A variety of acute injuries can result in critical illness and the need for ICU care. In the following material, we classify these "stresses" as related to a few main categories: surgery and trauma, metabolic disorders, and infection. In many patients, as in the patient just described, multiple stresses (eg, surgery, inflammation, and infection) coexist.
Direct Tissue Injury during Surgery and Trauma
Direct tissue injury during surgery and trauma can produce major perturbations of the body's homeostasis, including hemodynamic instability, respiratory abnormalities, and marked fluid shifts. Pain, immobility, and prolonged bed rest can contribute to perioperative morbidity. Only a few decades ago, these phenomena constituted a formidable challenge for surgeons and anesthesiologists, and they made many surgical procedures complex and dangerous for the patient. Today, the physiologic changes associated with so-called "routine" surgery can be flawlessly managed by the proper administration of perioperative anesthesia care. However, certain situations still carry a significant risk of perioperative complications, including complex elective procedures (eg, pneumonectomy, thoracoabdominal aneurysm repair), major trauma, emergency surgery, and procedures performed in patients with significant comorbidity. These patients constitute most of the population admitted to a surgical ICU.
Trauma is the primary cause of death in individuals younger than 40 years in the United States.1 In underdeveloped countries, trauma victims may have limited or no access to the type of structured intensive care that could save thousands of lives every year. Traumatic injuries are classified as penetrating and blunt injuries (see Chapter 76). Penetrating injuries (stab and gunshot wounds) require immediate control of hemorrhage, drainage of blood or air under pressure, and rapid transfer to a trauma center. Immediate appropriate care increases survival and can reduce the need for intensive care.2 Blunt trauma (eg, motor vehicle accidents, falls) can produce a combination of injuries that may require immediate treatment, such as a ruptured spleen or an open bone fracture, and others that are best treated conservatively. A damage control approach minimizes the time of surgical intervention and emphasizes perioperative surgical ICU care, including volume resuscitation, temperature control, hemodynamic monitoring, nutrition, and protocols for the prevention of nosocomial infectious complications. The injuries associated with major surgery and trauma derive from three main mechanisms: hemorrhage, tissue injury, and hypoperfusion.
Hemorrhage causes an immediate physiologic response to preserve oxygen delivery to vital organs. Using the large venous reservoir of the splanchnic and cutaneous circulation, the body maintains venous return and thus cardiac output to a certain extent.3 In healthy individuals, symptoms of shock develop when acute blood loss exceeds 20% of the blood volume (approximately 1 L of blood in a 70-kg adult). Immediate resuscitation is necessary to prevent cardiovascular collapse and death. Even at the low hemoglobin (Hgb) levels that accompany this degree of bleeding, what limits the tolerability of hemorrhage is the reduced blood volume and cardiac output, not the decreased oxygen-carrying capacity of the blood. For example, a 30% to 40% blood loss would eventually reduce the plasma Hgb concentration to a level that still produces ample delivery of oxygen to the tissues. With an adequate cardiac output and arterial oxygen tension (PaO2), a Hgb concentration as low as 5 g/dL still provides ample oxygen delivery to tissues supplied by normal vessels (Table 73-1).
Table 73-1 Values of Oxygen Delivery at Different Levels of Anemia ||Download (.pdf)
Table 73-1 Values of Oxygen Delivery at Different Levels of Anemia
|Hgb (g/dL)||CO (L/min)||ḊO2 (mL/min)|
Implementing early and effective therapies carry great importance in determining the subsequent clinical course. Despite a long-standing belief that aggressive volume resuscitation should be included in the initial care of the bleeding patient, this approach is now being revised for several reasons. First, the infusion of large volumes of crystalloids can cause a dilutional coagulopathy, characterized by thrombocytopenia and decreased concentrations of circulating clotting factors.4 Counteracting these defects by infusing platelets and fresh-frozen plasma, in conjunction with massive crystalloid resuscitation,5 results in intravascular volume overload and in edema of organs. Second, there is evidence that massive volume resuscitation for penetrating trauma of the torso may exacerbate bleeding from the site of injury and actually increase mortality.6 Third, transfusion of blood products may have immunosuppressive effects leading to an increased risk of infection, cause acute lung injury/acute respiratory distress syndrome (ALI/ARDS), and death.7,8
Tissue injury produces local and systemic perturbations that are minimized during elective surgery by using proper anesthetic and surgical techniques but can produce major damage in the random, unprotected situation of a traumatic injury. Tissue damage, loss of perfusion, and cell necrosis result in the immediate release of tissue factors into the bloodstream, which trigger a systemic inflammatory response characterized by the synthesis and release of cytokines. Tumor necrosis factor (TNF)-α and interleukin (IL)-6 are among the earliest cytokines to appear in the systemic circulation immediately after tissue trauma, and they amplify the complex inflammatory response that is an integral part of critical illness.9
Tissue trauma of different types can produce both direct and systemic effects leading to critical illness. One well-documented example occurs in injuries to the lung. In our case report, the initial cause of the patient's complex critical illness was a chemical injury to the alveolar epithelium caused by the aspiration of gastric contents. A similar evolution to critical illness can occur with other lung injuries, such as a lung contusion from blunt chest trauma or a pneumonia. Despite the variety of inciting factors, the lung responds to acute injury in a stereotypical fashion, leading to the pathologic picture of diffuse alveolar damange10 and the clinical picture of ALI/ARDS, which is a syndrome combining local and systemic inflammation.11 Although not as well studied, a similar sequence of events appears to follow major acute injury to the kidneys12,13 and the gut.14
Hypoperfusion and ischemia may result from direct tissue trauma, impaired regional blood flow, or a generalized decrease of blood flow: a low-flow state. A severe reduction of oxygen supplied to the tissues is marked by the local production of lactate from anaerobic glycolysis and may cause or exacerbate metabolic acidosis. However, even when profound ischemia occurs, tissue viability can be reestablished. The effects of restoration of blood flow after ischemic injury has been best characterized in the heart, where reversal of arterial occlusion is common with advanced techniques of coronary revascularization.15 Myocardial stunning describes the acute ischemic dysfunction caused by acute cessation of regional coronary circulation and can be reversed by rapid restoration of blood flow.16 Myocardial hibernation, a chronic state of dysfunction caused by insufficient coronary perfusion, can also, but less predictably, be improved with coronary revascularization procedures.17 However, global hypoperfusion is often irreversible: In the "postresuscitation syndrome" that occurs following prolonged cardiopulmonary resuscitation, stunning of the cardiac muscle (stony heart)15 is largely responsible for the high fatality rate observed early after cardiopulmonary resuscitation, and it is characterized by severely depressed contractility and malignant arrhythmias.
Although restoration of tissue oxygen supply may prevent cell death and reestablish function, acute reperfusion of ischemic tissues can cause significant cellular injury, known as ischemia-reperfusion injury. In the absence of adequate oxygen supply, mitochondrial production of adenosine triphosphate (ATP) decreases, causing an increase in adenosine monophosphate and its by-product hypoxanthine, and the conversion of the enzyme xanthine dehydrogenase to xanthine oxidase. Upon reperfusion with oxygen-rich blood, hypoxanthine is oxidized by xanthine oxidase at a high rate, producing large quantities of cytotoxic oxygen free radicals, including molecular oxygen, superoxide, and hydrogen peroxide ions.18 Ischemia-reperfusion injury has been described in patients with the crush syndrome,19 organ transplantation,20 restoration of blood flow to limbs or splanchnic organs,21 and during experimental alterations of ventilation and perfusion of the lung.22,23
Metabolic failure is a less common reason for admission to a surgical ICU. The most representative metabolic derangements include the consequences of severe malnutrition, such as extreme weight loss, kwashiorkor, and avitaminosis. These diseases are rarely seen in industrialized societies.
A different metabolic derangement, morbid obesity, has become more prevalent in the United States and other industrialized countries.24 Morbid obesity (defined as weight 30% in excess of ideal body weight, or a body mass index >40 [body mass index = weight in kg ÷ height in m2]) increases the risk of complications related to surgery and anesthesia. Morbidly obese patients are increasingly admitted to the ICU because of complications following bariatric surgery or unrelated events, such as trauma. Prevalent comorbidities of obesity include hypertension, diabetes mellitus, obstructive sleep apnea, chronic lung disease, and heart failure, which increase the rate of postoperative cardiovascular and respiratory complications. In addition, morbid obesity often presents logistical problems, such as the need for a special bed, a limited ability to perform important diagnostic tests such as magnetic resonance imaging and computed tomography scans, difficulty of vascular access and monitoring,25,26 and complex issues of proper drug dosing.27
Common metabolic derangements requiring ICU care include those related to chronic diseases such as diabetes mellitus, diabetic ketoacidosis, and hyperosmolar nonketotic coma. See Chapter 13 for management recommendations for diabetes mellitus and its complications.
Infection contributes importantly to both the onset and the progression of critical illness. In a survey of 198 European ICUs, sepsis was responsible for 25% of the ICU admissions, and 37% of ICU patients experienced sepsis and septic shock at some time during their stay.28 Infection is the leading cause of death in ICU patients. It is estimated that approximately 750 000 people develop sepsis annually in the United States, and 30% to 40% of these patients will die.29 The specific entity of severe sepsis following elective surgery has recently been reported to have an incidence of 0.5% to 1%, and a mortality rate that has decreased from 44% to 34% over the present decade.30 The presence of a proven infection in patients with ICU length of stays of more than 48 hours increases the mortality rate from 22% to 35%.31 The terms sepsis, severe sepsis, septic shock, and refractory septic shock describe the spectrum of severity of sepsis. Multiorgan dysfunction syndrome (MODS) is a common complication of sepsis and other inflammation-driven critical illnesses. MODS is associated with a high mortality. These terms were reviewed in a consensus conference of the Society of Critical Care Medicine and the American College of Chest Physicians32 and are thoroughly discussed in Chapter 72.
The most common community-acquired infections that require ICU admission include pneumonia, urosepsis, and peritonitis. Microorganisms involved in these infections are highly susceptible to antibiotic therapy when used properly. However, recent spread of multiresistant microorganisms outside health care institutions into the community has occurred, as exemplified by the case of methicillin- resistant staphylococcus aureus (MRSA). Community-acquired MRSA pneumonia is emerging as a particularly virulent infection due to the production of bacterial toxins, which is not well treated by vancomycin.33 Infections are also important because of their enormous impact on public health, current (tuberculosis, malaria, and AIDS) or potential (severe acute respiratory syndrome, avian influenza, and H1N1 influenza), and are summarized in Table 73-2.
Table 73-2 Infections that Constitute a Public Health Threat ||Download (.pdf)
Table 73-2 Infections that Constitute a Public Health Threat
|TB (bacterial)||Person-to-person droplets||14000 cases in the United States in 2003; enormous public health problem in Africa, Asia; on the rise in Europe; association with HIV||Antibacterial combinations are effective, but induced resistance develops|
|Malaria (parasite)||Anopheles (mosquito) bites||Widespread to warm and humid areas; sub-Saharan Africa has highest prevalence||Prevention and treatment with oral chloroquine and IV quinine; resistance is a problem|
|AIDS (virus)||Blood and body fluids, sexual||Relatively contained in United States; enormous public health problem in Africa, Asia, South America||Antiretroviral therapy slows progression but is not universally available|
|SARS (virus)||Person-to-person droplets||Worldwide outbreak in 2003; little in United States, now quiescent||Supportive|
|Avian flu||Birds to humans; sporadically person to person||Isolated cases; small outbreaks in Asia and Eastern Europe||Supportive|
|H1N1 flu||Person-to-person droplets||Worldwide outbreak in 2009, 2010||Supportive; antiviral therapy for high-risk group; prophylaxis: vaccination|
Health-care-acquired, or "nosocomial" infections (Table 73-3), are prevalent in the ICU and increase the mortality rate of critically ill patients.34-39 In our case report, the development of a Pseudomonas aeruginosa pneumonia acquired in the ICU halted the course of recovery from ARDS and prolonged the patient's time on the ventilator and in the ICU. Nosocomial infections are often caused by multiresistant bacteria such as P. aeruginosa, MRSA, vancomycin-resistant Enterococcus, and various enteric gram-negative bacteria, many of which have become difficult to eradicate. Independent risk factors for developing nosocomial infections such as VAP include the severity of the patient's underlying illness, its endogenous microflora, and the performance of invasive procedures. In turn, the patient's own microflora is affected by general practices of antibiotic therapy and by the transmission of nosocomial bacteria from patient to patient through breaches in proper infection-control measures.38,39 The most frequent ports of entry of nosocomial bacteria are indwelling devices such as central venous lines and urinary catheters. It has been clearly demonstrated that the incidence and related morbidity of nosocomial infections can be significantly curtailed by adopting simple procedures of sterile insertion and maintenance, and by removing devices as soon as they are no longer necessary.42
Table 73-3 Nosocomial Infections ||Download (.pdf)
Table 73-3 Nosocomial Infections
|Estimated Incidence||Estimated Mortality||Suggested Interventions|
|Ventilator-associated pneumonia34,35||5-10 per 1000 ventilator days36,39||10%-50%37|
Continuous aspiration of subglottic secretions40
Prophylactic "bundled" interventions41
|Central line–associated bloodstream infection35||1-5 per 1000 central line days36,39,42||30%-35%42||Hand wash, full sterile attire, alcohol-based prep, full-body sterile draping, discontinuing the line as soon as possible42|
|Catheter-associated urinary tract infection35||2-8 per 1000 catheter days36,39||Unknown; very low||Discontinuing the catheter as soon as possible|