Uterine atony, the inability of uterine myometrium to contract following delivery, remains the primary cause of postpartum hemorrhage (PPH).
Severe bleeding due to uterine atony increases potential risk of development of circulatory collapse. Therefore, assessment of patient's signs and symptoms along with physical examination is highly important . Physical examination of the patient's abdomen reveals distended and grossly palpable uterus, which is suggestive of uterine atony. If the urinary bladder is overdistended and palpable, it may indicate hindered uterine contraction and retraction. The bimanual examination of the uterus reveals uterine atony with enlargement and large amount of accumulated blood inside the organ.
Bleeding after other surgeries, or bleeding problems in other family members, or easy bruising, etc are more concerning and should be reported to your plastic surgeon and PCP. Best regards, -Erik Hoy, M.D. [realself.com]
Classically, the clinical manifestations include epistaxis, menorrhagia, easy bruising, recurrent anaemia and obstetric or surgical bleeding. [casesjournal.biomedcentral.com]
The bleeding that ensues uterine atony and resultant postpartum hemorrhage can develop an emergency situation if not promptly managed. Therefore, it is highly imperative to control atony instead of sparing time in determining other causes. Uterine atony is diagnosed by assessment of the uterine tone and size during physical examination of the organ. The uterine wall, on examination, reveals a boggy uterus, heavy vaginal bleeding or augmented uterus size which confirms the diagnosis of uterine atony.
Treatment of uterine atony requires initial management of vital signs, uterine massage and administration of uterotonic drugs. Surgical intervention is required when all of the other medical interventions do not respond with a positive outcome .
Maintenance of the patient's vital signs prior to initiating treatment is extremely important as the situation of uterine atony and the following bleeding requires management similar to that of hemorrhagic shock. The patient's airway, breathing and circulation (ABCs) must be assessed by a physical examination and inquiring about signs and symptoms . With intact airway, the patient is capable of speaking easily. If bradypnea is detected, the patient should be provided with supplemental oxygen to normalize breathing. During final assessment of vital signs, smooth blood circulation is assured by evaluation of heart rate, blood pressure and perineal examination of the origin of bleeding.
The primary assessment of physical examination is promptly followed by immediate medical interventions. The patient is given bimanual uterine massage to stimulate uterine contractions by gently compressing fundus with one hand and placing another hand into the lower uterus, pushing against the body of the uterus and extracting any large blood clots or tissues that may impede contractions. The uterine massage typically takes 15-30 minutes and if done properly, hastens bleeding and delivers the placenta. In case the uterus does not contract with gentle massage, vigorous massage should be commenced along with administration of therapeutic oxytocin. The drug can be administered by intravenous, intramuscular or intrauterine route or as a continuous infusion. Typically, oxytocin is administered as a 5 unit intravenous bolus, as 20 units in 1 liter of normal saline (intravenous) or as 10 units (intrauterine). If bleeding persists, the massage is followed by fluid resuscitation with crystalloids.
When the non pharmacological approach fails to facilitate uterine contraction, use of uterotonic drugs is required. Apart from oxytocin, ergot alkaloids (ergonovine and methlyergonovine) in a dose of 0.2 mg administered intramuscularly every 2-4 hours, may also be used to stimulate atonic uterus . The ergotamine class of drugs carry an adverse effect of elevating blood pressure and are contraindicated in hypertension and eclampsia. Carpoprost (15-methyl-prostaglandin) may be used alternatively in cases where ergotamines are contraindicated. The drug is administered in 250 mcg through intramuscular or intrauterine route every 15-90 minutes without exceeding a maximum of eight doses. Another alternative treatment for postpartum hemorrhage in conditions refractory to or not suitable to oxytocin is the use of misoprostol (prostaglandin E1 analogue) .
Persistent bleeding following administration of uterotonic agents necessitates the use of recombinant activated factor VII (synthetic vitamin K dependant protein) and transfusion of blood and blood products. When postpartum hemorrhage fails to manage by the pharmacological interventions, hysterectomy is ultimately required .
The duration of postpartum hemorrhage and the resultant volume of blood loss, presence of comorbidities and availability of adequate resources determine prognosis. Immediate diagnosis, appropriate treatment and continuous monitoring of the patient's condition are of paramount importance in order to achieve positive outcome. Typically, the condition is well controlled with prompt management.
Uterine atony is the primary cause of postpartum hemorrhage. Risk factors that may lead to the development of uterine atony comprise conditions that cause overdistended uterus (multiple gestations, fetal macrosomia, polyhydraminos), extremely fatigued uterus (resulting from prolonged labor, amnionitis, administration of uterine tocolytics) and impeded uterus (obstruction within uterus that may occur due to retention of placenta or fetal parts inside uterus, placenta accreta and excessively distended bladder).
Uterine atony is the major cause of postpartum hemorrhage, the second leading cause of maternal mortality in the world .
During pregnancy, blood flow to the uterus and placenta is increased by volume of 500-800 ml per minute. By the time third the trimester is approached, the maternal blood volume increases up to 50%, which poses a risk of sufficient uterine bleeding if not physiologically controlled. Once the fetus is delivered, the uterus contracts and relaxes which results in the separation of the placenta from the uterine muscles and reduction in blood volume. Separation of placenta is followed by a series of contraction and retraction cycles by the uterine muscles. Failure of uterine myomertrium to contract and retract following expulsion of the fetus results in postpartum hemorrhage. It has been estimated that approximately 80% incidences of postpartum hemorrhage occurring immediately after delivery are due to uterine atony.
Assessment of risk factors, accurate diagnosis of labor and justified use of oxytocin for induction of labor is recommended to prevent uterine atony.
Health care centers, where the patient's delivery is arranged, must be adequately equipped along with availability of pharmacologic uterotonic agents in order to prevent delay in patient management during postpartum hemorrhage. Internationally, measures have been taken to promote positive outcomes and prevent complications during delivery by training midwives and medical attendants on active management of labor   .
Obese women who conceive after 35 years of age are at an increased risk of developing uterine atony. Potential risk factors that are found to be linked to uterine atony comprise multiple pregnancy, polyhydramnios, fetal macrosomia, prolonged or precipitate labor, extended exposure to oxytocin, manual removal of placenta, previous postpartum hemorrhage and antepartum hemorrhage. Irrational use of certain uterine relaxants such as deep anesthesia, magnesium sulfate and intrinsic factors can also result in atonic uterus.
Uterine atony is referred to as a condition of the uterus in which myometrium fails to contract and retract following delivery. Maintenance of tonicity of myometrium is essential to halt bleeding and in the absence of powerful myometrial contractions, the uterus becomes soft and palpable resulting in blood loss from the vagina.
Uterine atony is the leading cause of primary postpartum hemorrhage (PPH), a condition characterized by excessive bleeding from the genital tract with a blood loss of more than 500ml after vaginal delivery or more than 1000ml following cesarean delivery within 24 hours of birth .
Careful monitoring of the patient's condition, admission into a well equipped hospital setting, availability of supplemental oxygen, blood, blood products and uterotonic agents and presence of trained midwifes is paramount in achieving good prognosis with prompt management of uterine atony and the ensuing postpartum hemorrhage. Identification of risk factors that may lead to atonic uterus can help in prophylactic management. Conditions that cause over distension or obstruction of uterus or fatigued uterus carry a risk of developing uterine atony.
Once diagnosed, immediate management of uterine atony is suggested to preserve vital functions as exacerbation of postpartum hemorrhage may lead to circulatory collapse. Assurance of controlled airway, breathing and circulation is followed by treatment and control of myometrial bleeding which requires promotion of uterine contraction. Initial bimanual uterine compression and massage is applied followed by administration of uterotonic agents. It has been recognized that prophylactic administration of oxytocin and its controlled use after delivery lessens the risk for development of postpartum hemorrhage by 40%. To date, oxytocin is recognized as the most effective first-line agent for treating postpartum hemorrhage. Alternative uterotonic drugs that can be used include ergotamines (ergometrine, ergonovine, methylergonovine), which promote tetanic contraction of uterine smooth muscles and prostaglandins (15-methyl prostaglandin F2A), which augment uterine contractility and cause vasoconstriction.
Uterine atony is the condition in which the muscles of the uterus fail to contract after birth and the delivery of placenta. It is the main cause of postpartum hemorrhage (PPH). In postpartum hemorrhage, brisk bleeding from the vaginal tract continues after delivery which can result in considerable loss of blood causing an emergency situation. Uterine atony accounts for 90% of all postpartum hemorrhage cases. It is the second leading cause of maternal death globally.
During normal pregnancy, the blood vessels that supply blood to the placenta are increased. When the placenta separates from the wall of the uterus after the birth of the baby, the blood vessels are severed which results in normal bleeding that ensues labor. The uterus then contracts which results in compression of the blood vessels and the bleeding stops. In uterine atony, the uterine muscles do not contract adequately and the bleeding continues leading to significant loss of blood after birth.
There are several factors that prevent uterine muscles from contracting normally after birth. They include abnormal labor, prolonged labor, multiple births, history of more than five pregnancies, large amount of amniotic fluid during pregnancy and delivery of a large baby. Moreover, improper use of oxytocin during labor can also result in atonic uterus. Other medicines that may cause uterine atony are general anesthetics, magnesium sulfate and instrinsic factors.
Management of uterine atony at the right time is imperative in preventing serious complications. Uterine atony is typically diagnosed by the presence of a boggy uterus during physical examination and heavy vaginal bleeding. It is very important to maintain the patient's vital signs along with providing treatment. Normally, as soon as the patient is diagnosed with uterine atony, the patient's airway, breathing and circulation is sustained and uterine massage is given to promote contraction of the uterine muscles. If uterine atony persists, the massage is followed by administration of medicines that stimulate contraction of uterus. Commonly used medicines for treating uterine atony include oxytocin, ergonovine, methylergonovine and carboprost. In rare cases when the condition is not controlled by uterine massage and medicines, surgery is required.
- Baskett TF. Complications of the third stage of labour. In: Essential Management of Obstetrical Emergencies. 3rd ed. Bristol, England: Clinical Press; 1999:196-201.
- Minino AM, Heron MP, Murphy SL, et al. National Vital Statistic Reports: Deaths 2004. US Department of Health and Human Services and the Center for Disease Control and Prevention. http://www.cdc.gov/nchs/data/nvsr/nvsr55/nvsr55_19.pdf. Published August 21, 2007.
- Tintinalli JE, Kelen GD, Stapczynski JS. Gynecology and Obstetrics: Post Partum Hemorrhage. In: A Comprehensive Study Guide. 6th ed. New York, NY: McGraw Hill; 2004:682.
- Soriano D, Dulitzki M, Schiff E, Barkai G, Mashiach S, Seidman DS. A prospective cohort study of oxytocin plus ergometrine compared with oxytocin alone for prevention of postpartum haemorrhage. Br J Obstet Gynaecol. 1996;103(11):1068-1073.
- Winikoff B, Dabash R, Durocher J, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women not exposed to oxytocin during labour: a double-blind, randomised, non-inferiority trial. Lancet. 2010;375(9710):210-216.
- Breathnach F, Geary M. Uterine atony: definition, prevention, nonsurgical management, and uterine tamponade. Seminars in perinatology. 2009;33(2):82-87.
- USAID (United States Agency for International Development). Postpartum Hemorrhage Prevention. USAID Postpartum Hemorrhage Prevention Initiative (POPPHI). http://www.pphprevention.org/briefs_newsletters.php. Published September 9, 2008.
- PATH. Saving Mother's Lives: Initiative promotes proven strategy for preventing postpartum hemorrhage. PATH: Preventing Postpartum Hemorrhage. http://www.path.org/projects/preventing_postpartum_hemorrhage.php Punlished September 9, 2008.
- Miller S, Lester F, Hensleigh P. Prevention and treatment of postpartum hemorrhage: new advances for low-resource settings. J Midwifery Womens Health. 2004;49(4):283-292.