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vaginal bleeding

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vaginal bleeding Empty vaginal bleeding

Post by mandible Thu Apr 29, 2010 12:51 pm

Vaginal Bleeding In Pregnancy

1-Placenta previa excludes :
a- Painless vaginal bleeding
b- Tone increased of uterus
c- Lower segmental abnormality
d- Early 3rd trimester

Placenta Previa
Essentials of Diagnosis
• Spotting during first and second trimesters.
• Sudden, painless, profuse bleeding in third trimester.
• Initial cramping in 10% of cases.
In placenta previa, the placenta is implanted in the lower uterine segment within the zone of effacement and dilatation of the cervix, constituting an obstruction to descent of the presenting part. Placenta previa is encountered in approximately 1 in 200 births, but only 20% are complete (placenta over the entire cervix). Approximately 90% of patients will be parous. Among grand multiparas the incidence may be as high as 1 in 20.

Etiology
The incidence of placenta previa is increased by
1. multiparity,
2. advancing age, and
3. previous cesarean delivery.

Thus, possible etiologic factors include
1. scarred or poorly vascularized endometrium in the corpus,
2. a large placenta, and
3. abnormal forms of placentation such as succenturiate lobe.

• The incidence of placenta previa is slightly higher in multiple gestation.
• A cesarean section scar triples the incidence of placenta previa.
• Another contributory factor is an increased average surface area of a placenta implanted in the lower uterine segment, possibly because these tissues are less well suited for nidation.

Bleeding in placenta previa may be due to any of the following causes:
1. mechanical separation of the placenta from its implantation site, either during the formation of the lower uterine segment or during effacement and dilatation of the cervix in labor, or as a result of intravaginal manipulation;
2. placentitis; or
3. rupture of poorly supported venous lakes in the decidua basalis that have become engorged with venous blood.

Classification
1. Complete placenta previa: The placenta completely covers the internal cervical os.
2. Marginal placenta previa: The placenta is implanted at the margin of the internal cervical os, within 2 cm. If the placenta is seen to be more than 2 cm from the internal os, the rate of antepartum or intrapartum hemorrhage is not increased.



Diagnosis
Every patient suspected of placenta previa should be hospitalized, and cross-matched blood should be at hand. To avoid provoking hemorrhage, both vaginal and rectal examination should not be performed.

Symptoms and Signs
1. Painless hemorrhage is the cardinal sign of placenta previa. Although spotting may occur during the first and second trimesters of pregnancy, the first episode of hemorrhage usually begins after the 28th week and is characteristically described as sudden, painless, and profuse. With the initial bleeding episode, clothing or bedding may be soaked by an impressive amount of bright red, clotted blood, but the blood loss usually is not extensive, seldom produces shock, and almost never is fatal.
2. In approximately 10% of cases there is some initial pain, probably because of coexisting placental separation and localized uterine contractions.Spontaneous labor can be expected over the next few days in 25% of patients. In a small minority of cases, bleeding is less dramatic or does not begin until after spontaneous rupture of the membranes or the onset of labor. A few nulliparous patients even reach term without bleeding, possibly because the placenta has been protected by an uneffaced cervix.
3. The uterus usually is soft, relaxed, and nontender.
4. A high presenting part cannot be pressed into the pelvic inlet.
5. The infant will present in an oblique or transverse lie in approximately 15% of cases.
6. FHR abnormalities are unlikely unless there are complications such as hypovolemic shock, placental separation, or a cord accident.

Ultrasonography
Bedside transabdominal ultrasonography can definitively identify 95% of placenta previas. Transvaginal or transperineal studies can make the diagnosis in virtually every case. This approach is particularly helpful with the posterior placenta previa.
During the middle of the second trimester, the placenta is observed by ultrasound to cover the internal cervical os in approximately 30% of cases. With development of the lower uterine segment, almost all of these low implantations will be carried to a higher station. An early ultrasonic diagnosis of placenta previa requires the confirmation of an additional study before definitive action is taken.

Differential Diagnosis
Placental causes of bleeding other than placenta previa include
1. partial premature separation of the normally implanted placenta or
2. circumvallate placenta.

Treatment
The treatment depends on the amount of uterine bleeding; the duration of pregnancy and viability of the fetus; the degree of placenta previa; the presentation, position, and station of the fetus; the gravidity and parity of the patient; the status of the cervix; and whether or not labor has begun. The patient must be admitted to the hospital to establish the diagnosis and ideally should remain in the hospital once the diagnosis is made. Blood should be readily available for transfusion.

Expectant Therapy
The initial hemorrhage of placenta previa may occur before pulmonary maturity is established. In such cases, fetal survival can often be enhanced by expectant therapy.

Early in pregnancy, transfusions to replace blood loss and the use of tocolytic agents to prevent premature labor are indicated to prolong pregnancy to at least 32–34 weeks. After 34 weeks, the benefits of further maturation must be weighed against the risk of major hemorrhage. The possibility that repeated small hemorrhages may be accompanied by intrauterine growth retardation also must be considered. Approximately 75% of cases of placenta previa are now delivered between 36 and 40 weeks.

In selecting the optimum time for delivery, tests of fetal lung maturation, including assessment of amniotic fluid surfactants and ultrasonic growth measurements, are valuable adjuvants.

If the patient is between 24 and 34 weeks' gestational age, a single course of betamethasone (2 doses of 12 mg intramuscularly separated by 24 hours) or dexamethasone (4 doses of 6 mg intravenously or intramuscularly separated by 12 hours) should be given to promote fetal lung maturity. Repeat courses of steroids are not necessary and usually are considered only for patients who initially present and receive treatment with steroids at less than 24 weeks.

Because of the costs of hospitalization, patients with a presumptive diagnosis of placenta previa are sometimes sent home on strict bed rest after their condition has become stable under ideal, controlled circumstances. Such a policy is always a calculated risk in view of the unpredictability of further hemorrhage, but the practice has been studied and is an acceptable alternative.

Delivery

Cesarean Section
Cesarean section is the delivery method of choice with placenta previa. Cesarean section has proved to be the most important factor in lowering maternal and perinatal mortality rates (more so than blood transfusion or better neonatal care).
If possible, hypovolemic shock should be corrected by administration of intravenous fluids and blood before the operation is started. Not only will the mother be better protected, but an at-risk fetus will recover more quickly in utero than if born while the mother is still in shock.
The choice of anesthesia depends on current and anticipated blood loss. A combination of rapid induction, endotracheal intubation, succinylcholine, and nitrous oxide is a suitable method for proceeding in the presence of active bleeding.
The choice of operative technique is of importance because of the placental location and the development of the lower uterine segment. If the incision passes through the site of placental implantation, there is a strong possibility that the fetus will lose a significant amount of blood—even enough to require subsequent transfusion. With posterior implantation of the placenta, a low-transverse incision may be best if the lower uterine segment is well developed. Otherwise, a classic incision may be required to secure sufficient room and to avoid incision through the placenta. Preparations should be made for care and resuscitation of the infant if it becomes necessary. In addition, the possibility of blood loss should be monitored in the newborn if the placenta has been incised.
In a small percentage of cases, hemostasis in the placental bed is unsatisfactory because of the poor contractility of the lower uterine segment. Mattress sutures or packing may be required in addition to the usual oxytocin, prostaglandins, and methylergonovine. If placenta previa accreta is found, hemostasis may necessitate a total hysterectomy. Puerperal infection and anemia are the most likely postoperative complications.

Vaginal Delivery
Vaginal delivery usually is reserved for patients with a marginal implantation and a cephalic presentation.
1. If vaginal delivery is elected, the membranes should be artificially ruptured prior to any attempt to stimulate labor (oxytocin given before amniotomy likely will cause further bleeding). Tamponade of the presenting part against the placental edge usually reduces bleeding as labor progresses.
2. Because of the possibility of fetal hypoxemia due to either placental separation or a cord accident (as a result of either prolapse or compression of low insertion of the cord by the descending presenting part), continuous fetal monitoring must be used. If FHR abnormalities develop, a rapid cesarean section should be performed unless vaginal delivery is imminent.
3. Deliver the patient in the easiest and most expeditious manner as soon as the cervix is fully dilated and the presenting part is on the perineum. For this purpose, a vacuum extractor is particularly valuable because it expedites delivery without risking rupture of the lower uterine segment.

Complications
Maternal
1. Maternal hemorrhage, shock, and death may follow severe antepartum bleeding resulting from placenta previa. Death may occur as a result of intrapartum and postpartum bleeding, operative trauma, infection, or embolism.
2. Premature separation of a portion of a placenta previa occurs in virtually every case and causes excessive external bleeding without pain; however, complete or wide separation of the placenta before full dilatation of the cervix is uncommon.
3. Placenta previa accreta is a serious abnormality in which the sparse endometrium and the myometrium of the lower uterine segment are penetrated by the trophoblast in a manner similar to placenta accreta higher in the uterus. In patients with 1 prior cesarean section, the rate of accreta in the presence of previa is 20–25% and rises to 50% with 2 or more prior cesarean sections.

Fetal
1. Prematurity (gestational age < 36 weeks) accounts for 60% of perinatal deaths due to placenta previa.
2. The fetus may die as a result of decreased oxygen delivery intrapartum or birth injury.
3. Fetal hemorrhage due to tearing of the placenta occurs with vaginal manipulation and especially upon entry into the uterine cavity as cesarean section is done for placenta previa. About half of these cesarean babies lose some blood. Fetal blood loss is directly proportional to the time that elapses between lacerating the cotyledon and clamping the cord.

Prognosis
1. Maternal : With rapid recourse to cesarean section, use of banked blood, and expertly administered anesthesia, the overall maternal mortality has fallen to less than 1 in 1000.
2. Fetal : The perinatal mortality rate associated with placenta previa has declined to approximately 1%. Although premature labor, placental separation, cord accidents, and uncontrollable hemorrhage cannot be avoided, the mortality rate can be greatly reduced if ideal obstetric and newborn care is given.


- Placenta previa, all true except :
a) Shock out of proportion of bleeding
b) Malpresentation
c) Head not engaged
d) Painless bleeding

2- A 34wk GA lady presented with vaginal bleeding of an amount more of that of her normal cycle. O/E utrine contracts every 4 min, bulged membrane, the cervix is 3 cm dilated, fetus is in a high transverse lie and the placenta is on the posterior fundus. US showed translucency behind the placenta and the CTG (Cardiotocography) showed FHR of 170, the best line of management is:
• C/S immediately.
• give oxytocin.
• do rupture of the membrane.
• amniocentisis.

Premature Separation of the Placenta (Abruptio Placentae, Marginal Sinus Bleed)

Essentials of Diagnosis
• Unremitting abdominal (uterine) or back pain.
• Irritable, tender, and often hypertonic uterus.
• Visible or concealed hemorrhage.
• Evidence of fetal distress may or may not be present, depending on the severity of the process.

General Considerations
Premature separation of the placenta is defined as separation from the site of uterine implantation before delivery of the fetus (approximately 1 in 77–89 deliveries). The severe form (resulting in fetal death) has an incidence of approximately 1 in 500–750 deliveries.

Two principal forms of premature separation of the placenta can be recognized, depending on whether the resulting hemorrhage is external or concealed (Fig 20–2).
1. In the concealed form (20%), the hemorrhage is confined within the uterine cavity, detachment of the placenta may be complete, and the complications often are severe. Approximately 10% of abruptions are associated with clinically significant coagulopathies (disseminated intravascular coagulation [DIC]), but 40% of those severe enough to cause fetal death are associated with coagulopathy.
2. In the external form (80%), the blood drains through the cervix, placental detachment is more likely to be incomplete, and the complications are fewer and less severe. Occasionally, the placental detachment involves only the margin or placental rim. Here, the most important complication is the possibility of premature labor.


Types of premature separation of the placenta.

















Approximately 30% of cases of third-trimester bleeding are due to placental separation, with the initial hemorrhage usually encountered after the 26th week. Placental separation in early pregnancy cannot be distinguished from other causes of abortion. Approximately 50% of separations occur before the onset of labor, and 10–15% are not diagnosed before the second stage of labor.

Etiology
The exact causes of placental separation are often difficult to ascertain, although there are a number of predisposing and precipitating factors. A common predisposing factor is previous placental separation. Following 1 episode, the incidence of recurrence is 10–17%. Following 2 episodes, the incidence of recurrence exceeds 20%. The hypertensive states of pregnancy are associated with 2.5–17.9% incidence of placental separation. In abruptio placentae extensive enough to cause fetal death, approximately 50% of cases are associated with hypertensive states of pregnancy. Approximately half of these cases have chronic hypertension and half pregnancy-induced hypertension. Other predisposing factors include advanced maternal age, multiparity, uterine distention (eg, multiple gestation, hydramnios), vascular disease (eg, diabetes mellitus, systemic lupus erythematosus), thrombophilias, uterine anomalies or tumors (eg, leiomyoma), cigarette smoking, alcohol consumption (> 14 drinks per week), cocaine use, and possibly maternal type O blood.

Precipitating causes of premature separation of the placenta, although more direct and definable, are no less diverse. All are rare.
1. Circumvallate placenta,
2. trauma (eg, external or internal version, automobile accident, abdominal trauma directly transmitted to an anterior placenta),
3. sudden reduction in uterine volume (eg, rapid amniotic fluid loss, delivery of a first twin),
4. abnormally short cord (usually only a problem during delivery, when traction is exerted on the cord as the fetus moves down the birth canal), and
5. increased venous pressure (usually only problematic with abrupt or extreme alterations) are included in this category.

Pathophysiology & Pathology
Several mechanisms are thought to be important in the pathophysiology of premature placental separation.
1. One mechanism is local vascular injury that results in vascular rupture into the decidua basalis, bleeding, and hematoma formation. The hematoma shears off adjacent denuded vessels, producing further bleeding and enlargement of the area of separation. Another mechanism is initiated by an abrupt rise in uterine venous pressure transmitted to the intervillous space. This results in engorgement of the venous bed and separation of all or a portion of the placenta. Conditions predisposing to vascular injury and known to be associated with an increased incidence of placental separation are preeclampsia–eclampsia, chronic hypertension, diabetes mellitus, chronic renal disease, cigarette smoking, and cocaine use. Factors that may predispose to a disturbed vascular equilibrium and the possibility of passive congestion of the venous bed in response to an abrupt rise in uterine venous pressure are vasodilatation secondary to shock, compensatory hypertension as a result of aortic compression, and paralytic vasodilatation of conduction anesthesia.
2. Mechanical factors causing premature separation are rare (1–5%). They include transabdominal trauma, sudden decompression of the uterus, such as with the delivery of a first twin or rupture of the membranes in hydramnios, or traction on a short umbilical cord.
3. Another possible mechanism is initiation of the coagulation cascade. This may occur, for example, with trauma causing release of tissue thromboplastin. These activated coagulation factors in turn may act to initiate clot formation in the relative hemodynamic stasis occurring in the placental pool.
Anatomically, placental abruption may occur by hemorrhage into the decidual basalis, which splits, leaving a thin layer adjacent to the myometrium. This decidual hematoma leads to separation, compression, and further bleeding. Alternatively, a spiral artery may rupture, creating a retroplacental hematoma. In either case, bleeding occurs, a clot forms, and the placental surface can no longer provide metabolic exchange between mother and fetus.
The clot depresses the adjacent placenta. Nonclotted blood courses from the site of injury. In concealed hemorrhage, this effusion may be totally retained behind the placental margins, behind the membrane attachment to the uterine wall, or behind a closely applied fetal presenting part. The blood may rupture through the membranes or placenta and gain access to the amniotic fluid (and vice versa). The tissue disruption by bleeding may allow maternofetal hemorrhage, fetomaternal hemorrhage, maternal bleeding into the amniotic fluid, or amniotic fluid embolus, depending on the areas disrupted and their relative pressure differences.
Concealed hemorrhage is more likely to be associated with complete placental detachment. If the placental margins remain adherent, central placental separation may result in hemorrhage that infiltrates the uterine wall. Uterine tetany may follow. Occasionally, extensive intramyometrial bleeding results in uteroplacental apoplexy—so-called Couvelaire uterus, a purplish and copper-colored, ecchymotic, indurated organ that may lose its contractile force because of disruption of the muscle bundles.
In the more severe cases of separation, there may be a clinically significant amount of DIC associated with depletion of fibrinogen and platelets as well as other clotting factors. The mother may then develop a hemorrhagic diathesis that is manifested by widespread petechiae, active bleeding, hypovolemic shock, and failure of the normal clotting mechanism. In addition, fibrin deposits in small capillaries (along with the hypoxic vascular damage of shock) can result in potentially lethal complications, including acute cor pulmonale, renal cortical and tubular necrosis, and anterior pituitary infarction (Sheehan's syndrome).
The likelihood of fetal hypoxia and fetal death depends on the amount and duration of placental separation and, in severe cases, the loss of a significant amount of fetal blood.

Clinical Findings

Symptoms and Signs
In general, the clinical findings correspond to the degree of separation. Approximately 30% of separations are small, produce few or no symptoms, and usually are not noted until the placenta is inspected. Larger separations are accompanied by abdominal pain and uterine irritability.
Hemorrhage may be visible or concealed. If the process is extensive, evidence of fetal distress, uterine tetany, DIC, or hypovolemic shock may be seen. Increased uterine tonus and frequency of contractions may provide early clues of abruption.
1. Approximately 80% of patients will present with vaginal bleeding, and
2. two-thirds will have uterine tenderness and abdominal or back pain.
3. One-third will have abnormal contractions; about half of these will have high-frequency contractions and half hypertonus.
4. More than 20% of patients with abruptio placentae will be diagnosed erroneously as having idiopathic premature labor.
5. Fetal distress will be present in more than 50% of cases, and 15% will present with fetal demise.

If placental separation is marginal, there will be only minimal irritability and no uterine tenderness or fetal distress. There may be a limited amount of external bleeding (50–150 mL), either bright or dark red depending on the rapidity of its appearance.



Laboratory and Imaging Findings
The degree of anemia probably will be considerably less than would seem to be justified by the amount of blood loss because changes in hemoglobin and hematocrit are delayed during acute blood loss until secondary hemodilution has occurred. A peripheral blood smear may show a reduced platelet count; the presence of schistocytes, suggesting intravascular coagulation; and fibrinogen depletion with release of fibrin split products. If serial laboratory determinations of fibrinogen levels are not available, the clot observation test, a simple but invaluable bedside procedure, can be performed. A venous blood sample is drawn every hour, placed in a clean test tube, and observed for clot formation and clot lysis. Failure of clot formation within 5–10 minutes or dissolution of a formed clot when the tube is gently shaken is proof of a clotting deficiency that almost surely is due principally to a lack of fibrinogen and platelets.
More sophisticated studies should be available on an emergency basis in most hospitals. The following tests will assist in determining coagulation status: prothrombin time and partial thromboplastin time, platelet count, fibrinogen, and fibrin split products.
Ultrasonography may be considered in the diagnosis of placental abruption but often is inconclusive. Possible findings include hyperechoic foci posterior to the placenta suggestive of a collection of fresh blood or a hypoechoic area suggestive of a formed clot. Lack of findings does not provide reassurance, and use of ultrasound should not be substituted for clinical judgment, especially in the face of a concerning clinical situation.
Treatment
Expectant Therapy
Expectant management of suspected placental abruption is the exception, not the rule. This management pathway should be attempted only with careful observation of the patient and a clear clinical picture. In general, expectant management may be appropriate when the mother is stable, the fetus is immature, and the fetal heart tracing is reassuring. The patient should be observed in the labor and delivery suite for 24–48 hours to ensure that further placental separation is not occurring. Continuous fetal and uterine monitoring should be maintained. Changes in fetal status may be the earliest indication of an expanding abruption.
In retrospective studies of women with placental abruption, tocolytic use was associated with increasing gestational age at delivery. Tocolytic use did not increase the incidence of hemorrhage, fetal distress, or stillbirth. Currently no prospective trials addressing the efficacy of tocolytic therapy in preventing an abruption from expanding have been reported.
Once the patient is stable, the decision to manage the patient as an outpatient should be tailored to the clinical situation. If outpatient surveillance is selected, the fetus should be followed closely with nonstress testing.
Emergency Measures
Most cases of placental abruption are diagnosed as an acute event (upon presentation to labor and delivery or during the intrapartum period), making immediate intervention necessary. If the patient exhibits clinical findings that become progressively more severe or if a major placental separation is suspected as manifested by hemorrhage, uterine spasm, or fetal distress, an acute emergency exists.
Blood should be drawn for laboratory studies and at least 4 units of PRBCs typed and crossed. Two large-bore intravenous catheters should be placed and crystalloid administered.
Vaginal Delivery
An attempt at vaginal delivery is indicated if the degree of separation appears to be limited and if the continuous FHR tracing is reassuring. When placental separation is extensive but the fetus is dead or of dubious viability, vaginal delivery is indicated. The exception to vaginal delivery is the patient in whom hemorrhage is uncontrollable and operative delivery is necessary to save the life of the fetus or mother.
Induction of labor with an oxytocin infusion should be instituted if active labor does not begin shortly after amniotomy. In practice, augmentation often is not needed because usually the uterus is already excessively irritable. If the uterus is extremely spastic, uterine contractions cannot be clearly identified unless an internal monitor is used, and the progress of labor must be judged by observing cervical dilatation. Pudendal block anesthesia is recommended. Conduction anesthesia is to be avoided in the face of significant hemorrhage because profound, persistent hypotension may result. However, in the volume-repleted patient in early labor, a preemptive epidural should be considered because rapid deterioration of maternal or fetal status can occur as labor progresses.
Cesarean Section
The indications for cesarean section are both fetal and maternal. Abdominal delivery should be selected whenever delivery is not imminent for a fetus with a reasonable chance of survival who exhibits persistent evidence of distress. Cesarean section also is indicated if the fetus is in good condition but the situation is not favorable for rapid delivery in the face of progressive or severe placental separation. This includes most nulliparous patients with less than 3–4 cm of cervical dilatation. Maternal indications for cesarean section are uncontrollable hemorrhage from a contracting uterus, rapidly expanding uterus with concealed hemorrhage (with or without a live fetus) when delivery is not imminent, uterine apoplexy as manifested by hemorrhage with secondary relaxation of a previously spastic uterus, or refractory uterus with delivery necessary (20%).
Complications
Disseminated Intravascular Coagulation
Placental abruption can lead to initiation of the coagulation cascade by release of tissue thromboplastin into the maternal circulation. Consumption of coagulation factors and platelets is followed by coagulopathic hemorrhage. A cycle ensues as further bleeding worsens the depletion of coagulation factors. Continuous monitoring for evidence of a clotting deficiency is mandatory from the time the diagnosis of placental abruption is considered well into the postpartum period. Treatment will depend not only on the demonstration of hematologic deficiencies but also on the amount of active bleeding and the anticipated route of delivery.
1. Fresh whole blood—Fresh whole blood is generally reserved for massive hemorrhage (more than 5–6 L blood loss in a 24-hour period). Each unit has a volume of 500 cc and contains red blood cells, white blood cells, coagulation factors, and other plasma proteins. Like PRBCs, 1 unit can be expected to raise the hematocrit by 3%.
2. Packed red blood cells—PRBCs are satisfactory for immediate replacement of blood loss, but they do not contain clotting factors. Each unit has a volume of 250 cc. Because the amount of white blood cells and plasma proteins is less than in whole blood, the chance of transfusion reaction is decreased.
3. Fresh-frozen plasma—Fresh-frozen plasma is a preparation of unconcentrated clotting factors without platelets. Each unit has a volume of 250 cc and can be expected to raise any clotting factor concentration by 2–3%. Fibrinogen concentration is raised by 10 mg% per unit. Fresh-frozen plasma usually is given in increments of 2 units.
4. Cryoprecipitate packs—Cryoprecipitate is prepared as a concentrate of fresh-frozen plasma and contains all the necessary labile coagulation factors. Because each unit contains a volume of only 40 cc, it is useful in avoiding fluid overload when treating hypofibrinogenemia.
5. Platelets—During active bleeding, transfusion of platelets often is the best practical means of counteracting a clotting deficiency. Each unit of platelets has a volume of 40–50 cc and can be expected to raise the platelet count by 10,000. Transfusions are customarily ordered as a minimum of 6–8 units.
6. Heparin—Prophylactic administration of heparin to block conversion of prothrombin to thrombin (and thereby reduce the consumption of coagulation factors) has been used successfully in the management of DIC associated with fetal death ("dead fetus syndrome"). With prompt diagnosis of fetal death and uterine evacuation, this syndrome is rarely seen. There is no role for heparin in treatment of DIC related to abruption.
7. Preparation for surgery—If cesarean section is indicated, preparation for surgery must be completed quickly. Two to 4 units of PRBCs should be secured from the moment the diagnosis is entertained. Fresh-frozen plasma can be ordered as indicated by coagulation studies. Empiric treatment of a clotting disorder may be necessary if intraoperative findings suggest abnormal coagulation and confirmatory laboratory results are not readily available. In cases of uncontrollable hemorrhage, despite maximal attempts to correct coagulopathy, alternatives include whole pelvis embolization, intrauterine balloon tamponade, and abdominal packing. Rarely, hysterectomy is necessary to control bleeding, even in the presence of some degree of coagulopathy.
Renal Cortical and Tubular Necrosis
The possibility of renal cortical or tubular necrosis must be considered if oliguria persists after an adequate blood volume has been restored. An attempt should be made to improve renal circulation and promote diuresis by increasing fluid volume (with the aid of monitoring). If oliguria or anuria persists, renal necrosis is probable, and fluid intake and output must be carefully monitored. Continuing impairment of renal function may require peritoneal dialysis or hemodialysis.
Uterine Atony
Extensive infiltration of the myometrial wall with blood may result in loss of myometrial contractility. If, as a result, bleeding from the placental bed is not controlled, hysterectomy may be necessary. If future childbearing is an important consideration, bilateral ligation of the ascending branches of the uterine arteries should be accomplished before resorting to hysterectomy. Not only will blood flow be reduced, but the relative ischemia produced may result in a satisfactory contraction of the damaged uterus. If ligation of the uterine vessels proves ineffective, bilateral ligation of the hypogastric arteries, reducing arterial pressure within the uterus to venous levels, may effect hemostasis. Following ligation of either the uterine or hypogastric arteries, collateral circulation should be adequate to preserve uterine function, including subsequent pregnancies.
A relatively new approach to uterine atony is the B-Lynch suture. This technique involves mechanical involution of an atonic uterus with chromic suture, mimicking the hemostasis obtained with bimanual compression. The B-Lynch technique is quick, easy to learn, and safe, providing a useful alternative to performing a hysterectomy.
Prognosis
External or concealed bleeding, excessive blood loss, shock, nulliparity, a closed cervix, absence of labor, and delayed diagnosis and treatment are unfavorable prognostic factors. Maternal mortality rates ranging from 0.5–5% are currently reported from various parts of the world. Most women die of hemorrhage (immediate or delayed) or cardiac or renal failure. A high degree of suspicion, early diagnosis, and definitive therapy should reduce the maternal mortality rate to 0.5–1%.
The perinatal mortality rate reported with abruption overall is approximately 5%. With severe abruption, the rate is much higher. In approximately 15% of cases, no fetal heartbeat can be heard on admission to the hospital, and in another 50% an abnormal FHR pattern is noted early. In cases in which transfusion of the mother is urgently required, the fetal mortality rate probably will be at least 50%. Liveborn infants have a high rate of morbidity resulting from predelivery hypoxia, birth trauma, and the hazards of prematurity (40–50%).


3- PPH happens more commonly with:
• multiple pregnancies.
• anaemia.
• preterm delivery.
• antithrombin III deficiency.

Uterine atony occurs in 90% of cases of postpartum hemorrhage. Postpartum uterine bleeding is typically controlled by compression of vessels by uterine contraction, so atony leads to rapid blood loss. Predisposing factors include overdistension of the uterus from multiple gestation, polyhydramnios, or macrosomia; rapid or prolonged labor; grand multiparity; chorioamnionitis; use of general anesthesia or tocolytic agents; and use of oxytocin (Pitocin) during labor.

4- The most common cause of Post Partum Hemorrhage is:
-Uterine Atony
-Multiple Pregnancy.
-Pre Eclampsia.

- Most important cause of immediate post partum hemorrhage:
a) laceration of cervix
b) laceration of vagin
c) uterine atony
d) placental fragment trtention

- most common cause of postpartum hemorrhage:
a) Uterin atony
b) Retained placental fragment
c) Cervical laceration
d) Nonofthe above


5-The most accurate Dx of Ectopic Pregnancy is:
a. Culdocentesis
b. Pelvic U/S
c. Endometrial Biobsy
d. Serial B-HCG
e. Laproscopy

Ultrasound—Ultrasound is useful in evaluating patients at risk for ectopic pregnancy, namely, by documenting the presence or absence of an intrauterine pregnancy. β-hCG titers and ultrasound complement each another in detecting ectopic pregnancy and have led to earlier detection with a subsequent decrease in adverse outcome. By correlating β-hCG titers with ultrasound findings, an ectopic pregnancy often can be differentiated from an intrauterine pregnancy. Furthermore, ultrasound can help distinguish a normal intrauterine pregnancy from a blighted ovum, incomplete abortion, or complete abortion.

A normal intrauterine sac appears regular and well defined on ultrasound. It has been described as a "double ring," which represents the decidual lining and the amniotic sac. In ectopic pregnancy, ultrasound may reveal only a thickened, decidualized endometrium. With more advanced ectopics, decidual sloughing with resultant intracavitary fluid or blood may create a so-called "pseudogestational sac," a small and irregular structure that may be confused with an intrauterine gestation.

An intrauterine sac should be visible by transvaginal ultrasound when the β-hCG level is approximately 1000 mIU/mL and by transabdominal ultrasound approximately 1 week later, when the β-hCG level is 1800–3600 mIU/mL. Thus, when an empty uterine cavity is seen with a β-hCG titer above this threshold, an ectopic pregnancy is more likely.

The presence of an adnexal mass with an empty uterus raises the suspicion for an ectopic pregnancy, especially if the β-hCG titers are above the discriminatory zone. Although direct visualization of an adnexal gestational sac along with a yolk sac or embryo secures the diagnosis, it is more likely to detect a "tubal ring" or complex mass adjacent to, but separate from, both the uterus and ovary. If rupture has occurred, a dilated fallopian tube with fluid in the cul-de-sac may be visualized. Ultrasound is increasingly being relied upon to differentiate several less common types of ectopic pregnancies. Both interstitial tubal and cesarean section scar pregnancies can masquerade as intrauterine gestations because of their proximity to the intrauterine cavity.
The most likely alternative diagnosis to an adnexal mass in early pregnancy is a corpus luteum cyst, which can rupture and bleed, thus contributing to a highly confusing clinical picture.

β-hCG: The qualitative serum or urine β-hCG assay is positive in virtually 100% of ectopic pregnancies. The value of this test is limited, however, because a positive result does not help to elicit the location of the pregnancy. More helpful is a quantitative β-hCG value that, in conjunction with transvaginal ultrasound, can usually make the diagnosis. In an unclear clinical picture, serial titers can be followed that, in the face of a normal pregnancy, should double every 2 days. Two-thirds of ectopic pregnancies have abnormally rising values, whereas the remaining third show a normal progression.

Laparoscopy—The need for laparoscopy in the diagnosis of ectopic pregnancy has declined with the increasing use of ultrasound. However, it still is useful in certain situations where a definitive diagnosis is difficult, especially in the case of a desired, potentially viable intrauterine pregnancy when a D&C is contraindicated. Laparoscopy may also be used as definitive management in early ectopic gestation.

6-A pregnant women with anterior lateral placenta on US, examiner finger cannot reach the placenta . the placenta is:
a) Low lying
b) Marginal placenta Previa
c) Partial Placenta Previa
d) Lateral Placenta Previa






7- About antepartum hemorrhage:
a) Need immediate assessment by vaginal exam
b) Mother risk is more than fetal risk (bcz its one of the leading cause of maternal death)

8- U/S of pregnant lady showed posterior wall placenta. It dose not reach examining finger by vaginal exam. Which of the following is true?
a) Complete placenta previa
b) Normal site placenta
c) Low lying placenta
d) Placenta previa marginalis
e) Incomplete centralis

9- Pt with post partum hemorhage & infertility, all can be found except :
A) Balloning of sella turcica
b) Decrease Na
c) Hypoglycemia
d) Decreased T4
e) Decreased iodine uptake thyroid

10- The most dangerous symptom during pregnancy is:
• PV bleeding
• Ankle swelling
• Hyperemesis
• Cramps

11- Physical exam reveals the uterus to be about 6 wk size. Vaginal bleeding is scant with no discernible tissue in the cervical os. There are no palpable adnexal masses. The uterus is mildly tender. Ultrasonographic exam does not reveal a gestational sac. Which of the following should be recommended?
a- Dilatation & curettage.
b- Culdocentesis.
c- Observation followed by serial B-HCG determinations.
d- Diagnostic laparoscopy.
e- Laparotomy.

12- If the above pt presented at 8 wk gestation & pelvic exam revealed unilateral adnexal tenderness w/o discernible mass, consideration should be given:
a- Observation.
b- Culdocentesis.
c- Laparoscopy.
d- Dilatation & curettage.
e- Laparotomy.

2. Laparoscopy—The need for laparoscopy in the diagnosis of ectopic pregnancy has declined with the increasing use of ultrasound. However, it still is useful in certain situations where a definitive diagnosis is difficult, especially in the case of a desired, potentially viable intrauterine pregnancy when a D&C is contraindicated. Laparoscopy may also be used as definitive management in early ectopic gestation.
3. D&C—D&C may confirm or exclude intrauterine pregnancy in the case of an undesired pregnancy. D&C may interrupt an intrauterine gestation and should not be performed if the pregnancy is desired, unless the -hCG titers have plateaued or fallen and the pregnancy is definitely abnormal. When chorionic villi are recovered, the diagnosis of an intrauterine pregnancy is confirmed. On the other hand, if only decidua is obtained on D&C, ectopic pregnancy is highly likely.
4. Laparotomy—Laparotomy is indicated when the presumptive diagnosis of ectopic pregnancy in an unstable patient necessitates immediate surgery, or when definitive therapy is not possible by medical management or laparoscopy.
5. Culdocentesis—Culdocentesis, the transvaginal passage of a needle into the posterior cul-de-sac in order to determine whether free blood is present in the abdomen (Fig 14–Cool, has largely been replaced by transvaginal ultrasound.
6. Magnetic resonance imaging—Magnetic resonance imaging is a useful adjunct to ultrasound in cases where an unusual ectopic location is suspected. An accurate diagnosis of cervical, cesarean scar, or interstitial pregnancy urges conservative intervention with methotrexate (MTX) in order to avoid the potentially catastrophic hemorrhage associated with surgical management of these sites.

3-Most common cause of post-partum bleeding:
A-Uterine atony
5-Laceration
C-Retained placental tissue
D-Uterine inversion



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vaginal bleeding Empty Re: vaginal bleeding

Post by wafyazaz Fri Nov 12, 2010 9:47 pm

جزاك الله خيرا
wafyazaz
wafyazaz
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vaginal bleeding Empty Re: vaginal bleeding

Post by ahmed bassett Thu Nov 17, 2011 12:51 pm

knwolloge is good
ahmed bassett
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