Principles of Critical Care
The last two decades have seen great advances in the care of the injured patient, both in prehospital triage and transport and in the intensive care unit (ICU). More than ever, the outcome of these patients, in terms of both morbidity and mortality, is very dependent on a solid understanding of the pathophysiology and also of the evolution of certain injuries. Attention to detail is critical and an awareness of the pitfalls is essential, if one has to be successful in avoiding preventable morbidity and mortality.
Excluding early deaths in the operating room, most complications and subsequent deaths following injury will occur in the ICU. Care in the ICU is designed to reestablish normal homeostasis and minimize complications of primary, secondary, and iatrogenic injury. Surgical critical care is inherently different from medical intensive care insofar as surgical patients, and particularly trauma patients, require intensive care as the result of an acute surgical intervention or injury and not as part of the (often inexorable) progression or exacerbation of chronic disease. This fundamental difference affects a multitude of patient management practices and decisions.
In the last several years, increasing emphasis has been placed on quality of care indicators and physician staffing models for ICUs. Therefore, a modern surgical ICU in the 21st century has to provide evidence-based care using algorithms, clinical management guidelines (CMGs), and checklists, use cutting-edge technology for physiologic monitoring, and has to have a robust continuous quality improvement process to constantly 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.
ORGANIZATION OF 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. Most medical ICUs are staffed in this manner along with some surgical ICUs where the ICU team is directed by another surgeon.
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, with or without house staff. 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 ICUs have a “semi-open” or transitional unit plan of practice whereby the ICU is staffed, 24 hours a day, 7 days a week, with dedicated on-site ICU physicians. On-call physicians are often attending-supervised house staff in larger teaching centers, and responsibility for care is shared between the ICU team and the primary specialty service. With the 24/7 in-unit staffing in the semi-open model, critical care team involvement in 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 conscious sedation. In these units, the ultimate responsibility for the patient remains with the primary team, but patient care is a collaborative effort. This semi-open model combines the advantages of maintaining a separate in-house critical care team 24 hours per day 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 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 outcome. 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 ICU physician staffing and mandatory ICU team involvement with patient management. This includes all closed units and most semi-open units (as previously defined). The remaining “open” units typically involve “low-intensity” ICU physician staffing. The principal hypothesis is that dedicated, higher-intensity intensivist staffing for ICU patients will ultimately improve outcome 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 This validated previous work done by the same author.3,4 Similar results were found by Nathens et al. who specifically examined the effect of high-intensity staffing on outcome from major trauma.5 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 (semi-open) by board-certified intensivists. The effect of dedicated intensivist involvement seems to extend also to neurology and neurosurgical patients, with reports demonstrating improved overall mortality and length of stay.6,7
These and other observations have led to attempts to improve patient safety in the ICU. 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 the ICU that involves the presence of experienced intensivists providing daytime care and response requirements for off-hours care.8 The intent of the Leapfrog initiative is to provide market incentives designed to stimulate preferential use of institutions adhering to these types of guidelines. However, the current shortage of critical care specialists makes it impossible to maintain care in “closed” units.
CONTINUOUS QUALITY IMPROVEMENT IN THE SURGICAL ICU
Quality assurance and performance improvement in a surgical CCU 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, to a significant degree, on specialization (critical care specialists), provider education and training, and 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 (e.g., percentage of eligible patients receiving deep venous thrombosis prophylaxis in a timely manner), and outcome measures (complicaton rate [%] for central venous line sepsis). Illness severity indices have been developed for the purpose of predicting outcome of critically ill patients and are being increasingly used as benchmarking tools, allowing participating units, through the use of statistical comparisons, 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 outcome, the development and implementation of clinical protocols and CMGs9,10 directed at reducing undesirable treatment variability will be linked to CCU 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 subsequently modified and further developed as part of the overall programs in performance improvement and cost control.
The effectiveness of protocols and CMGs has been demonstrated for a variety of problems and conditions including ventilator weaning, pneumonia, nutrition, and sedation.11–17 The difficulties that most institutions experience, however, relate more to the implementation of CMGs rather than to their development. Current methods of improving implementation of and compliance with CMGs include ongoing education, standing (preprinted) order forms, the assignment of some management responsibilities to specialized teams (e.g., nutrition, respiratory therapy), and the use of advance practice staff (nurse practitioners, physician’s assistants).
More recently, several fields in medicine, motivated by an increased awareness about errors in medical care delivery and mandatory reporting of quality measures, 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 as part of a continuous quality process.18,19 A detailed description of how to develop and implement a quality improvement program in the ICU is beyond the scope of this chapter but important information can be found in the excellent reviews by Curtis et al.,15 and McMillan and Hyzy.20
Inspired by an article by Vincent21 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 use 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 (e.g., 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. Other variations of the original mnemonic have been reported recently.22
PHYSIOLOGIC MONITORING IN THE CRITICAL CARE UNIT
One of the characteristics of the ICU is the utilization of intensive physiologic monitoring. In past years there were a limited number of types of ICU monitoring available. There has been a dramatic increase in recent years in the ability to monitor a wider variety of physiologic parameters. Today significant issues for trauma surgeons deciding which monitoring to use include lack of familiarity and required training, maintenance, acquisition costs, safety, and efficacy.
Patients admitted to the ICU will have an anticipated and possibly optimal clinical “trajectory” that will be the expectation of the experienced clinician. A considerable effort is expended by the critical care physician in determining if the patient is following the anticipated trajectory, and in anticipating and detecting complications. Monitoring is used to determine that the patient has stable organ function, and detect anomalies that may indicate organ dysfunction and incipient or actual complications. Monitors can be useful in determining if a patient trajectory is deviating from the anticipated or optimal course; however, any monitor’s output requires interpretation and integration with the clinical picture and clinical experience. Monitoring itself is associated with serious and lethal complications, including complications associated with invasive monitoring, and errors in interpretation of results that can lead to error 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, pulmonary arterial (PA) pressure, and cardiac output 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 postinjury inflammatory response syndrome and multiple organ failure (see Chapter 61). However, the phenomenon of regional circulation and inadequate perfusion of some organs, particularly the gut, in the presence of normal arterial pressures remains a concern. Direct monitoring of tissue perfusion, particularly in potentially comprised capillary beds such as the intestine, is more difficult and not commonly performed. New types of monitors are becoming available that have some promise to determine perfusion at the tissue level in organs of interest.
Arterial Pressure Monitoring
Noninvasive blood pressure monitoring is available throughout the Medical Center by the use of the automated blood pressure cuff. These devices can be set to do repetitive blood pressure measurements as frequently as every minute. However, these are usually considered insufficient in patients who are having significant hypotension due to the lack of sensitivity of the cuff 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 display of arterial blood pressure, even at very low blood pressures. Arterial lines are the preferred method of arterial blood pressure management in patients receiving continuous drips of vasoactive drugs as they allow better drug titration and have a wide variety of indications (Table 55-2). They also allow for the ready sampling of arterial blood for laboratory testing including arterial blood gas and lactate. Arterial lines are typically placed in the radial artery, although they can also be placed in the femoral artery or brachial artery. 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 infectious complications. Thrombotic complications can occur at any arterial line site; these may be as common as 30–40% and may lead to tissue loss, including loss of digits. This is particularly common in patients who had prolonged hypotension or sepsis or who have been treated with pressors. 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 look at variation in area under the arterial pressure waveform as a surrogate for stroke volume variation with respiration. These devices can provide an estimate of cardiac output without need of a PA catheter, although they are subject to error.
Central Venous Pressure Monitoring
Monitoring central venous pressure is most useful in patients at high risk of overresuscitation or underresuscitation (see Chapter 56). These include patients with limited cardiac reserve, including elderly patients and patients with cardiac disease. Patients with traumatic brain injury are another group in whom central venous pressure monitoring is frequently performed to avoid hypotension associated with underresuscitation or overresuscitation resulting in increased cerebral edema. Patients with pulmonary contusions can suffer from overresuscitation, which can lead to increased lung water and worsening respiratory status. Interpretation of the central venous pressure in a ventilated patient should optimally be done while the patient has been removed from positive end-expiratory pressure (PEEP). Central venous pressure can also be approximated by subtracting the level of PEEP in excess of 5 mm Hg from the CVP measurement. The central venous catheter can also be used to obtain a central venous blood sample; this can be used to obtain a mixed venous blood gas measurement. Since the mixed venous oxygen saturation (MVO2) is usually slightly lower in the SVC as compared with that in the 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. MVO2 is sometimes used as a surrogate for global perfusion; falling MVO2 is frequently associated with hypovolemic shock and worsening tissue perfusion.23 A rise in MVO2 above baseline may represent decreased VO2 such as in sepsis or poisoning. Central venous catheters that have an oximetric tip can measure the saturation of blood at the tip of the central venous catheter or ScvO2. This allows another surrogate measure of global perfusion on a continuous basis. Combination of the oximetric CVP catheter data and the stroke volume variation from arterial line catheter waveform analysis data in a commercially available monitor can allow continuous estimates of cardiac output, SVR, and stroke volume without the use of a PA catheter.24 Initial validation studies of one system (FloTrac/Vigileo) were disappointing, but better results may be obtained with improved software.25
Pulmonary Artery Catheters
The introduction of the Swan Ganz PA catheter in 1970 was followed by wide adoption in critical care units. However, in the mid-1990s there were a number of reports questioning their efficacy and safety. A study by Connors et al. concluded that use of PA catheters increased mortality and led to increased utilization of resources.26 A more recent meta-analysis has not demonstrated increased major adverse sequelae associated with the PA catheter27; however, its utilization in ICUs has decreased significantly. ICUs typically restrict use of the PA catheter to patients who have known or possible myocardial dysfunction, or in those patients who are thought to be sensitive to changes in preload, contractility, or afterload.28 In 2000 an NHLBI workshop report on PA catheters and clinical outcomes produced a consensus statement that indicated that a clinician’s ability to obtain and interpret PA catheter data and intervene appropriately is an important determinant of outcome.29 An assumption is that if the PA catheter use changes therapy and is used to correct physiologic deficits, mortality and morbidity can be reduced. In surgical patients it appears that monitoring data obtained through the PA catheter results in therapy changes in 30–60% of cases. Of these, estimated at 25–30%, are major therapeutic changes. Since there is less experience available in interpretation of PA catheter data for trainees in critical care, courses and online training are available that allow interpretation of simulated data to improve understanding of PA catheter data. A useful tool that can help validate the data obtained with the PA catheter at insertion and at intervals thereafter is the use of echocardiography.
Echocardiography has been available in the ICU for years, usually as a service performed by the hospital’s cardiology service. The formal transthoracic echocardiogram (TTE) can be invaluable in determining the function and structure of the heart as well as the health of its components including valves and chambers. Patients in the operating room undergoing major procedures such as coronary artery bypass grafting or liver transplantation and patients with major trauma procedures are frequently monitored using transesophageal echocardiography (TEE). TEE has been used in the ICU to provide excellent visualization of the heart and its functions as well as detection of such injuries as blunt aortic rupture (see Chapter 26).30,31 However, frequent use of TEE in the ICU is usually limited due to the availability of the devices, cleaning requirements, and the skill required by the operator. Repeated measurements with the TEE are usually impractical for these reasons. However, there are now FDA-approved TEE devices using a disposable probe that can be left in the esophagus and stomach for up to 72 hours that allow for repeated measurements. This can permit observation of ventricular function and ejection fraction over time, and may have a safety advantage over PA catheters. The increasing utilization of ultrasonography by critical care clinicians now means many North American ICUs have clinician-performed ultrasound available. This has led to a number of studies and protocols utilizing a limited TTE by noncardiologists in trauma and critical care patients who may be too hemodynamically unstable to wait for formal TTE. In a patient who is hypotensive with an unclear etiology, visualization of ventricular size and function can be very useful in determining whether shock has a hypovolemic or cardiogenic origin. Limited TTE can also detect such conditions as pneumothorax and pleural effusions. However, in about 50% of trauma patients it is difficult or impossible to perform a complete TTE exam due to issues such as chest trauma, subcutaneous air, obesity, and dressings. Despite this, clinicians often attempt limited TTE in patients with hypotension or during cardiac arrest, due the utility of visualizing cardiac motion in successful examinations. Simplified protocols such as the “focus assessed transthoracic echo” (FATE) or the “bedside echocardiographic assessment in trauma/critical care (BEAT)” can be utilized by trauma and critical care physician to rapidly determine the cause of hemodynamic instability.
Other Monitoring Modalities
Gastric tonometry is one of the few modalities utilizing a direct measurement of gut perfusion as end point in resuscitation. The rationale for measuring the intramucosal pH (pHi) is based on the observation that splanchnic perfusion can be impaired in the setting of adequate blood pressure and cardiac output, leading to impaired GI mucosal barrier function that may induce multiple organ dysfunction (see Chapter 61). The catheter used resembles an NG tube with a saline-filled silicone balloon at the tip. When the balloon is in contact with the stomach wall, oxygen and carbon dioxide in the saline-filled balloon will equilibrate with oxygen and carbon dioxide in the stomach mucosa. Measurement of the pCO2 of the saline in the balloon allows determination of pHi via the Henderson–Hasselbalch equation. Gastric tonometry has not demonstrated a clear advantage compared with conventional resuscitation end points and its use has not been widely adopted.32,33
Transthoracic impedance, also known as bioimpedance cardiography, as a method to continuously measure cardiac output has been evaluated for decades. A high-frequency, low-alternating electrical current is applied to the thorax, and changes in bioimpedance to this current are related to cardiac events and blood flow in the thorax. The technique has been refined by looking at differing algorithms and different parts of the signal such as electrical velocimetry, phase, or frequency. However, results of studies have led to conflicting and inconclusive results, which may lead to inappropriate clinical interventions. As a result, transthoracic impedance has not yet been widely adopted as a method to measure cardiac output in noninvestigational settings. A new device is available that utilizes impedance electrodes on the outside surface of an endotracheal tube.34 This allows impedance measurements in the trachea immediately adjacent to the aorta. This has had promising results in initial studies in cardiac surgery patients.
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.35
Blood transfusions independent of shock or injury/disease severity are associated with worse outcomes. Increased infection, multiple organ dysfunction, and mortality are correlated with the amount of blood transfused and pH of transfused blood. Blood transfusions are common in the ICU with 40–45% of critically ill patients receiving an average of 5 U of packed red blood cells. 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.36 In a medical population, the trial by Rivers et al. found a 30% relative survival advantage for a bundle of interventions, including inotropes and transfusion to maintain a central venous oxygenation of 70%.37 Based on this, the “Surviving Sepsis” guidelines currently recommend to “transfuse packed red cells if necessary to hematocrit of >30%.”38 However, the TRiCC guidelines have been more recently reaffirmed by a guideline from the Eastern Association for the Surgery of Trauma and Society of Critical Care Medicine (EAST-SCCM), referring to multiple studies that failed to find physiologic benefit from red cell transfusion in septic patients.39 The EAST-SCCM guidelines do support aggressive, empirical transfusion in trauma and other surgical patients with uncontrolled hemorrhage. 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 anatomic hemorrhage control is achieved and laboratory values stabilize. Coagulopathy associated with trauma and massive transfusion may require the early ministration of plasma at a 1:1 ratio with packed red cells (see Chapter 13).
Erythropoiesis-Stimulating Agents (ESAs)
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, ESAs, have been widely accepted for the indication of anemia due to chronic kidney disease, these agents are also attractive for anemia of acute critical illness as they may allow more rapid restoration of hemoglobin levels without transfusion. However, the optimal hemoglobin targets and dosing have not been established and clinical trials have used target hemoglobins higher than those suggested by TRiCC. The Normal Hematocrit Study used larger doses of epoetin alfa to increase hematocrit to 42 ± 3% or to continue epoetin alfa therapy to maintain a hematocrit value of 30 ± 3%; the trial was stopped early due to 1.3 times increased mortality and nonfatal myocardial infarction in the 42 ± 3% hematocrit group.40 Increased adverse outcomes have been seen in subsequent ESA trials, the Correction of Hemoglobin and Outcomes in Renal Insufficiency (CHOIR) trial, using a target of 13.5 g/dL, and the Trial to Reduce Cardiovascular Events with Aranesp Therapy (TREAT) at a 13.0 g/dL target.41,42 CHOIR was halted at an interim analysis when mortality reached 17.5% of patients in the high-hemoglobin group and in 13.5% of patients in the low-hemoglobin group (hazard ratio, 1.34; 95% CI, 1.03–1.74; P = .03). TREAT showed no increase in mortality but there were significant increased risks of fatal and nonfatal stroke and thromboembolic complications. Studies of ESAs in critical illness have sometimes shown a reduction in need for transfusions. The EPO-1 pilot study (n = 160) demonstrated a reduction in red blood cell transfusion and a rise in hemoglobin with epoetin alfa treatment using a dose of 300 U/kg per day for 5 days and then every other day.43 The follow-up study (EPO-2, 1,302 patients), using a significantly lower dose of epoetin alfa (40,000 U per week), confirmed the transfusion findings.44 A third randomized study (EPO-3, 1,460 patients) was performed using a weekly epoetin alfa dose of 40,000 U in which the primary outcome was again transfusion reduction.45 No transfusion reduction was identified with epoetin alfa treatment in this third trial, although hemoglobin concentration did rise. A subsequent 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.46 There is no clear consensus on ESA dosing in trauma patients. A multicenter study in anemic (Hb <12 g/dL) ICU patients (n = 60) examined six different dosing regimens, intravenous or subcutaneous for epoetin alfa administered for a duration of 15 days.47 Only 30 patients were evaluable. Erythropoietin serum concentrations were 10–45 times greater for intravenous compared with subcutaneous dosing. Mean absolute reticulocyte count peaked on day 11 or 15, and absolute reticulocyte count was greater for subcutaneous dosing, but the pharmacokinetics did not predict pharmacodynamic response in these anemic critically ill patients. More frequent administration of lower doses of epoetin alfa was not superior to less frequent administration of larger doses, but the total cumulative doses of epoetin alfa were similar in all groups (120,000–170,000 IU). This would suggest that subcutaneous, weekly dosing is as effective as other regimens, although the optimal dosing regimen and route of administration of ESAs in critically ill patients for the treatment of anemia are yet to be determined. 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. Overall the benefits of ESAs appear to be related to a reduced need for transfusion rather than an improvement in other outcomes. A retrospective study of a revised trauma practice guideline for anemia after deletion of ESAs showed a significant cost reduction and no increase in blood product utilization.48
One of the principal indications for admission to the ICU for trauma patients is in 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: one, the avoidance of secondary brain injury by avoidance of hypoxia and hypotension and maintenance of cerebral perfusion; and second, the detection of increased intracranial pressure (ICP) due to posttraumatic phenomenon such as cerebral edema or expanding intracranial hematomas. The neurologic assessments are composed of the Glasgow Coma Scale for assessment of the verbal, motor, and ocular responses in association with pupillary exam. Patients with coma and patients requiring sedation and ventilation require frequent assessment of brainstem reflexes. Reassessment is done frequently as even subtle changes may herald increases in ICP or cerebral ischemia.
Intracranial Pressure Monitoring
ICP monitoring with a ventriculostomy catheter or through a subdural bolt is a common practice in most major centers for patients who have neurologic exam that is unavailable or unreliable following traumatic brain injury. The Brain Trauma Foundation 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.49 Monitoring of the ICP and CPP can be used to guide therapy such as vasopressors or opening the ventriculostomy catheter to drainage and to provide surveillance for increasing cerebral edema or intracranial hemorrhage. ICP monitoring in a large population of traumatic brain injury patients was found to improve survival versus those who did not receive ICP monitoring despite a higher severity of injury in the ICP-monitored group, 51% versus 35%.50 Investigational noninvasive monitoring systems for ICP include transocular ultrasound monitoring of optic nerve sheath diameter (ONSD).51,52 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 monitoring of cerebral vessels is another investigational approach for ICU monitoring of traumatic brain injury.
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 monitoring should begin with an assessment of the degree of preinjury malnutrition as well as current requirements. Weekly assessments in the ICU should include a calculation of nitrogen balance; this calculation takes a difference between excreted nitrogen from a 24-hour urine urea nitrogen and the ingested nitrogen. An overall goal is to have the patient had a 2–4 g positive nitrogen balance if possible. Indirect calorimetry (metabolic cart) provides an assessment of caloric requirements and metabolic rate. It may be significantly more accurate than predictions based on formulae such as the Harris–Benedict equation.53 This technique uses the rate at which gases are produced in the intubated patient to estimate caloric expenditure. 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.
TIGHT GLYCEMIC CONTROL IN THE ICU
Hyperglycemia with or without insulin resistance appears to be a common phenomenon in the critically ill patients. Based on literature that indicated outcomes were improved if blood sugars were maintained below 215 mg/dL, van den Berghe et al. hypothesized that hyperglycemia leads to worse outcomes in a critically ill population.54 In their prospective randomized controlled trial, their group demonstrated that tightly controlled blood glucose levels (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. The adverse consequences of hyperglycemia may be associated with even worse mortality in trauma patients. A retrospective analysis of 12 years of data on trauma and on trauma patients showed that hyperglycemia in trauma patients correlated with higher mortality rates than in other surgical patients.55 The intensive insulin regimen initially proposed by van den Berghe et al. has been associated with increased hypoglycemic complications and lack of benefit in subsequent multi-institutional studies such as VISEP, GLUCONTROL, and Normoglycemia in Intensive Care Evaluation Survival Using Glucose Algorithm Regulation (NICE-SUGAR).56–58 The NICE-SUGAR trial showed the primary outcome variable of 90-day mortality was actually increased in patients randomly 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 major centers; however, a less intensive insulin protocol than that suggested by van den Berghe et al. may be prudent in avoiding the likelihood of severe hypoglycemia.
The normal response to physiologic stress leads to increased levels of tissue corticosteroids; this is also seen in the patient’s 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. The use of steroid therapy in sepsis and critical illness has been a topic of an extensive literature and pendulum has swung between apparent benefit and apparent risk. Identification of patients with acute adrenal insufficiency can be difficult; random cortisol sampling (<15 μg/dL) and corticotropin stimulation tests (15–34 mg/dL) were often used to identify patients suitable for low-dose steroids (100–300 mg per day hydrocortisone). Patients with abnormal stimulation tests (increases <9 mg/dL) were felt to require corticosteroid supplementation. While a 2002 study by Annane et al. suggested benefit to low-dose steroids in sepsis, the 2008 multi-institutional CORTICUS trial did not show any 28-day mortality benefit with 300 mg per day of hydrocortisone in patients with septic shock, either overall or in patients who did not have a response to corticotropin.59,60 However, hydrocortisone did hasten reversal of shock in CORTICUS study patients. Lacking adequately powered positive studies, low-dose steroid therapy should probably be limited to patients with septic shock whose blood pressure is poorly responsive to fluid resuscitation and vasopressor therapy. Corticotropin stimulation probably has no role in determining steroid use in patients with septic shock. Steroids should be discontinued if the patient does not respond to treatment given the potential risks of infection, hyperglycemia, and critical illness polyneuropathy (CIP).
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.61 Infectious complications of major injury (see Chapter 18) may be due to the results of the injury itself (e.g., open fractures), as a result of complications of treatment (e.g., anastomotic leak), or as iatrogenic complications of critical care management (e.g., ventilator-associated pneumonia [VAP], central line infection). Specific monitoring for infections will depend on injury type and severity, types of interventions performed, and the duration of postinjury 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), which is required in some states. In a study using multiple regression analysis, the most common variables for infection were found to be central venous catheters, mechanical ventilation, chest tubes, and trauma with open fractures.62 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 in 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, at defined end point for culture-negative patients and applied and reviewed with sensitivity- and spectrum-based adjustment when final culture information is available. Importantly, all critically injured trauma patients with unexplained fevers do not require antibiotics. Persistently febrile, culture-negative patients often present a difficult diagnostic and therapeutic challenge. 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 immuno-suppression.
MECHANICAL VENTILATION: GENERAL PRINCIPLES
The need for mechanical ventilation is the most common indication for admission to the ICU. Familiarity and advanced understanding of mechanical ventilation principles is the lynchpin to managing severely injured patients in the ICU. 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 physiologic pathology.
Providing a secure airway via endotracheal intubation generally happens early during the initial resuscitation. Even though intubation for airway security can be secondary to ventilatory insufficiency, the two can be mutually exclusive. 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
Since the development of modern ventilatory support in the 1960s, significant technological advancements have been made to improve the ventilators themselves. Using contemporary ventilator technologies, new modes of mechanical ventilation are often introduced, each with an acronym and specific terminology. Despite these advancements, the essential physical principle of mechanical ventilation remains constant, which, simply put, is pushing oxygen-rich air into the lungs by positive pressure and removal of waste CO2 by negative pressure. Understanding this fundamental principle simplifies even the most “advanced” modes of ventilation and therefore allows the surgeon a streamlined method to manage complex ICU patients with clarity and an evidence-based approach.
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 is driven from the alveolar airspace into the pulmonary capillaries primarily due to the difference in the O2 diffusion gradient between the respective tissue beds. Measuring PaO2 quickly and reliably from arterial blood gas samples may be taken for granted in modern ICU care. The physical basis for measuring PaO2 is a result from the development of the oxygen electrode and measuring resultant electrical current that is directly proportional to oxygen concentration.63 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 (see below). 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.64 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. Finally, SaO2 is not indicative of ventilation. A rising PaCO2 and subsequent acidosis may not initially affect SaO2 especially if a patient is on high FiO2 settings. For these reasons, it is important to interpret SaO2 in combination with appropriate PaO2 measurements to individually determine a patient’s ability for oxygen exchange.
Adequate pulmonary exchange, exhalation of CO2, and resultant arterial CO2 tension (PCO2) have important physiologic and clinical implications. The immediate detection of CO2 through disposable endotracheal 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 < 0.5%, whereas a yellow color change is equivalent to EtCO2 of >2.0%.65 Normal EtCO2 is >4%; therefore, capnography turns yellow when the endotracheal tube is positioned correctly. The accuracy of 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 also give a false impression of successful endotracheal intubation even though it is the esophagus that has been intubated. In these circumstances, initial detection of EtCO2 decreases rapidly with subsequent tidal volumes. Clogging of the capnograph with mucous and enteric contents can also give false readings.
The measurement of PCO2, through blood gas analysis, remains the most accurate measure of assessing ventilation. Continuous capnography analyzes EtCO2 and, depending on the alveolar–arterial gradient, can give an indication of the arterial PCO2. After anatomic dead space has been cleared, EtCO2 rises until the end of exhalation. This rise is generally steep but plateaus during the alveolar phase of ventilation. In patients without preexisting pulmonary disease, the normal alveolar–arterial gradient is between 1 and 3 mm Hg. Therefore, using continuous capnography in a ventilated patient estimates the patient’s PCO2 especially during the initial resuscitation phase. Utilizing capnography can be helpful particularly 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.66 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 >40 mm Hg 80% of the time, and a PCO2 >50 mm Hg 30% of the time. In severely injured patients, where an increase in pulmonary shunt may exist, appropriate confirmation of EtCO2 by blood gas sampling is important.
Causes of hypoventilation can be multifactorial. Severe thoracic injury resulting in pulmonary contusion or flail chest can be a factor warranting expedient intubation. Increased dead space from pulmonary contusion, ALI, acute 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
The mechanically ventilated lung is an active continuum that reflects real-time physiologic complexities of an ICU patient. Assessing specific 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 as is 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 and peak inspiratory pressures (PIPs) for a given tidal volume as seen in pneumothorax or in abdominal compartment syndrome. However, measuring the individual changes of either static or dynamic compliance may indicate specific pulmonary pathology.
If the respiratory system is reduced to a simple model of a straw and a balloon, the straw would represent the airway, and its resistance, and the balloon would represent the elastic recoil of the lung and the chest wall. In static compliance, the change of volume produced is measured from the inspiratory hold pressures or plateau pressure using the following formula: Compliancestatic = Volumetidal/Pressureplateau – PEEP. Thereby static compliance measures the pressure resistance of the alveoli and chest wall, not of 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 acute respiratory distress syndrome (ARDS), ALI, and pulmonary edema.
Dynamic compliance measures compliance by equating the pressure, PIP, needed to overcome the resistance of the airways or the straw using the balloon analogy (Compliancedynamic = Volumetidal/PIP – PEEP). Cases of a sudden decrease in dynamic compliance or a measured difference between static and dynamic compliance are a reflection of increased airway resistance during bronchospasm, mucous plugging, kinked endotracheal tube, or foreign body aspiration.
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 Pflex (Fig. 55-1). This point, corresponding to the transition between the curve’s flat portion and linear portion during inhalation, represents the critical pressure needed to open collapsed alveoli and corresponds to the zone of optimal alveolar recruitment and gas exchange. Initial driving pressure therefore precedes alveolar filling and corresponds to gas flow within the airways. The pressure reading at the inflection point may reflect an optimal PEEP setting. In healthy lungs with normal compliance, oxygenation and ventilation is achieved with modest PEEP (5 cm H2O) and plateau pressures (Pmax) less than 30 cm H2O. 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 increasing PEEP are often employed to maximize gas exchange in the zone of optimal ventilation. However, using pressure–volume curves alone in clinical decision making has been neither shown to be efficacious nor shown to improve outcomes. There are significant inconsistencies in curve interpretation, which leads to significant operator variability. A standardized method of pressure curve interpretation may aid in predicting the development of ALI and ARDS.
FIGURE 55-1 Pressure–volume curves.
Assessing ventilatory capacity in the mechanically ventilated patient can be an important physiologic indicator to monitor clinical improvement and predict successful extubation. Its use is particularly applicable in patients who have been intubated for prolonged periods of time, have spinal cord injury or injury to the thorax such as flail chest or rib fractures, or patients with neuropathic disease (i.e., Guillain–Barré syndrome, myasthenia gravis). A forced vital capacity (FVC) and a negative inspiratory force (NIF) are the most frequent measured indices of ventilator capacity. A normal vital capacity, which consists of both inspiratory capacity and expiratory reserve, is between 65 and 75 cm3/kg depending on ideal body weight and sex. An FVC of 10–15 cm3/kg is an acceptable value to predict successful extubation.67
The NIF, in conjunction with FVC and the rapid shallow breathing index (RSBI; see below), is also an important variable during weaning. Despite the need for a cooperative and awake patient, the NIF estimates inspiratory muscle strength using a one-way valve manometer attached to the airway. The inspiratory force is then calculated based on the negative force generated by the patient during occlusion of the valve. A value of –25 to –30 cm H2O is indicative of adequate inspiratory force to maintain airflow after extubation.67
Despite estimating ventilatory capacity and other respiratory parameters, there exists great variability in practice in when and how parameters are determined. In a survey of nine Los Angeles area ICUs, Soo Hoo and Park found significant variability in the method and frequency of both NIF and FVC measurements. This study only further underscores the notion that current weaning practice is just as much art as science.68
VENTILATOR-INDUCED LUNG INJURY
It is well established that high airway pressures during positive pressure ventilation can cause lung injury secondary to overdistension and alveoli rupture (see Chapter 57).69 Ventilator-induced lung injury can be delineated into mechanical and inflammatory categories since these processes differ in their pathophysiology and treatment.
Repetitive distention and collapse of lung tissue from mechanical ventilation is the basic mechanical pathophysiology that is thought to cause ventilator-induced lung injury from inflammatory changes. Pathologic features of ventilator-induced lung injury include edema and an upregulation of inflammatory cytokines and cells, the combination of which can further damage pulmonary tissue and progressively lead to pneumonia and sepsis. Webb and Tierney conducted the first comprehensive study in rats demonstrating that 1 hour of positive pressure ventilation, with peak pressure at 30 cm H2O or higher, caused pulmonary edema.70 Several other experiments also show pulmonary edema with a progressive increase in inflammatory cytokines, such as IL-1, TNF-α, and IL-8, following mechanical ventilation, although larger animals and humans require longer periods of intubation for these inflammatory changes to occur.71 Given these initial experimental observations, several human studies were initiated with the intent to demonstrate that decreasing alveolar stretch by lower tidal volumes will prevent ongoing lung injury and improve ICU outcomes. A detailed description of current ventilating modalities used in the management of ARDS is beyond the scope of this chapter (see Chapter 57).
Spontaneous breathing utilizes negative intrathoracic pressure to fill alveoli (Fig. 55-2). In contrast, mechanical ventilation utilizes the principles of external insufflation generating 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, and improving areas of ventilation/perfusion mismatch, and thereby decreases 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. As previously mentioned, the physical simplicity of mechanical ventilation is often lost within the technical jargon of individual ventilator modes. 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 outcome. 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.
FIGURE 55-2 Spontaneous breathing mode of ventilation.