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How I Evaluate the Peri-Partum Mare with Colic: Special Considerations
T. Mair
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Take Home Message
Many mares show signs of abdominal pain at some stage during gestation or around the time of parturition. The most serious causes of colic during the peri-partum period (excluding colic associated with stage III labour) include rupture of the uterine, utero-ovarian or external iliac arteries, damage to the small colon and its mesentery, perineal injuries, large colon displacements and torsion, uterine rupture and inversion of the uterine horn. Consideration must be given to all these possibilities during the examination.
Introduction
Colic in the broodmare presents both diagnostic and treatment challenges. In the pregnant mare, we are faced with not only one but potentially two patients simultaneously, and the best course of treatment for one may not necessarily be what is best for the other. The goals of treating the pregnant mare with colic are to identify and correct whatever abnormality is present as soon as possible, and to support placental function to maintain fetal viability throughout the remaining period of gestation. The goal for the foal is to keep the maternal environment optimal to maintain the pregnancy so it may be born with a reasonable chance of survival outside of the uterus
Although many different causes of colic can be encountered in the peri-parturient mare, there are certain specific diseases that are more commonly encountered at this time. This review will focus on some of these conditions.
Arterial Rupture
Rupture of the middle uterine, utero-ovarian, or the external ileac arteries at or around the time of foaling is a significant cause of colic and death in older (>11 years) foaling mares. Rupture of the middle uterine artery or utero-ovarian artery may result in the formation of a large, painful haematoma in the ipsilateral broad ligament that may dissect below the serosal uterine surface if the hemorrhage is contained within these structures. Pain results from the stretching of, and pulling on, these structures as the hematoma forms. If the broad ligament or serosa subsequently rupture and the haemorrhage is no longer contained, then the mare will rapidly bleed out into her abdominal cavity. Rupture of the external ileac artery, due to its anatomic location, results in the mare directly and fatally bleeding into her abdomen. Fatal bleeds are most common in aged mares (>18 years), and unfortunately the first occurrence of this disorder may be fatal.
The right middle uterine artery has been reported to be the most frequently affected of the susceptible vessels. There may be increased stress placed on this artery as a result of stretching
of the right broad ligament due to pressure from a full cecum. Uterine artery rupture may also occur secondary to uterine torsion. Findings of aneurisms and intimal fibrosis in affected middle uterine and utero-ovarian arteries on post mortem examination have been reported, and support the theory that age related vascular changes predispose older mares to arterial ruptures
Mares with uterine artery rupture demonstrate signs of colic, sweating, tachycardia, tachypnea, pale mucous membranes, thready pulse, cool extremities, depression, weakness and collapse. Initially, affected mares demonstrating signs of colic may be mistaken for mares sensitive to “after cramps”, but the signs of persistent pain and deterioration in the mares’ cardiovascular status and mucous membrane appearance readily distinguish them. Affected mares may also have swelling and edema in their vulva and perineal region more than that typically observed in a normal post foaling mare.
During the early course of a hemorrhage, the PCV usually remains normal. After 8-24 hours post acute hemorrhage, retention of sodium and water by the kidneys in an effort to correct hypovolemia result in a decrease in the PCV that will more accurately reflect the mare’s actual circulating red blood cell mass. Therefore, it is best to monitor affected mares with serial PCV measurements in order to accurately assess the actual degree of the mare’s anemia.
Mares whose hematomas rupture or who directly bleed into their abdomen from the start demonstrate rapid signs of shock and death. Mares whose bleeds are initially contained within the broad ligament may still die if the blood loss has been severe enough, or if the clot is disturbed and subsequently ruptures during the recovery phase (up to 2 weeks later).
Rectal palpation and ultrasound identifies a painful swelling of the haematoma within the broad ligament and over the uterus. Direct blood loss into the abdomen may be identified via transabdominal ultrasound. Free blood in the abdomen appears as a hypoechoic fluid with swirling echogenicity. Abdominocentesis will confirm these findings; abdominal fluid with a PCV >5% and a total protein > or = 3.5 g/dl supports a finding of frank haemorrhage into the abdomen.
Treatment of mares with extensive or uncontained uterine artery rupture is often unsuccessful. Attempts at surgical ligation are typically unsuccessful due to poor surgical access and the difficulty in finding the damaged arterial site within the volume of the haematoma. Also affected mares are very poor anaesthetic risks due to their poor cardiovascular status.
There are two approaches to managing affected mares that survive the initial stages of the hemorrhage – one conservative, the other more aggressive. Regardless of which therapeutic option is chosen, the mare must be kept as quiet as possible so as to minimize excessive increases in her arterial pressure. The conservative approach to treatment involves minimizing stress or excitement of the affected mare. The mare is kept in a quiet, darkened stall with or without her foal (depending on which is least stressful to the mare). Transportation of the mare is generally contraindicated. Tranquilizers are used judiciously as needed to help keep the mare calm, and, in the case of acepromazine, to help reduce arterial pressure directly. Naloxone (8-32mg/500 kg iv) has been anecdotally reported to be helpful in some mares. Aminocaproic acid (Amicar) (20 g in intravenous fluids as loading dose, followed by 10 g every 6 hours) has also been recommended; this drug acts by inhibiting fibrinolysis. Analgesics (butorphanol .01-.04 mg/kg IM) are also used as needed to control the mare’s pain. Attempts at volume re-expansion with fluids or whole blood transfusions are indicated to preserve cardiac output and perfusion, but may increase arterial pressure and disturb haemostasis. [...]
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