Hemorrhagic Bullae Research Articles

Postoperative bleeding adversely affects total knee arthroplasty outcomes in hemophilia

BackgroundHemophilic arthropathy can result in severe degenerative arthritis and functional limitations in the knees of relatively young patients. Total knee arthroplasty (TKA) provides pain relief and gain of function in advanced-stage hemophilic arthropathy cases. However, little is known about the long-term effects of early major postoperative bleeding (MPOB) in people with hemophilia (PWH). The aim of this study was to evaluate the effects of early MPOB on the final functional outcome, complications, and implant survival of TKA in a single-center hemophilia cohort. MethodPWH who underwent TKA between 1998 and 2019 in a single center were reviewed. Demographic data, clinical data, and radiographic images were evaluated. Hospital for Special Surgery (HSS), Knee Society Score (KSS), and Knee Society Function Score (KSS-F) scores were used to determine function. Patients with early bleeding complications (wound dehiscence, ecchymosis, hemarthrosis, hematoma formation, prolonged or recurrent bleeding attacks) were defined as the bleeding group. Patients who did not experience these complications were assigned to the control group. The bleeding group was compared with controls. Survival of the primary arthroplasty was analyzed by Kaplan–Meier curves. ResultsForty-five TKAs in 29 patients were included in the study. TKA led to an increase in the mean range of motion from 46.08° to 84.59° (P < 0.01). HSS scores increased from 48.33 preoperatively to 82.67 postoperatively (P < 0.01). There were improvements in both KSS and KSS-F scores from 34.22 and 53.3 preoperatively to 82.00 and 84.63 (P < 0.01), respectively. Ten patients (10 TKAs) (34%) experienced major bleeding during the postoperative period. Six of these patients had moderate hemophilia, and four had severe hemophilia. Three of these patients had hemarthroses (10.2%), one patient had a hematoma (3.4%), one patient had hemorrhagic bullae formation (3.4%), and five had excessive/prolonged bleeding from the wound (17%). The bleeding group (34%) had significantly worse HSS (63.78 vs 92.75, P < 0.001), KSS (61.78 vs 93.25, P < 0.001), and KSS-F (60.71 vs 96.25, P = 0.005) scores compared with controls. Preoperative and postoperative flexion contractures were positively correlated (+0.33, P = 0.003). One of the patients with postoperative hemarthrosis also had an accompanying transient common peroneal nerve palsy, and one patient (3.4%) had a periprosthetic fracture. Three knees (6.6%), two of whom were in the bleeding group, developed periprosthetic infections. Four knees (8.8%) in three patients underwent revision surgery, and two knees (4.4%) ended up in arthrodeses. Kaplan–Meier analysis revealed a mean survival duration of 17.04 years for the bleeding group and 22.15 years for the control group (P = 0.83). Survival rates were 80.0% for the bleeding group and 96.4% for the control group (P = 0.83). ConclusionsIn this study, MPOB after TKA in PWH was common and led to significantly worse function. MPOB after TKA in PWH was associated with a higher rate of complications and lower survival rates, although the differences were not statistically significant. Efforts must be made to avoid MPOB after TKA in PWH.

An update on oral clinical courses among patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection: A clinical follow-up (a prospective prevalent cohort) study.

Contemporary literature has revealed that Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) causes acute sialadenitis and related symptoms, such as discomfort, pain, swelling, and secretory dysfunction in salivary glands. The secretory dysfunction is due to SARS-CoV-2 infection-induced xerostomia and other associated clinical courses such as sore tongue, mucosal ulcer, and gingivitis in the oral cavity. Furthermore, it has been reported that COVID-19 causes the development of other oral manifestations. A prospective clinical follow-up (a prevalent cohort) study was conducted to identify the possible oral manifestations of SARS-CoV-2 infection among patients admitted toat the Eka General Hospital COVID-19 treatment center. Furthermore, the study aimed to calculate the prevalence rate of oral clinical courses in the cohorts. The study consisted of two follow-up phases: Hospital and patient-home-based. A total of 55 patients (36 males and 19 females) met the inclusion criteria and were followed for 7.5 weeks. The 3.5 weeks hospital-based prospective follow-up study documented an 18% (n = 10) prevalence rate of oral clinical courses among the cohorts. Twelve oral symptoms appeared in these ten patients. The manifested oral symptoms were oral mucosal lesions (n = 6), xerostomia (n = 5), and thickening of saliva (n = 1). The oral mucosal lesions per se consisted of aphthous lesions (n = 3), candidiasis (n = 1), geographic tongue (n = 1), and localized gingivitis (n = 1). The four weeks' home-based follow-up study disclosed four newly manifested oral symptoms: hemorrhagic crust, bulla, buccal mucositis, and petechiae. These manifestations appeared among six patients (four males and two females) who had not manifested any oral symptoms during the hospital-based follow-up. Accordingly, the overall prevalence of oral clinical courses among patients presented with SARS-CoV-2 is raised from 18% (n = 10) to 29% (n = 16). Similarly, the number of clinical courses increased from 12 to 16 after four additional weeks of follow-up. The study's findings suggest the importance of initiating oral health care for patients with COVID-19. Therefore, multidisciplinary healthcare approaches should be delivered to assure optimal health outcomes. Accordingly, oral health professionals must be a substantial part of the interdisciplinary approach in caring for patients with COVID-19.

S2772 Subcutaneous Sweet Syndrome Successfully Treated With Ustekinumab in Patient With Ulcerative Colitis

Introduction: Extraintestinal manifestations (EIMs) of inflammatory bowel disease (IBD) are well-established. Sweet syndrome (SS), or acute febrile neutrophilic dermatosis, is a reactive mucocutaneous manifestation of IBD presenting as erythematous papules/plauqes with associated fever and arthomyalgias. There is limited evidence regarding efficacy of Ustekinumab in management of EIMs of UC, particularly SS. Case Description/Methods: The patient is a 50-year-old woman with left-sided UC (Montreal classification E2) that previously failed several therapies, including mesalamine, azathioprine, infliximab, adalimumab, vedolizumab, and a fecal microbiota transplant trial. She presented with worsening abdominal pain, diarrhea/hematochezia, and bilateral lower extremity pain. She was febrile and tachycardic with tender, violaceous, and ulcerated subcutaneous nodules on the bilateral ankles with hemorrhagic bullae (FigureA). Labs revealed negative C. diff, elevated ESR/CRP, thrombocytosis, and borderline leukocytosis with neutrophilic predominance. Lower extremity MR imaging and bone biopsy revealed multifocal sterile osteomyelitis with adjacent abscess; skin biopsy demonstrated dense granulomatous/neutrophilic infiltrate in the deep dermis/subcutis without microorganisms, consistent with subcutaneous SS (FigureB). A restaging colonoscopy demonstrated severe proctosigmoid ulcerative colitis (FigureC). Given that the patient had failed several immunomodulators and biologic therapies, she was started on prednisone and Ustekinumab. Four months later, she reported complete resolution of her cutaneous SS off steroids and improving UC symptoms (less frequent and more formed stools, minimal hematochezia). Repeat MRI demonstrated resolution of the sterile osteomyelitis and abscess. Discussion: Our case highlights the novel use of Ustekinumab in the treatment of subcutaneous SS with sterile osteomyelitis in a patient with flaring UC. SS is a neutrophilic dermatosis that is a rare EIM of IBD, classically characterized by tender cutaneous lesions. There is limited evidence supporting the use of Ustekinumab in treating EIMs of CD, and a lack of data regarding its efficacy in treating EIMs of UC. Our case fills a major gap in the literature and highlights the clinical efficacy of Ustekinumab for SS and UC especially in patients that have a contraindication to, failed previous treatment with, or otherwise cannot tolerate corticosteroids and TNF-alpha antagonists.Figure 1.: 1A. Right lateral malleolus with 2.5 cm shallow erosion with slightly violaceous borders and central bright yellow fibrinous debris. There was slight atrophy of surrounding skin with mild edema and hyperpigmentation (left image). Left medial malleolus/dorsal foot with grouped irregular shallow ulcers with surrounding mild violaceous erythema (middle and right image). 1B. Left ankle biopsies showed mixed septal and lobular panniculitis with granulomatous and neutrophilic inflammation. Histologic sections show a mildly spongiotic epidermis with dense granulomatous and neutrophilic inflammatory infiltrate in the deep dermis and subcutis (left image). The inflammatory infiltrate, which consists of prominent neutrophils, histiocytes, and scattered lymphocytes, surrounds vascular and adnexal structures, as well as adipocyte lobules. Definitive features of vasculitis are not seen. PASd (periodic acid-Schiff-diastase), GMS (Grocott’s methenamine silver), Gram, and Fite staining fail to highlight microorganisms (right image). 1C. Colonoscopy demonstrated severe (Mayo Endoscopy Score 3) proctosigmoid ulcerative colitis to 30 cm (left image). Sigmoid biopsies showed significant immune cell infiltration with crypt architectural distortion concerning for severe chronic active colitis. No evidence of granulomas, dysplasia or cytomegalovirus (right image).

S2766 Purpura Fulminans in Acute Severe Ulcerative Colitis Successfully Treated With Infliximab

Introduction: Several extra-intestinal dermatological manifestations can be seen in patients with ulcerative colitis (UC). We report a rare case of purpura fulminans in the setting of acute, severe UC (ASUC). A few reports have shown improvement of this entity only with colectomy. We describe a case of purpura fulminans that developed in the setting of ASUC that responded with infliximab (IFX) therapy. Case Description/Methods: A 50-year-old Female with mild pan-UC and no previous dermatologic morbidity managed with oral mesalamine therapy for 18 months developed exacerbation of symptoms. Colonoscopy reveled moderate pancolitis (Endoscopic Mayo 2). She was started on prednisone and vedolizumab but after a partial response, lost response and developed worsening gastrointestinal (GI) symptoms and presented with vesiculated, hemorrhagic bullae involving both feet, left arm and back (FigureA). White blood cell count on admission was 35,700, International normalized ratio (INR) 1.7, C-reaction protein (CRP) 227 mg/L and fibrinogen 129 (mg/dl). Skin biopsy showed microthrombi but no pus. Patient was started on corticosteroids, with mild improvement in GI symptoms but worsening skin lesions. Given case reports of purpura fulminans resolving with colectomy, the procedure was offered but declined by the patient. She was started on IFX (10 mg/Kg). Her GI symptoms improved and her skin lesions stabilized. After discharge, the skin lesions on her back and arm healed, but both feet developed skin necrosis and dry gangrene, requiring a bilateral below the knee amputations (FigureB). After 14 weeks of IFX therapy, the patient is in clinical remission, normalized CRP and only with a limited area of mucosal inflammation in the sigmoid on colonoscopy. Discussion: To our knowledge, this is the first case of purpura fulminans in association with ASUC that responded to infliximab. While the patient required amputation, therapy with infliximab slowed the progression of her disease, limiting the areas of necrosis and potentially avoiding sepsis. Pupura fulminans is characterized by skin necrosis with thrombosis in the dermal vessels and consumptive coagulopathy. Limb ischemia is a devastating complication and amputation may be necessary to reduce mortality. In conclusion, patients with ASUC that develop purpura fulminans may benefit of early and aggressive medical therapy with IFX, sparing the need for colectomy.Figure 1.: Purpura fulminant at presentation and follow-up.

S3197 Warfarin-Induced Skin Necrosis Following Routine Endoscopy in a Patient With Cirrhosis

Introduction: Warfarin-induced skin necrosis (WISN) is rare, and most cases are caused by inherited deficiencies of protein C. Acquired protein C deficiency has been associated with advanced liver disease, ulcerative colitis (UC), and malignancies. Due to its rarity, clinicians must have a high index of suspicion for WISN to avoid delays in diagnosis or treatment. Case Description/Methods: A 67-year-old male with UC, cirrhosis due to primary biliary cholangitis, and prior pulmonary embolism on warfarin underwent surveillance EGD and colonoscopy. Warfarin was held for five days prior to the procedures without bridging. EGD was unremarkable and colonoscopy revealed active UC. He resumed warfarin therapy the next day. Two days later, he developed significant tenderness and bruising on his abdomen, flank, and outer thighs. After evaluation by multiple providers, his pain was attributed to central sensitization, and he was prescribed gabapentin. Over the next several days, he developed extensive painful retiform purpura and expanding areas of superficial necrosis (Figure 1). He was admitted to the hospital for multidisciplinary evaluation. Extensive workup assessed potential causes, such as WISN, sepsis, vasculitis, disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), or cryoglobulinemia. Given the characteristic appearance and temporal association with restarting warfarin, WISN was thought to be the most likely etiology. Protein C activity was low at 22% (normal 70-150%). Genetic testing for inherited protein C deficiency was negative, confirming an acquired deficiency. For management of WISN, warfarin was discontinued, heparin was initiated, and protein C was repleted with fresh frozen plasma (FFP). He was discharged on warfarin after bridging with heparin. He later had recurrence of his necrotic rash, and an excisional biopsy confirmed WISN. Warfarin was then discontinued in favor of lifelong enoxaparin. Discussion: Our case highlights a rare but devastating complication of warfarin use. In WISN, protein C is depleted prior to other vitamin K-dependent factors, leading to a transient hypercoagulable state, microvascular occlusion, and tissue necrosis. Despite our patient’s risk factors (liver disease and active UC) and characteristic presentation, diagnosis of WISN was delayed. Prompt recognition and treatment (discontinuation of warfarin, IV heparin, vitamin K and FFP) is crucial for tissue preservation and avoidance of morbid surgical interventions.Figure 1.: Images of the patient’s abdomen and right thigh (left) and left hip (right). The skin is extensively involved with painful retiform purpura and areas of superficial necrosis with associated hemorrhagic bullae.

P259 Rare presentations of Cryptococcosis: a case series

Poster session 2, September 22, 2022, 12:30 PM - 1:30 PM Objectives Cryptococcus spp. is usually opportunistic pathogens affecting immunocompromised individuals causing meningitis primarily. Non-CNS presentations are a rare entity and we hereby present a series of 3 cases in the past 1 year (2021-2022).MethodsCase records of the three patients were studied. Detailed history, demographic details, investigations, treatment were noted.ResultsPatient-1 was a 14-year-old girl who came with complaints of fever, pain, swelling, and restricted movements of the right wrist, elbow, and ankle joints with multiple subcutaneous swellings initially on the thigh followed by elbows, arms, and forearms. The swellings became hemorrhagic bullae bursting to form ulcers. She had a history of being treated 4 times for tuberculous lymphadenopathy. KOH-Calcofluor white mount of biopsy and pus aspirate samples showed circular yeast cells which were confirmed by cryptococcal antigen detection. All the samples had grown Cryptococcus neoformans on culture except blood, BAL, and CSF. She responded to Liposomal amphotericin-B drastically. Retesting of pus swabs from the ulcers after a week of antifungal therapy were negative for C. neoformans. Subcutaneous nodules and joint swellings decreased but she developed reactions to amphotericin B and was changed to fluconazole. She is on regular follow-up with no recurrence.Patient-2 was a 22-year-old male, a known case of Hodgkin Lymphoma stage 4 who underwent Autologous stem cell transplantation (ASCT) and was on immunosuppressants. He presented with fever, dyspnea, and cough which got worsened along with multiple cervical, hilar and abdominal lymphadenopathy. KOH-Calcofluor white mount of biopsy samples demonstrated circular yeast cells which were confirmed by cryptococcal antigen detection test of biopsy and BAL samples. Cryptococcus neoformans was grown on culture from all the samples. He succumbed to ARDS and cardiorespiratory arrest before any treatment could be initiated.Patient-3 was a 38-year-old female, known case of SLE with lupus nephritis, presented with intermittent fever, dyspnea, chest pain, decreased urinary output, and gradual swelling of the body starting from the face and progressing to the whole body. She further developed synpneumonic effusion, multiple erythematous tender papules over the right thigh, and cellulitis of the right lower limb. She was started on voriconazole in view of HRCT findings suggestive of fungal pneumonia. As galactomannan antigen test was negative, voriconazole was stopped. Pleural tap fluid flagged positive in Bactec and C. neoformans grown on subculture. Her condition worsened with septic shock and succumbed to the disease before any treatment could be initiated.ConclusionSubcutaneous, joint, and pulmonary involvement is rare, without a primary focus on the central nervous system. Culture and antigen detection can aid in early detection and hence early initiation of therapy.

Lucio Phenomenon in a Case of Lepromatous Leprosy

Leprosy is a chronic infectious disease caused by Mycobacterium leprae (M. leprae), mainly affecting skin and nerves. Lucio leprosy (LuLp) is a pure primitive diffuse nonnodular form of leprosy. Lucio phenomenon (LP) is a type of necrotizing reaction seen in untreated or inadequately treated cases of LuLp. We present a case of LP in a patient of lepromatous leprosy. A 55-year-old male presented with hemorrhagic bullae, angulated ulcers with jagged margins on lower limbs, purpuric patches on extremities, trunk, and face, and erythematous plaques with intact sensations on back. LP was diagnosed on the basis of clinicohistopathological features.

Ecthyma gangrenosum as a presenting feature of X-linked agammaglobulinemia: A case study.

A previously healthy 5-year-old boy presented with symptoms of fever, vomiting, and diarrhea for three days. He had extensive erythematous skin lesions mainly over his bilateral lower limbs. His parents were nonconsanguineous, and his two younger sisters were healthy. On arrival, he was in septic shock, thus requiring multiple fluid boluses, triple inotropes, and ventilation. The skin lesions started as macules that enlarged into papules and vesicles. Over the next 24 h, they rapidly evolved into multiple hemorrhagic bullae (Fig. 1A), which ruptured to form a gangrenous ulcer with gray-black eschar surrounded by an erythematous halo (Fig. 1B).

Acute Lower-Extremity Posterior Compartment Syndrome: A Rare Complication of Apixaban Use

Apixaban is an oral anticoagulant that directly inhibits factor Xa and is indicated for the prophylaxis and treatment of deep venous thrombosis and stroke prevention in nonvalvular atrial fibrillation. Acute lower-extremity posterior compartment syndrome is a rare complication of apixaban use. We present a 78-year-old man with significant medical morbidities taking apixaban for atrial fibrillation presenting with posttraumatic extensive hemorrhagic bullae on the left proximal pretibial region secondary to anticoagulation. We recommend that clinicians develop awareness of the potential for serious bleeding complications of anticoagulants and devise strategies to identify the need for early recognition and prompt management.

Finger Test for the Diagnosis of a Critically Ill Patient with Necrotizing Fasciitis

BackgroundNecrotizing fasciitis is a life-threatening soft-tissue infection, often characterized by soft-tissue destruction, systemic toxicity, and high mortality. No single laboratory value can diagnose necrotizing fasciitis; ultimately, necrotizing fasciitis is a clinical diagnosis and therefore presents a diagnostic dilemma for many physicians. The finger probe test is useful in confirming the diagnosis when imaging studies are unobtainable or nondiagnostic. Case ReportWe present the case of a 70-year-old woman presenting nonverbal and obtunded with a soft-tissue infection of the right lower extremity. The only pertinent positive vital sign was tachypnea with a respiratory rate of 22 breaths/min. Physical examination revealed nonpitting edema, cold-to-touch lower extremity, and Nikolsky-positive hemorrhagic bullae. Initial laboratory test results showed white blood cell count of 38 x 109/L and lactic acid of 8.2 mg/dL. Advanced imaging was unobtainable, given the patient's worsening clinical status, and the decision was made to perform the finger probe test, which revealed absence of bleeding and presence of friable tissue and “dishwater” discharge. Consequently, the general surgery team took the patient to the operating room and performed an above-the-knee amputation and surgical debridement. Postoperative report noted nonviable tissue consistent with necrotizing fasciitis. Why Should an Emergency Physician Be Aware of This?Necrotizing fasciitis is a life-threatening emergency that can destroy soft-tissue at a rate of 1 inch/h. When imaging is unobtainable or nondiagnostic, the finger probe test can be used in select patients to aid with diagnosis.

Clinico-epidemiology and management of hump-nosed pit viper (Hypnale spp.) bites in dogs

Human envenoming from the bite of the abundant hump-nosed pit viper (Hypnale spp.) (HNPV) is a frequent occurrence with victims experiencing unpleasant and sometimes life-threatening consequences. Further, clinico-pathology, treatment and management measures in HNPV envenomed dogs are under recognized. Prospective investigations were performed to assess the clinico-pathology and management options for HNPV envenomed dogs brought to the University of Peradeniya’s Veterinary Teaching Hospital from January, 2012 to March 2018. We recorded the local and systemic manifestations, hematological and urinary abnormalities of 78 dogs in which HNPV bite had been witnessed by the owner. Mild swelling, extensive swelling, hemorrhagic blistering and hemorrhagic bullae at the site of bite were observed in 59%, 31%, 6% and 4% of the dogs, respectively. Some dogs were subjected to surgical excision of necrotized tissue including limb amputation. We observed the following systemic clinical effects in envenomed dogs: neurotoxicity (13%), acute kidney injury (AKI) (14%) and coagulopathy (16%). All dogs showed leukocytosis with mean white blood cell count of 25.25 × 103/µL. Mild anemia and thrombocytopenia were detected in 29% of the dogs. There was a significant correlation between extent of local tissue injuries with length of hospitalization (LH). The mean time of coagulopathy observed was 21.3 h (IQR: 8–48 h). In coagulopathic dogs, there was a strong correlation between LH and extent of local tissue injury (rs = 0.7751, P < 0.0001); LH and whole blood clotting time(CT) (rs = 1.0, P < 0.0001); PT and aPTT (rs = 0.4712, P < 0.001). LH was significantly correlated with the development of AKI (p = 0.0013). Lack of specific antivenom (AVS) for HNPV envenoming provided an opportunity to study the remaining treatment options. Therefore, the study allowed the identification of local and systemic effects, hematological abnormalities, possible supportive treatments and drawbacks of management measures for envenomed dogs.

Acute Lower Extremity Posterior Compartment Syndrome: A Rare Complication of Apixaban Use

Apixaban is an oral anticoagulant that directly inhibits Factor Xa and is indicated for the prophylaxis and treatment of deep venous thrombosis and stroke prevention in non-valvular atrial fibrillation. Acute lower extremity Posterior Compartment Syndrome is a rare complication of Apixaban use. We present a 78-year-old male with significant medical morbidities taking Apixaban for Atrial Fibrillation presenting with post-traumatic extensive hemorrhagic bullae on the left proximal pretibial region secondary to anticoagulation.

WITHDRAWN: Eruption of hemorrhagic bullae and vesicles

WITHDRAWN: Eruption of hemorrhagic bullae and vesicles

Ecthyma gangrenosum in a patient with febrile pancytopenia

Ecthyma gangrenosum (EG) is a cutaneous infection most commonly associated with Pseudomonas bacteremia and usually occurring in immunocompromised patients [1]. The infection progresses sequentially from a maculopapular rash to hemorrhagic bullae, then to necrotic ulcerations with surrounding erythema [2]. Herein, we report a case of ecthyma gangrenosum in an immunologically compromised patient. A 65-year-old female was admitted to the oncohematology department for febrile pancytopenia. Blood work revealed severe thrombocytopenia at 15,000/mm³), an absolute neutrophil count of 180 cells/mm³, and anemia. A sternal bone marrow puncture found 15% of plasma cells. Four days after the admission, the patient had a painful, quickly extending lesion on the abdomen. She described erythema that progressed to pustules, then ulcerations. On general clinical evaluation, the patient was feverish at 40°C. A dermatological examination revealed the presence of a 6 cm purpuric patch on the left flank with a central necrotic eschar (Fig. 1). The diagnosis of ecthyma gangrenosum was reached and the patient was treated with ceftazidime and vancomycin. Unfortunately, having gone into septic shock, the patient died one week later.

From the morphology of skin lesions to diagnosis: Inspection is like reading a book

Leprosy presents a varied clinical spectrum. Lucius phenomenon is a rare leprosy reaction characterized by erythematous, painful, slightly infiltrated macules and hemorrhagic bullae that progress to ulceration. This case report describes a patient whose diagnosis of leprosy occurred in the presence of Lucius phenomenon. Late diagnosis and delay in the implementation of specific therapy contributed to an unfavorable outcome, highlighting the importance of early identification and treatment of this disease, as well as its complications.

A Fatal Case of Febrile Ulceronecrotic Mucha-Habermann Disease in a 10-Year-Old Boy.

A Fatal Case of Febrile Ulceronecrotic Mucha-Habermann Disease in a 10-Year-Old Boy.

Haemorrhagic bullae and purpura associated with the Bruton tyrosine kinase inhibitor ibrutinib

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Bilateral carpal tunnel syndrome preceding haemorrhagic bullae in an older adult.

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Bullous Hemorrhagic Dermatosis Induced By Heparin: An Indonesian Case Report

Introduction: Bullous haemorrhagic dermatosis is a rare clinical disorder which is usually related to a treatment with unfractionated heparin (UFH) or low molecular weight heparin (LMWH), characterized by multiple intra-epidermal haemorrhages distant from the site of injection.&#x0D; Presentation of Case: A 62-year-old male patient with coronary heart disease who received heparin treatment experienced several tense, haemorrhagic bullae located on the right arm area, close to the injection site, and followed by the formation of several hematomas on his back trunk 2 days after he had received UFH. The lesions regressed after discontinuation of heparin and supportive topical treatments.&#x0D; Discussion: The lesions in this patient have similar characteristic with heparin-induced skin necrosis and demonstrate thrombocytopenia probably related to heparin. There are some proposed hypotheses of pathophysiology which include hypersensitivity reaction and idiosyncratic dose-related reaction. Given the clinically course, the discontinuation of heparin treatment was essential for lesion regression in addition other supportive measures.&#x0D; Conclusion: Heparin-induced skin lesions may indicate the presence of life-threatening heparin-induced thrombocytopenia. An early diagnosis is crucial to enable discontinuation of heparin if required.

Ruptured hemorrhagic bulla in a patient with a HeartMate 3 treated with an Amplatzer device

Ruptured hemorrhagic bulla in a patient with a HeartMate 3 treated with an Amplatzer device