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Deep vein thrombosis following calf strain: a case study
Case Study
Deep vein thrombosis following calf strain: a case study Alan J. Taylor Deep vein thrombosis (DVT) has been the subject of considerable media attention after a number of deaths and scares in apparently low risk individuals following long haul ¯ights. While many contributory factors have been put forward for the development of DVT, few cases have been reported following muscle strain. The recent publicity surrounding the calf strain sustained by Steve Waugh, the Australian cricket captain, during the Ashes series was initially unremarkable. The case was however, subsequently complicated by the development of DVT following his return (long haul) ¯ight to Australia. Latest reports indicate that following anticoagulant treatment he has made a full recovery and returned to playing. This case could easily be dismissed as a `one off' or an unusual set of circumstances. The following case report illustrates that DVT following calf strain is by no means unique. The rami®cations of these cases may have serious implications for c 2002 Elsevier Science Ltd. All rights Physicians and manual therapists working in sports medicine. * reserved
Case study
Alan J. Taylor Nottingham Nuf®eld Hospital, 748 Mans®eld Road, Woodthorpe, Nottingham NG5 3FZ, UK Tel: 44-115-9209209; fax: 44-115967-3005; E-mail: aj. taylor21@ntlworld. com
110
This case study was compiled from the history and records of the patient obtained with prior consent. An untrained 39-year-old female Publican took part in a charity football match. During the second half, whilst running she sustained a sudden onset of acute left sided calf pain, swelling and inability to weight bear. She was carried off the pitch and eventually transported to Accident and Emergency where she was diagnosed with a `torn calf muscle'. She was advised ice, rest and elevation. She was provided with a pair of crutches and advised to remain non-weight bearing (NWB) until her follow up appointment. No compressive bandage or Tubigrip was supplied. A follow up physiotherapy appointment followed four days later at which stage the swelling remained and the patient had developed marked bruising in the lower calf and foot. She reported that the treatment involved education and advice, gentle NWB exercise for the calf and the application of Pulsed Short Wave Diathermy (PSWD). A heel pad was provided and she was encouraged to
Physical Therapy in Sport
(2002) 3, 110±113
doi : 10.1054/ptsp.2002.0106, available online at http://www.idealibrary.com on
gradually weight bear. A further six treatments followed involving further PSWD together with speci®c graduated stretches and strengthening for gastrocnemius and soleus. The condition appeared initially to make an uneventful recovery as local treatment and rehabilitation progressed. The patient recalled complaining of discomfort in the region of the popliteal fossa (the focal point of the muscle strain was mid calf and described as deep) during the third week of rehabilitation. This fact was noted and explained logically to the patient as a natural response to the injury and subsequent weight bearing stretching exercises. Her ability to weight bear improved signi®cantly and she reported a return to a normal gait pattern 4 weeks following the injury. Despite her improved function she became increasingly aware that the swelling of the limb below the knee was not reducing in size with her concomitant improvement in function. Six weeks following her injury and having returned to full activity in her job as a Publican, she noted an increase in the lower limb oedema and discomfort. She reported this at her ®nal
c 2002 Elsevier Science Ltd. All rights reserved *
1466-853X/02/$ - see front matter
Deep vein thrombosis following calf strain: a case study
follow up appointment at the physiotherapy clinic. She was examined and advised to visit her GP the same day. The GP sent her for an emergency ultrasound scan the following day. The scan revealed the presence of signi®cant thrombus formation in the region of the poplital fossa, together with small clots in the veins of the calf. She was considered for admission, but as no beds were available she was managed as an out-patient with sub cutaneous Heparin initially and Warfarin by mouth. Five months post injury she reported that she was still taking Warfarin and had developed post thrombotic syndrome, i.e. the limb remains swollen, discoloured and she complained of prominent super®cial veins and ongoing muscle cramps.
Discussion The risk factors for DVT are well documented (Church 2000). Muscle strain and the pathological response to it interestingly provide many of the conditions under which DVT may occur. The classical risk factors of Virchows triad ± venous stasis, vessel wall injury and clotting abnormalities (Davies & Salzman 1979) may all occur during or following muscle injury. In this case due to pain and on medical advice the patient was advised to remain NWB for the ®rst 72 h and indeed reported moving the affected calf muscle very little during that phase (mainly due to the restriction of pain and swelling). These circumstances provide the conditions for venous stasis. The combination of lack of movement, disuse of the muscle pump and the compressive effect of swelling may all lead to venous dilatation, pooling and a decrease in the velocity of blood ¯ow. It is usually unknown at the time of muscle injury whether concomitant blood vessel injury has occurred unless magnetic resonance imaging or speci®c diagnostic tests are used (this process is rare and may still miss intravascular trauma). This raises the question of whether the diagnosis of isolated muscle strain can safely be made in the presence of clinical testing alone. Blood vessels are delicate and commonly injured as a result of trauma in all areas of the body (Taylor et al. 1997; Vlychou et al. 2001). The force required to damage muscle tissue or the
c 2002 Elsevier Science Ltd. All rights reserved *
compressive effects of oedema may be suf®cient to cause intravascular damage or micro-tears leading to roughening of the vessel wall. These are the classical conditions which may lead to platelet aggregation and thrombus formation. Indeed it is of interest to note that the patient reported discomfort in the region of the popliteal fossa during the third week post injury. This is not an unusual complaint during the rehabilitation of patients following calf strain. As the muscle unit and tight ®brous scar tissue are stretched, the muscle attachments may be stressed during elongation. It is reasonable to consider that discomfort in the popliteal fossa or posterior knee region is due to the local stress of soft tissue in that region. What is clear in this case is that the thrombus was eventually found to be located in the popliteal fossa. There is some debate as to whether the patient symptoms at the third week post injury were the early signs of the development of DVT. Following injury, trauma or surgery the body mobilises the in¯ammatory and healing processes which are well documented (ACPSM 1998). Part of this process involves the mobilisation of clotting factors to halt bleeding and the release of ®brin to form a wound or scar. The extent of this of course depends on the severity of the injury but suf®ce to say clotting factors are triggered following any trauma involving bleeding of tissue, as part of the healing process (Evans 1980). In this case the patient reported signi®cant swelling initially post injury which appeared very slow to settle as the rest of the signs, symptoms and dysfunction resolved. It is not unreasonable to consider therefore, following signi®cant muscle injury, that potentially two or even three of the known risk or causative factors of DVT may exist. If patient history and examination reveals other factors such as Inherent risk factors ± family history, previous vascular problems Recent surgery or immobilisation? Trauma or potential vascular compromise Recent travel? ± long haul ¯ights, train, car Altered clotting factors ± i.e. oestrogen use then there is a potential increased risk of thrombus formation. In this case study the patient was both using oral contraceptives and
Physical Therapy In Sport
(2002) 3, 110±113
111
Physical Therapy in Sport
also related to a family history of vascular problems (her mother had previously suffered DVT and post thrombotic syndrome). These facts combined with the slow resolution of swelling and the description of popliteal discomfort could be interpreted as warning signs of the patient's developing pathology. A genetic component with regard to susceptibility has been suggested in the literature (Lensen et al. 2001). This raises the question of whether we should routinely probe further into family history for risk factors in cases of recalcitrant limb oedema following soft tissue injury. A few cases of venous thrombosis have been reported in the sports medicine literature. Wong and Bracker (1993) presented a raquetball player complaining of persistent calf pain which failed to respond to treatment in a `timely fashion'. Recalcitrant calf pain ought to `alert the clinician to rethink the original diagnosis and consider more unusual causes of leg pain'. Gorard (1990) and Schobi et al. (1983), respectively, reported cases in an American footballer and a skier but in the absence of frank injury or trauma attributed the thrombosis to `effort thrombosis' which is more commonly described in the upper limb. It is the authors belief that such cases and those following actual injury are under reported and that there may be two potential sources of error 1. Genuine DVT cases which are initially misdiagnosed as calf strains and treated as such, usually until failed resolution or indeed worsening of the condition reveals alarm bells. 2. Genuine calf strains with a bona ®de history of acute trauma which go on following initial immobilisation to develop DVT, only revealed after failed resolution or more usually worsening of symptoms. It is currently unknown what effect physical therapy treatments including ice, compression, elevation, electrotherapy and soft tissue massage may have on a misdiagnosed calf thromboembolism. What is known, is that delays in the recognition of DVT may lead to post thrombotic syndrome or at worst, have potentially fatal consequences. The guidelines of the ACPSM rightly advise referral on to a GP or Sports Physician where any doubt exists
112
Physical Therapy in Sport
(2002) 3, 110±113
about the condition or indeed the subsequent recovery rate. At the very least there is a requirement for practitioner awareness, but more importantly there may be a need for changes in clinical practice to encompass DVT risk assessment as part of routine subjective assessment. In sport history taking should include routine questioning with regard to family history of vascular conditions and recent long haul travel (because this is common amongst athletes). Clearly consistent monitoring of expected physical signs and recovery rates in all patients following (apparent) calf muscle tears is essential. A failure to respond fully to treatment within the expected time frame ( for the severity of the lesion) should ring alarm bells for the clinician. Little is known about the true mechanism of DVT formation following muscle injury, however this case and that of Steve Waugh (Australian cricket captain) illustrate a link between the conditions which exist during and after muscle injury and those which may lead to the evolution of thromboembolism. The rami®cations of this link may be of some signi®cance for referring physicians and manual therapists involved in the treatment of apparently benign muscle tears. Above all an over focus on one particular type of assessment, system or structure at the expense of others should be avoided. Careful assessment, history taking and clinical reasoning in all cases of lower limb pain is as always the key. Whilst cases of DVT following injury appear rare, practitioners in sports medicine should be aware that young apparently low risk patients may be affected by venous thromboembolism. It is currently unknown whether there is a link between soft tissue trauma and the pathogenesis of DVT.
References ACPSM/CSP1998 Guidelines for the management of soft tissue (musculoskeletal) injury Church V 2000 Staying on guard for deep vein thrombosis and pulmonary embolism. Nursing 30 (2): 34±42 Davies G S, Salzman E W 1979 The pathogenesis of deep vein thrombosis. In: Joist J H, Sherman L A (eds). Venous and arterial thrombosis: Pathogenesis, diagnosis, prevention and therapy, pp. 1±22. New York: Grune and Stratton
c 2002 Elsevier Science Ltd. All rights reserved *
Deep vein thrombosis following calf strain: a case study
Evans P 1980 The healing process at cellular level: a review. Physiotherapy 66 (8): 256±259 Gorard D A 1990 Effort thrombosis in an American Football Player. British Journal of Sports Medicine 24 (1): 15 Lensen R, Bertina R M, Vandenbroucke J P, Rosendaal F R 2001 High factor VIII levels contribute to the thrombotic risk in families with factor V Leiden. British Journal of Haematology 114 (2): 380±386 Schobi R, Kocher F, Vorburger C 1983 Deep leg vein thrombosis during skiing. A case report. Schweiz Med Wochenschr 113 (39): 1402±1403
c 2002 Elsevier Science Ltd. All rights reserved *
Taylor A J, Tennant W G, Batt M E, Wallace W A 1997 Traumatic occlusion of the external iliac artery in a racing cyclist: A cause of ill de®ned leg pain. British Journal of Sports Medicine 31: 155±156 Vlychou M, Spanomychos G, Chatziioannou A, Georganas M, Zavras G M 2001 Embolization of a traumatic aneurysm of the posterior circum¯ex artery in a volleyball player. British Journal of Sports Medicine 35: 136±137 Wong C, Bracker M 1993 Coagulopathy presenting as calf pain in a raquetball player. Journal Family Pratt 37 (4): 390±393
Physical Therapy In Sport
(2002) 3, 110±113
113
Deep vein thrombosis following calf strain: a case study Alan J. Taylor Deep vein thrombosis (DVT) has been the subject of considerable media attention after a number of deaths and scares in apparently low risk individuals following long haul ¯ights. While many contributory factors have been put forward for the development of DVT, few cases have been reported following muscle strain. The recent publicity surrounding the calf strain sustained by Steve Waugh, the Australian cricket captain, during the Ashes series was initially unremarkable. The case was however, subsequently complicated by the development of DVT following his return (long haul) ¯ight to Australia. Latest reports indicate that following anticoagulant treatment he has made a full recovery and returned to playing. This case could easily be dismissed as a `one off' or an unusual set of circumstances. The following case report illustrates that DVT following calf strain is by no means unique. The rami®cations of these cases may have serious implications for c 2002 Elsevier Science Ltd. All rights Physicians and manual therapists working in sports medicine. * reserved
Case study
Alan J. Taylor Nottingham Nuf®eld Hospital, 748 Mans®eld Road, Woodthorpe, Nottingham NG5 3FZ, UK Tel: 44-115-9209209; fax: 44-115967-3005; E-mail: aj. taylor21@ntlworld. com
110
This case study was compiled from the history and records of the patient obtained with prior consent. An untrained 39-year-old female Publican took part in a charity football match. During the second half, whilst running she sustained a sudden onset of acute left sided calf pain, swelling and inability to weight bear. She was carried off the pitch and eventually transported to Accident and Emergency where she was diagnosed with a `torn calf muscle'. She was advised ice, rest and elevation. She was provided with a pair of crutches and advised to remain non-weight bearing (NWB) until her follow up appointment. No compressive bandage or Tubigrip was supplied. A follow up physiotherapy appointment followed four days later at which stage the swelling remained and the patient had developed marked bruising in the lower calf and foot. She reported that the treatment involved education and advice, gentle NWB exercise for the calf and the application of Pulsed Short Wave Diathermy (PSWD). A heel pad was provided and she was encouraged to
Physical Therapy in Sport
(2002) 3, 110±113
doi : 10.1054/ptsp.2002.0106, available online at http://www.idealibrary.com on
gradually weight bear. A further six treatments followed involving further PSWD together with speci®c graduated stretches and strengthening for gastrocnemius and soleus. The condition appeared initially to make an uneventful recovery as local treatment and rehabilitation progressed. The patient recalled complaining of discomfort in the region of the popliteal fossa (the focal point of the muscle strain was mid calf and described as deep) during the third week of rehabilitation. This fact was noted and explained logically to the patient as a natural response to the injury and subsequent weight bearing stretching exercises. Her ability to weight bear improved signi®cantly and she reported a return to a normal gait pattern 4 weeks following the injury. Despite her improved function she became increasingly aware that the swelling of the limb below the knee was not reducing in size with her concomitant improvement in function. Six weeks following her injury and having returned to full activity in her job as a Publican, she noted an increase in the lower limb oedema and discomfort. She reported this at her ®nal
c 2002 Elsevier Science Ltd. All rights reserved *
1466-853X/02/$ - see front matter
Deep vein thrombosis following calf strain: a case study
follow up appointment at the physiotherapy clinic. She was examined and advised to visit her GP the same day. The GP sent her for an emergency ultrasound scan the following day. The scan revealed the presence of signi®cant thrombus formation in the region of the poplital fossa, together with small clots in the veins of the calf. She was considered for admission, but as no beds were available she was managed as an out-patient with sub cutaneous Heparin initially and Warfarin by mouth. Five months post injury she reported that she was still taking Warfarin and had developed post thrombotic syndrome, i.e. the limb remains swollen, discoloured and she complained of prominent super®cial veins and ongoing muscle cramps.
Discussion The risk factors for DVT are well documented (Church 2000). Muscle strain and the pathological response to it interestingly provide many of the conditions under which DVT may occur. The classical risk factors of Virchows triad ± venous stasis, vessel wall injury and clotting abnormalities (Davies & Salzman 1979) may all occur during or following muscle injury. In this case due to pain and on medical advice the patient was advised to remain NWB for the ®rst 72 h and indeed reported moving the affected calf muscle very little during that phase (mainly due to the restriction of pain and swelling). These circumstances provide the conditions for venous stasis. The combination of lack of movement, disuse of the muscle pump and the compressive effect of swelling may all lead to venous dilatation, pooling and a decrease in the velocity of blood ¯ow. It is usually unknown at the time of muscle injury whether concomitant blood vessel injury has occurred unless magnetic resonance imaging or speci®c diagnostic tests are used (this process is rare and may still miss intravascular trauma). This raises the question of whether the diagnosis of isolated muscle strain can safely be made in the presence of clinical testing alone. Blood vessels are delicate and commonly injured as a result of trauma in all areas of the body (Taylor et al. 1997; Vlychou et al. 2001). The force required to damage muscle tissue or the
c 2002 Elsevier Science Ltd. All rights reserved *
compressive effects of oedema may be suf®cient to cause intravascular damage or micro-tears leading to roughening of the vessel wall. These are the classical conditions which may lead to platelet aggregation and thrombus formation. Indeed it is of interest to note that the patient reported discomfort in the region of the popliteal fossa during the third week post injury. This is not an unusual complaint during the rehabilitation of patients following calf strain. As the muscle unit and tight ®brous scar tissue are stretched, the muscle attachments may be stressed during elongation. It is reasonable to consider that discomfort in the popliteal fossa or posterior knee region is due to the local stress of soft tissue in that region. What is clear in this case is that the thrombus was eventually found to be located in the popliteal fossa. There is some debate as to whether the patient symptoms at the third week post injury were the early signs of the development of DVT. Following injury, trauma or surgery the body mobilises the in¯ammatory and healing processes which are well documented (ACPSM 1998). Part of this process involves the mobilisation of clotting factors to halt bleeding and the release of ®brin to form a wound or scar. The extent of this of course depends on the severity of the injury but suf®ce to say clotting factors are triggered following any trauma involving bleeding of tissue, as part of the healing process (Evans 1980). In this case the patient reported signi®cant swelling initially post injury which appeared very slow to settle as the rest of the signs, symptoms and dysfunction resolved. It is not unreasonable to consider therefore, following signi®cant muscle injury, that potentially two or even three of the known risk or causative factors of DVT may exist. If patient history and examination reveals other factors such as Inherent risk factors ± family history, previous vascular problems Recent surgery or immobilisation? Trauma or potential vascular compromise Recent travel? ± long haul ¯ights, train, car Altered clotting factors ± i.e. oestrogen use then there is a potential increased risk of thrombus formation. In this case study the patient was both using oral contraceptives and
Physical Therapy In Sport
(2002) 3, 110±113
111
Physical Therapy in Sport
also related to a family history of vascular problems (her mother had previously suffered DVT and post thrombotic syndrome). These facts combined with the slow resolution of swelling and the description of popliteal discomfort could be interpreted as warning signs of the patient's developing pathology. A genetic component with regard to susceptibility has been suggested in the literature (Lensen et al. 2001). This raises the question of whether we should routinely probe further into family history for risk factors in cases of recalcitrant limb oedema following soft tissue injury. A few cases of venous thrombosis have been reported in the sports medicine literature. Wong and Bracker (1993) presented a raquetball player complaining of persistent calf pain which failed to respond to treatment in a `timely fashion'. Recalcitrant calf pain ought to `alert the clinician to rethink the original diagnosis and consider more unusual causes of leg pain'. Gorard (1990) and Schobi et al. (1983), respectively, reported cases in an American footballer and a skier but in the absence of frank injury or trauma attributed the thrombosis to `effort thrombosis' which is more commonly described in the upper limb. It is the authors belief that such cases and those following actual injury are under reported and that there may be two potential sources of error 1. Genuine DVT cases which are initially misdiagnosed as calf strains and treated as such, usually until failed resolution or indeed worsening of the condition reveals alarm bells. 2. Genuine calf strains with a bona ®de history of acute trauma which go on following initial immobilisation to develop DVT, only revealed after failed resolution or more usually worsening of symptoms. It is currently unknown what effect physical therapy treatments including ice, compression, elevation, electrotherapy and soft tissue massage may have on a misdiagnosed calf thromboembolism. What is known, is that delays in the recognition of DVT may lead to post thrombotic syndrome or at worst, have potentially fatal consequences. The guidelines of the ACPSM rightly advise referral on to a GP or Sports Physician where any doubt exists
112
Physical Therapy in Sport
(2002) 3, 110±113
about the condition or indeed the subsequent recovery rate. At the very least there is a requirement for practitioner awareness, but more importantly there may be a need for changes in clinical practice to encompass DVT risk assessment as part of routine subjective assessment. In sport history taking should include routine questioning with regard to family history of vascular conditions and recent long haul travel (because this is common amongst athletes). Clearly consistent monitoring of expected physical signs and recovery rates in all patients following (apparent) calf muscle tears is essential. A failure to respond fully to treatment within the expected time frame ( for the severity of the lesion) should ring alarm bells for the clinician. Little is known about the true mechanism of DVT formation following muscle injury, however this case and that of Steve Waugh (Australian cricket captain) illustrate a link between the conditions which exist during and after muscle injury and those which may lead to the evolution of thromboembolism. The rami®cations of this link may be of some signi®cance for referring physicians and manual therapists involved in the treatment of apparently benign muscle tears. Above all an over focus on one particular type of assessment, system or structure at the expense of others should be avoided. Careful assessment, history taking and clinical reasoning in all cases of lower limb pain is as always the key. Whilst cases of DVT following injury appear rare, practitioners in sports medicine should be aware that young apparently low risk patients may be affected by venous thromboembolism. It is currently unknown whether there is a link between soft tissue trauma and the pathogenesis of DVT.
References ACPSM/CSP1998 Guidelines for the management of soft tissue (musculoskeletal) injury Church V 2000 Staying on guard for deep vein thrombosis and pulmonary embolism. Nursing 30 (2): 34±42 Davies G S, Salzman E W 1979 The pathogenesis of deep vein thrombosis. In: Joist J H, Sherman L A (eds). Venous and arterial thrombosis: Pathogenesis, diagnosis, prevention and therapy, pp. 1±22. New York: Grune and Stratton
c 2002 Elsevier Science Ltd. All rights reserved *
Deep vein thrombosis following calf strain: a case study
Evans P 1980 The healing process at cellular level: a review. Physiotherapy 66 (8): 256±259 Gorard D A 1990 Effort thrombosis in an American Football Player. British Journal of Sports Medicine 24 (1): 15 Lensen R, Bertina R M, Vandenbroucke J P, Rosendaal F R 2001 High factor VIII levels contribute to the thrombotic risk in families with factor V Leiden. British Journal of Haematology 114 (2): 380±386 Schobi R, Kocher F, Vorburger C 1983 Deep leg vein thrombosis during skiing. A case report. Schweiz Med Wochenschr 113 (39): 1402±1403
c 2002 Elsevier Science Ltd. All rights reserved *
Taylor A J, Tennant W G, Batt M E, Wallace W A 1997 Traumatic occlusion of the external iliac artery in a racing cyclist: A cause of ill de®ned leg pain. British Journal of Sports Medicine 31: 155±156 Vlychou M, Spanomychos G, Chatziioannou A, Georganas M, Zavras G M 2001 Embolization of a traumatic aneurysm of the posterior circum¯ex artery in a volleyball player. British Journal of Sports Medicine 35: 136±137 Wong C, Bracker M 1993 Coagulopathy presenting as calf pain in a raquetball player. Journal Family Pratt 37 (4): 390±393
Physical Therapy In Sport
(2002) 3, 110±113
113