Coagulopathy and inhospital deaths in patients with acute subdural hematoma

Bershad, Eric M.; Farhadi, Saeed; Suri, M. Fareed K.; Feen, Eliahu S.; Hernández, O; Selman, Warren R.; Suárez, José I.

doi:10.3171/jns/2008/109/10/0664

Cited by 42 publications

(34 citation statements)

References 23 publications

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“…In acute subdural hematoma patients with coagulopathy (INR >1.2), mortality rates are higher than those in patients without coagulopathy; the underlying reasons cannot be clearly explained. However, rapid increase in the hematoma diameter, mass effect, increased intracranial pressure are considered as factors (20). Using PCC in the emergency room, surgery could be performed in all of our cases with subdural hematoma within the first 1 h without delay.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Prothrombin Complex Concentrates for Oral Anticoagulant Therapy-related Major Hemorrhage

Çavuş¹,

Yıldırım²,

Yurtseven³

et al. 2015

JAEM

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In patients admitted to accident and emergency departments for anticoagulant use-related major hemorrhage and requiring urgent surgery or life-saving invasive intervention, the international normalized ration (INR) value should be rapidly corrected and bleeding should be controlled. With prothrombin complex concentrate (PCC), when used at optimal dose levels, target INR values are achieved within 15 min. In this study, we aimed to discuss the efficacy of the used four-factor PCC in 10 patients who were admitted to the accident and emergency department because of oral anticoagulant use-related major bleeding. Of all the patients to whom PCC treatment was administered, targeted INR levels could not be attained in 2 patients (20%). For our cases with gastrointestinal bleeding, the average baseline INR value was 7.3, while the average INR value after PCC administration was 1.9. For our subdural hematoma cases, the median baseline INR value was 2.5, while the median INR value after PCC administration was 1.3. We believe that PCCs used in eligible patient groups, as in this case series, may provide the desired results at lower doses and that they may be safer with regard to complications. (JAEM 2015; 14: 37-40)

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Section: Discussionmentioning

confidence: 99%

Efficacy of Prothrombin Complex Concentrates for Oral Anticoagulant Therapy-related Major Hemorrhage

Çavuş¹,

Yıldırım²,

Yurtseven³

et al. 2015

JAEM

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“…Outcomes are worse in patients with ASDHs and coagulopathy. 1 However, Bershard et al did not demonstrate that traumatic ASDHs were larger in patients with coagulopathy; other factors, such as delay in surgery, could be responsible for the worse outcomes. Nontraumatic ASDHs have been shown to have greater thicknesses in the presence of coagulopathy.…”

Section: Cessation Of Asdh Enlargementmentioning

confidence: 96%

Acute subdural hematoma from bridging vein rupture: a potential mechanism for growth

Miller

Nader

2014

JNS

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Most acute subdural hematomas (ASDHs) develop after rupture of a bridging vein or veins. The anatomy of the bridging vein predisposes to its tearing within the border cell layer of the dura mater. Thus, the subdural hematoma actually forms within the dura. The hematoma grows by continued bleeding into the border cell layer. However, the venous pressure would not be expected to cause a large hematoma. Therefore, some type of mechanism must account for the hematoma's expansion. Cerebral venous pressure (CVP) has been demonstrated in animal models to be slightly higher than intracranial pressure (ICP), and CVP tracks the ICP as pressure variations occur. The elevation of CVP as the ICP increases is thought to result from an increase in outflow resistance of the terminal portion of the bridging veins. This probably results from a Starling resistor model or, less likely, from a muscular sphincter. A hypothesis is derived to explain the mechanism of ASDH enlargement. Tearing of one or more bridging veins causes these vessels to bleed into the dural border cell layer. Subsequent ICP elevation from the ASDH, cerebral swelling, or other cause results in elevation of the CVP by increased outflow resistance in the intact bridging veins. The increased ICP causes further bleeding into the hematoma cavity via the torn bridging veins. Thus, the ASDH enlarges via a positive feedback mechanism. Enlargement of an ASDH would cease as blood within the hematoma cavity coagulates. This would stop the dissection of the dural border cell layer, and pressure within the hematoma cavity would equalize with that in the torn bridging vein or veins.

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“…All of these data support a need for an early and rapid INR correction [13]. In patients with acute SDH, a coagulopathic state may further worse outcome [14]. For example, among 248 patients with acute SDH patients, coagulopathy (INR > 1.2) independently predicted higher inhospital mortality [14].…”

Section: Introductionmentioning

confidence: 96%

“…In patients with acute SDH, a coagulopathic state may further worse outcome [14]. For example, among 248 patients with acute SDH patients, coagulopathy (INR > 1.2) independently predicted higher inhospital mortality [14]. The reasons for the association of coagulopathy with worse outcome in SDH patients is not well studied, but may be related to further expansion of the hematoma, worsening mass effect, and elevation of intracranial pressure (ICP).…”

Section: Introductionmentioning

confidence: 98%

Prothrombin Complex Concentrates for Oral Anticoagulant Therapy-Related Intracranial Hemorrhage: A Review of the Literature

Bershad

Suárez

2009

Neurocrit Care

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Warfarin-related intracranial hemorrhage carries a high mortality and poor neurological outcome. Rapid reversal of coagulopathy is a cornerstone of medical therapy to halt bleeding progression; however the optimal approach remains undefined. Prothrombin complex concentrates have promising features that may rapidly reverse coagulopathy, but remain relatively unstudied. We aim to review the literature regarding the use of prothrombin complex concentrates in patients with warfarin-related intracranial hemorrhage. A comprehensive review of the literature was conducted using PUBMED and Google Scholar databases to identify the use of PCC in patients with warfarin-related intracranial hemorrhage. The characteristics abstracted included the type of PCC, dosing, study design, type of intracranial hemorrhage, changes in the INR, and adverse effects. Prothrombin complex concentrates are heterogeneous in regards to factor concentration. PCC consistently reversed the INR in patients with intracranial hemorrhage. There is some evidence that PCC may reverse the INR more rapidly compared to fresh frozen plasma. Serious adverse effects were uncommon and included mainly thromboembolism. PCC has features which make it a promising therapy for patients with warfarin-related intracranial hemorrhage, and deserves more rigorous study in prospective-randomized controlled trials.

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Coagulopathy and inhospital deaths in patients with acute subdural hematoma

Abstract: Coagulopathy is independently associated with inhospital death in patients with acute SDH. Time to treatment to correct coagulopathy using fresh frozen plasma and/or vitamin K was prolonged.

Cited by 42 publications

References 23 publications

Efficacy of Prothrombin Complex Concentrates for Oral Anticoagulant Therapy-related Major Hemorrhage

Efficacy of Prothrombin Complex Concentrates for Oral Anticoagulant Therapy-related Major Hemorrhage

Acute subdural hematoma from bridging vein rupture: a potential mechanism for growth

Prothrombin Complex Concentrates for Oral Anticoagulant Therapy-Related Intracranial Hemorrhage: A Review of the Literature

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