ARTHRITIS AFTER FROSTBITE INJURY IN CHILDREN

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1 1082 ARTHRITIS AFTER FROSTBITE INJURY IN CHILDREN GUILLERMO F. CARRERA, FRANKLIN KOZIN, and DANIEL J. MCCARTY Two patients who suffered frostbite injury to their hands as children were recently observed. The characteristic clinical and radiographic features of arthritis secondary to frostbite are described. Joint changes may be the result of direct chondrocyte injury during cold exposure. Current theories of the pathogenesis and treatment of frostbite injury are reviewed briefly. The consequences of frostbite injury to the hands of adults have been widely studied and reported. Much of this experience comes from the study of patients injured under battlefield conditions (1,2) or living in far northern latitudes (3). But only 4 cases of frostbite injury during childhood leading to arthritis have been reported in the United States literature (4). We have recently encountered 2 such cases and report them here to illustrate the characteristic sequelae of severe frostbite to the hands of growing children. The increasing popularity of outdoor winter activities for all age groups underscores the importance of early recognition of frostbite by the clinician. From the Department of Radiology and Section of Rheumatology, Department of Medicine, The Medical College of Wisconsin, Milwaukee County Medical Complex, Milwaukee, Wisconsin. Supported in part by a Clinical Research Center Grant, the Arthritis Foundation, and USPHS Grant No. AM-GQ Guillermo F. Carrera, MD Assistant Professor of Radiology; Franklin Kozin, MD Associate Professor of Medicine; Daniel J. McCarty, MD: Professor and Chairman, Department of Medicine. Address reprint requests to G.F. Carrera, MD, Department of Radiology, 8700 W. Wisconsin Avenue, Milwaukee, Wisconsin Submitted for publication May 4, 1979; accepted June 18, CASE REPORTS Case 1. TB is a 14-year-old boy who suffered a frostbite injury to both hands when he was 13 years old. He was trapped in a sewer by a fire in its entrance, and since he was not wearing gloves, was exposed to an ambient temperature of approximately -1 8 C for several hours. At the time of the initial medical evaluation by his personal physician, his hands appeared edematous and dusky. He had lost sensation of the tips of several fingers. He was hospitalized for 1 week; treatment included hand elevation, intravenous infusion of low molecular weight dextran, and antibacterial agents. Sensation gradually returned to his fingers over the first 24 hours, and his skin blistered over all but the left fifth finger. Skin on the affected fingers re-epithelialized within 2 months. New nail growth was noted 3 months after the cold exposure. Approximately 18 months later the patient noted swollen distal and proximal interphalangeal joints in all but his left fifth finger, and morning stiffness in the hands lasting for about 15 minutes. He was referred to the Rheumatology Service at the Milwaukee County General Hospital for evaluation. In addition to confirming the history, it was as- certained that the patient had grown rapidly after the -. cold injury, i.e., he had his pubertal growth spurt, There was evidence of vasomotor instability of both hands. Grip strengths, as measured with a rolledup sphygmomanometer cuff, were normal bilaterally. There was tenderness of the second, third, fourth, and fifth proximal interphalangeal (PIP) joints on the right Arthritis and Rheumatism, Vol. 22, No. 10 (October 1979)

Marked swelling is present in the second and third proximal and distal interphalangeal joints of both hands. B A Figure 2.

2 ARTHRITIS AFTER FROSTBITE 1083 A Figure 1. Photographs of A the left and B right hand of TB (case I), taken 18 months after frostbite injury. Considerable shortening and deformity of all fingers, except the left fifth, which had escaped frostbite, is evident. Marked swelling is present in the second and third proximal and distal interphalangeal joints of both hands. B A Figure 2. Radiographs of A the left and B right hand of TB (case l), obtained 18 months after frostbite injury, show premature fusion of the growth plates of all middle and distal phalanges except the left fifth and the left first distal phalanx. The proximal epiphyses and wrist are normal. B

3 1084 CARRERA ET AL Figure 3. An enlarged view of the right second and third fingers of TB (case 1) shows the irregularity of the articular surfaces of the third proximal and second distal interphalangeal joints (solid arrows) and early subchondral lucencies resembling cysts (open arrows). These findings are indicative of damage of articular cartilage and subchondral bone. and the second left PIP joint. The right second and left third distal interphalangeal (DIP) joints were also tender. There was a swan-neck deformity of the right index finger and thickening of the third right PIP joint (8 mm greater than the contralateral joint, as measured with a jeweler s tape). The third right PIP joint showed lateral deviation (Figure 1). There was limitation of flexion of the fourth and fifth fingers of the right hand. The fifth finger of the left hand measured 4 mm longer than the right fifth finger from the volar flexion crease to the tip. Radiographs of the hands (Figures 2 and 3) showed characteristic late findings of epiphyseal injury in a growing child. There was soft tissue swelling over the second to fourth PIP joints of the right hand, the second PIP joint of the left hand, all the DIP joints of the right hand, and the second to fourth DIP joints of the left hand. The middle and distal epiphyses have fused prematurely in all but the left fifth finger, which also had minimal skin changes. The articular surfaces of the proximal and distal interphalangeal joints of the right second to fifth and the left second to fourth fingers were irregular, indicating an injury to developing subchondral bone. These findings represent the earliest stage of cold-induced arthritis. Case 2. JS is a 25-year-old man who suffered a frostbite injury to the left hand when he was 5 years old. He had lost his glove while playing in the snow; the ambient temperature was below zero. Although the exact duration of his exposure is not clear, his parents estimated that he was outdoors at least 30 minutes without his glove. The skin over the distal phalanges was hard and white; severe blistering occurred within 48 hours. Healing was noted gradually over several months. Painless flexion deformities developed in the DIP joints, and distal phalangeal growth lagged behind that of the unexposed right hand. At age 21 he was found to have flexion deformities in the fourth and fifth PIP joints on the left as well. He was referred to the Rheumatology Service, Milwaukee County General Hospital, at age 25 because of increasing pain and stiffness involving the fourth and fifth left DIP joints. Flexion deformities were present in the second to fifth DIP joints and typical swan-neck changes were noted in the fourth and fifth fingers of the left hand (Figure 4). Crepitation (grating) was present on lateral movement of the DIP joints and locking occurred in the fourth and fifth fingers after forceful flexion. He underwent surgical fusion of the fourth and fifth DIP joints, with excellent symptomatic relief. Radiographs of his hands demonstrated the late sequelae of childhood frostbite injury (Figures 5 and 6). Epiphyseal damage and premature closure had produced dwarfing and malformation of the distal phalanges of the left second to fifth fingers. There is a radial clinodactyly of the left fifth distal phalanx. The articular surfaces of the DIP joints of the left hand are irregular and subchondral sclerosis has developed in the left second, third, and fifth DIP joints. The patient s right hand, which did not suffer frostbite, is normal. DISCUSSION The degree of frostbite injury to an extremity can be graded clinically at the time of initial evaluation. Orr

The fingers of the left hand are shortened.

4 ARTHRITIS AFTER FROSTBITE 1085 Figure 4. Photograph of the hands of patient JS (case 2), taken 20 years after frostbite injury of the left hand. The fingers of the left hand are shortened. Deformity of the left fourth and fifth fingers and radial clinodactyly of the fifth DIP joint is evident. A Figure 5. Radiographs of A the left and B right hand of patient JS (case 2), 20 years after a frostbite injury, show dwarfing of the left second to fifth distal and fourth and fifth middle phalanges. Radial clinodactyly of the fourth and fifth DIP joints is apparent. B

subchondral sclerosis, and lucencies (arrows).

5 1086 CARRERA ET AL Figure 6. Enlarged view of the left fourth and fifth fingers of JS (case 2), shows a squared off appearance of the fourth and fifth distal interphalangeal joints, irregularity of their articular surfaces, mild subchondral sclerosis, and lucencies (arrows). and Fainer divided frostbite injuries into four stages, based upon their extensive battlefield experience (1): Stage 1) erythema, edema, and peeling of superficial skin, Stage 2) vesiculation and loss of partial-thickness skin, Stage 3) loss of full-thickness skin with icy, white digits; and Stage 4) immediate bone involvement, leading to acute loss of a part. The consequences of frostbite in the adult hand have been well studied and summarized in the literature (33). Initially, soft tissue swelling and erythema occur and may be complicated by soft tissue emphysema produced by infection with gas-forming bacteria. Bone and joint changes may occur from a few weeks to several months after the frostbite. Demineralization is noted first and is most severe where the soft tissue damage was greatest. Late bony changes may not become apparent for months or years after the injury. These consist of small areas of increased bone density, particularly in the phalangeal tufts, cysts, and surface irregularities in juxtaarticular and subchondral bone, and occasionally subchondral sclerosis or frank bony ankylosis. Osteophyte formation is not common. In the growing hand, frostbite injury produces a combination of abnormal growth and development (33-7), as illustrated by the 2 cases reported here. Bone and joint abnormalities are usually found in subjects who suffer severe soft tissue damage initially (advanced Stage 2 or 3 injury) and become manifest several months to years later. The changes consist of premature epiphyseal fusion and abnormal epiphyseal growth, with consequent dwarfing and malformation of the phalanges. Clinodactyly may result from asymmetric epiphyseal growth. Injury to developing subchondral bone and articular cartilage leads to an arthritis which may be symptomatic and partially disabling for fine prehensile movement (7). Prominence of juxtaarticular bone and subchondral cysts on radiographs may indicate osteoarthritis; however, frostbite arthritis may be ditrerentiated by the absence of bony sclerosis and osteophytes and by its frequent asymmetry. When this characteristic lesion is present, particularly in a young individual, the possibility of frostbite injury should be recognized. The paucity of reported cases in children and young adults suggests that many cases of childhood frostbite are undiagnosed. A number of theories have been proposed to explain the pathophysiology of frostbite (8). Studies performed with rapid freezing techniques suggest that the formation of intra- and extracellular ice crystals may disrupt cells directly or through an ionic shock produced by marked changes in transcellular ionic strength (resulting from water loss through crystallization). Other studies, using gradual cooling methods, have implicated intravascular changes as the primary cause of tissue damage. Two phases of vascular hemostasis have been observed: an early, transient phase caused by platelet aggregation followed by a second, prolonged phase due to endothelial necrosis and swelling (9). Most of these reports examined the soft tissues rather than bone or cartilage. Since chondrocyte metabolism is largely glycolytic, it seems likely that these cells would be less susceptible to transient interruption of blood flow and more susceptible to ice crystal formation. Further studies are needed to determine the mechanism of cartilage damage from frostbite. Important advances in the treatment of frostbite injury have recently been reviewed (8,lO). Early, rapid rewarming of the frostbitten part in a water bath maintained at 40-42OC ( F) is essential in mini-

6 ARTHRITIS AFTER FROSTBITE 1087 mizing tissue loss. Anti-sludging agents such as low molecular weight dextran or heparin infusion also may be helpful. Recent studies have shown a beneficial effect of sympathectomy or intraarterial infusion of sympathetic blocking drugs; these drugs appear to reverse or prevent the microcirculatory collapse and their effects can be monitored angiographically (1 1). Physicians treating patients with possible frostbite injury should be aware of the risk of bone and joint abnormalities. These appear months to years after the exposure and have a characteristic appearance. A clear understanding of the lesions that follow frostbite will help determine prognosis and will encourage greater attention to its prevalence. REFERENCES I. Orr KD, Fainer DC: Cold injury in Korea during winter of Medicine 31: , Vincent HA, Schatzki R: Roentgenologic bone changes encountered in frostbite, Korea, Radiology 63: , Tishler JM: The soft-tissue and bone changes in frostbite injuries. Radiology , Seke AC Jr.: Destruction of phalangeal epiphyses by frostbite. Radiology 93: , Dreyfuss JR, Glimscher MJ: Epiphyseal injury following frostbite. N Engl J Med 253: , Thelander HE Epiphyseal destruction by frostbite. J Pediatr 36: , Bigelow DR, Ritchie GW The effects of frostbite in childhood. J Bone Joint Surg 45B: , Jarrett F: Frostbite: current concepts of pathogenesis and treatment. Rev Surg 31:71-74, Rabb JM, Renaud ML, Brandt PA, Witt CW: Effect of freezing and thawing on the microcirculation and capillary endothelium of the hamster cheek pouch. Cryobiol- Ogy 11: , Mills WJ, Gregory RT, Grossheim RL: Frostbite and hypothermia: current concepts. Alaska Medicine 15:26-59, Porter JM, Weschke DH, Roschbour GM: Intra-arterial sympathetic blockade in the treatment of clinical frostbite. Am J Surg 132: , 1976

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