiarity in dosing and low cost. It penetrates the blood brain barrier slowly to its poor lipid solubility. This results in a delayed peak effect and a long-acting effect as compared with more lipid-soluble agents such as fentanyl. Morphine does not have a direct negative inotropic effect; however, it has predictable effects of arterial and venous dilation. These effects suggest morphine may be advantageous in the hemodynamically stable or hypertensive patient with myocardial ischemia or cardiogenic pulmonary edema. Disadvantages of morphine and other opioid agonists are the opioid receptor–associated side effects, the most serious of which is centrally mediated respiratory depression. Other effects include sedation, nausea, and sphincter of Oddi spasm. Adverse effects can be reversed if necessary with careful titration of the opioid receptor antagonist naloxone. Naloxone must be administered with care as access effect is associated with undesirable hemodynamic effects such as hypertension, tachycardia, and myocardial ischemia as well as acute pulmonary edema. Morphine is also associated with a non-receptor-associated effect of histamine release, and this can result in undesired hypotension, tachycardia, and possibly exacerbating bronchospasm in patients with reactive airway disease. Prolonged use of morphine, especially in renal impairment, can result in the accumulation of a metabolite, morphine-6 glucuronide, and may result in a prolonged sedative effect.

Fentanyl is a lipid-soluble synthetic opioid having a more rapid onset of action than morphine. It is also inexpensive with costs similar to morphine. With small doses the duration of action is short due to redistribution. When large doses are administered, especially by continuous infusion, termination of effect requires elimination, probably due to the saturation of poorly perfused adipose tissue. The pharmacokinetics of fentanyl is not much altered by the presence of cirrhosis, and clearance appears to remain normal in renal failure. Hemodynamically fentanyl maintains cardiovascular stability and does not have significant negative inotropic effect. In the presence of high sympathetic tone, fentanyl may decrease blood pressure indirectly by decreasing central sympathetic output. Fentanyl also predictably causes a decrease in heart rate by a central vagotonic effect. The receptor-associated side effects of fentanyl and their management are the same as described for morphine. Fentanyl is 10 times more potent than morphine and has a more rapid onset of action, requiring vigilance with its use. Unlike morphine, fentanyl does not release histamine and therefore may be a better choice in patients who are hemodynamically unstable or who have reactive airway disease. For ICU patients, fentanyl has been recommended as an alternative to morphine in situations of hemodynamic instability, known allergy to morphine, or previous histamine release with morphine.⁷⁹

Hydromorphone is a semisynthetic opioid agent that is lipophilic and 5–10 times more potent than morphine. Time to onset of action and duration of action are similar to those of morphine, and hydromorphone’s terminal half-life is 184 minutes. Hydromorphone appears to have minimal hemodynamic effect and does not result in release of histamine. Like morphine and fentanyl, hydromorphone is inexpensive, and is recommended as a third-line agent after morphine and fentanyl.⁷⁹

Critical care practice guidelines for pain, sedation, and delirium, such as those developed by the SCCM, recommend regular assessment and response to therapy.⁷⁹ The appropriate target level of sedation is a calm patient who can be easily aroused with maintenance of the normal sleep–wake cycle. Some patients require deeper levels of sedation to facilitate mechanical ventilation or reduce ICP. Use of a sedation scale such as the Richmond Agitation Sedation Scale (RASS) or Riker Sedation Agitation Scale (SAS) is common in most ICUs.⁸² The choice of intermittent or continuous sedation is important; intermittent sedation relies on recognition of agitation and subsequent administration of a sedative. Continuous sedation reduces the likelihood of delay in administration of sedatives; however, continuous sedative infusions for ICU patients have been shown to increase the duration of mechanical ventilation and length of ICU stay. Weaning of patients from mechanical ventilation is often hampered by oversedation. The benzodiazepines (midazolam and lorazepam) are the most commonly used agents in the ICU for sedation. Propofol and dexmedetomidine have expanded the number of agents available for ICU sedation. The provision of anxiolysis and amnesia are of major importance for critical care patients undergoing intermittently painful procedures or mechanical ventilation. It has been demonstrated that the majority of patients surviving prolonged mechanical ventilation found memory of the experience to be unpleasant. Recent recommendations suggest the use of propofol or dexmedetomidine and reduced use of benzodiazepines for routine sedation due to a possible increased risk of delirium and mortality.⁷⁹ A meta-analysis of six trials ranked as moderate to high quality suggested that sedation with benzodiazepines may increase ICU LOS by approximately 1.62 days (p = 0.0007) and duration of mechanical ventilation by 1.9 days (p < 0.00001) compared with non-benzodiazepine sedation.⁸³ Benzodiazepines may have their greatest utility in the ICU for procedural sedation and in management of substance abuse withdrawal. Characteristics of commonly used benzodiazepines, dexmedetomidine, and propofol are found in Table 55-7.

Propofol is a lipid-soluble alkyl phenol intravenous anesthetic that is insoluble in water and formulated in a lipid emulsion. It has hypnotic, amnestic, and antiemetic properties but is devoid of analgesic effect. Propofol has minimal active metabolites, even with repeated administration. The sedative effect is rapid and predictable and recovery occurs quickly when the drug is terminated. Compared to benzodiazepines duration of mechanical ventilation is significantly shorter (2.6 days) in the patients sedated with propofol.⁸³ Propofol has predictable hemodynamic effects, including arterial and venous dilation, decreased inotropic effect, and decrease of systolic blood pressure of 20–30%. Propofol given as a loading dose will cause profound ventilatory depression. For this reason it is typically limited to mechanically ventilated patients only. SCCM guidelines recommend the use of propofol as a first line sedative agent.⁷⁹ Patients on propofol for longer than 24 hours need to be monitored carefully for propofol infusion syndrome. Hypertriglyceridemia and lipid-induced pancreatitis have been reported during prolonged infusion of propofol in the ICU, suggesting that serum triglyceride levels should be monitored in these patients. A lipid solution of propofol also supports rapid bacterial growth at room temperature, and a number of postoperative bacteremias had been linked to poor administration technique.

Dexmedetomidine is an imidazole compound that is a highly selective agonist of the α₂-adrenergic receptor with eight times greater affinity than clonidine. It is also shorter acting than clonidine allowing use as an intravenous infusion. Initially evaluated as an anesthetic, it was found to be associated with excess bradycardia and hypotension. Lower doses produce reliable sedation and dexmedetomidine is approved in the adult ICU as a sedative infusion. Patient selection and proper drug infusion are needed to avoid significant hemodynamic effects. Avoiding the initial bolus dose can reduce the incidence of significant bradycardia and hypotension on administration. Dexmedetomidine produces sedation but easy arousal, analgesic-sparing effect, and minimal depression of the respiratory drive. These characteristics are unique in that patients appear to be sedated but are readily roused and interactive and can follow commands. This makes the drug highly suited for patients who are being weaned from the ventilator, especially those who become agitated when other sedation is reduced. Dexmedetomidine is more expensive than benzodiazepines or propofol; however, studies suggest it is cost-effective as it reduces patient ventilator days, delirium, and ICU length of stay as compared with midazolam.⁸³

Monitoring of sedation within the ICU can be performed by the Ramsey or RASS scales (Table 55-8). The scales have midrange scores that indicate a calm, cooperative patient with high and low scores indicating excess agitation or oversedation. A common sedation scale should be used throughout the institution for consistent and effective use. Daily interruption of continuous IV sedation until awakening of mechanically ventilated patients decreases duration of mechanical ventilation and ICU length of stay. Combination of daily awakening with spontaneous breathing trials results in patients spending less time on mechanical ventilation, less time in a sedative coma, and less time in the ICU and in the hospital. Daily awakening trials are most effective when following a standardized nurse-driven protocol. Patients who should be excluded from a daily awakening trial include those with increased ICP or neuromuscular blockade, those requiring high levels of ventilatory support, and those who are postcoronary artery bypass grafting.

The daily awakening period should be synchronized with spontaneous breathing trials; in a study of 336 mechanically ventilated ICU patients, doing so achieved significant reduction in ventilator-free days and ICU and hospital length of stay.⁸⁴ The daily awakening also provides an opportunity for early exercise and mobilization (physical and occupational therapy) (Table 55-9). A recent study of early mobilization during daily awakening in 104 mechanically ventilated patients demonstrated increased independent functional status at hospital discharge, shorter duration of delirium, and fewer ventilator-free days during the 28-day follow-up period than those observed in controls.⁸⁵ An example of the recent trends toward less use of continuous sedation includes a recent trial of “no sedation” in mechanically ventilated patients.⁸⁶ In that study, the intervention group patients receiving no sedative medications were compared with control patients on continuous midazolam drips. The majority of the eligible ICU patients could not be enrolled as they had medical indications for deep sedation. Patients in the “no sedation” group were allowed morphine boluses and had frequent nonpharmacologic antianxiety interventions such as reassurance by nurses and reassessment by physicians of pain orders and the need for tubes and catheters. Patients in the “no sedation” group had significantly shorter ventilator days and hospital and ICU length of stay, but did have increased delirium and increased use of haloperidol.

Delirium is defined as fluctuation in mental status such as inattention, disorganized thinking, hallucinations, disorientation, and an altered level of consciousness. It occurs in up to 65% of hospitalized patients, and up to 87% of patients admitted to the ICU. Delirium in the elderly patient is associated with a doubling of mortality.⁸⁷ Delirium can increase hospital length of stay and increase health care cost. There has been discussion of ICU delirium rates as being a possible quality measure. Delirium must be considered when assessing pain and sedation in the ICU. It may occur in up to 54% of patients and can be further defined as (1) hyperactive delirium: characterized by hypervigilance, restlessness, anger, irritability, and uncooperativeness, and is associated with better overall outcomes; (2) hypoactive delirium: the more common and deleterious, characterized by a lack of awareness, decreased alertness, sparse or slow speech, lethargy, decreased motor activity, and apathy; and (3) mixed delirium: apparent in patients with a mixed clinical picture. Hypoactive delirium may be mistaken for depression or stupor and therefore is often not recognized which may contribute to higher 6-month mortality 32.0% versus 8.7% for mixed delirium.⁸⁸ Delirium occurs in patients typically 24–72 hours after admission to the ICU. Preexisting risk factors for delirium include cognitive impairment, chronic illness (including hypertension), age greater than 65 years, depression, smoking, alcoholism, and severity of illness. Risk factors arising during hospitalization include congestive heart failure, sepsis, prolonged restraint use, immobility, withdrawal from substance abuse, seizures, dehydration, hyperthermia, head trauma, intracranial mass lesions, and the use of lorazepam, midazolam, morphine, fentanyl, and propofol. Assessment of delirium should be carried out in association with pain and sedation assessments and can be facilitated by the use of a validated delirium score such as the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) or the Intensive Care Delirium Screening Checklist (ICDSC); these tools may be most usefully administered during a daily awakening.⁷⁹ In addition, the patient should be assessed for QTc prolongation on ECG if therapy is being considered as many antidelirium agents are associated with QTc prolongation and risk of torsade de pointes. CAM-ICU and ICDSC allow rapid consistent assessment for altered level of consciousness, disorganized thinking, inattention, and other delirium features. Nonpharmacologic measures are the primary treatment used to manage delirium and include daily awakening trials, continuous reorientation of the patient by nursing staff, keeping clocks and calendars visible to the patient, promoting effective sleep/awake cycles, timely removal of restraints and catheters, ensuring use of glasses and hearing aids, minimizing ICU noise and stimulation, and avoiding use of benzodiazepines. There are no double-blind, randomized, placebo-controlled trials which are adequately powered to prove the efficacy or safety of any antipsychotic agent in the management of delirium in ICU patients, although these are still commonly used by intensivists in the United States (Table 55-10).⁸⁹ Intravenous drugs include dexmedetomidine, which may be especially useful in patients failing spontaneous breathing trials secondary to agitation, and intravenous haloperidol. Haloperidol has been associated with a reduced seizure threshold, extrapyramidal reactions (dyskinesia), and laryngeal dystonia. It has also been associated with malignant neuroleptic syndrome. Large doses of intravenous haloperidol should only be administered in a monitored critical care setting and with monitoring of QTc intervals. In patients with hypoactive delirium, the dose of haloperidol may need to be reduced. Oral agents are longer acting and include aripiprazole, risperidone, or oral haloperidol. These agents are associated with QTc prolongation and should only be administered if the measured ECG QTc is less than 440 milliseconds. Another oral delirium agent with greater sedative properties is quetiapine; it is not strongly associated with QTc prolongation.

Critical care complications interpose a substantial cost burden to the health care institution and society and worsen patient outcomes. There is increasing public awareness of this issue; preventable complications are often reportable to regulatory authorities and many insurers, including Medicare, may refuse to pay hospital or physician charges in case of patients with certain preventable critical care complications. Health care consumers can readily obtain ICU complication rates for their health care institutions from a variety of media. The need to reduce preventable complications of critical care has resulted in a number of guidelines released by professional and regulatory organizations and local hospitals.^7,16

Infectious Complications

Two particularly troublesome and expensive nosocomial infections that occur during critical care after major trauma are CLABSI and VAP. One of the principal issues regarding VAP is its effect on outcome after major injury. There is evidence that pneumonia may exacerbate multiple organ failure and ARDS and could be associated with increased mortality, as has been found in other studies. CLABSI rates range from 1.2 to 5.6 per 1000 central venous catheter days with a marked increase in risk after 9 catheter days. CLABSI are also associated with longer length of stay, increased cost and an attributable mortality of 12–25%.⁹⁰ Both CLABSI and VAP are discussed in detail elsewhere (see Chapter 18).

Critical Illness Polyneuropathy

Prolonged neuromuscular weakness associated with critical illness was reported as early as the 1950s. Found to be associated with sepsis, hypotension, or multiple organ dysfunction, Critical illness polyneuropathy (CIP) may prolong weaning from mechanical ventilation, delay return to ambulation, and significantly affect overall recovery from post-traumatic critical illness. The syndrome is characterized by the development of diffuse neurogenic muscle weakness over a several-week course of severe critical illness. The neurologic manifestations may include unexplained failure to wean from mechanical ventilation, decreased/absent deep tendon reflexes, tetraparesis, muscle atrophy, decreased fibrillations, compound muscle action potentials, and axonal damage on electrophysiologic testing. Nerve conduction velocities are near normal, and histologic evaluation of peripheral nerves has shown acute diffuse neurogenic atrophy in muscles and axonal degeneration in nerve tissue. CIP may be far more common than is currently recognized and may frequently affect ventilator weaning and recovery.⁹¹ It should be considered as a cause of weaning failures or generalized weakness in the setting of critical illness. Electrophysiologic evaluation of muscle and nerve function is important for the diagnosis. Although not conclusive, available data suggest that the avoidance of long-term use of neuromuscular blocking agents (eg, pancuronium and vecuronium), particularly in combination with corticosteroids or aminoglycoside antibiotics, may be an important preventative measure. Recovery from CIP, although prolonged, may be nearly complete from a clinical standpoint. Follow-up electromyographic studies have shown changes with chronic neurogenic damage, however.

The Geriatric Trauma Patient in the ICU

Mortality in elderly trauma patients is significantly higher than that of their younger counterparts and has been associated with cardiovascular and septic complications.⁹² Therefore, aggressive monitoring is warranted as it may help in diagnosing physiologic deterioration and in assessing the effectiveness of a number of therapies deployed in an attempt to improve outcomes (see Chapter 44). End of life and goals of care discussions (see below in this chapter) are also particularly important in this patient population.

Sepsis and subsequent multiple organ system failure cause most late deaths following trauma in the elderly. Urosepsis and pneumonia are common in elderly trauma patients and what would be otherwise a relatively simple problem to treat in the young healthy individual may be the trigger to a cascade of events in the elderly patient, which may culminate with multiple organ dysfunction and death. For these reasons, aggressive and early treatment of these infections, initially with broad-spectrum antibiotics followed by culture-based deescalation or adjustment of therapy, is a critical determinant of good outcome.

One of the most common causes of death in the geriatric trauma population is pneumonia following blunt chest trauma and rib fractures. Due to decreased pulmonary reserve and associated comorbidities, the elderly trauma patient is generally more susceptible to the development of pneumonia due to an inability to effectively clear secretions and take deep breaths. Two aspects in the early initial care in the ICU in these patients are important: avoidance of fluid overload and adequate analgesia. To this end, patient-controlled narcotic analgesia and/or epidural administration of opiate analgesics or local anesthetics (rib blocks or chest wall pain catheters) may be helpful in appropriately selected trauma patients. Another option is surgical stabilization of rib fractures, but indications are not agreed upon, and data to date have not been able to demonstrate a consistent outcomes benefit.⁹³

Geriatric patients are also at increased risk for thromboembolic complications following trauma. Patients in the high-risk group for thromboembolic events (traumatic brain injury, spinal cord injury, complex pelvic fractures, bilateral lower extremity fractures, prolonged immobilization, or a previous history of deep venous thrombosis or pulmonary embolism) should receive pharmacologic prophylaxis with low-molecular-weight heparin, and/or inferior vena caval filter placement when the risk of bleeding has passed.

More recently, trauma centers in the United States have experienced an epidemic of elderly falls. The main clinical trials on anticoagulant therapies rarely include the frail elderly; however, many such patients arrive after taking these drugs. Common agents such as aspirin, clopidogrel, and warfarin have been joined by novel oral anticoagulants (NOAC) such as dabigatran and rivaroboxan. NOACs may require specific antidotes, if available or use of concentrated clotting factors such a prothrombin complex concentrates (PCC). Even patients with mild to moderate traumatic brain injury are at a much higher risk of developing fatal intracranial hemorrhage due to the use of these drugs and because of “increased space” for hematoma expansion due to brain atrophy. Rapidly obtaining a brain CT scan and quickly assessing coagulation parameters for reversal of anticoagulation are critical in early management. Those individuals who need an immediate craniotomy may benefit from rapid reversal with PCC.

Missed Injuries

The initial evaluation of the trauma patient centers on recognizing abnormal physiology and the pattern of injury. Missed injuries are the most common cause of preventable death; however, the true incidence of missed injury is difficult to determine. Surgical intensivists caring for trauma patients must recognize potential injuries likely to occur given a particular mechanism. The challenge becomes the rapid identification of occult injuries before the clinical condition of the patient deteriorates. Missed injury is a major pitfall in the care of trauma and an unexpected deterioration in the condition of the patient in the ICU should prompt a reexamination for possible missed injury, among other causes. Trauma patients in the ICU should undergo a tertiary survey and careful review of imaging results to reduce the risk of missed injury.⁹⁴

Postresuscitation Hypotension in the ICU

Any patient developing hypotension postresuscitation is bleeding until proven otherwise and aggressive investigation of the etiology is mandatory. Such episodes should prompt a reevaluation of the patient’s workup and raise the specter of a missed intra-abdominal injury or solid organ injury rebleeding due to overresuscitation and dislodgment of the initial hemostatic clot. It is a common pitfall to ignore such an episode, and assume that resuscitation has been completed and hypotension is due to other causes such as traumatic brain injury or bleeding due to long bone fractures.

There are certain injuries that may require ongoing resuscitation with blood products, most prominent among them a vertical shear-type posterior element pelvic fracture (see Chapter 35). However, in the absence of any such known injury, a diligent attempt must be made to exclude a missed injury in the abdomen or perhaps an injury whose magnitude was underestimated.

The traditional end points of resuscitation include an adequate urinary output, the trend of the base deficit on the arterial blood gas, and normalization of arterial lactate levels. There are situations in which the urinary output may be misleading. The intoxicated patient will have good urinary output even in the face of hypovolemia, because alcohol inhibits the release of ADH from the posterior pituitary; in addition, it is hypertonic and leads to peripheral arterial vasodilation. Another situation in which the urinary output will be misleadingly elevated is in the setting of hyperglycemia. Whether the patient is a diabetic or he or she has received high-dose steroids for a spinal cord injury, the resultant hyperglycemia will cause a misleadingly comforting urinary output. A serum blood sugar over approximately 180–190 mg/dL results in glycosuria and this pitfall must be recognized.

Similarly, the base deficit can also be misinterpreted. The etiology of metabolic acidosis in the injured patient is, until proven otherwise, due to hypoperfusion from hemorrhagic shock; it must be understood, however, that the base deficit can be due to ketosis, nonanion gap acidosis including hyperchloremia due to excess saline infusion and sepsis.

Hypoxemia and Pulmonary Contusion

Parenchymal disease is the most common cause of hypoxemia (see Chapter 57). The causes include aspiration pneumonia, hospital-acquired pneumonia, pulmonary contusion, or the ARDS. Pneumothorax and/or hemothorax may also manifest as hypoxemia but generally occur during the initial phase of the resuscitation and less often in the ICU. Pulmonary contusion consists of a direct injury to the lung the contusion evolves over the first 24 hours as alveolar hemorrhage and edema accumulate, such that the Po₂ progressively decreases during that time period. The contused lung has leaky capillaries and aggressive fluid resuscitation, particularly with colloids, may result in further deterioration of pulmonary function. The biggest pitfall in the management of pulmonary contusions is failure to anticipate injury progression. Some new evidence suggests CT scanning of the chest can be used to estimate the amount of injured lung and need for mechanical ventilation.⁹⁵

SIRS, Sepsis, Severe Sepsis, and Septic Shock

Injury leads to the activation of the inflammatory response, which may be aggravated by the severity of shock, degree of tissue injury, and secondary insults (see Chapter 12). To some extent, severely injured patients invariably develop an SIRS. SIRS is defined by manifestation of two or more of the following conditions: (1) temperature greater than 38°C or less than 36°C; (2) heart rate greater than 90 beats/min, (3) respiratory rate greater than 20 breaths/min or Paco₂ less than 32 mm Hg, and (4) white blood cell count greater than 12,000/mm³, less than 4000/mm³, or greater than 10% immature forms. The treatment of SIRS is supportive.¹⁶

Sepsis is defined as the presence of a proven infection in a patient with SIRS. Severe sepsis includes sepsis and organ dysfunction, while septic shock encompasses severe sepsis accompanied by hypotension and hypoperfusion, refractory to volume replacement and requiring inotropes. The hemodynamic derangements in sepsis, or, more properly, severe sepsis, are classically hypotension, high CO, a low SVR, and metabolic acidosis. Persistent SIRS and sepsis may ultimately lead to multiple organ dysfunction (discussed in another chapter).¹⁶

The source of sepsis in the injured patient relates to the type of injuries. It is extremely rare for a patient to have septic shock early, unless there is an obvious infection, such as an aspiration pneumonia or perforated viscus. The patient who has leukocytosis with bandemia, fever, and clinical deterioration must be investigated closely for a source of infection. The diagnosis of an infection following major trauma is the biggest pitfall since the cardinal signs of infection such as fever, leukocytosis, and hyperdynamic hemodynamic state can, and frequently are, the result of the inflammatory cascade in response to tissue trauma. The pitfall lies in the differentiation between sepsis and SIRS. The consequences of liberal use of antibiotics to broadly cover for presumptive sepsis are real, including drug resistance, antibiotic-related colitis, and fungemia. The consequences of not treating a patient with fever, hyperdynamic state, and signs and symptoms of infection, in the absence of positive cultures or a clear source, are equally daunting, as the patient may indeed be harboring an infection, but the yield of blood cultures and the other surveillance tests are poor. Unfortunately, there is no reliable method to clinically distinguish between the entities of sepsis and SIRS until a clear source of infection is identified. The usual sources of infection in the ICU are the lungs, indwelling vascular catheters, the urinary tract, and wounds. Each of these sites must be surveyed for infection.

The optimal management of septic complications is prevention, the Surviving Sepsis campaign provides a bundle of prophylactic and treatment measures to reduce the incidence and impact of sepsis.¹⁶ Lower mortality was observed in high (29.0%) versus low (38.6%) resuscitation bundle compliance sites (p < 0.001) and between high (33.4%) and low (32.3%) management bundle compliance sites (p = 0.039).⁹⁶

Acalculous Cholecystitis

Acalculous cholecystitis is a “hidden” cause of fever in the ICU. Changes in gastrointestinal motility, characterized by increased gastric residuals and intolerance to enteral nutrition, imply the onset of an infection and one potential source of such infection is the gallbladder. Acalculous cholecystitis is a disease of the critically ill patient; most of these patients have had major trauma or extensive burns, or are recovering from major surgery. The diagnosis can be difficult because patients who develop acalculous cholecystitis tend to be critically ill or severely injured and are frequently unable to react to physical examination. An ultrasound will typically show a thickened gallbladder wall without stones. The diagnostic test of choice is the HIDA scan, which will demonstrate a lack of emptying of the gallbladder in response to administration of cholecystokinin. The initial treatment for acalculous cholecystitis is conservative (bowel rest, antibiotics, and intravenous fluids), although some patients will require operative intervention. Alternatively, for those patients who are too sick to tolerate an operation, a percutaneous cholecystostomy tube placement is the best option.

Ethics may be regarded, in part, as a series of societal formulations predicated on moral values designed to produce a theoretical “optimal good.” With the ability of modern ICUs to maintain physiologic support and homeostasis well beyond the bounds of reasonable sentient existence, physicians are increasingly called on to participate in sometimes difficult live-or-die, withdraw/withhold support decisions. While ICU ethics also include other considerations, such as consent issues and donor organ procurement (see Chapter 50), this section focuses on the withdrawal/withholding of physiologic support including the application of do not resuscitate (DNR) orders in the surgical ICU.

Ethical Principles Applicable to Medical Decision Making

Ethical decision making should involve the careful application of established principles. The temptation to apply one’s individual value system to the decision-making process is strong, but the personal values of the patient are paramount, and the personal judgments of both family members and physicians must be considered in the context of the ethical principles involved. With the possible exception of the principle of distributive justice, each of the following principles should be applied in any given decision-making process:

• Beneficence : The principle of “doing good” as applies to a particular patient, individual, or situation.

• Nonmaleficence: The principle of avoiding harm or wrongdoing, as applied to a particular situation or individual.

• Autonomy: Perhaps the most important operative principle in critical care ethics is the right of self-determination—the inherent right of individuals to make decisions regarding their own treatment options (or withholding thereof) and ultimately make decisions that will impact their survival.

• Full disclosure: The principle of accurate communication of information that will allow individuals (or their surrogates) to exercise autonomy or surrogate decision making.

• Social (distributive) justice: The principle whereby benefits to an individual, if associated with burdens to another individual or individuals must be weighed in terms of the most “good” done to the society or group as a whole. This last principle typically involves decisions regarding the distribution of scarce resources to allow the “optimum” treatment of not a single individual, but a population of individuals (society). Such a principle may apply during wartime casualty triage or civilian mass-casualty triage.

Withdrawal/Withhold Support Decisions

Modern ICUs have developed the increasing technical capability to support homeostasis, even in the face of what would otherwise be overwhelming disease. Increasingly in the trauma population of ICU patients, patient demise is the result of a decision to withdraw or withhold life support. The consequences and irreversibility of such withdraw/withhold decisions in the ICU mandate that they be considered very carefully and predicted on the careful application of ethical and legal principles.

The importance and impact of withdraw/withhold decisions is considerable. In a review of such decision, Smedira et al found that in a mixed population of surgical and medical ICU patients, support was withheld in 1% and withdrawn in 5%. The resultant deaths accounted for 45% of all ICU deaths in the two institutions under study.⁹⁷ The general setting under which withdraw/withhold decisions are made is poor prognosis, which would include a low chance of survival and high likelihood of poor cognitive function. Specific criteria that may allow withdrawal/withholding include the following:

• Provision of further treatment is considered medically futile with respect to achieving well-defined therapeutic goals.

• The patient with decision-making capacity (DMC), in exercising his or her autonomy, chooses to have support withdrawn/withheld.

• A legal surrogate decision maker (legal guardian or durable power of attorney) chooses to have support withdrawn/withheld under medically appropriate circumstances.

• The decision is made on the basis of a prior written medical directive stipulating circumstances under which support may be withdrawn/withheld.

• The physician, acting as a surrogate decision maker in conjunction with next of kin, other consultants, and possibly an ethics committee, elects to withdraw/withhold support. The decision should be based on the following considerations:

  • Information regarding the patient’s wishes: What the patient would be likely to decide if he or she had DMC. This may be obtained from family, friends, or other providers with a history of relevant contact with the patient.

  • The benefits/burdens test: The benefits of continued treatment are outweighed by the burdens to the patient of such treatment in accomplishing the defined therapeutic goals.

  • Substituted judgment: The “reasonable person test.” In the absence of other available information regarding a patient’s wishes, a withdraw/withhold decision should be regarded as one likely to be made by any “reasonable person.”

  • Best interests test: The decision to withdraw/withhold must be medically appropriate and should not significantly diminish opportunity for recovery within the bounds of benefits/burdens.

The concept of futility refers to the inability to accomplish a therapeutic goal through medical interventions regardless of the duration of such interventions or the frequency with which they are repeated. The concept of futility is central to initial withdraw/withhold support decisions. Determination of futility requires two elements: (1) the establishment of an agreed-upon therapeutic goal and (2) determination of the probability, given the application of medical therapy, of reaching these therapeutic goals. Therapeutic goals should be outlined as specifically as possible and may incorporate elements of both physical and cognitive functions. Patients with DMC must be allowed to define their own therapeutic goals, regardless of how “unreasonable” or stringent these goals may seem. The determination of the probability of medical therapy in achieving those goals should be left to the team of treating physicians. Once a given treatment or treatments are deemed to be futile, based on established therapeutic goals, the physician is under no legal or ethical obligation to provide such treatment. Current writing in medical ethics, public policy, and more recently by case law has supported this perspective, although some ethicists do not support this medical prerogative. Individual circumstances, however, particularly in regard to family considerations and consistent with the principle of beneficence, may occasionally be indications for short-term delivery of what otherwise would be considered medically futile care.

During the early ICU phase of care, determination of futility often is achieved in patients with severe nonsurvivable brain injuries (transaxial gunshot injuries or open skull fractures with loss of brain tissue and GCS = 3).

Patients with significant comorbidities, particularly those with end-stage liver or renal disease, and those with malignancies are not candidates for extreme resuscitation efforts or massive transfusion. To the same extent, blunt trauma victims with significant intra-abdominal bleeding and associated nonsurvivable brain injury, greater than 60% TBSA burns, and cervical spinal cord transactions should not be aggressively resuscitated. Even if some of these patients survive, they will do so with a very poor quality of life and it is the trauma surgeon’s responsibility to provide the family with such information.

Patients who received massive blood transfusions in the OR without complete hemostasis usually present to the ICU as hypothermic, acidotic, and coagulopathic (see Chapter 13). Although difficult to estimate, the rapidity of bleeding and transfusion requirements greater than two blood volumes have traditionally been used as markers of irreversibility and most surgeons would agree that in these circumstances, if bleeding is nonmechanical and hypothermia and coagulopathy have not improved over a period of 6–8 hours, further resuscitation efforts are probably futile and will serve only to consume precious resources.⁹⁸

Late in the course of ICU care, defining futility in patients with neurologic injury is difficult, as it is almost impossible to predict those who will not achieve a meaningful recovery. Age and comorbidities should be considered when presenting the facts to family members, and they may facilitate the family’s decision to withdraw care.

In patients with multiple organ dysfunction, determination of futility is often achieved in those with three or more organ failures as mortality in these circumstances approaches 100%.

DMC, which has different implications than the legal term competent, requires the following:

• The patient must be able to comprehend and communicate information relevant to making a decision.

• The patient must be able to comprehend his or her alternatives and the benefits and burdens (risks) associated with each.

• The patient must be able to reason and deliberate about these alternatives against a background of stable personal values.

The determination of DMC may generally be made by the primary physician or team, but occasionally, particularly in the presence of underlying psychiatric illness, psychiatric consultation may be of benefit in making this determination. The exercise of autonomy is best accomplished by allowing any patient with DMC to participate in withdraw/withhold or DNR decisions. In many cases, a patient’s specific wishes may not be known and legal surrogates or medical directives may be unavailable. With careful adjustment (lightening to the extent possible) of any conscious sedation and directed efforts made in communicating the alternatives (full disclosure), many patients can make decisions or at least provide valuable information allowing surrogates to do so.

The written medical directive provides an alternative means by which a patient may exercise autonomy. Medical directives may be structured in a variety of ways—depending on known medical conditions, age of the patient, and so forth—but they typically contain language stipulating preferences (or not) for life-sustaining treatment as a function of expected physical and cognitive outcomes.⁹⁹

In situations where the patient does not have DMC and no specific medical directive is available, a surrogate decision-making process is utilized. Participants in the surrogate decision-making process may include family members, friends, other health care providers, clergy, and members of the institutional ethics committee. Family members invested with durable power of attorney may make clinically appropriate decisions independently on behalf of the patient. Surrogate decision making should involve close collaboration and extensive documented communication between health care providers and the family to the extent possible. The specific role of the family, however, in the absence of durable power, is not to actually make withdraw/withhold decisions but to provide information allowing providers to best formulate decisions consistent with what the patient’s desires would be. This information may include knowledge of the patient’s values, goals, religious or philosophical beliefs, or previously expressed wishes with respect to medical care. The importance of this information should not be underestimated; in the absence of durable power of attorney, family members have no recognized legal authority to dictate care or to make decisions that are medically or ethically inappropriate. Health care professionals also have a primary responsibility to act in what they perceive to be the best interests of the patient, which may occasionally be in conflict with wishes expressed by the family or, on rare occasions, the wishes expressed by a durable power agent.

In the absence of any information pertaining to the presumptive wishes of the patient, substituted judgment may be applied based on several considerations:

• What would a “reasonable” person want under similar circumstances? Physicians should rarely be making this judgment independently, and the involvement of colleagues or a formal ethics committee consultation may be appropriate.

• What would the likely benefits of continued treatment be (treatment outcome), weighed against the burdens imposed by both the treatment and the treatment outcome? The anticipated degree of functional recovery and resultant quality of life are important factors in this consideration. Therapeutic intervention designed to prolong life in a setting in which the quality of that life—because of severity of pain, lack of cognitive function, and so forth—is regarded as being excessively burdensome to an individual may not be medically appropriate.

In many cases, the outcome from a critical illness and specific degree of disability, at a given point in time, cannot be predicted with any degree of certainty. The best interests test prevents premature withdraw/withhold decisions from being made that might deprive a patient of an opportunity for satisfactory recovery. Additional professional consultation, including the institutional ethics committee, may help resolve the more difficult cases.

With good ongoing communication, full disclosure of relevant information and prognosis, and sensitivity to patient/family dynamics, withdraw/withhold support decisions can generally be made smoothly. The liberal use of consultants, particularly those involving the neurosciences, may be a valuable adjunct under such circumstances. Ethics consultation services have also been shown to affect management outcome when they are made available. Conflicts may arise, however, over issues of futility, therapeutic goals, and the conduct of surrogate decision making. These conflicts are often based on misunderstanding or mistrust and exacerbated by the lack of good communication.

In situations in which conflict between care providers and family members appears to be irreconcilable, even with ethics committee and institutional risk management/legal consultation, a number of alternatives should be offered to the family. These alternatives may include the following: (1) procurement of additional intramural or extramural medical, religious, or ethical consultations; (2) transferring the care of the patient to another provider within the institution; (3) transfer of the patient to another institution, under the care of another provider; and (4) procurement of a court order mandating a course of treatment.

The institution of DNR medical directives has been primarily based on the desire to avoid the indignity of futile cardiopulmonary resuscitation in the setting of inexorable progression of underlying known disease processes. Such orders are frequently applied to patients with long-standing terminal disease (eg, cancer, end-stage AIDS, and irreversible multiple organ failure). DNR orders are implicitly coupled to futility judgments about the benefit of cardiopulmonary resuscitation to achieve prospectively defined therapeutic goals. Under such circumstances, these orders are entirely appropriate and desirable in the variety of clinical disease states. The intensity of critical care interventions with mechanical ventilators and the use of complex drug regimens, including vasoactive drugs, may lead to unexpected (iatrogenic) complications unrelated directly to the underlying disease process for which a DNR order may have been originally placed. In addition, the critical illness being treated in the surgical ICU, particularly for trauma patients, results from a discreet event (surgery or injury) as opposed to complications or exacerbations of chronic disease, as is often the case for medical patients. The presumed reversibility of the physiologic sequelae constitutes a basis for ICU treatment of the trauma patient. As such, DNR for the trauma patient should be applied very carefully to expected complications, or physiologic changes due to inexorable progression of known underlying disease, as opposed to unexpected, very reversible iatrogenic complications.

DNR orders for trauma patients may be more appropriately linked to withdraw/withhold support conditions than more generally to patients with a poor but potentially reversible prognosis. The variability with which DNR orders are interpreted and the “message” such orders send to providers also raises concerns about their applicability for trauma patients. In addition to the potential for the inappropriate application of DNR orders in an ICU, application may result in less aggressive care on the part of ancillary providers.^100,101

DNR orders constitute the prospective application of a specific “withhold support” decision and should be made with the same care and consideration, as described in the above section, as any decision involving the limitation of critical care.