Cor pulmonale is defined as an alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system. Pulmonary hypertension is the common link between lung dysfunction and the heart in cor pulmonale. Right-sided ventricular disease caused by a primary abnormality of the left side of the heart or congenital heart disease is not considered cor pulmonale, but cor pulmonale can develop secondary to a wide variety of cardiopulmonary disease processes. Although cor pulmonale commonly has a chronic and slowly progressive course, acute onset or worsening cor pulmonale with life-threatening complications can occur.
Pathophysiology: Several different pathophysiologic mechanisms can lead to pulmonary hypertension and, subsequently, to cor pulmonale. These pathogenetic mechanisms include (1) pulmonary vasoconstriction due to alveolar hypoxia or blood acidemia; (2) anatomic compromise of the pulmonary vascular bed secondary to lung disorders, eg, emphysema, pulmonary thromboembolism, interstitial lung disease; (3) increased blood viscosity secondary to blood disorders, eg, polycythemia vera, sickle cell disease, macroglobulinemia; and (4) idiopathic primary pulmonary hypertension. The result is increased pulmonary arterial pressure.
The right ventricle (RV) is a thin-walled chamber that is more a volume pump than a pressure pump. It adapts better to changing preloads than afterloads. With an increase in afterload, the RV increases systolic pressure to keep the gradient. At a point, further increase in the degree of pulmonary arterial pressure brings significant RV dilation, an increase in RV end-diastolic pressure, and circulatory collapse. A decrease in RV output with a decrease in diastolic left ventricle (LV) volume results in decreased LV output. Since the right coronary artery, which supplies the RV free wall, originates from the aorta, decreased LV output diminishes blood pressure in the aorta and decreases right coronary blood flow. This is a vicious cycle between decreases in LV and RV output.
Right ventricular overload is associated with septal displacement toward the left ventricle. Septal displacement, which is seen in echocardiography, can be another factor that decreases LV volume and output in the setting of cor pulmonale and right ventricular enlargement. Several pulmonary diseases cause cor pulmonale, which may involve interstitial and alveolar tissues with a secondary effect on pulmonary vasculature or may primarily involve pulmonary vasculature. Chronic obstructive pulmonary disease (COPD) is the most common cause of cor pulmonale in the United States.
Cor pulmonale usually presents chronically, but 2 main conditions can cause acute cor pulmonale: massive pulmonary embolism (more common) and acute respiratory distress syndrome (ARDS). The underlying pathophysiology in massive pulmonary embolism causing cor pulmonale is the sudden increase in pulmonary resistance. In ARDS, 2 factors cause RV overload: the pathologic features of the syndrome itself and mechanical ventilation. Mechanical ventilation, especially higher tidal volume, requires a higher transpulmonary pressure. In chronic cor pulmonale, right ventricular hypertrophy (RVH) generally predominates. In acute cor pulmonale, right ventricular dilatation mainly occurs.
Frequency:
In the US: Cor pulmonale is estimated to account for 6-7% of all types of adult heart disease in the United States, with chronic obstructive pulmonary disease (COPD) due to chronic bronchitis or emphysema the causative factor in more than 50% of cases. Although the prevalence of COPD in the United States is about 15 million, the exact prevalence of cor pulmonale is difficult to determine because it does not occur in all cases of COPD and the physical examination and routine tests are relatively insensitive for the detection of pulmonary hypertension. In contrast, acute cor pulmonale usually is secondary to massive pulmonary embolism. Acute massive pulmonary thromboembolism is the most common cause of acute life-threatening cor pulmonale in adults. In the United States, 50,000 deaths are estimated to occur per year from pulmonary emboli and about half occur within the first hour due to acute right heart failure.
Internationally: Incidence of cor pulmonale varies among different countries depending on the prevalence of cigarette smoking, air pollution, and other risk factors for various lung diseases.
Mortality/Morbidity: Development of cor pulmonale as a result of a primary pulmonary disease usually heralds a poorer prognosis. For example, patients with COPD who develop cor pulmonale have a 30% chance of surviving 5 years. However, whether cor pulmonale carries an independent prognostic value or it is simply reflecting the severity of underlying COPD or other pulmonary disease is not clear. Prognosis in the acute setting due to massive pulmonary embolism or ARDS has not been shown to be dependent on presence or absence of cor pulmonale.
Showing posts with label Gynecology. Show all posts
Showing posts with label Gynecology. Show all posts
Thursday, 26 June 2008
Tuesday, 3 June 2008
Dysmenorrhea
Dysmenorrhea refers to the syndrome of painful menstruation. Primary dysmenorrhea occurs in the absence of pelvic pathology, whereas secondary dysmenorrhea results from identifiable organic diseases, most typically endometriosis, uterine fibroids, uterine adenomyosis, or chronic pelvic inflammatory disease. The prevalence of dysmenorrhea is estimated to be between 45 and 95% among reproductive-aged women. Although not life threatening, dysmenorrhea can be debilitating and psychologically taxing for many women and is one of the leading causes of absenteeism from work and school.
Pathophysiology
Historical attitudes toward menstrual pain were often dismissive. Pain was often attributed to women's emotional or psychological states, misconceptions about sex, and unhealthy maternal relations. Research has now established concrete physiologic explanations for dysmenorrhea, which discredit these prior theories.
Primary dysmenorrhea usually begins within the first 6-12 months after menarche once a regular ovulatory cycle has been established. During menstruation, sloughing endometrial cells release prostaglandins, which cause uterine ischemia through myometrial contraction and vasoconstriction. Elevated levels of prostaglandins have been measured in the menstrual fluid of women with severe dysmenorrhea. These levels are especially high during the first 2 days of menstruation. Vasopressin may also play a similar role.
Secondary dysmenorrhea may present at any time after menarche, but most commonly arises when a woman is in her 20s or 30s, after years of normal, relatively painless cycles. Elevated prostaglandins may also play a role in secondary dysmenorrhea, but, by definition, concomitant pelvic pathology must also be present. Common causes include endometriosis, leiomyomata (fibroids), adenomyosis, endometrial polyps, chronic pelvic inflammatory disease, and IUD use.
Frequency
United States
The prevalence of dysmenorrhea is estimated at 45-90%. This wide range can be explained by an assumed underreporting of symptoms. Many women self-medicate at home and never seek medical attention for their pain. As mentioned above, dysmenorrhea is responsible for significant absenteeism from work and school; 13-51% of women have been absent at least once, and 5-14% are repeatedly absent.
International
One longitudinal study from Sweden reported dysmenorrhea in 90% of women younger than 19 years and in 67% of women aged 24 years (French, 2005).
Mortality/Morbidity
Dysmenorrhea itself is not life threatening, but it can have a profoundly negative impact on a woman's day-to-day life. In addition to missing work or school, she may be unable to participate in sports or other activities, compounding the emotional distress brought on by the pain.
Race
No significant difference is apparent in the prevalence of dysmenorrhea among different populations.
Sex
Despite prevailing trends toward equality in the sexes, men are not yet known to experience dysmenorrhea.
Age
See Frequency above.
Read more HERE
Pathophysiology
Historical attitudes toward menstrual pain were often dismissive. Pain was often attributed to women's emotional or psychological states, misconceptions about sex, and unhealthy maternal relations. Research has now established concrete physiologic explanations for dysmenorrhea, which discredit these prior theories.
Primary dysmenorrhea usually begins within the first 6-12 months after menarche once a regular ovulatory cycle has been established. During menstruation, sloughing endometrial cells release prostaglandins, which cause uterine ischemia through myometrial contraction and vasoconstriction. Elevated levels of prostaglandins have been measured in the menstrual fluid of women with severe dysmenorrhea. These levels are especially high during the first 2 days of menstruation. Vasopressin may also play a similar role.
Secondary dysmenorrhea may present at any time after menarche, but most commonly arises when a woman is in her 20s or 30s, after years of normal, relatively painless cycles. Elevated prostaglandins may also play a role in secondary dysmenorrhea, but, by definition, concomitant pelvic pathology must also be present. Common causes include endometriosis, leiomyomata (fibroids), adenomyosis, endometrial polyps, chronic pelvic inflammatory disease, and IUD use.
Frequency
United States
The prevalence of dysmenorrhea is estimated at 45-90%. This wide range can be explained by an assumed underreporting of symptoms. Many women self-medicate at home and never seek medical attention for their pain. As mentioned above, dysmenorrhea is responsible for significant absenteeism from work and school; 13-51% of women have been absent at least once, and 5-14% are repeatedly absent.
International
One longitudinal study from Sweden reported dysmenorrhea in 90% of women younger than 19 years and in 67% of women aged 24 years (French, 2005).
Mortality/Morbidity
Dysmenorrhea itself is not life threatening, but it can have a profoundly negative impact on a woman's day-to-day life. In addition to missing work or school, she may be unable to participate in sports or other activities, compounding the emotional distress brought on by the pain.
Race
No significant difference is apparent in the prevalence of dysmenorrhea among different populations.
Sex
Despite prevailing trends toward equality in the sexes, men are not yet known to experience dysmenorrhea.
Age
See Frequency above.
Read more HERE
Monday, 2 June 2008
Rh Incompatibility
The Rh factor (ie, Rhesus factor) is a red blood cell surface antigen that was named after the monkeys in which it was first discovered. Rh incompatibility, also known as Rh disease, is a condition that occurs when a woman with Rh-negative blood type is exposed to Rh-positive blood cells, leading to the development of Rh antibodies.
Rh incompatibility can occur by 2 main mechanisms. The most common type occurs when an Rh-negative pregnant mother is exposed to Rh-positive fetal red blood cells secondary to fetomaternal hemorrhage during the course of pregnancy from spontaneous or induced abortion, trauma, invasive obstetric procedures, or normal delivery. Rh incompatibility can also occur when an Rh-negative female receives an Rh-positive blood transfusion. In part, this is the reason that blood banks prefer using blood type "O negative" or "type O, Rh negative," as the universal donor type in emergency situations when there is no time to type and crossmatch blood.
The most common cause of Rh incompatibility is exposure from an Rh-negative mother by Rh-positive fetal blood during pregnancy or delivery. As a consequence, blood from the fetal circulation may leak into the maternal circulation, and, after a significant exposure, sensitization occurs leading to maternal antibody production against the foreign Rh antigen.
Once produced, maternal Rh immunoglobulin G (IgG) antibodies may cross freely from the placenta to the fetal circulation, where they form antigen-antibody complexes with Rh-positive fetal erythrocytes and eventually are destroyed, resulting in a fetal alloimmune-induced hemolytic anemia. Although the Rh blood group systems consist of several antigens (eg, D, C, c, E, e), the D antigen is the most immunogenic; therefore, it most commonly is involved in Rh incompatibility.
Pathophysiology
The amount of fetal blood necessary to produce Rh incompatibility varies. In one study, less than 1 mL of Rh-positive blood was shown to sensitize volunteers with Rh-negative blood. Conversely, other studies have suggested that 30% of persons with Rh-negative blood never develop Rh incompatibility, even when challenged with large volumes of Rh-positive blood. Once sensitized, it takes approximately one month for Rh antibodies in the maternal circulation to equilibrate in the fetal circulation. In 90% of cases, sensitization occurs during delivery. Therefore, most firstborn infants with Rh-positive blood type are not affected because the short period from first exposure of Rh-positive fetal erythrocytes to the birth of the infant is insufficient to produce a significant maternal IgG antibody response.
The risk and severity of sensitization response increases with each subsequent pregnancy involving a fetus with Rh-positive blood. In women who are prone to Rh incompatibility, the second pregnancy with an Rh-positive fetus often produces a mildly anemic infant, whereas succeeding pregnancies produce more seriously affected infants who ultimately may die in utero from massive antibody-induced hemolytic anemia.
Risk of sensitization depends largely upon the following 3 factors:
Volume of transplacental hemorrhage
Extent of the maternal immune response
Concurrent presence of ABO incompatibility
The incidence of Rh incompatibility in the Rh-negative mother who is also ABO incompatible is reduced dramatically to 1-2% and is believed to occur because the mother's serum contains antibodies against the ABO blood group of the fetus. The few fetal red blood cells that are mixed with the maternal circulation are destroyed before Rh sensitization can proceed to a significant extent. Fortunately, ABO incompatibility usually does not cause serious sequela.
Rh incompatibility is only of medical concern for females who are pregnant or plan to have children in the future. Rh-positive antibodies circulating in the bloodstream of an Rh-negative woman otherwise have no adverse effects.
Frequency
United States
Only 15% of the population lack the Rh erythrocyte surface antigen and are considered Rh-negative. The vast majority (85%) of individuals are considered Rh positive. Rh sensitization occurs in approximately 1 per 1000 births to women who are Rh negative. The Southwest United States has an incidence approximately 1.5 times the national average, which likely is caused by immigration factors and limited access to medical care since blood typing is a routine part of prenatal care. Even so, only 17% of pregnant women with Rh-negative blood who are exposed to Rh-positive fetal blood cells ever develop Rh antibodies.
Mortality/Morbidity
During the course of Rh incompatibility, the fetus is primarily affected. The binding of maternal Rh antibodies produced after sensitization with fetal Rh-positive erythrocytes results in fetal autoimmune hemolysis. As a consequence, large amounts of bilirubin are produced from the breakdown of fetal hemoglobin and are transferred via the placenta to the mother where they are subsequently conjugated and excreted by the mother. However, once delivered, low levels of glucuronyl transferase in the infant preclude the conjugation of large amounts of bilirubin and may result in dangerously elevated levels of serum bilirubin and severe jaundice.
Mildly affected infants may have little or no anemia and may exhibit only hyperbilirubinemia secondary to the continuing hemolytic effect of Rh antibodies that have crossed the placenta.
Moderately affected infants may have a combination of anemia and hyperbilirubinemia/jaundice.
In severe cases of fetal hyperbilirubinemia, kernicterus develops. Kernicterus is a neurologic syndrome caused by deposition of bilirubin into central nervous system tissues. Kernicterus usually occurs several days after delivery and is characterized by loss of the Moro (ie, startle) reflex, posturing, poor feeding, inactivity, a bulging fontanelle, a high-pitched shrill cry, and seizures. Infants who survive kernicterus may go on to develop hypotonia, hearing loss, and mental retardation.
Another serious life-threatening condition observed in infants affected by Rh incompatibility is erythroblastosis fetalis, which is characterized by severe hemolytic anemia and jaundice. The most severe form of erythroblastosis fetalis is hydrops fetalis, which is characterized by high output cardiac failure, edema, ascites, pericardial effusion, and extramedullary hematopoiesis. Newborns with hydrops fetalis are extremely pale with hematocrits usually less than 5. Hydrops fetalis often results in death of the infant shortly before or after delivery and requires an emergent exchange transfusion by a neonatologist if there is to be any chance of infant survival.
Race
Approximately 15-20% of Caucasians, as opposed to 5-10% of African Americans, have the Rh-negative blood type.
Among individuals of Chinese and American Indian descent, the incidence of Rh-negative blood type is less than 5%.
CLINICAL
History of prior blood transfusion
Rh blood type of the mother
Rh blood type of the father (55% of Rh-positive men are genetically heterozygous for the Rh antigen and, therefore, produce Rh-negative offspring when mating with Rh-negative women 50% of the time.)
Previous pregnancies, including spontaneous and elective abortions
Previous administration of Rh IgG (RhoGAM)
Mechanism of injury in cases of maternal trauma during pregnancy
Presence of vaginal bleeding and/or amniotic discharge
Previous invasive obstetric procedures, such as amniocentesis, cordocentesis, chorionic villous sampling, or ectopic pregnancy
Note that a large fetal-maternal hemorrhage may occur without symptoms and with little or no evidence of trauma. Therefore, a high index of suspicion is warranted and a low threshold for treatment is indicated.
Physical
Evaluation of the vital signs and primary survey of the airway and cardiovascular system are indicated to ensure maternal stability.
A thorough pelvic examination is required.
In situations in which abdominal and/or pelvic trauma is a consideration, inspect for evidence of bruising that may suggest the possibility of significant fetomaternal hemorrhage.
When an infant with an Rh-negative mother is delivered in the emergency department, a thorough physical examination of the infant must be performed after initial stabilization, and a neonatologist must be consulted immediately.
Physical findings may vary from mild jaundice to extreme pallor and anemia with hydrops fetalis.
Causes
Factors that influence an Rh-negative pregnant female's chances of developing Rh incompatibility include the following:
Ectopic pregnancy
Placenta previa
Placental abruption
Abdominal/pelvic trauma
In utero fetal death
Any invasive obstetric procedure (eg, amniocentesis)
Lack of prenatal care
Spontaneous abortion
DIFFERENTIALS
Other Problems to be Considered
ABO incompatibility Autoimmune hemolytic anemia Microangiopathic hemolytic anemia Spherocytosis Hereditary enzyme deficiencies Alpha thalassemia Chronic fetomaternal hemorrhage Twin-twin transfusion Erythroblastosis fetalis Hydrops fetalis
Read more HERE
Rh incompatibility can occur by 2 main mechanisms. The most common type occurs when an Rh-negative pregnant mother is exposed to Rh-positive fetal red blood cells secondary to fetomaternal hemorrhage during the course of pregnancy from spontaneous or induced abortion, trauma, invasive obstetric procedures, or normal delivery. Rh incompatibility can also occur when an Rh-negative female receives an Rh-positive blood transfusion. In part, this is the reason that blood banks prefer using blood type "O negative" or "type O, Rh negative," as the universal donor type in emergency situations when there is no time to type and crossmatch blood.
The most common cause of Rh incompatibility is exposure from an Rh-negative mother by Rh-positive fetal blood during pregnancy or delivery. As a consequence, blood from the fetal circulation may leak into the maternal circulation, and, after a significant exposure, sensitization occurs leading to maternal antibody production against the foreign Rh antigen.
Once produced, maternal Rh immunoglobulin G (IgG) antibodies may cross freely from the placenta to the fetal circulation, where they form antigen-antibody complexes with Rh-positive fetal erythrocytes and eventually are destroyed, resulting in a fetal alloimmune-induced hemolytic anemia. Although the Rh blood group systems consist of several antigens (eg, D, C, c, E, e), the D antigen is the most immunogenic; therefore, it most commonly is involved in Rh incompatibility.
Pathophysiology
The amount of fetal blood necessary to produce Rh incompatibility varies. In one study, less than 1 mL of Rh-positive blood was shown to sensitize volunteers with Rh-negative blood. Conversely, other studies have suggested that 30% of persons with Rh-negative blood never develop Rh incompatibility, even when challenged with large volumes of Rh-positive blood. Once sensitized, it takes approximately one month for Rh antibodies in the maternal circulation to equilibrate in the fetal circulation. In 90% of cases, sensitization occurs during delivery. Therefore, most firstborn infants with Rh-positive blood type are not affected because the short period from first exposure of Rh-positive fetal erythrocytes to the birth of the infant is insufficient to produce a significant maternal IgG antibody response.
The risk and severity of sensitization response increases with each subsequent pregnancy involving a fetus with Rh-positive blood. In women who are prone to Rh incompatibility, the second pregnancy with an Rh-positive fetus often produces a mildly anemic infant, whereas succeeding pregnancies produce more seriously affected infants who ultimately may die in utero from massive antibody-induced hemolytic anemia.
Risk of sensitization depends largely upon the following 3 factors:
Volume of transplacental hemorrhage
Extent of the maternal immune response
Concurrent presence of ABO incompatibility
The incidence of Rh incompatibility in the Rh-negative mother who is also ABO incompatible is reduced dramatically to 1-2% and is believed to occur because the mother's serum contains antibodies against the ABO blood group of the fetus. The few fetal red blood cells that are mixed with the maternal circulation are destroyed before Rh sensitization can proceed to a significant extent. Fortunately, ABO incompatibility usually does not cause serious sequela.
Rh incompatibility is only of medical concern for females who are pregnant or plan to have children in the future. Rh-positive antibodies circulating in the bloodstream of an Rh-negative woman otherwise have no adverse effects.
Frequency
United States
Only 15% of the population lack the Rh erythrocyte surface antigen and are considered Rh-negative. The vast majority (85%) of individuals are considered Rh positive. Rh sensitization occurs in approximately 1 per 1000 births to women who are Rh negative. The Southwest United States has an incidence approximately 1.5 times the national average, which likely is caused by immigration factors and limited access to medical care since blood typing is a routine part of prenatal care. Even so, only 17% of pregnant women with Rh-negative blood who are exposed to Rh-positive fetal blood cells ever develop Rh antibodies.
Mortality/Morbidity
During the course of Rh incompatibility, the fetus is primarily affected. The binding of maternal Rh antibodies produced after sensitization with fetal Rh-positive erythrocytes results in fetal autoimmune hemolysis. As a consequence, large amounts of bilirubin are produced from the breakdown of fetal hemoglobin and are transferred via the placenta to the mother where they are subsequently conjugated and excreted by the mother. However, once delivered, low levels of glucuronyl transferase in the infant preclude the conjugation of large amounts of bilirubin and may result in dangerously elevated levels of serum bilirubin and severe jaundice.
Mildly affected infants may have little or no anemia and may exhibit only hyperbilirubinemia secondary to the continuing hemolytic effect of Rh antibodies that have crossed the placenta.
Moderately affected infants may have a combination of anemia and hyperbilirubinemia/jaundice.
In severe cases of fetal hyperbilirubinemia, kernicterus develops. Kernicterus is a neurologic syndrome caused by deposition of bilirubin into central nervous system tissues. Kernicterus usually occurs several days after delivery and is characterized by loss of the Moro (ie, startle) reflex, posturing, poor feeding, inactivity, a bulging fontanelle, a high-pitched shrill cry, and seizures. Infants who survive kernicterus may go on to develop hypotonia, hearing loss, and mental retardation.
Another serious life-threatening condition observed in infants affected by Rh incompatibility is erythroblastosis fetalis, which is characterized by severe hemolytic anemia and jaundice. The most severe form of erythroblastosis fetalis is hydrops fetalis, which is characterized by high output cardiac failure, edema, ascites, pericardial effusion, and extramedullary hematopoiesis. Newborns with hydrops fetalis are extremely pale with hematocrits usually less than 5. Hydrops fetalis often results in death of the infant shortly before or after delivery and requires an emergent exchange transfusion by a neonatologist if there is to be any chance of infant survival.
Race
Approximately 15-20% of Caucasians, as opposed to 5-10% of African Americans, have the Rh-negative blood type.
Among individuals of Chinese and American Indian descent, the incidence of Rh-negative blood type is less than 5%.
CLINICAL
History of prior blood transfusion
Rh blood type of the mother
Rh blood type of the father (55% of Rh-positive men are genetically heterozygous for the Rh antigen and, therefore, produce Rh-negative offspring when mating with Rh-negative women 50% of the time.)
Previous pregnancies, including spontaneous and elective abortions
Previous administration of Rh IgG (RhoGAM)
Mechanism of injury in cases of maternal trauma during pregnancy
Presence of vaginal bleeding and/or amniotic discharge
Previous invasive obstetric procedures, such as amniocentesis, cordocentesis, chorionic villous sampling, or ectopic pregnancy
Note that a large fetal-maternal hemorrhage may occur without symptoms and with little or no evidence of trauma. Therefore, a high index of suspicion is warranted and a low threshold for treatment is indicated.
Physical
Evaluation of the vital signs and primary survey of the airway and cardiovascular system are indicated to ensure maternal stability.
A thorough pelvic examination is required.
In situations in which abdominal and/or pelvic trauma is a consideration, inspect for evidence of bruising that may suggest the possibility of significant fetomaternal hemorrhage.
When an infant with an Rh-negative mother is delivered in the emergency department, a thorough physical examination of the infant must be performed after initial stabilization, and a neonatologist must be consulted immediately.
Physical findings may vary from mild jaundice to extreme pallor and anemia with hydrops fetalis.
Causes
Factors that influence an Rh-negative pregnant female's chances of developing Rh incompatibility include the following:
Ectopic pregnancy
Placenta previa
Placental abruption
Abdominal/pelvic trauma
In utero fetal death
Any invasive obstetric procedure (eg, amniocentesis)
Lack of prenatal care
Spontaneous abortion
DIFFERENTIALS
Other Problems to be Considered
ABO incompatibility Autoimmune hemolytic anemia Microangiopathic hemolytic anemia Spherocytosis Hereditary enzyme deficiencies Alpha thalassemia Chronic fetomaternal hemorrhage Twin-twin transfusion Erythroblastosis fetalis Hydrops fetalis
Read more HERE
Friday, 30 May 2008
Corpus Luteum Rupture
Ruptured corpus luteum is a common phenomenon with presentation ranging from no symptoms to symptoms mimicking an acute abdomen. Sequelae vary. Resolution may be spontaneous (most often); intraperitoneal hemorrhage and death may occur. Although most patients require only observation, some need laparoscopy or laparotomy to achieve hemostasis.
Pathophysiology
Each month, a mature ovarian follicle ruptures, releasing an ovum so the process of fertilization can begin. Occasionally, this rupture site may bleed, causing abdominal pain and signs of hemorrhage. The etiology of this increased bleeding is unknown, although abdominal trauma and anticoagulation treatments may increase the risk.
Frequency
United States
Occurrence is unknown but is likely quite frequent and without symptoms.
International
Occurrence is unknown but is likely quite frequent and without symptoms.
Mortality/Morbidity
Although circulatory collapse, hemorrhagic shock, disseminated intravascular coagulation (DIC), and death have been reported, these are rare. Most cases are self-limiting, with abdominal pain relieved with analgesics.
Race
No differences in frequency are reported by race or socioeconomic standing.
Sex
Ruptured corpus luteum occurs only in females.
Age
The condition most commonly occurs in women aged 18-35 years (peak reproductive years).
Read more HERE
Pathophysiology
Each month, a mature ovarian follicle ruptures, releasing an ovum so the process of fertilization can begin. Occasionally, this rupture site may bleed, causing abdominal pain and signs of hemorrhage. The etiology of this increased bleeding is unknown, although abdominal trauma and anticoagulation treatments may increase the risk.
Frequency
United States
Occurrence is unknown but is likely quite frequent and without symptoms.
International
Occurrence is unknown but is likely quite frequent and without symptoms.
Mortality/Morbidity
Although circulatory collapse, hemorrhagic shock, disseminated intravascular coagulation (DIC), and death have been reported, these are rare. Most cases are self-limiting, with abdominal pain relieved with analgesics.
Race
No differences in frequency are reported by race or socioeconomic standing.
Sex
Ruptured corpus luteum occurs only in females.
Age
The condition most commonly occurs in women aged 18-35 years (peak reproductive years).
Read more HERE
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