Acute Traumatic Coagulopathy/ Trauma-Associated Coagulopathy

Philip R Judge BVSc MVS PG Cert Vet Stud MACVSc (Veterinary Emergency and Critical Care; Medicine of Dogs)

Introduction

Acute traumatic coagulopathy (trauma associated coagulopathy) is a severe coagulopathy that can occur following acute trauma1-3.

In humans, coagulation abnormalities are present in up to 34% of major trauma victims at the time of hospital presentation, and the presence of coagulopathy on admission is associated with increased morbidity and mortality1-3.

Whilst haemodilution of coagulation factors during fluid therapy resuscitation can contribute to coagulopathy in the trauma patient, coagulopathy is also observed in patients without significant blood volume expansion1-3.

The term “Acute Traumatic Coagulopathy” has been used to describe endogenous coagulopathy following traumatic injury occurring prior to resuscitation4.

There are a small number of studies, which show that both hypercoagulation and hypo-coagulation may occur following trauma both in dogs and cats, and that for dogs, increasing trauma severity, as determined by the animal trauma triage (ATT) score, was associated with increased coagulation times5-10.

Pathophysiology of Acute Traumatic Coagulopathy

Acute trauma coagulopathy is thought to have the following underlying pathophysiological causes1-4,11,12:

  1. Tissue damage and inflammation – initial tissue damage following trauma results in increased activation of the coagulation cascade. Tissue inflammation occurs following any tissue injury or damage, and results in cytokine-mediated augmentation of coagulation system activation (platelet activating factor, etc.), and further consumption of coagulation factors. Additionally, accelerated fibrinolysis occurs. When tissue damage is widespread or severe, mediators of coagulation and fibrinolysis are disseminated in systemic circulation. Additionally, severe trauma results in catecholamine-mediated increases in endothelial cell activation and expression of thrombomodulin, which is a co-factor for thrombin that converts thrombin to an anticoagulant co-factor that activates the anticoagulant protein, Protein C, thereby reducing clot duration at sites of vascular injury.
  2. Glycocalyx damage – occurs secondary to catecholamine release in severe trauma. This causes hypercoagulation, with subsequent release of anti-coagulant mediators such as tissue plasminogen activator, resulting in systemic anticoagulation and hyperfibrinolysis.
  3. Platelet dysfunction – can occur following trauma. Accelerated ADP release from damaged tissues can promote platelet activation in circulation, thereby reducing activity of platelets at sites of vascular injury.
  4. Hypoperfusion – hypoperfusion of regional vascular beds is common in patients with haemorrhagic shock, which results in reduced oxygen delivery to tissues, and subsequent loss of vascular wall integrity in those tissues, and activation of coagulation.
  5. Hypothermia – occurs commonly in patients following trauma (and treatment with cool intravenous fluids), and contributes to prolonged clotting times, vasodilatation and reduced tissue oxygen delivery.
  6. Acidosis – metabolic acidosis commonly occurs in patients following trauma. Acidosis reduces activity of enzymes involved in coagulation, thereby prolonging clotting times. Acidosis may also lead to increased rates of fibrinogen breakdown.

Additionally, as previously mentioned, coagulopathy in the trauma patient may be exacerbated following treatment with intravenous fluid therapy, which may result in dilution of coagulation factors, which reduces clot strength, as well as exacerbation of haemorrhage due to blood pressure elevations6,8.

Acute Traumatic Coagulopathy Blog

Diagnosis of Acute Traumatic Coagulopathy

In both humans and animals, the use of traditional coagulation tests, such as pro-thrombin time, activated partial thromboplastin time, activated clotting time, fibrinogen and platelet count has been used to characterise acute traumatic coagulopathy11.

In humans, values used for defining acute traumatic coagulopathy using these parameters include a greater than 50% prolongation of aPTT or PT, and fibrinogen of less than 1 g/L. More recently, a PT ratio (patient PT/mean laboratory PT) of greater than 1.2 was shown to provide greater prediction of mortality and transfusion requirements11.

Due to several factors, including lack of compensation for acidosis, hypothermia or the dynamic and multifactorial aetiology of acute traumatic coagulopathy, aPTT and PT are considered to carry poor predictive value in the detection of the disorder11.

Thromboelastography (TEG) and rotational thromboelastometry (ROTEM) coagulation tests are able to evaluate all components of the coagulation process, including hypocoagulation, hypercoagulation and hyperfibrinolysis11. These tests reveal that acute traumatic coagulopathy results in abnormalities in clot strength. Additionally, they show that in acute trauma, coagulopathy progresses through a dynamic series of events, from hypercoagulation, to hypocoagulation and hyperfibrinolysis, as the degree of tissue injury increases13,14. However, these tests also do not take into account [AS1] endothelial health and function, acid-base status and shear forces in blood vessels that may be present in the patient and are therefore still less than ideal tests11. Additionally, many veterinary facilities lack the ability to utilise TEG or ROTEM in the emergency setting.

Making a diagnosis of acute traumatic coagulopathy in veterinary patients is currently challenging. It has been proposed that the presence of the following would be highly suggestive of acute traumatic coagulopathy11:

  • The presence of severe trauma with significant tissue injury
  • The presence of hypotension (systolic arterial pressure <80 mm Hg)
  • The presence of marked hyperlactataemia > 6 mmol/L
  • The presence of haemorrhagic shock, with uncontrollable intra-cavitary bleeding, or spontaneous bleeding from wound or catheter sites
  • Prolonged aPTT or PT greater than 1.5 x laboratory mean
  • ROTEM or TEG evidence of greater than 40% decrease in clot strength

Treatment of Acute Traumatic Coagulopathy

Acute traumatic coagulopathy may be managed using principles of damage control resuscitation to arrest haemorrhage, the use of early transfusion therapy and through the use of anti-thrombolytic agents such as tranexamic acid, to slow removal of blood clots – particularly of use where large organs have suffered contusion e.g. lungs, liver, spleen, etc.

Haemostasis control is one of the main strategies in management of haemorrhagic shock. Superficial wounds should have compressive bandages, topical coagulation agents or direct ligation of bleeding vessels applied at the earliest opportunity15. In patients with non-compressible haemorrhage, such as haemorrhage into the peritoneal cavity, application of an abdominal compression bandage should be considered, and is associated with reduced haemorrhage, slower reduction in mean arterial pressure, and greater survival than in patients without abdominal compression bandages16. In patients showing evidence of ongoing haemorrhage and decompensation despite abdominal pressure, surgical exploration to achieve direct haemostasis by direct pressure and damage control surgery is indicated15.

The concept of hypotensive, or permissive hypotension has been investigated in both humans and dogs and has potential to reduce the risk of dilutional coagulopathy in the presence of active haemorrhage, and the dislodgement of blood clots in traumatised tissue that can occur as the patient’s blood pressure increases, following use of large volumes of crystalloid fluid therapy in the treatment of hypovolaemia. However, at present, current recommendations are not widely either available or accepted in veterinary medicine, due to the lack of clarity in the evidence-base. In humans without traumatic brain injury, cardiovascular disease or other co-morbidities such as kidney injury, hypotensive resuscitation is applied using isotonic crystalloid, hypertonic saline or synthetic colloid fluids, to achieve systolic arterial blood pressures of 90 mm Hg, or mean arterial blood pressures of 60-70 mm Hg, until definitive haemostasis or damage control surgery can be performed15.

Damage control resuscitation is another concept that may offer benefit in acute traumatic coagulopathy, in which crystalloid or colloid fluids are administered as in hypotensive resuscitation, but are combined with the use of blood products to normalise coagulation and provide red cell replacement in cases of severe exsanguination, alongside damage control surgery5. Early transfusion therapy in patients with evidence of significant trauma and acute traumatic coagulopathy is associated with improved survival, reduced blood component use, and reduced organ failure over patients with delayed transfusion15.

Damage control surgery is an abbreviated surgical procedure designed to achieve rapid control of haemorrhage and contamination in the abdominal cavity in patients with uncontrollable abdominal haemorrhage, and involves packing the abdominal cavity with sponges to compress areas of haemorrhage, providing definitive ligation of bleeding vessels if identified, and temporary closure of the abdomen, whilst leaving abdominal sponges in place if the source of haemorrhage is unable to be identified or ligated (as in the case of organ contusion), followed by subsequent re-exploration once the patient is stable15.

Pharmacological adjunctive therapy may also be of benefit in the patient with acute traumatic coagulopathy. To date, anti-thrombolytic drugs such as aminocaproic acid and tranexamic acid have been the most widely recommended for use in dogs15.

Conclusion

Acute traumatic coagulopathy represents a potentially life-threatening complication in the patient with significant trauma. Current diagnostic tests are relatively insensitive, and do not provide a dynamic and holistic view of the entirety of the condition. However, prolongation of clotting times in the presence of significant trauma suggest acute traumatic coagulopathy is likely. Treatment should include attention to arrest of haemorrhage, the careful titration of intravenous fluid therapy, early transfusion therapy, damage control surgery, and the use of anti-thrombolytic agents as indicated by the patient response to each step of the treatments outlined above. More research into acute traumatic coagulopathy, including refinement of fluid therapy and transfusion guidelines will inform clearer recommendations in time11,15.

References

  1. Maegele, Marc, Rolf Lefering, Nedim Yucel, Thorsten Tjardes, Dieter Rixen, Thomas Paffrath, Christian Simanski, Edmund Neugebauer, Bertil Bouillon, and AG Polytrauma of the German Trauma Society (DGU. “Early coagulopathy in multiple injury: an analysis from the German Trauma Registry on 8724 patients.” Injury 38, no. 3 (2007): 298-304.
  2. MacLeod, Jana BA, Mauricio Lynn, Mark G. McKenney, Stephen M. Cohn, and Mary Murtha. “Early coagulopathy predicts mortality in trauma.” Journal of Trauma and Acute Care Surgery 55, no. 1 (2003): 39-44.
  3. Brohi, Karim, Mitchell J. Cohen, and Ross A. Davenport. “Acute coagulopathy of trauma: mechanism, identification and effect.” Current opinion in critical care 13, no. 6 (2007): 680-685.
  4. Hess, John R., Karim Brohi, Richard P. Dutton, Carl J. Hauser, John B. Holcomb, Yoram Kluger, Kevin Mackway-Jones et al. “The coagulopathy of trauma: a review of mechanisms.” Journal of Trauma and Acute Care Surgery 65, no. 4 (2008): 748-754.
  5. Gottlieb, Dara L., Jennifer Prittie, Yekaterina Buriko, and Kenneth E. Lamb. “Evaluation of acute traumatic coagulopathy in dogs and cats following blunt force trauma.” Journal of veterinary emergency and critical care 27, no. 1 (2017): 35-43.
  6. Abelson, Amanda L., Therese E. O’Toole, Andrea Johnston, Meghan Respess, and Armelle M. de Laforcade. “Hypoperfusion and acute traumatic coagulopathy in severely traumatized canine patients.” Journal of Veterinary Emergency and Critical Care 23, no. 4 (2013): 395-401.
  7. Holowaychuk, Marie K., Rita M. Hanel, R. Darren Wood, Lindsey Rogers, Karen O’Keefe, and Gabrielle Monteith. “Prospective multicenter evaluation of coagulation abnormalities in dogs following severe acute trauma.” Journal of veterinary emergency and critical care 24, no. 1 (2014): 93-104.
  8. Herrero, Yaiza, Rahel Jud Schefer, Benjamin M. Muri, and Nadja E. Sigrist. “Prevalence of acute traumatic coagulopathy in acutely traumatized dogs and association with clinical and laboratory parameters at presentation.” Veterinary and Comparative Orthopaedics and Traumatology 34, no. 03 (2021): 214-222.
  9. Herrero, Yaiza, Rahel Jud Schefer, Benjamin M. Muri, and Nadja E. Sigrist. “Serial Evaluation of Haemostasis Following Acute Trauma Using Rotational Thromboelastometry in Dogs.” Veterinary and Comparative Orthopaedics and Traumatology 34, no. 03 (2021): 206-213.
  10. Muri, Benjamin M., Rahel Jud Schefer, and Nadja E. Sigrist. “Serial evaluation of haemostasis following acute trauma using rotational thromboelastometry in cats.” Veterinary and Comparative Orthopaedics and Traumatology 32, no. 04 (2019): 289-296.
  11. Davenport, Ross. “Pathogenesis of acute traumatic coagulopathy.” Transfusion 53 (2013): 23S-27S.
  12. Palmer, Lee, and Linda Martin. “Traumatic coagulopathy‐Part 1: Pathophysiology and diagnosis.” Journal of Veterinary Emergency and Critical Care 24, no. 1 (2014): 63-74.
  13. Ganter, Michael T., and Christoph K. Hofer. “Coagulation monitoring: current techniques and clinical use of viscoelastic point-of-care coagulation devices.” Anesthesia & Analgesia 106, no. 5 (2008): 1366-1375.
  14. Johansson, Pär I. “Coagulation monitoring of the bleeding traumatized patient.” Current Opinion in Anesthesiology 25, no. 2 (2012): 235-241.
  15. Palmer, Lee, and Linda Martin. “Traumatic Coagulopathy‐Part 2: Resuscitative strategies.” Journal of Veterinary Emergency and Critical Care 24, no. 1 (2014): 75-92.
  16. McAnulty, J. F., and G. K. Smith. “Circumferential external counterpressure by abdominal wrapping and its effect on simulated intra‐abdominal hemorrhage.” Veterinary Surgery 15, no. 3 (1986): 270-274.

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