These glands are discharged by the anal ducts which are mainly lined columnar epithelium mebendazole 100mg free shipping. These glands can be considered as diverticula of the anal canal like diverticula in any part of the alimentary track order online mebendazole. As the duct passes through the internal sphincter purchase 100 mg mebendazole amex, this may not be able to discharge the contents of the gland so readily as the muscle tone will tend to compress their lumen mebendazole 100mg on-line. Cystic dilatation and abscess formation is not uncommon due to stasis and secondary infection. So such abscesses are always deep to the internal sphincter muscle in the intersphincteric zone. These glands may become infected with the result that an abscess or subsequently a fistula may be developed. The imaginary line along which the anal valves are situated is popularly known as pectinate line (dentate line). It indicates the site at which the anal membrane is situated in foetus and is thus the junction of the entodermal part and the ectodermal part. Sometimes small epithelial projections known as anal papillae are present on the edges of the anal valves. The epithelium above this line is supplied by sensory fibres from autonomic nervous system and therefore insensitive to painful stimuli such as cutting or cauterization. The epithelium below this line is innervated by spinal nerves and has somatic sensation. Submucosa contains fairly tough connective tissue which anchors the lining of the pecten to the muscle coat firmly. The line below the transitional zone is known as White line of Hilton, which according to some, is the junction of the entoderm and the ectoderm. The internal sphincter is the thickened continuation of the circular muscle coat of the rectum. This is an involuntary muscle and continuous above with the circular muscle of rectum through the pelvic diaphragm. When exposed, it is pearly white in colour and its transversely placed fibres can be seen clearly. Spasm and contracture of this muscle play a major part in formation of fissure and other anal conditions. The longitudinal muscle is the continuation of the longitudinal muscle coat of rectum. At the anorectal junction, the puborectalis fibres of the levator ani fuse with the longitudinal unstriped muscle coat of the rectum to form a conjoined longitudinal muscle coat for anal canal between the internal and external sphincters. Distally, this conjoined coat becomes increasingly fibroelastic and at the level of the ‘White line’ it breaks up into a number (9 to 12) of fibroelastic septa which spread out fanwise and pass mainly through the subcutaneous part of the external sphincter to become attached to the corium of the skin around the anus. These septa mainly consist of yellow elastic fibres and the most lateral septum passes between the subcutaneous and superficial parts of the external sphincter and becomes lost in the fat of the ischiorectal fossa. It is usually divided into 3 parts — the subcutaneous part, the superficial part and the deep part. The deep part of this sphincter is a thick annular band which surrounds the upper part of the internal sphincter. In front, its fibres decussate and become continuous with the superficial transverse perineal muscles. The superficial part is attached posteriorly to the terminal piece of the coccyx, the only bony attachment of this sphincter. The subcutaneous part surrounds the lowest part of the anal canal and itlies below the lower border of the internal sphincter and Hilton’s line. Anteriorly, its fibres are attached to the perineal body and posteriorly to the anococcygeal ligament. Lymphatics from the lower end of the anal canal, which is developed from the proctoderm, are drained into the superficial inguinal group of lymph nodes of both sides. The lower part of the anal canal which is developed from the proctodeum, is sensitive and is supplied by the inferiorrectal nerve, a somatic nerve. This nerve also supplies the external sphincter and sphincter urethrae and so any irritation of the lower part of the anal canal will cause these sphincters to go into spasm. It is a pyramidal space, whose apex is directed upwards and the base which is formed by the septum of the ischiorectal fossa is directed downwards. Its outer wall is vertical and is formed by the obturator intemus muscle and the fascia covering it. About l’/2 inches above the lower border of the ischial tuberosity in this fascia covering obturator intemus lies the Alcock’s canal (pudendal canal) containing the internal pudendal vessels and the pudendal nerve. Its inner wall is oblique and formed by the levator ani muscle and the deep and superficial parts of the external sphincter muscle. Anteriorly, it is bounded by the base of urogenital diaphragm and transverse perineal muscles. Posteriorly, it is bounded by the lower margin of the gluteus maximus muscle and the sacrotuberous ligament. It is now obvious from the concept of the boundaries of the fossa that the pus from one ischiorectal fossa can pass to the opposite fossa breaking the attachment of the levator ani to the anococcygeal ligament. Pus from this space may make its way to the ischiorectal fossa through the hiatus of Schwalbe, a gap between the obturator fascia to the attachment of the levator ani muscle. The pus from the ischiorectal fossa can also go up through this hiatus to the pelvi-rectal space resulting in a high fistula. If this prolapsed mass is palpated with one finger inside the anus and the thumb on the outside of the mass, it will be evident that it is composed of two layers of mucous membrane with submucosa in between. If a large portion of muscle is divided or if excessive stretching of anal sphincter is done, it may cause such prolapse. Such prolapse is usually localised to the affected quadrant and usually heal by itself. Any aetiological factor of complete prolapse may cause partial prolapse in the beginning before it turns into complete prolapse. The mother is taught how to replace the protruded bowel through the anal sphincter. By the index finger the protrusion is pushed up through the anal canal and the finger is gradually withdrawn. Attention of bowel habit, avoiding straining at stools, control of diarrhoea and dietatic adjustments in case of malnutrition are supportive treatments to be followed. This submucous injection treatment may also be tried in adults in early partial prolapse. The apex of the prolapse is injected circularly and the tip of the needle should reach the submucosa. The base of the prolapse should also be injected similarly and the needle must reach the submucosa. Aseptic inflammation following these injections will lead to fibrosis and the mucous membrane becomes fixed to the muscular coat and is drawn in. Two small midline incisions are made one in front and the another behind the anal opening about V inch away from it. A piece of silver wire or stainless steel wire 20 gauze is threaded through the eye of this needle. The needle is brought out through the anterior incision and now the wire traverses V of the2 circumference of the anus. The needle is reinserted through the same incision behind the anus and passed round the opposite side of the anus to emerge through the incision in front of the anus. The other end of the wire is threaded and the needle is withdrawn through the anterior incision. When the finger can be just sufficiently passed through the anus, the twisted wire ends are cut short. This gives not only a mechanical support but also a chemical support by the fibrous deposits around the anal canal. In this case strong chromic catgut may be used instead of silver or stainless steel wire. The main complication of this operation is that the wound may be complicated with the result of a discharging sinus. In this case the wire must be removed and usually by that time fibrosis has occurred to prevent further prolapse. By this the base of the prolapse is transfixed twice and the ligature is then tightened. Now the redundant mucosa is excised and if required the cut margins are sutured interruptedly.
This defect is usually associated with incomplete formation of mitral and tricuspid valves purchase mebendazole 100mg mastercard. Initially the cleft in the mitral valve is closed with interrupted sutures placed from the ventricular septum out to the free margin of the mitral orifice buy discount mebendazole line. After repair of the cleft mitral valve best 100mg mebendazole, the septal defect is repaired with a patch of pericardium inserted with interrupted sutures mebendazole 100mg. A defect in the tricuspid valve is frequent but usually not amenable to repair by direct suturing. The right pulmonary veins usually enter the superior vena cava inferior to the point of entry of azygos vein, or enter into the right atrium or into the inferior vena cava. When treatment is required, the anomalous veins can be corrected by insertion of prosthetic patch so that the defect is closed and the pulmonary veins are made to enter the left atrium. Ventricular defect is mostly situated in the membranous part or fibrous part of the septum. The membranous septal defects are either located posteriorly or anteriorly in relation to the crista supraventricularis. The posterior defects are close to the tricuspid valve on the right and the mitral valve on the left. The anterior defect is safely away from the conduction bundle and its closure is easier than that of the posterior defect. The defects smaller than 1 cm is called ‘small’ defect and larger than 1 cm is called ‘large’ defect. The defect allows passage of blood from the left to the right ventricle resulting in over-filling of the right heart and pulmonary hypertension. But those with larger defects are usually symptomatic and the first and most common symptom is dyspnoea on exertion. On Physical examination a loud pansystolic murmur is typically present in the 3rd and 4th intercostal space along the left sternal border. Enlargement of pulmonary artery and its tributaries and pulmonary congestion may be visible in X-ray. Cardiac catheterisation confirms the diagnosis and it also assesses the extent of left to right shunt. If symptoms are not disabling, the time for operation may be deferred to 4 to 6 years. A longitudinal ventriculotomy is performed usually in the infundibular part of the right ventricle and near the anterior descending coronary artery. The alternate approach is through the right atrium, particularly when pulmonary vascular resistance is significantly increased. The defect is usually closed with an oval patch of knitted Dacron by mattress sutures (prolene) posteriorly and continuous suture (prolene) anteriorly. Postoperatively, Digitalis is usually given, as some degree of right ventricular failure is common. The risk of operation increases somewhat if pulmonary vascular resistance is increased. Earlier diagnosis and treatment have brought down operative mortality to as low as 1 to 2%. The right ventricular obstruction increases right ventricular systolic pressure equal to that of the left ventricle. The right ventricular obstruction may be an infundibular stenosis or a valvular stenosis or a combination of the two. In this condition due to obstruction in the right ventricular outflow and presence of ventricular septal defect, the venous blood entering thcright ventricle is shunted direcdy into the aorta to produce cyanosis. This condition also decreases pulmonary blood flow and thus limits and ability to absorb oxygen. Due to presence of large ventricular septal defect, right ventricular pressure can never exceed left ventricular pressure inspite of presence of pulmonary stenosis. Arterial oxygen saturation may come down to 30 to 35%, when the body can walk only a short distance. Very low saturations of 10 to 20% is also seen in rare cases when the infant is not only unable to walk, but also may lose consciousness due to cerebral anoxia. Chronic anoxia may produce compensatory polycythemia and eventually clubbing of the extremities. About l/3rd of patients are cyanotic at birth, these patients often do not survive infancy unless operation is performed quickly. Walking for short distances, interrupted by squatting, is a pathognomonic symptom of this condition. He created an anastomosis between the left subclavian artery and the left pulmonary artery. In fact the subclavian artery is divided at a distance from its origin and the cut proximal end of the subclavian artery is then anastomosed to the upper border of the left pulmonary artery which is already mobilised and doubly clampped for convenience of performing the anastomosis. A continuous thrill is felt over the anastomosis as soon as the clamps are released. A side-to-side anastomosis between the ascending aorta and the right pulmonary artery was advocated by Waterson. An anastomosis is made between the descending aorta and left pulmonary artery (Pott’s). Superior vena cava is sometimes anastomosed with the right pulmonary artery (Glenn). A high vertical ventriculotomy is performed which stops near the pulmonary annulus and is limited to the infundibular portion of the right ventricle. Through this incision the ventricular septal defect is closed with a Dacron patch. The pulmonary vulvular and infundibular obstruction is also widened with a patch graft of Dacron. Following closure of the ventriculotomy and removal of air from all cardiac chambers, extracorporeal circulation is stopped. Now the intracardiac pressure is measured to confirm that the right ventricular systolic pressure is reduced to less than 60 to 70% of that of the left ventricle. If right ventricular pressure is still elevated, more correction of the ventricular obstruction becomes necessary. While the risk is about 10% for smaller children, it is only 2 to 5% in older children. As a result venous blood is ejected through the aorta and the oxygenated blood returning from the lungs into the left atrium enters the left ventricle and is again pumped through the pulmonary artery to the lungs. This is obviously incompatible with life except for if a communication exists between the pulmonary and systemic circulations in the form of a patent ductus arteriosus, an atrial septal defect or a ventricular septal defect. One or more of these congenital anomalies must exist for the infant to survive even a few hours after birth. Transposition of the great vessels is often associated with other congenital abnormalities e. The children who survive beyond first 2 years of life, clubbing and polycythemia appear. Signs of congestive failure are always found with pulmonary congestion, cardiac enlargement and hepatomegaly. The simplest procedure is the Balloon Septostomy, in which the atrial septal defect already present is enlarged by passing a deflated balloon catheter through the defect into the left atrium, and after inflating the balloon it is forcefully pulled across the septum to enlarge the opening. This technique was first developed by Rashkind and it is almost always done at the time of cardiac catheterisation. If Balloon Septostomy is ineffective, atrial septal defect may be created by the Blalock-Hanlon technique. A portion of the atrial septum is excised and the two incisions are now anastomosed. This is achieved by switching over the aorta and pulmonary arteries with transposition of the abnormal coronary arteries. After the initial episode of rheumatic fever, symptoms of mitral stenosis may not appear for 10 years or more. It is suggested that scarring of the mitral valve due to rheumatic fever causes turbulent flow of blood which in tum causes more scarring and contraction over many years. Usually severe mitral stenosis takes about 20 to 30 years to develop after the last known bout of rheumatic fever.
Chilaiditi syndrome Congenital anomaly in which there is interposition of a portion of the colon (less frequently purchase mebendazole us, the small bowel) between the liver and the right hemidiaphragm buy mebendazole 100mg with amex. The perihepatic ligaments may be affected by direct invasion buy line mebendazole, subperitoneal extension buy generic mebendazole on line, or extension along lymphatics. Sudden rupture of cyst contents causes an acute peritonitis and typically appears as discontinuity of the wall of the tumor. A chronically leaking teratoma cause chronic granulomatous peritonitis, which produces a pattern of ascites, hazy omental infiltration, and an inflammatory omental mass that simulates carcinomatous or tuberculous peritonitis. The demonstration of fatty implants within the peritoneal cavity strongly suggests this diagnosis. Lipoma/liposarcoma Liposarcoma is one of the most common malignant tumors in the retroperitoneum, and a fatty mass in this region can be confused with a perihepatic mass. The differentiation between lipoma and liposarcoma may be extremely difficult on imaging studies. It is thought to arise from a detached piece of colonic fat (an epiploic appendage) that degen- erates and becomes covered by a fibrous capsule before lodging between the diaphragm and the superior aspect of the liver. Usually occur- ring on the right, proposed etiologies include an anomalous arterial supply to the omentum, kinking of veins secondary to increased intra- abdominal pressure, and postprandial vascular congestion. The initial high attenuation of acute intraperitoneal blood decreases within several days due to clot lysis. Other causes of high-attenuation ascites include tuberculosis (high protein and cellular contents) and extravasated contrast material from the gastrointestinal or urinary tract. Contrast scan shows a fatty lesion (arrow) 161 adjacent to the intrahepatic vena cava. Peritonitis is an inflammation of the serosal membrane lining the peritoneal cavity and the organs within it, while perihepatitis is the term used to refer to localized inflammation of the liver capsule. This is a manifestation of the fact that the major route of the flow of peritoneal fluid from the pelvis is through the right paracolic gutter, since the left paracolic gutter is shallow and spread on the left is limited due to the phrenicolic ligament. Morison’s pouch is the most common site of perihepatic abscess, because it is the most dependent recess. Infected material can extend around the inferior edge of the liver or laterally from Morrison’s pouch to the right subphrenic space. Tuberculosis, actinomycosis, and echinococcosis are important causes of perihepatic abscesses. The typical symptoms of sudden onset of sharp right upper quadrant pain can be confused with acute chole- cystitis or pleurisy. Intense enhancement along the anterior surface of the liver may be demonstrated on early-phase images (increased blood flow related to inflammation) or on delayed scans (early capsular fibrosis). Enhancement of the liver capsule may also be a manifestation of other inflammatory conditions (tuberculous peritonitis, perforated hepatic abscess, or cholecystisis), sys- temic lupus erythematosus, radiation, and perito- neal carcinomatosis. This appearance is consistent with an abscess in the posterior right subhepatic space. It produces large amounts of ascites, which is often loculated, and characteristic nodular peritoneal thickening and enhancement. Implants on the liver and spleen often cause scalloping of the surface by the masses. The irregular studding of the peritoneum differ- entiates this condition from the diffusely smooth peritoneal thickening related to tuberculous peritonitis. Calcified peritoneal carcinomatois may occur in ovarian, colon, and gastric cancer. Contrast scan (arterial with focal areas of low attenuation in the anterior phase) shows enhancement of the capsule of the left right subhepatic space, findings suggestive of a small hepatic lobe (arrowhead). This permits the spread of disease not only between the intraperitoneal structures, but also between extraperitoneal and intraperitoneal sites. Gas, in- flammation, tumor, or proliferative disease can extend along the subperitoneum. Contrast scan shows that gas origi- nating from a gallbladder perforation has diffused along the hepato- duodenal ligament to the Glisson sheath (arrow). Contrast scan shows the inflammatory changes of pancreatitis extending upward along the portal vein (arrows) to the ligamentum teres (arrowhead). Other sonographic findings suggesting malignancy include liver and nodal metastases, venous compression or obstruction, and ascites. Langerhans is located (unlike carcinoma, which most commonly affects the head of the pancreas). Longitudinal sonogram demon- verse sonogram shows an enlarged liver containing multiple strates an irregular mass (M) with a semisolid pattern of intrinsic metastatic lesions (arrowheads). This cystic mass in the head of the Diffuse enlargement of the pancreas (P) with enlarged hypoe- pancreas shows acoustic enhancement without evidence of debris. They frequently are located posterior to and cause anterior displacement of the splenic and portal veins (primary carcinoma tends to be located more anteriorly and to cause posterior displacement of these vessels). Lymphoma Solid mass that is relatively anechoic and, when Primarily involves the region of the head and body round, may initially appear to be cystic until (where the main lymphatic chains are located). It frequently is located posterior to and causes anterior displacement of the splenic and portal veins (primary carcinoma tends to be located more anteriorly and causes posterior displacement of these vessels). Nodularity and papillary projections may be demonstrated along the internal wall of the cysts. Cystadenoma/ Predominantly cystic mass with septations and Uncommon tumors, usually occurring in women cystadenocarcinoma thick irregular walls. Multiloculated cystic mass with echogenic internal septa within the tail of the pancreas. Echogenic foci with shadowing that correspond to calcifications are noted along the septa (arrow). Although most have thick walls, be multiloculated, and contain commonly located in the peripancreatic region, internal debris and be difficult to differentiate pseudocysts may develop apart from the pancreas from cystadenoma, cystadenocarcinoma, or (the lesser sac, or anywhere from the mediastinum abscess. Sonogram shows a mass of low echo- right upper quadrant demonstrates an irregularly genicity due to the interfaces between the tiny cysts. Although the presence of gas in the echoes in the mass (representing gas) confirm pancreatic bed strongly suggests a pancreatic the diagnosis of an abscess. Atrophy of the pancreas patients, though more than 90% of the exocrine without fibrofatty replacement may occur. Transverse sonogram at the level of the echoic mass (M) in the peripancreatic region. Note the multiple cysts (*) of different sizes adjacent to the liver (L) and stomach (St). Fine lobulations fication, is considered virtually pathognomic for are common, and enhancement of septa and serous cystadenoma. Most are located appearance with septations and sometimes in the pancreatic body and tail, are frequently calcification scattered throughout the mass clinically silent, and can therefore attain sizes greater than 10 cm before becoming palpable. Although not frequently seen, peripheral and septal calcifications are highly specific for mucinous cystic neoplasm and strongly suggestive of malignancy. The peripheral and septal calcification (arrowheads) indicate the malignant nature of the lesion. On contrast studies, chronic pancreatitis, a diagnosis of carcinoma the relatively avascular tumor appears as an requires evidence of secondary signs of malignancy area of decreased attenuation when compared such as obliteration of peripancreatic fat planes with the normal pancreas. Larger tumors may contain the transient increase in contrast enhancement low-density areas due to foci of tumor necrosis. Contrast scan in an elderly man with watery diar- elderly man who presented with life-threatening hyper- rhea shows a huge mass with internal septa and calcification 170 in the body and tail of the pancreas. Variety of internal appearances ranging malignant potential with a favorable prognosis. Metastases Local invasion Obliteration of the fat planes that normally Hepatomas and carcinoma of the stomach or separate the pancreas from adjacent organs. Lesions of the left adrenal and kidney may displace the tail of the pancreas, destroy surrounding fat, and occlude the splenic vein. Peripancreatic lymph Lobulated mass or masses impinging on the Enlargement of peripancreatic nodes (metastatic node involvement pancreas.
Target heart rate is 85% of predicted maximum heart rate: 85% × (220 – patient’s age) mebendazole 100mg for sale. Patients who are unable to exercise or walk should be considered for chemical stress testing cheapest generic mebendazole uk, such as dipyridamole (Persantine) or dobutamine stress test buy cheap mebendazole 100mg on line. In those cases patients should be evaluated by nuclear stress imaging instead of the exercise stress test purchase mebendazole online. In most cases, medications should not be withheld in preparation for an exercise stress test. Certain medications require special consideration: Beta blockers may blunt the heart rate during exercise and thus should be held 24 hours prior to the test. While patients receiving beta blockers may perform the exercise required for the test, the usual age-adjusted target heart rate may not be a realistic end point for them. Also, the antihypertensive effect of beta blockers, alpha blockers, and nitroglycerin may cause significant hypotension during exercise. A number of other situations or conditions may reduce the validity of the exercise stress test. She has no history of chest pain, and she exercises routinely (runs 2–3 miles per day, 3 times per week). Other types of stress tests include: Nuclear stress test: A radioactive substance is injected into the patient and perfusion of heart tissue is visualized. An abnormal amount of thallium will be seen in those areas of the heart that have a decreased blood supply. Compared to regular stress tests, the nuclear stress tests have higher sensitivity and specificity (92% sensitivity, 95% specificity vs. The latter can recognize abnormal movement of the walls of the left ventricle (wall motion abnormalities) that are induced by exercise. Invasive techniques: Cardiac catheterization is also used in patients with stable angina for (1) diagnosis and (2) prognosis/risk stratification. Angiography is an appropriate diagnostic test when noninvasive tests are contraindicated or inadequate due to the patient’s illness or physical characteristics (e. Cardiac angiography is also used after conventional stress tests are positive to identify patients that will benefit from stent placement or bypass surgery. Other medications patients with stable angina should be taking, unless contraindicated, include aspirin and statins (for lipid lowering). Also, modify the risk factors (tobacco cessation, exercise, control of hypertension, etc. Most patients will require both pharmacologic and nonpharmacologic interventions to reach target goals. These are patients with established cardiovascular disease plus diabetes and patients with acute coronary syndromes. Every effort should be made to ensure that patients with coronary artery disease receive optimal lipid therapy. Statin medications are strongly supported as first- line medications due to compelling evidence of mortality reduction from multiple clinical trials. Typically, this means patients with left main disease or triple-vessel disease and low ejection fraction. The procedure involves the construction of 1 or more grafts between the arterial and coronary circulations. Potential consequences of graft failure (loss of patency) include the development of angina, myocardial infarction, or cardiac death. Collectively they represent one of the most common causes of acute medical admission to U. The natural course of coronary atherosclerotic plaque development and subsequent occlusion does not proceed in a step-wise, uniform manner, gradually progressing to luminal obstruction (and symptoms) over many years. Sudden change in the pattern of angina usually means a physical change within the coronary arteries, such as hemorrhage into an atherosclerotic plaque or rupture of a plaque with intermittent thrombus formation. High-risk patients should be treated with aggressive medical management and arrangements should be made for coronary angiography and possible revascularization, except in those with severe comorbidities. Medical management Aspirin is recommended (unless contraindicated) in all patients. Antiplatelet therapy (beyond aspirin): Early treatment should be initiated with aspirin and clopidogrel, prasugrel, or ticagrelor with the following considerations: Avoid clopidogrel in patients likely to require emergency coronary bypass surgery. Antithrombin therapy: Give unfractionated heparin or subcutaneous enoxaparin until angiography or for 48–72 hours. Give beta blockers on admission unless there are contraindications (severe asthma or cardiogenic shock). The use of these agents provides a more comprehensive platelet blockade than the combination of aspirin and heparin alone. Concomitant tirofiban is particularly beneficial and recommended in patients with diabetes. In patients with diabetes, good glycemic control should be targeted in the hospital and after discharge. Pain or ischemia refractory to medical therapy and high-risk features on early exercise testing can also identify patients suitable for early invasive therapy. Clinical Recall Which of the following medications must be withheld before performing an exercise stress test? Often, the pain is accompanied by additional symptoms, such as dizziness (lightheadedness), nausea or vomiting, diaphoresis, or shortness of breath (dyspnea). Women, elderly, and diabetic patients are prone to atypical symptoms such as nausea or dyspnea as the sole symptoms of infarction. Pulse rate may be normal, but often bradycardia is present in inferior infarctions. Restoring coronary patency (emergency reperfusion) as promptly as possible is a key determinant of short-term and long-term outcomes. Prolonged persistence of antibodies to streptokinase may reduce the effectiveness of subsequent treatment; therefore, streptokinase should not be used if used within the previous 12 months in the same patient. In patients selected for fibrinolytic therapy, clopidogrel should be given in addition to aspirin, unless contraindicated. Clopidogrel should be continued for at least a month after fibrinolytic therapy, or for up to 9–12 months after stent implantation, depending on the type of stent used. It may be advisable to give a bolus of heparin while the patient is in transit to the catheterization laboratory. With fibrinolysis: Antithrombin therapy should be used with fibrin-specific fibrinolytic agents. There is no significant advantage over full-dose fibrinolytic therapy alone, and the risk of bleeding is increased, particularly in the elderly. Clopidogrel: There is evidence that clopidogrel or prasugrel should be prescribed for up to 9–12 months after acute myocardial infarction, particularly after stent placement. Clopidogrel may also be prescribed as an alternative when aspirin is contraindicated, or to those intolerant to aspirin, in patients with recurrent cardiac events. Its use should be reviewed later on the course of the patient and discontinued if the heart failure resolves. Secondary prevention through the control or elimination of known risk factors for coronary artery disease (e. You are asked by your patient, who has a history of ischemic heart disease, about drug treatments that have been shown to decrease mortality in his case. It is used to assess prognosis and to identify those patients with reversible ischemia who should then have an angiogram (if one has not been done) to assess the need for coronary artery bypass graft. Myocardial perfusion imaging can be performed before hospital discharge to assess the extent of residual ischemia if the patient has not already undergone cardiac catheterization and angiography. Thromboembolic Mural thrombus with systemic embolism Deep vein thrombosis with prolonged immobilization Sudden cardiac death Most often due to arrhythmia. Beyond the accompanying emotional distress and suffering, depression also increases one’s risk of having another heart attack or dying over the ensuing months and years. Cognitive behavior therapy has also been found to be effective in treating depression. Cocaine use has been documented to induce coronary vasoconstriction in nondiseased coronary segments but is more pronounced in atherosclerotic segments. As opposed to typical angina, Prinzmetal angina usually occurs during periods of rest, most often at night and in the early morning hours. In men, Prinzmetal angina is often associated with atherosclerosis; in women it is not. Ergonovine has been used to trigger coronary artery spasm in susceptible patients, confirming the diagnosis.
Hypoxiaproduces cerebral confusion and restlessness mebendazole 100 mg sale, followed by unconscious ness in severe cases cheap mebendazole 100 mg free shipping. Position of the mediastinum should be assessed to detect whether there is pneumothorax or haemot horax or massive collapse of the lung mebendazole 100mg with mastercard. The chest wall is examined for rib fractures order 100 mg mebendazole, paradoxical movements, depression (stove-in chest) or presence of sucking wounds. Stabilisation of the chest wall should be done immediately as mentioned in the section of ‘flail chest 5. Relief of pain should be given with analgesics, morphine and/or intercostal nerve block. Removal of blood or air from the pleural cavity is essential with continuous water-seal drainage. It permits repeated aspiration of the tracheobronchial tree, eliminates dead space and allows intermittent positive pressure respiration. This positive pressure respiration should be continued till the blood gas estimations confirm achievement of normalcy. This usually takes about 10 to 14 days, which cannot be maintained with an endotracheal tube, so tracheostomy becomes necessary in all severe cases of crush injuries. Fluid replacement is highly important which should be supplemented with blood transfusion if considerable blood has been lost due to injury. This fluid is exudated by the visceral pleura and is absorbed by the parietal pleural. Any disturbance in the balance of secretion and absorption may result in accumulation of fluid in the pleural cavity, which is known as pleural effusion. A minimum of about 300 ml of pleural fluid is generally required before one can radiographically diagnose a case of pleural effusion. The first indication of which is blunting or abolition of costophrenic sinus or angle. So when a diagnosis of small pleural effusion is noted on a thoracic roentgenogram, usually considerable fluid is already present and can be obtained by a carefully performed thoracentesis. So radiographers often prescribe a lateral decubitus chest X-ray to be obtained to detect small volume of effusion. Pleural effusions can be classified into 2 groups — (i) Transudates and (ii) Exudates. The common causes of formation of such transudate are congestive cardiac failure, nephrotic syndrome, ascites and atelectasis. Such exudates are caused, by inflammatory diseases and neoplasms of both pleura and lungs and pulmonary infarction. A haemorrhagic pleural effusion is not included in transudate or exudate group and it is usually caused by neoplastic invasion of the pleura, pulmonary infarction, tuberculosis or unrevealed trauma. Stony dullness on percussion, absent breath sounds and absent vocal fremitus on auscultation are the significant signs of pleural effusion. If the effusion is massive, the mediastinum is shifted to the opposite side causing compression to the opposite lung. Severe cardiorespiratory embarrassment with cyanosis may also result in massive pleural effusion. Diagnostic thoracentesis is indicated in most patients with pleural effusion, unless the cause is already known. Thoracentesis is best done after careful localisation of the effusion by roentgenogram in frontal, lateral and oblique planes or by the use of fluoroscopic image intensifier. After thorough infiltration of the skin, intercostal muscles and the parietal pleural with a local anaesthetic agent, the needle of appropriate calibre and length is directed j ust above the superior border of the lower rib of the appropriate intercostal space. During aspiration low in the costophrenic angle, the needle tip should be directed upwards to avoid puncture of the diaphragm. Removal of all available fluid usually presents no difficulty unless sometimes after complete evacuation of a massive acute effusion, pain, discomfort and severe coughing may be initiated. Usually no more than 1500 ml should be aspirated in first attempt in a case of massive pleural effusion. Here I am giving a short list of the various causes of pleural effusion of surgical interest according to frequency :— 1. Of the above causes, subdiaphragmatic or intra-abdominal pathologies as the cause of pleural effusion deserve special mention. Cirrhosis of the liver and pancreatitis are also known to cause pleural effusion in certain percentage of cases. The method of formation of pleural effusion in these cases are still not clearly known. It may be that passage of fluid from the peritoneal cavity into the pleural cavity occurs through the lymphatics, whereas others hold the view that the passage of fluid occurs through recognised or unrecognised openings in the diaphragm. A collection of purulent fluid in the pleural space is called ‘empyema’ in wider sense. In fact all phases of pleural infection from an infected turbid effusion to a mature abscess containing thick pus are included in this term. The infective process usually extend to the pleura either directly or by the lymphatics, or by blood (haematogenous) spread or by rupture of necrotic pulmonary parenchyma. Lung infection may itself be secondary to bronchial obstruction either due to bronchogenic carcinoma or bronchiec tasis. A ruptured emphysematous bleb with spontaneous pneumothorax may also result in an empyema. So to narrate the sources of infection which may cause empyema are briefly as follows :— (a) Lung (pneumonia, lung abscess, bronchogenic carcinoma, bronchiectasis, tuberculosis). The most common organisms responsible for empyemas are the pneumococci, streptococci and staphylo coccus aureus. The last named organism is gradually moving to the top position so far as frequency of its existence and its virulence are concerned. Staphylococcal empyemas are often becoming antibiotic-resistant and causing real problem to the surgeons. A few gram-negative organisms are also causing empyema and these are Pseudomonas, Klebsiella pneumoniae, Esch. Previously two types of empyema were considered — syn-pneumonic and metapneumonic. The syn-pneuinonic empyema occurs secondary to streptococcal bronchopneumonia and the empyema occurs simultaneous with the bron chopneumonia. In case of empyema the actual pleural infection is preceded by the development of a serous effusion. The next stage is the starting of inflammatory changes in the pleura with exudation of fluid from the pleura. In the next stage fibrin is deposited on the surface of the pleura and the nature will try to encircle the septic area with a barrier of fibrous tissue. At the initial stage the visceral pleura will fuse with the parietal pleura at the periphery of the collection of fluid. Gradually the fibrin deposits on the pleura are invaded by blood vessels from the adjacent lung and chest wall. Granulation tissue is gradually formed which is replaced by fibrous tissue later on. Thick pus is an indication that the empyema is localised and cannot spread further. Later on in a case of chronic empyema there is a layer of fibrous tissue superficial to the visceral pleura and deep to the parietal pleura to encircle the empyema. A plane of clevage exists between this wall of fibrous tissue and the visceral pleura or the parietal pleura. The secondary changes in case of chronic empyema are that the lung is encased in a rigid cover of fibrous tissue and that segment of the lung becomes immobile and functionless. In streptococcal infections the pus is at first thin and watery and later on it is more serous than purulent, though it contains large number of organisms. The clinical signs of fluid in the pleural cavity are — (i) stony dullness on percussion, (ii) diminished breath sounds and vocal resonance on auscultation, (iii) mediastinum is displaced to the opposite side (this is not very prominent in case of empyema), (iv) diminished chest movement on the affected side. Diagnosis is confirmed by (i) chest X-ray, which shows fluid in the pleural cavity and (ii) aspiration of the pleural cavity.
It is 1 to 2 seconds in case of normal limb and it will be delayed in case of arterial occlusive disease and it may never appear in case of severely ischaemic limb 100mg mebendazole amex. Atherosclerosis is a generalized disease and the patient must be examined thoroughly to exclude ischaemic heart disease purchase mebendazole 100mg amex, cerebro-vascular disease mebendazole 100 mg without a prescription, hypertension buy mebendazole paypal, renal artery stenosis etc. In embolic manifestation, the heart is examined for presence of cardiac murmur, which may indicate certain lesion to cause embolus formation. Estimation of serum P-lipoprotein, triglyceride and cholesterol should be performed when atherosclerosis is suspected. The common femoral artery is used for aortoiliac, renal, mesenteric and femoropopliteal arteriography, whereas the brachial artery is used for subclavian, vertebral, carotid and thoracic angiography. The needle is now withdrawn and a flexible guide wire is threaded through the cannula. The cannula is withdrawn and a polythene catheter is passed over the guide wire into the artery for a distance. Series of X-ray exposures are made to see particularly the whole length of the arterial tree, the origins and the adjacent part of its branches. In selective angiogram the tip of the catheter is introduced into the corresponding artery to delineate the artery and its branches precisely. Abdominal aorta (translumbar route) may be chosen for aortoiliac and femoropopliteal arteriography when the femoral arteries are occluded or the retrograde method has failed to produce necessary information. In patients with occlusive lesion, abnormal signals can be obtained distal to the block and will be lost entirely over the site of the block. The second and third sounds are absent when the flow signals are detected just below the stenotic lesion where high velocity flow is present, a single high-pitched continuous sound is present indicating turbulent flow. This simple apparatus can be used to measure blood pressure at the ankle and at the arm. Normally the ankle systolic blood pressure is greater than the brachial (arm) systolic blood pressure by 5 to 15 mm Hg. If this pressure index becomes less than one it indicates some degree of arterial occlusion. Recently Technetium 99 has become the isotope of choice though the technique remains essentially the same. More recently intravenous injection of isotope has been used to get a direct arterial visualization. Two electrodes are placed diametrically opposite to each other in contact with the arterial wall. The electrodes on the surface of the artery pick up an electromotive force induced in the blood by its motion through the magnetic field and feed it back to suitable electronic amplification. But the greatest disadvantage of this technique is that the artery has to be exposed. Many of these patients are diabetic, though they may not show increased level of sugar in the blood. Later on organic changes develop and sympathectomy does not do much good to the patient. So, importance of finding out the degree of vasospasm cannot be overemphasized to assess the value of sympathectomy. Any rise of skin temperature is recorded and is compared with the rise of mouth temperature. Venous outflow from a limb is briefly arrested while allowing arterial inflow to measure the volume change in the limb which is proportional to the arterial inflow. But it has rarely been found suitable for screening method for surgery, as the surgeon is more interested to know the site of the arterial block rather than to measure the blood flow as such. Recently segmental plethysmography has been introduced by placing venous occlusion cuffs around the thigh, calf and ankle. The cuffs are inflated to 65 mm Hg and the pulsation is the quantitative measure of the arterial diseases. In embolism, a sudden decrease in the movement of its needle is obtained at the level of arterial occlusion. In thromboangiitis obliterans, if no pulsation is obtained in the leg, amputation should be performed in the thigh. The affected part becomes dry, shrivelled, hard, mummified and discoloured from disintegration of haemoglobin. Due to infection and putrefaction the affected part becomes oedematous with blebs. The term ‘Pregangrene’ is used to describe the changes in the tissue to indicate that its blood supply is so precarious that it will soon be inadequate to keep the tissue alive. Syringomyelia, tabes dorsalis, peripheral neuritis, leprosy, caries spine, fracture-dislocation of spine etc. Various special investigations as stated above will help the clinician to diagnose the condition and the level of the block. It is the inflammatory reaction in the arterial wall with involvement of the neighbouring vein and nerve, terminating in thrombosis of the artery. In lower extremity the disease generally occurs beyond popliteal artery, starting in tibial arteries extending to the vessels of the foot. So far as aetiology is concerned this disease has a striking association with cigarette smoking. An autoimmune aetiology has been postulated and familial predisposition has been reported. The pedal arteries are involved first and the patients complain of pain while walking at the arch of the foot (foot claudication), somewhat less often at the calf of the leg, but never at the thigh or buttock (which is common in atherosclerosis). Gradually postural colour changes appear followed by trophic changes and eventually ulceration and gangrene of one or more digits and finally of the entire foot or hand may ensue. It is differentiated from senile gangrene by the age, by its association with superficial phlebitis and pitting oedema. Characteristic arteriographic appearance of this disease is the smooth and normal appearance of larger arteries combined with extensive occlusion of the smaller arteries alongwith extensive collateral circulation. Presence of localized tenderness at the site of embolus and complete disappearance of pulse below this level are the pathognomonic features of this disease. The heart when examined carefully often gives an indication of the source of the embolus. It may be caused by (i) cervical rib, (ii) scalenus anticus muscle, (iii) costoclavicular syndrome, (iv) pectoralis minor syndrome, (v) wide first thoracic rib, and (vi) fracture of the first rib or clavicle. Neurologic symptoms are pain, paraesthesia and numbness in the fingers and hand in the ulnar nerve distribution. The symptoms gradually appear due to sagging down of the shoulder girdle with the advent of puberty. Sometimes symptoms appear later in life due to weakness of the muscles of the shoulder girdle. Presence of cervical rib does not always reveal symptoms or brings the patient to the surgeon. Symptoms of the cervical rib are mainly caused by angulation of the subclavian artery over the cervical rib and by the pressure irritation of the lowest trunk of the brachial plexus which contains the sympathetic nerve fibres to the upper limb. These symptoms will only appear when the muscles of the shoulder girdle will become weak and both the artery and the nerve trunk will be compressed on the cervical rib. When the hand is elevated it looks pale and it becomes blue on prolonged dependent position due to cyanotic congestion. Numbness of the fingers is complained of and the radial pulse becomes feeble on the affected side. X-ray often reveals the cervical rib, though sometimes a fibrous band in its place causes the symptoms like cervical rib and will not be seen by X-ray. The scalenus anticus syndrome is one in which the clinical pictures very much resemble those of the cervical rib. Here the pull of the scalenus anterior muscle, which compresses the subclavian artery and the lower trunk of the brachial plexus, is responsible for the symptoms. Negroes, people of Central Africa, Central America and the East are more prone to be affected. It usually affects the little toe, sometimes the fourth and rarely the third, second or the great toe. Though it is rare in upper limbs yet cases are on the record when the terminal phalanx of the little finger has been involved. The disease starts as a linear groove in the skin on the inner and plantar side of the root of the toe. Frequently the involvement is bilateral affecting both the feet simultaneously or one after the other.
Cross fluctuation between the two sacs of the hydrocele is the most pathognomonic sign of this condition discount mebendazole uk. The steps of operation are — (a) The sac is dissected off the spermatic cord buy cheap mebendazole 100mg on line, (b) The sac is opened and the fluid is drained order cheapest mebendazole and mebendazole, (c) The inside of the sac is inspected order 100mg mebendazole otc, (d) The sac is ligated at the deep inguinal ring and divided, (e) The distal part of the sac is pulled out through the inguinal incision, (f) The testis is inspected, (g) The tunica vaginalis is everted, (h) The testis is pushed into the scrotum, (i) The sac i. J In the last condition secondary hydrocele is due to damage of the lymphatic vessels of the tunica vaginalis, which pass with those of the testis along the spermatic cord. If the testis and the epididymis are not palpable due to excess collection of fluid, diagnosis of secondaiy hydrocele is only possible after the fluid of the hydrocele has been aspirated out. Recent haematocele is almost always ushered with recent trauma followed by pain and swelling. Whether it is from trauma or from tapping of a hydrocele, a recent haematocele should always be treated with urgent operation and exploration. If rupture of the testis has occurred, a linear rupture should be carefully sutured. When a segment of the testis has been damaged, that segment is wedge resected and the tunica albuginea at the margins of the wedge are sutured carefully. It is sometimes difficult to differentiate this condition from neoplasm of the testis unless exposed. The testis is often disorganised and damaged and orchidectomy should be called for in these cases. These tumours comprise slightly more than 1 % of all malignant tumours in the male. But these tumours are the commonest form of malignancy encountered in males between 25 and 35 years of age. The incidence of teratomas peak between 20 and 30 years of age and seminoma occurs mostly between 30 and 40 years. Cryptorchidism-associated tumours are much higher amongst black (40%), although overall testicular cancer is rare in blacks. Approximately 10% of tumours occur in testes that are or have been maldescended, indicating that males with cryptorchidism have a chance of developing testicular malignancy which is increased about 35 times compared with normal population. The risk is 6 times greater for intra-abdominal testes than for lower-lying testes. Another peculiar feature which has been noticed is that a person with cryptorchidism testis is more liable to have a tumour in the opposite normal testis than is a person without cryptorchidism. Approximately one in five tumours occurring in patients with unilateral maldescence appear in a normally descended testis. Orchidopexy if performed after 6 years of age has no influence in minimising development of tumours in testis. According to the others the risk remains the same and that age of orchidopexy has no effect on the risk of cancer. Bilateral cryptorchidism is associated with the secretion of excessive quantities of gonadotrophins and that the undescended testis functions abnormally and reacts in a peculiar fashion to androgens and gonadotrophins. This may give some clue as to the cause of more chance of testicular tumours in maldescended testis. It may be possible that in some cases it may hasten the growth of pre-existing tumour. The peak incidence seen after puberty suggests a link with testosterone or pituitary hormones. Exposure to maternal oestrogen occurs in utero, in which dizygous twin pregnancies, known to have higher maternal oestrogen levels than monozygous twins, are associated with a higher incidence of testicular cancer. The main sites of oestrogen action in males occur in the testis, prostate and associated organs, though oestrogen receptors are^also widespread in the gut, brain, heart etc. The enzyme aromatase is found in the former sites and is responsible for catalysing the final step in the conversion of androgens to oestradiol. Conversely having a brother or father affected constitutes 3 to 4 fold increased relative risk. The commonest chromosomal abnormality is presence of an isochrome of the short arm of chromosome 12, which is seen in 90% of cases. The pick incidence of teratoma is between 25 and 30 years of age and that for seminoma is between 35 and 45 years of age and combined tumours occupy an intermediate age distribution. Germinal tumours, constituting nearly 98% of the total and are presumed to arise from primordial sex or germ cells. Non-germinal tumours, constituting the remaining less than 2% of cases which take origin from the non-germinal elements of testis. For obscure reasons, the typical seminoma is somewhat more frequent in the right testis than in the left. Seminoma starts in the mediastinum of the testis and as it grows it compresses the surrounding testicular tissue. Macroscopically, it has a homogeneous grey-white or pink coloured lobulated cut surface, usually devoid of haemorrhages or necroses. The spermatocytic pattern is more likely to be slightly mucoid and may exhibit small areas of cystic necrosis and sometimes focal haemorrhages. Microscopically, there are three types of seminoma — (i) typical seminoma, (ii) anaplastic seminoma and (iii) spermatocytic seminoma. The classic ‘seminoma cell’ is large and round to polyhedral, has a distinct cell membrane, a clear cytoplasm and a large central hyperchromatic nucleus with one or two prominent nucleoli. The amount of stroma varies greatly — sometimes it is scanty and other times it is abundant. These lymphocytes are believed to reflect an autoimmune response and there is evidence that more lymphocytes mean better prognosis. These giant cells are much bigger than the seminoma cells and mitoses are always present. This tumour may occur at any age from infancy to adult life, though the highest incidence is between 25 and 35 years of age. Its cut surface shows multiple cysts, haemorrhages and varying consistency in different parts. Cystic teratomas are relatively infrequent in the testis but are the most common form of teratoma in the ovary. Mature solid teratomas are composed of heterogeneous collection of differentiated cells e. In more benign form all elements are differentiated and present no elements of potentially malignant embryonic cells. Sometimes these malignant foci reproduce the pattern of embryonal carcinoma or choriocarcinoma. Thus embryonal carcinoma may present a bewildering array of histologic patterns recapitulating all of the embryonic or differentiated cell types derived from ectoderm, mesoderm and entoderm. In the adult form there is a small tumour that does not replace the entire testis, but bulky tumours may be found. On cut surface the tumour is basically grey-white, poorly demarcated with foci of haemorrhages and necroses. Histologically the cells grow in alveolar, glandular, tubular or papillary patterns. The neoplastic cells have epithelial appearance and are anaplastic with hyperchromatic nuclei having prominent nucleoli. Microscopically there are varying spaces lined by flattened embryonal epithelial cells. The individual tumour cells are quite anaplastic and contain vacuoles and granules of alpha-fetoprotein. Due to relatively rapid growth of the tumour, haemorrhage and necrosis are common. The lesion is usually very small and often they cause no testicular enlargement, only small palpable nodule may be detected. The primary lesion may be a haemorrhagic or a clotted mass in which bits of grey tumour can tr seen. Microscopically the syncytiotrophoblastic cell is large with many irregular hyperchromatic nuclei and an abundant eosinophilic vacuolated cytoplasm. The cytotrophoblastic cells are more regular, polygonal with distinct cell border with a single fairly uniform nucleus. These grow in cords or masses usually the syncytial cells form a cap around a cluster of cytotrophoblastic cells. Majority of these cancers metastasise widely by haematogenous route virtually to any organ in the body. The primary testicular focus may be difficult to detect and disseminated metastases steal the show.