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After division of the scalenus anterior muscle the subclavian artery and the brachial plexus will slide forward and will be relieved of compression order cheapest silvitra erectile dysfunction treatment options. The subclavian artery and the lower trunk of the brachial plexus should be examined carefully whether they are really relieved of any stretching or compression generic 120 mg silvitra with amex erectile dysfunction 34. Sometimes the nerve trunk appears to be stretched over the medial tendinous fibres of the scalenus medius discount silvitra amex erectile dysfunction effects on women. A thorough search should be made for presence of a fibrous band in the substance of the scalenus medius muscle or neighbourhood. Two types of embolization are seen — (i) cardioarterial embolization and (ii) arterioarterial embolization. The main three causes are — atrial fibrillation, mitral stenosis and myocardial infarction. It may also occur from atherosclerosis without mitral stenosis particularly in older patients. With mitral stenosis emboli originate from thrombi which are formed in the left atrium because of restriction of blood flow through the stenotic mitral valve. These patients may also have atrial fibrillation which may be the cause of emboli formation. In myocardial infarction emboli originate from mural thrombi which are formed over the endocardial surfaces of the infarcts. Other rare causes of cardioarterial embolization are bacterial endocarditis and atrial myxoma. Another 5% emboli lodge in the visceral arteries — the superior mesenteric, renal etc. Emboli of the lower extremity usually lodge at bifurcation of major arteries where the diameter abruptly narrows. The common sites according to frequency of occurrence are : at the bifurcation of common femoral artery (about 35%), at the bifurcation of popliteal artery (15%), at the bifurcation of the common iliac artery (14%), at the bifurcation of the aorta (10%). In the superior extremity the commonest site is at the bifurcation of the brachial artery (about 10%), followed by axillary artery near shoulder joint (4. If untreated, gangrene occurs in about 50% of cases depending upon the artery involved. Striated muscles are less susceptible to oxygen deprivation and necrosis only appears after 4 to 6 hours. This time of course varies depending on the size of the artery occluded, axillary 4. These emboli may embolus lodgement, lodge anywhere, either near the atherosclerotic artery of some distance away from it. Emboli at the ends of anterior tibial and posterior tibial arteries may originate from the atherosclerotic plaques in the abdominal or thoracic aorta. Sometimes progressive ischaemia occurs which terminate to gangrene or repeated embolic episodes are seen with almost complete recovery between the episodes. Most arterial injuries result from penetrating wounds which partly or completely disrupt the walls of the arteries. Penetrating injuries may be associated with fractures in the adjacent bones which cause arterial blockage. Most arterial injuries are either lacerations or transections of the arterial wall. Rarer causes may be simple spasm of the arterial wall in association with fractures and/or extensive soft tissue injuries from blunt trauma. Sometimes swelling of the surrounding soft tissues may cause blockage of the artery within the fixed fascial compartments, which are known as a compartmental syndrome (see above). The best way to distinguish between arterial embolism and other causes of acute limb ischaemia is to take proper history and to examine the rest of the patient. Valvular heart disease and recent myocardial ischaemia account for majority of causes. Presence of atrial fibrillation should always give rise to the suspicion of cardio-genic embolism. In 80% of cases there is severe pain referred to the most peripheral portions of the limb. Alongwith the pain, the colour of the affected extremity becomes extremely pallor or mottling due to alternate areas of pallor and cyanosis, Neurologic symptoms carry a prognostic value. In majority of cases there may be some sensory disturbances which vary from paraesthesia to anaesthesia. Sometimes paralysis with anaesthesia may elude the clinician to divert his attention towards neurologic disease. Palpation of arterial pulse is the most important examination to know the site of obstruction. The pulse of the main artery if traced down, suddenly the pulsation will be lost at the point of obstruction. It must also be noted that at the site of lodgement of embolus the artery feels firm and often tender. For practical purposes this means that if the common femoral pulse is absent, the embolus is either lodged there in which case the artery becomes firm and tender or higher up most probably in the common iliac in which case the femoral artery is soft and non tender. Similarly the popliteal pulse becomes absent and the artery is tender when the embolism is within it. Sometimes the popliteal pulse is full and bounding, even stronger than the normal side. This happens when a small embolus impacts at the bifurcation of the artery below the level of the knee. The pulse can usually be traced down to the point where it meets the obstruction; here there is often a tender small swelling and the pulse is lost. However the level of ischaemia does not correspond to the level of site of occlusion. An iliac embolus produces ischaemia at the level of the hip joint, while a common femoral embolus produces ischaemia distal to the knee. The importance of this feeling is that when the muscles are soft the extremity can be salvaged with effective embolectomy, regardless of how long the embolus has been present. With continuing ischaemia, the muscle progresses to necrosis and finally to rigor mortis, at this time the muscles feel stiff. The most important aspect of physical examination is the cardiac examination, which should not be missed. Intraoperative angiography is alternative, which is particularly useful where the site of embolus is uncertain. As soon as the diagnosis is confirmed and the decision for operation is taken, Heparin, 5000 to 10000 units is given intravenously by continuous I. Some surgeons recommend administration of large doses of Heparin to promote lysis of emboli and thereby improve the chances of operative success. Only when the patient is clinically well and the anaesthetist or cardiologist gives his approval, a general anaesthetic should be considered. With the lower limb fully prepared and toweled as for a varicose vein operation, a longitudinal incision is made over the common femoral artery.
Use downward traction on this stitch to pull the diaphragm inferiorly and allow better visualization of the lower esophagus and hiatus order silvitra 120 mg impotence with condoms. Dissect the mediastinal pleura anteriorly along the plane between the edge of the lung and the the esophagus (Fig 120 mg silvitra with visa erectile dysfunction va rating. Take care to avoid injury to the esophagus and resect it with the specimen up to the azy- posterior membrane of the right main stem bronchus buy silvitra canada erectile dysfunction commercial, gous vein. Tributaries from the thoracic duct to the esophagus may be divided in this tissue, with risk for subsequent postoperative chylous leak. All surrounding soft tissue is taken with the esophagus, including the lymph node packets. Once the dis- section reaches the divided azygous vein, divide the vagus nerve and keep the dissection plane close to the esophagus. By dissecting the surrounding tissue away from the esopha- gus, traction on the vagus nerve is minimized, and the risk of recurrent nerve injury is decreased. This precaution is an aid to maintaining the gastric tube in the mediastinum and seals the surrounding tissue to minimize leakage of any cervical drainage into the chest. Move the Penrose drain up to the thoracic inlet to facilitate retrieval of the cervical esophagus during the neck dissection. We inject bupivacaine around the intercostal nerve to provide regional anesthesia. Place a 28-F chest tube through the camera port while the other ports are closed with Vicryl sutures. Of note, however, adequate periesophageal dissection well into the thoracic inlet and low dissection toward the hiatus will decrease the time spent in the neck and abdomen. Intrathoracic Anastomosis The intrathoracic anastomoses can be completed in one of several ways. A traditional hand-sewn anastomoses can be done although technically more challenging when performed using minimally invasive techniques. Make a small esoph- agotomy and then pass the OrVil through the mouth into the esophagus and out of the esophagotomy. Dock the spike to the OrVil and complete the anastomosis Carry this dissection up to the azygous vein. The staple line this drain to provide retraction away from the posterior along the lesser curve of the stomach can then be oversewn 17 Minimally Invasive Esophagectomy 175 with the use of an Endostitch device. Begin the incision at the mid- tube after submerging the anastomosis with irrigation ﬂuid. At this time, if the situation appears favorable for resec- If indicated, a cervical anastomosis can be created instead of tion, mobilize the duodenum with a Kocher maneuver to an intrathoracic one (see subsequent section). Once the Kocher maneuver is completed, position the Transhiatal Approach GelPort, establish 14-mmHg pneumoperitoneum, and insert a camera through the GelPort. In nonobese patient this port is generally located sequential compression devices. This port will be A double-lumen tube should be used for endobronchial used for the camera and occasionally for staplers. Place a intubation: if thoracoscopy is planned, right lung isolation is 5-mm port in the left upper quadrant (~4 cm below the rib necessary for adequate visualization and mobilization of the cage at the left midclavicular line) to be used for the right esophagus. Place an additional 5-mm port below the left double-lumen endotracheal tube in place will provide the rib cage along the anterior axillary line. This will be used by ability to collapse the right lung quickly, should emergency the assistant for retraction. Divide the gas- The whole abdomen, the chest, and the neck are prepped trocolic ligament in a right-to-left direction using the har- with chlorhexidine-based products and draped into the surgi- monic scalpel, therefore entering the lesser sac. Abdominal Portion During this maneuver it is important not only to preserve the gastroepiploic vessels but also to take care not to As previously mentioned, the abdominal steps of a mini- injure the transverse colon. Use a bowel grasper introduced mally invasive esophagectomy are common for both tran- through the port at the left axillary line to retract the trans- shiatal and transthoracic approach and will be described ﬁrst. We ﬁnd that the minilaparotomy the upper third of the greater curvature with the division of used for the GelPort is also helpful during blunt transhiatal the left gastroepiploic vessels and then the gastrosplenic esophageal dissection as well for removal of the specimen. This portion of the Other surgeons prefer to perform a fully laparoscopic tran- dissection is greatly facilitated by using the left hand to bring shiatal esophagectomy and remove the surgical specimen the stomach down and rolling it up to expose the back wall through the neck incision. At this time it is usually necessary to divide the avascular with the harmonic scalpel in order to facilitate transhiatal posterior gastropancreatic adhesions that are almost always dissection and to prevent venous stasis of the gastric tube. At this The esophagus is connected to the surrounding structures time the left crus and part of the hiatus with the distal esoph- mainly by loose areolar tissue. Using the Penrose to Still using the harmonic scalpel (or other equivalent pull down stomach and distal esophagus, continue the tran- sealing device) for dissection, divide the lateral portion of shiatal dissection as high as possible under direct laparo- the phrenoesophageal ligament and expose the ﬁbers of the scopic vision (generally to the level of the tracheal carina). In case of tumors of the gastroesophageal junction, If the gastric mobilization has been adequate, the pylorus it may be advisable to perform a wider dissection around the should easily reach the right crus. We generally do not perform a pyloromyotomy or pyloro- Once the left crus is exposed, have the assistant retract the plasty. The vast identify and preserve an accessory or replaced left hepatic majority of patients will do well without pyloromyotomy. Free the gas- endoscopic dilation of the pylorus can be performed postop- troesophageal junction from the hiatus by dissection up the eratively in patients with delayed gastric emptying. Take down the phrenoesophageal ligament and The laparoscopic portion of the esophagectomy is now proceed through the connective tissue posterior to the esoph- completed, and the operation will continue with either the agus to extend the dissection toward the left crus. At depending on whether a transhiatal or a transthoracic esoph- this point, with the gastroesophageal junction dissected on agectomy is being performed. With the patient’s head turned slightly to the right, make an The assistant may now use the Penrose drain to retract the oblique incision along the anterior border of the left sterno- esophagus caudally and increase exposure of the hiatal mastoid muscle and carried deeper through the platysma. Complete the dissection of the lower esophagus Identify and transect the omohyoid muscle. If the middle thyroid vein is encountered, ligate and ing the greater curvature in a cephalad direction. The left gastric Identify and protect the recurrent laryngeal nerve in the vessels at this time should be readily identiﬁable caudad to trachea-esophageal groove. Pass your index ﬁnger between the esopha- Sweep the connective and lymphatic tissue around the left gus and the prevertebral fascia, then back between the esoph- gastric vessels toward the specimen with a combination of agus and the trachea to encircle the esophagus. Insert the stapler through erwise the left recurrent laryngeal nerve might be injured. In the latter case it will be necessary to use a 5-mm tially, encircle it with a Penrose drain and apply cephalad camera introduced through one of the other ports. Use gentle ﬁnger dissection, applying the pads of Division of the left gastric artery enhances subsequent your ﬁngers on the esophageal wall to gently dissect the exposure so that dissection of the intrathoracic esophagus esophagus away from the overlying trachea and the posterior can be performed under direct vision. The nasogastric tube is used for cephalad retraction along the length of the esophagus, very helpful in providing tactile feedback of the relationship of with its proximal end about 3 cm above the level chosen for the esophagus with the surrounding structures. Simultaneously divide both the esophagus section the index ﬁnger can reach down to the tracheal carina. The short portion of Penrose stapled to the esophageal stump can be used to locate the stump easily in case it retracts into the neck. Leave the Transhiatal Dissection longer part of the Penrose stapled to the distal esophagus. Gently grasp the stomach with your hand and deliver it Once the cervical dissection has been completed as far distal outside the abdomen through the right subcostal minilapa- in the chest as possible, reposition your hand through the rotomy (with the wound protector portion of the GelPort still GelPort to complete the transhiatal dissection.
The overall effect appears to be one of lacing the wound edges together by a 3-dimensional weave discount silvitra 120mg otc impotence under 40. There is one of replacing granulation tissue discount silvitra master card erectile dysfunction treatment hyderabad, allowing the surface to become covered with epithelium and filling the remaining skin defect with scar tissue after contraction is complete purchase genuine silvitra on line erectile dysfunction pills nz. As far as the filling of the defect is concerned, contraction is the major influence. The central scar seems to remodel itself to fill the defect after contraction is over. Development of tensile strength (strength of per unit of scar tissue) and burst strength (strength of the entire wound) is the result initially of blood vessels growing across the wound, epithelialization and aggregation of globular protein. There is an almost imperceptable gain in tensile strength for 2 years subsequent to that. Collagen content of the wound tissue rises rapidly between the 6th and 17th days, but increases very little after 17 days. It must be remembered that secondary wounds contain slightly less collagen than primary wound of the same age. More effective cross-linking of better physical weave of collagen subunits is responsible for rapid gain in strength for secondary wounds. Experimentally it may be estimated by measuring the force necessary to disrupt the wound. In the first few days the strength of a wound is only that of the clot which cements the cut surfaces together. Later on various changes take place in the wound healing process as mentioned above and at the end the tensile strength of the wound corresponds to the increase in amount of collagen present. Tensile strength of the wound becomes more when this is parallel to the lines of Langer. That is why the transverse abdominal incisions produce stronger scar than the longitudinal ones. This effect is well accepted in the experimental animals, but corticosteroid in normal dosage may not influence wound healing in human beings. Healing of a clean incised wound, the edges of which are closed (closed wound) — takes place by a process known as healing by first intention. The following changes take place — (i) initial haemorrhage results in the formation of a fibrin-rich haematoma. In the first 24 hours basal cells mobilise from the undersurface of the epidermis. By 48 hours the advancing epithelial edge undergoes cellular hypertrophy and mitosis. Epithelial cells gradually line the wound deep to the fibrin clot and it also lines the suture tracks. The use of adhesive tapes instead of sutures for closing wounds avoids these marks and gives better cosmetic result. The main bulk of tissue which performs the healing process is the granulation tissue and that is why this type of healing is also called healing by granulation. But this does not mean that granulations are not formed in the simple incised wounds. The followings are the various important processes of this type of wound healing :— (i) Initial inflammatory phase affects the surrounding tissues and the wound is filled with coagulum. It must be remembered that the skin wound contracts by stretching the surrounding skin to close the defect and not by the production of new skin. Between 5 and 10 days, the wound edges move rapidly and after 2 weeks it becomes slowed down again. In fact this granulation tissue forms a temporary protective layer against infection until the surface is covered by epithelium. It must be remembered that specialised epithelial structures like interpapillary processes, hair follicles and sebaceous glands are not reformed. The epithelial cells in fact slide into the wound forming a thin tongue of cells between the granulation tissue and the clot. Gradually as the epithelialization continues, there is also remodelling of the granulation tissue and scar, so that the wounded area which was at first depressed, ultimately forms a flat scar. This may be due to uncontrolled growth with invasive potentiality of the surrounding epithelial cells which are concerned with epithelialization. In these cases there is not only mitosis, but there is pleomorphism, disorganization and loss of polarity. It should be noted that it is not always due to inadequate intake, but may be due to excessive loss e. Cortisone and its derivatives decrease the rate of protein synthesis, stabilize liposomal membranes and inhibit the normal inflammatory reaction. High doses of corticoids limit capillary budding, inhibit fibroblast proliferation and decrease the rate of epithelialization. Any agent that inhibit the division of local fibroblasts or epithelial cells should prevent or delay healing. Similarly high doses of radiation especially during first 3 days delay strength of the wound significantly. That is why wounds in the pretibial region take much more time to heal than those in the face, which are well vascularized. Due to infection, fibroblasts face tough time to persist as they have to compete with inflammatory cells and bacteria for oxygen and nutrients. The delicate capillary loops of the granulation tissue and the delicate epithelium are damaged due to movement. Frequent change of dressing also has the same adverse effect and should be avoided. Adhesions to bony surfaces cause delay in wound healing probably by preventing proper wound contraction. Faulty technique of wound closure is obviously responsible for delay in wound healing in many cases. It is a peripheral circulatory failure which results from a discrepancy in the size of the vascular bed and the volume of the intravascular fluid. It is a clinical condition which is characterized by signs and symptoms arising when the cardiac output is insufficient to fill the arterial tree with blood under sufficient pressure to provide all the organs and tissues with adequate blood flow. The characteristic features are decreased filling pressure of the heart, decreased systemic arterial pressure, tachycardia and increased vascular resistance. This is clinically manifested by low cardiac output, tachycardia, low blood pressure and vasoconstriction revealed by cold clammy extremities. In this type of shock there is hypovolaemia due to bleeding both externally and internally (intraperitoneal haemorrhage) from ruptured liver or spleen or from torn vessels of the mesentery alongwith toxic factors resulting from fragments of tissue entering the blood stream. Injury to the chest may cause damage to the respiratory system resulting in hypoxia and shock. Chest injury may also lead to contusion of the heart which may cause failure of pump resulting in shock.
No benign oesophageal tumours produce characteristic features in barium swallow examination silvitra 120mg visa erectile dysfunction pills generic. In case of polyps there is also characteristic filling defect detected in this examination cheap 120 mg silvitra visa erectile dysfunction at 20. In gastro-oesophageal reflux during the course of barium swallow examination reflux can be demonstrated 120mg silvitra mastercard impotence journal. This study shows multiphasic, repeatitive and high-amplitude contractions that occur after swallowing in the smooth muscles of the oesophagus. In case of gastro-oesophageal reflux, pH recording in the oesophagus 5 cm above the distal oesophageal high-pressure zone shows decline in pH to less than 4, which is a clear evidence of gastro-oesophageal reflux. These investigations however may find out abnormal masses in the mediastinum and aortic aneurysm which may press on the oesophagus to cause dysphagia. The proximal oesophagus ends as a blind tube and the distal oesophagus is joined to the lower part of the trachea with a tracheo- oesophageal fistula. During foetal life this condition may be recognized by presence of hydramnios, but this may not be present. When the tip of this tube is radio-opaque, straight X-ray is situ can diagnose this condition. Straight X-ray also reveals intestinal gas which indicates communication of distal trachea with distal oesophagus. The greatest risk of this condition is that there is a great possibility of aspiration of gastric juice, which is highly injurious to the lungs. The patient is nearly always a middle-aged woman who presents with difficulty in swallowing. Dysphagia is due to spasm of the circular muscle fibres at the extreme upper portion of the oesophagus. It may be considered as a Pulsion diverticulum — herniation of the oesophageal mucosa and sub mucosa through the weakened area. Note the long age and more of the oesophagus above the smooth irregular narrowing with slight dilatation of frequently men narrowing of the lower end of the the oesophagus above the stricture. Sometimes the patients may wake up from sleep with a feeling of suffocation followed by a severe cough. When the pouch enlarges it tends to compress the oesophagus which leads to dysphagia. When the patient drinks the pouch can be seen to be enlarging with gurgling noise in the neck. X-ray with a very thin barium emulsion should be performed as thick mixture refuses to be washed out from the pouch following examination. Traction diverticula may be occasionally seen in the middle portion of the oesophagus near tracheal bifurcation. These result from pull of scar tissue from an adjacent inflammatory process, usually tuberculous lymph nodes. X-ray with barium meal will show a long tortuous stricture with some dilatation of the proximal oesophagus and without any shouldering at the proximal end of the stricture. Some sort of emotional stress and anxiety are often associated with along chest pain and dysphagia. There is also regurgitation of food, though many patients experience regurgitation of intraoesophageal saliva during oesophageal colic. Irritable bowel syndrome, pylorospasm, peptic ulcer disease, gallstone and pancreatitis may stimulate diffuse oesophageal spasm. Oesophageal manometry has been considered the ultimate test in the diagnosis of this condition. This is due to fibrous replacement of oesophageal smooth muscle and then the distal oesophagus loses its tone and normal response to swallowing and gastro-oesophageal reflux occurs. In distal 2/3rds or 3/4ths of the oesophagus normal peristalsis gives way to weak nonpropulsive contractions. At its most upper part at the pharyngo- oesophageal junction and is known as pharyngo- oesophageal diverticulum or pharyngeal pouch which has been discussed above. This occurs in association with tuberculosis or histoplasmosis of the subcarina and parabronchial lymph nodes to which this diverticulum becomes adherent. This condition rarely causes symptom and is discovered accidentally on barium oesophagogram. This is due to oesophageal motor dysfunction of the distal oesophagus leading to mechanical distal obstruction. There is virtually no the mucosa and submucosa of the oesophagus dilatation of the oesophagus above the growth. Many patients may remain constricted part is very much irregular — ‘rat-tail’ deformity of the lower end of the oesophagus. This condition is diagnosed by barium oesophagogram, though oesophageal manometry should be performed to identify the exact motor disturbance. It is generally located at the oesophagogastric junction and has squamous epithelium on one side, gastric mucosa on the other side and fibrous tissues in the centre. Due to sloughing of a portion of the growth dysphagia may be eased out temporarily. Regurgitated material is usually alkaline mixed with saliva and streaked with blood from malignant growth. Anorexia is another symptom but more often seen in growths at the lower end of the oesophagus. Exfoliative cytology from oesophageal lavage may clinch the diagnosis very early even when radiology has not been positive. In late stages pressure on recurrent laryngeal nerve may cause hoarseness of voice or erosion of bronchus may lead to broncho-oesophageal fistula. If symptoms occur these are usually fullness after meals, early satiety and post prandial vomiting. Gastro-oesophageal reflux, which is a very common occurrence in sliding or axial or type I hiatus hernia, does not take place in this condition. The filling defect is then it courses behind the oesophagus (or in rare instances usually more irregular than is shown in front of the oesophagus between the oesophagus and the in this case. It is only when reflux occurs with increased frequency and at times when the stomach is not distended that pathologic gastro-oesophageal reflux is considered. The symptoms of this reflux are heart-burn and regurgitation aggravated by postural change. These are associated with dysphagia, substernal chest pain, sensation of something sticking in the throat and bleeding. Reflux of gastric contents irritates the oesophagus causing secondary muscle spasm alongwith inflammation of the mucosa leading to fibrosis and stricture. Closed injuries are due to waves of shock or direct compression of a viscus against a bony prominence. If a large segment of the abdomen or abdominothoracic wall is compressed it may burst or split organs like liver and spleen. It should be remembered that a similar force, particularly if the breath is held and the diaphragm is tense, may split the diaphragm.