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Umbilical Cord Torsion (in Horses)
Disease conditions involving the fetal membranes (placenta) are a major
cause of fetal loss and neonatal illness and include umbilical cord
torsion. The umbilical cord is the fetal structure through which blood
flows from the fetus to the placenta for oxygen and nutrient exchange.
The cord also contains the urachus that transports fetal urine from the
bladder to the allantoic sac.
Umbilical cord torsion refers to occlusion of the structures in the cord
as a result of either excessive twisting of the cord or strangulation
due to wrapping of the cord around the fetus. This occlusion can result
in death of the fetus, or, if only urachal obstruction occurs, the
bladder may not seal properly following birth resulting in a pervious
urachus.
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Care must be taken in evaluating the expelled placenta, as twisting
alone is not sufficient for a diagnosis. Twisting of the umbilical cord
indicates normal fetal mobility. Studies have shown that 78% of cords
have twists with an average of 4.4 twists per cord. (Ginther 1992.
Reproductive biology of the mare. 2nd ed. Equiservices, Cross Plains,
Wisconsin). Twists were detected as early as 68 days of gestation and
the amount of normal twisting remained constant each month of gestation.
Small fluid-filled swellings, representing urachal dilatations caused by
mild obstruction of the urachus at a twist, can also be present in the
wall of the umbilical cord of normal foals.
To be considered pathologic, twisting has to be excessive with occlusion
of the vessels. This is evidenced by constriction of the umbilical
vessels at sites of torsion, tearing of the intima of the vessels,
hemorrhage into the wall of the cord, aneurysms and thrombosis of the
vessels, and kinking of the cord following manual unwinding. (Whitwell
1975. Morphology and pathology of the equine umbilical cord. J. Reprod.
Fert. Suppl. 23:599-603)
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The fetus is usually autolyzed since death of the fetus precedes
abortion, and abnormalities of the urinary bladder may be present.
Microscopic examination typically reveals mineral deposits in the blood
vessels of the placenta.
Most abortions due to umbilical cord torsion occur in months 6-8 of
gestation (Whitwell 1975). High fetal mobility in months 4-7 of
gestation provides the greatest opportunity for torsion, with mobility
diminishing greatly after 7 months (Ginther 1992).
The only identified risk factor for umbilical cord torsion is excessive
length of the cord. Ninety-five percent of umbilical cords from normal
Thoroughbred foalings measured between 36 and 83 cm in length with a
mean of 55 cm, while cords from cases of torsion averaged greater than
85 cm in length (Whitwell 1975, Whitwell and Jeffcott. 1975.
Morphological studies on the fetal membranes of the normal singleton
foal at term. Res. Vet. Sci. 19:44-55).
The University of Kentucky Livestock Disease Diagnostic Center diagnosed
168 cases of umbilical cord torsion over a 5-year period (Figure 4),
representing 6% of equine fetus accessions during that period. The
majority was in Thoroughbreds with five other breeds represented. The
gestational age of the fetuses ranged from 5-10 months with a mean of
7.5 months (Figure 5).
The umbilical cord lengths varied from 62 to 125 cm with an average of
96 cm. The cords typically were highly twisted with areas of
constriction, edema, hemorrhage, and fluid-filled sacculations. The
fetuses were slightly to moderately autolyzed, indicating death of the
fetus prior to expulsion. No other changes were seen except for dilation
of the urinary bladder in some cases. The principal microscopic change
was deposition of calcified material in the blood vessels of the
allantochorion.
Methods to prevent umbilical cord torsion are not known, and factors
causing excessive cord length have not been identified. Torsion is
sporadic with no apparent increased risk for future problems in mares
that loose a foal due to this condition.
CONTACT:
Neil M. Williams, (859) 253-0571, nmwillia@uky.edu
Livestock Disease Diagnostic Center, University of Kentucky, Lexington,
Kentucky
Article appeared in the Equine Disease Quarterly -
University of Kentucky, College of Agriculture, Department of
Veterinary Science: April 2002 Issue; Volume 10, Number 3
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