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As preparations are being made for defibrillation antibiotic blue capsule purchase 500mg trimox with amex, consider performing 5 cycles of 30: 2 compressions to ventilations before performing defibrillation antibiotic before surgery discount trimox 250 mg with visa. Turn the device on infection gums order trimox from india, apply the patient electrodes in the appropriate positions treatment for glaucoma dogs cheapest generic trimox uk, analyze the rhythm antibiotics for ear infection purchase trimox no prescription, and deliver a shock if a shockable rhythm is present antibiotics like amoxicillin discount 250mg trimox otc. The pediatric resuscitation guidelines incorporated findings from a comprehensive review of the data. To perform pediatric defibrillation, a defibrillator monitor capable of adjustments in energy appropriate for children is needed. To acquire the electrical rhythm and subsequently administer an effective defibrillatory shock, place the appropriate-sized pads and paddles correctly on the chest. Furthermore, appropriate pad or paddle size-the largest surface area possible without direct electrode-to-electrode contact-will decrease transthoracic impedance and enhance defibrillation. If contact is made between the paddles, an electrical arc or short circuit could occur. Never use dry paddles because the resistance to flow of current will be very large. However, refrain from using saline-soaked pads in children because they may cause arcing as a result of the proximity of the pads on the chest. Remember that electricity will take the path of least resistance and that the current from defibrillation will travel across the chest if there is a saline bridge between the electrodes. In addition, the use of ultrasound gel and alcohol pads is discouraged because of poor electrical conductivity and potentially high impedance. Pediatric Sudden Cardiac Arrest When cardiac arrest occurs in a child, it is usually a terminal event associated with respiratory compromise or shock. Shock energy for defibrillation First shock 2 J/kg, second shock 4 J/kg, subsequent shocks 4 J/kg, maximum 10 J/kg or adult dose. Maintenance: 20-50 mcg/kg per minute infusion (repeat bolus dose if infusion initiated >15 minutes after intial bolus therapy). Note: the use of epinephrine and its safety and beneficial effects for an improved cardiac arrest outcome have recently been questioned. If the victim is unresponsive to verbal and tactile stimuli, begin chest compressions immediately (30: 2) at a rate greater than 100/min. If a spinal cord injury is suspected, use the jaw-thrust maneuver without head tilt. If there is no perceivable evidence of breathing, provide two slow rescue breaths (1 breath/ sec) that make the chest rise. Do not use excessive force when ventilating because this could cause regurgitation or aspiration, impede venous return to the heart, and decrease coronary blood flow as a result of increased intrathoracic pressure. After interposing the breaths, proceed to assess the circulation by checking for a pulse in either the carotid or femoral artery (<10 seconds). If there is no palpable pulse or a very slow pulse less than 60 beats/min in very young children after 10 seconds of attempting to feel a pulse, initiate chest compressions. If a single rescuer is performing the compressions and ventilations, the compressionto-ventilation ratio should be 30: 2. If two rescuers are available, the compression-to-ventilation ratio should be 15: 2. If an adequate pulse is present, interpose 12 to 20 breaths/ min (1 breath every 3 to 5 seconds). If self-adhesive multifunctional electrode pads are used, there is no need to use conductive gel. Make sure that the input selector switch is reading from the appropriate source. As mentioned earlier in the adult section of the chapter, two types of defibrillators are available: biphasic and monophasic. As of this writing, there is no specific, detailed differentiation between energy levels to be used by either type of defibrillator. However, the caveat that biphasic shocks are at least as effective as monophasic shocks and that they are less damaging to the myocardium still applies. Based on a review of adult and pediatric animal data, when a manual defibrillator is used for the first shock attempt, an energy level of 2 J/kg should be used with either a biphasic or a monophasic defibrillator. If a second or subsequent defibrillation is indicated, 4 J/kg should be used with either type. Before defibrillation, check to make sure that the defibrillator is set to the unsynchronized mode. Once the defibrillator has been charged and the patient cleared, apply firm pressure to the defibrillation paddles (25 lb) to increase contact and deflate the lungs to the end-expiration state. This will usually be followed by a perceptible whole-body muscle twitch by the patient. If no obvious response or twitch of the patient is seen, check the defibrillator controls to make sure that it is in the unsynchronized mode and that the paddles are activated. Once the shock has been delivered, resume resuscitation with immediate chest compressions. If two rescuers are available, use a 15: 2 ratio and switch compressors when the first compressor fatigues. If additional monitoring devices are in place in the hospital setting, modify this step accordingly as decided by the resuscitation team leader. If no pulse is palpable, resume compressions immediately and prepare to deliver a second defibrillatory shock. While the operator is preparing for the second shock, other members of the resuscitation team can work on securing the airway via endotracheal intubation, a laryngeal mask airway, or another appropriate device. The goal is to maintain chest compressions and avoid any unnecessary interruptions. Once an advanced airway has been secured, compression and ventilation cycles are no longer delivered. Now, the compressor will continue to deliver compressions at a rate of 100/min continuously without pausing for interposition of ventilations. When delivering the ventilations, provide 8 to 10 breaths/min, but be careful to not overinflate the chest or use too much force during ventilation to avoid overpressurizing the airways and esophagus and potentiating reflux. The same caveats concerning the lack of proven benefit of any medications to improve long-term survival in adults also applies to children. If a pediatric dose attenuator is not immediately available, a standard defibrillator should be used at the lowest appropriate setting. A patient with significant tachycardia may be asymptomatic or may complain of chest pain or discomfort, light-headedness, or shortness of breath. Rapid cardiac rhythms allow less time for ventricular filling and thereby result in reduced preload and hypotension. Pulmonary capillary wedge pressure may also rise despite the shortened filling time because of reduced ventricular compliance secondary to ventricular ischemia. Termination of rapid rhythms to alleviate or prevent these symptoms must occur quickly to prevent further deterioration. Carotid sinus message drug therapy, rapid cardiac pacing, and cardioversion are the methods available to terminate tachydysrhythmias. Cardioversion is effective almost immediately, has few side effects, and is often more successful than drug therapy in terminating dysrhythmias. In addition, the effective dose of many antidysrhythmic medications is variable, and there is often a small margin between therapeutic and toxic dosages. Although they can often suppress an undesirable rhythm, drugs may also suppress a normal sinus mechanism or may create toxic manifestations that are more severe than the dysrhythmia being treated. In the clinical setting of hypotension or acute cardiopulmonary collapse, cardioversion may be lifesaving, and is preferred over drug therapy. Indications and Contraindications All decisions regarding the need for cardioversion are best made at the bedside by the clinician assessing the given scenario. There are no firm guidelines on exactly what defines an unstable clinical situation, and definitions are relative terms that lend themselves to real-time clinical decision making and clinician interpretation. Cardioversion is often indicated whenever a reentrant tachycardia is causing chest pain, pulmonary edema, light-headedness, or hypotension. This excludes tachydysrhythmias that are known to be caused by digitalis toxicity, as well as a known sinus tachycardia. It is also indicated in less urgent circumstances when medical therapy has failed. In elderly patients, in whom a prolonged rapid heartbeat can be anticipated to cause complications. In the unusual case of sinus node reentrant tachycardia, rapid onset and offset may be the only clues. Ventricular rates in excess of those predicted for age strongly suggest an accessory pathway. Dysrhythmias caused by enhanced automaticity will not be terminated by uniformly depolarizing myocardial tissue because a homogeneous depolarization state already exists. Although cardioversion will not work in these cases, medications that suppress automaticity, including potassium and magnesium, may be useful. Digoxin is still generally withheld for 24 hours before cardioversion as a precaution against inadvertently elevated levels. Although many of these drugs are not used routinely, if they are needed, timing is likely to be critical. A significant and preventable complication of procedures involving sedation is hypoventilation leading to hypoxia. A pulse oximeter is generally recommended for patients undergoing conscious sedation. Synchronized monophasic or biphasic cardioversion is the appropriate first choice of treatment for unstable patients. Check to see that the machine is correctly identifying the R wave of the complexes (arrow). Sedative medications should be ready for use in labeled syringes, along with a prefilled saline syringe for flushing the catheter. If a patient has metabolic acidosis, compensatory hyperventilation after endotracheal intubation may be indicated before cardioversion. Administer the anesthetic agent or agents intravenously over a period of approximately 30 seconds and wait until the patient is unable to follow simple commands and loss of the eyelash reflex is noted. Administering the agent too quickly may result in hypotension; administering it too slowly may not allow blood levels to reach a therapeutic range if the agent has a rapid rate of metabolism. In the synchronized mode, the cardioverter searches for a large positive or negative deflection, which it interprets as the R or S wave. Once the cardioverter is set to synchronize, a brief delay will occur after the buttons are pushed for discharge as the machine searches for an R wave. If concern exists about whether the R wave is large enough to trigger the electrical discharge, the clinician can place the lubricated paddles together and press the discharge button. When the R- or S-wave deflection is too small to trigger firing, change the lead that the monitor is reading or move the arm leads closer to the chest. Electrode Position: Same as for Defibrillation Electrode paddles may be positioned just as they are for defibrillation. Any staff member acting as a ground for the electrical discharge can be seriously injured. The operator must announce "all clear" and give staff a chance to move away from the bed before discharging the paddles. Care must be taken to clean up spills of saline or water because they may create a conductive path to a staff person at the bedside. Obese patients may require a higher energy level for cardioversion, and the anteroposterior paddle position is sometimes more effective in these patients. If patients are shocked while in the expiratory phase of their respiratory cycle, energy requirements may also be lower. Cardioversion will be accomplished with 50 J in 90% of cases, and conversion should initially be attempted at this energy level. If the initial attempts at electrical cardioversion Methohexital 1 mg/kg Etomidate Propofol Thiopental Fentanyl 0. Midazolam is probably the most commonly used agent, with induction occurring approximately 2 minutes after a dose of approximately 0. Although induction with midazolam takes slightly longer than with the other medications, it has the advantage that a commercial antagonist, flumazenil, is available for reversal if necessary. Fentanyl can cause respiratory depression, but its action can be reversed with naloxone. Methohexital has the advantage of quick onset and a somewhat shorter duration of action than midazolam does, but it has a rare association with laryngospasm. All the drugs except etomidate and ketamine may cause a small drop in blood pressure, and infusion of propofol and etomidate is painful. If they do not, or if urgent conversion is needed because of a high ventricular rate, an electrical countershock should be administered in the synchronized mode at 50 J and doubled if necessary. Patients with ischemia or known coronary artery disease appear to be at much higher risk for significant post-shock bradycardia, with rate support pacing being required after 13 of 99 shocks in the aforementioned study. Therefore the proclivity for dysrhythmias is greater with high-dose cardioversion of an ischemic heart. Conclusion Cardioversion is a safe and effective method of quickly terminating reentrant tachycardia. Complications related to psychological trauma, respiratory depression, and unintentional shock in health care workers can be avoided with proper precautions. Synchronized shock should be administered after close scrutiny of the lead used for sensing to be sure that the R or S wave is significantly larger than the T wave. Atropine and temporary pacing equipment should be available to treat post-shock bradycardia, especially in patients with myocardial ischemia or infarction. Complications Complications of cardioversion may affect the patient, particularly those with a cardiac pacemaker, as well as health care personnel at the bedside.
Zoll and colleagues reported 25 humans paced for up to 108 hours with impulses of 20-msec duration antimicrobial laundry soap buy trimox online pills. Leatham and colleagues paced one patient for 68 hours with impulses 20 msec in duration antibiotic yellow teeth buy genuine trimox on line. Madsen and colleagues paced 10 healthy volunteers at threshold for 30 minutes and found no enzyme or echocardiographic abnormalities antibiotics for chest infection buy 250 mg trimox fast delivery. Soft tissue discomfort with potential injury may still occur with current transcutaneous pacemakers antibiotics brands discount trimox online. Most patients are able to tolerate the discomfort virus encyclopedia discount trimox online mastercard, especially after sedation and analgesia antibiotic resistant bacteria evolution purchase genuine trimox line, which should be routine. Nonetheless, prolonged use may still induce local cutaneous injury, particularly in pediatric patients because of the use of smaller electrodes. Furman S, Robinson G: the use of intracardiac pacemaker in the correction of total heart block. Piela N, Kornweiss S, Sacchetti A, et al: Outcomes of emergency department placement of transvenous pacemakers. Part 6: electrical therapies-automated external defibrillators, defibrillation, cardioversion, and pacing. In Braunwald E, editor: Heart disease: a textbook of cardiovascular medicine, Philadelphia, 1980, Saunders, p 749. Suleyman T, Tevfik P, Abdulkadir G, et al: Complete atrioventricular block and ventricular tachyarrhythmia associated with donepezil. Laczika K, Thalhammer F, Locker G, et al: Safe and efficient emergency transvenous ventricular pacing via the right supraclavicular route. Altamura G, Bianconi L, Boccadamo R, et al: Treatment of ventricular and supraventricular tachyarrhythmias by transcutaneous cardiac pacing. Monraba R, Sala C: Percutaneous overdrive pacing in the out-of-hospital treatment of torsades de pointes. Barthell E, Troiano P, Olson D, et al: Prehospital external cardiac pacing: a prospective, randomized, controlled clinical trial. Pinneri F, Frea S, Najd K, et al: Echocardiography-guided versus fluoroscopy-guided temporary pacing in the emergency setting: an observational study. Mehra R, Furman S, Crump J: Vulnerability of the mildly ischemic ventricle to cathodal, anodal, and bipolar stimulation. Electrical therapies: automated external defibrillators, defibrillation, cardioversion and pacing. Somani R, DeJong P, Michael K, et al: unnecessary shock from an implantable cardioverter-defibrillator following transcutaneous pacing. As fluid accumulates, a critical point is reached at which pericardial pressure negatively affects cardiac filling and causes circulatory insufficiency. Once compensatory mechanisms begin to fail, obstructive shock ensues and a failure to restore hemodynamics eventually leads to cardiac arrest. These properties limit the amount of cardiac dilation that is possible during diastole and enhance mechanical interactions between the atria and ventricles during systole. Cardiac tamponade typically occurs with an intrapericardial pressure of 15 to 20 mm Hg. No specific pericardial volume predicts the hemodynamic consequences of an effusion; such consequences depend on the acuity of the accumulation of the fluid. Pericardiocentesis Indications Diagnostic Determining the cause of pericardial effusion Therapeutic Shock/hemodynamic instability Cardiac arrest, pulseless electrical activity Equipment Contraindications Absolute None (if hypotension or hypoperfusion is evident or if the patient is in cardiac arrest) Relative Coagulopathy Prosthetic heart valve Pacemakers and cardiac devices Lack of direct visualization. Once critical volumes are reached, very small increases cause significant hemodynamic compromise. Note the initial slow changes, then the rapid decrease in systolic pressures once critical pericardial volume and pressure are reached. Early in tamponade, these compensatory mechanisms are usually effective in maintaining adequate cardiac output. Effusion may also be associated with aortic disease, connective tissue disease, or idiopathic causes. It is often difficult to report the exact incidence of each type of pericardial effusion because of variations in patient populations, local epidemiology, and the diagnostic protocols used during evaluation. The prevalence of a chronic effusion is also difficult to ascertain because it is often asymptomatic and underreported. Pressure drops rapidly when a small amount of fluid is removed, hence the initial significant benefit of pericardiocentesis. It is one of the most feared causes of tamponade because the semi-elastic pericardium cannot accommodate acute increases in pericardial fluid and clinical deterioration can be rapid. This diagnosis can be challenging to make because there may be little or no evidence during the initial evaluation. Common causes include trauma and aortic dissection retrograde into the pericardial sac. Traumatic Hemopericardium Penetrating cardiac trauma can cause acute hemopericardium by either external forces. External cardiac puncture is associated with stab wounds or projectile injuries. Tamponade develops in 80% to 90% of patients with cardiac stab wounds as opposed to 20% of those with gunshot wounds. Internal penetrating trauma is typically caused by invasive diagnostic or therapeutic procedures. The procedures most often associated with this injury are cardiac catheterization (angioplasty or valvuloplasty) and pacemaker insertion. Ironically, pericardiocentesis itself (treatment of a pericardial effusion) can cause hemopericardium if a coronary vessel or the myocardium is injured during the procedure. Interestingly, the pressure-volume relationship of the pericardial space demonstrates hysteresis; that is, withdrawing a certain quantity of fluid reduces intrapericardial pressure more than addition of the same amount of fluid increases intrapericardial pressure. This could be detrimental for patients with tamponade because right-sided filling is already compromised and further reductions can lead to severe hemodynamic instability. Low-pressure pericardial tamponade is defined as a hemodynamically significant effusion with an intrapericardial pressure that is lower than expected. Acute myocardial infarction dissecting aortic aneurysm Congestive heart failure Coronary aneurysm Internal jugular and subclavian venous catheters. Hemopericardium can occur immediately or can be delayed for days subsequent to erosion of the catheter through myocardial or vascular tissue. Major blunt chest trauma can cause hemopericardium with or without obvious signs of injury, from rupture of a cardiac chamber or, less commonly, damage to a coronary artery. Maintain a high index of suspicion for this condition in patients with risk factors, such as certain malignancies. The dissection may expand in a retrograde fashion by extending to the base of the aorta and into the pericardial sac. This is a very difficult diagnosis, and best visualized and comfirmed by bedside ultrasound. Risk factors for aortic dissection include hypertension, atherosclerosis, vasculitis. This complication is less common today than in the past (<1%)39 secondary to improved revascularization techniques, better therapeutic medications, and faster intervention times (shorter door-to-balloon times) for coronary ischemia. Radiation Pericardial effusions (secondary to radiation-induced pericarditis) can develop acutely during radiation therapy or may be delayed for years. Risk factors include the radiation dose, duration of exposure, and age of the patient. Chronic fluid accumulation allows the pericardium to stretch circumferentially and accommodate up to 2000 mL of fluid without any hemodynamic compromise. Thus, asymptomatic patients with moderate to large effusions may not need emergency pericardiocentesis, in contrast to patients with acute hemopericardium. Common causes of nonhemorrhagic effusions are discussed in the following sections. Any sign of hemodynamic compromise, however, warrants strong consideration of pericardiocentesis. Hypothyroidism Hypothyroid patients are at risk for pericardial effusions (up to 30%), but the fluid accumulates gradually, so tamponade develops in only a few patients. Medically managing the underlying hypothyroidism often reverses the effusion without the need for pericardiocentesis. Special Considerations in Pericardial Disease Pericardial tamponade is classically described as being secondary to circumferential effusion, which causes a generalized increase in pericardial pressure and compression of multiple cardiac chambers. Loculated effusions (caused by a local hematoma or an infectious process) or pericardial adhesions (from previous inflammation) can lead to tamponade by compressing one or more cardiac chambers and thus reducing both cardiac filling and cardiac output. These processes cause scarring, fibrosis, or calcification, and the pericardium eventually becomes a nonelastic and "constrictive" sac around the heart. Myocardial relaxation and cardiac filling are impaired, and diastolic dysfunction ensues. Without echocardiography, constrictive pericarditis can be difficult to distinguish from pericardial tamponade. It may be quite difficult to differentiate between effusiveconstrictive pericarditis and pericardial tamponade in stable patients because both are associated with effusions. Once a pericardial effusion is suspected (or diagnosed), the next step is to determine its size and hemodynamic significance and presence of underlying or associated diseases. History: Patient Profile and Symptoms the historical features of pericardial effusions are nonspecific and the diagnosis may easily be overlooked. Patients are likely to present with symptoms relating to the underlying disease rather than the pericardial effusion itself. If the history suggests pericardial effusion, the physical examination should focus on determining the underlying cause. Ironically, many pericardial effusions are not diagnosed from the history or findings on physical examination but are found incidentally during the evaluation for other diseases. In 1935, Beck characterized the physical manifestations of tamponade with two triads, one for chronic and one for acute tamponade. Almost 90% of patients have one or more of these "acute" signs,86 but only approximately 33% demonstrate the complete triad. It would be clinically desirable to identify patients in early tamponade, before hemodynamic collapse. They may be agitated, panic-stricken, confused, uncooperative, restless, cyanotic, diaphoretic, acutely dyspneic, or hemodynamically unstable. Such patients should undergo a brief and focused physical examination followed by a rapid hemodynamic assessment with bedside ultrasound because the time between initial evaluation and full arrest may be brief. Some of the findings on physical examination associated with tamponade are described later. Vital Sign Abnormalities There are three sequential stages that are typically described to reflect the natural history of acute tamponade (Table 16. Some patients are stable within a given stage for hours, whereas others proceed through all three stages and develop cardiac arrest within minutes. Nearly all patients with tamponade present with sinus tachycardia, although its specificity is low. Exceptions to the pairing of tachycardia with tamponade usually relate to the underlying cause of the effusion. Adding to the diagnostic complexity, not all patients in tamponade have a reduction in blood pressure. In fact, Brown and co-workers90 described several tamponade patients with elevated blood pressure. These patients were previously hypertensive and paradoxically had reduced systolic blood pressure following pericardiocentesis. The absence of distended neck veins may also result from severe venoconstriction secondary to intrinsic sympathetic discharge, vasopressor use, or severe hypovolemia. Bedside ultrasound is the fastest and most reliable diagnostic tool because it is noninvasive, does not emit radiation, and can be performed at the bedside without transporting unstable patients outside the Ed. As discussed previously, pericardial effusions are occasionally discovered incidentally during evaluation for other disorders. If neither diagnosis is more likely than the other, dual workups may be necessary. Chest Radiography Chest radiographs are not diagnostically useful in patients with acute traumatic tamponade because the pericardium does not have sufficient time to change size or shape (see section on Pathophysiology of Pericardial Tamponade). Radiographs, however, may reveal other associated findings such as hemothorax, bullets in the thorax, or even pneumopericardium. A, Top, the normal situation in which changes in intrathoracic pressure are transmitted to both the pericardial sac and the pulmonary veins. Bottom, Cardiac tamponade in which changes in intrathoracic pressure are transmitted to the pulmonary veins but not to the pericardial sac. To assess for pulsus paradoxus, have the patient breathe normally while lying at a 45-degree angle. Inflate the blood pressure cuff well above systolic pressure and slowly deflate it. A difference of more than 12 mm Hg between the two values indicates pulsus paradoxus. Its description here is for historical value and for use in hemodynamically stable patients. An apical view of a large pericardial effusion in early ventricular diastole reveals marked right atrial collapse. C, Chest radiograph showing an enlarged, globular cardiac silhouette (water-bottle heart) in a patient with tamponade caused by a malignant effusion. The chest film has minimal value in diagnosing tamponade but is usually abnormal when significant chronic effusions are present.
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The chest of a tiny infant may not accommodate all the precordial electrodes; in such cases the following array is recommended: V3R or V4R antibiotics essential oils generic trimox 500 mg with visa, V1 infection question generic trimox 500mg amex, V3 virus under microscope discount trimox 250 mg on line, and V6 bacteria in mouth buy 250 mg trimox. On some tracings virus x 2010 cheap trimox 500mg line, a computer-generated interpretation antibiotic otic drops generic 250mg trimox, or "reading," will also be displayed at the top of the tracing. A sample of nine of these programs was compared with the readings of eight cardiologists; the gold standard in this study was clinical diagnosis made independently of the interpretations of these tracings based on other objective data. The performance of the programs was good, with correct interpretations in a median of 91% of cases, but the cardiologists were significantly better (median of 96% correct). Note the box-shaped mark to the left of the complexes (arrows); this is a graphic representation of the calibration for the tracing. The calibration in this tracing was (inexplicably and unexpectedly) changed to 20 mm/ mV by the computer, not by the operator. A was recorded minutes later with correction of calibration to the standard 10 mm/mV and was unchanged from baseline tracings. These additional, or nontraditional, leads include posterior leads (V7, V8, and V9), right ventricular leads (especially V4R), and procedural leads (transvenous pacemaker wire placement and pericardiocentesis). Place leads V7, V8, and V9 on the same horizontal plane as V6, with V7 at the posterior axillary line, V8 at the tip of the left scapula, and V9 near the border of the left paraspinal muscles. Place right-sided leads V1R to V6R on the chest as a mirror image of the standard precordial leads. This alteration in lead placement is used to investigate the possibility of a right-sided acute myocardial infarction that may not be appreciated with normal lead placement. This tracing displays the right-sided precordial leads in an elderly man with chest pain, and they are consistent with acute coronary syndrome. This patient was found to have a subtotal proximal occlusive lesion of his right coronary artery at cardiac catheterization. If a balloon-tipped flotation catheter is used, deflate the balloon once it is in the right ventricle. Next, advance it until contact is made with the endocardium and the ventricle is captured. This form of monitoring will assist in correct positioning of the catheter in the pericardial space. In such instances, it may be necessary to place the pacing wire without the benefit of fluoroscopy. In such cases the recommendation is to advance the wire under electrocardiographic guidance with the patient connected to the limb leads of a grounded electrocardiographic machine and the pacing wire connected to the V lead (see Chapter 15). Importantly, this reduction in time to management is seen in urban, suburban, and rural settings, regardless of the transport time or type of reperfusion strategy selected for the particular patient. Alteration in Amplitude and Paper Speed Most 12-lead electrocardiography machines today allow alteration of both amplitude and paper speed from the basic 10-mm/ mV and 25-mm/sec standards, respectively. This technique is most advantageous when assessing patients with marked atrial or ventricular tachycardia. Increasing the paper speed exaggerates any existing irregularity (such as in atrial fibrillation) and can improve recognition of smaller deflections, such as P waves, in the presence of a significant tachycardia. A number of alternative lead systems requiring fewer electrodes have been described. Although continuous 12-lead electrocardiographic rhythm monitoring has the advantage of recording cardiac activity over multiple leads (thus maximizing atrial and ventricular monitoring), it is often impractical. Because of the rapid rate, the actual P waves are difficult to discern, thus making determination of the rhythm difficult. Limb-Precordium Leads A sequential pattern of bipolar leads on the chest, termed limb-precordium leads, has been proposed in combination with the original Einthoven limb leads. Esophageal Leads the esophageal lead (E) was first described by Brown in the 1930s. Once in the esophagus, the location of the electrode is determined either by fluoroscopy or by making a series of low to high esophageal recordings. The position of the electrode in the esophagus is adjusted by slowly pulling the electrode wire out the nares or mouth. Central Venous Catheter Intracardiac Leads For patients in whom a central venous catheter was placed for vascular access (or for other reasons such as cardiac pacing, hemodialysis, or Swan-Ganz monitoring) that catheter, when filled with saline, can be used as a modified intracardiac electrode for recording of atrial activity. Once filled with saline, a needle was then left in a side access port of the catheter and attached via an alligator clip to lead V1. This could suggest dextrocardia, but the precordial leads demonstrate a normal transition, which is not consistent with dextrocardia. A multitude of possibilities for misconnection of the limb electrodes exists; some of the most likely are summarized here. Reversal of the leg electrodes is largely insignificant in that the potentials at the left and right legs are essentially the same. A patient with a history consistent with acute coronary syndrome was brought to the emergency department after this electrocardiogram was recorded in a clinic. Precordial Electrode Misplacement and Misconnection unlike the limb electrodes, the precordial electrodes are more prone to misplacement, especially when variations in body habitus. This may cause some variability in the amplitude and morphology of the complexes in the precordial leads. However, these changes are not usually grossly abnormal and therefore can be difficult to detect. In such cases, it is useful to go to the bedside and examine where the electrodes were positioned relative to the recommended placement (see section on Electrode Placement earlier in this chapter). Note that the usual precordial progression of R-wave growth in leads V2 and V3 is disrupted in the tracing displayed in A. It has been observed that leads V1 and V2 are typically placed too high and that the lateral leads are placed too laterally and too low. McCann and colleagues56 demonstrated a high degree of variability between experienced clinicians in identifying anatomic landmarks for precordial electrocardiographic electrode placement. There was frequently a large difference in the measured distance from the actual to the "standardized" electrode position that ranged between 0 and 105 mm in the vertical direction (mean, 14 mm; median, 10 mm), and between 0 and 120 mm in the horizontal plane (mean, 17 mm; median, 10 mm). An abrupt change in wave morphology evolution- followed by a seeming return to normalcy in the next lead-is a good clue to misconnection of the precordial electrodes. It can be attributed to either physiologic (internal) or nonphysiologic (external) sources; the former includes muscle activity, patient motion, and poor electrode contact with the skin. Minimizing skin impedance and artifact may be achieved by: (1) avoiding electrode placement over bony prominences, major muscles, or pulsating arteries; (2) clipping rather than shaving thick hair at electrode sites; and (3) cleaning, and most importantly, drying the skin surface before reapplying the electrode if the tracing features substantial artifact. Nonphysiologic artifact is most often caused by 60-Hz electrical interference, which is ascribable to various other sources of alternating current near the patient. The electrocardiogram demonstrates a marked artifact that is giving the appearance of atrial flutter in lead V1. As a clue to the artifact, the patient was clinically stable and asymptomatic during the event, except for his rigors. Electrocardiographic artifact should be considered when the clinical picture indicates stability, and status quo and coincident procedures are in progress. Differentiation of artifact from true electrocardiographic abnormality is intuitively important; moreover, clinical consequences have been reported that are directly attributable to confusion of artifact with disease. Brady W, Adams M, Perron A, et al: the impact of the 12-lead electrocardiogram in the evaluation of the emergency department patient [abstract]. Surawicz B, uhley H, Borun R, et al: Task Force I: standardization of terminology and interpretation. American Heart Association Committee Report: Recommendations for standardization of leads and of specifications for instruments in electrocardiography and vectorcardiography. Lapostolle F, Petrovic T, Bernot B, et al: Comparison of the use of conventional and prewired electrodes for electrocardiography in an emergency setting: the Spaghetti Study. Thaler T, Tempelmann V, Maggiorini M, et al: the frequency of electrocardiographic errors due to electrode cable switches: a before and after study. Transcutaneous pacing is generally a temporizing measure that may precede transvenous cardiac pacing. Although it is not an expectation that all emergency clinicians will be adept at placing temporary transvenous cardiac pacemakers, many have mastered the techniques and are often the only clinicians available to perform this lifesaving procedure. Emergency cardiac pacing may be instituted either prophylactically or therapeutically. Therapeutic indications include symptomatic bradyarrhythmias and overdrive pacing. Pacing for asystole has very minimal success but it has been used for this condition. Several approaches to pacing can be taken, including transcutaneous, transvenous, transthoracic, epicardial, endocardial, and esophageal. Transvenous pacing should be reserved for patients who require prolonged pacing T the transvenous method of endocardial pacing is commonly used and is both safe and effective. However, in some instances, anatomic, logistic, and hemodynamic impediments can prohibit successful pacing by even the most skilled clinician. As with other medical procedures, it should not be performed without a thorough understanding of its indications, contraindications, and complications. Transvenous Cardiac Pacing Indications Bradycardias Symptomatic sinus node dysfunction Second- and third-degree heart block Atrial fibrillation with a slow ventricular response With myocardial infarction: new left bundle branch block, bifasicular block, alternating bundle branch block Malfunction of an implanted pacemaker Tachycardias Supraventricular dysrhythmias Ventricular dysrhythmias Equipment Sheath introducer Connecting cable Sterile sleeve Adapter pins Alligator clamp Pacing generator Contraindications Prosthetic tricuspid valve Severe hypothermia Complications Inadvertent arterial puncture Venous thrombosis/thrombophlebitis Pneumothorax/other anatomic injury Ventricular arrhythmia Misplacement of the pacing catheter Myocardial/pericardial perforation Entanglement of the pacing catheter Transvenous pacing catheter 3-mL syringe the contents of a typical transvenous pacemaker kit are shown here. Additional equipment required for insertion of the sheath introducer is reviewed in Chapter 22. Individual kits may vary by manufacturer; be familiar with the equipment available at your institution before performing the procedure. Initial efforts focused on the transcutaneous approach (see later in this section). Over the succeeding years several scattered experiments were reported, and in 1951 Callaghan and Bigelow first used the transvenous approach to stimulate asystolic hearts in hypothermic dogs. In 1964 Vogel and coworkers demonstrated the use of a flexible catheter passed without fluoroscopic guidance for intracardiac electrocardiography. During the same year, Harris and colleagues confirmed the ease and speed with which this procedure could be accomplished. Asynchronous pacing frequently resulted in the pacemaker firing during the vulnerable period of an intrinsic depolarization; this occasionally caused ventricular tachycardia or fibrillation. In 1967 a demand pacemaker generator that sensed intrinsic depolarizations and inhibited the pacemaker for a predetermined period was used successfully by Zuckerman and associates in six patients. Rosenberg and coworkers introduced an improved pacing catheter known as the Elecath semifloating pacing wire. Rosenberg and coworkers1 achieved pacing in 72% of their patients with an average procedure time of 18 minutes. In 1970, Swan and Ganz introduced the technique of heart catheterization with a flowdirected balloon-tipped catheter. They concluded that the balloon-tipped catheter was the method of choice for temporary transvenous pacing. In most cases the specific indications for cardiac pacing are clear; however, some areas are still controversial. Controversy exists throughout the literature, and this discussion is not meant to set a standard of care for individual circumstances. In general, the indications can be grouped into those that cause either tachycardias or bradycardias (see Review Box 15. Sinus node dysfunction may be manifested as sinus arrest, tachybrady (sick sinus) syndrome, or sinus bradycardia. Although symptomatic sinus node dysfunction is a common indication for elective permanent pacing, it is seldom cause for emergency pacemaker insertion. However, sinus bradycardia is not a benign rhythm in this situation; it has a mortality rate of 2% with inferior infarction and 9% with anterior infarction. Transvenous pacing in an asystolic or bradyasystolic patient has little value and is not recommended. Early pacing is essential when done for this purpose if success is to be achieved20 (see later in this section). Because these patients tend to progress to high-degree block without warning, a pacemaker is often placed prophylactically. Some patients are prophylactically Sinus Node Dysfunction Bradycardias paced on a temporary basis, even in the absence of hemodynamic compromise. These conduction abnormalities frequently result in hemodynamically tolerable escape rhythms because of sparing of the bundle branches. A hemodynamically unstable patient who is unresponsive to medical therapy should be paced promptly. Whether and when stable patients should be paced is unclear, but placing a transcutaneous pacer is one option that can be attempted before placing a transvenous pacing catheter. Pacing is not a standard intervention in traumatic cardiac arrest, but in selected cases it may be considered. Several rhythm and conduction disturbances have been documented in patients with nonpenetrating chest trauma. In these patients, traumatic injury to the specialized conduction system may predispose to life-threatening dysrhythmias and blocks that can be treated by cardiac pacing. Transvenous pacing is also useful in patients with digitalis-induced dysrhythmias, in whom direct current cardioversion may be dangerous, or in patients in whom there is further concern about myocardial depression with drugs. Because these drugs have direct effects on cells of the myocardial pacemaker and conduction system, cardiac pacing is usually of little therapeutic value. Tachycardic rhythms from amphetamines, cocaine, anticholinergics, cyclic antidepressants, theophylline, and other drugs do not benefit from cardiac pacing.
Rabies is a viral disease of mammals transmitted through the bite of a rabid animal infection lining of lungs generic trimox 500mg on line. The majority of rabies cases occur in wild animals such as raccoons virus neutralization assay buy discount trimox 250 mg on line, skunks negative effects of antibiotics for acne generic trimox 250mg with amex, bats infection 1 game order cheap trimox on line, and foxes antimicrobial halogens buy 250 mg trimox with mastercard. The rabies virus infects the central nervous system of humans oral antibiotics for acne minocycline cheap 500mg trimox amex, ultimately involving the brain and leading to death. As the disease progresses, more specific symptoms appear, including insomnia, anxiety, confusion, partial paralysis, hallucinations, hypersalivation (increased saliva), difficulty swallowing, and hydrophobia (fear of water). Once clinical signs of rabies appear, the disease is nearly always fatal, and treatment is mainly supportive. Thorough wound cleansing has been shown to markedly reduce the likelihood of contracting rabies. A tetanus shot should be given if the infected person has not received one within the previous ten years. Persons not previously vaccinated should receive a postexposure vaccination against rabies that includes administration of both passive antibody and vaccine. Bacterial Infections Zoonotic diseases caused by bacterial infections include the following: Anthrax. Anthrax is an acute infectious disease caused by the bacterium Bacillus anthracis. It most commonly occurs in wild and domestic mammals such as cattle, sheep, and goats, but it also can occur in humans who are exposed to infected animals or to tissue from infected animals. Humans can become infected by handling products from infected animals or by inhaling anthrax spores in contaminated animal products. Anthrax infections can be of three types: cutaneous (skin), inhalation, and gastrointestinal. Most cutaneous infections occur when the bacterium enters a cut or abrasion on the skin. About 20 percent of Infectious Diseases and Conditions untreated cases of cutaneous anthrax result in death, but death is rare with antimicrobial therapy. The first symptoms of inhalation infection resemble a common cold, but after several days, the symptoms may progress to severe breathing problems. The gastrointestinal form of anthrax follows the eating of contaminated meat and is followed by an acute inflammation of the intestinal tract. Lyme disease is caused by the bacterium Borrelia burgdorferi and is transmitted to humans by the bite of infected blacklegged ticks. The Lyme disease bacterium lives in deer, mice, squirrels, and other small animals, and ticks become infected by feeding on these animals. In the northeastern and north-central United States, Lyme disease is transmitted by the deer tick Ixodes scapularis. In the Pacific Northwest, the disease is spread by the Western blacklegged tick (I. In approximately 70 to 80 percent of infected persons, the first sign of infection is usually a circular rash that appears three to thirty days after the tick bite. Other early symptoms include fever, chills, headache, fatigue, swollen lymph nodes, and joint and muscle aches. Symptoms of late-stage Lyme disease include painful, swollen joints; severe headaches and neck stiffness from meningitis; and nervous system problems, such as impaired concentration and memory loss. Several laboratory tests for Lyme disease are available to measure antibodies to the infection. These tests may return false-negative results in persons with early disease, but they are reliable for diagnosing later stages of disease. Plague is an infectious disease of animals and humans caused by the bacterium Yersinia pestis. It is transmitted from animal to animal and from animal to human by the bites of infected fleas. Humans usually contract plague from being bitten by a rodent flea that is carrying the plague bacterium or by handling an infected animal. Fleas become infected by feeding on rodents, such as chipmunks, prairie dogs, ground squirrels, mice, and other mammals that are infected with the bacterium. Fleas transmit the plague bacterium to humans and other mammals during the feeding process. The characteristic sign of plague is a very painful, swollen lymph node called a bubo. This sign, accompanied with fever, extreme exhaustion, headache, and a history of possible exposure to rodent fleas, should lead to suspicion of plague. The disease progresses rapidly; the bacteria can then invade the bloodstream and produce a severe form of the illness called septicemic plague, as well as lung infection. Once a human is infected, a progressive and potentially fatal illness generally results unless specific antibiotic therapy is given. It is caused by infection with the bacterial organism Rickettsia rickettsii, which is transmitted by the bite of an infected tick. Initial symptoms may include severe headache, lack of appetite, muscle pain, nausea, and fever. Diagnosis is based on a combination of clinical signs and symptoms and laboratory tests. Salmonellosis is an infection with the bacterium Salmonella, which lives in the intestinal tracts of humans, animals, and birds. Salmonella is usually transmitted to humans through foods contaminated with animal feces. Contaminated foods are usually of animal origin and include beef, poultry, milk, and eggs, but any food, including vegetables, may become contaminated. People should always wash their hands immediately after handling one of these animals, even if it appears healthy. Most persons infected with Salmonella develop diarrhea, fever, and abdominal cramps twelve to seventy-two hours after infection. The illness usually lasts four to seven days, and most persons recover without treatment. Parasitic Infections Zoonotic diseases caused by parasitic infections include the following: Cryptosporidiosis. The parasite is protected by an outer shell that allows it to survive outside the body for long periods of time. Crypto is one of the most frequent causes of waterborne disease among humans in the United States and throughout the world. Crypto is found in soil, food, water, or surfaces that have been contaminated with the feces from infected humans or animals. Some people with crypto have no symptoms, but the most common symptom is watery diarrhea. Other symptoms include stomach cramps, dehydration, diarrhea, nausea, fever, or weight loss. Infection occurs when the tapeworm larvae enter the body and form cysticerci (cysts). When cysticerci are found in the brain, the condition is called neurocysticercosis. The tapeworm that causes cysticercosis is most often found in rural, developing countries where pigs are allowed to roam freely and eat human feces. When pigs swallow pork tapeworm eggs, the eggs are passed through the bowel movement. Once inside the stomach, the tapeworm egg hatches, penetrates the intestine, travels through the bloodstream, and may develop into larvae in the muscles, brain, or eyes. Although rare, larvae may float in the eye and cause swelling or detachment of the retina. Symptoms of neurocysticercosis can include seizures, headaches, confusion, lack of Salem Health attention, or difficulty with balance. Infections are generally treated with antiparasitic drugs in combination with anti-inflammatory drugs. Trichinellosis, also called trichinosis, is caused by eating the raw or undercooked meat of animals infected with the larvae of a species of worm called Trichinella. When an animal eats meat that contains Trichinella cysts (larvae), their stomach acid dissolves the hard covering of the cyst and releases the worms. After mating, adult females lay eggs that develop into immature worms and travel through the arteries to muscles. The first symptoms of trichinellosis include nausea, diarrhea, vomiting, fatigue, fever, and abdominal discomfort. These first symptoms are later followed by headaches, fevers, chills, cough, eye swelling, aching joints, muscle pains, itchy skin, or diarrhea. For mild to moderate infections, most symptoms subside within a few months, although fatigue, weakness, and diarrhea may last for months afterward. Impact Zoonotic diseases have the potential to spread efficiently across international boundaries, thereby affecting not only human health and well-being but also international travel and trade. More than 60 percent of the newly identified infectious agents that have affected people since the mid-twentieth century have been caused by pathogens originating from animals or animal products. This rare, potentially fatal, infection primarily affects the sinuses, brain, and lungs in persons with immune disorders. Causes Two orders of Zygomycetes cause human disease: Mucorales and Entomophthorales. Infection occurs through inhalation of mold spores, through ingestion, or through local skin trauma. These opportunistic fungi grow rapidly, targeting arteries to impede blood flow, causing bloodclots (thrombosis), and premature tissue death (necrosis). Rhinocerebral zygomycosis is the most common form of infection affecting the nose, eyes, sinuses, and brain. Cutaneous, gastrointestinal, and widespread (disseminated) zygomycosis occur but with less frequency. Risk Factors Exposure to these fungi occurs regularly, but many healthy persons have a natural immunity. Immunocompromised persons are more susceptible to this type of invasive infection. Conditions most commonly associated with a risk for zygomycosis include uncontrolled diabetes, malnutrition, bodily burns, steroid or intravenous drug use, metabolic acidosis, organ or stem-cell transplantation, leukemia or lymphoma, deferoxamine (iron chelator) treatment, and acquired immunodeficiency syndrome. Symptoms Rhinocerebral zygomycosis is indicated by fever, face pain, sinus congestion, headaches, eye swelling, visual disturbances, and nasal discharge. Symptoms of pulmonary zygomycosis include fever, chest pain, cough, and difficulty breathing. Gastrointestinal zygomycosis is indicated by abdominal pain and swelling, stomach upset, vomiting, diarrhea, and bloody stools, and it typically results in stomach and colon necrosis. Symptoms of cutaneous zygomycosis include a painful hardening of the skin with a blackened center. Disseminated zygomycosis usually begins in the lungs and spreads to the nervous system and includes fever, headaches, visual problems, and changes in brain function. Immunocompromised persons should seek immediate medical care if disease symptoms appear. Primar y care physicians should consult with an infectious disease or ear-nosethroat specialist for diagnosis and treatment. Diagnostic tests may include computed tomography or magnetic resonance imaging scans. Conclusive diagnosis of zygomycosis requires the isolation, analysis, and identification of the fungus in culture. Treatment and Therapy Persons with zygomycosis should be treated promptly to avoid blindness, thrombosis, nerve injuries, extensive surgery, disfigurement, and death. Intravenous amphotericin B is the antifungal therapy of choice, along with surgery to remove dead and infected tissue. Prevention and Outcomes the fungi that cause zygomycosis are everywhere in the environment. The best preventive measures involve better management of underlying illnesses associated with the disease, improvement of culture-based detection of the disease, and close Salem Health monitoring of at-risk persons for the earliest possible diagnosis. B cells: a class of white blood cells (lymphocytes) derived from bone marrow and responsible for antibody-directed immunity. IgG:immunoglobulin,classG;themostcommonand abundant immunoglobulin (antibody); reacts against bacteria and viruses. Most common symptoms include sudden severe sore throat, pain when swallowing, fever, swollen tonsils, swollen lymph nodes, and spots on the back of the throat; infection lasts from three to seven days and disappears without medication. Streptococcus pneumonia: a bacterium that is the leading cause of pneumonia and otitis media, or middle-ear infection. Salem Health West Nile virus: a virus spread by a mosquito; indigenous to eastern Africa; symptoms include fever, headache, body aches, skin rash, and swollen lymph nodes; severe forms of the disease cause meningitis and can be life-threatening; no specific treatment is available.
If possible bacteria blood purchase 250 mg trimox overnight delivery, one should avoid contact with people who have the condition; wash hands thoroughly with warm water and soap (and help children wash their hands thoroughly); use bleach to disinfect contaminated surfaces in the home antibiotic resistant gonorrhea 2015 best order trimox, including toilets Viral gastroenteritis Category: Diseases and conditions Anatomy or system affected: Abdomen antibiotic mouthwash prescription generic trimox 250mg visa, digestive system antibiotic 7169 trimox 250 mg mastercard, gastrointestinal system antibiotic 2013 trimox 250 mg, intestines antibiotics with pseudomonas coverage buy trimox 500mg line, stomach Also known as: Stomach bug, stomach flu Definition Viral gastroenteritis is an infection of the intestines caused by a virus. Causes Viral gastroenteritis is caused by one of several viruses that assault the intestines. The viruses are usually spread through contact with someone who is infected or with something the infected person touched. Symptoms the symptoms of viral gastroenteritis usually begin one to two days after exposure to the virus. Symptoms may include watery diarrhea, nausea, vomiting, abdominal cramps, fever, muscle aches, and headache. Blood tests and a Infectious Diseases and Conditions and sink faucets; and avoid sharing personal items such as toothbrushes, towels, and drinking glasses. Also, one should take special care when traveling to countries that are more likely to have contaminated food and water. Experts recommend that travelers drink only bottled water, avoid ice cubes, and avoid eating raw foods, including vegetables. Nausea and Vomiting: Overview, Challenges, Practical Treatments, and New Perspectives. Causes Progressive and chronic viral hepatitis is caused by toxins and by heavy drinking of alcohol. Risk Factors It is possible to develop viral hepatitis with or without the common risk factors listed here. However, the more risk factors, the greater the likelihood that a person will develop viral hepatitis. Persons at a greater risk include infants born to women with hepatitis B or hepatitis C and children in day-care centers. Also at greater risk are child-care workers (especially if one changes diapers or toilettrains toddlers), first aid and emergency workers, funeral home staff, health care workers, dentists and dental assistants, firefighters, and police personnel. For hepatitis A or hepatitis E, risk factors include traveling to (or spending long periods of time in) a country where hepatitis A or E are common or where there is poor sanitation. Screening tests are usually administered to people without current symptoms but who may be at high risk for certain diseases or conditions. Screening for hepatitis is a method of finding out if a person has hepatitis before he or she begins to have symptoms. Treatment and Therapy Treatment for hepatitis involves behavioral changes, medications, and alternative and complementary therapies. Also, one should donate his or her own blood before elective surgery so it can be used if a blood transfusion is necessary. Health care professionals should always follow routine barrier precautions and safely handle needles and other sharp instruments and dispose of them properly. One should wear gloves when touching or cleaning up bodily fluids on personal items, such as Salem Health bandages, tampons, sanitary pads, diapers, and linens and towels. One should cover open cuts or wounds and use only sterile needles for drug injections, blood draws, ear piercing, and tattooing. Infants born to women with hepatitis B should be treated within twelve hours of birth. When traveling to countries where the risk of hepatitis is higher, one should follow proper precautions, such as drinking bottled water only, avoiding ice cubes, and avoiding certain foods, such as shellfish, unpasteurized milk products, and fresh fruits and vegetables. The following people also should be vaccinated: persons traveling to areas where hepatitis A is prevalent, persons who engage in anal sex, drug users, people with chronic liver disease or blood-clotting disorders (such as hemophilia), children who live in areas where hepatitis A is prevalent, and people who will have close contact with an adopted child from a medium- or high-risk area. Hepatitis B vaccine is recommended for all children and for adults who are at risk. This shot is usually given before exposure to the virus or as soon as possible after exposure to the virus. Viruses do this repeatedly, not to kill cells but to reproduce in them and to do so rapidly. Viruses continue this process until they have taken over their unwitting host or a specific organ system in the body, often interrupting normal organ function. Viruses, such as West Nile, also can affect the nervous system; other viruses cause diseases such as rabies and encephalitis. The hepatitis viruses include hepatitis A, B, C, D, and E, of which hepatitis C results in the most prevalent blood-borne illness globally. Some viruses remain in human cells, resulting in lifelong episodes of infection and alternating with long periods of inactivity. The Universal Virus Database, an international compilation of viruses that is updated often by the International Committee on Taxonomy of Viruses to include newly discovered viruses, lists hundreds of virus families and their members, sometimes dozens in one family. Specific viruses cause specific types of illness because they characteristically infect a specific type of cell. Cold viruses, for example, infect cells in the respiratory tract and certain enteroviruses affect Viral infections Category: Diseases and conditions Anatomy or system affected: All Definition Viral infections are illnesses that arise from the presence of pathogens known as viruses in the cells of living organisms, including plants, birds, humans, and nonhuman animals. Because they do not absorb or metabolize nutrients to sustain themselves, as do bacteria, they need living cells in which to carry out their only function, reproduction. Viruses spread from person to person through direct human contact (skin, sexual, or blood transfusion) or through being inhaled or ingested in airborne droplets expelled during a sneeze or cough. Insects and parasites, such as mosquitoes and ticks, also carry and transmit certain viruses. Symptoms Symptoms vary widely depending on which virus has caused infection and what part of the body it has affected. Respiratory infections in the nose, throat, sinuses, and lungs may produce symptoms such as a sore throat, runny nose, painful sinuses, cough, and production of phlegm that can block the upper airways. Viruses affecting the skin may produce warts or a rash or skin eruptions and inflammation. With the outbreak of a viral epidemic, such as influenza, the prevailing symptoms among other cases may help identify the virus in new cases. Treatment and Therapy Viruses are difficult to approach with medications because they have built-in protection from the walls of the cells within which they are encased. Because they live inside human cells, they also do not respond to most antibiotics, which are designed to kill living Salem Health bacteria that reproduce outside cells. Often used instead are antiviral drugs, which do not destroy the virus directly but interfere with the ability of viruses to reproduce. Cells already occupied by viruses manufacture substances called interferons, which can increase the resistance of unoccupied cells to virus infection. Immune defenses include the release of infectionfighting white blood cells (lymphocytes, monocytes, and specialized killer T cells), which can defeat the virus attack and protect against subsequent exposure to the same virus. Examineshowsome viruses establish a permanent host relationship and recurrent infection by avoiding immune system actions. Covers later discoveries concerning the replication, molecular biology, pathogenesis, and medical aspects of viruses. Describes viruses responsible for respiratory conditions, including prevalence and manifestation of respiratory virus infection. The author examines twelve of the most common viral infections to demonstrate how viruses devise various solutions to stay alive. Viral meningitis Category: Diseases and conditions Anatomy or system affected: Brain, central nervous system, spinal cord, tissue Definition the brain and spinal cord are encased by layers of tissue called the meninges. Most of these viruses can also cause encephalitis, an inflammation of the brain tissue. Enteroviruses are spread through direct contact with respiratory secretions of an infected person, and through feces. Other viruses (mumps, herpes, chickenpox) are spread through close personal contact or through the air. Symptoms Classic symptoms of viral meningitis include high fever, headache, stiff, sore neck, nausea, vomiting, sensitivity to bright lights, and sleepiness. In newborns and infants, symptoms include inactivity, high fever (especially unexplained high fever), irritability, vomiting, feeding poorly or refusing to eat, tautness or bulging of soft spots between skull bones, and difficulty awakening. To rule out bacterial meningitis, the doctor may order a lumbar puncture (spinal tap), which removes fluid from the lower spinal column to be tested for bacteria (bacterial cultures), or the doctor may order other cultures, such as blood, urine, mucus, and pus from skin infections. Aspirin, Salem Health however, is not recommended for children with a current or recent viral infection. Antibiotics may be given for two to three days while waiting for bacterial cultures to be reported as negative. Prevention and Outcomes To help prevent infection, one should wash his or her hands often if in close contact with an infected person, after changing the diaper of an infected infant, or if working in a child-care setting; and should regularly wash objects and surfaces touched by children using a diluted bleach solution. Persons who have not had measles, mumps, rubella, or chickenpox should consider being vaccinated. If thinking about pregnancy, one should ensure protection (such as a chickenpox vaccine) from common diseases. Also, one should avoid all contact with rodents during pregnancy because lymphocytic choriomeningitis virus can be acquired from pet hamsters, mice, or other rodents. Pregnant women who have a pet rodent should consider finding another home for the rodent for the duration of the pregnancy. Symptoms Symptoms of viral pharyngitis include a sore, red, swollen throat; trouble swallowing; decreased appetite; fatigue; and swollen, tender lymph nodes in the neck and behind the ears. Most viral sore throats are diagnosed based on the symptoms and examination of the throat. Often, the throat will be swabbed to rule out a streptococcal infection, which would require treatment with antibiotics. A viral sore throat is a diagnosis of exclusion; that is, it is made when a sore throat is present and strep throat is unlikely. Even in the absence of strep, some types of sore throats need further tests or treatment. Treatments to relieve symptoms until the infection heals include over-the-counter pain medication, such as acetaminophen or ibuprofen. Other treatments are gargling with warm salt-water and using throat lozenges every couple of hours; drinking increased amounts of fluids (including hot drinks and soups); and running a cool-mist humidifier, which can help keep nasal passages moist and reduce congestion, two factors that can worsen a sore throat. Prevention and Outcomes To reduce the chance of getting a viral sore throat, one should practice good hygiene, including careful handwashing; should avoid sharing food or beverages; and should avoid areas where people are smoking. One should seek medical care if the sore throat worsens; if the sore throat is associated with new or serious symptoms, especially difficult breathing, weakness, or chills; or if the sore throat Viral pharyngitis Category: Diseases and conditions Anatomy or system affected: Pharynx, throat, upper respiratory tract Also known as: Sore throat, viral sore throat Definition Viral pharyngitis is a sore, inflamed throat caused by infection with a virus. Salem Health Viral upper respiratory infections Category: Diseases and conditions Anatomy or system affected: Ears, lungs, muscles, nose, throat, upper respiratory tract Also known as: Cold, common cold, influenza, the flu Definition Viral upper respiratory infection comprises the common cold and influenza. A common cold is a viral infection that irritates the upper respiratory tract (nose and throat). Colds are commonly mistaken for influenza, a more severe viral disease that affects the respiratory system and includes a high fever and extreme fatigue, among other symptoms. Causes the common cold is caused by any of about two hundred viruses, including rhinovirus, coronavirus, adenovirus, coxsackie virus, paramyxovirus, parainfluenza virus, and respiratory syncytial virus. There are two significant types of influenza viruses: A and B (influenza virus type C causes minor infections). The vast majority of the population in any given area may get colds or influenza during the course of a year. The average rate for adults in the United States is three or four infections per person per year. Another risk factor for the common cold (and influenza) is living in crowded conditions. For the seasonal flu, people younger than age five years or older than age sixty-five years are most at risk for contracting the flu, as are health care workers. Symptoms Common cold symptoms, which usually resolve on their own within one to two weeks, include a sore throat or scratchy throat; stuffy nose (hard to breathe through nose); runny nose; sneezing; itchy, stuffed sensation in the ears; watery eyes; slight cough; headache; aches and pains; low energy and malaise; and low-grade fever. The classic symptoms of the flu, which can take up to four days (in adults) from the time of infection to appear, are high fever and chills, sore throat, dry cough, runny nose, watery eyes, severe muscle aches, severe fatigue and malaise, decreased appetite, and headache. Muscle aches are most common in the legs, though they can appear anywhere in the body. Nausea, vomiting, and diarrhea can occur in people with the flu and are especially common in children. Most flu symptoms disappear in five to six days, though full recovery takes longer; the fatigue may last several weeks. Most people are familiar with cold and flu symptoms; however, one should be aware of a few specifics. Having a runny nose in which the discharge is yellow or green and combined with a fever, sore face or teeth, and persistent symptoms may signal the onset of a sinus infection. Blood in the mucus or phlegm and a headache are even more likely to be the result of a sinus infection.
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