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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pregnancy-induced hypertension is a disorder of unknown etiology unique to pregnant women. Classic clinical manifestations include hypertension, proteinuria, and edema. Early recognition and proper management of this disease may serve to avoid serious maternal complications. Ultimate maternal treatment depends on delivery of the fetus and placenta. Advanced stages of this disease result in multi-organ system dysfunction that may be life-threatening to the mother and her fetus. Such maternal complications of PIH include severe hypertension, oliguria or anuria, HELLP syndrome, eclamptic seizures, liver rupture, pulmonary edema, cerebral edema, and abruptio placentae. A multidisciplinary approach of the critical care team often will effect a reduction in maternal morbidity and mortality.
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PMID:Management of severe preeclampsia and eclampsia. 174 3

Many neurologic disorders, such as eclampsia, pseudotumor cerebri, stroke, obstetric nerve palsies, subarachnoid hemorrhage, pituitary tumors, and choriocarcinoma, can develop in the pregnant patient. Maternal mortality from eclampsia, which ranges from 0 to 14%, can be due to intracerebral hemorrhage, pulmonary edema, disseminated intravascular coagulation, abruptio placentae, or failure of the liver or kidneys. Associated fetal mortality ranges from 10 to 28% and is directly related to decreased placental perfusion. Pseudotumor cerebri can be associated with serious visual complications; thus, the therapeutic goal is to prevent loss of vision. The risk of stroke in the pregnant patient is 13 times the risk in the nonpregnant patient of the same age. The major causes of stroke in pregnant patients are arterial occlusion and cerebral venous thrombosis. Lumbar disk prolapse is common in pregnant patients, and lumbosacral plexus injuries can occur during labor or delivery. In addition, peripheral nerve compression or entrapment syndromes are thought to be caused by the retention of fluid during pregnancy. The incidence of subarachnoid hemorrhage during pregnancy is 1 in every 10,000 patients, a rate 5 times higher than in nonpregnant women. Because of a proliferation of prolactin-secreting cells, the pituitary gland can enlarge dramatically during pregnancy, a change that can disclose a previously unknown tumor or cause a known pituitary tumor to become symptomatic. The incidence of choriocarcinoma is 1 in 50,000 full-term pregnancies but 1 in 30 molar pregnancies. This malignant tumor has a high rate of cerebral metastatic lesions. In addition to these disorders that develop during pregnancy, the pregnant state can affect numerous preexisting neurologic conditions, including epilepsy, headaches, multiple sclerosis, myasthenia gravis, spinal cord injury, and brain tumors. We discuss advice for patients with such conditions who wish to become pregnant, recommendations for medical and surgical management, and surgical considerations for neurologic complications during pregnancy.
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PMID:Selected neurologic complications of pregnancy. 225 22

During a 12-year period, 254 cases of eclampsia were managed at this center. Eighty patients (32%) did not have edema, 58 (23%) had "relative hypertension," and 49 (19%) did not have proteinuria at the time of convulsions. Eclampsia developed at less than or equal to 20 weeks in 6 patients and beyond 48 hours post partum in 40 (16%). Convulsions developed in 33 while they were receiving standard doses of magnesium sulfate for preeclampsia during or after birth, and subsequent seizures developed in 36 (14%) after magnesium sulfate therapy was started. There was one maternal death (0.4%) and morbidity was frequent (acute renal failure, 4.7%; pulmonary edema, 4.3%; cardiorespiratory arrest, 3.1%; and aspiration, 2%. The use of multiple drug therapy was associated with significant maternal and neonatal complications. The total perinatal mortality was 11.8%, with the majority of them related to either abruptio placentae or extreme prematurity. These findings emphasize the need for intensive monitoring of women with preeclampsia throughout hospitalization and underscore the importance of maternal stabilization before and during transfer.
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PMID:Eclampsia. VI. Maternal-perinatal outcome in 254 consecutive cases. 240 30

During approximately a 9-year period, 37 severe preeclamptic-eclamptic patients had pulmonary edema for an incidence of 2.9%. The incidence was significantly higher in older patients (p less than 0.0001) and in multigravid patients (p less than 0.05). Eleven (30%) had antepartum edema with 10 (90%) of the 11 having preexisting chronic hypertension. Twenty-six (70%) had postpartum edema with an average onset of 71 hours post partum. The majority of these patients had excessive colloid and crystalloid infusions for various medical, surgical, and obstetric complications. There were four maternal deaths and morbidity was significant. Eighteen patients had disseminated intravascular coagulopathy, 17 had sepsis, 12 had abruptio placentae, 10 had acute renal failure, six had hypertensive crisis, five had cardiopulmonary arrest, two had rupture of the liver, and two had ischemic cerebral damage. The overall perinatal mortality was 530/1000 and neonatal morbidity was significant. Pulmonary edema is infrequent in severe preeclampsia-eclampsia without associated medical, surgical and obstetric complications. The occurrence of pulmonary edema in such patients is associated with high maternal and perinatal mortality and morbidity.
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PMID:Pulmonary edema in severe preeclampsia-eclampsia: analysis of thirty-seven consecutive cases. 357 33

Liver pathology is one of the main features of HELLP syndrome and develops on the basis of a generalised activation of intravascular coagulation. Fibrin deposits and haemorrhagic necrosis predominantly develop in the periportal areas and may eventually lead to subcapsular haematomas or even rupture of the liver. While the compensated form of activation of intravascular coagulation, which is diagnosed by a decrease in antithrombin III and an increase in thrombin-antithrombin III complex (TAT) and the appearance of fibrin, monomers and D-dimers, is found in almost all cases of HELLP syndrome, the decompensated form of intravascular coagulation with prolonged bleeding time (PT, PTT) and drop in fibrinogen is found only in the most severe forms. The development of a decompensation of coagulation correlates with the appearance of severe complications such as liver haematoma, abruptio placentae, renal failure and pulmonary oedema. The best prophylaxis against the development of life-threatening complications is early diagnosis and termination of pregnancy after stabilisation of the maternal condition, consisting of magnesium sulphate infusion, antihypertensive treatment with dihydralazine or calcium antagonists, steroids etc. Severe complications of HELLP syndrome have occasionally been observed in the postpartum period. As prophylaxis against postpartal worsening of HELLP syndrome, curettage of the uterus and continuation of the treatment with calcium antagonists and dexamethasone have been recommended.
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PMID:[Liver pathology within the scope of HELLP syndrome]. 784 9

Fifty patients with severe pre-eclampsia who presented before 32 weeks' gestation were managed conservatively (sedation, bed rest, antihypertensive therapy and intensive fetal and maternal monitoring) until intervention was indicated. Twelve patients presented before 26 weeks of pregnancy and there were no fetal survivors in this group; 23 presented between 26 and 29 weeks and 8(34,8%) of the babies in this group survived. The rate of perinatal loss in those presenting between 30 and 32 weeks was 26,6% (N = 4). Patients who had a history of a hypertensive disorder in their previous pregnancy(ies) had a higher perinatal mortality rate; 23 such mothers experienced 16 perinatal losses compared with 27 mothers who had no such history and who had only 8 perinatal losses. There was 1 maternal death, there were 2 cases of eclampsia, 3 of pulmonary oedema, 4 of abruptio placentae and 1 case of renal failure; 2 patients had disseminated intravascular coagulation. The local indigent and underprivileged black population have a more aggressive form of early onset of severe pre-eclampsia than that reported for other population groups. The high maternal complication rate of 30,8% and the low fetal survival rate before 26 weeks indicate that there is no place in our setting for expectant management of severe pre-eclampsia in patients presenting before 26 weeks. This applies particularly to those with a previous history of hypertension in pregnancy.
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PMID:Expectant management of early onset of severe pre-eclampsia in Durban. 821 21

Nineteen adolescent patients with eclampsia were studied in the course of 6 years. In 68% of the cases eclampsia (E) occurred antepartum, in 5% intrapartum. Maternal mortality was 52.65% (one patient with HELLP syndrome). Serious maternal morbidity included disseminated intravascular coagulations (10.52%), abruptio placentae (15.8%), pulmonary edema (5.26%) and acute renal failure (5.26%). Abruptio placentae was strongly correlated with the development of disseminated intravascular coagulation (p 0.0001), acute renal failure (p 0.001) and pulmonary edema (p 0.001). Eclampsia and HELLP syndrome were the most dangerous complications in adolescent pregnancies. They are associated with a serious maternal morbidity, especially when it arises in the postpartum period.
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PMID:[The perinatal outcome in adolescents with eclampsia and the HELLP syndrome]. 896 29

HELLP syndrome in the parturient (hemolysis, elevated liver enzymes, and low platelet count) is associated with poor maternal and fetal outcomes. Maternal mortality has been estimated to be as high as 24%. Patients with HELLP syndrome are also at greater risk of pulmonary edema, adult respiratory distress syndrome, abruptio placentae, disseminated intravascular coagulation, ruptured liver hematomas, and acute renal failure. Perinatal mortality is equally high, ranging from 79 to 367 per 1,000 live births, and neonatal complications correlate with the severity of maternal disease. Many clinicians view HELLP syndrome as an entity of preeclampsia, and because of varied symptomatology, the initial diagnosis may be obscured. Prodromal signs include: (1) weakness and fatigue, (2) nausea and vomiting, (3) right upper quadrant and/or epigastric pain, (4) headache, (5) changes in vision, (6) increased tendency to bleed from minor trauma, (7) jaundice, (8) diarrhea, and (9) shoulder or neck pain. Before delivery, aggressive obstetric management is directed toward stabilization of the affected organ systems, if possible, and timely interruption of the pregnancy in the early phase of the accelerated disease progression. Definitive therapy is delivery. Parturients with HELLP syndrome are often critically ill; their infants are frequently premature and their conditions are compromised. Management criteria should include a multidisciplinary approach in a tertiary care center. Obstetric anesthesia personnel should perform a thorough preanesthetic evaluation and be familiar with the pathophysiologic changes of this syndrome. Determining the anesthetic of choice depends on the patient's condition, fetal well-being, and the urgency of the situation. In the presence of severe coagulopathy, regional anesthesia is contraindicated.
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PMID:HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) pathophysiology and anesthetic considerations. 922 38

We studied 19 peripartum patients with acute respiratory failure associated with pregnancy. Although it is an uncommon event, noncardiogenic pulmonary edema is the most common cause of respiratory failure in the peripartum period. This acute lung injury syndrome was observed to be associated with a variety of complications of pregnancy including premature labor, the use of tocolytics, infection, hypertension, leukoagglutinin reactions, aspiration, abruptio placentae, and amniotic fluid embolism. From 1989 through 1992 there were 10,852 deliveries and 19 patients with noncardiogenic pulmonary edema at our institution. Analyzing these cases has led us to favor the hypothesis that the respiratory failure associated with the various complications of pregnancy primarily represents the fatal and nonfatal cases of amniotic fluid embolism that Steiner and Lushbaugh initially believed undoubtedly to exist. Moreover, we suggest, as have others, that the nonspecific symptom complex of inflammation, coagulopathy, and cardiopulmonary failure represents the release of soluble mediators into the maternal circulation. It is not clear what the predominant mediator is, but we have focused on platelet activating factor. It is also not established whether the mediator(s) is of amniotic fluid origin or a result of maternal anaphylactoid-type of response to a fetal or amnioplacental antigen. In conclusion, monitoring maternal oxygenation either directly or indirectly by oximetry should be considered routinely in the peripartum period, especially in complicated pregnancies, to detect at an early stage "asymptomatic" or preclinical cases of noncardiogenic pulmonary edema, in hopes of then modifying management to prevent their progression.
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PMID:Acute respiratory failure in pregnancy. An analysis of 19 cases. 946 62

Chronic hypertension in pregnancy is associated with increased rates of adverse maternal and fetal outcomes both acute and long term. These adverse outcomes are particularly seen in women with uncontrolled severe hypertension, in those with target organ damage, and in those who are noncompliant with prenatal visits. In addition, adverse outcomes are substantially increased in women who develop superimposed preeclampsia or abruptio placentae. Women with chronic hypertension should be evaluated either before conception or at time of first prenatal visit. Depending on this evaluation, they can be divided into categories of either "high risk" or "low risk" chronic hypertension. High-risk women should receive aggressive antihypertensive therapy and frequent evaluations of maternal and fetal well-being, and doctors should recommend lifestyle changes. In addition, these women are at increased risk for postpartum complications such as pulmonary edema, renal failure, and hypertensive encephalopathy for which they should receive aggressive control of blood pressure as well as close monitoring. In women with low-risk (essential uncomplicated) chronic hypertension, there is uncertainty regarding the benefits or risks of antihypertensive therapy. In my experience, the majority of these women will have good pregnancy outcomes without the use of antihypertensive medications. Antihypertensive agents are recommended and are widely used in these women despite absent evidence of either benefits or harm from this therapy. These recommendations are based on dogma and consensus rather than on scientific evidence. There is an urgent need to conduct randomized trials in women with mild chronic hypertension in pregnancy.
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PMID:Chronic hypertension in pregnancy. 1246 90


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