By P. Vibald. Stanford University. 2019.
During the past 20 to 25 years buy 1mg coumadin mastercard, candidiasis became Clin Infect Dis 2008; 46:1206−1213 a common problem in severely immunocompro- Discusses the fate on non-albicans Candida sp infections discount 2mg coumadin. In Elaborates on the various immunosuppressive regimens that addition to Candida sepsis 2mg coumadin with mastercard, other organs may appear to predispose to the development of progressive dis- become infected with the fungus best purchase coumadin. Epidemiology of Can- components of the fungal wall, and it may be dida species infections in critically ill non-immunosup- positive in candidiasis as well as other fungal infec- pressed patients. Of the three classes of antifungal agents A very careful review of the pertinent literature on the available, ie, polyenes, azoles, and echinocandins, subject. Dis- multicenter clinical evaluation of the (1-3)beta-D-glu- seminated histoplasmosis: clinical and pathologic cor- can assay as an aid to diagnosis of fungal infections in relations. Clin Infect Dis 2009; 48:503−535 ﬁndings in acute invasive pulmonary aspergillosis: Comprehensive recommendations for the treatment of both clinical signiﬁcance of the halo sign. Semin Respir Crit Care Med 2004; 25:203−219 A large contemporary series exploring the surgical option An excellent and comprehensive treatise on the subject. Emerg Infect Dis 2006; 12:958−962 in association with the largest outbreak of blastomycosis to An important consideration for practitioners in the endemic date. Patients almost always are treated severe disease (pulmonary arterial systolic pressure with analgesics, are hydrated to prevent hemocon- 45 mm Hg) in 10%. Portopulmonary Hypertension Hypoxemia is caused by precapillary and capillary dilation and pulmonary and pleural arteriovenous Up to 20% of patients with cirrhosis and portal anastomoses. The most common presenting symp- hypertension have modestly increased pulmonary tom is dyspnea, but the presence of stigmata of arterial systolic pressures ( 25 mm Hg at rest or chronic liver disease (spider nevi, clubbing) and 30 mm Hg with exercise) that are caused by severe hypoxemia strongly suggest the diagnosis. However, porto- while upright) because of increased shunting of pulmonary hypertension, with pulmonary pulmonary blood to the systemic circulation vasoconstriction and pathologic changes indistin- through spider nevi in the lung bases. Vascular dilations 25 mm Hg, mean pulmonary arterial occlusion probably cause hypoxemia by diffusion-perfusion pressure 15 mm Hg, and pulmonary vascular impairment, in which oxygen may not diffuse all resistance 250 dynes ⋅ s ⋅ cm-5. Unfortunately, and for unknown reasons, the regulated vasoactive mediators leaving the liver response of patients with portopulmonary hyper- and entering the lungs, causing remodeling of the tension to liver transplantation is unpredictable, pulmonary vessels. It is diagnosed by use of the fol- lowing criteria: portal hypertension (with or The pulmonary manifestations of this genetic without cirrhosis); arterial hypoxemia (alveolar- defect are actually the result of a primary hepatic arterial oxygen difference, 15 mm Hg); and abnormality. With a gene mutation, abnormal α - 1 pulmonary vascular dilation demonstrated by the protein levels accumulate in hepatocytes and are echocardiographic appearance of microbubbles in not released from the liver. The resulting low cir- the left atrium within three to six cycles after the culating concentration of this protective protease injection of hand-agitated circulation into a periph- inhibitor leads to excessive neutrophil elastase eral vein or abnormal brain uptake seen on radio- activity in the lungs and the destruction of pulmo- nuclide scanning. A Pao2 60 mm pleural space, causing the accumulation of pleural Hg is considered to be an indication for transplan- ﬂuid with the same characteristics as the ascites. Sponta- Oxygen radicals have a beneﬁcial role because they neous bacterial empyema may occur with or are used by neutrophils during phagocytosis and without spontaneous bacterial peritonitis. Thoracentesis may be excessive production of these molecules (termed helpful to relieve dyspnea and hypoxemia acutely; oxidative stress), leading to damage to cellular and however, the ﬂuid usually reaccumulates. Pleurodesis is generally unsuccess- sufﬁcient oxidative stress stop dividing and die, ful because the ﬂuid usually reaccumulates too some by entering apoptotic pathways and commit- rapidly for the pleural surfaces to come together ting “suicide,” others by oxidation-induced necro- and adhere. This may be the case with ischemia-reperfusion defects by videothoracoscopy can be attempted, injury in patients with myocardial infarction and but few centers are experienced in performing stroke. Intracellular enzymes that reduce because the pleural space has a lower pressure than oxidant activity include superoxide dismutase the venous system and because ﬂuid moves pref- (eliminates superoxide anion), catalase (metabo- erentially to the pleural space. The transjugular lizes H2O2), and glutathione peroxidases (reduces intrahepatic portosystemic shunt is an option in levels of H2O2 and lipid peroxides). Vitamin E patients who have recurrent hydrothorax despite inhibits lipid peroxidation in membranes, and receiving diuretic therapy and undergoing repeated deﬁciencies of vitamin E result in the increased thoracenteses. The lung and capillary endothelium are the only tissues that can be exposed to high concentra- Oxygen Toxicity tions of oxygen because other tissues consume more oxygen than is dissolved in the blood. Thus, Oxygen is necessary for life, but it also has the lung cells may be exposed to a Po2 of 600 mm potential to be toxic through the generation of free- Hg in a pure oxygen atmosphere under normobaric radical intermediates. A balance of oxidative and conditions, but other tissues are rarely exposed to antioxidant processes maintains life while main- oxygen tensions that are 10 mm Hg above nor- taining organ function. In experimental models, endotoxin also induces anti- The stepwise reduction of oxygen to water oxidant enzyme activity and increases tolerance to produces free radicals that in turn are injurious to high concentrations of O2. The latter is among the most reac- effects on the lung, probably because bleomycin tive biological molecules known and is capable of increases the generation of free O2 radicals. Killing tumor cells is accompanied by the destruction of surrounding normal lung tissue, Patients may notice retrosternal pain after leading to the following two clinical syndromes: inhaling pure oxygen for a few hours, and tracheo- radiation pneumonitis and radiation fibrosis. Muco- Although many patients who receive radiotherapy ciliary velocity is impaired, possibly as the result have radiographic changes, symptoms develop of damage to ciliated airway epithelium. With advances in com- ﬁcult to diagnose parenchymal oxygen toxicity in bined chemotherapy and radiation therapy for humans because the clinical picture is always cancers, this disorder should become even less obscured by the disease that prompted the need common. In experimental models, dam- age to type I pneumocytes increases permeability Pathogenesis and leads to the recruitment of inﬂammatory cells into capillaries and alveolar septae. Tissue injury There is no treatment for oxygen-induced lung also causes a cytokine response that recruits injury; therefore, the best strategy should be to immune cells to perpetuate the inflammatory prevent it by minimizing exposure. In studies of experimental lung injury, even 50% O2 enhances The magnitude of lung injury depends on sev- lung damage, and that concentration is the thresh- eral factors: old at which the replication of human pulmonary epithelial cells is inhibited. Irradiated volume of lung tissue: The risk of bleomycin, any supplemental O is deemed to pneumonitis increases with the volume of 2 be potentially hazardous. Thermal and Toxic Injury A progression of chest radiographic ﬁndings is typical, manifesting as ground-glass opacities that The same high temperatures that burn the skin may progress to consolidation, coalescing to form may injure the upper airways, and inhalation a sharply demarcated opacity corresponding to the injury is an important predictor of mortality in ﬁeld of radiation. The peripheral airways and alveoli outside the radiation ﬁeld, perhaps attributable to are not burned unless steam is inhaled because the a lymphocyte-mediated hypersensitivity reaction. Smoke inhalation is associated with bron- data and clinical experience indicate that therapy chospasm, impaired mucociliary function, mucus with corticosteroids is an effective treatment in hypersecretion, inflammation, and edema. The presence of edema and 6 months after exposure, may take up to 2 years to blistering should prompt intubation, but if the evolve, and generally remains stable thereafter. In the absence of a signiﬁcant ﬁbrosis, ranging from no symptoms to severe dys- airway burn, intubated patients can usually be pnea, hypoxemia, and death. Corticosteroid administration does not strictive pericarditis, and exposure of the coronary attenuate the course of pulmonary injury and arteries to the beam may cause obstruction. Herpes simplex against the development of delayed neuropsychi- tracheobronchitis is common, perhaps due to direct atric dysfunction, although this issue remains a extension from an oral source in patients who are contentious one. Pao may be convert the ferrous iron (Fe2+) in hemoglobin to the 2 normal, and pulse oximetry overestimates arterial ferric form (Fe3+), creating methemoglobin. When oxygen saturation because most devices do not oxidizing agents are administered in excess or to reliably distinguish oxyhemoglobin from carboxy- patients with deﬁciency in enzyme systems that hemoglobin. Thus, ment, but they do not necessarily correlate with both the decreased oxygen content of arterial blood clinical abnormalities, especially when measured and the increased afﬁnity of oxygen for hemoglo- hours after exposure. In asymptomatic persons, bin lead to reduced tissue oxygenation and the levels up to 20% may require no treatment, but symptoms associated with methemoglobinemia. High tion of acute symptoms, and there are some studies levels of methemoglobin turn blood brown, and that support the notion that it protects the patient the blood does not turn red when exposed to air. Dysregulated argi- Pulse oximeters may read falsely high oxyhemo- nine metabolism, hemolysis-associated pulmonary globin levels, and when methemoglobin levels of hypertension and mortality in sickle cell disease. Sickle is established using cooximetry, which measures cell chronic lung disease: prior morbidity and the oxyhemoglobin, deoxyhemoglobin, carboxyhemo- risk of pulmonary failure. J Clin Gastro- This “state of the art” article develops the hypothesis that enterol 2004; 38:52−58 oxidant-antioxidant disturbances are pivotal to the develop- Useful review of current concepts. Patients had histology Engl J Med 2008; 358:2378−2387 of bronchiolitis obliterans organizing pneumonia, suggest- Thorough review of the mechanisms, clinical features, diag- ing an immunologic mechanism. Radiographics 2004; 24:861−880 24: 985−997 Reviews hepatopulmonary syndrome and portopulmonary Review of radiation techniques and types of radiation- hypertension, with recommendations for diagnosis and induced injury, with excellent images. The daily fraction size, number of daily frac- Review of the histopathology associated with oxygen pulmo- tions, and total dose were associated with the risk of radia- nary injury. Chest Med 2002; 347:1057−1067 1997; 111:671−675 Three hyperbaric oxygen treatments reduced the incidence Emphasizes the value of laryngoscopy in patients with smoke of the delayed emergence of cognitive dysfunction by almost inhalation. Methemoglobin- of inhalational airway disorders than clinical, laboratory, emia complicating topical lidocaine used during endo- and radiographic ﬁndings. Benzo- In a retrospective review of 1,665 patients with acute burn caine-induced methemoglobinemia: experience from a injuries, three risk factors for death were identiﬁed: age 60 high-volume transesophageal echocardiography labo- years, 40% of body surface area burned, and inhalation ratory. Although some sta- Key words: medical statistics; probability; receiver operator curves tistical tests are fairly rigorous (ie, insensitive to the violation of assumptions), the results will be ques- tionable if an incorrect statistical test is used. Minor study ﬂaws (eg, randomization, Introduction use of appropriate controls, and double blinding) will limit conﬁdence in the results that have been A ﬁrm understanding of medical statistics is analyzed, even those that use the proper statistical vitally important for interpreting the medical lit- tests.
Hence buy 2 mg coumadin, from clinical data 2mg coumadin mastercard, a judgment needs to be rendered regarding how far along one is on the road of: Make a Dx → Stage the disease → Treat based on stage → Follow response Frequently purchase coumadin discount, the student is “taught” to regurgitate the same information that someone has written about a particular disease purchase coumadin online now, but is not skilled at giving the next step. This talent is learned optimally at the bedside, in a supportive envi- ronment, with freedom to make educated guesses, and with constructive feed- back. Smith has stable angina because he has retrosternal chest pain when he walks three blocks, but it is relieved within minutes by rest and with sub- lingual nitroglycerin. Stage the disease: “I don’t believe that this is severe disease because he does not have pain lasting for more than 5 minutes, angina at rest, or conges- tive heart failure. Treat based on stage: “Therefore, my next step is to treat with aspirin, beta- blockers, and sublingual nitroglycerin as needed, as well as lifestyle changes. Follow response: “I want to follow the treatment by assessing his pain (I will ask him about the degree of exercise he is able to perform without chest pain), performing a cardiac stress test, and reassessing him after the test is done. This question goes further than making the diagnosis, but also requires the student to understand the underlying mechanism for the process. The student is advised to learn the mechanisms for each disease process, and not merely memorize a constellation of symptoms. The platelets-antibody complexes are then taken from the circula- tion in the spleen. Because the disease process is specific for platelets, the other two cell lines (erythrocytes and leukocytes) are normal. Also, because the thrombocytopenia is caused by excessive platelet peripheral destruction, the bone marrow will show increased megakaryocytes (platelet precursors). Understanding the risk factors helps the practitioner to establish a diagnosis and to determine how to interpret tests. For example, understanding the risk factor analysis may help to manage a 45-year-old obese woman with sudden onset of dyspnea and pleuritic chest pain following an orthopedic surgery for a femur fracture. This patient has numerous risk factors for deep venous throm- bosis and pulmonary embolism. The physician may want to pursue angiography Clinical Pearl ➤ When the pretest probability of a disease is high based on risk factors,even with a negative initial test, more definitive testing may be indicated. Thus, the num- ber of risk factors helps to categorize the likelihood of a disease process. A clinician must understand the complications of a disease so that one may monitor the patient. Sometimes the student has to make the diagnosis from clinical clues and then apply his/her knowledge of the sequelae of the patho- logical process. For example, the student should know that chronic hyperten- sion may affect various end organs, such as the brain (encephalopathy or stroke), the eyes (vascular changes), the kidneys, and the heart. Understanding the types of consequences also helps the clinician to be aware of the dangers to a patient. The clinician is acutely aware of the need to monitor for the end-organ involvement and undertakes the appropriate intervention when involvement is present. To answer this question, the clinician needs to reach the correct diagnosis, assess the severity of the condition, and weigh the situation to reach the appro- priate intervention. For the student, knowing exact dosages is not as important as understanding the best medication, the route of delivery, mechanism of action, and possible complications. It is important for the student to be able to verbalize the diagnosis and the rationale for the therapy. A common error is for the student to “jump to a treatment,” like a random guess, and therefore being given “right or wrong” feedback. In fact, the student’s guess may be correct, but for the wrong reason; conversely, the answer may be a very reasonable one, with only one small error in thinking. Instead, the student should verbalize the steps so that feedback may be given at every reasoning point. For example, if the question is, “What is the best therapy for a 25-year-old man who complains of a nontender penile ulcer? Therefore, the best treatment for this man with probable syphilis is intramuscular penicillin (but I would want to confirm the diagnosis). In the scenario above, the man with a nontender penile ulcer is likely to have syphilis. Knowing the lim- itations of diagnostic tests and the manifestations of disease aids in this area. There are four steps to the clinical approach to the patient: making the diagnosis, assessing severity, treating based on severity, and following response. Assessment of pretest probability and knowledge of test characteristics are essential in the application of test results to the clinical situation. There are seven questions that help to bridge the gap between the text- book and the clinical arena. He describes the discomfort as a severe, retrosternal pressure sensation that had awakened him from sleep 3 hours earlier. He previously had been well but has a medical history of hypercholesterolemia and a 40- pack-per-year history of smoking. On examination, he appears uncom- fortable and diaphoretic, with a heart rate of 116 bpm, blood pressure 166/102 mm Hg, respiratory rate 22 breaths per minute, and oxygen satu- ration of 96% on room air. Auscultation of the chest reveals clear lung fields, a regular rhythm with an S4 gallop, and no murmurs or rubs. Cardiac examination reveals an S4 gallop, which may be seen with myocardial ischemia because of relative noncompliance of the ischemic heart, as well as hypertension, tachycardia, and diaphoresis, which all may represent sympathetic activation. Know which patients should receive thrombolytics or undergo percuta- neous coronary intervention, which may reduce mortality. Occasionally, they are caused by embolic occlusion, coronary vasospasm, vas- culitis, aortic root or coronary artery dissection, or cocaine use (which pro- motes both vasospasm and thrombosis). The resultant clinical syndrome is related to both the degree of atherosclerotic stenosis in the artery and to the duration and extent of sudden thrombotic occlusion of the artery. If the occlu- sion is incomplete or if the thrombus undergoes spontaneous lysis, unstable angina occurs. If the occlusion is complete and remains for more than 30 min- utes, infarction occurs. In contrast, the mechanism of chronic stable angina usually is a flow-limiting stenosis caused by atherosclerotic plaque that causes ischemia during exercise without acute thrombosis (Table 1–1). It is of the same character as angina pectoris—described as heavy, squeezing, or crushing—and is localized to the retrosternal area or epigastrium, sometimes with radiation to the arm, lower jaw, or neck. In contrast to stable angina, however, it persists for more than 30 minutes and is not relieved by rest. Cardiac auscultation may reveal an S4 gallop, reflecting myocardial noncompliance because of ischemia; an S3 gallop, representing severe systolic dysfunction; or a new apical systolic mur- mur of mitral regurgitation caused by ischemic papillary muscle dysfunction. The earliest changes are tall, positive, hyperacute T waves in the ischemic vascular territory. Cardiac-specific troponin I (cTnI) and cardiac-specific troponin T (cTnT) are more specific to heart muscle and are the preferred markers of myocardial injury. Cardiac-specific troponin I levels may remain elevated for 7 to 10 days and cTnT levels for 10 to 14 days. They are very sensitive indicators of myocardial injury, and their levels may be elevated with even small amounts of myocardial necrosis. Aortic dissection often presents with unequal pulses or blood pressures in the arms, a new murmur of aortic insufficiency, or a widened mediastinum on chest X-ray film. Because the process is caused by acute thrombosis, antiplatelet agents such as aspirin and anticoagulation with heparin are used. To limit infarct size, beta-blockers are used to decrease myocardial oxygen demand, and nitrates are given to increase coronary blood flow. In addition, morphine may be given to reduce pain and the consequent tachycardia, and patients are placed on supplemental oxygen (Figure 1–4). Because myocardium can be salvaged only before it is irreversibly injured (“time is muscle”), patients benefit maximally when the drug is given early, for example, within 1 to 3 hours after the onset of chest pain, and the relative benefits decline with time. Because systemic coag- ulopathy may develop, the major risk of thrombolytics is bleeding, which can be potentially disastrous, for example, intracranial hemorrhage. The risk of hemorrhage is relatively constant, so the risk begins to outweigh the benefit by 12 hours, at which time most infarctions are completed, that is, the at-risk myocardium is dead. Sometimes intraluminal expandable stents are deployed which may improve vessel patency. This has diminished in recent years with earlier and more aggressive treatment of ischemia and arrhythmias. Electrolyte deficiency, such as hypokalemia or hypomagnesemia, which can potentiate ventricular arrhyth- mias, should be corrected.
Psychometric properties of the Drug Abuse Screening Test in psychiatric outpatients cheap 2 mg coumadin mastercard. Prevalence of mental disorders discount coumadin 5mg visa, psychological distress order 5mg coumadin visa, and mental health services use among lesbian buy discount coumadin 1mg on line, gay, and bisexual adults in the United States. Measuring nicotine dependence among youth: A review of available approaches and instruments. Pharmacotherapy treatment of alcoholism and drug addiction: Overview and bibliography. How the recession has left millions of workers without health insurance, and how health reform will bring relief. Abuse liability of intravenous buprenorphine/naloxone and buprenorphine alone in buprenorphine- maintained intravenous heroin abusers. Injectable, sustained-release naltrexone for the treatment of opioid dependence: A randomized, placebo-controlled trial. Substance use screening, brief intervention, and referral to treatment for pediatricians. 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It is likely due to a hereditary hypofixation of the cecum to the posterior abdominal wall buy coumadin 5mg overnight delivery. Clinical Presentation and Diagnoses • Acute onset of severe intermittent abdominal pain followed by nausea and vomiting is the common clinical manifestation order genuine coumadin line. Obstipation may be absent early on or in a partial obstruction cheap coumadin online visa, and its absence does not exclude the diagnosis buy coumadin with visa. A supine abdominal film along with either a lateral decubitus or upright abdominal films are minimally needed for diagnosis. An upright chest film may be added to search for free air under the dia- phragm indicating a perforated viscous. The small bowel is differentiated from the large bowel by the presence of “valvulae conniventes” which are numerous, narrowly spaced and cross the entire lu- men. A “string of pearls” sign is highly suggestive of small bowel obstruction and is described as a line of air pockets in a fluid filled small bowel. Air fluid levels in a stepladder pattern are also suggestive of a small bowel obstruction. If not, sigmoid volvulus can be diagnosed by the classic “birds beak” sign on barium enema. Distended large bowel in the left lower quadrant with absence of right-sided gas may indicate a cecal volvulus. The intermittent nature of the pain is suggestive of bowel obstruction but is also present in mesenteric ischemia. Treatment • Early nasogastric decompression, aggressive fluid resuscitation, broad spectrum anti- biotics including coverage of Gram negatives and anaerobes, and early surgical consul- tation are the mainstays of treatment of small and large bowel obstructions. Up to 75% of partial small bowel obstructions and up to one-third of complete small bowel obstructions will resolve with decompression and fluid resuscitation alone. Strangu- lated obstructions indicated by fever, tachycardia, and/or localized tenderness are op- erative cases. Uncomplicated obstructions are usually initially treated conservatively, with surgery reserved for treatment failures. Disposition • These patients are all admitted to the hospital, almost always under the care of a surgeon. The highest incidence occurs in 10-30 yr olds, with atypical presentations more common in the very young or very old and women of child-bearing age. Clinical Presentation and Diagnoses • The classic description is of periumbilical, epigastric, or diffuse dull pain migrating over several hours to McBurney’s point in the right lower quadrant, with the pain changing in character from dull to sharp as the overlying peritoneum becomes in- flamed. Peritoneal signs, including involuntary guarding, rigidity and diffuse percus- sion tenderness may indicate perforation. Less specific and less frequently associated symptoms include fever, chills, diarrhea, dysuria and frequency, and constipation. A pelvic appendix may irritate the bladder, result- ing in suprapubic pain or dysuria, while a retroileal appendix may irritate the ureter, causing testicular pain. More than two-thirds of appendices lie within 5 cm of McBurney’s point, with more inferior and medial. Perforation is the most common malpractice claim for ab- dominal emergencies and the fifth most expensive claim overall in emergency medicine. Abdominal plain films have little or no utility and should not be routinely ordered, as even the finding of an appendicolith are neither sensitive nor specific for appendicitis. Ultrasound has reported sensitivity up to 93% and specific- ity up to 95% and is the preferred test in children and pregnant women. Other diagnoses to consider include testicular torsion, ruptured ectopic pregnancy, peptic ulcer disease, billiary tract disease, diverticulitis, abscesses, renal colic, pyelonephritis, bowel obstruction, and abdominal aortic aneurysm. Colonic Diverticulitis Risk Factors/Etiology • 96% of patients are older than 40 yr of age. Microperforations in the colon then occur producing a pericolic abscess or even peritonitis. Clinical Presentation and Diagnoses • Persistent abdominal pain, initially vague and diffuse, later localizing to the left lower quadrant is the most common presentation of sigmoid diverticulitis. Dysuria and frequency are also common due to irritation of the nearby bladder and ureter. The rectal exam may reveal local tenderness and will often be fecal occult blood positive. Iron deficiency anemia is un- common and should prompt a look for other causes, such as carcinoma. An upright chest X-ray may also be obtained to look for free air under the diaphragm, signaling a perforated viscus. Other diagnoses high in the differential include colon carcinoma with localized perforation, ischemic colitis, ulcerative colitis, and bacterial colitis. Colovesicular fistulas present with pneumaturia, fecaluria, dysuria, frequency, or incontinence. Acute Pancreatitis Risk Factors/Etiology • The underlying etiology of pancreatitis is most commonly due to gallstones or alco- holism. Clinical Presentation and Diagnoses • The typical presentation of pancreatitis is epigastric pain radiating to the back. Amylase is both of salivary and pancreatic origin, but most labs do not differentiate between the two. Caution should be used with administration of insulin as there is exaggerated response with pancreatitis and profound hypoglycemia may result. Cimetidine, glucagon and atropine fail to show any benefit in alleviating symptoms or complications. Autopsy studies have shown many missed cases of fatal pancreatitis in this subgroup of patients. It had been thought that cooling would cause vasoconstriction and accelerate cessation of bleed- ing, but this is now known to cause arrhythmias without decreasing bleeding. While evacuation of blood from the gut may be one benefit from nasogastric lavage, this procedure can cause great discomfort. H2 Blockers and Proton Pump Inhibitors • Proton pump inhibitors and H2 blockers are not effective in the acute phase of bleed- ing. Bleeding, Low systolic blood pressure, Elevated pro- thrombin time, Erratic mental status, Disease comorbid. Type O blood should follow the first 2 L via rapid transfuser, until type-specific and then cross-matched blood is available. Cholecystitis Risk Factors/Etiology • Common illness with over 15 million Americans affected. While uncommon in children, presence may suggest underlying disorder (sickle cell, hemolytic anemia). First line antibiotics include amp/sulbactam, flouroquinolone and flagyl or pipercillin/tz. Hernias Risk Factors/Etiology • A hernia occurs when a viscus internally or externally protrudes from its normal cavity. Clinical Presentation and Diagnosis • An asymptomatic hernia presents without pain or tenderness, is reducible, and will enlarge with standing or increased intra-abdominal pressure. It may or may not present with symptoms of bowel obstruction, including nausea and vomiting. If necrotic bowel is suspected do not attempt to reduce the hernia and return the dead bowel into the abdomen. Treatment • An incarcerated hernia without signs of bowel obstruction may be reduced with pain meds and gravity and referred for surgical follow-up. In contrast, umbilical hernias often have a benign course and do not require urgent referral. Esophageal Emergencies Risk/Factors Etiology • 75% of esophageal perforations are due to iatrogenic perforations. Most perforations occurs in the lower third of the esophagus in the left posterolat- eral region. Clinical Presentation and Diagnosis • Delay in diagnoses of Boerhaave syndrome is common and leads to a high mortality rate. Classic presentation for spontaneous rupture is vomiting followed by severe chest pain.
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