Thromboelastometry identifies coagulopathy associated with liver failure and disseminated intravascular coagulation caused by yellow fever, guiding specific hemostatic therapy: a case report. / A tromboelastometria identifica coagulopatia associada à insuficiência hepática e coagulação intravascular disseminada causadas por febre amarela, orientando a terapia hemostática específica: um relato de caso.

This case report a severe case of yellow fever complicated by liver failure and disseminated intravascular coagulation. Thromboelastometry was capable of identifying clotting disorders and guiding hemostatic therapy. We report the case of a 23-year-old male admitted to the Intensive Care Unit with sudden onset of fever, generalized muscle pain associated with liver failure, and disseminated intravascular coagulation. The results of conventional laboratory tests showed thrombocytopenia, whereas thromboelastometry suggested coagulopathy with slight hypofibrinogenemia, clotting factor consumption, and, consequently, an increased risk of bleeding. Unlike conventional laboratory tests, thromboelastometry identified the specific coagulation disorder and thereby guided hemostatic therapy. Both fibrinogen concentrates and vitamin K were administered, and no blood component transfusion was required, even in the presence of thrombocytopenia. Administration of hemostatic drugs, including fibrinogen concentrate and vitamin K, improved thromboelastometric parameters, correcting the complex coagulation disorder. Blood component transfusion was not performed, and there was no bleeding.

Este relato de caso detalha um caso grave de febre amarela complicada por insuficiência hepática e coagulação intravascular disseminada. A tromboelastometria foi capaz de identificar os distúrbios da coagulação e orientar o tratamento hemostático. Relatamos o caso de um homem com 23 anos de idade admitido na unidade de terapia intensiva com quadro com início abrupto de febre e dor muscular generalizada associados a insuficiência hepática e coagulação intravascular disseminada. Os resultados dos exames laboratoriais convencionais revelaram trombocitopenia, enquanto a tromboelastometria sugeriu coagulopatia com discreta hipofibrinogenemia, consumo de fatores de coagulação e, consequentemente, aumento do risco de sangramento. Diferentemente dos exames laboratoriais convencionais, a tromboelastometria identificou o distúrbio de coagulação específico e, assim, orientou o tratamento hemostático. Administraram-se concentrados de fibrinogênio e vitamina K, não sendo necessária a transfusão de qualquer componente do sangue, mesmo na presença de trombocitopenia. A tromboelastometria permitiu a identificação precoce da coagulopatia e ajudou a orientar a terapêutica hemostática. A administração de fármacos hemostáticos, incluindo concentrados de fibrinogênio e vitamina K, melhorou os parâmetros tromboelastométricos, com correção do transtorno da coagulação. Não se realizou transfusão de hemocomponentes, e não ocorreu qualquer sangramento.

A tromboelastometria identifica coagulopatia associada à insuficiência hepática e coagulação intravascular disseminada causadas por febre amarela, orientando a terapia hemostática específica: um relato de caso / Thromboelastometry identifies coagulopathy associated with liver failure and disseminated intravascular coagulation caused by yellow fever, guiding specific hemostatic therapy: a case report

RESUMO Este relato de caso detalha um caso grave de febre amarela complicada por insuficiência hepática e coagulação intravascular disseminada. A tromboelastometria foi capaz de identificar os distúrbios da coagulação e orientar o tratamento hemostático. Relatamos o caso de um homem com 23 anos de idade admitido na unidade de terapia intensiva com quadro com início abrupto de febre e dor muscular generalizada associados a insuficiência hepática e coagulação intravascular disseminada. Os resultados dos exames laboratoriais convencionais revelaram trombocitopenia, enquanto a tromboelastometria sugeriu coagulopatia com discreta hipofibrinogenemia, consumo de fatores de coagulação e, consequentemente, aumento do risco de sangramento. Diferentemente dos exames laboratoriais convencionais, a tromboelastometria identificou o distúrbio de coagulação específico e, assim, orientou o tratamento hemostático. Administraram-se concentrados de fibrinogênio e vitamina K, não sendo necessária a transfusão de qualquer componente do sangue, mesmo na presença de trombocitopenia. A tromboelastometria permitiu a identificação precoce da coagulopatia e ajudou a orientar a terapêutica hemostática. A administração de fármacos hemostáticos, incluindo concentrados de fibrinogênio e vitamina K, melhorou os parâmetros tromboelastométricos, com correção do transtorno da coagulação. Não se realizou transfusão de hemocomponentes, e não ocorreu qualquer sangramento.

Abstract This case report a severe case of yellow fever complicated by liver failure and disseminated intravascular coagulation. Thromboelastometry was capable of identifying clotting disorders and guiding hemostatic therapy. We report the case of a 23-year-old male admitted to the Intensive Care Unit with sudden onset of fever, generalized muscle pain associated with liver failure, and disseminated intravascular coagulation. The results of conventional laboratory tests showed thrombocytopenia, whereas thromboelastometry suggested coagulopathy with slight hypofibrinogenemia, clotting factor consumption, and, consequently, an increased risk of bleeding. Unlike conventional laboratory tests, thromboelastometry identified the specific coagulation disorder and thereby guided hemostatic therapy. Both fibrinogen concentrates and vitamin K were administered, and no blood component transfusion was required, even in the presence of thrombocytopenia. Administration of hemostatic drugs, including fibrinogen concentrate and vitamin K, improved thromboelastometric parameters, correcting the complex coagulation disorder. Blood component transfusion was not performed, and there was no bleeding.

Gastrointestinal ischemia: endoscopic findings in the context of vascular insufficiency.

Gastrointestinal ischemia may result from different causes: hemodynamic shock, thromboembolism, endoscopic or surgical complications, among other causes. Its symptoms are pain, vomiting, bleeding and bloating. Endoscopic findings are pale or blackened mucosa, and exudative and confluent ulcerative lesions. This paper aims to report a case of gastroduodenal ischemia associated with hemodynamic shock and disseminated intravascular coagulation (DIC). This is a case of a 56-years- old male with multiple comorbidities, presenting with refractory septic shock and DIC. He underwent an upper gastrointestinal endoscopy (UGE) for investigation of melena, which revealed an extensive deep and exudative gastric ulcer, associated with edematous purplish duodenal mucosa. Due to the severity of the underlying condition, the patient evolved to death, evidencing septic shock as cause of death. Gastroduodenal ischemia is associated with a poor prognosis, in which early diagnosis by UGE is fundamental to guide potential interventions.

Successful treatment of hemophagocytic lymphohistiocytosis and disseminated intravascular coagulation secondary to histoplasmosis in a patient with HIV/AIDS.

Haemophagocytic lymphohistiocytosis is an uncommon syndrome that results from an uncontrolled activation of macrophages and lymphocytes resulting in the compromise of multiple organs that is potentially fatal without timely treatment. It can be hereditary or a secondary result of infectious processes, neoplasms or autoimmune conditions. We present the case of a patient with HIV/AIDS who developed hemophagocytic lymphohistiocytosis as well as disseminated intravascular coagulation associated with histoplasmosis and who was successfully treated with amphotericin B, steroids and transitory dialytic support.

Deficiencia congénita de proteína C en un recién nacido con trombosis y necrosis de tejidos extensa / Congenital C protein deficiency in a newborn with extensive thrombosis and necrosis of tissues

Uno de los trastornos hematológicos más graves del período neonatal es la deficiencia congénita de proteína C, de presentación muy rara, y causa de enfermedad tromboembólica severa y púrpura fulminante en recién nacidos. Se puede sintetizar como una entidad clínico-patológica, de aparición aguda, con trombosis de la vasculatura de la dermis, lo cual conduce a necrosis hemorrágica y progresiva de la piel, asociada a coagulación intravascular diseminada y hemorragia perivascular, que ocurre en el período neonatal. El paciente presentado exhibe los elementos clínico-patológicos que caracterizan la púrpura fulminante, cuyo origen se debe a una deficiencia hereditaria de proteína C, lo cual condujo a la aparición de complicaciones trombóticas severas(AU)

One of the most serious hematological disorders of the neonatal period is congenital C protein deficiency of very rare occurrence and the main cause of severe thromboembolic disease and purpura fulminans in newborns. It may be summarized as a clinical and pathological entity of acute occurrence, with dermis vasculature thrombosis that leads to progressive hemorrhagic necrosis of the skin, associated to disseminate intravascular coagulation and perivascular hemorrhage in the neonatal period. The patient of this report showed the clinical and pathological elements characterizing purpura fulminans the origin of which is due to hereditary C protein deficiency that led to onset of severe thrombotic complications in this patient(AU)

Accident involving a 2-year-old child and Lonomia obliqua venom: clinical and coagulation abnormalities

Poisons of caterpillars have different effects on inflammatory and coagulation systems. This is a case report of a 2-year-old child that accidentally came in contact with several caterpillars of the species Lonomia obliqua. At first, the patient's exams presented abnormal coagulation and decreased fibrinogen, but the patient did not evolve to active bleeding or acute renal failure. The patient received antilonomic serum 15 h after the accident and the treatment was repeated after another 12 h due to persistent alterations shown by the coagulation exams. The venom of L. obliqua has several substances that act on the coagulation and inflammatory systems. The event is characterized by a hemorrhagic syndrome with decreases in fibrinogen. L. obliqua Stuart-factor activator (Losac) and L. obliqua prothrombin activator protease (Lopap) are components that act with procoagulatory effects. The pro-inflammatory action occurs due to metalloproteases, hyaluronidases and other substances with inflammatory activity. Studies on caterpillar venom can give new perspectives on the treatment of cancer and other diseases that cause dysfunction of the extra-cellular matrix...

[Protein C deficiency in patient with sepsis-associated disseminated intravascular coagulation and deep vein thrombosis]. / Déficit de proteína C en un paciente con coagulación intravascular diseminada asociada a sepsis y trombosis venosa profunda: Case report.

Disseminate intravascular coagulation (DIC) is a clinical pathological syndrome associated to several diseases. Sepsis is the most common cause in infants and children. DIC results from the anomalous activation of blood coagulation, widespread formation of thrombi in the microcirculation, and consumption of clotting factors and platelets. Clinical findings are variable; the most common is bleeding, followed by purpura and acral gangrene (purpura fulminans). We report a patient with sepsis associated-DIC and concurrent deep venous thrombosis. The diagnostic evaluation allowed to discover inherited thrombophilia associated to protein C deficiency.

Déficit de proteína C en un paciente con coagulación intravascular diseminada asociada a sepsis y trombosis venosa profunda: Case report / Protein C deficiency in patient with sepsis-associated disseminated intravascular coagulation and deep vein thrombosis

La coagulación intravascular diseminada es un síndrome clinicopatológico que complica a varias enfermedades graves; la sepsis es la causa más común en los pacientes pediátricos. Resulta de una anormal activación del sistema de coagulación, que conduce a la formación de trombos en la microcirculación, y al consumo de plaquetas y factores de la coagulación. Los hallazgos clínicos son variables; las hemorragias son la presentación más frecuente, seguidas de la púrpura y la gangrena de las extremidades (púrpura fulminante). Se presenta el caso de un paciente con coagulación intravascular diseminada asociada a sepsis, con trombosis venosa profunda concomitante. Los estudios permitieron diagnosticar una trombofilia hereditaria asociada a déficit hereditario de proteína C.

Disseminate intravascular coagulation (DIC) is a clinical pathological syndrome associated to several diseases. Sepsis is the most common cause in infants and children. DIC results from the anomalous activation of blood coagulation, widespread formation of thrombi in the microcirculation, and consumption of clotting factors and platelets. Clinical findings are variable; the most common is bleeding, followed by purpura and acral gangrene (purpura fulminans). We report a patient with sepsis associated-DIC and concurrent deep venous thrombosis. The diagnostic evaluation allowed to discover inherited thrombophilia associated to protein C deficiency.

Déficit de proteína C en un paciente con coagulación intravascular diseminada asociada a sepsis y trombosis venosa profunda: Case report / Protein C deficiency in patient with sepsis-associated disseminated intravascular coagulation and deep vein thrombosis

La coagulación intravascular diseminada es un síndrome clinicopatológico que complica a varias enfermedades graves; la sepsis es la causa más común en los pacientes pediátricos. Resulta de una anormal activación del sistema de coagulación, que conduce a la formación de trombos en la microcirculación, y al consumo de plaquetas y factores de la coagulación. Los hallazgos clínicos son variables; las hemorragias son la presentación más frecuente, seguidas de la púrpura y la gangrena de las extremidades (púrpura fulminante). Se presenta el caso de un paciente con coagulación intravascular diseminada asociada a sepsis, con trombosis venosa profunda concomitante. Los estudios permitieron diagnosticar una trombofilia hereditaria asociada a déficit hereditario de proteína C.(AU)

Disseminate intravascular coagulation (DIC) is a clinical pathological syndrome associated to several diseases. Sepsis is the most common cause in infants and children. DIC results from the anomalous activation of blood coagulation, widespread formation of thrombi in the microcirculation, and consumption of clotting factors and platelets. Clinical findings are variable; the most common is bleeding, followed by purpura and acral gangrene (purpura fulminans). We report a patient with sepsis associated-DIC and concurrent deep venous thrombosis. The diagnostic evaluation allowed to discover inherited thrombophilia associated to protein C deficiency.(AU)

Hemophagocytic lymphohistiocytosis associated with visceral leishmaniasis in late adulthood.

We describe a case of hemophagocytic lymphohistiocytosis related to visceral leishmaniasis in late adulthood. Because clinical features of visceral leishmaniasis can mimic those of hemophagocytic lymphohistiocytosis, diagnosing leishmaniasis as the underlying etiology can be quite challenging. In our case, treatment with amphotericin B resulted in a dramatic resolution of clinical abnormalities.

Déficit de proteína C en un paciente con coagulación intravascular diseminada asociada a sepsis y trombosis venosa profunda: Case report. / [Protein C deficiency in patient with sepsis-associated disseminated intravascular coagulation and deep vein thrombosis].

Disseminate intravascular coagulation (DIC) is a clinical pathological syndrome associated to several diseases. Sepsis is the most common cause in infants and children. DIC results from the anomalous activation of blood coagulation, widespread formation of thrombi in the microcirculation, and consumption of clotting factors and platelets. Clinical findings are variable; the most common is bleeding, followed by purpura and acral gangrene (purpura fulminans). We report a patient with sepsis associated-DIC and concurrent deep venous thrombosis. The diagnostic evaluation allowed to discover inherited thrombophilia associated to protein C deficiency.

Kocher-Debré-Sémélaigne syndrome diagnosed by autopsy associated with disseminated intravascular coagulation.

Kocher-Debré-Sémélaigne syndrome is a rare disease with little literature, which develops with myopathy in infancy associated with neuromuscular alterations, polymyositis with symmetrical proximal muscle weakness, pseudohypertrophy, muscular rigidity and spasms, exercise intolerance, myxoedema, short stature, and cretinism. Male patient aged 18 years old, 1.52 m in height, admitted in the General Hospital of Triângulo Mineiro Federal University on November 11, 2003, complaining of intense diffuse abdominal pain like severe cramps, without triggering factors, associated with asthenia and hyporexia. This seems to be one of the few reports of KDS syndrome diagnoses by autopsy, where alterations in the thyroid gland connected with hypotrophy and probable congenital hypothyroidism were described and resulted in complications such as disseminated intravascular coagulation and hemophagocytic syndrome with fast progression to death of an 18-year-old patient.

[Massive transfusion and trauma patient management: pathophysiological approach to treatment].

Bleeding that requires massive blood transfusion is one of the main causes of cardiac arrest and death in the operating room. Its mortality varies widely between 15 and 54%, and it is strongly related to multiple factors such as acidosis, hypothermia and hypocoagulation. We undertook this study to describe the mechanisms that perpetuate bleeding during massive hemorrhage and the particular issues under the different clinical conditions of controlled and uncontrolled tissue damage. Laboratory tests for coagulation status diagnosis as well as treatment guidelines for usage of different fluid replacement solutions and hemoderivatives are described. A well-established response plan is needed by the surgical team and the blood bank in order to quickly facilitate blood products to the patient. Measures to avoid hypothermia and availability of rapid infusion systems are also necessary.

Embolia amniótica durante parto normal sob analgesia: relato de caso / Amniotic fluid embolism during vaginal delivery under analgesia: case report / Embolia amniótica durante parto normal bajo analgesia: relato de caso

JUSTIFICATIVA E OBJETIVOS: A embolia amniótica é rara, sendo quadro clínico de início súbito e elevada morbidade. O objetivo deste trabalho foi apresentar um caso de embolia amniótica em paciente primigesta, submetida à analgesia para parto normal. RELATO DO CASO: Gestante de 38 anos, bolsa rota e 5 cm de dilatação do colo uterino. Apresentava-se com muita dor, agitação, sudorese, taquissistolia e venóclise com Ringer com lactato associado a 5 UI de ocitocina em gotejamento lento, pressão arterial (PA) de 110 × 70 mmHg, freqüência cardíaca (FC) 115 bpm, em ritmo sinusal e SpO2 de 98 por cento. Optou-se por técnica combinada, empregando-se 2,5 mg de bupivacaína pesada e 20 µg de fentanil no espaço subaracnóideo e cateter no espaço peridural. Após 20 minutos do início da analgesia a paciente referiu prurido súbito e intenso, apresentou agitação, vômito e palidez, FC 160 bpm, taquipnéia, SpO2 80 por cento e PA inaudível. Administrou-se solução fisiológica a 0,9 por cento (500 mL) associada à hidrocortisona, efedrina (50 mg) e oxigênio sob máscara facial com fluxo de 10 L.min-1. Nesse momento, a PA era 60 × 30 mmHg, a FC 150 bpm e a SpO2 92 por cento. Como a PA tendia a diminuir, foi administrado um total de 7 mg de metaraminol, divididos em várias doses. Após o parto vaginal, a paciente foi encaminhada à UTI com PA 90 × 60 mmHg, FC 110 bpm e taquipnéia. Duas horas após apresentou sangramento e hipotensão arterial, sendo diagnosticado coagulação intravascular disseminada (CIVD), tratada com cristalóides, concentrado de hemácias e plasma fresco congelado. Alta da UTI no terceiro dia de pós-operatório. CONCLUSÕES: Em decorrência da dramaticidade, gravidade e instalação abrupta do quadro, a rapidez e objetividade de medidas para manter sinais vitais são fundamentais e decisivos para a sobrevida das gestantes. Alerta-se para a importância de monitoração durante a analgesia de parto.

BACKGROUND AND OBJECTIVES: Amniotic fluid embolism is a rare occurrence; it has a sudden onset and high morbidity. The objective of this report was to present a case of amniotic fluid embolism in a primipara undergoing analgesia for vaginal delivery. CASE REPORT: This is a 38-year old pregnant woman with amniotic sac ruptured, cervix with 5-cm dilation, complaining of severe pain; the patient was agitated, diaphoretic, and with tachysystoly. After venipuncture, Ringer's lactate with 5 IU of oxytocin was infused slowly, blood pressure (BP) 110 × 70 mmHg, heart rate (HR) 115 bpm with sinus rhythm, and SpO2 98 percent. It was decided to use a combined technique: 2.5 mg of heavy bupivacaine and 20 µg of fentanyl were administered in the subarachnoid space and a catheter was inserted into the epidural space. Twenty minutes after the institution of analgesia, the patient complained of sudden onset of severe pruritus, she was agitated, with nausea and vomiting, pale, HR 160 bpm, tachypneic, SpO2 80 percent, and BP could not be detected. Normal saline (500 mL) associated with hydrocortisone, ephedrine (50 mg), and oxygen with a face mask at 10 L.min-1 were administered. At that moment, she presented BP 60 × 30 mmHg, HR 150 bpm, and SpO2 92 percent. Since BP tended to decrease, a total of 7 mg of metaraminol were administered divided in several doses. After vaginal delivery, the patient was transferred to the ICU with BP 90 × 60 mmHg, HR 110, and tachypnea. Two hours later, she developed bleeding and hypotension; disseminated intravascular coagulation (DIC) was diagnosed and the patient treated with crystalloid solutions, packed red blood cells and fresh frozen plasma. She was discharged from the ICU in the 3rd postoperative day (PO). CONCLUSIONS: Due to the dramatic presentation, severity, and fast installation of the symptoms, the speed and objectivity of the measures instituted to maintain vital signs are fundamental and decisive for survival...

JUSTIFICATIVA Y OBJETIVOS: La embolia amniótica es rara siendo un cuadro clínico de inicio súbito y de elevada morbidez. El objetivo de este trabajo fue presentar un caso de embolia amniótica en paciente primigesta, sometida a la analgesia para parto normal. RELATO DEL CASO: Embarazada de 38 años, bolsa rota y 5 cm de dilatación del cuello uterino. Se presentó con mucho dolor, agitación, sudoración, taquisistolia y venoclisis con Ringer con lactato asociado a 5 UI de ocitocina en goteo lento, presión arterial (PA) de 110 × 70 mmHg, frecuencia cardíaca (FC) 115 lpm, en ritmo sinusal y SpO2 de un 98 por ciento. Se optó por técnica combinada: empleando 2,5 mg de bupivacaína pesada y 20 µg de fentanil en el espacio subaracnoideo y catéter en el espacio epidural. Después de 20 minutos del inicio de la analgesia la paciente refirió prurito súbito e intenso, presentó agitación, vómito y palidez, FC 160 lpm, taquipnea, SpO2 80 por ciento y PA inaudible. Se administró una solución fisiológica a un 0,9 por ciento (500 mL) asociada a la hidrocortisona, efedrina (50 mg) y oxígeno bajo máscara facial con flujo de 10 L.min-1. En ese momento la PA era 60 × 30 mmHg, la FC 150 lpm y la SpO2 un 92 por ciento. Como la PA tendía a disminuir, se administró un total de 7 mg de metaraminol, divididos en varias dosis. Después del parto vaginal, la paciente se remitió a la UCI con PA 90 × 60 mmHg, FC 110 lpm y taquipnea. Dos horas después presentó sangramiento e hipotensión arterial, siendo diagnosticado coagulación intravascular diseminada (CIVD) y tratada con cristaloides, concentrado de glóbulos rojos y plasma fresco congelado. Alta de la UCI en el 3º PO. CONCLUSIONES: Debido al dramatismo, a la gravedad e instalación abrupta del cuadro, la rapidez y objetividad de las medidas para mantener las señales vitales son fundamentales y decisivas para la sobrevida de las embarazadas. Se avisa sobre la importancia de la monitorización durante la analgesia de parto.

Biochemical and biological properties of Lonomia obliqua bristle extract

Lonomia obliqua caterpillar is frequently seen in accidents with humans especially in the south of Brazil. Patients develop a hemorrhagic syndrome that can be treated with specific antilonomic serum. A consumptive coagulopathy was found to be the main cause of bleeding complications observed in patients after contact with L. obliqua. Studies revealed that L. obliqua caterpillar bristle extract (LOCBE) displays a procoagulant activity that leads to intravascular thrombin formation, resulting in a special form of disseminated intravascular coagulation (DIC). Fibrinolysis seems to be secondary to the fibrin production, since no direct fibrinolytic activity was found in LOCBE. Two procoagulant toxins, a factor X activator (Losac) and a prothrombin activator (Lopap), were isolated from LOCBE and characterized. Infusion of Lopap into experimental animals triggered a condition similar to that observed in human envenomation

Pregnancy complicated by acute pulmonary lymphangitic adenomatosis, metastasis and disseminated intravascular coagulation. A case report.

BACKGROUND: The association of pregnancy and cancer is a rare event, occurring in less than 1 case per 5,000 pregnancies, and is a cause of maternal mortality in about 5% of cases. CASE: A 33-year-old, Japanese woman presented at the end of pregnancy with clinical manifestations of pneumonia and developed fatal disseminated intravascular coagulation in the postpartum period. The pathologic findings suggested the existence of a primary cancer in the gastrointestinal tract with pulmonary and placental metastases. CONCLUSION: The biologic course of malignancies in pregnancy is complex. In gastrointestinal cancer, normal pregnancy symptoms can mask and delay the diagnosis. As in this patient, very rare presentations are possible.

Childhood acute promyelocytic leukemia: no benefit of all-trans-retinoic acid administered in a short-course schedule.

From January 1990 to August 1997, 29 consecutive patients were treated with newly diagnosed primary acute promyelocytic leukemia (APL) at the authors' Institution. Of these, 27 (16 boys and 11 girls) were evaluable. Median age at diagnosis was 6.3 (range: 1.9-15.7) years. This population was treated with two consecutive protocols: 13 patients were included in the AML-HPG-90 protocol and 14 in the AML-HPG-95. The initial treatment was the same for both protocols: an induction 8-day phase with cytarabine, idarubicin, and etoposide was followed by a consolidation with cyclophosphamide, cytarabine, 6-mercaptopurine, vincristine, doxorubicin, and prednisone. Two courses of intensification with high-dose (HD) cytarabine and etoposide were given in the first study. Only one intensification course was administered in the second study, with HD cytarabine plus idarubicin or etoposide decided by randomization. Complete remission was achieved in 67% (18/27) of cases. Mortality on induction was quite high, 30% (8/27) mainly due to hemorrhages from disseminated intravascular coagulation (DIC). The event-free survival estimate for all patients was 0.47 (SE: 0.1). From April 1994, all-trans-retinoic acid (ATRA) was administered just during the first days of the induction phase (median: 9, range: 2-27) to stop or prevent DIC. Eighteen patients received ATRA and 9 did not. Three patients developed signs of ATRA syndrome during the first days of administration but no one died due to this toxicity. The impact of a short course of ATRA on early control of DIC was studied by analyzing the number of platelet, cryoprecipitate, and fresh frozen plasma transfusions during the induction phase in both groups. No statistical differences in complete remission rate, early mortality, need of transfusion of blood components for DIC, and survival estimates could be established between patients who received ATRA and those who did not. ATRA used in a short-course schedule during induction of APL did not stop early mortality due to DIC. Moreover, survival results did not improve with this method of ATRA usage. Longer periods of ATRA administration during APL therapy are strongly recommended.