By W. Vandorn. Coe College.
If colon bacilli are injected intravenously into rabits in which one ureter had been partially ligated buy silvitra online pills, acute pyelonephritis develops in the obstructed kidney in 75% of cases buy 120mg silvitra amex, but never in the unobstructed kidney discount 120 mg silvitra fast delivery. Under the capsule there are numerous yellow spots representing areas of suppuration. Patchy areas of suppuration are seen which are spherical in the cortex and linear in the pyramids. Wedge shaped areas of larger size are suggestive of infarcts, and represent upward extension of infection. If suppuration is progressive, abscess cavities ftre formed with destruction of renal tissue. The outline of the calyces is destroyed and the resulting distortion is seen in X-ray film, which is an important feature of diagnosis. There is diffuse or spoty inflammation characterised by oedema and small haemorrhagic areas. There are also linear round cell infiltration with admixture of polymorphonuclears. There is destruction of the renal tubules with gradual replacement by scar tissue. The pathological process is characteristically patchy with intervening areas of the tubules which are either normal or dilated filled with pink staining colloid like material. In fact they are peculiarly immune to inflammatory change, though there may be some periglomerular fibrosis. The arteries show two types of changes — (a) endarteritis obliterans, a fibrous thickening of the intima with narrowing of the lumen and (b) thickening and hyalinization of all layers of the arterioles, which may cause renal hypertension. Peculiarly enough this condition affects right side more often than the left but it may be bilateral. The pain may radiate to the lower abdomen or to the groin mimicking ureteric colic. Sometimes anterior tenderness is not so easily palpable due to muscle spasm (iii) Percussion over the renal angle may be painful. Serial blood cultures should be done on any patient with high fever, chills and rigor as bacteraemia is not uncommon. When the condition is present for more than a day, the number of pus cells increases. Quantitative estimations of pus cells and bacteria are important in finding out the severity of the case. Culture of the specimen and sensitivity of the organism to antibiotics are highly important to find out proper chemotherapeutic agent 3. The pelvis and calyces on the affected side may be smaller, may be due to secretion of small volume of urine in the affected side. When infection is severe, it shows less concentration of dye on the affected side, which returns to normal after appropriate therapy. It should be borne in mind that excretory urography should not be used to diagnose this condition, neit her cystography should be performed for diagnosis. If diagnosis is delayed and treatment is inadequate, the condition may turn to be chronic. Such chronic form is not easy to diagnose as not only this condition is silent, but also there is few or no pus cell in the urine, however bacteria may be detected with difficulty. Such chronic form may gradually lead to (i) renal insufficiency, (ii) renal ischaemia and hypertension. Bacteraemic shock may be seen particularly when gram negative rods are the infecting organisms Differential Diagnosis. However change of bowel habit, normal urine and characteristic changes in barium enema will diagnose this condition. Skin hypersensit ivity and absence of pyuria are diagnostic points in its favour Treatment. Patient shoud be instructed to drink large quantities of bland fluid, at least 3 litres a day. In severe cases with vomiting and dehydration, intravenous dextrose saline may be required. If the urine is acid, which is common in coliform infections, alkalisation of the urine is beneficial to relieve symptoms. Potassium citrate with hyoscyamus in the form of mixture given 4 times a day is very useful treatment in this regard. Preferably the antibiotic chosen should reach a high concentration in urine and renal tissue. Such antibiotics are tetracycline, ampicillin, cotrimoxazole, polymyxin B, gentamicin. Once the culture and sensitivity reports are in hand, the proper antibiotic should be started in high dose for at least 10 days, till the urine is rendered sterile. It is better to administer another antibiotic of similar sensitivity for a further 10 days and again urine examination is performed. A few recently available antibiotics are quite effective and these are carbenicillin, cephalosporins (1st generation — cephalexin. If ureterovesical junction is grossly abnormal bacteria in the bladder reach the kidney and true chronic pyelonephritis continues. So treatment should be considered in this direction if permanent relief is to be obtained. The cut surface shows fair demarcation between the cortex and the medulla, but the kidney tissue is pale and fibrotic. Many of these become destroyed and disappear in the scar tissue The glomeruli however remain normal until late in the disease, when they may be hyalinized and fibrotic. Considerable thickening of the arteries and arterioles is evident and this is the cause of renal hypertension which is seen in half the cases. While majority of the females are below 40 years of age, majority of the males affected are above 40 years of age. Urinary sediment may or may not contain numerous white cells, but some bacteria are always present Renal function tests should always be performed. Voiding cystourethrography should be performed which demonstrates vesicoureteral reflux in at least half the cases. Suitable drugs include — Mandelic acid and its salts are quite effective against coliform organisms and Strept. Ammonium chloride of about 2 g may be given together with the previous drug 6 hourly. In about half the cases infection is by one organism, though after treatment with antibiotic it may be replaced by another organism. It needs only passing mention as it does not ordinarily lead itself to surgical treatment. It results in interstitial inflammation which leads to pressure necrosis of the papillae. Recurrent renal colic is complained of as sloughed papillae are passed through the ureter. Excretory urography may not reveal any definite clue to the diagnosis, except that satisfactory excretion of dye may not be present.
It is interesting to note that patients with lactescent serum usually have falsely normal serum amylase level making it a valuable diagnostic indicator of acute pancreatitis buy silvitra 120mg line. Explanation of low serum calcium in virulent acute pancreatitis includes (a) deposition of calcium in the peripancreatic retroperitoneal tissues order silvitra 120 mg visa, (b) a loss of serum albumin purchase silvitra 120mg without a prescription, (c) inadequate parathormone response at the bone level, (d) excess calcitonin secretion and (e) due to hyperglucagonaemia of pancreatitis. In case of severe attacks pulmonary dysfunction marked by dramatic hypoxemia and hyperventilation may occur. Increased amylase and lipase in the aspirated fluid may be detected when their respective serum levels are normal. However diagnostic paracentesis is not an ideal test for the confirmation of the diagnosis due to its poten tial complications and lack of specificity. Deoxyribonuclease /values are markedly elevated in the blood only in pancreatic necrosis. So increased concentration of this enzyme in the serum will reflect the presence of pancreatic disease, but its sensitivity is less than the values of serum amylase. Elevation of this enzyme in the serum correlates well with acute pancreatitis in the same manner as increased level of serum amylase and lipase. Occasionally air-fluid level may be detected in severe cases, (iii) There is often mild distension of the transverse colon due to vicinity of this organ to the inflamed pancreas, which may be revealed in straight X-ray. So air-fluid distended transverse colon is seen to be cut-off suddenly and this is known as the ‘cut-off sign’, (iv) Other possible findings are gallstones in the gallbladder and obliteration of the psoas margin due to retroperitoneal oedema. These findings may support the diagnosis of acute pancreatitis and eliminate other diagnoses. On lateral films, the stomach may be seen displaced forward due to extensive peripancreatic oedema. Such anterior displacement is more obvious due to accumulation of fluid in the lesser sac. In acute pancreatitis, swelling of the gland, loss of internal echoes and loss of the cleavage plane between the splenic vein and the pancreas may occur. Ultrasonography determines whether or not the bile duct is dilated with or without coexistence of gallstones. Computed tomography also gives an indication to acute pancreatitis by changes in the size or shape of the organ, decreased density, loss of sharp peripancreatic soft tissue planes due to extension of the inflam matory process into the adjacent retroperitoneum. Peripancreatic changes include thickening of the surrounding tissue planes, presence of fluid collec tions and blurring. Peripancreatic necrosis is usually more than pancreatic as the pan creas does not have a complete fibrous capsule and hence extravasation of pancreatic secretion into retroperitoneum and related areas occurs early. The cut-off value for diagnosing acute pancreatitis is three times the upper limit of the laboratory normal range for amylase or twice normal for lipase. About 5% of patients can have imaging evidence of acute pancreatitis in the absence of raised amylase levels. It is now generally agreed that immediate operation is unwise, provided other acute surgical emergencies can be excluded. The remaining 20% of attacks are severe with a pro tracted course and a mortality rate of 50%. The severe group needs more vigorous resuscitation and monitoring including intensive care facilities. Aggressive treatment such as early surgery, perito neal lavage or endoscopic sphincterotomy might be justified in patients with a poor outlook. Unfor tunately in no other abdominal condition is the outcome so unpredictable at the outset. So a multi factor prognostic scoring system (Ranson) has been used to detect the severity of the condition. Drawbacks of Ranson’s system are — (i) it requires 48 hours observation period, (ii) usually ‘one time’ assessment is necessary, (iii) some laboratory tests are not routinely performed, (iv) it has not taken into consideration obe sity which is an adverse factor. An Apache score of 6 or more may indicate chance of development of complications in almost 95% of cases. Careful monitoring of fluid balance by central venous pressure and hourly measurement of urinary volume assists accurate replacement. About 1 /3rd of the circulating blood volume may be sequestered as a result of acute pancreatitis. Nothing is permitted by mouth so gastric aspiration should also be added alongwith invisible water loss through lungs and skin and estimated fluid loss from the disease should be considered totally. The adequacy of volume replacement is assessed by the response of the heart rate, blood pressure and urinary output. In patients with pre-existing cardiac or pulmonary disease or in patients with severe pancreatitis, invasive monitoring including urethral catheterisation, cen tral venous pressure measurement, measurement of cardiac output and cardiac filling pressures via a Swan-Ganz catheter is necessary. Shock in acute pancreatitis is mainly due to massive fluid se questration and accumulation of fluid within bowel lumen secondary to paralytic ileus and due to marked oedema in the peripancreatic region. When there is hypocalcaemia calcium gluconate will need to be added to the parenteral fluid. Hypomagnesemia may also be observed and should be corrected as this may hasten the normalisation of serum ionised calcium. This now appears to be false, and indeed it seems that depriving the gut lumen of nutrients is likely to impair gut mucosal barrier function and exacerbate the problem of translocation. In clinical trials it is shown that patients with severe acute pancreatitis can tolerate enteral nutrition delivered either by oral intake or by nasoenteric tube feeding with no adverse effect. Pain is very severe and agonising in acute pancreatitis, so it should be relieved as soon as possible. Moreover pain is frequently accompanied by vasoconstriction which may be harmful to the myocardium and may reduce the blood supply to the pancreas to convert simple oedema to necrosis. Morphine, which is quite effective in relieving severe pain, cannot be given in acute pancreatitis as this causes spasm of sphincter of Oddi. Moreover, administration of morphine is frequently followed by nausea and vomiting. Demerol (Meperidine hydrochloride) in a dose of 50 to 100 mg every 4 hours is considered to be the analgesic of choice because of its anticholinergic action. It may be used in combination with Papaverine (100 mg intravenously) or Nitroglycerine. In only extreme cases bilateral paravertebral splanchnic block or epidural block may be necessary. This can be performed (i) by stopping everything by mouth, (ii) by nasogastric aspiration and (iii) by non-absorbable liquid antacid (preferably a combination of mag nesium trisilicate and aluminium hydroxide as a liquid gel). Cimetidine may be effective as an antacid, (iv) An adequate dose of anticholinergic drug such as probanthine 30 mg every 8 hours or atropine sulphate 0. But its general acceptances is still awaited, (vii) Calcitonin also suppresses pancre atic exocrine and gastric acid secretion, so this drug can also be used. Aprotinin is a specific drug which is being used in this condition with improved prognosis, (viii) Somatostatin is a potent in hibitor of pancreatic exocrine secretion and gastric acid output.
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