What is Uterine Atony?
Uterine atony is a serious and potentially life-threatening obstetric condition characterized by the inability of the uterus to contract effectively after childbirth. This failure of uterine muscle contraction results in excessive postpartum bleeding, making uterine atony the leading cause of primary postpartum hemorrhage (PPH). Prompt recognition and management are critical to prevent maternal morbidity and mortality.
.png "Uterine Atony - A Common Cause of PPH")
Table of Contents
Normal Physiology of Uterine Contraction Postpartum
The uterus is a highly muscular organ composed mainly of smooth muscle fibers called the myometrium. During pregnancy, the uterus expands dramatically to accommodate the growing fetus. After delivery of the baby and placenta, the uterus normally undergoes a process called involution, where it contracts and reduces in size to return to its pre-pregnancy state.
The key function of postpartum uterine contraction is to compress the spiral arteries and blood vessels at the site of placental attachment, effectively sealing off these vessels and preventing excessive bleeding. This contraction is mediated by rhythmic, sustained contractions of the myometrium, which occur in response to various hormonal and mechanical signals.
Oxytocin, a hormone released from the posterior pituitary gland during and after labor, plays a pivotal role by stimulating uterine muscle contraction. Additionally, the mechanical stimulation of the uterus during delivery and the sudden drop in progesterone levels contribute to the increased contractility of the myometrium.
The contracted uterus becomes firm and globular on palpation and typically lies near or just below the level of the umbilicus immediately after delivery. This tone is crucial to maintaining hemostasis at the placental site. Efficient uterine contraction also helps expel clots and debris and reduces the risk of postpartum hemorrhage.
Pathophysiology of Uterine Atony
In contrast, uterine atony occurs when the myometrium fails to contract effectively after delivery. Instead of becoming firm and compact, the uterus remains soft, enlarged, and poorly contracted, which impairs its ability to compress the maternal blood vessels that supply the placenta.
The underlying problem in uterine atony is a loss of myometrial tone and contractile force. This may result from excessive stretching of the uterine muscles, muscle fatigue, or interference with the normal biochemical pathways that trigger contraction. Without adequate contraction, the spiral arteries remain open, leading to ongoing bleeding from the placental bed.
From a physiological perspective, several mechanisms contribute to atony:
🔹 Myometrial exhaustion or damage: Overdistension from multiple pregnancies or large babies can thin the uterine muscle fibers, reducing their ability to contract.
🔹 Hormonal interference: Drugs like magnesium sulfate or anesthesia agents can relax smooth muscle tone.
🔹 Oxytocin receptor desensitization: Prolonged or excessive oxytocin administration during labor can lead to reduced responsiveness of the uterus to further oxytocin stimulation postpartum.
🔹 Retained placental fragments or infection: These can disrupt the contractile response through mechanical or inflammatory pathways.
Clinically, the uterus in atony is palpably boggy, often larger than expected for the postpartum period, and can be displaced if a large clot is present. The inability of the uterus to clamp down on blood vessels leads to significant postpartum hemorrhage, which is a major cause of maternal morbidity and mortality worldwide.
Read more: Postpartum Hemorrhage
Causes and Risk Factors for Developing Uterine Atony
While uterine atony can occur without any identifiable risk factors, certain conditions increase the likelihood of it happening. These risk factors often involve the uterus being overstretched or exhausted, or an impaired ability of the uterine muscle to respond to contractions.
1. Uterine Overdistension
Overdistension of the uterus is one of the most well-established causes of uterine atony. When the uterus has been excessively stretched during pregnancy, the muscle fibers can become too thin and ineffective at contracting after delivery.
✔ Multiple gestation (twins or more) increases uterine size and mass.
✔ Polyhydramnios, the presence of too much amniotic fluid, places added stress on the uterus.
✔ Macrosomia, a baby with excessive birth weight (typically over 4000 g), also contributes to overdistension.
✔ Fetal anomalies that result in increased uterine volume may have similar effects.
These conditions lead to a mechanically weakened myometrium that struggles to contract efficiently postpartum.
2. Prolonged or Rapid Labor
Both prolonged labor and precipitous (very fast) labor can increase the risk of uterine atony, although through different mechanisms. In prolonged labor, the uterus becomes fatigued and overworked, reducing its contractile strength. On the other hand, precipitous labor may not allow the uterus adequate time to prepare for effective postpartum contraction, leading to failure of myometrial tone.
Prolonged second or third stages of labor, especially if augmented with medications like oxytocin, can also exhaust uterine muscle responsiveness.
3. Use of Uterine Relaxant Medications
Certain medications used during labor or in the postpartum period can contribute to uterine atony by inhibiting uterine muscle contractions:
✔ Magnesium sulfate, commonly used to prevent seizures in preeclampsia/eclampsia, acts as a smooth muscle relaxant.
✔ General anesthesia, especially halogenated anesthetic agents like halothane and isoflurane, can relax uterine smooth muscle.
✔ Tocolytics such as terbutaline and nifedipine, given to delay preterm labor, may persist in the system and impair contraction postpartum.
These agents can prevent the uterus from effectively contracting and securing hemostasis.
4. Retained Placental Tissue
Incomplete delivery of the placenta or retention of placental fragments is a significant cause of uterine atony. Retained tissue can mechanically prevent uterine contraction or interfere with the normal physiologic signal for the uterus to contract. Placental accreta (abnormal adherence of the placenta to the uterine wall) can also make placental separation incomplete or difficult, contributing to atony.
This situation is particularly dangerous because retained tissue may go unnoticed unless actively investigated via examination or ultrasound.
5. Infection and Inflammation
Infections such as chorioamnionitis (infection of the fetal membranes) and endometritis (infection of the uterine lining postpartum) can compromise uterine muscle contractility. Inflammatory processes disrupt the normal myometrial function, making contraction inefficient or absent.
These infections can arise during prolonged labor, prolonged rupture of membranes, or after retained products of conception, increasing the risk of uterine atony and subsequent hemorrhage.
6. Multiparity
Women who have had multiple prior deliveries (grand multiparity) are at increased risk of uterine atony. Repeated stretching and contracting of the uterine wall over several pregnancies can reduce the uterus’s ability to contract effectively after birth due to loss of muscle tone and elasticity.
Multiparous uteri may also respond less effectively to oxytocin, making pharmacologic support less successful in preventing atony.
7. Previous History of Uterine Atony
A history of uterine atony in a previous delivery significantly raises the likelihood of recurrence. The same physiological or anatomical factors that contributed to the first occurrence may still be present, and close monitoring is warranted in subsequent deliveries.
8. Prolonged Use or High Dose of Oxytocin During Labor
While oxytocin is used to stimulate uterine contractions during labor, prolonged or excessive exposure can lead to receptor desensitization, rendering the uterus unresponsive to further oxytocin stimulation postpartum. This paradoxical effect means that even when oxytocin is given after delivery, the uterus may not contract adequately due to receptor fatigue.
9. Other Risk Factors
✔ Obesity: Associated with longer labor and increased risk of complications.
✔ Coagulation disorders: Although not a direct cause of atony, they can worsen bleeding associated with it.
✔ Placenta previa or accreta: Abnormal placentation can make placental separation more difficult and increase atony risk.
Uterine atony arises from a combination of mechanical, pharmacologic, infectious, and physiological factors. Risk factors such as overdistension, labor abnormalities, certain medications, and retained placental tissue play a pivotal role in impairing the uterus’s ability to contract after delivery. Clinicians must identify and monitor at-risk patients proactively, allowing for timely interventions to prevent postpartum hemorrhage and its life-threatening consequences.(alert-passed)
Clinical Features of Uterine Atony
Uterine atony is primarily characterized by the uterus’s failure to contract effectively after delivery, leading to significant clinical manifestations largely centered around postpartum hemorrhage (PPH).
1. Excessive Vaginal Bleeding
The hallmark clinical feature of uterine atony is heavy vaginal bleeding that occurs shortly after the delivery of the placenta. The bleeding is often bright red and profuse, as the uterus fails to contract and compress the blood vessels at the placental site. This blood loss can be sudden and rapid, sometimes leading to hypovolemic shock if not managed in a timely manner.
Unlike normal postpartum bleeding (lochia), which gradually decreases over days to weeks, the bleeding in uterine atony is abnormal in both quantity and speed, often overwhelming the normal physiological hemostasis mechanisms.
2. Uterine Tone and Palpation
On physical examination, the uterus in uterine atony is typically soft, enlarged, and poorly contracted, often described as boggy. Instead of feeling firm and well-contracted (like a tennis ball), the uterus feels flaccid and may be difficult to locate due to its distended state.
The uterine size may be larger than expected for the stage of involution due to retained blood or clots within the uterine cavity, which can contribute to the softness and enlargement.
3. Uterine Displacement
Because of its flaccidity, the uterus may be displaced from the midline of the abdomen. A displaced uterus—often deviated to one side—is frequently associated with a full bladder, which itself can worsen uterine atony by preventing adequate uterine contraction.
Therefore, assessment of bladder fullness and catheterization to relieve urinary retention is an essential steps in managing uterine atony.
4. Signs of Hypovolemia and Shock
With ongoing significant blood loss, signs of hypovolemia develop rapidly. These include tachycardia (fast pulse), hypotension (low blood pressure), pallor, sweating, dizziness, and weakness. In severe cases, the patient may experience altered mental status or loss of consciousness due to inadequate cerebral perfusion.
The severity of hypovolemic shock depends on the rate and amount of blood loss. Early recognition of these systemic signs is crucial to initiate resuscitation.
5. Associated Features
In some cases, uterine atony may be accompanied by:
✔ Retained clots or placental fragments: These may exacerbate the uterine enlargement and bogginess.
✔ Coagulopathy: Massive hemorrhage can lead to depletion of clotting factors, further complicating the bleeding.
✔ Signs of anemia: Over time, if bleeding continues, pallor, fatigue, and shortness of breath develop due to reduced oxygen-carrying capacity.
Timely clinical recognition of these features is essential for prompt management of uterine atony and prevention of life-threatening complications.(alert-passed)
Complications of Uterine Atony
Uterine atony is the leading cause of primary postpartum hemorrhage (PPH), which can rapidly escalate into serious and potentially life-threatening complications if not managed promptly and effectively. The failure of the uterus to contract adequately after delivery results in continued bleeding from the placental site, setting off a cascade of adverse outcomes that can impact maternal health profoundly.
1. Severe Postpartum Hemorrhage and Hypovolemic Shock
The most immediate and critical complication of uterine atony is severe postpartum hemorrhage. The uterus normally contracts after childbirth to compress the spiral arteries where the placenta was attached, minimizing blood loss. When atony occurs, these blood vessels remain open and bleed freely, leading to significant blood loss.
Excessive hemorrhage can quickly lead to hypovolemic shock, characterized by decreased circulating blood volume, reduced tissue perfusion, and subsequent multi-organ dysfunction. If untreated, hypovolemic shock can progress to cardiovascular collapse and death.
2. Coagulopathy and Disseminated Intravascular Coagulation (DIC)
Massive blood loss associated with uterine atony may cause consumption coagulopathy, where clotting factors and platelets are depleted due to ongoing bleeding and clot formation. This can evolve into disseminated intravascular coagulation (DIC), a severe systemic disorder marked by widespread clotting and bleeding.
DIC complicates the clinical picture by making bleeding more difficult to control, increasing the risk of further hemorrhage, and complicating surgical interventions.
3. Anemia and Related Morbidities
Due to the substantial blood loss, women with uterine atony often develop acute anemia. The decrease in red blood cell mass reduces oxygen delivery to tissues, leading to symptoms like fatigue, weakness, dizziness, and tachycardia. Severe anemia can impair recovery and worsen the overall prognosis, sometimes requiring blood transfusions to restore adequate oxygen-carrying capacity.
4. Organ Hypoperfusion and Failure
Prolonged hypovolemia resulting from uterine atony-induced hemorrhage can cause hypoperfusion of vital organs. Kidneys are particularly vulnerable, and acute kidney injury (AKI) may develop due to ischemia. The brain and heart may also suffer from insufficient blood flow, leading to confusion, altered consciousness, arrhythmias, or cardiac ischemia.
These complications significantly increase maternal morbidity and may have long-term health consequences.
5. Need for Surgical Interventions
When medical management of uterine atony fails, surgical interventions may become necessary. This can include uterine artery ligation, balloon tamponade, or even hysterectomy (removal of the uterus) as a life-saving measure.
Hysterectomy, while controlling hemorrhage, results in loss of fertility and can have significant psychological impacts. Surgical procedures carry risks of infection, anesthetic complications, and longer hospital stays.
6. Infection and Sepsis
Excessive bleeding and prolonged hospitalization increase the risk of postpartum infections such as endometritis, wound infections, or pelvic abscesses. If infections are not promptly treated, they can progress to sepsis, a systemic inflammatory response that can be fatal.
7. Psychological Impact
The experience of severe hemorrhage and emergency interventions can lead to significant psychological distress, including post-traumatic stress disorder (PTSD), anxiety, and depression. The impact on mental health is an important consideration during recovery and requires appropriate support and counseling.
Diagnosis of Uterine Atony
The diagnosis of uterine atony is primarily clinical and hinges on the recognition of its hallmark signs and symptoms in the postpartum period. It is often made quickly in the context of excessive vaginal bleeding following delivery, especially within the first 24 hours, when most cases of primary postpartum hemorrhage occur.
A. Clinical Presentation
The key diagnostic clue is excessive postpartum bleeding that is disproportionate to the expected blood loss after vaginal or cesarean delivery. Clinicians should suspect uterine atony when a woman experiences heavy vaginal bleeding accompanied by a uterus that feels soft, enlarged, and poorly contracted on abdominal palpation. Normally, after delivery, the uterus should be firm and contracted, palpable around or below the level of the umbilicus, depending on the timing. In uterine atony, the uterus remains “boggy” or flaccid, failing to contract adequately to compress the blood vessels at the placental site.
B. Physical Examination
On physical examination, the provider will assess the fundal tone by placing one hand on the lower abdomen just above the pubic bone. A boggy, relaxed uterus that fails to respond to uterine massage is highly suggestive of atony. The presence of continuous or large-volume vaginal bleeding despite uterine massage further supports the diagnosis.
The clinician also assesses the patient’s vital signs for evidence of hypovolemia such as tachycardia, hypotension, pallor, and diaphoresis, which reflect the severity of blood loss. Examination of the vaginal canal and cervix is important to rule out other causes of hemorrhage such as retained placental fragments, genital tract trauma, or lacerations.
C. Exclusion of Other Causes
Since postpartum hemorrhage can have multiple etiologies, diagnosis of uterine atony requires exclusion of other common causes such as:
✔ Retained placenta or placental fragments may prevent proper uterine contraction.
✔ Genital tract trauma, including cervical, vaginal, or perineal lacerations.
✔ Coagulopathies, either pre-existing or acquired, that impair clot formation.
✔ Uterine rupture or inversion, which present with bleeding and abnormal uterine contour.
Ultrasound imaging may be used in uncertain cases to evaluate for retained products or abnormal uterine anatomy.
D. Laboratory and Imaging Studies
Laboratory tests are not diagnostic for uterine atony per se, but are important in evaluating the patient’s condition and guiding management. A complete blood count (CBC) helps assess the degree of anemia. Coagulation studies may be warranted if bleeding is severe or if a coagulopathy is suspected.
Ultrasound can be used to confirm an empty uterus and exclude retained placental tissue or clots that might be contributing to bleeding. However, a normal ultrasound does not exclude uterine atony.
The diagnosis of uterine atony relies mainly on clinical assessment, characterized by excessive postpartum bleeding and a soft, poorly contracted (boggy) uterus on physical exam. Prompt recognition is crucial to initiate appropriate management to prevent severe hemorrhage and related complications. Exclusion of other causes of postpartum hemorrhage is essential to ensure correct diagnosis and treatment.(alert-passed)
Management of Uterine Atony
The goal of treatment is to control bleeding by stimulating uterine contractions, restoring circulating blood volume, and preventing further complications. Management involves a stepwise approach, starting with conservative measures and escalating to surgical interventions if necessary.
A. Initial Resuscitation and Stabilization
The first priority in managing uterine atony is stabilizing the patient. This involves securing the airway, breathing, and circulation (the ABCs). Intravenous access should be established promptly with at least two large-bore cannulas to allow rapid fluid and blood product administration. Isotonic crystalloids (e.g., normal saline or lactated Ringer’s solution) are infused to maintain blood pressure and tissue perfusion. Simultaneously, blood samples should be taken for complete blood count, blood typing, cross-matching, and coagulation studies to guide transfusion therapy.
Close monitoring of vital signs is essential, including heart rate, blood pressure, respiratory rate, oxygen saturation, and urine output, to assess the response to resuscitation and detect early signs of shock.
Read more: Postpartum Hemorrhage
B. Uterine Massage and Pharmacologic Therapy
Once the patient is stabilized, the next step is to stimulate uterine contractions to control bleeding. Uterine massage is a simple and immediate intervention where the provider manually massages the uterus through the abdominal wall to encourage contraction and reduce uterine bleeding. A firm, contracted uterus significantly reduces blood loss.
Pharmacologic agents, primarily uterotonic drugs, are then administered. The first-line medication is usually intramuscular or intravenous oxytocin, which promotes uterine muscle contraction. Oxytocin infusion can be titrated based on response.
If oxytocin alone is insufficient, additional uterotonics may be used, including:
🔹 Ergometrine (methylergometrine): A potent uterotonic that causes sustained uterine contractions, usually given intramuscularly. It is contraindicated in patients with hypertension or preeclampsia due to its vasoconstrictive effects.
🔹 Prostaglandins: Such as carboprost tromethamine (a prostaglandin F2α analogue) and misoprostol (a prostaglandin E1 analogue), are effective in stimulating uterine contractions. Carboprost is given intramuscularly, and misoprostol can be administered orally, sublingually, or rectally. Both are useful when oxytocin and ergometrine fail.
C. Identification and Correction of Underlying Causes
Concurrent with uterotonic therapy, the clinician must evaluate and address other potential causes of postpartum hemorrhage. Examination of the birth canal is performed to identify and repair any genital tract lacerations or hematomas. If placental fragments remain, manual removal or curettage under ultrasound guidance may be necessary.
D. Advanced Mechanical and Surgical Interventions
If pharmacologic measures fail to achieve uterine contraction and bleeding continues, more invasive interventions are required. Uterine tamponade using devices like a balloon catheter (e.g., Bakri balloon) can provide internal pressure to compress bleeding vessels and help control hemorrhage.
Surgical options include:
🔹 Uterine artery ligation or internal iliac artery ligation to reduce pelvic blood flow.
🔹 Compression sutures (such as B-Lynch sutures) are applied to the uterus to mechanically compress the bleeding surface.
🔹 As a last resort, hysterectomy may be necessary to save the patient’s life when bleeding is uncontrollable by other means.
E. Blood Transfusion and Supportive Care
Patients with significant blood loss may require blood transfusions to replace red blood cells and coagulation factors. Fresh frozen plasma, platelets, and cryoprecipitate might be needed if coagulopathy develops. Supportive care includes oxygen therapy, monitoring for signs of shock, and managing electrolyte imbalances.
F. Multidisciplinary Approach and Prevention
Management of uterine atony often involves a team including obstetricians, anesthesiologists, hematologists, and critical care specialists. Prevention strategies include active management of the third stage of labor with prophylactic oxytocin to reduce the risk of atony.
The management of uterine atony is urgent and involves stabilization, uterine massage, uterotonic drugs, correction of underlying causes, advanced mechanical or surgical interventions if needed, and supportive care, including blood transfusions. Early recognition and prompt, coordinated treatment are crucial to reducing morbidity and mortality.(alert-passed)
Prevention of Uterine Atony
Uterine atony, the failure of the uterus to contract effectively after childbirth, is the leading cause of postpartum hemorrhage (PPH). Because of its significant contribution to maternal morbidity and mortality, especially in low-resource settings, prevention is a critical aspect of obstetric care. Prevention strategies focus on both risk reduction before delivery and active management during and after the third stage of labor.
1. Risk Assessment and Antenatal Preparation
Preventing uterine atony begins with the identification of risk factors during the antenatal period. Women with a history of uterine atony, high parity (especially grand multiparity), prolonged labor, overdistended uterus (due to multiple gestation, polyhydramnios, or a large baby), and those undergoing labor augmentation or induction with oxytocin are considered high-risk. Early identification allows clinicians to plan deliveries in facilities equipped with the resources to manage PPH, such as blood banks, uterotonic agents, and surgical intervention capabilities.
2. Active Management of the Third Stage of Labor (AMTSL)
The most effective strategy for preventing uterine atony is the active management of the third stage of labor (AMTSL). This includes a combination of three main interventions:
✔ Administration of a prophylactic uterotonic drug immediately after the delivery of the baby (usually within one minute).
✔ Controlled cord traction (CCT) to deliver the placenta safely.
✔ Uterine massage after delivery of the placenta to stimulate uterine contraction.
These steps significantly reduce the incidence of uterine atony and associated hemorrhage. Oxytocin (10 IU intramuscular or intravenous) is the first-line uterotonic due to its efficacy and safety profile. In cases where oxytocin is not available or contraindicated, alternatives such as misoprostol, ergometrine, or carbetocin may be used.
3. Judicious Use of Oxytocin During Labor
While oxytocin is beneficial for inducing or augmenting labor, overuse or inappropriate dosing can lead to uterine fatigue and poor contractility after delivery. Therefore, clinicians must carefully monitor and titrate oxytocin to avoid uterine exhaustion. Similarly, avoiding prolonged or obstructed labor can prevent excessive uterine stretching and dysfunction.
4. Prevention and Management of Uterine Overdistension
Preventing overdistension of the uterus can help reduce the risk of atony. This involves careful monitoring in women with:
✔ Multiple pregnancies
✔ Macrosomia (large fetus)
✔ Polyhydramnios
Amnioreduction (removal of excess amniotic fluid) or timely delivery decisions may be considered in selected cases.
5. Optimal Management of the Placenta
Retained placental fragments can inhibit uterine contraction. Ensuring complete delivery of the placenta and membranes is essential. Manual removal may be necessary if placental separation does not occur spontaneously, but should be done under sterile and controlled conditions.
6. Uterine Massage and Monitoring After Delivery
Routine uterine massage after delivery helps promote uterine contraction. Continued assessment of uterine tone and lochia (vaginal bleeding) during the immediate postpartum period allows for early detection of uterine relaxation. Nurses and midwives should be trained to monitor fundal height, tone, and bleeding regularly.
7. Adequate Hydration and Correction of Anemia
Ensuring that the mother is well-hydrated and does not have untreated antenatal anemia enhances her physiological reserve in case of bleeding. Iron supplementation and nutritional support during pregnancy are basic but effective strategies to mitigate risk.
8. Staff Training and Emergency Preparedness
Prevention is also dependent on the preparedness of the healthcare team. All birth attendants must be trained in the early recognition of uterine atony and the use of emergency protocols, including the administration of uterotonic drugs, bimanual uterine massage, and rapid response for surgical intervention if needed.
Simulation drills, standardized protocols, and checklists for the management of postpartum hemorrhage can improve readiness and reduce delays in intervention.
Uterine atony is a preventable cause of postpartum hemorrhage and maternal death. By combining antenatal risk identification with proactive measures such as AMTSL, judicious labor management, prompt monitoring, and ensuring well-trained staff, the risk of uterine atony can be significantly reduced. Preventive strategies are particularly vital in low-resource settings where delays in recognition and treatment can be fatal.(alert-passed)
Prognosis of Uterine Atony
The prognosis of uterine atony largely depends on the promptness of diagnosis and the effectiveness of management. Uterine atony is the most common cause of postpartum hemorrhage (PPH), which remains a leading cause of maternal morbidity and mortality worldwide. Early recognition and aggressive treatment are crucial factors that improve outcomes.
Factors Influencing Prognosis
Several factors influence the prognosis of uterine atony. These include the severity of hemorrhage, the speed at which bleeding is controlled, availability of skilled healthcare providers, access to blood transfusion services, and the presence of underlying maternal conditions such as anemia or coagulopathies. Delay in intervention or inadequate treatment can lead to severe hypovolemic shock, organ failure, disseminated intravascular coagulation (DIC), and even maternal death.
Maternal Outcomes
With timely and appropriate management, most women with uterine atony recover without long-term complications. However, in cases of massive hemorrhage or delayed treatment, there can be significant maternal morbidity, including:
🔸 Hypovolemic shock: Caused by severe blood loss, which can impair perfusion to vital organs.
🔸 Coagulopathy and disseminated intravascular coagulation (DIC): Excessive bleeding can consume clotting factors, leading to a life-threatening coagulopathy.
🔸 Multi-organ failure: Prolonged shock may result in kidney injury, liver dysfunction, or respiratory failure.
🔸 Need for surgical interventions: Including hysterectomy, which can lead to loss of fertility and psychological impact.
🔸 Transfusion-related complications: Such as allergic reactions or infections.
Mortality rates have declined with improvements in obstetric care, but uterine atony still accounts for a significant proportion of maternal deaths in low-resource settings.
Fetal Outcomes
Fetal prognosis depends primarily on the timing and severity of maternal hemorrhage. Severe maternal blood loss can lead to maternal hypoxia and hemodynamic instability, which may reduce placental perfusion and cause fetal distress, hypoxia, or even intrauterine fetal demise. Additionally, emergency cesarean delivery or preterm birth may be required if uterine atony occurs during labor or immediately postpartum, potentially affecting neonatal outcomes.
Long-Term Prognosis and Prevention
In survivors, long-term prognosis is generally good if complications are avoided. However, women who have experienced uterine atony and PPH are at increased risk for recurrence in subsequent pregnancies. Preventive strategies such as active management of the third stage of labor and careful monitoring in future deliveries are recommended.
The prognosis of uterine atony depends on rapid diagnosis and effective management. While most women recover well with timely intervention, delays can lead to serious complications, increased maternal and fetal morbidity, and even mortality.(alert-passed)
