Scurvy, caused by a deficiency in vitamin C (ascorbic acid), is a rare but still relevant diagnosis, particularly in individuals with poor dietary habits or certain social vulnerabilities.
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Scurvy,1 caused by a deficiency in vitamin C (ascorbic acid), is a rare but still relevant diagnosis, particularly in individuals with poor dietary habits or certain social vulnerabilities. The condition results from insufficient vitamin C, which plays a key role in collagen synthesis, wound healing and maintaining the integrity of connective tissues. Although scurvy was once common among sailors and soldiers who lacked access to fresh fruit and vegetables,2 it remains an occasional diagnosis in contemporary clinical practice, especially among those who have an unbalanced diet, social vulnerability, alcoholism and severe psychiatric disorders.3 We report the case of a 62-year-old male who presented with right leg swelling, bruising and anaemia, initially suspected of having deep vein thrombosis (DVT) or a coagulation disorder, but was later diagnosed with scurvy.
A 62-year-old NZ European male presented to the emergency department (ED) with a 1-week history of right leg swelling and bruising, without any history of trauma. His past medical history included previous treatment for stage T4a N2a squamous cell carcinoma of the right tonsil in 2007, treated with chemoradiotherapy. He also had chronic thoracic back pain from a prior trauma. He was an ex-smoker, having quit 14 years ago, and denied alcohol consumption, over-the-counter medications, supplements or herbal remedies.
Upon presentation, the patient reported initially noticing small red spots on his right knee a week earlier, which had progressed to significant bruising and swelling of the right leg. He also described similar lesions on his left leg. Over the following days, he developed shortness of breath on exertion and dizziness upon standing. However, he denied any gastrointestinal bleeding, including melena, haematuria or oral bleeding. He also denied any recent infections or prior bleeding episodes, and there was no family history of bleeding disorders.
The patient appeared alert and comfortable, with a slim build. His blood pressure was 140/90mmHg in the supine position, dropping to 87/67mmHg upon standing, with a heart rate of 100 beats per minute. Examination revealed non-palpable, non-tender petechiae on the left leg, alongside extensive ecchymoses and swelling of the right leg. The oral mucosa was normal, and there were no signs of bleeding from the gums. Otherwise, his examination was unremarkable.
Initial blood tests revealed normocytic normochromic anaemia with a high reticulocyte count and normal iron studies, B12 and folate levels. Peripheral blood smear showed normocytic red cells with increased polychromatic cells and target cells, but no fragments or spherocytosis. Liver function tests were normal apart from mildly raised total bilirubin (34µmol/L) and conjugated bilirubin (15µmol/L), with a slight increase in haptoglobin levels. Lactate dehydrogenase (LDH) was normal, and renal function was intact. Coombs test was negative. Given the patient’s shortness of breath and dizziness, a computed tomography pulmonary angiogram (CTPA) was performed by the ED doctor, which ruled out pulmonary embolism. Ultrasound of the right leg excluded deep vein thrombosis (DVT). A dermatology consult was requested for probable cutaneous vasculitis causing extensive bruises and swelling. The patient exhibited perifollicular haemorrhages and corkscrew hairs on the right leg, which were strongly suggestive of scurvy. The absence of bleeding in the oral mucosa, gums or other mucosal surfaces and the patient’s poor dietary intake led to a diagnosis of scurvy. The lack of typical findings for vasculitis, such as oral ulceration or systemic symptoms, further supported this diagnosis.
The diagnosis of scurvy was confirmed after the patient’s vitamin C levels were found to be severely low (<1µmol/L; normal range: 26–85µmol/L). Given the clinical features, including the characteristic dermatological signs and the patient’s inadequate intake of fruit and vegetables, treatment with high-dose vitamin C (250mg twice daily) was initiated. Over the following days, the patient’s bruising and leg swelling improved significantly, and he reported a reduction in his symptoms of shortness of breath and dizziness.
Scurvy is a disease that results from a deficiency of vitamin C, which is essential for the hydroxylation of proline and lysine residues in collagen. This deficiency leads to impaired collagen synthesis, resulting in weakened blood vessels, which can cause bruising, petechiae and poor wound healing.3 In severe cases, scurvy can lead to spontaneous bleeding, bone pain and anaemia. It is most commonly seen in individuals with limited access to fresh fruit and vegetables, or those with psychiatric disorders, alcoholism or eating disorders.3
In this case, the patient’s clinical presentation—marked by easy bruising, leg swelling and anaemia—initially raised concerns of a coagulopathy, DVT or vasculitis. However, the absence of systemic inflammatory signs, the patient’s lack of trauma and the characteristic dermatological signs led to the diagnosis of scurvy. Notably, scurvy can mimic vasculitis, especially in patients presenting with purpura or ecchymosis, making it important to consider in the differential diagnosis.
Scurvy remains an important diagnosis in patients with unexplained bruising, anaemia and impaired wound healing, especially those with poor nutritional intake or risk factors for vitamin C deficiency. Early recognition and treatment with vitamin C supplementation can result in rapid improvement and prevent complications. This case highlights the importance of obtaining a detailed dietary history and considering nutritional deficiencies in the differential diagnosis of bleeding disorders.
View Figure 1.
The authors would like to acknowledge the Department of Dermatology for their valuable contribution and help in management of this patient.
Akram Shmendi: Consultant Physician, General Medicine Department, Middlemore Hospital, Auckland.
None declared.
1) Hodges RE, Hood J, Canham JE, et al. Clinical manifestations of ascorbic acid deficiency in man. Am J Clin Nutr. 1971;24(4):432-43. doi: 10.1093/ajcn/24.4.432.
2) Magiorkinis E, Beloukas A, Diamantis A. Scurvy: past, present and future. Eur J Intern Med. 2011;22(2):147-52. doi: 10.1016/j.ejim.2010.10.006.
3) Léger D. Scurvy: reemergence of nutritional deficiencies. Can Fam Physician. 2008;54(10):1403-6.
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