Coagulation and platelet changes after thermal injury in man

Bartlett, Robert H.; Fong, Susie W.; Marrujo, Greg; Hardeman, James; Anderson, Wayne H.

doi:10.1016/0305-4179(81)90013-9

Cited by 36 publications

(27 citation statements)

References 16 publications

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“…Further, alterations in circulating platelet counts after injury, with an acute thrombocytopenia and subsequent recovery with thrombocytosis, are also well supported in both human (14, 15) and murine studies (16, 26, 27). Thromboelastometry has not been previously utilized in murine models of thermal injury; however, our results are consistent with increased clot strength seen in human studies (5, 12).…”

Section: Discussionmentioning

confidence: 72%

“…Although human and animal studies have consistently found that platelet populations are altered after injury (14–16, 26, 27), no previous models of scald injury have examined platelet function and shown temporal changes after scald injury. Although ROTEM changes have been previously described in other murine trauma models (5, 12), this is the first murine scald model that has demonstrated hypercoagulability on thromboelastometry.…”

Section: Discussionmentioning

confidence: 99%

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Impact of Platelets and Platelet-Derived Microparticles on Hypercoagulability Following Burn Injury

Kuethe

Rice

Veile

et al. 2016

Shock

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An acute burn induced coagulopathy develops after scald injury, which evolves into a subacute, hypercoagulable state. Microparticles, specifically platelet-derived MPs (PMPs), have been suggested as possible contributors. We first developed a model of burn-induced coagulopathy and then sought to investigate the role of platelets and PMPs in coagulation after burn. We hypothesized that changes in circulating platelet and PMP populations after injury would contribute to the post-burn, hypercoagulable state. A murine scald model with 28% TBSA full thickness burn injury was utilized and blood samples were collected at intervals after injury. Circulating MP populations, platelet counts, overall coagulation, and platelet function were determined. Burn injury led to hypercoagulability on post-burn day one (PBD1), which persisted 6 days after injury (PBD6). On PBD1, there was a significant decrease in platelet numbers and a decline in platelet contribution to clot formation with a concomitant increase in circulating procoagulant PMPs. On PBD6, there was a significant increase in platelet numbers and in platelet activation with no change in PMPs compared with sham. Further, on PBD1 decreased ADP-induced platelet activation was observed with a contrasting increase in ADP-induced platelet activation on PBD6. We therefore concluded that there was a temporal change in the mechanisms leading to a hypercoagulable state after scald injury, that PMPs are responsible for changes seen on PBD1, and finally that ADP-induced platelet activation was key to the augmented clotting mechanisms 6 days after burn.

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Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Impact of Platelets and Platelet-Derived Microparticles on Hypercoagulability Following Burn Injury

Kuethe

Rice

Veile

et al. 2016

Shock

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“…This PLT trend was similarly shown in a previous study, which also demonstrated that the results of platelet function studies were abnormally decreased when PLT was low and that platelets may actually increase to abnormally high levels beyond the first week of injury. 25 Other possible factors contributing to transient thrombocytopenia include increased platelet consumption and decreased platelet production. 9,22 …”

Section: Discussionmentioning

confidence: 99%

Major burn injury is not associated with acute traumatic coagulopathy

Lin

et al. 2013

Journal of Trauma and Acute Care Surgery

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BACKGROUND The pathophysiology and time course of coagulopathy after major burns are inadequately understood. Our study objectives were to determine whether acute traumatic coagulopathy (ATC) is seen in burn patients on admission and to determine the changes in international normalized ratio (INR), activated partial thromboplastin time (aPTT), platelet count (PLT), and hemoglobin (Hgb) in the first 7 days after injury. METHODS We conducted a retrospective study of patients with at least 15% total body surface area (TBSA) burn who presented to the University of North Carolina. Data on patient demographics, injury characteristics, and laboratory data (INR, aPTT, PLT, and Hgb) on admission and within the first 7 days after injury were recorded. We defined ATC as INR ≥ 1.3, aPTT ≥ 1.5 times the mean normal limit, and normal PLT on admission. RESULTS We studied the hematologic profile of 102 patients with 15–100% TBSA burn, but did not identify a single patient with ATC on admission. The screening hematologic profile on admission was not influenced by burn severity. In the first 7 days after injury, the INR and aPTT were relatively preserved, while the PLT quickly recovered to baseline after an early decline and the Hgb remained stable at around 10 g/dL; all these changes occurred during the time when the burn patients had received large amounts of fluid resuscitation. CONCLUSION The screening hematologic profile of burn patients on admission is normal and the standard screening assays do not suggest the existence of ATC on admission. While this is a relatively small study, it provides evidence to suggest that ATC is unique to trauma patients. LEVEL OF EVIDENCE III, Prognostic and Epidemiological

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“…There is not only an increase in prothrombotic factors including factors V and VIII, but also a dramatic rise in platelet count and fibrinogen levels [1][2][3][4]. Conversely, the levels of antithrombotic factors including antithrombin III, protein C and protein S are decreased [1,5].…”

Section: Introductionmentioning

confidence: 99%