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Activated protein C Human recombinant activated protein C has been shown in a large multicentre trial to improve survival in patients with severe sepsis and a high risk of death cheap malegra dxt 130 mg online erectile dysfunction treatment auckland. Severe sepsis & septic shock 76 Handbook of Critical Care Medicine Bleeding is the most important side effect buy generic malegra dxt 130mg on line impotence leaflets. Correction of haemoglobin and blood product administration Blood transfusion is not recommended unless the haemoglobin drops to 7g/dL cheap 130 mg malegra dxt fast delivery erectile dysfunction medication australia. A haemoglobin of over 10g/dL is required only in patients with ischaemic heart disease. Platelet transfusion is 3 required only if the platelet count drops below 5000/mm in the absence of 3 bleeding, and below 30000/mm with active bleeding. Stress ulcer prophylaxis Stress ulcer prophylaxis should generally be given; proton pump inhibitors are more effective than H2 receptor blockers. The above therapies are based on clinical evidence, and contribute to better outcome. Recommendations are based on the Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock 2008. Consideration for limitation of support In spite of the best of care, severe sepsis and septic shock has a high mortality. The patient becomes progressively worse, and generally resistant hypotension develops as a terminal event. Severe sepsis & septic shock 77 Handbook of Critical Care Medicine It is important to discuss severity of illness and possible adverse outcome with the patient’s family, and make sure that expectations are realistic. If recovery seems unlikely, decisions of limitation or withdrawal of support should be considered. Since severe sepsis can suddenly affect previously well patients, this is all the more difficult. Severe sepsis & septic shock 78 Handbook of Critical Care Medicine Evaluating respiratory disease & airway management This section discusses the structure of the respiratory system and how to evaluate respiratory disease, and also deals with how to manage the airway. The respiratory system is divided into two parts – the upper and lower respiratory tract. The respiratory centres are stimulated by hypoxia, hypercapnoea, acidosis, and through various receptors within the lungs. The history, examination and investigations help to identify the abnormality in the respiratory system, diagnose its cause, and fine tune management appropriate to the patient. History Ask for a history of previous lung disease: x Asthma: duration, severity, compliance with medications, severity of exacerbations, previous intubation. Calculate the number of pack years (1 pack or 20 cigarettes for 1 year = one pack year). Has the patient Evaluating respiratory disease 79 Handbook of Critical Care Medicine stopped smoking now? Endocrine diseases: Cushing’s disease results in impaired immunity and increased risk of lung infections. Drug induced lung diseases: x Beta blockers: obstructive airways disease x Methotrexate, amiodarone: lung fibrosis x Corticosteroids and other immunosuppressive agents: increased risk of lung infections Cardiac diseases: valvular and congenital heart disease resulting in cor- pulmonale Previous lung surgery: patients maybe left with reduced lung reserve. Family history: Cystic fibrosis, alpha-1 antitrypsin deficiency, Kartegener’s syndrome, primary pulmonary hypertension Evaluating respiratory disease 80 Handbook of Critical Care Medicine Symptoms and signs Cough: the commonest respiratory symptom. Dry cough is seen in lung fibrosis, certain types of bronchiectasis, and pleurisy. Productive cough with purulent sputum is seen in bacterial infections of the lung. Cough can also be present in upper respiratory infections, such as laryngitis, pharyngitis, tonsillitis, sinusitis with post nasal drip. Sputum: most bacterial infections of the lung cause sputum production, which can be very variable depending on the type and severity of infection. The sputum is characteristically yellow in pyogenic infection, and is due to the presence of neutrophils. Yellow sputum is also seen in asthma due to large numbers of eosinophils in the sputum. The sputum in pneumonia is characteristically ‘rusty’, due to the presence of red blood cells. In lung abscess, the sputum is purulent and offensive, and halitosis is often present. In the past, amoebic liver abscesses were known to rupture into the lung, producing the characteristic ‘anchovy sauce’ sputum. Haemoptysis is always a serious symptom, and may be due to a sinister cause such as pulmonary tuberculosis, bronchial carcinoma, bronchiectasis, or pulmonary infarction. Dyspnoea is an important symptom of respiratory disease; it can be caused by anything that stimulates or increases the work of breathing – hypoxia, hypercapnoea, acidosis, consolidation, pneumothorax, pleural effusion, heart failure etc. Inflammatory conditions of the lung may involve the pleura and cause pleuritic chest pain, which characteristically worsens on breathing in and out. Cyanosis: this is the presence of more than 5g/dL of deoxygenated haemoglobin in the blood. Central cyanosis can be caused by any lung Evaluating respiratory disease 81 Handbook of Critical Care Medicine condition which causes severe hypoxia, or by cardiac right to left shunts. Peripheral cyanosis is caused by conditions which slow the peripheral circulation resulting in increased extraction of oxygen from haemoglobin – vasoconstriction, low cardiac output states. Clubbing: clubbing is seen in squamous cell bronchial carcinoma, suppurative lung disease (bronchiectasis, lung abscess, empyema), fibrosing alveolitis, and congenital or acquired cyanotic heart diseases (where a right- to-left shunt is present). Examination of the chest: The standard examination of the chest will reveal conditions such as pleural effusions, pneumothorax, localised consolidation, basal fibrosis, bronchiectasis etc. Investigations Chest radiograph An essential investigation in diagnosing respiratory disease. Because of this, it is prudent to be careful when interpreting subtle and minor radiological appearances which could be artefactual. It is mandatory that the person who did the procedure checks the chest radiograph. Always look carefully at the margins of the lung fields for air in the pleural space. PaO2 The partial pressure of oxygen determines the degree of oxygen saturation of haemoglobin (SaO ). The arterial oxygen content is dependent on the2 oxygen saturation and the haemoglobin. Thus the arterial oxygen content is determined by the following formula: Arterial O content = (SaO x Hb x 1. A small2 2 fall in PaO will not drop the SaO much, and hence, will not affect arterial2 2 oxygen content. Oxygen delivery to the tissues is dependent on the arterial oxygen content and the cardiac output. If the blood pressure is low, even though the arterial oxygen content is adequate, tissue oxygen delivery will be low. If oxygen utilisation in the tissues exceeds oxygen delivery, the cells revert to anaerobic metabolism, leading to lactic acidosis.

It would seem that Wellcome wanted to stop general practitioners from either treating patients themselves or referring them to community-based alternative practitioners purchase generic malegra dxt online what if erectile dysfunction drugs don't work. The dispute was finally resolved in high level negotiations between President Ronald Reagan and French Premier Jacques Chirac purchase malegra dxt 130 mg without a prescription impotence natural home remedies. Weiss had offered Wellcome his ideas about diagnostic testing kits and had then gone into business with them to produce these kits buy 130mg malegra dxt otc erectile dysfunction statistics singapore. In 1985, it was estimated that the British market for diagnostic kits was worth between £3 million and £4 million, and a world-wide market worth £180 million. The Surrey University department which Professor Marks heads has received over half a million pounds from Wellcome since 1985. Was it because of a genuine paternalistic concern for those who may test positive? Or could it have been that the drug companies feared that self-testing might lead to self-medication? In March 1992, the Department of Health banned the public sale of home testing kits in Britain. A journal on medical history published by the British Medical Association is perhaps more prestigious than a journal on the history of medicine published by a drug - company, or a Trust associated with a drug company. On his retirement in 1991, he took up a position as an associate research worker at the Wellcome Institute. In the early months of March 1988, Wellcome gave a covenant, amounting to £36,000 annually for four years and totalling £144,000, to the Foundation. It was expected that Wellcome representatives, together with Calmicff sales representatives, would be showing the videos and promoting the free package in all 11,000 surgeries in Britain. Dr John Marks is the brother of Vincent Marks, a keen member of the Campaign Against Health Fraud and prominent member of the Medical Research Council. In August 1988, the Medical Research Council published the detailed protocols for the Concorde trials. The Wellcome position was based upon the life history of the classic virus, which first infects the subject then proliferates within the body. Such people believed that co-factors probably played some part in all three circumstances. There were, as well, those who were adamant that the introduction of chemicals to the body, especially ones which actually destroyed the same cells that the infection itself was killing, was just such a co-factor. The agreement which set up Concorde was between Wellcome, the Medical Research Council and the Department of Health. In order to give drug trials a patina of independence, they are usually agreed between a university or hospital and the company producing the drug. Because Concorde was such a large trial, using considerable Health Department facilities, and because the whole issue of trialing a drug for what appeared to be a terminal illness was an issue designed to create moral panic, the Department of Health was, from the beginning, deeply involved. There is inevitably, therefore, a high degree of government interest in its programmes and strategies. Because of this interest, and the considerable involvement of the Department of Health, it would be accurate to say that the agreement for the Concorde trial was in fact a partnership between Wellcome and the British government. The matter of how the Concorde trial was run, its efficacy, its scientific conduct and its ultimate plausibility, became, 12 from August 1988, the date that the detailed protocol was finished, an affair of State. In a truly ethical situation, no one supported by Wellcome or receiving money from them, would have been involved in the administration of the trials. Usually, pharmaceutical companies provide the drug for trial and then pay the hospital or the academic institution per head for the treatment of trial subjects. Any hospital doctor who is contracted to trial a drug by a pharmaceutical company is in danger of mixing two sets of patients. Many patients were not given information about the possible range of treatments, but were taken straight into the Concorde trials. Detailed information was important, considering that by 1989 there had been reports of serious adverse effects upon patients; these included muscle wasting, serious anaemia, loss of white blood cells and impotence. In Britain and France, however, the clinicians involved in Concorde continued to give trial subjects l,000mg a day up to the completion of the trial in 1992. They argued that as the study was blinded, it would have been impossible to reduce the dosage without destroying the trial. Was it ethically correct to continue with the trial, once it had been suggested that at 1,000 mg a day there might possibly be a chance of serious adverse effects? The Concorde trial was not, however, just another small trial where the drug company could easily control the clinicians. Although ending up with a weaker settlement than it had set out to achieve, Wellcome did manage to negotiate a clause in the protocols which gave it complete control over any final report for uses other than publication. Ostensibly these two items gave Wellcome control over all draft reports and final 14 reports for all official uses other than publication. As publication was the very last stage in the process and might never actually happen, all report writing was in effect in the hands of Wellcome, despite the massive financial input into the trials by the British government. No other publications, either in writing or verbally, will be made before the definitive manuscript has been agreed and accepted for publication... The Wellcome Research Laboratories will prepare a detailed report of the Study for internal use and for submission to regulatory authorities. With government cuts in the eighties, Wellcome frequently protested as it saw itself increasingly stepping into the breach to support medical research. The gradual dominance of private finance in research was, however, a political as well as an economic trend and had the advantage that private interests were able to have access to research and results. By the late eighties, medical research in Britain was controlled by a partnership between Wellcome and the government. He was leader of the House of Lords from 19701973 and a member of the All-Party Group for the Chemical Industry. Lord Jellicoe is involved in all those things in which someone dedicated to medical research and health would be expected to be involved. Lord Jellicoe is also involved with Rockefeller interests especially through his directorship of Morgan Crucible. When he left the Department of Health, he took up a post at the London School of Hygiene and Tropical Medicine. Sir Austin Bide was the Chief Executive at the drug company Glaxo from 1973 to 1980, he then became first the Chairman of the Board and in 1985their Honorary President. He too has an interest in confectionery, having been a director of J Lyons & Co in the late seventies. He too was a member of the Society of the Chemical Industry, and chairman of the All-Party Group for the Chemical Industry for almost twenty years, from 1970 to 1987. He was a director of the pharmaceutical company Pfizer Ltd, for over twenty years, from 1966 to 1987.

Valve replacement should be considered for patients with symptoms and severe aortic stenosis generic malegra dxt 130 mg with visa erectile dysfunction foundation, for example buy malegra dxt 130mg free shipping erectile dysfunction at age 20, an aortic valve area less than 1 cm2 purchase 130 mg malegra dxt with amex erectile dysfunction 30 years old. Case 3 A 26-year-old woman presents to the emergency room complaining of sudden onset of palpitations and severe shortness of breath and cough- ing. She reports that she has experienced several episodes of palpitations in the past, often lasting a day or two, but never with dyspnea like this. On examination, her heart rate is between 110 and 130 bpm and is irregularly irregular, with blood pressure 92/65 mm Hg, respiratory rate 24 breaths per minute, and oxygen saturation of 94% on room air. On cardiac examination, her heart rhythm is irregularly irregular with a loud S1 and low-pitched diastolic murmur at the apex. She has a diastolic rumble and “ruddy cheeks,” both features of mitral stenosis, which is the likely cause of her atrial fibrillation as a result of left atrial enlargement. Because of the increased blood volume asso- ciated with pregnancy and the onset of tachycardia and loss of atrial contrac- tion, the atrial fibrillation has caused her to develop pulmonary edema. Understand the management of acute atrial fibrillation with rapid ventric- ular response. Know the typical cardiac lesions of rheumatic heart disease and the physi- cal findings in mitral stenosis. Understand the physiologic basis of Wolff-Parkinson-White syndrome and the special considerations in atrial fibrillation. The four major goals are (1) stabilization, (2) rate control, (3) conversion to sinus rhythm, and (4) anticoagulation. This may occur spontaneously or after correction of underlying abnormalities, or it may require pharmacologic or electrical cardioversion. Cardioverting the patient back to sinus rhythm, the return of coordinated atrial contraction in the presence of an atrial thrombus, may result in clot embolization, leading to a cerebral infarction or other distant ischemic event. Alternatively, low-risk patients can undergo transesophageal echocardiography to exclude the presence of an atrial appendage thrombus prior to cardioversion. Postcardioversion anticoagulation is still required for 4 weeks, because even though the rhythm returns to sinus, the atria do not con- tract normally for some time. Pharmacologic cardioverting agents, though not as effective, include procainamide, sotalol, and amiodarone. The longer the patient is in fibrillation, the more likely the patient is to stay there (“atrial fibrillation begets atrial fibrillation”) as a consequence of electrical remodeling of the heart. The major complication of warfarin therapy is bleeding as a consequence of excessive anticoagulation. If clinically significant bleeding is present, warfarin toxicity can be rapidly reversed with administration of vitamin K and fresh-frozen plasma to replace clotting factors and provide intravascular volume replacement. Because she has a history of acute rheumatic fever, her mitral stenosis almost certainly is a result of rheumatic heart disease. Rheumatic heart disease is a late sequela of acute rheumatic fever, arising many years after the original attack. The aortic valve may also develop stenosis, but usually in combination with the mitral valve. Almost all cases of mitral stenosis in adults are secondary to rheumatic heart disease, usually involving women. The physical signs of mitral stenosis are a loud S1 and an opening snap following S2. There is a low-pitched diastolic rumble after the opening snap, heard best at the apex with the bell of the stethoscope. Because of the stenotic valve, pres- sure in the left atrium is increased, leading to left atrial dilation and, ulti- mately, to pulmonary hypertension. Pulmonary hypertension can cause hemoptysis and signs of right-sided heart failure such as peripheral edema. Rate control with intravenous digoxin, beta-blockers, or calcium channel blockers is essential to relief of pulmonary symptoms. A portion of ventricular activation occurs over the accessory pathway, with the remaining occurring normally through the His-Purkinje system. If hemodynamically stable, the agent of choice is procainamide or ibutilide, to slow conduction and convert the rhythm to sinus. He reviews the charts of several patients with atrial fibrillation currently taking Coumadin. Which of the following patients is best suited to have anticoagulation discontinued? A 45-year-old man who has normal echocardiographic findings and no history of heart disease or hypertension, but a family his- tory of hyperlipidemia B. A 62-year-old man with mild chronic hypertension and dilated left atrium, but normal ejection fraction C. A 75-year-old woman who is in good health except for a prior stroke, from which she has recovered nearly all function D. The emergency room physician counsels the patient regarding cardioversion, but the patient declines. The early diastolic decrescendo murmur is typical of aortic regurgi- tation, holosystolic murmur at the apex that of mitral regurgitation, and late-peaking systolic murmur at the upper sternal border that of aortic stenosis. Conditions associated with a high risk for embolic stroke include a dilated left atrium, congestive heart failure, prior stroke, and the presence of a thrombus by echocardiogram. The man in answer A has “lone atrial fibrillation” and has a low risk for stroke and thus would not benefit from anticoagulation. If the patient is stable, initial management is ventricu- lar rate control with an atrioventricular nodal-blocking agent, such as digoxin, beta-blockers, diltiazem, or verapamil. Management of newly detected atrial fibrillation: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. This page intentionally left blank Case 4 A 37-year-old executive returns to your office for follow-up of recurrent upper abdominal pain. He initially presented 6 weeks ago, complaining of an increase in frequency and severity of burning epigastric pain, which he has experienced occasionally for more than 2 years. Now the pain occurs three or four times per week, usually when he has an empty stomach, and it often awakens him at night. The pain usually is relieved within minutes by food or over-the-counter antacids but then recurs within 2 to 3 hours. He admitted that stress at work had recently increased and that because of long working hours, he was drinking more caffeine and eating a lot of take-out foods. His medical history and review of systems were otherwise unremarkable, and, other than the antacids, he takes no medications. His physical examination was nor- mal, including stool guaiac that was negative for occult blood. His symp- toms resolved completely with the diet changes and daily use of the medication. Results of laboratory tests performed at his first visit show no anemia, but his serum Helicobacter pylori antibody test was positive.