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However buy 75mg amitriptyline with visa, the liver can be damaged by cytokines released by Kupffer cells as well as by factors released from activated neutrophils buy amitriptyline 25 mg without prescription. The subsequent fibrin deposition and hepatocyte damage can adversely affect the microcirculation of the liver cheap 25 mg amitriptyline free shipping, thereby leading to progressive liver damage and systemic toxicity [52] purchase amitriptyline 25 mg with visa. The role that the liver plays in the immune and metabolic responses to infection can lead to significant clinical sequelae. Aminotransferase elevation is characteristic in this setting and is reflective of cellular and mitochondrial injury. Prompt treatment of sepsis with supportive care and antibiotic therapy can result in normalization of enzymes and reversal of the associated hepatic dysfunction. There is no current evidence to support the use of antibodies directed toward endotoxins or cytokines for management [54]. The use of a stress dose of steroids has been found to favorably affect host defenses and reduce bacterial colonization of the liver during endotoxemia, but its use in sepsis without shock is controversial and does not appear to be beneficial [55,56]. Sepsis, hemorrhage, severe trauma, or tissue injury such as pancreatitis can precipitate this clinical picture. Hepatic hypermetabolism leads to relative systemic hypoperfusion, and multiple organ injury develops because tissue perfusion is continually compromised. In these conditions, the liver reduces protein synthesis, increases protein catabolism, and decreases detoxification potential. Disproportionately high bilirubin levels compared with aminotransferase levels develop among patients with hepatic dysfunction. Patients with elevations in serum bilirubin greater than 8 mg per dL, without the presence of hemolysis or biliary obstruction, have a mortality rate greater than 90% [56]. Prompt reversal of hypotension can greatly reduce hepatic necrosis, bacterial translocation, and impaired Kupffer cell activity seen in patients with shock. This is most likely owing to underdiagnosis and underreporting because the abnormalities range from asymptomatic liver chemistry abnormalities with a small potential impact to life or function to fulminant hepatic failure with high morbidity and mortality. The culprit drug or medication may be difficult to identify especially in the setting of polypharmacy. A thorough medication history obtained from the patient, relatives, friends, caregivers, and pharmacy records is essential to identify the most likely precipitating agent. Overall, the combined rate of death and need for transplantation is estimated to be approximately 10%. Injury develops from the direct effect of the drugs or their metabolites during hepatic detoxification process through cell stress, mitochondrial inhibition, and/or immune activation. Toxic by- products produced by the cytochrome P450 system or through conjugation can alter cell plasma membranes, cellular enzyme activity, or mitochondria. Drugs and their metabolites can also induce a host immune defense response with inflammatory cytokines, complement system activation, and nitric oxide, playing integral roles in the development of hepatocyte damage. With the inception of the Drug Induced Liver Injury Network, the pace of research in the field has grown exponentially. Although categorization was historically presented as either intrinsic (dose dependent and predictable) and idiosyncratic (unpredictable), our current understanding has evolved to consider multiple factors including host metabolism, drug exposure, environmental factors, immune responses, hepatic repair, and genetic polymorphisms [60]. Injury patterns are described as hepatocellular, cholestatic, or mixed hepatocellular-cholestatic based on liver biochemical parameters. Recognizing these patterns can be helpful for narrowing the differential diagnosis, although different patterns can be caused by the same medication (e. Isolated serum enzyme abnormalities can be simply related to induction of cytochrome P450 enzymes and are not necessarily indicative of hepatotoxicity. Cholestasis can occur with hepatocellular inflammation and necrosis, with associated systemic symptoms such as fever, myalgias, arthropathy, and rash. Toxicity from erythromycin, chlorpromazine, or oral hypoglycemic agents can present with this clinical picture. Cholestasis with minimal or no systemic symptoms can also occur and is the presentation typically associated with anabolic steroid or estrogen use [62]. Because the presentation of drug-induced cholestasis can resemble biliary obstruction, hepatobiliary imaging is often necessary to exclude biliary ductal dilation or a hepatic or pancreatic mass. Approximately 50% of cases of fulminant hepatic failure are attributed to acetaminophen and 11% are attributed to non-acetaminophen drugs. Continuous and/or repeated exposures to various drugs (such as amiodarone or methotrexate) can also result in chronic liver injury resembling other causes of chronic liver disease, such as autoimmune hepatitis or alcoholic liver disease [59,63]. Initially, the syndrome was thought to occur primarily as a result of injury directed toward the hepatic venules, with progressive venular obliteration, hepatocyte necrosis, and fibrosis. More recent studies indicate that venular involvement is not essential to pathogenesis and that sinusoidal obstruction is the primary mechanism behind disease development [68,69]. Classically, 3 to 4 weeks after the triggering event, the affected patient develops weight gain (fluid retention and ascites), right upper quadrant pain (tender hepatomegaly), and jaundice. Laboratory abnormalities begin with isolated hyperbilirubinemia (mostly conjugated or direct), followed by elevations in alkaline phosphatase and aminotransferases [70,71]. A high index of clinical suspicion must be maintained for a successful diagnosis because several other conditions have similar presentations. The major histologic features are sinusoidal congestion and fibrosis, necrosis of pericentral hepatocytes, narrowing and eventually fibrosis, and obliteration of sublobular and central venules [74]. A transjugular approach to measure the hepatic venous pressure gradient (>10 mm Hg) may have diagnostic and prognostic implications and facilitates obtaining a liver biopsy. Mild to moderate disease is characterized by eventual resolution of liver dysfunction, whereas severe disease is associated with multiorgan failure and a mortality rate approaching 100%. Risk factors include underlying hepatic disease, age, source of stem cells, conditioning regimen, age, sex, and metastatic malignancy. The strongest evidence exists for the use of defibrotide and ursodeoxycholic acid for prophylaxis, whereas agents such as pentoxifylline, prostaglandin E1, heparin, and antithrombin are not recommended because if mixed data and lack of randomized controlled trials [78–80]. Diagnosis is generally clinical and should be considered in any patient who presents with abdominal pain with diarrhea, classic rash, and/or rising bilirubin within 100 days following transplantation [88]. Patients who do not respond or progress within the first 5 to 7 days are considered steroid refractory and carry a poor prognosis [91]. Chronic viral hepatitis is arbitrarily defined as the presence of persistent liver inflammation, liver chemistry abnormalities, and positive serologic and molecular markers for more than 6 months. Damage to the hepatic parenchyma, with or without fibrosis, is a common outcome of chronic liver disease. Regardless of whether the insult to the hepatocytes, the biliary ducts, or the hepatic vasculature is toxic, viral, metabolic, autoimmune, or ischemic, the reparative process often leads to similar outcomes. Cirrhosis is a chronic diffuse condition characterized by replacement of liver cells by fibrotic tissue, which creates a nodular-appearing distortion of the normal liver architecture. Highly potent direct acting antivirals with cure rates >90% in most cases are creating a significant impact on patients with chronic hepatitis C [99,100]. It is the most common cause of liver cancer worldwide; and it is unevenly distributed throughout the world. In endemic areas (East Asia and sub-Saharan Africa), the infection is predominantly vertically transmitted from the mother to the infant. Although alcohol exerts a direct toxic effect on the liver, significant liver damage develops among only 10% to 20% of those patients with chronic alcohol abuse. Severe alcoholic hepatitis is a form of alcoholic liver disease associated with jaundice and coagulopathy, with a 30% to 50% 1-month mortality [104]. Alcoholic hepatitis–related hospitalization increased from 2002 to 2010, and inpatient mortality decreased during this period [105]. Alcoholic liver disease alone or in combination with other liver-related disease is one of the most common indications for liver transplant in the United States [106]. It is important to recognize acute decompensation in Wilson disease because this condition is universally fatal without a liver transplant. Clinical Manifestations and Diagnosis Clinical manifestations of chronic liver disease vary according to the functional and histologic stage of the liver disease. Physical findings described in patients with cirrhosis include temporal wasting, jaundice, telangiectasia, gynecomastia, ascites, splenomegaly, caput medusae, palmar erythema, and testicular atrophy. These markers may reflect the degree and progression of chronic liver disease and play an important role in determining patient prognosis. There is significant progress in noninvasive fibrosis staging and diagnosis of cirrhosis with the use of serum markers and tools such as elastography.

K2 cheap amitriptyline 75 mg line, also known as Spice or synthetic cannabis proven amitriptyline 25 mg, is dried plant material order amitriptyline 25 mg on line, which has been sprayed with synthetic chemicals that cause psychoactive effects amitriptyline 75mg with amex. Cocaine and methamphetamine have similar stimulant effects such as alertness, anxiety, tachycardia, hypertension, and hyperthermia. Ethanol is a depressant, which often will produce the opposite effects of stimulants including relaxation, drowsiness, and in high doses hypothermia. Cocaine combined with ethanol forms cocaethylene, which may lead to aggressive and impulsive behaviors as well as the potential for sudden myocardial infarction. Fentanyl derivatives are often many times more potent than heroin or fentanyl, which has led to an alarming number of overdoses in recent years. Overview Protozoan parasites that cause human diseases are prevalent in underdeveloped tropical and subtropical countries, where sanitary conditions, hygienic practices, and control of the vectors of transmission are inadequate. However, with increased world travel, protozoal diseases are no longer confined to specific geographic locales. Because they are unicellular eukaryotes, the protozoal cells have metabolic processes closer to those of the human host than to prokaryotic bacterial pathogens. Therefore, protozoal diseases are less easily treated than bacterial infections, and many of the antiprotozoal drugs cause serious toxic effects in the host, particularly on cells showing high metabolic activity. Chemotherapy for Amebiasis Amebiasis (amebic dysentery) is an infection of the intestinal tract caused by Entamoeba histolytica. Most infected individuals are asymptomatic but can exhibit varying degrees of illness depending on host factors and formation of trophozoites. Due to the risk of developing invasive disease and acting as a potential source of infection for others, therapy is indicated for acutely ill patients and asymptomatic carriers of E. Therapeutic agents for amebiasis are classified as luminal, systemic, or mixed amebicides according to the site of action (ure 46. For example, luminal amebicides act on the parasite in the lumen of the bowel, whereas systemic amebicides are effective against amebas in the intestinal wall and liver. Mixed amebicides are effective against both the luminal and systemic forms of the disease, although luminal concentrations are too low for single-drug treatment. Mechanism of action Amebas possess ferredoxin-like, low-redox-potential, electron transport proteins that participate in metabolic electron removal reactions. Pharmacokinetics Metronidazole is completely and rapidly absorbed after oral administration. Metabolism of the drug depends on hepatic oxidation of the metronidazole side chain by mixed-function oxidase, followed by glucuronidation. Therefore, concomitant treatment with inducers of the cytochrome P450, such as phenobarbital, enhances the rate of metabolism, and inhibitors, such as cimetidine, prolong the plasma half-life of metronidazole. Adverse effects the most common adverse effects are nausea, vomiting, epigastric distress, and abdominal cramps (ure 46. Other effects include oral moniliasis (yeast infection of the mouth) and, rarely, neurotoxicity (dizziness, vertigo, and numbness or paresthesia), which may necessitate discontinuation of the drug. It is used for treatment of amebiasis, amebic liver abscess, giardiasis, and trichomoniasis. Luminal amebicides After treatment of invasive intestinal or extraintestinal amebic disease is complete, a luminal agent, such as iodoquinol, diloxanide furoate, or paromomycin, should be administered for treatment of the asymptomatic colonization state. Adverse effects of iodoquinol include rash, diarrhea, and dose-related peripheral neuropathy, including a rare optic neuritis. Paromomycin is directly amebicidal and also exerts its antiamebic actions by reducing the population of intestinal flora. Systemic amebicides These drugs are useful for treating extraintestinal amebiasis, such as liver abscesses, and intestinal wall infections caused by amebas. It eliminates trophozoites in liver abscesses, but it is not useful in treating luminal amebiasis. The use of this ipecac alkaloid is limited by its toxicity, and it has largely been replaced by metronidazole. Adverse effects include pain at the site of injection, nausea, cardiotoxicity (arrhythmias and congestive heart failure), neuromuscular weakness, dizziness, and rash. Chemotherapy for Malaria Malaria is an acute infectious disease caused by five species of the protozoal genus Plasmodium. The classic presentation of malaria begins with headache and fatigue, followed by fever, chills, and sweats. Plasmodium falciparum is the most dangerous species and the primary cause of severe malaria, causing an acute, rapidly fulminating disease characterized by persistent high fever, hyperparasitemia, and organ system dysfunction. Plasmodium falciparum infection can lead to capillary obstruction, cerebral malaria, and death within days without prompt treatment. Plasmodium vivax, malariae, and ovale cause a milder form of the disease; however, the P. Plasmodium knowlesi is an uncommon form of malaria, previously thought to infect only nonhuman primates, which causes human infections, sometimes severe, in Southeast Asia. Resistance acquired by Plasmodium to antiprotozoal drugs has led to new therapeutic challenges, particularly in the treatment of P. A summary of the life cycle of the parasite and the sites of action of the antimalarial drugs are presented in ure 46. Mechanism of action While not completely understood, metabolites of primaquine are believed to act as oxidants that severely disrupt the metabolic processes of plasmodial mitochondria. The metabolites are responsible for the schizonticidal action, as well as for the hemolysis and methemoglobinemia encountered as toxicities. Pharmacokinetics Primaquine is well absorbed after oral administration and is not concentrated in tissues. Adverse effects Primaquine is associated with drug-induced hemolytic anemia in patients with glucose-6-phosphate dehydrogenase deficiency (ure 46. Large doses of the drug may cause abdominal discomfort (especially when administered in combination with chloroquine) and occasional methemoglobinemia. Chloroquine Chloroquine is a synthetic 4-aminoquinoline that had been the mainstay of antimalarial therapy for many years; however, the use is now limited due to P. Chloroquine is used in the prophylaxis of malaria for travel to areas with known chloroquine-sensitive malaria. Mechanism of action Although the mechanism of action is not fully understood, the processes essential for the antimalarial action of chloroquine are outlined in ure 46. After traversing the erythrocytic and plasmodial membranes, chloroquine (a diprotic weak base) is concentrated in the acidic food vacuole of the malarial parasite, primarily by ion trapping. In the food vacuole, the parasite digests the host cell’s hemoglobin to obtain essential amino acids. However, this process also releases large amounts of soluble heme, which is toxic to the parasite. To protect itself, the parasite polymerizes the heme to hemozoin (a pigment), which is sequestered in the food vacuole. Chloroquine specifically binds to heme, preventing its polymerization to hemozoin. The increased pH and the accumulation of heme result in oxidative damage to the phospholipid membranes, leading to lysis of both the parasite and the red blood cell. Pharmacokinetics Chloroquine is rapidly and completely absorbed following oral administration. The drug has a very large volume of distribution and concentrates in erythrocytes, liver, spleen, kidney, lung, melanin-containing tissues, and leukocytes. Chloroquine is dealkylated by the hepatic mixed-function oxidase system, and some metabolic products retain antimalarial activity. At higher doses, gastrointestinal upset, pruritus, headaches, and blurred vision may occur (ure 46. An ophthalmologic examination should be routinely performed during extended use due to potential retinal toxicity. Discoloration of the nail beds and mucous membranes may be seen on chronic administration. Chloroquine should be used cautiously in patients with hepatic dysfunction, severe gastrointestinal problems, or neurologic disorders.

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These drugs are coformulated with β-lactamase inhibitors cheap 10 mg amitriptyline free shipping, such as clavulanic acid or sulbactam amitriptyline 25 mg for sale, to combat infections caused by β-lactamase–producing organisms generic amitriptyline 50 mg line. Resistance in the form of plasmid-mediated penicillinases is a major clinical problem discount 10mg amitriptyline visa, which limits use of aminopenicillins with some gram- negative organisms. Formulation of piperacillin with tazobactam extends the antimicrobial spectrum to include penicillinase-producing organisms (for example, most Enterobacteriaceae and Bacteroides species). Resistance Survival of bacteria in the presence of β-lactam antibiotics occurs due to the following: 1. They are the major cause of resistance to the penicillins and are an increasing problem. Some of the β-lactam antibiotics are poor substrates for β-lactamases and resist hydrolysis, thus retaining their activity against β-lactamase–producing organisms. In gram-positive bacteria, the peptidoglycan layer is near the surface of the bacteria and there are few barriers for the drug to reach its target. Reduced penetration of drug into the cell is a greater concern in gram-negative organisms, which have a complex cell wall that includes aqueous channels called porins. An excellent example of a pathogen lacking high permeability porins is Pseudomonas aeruginosa. The presence of an efflux pump, which actively removes antibiotics from the site of action, can also reduce the amount of intracellular drug (for example, Klebsiella pneumoniae). Antibiotic exposure can prevent cell wall synthesis and can lead to morphologic changes or lysis of susceptible bacteria. Administration the route of administration of a β-lactam antibiotic is determined by the stability of the drug to gastric acid and by the severity of the infection. Penicillin V, amoxicillin, and dicloxacillin are available only as oral preparations. They are slowly absorbed into the circulation and persist at low levels over a long time period. Absorption the acidic environment within the intestinal tract is unfavorable for the absorption of penicillins. In the case of penicillin V, only one-third of an oral dose is absorbed under the best of conditions. Food decreases the absorption of the penicillinase-resistant penicillin dicloxacillin because as gastric emptying time increases, the drug is destroyed by stomach acid. All the penicillins cross the placental barrier, but none have been shown to have teratogenic effects. Metabolism Host metabolism of the β-lactam antibiotics is usually insignificant, but some metabolism of penicillin G may occur in patients with impaired renal function. Nafcillin and oxacillin are exceptions to the rule and are primarily metabolized in the liver. Excretion the primary route of excretion is through the organic acid (tubular) secretory system of the kidney as well as by glomerular filtration. Because nafcillin and oxacillin are primarily metabolized in the liver, they do not require dose adjustment for renal insufficiency. Probenecid inhibits the secretion of penicillins by competing for active tubular secretion via the organic acid transporter and, thus, can increase blood levels. Reactions range from rashes to angioedema (marked swelling of the lips, tongue, and periorbital area) and anaphylaxis. To determine whether treatment with a β-lactam is safe when an allergy is noted, patient history regarding severity of previous reaction is essential. Diarrhea Diarrhea is a common problem that is caused by a disruption of the normal balance of intestinal microorganisms. It occurs to a greater extent with those agents that are incompletely absorbed and have an extended antibacterial spectrum. Pseudomembranous colitis from Clostridium difficile and other organisms may occur with penicillin use. Nephritis Penicillins, particularly methicillin, have the potential to cause acute interstitial nephritis. Neurotoxicity the penicillins are irritating to neuronal tissue, and they can provoke seizures if injected intrathecally or if very high blood levels are reached. Hematologic toxicities Decreased coagulation may be observed with high doses of piperacillin and nafcillin (and, to some extent, with penicillin G). Cytopenias have been associated with therapy of greater than 2 weeks, and therefore, blood counts should be monitored weekly for such patients. Cephalosporins the cephalosporins are β-lactam antibiotics closely related both structurally and functionally to penicillins. Most cephalosporins are produced semisynthetically by the chemical attachment of side chains to 7-aminocephalosporanic acid. Structural changes on the acyl side chain at the 7-position alter antibacterial activity and variations at the 3- position modify the pharmacokinetic profile (ure 29. Cephalosporins have the same mode of action as penicillins, and they are affected by the same resistance mechanisms. However, they tend to be more resistant than the penicillins to certain β-lactamases. Antibacterial spectrum Cephalosporins have been classified as first, second, third, fourth, and advanced generation, based largely on their bacterial susceptibility patterns and resistance to β-lactamases (ure 29. First generation the first-generation cephalosporins act as penicillin G substitutes. Most oral cavity anaerobes like Peptostreptococcus are sensitive, but the Bacteroides fragilis group is resistant. Second generation the second-generation cephalosporins display greater activity against gram-negative organisms, such as H. They are the only cephalosporins commercially available with appreciable activity against gram-negative anaerobic bacteria. However, neither drug is first line because of the increasing prevalence of resistance among B. Third generation These cephalosporins have assumed an important role in the treatment of infectious diseases. The spectrum of activity of this class includes enteric organisms, such as Serratia marcescens and Providencia species. Third-generation cephalosporins must be used with caution, as they are associated with significant “collateral damage,” including the induction of antimicrobial resistance and development of Clostridium difficile infection. Cefepime has a wide antibacterial spectrum, with activity against streptococci and staphylococci (but only those that are methicillin susceptible). Cefepime is also effective against aerobic gram-negative organisms, such as Enterobacter species, E. In addition to its broad gram-positive activity, it also has similar gram-negative activity to the third-generation cephalosporin ceftriaxone. The twice-daily dosing regimen also limits use outside of an institutional setting. For example, ceftriaxone and cefotaxime are effective in the treatment of neonatal and childhood meningitis caused by H. Elimination Cephalosporins are eliminated through tubular secretion and/or glomerular filtration (ure 29. Therefore, doses must be adjusted in renal dysfunction to guard against accumulation and toxicity. One exception is ceftriaxone, which is excreted through the bile into the feces and, therefore, is frequently employed in patients with renal insufficiency. Adverse effects Like the penicillins, the cephalosporins are generally well tolerated. Patients who have had an anaphylactic response, Stevens-Johnson syndrome, or toxic epidermal necrolysis to penicillins should not receive cephalosporins. Cephalosporins should be avoided or used with caution in individuals with penicillin allergy. Current data suggest that the cross-reactivity between penicillin and cephalosporins is around 3% to 5% and is determined by the similarity in the side chain, not the β-lactam structure. The highest rate of allergic cross-sensitivity is between penicillin and first-generation cephalosporins. Carbapenems Carbapenems are synthetic β-lactam antibiotics that differ in structure from the penicillins in that the sulfur atom of the thiazolidine ring (ure 29.

Patient Expectations Treatment of benign pigmented may be performed on virtually any body region where photodamage is present 10 mg amitriptyline visa. Noticeable results are evident after a single treatment in properly selected candidates cheap 25 mg amitriptyline visa, but typically a series of 3–5 treatments are required for optimal results cheap amitriptyline 10mg otc. After treatment cheap amitriptyline 25mg online, pigmented lesions typically darken and become more noticeable for 1–2 weeks before flaking off to reveal lightened or resolved lesions. It is important for patients to understand that treated lesions will temporarily look worse before they look better. Indications • Lentigines • Ephelides • Mottled pigmentation • Postinflammatory hyperpigmentation • Poikiloderma of Civatte • Melasma Melasma can respond unpredictably with lasers. Paradoxical darkening of melasma can occur particularly with laser treatments that excessively heat the skin using aggressive parameters or short intervals between treatments. Alternative Therapies Nonlaser treatment options for benign pigmented lesions include liquid nitrogen, exfoliation treatments such as microdermabrasion and chemical peels, and topical skin- lightening products such as hydroquinone and azelaic acid. Liquid nitrogen is much less costly than lasers; however, it is frequently associated with hyperpigmentation and hypopigmentation posttreatment and it is advisable to restrict use to lighter skin types. Exfoliation and topical therapies are slower to achieve improvements and results are rarely comparable to lasers. Devices Currently Available for Treatment of Pigmented Lesions Lasers used for treatment of benign pigmented lesions can be broken down into 2 broad categories based on their cutaneous target: Pigment specific lasers target the melanin chromophore (s. Lesions at different depths are also targeted where shorter wavelengths target more superficial lesions and the longer wavelengths target deeper lesions. High-quality devices use built-in cooling for epidermal protection, which provides some anesthesia as well. Due to the short wavelength and high melanin absorption, this laser targets lesions located in the epidermis such as lentigines and ephelides. The disadvantage of this superficial target depth is the formation of purpura and epidermal injury with associated hyperpigmentation and hypopigmentation, which has limited their use in the past. Translucent compression spoons may be used to depress pigmented lesions, which reduce vascular target in the treatment area, thereby reducing risks of purpura and overtreatment. Ruby lasers (694 nm) were one of the first long pulse lasers to be used for treatment of pigmented lesions, but they had a high incidence of hypopigmentation and are rarely used today. Alexandrite lasers (755 nm) are commonly used for hair removal but are also effective for treatment of epidermal pigmented lesions. They typically use a cryogen spray for cooling; these cannisters are disposable and have an associated cost. Diode lasers (810 nm) are also primarily used for hair removal and, like alexandrite lasers, their high melanin absorption also makes them effective for treatment of discrete epidermal pigmented lesions. They can be used in darker skin types more safely than alexandrite lasers due to their longer wavelength with deeper penetration, and built-in cooling. Part of their appeal and popularity is due to their relatively compact size and lack of disposable parts. Melanosomes are very small in size (approximately 1 μm) and respond well to these extremely short pulse widths. When treating discrete lesions with these wavelengths, spot size is chosen to match the size of the lesion to avoid pigmentary changes to the surrounding skin. Skin Resurfacing Lasers Skin resurfacing lasers are primarily used for collagen remodeling effects to treat wrinkles and acne scars but can also reduce pigmentation. They are used to treat large areas confluently for diffuse pigmentation, rather than for discrete pigmented lesions. While they do not generate a wound as ablative lasers do, the skin is disrupted and requires some downtime for healing. Treatments are painful and patients typically require topical anesthetic and may also require oral analgesics. The nonablative fractional thulium laser (1927 nm) has greater absorption by water than the other nonablative fractional lasers, which result in more superficial penetration and more effective targeting of epidermal pigmentation. There is more downtime with 1927 nm than other nonablative fractional lasers and otherwise it has similar complication rates. Ablative lasers (2790 nm, 2940 nm, 10600 nm) are the most aggressive lasers and are primarily used for resurfacing to reduce wrinkles and laxity but can also treat epidermal pigmented lesions. Ablative lasers create a wound and have risks of pigmentary changes such as hyperpigmentation and hypopigmentation, scarring, and infection. Treatments are painful and patients typically require oral analgesics, anxiolytics, and topical anesthetics. Fractional ablative lasers, relative to nonfractional ablative lasers, have shorter recover times and similar types of complications, but with significantly lower incidences and reduced severity. Lesions suspicious for melanoma may be asymmetric, have irregular borders, variegated color, diameter greater than 6 mm, changing or new characteristics such as enlargement or bleeding. Topical prescription skin-lightening products can be used such as hydroquinone cream 4–8% or over-the-counter cosmeceutical products containing kojic acid, arbutin, niacinamide, and azelaic acid (which are less effective) once or twice daily for 1 month prior to treatment. Test spot parameters are selected based on the patient’s Fitzpatrick skin type and pigment characteristics following the manufacturer’s guidelines for wavelength, spot size, fluence, and pulse width. Test spots are viewed 3–5 days after placement for evidence of erythema, blister, crust, or other adverse effect. Patients should be informed that lack of an adverse reaction with test spots does not ensure that a side effect or complication will not occur with a treatment. In addition, anesthesia can interfere with patient feedback, an important component for selecting appropriate treatment parameters. For patients with low pain thresholds, consider an oral analgesic such as tramadol (Ultram™) 50 mg 1–2 tablets 1 hour prior to procedure. Selecting Initial Laser Parameters for Treatment Many clinical factors influence laser parameter selection for treatment including: • Fitzpatrick skin type. A patient having the same Fitzpatrick skin type2 with sparse light brown lentigines may use a pulse width of 15 ms and fluence of 34–36 J/cm. When assessing the skin it is important to take all chromophores that are potentially targeted by the wavelength used into account. In addition to pigmented lesions, photodamaged skin often has red vascular lesions and may also have dark hair present. For example, if the treatment area has sparse, faintly pigmented lesions that overlie intense erythema, conservative laser parameters are used. For example, if the treatment area has sparse, faintly pigmented lentigines that overlie an area with dense dark hair such as a man’s beard, the discrete lentigines can be spot treated using an opaque paper “mask” to cover skin surrounding the lentigines. In addition, hair is shaved prior to treatment to reduce excessive heating from singed hair on the skin surface. Treating over darkly colored hair may cause permanent hair reduction and patients need to be informed of this risk prior to treatment. Areas such as the extremities, neck and chest are treated using more conservative parameters than the face, due to slower healing times and greater risk of complications. Initially, it is advisable to avoid lips and as skill improves, providers may choose to treat lips for lesions such as lentigines. When treating the upper lip, discomfort can be reduced by having the patient place their tongue over their teeth while keeping their lips closed. Desirable Clinical Endpoints When optimal parameters are used for treatment of pigmented lesions, one or more of the following clinical endpoints may be observed on the skin: • Darkening of the lesion and enhanced demarcation against the background skin. Providers are advised to follow manufacturer guidelines specific to the device used at the time of treatment. If the patient is recently sun exposed or has tanned skin in the treatment area, it is advisable to wait 1 month before treating to reduce the risk of complications. Position the patient comfortably on the treatment table, prone or supine, to allow for exposure of the treatment area. If working on the face provide the patient with extraocular lead goggles and have the patient remove contact lenses. Always operate the laser in accordance with your clinic’s laser safety policies and procedures and the manufacturer’s guidelines. The laser technician is comfortably positioned, usually seated, to allow for precise manipulation of the handpiece while depressing the foot pedal. Select the pulse width and fluence based on the patient’s Fitzpatrick skin type and pigmented lesion characteristics in the treatment area taking into account lesion darkness and density; and the presence of other targets in the treatment area such as vascularities and dark hair (see Selecting Initial Laser Parameters for Treatment section). Select the repetition rate based on the size and contour of the treatment area (see Selecting Initial Laser Parameters for Treatment section). Place the device treatment tip firmly on the skin, making certain that the handpiece is perpendicular to the skin surface and the entire tip is in contact with the skin.

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