David Childs, MD

• Assistant Professor of Radiology
• Abdominal Imaging Section
• Wake Forest University School of Medicine
• Winston-Salem, North Carolina

Emesis and activated charcoal are generally not necessary following corticosteroid overdose erectile dysfunction levitra order genuine levitra super active line. Consider activated charcoal if co-ingestants with the potential for significant toxicity are involved erectile dysfunction treatment cream 40 mg levitra super active with amex. Acute adrenal insufficiency: Administration of water erectile dysfunction inventory of treatment satisfaction edits buy genuine levitra super active, sodium chloride erectile dysfunction caused by fatigue trusted levitra super active 40mg, glucose erectile dysfunction treatment needles discount levitra super active 40mg overnight delivery, and cortisol impotence meaning in english order cheap levitra super active online. Chronic primary adrenal insufficiency: Administration of hydrocortisone, liberal salt intake. Psychiatric manifestations: Tapered withdrawal and administration of neuroleptic drugs. Avoid chronic daily dosage of corticosteroids for durations greater than 3 weeks when possible. When chronic doses for periods greater than 3 weeks are essential, attempts should be made to manage the underlying disease with alternate day dosage. Single daily doses of shorter-acting preparations such as prednisone, prednisolone, or methylprednisolone on alternate mornings may be used. Adverse effects appear to be more common and more severe with the preparations having longer duration of effect, or when shorter-acting preparations are administered in multiple daily doses. The diet should have adequate protein content but caloric restrictions should be considered because of the apparent appetite stimulation properties of corticosteroids. Commercial preparations are available for either subcutaneous or intravenous injection which differ in respect to onset and duration of action. The onset and duration of action vary considerably depending on the preparation (Table 31. Insulin is reabsorbed in the proximal renal tubule (upto 98%), and 60% is returned to the venous blood. Section 9 Adverse Effects Hypoglycaemia: this remains one of the potential hazards of insulin therapy, and is invariably the result of inadvertent overdose. Symptoms will depend on the extent of overdose and the time elapsed since administration (Table 31. Prolonged hypoglycaemia can produce behaviour disturbances, convulsions, coma, and death. Irreversible neurologic sequelae are likely to occur when the duration of untreated hypoglycaemia approaches 7 hours following overdose. While there is little correlation between insulin dose and severity of hypoglycaemia, serious sequelae are common when insulin is combined with other agents such as barbiturates. Sensitivity reactions: these are more common with bovine preparations than with porcine insulin, while human insulin is associated with negligible incidence of allergic reactions. Cutaneous manifestations are most common, while in some cases there may be systemic effects. Lipoatrophy and lipohypertrophy: the former is said to be a variant of an immune response to insulin, while the latter is because of lipogenic action of high local concentrations of insulin. It is advisable to rotate the site of injection frequently to avoid these effects. Insulin oedema: Sodium retention consequent to insulin administration can result in oedema, abdominal bloating, weight gain, and blurred vision. Insulin was first extracted successfully from the pancreatic islets by a young Canadian surgeon Frederick G Banting, together with a medical student Charles H Best, in 1921. Therefore when the Nobel prize in Medicine (Physiology) was awarded to Banting Table 31. Clinical (Toxic) Features Acute Poisoning: General- Patients with intermediate or extended insulin overdose may not develop symptoms for 18 to 36 hours except for vomiting and lethargy. With long acting insulin, there is a compensatory mechanism in the first 24 hours which helps to maintain normoglycaemia. Later this is exhausted, leading to irreversible brain and myocardial damage due to severe hypoglycaemia. After an insulin overdose, upto 12 days of treatment may be required before insulin needs return to normal. Hypoglycaemia can occur with therapeutic doses of insulin in diabetics on an uncontrolled diet, with too much exercise, or in patients with brittle diabetes. It is difficult to predict the minimum toxic or lethal dose of insulin and severity of intoxication must be based on clinical findings. Aphasia, maniacal behaviour, and other personality changes secondary to hypoglycaemia can also occur. Hypokalaemia may occur along with other electrolyte abnormalities following massive insulin overdose. Chronic Poisoning this is usually the result of chronic overtreatment with insulin. There is recurrent, episodic hypoglycaemia characterised by Y Pallor, restlessness, stertorous respiration, depression, inattentiveness. Urinary glucose and acetone determination are also diagnostic for diabetic ketoacidosis. Immediate differentiation between hypoglycaemia and ketoacidosis is accomplished by the use of a bedside blood glucose testing strip. Chronic insulin-induced hypoglycaemia is often associated with the presence of insulin-binding antibodies and low C-peptide levels. Stabilisation: Airway, breathing and circulation must be established and maintained. Antidote: Glucose is the specific antidote and must be administered without delay. Follow this up with continuous glucose infusion of 5% or 10% dextrose in water, sufficient to maintain slight hyperglycaemia. Monitor blood glucose levels regularly to maintain a blood glucose level of 100 mg/dL. Some investigators have achieved success by surgically excising visible injection sites down to the muscle layer. Administer 300 grams daily or more of carbohydrates when the patient awakens, to supplement intravenous glucose and prevent secondary hypoglycaemia. Excision of the skin and fat down to the muscle wall of an insulin injection site using local anaesthetic has been utilised in the management of injected insulin overdoses. Permanent brain damage has been reported following injection of 800 and 3200 units of insulin in diabetic patients. Oral hypoglycaemics Classification Sulfonylureas- First generation analogues: tolbutamide, chlorpropamide, tolazamide, acetohexamide. Second generation analogues: glibenclamide (glyburide), glimepiride, glipizide, gliclazide. Miscellaneous Drugs and Poisons Treatment Sulfonylureas Sulfonylureas are antidiabetic agents that lower blood glucose in non-insulin dependant diabetics by directly stimulating the acute release of insulin from functioning beta cells of pancreatic islet tissue. Section 9 Toxicokinetics Sulfonylureas are rapidly absorbed on oral administration, are highly protein-bound, and are subjected to extensive hepatic metabolism Adverse Effects Severe hypoglycaemia, especially in elderly patients and those with hepatic or renal impairment. Hypoglycaemic effect is reduced by barbiturates, phenytoin, rifampicin, oestrogens, corticosteroids, furosemide, thiazides, and sympathomimetic drugs. Some investigators claim that such a reaction can also occur with second generation drugs such as glipizide and glibenclamide. There are indications that long-term use of tolbutamide may be associated with increased susceptibility to myocardial infarction. The following have been reported -monoplegia, hemiplegia, ataxia, extensor plantar response, absent deep tendon reflexes, and athetoid movements. Though sulfonylureas are generally not recommended to be given in pregnancy, some reports indicate that drugs such as glyburide may be relatively safe. Arterial blood gases and serum potassium levels may reveal a hypokalaemic metabolic acidosis. Treatment of hypoglycaemia: Hypoglycaemic episodes may last for several days; prolonged treatment may be required. Y Diazoxide: It is an inhibitor of insulin secretion, and can be given orally (200 mg every 4 hours), for several days. Y Dexamethasone: Some reports suggest beneficial effects with dexamethasone when administered early. Alkaline diuresis: Sodium bicarbonate has been shown to enhance elimination of chlorpropamide. Decontamination: Emesis can be induced in the alert patient if seen within 4 to 8 hours. In the convulsive or comatose patient, gastric lavage can be done (after endotracheal intubation). Other measures: Octreotide has been shown to be beneficial in suppressing plasma insulin. While both drugs are used widely in India, phenformin has been withdrawn from several countries in the West because of the serious risk of lactic acidosis (64 cases/100,000 patient years). Metformin is said to be relatively safe in pregnancy Gastrointestinal and Endocrinal Drugs Diagnosis Toxicokinetics these drugs are absorbed from the small intestine, do not bind to plasma proteins, and are excreted unchanged in the urine. Mode of Action Biguanides induce increase in peripheral glucose utilisation, decrease in hepatic gluconeogenesis, and decrease in intestinal absorption of glucose, vitamin B and bile acids. They usually do not lower the blood sugar in normal individuals (unless other hypoglycaemic agents or ethanol has been concomitantly ingested). Lactic acidosis: While phenformin is associated with a greater risk of lactic acidosis, the other biguanides can also cause it in the presence of renal or hepatic impairment, cardiac failure, or chronic hypoxic lung disease. Y Manifestations: Acute onset of diarrhoea, vomiting, hyperventilation, and alteration of consciousness. Y Diagnosis: Anion gap metabolic acidosis, low serum pH and bicarbonate, elevated serum potassium, normal or depressed serum chloride, increased blood lactate and lactate/pyruvate. Lactic acidosis is characterised by a number of abnormal laboratory values (vide supra). Stabilisation-Establish airway, undertake endotracheal intubation, and perform assisted ventilation (if necessary). Pressor amines such as dopamine must be used with caution, since they can aggravate lactic acidosis. Diagnosis Miscellaneous Drugs and Poisons Treatment often be obtained on the "black market" by users identified as anabolic androgenic steroid injectors to promote anabolic processes and inhibit catabolism. In fact deliberate overdose with these agents in diabetics appears to occur more often than selfpoisoning with insulin. Sometimes inadvertent name confusion leads to unpredicted and unwanted hypoglycaemic effects. Indigenous medicines reputed to be effective in diabetes can contain one of these compounds. While homicidal poisoning with insulin and oral hypoglycaemics is quite rare, a few notable cases have been reported from around the world. Omeprazole and excessive sweating, if unrecognised, may lead to unnecessary investigations. Other hypoglycaemics Acarbose Acarbose is an alpha-glucosidase inhibitor which reduces intestinal absorption of starch, dextrin, and disaccharides by inhibiting the action of intestinal brush-border alpha-glucosidase. This results in depressed absorption of carbohydrates with blunting of postprandial rise of plasma glucose. Adverse effects include flatulence, gastritis, abdominal pain, nausea, anorexia, stool discolouration, hepatitis, and dermal reactions (urticaria, exanthema). Troglitazone, Ciglitazone, Pioglitazone these drugs are thiazolidinediones and have been recently introduced in the treatment of insulin-resistant diabetes. They do not cause hypoglycaemia in diabetic or normal persons, but may produce hepatotoxicity. Section 9 Forensic Issues Most cases of toxicity are iatrogenic due to inadvertent overdoses. However there have been several cases of intentional insulin overdose among depressed patients intent on committing suicide. Surreptitious insulin administration may be a symptom of serious underlying psychiatric disorder (especially in adolescents with insulin-dependant diabetes mellitus). Other Drugs Dobutamine Dobutamine resembles dopamine in its structure, but possesses an aromatic substitute on the amino group. It is used for shortterm treatment of cardiac decompensation due to depressed contractility. Infusion of dobutamine in combination with echocardiography is useful in the non-invasive assessment of patients with coronary artery disease. Dobutamine is a beta1-adrenergic agonist, and also induces alpha1-adrenoceptor-mediated vasoconstriction, as well as beta2-adrenoceptor-mediated vasodilation. Adverse effects include nausea, tachycardia, palpitations, angina, dyspnoea, headache, and hypotension. Overdose results in hypotension, oliguria, supraventricular tachycardia, stuffy nose, hoarseness, flushing of skin, tachypnoea, palpitations, anginal pain, paraesthesias, and urinary i ncontinence. Beta2-selective adrenergic agonists are much more useful in the treatment of asthma than beta-adrenergic agonists, because unlike the latter, they do not stimulate beta1-adrenergic receptors in the heart that can result in serious cardiac effects. Another advantage is that these drugs have enhanced oral bioavailability, and hence can be given orally. However, inhalation of small doses in aerosol form affords best protection against adverse effects. Cromolyn sodium and Nedocromil Bronchodilators Beta-Adrenergic Agonists Beta-adrenergic agonists have an important role as cardiac stimulants owing to both chronotropic and inotropic effects on the heart, and are (relatively) rarely used as bronchodilators today, so their inclusion here may appear incongruous. Isoproterenol (Isopropylarterenol, Isoprenaline, Isopropylnoradrenaline) this drug is used to stimulate heart rate in bradycardia or heart block as an emergency measure, and occasionally for the treatment of asthma. It acts by lowering peripheral vascular resistance and mean arterial pressure, while increasing cardiac output and relaxing smooth muscles. Beta2-Selective Adrenergic Agonists 488 Examples Metaproterenol (orciprenaline), terbutaline, albuterol (salbutamol), isoetharine, isoxsuprine, pirbuterol, bitolterol, fenoterol, formoterol, procaterol, salmeterol and ritodrine. Ritodrine is more commonly used for inhibition of uterine contractions (in premature labour). Decontamination-Stomach wash may be done if the patient is seen within 4 to 6 hours.

In 1984 erectile dysfunction treatment kerala order levitra super active master card, Kanji Inoue from Japan and in 1985 erectile dysfunction drugs market cheap levitra super active 40 mg, James E Lock erectile dysfunction causes and treatment cheap levitra super active 40mg on line, contemporary Professor of Pediatric Cardiology erectile dysfunction doctors in brooklyn buy levitra super active 40mg with amex, Harvard Medical School erectile dysfunction medication online pharmacy buy levitra super active 40 mg low price, and colleagues introduced balloon valvuloplasty for mitral stenosis erectile dysfunction kidney disease discount levitra super active 40mg fast delivery. Obtain a history of myocardial infarction, rheumatic fever, connective tissue dis-order, infective endocarditis. Apex beat will be displaced downwards and outwards and will be forceful in character. Pansystolic murmur (Hope murmur) conducted to the axilla, best detected with the diaphragm and on expiration. When mitral regurgitation is caused by left ventricular dilatation and dim-inished cardiac contractility, the systolic murmur may be mid, late or pansystolic. Other causes of short systolic murmurs at the apex include mitral valve prolapse, papillary muscle dysfunction and aortic stenosis. In calcific aortic stenosis of the elderly, the murmur may be more prominent in the apex and may be confused with mitral regurgitation. In such instances try to listen to the murmur after a pause with pre-mature beat or listen to the beat after a pause with atrial fibrillation. The murmur of aortic stenosis becomes louder, whereas that of mitral regurgitation shows little change. When coronary artery disease is the cause, there is often evidence of inferior or posterior wall myocardial infarction. Chest radiograph, looking for pulmonary congestion, large heart, left atrial en-largement and pulmonary artery enlargement (if severe and longstanding). Echocardiogram to determine the anatomy of the mitral valve apparatus, left atrial and left ventricular size and function (typical features include large left atrium, large left ventricle, increased fractional shortening, regurgitant jet on colour Doppler, leaflet prolapse, floppy valve or flail leaflet). The echocardiogram provides baseline estimation of left ventricle and left atrial volume, an estimation of left ventricular ejection fraction, and an approximation of the severity of regurgitation. How would you differentiate between mitral regurgitation and tricuspid regurgitation Because of reduced systolic ejection time, secondary to a large volume of blood regurgitating into the left atrium. Rarely, due to involvement of the posterior mitral leaflet or to ruptured chordae tendineae, the regurgitant jet strikes the left atrial wall adjacent to the aortic root and the murmur radiates to the base of the heart, and therefore may be confused with the murmur of aortic stenosis. Grade 6: Murmur is loud enough to be heard with the stethoscope just removed from contact with the chest wall. However, echocardiography provides only a semi-quantitative estimate of the severity of regurgitation. Left ventriculography performed during cardiac catheterization provides an additional but also im-perfect estimate of the severity of mitral regurgitation. The prevalence of third heart sounds increases with the severity of mitral regur-gitation. However, in patients with mitral regurgitation, the third heart sound is due to rapid ventricular filling and does not necessarily reflect left ventricular systolic dysfunction or increased filling pressure. In this situation S3 is caused by rapid filling of the left ventricle by the large volume et blood stored in the left atrium in diastole. Patients with minimal or no symptoms should be followed up every 6 months by echocardiographic or radionuclide assessment of left ventricular size and systolic function. Remember that ischaemic mitral regurgitation carries the worse prognosis: operative mortality is 10-20% and long-term survival is substantially lower than with non-ischaemic mitral regurgitation (J Thorac Cardiovasc Surg 1986; 91: 379-88; Ann Thorac Surg 1994; 58: 668-75). It is less likely when the aetiology is ischaemic, infectious or rheumatic, when there is significant calcification, when the prolapse is bileaflet or anterior. In patients with mitral regurgitation due to flail leaflet, the lesion usually results in high degrees of regurgitation (J Am Coil Cardiol 1990; 16: 232-9). In Western countries flail leaflet is the most frequent cause of mitral regurgitation requiring surgical correction (Mayo Clinic Proc 1987; 62: 22-34; Eur Heart J 1991; 12 suppl B: 2-4). When treated medically, mitral regurgitation due to flail leaflet is associated with excess mortality and high morbidity. Surgery is almost unavoidable within 10 years after the diagnosis and appears to be associated with an improved prog-nosis, suggesting that surgery should be considered early in the course of the disease (N Engl J Med 1996; 335: 1417-23). Levine was Professor of Cardiology at Harvard Medical School and Peter Bent Brigham Hospital in Boston. Proceed as follows: Look carefully for surgical scars of mitral valvotomy in all patients (scars under the left breast in female patients are often missed). A third heart sound in mitral regurgitation indicates that any associated mitral stenosis is insignificant. There may be patients who do not have clear-cut signs such as a loud first heart sound with a displaced apex; in such cases you must say that it is difficult to ascertain clinically the dominant lesion and that cardiac catheterization should resolve the issue. Read these papers for further information: Circulation 1973; 48: 357; Ann Intern Med 1972: 77: 939. What are the approximate frequencies with which various valves are affected by rheumatic heart disease In the absence of mitral stenosis it suggests that there is high diastolic transmitral flow and severe mitral regur-gitation. Inhalation of amyl nitrate increases both the duration and intensity of the diastolic murmur due to mitral stenosis whereas it decreases them if the diastolic rumble is caused solely by mitral regurgitation. Also the presence of an opening snap suggests mitral stenosis as the cause of the diastolic rumble. In patients with mitral regurgitation and a diastolic rumble, what does the presence of a giant left atrium indicate Perloff is contemporary Professor of Cardiology, Los Angeles; his chief interest is congenital heart disease. Examination Pulse Collapsing pulse (large volume, rapid fall with low diastolic pressure). When the ascending aorta is dilated and displaced to the right, the murmur may be heard along the right sternal border as well. This murmur may be as loud as grade 5 or 6, and underlying organic stenosis can be ruled out only by investigations. It is typically low-pitched, similar to the murmur of mitral stenosis but without a preceding opening snap. Radionuclide angiography is useful in asymptomatic patients with poor quality echocardiographic images. According to the Helsinki Ageing Study, 13% of persons aged 75-86 years have moderate to severe aortic regurgitation (J Am Coll Cardiol 1993; 21: 1220-5). In mild aortic regurgitation the difference is less than 20 mmHg, in moderate regurgitation it is between 20 and 40 mmHg and in severe regurgitation it is over 60 mmHg. In mild aortic regurgitation the murmur is short but, as the severity of the regur-gitation increases, the murmur becomes longer and louder. It is an apical, low-pitched, diastolic murmur caused by vibration of the anterior mitral cusp in the regurgitant jet, and is heard at the apex. About 4% of patients develop symptoms, left ventricular dysfunction, or both, every year. In chronic aortic regurgitation there is slow and progressive left ventricular dilatation and hypertrophy in an attempt to normalize wall stress. The heart may thus become larger and heavier than in any other form of chronic heart disease - cor bovinum (bovine or ox heart). Patients in whom left ventricular dys-function developed when treated with nifedipine respond favourably to valve replacement in terms of both survival and normalization of ejection fraction. The timing of surgery is important and depends on severity of symptoms and extent of left ventricular dysfunction (Circulation 1998; 98: 1949-84). Valve replacement should be performed as soon as possible after the onset of ventricular dysfunction. Indications for surgery include: Symptoms of heart failure and diminished left ventricular function (an ejection fraction of less than 50% but more than 20-30%). A reduction in exercise ejection traction (as estimated with radionuclide ventriculography and exercise testing) of 5% or more is considered by some to be an indication for surgery, even in the absence of symptoms. Several investigators have suggested an end-systolic dimension of 55 mm to represent the limit of surgically reversible dilatation of the left ventricle, so that aortic valve replacement is performed before this chamber size is exceeded. Others have challenged the validity of the 55 mm systolic limit, as postoperative reduction in chamber size remains variable. In the elderly and in those for whom anticoagulants are contraindicated, tissue valves are preferred. Patients who have had valve replacement should also be seen regularly and monitored for signs of failure of the aortic valve prosthesis (particularly in patients with biological valves) and endocarditis (Circulation 1998; 98:1949-84). Alfred de Musset was a French poet whose nodding movements were described by his brother in a biography. When told of this, Alfred put his thumb and forefinger on his neck and his head stopped bobbing. Austin Flint (1812-1886) was one of the founders of Buffalo Medical College, New York, and reported the murmur in two patients with aortic regurgitation, confirmed by autopsy. Quincke (1842-1922) was a German physician who described angioneurotic oedema and benign intracranial hypertension. Duroziez (1826-1897), a French physician, was widely acclaimed for his articles on mitral stenosis. Traube (1818-1876), a German physician, was the first to describe pulsus bigeminus. Antonio Maria Valsalva (1666-1723) was an Italian anatomist and surgeon who discovered the labyrinth and developed the Valsalva manoeuvre to remove foreign bodies from the ear. Syncope (in 25% of patients, during or immediately after exercise; average survival after onset of syncope ix 3 years). Dyspnoea is a common presenting symptom (suggests left ventricular dys-function; heart failure reduces life expectancy to less than 2 years). This is due to a reduction in systolic pressure and a gradual decline in diastolic pressure. General examination Check the blood pressure, keeping in mind that the pulse pressure is low in moderate to severe stenosis. Aortic sclerosis is seen in the elderly; the pulse is normal volume, the apex beat is not shifted and the murmur is localized. A single second heart sound may be heard when there is fibrosis and fusion of the valve leaflets. Reversed splitting of the second sound indicates mechanical or electrical pro-longation of ventricular systole. It is a crescendo-decrescendo murmur which begins after the first heart sound (or after the ejection click when present), peaks in mid or late systole and ends before the second heart sound. No, the loudness of the murmur is related more to the cardiac output and the systolic turbulence surrounding the valve than to the severity of the stenosis. Thus, a loud murmur may be associated with trivial stenosis and, in severe heart failure, the mur-mur may be soft because of decreased flow across the valve from the diminished cardiac output. According to the Helsinki Ageing Study, almost 3%, of individuals aged between 75 and 86 years have critical aortic stenosis (J Am Coil Cardiol 1993; 21: 1220-5). Marked peripheral vasodilatation without a concomitant increase in cardiac out-put. Chest radiograph May show cardiac enlargement, post-stenotic dilatation of aorta (a bicuspid valve should be suspected if the proximal aorta is greatly enlarged), calcification of aortic valve (particularly in older patients). In selected patients it may be useful to provide a basis for advice about physical activity. Cardiac catheterization this is done to assess the coronary circulation and to confirm or clarify the diagnosis. When the echocardiogram is inadequate, cardiac haemodynamics using both left and right heart catheterization is indicated and requires: (1) measurement of transvalvular flow, (2) determination of transvalvular pressure gradient and (3) calculation of the effective valve area. If the patient is asymptomatic and the valvular gradient is less than 50 mmHg, then observe the patient. Valve replacement in the following circumstances: the patient is symptomaticor the valvular gradient is more than 50 mmHg. Patients with severe aortic stenosis should have valve replacement early to avoid deterioration. Balloon valvuloplasty should be limited to moribund patients requiring emergency intervention or those with a very poor life expectancy due to other pathology. In one study, although in-hospital mortality rates were similar to those following conventional surgical replacement, there were more deaths in the valvuloplasty group in the subsequent follow-up period (d Am Coil Cardiol 1992; 20:796-801). If a young person presents with signs and symptoms of aortic stenosis but the aortic valve is normal on echocardiography which condition would you suspect Studies suggest that mutation in the elastin gene causes supravalvular stenosis (Cell 1993; 73: 159). If the patient was icteric and had haemolytic anaemia, what would the mechanism be Microangiopathic haemolysis has been described in severe calcified aortic stenosis manifesting with anaemia and icterus (Semin Hemato/ 1969; 6: 133). The high-frequency components of the ejection systolic murmur may radiate to the apex, falsely suggesting mitral regurgitation. Proceed as follows: Tell the examiner that you would like to check the blood pressure, in particular to determine the pulse pressure (systolic minus diastolic pressure). When aortic stenosis predominates, the pathophysiology and, therefore, the management resembles that of pure aortic stenosis (J Am Coil Cardiol 1998; 32: 1486-588). The timing of aortic valve replacement (as in pure aortic stenosis) depends on symptoms (Circulation 1998; 98: 1949-84). Theretore, although neither lesion by itself is sufficiently severe to merit surgery, both together produce substantial haemodynamic compromise and require surgery (Circulation 1998; 98: 1949-84). Because the transvalvular gradient varies with the square of the transvalvular flow (Am Heart J 1951; 41: 1-29), a high gradient in predominant regurgitation may be predicted primarily on excess transvalvular flow rather than on a severely com-promised orifice area (Circulation 1998; 98: 1949-84). In mixed aortic valve disease is cardiac catheterization more accurate than Doppler echocardiography to measure valve area Aortic valve area will be measured inaccurately at the time of cardiac catheteriz-ation in mixed aortic valve lesions if the cardiac output is measured either by the Fick or the thermodilution method as both these methods usually underestimate total valve flow. The valve area can be measured more accurately using Doppler echocardiography (by continuity equation) in mixed aortic stenosis and aortic regurgitation. However, the confusing nature of mixed valve disease makes cardiac catheterization necessary to obtain additional haemodynamic information in most patients (including coronary anatomy) (Circulation 1998; 98:1949 84). Early diastolic murmur of aortic regurgitation heard on end expiration with the patient sitting forward. Note If the apex beat is not displaced in such mixed lesions then mitral stenosis is the dominant lesion.

Some observations on the toxicity and antipyretic activity of crude and processed aconite roots erectile dysfunction pills sold at gnc buy levitra super active 40 mg overnight delivery. Cardiotoxic Plants Forensic Issues Cerberin is difficult to detect in autopsies and its taste can be masked with strong spices online erectile dysfunction drugs reviews purchase cheap levitra super active on line. Simple Asphyxiants-These gases displace oxygen from the ambient air and reduce the partial pressure of available oxygen erectile dysfunction icd 9 code 2012 buy levitra super active 40 mg without a prescription. Examples include carbon dioxide acupuncture protocol erectile dysfunction order genuine levitra super active, nitrogen xyrem erectile dysfunction order cheapest levitra super active, aliphatic hydrocarbon gases (butane erectile dysfunction neurological causes discount levitra super active 40 mg without a prescription, ethane, methane, and propane), and noble gases (argon, helium, neon, radon, and xenon). Respiratory Irritants-These gases damage the respiratory tract by destroying the integrity of the mucosal barrier. Examples include acrolein, ammonia, chloramine, chlorine, formaldehyde, hydrogen sulfide, methyl bromide, methyl isocyanate, oxides of nitrogen, osmium tetroxide, ozone, phosgene, and sulfur dioxide. Heavy metal-related gases also come under this category (cadmium fumes, copper fumes, mercury vapour, zinc chloride and zinc oxide). Systemic Asphyxiants-These gases produce significant systemic toxicity by specialised mechanisms. It must be noted that systemic toxicity may also be observed in the case of some simple asphyxiants and respiratory irritants, though it is not the predominant feature. Discussion of toxicity of the examples mentioned under the various categories now follows, while pointing out that some of them have been discussed elsewhere (consult Index). Concentrations above 35% have a depressing effect upon both circulation and respiration. Bradycardia progressing to asystole may occur in the absence of signs of cyanosis following inhalation exposure to 99. Investigators suggest hypercapnia and acidosis may contribute to the cause of cardiac arrest. Forensic Issues Diagnosis Asphyxiant Poisons Arterial blood gases are useful to assess the degree of hypoxaemia. Administer 100% humidified supplemental oxygen, perform endotracheal intubation, and provide assisted ventilation as required. If hypoxia has been severe or prolonged, carefully evaluate for neurologic sequelae and provide supportive treatment as indicated. Freeze injury associated with dermal exposure to "dry ice" is unlike frostbite in that the damage occurs within seconds and rewarming is not beneficial. Some investigators suggest that freeze injuries of this nature should be managed much like a thermal burn. Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 420C for 15 to 30 minutes until thawing is complete. Some authors suggest that an antibacterial (hexachlorophene or povidone-iodine) be added to the bath water. Survivors of the Lake Nyos disaster in August, 1986 were noted to have superficial blisters which healed rapidly. Characteristics of the blisters suggested that they were the result of depriving the skin of oxygen. Hospitalised and outpatient survivors had symptoms compatible with exposure to a suffocating gas. Many survivors had lost consciousness for hours (6 to 36 hours) after the incident. Cough, headache, fever, weakness or malaise, and limb swelling were frequently noted (10% or more incidence) among the victims. Evidence after the incident suggested a slow build-up of carbon dioxide deep in the lake, followed by its release as a cold, suffocating aerosol. Dogs, cats, cattle, goats, chickens, snakes, and frogs were also found dead in their tracks. Insect life was noted to be absent for approximately 24 hours following the incident. Excess levels of carbon dioxide, ammonia, and other asphyxiant gases have been theorised to accumulate at the face of a sleeping infant. Section 7 Aliphatic Hydrocarbon Gases Ethane is an odourless gas which is used as a refrigerant and as a component of natural gas. Conversion of domestic gas from coal gas (mostly carbon monoxide) to natural gas (mostly methane) has significantly reduced mortality from domestic gas leaks, since methane is much less toxic as compared to carbon monoxide. Methane being odourless, a stenching agent (alkyl mercaptan) is deliberately added to domestic gas so that leaks can be immediately recognised. Most explosions in mines (as well as homes using natural gas as fuel) occur because of this reason. Butane, liquefied petroleum gas, propane, and propylene have a faint petroleum-like odour and may be stenched with mercaptans for transport and storage. Butane is used as a raw material for automobile fuels, in organic synthesis, and as a solvent, refrigerant, and aerosol. Propane is used as a raw material in organic synthesis, as a component of industrial and domestic fuels, as an extractant, a solvent, and a refrigerant, and in the manufacture of ethylene. Incomplete combustion of these agents can release carbon monoxide into the ambient air. Butane is often abused by adolescents in the form of inhalation (see "glue sniffing", page no 576). Propylene is a raw material in polypropylene, isopropyl alcohol, isopropylbenzene, acetone, and propylene oxide manufacturing. Most of the aliphatic hydrocarbon gases act as simple asphyxiants (vide supra), in addition to additional specific toxicities. It is highly water soluble (forming ammonium hydroxide which is an alkaline corrosive). When heated to decomposition, it emits toxic fumes of ammonia and oxides of nitrogen. Uses Agriculture (fertiliser) Mining Manufacture of plastics and explosives Refrigerant Cleaning and bleaching agent Treatment of syncope in the form of smelling salts (page no 57). Management is best effected by immediate (and permanent) exclusion from the source of exposure and symptomatic measures, though the response to beta2 adrenergic agonist therapy is not as good as in occupational asthma. Ingestion of ammonia solution produces corrosion of the alimentary tract and aspiration pneumonia. Swelling of the lips, mouth, and larynx, and oral or oesophageal burns may occur if concentrated ammonia solutions are ingested. Exposure to anhydrous ammonia stored at minus 280 F may produce frostbite injury with thrombosis of surface vessels and subsequent ischaemia and necrosis. Ocular exposure can result in immediate and serious chemical burn with rapid penetration into the interior of the eye. Conjunctivitis, lacrimation, corneal irritation, and temporary or permanent blindness can result. Ammonia has greater tendency than other alkalies to penetrate and damage the iris, and to cause burns and cataracts in cases of severe exposure. Iritis may be accompanied by hypopyon or haemorrhages, extensive loss of pigment, and severe glaucoma. Chronic exposure in workers may lead to initial complaints of chronic cough, dyspnoea on effort, bilateral infiltrates on chest X-ray, and lung function indices reflecting ventilatory and diffusion abnormalities Asthma and laryngitis have been reported in workers chronically exposed to ammonia. Inhalation produces such severe upper airway irritation that the victim seldom remains exposed for more than an instant, unless he is trapped. There is glottic and laryngeal oedema, sloughing of bronchial mucosa, and chemical pneumonitis with pulmonary oedema. This is a persistent, asthma-like syndrome and is also referred to as irritant induced asthma. Fatalities may also occur from exposure to ammonia concentrations of 2500 to 4500 ppm if inhaled for 30 minutes. Mixing of ammonia with hypochlorite bleach results in the formation of chloramine, which causes a toxic pneumonitis (pulmonary oedema) following inhalation, and may produce residual pulmonary function abnormalities. The determination of ammonia in air may be done using an ammoniaspecific electrode, second derivatives spectroscopy, ion chromatography, or colourimetrically. There can be a four-fold or greater rise in blood ammonia in some toxic liver diseases because the urease needed to convert ammonia to urea is found only in the liver. Ocular exposure should be treated with prolonged irrigation with water (30 minutes or more) until the eye reaches neutral pH as tested with a litmus paper in the conjunctival sac. Dermal exposure requires washing with soap and water, followed by copious irrigation with water alone. Intubation or tracheostomy may be life-saving following severe exposure if stridor, indicating laryngeal oedema, is present. If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents. In the case of ingestion, a small quantity of water or milk can be administered as a first-aid measure to dilute the chemical. Activated charcoal is of no benefit, and may induce vomiting and obscure endoscopy findings. Formaldehyde Synonyms Dormol, fannoform, formalin, formalith, formic aldehyde, formol, lysoform, methanal, methyl aldehyde, methylene oxide, morbicid, oxomethane, oxymethylene. Formalin is an aqueous solution of formaldehyde containing 37 to 40% formaldehyde and 10 to 15% methanol. Therefore 10% formalin would actually mean a 1: 10 dilution of such a commercial preparation and contains 3. Some formaldehyde aqueous solutions can be amber to dark brown or even reddish in colour. Formaldehyde is also available as a solid polymer, paraformaldehyde, in a powder or flaked form containing from 90 to 93% formaldehyde, and as its cyclic trimer, trioxane. Industrial/Household: Formaldehyde is used in fertilisers, pesticides, sewage treatment, paper-making, preservatives, embalming fluids, disinfectants, foam insulation, urea and melamine resins, artificial silk and cellulose esters, explosives, particle board, plywood, air fresheners, cosmetics, fingernail polishes, water-based paints, tanning and preserving hides, and as a chemical intermediate. It is also used as a preservative and coagulant in latex rubber, and in photograph developing processes and chrome printing. Medical/Veterinary: Therapeutically, formaldehyde has been used to treat massive haemorrhagic cystitis and hydatid cysts of the liver. Dialysis patients using dialyser machines sterilised with formaldehyde receive a small dose with each treatment. The most frequent sequelae is a type of autoimmune haemolytic anaemia; rarely, peripheral eosinophilia may occur. Severe hypersensitivity reactions have been observed in a few of these dialysis patients, though the exact relationship of this to formaldehyde-sterilised equipment is unclear. Currently other sterilisers are in use such as a mixture of hydrogen peroxide and peracetic acid. Formaldehyde is a common contaminant of smoke and is even present to a significant extent in tobacco smoke. Burning wood, cigarette smoking, and other forms of incomplete combustion emit formaldehyde. Addicts sometimes dip cigarettes of tobacco or cannabis in formaldehyde ("amp" or "dank") before smoking, in the belief that this produces a hallucinogenic effect and "body numbness". It is a dangerous practice and can result in encephalopathy, pulmonary oedema, rhabdomyolysis and coma. While poisoning with ammonia is not very common, most of the cases reported are suicidal in nature. Since the solution or gas even when weak has a distinct irritant smell, accidental poisoning is unlikely. However, of late ammonia is being used as a spray to incapacitate victims of robbery. Other inhibitors of polymerisation used with formaldehyde include ethyl cellulose, methyl cellulose, hydroxypropyl methyl cellulose, and isophthalobisguanamine. Due to conversion in the body to formic acid there is usually profound metabolic acidosis, and this is aggravated by the concomitant presence of methanol (a common additive in formalin solutions) which is also broken down to formic acid. Delayed absorption of methanol might occur following ingestion of formalin if the formaldehyde causes fixation of the stomach. Ingestion of as little as 30 ml of 37% (approximately 2 tablespoons) formaldehyde solution (formalin) has been reported to cause death in an adult. Exposure to air concentrations as low as 2 ppm can cause eye and upper respiratory irritation. Dermal exposure to formalin can result in irritation (acute), or allergic dermatitis (chronic) in susceptible individuals. Exposure to solutions of 2 to 10% may result in blisters, fissures, and urticaria. Inhalation-cough, lacrimation, dyspnoea, chest pain, wheezing, rhinitis, anosmia, tracheitis, bronchitis, laryngospasm, pulmonary oedema, headache, weakness, dizziness, and palpitations. Ingestion-severe abdominal pain, vomiting, diarrhoea, haematemesis, tachypnoea, hypotension, cyanosis, altered mental status, and coma.

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