Trauma Pediatric - part 4 ppt

A prospective, randomized trial of Poly SFH- P in trauma patients demonstrated that the use of a red blood cell substitutefor the treatment of acute blood loss reduced the need for red b

by the rapid onset of fever, chills, rigors, chest or abdominal pain progressing torespiratory distress, and circulatory shock Hemoglobin is present in the plasmaand urine Renal failure may ensue Once recognized, the transfusion should imme-diately be discontinued Aggressive resuscitation should be instituted to support thecirculation and achieve a urine output of >60 mL/hr.

Transfusion-Transmitted Disease

Viral infection, the most feared complication, is the most common cause of latedeath from transfusion (Table 2) The first descriptions of transfusion-associatedHIV infection occurred in late 1982 Improved screening and detection hasreduced the current frequency of HIV infection to approximately to 1/250,000–1/2,000,000 units The most common serious viral infection is hepatitis C (HCV),estimated to occur in 1/30,000–1/150,000 units Eighty-five percent of posttransfu-sion HCV infections become chronic, 20% of infected patients develop cirrhosis,and 1% progress to hepatocellular carcinoma Hepatitis B (HBV) infection isestimated to occur in 1/30,000–1/250,000 units In 1975 new screening tests wereimplemented, reducing transfusion-transmitted HBV infection The HBV nowaccounts 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 platelettransfusion (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 at20–24C, which facilitate bacterial growth, while red blood cells are generally stored

at much lower temperatures The most common organism associated with RBCcontamination is Yersinia enterocolitica, while Staphylococcus aureus, Klebsiellapneumoniae, Serratia marcescens, and S epidermidis infections are most frequentlyobserved in platelet-associated infection (2)

Delayed hemolytic transfusion reaction 1:1000

Fatal hemolytic transfusion reaction 1:250,000–1:1,000,000

Source: Adapted from Ref 2.

Children are prone to hypothermia and may become profoundly hypothermic withthe infusion of cold fluids and blood products Hypothermia not only increasesmetabolic demand but also worsens coagulopathy Infants and small children should

be maintained in a warm environment and given warmed fluids and blood products.Rapid infusion can also produce severe electrolyte disturbances Hypocalcemia orhyperkalemia may arise after large- or rapid-volume infusion and, therefore, serumelectrolytes should be periodically evaluated

RED BLOOD CELL SUBSTITUTES

Due to the risks and costs of blood transfusion, efforts have been directed towardthe development of hemoglobin-based red cell substitutes Red cell substitutes donot transmit viral pathogens and have lower viscosities than blood while maintain-ing the same-oxygen carrying capacity of allogenic blood Free hemoglobin has anextremely 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 insynthetic hemoglobin with a P50 of natural hemoglobin, a plasma half-life up to

30 hours, and normal oncotic pressure (50) The absence of a red cell membraneeliminates the need for blood typing and crossmatching, as well as the immunologiceffects attributed to surface antigens or white blood 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, P50 of28–30 torr and t1/2 of one day A phase-II trial of Poly SFH-P demonstratedits 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 substitutefor 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 maintain carrying capacity in the setting of acute hemorrhagic shock, even with transfusionrequirements up to 20 units (52) Mortality (25%) was substantially lowered atcritical hemoglobin levels3 g/dL relative to historic controls (64.5%) who refusedred blood cells on religious grounds Remarkably 9/12 patients who sustainedlethal blood loss (RBC Hb 1 g/dL) survived with the administration of PolySFH-P and resultant total hemoglobin concentration (RBC Hb þ Poly SFH-P)7–10 g/dL

oxygen-Although these results are encouraging, the abrupt end of the diaspirin linked hemoglobin (DCLHb) trial suggests that the various red blood substitutesunder development are not homogenous Unlike the Poly SFH-P trials, a phase-IItrial of DCLHb administration was associated with a 72% increase in morbidity(Multiple Organ Dysfunction Score) and a threefold fold increase in mortality inthe treatment group (46%) relative to the control group (17%) (53) It is speculatedthat selected red blood substitutes (e.g., DCLHb) bind nitric oxide, which causesthe undesirable side effects of vasoconstriction and pulmonary hypertension Never-theless, efforts to develop a safe and effective red cell substitute continue given theadvantages of a readily available, oxygen-carrying, resuscitative fluid that eliminatesthe delay and risks of allogenic blood

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 hipfracture 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 TrialsGroup 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 transfusionrequirements 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 transfusionpolicies 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 ment Am J Surg 1995; 170(suppl):16S–20S

manage-14 Grupp-Phelan J, Tanz RR How rational is the crossmatching of blood in a pediatricemergency department? Arch Pediatr Adolesc Med 1996:150(11):1140–1144

15 Wallace EL, Churchill WH, Surgenor DM, Cho GS, McGurk S Collection and sion of blood and blood components in the United States, 1994 [see comments] Transfu-sion 1998; 38(7):625–636

transfu-16 Orliaguet GA, Meyer PG, Blanot S, Jarreau MM, Charron B, Buisson C, Carli PA dictive factors of outcome in severely traumatized children Anesth Analg 1998;87(3):537–542

Pre-17 Stylianos S Evidence-based guidelines for resource utilization in children with isolatedspleen 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 withtraumatic 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 oftraumatic splenic injuries J Trauma 1992; 33:340–348

20 Avanoglu A, Ulman I, Ergun O, Ozcan C, Demircan M, Ozok G, Erdener A Bloodtransfusion requirements in children with blunt spleen and liver injuries Eur J PediatrSurg 1998; 8(6):322–325.

21 Patrick DA, Bensard DD, Moore EE, Karrer FM Nonoperative management of solidorgan 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 sion requirements and length of hospitalization for laparotomy versus observation

geo-29 Greenberg A A physiologic basis for red blood cell transfusion decisions Am J Surg1995; 170:44s–48s

30 Carson JL, Noveck H, Berlin JA, Gould SA Mortality and morbidity in patients withlow 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 patientswho 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 toacute, 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 forpostinjury 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 ofpostinjury multiple organ failure Arch Surg 1994; 129(1):39–45

37 Siliman C, Paterson A, Dickey W The association of biologically active lipids with thedevelopment of transfusion related acute lung injury: a retrospective study Transfusion1997; 37:719–726

38 Zallen G, Offner PJ, et al Age of transfused blood is an independent risk factor for injury multiple organ failure Am J Surg 1999; 178(6):570–572

post-39 Sauaia A, Moore F, Moore E, Moser K, Brennan R, Read R, Pons P Epidemiology oftrauma deaths: a reassessment J Trauma 1995; 38:185–193

40 Advanced trauma life support student manual Sixth ed Chicago: American College ofSurgeons, 1997

41 Kivioja A, Myllynen P, Rokkanen P Survival after massive transfusions exceeding fourblood volumes in patients with blunt injuries Am Surg 1991; 57(6):398–401

42 Wudel JH, Morris JA Jr, Yates K, Wilson A, Bass SM Massive transfusion: outcome inblunt trauma patients J Trauma 1991; 31(1):1–7.

43 Ciavarella D, Reed F, Counts R Clotting factor levels and the risk of diffuse cular bleeding in the massively transfused patient Br J Haematol 1987; 67:365–368

microvas-44 Cathey KL, Brady WJ Jr, Butler K, Blow O, Cephas GA, Young JS Blunt splenictrauma: 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 deficitpredicts 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 ofacidosis after traumatic shock J Trauma 1998; 44(1):114–118

47 Mikulaschek A, Henry SM, Donovan R, Scalea TM Serum lactate is not predicted byanion 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 silverday: detection and correction of occult hypoperfusion within 24 hours improves outcomefrom major trauma J Trauma 1999; 47(5):964–969

49 Dabrowski G, Steinberg S, Ferrara J, Flint L A critical assessment of endpoints of shockresuscitation Surg Clinics N Amer 2000; 80:825–844

50 Creteur J, Sibbald W, Vincent J Hemoglobin solutions-not just red blood cell tutes Crit Care Med 2000; 28:3025–3034

substi-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 substituteafter 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 hemoglobinwhen 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 aspirin cross-linked hemoglobin (DCHLb) in the treatment of severe traumatic hemor-rhagic shock: a randomized controlled efficacy trial JAMA 1999; 282:1857–1864

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 frequentlyneed intensive care The criteria for intensive care unit (ICU) admission will varyfrom institution to institution, but some commonality can be suggested Those withmulti-system trauma or hemodynamic instability will benefit from intensive care.Others with a Pediatric Trauma Score of seven or less; isolated but significant headtrauma and an altered mental status; liver, or splenic lacerations of grade III orgreater; significant pancreatic injuries, multiple orthopedic injuries; and injuries, thatmay not be readily cared for on the ward because of local institutional factors maybest be cared for initially in the ICU

MONITORING

Basic monitoring is required for all pediatric trauma patients in the ICU This includesmeasurement of vital signs: determination of heart rate and respiratory rate, continu-ous electrocardiography, noninvasive blood pressure determination, and temperaturemeasurement According to recent pediatric literature, pulse oximetry should be con-sidered a fifth vital sign, and capnography should also be included for intubatedpatients (1)

Cardiovascular Monitoring

Usually, noninvasive blood pressure monitoring is utilized in the pediatric population.Noninvasive monitoring in the child may be quite accurate if the proper cuff size isutilized The American Heart Association has set guidelines for proper cuff fit Theyrecommend 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 mustalso be aware of the age-related norms for blood pressures (Table 1)

123

In most modern pediatric intensive care units (PICU), automated arterial bloodpressure 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 framemay be missed

Access for invasive blood pressure monitoring may be accomplished in allchildren This is performed either through percutaneous arterial cannulation or byarterial 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 quickestaccess 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 invasivemonitoring include limb ischemia (femoral artery), cannula compression, and kink-ing or clot formation It is therefore wise to correlate invasive with noninvasivemonitoring in the critically ill trauma patient Benefits of invasive monitoring includecontinuous direct waveform display of the arterial blood pressure and access forarterial blood sampling for blood gases

Electrocardiography (ECG) monitors the heart rate and rhythm of cardiacconduction Rhythm disturbances associated with trauma may include atrial tachycar-dia, ventricular tachycardia (subarachnoid hemorrhage), persistent sinus bradycardia(cerebral hypoxia/arrest at the scene/airway obstruction/tracheal disruption/increasedintracranial pressure secondary to head trauma/hypothermia due to cold exposure), andsinus tachycardia (hypovolemic shock) Also, many teenage trauma patients have takendrugs that alter the ECG: tricyclic antidepressants, cocaine, opiates, and amphetamines

Oxygen Saturation

Pulse oximetry is currently being advocated as an accurate, simple, and noninvasivemethod 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 nmwavelength and transmits red light at the 660 nm wavelength The pulse oximetryprobe has two light-emitting diodes that pass light at these wavelengths through theperfused tissue to a photodetector on the other side The photodiode then comparesthe amount of infrared, red, and ambient light that reaches it and calculates the oxygensaturation (SaO2) (2) A small sensor (probe) is placed on the finger, toe, earlobe, fore-head, or any convenient place Most devices demonstrate the SaO2as well as pulserate continuously

The pulse oximeter has been demonstrated to reflect moderate hypoxia(SaO2<89%) before an increase in ventilatory drive is demonstrated (1) This, aswell as its noninvasive, continuous monitoring of the SaO , has made it a critical

Table 1 Abnormal Vital Signs

component of PICU monitoring in the pediatric trauma patient It provides a uous reflection of hemoglobin saturation and provides the trauma surgeon withknowledge that sufficient oxygen is being delivered to the injured tissues.

contin-A disadvantage of pulse oximetry has been decreased accuracy at low saturations(defined as SaO2<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 PaO2 should be done at lower saturations(4) If the oxygen saturation is below 70% on multiple pulse oximeter determinationsthen the arterial blood should be sampled because the true oxygen saturation is usuallyunderestimated by most oximeters Other disadvantages of some pulse oximeter modelsinclude motion artifact, placement of sensor below blood pressure cuff, and poor tissueperfusion of a distal extremity (3,5)

When elevations of carboxyhemoglobin (COHb) are seen in the setting ofcarbon monooxide (CO) poisoning, the pulse oximetry reading remains in the nor-mal range, despite markedly reduced actual oxygenated hemoglobin (O2Hb) 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 cannotdifferentiate between the COHb and O2Hb at the red wavelength, and the combinedvalue is applied to the calculation of the oxygen saturation As a result, the pulse oxi-meter overestimates the actual oxyhemoglobin saturation (SaO2) so that it is unreli-able in patients with CO poisoning (6)

Ventilation

End tidal carbon dioxide (EtCO2) monitoring, known as capnometry, is a noninvasivemethod for measuring the PaCO2in expired gas Similar to pulse oximetry-measuringdevices, the exhaled gas passing through a sampling chamber, which has an infraredlight source on one side and a photodetector on the other, measures the carbon dioxide(CO2) CO2absorbs light at the infrared wavelength (940 nm) The CO2present in theexpired gas may be calculated from the amount of infrared light that reaches the photo-detector EtCO2is 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 fromthe PICU for early detection of endotracheal tube dislodgment (7) It is currentlyrecommended by several sources, including the American Academy of Pediatrics, thatall children who are intubated and being transported have an EtCO2(8)

MANAGEMENT OF PICU TRANSFUSIONS

In the unstable trauma patient, hemoglobin and hematocrit should be measured everyfour hours and one hour after every transfusion until vital signs stabilize and urineoutput is adequate To restore blood volume and O2-carrying capacity to a pediatrictrauma patient that has lost a large volume of blood, it is essential to transfuse oneunit 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 acuteblood loss For severe hemorrhage, plasma substitutes are required when packedred blood cells are transfused to compensate for dilution of coagulation proteins.Massive transfusions that involve replacing an amount of blood equal to thepatient’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

from decreased 2,3 disphosglycerate content, pulmonary microembolism, decreasedcore 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 ofthe side effects of massive transfusion should be initiated For every blood volumelost, it is often necessary to administer fresh frozen plasma (20 mL/kg), sodiumbicarbonate (1–3 meq/kg if pH <7.3), calcium chloride 10% (10–20 mg/kg if ionizedcalcium <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 largeamounts of blood and crystalloid are transfused to decrease the incidence ofhypothermia In addition, most PICU beds have thermal blankets and externalwarming sources to minimize heat loss

of the patient, and a small amount of jejunal feeds can be continued to maintaingut integrity

COMMONLY USED MEDICATIONS

Table 2 shows the commonly used medications

ACUTE RESPIRATORY FAILURE

Acute lung injury leading to respiratory insufficiency is a frequent complicationfound in the trauma patient Its etiology is varied and includes atelectasis, aspiration,infection, the acute respiratory distress syndrome (ARDS) as well as others Of theseARDS has the most potential for significant morbidity and mortality Therapy may

be as simple as supplying oxygen and pulmonary physiotherapy or as complicated asproviding extracorporeal life support (ECLS) The pulmonary injury precedingARDS 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

In an early description Asbaugh et al termed the clinical picture of progressive 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

hypox-to four days of the original inciting event This clinical entity describes a final commonpathway with definable lung pathology from a wide spectrum of significant injuries.Early beliefs were that ARDS results in a disseminated and homogeneous pulmonaryprocess, as suggested by conventional chest X rays (CXR) (Fig 1) It has since beenshown 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 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 thusreceive an inordinate amount of the minute ventilation This is because gases all flowvia the path of least resistance As the syndrome progresses, so does the opacification

depen-on CXR Gattidepen-onni et al showed that as little as depen-one third of the lung is actually lated and called this condition ‘‘baby lung’’ (16) Mechanical ventilation in this clinicalsetting leads to regional over-distension of nondependent lung, reduces capillaryperfusion, increases pulmonary dead space, and exacerbates the already presentventilation perfusion mismatch

venti-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 tovolutrauma Webb and Tierny have also shown that regional over-distension ofalveoli with mechanical ventilation leads to injury (19) This is most closely associatedwith high peak inspiratory pressures, greater than 40 cm H2O, and repeated openingand closing of collapsed alveoli This alveolar over-distension leads to stress failure ofalveolar capillary membranes, which leads to increased microvascular permeabilityand edema Although the evidence is circumstantial, it is felt that this volutrauma

Table 2 Commonly Used Medications

on top of the existing ARDS significantly complicates the syndrome A recentmulticenter study showed a significant difference in mortality and ventilator dayswhen lung protective strategies (tidal volume <6 cc/kg and plateau pressures <30 cm

H2O) were used (20)

Etiology

Two groups of patients with ARDS are differentiated by the etiology of their pulmonarydisease A primary lung insult such as pneumonia may lead to a reduction in lungbut not chest wall compliance Here, consolidation is the main pathology These patientsare less responsive to lung recruitment measures such as positive end expiratory pres-sure (PEEP) and prone positioning These patients are more susceptible to regional

Figure 1 Chest X ray CXR showing diffuse bilateral pulmonary infiltrates

Figure 2 CT scan showing the inhomogeneity of ARDS

hyperinflation so that peak pressures must be watched very closely Indirect causes ofARDS, such as trauma and sepsis, lead to secondary lung injury These patients have

a reduction in both their lung and chest wall compliance The major pathologic findingsare interstitial edema and alveolar collapse These patients are usually more responsive

to PEEP and prone positioning If not careful, however, these measures may put them atrisk for hemodynamic instability

Diagnosis

Making the diagnosis of ARDS is not usually difficult if one considers it in thosepatients who have suffered significant trauma or develop sepsis or pneumoniafollowing trauma Physicians do not universally agree on all of the necessary findingsbut there are some commonalities The American European Consensus Conferenceattempted to simplify this and includes:

1 an acute onset,

2 a PaO2/ fraction of expired oxygen (FiO2) <300,

3 bilateral pulmonary infiltrates on CXR,

4 pulmonary capillary wedge pressure (PCWP) <18 mmHg or no clinicalevidence of left atrial hypertension (21)

Clinical Course

There is a series of phases in the course of ARDS The initial phase is characterized

by tachypnea and dyspnea with hypocarbia from hyperventilation The partial sure of oxygen (pO2) is usually normal Microscopically there is neutrophil seques-tration and platelet aggregation within the pulmonary vasculature Within 12 to

pres-24 hours progressive hypoxemia and worsening respiratory symptoms develop Achest X ray will show bilateral infiltrates There is worsening endothelial injury andincreased permeability with leaky capillaries Neutrophils marginate to the intersti-tium, where there is already an abnormally high protein content Damage to the alveo-lar epithelial integrity continues and fluid floods the alveolar space There is continuedfibrin and platelet aggregation and worsening microvascular occlusion At this pointthe clinical entity is still reversible if the initiating factors are discovered, treated, andeliminated The next phase occurs if there are repeated or sustained insults This takesplace over the next several days Respiratory failure continues with an increase in theventilation perfusion mismatch and intrapulmonary shunting Hypoxemia is now moresevere and less responsive to increases in FiO2 This necessitates increased ventilationsupport in the face of worsening pulmonary compliance Continued infiltration withneutrophils and now mononuclear cells, lymphocytes, and fibroblasts worsen the inter-stitial milieu Surfactant destruction occurs as well as further alveolar collapse Macro-phages release monokines, which activate other inflammatory cells, thus worsening theentire picture The final phase is more chronic in nature There is a worsening pulmo-nary fibrosis, and with recurrent pneumonias, lung compliance and gas exchange fail toimprove The usual endpoint is significant morbidity if not mortality

Management

There is no specific therapy for ARDS Most measures are directed towards support ofthe patient’s respiratory status as well as the treatment of any underlying problems,such as pneumonia and sepsis In the past most respiratory therapies were directed

toward normalization of blood gases Today, most critical care physicians attempt toachieve adequate gas exchange and prevent further lung injury, which may assist withlung healing Mechanical ventilation is probably the most important supportive ther-apy in treating patients with ARDS Criteria for its utilization include hypoxemia unre-sponsive to supplemental O2and the need to recruit atelectatic alveoli On occasioncontinuous positive airway pressure (CPAP) will be adequate; however, there areseveral limitations with this type of assistance It requires a very tight-fitting maskand a very cooperative patient If the amount of pressure required exceeds 10 cm

H2O, then the success rate is not high

it may be detrimental It increases mean airway pressure and intrathoracic pressureand decreases venous return, which may lead to a decrease in cardiac output Itmay also impact intracranial pressure as well as hepatic and renal perfusion Thesecomplications are rare if PEEP is kept below 10 cm H2O If higher levels of PEEPare necessary then the use of a Swan–Ganz catheter or oximetric pulmonary arterycatheter should be considered The best level of PEEP can be calculated from staticpressure volume curves (Fig 3) (23) Looking at the lower and higher inflection pointsfacilitates setting both the best PEEP and peak inspiratory pressures This limits over-distension on inspiration and alveolar collapse on expiration, which may prevent thealveolar stretch injury associated with repeated opening and closing of alveoli withinflation and deflation

Figure 3 An inflation pressure versus volume curve showing the upper (peak inspiratorypressure point) and lower (ideal PEEP) inflection points

In the past, average volumes of 10–15 cc/kg were used in attempts to adequatelyventilate patients More recently evidence suggests that this is more than is reallynecessary (20) Six to ten cc/kg may be adequate Much of the consolidated lung willnot ventilate, so the portions of lung that can be ventilated are actually overstretchedand damaged We attempt to keep our peak inspiratory pressures <40 In sometrauma patients (indirect lung injury) it is the chest wall that may be noncompliant

If this is the case then higher pressures may be better tolerated and necessary The ity to maintain gas exchange is often difficult while staying within airway pressure andtidal volume guidelines The question to ask is whether to change the guidelines or gasexchange expectations Normocapnia may not be possible and it may be necessary toaccept higher levels of partial pressure exected by CO2in mmHg (pCO2) This idea ofpermissive hypercapnia is not new Sudden elevations in pCO2, however, are also det-rimental and result in cardiac depression, increases in intracranial pressure, and mayworsen intracellular acidosis An absolute endpoint is uncertain but a pH as low as 7.2seems to be well tolerated This often requires heavy sedation and even paralysis

abil-Ventilation Modes

The two common modes of ventilation are based on airway pressure and tidal volume,respectively Each has advantages and disadvantages Pressure control allows for rapidvariable flow and provides peak inspiratory pressure throughout the entirety of theinspiratory time Volume control allows for a constant tidal volume and minute ven-tilation regardless of the changes in pulmonary compliance There are some newmodes that allow for a combination of both and also allow for changes breath tobreath Pressure-regulated volume control is one that sets a target tidal volume andinspiratory time and allows the ventilator to adjust the flow rate Waveform and peakinspiratory pressure vary from breath to breath as pulmonary compliance, resistance,and patient cooperation change This is our preferred method of ventilation in themore critical patients with ARDS

High-frequency ventilation allows for continual high airway pressures, verylow tidal volumes, and very fast rates Gas exchange occurs via Brownian motion.These modes are helpful as trials when other modes fail, as well as in cases of persis-tent pneumothoraces or chronic bronchopleural fistulas Their efficacy in the pedia-tric patient with ARDS has not been shown

Prone Positioning

Prone positioning was tried first by Brian 25 years ago and seems to be quite popular

in Europe (24) The idea is to reduce ventilation perfusion inequality by redistributingblood flow from unventilated areas of lung to those with a more normal ventilation-perfusion ratio (V/Q) match It may also recruit previously atelectatic lung areas Thepatient is rotated from the supine to the prone position on a schedule whose timeinterval varies from institution to institution from every hour to once a day Patientrepositioning is labor-intensive and this effort must be monitored closely Pressurepoints must be protected and the most common complication is dislodgement of linesand endotracheal tubes, which can be a serious problem if the patient has just beenplaced in the prone position

Nitric Oxide

Nitric oxide (NO), initially named endothelium-derived relaxing factor, has beenshown to dilate pulmonary arteries and has been used extensively in treating pulmo-nary hypertension Its use in ARDS is based on two principles First is the treatment

of pulmonary hypertension, and the second is to direct blood flow towards ventilatedalveoli, thus decreasing the ventilation perfusion mismatch Initially, studies byRoissant et al showed an improvement in oxygenation, reduced pulmonary arterypressure, and reduced shunt fraction (25) It appears though the ideal dose range isbetween 1 and 10 ppm (26) Its use is well tolerated and the adverse reactions arefew and limited Papazian demonstrated a beneficial effect of inhaled NO when com-bined with prone positioning (27) Each modality increased the PaO2/FiO2, but thehighest change was found when the two were combined

Partial Liquid Ventilation

Perfluorocarbons have been investigated for years due to their significant affinity foroxygen Recently, they have been used clinically in treating ARDS in both Phase 2and 3 trials Perflubron is one such chemical that has low viscosity, low surfacetension, high density, and a high oxygen solubility and CO2-carrying ability Partialliquid ventilation is a technique where a volume of chemical equal to the functionalresidual capacity of a patient is used in combination with conventional ventilation.The perfluorocarbon’s high density assists its ability to collect in the dependentportions of the lung, which are poorly ventilated With this characteristic it has beenshown to displace alveolar transudate within the dependent consolidated lung, thusrecruiting alveoli Exudate is then lavaged out of the lung, clearing cellular debrisand mucous plugs The most recent multicenter trial looking at its use in ARDS inadults has closed and the data are not yet available

Steroids

Corticosteroids have been shown to modulate a number of mediators, which pate in the inflammatory cascade that is a component of ARDS Most agree that theiruse in the early phases of ARDS has no benefit We believe, however, that their efficacy

partici-in the later fibroproliferative phase of ARDS has still not been answered Meduri

et al has shown positive effects of their use in those who have failed to respond toconventional ventilation after seven days (28)

Extracorporeal Membrane Oxygenation (ECMO)

When all of the above interventional modalities fail to show improvement in patientswith ARDS, their survival has most likely been reduced to 20% to 30% A trial ofECMO is warranted in this instance and some would argue that it should be consid-ered sooner rather that later The survival as reported by the Extracorporeal LifeSupport Organization is between 50% and 60% in, pediatric patients with respiratoryfailure (29) In short, ECMO supports the patient’s pulmonary function (veno-venous) or pulmonary and cardiac function (venoarterial) in hopes that lung restand healing can take place It is not in the scope of this chapter to explain in detailthe intricacies of ECMO, which can be found in one of the textbooks written on thissubject (30)

1 Mower WR, Sachs C, Nicklin EL, Myers G, Kearin KT, Baraff LJ Pulse oximetry as afifth pediatric vital sign Pediatrics 1997; 99:681–686

2 Stafford MA Cardiovascular physiology and care In: O’Neill JA, Rowe ML, Grosfeld

EW, Fonkalsrud EW, Coran AG, eds Pediatric Surgery Vol 1 St Louis: Mosby-YearBook Inc., 1998

3 American College of Surgeons, Advanced Trauma Life Support for Physicians, 6th ed 1997

4 Carter BC, Carlin JB, Tibballs J, Mead H, Hochmann M, Osborne A Accuracy of twopulse oximeters at low arterial hemoglobin-oxygen saturation Crit Care Med 1998;26:1128–1133

5 Tremper KK Pulse Oximetry’s final frontier Crit Care Med 2000; 28:1684–1685

6 Bozeman WP, Myers RA, Barish RA Confirmation of the pulse oximetry gap in carbonmonoxide poisoning Ann Emerg Med 1997; 30:608–611

7 Bhende MS, Karr VA, Wilsie DC, Orr RA Evaluation of a portable infrared end-tidal bon dioxide monitor during pediatric interhospital transport Pediatrics 1995; 95:875–878

car-8 Task Force on Interhospital Transport, American Academy of Pediatrics Guidelines forair and ground transportation of neonatal and pediatric patients Elk Grove Village, IL:American Academy of Pediatrics, 1993

9 Hutchinson RJ Surgical implications of hematologic disease In: O’Neill JA, Rowe ML,Grosfeld EW, Fonkalsrud EW, Coran AG, eds Pediatric Surgery Vol 1 St Louis:Mosby-Year Book Inc., 1998

10 Moore E, Jones T Benefits of immediate jejunostomy feeding after major abdominaltrauma: A prospective, randomized study J Trauma 1986; 26:874–880

11 Chellis MJ, Sanders SV, Webster H, Dean JM, Jackson D Early enteral feeding in thepediatric intensive care unit J Parenter Enteral Nutr 1996; 20:71–73

12 Panadero E, Lopez-Herce J, Caro L, Sanchez A, Cueto E, Bustinza A, Moral R, Carrillo A,Sancho L Transpyloric enteral feeding in critically III children J Pediatr GastroenterolNutr 1998; 26:43–48

13 Ashbaugh DG, Bigelow DB, Petty TL, Levine BE Adult respiratory distress Lancet1967; 2:319–323

14 Pelosi P, Crotti S, Brazzi L Computed tomography in adult respiratory distress syndrome:what it has taught us? Eur Respir J 1996; 9:1055–1062

15 Gattinoni L, Pesenti A, Torresin A, Baglioni S, Rivolta M, Rossi F, Scarani F, Marcolin R,Cappelletti G Adult respiratory distress syndrome profiles by computed tomography

J Thorac Imag 1986; 1:25–30

16 Gattiononi L, Pesenti A, Bombino M, Baglioni S, Rivolta M, Rossi F, Rossi G,Fumangalli R, Marcolin R, Mascheroni D Relationships between lung computed tomo-graphic density, gas exchange and PEEP in acute respiratory failure Anesthesiology1988; 69:824–832

17 Dreyfuss D, Saumon G Ventilator-induced lung injury-Lessons from experimentalstudies Am J Respir Crit Care Med 1998; 157:294–323

18 Parker JC, Hernandez LA, Peevy KJ Mechanisms of ventilator-induced lung injury CritCare Med 1993; 21:131–143

19 Webb HH, Tierney DF Experimental pulmonary edema due to intermittent positivepressure ventilation with high inflation pressures: Protection by positive end-expiratorypressures Am Rev Respir Dis 1974; 110:556–565

20 The Acute Respiratory Distress Syndrome Network Ventilation with lower tidal volumes

as compared with conventional tidal volumes for acute lung injury and the acute tory distress syndrome N Engl J Med 2000; 342(18):1301–1308

respira-21 Bernard GR, Artigas A, Bringham KL, Carlet J, Falke K, Hudson L, Lamy M, LeGall

JR, Morris A, Spragg R The American-European consensus conference on ARDS Am JRespir Crit Care Med 1994; 149:818

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 1984; 311:281

23 Levy P, Similowski T, Corbeil C A method for studying the static-pressure volumecurves of the respiratory 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 PronePosition for ARDS Anaesthesist 1994; 43(7):454–62

25 Rossaint R, Falke KJ, Lopez F, Slama K, Pison U, Zapol WM Inhaled nitric oxide forthe adult respiratory distress syndrome N Engl J Med 1993; 328:399–405

26 BigatelIo LM, Hurdord WE, Kacmarek RM, Roberts JD, Zapol WM Prolonged tion of low concentrations of nitric oxide in patients with severe adult respiratory distresssyndrome: Effects on pulmonary hemodynamics and oxygenation Anesthesiology 1994;80:761–770

inhila-27 Papazian L, Bregeon F, Gaillat F, Thirion X, Gainnier M, Gregoire R, Saux P, Gouin F,Jammes Y, Auffray J Respective and combined effects of prone position and inhalednitric oxide in patients with acute respiratory distress syndrome Am J Respir Crit CareMed 1998; 157:580–585

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29 Extracorporeal Life Support Organization, International Summary, January 2002

30 Zwischenberger J, Bartlett R Extracorporeal Cardiopulmonary Support in Critical Care.Extracorporeal Life Support Organization, 1995

Nutritional Support for the Pediatric

Trauma Patient

Tom Jaksic and Biren P Modi

Department of Surgery, Children’s Hospital Boston, Boston, Massachusetts, U.S.A

INTRODUCTION

Trauma is accompanied by a set of metabolic aberrations that are profound butpredictable Over 65 years ago Sir David Cuthbertson described the fundamentalaspects of this metabolic response to injury in adults (1) Although the metabolicsequelae of trauma in children qualitatively resemble those of adults, marked quan-titative differences exist

An understanding of the metabolic events that accompany trauma is the firststep in nutritional support therapy An individualized determination of nutrientrequirements must be made and an appropriate route of delivery selected Nutri-tional support of the injured child should be instituted promptly and be designed

to limit the deleterious consequences of structural protein loss while facilitatingwound healing and the immune response

THE METABOLIC RESPONSE TO TRAUMA

During the period immediately following severe injury, aggressive fluid, electrolyte,and blood replacement is often required for survival This period is termed the ‘‘ebbphase’’ of the metabolic response to trauma and is characterized by a decrease incardiac output and a reduction in metabolic rate Once the patient has beenadequately resuscitated, the ‘‘flow phase’’ of injury is entered The metabolic responseduring the flow phase is summarized in Figure 1 and consists of an increase in netmuscle protein breakdown and the enhanced movement of amino acids throughthe circulation This provides the amino acids needed for the rapid synthesis ofproteins for the inflammatory response and tissue repair Those amino acids not usedfor protein synthesis are channeled through the liver to create glucose from theircarbon skeletons by gluconeogenesis Glucose requirements are effectively met by thismechanism In a coupled hepatic process the amino portions of the amino acids arecleaved and detoxified by the urea cycle There is a marked rise in the circulation

of hepatically derived acute-phase proteins (i.e., C-reactive protein, fibrinogen,

135

haptoglobin, alpha-1 antitrypsin, and alpha-1 acid glycoprotein) and a concomitantdecrease in hepatically derived nutrient transport proteins such as albumin and retinol-binding protein.

The metabolic response to major trauma is associated with a consistent monal and cytokine profile regardless of the specific pattern of injury Traumatizedpatients demonstrate a very transient decrease in insulin concentrations followed by

hor-a persistent elevhor-ation Despite higher insulin levels, which, in theory, should promoteanabolism, accelerated net protein breakdown continues This may be explained, inpart, by the elevated concentrations of the catabolic hormones (glucagon, catechola-mines, and cortisol) found during the period of acute injury Increases in the cytokinesinterleukin-6 (IL-6) and tumor necrosis factor, both of which are released by activatedmacrophages, also occur IL-6 levels are correlated with increased protein turnover,protein catabolism and the synthesis of acute phase proteins, and increased mortality

Figure 1 Substrate metabolism in patients following major trauma

(2,3) The release of IL-2, IL-8, gamma interferon, and many growth factors is alsoknown to augment the immunologic and hormonal response to injury.

The catabolism of skeletal muscle to generate the amino acids needed forwound healing and to produce glucose for energy production is an excellent short-term adaptation in children However, it cannot be sustained for long periods due

to the lack of body protein stores The progressive loss of skeletal muscle proteinleads to respiratory compromise, cardiac dysfunction, increased susceptibility toinfection and, ultimately, increased mortality (4) Hence minimizing the protein lossassociated with trauma is of major clinical importance

NUTRITIONAL NEEDS

Once a decision has been made to commence nutritional support in the injured child

an accurate individualized determination of nutrient requirements is needed Thisassessment should include estimates of protein, total energy, carbohydrate, lipid,electrolyte, and micronutrient needs

Protein Requirements

Amino acids are the key building blocks required for growth and tissue repair Thevast majority of amino acids reside in proteins, with the remainder being in the freeamino acid pool Proteins themselves are not static as they are continually degradedand synthesized in a process termed ‘‘protein turnover.’’ The reutilization of aminoacids released from protein breakdown is extensive Protein turnover contributes to

Table 1 The Body Composition of Neonates, Children, and Non-obese Adults as a Percent

of Total Body Weight

protein synthesis more than twice the amount of amino acids derived from proteinintake In traumatized children, such as those with severe burn injury, or in ill child-ren with cardiorespiratory failure requiring extracorporeal membrane oxygenation(ECMO), protein turnover is twice that of normal children (9) Generally, in severeillness amino acids are redistributed away from skeletal muscle to injured tissues, cellsinvolved in the inflammatory response, and the liver Acutely needed enzymes, serumproteins, and glucose (by way of gluconeogenesis) are thus synthesized A salientadvantage of high-protein turnover is that it allows for the immediate synthesis ofproteins needed for the inflammatory response and tissue repair The process doesrequire energy, hence either an increase in resting energy expenditure or a redistribu-tion of energy normally used for growth is required Although critically ill childrendemonstrate both an increase in whole-body protein degradation and whole-body synthesis, it is the former that predominates Thus, these patients manifest netnegative protein balance, which clinically may be noted by weight loss and skeletalmuscle wasting.

The catabolism of skeletal muscle to generate glucose is necessary as glucose isthe preferred energy source for the brain, red blood cells, and renal medulla Illnessenhances gluconeogenesis in adults, children, and neonates On a per kilogram bodyweight basis, gluconeogenesis seems to be particularly elevated in very small children(presumably because of their relatively large brain-to-body-weight ratio) (10) Inter-estingly, the provision of dietary glucose is relatively ineffective in quelling endoge-nous glucose production in the stressed state (11)

Without elimination of the inciting stress for catabolism, the progressive loss ofdiaphragmatic and intercostal muscle as well as cardiac muscle may cause cardiopul-monary failure Fortunately, amino acid supplementation does improve proteinbalance The mechanism for this change in ill patients appears to be an increase inprotein synthesis with little change in protein degradation (12)

The amount of protein required to optimally enhance protein accretion ishigher in unwell than in healthy children Infants demonstrate 25% higher proteindegradation after surgery, 100% increase in urinary nitrogen excretion with bacterialsepsis, and 100% increase in protein breakdown if they are ill enough to requireECMO (9) The provision of dietary protein sufficient to optimize protein synthesis,facilitate wound healing and the inflammatory response, as well as to preserve ske-letal muscle protein mass, is the single most important nutritional intervention

in injured children The quantity of protein (or amino acid solution) administered

in critical illness should be 2–3 g/kg/day for infants up to the age of one year and1.5 g/kg/day for older children Certain severely stressed states (i.e., severe burninjury) may require additional protein supplementation (2.0–2.5 g/kg/day) Exces-sive protein administration should be avoided because toxicity, particularly inpatients with marginal renal and hepatic function, is possible Even relatively wellneonates fed protein allotments of 6 g/kg/day have developed azotemia, pyrexia,

a higher incidence of strabismus, and lower IQ (13,14)

Two important issues regarding the protein metabolism of critically ill childrenremain to be elucidated At present there is no specific recommendation possibleregarding any special amino acid composition that may be of specific benefit toseverely injured children (15) The use of enteral glutamine supplementation (withand without other ‘‘immune enhancing’’ nutrients such as arginine, omega-3 fattyacids, and nucleotides) has been used in an effort to limit septic complications asso-ciated with trauma However, this approach remains investigational and larger-scalestudies are needed (16,17) Similarly, quelling the extreme protein catabolism found

in children with major injuries utilizing hormonal modulation, particularly insulinadministration, is also being actively investigated (18).

Energy Requirements

A careful appraisal of energy requirements in critically ill children is required asboth too much and too little energy may have potentially deleterious consequences.Inadequate caloric intake will result in poor protein retention, especially if proteinadministration is marginal In contradistinction, the provision of excess glucosecalories in critically ill patients results in increased carbon dioxide (CO2) productionrates (hence exacerbating ventilatory failure) and a possible paradoxical increase innet protein degradation (15,19)

The severity and duration of the illness or injury governs the energy needs ofcritically ill patients Recent data suggest that energy needs are far less than previouslythought for most types of trauma The resting energy expenditure in the flow phase ofinjury is increased by 50% in children with severe burns However, it returns tonormal during convalescence (20) If illness increases work of breathing, such as inneonates with bronchopulmonary dysplasia, a persistent elevation in energy expendi-ture up to 25% over expected values is evident (21) Newborns undergoing majoroperations have only a transient 20% increase in energy expenditure that returns tobaseline levels within 12 hours and remains at baseline unless major complicationsdevelop (22,23) Adequate anesthetic and analgesic management also plays a signifi-cant role in muting the stress response, as evidenced by neonates undergoing patentductus arteriosus (PDA) ligation who do not manifest any discernable increase inresting energy expenditure postoperatively with fentanyl anesthesia and subsequentintravenous analgesia (24) Adult intensive care unit patients also do not have an ele-vation of resting energy expenditure over expected values (25) Head injury produces

a variable elevation in resting energy expenditure, presumably due to a marked rise incirculating catecholamines Again patients who are sedated, in phenobarbitol coma,

or have been given neuromuscular relaxants manifest no such elevation in energyexpenditure (26)

Total energy requirements include resting energy expenditure, energy neededfor physical activity, and diet-induced thermogenesis Resting energy expenditureitself includes the caloric requirement for growth Although critically ill childrenhave increased protein turnover, their growth is often halted during extreme physio-logic stress Additionally, levels of physical activity are typically low following severeinjury The mean energy expenditures of critically ill neonates on ECMO were found

to be nearly identical to age- and diet-matched, non-stressed controls (27) Thecritically ill cohort did, however, have a greater variability in energy expenditure(27) Further, a surfeit of calories in critically ill neonates does not necessarily result

in improved protein accretion (15) Thus, for practical purposes the recommendeddietary caloric intake for healthy children affords a reasonable starting point for cri-tically injured patients (28) Table 2 outlines safe caloric provisions for injured chil-dren at various ages Enterally fed traumatized children, as a rule, require a further10% increment in calories due to obligate malabsorption In any injured child withprotracted illness the actual measurement of resting energy expenditure, by portableindirect calorimetry, is advised due to the high-interindividual variability in energyexpenditure Predictive equations used in conjunction with stress factors to accountfor degree of illness have been shown to be inaccurate in determining individualenergy expenditures in intensive care unit patients and are not recommended (25)