By W. Copper. Southern Illinois University Medical School at Springsfield. 2019.
However best prednisolone 10 mg allergy treatment while breastfeeding, vigorous lavage of adherent clot can uncover stigmata requiring endoscopic treatment in nearly half of patients and can be performed at the discretion of the endoscopist  trusted prednisolone 5 mg allergy forecast lubbock. The most common modalities of endoscopic therapy used are thermal therapy (heater probe prednisolone 10mg visa allergy testing when pregnant, bipolar probe, argon plasma coagulation), injection therapy (epinephrine, hypertonic saline, sclerosing solutions), and mechanical therapy (hemoclips, endoloops, and band ligation). Newer endoscopic techniques, including over-the-scope clips, endoscopic suturing, mucosal ablation devices, fibrin glue injection, hemostatic spray, and endoscopic ultrasound-guided angiotherapy, may improve success rates in treatment of high-risk lesions . The treatment modalities are generally comparable with respect to efficacy and safety even when used in combination . The Baylor bleeding score, using patient age, number of illnesses, illness severity, site of bleeding, and stigmata of bleeding, has been proposed to predict the likelihood of rebleeding  and may be useful in determining which patients may benefit from second-look endoscopy . Angiotherapy Intra-arterial vasopressin and/or embolization are used for angiographic control of various bleeding lesions [8,55]. A recent randomized study comparing urgent colonoscopy to radionuclide scanning followed by angiography demonstrated no differences in hospital stay and transfusion requirements despite the fact that colonoscopy identified a definitive bleeding source more often. However, this study used only vasopressin infusion and did not use embolization as a mode of angiotherapy . Gelfoam and metal coils used for embolic therapy after superselective cannulation of the bleeding artery are effective because they can be delivered close to the terminal bleeding vessel and result in localized thrombosis with vessel occlusion. Embolization successfully controls bleeding in 52% to 94% of patients, with approximately 10% of these patients requiring repeat embolization for recurrent bleeding . There is a risk of bowel ischemia following embolization, but this is usually minor and self- limited . Angiotherapy can be comparable to surgical intervention when endoscopic therapy fails for bleeding peptic ulcers. A retrospective analysis demonstrated no difference between embolization and surgery in recurrent bleeding (29. The timing for the use of angiography and angiotherapy must be individualized and usually is a consensus decision by the involved physicians. Surgical Therapy the appropriate timing of when a surgeon should be involved in the care of a bleeding patient is physician and institution dependent, and ranges from an early team approach at presentation to involvement once the risk of significant morbidity and mortality are established after a poor response to medical and endoscopic therapy. Surgical intervention is an effective and safe alternative for patients with uncontrollable bleeding or those unable to tolerate additional bleeding . Prior to surgical intervention, a repeat endoscopy for a patient with persistent or recurrent bleeding can be considered owing to lower risks of side effects from endoscopy compared to surgery [60,61]. A possible exception may be ulcers >2 cm in hypotensive patients where the risk of rebleeding is extremely high with repeat endoscopic therapy [26,61]. Patients with massive hemorrhage that overwhelms the resuscitation effort may need to proceed directly to the surgical suite during ongoing resuscitation. If these patients are high-risk surgical candidates, angiotherapy or a percutaneously or surgically placed portal-hepatic shunt for variceal bleeding may be alternatives. Bleeding from gastroesophageal varices characteristically is brisk and typically presents as hematemesis, melena, or hematochezia in association with hemodynamic instability. The presentation may be less dramatic because acute blood loss can be self- limited in 50% to 60% of cases . Once active bleeding stops, the likelihood of recurrent variceal hemorrhage is 40% within 72 hours and 60% within 10 days if no definitive treatment is pursued . Risk factors associated with variceal rupture include a portal pressure gradient greater than 12 mm Hg, large variceal size (greater than 5 mm), and progressive hepatic dysfunction . Endoscopic findings that implicate esophageal or gastric varices as the bleeding source include the red sign, where one varix is brighter red than the others from microtelangiectasia (red-sign variants include red- wale marks, cherry-red spots, hematocystic spots, and diffuse redness of varix), and the white-nipple sign, in which a fresh fibrin clot may be seen protruding from a varix [66,67]. Endotracheal intubation protects the airway from aspiration of blood in obtunded patients, especially in the setting of massive bleeding . Additional complications that must be addressed include alcohol withdrawal, aspiration, infection, and electrolyte imbalances. Octreotide is a somatostatin analog that decreases splanchnic blood flow and portal pressure, controlling variceal bleeding in as many as 85% of patients [69,70] with an efficacy approaching that of endoscopic therapy and providing improved visibility during subsequent endoscopy [70–72]. Aside from transient nausea and abdominal pain with bolus doses, significant adverse effects from octreotide are rare. Vasopressin, once widely used in this setting, has a significant cardiovascular side effect profile and for this reason has been replaced by octreotide. Endoscopic evaluation should be performed urgently (within 12 hours) in patients in whom variceal bleeding is suspected . Endoscopic band ligation has gained acceptance as the preferred endoscopic treatment for patients with bleeding esophageal varices, with rapid obliteration of varices, and low rates of complications and rebleeding (Table 203. Endoscopic variceal sclerotherapy (injecting a sclerosing solution into the variceal lumen or into the adjacent submucosa), although successful in controlling variceal bleeding, is associated with a 20% to 40% incidence of complications, and has largely been relegated to a second-line therapeutic modality, reserved for patients in whom band ligation is technically difficult [66,81]. Complications of band ligation include recurrent bleeding from treatment-induced esophageal ulcers, stricture formation, esophageal perforation, and acceleration of portal hypertensive gastropathy . Repeat variceal band ligation is performed until varices are obliterated because this approach reduces the incidence of rebleeding . Appropriate interval for repeat band ligation is controversial, with recommendations ranging from 1 to 8 weeks . Gastric varices are detected in approximately 20% of patients with portal hypertension, but can also occur from splenic vein thrombosis. Gastric varices bleed less often, but blood loss can be more substantial compared to esophageal varices . Complications include a propensity for embolic phenomenon posttreatment, including massive pulmonary embolism . Embolization of the short gastric veins and varices is a potential management option for isolated gastric varices. Complications include transient deterioration of liver function, new or worsened hepatic encephalopathy (25%), and shunt insufficiency from thrombosis or stenosis . When placed in an emergency setting to control active bleeding, a 10% in-hospital mortality and 40% 30-day mortality have been reported [86,88,89]. This technique requires a natural gastrorenal or gastrophrenic shunt, which occur in 95% of cases of gastric varices . A balloon catheter is used to occlude the shunt, following which a sclerosant, for example, ethanolamine is injected into the varix . A recent meta-analysis found a pooled clinical success rate of 97% with a major complication rate of 2. Surgically created shunts reliably control acute bleeding (>90%) and prevent rebleeding (<10%) [92,93] but are limited by high operative mortality and postprocedure encephalopathy. Therefore, surgical shunts are only considered in well-compensated cirrhotic patients with good long-term prognoses . Esophageal or gastric balloon devices may be used for direct tamponade of the bleeding source when definitive therapy is not immediately available. There are two basic types of balloon tubes: those with gastric and esophageal balloons (Sengstaken–Blakemore and Minnesota tubes) and those with a large gastric balloon alone (Linton– Nachlas).
A long beard clings to his chin 10 mg prednisolone fast delivery allergy and treats, giving those who observe him a pronounced feeling of the utmost respect safe 20mg prednisolone allergy symptoms vs flu symptoms. Except in the winter order prednisolone 40 mg overnight delivery allergy medicine good for high blood pressure, when the snow or ice prevents, he slowly takes a short walk in the open air each day. There are several reasons why nutrition is impor- tant in movement disorders: ▪ Nutrition may impact mobility, cognition, and swallowing function. Move- ment disorders, by defnition, result in changes in mobility and may lead to a decreased capacity to perform activities of daily living, such as cooking and shopping. Con- versely, decreased levels of activity may lead to a sedentary lifestyle and obesity, exacerbating the underlying neurological disability. All of the reasons listed above suggest that physicians caring for individuals with movement disorders should be familiar with appropriate nutritional strategies for these patients. The lasing medium is a substance, which, when stimulated by an external energy source, emits a particular wavelength of light. In other words, the lasing medium has properties that allow it to amplify light through an internal process of stimulated emission. For example, a laser containing an alexandrite rod lasing medium will be referred to as a 755 nm alexandrite laser. In addition to the lasing medium, all lasers have an optical cavity surrounding the lasing medium that contains the amplification process, a power supply or “pump” that supplies energy to the lasing medium, and a delivery system such as a fiber optic cable or articulated arm with mirrors that precisely delivers laser energy to the skin. ures 5 and 6 in Key References list lasers used for treatment of photoaged skin including their lasing medium and wavelength. By appropriately selecting laser parameters of wavelength, fluence, pulse width, and spot size, specific lesions can be targeted with maximal efficacy and safety. Short wavelengths penetrate superficially due to greater scattering of the laser beam and longer wavelengths penetrate deeper. Very high fluences can be associated with undesirable thermal injury to tissue surrounding the targeted lesion while very low fluences may not be effective for lesion removal. Additionally, short pulse widths are used for small lesions and long pulse widths are used for larger lesions. Small spot sizes penetrate superficially due to greater scattering of the laser beam and larger spot sizes penetrate deeper. Spot sizes used with fractional devices, also referred to as pixels, are very small (measured in μm) and are not adjustable. Pixels can penetrate very deeply and the principle of larger spot sizes having increased depth of penetration does not hold true when considering the tiny spot sizes used with fractional lasers. Fast repetition rates allow for more rapid coverage of large, flat treatment areas and can shorten treatment times. Slower repetition rates aid in precise placement of laser pulses and are useful for treatment of single, discrete lesions or contoured treatment areas. These variables are not adjusted during treatments but rather are discussed when comparing different laser devices. Some lasers utilize cooling methods such as cryogen sprays and contact cooling to protect the epidermis during treatment; external forced refrigerated air is also used. Some devices, particularly for ablative resurfacing, utilize scanners and computer software to “randomly” deliver pulses within a set pattern so that the pulses are not adjacent to one another. Using nonadjacent pulses allows for high energies to be delivered to the skin without the effects of bulk heating and associated risk of thermal injury. Fractional devices also have a density setting which determines the percentage of skin that is treated with a pulse. High-density settings are associated with more intense treatments, have longer healing times, and potentially greater improvements. In addition, the overall pulse width is lengthened in multipulse modes and they are used to treat deeper lesions. Other laser components used for treatments are also shown in ure 10 including the laser arm, handpiece, and distance guide that aids in maintaining a constant distance between the laser tip and skin. Thermal Relaxation Time To understand how pulse width contributes to selectively targeting lesions, one must first understand the concept of thermal relaxation time. Thermal relaxation time is the time it takes a lesion to dissipate ∼50% of its energy into the surrounding tissue. The most selective heating of a target lesion is achieved when laser energy is delivered to the target at a rate faster than the rate of heat dissipation away from the target. In other words, laser energy is confined to the target when the laser pulse width is shorter than the thermal relaxation time of the target. The ideal pulse width is long enough to heat the desired target, while short enough to limit transfer of damaging heat to surrounding tissues. Small targets, such as fine telangiectasias, have short thermal relaxation times and require short pulse widths for treatment; larger caliber vessels have longer thermal relaxation times and require longer pulse widths for treatment. By choosing a wavelength that is selectively absorbed by the chromophore in the lesion, using adequate fluence to damage the lesion, and choosing a pulse width that allows for heating of the lesion rather than adjacent tissue, lasers selectively destroy lesions with minimal nonspecific thermal damage to surrounding skin. Depth of Penetration Deep penetration of laser energy is safer for the epidermis as it reduces superficial absorption of heat and the likelihood of epidermal thermal injury. In addition, understanding how laser parameters affect the depth of penetration allows providers to better target lesions at different depths in the skin. Superficial penetration is associated with short wavelengths, short pulse widths, low fluences, and small spot sizes. Deeper penetration is associated with long wavelengths, long pulse widths, high fluences, and large spot sizes. High fluences and wavelengths poorly absorbed by the water chromophore, have deep cutaneous penetration (see Wrinkles—Nonablative Resurfacing, Chapter 5 for further discussion). The epidermis is the top layer of the skin and is composed of the outermost nonliving layer, the stratum corneum, and the living cellular layers of the stratum granulosum, stratum spinosum, and stratum basale. The stratum corneum is composed of corneocytes (nonliving keratinocytes) and lipids and is often referred to as the epidermal barrier. In healthy young skin, it takes approximately 1 month for keratinocytes to migrate from the living basal layer of the epidermis to the stratum corneum surface and desquamate during the process of epidermal renewal. Melanin pigment, which determines skin color and dyschromias, is primarily concentrated within the epidermis, and in some conditions is found in the dermis (e. The number of melanocytes is similar for both light and dark skin; however, the type and distribution of melanin within the epidermis differ. The key regulatory step in melanin synthesis (melanogenesis) is the enzymatic conversion of tyrosine to melanin by tyrosinase. Once synthesized, melanin is packaged into intracellular organelles called melanosomes that are distributed within the melanocyte and to surrounding epidermal keratinocytes. The dermis lies beneath the epidermis and is divided into the more superficial papillary dermis and deeper reticular dermis.
Gastrointestinal absorption is slow; therefore order generic prednisolone on-line allergy symptoms stuffy ears, when given orally purchase prednisolone with paypal allergy symptoms lymph nodes, the onset of action is delayed while the drug slowly accumulates in adipose tissue generic prednisolone 5 mg on-line allergy yellow jacket. Amiodarone decreases myocardial contractility and also causes vasodilatation, which counterbalances the decrease in contractility. In a major study of out-of-hospital cardiac arrest due to ventricular arrhythmias refractory to shock, patients were initially treated with either amiodarone (246 patients) or placebo (258 patients). On the basis of this study, amiodarone has been given status as an option for use after defibrillation attempts and epinephrine therapy in refractory ventricular arrhythmias during cardiac arrest. It is also an option for ventricular rate control in rapid atrial arrhythmias in patients with impaired left ventricular function. Supplemental infusions of 150 mg may be given for recurrent or resistant arrhythmias to a total maximum dose of 2 g for 24 hours. Premature ventricular complexes are not unusual in apparently healthy people and most often are benign. If the patient has suffered an acute myocardial infarction and has had ventricular arrhythmias, the infusion is continued for hours to days and tapered slowly. The dosage should be reduced in patients with low cardiac output, congestive failure, hepatic failure, and age older than 70 years because of the decreased liver metabolism of the drug. Toxic manifestations are usually neurologic, and can vary from slurred speech, tinnitus, sleepiness, and dysphoria to localizing neurologic symptoms. Frank seizures may occur with or without preceding neurologic symptoms and may be controlled with short-acting barbiturates or benzodiazepines. Conscious patients should be warned about possible symptoms of neurologic toxicity and asked to report them immediately if they occur. Adenosine may also be used in the diagnosis and treatment of stable and unstable narrow complex tachycardias. Side effects caused by adenosine are transient and may include flushing, dyspnea, bronchoconstriction, and angina-like chest pain (even in the absence of coronary disease). The reentrant tachycardia may recur after the effect of adenosine has dissipated and may require additional doses of adenosine or a longer acting drug, such as verapamil or diltiazem. Theophylline and other methylxanthines, such as theobromine and caffeine, block the receptor responsible for adenosine’s electrophysiologic effect; therefore, higher doses may be required in their presence. Dipyridamole and carbamazepine, on the other hand, potentiate and may prolong the effect of adenosine; therefore, other forms of therapy may be advisable. These drugs may also slow the ventricular response of patients with atrial flutter or fibrillation and even for patients with multifocal atrial tachycardia. They should be used only for patients for whom the tachycardia is known to be supraventricular in origin. In the absence of a response, additional doses of 5 to 10 mg may be given at 15- to 30-minute intervals to a maximum of 20 mg. A maintenance infusion of 5 to 15 mg per hour may be used to control the rate of ventricular response in atrial fibrillation. Verapamil and diltiazem should be used for arrhythmias known to be supraventricular in origin and in the absence of preexcitation. Both verapamil and diltiazem may decrease myocardial contractility and worsen congestive heart failure or even provoke cardiogenic shock in patients with significant left ventricular dysfunction. They should, therefore, be used with caution in patients with known cardiac failure or suspected diminished cardiac reserve and in the elderly. If worsened failure or hypotension develops after the use of these agents, calcium should be administered, as described in the section “Other Agents. Magnesium may be of value for patients with torsades de pointes, even in the absence of hypomagnesemia. A 24-hour5 infusion of magnesium may be used for periinfarction patients with documented hypomagnesemia. A loading dose of 1 to 2 g is diluted in 100 mL D W and slowly given for 5 minutes to 1 hour, followed by an infusion5 of 0. Many other drugs may be required in particular circumstances and are discussed in other parts of this text. An incomplete list of these drugs includes beta-blockers, ibutilide, propafenone, flecainide, sotalol, digoxin, antibiotics, thiamine, thyroxine, morphine, naloxone, adrenocorticoids, fibrinolytic agents, anticoagulants, antiplatelet agents, and dextrose. Atropine is indicated primarily for bradycardias causing hemodynamic difficulty or associated with ventricular arrhythmias. If a satisfactory response has not occurred within 3 to 5 minutes, additional 1-mg doses should be given in a bolus, to a maximum dose of 3 mg (0. Precautions for atropine include the requirement that an inordinately rapid heart rate not be produced. Patients with ischemic heart disease are likely to have worsened ischemia or ventricular arrhythmias if the rate is too rapid. Uncommonly, a patient will have a paradoxic slowing of rate with atropine; this is more likely to occur with smaller first doses and is caused by a central vagal effect. If additional atropine does not correct the problem, the patient may require judicious use of isoproterenol or pacemaker therapy. The contractile state of the myocardium depends in part on the intracellular concentration of the calcium ion. Transmembrane calcium flux serves an important regulatory function in both active contraction and active relaxation. The use of calcium in cardiac arrest is based on an early report by Kay and Blalock  in which several pediatric cardiac surgical patients were successfully resuscitated, apparently with the aid of calcium. However, several field studies have failed to demonstrate an improvement in survival or neurologic outcome with the use of calcium versus a control . In addition, after standard doses of calcium administered during cardiac arrest, many patients are found to have very high calcium blood levels . This is apparently due to the markedly contracted volume of distribution of the ion in the arrested organism. In addition, calcium has the theoretic disadvantage of facilitating postanoxic tissue damage, especially in the brain and heart. Calcium is indicated only in specific circumstances: calcium channel blocker toxicity, severe hyperkalemia, severe hypocalcemia, arrest after multiple transfusions with citrated blood, fluoride toxicity, and while coming off heart–lung bypass after cardioplegic arrest. It is highly irritating to tissues and must be injected into a large vein with precautions to avoid extravasation. If bicarbonate has been administered through the same line, it must be cleared before introducing the calcium. The following sections focus on the pharmacologic and electric interventions appropriate to various clinical settings common in cardiac arrest. Special Situations Patients who have nearly drowned in cold water may recover after prolonged periods of submersion. Apparently, the hypothermia and bradycardia of the diving reflex may serve to protect against organ damage . The body’s ability to maintain temperature is diminished by alcohol, sedation, antidepressants, neurologic problems, and advanced age. Because of the associated bradycardia and oxygen- sparing effects, prolonged hypothermia and arrest may be tolerated with complete recovery. A longer period may be needed to establish breathlessness and pulselessness because of profound bradycardia and slowed respiratory rate.
However cheap prednisolone 20mg with amex allergy medicine erowid, neither anemia nor basophilic stippling is a sensitive or specific indicator of lead intoxication cheap 5 mg prednisolone mastercard allergy treatment in children. Lead-induced anemia results from either a prolonged exposure or a concentrated short-term exposure with a latent period of several weeks cheap 20 mg prednisolone free shipping allergy testing ige. Lead toxicity produces anatomic lesions in the proximal tubule and loops of Henle, which is characterized by round acidophilic intranuclear inclusion bodies. Most often, lead-induced renal injury is associated with prolonged exposure to large amounts of lead, resulting in progressive renal insufficiency. Peripheral nervous system toxicity is known as lead palsy and is due to the degenerative changes in the motoneurons and their axons, with secondary effects involving the myelin sheaths . Clinical Toxicity Poisoning is usually the result of continued exposure to small amounts of lead rather than a single acute event. Usually, the clinical presentation of acute lead toxicity appears to be associated with a sharp incremental rise in the concentration of lead in various soft tissues, and this often occurs against the background of chronic lead poisoning. The multisystemic toxicity of lead presents a spectrum of clinical findings ranging from overt, life-threatening intoxication to subtle, subclinical deficits. Acute ingestion of very large quantities of lead (gram quantities) may cause abdominal pain, toxic hepatitis, and anemia (usually hemolytic). Subacute or chronic exposure causes nonspecific constitutional symptoms such as fatigue, arthralgias, decreased libido, irritability, impotence, depression, anorexia, malaise, myalgias, weight loss, and insomnia . Central nervous system findings range from impaired concentration, visual–motor coordination, and headache, to severe, life-threatening encephalopathy characterized by vomiting, tremors, hyperirritability, ataxia, confusion, delirium, lethargy, obtundation, convulsions, coma, and death. A peripheral motor neuropathy, predominantly affecting the upper extremities, may result in extensor weakness. Nephrotoxic effects include overt reversible acute tubular dysfunction, in particular, Fanconi-like aminoaciduria in children, and chronic progressive renal interstitial fibrosis following heavy long-term exposure in lead workers. Sometimes hyperuricemia, with or without evidence of gout, may be associated with the renal insufficiency. Diagnostic Evaluation Although encephalopathy and abdominal colic following a suspect activity may readily suggest the diagnosis of severe lead intoxication, the nonspecific nature of mild-to-moderate intoxication frequently presents a diagnostic challenge. Exposure is often not suspected, and symptoms are commonly attributed to a “nonspecific viral illness. Lead encephalopathy should be considered in any child with delirium or seizures, and milder degrees of intoxication should be considered in children with neurobehavioral deficits or developmental delays. Lead encephalopathy has usually been associated with blood lead concentrations of 100 μg per dL or more . Whole blood lead concentration is the most useful screening and diagnostic test for acute or recent lead exposure. This test does not measure total-body lead burden, but it does reflect abrupt changes in lead exposure. However, it was subsequently shown that other porphyrins were measured in minute amounts, and most protoporphyrin had nonenzymatically bound zinc and was therefore not “free. Urinary lead excretion reflects the plasma lead concentration, which increases and decreases more rapidly than does blood lead concentration. Management Acute lead encephalopathy is a medical emergency that requires intensive care and monitoring of the patient. It has long been recommended that any child who is symptomatic from lead poisoning or has a whole blood lead concentration >80 μg per dL should be hospitalized immediately and treated as a medical emergency . More recently, the Centers for Disease Control and Prevention has issued a statement that children with blood lead concentrations of 70 μg per dL or greater require immediate chelation therapy . Although present-day recommendations for the treatment of lead encephalopathy were derived from experiences in managing children [22,24–26], they have been extrapolated to adults. As with any potential life-threatening emergency, assessment and aggressive management of the airway, breathing, and circulation should be paramount. Ultimately, the chief priority is to identify and eradicate the source of lead exposure and institute control measures to prevent repeated intoxication. Lead-containing buckshot, shrapnel, or bullets in or adjacent to synovial spaces should be surgically removed if possible, especially if associated with evidence of systemic lead absorption. In a child presenting with encephalopathy, immediate treatment should begin with establishing an adequate urine output . If this fails to produce a urine output, infusion of a 20% mannitol solution (1 to 2 g per kg) is recommended at 1 mL per minute. Such management is designed to avoid excessive fluid administration and prevent further development of cerebral edema. However, when cerebral edema occurs in the presence of encephalopathy, there is further insult to the brain, and it may be the immediate cause of death. If paralysis with sedation or general anesthesia is required for controlling seizure activities, a bedside electroencephalogram should be obtained to rule out electrical status. Because high doses of phenytoin and phenobarbital were often required to control the initial seizures in lead encephalopathy, paraldehyde was formerly used. However, barbiturates were recommended in the prevention of seizures during the early convalescent phase of lead encephalopathy. Repeated seizures and hypoxia can exacerbate cerebral edema, and so it was suggested that anticonvulsants be administered when there is evidence of increased muscle tone or muscle twitching; one should not wait for obvious seizure activity . Computed tomography scan of the head should be performed in patients presenting with encephalopathy to screen for cerebral edema. The benefit of glucocorticoids for treating perifocal vasogenic edema due to an intrinsic intracranial mass lesion is well established. However, glucocorticoids have not been proved beneficial in models of intracellular cytotoxic edema, and neurologic outcome studies do not support the routine use of glucocorticoids following head injury, global brain ischemia, or cerebral vascular accidents . If the cerebral edema associated with lead encephalopathy is believed to be vasogenic in origin, the empiric use of dexamethasone should be considered. Chelating agents have been shown to decrease blood lead concentrations and increase urinary lead excretion. However, controlled clinical trials demonstrating therapeutic efficacy is lacking, and treatment recommendations have been largely empiric. If severe anemia requires prompt intervention during chelation therapy, transfusion would be preferable. Increased urinary lead excretion begins within 1 hour and is followed by a decrease in whole blood lead concentration over the course of treatment. For patients with high body lead burdens, cessation of chelation is often followed by a rebound in blood lead concentrations as bone stores equilibrate with lower soft-tissue concentrations. A third course may be required if the whole blood concentration rebounds to 50 mg per dL or greater within 48 hours after the second chelation treatment. A second or third course of chelation may be considered on the basis of the same guidelines as discussed in the previous paragraph. It has an insignificant effect on elimination of the endogenous minerals calcium, iron, and magnesium. The drug is predominantly cleared by the kidneys, with peak urinary elimination of the parent drug and its metabolites occurring between 1 and 4 hours. An additional course of treatment may be considered on the basis of posttreatment whole blood lead concentrations and the persistence or recurrence of symptoms.