Severe Disseminated Intravascular Coagulation Research Articles

Uterine balloon tamponade in combination with topical administration of tranexamic Acid for management of postpartum hemorrhage.

While uterine balloon tamponade is an effective modality for control of postpartum hemorrhage, the reported success rates have ranged from the level of 60% to the level of 80%. In unsuccessful cases, more invasive interventions are needed, including hysterectomy as a last resort. We developed a modified tamponade method and applied it to two cases of refractory postpartum hemorrhage after vaginal delivery. The first case was accompanied by uterine myoma and low-lying placenta. After an induced delivery, the patient had excessive hemorrhage due to uterine atony. Despite oxytocin infusion and bimanual uterine compression, the total blood loss was estimated at 2,800 mL or more. The second case was diagnosed as placental abruption complicated by fetal death and severe disseminated intravascular coagulation, subsequently. A profuse hemorrhage continued despite administration of uterotonics, fluid, and blood transfusion. The total blood loss was more than 5,000 mL. In each case, an intrauterine balloon catheter was wrapped in gauze impregnated with tranexamic acid, inserted into the uterus, and inflated sufficiently with sterile water. In this way, mechanical compression by a balloon and a topical antifibrinolytic agent were combined together. This method brought complete hemostasis and no further treatments were needed. Both the women left hospital in stable condition.

Effect of antivenom therapy of Rhabdophis tigrinus (Yamakagashi snake) bites.

BackgroundRhabdophis tigrinus (Yamakagashi snake) is a rear-fanged colubrid snake present throughout Russia and Asia. Its venom induces life-threatening hemorrhagic symptoms and severe disseminated intravascular coagulation with a fibrinolytic phenotype.R. tigrinus antivenom manufactured by the immunization of horses to neutralize the venom has the risk of adverse events such as anaphylaxis and serum sickness disease. It should be used when benefit is greater than the risk of adverse effects; however, its efficacy has not been well evaluated.Although our previous survey of nine cases demonstrated that seven of all cases treated with antivenom survived, the clinical characteristics and prognosis without antivenom administration remained unclear. We assumed that R. tigrinus antivenom administration overlaps self-recovery with supportive care. We aimed to determine the association between antivenom administration and outcome with further analyzed cases.MethodsWe retrospectively reviewed the records of the Japan Snake Institute between January 1, 1973 and December 31, 2013. Antivenom and without antivenom groups were compared with regard to baseline demographic features, treatment-related factors, and outcomes.ResultsIn total, 34 patients were analyzed (97% male, median age 37.5 years). Twenty-five patients were further examined from our previous study. On admission, the median levels of fibrinogen and fibrinogen degradation products were 35 mg/dL and 200 μg/mL, respectively, and platelet counts were 107,000/mm3. The median disseminated intravascular coagulation score (defined by the Japanese Association of Acute Medicine) was 5. Antivenom was administered to 19 patients, with a median interval of 32 h between bite and antivenom administration. The in-hospital mortality rate was 12%. In univariate analysis, baseline characteristics and laboratory data were not significantly different between the antivenom and without antivenom groups. Hospital mortality in the antivenom group was significantly better than that in the without antivenom group (0% vs. 26.7%, P = 0.03). Moreover, the number of patients developing renal failure requiring hemodialysis was significantly lower in the antivenom group (5.3% vs. 40.0%, P = 0.03).ConclusionsIn our small retrospective study, antivenom administration was likely to be effective in the management of R. tigrinus bites. Apparently, further research is required to confirm its efficacy.

New diagnostic strategy for sepsis-induced disseminated intravascular coagulation: a prospective single-center observational study

IntroductionInflammation and coagulation are closely interrelated pathophysiologic processes in the pathogenesis of sepsis. However, the diagnostic criteria of sepsis and disseminated intravascular coagulation (DIC) are different. This study aimed to define a biomarker panel to predict sepsis-induced DIC in emergency department patients.MethodsEighty-two patients who were admitted to the emergency department of a tertiary university hospital were included in this study. The inclusion criteria were as follows: (1) age >18 years; (2) ≥1 systemic inflammatory response syndrome (SIRS) criteria. Patients were excluded if they lacked biomarker data or apparent clinical manifestations. Eleven biomarkers were assayed from blood drawn on ED admission. Receiver operating curve (ROC) analysis including the area under the ROC and multivariable logistic regression were used to identify an optimal combination of biomarkers to create a diagnostic panel. The derived formula for weighting biomarker values was used to determine the severity of sepsis-induced DIC, which was divided into three categories: mild, moderate, and severe. We also investigated the ability of this classification to predict secondary outcome measures of rates of sepsis and DIC, DIC score, acute physiology and chronic health evaluation (APACHE) II score, sequential organ failure score (SOFA) score, and 28-day all-cause mortality.ResultsAmong the 11 biomarkers tested, the optimal 2-marker panel comprised presepsin and protein C. The area under the curve for the accuracies of predicting sepsis and DIC from these two biomarkers were 0.913 and 0.880, respectively. When patients were divided according to the severity of sepsis-induced DIC, all secondary outcomes except for mortality were significantly higher depending on the severity (P < .0001). The overall mortality rates of mild, moderate, and severe sepsis-induced DIC were 7.14%, 15.4%, and 28.6%, respectively (P = .0994).ConclusionsA biomarker panel of presepsin and protein C is predictive of the severity of sepsis-induced DIC in suspected ED patients. These criteria for sepsis-induced DIC are very simple, easy to implement, and can be used in intensive care units as a point-of-care test.

Use of Recombinant Thrombomodulin in Disseminated Intravascular Coagulation Complicated Hemophagocytic Lymphohistiocytosis

Hemophagocytic lymphohistiocytosis (HLH) is frequently lethal in its early phase due to complicating disseminated intravascular coagulation (DIC). The authors report a 14-mo-old girl with severe DIC complicating Epstein-Barr virus associated HLH. She was successfully treated with immunochemotherapy consisting mainly of etoposide and additional recombinant thrombomodulin (r-TM), a newly developed anticoagulant. Although the efficacy of r-TM cannot be proven in a single case report, additional anticoagulation therapy with r-TM is safe and may reduce early deaths in patients with DIC-complicated severe HLH. More clinical experience is required, although r-TM is currently licensed only in Japan.

Successful renal transplantation from a brain-dead deceased donor with head injury, disseminated intravascular coagulation and deranged renal functions

Deceased donors (DDs) with the brain death due to head injury are the major source of organs for transplantation. The incidence of post-head injury disseminated intravascular coagulation (DIC) ranges from 24% to 50%. Many centers do not accept organs from donors with DIC due to increased risk of primary graft non-function and/or high chances of morbidity/mortality. We performed two successful renal transplants from a DD with head injury with DIC and deranged renal function. One of the recipients developed transient thrombocytopenia, but there was no evidence of DIC or delayed graft functions in either of the recipients. Over a follow-up of 1 month, both are doing well with stable graft function and hematological profile. Thus, a carefully selected DD with severe DIC even with deranged renal function is not a contraindication for organ donation if other risk factors for primary non-function are excluded. This approach will also help in overcoming organ shortage.

Application of Massive Transfusion Protocol is Associated with a Low Incidence of Coagulopathy and Mortality Rate

Background: Massive haemorrhage and subsequent Massive Transfusion (MT) are associated with serious, often fatal complications including intractable Disseminated Intravascular Coagulation (DIC). Historically undesirable outcomes demonstrate the need to improve the management approach of MT. It is clear that evidence-based guidelines and protocols should be developed with the aim of improving MT-outcome. Methods: We implemented an evidence-based MT-Protocol (MTP) in 2007 and studied all patients (105) from Jan 2008 to Jan 2011 who required MT and were treated with the MTP at our institution. The MTP includes two phases and incorporates a fixed volume of Fresh Frozen Plasma (FFP), cryoprecipitate and platelets in addition to Packed Red Blood Cells (PRBC). Results: The median age of patients was 57 years (range, 18-86). The male to female ratio was 74:31. Median Hb was 90 g/L (range, 44-110) and platelet count was 190/nl (range, 34-817). Thirteen patients developed mild DIC; 22 moderate DIC and one severe DIC. D-dimer showed average increase of 7.9 mg/L with a range between 0.6-35 mg/L (Normal <0.5). Average INR was 1.97, (range, 1.2-7.2), while average APTT was 36 seconds (range, 22-88s). The mortality rate was 11.4% (12/105) and these were mainly related to underlying trauma rather than DIC with the exception of 1 patient. The average number of transfused PRBC was 15 units (range, 6-42); cryoprecipitate, 20(range, 10-60); platelets, 2(range, 1-7) and FFP, 8(range, 2-20). Conclusion: Despite serious bleeding secondary to trauma or surgery, the implementation of MTP seems to have reduced the occurrence of severe DIC and was associated with a relatively low mortality-rate. Further studies to confirm these findings are warranted.

Uso de Terapia VAC® en paciente pediátrico con exposición ósea postamputación tras púrpura fulminans

Meningococcal sepsis is associated with a high mortality rate. These patients may show severe disseminated intravascular coagulation (DIC) and skin, subcutan...

In vivo anticoagulant effect of ethyl pyruvate in endotoxemic rats

Introduction Disseminated intravascular coagulation (DIC), a disorder of the blood coagulation function, is a common complication of severe sepsis. Ethyl pyruvate (EP), a derivative of pyruvate, is known for its anti-inflammatory and antioxidant properties. Recently, EP showed anticoagulant effects in vitro. Therefore, the aim of study is to investigate the in vivo anticoagulant effect of EP on a severe DIC model induced by lipopolysaccharide (LPS) in anesthetized Wistar rats. Materials and Methods The animals were intravenously infused with LPS (30 mg/kg) over a period of 4 h. One hour after LPS initiation, rats were treated with EP in three dosages (20, 40 and 60 mg/kg/4 h, i.v.). Results The intermediate and high doses of EP (40 and 60 mg/kg) prevented circulatory failure, improved renal and hepatic function, and reduced the plasma levels of TNF-α and IL-6 after LPS administration. All used doses of EP significantly prevented prothrombin time prolongation, and reduced mRNA expression of tissue factor in lung tissue induced by LPS. The two higher doses of EP attenuated plasma concentrations of thrombin-antithrombin complex. The high dose of EP (60 mg/kg) significantly preserved platelet counts, and improved survival rate. However, EP did not reduce the elevation of plasma plasminogen activator inhibitor-1 during endotoxemia. Conclusion EP demonstrates the in vivo anticoagulant effect and improved organ functions in a severe DIC model in rats, which is likely associated with the inhibitory effect on tissue factor mRNA expression and cytokines release. Its effectiveness in preventing DIC is not mediated by increase in fibrinolysis.

Guidelines for the diagnosis and management of disseminated intravascular coagulation

The diagnosis of disseminated intravascular coagulation (DIC) should encompass both clinical and laboratory information. The International Society for Thrombosis and Haemostasis (ISTH) DIC scoring system provides objective measurement of DIC. Where DIC is present the scoring system correlates with key clinical observations and outcomes. It is important to repeat the tests to monitor the dynamically changing scenario based on laboratory results and clinical observations. The cornerstone of the treatment of DIC is treatment of the underlying condition. Transfusion of platelets or plasma (components) in patients with DIC should not primarily be based on laboratory results and should in general be reserved for patients who present with bleeding. In patients with DIC and bleeding or at high risk of bleeding (e.g. postoperative patients or patients due to undergo an invasive procedure) and a platelet count of <50 x 10(9)/l transfusion of platelets should be considered. In non-bleeding patients with DIC, prophylactic platelet transfusion is not given unless it is perceived that there is a high risk of bleeding. In bleeding patients with DIC and prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), administration of fresh frozen plasma (FFP) may be useful. It should not be instituted based on laboratory tests alone but should be considered in those with active bleeding and in those requiring an invasive procedure. There is no evidence that infusion of plasma stimulates the ongoing activation of coagulation. If transfusion of FFP is not possible in patients with bleeding because of fluid overload, consider using factor concentrates such as prothrombin complex concentrate, recognising that these will only partially correct the defect because they contain only selected factors, whereas in DIC there is a global deficiency of coagulation factors. Severe hypofibrinogenaemia (<1 g/l) that persists despite FFP replacement may be treated with fibrinogen concentrate or cryoprecipitate. In cases of DIC where thrombosis predominates, such as arterial or venous thromboembolism, severe purpura fulminans associated with acral ischemia or vascular skin infarction, therapeutic doses of heparin should be considered. In these patients where there is perceived to be a co-existing high risk of bleeding there may be benefits in using continuous infusion unfractionated heparin (UFH) due to its short half-life and reversibility. Weight adjusted doses (e.g. 10 mu/kg/h) may be used without the intention of prolonging the APTT ratio to 1.5-2.5 times the control. Monitoring the APTT in these cases may be complicated and clinical observation for signs of bleeding is important. In critically ill, non-bleeding patients with DIC, prophylaxis for venous thromboembolism with prophylactic doses of heparin or low molecular weight heparin is recommended. Consider treating patients with severe sepsis and DIC with recombinant human activated protein C (continuous infusion, 24 microg/kg/h for 4 d). Patients at high risk of bleeding should not be given recombinant human activated protein C. Current manufacturers guidance advises against using this product in patients with platelet counts of <30 x 10(9)/l. In the event of invasive procedures, administration of recombinant human activated protein C should be discontinued shortly before the intervention (elimination half-life approximately 20 min) and may be resumed a few hours later, dependent on the clinical situation. In the absence of further prospective evidence from randomised controlled trials confirming a beneficial effect of antithrombin concentrate on clinically relevant endpoints in patients with DIC and not receiving heparin, administration of antithrombin cannot be recommended. In general, patients with DIC should not be treated with antifibrinolytic agents. Patients with DIC that is characterised by a primary hyperfibrinolytic state and who present with severe bleeding could be treated with lysine analogues, such as tranexamic acid (e.g. 1 g every 8 h).

Dissemenated Intravascular Coagulation in Patients with Septic Shock: Impact of Coagulation Markers on Prediction of the Mortality

Background: Patients with severe sepsis usually present with a generalized activation of the innate immune response that triggers coagulation and inhibits fibrinolysis. Haemostatic abnormalities associated with severe sepsis may vary from subtle laboratory evidence of coagulation activation to clinically overt, severe disseminated intravascular coagulation (DIC). Clinically, severe DIC may contribute to multiple organ dysfunctions by microvascular thrombotic complications. Despite its obvious effects on microcirculatory conditions, the impact of these modifications on mortality prediction is not clear. The International Society on Thrombosis and Haemostasis (ISTH) has proposed a diagnostic scoring algorithm for overt DIC based on routine laboratory test. These templates have been validated prospectively in independent patient populations, both as a tool for defining diagnostic scores for DIC, and as a method to demonstrate prognostic associations for DIC scores with mortality risk. We aimed to study, in patients entering an intensive care unit with septic shock, prognosis performances of two DIC scores D-Dimers (D-Di) and soluble fibrin monomers (SFMC) calculated with an informative cut-off of D-Di or SFMC.Methods: One hundred fifty-eight consecutive patients with septic shock entering our institutions ICU were investigated on the first day of admission, and two DIC scores (D-Di and SFMC) were registered at the admission and during the first five days. We evaluated the blood cell count and haemostasis-related parameters on the initial blood sample: aPTT ratio, TP ratio, fibrinogen Fg; antithrombin; factor VII, X, II, II; D-Di and SFMC. The diagnosis of overt-DIC was performed according to the recommendations of the ISTH. We used a test trend (Cochran-Armitage) on mortality to analyze prognostic associations for the two DIC scores with mortality risk, according different D-Di and SFMC cut-off.Results: Eighteen patients died on the first day of inclusion (mortality 11.5%), 35 patients during the first week (22.2%). Sixty-one patients were transfused (38.6%). No AT concentrates were given, Fg concentrates were used for two patients and recombinant activated human protein C (Xigris; Eli Lilly and Co., Indianapolis, USA) was given to 18 patients after the initial blood sampling (11.4%; six of them died). A trend on mortality was detected (p<0.05) according to the two DIC scores (D-Di or SFMC) with a cut-off equal to 2 and to 10 for D-Di and SFMC respectively. We identified with this cut-off that all the patients with a DIC score (D-Di) ≤ 2 (n=19/19) survived [negative predictive value (NVP) equal to 100% (95%CI: [82.4–100.0]. Similarly, with a SFMC cutoff of 10, 71/84 patients with a DIC score (SFMC) ≤ 2 survived corresponding to a NVP 84.5 % (95%CI: [75.0–91.5].Conclusion: This single-institution study demonstrates that the mortality of patients with septic shock is related to DIC scores (D-Di and SFMC). We proposed a significant cut-off for D-Di and SFMC scores that allowed identifying with an excellent NVP patients with a low risk of death.

Protein C deficiency

Severe protein C deficiency (i.e. protein C activity <1 IU dL(-1)) is a rare autosomal recessive disorder that usually presents in the neonatal period with purpura fulminans (PF) and severe disseminated intravascular coagulation (DIC), often with concomitant venous thromboembolism (VTE). Recurrent thrombotic episodes (PF, DIC, or VTE) are common. Homozygotes and compound heterozygotes often possess a similar phenotype of severe protein C deficiency. Mild (i.e. simple heterozygous) protein C deficiency, by contrast, is often asymptomatic but may involve recurrent VTE episodes, most often triggered by clinical risk factors. The coagulopathy in protein C deficiency is caused by impaired inactivation of factors Va and VIIIa by activated protein C after the propagation phase of coagulation activation. Mutational analysis of symptomatic patients shows a wide range of genetic mutations. Management of acute thrombotic events in severe protein C deficiency typically requires replacement with protein C concentrate while maintaining therapeutic anticoagulation; protein C replacement is also used for prevention of these complications around surgery. Long-term management in severe protein C deficiency involves anticoagulation with or without a protein C replacement regimen. Although many patients with severe protein C deficiency are born with evidence of in utero thrombosis and experience multiple further events, intensive treatment and monitoring can enable these individuals to thrive. Further research is needed to better delineate optimal preventive and therapeutic strategies.

Systemic AL amyloidosis with disseminated intravascular coagulation associated with hyperfibrinolysis

Many coagulation abnormalities are known to coexist in patients with AL amyloidosis; however, disseminated intravascular coagulation (DIC) is rarely observed. We describe the case of a 61-year-old woman who presented with systemic purpura, macroscopic hematuria, and hepatosplenomegaly as the initial manifestations of systemic AL amyloidosis. A coagulation study revealed severe DIC associated with fibrinolysis. The patient was treated for DIC with gabexate mesilate (GM); however, her bleeding symptoms and thrombocytopenia continued to worsen. The treatment was changed from GM to nafamostat mesilate (NM); DIC improved gradually, and the platelet count normalized in 1 week. After the tapering and cessation of NM therapy, deterioration of DIC did not occur. She underwent autologous peripheral blood stem cell transplantation twice following high-dose melphalan therapy, and received maintenance therapy with thalidomide. Hepatosplenomegaly progression appears to have been halted, and DIC has not recurred. This is the first reported case of AL amyloidosis showing severe DIC with excessive fibrinolysis. The clinical observation that NM was considerably more effective than GM in our patient suggests that NM may be more suitable for the treatment of DIC with a hyperfibrinolytic condition in AL amyloidosis patients.

Microangiopathies thrombotiques : physiopathologie, diagnostic et traitement

Thrombotic microangiopathies (TMA) consist in a syndrome characterized by a mechanical hemolytic anemia, a consumption thrombocytopenia and multivisceral ischemia. Thrombotic thrombocytopenic purpura (TTP) is a multisystemic form of TMA which prognosis may be severe; hemolytic uremic syndrome (HUS) is a TMA which renal involvement is predominant. A TMA syndrome may also be observed in association with other clinical contexts such as the HELLP (Hemolysis, Elevated Liver enzymes, Low Platelet count) syndrome, cancers, organ transplantations, Human Immunodeficiency Virus infection, catastrophic antiphospholipid syndrome or severe disseminated intravascular coagulation. The pathophysiology for TMA has been recently better elucidated, allowing a more appropriate classification of the various forms of this syndrome. TTP is characterized by a severe enzymatic deficiency of the specific von Willebrand factor (VWF)-cleaving protease named ADAMTS13; this deficiency which is either acquired via autoantibodies or inherited via ADAMTS13 gene mutations, leads to the accumulation of hyperadhesive forms of VWF in plasma inducing the spontaneous formation of platelet thrombi in the microvasculature. Pathophysiology for HUS may involve either verotoxin-producing bacteria (post-diarrheal HUS) or inherited complement proteins deficiencies (factor H, factor I, CD46/MCP-1). Diagnosis and therapeutic management of TMA both remain an emergency. The first intention treatment is plasmatherapy (mainly plasma exchanges) while immunosuppressive drugs, specific treatment for an underlying disease and intensive care procedures may be required as a function of the clinical context. The global prognosis of TMA remains difficult to establish considering the heterogeneity of the different forms of this syndrome.

Two cases of hemorrhage secondary to amniotic fluid embolus managed with uterine artery embolization.

To describe the anesthetic management of two cases of amniotic fluid embolus (AFE) and disseminated intravascular coagulation (DIC) who underwent bilateral uterine artery embolization to control their postpartum hemorrhage. We report the clinical course and management of two women who suffered sudden cardiorespiratory events during labour. The first patient had a cardiac arrest whereas the second developed respiratory failure and altered neurological status. They were diagnosed as having had an AFE. Both of these events were accompanied by severe postpartum hemorrhage and DIC. They suffered prolonged bleeding and received massive transfusions. Successful management of hemorrhage was optimized by uterine artery embolization, thus avoiding ongoing problems with bleeding and possible hysterectomy. The role of uterine artery embolization is described, along with its advantages and anesthetic considerations. Women with severe postpartum hemorrhage, with or without DIC, should be considered for uterine artery embolization.

Aggravation of endotoxin-induced disseminated intravascular coagulation and cytokine activation in heterozygous protein-C–deficient mice

AbstractIn the pathogenesis of sepsis and disseminated intravascular coagulation (DIC), dysfunctional anticoagulant pathways are important. The function of the protein C system in DIC is impaired because of low levels of protein C and down-regulation of thrombomodulin. The administration of (activated) protein C results in an improved outcome in experimental and clinical studies of DIC. It is unknown whether congenital deficiencies in the protein C system are associated with more severe DIC. The aim of the present study was to investigate the effect of a heterozygous deficiency of protein C on experimental DIC in mice. Mice with single-allele targeted disruption of the protein C gene (PC+/–) mice and wild-type littermates (PC+/+) were injected with Escherichia coli endotoxin (50 mg/kg) intraperitoneally. PC+/–mice had more severe DIC, as evidenced by a greater decrease in fibrinogen level and a larger drop in platelet count. Histologic examination showed more fibrin deposition in lungs, kidneys, and liver in mice with a heterozygous deficiency of protein C. Interestingly, PC+/– mice had significantly higher levels of proinflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β, indicating an interaction between the protein C system and the inflammatory response. Survival was lower at 12 and 24 hours after endotoxin in the PC+/– mice. These results confirm the important role of the protein C system in the coagulative-inflammatory response on endotoxemia and may suggest that congenital deficiencies in the protein C system are associated with more severe DIC and adverse outcome in sepsis.

Haematology in dengue and dengue haemorrhagic fever

Dengue fever (DF) and dengue haemorrhagic fever (DHF) are caused by the dengue virus. The major pathophysiological hallmark that distinguishes DHF from DF is plasma leakage as a result of increased vascular permeability. Following this leakage, hypovolaemic shock occurs as a consequence of a critical plasma volume loss. Constant haematological abnormalities occurring in DHF and frequently include bone marrow suppression, leucopenia and thrombocytopenia. An enhanced immune response of the host to a secondary DV infection is a feature of DHF and leads to many consequences. These are immune complex formation, complement activation, increased histamine release and a massive release of many cytokines into the circulation, leading to shock, vasculopathy, thrombopathy and disseminated intravascular coagulation (DIC).The mechanisms underlying the bleeding in DHF are multiple. These are vasculopathy, thrombopathy and DIC. Thrombopathy consists of thrombocytopenia and platelet dysfunction. DIC is prominent in patients with shock. The most severe DIC and massive bleeding are the result of prolonged shock and cause a fatal outcome. The mechanisms of thrombopathy and DIC and the proper management of DHF are reviewed and discussed.

Disseminated intravascular coagulation after Cerastes vipera envenomation in a 3-year-old child: a case report

This study presents a case of severe disseminated intravascular coagulation (DIC) in a 3-year-old child following envenomation by the snake, Cerastes vipera. A literature search revealed very few similar cases. We describe a child who was bitten in his left foot by a snake identified as a C. vipera. Initial symptoms were relatively benign. Local signs included a hemorrhagic vesicle at the site of the bite with marked swelling of the entire leg. Twenty-four hours later, the child developed severe bleeding due to DIC, which lasted 5 days and required repeated administration of blood and blood products and total exchange transfusion. The patient was discharged from the hospital after 7 days in good condition. To the best of our knowledge, severe DIC following envenomation by a C. vipera has not been previously described in the literature. Treatment was essentially supportive. The case report indicates that a specific antivenin against this snake's venom should be made available in our area.

Cellular origin and procoagulant properties of microparticles in meningococcal sepsis

Patients with meningococcal sepsis generally suffer from disseminated intravascular coagulation (DIC). The aim of this study was to address whether these patients have elevated numbers of circulating microparticles that contribute to the development of DIC. Plasma samples from 5 survivors, 2 nonsurvivors, and 5 healthy volunteers were analyzed for the presence of microparticles by flow cytometry. Ongoing coagulation activation in vivo was quantified by enzyme-linked immunosorbent assay of plasma prothrombin fragment F(1 + 2), and procoagulant properties of microparticles in vitro were estimated by thrombin-generation assay. On admission, all patients had increased numbers of microparticles originating from platelets or granulocytes when compared with controls (P =.004 and P =.008, respectively). Patients had elevated levels of F(1 + 2) (P =.004), and their microparticles supported thrombin generation more strongly in vitro (P =.003) than those of controls. Plasma from the patient with the most fulminant disease course and severe DIC contained microparticles that expressed both CD14 and tissue factor, and these microparticles demonstrated extreme thrombin generation in vitro. We conclude that patients with meningococcal sepsis have elevated numbers of circulating microparticles that are procoagulant. These findings may suggest a novel therapeutic approach to combat clinical conditions with excessive coagulation activation.

Severe neonatal echovirus 17 infection during a nursery outbreak.

Severe neonatal echovirus 17 infection during a nursery outbreak.

Surgical treatment of extensive skin necrosis secondary to purpura fulminans in a patient with meningococcal sepsis

Meningococcal sepsis is associated with a high mortality rate. These patients may show severe disseminated intravascular coagulation (DIC) and skin necrosis. There is very little published experience regarding the surgical treatment of this complication. The similarity between skin necrosis secondary to DIC and full thickness cutaneouos burns provides the rationale for its treatment as if it was a deep burn. We report the surgical treatment of extensive skin necrosis in a patient with meningococcal sepsis and DIC. This treatment is similar to that used in full thickness burns, including excision of necrotic tissue and coverage with autografts, as well as amputation of extremities if distal coverage is not possible.