Disordered Hemostasis in Liver Damage from Paracetamol Overdose

Clark, Russell D.; Borirakchanyavat, V.; Gazzard, B. G.; Rake, M. O.; Shilkin, K. B.; Flute, P.T.; Williams, Roger

doi:10.1016/s0016-5085(19)33015-x

Cited by 33 publications

(7 citation statements)

References 14 publications

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“…However, the prothrombin time reverted to normal over a few days with both treatment schedules and it could be that the duration of the synthetic defect and of intravascular coagulation is too short for the development of a clinical bleeding disorder. The frequency with which intravascular coagulation was found in the present series is similar to that found in an earlier analysis of 39 cases of paracetamol-induced hepatic necrosis (Clark et al, 1973b). In that series an increased catabolic rate of fibrinogen was demonstrated in many of the patients.…”

Section: Discussionsupporting

confidence: 90%

“…This is in keeping with the other evidence of severe liver damage, ie, the presence of hepatic encephalopathy in half of the patients at some time during the illness. There was also evidence of intravascular coagulation in a significant percentage and the development of this is closely dependent on the severity of hepatic necrosis (Clark, Borirakchanyavat, Gazzard, Rake, Shilkin, Flute, and Williams, 1973b). However, the prothrombin time reverted to normal over a few days with both treatment schedules and it could be that the duration of the synthetic defect and of intravascular coagulation is too short for the development of a clinical bleeding disorder.…”

Section: Discussionmentioning

confidence: 99%

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A controlled trial of heparin therapy in the coagulation defect of paracetamol-induced hepatic necrosis

Gazzard¹,

Clark²,

Borirakchanyavat³

et al. 1974

Gut

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

A controlled trial of heparin therapy in the coagulation defect of paracetamol-induced hepatic necrosis

Gazzard¹,

Clark²,

Borirakchanyavat³

et al. 1974

Gut

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“…Similar results were obtained by Rapaport [91] and Cederblad [15]. Low values of factor XI [17,73] and of factor XII [73] were found in toxic liver failure. Factor XI and XII levels are elevated in biliary cirrhosis and obstructive jaundice [15].…”

supporting

confidence: 82%

Coagulation Abnormalities in Liver Disease

Lechner¹,

Niessner²,

Thaler³

2008

Semin Thromb Hemost

100

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“…Standard liver function tests were carried out at this time and then daily. Those patients who developed a plasma bilirubin concentration of more than 69 ,umol/l were classified as having severe hepatic damage, as we have previously shown that these are the patients in whom encephalopathy and other signs of fulminant hepatic failure are most likely to occur (Clark, Borirakchanyavat, Gazzard, Rake, Shilkin, Flute, and Williams, 1973b). Indeed, the nine deaths in the series were all from this group.…”

Section: Methodsmentioning

confidence: 99%

Early changes in coagulation following a paracetamol overdose and a controlled trial of fresh frozen plasma therapy.

Gazzard¹,

Henderson²,

Williams³

1975

Gut

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SUMMARY Early changes in coagulation were found in patients following a paracetamol overdose. Low levels of clotting factors II, V and VII were present within 24 hours of the overdose. As the levels of factor II correlated with plasma fibrinogen values at this time, it is possible that they were consumed in the process of intravascular coagulation, although this was not supported by the presence of raised titres of fibrin degradation products. The prothrombin time ratio was greater than 2-2 within 30 hours of ingestion of the overdose in all patients who eventually died, whereas it was less than this in those developing only moderate liver damage. The administration of fresh frozen plasma to patients did appear to reduce the maximum abnormality of the prothrombin time ratio, which was significantly less three days after the overdose in the group receiving fresh frozen plasma. However, the coagulation disturbance was of short duration, and the prothrombin time ratio had also returned to normal within one week of the overdose in the control patients, and the administration of fresh frozen plasma did not appear to reduce the morbidity or mortality in the treated patients.Paracetamol is frequently taken as an overdose in suicidal attempts, and hepatic damage of all grades of severity, from minor to fulminant hepatic failure, may result (Prescott, Wright, Roscoe, and Brown, 1971). In the latter group bleeding is often a major problem and is not infrequently the direct cause of death. It is thought to be due in part to low levels of clotting factors resulting both from impaired hepatic synthesis and increased consumption from intravascular coagulation (Rake, Flute, Shilkin, Lewis, Winch, and Williams, 1971). To replace this synthetic deficiency we have advocated the regular use offresh frozen plasma (FFP), although controlled evidence of its value was lacking.In this paper we describe detailed studies, including individual clotting factor assays, in 66 patients seen shortly after a paracetamol overdose, together with the results of a controlled trial of FFP in those patients in whom a severe coagulation disturbance subsequently developed.

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Disordered Hemostasis in Liver Damage from Paracetamol Overdose

Cited by 33 publications

References 14 publications

A controlled trial of heparin therapy in the coagulation defect of paracetamol-induced hepatic necrosis

A controlled trial of heparin therapy in the coagulation defect of paracetamol-induced hepatic necrosis

Coagulation Abnormalities in Liver Disease

Early changes in coagulation following a paracetamol overdose and a controlled trial of fresh frozen plasma therapy.

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