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Gelatin sponge embolization. a method for the management of iatrogenic preterm premature rupture of the membranes.

Despite the morbidity and mortality associated with early midtrimester premature rupture of the membranes (PROM), limited therapeutic options currently exist for its treatment. A new operative approach to this condition termed embolization involves intra-uterine administration of a gelatin sponge which can remarkably reduce or eliminate further loss of amniotic fluid. A successful case of embolization for the treatment of iatrogenic previable PROM complicating therapeutic fetoscopy is described.

Adult↗

Maternal mortality in Iowa from 1952 to 1986.

The frequency of maternal death is decreasing in Iowa, particularly in the category of direct obstetric causes, such as hemorrhage, infection, pre-eclampsia and eclampsia. Unfortunately, concurrent linkage of vital statistics records was not performed during the study period, precluding any certain conclusion that all maternal deaths were actually identified (29). In addition, there has been, at best, only a modest decrease in the proportion of direct obstetric deaths that are preventable, suggesting that the educational goals of the maternal mortality review process are as yet far from fulfilled. In particular, the number of embolic deaths, both from pulmonary emboli and amniotic fluid emboli, has remained constant. We now appreciate many predisposing risk factors for pulmonary embolization and must seriously consider prophylactic anticoagulation in pregnant or puerperal women at increased risk. We also need further studies in the pathogenesis, treatment and prevention of amniotic fluid emboli. Although associated with lower proportions of preventability than with direct causes of obstetric deaths, the indirect and nonobstetric categories of maternal deaths have also been associated with a less dramatic decline in numbers. In particular, trauma remains a persistent cause of preventable maternal death. Continued public education as well as legislation for mandatory safety restraints in automobiles may reverse this trend. This suggests that considerable room for improvement exists in the field of education of patients and of health care professionals who routinely care for patients with complicated obstetric problems.

Adolescent↗

Crisis management during anaesthesia: embolism.

BACKGROUND: Embolism with gas, thrombus, fat, amniotic fluid, or particulate matter may occur suddenly and unexpectedly during anaesthesia, posing a diagnostic and management problem for the anaesthetist. OBJECTIVES: To examine the role of a previously described core algorithm "COVER ABCD-A SWIFT CHECK" supplemented by a specific sub-algorithm for embolism, in the management of embolism occurring in association with anaesthesia. METHODS: The potential performance of this structured approach for each of the relevant incidents among the first 4000 reported to the Australian Incident Monitoring Study (AIMS) was compared with the actual management as reported by the anaesthetists involved. RESULTS: Among the first 4000 incidents reported to AIMS, 38 reports of embolism were found. A sudden fall in end-tidal carbon dioxide and oxygen saturation were the cardinal signs of embolism, each occurring in about two thirds of cases, with hypotension and electrocardiographic changes each occurring in about one third of cases. CONCLUSION: The potential value of an explicit structured approach to the diagnosis and management of embolism was assessed in the light of AIMS reports. It was considered that, correctly applied, it potentially would have led to earlier recognition of the problem and/or better management in over 40% of cases.

Algorithms↗

[Clinico-laboratory and pathomorphologic study of intravascular blood coagulation syndrome in experimental amniotic embolism].

The time-course of hemocoagulative and morphological changes affected by intravenous administration of amniotic fluids was examined in experiments on Chinchilla rabbits weighing 2.0-2.5 kg. Laboratory studies revealed profound phasic changes in hemocoagulation (hyper- and hypocoagulation) which were typical of the DIC syndrome. At the same time, pronounced hemocirculatory abnormalities were pathomorphologically detected chiefly in the lung; there were also highly moderate phenomena of platelet aggregation and thrombus formation. These findings suggest that the contribution made by the demands of coagulative factors is not so significant in the pathogenesis of microcirculatory abnormalities in amniotic embolism as it is generally accepted today. The paper provides evidence for expediency of performing special investigations to elucidate the real role which the DIC syndrome plays in the pathogenesis of microcirculatory abnormalities in other diseases.

Animals↗

Acute circulatory and respiratory collapse in obstetrical patients: a case report and review of the literature.

Venous air embolism is the entrapment of air into the venous system producing signs and symptoms due to obstruction of pulmonary arterial blood flow. We present a healthy, 27-year-old, full-term parturient admitted for postdate induction of labor. Cesarean delivery was required following fetal distress. During delivery, the mother became bradycardic and required advanced cardiac life support for resuscitation. Serial hemoglobin values, electrocardiograms, echocardiograms, and a magnetic resonance image of the head were all normal. No fetal squamous cells were found in the patient's blood. She required 6 days of ventilation, was successfully extubated, and was discharged 14 days after the cesarean delivery. The differential diagnosis in this patient's care centered on a pulmonary embolic event. Thromboembolism was unlikely, based upon the patient's rapid clinical improvement without definitive therapy for thrombotic disease or detection of peripheral thrombosis. Amniotic fluid embolus was unlikely, although not excluded, by the absence of fetal cells in the maternal circulation and the lack of an accompanying intravascular coagulopathy. Air embolism may occur in up to 50% of women undergoing cesarean delivery. A lethal embolism may follow a bolus of 3 to 5 mL/kg of air. Chief among the many symptoms of air embolism are tachypnea, chest pain, and gasping. The diagnosis may be facilitated by precordial Doppler monitoring, transesophageal echocardiography, or by the identification of air when aspirating from a right heart catheter. Management includes optimum patient positioning, aspiration of air, discontinuation of nitrous oxide, administration of 100% oxygen, and flooding the surgical site with saline to avoid further air entry. Preventive strategies are also discussed.

Acute Disease↗

Effects of intrauterine growth restriction and intraamniotic insulin-like growth factor-I treatment on blood and amniotic fluid concentrations and on fetal gut uptake of amino acids in late-gestation ovine fetuses.

OBJECTIVES: To investigate, in the late-gestation ovine fetus: 1) amino acid concentrations in blood and amniotic fluid, 2) the effects of intrauterine growth restriction (IUGR) induced by placental embolization on these concentrations, 3) fetal gut uptake of glutamine in healthy and IUGR fetuses, and 4) the effects of intraamniotic insulin-like growth factor-I (IGF-1) treatment on these parameters. METHODS: Fetuses were randomly assigned to control (n = 9), IUGR + saline (n = 9), or IUGR + IGF-1 (n = 11) groups. IUGR was induced by uteroplacental embolization from 114 to 119 days (term = 145 days). IUGR fetuses received daily intraamniotic injections of saline or IGF-1 (20 microg/d) from 120 to 130 days. RESULTS: Baseline amino acid concentration was higher in fetal blood than amniotic fluid for all essential amino acids except lysine and histidine, but was lower for serine, alanine, and methylhistidine. Embolization reduced total amino acid concentration in blood and amniotic fluid by approximately 15%. Concentrations were reduced for serine, glutamine, and methylhistidine in blood and for serine in amniotic fluid, but were increased for glycine, alanine, and asparagine in blood and for alanine in amniotic fluid. Glutamine was taken up by the fetal gut (glutamine:oxygen quotient of 0.65) and citrulline was released by the gut. IGF-1 treatment did not alter amino acid concentration in blood or amniotic fluid, but reduced gut uptake of glutamine from blood and the gut glutamine:oxygen quotient by 15%. Citrulline release was unchanged. CONCLUSIONS: These data suggest that amniotic fluid amino acids are not simply filtered from fetal blood and may provide an important pool of nutrients for the fetus. They demonstrate for the first time that glutamine is taken up by the fetal gut. IGF-1 treatment may promote gut utilization of amino acids from the amniotic fluid pool.

Amino Acids↗

Is there a place for inhaled nitric oxide in the therapy of acute pulmonary embolism?

Acute pulmonary embolism (PE) is a serious complication resulting from the migration of emboli to the lungs. Although deep venous thrombi are the most common source of emboli to the lungs, other important sources include air, amniotic fluid, fat and bone marrow. Regardless of the specific source of the emboli, very little progress has been made in the pharmacological management of this high mortality condition. Because the prognosis is linked to the degree of elevation of pulmonary vascular resistance, any therapeutic intervention to improve the hemodynamics would probably increase the low survival rate of this critical condition. Inhaled nitric oxide (iNO) has been widely tested and used in cases of pulmonary hypertension of different causes. In the last few years some authors have described beneficial effects of iNO in animal models of acute PE and in anecdotal cases of massive PE. The primary cause of death in massive PE that is caused by deep venous thrombi, gas or amniotic fluid, is acute right heart failure and circulatory shock. Increased pulmonary vascular resistance following acute PE is the cumulative result of mechanical obstruction of pulmonary vessels and pulmonary arteriolar constriction (attributable to a neurogenic reflex and to the release of vasoconstrictors). As such, the vasodilator effects of iNO could actively oppose the pulmonary hypertension following PE. This hypothesis is consistently supported by experimental studies in different animal models of PE, which demonstrated that iNO decreased (by 10 to 20%) the pulmonary artery pressure without improving pulmonary gas exchange. Although maximal vasodilatory effects are probably achieved by less than 5 parts per million iNO, which is a relatively low concentration, no dose-response study has been published so far. In addition to the animal studies, a few anecdotal reports in the literature suggest that iNO may improve the hemodynamics during acute PE. However, no prospective, controlled, randomized clinical trial addressing this issue has been conducted to date. Future investigations addressing the effects of iNO combined with other drugs such as vasoconstrictors and inhibitors of phosphodiesterase III or V, may increase the responsiveness to iNO in acute PE.

Acute Disease↗

Amniotic fluid and fetal urinary responses to severe placental insufficiency in sheep.

OBJECTIVE: Our purpose was to test the hypothesis that severe placental insufficiency leads to reductions in fetal urine production and amniotic fluid volume in late-gestation fetal sheep. STUDY DESIGN: At 0.85 of gestation, chronically catheterized fetal sheep with ligated urachus were either embolized for 5 days by repeated injection of boluses of 15-microm microspheres into the common fetal umbilical artery until fetal arterial oxygen content was reduced by 50% (n = 6) or were infused with saline solution (n = 6). Amniotic fluid volume was measured daily before embolization by means of an indicator dilution technique and by drainage at autopsy. Fetal urine production, heart rate, and mean arterial blood pressure were measured continuously for 1 hour before embolization and 1 hour after embolization each day. Fetal arterial blood gases, oxygen content, electrolytes, and osmolality were also monitored. RESULTS: Five days of placental insufficiency, which reduced fetal arterial oxygen content by 50% and arrested fetal growth, resulted in a reduced amniotic fluid volume without a reduction in fetal urine production. Compared with that of controls, amniotic fluid volume was reduced over the 5-day period by 547 +/- 144 mL (-62%, P <.01). Amniotic fluid composition was also altered, with a significant increase in lactate and sodium concentrations and osmolality on days 4 to 5. On days 2 to 5, there was a progressive increase in amniotic fluid osmolality above that of controls, which paralleled the changes in amniotic fluid sodium concentration (P <.05). Fetuses became hypertensive on days 2 to 4 of embolization, although this response was attenuated by day 5. CONCLUSIONS: Chronic severe placental insufficiency caused a reduction in amniotic fluid volume not attributable to reduced fetal urine production. Changes in amniotic fluid composition induced by placental insufficiency suggest an excess intramembranous absorption of amniotic fluid water, in relation to solutes, into the fetal and maternal compartments, which may lead to the development of oligohydramnios.

Amniotic Fluid↗

Intrapulmonary neuroglial heterotopia.

Nonteratomatous intrapulmonary neuroglial heterotopia not associated with birth trauma or frank vascular embolization has been described rarely. This article briefly reviews the literature, and presents two additional cases of intrapulmonary neuroglial heterotopia. We found 14 cases in the literature. Twelve of these cases had central nervous system disruption, where neuroglial elements were in direct contact with amniotic fluid. Several hypotheses have been proposed, including fetal aspiration of detached neural fragments within amniotic fluid, neural crest migration defects, and vascular embolization with implantation. Of our two cases, one represents the first occurrence where central nervous system abnormalities were secondary to mechanical disruption, rather than to a primary neural tube defect. Our second case represents the youngest documented occurrence (17 weeks gestation) of intrapulmonary neuroglial heterotopia. Additionally, immunohistochemical studies were performed on these lesions, the results of which favor their neural origin. We present these findings and suggest they support the aspiration mechanism for neuroglial heterotopia in lung tissue.

Abnormalities, Multiple↗

[Perioperative pulmonary embolism: a nationwide survey in Japan].

Pulmonary embolism is a leading cause of death and morbidity in the perioperative period. To obtain a contemporary overview of the epidemiology of acute pulmonary embolism, a questionnaire was mailed to anesthesia department chair-persons at 179 hospitals in Japan. The 158 cases were reported from the 88 hospitals. The cause of embolism was thromboembolism 127, gas 13, fat 9, amniotic fluid 4 and tumor 3. The mortality rate for patients with thromboembolism was high (29%). Dyspnea was the most frequent symptom (60%) and hypotension was the most frequent clinical sign (54%). The signs which suggested massive pulmonary embolism, such as hypotension, cyanosis (53%), syncope (39%) and cardiac arrest (29%) were frequently seen. Most of the pulmonary embolisms occurred during the operation and within 7 days after the operation. The high risk factors associated with thromboembolism were age, malignancy, obesity and the type of surgery performed. Treatment performed included anticoagulation 81%, catecholamine infusion 66%, thrombolysis 14%, surgical embolectomy 8% and extra-corporeal circulation 4%. This study indicates that the perioperative pulmonary embolism is still associated with high mortality and requires an immediate diagnosis and intensive therapy.

Adolescent↗

The missing link. An unusual case of embolization.

Embolization is a well-recognized phenomenon in medicine and forensic pathology and generally involves formed blood elements, bone, air, amniotic fluid, or more exotic items such as bullets. We report the embolization of a chain-saw link. The case demonstrates how, without complete autopsy and investigation, a penetrating sharp-force injury could be misdiagnosed and a false conclusion as to the commission of a crime could occur. Although the forensic literature is replete with examples of bizarre emboli, from bullets to suspected crystals of methylmethacrylate, a literature review failed to find a single case of penetrating chain-saw-link injury as a cause of traumatic death. Most reports of chain-saw incidents cite accidental injuries to hands and arms or dramatic facial injuries due to entrapment and recoil (1,2). One fatality occurred from a skull fracture and cerebral injury when a 19-year-old man fell onto a saw.

Aged↗

[Ectopic neuroglial tissue associated with intrapulmonary congenital cystic adenomatoid malformation].

BACKGROUND: Few cases of ectopic neurological tissue have been reported in the lung. The aim of the present study was to give a brief overview of these cases and to examine an additional case of intrapulmonary neuroglial heterotopia. We have identified only sixteen similar cases in the literature. CASE DESCRIPTION: The object of our study was a male fetus of Asian parents at the 23rd week of gestation, in which ultrasound tests revealed the presence of anterior encephalocele. Routine postmortem examination of lung samples showed neuroglial tissue and a congenital adenomatoid cystic malformation of type II. The lesion was made up of multiple small cysts lined with columnar or ciliated cuboidal epithelium. A possible link between adenomatoid malformation and intrapulmonary neurological tissue has not so far been reported in the literature. Immunohistochemical analysis showed the presence in the pulmonary parenchyma of neuronal cells (neuron-specific enolase positive), astrocytes (glial fibrillary acidic protein positive) and intra-alveolar squamous cells (citokeratines positive), indicative of fetal aspiration of amniotic fluid. CONCLUSIONS: There are several possible explanations for the presence of intrapulmonary neuroglial heterotopia: fetal aspiration, neural crest migration defects or vascular embolization with implantation. However, in the view of the microscopic findings and at the same time recognizing the intrapulmonary aspiration of amniotic fluid, the authors maintain that the most likely explanation for the heterotopia is that of consequential multiple malformations. Moreover neuroglial ectopy and cystic adenomatoid congenital malformation of the lung could have appeared simultaneously, due to embryologic insult between the 4th and the 20th week of gestation.

Choristoma↗

Sources of amniotic fluid erythropoietin during normoxia and hypoxia in fetal sheep.

OBJECTIVE: Erythropoietin is present in human amniotic fluid and has been suggested as a marker of fetal hypoxia. The objectives of the present study were to determine whether erythropoietin is present in ovine amniotic fluid, fetal urine, and/or lung liquid and whether concentrations in these compartments change in parallel with endogenous fetal plasma erythropoietin concentration when the latter is increased experimentally. STUDY DESIGN: In late gestation chronically catheterized fetal sheep, samples of amniotic fluid and plasma, urine and plasma, lung liquid, amniotic fluid, and plasma were collected before and up to 7 days after induction of 4 types of fetal hypoxia: (1) acute anemic hypoxia that was induced by a single fetal hemorrhage, (2) progressive anemic hypoxia that was induced by daily exchange transfusion, (3) acute hypoxic hypoxia that was induced by the reduction of maternal inspired oxygen content, or (4) chronic placental insufficiency that was induced by daily umbilicoplacental embolization for 4 days. Erythropoietin concentrations were determined by radioimmunoassay. Statistical testing included analysis of variance and least squares regression. RESULTS: Under basal, nonhypoxic conditions, amniotic fluid erythropoietin concentration averaged 33.2% +/- 1.6% (SE) of fetal plasma erythropoietin concentration, and basal fetal urine and lung liquid erythropoietin concentrations ranged from low (<10% of plasma concentration) to nondetectable. Unlike the strong correlation in humans, basal amniotic fluid and plasma erythropoietin concentrations were correlated only weakly (r = 0.259; r2 = 6.7%; P = .0027; n = 132). Amniotic fluid erythropoietin concentration approximately doubled after 12 hours of severe hypoxic hypoxia or after 24 hours of embolization-induced severe hypoxia but was unchanged after 12 hours of mild-moderate hypoxic hypoxia or 24 hours of anemic hypoxia. Concomitant fetal plasma erythropoietin concentrations increased to 28.1 +/- 5.3, 12.5 +/- 2.7, 10.8 +/- 4.6, and 10.0 +/- 1.3 times basal values, respectively. During progressive fetal anemia, urinary erythropoietin concentration increased almost 10-fold (P = .0023) but remained a small fraction (3.7% +/- 0.4%) of plasma concentration; at 12 hours of hypoxic hypoxia, lung liquid erythropoietin concentration did not vary with the severity of the hypoxia and remained low relative to plasma concentration (4.2% +/- 2.1%). CONCLUSION: Erythropoietin is present in ovine amniotic fluid, urine, and lung liquid. With only 3 potential sources, the fetal membranes appear to be the primary source of amniotic fluid erythropoietin in the nonhypoxic ovine fetus because basal urine and lung liquid erythropoietin concentrations are much lower than amniotic fluid concentrations. Although unchanged during mild-to-moderate fetal hypoxia, amniotic fluid erythropoietin concentration increases modestly during severe fetal hypoxia. In sheep, fetal urinary erythropoietin may contribute to this rise in amniotic fluid erythropoietin concentration during severe hypoxia, because fetal urinary and plasma concentrations increase in parallel during anemia.

Amniotic Fluid↗

An assessment of the effects on coagulation of midtrimester and final-trimester amniotic fluid on whole blood by Thrombelastograph analysis.

UNLABELLED: The Thrombelastograph((R)) test (TEG; Haemoscope Corporation, Skokie, IL) was used to assess the effects of midtrimester and final-trimester amniotic fluid (AF) on whole blood coagulation. Different volumes of midtrimester and final-trimester AF were added to whole blood from nonpregnant volunteers in a series of TEG tests. The addition of both midtrimester and final-trimester AF resulted in significant decreases in reaction time (P < 0.001) and time from reaction to a fixed level of clot firmness (P < 0.05) and significant increases in angle (P < 0.05) and coagulation index (P < 0.05) values. This reflects accelerated clot initiation and propagation. There was no significant change in the maximal amplitude or % lysis at 30 and 60 min with the addition of either midtrimester or final-trimester AF. There was no significant difference between the effects of midtrimester and final-trimester AF on whole blood TEG. TEG may be an additional useful tool in the treatment of coagulopathy in AF embolism. IMPLICATIONS: We used the Thrombelastograph((R)) test (Haemoscope Corporation, Skokie, IL) to assess the effects of midtrimester and final-trimester amniotic fluid (AF) on whole blood coagulation. Results demonstrate that AF accelerates clot initiation and propagation. The Thrombelastograph((R)) test may be useful in assessing coagulopathy in patients with AF embolism.

Adult↗