Postpartum eclampsia and fulminant HELLP syndrome.
Summary of "Postpartum eclampsia and fulminant HELLP syndrome."
Postpartum onset of eclampsia and HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome is a rare but life-threatening complication for both mother and fetus. A case of a 38-year-old parturient (gravida 2, para 1) who was asymptomatic prior to delivery is reported. Emergency cesarian section had to be performed due to sudden onset of fetal bradycardia as a result of partial placental separation. The perioperative course was characterized by new onset hypertension, nausea and restlessness; within 2 h the patient suffered a generalized seizure which was treated with magnesium sulfate and hydralazine. Despite management in accordance with current guidelines, the condition deteriorated with hypotension, anemia and renal failure. On further examination hematomas in the abdominal cavity and walls were identified and laboratory tests confirmed HELLP syndrome with severe coagulopathy. Explorative laparotomy revealed diffuse bleeding without a significant isolated source or postpartum uterine hemorrhage. Retrospectively, the anemia could be ascribed to severe hemolysis and diffuse bleeding from coagulopathy. The patient required packed red cells, platelets, fresh frozen plasma and prothrombin complex. After admission to the intensive care unit persistent diffuse bleeding mainly caused by hyperfibrinolysis and renal failure occurred, which required blood transfusion, antifibrinolytic (tranexamic acid) and renal replacement therapy (continuous veno-venous hemodiafiltration with citrate) for 6 days. The patient recovered without any sequelae and was discharged 26 days later. Placental separation with new onset peripartum hypertension is to be interpreted as a precursor of severe gestosis and associated complications, especially dissiminated intravascular coagulation (DIC), acute renal failure and pleural effusion. A differentiation between a rapid drop in hemoglobin concentration secondary to hemolysis in postpartum HELLP syndrome rather than postpartum hemorrhage can be challenging. In addition, HELLP syndrome can lead to rapidly developing, fulminant hyperfibrinolysis in the context of DIC. Keys to successful management of postpartum gestosis and associated complications are early detection and perception of clinical and laboratory warning signs, a multidisciplinary approach with rapid and consistent targeted symptomatic therapy to save the mother and fetus.
Klinik für Anaesthesiologie, Intensivmedizin und Schmerztherapie, Klinikum Nordstadt, Klinikum Region Hannover, Haltenhoffstr. 41, 30167, Hannover, Deutschland, firstname.lastname@example.org.
This article was published in the following journal.
Name: Der Anaesthesist
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/21184033
- DOI: http://dx.doi.org/10.1007/s00101-010-1837-0
Medical and Biotech [MESH] Definitions
A syndrome of HEMOLYSIS, elevated liver ENZYMES, and low blood platelets count (THROMBOCYTOPENIA). HELLP syndrome is observed in pregnant women with PRE-ECLAMPSIA or ECLAMPSIA who also exhibit LIVER damage and abnormalities in BLOOD COAGULATION.
Onset of HYPERREFLEXIA; SEIZURES; or COMA in a previously diagnosed pre-eclamptic patient (PRE-ECLAMPSIA).
Transient autoimmune thyroiditis occurring in the POSTPARTUM PERIOD. It is characterized by the presence of high titers of AUTOANTIBODIES against THYROID PEROXIDASE and THYROGLOBULIN. Clinical signs include the triphasic thyroid hormone pattern: beginning with THYROTOXICOSIS, followed with HYPOTHYROIDISM, then return to euthyroid state by 1 year postpartum.
A complication of PREGNANCY, characterized by a complex of symptoms including maternal HYPERTENSION and PROTEINURIA with or without pathological EDEMA. Symptoms may range between mild and severe. Pre-eclampsia usually occurs after the 20th week of gestation, but may develop before this time in the presence of trophoblastic disease.
A small colorless crystal used as an anticonvulsant, a cathartic, and an electrolyte replenisher in the treatment of pre-eclampsia and eclampsia. It causes direct inhibition of action potentials in myometrial muscle cells. Excitation and contraction are uncoupled, which decreases the frequency and force of contractions. (From AMA Drug Evaluations Annual, 1992, p1083)
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