MRI evaluation and follow-up of bone necrosis after meningococcal infection and disseminated intravascular coagulation

1993 ◽  
Vol 23 (6) ◽  
pp. 429-431 ◽  
Author(s):  
N. Damry ◽  
T. Schurmans ◽  
N. Perlmutter
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Meningococcal Infection ◽  
Bone Necrosis ◽  
Intravascular Coagulation ◽  
Mri Evaluation

Increased Tissue Thromboplastin Activity in Monocytes of Patients with Meningococcal Infection: Related to an Unfavourable Prognosis

1983 ◽  
Vol 49 (01) ◽  
pp. 005-007 ◽  
Author(s):  
B Østerud ◽  
T Flægstad
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Fold Increase ◽  
Meningococcal Infection ◽  
High Concentration ◽  
Intravascular Coagulation ◽  
Tissue Thromboplastin ◽  
Unfavourable Prognosis

SummaryIn 16 patients, 13 with meningococcal infection and 3 suspected to have this infection, 8 patients were found to possess significant higher level of tissue thromboplastin activity of their monocytes isolated from the blood at the admission to the hospital than normal. Five of those 8 patients had an extremely high concentration, > 60-300 fold increase, and all these patients died. The exposed tissue thromboplastin activity on the surface of the endotoxin stimulated monocytes is probably the direct inducer of disseminated intravascular coagulation (DIC) in meningococcal infection.

scholarly journals Avascular osteonecrosis of the premaxilla secondary to disseminated intravascular coagulation: a case report

2018 ◽  
Vol 24 (4) ◽  
pp. 173-177
Author(s):  
Alizée Mouraret ◽  
Eric Gérard ◽  
Joey Le Gall ◽  
Rémi Curien
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Oral Surgery ◽  
Disease Process ◽  
Vascular Supply ◽  
Pathological State ◽  
Avascular Osteonecrosis ◽  
Bone Necrosis ◽  
Intravascular Coagulation ◽  
Severity Of The Disease ◽  
Surgery Department

Introduction:Disseminated intravascular coagulation (DIC) is a complexe systemic disorder characterized by a widespread activation of the coagulation, that may lead to thrombosis, ischemia and finally, end-organ failure. The clinical presentation of DIC depends on the site of intravascular coagulation and the severity of the disease process. Avascular osteonecrosis is a pathological state, that can occur secondary to DIC and where a reduced vascular supply leads to ischemia and bone necrosis.Observation:A 83 years old patient was sent to the oral surgery department for tooth mobility in the premaxilla, following the diagnosis of sepsis and DIC induced acute myeloid leukemia, one month ago. The examination showed an exposed avascular bone behind the 12-11-21. A diagnosis of DIC induced osteonecrosis of the premaxilla was made. A resection surgery was then programmed.Discussion:DIC may generates thrombi that might occlude intraosseous vessels in the premaxilla, and lead to bone necrosis. The maxilla is supplied by multiple branches of external carotide artery, therefore, usually, there is a lower risk of osteonecrosis in the maxilla. Nevertheless, since 1993, 4 cases of avascular necrosis of the maxilla secondary to DIC are repported in literature.Conclusion:This kind of complication, although being rare, can be dramatic for the patient as bone and aesthetic defects. Early support and management of these complications is necessary.

Serum procalcitonin levels predict disseminated intravascular coagulation in patients with sepsis shock: A retrospective cohort study

2020 ◽  
Author(s):  
Guang Fu ◽  
Xi-si He ◽  
Hao-li Li ◽  
Hai-chao Zhan ◽  
Jun-fu Lu ◽  
...  
Keyword(s):  
Risk Factors ◽  
Septic Shock ◽  
Cohort Study ◽  
Disseminated Intravascular Coagulation ◽  
Area Under The Curve ◽  
Multivariable Logistic Regression Model ◽  
Intravascular Coagulation ◽  
The Relationship ◽  
Conventional Risk Factors

Abstract Background Complication of disseminated intravascular coagulation (DIC) is a determinant of the prognosis in patients with sepsis shock. Procalcitonin (PCT) has been advocated as a marker of bacterial sepsis. The purpose of this study was to evaluate the relationship between serum PCT levels and DIC with sepsis shock Methods A cohort study was designed which included patients that admitted in intensive care unit (ICU) between January 1, 2015 and December 31, 2018 and the follow-up to discharge. 164 septic shock patients were divided into DIC and non-DIC groups according to international society of thrombosis and homeostasis (ISTH). PCT was measured at the admission to ICU, and all the participants received routine biochemical coagulation test subsequently. Results PCT levels were considerably higher in septic shock patients who developed DIC than those who did not (54.6[13.6–200]vs12.6[2.4–53.3]ng/ml), respectively, P < 0.001). Multivariable logistic regression model revealed that PCT level was significantly associated with risk of DIC independent of conventional risk factors. In addition, curve fitting showed a linear relationship between PCT and DIC score. The Receiver Operating characteristic(ROC) curve suggested that the optimal cut-off point for PCT to predicting DIC induced by septic shock was 42.0 ng/ml, and the area under the curve (AUC) was 0.701(95% CI [0.619–0.784], P < 0.001). More importantly, incorporating PCT with other risk factors into the prediction model significantly increased the AUC for prediction of DIC induced by sepsis shock (0.801vs 0.706; P = 0.012). Conclusions Our study suggests that PCT levels on admission is significantly and independently associated with DIC development subsequently with septic shock, combining PCT levels with other risk factors could significantly improve the prediction of DIC induced by sepsis shock.

scholarly journals Successful treatment of an adult with Kasabach-Merritt syndrome using thalidomide, vincristine, and prednisone

2019 ◽  
Vol 47 (4) ◽  
pp. 1810-1814
Author(s):  
Yue-Hua Huang ◽  
Dao-Bin Zhou ◽  
Bing Han ◽  
Tian Li ◽  
Shu-Jie Wang
Keyword(s):  
Treatment Regimen ◽  
Disseminated Intravascular Coagulation ◽  
Tumor Regression ◽  
Severe Bleeding ◽  
Intravascular Coagulation ◽  
Subcutaneous Mass ◽  
Low Incidence ◽  
Disease Free ◽  
Novel Therapeutic

Objective Kasabach-Merritt syndrome is a rare disease that mainly occurs in infants and adolescents. It usually manifests as disseminated intravascular coagulation and severe bleeding, and is associated with high mortality. However, its low incidence and clinical rarity in adults mean that there is currently no well-verified treatment regimen for this disease. We report on an effective novel therapeutic regimen in a patient with Kasabach-Merritt syndrome. Methods A woman with Kasabach-Merritt syndrome presented with a recurrent subcutaneous mass and disseminated intravascular coagulation, and was treated with prednisone, vincristine and thalidomide. Results This treatment regimen successfully resolved the patient’s symptoms, with tumor regression. The patient remained disease-free after 6 years of follow-up. Conclusions Prednisone combined with vincristine and thalidomide may be an effective treatment for Kasabach-Merritt syndrome, but further studies are needed to verify the use of this regimen.

Diffuse Cutaneous Bullous Mastocytosis and Disseminated Intravascular Coagulation Postvaccination

2016 ◽  
Vol 20 (6) ◽  
pp. 596-599 ◽  
Author(s):  
Alexandra Hudson ◽  
Laura Finlayson
Keyword(s):  
Mast Cell ◽  
Disseminated Intravascular Coagulation ◽  
Rare Condition ◽  
Intravascular Coagulation ◽  
Tubular Necrosis ◽  
Skin Infiltration ◽  
Suboptimal Dose ◽  
Cutaneous Mastocytosis ◽  
Bullous Mastocytosis

Background: Diffuse cutaneous bullous mastocytosis is the most rare subtype of cutaneous mastocytosis, characterized by generalized skin infiltration with mast cells and blistering. Objective: To increase the awareness of the natural history and potential adverse complications of this rare cutaneous condition. Method and Results: We report a case of a male diagnosed on day 7 of life with follow-up of his progression over 6 years. When he was 2.5 months old, he was admitted to hospital postvaccinations with a flare of his blistering that was complicated by disseminated intravascular coagulation and polyuric acute tubular necrosis. Blistering ceased at 3 years, but at 6 years, extensive urtication continued in response to known triggers and a suboptimal dose of mast cell membrane stabilizers and histamine-1 and -2 receptor antagonists. Conclusion: This case discusses the progression of this rare condition over 6 years and highlights the importance of reaching optimal pharmacologic blockage of histamine-1 and -2 receptors and stabilization of mast cell membranes in patients persistently experiencing ongoing pruritus, urtication, and flushing symptoms.

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