It appears that the patient has erythema nodosum lesions associated with a flare of his disease, which is common. Treatment of the disease and its control usually improves the cutaneous lesions. The lesions should not be biopsied.

A 17-year-old boy with Crohn's disease with colonic involvement of 2 years of evolution, in maintenance treatment with azathioprine, consults for the appearance since 5 days ago of purplish-red, hot, painful, bilateral subcutaneous nodules of pretibial location, associated with an increase in the number of stools and abdominal pain. The most appropriate approach in this case is:

Recommend relative rest and warm cloths on both legs and add antidepressant treatment.

Biopsy skin areas away from the injured areas and prescribe opioid analgesics at the beginning.

Suspect bilateral lower extremity ischemia of drug origin.

Adjustment of the treatment of the disease.

An unusual cutaneous manifestation of Crohn's disease.

A 61-year-old man with a 12-year history of quiescent Crohn's disease on mesalamine presented to his gastroenterologist in April 2009, complaining of abdominal cramping, diarrhea, and a 25-lb weight loss over 6 weeks. He did not respond to prednisone 50 mg and 6-mercaptopurine 100 mg daily. Abdominal computed tomography findings revealed diffuse submucosal edema consistent with extensive colitis. Colonoscopy demonstrated diffuse inflammation with erythema, friability, and shallow ulcerations in the rectum and colon. Biopsies were consistent with Crohn's colitis. He was admitted for infliximab infusion for his unremitting diarrhea. Five days before admission, the patient noted mild swelling and redness of the left lower eyelid, which progressed to involve the right lower eyelid with frank pus draining from both eyes. He had no visual impairment or eye pain. Two days before admission, an ophthalmologist prescribed a steroid eyedrop with no relief. He also complained of seropurulent painful skin lesions on his face and scalp, which spread to involve his upper trunk and proximal arms. On admission to the hospital, dermatology, ophthalmology, and infectious disease consultations were obtained to rule out disseminated infection before initiation of infliximab therapy. The patient was afebrile and hemodynamically stable. His oral mucosa was normal. He had prominent bilateral lower eyelid edema, erythema, and superficial erosions with hemorrhagic crusting and frank green purulent drainage from both eyes, with crusting along the lower lash line and bilateral sclera injection (Figure 1). On his scalp, face, trunk, and proximal extremities, he had 25 to 30 erythematous, 4- to 8-mm papulopustules with narrow red halos, some with central necrosis and crusting (Figure 2). Cultures from the purulent ocular drainage and pustules on the trunk and arms were all negative for bacteria, virus, and fungi. Gram stain from the eye drainage showed polymorphonuclear leukocytes without organisms. Tissue cultures were negative for bacterial, fungal, and mycobacterial infection. Skin biopsy taken from the central upper back demonstrated subcorneal pustules with areas of eroded epidermis and collections of neutrophils in the superficial dermis (Figure 3). Special stains were negative for organisms. He received infliximab infusion 5 mg/kg for a total dose of 420 mg over 2 hours. Within 48 hours of infusion, there was notable decrease in size of lesions, in addition to reduction of purulent drainage from both eyes. The patient was discharged home following infliximab infusion. His skin lesions resolved during a period of 2 weeks, leaving small pink atrophic scars. He received his second infusion of infliximab 2 weeks after discharge with continued improvement in his gastrointestinal symptoms.

A Rare Case of <i>Helicobacter pylori</i> Infection Complicated by Henoch-Schonlein Purpura in an Adult Patient.

Henoch-Schonlein purpura (HSP) is known as a leukocytoclastic vasculitis of small vessels, resulting in skin, joint, gastrointestinal (GI) and renal involvement. It is the most common acute vasculitis in children but is relatively uncommon in adults. The pathogenesis of HSP remains unclear, but a wide variety of conditions such as bacterial or viral infections, vaccinations, drugs and other environmental exposures may be responsible for the onset. A few previous case reports have described an association between gastric <iHelicobacter pylori</i (HP) infection and HSP. A 30-year-old Indian man who migrated to the USA from India 3 years prior to this presentation with a past medical history of psoriasis on remission, not on any medications presented to the emergency department with sudden onset constant abdominal pain for 5 days. The pain was in the right upper quadrant, spasmodic in nature. The abdominal examination was normal. The patient was evaluated with complete blood count, comprehensive metabolic panel, urinalysis, computed tomography scan of abdomen and pelvis, and right upper quadrant ultrasound, all of which were negative except for leukocytosis. He was discharged on pantoprazole and tramadol. Pain continued despite treatment. Patient was readmitted 2 days later, when he noticed a new maculopapular rash on both legs. Upper GI endoscopy was done showing non-bleeding small gastric ulcer with multiple duodenal erosions. Gastric biopsy came back positive for HP and he was started on clarithromycin, amoxicillin and lansoprazole. Pain persisted after finishing antibiotic course. Rash continued to spread to involve the thighs, flanks, around the umbilicus and extensor surfaces of arms. Immunological workup was negative. A skin biopsy of the skin rash came back positive for leukocytoclastic vasculitis. HSP diagnosis was made by exclusion. Patient was started on prednisone 40 mg daily and improved drastically on the following day. He was continued steroids taper for 8 weeks. Rash as well as abdominal pain resolved completely. In conclusion, HSP involves the skin, GI tract, joints and kidneys. It is a pediatric disease and rarely occurs in adults. It can be associated with underlying malignancy in adults. HP infection can trigger HSP in pediatric and adult patients. Detection of the carrier state is crucial in HSP patients in areas where HP is endemic. Eradication of HP infection is usually associated with the resolution of HSP. In resistant cases with GI and renal involvement, corticosteroids use results in resolution of symptoms and reduction of the duration of mild nephritis.

Nicolau's syndrome: A rare but preventable iatrogenic disease.

Dear Editor, Nicolau's syndrome, also called embolia cutis medicamentosa or livedoid dermatitis, is a rare injection site reaction characterized by immediate intense pain at the injection site followed by erythema and a hemorrhagic patch with a livedoid reticular pattern after injections of non-steroidal anti-inflammatory drugs (NSAIDS), antiepileptics, antibiotics, antihistaminics, corticosteroids, etc. (1). To the best of our knowledge, only one case of Nicolau's syndrome has been reported after the use of triamcinolone acetonide. Herein we report two cases of Nicolau's syndrome caused by intramuscular injections of triamcinolone acetonide and diclofenac sodium, respectively. CASE 1 A 24-year-old male patient presented with severe pain and bluish discoloration of the right arm for 2 days, which he had noticed shortly after receiving an intramuscular injection of triamcinolone for recurrent episodes of urticaria by a local practitioner in the right deltoid region. On examination, there was a livedoid pattern of non-blanchable, violaceous discoloration extending from the deltoid area to the distal third of the forearm with associated induration (Figure 1, a, b). The local area was warm and tender to the touch. There was no regional lymphadenopathy, and the rest of the examination was normal. The patient's platelet count, bleeding and clotting times, prothrombin time, and international normalized ratio (INR) were unremarkable. There was no previous history of any bleeding disorder. The patient denied any intake of drugs like aspirin, warfarin, etc. Subsequently, the patient developed an ulcer on the forearm, which was managed by topical and systemic antibiotics to prevent any secondary infection of the wound. CASE 2 A 40-year-old female patient presented with complaints of pain and discoloration of the left gluteal region after receiving an intramuscular injection of diclofenac sodium for her arthralgia. A large ecchymotic patch with reticular borders was found on the gluteal region, extending to the lateral aspect of thigh (Figure 2). It was tender to the touch, non-indurated, and the local temperature was raised. There was no regional lymphadenopathy. No other abnormality was detected on examination. All routine investigations were within normal limits. Platelet count, bleeding, clotting and prothrombin times, and international normalized ratio (INR) were within normal limits. The lesions resolved within few weeks without any complications. Nicolau syndrome was first described in the early 1920s by Freudenthal and Nicolau as an adverse effect of using intramuscular injections of bismuth salts in the treatment of syphilis. Since then, several case reports of this disease occurring after intramuscular, intra-articular, intravenous, and subcutaneous injections have appeared in the literature associated with a variety of drugs like NSAIDs, vitamin K, penicillin, antihistamines, corticosteroids, local anesthetics, vaccines, polidocanol, and pegylated interferon alpha (1). The pathogenesis of Nicolau syndrome is unknown, though intra and periarterial injection of the drug is a possible cause. Stimulation of the sympathetic nerve due to periarterial injection causes spasms and consequent ischemia. Inadvertent intra-arterial injections may cause emboli and occlusion. A lipophilic drug may penetrate the vessel and produce physical occlusion like fat embolism. Cytotoxic drugs may produce perivascular inflammation and ischemic necrosis. NSAIDs are believed to additionally induce ischemic necrosis due to their inhibition of cyclooxygenase and, consequently, prostaglandins (2). The clinical features of the disease have been divided into three phases in a review by Kim et al. (3). The authors describe an initial phase characterized by intense pain with subsequent erythema. This is followed 1-3 days later by an acute phase, when an indurated, tender plaque with livedoid pattern develops. The final phase occurs between 5 days and 2 weeks later. Necrosis ensues in this stage, with possible ulceration. Diagnosis is chiefly clinical, and histopathology shows necrotic changes and vascular thrombosis. However, a biopsy was not performed in our cases because both lesions were painful. Management strategies are variable and range from conservative management with analgesics and antibiotics to active surgical debridement (4). Complications include deformities, contractures or even death. The patient in our first case developed ulceration which healed normally, while the second case resolved without any complications. Nicolau syndrome can be avoided by precautions such as aspirating the needle before injecting to check for blood, use of Z-track injection technique, proper site of injection, avoiding large doses at a single site, and regular change of sites if multiple injections are to be given (5). Nicolau syndrome is a rare disease. There are a few case reports of it occurring after diclofenac injection (1-5). We could only find one case report of this syndrome after intramuscular injection (IM) of triamcinolone in a patient with lichen planus (3), and our case is the second reported case of this syndrome as a result of triamcinolone acetonide injection, which adds to the significance to the present article.

Extraintestinal Manifestations of Inflammatory Bowel Disease -- Introduction -- Cutaneous Manifestations

Cutaneous manifestations of IBD occur in up to 15% of IBD patients. [4] The most common conditions include EN, pyoderma gangrenosum, Sweet syndrome, and oral aphthous lesions. EN frequently arises as tender raised subcutaneous nodules on the lower extremities. These nodules appear red/purple, measuring 1-5 cm in size, and occurs more commonly in females than males. EN is a self-limited condition that coincides with intestinal-IBD activity and improves with IBD treatment. Specific treatment options for mild EN include leg elevation, compression stockings, analgesic, and anti-inflammatory medication. [7]

Generalized Pyoderma Gangrenosum Associated with Ulcerative Colitis: Successful Treatment with Infliximab and Azathioprine.

Pyoderma gangrenosum (PG) is a rare ulcerative skin disease, part of the spectrum of neutrophilic and auto-inflammatory dermatoses. Its pathogenesis is unknown, although immune pathways have been implicated. Lesion biopsies show a predominantly neutrophilic infiltrate. The incidence of PG is uncertain, but it is estimated to be 3-10 per million per year, occurring at any age but most commonly between 20 and 50 years with a possible slightly higher incidence in women. Approximately 50% of patients with PG also have another disease associated with PG. The most common is inflammatory bowel disease (IBD), particularly Crohn's and ulcerative colitis (UC). Local treatment may be sufficient for mild cases, while for severe cases systemic immunosuppressants are the mainstay (1,2). We report the case of a patient with bullous PG and UC successfully treated with infliximab and azathioprine. A 32-year-old male Caucasian patient presented with painful violaceous vesicles and enlarging bullae of various sizes and with acute onset, located on the trunk and bilaterally on both the lower and the upper extremities. Lesions on the trunk were composed of hemorrhagic pustules with a surrounding erythematous overhanging border. Some of the lesions had undergone central necrosis and ulceration (Figure 1, a-d). The patient reported of the lesions had appeared one week ago, simultaneously with the exacerbation of a known inflammatory bowel disease with hemorrhagic mucoid diarrhea and fever of up to 38.5°C. The patient's medical history included UC affecting the whole colon (pancolitis), diagnosed 5 months prior to the onset of the epidermal lesions, for which the patient was receiving treatment with oral prednisolone 10 mg/day and mesalazine granules. Blood tests showed severe anemia, leukocytosis, and increased inflammatory markers (C-reactive protein, erythrocyte sedimentation rate). Antinuclear antibodies (ANA), anti-double stranded DNA (anti-dsDNA) andtibodies, antineutrophil cytoplasmic antibodies (cANCA), perinuclear neutrophil antibodies (p-ANCA), antiphospholipid antibodies, and tumor markers were within normal limits. The patient was negative for cryoglobulins, viral hepatitis (B, C) and human immunodeficiency virus (HIV). Blood cultures were negative. Microscopy and cultures for mycobacteria and fungi gave negative results. Stool samples tested negative for infections agents. The Mantoux skin test was negative. Colonoscopy showed severe pancolitis, and biopsies from the rectum and sigmoid colon were consistent with chronic ulcerative colitis. Abdominal ultrasound and chest and abdominal X-rays did not result in significant findings. Because of severe anemia, the patient received 2 blood transfusions. The histopathologic examination carried out on the erythematous border of a lesion on the lower leg showed a neutrophilic infiltrate, confined to the dermis. On the basis of clinical findings, the diagnosis of PG was established. Topical wound care consisted of local wound care and a topical corticosteroid. Systemic therapy was initiated with 40 mg/day methylprednisolone for 7 days, 30 mg/day for 7 days, then 25 mg/day, and then tapered down further. The patient received an infusion of infliximab 7.5 mg/kg at weeks 0, 2, and 6 and every 8 weeks thereafter. After week 2, oral azathioprine 2.5 mg/kg daily was added to the treatment. The patient also received mesalazine tablets (2 g ×2/day) and mesalazine enema (1-2/day). The patient showed good response to treatment, with clinical remission of skin lesions. Lesions healed with characteristic thin, atrophic scars (Figure 2, a-d). At 7-month follow-up the patient was continuing with infusions of infliximab 7.5 mg/kg and azathioprine 2.5 mg/kg and was still in remission. We reported our experience with a case of generalized bullous pyoderma gangrenosum associated with ulcerative colitis. Generalized pyoderma gangrenosum is very rare. Bullous or atypical PG was first described by Perry and Winklemann in 1972 (1). Brunsting et al. coined the term pyoderma gangrenosum (PG) to describe a series of patients with recurrent ulcerations (3). The incidence of this disease is uncertain. Its pathogenesis is unknown, but an immunological background has been suggested. In approximately 50% of patients, an underlying immunological disease is present, commonly inflammatory bowel disease (IBD) (4-6). In larger series of patients with PG, approximately 50% present with a primary disorder. Ulcerative colitis is found in 10-15% of cases. Crohn's disease is associated with PG closed than UC. Less than 3% of patients with Crohn's disease or UC develop PG (6). PG is characterized by cutaneous ulcerations with mucopurulent or hemorrhagic exudate. It begins as an inflammatory pustule with a surrounding halo that enlarges and begins to ulcerate. These very painful ulcers present with undermined bluish borders with surrounding erythema. The lesions of PG most commonly occur on the legs, but they may occur anywhere on the body. The clinical picture of PG is very characteristic. Therefore the diagnosis of PG is based firstly on clinical signs and on the patient's history of underlying diseases and then supported by biopsy. PG has four distinctive clinical and histological variants. Some have morphological and histological features that overlap with other reactive neutrophilic skin conditions. There are no diagnostic serologic features (6,7). There is no evidence that the efficacy of treatment strategies for PG differs between IBD and non-IBD patients. For patients with a diffuse disease or rapidly progressive process, systemic treatment is essential. Immunosuppression is the mainstay of treatment. Traditionally, the most commonly used drugs with the best clinical experience are systemic corticosteroids. Corticosteroids have been considered as first line treatment (6,8). As reported by the European Crohn's and Colitis Organisation (ECCO) in 2008, an evidence-based consensus on the management of special situations in patients with ulcerative colitis, systemic corticosteroids are recommended (9). Treatment with corticosteroids (e.g. prednisolone 1-2 mg per kg/day or pulse therapy with 1 g of methylprednisolone) aims to prevent progression and rapidly stop inflammation (6). Additional mesalamine and corticosteroids may be effective in patients with bowel disease (10). In recent years, tumor necrosis alpha (TNF-α) inhibitors, such as infliximab and adalimumab, were reported to be effective for PG associated with IBD. These drugs block the biological activity of TNF-α, which effects regulatory T cells, restoring their capacity to inhibit cytokine production. The TNF-α inhibitors thus suppress the inflammatory processes that is involved in the pathogenesis of PG (11). Infliximab, a chimeric monoclonal antibody, is given by infusion at weeks 0, 2, and 6 and then every 8 weeks, usually at a dosage of 5 mg/kg. UC of patients with frequent disease relapse or those that are resistant or dependent on corticosteroids is often treated with purine antimetabolites, such as azathioprine (AZA) (10). AZA, a purine antimetabolite (2.5 mg per kg/day) is administered for its steroid-sparing effects. The response occurs after 2 to 4 weeks (6, 10). Infliximab can be combined with AZA. Patients with UC treated with infliximab plus AZA were more likely to achieve corticosteroid-free remission at 16 weeks than those receiving either monotherapy (10,12).

[Cutaneous complications in idiopathic inflammatory bowel disease].

A 29-year-old male patient with the anamnesis of inflammatory bowel disease and Grave-Basedowov disease was hospitalized because of rapidly spreading skin defect with affected muscle on the left shin. This skin defect appeared after the significant decreasing of corticoids. The small skin trauma preceded the pyoderma gangrenosum. First the skin disease was not right diagnosed and patient was cured by the excision of the defect. It caused tissue disintegration, muscle necrosis and extension of the defect. The whole leg was endangered. Patient was cured with corticoids and cyclosporin A after the right diagnosis. The defect healed and laboratory inflammatory markers decreased. The immunosuppresive therapy was changed to azathioprin, the corticoid therapy was interrupted. After three months the defect was healed.

InternalMed_Harrison

Patients with SJS, SJS/TEN, or TEN initially present with acute onset of painful skin lesions, fever >39°C (102.2°F), sore throat, and conjunctivitis resulting from mucosal lesions. Intestinal and pulmonary involvement is associated with a poor prognosis, as are a greater extent of epidermal detachment and older age. About 10% and 30% of SJSand TEN-affected persons die from their disease, respectively. Drugs that most commonly cause SJS or TEN are sulfonamides, nevirapine (1 in 1000 risk of SJS or TEN), allopurinol, lamotrigine, aromatic anticonvulsants, and NSAIDs, specifically oxicam. Frozen-section skin biopsy may aid in rapid diagnosis. At this time, SJS and TEN have no proven effective treatment. The best results come from early diagnosis, immediate discontinuation of any suspected drug, supportive therapy, and paying close attention to ocular complications and infection. Systemic glucocorticoid therapy (prednisone 1–2 mg/kg) may be useful early in the evolution of the disease,

Atypical Forms of Pyoderma Gangrenosum in Inflammatory Bowel Disease: Report of Four Cases and Literature Review.

Cutaneous involvement is the second-most frequent extraintestinal manifestation of inflammatory bowel disease, with pyoderma gangrenosum (PG) a particularly relevant form because of its frequency, morbidity, and recurrence. The limited number of clinical trials involving PG increases the challenge to gastroenterologists in the management of this condition. Four cases of atypical presentations of PG are reported. A 25-year-old patient with ulcerative colitis presented an extensive chronic ulcerative lesion on her left leg that was associated with significant bleeding; the intestinal disease was in remission under the use of azathioprine. The patient was on long-term use of 60 mg corticosteroid with no improvement in the skin disease; however, initiation of cyclosporine induced remission. In the second case, a 52-year-old woman was a carrier of Crohn's disease, with a history of partial colectomy. The patient's skin condition had evolved with a cutaneous lesion localized in the perineal region, buttocks, and colostomy pouch, simulating a case of impetigo, and this had been treated with antibiotic cycles without improvement. Lesion biopsy suggested a diagnosis of PG. Consequently, the patient was started on biological therapy with infliximab, and the PG regressed. In the third case, a 38-year-old woman with a history of pancolitis presented a picture of PG with an extensive and deep ulcerative lesion in the right breast. The lesion regressed after treatment with oral corticosteroid. The final case was a 44-year-old woman with Crohn's disease suffering from Crohn's disease pancolitis. The patient's condition evolved with a mixed pattern with pustules, bullae, and ulcerative lesions in the vulva, oral cavity, gluteus, right auricular region, scalp, and left flank, and was resolved by administration of adalimumab. PG is an important and frequent manifestation of inflammatory bowel disease, with a spectrum of clinical variants, significant morbidity, and requiring a variety of therapeutic approaches.

Hardness and Painful Lesion of the Breast.

Dear Editor, Lupus panniculitis or lupus profundus is a rare inflammatory complication found in patients with systemic lupus erythematosus (SLE), or discoid lupus erythematosus (DLE) (1). When the breast is involved, the term lupus mastitis (LM) is used. This disease involving the breast is rare, and the lesions may precede, coincide with, or occur later than the onset of other lupus lesions. Tissue biopsy is required to confirm the suspected diagnoses of LM. We report a case of a patient with lupus mastitis due to the important differential diagnosis. A 60-year-old woman presented with a painful nodular lesion in her left breast that had appeared 15 days ago (Figure 1, a). She had been previously diagnosed with discoid lupus erythematosus 3 years ago. Physical examination revealed a deep and firm erythematous subcutaneous nodule without overlying skin involvement in the lower-central portion of the left breast. Laboratory findings were positive for antinuclear antibodies (1:80) and double-stranded deoxynucleic acid antibodies (1:10). Mammography and ultrasounds showed an area of increased density and irregular breast tissue along with an important thickening of the overlying skin (Figure 1, b). On suspicion of malignancy, a needle biopsy of the breast lesion was performed and showed vacuolar alteration and lymphocytic infiltrate in the basal layer. Subcutaneous fat showed a lobular panniculitis with a prominent lymphocytic infiltrate and hyalinization of the fat lobules (hyaline fat necrosis). Direct immunofluorescence of the face biopsy revealed IgA, IgG, IgM, and C3 granular deposition. Based on these results, a diagnosis of lupus mastitis associated with DLE was established. Antimalarial therapy resulted in complete resolution of the clinical features. Three years later, the patient presented with a disfiguring atrophy with retraction in the damaged areas of the breast (Figure 2). Lupus mastitis is a very unusual disease that most commonly affects middle-aged women. The first case of LM was described by Tuffanelli in 1971. The lesions usually present following the diagnosis of SLE/DLE; however, on rare occasions they may be observed earlier (2). The histophysiology of this disease remains unclear, but the predominant theory suggests an autoimmune-related etiology. Corroborating evidence for this theory includes the finding of immune complexes, both at the basement membrane of the dermal-epidermal junction and in the blood vessels in the areas of panniculitis (3). Lupus mastitis may be present in the breast as single or multiple subcutaneous nodules that may be tender or painful and can progress to chronic ulcers over time or resolve, leaving atrophic scars. The overlying skin can be normal, erythematous, poikilodermic or ulcerated. When skin changes are prominent, the lesion may clinically and radiologically mimic inflammatory breast carcinoma. Mammographic and ultrasounds findings include an ill-defined breast density with or without associated microcalcifications (4). Histologically, this disease is characterized by lobular lymphocytic panniculitis and predominantly involves the fat lobule and the presence of anucleated adipocytes in a background of a glassy-appearing collagenous stroma (hyaline fat necrosis). Fibrinoid necrosis of the vessel wall has also been reported, but is usually absent (5). Differential diagnosis of lupus mastitis includes inflammatory breast carcinoma, primary medullary carcinoma, and other immune-mediated inflammatory conditions such as diabetic mastopathy. The first line of treatment the use of antimalarial drugs such as hydroxychloroquine. Systemic steroids and cyclophosphamide have also been used. Surgical treatment should be considered only in patients who do not respond to management with medications. In summary, we reported a case of lupus mastitis in a patient with discoid lupus erythematosus. This dermatosis should be considered in the differential diagnosis of breast lesions in lupus patients, and a biopsy of the breast lesion is essential to reject suspected malignancy. If the disease is left untreated, unsightly atrophy will appear; it is thus important to diagnose early on. The course of the disease tends to be chronic with remission and flares, so patients should be followed-up regularly due to the risk of recurrences in the same area or in a different location.

[Atypical recurrent aseptic cutaneous abscesses as the presenting manifestation of Crohn's disease].

We report here a case of chronic inflammatory bowel disease revealed by multiple large cutaneous aseptic distal necrotic ulcers. A 44-year-old male presented with high fever at 40°C associated with multiple necrotic abcesses located on the distal part of his limbs. They were treated successfully by debridment and dressings associated with antibiotics allowing complete healing after 1 month. Six months later, the patient relapsed on his left hand with a short episode of diarrhoea. A total coloscopy revealed a Crohn's disease. Systemic corticotherapy and azathioprine were administered and complete remission was obtained with a 1-year follow-up. Skin manifestations that this patient presented were atypical because of their number, size, and location, exclusively distally on the limbs. This report illustrates an unusual presentation of Crohn's disease with multiple necrotic ulcers only located on the patient extremities.

Xanthoma-like Skin Changes in an Elderly Woman with a Normal Lipid Profile.

Dear Editor, An 83-year-old woman developed yellow-brownish infiltrates, nodules, and tumors mimicking xanthomas, mostly involving the periorbital and chest area within three months (Figure 1). She had no abnormalities in serum cholesterol or triglycerides levels. A detailed laboratory analysis revealed the presence of mild monoclonal gammopathy with a presence of immunoglobulin G (IgG) kappa light chains; however, according to hematologist consultation, it did not require medical intervention. Imaging assessment and ultrasound examination did not show any specific involvement of internal organs. The skin biopsy demonstrated necrobiotic areas alternated with foci of xanthogranulomatous infiltration throughout the reticular dermis with extension into subcutaneous tissue. The granulomatous infiltrate was composed of epithelioid, foamy histiocytes in addition to conspicuous giant cells of the Touton type and foreign body type, as well as variable numbers of lymphocytes, plasma cells, and neutrophiles. Lipid vacuoles were seen within the foci of necrobiosis and xanthogranulomatous infiltration (Figure 2). Two months after first admission to our department, the first signs of necrosis within the lesions were noted, and massive necrosis of skin lesions occurred after the following 5 months (Figure 1). Based on the clinical manifestation and histological and laboratory findings, the diagnosis of necrobiotic xanthogranuloma (NXG) was established. In our patient, the extremely late onset of the disease, its very aggressive course, and the absence of malignant hematological disorder were remarkable. The general condition improved after local treatment and a low dose of prednisone. However, patient anamnesis revealed myocardial infarction in the past, congestive heart failure, and atrial fibrillation. Eventually, the patient died due to acute heart failure before alkylating agents could be administered; we consider the patient's death to have been unrelated to NXG. NXG is a rare, chronic granulomatous disorder which was first described in 1980 by Kossard and Winkelmann (1). Currently, less than one hundred fifty cases of this syndrome have been reported in the literature worldwide (2,3). The disease occurs during adulthood, slightly more frequently in women, and usually after the age of 60 years, although the youngest reported patient was 17 years old (3). The disease initially manifests as xanthoma-like eruptions of yellowish or red-orange papules and nodules that coalesce into indurated plaques (4). The size of the lesions typically increases over time or with the next recurrences. In comparison to hyperlipemic and normolipemic xanthomas, the lesions are firmer, more prominent, and more polymorphic (3) with superficial telangiectasias, sometimes erythematous and/or violaceous borders, and atrophy (5). Ulcerations of the lesions were observed in about 50% of patients and tended to be extensive and progressive (4). Skin lesions of NXG can occur anywhere on the body. However, about two-thirds of patients had periorbital involvement, particularly on the upper and/or lower eyelids or elsewhere on the face. The second most commonly affected site was the trunk, predominantly the chest (3-6). However, many skin lesions first appear on the trunk or extremities and subsequently involve the periorbital area (4). More than one body area was affected in about 90% of the published cases (3,4). In individual cases, the occurrence of NXG was noted within scars, after trauma, or in a previously X-ray irradiated area (5). Lesions may be asymptomatic; however, over half of patients asked reported various symptoms, predominantly itching but also burning, tenderness, and even pain (4,5). Periorbital skin lesions are often accompanied by ophthalmic manifestations, mainly scleritis, choroiditis, or conjunctivitis (3), and with complications such as blepharoptosis, restricted ocular motility, and proptosis (4,5). Extracutaneous lesions are most commonly seen in the respiratory tract, including the lungs and larynx, followed by the myocardium, oral cavity, skeletal muscles, kidneys, ovaries, intestine, and other sites (5,6). Extracutaneous involvement was reported in less than 20% of cases (3), but its frequency seems to have increased in recent years (5). Regarding laboratory abnormalities, the majority of patients with NXG (70% and up to 90% depending on the studied population) have a monoclonal gammopathy (more often IgG-kappa than IgG-lambda). Elevated erythrocyte sedimentation rate, anemia, leukopenia, low C1 and C4 levels, and cryoglobulinemia are also frequently present (3-6). Incisional biopsy is recommended to confirm the diagnosis of NXG, but correlations between the clinical presentation and specific histopathologic findings have been poorly characterized so far. The histopathology shows an inflammatory infiltrate composed of macrophages, foam cells, plasma cells, and other inflammatory cells as well as Touton and foreign body-type giant cells in the dermis and subcutaneous tissue. Necrobiosis is usually present, and nodular lymphoid aggregates are common. Cholesterol clefts or asteroid bodies are rare or absent. The epidermis may be atrophic or normal. Special stains are not helpful in establishing the diagnosis of NXG, but immunohistochemistry for CD68 is positive while it is always for CD1a and PS100 negative, like in non-X histiocytosis (4,5). In patients without a known myeloproliferative disorder, bone marrow biopsy may reveal atypical or increased plasma cells and, very rarely, true multiple myeloma (5). As mentioned above, NXG can be a manifestation of multiple myeloma. However, chronic lymphocyte leukemia, B-cell lymphoma, and other lymphoproliferative diseases have also been reported in patients with NXG (3). Remarkably, hematological disorders may emerge many years before or after the onset of skin lesions (even up to 11 years) (4). According to available literature data, the course of the disease is usually chronic and slowly progressive, and the prognosis is relatively good in the absence of co-occurrence of malignant hematological disorders ([5-7). Aside from hyperlipemic and normolipemic xanthomas, the differential diagnosis of NXG includes multifocal necrobiosis lipoidica, granuloma annulare, foreign-body granuloma, juvenile xanthogranuloma, rheumatoid nodules, and amyloidosis (4). In 5 cases from the literature, xanthoma and NXG were present at the same time (3). Despite several hypotheses, the etiopathogenesis of NXG remains unknown (3,4,8). For that reason and due to the rarity of the disease, the optimal therapy has not been not defined. Frequently, chlorambucil or melphalan have been used alone or in combination with prednisone (4). Treatment may result in remission of symptoms on the skin, but it does not provide a permanent cure (8). There are also single reports of the successful use of thalidomide, lenalidomide, cyclophosphamide, dexamethasone, interferon 2a and 2b, plasmapheresis and hydroxychloroquine, azathioprine, infliximab, and autologous bone marrow transplantation (3). Methotrexate seems to be ineffective (9). Local therapy, including local steroids, laser CO2, or radiotherapy, results in partial improvement (3,4). Skin lesions which relapsed or were unresponsive to treatment could be excised surgically and the defects resurfaced with skin grafts. [2].

Undertreatment of pain

facilities with principally minority patients were three times more likely to be undermedicated than patients treated in non-minority facilities. Furthermore, a follow-up study that investigated pain treatment in minority patients with recurrent or metastatic cancer found that 74% of Latinx and 59% of African American patients experiencing pain were not given the adequate analgesics. Minority patients, when compared to non-minority patients, were not as likely to be appropriately evaluated for their pain and reported less pain relief. Although the prescription of opioid analgesics in response to pain-related visits grew from 1993 to 2005, disparities in prescribing to racial and ethnic minorities persisted. White patients experiencing pain were considerably more likely to be prescribed an opioid analgesic when compared to Black, Hispanic or Asian patients. Specifically, 40% of white patients were prescribed opioid analgesics in 2005, while only 32% of nonwhite patients experiencing

Atrophie blanche. A clinicopathological study of 27 patients.

Twenty seven patients (8 males and 19 females) with atrophie blanche were observed in the past 7-years. The mean age at onset was 32 years (ranging from 23 years to 57 years) and 19 years (ranging from 11 years to 36 years) for male and female patient, respectively. The mean disease duration was 2.5 years (ranging from 2 months to 16 years) prior to their consultation. Sixty-three percent of them had summer exacerbation. Four patients had essential cryoglobulinemia, one of whom also developed bilateral iliofemoral artery stenosis one year later. Twelve patients also manifested concurrent purpura pigmentosa chronica (PPC)-like lesions. The observation of the natural course and clinical morphology, being divided into white atrophy-predominant and ulcer-predominant type, led to the impression that atrophie blanche and livedo vasculitis are synonyms with the same disease spectrum. Furthermore, white atrophy is not ulcer scars but lesions de novo suggesting dermal vasculopathy. An attempt was made to explain the uniqueness of clinical morphology. First line treatment included local wound care, bed rest and low-dose aspirin plus dipyridamole. Thirteen patients responded to these treatment either at the first attack or the recurrent episodes. Heparin (5000 units subcutaneous injection once daily) was effective for control of intractable painful ulceration in active stage in 70% of the remaining patients.

Subcutaneous histiocytoid sweet syndrome associated with crohn disease in an adolescent.

We report a case of subcutaneous histiocytoid Sweet syndrome in an adolescent with Crohn disease. A 14-year-old boy with a 1-year history of ileocolonic and perianal Crohn disease, treated with infliximab and azathioprine, was admitted to the Pediatrics Department with malaise, abdominal pain, bloody diarrhea, and fever (39°C) from 15 days ago. Two days later, he developed cutaneous lesions consisting of tender, erythematous, and violaceous papules and nodules scattered over his legs, soles, and upper extremities. Laboratory studies revealed neutrophilia, microcytic anemia, and elevation of both erythrocyte sedimentation rate and C-reactive protein rate. A skin biopsy specimen showed deep dermal and predominantly septal inflammatory infiltrate in the subcutaneous tissue composed of polymorphonuclears, eosinophils, and mononuclear cells of histiocytic appearance. These histiocytoid cells stained positive for myeloperoxidase. Subcutaneous Sweet syndrome is a rare subtype of acute neutrophilic dermatosis, in which the infiltrate is exclusively or predominantly located in the subcutaneous tissue, causing lobular or septal panniculitis. It is often described in patients with an underlying haematological disorder or caused by drugs, but very rare in patients with inflammatory bowel disease, especially in childhood or adolescence. To our knowledge, this is the first case of subcutaneous histiocytoid type in a paediatric patient.

[Ileocecal manifestation of Schoenlein-Henoch purpura as a rare differential Crohn disease diagnosis].

In the case of a 21-year-old patient gastroscopy and coloscopy were performed because of recurrent abdominal pain with diarrhea and vomiting. Colonoscopy showed moderate signs of inflammation of the rectum and aphthoid ulcerations in the terminal ileum. Since the macroscopic and clinical presentation was compatible with Crohn's disease, therapy with sulfasalacine was started. Because histology showed only lymphoid hyperplasia and the patient was asymptomatic at that time, the medication was ceased. Recurrence of abdominal pain and weight loss, proteinuria and a recurrent palpable purpura of the shanks in synopsis with the result of the previous colonoscopy led to a suspected diagnosis of Schoenlein-Henoch purpura with cutaneous, renal and abdominal manifestation which was confirmed by dermal and renal biopsies.

Indurated Plaques on the Legs: Think Lymphoma.

Dear Editor, Primary cutaneous diffuse large B-cell lymphoma, leg-type (PCDLBCL-LT) is a rare and aggressive neoplasm. A timely diagnosis may prevent fatal outcomes; physicians should take this entity into consideration when assessing non-specific lesions on the lower limbs. We present a 69-year-old woman with a 1-month history of a firm plaque on her left leg. Physical examination revealed an asymptomatic, indurated, smooth, and erythematous plaque on the pretibial region of her left extremity (Figure 1, a). The rest of the physical examination was normal. Histological examination revealed cohesive sheets of a dense cell infiltrate in the dermis, composed of large round immunoblast-type cells with prominent nucleoli, and the presence of mitoses. Immunohistochemical stains were positive for CD20, Bcl2, and MUM1 (Figure 1, b-d). Additionally, c-MYC and Ki67 exhibited a 20% positivity; CD3 and CD10 were negative. The diagnosis of PCDLBCL-LT was established. Imaging and blood workup ruled out systemic involvement. Treatment with R-CHOP chemotherapy was initiated, with complete tumor regression by the third cycle. The patient completed 6 cycles and has remained disease-free after 18 months. Primary cutaneous B-cell lymphomas (CBCL) are lymphoproliferative disorders that appear on the skin without evidence of extracutaneous manifestations at the time of diagnosis (1). They represent 25 to 35% of all primary cutaneous lymphomas (2). In 2018, an updated version of the 2008 WHO-EORTC classification divided CBCLs into 5 subtypes: PCDLBCL-LT, primary cutaneous marginal zone B-cell lymphoma (PCMZL), primary cutaneous follicle center lymphoma (PCFCL), Epstein-Barr virus-positive mucocutaneous ulcer (EBVMCU), and intravascular large B-cell lymphoma (3). PCDLBCL-LT is the least common subtype, representing approximately 10% of all CBCLs and only 4% of all cutaneous lymphomas (2,3). Although the pathogenesis for most CBCLs is still unknown, positive serology for Lyme disease in a significant number of patients has been recognized as a probable etiologic association (4). PCDLBCL-LT is more frequent in women, and the mean age of presentation is 76 years. It usually presents as erythematous or bluish nodules, and up to 75% of the cases appears on one or both legs (1). Although infrequent, other locations have been reported, including the head, neck, trunk, and upper extremities (5). Workup should include a complete physical exam, skin biopsy, blood tests, and imaging (2,3). Histopathology shows a diffuse infiltrate in the dermis composed of large B-cells (centroblasts and/or immunoblasts) with extension to subcutaneous cellular tissue. These cells have round nuclei that are more than twice the size of normal lymphocytes, with prominent nucleoli. The immunophenotype of PCDLBCL-LT is CD20+, CD79a+, CD10-, and Bcl-6+/-, and strongly expresses Bcl-2, MUM1/IRF4, and FOX-P1 (1-3). Unlike the other indolent subtypes, PCDLBCL-LT is generally more aggressive with a poor prognosis. The 5-year disease survival rate is of approximately 50% (5). Management depends on the body surface area, location, and the patient's age and general health. To date, chemotherapy with R-CHOP remains the first line of therapy for PCDLBCL-LT, resulting in complete remission in up to 92% of cases (2). The prognostic characteristics of most PCDLBCL-LTs require timely and appropriate diagnosis and treatment.

[Emétine and quinine, a therapy to rescue Bellini in 1835].

At the moment when his operas got a European celebrity, Vincenzo Bellini born in 1801 rapidly died in September 1835 after a three weeks digestive illness, with mainly dysenteria. Young and healthy, this unexpected event questioned the authorities in Paris. The post mortem examination showed that the colonic mucosa was covered by numerous ulcers, and that a large abcess existed in the liver. All other parts of the body were absolutely sound. These results came out from the autopsy performed by Adolphe Dalmas (1799-1844), professor agrégé at the Faculty of medicine of Paris, formerly member of the special committee in charge of fighting the cholera in 1831 and 1832, who studied its medical aspects during the epidemic attack in Russia, Poland, Germany and Great Britain. With a wide knowledge in the field of the intestinal pathology, his conclusions established that the death came from an inflammation of the bowel, excluding clearly any touch of cholera or poisoning. Nowadays, it is obvious that this dysenteria syndome associated to such anatomic disorders would belong to the chronic amebic disease. Probably contaminated in 1828, Bellini developed a severe episode in 1830, necessitating a long rest during several months, spent at Moltrasio along the side of the Lake of Como. At the time, he composed La Sonnambula and Norma. In 1833 after staying in London from April to August, he came to Paris preparing a new work I Puritani (The Puritains). At summer time, he usually suffered slight recurring episodes, that he treated by applying vesicatories. For frequent periods, he lived outside Paris in a villa standing along the Seine in Puteaux rented by his British friends the Levys. Early in September 1835, these symptoms came again and and suddenly worsened with pain, fever and loss of rest at night. Deserted and lonely as the Levys often left the villa, his critical condition exhibiting tremendous sufferings led to death on the 23rd of September. During the final days, he was not granted any relevant medical support, except the poor cares given by the Italian physician Montallegri, not authorised at that time to practice in France. As emetine and quinine since 1822 were both available as pure alcaloids, produced by the pharmacist Joseph Pelletier, it is assumed that Bellini might have recovered after an intensive treatment implementing these substances by oral, local and rectal routes (enemas and suppositories). At that time, apart from the academic teaching inherited from Broussais, the tropical practitioners currently used them in the treatment of dysenteria and tropical liver abcesses (Annesley, Segond and Dutroulau), as decocted ipeca roots and cinchona barks. Later on when the amebic disease has gained its proper nosography, the clinicians underlined the dangerous and unpredictable issues of the hyperacute hepatic syndromes, unexpected and occurring by apparently healthy individuals. By 1960, its treatment was still obtained by the emetine derivatives.

Betty Ford

In January 1984, Betty Ford said the six years since beginning her alcohol and drug abuse treatment "have been the best years in my life from the standpoint of feeling healthier and feeling more comfortable with myself" during an address at a program in Michigan. The Betty Ford Center In 1978, the Ford family staged an intervention and forced her to confront her alcoholism and an addiction to opioid analgesics, which had been prescribed in the early 1960s for a pinched nerve. "I liked alcohol," she wrote in her 1987 memoir. "It made me feel warm. And I loved pills. They took away my tension and my pain". She went into treatment for substance abuse.

InternalMed_Harrison

Pyoderma gangrenosum (PG) is seen in 1–12% of UC patients and less commonly in Crohn’s colitis. Although it usually presents after the diagnosis of IBD, PG may occur years before the onset of bowel symptoms, run a course independent of the bowel disease, respond poorly to colectomy, and even develop years after proctocolectomy. It is usually associated with severe disease. Lesions are commonly found on the dorsal surface of the feet and legs but may occur on the arms, chest, stoma, and even the face. PG usually begins as a pustule and then spreads concentrically to rapidly undermine healthy skin. Lesions then ulcerate, with violaceous edges surrounded by a margin of erythema. Centrally, they contain necrotic tissue with blood and exudates. Lesions may be single or multiple and grow as large as 30 cm. They are sometimes very difficult to treat and often require IV antibiotics, IV glucocorticoids, dapsone, azathioprine, thalidomide, IV cyclosporine, or infliximab.

Autosomal dominant polycystic kidney disease

Treatment Currently, the only pharmacological treatment available for ADPKD consists in reducing the speed in gain of total kidney volume (TKV) with vasopressin receptor 2 (V2) antagonists (i.e. tolvaptan). Tolvaptan treatment does not halt or reverse disease progression and patients still progress towards renal failure. Palliative treatment modalities involve symptomatic medications (nonopioid and opioid analgesics) for abdominal/retroperitoneal pain. Options for analgesic-resistant pain include simple or complex surgical procedures (i.e. renal cyst aspiration, cyst decortication, renal denervation and nephrectomy), which can result in complications inherent to surgery. Recent research suggests that ketogenic dietary interventions beneficially affect the progression and symptoms in individuals with ADPKD. Mild weight loss favorably affects pain indicating the benefit of dietary and lifestyle changes.

InternalMed_Harrison

IdIOPATHIC INFLAMMATORY BOwEL dISEASE The illnesses in this category, which include Crohn’s disease and chronic ulcerative colitis, are among the most common organic causes of chronic diarrhea in adults and range in severity from mild to fulminant and life-threatening. They may be associated with uveitis, polyarthralgias, cholestatic liver disease (primary sclerosing cholangitis), and skin lesions (erythema nodosum, pyoderma gangrenosum). Microscopic colitis, including both lymphocytic and collagenous colitis, is an increasingly recognized cause of chronic watery diarrhea, especially in middle-aged women and those on NSAIDs, statins, proton pump inhibitors (PPIs), and selective serotonin reuptake inhibitors (SSRIs); biopsy of a normal-appearing colon is required for histologic diagnosis. It may coexist with symptoms suggesting IBS or with celiac sprue or drug-induced enteropathy. It typically responds well to anti-inflammatory drugs (e.g., bismuth), to the opioid agonist loperamide,

First_Aid_Step2

The differential also includes graft-versus-host reaction (usually after bone marrow transplant), radiation therapy, and burns. Patients have the same complications as burn victims, including thermoregulatory difficulties, electrolyte disturbances, and 2° infections. Treatment includes skin coverage and maintenance of ﬂuid and electrolyte balance. Controversial treatments include systemic corticosteroids in the early stages of SJS/ TEN or IVIG. There is a high risk of mortality. A panniculitis whose triggers include infection (e.g., Streptococcus, Coccidioides, Yersinia, TB), drug reactions (e.g., sulfonamides, various antibiotics, OCPs), and chronic inﬂ ammatory diseases (e.g., sarcoidosis, Crohn’s disease, ulcerative colitis, Behçet’s disease). Painful, erythematous nodules appear on the patient’s lower legs (see Figure 2.2-6) and slowly spread, turning brown or gray. Patients may present with fever and joint pain. FIGURE 2.2-6. Erythema nodosum.

Methadone clinic

A methadone clinic, or substance use disorder services clinic (SUDS), is a clinic which has been established for the dispensing of medications used in the treatment of opiate dependence —historically and most commonly methadone, although buprenorphine is also increasingly prescribed. Medically assisted drug therapy treatment is indicated in patients who are opioid-dependent or have a history of opioid dependence. Methadone is a schedule II (USA) opioid analgesic, that is also prescribed for pain management. It is a long-acting opioid that can delay the opioid withdrawal symptoms that patients experience from taking short-acting opioids, like heroin, and allow time for detoxification. In the United States, by law, patients must receive methadone under the supervision of a physician, and dispensed through an opioid treatment program certified by Substance Abuse and Mental Health Services Administration and registered with the Drug Enforcement Administration.

Erythromelalgia

Pain relief Patients find relief by cooling the skin. All patients must be notified to not apply ice directly on to the skin, since this can cause maceration of the skin, nonhealing ulcers, infection, necrosis, and even amputation in severe cases. Mild sufferers may find sufficient pain relief with tramadol or amitriptyline. Sufferers of more severe and widespread EM symptoms, however, may obtain relief only from opioid drugs. Opana ER has been found to be effective for many in the USA, whilst in the UK slow-release morphine has proved to be effective. These powerful and potentially-addictive drugs may be prescribed to patients only after they have tried almost every other type of analgesia to no avail. (This delay in appropriate pain management can be a result of insurer-mandated or legally-required step therapy, or merely overly-cautious prescribing on the part of sufferers' doctors.)

Pain management in children

After treatment Post-procedural treatment in children is primarily prescription opioids. Morphine is effective and relatively safe, and is often used with moderate to severe pain. Codeine and tramadol should be avoided especially in children younger than 12 years old since metabolism varies due to genetic differences between individuals, and, in the case of tramadol, this medication has not been well studied in children. However, other interventions include medications classified as non-opioid analgesics, which are useful in post surgical treatment. For example, acetaminophen or ibuprofen can be used as a non-opioid analgesics. Unlike acetaminophen, ibuprofen has anti-inflammatory property which can be useful for pain in inflammatory conditions. Aspirin is not used in pediatric population due to its association with Reye's syndrome. Management

Umbilical spider's web.

We report the case of a 38y old woman who consulted for chronic diffuse abdominal pain related to previous irritable bowel syndrome diagnosis. Physical examination showed nonblanching reddish hyperpigmented reticular peri-umbilical skin patch (figure 1). What's your diagnosis? The diagnosis of erythema ab igne was made. Additional investigations confirmed repeated use of hot water bottles applied on abdominal wall for 3 weeks overnight for pain relief. Erythema ab igne is a pathognomonic cutaneous presentation of long-lasting exposure to heat sources (1). The pathophysiology of erythema ab igne remains uncertain. It has been suggested that heat exposure damages dermal vascular plexus and subsequent hemosiderin deposition leading to spider's web-like hyperpigmentation. Differential diagnosis of peri -umbilical dermatological manifestations includes digestive-related entities as caput medusae's sign (related to portal hypertension), Cullen's sign or Walzel's sign (related to acute pancreatitis); and non-digestive-related entities such as livedo reticularis (2). Erythema ab igne is well known from the dermatologists, mostly located on the lower limbs due to prolonged close exposition to heaters or on thighs due to laptop batteries (3). Erythema ab igne is usually of benign course, most often self-resolving after heat exposure discontinuation (3). We believe that it is of paramount to take into consideration the patients' pain and to propose an adapted management to avoid self-treatment.

Chronic wound

If local treatment does not provide adequate pain reduction, it may be necessary for patients with chronic painful wounds to be prescribed additional systemic treatment for the physical component of their pain. Clinicians should consult with their prescribing colleagues referring to the WHO pain relief ladder of systemic treatment options for guidance. For every pharmacological intervention there are possible benefits and adverse events that the prescribing clinician will need to consider in conjunction with the wound care treatment team. Ischemia and hypoxia Blood vessels constrict in tissue that becomes cold and dilate in warm tissue, altering blood flow to the area. Thus keeping the tissues warm is probably necessary to fight both infection and ischemia. Some healthcare professionals use ‘radiant bandages’ to keep the area warm, and care must be taken during surgery to prevent hypothermia, which increases rates of post-surgical infection.

[Clinical features of Crohn's disease: its diagnosis and treatment].

To enhance our understanding of Crohn's disease and improve its early diagnostic accuracy and therapeutic efficacy. Thirty-one patients with active Crohn's disease were studied. All their diagnostic and therapeutic results were analyzed. Most patients were young adults, with a 1.14:1 female predominance in prevalence. The disease affects any segment or a combination of segments of the alimentary tract from the mouth to the anus. However, the colon and the small bowel were the major sites involved. Recurrent episodes of abdominal pain and watery diarrhea were the most common symptoms. In addition, low grade fever, emaciation, anemia, and symptoms with skin, joints or perianal complications could be discovered if attention was paid. An endoscopy combined with histologic examination in biopsy specimens provided characteristic features with a diagnostic accuracy of 62.9%. Granulomas were identifiable in 30.8% of all biopsy specimens. Transabdominal bowel sonography (TABS) accurately detected intestinal complications. Factors causing misdiagnosis were: insufficient attention of the disease, diverse clinical presentations, or over emphasis of the diagnostic value of granulomas. Oral prednisone therapy for mild to moderate disease was more rapid to receive clinical remission when compared to oral aminosalicylates (SASP or 5-ASA). Nutrition support therapy was given in 20 cases with active disease and received beneficial effects on host nutritional status. Immunosuppressives were used on an individual basis, and showed variable effects with limited experience. Sixteen patients had operations due to intestinal obstruction or failure to respond to drug therapies. Rapid improvement after operations was achieved. Crohn's diseases not uncommon in China. Abdominal pain and watery diarrhea are two hallmark symptoms. Endoscopy (with biopsy), and TABS were both valuable procedures for diagnosis. Prednisone and SASP/5-ASA were effective as inductive therapies. Surgery, as an alternative and effective treatment, provided another choice in well selected patients.

Pain Management for Pediatric Burns in the Outpatient Setting: A Changing Paradigm?

Childhood burns are common and distressing for children and their parents. Pain is the most common complaint and often thought to be undertreated, which can negatively influence the child's care and increase the risk of posttraumatic stress disorder. There is limited literature on the role of opioids and multimodal therapy in the treatment of pediatric outpatient burns. We sought to evaluate the current use of opioids (including the use of multimodal therapies), storage, and disposal of opioids in this patient population. Parents of burn-injured children 8 months to 18 years old, who were seen in an outpatient setting within 2 weeks of their burn injury, were queried from April to December 2019 regarding their child's pain control, opioid medication use, over-the-counter pain medication use, opioid storage, and disposal. A total of 142 parents of burn-injured children and their parents were surveyed. The median age of the burn-injured children was 2.7 years old and the majority (54.2%; 77/142) were male. The mean total body surface area (TBSA) was 1.8% and half sustained burn injuries to one or both hands. The most frequently used regimens for constant and/or breakthrough pain control were acetaminophen (62.7%) and nonsteroidal anti-inflammatory drugs (NSAIDs; 68.3%). Less than one fifth (26/142;18%) of patients were prescribed opioids and 88% filled their prescription. The median number of doses of opioids prescribed was eight doses, with a median of four doses of opioids unused. Only three patients used all of their prescribed opioids and no patient ≥12 years old used their entire prescription. Burns greater than 3% TBSA, irrespective of burn injury location, were associated with opioid prescription (P = .003). Approximately 40% (10/26) of parents who filled their child's opioid prescription stored the opioid in a locked area. Fewer than one third (7/26) of patients were educated on how to dispose of excess opioid pain medication. Overall, most pediatric outpatient burn injuries can be successfully managed with over-the-counter medications. Providers, who care for burn-injured children ≤ 12 years old with burns that cover ≥3% TBSA in the outpatient setting, should consider no more than four opioid doses for initial pain control. This guideline, coupled with family and provider-centered education on multimodal therapy at the time of initial presentation and safe use of opioids, are important first steps to minimizing the use of opioids in the management of small area burns in children.

[Acute abdominal pain as the first sign of Henoch-Schönlein purpura; a hidden diagnosis in the absence of purpura].

2 girls with abdominal pain, aged 7 and 9 years, were admitted and underwent extensive evaluation: the first girl underwent colonoscopy and the second appendectomy, in which a negative appendix was removed. After 6 and 14 days, respectively, they developed skin lesions that did not disappear on pressure, characteristic of Henoch-Schönlein purpura (HSP). They recovered after treatment with prednisone. HSP is a systemic vasculitis, which can be diagnosed by its characteristic purpura of the skin. Diagnosis is more difficult if the patient does not present with skin lesions. HSP presenting with acute abdominal pain as an initial symptom can give rise to unnecessary additional investigation and even laparotomy. Apart from the other clinical features of HSP, i.e. bloody stools, oligo-articular arthritis and (microscopic) haematuria, diagnosis can be made earlier if biopsies of the normal skin or duodenum are taken and assessed for IgA depositions. Treatment of the abdominal pain with corticosteroids can be considered.

Levomepromazine

Medical uses It can be used as an analgesic for moderate to severe pain in non-ambulant patients (the latter being because of its strong sedative effects). Levomepromazine is also used at lower doses for the treatment of nausea and insomnia. Levomepromazine is frequently prescribed and valued worldwide in palliative care medicine for its multimodal action, to treat intractable nausea or vomiting, and for severe delirium/agitation in the last days of life. Palliative care physicians will commonly prescribe it orally or via subcutaneous syringe drivers in combination with opioid analgesics such as hydromorphone.

First_Aid_Step2

FIGURE 2.2-6. Erythema nodosum. Erythematous plaques and nodules are commonly located on pretibial areas. Lesions are pain ful and indurated but heal spontaneously without ulceration. (Reproduced, with permission, from Hurwitz RM. Pathology of the Skin: Atlas of Clinical-Pathological Correlation, 2nd ed. Stamford, CT: Appleton & Lange, 1998: 132.) Diagnosed by clinical impression. Histology shows nonspecific septal panniculitis. Workup should include an ASO titer, a PPD test in patients who are high risk, a CXR to rule out sarcoid, and a small bowel series to rule out IBD in patients with GI symptoms. Remove the triggering factor and treat the underlying disease where possible. NSAIDs can be used but may lead to erythema multiforme.