A Case of Vaginal Tearing and Peritonitis in a Pony Mare
Caitlin Hokanson
Dr. Gillian Perkins
Dr. Robert Gilbert
Senior Seminar paper
Cornell University College of Veterinary Medicine
March 5, 2014
Key words: Vaginal Tear, Peritonitis, Laminitis, Equine Metabolic Syndrome
Signalment and Case History:
A fifteen-year old maiden Welsh Pony mare presented to Cornell’s Equine
Hospital on 6/18/2013 following a three-day history of intermittent colic, lethargy, and
fever after an unplanned mating with a horse-sized stallion. On the morning of 6/15/13
the owner visualized copulation followed by frank blood from and distension of the
vulva. Following the breeding the mare was observed to be lethargic and show bouts of
colic like activity including pawing, flank watching, and increased frequency of lying
down. She had decreased appetite and passage of manure. On the morning of 6/18/13
the referring veterinarian arrived at the farm to do a complete colic work up but following
the history and physical exam findings of fever she administered a dose of non-steroidal
anti-inflammatories (flunixin meglumine) and referred the pony. Historical problems
included chronic laminitis that was being conservatively managed at home and suspect
equine metabolic syndrome (EMS).
Presentation and Diagnostics:
On presentation she was quiet, alert, and responsive. She was over-conditioned
with a weight of 261 kg and a body condition score of 8/9, ideal being 4.5/9. She was
moderately tachycardic (52 beats per minute) however she was eupneic (18 breaths per
minute) and normothermic (100.7F). Mucus membranes were pink but tacky with a
capillary refill time of less than two seconds. She was estimated at 5% dehydration.
Normal borborygmi were auscultated in all 4 gastrointestinal quadrants and digital pulses
were within normal limits. The rest of the physical examination was unremarkable.
Pertinent hemogram abnormalities on entering assessment included a mild anemia
[hematocrit 32% (34-44)], decreased hemoglobin 11.3 g/dL (11.8-15.9) and decreased
red blood cell count 5.5 mill/uL (6.6-9.77). Additionally there was a mild neutropenia
present [5.0thou/uL neutrophils (5.2-10.1)]. Fibrinogen was at the upper end of the
reference range at 200mg/dL (0-200), indicative of the start of an inflammatory response.
The neutropenia was likely due to a septic consumptive processes associated with the
physical examination findings of vaginal and peritoneal tearing discussed below. The
fibrinogen levels at the cusp of elevation support this interpretation. Decreased
hematocrit is consistent with recent low-grade hemorrhage.
Abnormalities on serum blood chemistry included a moderate hyperglycemia
185mg/dL (71-113) and a decreased albumin:globulin ratio 0.7 (0.8-1.4) that was
contributed to the concurrent mild hypoalbuminemia 2.9 g/dL (3-3.7). There were
slightly elevated triglycerides 88mg/dL (14-77) and an elevated indirect bilirubin
2.4mg/dL (0.3-2.3). Additionally there were mild electrolyte abnormalities attributed to
historical anorexia and decreased intake.
Hypoalbuminemia and the decreased albumin:globulin ratio can be explained by
protein loss into the peritoneal cavity secondary to peritonitis. Elevated triglycerides can
be attributed to both her physical findings suggestive of EMS coupled with her recent
period of anorexia spanning several days. Elevated indirect bilirubin is frequently seen
within 12 hours of the onset of anorexia in the horse.
A trans-abdominal ultrasound was performed and all abdominal viscera appeared
to be of normal size and echogenicity. The organs were in the correct anatomical
positions with appropriate motility and wall thickness. No gas was observed within the
abdomen however there was a trace amount of free fluid visualized along the ventrum.
On trans-rectal palpation the uterus and cervix were found to be soft, consistent
with estrus. Ultrasonography revealed a uterus free of fluid and lacking edema in the
walls. A corpus luteum, indicating recent ovulation was visible on the left ovary. Its
presence was important to the owner who was concerned about possible fertilization and
an embryo. A large fluid filled mass was visualized beneath the uterine body cranial to
the bladder, presumed to be a hematoma.
A vaginal speculum examination was performed and the entrance to the urethra
was visualized and found to be intact and without obvious trauma. The vestibulovaginal
sphincter was tight, closed, and intact. When the vaginal speculum was passed through
the sphincter, a large amount of malodorous reddish-brown fluid was passed. A large
tear in the vaginal wall to the left of the cervix running in a dorsal to ventral fashion was
visualized. A sterile glove was then passed through the tear in the vaginal wall and into
the abdominal cavity where viscera was palpable immediately adjacent to the tear
indicating that peritoneum, in addition to vaginal wall had been torn by the stallion’s
penis.
In light of the above findings abdominocentesis was indicated to collect a sample
of the peritoneal fluid for cytology, analysis, gram stain and culture. Using
ultrasonographic guidance a small pocket of free fluid was located in the abdomen along
the ventral midline just caudal to the xiphoid. Gross analysis of the peritoneal fluid
showed opaque fluid medium yellow in color. The nucleated cell count was 451,200 /uL
(<10,000), total red cell count of the fluid was 52,300/uL, and the total protein of the
peritoneal fluid was 6.3 g/dL (<2.5). Microscopic examination of the fluid showed high
cellularity composed of a population of over 90% non-degenerate neutrophils, a few
macrophages, and occasional small lymphocytes. Neither spermatozoa nor bacteria were
identified on fluid evaluation. The peritoneal fluid evaluation revealed a supportive
inflammation.
Management:
The primary problem to be addressed was the vaginal tear followed by the
associated peritonitis. In addition, sequela of the peritonitis including laminitis and intraabdominal adhesions needed to be prevented and historical conditions such as EMS also
needed attention during hospitalization.
Conservative medical management, or second intention healing, was the elected
treatment of choice for the vaginal tear. The vagina is a very elastic structure capable of
rapid healing if motion and pressure within the abdominal cavity are kept minimized.
The mare was tied using a suspension line from the ceiling of the stall to the poll portion
of the halter. This would prevent her from lying down for 10-14 days. Standing from
sternal or laterally recumbent position would allow both an increase in abdominal
pressure coupled with gravity’s effects leading to herniation of the bowel.
The mare was administered broad-spectrum anti-microbial therapy as a precaution
due to the traumatic nature of her injury and suspect bacterial contamination of the
peritoneum. Intravenous enrofloxacin is a concentration dependent fluoroquinolone
antibiotic with bactericidal activity against both gram negative and positive bacteria.
Intravenous potassium penicillin is a cidal time-dependent beta lactam antibiotic that
targets gram-positive organisms. Finally, oral metronidazole was administered for
anaerobic coverage. Due to the large number of antibiotics being administered,
Saccharomyces cerevisiae in addition to yogurt were given orally to prevent secondary
colitis due to disruption of the microflora.
Acute laminitis secondary to peritonitis and systemic inflammation was a concern
in this mare. Consequently prophylactic laminitis treatments were used. Pentoxifylline,
a methylxanthine derivative with properties thought to improve digital blood flow and
decrease inflammatory cytokine production was given orally. In addition, low-dose
flunixin meglumine was administered intravenously. These two drugs are more effective
at preventing acute laminitis when administered together.1 Ice boots were placed on all
four limbs spanning from below the coronary band to above the carpus and tarsus. These
boots were kept constantly full for an entire 5 days.
During hospitalization lateral radiographs were taken of all four feet and showed
evidence of chronic disease but nothing to suggest acute overt rotation. There were small
amounts of new bone deposition the distal aspect of the third phalanx known as “ski
tipping”, on all four digits. In addition there was slight rotation of the third phalanx in all
four digits. These changes are both consistent with the history of chronic disease.
Intravenous heparin was administered intravenously for three days in an effort to
prevent the formation of intra-abdominal adhesions between the viscera within her
abdominal cavity. 6 With systemic inflammation secondary to peritonitis there is an
increased production of systemic fibrin within the vasculature. Fibrin then is able to
cross the endothelium and infiltrate the abdominal cavity setting up fibrinous, and then
fibrous adhesions between organs.
Serial physical examinations, blood chemistries, hemograms, and peritoneal fluid
analyses were drawn to monitor the mare’s response to therapy, her degree of systemic
inflammation, and trends in the systemic and peritoneal fluid cell counts. On 6/19/14
pertinent hemogram abnormalities included a leukopenia 4.2thou/uL (5.2-10.1),
characterized by a neutropenia 2.3thou/uL (2.7-6.6), a left shift 0.1 thou/uL (0), and
hyperfibrinogenemia 500mg/dL (0-200). The mare had an ongoing severe inflammatory
response with consumption of neutrophils in the abdominal cavity.
On 6/20/14 there was a continuation of the left shift 0.3 thou/uL (0), a
hyperproteinemia 8 g/dL (5.2-7.8), and hyperfibrinogenemia 400 mg/dL (0-200). The
body continued to release band neutrophils prematurely in an effort to combat the
consumptive process within the peritoneal cavity and reduce abdominal contamination.
Total protein and fibrinogen were elevated in response to inflammation and likely the
production of large amounts of globulins six days out from the initial insult. Blood
chemistry from 6/20/13 showed mild electrolyte abnormalities in addition to elevated
globulins 4.5g/dL (2.4-4.4), a decreased A/G Ratio of 0.7 (0.8-1.4).
On 6/22/13 the hemogram revealed a lymphopenia 1.1 thou/uL (1.2-4.9) and
hyperfibrinogenemia 500 mg/dL (0-200). The continued lymphopenia was secondary to
consumption of white cells within the peritoneal cavity and the elevated fibrinogen levels
were a result of systemic inflammation.
The hemogram from 6/24/13 was the final one prior to discharge. At that time all
leukogram abnormalities had resolved. Hyperproteinemia 8.2g/dL (RR 5.2-7.8 g/dL) and
a hyperfibrinogenemia 600 mg/dL (RR 0-200 mg/dL) were still present, both consistent
with a chronic inflammatory process.
Peritoneal fluid analysis done that same day was much improved. The fluid was a
medium yellow and opaque with a total protein of 3.2 g/dL and a nucleated cell count of
12.2 (thou/uL). The fluid contained a mixture of inflammatory cells dominated by nondegenerate neutrophils (75%) and containing fewer macrophages (16%) demonstrating
prominent leukophagia, and a low number of lymphocytes (9%). Some of the
lymphocytes were reactive or in granular forms. There were also low numbers of
erythrocytes. No infectious agents were seen at the time of this sample and the
interpretation of the smear was peritonitis.
Prior to discharge, an endoscopic examination of the vagina was performed to
observe the healing of the vaginal tear. The area of the urethra was normal. The
endoscope was then advanced through the vestibulo-vaginal sphincter into the vagina.
The region of the tear was still visible to the left of the cervix. There was only a slight
amount of brownish-red fluid pooling at the base of the vaginal vault. Large deposits of a
fibrin like material were seen over the vaginal wall where the tear was and there was
remodeling evident along the torn edges. Due to the rapid healing of the vagina it was
determined that the mare could be released from her tie rope without fear of bowel
herniation.
The mare had a good appetite and attitude, the vaginal tear was healing, and the
peritonitis was resolving and she no longer required critical care. The mare was
discharged with instructions to treat with oral antimicrobials and to closely monitor for
signs of laminitis and colic. Chloramphenicol was chosen as the antibiotic of choice due
to its broad-spectrum coverage, its ability to penetrate tissues and thick walled abscesses,
and finally due to its ease of administration.
Unfortunately the mare returned to the Equine Hospital two days following
discharge for presumptive acute laminitis. She was immediately placed in soft ride boots
in a sand stall and cryotherapy administered (ice boots). She had a mild episode of
impaction colic that same day and was managed conservatively with intravenous fluids
and nasogastric administration of water, electrolytes, and mineral oil rotated every four
hours. Blood submitted for ACTH levels and found to be within normal limits ruling out
Cushing’s disease as the cause of the observed metabolic signs. Following resolution of
impaction and suspect acute laminitis the patient was again discharged without further
complication.
DISCUSSION:
Vaginal tears in mares are most commonly associated with aggressive breeding
by stallions but may also happen during dystocia. They are thought to be under
diagnosed complications as they can be easily missed without evidence of external
hemorrhage following copulation. When evident they most frequently involve the cranial
dorsal portion of the vagina near the cervix and usually are less than 5 centimeters in
length. If the laceration is minor and left to heal on its own it will do so rapidly and be
virtually undetectable by the start of the next estrus cycle. More severe tears however
may need to be closed surgically as evisceration of bowel or urinary bladder through the
tear is possible. 3
It is a very rare finding, but in mares with a traumatic breeding peritonitis
macrophages with phagocytized spermatozoa may be found in the peritoneal fluid. This
is concrete evidence of ejaculation within the peritoneal cavity. This is an important
finding as the ejaculatory contents are extremely irritating and will initiate
chemical/irritant peritonitis. Normal semen is not sterile containing up to 5.1x 109
bacteria/liter. In addition to the pathogens within the semen, other components of the
semen including prostaglandins, proteins, a variety of enzymes, lipids, and acids are all
extremely irritating and can play a large role in the degree of peritonitis observed. 3
Although conservative medical management was elected for this mare, surgical
management of the vaginal tear was an option as well. With the widespread
inflammation within the abdomen and the herniated loops of bowel, an exploratory
celiotomy and peritoneal lavage was appropriate. Peritoneal lavage would have allowed
for the removal of a majority of the inflammatory contents from the peritoneum in
addition to whatever bacteria might have been present though uncultured. Additionally
the celiotomy would have offered the opportunity to explore the herniated loops of bowel
and ensure that there was no damage and allowed for possible closure of the peritoneum.3
Primary closure of the peritoneal and vaginal tears was not ideal in this instance as the
loops of bowel were adjacent to the tear and the risk of perforation of the bowel with the
needle for closure was too considered too high.
Case reports in the literature of similarly identified vaginal and peritoneal tears
indicated a predisposition for loops of bowel to leave the abdominal cavity by way of the
vaginal tear leading to evisceration and death.3 This effect is seen most frequently as the
horses stand up following resting in sternal or lateral decumbency due to the combined
effects of gravity and abdominal push leading to increased abdominal pressure. As a
preventative measure, the mare was tied at all times in her stall using a suspension rope to
prevent her from lying down. It was recommended this therapy be continued for 17-14
days to allow mending of the vaginal wall.3
Peritonitis is the inflammation of the mesothelium lining the peritoneal cavity. It
can be caused by a variety of different insults including chemical damage, mechanical
trauma, or infectious agents. 8 The most common clinical manifestation is acute diffuse
septic peritonitis usually related to gastrointestinal disease and ruptured bowel.
Traumatic events such as vaginal tearing during breeding or foaling are fairly uncommon
causes of septic peritonitis. Clinical signs frequently associated with peritonitis can vary
and may include fever, depression, diarrhea, and abdominal pain leading to signs
consistent with colic. 8
Definitive diagnosis of peritonitis is based on analysis of free peritoneal fluid.
Elevated total nucleated cell count (greater than 10,000/uL) is confirmation of diagnosis.
Concern over a septic cause of peritonitis warrants culture. However, a negative culture
of a peritoneal sample does not rule out infectious organisms, as there is currently low
sensitivity with culture and only 9.5-32.5% of samples culture positive. 8 Consequently
broad-spectrum antibiotic therapy was initiated, as we could not definitively rule out a
septic component. If unable to culture an organism but history lends toward suspicion of
septic peritonitis additional parameters must be evaluated including clinical signs,
amount of fluid within the abdomen, and cytological and chemical analysis of the fluid.
In this case, broad-spectrum antibiotics were begun before culture results were available
because of the known environmental contamination of the abdominal cavity. 8
Peritonitis is by itself a deadly disease and the secondary complications associated
with it can be devastating. One of these complications is acute laminitis that is defined as
a compromise of the suspensory apparatus of the third phalanx within the hoof capsule. It
is a disease process associated with constant pain and lameness.
The suspensory apparatus of the third phalanx is composed of a connective tissue
called lamellae (both sensitive and insensitive) that act by increasing surface area and
consequently increasing the degree of attachment to the surface of the distal phalanx. As
the attachment between the corium of the bone and the epidermal lamellae becomes
compromised, the epidermal lamella releases its hold on the outer surface of the distal
phalanx. This allows the third phalanx to sink towards the ground due to the constant
weight of the horse pressing down on the bone and rotate because of the tension on the
deep digital flexor tendon. 7
As a disease process, laminitis can be acute or chronic. A number of triggers for
the disease have been identified including endotoxemia and inflammation,
hyperinsulinemia, EMS, bacterial factors, Cushing’s disease, exogenous steroids, black
walnut residue, and carbohydrate overload. In the current case, prevention of an episode
of acute laminitis was at the forefront of the mare’s therapy. This mare had a history of
chronic laminitis, likely linked to EMS. At the time of presentation acute laminitis was
the primary concern following massive, widespread inflammation and the possible septic
process suspected within the abdomen. 7
The connection between the processes of inflammation and laminitis in the horse
is clear. However, the actual mechanism in which inflammation actually causes acute
laminitis is not yet clear to the veterinary community. There are a number of current
hypotheses of how a horse undergoing a systemic inflammatory develops laminitis. The
current most widely accepted theory is that inflammatory cells and the cytokines they
produce play an important role in the failure of the laminar dermal–epidermal interface.
Most studies involving the prodromal phases of laminitis are performed using
either carbohydrate overload or exposure to concentrated black walnut and they have
found that there is a 30-40 hour period prior to the onset clinical signs where the lamina
begin to be damaged. Carbohydrate overload is the most successful and reliable method
of laminitis induction. The large amount of fermentable carbohydrates in the hindgut
alters the wall of the cecum allowing it to become leaky. Once the wall is damaged it
allows for passage of endotoxin and other bacterial components from gut lumen to
bloodstream. 7 The prodromal phase then merges into acute laminitis with the onset of
obvious foot pain and clinical signs. As the disease processes continues on, the hoof wall
and the distal phalanx lose their parallel orientation and the distal phalanx become more
and more detached. By the time that foot pain or other clinical signs are observed,
lamellar pathology has already begun and the acute phase has started. 7
The onset mechanism with the most widespread support amongst the veterinary
community currently involves altered lamellar blood flow. It is hypothesized that during
the prodromal stage of laminitis altered blood flow leads to ischemia and consequently
necrosis of the lamellar tissues. Despite the support for alteration in lamellar blood flow
as the mechanism of disease, literature is not currently united as to whether it is
vasodilation or vasoconstriction or vascular shunting that causes the disease. Both of
these processes have been observed in prodromal and acute clinical laminitis. 7
Vasodilation may allow for increased exposure to toxic agents in addition to self
produced inflammatory mediators. The inflammatory mediators are produced by
increased numbers of white blood cells and include chemokines and cytokines.
Interleukin-1b (IL-1b) is a cytokine produced by leukocytes during inflammation that has
been found to be elevated in the laminar tissue during disease development. IL-1b is
involved in the production of pro-coagulant, pro-inflammatory, and vasoactive mediators
in addition to matrix metalloproteinase. IL-1b is also involved in the production of IL-6,
another cytokine involved in the production of cyclooxygenase 2 (COX2) a major
inflammatory enzyme. 9 Uncontrolled matrix metalloproteinase production coupled with
COX2 production from the inflammatory cascade leads to damage of the basement
membrane zone and initiates lamellar detachment.
The mare discussed had a predisposing condition for developing acute laminitis
with EMS, a syndrome composed of obesity, insulin resistance, and chronic laminitis. 2
She had been contending with laminitis for several years making acute recrudescence
with peritonitis more likely. Horses suffering from EMS have a fairly typical phenotype
consisting of either regional or generalized adiposity. Regionalized adiposity involves fat
deposits along the nuchal ligament, the tail head, behind the shoulder, and within the
mammary gland or prepuce. These horses are frequently insulin resistant with an
abnormal glycemic response when challenged orally with glucose. Additional
biochemical findings in these horses include hypertriglyceridemia, elevated leptin levels,
arterial hypertension, and altered reproductive cycles in mares. 2
Diagnosis of EMS is made primarily from the history (previous bouts of laminitis,
being an “easy keeper”), physical exam findings of obesity, foot radiographs to identify
chronic laminitis, and laboratory tests looking at glucose and insulin levels in the blood.
Welsh, Dartmoor, and Shetland ponies, in addition to Morgans, Paso Finos, Arabians,
and Saddlebreds that are within 5-15 years of age are the most commonly afflicted
demographic. They frequently present for seasonal laminitis and must be differentiated
from horses with Cushing’s disease that may present with similar clinical signs. 2
Laminitis associated with EMS is considered an endocrinopathic laminitis, with
obesity and insulin resistance being the two most common endocrinopathic
predispositions. EMS laminitis is a chronic form of laminitis. Onset is hypothesized to
include glucose dysregulation and inflammation. Glucose dysregulation in insulin
resistant horses leads to a vascular endotheliopathy allowing for vasoconstriction and
thrombosis in conjunction with elevated insulin levels that also promote vasoconstriction.
Also, the state of obesity is a constant inflammatory state as inflammatory signals are
produced at high levels by adipose tissue. 4
Laminitis secondary to this disease process is best managed by controlling the
overall syndrome. Dietary management is a mainstay of therapy having these horses
avoid lush pastures and large amounts of fermentable carbohydrates and easily digestible
energy. Grazing muzzles should be employed if pasture is unavoidable and a weight loss
plan to lower adiposity and hopefully systemic inflammation should be employed.
Physical activity is essential to aid in weight loss so long as the horse’s feet are up to
activity and not undergoing a severe laminitis episode. Additionally, thyroid
supplementation is a possibility to help speed the weight loss process. 2
Conclusion:
Vaginal tearing and peritonitis is a rare condition seen in mares following
aggressive breeding by a stallion. In the case of this mare, the known historic diseases
coupled with the vaginal tear and its sequella made for a challenging case management.
All therapies employed were designed to minimize disease and prevent further from
occurring allowing for a successful discharge with a good prognosis for health and future
breeding soundness.
References:
1.
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in equine medicine. St. Louis, Mo: Saunders Elsevier, 2009; 30-45.
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