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POSTOPERATIVE CARE OF THE TRAUMA PATIENT
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TRAUMA
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POSTOPERATIVE CARE OF THE TRAUMA PATIENT Steven N. Vaslef, MD, PhD, FACS, and Jeffery S. Vender, MD
The postoperative care of seriously injured trauma patients can be challenging and frustrating, yet very satisfying. Recent advances in critical care have been spurred on by improvements in technology, as well as by refinements of our understanding of the basic sciences such as physiology, microbiology, pharmacology, and molecular biology. As the prehospital and initial hospital care of injured patients improves, the role of postoperative care in reducing postinjury mortality is expected to expand. Improved care in intensive care units (ICUs) may contribute to decreases in preventable trauma death rates, particularly in regionalized trauma centers.'*,13, 75 Because postoperative complications are the rule rather than the exception in severely injured patients, anesthesiologists and surgeons caring for critically ill trauma victims in the postoperative period must be vigilant and prepared to diagnose and treat problems,as they arise. This article reviews current concepts in the "routine" postoperative care of the trauma patient and in the management of some of the more common postoperative complications. The reader is encouraged to consult other sources for more thorough discussions of this topic, includ49, h7, 71 ing trauma in elderly, pregnant, or pediatric ANALGESIA
The goals of postoperative analgesia are to provide adequate pain control and to minimize postoperative complications with a low inciFrom the Department of Surgery, Duke University Medical Center, Durham, North Carolina (SNV); and the Department of Anesthesiology, Northwestern University Medical School, Chicago, and Evanston Hospital, Evanston, Illinois (JSV)
ANESTHESIOLOGY CLINICS OF NORTH AMERICA VOLUME 14 NUMBER 1 * MARCH 1996
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dence of side effects.35Effective analgesia improves clinical outcome by reducing pulmonary complications, modulating the stress response to injury, and possibly reducing the incidence of perioperative myocardial ischemia, deep venous thrombosis (DVT), and pulmonary embolism (PE).’” 37,47, 58 The preferred route of analgesic administration varies from patient to patient, depending on the nature and sites of injury. Newer modalities of analgesic management have become available in recent years and offer alternatives to intravenous or intramuscular boluses of opioids. The box below summarizes some of the possible routes of postoperative analgesic administration.
Common Routes of Postoperative Analgesic Administration Oral Intramuscular Intravenous Continuous Intermittent Nurse controlled Patient controlled Epidural lnterpleural Intercostal block Axillary block
Opioid Analgesics Intravenous opioid injection may be either continuous or intermittent. Continuous opioid infusion ordinarily requires monitoring in the ICU because of the risks of respiratory depression, oversedation, hemodynamic instability, and inability to predict an optimal infusion rate. Intermittent intravenous administration of either meperidine or morphine, on the other hand, can be safe and effective outside the ICU setting. Patient-controlled analgesia (PCA), whereby the patient receives low-dose opioids on demand, emerged as a response to reports of the undertreatment of pain in hospitalized patients?], 48 In this technique, the patient triggers an electronic infusion pump to deliver a preset amount of analgesic, usually meperidine or morphine, whenever he or she experiences pain. A lockout interval of between 5 and 15 minutes prevents the administration of another dose until the first has exerted its maximal analgesic effect. Advantages of PCA over conventional cyclical analgesic regimens are improved pain control, less sedation, improved results in pulmonary function tests, reduced demand on nursing staff, and possible psychological advantages to the patient.31Table 1 compares the pharmacology of several commonly used intravenous opioids. Fentanyl has a rapid onset of action and a shorter duration of
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Table 1. COMPARISON OF COMMONLY USED INTRAVENOUS OPlOlDS
Equianalgesic dose (rng) Peak effect (min) Duration of action (hr) Adult dose Bolus (rng)* Continuous infusion (WWt PCA bolus (mg)*
Morphine
Meperidine
10 20-30 3-4
75 5-7 2-3
Fentanyl 0.1 3-5 0.5-1
2-1 0
25-50
25-1 00'
1-10 1-4
15-35 5-20
25-1 O O t 10-50*
'Units for fentanyl: pg t Units for fentanyl: pg/hr PCA = patient-controlled analgesia. Data from Bailey PL, Stanley TH: Intravenous opioid anesthetics. In Miller RD (ed): Anesthesia, ed 4. New York, Churchill Livingstone, 1994, p 291; and Raj PR, Hartrick C, Pither CE: Pain management of the injured. In Capan LM, Miller SM, Turndorf H (eds): Trauma: Anesthesia and Intensive Care. Philadelphia, JB Lippincott, 1991I p 685.
action than either morphine or meperidine, but like the latter two opioids, accumulation may occur with repeated intravenous boluses or prolonged continuous intravenous infusion. Fentanyl also has fewer hemodynamic and histamine-releasing effects than morphine or meperidine. Epidural analgesia is an attractive mode of pain control, particularly after blunt injuries to the chest or after thoracic or upper abdominal operations that adversely affect pulmonary function the most. Studies of epidural opioid delivery after thoracic trauma have shown that ventilatory function is improved, pulmonary complications are reduced, and mortality, at least in elderly patients, is reduced.46, 83 Most experience with continuous epidural analgesia has been with opioids, although the combination of opioids (0.1 mg/mL of morphine or 1 pg/mL of fentanyl) with a long-acting local anesthetic (for example, 0.1% bupivacaine) may be better than either agent alone in achieving effective a n a 1 g e ~ i a . l ~ ~ ~ ~ Epidural bupivacaine may be associated with excessive sympathetic and motor blockade, hypotension, and urinary retention. Epidural fentanyl may be preferable to epidural morphine because of its increased lipophilicity, short onset of action, short serum half-life, and lower incidence of complications (Table 2). Patient-controlled epidural analgesia also has been used successfully, combining continuous and demand modes.30 Relative contraindications to the use of epidural analgesia include hypotension, sepsis, local infection, and coagulopathy. Local Anesthetic Techniques
Interpleural analgesia with 0.25% to 0.5% bupivacaine has been reported after multiple rib fractures or thora~otomy.~~ Pneumothorax and unilateral Horner's syndrome are potential complications of this
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Table 2. COMPARISON OF EPIDURAL MORPHINE AND FENTANYL
Dose range Bolus (mg/kg)* Infusion (mg/kg/hr)t Onset of action (min) Duration of action (hr) Side effects Nausea Pruritus Sedation Urinary retention Delayed respiratory depression
Morphine
Fentanyl
0.05-0.1 0.005-0.0 1 30-90 12-24
1-1.5* 0.5-2t 10-15 2-4
+++
+++ ++ + +
+ + + +
'Units for fentanyl: pg/kg tunits for fentanyl: pg/kg/hr Data from Grass JA: Fentanyl: Clinical use as a postoperative analgesia-epiduraVintrathecal route. J Pain Symptom Manage 7:419, 1992; and Raj PR, Hartrick C, Pither CE: Pain management of the injured. In Capan LM, Miller SM, Turndoif H (eds): Trauma: Anesthesia and Intensive Care. Philadelphia, JB Lippincott, 1991, p 685.
technique, which needs further study before its use can be widely recommended in trauma patients. Intercostal nerve blocks using long-acting local anesthetics can provide effective analgesia after rib fractures, thoracotomy, or flank incisions. Side effects are infrequent, and the benefits derived from improved ventilatory function and reduced narcotic requirements seem to 55 The limited duration of action of the analgesic effect be significant.l0* and the necessity for multiple injections for multiple rib fractures are drawbacks of this technique. Axillary blockade after injury or operation involving the upper extremity may be accomplished by either bolus injection of 30 to 40 mL of 0.25% bupivacaine or continuous infusion of 0.125% bupivacaine at 8 to 10 mL/hr after an initial bolus.45This dosage allows pain relief while preserving motor function. Nerve or vascular injury, dislodgement of the catheter, and infection are potential complications with this procedure.
Ketorolac Ketorolac is a nonsteroidal anti-inflammatory drug (NSAID) that is currently approved for oral or intramuscular administration. Intramuscular ketorolac provides an analgesic level equivalent to intramuscular morphine, but without the side effects of o p i o i d ~Like . ~ ~ other NSAIDs, however, ketorolac inhibits platelet aggregation; thus the potential for bleeding is of concern. In hypovolemic patients, renal impairment can occur, thereby possibly limiting the use of ketorolac in trauma patients.
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SEDATION
Severely injured patients frequently require the administration of sedative agents because of the anxiety they experience due to their injuries, ICU stay, and mechanical ventilation. The practice of administering a sedative in combination with an opioid analgesic is common, especially in intubated patients. Extra caution should be exercised when using combination drugs because of the added risks of prolonged sedation, cardiovascular instability, and respiratory depression. Benzodiazepines The benzodiazepines are widely used as sedatives in the ICU.32 Their sedative, anxiolytic, amnesic, and anticonvulsant actions make them particularly appealing agents for use in the critical care setting. Diazepam has been virtually replaced by midazolam because of midazolam’s rapid onset of action and relatively short elimination halflife (1.5 to 3.5 Drug accumulation of midazolam, especially in elderly patients, in patients with hepatic dysfunction, or after long periods of intravenous infusion, may lead to prolonged A wide variability exists in the level of plasma midazolam and clinical response between individuals. Furthermore, tolerance to the drug may develop. Although the cardiovascular effects of midazolam are usually minimal and well tolerated, hypotension has been observed when midazolam has been administered to hypovolemic patients. The recent availability of flumazenil to reverse the sedation associated with benzodiazepines may improve the safety margin of these sedative agents and additionally even allows for periodic neurologic evaluation of patients with significant drug accumulation. Lorazepam is an intermediate-acting benzodiazepine that has an elimination half-life (10 to 20 hours) longer than that of midazolam but shorter than that of diazepam. Its primary usefulness may be in patients with serious liver dysfunction because of its reduced potential for side effects in these patients. Propofol Propofol, an alklyl phenol administered as a lipid emulsion, is used extensively in the operating room as an anesthetic induction agent. It also is increasingly being used postoperatively for sedation of intubated, critically ill patients.72Its pharmacokinetic profile lends itself well to continuous infusion in the postoperative period. Onset of action is rapid after intravenous administration, and the elimination half-life is only 1 to 3 hours, without any apparent significant drug accumulation or significant active metabolites. A rapid recovery time, generally less than 30 minutes, is observed after the termination of propofol infusion. The
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recommended dose for continuous propofol infusion for postoperative sedation is 1 to 3 mg/kg/hr.7z Tolerance to the drug may develop, necessitating higher rates of infusion, which may increase the risk of developing hyperlipidemia. Hypotension may be seen, particularly after bolus injection; however, the cardiovascular effects seem to be similar to those seen with other agents such as midazolam.2 Ketamine Ketamine is a phencyclidine compound that produces sedation, analgesia, and a dissociative state when used in subanesthetic doses. It has a rapid onset of action when given intravenously at doses of 0.2 to 0.8 mg/kg and provides analgesia for up to 20 minutes.14* Ketamine, therefore, is a useful agent in the ICU to provide sedation and analgesia during short, intense procedures, such as major dressing changes. The combination of midazolam and ketamine may decrease the dose requirement of both agents and reduce the incidence of emergence reactions seen with ketamine. Ketamine induces a sympathetic response, which may have a beneficial effect in patients with cardiovascular instability, but may have a detrimental effect in patients with head injuries because it increases intracranial pressure. NEUROMUSCULAR BLOCKADE The primary indications for the use of nondepolarizing muscle relaxants in the postinjury or postoperative period are (1) as an adjunctive measure in the management of severe respiratory failure; (2) to decrease muscle activity and oxygen consumption in certain septic or hypoxic patients to improve oxygen balance; and infrequently (3) to control intracranial pressure surges that occur in response to muscle activity. Sedatives and analgesics must be administered concomitantly with neuromuscular blocking agents to avoid conscious paralysis. Furthermore, the use of a peripheral nerve stimulator is recommended so that the degree of neuromuscular blockade can be titrated to a single twitch during Train-of-Four m ~ n i t o r i n gTable . ~ ~ 3 compares several commonly used neuromuscular blocking agents. Pancuronium is a longacting agent, whereas vecuronium and atracurium have shorter durations of action. Both pancuronium and vecuronium are eliminated largely by biliary excretion, whereas atracurium does not depend on hepatic or renal elimination. Atracurium, therefore, has been postulated to be useful in cases of multiple organ failure.8 All three agents have been reported to cause prolonged paralysis after discontinuation of their use?, 8o The cause of prolonged neuromuscular blockade is not always clear, but associations with organ dysfunction, concomitant drug use, injury severity, and length of therapy have been made. Vecuronium appears to have fewer cardiovascular side effects than either pancuro-
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POSTOPERATIVE CARE OF THE TRAUMA PATIENT
Table 3. NEUROMUSCULAR BLOCKING AGENTS
Duration of action after bolus (min) Adult dose Bolus (mg/kg) Continuous infusion (mg/kg/hr) Elimination
Pancuronium
Vecuronium
Atracurium
45-60
30-45
30-45
0.05-0.1
0.3-0.5
0.08-0.1
0.02404 Hepatic > Renal
0.05-0.1 Hepatic > Renal
+
++
Relative cost
0.5-1 .O Hoffmann degradation
+++
Data from Durbin CG Jr: Neuromuscular blocking agents and sedative drugs: Clinical uses and toxic effects in the critical care unit. Crit Care Clin 7:489. 1991; Khuenl-Brady KS. Reitstatter 6.Schlager A, et al: Long-term administration of pancuronium and pipecuronium in the intensive care unit. Anesth Analg 78:1082.1994; and Wadon AJ, Dogra S, Anand S Atracurium infusion in the intensive care unit. Br J Anaesth 58:564, 1986.
nium or atracurium. Cost should also be taken into account when choosing a neuromuscular blocking agent because the cost of a daily infusion of pancuronium is only a fraction of the cost of infusions of vecuronium or atracurium. NUTRITIONAL SUPPORT The provision of adequate nutritional support plays a critical role in the management of trauma patients. The hypermetabolic and catabolic state that characterizes the early postinjury phase may be significantly ameliorated by the administration of nutrient substrates.' The goal of nutritional care is to provide an individualized, balanced diet on the basis of the metabolic requirements, fluid and electrolyte status, and degree of organ dysfunction of each patient. Nutritional Requirements Caloric needs may be estimated by a number of techniques, including calculations of resting energy expenditure based on modifications of the Harris-Benedict equation or on indirect calorimetry measurements of oxygen consumption and carbon dioxide produ~tion.~~, 69 In general, the energy expenditure for intubated patients in the ICU is the sum of the basal metabolic rate, normally between 30 to 40 kcal/m2/hr for adults, and the energy expenditure due to stress, which for severely injured patients may be an additional 30% to 50% of the basal rate. Thermally injured or septic patients may have even higher energy requirements. Protein requirements are proportional to the severity of injury, and higher protein formulations are frequently used in trauma patients to minimize visceral. protein catabolism. The optimal nitrogen:calorie ratio increases from approximately 1 g N,/300 nonprotein kcal in the mini-
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mally stressed patient to approximately 1:150 in more severely injured patients. Route of Feeding Convincing evidence exists that the route of feeding influences immunologic and metabolic responses after injury.@The gastrointestinal tract has emerged as a central system in the stressed patient.7,81 Enteral feeding, when compared to total parenteral nutrition (TPN), is associated with fewer septic complications, fewer metabolic complications, such as hyperglycemia and electrolyte disturbances, and better clinical out23, 40,56 Therefore, enteral feeding is the preferred route of feeding come~.'~, whenever possible. Several high protein enteral formulations are available, including preparations that incorporate substrates that promote enterocyte and immunologic function. Various specialized enteral formulas also are available for patients with respiratory, hepatic, or renal insufficiency. Occasionally, patients experience abdominal distention after early postoperative enteral feeding that precludes further feeding by this route; however, most patients tolerate enteral feeding. POSTINJURY COMPLICATIONS
Complications in the postinjury period are common in severely injured patients. Early diagnosis and prompt intervention are critical to successful clinical outcomes. A comprehensive discussion of postinjury or postoperative complications is beyond the scope of this article, but some of the more frequent complications are reviewed. Missed Injuries Despite attempts to complete an accurate primary and secondary survey of the trauma victim, the rate of missed injuries in patients with multisystem trauma is at least Several factors can be identified that contribute to the rate of missed injuries: low index of suspicion; failure to perform a thorough examination; and failure to order, perform, or accurately interpret diagnostic tests.4I During the excitement of a resuscitation, the immediately life-threatening injuries (as well as airway, breathing, and circulation) are addressed first, and other injuries, whether clinically significant or not, may be overlooked. Sometimes the first chance of completing the secondary survey or obtaining radiographs is postoperatively in the ICU. Alteration of consciousness due to head injury, drug or alcohol intoxication, or general anesthesia frequently preclude a complete, reliable physical examination; thus a high index of suspicion must be maintained in this group of patients. In such
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instances, other modalities to rule out injuries must be used, such as CT scanning or diagnostic peritoneal lavage. Musculoskeletal injuries excluding spinal injuries made up 50% of missed injuries in one s t ~ d y . 2Spinal ~ and facial fractures and thoracic and abdominal injuries comprise most of the remaining missed injuries. Cervical spine fractures are perhaps the most feared missed injuries, but in alert, nonintoxicated patients without cervical spine pain, injury is usually, but not always, excluded if the radiographs are normal.50The incidence of missed intracranial head injuries may be relatively low in the United States because of the availability of and reliance on CT scanning. The importance of frequent, thorough examinations in the postinjury period cannot be overemphasized. Sedation should be reversed periodically, if necessary and appropriate, to conduct a complete examination. Radiographs or other diagnostic tests should be obtained on the basis of the findings of the physical examination. Serial laboratory tests are used to determine the presence of ongoing bleeding or infection. If a high index of suspicion for associated injuries is maintained, the incidence of adverse outcomes due to missed injuries may be reduced. Postoperative Bleeding
Postoperative hemorrhage after major trauma may be due to coagulopathy or surgical bleeding. Traumatic coagulopathies are discussed in detail elsewhere in this issue. The distinction between nonsurgical and surgical causes of bleeding is important because early re-operation in the latter case may be lifesaving. The diagnosis of surgically correctable causes of postoperative bleeding, however, may be elusive. Direct evidence of hemorrhage, such as continued output from a chest tube or abdominal drain, and indirect signs of blood loss, such as hemodynamic instability, drop in hematocrit, or abdominal distention, do not always indicate active bleeding that requires re-operation. The operating surgeon is responsible for deciding if and when a patient needs to be returned to the operating room. It is becoming more popular among trauma surgeons to perform an abbreviated laparotomy in cases of extreme physiologic instability and imminent intraoperative death.27,77 The abdomen is packed with laparotomy pads to tamponade bleeding and the patient is taken to the ICU for resuscitation. If the patient survives the immediate postoperative period, he or she is returned to the operating room, usually within 48 hours, for definitive laparotomy. Unfortunately, despite vigorous resuscitative attempts to correct hypothermia, metabolic acidosis, coagulopathy, and hemodynamic instability, many of these patients die in the ICU before the planned re-operation.ll Interestingly, in a large series of patients who had undergone abbreviated laparotomy and subsequent re-operation for hemorrhage, only 4% were found to have diffuse oozing at re-exploration, while over 90% were found to have surgically correcta-
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ble causes of bleeding.34Thus, a low threshold for re-operation should be the rule in patients who survive the immediate postoperative period but continue to bleed despite the correction of hypothermia, acidosis, and coagulopathy. The goal of transfusing perioperative packed red blood cells (PRBCs) is to restore hemodynamic stability by improving oxygencarrying capacity. Critically ill patients may exhibit a pathologic dependence of oxygen delivery on oxygen supply.7oHence, increasing oxygencarrying capacity by PRBC transfusion is an effective way to improve oxygen delivery and possibly reduce the pathologic supply dependence of oxygen uptake. Even with massive transfusion (> 20 units PRBCs), survival rates of 50% in trauma patients have been reported.84 Deep Venous Thrombosis and Pulmonary Embolism The true incidence of venous thromboembolism in trauma patients is not well defined but is thought to be high, at least in certain subgroups.62Autopsy studies have found evidence of DVT in as many as 65% of patients who died after injury, and 15% to 20% had evidence of PE.73Attempts have been made to identify trauma patients who are at high risk for developing DVT or PE, but the data are ~onflicting.~~, 60, 74 The presence of one or more risk factors listed in the box below may predispose trauma patients to the development of complications of DVT or PE.
Possible Risk Factors for the Development of Venous Thromboembolism in Trauma Patients Age > 45 years Prolonged immobilization Previous history of clotting abnormalities Severe head injurylcoma Spinal cord injury Pelvis fracture Long bone fracture Repair of major vein in lower extremity Central vein cannulation Multiple transfusions
Prophylaxis of venous thromboembolism in trauma patients is incompletely understood. A significant number of these patients have contraindications to the use of low-dose heparin or are unable to wear compression hose and pneumatic compression boots because of extremity injuries. Furthermore, the use of pneumatic compression devices may increase the risk of bleeding due to activation of the fibrinolytic system?
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When suspected, DVT may be diagnosed with Doppler ultrasound or impedance plethysmography. Pulmonary embolism may be diagnosed by radionuclide imaging or pulmonary arteriography. Patients in whom DVT or PE is diagnosed require intervention to prevent further pulmonary thromboembolic complications. The risks of anticoagulation must be assessed, and if prohibitive, a vena cava filter should be inserted. Recently, a prospective study has shown that insertion of a prophylactic vena cava filter in high risk patients decreases the incidence of PE in trauma patients from 1%to 0.25Y0.~~ Fat Embolism Syndrome Fat embolism syndrome is relatively infrequently diagnosed, yet it may occur with an incidence of at least 10% in patients with long bone or pelvic fracture.26The syndrome is characterized by hypoxemia with an increased alveolar/arterial PO, gradient, changes in mental status, and a petechial rash. Onset typically occurs 12 to 72 hours after injury. Detection of urinary fat bodies can confirm the diagnosis. Prophylactic approaches in high risk patients have been tried, including the use of corticosteroids, but currently the best strategy is early fixation of fractures. Treatment of the syndrome consists of supportive measures directed at treating the pulmonary complications of fat embolism. Renal Failure Acute renal failure after trauma is uncommon. A retrospective multicenter review of trauma admissions noted a 0.1% incidence of renal failure requiring hem~dialysis.~~ The causes of posttraumatic renal failure include shock, multiple organ dysfunction syndrome, sepsis, nephrotoxins, rhabdomyolysis, and rarely, postrenal obstruction. Renal failure that develops within several days of injury is thought to be due to inadequate resuscitation, whereas late onset renal failure, which occurs twice as often as early onset renal failure, is most frequently caused by multiple organ dysfunction or sepsis.57 The contributory role of iatrogenically delivered nephrotoxins in causing acute renal failure cannot be overlooked. Many diagnostic or therapeutic agents that are frequently used in trauma patients can induce renal failure. Radiographic contrast agents, antibiotics, particularly the aminoglycosides, NSAIDs, and vasoconstrictors are potentially nephrotoxic, especially in patients with hypovolemia or preexisting risk factors such as diabetes mellitus, renal insufficiency, congestive heart failure, or advanced age. Although the incidence of radiocontrast-induced nephropathy is less than 5% in low risk individuals, the incidence sharply rises in high risk patients.,O Iatrogenically induced renal failure is a complication that can be prevented or minimized by ensuring adequate volume expansion before and after a radiographic procedure in which
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contrast dye is used, by minimizing the amount of contrast agent used, by maintaining an adequate urine output with hydration and diuretics, if needed, and by avoiding nephrotoxic drugs in high risk individuals? Rhabdomyolysis may rapidly lead to acute renal failure unless it is aggressively treated. Causes of traumatic rhabdomyolysis include crush injury, burns, electrical injury, and compartment syndrome. In the presence of aciduria (pH < 5.6), released myoglobin is converted to ferrihemate, which may produce renal failure by direct toxicity to renal tubules and by tubular plugging. Diagnosis is made by the laboratory findings of elevated concentrations of plasma creatine kinase (CK) and myoglobinuria. Treatment must be expeditious and should include reversal of the underlying cause and forced alkaline diuresis.5 Normal saline infusion should be instituted to achieve a urine output of at least 200 mL/hr. Mannitol (25 g every 6 hours) may be given after volume replenishment if urine output is low. Sodium bicarbonate should be administered, as necessary, to keep urine pH levels greater than 6. Treatment should continue until myoglobinuria has resolved and plasma CK levels fall below 1000 IU/L. The diagnosis of acute renal failure is usually obvious from the history, physical examination, and clinical course, but differentiating prerenal azotemia from acute tubular necrosis is occasionally difficult. Table 4 lists some diagnostic indices that can help to differentiate these two entities. Nonoliguric renal failure (urine output > 500 mL/day) may have a milder clinical course and is somewhat easier to manage than oliguric renal failure (urine output > 500 mL/day). The rationale, therefore, to attempt to induce a diuresis in oliguric acute renal failure may be valid. The combination of furosemide (100 to 200 mg every 6 to 8 hours) and Table 4. URINARY DIAGNOSTIC INDICES Prerenal Azotemia Urine sodium (mEq/L) Urine osmolality (mOsm/L) Urine/plasma creatinine Plasma uredplasma creatinine Fractional excretion of sodium' Renal failure indext .Fractional excretion of sodium
tRenal failure index =
=
Acute Tubular Necrosis
<20 >500
>40
>40
<20
>20
<20 >2
<400
<1 <1
urine sodium x plasma creatinine plasma sodium x urine creatinine
>2
x 100%
urine sodium x plasma creatinine urine creatinine
Data from Fischer RP, Reed RL 11, Yatsu JS: Renal failure. In Mattox KL (ed): Complications of Trauma. New York, Churchill Livingstone, 1994, p 41; Miller TR, Anderson RJ, Linas SL, et al: Urinary diagnostic indices in acute renal failure: A prospective study. Ann Intern Med 89:47, 1978; and Zarich S, Fang LST, Diamond JR: Fractional excretion of sodium: Exceptions to its diagnostic value. Arch Intern Med 145:108, 1985.
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low-dose dopamine (1-3 pg/kg/min) may be synergistic in inducing di~resis.~~ Acute renal failure is treated by volume restriction, nutritional replenishment, electrolyte correction, and adjustments in dosages of medications. Dialysis may be indicated for uremia (blood urea nitrogen [BUN] > 100 mg/dL or central nervous system manifestations of uremia), volume overload, or severe electrolyte imbalance (including refractory hyperkalemia and uncontrollable metabolic acidosis). A description of the various types of dialysis and hemofiltration procedures is beyond the scope of this article but is reviewed e l ~ e w h e r e . ~ ~
Pulmonary lnsufficiency Pulmonary dysfunction in the traumatized patient is discussed elsewhere in this issue and is only mentioned here to emphasize that practically all trauma patients who sustain moderate or severe injuries will develop some degree of pulmonary insufficiency. Both infectious and noninfectious pulmonary complications are seen frequently. Patients with altered consciousness, prolonged intubation, or with altered flora in the gastrointestinal tract seem to be at increased risk for developing pne~monia.’~ Aspiration in such patients should always be suspected, but the role of bacterial translocation from the gastrointestinal tract cannot be overlooked as a potential septic source.28The spectrum of standard and nonstandard treatments for respiratory failure is wide, and particular treatment approaches must be individualized on the basis of training, experience, and ICU resources.
Sepsis and Multiple Organ Dysfunction Sepsis or multiple organ dysfunction remain the major cause of late deaths after injury. The incidence of infectious complications in trauma patients is estimated to be about 20% but may be even higher in mechanically ventilated patients.65 Single or multiple organ dysfunction may result from infection but may also arise from noninfectious causes. These causes of organ dysfunction may be either primary (as in lung contusion) or secondary (as a result of a systemic host response to injury). The literature has been replete in recent years with confounding definitions of ”sepsis,” “sepsis syndrome,” and ”multiple organ failure;” thus standardization of terminology has been proposed.5Z Systemic inflamrnatoy response syndrome (SIRS) is the systemic inflammatory response to injury or other noninfectious insults to the host that results from activation of cytokines and other endogenous mediators. Systemic inflammatory response syndrome is characterized by two or more of the following: (1) temperature greater than 38°C or less than 36”C, (2) heart rate greater than 90/minute, (3) respiratory rate greater than 20/minute or PaC02 less than 32 torr, and (4) white blood cell
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count greater than 12,000/mm3, less than 4000/mm3, or more than 10% band forms. Sepsis is defined as the systemic inflammatory response associated with infection. Sepsis has the same clinical manifestations as SIRS, along with microbial evidence that an infectious process plays a direct part in the systemic inflammatory response. Multiple organ dysfunction syndrome (MODS) is the ”presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without interventi~n.”~~ The rationale for defining MODS in this fashion, rather than delineating clinical parameters of organ failure, is that if MODS is regarded as a continuum of organ dysfunction, earlier recognition of the syndrome, hence earlier therapeutic interventions, may be possible. Prevention of septic complications and the development of MODS begins in the emergency department at the time of admission, is continued in the operating room at the time of surgery, and remains a vital role in the ICU in the postoperative period. Expeditious resuscitative measures to restore intravascular volume, oxygen delivery, and tissue perfusion are important factors in reducing the incidence of organ dysfunction.33Nutritional and metabolic support, as previously outlined, are vital.16 Prophylactic antibiotics should be administered, when indicated, but indiscriminate use of antimicrobial agents should be avoided to prevent the complications of superinfection and the emergence of resistant microbial organisms. Lines for vascular access or hemodynamic monitoring should be routinely inspected, inserted, and dressed using aseptic technique. Once sepsis or MODS is suspected, a vigilant search to identify infectious causes of organ dysfunction should be made. Thorough physical examination is supplemented by appropriate ordering of laboratory tests, plain radiographs, CT scans, or other diagnostic tests. Certain patterns of injury may help guide the search for infection. Patients who underwent laparotomy for blunt or penetrating injury were found in one study to have an approximately 7.5% incidence of abdominal sepsis.18 Patients with chest or head injuries or with a history of blunt trauma have a higher incidence of developing pneurn0nia.6~The need and the duration of mechanical ventilation also increase the risk of developing pneurn0nia.6~Soft-tissue infections require drainage, antibiotics, local wound care, and debridement of infected and devitalized tissue. Empiric broad-spectrum antibiotics should be administered when the diagnosis of sepsis is considered. The antibiotic regimen may be changed once culture results become available. When MODS is diagnosed, organ-specific supportive care currently is the cornerstone of treatment. Newer modalities of treatment are being intensely investigated. Some of the innovative therapies being evaluated include the use of monoclonal antibodies (for example, anti-TNF-a), oxidant scavengers, growth factors, and NSAIDs or other pharmacologic agents. Such agents modulate specific steps in the biosynthetic pathways
POSTOPERATIVE CARE OF THE TRAUMA PATIENT
253
Further that are responsible for the systemic inflammatory studies of these potential treatments for MODS are anxiously awaited.
SUMMARY The postoperative care of the trauma patient requires an understanding of the use of analgesics, sedatives, and neuromuscular blocking agents, as well as principles of nutritional and metabolic support. Complications in the postoperative period, despite attempts to prevent them, are common. Anticipation, early recognition, and treatment of complications are essential to successful clinical outcomes.
References 1. Abbott WC, Echenique MM, Bistrian BR, et al: Nutritional care of the trauma patient. Surg Gynecol Obstet 157585, 1983 2. Aitkenhead AR, Pepperman ML, Willatts SM, et al: Comparison of propofol and midazolam for sedation in critically ill patients. Lancet 2704, 1989 3. Allenby F, Boardman L, Pflug JJ, et al: The effects of external pneumatic intermittent compression on fibrinolysis in man. Lancet 21412, 1973 4. Bailey PL, Stanley TH: Intravenous opioid anesthetics. In Miller RD (ed): Anesthesia, ed 4. New York, Churchill Livingstone, 1994, p 291 5. Better OS, Stein JH: Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med 322825, 1990 6. Boras-Uber LA, Brackett NC: Ketorolac-induced acute renal failure. Am J Med 92450, 1992 7. Border JR, Hassett J, LaDuca J, et al: The gut origin septic states in blunt multiple trauma (ISS=40) in the ICU. Ann Surg 206427,1987 8. Branney SW, Haenel JB, Moore FA, et al: Prolonged paralysis with atracurium infusion: A case report. Crit Care Med 221699, 1994 9. Brezis M, Epstein F H A closer look at radiocontrast-induced nephropathy. N Engl J Med 320:179,1989 10. Bridenbaugh PO, DuPen SL, Moore DC, et al: Postoperative intercostal nerve block analgesia versus narcotic analgesia. Anesth Analg 5281, 1973 11. Burch JM, Ortiz VB, Richardson RJ, et al: Abbreviated laparotomy and planned reoperation for critically injured patients. Ann Surg 215476, 1992 12. Cales RH, Trunkey DD: Preventable trauma deaths: A review of trauma care systems development. JAMA 254:1059,1985 13. Cales RH: Trauma mortality in Orange County: The effect of implementation of a regional trauma system. Ann Emerg Med 13:1, 1984 14. Capan LM, Gottlieb G , Rosenberg A: General principles of anesthesia for major acute trauma. In Capan LM, Miller SM, Tumdorf H (eds): Trauma: Anesthesia and Intensive Care. Philadelphia, JB Lippincott, 1991, p 259 15. Cerra FB Role of nutrition in the management of malnutrition and immune dysfunction in trauma. J Am Coll Nutr 11:512, 1992 16. Cerra FB: Hypermetabolism, organ failure, and metabolic support. Surgery 101:1, 1987 17. Craig P: Postoperative recovery of pulmonary function. Anesth Analg 60:46, 1981 18. Croce MA, Fabian TC, Stewart RM, et al: Correlation of abdominal trauma index and injury severity score with abdominal septic complications in penetrating and blunt trauma. J Trauma 32380, 1992 19. Cullen ML, Staren ED, El-Ganzouri A, et al: Continuous epidural infusion for analgesia
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20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33.
34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47.
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after major abdominal operations: A randomized, prospective, double-blind study. Surgery 98:718, 1985 D’Elia JA, Gleason RE, Alday M, et al: Nephrotoxicity from angiographic contrast material: A prospective study. Am J Med 72:719, 1982 Donovan M, Dillon P, McGuire L Incidence and characteristics of pain in a sample of medical-surgical inpatients. Pain 30:69, 1987 Durbin CG Jr: Neuromuscular blocking agents and sedative drugs: Clinical uses and toxic effects in the critical care unit. Crit Care Clin 7489, 1991 Ellis LM, Copeland EM 111, Souba W. Perioperative nutritional support. Surg Clin North Am 71:493, 1991 Enderson BL, Maul1 KI: Missed injuries: The trauma surgeon’s nemesis. Surg Clin North Am 71:399, 1991 Enderson BL, Reath DB, Meadors J, et al: The tertiary trauma survey: A prospective study of missed injuries. J Trauma 30:666, 1990 Fabian TC, Hoots AV, Stanford DS, et al: Fat embolism syndrome: Prospective evaluation in 92 fracture patients. Crit Care Med 18:42, 1990 Feliciano DV, Mattox KL, Burch JM: Packing for control of hepatic hemorrhage. J Trauma 26:738, 1986 Fiddian-Green R, Baker S Nosocomial pneumonia in the critically ill: Product of aspiration or translocation? Crit Care Med 19:942, 1991 Fischer RP, Reed RL 11, Yatsu JS: Renal failure. In Mattox KL (ed): Complications of Trauma. New York, Churchill Livingstone, 1994, p 41 Grass JA: Fentanyl: Clinical use as postoperative analgesic-epidural/intrathecalroute. J Pain Symptom Manage 7419,1992 Graves DA, Foster TS, Batenhorst RL, et al: Patient-controlled analgesia. Ann Intern Med 99:360, 1983 Hansen-Flaschen JH, Brazinsky S, Basile C, et a1 Use of sedating drugs and neuromuscular blocking agents in patients requiring mechanical ventilation for respiratory failure: A national survey. JAMA 266:2870, 1991 Henao FJ, Daes JE, Dennis RJ: Risk factors for multiorgan failure: A case-controlled study. J Trauma 31:74, 1991 Hirshberg A, Wall MJ Jr, Ramchandani MK, et al: Reoperation for bleeding in trauma. Arch Surg 128:1163, 1993 Hopf Hw, Weitz S: Postoperative pain management. Arch Surg 129:128,1994 Ireton-Jones C, Turner WW Jr: The energy equations: Formulae for estimating energy expenditures in hospitalized patients. Journal of Parenteral and Enteral Nutrition 13(suppl):2OS, 1989 Kehlet H The modifying effect of general and regional anesthesia on the endocrine and metabolic response to surgery. Reg Anesth 7539, 1982 Khuenl-Brady KS, Reitstatter B, Schlager A, et al: Long-term administration of pancuronium and pipecuronium in the intensive care unit. Anesth Analg 78:1082, 1994 Knudson MM, Collins JA, Goodman SB, et al: Thromboembolism following multiple trauma. J Trauma 322,1992 Kudsk KA, Croce MA, Fabian TC, et al: Enteral versus parenteral feeding. Effects on septic morbidity after blunt and penetrating abdominal trauma. Ann Surg 215:503,1992 Laasonen EM, Kivioja A Delayed diagnosis of extremity injuries in patients with multiple injuries. J Trauma 31:257, 1991 Levy DB, Hanlon DP, Townsend RN: Geriatric trauma. Clin Geriatr Med 9:601, 1993 Lindner A: Synergism of dopamine and furosemide in diuretic-resistant, oliguric acute renal failure. Nephron 33:121, 1983 Lowry SF: The route of feeding influences injury responses. J Trauma 3Oofsuppl 12):10S, 1990 Lutz LJ, Lamer TJ: Management of postoperative pain: Review of current techniques and methods. Mayo Clin Proc 65:584,1990 Mackersie RC, Shackford SR, Hoyt DB, et a1 Continuous epidural fentanyl analgesia: Ventilatory function improvement with routine use in treatment of blunt chest injury. J Trauma 271207,1987 Mangano D, Hollenberg M, Fegert G, et a1 Perioperative myocardial ischemia in
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patients undergoing noncardiac surgery-I: Incidence and severity during the 4-day perioperative period. J Am Coll Cardiol 17843, 1991 48. Marks RM, Sachar EJ: Undertreatment of medical inpatients with narcotic analgesics. Ann Intern Med 78:173, 1973 49. Mattox KL (ed): Complications of Trauma. New York, Churchill Livingstone, 1994 50. Maul1 KI, Sachatello C R Avoiding a pitfall in resuscitation: The painless cervical fracture. South Med J 4:477, 1977 51. McGuire GP, Pearl RG: Sepsis and the trauma patient. Crit Care Clin 6121, 1990 52. Members of the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference Committee: American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 20864, 1992 53. Mendel PR, M i t e PF: Sedation of the critically ill patient. Int Anesthesiol Clin 31:185, 1993 54. Miller TR, Anderson RJ, Linas SL, et al: Urinary diagnostic indices in acute renal failure: A prospective study. Ann Intern Med 89:47, 1978 55. Moore DC, Bridenbaugh L D Intercostal nerve block in 4333 patients: Indications, technique, and complications. Anesth Analg 41:1, 1962 56. Moore FA, Moore EE, Jones TN, et al: TEN versus TPN following major abdominal trauma-reduced septic morbidity. J Trauma 29:916, 1989 57. Morris JA Jr, Mucha P Jr, Ross SE, et a 1 Acute posttraumatic renal failure: A multicenter perspective. J Trauma 31:1584, 1991 58. Nielsen T, Nielsen H, Husted S, et al: Stress response and platelet function in minor surgery during epidural bupivacaine and general anesthesia: Effect of epidural morphine addition. Eur J Anaesthesiol 6:409, 1989 59. OHara DA, Fragen RJ, Kinzer M, et al: Ketorolac tromethamine as compared with morphine sulfate for treatment of postoperative pain. Clin Pharmacol Ther 41:556,1987 60. OMalley KF, Ross SE: Pulmonary embolism in major trauma patients. J Trauma 30748, 1990 61. Raj PR, Hartrick C, Pither CE: Pain management of the injured. In Capan LM, Miller SM, Turndorf H (eds): Trauma: Anesthesia and Intensive Care. Philadelphia, JB Lippincott, 1991, p 685 62. Rehm CG, Spence RK, Ross SE: Venous thromboembolism in trauma patients. NJ Med 89:755, 1992 63. Ritz R Benzodiazepine sedation in adult ICU patients. Intensive Care Med 17(suppl l):llS, 1991 64. Rocco A, Reiestad F, Gudman J, et a1 Intrapleural administration of local anesthetics for pain relief in patients with multiple rib fractures. Reg Anesth 1210,1987 65. Rodriguez JL, Gibbons KJ, Bitzer LG, et al: Pneumonia: Incidence, risk factors, and outcome in injured patients. J Trauma 31:907, 1991 66. Rogers FB, Shackford SR, Wilson J, et al: Prophylactic vena cava filter insertion in severely injured trauma patients: Indications and preliminary results. J Trauma 35:637, 1993 67. Rouse TM, Eichelberger MR Trends in pediatric trauma management. Surg Clin North Am 721347, 1992 68. Rozycki G: Trauma during pregnancy: Predicting pregnancy outcome. Arch Gynecol Obstet 253(suppl):15S, 1993 69. Saffle JR, Medina E, Raymond J, et al: Use of indirect calorimetry in the nutritional management of burned patients. J Trauma 2532,1985 70. Samsel RW, Schumacker P T Pathologic supply dependence of oxygen utilization. In Hall JB, Schmidt GA, Wood LDH (eds): Principles of Critical Care. New York, McGraw-Hill, 1992, p 667 71. Santora TA, Schinco MA, Trooskin SZ: Management of trauma in the elderly patient. Surg Clin North Am 74163, 1994 72. Sebel P, Lowdon J D Propofol A new intravenous anesthetic. Anesthesiology 71260, 1989 73. Sevitt S, Gallagher NG: Prevention of venous thrombosis and pulmonary embolism in injured patients. Lancet 2981, 1959
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74. Shackford SR, Davis JW, Hollingsworth-Fridlud P, et al: Venous thromboembolism in patients with major trauma. Am J Surg 159:365, 1990 75. Shackford SR, Mackersie RC, Hoyt DB, et al: Impact of a trauma system on outcome of severely injured patients. Arch Surg 122523, 1987 76. Staren ED, Cullen ML: Epidural catheter analgesia for the management of postoperative pain. Surg Gynecol Obstet 162389, 1986 77. Stone HH, Strom PR, Mullins RJ: Management of the major coagulopathy with onset during laparotomy. Ann Surg 197532, 1983 78. Tran DD, Cuesta MA, Van Leeuwen PAM, et al: Risk factors for multiple organ system failure and death in critically injured patients. Surgery 11421, 1993 79. Wadon AJ, Dogra S, Anand S Atracurium infusion in the intensive care unit. Br J Anaesth 58S64, 1986 80. Watling SM, Dasta JF: Prolonged paralysis in intensive care unit patients after the use of neuromuscular blocking agents: A review of the literature. Crit Care Med 22884, 1994 81. Wilmore DW, Smith RJ, ODwyer ST, et al: The gut: A central organ after surgical stress. Surgery 104:917, 1988 82. Wisner D H A stepwise logistic regression analysis of factors affecting morbidity and mortality after thoracic trauma: Effect of epidural analgesia. J Trauma 30799, 1990 83. Worthley LIG: Thoracic epidural in the management of chest trauma: A study of 161 cases. Intensive Care Med 11:312, 1985 84. Wudel JH, Morris JA Jr, Yates K, et al: Massive transfusion: Outcome in blunt trauma patients. J Trauma 31:1, 1991 85. Zarich S, Fang LST, Diamond J R Fractional excretion of sodium: Exceptions to its diagnostic value. Arch Intern Med 145:108, 1985
Address reprint requests to Steven N. Vaslef, MD, PhD Department of Surgery Duke University Medical Center Box 2601 Durham, NC 27710
TRAUMA
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POSTOPERATIVE CARE OF THE TRAUMA PATIENT Steven N. Vaslef, MD, PhD, FACS, and Jeffery S. Vender, MD
The postoperative care of seriously injured trauma patients can be challenging and frustrating, yet very satisfying. Recent advances in critical care have been spurred on by improvements in technology, as well as by refinements of our understanding of the basic sciences such as physiology, microbiology, pharmacology, and molecular biology. As the prehospital and initial hospital care of injured patients improves, the role of postoperative care in reducing postinjury mortality is expected to expand. Improved care in intensive care units (ICUs) may contribute to decreases in preventable trauma death rates, particularly in regionalized trauma centers.'*,13, 75 Because postoperative complications are the rule rather than the exception in severely injured patients, anesthesiologists and surgeons caring for critically ill trauma victims in the postoperative period must be vigilant and prepared to diagnose and treat problems,as they arise. This article reviews current concepts in the "routine" postoperative care of the trauma patient and in the management of some of the more common postoperative complications. The reader is encouraged to consult other sources for more thorough discussions of this topic, includ49, h7, 71 ing trauma in elderly, pregnant, or pediatric ANALGESIA
The goals of postoperative analgesia are to provide adequate pain control and to minimize postoperative complications with a low inciFrom the Department of Surgery, Duke University Medical Center, Durham, North Carolina (SNV); and the Department of Anesthesiology, Northwestern University Medical School, Chicago, and Evanston Hospital, Evanston, Illinois (JSV)
ANESTHESIOLOGY CLINICS OF NORTH AMERICA VOLUME 14 NUMBER 1 * MARCH 1996
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dence of side effects.35Effective analgesia improves clinical outcome by reducing pulmonary complications, modulating the stress response to injury, and possibly reducing the incidence of perioperative myocardial ischemia, deep venous thrombosis (DVT), and pulmonary embolism (PE).’” 37,47, 58 The preferred route of analgesic administration varies from patient to patient, depending on the nature and sites of injury. Newer modalities of analgesic management have become available in recent years and offer alternatives to intravenous or intramuscular boluses of opioids. The box below summarizes some of the possible routes of postoperative analgesic administration.
Common Routes of Postoperative Analgesic Administration Oral Intramuscular Intravenous Continuous Intermittent Nurse controlled Patient controlled Epidural lnterpleural Intercostal block Axillary block
Opioid Analgesics Intravenous opioid injection may be either continuous or intermittent. Continuous opioid infusion ordinarily requires monitoring in the ICU because of the risks of respiratory depression, oversedation, hemodynamic instability, and inability to predict an optimal infusion rate. Intermittent intravenous administration of either meperidine or morphine, on the other hand, can be safe and effective outside the ICU setting. Patient-controlled analgesia (PCA), whereby the patient receives low-dose opioids on demand, emerged as a response to reports of the undertreatment of pain in hospitalized patients?], 48 In this technique, the patient triggers an electronic infusion pump to deliver a preset amount of analgesic, usually meperidine or morphine, whenever he or she experiences pain. A lockout interval of between 5 and 15 minutes prevents the administration of another dose until the first has exerted its maximal analgesic effect. Advantages of PCA over conventional cyclical analgesic regimens are improved pain control, less sedation, improved results in pulmonary function tests, reduced demand on nursing staff, and possible psychological advantages to the patient.31Table 1 compares the pharmacology of several commonly used intravenous opioids. Fentanyl has a rapid onset of action and a shorter duration of
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Table 1. COMPARISON OF COMMONLY USED INTRAVENOUS OPlOlDS
Equianalgesic dose (rng) Peak effect (min) Duration of action (hr) Adult dose Bolus (rng)* Continuous infusion (WWt PCA bolus (mg)*
Morphine
Meperidine
10 20-30 3-4
75 5-7 2-3
Fentanyl 0.1 3-5 0.5-1
2-1 0
25-50
25-1 00'
1-10 1-4
15-35 5-20
25-1 O O t 10-50*
'Units for fentanyl: pg t Units for fentanyl: pg/hr PCA = patient-controlled analgesia. Data from Bailey PL, Stanley TH: Intravenous opioid anesthetics. In Miller RD (ed): Anesthesia, ed 4. New York, Churchill Livingstone, 1994, p 291; and Raj PR, Hartrick C, Pither CE: Pain management of the injured. In Capan LM, Miller SM, Turndorf H (eds): Trauma: Anesthesia and Intensive Care. Philadelphia, JB Lippincott, 1991I p 685.
action than either morphine or meperidine, but like the latter two opioids, accumulation may occur with repeated intravenous boluses or prolonged continuous intravenous infusion. Fentanyl also has fewer hemodynamic and histamine-releasing effects than morphine or meperidine. Epidural analgesia is an attractive mode of pain control, particularly after blunt injuries to the chest or after thoracic or upper abdominal operations that adversely affect pulmonary function the most. Studies of epidural opioid delivery after thoracic trauma have shown that ventilatory function is improved, pulmonary complications are reduced, and mortality, at least in elderly patients, is reduced.46, 83 Most experience with continuous epidural analgesia has been with opioids, although the combination of opioids (0.1 mg/mL of morphine or 1 pg/mL of fentanyl) with a long-acting local anesthetic (for example, 0.1% bupivacaine) may be better than either agent alone in achieving effective a n a 1 g e ~ i a . l ~ ~ ~ ~ Epidural bupivacaine may be associated with excessive sympathetic and motor blockade, hypotension, and urinary retention. Epidural fentanyl may be preferable to epidural morphine because of its increased lipophilicity, short onset of action, short serum half-life, and lower incidence of complications (Table 2). Patient-controlled epidural analgesia also has been used successfully, combining continuous and demand modes.30 Relative contraindications to the use of epidural analgesia include hypotension, sepsis, local infection, and coagulopathy. Local Anesthetic Techniques
Interpleural analgesia with 0.25% to 0.5% bupivacaine has been reported after multiple rib fractures or thora~otomy.~~ Pneumothorax and unilateral Horner's syndrome are potential complications of this
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Table 2. COMPARISON OF EPIDURAL MORPHINE AND FENTANYL
Dose range Bolus (mg/kg)* Infusion (mg/kg/hr)t Onset of action (min) Duration of action (hr) Side effects Nausea Pruritus Sedation Urinary retention Delayed respiratory depression
Morphine
Fentanyl
0.05-0.1 0.005-0.0 1 30-90 12-24
1-1.5* 0.5-2t 10-15 2-4
+++
+++ ++ + +
+ + + +
'Units for fentanyl: pg/kg tunits for fentanyl: pg/kg/hr Data from Grass JA: Fentanyl: Clinical use as a postoperative analgesia-epiduraVintrathecal route. J Pain Symptom Manage 7:419, 1992; and Raj PR, Hartrick C, Pither CE: Pain management of the injured. In Capan LM, Miller SM, Turndoif H (eds): Trauma: Anesthesia and Intensive Care. Philadelphia, JB Lippincott, 1991, p 685.
technique, which needs further study before its use can be widely recommended in trauma patients. Intercostal nerve blocks using long-acting local anesthetics can provide effective analgesia after rib fractures, thoracotomy, or flank incisions. Side effects are infrequent, and the benefits derived from improved ventilatory function and reduced narcotic requirements seem to 55 The limited duration of action of the analgesic effect be significant.l0* and the necessity for multiple injections for multiple rib fractures are drawbacks of this technique. Axillary blockade after injury or operation involving the upper extremity may be accomplished by either bolus injection of 30 to 40 mL of 0.25% bupivacaine or continuous infusion of 0.125% bupivacaine at 8 to 10 mL/hr after an initial bolus.45This dosage allows pain relief while preserving motor function. Nerve or vascular injury, dislodgement of the catheter, and infection are potential complications with this procedure.
Ketorolac Ketorolac is a nonsteroidal anti-inflammatory drug (NSAID) that is currently approved for oral or intramuscular administration. Intramuscular ketorolac provides an analgesic level equivalent to intramuscular morphine, but without the side effects of o p i o i d ~Like . ~ ~ other NSAIDs, however, ketorolac inhibits platelet aggregation; thus the potential for bleeding is of concern. In hypovolemic patients, renal impairment can occur, thereby possibly limiting the use of ketorolac in trauma patients.
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SEDATION
Severely injured patients frequently require the administration of sedative agents because of the anxiety they experience due to their injuries, ICU stay, and mechanical ventilation. The practice of administering a sedative in combination with an opioid analgesic is common, especially in intubated patients. Extra caution should be exercised when using combination drugs because of the added risks of prolonged sedation, cardiovascular instability, and respiratory depression. Benzodiazepines The benzodiazepines are widely used as sedatives in the ICU.32 Their sedative, anxiolytic, amnesic, and anticonvulsant actions make them particularly appealing agents for use in the critical care setting. Diazepam has been virtually replaced by midazolam because of midazolam’s rapid onset of action and relatively short elimination halflife (1.5 to 3.5 Drug accumulation of midazolam, especially in elderly patients, in patients with hepatic dysfunction, or after long periods of intravenous infusion, may lead to prolonged A wide variability exists in the level of plasma midazolam and clinical response between individuals. Furthermore, tolerance to the drug may develop. Although the cardiovascular effects of midazolam are usually minimal and well tolerated, hypotension has been observed when midazolam has been administered to hypovolemic patients. The recent availability of flumazenil to reverse the sedation associated with benzodiazepines may improve the safety margin of these sedative agents and additionally even allows for periodic neurologic evaluation of patients with significant drug accumulation. Lorazepam is an intermediate-acting benzodiazepine that has an elimination half-life (10 to 20 hours) longer than that of midazolam but shorter than that of diazepam. Its primary usefulness may be in patients with serious liver dysfunction because of its reduced potential for side effects in these patients. Propofol Propofol, an alklyl phenol administered as a lipid emulsion, is used extensively in the operating room as an anesthetic induction agent. It also is increasingly being used postoperatively for sedation of intubated, critically ill patients.72Its pharmacokinetic profile lends itself well to continuous infusion in the postoperative period. Onset of action is rapid after intravenous administration, and the elimination half-life is only 1 to 3 hours, without any apparent significant drug accumulation or significant active metabolites. A rapid recovery time, generally less than 30 minutes, is observed after the termination of propofol infusion. The
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recommended dose for continuous propofol infusion for postoperative sedation is 1 to 3 mg/kg/hr.7z Tolerance to the drug may develop, necessitating higher rates of infusion, which may increase the risk of developing hyperlipidemia. Hypotension may be seen, particularly after bolus injection; however, the cardiovascular effects seem to be similar to those seen with other agents such as midazolam.2 Ketamine Ketamine is a phencyclidine compound that produces sedation, analgesia, and a dissociative state when used in subanesthetic doses. It has a rapid onset of action when given intravenously at doses of 0.2 to 0.8 mg/kg and provides analgesia for up to 20 minutes.14* Ketamine, therefore, is a useful agent in the ICU to provide sedation and analgesia during short, intense procedures, such as major dressing changes. The combination of midazolam and ketamine may decrease the dose requirement of both agents and reduce the incidence of emergence reactions seen with ketamine. Ketamine induces a sympathetic response, which may have a beneficial effect in patients with cardiovascular instability, but may have a detrimental effect in patients with head injuries because it increases intracranial pressure. NEUROMUSCULAR BLOCKADE The primary indications for the use of nondepolarizing muscle relaxants in the postinjury or postoperative period are (1) as an adjunctive measure in the management of severe respiratory failure; (2) to decrease muscle activity and oxygen consumption in certain septic or hypoxic patients to improve oxygen balance; and infrequently (3) to control intracranial pressure surges that occur in response to muscle activity. Sedatives and analgesics must be administered concomitantly with neuromuscular blocking agents to avoid conscious paralysis. Furthermore, the use of a peripheral nerve stimulator is recommended so that the degree of neuromuscular blockade can be titrated to a single twitch during Train-of-Four m ~ n i t o r i n gTable . ~ ~ 3 compares several commonly used neuromuscular blocking agents. Pancuronium is a longacting agent, whereas vecuronium and atracurium have shorter durations of action. Both pancuronium and vecuronium are eliminated largely by biliary excretion, whereas atracurium does not depend on hepatic or renal elimination. Atracurium, therefore, has been postulated to be useful in cases of multiple organ failure.8 All three agents have been reported to cause prolonged paralysis after discontinuation of their use?, 8o The cause of prolonged neuromuscular blockade is not always clear, but associations with organ dysfunction, concomitant drug use, injury severity, and length of therapy have been made. Vecuronium appears to have fewer cardiovascular side effects than either pancuro-
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Table 3. NEUROMUSCULAR BLOCKING AGENTS
Duration of action after bolus (min) Adult dose Bolus (mg/kg) Continuous infusion (mg/kg/hr) Elimination
Pancuronium
Vecuronium
Atracurium
45-60
30-45
30-45
0.05-0.1
0.3-0.5
0.08-0.1
0.02404 Hepatic > Renal
0.05-0.1 Hepatic > Renal
+
++
Relative cost
0.5-1 .O Hoffmann degradation
+++
Data from Durbin CG Jr: Neuromuscular blocking agents and sedative drugs: Clinical uses and toxic effects in the critical care unit. Crit Care Clin 7:489. 1991; Khuenl-Brady KS. Reitstatter 6.Schlager A, et al: Long-term administration of pancuronium and pipecuronium in the intensive care unit. Anesth Analg 78:1082.1994; and Wadon AJ, Dogra S, Anand S Atracurium infusion in the intensive care unit. Br J Anaesth 58:564, 1986.
nium or atracurium. Cost should also be taken into account when choosing a neuromuscular blocking agent because the cost of a daily infusion of pancuronium is only a fraction of the cost of infusions of vecuronium or atracurium. NUTRITIONAL SUPPORT The provision of adequate nutritional support plays a critical role in the management of trauma patients. The hypermetabolic and catabolic state that characterizes the early postinjury phase may be significantly ameliorated by the administration of nutrient substrates.' The goal of nutritional care is to provide an individualized, balanced diet on the basis of the metabolic requirements, fluid and electrolyte status, and degree of organ dysfunction of each patient. Nutritional Requirements Caloric needs may be estimated by a number of techniques, including calculations of resting energy expenditure based on modifications of the Harris-Benedict equation or on indirect calorimetry measurements of oxygen consumption and carbon dioxide produ~tion.~~, 69 In general, the energy expenditure for intubated patients in the ICU is the sum of the basal metabolic rate, normally between 30 to 40 kcal/m2/hr for adults, and the energy expenditure due to stress, which for severely injured patients may be an additional 30% to 50% of the basal rate. Thermally injured or septic patients may have even higher energy requirements. Protein requirements are proportional to the severity of injury, and higher protein formulations are frequently used in trauma patients to minimize visceral. protein catabolism. The optimal nitrogen:calorie ratio increases from approximately 1 g N,/300 nonprotein kcal in the mini-
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mally stressed patient to approximately 1:150 in more severely injured patients. Route of Feeding Convincing evidence exists that the route of feeding influences immunologic and metabolic responses after injury.@The gastrointestinal tract has emerged as a central system in the stressed patient.7,81 Enteral feeding, when compared to total parenteral nutrition (TPN), is associated with fewer septic complications, fewer metabolic complications, such as hyperglycemia and electrolyte disturbances, and better clinical out23, 40,56 Therefore, enteral feeding is the preferred route of feeding come~.'~, whenever possible. Several high protein enteral formulations are available, including preparations that incorporate substrates that promote enterocyte and immunologic function. Various specialized enteral formulas also are available for patients with respiratory, hepatic, or renal insufficiency. Occasionally, patients experience abdominal distention after early postoperative enteral feeding that precludes further feeding by this route; however, most patients tolerate enteral feeding. POSTINJURY COMPLICATIONS
Complications in the postinjury period are common in severely injured patients. Early diagnosis and prompt intervention are critical to successful clinical outcomes. A comprehensive discussion of postinjury or postoperative complications is beyond the scope of this article, but some of the more frequent complications are reviewed. Missed Injuries Despite attempts to complete an accurate primary and secondary survey of the trauma victim, the rate of missed injuries in patients with multisystem trauma is at least Several factors can be identified that contribute to the rate of missed injuries: low index of suspicion; failure to perform a thorough examination; and failure to order, perform, or accurately interpret diagnostic tests.4I During the excitement of a resuscitation, the immediately life-threatening injuries (as well as airway, breathing, and circulation) are addressed first, and other injuries, whether clinically significant or not, may be overlooked. Sometimes the first chance of completing the secondary survey or obtaining radiographs is postoperatively in the ICU. Alteration of consciousness due to head injury, drug or alcohol intoxication, or general anesthesia frequently preclude a complete, reliable physical examination; thus a high index of suspicion must be maintained in this group of patients. In such
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instances, other modalities to rule out injuries must be used, such as CT scanning or diagnostic peritoneal lavage. Musculoskeletal injuries excluding spinal injuries made up 50% of missed injuries in one s t ~ d y . 2Spinal ~ and facial fractures and thoracic and abdominal injuries comprise most of the remaining missed injuries. Cervical spine fractures are perhaps the most feared missed injuries, but in alert, nonintoxicated patients without cervical spine pain, injury is usually, but not always, excluded if the radiographs are normal.50The incidence of missed intracranial head injuries may be relatively low in the United States because of the availability of and reliance on CT scanning. The importance of frequent, thorough examinations in the postinjury period cannot be overemphasized. Sedation should be reversed periodically, if necessary and appropriate, to conduct a complete examination. Radiographs or other diagnostic tests should be obtained on the basis of the findings of the physical examination. Serial laboratory tests are used to determine the presence of ongoing bleeding or infection. If a high index of suspicion for associated injuries is maintained, the incidence of adverse outcomes due to missed injuries may be reduced. Postoperative Bleeding
Postoperative hemorrhage after major trauma may be due to coagulopathy or surgical bleeding. Traumatic coagulopathies are discussed in detail elsewhere in this issue. The distinction between nonsurgical and surgical causes of bleeding is important because early re-operation in the latter case may be lifesaving. The diagnosis of surgically correctable causes of postoperative bleeding, however, may be elusive. Direct evidence of hemorrhage, such as continued output from a chest tube or abdominal drain, and indirect signs of blood loss, such as hemodynamic instability, drop in hematocrit, or abdominal distention, do not always indicate active bleeding that requires re-operation. The operating surgeon is responsible for deciding if and when a patient needs to be returned to the operating room. It is becoming more popular among trauma surgeons to perform an abbreviated laparotomy in cases of extreme physiologic instability and imminent intraoperative death.27,77 The abdomen is packed with laparotomy pads to tamponade bleeding and the patient is taken to the ICU for resuscitation. If the patient survives the immediate postoperative period, he or she is returned to the operating room, usually within 48 hours, for definitive laparotomy. Unfortunately, despite vigorous resuscitative attempts to correct hypothermia, metabolic acidosis, coagulopathy, and hemodynamic instability, many of these patients die in the ICU before the planned re-operation.ll Interestingly, in a large series of patients who had undergone abbreviated laparotomy and subsequent re-operation for hemorrhage, only 4% were found to have diffuse oozing at re-exploration, while over 90% were found to have surgically correcta-
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ble causes of bleeding.34Thus, a low threshold for re-operation should be the rule in patients who survive the immediate postoperative period but continue to bleed despite the correction of hypothermia, acidosis, and coagulopathy. The goal of transfusing perioperative packed red blood cells (PRBCs) is to restore hemodynamic stability by improving oxygencarrying capacity. Critically ill patients may exhibit a pathologic dependence of oxygen delivery on oxygen supply.7oHence, increasing oxygencarrying capacity by PRBC transfusion is an effective way to improve oxygen delivery and possibly reduce the pathologic supply dependence of oxygen uptake. Even with massive transfusion (> 20 units PRBCs), survival rates of 50% in trauma patients have been reported.84 Deep Venous Thrombosis and Pulmonary Embolism The true incidence of venous thromboembolism in trauma patients is not well defined but is thought to be high, at least in certain subgroups.62Autopsy studies have found evidence of DVT in as many as 65% of patients who died after injury, and 15% to 20% had evidence of PE.73Attempts have been made to identify trauma patients who are at high risk for developing DVT or PE, but the data are ~onflicting.~~, 60, 74 The presence of one or more risk factors listed in the box below may predispose trauma patients to the development of complications of DVT or PE.
Possible Risk Factors for the Development of Venous Thromboembolism in Trauma Patients Age > 45 years Prolonged immobilization Previous history of clotting abnormalities Severe head injurylcoma Spinal cord injury Pelvis fracture Long bone fracture Repair of major vein in lower extremity Central vein cannulation Multiple transfusions
Prophylaxis of venous thromboembolism in trauma patients is incompletely understood. A significant number of these patients have contraindications to the use of low-dose heparin or are unable to wear compression hose and pneumatic compression boots because of extremity injuries. Furthermore, the use of pneumatic compression devices may increase the risk of bleeding due to activation of the fibrinolytic system?
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When suspected, DVT may be diagnosed with Doppler ultrasound or impedance plethysmography. Pulmonary embolism may be diagnosed by radionuclide imaging or pulmonary arteriography. Patients in whom DVT or PE is diagnosed require intervention to prevent further pulmonary thromboembolic complications. The risks of anticoagulation must be assessed, and if prohibitive, a vena cava filter should be inserted. Recently, a prospective study has shown that insertion of a prophylactic vena cava filter in high risk patients decreases the incidence of PE in trauma patients from 1%to 0.25Y0.~~ Fat Embolism Syndrome Fat embolism syndrome is relatively infrequently diagnosed, yet it may occur with an incidence of at least 10% in patients with long bone or pelvic fracture.26The syndrome is characterized by hypoxemia with an increased alveolar/arterial PO, gradient, changes in mental status, and a petechial rash. Onset typically occurs 12 to 72 hours after injury. Detection of urinary fat bodies can confirm the diagnosis. Prophylactic approaches in high risk patients have been tried, including the use of corticosteroids, but currently the best strategy is early fixation of fractures. Treatment of the syndrome consists of supportive measures directed at treating the pulmonary complications of fat embolism. Renal Failure Acute renal failure after trauma is uncommon. A retrospective multicenter review of trauma admissions noted a 0.1% incidence of renal failure requiring hem~dialysis.~~ The causes of posttraumatic renal failure include shock, multiple organ dysfunction syndrome, sepsis, nephrotoxins, rhabdomyolysis, and rarely, postrenal obstruction. Renal failure that develops within several days of injury is thought to be due to inadequate resuscitation, whereas late onset renal failure, which occurs twice as often as early onset renal failure, is most frequently caused by multiple organ dysfunction or sepsis.57 The contributory role of iatrogenically delivered nephrotoxins in causing acute renal failure cannot be overlooked. Many diagnostic or therapeutic agents that are frequently used in trauma patients can induce renal failure. Radiographic contrast agents, antibiotics, particularly the aminoglycosides, NSAIDs, and vasoconstrictors are potentially nephrotoxic, especially in patients with hypovolemia or preexisting risk factors such as diabetes mellitus, renal insufficiency, congestive heart failure, or advanced age. Although the incidence of radiocontrast-induced nephropathy is less than 5% in low risk individuals, the incidence sharply rises in high risk patients.,O Iatrogenically induced renal failure is a complication that can be prevented or minimized by ensuring adequate volume expansion before and after a radiographic procedure in which
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contrast dye is used, by minimizing the amount of contrast agent used, by maintaining an adequate urine output with hydration and diuretics, if needed, and by avoiding nephrotoxic drugs in high risk individuals? Rhabdomyolysis may rapidly lead to acute renal failure unless it is aggressively treated. Causes of traumatic rhabdomyolysis include crush injury, burns, electrical injury, and compartment syndrome. In the presence of aciduria (pH < 5.6), released myoglobin is converted to ferrihemate, which may produce renal failure by direct toxicity to renal tubules and by tubular plugging. Diagnosis is made by the laboratory findings of elevated concentrations of plasma creatine kinase (CK) and myoglobinuria. Treatment must be expeditious and should include reversal of the underlying cause and forced alkaline diuresis.5 Normal saline infusion should be instituted to achieve a urine output of at least 200 mL/hr. Mannitol (25 g every 6 hours) may be given after volume replenishment if urine output is low. Sodium bicarbonate should be administered, as necessary, to keep urine pH levels greater than 6. Treatment should continue until myoglobinuria has resolved and plasma CK levels fall below 1000 IU/L. The diagnosis of acute renal failure is usually obvious from the history, physical examination, and clinical course, but differentiating prerenal azotemia from acute tubular necrosis is occasionally difficult. Table 4 lists some diagnostic indices that can help to differentiate these two entities. Nonoliguric renal failure (urine output > 500 mL/day) may have a milder clinical course and is somewhat easier to manage than oliguric renal failure (urine output > 500 mL/day). The rationale, therefore, to attempt to induce a diuresis in oliguric acute renal failure may be valid. The combination of furosemide (100 to 200 mg every 6 to 8 hours) and Table 4. URINARY DIAGNOSTIC INDICES Prerenal Azotemia Urine sodium (mEq/L) Urine osmolality (mOsm/L) Urine/plasma creatinine Plasma uredplasma creatinine Fractional excretion of sodium' Renal failure indext .Fractional excretion of sodium
tRenal failure index =
=
Acute Tubular Necrosis
<20 >500
>40
>40
<20
>20
<20 >2
<400
<1 <1
urine sodium x plasma creatinine plasma sodium x urine creatinine
>2
x 100%
urine sodium x plasma creatinine urine creatinine
Data from Fischer RP, Reed RL 11, Yatsu JS: Renal failure. In Mattox KL (ed): Complications of Trauma. New York, Churchill Livingstone, 1994, p 41; Miller TR, Anderson RJ, Linas SL, et al: Urinary diagnostic indices in acute renal failure: A prospective study. Ann Intern Med 89:47, 1978; and Zarich S, Fang LST, Diamond JR: Fractional excretion of sodium: Exceptions to its diagnostic value. Arch Intern Med 145:108, 1985.
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low-dose dopamine (1-3 pg/kg/min) may be synergistic in inducing di~resis.~~ Acute renal failure is treated by volume restriction, nutritional replenishment, electrolyte correction, and adjustments in dosages of medications. Dialysis may be indicated for uremia (blood urea nitrogen [BUN] > 100 mg/dL or central nervous system manifestations of uremia), volume overload, or severe electrolyte imbalance (including refractory hyperkalemia and uncontrollable metabolic acidosis). A description of the various types of dialysis and hemofiltration procedures is beyond the scope of this article but is reviewed e l ~ e w h e r e . ~ ~
Pulmonary lnsufficiency Pulmonary dysfunction in the traumatized patient is discussed elsewhere in this issue and is only mentioned here to emphasize that practically all trauma patients who sustain moderate or severe injuries will develop some degree of pulmonary insufficiency. Both infectious and noninfectious pulmonary complications are seen frequently. Patients with altered consciousness, prolonged intubation, or with altered flora in the gastrointestinal tract seem to be at increased risk for developing pne~monia.’~ Aspiration in such patients should always be suspected, but the role of bacterial translocation from the gastrointestinal tract cannot be overlooked as a potential septic source.28The spectrum of standard and nonstandard treatments for respiratory failure is wide, and particular treatment approaches must be individualized on the basis of training, experience, and ICU resources.
Sepsis and Multiple Organ Dysfunction Sepsis or multiple organ dysfunction remain the major cause of late deaths after injury. The incidence of infectious complications in trauma patients is estimated to be about 20% but may be even higher in mechanically ventilated patients.65 Single or multiple organ dysfunction may result from infection but may also arise from noninfectious causes. These causes of organ dysfunction may be either primary (as in lung contusion) or secondary (as a result of a systemic host response to injury). The literature has been replete in recent years with confounding definitions of ”sepsis,” “sepsis syndrome,” and ”multiple organ failure;” thus standardization of terminology has been proposed.5Z Systemic inflamrnatoy response syndrome (SIRS) is the systemic inflammatory response to injury or other noninfectious insults to the host that results from activation of cytokines and other endogenous mediators. Systemic inflammatory response syndrome is characterized by two or more of the following: (1) temperature greater than 38°C or less than 36”C, (2) heart rate greater than 90/minute, (3) respiratory rate greater than 20/minute or PaC02 less than 32 torr, and (4) white blood cell
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count greater than 12,000/mm3, less than 4000/mm3, or more than 10% band forms. Sepsis is defined as the systemic inflammatory response associated with infection. Sepsis has the same clinical manifestations as SIRS, along with microbial evidence that an infectious process plays a direct part in the systemic inflammatory response. Multiple organ dysfunction syndrome (MODS) is the ”presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without interventi~n.”~~ The rationale for defining MODS in this fashion, rather than delineating clinical parameters of organ failure, is that if MODS is regarded as a continuum of organ dysfunction, earlier recognition of the syndrome, hence earlier therapeutic interventions, may be possible. Prevention of septic complications and the development of MODS begins in the emergency department at the time of admission, is continued in the operating room at the time of surgery, and remains a vital role in the ICU in the postoperative period. Expeditious resuscitative measures to restore intravascular volume, oxygen delivery, and tissue perfusion are important factors in reducing the incidence of organ dysfunction.33Nutritional and metabolic support, as previously outlined, are vital.16 Prophylactic antibiotics should be administered, when indicated, but indiscriminate use of antimicrobial agents should be avoided to prevent the complications of superinfection and the emergence of resistant microbial organisms. Lines for vascular access or hemodynamic monitoring should be routinely inspected, inserted, and dressed using aseptic technique. Once sepsis or MODS is suspected, a vigilant search to identify infectious causes of organ dysfunction should be made. Thorough physical examination is supplemented by appropriate ordering of laboratory tests, plain radiographs, CT scans, or other diagnostic tests. Certain patterns of injury may help guide the search for infection. Patients who underwent laparotomy for blunt or penetrating injury were found in one study to have an approximately 7.5% incidence of abdominal sepsis.18 Patients with chest or head injuries or with a history of blunt trauma have a higher incidence of developing pneurn0nia.6~The need and the duration of mechanical ventilation also increase the risk of developing pneurn0nia.6~Soft-tissue infections require drainage, antibiotics, local wound care, and debridement of infected and devitalized tissue. Empiric broad-spectrum antibiotics should be administered when the diagnosis of sepsis is considered. The antibiotic regimen may be changed once culture results become available. When MODS is diagnosed, organ-specific supportive care currently is the cornerstone of treatment. Newer modalities of treatment are being intensely investigated. Some of the innovative therapies being evaluated include the use of monoclonal antibodies (for example, anti-TNF-a), oxidant scavengers, growth factors, and NSAIDs or other pharmacologic agents. Such agents modulate specific steps in the biosynthetic pathways
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Further that are responsible for the systemic inflammatory studies of these potential treatments for MODS are anxiously awaited.
SUMMARY The postoperative care of the trauma patient requires an understanding of the use of analgesics, sedatives, and neuromuscular blocking agents, as well as principles of nutritional and metabolic support. Complications in the postoperative period, despite attempts to prevent them, are common. Anticipation, early recognition, and treatment of complications are essential to successful clinical outcomes.
References 1. Abbott WC, Echenique MM, Bistrian BR, et al: Nutritional care of the trauma patient. Surg Gynecol Obstet 157585, 1983 2. Aitkenhead AR, Pepperman ML, Willatts SM, et al: Comparison of propofol and midazolam for sedation in critically ill patients. Lancet 2704, 1989 3. Allenby F, Boardman L, Pflug JJ, et al: The effects of external pneumatic intermittent compression on fibrinolysis in man. Lancet 21412, 1973 4. Bailey PL, Stanley TH: Intravenous opioid anesthetics. In Miller RD (ed): Anesthesia, ed 4. New York, Churchill Livingstone, 1994, p 291 5. Better OS, Stein JH: Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med 322825, 1990 6. Boras-Uber LA, Brackett NC: Ketorolac-induced acute renal failure. Am J Med 92450, 1992 7. Border JR, Hassett J, LaDuca J, et al: The gut origin septic states in blunt multiple trauma (ISS=40) in the ICU. Ann Surg 206427,1987 8. Branney SW, Haenel JB, Moore FA, et al: Prolonged paralysis with atracurium infusion: A case report. Crit Care Med 221699, 1994 9. Brezis M, Epstein F H A closer look at radiocontrast-induced nephropathy. N Engl J Med 320:179,1989 10. Bridenbaugh PO, DuPen SL, Moore DC, et al: Postoperative intercostal nerve block analgesia versus narcotic analgesia. Anesth Analg 5281, 1973 11. Burch JM, Ortiz VB, Richardson RJ, et al: Abbreviated laparotomy and planned reoperation for critically injured patients. Ann Surg 215476, 1992 12. Cales RH, Trunkey DD: Preventable trauma deaths: A review of trauma care systems development. JAMA 254:1059,1985 13. Cales RH: Trauma mortality in Orange County: The effect of implementation of a regional trauma system. Ann Emerg Med 13:1, 1984 14. Capan LM, Gottlieb G , Rosenberg A: General principles of anesthesia for major acute trauma. In Capan LM, Miller SM, Tumdorf H (eds): Trauma: Anesthesia and Intensive Care. Philadelphia, JB Lippincott, 1991, p 259 15. Cerra FB Role of nutrition in the management of malnutrition and immune dysfunction in trauma. J Am Coll Nutr 11:512, 1992 16. Cerra FB: Hypermetabolism, organ failure, and metabolic support. Surgery 101:1, 1987 17. Craig P: Postoperative recovery of pulmonary function. Anesth Analg 60:46, 1981 18. Croce MA, Fabian TC, Stewart RM, et al: Correlation of abdominal trauma index and injury severity score with abdominal septic complications in penetrating and blunt trauma. J Trauma 32380, 1992 19. Cullen ML, Staren ED, El-Ganzouri A, et al: Continuous epidural infusion for analgesia
254
20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33.
34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47.
VASLEF & VENDER
after major abdominal operations: A randomized, prospective, double-blind study. Surgery 98:718, 1985 D’Elia JA, Gleason RE, Alday M, et al: Nephrotoxicity from angiographic contrast material: A prospective study. Am J Med 72:719, 1982 Donovan M, Dillon P, McGuire L Incidence and characteristics of pain in a sample of medical-surgical inpatients. Pain 30:69, 1987 Durbin CG Jr: Neuromuscular blocking agents and sedative drugs: Clinical uses and toxic effects in the critical care unit. Crit Care Clin 7489, 1991 Ellis LM, Copeland EM 111, Souba W. Perioperative nutritional support. Surg Clin North Am 71:493, 1991 Enderson BL, Maul1 KI: Missed injuries: The trauma surgeon’s nemesis. Surg Clin North Am 71:399, 1991 Enderson BL, Reath DB, Meadors J, et al: The tertiary trauma survey: A prospective study of missed injuries. J Trauma 30:666, 1990 Fabian TC, Hoots AV, Stanford DS, et al: Fat embolism syndrome: Prospective evaluation in 92 fracture patients. Crit Care Med 18:42, 1990 Feliciano DV, Mattox KL, Burch JM: Packing for control of hepatic hemorrhage. J Trauma 26:738, 1986 Fiddian-Green R, Baker S Nosocomial pneumonia in the critically ill: Product of aspiration or translocation? Crit Care Med 19:942, 1991 Fischer RP, Reed RL 11, Yatsu JS: Renal failure. In Mattox KL (ed): Complications of Trauma. New York, Churchill Livingstone, 1994, p 41 Grass JA: Fentanyl: Clinical use as postoperative analgesic-epidural/intrathecalroute. J Pain Symptom Manage 7419,1992 Graves DA, Foster TS, Batenhorst RL, et al: Patient-controlled analgesia. Ann Intern Med 99:360, 1983 Hansen-Flaschen JH, Brazinsky S, Basile C, et a1 Use of sedating drugs and neuromuscular blocking agents in patients requiring mechanical ventilation for respiratory failure: A national survey. JAMA 266:2870, 1991 Henao FJ, Daes JE, Dennis RJ: Risk factors for multiorgan failure: A case-controlled study. J Trauma 31:74, 1991 Hirshberg A, Wall MJ Jr, Ramchandani MK, et al: Reoperation for bleeding in trauma. Arch Surg 128:1163, 1993 Hopf Hw, Weitz S: Postoperative pain management. Arch Surg 129:128,1994 Ireton-Jones C, Turner WW Jr: The energy equations: Formulae for estimating energy expenditures in hospitalized patients. Journal of Parenteral and Enteral Nutrition 13(suppl):2OS, 1989 Kehlet H The modifying effect of general and regional anesthesia on the endocrine and metabolic response to surgery. Reg Anesth 7539, 1982 Khuenl-Brady KS, Reitstatter B, Schlager A, et al: Long-term administration of pancuronium and pipecuronium in the intensive care unit. Anesth Analg 78:1082, 1994 Knudson MM, Collins JA, Goodman SB, et al: Thromboembolism following multiple trauma. J Trauma 322,1992 Kudsk KA, Croce MA, Fabian TC, et al: Enteral versus parenteral feeding. Effects on septic morbidity after blunt and penetrating abdominal trauma. Ann Surg 215:503,1992 Laasonen EM, Kivioja A Delayed diagnosis of extremity injuries in patients with multiple injuries. J Trauma 31:257, 1991 Levy DB, Hanlon DP, Townsend RN: Geriatric trauma. Clin Geriatr Med 9:601, 1993 Lindner A: Synergism of dopamine and furosemide in diuretic-resistant, oliguric acute renal failure. Nephron 33:121, 1983 Lowry SF: The route of feeding influences injury responses. J Trauma 3Oofsuppl 12):10S, 1990 Lutz LJ, Lamer TJ: Management of postoperative pain: Review of current techniques and methods. Mayo Clin Proc 65:584,1990 Mackersie RC, Shackford SR, Hoyt DB, et a1 Continuous epidural fentanyl analgesia: Ventilatory function improvement with routine use in treatment of blunt chest injury. J Trauma 271207,1987 Mangano D, Hollenberg M, Fegert G, et a1 Perioperative myocardial ischemia in
POSTOPERATIVE CARE OF THE TRAUMA PATIENT
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patients undergoing noncardiac surgery-I: Incidence and severity during the 4-day perioperative period. J Am Coll Cardiol 17843, 1991 48. Marks RM, Sachar EJ: Undertreatment of medical inpatients with narcotic analgesics. Ann Intern Med 78:173, 1973 49. Mattox KL (ed): Complications of Trauma. New York, Churchill Livingstone, 1994 50. Maul1 KI, Sachatello C R Avoiding a pitfall in resuscitation: The painless cervical fracture. South Med J 4:477, 1977 51. McGuire GP, Pearl RG: Sepsis and the trauma patient. Crit Care Clin 6121, 1990 52. Members of the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference Committee: American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 20864, 1992 53. Mendel PR, M i t e PF: Sedation of the critically ill patient. Int Anesthesiol Clin 31:185, 1993 54. Miller TR, Anderson RJ, Linas SL, et al: Urinary diagnostic indices in acute renal failure: A prospective study. Ann Intern Med 89:47, 1978 55. Moore DC, Bridenbaugh L D Intercostal nerve block in 4333 patients: Indications, technique, and complications. Anesth Analg 41:1, 1962 56. Moore FA, Moore EE, Jones TN, et al: TEN versus TPN following major abdominal trauma-reduced septic morbidity. J Trauma 29:916, 1989 57. Morris JA Jr, Mucha P Jr, Ross SE, et a 1 Acute posttraumatic renal failure: A multicenter perspective. J Trauma 31:1584, 1991 58. Nielsen T, Nielsen H, Husted S, et al: Stress response and platelet function in minor surgery during epidural bupivacaine and general anesthesia: Effect of epidural morphine addition. Eur J Anaesthesiol 6:409, 1989 59. OHara DA, Fragen RJ, Kinzer M, et al: Ketorolac tromethamine as compared with morphine sulfate for treatment of postoperative pain. Clin Pharmacol Ther 41:556,1987 60. OMalley KF, Ross SE: Pulmonary embolism in major trauma patients. J Trauma 30748, 1990 61. Raj PR, Hartrick C, Pither CE: Pain management of the injured. In Capan LM, Miller SM, Turndorf H (eds): Trauma: Anesthesia and Intensive Care. Philadelphia, JB Lippincott, 1991, p 685 62. Rehm CG, Spence RK, Ross SE: Venous thromboembolism in trauma patients. NJ Med 89:755, 1992 63. Ritz R Benzodiazepine sedation in adult ICU patients. Intensive Care Med 17(suppl l):llS, 1991 64. Rocco A, Reiestad F, Gudman J, et a1 Intrapleural administration of local anesthetics for pain relief in patients with multiple rib fractures. Reg Anesth 1210,1987 65. Rodriguez JL, Gibbons KJ, Bitzer LG, et al: Pneumonia: Incidence, risk factors, and outcome in injured patients. J Trauma 31:907, 1991 66. Rogers FB, Shackford SR, Wilson J, et al: Prophylactic vena cava filter insertion in severely injured trauma patients: Indications and preliminary results. J Trauma 35:637, 1993 67. Rouse TM, Eichelberger MR Trends in pediatric trauma management. Surg Clin North Am 721347, 1992 68. Rozycki G: Trauma during pregnancy: Predicting pregnancy outcome. Arch Gynecol Obstet 253(suppl):15S, 1993 69. Saffle JR, Medina E, Raymond J, et al: Use of indirect calorimetry in the nutritional management of burned patients. J Trauma 2532,1985 70. Samsel RW, Schumacker P T Pathologic supply dependence of oxygen utilization. In Hall JB, Schmidt GA, Wood LDH (eds): Principles of Critical Care. New York, McGraw-Hill, 1992, p 667 71. Santora TA, Schinco MA, Trooskin SZ: Management of trauma in the elderly patient. Surg Clin North Am 74163, 1994 72. Sebel P, Lowdon J D Propofol A new intravenous anesthetic. Anesthesiology 71260, 1989 73. Sevitt S, Gallagher NG: Prevention of venous thrombosis and pulmonary embolism in injured patients. Lancet 2981, 1959
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74. Shackford SR, Davis JW, Hollingsworth-Fridlud P, et al: Venous thromboembolism in patients with major trauma. Am J Surg 159:365, 1990 75. Shackford SR, Mackersie RC, Hoyt DB, et al: Impact of a trauma system on outcome of severely injured patients. Arch Surg 122523, 1987 76. Staren ED, Cullen ML: Epidural catheter analgesia for the management of postoperative pain. Surg Gynecol Obstet 162389, 1986 77. Stone HH, Strom PR, Mullins RJ: Management of the major coagulopathy with onset during laparotomy. Ann Surg 197532, 1983 78. Tran DD, Cuesta MA, Van Leeuwen PAM, et al: Risk factors for multiple organ system failure and death in critically injured patients. Surgery 11421, 1993 79. Wadon AJ, Dogra S, Anand S Atracurium infusion in the intensive care unit. Br J Anaesth 58S64, 1986 80. Watling SM, Dasta JF: Prolonged paralysis in intensive care unit patients after the use of neuromuscular blocking agents: A review of the literature. Crit Care Med 22884, 1994 81. Wilmore DW, Smith RJ, ODwyer ST, et al: The gut: A central organ after surgical stress. Surgery 104:917, 1988 82. Wisner D H A stepwise logistic regression analysis of factors affecting morbidity and mortality after thoracic trauma: Effect of epidural analgesia. J Trauma 30799, 1990 83. Worthley LIG: Thoracic epidural in the management of chest trauma: A study of 161 cases. Intensive Care Med 11:312, 1985 84. Wudel JH, Morris JA Jr, Yates K, et al: Massive transfusion: Outcome in blunt trauma patients. J Trauma 31:1, 1991 85. Zarich S, Fang LST, Diamond J R Fractional excretion of sodium: Exceptions to its diagnostic value. Arch Intern Med 145:108, 1985
Address reprint requests to Steven N. Vaslef, MD, PhD Department of Surgery Duke University Medical Center Box 2601 Durham, NC 27710