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By U. Derek. The College of Insurance. 2019.

Pregnant women and the immunosuppressed were particularly affected in the 2009 pandemic discount 120mg silvitra otc, comprising from 4% to 10% of hospitalizations and fatalities discount generic silvitra uk. In the United States 120 mg silvitra visa, 15 million infections occur annually in young people and 4 million in older adults. Avian influenza (“bird flu”) is a concern: a) the 1918 pandemic strain may have evolved from an avian strain. The patient can often say exactly when they fell ill with fever, headache, shaking chills, and myalgias. Fever and systemic symptoms predominate in the clinical picture, but a dry cough is invariably present and usually persists after the fever is gone. Recovery can be prolonged, taking up to 3 weeks or even longer; during this period, the patient experiences cough and persistent fatigue. Is characterized by abrupt onset of high fever, shaking chills, headache, myalgias, pharyngitis, and rhinorrhea. Once influenza virus infects the respiratory epithelium, it kills the host cell as it replicates. The virus multiplies rapidly, producing large numbers of infectious viruses in the respiratory secretions and causing diffuse inflammation and damage. Pulmonary function is abnormal even in normal hosts and may remain abnormal for a period of weeks after recovery. It has become recognized that influenza may also cause a milder febrile upper respiratory disease or even mild illness without fever. The extent to which influenza causes milder diseases is not well characterized, due to the likelihood that the majority of such cases are not reported. Human cases of avian influenza differ from typical human influenza in several ways. Although experience with H5N1 avian influenza remains limited, the disease typically presents with fever, cough, and respiratory failure, often accompanied by diarrhea. Almost all cases report close contact with poultry, and the virus has predominantly infected children. Mortality has been high among hospitalized cases, although the full clinical spectrum of infection is not well established. Unlike most previous influenza strains, H5N1 is particularly virulent in children over the age of 12 years with no underlying diseases (those that would be predicted to have a strong immune system). Within 6–29 days of the onset of fever, many of these patients develop a respiratory distress syndrome and die of respiratory failure. Subsequently, cases were reported in Azerbaijan, Djibouti, Egypt, Indonesia, Iraq, Laos, Nigeria, and Turkey. The virus exhibits a greater propensity to replicate in lower respiratory epithelium, possibly explaining the high incidence of pneumonia that led to hospitalization during the initial pandemic. Complications the major complications of influenza are viral pneumonia and secondary bacterial pneumonia. The lungs are hemorrhagic, and there is diffuse involvement, but little inflammation. This complication was a major cause of death among young adults during the 1918 pandemic, but is rarely seen today. However, recent experience with avian influenza virus suggests that, if the H5N1 strain adapts to humans, the incidence of this complication could greatly increase. In some cases of influenza pneumonia, patients initially appear to be recovering from the virus, but then suddenly relapse with fever and typical signs of bacterial pneumonia (see Chapter 4, case 4. As a consequence of damage to the tracheobronchial epithelial lining, secondary bacterial pneumonia develops, with Staphylococcus aureus, Haemophilus influenzae, and Streptococcus pneumoniae being the most common offenders (see Chapter 4). As noted with varicella virus, use of aspirin during influenza has been associated with the development of Reye syndrome. Reye syndrome is characterized by fatty infiltration of the liver and changes in mental status, such as lethargy or even delirium and coma. No specific treatment of Reye syndrome is available other than correction of metabolic abnormalities and reduction in elevated intracranial pressure. Diagnosis the most useful characteristic distinguishing influenza from other respiratory illnesses is the predominance of the systemic symptoms. In addition, the epidemic nature of the disease in the community is helpful in making a diagnosis. When influenza is circulating in a community, an adult displaying the symptoms described earlier is highly likely to have influenza. However, the sensitivity of these tests is somewhat variable, depending on the source and quality of the specimen and on other factors, possibly being as low as 60%. Further, the likelihood of false positives is high when influenza incidence is low and, conversely, the likelihood of a false negative is high when influenza is circulating in the community. When to Consider Further Influenza Testing Treatment Amantadine and rimantadine inhibit influenza A virus infection by binding to a virus membrane protein. However, influenza A is now widely resistant to both amantadine and rimantadine, and the U. Advisory Committee on Immunization Practices therefore recommends that amantadine and rimantadine not be used for the treatment or chemoprophylaxis of influenza A in the United States. Both agents can be used for prophylaxis and treatment, and they are most effective when administered soon after the onset of infection. Recently, rare but serious psychiatric and neurologic side effects have been associated with oseltamivir, particularly in pediatric patients. These side effects include panic attacks, delusions, delirium, convulsions, depression, loss of consciousness, and suicide. Both oseltamivir and zanamivir are active against H5N1 avian influenza in animal and in vitro models. Whether widespread resistance to oseltamivir will present a significant obstacle in the management of an avian influenza outbreak is unknown. Recently, however, multidrug resistant strains have been reported, complicating the choice of antiviral regimens. Infectious disease consultation is recommended for all severely ill influenza patients. Commercial immunodetection methods are available for early diagnosis; viral culture is confirmatory. Treatment should not be withheld when clinically indicated based on the results of rapid diagnostic tests or while awaiting test results. Amantadine and rimantadine should no longer be used because of widespread resistance. Neuraminidase inhibitors zanamivir and oseltamivir are effective for types A and B influenza alike.

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The brain Hyponatremia can occur in patients with congestive cardiac does not have the opportunity to adjust to the change order silvitra overnight, and failure order silvitra discount, nephrotic syndrome buy 120mg silvitra, or hepatic failure due to greater brainstem herniation may occur. The total body sodium in these patients is high and urinary sodium is often less than 5 mEq/L; there is relative excess of Treatment of acute symptomatic hyponatremia (with free water in conjunction with an underlying condition that seizures/impaired consciousness) and serum sodium less impairs the ability to excrete free water. Rest of the correction should be achieved slowly by Hyponatremia due to syndrome of inappropriate anti­ administration of saline (0. In asymptomatic Barré syndrome, cerebral malformations, and intracranial hyponatremia, sodium deficit is calculated as above but the hemorrhage), pulmonary infections, cystic fibrosis, correction is achieved over a period of 48–72 hours. Syndrome of inappropriate antidiuretic hormone secretion : Initial aim is to correct the underlying has well­defined diagnostic criteria and need to be cause. Since blood volume is already expanded, fluid administration may lead to pulmonary edema and heart failure. It represents a deficit of water with respect to body’s sodium stores and can result from gastric aspiration), urinary losses (prolonged use of diuretics, a net water loss (diarrhea, vomiting, diuresis and burns) or renal tubular acidosis, hyperaldosteronism, steroid therapy) excessive sodium intake. It can, therefore, be associated hypomagnesaemia, intracellular K+ shift (alkalosis, therapy with any state of hydration; dehydration, overhydration or with E­agonists, insulin, and diabetic ketoacidosis), protein­ normal hydration. Hyperventilation, fever, and inadequate water intake are Potassium mainly affects bioelectric processes, including other factors contributory to hypernatremia. Electrocardiography severe hyperosmolality may cause cerebral damage with changes may not correlate with serum potassium level. Long widespread cerebral hemorrhages, thromboses or subdural standing hypokalemia decreases the concentrating capacity effusion. Child of kidneys (Hypokalemic nephropathy) Respiratory paralysis is hyperirritable with high­pitched shrill cry. Slow correction is advisable in patients Around 100 mL of stock solution is made by adding 90 with hypernatremia of longer duration. In such cases 3–5 mL/kg of 3% saline or 20% t Mg repletion if Mg deficiency is present t K+ sparing diuretics can be added. In severe cholera, seen in metabolic acidosis, sepsis, acute hemolysis, acute stool potassium is <10 mEq/L, stomach: 10 mEq/L, biliary rhabdomyolysis, and tumor lysis syndrome and tissue drainage, duodenal and ileal secretions: 5 mEq/L necrosis. Hypokalemia is defined as a serum potassium level below Mild hyperkalemia is often asymptomatic. Calcium chloride 10% solution, absent P waves, first­degree heart block, sine wave (bizarre contains 1. Normal serum Mg++ concentration t Check the drugs and stop those that can precipitate range between 1. It may potentiate dysrhythmia different options available in the order of efficacy. About twice the estimated magnesium deficit is Sepsis is often associated with hypocalcemia, mild replaced at a rate of 1 mEq/kg for the first 24 hours and 0. Symptomatic ionized hypocalcemia presents with neurological and cardiovascular features. Parenteral fluid therapy may be required in a wide variety One should treat hypocalcemia if symptomatic or if the of clinical situations to provide normal or adjusted ionized calcium concentration is <0. Close monitoring is required is thought to contribute to oxygenation failure by especially when osmotic diuretic such as mannitol is used. Maintenance fluid calculated by Holliday­Segar formula may often : It is a hyperosmolar state and for all overestimate the fluid requirement in acute illness state. These patients have neurohormonal response along with increased fluid moderately low sodium, normal potassium and total administration contributes to fluid overload in this patient body depletion of phosphate. While timely administration of fluids is lifesaving, If in shock, patient needs fluids not insulin. Give one positive fluid balance after hemodynamic stabilization is 20 mL/kg normal saline or Ringer’s lactate boluses in an detrimental to organ function and negatively influences hour till pulse volume returns to normal. Accurate and : If the child has >10% of cumulative fluid frequent monitoring is essential. Frequent (6–12 hourly) fluid balance calculation would Non­urinary fluid losses are replaced by 10% glucose help to make such decisions at the earliest. Patients with clinical evidences of poor peripheral perfusion should receive volume expanders (saline, Ringer’s lactate) at a rapid rate. Monitoring of the central venous pressure t Information about patient’s immediate environment– and acid­base values are mandatory to guide the initial —FiO, barometric pressure 2 therapy. Subsequent fluid and electrolyte therapy depends t Clinical information, including the history and physical upon the status of serum electrolytes and complications examination with emphasis on patient’s respiratory such as cerebral edema. Acid is a substance that tends to dissociate or give a hydrogen ion (proton donor) whereas base is a substance that tends to bind or associate a hydrogen ion t : High/low (proton acceptor). In contrast if the disturbance is predominantly from 8 mEq/L to 16 mEq/L (12 ± 4) but it is variable in different 3 laboratories. The patient may have high anion gap metabolic fatigue, muscle cramps, lethargy, hyporeflexia, muscular acidosis when the calculated anion gap is more than 16. Increased work of breathing (Kussmaul’s breathing) may In respiratory acidosis there is decreased elimination of predispose to superimposed respiratory acidosis. Chronic carbon dioxide from the body due to poor ventilation, which acidemia results in osteopenia, muscle wasting, and growth leads to accumulation of carbon dioxide. Oxygen administration with high flow rates metabolic acidosis if severe or if associated with renal may help to wash out carbon dioxide. Symptoms are due to hypokalemia and decreased ionized Acute respiratory alkalosis last no longer than 6–12 calcium levels. Usually there is hyperventilation with features of tetany as alkalosis decreases blood levels of ionized calcium. Mixed acid­base disturbances are conditions where more than one primary acid disturbance occurs. The four commonly encountered mixed acid­base disorders are: (1) respiratory acidosis + metabolic acidosis, (2) respiratory acidosis + metabolic alkalosis, (3) respiratory alkalosis + metabolic acidosis and (4) respiratory alkalosis + metabolic alkalosis (Table 17. The most serious acid­base disorders are of mixed type when respiratory and metabolic disturbances result in a pH change in the same direction. During intravenous infusion in early resuscitation phase (0–2 hours) pulse rate, blood pressure, capillary refill time and sensorium should be monitored continuously and urine output, hourly. Subsequently recording intake and output, body weight to detect renal compensatory mechanisms or consequences due to fluid excess or deficit are the most important concerns. A chart should be maintained to record the relevant parameters at regular intervals. Disorders of body water homeostasis in and laboratory tests every 12–24 hours to adjust intake of critical illness. Fluids, electrolytes and acid­base to concentrate maximally, but provide enough fluids to disorders second edition, 1995. The reverse situation will cause hypermetropia; rays introduction of parallel light are brought to a focus behind the retina. Eye development is critical in the first few months of life; Accommodation (increasing the curvature of the lens) shifts processes that interfere with development may seriously the focus anteriorly so that a clear image is formed on the impact vision. Constant accommodation in hypermetropes causes first eye screening at birth, followed by an assessment at headaches, eyestrain and excessive convergence (causing 6 months, and thereafter, at every visit to the pediatrician convergent squint). Check vision using objects by 6 months of age) Snellen’s chart; repeat using a pinhole.

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Although there may be a subjective coexisting tremor that gives a feeling of cogwheel- ing order silvitra with visa, true cogwheeling is a form of rigidity independent of tremor discount silvitra 120mg visa. They develop some retropulsion later on buy silvitra 120 mg lowest price, in which they may take two to three steps back but can still correct themselves. This syndrome can result from extensive, bilateral ischemic white matter disease (ath- erosclerotic/vascular parkinsonism), hydrocephalus, or other frontal lobe disorders. The patient’s pace, stance, stride, initiation, and performance in special maneuvers (eg, turn- ing) should be noted. Although failure to stand without assistance can result from proximal muscle weakness of the lower extremities (eg, a myopathic condition), the same problem is often appreciated in moderate and severe stages of parkinsonism. Hallucinations occur later and after Hallucinations occur earlier and Parkinson’s disease medication use. Gait ignition failure/primary progressive freezing of gait–like vari- ant may present with minimal parkinsonian features, at least initially, and mainly with gait freezing. Secondary Parkinsonism ▪ Vascular parkinsonism45–47 ○ Vascular parkinsonism is also known as lower body parkinsonism. Classically, the presentation was described as having an acute onset, symmetric and without tremor, but with postural instability and a poor response to dopamine replacement therapy. In one series, only about a quarter of cases of vascular parkinsonism were considered to have an acute onset with a new isch- emic stroke event, but even here, the new event may have unmasked an insidious process. Subcortical arteriosclerotic encephalopathy (Binswanger dis- ease) is clinically associated with a progressive gait disorder and dementia. In clinical practice, it is appropriate to try levodopa, often up to the maximum tolerated dose, and to continue treatment if there is clinical beneft but discontinue it if there is no response, or if adverse effects outweigh any beneft. However, the risks of surgery may outweigh the potential beneft, particularly when poor prognos- tic features, including dementia, long-standing symptoms, and cortical atrophy, are present. Other Neurodegenerative Disorders Presenting With Parkinsonism ▪ Wilson’s disease55–58 ○ Wilson’s disease is an autosomal recessive genetic disorder of copper metabolism. Is there history of Consider vascular Lower-body parkinsonism is cerebrovascular parkinsonism, usually a presentation of disease? Corticobasal ganglionic degeneration and pro- gressive supranuclear palsy presenting with cognitive decline. Is 6 months of neuroleptic withdrawal suffcient to distinguish drug-induced parkinsonism from Parkinson’s disease? Diagnosis and management of idiopathic normal-pressure hydrocephalus: a prospective study in 151 patients. Selegiline Tetrud and 54 Need for Early selegiline therapy (deprenyl)40 Langston levodopa delays the requirement for antiparkinsonian medications, possibly by slowing progression of the disease. These fndings are not readily explained by the drug’s symptomatic effects and are consistent with the hypothesis that deprenyl has a neuroprotective effect. After a 2-month washout period (before the start of levodopa therapy), no signifcant symptomatic effect of selegiline was seen in comparison with the pla- cebo group, supporting the concept of neuroprotective properties of the drug. Less disability developed in subjects assigned to coenzyme Q10 than in those assigned to placebo, and the beneft was greatest in subjects receiving the highest dose. It was futile to complete the study because it was very unlikely to demonstrate a statistically signifcant beneft of active treatment over placebo. Antiexcitotoxic and antiglutaminergic agents Amantadine49 Amantadine 836 Better survival the association of improved (retrospec- (higher survival with amantadine tive, 10-year use may stem from unblinded expected symptomatic beneft or may study) survival, refect a “neuroprotective” absence of effect. Additional factors (cost, availability of other agents, more recent data on placebo outcomes, other ongoing trials) should also be considered in the selection of agents for phase 3 studies. In this case, lessening/improving the wearing-off state through dopaminergic medication adjustments may also improve the nonmotor features. However, anxiety, apathy, depression, fatigue, and urinary, speech, swallow, and sleep disturbances are also fairly common. Evidence shows that the intervention has a positive effect on studied outcomes; supported by data from at least one high-quality (score ≥ 75%) randomized controlled trial without conficting level 1 data. Evidence suggests, but is not suffcient to show, that the intervention has a positive effect on studied outcomes; supported by data from any level 1 trial without conficting level 1 data. Evidence suggests that the intervention does not have a positive effect on studied outcomes; supported by data from any level 1 trial without conficting level 1 data. Evidence shows that the intervention does not have a positive side effect on studied outcomes; supported by data from at least one high-quality (score ≥ 75%) randomized controlled trial with- out conficting level 1 data. The Movement Disorder Society Evidence-Based Medicine Review Update: Treatments for the non-motor symptoms of Parkinson’s disease. The Movement Disorder Society Evidence-Based Medicine Review Update: Treatments for the non-motor symptoms of Parkinson’s disease. The Movement Disorder Society Evidence-Based Medicine Review Update: Treatments for the non-motor symptoms of Parkinson’s disease. The Movement Disorder Society Evidence-Based Medicine Review Update: Treatments for the non-motor symptoms of Parkinson’s disease. Motor Fluctuations ▪ About 40% of patients treated with levodopa develop motor fuctuations and/or dyskinesias within 4 to 6 years of initiating therapy. The Movement Disorder Society Evidence-Based Medicine Review Update: Treatments for the non-motor symptoms of Parkinson’s disease. The Movement Disorder Society Evidence-Based Medicine Review Update: Treatments for the non-motor symptoms of Parkinson’s disease. The Movement Disorder Society Evidence-Based Medicine Review Update: Treatments for the non-motor symptoms of Parkinson’s disease. In addition, this stage can be domi- nated by nonmotor features (eg, cognitive decline or dementia, psychosis). T M ed ica her p y for P a ki on iea e M edicat in up a M edicat in s vail abl e ses ide ffect s n dicat in san d ecaut in s L evodopa C arbidopa/ levodopa mg, N ausea, vomitin g, hypoten sion, • osteffcacioustreatmen tforP D ( Sin emet mg, mg hallucin ation ssomn olen ce “gold stan dard”) dyskin esias • reaterlikelihood for developmen tofmotor C arbidopa/ levodopa mg N ausea, vomitin g, hypoten sion, complication sdyskin esias con trolled release hallucin ation, somn olen ce • ettertolerated compared with ( Sin emetC R dyskin esias dopamin eagon ists especiallyin C arbidopa/ mg, N ausea, vomitin g, hypoten sion, theelderly levodopa/ mg, hallucin ation, dyskin esiassom- en tacapon e Stalevo) mg n olen cediarrhea, oran geurin e D opamin eagon ist romocriptin e mg, mg N ausea, vomitin g, legedema, • L esseffcaciousthan levodopa/ ( ergot somn olen cevalvularfbrosis carbidopa • P ramipexolehasbeen shown to D opamin eagon ists P ramipexole mg, N ausea, vomitin g, legedema, beeffectivein tremor an d ( n on ergot irapex) mg, somn olen ceimpulsecon trol haspossiblean tidepressan teffect 0 mg, mg, disorderweightgain • L esstolerated than levodopa 1 mg ( moresedation, hallucin ation s R opin irole R equip) mg, mg, N ausea, vomitin g, legedema, edema) mg, mg, mg, somn olen ceimpulsecon trol • W atchforidiosyn craticclassside 4 mg, mg disorderweightgain effectspedaledema, impulse P iribedilTrivastal mg N ausea, vomitin g, legedema, con troldisorder, “sleepattacks” somn olen ceimpulsecon trol iesudden lyfallin gasleep disorderweightgain withoutwarn in g) weightgain co nt inu ed T M ed ica her p y for P a ki on iea e M edicat in up a M edicat in s vail abl e ses ide ffect s n dicat in san d ecaut in s P ramipexole mg, 0 mg, N ausea, vomitin g, legedema, exten ded release. Increased nigral iron content and alterations in other metal ions occurring in brain in Parkinson’s disease. Environmental, life-style, and physical pre- cursors of clinical Parkinson’s disease: recent fndings from the Honolulu-Asia Aging Study. A 2-year, multicenter, placebo-controlled, double-blind, parallel-group study of the effect of riluzole on Parkinson’s disease progression. Dopamine transporter brain imaging to assess the effects of pramipexole vs levodopa on Parkinson disease progression. A randomized, double-blind, futility clinical trial of creatine and minocycline in early Parkinson disease. Randomized controlled trial of intraputaminal glial cell line-derived neurotrophic factor infusion in Parkinson disease. The Movement Disorder Society Evidence- Based Medicine Review Update: Treatments for the non-motor symptoms of Parkin- son’s disease.

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Toxicities include cytopenias buy cheap silvitra on line, dyslipidemia buy silvitra 120mg otc, elevations in creatinine and transaminases cheap silvitra 120 mg on-line, and immunosuppressive effects, including reactivation of latent tuberculosis. The most common adverse events are gastrointestinal (typically diarrhea and nausea), and they usually occur early and are self-limiting. There has been no significant increase in major adverse cardiac events, serious or opportunistic infections, malignancies, or laboratory abnormalities compared to placebo [22]. The favorable infection profile and decreased need for regular lab monitoring make this drug desirable. Late adverse reactions are quite rare but can include thromboembolic events in up to 2% of patients [24]. Abatacept, rituximab, belimumab, tocilizumab, tofacitinib, and apremilast are all class C (risk cannot be ruled out). Use of these biologic agents should be avoided during pregnancy unless no alternative therapies are available. In addition, other toxicities of these drugs can include cytopenias, liver function abnormalities, atypical neurologic symptoms, and congestive heart failure. Wolfe F, Michaud K: Lymphoma in rheumatoid arthritis: the effect of methotrexate and anti-tumor necrosis factor therapy in 18,572 patients. Masala A, Faedda R, Alagna S, et al: Use of testosterone to prevent cyclophosphamide-induced azoospermia. Frieri M, Heuser W, Bliss J: Efficacy of novel monoclonal antibody belimumab in the treatment of lupus nephritis. Orbach H, Katz U, Sherer Y, et al: Intravenous immunoglobulin: adverse effects and safe administration. It describes the shock-like state that is caused by contact with a substance and contrasts with the term prophylaxis, which denotes a beneficial or protective state resulting from contact with a substance. The clinical features of anaphylactic reactions are the physiologic sequelae of release of chemical mediators from tissue-based mast cells and circulating basophils and include a potential for life-threatening vascular collapse and respiratory obstruction [2,3]. A clinically and physiologically indistinguishable hypersensitivity reaction, which is called an anaphylactoid reaction, differs from anaphylactic reactions only because the chemical mediators are released by nonimmunologic mechanisms. Since the clinical features are indistinguishable, both will be referred to collectively as anaphylactic reactions [4]. Estimation of the annual incidence of anaphylactic reactions from administrative sources is hampered by complex coding and incomplete reporting. In a separate study, examination of a United States database identified 2,458 deaths from anaphylaxis from 1999 to 2010 [7]. First, contact with an antigen stimulates the generation of antibodies of the immunoglobulin E (IgE) class. Next, the IgE molecules bind by way of their Fc receptor to a glycoprotein receptor on the cell-surface membrane of tissue mast cells and blood-borne basophils, the so-called target cells. As many as 4,000 to 100,000 IgE molecules normally bind to a single target cell, and up to 100,000 to 500,000 among atopic individuals [7,8]. When two IgE molecules with the same Fab-binding (antigen-recognition) specificity are in close proximity on the surface of mast cells and basophils, the cells are termed sensitized. For subsequent antigenic exposure to stimulate the release of mediators from mast cells and basophils, the specific antigen must bind to the Fab portion of two IgE molecules fixed to the surface of the target cell. This bridging of two IgE molecules initiates a series of biochemical modifications called the activation–secretion response. When two IgE molecules are bridged by an antigen that is specifically recognized by those IgE molecules, a cascade of transmembrane and intracellular events is triggered. The result is the extrusion of granule contents (mediators) into the extracellular space and elaboration of other, newly formed mediators. Tyrosine kinase appears to be an important intramembrane messenger that initiates the intracellular cascades. A variety of substances can induce IgE antibody formation and, on subsequent challenge, provoke anaphylactic reactions [9]. Non–IgE-mediated anaphylaxis occurs when certain ingested or infused substances cause direct mast cell and basophil activation. The administration of blood, serum, or immunoglobulins to patients who are IgA deficient can result in immune complex formation between donor IgA and recipient IgG anti-IgA antibodies [4,12]. These immune complexes fix complement causing activation of the complement cascade with release of the C3a and C5a complement fragments. The contribution of multiple mediators other than histamine explains the limited benefit of antihistamines alone in treating anaphylaxis. Studies of histamine infusion into normal human volunteers suggest that vasodilatation is mediated by both H and H receptors,1 2 whereas bronchoconstriction and tachycardia are mediated by H1 receptors alone [15]. Thus, the physiologic consequences of chemical mediator release during anaphylaxis are (a) an increased vascular permeability; (b) an increased secretion from nasal and bronchiolar mucous glands; (c) smooth muscle contraction in the blood vessels, the bronchioles, the gastrointestinal tract, and the uterus; (d) migration–attraction of eosinophils and neutrophils; (e) bradykinin generation stimulated by kallikrein substances; and (f) induction of platelet aggregation and degranulation. These events act synergistically to increase the vascular permeability that in turn permits the access of a variety of plasma proteins (antibodies, complement, kinins, and coagulation proteins) to tissue sites, which further contributes to the observed inflammation. Urticaria, angioedema, respiratory obstruction (cough, wheezing, stridor, or breathlessness), and vascular collapse are the most important clinical features of anaphylaxis, and these signs and symptoms are due to the direct effects of mast cell and basophil-derived mediators on affected organ systems. Other clinical manifestations may include (a) a sense of fright or impending doom, (b) weakness or dizziness, (c) sweating, (d) sneezing, (e) rhinorrhea, (f) conjunctivitis, (g) generalized pruritus and swelling, (h) flushing, (i) hypoxemia, (j) choking, (k) dysphagia, (l) vomiting or diarrhea, (m) abdominal pain, (n) incontinence, (o) uterine cramps, and (p) loss of consciousness. Profound hypotension and shock may develop as a result of significant arteriolar vasodilatation, increased vascular permeability, cardiac arrhythmias, or irreversible cardiac failure, even in the absence of respiratory or other symptoms [3,10]. Furthermore, transient or sustained hypotension may result in local tissue ischemia, stroke, myocardial infarction, or death [10]. Structures throughout the respiratory tract may be affected, but respiratory failure is generally the result of upper respiratory tract obstruction due to laryngeal edema or obstruction of small airways due to bronchoconstriction, mucosal edema, and hypersecretion of mucus [21,22]. The physical examination of a patient with anaphylactic shock may reveal one or more of the following: a rapid, weak, irregular, or unobtainable pulse, tachypnea, respiratory distress, cyanosis, hoarseness, stridor, dysphagia, diminished breath sounds, crackles, cough, wheezes, hyperinflated lungs, urticaria, angioedema, or conjunctival edema (Table 69. A given patient may manifest only a subset of these findings, sometimes only cardiovascular collapse or only stridor and breathlessness. Biochemical abnormalities in anaphylaxis include elevation of plasma histamine, serum or plasma tryptase, and depression of serum complement components [9,10]. Although these biochemical abnormalities codify our understanding of the pathophysiology of anaphylaxis, they are rarely evaluated in the acute management of clinically established anaphylaxis. Plasma histamine peaks by 15 minutes after the onset of anaphylaxis and returns to baseline by 60 minutes; measurement is generally not feasible unless anaphylaxis develops in the hospital. As discussed in the next section, serum or plasma tryptase may be helpful retrospectively when the diagnosis is uncertain [9,25]. Although there have been no systematic reviews of electrocardiographic findings, reports describe disturbances in rate, rhythm, repolarization, and ectopy [26–28], as well as myocardial infarction [29,30]. The setting is often suggestive as well: a patient who has just received an antibiotic or radiographic contrast media infusion or one who presents to the emergency room after a yellow jacket sting. Clinical criteria have been developed to help clinicians recognize the variable presentations of anaphylaxis [2,31]. A diagnosis of anaphylaxis is likely when any one of the following three criteria is present: (1) the rapid onset (minutes to several hours) of an illness with involvement of skin and/or mucosa (angioedema, flushing, pruritus, urticaria), and either respiratory compromise (dyspnea, wheeze, decreased peak flow, stridor, hypoxemia) or hypotension or end-organ dysfunction (collapse, syncope, incontinence); (2) onset of two or more of the following features after exposure to a likely allergen: skin and/or mucosa (angioedema, flushing, pruritus, urticaria), respiratory compromise (dyspnea, wheeze, decreased peak flow, stridor, hypoxemia), hypotension or end-organ dysfunction (collapse, syncope, incontinence), or persistent gastrointestinal symptoms (vomiting, crampy abdominal pain, diarrhea); or (3) onset of hypotension minutes to several hours after exposure to a known allergen for that patient [31]. Recognition of the early signs and symptoms of anaphylaxis and prompt treatment are imperative to prevent progression to irreversible shock and death [9].

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