6: Critical Care for the Thoracic Surgery Patient

The thoracic surgery patient population can present significant challenges to clinical care. Patients often are older, current, or former smokers, and sicker than other surgical populations. It is not uncommon for these patients to present with underlying chronic lung disease, some form of arteriovascular disease, hypertension, diabetes, and baseline renal insufficiency. They have diminished physiologic reserve and more limited ability to recover from perioperative complications. In particular, they are prone to pulmonary complications, which are very poorly tolerated. As a result, they may require the services of an intensive care unit (ICU) and its highly trained, specialized staff more frequently than other patient populations. This chapter reviews critical care issues specific to thoracic surgery patients, general issues of management related to sepsis and acute respiratory distress syndrome (ARDS), and strategies for avoiding the common nosocomial complications of critical care.

Secretion Retention, Atelectasis, Pneumonia

Thoracic surgery patients are at increased risk of secretion retention and atelectasis. General anesthesia, particularly when accompanied by one lung ventilation (OLV), causes a marked decrease in functional residual capacity (FRC), which promotes atelectasis. Surgical manipulation of the lung can lead to retained blood and secretions, with partial or complete airway obstruction. Gas flow is further hindered by bronchospasm and decreased compliance of the operative lung. Splinting from postoperative pain, or conversely, respiratory depression from opiates or benzodiazepines further limit lung expansion. Patients with preexisting chronic obstructive pulmonary disease (COPD), asthma, bronchitis, or pneumonia will be at greatest risk. Similarly, patients with impaired cough reflexes, including those who have had airway resection with anastomosis (e.g., sleeve resection) would be expected to have greater difficulty clearing secretions. Secretion retention over time results in both hypoxemia and hypercarbia. It also predisposes the patient to pneumonia.

Preventing secretion retention and atelectasis requires a systematic, multidisciplinary approach. Time under general anesthesia should be limited to the minimum required to complete the procedure. Patients should be extubated immediately whenever possible. Fiberoptic bronchoscopy immediately before extubation facilitates the removal of blood and secretions from the proximal airways. Excellent analgesia combined with aggressive early ambulation will promote recruitment of lung volume and clearance of secretions. Chest physiotherapy further aids this process. Any patient with a preoperative pulmonary infection should undergo aggressive, culture-directed, antibiotic therapy during the immediate perioperative period.

Treatment of retained secretions and atelectasis includes aggressive chest physiotherapy and mobilization. Humidified oxygen, nebulized saline, and bronchodilators can help thin secretions and promote gas flow. Patients with copious, thick secretions may benefit from nebulized N-acetylcysteine or dornase (DNAse), with bronchodilator pretreatment to mitigate treatment-induced bronchospasm. Any patient having significant trouble clearing their secretions should be evaluated for the possibility of vocal cord dysfunction, which is a known complication of certain thoracic surgical procedures and results in a markedly impaired cough. A small subset of patients may require more aggressive interventions including repeated awake fiberoptic bronchoscopy, intermittent noninvasive ventilation, use of an Acapella® device or vibratory vest, assisted cough using an inexuflator device, or in the most severe cases, intubation and mechanical ventilation. Patients who require intubation primarily for secretion clearance should be evaluated for early tracheostomy.

Postpneumonectomy Pulmonary Edema

Approximately 2% to 9% of pneumonectomy patients will experience early onset idiopathic acute lung injury (ALI). It is characterized by the development of diffuse infiltrates followed by significant hypoxemia in the first 1 to 3 days postoperatively. In contrast to late onset ALI, no etiology is readily apparent. Pulmonary capillary wedge pressures are normal to low, and the alveolar fluid has high protein content. Studies using radiolabeled albumin have been consistent with a pulmonary capillary leak syndrome.¹ The relative rarity of this event has precluded the possibility of prospective analysis.

Retrospective analyses have identified multiple factors associated with the development of postpneumonectomy pulmonary edema (Table 6-1).² The exact etiology remains unknown. It has been postulated that ventilator-induced lung injury, oxygen toxicity, tissue injury with cytokine release, loss of lymphatic drainage, pulmonary hypertension, and shear injury to the capillary endothelium from increased blood flow through the remaining pulmonary artery all contribute to the development of capillary leak and the subsequent accrual of interstitial lung water. Once a capillary leak develops, movement of fluid from the pulmonary vasculature to the interstitium is governed by hydrostatic and colloid osmotic pressures, as described by Starling's law. Few recommendations can be made regarding strategies to prevent postpneumonectomy pulmonary edema, but it would seem prudent to use lung-sparing ventilation with lower tidal volumes and plateau pressures and to limit intravascular fluid to the minimum needed to support end-organ perfusion. Likewise, hypercarbia, hypoxia, and pain should be avoided because of the propensity to increase pulmonary arterial pressures. Once established, postpneumonectomy pulmonary edema is treated the same as any other case of ALI or ARDS, with lung-sparing ventilation and good supportive care.

Atrial Arrhythmias

Atrial fibrillation and atrial flutter are common after thoracic surgery. The incidence can be as high as 44% following extrapleural pneumonectomy.³ A number of factors have been associated with the occurrence of atrial arrhythmias (Table 6-2). Etiologies may include elevated catecholamines, myocardial ischemia, pulmonary hypertension, atrial enlargement, hypoxemia, electrolyte imbalances, mechanical displacement of the heart, and vagal nerve irritation. Trials in the cardiac surgery population have shown that prophylaxis with beta blockers, calcium channel blockers, sotalol, amiodarone, statins, or corticosteroids may decrease the incidence of atrial fibrillation.^4,5

The few clinical trials performed in lung resection patients suggest that both calcium channel blockers and beta blockers, given prophylactically, decrease the incidence of atrial tachydysrhythmia by roughly 50%.⁶ Hemodynamically stable patients with atrial arrhythmias can be treated with beta blockers or calcium channel blockers to achieve rate control. The ability of calcium channel blockers to reduce pulmonary vascular resistance (PVR) and right ventricular pressures makes this drug class an appealing choice for primary treatment in lung resection patients.

Digoxin may be used as an additional agent to improve rate control but care must be taken to avoid toxicity, particularly in the setting of renal insufficiency. Amiodarone is a useful agent for those patients who maintain a high ventricular response rate despite maximum therapy with other agents or who become hypotensive with first line agents. However, amiodarone can cause primary acute lung toxicity in patients who have undergone thoracic resections, and, therefore should be reserved as a second line therapy.⁷

The risk of third-degree heart block must be carefully evaluated if more than one nodal blocking agent is to be used simultaneously. Unstable patients may require electrical cardioversion to restore sinus rhythm. Unfortunately, the factors that led to the atrial arrhythmia are usually still present after surgery, and recurrence of the arrhythmia is common after either electrical or initial chemical cardioversion. Of note, however, the majority of patients with new onset atrial arrhythmia after surgery will be back in sinus rhythm within 6 weeks. This makes rate control with anticoagulation, if not otherwise contraindicated, a practical approach in this patient population.

Bronchospasm and Chronic Obstructive Pulmonary Disease Exacerbation

COPD is a common comorbidity in the thoracic surgery patient population. Intubation and airway manipulation can exacerbate a patient's COPD. The increased resistance to airflow increases the work of breathing and may result in frank respiratory distress. Associated “auto-peep” or dynamic hyperinflation, resulting from trapped alveolar gas, further increases the work of breathing, adversely affects gas exchange, and causes hemodynamic instability if venous return is impaired. Patients with COPD should be maintained on their home bronchodilator and inhaled steroid regimen throughout the perioperative period. The rare patient will require systemic steroids to treat an exacerbation of their COPD. Early extubation followed by aggressive mobilization is critical to avoiding the cycle of airway irritability, bronchospasm, dynamic hyperinflation, and respiratory distress.

Hypotension

Postoperative hypotension can be categorized as problems of pump function or venous return. Myocardial ischemia is a cause of acute ventricular dysfunction. Likewise, acute onset or worsening of pulmonary hypertension can lead to right ventricular failure (see Hyperglycemia). Venous return problems limiting effective diastolic filling of the heart are more common. Dehydration or acute hemorrhage leads to absolute hypovolemia. Tension pneumothorax, pericardial tamponade, pulmonary embolism, severe dynamic hyperinflation, mediastinal shift, and cardiac herniation will limit venous return despite normal intravascular volume. Finally, some patients may exhibit hypotension with a normal cardiac output and a low systemic vascular resistance. The increase in venous capacitance creates a state of relative hypovolemia. This low-tone state is typical of sepsis, but may also be seen with sympathectomies that are either pharmacologically induced from local anesthetics given via a thoracic epidural, or mechanically induced from trauma to the sympathetic chain during surgery. Central venous pressure (CVP) monitoring can be very helpful in distinguishing between the various causes of postoperative hypotension. If pulmonary hypertension and right heart failure is suspected, early placement of a pulmonary artery catheter (PAC) is advised.

Pulmonary Hypertension and Right Ventricular Failure

Acute onset of pulmonary hypertension with subsequent right ventricular failure is one of the most dreaded perioperative complications following thoracic surgery. Unless it is immediately recognized and successfully managed it can become rapidly fatal. Preexisting COPD, with its intrinsic loss of pulmonary microvasculature, limits the ability of the remaining lung to compensate for an abrupt increase in pulmonary blood flow following pulmonary resection and predisposes the patient to acute perioperative pulmonary hypertension. Preoperative evaluation, including echocardiography and cardiac catheterization can help to identify those patients with significant preoperative pulmonary hypertension. It should be understood, however, that these tests are done at rest, and sometimes under conscious sedation; therefore, may not accurately predict the pulmonary artery pressures that may occur postoperatively under the conditions of stress and hypermetabolism. Even a reassuring preoperative catheterization with a balloon occlusion trial does not completely rule out the possibility of postoperative right ventricular failure.

Patients with acute right ventricular failure will often present with hypotension and evidence of low cardiac output including oliguria, a high CVP and peripheral edema. Patients also may complain of dyspnea and lightheadedness, particularly with exertion. Unlike patients with biventricular failure, there generally is an absence of pulmonary edema, and left atrial pressures are low. Right ventricular dysfunction can occur in the setting of right ventricular pressure overload, volume overload, or impaired contractility. An electrocardiogram and echocardiogram will help exclude right ventricular ischemia or infarction, which if present, may require urgent therapy to treat an acute coronary syndrome. Likewise, the patient should be assessed for the likelihood of acute pulmonary embolism, as this can cause pulmonary hypertension and right ventricular failure and requires specific therapy.

Initial treatment of right ventricular failure is aimed at correcting reversible causes of pulmonary hypertension including hypoxia, hypercarbia, and acidosis. Pain and fever, because of their associated hypermetabolic state, can also cause pulmonary hypertension and should be rapidly treated. Volume management can be complex. Cardiac output is preload dependent; however, right-sided volume overload can adversely affect left ventricular output through septal shift and intraventricular dependence. The combination of echocardiography and PAC measurements can be helpful in identifying the optimum volume status for each patient. Right ventricular function and systemic blood pressure can be supported with the use of inotropes (dopamine, epinephrine, and norepinephrine) and inodilators (dobutamine, milrinone). A PAC is helpful for titrating therapy. If an inodilator results in an improved cardiac output but worsened systemic hypotension, low-dose vasopressin may be used to maintain systemic blood pressure without increasing pulmonary artery pressures. Unfortunately, the inotropes and inodilators are all arrhythmogenic and also increase myocardial oxygen consumption.

Pulmonary vasodilators reduce PVR and increase the right ventricular cardiac output without causing arrhythmias or increasing myocardial oxygen consumption. Unfortunately, the common vasodilators, including nitroglycerine, sodium nitroprusside, and hydralazine, usually result in significant systemic hypotension. Inhaled nitric oxide can decrease PVR and does not cause systemic hypotension. Recent experience has shown that many patients respond well to inhaled epoprostenol, which is considerably less costly than nitric oxide. Intravenous epoprostenol or enteral sildenafil may also be useful. Patients who develop chronic pulmonary hypertension should be evaluated by specialists with expertise in long-term management of pulmonary hypertension. Options for long-term management include: prostanoids (epoprosentol, treprostinil, and iloprost), endothelin receptor antagonists (bosentan, ambrisentan), and phosphodiesterase-5 inhibitors (sildenafil, tadalafil, vardenafil).⁸

Massive Hemoptysis

Massive hemoptysis defined as more than 600 mL of blood loss in 24 hours, is uncommon but can be rapidly fatal. It is associated with pulmonary infections, bronchiectasis, tumor erosion into a pulmonary or bronchial artery, pulmonary artery rupture during pulmonary artery catheterization, and trauma. Patients with massive hemoptysis are at imminent risk of death from asphyxiation. The patient should be turned bleeding side down to protect the good lung and intubated early rather than late. A bronchial blocker can be used to isolate the site of bleeding. Although double-lumen endotracheal tubes do allow for lung isolation, difficult positioning and very small internal lumens make them difficult to use in this setting. Once the patient is stabilized, focus should shift to determining the source of bleeding. Bronchoscopy, CT scanning, and angiography all may be useful. Further management is dictated by the specific cause of the hemoptysis.

Bronchopleural Fistula

The breakdown of an airway anastomosis or stump can result in the formation of a large proximal bronchopleural fistula (BPF). Alveolar rupture, persistent leak at a resection margin, or traumatic injury to the pulmonary parenchyma will create a more distal air leak. Empyema, tumor recurrence, irradiation, and poor wound healing all contribute to BPF formation. Early aggressive treatment of infection is critical. Maximizing the patient's nutritional status is a priority. Every effort should be made to keep patients ambulatory and breathing without mechanical assistance. If a patient requires mechanical ventilation, volume loss through the BPF can be quantified by comparing the inspiratory and expiratory tidal volumes recorded on the volume versus time loop of the ventilator graphics. Patients with significant volume loss may be easier to ventilate using pressure modes of ventilation. If the patient is awake, pressure support can be used if the ventilator model permits adjustment of the expiratory flow cut-off. Failure to increase the expiratory flow cut-off above the standard 25% may result in a sustained inspiration and subsequent ventilator dyssynchrony. No matter which ventilator mode is used, inspiratory pressure and volume should be minimized to limit the airflow across the BPF. In some cases, lung isolation may be required to permit adequate ventilation. This is particularly true for BPFs that occur after pneumonectomy, especially if the remaining lung is compromised. In this setting, double-lumen endotracheal tubes, endobronchial tubes or specially made tracheotomy tubes that are custom measured to sit below the carina will allow exclusion of the BPF. Unfortunately, it is difficult to maintain any of these tubes in constant position, and the emergent need to reposition these tubes occurs with some frequency.

Meticulous supportive care remains the mainstay of treatment for patients with ARDS. It is vitally important to manage the mechanical ventilation with a view toward avoiding ventilator-induced lung injury. The ARMA trial, published in 2000, showed that low tidal volume ventilation (6 mL/kg ideal body weight), with a plateau pressure of 30 cm H₂O or less, resulted in an 8% decrease in absolute mortality.⁹ This has now become the standard of care for patients with, or at risk of developing, ARDS. Ideally, the level of positive end-expiratory pressure (PEEP) should be set to prevent cyclic alveolar collapse at end expiration. Unfortunately, at this time there is no clear consensus on how to determine optimum PEEP in routine clinical practice. A pragmatic approach is to titrate the PEEP up until maximum pulmonary compliance and best oxygenation is achieved.

During the late 1970s and early 1980s, a number of trials were undertaken to investigate the use of high-dose corticosteroids in early ARDS.¹⁰ All of these studies were negative, with some actually resulting in increased mortality. The steroid debate reemerged in 1998 with the publication of a very small single center trial of prolonged methylprednisolone for late-stage ARDS.¹¹ This trial reported a significant decrease in mortality in the treatment group but was plagued by serious methodological problems in the trial design and execution. In 2006, the ARDSNet trials group published the results of a large, multicenter randomized trial of steroids for late ARDS.¹² The treatment group did, in the initial 4 weeks of treatment, have more ventilator-free and shock-free days, as well as improved oxygenation and pulmonary compliance. There was no difference in mortality at 60 or 180 days. Of note, if methylprednisolone was started more than 14 days after the onset of ARDS, there was a significant increase in mortality at both 60 and 180 days. The only subgroup that appeared to benefit from treatment was the group with elevated procollagen III levels in the alveolar fluid at the time of enrollment. At this time corticosteroids cannot be recommended for routine treatment of ARDS.

The ARDSNet Trials Group recently completed a complex but well-designed trial comparing a liberal versus restrictive fluid policy for patients with ARDS.¹³ The restrictive protocol targeted a CVP of 4 mm Hg or less provided the patient was not in shock and did not display signs of end-organ hypoperfusion. The liberal protocol targeted pressures of 10 to 14 mm Hg. There was no difference in mortality, but the restrictive protocol resulted in earlier liberation for the ventilator and earlier discharge from the ICU without any increase in organ failure. Another arm of the study executed the same fluid interventions but used a PAC rather than a central venous catheter. There was no advantage to PAC use in ARDS. This study reassuringly supports the common clinical practice of moderate fluid restriction.

Historically, mortality from septic shock has exceeded 40%. In 2001, Emanuel Rivers published a randomized prospective clinical trial of early goal-directed therapy. He focused on protocol-driven resuscitation within the first 6 hours of presentation.¹⁴ Mortality in this clinical setting was decreased from 46.5% to 30.5%. Bernard et al. published another study in 2001 regarding the results of a randomized, prospective trial of activated protein C (APC). APC led to a 6% absolute reduction in mortality, making APC the first pharmacologic substance to have proven efficacy in sepsis.¹⁵

In 2004, the Society of Critical Care Medicine, in conjunction with multiple other organizations, launched the Surviving Sepsis Campaign, which underwent substantial revision in 2008.¹⁶ The guidelines integrate findings from all recent high-quality sepsis trials. Care goals are bundled into the first 6 hours and the first 24 hours, reflecting increasing evidence that outcomes from sepsis are dependent on the timeliness of treatment.

Within the first 6 hours the focus should be on obtaining cultures, starting an appropriate broad-spectrum antibiotic regime, and executing rapid and effective fluid resuscitation. Specific recommendations for fluid resuscitation include the early placement of an arterial line and central venous line. Either crystalloids or colloids may be used to reach a CVP target of 8 to 12 mm Hg. If the patient is mechanically ventilated, a higher goal of 12 to 15 mm Hg is appropriate. Mean arterial pressure (MAP) should be maintained at greater than 65 mm Hg. If the target CVP has been reached and the MAP is still low, the patient should be started on vasopressors. Urine output (at least 0.5 mL/kg/h), trends in lactic acid levels, and the central venous oxygen saturation (SvcO₂) are followed for evidence of tissue hypoperfusion. If the SvcO₂ is less than 70%, the urine output remains low, or lactic acid levels are climbing, the patient may be a candidate for inotropic therapy and/or transfusion to a hematocrit of 30%, with the goal being to increase cardiac output and oxygen delivery.¹⁴ Norepinephrine and dopamine are considered the vasopressors of choice and dobutamine is the inotrope of choice. Source control is vital to the successful treatment of sepsis and any focal area of infection amenable to drainage or debridement should be addressed early.

Mechanically ventilated patients should be treated using the lung protective strategies outlined in the previous section. Appropriate glucose control should be instituted (see Hyperglycemia below). Routine evaluation for adrenal insufficiency is no longer recommended on the basis of the results of the CORTICUS trial.¹⁷ Corticosteroid therapy should be reserved for those septic shock patients who are poorly responsive to both fluid and vasopressors.

In many situations, a critically ill patient may survive their initial illness only to succumb to complications of their care. There are a number of well-recognized nosocomial complications that are common to ICU patients throughout the world. Most are preventable with appropriate attention to detail and protocolized care. The most common and significant nosocomial complications are discussed below.

Thromboembolism

Deep venous thrombosis (DVT) initially is a silent disease, and when accompanied by pulmonary embolism, it can be quite morbid in the thoracic surgery population because of limited pulmonary reserve. Virtually all thoracic surgery patients should receive aggressive prophylaxis for DVT, including mechanical venous compression devices and pharmacologic therapy with either low-dose unfractionated heparin or low-molecular-weight heparin. Even with appropriate prophylaxis, DVT does occur, and it is necessary to maintain a high index of suspicion for thrombotic and thromboembolic events in this population.

Stress Ulcers

Shallow gastric mucosal ulcerations, usually located in the proximal stomach, are common in ICU patients and develop rapidly after the onset of acute illness. In a small percentage, the ulceration will progress to involve the submucosal layers and can result in bleeding or perforation. Histamine-2-receptor antagonists are the mainstay of prophylaxis in the ICU setting. They have been shown to effectively decrease the rate of clinical bleeding from stress ulcers. Proton-pump inhibitors have also been used for this purpose. Unfortunately, both of these classes of drugs result in alkalization of the stomach resulting in overgrowth with gram-negative bacilli. A growing body of evidence shows that stress ulcer prophylaxis with pH-modifying drugs increases the rate of ventilator-associated pneumonia (VAP).^18,19

Pressure Sores

Pressure sores remain a troublesome issue for ICU patients. Many patients have multiple risk factors including immobility, heavy sedation, poor nutrition, impaired tissue perfusion, and frequent incontinence. Pressure sores are both morbid and costly to treat. Early identification of at-risk patients, combined with aggressive efforts at prevention, is needed. Preventative measures include correcting nutritional deficits, restoring tissue perfusion, minimizing sedation, and emphasizing early return to mobility even for ventilated patients. For patients who are immobile, redistributing body weight over bony prominences at least every 2 hours is mandatory. In addition, the skin must be kept clean and dry, and care must be taken to avoid sheer injury to the skin during turns. High-risk patients may benefit from special low air loss therapy beds.

Malnutrition

Inadequate nutrition is an insidious problem that can ultimately lead to severe consequences. It contributes to wound breakdown and infection, the development of pressure sores, immune suppression, and generalized weakness which in turn limits mobility and impairs weaning from mechanical ventilation. In addition, malnourished patients tend to have lower colloid osmotic pressures and more trouble mobilizing edema fluid. Corticosteroid use, when necessary, will further compound muscle catabolism and amplify the systemic effects of malnutrition. It is vitally important to begin nutritional repletion as soon as possible in all ICU patients. Enteral feeding is strongly preferred. Theoretically, postpyloric feeding should be associated with a lower risk of aspiration and improved ability to reach nutritional goals. Unfortunately, multiple trials have failed to demonstrate this benefit.²⁰ Decisions about enteral access should be made on an individual patient basis. Those patients who are not candidates for enteral feeding in the short term should be supported with total parenteral nutrition (TPN). Since TPN is associated with significant complications, initiation of TPN should be done concomitantly with reassessment of options to promote enteric function and allow for a rapid transition to enteric feeding. Critically ill patients should be regularly reevaluated to determine if their nutritional needs are being adequately met.

Hyperglycemia

Surgery and critical illness both result in a systemic stress response. Even nondiabetic patients will develop insulin resistance and hyperglycemia. A single center trial showed promising results with tight control targeting blood glucose of 80 to 110 mg/dL in critically ill patients.²¹ Unfortunately, subsequent studies, including the NICE-SUGAR trial,²² which enrolled 6104 patients have not confirmed these results. Currently the consensus recommendations from the American Diabetes Association and the American Association of Clinical Endocrinologists²³ recommend starting an insulin infusion for blood glucose greater than 180 mg/dL and targeting glucose of 140 to 180 mg/dL for critically ill patients. Further research is needed to identify the optimum blood glucose target in different populations and to test closed-loop systems that continuously monitor blood glucose and automatically titrate insulin.

Nosocomial Blood Stream Infection

Catheter-related blood stream infections (CRBSIs) are associated with an increased length of stay, increased cost of care, and significant attributable mortality. Recent research indicates that catheter-related blood stream infections are nearly completely preventable. The Centers for Disease Control and Prevention (CDC) publishes practice-based guidelines with which all clinicians caring for patients with central lines should be familiar.²⁴ A bundled approach that emphasizes hand hygiene, full body draping during insertion, chlorhexidine skin preparation, avoidance of the femoral site, use of a real-time checklist, and daily assessment for catheter removal has been remarkably effective at decreasing CRBSI rates in multiple institutions.²⁵

Ventilator-Associated Pneumonia

Certain thoracic surgical patients will require postoperative mechanical ventilation. Up to 25% of ventilated patients develop VAP. VAP is associated with significant morbidity and mortality and therefore prevention of VAP should be a priority for all ICUs. A number of simple interventions can reduce the incidence of VAP. Patients should be nursed in the semi-recumbent position, with the head of bed elevated at least 30 degrees at all times. Routine oral care, including twice daily chlorhexidine, has been shown to have a significant impact on VAP rates. Each institution should develop a standardized policy for mouth care of intubated patients. All patients should undergo standardized daily assessment for readiness to extubate, which may include the measurement of the rapid shallow breathing index (RISBI) or a spontaneous breathing trial. Any patient on continuous sedation should have a daily sedation holiday, unless contraindicated, with the assessment for readiness to be extubated timed to the sedation holiday. As mentioned previously, some evidence supports the use of sucralfate rather than pH-modifying agents for stress ulcer prophylaxis. Use of specialized endotracheal tubes with subglottic suctioning or silver impregnation may be appropriate for patients likely to be intubated for greater than 72 hours. Finally, the CDC has published guidelines on the care of respiratory equipment, including humidifiers, nebulizers, and tonsil tip suction devices. Institutional practices should be periodically reviewed to verify compliance with these guidelines in an effort to prevent such equipment from serving as a nidus of infection. Institutions that have bundled interventions to prevent VAP with universal training and frequent monitoring and feedback have been able to significantly reduce VAP rates across all patient populations.

Delirium and Over Sedation

For years, physicians and nurses have sedated mechanically ventilated patients to minimize the physiologic stress response and maximize patient comfort. Although these are laudable goals, these practices have resulted in the unexpected complications of increased delirium, delayed ventilator weaning, increased VAP, and severe physical deconditioning. Delirium in turn is associated with increased length of stay and higher mortality. All ICUs should use standardized sedation scores (e.g., RASS) and delirium assessment tools (e.g., CAM-ICU).^26,27 These standardized tools help to prevent over sedation and allow for early diagnosis and intervention for delirium. Writing sedation orders to target a specific sedation score, combined with daily interruption of sedative infusions, is particularly effective at minimizing over sedation and promoting early extubation. Patients who require heavy sedation to tolerate oral intubation should be evaluated for early tracheostomy.

Renal Dysfunction

Acute renal failure is a common complication in critically ill patients. Unfortunately, it is also a highly morbid one, with reported mortality rates greater than 50% in some trials. Prerenal azotemia refers to compromised renal function secondary to impaired renal perfusion but absent any actual damage to the nephron. This occurs in patients who are hypovolemic or have severely decreased cardiac output. It is rapidly reversible provided the underlying condition is recognized and corrected. Persistent renal hypoperfusion, such as that occurs in shock states, can result in cellular damage to the nephron or glomerulus, thus converting prerenal azotemia into intrinsic renal failure. Administration of nephrotoxic agents can amplify the injury or even result in de novo injury to the nephron in the absence of renal ischemia. Finally, the clinician must remember to evaluate every patient with acute renal failure for potential postrenal obstructive processes.

Close attention should be paid to avoiding renal injury in critically ill patients. Nephrotoxic drugs should be avoided whenever possible. Consideration should be given to pretreatment with n-acetylcysteine or sodium bicarbonate before intravenous contrast administration. Hypotension, hypovolemia, and hypoxia must be rapidly corrected. Patients with new onset of acute renal failure should have urine electrolytes and urine sediment evaluated. CVP monitoring may be helpful in detecting hypovolemia. An echocardiogram can provide a rapid assessment of overall cardiac function. If there is any concern for obstructive pathology, an immediate renal ultrasound should be performed. Although positive findings are rare, often they are amenable to intervention. It is important to carefully review the patient's medication list, eliminating all potentially nephrotoxic agents and renally dosing the rest. Should renal replacement therapy be needed, most critically ill patients tolerate a continuously administered replacement best. It is important to appreciate that it may take weeks for renal function to recover and it is impossible to accurately predict renal recovery.

Critical Illness Polyneuropathy and Acute Myopathy

Critical illness polyneuropathy occurs in up to 50% of patients who are septic for more than 2 weeks. The etiology remains unknown. Clinically, it presents as severe muscle weakness (distal worse than proximal), respiratory muscle weakness with difficulty weaning from mechanical ventilation, and decreased deep tendon reflexes. Pathologically, it is a disease of axonal degeneration and denervation. Nerve conduction studies show normal conduction velocities with prominent denervation. Patients who survive their underlying illness will regain muscle strength over a period of weeks to months. Treatment and prevention focus on avoiding compounding factors such as unnecessary use of corticosteroids or nondepolarizing neuromuscular blockers, both of which are thought to cause acute myopathy.²⁸ If paralytic agents cannot be avoided, every effort should be made to limit the duration of use to less than 48 hours. Beyond 48 hours, the incidence of myopathy becomes quite high. Malnutrition, heavy sedation, and prolonged immobility need to be avoided. At-risk patients should receive daily physical therapy with the goal of early resumption of mobility, even in the setting of prolonged mechanical ventilation. Ventilated patients may be ambulated with the help of a walker and either an Ambu bag or portable mechanical ventilator.

The management of the critically ill patient requiring thoracic surgery is facilitated by a partnership between a thoracic intensivist and a thoracic surgeon. Furthermore, this patient population frequently requires daily interventions, such as bronchoscopy, invasive monitoring, and nutritional support. This concise chapter provides clear instruction in the management of the most common issues, including secretion retention, arrhythmias, and avoidance of secondary complications. Management of pulmonary hypertension is frequently the focus of therapeutic intervention, and I call the reader's attention to this particular area. Specifics in ventilator management are discussed in Chapter 7.