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Post-Traumatic Raynaud's Phenomenon Following Volar Plate

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Post-Traumatic Raynaud's Phenomenon Following Volar Plate CONTRIBUTION Post-Traumatic Raynaud’s Phenomenon Following Volar Plate Injury YOSEF G. CHODAKIEWITZ, BA, MD’15; ALAN H. DANIELS, MD; ROBIN N. KAMAL, MD; ARNOLD-PETER C. WEISS, MD 24 26 EN ABSTRACT Figure 1. Clinical photograph: index finger Raynaud’s phenomenon with Post-traumatic Raynaud’s phenomenon following sharp demarcated pallor at level of volar plate injury. non-penetrating or non-repetitive injury is rare. We re- port a case of Raynaud’s phenomenon occurring in a sin- gle digit 3 months following volar plate avulsion injury. Daily episodes of painless pallor of the digit occurred for 1 month upon any exposure to cold, resolving with warm water therapy. Symptoms resolved after the initiation of hand therapy, splinting, and range-of- motion exercises. KEYWORDS: Raynaud’s phenomenon, Volar plate injury, Raynaud’s syndrome INTRODUCTION Raynaud’s phenomenon is a condition in which a digit expe- riences episodic vasospasm, producing sharply demarcated pallor, coolness, paresthesias, and numbness in the digit dis- tal to the affected vessels. The episodes are typically induced by exposure to cold temperatures and may represent an exaggerated cold response in the affected digit. Diagnosis of Raynaud’s relies solely on physical exam and history. Raynaud’s phenomenon involves an increased vascu- lar contractile response to sudden cooling and alpha-2-ad- renergic agonists, which is particularly pronounced in the acral body parts because of their major thermoregulatory requirements.1 The condition may be idiopathic or second- Secondary Raynaud’s phenomenon also may occur after ary to an underlying pathology. In idiopathic Raynaud’s, also trauma, such as after digital replantation6 or after prolonged called primary Raynaud’s phenomenon, patients are typical- repetitive vibration trauma, as in the Vibration White Fin- ly female, in their second or third decade of life.2 When an ger (VWF) syndrome typically seen in construction workers underlying disorder is identified as the cause of Raynaud’s working with vibrating power tools.7,8 Raynaud’s phenome- phenomenon it is called secondary Raynaud’s phenomenon. non secondary to these types of trauma appears to be driven The most common causes of secondary Raynaud’s phe- by perivascular nerve damage. Loss of calcitonin-gene-re- nomenon are systemic rheumatic disorders, such as sclero- lated-peptide (CGRP) nerve fibers in digital cutaneous peri- derma or systemic lupus erythematosus.2,3 Raynaud’s vascular nerves has been observed in patients with VWF.8,9 phenomenon secondary to scleroderma, which is the most CGRP is a potent vasodilator and its loss leads to the vaso- studied presentation, involves a vasculopathy consisting of regulatory imbalance characteristic of Raynaud’s phenome- diffuse intimal fibrosis, activation of smooth muscle cells, non. In VWF, endothelial cells may play an additional role and endothelial cell perturbations.4 Endothelial cell autoan- in further driving this misbalance, as it has been shown that tibodies have been found in high frequency in scleroderma oscillatory mechanical forces can induce increased expres- patients,5 and it has been postulated that activation or apop- sion and release of endothelin-1, a potent vasoconstrictor, tosis of endothelial cells due to action of these antibodies from cultured endothelial cells.10,11 could lead to the release of vasoconstrictors and decreased While post-traumatic Raynaud’s phenomenon has been production of vasodilators.4 reported to occur after penetrating trauma or prolonged WWW.RIMED.ORG | RIMJ ARCHIVES | APRIL WEBPAGE APRIL 2014 RHODE ISLAND MEDICAL JOURNAL 24 CONTRIBUTION vibration trauma, there are no English- Figure 2. Lateral radiograph of index finger 3 delay of 2 months after the inciting language reports, to our knowledge, months following injury revealed volar plate injury, and it resolved promptly with that describe the presentation and avulsion fracture (arrow) and 10-degree prox- range-of-motion exercises. In general, management of secondary Raynaud’s imal interphalangeal joint contracture. symptoms of Raynaud’s do not resolve phenomenon following an isolated quickly in the majority of patients and blunt trauma to a digit. the etiology following blunt trauma may involve non-neurogenic factors as well. CASE REPORT Treatment of Raynaud’s syndrome A 26-year-old nonsmoking male uni- using a dihydropyridine calcium-chan- versity student presented to our office nel antagonist has been reported to be with diminished flexion and exten- successful, depending on patient tol- sion of the right index finger at the erability of the drug.12-14 However, it proximal interphalangeal joint (PIP). is preferable to first try conservative He reported that he “jammed” his measures involving simple risk-factor finger three months prior to presenta- avoidance, such as smoking cessation tion while playing basketball. He also and avoidance of cold-exposure in complained of recurrent transient epi- an effort to reduce attack frequency sodes of sharply demarcated pallor and and avoid the need for pharmacolog- numbness just distal to the injured PIP ical treatment. These more conser- when exposed to cold, which began vative methods are often successful, abruptly 2 months following injury and pharmacological intervention (Figure 1). becomes unnecessary.15-17 Radiographic examination of the In the case of our patient, our ini- index finger revealed an avulsion frac- tial therapy involved conservative ture fragment at the base of the volar non-pharmacological methods. How- surface of its middle phalanx consis- ever, in addition to recommending tent with a volar plate injury (Figure risk-factor avoidance, we also initiat- 2). Physical examination revealed soft ed hand therapy to improve range of tissue swelling about the PIP joint, motion in the patient’s injured finger. and limited range of motion from 100 The patient eventually regained full to 800. No skin abnormalities, oth- range of motion, as well as complete er joint abnormalities, or other signs reduction in finger swelling, after of systemic conditions were found completing the prescribed therapy regi- on physical exam. The likelihood of scleroderma, SLE, or men. Furthermore, at one year following initial presentation, other connective tisue disease was deemed very unlikely the patient reported that he no longer avoids cold-exposure due to lack of suggestive history or physical findings. There- and was free of Raynaud’s symptoms. This case illustrates fore he was diagnosed with isolated Raynaud’s secondary to the value of a trial of conservative measures before prescrib- local blunt trauma. We recommended cold avoidance, and ing pharmacological interventions in patients who present referred the patient for hand therapy for splinting, aggressive with secondary Raynaud’s syndrome from trauma. range-of-motion exercise, and a home stretching program. On follow-up one month later, after two hand therapy ses- sions and daily regimen of self-directed exercises, the patient had improving range of motion of the injured PIP from 50 References 0 1. Sunderkotter C, Riemekasten G. Pathophysiology and clinical to 95 . He reported resolution of the episodes of Raynaud’s consequences of Raynaud’s phenomenon related to systemic phenomenon since the initiation of hand therapy. At one- sclerosis. Rheumatology (Oxford). Oct 2006;45 Suppl 3:iii33-35. year follow-up, the patient continued to be free of Raynaud’s 2. Block JA, Sequeira W. Raynaud’s phenomenon. Lancet. Jun 23 symptoms. Physical examination revealed resolved soft 2001;357(9273):2042-2048. tissue swelling and normal range of motion of 00 to 1150. 3. Gayraud M. Raynaud’s phenomenon. Joint Bone Spine. Jan 2007;74(1):e1-8. 4. Grader-Beck T, Wigley FM. Raynaud’s phenomenon in mixed connective tissue disease. Rheum Dis Clin North Am. Aug DISCUSSION 2005;31(3):465-481, vi. Raynaud’s syndrome secondary to isolated blunt non-pen- 5. Sgonc R, Gruschwitz MS, Boeck G, Sepp N, Gruber J, Wick G. Endothelial cell apoptosis in systemic sclerosis is induced by etrating trauma to a finger appears to be exceedingly rare. antibody-dependent cell-mediated cytotoxicity via CD95. Ar- Interestingly, the onset of symptoms in our patient had a thritis Rheum. Nov 2000;43(11):2550-2562. WWW.RIMED.ORG | RIMJ ARCHIVES | APRIL WEBPAGE APRIL 2014 RHODE ISLAND MEDICAL JOURNAL 25 CONTRIBUTION 6. Povlsen B. Cold-induced vasospasm after finger replantation; Authors abnormal sensory regeneration and sensitisation of cold nociceptors. Yosef G. Chodakiewitz, BA, MD’15, The Warren Alpert Medical Scand J Plast Reconstr Surg Hand Surg. Mar 1996;30(1):63-66. School, Brown University, Providence, RI 7. Stoyneva Z, Lyapina M, Tzvetkov D, Vodenicharov E. Current Alan H. Daniels, MD, Department of Orthopaedics, The Warren pathophysiological views on vibration-induced Raynaud’s phe- Alpert Medical School, Brown University, Providence, RI nomenon. Cardiovasc Res. Mar 2003;57(3):615-624. 8. Noel B. Pathophysiology and classification of the vibration white Robin N. Kamal, MD, Department of Orthopaedics, The Warren finger.Int Arch Occup Environ Health. Apr 2000;73(3):150-155. Alpert Medical School, Brown University, Providence, RI 9. Goldsmith PC, Molina FA, Bunker CB, et al. Cutaneous nerve Arnold-Peter C. Weiss, MD, Department of Orthopaedics, fibre depletion in vibration white finger. J R Soc Med. Jul The Warren Alpert Medical School, Brown University, 1994;87(7):377-381. Providence, RI 10. Ziegler T, Bouzourene K, Harrison VJ, Brunner HR, Hayoz D. Correspondence Influence of oscillatory and unidirectional flow environments on the expression of endothelin and nitric oxide synthase in Arnold-Peter C. Weiss, MD cultured endothelial cells. Arterioscl Thromb Vasc Biol. May Professor, Department of Orthopaedics 1998;18(5):686-692. Warren Alpert Medical School, Brown University 11. White CR, Haidekker MA, Stevens HY, Frangos JA. Extracellu- 2 Dudley St. lar signal-regulated kinase activation and endothelin-1 produc- Providence, RI 02905 tion in human endothelial cells exposed to vibration. Journal 401-457-1520 Physiol. Mar 1 2004;555(Pt 2):565-572. Fax 401-831-5874 12.
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