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J Oral Maxillofac Surg68:195-200, 2010

Spontaneous Intraoral Hemorrhage asManifestation of Thoracoabdominal

Aortic Aneurysm-Associated DisseminatedIntravascular Coagulation: Case Report

and ReviewTomoaki Imai, DDS, PhD,* Masahiro Michizawa, DDS, PhD,†

Hidetaka Shimizu, DDS, PhD,‡ Yoshiaki Yura, DDS, PhD,§ and

Yasuji Doi, MD, PhD�

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ntraoral bleeding from the gingiva or alveolar mucosas a common symptom in dental and oral surgeryutpatients. The bleeding is relatively easy to controlith professional dental treatment, because it is al-ost always from local causes, such as inflammation

r application of extreme external force to the mu-osa. Occasionally, persistent or intermittent hemor-hage refractory to treatment indicates a general he-ostatic disturbance, including coagulation factor

eficiencies, fibrinolytic defects, and platelet or vas-ular disorders.1,2

Disseminated intravascular coagulation (DIC) is ancquired consumptive coagulopathy caused by vari-us underlying factors, including sepsis, trauma, ma-

ignant neoplasms, obstetric complications, severe he-atic failure, severe toxic or immunologic reactions,nd vascular abnormalities.3,4 In typical acute DIC

*Clinical Fellow, Department of Oral and Maxillofacial Surgery,

aiseikai Senri Hospital, Suita, Osaka, Japan.

†Head, Department of Oral and Maxillofacial Surgery, Saiseikai

enri Hospital, Suita, Osaka, Japan.

‡Assistant Professor, Department of Oral and Maxillofacial Sur-

ery II, Osaka University Graduate School of Dentistry, Suita, Osaka,

apan.

§Professor, Department of Oral and Maxillofacial Surgery II,

saka University Graduate School of Dentistry, Suita, Osaka, Japan.

�Head, Division of Cardiology, Department of Internal Medicine,

aiseikai Senri Hospital, Suita, Osaka, Japan.

Address correspondence and reprint requests to Dr Imai: De-

artment of Oral and Maxillofacial Surgery, Saiseikai Senri Hospital,

-1 Tsukumodai, Suita, Osaka 565-0862 Japan; e-mail: hsc12@

otmail.com

2010 American Association of Oral and Maxillofacial Surgeons

278-2391/10/6801-0032$36.00/0

aoi:10.1016/j.joms.2009.04.045

econdary to trauma or infection, multiple thrombire formed in the vascular system, often leading toultiple organ failure. Less commonly, DIC can stem

rom a chronic progressive disease, such as certainypes of malignant neoplasms or vascular disorders,nd usually remains in a chronic compensated state.3

n vascular disorders, such as aortic aneurysm (AA),he coagulation cascade is locally activated, occasion-lly resulting in the local consumption of platelets andoagulation factors with systemic hyperfibrinolysis, inurn contributing to a predominant hemorrhagic ten-ency.3,5,6

Fine et al7 reported the first case of AA-induced DICn 1967, and several investigators have since identi-ed a clinically overt form of DIC.6,8,9 However, littleention has been made in published reports from an

ral surgery viewpoint regarding chronic DIC, partic-larly DIC secondary to AA10,11 and its management.e describe an unusual case of spontaneous intraoral

emorrhage as a manifestation of thoracoabdominal AA-ssociated DIC and review the published reports of DICases concerning oral and maxillofacial surgery.

eport of a Case

In 2003, an elderly man had undergone extraction of theight upper first and second premolars by a private dentalractitioner. Although he experienced no postextractionemorrhage, he subsequently experienced slight, occa-ional bleeding from the surgery site after eating or brush-ng. In 2007, on noticing a small amount of accumulatedlood in his mouth, the 88-year-old man attended Saiseikaienri Hospital reporting hemorrhage from the dental alve-lus. The patient had a history of gastric ulcers, benignrostatic hyperplasia, and brain infarction with administra-ion of aspirin and had been diagnosed with thoracoabdomi-al AA 3 years previously that was under conservative man-

gement by an internalist.

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On examination, the alveolar mucosa in the right upperremolars was found to have a small, nonhemorrhaging slitovered with a tiny clot. A dental x-ray revealed submucosalequestra in the premolars (Fig 1). The patient was sched-led for medical consultation with the attending physiciano address removal of the sequestra. Two days later, theatient revisited our hospital with persistent hemorrhagend reported difficulty eating and fatigue (Fig 2). The bleed-ng site was sutured with the patient under local anesthesiand covered with an absorbable oxycellulose dressing totaunch the blood flow. The patient was afebrile, and themergency laboratory tests showed a platelet count of5,000/�L, prothrombin time-international normalized ratiof 2.44, fibrinogen of 33 mg/dL, and D-dimer level of 25g/mL (Table 1). A previous blood test administered ap-roximately 1 year earlier had revealed a platelet count of27,000/�L and D-dimer level of 21 �g/mL. These findingsere suggestive of chronic consumptive coagulopathy.

IGURE 1. Dental x-ray with submucosal sequestra (arrows) sub-equent to dental extraction.

mai et al. Spontaneous Intraoral Hemorrhage. J Oral Maxillofacurg 2010.

IGURE 2. Intraoral appearance of patient on admission showingersistent hemorrhage from alveolar slit.

emai et al. Spontaneous Intraoral Hemorrhage. J Oral Maxillofacurg 2010.

The patient was admitted for observation of the oralleeding, additional investigation into the cause of the co-gulopathy, and correction of the poor feeding condition. Ahest x-ray showed clear lung fields and the abnormal con-our of a tortuous aorta. The electrocardiographic findingsere normal, but computed tomography of the chest, ab-omen, and pelvis showed extensive aneurysmal dilation ofhe thoracic and abdominal aorta. The greatest dimension ofhe aneurysm was 46 mm, an increase from the previouseasurement 2 years earlier, and extending downward as

ar as the bifurcation of the common iliac arteries (Fig 3).dditionally, ultrasound abdominal images showed an inti-al flap in the abdominal aorta. No evidence of any abnor-al mass formation or sign of infection was seen on com-uted tomography. The echocardiographic findings ruledut endocarditis, intracardiac tumor, and thrombi. Fromhese findings, the patient was diagnosed by a cardiolo-ist as having thoracoabdominal AA complicated by acute

Table 1. LABORATORY DATA ON ADMISSION ANDAT DISCHARGE AFTER 3 MONTHS

Examination

Admission(July 5,2007)

After Discharge(December 10,

2007)NormalRange

omplete bloodcell count

WBC (�103/�L) 8.3 5.5 4.0-8.0RBC (�106/�L) 2.38 3.20 4.0-5.5Hematocrit (%) 23.5 31.2 40-50Hemoglobin

(g/dL) 7.8 10.3 13.0-16.0Platelets

(�104/�L) 5.5 17.2 15.0-36.0lood chemistryAST (U/L) 14 15 8-37ALT (U/L) 11 7 0-39BUN (mg/dL) 74 22 9-20Creatine (mg/dL) 2.0 1.8 0.5-1.2Na (mEq/L) 140 139 138-146K (mEq/L) 4.6 4.1 3.8-5.1Antiplatelet

antibody Negative Negativeoagulation testsPT% 34 30 75-125PT-INR 2.17 2.38 0.80-1.20aPTT (s) 37 25-45Fbg (mg/dL) 34 300 200-450FDP (�g/mL) 75 �5.0D-dimer (�g/mL) 24.5 7.5 �1.0�2-PI (%) 38 82 80-125Plasminogen (%) 65 75-125AT-III (%) 69 75-125

Abbreviations: WBC, white blood cell (count); RBC, redlood cell (count); AST, aspartate aminotransferase; ALT,lanine aminotransferase; BUN, blood urea nitrogen; PT%,rothrombin time activity; PT-INR, prothrombin time-

nternational normalized ratio; aPTT, activated partialhromboplastin time; Fbg, fibrinogen; FDP, fibrin/fibrino-en degradation products; �2-PI, �2-plasmin inhibitor; AT,ntithrombin.

mai et al. Spontaneous Intraoral Hemorrhage. J Oral Maxillofacurg 2010.

xacerbation of chronic DIC. The patient was adminis-

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IMAI ET AL 197

ered continuous intravenous 1.0 g gabexate mesilateaily (Fig 4).On the third day of hospitalization, the patient had de-

eloped ecchymoma on the extremities (Fig 5), and the

IGURE 3. Plain axial computed tomography scan showing A,hest and B, abdomen. Arrows indicate aneurysmal dilations.

mai et al. Spontaneous Intraoral Hemorrhage. J Oral Maxillofacurg 2010.

IGURE 4. Clinical course during hospitalization. On improvemeabexate mesilate, sequestra were removed, and administration whowed temporary deterioration in DIC, DIC was eventually contrabexate mesilate 1.0 g daily, camostat mesilate 600 mg daily, ted blood cell concentrate in a mannitol-adenine-phosphate solutio

mai et al. Spontaneous Intraoral Hemorrhage. J Oral Maxillofac Surg

ntraoral bleeding had stopped completely. The hemoglo-in count had decreased to 6.3 g/dL owing to hemorrhagicnemia and the dilution effect from fluid administration.he patient developed postexertional fatigue and was ad-inistered a blood transfusion of 2 U of red blood cell

oncentrate in a mannitol-adenine-phosphate solution onay 5. On day 11, the hemoglobin, platelet count, androthrombin time-international normalized ratio had im-roved to 8.3 g/dL, 99,000/�L, and 1.33, respectively. Theubmucosal sequestera, the source of the intraoral bleeding,ere surgically removed with the patient under local anes-

hesia, filled with oxycellulose, and sutured. A surgicalplint was applied to cover the hard palate and wound, andomplete hemostasis was attained after 3 days.A cardiovascular surgeon considered surgery to repair the

A; however, owing to the patient’s uncontrollable hemor-hagic tendency, cerebrovascular complications, and im-

IC with continuous intravenous administration of protein inhibitor,hed to oral camostat mesilate. Although hematologic examinationith additional orally administered warfarin and tranexamic acid:mic acid 750 mg daily. Fbg, fibrinogen; PLT, platelet; RCC-MAP,v., drip of intravenous; p.o., by mouth.

FIGURE 5. Ecchymoma of anterior surface of leg.

mai et al. Spontaneous Intraoral Hemorrhage. J Oral Maxillofacurg 2010.

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198 SPONTANEOUS INTRAORAL HEMORRHAGE

aired renal function (creatinine clearance 21 mL/min),onsurgical medication therapy was prescribed. On day 19,he continuous administration of gabexate mesilate washanged to peroral administration of camostat mesilate at00 mg daily. However, hematologic examination revealedeterioration of the DIC, characterized by a decrease in thelatelet count and fibrinogen levels and an increase in the-dimer level. Warfarin and tranexamic acid were then orallydministered from day 32 and day 45, respectively, with im-rovement in coagulation and the fibrinolytic system. Warfarinas administered at a low starting dose of 1.0 mg, with a

radual increase to 3.0 mg. The lack of hemorrhage in thepper and lower gastrointestinal tract was confirmed by en-oscopy, and the patient was discharged on day 60.At 3 months after discharge, the private dental practi-

ioner attending the patient recommended the upper leftrst premolar be extracted owing to progressive periodon-itis. Hematologic tests showed that the ongoing oral ad-inistration of anticoagulant and antifibrinolytic drugs was

ffectively keeping the hemostatic system under controlTable 1); thus, the tooth was easily extracted, with no needor a dosage adjustment of the medication. The extractionpace was filled with oxycellulose, and complete hemosta-is was attained the same day without any complications.

iscussion

DIC ASSOCIATED WITH AORTIC ANEURYSM

The pathogenesis from local activation of coagula-ion system because of DIC has been reported toesult from multiple mechanisms. ten Cate et al5 de-cribed 3 mechanisms: activation of the intrinsic co-gulation system by subendothelial tissues; activationf the extrinsic pathway by thromboplastic tissue fromhe aortic wall; and hyperfibrinolysis triggered by theelease of fibrinolytic activators. Furthermore, inflamma-ory cells recruited to the aortic wall because of athero-clerosis have been shown to release various kinds ofytokines (interleukin [IL]-1�, IL-2, IL-4, IL-6, IL-10,umor necrosis factor-�, and tissue factor), some ofhich can induce systemic coagulation and fibrinoly-

is.12 These processes develop continuously or inter-ittently and can lead to chronic DIC in a compen-

ated state, in which the compensatory mechanismsf the liver and bone marrow function successfully.bout 0.5% to 4% of patients with AA have clinicallyvert DIC with hemorrhagic complications.3,8 Jelen-ka13 reported that overt DIC seems to be more fre-uent in patients with thoracoabdominal AA than inhose with abdominal AA.

DIC can be diagnosed from the laboratory findingsombined with knowledge of the underlying disease.3,4

he most frequent and elemental changes broughtbout by DIC are thrombocytopenia, increased fibrino-en degradation product levels, and consumption ofoagulation factors (prothrombin time, activated partialhromboplastin time, thromboplastin time). Further-ore, measurement of D-dimers, antithrombin-III, plas-

inogen, and �2-antiplasmin activity can be confirma- a

ory if the screening hematologic examination findingsuggest previous evidence of DIC.3,4,6 In addition to thelinical symptoms and laboratory evidence for DIC,iebert and Natelson14 advocated that confirmation re-uires correction of hemostatic abnormalities by suc-essfully repairing the AA. However, adequate evalu-tion of an inoperable case, such as in the presentatient, is impossible. We thus eliminated the possi-ility of another underlying disease causing the DIChrough various examinations and concluded that theatient had a collapsed state of compensated DICgainst AA.

Definitive treatment of DIC requires correction ofhe causative underlying disorder.3,4 No widely ac-epted optimal therapeutic guideline is available, par-icularly pertaining to supportive treatment.6 An indi-idualized therapeutic modality should thus beetermined by closely monitoring the clinical condi-ion and hemostasis, in line with the patient’s wishes,articularly in patients with chronic disease, theealth care system, and the current social conditions.urgery is the most effective treatment for AA-inducedIC after optimization of the patient’s general conditionith blood transfusion or administration of anticoagu-

ant agents such as heparin.9 Because of his high-riskrofile, our present patient was not a candidate forurgical intervention and instead received only pharma-ologic treatment. Synthetic protease inhibitors such asabexate mesilate with the properties of antiplasminnd antithrombin activity are widely prescribed for bothcute and chronic DIC in Japan.15,16 Protease inhibitorsave the advantage of not requiring antithrombin-III forctivity, which heparin does. With regard to patientobility, subcutaneously applied low-molecular-weighteparin17 and warfarin18 do not restrict patient move-ent; however, unfractionated heparin and gabexateesilate are given by continuous infusion and, thus, do

estrict movement.19 Successful treatment of AA-in-uced DIC by systemic administration of tranexamiccid, a major antifibrinolytic agent, in conjunction withnticoagulant drugs has also been reported.20,21 How-ver, the possibility of thrombotic complications on clotissolution has called the clinical efficacy and safety ofranexamic acid into question.9

The improvement seen in our patient’s DIC withntravenous administration of gabexate mesilatetopped when the administration was switched toral camostat mesilate and the condition tended to-ard regression. Considering both the intestinal ab-

orption efficiency and the bioavailability of the drugith oral administration, as well as the decrease inosage of the protease inhibitor, the regression ap-eared to result from a lower therapeutic dosage withhe oral form. Rather than escalating the dose of theame agent in monotherapy, however, we elected to

dminister another drug with a different mechanism

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f action (warfarin and tranexamic acid). The DICas controlled with orally administered agents, sug-

esting a convenient and affordable approach toong-term outpatient management of inoperablehronic DIC. In patients in whom oral treatmentroves ineffective, other anticoagulant agents suchs low-molecular-weight heparin17,19 or danaparoidodium,21 a mixture of sulfated glycosaminogly-ans, might be considered.

DIC IN RELATION TO ORAL ANDMAXILLOFACIAL SURGERY

A few DIC cases pertaining to oral and maxillo-acial surgery have been reported in English studiesTable 2).10,11,22-36 The most prevalent underlyingisease was prostate carcinoma (5 cases), known toe an insidious tumor. The tumor tissue releases ahromboplastic substance that provokes hyperfibri-olysis, with an increased risk of persistent hemor-hage.37 DIC derived from vascular abnormalities andbruption also has a high tendency to display hemor-hage as a primary symptom. This characteristic dis-inguishes this DIC from DIC secondary to otherolid neoplasms or sepsis, which are usually asso-iated with predominant thrombotic phenomena.3

hemorrhagic manifestation might be the onlynitial clinical marker of deteriorating compensatedIC rather than of typical acute DIC. To our knowl-dge, the present case is the first report of sponta-eous intraoral hemorrhage directly resulting in a

Table 2. DIC RELEVANT TO ORAL AND MAXILLOFACIAL

Causative Underlying Disease C

Malignancy (prostate cancer) Falace et al,McKechnie,CatramboneMcLoughlinSawaki et al

Vascular disorderKTW syndrome Ita et al,27 2Aortic aneurysm Herold et al

Peters et al,Obstetrics

Abruption Samman,28

SepticemiaSubmandibular abscess Rawson et aInfection in maxillary cancer Saito et al,31

Alveolar abscess Currie et al,Parotitis Mehra et al,

None Marshall etChristiansenCho et al,36

Vascular disorderAortic aneurysm Present case

bbreviation: KTW, Klippel-Trenaunay-Weber.

mai et al. Spontaneous Intraoral Hemorrhage. J Oral Maxillofac Surg

ubsequent diagnosis of DIC, because the previ-usly reported cases were diagnosed in the wake ofersistent hemorrhage after therapeutic interventionr trauma10,11,22-28,33-36 or were recognized by systemicymptoms such as hypoxia, hypotension, or pyrexiaith rigor in acute DIC with or without hemor-

hage.29-32 Given that the underlying AA in our patientas inoperable and remained as the cause of chronicIC, surgical intervention to remove the sequestra, inonjunction with improvement of the DIC in ad-ance, was valuable, because it precluded the possi-ility of recurrent oral bleeding.Localized triggering events that injure tissue and

esult in the overactivation of systemic fibrinolysisould exacerbate compensated DIC to decompen-ated DIC, particularly in already compromised pa-ients.38 Furthermore, Marshall et al34 reported aatal case of DIC developing after dental extractionespite the absence of an underlying disease. Thisase was attributed to a generalized Schwartzmaneaction inducing fatal disordered coagulation. Al-hough the present case had no clear precipitatingvent, we believe the etiology was as follows: theesidual sequestra under the alveolar mucosaaused chronic inflammation, resulting in a local-zed tendency to bleeding, and constant abrasion ofhe mucosa by the denture, compounded by inef-ective oral hygiene. The extensive and steadilyxpanding thoracoabdominal AA created potentialisks because of imbalanced coagulation, and this,

ERY

Local Hemorrhagic Trigger in Oraland Maxillofacial Area

6 Dental extraction9 Dental extraction

24 1990 Preauricular biopsy5 1994 Facial injury9 Dental extraction

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200 SPONTANEOUS INTRAORAL HEMORRHAGE

ombined with the spontaneous bleeding of thelveolar mucosa, however slight or temporary itight have been, resulted in intermittent bleeding,

esulting in a loss of appetite and exacerbating theatient’s general condition, with compromised re-al function and a lapse into clinically overt DICith continuous intraoral hemorrhage.With the steady aging of the population world-ide, the increase in the number of patients withrostate cancer and aneurysms is likely to continue.his, in turn, will produce an increasing numberf patients with underlying DIC. Oral surgeonshould ensure they are equipped to properly diag-ose the oral manifestation of chronic DIC11 andre attentive to the possibility that even minorurgery can predispose these patients to develop-ng decompensated DIC.38 In the present patient,ental extraction was performed 3 months after dis-harge without any complications using long-term ad-inistration of anticoagulant and antifibrinolytic agents

o maintain control of the hemostatic conditions. Closengoing cooperation with hematologists and special-sts in internal medicine will allow the developmentf systemic and topical prophylactic strategies toinimize the postoperative complications associ-

ted with chronic DIC.

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