Critical care complications interpose a substantial cost burden to the health care institution and society and worsen patient outcomes. There is increasing public awareness of this issue; preventable complications are often reportable to regulatory authorities and many insurers, including Medicare, may refuse to pay hospital or physician charges in case of patients with certain preventable critical care complications. Health care consumers can readily obtain ICU complication rates for their health care institutions from a variety of media. The need to reduce preventable complications of critical care has resulted in a number of guidelines released by professional and regulatory organizations and local hospitals.7,16
Two particularly troublesome and expensive nosocomial infections that occur during critical care after major trauma are CLABSI and VAP. One of the principal issues regarding VAP is its effect on outcome after major injury. There is evidence that pneumonia may exacerbate multiple organ failure and ARDS and could be associated with increased mortality, as has been found in other studies. CLABSI rates range from 1.2 to 5.6 per 1000 central venous catheter days with a marked increase in risk after 9 catheter days. CLABSI are also associated with longer length of stay, increased cost and an attributable mortality of 12–25%.90 Both CLABSI and VAP are discussed in detail elsewhere (see Chapter 18).
Critical Illness Polyneuropathy
Prolonged neuromuscular weakness associated with critical illness was reported as early as the 1950s. Found to be associated with sepsis, hypotension, or multiple organ dysfunction, Critical illness polyneuropathy (CIP) may prolong weaning from mechanical ventilation, delay return to ambulation, and significantly affect overall recovery from post-traumatic critical illness. The syndrome is characterized by the development of diffuse neurogenic muscle weakness over a several-week course of severe critical illness. The neurologic manifestations may include unexplained failure to wean from mechanical ventilation, decreased/absent deep tendon reflexes, tetraparesis, muscle atrophy, decreased fibrillations, compound muscle action potentials, and axonal damage on electrophysiologic testing. Nerve conduction velocities are near normal, and histologic evaluation of peripheral nerves has shown acute diffuse neurogenic atrophy in muscles and axonal degeneration in nerve tissue. CIP may be far more common than is currently recognized and may frequently affect ventilator weaning and recovery.91 It should be considered as a cause of weaning failures or generalized weakness in the setting of critical illness. Electrophysiologic evaluation of muscle and nerve function is important for the diagnosis. Although not conclusive, available data suggest that the avoidance of long-term use of neuromuscular blocking agents (eg, pancuronium and vecuronium), particularly in combination with corticosteroids or aminoglycoside antibiotics, may be an important preventative measure. Recovery from CIP, although prolonged, may be nearly complete from a clinical standpoint. Follow-up electromyographic studies have shown changes with chronic neurogenic damage, however.
The Geriatric Trauma Patient in the ICU
Mortality in elderly trauma patients is significantly higher than that of their younger counterparts and has been associated with cardiovascular and septic complications.92 Therefore, aggressive monitoring is warranted as it may help in diagnosing physiologic deterioration and in assessing the effectiveness of a number of therapies deployed in an attempt to improve outcomes (see Chapter 44). End of life and goals of care discussions (see below in this chapter) are also particularly important in this patient population.
Sepsis and subsequent multiple organ system failure cause most late deaths following trauma in the elderly. Urosepsis and pneumonia are common in elderly trauma patients and what would be otherwise a relatively simple problem to treat in the young healthy individual may be the trigger to a cascade of events in the elderly patient, which may culminate with multiple organ dysfunction and death. For these reasons, aggressive and early treatment of these infections, initially with broad-spectrum antibiotics followed by culture-based deescalation or adjustment of therapy, is a critical determinant of good outcome.
One of the most common causes of death in the geriatric trauma population is pneumonia following blunt chest trauma and rib fractures. Due to decreased pulmonary reserve and associated comorbidities, the elderly trauma patient is generally more susceptible to the development of pneumonia due to an inability to effectively clear secretions and take deep breaths. Two aspects in the early initial care in the ICU in these patients are important: avoidance of fluid overload and adequate analgesia. To this end, patient-controlled narcotic analgesia and/or epidural administration of opiate analgesics or local anesthetics (rib blocks or chest wall pain catheters) may be helpful in appropriately selected trauma patients. Another option is surgical stabilization of rib fractures, but indications are not agreed upon, and data to date have not been able to demonstrate a consistent outcomes benefit.93
Geriatric patients are also at increased risk for thromboembolic complications following trauma. Patients in the high-risk group for thromboembolic events (traumatic brain injury, spinal cord injury, complex pelvic fractures, bilateral lower extremity fractures, prolonged immobilization, or a previous history of deep venous thrombosis or pulmonary embolism) should receive pharmacologic prophylaxis with low-molecular-weight heparin, and/or inferior vena caval filter placement when the risk of bleeding has passed.
More recently, trauma centers in the United States have experienced an epidemic of elderly falls. The main clinical trials on anticoagulant therapies rarely include the frail elderly; however, many such patients arrive after taking these drugs. Common agents such as aspirin, clopidogrel, and warfarin have been joined by novel oral anticoagulants (NOAC) such as dabigatran and rivaroboxan. NOACs may require specific antidotes, if available or use of concentrated clotting factors such a prothrombin complex concentrates (PCC). Even patients with mild to moderate traumatic brain injury are at a much higher risk of developing fatal intracranial hemorrhage due to the use of these drugs and because of “increased space” for hematoma expansion due to brain atrophy. Rapidly obtaining a brain CT scan and quickly assessing coagulation parameters for reversal of anticoagulation are critical in early management. Those individuals who need an immediate craniotomy may benefit from rapid reversal with PCC.
The initial evaluation of the trauma patient centers on recognizing abnormal physiology and the pattern of injury. Missed injuries are the most common cause of preventable death; however, the true incidence of missed injury is difficult to determine. Surgical intensivists caring for trauma patients must recognize potential injuries likely to occur given a particular mechanism. The challenge becomes the rapid identification of occult injuries before the clinical condition of the patient deteriorates. Missed injury is a major pitfall in the care of trauma and an unexpected deterioration in the condition of the patient in the ICU should prompt a reexamination for possible missed injury, among other causes. Trauma patients in the ICU should undergo a tertiary survey and careful review of imaging results to reduce the risk of missed injury.94
Postresuscitation Hypotension in the ICU
Any patient developing hypotension postresuscitation is bleeding until proven otherwise and aggressive investigation of the etiology is mandatory. Such episodes should prompt a reevaluation of the patient’s workup and raise the specter of a missed intra-abdominal injury or solid organ injury rebleeding due to overresuscitation and dislodgment of the initial hemostatic clot. It is a common pitfall to ignore such an episode, and assume that resuscitation has been completed and hypotension is due to other causes such as traumatic brain injury or bleeding due to long bone fractures.
There are certain injuries that may require ongoing resuscitation with blood products, most prominent among them a vertical shear-type posterior element pelvic fracture (see Chapter 35). However, in the absence of any such known injury, a diligent attempt must be made to exclude a missed injury in the abdomen or perhaps an injury whose magnitude was underestimated.
The traditional end points of resuscitation include an adequate urinary output, the trend of the base deficit on the arterial blood gas, and normalization of arterial lactate levels. There are situations in which the urinary output may be misleading. The intoxicated patient will have good urinary output even in the face of hypovolemia, because alcohol inhibits the release of ADH from the posterior pituitary; in addition, it is hypertonic and leads to peripheral arterial vasodilation. Another situation in which the urinary output will be misleadingly elevated is in the setting of hyperglycemia. Whether the patient is a diabetic or he or she has received high-dose steroids for a spinal cord injury, the resultant hyperglycemia will cause a misleadingly comforting urinary output. A serum blood sugar over approximately 180–190 mg/dL results in glycosuria and this pitfall must be recognized.
Similarly, the base deficit can also be misinterpreted. The etiology of metabolic acidosis in the injured patient is, until proven otherwise, due to hypoperfusion from hemorrhagic shock; it must be understood, however, that the base deficit can be due to ketosis, nonanion gap acidosis including hyperchloremia due to excess saline infusion and sepsis.
Hypoxemia and Pulmonary Contusion
Parenchymal disease is the most common cause of hypoxemia (see Chapter 57). The causes include aspiration pneumonia, hospital-acquired pneumonia, pulmonary contusion, or the ARDS. Pneumothorax and/or hemothorax may also manifest as hypoxemia but generally occur during the initial phase of the resuscitation and less often in the ICU. Pulmonary contusion consists of a direct injury to the lung the contusion evolves over the first 24 hours as alveolar hemorrhage and edema accumulate, such that the Po2 progressively decreases during that time period. The contused lung has leaky capillaries and aggressive fluid resuscitation, particularly with colloids, may result in further deterioration of pulmonary function. The biggest pitfall in the management of pulmonary contusions is failure to anticipate injury progression. Some new evidence suggests CT scanning of the chest can be used to estimate the amount of injured lung and need for mechanical ventilation.95
SIRS, Sepsis, Severe Sepsis, and Septic Shock
Injury leads to the activation of the inflammatory response, which may be aggravated by the severity of shock, degree of tissue injury, and secondary insults (see Chapter 12). To some extent, severely injured patients invariably develop an SIRS. SIRS is defined by manifestation of two or more of the following conditions: (1) temperature greater than 38°C or less than 36°C; (2) heart rate greater than 90 beats/min, (3) respiratory rate greater than 20 breaths/min or Paco2 less than 32 mm Hg, and (4) white blood cell count greater than 12,000/mm3, less than 4000/mm3, or greater than 10% immature forms. The treatment of SIRS is supportive.16
Sepsis is defined as the presence of a proven infection in a patient with SIRS. Severe sepsis includes sepsis and organ dysfunction, while septic shock encompasses severe sepsis accompanied by hypotension and hypoperfusion, refractory to volume replacement and requiring inotropes. The hemodynamic derangements in sepsis, or, more properly, severe sepsis, are classically hypotension, high CO, a low SVR, and metabolic acidosis. Persistent SIRS and sepsis may ultimately lead to multiple organ dysfunction (discussed in another chapter).16
The source of sepsis in the injured patient relates to the type of injuries. It is extremely rare for a patient to have septic shock early, unless there is an obvious infection, such as an aspiration pneumonia or perforated viscus. The patient who has leukocytosis with bandemia, fever, and clinical deterioration must be investigated closely for a source of infection. The diagnosis of an infection following major trauma is the biggest pitfall since the cardinal signs of infection such as fever, leukocytosis, and hyperdynamic hemodynamic state can, and frequently are, the result of the inflammatory cascade in response to tissue trauma. The pitfall lies in the differentiation between sepsis and SIRS. The consequences of liberal use of antibiotics to broadly cover for presumptive sepsis are real, including drug resistance, antibiotic-related colitis, and fungemia. The consequences of not treating a patient with fever, hyperdynamic state, and signs and symptoms of infection, in the absence of positive cultures or a clear source, are equally daunting, as the patient may indeed be harboring an infection, but the yield of blood cultures and the other surveillance tests are poor. Unfortunately, there is no reliable method to clinically distinguish between the entities of sepsis and SIRS until a clear source of infection is identified. The usual sources of infection in the ICU are the lungs, indwelling vascular catheters, the urinary tract, and wounds. Each of these sites must be surveyed for infection.
The optimal management of septic complications is prevention, the Surviving Sepsis campaign provides a bundle of prophylactic and treatment measures to reduce the incidence and impact of sepsis.16 Lower mortality was observed in high (29.0%) versus low (38.6%) resuscitation bundle compliance sites (p < 0.001) and between high (33.4%) and low (32.3%) management bundle compliance sites (p = 0.039).96
Acalculous cholecystitis is a “hidden” cause of fever in the ICU. Changes in gastrointestinal motility, characterized by increased gastric residuals and intolerance to enteral nutrition, imply the onset of an infection and one potential source of such infection is the gallbladder. Acalculous cholecystitis is a disease of the critically ill patient; most of these patients have had major trauma or extensive burns, or are recovering from major surgery. The diagnosis can be difficult because patients who develop acalculous cholecystitis tend to be critically ill or severely injured and are frequently unable to react to physical examination. An ultrasound will typically show a thickened gallbladder wall without stones. The diagnostic test of choice is the HIDA scan, which will demonstrate a lack of emptying of the gallbladder in response to administration of cholecystokinin. The initial treatment for acalculous cholecystitis is conservative (bowel rest, antibiotics, and intravenous fluids), although some patients will require operative intervention. Alternatively, for those patients who are too sick to tolerate an operation, a percutaneous cholecystostomy tube placement is the best option.