Uterine atony

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Adnan Ezici, M.D[2]

Synonyms and keywords:

Overview

Physiologically, contraction of the myometrium occurs in response to oxytocin, therefore, mediates the uterine hemostasis by mechanically compressing the blood vessels supplying the placenta. The uterine atony is caused by inadequate contraction of the myometrium following the delivery. Uterine atony must be differentiated from other diseases that cause postpartum hemorrhage, such as retained placental tissue, obstetric lacerations, placenta accreta spectrum (placenta accreta, increta, and percreta), uterine inversion, maternal coagulation defects, and disseminated intravascular coagulation (DIC). Uterine atony is responsible for up to 80% of cases of postpartum hemorrhage, and approximately 25% of maternal deaths are due to postpartum hemorrhage, which is the leading cause of maternal deaths. The presence of a large, soft and boggy uterus on physical examination is highly suggestive of uterine atony. The mainstay of treatment for uterine atony is bimanual uterine massage with the administration of oxytocin (IV or IM) simultaneously. If oxytocin fails, second-line pharmacologic agents (methylergonovine or carboprost) should be considered. If medical therapy fails, surgical procedures such as uterine compression sutures (brace sutures) should be considered.

Historical Perspective

In 1953, Du Vigneaud et al. were the first to discover the aminoacid sequence of oxytocin and its biochemical synthesis. Following his discoveries about polypeptide hormones, The Nobel Prize for chemistry was awarded to Vincent du Vigneaud in 1955.[1][2]

Classification

There is no established system for the classification of uterine atony.

Pathophysiology

It is thought that the uterine atony is caused by inadequate contraction of the myometrium following the delivery. Physiologically, contraction of the myometrium occurs in response to oxytocin, therefore, mediates the uterine hemostasis by mechanically compressing the blood vessels supplying the placenta.[3]

Causes and Risk Factors

Common risk factors in the development of uterine atony include:[4][5][6]

Differentiating Uterine Atony from other Diseases

Uterine atony must be differentiated from other diseases that cause postpartum hemorrhage, such as retained placental tissue, obstetric lacerations, placenta accreta spectrum (placenta accreta, increta, and percreta), uterine inversion, maternal coagulation defects, and disseminated intravascular coagulation (DIC)[7]

  • Detection of the uterine atony might be challenging in the presence of uterine inversion which causes the absence of typical findings of uterine atony such as soft and boggy uterus. The specific finding of uterine inversion is a visible protruding mass through the vagina.[3]

Epidemiology and Demographics

Uterine atony is responsible for up to 80% of cases of postpartum hemorrhage, and approximately 25% of maternal deaths are due to postpartum hemorrhage, which is the leading cause of maternal deaths.[4][8]

Screening

There is insufficient evidence to recommend routine screening for uterine atony. However, identifying the risk factors might provide a better prediction of women at risk for uterine atony, therefore, planning and preparation might be provided more sufficiently.[4]

Natural History, Complications, and Prognosis

Sheehan syndrome, a possible late complication of uterine atony. Enlarged pituitary gland, with low T1, and high T2 homogenous signal on MRI. Case courtesy of Dr Hani Makky Al Salam, <a href="https://radiopaedia.org/">Radiopaedia.org</a>. From the case <a href="https://radiopaedia.org/cases/8518">rID: 8518</a>

Diagnosis

Diagnostic Study of Choice

For the diagnostic definition of postpartum hemorrhage, click here.

History and Symptoms

  • A detailed prenatal history is important for the detection of risk factors in the development of uterine atony.[3]
  • The hallmark of postpartum hemorrhage is hypovolemia. For more symptoms of postpartum hemorrhage, click here.

Physical Examination

Abdominal examination by palpation is one of the main methods of physical examination in the diagnosis of uterine atony. Palpation of the uterus might be either direct (following the cesarean delivery) or indirect (bimanual examination after the vaginal delivery).[3]

  • The presence of a large, soft and boggy uterus on physical examination is highly suggestive of uterine atony.[11]
  • In case of focal localized atony of the uterine lower segments with normal contraction of uterine fundus, it might be challenging to detect the uterine atony with abdominal examination. Thus, manual exploration of the uterine cavity or ultrasound imaging might be useful in suspected cases.

Laboratory Findings

Laboratory findings consistent with the diagnosis of uterine atony include a decreased concentration of hemoglobin and hematocrit.[12]

  • Severe anemia (Hb ⩽ 7 g/dl) might decrease the ability of contraction of the myometrium. Therefore, low maternal hemoglobin levels at the beginning of the delivery might predict the possibility and the severity of the uterine atony.[13]

Electrocardiogram

There are no ECG findings associated with uterine atony.

X-ray

There are no x-ray findings associated with uterine atony.

Ultrasound

Ultrasound may be helpful in the diagnosis of uterine atony. Findings on ultrasound suggestive of uterine atony include echogenic endometrial stripe and intrauterine blood clots with no intrinsic vascularity.[14]

CT scan

Dynamic CT (dCT) scan may be helpful in the detection of intractable uterine atony. Findings on dCT scan suggestive of intractable uterine atony include arterial contrast extravasation and significant difference of size and shape between the upper and lower uterine cavity.[15]

  • The eventual requirement of embolization might be predicted by the presence of arterial contrast extravasation on dynamic CT scan.

MRI

There are no MRI findings associated with uterine atony.

Other Imaging Findings

There are no other imaging findings associated with uterine atony.

Other Diagnostic Studies

There are no other diagnostic studies associated with uterine atony.

Treatment

Medical Therapy

The mainstay of treatment for uterine atony is bimanual uterine massage with the administration of oxytocin (IV or IM) simultaneously.[9]

  • It is thought that the stimulation of uterine contractions can be mediated by bimanual uterine massage by the secretion of endogenous prostaglandins.

If oxytocin fails, second-line pharmacologic agents (methylergonovine or carboprost) should be considered.

If pharmacotherapy fails, uterine compression sutures or placement of a uterine balloon tamponade (success rate >85%) such as Bakri balloon tamponade may be considered.


Surgery

Surgery is not the first-line treatment option for patients with uterine atony. Surgery is usually reserved for patients with bleeding resistant to the medical therapy.[9]

  • Uterine compression sutures (brace sutures) such as the B-Lynch method is recommended in patients with uterine atony resistant to the medical therapy (bimanual uterine massage, administration of uterotonic agents, etc.).
  • If uterine compression sutures or balloon tamponades fail, bilateral uterine artery ligation should be considered as a next step treatment approach.
  • If the bleeding is still poorly controlled, the next step should be the ligation of the bilateral utero-ovarian artery.
  • If the bleeding continues, ligation of the internal iliac artery should be considered.
  • If all the abovementioned procedures are not successful for the bleeding control (might be considered at an earlier step for patients without fertility desires), hysterectomy (total or supracervical) should be considered as a life-saving measure.

Prevention

For the prevention of postpartum hemorrhage, click here.

References

  1. Prata N, Bell S, Weidert K (2013). "Prevention of postpartum hemorrhage in low-resource settings: current perspectives". Int J Womens Health. 5: 737–52. doi:10.2147/IJWH.S51661. PMC 3833941. PMID 24259988.
  2. Ragnarsson U (July 2007). "The Nobel trail of Vincent du Vigneaud". J Pept Sci. 13 (7): 431–3. doi:10.1002/psc.864. PMID 17554806.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 Gill P, Patel A, Van Hook JW. PMID 29630290. Missing or empty |title= (help)
  4. 4.0 4.1 4.2 Wetta LA, Szychowski JM, Seals S, Mancuso MS, Biggio JR, Tita AT (July 2013). "Risk factors for uterine atony/postpartum hemorrhage requiring treatment after vaginal delivery". Am J Obstet Gynecol. 209 (1): 51.e1–6. doi:10.1016/j.ajog.2013.03.011. PMC 3788839. PMID 23507549.
  5. Oyelese Y, Ananth CV (March 2010). "Postpartum hemorrhage: epidemiology, risk factors, and causes". Clin Obstet Gynecol. 53 (1): 147–56. doi:10.1097/GRF.0b013e3181cc406d. PMID 20142652.
  6. Breathnach F, Geary M (April 2009). "Uterine atony: definition, prevention, nonsurgical management, and uterine tamponade". Semin Perinatol. 33 (2): 82–7. doi:10.1053/j.semperi.2008.12.001. PMID 19324236.
  7. "ACOG Practice Bulletin: Clinical Management Guidelines for Obstetrician-Gynecologists Number 76, October 2006: postpartum hemorrhage". Obstet Gynecol. 108 (4): 1039–47. October 2006. doi:10.1097/00006250-200610000-00046. PMID 17012482.
  8. Fukami T, Koga H, Goto M, Ando M, Matsuoka S, Tohyama A, Yamamoto H, Nakamura S, Koyanagi T, To Y, Kondo H, Eguchi F, Tsujioka H (2019). "Incidence and risk factors for postpartum hemorrhage among transvaginal deliveries at a tertiary perinatal medical facility in Japan". PLoS One. 14 (1): e0208873. doi:10.1371/journal.pone.0208873. PMC 6326562. PMID 30625154.
  9. 9.0 9.1 9.2 Bienstock JL, Eke AC, Hueppchen NA (2021). "Postpartum Hemorrhage". N Engl J Med. 384 (17): 1635–1645. doi:10.1056/NEJMra1513247. PMID 33913640 Check |pmid= value (help).
  10. Kaya B, Tuten A, Daglar K, Onkun M, Sucu S, Dogan A, Unal O, Guralp O (May 2015). "B-Lynch uterine compression sutures in the conservative surgical management of uterine atony". Arch Gynecol Obstet. 291 (5): 1005–14. doi:10.1007/s00404-014-3511-2. PMID 25315382.
  11. Quiñones JN, Uxer JB, Gogle J, Scorza WE, Smulian JC (March 2010). "Clinical evaluation during postpartum hemorrhage". Clin Obstet Gynecol. 53 (1): 157–64. doi:10.1097/GRF.0b013e3181cd5d36. PMID 20142653.
  12. Rath WH (May 2011). "Postpartum hemorrhage--update on problems of definitions and diagnosis". Acta Obstet Gynecol Scand. 90 (5): 421–8. doi:10.1111/j.1600-0412.2011.01107.x. PMID 21332452.
  13. Kamaya A, Ro K, Benedetti NJ, Chang PL, Desser TS (September 2009). "Imaging and diagnosis of postpartum complications: sonography and other imaging modalities". Ultrasound Q. 25 (3): 151–62. doi:10.1097/RUQ.0b013e3181b5451e. PMID 19730078.
  14. Ikeda A, Kondoh E, Chigusa Y, Mogami H, Kameyama Nakao K, Kido A, Horie A, Baba T, Hamanishi J, Mandai M (October 2020). "Novel subtype of atonic postpartum hemorrhage: dynamic computed tomography evaluation of bleeding characteristics and the uterine cavity". J Matern Fetal Neonatal Med. 33 (19): 3286–3292. doi:10.1080/14767058.2019.1571033. PMID 30651015.
  15. Ramdhan RC, Loukas M, Tubbs RS (October 2017). "Anatomical complications of hysterectomy: A review". Clin Anat. 30 (7): 946–952. doi:10.1002/ca.22962. PMID 28762535.


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