Approaching acute haemorrhage in horses

The degree of blood loss will dictate if the patient needs a specific therapy and if this should take priority before surgery

01 October 2020, at 8:25am

Imagine this scenario: You are called to attend an eight-year-old TB gelding who has suffered a deep laceration to the plantar and lateral aspect of his right-hind pastern in the field. The owner is concerned about the amount of blood loss and the fact the wound is continuing to bleed. Clinical examination reveals a quiet but alert and respon­sive horse with tachycardia (heart rate 80 bpm), tachypnoea (44 bpm), hypothermia (35.8°C), pale mucous membranes and a capillary refill time of two seconds. On examination of the wound, you are concerned about digital flexor tendon sheath (DFTS), distal and proximal interphalangeal joint involvement and notice there is an arterial bleed from the lateral digital artery.

This horse needs to have the clinical implications of the wound with respect to the DFTS and joint involvement inves­tigated, and potential synovial surgical flushing and debride­ment needs to be performed. However, decisions also need to be made on the degree of blood loss and if the patient needs any specific therapy for this, and if this should take pri­ority before surgery. This article will focus on the treatment and management of the acute blood loss; it is beyond the scope of this article to comment in depth on the management of the deep laceration, tendon sheath or joint issues.

With acute haemorrhage it is important to monitor for clinical signs of hypovolaemia, laboratory evidence of tissue hypoperfusion and laboratory evidence of acute blood loss.


Hypovolaemic shock occurs when there is a decreased circulating blood volume, as a result of external or internal loss, or plasma volume third spacing. Decreased venous return to the heart ensues, in turn reducing stroke volume and decreasing cardiac output, if heart rate alterations fail to compensate. The body’s response to hypovolaemic shock includes increase in heart rate, peripheral vasoconstriction and fluid movement into the plasma to increase intravascular pressure and maintain perfusion of vital organs. If hypovol­aemia is severe or prolonged, tissue hypoperfusion occurs with a shift from aerobic to anaerobic metabolism, production of lactate and progressive cellular damage. Overproduction of lactic acid inhibits normal cell function and leads to meta­bolic acidosis. If shock continues, irreversible tissue damage starts to occur.

In adult horses, the clinical signs of hypovolaemia reflect­ing these pathophysiological compensatory mechanisms include hypotension (low blood pressure), tachycardia (increased heart rate), weak peripheral pulse, tachypnoea (increased breathing rate), reduced urine output (oliguria) and hypothermia (reduced body temperature).

The horse in this clinical scenario has tachycardia, tachypnoea and hypothermia; thus, along with the known history of acute haemorrhage, hypovolaemic shock should be presumed. It is critical to pay attention to clinical exami­nation findings in these cases which can direct you to diag­nosing hypovolaemic shock. It is important to bear in mind that in neonatal foals, the clinical signs of hypovolaemia can be much less apparent.

Laboratory evidence of tissue hypoperfusion and acute blood loss

It is important to gauge for the degree of blood loss and the effect of the hypovolaemia on the body’s function. Some rapid, cheap and easy to perform tests can help to estab­lish the current state and be useful for ongoing monitoring response to therapy (Table 1).

Table of contents
TABLE (1) A venous blood sample should be collected to perform tests useful to establish the current state of the animal and monitor response to therapy

Laboratory tests performed on the horse in this scenario were as follows:

  • PCV: 32 percent – within reference range
  • TP: 33 g/l – hypoproteinaemia
  • Blood lactate: 6.9 mmol/l – hyperlactataemia

Hyperlactataemia indicates hypoperfusion and anaerobic metabolism are occurring. Blood lactate concentration is a useful and sensitive indicator of acute blood loss in horses (Magdesian et al., 2006; Hurcombe et al., 2007). This informa­tion combined with the clinical signs indicates the need for urgent treatment of hypovolaemic shock.

The PCV appears to be within the normal range, whilst the TP is decreased. This is not surprising, since the effect of the blood loss will only be reflected in the PCV once the lost volume has been replaced by interstitial fluid. TP tends to decrease first before changes in PCV are seen clinically. Therefore, the PCV measurement in itself is of little value in initial assessment of acute haemorrhage, but it is an impor­tant tool for monitoring changes.

Initial management

Horse blood volume is 6 to 10 percent of body weight, depending on breed (Marcilese et al., 1964). Horses can tolerate up to 15 percent blood loss without the need for transfusion, and up to 20 to 30 percent blood loss may be tolerated by some individuals before a transfusion is needed. So, for a 500kg horse, blood volume is 30 to 50 litres, so a loss of 4.5 to 7.5 litres and up to 15 litres in some individuals may be tolerated. Blood transfusion decision making depends not only on the volume of blood lost but also the speed of blood loss, as animals adapt to chronic anaemia with low PCV and cope better than in sudden volume loss. As a general rule, a blood transfusion should be considered in any horse with a PCV less than 18 percent and is crucial if the PCV drops to 12 percent.

The case here presents with acute haemorrhage, so blood transfusion may indeed be indicated if the oxygen carrying capacity of the blood is decreased, compromising oxygen tissue delivery. However, in all cases of acute haemor­rhage, hypovolaemia should be corrected first, as this is the immediately life-threatening event that needs addressing as a priority. Several studies have indicated that immediate surgical treatment of synovial penetration is not neces­sary for a positive outcome, and furthermore, anaesthetic induction for treatment of synovial sepsis outside of normal working hours has been associated with death (Smith et al., 2006; Walmsley et al., 2011; Milner et al., 2014; Crosby et al., 2019). Thus, it would be prudent to delay surgery until the patient is haemodynamically stable. In the interim, the wound should be cleaned of organic debris as far as possible and a pressure bandage applied to stem the bleeding. If bleeding cannot be controlled, the arterial bleed should be located and ligated. If a horse is suffering from uncontrolled haemor­rhage (usually an internal bleed), then aggressive fluid ther­apy to correct hypovolaemia should be avoided, since a rapid increase in blood pressure can destabilise clot formation.

Hypovolaemia treatment

There are a variety of different fluid types that can be used to treat hypovolaemia, but the essence of treatment is rapid replacement of intravascular fluid volume. Thus, a wide gauge intravenous catheter (or two) should be placed and preferably wide-bore tubing used if possible to facilitate rapid fluid administration.

The easy to use principle of “shock dose” of fluids should be applied. An adult horse shock dose, applied over 60 to 90 minutes, corresponds to 60 to 80ml/kg of crystalloid fluids (30 to 40 litres for a 500kg horse), 10 to 15ml/kg pentastarch (5 to 7.5 litres for a 500kg horse), 10ml/kg hetastarch (5 litres for a 500kg horse) or 2 to 4 ml/kg of 7% hypertonic saline (1 to 2 litres for a 500kg horse). Initially, a bolus of 0.25 to 0.5 of the total shock dose is given, followed by reassessment of the clinical signs of hypovolaemia, and further 0.25 doses of the shock dose given up to the full dose if necessary.

Fluids that will draw extracellular fluid into the intravascular space are preferable to isotonic crystalloid fluids for rapid volume replacement in adult horses for the simple reason that a smaller volume can practically be delivered in a short period of time. Hypertonic saline will draw intravascular fluid rapidly into the vasculature and replace blood volume, but the effect will be short-lived (30 minutes) and thus replace­ment of fluid with large volumes of crystalloid fluids must follow hypertonic saline administration (within 2.5 hours). Colloids (synthetic or plasma) will draw extravascular fluid into the vascular space by means of oncotic pressure, and since the large molecules will be slower to leave the vascu­lar space than saline, exert their effect for a more prolonged period of time. In any case, it is important to remember to continue to treat dehydration after hypovolaemia has been corrected. This will normally require intravenous crystalloid therapy over the following 12 to 24 hours.

The case here was treated with a hydroxyethyl starch synthetic colloid preparation (pentastarch), at a dose of 5ml/kg (2.5 litres for a 500kg horse) bolused in (by squeez­ing the bags attached to the drip line) over 20 minutes. The horse was then reassessed for signs of hypovolaemia. Heart rate was 60 bpm, respiratory rate 28 bpm and tem­perature 36.5°C. Thus, there was a marked improvement in the clinical signs of hypovolaemia, and a further 2.5ml/ kg (1.25 litres for a 500kg horse) of pentastarch was given over a further 10 minutes. This further improved the clinical signs of hypovolaemia (heart rate 44 bpm, respiratory rate 16 bpm, temperature 37.0°C). At four hours post initiation of treatment, laboratory tests were repeated:

  • PCV: 26 percent
  • TP: 40g/l
  • Blood lactate: 2.1mmol/l

Intravenous crystalloid fluids were continued for a further 12 hours at a rate of 4ml/kg/hour. Measurements repeated at 12 hours revealed:

  • PCV: 24 percent – low
  • TP: 47g/l – hypoproteinaemia
  • Blood lactate: 1.5 mmol/l – within reference range

The horse was considered a more stable candidate for general anaesthesia and surgery at this stage, and a blood transfusion was not deemed necessary in this case, based on the clinical and laboratory findings.

It is important to be able to recognise the clinical signs of hypovolaemia that accompany acute haemorrhage and understand how to address this rapidly in order to pre­serve organ function. Not every case of acute haemorrhage needs a blood transfusion, but it is important to monitor for changes in clinical and laboratory parameters that might indicate tissue oxygen demand is not being met.

Author Year Title
Crosby, D., Labens, R., Hughes, K., Nielsen, S. and Hilbert, B. 2019 Factors associated with survival and return to function following synovial infections in horses. Frontiers in Veterinary Science, 6, 367
Hurcombe, S., Mudge, M. and Hinchcliff, K. 2007 Clinical and clinicopathologic variables in adult horses receiving blood transfusions: 31 cases (1999–2005). Journal of the American Veterinary Medical Association, 231, 267-274
Magdesian, K., Fielding, C., Rhodes, D. and Ruby, R. 2006 Changes in central venous pressure and blood lactate concentration in response to acute blood loss in horses. Journal of the American Veterinary Medical Association, 229, 1458-1462
Marcilese, N., Valsecchi, R., Figueiras, H., Camberos, H. and Varela, J. 1964 Normal blood volumes in the horse. American Journal of Physiology – Legacy Content, 207, 223-227
Milner, P., Bardell, D., Warner, L., Packer, M., Senior, J., Singer, E. and Archer, D. 2014 Factors associated with survival to hospital discharge following endoscopic treatment for synovial sepsis in 214 horses. Equine Veterinary Journal, 46, 701-705
Smith, L., Mellor, D., Marr, C. and Mair, T. 2010 What is the likelihood that a horse treated for septic digital tenosynovitis will return to its previous level of athletic function? Equine Veterinary Journal, 38, 337-341
Walmsley, E., Anderson, G., Muurlink, M. and Whitton, R. 2011 Retrospective investigation of prognostic indicators for adult horses with infection of a synovial structure. Australian Veterinary Journal, 89, 226-231

Adele Williams, BVSc, MRCVS, DipECEIM, PhD, is a European and RCVS specialist in equine internal medicine. She is head of equine at Vet-AI and works as a consultant specialist for Virtual Veterinary Specialists.

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