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American Journal of Emergency Medicine

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American Journal of Emergency Medicine 32 (2014) 288.e1-288.e3

Rotational thromboelastometry along with thromboelastography plays a critical role in the management of traumatic bleeding

Abstract

Massive posttraumatic bleeding is the leading cause of potentially Preventable death among patients with severe trauma. Immediate diagnosis and treatment of traumatic coagulopathy and its differen- tiation from surgical bleeding after major trauma are critical in the management of such patients. In this case report, we present a 33- year-old woman who had multiple injuries to the head and trunk in motor vehicle collision, resulting in severe bleeding and necessitating emergency surgery. We demonstrate how repeated rotational throm- boelastometry and thromboelastography analyses were used to direct the choice of therapy to stabilize her circulatory system for surgery and to differentiate surgical bleed from coagulopathy. Therapy based on massive transfusion protocol and on laboratory coagulation tests would be insufficient to stop bleeding. We conclude that rotational thromboelastometry/thromboelastography analysis plays a critical role in the management of traumatic bleeding and helps us provide more aggressive and targeted therapy for coagulopathy both in the acute and later phases of treatment of severe bleeding.

Massive posttraumatic bleeding is the leading cause of potentially preventable death among patients with severe trauma [1]. Immediate diagnosis and treatment of traumatic coagulopathy and its differen- tiation from surgical bleeding after major trauma are critical in the management of such patients. In this case, we want to show that Rotational thromboelastometry along with thromboelasto- graphy (TEG) plays a critical role in the management of severe traumatic bleeding. The patient has given her consent to the publication of the case.

We present the case of a 33-year-old woman who had severe trauma (Injury Severity Score [ISS], 59) in a motor vehicle collision. Because of unconsciousness on the spot, she was immediately intubated and artificially ventilated and had received norepinephrine in an attempt to restore arterial pressure during the Ambulance transfer to hospital because of low blood pressure of 70/40 mm Hg not reacting to fluids. On arrival, she had severe bleeding from an open wound to the occiput, left eye mydriasis with no photoreaction, and an open fracture of the left thigh. To obtain a palpable pulse at the femoral artery, norepinephrine was infused at 0.75 ug kg^-1 min^-1 and mean arterial blood pressure was maintained at 80 to 90 Torr. Ultrasonography detected free fluid in the patient’s peritoneal cavity, and so she was immediately referred for surgical laparotomy.

The patient’s temperature was 35.9?C. A blood sample was subjected to hematologic, biochemical, and ROTEM analysis at 37?C [ROTEM-extrinsic haemostasis system (EXTEM); Pentapharm GmbH, Munich, Germany]. plasma lactate concentration was 7.8 mmol/L (no

alcohol detected), pH was 7.0, and the base excess was -18.5 mmol/L. The patient was therefore given 2 g of Tranexamic acid, 4 g of fibrinogen, 4 units of fresh-frozen plasma , 4 units of red blood cells, 2000 mL of crystalloids, 500 mL of colloids, and 100 mmol of sodium bicarbonate solution. After this therapy, the norepinephrine dose was reduced to 0.12 ug kg^-1 min^-1.

Because EXTEM analysis showed prolongation of clotting time

(CT) of 112 seconds (Fig. 1A), FFP and red blood cells were administered continuously in a 1:1 ratio while the patient was in the operating theater, according to the massive transfusion protocol [2]. After 1 hour, however, there was no decrease in bleeding, and another EXTEM analysis was performed. This found severe coagulo- pathy, with a CT prolongation of 114 seconds, a Clot formation time of 482 seconds, and an ? angle of 36^o. Amplitude of clot firmness at 10 minutes was 22 mm, and maximal clot firmness (MCF) was 35 mm. Maximum lysis was only 2%. functional Fibrinogen level (FIBTEM) analysis also showed a low MCF of 5 mm (Fig. 1B, C).

The patient was immediately given another 4 g fibrinogen (to increase fibtem MCF to 13 mm) with 1200 units of prothrombin complex concentrate (to correct CT time), 4 units of platelets (because EXTEM MCF was only 35 mm, thus indicative of low platelets function), and calcium and magnesium supplements. When the results of laboratory tests ordered when the patient was admitted became available, they showed platelet counts of 189 x 10⁹/L, an International normalized ratio of 2.5, an activated partial thromboplastin time of 103 seconds, and fibrinogen levels of 1.27 g/L. In the operating theater, the general surgeons found severe bleeding from the spleen, liver, and omentum. A splenectomy and an omentectomy were performed, and the liver was packed and sutured. Meanwhile, the trauma surgeon sutured a 20-cm-long occipital wound, over a fracture of the lamina externa cranii. Severe bleeding from this wound required the insertion of a drain; however, this stopped after the treatment indicated by the ROTEM results. Because the patient’s circulation was still unstable, the surgeon suspected that she was bleeding from the thigh, and osteosynthesis of the fracture was performed after abdominal surgery. This still did not correct the instability; however, and EXTEM and FIBTEM were performed again (Fig. 1D). No coagulopathy was found; pH was 7.37, base excess was -4.1mmol/L, and lactate concentration was

3.5mmol/L. At this point, we decided to perform classical TEG analysis

(ie, using nonactivated blood treated with sodium citrate; TEG Hemostasis System; Haemoscope Corp, Niles, IL) at both the patient’s body temperature (33?C) and at 37?C. The curves were almost identical (Fig. 2), which eliminated hypothermic coagulopathy as a cause and suggested surgical bleeding. Contrast computed tomogra- phy was performed, which showed that the source of the bleeding

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288.e2 M. Durila, M. Malosek / American Journal of Emergency Medicine 32 (2014) 288.e1-288.e3

Fig. 1. ROTEM measurements. A, EXTEM before surgical intervention followed by administering of FFP. EXTEM (B) and FIBTEM (C) at 1 hour after continuously administering FFP followed by more aggressive therapy. D, EXTEM after adequate therapy. Reference ranges for EXTEM: CT = 38-79 seconds; CFT = 34-159 seconds; ? angle = 63?-83?; and MCF = 50-72 mm. Reference range for FIBTEM: MCF = 9-25 mm.

was in the spleen. Besides this finding, a number of brain injuries were diagnosed: a 3-mm fracture of the occipital bone, bilateral contusions of the cerebellum as well as occipital and parietal contusions, contusion with bleeding (13 mm x 8 mm) in the frontal brain, and an acute ischemic focus (4 cm x 2 cm) in the right cereberal hemisphere. The patient also had minimal contusion of the lungs, grade V lacerations of both liver lobes, L2 to L4 abruption of transverse processes, and fractures of the acetabulum and upper arm of the symphysis. A surgeon was contacted immediately, and the patient underwent another intervention. During laparotomy, the source of bleeding was found in a small branch of the spleen artery; once this was treated, the patient’s circulatory system stabilized with norepi- nephrine 0.07ug kg^-1 min^-1.

In total, during this period (8 hours), the patient received 26 units of FFP, 30 transfusion unit of erythrocytes, 4000 mL of crystalloids, and 1500 mL of colloids. A final blood analysis found a platelet count of 67 x 10⁹/L, an INR of 1.32, an activated partial thromboplastin time of 31.5 seconds, and a fibrinogen level of 1.46 g/L. Analysis of EXTEM found normal CT (51 seconds) and slightly prolonged CFT (163 seconds). The ? angle was slightly lower (60?) than previously, but the amplitude of clot firmness at 10 minutes was significantly lower (39 mm) and the boundary MCF was 50 mm, with no sign of fibrinolysis. Using FIBTEM, a low MCF of 4 mm was detected.

Only a further dose of 2 g fibrinogen (to increase FIBTEM MCF to 8 mm) was administered to the patient to maintain EXTEM findings

Fig. 2. TEG measurements. Black curve obtained after measuring at 37?C and green curve obtained after measuring at 33?C. Almost identical results eliminate hypothermic coagulopathy as the cause of bleeding.

M. Durila, M. Malosek / American Journal of Emergency Medicine 32 (2014) 288.e1-288.e3 288.e3

Fig. 3. ROTEM intervention scheme.

within reference ranges, with an MCF of 57 mm as checked afterward. At that point, we were able to introduce a sensor for measuring intracranial pressure without any Bleeding complications. Computed tomography performed on the following day found no progression of Pathological findings or new bleeding, even in the area where the sensor had been introduced. Two days after the abdominal revision, the packing was removed, again without any bleeding complications. After this, sedation was withdrawn, and the patient was successfully extubated on the sixth day after admission with no neurologic deficit. No other complications such as transfusion-related acute lung injury, acute kidney injury, or intestinal distress syndrome were observed.

Although we adhered to the massive transfusion protocol [2] at the beginning of the patient’s treatment, it was not sufficient to stop her bleeding. Rotational thromboelastometry analysis provided addition- al information that guided our choice of successful therapy. We used the protocol of Lier et al [3] and Schochl et al [4] but adjusted it to a simplified formula (Fig. 3). Of note, although this patient had multiple-trauma injury, including cranial trauma, and her platelet count was 67 x 10⁹/L and prothrombin time INR was 1.32 after general stabilization, she did not receive a platelet transfusion or FFP because EXTEM indicated that MCF and CT were in the reference range. Having in common with other authors [5,6], we believe that it is not low platelet counts (b 100 x 10⁹) that jeopardize patients with cranial or multiple trauma and ROTEM values in the reference range, but rather hypoperfusion, low fibrinogen levels, and fibrinolysis.

We conclude that ROTEM/TEG analysis plays a critical role in the management of traumatic bleeding and helps us provide more aggressive and targeted therapy for coagulopathy both in the acute and later phases of treatment of severe bleeding. It is an inexpensive technique that can be easily performed at the patient’s bedside, repeatedly if necessary, and that provides rapid results.

Acknowledgments

The authors thank colleagues Jiri Petruska, MD, and Tomas Vymazal, MD (both from the Department of Anesthesiology and Critical Care Medicine, Second Faculty of Medicine, Charles University in Prague, Czech Republic) for consultation.

Miroslav Durila PhD Martin Malosek MD

Department of Anesthesiology and Critical Care Medicine Second Faculty of Medicine, Charles University in Prague, Czech Republic

E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2013.09.038

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