Disseminated intravascular coagulation

Letsky, Elizabeth A.

doi:10.1053/beog.2001.0204

Cited by 60 publications

(41 citation statements)

References 82 publications

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“…Examples of sudden death syndrome from the medical literature support our hypothesis, including thrombohemorrhagic phenomena (THP), such as anaphylaxis [229,230,[237][238][239], disseminated intravascular coagulation (DIC) [240,241], HELLP syndrome [242], acute liver necrosis [243], Waterhouse-Friderichsen's syndrome, hemolytic uremic anemia, idiopathic pulmonary hemorrhage [244], acute pancreatitis [245], acute pituitary necrosis [246], pseudomembranous colitis, thrombotic thrombocytopenic purpura (TTP), Sanarelli-Shwartzman phenomenon (SSP), Henoch-Schonlein purpura (HSP), eclampsia [238], serum sickness, hemolytic anemia, preeclampsia, and stillbirths [247].…”

Section: Zeta Potential and Cardiovascular Diseasementioning

confidence: 79%

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Davidson¹,

Seneff²

2012

Entropy

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Abstract:In reviewing the literature pertaining to interfacial water, colloidal stability, and cell membrane function, we are led to propose that a cascade of events that begins with acute exogenous surfactant-induced interfacial water stress can explain the etiology of sudden death syndrome (SDS), as well as many other diseases associated with modern times. A systemic lowering of serum zeta potential mediated by exogenous cationic surfactant administration is the common underlying pathophysiology. The cascade leads to subsequent inflammation, serum sickness, thrombohemorrhagic phenomena, colloidal instability, and ultimately even death. We propose that a sufficient precondition for sudden death is lowered bioavailability of certain endogenous sterol sulfates, sulfated glycolipids, and sulfated glycosaminoglycans, which are essential in maintaining biological equipose, energy metabolism, membrane function, and thermodynamic stability in living organisms. Our literature review provides the basis for the presentation of a novel hypothesis as to the origin of endogenous bio-sulfates which involves energy transduction from sunlight. Our hypothesis is amply supported by a growing body of data showing that parenteral administration of substances that lower serum zeta potential results in kosmotropic cationic and/or chaotropic anionic interfacial water stress, and the resulting cascade.Keywords: inflammation; serum sickness; colloidal instability; interfacial water stress; bio-sulfates; Shwartzman phenomena; sudden death syndrome Glossary of TermsAnaphylaxis a severe, rapidly progressing, life-threatening, generalized allergic reaction. Biological equipoise a stable, non-equilibrium, dissipative system synonymous with life. Cholesterol sulfate (Ch-S)quantitatively the most important known sterol sulfate in human plasma where it regulates the activity of the serine proteases, in cell membranes where it has a stabilizing role, and in platelet membranes where it supports platelet adhesion. Coherence domain (CD)a water CD is a collection of liquid water molecules which oscillate in unison in tune with a self-trapped electromagnetic field at a well-defined frequency. The coherent oscillations produce an ensemble of quasi-free electrons, able to collect noise energy from the environment and transform it into high-grade coherent energy in the form of electron vortices. This high-grade energy may then activate biomolecules resonating with the water CD. Colloidal instabilitya property attributed to a colloidal suspension that develops when stabilizing repulsive steric and electrostatic forces between colliding particles are insufficient to prevent their natural tendency to aggregate into masses large enough to precipitate.Colloidal suspension a colloid that has a continuous liquid phase in which a solid is suspended in a liquid, e.g., our flowing blood. Exclusion zone (EZ)a glass-like, gel phase consisting of water CDs resonating in-phase, adjacent to hydrophilic surfaces, several hundred micrometers wide which excludes colloi...

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Section: Zeta Potential and Cardiovascular Diseasementioning

confidence: 79%

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Davidson¹,

Seneff²

2012

Entropy

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“…Postpartum hemorrhage must be anticipated following a severe placental abruption and prophylactic uterotonic drugs should be considered. Myometrial contractility is impaired by fibrin degradation products rather than by presence of extravasated blood [8]. Some potential precipitators of ARDS associated with pregnancy includes infection, preeclampsia/eclampsia, hemorrhage and amniotic fluid embolism.…”

Section: Discussionmentioning

confidence: 99%

Abruptio Placentae Leading to Fetal Death and Adult Respiratory Distress Syndrome

Singh

Shankar

Rohatgi

2008

Medical Journal Armed Forces India

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“…This should be followed immediately with red cell replacement using packed RBCs to restore the oxygen carrying capacity, with the goal of maintaining hemoglobin at 7-10 g/dL. Lastly, clotting factors and platelets should be replaced in order to prevent or correct coagulopathy [32,33]. This replacement should begin with fresh, frozen plasma and be followed by cryoprecipitate and platelets.…”

Section: Hemorrhagementioning

confidence: 99%

Fluid Management in Obstetric Patients

Frigo¹,

Pumpo

2013

Body Fluid Management

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In pregnancy, hemodynamic and cardiovascular changes occur that prevent blood loss during delivery. In fact, there is an increase in blood volume, during the first trimester [1]. The volume of blood continues to expand rapidly in the second trimester before reaching a plateau in the last trimester. At the same time, the increase in Red Blood Cell (RBC) mass occurs more slowly, leading to a relative anemia and hemodilution [2], with the latter peaking by 30-32 weeks of gestation. Dilutional anemia is therefore common, especially between 28 and 34 weeks gestation, when hemoglobin concentrations are lowest. The accretion in RBC mass results in an 18-25% increase in the first months of pregnancy, followed by a drop after childbirth due to hemorrhage [3][4][5]. The increase in red cell volume provides for the extra oxygen demands of the mother and fetus. The lower end of the normal range for hemoglobin in pregnancy is 11-12 g/dL. These physiological responses have considerable advantages during pregnancy: improved placental perfusion, decreased risk of thrombosis and an adequate blood supply despite the bleeding that occurs with childbirth [6][7][8].The White Blood Cell (WBC) count increases in pregnancy beginning in the first trimester, as a result of selective marrow erythropoiesis. This causes a left shift, with granulocytosis and more immature white cells in the circulation. The normal WBC count for pregnancy is 5000-12,000 WBC/mm 3 , although values as high as 15,000 WBC/mm 3 are not uncommon [9].

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Disseminated intravascular coagulation

Cited by 60 publications

References 82 publications

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Abruptio Placentae Leading to Fetal Death and Adult Respiratory Distress Syndrome

Fluid Management in Obstetric Patients

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