Uterine atony

Uterine atony
Specialty	Obstetrics and gynaecology

Uterine atony is a loss of tone in the uterine musculature. Normally, contraction of the uterine muscles during labor compresses the blood vessels and reduces flow, thereby increasing the likelihood of coagulation and preventing hemorrhage. A lack of uterine muscle contraction, however, can lead to an acute hemorrhage, as the uterine blood vessels are not sufficiently compressed. Clinically, 75-80% of postpartum hemorrhages are due to uterine atony.

Risk factors

Many factors can contribute to the loss of uterine muscle tone, including:

- overdistention of the uterus
- multiple gestations
- polyhydramnios
- fetal macrosomia
- prolonged labor
- oxytocin augmentation of labor
- grand multiparity (having given birth 5 or more times)
- precipitous labor (labor lasting less than 3 hours)
- magnesium sulfate treatment of preeclampsia
- chorioamnionitis
- halogenated anesthetics
- uterine leiomyomata

- full bladder

- retained colyledon, placental fragments

- placenta previa

- placental abruption

- constriction ring

- incomplete separation of the placenta

Treatment

The first step in management of uterine atony is uterine massage. The next step is pharmacological therapies, the first of which is oxytocin, used because it initiates rhythmic contractions of the uterus, compressing the spiral arteries which should reduce bleeding. The next step in the pharmacological management is the use of methylergometrine, which is an ergot derivative, much like that use in the abortive treatment of migraines. Its side effect of hypertension means its use should not be used in those with hypertension or pre-eclampsia. In those with hypertension, the use of prostaglandin F_2α is indicated (but beware of its use in patients with asthma). Another option Carbetocin and Carboprost where Oxytocin and ergometrin is inappropriate.

References

• Hacker, Neville, J. G. Moore, and Joseph Gambone. Essentials of Obstetrics and Gynecology. 4th ed. Vol. 1. Philadelphia: Elsevier Inc., 2004. 151.