Coagulación Intravascular Diseminada (CID)

Presentado porManuel Pineda Estudiante de III enfermeríaFundación universitaria de ciencias de la salud

Plaquetas

•Las plaquetas son fragmentos de células encargadas de los procesos de coagulación lo que ayuda a prevenir y controlar las hemorragias representa el 5% de la sangre

Factor Nombre

I Fibrinógeno

II Protrombina

III Tromboplastina o factor tisular

IV Ión Calcio

V proacelerina (leiden)

VII Proconvertina

IX Factor Christmas

X Factor Stuart-Prower

XITromboplastina plasmática o antecedente trombo plastínico de plasma

XII Factor Hageman

XIIIPretransglutaminidasa o factor Laili-Lorand

Definición.•Es la alteración de la coagulación del

factor V(protombina) y VII(fibrina).

Es una enfermedad caracterizada por la producción de una excesiva cantidad de pequeños coágulos intravasculares, con componentes defectuosos y disfunción endotelial en los vasos periféricos del cuerpo , los cuales causan trombos en los pequeños vasos sanguíneos.

Fisiopatología

•El una enfermedad donde se alteran todas las proteínas que ayudan en la coagulación, (fibrina) formando trombos pequeños en las partes distales del cuerpo.

Factores de riesgo

bactriano viruscongénito

Proceso

•Purpura.•Enfermedad de la membrana hialina •Cianosis cardiaca congestiva •Síndrome hemolítico.

•La sangres presenta factores de coagulación

que se desencadenan en cascada o cadena

para formar el coagulo y para la detener la hemorragia. En la coagulación

disemina intravascular algunos de estos factores no trabajan adecuadamente formando trombos en la partes distales del cuerpo

Tratamiento

1. Transfusión sanguínea (plaquetas)2. Anticoagulantes

Artículos de investigación

EBSCOHOSTPubMed

Nonbacterial purpura fulminans and severe autoimmune acquired protein S deficiency associated

with human herpesvirus-6 active replication.

• Nonbacterial purpura fulminans (PF) is rare, usually follows viral infection in young children, and is characterized by specific coagulation disorders, requiring specific therapy. Following a transient rash, a 2-year-old previously healthy girl developed PF without haemodynamic impairment. Laboratory data revealed disseminated intravascular coagulation and a severe transient protein S deficiency. Antiprotein S autoantibodies and active human herpesvirus-6 (HHV6) replication were demonstrated. Purpuric skin lesions spread very rapidly despite broad-spectrum antibiotics and right leg amputation. Plasmapheresis and intravenous immunoglobulins gave complete clinical recovery and normalization of protein S level within 10 days, with progressive clearance of antiprotein S autoantibodies. Transient severe protein S deficiencies have previously been reported in patients with nonbacterial PF, usually after varicella infection. This is the first documented case of PF after HHV6 infection. [ABSTRACT FROM AUTHOR]

Disseminated Intravascular Coagulation•A disorder characterized by procoagulant

substances entering the general circulation causing a systemic thrombotic process. The activation of the clotting mechanism may arise from any of a number of disorders. A majority of the patients manifest skin lesions, sometimes leading to PURPURA FULMINANS

• Coagulación intravascular diseminada que complica la infección por virus Epstein-Barr en un paciente trasplantado cardíaco:

.• O'Connor DS, Elmariah S, Aledort LM, Pinney SP.• El Monte Sinaí Escuela de Medicina de Nueva York, Nueva York,

EE.UU. .• Resumen• Las infecciones virales son particularmente frecuentes después

del trasplante cardíaco. En esto hemos presentado un caso de infección por virus de Epstein- Barr, que presenta como un síndrome viral con síntomas respiratorios , pero se vio complicada por fallo multiorgánico y coagulación intravascular diseminada . los médicos de trasplante deben ser conscientes de esta complicación única de una infección de otro modo auto- limitada.

• PMID: 20620559 [ PubMed - en proceso]

• http://www.ncbi.nlm.nih.gov/pubmed/20620559

• Detection of disseminated intravascular coagulation with the help of the conception of constant intravascular microcoagulation.

• Bokarev I, Popova L.• I. M. Sechenov Moscow Medical Academy, Moscow, Russia. bokarev@online.ru• Abstract• The possibility of intravascular blood coagulation existence in the

microvascular vessels and capillaries without the presence of a large thrombus in the arteries and veins has been known from the middle of 19th century. It is impossible to know exactly about the prevalence of this pathology, because there is a jumble in terminology that does not help statistics to be exact. One of the reasons of so high mortality from disseminated intravascular coagulation (DIC) is due to the impossibility to always make exact diagnosis, and as M. Levi thinks it is provoked in the absence of generally accepted idea of DIC syndrome. We investigated these markers and the intensity of intravascular blood coagulation in a number of patients. Our understanding of the problems of DIC was formulated on the grounds of a thirty-year study of the problem involving over 1,500 patients. Thereby, the conception of constant intravascular microcoagulation (CIMC) was developed with the following aims: to report the existing material and bring to researchers and doctors in practice information about the presence of the phenomenon of CIMC and to resolve debatable questions of definitions and practical usage of up-to-date information about DIC with the help of CIMC conception.

• PMID: 20229684 [PubMed - indexed for MEDLINE] • http://www.ncbi.nlm.nih.gov/pubmed/20229684

Thrombocytopenia and thrombosis in disseminated intravascular coagulation (DIC).

• Kitchens CS.• University of Florida, Gainesville, FL 32610, USA.

craig.kitchens@medicine.ufl.edu• Abstract• Disseminated intravascular coagulation (DIC) is the physiologic result

of pathologic overstimulation of the coagulation system. Despite multiple triggers, a myriad of laboratory abnormalities, and a clinical presentation ranging from gross hemostatic failure to life-threatening thrombosis, or even both simultaneously, a simplified clinical approach augmented by a few readily available tests allows prompt identification of the process and elucidation of treatment opportunities. Platelet counts in DIC may be low, especially in acute sepsis-associated DIC, yet increased in malignancy-associated chronic DIC. Thrombotic risk is not a function of the platelet count, and thrombocytopenia does not protect the patient from thrombosis. The stratification of both thrombotic risk and hemorrhagic risk will be addressed.

Nonbacterial purpura fulminans• Nonbacterial purpura fulminans (PF) is rare, usually follows viral infection in

young children, and is characterized by specific coagulation disorders, requiring specific therapy. Following a transient rash, a 2-year-old previously healthy girl developed PF without haemodynamic impairment. Laboratory data revealed disseminated intravascular coagulation and a severe transient protein S deficiency. Antiprotein S autoantibodies and active human herpesvirus-6 (HHV6) replication were demonstrated. Purpuric skin lesions spread very rapidly despite broad-spectrum antibiotics and right leg amputation. Plasmapheresis and intravenous immunoglobulins gave complete clinical recovery and normalization of protein S level within 10 days, with progressive clearance of antiprotein S autoantibodies. Transient severe protein S deficiencies have previously been reported in patients with nonbacterial PF, usually after varicella infection. This is the first documented case of PF after HHV6 infection. [ABSTRACT FROM AUTHOR]   Copyright of British Journal of Dermatology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The host response to sepsis and developmental impact.• Wynn J, Cornell TT, Wong HR, Shanley TP, Wheeler DS.• Division of Neonatology, Duke University Children's Hospital, Durham, North Carolina,

USA.• Abstract• Invasion of the human by a pathogen necessitates an immune response to control and

eradicate the microorganism. When this response is inadequately regulated, systemic manifestations can result in physiologic changes described as "sepsis." Recognition, diagnosis, and management of sepsis remain among the greatest challenges shared by the fields of neonatology and pediatric critical care medicine. Sepsis remains among the leading causes of death in both developed and underdeveloped countries and has an incidence that is predicted to increase each year. Despite these sobering statistics, promising therapies derived from preclinical models have universally failed to obviate the substantial mortality and morbidity associated with sepsis. Thus, there remains a need for well-designed epidemiologic and mechanistic studies of neonatal and pediatric sepsis to improve our understanding of the causes (both early and late) of deaths attributed to the syndrome. In reviewing the definitions and epidemiology, developmental influences, and regulation of the host response to sepsis, it is anticipated that an improved understanding of this host response will assist clinician-investigators in identifying improved therapeutic strategies.

TREM-like transcript-1 protects against inflammation-associated hemorrhage by facilitating platelet aggregation in mice and humans.

• Triggering receptor expressed on myeloid cells-like (TREM-like) transcript-1 (TLT-1), a type 1 single Ig domain orphan receptor specific to platelet and megakaryocyte α-granules, relocates to the platelet surface upon platelet stimulation. We found here that patients diagnosed with sepsis, in contrast to healthy individuals, had substantial levels of soluble TLT-1 (sTLT-1) in their plasma that correlated with the presence of disseminated intravascular coagulation. sTLT-1 bound to fibrinogen and augmented platelet aggregation in vitro. Furthermore, the cytoplasmic domain of TLT-1 could also bind ezrin/radixin/moesin family proteins, suggesting its ability to link fibrinogen to the platelet cytoskeleton. Accordingly, platelets of Treml1^-/- mice failed to aggregate efficiently, extending tail-bleeding times. Lipopolysaccharide-treated Treml1^-/- mice developed higher plasma levels of TNF and D-dimers than wild-type mice and were more likely to succumb during challenge. Finally, Treml1^-/- mice were predisposed to hemorrhage associated with localized inflammatory lesions. Taken together, our findings suggest that TLT-1 plays a protective role during inflammation by dampening the inflammatory response and facilitating platelet aggregation at sites of vascular injury. Therefore, therapeutic modulation of TLT-1-mediated effects may provide clinical benefit to patients with hypercoagulatory conditions, including those associated with inflammation. [ABSTRACT FROM AUTHOR]   Copyright of Journal of Clinical Investigation is the property of American Society for Clinical Investigation and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Conclusión

•Podemos concluir que en las investigaciones realizadas, las coagulación diseminada intravascular se puede dar por varios

factores no solo congénito, también puede ser producida por agentes

patógenos, por mala asepsias en la técnicas de

procedimientos invasivos.

Bibliografía 1. http://www.ncbi.nlm.nih.gov/pubmed/206205592. http://www.ncbi.nlm.nih.gov/pubmed/202296843. http://

biblioteca.fucsalud.edu.co:2080/ehost/detail?vid=4&hid=7&sid=5ce41808-8187-4681-aa9d-ed6bf09f23d5%40sessionmgr12&bdata=Jmxhbmc9ZXMmc2l0ZT1laG9zdC1saXZl#db=byh&AN=41889052

4. Biomedical Reference Collection: Comprehensive5. Wynn J, Cornell TT, Wong HR, Shanley TP, Wheeler DS.6. http://

biblioteca.fucsalud.edu.co:2080/ehost/detail?vid=4&hid=105&sid=ab583119-a6db-4c85-af8c-bbfa5b8c5617%40sessionmgr104&bdata=Jmxhbmc9ZXMmc2l0ZT1laG9zdC1saXZl#db=byh&AN=41522147

Gracia

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