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18 nederlands tijdschrift voor anesthesiologie | januari '10 Secondary bleeding in traumatic brain injury: a case report S. Greuters, Drs. (MD) A. van den Berg, BSc C.M.J. van der Rijst, BSc V. Viersen, Drs. (MD) L.A. Schwarte, Dr. (MD) C. Boer, Dr. Acute coagulopathy is a severe complication of trauma and may contribute to secondary injury [1]. In the case of traumatic brain injury (TBI), coagulopathy in combination with hypothermia and acidosis may lead to cerebral hypoperfusion and consequent hypoxia, leading to impaired outcome. In 1974, it was already suggested by Goodnight et al. that TBI induces cerebral tissue thromboplastin release, independent of bleeding, which initiates the coagulation pathway [2]. Although subsequent fibrin clot formation matches with fibrinolytic activity, this finally leads to coagulation factor consumption and thus increases the risk for delayed bleeding. Here we report the hemostatic changes observed in a TBI patient who was presented without an apparent bleeding disorder and discuss the possible mechanisms underlying trauma-induced coagulopathy when brain injury is involved. Case report A 63 year old male without previous medical history was admitted to the Emergency Department (ED) of the VU University Medical Center. While riding a scooter without head protection he collided upon a stationary vehicle. He was found by ambulance paramedics gasping for breath. His vital parameters were: a SpO 2 of 70%, a heart rate of 100 beats per minute and a blood pressure of 100 over 70 mmHg. Neurological investigation revealed a Glasgow Coma Scale (GCS) of E1M1V1 and light-reactive pupils on both sides. Because of his severe neurological condition and threatened airway he was endotracheally intubated by the physician-based mobile medical team (MMT) after a rapid sequence induction. Thousand ml of NaCl (0.9%), 500 ml mannitol 10% and 250 ml of 7.2% saline in 6% hydroxyethyl starch (HyperHAES ® Fresenius Kabi AG, Bad Homburg v.d.H., Germany) were given in the prehospital phase. Upon ED arrival the patient was mechanically ventilated and hemodynamically stable with light-reactive pupils. Physical examination revealed some blood loss from the left ear, an open cruris facture of the right leg and a wound on his left knee. Blood was drawn immediately after ED admission (T=0) and the results from routine coagulation tests (activated partial thromboplastin time (aPTT), prothrombine time (PT) and Clauss fibrinogen test) and thromboelastometry (ROTEM ® , Pentapharm, Munich) are represented in table 1 and Department of Anesthesiology Institute for Cardiovascular Research VU University Medical Center Amsterdam The Netherlands contactinformation S. Greuters, MD Department of Anesthesiology VU University Medical Center De Boelelaan 1117 1081 HV Amsterdam The Netherlands Tel. +31 20 4444386 Email s.greuters@vumc.nl 2, respectively. The background of ROTEM measurements is explained in the insert, and ROTEM output is depicted in figure 1. Radiological investigation showed severe TBI with distinct contusion focuses, subarachnoid and subdural haemorrhage and an impression fracture of the os parietale with pneumocephaly. Moreover, the patient suffered from a rib fracture and a pertrochanteric fracture of the femur. Surgical intervention comprised decompression craniotomy, placement of an intracranial pressure measuring catheter and external fixation of the cruris fracture. Preoperative and perioperative blood loss were estimated to be 800 ml in about 4 hours. Subsequent blood analysis was performed at 2 and 4 hours after ED arrival, showing a coagulopathy that worsened over time as represented by an increased aPTT and PT and lowered plasma fibrinogen levels (table 1). Simultaneously, ROTEM values changed accordingly as represented in table 2 and figure 1. Thromboelastometry demonstrated a decrease in maximum clot formation (MCF) in the fibrinogen test (FIBTEM) from 13 mm at T= 0 to 3 and 2 mm at T=2 and T=4, respectively. The INTEM assay showed prolonged clot formation
januari '10 | nederlands tijdschrift voor anesthesiologie 19 time (CFT) whereas the EXTEM assay revealed an extended clotting time and CFT, a decreased α-angle and a decreased maximum clot formation (MCF). There was no sign of hyperfibrinolysis in all four ROTEM analyses. The diagnosed hypofibrinogenemia was paralleled by clinical bleeding and blood oozed from the neurosurgical site and the insert of the intravenous catheters. Before T=4, coagulopathy was treated by 2 units fresh frozen plasma (FFP), 3 units of packed cells (PC), 2 gram tranexamic acid and 1.4 gram calciumgluconate. Despite this effort to correct the coagulopathy, routine and ROTEM coagulation tests were even more aggravated at T=4 and the patient was subsequently treated with 2 gram tranexamic acid and 2 gram fibrinogen (Haemocomplettan P, CSL Behring, Breda, the Netherlands), which resulted in reduced oozing and improved hemostasis as shown at T=8 (table 1). At T=24, ROTEM was repeated and showed a normal coagulation (table 2, figure 1). The patient was subsequently admitted to the Intensive Care Unit with stable hemostasis. During his ICU admission his neurological condition however did not improve and it was decided to withhold further treatment. The patient died 12 days post-trauma. Discussion Current literature proposes several mechanisms underlying the development of trauma-induced coagulopathy in patients with brain injury which involve alterations in thrombin generation, fibrinogen levels, thrombocyte function and hyperfibrinolysis [1-3]. Here we discuss possible mechanisms contributing to the coagulopathy as seen in our patient. TBI involves a state of hypercoagulability which is presumed to be initiated by an abundant release of tissue factor [1, 4]. This increased tissue factor release presumably may lead to disseminated intravascular coagulation (DIC), cerebral microthrombi and a consumption coagulopathy [1, 5]. In particular, coagulation factor consumption may subsequently promote a tendency towards bleeding in TBI patients. A second mechanism underlying TBI-associated coagulopathy is based on the association between systemic hypoperfusion and the initiation of anticoagulation and hyperfibrinolysis [6]. Hypoperfusion promotes endothelial thrombomodulin expression which binds thrombin and thereby results in inhibition of fibrin generation from fibrinogen. The thrombomodulin-thrombin complex additionally activates protein C, which inhibits plasminogen activator inhibitor 1 (PAI-1) and the coagulation factors Va and VIIIa. Simultaneously, t-PA is released from the endothelium which further contributes to fibrinolysis [7]. In addition to hypercoagulability and hyperfibrinolysis, trauma patients frequently suffer from hypothermia and acidosis which both contribute to a disturbed coagulation and impaired outcome [8, 9]. Severe hypothermia (< 32 o C) specifically influences the initiation of the coagulation cascade, whereas acidosis impairs the propagation phase that is necessary for clot formation. Both hypothermia and acidosis contribute to impaired platelet function, fibrinogen levels and fibrin generation [10]. Traumatic coagulopathy is often attributed to hemodilution from fluid resuscitation, which implicates that at least part of the observed coagulation problems are actually caused by the treatment given instead of the trauma itself. There have been numerous in vitro studies trying to find the mechanism responsible for volume therapy-related coagulopathy. A recent study by Fenger-Eriksen et al. showed that an in vivo dilution of 30% dilution with 130/0.4 hydroxyethyl starch (HES) caused a severe reduction of all coagulation factors. They further provided evidence of fibrinogen deficiency as being a major determinant in dilutional coagulopathy [11]. We present a patient with severe TBI and concomitant injuries, who developed trauma-induced coagulopathy (TIC) that was not initially caused by massive bleeding. Our patient was admit- case report T=0 T=2 T=4 T=8 Hemoglobin (mmol/l) 5.9 5.0 - 5.9 Hematocrit 0.29 0.24 - 0.28 Thrombocytes (109/l) 177 157 - 133 PT (INR) 1.32 1.66 1.83 1.23 APTT (s) 43 51 50 38 D-dimer (mg) 26.4 - 40.9 - Fibrinogen (g/l) 1.9 1.3 1 - pH 7.32 7.24 7.3 7.22 PaO2 (mm Hg) 496 343 268 268 PaCO2 (mm Hg) 50 62.6 55 66 HCO3 (mmol/l) 24.9 26 26.6 25.7 B.E. (mmol/l) -0.9 -4.2 -0.3 -2.3 Lactate (mmol/l) 1.0 0.87 1.37 1.1 Table 1. Laboratory values measured at different time points post-trauma APTT: activated partial thromboplastin time. PT: prothrombine time. BE: base deficit. Reference values T= 0 T= 2 T= 4 T= 24 CT INTEM (s) 100-240 155 190 179 181 CFT INTEM (s) 30-110 93 150 217 105 α INTEM (o) 70-83 71 62 55 73 MCF INTEM (mm) 50-72 57 52 47 58 CT EXTEM (s) 38-79 57 99 152 67 CFT EXTEM (s) 34-159 169 202 223 120 α EXTEM (o) 63-83 58 54 54 71 MCF EXTEM (mm) 50-72 53 48 43 61 MCF FIBTEM (mm) 9-25 13 3 2 18 Table 2. ROTEM values at different time points post-trauma. CT: clotting time; CFT: clot formation time; α: α-angle; MCF: maximum clot formation; INTEM: intrinsic coagulation; EXTEM: extrinsic coagulation; FIBTEM: fibrinogen component of clot formation.
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