2019, University of Guam, Pyran's review: "Order Frumil online in USA - Discount online Frumil no RX".

A renal transplant has even been per- toxic infections; and stable function with non‐terato- formed with surgeons unaware that the recipient was in genic immunosuppression [2] 5 mg frumil with visa. Obstetric success in such cases does not a wait of at least 1 year after transplantation generic frumil 5 mg visa. By then cheap frumil 5 mg without a prescription, the negate the importance of contraception counselling for patient will have recovered from the surgery and any all patients with renal failure and the exclusion of preg- sequelae, graft function will have stabilized, and imuno- nancy prior to the surgery. Also, if func- tion is well maintained at 2 years, there is a high probability of allograft survival at 5 years (Table 11. Antenatal strategy and decision‐making ● Serial assessment of renal function is essential along Management requires serial assessment of renal func- with early diagnosis and treatment of rejection (~2%), tion, early diagnosis and treatment of rejection, blood blood pressure control and treatment of infection. Good general health for about 1 year after transplantation Stature compatible with good obstetric outcome No or minimal proteinuria A woman should be counselled from the time the vari- No or well‐controlled hypertension ous treatments for renal failure and the potential for No evidence of graft rejection optimal rehabilitation are discussed [1,22]. As men- No pelvicalyceal distension on recent ultrasound or intravenous tioned at the start of this chapter, couples who want a urography child should be encouraged to discuss all the implica- Stable graft function: Scr ≤160 µmol/L, preferably ≤125 µmol/L tions, including the harsh realities of maternal survival Drug therapy at maintenance levels: prednisolone, azathioprine, prospects. Guidelines vary, with the European Best cyclosporin and tacrolimus are ‘safe’ Practice Guidelines recommending a delay of 24 months Mycophenolate mofetil and sirolimus are contraindicated before conception [71], whilst the American Society of Source: Newcastle upon Tyne 1976, revised 1987 and 2006. Loss of >25% renal function Scr Fetal growth Preterm Pre‐eclampsia Perinatal Pregnancy Persists post End‐stage failure in (µmol/L) restriction (%) delivery (%) (%) deaths (%) (%) partum (%) 1 year (%) ≤125 30 35 24 3 15 4 – 125–160 50 70 45 7 20 7 10 ≥160 60 90 60 12 45 35 70 Estimates based on literature review (1991–2007) from 1076 women in 1498 pregnancies, with all pregnancies attaining at least 24 weeks’ gestation. Haematinics are needed if the transplant, with appropriate and reliable contraception various haematological indices show deficiency. However, significant renal functional Mycophenolate mofetil and sirolimus contraindicated impairment can develop in some patients during preg- Comorbidities (e. No live a gradual decline in function is common in non‐preg- vaccines can be given to any patient on immunosuppression. Most agree that pregnancy does not com- appropriate Discuss the effect of pregnancy on graft function promise long‐term graft progression unless graft dys- Discuss the risks of fetal growth restriction, preterm delivery function was already present before pregnancy [22,74,75]. Delineating late‐onset proteinuria Early diagnosis and dating of pregnancy from pre‐eclampsia remains a challenge but if hyperten- Clincial and laboratory monitoring of the graft and sion is present, then it is usually safer to assume superim- immunosuppressive drug levels every 2–4 weeks until 32 posed pre‐eclampsia. In the future, angiogenic factor weeks, then every 1–2 weeks until delivery levels may assist in differentiating pre‐eclampsia from Surveillance for rejection, with transplant biopsy considered if it is suspected other causes of proteinuria [76] though more recent Surveillance for bacterial or viral infection (e. Whether cal- cytomegalovirus, toxoplasmosis, hepatitis in first trimester cineurin inhibitors are more nephrotoxic in the pregnant and repeat if signs of rejection or tenderness over graft site) compared with the non‐pregnant patient is not known. For kidney recipients: episiotomy on side opposite to graft; caesarean section may not be easy Should discuss operative approach with transplant surgeon in Immunosuppressive therapy (Table 11. Monitor immunosuppressive drug levels for 3–4 weeks after Immunosuppressive therapy needs to be adjusted to delivery, with adjustment as needed ensure that teratogenic medications are ceased well Breastfeeding is appropriate (unless mycophenolate mofetil before conception and that appropriate doses of others restarted); monitor fetal drug levels if there are concerns e. However, azathioprine is widely used in pregnancy and is generally considered safe. B, no fetal risk, no controlled studies; C, fetal risk cannot be ruled out; D, evidence of fetal risk. Numerous adverse anomalies, corpus callosum agenesis, heart defects, kid- effects are attributed to calcineurin inhibitors in non‐ ney malformations and diaphragmatic hernia could also pregnant transplant recipients, including renal toxicity, be a part of the phenotypic spectrum, which is sup- hepatic dysfunction, chronic hypertension, tremor, con- ported by experimental animal studies. To date, in the vulsions, diabetogenic effects, haemolytic uraemic syn- babies, psychomotor development and growth have drome, and neoplasia. There was good evidence suggesting that Medicines and Healthcare products Regulatory Agency patients had more hypertension and smaller babies (https://www. In the cur- not be used in pregnancy unless there is no suitable rent era, lower doses are used. Caesarean section should Hypertension, particularly before 28 weeks’ gestation, is be undertaken for obstetric reasons only and may not be associated with adverse perinatal outcome. The operative approach should be discussed with a due to covert cardiovascular changes that accompany, transplant surgeon in advance and ideally he or she and/or are aggravated by, chronic hypertension. The would be present at delivery to ensure that the kidney appearance of hypertension in the third trimester, its and/or pancreas transplant is protected. Pre‐eclampsia is actually Paediatric management diagnosed clinically in about 20–30% of pregnancies in Over 50% of liveborns have no neonatal problems. Preterm delivery is common (45–60%), as is fetal growth restriction (20–30%), and occasionally the two problems Infections coexist. Lower birthweights are seen in infants born to Throughout pregnancy patients should be monitored mothers who received their transplant less than 2 years carefully for bacterial and viral infection. Prophylactic previously and the use of calcineurin inhibitors can be antibiotics must be given before any surgical procedure, associated with lower birth weights [84]. Asymptomatic bacteriuria is common, should be treated and, if recurrent, merits prophylactic Breastfeeding antibiotics during pregnancy. It could be argued that because the baby has been exposed to Diabetes mellitus immunosuppressive agents and their metabolites in preg- In general, women are having their children at an older nancy, breastfeeding should not be allowed. For cyclo- age, which makes it more likely that patients with type 1 sporin levels in breast milk are usually greater than those diabetes mellitus have reached end‐stage renal failure in a simultaneously taken blood sample. There be due to the presence of generalized cardiovascular is a view that mothers who want to breastfeed should be pathology, which is part of the metabolic risk factor syn- encouraged, so long as the baby is thriving [87,88] and drome. Successful pregnancies have been reported after monitoring fetal drug levels could be undertaken if there combined pancreas–kidney allografts [86]. Preterm delivery is com- immunosuppressive agents, with eventual development mon (45–60%) because of intervention for obstetric rea- of malignant tumours in affected offspring, autoimmune sons and the common occurrence of preterm labour or complications and/or abnormalities in reproductive per- preterm rupture of membranes. Thus paediatric follow‐ monly associated with poor renal function, but in some it up is needed (Table 11. To date, information about has been postulated that long‐term immunosuppression general progress in early childhood has been good. Unless there are problems, spontaneous Preterm delivery and/or small for gestational age onset of labour can be awaited but most advise not Respiratory distress syndrome exceeding 38–39 weeks’ gestation. During labour careful Adrenocortical insufficiency monitoring of fluid balance, cardiovascular status and Septicaemia temperature is mandatory. Surgical induction of labour (by Depressed haematopoiesis amniotomy) and episiotomy warrant antibiotic cover. Reduced T lymphocyte and immunoglobulin levels Augmentation of steroids should not be overlooked. The ultimate measure of transplant success is the long‐ term survival of the patient and the graft. As it is only 40 Gynaecological problems years since this procedure became widely employed in There is a danger that symptoms secondary to genuine the management of end‐stage renal failure, few long‐ pelvic pathology may be erroneously attributed to the term data from sufficiently large series exist from which transplant because of its location near the pelvis [5]. Furthermore, the long‐term results Transplant recipients receiving immunosuppressive for renal transplantation relate to a period when many therapy have a malignancy rate estimated to be 100 times aspects of management would be unacceptable by pre- greater than normal and the female genital tract is no sent‐day standards. This association is probably related to factors numbers of patients worldwide indicate that about 95% such as loss of immune surveillance, chronic immuno- of recipients of kidneys from related living donors are suppression allowing tumour proliferation (especially if alive 5 years after transplantation. With cadaver kidneys, virally driven) and/or prolonged antigenic stimulation of the figure is approximately 89%.

purchase 5 mg frumil visa

cheap frumil 5mg free shipping

Most often frumil 5mg without prescription, etiology is infection with Escherichia coli O157:H7 but increasingly other serotypes such as O26 and O104:H4 are being reported frumil 5mg online. Patients come to medical attention either because of the diarrhea or because of symptoms of renal failure generic frumil 5mg free shipping. Treatment of severe cases or those with prominent extrarenal manifestations is controversial, as studies suggest no benefit with plasma exchange [39]. Some patients may transiently respond to plasma exchange, but then relapse with relentless decline in renal function. Proof of the role of complement activation is the dramatic response seen in patients with complement inhibitor treatment. Patients receiving this agent should be vaccinated for meningococcal infections as the risk of these infections is increased with blockade of the terminal part of complement. One is “multiorgan fulminant” which occurs early (20 to 60 days posttransplant), has multiorgan system involvement, and is often fatal. Pregnancy-Related Thrombocytopenic Syndromes One should consider three syndromes in the critically ill pregnant woman who presents with thrombocytopenia. Fatty liver of pregnancy also occurs late in pregnancy and is only associated with preeclampsia in 50% of cases [55,59]. Patients present with nonspecific symptoms of nausea and vomiting, but can progress to fulminant liver failure. Hypoglycemia, low antithrombin, and high ammonia levels can help distinguish fatty liver from other pregnancy complications [59]. Therapy includes termination of pregnancy or supporting the patient with plasma exchange until the fetus is viable. The bleeding is caused by a combination of factor depletion, platelet dysfunction, thrombocytopenia, and excessive fibrinolysis. Most often the thrombosis is venous, but arterial thrombosis and nonbacterial thrombotic endocarditis have been reported [65]. Measurement of laboratory tests that will reflect the basic parameters essential for both blood volume and hemostasis is helpful. Replacement therapy is based on the results of these laboratories and the clinical situation of the patient (Table 91. Additional discussion regarding transfusion of blood products in critically ill patients is found in Chapter 116. In this case, the purpura fulminans starts with a painful red area on the lower extremities that rapidly progresses to a black ischemic lesion. Secondary purpura fulminans is most often associated with meningococcemia infections, but it can occur in any patient with overwhelming infection [70]. Post-splenectomy sepsis syndrome patients and those with functional hyposplenism due to chronic liver diseases are also at risk [71]. Patients present with signs of sepsis, and the skin lesions often involve the extremities and may lead to amputation. As opposed to primary purpura fulminans, those with secondary purpura fulminans will have symmetrical ischemic lesions at the distal parts of the body (toes and fingers) that ascend as the process progresses. Adrenal infarction (Waterhouse–Friderichsen syndrome) can occur which leads to severe hypotension [72]. Primary purpura fulminans, especially cases with post-varicella autoimmune protein S deficiency, may respond to plasma infusion titrated to keep the protein S level more than 25% [67]. Critically ill patients with secondary purpura fulminans have been treated with plasma drips, plasmapheresis, and continuous plasma ultrafiltration. Much attention has been given to replacement of natural anticoagulants such as antithrombin as therapy for purpura fulminans, but randomized trials using antithrombin have shown mostly negative results [75]. Many patients need debridement and amputation; in one review, approximately 66% of patient required amputation [76]. The syndrome has occurred in association with the use of advanced-generation cephalosporins (notably cefotetan and ceftriaxone), and it has been reported with carboplatin and oxaliplatin [77]. The clinical syndrome associated with cephalosporin starts 7 to 10 days after receiving the drug and may occur following a single dose given as surgical prophylaxis. The patient may be misdiagnosed as having sepsis and be reexposed to the cephalosporin, resulting in worsening of the clinical picture. Approximately 24 to 96 hours after quinine exposure, the patient becomes acutely ill with nausea and vomiting. Some patients, besides having antiplatelet antibodies, also have antibodies that bind to red cells and neutrophils that may lead to the more severe syndrome. Early recognition of the hemolytic anemia (and the suspicion that it is drug-related) is important for early diagnosis so that the culprit drug can be discontinued. One of the agents most commonly associated with drug-induced thrombocytopenia in the critical care setting is vancomycin. The 9 thrombocytopenia is acute and severe (below <10 × 10 per L), is durably refractory to platelet transfusions, and resolves within days of stopping the drug [80]. In patients with a possible drug-induced thrombocytopenia, the primary therapy is to stop the suspect drug. Patients with severe thrombocytopenia should receive platelet transfusions because of the risk of fatal bleeding [81]. However, with vancomycin-induced thrombocytopenia, the patient may be refractory to platelet transfusion [80]. If there are multiple risk medications, the best approach is to stop any drug that is strongly associated with thrombocytopenia (Table 91. Patients with hemophagocytosis appear to have higher rates of multiple organ system failure and higher mortality rates. Inflammatory cytokines, especially monocyte-colony stimulating factor, are thought responsible for inducing the hemophagocytosis. Three members of the Ehrlichia/anaplasma family have been reported to cause infections in humans [85]. Patients may have central nervous system signs and marked elevation of the serum levels of liver enzymes. In many patients, the buffy coat reveals the organisms bundled in a 2 to 5 µm morula in the cytoplasm of the granulocytes or monocytes. Consideration of ehrlichiosis is important because highly specific therapy is doxycycline, which is a drug not routinely used for therapy of sepsis syndrome. Patients suffer a flu-like prodrome and then rapidly develop a noncardiac pulmonary edema resulting in profound respiratory failure [89]. Marked hemoconcentration is also present because of capillary leak syndrome with the hematocrit reaching in some patients as high as 68%. In the southern United States, dengue is becoming an increasing problem, and fatal cases of arenavirus have been reported in California [93].

order 5 mg frumil free shipping

Arendse R order frumil 5 mg without prescription, Irusen E: An atropine and glycopyrrolate combination reduces mortality in organophosphate poisoning purchase 5mg frumil overnight delivery. Eddleston M cheap frumil 5mg without a prescription, Eyer P, Worek F, et al: Pralidoxime in acute organophosphorus insecticide poisoning–a randomised controlled trial. Sundwall A: Minimum concentrations of N-methylpyridinium-2- aldoxime methane sulphonate (P2 S) which reverse neuromuscular block. Eyer P, Worek F, Thiermann H, et al: Paradox findings may challenge orthodox reasoning in acute organophosphate poisoning. Eyer F, Worek F, Eyer P, et al: Obidoxime in acute organophosphate poisoning: 1—clinical effectiveness. Ashani Y, Rothschild N, Segall Y, et al: Prophylaxis against organophosphate poisoning by an enzyme hydrolysing organophosphorus compounds in mice. Raveh L, Segall Y, Leader H, et al: Protection against tabun toxicity in mice by prophylaxis with an enzyme hydrolyzing organophosphate esters. Ashani Y, Leader H, Rothschild N, et al: Combined effect of organophosphorus hydrolase and oxime on the reactivation rate of diethylphosphoryl-acetylcholinesterase conjugates. Sener S, Ozsarac M: Case of the month: rivastigmine (Exelon) toxicity with evidence of respiratory depression. Other than alcohol, cocaine is the most common cause of acute drug-related emergency department visits, accounting for 31% of all visits to the emergency department related to drug misuse or abuse [2]. Blockade of the fast sodium channels stabilizes axonal membranes, producing a local anesthetic-like effect and a type I antidysrhythmic effect on the myocardium. Cocaine is well absorbed through the mucosa of the respiratory, gastrointestinal, and genitourinary tracts, including less common routes of absorption such as the urethra, bladder, and vagina. Crack cocaine and cocaine freebase are alkaloid forms of cocaine that are produced by an extraction process. It is rapidly hydrolyzed to the inactive metabolites ecgonine methyl ester and benzoylecgonine, which account for 80% of cocaine metabolism. These compounds have half-lives of 4 to 8 hours and have some cardiovascular effects that are similar to the parent compound. Urinary toxicology screens for recreational drugs typically assess for the presence of benzoylecgonine, which is usually present for 48 to 72 hours after cocaine use [3]. The metabolism of cocaine in the presence of ethanol produces cocaethylene, which has additional cardiovascular and behavioral effects [4]. Human studies demonstrate that cocaethylene produces milder subjective effects and similar hemodynamic effects when compared with cocaine. Cocaine toxicity is due to an exaggeration of its pharmacologic effects, resulting in myriad consequences that have an impact on every organ system. The widespread effects of cocaine are related to its ability to stimulate the peripheral and central sympathetic nervous systems, in addition to local anesthetic-like effects. Cocaine causes vascular effects through multiple pathophysiologic mechanisms that have been best described in the heart [6–8]. These include arterial vasoconstriction, in situ thrombus formation, platelet activation, and inhibition of endogenous fibrinolysis. In addition, myocardial oxygen demand is increased by cocaine-induced tachycardia and hypertension [6–9]. The direct local anesthetic-like effect of cocaine or secondary cocaine-induced myocardial ischemia [6,10] may be responsible for cardiac conduction disturbances [10] and dysrhythmias. Most severe cocaine-related toxicity and cocaine- related deaths are manifested by signs of sympathomimetic overdrive (e. This increased psychomotor activity causes increased heat production and can lead to severe hyperthermia and rhabdomyolysis [11]. Although most of the patients do not have serious underlying etiology, myocardial infarction due to cocaine is a well-established entity and needs to be excluded [12,13]. Cocaine-associated myocardial infarction typically occurs in patients aged 18 to 60 years without apparent massive cocaine exposure or without evidence of cocaine toxicity. Patients with cocaine-associated myocardial infarctions frequently have atypical chest pain or chest pain that is delayed hours to days after their most recent cocaine use [6,12]. The stimulatory effects of cocaine can lead to seizures, cerebral infarction, intracerebral bleeding, subarachnoid hemorrhage, transient ischemic attacks, migraine-type headache syndromes, cerebral vasculitis, anterior spinal artery syndrome, and psychiatric manifestations [20–24, 24a]. Cocaine-induced seizures are typically single, brief, generalized, self- limited, and not associated with permanent neurologic deficit [24,24a]. These seizures may occur in the presence or absence of concurrent structural disease, such as infarction or hemorrhage. Multiple or focal seizures are usually associated with concomitant drug use or an underlying seizure disorder [20]. Cocaine has a number of direct and indirect effects on the lungs, and they are associated with how the drug is used [25]. These effects include asthma exacerbations, pneumothorax, pneumomediastinum, noncardiogenic pulmonary edema, alveolar hemorrhage, pulmonary infarction, pulmonary artery hypertrophy, and acute respiratory failure [26,27]. Asthma exacerbations are more common with crack cocaine usage, most likely due to particulate by-products of combustion [27]. Inhalation of cocaine is typically associated with deep Valsalva maneuvers to maximize drug delivery and can cause pneumothorax, pneumomediastinum, and noncardiogenic pulmonary edema. The most deadly gastrointestinal manifestation of cocaine usage is seen in the patient who presents after ingesting packets filled with cocaine. Body packers are patients who swallow carefully prepared condom or latex packets filled with large quantities of highly purified cocaine for the purposes of smuggling this drug into the country. In contrast, body stuffers are typically “street” drug dealers who swallow packets of cocaine while fleeing the police. These packets are generally prepared for distribution to individual customers and not to protect the body stuffer from absorbing cocaine. It was previously thought that cocaine ingested orally was metabolized in the gastrointestinal track and did not lead to systemic toxicity. This is clearly not the case and toxicity can develop in body stuffers and packers from cocaine leaking out of the swallowed packets. The dosage of cocaine exposure in body stuffers is generally substantially less than that of a body packer. Although massive exposure to leakage from a condom or latex-filled packet of a body packer can occur, most body packers identified by airport immigration officers do not develop clinical toxicity. However, any patient identified as a body packer who has developed any signs of systemic cocaine toxicity (tachycardia, hypertension, diaphoresis, etc. These patients, when identified, have a high potential for progressively worsening toxicity and mortality [29]. Further, cocaine-induced left ventricular dysfunction can lead to hypertrophy and eventually a dilated cardiomyopathy and congestive heart failure [6]. Cocaine-associated dilated cardiomyopathy appears to have a reversible component, and some patients have demonstrated improvement after cessation of cocaine use [6]. Chronic severe cocaine users can present with lethargy and a depressed mental status that is not attributable to any other etiology (diagnosis of exclusion), the “cocaine washout syndrome. Chronic cocaine usage during pregnancy increases the chance of premature delivery and abruptio placentae [32]. Maternal cocaine usage is associated with low birth weight, small head circumference, developmental problems, and birth defects in the neonate [33–35].

cheap frumil 5 mg

frumil 5 mg line

Pancreatic effects of iron deposition affects mostly the beta cells leading to glucose intolerance and eventually overt dia- betes buy 5mg frumil free shipping. Joint pain (arthralgia) and arthritis are also common (25–50 percent of patients) in Case 24: Man with painful knees 111 haemochromatosis due to local deposition (as in this patient) generic 5mg frumil with visa. Erectile dysfunction may be seen in haemochromatosis due to either testicular or pituitary involvement discount 5 mg frumil visa. One of the possible late manifestations of hereditary haemochromatosis is referred to as ‘bronze diabetes’. This condition occurs when the disease involves the skin (bronze appearance) and the pancreas (diabetes). In the last two months, she also reports intermittent abdominal disten- sion and ‘squeezing’ pain, sometimes associated with vomiting. Regular medicines are peppermint oil capsules, mebeverine, citalopram 10 mg per day and a salbutamol inhaler. The clinical suspicion is that of inflammatory bowel disease, either Crohn’s disease or ulcerative colitis. The differential diagnoses in this case would include appendici- this, intra-abdominal infection or possible ovarian pathology. The patient is young and of child-bearing age (note negative pregnancy test) – any imaging should ideally keep ionizing radiation to a minimum. Abdominal x-ray indicated if any suggestion of ileus/obstruction, megacolon or perforation (where combined with an erect chest film to demonstrate free intra- peritoneal air). It is accurate in these groups for appendicitis/terminal ileal disease and also for renal/ pelvic cases of pain. Barium studies (small bowel meal/follow-through) are used for the further inves- tigation of suspected small bowel Crohn’s disease. There is inflammatory change in the perimesenteric fatty tissue around the involved segment which suggests inflammation affecting the full thick- ness of the bowel wall. Case 25: Woman with abdominal pain 119 A long irregular stricture is seen in the region of the terminal ileum (ure 25. The barium meal and follow-through shows appearances consistent with a Crohn’s stricture of the terminal ileum. Crohn’s disease is a chronic, relapsing inflammatory condition that can affect any part of the gastrointestinal tract from mouth to anus. Patients with small bowel involvement often present with abdominal pain, diarrhoea and weight loss and often there is a mass in the right iliac fossa. Eighty per cent of Crohn’s patients have small bowel involvement and the terminal ileum is the most common site. Other barium study findings in Crohn’s disease may be small bowel fold thicken- ing (caused by increase in the volume or fluid of cells in the mucosal or submu- cosal region) and hyperplasia of lymphoid tissue with or without mucosal erosions (aphthous ulcers). Aphthous ulcers may enlarge and deepen across the bowel wall causing the characteristic ‘rose-thorn’ ulceration. Late signs include deep fissures or ulcers, pseudopolyps, ‘cobblestone’ pattern caused by transverse and longitu- dinal fissures around pseudopolyps, and separation of oedematous bowel loops. Characteristic ‘skip lesions’ refer to the manner in which lesions occur in multiple sites along the bowel. Strictures are common, especially in the terminal ileum, and are a result of the inflammatory process, and fistulae are also common. Both Crohn’s and ulcerative colitis are associated with extraintestinal manifesta- tions, including: • Clubbing • Fatty liver, chronic active hepatitis, sclerosing cholangitis • Erythema nodosum, pyoderma gangrenosum • Amyloidosis, ankylosing spondylitis, seronegative arthritis • Uveitis, episcleritis, iritis. Magnetic resonance enterography with gadolinium contrast is an imaging modal- ity that is being increasingly used in Crohn’s disease, being useful for assessing the extent of both non-active disease and active disease. Case 25: Woman with abdominal pain 121 Features which may help differentiate Crohn’s disease from ulcerative colitis Crohn’s disease Ulcerative colitis Distribution Mouth–anus Colon/ileum (back wash ileitis) Colon involvement Right-sided Left-sided Ulcers Deep (rose-thorn) Superficial (collar stud) Ileocaeal valve Thickened Gaping Fistulae Yes No Skip lesions Yes No Risk of carcinoma Slight ↑ Marked ↑ Megacolon Unusual More common Rectum involved 14–50% 95% There is also an increased risk of small bowel lymphoma and adenocarcinoma in Crohn’s disease. She is a current smoker with a 40 pack-year history, she is a social drinker with no other significant history. Her respiratory rate is 18 per minute and there is reduced air entry in the right upper zone of the chest. Primary or secondary squamous cell carcinomas are the most common causes – remember head, neck and cervix as possible pri- mary sites. Tuberculosis, Staphylococcus aureus and Klebsiella also cause cavitation, although the patient would be systemically unwell. Hypercalcaemia may also be related to bone metastases which should be considered and excluded (radionuclide bone scan). A chest film 4 hours post-procedure should always be performed to ensure there is no latent pneumotho- rax (remember to review this, or arrange review and document your findings in the patient’s notes). In the right upper lobe, adjacent to the vertebral body, there is a large soft tissue lesion which contains an air – fluid level (arrow A). Note vertebral Case 26: Woman with cough and weight loss 125 body (arrow B), trachea (arrow C) and a left upper lobe bulla (arrow D). Adenocarcinoma is most commonly seen in non-smokers and females, is peripher- ally located in the lung, grows slowly but may metastasize early. Bronchoalveolar carcinoma is a subtype of adenocarcinoma which may present as a nodule or a focus of consolidation on a chest film. It may develop within an area of scarred lung fibrosis secondary to tuberculosis, bronchiectasis or scleroderma. Persistent consolidation 6–8 weeks after antibiotic therapy should raise the suspicion of cancer and patients require further investigation. Undifferentiated large cell carcinoma is associated with smoking, is usually large, centrally or peripherally located, grows rapidly and metastasizes early. Risk factors for lung cancer include cigarette smoking, male gender, scarred lung fibrosis and exposure to asbestos, uranium and radon gas. Radon gas is a colour- less, radioactive gas which is produced by the radioactive decay of uranium in soil and rocks. A relevant occupational and social history is therefore necessary when presenting symptoms suggest bron- chogenic carcinoma. She notes also a one-month history of intermittent bouts of central chest pain worse after food and notes a 2-week history of cough at night, which is non-productive but worsening. Examination Clinical examination revealed no haemodynamic compromise, respiratory examination revealed scattered coarse crepitations in the base of the right lung, but no evidence of respiratory distress. Investigations Blood tests showed no evidence of anaemia or infection with normal renal and liver function. There is a tight, ‘bird beak’-like stricture at the lower oesophageal sphincter (arrow A) with dilatation of the proximal oesophagus containing food debris (arrow B). Distal to the stricture barium contrast is seen in the stomach suggesting that fluid can traverse the stricture (arrow C). This diagnosis is made in the absence of other pathologies such as carcinoma of the oesophagus or fibrosis.