vitamin-k-semiquinone-radical and Shock--Septic

Topics: Bacterial Vaccines; Bicarbonates; Brain Edema; Diagnosis, Differential; Diazepam; Digoxin; Fever; Gastrointestinal Hemorrhage; Heparin; Humans; Hydrocortisone; Infant; Infant, Newborn; Isoproterenol; Mannitol; Meningitis; Meningitis, Meningococcal; Meningitis, Viral; Phenytoin; Seizures; Shock, Septic; Vitamin K

Topics: Ascorbic Acid; Humans; Pilot Projects; Shock, Septic; Thiamine; Vitamin A; Vitamin K; Vitamins

Since the mid-1980s, an increase in incidence of invasive disease caused by group A streptococci has been noted among adults and children. The characteristic clinical and laboratory features of the streptococcal toxic shock syndrome include deep-seated infection associated with shock, skin manifestation, and multiorgan failure. However, bullous impetigo is invariably considered to be a staphylococcal disease. Staphylococcus aureus produces an epidermolytic toxin, assumed to be the cause of bullous formation in the skin. Here, we present a case of bullous impetigo in an infant with streptococcal toxic shock syndrome. This is a rare presentation of bullous impetigo caused by group A streptococcus.

Topics: Anti-Bacterial Agents; Cardiotonic Agents; Cefotaxime; Clindamycin; Colloids; Combined Modality Therapy; Disseminated Intravascular Coagulation; Female; Humans; Impetigo; Infant; Plasma; Respiration, Artificial; Shock, Septic; Skin Diseases, Vesiculobullous; Streptococcal Infections; Streptococcus pyogenes; Vancomycin; Vitamin K

Group A beta-hemolytic Streptococcus (pyogenes) has been associated recently with toxic-shock-like syndrome similar to staphylococcal toxic shock as described originally in 1978. A group A beta-hemolytic streptococcal infection occurred in a recent postpartum patient and clinically resembled staphylococcal toxic shock.

Topics: Adult; Blood Gas Analysis; Drainage; Empyema; Female; Humans; Penicillin G; Pleural Effusion; Radiography; Shock, Septic; Streptococcal Infections; Streptococcus pyogenes; Vitamin K

Vascular endothelium plays an active role in preventing blood clot formation in vivo. One mechanism by which prevention is achieved involves a cell surface thrombin-binding protein, thrombomodulin, which converts thrombin into a protein C activator. Activated protein C then functions as an anticoagulant by inactivating two regulatory proteins of the coagulation system, factors Va and VIIIa. The physiological relevance of the protein C anticoagulant pathway is demonstrated by the identification of homozygous protein C--deficient infants with severe thrombotic complications. Recent studies suggest that this pathway provides a link between inflammation and coagulation.

Topics: Animals; Blood Coagulation; Chemical Phenomena; Chemistry; Glycoproteins; Homeostasis; Humans; Liposomes; Papio; Protein C; Protein S; Receptors, Cell Surface; Receptors, Thrombin; Shock, Septic; Thrombin; Thrombosis; Vitamin K

Authors present their adopted measures, in the different clinical stages of endotoxic shock with a phisiological approach, paying special attention to those secondary to meningococcal infections.

Topics: Adrenal Cortex Hormones; Anti-Bacterial Agents; Cardiovascular Agents; Combined Modality Therapy; Fluid Therapy; Humans; Intensive Care Units; Meningococcal Infections; Shock, Septic; Vitamin K