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232 PART IV MANAGEMENTCONSIDERATIONS
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often produced by the Herpesviridae family (i.e., herpes simplex, varicella zoster virus, and cytomegalovirus). The clinical presentation of these infections is typically an acute, vesiculobullous lesion with a
lack of inflammatory response in leukopenic patients. If not treated aggressively with antiviral agents,
suchasacyclovir,valaciclovir(Valtrex),organciclovir,theseinfectionscanleadtosignicantlocaland
possible systemic morbidity.
Among fungal infections, Candida albicans is the most common fungal pathogen, but others
such as Aspergillus and Cryptococcus are commonly encountered. The more aggressive fungi show
an invasive behavior that often involves deeper tissues. Patients should be monitored carefully for
signs of local tissue trauma that may predispose them to viral or fungal colonization.
15. What are the characteristics of bacterial oral infections in immunocompromised
patients?
Oral infections in immunocompromised patients typically occur with significant local symptoms and
may spread to involve adjacent or distant anatomic sites. These infections tend to progress more
rapidly and may produce systemic symptoms or local osteomyelitis. Infections may be caused by
gram-negative enteric flora secondary to colonization of these organisms in the oral cavity. These bacteria are often resistant to penicillin and cephalosporins. Broad-spectrum antibiotic prophylaxis should
be used empirically before definitive identification of the causative microorganism in immunocompromised patients with evidence of infection.
16. What are the general principles of the preoperative evaluation of immunocompromised patients?
Immunosuppression is not in itself a contraindication to well-planned surgery. The general approach
to the care of these patients when they are to undergo surgery is to increase host resistance to
infection and to maximize wound healing. The patient’s immune status should be evaluated by means
of a history, physical exam, and lab studies. The history should include questions about the patient’s
underlying disease, previous infections, use of medications and other therapy, previous anesthesia,
and trauma. The physical exam should also determine the patient’s nutritional status and include a
search for signs of existing infection and lymphadenopathy.
High-risk patients should have elective procedures scheduled at the beginning of the day. The
possibility of reducing the dosages of immunosuppressive drugs must be weighed against the effect
this might have on the reason why the patient is being treated with these agents. Other considerations include the removal of any infected foreign bodies; assessment of the need of invasive
devices; restoration of cardiac and renal function, including tissue perfusion; correction of nutritional
deficiencies, if present; assessment of the patient’s need for vaccinations; and administration
of prophylactic antibiotics. Also, regardless of the etiology, hemostasis should be achieved with
pressure,packing,orsuturing,andiftheplateletcountisbelow50,000/mm3, platelet transfu-
sion should be considered. In the case of dental extractions, alveolectomy and primary closure are
recommended.Ifplateletcountsare<40,000/mm3,plateletsshouldbetransfused30minutesbefore
surgerytoachieveplateletlevelsofmorethan40,000/mm3. One unit (pack) of platelets typically
raisestheplateletcountby10,000/mm3. Although correcting the patient’s immunodeficiency is
usually difficult or impossible, defects in B-cell function may be partially treated by administering
immunoglobulin.
17. What preoperative lab studies should be included in evaluation of immunocompromised patients?
• Chestradiograph
• Urinalysis
• Serumalbumindetermination
• Liverandkidneyfunctiontests
• Cultureofmaterialfromanyinfectedsites
• Completebloodcountwithplateletcount
• Absoluteneutrophilcount(ANC)
• Prothrombintime(PT)
• Partialthromboplastintime(PTT)
Because some of these patients may present with neutropenia as well as thrombocytopenia,
other tests include:
Specictestingofthepatient’sT-cells,B-cells,PMNs,andcomplementshouldbechecked
before surgery.
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18. What are the effects of chemotherapeutic and immunosuppressant drugs on the
immune system?
Theeffectsofthesedrugsvaryfromagenttoagent.Forexample,chemotherapeuticagentsdepress
the number and activity of the neutrophilic leukocytes (leukopenia). The nadir of white cell counts
varies with the agents used but generally occurs 10-20 days after administration. The patient is
susceptibletoinfectionwhentheANCfallsbelow1500/mm3. The susceptibility increases significantly
whenthecountfallsbelow500/mm3. Corticosteroids, on the other hand, decrease the leukocyte
response to inflamed tissue and depress T-cell function. Wound healing is slowed, and the ability to
localize infection is reduced. Cyclosporine has almost no effect on the local inflammatory reaction but
causes the initiation of interleukin-2 production and the suppression of T-helper and cytotoxic cells.
Antilymphocyte antibodies appear to work by lysing target cells. With all these agents, increased dosage is associated with increased predisposition to infection. These patients should receive prophylactic antibiotics before most surgical procedures.
19. When should prophylactic antibiotics be used in a chemotherapy patient?
Prophylacticantibioticsshouldbeconsideredifthegranulocytecountis<2000/mm3. Surgery gener-
allyshouldbeperformedatleast3daysbeforechemotherapyisinitiatedincancerpatientsbecause
granulocytelevelsmayfallbelow500/mm3 one week after the initiation of many types of chemo-
therapeutic agents. When surgery needs to be performed during severe neutropenia (granulocyte
counts<500/mm3), it is recommended that the procedure be performed in a hospital setting with
broad-spectrum antibiotic prophylaxis administered during the perioperative period.
20. What type of virus is HIV, and what is its cell target?
Humanimmunodeciencyviruses(HIVs)areagroupofretrovirusesthatcanbeacquiredbythe
transmission of body fluids, including transfusions, and through the infection of infants by infected
mothers.ThespecictargetofthevirusistheCD4T-celllymphocytes.Thevirusmultipliesinthecell
and eventually destroys it. Cell-mediated immunity is thereby severely affected.
21. What are the general categories of HIV-infected patients?
• AsymptomaticpatientswithevidenceofHIVinfectiondemonstratedbythepresenceofHIVanti-
bodies in the serum or in the secretions of these patients
• PatientswithAIDS-relatedcomplex(ARC),manifestedbythepresenceofsymptomsincluding
lymphadenopathy, unexplained fever, weight loss, and hematologic and neurologic abnormalities
• PatientswithAIDSasdenedbytheCentersforDiseaseControlandPrevention(CDC)(i.e.,HIV
infectionandCD4lymphocytecount<200)
22. What are the lab tests to determine the status of the HIV patient?
DiagnosisofHIVinfectionismadebydetectionofantibodiestoHIV.AntibodiestoHIVaredetermined
bytheenzyme-linkedimmunosorbentassay(ELISA)methodorbytheWesternblotmethod;bothtests
require the patient’s consent in many states.
ThestatusofpatientswithHIVinfectionandpotentialriskofsurgeryareevaluatedbyassessing
theviralloadandtheCD4+lymphocytecount.Theviralload,determinedbytheHIVRNA,shouldideallybeundetectable.TheCD4+lymphocytecountshouldbegreaterthan200andideallygreaterthan
400.Informationregardingtheoverallphysicalstatusofthepatientandthepatient’ssymptomatic
andphysicalmanifestationsofHIV-relateddiseasesarealsohelpfulinassessingtheHIVpatient’srisk
for surgery.
Viralloadmeasurementsgiveanindicationoftheamountofcurrentviralactivityandhavebeen
shown to correlate with disease progression. Studies have demonstrated that viral loads of more than
30,000-50,000HIVRNAcopies/mLofplasmacorrelatewithapoorprognosis,whereasviralloadsof
<5000copies/mLcorrelatewithbettershort-termprognosis.
TheCD4+lymphocytegivesanindicationofthedegreeofimmunologicdestruction.Labndings
inpatientswithAIDSincludelowlymphocytecountsanddepressedCD4T-cells,withtheCD4-to-CD8
ratioof1:0orless(normally1.8:2.2).
23. What are the clinical manifestations of AIDS?
Signs and Symptoms Opportunistic Infections
Lymphadenopathy P. jiroveci (pulmonary)
Weight loss Toxoplasmosis (cerebral)
Diarrhea Cryptosporidiosis (diarrhea)
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Signs and Symptoms Opportunistic Infections
Thrombocytopenia Candidiasis (esophageal)
Anemia Cryptococcus (meningitis)
Leukopenia Herpes
Neurologic abnormalities Varicellaviruses(skin)
Dementia Histoplasmosis
Encephalopathy Tuberculosis
Central nervous system toxoplasmosis Neoplasms
Lymphoma Kaposi’ssarcoma
24. What are the principles of drug therapy of AIDS patients?
ThemajorgoaloftherapyofpatientswithAIDSistreatmentoftheopportunisticinfections,
includingantiviraltherapy.ProphylaxisisessentialforallpersonswithsymptomaticHIVdisease,
AIDS,orCD4+counts<200/μL.SurvivalhasalsobeenprolongedinHIV-positivepatientsby
prophylaxis against opportunistic infections such as P. jiroveci pneumonia (PJP), the mycobac-
terium aviumcomplex(MAC),andotherfungalinfections.PJPprophylaxiscommonlyiswith
trimethoprim- sulfamethoxazole, although dapsone-trimethoprim or clindamycin-primaquine may be
usedalternately.ProphylaxisforMACusuallyconsistsofamacrolideantibiotic,clarithromycin,or
azithromycinandisrecommendedwhentheCD4+cellcountfallsbelow75or50/mL.Prophylaxis
against Candida or other fungal diseases is currently not recommended, although many immunocompromised patients may be taking an antifungal medication, such as fluconazole or another
azole, when they have manifestations of fungal infection. Current antiretroviral therapies have been
shown to reduce viral counts and slow disease progression, and they can be effective in raising
theCD4+lymphocytecountsconsiderably.Themosteffectiveantiretroviraltreatmentstrategies
are multiple drug therapies that combine nucleoside analogue drugs with protease inhibitors and,
when patients are able to tolerate these regimens, triple drug therapy with two nucleoside analogue
drugs plus a protease inhibitor.
25. What are the considerations in the surgical treatment of an HIV-infected person?
PatientswithearlyHIVinfectionandwithnoimmunologicimpairmentgenerallytolerateelectiveoral
surgical procedures well, and recent studies have demonstrated no increased incidence in infection,
bleeding, or dry socket in extractions. In fact, routine prophylactic antibiotics are not indicated for
these patients and may even further predispose them to candidiasis or drug reactions. In contrast,
patientswithAIDSandARCarenotgoodsurgicalcandidatesbecauseoftheirhematologicabnormalitiesandpredispositiontoAIDSinfection.PatientswithmandibularfractureswhohaveAIDSinfection
haveanincreasedincidenceofpostoperativeinfectionscomparedwithasymptomaticHIV-positive
patients.Accordingly,itisrecommendedthatpatientswithAIDS(asdenedbyCD4+countof<200
cells/mLorhistoryofAIDS-deningillnesssuchaslymphoma,tuberculosis,orP. jiroveci ) should not
undergo elective surgery. When urgent and emergency surgery is necessary, these patients should
receive broad-spectrum prophylactic antibiotics before undergoing any surgical procedure, and proper
attention to the prevention of wound infection must be given to prevent transmission of the virus to
personnel caring for the patient.
26. What are the potential drug interactions in HIV-infected patients?
See Table 22-1.
27. What is the management of health care workers exposed to HIV-infected blood or
body fluids?
TherateofseroconversionofhealthcareworkersexposedtoHIV-infectedbloodorbodyuidhas
beenreportedtobe0.42%.Themanagementofoccupationalexposuresofcontaminatedorsuspectedcontaminateduidsiscontroversial.Currently,theCDCrecommendsthat,afterinformedconsentisobtained,thepatientshouldbetestedforHIV.IfthepatientisHIV-positive,theexposedhealth
careworkershouldundergoHIVtestingimmediatelyandthenat6weeks,12weeks,and6months.
Initiation of zidovudine prophylaxis after exposure remains controversial because of its yet unproven
efficacy.
Lymphoma
Table 22-1. Potential Interactions of Drugs Used by HIV-Infected Patients
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DRUG DRUG USED TO TREAT HIV
Benzodiazepines Ritonavir,indinavir(protease
Cisapride Azole antifungals, clarithromycin,
Clarithromycin Ritonavir,indinavir Inhibition of hepatic
Didanosine(nucleoside
analogue)
Ganciclovir Zidovudine (thymidine analogue) Pharmacodynamic
Ketoconazole Saquinavir (protease inhibitor) Inhibition of hepatic
Metronidazole Ritonavir(liquidonly) Alcohol in liquid
Opiate analgesics
(especially meperidine,
propoxyphene, fentanyl)
Terfenadine, astemizole (H1
antihistamines)
G-CSF, Granulocyte colony-stimulating factor.
Adapted from Sandler NA, Braun TW: Current surgical management of the immunocompromised patient, Oral Maxillofac Surg Clin North Am 10:445–455, 1998.
inhibitors)
ritonavir, indinavir
Oral ganciclovir Unknown ↑Didanosine Monitorfordidanosinetoxicity;dosagereduc-
Ritonavir Inhibition of hepatic
Azole antifungals, clarithromycin,
ritonavir
MECHANISM OF
INTERACTION EFFECT RECOMMENDATION
Inhibition of hepatic
metabolism
Inhibition of hepatic
metabolism
metabolism
interaction
metabolism
formulation
metabolism
Inhibition of hepatic
metabolism
↑ Concentration of benzodiaz-
epines
Cardiotoxic effects (including
fatal arrhythmias)
↑ Concentration of clarithro-
mycin
Enhancedbonemarrowtoxicity Mayrequiredecreaseddoseofzidovudineor
↑ Saquinavir concentration Underinvestigationtomaximizesaquinavir
Disulram-likereaction Monitorfortoxicity;changeformofritonavir
↑ Opiate concentration Usealternatepainmedication;monitorfor
Accumulation of cardiotoxic
unmetabolized antihistamine
Adjust benzodiazepine dosage, use alternate
agent, or monitor closely for toxicity
Avoid concomitant use
Dosagereductionnotrequiredforpatientswith
normal renal function
tion may be required
concomitantG-CSF
exposure
toxicity
Avoid concomitant use
CHAPTER 22 THEIMMUNOCOMPROMISEDSURGICALPATIENT 235
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Antigen
Antigenpresenting
cell
Corticosteroids
Figure 22-1. Sites of action of immunosuppressive drugs used in transplant patients. IL, Interleukin. (Modified from
Sandler NA, Braun TW: Current surgical management of the immunocompromised patient, OralMaxillofacSurgClinNorth
Am 10:445–455, 1998.)
28. What is the mechanism of action of immunosuppressive agents used in transplant
patients?
The drugs listed in Figure22-1 suppress the immune system at sites complementary to traditional
immunosuppressivemedications.Manytransplantpatientscurrentlyareontwoormoreofthese
drugs in an attempt to prevent rejection. This may predispose the patient to overimmunosuppression
or potential drug interactions.
29. What is graft-versus-host disease (GVHD)?
GVHDresultswhenimmunecellsortissuestransplantedfromadonoracttowardthetransplant
recipient as foreign, thereby initiating an immune reaction that causes disease in the transplant recipient. It is primarily a T-cell-mediated immune process.
30. What are the common immunosuppressive agents used to treat GVHD?
MedicationsusedforthepreventionandtreatmentofGVHDincludeimmunosuppressivedrugs,such
as corticosteroids and methotrexate, as well as more specific T-cell immunosuppressive drugs, such
as cyclosporine and tacrolimus. Corticosteroids are the most widely used front-line therapy for the
treatmentofclinicalGVHD,commonlyadministeredincombinationwiththerapeuticdosesofcyclosporine or tacrolimus.
31. What oral manifestation may indicate an overdosage of methotrexate in patients
being treated for GVHD?
GradeIII/IVmucositis.
32. What are some of the common post-transplantation immunosuppressive drugs?
Post-transplantation immunosuppressive drugs are several and include:
Nonspecific
• Corticosteroids: The most commonly utilized corticosteroid is methylprednisolone.
• Methotrexate: An antimetabolite with primary goal to cause cell death. It can induce tolerance
following marrow transplantation.
Specific T-Cell Immunosuppressive Drugs
• Cyclosporine: Blocks the calcium-dependent signal transduction pathways distal to engagement
of the T-cell receptor. This block interrupts the activation of T-cells.
• Tacrolimus: This is a macrolide antibiotic. It inhibits the signaling through the T-cell receptor. See
question33formoredetails.
• Sirolimus: (rapamycin) is a lipophilic macrolide antibiotic.
• Mycophenolate:MycophenolateMofetil(MMF,CellCept)isamorpholinoethylesterofmycopheno-
licacid(MPA).
Antibodies
• Mostofthepromisingresultshavecomefromstudiesusingselectedmonoclonalantibodies.
DirectedMuromonab-CD3 (OKT3) is a monoclonal mouse antibody licensed for the therapy of
allograft rejection. High incidences of infection have discouraged the use of this antibody.
IL-1
CD-4
T-helper
cell
Cyclosporine
Tacrolimus
Monoclonal
antibodies
IL-2 B-cells Plasma
T-cells
Sirolimus Gusperimus
Azathioprine
Mycophenolate
mofetil
cells
Activated
T-cells
CHAPTER 22 THEIMMUNOCOMPROMISEDSURGICALPATIENT 237
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Table 22-2. Side Effects of Immunosuppressive Drugs Used in Transplant Patients
MEDICATION POTENTIAL SIDE EFFECTS
Corticosteroids Cushing’s syndrome, adrenal insufficiency
Azathioprine Myelodepression(leukopenia,thrombocytopenia)
Cyclosporine Nephrotoxicity,neurotoxicity,hypertension,hepatotoxicity
Tacrolimus Nephrotoxicity,neurotoxicity,diabetogeniceffects
Mycophenolatemofetil Myelodepression(leukopenia,anemia),gastrointestinal(diarrhea,emesis)
Sirolimus Myelodepression(leukopenia,thrombocytopenia),potentialnephrotoxicity
Gusperimus Myelodepression(leukopenia,anemia,thrombocytopenia)
Monoclonalantibodies Central nervous system (seizure, encephalopathy, psychosis)*
*Increased risk of encephalopathy and psychosis reported with indomethacin use.
Adapted from Sandler NA, Braun TW: Current surgical management of the immunocompromised patient, Oral
Maxillofac Surg Clin North Am 10:445–455, 1998.
• Antithymocyte globulin is a polyclonal immunoglobulin prepared by injecting various cellular
preparations into animals. The antibodies produced are capable of destroying human leukocytes.
• Rituximabisananti-CD20monoclonalantibodyusedtodecreaseallogeneicdonorB-cell
immunity.
Thalidomide
• Thalidomide is an immunomodulator that lacks a global inhibitory effect upon lymphocyte prolif-
erationanddoesnotimpairDTH.
Novel Agents
• Anti-cytokinestoTNF-alpha,IL-1,andgamma-interferon
• Induction of anergy
• Other approaches:Drugsornonpharmacologicaltreatmentoptionsthatappeartobepromising
includeclofazimine,psoralenandultravioletlightA(PUVA),photopheresis,radiationtherapy,and
novelmoleculessuchasafusionimmunotoxindirectedagainstCD3.
33. What are the side effects of immunosuppressive drugs in transplant patients?
See Table 22-2.
34. What are the oral manifestations of cyclosporine use?
Cyclosporine is associated with gingival hyperplasia in the dental papillae of the anterior teeth, which
typicallyoccursafter3-6monthsofimmunosuppressanttherapy.Studiessuggestthatapproximately
30%ofpatientsmedicatedwithcyclosporinealoneexperiencesignicantgingivalchanges.Calcium
channel blocking agents that may be prescribed to counter the hypertension caused by cyclosporine
may also induce gingival hyperplasia with an additive effect to that of cyclosporine. When the two drugs
areusedsimultaneously,theycanresultinanearly40%incidenceofgingivalhyperplasia.Othersignificant risk factors that influence gingival overgrowth include age and sex (with younger men having
anincreasedsusceptibility),durationoftherapy,serumcreatininelevels,andtheHLA-B37haplotype.
35. How is cyclosporine-induced gingival hyperplasia treated?
Decreasesinthedosageofthedrugordiscontinuingthedrugearlymayresultinreversalofthisside
effect. However, surgical intervention that consists of gingivectomy and tissue re-contouring is often
necessary to improve aesthetics and function.
36. What are the different drug interactions of cyclosporine/tacrolimus?
See Table22-3.
37. What is tacrolimus, and what are its major side effects?
Tacrolimus(FK-506)isamacrolideimmunosuppressantisolatedfromStreptomyces tsukubaensis
in1984.Thisdrugis50-100timesmorepotentthancyclosporine.Initiallyusedduringepisodesof
severe graft rejection, it is now used for baseline immunosuppression.
The principal adverse effects associated with tacrolimus are similar to those of cyclosporine and
include nephrotoxicity and neurotoxicity. In addition, diabetogenic effects are seen. The mechanism
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Table 22-3. Drug Interactions of Cyclosporine and Tacrolimus
DRUG CLASS MECHANISM
Increased Cyclosporine
Metoclopramide Prokinetic ↑ cyclosporine absorption
Cisapride Prokinetic ↑ cyclosporine absorption
Erythromycin Macrolideantibiotic Mechanismunclear
Increased Cyclosporine/Tacrolimus
Clotrimazole Imidazole InhibitcytochromeP450
Fluconazole Antifungal InhibitcytochromeP450
Corticosterone Corticosteroid InhibitcytochromeP450
Dexamethasone Corticosteroid InhibitcytochromeP450
Bromocriptine Dopamineagonist InhibitcytochromeP450
Cyclosporine/tacrolimus Immunosuppressant InhibitcytochromeP450
Ergotamine Alpha blocker InhibitcytochromeP450
Nifedipine Ca channel blocker InhibitcytochromeP450
Diltiazem Ca channel blocker InhibitcytochromeP450
Verapamil Ca channel blocker InhibitcytochromeP450
Cimetidine H2 blocker InhibitcytochromeP450
Omeprazole H/KATPaseblocker InhibitcytochromeP450
Increased Tacrolimus
Danazol Androgen ↑Renalimpairment
Grapefruitjuice InhibitintestinalcytochromeP450
Decreased Cyclosporine/Tacrolimus
Rifampin Antibiotic ↑CytochromeP450activity
Phenytoin Anticonvulsant ↑CytochromeP450activity
Phenobarbital Anticonvulsant ↑CytochromeP450activity
Decreased Cyclosporine
Sulfadimidine Antibiotic ↑CytochromeP450activity
Trimethoprim Antibiotic ↑CytochromeP450activity
Decreased Tacrolimus
Carbamazepine Anticonvulsant ↑CytochromeP450activity
Primidone Anticonvulsant ↑CytochromeP450activity
ATPase, Adenosine triphosphatase.
Adapted from Sandler NA, Braun TW: Current surgical management of the immunocompromised patient,
Oral Maxillofac Surg Clin North Am 10:445–455, 1998.
by which tacrolimus causes nephrotoxicity is related to an alteration of prostaglandin metabolism,
by inducing vasoconstriction, and reduction in renal blood flow and a resultant decreased glomerular
ltrationrate.Withtheadditionofanonsteroidalantiinammatorydrug(NSAID),therenalbloodow
canbecomeevenmoreimpaired.Therefore,theroutineprescriptionofNSAIDstopatientsontacrolimusshouldbeavoided.Drugsthatmayinducenephrotoxicityandcontributetorenalimpairment,
such as aminoglycosides, trimethoprim-sulfamethoxazole, amphotericin B, and acyclovir, also should
be avoided in patients who are taking tacrolimus.
38. Does tacrolimus interact with any drugs that are routinely used in oral and maxil-
lofacial surgery patients?
Yes.TacrolimusiseliminatedintheliverbycytochromeP450isoenzymesand,therefore,mayshow
a rise in concentration with the concomitant use of macrolide antibiotics, such as erythromycin
CHAPTER 22 THEIMMUNOCOMPROMISEDSURGICALPATIENT 239
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or clarithromycin, azole antifungal agents, or corticosteroids. Also, the antihistamines terfenadine
(Seldane) and astemizole (Hismanal) have been associated with cardiac arrhythmias after coadmin-
istrationwithtacrolimusorcyclosporine.ConcurrentuseofNSAIDsornephrotoxicantibioticsand
tacrolimus also increases the potential for nephrotoxicity.
39. What are the oral manifestations of GVHD in the transplant patient?
Theoralcavitycanbeaffected,alongwiththeliver,skin,andgastrointestinaltract.Morethan80%
ofpatientswithGVHDhaveorallesions,whichinmanycasesmaybetherstsymptom.Theclinical
presentationoforalGVHDresemblesthatofothercollagenvasculardiseases,suchassystemiclupus
erythematosus or lichen planus. The oral mucosa may show erythema, ulceration, white striations,
atrophy, or a pseudomembranous covering. Symptoms may range from mild discomfort to burning
andseverepainandsalivarydysfunction.GVHDistreatedbyaugmentingimmunosuppressivetherapy. Careful monitoring of the patient for signs of overimmunosuppression should also be performed
during this period.
40. What are the perioperative considerations of post-splenectomy patients?
Post-splenectomy patients have the potential to develop overwhelming sepsis with shock and dis-
seminatedintravascularcoagulation(DIC).Themostcommonorganismscausingsuchinfectionsare
Pneumococcus, Meningococcus, and Haemophilus. Therefore, before splenectomy, patients should
receive vaccination with pneumococcal polysaccharide. Prophylactic antibiotics should be given
beforesurgicalproceduresincontaminatedsites,suchastheoralcavity.Earlyaggressivetreatment
of infections in these patients is recommended.
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