A method of tissue ablation and bleeding control that uses ARGON plasma (ionized argon gas) to deliver a current of thermocoagulating energy to the area of tissue to be coagulated.

Argon. A noble gas with the atomic symbol Ar, atomic number 18, and atomic weight 39.948. It is used in fluorescent tubes and wherever an inert atmosphere is desired and nitrogen cannot be used.

Procedures using an electrically heated wire or scalpel to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. It is different from ELECTROSURGERY which is used more for cutting tissue than destroying and in which the patient is part of the electric circuit.

Control of bleeding performed through the channel of the endoscope. Techniques include use of lasers, heater probes, bipolar electrocoagulation, and local injection. Endoscopic hemostasis is commonly used to treat bleeding esophageal and gastrointestinal varices and ulcers.

The use of green light-producing LASERS to stop bleeding. The green light is selectively absorbed by HEMOGLOBIN, thus triggering BLOOD COAGULATION.

INFLAMMATION of the MUCOUS MEMBRANE of the RECTUM, the distal end of the large intestine (INTESTINE, LARGE).

A distinct vascular lesion in the PYLORIC ANTRUM that is characterized by tortuous dilated blood vessels (ectasia) radiating outward from the PYLORUS. The vessel pattern resembles the stripes on the surface of a watermelon. This lesion causes both acute and chronic GASTROINTESTINAL HEMORRHAGE.

Acquired degenerative dilation or expansion (ectasia) of normal BLOOD VESSELS, often associated with aging. They are isolated, tortuous, thin-walled vessels and sources of bleeding. They occur most often in mucosal capillaries of the GASTROINTESTINAL TRACT leading to GASTROINTESTINAL HEMORRHAGE and ANEMIA.

Bleeding in any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM.

The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.

A condition with damage to the lining of the lower ESOPHAGUS resulting from chronic acid reflux (ESOPHAGITIS, REFLUX). Through the process of metaplasia, the squamous cells are replaced by a columnar epithelium with cells resembling those of the INTESTINE or the salmon-pink mucosa of the STOMACH. Barrett's columnar epithelium is a marker for severe reflux and precursor to ADENOCARCINOMA of the esophagus.

Endoscopic examination, therapy or surgery of the esophagus.

Ionized gases, consisting of free electrons and ionized atoms or molecules which collectively behave differently than gas, solid, or liquid. Plasma gases are used in biomedical fields in surface modification; biological decontamination; dentistry (e.g., PLASMA ARC DENTAL CURING LIGHTS); and in other treatments (e.g., ARGON PLASMA COAGULATION).

A condition with trapped gas or air in the PERITONEAL CAVITY, usually secondary to perforation of the internal organs such as the LUNG and the GASTROINTESTINAL TRACT, or to recent surgery. Pneumoperitoneum may be purposely introduced to aid radiological examination.

Injuries caused by electric currents. The concept excludes electric burns (BURNS, ELECTRIC), but includes accidental electrocution and electric shock.

Harmful effects of non-experimental exposure to ionizing or non-ionizing radiation in VERTEBRATES.

Endoscopic examination, therapy or surgery of the gastrointestinal tract.

Endoscopic examination, therapy or surgery of the interior of the stomach.

Endoscopic examination, therapy or surgery of the bronchi.

A compound produced from succinyl-CoA and GLYCINE as an intermediate in heme synthesis. It is used as a PHOTOCHEMOTHERAPY for actinic KERATOSIS.

Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.

Drugs that are pharmacologically inactive but when exposed to ultraviolet radiation or sunlight are converted to their active metabolite to produce a beneficial reaction affecting the diseased tissue. These compounds can be administered topically or systemically and have been used therapeutically to treat psoriasis and various types of neoplasms.

Laboratory tests for evaluating the individual's clotting mechanism.

Therapy using oral or topical photosensitizing agents with subsequent exposure to light.

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.

Endogenous substances, usually proteins, that are involved in the blood coagulation process.

Tumors or cancer of the ESOPHAGUS.

Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.

Clotting time of PLASMA recalcified in the presence of excess TISSUE THROMBOPLASTIN. Factors measured are FIBRINOGEN; PROTHROMBIN; FACTOR V; FACTOR VII; and FACTOR X. It is used for monitoring anticoagulant therapy with COUMARINS.

Hemorrhagic and thrombotic disorders that occur as a consequence of abnormalities in blood coagulation due to a variety of factors such as COAGULATION PROTEIN DISORDERS; BLOOD PLATELET DISORDERS; BLOOD PROTEIN DISORDERS or nutritional conditions.

Constituent composed of protein and phospholipid that is widely distributed in many tissues. It serves as a cofactor with factor VIIa to activate factor X in the extrinsic pathway of blood coagulation.

A low-osmolar, ionic contrast medium used in various radiographic procedures.

Heat- and storage-stable plasma protein that is activated by tissue thromboplastin to form factor VIIa in the extrinsic pathway of blood coagulation. The activated form then catalyzes the activation of factor X to factor Xa.

The residual portion of BLOOD that is left after removal of BLOOD CELLS by CENTRIFUGATION without prior BLOOD COAGULATION.

A fibrin-stabilizing plasma enzyme (TRANSGLUTAMINASES) that is activated by THROMBIN and CALCIUM to form FACTOR XIIIA. It is important for stabilizing the formation of the fibrin polymer (clot) which culminates the coagulation cascade.

Tumors or cancer of the pelvic region.

Stable blood coagulation factor activated by contact with the subendothelial surface of an injured vessel. Along with prekallikrein, it serves as the contact factor that initiates the intrinsic pathway of blood coagulation. Kallikrein activates factor XII to XIIa. Deficiency of factor XII, also called the Hageman trait, leads to increased incidence of thromboembolic disease. Mutations in the gene for factor XII that appear to increase factor XII amidolytic activity are associated with HEREDITARY ANGIOEDEMA TYPE III.

The use of photothermal effects of LASERS to coagulate, incise, vaporize, resect, dissect, or resurface tissue.

The time required for the appearance of FIBRIN strands following the mixing of PLASMA with phospholipid platelet substitute (e.g., crude cephalins, soybean phosphatides). It is a test of the intrinsic pathway (factors VIII, IX, XI, and XII) and the common pathway (fibrinogen, prothrombin, factors V and X) of BLOOD COAGULATION. It is used as a screening test and to monitor HEPARIN therapy.

A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia.

Storage-stable blood coagulation factor acting in the intrinsic pathway. Its activated form, IXa, forms a complex with factor VIII and calcium on platelet factor 3 to activate factor X to Xa. Deficiency of factor IX results in HEMOPHILIA B (Christmas Disease).

Blood-coagulation factor VIII. Antihemophilic factor that is part of the factor VIII/von Willebrand factor complex. Factor VIII is produced in the liver and acts in the intrinsic pathway of blood coagulation. It serves as a cofactor in factor X activation and this action is markedly enhanced by small amounts of thrombin.