DOCSLIB.ORG

How to Differentiate Hemosiderin Staining

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

What’s causing your patient’s lower-extremity redness? How to differentiate hemosiderin staining, lipodermatosclerosis, In left image, note pronounced varicose veins and hemosiderin staining in gaiter area (ankle to venous dermatitis, and knee) of light-skinned patient. In right image, note similar conditions hemosiderin staining in dark-skinned patient and medial ankle flare of dilated small veins By Robyn Bjork, MPT, CWS, WCC, CLT-LANA associated with chronic venous hypertension. he ability to understand or “read” lower-extremity redness in your pa - Ttient is essential to determining its cause and providing effective treatment. Redness can occur in multiple condi - tions—hemosiderin staining, lipoder - matosclerosis, venous dermatitis, chronic inflammation, cellulitis, and dependent ru - Note inverted champagne-bottle appearance of bor. This article provides clues to help you leg and ankle, indicating chronic lipodermato - sclerosis. Also note lumpy, bumpy skin (papillo - differentiate these conditions and identify matosis) and thickened, fibrotic skin with positive the specific cause of your patient’s lower- Stemmer’s sign, which indicate secondary phle - extremity redness. bolymphedema. Redness results from chronic in - flammation and resolves with compression ther - Hemosiderin staining and apy and manual lymphatic drainage. lipodermatosclerosis Hemosiderin staining is dark purple or dermatosclerosis may be misdiagnosed as rusty discoloration of the lower legs cellulitis. Active lipodermatosclerosis caus - caused by chronic venous disease. A 2010 es painful, sharply demarcated red patch - study found hemosiderin staining in all es on medial aspects of the lower leg. subjects with lipodermatosclerosis and ve - Unlike in cellulitis, redness in lipoder - nous ulcers. When vein valves fail, regurgi - matosclerosis is localized to areas of he - tated blood forces red blood cells (RBCs) mosiderin staining and induration. Also, out of capillaries. Dead RBCs release iron, the skin isn’t hot and the patient is which is stored in tissues as hemosiderin, afebrile and unresponsive to antibiotics. staining the skin. Lipodermatosclerosis progresses to fibro - Hemosiderin staining and active lipo - sis and constriction, causing an inverted 16 www.WoundCareAdvisor.com Wound Care Advisor July/August 2013 • Volume 2, Number 4 • champagne-bottle appearance of the legs. common in patients with lower-extremity Treat active lipodermatosclerosis with venous disease. Signs and symptoms in - compression therapy and topical corticos - clude scaling, crusting, weeping, erythema, teroids, if needed. Control chronic venous erosions, and intense itching. This disorder hypertension with compression, and he - increases the risk of contact sensitivity. Ad - mosiderin staining will fade. Refer the pa - vise the patient to avoid such products as tient for potential corrective venous surgi - lanolin, balsam of Peru, rubber, adhesives, cal procedures. fragrances, dyes, preservatives, skin sealants, silver sulfadiazine, neomycin, and Venous dermatitis bacitracin—all known to exacerbate ve - Defined as inflammation of the epidermis nous dermatitis. and dermis, venous (stasis) dermatitis is Venous dermatitis commonly is con - fused with cellulitis. A 2011 study found that 28% of 145 patients hospitalized for cellulitis had been misdiagnosed. The most common mistaken diagnosis was venous dermatitis. Unlike cellulitis, venous der - matitis causes itching and crusting; also, the skin isn’t acutely painful or hot and the patient is afebrile. Treat acute venous dermatitis with com - pression therapy and mild-potency topical corticosteroids. Apply corticosteroids spar - ingly to affected areas once or twice daily for 2 weeks; be aware that premature dis - continuation can lead to recurrence, while prolonged use can cause skin thinning and reduced efficacy. Domeboro soaks also de - crease weeping, irritation, and itching. Paste bandages impregnated with calamine or zinc oxide are soothing and drying. However, some patients may react to the preservatives in paste bandages, so a patch test is prudent. Top image shows redness, weeping, and crust - ing from acute venous dermatitis, coupled with secondary phlebolymphedema. Bottom image Chronic inflammation shows scaling from venous dermatitis on right leg Lymphedema causes chronic inflammation. and hemosiderin staining on left leg. Notice skin About 50% of plasma proteins leak into pallor on left leg (top of image), which becomes the interstitial space daily and are recycled more prominent with leg elevation, indicating through the lymphatics. Lymphatic failure concurrent peripheral arterial disease. Redness traps proteins in the tissues; the proteins from stasis dermatitis obscures arterial disease on right leg. Skin tears on right ankle result from pa - act like sponges, attracting and binding tient tearing off itchy, flaky scales. fluid. The proteins then denature, trigger - Wound Care Advisor www.WoundCareAdvisor.com 17 • July/August 2013 • Volume 2, Number 4 Stemmer’s sign confirms lymphedema. Complete decongestive physiotherapy pro - motes protein reabsorption and resolves chronic inflammation. Cellulitis Cellulitis is a rapidly spreading infection of the dermis and subcutaneous tissue. In adults, it most commonly stems from Staphylococcus aureus infection of the legs. Erysipelas, a superficial form of cel - lulitis, involves the lymphatic system and is differentiated by “streaking” toward a re - gional lymph node. Cellulitic skin is hot, acutely painful, edematous, and indurated. Redness spreads and the borders usually are irreg - ular, sharply defined, and slightly elevat - ed. Blisters, hemorrhagic bullae, abscesses, erosions, and necrosis may develop. About 30% to 80% of patients with lower limb cellulitis are afebrile. The white Top image demonstrates phlebolipolym - blood cell count, erythrocyte sedimenta - phedema, a combination of venous disease (phlebo), lipedema (lipo), and early secondary tion rate, and C-reactive protein levels lymphedema. Note the chronic inflammation just commonly are elevated, but normal values above the ankle, where there is significant lym - don’t rule out cellulitis. phatic congestion. Also note the dilated veins Treat cellulitis with oral antibiotics effec - near the medial heel, which indicate venous hy - tive against staphylococcus and streptococ - pertension. The foot appears spared of swelling cus. Adding a brief course of oral corticos - compared to the rest of the leg, indicating li - pedema. The redness resolves with compression teroids significantly shortens cellulitis therapy. In the bottom image, note the scale and duration. Severe cases may necessitate crust of chronic venous dermatitis on the lateral hospitalization and I.V. antibiotics, plus ab - aspect of the left ankle. scess incision and drainage. Control edema with bed rest and leg elevation. ing a chronic inflammatory response. This Recurrent cellulitis is common in patients response sometimes is misdiagnosed and with lymphedema. With compromised skin treated as chronic cellulitis. immunity, bacteria invade and spread with Compared to cellulitis, high-protein little resistance. If lymphedema is present, chronic inflammation is diffuse and non - refer the patient for treatment after acute tender, with light redness and mildly in - cellulitis resolves. If the patient already is creased warmth. Local skin changes may being treated for lymphedema, suspend include thickening or papillomatosis (a manual lymphatic drainage and compres - lumpy, bumpy appearance). A positive sion until acute cellulitis resolves. 18 www.WoundCareAdvisor.com Wound Care Advisor July/August 2013 • Volume 2, Number 4 • The most common disorders mistaken veins when the leg is elevated and regurgi - for lower-limb cellulitis are venous der - tates back into the tissues when the leg is matitis, lipodermatosclerosis, irritant der - dependent. matitis, and lymphedema. It also may be If you detect dependent rubor, obtain mistaken for deep vein thrombosis (DVT) the ankle-brachial index (ABI) to confirm or dependent rubor. Rule out DVT using PAD. For moderate PAD (ABI of 0.5 to venous duplex ultrasound. Dependent ru - 0.79), refer the patient for a routine vascu - bor disappears with leg elevation, whereas lar specialist consultation. For severe PAD cellulitic redness doesn’t. (ABI below 0.5), maintain dry, stable Click here to view image of cellulitis. wound eschar and urgently refer the pa - tient to a vascular specialist for potential Dependent rubor revascularization. Dependent rubor is a fiery to dusky-red Click here to view images and read a case coloration visible when the leg is in a de - study on dependent rubor. pendent position but not when it’s elevat - ed above the heart. The underlying cause Knowledge summary is peripheral arterial disease (PAD), so the “Reading” the common causes of leg red - extremity is cool to the touch. To test for ness helps you determine what’s causing dependent rubor, position the patient your patient’s redness so you can provide supine and elevate the legs 60 degrees for effective treatment. Remember—chronic 1 minute; then examine sole color. PAD venous disease causes hemosiderin stain - causes the soles to change from pink to ing, lipodermatosclerosis, and venous der - pale in fair-skinned people and to gray or matitis. Dermatitis is itchy and crusty; lipo - ashen in dark-skinned people. The faster dermatosclerosis causes sclerosis and an the pallor appears, the worse the PAD. Pal - inverted champagne-bottle
Recommended publications
  • Section 8: Hematology CHAPTER 47: ANEMIA

    Section 8: Hematology CHAPTER 47: ANEMIA

    Section 8: Hematology CHAPTER 47: ANEMIA Q.1. A 56-year-old man presents with symptoms of severe dyspnea on exertion and fatigue. His laboratory values are as follows: Hemoglobin 6.0 g/dL (normal: 12–15 g/dL) Hematocrit 18% (normal: 36%–46%) RBC count 2 million/L (normal: 4–5.2 million/L) Reticulocyte count 3% (normal: 0.5%–1.5%) Which of the following caused this man’s anemia? A. Decreased red cell production B. Increased red cell destruction C. Acute blood loss (hemorrhage) D. There is insufficient information to make a determination Answer: A. This man presents with anemia and an elevated reticulocyte count which seems to suggest a hemolytic process. His reticulocyte count, however, has not been corrected for the degree of anemia he displays. This can be done by calculating his corrected reticulocyte count ([3% × (18%/45%)] = 1.2%), which is less than 2 and thus suggestive of a hypoproliferative process (decreased red cell production). Q.2. A 25-year-old man with pancytopenia undergoes bone marrow aspiration and biopsy, which reveals profound hypocellularity and virtual absence of hematopoietic cells. Cytogenetic analysis of the bone marrow does not reveal any abnormalities. Despite red blood cell and platelet transfusions, his pancytopenia worsens. Histocompatibility testing of his only sister fails to reveal a match. What would be the most appropriate course of therapy? A. Antithymocyte globulin, cyclosporine, and prednisone B. Prednisone alone C. Supportive therapy with chronic blood and platelet transfusions only D. Methotrexate and prednisone E. Bone marrow transplant Answer: A. Although supportive care with transfusions is necessary for treating this patient with aplastic anemia, most cases are not self-limited.
  • Obesity and Chronic Inflammation in Phlebological and Lymphatic Diseases

    Obesity and Chronic Inflammation in Phlebological and Lymphatic Diseases

    Review 55 Obesity and chronic inflammation in phlebological and lymphatic diseases G. Faerber Centre for Vascular Medicine, Hamburg Keywords increase in intra-abdominal and intertriginous ten mit venösen oder lymphatischen Erkran- Obesity-associated functional venous insuffi- pressure, which in turn leads to an increase in kungen, die gleichzeitig schwer adipös und ciency, obesity-associated lymphoedema, vis- venous pressure in leg vessels, these relation- häufig multimorbide sind, überproportional ceral obesity, chronic inflammation, insulin ships are mainly caused by the metabolic, an. Die Adipositas, vor allem die viszerale, resistance chronic inflammatory and prothrombotic pro- verschlechtert alle Ödemerkrankungen, er- cesses that result from the increase of visceral höht das Risiko für thromboembolische Er- Summary adipose tissue. These processes can be ident- krankungen und postthrombotisches Syn- The prevalence of obesity has continued to ified by low levels of adiponectin and high lev- drom und kann alleinige Ursache sein für die increase considerably during the past 15 els of leptin, insulin, intact proinsulin, PAI-1 Adipositas-assoziierte funktionelle Venenin- years. Particularly noticeable is the marked and proinflammatory cytokines (IL-6, IL-8, suffizienz ohne Nachweis von Obstruktion increase in morbid obesity, which is in turn TNF-α). Therapeutic measures must therefore oder Reflux. Das Adipositas-assoziierte particularly pronounced among the elderly. be aimed primarily at reducing visceral obesity Lymphödem stellt inzwischen den größten Since the prevalence of venous thromboem- and with it hyperinsulinemia or insulin resis- Anteil unter den sekundären Lymphödemen. bolism, chronic venous insufficiency and sec- tance as well as at fighting chronic inflam- Mehr als 50 Prozent der Lipödempatientin- ondary lymphoedema also increases with mation.
  • The Nature of Storage Iron in Idiopathic Hemochromatosis and in Hemosiderosis

    The Nature of Storage Iron in Idiopathic Hemochromatosis and in Hemosiderosis

    THE NATURE OF STORAGE IRON IN IDIOPATHIC HEMOCHROMATOSIS AND IN HEMOSIDEROSIS ELECTRON OPTICAL, CHEMICAL, AND SEROLOGIC STUDIES ON ISOLATED HEMOSIDERIN GRANULES* BY GOETZ W. RICHTER, M.D. (From the Department of Pathology, Cornell University Medical College, New York) PLATES 47 TO 51 (Received for publication, April 21, 1960) Although ferritin has long been recognized as an important iron storage compound and as an intermediary in normal iron metabolism, its role in idiopathic hemochromatosis and in secondary hemosiderosis is still unkuown. Diverse means have been employed to gain more knowledge on the pathway of iron in these conditions, and numerous publications attest the difficulties inherent in trying to distinguish between normal and abnormal storage of iron in cells of various sorts. Histochemical studies have provided evidence that inorganic compounds of iron stored in cells as hemosiderin are combined with an organic carrier substance that contains variable quantities of protein, lipid, and carbohydrate (1, 2). Results of chemical analyses led Ludewig to emphasize the heterogeneity of hemosiderin granules (3); his findings have provided qualitative and quantitative data on the carbohydrate, lipid, protein, and iron content of various hemosiderin preparations. The term "hemosiderin" has been used rather loosely; generally it refers to granules that are visible in the light micro- scope, brown when unstained, and give a positive Prussian blue test. Iron that gives a positive Prussian blue test with potassium ferrocyanide without the previous application of oxidizing agents must be in the trivalent (ferric) state. This is true of the bulk of iron in hemosiderin granules; it is also true of the iron hydroxide present in ferritin (4, 5, 7).
  • Visualization of Microbleeds with Optical Histology in Mouse Model of Cerebral Amyloid Angiopathy

    Visualization of Microbleeds with Optical Histology in Mouse Model of Cerebral Amyloid Angiopathy

    Microvascular Research 105 (2016) 109–113 Contents lists available at ScienceDirect Microvascular Research journal homepage: www.elsevier.com/locate/ymvre Visualization of microbleeds with optical histology in mouse model of cerebral amyloid angiopathy Patrick Lo a,b, Christian Crouzet a,b, Vitaly Vasilevko c,1,BernardChoia,b,d,⁎,1 a Beckman Laser Institute and Medical Clinic, University of California, Irvine, 1002 Health Sciences Road East, Irvine, CA 92612, USA b Department of Biomedical Engineering, University of California, Irvine, 3120 Natural Sciences II, Irvine, CA 92697, USA c Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, 1207 Gillespie NRF, Irvine, CA 92697-4540, USA d Edwards Lifesciences Center for Advanced Cardiovascular Technology, University of California, Irvine, 2400 Engineering Hall, Irvine, CA 92697, USA article info abstract Article history: Cerebral amyloid angiopathy (CAA) is a neurovascular disease that is strongly associated with an increase in the Received 14 May 2015 number and size of spontaneous microbleeds. Conventional methods of magnetic resonance imaging for detec- Revised 3 February 2016 tion of microbleeds, and positron emission tomography with Pittsburgh Compound B imaging for amyloid Accepted 4 February 2016 deposits, can separately demonstrate the presence of microbleeds and CAA in affected brains in vivo;however, Available online 10 February 2016 there still is a critical need for strong evidence that shows involvement of CAA in microbleed formation. Here, we show in a Tg2576 mouse model of Alzheimer's disease, that the combination of histochemical staining and Keywords: Intracerebral hemorrhage an optical clearing method called optical histology, enables simultaneous, co-registered three-dimensional visu- DiI alization of cerebral microvasculature, microbleeds, and amyloid deposits.
  • Brain Metastasis from Unknown Primary Tumour: Moving from Old Retrospective Studies to Clinical Trials on Targeted Agents

    Brain Metastasis from Unknown Primary Tumour: Moving from Old Retrospective Studies to Clinical Trials on Targeted Agents

    cancers Review Brain Metastasis from Unknown Primary Tumour: Moving from Old Retrospective Studies to Clinical Trials on Targeted Agents Roberta Balestrino 1,* , Roberta Rudà 2,3 and Riccardo Soffietti 3 1 Department of Neuroscience, University of Turin, Via Cherasco 15, 10121 Turin, Italy 2 Department of Neurology, Castelfranco Veneto/Treviso Hospital, Via dei Carpani, 16/Z, 31033 Castelfranco Veneto, Italy; [email protected] 3 Department of Neuro-Oncology, University of Turin, Via Cherasco 15, 10121 Turin, Italy; riccardo.soffi[email protected] * Correspondence: [email protected] Received: 13 October 2020; Accepted: 9 November 2020; Published: 12 November 2020 Simple Summary: Brain metastases (BMs) are the most common intracranial tumours in adults and occur up to 3–10 times more frequently than primary brain tumours. In up to 15% of patients with BM, the primary tumour cannot be identified. These cases are known as BM of cancer of unknown primary (CUP) (BM-CUP). The understanding of BM-CUP, despite its relative frequency and unfavourable outcome, is still incomplete and clear indications on management are missing. The aim of this review is to summarize current evidence on the diagnosis and treatment of BM-CUP. Abstract: Brain metastases (BMs) are the most common intracranial tumours in adults and occur up to 3–10 times more frequently than primary brain tumours. BMs may be the cause of the neurological presenting symptoms in patients with otherwise previously undiagnosed cancer. In up to 15% of patients with BMs, the primary tumour cannot be identified. These cases are known as BM of cancer of unknown primary (CUP) (BM-CUP).
  • A Case Report of Chronic Sclerosing Panniculitis Hadiuzzaman*, M

    A Case Report of Chronic Sclerosing Panniculitis Hadiuzzaman*, M

    Journal of Pakistan Association of Dermatologists 2010; 20 : 246-248. Case Report A case report of chronic sclerosing panniculitis Hadiuzzaman*, M. Hasibur Rahman*, Nazma Parvin Ansari**, Aminul Islam† *Department of Dermatology, Community Based Medical College, Bangladesh, Mymensingh, Bangladesh. **Department of Pathology, Community Based Medical College, Bangladesh, Mymensingh, Bangladesh †Department of Medicine, Community Based Medical College, Bangladesh, Mymensingh, Bangladesh Abstract Sclerosing panniculitis is a fibrotic process that usually occurs on the legs, commonly in women older than 40. The principal features are indurated woody plaques with erythema, edema, telangiectasia, and hyperpigmentation. Although the exact pathogenesis is uncertain, it is thought to occur as a result of ischemic changes. We present a 28-year-old married female who had a 10- year history of painful sclerotic plaques, repeated ulceration and healing with fibrosis of the both lower legs and abdomen. Venogram and Doppler investigations were normal. Skin biopsy from the edge of the ulcer demonstrated the feature of chronic sclerosing panniculitis. Satisfactory improvement was found with methotrexate 7.5mg weekly for 4 months. No recurrence was noted within 1 year follow up. Key words Sclerosing panniculitis, lipodermatosclerosis. Case report Mild swelling of the legs worse at the end of the day was also reported. Tenderness of the ulcer A 28-year-old married female presented to was worse with dependency. There was no dermatology outpatient, Community Based history of previous trauma to the area, joint Medical College, Bangladesh, with a 10-year complaint, pancreatic disease, or other tender history of painful repeated ulceration and nodular lesions or ulcerations. There was no healing with fibrosis of the both lower legs and significant history of fever and night sweating.
  • 2016 Essentials of Dermatopathology Slide Library Handout Book

    2016 Essentials of Dermatopathology Slide Library Handout Book

    2016 Essentials of Dermatopathology Slide Library Handout Book April 8-10, 2016 JW Marriott Houston Downtown Houston, TX USA CASE #01 -- SLIDE #01 Diagnosis: Nodular fasciitis Case Summary: 12 year old male with a rapidly growing temple mass. Present for 4 weeks. Nodular fasciitis is a self-limited pseudosarcomatous proliferation that may cause clinical alarm due to its rapid growth. It is most common in young adults but occurs across a wide age range. This lesion is typically 3-5 cm and composed of bland fibroblasts and myofibroblasts without significant cytologic atypia arranged in a loose storiform pattern with areas of extravasated red blood cells. Mitoses may be numerous, but atypical mitotic figures are absent. Nodular fasciitis is a benign process, and recurrence is very rare (1%). Recent work has shown that the MYH9-USP6 gene fusion is present in approximately 90% of cases, and molecular techniques to show USP6 gene rearrangement may be a helpful ancillary tool in difficult cases or on small biopsy samples. Weiss SW, Goldblum JR. Enzinger and Weiss’s Soft Tissue Tumors, 5th edition. Mosby Elsevier. 2008. Erickson-Johnson MR, Chou MM, Evers BR, Roth CW, Seys AR, Jin L, Ye Y, Lau AW, Wang X, Oliveira AM. Nodular fasciitis: a novel model of transient neoplasia induced by MYH9-USP6 gene fusion. Lab Invest. 2011 Oct;91(10):1427-33. Amary MF, Ye H, Berisha F, Tirabosco R, Presneau N, Flanagan AM. Detection of USP6 gene rearrangement in nodular fasciitis: an important diagnostic tool. Virchows Arch. 2013 Jul;463(1):97-8. CONTRIBUTED BY KAREN FRITCHIE, MD 1 CASE #02 -- SLIDE #02 Diagnosis: Cellular fibrous histiocytoma Case Summary: 12 year old female with wrist mass.
  • Panniculitis Martin C

    Panniculitis Martin C

    Panniculitis Martin C. Mihm M.D. Director – Mihm Cutaneous Pathology Consultative Service (MCPCS) Brigham and Women’s Hospital Director – Melanoma Program Brigham and Women’s Hospital and Harvard Medical School Co-Director – Melanoma Program Dana-Farber Cancer Institute and Harvard Medical School Conflicts of Interest • Chairman Scientific Advisory Board – Caliber I.D. Inc. • Member Scientific Advisory Board – MELA Sciences Inc. • Consultant – Novartis • Consultant – Alnylam Disorders of the Subcutis • Septal • Lobular • Mixed • Inflammatory (N/G/L) • Pauci-inflammatory 1 Septal Panniculitis • Erythema nodosum • Necrobiosis lipoidica • Morphea profundus Erythema Nodosum Clinical Features • Young adults • Nodular or plaque like lesions • Anterior aspect of lower legs (common) • Arms or abdomen (occurs occasionally) • Clinical course • Initially erythematous, painful area • Evolves into nodule or plaque • Lasts 10 days to 8 weeks • Fever, malaise, arthralgias (variable s/s) Erythema Nodosum Clinical Features Causation • Systemic diseases: CTD, Behcet’s, Sweet’s, sarcoidosis,etc. • Drugs: Numerous drugs have been associated: penicillin, sulfa, Cipro, isotretinoin, etc. • 30%: idiopathic or of unknown cause.. 2 3 Erythema nodosum : Well Developed Lesion • Septal fibrosis • Septal chronic inflammation • Lymphocytes • Frank Vasculitis may not be present • Granulomatous changes • Small granulomatous aggregates of histiocytes • Miescher’s radial granuloma • Multinucleated giant cells 4 5 6 Erythema nodosum : Morphologic Clues to underlying etiology
  • Urine Hemosiderin: a Novel Marker to Assess the Severity of Chronic Venous Disease

    Urine Hemosiderin: a Novel Marker to Assess the Severity of Chronic Venous Disease

    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Urine hemosiderin: A novel marker to assess the severity of chronic venous disease Paolo Zamboni, MD,a Marcello Izzo, MD,a Luisella Fogato, MD,a Sergio Carandina, MD,a and Vincenzo Lanzara, PhD,b Ferrara, Italy Objective: Impaired venous drainage in severe chronic venous insufficiency (CVI) leads to microcirculatory overload, characterized by erythrocyte diapedesis and subsequent extravascular hemolysis, resulting in typical dermal hemosiderin deposition. We hypothesized that hemosiderin, normally absent, could be present in the urine in CVI. Methods: The three-phase study included 117 patients with CVI and 12 healthy control subjects, all of whom had undergone clinical examination and duplex scanning. In phase 1, current methods were used to test urine for hemosiderin in 61 persons: 12 healthy control subjects, 24 patients with mild CVI (clinical class C1 to C3), and 25 patients with severe CVI (clinical class C4 to C6). In phase 2, the concentration of urinary hemosiderin was determined in 45 consecutive patients with CVI, CEAP class 1 to 6. A score of 0 was assigned when typical hemosiderin granules were absent at microscopic examination, a score of 1 when one to three granules per field were detected; 2 when four to six granules were detected; and 3 when more than six granules were observed. Phase 3 included 23 patients with CVI (clinical class 2 to 6). Hemosiderin concentration was determined and a score assigned before patients underwent surgical procedures to correct primary CVI. Both hemosiderin testing and duplex scanning were repeated after 6 months.
  • The Biophysical Role of Hemodynamics in the Pathogenesis of Cerebral Aneurysm Formation and Rupture

    The Biophysical Role of Hemodynamics in the Pathogenesis of Cerebral Aneurysm Formation and Rupture

    NEUROSURGICAL FOCUS Neurosurg Focus 47 (1):E11, 2019 The biophysical role of hemodynamics in the pathogenesis of cerebral aneurysm formation and rupture Sauson Soldozy, BA, Pedro Norat, MD, Mazin Elsarrag, MS, Ajay Chatrath, MS, John S. Costello, BA, Jennifer D. Sokolowski, MD, PhD, Petr Tvrdik, PhD, M. Yashar S. Kalani, MD, PhD, and Min S. Park, MD Department of Neurological Surgery, University of Virginia Health System, Charlottesville, Virginia The pathogenesis of intracranial aneurysms remains complex and multifactorial. While vascular, genetic, and epidemio- logical factors play a role, nascent aneurysm formation is believed to be induced by hemodynamic forces. Hemodynamic stresses and vascular insults lead to additional aneurysm and vessel remodeling. Advanced imaging techniques allow us to better define the roles of aneurysm and vessel morphology and hemodynamic parameters, such as wall shear stress, oscillatory shear index, and patterns of flow on aneurysm formation, growth, and rupture. While a complete understand- ing of the interplay between these hemodynamic variables remains elusive, the authors review the efforts that have been made over the past several decades in an attempt to elucidate the physical and biological interactions that govern aneurysm pathophysiology. Furthermore, the current clinical utility of hemodynamics in predicting aneurysm rupture is discussed. https://thejns.org/doi/abs/10.3171/2019.4.FOCUS19232 KEYWORDS cerebral aneurysm; hemodynamics; wall shear stress; computational fluid dynamics; vascular remodeling NTRACRANIAL aneurysms (IAs) are acquired outpouch- cades and, ultimately, a wide range of transcriptional and ings of arteries that occur in 1%–2% of the popula- signaling changes that lead to vascular wall remodeling. tion.36 Likely as a result of improved imaging modali- The advent of computational and radiographic modeling Ities, the incidence of unruptured IAs has increased.
  • Path Pulmonary Outline

    Path Pulmonary Outline

    Pathology Pulmonary ATELECTASIS Neonatal Atelectasis ‐ The lungs of the neonate never inflate, a consequence of congenital defect, premature birth (insufficient surfactant), or other consequence, also called Patchy Atelectasis Adult or Acquired Atelectasis ‐ Collapse of Previously Inflated lung, creating areas of “airless parenchyma” ‐ Produces a well‐perfused but poorly‐ventilated region, predisposing for infection Decreased Volume ‐ Is a reversible disorder (except in the case of contraction) outside pleural space ‐ Resorption Atelectasis o Consequence of complete obstruction without impairment to blood flow Blockage o A decreased lung volume results in a mediastinal shift towards affected lung o Caused by a mucous plug associated with Asthma, Bronchitis, or Aspiration Pneumonia ‐ Compression Atelectasis o Consequence of partially or totally filled pleura with exudate (CHF), tumor, air (pneumothorax), blood (hemothorax), when air pressure threatens the function of lungs and great vessels (tension pneumothorax), or with an extra‐pulmonary mass compressing Something within lung parenchyma. pleural space compressing o Compressed lung tissue cannot expand and is therefore poorly ventilated. parenchyma o Compression pushes lung resulting in a mediastinal shift away from affected lung ‐ Contraction Atelectasis o Fibrotic changes prevent expansion, resulting in reduced lung volume and ventilation Fibrotic o This form is irreversible Changes are Irreversible PULMONARY EDEMA Pulmonary Edema is simply the accumulation of fluid in the alveolar
  • Hemosiderin-Laden Macrophages Are an Independent Factor Correlated with Pulmonary Vascular Resistance in Idiopathic Pulmonary Fi

    Hemosiderin-Laden Macrophages Are an Independent Factor Correlated with Pulmonary Vascular Resistance in Idiopathic Pulmonary Fi

    Fukihara et al. BMC Pulmonary Medicine (2017) 17:30 DOI 10.1186/s12890-017-0376-8 RESEARCHARTICLE Open Access Hemosiderin-laden macrophages are an independent factor correlated with pulmonary vascular resistance in idiopathic pulmonary fibrosis: a case control study Jun Fukihara1, Hiroyuki Taniguchi1*, Masahiko Ando2, Yasuhiro Kondoh1, Tomoki Kimura1, Kensuke Kataoka1, Taiki Furukawa1, Takeshi Johkoh3, Junya Fukuoka4, Koji Sakamoto5 and Yoshinori Hasegawa5 Abstract Background: Increases in hemosiderin-laden macrophages (HLM) are reported to be observed in idiopathic pulmonary fibrosis (IPF). According to a recent study, significant correlation between hemosiderin deposition in the lung tissue of IPF and pulmonary hypertension evaluated by echocardiography has been suspected. In this study, we aimed to evaluate whether HLM in bronchoalveolar lavage fluid (BALF) is a factor correlated with pulmonary hemodynamic parameters evaluated by right heart catheterization in patients with IPF. Methods: Initial data from 103 consecutive patients with IPF who underwent surgical lung biopsy between November 2007 and March 2014 were retrospectively analyzed. The “HLM score” of BALF was established by dividing the number of Perls’ Prussian blue stain positive macrophages by the total number of macrophages counted. Results: BALF showed an elevated HLM score (38.2%). Right heart catheterization revealed mean pulmonary arterial pressure (mPAP) of 16.3 mmHg and pulmonary vascular resistance (PVR) of 1.55 Wood units. HLM score was positively correlated with mPAP (ρ = 0.204; p = 0.038) and PVR (ρ = 0.349, p < 0.001). In multivariate analysis, 6-min walk distance (standardized partial regression coefficient [β], −0.391; p < 0.001), minimum oxygen saturation during 6-min walk distance (β, −0.294; p = 0.001) and HLM score (β, 0.265; p = 0.002) were independently correlated with PVR.