Thromboelastometry-guided hemostatic therapy for hemorrhagic shock in the postoperative period of vascular surgery: a case report

Thromboelastometry-guided hemostatic therapy for hemorrhagic shock in the postoperative period of... Background: Hemorrhagic shock is a medical emergency that often complicates vascular surgery and can lead to death. Hemorrhagic shock is characterized by hypoperfusion and hemodynamic abnormalities leading to the collapse of homeostasis due to massive blood loss. Early diagnosis is critical for a favorable outcome. Thromboelastometry has been considered an effective tool for bleeding management in critically ill patients. Thromboelastometry can guide transfusion therapy quickly, reducing the need for blood products. Therefore, it could be an alternative test to guide hemostatic therapy in complex cases of hemorrhagic shock as a result of vascular surgeries. We report our successful experience with a case of hemorrhagic shock in postoperative care in vascular surgery, in which bleeding management was guided by thromboelastometry and bleeding control was achieved with hemostatic drugs and coagulation factor concentrates. Case presentation: We report a case of an 82-year-old Afro-Brazilian man who presented to the intensive care unit with hemorrhagic shock in the postoperative period of vascular surgery. He underwent surgery for correction of iliac artery aneurysm with endoleak. His laboratory tests revealed severe anemia (hemoglobin 7.4 mg/dL), metabolic acidosis (bicarbonate 10 mEq/L, pH 7.11), acute kidney injury (creatinine 3.1 mg/dL), thrombocytopenia 3 3 (platelets count 83 × 10 /mm ), hypofibrinogenemia (70 mg/dL), international nationalized ratio 1.95, activated partial thromboplastin time 64.5 seconds, and lactate 87 mmol/L. There was active bleeding in surgical site. Bleeding management was guided by thromboelastometry. The first test showed fulminant hyperfibrinolysis, which was corrected with the administration of tranexamic acid. The second thromboelastometry test showed improvement of hyperfibrinolysis but severe hypocoagulability. Fibrinogen concentrate, platelet apheresis, cryoprecipitate, and prothrombin complex concentrate were sequentially administrated. Thromboelastometry was completely corrected after 2 hours. Arteriography to evaluate mechanical cause of bleeding was normal. No more bleeding was identified, and neither was any further transfusion needed. He was discharged from the intensive care unit from the ward 3 days after admission. Conclusions: Thromboelastometry may be considered a useful, feasible and safe tool to monitor and manage coagulopathy in patients with hemorrhagic shock. Moreover, it has the potential benefit of allowing rapid diagnosis, goal-directed therapy with hemostatic drugs and coagulation factor concentrates and thus, avoiding unnecessary blood component transfusion. Keywords: Thromboelastography, Thromboelastometry, Viscoelastic tests, Hemorrhagic shock, Vascular surgery, Postoperative bleeding, Hemostatic therapy * Correspondence: tomazcr@gmail.com Hospital Israelita Albert Einstein – Intensive Care Unit, Av. Albert Einstein, 627, Morumbi, São Paulo, SP CEP: 05651-901, Brazil © The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 2 of 8 Background transfusion with blood components does not focus on Hemorrhagic shock is a medical emergency related to sur- the specific disorders of coagulation [8, 9]. Furthermore, gery, invasive procedures, and trauma. Ongoing severe currently there is a trend in major centers in Europe to bleeding is associated with increased morbidity and mor- avoid the use of blood components due to the high risk tality, and may promptly require additional surgery. Early of adverse events. Possible complications associated with diagnosis of hemorrhagic shock is critical for a favorable transfusion of blood components include transfusion- outcome [1, 2]. Hemorrhagic shock represents a clinical related acute lung injury (TRALI), transfusion associated condition of impaired tissue perfusion resulting from circulatory overload (TACO), nosocomial infections, acute reduction in intravascular blood volume, sepsis, transfusion-related immunomodulation (TRIM), hemodynamic instability, decreased oxygen delivery, cellu- and organ dysfunction [10, 11]. lar hypoxia, organ dysfunction, and death [3]. Resuscita- CCT such as prothrombin time (PT)/international na- tion involves interrupting the source of bleeding and tionalized ratio (INR) and activated partial thromboplas- restoring the circulation of blood volume. Fluids are the tin time (aPTT) are poor predictors of bleeding. CCT first-line therapeutic option to restore intravascular blood fail to identify specific coagulation disorders such as volume but there is still a lack of consensus in the litera- hyperfibrinolysis, hypercoagulability, and the platelet ture concerning the optimal fluid used in patients present- component [12]. In fact, CCT were originally indicated ing hemorrhagic shock. Fluids should be administered to to monitor anticoagulant drugs including heparin and improve perfusion parameters such as blood pressure, warfarin. On the other hand, POCT such as thromboe- urine output, or lactate [4]. Anemia should be promptly lastometry (ROTEM™) has been associated with a reduc- corrected with red blood cells (RBC) to restore blood loss tion in the need for blood component transfusion in [5]. However, quantifying blood loss can be a difficult task. different clinical settings [13]. Thromboelastometry al- Transfusion of allogeneic blood components is necessary lows rapid identification of a specific coagulation dis- when the estimated blood loss from hemorrhage exceeds order in order to predict early massive transfusion and 30% of blood volume (class III hemorrhage) [1]. A guide goal-directed therapy with specific hemostatic hemoglobin level of 7–8 g/dl has been considered an ap- drugs and coagulation factor concentrates [14, 15]. propriate threshold for transfusion in critically ill patients These results were recently confirmed by a prospective with no risk factors for tissue hypoxia [5]. Maintaining randomized clinical trial in cardiac surgery demonstrat- hemoglobin level between 9 and 10 g/dl seems a reason- ing a significant reduction in transfusion requirements, able goal for patients with active bleeding or with high risk transfusion-associated adverse events, costs, as well as of myocardial infarction. The ability to quickly diagnose improved outcomes including 6-month mortality in the hemorrhagic shock is critical and necessary for favorable point-of-care group compared to the control group [16]. outcomes. The clinical setting is usually characterized by: We aimed to report an interesting case where bleed- severe hypotension (systolic blood pressure < 90 mmHg); ing management associated with hemorrhagic shock in tachycardia, that is, heart rate > 120 beats per minute the postoperative period of vascular surgery was success- (bpm); metabolic acidosis (blood lactate > 2–3 mmol/L or fully reversed guided by ROTEM at the bedside. Throm- base deficit < 4 mmol/L); decreased pulse pressure; cold boelastometry enabled the early identification of specific skin; and impaired consciousness [6]. coagulation disorders associated with hemorrhagic shock Traditional therapeutic options for bleeding control as- and, therefore, guided hemostatic therapy by goals. sociated with hemorrhagic shock include transfusion of RBC and allogeneic blood products, such as fresh frozen Case presentation plasma (FFP), platelet concentrates (PC), and cryoprecipi- We report the case of an 82-year-old Afro-Brazilian man tate (Cryo). Nowadays, coagulation factor concentrates (weight 72 kg) who presented to the intensive care unit and hemostatic drugs have been considered a good alter- (ICU) in the immediate postoperative period of elective native since blood components transfusion is associated surgery with signs of hemorrhagic shock. This surgery with serious adverse events and increased mortality [7]. was performed to treat iliac artery aneurysm with endo- Hemostatic therapy might be empiric in fixed ratio, based leak type 1 to 1B with placement of Endurant™ IIS tri- on conventional coagulation tests (CCT) or guided by modular prosthesis. His previous medical history point-of-care testing (POCT). The main goal in the man- included dementia, arterial hypertension, tobacco smok- agement of hemorrhagic shock should be bleeding control ing, ischemic heart disease, and aortic insufficiency. He without increasing the risk of thrombotic events. denied consuming alcohol. At home, he was stable and There is a lack in scientific literature of high quality felt well. He was calm and performed his daily activities evidence concerning efficacy of the traditional practice under medical supervision, despite early stage dementia. of transfusion in fixed ratio of RBC and FFP of 1:1 to He had no motor deficit, only idle speed typical of the treat life-threatening bleeding. In addition, traditional elderly. His blood pressure was controlled, with no Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 3 of 8 clinical signs of heart failure. According to his family, he RBC was urgently performed according to estimated blood had a good quality of life. Three months earlier he had loss. Norepinephrine infusion was associated due to undergone vascular surgery to treat an aneurysm in his hemodynamic instability to maintain a mean blood common iliac artery with endoprosthesis. The surgery pressure above 65 mmHg. The coagulopathy treatment was had no complications and he was rehabilitated at home. performed guided by ROTEM. However, 3 days prior to hospital admission he had a A ROTEM (ROTEM®; Pentapharm Co., Munich, computed tomography scan. The result of imaging Germany) was performed in the immediate postopera- showed an increase in aneurysm size in his common tive period in the ICU. The first thromboelastometry iliac artery. Then a new surgery was indicated for the analysis showed fulminant hyperfibrinolysis in the pres- treatment of the aneurysm. ence of active bleeding. The FIBTEM revealed severe The present surgery was performed under general impairment in the fibrinogen function (Fig. 1). Based on anesthesia, with hemodynamic instability throughout the maximum lysis (ML = 99%) in EXTEM, 1.0 g of tranex- procedure, which required norepinephrine. Iliac dissection amic acid was administered in bolus. A second throm- technique was difficult; there was loss of blood and a need boelastometry analysis was performed 30 minutes after forsutureand compressivedressing.Cefuroximewas ad- tranexamic acid infusion due to continuous bleeding, ministered intravenously in the operating room at 1.5 g showing a severe hypocoagulation in EXTEM with max- intravenously and maintained every 8 hours postopera- imum clot firmness (MCF) EXTEM 32 mm and FIB- tively. In addition, 3500 ml of crystalloid, and 1 unit of RBC TEM with MCF FIBTEM 4 mm (Fig. 2a, b). Based on were administered. Our patient left the surgery without a these tests, 6.0 g of fibrinogen concentrate (FC; Haemo- distal pulse; 31 mL of contrast was needed. He presented complettan® P; CSL Behring, Marburg, Germany) and 1 hypotension and alteration of consciousness after platelet apheresis were administered. A third ROTEM anesthesia wore off. His low blood pressure was increased was performed due to persistent bleeding, showing a with metaraminol use, a sympathomimetic drug that pro- prolonged clotting time (CT) in EXTEM and reduced duces peripheral vasoconstriction (compresses peripheral MCF in FIBTEM (Fig. 2c, d). According to the third vessels) by direct action on alpha-adrenergic receptors. An ROTEM, 9 units of Cryo and 1500 UI of prothrombin infusion of norepinephrine was needed after initial recovery complex concentrate (PCC; Beriplex ® P/N 500 UI; CSL of blood pressure. After his blood pressure had improved Behring, Marburg, Germany) were administered. The and he regained consciousness, the anesthesiologist opted last thromboelastometry was completely corrected for extubation in the operation room. At the ICU, he pre- after 2 hours of treatment, and bleeding was con- sented fast clinical worsening. He showed an altered level trolled (Table 1 and Fig. 2e, f). Our patient presented of consciousness (Glasgow Coma Scale of 9), agitation, de- clinical and hemodynamic stability with dose reduc- lirium, and mental confusion. His arterial blood pressure tion of norepinephrine. Arteriography performed to was 70/35 mmHg, heart rate was 145 bpm, and respiratory evaluate mechanical cause of bleeding was normal. rate 42 breaths per minute. He presented active bleeding in No active bleeding was identified. Hemodialysis was the femoral region, at the arterial puncture site. started within 24 to 36 hours. There was no additional Hypothermia (34 °C), sweating, oliguria, bleached mucosa, need for blood components transfusion on subsequent cold extremities, and signs of severe tissue hypoperfusion days. He was discharged from our ICU and cleared for a completed the clinical scenario. The clinical picture was ward 3 days after admission. No new organ dysfunction or strongly suggestive of hemorrhagic shock. Laboratory tests infection was identified, and the result of the microbiology revealed acidosis and severe anemia with hemoglobin of 7. was negative. He was transferred to a ward for clinical re- 4 g/dL. CCT were greatly altered, platelets count 83 × 10 / habilitation. At follow-up, he required conventional mm , plasma fibrinogen concentration 70 mg/dL, and hemodialysis for 5 days. He was treated for pneumonia prolonged INR 1.95. General blood tests showed total with piperacillin-tazobactam, oxygen supplementation, bilirubin 1.1 mg/dL, serum creatinine 3.1 mg/dL, serum and respiratory and motor physiotherapy for 7 days. With aspartate aminotransferase (AST) 48 U/L, serum alanine improved renal function and recovery of urinary output, aminotransferase (ALT) 32 U/L, arterial bicarbonate and with no other signs of infection, he was discharged 10 mEq/L, arterial pH 7.11, blood glucose 98 mg/dL, ionic after 2 weeks in hospital. At follow-up after 6 months, he calcium 1.02 mmol/L, and lactate 87 mg/dl. Central vein was at home, in rehabilitation with physiotherapy, without catheterization and endotracheal intubation were dialysis or infection. performed due to circulatory shock, consciousness impairment, and airway patency protection. Our patient Discussion received an initial fluid load of 3000 mL of 0.9% saline We report this case of hemorrhagic shock complicating solution. He was warmed and calcium gluconate was postoperative vascular surgery for treatment of common administered. An initial transfusion therapy with 4 units of iliac artery aneurysm. Our patient presented clinical Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 4 of 8 Fig. 1 First Thromboelastometry (ROTEM®) analysis in intensive care unit. Both EXTEM (extrinsic coagulation pathway) and FIBTEM (cytochalasin D) tests showing fulminant hyperfibrinolysis. APTEM (aprotinin) is normal. APTEM uses aprotinin to inhibit fibrinolysis signs of low cardiac output and tissue hypoperfusion, in- allowed specific treatment with hemostatic drugs, coagu- cluding hypotension, mental alteration, and cold extrem- lation factor concentrates, and even allogeneic blood ities, in the presence of active bleeding at a surgical site components. in the right femoral region. Advanced life support with Hemorrhagic shock is an important cause of mortality orotracheal intubation for airway protection and partial in surgical patients; it is responsible for more than 80% hemodynamic stabilization with crystalloids and RBC of deaths in the operating room [1]. Hemorrhagic shock were immediately performed. He was warmed and given is a medical emergency characterized by inadequate calcium gluconate and calcium bicarbonate for biochem- tissue perfusion resulting from an acute decrease in ical balance. Bleeding management was successfully intravascular blood volume leading to hypovolemic state. guided by ROTEM at the bedside. Different clotting dis- The clinical picture includes severe hypotension (systolic orders such as hyperfibrinolysis, hypofibrinogenemia, blood pressure < 90 mmHg), tachycardia (heart rate > platelet disease, and clotting factor deficiency were iden- 120 bpm), metabolic acidosis (blood lactate > 2–3 mmol/L tified, sequentially. As a result, thromboelastometry or base deficit < 4 mmol/L), decreased pulse pressure, cold Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 5 of 8 a) EXTEM b) FIBTEM c) EXTEM d) FIBTEM f) FIBTEM e) EXTEM h) FIBTEM g) EXTEM Fig. 2 a-b) Second Thromboelastometry analysis (ROTEM®) 30 minutes after tranexamic acid showing kinect and structural hypocoagulability in both EXTEM (extrinsic coagulation pathway) and FIBTEM (cytochalasin D); c-d) Third Thromboelastometry analysis showing prolonged clotting time in EXTEM and maximum clot firmness reduced in FIBTEM; e-f) Fourth Thromboelastometry analysis corrected and bleeding was controlled; g-h) Thromboelastometry analysis control Table 1 Evolution of thromboelastometry parameters Time points Assays CT (seconds) CFT (seconds) A10 MCF (mm) ML (mm) (%) 0 minute EXTEM 111 323 28 32 99 FIBTEM 96 4 4 66 APTEM 134 311 29 41 2 30 minutes EXTEM 302 957 16 26 0 FIBTEM 4085 0 0 60 minutes EXTEM 252 601 20 31 9 FIBTEM 3674 0 0 90 minutes EXTEM 78 219 36 50 5 FIBTEM 86 6 7 0 120 minutes EXTEM 80 145 44 56 3 FIBTEM 77 11 14 2 A10 clot formation after 10 minutes, CT clotting time, CFT clot formation time, MCF maximum clot firmness, ML maximum lysis, EXTEM extrinsic coagulation pathway, INTEM intrinsic coagulation pathway, FIBTEM cytochalasin D, HEPTEM Heparinase, APTEM aprotinin Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 6 of 8 skin, sweating, and altered state of consciousness, includ- and the use of vasopressors and blood transfusion to ing drowsiness, torpor, disorientation, or confusion [8]. prevent or correct coagulopathy [21]. Multiple factors are considered a cause of bleeding in Currently, there is growing evidence in the literature surgical patients, including blood loss, hemodilution, showing that exposure to allogeneic blood transfusion has fibrinogen dysfunction, acquired platelet dysfunction, co- been associated with serious adverse events, such as agulation factor consumption, activation of fibrinolytic TRALI, TACO, nosocomial infections, sepsis, TRIM, and system, and hypothermia. Antiplatelet and anticoagulant organ dysfunction [22]. FFP was associated with an in- drugs can lead to coagulopathy during surgery compli- creased risk of infection in surgical patients [23]. Blood cating bleeding control. Surgical or mechanical bleeding transfusion can lead to pulmonary complications, which may occur due to an uncontrolled source in the absence are responsible for the majority of morbidity and mortal- of coagulopathy [9]. Immediately after tissue damage ity, associated with blood component transfusion in hospi- during major surgery, the exposure of the talized patients [24]. thromboplastin-rich subendothelial tissue to flowing CCT were originally intended to monitor the effect of blood induces the activation of coagulation and an initial anticoagulant drugs. Despite their extended use to identify hypercoagulable state [10]. Uncontrolled bleeding leads coagulopathy, CCT are weak predictors of bleeding in crit- to loss of coagulation factors and a later decrease in ically ill patients. In vivo coagulation system occurs pri- platelet counts. Hypovolemia due to intravascular blood marily on the surface of platelets. Tissue factor-bearing volume loss and shock leads to tissue hypoperfusion and cells and RBC also play a significant role in hemostasis. In endothelial dysfunction [11]. Thrombomodulin (TM) the absence of blood cells, which are removed by centrifu- expressed on vascular endothelium binds to thrombin gation, CCT are performed using plasma. Also, these tests forming a complex and it acts as an anticoagulant. In are stopped upon formation of the first fibrin strands addition, the thrombin-TM complex activates protein C when only 5% of the total thrombin has been generated to produce activated protein C (APC), which inactivates [8, 25]. Moreover, conventional coagulation tests do not factors VIIIa and Va in the presence of protein S, thereby assess the quality and the strength of clot and fail to iden- inhibiting further thrombin formation: a hypocoagulable tify hypercoagulability, hyperfibrinolysis, and platelet state [12]. Tissue injury in surgery may lead to the component. exposure of tissue plasminogen activator by the endothe- In contrast, viscoelastic tests are performed in whole lium, resulting in hyperfibrinolysis and impairing blood sample providing a better reflection of the in vivo hemostasis, thereby contributing to the exacerbation of coagulation, considering interaction between blood cells, bleeding [4]. Dilution of coagulation factors and platelets soluble coagulation factors, and platelets. Viscoelastic by fluids resuscitation and blood transfusion aggravates tests, such as ROTEM or thromboelastography (TEG) coagulopathy [14]. Hypothermia, which slows down en- have been associated with a reduction in the need for zymatic reactions, modifies platelet function, decreases blood components transfusion in critically ill patients in platelet counts, and stimulates fibrinolysis. Acidosis different clinical situations, including cardiac surgery, worsens fibrin polymerization and impairs clot strength. trauma, liver transplantation, and postpartum hemorrhage Low-ionized calcium due to massive RBC transfusions [26]. Viscoelastic tests allow global dynamic information containing citrate and low hematocrit further aggravates about clot formation process with rapid results. ROTEM bleeding diathesis [15, 17]. can predict massive transfusion, identifying the cause of The priority treatment of hemorrhagic shock is to con- coagulopathy. As a result, thromboelastometry can guide trol the source of bleeding as quickly as possible and to goal-directed therapy with specific hemostatic drugs, co- replace fluid and improve hemodynamics parameters agulation factor concentrates, and allogeneic blood prod- maintaining oxygen delivery to limit tissue hypoxia, in- ucts. Reagents tests such as EXTEM (extrinsic coagulation flammation, and organ dysfunction. There is a lack of lit- pathway activated by thromboplastin or tissue factor) and erature on what kind of fluid is superior to other fluids. INTEM (intrinsic coagulation pathway activated by con- Although colloids could induce a more rapid and per- tact phase – ellagic acid) are used for initial screening to sistent plasma expansion because of a larger increase in identify the presence of coagulopathy. FIBTEM (cytocha- oncotic pressure, colloids may impair the coagulation lasin D), HEPTEM (heparinase), and APTEM (aprotinin) system, decreasing factor VIII activity, von Willebrand tests are used to identify a specific diagnosis of coagulopa- factor (vWF) function, and fibrin polymerization [18]. thy, and thus guide transfusion therapy according to the On the other hand, resuscitation with large volumes of needs of each patient. The parameters analyzed for the in- crystalloids has been associated with tissue edema, an terpretation of the thromboelastometry curve, as in the increased incidence of abdominal compartment syn- EXTEM, include CT (in seconds), coagulation formation drome, and hyperchloremic metabolic acidosis [19, 20]. time (CFT) in seconds, MCF (in mm), and ML (in per- The resuscitative strategy still involves fluid resuscitation centage). CT demonstrates the period related to the initial Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 7 of 8 process of clot formation and fibrin polymerization. A coagulation tests, ROTEM allows rapid assessment of prolongation in CT suggests deficiency of coagulation fac- the whole clot formation process with early identifica- tors or heparin effect. CFT represents the period from tion of disturbance of coagulopathy. In this reported thrombin generation to MCF, which is determined mainly case, ROTEM identified hyperfibrinolysis, and thus by fibrinogen, platelets, and factor XIII. A prolongation in guided the specific therapy with hemostatic drug (tran- CFT indicates a hypofibrinogenemia, platelet dysfunction, examic acid). In severe acute bleeding management, the or factor XIII deficiency. MCF demonstrates clot strength. first step is to correct the clot stabilization process by Changes in MCF can identify a state of hypercoagulability administering an antifibrinolytic drug. Otherwise, con- or hypocoagulability. Finally, ML demonstrates the last tinued consumption of fibrinogen should be maintained. period of clot stabilization. ML reduced suggests the pres- The second step involves the correction of MCF or clot ence of hyperfibrinolysis, which can be confirmed com- strength, determined by fibrinogen, platelets, and factor paring EXTEM with APTEM. ML over 15% in EXTEM XIII. In this case, even after 6 g of FC, there was persist- that is corrected by aprotinin (APTEM test) confirms the ence in the hypocoagulability, which was corrected after diagnosis of hyperfibrinolysis [27]. transfusion of PC, but mainly with transfusion of Cryo, This case report describes a patient with hemorrhagic composed of fibrinogen but also factor XIII. The last shock in the immediate postoperative period of vascular step includes improving the initial thrombin generation surgery with signs of active bleeding at the surgical site process, through replacement of coagulation factors or in inguinal region. The initial approach included transfu- reversal of the effect of present heparin. sion of 4 units of RBC and fluid replacement with crys- In hemorrhagic shock, coagulation disorder is com- talloid and norepinephrine to achieve mean blood plex, dynamic, and variable over time. CCT take 45 to pressure around 65 mmHg and preserve tissue perfu- 60 minutes to read. CCT are unable to identify coagula- sion. Our patient underwent orotracheal intubation and tion disorders contemporaneously as in this reported a central venous access in deep jugular vein was case, that is, the presence of hyperfibrinolysis. The rapid inserted. Acidosis and hypocalcemia were corrected and interpretation of ROTEM associated with the use of he was heated. Transfusion therapy was guided by hemostatic drugs and coagulation factor concentrates al- ROTEM. An initial ROTEM examination showed early lows a more precise, individualized, and early treatment fulminant hyperfibrinolysis (ML in EXTEM greater than of bleeding. Traditional transfusion practice with blood 15% and ML normal in APTEM test). Unlike CCT, components such as RBC, FFP, Cryoprecipitate, and PC, ROTEM allowed an early diagnosis of this coagulopathy, requires time for blood typing, thawing, and transporta- within the first 5 to 10 minutes. Administration of 1 g of tion from the blood bank. This delay in administration tranexamic acid, a low-cost drug in bolus infusion, of blood component may be a determining factor for an quickly corrected the severe coagulation disorder. Thirty unfavorable outcome. Similarly, the empirical use of minutes after administration of the antifibrinolytic drug, blood components in the absence of ROTEM increases the second ROTEM showed a correction of the hyperfi- the risk of adverse effects to the patient and may fail to brinolysis, but a severe hypocoagulability (decreased correct the mechanism responsible for bleeding. MCF in EXTEM) in the presence of active bleeding was identified. In that moment, 6 g of FC and, after that, 1 Conclusions platelet apheresis were administered. Thirty minutes In summary, successful bleeding management of patients later, the sequential ROTEM test still showed a serious with hemorrhagic shock is still a challenge for anesthesiol- state of hypocoagulability, a delayed thrombin gener- ogists. Early recognition of the specific cause of coagulop- ation process, and maintenance of hemorrhage. At this athy followed by appropriate treatment is associated with time, 9 units of Cryo were administered to correct clot a favorable outcome. Thromboelastometry may be consid- strength and 1500 units of PCC to correct the initial ered a useful, feasible, and safe tool for rapid diagnosis of phase of thrombin generation. Finally, there was clinical different coagulation disorders associated with bleeding control, 30 minutes after using Cryo and PCC, hemorrhagic shock. Thromboelastometry still presents guided by ROTEM. In this case, ROTEM became nor- the potential benefit of allowing goal-guided hemostatic mal 120 minutes after the first ROTEM with therapy with hemostatic drugs and coagulation factor con- hyperfibrinolysis. centrates. Thus, this POCT could help avoid unnecessary Some aspects of this transfusion practice for the cor- transfusion in patients with hemorrhagic shock and active rection of coagulopathy should be highlighted. The order bleeding. Additional studies are expected to define the or sequence of the therapeutic approach in this scenario role and benefit of the use of thromboelastometry for of bleeding management is very important and can make diagnosis of coagulopathy and as a guide for transfusion a difference for the patient. First of all, ROTEM is a therapy with allogeneic blood products, coagulation factor POC testing performed at the bedside. Instead of concentrates, or hemostatic drugs. Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 8 of 8 Abbreviations 9. Rossaint R, Bouillon B, Cerny V, Coats TJ, Duranteau J, Fernández-Mondéjar ALT: Serum alanine aminotransferase; APC: Activated protein C; E, et al. Management of bleeding following major trauma: an updated aPTT: Activated partial thromboplastin time; AST: Serum aspartate European guideline. Crit Care. 2010;14(2):R52. aminotransferase; bpm: beats per minute; CCT: Conventional coagulation 10. Yau JW, Teoh H, Verma S. Endothelial cell control of thrombosis. BMC tests; CFT: Clot formation time; Cryo: Cryoprecipitate; CT: Clotting time; Cardiovasc Disord. 2015;15:130. FC: Fibrinogen concentrate; FFP: Fresh frozen plasma; ICU: Intensive care unit; 11. Jacob M, Kumar P. The challenge in management of hemorrhagic shock in INR: International nationalized ratio; MCF: Maximum clot firmness; trauma. Med J Armed Forces India. 2014;70(2):163–9. ML: Maximum lysis; PC: Platelet concentrates; PCC: Prothrombin complex 12. Ikezoe T. Thrombomodulin/activated protein C system in septic concentrate; POCT: Point-of-care testing; PT: Prothrombin time; RBC: Red disseminated intravascular coagulation. J Intensive Care. 2015;3(1):1. blood cells; ROTEM: Thromboelastometry; TACO: Transfusion associated 13. Wikkelsø A, Wetterslev J, Møller AM, Afshari A. Thromboelastography (TEG) circulatory overload; TEG: Thromboelastography; TM: Thrombomodulin; or thromboelastometry (ROTEM) to monitor haemostatic treatment versus TRALI: Transfusion-related acute lung injury; TRIM: Transfusion-related usual care in adults or children with bleeding. Cochrane Database Syst Rev. immunomodulation; vWF: Von Willebrand factor 2016;8:CD007871. 14. Bonanno FG. Hemorrhagic shock: The "physiology approach". J Emerg Trauma Shock. 2012;5(4):285–95. Acknowledgements 15. Dirkmann D, Hanke AA, Görlinger K, Peters J. Hypothermia and acidosis We thank Carolina Martinez Savioli and Helena Spalic for proofreading this synergistically impair coagulation in human whole blood. Anesth Analg. manuscript. 2008;106(6):1627–32. 16. Weber CF, Görlinger K, Meininger D, Herrmann E, Bingold T, Moritz A, et al. Funding Point-of-care testing: a prospective, randomized clinical trial of efficacy in Not applicable. No funding was received. coagulopathic cardiac surgery patients. Anesthesiology. 2012;117(3):531–47. 17. Van Poucke S, Stevens K, Marcus AE, Lancé M. Hypothermia: effects on Availability of data and materials platelet function and hemostasis. Thromb J 2014;12(1):31. The datasets used and/or analyzed during the current study are available 18. Kozek-Langenecker SA. Fluids and coagulation. Curr Opin Crit Care. 2015; from the corresponding author on reasonable request. 21(4):285–91. 19. Handy JM, Soni N. Physiological effects of hyperchloraemia and acidosis. Authors’ contributions Br J Anaesth. 2008;101(2):141–50. TC and FS devised the case report. TC and FS collected the data. TC and FS 20. Madigan MC, Kemp CD, Johnson JC, Cotton BA. Secondary abdominal wrote the first manuscript draft. TC critically revised the manuscript. TC and compartment syndrome after severe extremity injury: are early, aggressive FS approved the final manuscript. fluid resuscitation strategies to blame? J Trauma. 2008;64(2):280–5. 21. Bouglé A, Harrois A, Duranteau J. Resuscitative strategies in traumatic hemorrhagic shock. Ann Intensive Care. 2013;3(1):1. Ethics approval and consent to participate 22. Sahu S, Hemlata, Verma A. Adverse events related to blood transfusion. Not applicable. Indian J Anaesth. 2014;58(5):543–51. 23. Sarani B, Dunkman WJ, Dean L, Sonnad S, Rohrbach JI, Gracias VH. Consent for publication Transfusion of fresh frozen plasma in critically ill surgical patients is Written informed consent was obtained from the patient for publication of associated with an increased risk of infection. Crit Care Med. 2008;36(4): this case report and any accompanying images. A copy of the written 1114–8. consent is available for review by the Editor-in-Chief of this journal. 24. Benson AB. Pulmonary complications of transfused blood components. Crit Care Nurs Clin North Am. 2012;24(3):403–18. Competing interests 25. Mann KG. Thrombin formation. Chest. 2003;124(3 Suppl):4S–10S. The authors declare that they have no competing interests. 26. Haas T, Görlinger K, Grassetto A, Agostini V, Simioni P, Nardi G, et al. Thromboelastometry for guiding bleeding management of the critically ill patient: a systematic review of the literature. Minerva Anestesiol. 2014; Publisher’sNote 80(12):1320–35. Springer Nature remains neutral with regard to jurisdictional claims in 27. Crochemore T, Piza FMT, Rodrigues RDR, Guerra JCC, Ferraz LJR, Corrêa TD. published maps and institutional affiliations. A new era of thromboelastometry. Einstein (Sao Paulo). 2017;0 Received: 20 December 2017 Accepted: 19 March 2018 References 1. Gutierrez G, Reines HD, Wulf-Gutierrez ME. Clinical review: hemorrhagic shock. Crit Care. 2004;8(5):373–81. 2. Rossaint R, Cerny V, Coats TJ, Duranteau J, Fernández-Mondéjar E, Gordini G, et al. Key issues in advanced bleeding care in trauma. Shock. 2006;26(4): 322–31. 3. Bose EL, Hravnak M, Pinsky MR. The interface between monitoring and Submit your next manuscript to BioMed Central physiology at the bedside. Crit Care Clin. 2015;31(1):1–24. 4. Meißner A, Schlenke P. Massive Bleeding and Massive Transfusion. Transfus and we will help you at every step: Med Hemother. 2012;39(2):73–84. • We accept pre-submission inquiries 5. Kozek-Langenecker SA, Ahmed AB, Afshari A, Albaladejo P, Aldecoa C, Barauskas G, et al. Management of severe perioperative bleeding: guidelines � Our selector tool helps you to find the most relevant journal from the European Society of Anaesthesiology: First update 2016. Eur J � We provide round the clock customer support Anaesthesiol. 2017;34(6):332–95. � Convenient online submission 6. Gallimore E. Clinical features and management of haemorrhagic shock. Nurs Stand. 2015;30(1):51–8. quiz 60 � Thorough peer review 7. Schöchl H, Voelckel W, Schlimp CJ. Management of traumatic � Inclusion in PubMed and all major indexing services haemorrhage—the European perspective. Anaesthesia. 2015;70 Suppl 1: � Maximum visibility for your research 102–7. e35–7 8. Martel MJ, MacKinnon KJ, Arsenault MY, Bartellas E, Klein MC, Lane CA, et al. Submit your manuscript at Hemorrhagic shock. J Obstet Gynaecol Can. 2002;24(6):504–20. quiz 21-4 www.biomedcentral.com/submit http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Medical Case Reports Springer Journals

Thromboelastometry-guided hemostatic therapy for hemorrhagic shock in the postoperative period of vascular surgery: a case report

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Abstract

Background: Hemorrhagic shock is a medical emergency that often complicates vascular surgery and can lead to death. Hemorrhagic shock is characterized by hypoperfusion and hemodynamic abnormalities leading to the collapse of homeostasis due to massive blood loss. Early diagnosis is critical for a favorable outcome. Thromboelastometry has been considered an effective tool for bleeding management in critically ill patients. Thromboelastometry can guide transfusion therapy quickly, reducing the need for blood products. Therefore, it could be an alternative test to guide hemostatic therapy in complex cases of hemorrhagic shock as a result of vascular surgeries. We report our successful experience with a case of hemorrhagic shock in postoperative care in vascular surgery, in which bleeding management was guided by thromboelastometry and bleeding control was achieved with hemostatic drugs and coagulation factor concentrates. Case presentation: We report a case of an 82-year-old Afro-Brazilian man who presented to the intensive care unit with hemorrhagic shock in the postoperative period of vascular surgery. He underwent surgery for correction of iliac artery aneurysm with endoleak. His laboratory tests revealed severe anemia (hemoglobin 7.4 mg/dL), metabolic acidosis (bicarbonate 10 mEq/L, pH 7.11), acute kidney injury (creatinine 3.1 mg/dL), thrombocytopenia 3 3 (platelets count 83 × 10 /mm ), hypofibrinogenemia (70 mg/dL), international nationalized ratio 1.95, activated partial thromboplastin time 64.5 seconds, and lactate 87 mmol/L. There was active bleeding in surgical site. Bleeding management was guided by thromboelastometry. The first test showed fulminant hyperfibrinolysis, which was corrected with the administration of tranexamic acid. The second thromboelastometry test showed improvement of hyperfibrinolysis but severe hypocoagulability. Fibrinogen concentrate, platelet apheresis, cryoprecipitate, and prothrombin complex concentrate were sequentially administrated. Thromboelastometry was completely corrected after 2 hours. Arteriography to evaluate mechanical cause of bleeding was normal. No more bleeding was identified, and neither was any further transfusion needed. He was discharged from the intensive care unit from the ward 3 days after admission. Conclusions: Thromboelastometry may be considered a useful, feasible and safe tool to monitor and manage coagulopathy in patients with hemorrhagic shock. Moreover, it has the potential benefit of allowing rapid diagnosis, goal-directed therapy with hemostatic drugs and coagulation factor concentrates and thus, avoiding unnecessary blood component transfusion. Keywords: Thromboelastography, Thromboelastometry, Viscoelastic tests, Hemorrhagic shock, Vascular surgery, Postoperative bleeding, Hemostatic therapy * Correspondence: tomazcr@gmail.com Hospital Israelita Albert Einstein – Intensive Care Unit, Av. Albert Einstein, 627, Morumbi, São Paulo, SP CEP: 05651-901, Brazil © The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 2 of 8 Background transfusion with blood components does not focus on Hemorrhagic shock is a medical emergency related to sur- the specific disorders of coagulation [8, 9]. Furthermore, gery, invasive procedures, and trauma. Ongoing severe currently there is a trend in major centers in Europe to bleeding is associated with increased morbidity and mor- avoid the use of blood components due to the high risk tality, and may promptly require additional surgery. Early of adverse events. Possible complications associated with diagnosis of hemorrhagic shock is critical for a favorable transfusion of blood components include transfusion- outcome [1, 2]. Hemorrhagic shock represents a clinical related acute lung injury (TRALI), transfusion associated condition of impaired tissue perfusion resulting from circulatory overload (TACO), nosocomial infections, acute reduction in intravascular blood volume, sepsis, transfusion-related immunomodulation (TRIM), hemodynamic instability, decreased oxygen delivery, cellu- and organ dysfunction [10, 11]. lar hypoxia, organ dysfunction, and death [3]. Resuscita- CCT such as prothrombin time (PT)/international na- tion involves interrupting the source of bleeding and tionalized ratio (INR) and activated partial thromboplas- restoring the circulation of blood volume. Fluids are the tin time (aPTT) are poor predictors of bleeding. CCT first-line therapeutic option to restore intravascular blood fail to identify specific coagulation disorders such as volume but there is still a lack of consensus in the litera- hyperfibrinolysis, hypercoagulability, and the platelet ture concerning the optimal fluid used in patients present- component [12]. In fact, CCT were originally indicated ing hemorrhagic shock. Fluids should be administered to to monitor anticoagulant drugs including heparin and improve perfusion parameters such as blood pressure, warfarin. On the other hand, POCT such as thromboe- urine output, or lactate [4]. Anemia should be promptly lastometry (ROTEM™) has been associated with a reduc- corrected with red blood cells (RBC) to restore blood loss tion in the need for blood component transfusion in [5]. However, quantifying blood loss can be a difficult task. different clinical settings [13]. Thromboelastometry al- Transfusion of allogeneic blood components is necessary lows rapid identification of a specific coagulation dis- when the estimated blood loss from hemorrhage exceeds order in order to predict early massive transfusion and 30% of blood volume (class III hemorrhage) [1]. A guide goal-directed therapy with specific hemostatic hemoglobin level of 7–8 g/dl has been considered an ap- drugs and coagulation factor concentrates [14, 15]. propriate threshold for transfusion in critically ill patients These results were recently confirmed by a prospective with no risk factors for tissue hypoxia [5]. Maintaining randomized clinical trial in cardiac surgery demonstrat- hemoglobin level between 9 and 10 g/dl seems a reason- ing a significant reduction in transfusion requirements, able goal for patients with active bleeding or with high risk transfusion-associated adverse events, costs, as well as of myocardial infarction. The ability to quickly diagnose improved outcomes including 6-month mortality in the hemorrhagic shock is critical and necessary for favorable point-of-care group compared to the control group [16]. outcomes. The clinical setting is usually characterized by: We aimed to report an interesting case where bleed- severe hypotension (systolic blood pressure < 90 mmHg); ing management associated with hemorrhagic shock in tachycardia, that is, heart rate > 120 beats per minute the postoperative period of vascular surgery was success- (bpm); metabolic acidosis (blood lactate > 2–3 mmol/L or fully reversed guided by ROTEM at the bedside. Throm- base deficit < 4 mmol/L); decreased pulse pressure; cold boelastometry enabled the early identification of specific skin; and impaired consciousness [6]. coagulation disorders associated with hemorrhagic shock Traditional therapeutic options for bleeding control as- and, therefore, guided hemostatic therapy by goals. sociated with hemorrhagic shock include transfusion of RBC and allogeneic blood products, such as fresh frozen Case presentation plasma (FFP), platelet concentrates (PC), and cryoprecipi- We report the case of an 82-year-old Afro-Brazilian man tate (Cryo). Nowadays, coagulation factor concentrates (weight 72 kg) who presented to the intensive care unit and hemostatic drugs have been considered a good alter- (ICU) in the immediate postoperative period of elective native since blood components transfusion is associated surgery with signs of hemorrhagic shock. This surgery with serious adverse events and increased mortality [7]. was performed to treat iliac artery aneurysm with endo- Hemostatic therapy might be empiric in fixed ratio, based leak type 1 to 1B with placement of Endurant™ IIS tri- on conventional coagulation tests (CCT) or guided by modular prosthesis. His previous medical history point-of-care testing (POCT). The main goal in the man- included dementia, arterial hypertension, tobacco smok- agement of hemorrhagic shock should be bleeding control ing, ischemic heart disease, and aortic insufficiency. He without increasing the risk of thrombotic events. denied consuming alcohol. At home, he was stable and There is a lack in scientific literature of high quality felt well. He was calm and performed his daily activities evidence concerning efficacy of the traditional practice under medical supervision, despite early stage dementia. of transfusion in fixed ratio of RBC and FFP of 1:1 to He had no motor deficit, only idle speed typical of the treat life-threatening bleeding. In addition, traditional elderly. His blood pressure was controlled, with no Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 3 of 8 clinical signs of heart failure. According to his family, he RBC was urgently performed according to estimated blood had a good quality of life. Three months earlier he had loss. Norepinephrine infusion was associated due to undergone vascular surgery to treat an aneurysm in his hemodynamic instability to maintain a mean blood common iliac artery with endoprosthesis. The surgery pressure above 65 mmHg. The coagulopathy treatment was had no complications and he was rehabilitated at home. performed guided by ROTEM. However, 3 days prior to hospital admission he had a A ROTEM (ROTEM®; Pentapharm Co., Munich, computed tomography scan. The result of imaging Germany) was performed in the immediate postopera- showed an increase in aneurysm size in his common tive period in the ICU. The first thromboelastometry iliac artery. Then a new surgery was indicated for the analysis showed fulminant hyperfibrinolysis in the pres- treatment of the aneurysm. ence of active bleeding. The FIBTEM revealed severe The present surgery was performed under general impairment in the fibrinogen function (Fig. 1). Based on anesthesia, with hemodynamic instability throughout the maximum lysis (ML = 99%) in EXTEM, 1.0 g of tranex- procedure, which required norepinephrine. Iliac dissection amic acid was administered in bolus. A second throm- technique was difficult; there was loss of blood and a need boelastometry analysis was performed 30 minutes after forsutureand compressivedressing.Cefuroximewas ad- tranexamic acid infusion due to continuous bleeding, ministered intravenously in the operating room at 1.5 g showing a severe hypocoagulation in EXTEM with max- intravenously and maintained every 8 hours postopera- imum clot firmness (MCF) EXTEM 32 mm and FIB- tively. In addition, 3500 ml of crystalloid, and 1 unit of RBC TEM with MCF FIBTEM 4 mm (Fig. 2a, b). Based on were administered. Our patient left the surgery without a these tests, 6.0 g of fibrinogen concentrate (FC; Haemo- distal pulse; 31 mL of contrast was needed. He presented complettan® P; CSL Behring, Marburg, Germany) and 1 hypotension and alteration of consciousness after platelet apheresis were administered. A third ROTEM anesthesia wore off. His low blood pressure was increased was performed due to persistent bleeding, showing a with metaraminol use, a sympathomimetic drug that pro- prolonged clotting time (CT) in EXTEM and reduced duces peripheral vasoconstriction (compresses peripheral MCF in FIBTEM (Fig. 2c, d). According to the third vessels) by direct action on alpha-adrenergic receptors. An ROTEM, 9 units of Cryo and 1500 UI of prothrombin infusion of norepinephrine was needed after initial recovery complex concentrate (PCC; Beriplex ® P/N 500 UI; CSL of blood pressure. After his blood pressure had improved Behring, Marburg, Germany) were administered. The and he regained consciousness, the anesthesiologist opted last thromboelastometry was completely corrected for extubation in the operation room. At the ICU, he pre- after 2 hours of treatment, and bleeding was con- sented fast clinical worsening. He showed an altered level trolled (Table 1 and Fig. 2e, f). Our patient presented of consciousness (Glasgow Coma Scale of 9), agitation, de- clinical and hemodynamic stability with dose reduc- lirium, and mental confusion. His arterial blood pressure tion of norepinephrine. Arteriography performed to was 70/35 mmHg, heart rate was 145 bpm, and respiratory evaluate mechanical cause of bleeding was normal. rate 42 breaths per minute. He presented active bleeding in No active bleeding was identified. Hemodialysis was the femoral region, at the arterial puncture site. started within 24 to 36 hours. There was no additional Hypothermia (34 °C), sweating, oliguria, bleached mucosa, need for blood components transfusion on subsequent cold extremities, and signs of severe tissue hypoperfusion days. He was discharged from our ICU and cleared for a completed the clinical scenario. The clinical picture was ward 3 days after admission. No new organ dysfunction or strongly suggestive of hemorrhagic shock. Laboratory tests infection was identified, and the result of the microbiology revealed acidosis and severe anemia with hemoglobin of 7. was negative. He was transferred to a ward for clinical re- 4 g/dL. CCT were greatly altered, platelets count 83 × 10 / habilitation. At follow-up, he required conventional mm , plasma fibrinogen concentration 70 mg/dL, and hemodialysis for 5 days. He was treated for pneumonia prolonged INR 1.95. General blood tests showed total with piperacillin-tazobactam, oxygen supplementation, bilirubin 1.1 mg/dL, serum creatinine 3.1 mg/dL, serum and respiratory and motor physiotherapy for 7 days. With aspartate aminotransferase (AST) 48 U/L, serum alanine improved renal function and recovery of urinary output, aminotransferase (ALT) 32 U/L, arterial bicarbonate and with no other signs of infection, he was discharged 10 mEq/L, arterial pH 7.11, blood glucose 98 mg/dL, ionic after 2 weeks in hospital. At follow-up after 6 months, he calcium 1.02 mmol/L, and lactate 87 mg/dl. Central vein was at home, in rehabilitation with physiotherapy, without catheterization and endotracheal intubation were dialysis or infection. performed due to circulatory shock, consciousness impairment, and airway patency protection. Our patient Discussion received an initial fluid load of 3000 mL of 0.9% saline We report this case of hemorrhagic shock complicating solution. He was warmed and calcium gluconate was postoperative vascular surgery for treatment of common administered. An initial transfusion therapy with 4 units of iliac artery aneurysm. Our patient presented clinical Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 4 of 8 Fig. 1 First Thromboelastometry (ROTEM®) analysis in intensive care unit. Both EXTEM (extrinsic coagulation pathway) and FIBTEM (cytochalasin D) tests showing fulminant hyperfibrinolysis. APTEM (aprotinin) is normal. APTEM uses aprotinin to inhibit fibrinolysis signs of low cardiac output and tissue hypoperfusion, in- allowed specific treatment with hemostatic drugs, coagu- cluding hypotension, mental alteration, and cold extrem- lation factor concentrates, and even allogeneic blood ities, in the presence of active bleeding at a surgical site components. in the right femoral region. Advanced life support with Hemorrhagic shock is an important cause of mortality orotracheal intubation for airway protection and partial in surgical patients; it is responsible for more than 80% hemodynamic stabilization with crystalloids and RBC of deaths in the operating room [1]. Hemorrhagic shock were immediately performed. He was warmed and given is a medical emergency characterized by inadequate calcium gluconate and calcium bicarbonate for biochem- tissue perfusion resulting from an acute decrease in ical balance. Bleeding management was successfully intravascular blood volume leading to hypovolemic state. guided by ROTEM at the bedside. Different clotting dis- The clinical picture includes severe hypotension (systolic orders such as hyperfibrinolysis, hypofibrinogenemia, blood pressure < 90 mmHg), tachycardia (heart rate > platelet disease, and clotting factor deficiency were iden- 120 bpm), metabolic acidosis (blood lactate > 2–3 mmol/L tified, sequentially. As a result, thromboelastometry or base deficit < 4 mmol/L), decreased pulse pressure, cold Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 5 of 8 a) EXTEM b) FIBTEM c) EXTEM d) FIBTEM f) FIBTEM e) EXTEM h) FIBTEM g) EXTEM Fig. 2 a-b) Second Thromboelastometry analysis (ROTEM®) 30 minutes after tranexamic acid showing kinect and structural hypocoagulability in both EXTEM (extrinsic coagulation pathway) and FIBTEM (cytochalasin D); c-d) Third Thromboelastometry analysis showing prolonged clotting time in EXTEM and maximum clot firmness reduced in FIBTEM; e-f) Fourth Thromboelastometry analysis corrected and bleeding was controlled; g-h) Thromboelastometry analysis control Table 1 Evolution of thromboelastometry parameters Time points Assays CT (seconds) CFT (seconds) A10 MCF (mm) ML (mm) (%) 0 minute EXTEM 111 323 28 32 99 FIBTEM 96 4 4 66 APTEM 134 311 29 41 2 30 minutes EXTEM 302 957 16 26 0 FIBTEM 4085 0 0 60 minutes EXTEM 252 601 20 31 9 FIBTEM 3674 0 0 90 minutes EXTEM 78 219 36 50 5 FIBTEM 86 6 7 0 120 minutes EXTEM 80 145 44 56 3 FIBTEM 77 11 14 2 A10 clot formation after 10 minutes, CT clotting time, CFT clot formation time, MCF maximum clot firmness, ML maximum lysis, EXTEM extrinsic coagulation pathway, INTEM intrinsic coagulation pathway, FIBTEM cytochalasin D, HEPTEM Heparinase, APTEM aprotinin Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 6 of 8 skin, sweating, and altered state of consciousness, includ- and the use of vasopressors and blood transfusion to ing drowsiness, torpor, disorientation, or confusion [8]. prevent or correct coagulopathy [21]. Multiple factors are considered a cause of bleeding in Currently, there is growing evidence in the literature surgical patients, including blood loss, hemodilution, showing that exposure to allogeneic blood transfusion has fibrinogen dysfunction, acquired platelet dysfunction, co- been associated with serious adverse events, such as agulation factor consumption, activation of fibrinolytic TRALI, TACO, nosocomial infections, sepsis, TRIM, and system, and hypothermia. Antiplatelet and anticoagulant organ dysfunction [22]. FFP was associated with an in- drugs can lead to coagulopathy during surgery compli- creased risk of infection in surgical patients [23]. Blood cating bleeding control. Surgical or mechanical bleeding transfusion can lead to pulmonary complications, which may occur due to an uncontrolled source in the absence are responsible for the majority of morbidity and mortal- of coagulopathy [9]. Immediately after tissue damage ity, associated with blood component transfusion in hospi- during major surgery, the exposure of the talized patients [24]. thromboplastin-rich subendothelial tissue to flowing CCT were originally intended to monitor the effect of blood induces the activation of coagulation and an initial anticoagulant drugs. Despite their extended use to identify hypercoagulable state [10]. Uncontrolled bleeding leads coagulopathy, CCT are weak predictors of bleeding in crit- to loss of coagulation factors and a later decrease in ically ill patients. In vivo coagulation system occurs pri- platelet counts. Hypovolemia due to intravascular blood marily on the surface of platelets. Tissue factor-bearing volume loss and shock leads to tissue hypoperfusion and cells and RBC also play a significant role in hemostasis. In endothelial dysfunction [11]. Thrombomodulin (TM) the absence of blood cells, which are removed by centrifu- expressed on vascular endothelium binds to thrombin gation, CCT are performed using plasma. Also, these tests forming a complex and it acts as an anticoagulant. In are stopped upon formation of the first fibrin strands addition, the thrombin-TM complex activates protein C when only 5% of the total thrombin has been generated to produce activated protein C (APC), which inactivates [8, 25]. Moreover, conventional coagulation tests do not factors VIIIa and Va in the presence of protein S, thereby assess the quality and the strength of clot and fail to iden- inhibiting further thrombin formation: a hypocoagulable tify hypercoagulability, hyperfibrinolysis, and platelet state [12]. Tissue injury in surgery may lead to the component. exposure of tissue plasminogen activator by the endothe- In contrast, viscoelastic tests are performed in whole lium, resulting in hyperfibrinolysis and impairing blood sample providing a better reflection of the in vivo hemostasis, thereby contributing to the exacerbation of coagulation, considering interaction between blood cells, bleeding [4]. Dilution of coagulation factors and platelets soluble coagulation factors, and platelets. Viscoelastic by fluids resuscitation and blood transfusion aggravates tests, such as ROTEM or thromboelastography (TEG) coagulopathy [14]. Hypothermia, which slows down en- have been associated with a reduction in the need for zymatic reactions, modifies platelet function, decreases blood components transfusion in critically ill patients in platelet counts, and stimulates fibrinolysis. Acidosis different clinical situations, including cardiac surgery, worsens fibrin polymerization and impairs clot strength. trauma, liver transplantation, and postpartum hemorrhage Low-ionized calcium due to massive RBC transfusions [26]. Viscoelastic tests allow global dynamic information containing citrate and low hematocrit further aggravates about clot formation process with rapid results. ROTEM bleeding diathesis [15, 17]. can predict massive transfusion, identifying the cause of The priority treatment of hemorrhagic shock is to con- coagulopathy. As a result, thromboelastometry can guide trol the source of bleeding as quickly as possible and to goal-directed therapy with specific hemostatic drugs, co- replace fluid and improve hemodynamics parameters agulation factor concentrates, and allogeneic blood prod- maintaining oxygen delivery to limit tissue hypoxia, in- ucts. Reagents tests such as EXTEM (extrinsic coagulation flammation, and organ dysfunction. There is a lack of lit- pathway activated by thromboplastin or tissue factor) and erature on what kind of fluid is superior to other fluids. INTEM (intrinsic coagulation pathway activated by con- Although colloids could induce a more rapid and per- tact phase – ellagic acid) are used for initial screening to sistent plasma expansion because of a larger increase in identify the presence of coagulopathy. FIBTEM (cytocha- oncotic pressure, colloids may impair the coagulation lasin D), HEPTEM (heparinase), and APTEM (aprotinin) system, decreasing factor VIII activity, von Willebrand tests are used to identify a specific diagnosis of coagulopa- factor (vWF) function, and fibrin polymerization [18]. thy, and thus guide transfusion therapy according to the On the other hand, resuscitation with large volumes of needs of each patient. The parameters analyzed for the in- crystalloids has been associated with tissue edema, an terpretation of the thromboelastometry curve, as in the increased incidence of abdominal compartment syn- EXTEM, include CT (in seconds), coagulation formation drome, and hyperchloremic metabolic acidosis [19, 20]. time (CFT) in seconds, MCF (in mm), and ML (in per- The resuscitative strategy still involves fluid resuscitation centage). CT demonstrates the period related to the initial Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 7 of 8 process of clot formation and fibrin polymerization. A coagulation tests, ROTEM allows rapid assessment of prolongation in CT suggests deficiency of coagulation fac- the whole clot formation process with early identifica- tors or heparin effect. CFT represents the period from tion of disturbance of coagulopathy. In this reported thrombin generation to MCF, which is determined mainly case, ROTEM identified hyperfibrinolysis, and thus by fibrinogen, platelets, and factor XIII. A prolongation in guided the specific therapy with hemostatic drug (tran- CFT indicates a hypofibrinogenemia, platelet dysfunction, examic acid). In severe acute bleeding management, the or factor XIII deficiency. MCF demonstrates clot strength. first step is to correct the clot stabilization process by Changes in MCF can identify a state of hypercoagulability administering an antifibrinolytic drug. Otherwise, con- or hypocoagulability. Finally, ML demonstrates the last tinued consumption of fibrinogen should be maintained. period of clot stabilization. ML reduced suggests the pres- The second step involves the correction of MCF or clot ence of hyperfibrinolysis, which can be confirmed com- strength, determined by fibrinogen, platelets, and factor paring EXTEM with APTEM. ML over 15% in EXTEM XIII. In this case, even after 6 g of FC, there was persist- that is corrected by aprotinin (APTEM test) confirms the ence in the hypocoagulability, which was corrected after diagnosis of hyperfibrinolysis [27]. transfusion of PC, but mainly with transfusion of Cryo, This case report describes a patient with hemorrhagic composed of fibrinogen but also factor XIII. The last shock in the immediate postoperative period of vascular step includes improving the initial thrombin generation surgery with signs of active bleeding at the surgical site process, through replacement of coagulation factors or in inguinal region. The initial approach included transfu- reversal of the effect of present heparin. sion of 4 units of RBC and fluid replacement with crys- In hemorrhagic shock, coagulation disorder is com- talloid and norepinephrine to achieve mean blood plex, dynamic, and variable over time. CCT take 45 to pressure around 65 mmHg and preserve tissue perfu- 60 minutes to read. CCT are unable to identify coagula- sion. Our patient underwent orotracheal intubation and tion disorders contemporaneously as in this reported a central venous access in deep jugular vein was case, that is, the presence of hyperfibrinolysis. The rapid inserted. Acidosis and hypocalcemia were corrected and interpretation of ROTEM associated with the use of he was heated. Transfusion therapy was guided by hemostatic drugs and coagulation factor concentrates al- ROTEM. An initial ROTEM examination showed early lows a more precise, individualized, and early treatment fulminant hyperfibrinolysis (ML in EXTEM greater than of bleeding. Traditional transfusion practice with blood 15% and ML normal in APTEM test). Unlike CCT, components such as RBC, FFP, Cryoprecipitate, and PC, ROTEM allowed an early diagnosis of this coagulopathy, requires time for blood typing, thawing, and transporta- within the first 5 to 10 minutes. Administration of 1 g of tion from the blood bank. This delay in administration tranexamic acid, a low-cost drug in bolus infusion, of blood component may be a determining factor for an quickly corrected the severe coagulation disorder. Thirty unfavorable outcome. Similarly, the empirical use of minutes after administration of the antifibrinolytic drug, blood components in the absence of ROTEM increases the second ROTEM showed a correction of the hyperfi- the risk of adverse effects to the patient and may fail to brinolysis, but a severe hypocoagulability (decreased correct the mechanism responsible for bleeding. MCF in EXTEM) in the presence of active bleeding was identified. In that moment, 6 g of FC and, after that, 1 Conclusions platelet apheresis were administered. Thirty minutes In summary, successful bleeding management of patients later, the sequential ROTEM test still showed a serious with hemorrhagic shock is still a challenge for anesthesiol- state of hypocoagulability, a delayed thrombin gener- ogists. Early recognition of the specific cause of coagulop- ation process, and maintenance of hemorrhage. At this athy followed by appropriate treatment is associated with time, 9 units of Cryo were administered to correct clot a favorable outcome. Thromboelastometry may be consid- strength and 1500 units of PCC to correct the initial ered a useful, feasible, and safe tool for rapid diagnosis of phase of thrombin generation. Finally, there was clinical different coagulation disorders associated with bleeding control, 30 minutes after using Cryo and PCC, hemorrhagic shock. Thromboelastometry still presents guided by ROTEM. In this case, ROTEM became nor- the potential benefit of allowing goal-guided hemostatic mal 120 minutes after the first ROTEM with therapy with hemostatic drugs and coagulation factor con- hyperfibrinolysis. centrates. Thus, this POCT could help avoid unnecessary Some aspects of this transfusion practice for the cor- transfusion in patients with hemorrhagic shock and active rection of coagulopathy should be highlighted. The order bleeding. Additional studies are expected to define the or sequence of the therapeutic approach in this scenario role and benefit of the use of thromboelastometry for of bleeding management is very important and can make diagnosis of coagulopathy and as a guide for transfusion a difference for the patient. First of all, ROTEM is a therapy with allogeneic blood products, coagulation factor POC testing performed at the bedside. Instead of concentrates, or hemostatic drugs. Crochemore and Savioli Journal of Medical Case Reports (2018) 12:153 Page 8 of 8 Abbreviations 9. Rossaint R, Bouillon B, Cerny V, Coats TJ, Duranteau J, Fernández-Mondéjar ALT: Serum alanine aminotransferase; APC: Activated protein C; E, et al. Management of bleeding following major trauma: an updated aPTT: Activated partial thromboplastin time; AST: Serum aspartate European guideline. Crit Care. 2010;14(2):R52. aminotransferase; bpm: beats per minute; CCT: Conventional coagulation 10. Yau JW, Teoh H, Verma S. Endothelial cell control of thrombosis. BMC tests; CFT: Clot formation time; Cryo: Cryoprecipitate; CT: Clotting time; Cardiovasc Disord. 2015;15:130. FC: Fibrinogen concentrate; FFP: Fresh frozen plasma; ICU: Intensive care unit; 11. Jacob M, Kumar P. The challenge in management of hemorrhagic shock in INR: International nationalized ratio; MCF: Maximum clot firmness; trauma. Med J Armed Forces India. 2014;70(2):163–9. ML: Maximum lysis; PC: Platelet concentrates; PCC: Prothrombin complex 12. Ikezoe T. Thrombomodulin/activated protein C system in septic concentrate; POCT: Point-of-care testing; PT: Prothrombin time; RBC: Red disseminated intravascular coagulation. J Intensive Care. 2015;3(1):1. blood cells; ROTEM: Thromboelastometry; TACO: Transfusion associated 13. Wikkelsø A, Wetterslev J, Møller AM, Afshari A. Thromboelastography (TEG) circulatory overload; TEG: Thromboelastography; TM: Thrombomodulin; or thromboelastometry (ROTEM) to monitor haemostatic treatment versus TRALI: Transfusion-related acute lung injury; TRIM: Transfusion-related usual care in adults or children with bleeding. Cochrane Database Syst Rev. immunomodulation; vWF: Von Willebrand factor 2016;8:CD007871. 14. Bonanno FG. Hemorrhagic shock: The "physiology approach". J Emerg Trauma Shock. 2012;5(4):285–95. Acknowledgements 15. Dirkmann D, Hanke AA, Görlinger K, Peters J. Hypothermia and acidosis We thank Carolina Martinez Savioli and Helena Spalic for proofreading this synergistically impair coagulation in human whole blood. Anesth Analg. manuscript. 2008;106(6):1627–32. 16. Weber CF, Görlinger K, Meininger D, Herrmann E, Bingold T, Moritz A, et al. Funding Point-of-care testing: a prospective, randomized clinical trial of efficacy in Not applicable. No funding was received. coagulopathic cardiac surgery patients. Anesthesiology. 2012;117(3):531–47. 17. Van Poucke S, Stevens K, Marcus AE, Lancé M. Hypothermia: effects on Availability of data and materials platelet function and hemostasis. Thromb J 2014;12(1):31. The datasets used and/or analyzed during the current study are available 18. Kozek-Langenecker SA. Fluids and coagulation. Curr Opin Crit Care. 2015; from the corresponding author on reasonable request. 21(4):285–91. 19. Handy JM, Soni N. Physiological effects of hyperchloraemia and acidosis. Authors’ contributions Br J Anaesth. 2008;101(2):141–50. TC and FS devised the case report. TC and FS collected the data. TC and FS 20. Madigan MC, Kemp CD, Johnson JC, Cotton BA. Secondary abdominal wrote the first manuscript draft. TC critically revised the manuscript. TC and compartment syndrome after severe extremity injury: are early, aggressive FS approved the final manuscript. fluid resuscitation strategies to blame? J Trauma. 2008;64(2):280–5. 21. Bouglé A, Harrois A, Duranteau J. Resuscitative strategies in traumatic hemorrhagic shock. Ann Intensive Care. 2013;3(1):1. Ethics approval and consent to participate 22. Sahu S, Hemlata, Verma A. Adverse events related to blood transfusion. Not applicable. Indian J Anaesth. 2014;58(5):543–51. 23. Sarani B, Dunkman WJ, Dean L, Sonnad S, Rohrbach JI, Gracias VH. Consent for publication Transfusion of fresh frozen plasma in critically ill surgical patients is Written informed consent was obtained from the patient for publication of associated with an increased risk of infection. Crit Care Med. 2008;36(4): this case report and any accompanying images. A copy of the written 1114–8. consent is available for review by the Editor-in-Chief of this journal. 24. Benson AB. Pulmonary complications of transfused blood components. Crit Care Nurs Clin North Am. 2012;24(3):403–18. Competing interests 25. Mann KG. Thrombin formation. Chest. 2003;124(3 Suppl):4S–10S. The authors declare that they have no competing interests. 26. Haas T, Görlinger K, Grassetto A, Agostini V, Simioni P, Nardi G, et al. Thromboelastometry for guiding bleeding management of the critically ill patient: a systematic review of the literature. Minerva Anestesiol. 2014; Publisher’sNote 80(12):1320–35. Springer Nature remains neutral with regard to jurisdictional claims in 27. Crochemore T, Piza FMT, Rodrigues RDR, Guerra JCC, Ferraz LJR, Corrêa TD. published maps and institutional affiliations. A new era of thromboelastometry. Einstein (Sao Paulo). 2017;0 Received: 20 December 2017 Accepted: 19 March 2018 References 1. Gutierrez G, Reines HD, Wulf-Gutierrez ME. Clinical review: hemorrhagic shock. Crit Care. 2004;8(5):373–81. 2. Rossaint R, Cerny V, Coats TJ, Duranteau J, Fernández-Mondéjar E, Gordini G, et al. Key issues in advanced bleeding care in trauma. Shock. 2006;26(4): 322–31. 3. Bose EL, Hravnak M, Pinsky MR. The interface between monitoring and Submit your next manuscript to BioMed Central physiology at the bedside. Crit Care Clin. 2015;31(1):1–24. 4. Meißner A, Schlenke P. Massive Bleeding and Massive Transfusion. Transfus and we will help you at every step: Med Hemother. 2012;39(2):73–84. • We accept pre-submission inquiries 5. Kozek-Langenecker SA, Ahmed AB, Afshari A, Albaladejo P, Aldecoa C, Barauskas G, et al. Management of severe perioperative bleeding: guidelines � Our selector tool helps you to find the most relevant journal from the European Society of Anaesthesiology: First update 2016. Eur J � We provide round the clock customer support Anaesthesiol. 2017;34(6):332–95. � Convenient online submission 6. Gallimore E. Clinical features and management of haemorrhagic shock. Nurs Stand. 2015;30(1):51–8. quiz 60 � Thorough peer review 7. Schöchl H, Voelckel W, Schlimp CJ. Management of traumatic � Inclusion in PubMed and all major indexing services haemorrhage—the European perspective. Anaesthesia. 2015;70 Suppl 1: � Maximum visibility for your research 102–7. e35–7 8. Martel MJ, MacKinnon KJ, Arsenault MY, Bartellas E, Klein MC, Lane CA, et al. Submit your manuscript at Hemorrhagic shock. J Obstet Gynaecol Can. 2002;24(6):504–20. quiz 21-4 www.biomedcentral.com/submit

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