28/06/2023
Equine Periparturient Hemorrhage
Brian S. Burks, DVM
Diplomate, ABVP
Board-Certified in Equine Practice
The peripartum period is defined as the time just before, during, or immediately after parturition. Although the vast majority of mares foal without complications, there are certain disease processes that are more common and unique to the peripartum period. One such concern is periparturient hemorrhage (PPH). Important causes of hemorrhage in peripartum mares include arterial rupture, uterine rupture, vaginal varicose veins, cervical lacerations, and other forms of perineal trauma. Rupture of the external iliac artery, utero-ovarian artery, and uterine artery have all been attributed to the onset of PPH.
The reproductive organs are supplied by the ovarian, uterine, and vaginal arteries. Both the external iliac artery and utero-ovarian artery branch directly off the aorta and the uterine artery branches off the external iliac artery. The uterine arteries are in a band of tissue called the broad ligament, which suspends the uterus in the abdominal cavity. The broad ligament fans out from the uterine body, along the horns, and the ovaries in a ‘Y’ shape and is attached to the dorsal body wall.
Reproductive tract hemorrhage associated with pregnancy and parturition is a cause of morbidity and mortality in broodmares. The condition affects about 3% of broodmares and accounts for most mortalities in foaling-related deaths. Although most cases occur in the post-partum period, typically within 48 hours of foaling, some do occur pre-partum. The uterine artery (usually the right or the middle) in the broad ligament can have an aneurysm or rupture. If the hemorrhage is contained within the broad ligament, it is a hematoma. If the blood is not contained there, hemoabdomen results. Rupture of the external iliac artery, utero-ovarian artery, and terminal aorta has also been attributed to the onset of periparturient hemorrhage (PPH).
The exact cause of PPH is not well understood. There are degenerative changes in the affected vessel that may be related to age and parity. Add to that a late-term fetus or uterine contractions and the vessel can be further compromised by blood dissection and eventual rupture. The right uterine artery may be predisposed due to displacement to the left by the cecum, increasing tension in the right broad ligament. Low serum copper may also be a risk factor, as copper is needed to maintain elasticity and integrity of the vascular wall.
There may be direct hemorrhage into the peritoneal cavity, the broad ligament or serosal layer of the uterus. Hemorrhage may also occur into the uterine lumen, because of laceration of an artery within the uterine wall. Mare can have concurrent hemorrhage from more than one site.
Clinical signs of arterial rupture include mucus membrane pallor, prolonged capillary refill time, depression, weakness, elevated heart and respiratory rates, colic, cold extremities, sweating, trembling, and collapse followed by death. Mares may also periodically curl their lip upward (Flehmen response). Colic signs may predominate with pawing, rolling, and restlessness. Some mares may only show peracute death.
The severity and peracute onset of PPH constitutes a true emergency, require rapid response, efficient assessment, and proper therapy. Diagnosis is based upon history and physical examination, transabdominal ultrasonography, abdominocentesis, trans-rectal palpation. Blood can be seen swirling on ultrasound during active hemorrhage. Collection of blood is performed for a complete blood count and serum chemistry every 12-24 hours. Results of these tests direct future therapy.
Treatment of hemorrhagic shock involves maintaining or restoring vascular volume and supporting coagulation with formation of a clot. Tamponade from the tissues of the broad ligament may result in such a clot. Various medications can be given to promote clot formation, but there is little scientific support for such medications. Affected mares can be treated with hypertonic saline and isotonic crystalloid fluid replacement therapy, given with caution as a rapid rise in blood pressure may dislodge the clot, and even intensify hemorrhage. Some patients will require whole blood transfusions. Cross matching is advised, time permitting. Both cross matching and whole blood transfusion are performed in our hospital. Significant resources are required to treat mares with PPH, and treatment should proceed in the hospital setting.
The foal should be separated from the mare, confined where the mare can still see the foal, to prevent injury; however, some mares may become even more distressed, intensifying hemorrhage.
Mares may require pain control and/or sedation to facilitate examination. Acepromazine is contraindicated, as it can exacerbate hemorrhage.
Horses can sustain acute blood loss of up to 1/3 of blood volume before requiring blood transfusion. This is approximately 11 liters in the average sized horse. During early hemorrhage, true blood loss is not reflected in the hematocrit, but when the mare receives fluids, the red blood cells in circulation become diluted. In a normal mare the hematocrit should test at 45-50%. In hemorrhaging mares, the number often falls to 15-20%. Whole blood is required when the hematocrit fall to or below 15%. Fresh frozen plasma contains clotting factors which can help clot formation as the affected vascular site. Fox Run Equine Center maintains a store of fresh frozen plasma.
Pain control is also important, as this will decrease heart rate and blood pressure. A variety of pain medication can be used. There are medications to help stabilize clot formation, but their efficacy is uncertain.
Many will resolve with conservative treatment; however, in some cases, as a life-saving measure, the artery may need to be ligated directly. This requires surgery on a large artery, with a difficult surgical approach due to the size of the horse, and which requires reaching deep into the abdomen.
Broad spectrum antibiotics should be administered to prevent secondary complications, such as abscessation of a broad ligament hematoma or peritonitis. In some instances, supplemental oxygen is provided via nasal insufflation tube at 8-10 L/min. The environment around the stall should also be kept as quiet as possible to minimize stress and activity which would raise blood pressure and dislodge the thrombus.
Differential diagnoses include post-foaling colic associated with passage of fetal membranes and uterine contraction (usually short-lived) gastrointestinal causes of colic, particularly colon displacement or torsion, traumatic uterine rupture during foaling, incipient uterine prolapse, and uterine horn intussusception.
The prognosis is guarded, although early recognition often improves outcomes. Hemorrhage into the peritoneal cavity carries the worst prognosis, and into the uterus the best prognosis, as they do not suffer from profound hypovolemia. Younger mares are more likely to survive. Further hemorrhage can occur in the first few days, which may be fatal. Depending on the degree and duration of hypovolemia, there may be reperfusion injury to multiple organs, resulting in secondary complications such as renal failure or laminitis, which could require intensive and prolonged treatment. Excitement or movement of the mare may cause clot disruption, followed by uncontrolled fatal hemorrhage into the abdominal cavity. Mares can remain in critical condition for days to weeks.
Fox Run Equine Center
www.foxrunequine.com
(724) 727-3481
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