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The diagnosis of melanoma is usually delayed when the patient presents with bleeding or extension of the lesion to the adjacent structures such as the orbit erectile dysfunction treatment fruits buy cheap nizagara 100 mg line, brain or cranial nerves erectile dysfunction lotion buy cheap nizagara 50mg line. A skin cancer is easily seen and this has led to the conviction that we should be able to decrease mortality by clinical surveillance of highrisk populations. However, mortality has not decreased due to two important factors, which are often underestimated: the different biological aggressiveness of different melanomas, and the limited proportion of overall melanomas that arise within the highrisk groups. Screening in the general population Melanoma is not confined to the highrisk groups so screening of the general population makes rational sense. The proportion of primary melanoma, the prognosis of which can be influenced by early detection is actually unknown. The most aggressive tumours are fast growing and have a high Breslow thickness at presentation. Even with early detection there is no evidence that their prognosis could be changed by early surgery [155]. In contrast, less aggressive melanomas have a low mortality even if they are not detected early and, as they tend to grow slowly, are being picked up earlier and earlier. Screening therefore picks up less aggressive rather than the more aggressive subtypes and thus has no major impact on mortality. Occasional screening Melanoma days or similar services have been conducted in most developed countries in the last few decades. Their major interest is to increase the awareness of the population and doctors about melanoma. Difficulty of targeting the right population A successful strategy must address the highrisk population defined by phenotypic criteria such as light skin type, high number of naevi, etc. Medical system organization in different countries, plus societal and psychological factors, explain why some populations. Systematic periodic screening Periodic screening in the whole population is a high cost intervention with a high demand in terms of medical interventions. A recent experiment in SchleswigHolstein [195] has shown encouraging data including a reduction in mortality. This needs to be confirmed, and to be attributed with certainty to the systematic screening, not just to the increase in awareness induced by an intensive campaign which might achieve the same results at a much lower cost. Public health education Improving the ability of patients to recognize melanoma and to seek medical advice for suspicious lesions is crucial for early detection and improvement of melanoma prognosis in the general population [196,197] for several reasons. First, patients are responsible for most of the delay in melanoma diagnosis [198]. Second, twothirds of melanomas are selfdetected and only a third detected by doctors [199]. Third, the most dangerous melanomas [155,156] probably grow so fast that only patients can detect them early enough. Therefore this strategy of education of the community is probably a reasonable one in terms of costefficiency, and gives the higher probability to impact on mortality. The internet offers an easy opportunity to promote such cognitive training in the general population. Screening in the highrisk population Screening for melanoma in the highrisk population is a cost effective intervention; however, a major limitation is that it fails to pick up the majority of the more aggressive tumours. There is no agreement as to the frequency of this monitoring and to which population this operation should be limited to . Any lesion suspicious of melanoma must be completely removed and sent for pathological examination. The pathological analysis aims at confirming the malignancy and the melanocytic origin of the proliferation, but also to collect major prognostic information (see later). There is a great variability in the morphology and pattern of benign naevi as well as melanoma, which has resulted in the description of a great number of naevi, as well as many melanoma pathological subtypes. There remain ambiguous situations where there is doubt between a benign and malignant melanocytic tumour, some covered by a panel of names which do not always clarify the situation. In this complex situation, a few criteria should be highlighted which are the basis of the differential diagnosis between naevus and melanoma, none of them being specific.

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Acute affect of diphenoxylate with atropine (Lomotil) in patients with chronic diarrhea and fecal incontinence erectile dysfunction from diabetes treatment for buy nizagara 100mg lowest price. Cholestyramine-a useful adjunct for the treatment of patients with fecal incontinence impotence at 52 discount nizagara online visa. Efficacy of alosetron in irritable bowel syndrome: A meta-analysis of randomized controlled trails. The influence of estrogen replacement on fecal incontinence in postmenopausal women. Open study of low-dose amitriptyline in the treatment of patients with idiopathic fecal incontinence. Investigation of mode of action of biofeedback in treatment of fecal incontinence. Long-term outcome and objective changes of anorectal function after biofeedback therapy for fecal incontinence. A prospective, randomized study comparing the effect of augmented biofeedback with sensory biofeedback alone on fecal incontinence after obstetric trauma. Randomized controlled trial shows biofeedback to be superior to alternative treatments for patients with fecal incontinence [abstract]. A prospective randomised trial comparing four biofeedback techniques for patients with faecal incontinence. A randomized-controlled trial comparing an educational intervention alone vs education and biofeedback in the management of faecal incontinence in women. Randomized clinical trial of intra-anal electromyographic biofeedback physiotherapy with intra-anal electromyographic biofeedback augmented with electrical stimulation of the anal sphincter in the early treatment of postpartum fecal incontinence. Randomised, controlled trial of biofeedback with anal manometry, transanal ultrasound, or pelvic floor retraining with digital guidance alone in the treatment of mild to moderate fecal incontinence. Biofeedback and/or sphincter exercises for the treatment of faecal incontinence in adults. Tripletarget treatment versus low-frequency electrostimulation for anal incontinence: A randomized, controlled trial. Rectal balloon training as add-on therapy to pelvic floor muscle training in adults with fecal incontinence: a randomized controlled trial. Can manometric parameters predict response to biofeedback therapy in fecal incontinence Predictive factors which influence outcome of biofeedback therapy in fecal incontinence. Pudendal neuropathy and severity of incontinence but not presence of anal sphincter defect may determine the response to biofeedback therapy in fecal incontinence. Biofeedback therapy for excessive stool frequency and incontinence following anterior resection or total colectomy. Is a new biofeedback therapy effective for fecal incontinence in patients who have anorectal malformations The anal continence plug: A disposable device for patients with anorectal incontinence. The anal plug in the treatment of fecal incontinence in myelomeningocele patients: Results of the first clinical trial. Polytetrafluoroethylene injection for the treatment of partial fecal incontinence. Efficacy of dextranomer in stabilised hyaluronic acid for treatment of faecal incontinence: A randomised, sham-controlled trial. Is electrostimulation of the pelvic floor an effective treatment for neurogenic faecal incontinence Electrical stimulation and pelvic floor muscle training with biofeedback in patients with fecal incontinence: A cohort study of 281 patients. The effects of low-frequency endo-anal electrical stimulation on faecal incontinence: A prospective study. Overlapping anal sphincter repair for faecal incontinence due to sphincter trauma: Five-year follow-up functional results. Long-term results of overlapping anterior anal sphincter repair for obstetric trauma. Prospective study of the effects of postanal repair in neurogenic faecal incontinence.

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Malignant transformation most often occurs during childhood [26 erectile dysfunction drugs available over the counter cheap nizagara 25mg otc,28 erectile dysfunction doctor denver buy nizagara 100mg otc,31] and more rarely later, from the skin but also within the central nervous system [33]. Epidemiological trends in incidence and mortality the incidence of melanoma has been rising worldwide in developed countries over the past five decades usually attributed to increase in recreational sun exposure [7]. Increasing rates of melanoma are also observed in the age group >60 years, particularly in males [7,16]. Common naevi the annual risk of transformation of a naevus into a melanoma is very low and has been estimated around 1/200 000 before the age of 40 in both sexes and 1/30 000 for men older than 60 [35]. For a 20yearold individual, the estimated lifetime risks of transformation of any given mole is about 1/3000 for males and 1/10 000 for females. Genetics Familial melanoma the prevalence of reported family history of melanoma ranged from 1. In a large metaanalysis [43], family history of melanoma was overall associated with a twofold increased risk of melanoma. Phenotypic traits Skin pigmentation and tanning abilities Skin pigmentation and tanning abilities reflecting the skin sensitivity to sunlight exposure are wellknown risk factors for melanoma. Naevus phenotype the naevus phenotype can be defined by the number and the features of naevi, which depends on the genetic background of the individual but also on the amount of sun exposure since birth [46,47]. Among white people, a fairly large body of evidence suggested that the naevus phenotype (number, size and features of Practical consequences In the current situation, prophylactic surgical excision of naevi to prevent melanoma is not relevant, since none of the subtypes of naevi that we can identify fulfil the rate of transformation which would make it costefficient. Only preventative removal of selected large congenital naevi may be desirable for risk reduction and cosmesis though often surgery is impossible in practice due to the size and neurological extension of these lesions. The presence of any clinically atypical naevi gives a relative risk of 4, increasing to more than 6 for patients carrying more than five atypical naevi as compared to noncarriers [52]. The probability of finding a mutation increases with the number of melanoma cases within the family [56], with a young age at diagnosis (<50 years) [57] and with the presence of subjects with multiple melanoma. An excess of pancreatic [57] and even more rarely breast cancers [58] has also been reported. This variation as the result of geographical location suggests that other factors, such as degree of sun exposure or other coinherited gene modifiers, also contribute to the overall risk [62]. Only 2% of the families exhibited these mutations in the most extensive study of familial melanoma conducted by the Melanoma Genetics Consortium (GenoMel) [63]. Losses in function are thus associated with a switch in melanin production from eumelanin to phaeomelanin. Several other genes related to the production or transport of melanin, hair colour, tanning ability, naevus count or melanocyte Genes associated with melanoma risk General understanding of genetically driven risk factors A few major high penetrance genes confer a very high risk of melanoma and lead to familial aggregation of melanoma by a simple transmission of the gene, but they account only for a minority of melanoma. Most of the apparently sporadic cases may be genetically driven to a certain extent by the convergence in a given individual of different alleles of low penetrance genes, which contribute to facilitate melanoma development. The mutation has also been detected in patients affected by multiple primary melanomas or presenting with both melanoma and renal cell carcinoma [84,85]. The pattern of sun exposure varies according to the anatomical location of the melanoma: trunk melanomas are preferentially associated with intermittent patterns of sun exposure while head and neck melanoma like lentigo maligna are preferentially associated with chronic patterns of sun exposure [103]. The presence or history of premalignant and cancerous lesions (actinic keratosis, squamous cell carcinoma and basal cell carcinoma) confers a risk of 4. However, separating intermittent from chronic and cumulative exposure to sunlight is somewhat of an artificial oversimplification.

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If the tumour is solitary erectile dysfunction drugs non prescription buy generic nizagara 50mg line, surgical excision or curettage would be appropriate allowing for the best cosmetic result erectile dysfunction 50 buy nizagara 25 mg overnight delivery. Oral retinoids (acitretin) have been used successfully in a few reports to prevent and control the development of new tumours. Clinical variants In one case, lesions were strikingly confined to half of the body [10]. Other associated findings include severe pruritus, a Koebner reaction, masklike facial appearance, ectropion, and hoarseness due to nodules on the larynx. Complications and comorbidities Patients develop multiple tumours over their lifetime resulting in marked unsightly scars. Investigations Investigations are generally not required but biopsy of a nodule may be necessary to help with the diagnosis. Patients should be advised about signs of new tumour development and what to look out for: red or fleshcoloured nodules usually on lightexposed sites. If there are a small number of tumours, surgical excision or curettage would be appropriate allowing for the best cosmetic result. They may develop a masklike face, present with an ectropion and have hoarseness due to nodules in the larynx. The lesions grow rapidly, last a few weeks and then regress spontaneously leaving atrophic scarring. In these cases, there was evidence of infundibulocystic hyperplasia which developed in the context of hypertrophic lichen planus [2,3]. Torre in 1968 described a patient with multiple sebaceous adenomas and multiple primary visceral tumours [5]. Internal malignancy Most patients develop colorectal carcinoma and nearly 50% have two or more visceral carcinomas. Ten per cent have more than four primary tumours and patients with up to nine tumours have been reported in the literature. Other internal malignancies include carcinoma of the endometrium, stomach, small bowel, genitourinary tract, breast, ovary, pancreas, liver and kidney [6]. There are single reports of an association with nonsmall cell carcinoma of the lung. The sebaceous carcinomas in this syndrome, like the visceral malignancies, are less aggressive than their counterparts that occur independently. Age Although described from the second decade, most cases present with cutaneous and/or internal tumours after the fifth decade [6]. Pathophysiology Pathology See pathology section of sebaceous tumours in Chapter 138. Gardner syndrome is a subtype of familial adenomatous polyposis with a higher risk of colon carcinoma and multiple colon polyps. Clinical features History the majority of patients have a family history of cutaneous tumours and/or internal malignancy.

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A heterogenous disorder caused by a variety of abnormalities of smooth muscle or myenteric plexus what age can erectile dysfunction occur 25 mg nizagara with visa. Analysis of clinical manifestations of symptomatic acquired jejunoileal diverticular disease injections for erectile dysfunction video cheap 25mg nizagara mastercard. Capsule endoscopy versus push enteroscopy in patients with occult gastrointestinal bleeding. The clinical significance of jejunal diverticular disease diagnosed by double-balloon enteroscopy for obscure gastrointestinal bleeding. Complicated jejunal diverticulitis: A challenging diagnosis and difficult therapy. Enterolith ileus: Liberated large jejunal diverticulum enterolith causing small bowel obstruction in the setting of jejunal diverticulitis. Abdominal wall hernias protrude through the retaining walls of the abdomen and have 2 parts: (1) the orifice or defect in the aponeurotic wall of the abdomen and (2) the hernia sac, which consists of peritoneum and abdominal contents. Abdominal wall hernias are external if the sac protrudes through the abdominal wall or interparietal if the sac is contained within the abdominal wall. Internal hernias are contained within the abdominal cavity and do not always have a hernia sac. Hernias are reducible when the protruding contents can be returned to the abdomen and irreducible or incarcerated when they cannot. A hernia is strangulated when the vascular supply of the protruding organ is compromised, and as a consequence the organ becomes ischemic or necrotic. An incarcerated hernia is generally repaired because there is danger of strangulation. Because it can be difficult to determine whether a hernia is incarcerated or strangulated, incarcerated hernias are considered urgent and treated with surgical intervention. Etiology and Pathophysiology Sliding hiatal hernias (type I) occur when the gastroesophageal junction and some portion of the stomach are displaced above the diaphragm, but the orientation of the stomach axis is unchanged. The phrenoesophageal membrane anchors the gastroesophageal junction to the diaphragm (see Chapter 44). Hiatal hernias may be caused by age-related deterioration of this membrane, combined with normal positive intraabdominal pressure and traction of the esophagus on the stomach as the esophagus shortens during swallowing. The gastroesophageal junction remains in a normal position at the level of the diaphragm, because there is preservation of the posterior phrenoesophageal ligament and normal anchoring of the gastroesophageal junction, and only the stomach moves proximally. When diagnosing a hiatal or paraesophageal hernia, important questions for the radiologist to address include: (1) Does the gastroesophageal junction lie at or above the hiatus Hiatal and Paraesophageal Hernias the most common diaphragmatic hernias are sliding hernias of the stomach through the esophageal hiatus, which include hiatal and paraesophageal hernias. Technically, all these hernias are hiatal hernias because they pass through the esophageal hiatus of the diaphragm. Epidemiology Estimates of the prevalence of hiatal hernia vary widely, ranging from 14% to 84% of patients examined, depending on the patient population, method of diagnosis, and symptoms present. Barium study showing a paraesophageal hernia with a portion of the stomach above the diaphragm. The gastroesophageal junction remains in a relatively normal position below the diaphragm (arrow). C, the retroflexed endoscopic view of the proximal stomach demonstrates the endoscope traversing a sliding hiatal hernia adjacent to a large paraesophageal hernia. Patients with symptomatic paraesophageal hernias are most often middle-aged to older adults. Clinical Features, Diagnosis, and Complications Many patients with small simple sliding hiatal hernias are asymptomatic. The main clinical significance of the sliding hiatal hernia is its contribution to gastroesophageal reflux (see Chapter 44). In addition to heartburn and regurgitation, patients with large sliding hiatal hernias may complain of dysphagia or discomfort in the chest or upper abdomen. With chest radiography, a hiatal hernia may be noted as a soft tissue density or an air-fluid level in the retrocardiac area.

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The nodules on the auricle affect the antihelix but erectile dysfunction with age buy discount nizagara 50 mg line, as in polychondritis erectile dysfunction medication list order cheap nizagara online, spare the lobule [3]. Several therapies have been tried, including dapsone, corticosteroids and pentoxifylline. The diagnosis is established by biopsy, or by other associated changes, and appropriate radiology. Radiological bone changes include localized osteolysis or osteosclerosis and generalized osteopenia or osteosclerosis [1]. Spondyloarthritis is commoner in patients with mastocytosis than in the general population [3]. Treatment the progression of the acute relapse can be controlled with corticosteroids. An initial daily dose of 30 mg prednisolone can be gradually reduced and finally discontinued as remission develops. Immunosuppressive agents such as methotrexate and ciclosporin [7,12] may have a role. Other cytokine modulators used with success include rituximab and tocilizumab [2]. Skin and joint lesions may resolve spontaneously in a few weeks, may be recurrent or progress over many months or years [1,2]. Xrays reveal symmetrical, irregular periosteal ossification, predominantly affecting the distal ends of long bones [1]. Histology shows cutaneous sclerosis and hyalinosis, with perivascular infiltration by lymphoid cells in the dermis [2]. Cosmetic procedures such as facelift and botulinum toxin improve facial appearance [12]. Swelling and erythema resembling cellulitis occurs around the elbow or knee in some patients with rheumatoid arthritis and other inflammatory disorders such as Crohn disease; it may occur in the absence of systemic disease [4]. Several cases are reported affecting the tissues adjacent to an orthopaedic metal implant [5,6,7]; this may raise concern about infection or rejection. Typically asymptomatic poorly demarcated erythematous plaques or livedo reticularislike lesions develop near an elbow or knee. Histology shows dilated vascular structures in the reticular dermis, with an endothelial marker profile suggesting lymphatic origin. It has been suggested that the condition is related to reactive intravascular angioendotheliomatosis, forming part of the spectrum of cutaneous reactive angiomatosis [4,7,8]. It is a benign process, and although there are reports of the use of drugs such as infliximab [9], it can respond to simple pressure bandaging, suggesting that it may be related to local lymphostasis [10]. A better understanding of pharmacogenomics may enable screening atrisk patients in the future [2,3]. A pseudoporphyria, clinically resembling porphyria cutanea tarda, is seen in patients taking naproxen. Urticarial lesions may be induced by immunological or pharmacological mechanisms [3]. Crossreaction with octocrylene, a sunscreen ingredient, is often seen with ketoprofen photosensitivity [5]. An association with rheumatoid arthritis is reported in several cases, although the arthritis is often seronegative and nonerosive; in over 50% of patients it is progressive and destructive, resembling psoriatic arthritis [1,2]. Skincoloured, erythematous or violaceous papules, linear bands or plaques develop symmetrically on the lateral aspects of the trunk, proximal thighs or axillae. Palisaded neutrophilic and granulomatous dermatitis [3] is probably a variant, with papules and nodules on the extremities. The collagen bundles are thickened but there is also piecemeal fragmentation of collagen and elastic fibres [2,4,5]. Fortunately, the eruption often responds to topical therapy and, if not, generally resolves on changing to another biological agent.

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Therefore it is not surprising that both excessive and insufficient serum levels of T3 or thyroxine T4 can generate a plethora of dermatological signs and symptoms erectile dysfunction 27 buy genuine nizagara on-line. A hyperthyroid state most frequently results from Graves disease impotence merriam webster best 100mg nizagara, the most prevalent endocrinopathy after diabetes. It primarily affects women or occurs during the initial phase of autoimmune thyroiditis (Hashimoto type) [5,150]. While the latter eventually results in hypothyroidism, its first dermatological presentation can be due to hyperthyroidism. An additional, thyroid automimmunityrelated skin sign may be chronic urticaria, as it has been postulated to be inducible by IgE autoantibodies against thyroid peroxidase [365]. The cutaneous microcirculation also appears to be affected in patients with Graves disease [367]. Hashimoto thyroiditis, the main cause of hypothyroidism apart from dietary iodine deficiency, can be associated with a few additional characteristic signs, namely lateral sparseness of the eyebrows (the sign of Hertoghe; key differential diagnoses include atopic eczema, trichotillomania and ulerythema ophryogenes) and a yellowish hue of the skin due to carotene accumulation (aurantiasis cutis) [368]. If these are accompanied by carpal tunnel syndrome, ptosis and brittle, slowgrowing nails, this further indicates the presence of hypothyroidism [211,276]. With these characteristic signs, the diagnosis of hypothyroidism should not be challenging. Iatrogenic hypothyroidism used to be largely restricted to patients following thyroid surgery, thyroid radiation or thyrostatic drug therapy. More recently, however, another iatrogenic form of hypothyroidism must also be considered: bexarotene, a second line therapy for cutaneous Tcell lymphoma, can induce significant hypothyroidism [369,370], accompanied by the corresponding skin signs and symptoms (see Chapter 19). Hypoparathyroidism Hypoparathyroidsm used to arise predominantly as a surgical complication following thyroidectomy. It is clinically most obvious from the characteristic resultant tetanic muscle cramps. However, hypoparathyroidism can also be seen in polyglandular autoimmune endocrinopathies or rare genetic defects, where its onset and progression can be far more insidious. In both cases, hair and nail growth disorders and skin dryness are the most frequently associated dermatological phenomena. In a small Indian cohort of such patients, loss of axillary and pubic hair, coarsening of body hair, brittle and ridged nails and xerosis cutis were the most common skin signs observed [379]. Another study involved patients exposed to ionizing radiation following the nuclear reactor accident in Chernobyl who had had to undergo thyroidectomy and who developed permanent hypoparathyroidism as a surgical complication. Apart from frequently recurring paraesthesiae and joint pains, hair loss and progressively dry skin were the chief dermatological abnormalities [380]. A study in Brazilian women found hypoparathyroidism to be associated with a significantly reduced hair shaft content of calcium and phosphate, while these minerals were increased in patients with hyperparathyroidism or hyperthyroidism [381]. Primary hyperparathyroidism most commonly results from an autonomous parathormonesecreting adenoma; secondary hyperparathyroidism may arise from vitamin D deficiency or from disturbances of the calcium-phosphate balance, especially in patients with chronic kidney disease. This predisposes to calciphylaxis (calcific uraemic arteriolopathy), though not all patients with this frequently fatal condition have either abnormal parathormone levels or high calcium-phosphate products [5,120,211]. Calciphylaxis is characterized by widespread vascular calcification and thrombotic occlusion of cutaneous blood vessels with resultant extensive tissue necrosis. Calciphylaxis is a frequent complication of endstage renal insufficiency [371,372]. Given the very high mortality of calciphylaxis, its development requires rapid diagnostic action so as to ascertain its origin and treatability [373]. Rarely, hyperparathyroidism may result in metastatic calcification in the dermis and subcutis: this does not specifically affect blood vessels and, if treated promptly, is reversible. It again is commoner in patients with renal failure and typically presents as firm papules, nodules or plaques, particularly around large joints or flexural sites. Thus, hypoparathyroidism illustrates the principle that the skin phenotype seen in patients with a defined hormone deficiency, if interpreted in conjunction with the experimental literature, can highlight clinically relevant novel research frontiers in investigative dermatoendocrinology.

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The globalization of commerce has increased the frequency of once exotic infections in those without grossly obvious exposures erectile dysfunction epocrates order generic nizagara from india. Potential secondary gains from illness or a history of attempted weight loss and fixation on body image should raise the possibility of laxative abuse (see later) erectile dysfunction causes in young men discount 50mg nizagara amex. Functional diarrhea must also be distinguished from idiopathic secretory diarrhea (see later). Physical Examination Physical findings are usually more useful in determining the severity of diarrhea than in determining its cause. Rarely, the physical examination may provide more direct evidence of the cause of diarrhea. A complete blood count should be done to look for anemia, hemoconcentration, or an abnormal white blood cell count. Patients with a viral cause of diarrhea usually have normal white blood cell and differential counts or lymphocytosis, but those with bacterial infections-particularly those caused by organisms that invade the intestinal mucosa- have leukocytosis with an excess of immature white blood cells. Measurements of serum electrolyte concentrations and blood urea nitrogen and serum creatinine levels can be used to assess the extent of fluid and electrolyte depletion and its effect on kidney function. Stool samples should be examined for white blood cells to identify inflammatory diarrhea. Test accuracy depends on the experience and skill of the observer; false-positive and false-negative results are common. Tests for the neutrophil products calprotectin and lactoferrin are sensitive and specific for detecting neutrophils in stool and may be a useful alternative to microscopy. This approach may be of more value in outpatients than in patients hospitalized with diarrhea, because the latter have toxicity or have failed to resolve spontaneously within a few days and must have stool cultures sent. Routine stool cultures are of little use for hospitalized patients in whom acute diarrhea develops while the patient is in the hospital; testing for C. Advanced testing using molecular biological techniques may speed the diagnosis of infectious diarrhea. Abdominal x-rays should be obtained in toxic-appearing patients to assess for colitis and evidence of ileus or megacolon. Proctoscopy or flexible sigmoidoscopy should also be considered in patients who are clearly toxic with infection, have blood in the stool, or have persistent acute diarrhea. Sigmoidoscopy is probably adequate as an early investigation in such patients with severe acute diarrhea. Chapter 16 Diarrhea 231 Further Evaluation of Chronic Diarrhea Because the differential diagnosis of chronic diarrhea is more extensive than that of acute diarrhea, evaluation is more complex. The value of analyzing a timed collection is that stool weight, and therefore the output of stool components like fat, can be measured accurately. In the absence of a timed collection, however, assessment of other stool characteristics on a random or spot collection still provide many clues to the correct diagnosis. Although stool collections are often viewed by patients and physicians as messy and distasteful, they can usually be done easily and successfully at home or in the hospital. Perhaps the biggest hurdle is in dealing with laboratories that are inexperienced or uninterested in stool analysis. Commercially available collection units that fit into a commode and allow separation of stool and urine facilitate the collection, as does the use of preweighed plastic or metal containers and a small refrigerator or picnic cooler to keep the specimens cold. Patients should continue their regular activities and should consume a regular diet, including an intake of 80 to 100 g of fat daily, during the collection. When evaluating the results of timed stool collections, it is important to recognize that patients often do not eat diets sufficiently high in fat. During the collection, diagnostic tests that might alter stool output or composition, such as barium x-ray studies, should be avoided and only essential medications given. If stool output is not representative during that time, the collection can be extended. Occasionally, stool output is measured during fasting; if the diarrhea is caused by an ingested substance, fasting should abolish the diarrhea. Measurement of stool sodium and potassium concentrations allows calculation of an osmotic gap in stool water. The osmotic gap is calculated by subtracting twice the sum of the sodium and potassium concentrations from 290 mOsm/kg, the osmolality of stool in the body.