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Neurology India, Vol. 58, No. 5, September-October, 2010, pp. 756-757 Brief Report Hypofibrinogenemia in isolated traumatic brain injury in Indian patients Gaurav Chhabra1, Kanchana Rangarajan1, Arulselvi Subramanian1, Deepak Agrawal2, Subhadra Sharma1, AK Mukhopadhayay1 1 Department of Lab Medicine, Jai Prakash Narayan Apex Trauma Centre, AIIMS, Delhi, India Correspondence Address: Date of Acceptance: 08-Jul-2010 Code Number: ni10206 PMID: 21045504 DOI: 10.4103/0028-3886.72175 Abstract Coagulation abnormalities are common in patients with head injuries. However, the effect of brain injury on fibrinogen levels has not been well studied prospectively to assess coagulation abnormalities in patients with moderate and severe head injuries and correlate these abnormalities with the neurologic outcome. Consecutive patients with moderate (Glasgow Comma Scale (GCS),9-12) and severe (GCS≤8) head injuries were the subjects of this pilot study, All patients had coagulation parameters, including plasma fibrinogen levels measured. Clinical and computed tomography (CT) scan findings and immediate clinical outcome were analyzed. Of the 100 patients enrolled, only seven (7%) patients had hypofibrinogenemia (fibrinogen ≤200 mg/dL). The head injury was moderate in two patients and severe in five patients. Fibrinogen levels showed a progressively increasing trend in four patients (three with severe head injuries and one with moderate head injury). CT scan revealed subdural hematoma in five patients; extradural hematoma in one; and subarachnoid hemorrhage in another patient. Of the seven patients, two patients died during hospital. Large-scale prospective studies are needed to assess the fibrinogen level in patients with head injury and its impact on outcome.Keywords: Coagulopathy, head injury, hypofibrinogenemia Introduction There is enough observational data to suggest the association of coagulopathy with head trauma. [1] However, the role of fibrinogen in isolated traumatic head injury patients has not been fully explored. The aim of the present study was to evaluate the coagulation abnormalities in patients with moderate and severe head injuries and correlate these abnormalities with the neurologic outcome. Materials and Methods This prospective pilot study was carried out at a level-I trauma care center between May 2008 and October 2008. Informed consent was taken from all the patients enrolled in the study. Patients aged between 3 and 75 years with severe head injury [Glasgow Coma Score (GCS), ≤8] and those with moderate head injury (GCS, 9-12) and presenting within 24 hours of injury were included in the study. Patients with polytrauma, known hemorrhagic disorders, on anticoagulant therapy, or with liver disease, renal disease or any other comorbidity were excluded from the study. Plasma fibrinogen levels were measured at admission and on day 3 of injury in patients with moderate head injury; and additionally on day-5, in patients with severe head injury. Patients also had work-up for other coagulation parameters and platelet count. Clinical and computed tomography (CT) scan findings were also analyzed, and immediate outcome (discharged or death) was assessed. Results Of the 100 patients enrolled in the study, seven (7%) were found to have hypofibrinogenemia (fibrinogen, ≤200 mg/dL). The mean age of the patients was 21.8 years; all the patients were male. Among these seven patients, five had severe head injury and two had moderate head injury [Table - 1]. One patient had severe hypofibrinogenemia (<50 mg/dL), and six patients had moderate hypofibrinogenemia (50-200 mg/dL). Fibrinogen levels showed a progressively increasing trend in the four patients (three severe head injuries and one moderate head injury). D-dimer levels were found to be elevated in all these seven patients. Low platelet count (< 100×10 3 /mm 3 ) was seen in three patients. The other coagulation markers were within normal limits at the time of admission in all the patients. CT scan revealed subdural hematoma (SDH) in five patients; extradural hematoma (EDH) in one; and subarachnoid hemorrhage (SAH) in another patient, who died subsequently. Of the seven patients, two patients died during hospital stay. Discussion In this study, patients who succumbed to head injury had low or severely depleted fibrinogen levels. Fibrinogen levels could be affected post-trauma due to various causes [1],[2] and they include: ongoing hemorrhage leading to coagulopathy, acidosis and hypothermia. While hemorrhage and acidosis cause an acceleration of fibrinogen breakdown, hypothermia causes an inhibition of fibrinogen synthesis. [1],[2] Other studies have shown increased levels of fibrinopeptide, fibrin split products and d-Dimer following isolated head injury, and lower levels of fibrinogen and anti-thrombin. [3],[4] In our study the incidence of hypofibrinogenemia is low, even though the sample size was fairly large,, the reasons for which remain unclear. One factor may be the genetic variation of the Indian population leading to differences in post-trauma coagulation cascade activation. Similar to our study, low fibrinogen levels were associated with poor outcome and poorer prognosis in patients suffering from cranio-cerebral trauma. [5] A correlation between the CT findings, plasma fibrinogen degradation product (FDP) values and outcome was explored in 26 patients of head injury. [6] This study suggested that coagulation abnormalities were caused by the brain tissue destruction rather than by brain compression, and hence patients with severe contusion had more consistent and prolonged elevation of FDP levels than patients with mild contusion. We had similar results with patients of severe contusion on CT scan showing marked elevation of d-Dimer levels on admission in comparison to those with SDH or EDH. Conclusions Coagulation profile, especially for determining low fibrinogen levels if present, in head trauma patients needs assessment in a larger setting. Prospective large-scale trials are necessary to assess the quantum of coagulation abnormalities and their impact on outcome in these patients. Acknowledgment We would like to acknowledge the valuable support and help given by the technicians and attendants of the Department of Laboratory Medicine, Jai Prakash Narayan Apex Trauma Centre, especially, Vibha, Kiran, Santhosh, Suman, Adesh, Shiv kumar, Vinith and Kisan. References
Copyright 2010 - Neurology India The following images related to this document are available:Photo images[ni10206t1.jpg] |
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