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BOSTON – Venous thromboembolism is a common complication of traumatic brain injury, and pharmacologic thromboprophylaxis is considered to be the standard of care. But when that prophylaxis is interrupted for surgery or other procedures, the patient’s risk for VTE significantly increases, reported investigators at the annual meeting of the American Association for the Surgery of Trauma.
Among 480 patients with stable traumatic brain injury (TBI), those who received interrupted pharmacologic thromboprophylaxis (PTP) had a sevenfold higher risk for VTE than did patients who received continuous prophylaxis, said Dr. Patrick Offner of the trauma service at St. Anthony Central Hospital in Denver.
“We would suggest that interruption of PTP in patients with traumatic brain injury does increase the risk of venous thromboembolism, and all efforts should be made to not interrupt it once it’s started,” Dr. Offner said.
Patients with traumatic brain injury are at increased risk for VTE because of multiple mechanisms, some related to injury and some to treatment. But efforts to prevent VTE in these patients are particularly challenging, because prophylaxis with an agent such as low-molecular-weight heparin also increases risk of intracranial hemorrhage, he said.
Dr. Offner and colleagues recently published a study suggesting that PTP use is associated with a 13-fold increase in odds of further hemorrhage progression in patients with unstable TBI, defined as evidence of intracranial hemorrhage progression on a follow-up CT scan within 1 day of admission (J. Trauma 2010;68:886-94).
To get a better handle on the optimal administration of PTP in patients with stable TBI and to see whether late or interrupted PTP might increase the risk of VTE, the investigators conducted a retrospective cohort study.
They reviewed records on all adult patients admitted to two urban level 1 trauma centers with a diagnosis of TBI based on ICD-9 codes. Patients with hospital stays shorter than 3 days, new or aggressive intracranial hemorrhage within 24 hours, or VTE diagnosed within 24 hours of admission were excluded.
The VTE prophylaxis protocol included placement of bilateral sequential compression devices (unless precluded by lower-extremity injuries) on admission to the ICU, and Lovenox (enoxaparin) 30 mg subcutaneously every 12 hours beginning at 36 hours, unless it was specifically held by neurosurgeons or other members of the care team. The patients also received weekly duplex ultrasound surveillance of the lower extremities.
The authors collected data on development of deep vein thrombosis (DVT) or pulmonary embolism (PE), DVT prophylaxis timing and method, and demographics. The analysis included incidence of VTE, associations between VTE and PTP – any exposure, early exposure (within 72 hours) compared with late, and interrupted administration of PTP – and multivariate logistic regression modeling.
Information on a total of 480 patients was available. The median age was 53 years, 62% were men, and 48% of injuries were due to falls. The mean Injury Severity Score was 19.7, mean Abbreviated Injury Scale (AIS) score was 3.5, and mean Glasgow Coma Scale (GCS) score was 12.2.
There were 15 venous thromboembolic events: 12 DVT and 5 PE (two patients had DVT and PE). The incidence was lower than the investigators had anticipated, Dr. Offner said.
In all, 93% of the patients were treated with sequential compression, and 255 received PTP. Of these, 42% received PTP early, 58% received it late, 74% received it continuously, and 26% had PTP interrupted.
Factors significantly related to the subsequent development of VTE included a GCS score of 3-8, compared with 9-15 for patients who did not develop a VTE; severe head injury (AIS score = 5); chest or extremity injury (AIS score 3 or greater for each); and less ambulation before discharge.
“When we looked at the univariate association between VTE and PTP, we were surprised in that administration of PTP either at all or in a late or early fashion didn’t seem to affect the subsequent incidence of VTE. On the other hand, if PTP was interrupted after it was started, there was a fourfold increase [odds ratio, 4.53; P = .02] in the incidence of subsequent venous thromboembolism,” Dr. Offner said.
In logistic regression analyses controlling for various risk factors, the investigators first compared PTP with no PTP and VTE incidence, and found that the only significant risk factor was ambulation before discharge (OR, 0.19; P = .02). Severity of injuries, preinjury anticoagulant/platelet inhibitor use, low GCS score, or female sex were not significantly linked to VTE incidence, regardless of PTP use.
There were also no significant differences in VTE incidence in late, compared with early administration of PTP.
However, when they looked at interrupted compared with continuous administration, they found that interrupted administration was associated with a sevenfold increased risk for VTE (OR, 7.07; P = .04). None of the other variables were significantly linked to VTE risk in this subanalysis.
Dr. Offner noted that the study results were limited by the retrospective design, potential for surveillance bias, and relatively small number of VTE cases in the sample.
Invited discussant Dr. Thomas Esposito of the department of surgery at Loyola University Medical Center in Maywood, Ill., noted that there was a mismatch between the interrupted and continuous PTP administration groups. That called the data into question, he said, because differences between the groups might have significantly influenced the incidence of VTE and PE.
Dr. Offner acknowledged that the small numbers involved could have subjected the study to a type II statistical error. He also agreed that the interrupted therapy group was a higher-risk group and that those risk factors could in part explain the higher incidence of VTE.
The study was internally funded. Neither Dr. Offner nor Dr. Esposito had conflict of interest disclosures.
Patrick J. Offner
BOSTON – Venous thromboembolism is a common complication of traumatic brain injury, and pharmacologic thromboprophylaxis is considered to be the standard of care. But when that prophylaxis is interrupted for surgery or other procedures, the patient’s risk for VTE significantly increases, reported investigators at the annual meeting of the American Association for the Surgery of Trauma.
Among 480 patients with stable traumatic brain injury (TBI), those who received interrupted pharmacologic thromboprophylaxis (PTP) had a sevenfold higher risk for VTE than did patients who received continuous prophylaxis, said Dr. Patrick Offner of the trauma service at St. Anthony Central Hospital in Denver.
“We would suggest that interruption of PTP in patients with traumatic brain injury does increase the risk of venous thromboembolism, and all efforts should be made to not interrupt it once it’s started,” Dr. Offner said.
Patients with traumatic brain injury are at increased risk for VTE because of multiple mechanisms, some related to injury and some to treatment. But efforts to prevent VTE in these patients are particularly challenging, because prophylaxis with an agent such as low-molecular-weight heparin also increases risk of intracranial hemorrhage, he said.
Dr. Offner and colleagues recently published a study suggesting that PTP use is associated with a 13-fold increase in odds of further hemorrhage progression in patients with unstable TBI, defined as evidence of intracranial hemorrhage progression on a follow-up CT scan within 1 day of admission (J. Trauma 2010;68:886-94).
To get a better handle on the optimal administration of PTP in patients with stable TBI and to see whether late or interrupted PTP might increase the risk of VTE, the investigators conducted a retrospective cohort study.
They reviewed records on all adult patients admitted to two urban level 1 trauma centers with a diagnosis of TBI based on ICD-9 codes. Patients with hospital stays shorter than 3 days, new or aggressive intracranial hemorrhage within 24 hours, or VTE diagnosed within 24 hours of admission were excluded.
The VTE prophylaxis protocol included placement of bilateral sequential compression devices (unless precluded by lower-extremity injuries) on admission to the ICU, and Lovenox (enoxaparin) 30 mg subcutaneously every 12 hours beginning at 36 hours, unless it was specifically held by neurosurgeons or other members of the care team. The patients also received weekly duplex ultrasound surveillance of the lower extremities.
The authors collected data on development of deep vein thrombosis (DVT) or pulmonary embolism (PE), DVT prophylaxis timing and method, and demographics. The analysis included incidence of VTE, associations between VTE and PTP – any exposure, early exposure (within 72 hours) compared with late, and interrupted administration of PTP – and multivariate logistic regression modeling.
Information on a total of 480 patients was available. The median age was 53 years, 62% were men, and 48% of injuries were due to falls. The mean Injury Severity Score was 19.7, mean Abbreviated Injury Scale (AIS) score was 3.5, and mean Glasgow Coma Scale (GCS) score was 12.2.
There were 15 venous thromboembolic events: 12 DVT and 5 PE (two patients had DVT and PE). The incidence was lower than the investigators had anticipated, Dr. Offner said.
In all, 93% of the patients were treated with sequential compression, and 255 received PTP. Of these, 42% received PTP early, 58% received it late, 74% received it continuously, and 26% had PTP interrupted.
Factors significantly related to the subsequent development of VTE included a GCS score of 3-8, compared with 9-15 for patients who did not develop a VTE; severe head injury (AIS score = 5); chest or extremity injury (AIS score 3 or greater for each); and less ambulation before discharge.
“When we looked at the univariate association between VTE and PTP, we were surprised in that administration of PTP either at all or in a late or early fashion didn’t seem to affect the subsequent incidence of VTE. On the other hand, if PTP was interrupted after it was started, there was a fourfold increase [odds ratio, 4.53; P = .02] in the incidence of subsequent venous thromboembolism,” Dr. Offner said.
In logistic regression analyses controlling for various risk factors, the investigators first compared PTP with no PTP and VTE incidence, and found that the only significant risk factor was ambulation before discharge (OR, 0.19; P = .02). Severity of injuries, preinjury anticoagulant/platelet inhibitor use, low GCS score, or female sex were not significantly linked to VTE incidence, regardless of PTP use.
There were also no significant differences in VTE incidence in late, compared with early administration of PTP.
However, when they looked at interrupted compared with continuous administration, they found that interrupted administration was associated with a sevenfold increased risk for VTE (OR, 7.07; P = .04). None of the other variables were significantly linked to VTE risk in this subanalysis.
Dr. Offner noted that the study results were limited by the retrospective design, potential for surveillance bias, and relatively small number of VTE cases in the sample.
Invited discussant Dr. Thomas Esposito of the department of surgery at Loyola University Medical Center in Maywood, Ill., noted that there was a mismatch between the interrupted and continuous PTP administration groups. That called the data into question, he said, because differences between the groups might have significantly influenced the incidence of VTE and PE.
Dr. Offner acknowledged that the small numbers involved could have subjected the study to a type II statistical error. He also agreed that the interrupted therapy group was a higher-risk group and that those risk factors could in part explain the higher incidence of VTE.
The study was internally funded. Neither Dr. Offner nor Dr. Esposito had conflict of interest disclosures.
Patrick J. Offner
BOSTON – Venous thromboembolism is a common complication of traumatic brain injury, and pharmacologic thromboprophylaxis is considered to be the standard of care. But when that prophylaxis is interrupted for surgery or other procedures, the patient’s risk for VTE significantly increases, reported investigators at the annual meeting of the American Association for the Surgery of Trauma.
Among 480 patients with stable traumatic brain injury (TBI), those who received interrupted pharmacologic thromboprophylaxis (PTP) had a sevenfold higher risk for VTE than did patients who received continuous prophylaxis, said Dr. Patrick Offner of the trauma service at St. Anthony Central Hospital in Denver.
“We would suggest that interruption of PTP in patients with traumatic brain injury does increase the risk of venous thromboembolism, and all efforts should be made to not interrupt it once it’s started,” Dr. Offner said.
Patients with traumatic brain injury are at increased risk for VTE because of multiple mechanisms, some related to injury and some to treatment. But efforts to prevent VTE in these patients are particularly challenging, because prophylaxis with an agent such as low-molecular-weight heparin also increases risk of intracranial hemorrhage, he said.
Dr. Offner and colleagues recently published a study suggesting that PTP use is associated with a 13-fold increase in odds of further hemorrhage progression in patients with unstable TBI, defined as evidence of intracranial hemorrhage progression on a follow-up CT scan within 1 day of admission (J. Trauma 2010;68:886-94).
To get a better handle on the optimal administration of PTP in patients with stable TBI and to see whether late or interrupted PTP might increase the risk of VTE, the investigators conducted a retrospective cohort study.
They reviewed records on all adult patients admitted to two urban level 1 trauma centers with a diagnosis of TBI based on ICD-9 codes. Patients with hospital stays shorter than 3 days, new or aggressive intracranial hemorrhage within 24 hours, or VTE diagnosed within 24 hours of admission were excluded.
The VTE prophylaxis protocol included placement of bilateral sequential compression devices (unless precluded by lower-extremity injuries) on admission to the ICU, and Lovenox (enoxaparin) 30 mg subcutaneously every 12 hours beginning at 36 hours, unless it was specifically held by neurosurgeons or other members of the care team. The patients also received weekly duplex ultrasound surveillance of the lower extremities.
The authors collected data on development of deep vein thrombosis (DVT) or pulmonary embolism (PE), DVT prophylaxis timing and method, and demographics. The analysis included incidence of VTE, associations between VTE and PTP – any exposure, early exposure (within 72 hours) compared with late, and interrupted administration of PTP – and multivariate logistic regression modeling.
Information on a total of 480 patients was available. The median age was 53 years, 62% were men, and 48% of injuries were due to falls. The mean Injury Severity Score was 19.7, mean Abbreviated Injury Scale (AIS) score was 3.5, and mean Glasgow Coma Scale (GCS) score was 12.2.
There were 15 venous thromboembolic events: 12 DVT and 5 PE (two patients had DVT and PE). The incidence was lower than the investigators had anticipated, Dr. Offner said.
In all, 93% of the patients were treated with sequential compression, and 255 received PTP. Of these, 42% received PTP early, 58% received it late, 74% received it continuously, and 26% had PTP interrupted.
Factors significantly related to the subsequent development of VTE included a GCS score of 3-8, compared with 9-15 for patients who did not develop a VTE; severe head injury (AIS score = 5); chest or extremity injury (AIS score 3 or greater for each); and less ambulation before discharge.
“When we looked at the univariate association between VTE and PTP, we were surprised in that administration of PTP either at all or in a late or early fashion didn’t seem to affect the subsequent incidence of VTE. On the other hand, if PTP was interrupted after it was started, there was a fourfold increase [odds ratio, 4.53; P = .02] in the incidence of subsequent venous thromboembolism,” Dr. Offner said.
In logistic regression analyses controlling for various risk factors, the investigators first compared PTP with no PTP and VTE incidence, and found that the only significant risk factor was ambulation before discharge (OR, 0.19; P = .02). Severity of injuries, preinjury anticoagulant/platelet inhibitor use, low GCS score, or female sex were not significantly linked to VTE incidence, regardless of PTP use.
There were also no significant differences in VTE incidence in late, compared with early administration of PTP.
However, when they looked at interrupted compared with continuous administration, they found that interrupted administration was associated with a sevenfold increased risk for VTE (OR, 7.07; P = .04). None of the other variables were significantly linked to VTE risk in this subanalysis.
Dr. Offner noted that the study results were limited by the retrospective design, potential for surveillance bias, and relatively small number of VTE cases in the sample.
Invited discussant Dr. Thomas Esposito of the department of surgery at Loyola University Medical Center in Maywood, Ill., noted that there was a mismatch between the interrupted and continuous PTP administration groups. That called the data into question, he said, because differences between the groups might have significantly influenced the incidence of VTE and PE.
Dr. Offner acknowledged that the small numbers involved could have subjected the study to a type II statistical error. He also agreed that the interrupted therapy group was a higher-risk group and that those risk factors could in part explain the higher incidence of VTE.
The study was internally funded. Neither Dr. Offner nor Dr. Esposito had conflict of interest disclosures.
Patrick J. Offner