Surprisingly buy caverta master card, even patients without an apparent cardiopulmonary condition reported a high frequency of shortness of breath (Table 35 discount caverta 50mg without prescription. Dyspnea is a result of the interplay between physiologic factors and psychological cheap caverta 50mg with visa, social purchase caverta now, and environmental elements [5]. Afferent impulses originate in, or are at least modified by, receptors located in the skin, chest wall, respiratory muscles and tendons, airways, lungs, pulmonary vessels, carotid and aortic bodies, and medulla. At any given moment, it is likely that multiple inputs are generated, transmitted through different pathways, and leading to a variety of uncomfortable respiratory sensations collectively described as dyspnea. Dyspnea occurs when a subject perceives an imbalance between respiratory demand and ventilatory response. Treatment As demonstrated by its high prevalence among patients under hospice care, alleviation of dyspnea at the end of life is often inadequate [7]. There is general agreement that the initial focus of management should be on treating the underlying disease process responsible for this symptom [8]. We have divided nonspecific therapies into the following categories: first-line therapies (recommended), second-line therapies (probably effective, considered for refractory situations), and interventions of unknown efficacy. First-Line Therapies Systemic (oral or parenteral) opioids are effective for the treatment of dyspnea, and they are considered the primary therapies. Their mechanism of action likely involves depression of the respiratory drive and changes at the cortical level [5]. They can be associated with a variety of side effects including nausea, vomiting, constipation, and drowsiness. In nonacute situations, it is reasonable to start with a low dose (oral, immediate-release formulation) and transition to a long-acting dose once a steady state has been reached [5]. Its mechanism of action could involve a decrease in the work of breathing by increasing airflow at sites on airway narrowing by virtue of its lower density compared with air. The mechanism of action of furosemide is unknown but could involve desensitization of the respiratory epithelium. The use of oxygen with the intent to alleviate dyspnea should be considered for certain subgroups of patients. However, most of the subjects from these studies were either outpatients or had no respiratory distress. It is also unknown if medical air, used as placebo in these studies, could have exerted a therapeutic effect by cooling the nasal mucosa, for example. Until new evidence is available, we suggest considering the use of oxygen in patients with respiratory distress because it is a low-risk intervention with potential benefits. Furthermore, nausea and vomiting may hinder reaching nutritional goals by delaying initiation of enteral feeding and complicate medication delivery and absorption. Constipation Constipation is defined as infrequent or absent bowel movements that occur with difficulty of passing stool. Vasoactive drugs such as dopamine can cause constipation, and hemodynamic instability in the setting of hypoperfusion, shock, and endotoxin overproduction can decrease bowel motility. Opioids are regularly used for management of pain and sedation among critically ill patients and frequently cause constipation. Assessment It is important to elicit a careful history, including the past medical history, the past abdominal surgical history, and prior bowel habits to establish whether chronic constipation was present or the patient has risk factors for constipation. Inpatient medications and medical interventions performed during the hospitalization must also be reviewed. The timing, quality, quantity, and frequency of stools since admission will characterize the degree of constipation. The abdominal examination may show firmness, distension, and the presence of hyperactive or hypoactive bowel sounds. In some cases, fecal impaction may present as diarrhea with incontinence when fecal material higher in the colon is broken down into liquid form and flows past the mass. Patients with traumatic spinal cord injury often have neurogenic bowel, but clinicians may overlook it in nontraumatic etiologies such as multiple sclerosis, stroke, or cancer. In these patients, digital rectal and abdominal exams can help distinguish between upper motor neuron (a tight anal sphincter with peristalsis intact) and lower motor neuron lesions (a flaccid sphincter with no volitional contraction). In upper motor neuron injury, evacuation depends on stimulating the bowel wall digitally or with a suppository; by comparison, patients with lower motor neuron injury may need stool-bulking agents like fiber to control stool flow [23]. A plain abdominal radiograph can estimate the stool burden and differentiate between obstruction and constipation. In patients with continued symptoms and concern of alternative etiologies, computed tomography may aid in evaluation of small bowel obstruction, ileus, intra-abdominal abscess, bowel perforation or undiagnosed intraluminal or extraluminal abdominal masses. Treatments It can be effective to time medication use with a patient’s normal toileting schedule and take advantage of the gastrocolonic response with meals to improve outcomes. Hydration and high dietary fiber content are advantageous for healthy, active patients; however, additional dietary fiber such as psyllium may worsen constipation and should generally be avoided for critically ill patients who are not well hydrated. If constipation due to secondary causes is suspected, interventions aimed at treating and reversing underlying etiologies should be attempted. Pharmacologic therapies that utilize different mechanisms and combine oral and rectal interventions may yield effective results. The early use of supportive therapeutic agents is important and can be initiated independent of underlying pathology and bowel habits (see Table 35. Magnesium salts must be used cautiously in renal insufficiency as this may lead to magnesium toxicity. Lactulose passes unabsorbed into the colon where bacteria break it down, thus possibly causing bloating and abdominal cramping. Sodium phosphate enemas should be used with caution among elderly patients as they may cause hypotension, volume depletion, and electrolyte loss [24]. Metoclopramide is a prokinetic agent that antagonizes dopamine receptors, and it can be used in constipation that has not responded to other pharmacologic interventions. Methylnaltrexone is a peripheral opioid antagonist with limited ability to cross the blood–brain barrier and thus does not reverse centrally mediated analgesia. It is approved for treatment of opioid-induced constipation among patients with advanced illness and is effective for inducing laxation of palliative care patients with opioid-induced constipation where conventional laxatives have failed [25]. Nausea is a subjective sensation that precedes the need to vomit and may be associated with other symptoms including tachycardia, lightheadedness, diaphoresis, abdominal pain, and diarrhea. Retching is contraction of the abdominal musculature in the presence of a closed glottis and no expulsion of gastric contents. Any of these symptoms in the most severe form may result in electrolytes imbalances, dehydration, and feeding intolerance with subsequent malnutrition. The vomiting center additionally activates efferent pathways to the cranial nerves, diaphragm, and abdominal muscles [26,27]. Secondary causes of symptoms are adverse effects from medications, shock, abnormal lab values, renal failure, intracranial lesions, increased intracranial pressure, heart failure, and nonabdominal surgery [19]. Assessment Evaluation of nausea and vomiting in the critical care setting must involve patient assessment and corroboration of information from nursing staff. A thorough evaluation of the history, physical examination, laboratory, and radiographic data can frequently identify an etiology. Key components to assess are as follows: Symptoms of nausea, vomiting, retching, reflux, diarrhea, distension, abdominal pain, regurgitation, and constipation Timing, frequency, nature of the event (i. Bilious or fecal emesis associated with abdominal discomfort and constipation or absence of bowel movements can suggest bowel obstruction. Ileus occurs after abdominal surgery, and general anesthesia also contributes to nausea among postoperative patients. Treatment A successful approach to managing the symptomatic patient incorporates thorough patient assessment, knowledge of the emetic pathophysiologic pathways, and a comprehensive treatment plan including pharmacologic and emotional support [26]. Published guidelines currently focus on chemotherapy-related and postoperative nausea management [27,28]. The occurrence of encephalopathy during critical illness may result in clinicians treating signs of emesis rather than symptoms. Although targeted antiemetic treatment blocks the neurotransmitters implicated in the underlying cause, empiric therapy may be necessary without a clear etiology, usually with a dopamine or serotonin antagonist [26]. Phenothiazines are D antagonists but have broader activity than do2 metoclopramide, as they additionally block cholinergic and histamine receptors. These drugs have potent antiemetic activity, but are frequently associated with adverse effects including hypotension, sedation, dry mouth, and extrapyramidal effects. Prochlorperazine, promethazine, chlorpromazine, and levomepromazine are several phenothiazines that are available. Among terminal cancer patients, it is commonly used for the management of nausea and vomiting, and it has also been used for postoperative nausea and vomiting [29].

There is currently no widely available biomarker in use to detect vascular injury in the context of aneurysm or rupture discount caverta 100 mg overnight delivery. The type of repair is determined by the location of the rupture and the presence or absence of aortic valve involvement purchase caverta no prescription. Dacron grafts are generally placed to replace the diseased vessel segment caverta 50 mg lowest price, with various strategies for aortic valve repair or replacement when necessary discount caverta 50 mg otc. Recent work indicates that a less invasive form of repair, retrograde endovascular stent placement, may be useful for the repair of aneurysms of the descending aorta. Standard methods entail surgical replacement of diseased segments in a “staged” fashion; however, newer methods involving a hybrid approach of surgical replacement of the ascending aorta, with subsequent endovascular therapy of the distal segments, appear promising. It may be that a particular patient presents with complaints raising concern for a ruptured aortic aneurysm. In the event that no rupture is found and the patient is hemodynamically stable, it is possible that expansion of the aneurysm is responsible for the symptoms. In such a case, the focus of immediate clinical treatment should be to decrease aortic wall strain and systemic blood pressure through the use of β- blockers in the context of a critical care setting. This trend has been linked to the increased prevalence of atherosclerosis, which is thought to be the major etiology responsible for abdominal aneurysms. In general, the infrarenal segment of the aorta is most heavily affected by atherosclerosis, and this is also the segment where most abdominal aneurysms are observed. The risk factor most closely associated with abdominal aneurysms is smoking, followed by age, hypertension, and hyperlipidemia. Damage to the vessel wall, caused by atherosclerotic plaque, has been shown to cause local inflammation. This inflammatory process is thought to cause degradation of extracellular matrix proteins, notably elastin and collagen. In addition, it is thought that the proinflammatory cytokine milieu leads to cell death within the vessel wall. The full effects of smoking on aneurysm formation and expansion are not known, but increased atherosclerosis and hypertension are thought to be contributors. Such aneurysms are referred to as thoracoabdominal, and their management mirrors the management of aneurysms in the abdominal cavity. Aneurysms of the descending thoracic or abdominal aorta may also be caused by acute bacterial infections. Syphilis may also be associated with abdominal aneurysms, but it is more commonly associated with the ascending aorta. Connective tissue disorders, such as Marfan and Ehlers–Danlos syndromes, do not typically affect the abdominal aorta; however, some systemic inflammatory disorders, notably Takayasu arteritis or Behcet disease, may be associated with abdominal aneurysms. Clinical Manifestations As is the case with thoracic aneurysms, most abdominal aneurysms are asymptomatic and tend to be discovered with testing performed for other reasons. Those patients who do have aneurysm-related complaints tend to report pain in the hypogastric area and/or pain in the lower back. This pain is caused by the expansion of the aneurysm and tends to last for hours or days at a time, and is usually dull and steady. The most common consequence of aortic expansion is compression of the ureter or kidney, leading to hydronephrosis. An episode of rupture tends to be announced by a sudden onset or increase in abdominal and/or back pain. These patients may present with an initial episode of pain associated with the first rupture, followed by temporary tamponade of the retroperitoneal space. Consequently, the absence of a pulsatile mass on physical examination should not be interpreted as an absence of aneurysm. Laboratory analysis may reveal evidence of elevation in D-dimer or an elevation in cardiac biomarkers, due to demand-related myocardial ischemia. Imaging Transcutaneous ultrasound is a noninvasive and readily available technique for the evaluation of the abdominal aorta. This method is frequently used to track the size of abdominal aneurysms, though it is not the imaging modality of choice for the acute aortic syndromes. Open repair, with replacement of the diseased segment with a Dacron graft, is the most established technique. Retrograde endovascular stent placement is a promising technique [113–115], but it is not yet in common use in the acute setting [116,117]. Timely, but elective, surgical or endovascular intervention on the basis of size criteria, as assessed with longitudinal imaging, is the most effective means to prevent progression to rupture. Kuperstein R, Cahan T, Yoeli-Ullman R, et al: Risk of aortic dissection in pregnant patients with the marfan syndrome. Moza A, Al-Hudaif A, Sheikh M: Isolated aortic dissection during coronary intervention: rare but challenging. Girdauskas E, Rouman M, Disha K, et al: Aortic dissection after previous aortic valve replacement for bicuspid aortic valve disease. Ohlmann P, Morel O, Radulescu B, et al: D-dimer in ruling out acute aortic dissection: sensitivity is not 100%. Suzuki T, Katoh H, Tsuchio Y, et al: Diagnostic implications of elevated levels of smooth-muscle myosin heavy-chain protein in acute aortic dissection. Shinohara T, Suzuki K, Okada M, et al: Soluble elastin fragments in serum are elevated in acute aortic dissection. Bossone E, Evangelista A, Isselbacher E, et al: Prognostic role of transesophageal echocardiography in acute type A aortic dissection. Piccardo A, Regesta T, Zannis K, et al: Outcomes after surgical treatment for type A acute aortic dissection in octogenarians: a multicenter study. Li Z, Lu Q, Feng R, et al: Outcomes of endovascular repair of ascending aortic dissection in patients unsuitable for direct surgical repair. Fattori R, Cao P, De Rango P, et al: Interdisciplinary expert consensus document on management of type B aortic dissection. Midulla M, Renaud A, Martinelli T, et al: Endovascular fenestration in aortic dissection with acute malperfusion syndrome: immediate and late follow-up. Girish A, Padala M, Kalra K, et al: the impact of intimal tear location and partial false lumen thrombosis in acute type B aortic dissection. Kudo T, Mikamo A, Kurazumi H, et al: Predictors of late aortic events after stanford type B acute aortic dissection. Delsart P, Maldonado-Kauffmann P, Bic M, et al: Post aortic dissection: gap between activity recommendation and real life patients aerobic capacities. Kitai T, Kaji S, Yamamuro A, et al: Clinical outcomes of medical therapy and timely operation in initially diagnosed type A aortic intramural hematoma: a 20-year experience. Iida Y, Kawaguchi S, Koizumi N, et al: Thoracic endovascular aortic repair with aortic arch vessel revascularization. Garzon G, Fernandez-Velilla M, Marti M, et al: Endovascular stent- graft treatment of thoracic aortic disease. Larzon T, Lindgren R, Norgren L: Endovascular treatment of ruptured abdominal aortic aneurysms: a shift of the paradigm? Potential explanations for the higher prevalence of heart failure in the elderly include the high rate of hypertension; ventricular remodeling from prior myocardial infarction; age-related loss of functional myocytes; and increased extracellular matrix that contributes to alterations in left ventricular compliance. Several of these features combine to create a ventricular phenotype of “heart failure with preserved ejection fraction. The differentiation of new-onset decompensated heart failure from subacute or acute worsening of chronic heart failure is important, because their pathophysiologies differ. Patients with new- onset heart failure have intense sympathetic activation and enhanced microvascular permeability [4]. Consequently, jugular venous distention may be more difficult to assess in these patients because of venous vasoconstriction and redistribution of fluids. Although dramatic, only 5% to 10% of patients with acute decompensation present with “sudden-onset” pulmonary edema. Hemodynamic measurements typically reveal increased right- and left-sided ventricular filling pressures; cardiac index is often, but not always, depressed. Congestion may be related to poor adherence to diet or medications or progression of left ventricular dysfunction with concomitant activation of vasoconstrictor neurohormones and/or worsening renal function.

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However purchase caverta cheap, it should be noted that lasers are complex devices purchase caverta 100mg free shipping, laser–tissue interactions can vary with individual patients and even in the best of hands with the best technique purchase caverta cheap, complications can occur order caverta online pills. Hyperpigmentation, darkened skin coloration relative to surrounding skin, is a very common complication and has been reported with virtually every laser device. Hyperpigmentation usually resolves spontaneously over several months, although in rare instances it may be permanent. Hypopigmentation, lightened skin coloration relative to surrounding skin, is a less common but more significant complication than hyperpigmentation. Second degree burns extend into the dermis and are visible as erythema, edema and blisters that may rupture and form crusts or erosions. A keloid is defined as an abnormal scar that grows beyond the boundaries of the original site of skin injury. A hypertrophic scar is defined as a widened or raised scar that does not extend beyond the boundaries of the site of injury. An atrophic scar is a depressed well defined area, most commonly resulting from collagen destruction associated with inflammatory conditions such as cystic acne, or as a result of tension on a surgical wound. Interventions to prevent scarring are most effective at this stage and are reviewed in the Scarring section, Chapter 6. Scarring is a rare complication with the use of appropriate settings, but can result with any laser at sites that have been overtreated or burned, especially if healing has been complicated by infection or repetitive abrasion. Hypertrophic scarring is more common with laser treatments that create an open wound such as ablative lasers. Subtle textural changes commonly occur with Q-switched tattoo laser treatments due to epidermal injury from high absorption of laser energy by darkly pigmented targets. Recent use of isotretinoin, previous radiation therapy in the treatment area, and a history of keloid formation are also risk factors for hypertrophic and keloidal scarring. Certain areas of the body such as the lower eyelids, mandible, anterior neck and chest are more susceptible to scarring. Additionally, patients of Asian and African decent may have a greater predisposition to hypertrophic and keloidal scarring. Ocular injury is the most severe complication associated with laser use, and both patients and providers are at risk. These wavelengths can also be absorbed by the vitreous humor, forming ‘floaters’ that drift across the visual field. Wavelengths greater than 1100 nm are strongly absorbed by water in the cornea and can lead to corneal burns and cataract formation. Protective eye wear appropriate for the wavelengths used is essential for providers, patients, and personnel in the treatment room and is reviewed in Laser Safety. Most patients experience discomfort only when the laser pulses the skin, and this rapidly resolves once the pulse ceases. Structures in the midline of the face such as the lips, nose, and chin are more sensitive than the periphery of the face. While this is not usually problematic for women as makeup can be worn, erythema can be more of a concern for men. Erythema and edema are considered abnormal if they persist longer than or are more intense than routinely observed. Nonablative lasers generally have a shorter duration of postprocedure erythema usually lasting 3–4 days, ablative lasers have a longer duration of erythema, which can persist up to a few weeks or even months with deep nonfractional ablative resurfacing. Treated skin is vulnerable to irritation from various substances found in topical products such as preservatives and fragrances. Over-the-counter herbal and vitamin remedies such as vitamin E and aloe products are common causes of contact dermatitis. Herpes simplex eruptions are usually preceded by tingling and burning and appear as small vesicles on the lip (i. Prophylactic antiviral medications are given to reduce the occurrence in patients with a known history of viral infections in the treatment area. Bacterial infections are rare (apart from acne), and if they occur usually result from Streptococcus or Staphylococcus. Acne vulgaris infection due to Propionibacterium acnes is visible as erythematous papules and pustules and can occur following any laser treatment. Acne may be due to the laser treatment itself or postprocedure skin care, particularly with prolonged use of occlusive moisturizers. Impetigo is a superficial bacterial infection that can occur following treatments on the face and extremities; lesions progress from papules to vesicles, pustules, and crusts. The main pathogens are Staphylococcus aureus (methicillin-resistant Staphylococcus aureus is uncommon) and group A Streptococcus. Folliculitis is a superficial infection of hair follicles visible as small, erythematous papules and pustules that are less than 5 mm in diameter. Folliculitis most often occurs after vigorous exercise or shaving immediately following treatments and is due to S. Ablative laser treatments have the greatest risk of any infection as the skin is not intact posttreatment, and they have a greater risk of rapidly spreading. Furthermore, the appearance of infections in nonintact resurfaced skin does not always have the characteristic signs seen with intact skin. Tattoos and permanent makeup have concentrated ink pigments and treating over them with lasers that are not intended for tattoo removal can result in severe epidermal injury such as a full thickness skin burn (i. Hair growth structures are susceptible to thermal injury and reduction of hair growth can occur with most lasers, especially those that are absorbed by the melanin chromophore. In addition, when performing hair removal treatments, it is possible to reduce hair adjacent to the intended treatment area as hair follicles grow at angles to the skin. Petechiae and purpura (bruise) represent bleeding underneath the skin and usually appear a few minutes after treatment. They are defined based on size where petechiae are pinpoint dots less than 3 mm, purpura is 3–10 mm, and ecchymoses are greater than 10 mm. These commonly occur with lasers using short pulse widths such as Q-switched lasers and short wavelengths that are highly absorbed by oxyhemoglobin such as 532 nm and pulsed-dye lasers. While they are not a serious complication, purpura in particular, is an unsightly inconvenience due to the 2–3 week duration necessary for clearance. Learning Techniques When getting started with lasers or incorporating a new laser procedure into practice, it is advisable to treat friends, family and staff prior to treating patients. Home-use laser devices are a new area of laser medicine that’s expanding rapidly and are discussed below. The evidence behind these devices is limited and there is wide variation in effectiveness, safety, and quality. Home-use devices use lower parameters than office devices to reduce patient risks, and when compared to in-office devices, more treatments are required at frequent intervals to achieve effects. Lasers used for treatment of vascularities require relatively high energy and as yet there are no home devices for this indication. Although physicians may not use home laser devices directly, patients will likely seek guidance from healthcare professionals about these devices. For example, the Tria, which is one of the most popular and effective home devices for hair removal, is not indicated for use on the face, neck, or genital area. In addition, diminishment and redistribution of fat, hyperdynamic muscle contraction, volume loss and bone resorption also contribute to facial aging changes. To help improve the signs of photoaging and enhance overall aesthetic appearance, an array of minimally invasive cosmetic procedures are currently available including injectable botulinum toxin and dermal fillers, nonablative and ablative lasers, chemical peels and topical prescription, and cosmeceutical products. Some are performed together on the same day during one visit, others are incorporated into a multiple visit treatment plan. Following laser treatment of pigmented lesions such as lentigines, lesions clinically darken due to formation of microcrusts. Microcrusts will slough off spontaneously; however, the addition of an exfoliating microdermabrasion treatment expedites exfoliation and enhances overall skin appearance. Microdermabrasion is typically performed 2 weeks after nonablative laser treatment on the face and 3 weeks after treatment on nonfacial areas. This combination may be alternated every 2 weeks for the duration of the patient’s series of laser treatments.

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Treatment Once cholangitis is suspected purchase cheap caverta on-line, the patient should be treated empirically with broad-spectrum antibiotics with adequate biliary excretion such as ampicillin/sulbactam buy generic caverta 50mg, piperacillin/tazobactam buy caverta 100mg with mastercard, third- or fourth- generation cephalosporins buy caverta 100mg, a quinolone, or a carbapenem. Patients who have mild disease usually respond promptly to medical therapy and should undergo biliary decompression and/or definitive therapy for bile duct stones as early as possible, preferably within 24 to 48 hours. Patients who have severe or progressive obstructive biliary disease require urgent biliary drainage in addition to medical therapy. Selection of a particular approach should be tailored to the patient’s condition, local expertise, and the rapid availability of the procedure. It must be recognized that even with modern support, biliary decompression techniques, and broad-spectrum antibiotics, the mortality from acute fulminant cholangitis ranges from 10% to 50%. Surgical approaches are preferred for patients who are good operative candidates and who may have resectable malignancy. The extravasated bile may accumulate focally to form a biloma or freely flow within the peritoneal cavity. The resultant bile peritonitis is usually associated with abdominal pain, ascites, leukocytosis, and fever. The aim of endoscopic therapy is to decrease or abolish the tone of the sphincter of Oddi, which diverts bile flow away from the leak site. Rarely, if endoscopic therapy is unsuccessful for healing a bile leak, surgical repair may be required. A high degree of suspicion and prompt use of noninvasive testing, including ultrasonography and hepatobiliary scanning, are essential to arrive at a timely and correct diagnosis of this entity. In this setting, an aggressive diagnostic and therapeutic approach is essential because significant morbidity and even mortality continues to occur from complicated acalculous cholecystitis. Supportive measures should be undertaken while the patient is being evaluated with noninvasive testing. Antibiotic therapy with broad- spectrum coverage should be initiated for patients with clinical evidence of sepsis, leukocytosis, or fever. Percutaneous cholecystostomy has become the therapy of choice for patients with acute calculous or acalculous cholecystitis who do not respond to conservative therapy and are too unstable for operative cholecystectomy. A guidewire is passed through this needle and the tract is dilated, allowing placement of a drainage catheter, with success rates exceeding 95%. The primary advantage of percutaneous cholecystostomy is that it can be done at the bedside without general anesthesia. Percutaneous cholecystostomy is often helpful for patients with suspected gallbladder disease, even if cholecystitis is not found, by excluding the diagnosis. Therefore, percutaneous cholecystostomy should be performed early if gallbladder disease is suspected. The cholecystostomy drainage catheter is left in place until acute symptoms resolve, at which time an elective surgical cholecystectomy or, in the setting of a patent cystic duct and functioning gallbladder, simple tube removal may be performed. For patients with acute calculous cholecystitis and severe underlying medical problems, the gallstones can be removed through the percutaneous tract using various techniques [21]. Such percutaneous gallstone removal is an effective alternate therapy to cholecystectomy for patients with other significant medical conditions. It should be reserved for critically ill patients with severe comorbidities that preclude surgical cholecystectomy and/or patients with contraindications to placement of a percutaneous cholecystostomy tube in case of large-volume ascites, coagulopathy, or the presence of an intervening loop of bowel between the diaphragm and the liver that precludes percutaneous access [11]. Although most of the cases have an indolent course, about 25% of patients will develop clinically severe acute pancreatitis, usually because of necrotizing pancreatitis. There are several theories regarding the pathogenesis of gallstone pancreatitis, the most accepted being that stone passage or impaction in the ampulla is responsible for this entity. Gallstone pancreatitis should be considered and excluded during the evaluation of all patients with acute pancreatitis because it is a recurrent and treatable cause of this presentation. Standard abdominal ultrasound in combination with laboratory screening for biliary obstruction can be used to exclude gallstones as the cause for the pancreatitis for most patients [22]. Patients with acute pancreatitis should be classified into risk groups based on one of the accepted prognostic scales [23]. These prognostic scales allow physicians to identify patients who are at risk of developing severe pancreatitis and a complicated hospital course. Patients with acute pancreatitis from biliary stone disease should be managed initially as detailed in Chapter 209. Consultation with a skilled biliary endoscopist should be obtained early in the course for all patients with severe gallstone pancreatitis. In addition, sphincterotomy prevents recurrent pancreatitis in the interim to cholecystectomy, especially if cholecystectomy is not planned within the index admission because of advanced age or severe comorbid medical illnesses. An alternative to sphincterotomy for patients with coagulopathy is placement of a biliary stent to relieve jaundice and prevent stone impaction. Definitive therapy to prevent recurrent bouts may be accomplished by cholecystectomy or endoscopic sphincterotomy with stone extraction in nonoperative candidates. Although debate continues regarding the timing of surgery, it is generally accepted that all patients who are operative candidates should undergo cholecystectomy during the initial hospital admission after the pancreatitis has subsided [26]. Early operative intervention for patients with active severe gallstone pancreatitis has been associated with unacceptably high morbidity. In patients with cholangitis, empiric antibiotic therapy should be directed against gram-negative bacteria [17]. Percutaneous cholecystostomy offers an important therapeutic alternative for critically ill patients with acute cholecystitis [28]. Sugiyama M, Atomi Y: Endoscopic ultrasonography for diagnosing choledocholithiasis: a prospective comparative study with ultrasonography and computed tomography. Attasaranya S, Fogel E, Lehman G: Choledocholithiasis, ascending cholangitis, and gallstone pancreatitis. Kimura Y, Takada T, Kawarada Y, et al: Definitions, pathophysiology, and epidemiology of acute cholangitis and cholecystitis: Tokyo guidelines. Tse F, Yuan Y: Early routine endoscopic retrograde cholangiopancreatography strategy versus early conservative management strategy in acute gallstone pancreatitis. Acute pancreatitis is defined as an inflammatory process that occurs in a gland that was morphologically and functionally normal before the attack and can return to that state after resolution of the attack. The pathologic changes associated with acute pancreatitis vary to a great extent with the severity of the attack [1]. Nonsevere acute pancreatitis is associated with interstitial edema, a mild infiltration of inflammatory cells, and evidence of intrapancreatic or peripancreatic fat necrosis, or both. In contrast, severe acute pancreatitis is usually associated with acinar cell necrosis that may be either focal or diffuse. In addition, thrombosis of intrapancreatic vessels, vascular disruption with intraparenchymal hemorrhage, and abscess formation may be noted [2–5]. In developed countries, acute pancreatitis is caused by ethanol abuse or biliary tract disease in 70% to 80% of patients. No etiology can be identified in another 10% to 20% of patients, a condition referred to as idiopathic pancreatitis. In the less well-developed countries, particularly those in Africa and Asia, acute pancreatitis can develop as a result of malnutrition, ingestion of potentially toxic agents, or both; this type of acute pancreatitis has been called nutritional or tropical pancreatitis [9–12]. The mechanism by which stone passage triggers this gallstone pancreatitis has been the subject of considerable speculation and experimental investigation. The first was the “common channel” theory proposed by Opie [15] in 1901 after he noted gallstones impacted the ampulla of Vater when patients dying of gallstone pancreatitis underwent autopsy examination. He suggested that such stones might create a common biliopancreatic channel proximal to the stone-induced obstruction and that, as a consequence, bile could reflux into the pancreatic ductal system. Subsequent investigations by many groups, however, have challenged the validity of this theory pointing out that pancreatic duct pressure normally exceeds biliary duct pressure, and therefore pancreatic juice reflux into the biliary tract rather than bile reflux into the pancreas would be expected if an obstruction were to create a common channel [16]. Furthermore, many patients develop pancreatitis but lack a common channel that could permit reflux [17], and bile perfused into the pancreatic duct at normal pressure does not induce pancreatitis [18]. Another theory suggested that the stone passing through the sphincter of Oddi could render that sphincter incompetent and, as a result, permit reflux of duodenal juice containing activated digestive enzymes into the pancreas [19]. This “duodenal reflux” would seem to be an unlikely explanation for the development of pancreatitis because it is now clear that neither endoscopic nor surgical procedures that make the sphincter of Oddi incompetent lead to subsequent attacks of acute pancreatitis. The third theory suggests that either the stone or edema and inflammation resulting from stone passage cause pancreatic duct obstruction and that pancreatic duct obstruction is the event that triggers acute pancreatitis.

By X. Grobock. Missouri Valley College.