I will discuss some of the important features that will help you tell these two diseases apart medications without doctors prescription order cheapest disulfiram and disulfiram. Patients with smallpox have a severe medicine 5513 buy cheapest disulfiram, febrile prodrome that starts one to four days before the onset of the rash treatment lower back pain order disulfiram pills in toronto. People with varicella will have a short 5 medications order generic disulfiram line, mild prodrome medicine used to stop contractions buy generic disulfiram 500mg on line, and some of them will have no prodrome at all before the onset of their rash medications zoloft side effects cheap disulfiram. If there is no history of a febrile prodrome treatment zap trusted disulfiram 250mg, smallpox is not the likely diagnosis medicine natural buy disulfiram 250mg with visa. In addition to fever, the prodrome of smallpox is associated with one or more additional symptoms, such as prostration, headache, backache, chills, abdominal pain, or vomiting. Although there may be some overlap in the appearance of the lesions, particularly soon after rash onset, classic smallpox looks very different than varicella. By contrast, the varicella rash is supercial and the lesions appear to be delicate. In a typical case of smallpox, lesions evolve from macules to papules to vesicles and then to crusts, with each stage taking one or two days. By contrast with varicella, some lesions will have evolved from macules to crusts within 24 hours. Because of the slow rate of evolution of smallpox lesions, all the lesions on any one part of the body will be in the same stage of development, such as all vesicles or all pustules. Varicella lesions typically appear in crops and they evolve quickly, so in any one area of the body you will nd lesions in all stages of evolution: papules, vesicles, and crusting lesions. By contrast, the rash of varicella is generally most dense on the abdomen and back, and less dense on the extremities. Notice the concentration of lesions is highest on the back, and becomes less dense on the arms and the legs. Here you can see that the lesions are most concentrated on the arms and the legs, and there are fewer lesions on the back. Lesions on the palms or soles are seen in the majority of cases of smallpox, but are very rare in varicella. There are lesions on the face, but they look supercial, they are of different sizes, and they are all in different stages of evolution. Since second cases of varicella are really rare, asking whether a person has had chickenpox in the past helps in determining the likelihood that the rash you are evaluating is varicella. When varicella does occur in an adult it tends to be more severe than a typical childhood case. Generalized varicella is unlikely in a person who has received the varicella vaccine. Third, a history of exposure to a person with varicella or herpes zoster 10 to 21 days before rash onset. About 80% of children and half of adults with varicella will recall an exposure to a case of chickenpox or shingles. Since varicella is now a vaccine-preventable disease, we encourage health care providers to vaccinate susceptible children, adolescents, and adults. There are other illnesses and conditions to consider in the differential diagnosis of a person with a generalized rash illness. Drug eruptions can present with a variety of generalized rashes, and they may have concurrent symptoms, such as fever. For this reason it is important to take a detailed history of all medications including prescription and over-the-counter medications. Herpes zoster, or shingles, usually presents as a localized and painful rash in one or two dermatomes on one side of the body. In immunocompromised persons it can disseminated and can present with a generalized vesicular rash. Hand, Foot, and Mouth Disease is an enteroviral disease that most commonly occurs in the summer or the autumn. Ulcerative lesions can be seen in the mouth, and tender vesicular or pustular lesions on the hands and feet including the palms and soles. However the individual lesions are really easy to distinguish from the hard pustules of smallpox and the lesions clear up in about a week. Molluscum contagiosum is a common viral infection of the skin and mucous membranes and is caused by poxvirus. Molluscum contagiosum also occurs in healthy children, who are perfectly well and afebrile. Secondary syphilis can produce almost any type of generalized rash, including pustular rash. The rash may appear anywhere on the body, and they may involve the palms and soles. Fortunately syphilis is becoming a rare illness in the United States, but it should be ruled out in someone who is sexually active and has a generalized rash. There are many other causes of generalized rash illnesses, from common etiologies like insect bites, scabies, and contact dermatitis to less common conditions such as disseminated herpes simplex, or erythema multiforme. In addition there are some exceedingly rare causes, such as rickettsial pox and monkeypox. Although we have focused on differentiating smallpox from conditions that can present with generalized vesicular or pustular rashes, a small percentage of smallpox cases will present with either a hemorrhagic rash or at type rash. Always wear gloves when touching a patient with a rash illness, and institute respiratory precautions if there is any chance of airborne spread, as occurs with both varicella and smallpox. The next actions you take will depend on the likelihood that the person you are evaluating has smallpox. And if a person meets all three criteria he or she is considered a high-risk case. The rst criterion is that the person had a signicant febrile prodrome one to four days before rash onset. Second, the rash lesions are deep in the skin, rm or hard to the touch and well circumscribed. Third, on any one part of the body, all of the lesions are in the same stage of development. The distribution of the rash is centrifugal, meaning that the greatest concentration of lesions is on the face and distal extremities with relative sparing of the trunk. The rst lesions of the rash appeared on the oral mucosa or palate, or else on the face or forearms. Lesions progressed slowly, by which I mean that the individual lesions evolved from macules to papules to pustules over several days. A person is considered at high risk for smallpox if he or she meets all three major criteria. Immediate action should be taken to make sure that contact precautions and respiratory isolation are in place. A person is considered at moderate risk of smallpox if he or she had a febrile either a prodrome and either one other major criterion or at least four minor. These patients should be isolated and be evaluated urgently to determine the cause of the illness. We recommend that persons who are classied at high or moderate risk be seen in consultation with a specialist in infectious diseases and/or dermatology whenever possible. Any person who did not have a febrile prodrome is considered low risk, as are persons who had a febrile prodrome, but less than four minor criteria. The protocol includes a diagnostic algorithm, a chart with the major and minor criteria I just discussed, and a chart of common rash illnesses along with clinical and diagnostic clues. In addition there are photographs of the classic lesions of smallpox and varicella. Recent advances in serologic testing and culture will be useful for conrmation of an acute case. Laboratory testing should be done in consultation with an infectious disease or dermatology specialist. This technique is very sensitive and specic but is critically dependent on careful collection of material from a lesion. Currently, laboratory procedures for variola virus in clinical specimens should be done only by the Centers for Disease Control and Prevention in Atlanta. Personnel can be quickly deployed to assist in conrming the diagnosis by collecting clinical material for laboratory testing, and to assist in implementation of control measures if necessary. The diagnosis of orthopoxvirus infection in general can be made rapidly by electron microscopic examination of vesicular or pustular uid or scabs. Differentiation of orthopoxviruses is made by nucleic acid based testing, such as polymerase chain reaction, and by culture. So blood samples will be an important part of the laboratory evaluation of a suspected case. Detailed instructions for the collection and transport of specimens is available on the Bioterrorism Preparedness and National Immunization Program Web sites. We recommend you obtain these instructions, and familiarize yourself with the types of specimens and methods of collection. In 1796, Edward Jenner demonstrated that immunity to smallpox could be produced by inoculating a human with material from a lesion on the udder of a cow. Jenner called this infectious material "vaccine," and the procedure came to be called "vaccination. At some time during the 19th century, the virus used for smallpox vaccination ceased to be cowpox and changed to vaccinia. Vaccinia is in the same family as cowpox and variola, but is genetically distinct from both of them. The origin of vaccinia, and how it came to replace cowpox virus in the vaccine, is not known. The vaccine currently available in the United States was prepared in the early 1980s from calf lymph with a seed virus derived from the New York City Board of Health strain of vaccinia. The diluent used to reconstitute the vaccine is 50% glycerin, and contains the antibiotics polymyxin B, streptomycin, tetracycline and neomycin, and a small amount of phenol as a preservative. Approximately 15 million doses of smallpox vaccine are available now in the United States. More than 200 million additional doses of vaccine are being produced to be available in case of an introduction of smallpox. The new vaccine is being produced by cell culture methods similar to those used to produce other human vaccines. The efficacy of smallpox vaccine has never been measured precisely in controlled trials. But, protection has been determined in studies of people exposed to a smallpox patient in their households. There was a 90% reduction in smallpox among contacts with a vaccination scar compared to contacts without a scar. Epidemiologic studies demonstrated that this high level of protection against smallpox persists for up to ve years after primary vaccination and substantial but waning immunity can persist for 10 years or more. Although vaccination 30 or more years ago may not protect against smallpox, vaccinated people appear to have less severe disease. Studies of smallpox cases imported into Europe in the 1950s and 1960s showed fewer fatalities among vaccinated people compared to those who were unvaccinated. This graph shows the smallpox fatality rate among people vaccinated at various intervals before exposure to smallpox. The data are from a series of 680 smallpox cases resulting from importation into Europe between 1950 and 1971. The fatality rate among people vaccinated less than 10 years before exposure was 1. It was 7% among those vaccinated 11 to 20 years prior, and 11% among those vaccinated 20 or more years prior to infection. Administration of the vaccine within the rst few days after initial exposure to smallpox virus can reduce symptoms or prevent disease. Studies in Pakistan and India showed that secondary cases in households were reduced up to 91% compared to unvaccinated people, if the vaccine was administered less than seven days after exposure. A vesicle then forms, which becomes pustular by seven to 11 days after vaccination. A person is considered protected with the development of a pustule like this at the vaccination site. Vaccinia virus is present at the vaccination site beginning three to four days after vaccination until the scab separates. Care must be taken to avoid transferring virus to other parts of the body, such as the eye, or to other people. Vaccination is routinely recommended for laboratory workers who directly handle cultures or animals contaminated or infected with some strains of vaccinia and recombinant vaccinia viruses. Vaccination is also recommended for laboratory workers exposed to other orthopoxviruses that infect humans such as monkeypox or cowpox. Vaccination can be considered for other health care workers who come into contact with materials such as dressings that may be contaminated with vaccinia or recombinant vaccinia. This could occur, for example, in the course of a clinical trial in which humans were given vaccines containing recombinant vaccinia viruses. Persons at risk of exposure would include those involved in the direct medical or public health evaluation, care or transportation of conrmed or suspected smallpox patients; laboratory personnel who collect or process clinical specimens from conrmed or suspected smallpox patients; and people who may have contact with infectious materials. This includes those responsible for medical waste disposal, linen disposal or disinfection, and room disinfection in a facility where smallpox patients are present. Vaccination will be a key component of our response to an intentional release of variola virus. We will discuss vaccination strategies again later in the program in the context of the smallpox response plan. Vaccine Administration (video) Dip the bifurcated point of the needle into the vaccine solution so that the needle is perpendicular to the oor. The needle will pick up a drop of the vaccine in the space between the two prongs. Hold the skin on the arm taught and begin to prick the skin 15 times as shown here. This should be done rapidly in a perpendicular fashion within a 5 millimeter diameter area. Enough pressure should be used to produce a trace of blood at the vaccination site that appears 10 to 20 seconds after vaccination. This method allows the live vaccinia virus to penetrate the supercial layers of the skin so that viral multiplication can take place and immunity to smallpox will develop. Once the vaccine is administered you should dispose of the needle and cover the site with a piece of gauze. Smallpox vaccine complications, or adverse events, range from frequent and innocuous to rare and fatal. More severe complications are rare but occur more than 10 times more often among primary vaccinees than among revaccinees and are more frequent among infants than among older children and adults. Transfer, or autoinoculation, of vaccinia from the vaccination site is called inadvertent inoculation. When it occurs at the time when the primary lesion is well developed, small or attenuated lesions may be produced. Inadvertent inoculation accounts for approximately half of all complications of primary vaccination and revaccination. In our 1968 studies, inadvertent inoculation occurred once per 1,800 primary vaccinations. Lesions of inadvertent inoculation could occur anywhere on the body, but the most common sites involved were the face, eyelid, nose, mouth, genitalia, and rectum. This girl had severe periorbital swelling from vaccinial lesions on her right lower and upper eyelids. These lesions, as well as those on most other locations, heal without specic therapy. These rashes are referred to as erythema multiforme, roseola vaccinia, toxic erythema, and postvaccinial urticaria. They are at, erythematous, macular, or urticarial lesions, usually with microscopic vasculitis. Patients with erythematous urticarial rashes associated with vaccinia are generally not severely ill and are usually afebrile despite extensive skin involvement, except upon the rare occasions when Stevens-Johnson syndrome, or bullous erythema multiforme develops. He had extensive erythematous patches over his entire body except for relative sparing of the soles of the feet. Another type of rash following smallpox vaccination is labeled as generalized vaccinia. This condition is believed to result from a vaccinia viremia with implantations in the skin in persons without underlying illnesses. Rashes diagnosed as generalized vaccinia occurs at a rate of about once per 4,000 primary vaccinations. It consists of vesicles or pustules appearing on normal skin at a distance from the vaccination site. Most rashes labeled as generalized vaccinia produces only minor illness with little residual damage. This photograph shows typical vaccinial lesions on the legs of a 14-year-old primary vaccinee approximately eight days after vaccination. The lesions are similar to small vaccinations, but the child did not have considerable systemic symptoms.
Always check that the chest is rising and falling symmetrically with each squeeze of the bag medicine assistance programs disulfiram 250 mg without a prescription. Note the pressure needed to inflate the lungs: if it is increasing that may indicate a lung problem such as aspiration treatment zygomycetes purchase disulfiram 250mg without a prescription, bronchospasm or pneumothorax symptoms sinus infection purchase 500 mg disulfiram fast delivery. If a cardiorespiratory arrest occurs during an operation symptoms yeast infection disulfiram 500mg low price, make sure that the anaesthetic agents have been turned off and you are ventilating with the highest possible percentage of oxygen treatment vitiligo 500 mg disulfiram with mastercard. Unlike breathing symptoms 2 days before period order 500 mg disulfiram with amex, it is less obvious when there is no blood circulation medicine 027 pill buy disulfiram 250 mg low price, especially in patients with dark skins medicine school buy disulfiram 250 mg on-line. You must look for and make the specific diagnosis of circulatory arrest: Feel for a pulse in the carotid or femoral artery Feel for an apex heartbeat Listen at the apex with a stethoscope Look for cyanosis or pallor in the tongue. Some other treatment must be given and normal circulation must be restored if the patient is to survive. Assign a third person to feel for the femoral pulse and report to you if it returns. Very often, a device is present in the hospital but does not work when needed or it has to be brought from somewhere else, causing delay. Always use it once the diagnosis is made, even if you do not know the cause of the arrest. In order of frequency of occurrence in countries where ischaemic heart disease is rare, the cardiac arrest rhythms are as follows. You may see occasional widened complexes, but no pulse can be felt in the femoral artery. Asystole is the terminal event in many severe illnesses, but may be acutely caused by: Septicaemia Hypoxia Excessive vagal tone Electrolyte abnormalities Severe hypotension. There are many causes of this situation and, in the heat of the moment, you have to think clearly. Some of the important causes are: Overdose of anaesthetic agent Hypovolaemia/blood loss Hypoxia (or other ventilation problem) Septic or other toxaemia Pulmonary embolus Cardiac tamponade Tension pneumothorax Hypothermia. If you can withdraw or correct the cause of the arrest (by switching off halothane, increasing intravenous fluids, correcting a problem with the anaesthesia 13 circuit), this will be safer than giving an intravenous bolus of epinephrine. Ventricular fibrillation A coarse or fine jagged line denotes chaotic ventricular activity (Figure 13. Nodal rhythm Atrial fibrillation Pulsus bigeminus: alternate ventricular ectopics Multi-focal ventricular ectopics Ventricular fibrillation Figure 13. No one should be touching the patient or anything that is touching the patient, including the resuscitation bag, as most things conduct electricity. Prognosis is good, especially if the precipitating cause was halothane and epinephrine interaction or hypoxia. Bleeding into body cavities may be apparent only later; for example, when the circulation has been restored and the rise in blood pressure causes more bleeding and a second fall in blood pressure. The cause is usually one of the following: Tachycardia (may be the only sign in a child) Hypovolaemia (bleeding) Thready pulse Sepsis Narrow pulse pressure. Breathlessness and hyperventilation Confusion leading to There may be more than one cause of shock. In hypovolaemic shock, the circulating volume is reduced by loss of blood or other fluid. Rapid fluid replacement, starting with normal saline or Hartmanns solution, should restore the circulation towards normal. In septic shock, the circulating volume may be normal, but blood pressure is low and tissue circulation is inadequate. Support the circulation with volume infusion, but it may not respond as in hypovolaemic shock. Assess the response to stimuli, look at the pupils initially and re-examine them later to follow progress. Look for unequal pupils or other localizing signs that may show intracranial haematoma developing. In many instances, you may attend to and stabilize other systems first and await the return of consciousness as cerebral perfusion and oxygenation improves. The supine unconscious patient with a full stomach is at grave risk of regurgitation and aspiration due to the unprotected airway. However, if a comatose patient has a clear airway and vital signs are normal: Avoid intubation as this will involve drug administration and complicate the subsequent diagnosis Nurse the patient in the recovery position Monitor the airway and await progress and diagnosis (Figure 13. Guidance on further examination and assessment of the trauma patient and on treatment of these conditions is given in the Annex: Primary Trauma Care Manual. It is not possible to give any rigid rule on the lowest permissible value of haemoglobin below which transfusion is necessary or surgery cannot be carried out in a particular case. There is general agreement that a patient can tolerate a haemoglobin concentration well below the traditional value of 10 g/dl. A preoperative value of 7 or 8 g/dl is acceptable without the need for transfusion or making a request for blood. The following factors will make a patient less tolerant of anaemia than this: Significant blood loss anticipated Respiratory, cardiovascular disease or obesity Old age Recent blood loss or surgery. On the other hand, an emergency, actively bleeding case must go for life saving surgery without delay, no matter what the haemoglobin level. A critical haemoglobin concentration is 4 g/dl, below which significant reduction in oxygen consumption starts to occur. Convulsions are dangerous for the sufferer as there is breath-holding, hypoxia, collapse, biting of tongue or other physical damage. Convulsions are usually short lived (although continuous eclamptic fits do occur) and may have stopped by the time an anticonvulsant has been found and given. After a convulsion, most people are disorientated for several minutes or remain in coma. With a struggling baby, you may be There is almost no emergency unable to find a vein. In this case, it may be permissible to give inhalation case that can survive without a halothane or intramuscular ketamine. It is essential that the stomach is empty before starting inhalation induction by mask. This is a well-tolerated procedure and avoids the catastrophe of regurgitation into an unprotected airway. Often the best veins to use in emergencies are: Antecubital fossa Femoral vein Internal jugular vein. At this moment, you have to decide if the needle tip is in the middle of the vein, just entering or just exiting. Go further in with the needle fully inserted, take out the needle and connect the syringe directly to the cannula. Check for free flow of dark blood with no pressure (that is, it is not in the artery) when the final position has been selected. In both cases, the patient should be positioned head down (Trendelenburg position). The ease of successful puncture is directly proportional to the pressure of blood in the internal jugular vein. A patient in hypovolaemic shock should therefore be positioned more head down than one in congestive cardiac failure. The latter may not tolerate a head down position and cannulation can take place on a level bed. Patients suffering cardiac arrest invariably have distended neck veins and internal jugular vein cannulation is fortunately very easy in these crisis circumstances. Usually this point will be around the external jugular vein, which should be avoided. According to the circumstances, it may be appropriate 13 to put some local anaesthesia at the puncture point. If you are right handed, you must stand well over to the left of the patients head to get the correct angle (Figure 13. At this point, fix the syringe and needle with the right hand while using your left hand to slide the cannula with a rotating action into the internal jugular vein as far as it will go. Flow should be fast although it sometimes pauses when the patient breathes in; this respiratory effect is a sign of hypovolaemia and will stop when you have infused more fluid. Even then, you should continue to look for swelling in the neck which will indicate that the cannula has come out of the vein. If the cannula is in an artery, the drip may run at first if the blood pressure is low, but then backs up the giving set with bubbles seen in the bag as the blood pressure returns to normal. A misplaced cannula may be in the soft tissues, giving a swelling after a few minutes, or in the pleural cavity. In the latter case, it is possible to infuse litres of fluid into the pleural cavity by mistake. Using the same patient positioning as above, identify the triangle made by the sternal and clavicular heads of the sternomastoid muscle, left and right, and the clavicle, below. The internal jugular vein runs downwards just below the skin in this triangle, at the lateral side (below the medial edge of the Figure 13. The saphenous vein is the most common site of cutdown and can be used in both adults and children. All that is required is: Small scalpel Artery forceps Scissors Wide bore sterile catheter (a sterile infant feeding tube is one alternative). Make a transverse incision two finger breadths superior and two fingers anterior to the medial malleolus. Use the patients finger breadths to define the incision: this is particularly important in the infant or child. Do not suture the incision closed after catheter removal as the catheter is a foreign body. If purpose-designed intraosseous needles are unavailable, spinal, epidural or bone marrow biopsy needles offer an alternative. The intraosseous 13 route has been used in all age groups, but is generally most successful in children below about six years of age. Veins in babies and neonates Finding a vein in a baby can be one of the most difficult technical feats in the entire spectrum of medical practice as well as one of the most distressing for everyone involved. The anaesthetist usually is called in when everyone else has failed, so there are no easy veins and the child is very distressed by the previous attempts. Preferred approaches are: Back of hand (on the ulnar side) Scalp Ventral surface of wrist (very small veins) Femoral vein Saphenous vein. The saphenous vein is invariably anterior to the medial malleolus, even if it cannot be seen or felt, and a cut down here is possible. Great vein cannulation is difficult in babies because the large head makes the angle difficult. It is not recommended unless no other veins are available, such as after extensive burns. Replace with fluids of a similar volume and composition Add the patients daily the initial resuscitating fluid should be either normal saline (0. These fluids the fluid needed to replace are sometimes referred to as crystalloids. These are starch, Watch carefully for a response gelatin or macro-sugar based solutes dissolved in saline with other electrolytes. They have the osmotic effect of increasing fluid shift from the extravascular into the vascular space (circulating volume), causing a rise in blood pressure. It has no place in the restoration of circulating volume because it is rapidly distributed throughout the entire body water component of about 40 litres. Opinions differ on the volume of crystalloids and colloids that are needed to correct blood and other volume losses from the blood circulation. There are no absolute rules but most authorities agree that you should give about three times the estimated circulation loss as crystalloid fluid. It is far more common for a shocked or dehydrated patient to receive too little intravenous fluid than to receive too much. More important than any rule on the volume of replacement fluids is to observe the patients response to volume infusion. If, in an adult, the blood pressure has not responded to fluid therapy, or if blood loss is continuing after three or four litres of crystalloid, you may consider changing to a colloid infusion. These solutions usually come in 500 ml polythene containers and up to three (total 1500 ml) are usually given. After the above fluid therapy the patient will have been haemodiluted and, depending on any continuing blood loss, may also still be in shock. Recent research and experience has shown that a shocked patient with severe anaemia can still have a favourable outcome, provided blood pressure and circulating volume are maintained. Opinion has therefore moved towards giving volume first as crystalloid/colloid and blood transfusion later. In the case of extreme haemodilution (Hb <4 g/dl), there is a risk of heart failure which might then result in a low blood pressure and/or pulmonary congestion with lung crepitations. Meanwhile, make a rapid assessment of the actual deficit based on body weight, dehydration and continuing circulating volume losses. A 3 kg neonate should have 250 ml circulating blood volume, so the initial intravenous fluid load is about 20% of circulating volume. Recent studies of outcome in paediatric emergencies, especially where sepsis is present, have shown that generous fluid regimes giving up to 80 ml/kg in the first 12 hours, using a mixed crystalloid/colloid regimen, have given the best figures for patient survival. If the fluid runs too fast, the whole bag will be given, leading to a fatal overload. Always use a burette giving set; if you do not have a burette, use a syringe to inject measured volumes. Finally, closely watch the neck veins and the eyes, looking for signs of over transfusion. If the child was dehydrated with reduced skin turgor, this should have been corrected by fluid therapy. If hourly urine output is needed, insert a urinary catheter or, if there is no catheter, make sure you take account of urinary bladder filling by palpating and percussing the bladder before deciding on further fluid therapy. When giving blood for replacement in paediatric anaesthesia, the rate of flow is often less than you want, even with a pressure infuser, because the cannula is so small. A slow running drip overnight is the commonest reason for a dead patient in the morning. If the patient is in shock, you should give fluids as fast as the drip will run until the blood pressure responds, then reassess the 13 rate of flow. If the drip runs too slowly, either a pressure infuser bag may be needed to push it in, or a second drip. If you are supervising a fast running drip, with a continuous stream through the chamber, you must stay beside the patient until the flow rate can be slowed to a rate that is more usual on a ward with normal nursing supervision. A patient on the ward with a drip will usually be given 3 litres per day as a standard regime. Assume this will happen and make it absolutely clear to ward staff if you want some other regime. Depending on circumstances (such as if the patient is chronically dehydrated or debilitated), it may be preferable to get the blood pressure up to about 90 mmHg systolic over an hour or so before going into the operating room. On the other hand, an actively bleeding patient (for example, from a ruptured uterus, bleeding peptic ulcer, oesophageal varices, ruptured ectopic pregnancy, severed artery or other severe trauma) should have volume replacement, ketamine anaesthesia, tracheal intubation and surgery all at the same time. In severe haemorrhage, control of bleeding is the first priority, whatever the blood pressure or haemoglobin. If blood is haemorrhaging from one end of a patient, there is little point in pouring fluids in at the other end in the expectation that the blood pressure will come up. The only option is to rush the patient to the operating room and get surgical haemostasis. The only treatment for the non-breathing patient is to inflate the lungs mechanically, preferably with a resuscitation bag and mask or a tracheal tube. If you cannot decide whether to give a relaxant to intubate an unstable patient 13 who might deteriorate, think about the other conditions present and talk to the health care personnel looking after these complications to find out the next steps in their management plan. You should, however, bear in mind the side effects of suxamethonium, such as hyperkalaemia, a possible contribution to cardiac arrest. A potentially difficult airway (such as after severe facial trauma or soft tissue swelling) will make suxamethonium very hazardous: failure to intubate will mean certain death almost on the end of the needle seconds later. Drugs in resuscitation (adult doses) Drug Indication/action Dose Epinephrine Cardiac arrest 0. This is the standard dose for any cardiac arrest and also where the cause and/or rhythm are unknown. If you have any doubt that the needle or cannula is in the vein, dilute the 1 ml ampoule in 10 ml saline. For severe hypotension, provided circulating volume has been restored: Dilute 1 mg in 10 ml saline Give doses of 0. Epinephrine should be given as close to the heart as possible, such as into the internal jugular vein, while external cardiac massage is going on. This is to get the drug to the place where it is going to have an effect: the myocardium. Intra-cardiac epinephrine is not recommended, even as a final measure when all else has failed. Give atropine before epinephrine if: You see a severe bradycardia 13 You suspect excessive vagal tone as a cause (unusual) of asystole. Vasoconstrictors are sometimes used in septic shock, but usually with limited effect. Calcium chloride 10 mg in 10 ml during a cardiac arrest may be used to promote the effects of adrenaline and improve myocardial contractility. They can be used in conjunction with vasodilators such as hydralazine, nitrates and calcium blockers.
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No part of it may be reproduced, stored in a retrieval system, or transmitted in any frm or by any means, electronic, mechanical, photocopying, recording or otherwise, without written permission fom the copyright owner. Despite our best eforts t proofead and edit, mistakes ofn slip 1) Write in a conversational style frrapid assimiation. The most usefl is the Gram stain, which separates organisms into 2 groups: gram-positive bugs and gram-negative bugs. This stain also allows the I clinician to determine whether the organism is round or aa rod-shaped. Both gram-positive and gram-negative organisms 3) Wash of with water and then "decolorze" with have more than 1 layer protecting their cytoplasm and 95% alcohol. The layerjust outside the bacterial cytoplasmic membrane Wen the slide is studied microscopically, cells that is the peptidoglycan layer or cell wall. It is present absorb the crystal violet and hold onto it will appear in both gram-positive and gram-negative organisms. The peptidoglycan layer or cell wall is these cells will absorb the safanin and appear red. The antibiotic penicillin binds to the diferent stains are the result ofdiferences inthe and inhibits this enzyme. For this reason the enzyme is cell walls of gram-positive and gram-negative bacteria. The bacteral cytoplasmic membrane (unlike that of animals) has no cholesterol or other sterols. The gram-negative cell envelope has 3 layers, Figre 1-3 not including the periplasmic space. Gram-negative bacteria have a cell wall composed of complex cross-linked peptidoglycan, periplasmic space between the cytoplasmic membrane teichoic acid, polysaccharides, and other proteins. This lipoprotein is important because it orignates fom the peptidoglycan layer and extends outward to bind the unique third outer membrane. Ths part is called the 0-specifc side chain or the staining is a large dye complex that is trapped in the 0-antigen. Bacteria have 4 major shapes: Embedded in the gram-negative outer membrane are 1) Cocci: spherical. Axial fagella come out of the ends of the spirochete cell wall, but rather than protrude out ofthe outer membrane (like other bacteria shown in Figure 2-1), the fagella run sideways along the spirochete under the outer membrane sheath. Rotation of these periplasmic fagella spins the Ofthe gram-positives, 3 are cocci, and the other 4 are spirochete around and generates thrust, propelling rod-shaped (bacilli). The 3 gram-positive cocci both have the word coccus 3) Mycoplasma do not have a cell wall. Two important properties include: Bacterial ribosomes consist of 2 subunits, a large 1) how the organism deals with oxygen, and 2) what the subunit (50S) and a small subunit (30S). Antibiotics, such as properties include the diferent metabolic end-products eryhromycin and tetracycline, have been developed that bacteria produce such as acid and gas. There are 3 enzymes have the faculty to be anaerobic but prefer aerobic that some bacteria possess to break down these oxygen conditions. This is similar to the switch to anaerobic products: glycolysis that human muscle cells undergo during sprinting. One of these is an anaerobic growth media with Bacteria are classifed on a continuum. The oxygen spectrum ofthe major bacterial site end are bacteria which have no enzymes and pretty groups. Of the organisms Respiration is used with the aerobic and fcultative that use chemical sources, those that use inorganic anaerobic organisms. Others use organic carbon sources and port chain coupled with oxidative phosphorylation. These bacteria Ferentation (glycolysis) is used by many bacteria live in their host cell and cannot survive without fr oxygen metabolism. Lactic acid, ethanol, propionc acid, butyric acid, discussed in the chapters covering specifc organisms. This causes the ofcertain cell structures and on bacterial exotoxins and bacterial fagella to undulate in a coordinated manner endotoxins, all of which are virulence fctors. The basal body spans through fagella run sideways along the spirochete under their the entire cell wall, binding to the inner and outer cell unique outer membrane sheath. These specialized membrane in gram-negative bacteria and to the inner fagella are called periplasmic fagella. For example,Neisseriagonorrhea has pili that allow it to bind to cercal cells and buccal cells to cause gonorrhea. Escherichia coli and Campylobacterjejuni cannot cause diarrhea without their adhesins to bind to the intestinal epithelium, and Bordetella pertussis uses its adhesin to bind to ciliated respiratory cells and cause whooping cough. Bacteria that do not produce these pili cannot grab hold of their victim; they lose their virulence and thus cannot infct humans. Figre 2-2 Capsules these periplasmic fagella spins the spirochete around Capsules are protective walls that surround the and generates thrust, propelling them frward. One bacterium, Bacillus anthracis, is unique in that its capsule is made up of amino acid residues. Capsules enable bacteria to be more virulent because macrophages and neutrophils are unable to phagocytize the encapsulated buggers. When grown on media, these encapsulated bacteria appear as smooth (S) colonies that cause rapid death when injected into mice. These rough colonies have lost their virulence and when injected into mice do not cause death. A vaccine against Streptococcus bodies bind, the capsule swells with water, and this can pneumoniae contains antigens fom the 23 most common be visualized microscopically. Bioflms A bioflm is an extracellular polysaccharide network, similar to the capsule polysaccharides, that frms a mechanical scafold around bactera. The bioflm allows bactera to bind to prosthetic devces, like intravenous catheters, and protects them fom attack by antibiotics and the immune system. Staphylococcus epidermidis ofen frms bioflms on intravascular catheters and leaches out to cause bacteremia and catheter related sepsis. Imagine bacteria secreting their polysaccharide concrete around themselves t fr a biologcal bunker. The most efective way to cure an infection involving a prosthetic devce is to remove the device. Salmonella tphi the production of antibodies that protect the individual against fture infctions by this organism. Bruce/la Endospores are frmed by only 2 genera ofbacteria, both of which are gram-positive: the aerobic Bacillus 6. Endospores are metabolically dormant frms ofbacteria that are resistant to heat (boiling), cold, drying 8. One of these subunits Exotoxins (called B fr binding or H fr holding on) binds to the target cell. The other subunit (called A fr action Exotoxins are proteins that are released by both or L fr laser) then enters the cell and exerts the gram-positive and gram-negative bacteria. Picture these subunits as a key (B and H) and a gn (A and L) bound together by disulfde released by most of the major gram-positives. The key opens the cell, and then the gun does negative bacteria such as Vibrio cholera, Escherichia its damage. Remember fom the last chapter that endotoxin is Neurotoxins are exotoxins that act on the nerves or lipid A, which is a piece of the outer membrane motor endplates to cause paralysis. Endotoxin is also shed in steady inhibit NaCl resorption, activate NaCl secretion, or amounts fom living bacteria. The enterotoxins cause 2 disease the bacteria are lysed, releasing large quantities of manifstations: endotoxin. The diarrhea will continue until the bacteria that sort of sheds of, especially during lysis. Septic Shock 2) Food poisoning: Bacteria grow in fod and release enterotoxin in the fod. Septic shock: Sepsis that results in dangerous drops in blood pressure and organ dysfnction is called septic. May be responsible for hemolyic uremic syndrome absorption of fluid and electrolytes from the intestinal 3. Inhibits protein synthesis in a manner analogous to tract the antiribosomal antibiotics (erythromycin, tetracycline, etc. This toxin stimulates the macrophage to release tumor necrosis factor alpha and interleukin-1Beta, which contributes to death in anthrax. Pertussis toxin B Subunit bindsto target cells B Subunit: bindsto target cells A Subunit activates membrane G proteins A Subunit: inhibits phagocytosis to activate membrane bound adenylate 2. Extracytoplasmic adenylate cyclase: Similar epithelial cells to Bacilus anthracis edema factor, which 4. These cells, in response to the stimulus, the mortality rate fr septic shock is high: up to 40% release a host of proteins that are refrred to as of patients will die, even with intensive care and endogenous mediators of sepsis. For every organ system that fils the most fmous endogenous mediator of sepsis is the mortality rises. For each ing a wasting (weight loss) syndrome, called cachexia, additional organ filure (renal filure, etc. Ann Intern Med 1990; 113: matory agents such as ibuprofen and steroids, and a 227-42.
However treatment question generic disulfiram 500mg amex, with increased ability to safely characterize viruses treatment goals for depression order disulfiram online from canada, the relationship to other disease-causing arboviruses can be established with reduced exposure to the investigators medications hyperkalemia discount disulfiram 500 mg with amex. One criterion for a newly identifed arbovirus is a thorough description of how the virus will be handled and investigated 897 treatment plant rd buy disulfiram 250mg without prescription. For example treatment junctional rhythm best order disulfiram, experiments involving pure genetic analysis could be handled differently than those where the virus will be put into animals or arthropods treatment interstitial cystitis disulfiram 250mg line. While variable pathogenicity occurs frequently with naturally identifed strains medicine 5113 v buy disulfiram no prescription, it is of particular note for strains that are modifed in the laboratory symptoms 0f colon cancer order 500mg disulfiram overnight delivery. Chimeric, full-length viruses and truncated replicons have been constructed from numerous alphaviruses and faviviruses. For example, alphavirus replicons encoding foreign genes have been used Agent Summary Statements: Arboviruses and Related Zoonotic Viruses 239 widely as immunogens against bunyavirus, flovirus, arenavirus, and other antigens. These replicons have been safe and usually immunogenic in rodent hosts leading to their development as candidate human vaccines against several virus groups including retroviruses. This minimizes the possibility of mutations that could alter virulence properties. Because some chimeric strains incorporate genomic segments lacking gene regions or genetic elements critical for virulence, there may be limited possibility of laboratory recombination to generate strains exhibiting wild-type virulence. The attenuation of all chimeric strains should be verifed using the most rigorouscontainment requirements of the parental strains. The virus was frst isolated from a febrile adult woman in the West Nile District of Uganda in 1937. Virus amplifcation occurs during periods of adult mosquito blood feeding by continuous transmission between mosquito vectors and bird reservoir hosts. All three viruses can cause encephalitis often accompanied by long-term neurological sequelae. The classical epizootic varieties of the virus are not present in the United States. The primary laboratory hazards are parenteral inoculation, contact of the virus with broken skin or mucus membranes, bites of infected animals or arthropods, or aerosol inhalation. The largest of these was in 1977 to 1979 in Egypt with many thousands of human cases and 610 reported deaths. Hemorrhagic fever develops as the primary illness proceeds and is characterized by disseminated intravascular coagulation and hepatitis. Infected sheep and cattle suffer a mortality rate of 10-35%, and spontaneous abortion occurs virtually in all pregnant females. It is currently believed that the virus passes dry seasons in the ova of food-water Aedes mosquitoes. The vertebrate amplifers are usually sheep and cattle, with two caveats; as yet undefned native African vertebrate amplifer is thought to exist and very high viremias in humans are thought to play some role in viral amplifcations. Large numbers of infectious virus also are generated in cell cultures and laboratory animals. Agent Summary Statements: Arboviruses and Related Zoonotic Viruses-References 265 5. Vaccination of macaques against pathogenic simian immunodefciency virus with Venezuelan equine encephalitis virus replicon particles. Clinical proof of principle for ChimeriVax: recombinant live attenuated vaccines against favivirus infections. Isolation from human sera in Egypt of a virus apparently identical to West Nile virus. Rift valley fever: a report of three cases of laboratory infection and the experimental transmission of the disease to ferrets. The heavy chain enhances cell binding and translocation of the catalytic light chain across the vesicular membrane. Four of the serotypes (A, B, E and, less commonly, F) are responsible for most human poisoning through contaminated food, wound infection, or infant botulism, whereas livestock may be at greater risk for poisoning with serotypes B, C1 and D. Diagnosis of Laboratory Exposures Botulism is primarily clinically diagnosed through physician observations of signs and symptoms that are similar for all serotypes and all routes of intoxication. Laboratory Safety and Containment Recommendations Solutions of sodium hypochlorite (0. The intoxications were relatively mild, and all affected individuals recovered after a week of hospitalization. At higher exposure levels, intoxication progresses to hypovolemia, dehydration, vasodilatation in the kidneys, and lethal shock. The A-chain is an N-glycosidase enzyme and a potent inhibitor of protein synthesis, whereas the B-chain is a relatively non-toxic lectin that facilitates toxin binding and internalization to target cells. The latency period progresses rapidly to severe pulmonary distress, depending upon the exposure level. Most of the pathology occurs in the lung and upper respiratory tract, including infammation, bloody sputum, and pulmonary edema. Gastric ingestion of ricin causes nausea, vomiting, diarrhea, abdominal cramps and dehydration. Initial symptoms may appear more rapidly following gastric ingestion (1-5 h), but generally require exposure to much higher levels of toxin compared with the inhalation route. Following intramuscular injection of ricin, symptoms may persist for days and include nausea, vomiting, anorexia, and high fever. The site of ricin injection typically shows signs of infammation with marked swelling and induration. One case of poisoning by ricin injection resulted in fever, vomiting, irregular blood pressure, and death by vascular collapse after a period of several days; it is unclear in this case if the toxin was deposited intramuscularly or in the bloodstream. Additional supportive clinical or diagnostic features, after aerosol exposure to ricin, may include the following: bilateral infltrates on chest radiographs, arterial hypoxemia, neutrophilic leukocytosis, and a bronchial aspirate rich in protein. Precautions should be extended to handling potentially contaminated clinical, diagnostic and post-mortem samples because Agent Summary Statements: Toxin Agents 273 ricin may retain toxicity in the lesion fuids, respiratory secretions, or unfxed tissues of exposed animals. Laboratory coat, gloves, and full-face respirator should be worn if there is a potential for creating a toxin aerosol. Symptoms of human ingestion are expected to Agent Summary Statements: Toxin Agents 275 include paresthesias of the face, throat and fngers or toes, followed by dizziness, chills, muscle pains, nausea, gastroenteritis, and reduced heart rate. Metabolites of several marine toxins, including saxitoxin, tetrodotoxin, and brevetoxins, are well-studied as part of routine regulation of food supplies. Environmental and clinical samples can be tested using a gas liquid chromatography-mass spectrometry technique. Laboratory Safety and Containment Recommendations General considerations for the safe use and inactivation of toxins of biological origin are found in Appendix I. Special emphasis, therefore, must be placed upon proper decontamination of work surfaces and equipment. The use of respiratory protection should be considered if potential aerosolization of toxin exists. Effcacy of prophylactic and therapeutic administration of antitoxin for inhalation botulism. Tetrodotoxin, saxitoxin and their signifcance in the study of excitation phenomena. The only clear risk factor for disease transmission is the consumption of infected tissues such as human brain in the case of kuru, and meat including nervous tissue in the case of bovine spongiform encephalopathy and related diseases such as feline spongiform encephalopathy. After cross-species infection there is often a gradual adaptation of specifcity for the new host; however, infectivity for the original host may also be propagated for several passages over a time-span of years. The process of cross-species adaptation can also vary among individuals in the same species and the rate of adaptation and the fnal species specifcity is diffcult to predict with accuracy. Such considerations help to form the basis for the biosafety classifcation of different prions. However, when a prion from one species is inoculated into another the resultant infected animal should be treated according to the guidelines applying to the source of the inoculum. Although the exact mechanism of spread of scrapie among sheep and goats developing natural scrapie is unknown, there is considerable evidence that one of the primary sources is oral inoculation with placental membranes from infected ewes. However, the human prion diseases in this setting 284 Biosafety in Microbiological and Biomedical Laboratories are not communicable or contagious. Special Issues Inactivation of Prions Prions are characterized by resistance to conventional inactivation procedures including irradiation, boiling, dry heat, and chemicals (formalin, betapropiolactone, alcohols). The use of conventional autoclaves as the sole treatment has not resulted in complete inactivation of prions. Some investigators recommend that formalin-fxed tissues from suspected cases of prion disease be immersed for 30 min in 96% formic acid or phenol before histopathologic processing (Table 9), but such treatment may severely distort the microscopic neuropathology. The safest and most unambiguous method for ensuring that there is no risk of residual infectivity on contaminated instruments and other materials is to discard and destroy them by incineration. The highest concentrations of prions are in the central nervous system and its coverings. It is further strongly recommended that impervious gloves be worn for activities that provide the opportunity for skin contact with infectious tissues and fuids. Medical waste incinerators should comply with applicable state and federal regulations. Gloves, embedding molds, and all handling materials are disposed s regulated medical waste. Handling and processing of tissues from patients with suspected prion disease the special characteristics of work with prions require particular attention to the facilities, equipment, policies, and procedures involved. Rinse instruments with water, transfer to open pan and autoclave at 121C (gravity displacement) or 134C (porous load) for 1 hour. Transmissible spongiform encephalopathies in non-domestic animals: origin, transmission and risk factors. For example, high-speed blenders designed to reduce aerosol generation, needle-locking syringes, micro burners and safety centrifuge cups or sealed rotors are among the engineered devices that protect laboratory workers from biological hazards. An important piece of safety equipment is the biological safety cabinet in which manipulations of infectious microorganisms are performed. Therefore, these cubicles could not be used for handling infectious agents because the worker was in a contaminated air stream. To protect the worker during manipulations of infectious agents, a small workstation was needed that could be installed in existing laboratories with minimum modifcation to the room. They were characterized by mass airfow into the cabinets albeit with widely varying air volumes across openings. However, since the air was unfltered, the cabinet was contaminated with environmental microorganisms and other undesirable particulate matter. The flter medium is pleated to increase the overall surface area inside the flter frames and the pleats are often divided by corrugated aluminum separators (Figure 1). Depending on the confguration of these flters and the direction of the airfow, varying degrees of personnel, environmental and product protection can be achieved. Airfow is drawn into the front grille of Appendix A: Biological Safety Cabinets 293 the cabinet, providing personnel protection. Airfow provided in this manner reduces turbulence in the work zone and minimizes the potential for cross-contamination. The downward moving air splits as it approaches the work surface; the fan6 draws part of the air to the front grille and the remainder to the rear grille. The air is drawn through the front and rear grilles by a fan pushed into the space between the supply and exhaust flters. However, it must be done in a manner that does not alter the balance of the cabinet exhaust system, thereby disturbing the internal cabinet airfow. The proper method of connecting a Type A1 or A2 cabinet to the building exhaust system is through use of a canopy hood,8,10 which provides a small opening or air gap (usually 1 inch) around the cabinet exhaust flter housing (Figure 4). The airfow of the building exhaust must be suffcient to maintain the fow of room air into the gap between the canopy unit and the flter housing. The canopy must be removable or be designed to allow for operational testing of the cabinet. Carcinogens used in cell culture or microbial systems require both biological and chemical containment. This particulate-free air fows upward through a plenum at each side of the cabinet and then downward to the work area through a backpressure plate. As with the Type A1 and A2 cabinets, there is a split in the down-fowing air stream just above the work surface. Since this feature is not supplied by all cabinet manufacturers, it is prudent to install a sensor such as a fow monitor and alarm in the exhaust system as necessary. This cabinet provides simultaneous primary biological and chemical (small quantity) containment. The higher static air pressure required to operate this cabinet also results in additional costs associated with heavier gauge ductwork and higher capacity exhaust fan. All positive pressure contaminated plenums within the cabinet are surrounded by a negative air pressure plenum thus ensuring that any leakage from a contaminated plenum will be drawn into the cabinet and not released to the environment. For example, the front sash can be modifed by the manufacturer to accommodate the eyepieces of a microscope. Access for passage of materials into the cabinet is through a dunk tank, that is accessible through the cabinet foor, or double-door pass-through box. In order to determine the greatest chemical concentration, which might be entrained in the air stream following an accident or spill, it is necessary 298 Biosafety in Microbiological and Biomedical Laboratories to evaluate the quantities to be used. Moving arms in and out slowly, perpendicular to the face opening of the cabinet will reduce this risk. This allows the cabinet to stabilize, to air sweep the hands and arms, and to allow time for turbulence reduction. If the cabinet has been shut down, the blowers should be operated at least four minutes before beginning work to allow the cabinet to purge. The correct sash position (usually 8or 10above the base of the opening) should be indicated on the front of the cabinet. The frequent inward/outward movement needed to place objects in these containers is disruptive to the integrity of the cabinet air barrier and can compromise both personnel and product protection. Materials and supplies should be placed in the cabinet in such a way as to limit the movement of dirty items over clean ones. Investigators working with Petri dishes and tissue culture plates should hold the lid above the open sterile surface to minimize direct impaction of downward air. Open fames are not required in the near microbe-free environment of a biological safety cabinet. Inactivation of aspirated materials can be accomplished by placing suffcient chemical decontamination solution into the fask to inactivate the microorganisms as they are collected. Items should be introduced into the pan with minimum splatter and allowed appropriate contact time as per manufacturers instructions. It is a prudent practice to decontaminate the exterior surface of bags and pans just prior to removal from the cabinet. At the end of the workday, the fnal surface decontamination of the cabinet should include a wipe-down of the work surface, the cabinets sides and back and the interior of the glass. Any splatter onto items within the cabinet, as well as the cabinet interior, should be immediately cleaned up with a towel dampened with an appropriate decontaminating solution. Spills large enough to result in liquids fowing through the front or rear grilles require decontamination that is more extensive. The spilled fuid and disinfectant solution on the work surface should be absorbed with paper towels and discarded into a biohazard bag. A hose barb and fexible tube should be attached to the drain valve and be of suffcient length to allow the open end to be submerged in the disinfectant within the collection vessel. Periodic removal of the cabinetwork surface and/or grilles after the completion of drain pan decontamination may be justifed because of dirty drain pan surfaces and grilles, which ultimately could occlude the drain valve or block airfow. However, extreme caution should be observed on wiping these surfaces to avoid injury 304 Biosafety in Microbiological and Biomedical Laboratories from broken glass that may be present and sharp metal edges. The most common decontamination method uses formaldehyde gas, although more recently, hydrogen peroxide vapor21 and chlorine dioxide gas have been used successfully. Whenever possible, adequate clearance should be provided behind and on each side of the cabinet to allow easy access for maintenance and to ensure that the cabinet air re-circulated to the laboratory is not hindered. Note, however, that this requirement must be identifed at the time of purchase and installation; a bag-in/bag-out assembly cannot be added to a cabinet after the-fact without an extensive engineering evaluation. If in-house personnel are performing the certifcations, then these individuals should become accredited. Table 4 indicates where to fnd information regarding the conduct of selected tests. The purpose and acceptance level of the operational tests (Table 3) ensure the balance of infow and exhaust air, the distribution of air onto the work surface, and the integrity of the cabinet and the flters. Airfow Smoke Patterns Test: this test is performed to determine if: 1) the airfow along the entire perimeter of the work access opening is inward; 2) if airfow within the work area is downward with no dead spots or refuxing; 3) if ambient air passes onto or over the work surface; and 4) if there is no escape to the outside of the cabinet at the sides and top of the window. The aerosol is generated on the intake side of the flter and particles passing through the flter or around the seal are measured with a photometer on the discharge side. Cabinet integrity can also be checked using the bubble test; liquid soap can be spread along welds, gaskets and penetrations to visualize air leaks that may occur. It is appropriate to request the calibration information for the test equipment being used by the certifer. A Required for proper certifcation if the cabinet is new, has been moved or panels have been removed for maintenance. Note: There is a 1 gap between the canopy unit (D) and the exhaust flter housing (C), through which room air is exhausted. One method to protect a house vacuum system during aspiration of infectious fuids. The left suction fask (A) is used to collect the contaminated fuids into a suitable decontamination solution; the right fask (B) serves as a fuid overfow collection vessel. A bag-in-bag-out flter enclosure allows for the removal of the contaminated flter without worker exposure.
Aphasia is a relatively frequent condition and the amount of references throughout recent human history to the loss of speech associated with brain disorders and head injuries symptoms gallstones cheap 500 mg disulfiram fast delivery, is not surprising medications erectile dysfunction purchase disulfiram 500mg otc. Goldstein (1917) 86 treatment ideas practical strategies disulfiram 250 mg lowest price, Head (1926) medicine 75 yellow buy 250 mg disulfiram otc, and Nielsen (1936 medications mexico discount disulfiram 500 mg visa, 1938) are just some of the many clinicians that approached the question of aphasia rehabilitation during this time medicine rocks state park purchase cheap disulfiram. During the time of the war treatment yeast uti cheap 500mg disulfiram with amex, Luria was working in a rehabilitation hospital in the Urals (Russia); he had the specific goal of developing rehabilitation procedures for war-wounded soldiers 4d medications buy cheap disulfiram 250mg line. During the following years, this book was translated to many different languages and became a milestone, not only for language rehabilitation, but also for cognitive rehabilitation in general. Interest in aphasia recovery and rehabilitation has continued growing to the present day. Stages of language recovery After a pathological brain condition, some recovery is expected. This recovery, observed without the application of any language intervention techniques, is known as spontaneous recovery (Figure 11. Of course, spontaneous recovery is only observed after a stroke, a traumatic Aphasia Handbook 190 brain injury, or another static condition; when aphasia is due to a progressive condition, such as a brain tumor or a degenerative disease, no spontaneous recovery is observed. Two stages in spontaneous recovery are usually distinguished (Kertesz, 1988; Lomas & Kertesz, 1978): Stage 1 (early recovery) It refers to the rapid recovery observed during the initial weeks and month after the aphasia onset. Indeed, most of the spontaneous recovery is observed during the initial 3 months following the pathological brain condition. It has been assumed that some neurophysiological processes (such edema decrease, disappearance of hemorrhages, etc. An association between early recovery of spoken word comprehension and reperfusion (restoration of blood flow) of Wernickes area has been demonstrated in stroke aphasia patients (Hillis & Heidler, 2010). Stage 2 (late recovery) Language continues improving during the following months, but recovery is progressively slower and slower. It is usually accepted that after about 2-3 years, no further spontaneous recovery is observed. Relearning and reorganization of the language in the brain are considered the two basic mechanisms accounting for this late language recovery. Factors affecting recovery Aphasia Handbook 191 Various factors affect language recovery in aphasia. Some of them can be regarded as major factors, whereas others represent secondary factors. Lesion site Lesion site is associated with aphasia type; this means that left temporal lobe damage will result in a Wernickes-type aphasia, and a left posterior frontal pathology will be associated with a Brocas-type aphasia. Lesion size the association between language recovery and lesion size is obvious: the smaller the lesion, the milder the language defect and the larger the remaining intact brain tissue that can be used to re-learn and compensate the language deficit. Conversely, the larger the lesion, the greater the language defect and the smaller the remaining intact brain that can be used to re-learn and compensate the language deficit. Age Frequently, it has been assumed that children recover more rapidly than adults suffering from the same type of brain lesion; this assumption is known as the Kennard principle (Kennard, 1936). According to the Kennard Principle, there is a negative linear relation between age at brain injury and functional outcome. Other things being equal, the younger the lesioned organism, the better the outcome (Maureen, 2010; page 1043). Etiology Aphasia recovery tends to be better in the case of traumatic head injury than in cerebrovascular accidents. Aphasia associated with tumors is variable and recovery depends on the specific type of tumor. Recovery after tumor removal may be excellent in a usually benign tumor, such as meningioma. Recovery, however, is associated not only with the type of tumor, but also with other factors such as size, location, patients age, etc. In general, the larger the brain damage, the more severe the aphasia and the lesser the expected recovery. Some types of aphasia are considered to be very limited in their recovery; for instance, recovery in Brocas aphasia is frequently very modest. Furthermore, aphasia profile may change over time; for instance, a Wernickes aphasia can become an anomia. Temporal factors Temporal factors refer to the speed of the pathological process. Time from onset It is known that in aphasia, language therapy should begin as soon as possible. It is generally accepted that the sooner it begins, the better the recovery will be. During some time it was (wrongly) assumed that 2-3 years after the aphasia onset, the observed language defects were permanent and aphasia therapy was no longer effective. Handedness Frequently, it is assumed that left-handers as a group have a more bilateral representation of language; because of this more bilateral representation, language recovery in cases of aphasia is more rapid and more complete. Basso (1992) presents an extensive review of prognostic factor in aphasia recovery; she concludes that handedness and gender play just a minor role in recovery from aphasia Gender the influence of gender on aphasia recovery has been controversial. Assuming that females have a more bilateral representation of language, it has been suggested that they present a better aphasia recovery. Although no initial difference was found in severity of language disorders between sexes, females within the global aphasic group showed significantly greater improvement in three tests of language comprehension. It was suggested then that more bilateral representation of language functions in the female brain may account for this greater improvement. Treatment the effect of aphasia treatment represents a major factor affecting recovery. Motivation and personality It has been suggested that motivation and personality play a crucial role in aphasia recovery. For example, people used to reading will be especially motivated to recover their reading ability in the case of alexia. Associated disorders Aphasia is frequently associated with a diversity of disorders, such as hemiparesis, apraxia, acalculia, agnosia, amnesia, etc. Of course, a patient with hemiparesis (or other disorders) will have more limitations, and hence the recovery can be slower and the therapy harder to administer. Aphasia Handbook 193 Effects of therapy It has been well established that aphasia therapy results in a higher performance on diverse language tests at every moment of the aphasia evolution (Figure 11. In a pioneer study Basso et al (1979) selected 281 aphasics (162 reeducated and 119 controls); they were subjected to a second examination no less than six months after the first. Presence or absence of rehabilitation between first and subsequent examination was studied. It was found that rehabilitation had a significant positive effect on improvement in all language skills. This study was particularly important because of the large sample of participants; taking into consideration the size of the sample, potential confounding variables capable of affecting the results were randomly distributed. This positive effect of language therapy has been extensively corroborated using different methods. Brain damage symptoms Goldstein (1948) defines two types of symptoms observed after a brain pathological condition: 1. They represent a direct consequence of the brain damage; for example, word-finding difficulties due to pathology in the posterior left temporal lobe. They are affected by the previous personality and current environmental conditions. For instance, people with language understanding difficulties frequently attempt to pay an increased attention to some secondary information such as the gestures, the face expressions, and the lip movements. It is presumed that recovery is due to two major mechanisms: relearning (re-training) and compensatory techniques (reorganization of the functional system) (Levin & Grafman, 2000; Luria, 1980). Re-learning (re-training) Regardless of the brain damage, language can be re-learned to some extent. It is likely that homologous areas of the contralateral (right) hemisphere participate in this relearning process (Raboyeau et al. It has been observed that the practice in of ability (language or other) results in an increase in the size of the cortical brain area involved in that particular ability (Levin & Grafman, 2000). Compensatory techniques (reorganization of the functional system) this means that an alternative way to process the information is used to perform the task. The possibility of using alternative strategies is a consequence of the brains plasticity. For instance, the aphasic patient can use speech prosody in an extended way to communicate (prosody is potentially preserved in cases of aphasia; it is more related to the right hemisphere activity; Ross & Monnot, 2008; and prosody production and understanding are impaired in cases of right hemisphere pathology). Rehabilitation Goals A rehabilitation program for aphasia, as a matter of fact, has different goals. They can be summarized in the following five points: To keep the patient verbally active this is the basic rule in any type of rehabilitation: keep the patient active. Frequently, because of the communication difficulties, there is a certain tendency to verbally isolate the aphasic patient. If the aphasic patient is not intensively exposed to language, and is not required to practice in a continuous way, recovery will be limited. To re-learn language To a significant extent, therapy is directed at re-learning language. Regardless of age, and the abnormal brain condition, it is still possible to at least learn some language. This re-learning process has to follow a specific sequence: from the simpler to the more complex. To provide strategies to improve language Linguistic abilities can improve if certain strategies are used. These strategies depend on the particular type of aphasia and the specific conditions of the patient. For instance, so called Aphasia Handbook 195 Melodic Intonation Therapy (Albert et al. To teach the family to improve communication Language is used to communicate in different social contexts, but family represents the major and most significant communication context, particularly for an individual with some limitations. One major function of the speech/language therapist is to explain to the family how to maximize the effectiveness of communication with the patient. Communication with somebody capable of understanding them (the therapist) becomes particularly important and reinforcing. By the same token, the patient usually has important questions about the future (What is going to happen All of these difficulties and conflicts can be reflected in the rehabilitation context. Summary the recovery of language after a pathological brain condition is a question that has interested health professional for a long time. This recovery observed without the application of any language intervention technique is known as spontaneous recovery. There is a series of factors that have proven to affect recovery, including lesion site, size, age, etiology, aphasia profile, temporal factors, time from onset, handedness, gender, treatment, motivation and personality, and associated disorders. Two types of symptoms have been described after a brain pathological condition: direct and indirect. It is assumed that recovery is due to two major mechanisms: re-learning (re-training), and compensatory techniques (reorganization of the functional system). A rehabilitation program for aphasia has different goals, including: to keep the patient verbally active, to re-learn language, to provide strategies to improve language, to teach the family to improve communication, and to provide psychological support to the patient. Clinical remarks on cases of defects of expression (by words, writing, signs, etc) in diseases of the nervous system. Waxman (ed), Advances in Neurology, vol 47: Functional recovery in neurological diseases. Spontaneous recovery of language in patients with aphasia between 4 and 34 weeks after stroke. Patterns of spontaneous recovery in aphasic groups: a study of adult stroke patients. Right hemisphere activation in recovery from aphasia: lesion effect or function recruitment Neurology of affective prosody and its functional anatomic organization in right hemisphere. Aphasia Handbook 198 Chapter 12 Aphasia rehabilitation Introduction Patients with aphasia may present some spontaneous language improvement (so called spontaneous recovery), but systematic therapeutic programs can significantly contribute to a more rapid and complete language recovery. During the last decades, it has been observed that an increased number of aphasia patients have had the opportunity to participate in rehabilitation programs; this situation has resulted in a better quality of life for a significant number of aphasic individuals. Unfortunately, however, there are still many aphasic patients that, due to a range of conditions, cannot attend language therapeutic programs; language recovery for them is more limited, and the quality of life is somehow lower. By the same token, research in aphasia rehabilitation has significantly grown during the last decades. New research has contributed not only to having a better understanding of the rehabilitation processes, but has also proposed new avenues to treat speech and language disorders associated with brain pathology. New technological advances, such as contemporary neuroimaging techniques, have significantly increased our insight of the neurological processes underlying language recovery in aphasia. It can be anticipated that this interest in aphasia rehabilitation will continue growing toward the future. In this chapter some major general guidelines in aphasia rehabilitation will be analyzed. An attempt to integrate contemporary approaches to aphasia rehabilitation (Albert et al. Obviously, the starting point for any rehabilitation program is a good language evaluation in order to pinpoint the specific language components impaired in the patient. Rehabilitation programs should be tailored to the specific linguistic needs of each patient. However, it can be considered that language includes two major dimensions: lexical and grammatical (Ardila, 2011, 2012). The first one is mostly impaired in the sensory aphasias, whereas a disturbance of the second one is characteristic of Brocas aphasia. Basso (2003) specifically analyzes the rehabilitation of each one of these two language levels. Her rehabilitation strategies for each one of these components are presented below. Rehabilitation of lexical and sentence disorders Different specific components of the language lexicon can be distinguished (auditory analysis, word identification, semantics associations, etc. However, many components and/or processes are generally impaired in the same patient. Auditory analysis system Aphasia Handbook 199 According to Basso (2003) the same tasks used to evaluate the integrity of a component can also be used for its treatment. So, if the patient has difficulties in phoneme discrimination, pairs of phonemes can be presented in order to say whether they are the same or different. Initially both phonemes can be different in several features, such as, /p/ /r/ And progressively the task moves to phonemes that are different in only one feature, such as, /b/ /p/ Abstract letter identification the use of computers seems appropriate in cases of damage to the abstract letter identification system. The patient is shown pairs of letters in different fonts and has to say whether they represent the same letter or not. The task can become progressively more complex, as pairs of letters and words are introduced. Input lexicon (comprehension) It is interesting to note that comprehension disorders have been shown to be the first to recover spontaneously in a significant number of aphasic patients. Comprehension disorders are mostly associated with Wernickes-type fluent aphasias. A classical approach for the treatment of comprehension disorders has been word picture matching; this is when a word is orally presented. The task of choice for the evaluation of the input lexicons is the so-called lexical decision task; that is, determining whether or not a string of letters (or phonemes) corresponds to a real word or not. Written stimuli can be used for the orthographic system and spoken for the phonological system. Basso (2003) suggests that an exercise that the patient can do alone is to look up in a small dictionary containing only frequently used words, and focus on those that s/he is unsure about. The patient is encouraged to look the orthographic form and to read the definition. The semantic system Damage to the semantic system will prevent the correct performance of any task requiring the comprehension or production of words. The semantic system is mostly impaired in Wernickes aphasia and so-called transcortical (extrasylvian) sensory aphasia, which indeed can be regarded as a subtype of Wernickes aphasia. Aphasia Handbook 200 Tsvetkova (Hanninen, 1985) observed that patients with lesions in the temporal occipital area of the left hemisphere have significant difficulties in drawing the meaning of words. For instance, if these patients are required to draw a squirrel and a rabbit, they may know that both are animals; and animals have a head, ears, tail, body and legs; but these patients are unable to draw the specific features distinguishing both animals. Typical drawings of a squirrel and a rabbit in patients with left temporal-occipital lesions. The patient is unable to use the distinguishing features, characteristics of a squirrel and a rabbit. The complete knowledge that we have about a word, including visual aspects, function, sensory attributes, associated gestures, category, and so forth, correspond to the semantic system (concept) of that particular word. However, the sensory representations are different depending on the specific knowledge that we have about that particular word; indeed, they are modality-specific semantic systems. For instance, these are the associations of the following words: House: only has a visual representation Phone: has a visual and also an auditory representation Key: has visual, tactile, and auditory representations Ice cream: has a visual and a gustatory representation Flower: has a visual and an olfactory representation Classification tasks are frequently used to treat the semantic deficits in aphasia and restore the semantic representations of the words.
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