Trauma Pediatric - part 4 ppt

by the rapid onset of fever, chills, rigors, chest or abdominal pain progressing to respiratory distress, and circulatory shock. Hemoglobin is present in the plasm a and urine. Renal failure may ensue. Once recognized, the transfusion should imme- diately be discontinued. Aggressive resuscitation should be instituted to support the circulation and achieve a urine output of >60 mL/hr. Transfusion-Transmitted Diseas e Viral infection, the most feared complication, is the most common cause of late death from transfusion (Table 2). The first desc riptions of transfusion-associated HIV infec tion occurr ed in late 1982. Improved screening and detection has reduced the current frequency of HIV infection to ap proximately to 1/250, 000– 1/2,000,000 units. The most common serious viral infection is he patitis C (HCV), estimated to occur in 1/30,00 0–1/150,000 units. Eighty-five percent of posttransfu- sion HCV i nfections become chronic, 20% of infected patient s develop cirrhosis, and 1% progre ss t o hepatocellular carcinoma. Hepatitis B (HBV) infe ction is estimated to occur in 1/30,000–1/250,000 units. In 1975 new screening tes ts were implemented, reducing transfusion-transmitted HBV infection. The HBV now accounts for only 10% of all cases of posttransfusion hepatitis. Acute disease develops in 35% of persons infected with HBV. Up to 10% will develop chronic infection. Bacterial infection due to contamination most often occurs following platelet transfusion (1/12,000 units), but can also occur following RBC transfusion (1/500,00 units). The difference in frequency is attributed to storage of platelets at 20–24  C, which facilitate bacterial growth, while red blood cells are generally stored at much lower temperatures. The most common organism associated with RBC contamination is Yersinia enterocolitica, while Staphylococcus aureus, Klebsiella pneumoniae, Serratia marcescens, and S. epidermidis infections are most frequently observed in platelet-associated infection (2). Metabolic Complications Children may be more susceptible than adults to metabolic complications with rapid transfusion because of the higher ratio of transfused blood-to-blood volume. Table 2 Estimated Risks of Transfusion per Unit in the United States (1999) Febrile reaction 1:100 Bacterial contamination Platelets 1:12,000 Red blood cells 1:500,000 Viral infection Hepatitis A 1:1,000,000 Hepatitis B 1:30,000–1:250,000 Hepatitis C 1:30,000–1:150,000 HIV 1:200,000–1:2,000,000 Delayed hemolytic transfusion reaction 1:1000 Fatal hemolytic transfusion reaction 1:250,000–1:1,000,000 Source: Adapted from Ref. 2. 118 Bensard Children are prone to hypothermia and may become profoundly hypothermic with the infusion of cold fluids and blood products. Hypothermia not only increases metabolic demand but also worsens coagulopathy. Infant s and small childr en should be maintained in a warm environment and given warmed fluids and blood products. Rapid infusion can also produce severe electrolyte disturbances. Hypocalcemia or hyperkalemia may arise after large- or rapid-volume infusion and, therefore, serum electrolytes should be periodically evaluat ed. RED BLOOD CELL SUBSTITUTES Due to the risks and costs of blood transfusion, efforts have been directed toward the development of hemoglobin-based red cell substitutes. Red cell substitutes do not transmit viral pathogens and have lower viscosities than blood while maintain- ing the same-oxygen carrying capacity of allogenic blood. Free hemoglobin has an extremely high oxygen affinity that renders it ineffective for tissue oxygenation. Furthermore, once outside the protective red cell membrane the hemoglobin tetra- mer disassociates into its component a and b dimers, which are potentially nephro- toxic. Polymerization of bovine, human, and recombinant hemoglobin results in synthetic hemoglobin with a P 50 of natural hemogl obin, a plasma half-life up to 30 hours, and normal oncotic pressure (50). The absence of a red cell membrane eliminates the need for blood typing and crossmatchi ng, as well as the immunologic effects attributed to surface antigens or white bloo d cells, platelets, and debris pre- sent in red blood cell units. One unit (500 mL) of synthetic, polymerized, stroma-free hemoglobin (Poly SFH-P) is characterized by hemoglobin concentration of 10 g/dL, P 50 of 28–30 torr and t 1/2 of one day. A phase-II trial of Poly SFH-P demonstrated its safe use in acute trauma (51). A prospective, randomized trial of Poly SFH- P in trauma patients demonstrated that the use of a red blood cell substitute for the treatment of acute blood loss reduced the need for red blood cell transfu- sion, while maintaining parameters of oxygen transport (4). The most recent trial of Poly SFH-P confirms the ability of red blood cell substitutes to m aintain oxygen- carryingcapacityinthesettingofacutehemorrhagic shock, even with transfusion requirements up to 20 units (52). Mortality (25%) was substantially lowered at critical hemoglobin levels 3 g/dL relative to historic controls (64.5%) who refused red blood cells on religious grounds. Remarkably 9/12 patients who sustained lethal blood loss (RBC Hb 1 g/dL) survived with the administration of Poly SFH-P and resultant total hemoglobin concentration (RBC Hb þ Poly SFH-P) 7–10 g/dL. Although these results are encouraging, the abrupt en d of the diaspirin cross- linked hemoglobin (DCLHb) trial suggests that the various red blood substitutes under development are not homogenous. Unlike the Poly SFH-P trials, a phase-II trial of DCLHb administration was associated with a 72% increase in morbidity (Multiple Organ Dysfunction Score) and a threefold fold increase in mortality in the treatment group (46%) relative to the control group (17%) (53). It is speculated that selected red blood substitutes (e.g., DCLHb) bind nitric oxide, which causes the undesirable side effects of vasoconstriction and pulmonary hypertension. Never- theless, efforts to develop a safe and effective red cell substitute continue given the advantages of a readily available, oxygen-carrying, resuscitative fluid that eliminates the delay and risks of allogenic blood. Transfusion Therapy in Injured Children 119 REFERENCES 1. Rossi E, Simon T, Moss G, Gould S. A history of transfusion. In: Spiess B, Counts R, Gould S, eds. Perioperative Transfusion Medicine. Baltimore: Williams and Wilkins, 1997:3–12. 2. Goodnough L, Brecher M, Kanter M, AuBuchon J. Transfusion Medicine. NEJM 1999; 340:438–447. 3. Carson JL, Terrin ML, Barton FB, Aaron R, Greenburg AG, Heck DA, Magaziner J, Merlino FE, Bunce G, McClelland B, Duff A, Noveck H. A pilot randomized trial com- paring symptomatic vs. hemoglobin-level-driven red blood cell transfusions following hip fracture. Transfusion 1998; 38(6):522–529 4. Gould SA, Moore EE, Hoyt DB, Burch JM, Haenel JB, Garcia J, DeWoskin R, Moss GS. ‘‘The first randomized trial of human polymerized hemoglobin as a blood substitute in acute trauma and emergent surgery [see comments]. J Am Coll Surg 1998; 187(2):113– 120. 5. Hebert PC, Wells G, Marshall J, Martin C, Tweeddale M, Pagliarello G, Blajchman M. Transfusion requirements in critical care. A pilot study. Canadian Critical Care Trials Group. JAMA 1995; 273(18):1439–1444. 6. Hebert PC. Transfusion requirements in critical care (TRICC): a multicentre, randomized, controlled clinical study. Transfusion Requirements in Critical Care Inves- tigators and the Canadian Critical care Trials Group. Br J Anaesth 1998; 81(suppl 1): 25–33. 7. Hebert PC, Wells G, Blajchman MA, Marshall J, Martin C, Pagliarello G, Tweeddale M, Schweitzer I, Yetisir E. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group. N Engl J Med 1999; 340(6):409–417. 8. Tullis J. Office of Medical Applications of Research, National Institutes of Health: Fresh-frozen plasma: Indications and risks. JAMA 1985; 253:551–553. 9. Greenwalt T. Office of Medical Applications of Research, National Institutes of Health: Perioperative red blood cell transfusion. JAMA 1988; 260:2700–2703. 10. Aster R. Office of Medical Applications of Research, National Institutes of Health: Platelet transfusion therapy. JAMA 1987; 257:1777–1780. 11. Spence RK. Practice policies for surgical red blood cell transfusion: surgical transfusion policies. Semin Hematol 1996; 33(1 suppl 1):19–22. 12. Practice guidelines for blood component therapy. Anesthesiology 1996; 84:732–747. 13. Goodnough L, Despotis G. Establishing practice guidelines for surgical blood manage- ment. Am J Surg 1995; 170(suppl):16S–20S. 14. Grupp-Phelan J, Tanz RR. How rational is the crossmatching of blood in a pediatric emergency department? Arch Pediatr Adolesc Med 1996:150(11):1140–1144. 15. Wallace EL, Churchill WH, Surgenor DM, Cho GS, McGurk S. Collection and transfu- sion of blood and blood components in the United States, 1994 [see comments]. Transfu- sion 1998; 38(7):625–636. 16. Orliaguet GA, Meyer PG, Blanot S, Jarreau MM, Charron B, Buisson C, Carli PA. Pre- dictive factors of outcome in severely traumatized children. Anesth Analg 1998; 87(3):537–542. 17. Stylianos S. Evidence-based guidelines for resource utilization in children with isolated spleen or liver injury. The APSA Trauma Committee. J Pediatr Surg 2000; 35(2): 164–167; discussion 167–169. 18. Fallat M, Casale A. Practice patterns of pediatric surgeons caring for stable patients with traumatic solid organ injury. J Trauma 1997; 43:820–824. 19. Feliciano P, Mullins R, Trunkey D, Crass R, Beck J, Helfand M. A decision analysis of traumatic splenic injuries. J Trauma 1992; 33:340–348. 120 Bensard 20. Avanoglu A, Ulman I, Ergun O, Ozcan C, Demircan M, Ozok G, Erdener A. Blood transfusion requirements in children with blunt spleen and liver injuries. Eur J Pediatr Surg 1998; 8(6):322–325. 21. Patrick DA, Bensard DD, Moore EE, Karrer FM. Nonoperative management of solid organ injuries in children results in decreased blood utilization. J Pediatr Surg 1999; 34(11):1695–1699. 22. Schwartz MZ, Kangah R. Splenic injury in children after blunt trauma: blood transfu- sion requirements and length of hospitalization for laparotomy versus observation. J Pediatr Surg 1994; 29(5):596–598. 23. Shafi S, Gilbert JC, Carden S, Allen JE, Glick PL, Caty MG, Azizkhan RG. Risk of hemorrhage and appropriate use of blood transfusions in pediatric blunt splenic injuries. J Trauma 1997; 42(6):1029–1032. 24. Bond SJ, Eichelberger MR, Gotschall CS, Sivit CJ, Randolph JG. Nonoperative man- agement of blunt hepatic and splenic injury in children. Ann Surg 1996; 223(3):286–289. 25. Farion KJ, McLellan BA, Boulanger BR, Szalai JP. Changes in red cell transfusion prac- tice among adult trauma victims. J Trauma 1998; 44(4):583–587. 26. Lynch JM, Gardner MJ, Gains B. Hemodynamic significance of pediatric femur fractures. J Pediatr Surg 1996; 31(10):1358–1361. 27. Ciarallo L, Fleisher G. Femoral fractures: are children at risk for significant blood loss? Pediatr Emerg Care 1996; 12(5):343–346. 28. McIntyre RC Jr, Bensard DD, Moore EE, Chambers J, Moore FA. Pelvic fracture geo- metry predicts risk of life-threatening hemorrhage in children. J Trauma 1993; 35(3):423– 429. 29. Greenberg A. A physiologic basis for red blood cell transfusion decisions. Am J Surg 1995; 170:44s–48s. 30. Carson JL, Noveck H, Berlin JA, Gould SA. Mortality and morbidity in patients with low postoperative Hb levels who decline blood transfusion. Transfusion 2002; 42: 812–818. 31. Viele MK, Weiskopf RB. What can we learn about the need for transfusion from patients who refuse blood? The experience with Jehovah’s Witnesses. Transfusion 1994; 34(5):396–401. 32. Carson J. Morbidity risk assessment in the surgically anemic patient. Am J Surg 1995; 170:32s–35s. 33. Weiskopf RB, Viele MK, Feiner J, Kelley S, Lieberman J, Noorani M, Leung JM, Fisher DM, Murray WR, Toy P, Moore MA. Human cardiovascular and metabolic response to acute, severe isovolemic anemia. JAMA 1998; 279(3):217–221. 34. Carson JL, Duff A, Berlin JA, Lawrence VA, Poses RM, Huber EC, O’Hara DA, Noveck H, Srrom BL. Perioperative blood transfusion and postoperative mortality. JAMA 1998; 279(3):199–205. 35. Moore FA, Moore EE, Sauaia A. Blood transfusion. An independent risk factor for postinjury multiple organ failure. Arch Surg 1997; 132(6):620–624. 36. Sauaia A, Moore FA, Moore EE, Haenel JB, Read RA, Lezotte DC. Early predictors of postinjury multiple organ failure. Arch Surg 1994; 129(1):39–45. 37. Siliman C, Paterson A, Dickey W. The association of biologically active lipids with the development of transfusion related acute lung injury: a retrospective study. Transfusion 1997; 37:719–726. 38. Zallen G, Offner PJ, et al. Age of transfused blood is an independent risk factor for post- injury multiple organ failure. Am J Surg 1999; 178(6):570–572. 39. Sauaia A, Moore F, Moore E, Moser K, Brennan R, Read R, Pons P. Epidemiology of trauma deaths: a reassessment. J Trauma 1995; 38:185–193. 40. Advanced trauma life support student manual. Sixth ed. Chicago: American College of Surgeons, 1997. 41. Kivioja A, Myllynen P, Rokkanen P. Survival after massive transfusions exceeding four blood volumes in patients with blunt injuries. Am Surg 1991; 57(6):398–401. Transfusion Therapy in Injured Children 121 42. Wudel JH, Morris JA Jr, Yates K, Wilson A, Bass SM. Massive transfusion: outcome in blunt trauma patients. J Trauma 1991; 31(1):1–7. 43. Ciavarella D, Reed F, Counts R. Clotting factor levels and the risk of diffuse microvas- cular bleeding in the massively transfused patient. Br J Haematol 1987; 67:365–368. 44. Cathey KL, Brady WJ Jr, Butler K, Blow O, Cephas GA, Young JS. Blunt splenic trauma: characteristics of patients requiring urgent laparotomy. Am Surg 1998; 64(5):450–454. 45. Davis JW, Parks SN, Kaups KL, Gladen HE, O’Donnell-Nicol S. Admission base deficit predicts transfusion requirements and risk of complications. J Trauma 1996; 41(5):769– 774. 46. Davis JW, Kaups KL, Parks SN. Base deficit is superior to pH in evaluating clearance of acidosis after traumatic shock. J Trauma 1998; 44(1):114–118. 47. Mikulaschek A, Henry SM, Donovan R, Scalea TM. Serum lactate is not predicted by anion gap or base excess after trauma resuscitation. J Trauma 1996; 40(2):218–222. 48. Blow O, Magliore L, Claridge JA, Butler K, Young JS. The golden hour and the silver day: detection and correction of occult hypoperfusion within 24 hours improves outcome from major trauma. J Trauma 1999; 47(5):964–969. 49. Dabrowski G, Steinberg S, Ferrara J, Flint L. A critical assessment of endpoints of shock resuscitation. Surg Clinics N Amer 2000; 80:825–844. 50. Creteur J, Sibbald W, Vincent J. Hemoglobin solutions-not just red blood cell substi- tutes. Crit Care Med 2000; 28:3025–3034. 51. Gould SA, Moore EE, Moore FA, Haenel JB, Burch JM, Sehgal H, Sehgal L, DeWoskin R, Moss GS. Clinical utility of human polymerized hemoglobin as a blood substitute after acute trauma and urgent surgery. J Trauma 1997; 43(2):325–331. 52. Gould SA, Moore EE, Hoyt DB, Ness PM, Norris EJ, Carson JL, Hides GA, Freeman I, DeWoskin R, Moss GS. The life-sustaining capacity of human polymerized hemoglobin when red cells might be unavailable. J Am Coll Surg 2002; 195:445–455. 53. Sloan EP, Koenigsberg M, Gens D, Cipolle M, Runge J, Mallory MN, Rodman GJ. Dis- aspirin cross-linked hemoglobin (DCHLb) in the treatment of severe traumatic hemor- rhagic shock: a randomized controlled efficacy trial. JAMA 1999; 282:1857–1864. 122 Bensard 10 Pediatric ICU Management Cameron Mantor, Nikola Puffinbarger, and David Tuggle The Section of Pediatric Surgery, Department of Surgery, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma, U.S.A. ICU CARE Trauma continues to be the leading cause of death in the first several decades of life. Those surviving an accident but suffering from significant trauma will frequently need intensive care. The criteria for intensive care unit (ICU) admis sion will vary from institution to institution, but some commonality can be suggested. Those with multi-system trauma or hemodynamic instability will benefit from intensive care. Others with a Pediatric Trauma Score of seven or less; isolated but significant head trauma and an altered mental status; liver, or spleni c lacerations of grade III or greater; significant pancreatic injuries, multiple orthopedic injuries; and injuries, that may not be readily cared for on the ward because of local institutional factors may best be cared for initially in the ICU. MONITORING Basic monitoring is required for all pediatric trauma patients in the ICU. This includes measurement of vital signs: determination of heart rate and respiratory rate, continu- ous electrocardiography, noninvasive blood pressure determination, and temperature measurement. According to recent pediatric literature, pulse oximetry should be con- sidered a fifth vital sign, and capnography should also be included for intubated patients (1). Cardiovascular Monitoring Usually, noninvasive blood pressu re monitori ng is utilized in the pediatric population. Noninvasive monitoring in the child may be quite accurate if the proper cuff size is utilized. The American Heart Association has set guidelines for proper cuff fit. They recommend a cuff whose width is 40% of the circumference at the midpoint of the limb or 20% greater than the diameter of the extremity (2). The attending trauma team must also be aware o f the age-related norms for blood pressures (Table 1). 123 In most modern pediatric intensive care units (PICU), automated arterial blood pressure devices are utilized. These units measure heart rate and systolic, diastolic, and mean arterial blood pressure. Pitfalls of noninvasive monitoring include: 1. Diastolic pressures tend to be slightly higher with the noninvasive devices. 2. Dysrhythmias and wide variations in blood pressure over a short time frame may be missed. Access for invasive blood pressure monitoring may be accomplished in all children. This is performed either through percutaneous arterial cannulation or by arterial cutdown. The usual site in children is the radial artery. However, in an emer- gent situation in a crowded trauma bay, the ICU, or operating room the quickest access may be percutaneous cannulation of the femoral artery (3). After stabilization in the PICU the arterial site may be changed to the radial artery. Pitfalls of invasive monitoring include limb ischemia (femoral artery), cannula compression, and kink- ing or clot formation. It is therefore wise to correlate invasive with noninvasive monitoring in the critically ill trauma patient. Benefits of invasive monitoring include continuous direct waveform display of the arterial blood pressure and access for arterial blood sampling for blood gases. Electrocardiography (ECG) monitors the heart rate and rhythm of cardiac conduction. Rhythm disturbances associated with trauma may include atrial tachycar- dia, ventricular tachycardia (sub arachnoid hemorrhage), persistent s inus bradycardia (cerebral hypoxia/arrest at the scene/airway obstruction/tracheal disruption/increased intracranial pressure secondary to head trauma/hypothermia d ue to cold exposure), and sinus tachycardia (h ypovolemic shock). A lso, man y teen age t rauma p atients h ave taken drugs that alter the ECG: tricyclic antidepressants, cocaine, opiates, and amphetamines. Oxygen Saturation Pulse oximetry is currently being advocated as an accurate, simple, and noninvasive method of measuring the oxygen saturation of arterial blood. It is based on the spec- trophotometry of oxygenated hemoglobin, which absorbs infrared light at the 940 nm wavelength and transmits red light at the 660 nm wavelength. The pulse oximetry probe has two light-emitting diodes that pass light at these wavelengths through the perfused tissue to a photodetector on the other side. The photodiode then compares the amount of infrared, red, and ambient light that reaches it and calculates the oxygen saturation (SaO 2 ) (2). A small sensor (probe) is placed on the finger, toe, earlobe, fore- head, or any convenient place. Most devices demonstrate the SaO 2 as well as pulse rate continuously. The pulse oximeter has been demonstrated to reflect moderate hypoxia (SaO 2 < 89%) before an increase in ventilatory drive is demonstrated (1). This, as well as its noninvasive, continuous monitoring of the SaO 2 , has made it a critical Table 1 Abnormal Vital Signs RR Pulse BP Infant >40 >160 <60 Toddler >30 >140 <75 School age >25 >120 <85 Adolescent >20 >110 <90 124 Mantor et al. component of PICU monitoring in the pediatric trauma patient. It provides a contin- uous reflection of hemoglobin saturation and provides the trauma surgeon with knowledge that sufficient oxygen is being delivered to the injured tissues. A disadvantage of pulse oximetry has been decreased accuracy at low saturations (defined as SaO 2 < 70–75%). New generations of pulse oximeters perform better with- out deterioration of performance at saturations <75%. However, it is still recom- mended that frequent measurements of PaO 2 should be done at lower saturations (4). If the oxygen saturation is below 70% on multiple pulse oximeter determinations then the arterial blood should be sampled because the true oxygen saturation is usually underestimated by most oximeters. Other disadvantages of some pulse oximeter models include motion artifact, placement of sensor below blood pressure cuff, and poor tissue perfusion of a distal extremity (3,5). When elevations of carboxyhemoglobin (COHb) are seen in the setting of carbon monooxide (CO) poisoning, the pulse oximetry reading remains in the nor- mal range, despite markedly reduced actual oxygenated hemoglobin (O 2 Hb). This is because COHb does not absorb light at the infrared wavelength (940 nm), while it does transmit red light (wavelength 640 nm). As a result, the pulse oximeter cannot differentiate between the COHb and O 2 Hb at the red wavelength, and the combined value is applied to the calculation of the oxygen saturation. As a result, the pulse oxi- meter overestimates the actual oxyhemoglobin saturation (SaO 2 ) so that it is unreli- able in patients with CO poisoning (6). Ventilation End tidal carbon dioxide (EtCO 2 ) monitoring, known as capnometry, is a noninvasive method for measuring the PaCO 2 in expired gas. Similar to pulse oximetry-measuring devices, the exhaled gas passing through a sampling chamber, which has an infrared light source on one side and a photodetector on the other, measures the carbon dioxide (CO 2 ). CO 2 absorbs light at the infrared wavelength (940 nm). The CO 2 present in the expired gas may be calculated from the amount of infrared light that reaches the photo- detector . EtCO 2 is a reflection of alveolar ventilation, metabolic rate, and the pulmo- nary circulation. It also may be helpful in transport of the injured patient to and from the PICU for early detection of endotracheal tube dislodgment (7). It is currently recommended by several sources, including the American Academy of Pediatrics, that all children who are intubated and being transported have an EtCO 2 (8). MANAGEMENT OF PICU TRANSFUSIONS In the unstable trauma pa tient, hemoglobin and hematocrit should be measured every four hours and one hour after every trans fusion until vital signs stabilize and urine output is adequate. To restore blood volume and O 2 -carrying capacity to a pediatric trauma patient that has lost a large volume of blood, it is essential to transfuse one unit quickly in larger children ( >25 kg) or 10–15 mL/kg of blood in smaller children. Packed red blood cells are the product of choice for patients with moderate acute blood loss. For severe hemorrhage, plasma substitutes are requir ed when packed red blood cells are transfused to compensate for dilution of coagulation proteins. Massive transfusions that involve replacing an amount of blood equal to the patient’s blood volume in 24 hours involve several risks. These include citrate tox- icity, electrolyte imbalance, and decreased release of oxygen to the tissues resulting Pediatric ICU Management 125 from decreased 2,3 disphosglycerate content, pulmonary microembolism, decreas ed core temperature, and thrombocytopenia/disseminated intravascular coagulation (DIC). The total blood volume in a child is approximately 75 mL/kg. If this amount of blood has been given to a child in a 24-hour period or less then early treatment of the side effects of massive transfusion should be initiated. For every blood volume lost, it is often necessary to administer fresh frozen plasma (20 mL/kg), sodium bicarbonate (1–3 meq/kg if pH <7.3), calcium chloride 10% (10–20 mg/kg if ionized calcium <2), and platelets (platelet count <50,000/uL). In children, 0.1 unit of pla- telet concentrate/kg usually increases the platlets an increment of 40,000/uL (3,9). Transfusion pumps equipped with warming units should be used when large amounts of blood and crystalloid are transfused to decrease the incidence of hypothermia. In addition, most PICU beds have thermal blankets and external warming sources to minimize heat loss. NUTRITION Although gastric and colonic motility may be impaired for several days after trauma or stress, small intestinal motility and absorpt ive function remain intact. A prospective, randomized study by Moore and Jones demonstrated that enterally fed patients had fewer complications after major abdominal tr auma than patients receiving total parenteral nutrition (10). A recent study by Jackson, et al. demon- strated that early enteral feeding in PICU patients was feasible, well tolerated, and cost-effective without th e risk of aspiration or abdominal dis tension. Beds ide nasal jejunal tubes were pa ssed and caloric requirement s were met within 48 hours in most patients (11, 12). Placement of the tubes may be che cked by portab le kidney, ureter, and bladder (KUB) films and, if passage is difficult, may be performed under fluoroscopic guidance with minima l sedation in the fluoroscopy suite. In conc lusion, elemental feedings should be initiated early in the pe diatric trauma patient and are preferred over parenteral nutrition. If full enteral feeds are not tolerated then parenteral nutrition should be instituted to meet the caloric needs of the patient, and a small amount of jejunal feeds can be continued to maintain gut integrity. COMMONLY USED MEDICATIONS Table 2 shows the commonly used medications. ACUTE RESPIRATORY FAILURE Acute lung injury leading to respiratory insufficiency is a frequent complication found in the trauma patient. Its etiology is varied and includes atelectasis, aspiration, infection, the acute respiratory distress syndrome (ARDS) as well as others. Of these ARDS has the most potential for significant morbidity an d mortality. Therapy may be as simple as supplying oxygen and pulmonary physiotherapy or as complicated as providing extracorporeal life support (ECLS). The pulmonary injury preceding ARDS may be direct (pulmonary contusion and smoke inhalation) or indirect (shock and sepsis). It is important to understand the differences in both their effects as well as how each can be best treated. 126 Mantor et al. Pathophysiology In an early description Asbaugh et al. termed the clinical picture of progressive hypox- emia, tachypnea, and generalized patchy pulmonary infiltrates, in the absence of car- diac failure ARDS (13). These signs and symptoms are usually presented within one to four days of the original inciting event. This clinical entity describes a final common pathway with definable lung pathology from a wide spectrum of significant injuries. Early beliefs were that ARDS results in a disseminated and homogeneous pulmonary process, as suggested by conventional chest X rays (CXR) (Fig. 1). It has since been shown with computed tomography (CT) that this is not so (Fig. 2) (14,15). CT scans in patients with ARDS reveal the presence of atelectasis and edema in the more depen- dent portions of the lungs. This is felt to be due to compression of lung tissue. Nonde- pendent portions of the lungs have an increase in edema but are well aerated and thus receive an inordinate amount of the minute ventilation. This is because gases all flow via the path of least resistance. As the syndrome progresses, so does the opacification on CXR. Gattionni et al. showed that as little as one third of the lung is actually venti- lated and called this condition ‘‘baby lung’’ (16). Mechanical ventilation in this clinical setting leads to regional over-distension of nondependent lung, reduces capillary perfusion, increases pulmonary dead space, and exacerbates the already present ventilation perfusion mismatch. It has also been shown that mechanical ventilation itself can lead to lung injury (17,18). Initially termed barotrauma, this injury may more appropriately be due to volutrauma. Webb and Tierny have also shown that regional over-distension of alveoli with mechanical ventilation leads to injury (19). This is most closely associated with high peak inspiratory pressures, greater than 40 cm H 2 O, and repeated opening and closing of collapsed alveoli. This alveolar over-distension leads to stress failure of alveolar capillary membranes, which leads to increased microvascu lar permeability and edema. Although the evidence is circumstantial, it is felt that this volutrauma Table 2 Commonly Used Medications Pressors Dopamine Low dose 2–5 mcg/kg/min Intermediate 5–15 mcg/kg/min High 20 mcg/kg/min Dobutamine 2–15 mcg/kg/min Epinephrine 0.1–1.0 mcg/kg/min Analgesics Fentanyl 1–5 mcg/kg/hr Morphine 0.05–0.2 mg/kg/hr Sedation Ativan 0.05–0.2 mg/kg/hr Ketamine 0.5–2 mg/kg Versed 0.05–0.2 mg/kg/hr Paralysis Cisatracurium 1–2 mcg/kg/min Vecuronium 0.05–0.1 mg/kg/hr Bronchodilators Albuterol 0.05–15 mg/kg nebulized q 4 hr Racemic epinephrine 0.05 cc/kg/dose dilated to 3 cc NS nebulized q 4 hr Pediatric ICU Management 127 [...]... is a health risk (43 ,44 ) Nutritional Support for the Pediatric Trauma Patient 143 ROUTES OF NUTRIENT PROVISION In the traumatized child the enteral route of nutrient provision is preferable to the parenteral route whenever the gastrointestinal tract is functional Enteral nutrition is physiologic, safer, and cheaper (45 ) If there is a concern regarding aspiration, the use of post-pyloric feeding tubes... infants Pediatrics 1980; 66:26–30 42 Freeman J, Goldmann DA, Smith NE, Freeman J, Goldmann DA, Smith NE, Sidebottom DG, Epstein MF, Platt R 43 Marks J The safety of vitamins: an overview Int J Vitam Nutr Res 1989; 30:S12–S20 44 Foldin NW Micronutrient supplements: toxicity and drug interactions Prog Food Nutr Sci 1990; 14: 277–331 45 de Lucas C, Moreno M, Herce JL, Lopez-Herce J, Ruiz F, Perez-Palencia... 2000;30:175–180 46 Munshi IA, Steingrub JS, Wolpert L Small bowel necrosis associated with early postoperative jejunal feeding in a trauma patient J Trauma 2000; 49 :163–165 12 Anesthesia for Pediatric Trauma J Thomas and J Lerman Department of Anesthesia, Women and Children’s Hospital of Buffalo, SUNY at Buffalo, Buffalo, New York, U.S.A INTRODUCTION The role of anesthesia in pediatric trauma extends... the Pediatric Airway All anesthetic equipment should be inspected and operational before the child arrives in the operating room /trauma room A working source of oxygen and airway Anesthesia for Pediatric Trauma 149 suction, as well as backup supplies, should be available The oxygen source should have high flow capabilities (15 L/min for maximum oxygen delivery) and include a self-inflating bag-valve-mask... plasma cytokine elevations with mortality rate in children with sepsis J Pediatr 1992; 120:510– 515 4 Gump GE, Kinney JM Energy balance and weight loss in burned patients Arch Surg 1971; 103 :44 2 44 8 5 Forbes GB, Bruining GJ Urinary creatinine excretion and lean body mass Am J Clin Nutr 1976; 29:1359–1366  144 Jaksic and Modi 6 Foman SJ, Haschke F, Zeigler EE, Nelson SE Body composition of reference children... mediating the protein catabolism of burns and sepsis Am J Physiol 1989; 257:323–331 19 Askhanazi J, Rosenbaum SH, Hyman AI, Silverberg PA, Milic-Emili J, Kinney JM Respiratory changes induced by the large glucose loads of total parenteral nutrition JAMA 1980; 243 : 144 4– 144 7 20 Jahoor F, Desai M, Herndon DN, Wolfe RR Dynamics of the protein metabolic response to burn injury Metabolism 1988; 37:330–337 21 Weinstein... deficiency in the newborn Pediatrics 1976; 58: 640 – 649 39 Van Aerde JE, Sauer PJ, Pencharz PB, Smith JM, Heim T, Swyer PR Metabolic consequences of increasing energy intake by adding lipid to parenteral nutrition in full-term infants Am J Clin Nutr 19 94; 59:659–662 40 Cleary TG, Pickering LK Mechanisms of intralipid effect on polymorphonuclear leukocytes J Clin Lab Immunol 1983; 11:21–26 41 Perriera GR, Fox... system during mechanical ventilation J Crit Care 1989; 4: 83–89 24 Hormann C, Benzer H, Baum M, Wicke K, Putensen C, Putz G, Hartlieb S The Prone Position for ARDS Anaesthesist 19 94; 43 (7) :45 4–62 25 Rossaint R, Falke KJ, Lopez F, Slama K, Pison U, Zapol WM Inhaled nitric oxide for the adult respiratory distress syndrome N Engl J Med 1993; 328:399 40 5 26 BigatelIo LM, Hurdord WE, Kacmarek RM, Roberts... Increases in the cytokines interleukin-6 (IL-6) and tumor necrosis factor, both of which are released by activated macrophages, also occur IL-6 levels are correlated with increased protein turnover, protein catabolism and the synthesis of acute phase proteins, and increased mortality Nutritional Support for the Pediatric Trauma Patient 137 (2,3) The release of IL-2, IL-8, gamma interferon, and many growth... Morris A, Spragg R The American-European consensus conference on ARDS Am J Respir Crit Care Med 19 94; 149 :818 1 34 Mantor et al 22 Pepe PE, Hudson LD, Carrico CJ Early application of positive end-expiratory pressure in patients at risk for adult respiratory distress syndrome N Engl J Med 19 84; 311:281 23 Levy P, Similowski T, Corbeil C A method for studying the static-pressure volume curves of the . 1998; 64( 5) :45 0 45 4. 45 . Davis JW, Parks SN, Kaups KL, Gladen HE, O’Donnell-Nicol S. Admission base deficit predicts transfusion requirements and risk of complications. 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