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Basics

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BASICS

Definition!!navigator!!

Rapid loss of blood, usually over <24 h.

Pathophysiology!!navigator!!

  • Acute loss of >30% of circulating blood volume (12 L/500 kg) results in hypovolemic shock; immediate triggering of compensatory mechanisms
  • Rapid loss of >40–50% of circulating blood volume is a severe, irreversible physiologic insult; death is common
  • Compensatory mechanisms include vasoconstriction, increased cardiac contractility and rate, expansion of blood volume via increased water and sodium resorption, and fluid movements from the intracellular/interstitial spaces to the vascular pool
  • RBCs are released into the circulation via splenic contraction
  • PCV may not reflect total blood loss for up to 24 h. TP decreases in 6 h. With internal hemorrhage of RBCs are autotransfused to the circulation within 24–72 h
  • A regenerative bone marrow response is demonstrable from 3 to 42 days. Complete restoration of RBC mass requires 1–3 months
  • Replacement of plasma proteins is more rapid, with albumin taking 5–10 days and globulins 3–4 weeks

Systems Affected!!navigator!!

  • Cardiovascular and respiratory
  • Hemic/lymphatic/immune
  • Hepatobiliary, renal, GI, musculoskeletal, and central nervous

Genetics!!navigator!!

N/A

Incidence/Prevalence!!navigator!!

N/A

Geographic Distribution!!navigator!!

N/A

Signalment!!navigator!!

All ages/breeds.

Signs!!navigator!!

General Comments

Signs vary with the duration and severity of blood loss, site of hemorrhage, and underlying disease.

Historical Findings

  • Evidence of trauma
  • Recent dystocia in neonatal foals with hemothorax
  • Recent foaling; uterine artery rupture
  • Sudden collapse or distress in stallions; aortic root rupture
  • Recent intense exercise in racehorses (EIPH)

Physical Examination Findings

  • Signs of shock (loss of >30% of circulating blood volume) include tachycardia, tachypnea, mucous membrane pallor, systolic heart murmur, slowed jugular filling, reduced pulse pressure, and oliguria. Agitation, generalized weakness, and sweating may occur
  • Ataxia and collapse with >40% blood volume loss
  • Epistaxis, respiratory distress, decreased or absent ventral lung sounds, and pleurodynia if lung/thorax are involved
  • Signs of low-grade colic and decreased GI tract motility may occur with diminution of organ perfusion or intra-abdominal hemorrhage
  • Sudden death may be the only sign with aortic root rupture

Causes!!navigator!!

Internal Abdominal Hemorrhage and Hemoperitoneum

  • Splenic and hepatic rupture following trauma
  • Rupture of caudal vena cava (after incarceration of the small intestine in the epiploic foramen)
  • Rupture of the middle uterine artery following dystocia or uterine eversion/prolapse
  • Hemorrhage from ovarian arteries.
  • Iliac arterial rupture secondary to a displaced pelvic fracture. Neoplasia, e.g. hemangiosarcoma
  • Recent surgery or biopsy

Internal Thoracic Hemorrhage

  • Thoracic trauma, e.g. rib fractures, lacerated heart or vessels during lung biopsy
  • Aortic root/other large vessel rupture
  • Diaphragmatic hernia with vascular tearing
  • Pulmonary hemorrhage
  • Neoplasia
  • Coagulopathy

External Hemorrhage

  • Epistaxis due to guttural pouch mycosis with erosion of the carotid artery, EIPH, severe trauma
  • Trauma, e.g. wounds
  • Surgical complications, e.g. post castration
  • Umbilical hemorrhage
  • Coagulopathy

Risk Factors!!navigator!!

  • High-intensity exercise; risk of EIPH
  • Previous periparturient hemorrhage in mares; a risk in future pregnancies
  • Older breeding stallions and Friesians at higher risk for acute aortic root rupture
  • Neonatal foals at risk of rib fractures and umbilical hemorrhage

Diagnosis

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DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Low-grade colic differentiated by rectal examination, abdominal US, and abdominocentesis
  • Acute severe hemolytic anemia differentiated on basis of history, biochemistry, serology (Coggins), examination of blood smears, or Coombs test
  • Sudden death differentiated by history, physical, and postmortem examinations

CBC/Biochemistry/Urinalysis!!navigator!!

  • Decreases in TP usually precede decreases in PCV due to splenic contraction
  • Few changes in mean cell volume, mean cell hemoglobin, and mean cell hemoglobin concentration. Transient leukocytosis with neutrophilia
  • Increased serum creatinine and urea nitrogen concentrations reflect prerenal or renal azotemia. Increased aspartate aminotransferase and creatine kinase activities if significant musculoskeletal trauma has occurred
  • Oliguria and increased urine specific gravity (>1.040) with hypovolemic shock

Other Laboratory Tests!!navigator!!

  • Coagulation tests (e.g. platelet count, prothrombin time, activated partial thromboplastin time) should be performed if a coagulopathy is suspected
  • Blood lactate 4 mmol/L and oxygen extraction ratio 40%, with clinical signs of acute or ongoing blood loss, support a decision to transfuse

Imaging!!navigator!!

Radiography

Thoracic radiography if hemothorax, rib fractures, or pneumothorax are suspected.

US

US to demonstrate hemoabdomen/hemothorax or identify thoracic or abdominal masses and suspected aortic root rupture.

Other Diagnostic Procedures!!navigator!!

  • Abdominocentesis and thoracocentesis. Erythrophagocytosis rules out inadvertent splenic or subcutaneous vessel puncture during sampling
  • Rectal palpation if intra-abdominal hemorrhage suspected
  • Airway endoscopy to localize the source of epistaxis
  • Laparoscopy to differentiate causes of intra-abdominal hemorrhage
  • Systolic blood pressure <80 mmHg or mean pressure <60 mmHg indicates hypotension

Pathologic Findings!!navigator!!

Depends on underlying cause. Wounds, hemothorax, hemoperitoneum, ruptured vessels, broad ligament rupture, broken ribs, epistaxis, melena, cardiac tamponade.

Treatment

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TREATMENT

Appropriate Health Care!!navigator!!

  • Aims—preserve life; stop hemorrhage; restore vascular fluid and blood volumes; treat associated injuries/problems
  • Severe acute hemorrhage often constitutes an emergency
  • Controlling hemorrhage and replacing blood volume are priorities
  • External hemorrhage may be controlled by pressure bandages or ligating ruptured vessels
  • Control of internal hemorrhage is more difficult; use a “wait and see” approach

Fluid Therapy

  • Balanced isotonic IV fluid therapy (initially 20 mL/kg; 10 L/500 kg) indicated if tachycardia, poor pulse quality, and cool extremities and low blood pressure present. Total volume administered should be 2–3 times the estimated loss
  • If high-volume isotonic fluid replacement is not practical, give small volumes of hypertonic saline (7% NaCl at 2–4 mL/kg IV) over 15 min if hemorrhage has been controlled. Isotonic fluids in sufficient volume to replace estimated deficits should follow within a few hours
  • Hydroxyethyl starch (6%) (8–10 mL/kg IV) may be used when hemorrhage has been controlled

Blood Transfusion

  • Indications for blood transfusion include poor response to fluids, persistent severe tachycardia, profound hypotension, ongoing hemorrhage, PCV decreasing to <20% within 12 h or if it falls to <12% over 24–48 h
  • Donors should be selected based on compatibility testing. If an immediate transfusion is needed blood may be collected from a gelding of similar breed with no history of blood/plasma therapy. Initial transfusions rarely cause adverse reactions, but subsequent transfusions (after 3 days) may cause severe reactions. An adult horse can donate 8–10 L of blood (or 20–25% of total blood volume) every 4–5 weeks without adverse clinical or physiologic consequences. Blood should be collected into bags containing citrate anticoagulant, with acid–citrate–dextrose (ACD), citrate–phosphate–dextrose (CPD), or CPD with supplemental adenine
  • Transfusion volume should be based on degree of hypovolemia and estimates of blood loss. For adult horses weighing 500 kg, 6–8 L (or 15 mL/kg) usually is required. The initial transfusion volume should be 50% of the estimated blood loss. Transfusion should be slow for the first 15 min (0.1 mL/kg/min); if no adverse reactions occur increase to 20 mL/kg/h

Nursing Care, Activity!!navigator!!

  • Box stall rest with severe blood loss
  • Horses with severe, acute hemorrhage require inpatient care
  • With hemothorax and respiratory distress blood can be removed by thoracocentesis; rapid refilling may occur
  • Administration of oxygen is indicated in hypoxemic patients; this is not a replacement for blood transfusion

Diet!!navigator!!

Good quality.

Client Education!!navigator!!

Monitoring and adhere to treatment plan.

Surgical Considerations!!navigator!!

Horses with acute severe hemorrhage are poor anesthetic risks and should be stabilized prior to surgery.

Medications

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MEDICATIONS

Drug(s) of Choice!!navigator!!

Aminocaproic acid (10–40 mg/kg IV diluted in 0.9% saline and administered over 30–60 min, every 6 h) and tranexamic acid (5 g IV every 12 h). Smaller doses may be effective. Yunnan baiyao (Chinese herbal mixture) has been used. Flunixin meglumine (0.5–1.0 mg/kg every 8–12 h) for anti-inflammatory/analgesic activity.

Contraindications!!navigator!!

  • Oxytocin is contraindicated with hematoma of the broad ligament
  • Parenteral iron dextran preparations can cause death

Precautions!!navigator!!

  • Synthetic colloidal products (dextrans, hetastarch) may reduce platelet aggregation and coagulation protein efficacy
  • Acepromazine should be used with extreme caution in hypotensive animals.
  • Hypertonic saline in horses with uncontrolled hemorrhage may increase blood loss

Alternative Drugs!!navigator!!

Stroma-free bovine hemoglobin (30 mL/kg) has been used as an alternative to whole-blood transfusion.

Follow-up

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FOLLOW-UP

Patient Monitoring!!navigator!!

  • Heart rate, pulse quality, and blood pressure should be monitored frequently during the initial 12–24 h
  • Ongoing hemorrhage and bone marrow response can be assessed by determining PCV for 1–3 days after hemorrhage
  • A regenerative response is indicated by increases in PCV; PCV remaining low suggests continuing bleeding

Prevention/Avoidance!!navigator!!

Problematic due to myriad causes of hemorrhage.

Possible Complications!!navigator!!

Blood transfusion should be stopped if an immediate transfusion reaction occurs and appropriate therapy administered.

Expected Course and Prognosis!!navigator!!

  • Prognosis for acute hemorrhage depends on severity, rate, and cause of blood loss
  • Anemia can resolve within 4–12 weeks when hemorrhage is controlled
  • Rupture of major vessels (e.g. aorta, middle uterine artery) has a higher fatality rate

Miscellaneous

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MISCELLANEOUS

Associated Conditions!!navigator!!

N/A

Age-Related Factors!!navigator!!

Severe hypovolemic shock may compromise the fetus, particularly during the last trimester. Follow-up monitoring should include evaluation of fetal viability.

Zoonotic Potential!!navigator!!

N/A

Pregnancy/Fertility/Breeding!!navigator!!

Mares with previous rupture of the broad ligament are at risk of hemorrhage during subsequent pregnancies.

Synonyms!!navigator!!

Severe bleeding; major blood loss.

Abbreviations!!navigator!!

  • EIPH = exercise-induced pulmonary hemorrhage
  • GI = gastrointestinal
  • PCV = packed cell volume
  • RBC = red blood cell
  • TP = total protein
  • US = ultrasonography, ultrasound

Suggested Reading

Mudge MC. Acute hemorrhage and blood transfusions in horses. Vet Clin North Am Equine Pract 2014;30:427436.

Author(s)

Author: Margaret C. Mudge

Consulting Editors: David Hodgson, Harold C. McKenzie, and Jennifer L. Hodgson

Acknowledgment: The author and editors acknowledge the prior contribution of Nicholas Malikides.