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Spontaneous Acute Subdural Hematoma and Chronic Epidural Hematoma in a Child with F XIII Deficiency
The Journal of Emergency Medicine, Vol. 38, No. 1, pp. 25–29, 2010 Copyright © 2010 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/08 $–see front matter
doi:10.1016/j.jemermed.2007.11.041
Clinical Communications: Pediatrics SPONTANEOUS ACUTE SUBDURAL HEMATOMA AND CHRONIC EPIDURAL HEMATOMA IN A CHILD WITH F XIII DEFICIENCY Murat Vural,
MD,*
Coskun Yarar,
MD,†
Ramazan Durmaz,
MD,*
and Metin Ant Atasoy,
MD*
*Department of Neurosurgery and †Department of Pediatrics, Eskis¸ehir Osmangazi University Medical Faculty, Eskisehir, Turkey Reprint Address: Murat Vural, MD, Department of Neurosurgery, Eskis¸ehir Osmangazi University Medical Faculty, Deliklitas¸ Mh. Deliklitas¸ Cd. Huzur, Apt. No. 28/3, Eskisehir, Turkey
e Abstract—Factor XIII (F XIII) deficiency is a rare autosomal recessive congenital disorder that can cause spontaneous subdural or epidural hematomas. Due to its low incidence, F XIII deficiency may well be under-diagnosed. A 7-year-old girl with no history of medical problems presented with progressive headache of 3 days. Cerebral computed tomography (CT) scans revealed a large right acute parietooccipital subdural hematoma with a significant midline shift. After an emergent parietooccipital craniotomy and evacuation of the subdural hematoma, a screening test for factor XIII was performed. The results of the test were abnormal. She had full recovery and was discharged with a follow-up treatment of monthly transfusion of fresh frozen plasma as the replacement and prophylactic therapy. Ten months later, she was referred to our center with headache after a minor head trauma. Her medical history revealed that she had not received fresh frozen plasma for the last 2 months. CT scan showed a chronic right parietal epidural hematoma beneath the craniotomy flap. The present case indicates that although its incidence is very rare, F XIII deficiency can cause acute or chronic subdural and epidural hematomas. Therefore, in acute or chronic subdural and epidural hematomas with no underlying cause, the presence of a potential F XIII deficiency should be suspected as a cause of hemorrhagic diathesis. © 2010 Elsevier Inc.
tension, anticoagulant therapy, bleeding and coagulation disorders, cocaine-induced vasculitis, and bleeding from intracranial tumors or aneurysms (1,3,4). Epidural hematoma (EDH) often results from a local injury (5). Factor XIII (F XIII) is a transpeptidase that is necessary for normal blood hemostasis. In F XIII deficiency, blood clot is weak and thus unable to maintain a hemostatic plug, leading to hemorrhages (6,7). Intracerebral hemorrhages due to factor XIII deficiency have been shown in various case reports (8 –12). To the best of our knowledge, this is the first case of acute SDH and chronic EDH 10 months after the first operation.
CASE REPORT A 7-year-old girl was admitted to our hospital with complaints of progressing headache, nausea, and vomiting for the last 3 days. She had no significant past medical history. At the time of admission, she was disoriented but able to converse. Computed tomography (CT) scans showed a large hyperdense parietooccipital SDH with a significant midline shift. The hematoma was evacuated immediately (Figure 1). Her post-operative course was uneventful with complete neurological recovery. In consultation with the Department of Pediatrics, further investigations were made to determine the etiology of subdural hemorrhage. Platelet count, prothrombin time, activated partial thromboplastin time, international normalized ratio, bleeding time, and all coagulation factors were normal except for
e Keywords—F XIII deficiency; epidural hematoma; subdural hematoma; pediatric age
INTRODUCTION Spontaneous acute subdural hematoma (SDH) is a rare condition (1,2). Potential predisposing factors are hyper-
RECEIVED: 6 March 2007; FINAL ACCEPTED: 5 November 2007
SUBMISSION RECEIVED:
20 July 2007; 25
26
M. Vural et al.
Figure 1. Axial view of the large hyperdense parietooccipital subdural hematoma with a significant midline shift.
F XIII. The diagnosis of F XIII deficiency was made based on the positive clot solubility test using 5 M urea. However, no reliable data about the history of prolonged bleeding from the umbilical stump, a common symptom of F XIII deficiency at birth, were available. The patient was discharged without any neurological deficits, with a treatment of monthly transfusion of fresh frozen plasma as the replacement and prophylactic therapy. There was no residual or recurrent hemorrhage on control CT scans (Figure 2). Ten months after her discharge, the patient was referred to our clinic with a 3-week history of mild headache that had started after a minor head trauma. CT scan revealed a chronic right parietal EDH beneath the craniotomy flap (Figure 3). The patient’s neurological functions were intact. The hematological tests showed F XIII levels as low as in her first presentation. A detailed inquiry revealed that the patient had not received fresh frozen plasma for the last 2 months. The EDH was surgically removed while the patient was infused with fresh frozen plasma. Full recovery was achieved, and the post-operative CT scan of the patient demonstrated no residual hemorrhage (Figure 4).
DISCUSSION Acute SDH occurs in approximately 5–22% of patients with severe head injury and results from bleeding within
the subdural space due to stretching and tearing of the bridging veins that traverse the space between the cortical surface and the venous sinuses (13,14). Subdural hemorrhages also can result from injury to the surface of the brain with bleeding from cortical vessels into the subdural space (14). Epidural hematoma is a collection of blood between the inner table of the skull and the dura and occurs in ⬍ 2% of patients admitted with craniocerebral trauma (14). In infants and elderly people, EDHs are rare due to dura that is well attached to the skull, but in young children the dura-to-skull fibrovascular attachments decrease in density as the skull grows. EDHs, therefore, are the most common traumatic intracranial hematoma in young children, with about 3% of those hospitalized with head trauma (5). Acute spontaneous SDH is extremely rare. Its main etiological factors include anticoagulant therapy, hypertension, cocaine-induced vasculitis, bleeding from intracranial tumors or aneurysms, and bleeding and coagulation disorders (1,3,4). Deficiency of F XIII is a quite rare coagulation disorder and occurs as congenital or in acquired forms (15). The main causes of acquired F XIII deficiency are liver disease, inflammatory bowel disease, disseminated intravascular coagulopathy, HennochSchönlein purpura, and sepsis (15,16). Congenital form is an autosomal recessive disorder of hemostasis, with an estimated prevalence of approximately 1 in 3–5 million individuals (7). In our patient, there were no signs or
Epidural and Subdural Hematoma in a Child with F XIII Deficiency
27
Figure 2. Post-operative CT scans demonstrating no hemorrhage.
symptoms of those diseases mentioned above causing the acquired form. F XIII, found in plasma, platelets, and monocytes, is a transpeptidase that is necessary for normal hemostasis and wound healing. It converts hydrogenbonded fibrin monomers into covalently bonded fibrin polymers and cross-links between collagen and fibronectin (6,7,17). In addition, in F XIII deficiency, blood clot is weak and unable to maintain a hemostatic plug, leading to hemorrhages (7). Factor XIII deficiency is associated with a high incidence of life-threatening complications, particularly intracranial hemorrhages (8). There are several studies demonstrating that F XIII deficiency causes intracerebral hemorrhages, chronic subdural and post-traumatic EDHs; however, there are no reports in the literature regarding spontaneous acute SDH resulting from F XIII deficiency (8 –12,16).
Post-operative bleeding in the surgical field is also a serious problem, especially in neurological surgery (15). Although there are reported cases regarding bleeding around the surgery site, in our case no hemorrhages developed in the surgical field in the early post-operative period. However, chronic EDH detected beneath the craniotomy flap after a minor trauma 10 months after the first surgery might be related to insufficient replacement therapy for F XIII. The clinical presentation can vary based on the size, rapidity of growth of the SDH or EDH, and the severity of diffuse injury to the brain (14). In our patient, there was no history or signs of trauma at the time of first admission. Furthermore, the patient was awake and able to converse, but disoriented. The relatively good neurological condition of the patient at the first admission
Figure 3. Chronic epidural hematoma beneath the craniotomy flap.
28
M. Vural et al.
Figure 4. Post-operative CT scan demonstrating no hemorrhage.
despite the large SDH may have been due to the absence of traumatic direct impact to the brain surface. On her second admission, the patient was neurologically intact despite having a small hematoma that had developed after a minor head trauma due to a fall, which apparently did not cause noticeable damage. Umbilical cord bleeding is the most common symptom of F XIII deficiency and occurs in about 80% of patients. Recognition of this characteristic feature is vital for diagnosis of this rare congenital bleeding disorder (18). By the replacement and prophylactic therapy after the definitive diagnosis of F XIII deficiency, the mortal manifestations like intracranial hemorrhages, which occur in 25– 60% of patients not receiving therapy, could be prevented (18). The history of our patient involved no definitive data about umbilical cord bleeding; therefore, considering the development of spontaneous SDH, F XIII deficiency was the diagnosis. The treatment of F XIII deficiency includes F XIII concentrate and fresh frozen plasma administration (19). Our patient received fresh frozen plasma for the replacement and prophylactic therapy. Because the patient was living in another city, she came to our hospital monthly for transfusion. However, a detailed inquiry revealed that the patient had not received the last two plasma transfusions before her
second admission, which resulted in insufficient levels of F XIII. Consequently, an EDH after a minor head trauma was more likely to develop due to insufficient levels of F XIII. To the best of our knowledge, this report presents the first case of a spontaneous acute SDH and late posttraumatic EDH beneath the craniotomy flap in a child with F XIII deficiency. We present this case to raise awareness of the presence of a potential F XIII deficiency as a cause of hemorrhagic diathesis and spontaneous SDH.
REFERENCES 1. Agrawal D, Mahapatra AK. Spontaneous subdural hematoma in a young adult with hemophilia. Neurol India 2003;51:114 –5. 2. Avis SP. Nontraumatic acute subdural hematoma. A case report and review of the literature. Am J Forensic Med Pathol 1993;14: 130 – 4. 3. Drake CG. Subdural haematoma from arterial rupture. J Neurosurg 1961;18:597– 601. 4. Keller TM, Chappell ET. Spontaneous acute subdural hematoma precipitated by cocaine abuse: case report. Surg Neurol 1997;47: 12–5. 5. Piatt JH, Kernan JC. Intracranial hematomas. In: McLone DG, Reigel DH, eds. Pediatric neurosurgery. Philadelphia, PA: W.B. Saunders; 2001:634 – 45.
Epidural and Subdural Hematoma in a Child with F XIII Deficiency 6. Lorand L, Losowsky MS, Miloszewski KJ. Human factor XIII: fibrin-stabilizing factor. Prog Hemost Thromb 1980;5:245–90. 7. Pernod G, Barro C, Arnutti B, et al. Surgery in severe factor XIII deficiency: report of a case of epilepsy neurosurgery and review. Haemophilia 2003;9:121– 4. 8. Abbondanzo SL, Gootenberg JE, Lofts RS, McPherson RA. Intracranial hemorrhage in congenital deficiency of factor XIII. Am J Pediatr Hematol Oncol 1988;10:65– 8. 9. Donnet A, Trefouret S, Alessi MC, Harle JR, Graziani N, Grisoli F. Intradural hematoma of the foramen magnum associated with factor XIII deficiency. Rev Neurol (Paris) 1994;150:164 – 6. 10. Giraldi C, Creta S, Martini A, Ioppoli C, Valleriani A, Muratorio A. Spontaneous intracerebral hematoma in a adolescent with factor XIII deficiency. Case report. Ital J Neurol Sci 1989;10:579 – 82. 11. Larsen PD, Wallace JW, Frankel LS, Crisp D. Factor XIII deficiency and intracranial hemorrhages in infancy. Pediatr Neurol 1990;6:277– 8. 12. Shigemori M, Kojima T, Kojo N, et al. 3 operated cases of congenital deficiency of Factor XIII associated with intracranial hematomas [Japanese]. No Shinkei Geka 1984;12:1167–71.
29 13. Bailes JE, Hudson V. Classification of sport-related head trauma: a spectrum of mild to severe injury. J Athl Train 2001;36:236 – 43. 14. Samudrala S, Cooper PR. Traumatic intracranial hematomas. In: Wilkins RH, Rengachary SS, eds. Neurosurgery. New York: McGraw-Hill; 1996:2797– 807. 15. Gerlach R, Raabe A, Zimmermann M, Siegemund A, Seifert V. Factor XIII deficiency and postoperative hemorrhage after neurosurgical procedures. Surg Neurol 2000;54:260 – 6. 16. Albanese A, Tuttolomondo A, Anile C, et al. Spontaneous chronic subdural hematomas in young adults with a deficiency in coagulation factor XIII. Report of three cases. J Neurosurg 2005;102: 1130 –2. 17. Muszbek L, Adany R, Mikkola H. Novel aspects of blood coagulation factor XIII. I. Structure, distribution, activation, and function. Crit Rev Clin Lab Sci 1996;33:357– 421. 18. Nugent DJ. Prophylaxis in rare coagulation disorders—factor XIII deficiency. Thromb Res 2006;118(Suppl 1):S23– 8. 19. Bolton-Maggs PH, Perry DJ, Chalmers EA, et al. The rare coagulation disorders—review with guidelines for management from the United Kingdom Haemophilia Centre Doctors’ Organisation. Haemophilia 2004;10:593– 628.
doi:10.1016/j.jemermed.2007.11.041
Clinical Communications: Pediatrics SPONTANEOUS ACUTE SUBDURAL HEMATOMA AND CHRONIC EPIDURAL HEMATOMA IN A CHILD WITH F XIII DEFICIENCY Murat Vural,
MD,*
Coskun Yarar,
MD,†
Ramazan Durmaz,
MD,*
and Metin Ant Atasoy,
MD*
*Department of Neurosurgery and †Department of Pediatrics, Eskis¸ehir Osmangazi University Medical Faculty, Eskisehir, Turkey Reprint Address: Murat Vural, MD, Department of Neurosurgery, Eskis¸ehir Osmangazi University Medical Faculty, Deliklitas¸ Mh. Deliklitas¸ Cd. Huzur, Apt. No. 28/3, Eskisehir, Turkey
e Abstract—Factor XIII (F XIII) deficiency is a rare autosomal recessive congenital disorder that can cause spontaneous subdural or epidural hematomas. Due to its low incidence, F XIII deficiency may well be under-diagnosed. A 7-year-old girl with no history of medical problems presented with progressive headache of 3 days. Cerebral computed tomography (CT) scans revealed a large right acute parietooccipital subdural hematoma with a significant midline shift. After an emergent parietooccipital craniotomy and evacuation of the subdural hematoma, a screening test for factor XIII was performed. The results of the test were abnormal. She had full recovery and was discharged with a follow-up treatment of monthly transfusion of fresh frozen plasma as the replacement and prophylactic therapy. Ten months later, she was referred to our center with headache after a minor head trauma. Her medical history revealed that she had not received fresh frozen plasma for the last 2 months. CT scan showed a chronic right parietal epidural hematoma beneath the craniotomy flap. The present case indicates that although its incidence is very rare, F XIII deficiency can cause acute or chronic subdural and epidural hematomas. Therefore, in acute or chronic subdural and epidural hematomas with no underlying cause, the presence of a potential F XIII deficiency should be suspected as a cause of hemorrhagic diathesis. © 2010 Elsevier Inc.
tension, anticoagulant therapy, bleeding and coagulation disorders, cocaine-induced vasculitis, and bleeding from intracranial tumors or aneurysms (1,3,4). Epidural hematoma (EDH) often results from a local injury (5). Factor XIII (F XIII) is a transpeptidase that is necessary for normal blood hemostasis. In F XIII deficiency, blood clot is weak and thus unable to maintain a hemostatic plug, leading to hemorrhages (6,7). Intracerebral hemorrhages due to factor XIII deficiency have been shown in various case reports (8 –12). To the best of our knowledge, this is the first case of acute SDH and chronic EDH 10 months after the first operation.
CASE REPORT A 7-year-old girl was admitted to our hospital with complaints of progressing headache, nausea, and vomiting for the last 3 days. She had no significant past medical history. At the time of admission, she was disoriented but able to converse. Computed tomography (CT) scans showed a large hyperdense parietooccipital SDH with a significant midline shift. The hematoma was evacuated immediately (Figure 1). Her post-operative course was uneventful with complete neurological recovery. In consultation with the Department of Pediatrics, further investigations were made to determine the etiology of subdural hemorrhage. Platelet count, prothrombin time, activated partial thromboplastin time, international normalized ratio, bleeding time, and all coagulation factors were normal except for
e Keywords—F XIII deficiency; epidural hematoma; subdural hematoma; pediatric age
INTRODUCTION Spontaneous acute subdural hematoma (SDH) is a rare condition (1,2). Potential predisposing factors are hyper-
RECEIVED: 6 March 2007; FINAL ACCEPTED: 5 November 2007
SUBMISSION RECEIVED:
20 July 2007; 25
26
M. Vural et al.
Figure 1. Axial view of the large hyperdense parietooccipital subdural hematoma with a significant midline shift.
F XIII. The diagnosis of F XIII deficiency was made based on the positive clot solubility test using 5 M urea. However, no reliable data about the history of prolonged bleeding from the umbilical stump, a common symptom of F XIII deficiency at birth, were available. The patient was discharged without any neurological deficits, with a treatment of monthly transfusion of fresh frozen plasma as the replacement and prophylactic therapy. There was no residual or recurrent hemorrhage on control CT scans (Figure 2). Ten months after her discharge, the patient was referred to our clinic with a 3-week history of mild headache that had started after a minor head trauma. CT scan revealed a chronic right parietal EDH beneath the craniotomy flap (Figure 3). The patient’s neurological functions were intact. The hematological tests showed F XIII levels as low as in her first presentation. A detailed inquiry revealed that the patient had not received fresh frozen plasma for the last 2 months. The EDH was surgically removed while the patient was infused with fresh frozen plasma. Full recovery was achieved, and the post-operative CT scan of the patient demonstrated no residual hemorrhage (Figure 4).
DISCUSSION Acute SDH occurs in approximately 5–22% of patients with severe head injury and results from bleeding within
the subdural space due to stretching and tearing of the bridging veins that traverse the space between the cortical surface and the venous sinuses (13,14). Subdural hemorrhages also can result from injury to the surface of the brain with bleeding from cortical vessels into the subdural space (14). Epidural hematoma is a collection of blood between the inner table of the skull and the dura and occurs in ⬍ 2% of patients admitted with craniocerebral trauma (14). In infants and elderly people, EDHs are rare due to dura that is well attached to the skull, but in young children the dura-to-skull fibrovascular attachments decrease in density as the skull grows. EDHs, therefore, are the most common traumatic intracranial hematoma in young children, with about 3% of those hospitalized with head trauma (5). Acute spontaneous SDH is extremely rare. Its main etiological factors include anticoagulant therapy, hypertension, cocaine-induced vasculitis, bleeding from intracranial tumors or aneurysms, and bleeding and coagulation disorders (1,3,4). Deficiency of F XIII is a quite rare coagulation disorder and occurs as congenital or in acquired forms (15). The main causes of acquired F XIII deficiency are liver disease, inflammatory bowel disease, disseminated intravascular coagulopathy, HennochSchönlein purpura, and sepsis (15,16). Congenital form is an autosomal recessive disorder of hemostasis, with an estimated prevalence of approximately 1 in 3–5 million individuals (7). In our patient, there were no signs or
Epidural and Subdural Hematoma in a Child with F XIII Deficiency
27
Figure 2. Post-operative CT scans demonstrating no hemorrhage.
symptoms of those diseases mentioned above causing the acquired form. F XIII, found in plasma, platelets, and monocytes, is a transpeptidase that is necessary for normal hemostasis and wound healing. It converts hydrogenbonded fibrin monomers into covalently bonded fibrin polymers and cross-links between collagen and fibronectin (6,7,17). In addition, in F XIII deficiency, blood clot is weak and unable to maintain a hemostatic plug, leading to hemorrhages (7). Factor XIII deficiency is associated with a high incidence of life-threatening complications, particularly intracranial hemorrhages (8). There are several studies demonstrating that F XIII deficiency causes intracerebral hemorrhages, chronic subdural and post-traumatic EDHs; however, there are no reports in the literature regarding spontaneous acute SDH resulting from F XIII deficiency (8 –12,16).
Post-operative bleeding in the surgical field is also a serious problem, especially in neurological surgery (15). Although there are reported cases regarding bleeding around the surgery site, in our case no hemorrhages developed in the surgical field in the early post-operative period. However, chronic EDH detected beneath the craniotomy flap after a minor trauma 10 months after the first surgery might be related to insufficient replacement therapy for F XIII. The clinical presentation can vary based on the size, rapidity of growth of the SDH or EDH, and the severity of diffuse injury to the brain (14). In our patient, there was no history or signs of trauma at the time of first admission. Furthermore, the patient was awake and able to converse, but disoriented. The relatively good neurological condition of the patient at the first admission
Figure 3. Chronic epidural hematoma beneath the craniotomy flap.
28
M. Vural et al.
Figure 4. Post-operative CT scan demonstrating no hemorrhage.
despite the large SDH may have been due to the absence of traumatic direct impact to the brain surface. On her second admission, the patient was neurologically intact despite having a small hematoma that had developed after a minor head trauma due to a fall, which apparently did not cause noticeable damage. Umbilical cord bleeding is the most common symptom of F XIII deficiency and occurs in about 80% of patients. Recognition of this characteristic feature is vital for diagnosis of this rare congenital bleeding disorder (18). By the replacement and prophylactic therapy after the definitive diagnosis of F XIII deficiency, the mortal manifestations like intracranial hemorrhages, which occur in 25– 60% of patients not receiving therapy, could be prevented (18). The history of our patient involved no definitive data about umbilical cord bleeding; therefore, considering the development of spontaneous SDH, F XIII deficiency was the diagnosis. The treatment of F XIII deficiency includes F XIII concentrate and fresh frozen plasma administration (19). Our patient received fresh frozen plasma for the replacement and prophylactic therapy. Because the patient was living in another city, she came to our hospital monthly for transfusion. However, a detailed inquiry revealed that the patient had not received the last two plasma transfusions before her
second admission, which resulted in insufficient levels of F XIII. Consequently, an EDH after a minor head trauma was more likely to develop due to insufficient levels of F XIII. To the best of our knowledge, this report presents the first case of a spontaneous acute SDH and late posttraumatic EDH beneath the craniotomy flap in a child with F XIII deficiency. We present this case to raise awareness of the presence of a potential F XIII deficiency as a cause of hemorrhagic diathesis and spontaneous SDH.
REFERENCES 1. Agrawal D, Mahapatra AK. Spontaneous subdural hematoma in a young adult with hemophilia. Neurol India 2003;51:114 –5. 2. Avis SP. Nontraumatic acute subdural hematoma. A case report and review of the literature. Am J Forensic Med Pathol 1993;14: 130 – 4. 3. Drake CG. Subdural haematoma from arterial rupture. J Neurosurg 1961;18:597– 601. 4. Keller TM, Chappell ET. Spontaneous acute subdural hematoma precipitated by cocaine abuse: case report. Surg Neurol 1997;47: 12–5. 5. Piatt JH, Kernan JC. Intracranial hematomas. In: McLone DG, Reigel DH, eds. Pediatric neurosurgery. Philadelphia, PA: W.B. Saunders; 2001:634 – 45.
Epidural and Subdural Hematoma in a Child with F XIII Deficiency 6. Lorand L, Losowsky MS, Miloszewski KJ. Human factor XIII: fibrin-stabilizing factor. Prog Hemost Thromb 1980;5:245–90. 7. Pernod G, Barro C, Arnutti B, et al. Surgery in severe factor XIII deficiency: report of a case of epilepsy neurosurgery and review. Haemophilia 2003;9:121– 4. 8. Abbondanzo SL, Gootenberg JE, Lofts RS, McPherson RA. Intracranial hemorrhage in congenital deficiency of factor XIII. Am J Pediatr Hematol Oncol 1988;10:65– 8. 9. Donnet A, Trefouret S, Alessi MC, Harle JR, Graziani N, Grisoli F. Intradural hematoma of the foramen magnum associated with factor XIII deficiency. Rev Neurol (Paris) 1994;150:164 – 6. 10. Giraldi C, Creta S, Martini A, Ioppoli C, Valleriani A, Muratorio A. Spontaneous intracerebral hematoma in a adolescent with factor XIII deficiency. Case report. Ital J Neurol Sci 1989;10:579 – 82. 11. Larsen PD, Wallace JW, Frankel LS, Crisp D. Factor XIII deficiency and intracranial hemorrhages in infancy. Pediatr Neurol 1990;6:277– 8. 12. Shigemori M, Kojima T, Kojo N, et al. 3 operated cases of congenital deficiency of Factor XIII associated with intracranial hematomas [Japanese]. No Shinkei Geka 1984;12:1167–71.
29 13. Bailes JE, Hudson V. Classification of sport-related head trauma: a spectrum of mild to severe injury. J Athl Train 2001;36:236 – 43. 14. Samudrala S, Cooper PR. Traumatic intracranial hematomas. In: Wilkins RH, Rengachary SS, eds. Neurosurgery. New York: McGraw-Hill; 1996:2797– 807. 15. Gerlach R, Raabe A, Zimmermann M, Siegemund A, Seifert V. Factor XIII deficiency and postoperative hemorrhage after neurosurgical procedures. Surg Neurol 2000;54:260 – 6. 16. Albanese A, Tuttolomondo A, Anile C, et al. Spontaneous chronic subdural hematomas in young adults with a deficiency in coagulation factor XIII. Report of three cases. J Neurosurg 2005;102: 1130 –2. 17. Muszbek L, Adany R, Mikkola H. Novel aspects of blood coagulation factor XIII. I. Structure, distribution, activation, and function. Crit Rev Clin Lab Sci 1996;33:357– 421. 18. Nugent DJ. Prophylaxis in rare coagulation disorders—factor XIII deficiency. Thromb Res 2006;118(Suppl 1):S23– 8. 19. Bolton-Maggs PH, Perry DJ, Chalmers EA, et al. The rare coagulation disorders—review with guidelines for management from the United Kingdom Haemophilia Centre Doctors’ Organisation. Haemophilia 2004;10:593– 628.