Scurvy Imaging
No Results
No Results
processing….
The term scurvy is derived from the Nordic word skyrbjugr, meaning swelling or edema. It has also been suggested that the term is derived from the Old Icelandic words skyrbugr, scarby, or skurvic.
Scurvy is caused by a lack of vitamin C and manifests as collagen defects, hemorrhagic diathesis, abnormalities in bone maturation, epiphyseal disease, lifting of the periosteum, hemarthroses, irritability, decreased appetite, delayed development, and pseudoparalysis related to bone pain. [1, 2, 3, 4]
Scurvy is not a common condition, although, in one study, vitamin C deficiency was present in up to 23% of respondents. [5, 6] Young children and older persons are predisposed to scurvy because of their diets or the overpreparation of food (cooking destroys vitamin C). Smokers, non-Hispanic black males, and individuals who do not use vitamin supplements have an increased risk of vitamin C deficiency. [5] Gastric bypass surgery may be complicated by vitamin C deficiency within 29-90 days, if diet is not supplemented. [7]
Radiography is the preferred imaging examination for diagnosis. Serum vitamin C levels can be obtained to confirm the diagnosis of scurvy. Congenital syphilis and neuroblastoma produce findings similar to those of scurvy. The same findings may also be seen in a limb with residual palsy as a result of polio.
Some authors have suggested that the most diagnostic radiologic finding of vitamin C deficiency is a large, fluctuant, parietal swelling, which is apparently caused by subperiosteal hemorrhage. This author, however, considers long-bone changes to be better clinical identifiers of vitamin C deficiency than parietal swelling.
The epiphyses and periosteum also become easily detachable because of hemorrhage below the periosteum. Separation of the metaphyseal plate from the diaphysis, epiphyseal clefts, and malalignment of the metaphysis may also occur. A circular, opaque radiologic shadow often surrounds epiphyseal centers of ossification. This ring of increased opacity formed around the ossification center of long bone epiphyses is known as the Wimberger sign, which may result from bleeding or attachment movement.
Vitamin C deficiency is characterized by cortical thinning, which is sometimes described as a “pencil-point” cortex. Decreased trabeculae produce a decrease in radiopacity, resulting in a transparent aspect similar in appearance to ground glass (see image below).
The increased opacity of distal diaphysis may be accompanied by a subjacent zone of decreased opacity. The thickening is known as a Frankel line, and the lucent zone on the diaphyseal side of the Frankel line (secondary to poorly formed trabeculae) is known as the Trümmerfeld zone. Its origin might be related to vascular compromise, similar to increases in bone density noted with avascular necrosis.
Costochondral junctions of the first 6 or 8 thoracic ribs may be expanded; this change may be related to fracturing of the zone of provisional calcification during normal respiration. The costochondral junctions are rounded and appear smooth, knobby, and steplike. The enlargement of the costochondral junctions simulates that seen in rickets.
The zone of proliferating cartilage cells is distorted, producing spicules from the metaphysis into the epiphyseal plate region. The zone of temporary calcification broadens, producing a wide, radiopaque metaphyseal band. Subjacent to this is a zone of poor-quality trabeculae, which appears radiolucent. A steplike lateral projection is found at the epiphyseal line in patients who are severely affected. Scorbutic changes are radiologically more severe in the lower extremities, whereas scorbutic changes seen in rickets are allegedly more severe in the upper extremities.
Metaphyseal “beaks” and transverse lines of increased or decreased opacity may be seen in scurvy. The “beaks,” known as Pelkan spurs, are associated with fractures of the Trümmerfeld zone. They may be produced by lateral growth of the metaphyseal calcification zone and are associated with periosteal elevation. Subepithelial marginal clefts may also be present.
Skull changes may produce a porotic hyperostosis (“hair-on-end” appearance) or crew-cut appearance secondary to marrow hyperplasia in response to anemia. No sphenoid changes are reported. Sphenoid porosity has not been shown to be caused by scurvy.
Subperiosteal hemorrhages are visualized only in the healing phase of scurvy, and these are almost invariably paraepiphyseal in distribution. Epiphyseal separation often results. Healing scurvy also appears with the loss of the scurvy line, in which the only residual manifestation is a double line of ossification at the original active site.
Periosteal elevation and epiphyseal separation both appear to be relatively specific for scurvy. Osteoporosis is a nonspecific finding.
The periosteal reaction of syphilis is more generalized than that of scurvy and is usually thick or multilaminated. Syphilis, often called the great imitator, produces metaphyseal beaking similar to that noted in scurvy; however, syphilis does not produce radiopaque metaphyseal lines. Although periosteal elevation may occur and produce a linear elevated area in patients, a spiculated periosteal reaction does not occur in scurvy.
Metaphyseal lesions caused by syphilis are beaklike, whereas those caused by scurvy involve epiphyseal separation. Epiphyseal separation is a known complication of scurvy; however, it is also seen in cases of child abuse. The periosteal reaction resulting from child abuse is more generally distributed and is associated with a fracture.
Costochondral beading is more common with rickets than with scurvy.
Skull-marrow hyperplasia is more likely to result from hemolytic anemia or anemia related to parasitic infestation.
T1-weighted and PD/SPIR images reveal focal areas of metaphyseal marrow edema attributed to focal hemorrhage or infarcts.
Subperiosteal fluid and displacement of epiphyses has been reported. [8] Skull changes may be below the resolution of computed tomography (CT) or magnetic resonance imaging (MRI). A change in skull shape is not diagnostic, as this finding may also be seen with hemolytic anemia, other causes of bone marrow hyperplasia, and rickets. [9, 10, 11]
Technetium bone scans are not routinely performed in patients with scurvy; however, increased uptake at the distal metaphyses and the epiphyses and formation of a rachitic rosary are hypothetically possible.
Bohrer I, Roy M, Nager W, te Wildt B, Emrich HM, Ohlmeier MD. [Scurvy–a wrongly forgotten avitaminosis]. MMW Fortschr Med. 2007 Nov 8. 149(45):41-3. [Medline].
Léger D. Scurvy: reemergence of nutritional deficiencies. Can Fam Physician. 2008 Oct. 54(10):1403-6. [Medline].
Sommer A. Vitamin a deficiency and clinical disease: an historical overview. J Nutr. 2008 Oct. 138(10):1835-9. [Medline].
Hansen EP, Metzsche C, Henningsen E, Toft P. Severe scurvy after gastric bypass surgery and a poor postoperative diet. J Clin Med Res. 2012 Apr. 4(2):135-7. [Medline]. [Full Text].
Hampl JS, Taylor CA, Johnston CS. Vitamin C deficiency and depletion in the United States: the Third National Health and Nutrition Examination Survey, 1988 to 1994. Am J Public Health. 2004 May. 94(5):870-5. [Medline].
Velandia B, Centor RM, McConnell V, Shah M. Scurvy is still present in developed countries. J Gen Intern Med. 2008 Aug. 23(8):1281-4. [Medline].
Noordin S, Baloch N, Salat MS, Rashid Memon A, Ahmad T. Skeletal manifestations of scurvy: a case report from dubai. Case Rep Orthop. 2012. 2012:624628. [Medline]. [Full Text].
Karthiga S, Dubey S, Garber S, Watts R. Scurvy: MRI appearances. Rheumatology (Oxford). 2008 Jul. 47(7):1109. [Medline].
Polat AV, Bekci T, Say F, Bolukbas E, Selcuk MB. Osteoskeletal manifestations of scurvy: MRI and ultrasound findings. Skeletal Radiol. 2015 Aug. 44 (8):1161-4. [Medline].
Gulko E, Collins LK, Murphy RC, Thornhill BA, Taragin BH. MRI findings in pediatric patients with scurvy. Skeletal Radiol. 2015 Feb. 44 (2):291-7. [Medline].
Gongidi P, Johnson C, Dinan D. Scurvy in an autistic child: MRI findings. Pediatr Radiol. 2013 Oct. 43 (10):1396-9. [Medline].
Bruce M Rothschild, MD Professor of Medicine, West Virginia University School of Medicine; Research Associate, Carnegie Museum
Bruce M Rothschild, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Rheumatology, International Skeletal Society, New York Academy of Sciences, Sigma Xi, Society of Skeletal Radiology
Disclosure: Nothing to disclose.
Bernard D Coombs, MB, ChB, PhD Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.
Marta Hernanz-Schulman, MD, FAAP, FACR Professor, Radiology and Radiological Sciences, Professor of Pediatrics, Department of Radiology, Vice-Chair in Pediatrics, Medical Director, Diagnostic Imaging, Vanderbilt Children’s Hospital
Marta Hernanz-Schulman, MD, FAAP, FACR is a member of the following medical societies: American Institute of Ultrasound in Medicine, American Roentgen Ray Society
Disclosure: Nothing to disclose.
Felix S Chew, MD, MBA, MEd Professor, Department of Radiology, Vice Chairman for Academic Innovation, Section Head of Musculoskeletal Radiology, University of Washington School of Medicine
Felix S Chew, MD, MBA, MEd is a member of the following medical societies: American Roentgen Ray Society, Association of University Radiologists, Radiological Society of North America
Disclosure: Nothing to disclose.
Michael A Bruno, MD, MS, FACR Professor of Radiology and Medicine, Pennsylvania State University College of Medicine; Director, Radiology Quality Management Services, The Penn State Milton S Hershey Medical Center
Michael A Bruno, MD, MS, FACR is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Association of University Radiologists, Radiological Society of North America, Society of Nuclear Medicine and Molecular Imaging, Society of Skeletal Radiology
Disclosure: Received royalty from Oxford Press for book author/editor & reviewer; Received royalty from Elsevier Press for book author / editor.
Jeno Imre Sebes, MD Professor, Department of Radiology, University of Tennessee Health Science Center at Memphis
Jeno Imre Sebes, MD is a member of the following medical societies: American College of Chest Physicians, American College of Radiology, American Medical Association, American Roentgen Ray Society, Association of University Radiologists, International Skeletal Society, New York Academy of Sciences, Radiological Society of North America, Sigma Xi, Society of Skeletal Radiology, Tennessee Medical Association, andTennessee Radiological Society
Disclosure: Nothing to disclose.
Scurvy Imaging
Research & References of Scurvy Imaging|A&C Accounting And Tax Services
Source
0 Comments