fibrin and Shock

The authors' and literature data on the liver changes at different types of shock are summarized with consideration of the role of etiology and pathogenetic factors. Three groups of similar liver alterations reflecting the severity of impairment of the reticulo-endothelial system (RES), microcirculation and parenchyma are distinguished. No clear-cut dependence between the liver morphological changes and the severity of shock is noted. At the same time the characteristic structural alterations for some forms of shock differing at their early stages by a predominance of neuro-reflectoral, hypovolemic or toxic component are revealed. A rapidly developing hydropic degeneration, the absence of the compensatory changes, signs of the RES deficiency with the progressing necrobiotic and necrotic processes in the liver are characteristic for a neuro-reflectoral shock. Endotoxic shock is associated with widespread intravascular thrombi, liver cell necrosis, combination of the destruction of reticuloendotheliocytes with the signs of their preceding activation, foci of a smooth cytoplasmic network hyperplasia of centrolobular hepatocytes; hypovolemic shock is characterized by activation of compensatory processes.

Topics: Animals; Crush Syndrome; Disseminated Intravascular Coagulation; Energy Metabolism; Fibrin; Kupffer Cells; Liver; Microcirculation; Microscopy, Electron; Mitochondria, Liver; Pain; Phagocytosis; Platelet Aggregation; Rabbits; Rats; Shock; Shock, Hemorrhagic; Shock, Septic

The authors describe the pathophysiology of disseminated intravascular coagulation and the coagulopathy of utilization. The clinical and laboratory data on different types of shock are described. The efficacy of different antithrombotic agents in shock with disseminated intravascular coagulation is shown.

Topics: Blood Coagulation Disorders; Blood Platelets; Cyclic AMP; Disseminated Intravascular Coagulation; Fibrin; Fibrinolysis; Hemostasis; Humans; Microcirculation; Respiratory Distress Syndrome; Shock; Thrombocytopenia; Thrombosis

This report describes how a finding at the autopsy table led to the observation of a clinical syndrome. A synthesis of autopsy experience, clinical investigations, and experimental and biochemical studies were able to shed light on one factor in the pathogenesis of this syndrome, namely blood coagulation with pulmonary microemboli and release and delayed elimination of peptides from fibrin degradation extravascularly in the lungs. These peptides may both induce increased permeability in the microcirculation and stimulate fibroblast proliferation. Knowledge about the pathogenesis has led to improved prophylaxis and therapy and a reduction of the number of deaths.

Topics: Antifibrinolytic Agents; Autopsy; Blood Coagulation; Capillary Permeability; Cell Division; Embolism, Fat; Fibrin; Fibrin Fibrinogen Degradation Products; Fibroblasts; Humans; Microcirculation; Pulmonary Embolism; Shock; Syndrome

Topics: Abruptio Placentae; Animals; Blood Platelets; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinolysis; Heat Exhaustion; Hemolytic-Uremic Syndrome; Heparin; Humans; Polymers; Pregnancy; Shock

Topics: Adult; Aged; Autopsy; Brain; Central Venous Pressure; Colitis; Colon; Enteritis; Female; Fibrin; Heart Ventricles; Hemorrhage; Humans; Kidney; Kidney Glomerulus; Kidney Tubules; Liver; Lung; Male; Middle Aged; Myocardium; Necrosis; Pancreas; Shock; Thrombosis

Echis carinatus is the most important cause of morbidity and mortality from snake bite in Nigeria and in many other parts of the world. Forty-six patients with systemic poisoning by this snake were given echis antivenom made either by the South African Institute for Medical Research (S.A.I.M.R.) or by Behringwerke (North and West African polyvalent antivenom). A simple test of blood coagulability was used to assess whether an adequate neutralizing dose of antivenom had been given. An average of 15.2 ml S.A.I.M.R. antivenom restored normal coagulability permanently in all 23 patients in one group, but in the other group receiving an average dose of 37.9 ml Behringwerke antivenom normal clotting resulted in only 18 out of 23 patients. Local tissue swelling was similar in both groups, but local necrosis occurred in three patients treated with Behringwerke antivenom and in none given S.A.I.M.R. antivenom.

Topics: Acute Disease; Anemia; Antivenins; Blood Coagulation; Cerebral Hemorrhage; Codeine; Epinephrine; Fibrin; Fibrinogen; Hematocrit; Histamine H1 Antagonists; Humans; Hydrocortisone; Nigeria; Prednisone; Shock; Snake Bites; Snake Venoms

Topics: Accidents, Traffic; Body Temperature Regulation; Efficiency, Organizational; Emergency Medical Services; Fibrin; Humans; Infusions, Intravenous; Medical Records Systems, Computerized; Shock; Tissue Adhesives; Wounds and Injuries

Globular hyaline microthrombi are characterized by their diameter (2-30 micron), globular form, and positive PAS and PTAH reaction. They are a morphologic indicator of disturbed microcirculation and hemostasis, such as that occurring in shock. In two of our cases, we observed large globular hyaline microthrombi, some with central webbed degradation progressing to the formation of closed or open hollow globules. The electron microscopic findings were similar to those observed by other investigators in typical shock bodies. On the basis of the morphologic findings, the authors conclude that degradation phenomena start at the center of globular hyaline microthrombi and can progress to the surface where accelerated fibrinolysis is possible. The cellular elements that other investigators have described as a possible condensation center for fibrin precipitate proved to be structurally intact cells that are apparently located in niches of open hollow globules or in the center of circular hyaline microthrombi. The diagnostic relevance, vitality, and temporal classification are discussed.

Topics: Adult; Cerebral Veins; Fibrin; Hematoma, Subdural; Humans; Hyalin; Intracranial Embolism and Thrombosis; Male; Malignant Hyperthermia; Microscopy, Electron; Middle Aged; Portal Vein; Shock; Thrombosis

Disorders of the coagulation system in shock are caused by injuries of the endothelium, influx of thromboplastic material into the blood and stasis. In this way, the intrinsic and the extrinsic system is activated. Fibrin is generated in the blood stream and forms high molecular complexes together with fibrinogen (hypercoagulability). With progress of the shock fibrin can deposit in the small vessels with the consequence of impaired circulation. Finally clotting factors and inhibitors (e.g. antithrombin III) are consumed by disseminated intravascular coagulation. This results in a bleeding tendency (consumption coagulopathy). In this survey particular shock formes (endotoxin induced, cardiogenic, traumatic, hemorrhagic) are discussed with regard to the reflections of the blood coagulation. The therapy of shock-induced disorders of blood coagulation are focused on treatment of primary disease, prevention or elimination of microthrombi, substitution of blood respective plasma components.

Topics: Blood Coagulation; Fibrin; Hemostasis; Humans; Protease Inhibitors; Shock

The fibrinolytic activity of peritoneum was evaluated in 4-month-old calves before and after peritoneal trauma. In each calf, a peritoneal resection, abrasion, sutured incision, and nonsutured incision were performed. These 4 trauma sites were evaluated for fibrinolytic activity and adhesion formation at 1 of 6 posttrauma intervals (1, 2, 3, 5, 8, or 14 days). Peritoneal plasminogen activator and fibrinolytic inhibitor activities from pre- and posttrauma samples were evaluated, using a fibrin-slide incubation technique. Calf peritoneal specimens consistently had fibrinolytic inhibitor activity, but did not have plasminogen activator activity. Significant differences were not found between fibrinolytic activity before or after trauma and a significant correlation was not found between fibrinolytic activity and the presence of or severity of adhesions.

Topics: Animals; Cattle; Female; Fibrin; Fibrinolysis; Peritoneum; Plasminogen Activators; Shock

Topics: Disseminated Intravascular Coagulation; Fibrin; Histocytochemistry; Humans; Microcirculation; Microscopy, Electron; Shock; Thrombosis; Time Factors

First intravascular coagula were detected as early as in the pre-acidotic phase of artificially hypoxic rabbit foetuses used by the authors in experimental studies. Growing acidosis in circulating blood has been accompanied by excessive increase of fibrin precipitation in the terminal blood track. Further increase of intravascular coagulation was found to be discontinued by predominance of secondary fibrinolysis at blood pH around 6.9. Rising hydrogen ion concentration, as a reflection of a consumptional reaction, was found to be accompanied by decline in both the fibrinogen level and thrombocyte count in the foetal blood, fully in parallel with the above DIC.

Topics: Animals; Asphyxia; Blood Coagulation Tests; Disease Models, Animal; Disseminated Intravascular Coagulation; Female; Fibrin; Hydrogen-Ion Concentration; Pregnancy; Pregnancy Complications, Hematologic; Rabbits; Shock

In 56 placentas there were fibrin clots in the vessels of the chorionic plate and the stem villi. Fifty infants survived. The fibrin clots in the relatively large placental vessels are considered to be the result of intrauterine shock. A similar pathogenetic concept is postulated as in the well-known diseminated fibrin thromboembolism which is evident in the visceral organs of children who died in the perinatal period. This identification of these fibrin clots in the vessels of the stem villi, especially in cases of so-called risk deliveries, allows the risk for newborn to be determined during their first days of life (hyaline-membrane disease, hemorrhagic diathesis, etc.). One can testify the intrauterine shock by these findings, even in newborn who survive the respiratory distress syndrome.

Topics: Disseminated Intravascular Coagulation; Female; Fibrin; Humans; Hyaline Membrane Disease; Infant, Newborn; Placenta; Placenta Diseases; Pregnancy; Pregnancy Complications, Hematologic; Respiratory Distress Syndrome, Newborn; Shock; Thromboembolism

The ultrastructure of globular hyaline microthrombi (GHM) is characterized by a spherical space lattice of frequently interconnected bundles of fibres of different width, with a periodic transverse striation and the fibrin-characteristic axial periodicity of 23 nm. These are surrounded by plump or slender bundles of fibres spreading radially over the surface which are only ocassionally interlinked. These filamentary formations of the so-called corona are also characterized by the fibrin-characteristic periodicity. Part of the GHM, however, lacks this axial periodicity, and periodic striation is then only visible in the radially extending fibrils of the corona. The spherical sace lattices with their plump or slender fibrillary fibrin bundles are also replaced by mosaic-like or nearly amorphous fine-grained precipitates. All intermediate stages between these main types of GHM can be found. The disappearance of the axial periodicity and of the fibrillary structure of the spherical space lattices is considered to be the morphological equivalent of seocndary fibrinolysis, here called endolysis, in the centre of the GHM. The morphogenesis of the GHM in states of shock of different aetiologies is discussed.

Topics: Blood; Disseminated Intravascular Coagulation; Fibrin; Fibrin Fibrinogen Degradation Products; Humans; Microscopy, Electron; Rheology; Shock; Thrombosis

Topics: Blood Transfusion; Blood Vessels; Capillaries; Disseminated Intravascular Coagulation; Fibrin; Humans; Lung; Pancreas; Postoperative Complications; Shock; Thrombosis

In a post mortem study of shock-induced changes in the bone marrow, marrow from six different parts of the skeletal system was examined in a total of 109 patients. The comparison of a group of 64 subjects deceased in shock conditions with a control group of 25 deceased without shock showed: In 76,6% of all patients with shock, fibrin networks were found in the sinus and perisinoidal interstice of bone marrow. This can be demonstrated abundantly in every fourth patient with shock. Microthrombi and emboli occluding vessels in the marrow were seen in only 6.3% of the shock cases (controls 0%). The different forms of fibrin precipitates appear most commonly after shock caused by infection. Platelet aggregates in the vessels are seen in 28.2% of all cases with shock (controls 8%). 5% of the cases with shock showed infarction-like necroses of the bone marrow and a further 23% necroses of small cell groups. In every fifth patient with shock, a great number of nucleated blood cells and their precursors were found in the marrow sinus (controls 8%). In a third group of 20 patients with serious illness alledgedly without shock, 45 per cent had a fibrin network when compared with the control group. When several of these findings are present simultaneously, one can apply the term "shock marrow".

Topics: Adult; Aged; Autopsy; Bone Marrow; Bone Marrow Examination; Female; Fibrin; Humans; Male; Middle Aged; Platelet Aggregation; Shock; Shock, Septic; Thromboembolism

Topics: Aprotinin; Disseminated Intravascular Coagulation; Fibrin; Fibrinolysin; Humans; Lung Diseases; Pancreatitis; Shock

Topics: Adenosine Diphosphate; Animals; Antigens; Catheterization; Disseminated Intravascular Coagulation; Diuresis; Endothelium; Endotoxins; Fibrin; Glomerular Filtration Rate; Glucuronidase; Infusions, Parenteral; Kidney; Natriuresis; Osmolar Concentration; Potassium; Rabbits; Renal Artery; Shock; Sodium; Sodium Chloride; Thrombin; Trypsin; Urination; Urine; Water

Topics: Adolescent; Adult; Bone Marrow; Bone Marrow Cells; Bone Marrow Examination; Fibrin; Humans; Middle Aged; Shock

Topics: Animals; Blood Coagulation; Capillaries; Endothelium; Epithelial Cells; Extracorporeal Circulation; Fibrin; Humans; Lung; Lung Diseases; Lymphatic System; Microcirculation; Microscopy, Electron; Oxygen; Positive-Pressure Respiration; Pulmonary Circulation; Pulmonary Surfactants; Respiratory Insufficiency; Shock

Topics: Blood Proteins; Complement System Proteins; Dengue; Disseminated Intravascular Coagulation; Fibrin; Fibrinogen; Hemorrhagic Fevers, Viral; Humans; Shock; Syndrome; Thailand; Thrombocytopenia; Transferrin

Topics: Abruptio Placentae; Acute Kidney Injury; Animals; Anuria; Disseminated Intravascular Coagulation; Female; Fibrin; Iodine Radioisotopes; Kidney; Kidney Glomerulus; Mercury Poisoning; Methemoglobin; Pregnancy; Rabbits; Shock; Shwartzman Phenomenon; Tourniquets

Topics: Abortion, Missed; Abruptio Placentae; Blood Coagulation Tests; Collagen Diseases; Erythrocytes; Esters; Female; Fibrin; Fibrinolysis; Fluorides; Hemagglutination Inhibition Tests; Humans; Kidney Diseases; Latex Fixation Tests; Leukemia; Ovarian Neoplasms; Pre-Eclampsia; Pregnancy; Pyruvates; Shock; Staphylococcus; Uterine Neoplasms

Topics: Administration, Oral; Animals; Caseins; Diet Therapy; Dogs; Fibrin; Food; Humans; Nutritional Requirements; Osmolar Concentration; Parenteral Nutrition; Protein Hydrolysates; Shock

Topics: Adult; Anti-Bacterial Agents; Autoimmune Diseases; Blood Viscosity; Capillaries; Cell Membrane; Fibrin; Gas Poisoning; Glucocorticoids; Humans; Hypoxia; Male; Nitrogen Dioxide; Pulmonary Edema; Shock

Topics: Adrenal Glands; Adrenal Medulla; Autopsy; Blood Cell Count; Child; Child, Preschool; Disseminated Intravascular Coagulation; Female; Fibrin; Hemorrhage; Heparin; Histocytochemistry; Humans; Infant; Kidney; Kidney Glomerulus; Length of Stay; Male; Shock; Waterhouse-Friderichsen Syndrome

Topics: Animals; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Group Incompatibility; Dogs; Female; Fibrin; Fibrinogen; Fibrinolysis; Heparin; Immunoelectrophoresis; Male; Rats; Shock; Thrombelastography; Transfusion Reaction

Topics: Animals; Blood Coagulation; Blood Coagulation Factors; Blood Transfusion; Disseminated Intravascular Coagulation; Endotoxins; Female; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhage; Humans; Pregnancy; Pregnancy Complications, Cardiovascular; Shock; Surface-Active Agents; Surgical Procedures, Operative; Thrombosis; Venoms

Topics: Coronary Circulation; Disseminated Intravascular Coagulation; Erythrocyte Aggregation; Fibrin; Fibrinogen; Humans; Microcirculation; Shock; Shock, Septic

Topics: Aged; Agglutination; Animals; Blood Coagulation Disorders; Blood Platelets; Dogs; Female; Fibrin; Fibrinogen; Haplorhini; Humans; Middle Aged; Necrosis; Shock

Topics: Animals; Blood Coagulation Disorders; Blood Platelets; Busulfan; Fibrin; Fibrinogen; Hemolysis; Injections, Intravenous; Kidney Glomerulus; Models, Biological; Neoplasms; Platelet Adhesiveness; Purpura; Rabbits; Sepsis; Shock; Shwartzman Phenomenon; Sulfonic Acids; Thrombocytopenia

Topics: Amniotic Fluid; Animals; Embolism; Endocardium; Female; Fibrin; Lung; Pregnancy; Rabbits; Shock

Topics: Adaptation, Physiological; Adrenal Glands; Adrenocorticotropic Hormone; Blood Circulation; Blood Coagulation; Blood Flow Velocity; Endotoxins; Fibrin; Homeostasis; Humans; Hydrolases; Mononuclear Phagocyte System; Pathology; Radiation Injuries; Radiation Injuries, Experimental; Shock; Stress, Physiological

Topics: Afibrinogenemia; Animals; Blood Coagulation Disorders; Blood Coagulation Tests; Dogs; Epinephrine; Fibrin; Fibrinogen; Pharmacology; Postoperative Complications; Reserpine; Shock; Shock, Hemorrhagic; Thrombophilia

Topics: Blood Transfusion; Fibrin; Humans; Shock; Thrombolytic Therapy

Topics: Acetylcholine; Convulsive Therapy; Fibrin; Fibrinolysis; Humans; Shock

Topics: Anaphylaxis; Capillary Permeability; Fibrin; Humans; Hypersensitivity; Peptones; Serum; Shock

Topics: Blood Coagulation; Blood Coagulation Disorders; Embolism; Female; Fibrin; Hemorrhagic Disorders; Heparin; Humans; Infant, Newborn; Meconium; Placenta; Pregnancy; Shock

Topics: Blood Coagulation; Blood Physiological Phenomena; Blood Transfusion; Fibrin; Fibrinolysis; Humans; Platelet Transfusion; Shock

Topics: Adrenal Glands; Blood; Fibrin; Fibrinolysis; Peptones; Shock

Topics: Anaphylaxis; Animals; Blood; Dogs; Fibrin; Fibrinolysis; Hypersensitivity; Immune System Diseases; Peptones; Shock