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The pathophysiology of uncontrolled hemorrhage in horses.

Abstract: Hemorrhagic shock in horses may be classified in several ways. Hemorrhage may be considered internal versus external, controlled or uncontrolled, or described based on the severity of hypovolemic shock the patient is experiencing. Regardless of the cause, as the severity of hemorrhage worsens, homeostatic responses are stimulated to ameliorate the systemic and local effects of an oxygen debt. In mild to moderate cases of hemorrhage (<15% blood volume loss), physiological adaptations in the patient may not be clinically apparent. As hemorrhage worsens, often in the uncontrolled situation such as a vascular breach internally, the pathophysiological consequences are numerous. The patient mobilizes fluid and reserve blood volume, notably splenic stored and peripherally circulating erythrocytes, to preferentially supply oxygen to sensitive organs such as the brain and heart. When the global and local delivery of oxygen is insufficient to meet the metabolic needs of the tissues, a cascade of cellular, tissue, and organ dysfunction occurs. If left untreated, the patient dies of hemorrhagic anemic shock. Conclusions: An understanding of the pathophysiological consequences of hemorrhagic shock in horses and their clinical manifestations may help the practitioner understand the severity of blood volume loss, the need for referral, the need for transfusion, and potential outcome. In cases of severe acute uncontrolled hemorrhage, it is essential to recognize the clinical manifestations quickly to best treat the patient, which may include humane euthanasia. Conclusions: Uncontrolled hemorrhage may be defined as the development of a vascular breach and hemorrhage that cannot be controlled by interventional hemostasis methods such as external pressure, tourniquet, or ligation. Causes of uncontrolled hemorrhage in horses may be due to non-surgical trauma, surgical trauma, invasive diagnostic procedures including percutaneous organ biopsy, coagulopathy, hypertension, cardiovascular anomaly, vascular damage, neoplasia such as hemangiosarcoma, toxicity, or idiopathic in nature. When a critical volume of blood is lost, the respondent changes in heart rate, splenic blood mobilization, and microcirculatory control can no longer compensate for decreasing oxygen delivery to the tissues In spite of organ-specific microvascular responses (eg, myogenic responses, local mediator modulation of microvasculature, etc), all organs experience decreases in blood flow during severe hypovolemia Acute, fatal hemorrhagic shock is characterized by progressive metabolic acidosis, coagulopathy, and hypothermia, often termed the "triad of death," followed by circulatory collapse.
Publication Date: 2022-01-20 PubMed ID: 35044067DOI: 10.1111/vec.13122Google Scholar: Lookup
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  • Journal Article

Summary

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This study explores the physiological process and consequences of uncontrolled bleeding in horses. The research emphasizes the need to quickly recognize and adequately respond to this condition to improve the chances of survival, or regretfully, consider humane euthanasia in severe cases.

Explanation of Hemorrhagic Shock in Horses

  • The study starts by categorizing hemorrhagic shock in horses, meaning severe blood loss, based on several factors including whether it is internal versus external, controlled or uncontrolled, and the severity of the resultant hypovolemic shock, a condition characterized by decreased blood volume.
  • It explains that if a horse loses less than 15% of its total blood volume, the physiological adjustments might not be outwardly noticeable.

Pathophysiological Consequences of Severe Hemorrhage

  • However, if the bleeding worsens – an uncontrolled bleed, for example, due to internal vascular damage – the pathophysiological impacts are numerous.
  • The horse’s body tries to maintain oxygen delivery to critical organs like the brain and heart by mobilizing fluid and reserve blood volume, particularly stored blood from the spleen and circulating red blood cells.
  • When these adaptations fail to supply enough oxygen to meet tissue requirements, a cascade of cellular, tissue, and organ dysfunction begins. This can lead to fatal hemorrhagic anemic shock if not addressed.

Clinical Manifestations and Treatment

  • Understanding the pathophysiological implications of hemorrhagic shock and their clinical symptoms can be crucial in assessing the extent of blood volume loss, identifying the need for referral or transfusion, and informing on the potential outcome.
  • Timely recognition of severe acute uncontrolled hemorrhage is essential for effective treatment, which can unfortunately involve considering humane euthanasia in some circumstances.

Causes of Uncontrolled Hemorrhage

  • The research expands on the causes of uncontrolled bleeding in horses, outlining potential factors like non-surgical trauma, surgical trauma, invasive diagnostic procedures (like percutaneous organ biopsy), blood clotting disorders (coagulopathies), hypertension, cardiovascular anomaly, vascular damage, cancer (like hemangiosarcoma), toxicity, or idiopathic causes (unknown origins).
  • As hemorrhage intensifies and blood volume decreases, compensatory physiological responses such as increased heart rate, movement of splenic blood, and control of small blood vessels (microcirculation) can no longer maintain oxygen supply to tissues.
  • All organs experience decreased blood flow during severe blood loss, regardless of specific microvascular responses. Severe, fatal hemorrhagic shock is then characterized by a progression of metabolic acidosis (excess acid in body fluids), coagulopathy, and hypothermia, often referred to as the “triad of death,” followed by circulatory collapse.

Cite This Article

APA
Hurcombe SDA, Radcliffe RM, Cook VL, Divers TJ. (2022). The pathophysiology of uncontrolled hemorrhage in horses. J Vet Emerg Crit Care (San Antonio), 32(S1), 63-71. https://doi.org/10.1111/vec.13122

Publication

ISSN: 1476-4431
NlmUniqueID: 101152804
Country: United States
Language: English
Volume: 32
Issue: S1
Pages: 63-71

Researcher Affiliations

Hurcombe, Samuel D A
  • Emergency Surgery and Medicine, Cornell Ruffian Equine Specialists, Elmont, New York, USA.
Radcliffe, Rolfe M
  • Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA.
Cook, Vanessa L
  • Department of Large Animal Clinical Sciences, Michigan State University, East Lansing, Michigan, USA.
Divers, Thomas J
  • Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA.

MeSH Terms

  • Animals
  • Blood Coagulation Disorders / veterinary
  • Hemorrhage / etiology
  • Hemorrhage / therapy
  • Hemorrhage / veterinary
  • Horse Diseases / therapy
  • Horses
  • Hypovolemia / therapy
  • Hypovolemia / veterinary
  • Microcirculation
  • Shock, Hemorrhagic / therapy
  • Shock, Hemorrhagic / veterinary

References

This article includes 46 references
  1. Magdesian KG, Fielding CL, Rhodes DM. Changes in central venous pressure and blood lactate concentrations in response to acute blood loss in horses.. J Am Vet Med Assoc 2006; 229:1458-1462.
  2. Weld JM, Kamerling SG, Combie JD. The effects of naloxone on endotoxic and hemorrhagic shock in horses.. Res Commun Chem Pathol Pharmacol 1984; 44:227-238.
  3. Schmall LM, Muir WW, Robertson JT. Haemodynamic effects of small volume hypertonic saline in experimentally induced haemorrhagic shock.. Equine Vet J 1990; 22:273-277.
  4. Wilson DV, Rodenay Y, Shance PU. The cardiopulmonary effects of severe blood loss in anesthetized horses.. Vet Anaesth Analg 2003; 30:81-87.
  5. Arnold CE, Payne M, Thompson JA. Periparturient hemorrhage in mares: 73 cases (1998-2005).. J Am Vet Med Assoc 2008; 232:1345-1351.
  6. Pusterla N, Fecteau ME, Madigan JE. Acute hemoperitoneum in horses: a review of 19 cases (1992-2003).. J Vet Intern Med 2005; 19:344-347.
  7. Kishardt KK, Schumacher J, Finn-Bodner ST. Severe renal hemorrhage caused by pyelonephritis in 7 horses: clinical and ultrasonographic evaluation.. Can Vet J 1999; 40:571-576.
  8. Versnaeyen H, Saey V, Vermieren D. Intermittent haemotypsis due to an aortobronchial fistula in a Warmblood mare.. J Comp Pathol 2016; 155:213-217.
  9. Lyle CH, Uzal FA, McGorum BC. Sudden death in racing Thoroughbred horses: an international study of post mortem findings.. Equine Vet J 2011; 43:324-331.
  10. Gray SN, Dechant JE, LeJeune SS. Identification, management and outcome of postoperative hemoperitoneum in 23 horses after emergency exploratory celiotomy for gastrointestinal disease.. Vet Surg 2015; 44:379-385.
  11. Doyle AJ, Freeman DE, Rapp H. Life-threatening hemorrhage from enterotomies and anastomosis in 7 horses.. Vet Surg 2003; 32:553-558.
  12. Livesey MA, Little CB, Boyd C. Fatal hemorrhage associated with incarceration of small intestine by the epiploic foramen in three horses.. Can Vet J 1991; 32:434-436.
  13. Archer RM, Knight CG, Bishop WJ. Guttural pouch mycosis in six horses in New Zealand.. NZ Vet J 2012; 60:203-209.
  14. Freeman DE, Johnston JK, Baker GJ. An evaluation of the haemostatic suture in hysterotomy closure in the mare.. Equine Vet J 1999; 31:208-211.
  15. Waguespack R, Belknap J, Williams A. Laparoscopic management of postcastration haemorrhage.. Equine Vet J 2001; 33:510-513.
  16. Nickels FA. Nasal passages and paranasal sinuses.. Equine Surgery Elsevier; 2012, pp. 557-568.
  17. Troillet A, Bottcher D, Brehm W. Retrospective evaluation of hemithyroidectomy in 14 horses.. Vet Surg 2016; 45:949-954.
  18. Marrietta M, Facchini L, Pedrazzi P. Pathophysiology of bleeding in surgery.. Transplant Proc 2006; 38:812-814.
  19. Eddy VA, Morris JA, Culliname DC. Hypothermia, coagulopathy, acidosis.. Surg Clin North Am 2000; 80:845.
  20. Dutton RP. Current concepts in hemorrhagic shock.. Anesthesiol Clin 2007; 25(1):23-34.
  21. Gutierrez G, Reines HR, ME W-G. Clinical review: hemorrhagic shock.. Crit Care Med 2004; 8:373-381.
  22. Kline H, Foreman JH. Heart and spleen weights as a function of breed and somatotype.. Equine Exerc Physiol 1991; 3:17-21.
  23. Persson SGB, Ekman L, Lydin G. Circulatory effects of splenectomy in the horse. II. Effect of plasma volume and total and circulating red-cell volume.. Zentrabl Veterinarmed A 1973; 20:456-468.
  24. Nolen-Walston RD, Norton JL, Navas de Solis C. The effects of hypohydration on central venous pressure and splenic volume in adult horses.. J Vet Intern Med 2011; 25:570-574.
  25. Greenway CV, Stark RD. Vascular responses of the spleen to rapid haemorrhage in the anaesthetized cat.. J Physiol 1969; 204:169-179.
  26. Lynn M, Jeroukhimov I, Klein Y. Updates in the management of severe coagulopathy in trauma patients.. Intensive Care Med 2002; 28:S241.
  27. LaFarge CG, Miettinen OS. The estimation of oxygen consumption.. Cardiovasc Res 1970; 4:23-30.
  28. Ray CJ, Abbas MR, Coney AM, Marshall JM. Interactions of adenosine, prostaglandins and nitric oxide in hypoxia-induced vasodilatation: in vivo and in vitro studies.. J Physiol 2002; 544:195-209.
  29. Edmunds NJ, Marshall JM. Vasodilatation, oxygen delivery and oxygen consumption in rat hindlimb during systemic hypoxia: roles of nitric oxide.. J Physiol 2001; 532:251-259.
  30. Cain SM. Peripheral oxygen uptake and delivery in health and disease.. Clin Chest Med 1983; 4:139-148.
  31. Karpati PC, Rossignol M, Pirot M. High incidence of myocardial ischemia during postpartum hemorrhage.. Anesthesiology 2004; 100:30-36.
  32. Rossi TM, Pyle WG, Maxie MG. Troponin assays in the assessment of the equine myocardium.. Equine Vet J 2014; 46:270-275.
  33. Diaz OM, Durando MM, Birks EK. Cardiac troponin I concentrations in horses with colic.. J Am Vet Med Assoc 2014; 245:118-125.
  34. Nath LC, Anderson GA, Hinchcliff KW. Serum cardiac troponin I concentrations in horses with cardiac disease.. Aust Vet J 2012; 90:351-357.
  35. Navas de Solis C, Dallap Schaer B, Boston R. Myocardial insult and arrhythmias after acute hemorrhage in horses.. J Vet Emerg Crit Care 2015; 25:248-255.
  36. Rainer K, Rollwagen FM, Prueckner S. Effects of mild hypothermia on survival and serum cytokines in uncontrolled hemorrhagic shock in rats.. Shock 2002; 17:521-526.
  37. Schlichtig R, Kramer DJ, Pinsky MR. Flow distribution during progressive hemorrhage is a determinant of critical O2 delivery.. J Appl Physiol 1991; 70:169-178.
  38. Brohi K, Cohen MJ, Ganter MT. Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway?. Ann Surg 2007; 245:812-818.
  39. Meng ZH, Wolberg AS. The effect of temperature and pH on the activity of factor VIIa: implications for the efficacy of high-dose factor VIIa in hypothermic and acidotic patients.. J Trauma 2003; 55:886-891.
  40. Collicott PE. Advanced Trauma Life Support (ATLS); past, present, future-16th Stone Lecture, American Trauma Society.. J Trauma 1992; 33:749-753.
  41. Hurcombe SD, Mudge MC, Hinchcliff KW. Clinical and clinicopathologic variables in adult horses receiving blood transfusion: 31 cases (1999-2005).. J Am Vet Med Assoc 2007; 231:267-274.
  42. Dubin A, Estensoro E, Murias G. Effects of hemorrhage on gastrointestinal oxygenation.. Intensive Care Med 2001; 27:1931-1936.
  43. Mudge MC. Acute hemorrhage and blood transfusion in horses.. Vet Clin Equine 2014; 30:427-436.
  44. Babuin L, Vasile VC, Rio Perez JA. Elevated cardiac troponin is an independent risk factor for short- and long term mortality in medical intensive care unit patients.. Crit Care Med 2008; 36:759-765.
  45. De Robertis E, Kozek-Langenecker SA, Tufano R. Coagulopathy induced by acidosis, hypothermia and hypocalcemia in severe bleeding.. Minerv Anestesiol 2015; 81:65-75.
  46. Wang L, Song J, Buggs J. A new mouse model of hemorrhagic shock-induced acute kidney injury.. Am J Physiol Renal Physiol 2017; 312:F134-F142.

Citations

This article has been cited 1 times.
  1. Du J, Wang J, Xu T, Yao H, Yu L, Huang D. Hemostasis Strategies and Recent Advances in Nanomaterials for Hemostasis.. Molecules 2023 Jul 7;28(13).
    doi: 10.3390/molecules28135264pubmed: 37446923google scholar: lookup