Beardon v TAC [2003] VCAT 388 (24 February 2003)

Transport accident - assessment of impairment - AMA Guides to the Evaluation of Permanent Impairment (4th edition)- reflex sympathetic dystrophy

MEDIUM NEUTRAL CITATION: [2003] VCAT 388

1. The decision of the respondent made on 1 August 2001 is set aside and there is substituted therefor a determination that the applicant's whole person impairment arising out of her transport accident on 1 August 1998 is 22%.

Applicant Mr Nightingale of counsel instructed by Arnold Thomas & Becker

Respondent Mr Myers of counsel instructed by TAC Law

1. Ms Unita Beardon is a 34 year old bank officer who on 1 August 1998 was involved in a transport accident. She was a passenger in a taxi, seated in the rear of the vehicle. The vehicle was struck on the side where she was seated.

2. Her husband attended the scene of the accident and drove her to Royal Melbourne Hospital. The hospital report indicates complaint of left leg pain and right-sided back pain with tenderness over the L3/4 region. Radiological investigations of the left tibia and chest revealed no abnormality. She was discharged to the care of her general practitioner (Dr Williams) on whom she attended two days later.

3. Although she had occupied a full time position with the bank before the accident, that altered post-accident due, it is said, to restructuring in the bank. When she eventually returned to work her hours were 30 weekly. During the time she was away from work she had constant pain and shortly after her return to employment her left arm and hand turned very blue and cold.

4. Since then she has undergone a range of treatment; she attended a pain management clinic, she has received radio frequency denervation treatment, other nerve block procedures, she regularly attends a psychologist and throughout this entire period she has continued working.

5. On 1 August 2001 the respondent assessed the applicant's impairment due to the accident at 5% and the applicant now seeks to review that decision.

6. The applicant claims impairment in relation to an injury to her neck, and injury to her left shoulder and arm by way of reflex sympathetic dystrophy, injury of a gastrological nature as well as psychiatric injury.

7. In addition to the applicant's own viva voce evidence, the Tribunal heard from Dr Vivian, the applicant's treating musculo-skeletal specialist, Dr Stephen Williams, her current treating general practitioner and two medico-legal experts, Dr Colman, a gastroenterologist and Dr Peter Blombery, a vascular specialist with a special interest in reflex sympathetic dystrophy. By consent of the parties a large number of other medical reports were tendered to the Tribunal for consideration.

8. This case is concerned primarily with the question whether the applicant is entitled to an impairment assessment for what is variously described as Reflex Sympathetic Dystrophy or Complex Regional Pain Syndrome Type 1. Mr Myers of counsel who appeared for the respondent submits that she is not so entitled. The nub of his argument is that "unexplained pain" does not give rise to a rating simply because it is accompanied by signs of colour and temperature change in the applicant's affected limb. Further he submitted that amongst the factors to be taken into account were the lack of treatment since December 1999, the role of a stellate ganglion block administered at that time and the functional and variable nature of the applicant's symptoms.

9. There is agreement that the applicant's injury to her neck rates 5% impairment and I so find.

10. Both Drs Vivian and Blombery assessed the applicant's impairment resulting from reflex sympathetic dystrophy. The basis for assessment is set out at page 3/56 of the 4th edition of the American Medical Association Guides to the Evaluation of Permanent ("the Guides"). Under the heading Causalgia and Reflex Sympathetic Dystrophy the Guides provide -

Causalgia is a term that describes the constant and intense burning pain usually seen with reflex sympathetic dystrophy (RSD) when the causative lesion involves injury to a nerve.

The term "major causalgia" designates an extremely serious form of RSD produced by an injury to a major mixed nerve, usually in the proximal portion of the extremity. The term "minor causalgia" designates a more common form of RSD produced by an injury to the distal part of the extremity involving a purely sensory branch of a nerve.

Other forms of RSD not associated with injury of a peripheral nerve include minor traumatic dystrophy, shoulder-hand syndrome, and major traumatic dystrophy.

The four cardinal signs and symptoms of RSD are pain, swelling, stiffness and discoloration. The diagnosis of RSD may be supported with a three-phase nucleotide flow study, cold stress testing, recurrence of pain after previously successful stellate ganglion blocks, in which case Horner's syndrome must be present, or Bier blocks.

The impairment secondary to causalgia and RSD is derived as follows:

1. Rate the upper extremity impairment due to loss of motion of each joint involved (Sections 3.1f through 3.1j).

2. Rate the sensory deficit or pain impairment according to instructions in this section and Table 11a (p48).

3. Rate the motor deficit impairment of the injured peripheral nerve, if it applies (Table 12a, p.49).

4. The appropriate impairment percents for loss of motion, pain or sensory deficits, and motor deficits if present are combined using the Combined Values Chart (p.322) to determine the upper extremity impairment. Major causalgia may result in a complete loss of function and an impairment of the extremity as great as 100%.

11. From the evidence of Drs Vivian, Blombery and Hjorth I understand that the term "reflex sympathetic dystrophy" has largely disappeared from the medical lexicon or, at the very least, the term has been redefined. The result of that redefinition has led to a new description of complex regional pain syndrome ("CRPS"). CRPS Type l now replaces reflex sympathetic dystrophy and the term CRPS Type ll replaces causalgia. I also understand from their evidence that time and the development of medical science have led to an important distinction in that sympathetic dysfunction is no longer considered to be an essential feature of CRPS. Be that as it may, the terms RSD and CRPS1 were used interchangeably (and often confusingly so) in the evidence given before me. For instance, Mr Blombery's diagnosis was Complex Regional Pain Syndrome Type 1, Mr Hjorth thought mild Reflex Sympathetic Dystrophy and Dr Vivian hedged his bets by referring to Complex Regional Pain Syndrome Type l/ll but in any event placed more emphasis on his quest to ascertain the source of pain via facet joint denervation. During cross-examination he opined that the applicant has 90% CRPS Type 1 and 10% type 2 as well as thoracic outlet syndrome.

12. The current legislation requires that the Tribunal use the fourth edition of the Guides for the assessment of impairment notwithstanding the obvious anomalies arising from changing definitions and notwithstanding current received wisdom on the subject.

13. The wording set out above (para.10) in relation to the method of assessing impairment of RSD might, at first blush, appear relatively clear but a proper examination of those words and the tables to which they refer, renders the matter more that a little opaque. And before proceeding to the detail of the actual impairment it is necessary that I set out my understanding of what the Guides require.

14. In relation to paragraph (1), the upper extremity impairment due to loss of range of motion is, in this case, rated according to Table 38 found under Paragraph 3.1j on page 43 of the Guides.

15. Paragraph (2) requires sensory deficit or pain impairment to be rated according "to this section and Table 11a (p.48)" My understanding of what is meant by the term "this section" is that set out under the heading "Sensory Deficits and Pain" found on pp.3/46 and 3/48 and that is to be read and considered in conjunction with Table 11a at p.48. Of particular note on p.48 is the following paragraph -

Only persistent pain or discomfort that leads to permanent loss of function, in spite of maximum effort toward medical rehabilitation and allowing an optimal period of time for physiologic adjustment, should be evaluated as a permanent impairment. Pain that does not meet one or more of the above criteria is not considered to be within the scope of this section.

16. Table 11a is headed "Determining Impairment of the Upper Extremity Due to Pain or Sensory Deficit Resulting from Peripheral Nerve Disorders". Although one might conclude from the heading to Table 11 and from the procedure set out

in Table 11 that for a impairment to be rated, there must be some identified peripheral nerve disorder, that conclusion is probably overridden by the acceptance in the Guides of other forms of RSD that are not associated with injury to a peripheral nerve (e.g. minor traumatic dystrophy, shoulder-hand syndrome and major traumatic dystrophy) and by the generality of the procedural instructions in Table 11; e.g. "identify the area of involvement using the dermatome chart". None of other forms of RSD is contended for in the instant case.

17. The same conclusion cannot, in my view, be reached in relation to motor impairment. Paragraph (3) of the impairment method provides for a rating of "the motor deficit impairment of the injured peripheral nerve, if it applies (Table 12a, p.49). When one turns to Table 12a, one finds it is headed "Determining Impairment of the Upper Extremity Due to Loss of Power and Motor Deficits Resulting from Peripheral Disorders Based on Individual Muscle Rating." Again it seems to me that to rate for a motor impairment, there must be specific injury to a peripheral nerve and that the generality in relation to sensory impairment cannot be imparted here in the presence of a precise indicator requiring an injured peripheral nerve. Further the procedural instructions in Table 12 are quite specific in nature and require identification of individual movements, muscles and nerve structures.

18. The result of that is that I have concluded that the methodology in the instant case is to combine the percentage attributable to range of movement with any rating for sensory deficit. Motor impairment in the absence of specific verifiable nerve injury is excluded.

19. I will deal first with the range of motion of the left shoulder as indicated in paragraph (1) of the instructions. Taken chronologically the following observations (and in some cases assessments) were made:

* In October 1998, the treating orthopaedic surgeon Mr Mills found a full range of movement bilaterally;

* In February 1999 Dr Lefkovits (for TAC) found some restriction in forward elevation and abduction;

* In March 1999 the treater Dr Vivian found normal range of movement;

* In June 1999 Dr Vivian found abduction limited at 100º but a pain-free range of movement following injection;

* In December 1999, the treater Dr Hackman noted that range of movement was almost normal;

* In February 2000 Dr Lefkovits found full range of movement;

* In October 2000 Dr Mary Wyatt (for TAC) noted normal range of shoulder movement;

* In November 2000 Mr Henry Byrne (for TAC) found minimal restriction in forward flexion only;

* Dr Blombery (for the applicant) examined the applicant in June 2001 and found a full range of shoulder movement;

* In October 2001 Dr Vivian assessed loss of movement at 12% upper extremity;

* Mr Hjorth (for TAC) examined the applicant in November 2001 and he told the Tribunal that there was no restriction of mobility at the time of his examination;

* Mr Dunin (for the applicant) examined the applicant in March 2002 and found diminished movement and rated the impairment at 8% of the upper extremity.

* Mr Shannon (for TAC) examined the applicant in January 2003 and found some limitation in abduction and flexion although he thought the 12% impairment arose from loss of use.

20. I have included the observations of Drs Lefkovits, Wyatt and Dunin and Mr Byrne notwithstanding they were not called and their reports were not tendered. Their reports were of course to be found in the Tribunal book but their inclusion is really in an attempt to gain some sort of global picture of the development of the applicant's variable symptoms. The findings of Drs Mills and Hackman and Mr Shannon are to be found in the materials tendered to the Tribunal by consent.

21. It is trite to say that the duty of the Tribunal is to form a view about permanent impairment and that in the case of the musculoskeletal system, it must come to a concluded view of the typical presentation of the applicant excluding from consideration unusually good and unusually bad days.

22. I have formed the view that the applicant's typical presentation is not that demonstrated to Dr Vivian and Mr Shannon. I am fortified in that view by the evidence of Dr Blombery who found a full range of movement when he examined the applicant, from Dr Hjorth who found a normal range of movement and from the minimal restrictions noted by other practitioners over the years. Doing my best with the disparate evidence I find the applicant's impairment in relation to the range of shoulder movement is 6%.

23. The applicant's sensory deficit is the next matter to be considered. Table 11 requires the identification of the area of involvement using the dermatome charts, then the identification of the nerves that innervate those areas, then the severity is to be classified according to the descriptors set out in Table 11A.

24. Both Drs Vivian and Blombery identified the spinal nerves innervating C5, C6, C7, C8 and T1. The difference between the two assessments rests on each practitioner's placement in the list of descriptors. The third and fourth descriptors read as follows:

Decreased sensibility with or without abnormal sensation, which interferes with activity

Decreased sensibility with or without abnormal sensation or pain, which may prevent activity, and/or minor causalgia

26. Using Table 13 and the nerves identified by the practitioners, one comes to a total of 28%. Dr Blombery has calculated the upper extremity sensory impairment by taking 61% of 28, whereas Dr Vivian's calculation is 80% of 28. I have some difficulty with the methodology given the evidence that no nerve injury was found. But assuming it is correct procedure to identify those nerves referred to by the doctors (and although I am not entirely convinced that is absolutely correct on the basis of clinical supposition alone I accept their thesis for this purpose) then the applicant must fit the description at either the upper or lower end of category 4 for either of the doctors' assessments to be accepted.

27. I am not satisfied that this classification (category 4) is correct. There was no evidence before me that activity was prevented and there was evidence (Dr Blombery) that no causalgia existed. Notwithstanding the lack of evidence of actual nerve damage, it is clear there has been a history of some sort of intermittent sensory deficit. Dr Collins, a treating neurologist who first examined the applicant in November 1998 noted "glove distribution of subjective alteration to light touch and pinprick in the left hand"; he thought at that stage there were insufficient features to fit with a diagnosis of RSD. When he reviewed the applicant in December 1998, he noted the sensory symptoms remained unexplained. In November 1998 Dr Lisa Sherry noted decreased pinprick to region of C8, T1 and T2. The reports of Dr Lefkovits in February 1999 and 2000 indicate he found sensation intact.

28. Mr Henry Byrne examined the applicant in November 2000 and noted odd sensory changes extending from the left elbow to four lateral fingers on the left hand excluding the thumb. When Dr Blombery first examined the applicant in June 2001 he noted subjective reduction in sensation in entire left arm particularly over the ring and little fingers. In August 2001, the treater Dr Symington noted only altered sensation in the face. Dr Hjorth, another neurologist examined the applicant in November 2001 and found reduced pinprick sensation in the left arm ("in effect upper quadrant anaesthesia") which he opined was likely to be functional.

29. The evidence of the treating general practitioner (Dr Williams) in relation to RSD symptoms was of colour and temperature changes; he noted no sensory changes or motor deficits that were neurological in nature.

30. Doing my best with the evidence I have concluded that the applicant does suffer some sensory impairment; the question then arises whether that impairment is permanent. The applicant was involved in a transport accident in 1983 in which she injured her neck and left shoulder. She told the Tribunal it took approximately five years for the symptoms to resolve. In cross-examination she was asked whether she had symptoms of RSD as a result of that accident and she replied in the negative. That is at odds with the evidence of the treating general practitioner who told the Tribunal his understanding was that the applicant had suffered similar symptoms from the earlier accident. (There was no opportunity to put this to the applicant but in any event it is not of particular moment.) The report of Dr Sherry contained in the materials produced pursuant to subpoena also hints at the possibility of identical symptoms in the earlier accident. But the evidence is that by the time of this accident, she had totally recovered and in that regard I accept her testimony. It may well be that she retains some susceptibility to such symptoms but that is immaterial in the instant case.

31. Notwithstanding the variable nature of the sensory symptoms, I consider that on the balance of probabilities they are permanent for the purposes of the Guides. Although four and a half years have elapsed since the accident, and although she has received no treatment for the RSD since the stellate ganglion block administered in December 1999, she still suffers symptoms. They have not disappeared. What then is the proper classification for her sensory deficit? Again doing my best with the variable evidence I have come to the conclusion that the lower end of the third classification in Table 11 is appropriate. I have come to this view because, although there is some interference with some activity, the applicant did not give the impression that this was a serious problem nor was there any constancy of presentation to the many treaters and medico-legal specialists. I should also state that I was not persuaded that the result of the stellate ganglion block was significant. The evidence is clear that it is not necessarily a reliable investigative tool.

32. Although I have some reservation as expressed earlier about the global acceptance of the area of involvement (C5 through to T1) I think the benefit of the doubt should be given to the applicant having regard to the generality of the procedural instructions. The low end of the third grade of deficit being 26%, the appropriate upper extremity impairment is 28% of 26% which equals 7%.

33. As I indicated earlier I have formed the view that no impairment is applicable in relation to motor function. Even if I were wrong in my interpretation of the Guides I would not have found any impairment of motor function. Neither Dr Vivian nor Dr Blombery complied with the Guides in their methodology (see the precise procedure set out in Table 12) but more particularly I was swayed by the evidence of Dr Hjorth that he found no motor weakness. Dr Hjorth is an eminent neurologist and I accept his evidence on this matter in preference to that of Drs Vivian and Blombery, neither of whom is a neurological specialist. I do not accept Dr Vivian's hypothesis that more than likely there is injury at the C8 level. I was bolstered in my views by the report of orthopaedic surgeon Mr Bryne who found no motor weakness in November 2000.

34. The result of my findings is 10% impairment arising from the applicant's RSD. This is achieved by using table 3 on page 3/20 to convert 7% upper extremity impairment to 4% whole person; to this is added the 6% impairment for range of shoulder motion which results in 10% impairment arising from RSD. That is to be added to the 5% impairment in relation to the cervical spine to produce a total impairment of the musculoskeletal system of 15%.

34.The parties tendered the reports of two medico-legal psychiatric specialists. Dr Kaplan interviewed the applicant in November 2001 and assessed her impairment at 20%, and estimated that half of this impairment arose from the direct effects of the accident itself.

35.Dr Gayner first examined the applicant in November 2000. At the time he assessed impairment at 10% and opined that one half of that was due to the direct effects of the accident. He examined her again in February 2003 and at that time assessed her total impairment at 15%. He formed the view that the applicant had developed a somatization disorder and as I understand his report, he thought that it has pre-existed this accident although it was (as he described it) a "persistent and fluctuating disorder."

36 Using that diagnosis Dr Gayner divided the impairment assessment three ways - 5% to the direct effects of the accident, 5% arising from the response to physical injury and 5% unrelated being the somatization disorder.

37. The Tribunal also had available to it numerous reports from the treating psychologist, Ms Anna Sfyris. Ms Sfyris has treated the applicant since September 1998 and her most recent report was written in April 2002. It is clear from her reports that the applicant is significantly disabled by her emotional state although, being a determined and resilient woman she has battled with her pain and depression and battled to improve her life. Although some aspects of her emotional state have improved, her overall condition has not. There is little between the two practitioners in terms of collective impairment and giving the applicant the benefit of the slightly higher assessment, I accept the assessment made by Mr Kaplan at 20%. Although Dr Kaplan attributed half of that impairment to the direct effects of the accident I do not consider that apportionment is consonant with the overall picture of this applicant. In particular it is at odds with the treatment regime undertaken and the ongoing history given to the long-term treating psychologist Ms Sfyris. In my opinion one-third of the impairment arises from the direct effects of the accident and I find that applicant's psychiatric impairment is 8%.

38. Dr John Colman is a gastroenterologist who examined the applicant for medico-legal purposes on 13 September 2001. In his report dated the same day he stated -

In arriving at an evaluation of Permanent Impairment according to the AMA Guides.....I am handicapped as a gastroscopy has not been recently performed. I therefore request that this be done before I submit a final assessment. Currently she has a Class 1, 5% impairment of whole person. She certainly has symptoms of upper digestive tract disease, but anatomic alteration has not been demonstrated (which the performance of a gastroscopy would be able to do.) Continuous treatment is used by her but this consists of natural therapy. This impairment evaluation may alter on the basis of a gastroscopy.

39. On 20 February 2002 he prepared another report having viewed the report of upper endoscopy performed in October 2001 by Mr Paul Dumbrell. He also had access to a report of a gastroscopy conducted in February 1996 (more than two years prior to this accident) by Dr Kronborg who reported the presence of a "small hiatus hernia with irregular mucosal junction."

40.The most recent report of Mr Dumbrell indicated "the oesophagus was normal without reflux oesophagitis.The stomach showed no evidence or erosions and the duodenum was completely normal". He confirmed that no abnormality was seen on examination.

41. Notwithstanding this finding Dr Colman now allocated 9% impairment and stated that "symptoms but not signs of organic digestive disease are present, but no anatomical loss or alteration has been demonstrated. Drugs, however, are required to control her symptoms". By drugs, Dr Colman was referring to the ingestion by the applicant of a herbal remedy and peppermint tea.

42.Table 2 of the section of the Guides dealing with the digestive system (see p.10/39) provides for an impairment of 0% to 9% where "symptoms or signs of upper digestive tract disease are present, or there is anatomic loss or alteration and continuous treatment is not required and weight can be maintained at desirable level."

43.Dr Williams confirmed that as early as 1994 there was mention in the clinic's notes of the applicant's hiatus hernia and this was confirmed by in the gastroscopy performed by Dr Kronborg in 1996. (I note also that the copy of the hospital notes in relation to the 1983 accident located in Dr William's clinical file indicates a history was taken of hiatus hernia since 1995.) Dr Williams however has only treated the applicant since the accident. The applicant told the Tribunal she took Tagamet and Zantac for the earlier hernia but Dr Williams was neither the referring practitioner in relation to Dr Kronborg's tests nor the prescribing practitioner in relation to the medication. In fact the evidence of the identity of her pre-accident treating general practitioner and the identity of the practitioner who performed her gastric stapling was muddled - she was unable to remember names although later in her evidence she did identify someone but no one was called to give evidence in relation to her pre-accident gastric condition.

44. The applicant was asked in re-examination whether her gastric condition differed pre- and post-accident and she told the Tribunal it was much the same having already told the Tribunal she had no problems following the gastric by-pass.

45.Dr Williams told the Tribunal that following the Dumbrell endoscopy (which in his view disclosed no cause for concern) he prescribed Losec. The applicant told the Tribunal she did not take the medication, preferring herbal solutions.

46. I am not disposed to make any assessment in relation to the digestive system. There are a number of reasons for this. First, the applicant had an hiatus hernia that pre-dated the accident, second, the former treating practitioner in relation to gastric symptoms was not satisfactorily identified and in any event not called, third, Dr Williams recorded no complaint post-October 2001, fourth there was no demonstrated anatomic loss or alteration (the gastroscopy was entirely normal) and fifth, if there are any symptoms or signs there is no evidence before me to suggest they are permanent. Further I found Dr Colman's evidence logically inconsistent. I make no assessement under Chapter 10 of the Guides.

47. The applicant's collective impairment is 22% ascertained by combining 15% musculoskeletal impairment with 8% psychiatric impairment.

* The decision of the respondent made on 1 August 2001 is set aside and there is substituted therefor a determination that the applicant's whole person impairment arising out of the transport accident on 1 August 1998 is 22%