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Radial head fracture is given as 33% of elbow region while distal radius as 1/6 of fracture (not known) of what? If we refer all type B & C fracture for all fractures than how the patients in Village order red viagra 200mg fast delivery, Tehsil cheap 200 mg red viagra with amex, District will be treated as we do not have any networking of referral centers (they are all concentrated in the cities. Is it to stop small centers in cities to stop operating the particular type of fractures and force them to refer or to make a national policy for the overall effective management of the orthopaedic patients? Incidence & classification: Scaphoid fracture accounts for about 50-80% of carpal injuries. It is caused by a fall on the outstretched palm, resulting in severe hyperextension and slight radial deviation of the wrist. Tuberosity fractures and Nondisplaced distal third fractures: Conservative with scaphoid cast for 6-8 weeks 2. Hand Fractures: 35 Metacarpal and phalangeal fractures are common, comprising 10% of all fractures. There is a high degree of variation in mechanism of injury accounting for broad spectrum of patterns of fractures in hand. Incidence & classification: Distal phalanx fractures are most common of all hand fractures (45%) followed by metacarpal fractures (30%), proximal phalanx (15%) and middle phalanx (10%). For comminuted fractures, ligamentotaxis with external fixators or specialized reconstruction techniques can be used. Reasons for referral to higher centre: Lack of expertise, lack of infrastructure, Fracture dislocations Tendon Injuries 36 Extensor Tendon Injuries are usually treated with primary repair Flexor tendon injuries are treated according to zone of injuries: Zone 1: Direct Repair, tenodesis or arthrodesis in some cases Zone 2: Need expertise, primary repair or delayed grafting Zone 3: primary repair Zone 4: primary repair Zone 5: primary repair Complication include stiffness, rupture of the graft or repair site, bowstringing etc. Radial head fracture is given as 33% of elbow region while distal radius as 1/6 of fracture (not known) of what? If we refer all type B & C fracture for all fractures than how the patients in Village, Tehsil, District will be treated as we do not have any networking of referral centers (they are all concentrated in the cities. Is it to stop small centers in cities to stop operating the particular type of fractures and force them to refer or to make a national policy for the overall effective management of the orthopaedic patients? The treatment varies with the age of the patient, the level of the fracture and the displacement of the fragments. If union of the fracture is not likely to be achieved then what alternative method should be adopted which will suit the patient, keeping in mind his age, life style, profession and economic status. Majority of our patients are not covered by health insurances, hence all the expenditure has to be born by the patient himself. It is therefore desirable on the part of treating orthopaedic surgeon to choose a method which these patients can afford. Fracture neck femur is commonly seen in old people but in our country quite a good number of patients are young adults. Fracture neck femur whether intra-capsular or extra-capsular can be diagnosed and differentiated by clinical examination and confirmed by the roentgenograms. Any underlying pathologic condition like metastasis or osteoporosis if present can also be identified on roentgenograms. Fracture neck femur intra-capsular can be divided as per the following classifications: (A) Garden Classification  Type 1 is a stable fracture with impaction in valgus. The aim of treatment is to achieve union of the fracture and a durable hip joint afterwards. More than 21 days – Neglected fracure Management: Primary health centre level: The doctor on duty should recognise the features of fracture and disloction. The injured should be referred to the higher centre earliest feasible causing no further harm. Investigations: X-rays of the pelvis including both hip and knee joint and of other areas if required, General Investigations and specific if required according to the status of the health of the patient. Sub-capital and transcervical fractures should be fixed with multiple Kirschner (K) wires or Moore’s pins after closed reduction in valgus. Basicervical fractures can be fixed either by K wires, Moore’s pins or cancellous/cannulated lag screws. Age 16-50 years Sub-capital fractures: Undisplaced: Internal fixation with 2-3 cancellous/cannulated lag screws Displaced: Closed reduction and fixation with Lag screws.

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Thrombin purchase red viagra 200 mg with mastercard, when bound to a receptor on endothelial cells called thrombomodulin buy red viagra 200mg with mastercard, can cleave a small peptide from and thus activate protein C. Factor V Leiden is a genetic mutation (substitution of arginine with glutamine at position 506) that decreases degradation of factor Va by activated protein C. These clinical observations establish the physiologic importance of the protein C/protein S mechanism for regulating coagulation. A balance between fibrin deposition and lysis maintains and remolds the hemostatic seal during repair of an injured vessel wall. Plasmin arises from an inert plasma precursor, plasminogen, through cleavage of a single arginine-valine peptide bond. Fibrin is first degraded into large 360 Hematology fragments (X and Y) and then into smaller fragments (D and E). When fibrinogen is converted to fibrin, lysine residues become available on the molecule to which plasminogen can bind tightly by way of lysine-binding sites. Two types of plasminogen activators triggering lysis of intravascularly deposited fibrin are released from vascular endothelial cells. The second type, urokinase, exists in single-chain and double-chain forms with different functional properties. A trace concentration of plasmin cleaves single-chain to double-chain urokinase plasminogen activator, which is an equally potent activator of plasminogen in solution and of plasminogen bound to fibrin. Epithelial cells that line excretory ducts (eg, renal tubules, mammary ducts) also secrete urokinase, which is thought to be the physiologic activator of fibrinolysis in these channels. Streptokinase, a bacterial product not normally found in 361 Hematology the body, is another potent plasminogen activator. The primary plasmin inhibitor is 2-antiplasmin, which can very rapidly inactivate free plasmin escaping from a fibrin clot. Plasma also contains histidine-rich glycoprotein, which is not a serine protease inhibitor but competes for lysine-binding sites on plasminogen, thus reducing the plasma concentration of plasminogen molecules with free lysine-binding sites. Moreover, plasmin escaping from the fibrin surface is almost instantaneously neutralized by 2- antiplasmin. Their severe tissue bleeding after trivial injury establishes 2-antiplasmin as a key regulator of normal fibrinolysis. An occasional patient with decompensated chronic liver disease may bleed uncontrollably because of excessive fibrinolysis thought to partially stem from acquired severe 2-antiplasmin deficiency (secondary to diminished hepatocellular synthesis plus increased consumption caused by excessive plasminogen activator activity). Screening tests measure combined effects of factors that influence a particular phase of coagulation (eg, bleeding time). Additional tests may measure a product or effect of pathologic in vivo activation of platelets, coagulation, or fibrinolysis (eg, level of fibrin degradation products). Screening test results and knowledge of the clinical disorder guide the selection of more specific diagnostic tests. A disposable, spring-loaded bleeding time device is used to make a 6-mm × 1-mm incision on the volar aspect of the forearm. Plasma is incubated for 3 min with a reagent supplying procoagulant phospholipid and a surface-active powder (eg, micronized silica). Because the test is independent of the reactions that generate thrombin, it is used to screen specifically for abnormalities affecting the thrombin-fibrinogen reaction: heparin, large fibrin degradation products, and qualitative abnormalities of fibrinogen. It is particularly useful in establishing whether a plasma sample contains heparin (eg, residual heparin not neutralized after an extracorporeal bypass procedure or contaminated plasma obtained from blood drawn from a line kept open with heparin flushes). In plasma that contains heparin, the thrombin time will be prolonged, but a repeat test will be normal if the reagent batroxobin (a snake venom enzyme insensitive to heparin that directly converts fibrinogen to fibrin) is substituted for thrombin. A normal result does not rule out a milder yet potentially 368 Hematology clinically significant abnormality of fibrinolysis (eg, a reduced plasma 2-antiplasmin level in the 10 to 30% of normal range). One-tenth volume of 1% protamine sulfate is mixed with plasma, which, after a brief incubation at 37° C (98. A false-positive result may be caused by difficulty with venipuncture or by inadequate anticoagulation of a blood sample. In the D-dimer test, undiluted test plasma and diluted test plasma as necessary are mixed with latex particles coated with monoclonal antibodies that react exclusively with derivatives of fibrin that contain D-dimer, which are formed when plasmin degrades cross-linked fibrin. The antibodies will not react with fibrinogen itself, which is why the test can be performed on plasma, nor with fibrinogen degradation products because these are not cross-linked. Agglutination with a 1:20 dilution of serum indicates increased amounts (>= 40 µg/mL) of fibrin degradation products. A euglobulin lysis time is also often part of screening if increased fibrinolytic activity is suspected.

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La sangre derramada purchase red viagra 200 mg fast delivery, si no tiene fácil salida al exterior se acumula aumentando la presión local y cuando alcanza una tensión igual a la que existe en el interior del vaso contribuye a detener la hemorragia 200 mg red viagra mastercard. En caso de lesiones venosas como su pared es más delgada y su capa muscular fina, escasa y débil, este mecanismo no ocurrirá. Otro mecanismo defensivo es la formación local de un tapón hemostático de fibrina mediante la cascada de la coagulación de la sangre, dicha fibrina se produce en finas hebras, que se entretejen en una red de apretadas mallas que aprisionan plaquetas, hematíes y otros elementos para formar el coágulo. Puede ser copiosa y no verse, pero sí sospecharse por los signos y síntomas de choque en el lesionado. Signos - Palidez generalizada - Frialdad de las cuatro extremidades, nariz, orejas - Labios afilados, pálidos y cianóticos - Sudoración, a veces sutil en el mentón y la nariz - Pulso radial, o periféricos en general, imperceptibles o muy débiles - Taquicardia - Presión arterial baja y descendiendo Síntomas - Sed. Pide agua con ansiedad - Frío - Indiferencia - Inconsciencia Es posible sospechar la lesión de vasos sanguíneos en las extremidades cuando no existe comunicación hacia el exterior por la presencia de hematomas. En caso que sea una arteria la lesionada, se encontrará un hematoma pulsátil, con soplo sistólico. En la extremidad, por debajo de la lesión vascular, existen los signos de isquemia aguda. Mientras que en caso de lesión venosa de mediano o gran calibre existe un hematoma, no pulsátil, pero que crece muy rápidamente. Arterial, venosa o ambas La hemorragia externa se ve, es hacia fuera y puede ser arterial, venosa o ambas. En la venosa la sangre es del color del café o malta, oscura, brota espontáneamente, sin latidos, encharca al lesionado y la camilla. Algunas formas particulares de hemorragias externas - Epistaxis: hemorragia por las fosas nasales - Otorragia: Hemorragia proveniente del oído. Hemostasia provocada Son los métodos tanto temporales como definitivos que se utilizan para detener la hemorragia. Métodos temporales de control de la hemostasia en las hemorragias del tronco: tórax y abdomen Los métodos temporales de control no solucionan las hemorragias en las grandes cavidades. Las hemorragias internas en las cavidades necesitan de intervención quirúrgica de emergencia sin pretensión de lograr la estabilidad hemodinámica sin realizarla. Esto asegura la perfusión renal sin peligro de nueva o mayor hemorragia, mientras se alcanza el salón de operaciones que puede estar más o menos distante. Las causas más frecuentes de hemorragia interna son: 145 - Rotura de un embarazo ectópico (casi siempre tubario) - Rotura de un aneurisma de la aorta abdominal - Rotura traumática de víscera maciza: bazo (hipocondrio izquierdo), hígado (hipocondrio derecho) - Heridas y otros traumas - Ruptura de un folículo hemorrágico Medidas temporales de control de la hemostasia en las hemorragias de las extremidades Las medidas temporales para el control de la hemostasia serán mejores cuando se trata de extremidades con hemorragias externas. Cuando la hemorragia es severa y una arteria principal ha sido afectada, la presión manual puede resultar insuficiente y puede ser necesario colocar un torniquete. En los casos de hemorragia severa por herida arterial es posible que la presión sea insuficiente y se requiera un torniquete que es un método efectivo en las extremidades para detener la hemorragia; sin embargo, interrumpe la circulación hacia la porción inferior del miembro afectado y solo debe usarse cuando otros métodos, tales como los vendajes compresivos, hayan fracasado. Solamente se aplicará un torniquete, por personas con experiencia, para controlar la hemorragia de una herida arterial, como último recurso, y en situaciones que pongan en peligro la vida, como por ejemplo, en una copiosa hemorragia arterial que no cesa con la presión manual sostenida, pues puede hacer más mal que bien. Se debe aplicar el torniquete al miembro entre el área de la hemorragia arterial y el corazón. El mejor torniquete es un esfigmomanómetro, en su ausencia, para elaborar un torniquete, es preciso utilizar vendas de 5 a 8 cm de ancho y envolver el miembro con ellas varias veces, para luego atar un nudo medio y permitir que las puntas 147 sean lo suficientemente largas como para atar otro nudo. Se le hace girar hasta que la venda que se le realiza la torsión esté lo suficientemente apretada como para que cese la hemorragia. Es necesario inspeccionar el torniquete cada 10 a 15 minutos y, si al “abrirlo” la hemorragia está detenida, se le deja abierto “in situ”. El mejor torniquete en el consultorio u hospital es el esfigmomanómetro, porque es: - Ancho - Acolchado, es un manguito de aire - Atraumático - Puede controlarse la presión a la que se aplicará. Mejor torniquete en la calle Un cinto ancho, pañoleta de pionero, pañuelos, mecha de farol, cámara de bicicleta y otros. Utilizar sobre un apósito, pañuelo o paño de manera que sirvan de acolchamiento entre él y la piel del lesionado. Permanecer el menor tiempo posible, a los 10 ó 15 minutos se aflojará y si no hay nuevo sangramiento se dejará flojo, sin retirarse. Anotar en la hoja de remisión, hoja de traslado, tarjeta del lesionado o tarjeta del herido de guerra que está puesto y su hora de cierre, así como en la frente del lesionado con: - Tinta indeleble - Plumones permanentes - Pintura - Mercurocromo - Esparadrapo pegado escrito - Lápiz labial - Sangre del lesionado - Otros 149 Complicaciones del torniquete 1. Estado de cgoque por supresión del torniquete, que puede llegar a ser súbito e irreversible. Muerte Medios permanentes de control de la hemorragia Pinzas, ligaduras, electrocoagulación, láser, esponja de fibrina, surgicel, pegamentos biológicos, rafias, parches, sustituciones con vasos homólogos, sustituciones con prótesis vasculares. Cuerpos extraños en trayecto vascular En alguna ocasión el médico puede recibir en su consultorio, policlínico o cuerpo de guardia del hospital un herido con un cuerpo extraño en un trayecto vascular.

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