Rupture of the Uterus

Essentials of Diagnosis

• Fetal heart rate abnormalities.
• Increased suprapubic pain and tenderness with labor.
• Sudden cessation of uterine contractions with a "tearing" sensation.
• Vaginal bleeding (or bloody urine).
• Recession of the fetal presenting part.

General Considerations

Rupture of the pregnant uterus is a potential obstetric catastrophe and a major cause of maternal death. The incidence of uterine rupture is 0.8% for women with a prior low-transverse uterine scar and 4–8% for women with a prior classic scar. Complete rupture includes the entire thickness of the uterine wall and, in most cases, the overlying serosal peritoneum (broad ligament) (Fig 20–5). Occult or incomplete rupture is a term usually reserved for dehiscence of a uterine incision from previous surgery, in which the visceral peritoneum remains intact. Such defects usually are asymptomatic unless converted to complete rupture during the course of pregnancy or labor.

Risk factors

Risk factors for uterine rupture include history of hysterotomy (cesarean section, myomectomy, metroplasty, cornual resection), trauma (motor vehicle accident, rotational forceps, extension of a cervical laceration), uterine overdistention (hydramnios, multiple gestation, macrosomia), uterine anomalies, placenta percreta, and choriocarcinoma.

Ruptures usually occur during the course of labor. One notable exception is scars from a classic cesarean section (or hysterotomy), one-third of which rupture during the third trimester before term and before the onset of labor. Other causes of rupture without labor are placenta percreta, invasive mole, choriocarcinoma, and cornual pregnancy.

Complete ruptures can be classified as traumatic or spontaneous. Traumatic ruptures occur most commonly as a result of motor vehicle accidents, improper administration of an oxytocic agent, or an inept attempt at operative vaginal delivery. Breech extraction through an incompletely dilated cervix is the type of operative vaginal delivery most likely to produce uterine rupture. Other maneuvers that impose risk of rupture are internal podalic version and extraction, difficult forceps, destructive operations, and cephalic replacement to relieve shoulder dystocia. Neglected obstructed labor may be responsible for rupture of the uterus. Causes of obstructed labor include contracted pelvis, fetal macrosomia, brow or face presentation, hydrocephalus, or tumors involving the birth canal. The vast majority of uterine ruptures are associated with prior uterine surgery. Previous uterine surgery includes both classic and low cervical section, intramural or submucous myomectomy, resection of the uterine cornu, metroplasty, and trachelectomy. Other operative procedures that may have damaged the uterus are vigorous curettage, induced abortion, and manual removal of the placenta.

Clinical Findings

There are no reliable signs of impending uterine rupture that occurs before labor, although the sudden appearance of gross hematuria is suggestive.

Rupture may produce local pain and tenderness associated with increased uterine irritability and, in some cases, a small amount of vaginal bleeding. Premature labor may follow. As the extent of the rupture increases, more pain, more bleeding, and perhaps signs of hypovolemic shock will occur. Exsanguination prior to surgery is unlikely because of the reduced vascularity of scar tissue, but the placenta may be completely separated and the fetus extruded partially or completely into the abdominal cavity.

By far the most common clinical setting for rupture of the uterus is rupture of a low cervical scar; this almost always occurs during active labor. Clearly identifiable signs and symptoms may be lacking. However 78–90% of patients have FHR abnormalities as the first sign of rupture. Although it is possible that labor will progress to the vaginal birth of an unaffected infant, rupture may lacerate a uterine artery, producing exsanguination, or the fetus may be extruded into the abdominal cavity. If a defect is palpated in the lower uterine segment following vaginal delivery, laparotomy may be necessary to assess the damage. Laparotomy is mandatory if continuing hemorrhage is present. If such a defect is palpated in a stable patient who does not require exploration, a subsequent trial of labor is contraindicated.

Although much less common than FHR abnormalities, other findings of spontaneous rupture during labor are suprapubic pain and tenderness, cessation of uterine contractions, disappearance of fetal heart tones, recession of the presenting part, and vaginal hemorrhage—followed by the signs and symptoms of hypovolemic shock and hemoperitoneum. Ultrasound examination might confirm an abnormal fetal position or extension of the fetal extremities. Hemoperitoneum can sometimes be seen on ultrasound.

The clinical picture depends on the extent of rupture. Unfortunately, valuable time is often lost because the rupture was not diagnosed at the time of initial examination. Whenever a newly delivered patient exhibits persistent bleeding or shock, the uterus must be carefully reexamined for signs of a rupture that may have been difficult to palpate because of the soft, irregular tissue surfaces.

Whenever an operative delivery is performed—especially if the history includes events or problems that increase the likelihood of uterine rupture—the initial examination of the uterus and birth canal must be diligent. A dehiscence of the lower uterine segment contained only by a layer of visceral peritoneum is not an uncommon finding at time of repeat cesarean section.

Treatment

Treatment is dictated by clinical scenario and can range from simply repairing the defect and obtaining hemostasis to removing the entire uterus. If hysterectomy is deemed necessary, either total hysterectomy or the subtotal operation can be performed, depending on the site of rupture and the patient's condition. The most difficult cases are lateral ruptures involving the lower uterine segment and a uterine artery with hemorrhage and hematoma formation obscuring the operative field. Care must be taken to avoid ureteral damage by blind suturing at the base of the broad ligament. If there is a question of ureteral occlusion by a suture, it is best to perform cystotomy to observe the bilateral appearance of an intravenously injected dye such as indigo carmine. If doubt still exists, a retrograde ureteral catheter can be passed upward through the cystotomy wound.

If childbearing is important and the risks—both short and long term—are acceptable to the patient, rupture repair can be attempted. Many ruptures can be repaired. Successful pregnancies have been reported following uterine repair; however, the risk of rupture in a subsequent pregnancy is at least as high as the risk with a prior classic cesarean section. Occult ruptures of the lower uterine segment encountered at repeat section can be treated by freshening the wound edges and secondary repair, but the newly repaired incision is at increased risk for rupture, and a subsequent trial of labor is contraindicated.

Prevention

Most causes of uterine rupture can be avoided by carefully selecting patients for trial of labor. Thorough and well-documented informed consent that includes mention of fetal or maternal death is needed. The ideal candidate will have a single prior low-transverse cesarean for a nonrepetitive indication (eg, breech), will have a prior vaginal delivery, will present in active labor, and will not require augmentation during labor. The further the characteristics diverge from those of this ideal patient, the greater the chance of a failed trial of labor and complications including uterine rupture. Continuous FHR monitoring by fetal scalp electrode as soon as feasible is the best means of detecting evolving rupture during labor. Two-layer closure of the uterine incision and increasing interval between pregnancies appears to decrease the risk of subsequent rupture of the low-transverse scar.

Complications

The complications of ruptured uterus are hemorrhage, shock, postoperative infection, bladder or ureteral damage, thrombophlebitis, amniotic fluid embolus, DIC, pituitary failure, and death.

Prognosis

The maternal mortality rate is 4.2%. The perinatal mortality rate is approximately 46%

Rupture of the Uterus

Essentials of Diagnosis

• Fetal heart rate abnormalities.
• Increased suprapubic pain and tenderness with labor.
• Sudden cessation of uterine contractions with a "tearing" sensation.
• Vaginal bleeding (or bloody urine).
• Recession of the fetal presenting part.

General Considerations

Rupture of the pregnant uterus is a potential obstetric catastrophe and a major cause of maternal death. The incidence of uterine rupture is 0.8% for women with a prior low-transverse uterine scar and 4–8% for women with a prior classic scar. Complete rupture includes the entire thickness of the uterine wall and, in most cases, the overlying serosal peritoneum (broad ligament) (Fig 20–5). Occult or incomplete rupture is a term usually reserved for dehiscence of a uterine incision from previous surgery, in which the visceral peritoneum remains intact. Such defects usually are asymptomatic unless converted to complete rupture during the course of pregnancy or labor.

Risk factors

Risk factors for uterine rupture include history of hysterotomy (cesarean section, myomectomy, metroplasty, cornual resection), trauma (motor vehicle accident, rotational forceps, extension of a cervical laceration), uterine overdistention (hydramnios, multiple gestation, macrosomia), uterine anomalies, placenta percreta, and choriocarcinoma.

Ruptures usually occur during the course of labor. One notable exception is scars from a classic cesarean section (or hysterotomy), one-third of which rupture during the third trimester before term and before the onset of labor. Other causes of rupture without labor are placenta percreta, invasive mole, choriocarcinoma, and cornual pregnancy.

Complete ruptures can be classified as traumatic or spontaneous. Traumatic ruptures occur most commonly as a result of motor vehicle accidents, improper administration of an oxytocic agent, or an inept attempt at operative vaginal delivery. Breech extraction through an incompletely dilated cervix is the type of operative vaginal delivery most likely to produce uterine rupture. Other maneuvers that impose risk of rupture are internal podalic version and extraction, difficult forceps, destructive operations, and cephalic replacement to relieve shoulder dystocia. Neglected obstructed labor may be responsible for rupture of the uterus. Causes of obstructed labor include contracted pelvis, fetal macrosomia, brow or face presentation, hydrocephalus, or tumors involving the birth canal. The vast majority of uterine ruptures are associated with prior uterine surgery. Previous uterine surgery includes both classic and low cervical section, intramural or submucous myomectomy, resection of the uterine cornu, metroplasty, and trachelectomy. Other operative procedures that may have damaged the uterus are vigorous curettage, induced abortion, and manual removal of the placenta.

Clinical Findings

There are no reliable signs of impending uterine rupture that occurs before labor, although the sudden appearance of gross hematuria is suggestive.

Rupture may produce local pain and tenderness associated with increased uterine irritability and, in some cases, a small amount of vaginal bleeding. Premature labor may follow. As the extent of the rupture increases, more pain, more bleeding, and perhaps signs of hypovolemic shock will occur. Exsanguination prior to surgery is unlikely because of the reduced vascularity of scar tissue, but the placenta may be completely separated and the fetus extruded partially or completely into the abdominal cavity.

By far the most common clinical setting for rupture of the uterus is rupture of a low cervical scar; this almost always occurs during active labor. Clearly identifiable signs and symptoms may be lacking. However 78–90% of patients have FHR abnormalities as the first sign of rupture. Although it is possible that labor will progress to the vaginal birth of an unaffected infant, rupture may lacerate a uterine artery, producing exsanguination, or the fetus may be extruded into the abdominal cavity. If a defect is palpated in the lower uterine segment following vaginal delivery, laparotomy may be necessary to assess the damage. Laparotomy is mandatory if continuing hemorrhage is present. If such a defect is palpated in a stable patient who does not require exploration, a subsequent trial of labor is contraindicated.

Although much less common than FHR abnormalities, other findings of spontaneous rupture during labor are suprapubic pain and tenderness, cessation of uterine contractions, disappearance of fetal heart tones, recession of the presenting part, and vaginal hemorrhage—followed by the signs and symptoms of hypovolemic shock and hemoperitoneum. Ultrasound examination might confirm an abnormal fetal position or extension of the fetal extremities. Hemoperitoneum can sometimes be seen on ultrasound.

The clinical picture depends on the extent of rupture. Unfortunately, valuable time is often lost because the rupture was not diagnosed at the time of initial examination. Whenever a newly delivered patient exhibits persistent bleeding or shock, the uterus must be carefully reexamined for signs of a rupture that may have been difficult to palpate because of the soft, irregular tissue surfaces.

Whenever an operative delivery is performed—especially if the history includes events or problems that increase the likelihood of uterine rupture—the initial examination of the uterus and birth canal must be diligent. A dehiscence of the lower uterine segment contained only by a layer of visceral peritoneum is not an uncommon finding at time of repeat cesarean section.

Treatment

Treatment is dictated by clinical scenario and can range from simply repairing the defect and obtaining hemostasis to removing the entire uterus. If hysterectomy is deemed necessary, either total hysterectomy or the subtotal operation can be performed, depending on the site of rupture and the patient's condition. The most difficult cases are lateral ruptures involving the lower uterine segment and a uterine artery with hemorrhage and hematoma formation obscuring the operative field. Care must be taken to avoid ureteral damage by blind suturing at the base of the broad ligament. If there is a question of ureteral occlusion by a suture, it is best to perform cystotomy to observe the bilateral appearance of an intravenously injected dye such as indigo carmine. If doubt still exists, a retrograde ureteral catheter can be passed upward through the cystotomy wound.

If childbearing is important and the risks—both short and long term—are acceptable to the patient, rupture repair can be attempted. Many ruptures can be repaired. Successful pregnancies have been reported following uterine repair; however, the risk of rupture in a subsequent pregnancy is at least as high as the risk with a prior classic cesarean section. Occult ruptures of the lower uterine segment encountered at repeat section can be treated by freshening the wound edges and secondary repair, but the newly repaired incision is at increased risk for rupture, and a subsequent trial of labor is contraindicated.

Prevention

Most causes of uterine rupture can be avoided by carefully selecting patients for trial of labor. Thorough and well-documented informed consent that includes mention of fetal or maternal death is needed. The ideal candidate will have a single prior low-transverse cesarean for a nonrepetitive indication (eg, breech), will have a prior vaginal delivery, will present in active labor, and will not require augmentation during labor. The further the characteristics diverge from those of this ideal patient, the greater the chance of a failed trial of labor and complications including uterine rupture. Continuous FHR monitoring by fetal scalp electrode as soon as feasible is the best means of detecting evolving rupture during labor. Two-layer closure of the uterine incision and increasing interval between pregnancies appears to decrease the risk of subsequent rupture of the low-transverse scar.

Complications

The complications of ruptured uterus are hemorrhage, shock, postoperative infection, bladder or ureteral damage, thrombophlebitis, amniotic fluid embolus, DIC, pituitary failure, and death.

Prognosis

The maternal mortality rate is 4.2%. The perinatal mortality rate is approximately 46%

Rupture of the Uterus

Essentials of Diagnosis

• Fetal heart rate abnormalities.
• Increased suprapubic pain and tenderness with labor.
• Sudden cessation of uterine contractions with a "tearing" sensation.
• Vaginal bleeding (or bloody urine).
• Recession of the fetal presenting part.

General Considerations

Rupture of the pregnant uterus is a potential obstetric catastrophe and a major cause of maternal death. The incidence of uterine rupture is 0.8% for women with a prior low-transverse uterine scar and 4–8% for women with a prior classic scar. Complete rupture includes the entire thickness of the uterine wall and, in most cases, the overlying serosal peritoneum (broad ligament) (Fig 20–5). Occult or incomplete rupture is a term usually reserved for dehiscence of a uterine incision from previous surgery, in which the visceral peritoneum remains intact. Such defects usually are asymptomatic unless converted to complete rupture during the course of pregnancy or labor.

Risk factors

Risk factors for uterine rupture include history of hysterotomy (cesarean section, myomectomy, metroplasty, cornual resection), trauma (motor vehicle accident, rotational forceps, extension of a cervical laceration), uterine overdistention (hydramnios, multiple gestation, macrosomia), uterine anomalies, placenta percreta, and choriocarcinoma.

Ruptures usually occur during the course of labor. One notable exception is scars from a classic cesarean section (or hysterotomy), one-third of which rupture during the third trimester before term and before the onset of labor. Other causes of rupture without labor are placenta percreta, invasive mole, choriocarcinoma, and cornual pregnancy.

Complete ruptures can be classified as traumatic or spontaneous. Traumatic ruptures occur most commonly as a result of motor vehicle accidents, improper administration of an oxytocic agent, or an inept attempt at operative vaginal delivery. Breech extraction through an incompletely dilated cervix is the type of operative vaginal delivery most likely to produce uterine rupture. Other maneuvers that impose risk of rupture are internal podalic version and extraction, difficult forceps, destructive operations, and cephalic replacement to relieve shoulder dystocia. Neglected obstructed labor may be responsible for rupture of the uterus. Causes of obstructed labor include contracted pelvis, fetal macrosomia, brow or face presentation, hydrocephalus, or tumors involving the birth canal. The vast majority of uterine ruptures are associated with prior uterine surgery. Previous uterine surgery includes both classic and low cervical section, intramural or submucous myomectomy, resection of the uterine cornu, metroplasty, and trachelectomy. Other operative procedures that may have damaged the uterus are vigorous curettage, induced abortion, and manual removal of the placenta.

Clinical Findings

There are no reliable signs of impending uterine rupture that occurs before labor, although the sudden appearance of gross hematuria is suggestive.

Rupture may produce local pain and tenderness associated with increased uterine irritability and, in some cases, a small amount of vaginal bleeding. Premature labor may follow. As the extent of the rupture increases, more pain, more bleeding, and perhaps signs of hypovolemic shock will occur. Exsanguination prior to surgery is unlikely because of the reduced vascularity of scar tissue, but the placenta may be completely separated and the fetus extruded partially or completely into the abdominal cavity.

By far the most common clinical setting for rupture of the uterus is rupture of a low cervical scar; this almost always occurs during active labor. Clearly identifiable signs and symptoms may be lacking. However 78–90% of patients have FHR abnormalities as the first sign of rupture. Although it is possible that labor will progress to the vaginal birth of an unaffected infant, rupture may lacerate a uterine artery, producing exsanguination, or the fetus may be extruded into the abdominal cavity. If a defect is palpated in the lower uterine segment following vaginal delivery, laparotomy may be necessary to assess the damage. Laparotomy is mandatory if continuing hemorrhage is present. If such a defect is palpated in a stable patient who does not require exploration, a subsequent trial of labor is contraindicated.

Although much less common than FHR abnormalities, other findings of spontaneous rupture during labor are suprapubic pain and tenderness, cessation of uterine contractions, disappearance of fetal heart tones, recession of the presenting part, and vaginal hemorrhage—followed by the signs and symptoms of hypovolemic shock and hemoperitoneum. Ultrasound examination might confirm an abnormal fetal position or extension of the fetal extremities. Hemoperitoneum can sometimes be seen on ultrasound.

The clinical picture depends on the extent of rupture. Unfortunately, valuable time is often lost because the rupture was not diagnosed at the time of initial examination. Whenever a newly delivered patient exhibits persistent bleeding or shock, the uterus must be carefully reexamined for signs of a rupture that may have been difficult to palpate because of the soft, irregular tissue surfaces.

Whenever an operative delivery is performed—especially if the history includes events or problems that increase the likelihood of uterine rupture—the initial examination of the uterus and birth canal must be diligent. A dehiscence of the lower uterine segment contained only by a layer of visceral peritoneum is not an uncommon finding at time of repeat cesarean section.

Treatment

Treatment is dictated by clinical scenario and can range from simply repairing the defect and obtaining hemostasis to removing the entire uterus. If hysterectomy is deemed necessary, either total hysterectomy or the subtotal operation can be performed, depending on the site of rupture and the patient's condition. The most difficult cases are lateral ruptures involving the lower uterine segment and a uterine artery with hemorrhage and hematoma formation obscuring the operative field. Care must be taken to avoid ureteral damage by blind suturing at the base of the broad ligament. If there is a question of ureteral occlusion by a suture, it is best to perform cystotomy to observe the bilateral appearance of an intravenously injected dye such as indigo carmine. If doubt still exists, a retrograde ureteral catheter can be passed upward through the cystotomy wound.

If childbearing is important and the risks—both short and long term—are acceptable to the patient, rupture repair can be attempted. Many ruptures can be repaired. Successful pregnancies have been reported following uterine repair; however, the risk of rupture in a subsequent pregnancy is at least as high as the risk with a prior classic cesarean section. Occult ruptures of the lower uterine segment encountered at repeat section can be treated by freshening the wound edges and secondary repair, but the newly repaired incision is at increased risk for rupture, and a subsequent trial of labor is contraindicated.

Prevention

Most causes of uterine rupture can be avoided by carefully selecting patients for trial of labor. Thorough and well-documented informed consent that includes mention of fetal or maternal death is needed. The ideal candidate will have a single prior low-transverse cesarean for a nonrepetitive indication (eg, breech), will have a prior vaginal delivery, will present in active labor, and will not require augmentation during labor. The further the characteristics diverge from those of this ideal patient, the greater the chance of a failed trial of labor and complications including uterine rupture. Continuous FHR monitoring by fetal scalp electrode as soon as feasible is the best means of detecting evolving rupture during labor. Two-layer closure of the uterine incision and increasing interval between pregnancies appears to decrease the risk of subsequent rupture of the low-transverse scar.

Complications

The complications of ruptured uterus are hemorrhage, shock, postoperative infection, bladder or ureteral damage, thrombophlebitis, amniotic fluid embolus, DIC, pituitary failure, and death.

Prognosis

The maternal mortality rate is 4.2%. The perinatal mortality rate is approximately 46%

Rupture of the Uterus

Essentials of Diagnosis

• Fetal heart rate abnormalities.
• Increased suprapubic pain and tenderness with labor.
• Sudden cessation of uterine contractions with a "tearing" sensation.
• Vaginal bleeding (or bloody urine).
• Recession of the fetal presenting part.

General Considerations

Rupture of the pregnant uterus is a potential obstetric catastrophe and a major cause of maternal death. The incidence of uterine rupture is 0.8% for women with a prior low-transverse uterine scar and 4–8% for women with a prior classic scar. Complete rupture includes the entire thickness of the uterine wall and, in most cases, the overlying serosal peritoneum (broad ligament) (Fig 20–5). Occult or incomplete rupture is a term usually reserved for dehiscence of a uterine incision from previous surgery, in which the visceral peritoneum remains intact. Such defects usually are asymptomatic unless converted to complete rupture during the course of pregnancy or labor.

Risk factors

Risk factors for uterine rupture include history of hysterotomy (cesarean section, myomectomy, metroplasty, cornual resection), trauma (motor vehicle accident, rotational forceps, extension of a cervical laceration), uterine overdistention (hydramnios, multiple gestation, macrosomia), uterine anomalies, placenta percreta, and choriocarcinoma.

Ruptures usually occur during the course of labor. One notable exception is scars from a classic cesarean section (or hysterotomy), one-third of which rupture during the third trimester before term and before the onset of labor. Other causes of rupture without labor are placenta percreta, invasive mole, choriocarcinoma, and cornual pregnancy.

Complete ruptures can be classified as traumatic or spontaneous. Traumatic ruptures occur most commonly as a result of motor vehicle accidents, improper administration of an oxytocic agent, or an inept attempt at operative vaginal delivery. Breech extraction through an incompletely dilated cervix is the type of operative vaginal delivery most likely to produce uterine rupture. Other maneuvers that impose risk of rupture are internal podalic version and extraction, difficult forceps, destructive operations, and cephalic replacement to relieve shoulder dystocia. Neglected obstructed labor may be responsible for rupture of the uterus. Causes of obstructed labor include contracted pelvis, fetal macrosomia, brow or face presentation, hydrocephalus, or tumors involving the birth canal. The vast majority of uterine ruptures are associated with prior uterine surgery. Previous uterine surgery includes both classic and low cervical section, intramural or submucous myomectomy, resection of the uterine cornu, metroplasty, and trachelectomy. Other operative procedures that may have damaged the uterus are vigorous curettage, induced abortion, and manual removal of the placenta.

Clinical Findings

There are no reliable signs of impending uterine rupture that occurs before labor, although the sudden appearance of gross hematuria is suggestive.

Rupture may produce local pain and tenderness associated with increased uterine irritability and, in some cases, a small amount of vaginal bleeding. Premature labor may follow. As the extent of the rupture increases, more pain, more bleeding, and perhaps signs of hypovolemic shock will occur. Exsanguination prior to surgery is unlikely because of the reduced vascularity of scar tissue, but the placenta may be completely separated and the fetus extruded partially or completely into the abdominal cavity.

By far the most common clinical setting for rupture of the uterus is rupture of a low cervical scar; this almost always occurs during active labor. Clearly identifiable signs and symptoms may be lacking. However 78–90% of patients have FHR abnormalities as the first sign of rupture. Although it is possible that labor will progress to the vaginal birth of an unaffected infant, rupture may lacerate a uterine artery, producing exsanguination, or the fetus may be extruded into the abdominal cavity. If a defect is palpated in the lower uterine segment following vaginal delivery, laparotomy may be necessary to assess the damage. Laparotomy is mandatory if continuing hemorrhage is present. If such a defect is palpated in a stable patient who does not require exploration, a subsequent trial of labor is contraindicated.

Although much less common than FHR abnormalities, other findings of spontaneous rupture during labor are suprapubic pain and tenderness, cessation of uterine contractions, disappearance of fetal heart tones, recession of the presenting part, and vaginal hemorrhage—followed by the signs and symptoms of hypovolemic shock and hemoperitoneum. Ultrasound examination might confirm an abnormal fetal position or extension of the fetal extremities. Hemoperitoneum can sometimes be seen on ultrasound.

The clinical picture depends on the extent of rupture. Unfortunately, valuable time is often lost because the rupture was not diagnosed at the time of initial examination. Whenever a newly delivered patient exhibits persistent bleeding or shock, the uterus must be carefully reexamined for signs of a rupture that may have been difficult to palpate because of the soft, irregular tissue surfaces.

Whenever an operative delivery is performed—especially if the history includes events or problems that increase the likelihood of uterine rupture—the initial examination of the uterus and birth canal must be diligent. A dehiscence of the lower uterine segment contained only by a layer of visceral peritoneum is not an uncommon finding at time of repeat cesarean section.

Treatment

Treatment is dictated by clinical scenario and can range from simply repairing the defect and obtaining hemostasis to removing the entire uterus. If hysterectomy is deemed necessary, either total hysterectomy or the subtotal operation can be performed, depending on the site of rupture and the patient's condition. The most difficult cases are lateral ruptures involving the lower uterine segment and a uterine artery with hemorrhage and hematoma formation obscuring the operative field. Care must be taken to avoid ureteral damage by blind suturing at the base of the broad ligament. If there is a question of ureteral occlusion by a suture, it is best to perform cystotomy to observe the bilateral appearance of an intravenously injected dye such as indigo carmine. If doubt still exists, a retrograde ureteral catheter can be passed upward through the cystotomy wound.

If childbearing is important and the risks—both short and long term—are acceptable to the patient, rupture repair can be attempted. Many ruptures can be repaired. Successful pregnancies have been reported following uterine repair; however, the risk of rupture in a subsequent pregnancy is at least as high as the risk with a prior classic cesarean section. Occult ruptures of the lower uterine segment encountered at repeat section can be treated by freshening the wound edges and secondary repair, but the newly repaired incision is at increased risk for rupture, and a subsequent trial of labor is contraindicated.

Prevention

Most causes of uterine rupture can be avoided by carefully selecting patients for trial of labor. Thorough and well-documented informed consent that includes mention of fetal or maternal death is needed. The ideal candidate will have a single prior low-transverse cesarean for a nonrepetitive indication (eg, breech), will have a prior vaginal delivery, will present in active labor, and will not require augmentation during labor. The further the characteristics diverge from those of this ideal patient, the greater the chance of a failed trial of labor and complications including uterine rupture. Continuous FHR monitoring by fetal scalp electrode as soon as feasible is the best means of detecting evolving rupture during labor. Two-layer closure of the uterine incision and increasing interval between pregnancies appears to decrease the risk of subsequent rupture of the low-transverse scar.

Complications

The complications of ruptured uterus are hemorrhage, shock, postoperative infection, bladder or ureteral damage, thrombophlebitis, amniotic fluid embolus, DIC, pituitary failure, and death.

Prognosis

The maternal mortality rate is 4.2%. The perinatal mortality rate is approximately 46%

Rhinitis

definition

 is a medical term for irritation and inflammation of the mucous membrane inside the nose. Common symptoms of rhinitis are a stuffy nose, runny nose, and post-nasal drip. The most common kind of rhinitis is allergic rhinitis, which is usually triggered by airborne allergens such as pollen and dander. Allergic rhinitis may cause additional symptoms, such as sneezing and nasal itching, coughing, headache, fatigue, malaise, and cognitive impairment. The allergens may also affect the eyes, causing watery, reddened or itchy eyes and puffiness around the eyes^.

Rhinitis is very common. Allergic rhinitis is more common in some countries than others; in the United States, about 10%-30% of adults are affected annually.

In rhinitis, the inflammation of the mucous membrane is caused by viruses, bacteria, irritants or allergens. The inflammation results in the generation of large amounts of mucus, commonly producing a runny nose, as well as a stuffy nose and post-nasal drip. In the case of allergic rhinitis, the inflammation is caused by the degranulation of mast cells in the nose. When mast cells degranulate, they release histamine and other chemicals, starting an inflammatory process that can cause symptoms outside the nose, such as fatigue and malaise.

Contents 1 Types 1.1 Infectious 1.2 Vasomotor rhinitis 1.3 Allergic 1.4 Rhinitis medicamentosa 1.5 Chronic atrophic rhinitis 1.6 Rhinitis sicca 1.7 Polypous rhinitis 2 Management 3 References 4 External links

Types

Rhinitis is categorized into three types: (i) infective rhinitis includes acute and chronic bacterial infections; (ii) nonallergic (vasomotor) rhinitis includes autonomic, hormonal, drug-induced, atrophic, and gustatory rhinitis, as well as rhinitis medicamentosa; (iii) allergic rhinitis, triggered by pollen, mold, animal dander, dust and other similar inhaled allergens

Infectious

See also: Common cold and Sinusitis

Rhinitis is commonly caused by a viral or bacterial infection, including the common cold, which is caused by Rhinoviruses and Coronaviruses, or bacterial sinusitis. Symptoms of the common cold include rhinorrhea, sore throat (pharyngitis), cough, congestion, and slight headache 

Vasomotor rhinitis

Non-allergic rhinitis refers to runny nose that is not due to allergy. Non-allergic rhinitis can be classified as either non-inflammatory or inflammatory rhinitis. One very common type of non-inflammatory, non-allergic rhinitis that is sometimes confused with allergy is called vasomotor rhinitis, in which certain non-allergic triggers such as smells, fumes, smoke, dusts, and temperature changes, cause rhinitis. There is still much to be learned about this entity, but it is thought that these non-allergic triggers cause dilation of the blood vessels in the lining of the nose, which results in swelling, and drainage. Vasomotor rhinitis can coexist with allergic rhinitis, and this is called "mixed rhinitis." (Middleton's Allergy Principles and Practice, seventh edition.) The pathology of vasomotor rhinitis appears to involve neurogenic inflammation and is as yet not very well understood. Vasomotor rhinitis appears to be significantly more common in women than men, leading some researchers to believe that hormones play a role. In general, age of onset occurs after 20 years of age, in contrast to allergic rhinitis which can be developed at any age. Individuals suffering from vasomotor rhinitis typically experience symptoms year-round, though symptoms may be exacerbated in the spring and autumn when rapid weather changes are more common. An estimated 17 million United States citizens have vasomotor rhinitis. The antihistamines azelastine and olopatadine, applied as nasal sprays, may both be effective for vasomotor rhinitis. Fluticasone propionate or budesonide (both are steroids) in nostril spray form may also be used for symptomatic treatment.

Allergic

Main article: Allergic rhinitis

Pollen grains from a variety of common plants can cause hay fever.

Allergic rhinitis or hay fever is when an allergen such as pollen or dust is inhaled by an individual with a sensitized immune system, triggering antibody production. These antibodies mostly bind to mast cells, which contain histamine. When the mast cells are stimulated by pollen and dust, histamine (and other chemicals) are released. This causes itching, swelling, and mucus production. Symptoms vary in severity between individuals. Very sensitive individuals can experience hives or other rashes. Particulate matter in polluted air and chemicals such as chlorine and detergents, which can normally be tolerated, can greatly aggravate the condition.^{[citation needed]}

Characteristic physical findings in individuals who have allergic rhinitis include conjunctival swelling and erythema, eyelid swelling, lower eyelid venous stasis, lateral crease on the nose, swollen nasal turbinates, and middle ear effusion

Even if a person has negative skin-prick, intradermal and blood tests for allergies, they may still have allergic rhinitis, from a local allergy in the nose. This is called local allergic rhinitis. Many people who were previously diagnosed with nonallergic rhinitis may actually have local allergic rhinitis.

Rhinitis medicamentosa

Main article: Rhinitis medicamentosa

It is a condition of rebound nasal congestion brought on by extended use of topical decongestants (e.g., oxymetazoline, phenylephrine, xylometazoline, and naphazoline nasal sprays) that work by constricting blood vessels in the lining of the nose.

Chronic atrophic rhinitis

Main article: Chronic atrophic rhinitis

Chronic rhinitis in form of atrophy of the mucous membrane and glands.

Rhinitis sicca

Chronic form of dryness of the mucous membranes

Polypous rhinitis

Management

The management of rhinitis depends on the underlying cause. High-dose administration of Vitamin B12 has been additionally validated to stimulate the activity of the body's TH1 suppressor T-Cells, which then down-regulates the over-production of the allergen antibody IgE in allergic individuals which could decrease both near and long term manifestations of rhinitis symptomology.