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Taxonomy: Alcohol abusers tend to remain alcohol abusers and alcohol dependent patients tend to remain alcohol dependent cheap reglan generic gastritis binge eating. Alcoholism can be divided into Alcohol related problems - social purchase reglan with mastercard gastritis diet xtreme, psychological or physical Alcohol dependence - manifested similarly to any other physical dependence: Secretiveness Buying extra rounds Gulping drinks Drinking alone Stocking up Giving other activities up 2525 People who start smoking often experience disconcerting nausea purchase generic reglan line gastritis diet 7 up, cough, and dizziness and yet, if social pressure is strong enough, may persist with the habit to the point of dependence. Performance impairment, often subtle, is greater in older people than can be 2529 accounted for by blood alcohol concentration. Non-intoxication in the presence of a blood alcohol level in excess of 200 mg/dL is pathognomonic of alcoholism. Have you ever neglected your obligations, your family, or your work for 2 or more days in a row because you were drinking? The scores are not shown to the user in the form in which the questionnaire is used in practice, but they are given here for convenience sake. Have you ever had a drink first thing in the morning (eye-opener) to steady your nerves or to get rid of a hangover? One unit of alcohol equals a half-pint glass of beer, lager or stout, a glass of wine or sherry, or a single measure of spirits. Having excess drink on each occasion of drinking (say > 5 drinks) is as important as the overall intake when it comes to social and personal complications. The annual cost of alcohol misuse in Britain for 1990 was estimated at stg £2 bn if one includes ill health, crime, accidents and absenteeism. Treatment of illnesses and injuries due to alcohol costs the British Government in the early twenty-first century up to £176 bn annually, total costs (absenteeism, crime, etc) reaching as high as £20 bn. This takes no account of the effects on health, relationships, and child development. About 25% of acute male admissions to medical wards, and an even higher percentage in the case of acute surgical emergency admissions, are related to alcohol misuse. If someone looks sober with a high blood alcohol level this suggests a regular heavy alcohol intake - the 2536 levels can still be high 24 hours after the drinking has stopped. Reasons for misdiagnosis of excess alcohol consumption in the elderly (O’Connell ea, 2003) Non-disclosure Low index of clinical suspicion Low referral rate because seen as understandable (poor health and life changes) and untreatable Atypical (falls, confusion, depression) or masked (comorbid physical or psychiatric disorders) presentation Non-applicability of ‘sensible limits’ (metabolic changes, ill health, increased sensitivity to alcohol) Lack of consequences (social, legal, occupational) Focus on recent (rather than lifetime) intake by diagnostic criteria and screening instruments Self-disclosure of alcohol intake by elderly Irish interviewed in their homes showed a significant positive association between consumption and being male and widowed. It was held that 6- 20% of alcoholics commited suicide, although the accepted figure has dropped below the lower of these 2537 two figures in recent years. The alcoholic who was seen as at the highest risk for suicide was older, socially isolated, male, had made previous suicide attempts of serious intent, was physically ill and had a 2533 Gamma glutamyl transpeptidase levels are also elevated with hepatic disease, obesity, and a number of drugs (e. He also believes that 25% of suicides are solely due to alcohol (alcohol is present in the bodies of 58% of Irish suicides). Elder abuse is usually related to chronic stress and low support, but a minority is associated with drug and alcohol abuse, sociopathy, intellectual disability, and various psychiatric disorders in the abuser, e. Wrigley, 1991) Depression in alcohol misusers is often secondary to alcohol, although it may be primary in some cases (bipolar > unipolar depression). Opinion differs on how long a period of sobriety is required before an (alcohol-) independent diagnosis of depression can be made. Alcoholics are at high risk for marital breakdown, unemployment, accidents, doing physical or psychological harm to others, becoming involved in unwise sexual encounters, and of imprisonment. It may also causes gradual coarsening of the personality and the emergency of sociopathic traits. Syndromes associated with alcohol Alcoholic dementia: Lishman (1987) suggested that this condition might account for at least 10% of all end-stage dementias. Radiological studies revealed decreases in brain volume in many chronic alcoholics. This is at least partially and very slowly reversible with prolonged abstinence: it is debated as to whether reversal is due to rehydration of the brain or repair of neurones or myelin. In both cortical areas there was evidence that alcoholics had smaller, shrunken neurones than controls. Possible causes of cognitive disorders in alcoholics include premorbid intellectual deficit, direct ethanol neurotoxicity, neurological complications of alcohol (e. Korsakoff’s), thiamine or nicotinic acid deficiency, recurrent head trauma, and hepatocerebral degeneration. There is controversial evidence that light to moderate drinking may reduce the chances of developing dementia, even when other variables like smoking are controlled for. Most cases clear up quickly after drinking is stopped although hallucinations may return if drinking restarts. The patient may become paranoid, hostile or suicidal as a result, or he/she may take flight or hide. Treatment includes detoxification from alcohol and neuroleptics for hallucinations. Features include intense fear, restlessness, 2540 2541 illusions, delusions, visual hallucinations , tremulousness, ataxia, vestibular dysfunction , hypertension, tachycardia, leucocytosis, impaired hepatic function, and pyrexia. Fever may be part of the core syndrome or due to a complication such as aspiration pneumonia. High blood pressure, tachycardia, and tremor may be obscured by medication that the patient is taking, e. Death can be due to 2543 2544 cardiovascular collapse, infection, and self-injury when restless. Subdural haematoma, pneumonia, and meningitis should be considered in the disorientated alcoholic. Fluids should be replaced sparingly because alcoholics have a reduced ability to excrete water and a tendency to cerebral oedema. Black-outs: This refers to memory lapses (‘memory blackouts’) following a heavy bout of drinking despite observers not noting any significant change in level of consciousness. It is more likely to be abnormal if it occurs frequently or if the episodes of amnesia last for days. The drinker cannot remember where he left his car, who was with him at the time, and so on. Hypoglycaemia: Factors responsible include malnourishment (low hepatic stores of glycogen) and inhibition of hepatic gluconeogenesis by alcohol. Children who take alcohol (not necessarily in large quantity), binge drinkers, and chronic alcoholics have relatively little glycogen reserve in their livers and may present in a comatose state with hypothermia. Hypertension: About a quarter of alcoholics have systemic hypertension, often resolving (to various degrees) with abstention. Retrobulbar neuritis and optic atrophy: These are classically associated with methanol but can occur with ethanol. The retrobulbar neuritis usually comes on insidiously and causes central loss of vision, typically red-green blindness. Neuropathy: This is usually a polyneuropathy, with sensory, motor and autonomic signs: numbness, paraesthesiae, burning dysesthesia, pain, weakness, muscle cramps, gait ataxia, loss of tendon reflexes (including ankle jerks), defective perception of touch and vibration sensation. Treatment: if the patient stops drinking and if nutrition is improved the prognosis should be good. Myopathy: This is more common than one would think from the number of cases diagnosed in clinical practice. There are a variety of possible causes, such as a direct toxic effect of alcohol or hypokalaemia.
It is highly water-soluble purchase reglan 10 mg with amex gastritis diet x1, and is rapidly converted to phenytoin after ad- ministration reglan 10mg cheap gastritis jelovnik. It is rapidly and completely absorbed when given intramuscularly and can also be given intravenously at three times the rate of phenytoin buy reglan 10 mg granulomatous gastritis symptoms. Because it has no intrin- sic action before conversion, it is believed to have the same onset of action as phenytoin. It is generally reserved for cases in which benzodiazepines and phenytoin have failed. It has a rapid onset of action and a quick recovery time after the drug is discontinued. Patients will often require pressors because of significant hypotension and myocardial suppression. Kassinove Introduction Abdominal pain accounts for over five million visits annually to Emergency De- partments. In particular, women who are of child-bearing age or pregnant, chil- dren and elderly patients create a diagnostic challenge (due to atypical presenta- tions). Unfortunately, many of the disease processes share similar clinical presentations and may be difficult to sort out by history alone. Physical examination and labora- tory evaluation can both lack sensitivity, making the job of the emergency physician difficult. Therefore, the diagnosis of abdomen pain of unclear etiology is a common diagnosis made in cases where the underlying pathology is not clear. This obligates the physician to provide patients with adequate reexamination to monitor the pro- gression of the process. While the discussion of abdominal disorders in this chapter is not exhaustive, the most common etiologies are reveiwed. As a general rule, elderly patients presenting with abdominal pain form a unique group. Despite lack of identification of a focal disease process on initial presenta- tion, at least half will have a disorder requiring surgical intervention. Physical ex- amination will often lack sensitivity, as will laboratory evaluation. Women of child-bearing age and young children will have atypical presentations of common disorders, such as appendicitis and may require more observation time. Despite technology in imaging and laboratory diagnostics, a large portion of pa- tients will still have undifferentiated abdominal pain, requiring close follow-up and referral. Mesenteric Ischemia Risk Factors/Etiology • Age >50 yr old • Occlusive disease (80% of mesenteric ischemia) occurs 50% of the time from the sudden occlusion of the superior mesenteric artery originating from a proximal source and 25% of the time as local thrombosis. Prolonged occlusion can result in both proximal and distal reactive vasospasm, further aggravating the insult to the intestines. Mesenteric venous thrombosis occurs dur- ing the classic hypercoagulable states as well as during malignancy, abdominal trauma, and estrogen therapy. Additionally, regional vasospasm can result from use of vasoactive medications, such as digoxin, diuretics, cocaine, or vasopressin. Clinical Presentation and Diagnosis • The historical factors may be nonspecific, but the diagnosis should be pursued in any person >50 yr old with sudden onset of acute abdominal pain and with an associated low flow, atherosclerotic, or hypercoaguable disease state. Abdominal 5 distention and rectal bleeding may be the only initial complaint in up to 25% of the cases. The only initial abnormality on physical exam may be the presence of fecal occult blood, occurring in over half of the cases. Additionally, metabolic acidosis with a base deficit, an elevated amylase, and evidence of hemoconcentration are sensitive (present in more than half the cases) but nonspecific findings. They may show pneumatosis intestinalis, portal vein gas, or thumb printing in late disease. Angiography is contraindicated in shock states or with patients on vasopressor therapy because they confound the diagnosis of nonocclusive mesenteric ischemia. Common initial misdiagnoses include con- stipation, gastroenteritis, ileus, and small bowel obstruction. Younger pa- tients with collagen vascular disease are also at risk of aortic dissection. This dilatation is a mechanism of the artery to compensate for a proximal stenosis. Clinical Presentation • Classical presentation of pulsatile mass in the patient with abdominal pain and pulse deficits is not always present. Patients presenting with an abdominal aneurysm with abdominal pain are ruptured until proven otherwise and surgical consult is mandatory. Rupture unstable: surgical repair The differentiation between a stable and unstable rupture is trivial as the process is dynamic. The perioperative mortality is over 25% secondary acute myocardial infarction in emergent surgery compared to fewer than 5% for elective. Therefore it is preferred, but not always possible, to prime the patient for the operating room. Bowel Obstruction Risk Factors/Etiology • Small bowel obstruction is typically caused by postoperative adhesions, hernias, or tumors. It is likely due to a hereditary hypofixation of the cecum to the posterior abdominal wall. Clinical Presentation and Diagnoses • Acute onset of severe intermittent abdominal pain followed by nausea and vomiting is the common clinical manifestation. Obstipation may be absent early on or in a partial obstruction, and its absence does not exclude the diagnosis. 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.
Other causes of low output failure include valvular disease buy reglan 10mg cheap gastritis diet oatmeal cookies, myocarditis buy 10 mg reglan free shipping gastritis yahoo answers, chronic hypertension and cardiomyopathies (such as those caused by ethanol and cocaine abuse) order cheapest reglan gastritis symptoms and prevention. Decreasing stroke volume leads to the clinical effects of both backward and forward failure. Alterations in adrenergic tone redistribute blood flow to the brain and heart and reduce flow to other organs. This leads to increased sodium and water retention and a rise in both preload and afterload. Increased adrenergic tone leads to arteriolar vasoconstriction, which also contributes to increased afterload. Diagnosis and Evaluation Clinical Features • Left-sided failure symptoms include dyspnea (particularly with exertion), orthopnea, paroxysmal nocturnal dyspnea, fatigue and nocturia. The specific technique of delivery (nasal cannula, face mask, non-rebreather mask) should be guided by the severity of presentation and pulse oximetry values. Endotracheal intubation will be necessary in patients who become so somnolent that they are unable to protect their airway or in those who have tired of breathing and may have begun to have periods of apnea. They are used as a bridging therapy in the patient with severe cardiogenic pulmonary edema until pharmacologic therapy takes effect. These devices provide continuous or biphasic posi- tive airway pressure through a tight-fitting face mask. This positive pressure improves cardiac output by decreasing venous return and excessive preload. It also improves oxygenation by increasing alveolar recruitment and decreases the work and metabolic 2 requirement of breathing. These agents all increase myocardial oxygen consumption and ischemia, creating an additional risk for dysrhythmias. Adequate perfusion must always be assessed by using clinical indicators such as urine output, skin appearance and mental status. As each successive agent is introduced (at a pace commensurate with the severity of symptoms), close attention must be paid to vital signs, fluid bal- ance and symptomatic response to therapy. Adverse effects of diuretics include electrolyte imbalances, prerenal azotemia, contraction alkalosis and hypotension. However, little evidence for the effectiveness of morphine exists and its use is controversial. Respiratory depression with morphine may result in unnecessary intubation—a small dose (e. They inhibit the neu- rohormonal cascade and improve symptoms, especially in the setting of cardiac ischemia. However, they are not generally indi- cated in the treatment of acute heart failure and may result in acute decompensation. Dobutamine must be given with close hemodynamic monitoring and may initially result in hypotension. Two commonly used classification systems for severity of heart failure are given in (Table 2C. Disposition Patients diagnosed with acute heart failure or acute exacerbation of chronic heart failure most commonly require admission to hospital. It may also be appropriate to admit patients with mild exacerba- tions to short-stay or observational units or even to discharge them home with close follow-up when no acute serious underlying pathology is suspected and symp- toms have resolved. Effect of losartan compared with captopril on mortality in patients with symptomatic heart failure. Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. Attenuation of compensation of endogenous cardiac natriuretic peptide system in chronic heart failure: Prognostic role of plasma brain natriuretic peptide concentration in patients with chronic symptomatic left ven- tricular dysfunction. Part D: Endocarditis Epidemiology/Pathophysiology • Endocarditis is an infection of the heart valves which can present either acutely or as a chronic disease. It is a life threatening infectious disease that is difficult to diagnose with certainty in the Emergency Department. Other patients at risk include those with intracardiac devices (pacemakers, defibrillators), those with a history of endocarditis, 40 Emergency Medicine those with mitral valve prolapse and regurgitation, and patients with certain congeni- tal heart defects. Diagnosis and Evaluation • Diagnosis of endocarditis has traditionally been based on clinical findings and bacte- riologic criteria from blood cultures. The development and increased utilization of echocardiography has provided increased ability to diagnose endocarditis. The Duke criteria describes clinical, bacteriological and echocardiographic diagnostic criteria for endocarditis. History and Physical Exam • Endocarditis presents with a variety of clinical complaints. Laboratory and Studies • Laboratory findings include positive blood cultures as discussed above and a mild anemia. Blood cultures should be drawn before be- ginning antibiotics as antibiotics reduce the bacterial recovery rate of cultures by approximately one-third. Patients with a subacute course and native heart valves should receive either penicillin and an aminoglycoside or a penicillinase-resistant penicillin (nafcillin) and an aminoglycoside. Amoxicillin or erythromycin should be given 1 h before the procedure for proper prophylaxis. A Report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. Part E: Pericardial Diseases Pericardial disease is an important consideration in patients presenting with car- diopulmonary symptoms. The understanding of pericardial disease is important as these diseases not only cause significant morbidity, but they may also mimic other diseases which may require alternative treatment. Definitions • Pericarditis is an inflammation of the pericardial layer surrounding the heart. Pericarditis may also be idiopathic, but it is unclear if these represent undiagnosed viral pericarditis. As pericardial fluid accumulates, intrapericardial pressure increases exponentially. This leads to an increase in central venous pressure and a decreased cardiac output. Diagnosis and Evaluation History and Physical Examination • Pericarditis may be asymptomatic. Laboratory and Studies • Laboratory tests do not play a major role in the evaluation of pericardial disease. Echocardiography can detect as little as 15 ml of fluid and can be done at bedside in unstable patients. Treatment may continue on an outpatient basis in stable patients, but may require inpatient management in patients with severe pain, significant pericardial effusions, or any signs of hemodynamic instability. Part F: Structural Heart Disease The Emergency Physician must be comfortable managing patients with structural heart disease.