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G Gut Mucosal Atrophy functions, including digestion and nutrient absorption;itservesasabarrierandhasimmuno- IndraneilMukherjee1andKhanjanH. logical properties as well. It is also adaptable to Nagarsheth2 many situations like starvation, metabolic dis- 1TheSoutheasternCenterforDigestiveDisorders eases, and intestinal surgery. These adaptations &PancreaticCancer,AdvancedMinimally canbeeitherproliferativeoratrophic. Invasive&RoboticSurgery,FloridaHospital Enterocytes are the dominant cells that form Tampa,Tampa,FL,USA theintestinalbrushborder.Themicrovilliattheir 2RAdamsCowleyShockTraumaCenter, luminal end are the functional component UniversityofMarylandSchoolofMedicine, containing the enzymes and the glycocalyx coat Baltimore,MD,USA thatactsasaphysicalbarrier.Themucosalsurface forms villi by extensions of the lamina and then thesubmucosafoldstoformtheplicaecirculares. Synonyms Thisspecificanatomicalfeatureincreasesthesur- face area. The mucosa is formed by crypt-villus Intestinalepithelialapoptosis;Starvation-induced unitswhichincludethestemcells,whichgiverise smallbowelatrophy to the progenitor cells. These progenitor cells furtherdifferentiateintoabsorptiveandsecretory cells.Thestemcellsarepresentthroughoutlifein Definition thecrypts;theirproliferationisregulatedviamul- tiple signals ranging from external diet to hor- Mucosalatrophyisdefinedasanatomicalchanges monesandimmunity. in the intestinal mucosa such as reduced number In proliferation there is an increase in villus of cells, decreased surface area, and shortened height, crypt depth, and surface area. In the aug- villous height and crypt depth, with subsequent mentationofintestinalfunction,thereisincreased lossofintestinalfunction. functionofnotonlytheepithelialcellsbutalsothe deeper cells, such as blood vessels and secretory cells. PreexistingCondition Finally,thelastkindofadaptationisatrophy.It usually is a result of starvation which reduces The gut mucosa starts at the vermilion border at enteralnutrition.Supportingthepatientwithade- thelipandextendstothedentatelineattheanus. quate parenteral nutrition has been unsuccessful Theintestinalmucosa,inparticular,servesmany inpreventingatrophy.Theatrophicchangesresult #Springer-VerlagBerlinHeidelberg2016 P.J.Papadakos,M.L.Gestring(eds.),EncyclopediaofTraumaCare, DOI10.1007/978-3-642-36200-2_134-1 2 GutMucosalAtrophy inafailureoftheadaptivefunctionsofprolifera- therapyinextremecases.Therearemanyknown tion,augmentation,anddifferentiation aswellas side effects and complications associated with increasedapoptosis. chronicparenteralnutritionuse.Thesecomplica- Multipleanimalstudieshavefoundthatmuco- tions include catheter malfunctions, infections, salatrophyischaracterizedbyadecreaseinintes- andliverfailure.Insuchsituation,seriousconsid- tinal weight and nitrogen content. The intestine eration should be made about smallbowel trans- has fewer Peyer’s patches and T cells, thereby plant and management by a multidisciplinary decreasing the immunological capabilities. The team(Modietal.2008). mucosal hypoplasia is mediated by an alteration Thetherapyinthissituation shouldbegeared inthetumornecrosisfactor(TNF)-a/EGFsignal- towardreversingmucosalatrophyandpromoting ingpathway.Theuseoftotalparenteralnutrition adaptations by proliferation, augmentation, and (TPN) may actually cause enterocyte apoptosis differentiation. andstimulationofionsecretion,viaintraepithelial Even small amounts of enteral nutrition can lymphocyte-derivedinterferon-gamma,causinga improve intestinal epithelial growth, motility, decrease in the barrier function of the mucosa. and absorption (Perdikis and Basson 1997). Direct contact with luminal food and chyme has Lipids in the diet as well as its use in parenteral alsobeenfoundtobeimportantformucosalinteg- nutrition add significant benefit. Luminal lipids rity(Shawetal.2012). havebeenshowntoincreaseadaptationandfunc- Mucosalatrophyisasignificantprobleminthe tion of the mucosa. Short-chain fatty acids are settingofstarvation.Inthemilieuofmodern-day shown to reduce mucosal atrophy and promote healthcare,itisamajorprobleminthesettingof adaptation. Proteins and amino acids like gluta- trauma. In these scenarios, gut mucosal atrophy mine improve gut mucosal health by enhancing increases sepsis rates dramatically (Kudsk mucosalfunctionandretardatrophy.Supplements etal.1992).Itisalsoevidentinprolongedstarva- like retinoic acid and ornithine a-ketoglutarate tion for various medical conditions like pancrea- havealsoshowntoimproveadaption.Antibiotics titis and short bowel syndrome. Short bowel may reduce malabsorption and reverse mucosal syndromeisusuallysecondarytointestinalresec- atrophybyreducingbacterialovergrowth.Epider- tions for inflammatory bowel disease, ischemia, mal growth factor and glucagon-like peptide-2 and obstruction. In the pediatric age group, it is have also been used in many controlled settings mostly seen in cases of necrotizing enterocolitis, to improve adaptation. Experimental therapies intestinal malrotations, and atresias. Total paren- using leptin, bombesin, and ghrelin may be used teral nutrition is used to manage prolonged star- inthefutureforthispurpose. vation but may not be beneficial in this regard (Sax 2010). These can be significant enough to cause“intestinalfailure”andfailuretothrive.Itis Cross-References seen when the absorptive surface is so low that patientshavediarrhea,dehydration,malnutrition, ▶NutritionalDeficiency/Starvation andelectrolytedisturbance. ▶NutritionalSupport Application References Totalparenteralnutritionhasbeenthemainstayof KudskKA,CroceMA,FabianTC,MinardG,TolleyEA, management for intestinal failure. This form of PoretHA,KuhlMR,BrownRO(1992)Enteralversus nutritioniscriticalintheshorttermandinmany parenteral feeding. Effects on septic morbidity after blunt and penetrating abdominal trauma. Ann Surg cases is needed on a chronic basis to maintain 215:503–511,discussion511–513 homeostasisandelectrolytebalance.Totalparen- ModiBP,LangerM,ChingYA,ValimC,WaterfordSD, teral nutrition should only be used for long-term IglesiasJ,DuroD,LoC,JaksicT,DugganC(2008) GutMucosalAtrophy 3 Improved survival in a multidisciplinary short bowel SaxHC(2010)Managementofshortbowelsyndrome.In: syndrome program. J Pediatr Surg 43(1):20–24. CameronJL,CameronAM(eds)Currentsurgicalther- doi:10.1016/j.jpedsurg.2007.09.014 apy,10thedn.Elsevier,Philadelphia PerdikisDA,BassonMD(1997)Basalnutritionpromotes ShawD,GohilK,BassonMD(2012)Intestinalmucosal human intestinal epithelial (Caco-2) proliferation, atrophy and adaptation. World J Gastroenterol brush border enzyme activity, and motility. Crit Care 18(44):6357–6375 Med25:159–165 G Gastrointestinal Hemorrhage PreexistingCondition AndrewS.BrockandJosephRomagnuolo Epidemiology DivisionofGastroenterologyandHepatology, Gastrointestinal hemorrhage represents a signifi- MedicalUniversityofSouthCarolina, cant health problem worldwide. In 2009, the Charleston,SC,USA annualincidenceofhospitalizationsintheUnited StatesforupperandlowerGIbleedingwas60.6/ 100,000 and 35.7/100,000, respectively (Laine Synonyms et al. 2012). This represents a decline over the pastdecade,though thereasonfor thisdeclineis Gastrointestinal bleeding; GI bleeding; GI notclear. hemorrhage Etiology Therearemultiplecausesofgastrointestinalhem- orrhage(Table1).Pepticulcerdiseaseisthenum- Definition ber one cause of upper GI hemorrhage and diverticulardiseasethenumberonelowersource. Gastrointestinal (GI) hemorrhage is defined as Thishasremainedsteadyoverthelastdecade. bleeding from the GI tract, anywhere from the mouth to the anus. Traditional terminology uses Presentation the ligament of Treitz to demarcate upper from Patients with GI hemorrhage may present in a lower GI bleeding. The advent of technologies variety of ways, from fulminant, life-threatening capableofaccessingthesmallintestine,however, bleedingtoslow,occultoozingovermanymonths has led to the addition of “mid-gut” bleeding, resulting in unexplained iron deficiency anemia. whereby upper, mid-, and lower sources refer to Vomitingblood isdiagnosticofanupper source, areasaccessible toesophagogastroduodenoscopy while small amounts ofbrightred blood perrec- (EGD), enteroscopy, and colonoscopy, respec- tum in the absence of changes in hemodynamics tively. Thus, upper GI bleeding now refers to or hemoglobin represent an anorectal source. lesions proximal to the papilla of Vater, mid-GI Melena typically indicates an upper or mid-gut bleeding includes lesions distal to the papilla of source, but can also result from a right colon Vatertotheterminalileum,andlowerGIbleeding lesion. Lower GI bleeding usually presents with referstolesionsinthecolorectumandanus. hematochezia, but it also can represent a brisk upperormid-gutsource. #Springer-VerlagBerlinHeidelberg2016 P.J.Papadakos,M.L.Gestring(eds.),EncyclopediaofTraumaCare, DOI10.1007/978-3-642-36200-2_242-1 2 GastrointestinalHemorrhage GastrointestinalHemorrhage,Table1 CausesofGIhemorrhagebylocation Upper Midgut Lower Ulcer Angioectasia Diverticulosis Varices Erosions Colitis(ischemia,IBD,radiation) Gastritis Tumor Hemorrhoids Esophagitis Polyp Tumor Mallory-Weisstear Ulcer Post-polypectomy Dieulafoy Dieulafoy Angioectasia Angioectasia Crohn’sdisease Polyp GAVE Celiacdisease Ulcer Cameron’serosions Meckel’sdiverticulum Dieulafoy Tumor Diverticulosis Hemobilia Aortoentericfistula Hemosuccuspancreaticus Polyp Portalhypertensivegastropathy GAVEgastricantralvascularectasia,IBDinflammatoryboweldisease Cluestothesourceofbleedingmaybeelicited approximately25 %ofpatientswillhavelesions fromthemedicalhistory.Patientswithcirrhosisor withinreachofEGDorcolonoscopy. risk factors for liver disease may have a portal hypertensiveetiologyofhemorrhage,suchasvar- ices or gastric antral vascular ectasia (GAVE). Application Recent nonsteroidal anti-inflammatory drug (NSAID)usepredisposestopepticulcerdisease. InitialManagement Use of anticoagulants, such as warfarin or Vital signs must be monitored closely, with con- clopidogrel, should be noted. Patients who have sideration for intensive care unit monitoring, undergone gastrointestinal surgery are at risk for especiallyforpatientswithactivebleeding,hemo- anastomotic hemorrhage. Aortic stenosis and dynamiccompromise,high-risklesionsonendos- renal failure are risk factors for angioectasia. copy, suspected varices, advanced age, or major Malignant GI tumors can hemorrhage. Patients comorbidities.Labworkshouldinclude,atmini- with aortic grafts or aneurysms can develop mum, a complete blood count, basic metabolic aortoenteric fistulae. A history of retching might panel, hepatic panel, and prothrombin time with indicateaMallory-Weisstear.Recentendoscopic internationalionizedratio(INR).Aphysicalexam polypectomy or biliary/pancreatic should be performed, including a rectal exam to sphincterotomy should raise suspicion for bleed- assess stool color. Intravascular volume may be ingfromthosesites. gleaned from the vital signs; resting tachycardia, Five percent of patients will have obscure GI orthostasis, and hypotension are reflective of bleeding(OGIB).Thisisdefinedasbleedingthat depleted stores. Prognostic scales such as the isnotidentifiedonEGDandcolonoscopy.OGIB Blatchford(pre-endoscopy)andRockall(clinical is subdivided into obscure occult and obscure andendoscopic)scorescanaidintriagingpatients overtbleeding,withtheformerreferringtobleed- by stratifying them into high- and low-risk cate- ing from the GI tract resulting in iron deficiency gories(Barkunetal.2010).Placementofanaso- anemia and the latter as recurrent melena or gastric tube (NGT) has not been shown to hematochezia. The majority of patients with improveoutcomes;further,upto15 %ofpatients OGIB will have small bowel lesions, though without bloody aspirate will have high-risk GastrointestinalHemorrhage 3 lesions. However, NGT can help distinguish lesionswhengivenpriortoendoscopyandreduce upper and lower sources in patients with rebleeding, the need for surgery, and mortality hematochezia with significant hemoglobin drop after endoscopic therapy of high-risk lesions. and/ormildhypovolemia. This likely has little to no benefit in non-high- Two large-bore peripheral intravenous risklesions.H2receptorblockershavenotledto (IV) catheters or a single central catheter should improvedoutcomesandthusarenotindicatedfor be inserted. Patients with signs of intravascular acute upper GI bleeding. Use of a promotility depletionshouldberesuscitatedwithcrystalloids agent such as erythromycin or metoclopramide andbloodproductsasneeded.Transfusionshould can reduce the need for repeat endoscopy by also be given to patients with a hemoglobin less clearing the stomach of blood and, thus, should than 7.0 g/dL, though the threshold in patients beconsidered(Gralneketal.2008).IVoctreotide with underlying coronary artery disease or signs can be added in selected patients with ongoing of impaired myocardial perfusion may require bleeding(ImperialeandBirgisson1997). hemoglobin levels as high as 10.0 g/dL. Care Patientssuspectedofhavingvaricealbleeding mustbetakentoavoidovertransfusioninpatients should receive IV octreotide with a bolus of with known or suspected varices, as this can 50 mcg followed by an infusion at 50 mcg/h for increase portal pressures, thus worsening bleed- 3–5days(Burroughs1994).Patientswithcirrho- ing;atargethemoglobinof8.0g/dLisappropriate sis and GI bleeding should receive IVantibiotics inthesepatients. asprophylaxisforspontaneousbacterialperitoni- Anticoagulants and antiplatelet agents should tis. Acceptable choices include cephalosporins, beheld.Coagulopathyshouldbereversedifsafe such as ceftriaxone, and fluoroquinolones such todoso,aimingforaplateletcountofgreaterthan as ciprofloxacin. These should initially be given 50 and INR less than 1.5. However, if unsafe, IV,buttransitioncanbemadetooraladministra- endoscopycangenerallybeperformedinpatients tiononcethepatientisstabilizedtocompletethe with therapeutic coagulopathy. INR in patients recommended7-daycourse. with cirrhosis is not predictive of bleeding; thus, attempts at correction may simply lead to exces- EndoscopicTreatment sivevolumeexpansion.Consideration ofplatelet Consultation with a gastroenterologist should be transfusion should also be given to patients on made for all significant bleeds. Once the patient antiplatelet agents such as aspirin or clopidogrel has been hemodynamically stabilized, including who present with life-threatening bleeding. In endotracheal tube placementif necessary, endos- high-risk situations, such as mechanical valves copycanbeundertaken.Earlyendoscopy,defined or newly placed coronary stents, consultation as within 24 h of presentation, is recommended withacardiologistshouldbeundertaken. forpatientswithacuteupperGIbleeding(Barkun etal.2010).PatientswithbrisklowerGIbleeding MedicalTherapy may also warrant inpatient endoscopy, particu- Themostimportantlife-savingmedicaltreatment larly if the bleeding persists. Patients with self- for GI hemorrhage is proper resuscitation and limited hematochezia can undergo outpatient maneuverstoprotecttheairway;thisshouldpre- colonoscopy. cedeendoscopyandmostothertherapies.Patients The role of endoscopy in patients with GI with significant upper GI hemorrhage suspected hemorrhageistodiagnosethesourceofbleeding, ofhavingahigh-risklesiononendoscopyshould riskstratifythepatient,andtreatthesourcelesion receivehigh-doseIVprotonpumpinhibitor(PPI) if necessary. Lesions at low risk of rebleeding therapy(Dorwardetal.2006).High-dosetherapy include peptic ulcers with a clean base or flat includes omeprazole, esomeprazole, or spot, Mallory-Weiss tear, gastritis, esophagitis, pantoprazole in a bolus dose of 80 mg followed and non-bleeding angioectasia. Healthy patients byacontinuousinfusiondoseof8mg/hfor72h. at low risk of rebleeding can be discharged after This has been shown to downstage high-risk endoscopy. Endoscopic hemostasis should be 4 GastrointestinalHemorrhage attempted in patients with high-risk lesions, hemostasis. Mechanical hemostasis for ulcers including ulcers with active bleeding or visible consistsofhemostaticclips,whichworkbygrasp- vessel,Dieulafoylesions,bleedingangioectasias, ingthevesseltocutoffbloodflow.Thedecision diverticula with bleeding or visible vessel, and tousethermaltherapyversusclippingisbasedon varices amenable to endoscopic therapy. All position of lesion and endoscopist preference, as ulcerswithclotsshouldbeirrigated,buttreatment onehasnotbeenshowntobesuperiortotheother. ofulcerswithanadherentclotthatdoesnoteasily Further, whether one combines injection therapy wash with gentle irrigation is at the discretion of witheitherthermalormechanicaltherapyoruses theendoscopist,whereeitherendoscopictherapy thethermalormechanicaltechniquealoneisatthe or medical therapy is acceptable. Tumors are at discretion of the endoscopist as there is no evi- highriskofrebleeding,butarerarelyamenableto dence these approaches result in different endoscopic therapy. Other lesions may warrant rebleeding rates. A common approach is to use non-endoscopic therapy; for example, injectiontherapyfirstwhenthereisactivebleed- aortoenteric fistulae require surgery, hemosuccus ing (to clear the views) or into an adherent clot pancreaticus may necessitate angiography, and before removal (for prophylaxis against persistent bleeding from tumors may require bleeding). angiographicorradiationtherapy. The above techniques may also be used for There are various modalities of endoscopic other sources of GI hemorrhage. For example, therapy that may be used. Band ligation is the bleeding diverticula and Dieulafoy lesions may recommended first-line endoscopic therapy for be treated with any of the techniques mentioned esophageal varices, though sclerosants such as forulcerhemorrhage,orbybandligation.Endo- sodium morrhuate may be used when band liga- scopic clipping is often effective for Mallory- tionisnotfeasible(Garcia-Tsaoetal.2007).Cya- Weisstears.Angioectasiacanbetreatedwithther- noacrylate glue has recently been introduced for maltechniques,clipping,aswellasargonplasma thetreatmentofbleedinggastricvarices,thoughit coagulation (APC). APC is a noncontact tech- is only available at a limited number of United nique that uses a monopolar current. It is most Statesinstitutionsatthistime. effective for angioectasia, GAVE, and radiation The armamentarium is broader for proctitis. Hemospray (Cook Medical Inc, non-variceal hemorrhage. For peptic ulcers with Winston-Salem, NC) is a promising new tech- high-risk stigmata such as active bleeding or niquethathasnotyetreceivedapprovalfromthe non-bleeding visible vessel, there are three basic Food and Drug Administration. This technique categories of therapy: injection therapy, thermal, involves directly spraying a nanopowder onto and mechanical.Injection therapygenerallycon- thesourceofbleeding,withgoodefficacyinpre- sistsofnormalsalineorepinephrine,whichworks liminarytrials(Sungetal.2011). byatamponadeorvasoconstrictiveeffect,respec- Aspirintherapyshouldberestartedinlessthan tively.Injectiontherapyshouldnotbeusedalone 5–7 days, as soon as the cardiac risk outweighs asrebleedingratesaresignificantlylowerwhenit rebleeding risk. Helicobacter pylori should be is applied concurrently with either thermal or eradicated and NSAIDS avoided in both upper mechanical therapy. Contact thermal techniques andlowerbleedingsources. include bipolar electrocautery (e.g., Gold probe, Microvasive Boston Scientific, Natick, MA, and OtherTherapy BICAP,CirconACMI,Stamford,CN)andheater If rebleeding occurs once after successful endo- probe(OlympusCorp.,LakeSuccess,NY).These scopic hemostasis, randomized trial data shows methods work by coaptive coagulation, whereby repeatendoscopytobesaferthansurgery.Second the probe is applied directly to the lesion or third rebleeding episodes should have other (coaptation) and an electrical current is applied options considered. If endoscopic therapy fails, (coagulation). This compression of the vessel or thelesion isnotamenableto endoscopicther- with subsequent cautery enables effective apy, other modalities may be used. For example, GastrointestinalHemorrhage 5 transjugular intrahepatic portosystemic shunting include radionuclide scan, Meckel’s scan, com- (TIPS) is used in appropriate patients with puted tomographic (CT) angiography, CT variceal bleeding, with its most feared adverse enterography (CTE), and the newer triple-phase event being encephalopathy (30 %). CTE. Intraoperative enteroscopy is reserved for Angiography-guided hemostasis can be patientswithlife-threateningsmallbowelhemor- performedforhemorrhagefromulcers,Dieulafoy, rhagethatisnotresponsivetomoreconservative angioectasia, and diverticula, with contrast- therapies,asthisoperationcarriessignificantmor- induced nephropathy being the most important bidityandmortality. adverseevent.Asnoted above,radiationtherapy canbeusedfortumorhemorrhage.Surgeryisnow consideredalastresortforanyformofGIbleed- Cross-References ingandisrarelyneededcurrentlyduetoimprove- ments in medical and endoscopic therapy. An ▶Curling’sUlcer exceptionishemorrhagefromarecentanastomo- ▶Cushing’sUlcer sis,whichmayrequiresurgicalrevision;also,the ▶Gastritis airandstressontheanastomosisfromendoscopy ▶Gastrointestinal Bleeding: Indications for Pro- aregenerallycontraindicated. phylaxisPost-traumaandTreatment Patients with OGIB (negative EGD and colo- ▶Hemorrhage noscopy)shouldundergocapsuleendoscopyafter ▶HemorrhagicShock consideration is given to repeating EGD and/or ▶TransfusionThresholds colonoscopy. Repeat standard endoscopy is par- ticularly useful in cases where views on initial procedures were compromised due to blood, References poor prep, or other factors. It remains unclear if non-bleeding diverticula on colonoscopy in a BarkunAN,BardouM,KuipersEJetal(2010)Interna- patient with hematochezia defines a “negative” tionalconsensusrecommendationsonthemanagement of patients with nonvariceal upper gastrointestinal colonoscopyornot,givenitisthemostcommon bleeding.AnnInternMed152:101–113 lower source. If a lesion is identified on capsule BurroughsAK(1994)Octreotideinvaricealbleeding.Gut endoscopy,orthepatientcontinuestobleedfrom 35:S23–S27 DorwardS,SreedharanA,LeontiadisGIetal(2006)Pro- an unknown source, enteroscopy may be under- ton pump inhibitor treatment initiated prior to endo- taken.Theformofenteroscopyisdrivenbylesion scopic diagnosis in upper gastrointestinal bleeding. location,withtheoptionsbeingpushenteroscopy CochraneDatabaseSystRev7:CD005415 or deep enteroscopy. Deep enteroscopy consists Garcia-TsaoG,SanyalAJ,GraceNDetal(2007)Preven- tionandmanagementofgastroesophagealvaricesand of double-balloon enteroscopy, single-balloon variceal hemorrhage in cirrhosis. Hepatology enteroscopy, and spiral enteroscopy and may be 46:922–938 approachedfromanantegrade(peroral)orretro- GralnekIM,BarkunAN,BardouM(2008)Management grade(peranus)direction.Hemostaticcapabilities of acute bleeding from a peptic ulcer. NEJM 359:928–937 mirror those of standard endoscopy discussed Imperiale TF, Birgisson S (1997) Somatostatin or above, except banding, which cannot be accom- octreotidecomparedwithH2antagonistsandplacebo modated by enteroscopes. However, the efficacy inthemanagementofacutenonvaricealuppergastro- ofenteroscopictherapyislessclear,andrandom- intestinal hemorrhage: a meta-analysis. Ann Intern Med127:1062–1071 izedoutcomedataarelacking.Asianandyounger LaineL,YangH,ChangS-C,DattoC(2012)Trendsfor cohorts have a higher incidence of small bowel incidenceofhospitalizationanddeathduetoGIcom- tumors, which may require surgery after plicationsintheUnitedStatesfrom2001to2009.Am localization. JGastroenterol107:1190–1195 SungJJ,LuoD,WuJCetal(2011)Earlyclinicalexperi- Hemodynamically unstable patients with ence of the safety and effectiveness of hemospray in OGIB should undergo angiography. Other tests achievinghemostasisinpatientswithacutepepticulcer for patients without a bleeding source identified bleeding.Endoscopy43:291–295 O Organ Donor Management management practices in the intensive care unit in the pre-retrieval phase and the current state of LaveenaMunshi1andJeffreyM.Singh2 theevidence. 1ClinicalAssociate,CriticalCare,MountSinai HospitalandUniversityHealthNetwork, UniversityofToronto,Toronto,ON,Canada PreexistingCondition 2CriticalCareMedicine,UniversityHealth NetworkandAssistantProfessor,Divisionof Pathophysiology CriticalCare,UniversityofToronto,Toronto, Understandingthepathophysiologicchangesthat ON,Canada occur pre-, peri-, and post-brain death is impera- tive to ensure optimal management of this popu- lation. Brain injury is associated with Synonyms vasoregulatorydysfunction,multifactorialshock, andhormonederangements,allofwhichmakethe Brain-dead donor; Donation after cardiac death; managementofthepotential organdonorachal- Donormanagement;Neurologicdeterminationof lenge(Table1). death;Potentialorgandonor Neurologic:Brainstemischemiaisduetothe primary neurologic injury and further worsened byelevationsinintracranialpressurethatdevelop Definition duringbrain death. Prior toherniation,hyperten- sionmayoccurasacompensatorymechanismto Advancementsintransplantmedicine havefacil- protect cerebral perfusion in the face of rising itated lifesaving therapeutic options for patients intracranial pressure. As the organ donor pro- with end-stage organ failure. Despite major gresses to brain death, pontine ischemia occurs advancesinsurgicaltechniques,immunosuppres- first, resulting in mixed vagal and sympathetic sive pharmacology, ex vivo assessment and the stimulationthatmanifestsastheclassicCushing’s expansion of the donor pool using living-related responseofbradycardia,hypertension,andirreg- donors, the supply of donor organs continues to ular breathing. Unopposed sympathetic stimula- fall short of the demand for organs by potential tion follows during medullary ischemia which recipients.Meticulous intensivecaredonor man- resultsintransienthypertensionwithmassivecat- agement strategies can increase the number and echolamine release. Cerebral herniation and spi- quality of organs eligible for transplant. This nal cord ischemia are the final pathways which chapter will provide an overview of donor result in a blunted sympathetic nervous system, #HerMajestytheQueeninRightofCanada2016 P.J.Papadakos,M.L.Gestring(eds.),EncyclopediaofTraumaCare, DOI10.1007/978-3-642-36200-2_256-1 2 OrganDonorManagement OrganDonorManagement,Table1 Overviewofpathophysiologicchangesandmanagement Condition Mechanism Management Shock Hypovolemic Under-resuscitationpretransplant Fluid(crystalloidorcolloid) Diabetesinsipidus Endpoints:MAP>60–65,sBP>90, normalizedlactate,u/o>0.5cc/kg IdentificationandreversalofDI(desmopressin, vasopressin,fluids) Cardiogenic Myocardialnecrosis,subendocardialischemia, Cautiousadministrationoflowest-dose oxygen-freeradicals inotropicsupportneededtomaintainend-organ perfusion Vasodilatory Spinalcordischemiabluntingsympathetic Vasopressin responseandlossofcatecholamines Dopamine Norepinephrine Epinephrine Phenylephrine Hormone Lossofanteriorandposteriorpituitaryfunction AntidiureticHormone–fluid,desmopressin, therapy (antidiuretichormone,adrenocorticotropic vasopressin hormone,thyroidhormone,growthhormone) T3/T4–thyroidreplacementwith triiodothyronineorthyroxine(controversial) ACTH–methylprednisolonea Hyperglycemia–insulin Empiricapplicationofreplacementversus targetedversusinthesettingofhemodynamic instabilityvariesamongprograms Ventilation Ventilator- Associatedwithtraumaticbraininjury,micro- Preventionandtreatment associated aspiration,impairedhostdefensemechanism pneumonia Pulmonary Over-resuscitation Diuresis edema Cardiogenicfromimpairedcontractilityinsetting Cautiousfluidadministration ofbrainstemdeath Noroleforbetaagonists Cardiomyopathyassociatedwithneurologic injury Vasoconstrictioncrisisacutelyelevatingleft-sided cardiacpressure Ventilator- Volutrauma,biotrauma,atelectraumaleadingto Earlyresearchsuggestingbenefitoflung- associated systemicinflammation protectiveventilationstrategies lunginjury MAPmeanarterialpressure,ACTHadrenocorticotropinhormone aEvidencesurroundingwhattoreplace,whentoreplace,andhowtoreplacecontroversial decreaseincatecholaminesandvasculartone,and insufficiency), hypovolemic shock (diabetes vasodilatory shock. The transient hypertension insipidus, volume depletion, hemorrhage related followed by a profound drop in blood pressure to trauma), and cardiac dysfunction can threaten organ viability. Neurohormonal (catecholamine surge, hormonal derangements, changes ensue as posterior pituitary gland func- orsubendocardialischemia). tionisimpaired. Pulmonary: The lungs are especially vulnera- Cardiac: Cardiovascular changes that follow ble to injury during the process of death due to includevasodilatoryshock(inflammation/adrenal aspiration, trauma, and hydrostatic and

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