Case Report: Hemorrhage After Dental Extractions PDF

LIEBERMAN ET AL 2311
16. Spaulding WB: Methyltestosterone therapy for hereditary epi- 20. Pickering RJ, Good RA, Kelly JR, et al: Replacement therapy in
sodic edema (hereditary angioneurotic edema). Ann Intern hereditary angioedema. Successful treatment of two patients
Med 53:739, 1960 with fresh frozen plasma. Lancet 1:326, 1969
17. Gelfand JA, Sherins RJ, Alling DW, et al: Treatment of heredi- 21. Longhurst HJ: Emergency treatment of acute attacks in hered-
tary angioedema with danazol. Reversal of clinical and bio- itary angioedema due to C1 inhibitor deficiency: What is the
chemical abnormalities. N Engl J Med 295:1444, 1976 evidence? Int J Clin Pract 59:594, 2005
18. Leimbruger A, Jaques WA, Spaeth RJ: Hereditary angioedema 22. Moore GP, Hurley WT, Pace SA: Hereditary angioedema. Ann
uncomplicated maxillofacial surgery using short-term C1 inhibitor Emerg Med 17:1082, 1988
replacement therapy. Int Arch Allergy Immunol 101:107, 1993 23. Chiu AG, Newkirk KA, Davidson BJ, et al: Angiotensin-convert-
19. Jaffe CJ, Atkinson JP, Gelf JA, et al: Hereditary angioedema: The ing enzyme inhibitor-induced angioedema: A multicenter re-
use of fresh frozen plasma for prophylaxis in patients under- view and an algorithm for airway management. Ann Otol Rhi-
going oral surgery. J Allergy Clin Immunol 55:386, 1975 nol Laryngol 110:834, 2001
J Oral Maxillofac Surg

68:2311-2319, 2010
Control of Life-Threatening Head and

Neck Hemorrhage After Dental
Extractions: A Case Report
Benn Larkin Lieberman, DMD,* Michelle K. Kennedy, DMD,†
Dorothy R. Lorenzo, DMD,‡ Louis J. Reed, MD,§
Arthur K. Adamo, DDS,储 Vito A. Cardo, Jr, DDS,¶ and
Victor M. Badner, DMD, MPH**
Report of a Case patient denied taking any medications. He had no known

drug allergies but admitted to occasional alcohol use. He de-
A 54-year-old man presented to the North Central Bronx nied any drug or tobacco use on the medical intake question-
Hospital Dental Clinic (Bronx, NY) on October 30, 2007, naire and during the initial consultation. He noted a history of
with a complaint of pain in his right mandible. The patient’s bruising easily but reported having previous dental extractions
vital signs were unremarkable on presentation with a blood without incident. A panoramic radiograph (Fig 1) showed
pressure of 140/75 mm Hg and a pulse rate of 85 beats/min. multiple nonrestorable teeth (maxillary right third molar, max-
The patient reported having a stroke 10 years previously illary right first premolar, maxillary right canine, maxillary left
that was managed with aspirin therapy for 7 years. The second premolar, maxillary left first molar, mandibular left first
premolar, mandibular right second molar, and mandibular
right third molar) with bone loss consistent with generalized
Received from North Bronx Healthcare Network, Bronx, NY. periodontal disease. Clinical examination showed gross caries
and gross mobility of the maxillary right third molar, maxillary
*Director of Oral and Maxillofacial Surgery, North Central Bronx
right first premolar, maxillary right canine, maxillary left sec-
Hospital. ond premolar, maxillary left first molar, mandibular right sec-
†Former Resident; Currently, Attending, Oral and Maxillofacial ond molar and mandibular right third molar, as well as a
Surgery, Brookdale University Hospital. fractured crown and an exposed endodontic metal post in the
‡Chief Resident, Oral and Maxillofacial Surgery, Brookdale Uni-
versity Hospital.
§Associate Visiting Physician, Division of Hematology/Oncology,
Department of Medicine.
储Director, Oral and Maxillofacial Surgery.
¶Director, Oral and Maxillofacial Surgery, Brookdale Universtiy
Hospital; Former Chairman, Caritas Hospital.
**Chairman, Department of Dentistry/Oral and Maxillofacial
Surgery.
Address correspondence and reprint requests to Dr Lieberman:
North Bronx Healthcare Network, 1400 Pelham Pkwy S, Bldg 1,
Room 3N34, Bronx, NY 10461; e-mail: benn.lieberman@nbhn.net FIGURE 1. Preoperative panoramic radiograph (October 30,
© 2010 American Association of Oral and Maxillofacial Surgeons 2007).
0278-2391/10/6809-0040$36.00/0 Lieberman et al. Hemorrhage After Dental Extraction. J Oral
doi:10.1016/j.joms.2010.02.020 Maxillofac Surg 2010.
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2312 HEMORRHAGE AFTER DENTAL EXTRACTION
root of the mandibular left first premolar. The mandibular right extended to the patient’s right buccal and right submandib-
second and third molars were painful on palpation. ular spaces. Concurrently, the patient continued to have
After the radiographic and intraoral examination, at ap- oozing intraorally from both the left and right extraction
proximately 2:30 PM, informed consent was obtained for sites. At this time, the patient was sedated with propofol,
extraction of the mandibular left first premolar and mandi- and the airway was secured with an oral endotracheal tube.
bular right second and third molars. Approximately 7.2 mL It was estimated that the patient lost 500 mL of blood before
of 2% lidocaine with 1:100,000 epinephrine was adminis- intubation. The intubation was performed approximately 3
tered, and the mandibular right second and third molars hours after his extractions were completed.
were extracted with minimal force or disturbance of the The patient’s sister, who accompanied him to the oral
surrounding tissues by use of an elevator and forceps. The surgery clinic that afternoon, was consulted regarding her
surrounding granulation tissue was removed with a curette, brother’s medical history. Although she was not aware of
and gauze was packed over the extraction sites. Attention any pre-existing medical condition, she reported that her
was then drawn to the mandibular left first premolar. A brother had been an alcoholic for many years and, to her
full-thickness mucoperiosteal flap was reflected, and the knowledge, was not under the care of any physician.
tooth was extracted with the assistance of a surgical hand- Baseline laboratory values obtained in the ED showed a
piece. platelet count of 21,000/mm3 (normal range, 150-450,000/
It was noted after the extractions that the patient had mm3), hemoglobin level of 10.1 g/dL (normal range, 3.5-
persistent oozing from the posterior sites. The patient’s 17.5 g/dL), and hematocrit level of 30% (normal range,
medical history was reviewed again, but he did not disclose 41%-53%). In addition, liver function enzyme tests showed
any further information. On removal of the gauze, persistent an aspartate aminotransferase level of 308 U/L (normal
oozing of the extraction sites was seen. No pulsatile bleed- range, 8-20 U/L), alanine transferase level of 86 U/L (normal
ing was noted. The mandibular left first premolar extraction range, 0-35 U/L), alkaline phosphatase level of 141 U/L
site was also seen to be oozing unusually. Absorbable gela- (normal range, 20-70 U/L), and total bilirubin level of 2.0
tin powder (Gelfoam; Pharmacia, Kalamazoo, MI) was ini- mg/dL (normal, ⬍1 mg/dL). The decision was made to
tially placed into the sockets of the mandibular left first transfer the patient to the medical intensive care unit
premolar and mandibular right second and third molars to (MICU) for observation and hematologic evaluation. Before
attempt hemorrhage control. Gauze was then placed over admission to the MICU, the patient was transfused with 3 U
the sites and held firmly in place. This did not control the of pooled platelets and 2 U of fresh-frozen plasma (FFP).
bleeding. Oxidized regenerated cellulose (Surgicel; Ethicon, Ten milligrams of vitamin K were administered intramuscu-
Somerville, NJ) was then introduced into the sockets with larly. On admission to the MICU, the patient’s physical
gauze pressure over the sockets. The bleeding persisted, examination (with the exception of his head and neck
and microfibrillar collagen hemostat (Avitene; Davol, Cran- examination) was unremarkable. No hepatosplenomegaly
ston, RI) was obtained and placed into the sockets with was appreciated. His abdomen was soft and slightly dis-
placement of gauze soaked with topical thrombin of bovine tended, with no rebound or shifting dullness. His pulmo-
origin (Thrombin-JMI; GenTrac, Middletown, WI) over the nary and cardiovascular examinations were also normal.
sockets. This was removed temporarily to facilitate place- Overnight in the MICU, an additional 5 U of platelets, 4 U
ment of multiple sutures to obtain primary closure. of FFP, and 25 ␮g of desmopressin (DDAVP; Sinopep Phar-
During the course of this treatment, the patient ingested maceutical, Hangzhou, China) IV soluset were adminis-
blood, causing gastrointestinal distress. This resulted in an tered. Steroids were considered, but they were not admin-
episode of emesis. Monitors were applied to the patient to istered because they are only useful in cases of autoimmune
obtain a second set of vital signs. The blood pressure was splenic sequestration and do not have a role in alcohol-
recorded as 140/83 mm Hg with a heart rate of 81 beats/ induced sequestration. Piperacillin-tazobactam (Zosyn; Pfizer,
min. New York, NY) and vancomycin (Vancocin; Alpharma Phar-
Despite aggressive local measures, the slow oozing con- maceutical, Fort Lee, NJ) antibiotic therapy was initiated for
tinued. It was then decided to transport the patient to the pulmonary coverage and for potential infection of a hema-
emergency department (ED), where laboratory values could toma. Vital signs on admission to the MICU and for the next 24
be obtained and appropriate medical management could be hours were documented closely and are shown in Table 1.
instituted because a significant bleeding diathesis was sus- Despite these various pharmacologic coagulation and he-
pected. Shortly after the patient’s arrival in the ED, it was mostatic efforts, the patient continued to exhibit persistent
observed that the bleeding was causing elevation of the oozing from the extraction sites. He subsequently lost an
floor of the mouth. Because of the threat to the patient’s estimated 1,500 mL of blood in the following 12 hours. In
airway, anesthesiology was consulted. consultation with the hematology team, additional rounds
Members of the oral and maxillofacial surgery, anesthesi- of FFP, packed red blood cells (PRBCs), DDAVP, and plate-
ology, and emergency medicine teams agreed that the pa- lets were administered. Embolization of the bleeding was
tient should be intubated prophylactically for airway con- considered not to be an option because of the medical
trol. Before intubation, it was also noted that the edema had nature of the bleed. Aminocaproic acid (EACA) (Amicar;
Table 1. HEMODYNAMIC PARAMETERS (START TIME, OCTOBER 30, 6 PM)
1h 4h 8h 12 h 16 h 20 h 24 h 24-h Range
Blood pressure (mm Hg) 136/86 123/68 122/78 127/80 113/80 103/59 166/90 103-166/59-90
Heart rate (beats/min) 128 122 129 130 143 133 123 122-143
Temperature (°F) 101.6 103.2 101.8 100.9 101.5 101.8 101.3 100.9-103.2
Lieberman et al. Hemorrhage After Dental Extraction. J Oral Maxillofac Surg 2010.
Table 2. FLUIDS GAINED AND LOST (START TIME, OCTOBER 30, 6 PM)
1h 4h 8h 12 h 16 h 20 h 24 h 24-h Totals
Fluids 600 mL 600 mL 600 mL 600 mL 200 mL dextrose 200 mL dextrose 200 mL dextrose 3,150 mL
normal normal normal normal 5% in water 5% in water 5% in water normal
saline saline saline saline (50 mL/h) (50 mL/h) (50 mL/h) saline
(bolus) (150 mL/h) (150 mL/h) (150 mL/h) 250 mL normal 300 mL 200 mL 600 mL
saline / normal saline / normal saline / dextrose
aminocaproic aminocaproic aminocaproic 5% in
acid (bolus) acid acid water
(50 mL/h) (50 mL/h)
Blood 1,900 mL 2,050 mL 3,300 mL 7,250 mL
products
Urine output Not measured 260 mL initial ⬃50 mL/h ⬃38 mL/h ⬃30 mL/h ⬃25 mL/h ⬃37 mL/h 1,050 mL
Foley
output
Blood loss ⬃500 mL Not measured Not measured 1,500 mL Not measured Not measured 1,500 mL ⬃3,500 mL
Pfizer) was introduced as both a systemic and topical anti- goals (Table 5). The patient’s vital signs were labile (Table
fibrinolytic agent. The patient was administered an initial 2), and he exhibited severe cervicofacial edema and ana-
bolus dose of 4 g and received an additional 10 g of EACA sarca (a generalized infiltration of edema fluid into subcu-
infused over a period of 10 hours. Topically, gauze soaked taneous connective tissue) that confined him to intubation
with 5 g of EACA was placed at the extraction sites. in the MICU. A series of failed cuff-leak tests and computed
Over the course of 24 hours, the patient’s condition was tomography scans of the patient’s airway clearly showed
extremely guarded because of the onset of hypovolemic the severity of edema (Fig 4). A repeat computed tomogra-
shock. The patient exhibited a steady decrease in urine phy scan was completed before extubation (Fig 5). After 13
output and blood pressure, as well as a corresponding days, there was a clinical and radiographic decrease in
elevation in heart rate (Tables 1, 2). The patient was febrile upper airway edema, and the patient was extubated with-
throughout the night and had a maximum temperature of out complication on November 12, 2007, in the presence of
103.2°F. Despite aggressive replacement therapy, the pa- members of the respiratory, anesthesia, MICU, otolaryngol-
tient’s complete blood count showed little improvement ogy, and oral and maxillofacial surgery teams. The patient
because of the ongoing bleeding and the apparent splenic
was transferred from the MICU to the medicine service for
sequestration of platelets (Table 3). Compounding the pa-
further observation and management (Figs 6, 7).
tient’s deteriorating physiologic state, the extraction site
The patient was ultimately diagnosed with ethanol-in-
continued to ooze throughout the night. An estimated total
of 3,500 mL of blood loss was recorded over the 24-hour duced cirrhosis and secondary factor VII deficiency. The
period after extractions. results of hepatic viral tests did not indicate a significant
Twenty-four hours after the extractions, there was no role for active viral infection in the patient’s thrombocyto-
alleviation of the intraoral bleeding. The hematology team penia or liver dysfunction: hepatitis C, nonreactive; hepati-
recommended the use of recombinant factor VIIa (rFVIIa), tis B surface antigen, nonreactive; hepatitis B surface anti-
which was administered at a dose of 30 ␮g/kg. After the body, reactive (⬎10 IU/mL); hepatitis A antibody
administration of rFVIIa, the patient showed a substantial immunoglobulin, reactive; and hepatitis A antibody immu-
decrease in intraoral oozing and hemostasis was achieved noglobulin, nonreactive.
(Figs 2, 3). The first 24 hours’ transfusions are documented The patient was discharged from the hospital 34 days
in Table 4. postoperatively in stable condition with furosemide (Lasix;
The patient’s condition remained guarded as a result of DAVA Pharmaceuticals, Fort Lee, NJ) therapy and a daily
the physiologic sequelae of distributive shock, and further vitamin regimen including a multivitamin, folic acid, and
transfusions were administered in an attempt to meet target thiamine.
Table 3. COMPLETE BLOOD COUNT AND COAGULATION VALUES—FIRST 24 HOURS (START TIME, OCTOBER 30,
6 PM)
October 30: October 30: October 31: October 31: 18-24 h

0-6 h 6-12 h 12-18 h (After Factor rVIIa Administration)
Platelets 21 66 88 64
Hemoglobin 10.1 9.4 6.4 6.5
Hematocrit 30 27.3 18.7 19.1
White blood cells 4.8 6.4 6.8 2.4
Fibrinogen 173 157.6
Prothrombin time 15.3 14.7 14.0 9.9
International Normalized Ratio 1.52 1.45 1.38 0.94
Partial thromboplastin time 28.7 28.7 25.0 31.0
function are among the most commonly observed in

the alcoholic patient. Thrombocytopenia develops as
a combined result of bone marrow depression and
hypersplenism. Coagulopathies develop because of
impaired vitamin K absorption, thereby affecting the
synthesis of clotting factors II, VII, IX, and X.2 In fact,
factor VII plasma levels are among the first of the
coagulation factors to plummet in liver disease be-
cause of their short half-life of 3 to 6 hours.3
Although none was observed on examination, co-
agulation disorders may present themselves within
the oral cavity. Oral manifestations include oral mu-
cosal petechiae, hematoma, gingival bleeding, gingi-
val jaundice, and glossitis.1 In retrospect, if the pa-
tient had given a more accurate medical history, we
FIGURE 2. Post-intubation photograph (October 31, 2007). Note
severe facial swelling.
may have identified him as an alcoholic, therefore
altering the course of treatment. He acknowledged a
Lieberman et al. Hemorrhage After Dental Extraction. J Oral
Maxillofac Surg 2010. history of social drinking of 2 to 3 drinks per week
with no associated medical complications. A CAGE
(criticized, annoyed, guilty, eye-opener) question-
naire (Table 7) may have elicited a different response
As of April 2009, the patient continues to be followed up
by the hematology, medicine, and oral and maxillofacial
from the patient. Once a clear history of alcoholism is
surgery clinics on an outpatient basis. It should be noted established, the Child-Pugh classification (Tables 8, 9)
that he no longer abuses alcohol and is in stable physical may be used to determine the severity of liver disease
condition (Fig 8). As a result, his laboratory values have and life expectancy.
shown a considerable improvement in terms of hepatic Dental and surgical management of a known
function and hematologic parameters (Table 6). The patient
is scheduled to undergo additional extractions of his re-
alcoholic or a patient with liver disease should in-
maining nonrestorable teeth in the operating room under clude a thorough medical and dental survey. Specifi-
general anesthesia with rFVIIa on standby. cally, one should investigate for hepatitis, jaundice,
human immunodeficiency virus/acquired immunode-
ficiency syndrome, family history, medications, alco-
Discussion
Alcoholism can result in deleterious multiorgan sys-
tem disorders such as central nervous system defects,
hepatitis, cirrhosis, and coagulopathies. In our case re-
port of a patient with unidentified alcoholism with alco-
hol-induced liver hepatitis, occult coagulation disorders
led to a near-fatal intraoral hemorrhage after multiple
tooth extractions. This life-threatening bleed resulted in
prophylactic intubation and MICU admission of the pa-
tient during which time a variety of pharmacologic
agents and blood products were administered.
As exhibited in this case report, the physiologic
manifestations of chronic alcohol consumption can
cause detrimental effects on multiple major organ
systems. In the case of our patient, alcoholic liver
disease resulted in thrombocytopenia and a relative
factor VII deficiency.
Clinical manifestations of hepatitis and cirrhosis in-
clude malaise, jaundice, and portal hypertension. Result-
ant laboratory values include elevated transaminase
(alanine transferase/aspartate aminotransferase), el-
evated bilirubin, and decreased albumin levels. Al-
cohol reduces the intestinal absorption of glucose FIGURE 3. Photograph from November 2, 2007.
and vitamins, resulting in nutritional deficiencies and Lieberman et al. Hemorrhage After Dental Extraction. J Oral
hematologic disorders.1 Disorders of hematologic Maxillofac Surg 2010.
Table 4. BLOOD PRODUCTS AND PROCOAGULANTS ADMINISTERED—FIRST 24 HOURS (START TIME, OCTOBER 30,
6 PM)
October 30, October 31, Wednesday

Tuesday: 0-6 h 6-12 h 12-18 h 18-24 h 24-h Totals
FFP 2U 4U 6U 12 U
Pooled platelets 6U 2U 2U 10 U
Packed red blood cells 2U 4U 6U
DDAVP 25 ␮g 25 ␮g 50 ␮g
(desmopressin acetate)
Vitamin K 10 mg 5 mg IV 10 mg IV soluset 25 mg
intramuscular soluset
Amicar (EACA) 4 g IV soluset in 5 g IV soluset in 14 g systemic
250 mL normal 250 mL normal 10 g local/topical
saline (bolus) saline (1 g/h)
5 g IV soluset in Gauze soaked with
250 mL normal 5-g topical
saline (1 g/h) application
Gauze soaked with
5-g topical
application
rFVIIa 2.4 mg (30 ␮g/kg) 2.4 mg
Rho (D) immune 300 ␮g 300 ␮g
globulin
hol intake, recreational drug use, sexual history, and Platelet transfusion should be considered before
bleeding tendencies. Patient testing should include surgery in the thrombocytopenic patient. One unit of
complete blood count, prothrombin time, Interna- platelets yields an average increase of 5,000 to
tional Normalized Ratio, partial thromboplastin time, 8,000/␮L in 1 hour. Approximately one third of plate-
and liver function tests. Any abnormal values detected lets are sequestered in the spleen; therefore, the sur-
should be reviewed, and a primary care physician geon should be aware that patients with splenomeg-
should be consulted before any surgical treatment. A aly will sequester these transfused platelets more
platelet count of 100,000/␮L is desirable for major rapidly. Fifty-eight percent of platelet transfusions ad-
surgical procedures, and minor oral surgical proce- ministered to splenomegalic patients produce a cor-
dures may be performed with little risk with a platelet rected count increment of less than 7,500.4
count of 50,000/␮L.
Table 5. BLOOD PRODUCTS AND PROCOAGULANTS ADMINISTERED—HOSPITAL DAYS 3-7 (START DATE,
NOVEMBER 1)
November 1, November 2, November 3, November 4, November 5,

Thursday: 24-48 h Friday: 48-72 h Saturday Sunday Monday
FFP 2U 2U
Pooled platelets 1U 8U 1U
Packed red blood cells 1U
DDAVP
Vitamin K 10 mg 10 mg 10 mg 10 mg 10 mg
Amicar (EACA) 20 g IV soluset in 1 L 5 g IV soluset in
dextrose 5% in 500 mL dextrose
water (1 g/h) 5% in water (500
Gauze soaked with mg/h)
5-g topical Gauze soaked with
application 3 times 5-g topical
per day application 3
times per day
rFVIIa
Rho (D) immune globulin 300 ␮g
FIGURE 4. Computed tomography scan from November 5, 2007.

Note lack of air space around endotracheal tube.
FIGURE 6. Post-extubation extraoral photograph from November
16, 2007.
Maxillofac Surg 2010.
In cases in which platelet transfusion appears inade-
quate, systemic pharmacologic intervention may be nec-
essary. Recommended agents include DDAVP and lysine ulates the release of von Willebrand factor from plate-
analogs (EACA and tranexamic acid). DDAVP (desmo- lets. The recommended intravenous dose of desmopres-
pressin) is a synthetic analog of antidiuretic hormone sin to decrease bleeding time is 0.3 ␮g/kg. EACA and
that increases the plasma levels of factor VIII and stim- tranexamic acid are antifibrinolytics that inhibit plasmin-
ogen conversion to plasmin. Thus they prevent clot
lysis. The recommended loading dose of EACA is ap-
proximately 10 g, followed by a maintenance dose of 1
g/h. Tranexamic acid is approximately 10 times more
potent than EACA. The recommended loading dose of
tranexamic acid is also approximately 10 g, followed by
an infusion of 250 mg/h.5
FIGURE 5. Computed tomography scan from November 11,

2007. Note air space in vallecula and piriform sinuses around FIGURE 7. Post-extubation intraoral photograph from November
endotracheal tube. 16, 2007.
Lieberman et al. Hemorrhage After Dental Extraction. J Oral Lieberman et al. Hemorrhage After Dental Extraction. J Oral
Maxillofac Surg 2010. Maxillofac Surg 2010.
Table 7. CAGE (CRITICIZED, ANNOYED, GUILTY,

EYE-OPENER) QUESTIONNAIRE
Are you criticized about the amount of alcohol you

consume?
Are you annoyed or angered by this criticism?
Do you feel guilty about your drinking?
Do you need an “eye opener” in the morning to get you
going or to relieve a hangover?
the extrinsic pathway of the coagulation cascade on

the surface of activated platelets at the site of tissue
injury (NovoSeven package insert). NovoSeven was
initially developed for the treatment of bleeding in
patients with hemophilia who had antibodies inacti-
vating factor VIII or IX.6 Previous FVIII and FIX re-
placement therapies for patients with hemophilia A
and B resulted in the production of alloantibodies
(inhibitors), which rendered the therapy ineffective. It
was found that recombinant activated factor VII was
structurally similar to human plasma-derived factors VIII
and IX and showed an efficacy of 90% to 95% in
FIGURE 8. Five-month follow-up photograph from February 27,
2008. Note extreme change in facial form compared with Figure 2. the treatment of bleeding episodes in patients with con-
Lieberman et al. Hemorrhage After Dental Extraction. J Oral Max-
genital hemophilia without the production of alloanti-
illofac Surg 2010. bodies.7
Food and Drug Administration–approved usage
for rFVIIa is limited to the treatment and prophy-
In cases of acute hemorrhage in which local mea- laxis of bleeding episodes in patients with a known
sures failed to promote hemostasis, alternate methods hemophilia A or B inhibitor or deficiency. Anec-
of coagulation therapy have been suggested in dotal evidence and case reports have shown suc-
the literature. NovoSeven (Novo Nordisk, Princeton, cess in the treatment of life-threatening hemor-
NJ), a recombinant human coagulation factor VIIa rhage in patients with thrombocytopenia, trauma,
(rFVIIa), is a vitamin K– dependent glycoprotein struc- and liver disease.8 rFVIIa does not induce systemic
turally similar to human plasma-derived factors VIIa. It activation of the coagulation system and is not
is thought to promote local hemostasis by activating affected by circulating inhibitors, and its in vitro
Table 6. COMPLETE BLOOD COUNT, LIVER FUNCTION TESTS, AND COAGULATION VALUES
October 30, November 1, December 3, March 7, March 19,

2007: Admission 2007 2007: Discharge 2008: Follow-Up 2009
Platelets (/␮L) 21,000 13,000 72,000 87,000 108,000

Hemoglobin (g/dL) 10.1 8.8 9.9 13.1 15.0
Hematocrit (%) 30 24.7 29.2 36.6 44
White blood cells (/␮L) 4,800 4,300 9,800 5,900 5,800
Fibrinogen 173.0 Clotting 222.4
Prothrombin time 15.3 Clotting 19.7 13.5 12.3
International Normalized
Ratio 1.52 Clotting 2.01 1.32 1.21
Partial thromboplastin
time 28.7 Clotting 33.4 30.9 29.0
Aspartate aminotransferase 308 319 41 54 41
Alanine transferase 86 72 26 34 29
Total bilirubin 2.0 9.5 1.4 1.5 1.0
Albumin 2.3 2.1 2.0 3.4 4.0
Table 8. CHILD-PUGH CLASSIFICATION

of 8 patients who sustained blunt force trauma after
rFVIIa therapy and a substantial decrease in the
Points Assigned amount of transfused blood products as a result of the
Parameter 1 2 3 hemostasis.
The use of rFVIIa for the treatment of spontaneous
Ascites Absent Slight Moderate
or surgical bleeding has shown to be efficacious in
Bilirubin (mg/dL) ⬍2 2-3 ⬎3
Albumin (g/dL) ⬎3.5 2.8-3.5 ⬍2.8 obtaining hemostasis and decreasing the amount of
Prothrombin time blood products transfused in a number of case reports
Seconds over control 1-3 4-6 ⬎6 and clinical trials.13 It should be noted that dosages
INR ⬍1.8 1.8-2.3 ⬎2.3 and timing of administration are not standardized, and
Grades Grades
Encephalopathy None 1-2 3-4
off-label usage of this potent hemostatic agent should
be done with caution because detrimental thrombotic
Lieberman et al. Hemorrhage After Dental Extraction. J Oral events, though uncommon, can occur. In the case of
our patient, who had a persistent bleed after a routine
tooth extraction, recombinant FVIIa was used when
Table 9. CHILD-PUGH SURVIVAL
other local and systemic methods of hemostasis had
1-yr Patient 2-yr Patient failed.
Grade Points Survival (%) Survival (%) Off-label use of rFVIIa has grown extensively since
the original report of a nearly miraculous recovery of
A: Well-compensated
disease 5-6 100 85 a gunshot victim given rFVIIa after becoming coagu-
B: Significant lopathic.14 Indeed, a registry is now operational to
functional record the results of hemorrhage control using rFVIIa
compromise 7-9 80 60 off label.15 A number of randomized controlled trials
C: Decompensated have been carried out using rFVIIa or placebo in
disease 10-15 45 35
diverse coagulopathic patients without hemophilia. A
A total score of 5-6 is considered grade A (well-compensated meta-analysis of 22 such trials involving 3,184 patients
disease); 7-9 is grade B (significant functional compromise); showed that additional transfusions were significantly
and 10-15 is grade C (decompensated disease). These grades
correlate with 1- and 2-year patient survival.
less likely to be required in patients receiving rFVIIa
than those receiving placebo.16 However, use of
Maxillofac Surg 2010. rFVIIa in bleeding dental patients has seldom been
reported.
Life-threatening hemorrhage after a tooth extrac-
production eliminates the risk for transfusion infection is a rare and frightening event. The most effective
tion. These characteristics of rFVIIa make it an preparation for such a catastrophic event is preven-
appealing option for treatment of bleeding disor- tion. It may be necessary despite all attempts at
ders outside the realm of hemophilia.9 prevention to use alternate means to control such
The hypothetical interaction between platelets and bleeding. This may include both local and systemic
rFVIIa forms the basis of the therapeutic use of high- measures to achieve hemostasis.
dose factor VIIa in treating hemophilic patients with It is imperative to obtain a clear and comprehensive
inhibitory antibodies.10 High-dose factor VIIa has medical history on all patients who are to receive
been found to shorten the bleeding time in thrombo- surgical treatment. Vital signs should be recorded,
cytopenic patients who bleed despite receiving plate- and one must be able to recognize when a patient
let transfusions.11 Depending on the cause for the requires further preoperative testing. The risks and
thrombocytopenia, often a transfusion will increase benefits of more extensive preoperative testing
the quantity of platelets available to begin the hemo- should also always be considered. The urge to obtain
static process. In many cases of thrombocytopenia, screening-type preoperative tests must be tempered
however, the cause is splenic sequestration; transfu- by concerns about their sensitivity and specificity. In
sions will be ineffective or only partially effective in addition, crucial is the ability to sense a patient’s
overcoming this problem. In vitro evidence shows resistance to present a complete medical history, as
that rFVIIa increases thrombin generation on the ac- well as to be able to determine the safety of proceed-
tivated platelet surface and shortens the lag phase of ing with surgical treatment with the information at
further platelet activation.6 hand. In our case presentation, despite our patient’s
Several case reports exist showing success in reduc- severe coagulopathy, he did not manifest any overt
ing major blood loss in patients with trauma by ad- clinical signs or symptoms of liver disease.
ministering rFVIIa. Geeraedts et al12 report a com- The use of rFVIIa was initiated in this case after all
plete cessation of uncontrollable hemorrhaging in 6 local and systemic agents failed to alleviate the bleed-
ing. Although rFVIIa is not available in a private office 9. Ratko TA, Cummings JP, Matuszewski KA: Off-label use of
recombinant activated factor VII (NovoSeven). P and T 29:712,
setting, clinicians should be aware of its use to control
2004
hemorrhage. Originally developed for the prophylac- 10. Lau HK: The interaction between platelets and factor VII/VIIa.
tic treatment of hemophilic patients with inhibitors, Transfus Apher Sci 28:279, 2003
rFVIIa has been shown to be successful in a number 11. Kristensen J, Killander A, Hippe E, et al: Clinical experience
with recombinant factor VIIa in patients with thrombocytope-
of emergent bleeding situations in several anecdotal nia. Haemostasis 26:159, 1996
case reports. It should also be noted that the use of 12. Geeraedts LM Jr, Kamphuisen PW, Kaasjager HA, et al: The role
rFVIIa in cases of spontaneous and surgical bleeding is of recombinant factor VIIa in the treatment of life-threatening
not Food and Drug Administration approved, and an- haemorrhage in blunt trauma. Injury 36:495, 2005
13. Midathada MV, Mehta P, Waner M, et al: Recombinant factor VIIa
ecdotal evidence suggests varying therapeutic doses in the treatment of bleeding. Am J Clin Pathol 121:124, 2004
and possible uses for this life-saving pharmacologic 14. Kenet G, Walden R, Eldad A, et al: Treatment of traumatic
agent. This is one of only a handful of case reports of bleeding with recombinant factor VIIa. Lancet 354:1879,
1999
factor VIIa being used in the oral surgery setting for
15. Poon MC, d’Oiron R: Recombinant activated factor VII
either prevention17,18 or treatment19,20 of postsurgi- (NovoSeven) treatment of platelet-related bleeding disor-
cal hemorrhage. ders. International Registry on Recombinant Factor VIIa and
Congenital Platelet Disorders Group. Blood Coagul Fibrino-
lysis 11:S55, 2000 (suppl 1)
References 16. Hsia CC, Chin-Yee IH, McAlister VC: Use of recombinant acti-
vated factor VII in patients without hemophilia: A meta-analysis
1. Golla K, Epstein JB, Cabay RJ, et al: Liver disease: Current of randomized control trials. Ann Surg 1:61, 2008
perspectives on medical and dental management. Oral Surg 17. Chuansumrit A, Suwannuraks M, Sri-udomporn N, et al: Recom-
Oral Med Oral Pathol Oral Radiol Endod 98:516, 2004 binant activated factor VII combined with local measures in
2. Schreiber A. Alcoholism. Oral Surg Oral Med Oral Pathol Oral preventing bleeding from invasive dental procedures in pa-
Radiol Endod 92:127, 2001 tients with Glanzmann thrombasthenia. Blood Coagul Fibrino-
3. Henderson JM, Bergman S, Salama A, et al: Management of the
lysis 14:187, 2003
oral and maxillofacial surgery patient with thrombocytopenia.
18. Satoh K, Okamoto M, Torimura A, et al: Successful hemostasis
J Oral Maxillofac Surg 59:421, 2001
after dental extraction with the use of recombinant activated
4. Hussein MA, Lee EJ, Schiffer CA: Platelet transfusions adminis-
tered to patients with splenomegaly. Transfusion 6:508, 1990 factor VII in a factor VII deficient patient. Oral Sci Int 3:10,
5. Mannucci PM, Levi M, et al: Prevention and treatment of major 2006
blood loss. N Engl J Med 356:2301, 2007 19. Berthier AM, Guillygomarc’h A, Messner M, et al: Use of re-
6. Erhardtsen E: Ongoing NovoSeven trials. Intensive Care Med combinant factor VIIa to treat persistent bleeding following
28:S248, 2002 (suppl 2) dental extractions in two cirrhotic patients. Vox Sang 82:119,
7. Von Depka M: NovoSeven: Mode of action and use in acquired 2002
haemophilia. Intensive Care Med 28:S222, 2002 (suppl 2) 20. Heiland M, Weber M, Schmelzle R, et al: Life-threatening bleed-
8. Ho K, Hutter JJ, Eskridge J, et al: The management of life- ing after dental extraction in a hemophilia A patient with
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LIEBERMAN ET AL 2311

J Oral Maxillofac Surg

Control of Life-Threatening Head and

Report of a Case patient denied taking any medications. He had no known

Table 1. HEMODYNAMIC PARAMETERS (START TIME, OCTOBER 30, 6 PM)

October 30: October 30: October 31: October 31: 18-24 h

function are among the most commonly observed in

October 30, October 31, Wednesday

November 1, November 2, November 3, November 4, November 5,

FIGURE 4. Computed tomography scan from November 5, 2007.

FIGURE 5. Computed tomography scan from November 11,

Table 7. CAGE (CRITICIZED, ANNOYED, GUILTY,

Are you criticized about the amount of alcohol you

the extrinsic pathway of the coagulation cascade on

October 30, November 1, December 3, March 7, March 19,

Platelets (/␮L) 21,000 13,000 72,000 87,000 108,000

Table 8. CHILD-PUGH CLASSIFICATION

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