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Postoperative bleeding caused by aspirin
Journal of Dentistry,
6, No. 3,1978,
Postoperative aspirin Terence
McGaul,
pp. 207-209.
Printed
in Great Britain
bleeding caused by
BDS
Newcastle upon Tyne Dental Hospital
ABSTRACT Aspirin impairs platelet function and increases the bleeding time, even in normal subjects. Prolonged postoperative bleeding may occur when aspirin has been taken and particularly in certain aspirin-sensitive individuals. A case is described where full periodontal surgery was carried out in four stages, but postoperative bleeding only occurred at the third and fourth stages when aspirin had been taken.
INTRODUCTION
The fact that small doses of acetylsalicylic acid (aspirin) can cause a slight but significant increase in bleeding time has been well documented by Weiss et al. (1968) and Meilke et al. (1969). Aspirin produces this effect by impairing the formation of a platelet plug following tissue injury. In the normal sequence of events of haemostasis, a few platelets adhere to the exposed collagen of a traumatized vessel wall. Adenosine diphosphate (ADP) is released by the adherent platelets, inducing vast numbers of platelets to aggregate, forming a plug and hence sealing off the damaged part of the vessel. Aspirin inhibits the adherence of platelets to collagen and also inhibits the release of ADP. An Editorial (1969) in the British Medical Journal stated that a single dose of 3-4 aspirin tablets (900-1200 mg) will produce inhibition of platelet aggregation, beginning 2-3 hours after ingestion and persisting for 3-7 days. Schwartz and Pearson (1971) suggested that this effect on platelets is permanent and is only alleviated by platelet renewal. This acquired defect in platelet function is reflected in a significant increase in bleeding time. In fact, Weiss (1974) stated that a single dose of 300-1200 mg of aspirin prolongs the bleeding time by several minutes in normal subjects, and to an even greater degree in patients with bleeding disorders, and that this effect lasts for 4-7 days. It is interesting to note that sodium salicylate does not alter the bleeding time and it seems that it is the acetyl radical of aspirin which is implicated in this effect (Hussey, 1974). Three categories of patients are placed at risk by an aspirin-induced increase in bleeding time: those with intrinsic haemorrhagic defects, e.g. haemophilia, those on anticoagulant therapy and those undergoing surgical procedures (including tooth extraction). Aspirin should not be given to patients in the first two groups as it will cause further impairment of the haemostatic mechanisms. Schwartz and Bennett (1973) found some evidence to suggest that certain tidividuals are sensitive to aspirin, i.e. their platelets are intrinsically more easily inhibited by aspirin than those of a normal individual; a view supported by Mills et al. (1974). As a result they are more likely to bleed postoperatively provided that aspirin has been taken during the previous 7 days. Moreover, they may be quite numerous; to quote Quick (1970): ‘It is astounding that so many bleeding states characterised by easy bruising, nose bleeds and bleeding after tooth extraction, are strikingly ameliorated by discontinuing all medication containing
208
Journal of Dentistry, Vol. ~/NO. 3
aspirin’. Furthermore, Quick (1966) suggested that an aspirin tolerance test should be included in a complete haematological investigation. This may not be practicable routinely, especially where a large number of patients is involved. However, in the presence of a history of even slightly prolonged bleeding after tooth extraction, or of other evidence suggesting a mild haemostatic defect, the use of aspirin should be discouraged. Paracetamol may be recommended as a relatively safe alternative. The small doses of aspirin involved and the very minor nature of the operative procedures which may result in bleeding are emphasized in a paper by Foulke (1976). In this paper a case was described where severe haemorrhage lasted for several days following ultrasonic scaling. The patient had taken 2 aspirin tablets the night before the dental treatment. CASE REPORT A male patient aged 37 years required full mouth periodontal surgery and the extraction of lJ which was the abutment for a cantilever bridge replacing LI_ . Following a course of prophylaxis and plaque control, 1/ was extracted under local anaesthesia and an immediate replacement partial denture was fitted. On separate, subsequent occasions periodontal flap surgery was carried out in all quadrants. On each occasion lignocaine containing 1: 80000 adrenaline was used and the flaps replaced with black silk sutures. After the usual measures were taken to ensure haemostasis, a Coe-Pak dressing was applied. The upper quadrants were treated first; no postoperative discomfort or bleeding was experienced and healing took place readily. In the lower left quadrant the patient felt some postoperative discomfort and took 2,300-mg aspirin tablets. He presented on the next day with some bleeding and oedematous swelling in the buccal sulcus. On removing the dressing the haemorrhage was easily arrested by lateral pressure and an infdtration of lignocaine and adrenaline. The following day he returned with further bleeding which was controlled by prolonged fum pressure. Healing was then uneventful except for a slight haemorrhage 2 days later which the patient controlled himself by applying pressure. Three weeks later the lower right quadrant was treated in the same way as the others, except that a smaIl lingual flap was raised in the q region to curette a periodontal abscess. Postoperative discomfort was again experienced and this time 6 aspirin tablets were taken in three separate doses of 600 mg. He presented the next day with a small haematoma in the anterior region of the floor of the mouth and a very slight oozing from under the dressing. No haemostatic measures were deemed necessary. However, during the night the haemorrhage became quite severe and on two occasions he reported to the dental department of a general hospital where thrombin-impregnated pressure packs were used without any real success. As there was still a steady haemorrhage the next morning, it was decided to admit the patient for a complete haematological investigation, the results of which are as follows: bleeding time 3 min 31 s, prothrombm 12 s (control 12 s), prothrombin ratio 1 (control l), PTTK 66 s (control 52 s), thrombin time 13 s (control 13 s), factor I 350 mg, factor VIII 100 mg, factor IX 120 mg, platelets 300 X lo9 /l, WBC 12.5 x log/l, RBC 5 x 1Ol2/I, haemoglobin 14.8 g/dl, mean cell haemoglobin concentration 32.5 g/dl. The report also stated that platelet function was grossly impaired and the haematologist was able to say categorically that the patient had been taking aspirin. In the absence of other abnormal findings, an acrylic pressure splint with a gutta-pcrcha lining was fitted and left in situ for 4 days. The patient was discharged from inpatient care the morning after admission. Healing was subsequently uneventful and a good result was obtained.
DISCUSSION there would appear to be a direct correlation between aspirin ingestion and the occurrence of postoperative haemorrhage. According to Schwartz and Pearson (1971) a considerable proportion of bleeding after oral surgery is attributable to aspirin and they stressed the importance of detecting this fact in the history. The main problem for the dental practitioner is that many of his patients who present with toothache and require extraction will have taken aspirin to control the pain. It is the most commonly used analgesic and the most commonly used drug in the United States. However, having confirmed that the patient has taken aspirin, at least the practitioner is In the case described
209
McGaul: Postoperative bleeding caused by aspirin
and ready to institute the necessary haemostatic procedures. For obvious reasons, aspirin should not be recommended as an immediate postoperative analgesic. Perhaps aspirin is a more significant factor in the causation of postoperative haemorrhage than hitherto realized.
forewarned
Acknowledgements I am most grateful to Mr R. A. Howell and Mr J. G. Walton for their help and encouragement in preparing this paper. REFERENCES
Editorial (1969) Platelets and aspirin. Br. Med. J. 3, 37 l-372. Foulke C. N. (1976) Gingival haemorrhage related to aspirin ingestation.
J. PeriodontoZ. 47,
355-357.
Hussey H. H. (1974) Aspirin can be dangerous. JAMA 228, 609. Meilke C. H. jun, Kaneshiro M. M., Maher I. A. et al. (1969) The standard&d normal Ivy bleeding time and its prolongation by aspirin. BZood 34, 204-2 15. Mills D. G. Borda I. T., Philp R. B. et al. (1974) Effects of in vitro aspirin on blood platelets of gastrointestinal bleeders. Clin. Pharmacol. Ther. 15, 187- 192. Quick A. J. (1966) Salicylates and bleeding - the aspirin tolerance test. Am. J. Med. Sci. 252,265-269.
Quick A. J. (1970) Aspirin and bleeding time. JAMA 214, 1565. Schwartz H. J. and Bennett B. (1973) The differential effects of acetylsalicylic acid on in vitro aggregation of platelets from normal, asthmatic and aspirin sensitive subjects. ht. Arch. Allergy Appl. Immunol.
Schwartz
A. D. and Pearson
45, 899-904.
H. A. (1971)
Aspirin,
platelets
and bleeding.
J. Pediatr. 78,
558-560.
Weiss H. J. (1974) Aspirin - a dangerous drug? JAMA 229, 1221- 1222. Weiss H. J., Aledort L. M. and Kochwa S. (1968) The effects of salicylates on the haemostatic properties of platelets in man. J. Clin. Invest. 47, 2169-2180.
6, No. 3,1978,
Postoperative aspirin Terence
McGaul,
pp. 207-209.
Printed
in Great Britain
bleeding caused by
BDS
Newcastle upon Tyne Dental Hospital
ABSTRACT Aspirin impairs platelet function and increases the bleeding time, even in normal subjects. Prolonged postoperative bleeding may occur when aspirin has been taken and particularly in certain aspirin-sensitive individuals. A case is described where full periodontal surgery was carried out in four stages, but postoperative bleeding only occurred at the third and fourth stages when aspirin had been taken.
INTRODUCTION
The fact that small doses of acetylsalicylic acid (aspirin) can cause a slight but significant increase in bleeding time has been well documented by Weiss et al. (1968) and Meilke et al. (1969). Aspirin produces this effect by impairing the formation of a platelet plug following tissue injury. In the normal sequence of events of haemostasis, a few platelets adhere to the exposed collagen of a traumatized vessel wall. Adenosine diphosphate (ADP) is released by the adherent platelets, inducing vast numbers of platelets to aggregate, forming a plug and hence sealing off the damaged part of the vessel. Aspirin inhibits the adherence of platelets to collagen and also inhibits the release of ADP. An Editorial (1969) in the British Medical Journal stated that a single dose of 3-4 aspirin tablets (900-1200 mg) will produce inhibition of platelet aggregation, beginning 2-3 hours after ingestion and persisting for 3-7 days. Schwartz and Pearson (1971) suggested that this effect on platelets is permanent and is only alleviated by platelet renewal. This acquired defect in platelet function is reflected in a significant increase in bleeding time. In fact, Weiss (1974) stated that a single dose of 300-1200 mg of aspirin prolongs the bleeding time by several minutes in normal subjects, and to an even greater degree in patients with bleeding disorders, and that this effect lasts for 4-7 days. It is interesting to note that sodium salicylate does not alter the bleeding time and it seems that it is the acetyl radical of aspirin which is implicated in this effect (Hussey, 1974). Three categories of patients are placed at risk by an aspirin-induced increase in bleeding time: those with intrinsic haemorrhagic defects, e.g. haemophilia, those on anticoagulant therapy and those undergoing surgical procedures (including tooth extraction). Aspirin should not be given to patients in the first two groups as it will cause further impairment of the haemostatic mechanisms. Schwartz and Bennett (1973) found some evidence to suggest that certain tidividuals are sensitive to aspirin, i.e. their platelets are intrinsically more easily inhibited by aspirin than those of a normal individual; a view supported by Mills et al. (1974). As a result they are more likely to bleed postoperatively provided that aspirin has been taken during the previous 7 days. Moreover, they may be quite numerous; to quote Quick (1970): ‘It is astounding that so many bleeding states characterised by easy bruising, nose bleeds and bleeding after tooth extraction, are strikingly ameliorated by discontinuing all medication containing
208
Journal of Dentistry, Vol. ~/NO. 3
aspirin’. Furthermore, Quick (1966) suggested that an aspirin tolerance test should be included in a complete haematological investigation. This may not be practicable routinely, especially where a large number of patients is involved. However, in the presence of a history of even slightly prolonged bleeding after tooth extraction, or of other evidence suggesting a mild haemostatic defect, the use of aspirin should be discouraged. Paracetamol may be recommended as a relatively safe alternative. The small doses of aspirin involved and the very minor nature of the operative procedures which may result in bleeding are emphasized in a paper by Foulke (1976). In this paper a case was described where severe haemorrhage lasted for several days following ultrasonic scaling. The patient had taken 2 aspirin tablets the night before the dental treatment. CASE REPORT A male patient aged 37 years required full mouth periodontal surgery and the extraction of lJ which was the abutment for a cantilever bridge replacing LI_ . Following a course of prophylaxis and plaque control, 1/ was extracted under local anaesthesia and an immediate replacement partial denture was fitted. On separate, subsequent occasions periodontal flap surgery was carried out in all quadrants. On each occasion lignocaine containing 1: 80000 adrenaline was used and the flaps replaced with black silk sutures. After the usual measures were taken to ensure haemostasis, a Coe-Pak dressing was applied. The upper quadrants were treated first; no postoperative discomfort or bleeding was experienced and healing took place readily. In the lower left quadrant the patient felt some postoperative discomfort and took 2,300-mg aspirin tablets. He presented on the next day with some bleeding and oedematous swelling in the buccal sulcus. On removing the dressing the haemorrhage was easily arrested by lateral pressure and an infdtration of lignocaine and adrenaline. The following day he returned with further bleeding which was controlled by prolonged fum pressure. Healing was then uneventful except for a slight haemorrhage 2 days later which the patient controlled himself by applying pressure. Three weeks later the lower right quadrant was treated in the same way as the others, except that a smaIl lingual flap was raised in the q region to curette a periodontal abscess. Postoperative discomfort was again experienced and this time 6 aspirin tablets were taken in three separate doses of 600 mg. He presented the next day with a small haematoma in the anterior region of the floor of the mouth and a very slight oozing from under the dressing. No haemostatic measures were deemed necessary. However, during the night the haemorrhage became quite severe and on two occasions he reported to the dental department of a general hospital where thrombin-impregnated pressure packs were used without any real success. As there was still a steady haemorrhage the next morning, it was decided to admit the patient for a complete haematological investigation, the results of which are as follows: bleeding time 3 min 31 s, prothrombm 12 s (control 12 s), prothrombin ratio 1 (control l), PTTK 66 s (control 52 s), thrombin time 13 s (control 13 s), factor I 350 mg, factor VIII 100 mg, factor IX 120 mg, platelets 300 X lo9 /l, WBC 12.5 x log/l, RBC 5 x 1Ol2/I, haemoglobin 14.8 g/dl, mean cell haemoglobin concentration 32.5 g/dl. The report also stated that platelet function was grossly impaired and the haematologist was able to say categorically that the patient had been taking aspirin. In the absence of other abnormal findings, an acrylic pressure splint with a gutta-pcrcha lining was fitted and left in situ for 4 days. The patient was discharged from inpatient care the morning after admission. Healing was subsequently uneventful and a good result was obtained.
DISCUSSION there would appear to be a direct correlation between aspirin ingestion and the occurrence of postoperative haemorrhage. According to Schwartz and Pearson (1971) a considerable proportion of bleeding after oral surgery is attributable to aspirin and they stressed the importance of detecting this fact in the history. The main problem for the dental practitioner is that many of his patients who present with toothache and require extraction will have taken aspirin to control the pain. It is the most commonly used analgesic and the most commonly used drug in the United States. However, having confirmed that the patient has taken aspirin, at least the practitioner is In the case described
209
McGaul: Postoperative bleeding caused by aspirin
and ready to institute the necessary haemostatic procedures. For obvious reasons, aspirin should not be recommended as an immediate postoperative analgesic. Perhaps aspirin is a more significant factor in the causation of postoperative haemorrhage than hitherto realized.
forewarned
Acknowledgements I am most grateful to Mr R. A. Howell and Mr J. G. Walton for their help and encouragement in preparing this paper. REFERENCES
Editorial (1969) Platelets and aspirin. Br. Med. J. 3, 37 l-372. Foulke C. N. (1976) Gingival haemorrhage related to aspirin ingestation.
J. PeriodontoZ. 47,
355-357.
Hussey H. H. (1974) Aspirin can be dangerous. JAMA 228, 609. Meilke C. H. jun, Kaneshiro M. M., Maher I. A. et al. (1969) The standard&d normal Ivy bleeding time and its prolongation by aspirin. BZood 34, 204-2 15. Mills D. G. Borda I. T., Philp R. B. et al. (1974) Effects of in vitro aspirin on blood platelets of gastrointestinal bleeders. Clin. Pharmacol. Ther. 15, 187- 192. Quick A. J. (1966) Salicylates and bleeding - the aspirin tolerance test. Am. J. Med. Sci. 252,265-269.
Quick A. J. (1970) Aspirin and bleeding time. JAMA 214, 1565. Schwartz H. J. and Bennett B. (1973) The differential effects of acetylsalicylic acid on in vitro aggregation of platelets from normal, asthmatic and aspirin sensitive subjects. ht. Arch. Allergy Appl. Immunol.
Schwartz
A. D. and Pearson
45, 899-904.
H. A. (1971)
Aspirin,
platelets
and bleeding.
J. Pediatr. 78,
558-560.
Weiss H. J. (1974) Aspirin - a dangerous drug? JAMA 229, 1221- 1222. Weiss H. J., Aledort L. M. and Kochwa S. (1968) The effects of salicylates on the haemostatic properties of platelets in man. J. Clin. Invest. 47, 2169-2180.