Obstetric shock due to pulmonary emboli of amniotic fluid.
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The soluble fibrin monomer complexes (SFMC) in 154 obstetric patients with possible disseminated intravascular coagulation (DIC) were evaluated in SDS polyacrylamide gel electrophoresis (PAGE) after precipitation with B-alanine. Other coagulation tests were performed on these patients. The patients were classified into three groups: A) patients with a clinical history of DIC (6 cases); B) patients with only the analytical alterations of DIC (35 cases); and C) patients who showed pathological obstetric diagnoses but without a clinical nor analytical history of DIC (113 cases). In the three groups, well-defined bands of less electrophoretic mobility than fibrinogen were obtained. A significant increase in the second electrophoretic band was found in group A (5.1 per cent) when compared to group C (0.5 per cent). The second electrophoretic band appeared in greater proportion in the group of patients with an unfavorable clinical evolution.
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Pregnancy alters both the fibrinolytic system and coagulation cascade. In addition, pregnancy presents unique triggering mechanisms for DIC. Management of DIC in pregnancy should include removal of the triggering mechanism, blood, and factor replacement. Inherited coagulation defects, while rarely resulting in bleeding diathesis in the pregnant patient, do require monitoring of maternal factor levels. Genetic counseling should be offered to all patients with inheritable coagulation disorders.
This article presents current understanding of the causes, pathophysiology, clinical, and laboratory diagnosis, and management of fulminant and low-grade DIC, as they apply to obstetric, pregnant, and gynecologic patients. General medical complications leading to DIC, which may often be seen in these patients, are also discussed. Considerable attention has been given to interrelationships within the hemostasis system. Only by clearly understanding these pathophysiologic interrelationships can the obstetrician/gynecologist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. Objective clinical and laboratory criteria for diagnosis of DIC have been outlined to eliminate unnecessary confusion and the need to make empiric decisions regarding the diagnosis. Particularly in the obstetric patient, if a condition is observed that is associated with DIC, or if any suspicion of DIC arises from either clinical or laboratory findings, it is imperative to monitor the patient carefully with clinical and laboratory tools to assess any progression to a catastrophic event. In most instances of DIC in obstetric patients, the disease can be ameliorated easily at early stages. Many therapeutic decisions are straightforward, particularly in obstetric and gynecologic patients. For more serious and complicated cases of DIC in these patients, however, efficacy and choices of therapy will remain unclear until more information is published regarding response rates and survival patterns. Also, therapy must be highly individualized according to the nature of DIC, patient's age, origin of DIC, site and severity of hemorrhage or thrombosis, and hemodynamic and other clinical parameters. Finally, many syndromes that are often categorized as organ-specific disorders and are sometimes identified as independent disease entities, such as AFE syndrome, HELLP syndrome, adult shock lung syndrome, eclampsia, and many others, either share common pathophysiology with DIC or are simply a form of DIC. These entities represent the varied modes of clinical expression of DIC and illustrate the diverse clinical and anatomic manifestations of this syndrome.
A neurophysiological follow-up (EEG, exogenous and endogenous evoked potentials--EP) was performed over a 4-month period in a patient who presented a long-lasting coma following a cardiac arrest and an amniotic embolism. A pure anoxic aetiology was ruled out starting from the second day on the basis of a dissociation between mildly altered flash visual EP and markedly altered somatosensory EP, indicating focal brain-stem pathology. Endogenous EP reappeared after 12 days. This patient recovered consciousness after 51 days. Despite the absence of MRI abnormalities, we put forward the hypothesis that a brain-stem embolism had, in fact, worsened the clinical picture of an actually moderate anoxia. This case exemplifies the interest of an integrated neurophysiological approach (EEG, exogenous three-modality EP and endogenous EP) in the early evaluation of coma. It also illustrates the complement between structural imaging and functional assessment of the nervous system.
Vasovagal syncope refers to a reflex cardiovascular depression that gives rise to loss of consciousness with bradycardia and profound vasodilatation. This response commonly occurs during regional anesthesia, hemorrhage or supine inferior vena cava compression in pregnancy. The changes in circulatory response from the normal maintenance of arterial pressure to parasympathetic activation and sympathetic inhibition may cause severe hypotension. This change is triggered by reduced cardiac venous return as well as episodes of emotional stress, excitement or pain. Occasionally, these vasovagal responses may be unpredictable and may dramatically proceed to asystole with circulatory collapse, and may even result in death. In these circumstances, hypotension may be more severe than that caused by bradycardia alone, because of unappreciated vasodilatation. Regional anesthesia, decreased venous return, hemorrhage and abnormal fetal presentation cumulatively increase the risk of vasovagal syncope in cesarean section patients. When a vasovagal response occurs, ephedrine is the drug of first choice because of its combined action on the heart and peripheral blood vessels. Epinephrine must be used early in established cardiac arrest, especially after high regional anesthesia.
We report on a retrospective study of maternal deaths in Malaysia that occurred within 24 hours of delivery, abortion or operative termination of the pregnancy (defined as sudden deaths) in the years 1995-1996. There were 131 sudden maternal deaths (20.6% of all maternal deaths); postpartum hemorrhage, obstetric embolisms, trauma and hypertensive disorders of pregnancy were the main causes. There was a disproportionately increased risk of sudden maternal deaths in the Chinese and the 'other bumiputra' racial groups. The proportion of mothers who had no obstetric risk factors in the pregnancy that led to death was 16.8%. Fourteen mothers died in transit Twenty mothers died after a cesarean section. The findings of this review emphasize the fact that caregivers in obstetrics need to be forever vigilant. All maternity staff need to be well trained in emergency care and there needs to be quick referral to centers that can provide expertise in handling these emergencies.
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