Occluding Plug Research Articles

A Misdiagnosed Case of Endoleak Type-III Caused by Inadvertent Bilateral Limb Insertion in the Same Limb Gate of the Ovation Endograft.

We describe an infrequent case of endoleak Type-III due to an unrecognized, inadvertent bilateral limb deployment into the same limb gate of the Ovation aortic endograft, accompanied by thrombosis and acute ischemia. The following computed tomography angiography revealed the open limb gate with the characteristic of radio-opaque polymer in the sealing rings. Intraoperative angiographies via the brachial route identified the open limb gate and facilitated the successful use of an occluding plug to manage the Type-III endoleak.

Spontaneous Pneumomediastinum After Kidney Transplantation: Case Report

Spontaneous pneumomediastinum is a rare condition with nonspecific signs and symptoms. A 39-year-old underwent cadaver kidney transplantation. After an uncomplicated operation, progressive dyspnea of unknown origin developed. Findings at chest radiography suggested pneumomediastinum, which was confirmed at computed tomography. Esophageal or tracheal injury was ruled out. The rapidly developing atelectasis of the left lung necessitated urgent bronchoscopy, which revealed occlusion of the left main bronchus. After removal of the occluding mucus plug, the clinical symptoms immediately improved, and the spontaneous pneumomediastinum resolved within 3 days. Asymptomatic increase in airway secretions in patients receiving peritoneal dialysis may result in mucus plug formation during general anesthesia, which can cause spontaneous pneumomediastinum.

Stored erythrocytes have less capacity than normal erythrocytes to support primary haemostasis

Primary haemostasis is mediated by platelet aggregation. Red blood cells (RBCs) are involved in this process. We hypothesised that stored RBCs could have less capacity to support primary haemostasis. This was tested with RBC units from 17 healthy volunteers stored for 45 days. Fresh citrated blood was taken again from the same donors and platelet-rich plasma was prepared, in which RBCs were resuspended with a constant haematocrit (40%), but changing fractions of stored versus fresh autologous RBCs (0, 25, 50, 75, and 100%, respectively). A platelet function analyser PFA-100((R)) was used. In this instrument blood is aspirated through a membrane pore coated with collagen and either epinephrine (EPI) or ADP, which causes platelets to adhere, aggregate, and form an occluding plug, which stops blood flow and is measured as closure time (CT). We found that the CT increased with increasing fractions of stored blood. CT-EPI was 121 +/- 17 seconds [s], 129 +/- 32 s, 164 +/- 45 s (p < 0.000, ANOVA), 214 +/- 54 s (p < 0.0001), and 273 +/- 36 s (p < 0.0001) for 0, 25, 50, 75, and 100% stored RBCs. For CT-ADP the values were 91 +/- 22 s, 95 +/- 12 s, 101 +/- 13 s, 124 +/- 44 s (p = 0.004), and 191 +/- 72 s (p < 0.0001), respectively. We conclude that stored RBCs have less capacity than normal RBCs to support primary haemostasis by platelet aggregation in vitro, suggesting a decreased capacity of stored RBCs to bring platelets into close contact with the wall, which may contribute to sustained bleeding seen after mass transfusion.

Estudo comparativo da reação inflamatória renal entre álcool de polivinil - flocular e álcool de polivinil + acetato de polivinil - esférico: estudo experimental

OBJETIVO: Avaliar as características e os efeitos de um agente embólico, disponível comercialmente, consistindo de Polivinil Álcool (PVA) de morfologia flocular, e comparar com um agente esférico, de tecnologia nacional, consistindo de Polivinil Álcool e Polivinil Acetato (PVA + PVAc). MÉTODO: Foram utilizadas fêmeas de coelho albino "New Zealand", submetidas à embolização arterial renal. PVA-flocular foi usado em 24 animais, assim como PVA+PVAc-esférico. Seis animais foram utilizados como controle. Todos foram mantidos em cativeiro até a morte, por períodos pós-operatórios de 48 horas, cinco dias, 10 dias e 30 dias. RESULTADOS: Ambos os agentes promoveram oclusão do vaso e infarto do órgão. O estudo microscópico inicial das artérias embolizadas com PVA-flocular, mostra oclusão com trombo e PVA. Os vasos embolizados com PVA+PVAc-esférico, mostram os agentes ocupando praticamente todo o lúmen. No estudo de 30 dias, observa-se absorção do trombo e retração dos agentes de PVAflocular, criando espaços. E com PVA+PVAc-esférico, pode-se observar os agentes circundados por intensa fibrose. CONCLUSÕES: Ambas as partículas foram efetivas para causar isquemia tecidual. A reação inflamatória foi mais intensa com PVA+PVAc-esférico que também apresentou grau de penetração maior no sistema vascular.

Rapid sevoflurane induction compared with thiopental

Study objectives To examine whether the speed of induction of anesthesia with sevoflurane/nitrous oxide (N 2O) utilizing a 10-second vital capacity rapid inhalation induction (VCRII) followed by tidal breathing was similar or faster than cautious intravenous (IV) thiopental induction with inhaled N 2O. Design Prospective, randomized, double-blinded study. Setting Veterans Affairs Medical Center. Patients 50 male ASA physical status I, II, and III patients scheduled for general anesthesia. Interventions Patients were randomized to receive either 8% sevoflurane or IV thiopental. Patients were allocated to one of two groups of 25 patients each. In both groups, the breathing circuit was initially primed for 5 minutes with (4 L/min) and O 2 (2 L/min), while the Y-piece was occluded. In the sevoflurane group, the circuit was additionally primed with 8% sevoflurane. Patients were trained to perform a vital capacity breath. After maximal exhalation, the occluding plug was rapidly removed from the Y-piece and connected to the facemask. The patient then inspired to vital capacity, held his breath for 10 seconds, and then was allowed to breathe normally. At the end of the 10-second breathhold, and as the patient started normal breathing, either thiopental (thiopental group) or normal saline (sevoflurane group) was injected at a rate of 4 mL every 10 seconds. Measurements A study-blinded observer recorded the time to induction, as defined by the time to loss of eyelash reflex, and noted the occurrence of side effects. Main results The speed of induction was the same for both groups ( p > 0.05). An average of eight breaths was required before loss of eyelash reflex. Side effects occurred in 36% of the patients in the thiopental group, and 32% in the sevoflurane group ( p > 0.05); these were minor and did not affect induction. Conclusion Sevoflurane/N 2O VCRII as used in this investigation is an effective inhalation technique; it resulted in an induction time similar to that of slow IV thiopental with inhaled N 2O.

Recent insights on biochemical and molecular basis for developing antihaemostatic agents: A review

The normal coagulation process is initiated by disruption and exposure of the subendothelial components of blood vessels. Platelets adhere to subendothelium-bound von Willebrand factor via glycoprotein (GP) Ib complex. This initial interaction per se and the release of platelet agonists transduce signals that leads to the rise in intracellular Ca2+ which induces shape change, prostaglandin synthesis, release of granular contents and conformational changes in platelet Gp IIb-IIIa. Gp IIb-IIIa in activated platelets binds fibrinogen and other adhesive proteins and mediates platelet cohesion the primary haemostatic plug. Furthermore, the activated platelets due to aggregation, result in the formation of fibrin (secondary hemostasis). Normally the haemostatic process plays a delicate balance between keeping the blood in the fluid state to maintain flow and rapidly forming an occluding plug following vessel injury. Thrombosis occurs because of alteration in this delicate balance. Arterial thrombosis occurs in the setting of previous vessel wall injury mostly because of atherosclerosis, while venous thrombosis occurs in areas of stasis. The recent advances in understanding of the haemostatic process have led to a better understanding of the mechanism of action of many antithrombotic drugs and identification of new targets for drug development. The molecular target of the ticlopidine has been identified. Large numbers of IIb-IIIa inhibitors have been developed. The mechanism of action of heparin has been defined at the molecular level. As a result, a synthetic pentasaccharide, based on antithrombin-binding domain of heparin, has been developed and tested successfully in clinical trials. New generation direct thrombin inhibitors are being developed. Factor Xa has a critical position at the convergence of intrinsic and extrinsic pathway. The clinical tolerability and the efficacy of low molecular weight heparins has established that inhibition of further thrombin generation, by blocking factor Xa alone can be an effective way of preventing thrombus growth without inactivating thrombin. A large number of specific factor Xa inhibitors are under development. Some of these are in preliminary clinical trials and appear to be promising. Future clinical trials will determine whether these new drugs will provide better risk-benefit ratio in treatment of thrombotic disorders. Similarly role of thrombolytics has been clearly established in many diseases including coronary artery disease.

Pathologic Evaluation of a Spherical Polyvinyl Alcohol Embolic Agent in a Porcine Renal Model

To evaluate the effects of a spherical embolic agent consisting of polyvinyl alcohol (PVA) and to compare this agent with commercially available embolization agents. Eleven miniature pigs were included in the study population. The upper poles of both kidneys were selected as the target organs for embolization. PVA spheres (700-900 micro m) were used in nine kidneys, PVA particles (500-710 micro m) were used in six kidneys, gelatin spheres (700-900 micro m) were used in five kidneys, and gold-colored gelatin spheres (700-900 micro m) were used in three kidneys. Two animals were killed immediately after embolization. In the remaining animals, angiography was performed before sacrifice 7 days (in five pigs) or 28 days (in four pigs) after embolization. Pathologic and histologic evaluation of the kidneys was performed. All agents resulted in target vessel occlusion and end-organ infarction. All arteries embolized with spherical agents were recanalized at follow-up angiography. In vessels embolized with PVA particles, the occluding plug consisted of thrombus and PVA. In vessels embolized with spherical agents, the occluding plug consisted mostly of the embolic agent. PVA spheres were associated with the mildest inflammatory responses at 7 and 28 days when compared with PVA particles and gelatin-based microspheres. Arterial wall destruction was seen to a greater extent in kidneys embolized with gelatin-based microspheres than in those embolized with PVA-based agents. The spherical, PVA-based embolization agent resulted in target organ infarction and temporary arterial occlusion. The inflammatory response to PVA spheres was significantly less aggressive than the response to other agents tested. Further study with clinical and long-term pathologic follow-up is suggested to determine if these findings may have favorable clinical implications for patients undergoing embolization procedures.

New targets for antithrombotic drugs.

The normal hemostatic process is initiated by disruption in the vascular continuity and exposure of the subendothelial components. Platelets adhere to subendothelium-bound von Willebrand factor via glycoprotein (GP) Ib complex. This initial interaction per se and the release of platelet agonists transduce signals that lead to the rise in intracellular Ca(2+). The rise in Ca(2+) induces shape change, prostaglandin synthesis, release of granular contents and conformational changes in platelet Gp IIb-IIIa. Gp IIb-IIIa in activated platelets becomes competent to bind fibrinogen and other adhesive proteins and mediates platelet cohesion (primary hemostatic plug). Furthermore, the activated platelet surface provides an efficient catalytic surface for the coagulation reactions, ultimately resulting in the formation of fibrin (secondary hemostasis). Normally the hemostatic process plays a delicate balance between keeping the blood in the fluid state to maintain flow and rapidly forming an occluding plug following vessel injury. Thrombosis occurs because of alteration in this delicate balance. Consequences of thrombosis are a major cause of morbidity and mortality in industrialized countries. Arterial thrombosis occurs in the setting of previous vessel wall injury mostly because of atherosclerosis, while venous thrombosis occurs in areas of stasis. The recent advances in our understanding of the hemostatic process have led to a better elucidation of the mechanism of action of many antithrombotic drugs and identification of new targets for drug development. The molecular target of the well known antiplatelet drug ticlopidine has been identified. Large numbers of IIb-IIIa inhibitors have been developed based on the crystal structure of a potent antagonist echistatin. The mechanism of action of heparin has been defined at the molecular level. As a result a synthetic pentasaccharide, based on antithrombin-binding domain of heparin, has been developed and tested successfully in clinical trials. New generation direct thrombin inhibitors are being developed based on the crystal structure of thrombin. Factor Xa has a critical position at the convergence of intrinsic and extrinsic pathway ways. The clinical tolerability and the efficacy of low molecular weight heparins led to the concept that inhibition of further thrombin generation, by blocking factor Xa alone, can be an effective way of preventing thrombus growth without inactivating thrombin. A large number of specific factor Xa inhibitors are under development. Some of these drugs have already undergone preliminary clinical trials and appear to be promising. Future clinical trials will determine whether these new drugs will provide better risk-benefit ratio in treatment of thrombotic disorders.

Sneddonʼs Syndrome—An Inflammatory Disorder of Small Arteries Followed by Smooth Muscle Proliferation

Sneddon's syndrome is a rare, but potentially severe, arterioocclusive disorder characterized by generalized livedo racemosa of the skin and various central nervous symptoms due to occlusion of medium-sized arteries of unknown cause. We have recently shown that, in skin, small to medium-sized arteries of the dermis-subcutis boundary are affected in a stage-specific sequence. An initial phase (stage I), characterized by the attachment of lymphohistiocytic cells and detachment of endothelial cells (endothelitis), is followed by an early phase (stage II), which displays partial or complete occlusion of the lumen by a plug of lymphohistiocytic cells and fibrin. In an intermediate phase (stage III), the occluding plug is replaced by proliferating subendothelial cells accompanied by the occurrence of dilated capillaries in the adventitia of the occluded vessel. The late phase (stage IV) shows fibrosis and shrinkage of the affected vessels. We investigated sections of paraffin-embedded specimens of 18 patients by immunohistochemistry using a panel of antibodies to detect endothelial cells, macrophages, T cells, smooth muscle-specific actin, and intermediate filaments (vimentin, desmin). We found that the cells involved in subendothelial proliferation were vimentin and actin positive (smooth-muscle-specific), but desmin negative and thus displayed the phenotype characteristic of smooth muscle cells, which was confirmed by ultrastructural studies. CD3+, UCHL-1+, and HLA-DR+ cells constituted a significant proportion of the inflammatory infiltrate in the early stages. The endothelial cells in the dilated capillaries of the adventitia were strongly HLA-DR positive. In later stages, endothelial cells and leukocytes were scarce. The data confirm the hypothesis that Sneddon's syndrome starts as an inflammatory and possibly immunologically mediated disorder, leading to a migration and proliferation of smooth cells of small arteries, resulting in a partial or complete narrowing of the vessel lumen.

Induction of vascular haemostasis by Nd:YAG laser light in melanin-rich and melanin-free tissue.

Haemostasis was effected in vessels of melanin-rich (MR: choroid) and melanin-free (MF: mesentery) rabbit tissue irradiated with a cw-Nd:YAG laser. The following parameters were employed: - pulse duration: 200 ms (MR) and 100 ms (MF); focal spot diameter: 200 microns (MR) and 80 microns (MF); pulse energies: 100-250 mJ (MR) and 0.5-1 J (MF); irradiances: 1.6-4.0 kW cm-2 (MR) and 1-2 x 10(2) kW cm-2 (MF). In melanin-rich tissue, laser energy is absorbed principally by melanin granules contained within the stromal melanocytes. The heat generated in these structures radiates into the surrounding tissue where it is dissipated. The damage thus incurred by the endothelium of blood vessels encompassed within this field triggers the haemostatic mechanism whereby blood flow is arrested. This effect is realized by the formation of an occluding plug of platelets, which is stabilized by the deposition of fibrin, particularly in capillaries, and to a lesser degree in larger vessels of the vascular lamina. In melanin-free tissue, haemoglobin serves as the primary site of energy absorption, which is thus shifted from the stroma to the vessel lumen. Irradiation of vessels in such tissue leads to thermocoagulation of plasma proteins and consequent stasis of blood flow.

Life history of cutaneous vascular lesions in Sneddon's syndrome

Sneddon's syndrome is a potentially fatal arterio-occlusive disorder characterized by generalized livedo racemosa and cerebrovascular lesions. Skin biopsies often fail to yield diagnostic arterial lesions. In the present series, affected vessels were found in skin biopsies from 12 of 15 patients with Sneddon's syndrome. Selection of the correct biopsy site (seemingly uninvolved skin at the center of a livedo racemosa area), adequate biopsy size (1 to 2 cm), and serial sections are essential for the detection of relevant vascular pathology. Only small to medium-sized arteries of the dermis-subcutis boundary were found to be involved. Lesions follow a distinct course. The initial stage displays partial detachment of endothelial cells, adhesion of mononuclear cells interspersed with fibrin (“endothelitis”), a marked edema of the surrounding connective tissue with numerous dilated capillaries, and a predominantly lymphohistiocytic infiltrate with polymorphonuclear leukocytes. In the early phase a sponge-like plug is formed from mononuclear cells, fibrin, and red blood cells, leading to partial to complete obstruction. A perivascular inflammatory infiltrate, devoid of polymorphonuclear leukocytes, is located around affected arteries; in the adventitia of the occluded vessel, a very regular corona of dilated capillaries appears that is continuous with more peripheral dilated and branching vessels. Organization of the occluding plug ensues in the intermediate stage by “subendothelial cell proliferation,” most likely due to immigrating smooth muscle cells. In the final stage, the occluding artery undergoes fibrosis, shrinkage, and atrophy.

Strukturierende prinzipien hämostatischer prozesse

The formation of the hemostatic plug on areas of skin injury is characterized as a sequence of structure-forming processes ending in the formation of an impenetrable barrier. The morphology of this barrier is further elucidated by means of scanning- and transmission electron microscopy. Especially the fibrin coating of the injury shows a completely different formation than is deducible from the solely hemostaseologically orientated view of the formation of the hemostatic plug. These structure-forming processes are: activation of the intrinsic clotting system by means of explosion-like destruction of thrombocytes with an immediate formation of a fibrin clot within seconds after the injury. Later during the process the fibrin clot is then condensed and as a function of thrombocyte dependent retraction receives its final fibrin stabilisation and modellation towards an occluding plug. The very narrow net formation of fibrin fibers is interpreted as dependent on the destruction of thrombocyte pseudopodia using their round shape as a rail for fibrin fiber formation. Disturbances of clot formation of post-mortal clots compared to vital clots are interpreted as functional thrombocytic distortions, especially of the thrombocytic energy metabolism. Extracorporal clotting of blood drops after extreme ischemia resemble fibrin structures and fibrin structure formation distortions of postmortal origin.

Bone Conduction Threshold Measurements: Effects of Occlusion and Masking Devices

As shown by many investigators, occlusion of the external ear canals produces a lowering of the bone conduction threshold for normal ears at low frequencies. The present investigation shows that complete occlusion is not necessary to produce some threshold shift but that complete occlusion is necessary to give a maximal shift at a given frequency—also that if occlusion is complete, variation of the mass of the occluding plug does not cause a corresponding variation of the shift, the shift remaining almost constant. Small enclosures, placed over the ears and pressed tightly against them or the adjacent portion of the skull, coupling a small closed volume of air to the air of each external ear canal, also produce a lowering of the bone conduction threshold; but large enclosures, lined with absorptive material, do not. A similar, but smaller, shift arises for an enclosure over one ear. Earphones with rubber ear cushions to prevent air radiation have been used by some investigators to introduce thermal masking noise into one ear by air conduction while testing the acuity of the other ear by bone conduction. Such a masking device produces the type of bone conduction threshold shift. mentioned above if used on a normal ear or on one with small loss, and frequently causes a spurious bone conduction threshold for the ear being tested. A masking device has been developed which will introduce thermal masking noise into one ear by air conduction without causing a bone conduction threshold shift, thereby making possible accurate bone conduction threshold measurements on the opposite ear.