Insurance Australia Limited t/as NRMA Insurance v Georgiadis

DETERMINATION OF REVIEW PANEL
CITATION:	Insurance Australia Limited t/as NRMA Insurance v Georgiadis [2024] NSWPICMP 695
CLAIMANT:	Andrew Georgiadis
INSURER:	IAG Limited trading as NRMA Insurance
REVIEW PANEL
MEMBER:	Alexander Bolton
MEDICAL ASSESSOR:	Mark Burns
MEDICAL ASSESSOR:	Margaret Gibson
DATE OF DECISION:	4 October 2024
DATE OF AMENDMENT:	18 November 2024
CATCHWORDS:	MOTOR ACCIDENTS – Review of decision of Medical Assessor (MA) Grainge who assessed the claimant as having a 44% whole person impairment (WPI) but did not consider whether he had suffered a threshold injury with the claimant having been diagnosed as having a Non-Specific Interstitial Pneumonitis (NSIP); claimant had an accident on 19 April 2020 when he was riding a pushbike which collided with the insured car causing the claimant to fall off his bike and onto his left shoulder; claimant attended Bankstown Hospital and was then transferred to St George Hospital where he underwent rotator cuff surgery and following this he developed NSIP; claimant has had a documented lung condition since 2000 and is currently awaiting a double lung transplant; issue of causation and whether the surgery brought about NSIP which had also occurred following surgery in 2017; discussion of the claimant’s pre-accident medical condition and causation of an NSIP following surgery to his left shoulder after the accident; Medical Review Panel (Panel) concluded that the shoulder surgery which was a necessary consequence of the accident did bring about the condition of NSIP; Panel noted that surgery and anaesthesia can aggravate pulmonary interstitial pneumonitis; Held – the respiratory injury suffered by the claimant involved the lung parenchyma which is not a supporting structure but part of the lung which is an organ and this was not a soft tissue injury; the claimant has suffered a non-threshold injury and has a WPI assessment of 44%; certificate of MA Grainge revoked.
DETERMINATIONS MADE:	REPLACEMENT CERTIFICATE OF DETERMINATION 1. The Panel revokes the certificate of Medical Assessor Grainge dated 4 May 2023. 2. The Panel is satisfied that the condition of non-specific interstitial pneumonitis arises because of the accident and that this is a non-threshold injury 3. The Panel assesses the claimant’s whole person impairment at 44%.

STATEMENT OF REASONS

INTRODUCTION

There is a dispute between the claimant and the insurer about:
• whether the injury is a threshold injury under Schedule 2 section 2(e) of the Motor Accident Injuries Act2017 (the Act).
• the degree of permanent impairment under Schedule 2 section 2(a) of the Act
The following injuries were referred by the Personal Injury Commission (the Commission) for assessment:

Lung – Non-specific interstitial pneumonitis.
Medical Assessor Grainge found that the injuries caused by the accident gave rise to a permanent impairment of 44%.
While the Medical Assessor made a Whole Person Impairment (WPI) assessment of 44% he did not determine whether the injury suffered by the claimant was a threshold injury.
The insurer has sought a review of the certificate of Medical Assessor Grainge.

Bundles of documents

The parties have each presented their respective bundles of documents upon which they rely. The Panel have read all the documentation. If a particular document is not referred to by the Panel, this does not mean that the Panel or a Panel Member has not read it, in much the same manner as parties not referring to or not specifically relying on a document in their own bundle and submissions.
The Panel is not required to “analyse every piece of information from every opinion contained in a document with which he [it] was provided” – see Farr v Insurance Australia Limited t/as NRMA Insurance Ltd [2014] NSWSC 1435 at [46]. The Panel is to come to its own conclusion and to take its own history.

The accident

The claimant was riding his bicycle on 18 April 2020 when he was struck by the insured car and fell to the ground.
The claimant proceeded by himself to the Emergency Department at Bankstown Hospital with a complaint of left shoulder pain.
The Panel understands that the claimant is presently a candidate for a double lung transplant.

Threshold/minor injury

The Motor Accident Injuries Amendment Act 2022 (MAI Amendment Act) was assented on 28 November 2023 with various amendments commencing on 1 April 2023. From 1 April 2023 the MAI Amendment Act provides that a “minor injury” is known as a “threshold injury” and “minor injuries” are known as “threshold injuries”.
The definition of what constitutes a minor injury has not been amended and continues to apply to a threshold injury.
The original certificate was issued where the relevant term was “minor injury” which, because of the amendment, is now described as a threshold injury. The submissions and original medical assessment were written at a time when the term was “minor injury”.
Amongst other things, unless the claimant is found to have a non-threshold injury then she cannot make a claim for non-economic loss

LEGISLATIVE BACKGROUND

Jurisdiction

The claimant’s claim is governed by the provisions of the Act. This legislation provides a scheme for the compulsory third-party insurance of all motor vehicles registered in New South Wales and a scheme of statutory benefits (under Part 3) and compensation by way of lump sum damages (under Part 4) for persons injured in motor accidents in New South Wales.
It should also be noted that in a common law damages claim, no damages are recoverable if the claimant’s injuries are “threshold” injuries.
Pursuant to Schedule 2, cl 2 of the Act, various matters are declared to be a medical assessment matters, including (e) “whether the injury caused by the motor accident is a threshold injury for the purposes of the Act”.

Threshold injury

A threshold injury is defined in s 1.6 of the Act as a “soft tissue injury” and a “threshold psychological or psychiatric injury”. Section 1.6(2) of the MAI Act defines a soft tissue injury to mean:
“[A]n injury to tissue that connects, supports or surrounds other structures or organs of the body (such as muscles, tendons, ligaments, menisci, cartilage, fascia, fibrous tissues, fat, blood vessels and synovial membranes), but not an injury to nerves or a complete or partial rupture of tendons, ligaments, menisci or cartilage.”
In summary, if a person injured in a car accident has soft tissue injuries only then, unless one of those soft tissue injuries falls within the excluding clause of s 1.6(4), the injured person’s statutory benefits cease in accordance with ss 3.11 and 3.28. If a person injured in a car accident has an injury to a structure (such as a bone) or an injury to an organ, that injury will not be a non-threshold injury.
Section 1.6(4) provides that regulations may be made to exclude or include a specified injury from being a soft tissue injury or a threshold psychological or psychiatric injury. Part 1, cl 4 of the Motor Accident Injuries Regulation 2017 (the MAI Regulation) further defines threshold injury to include “an injury to the spinal nerve root that manifests in neurological signs (other than radiculopathy)” and an acute stress disorder and an adjustment disorder (in terms of psychiatric or psychological injuries).
Section 1.6(5) says that the Motor Accident Guidelines (the Guidelines) may provide for the assessment of whether or not an injury is a threshold injury.

Method of assessment

Part 5 of the Guidelines contain the procedure for assessing whether an injury resulting from the motor accident is a “threshold injury” for the purposes of the MAI Act. In respect of the medical assessment of whether an injury is a threshold injury or not, the Guidelines relevantly provide:
“5.3 The assessment will determine whether the injury related to the claim is a soft tissue injury or a threshold psychological or psychiatric injury caused by the motor accident.
5.5   Diagnostic imaging is not considered necessary to assess threshold injury.
5.5    A diagnosis for the purpose of a threshold injury decision must be based on a clinical assessment by a medical practitioner or other suitably qualified person independent from the insurer.
5.6    The assessment of whether an injury caused by the accident is a threshold injury for the purposes of the Act should be based on the evidence available and include all relevant findings derived from:
(a) a comprehensive accurate history, including pre-accident history and pre-existing conditions
(b) a review of all relevant records available at the assessment
(c)a comprehensive description of the injured person’s current symptoms
(d) a careful and thorough physical and/or psychological examination
(e) diagnostic tests available at the assessment. Imaging findings that are used to support the assessment should correspond with symptoms and findings on examination.”

Insurers submissions

The insurer says the Medical Assessor did not review all of the documents produced by the insurer for consideration. The insurer says that had the Medical Assessor reviewed those documents he would have found a history of lung disease.
Regarding the claimants pre-existing respiratory illness, the insurer says the Medical Assessor noted that the claimant was a smoker between the ages of 20 to 50, and that the claimant was diagnosed with pulmonary emboli in 2000 and 2002, following knee surgery and a long haul flight, respectively. The Medical Assessor further noted that the claimant had asthma since childhood.
Notwithstanding this pre-accident history, the insurer says the Medical Assessor reported that the claimant had no pre-existing respiratory illness or disease prior to the subject accident, and that claimant was an active individual who did not experience any shortness of breath.
The insurer submits that this is incorrect. The insurer says that had the Medical Assessor reviewed the documents lodged by it then he would have found a history of lung disease.
The insurer acknowledged that following the accident on 18 April 2020, the claimant injured his left shoulder, requiring surgery which was performed on 19 May 2020. Following this, the insurer acknowledges that the claimant developed NSIP (non-specific interstitial pneumonia).
The insurer says that the claimant’s treating respiratory physician, Professor Barnes, reported on 26 August 2021:
“The Claimant's diagnosis of NSIP, is based on his CT scan findings. A specific diagnosis would require a lung biopsy, but this is not usually required. Most cases of NSIP are of no known cause (i.e. idiopathic). It is sometimes due to connective tissue or autoimmune conditions like lupus, rheumatoid arthritis and scleroderma. You are asking whether it arose as a result of his MVA or his shoulder surgery. Both of those events are not known to cause NSIP but having said this most cases are idiopathic and therefore one cannot absolutely exclude the possibility of an association between either of these events and his subsequent NSIP. We do know that interstitial lung disease can be aggravated by surgery and general anaesthetic, and if he did have preexisting NSIP then that surgical intervention may have increased the severity of his NSIP. This is not able to be proven as he was not known to have any lung condition prior to the MVA or surgery.”
Noting this opinion, the insurer says that Professor Barnes does not appear aware of the claimant's history of lung disease, including Interstitial Pneumonitis.
The insurer submits that on 31 May 2017, three years before the accident, the claimant’s general practitioner (GP) Dr Chan, documented that the claimant had a follow-up CT scan of his lung which revealed interstitial disease with a subdural thickening and parenchymal reticulation and bronchiectasis interstitial pneumonias and infection.
The insurer says the claimant has a lengthy history, dating back to well before the accident, of recurrent pulmonary emboli and had been treated with long term warfarin.
The insurer noted that the claimant had been treated by a respiratory physician, Dr Freiberg, from about 2000. On 27 October 2000, Dr Freiberg reported;
“He had a pulmonary embolus earlier this year after knee surgery.”
The insurer submits that on 11 August 2009, Dr Freiberg reported that controlling the claimant’s sleep disordered breathing was important in a man with “underlying lung disease and pulmonary hypertension.”
By way of further pre-accident treatment, the insurer noted that Dr Calermajer documented suspicion of pulmonary thromboembolic disease in a report dated 17 January 2006. On
1 September 2006 he documented “mild to moderate pulmonary hypertension ? primary/secondary. Recurrent pulmonary emboli.”
The insurer noted the following medical events;
(a)    The claimant underwent a CT of the chest on 7 August 2020 which showed findings suggestive of a non-specific interstitial pneumonitis, not typical for a usual interstitial pneumonia (UIP) pattern of interstitial lung disease.
(b)    The claimant attended an initial consultation with Respiratory & Sleep Physician, Professor Barnes, on 17 August 2020. In a report of 17 August 2020, Professor Barnes noted that the claimant had a background of hypertension, pulmonary emboli, pulmonary hypertension, asthma, and Chronic Obstructive Pulmonary Disease (COPD). Professor Barnes provided a diagnosis of Non-Specific Interstitial Pneumonitis (NSIP). The claimant’s symptoms commenced following day surgery on 19 May 2020.
(c)    A high-resolution CT of the chest was performed on 17 August 2020 which showed interstitial lung disease not consistent with a UIP pattern of pulmonary fibrosis.
(d)    In report dated 7 September 2020, Professor Barnes noted that the claimant probably had a fibrosing form of NSIP.
(e)    In a report dated 23 November 2020 Professor Murrell noted that the claimant was 6 months post rotator cuff repair with a polytetrafluoroethylene (PTFE) patch to his left shoulder. On examination, the claimant had a good range of motion and was strong in strength testing. Professor Murrell noted a very good outcome.
(f)    A CT of the chest was performed on 20 May 2021 which showed interstitial lung changes with honeycombing and early bronchiectasis. The appearance carried the differential of NSIP and hypersensitivity pneumonitis.
The insurer noted that Dr Hsu from the Pulmonary Hypertension Clinic recorded that on
6 February 2009 that the claimant had pulmonary hypertension likely secondary to chronic recurrent pulmonary embolic disease.
The insurer reported that the claimant saw Dr Smillie, cardiologist between 18 July 2005 and 22 July 2013. She diagnosed:
(a)    “recurrent pulmonary emboli - long term warfarin recommended
(b)    echocardiogram dilated right side of heart, mildly impaired RV function, moderately severe pulmonary hypertension
(c)    obstructive sleep apnoea on CPAP
(d)    asthma
(e)    hypertension. Echocardiogram mild LVH
(f)    right heart cath 1/06 moderate PHT, LCWP 15 mm
(g)    thalassaemia trait”
The insurer submits that noting the pre-accident medical history of the claimant, it appears Professor Barnes did not know the claimant had an extensive history of lung disease, including Interstitial disease in May 2017.
The insurer says that Professor Barnes' opinion was that “interstitial lung disease can be aggravated by surgery and general anaesthetic, and if he did have pre-existing NSIP then that surgical intervention may have increased the severity of his NSIP.”
The insurer submits the Medical Assessor has failed to consider the documents lodged by the insurer which included, clinical notes showing the claimant’s pre-accident history.
The insurer submits that had Professor Barnes considered those documents he would have become aware of that history.
The insurer submits the accident and subsequent surgery did not cause the claimant's Non- Specific Interstitial Pneumonitis. The insurer submits that the surgery may only have aggravated it.
The insurer submits that any such aggravation would have been temporary and that this is consistent with the claimant having ongoing symptoms since, at least, 2000.
The insurer submits that based on the available medical evidence, the diagnosis of NSIP was not directly caused by the subject accident.

Claimant’s submissions

The claimant refers to the insurers submission that the Medical Assessor failed to consider the insurer’s documents on the basis that the Medical Assessor found no pre-existing respiratory illness. The claimant submits that the Medical Assessor did undertake a detailed assessment in relation to the claimant’s history including treatment and symptoms.
The claimant noted that the Medical Assessor pointed out that the claimant had a diagnosis of pulmonary emboli in 2000 and 2002. The claimant says that this is a condition which the insurer repeatedly refers to in its submissions as being one which the Medical Assessor failed to consider which the claimant submits is clearly incorrect.
The claimant says that the Medical Assessor therefore reviewed all available evidence and noted any related medical history of the claimant in his certificate.

Medical evidence

Dr Dryson in his report of 1 June 2021, noted that the claimant had audible rales in the lower lobe of the right lung. He diagnosed:
(a)    Rotator cuff tears – left shoulder – post surgery.
(b)    Tear of medial meniscus, left knee.
(c)    Nonspecific interstitial pneumonitis.
Within his report, Dr Dryson did not provide any background about how he concluded the claimant had NSIP. He did say though, when discussing his assessment, later in his report, of the claimant’s condition that having had no problems with the left shoulder since surgery seven years previously, there was complete or near complete rupture of all of the rotator cuff tendons. Dr Dryson said that the claimant developed a secondary flow on effect in relation to NSIP, secondary to the anaesthetic given for his shoulder surgery. This restricts his ability to exert himself particularly when negotiating slopes or inclines.
Dr Dryson noted that the surgery with anaesthetic would aggravate his NSIP.
Dr Dryson assessed WPI and 18% but this was only with respect to the claimant’s left shoulder, left knee and scarring. He made no allowance for NSIP as he stated he was not qualified to do so as he was not a respiratory physician
A CT pulmonary angiogram performed on 4 June 2020 found diffuse ground glass appearance and pulmonary fibrosis in both lungs.
The claimant underwent a CT of the chest on 7 August 2020 which showed findings suggestive of a non-specific interstitial pneumonitis, not typical for a UIP pattern of interstitial lung disease.
The claimant attended an initial consultation with respiratory and sleep physician, Professor Barnes, on 17 August 2020. In a report of the same date, Professor Barnes noted that the claimant had a background of hypertension, pulmonary emboli, pulmonary hypertension, asthma, and COPD. Professor Barnes provided a diagnosis of non-specific interstitial pneumonitis. The claimant’s symptoms commenced following day surgery on 19 May 2020.
A CT of the chest (high resolution) was performed on 17 August 2020 which showed interstitial lung disease not consistent with a Usual Interstitial Pneumonia (UIP) this pattern of pulmonary fibrosis.
In the report dated 7 September 2020, Professor Barnes noted that the claimant probably had a fibrosing form of NSIP.
A CT of the chest was performed on 20 May 2021 which showed interstitial lung changes with honeycombing and early bronchiectasis. The appearance carried the differential of NSIP and hypersensitivity pneumonitis.
A report of Dr Freiberg of 27 October 2000 noted the claimant smoked for 19 years on an average half a packet a day stopping two weeks earlier. He had a history of mild asthma and a pulmonary embolus earlier that year after knee surgery. A lung function test showed moderately severe airway obstruction with reversibility post bronchodilator indicating an asthmatic component. Concern was noted about a reduction in his diffusing capacity of the lungs for carbon monoxide (DLCO) indicating impairment of the pulmonary vascular bed. It was said that the reduction in the claimant’s lung function had the potential to worsen already very severe obstructive sleep apnoea.

A report of 9 June 2009 noted:
“A decade ago his DLCO, an indirect marker of pulmonary vascular bed function, was 73% of predicted normal. Today it is 48% of predicted normal.
A decade ago his oxygen saturations were normal during the day and normal on CPAP at night for what was severe co existing obstructive sleep apnoea. Now his oxygen saturation is 93% on room air and simple exertion results in oxygen desaturation.
The tipping point was an anaesthetic with sedation for orthopaedic surgery and he was noted to be hypoxic post operatively and has not fully recovered from this. ACT pulmonary angiogram showed no acute pulmonary emboli.”
The Panel notes that the claimant, at the time of re-examination by Medical Assessor Burns, did not believe that the date on the report was correct. Information was obtained from Dr Freiberg by the claimant’s legal representatives, who reported his clinical notes were scanned and some of the dates were altered. Considering the information in this report it is obvious that the correct date should be in 2020. This is supported by the general practitioner (GP) notes which do not support shortness of breath during this period.
CT of chest 30 May 2017:
“Impression:
i.No pulmonary emboli appreciated.
ii.Interstitial disease with subpleural thickening and parenchymal reticulation and mild traction bronchiectasis. Scattered non specific ground glass opacities a finding that may be seen with air trapping. interstitial pneumonias (i.e., UIP) and infection”.
Professor Barnes report 17 August 2020 – “
“It looks as though Andrew has some form of ILD and we need to sort out whether this is mainly inflammatory or fibrotic in nature. It is difficult to know what happened with respect to his surgery. He was normal before this intervention. The possibilities here include aspiration during anaesthetic induction, or perhaps an exacerbation of pre-existing ILD that was not previously apparent. He will have a connective tissue and autoimmune blood screen, detailed respiratory function tests, and a high-resolution CT scan”.
Professor Barnes report 12 May 2022:
“There is still a significant inflammatory component to his interstitial lung disease”
Dr Chan clinical notes:

31 May 2017 – surgery consultation: follow-up CT scan lung: interstitial disease with some pleural thickening and parenchymal reticulation and bronchiectasis interstitial pneumonias infection.
29 October 2020 – after walking his oxygen level drops to 80 to 82% only, resting 97%. Review by Professor Barnes 2 December 2020
15 June 2020 – I stated that his breathing is poor
5 June 2020 – pulmonary angiogram report – no PE, bilateral fibrosis noted – pain management view
25 May 2020 – had operation last Tuesday for left shoulder tater cuff repair but post op, in our blocked was used, post operation is breathing problem, transferred to St George public and end up in respiratory ward – discharge letter read and filed, leaving today is okay and colour normal
9 April 2021- review regarding post-accident recovery –
left rotator cuff complete tear? Muscle
Post op lung content catered breeding difficulty and oxygen saturation drop later investigation showed no specific interstitial pneumonitis
left medial meniscus tear
umbilical hernia developed due to lung complication post operation
surgical repair of this kiss tear and hernia not recommended due to lung complication

Letter from Associate Professor McGrady to Dr Chan dated 31 August 2023:
“We did a teleconference today just to make sure things have been followed through, and he was not sounding great on the phone. He has seen Professor Lau and is trying some new treatments for his pulmonary fibrosis, which is good. He is on 2L of oxygen at the moment. He is currently on a trial of Macitentan, which is causing fluid retention of several kilograms, so the diuretics increased and Spironolactone added. I think if he is no better, they may stop the Macitentan and try something else.”
Letter from Professor Barnes to Dr Chan dated 26 July 2023:
“A lot has happened since I last saw Andrew. He has been diagnosed with severe pulmonary hypertension and is about to commence pulmonary vasodilator therapy. Interestingly he was found to have mild pulmonary hypertension back in 2006 when he had an episode of pulmonary emboli. Currently he has been found to have borderline hypoxia and will require home oxygen therapy, particularly on exertion. His current oxygen saturation is 90%. He has basal crackles as well as a pansystolic murmur.”
Letter from Professor Barnes to Dr Chan dated 26 July 2023:
“A lot has happened since I last saw Andrew. He has been diagnosed with severe pulmonary hypertension and is about to commence pulmonary vasodilator therapy. Interestingly he was found to have mild pulmonary hypertension back in 2006 when he had an episode of pulmonary emboli. Currently he has been found to have borderline hypoxia and will require home oxygen therapy, particularly on exertion. His current oxygen saturation is 90%. He has basal crackles as well as a pansystolic murmur.
For his NSIP Andrew will continue on Prednisone 10 mg daily along with Mycophenolate 500 mg bd. He will continue on Symbicort and Spiriva for his COPD. He will supplement his CPAP therapy at night with oxygen. Hopefully he will respond to his therapy for pulmonary hypertension.”
Letter from Professor McGrady to Dr Chan dated 11 May 2023:
“Andrew has a background of pulmonary fibrosis, which was initially diagnosed in 2000 and has been relatively mild. He has been managed over the years by Professor Barnes. It has been quite significant, however, since 2022 after shoulder surgery. More recently, he has noticed a decrease in his exercise tolerance and now it is less than 100m. He does not get chest pain. He also reports every morning he has a cough with phlegm that is white. He has had ankle swelling since December 2020. It may well relate to the Amlodipine or steroids, but he has been on these medications for a long time. Andrew sleeps on one pillow and denies symptoms of PND though.
Andrew is not terribly active. He rides an e-bike occasionally and has a stationary bike that he might do once or twice a week.
Andrew's other significant past medical history is for recurrent PEs. He had a PE postoperatively in 2000 and then a PE following a flight in 2002. He has been on anticoagulants since this time. He had the second knee surgery in 2000. He has also had a motor vehicle accident when he was hit by a bike and had a shoulder tendon issue. He has a history of thalassaemia minor, he has pulmonary hypertension, sleep apnoea on CPAP, gout which is quiescent at the moment, psoriasis, hypertension, an inguinal hernia repair, and a kidney stone many years ago.
Andrew currently weighs 97kg with a waist circumference of 117cm. He is in sinus tachycardia. First and second ear sounds are normal. I could hear a harsh mitral regurgitant murmur across over the apex. Peripheral pulses are present, there was no peripheral oedema today, but he did have surgical stockings on. There was decreased air entry and crackles throughout the lower bases. Oxygen saturation was 81%, which Andrew tells me is normal for him. He is starting to get clubbing and looks slightly peripherally cyanosed.
The ECG shows sinus rhythm with right atrial enlargement and right ventricular hypertrophy.
Andrew’s echo shows that he has mild-to-moderately increased left ventricular wall thickness, a small cavity size and normal ejection fraction. He has a severely hypertrophied right ventricle with impaired contraction. There is mild coaptation of the tricuspid leaflets, and severe tricuspid regurgitation. The pulmonary artery pressures are severely elevated at 85mmHg, and probably underestimated given the degree of TR. The anterior mitral leaflet looks prolapsing, but it is difficult to visualise any regurgitant we can definitely see is trivial, but I thought I could hear more than that today. There is no aortic stenosis.”
Dr Keller provided a report of 31 May 2022:
“I have seen the report of Dr Dryson dated 1 June 2021. He diagnoses him with left shoulder cuff tear and surgery, left medial meniscal tear and interstitial pneumonitis. He does not appear to recognise the prior left shoulder cuff surgery or prior left knee surgery. I can see no medical reason for attributing the interstitial pneumonitis to the effects of the bicycle accident”
Medical Assessor Grainge provided a certificate and reasons of 29 August 2023.
He referred to pulmonary function tests from 16 February 2023. Incorrectly, the Medical Assessor said that the claimant had no documented respiratory illness or disease prior to his accident and yet he referred in his certificate to diagnoses of pulmonary emboli and suffering from asthma in childhood.
The Medical Assessor noted that the claimant cycled for recreation, for example cycling 30km in around two hours with his wife, not experiencing shortness of breath unexpected for that degree of activity. The claimant had said that he walked approximately 10km a day as part of his work with no breathlessness.
The Medical Assessor noted that following shoulder surgery after the accident, the claimant had an episode of respiratory distress and was transferred to St George Hospital for four days where a diagnosis of NSIP was made. Post-operatively on discharge from hospital, the claimant was reported to have been short of breath walking 20 metres on the flat and on walking that distance, his oxygen saturations fell from the mid-90s down to around 80%. The Medical assessor said that these results indicated very significant lung disease incompatible with the claimant’s previous level of function. To treat the claimant’s NSIP, he was started on immunosuppression by Professor Barnes,. This resulted in a minor improvement in his breathlessness, but he remained extremely limited by his respiratory function.
The Medical Assessor concluded that the claimant’s injury to his lung, diagnosed as NSIP, was caused by the accident. However, he failed to provide any information about how he reached this conclusion other than to say before the accident, the claimant walked and rode a bicycle with no issues. The Medical Assessor said that during or around the time of surgery to the claimant’s shoulder, caused by the accident, the claimant suffered an acute lung injury. This acute lung injury led to the development of an NSIP which he said would not have happened in the absence of his operative intervention for his shoulder injury.
The Medical Assessor assessed WPI at 44% as follows;

Body Part or System	AMA4 Guides/ Guidelines References (chapter/ page/table)	Permanent (YES/NO)	Current %WPI*	*%WPI from pre-existing OR subsequent causes**	*%WPI due to motor accident**
1	Lung – Non- specific interstitial pneumonitis	Using Table 5-4b	Yes	44%	0	44%

Regarding his assessment, the Medical Assessor said “PFTs (pulmonary function tests) from 16/02/2023 show that Mr Georgiadis is 61 years old, height 168cm, his FEV1 (forced exhaled volume in 1 second) is 2.40 litres, his FVC (forced vital capacity) 3.05 litres and his TLCO (total lung single breath diffusing capacity of carbon monoxide) 12.55. Using Table 5-4b of AMA4 the lower limit of normal for a man of his age and height for FEV1 is 2.408L, for FVC 2.985L and for TLCO 21.3. Mr Georgiadis is therefore above the lower limit of normal (LLN) for FEV1 and FVC, and his predicted normal for TCLO is 29.5. Mr Georgiadis is below LLN for TCLO and is 42.5% of predicted normal. This places him in Class 3 impairment of the whole person, between 26-50% impairment. Based on his symptoms and restriction in activity, I place him in the upper tertile of that range, at 42% whole person impairment”. An additional 2% WPI was added for the effects of treatment.

Claimants statement

The claimant has provided a number of statements concerning his injuries and damages. Relevantly, he said:
“In 2000 I underwent surgery to my knee. I cannot recall whether it was my left or right knee but I did not sustain any particular injury to my knee. I cannot recall the name of the surgeon as it was so long ago.
In 2000 I suffered from lung clots after the surgery to my knee and then again in 2002 after an international flight. I was taking Warfarin since then until my shoulder surgery and now have been taking Pradaxa as a blood thinner to prevent blood clots. The second clot in 2002 led to my having pulmonary hypertension which was kept under control.
I would say that I was in generally good health at the time of the accident. I was fit and healthy and quite active. I was an avid traveller both recreationally and for work and would do 20km bicycle rides regularly. I have not suffered from any prior injuries or medical conditions other than those mentioned above. I have not had any prior disabilities. I have not made any prior claims for compensation”.

Medical examination

The claimant was examined by Medical Assessor Burns on 13 September 2024. His report follows.
“Mr Andrew Georgiadis attended the PIC Medical Suites on 13 September 2024 for an Appeal Panel Re-examination. He attended with his son, Christopher Georgiadis.”
HISTORY
Mr Georgiadis confirmed the initial history taken by Assessor Grainge on 13 January 2023. This is as follows.
Mr Georgiadis was riding his bicycle on 18 April 2020 when he was struck by a car and fell to the ground. He then self-presented to the Emergency Department with left shoulder pain and no apparent fracture was seen initially. Of note, on the Case Records of Bankstown-Lidcombe Hospital the attending doctor noted no abnormality on clinical examination of his chest.
HISTORY OF SYMPTOMS AND TREATMENT FOLLOWING THE MOTOR ACCIDENT

Mr Georgiadis confirmed the history obtained by Assessor Grainge with one modification. He did not believe that the diagnosis of non-specific interstitial pneumonitis was made at St George Hospital but was made later by Dr Barnes, Respiratory Specialist. In the Medical Assessment Certificate, it was stated as, Mr Georgiadis’ left shoulder continued to cause him pain and restriction in movement following his accident on 18 April 2020 and on 27 April 2020 he saw Professor George Murrell, an Orthopaedic Surgeon who specialises in shoulder repairs, who noted that Mr Georgiadis had painful, moderately restricted range of shoulder movement with positive impingement signs and mechanical impingement. An ultrasound scan showed massive supraspinatus and infraspinatus rotator cuff tears. Professor Murrell then advised surgery, which was carried out on 19 May 2020.
In the peri-operative period, Mr Georgiadis had an episode of respiratory distress, and he was transferred to St George Hospital for 4 days where be believed that no diagnosis of his condition was made.
Postoperatively on discharge from hospital Mr Georgiadis was short of breath walking 20 meters on the flat and on walking that distance his oxygen saturations fell from the mid-90’s down to around 80% (these results indicate very significant lung disease incompatible with Mr Georgiadis’ previous level of function). In order to treat Mr Georgiadis’s non-specific interstitial pneumonitis (NSIP), Mr Georgiadis was commenced on immunosuppression by Dr Barnes, Respiratory Specialist. This resulted in a minor improvement in breathlessness, but he remains extremely limited by his respiratory function.
HISTORY SINCE INITIAL ASSESSMENT
Mr Georgiadis reported that over the last 18 months his respiratory condition has deteriorated. He reported that his non-specific interstitial pneumonitis has been associated with increasing pulmonary hypertension. His breathing has deteriorated. In September 2023 he commenced on supplementary oxygen via nasal prongs. He currently has 2 litres of oxygen per hour for 16 hours per day. He has recently been told that this may need to be increased to 18 hours per day.
Approximately 12 months ago he was referred to the Transplant Unit at St Vincent’s Hospital. He has been seeing Professor Lau as St Vincent’s Hospital as well as Dr Darley, a Cardiothoracic Surgeon. He was informed at that time that his life expectancy with his current condition would be approximately 2 years. He was placed on the waiting list at St Vincent’s Hospital for a double lung transplant. He currently goes to the hospital every 6 weeks to be reviewed.
PRE-ACCIDENT MEDICAL HISTORY AND RELEVANT PERSONAL DETAILS
The pre-existing history I obtained today from Mr Georgiadis was significantly greater than that, which was recorded by Assessor Grainge. Mr Georgiadis agreed with the information in the final paragraph, which stated, Mr Georgiadis had diagnoses of pulmonary emboli made in the year 2000 and the year 2002. In 2000 his pulmonary embolus was diagnosed following an operation for a knee condition and in 2002 following a long-haul flight. Mr Georgiadis has also been diagnosed with asthma in childhood and has been on Seretide but had minimal Ventolin use and had no restriction in his activity and no admissions to hospital.

The following information can be added to the above. Dr Freiberg, Respiratory Physician was initially seeing Mr Georgiadis since approximately 2000 after the first episode of pulmonary emboli. Dr Freiberg in his report dated 28 June 2005 recorded that he was commenced on anticoagulation with Warfarin for 6 months after this pulmonary embolus. Dr Freiberg also noted that his spirometry results in 2005 were moderately obstructive but stable compared to results in 2000 against his single breath estimate of total lung capacity and his gas exchange capacity. In 2005 they were better than 2000 and were within the normal range. I noted that following his second episode of pulmonary emboli in 2002 that he was eventually commenced on long term Warfarin. Further Ventilation Perfusion Scans were carried out in 2005, and it was noted that on 17 June 2005 that a scan revealed several areas of matched sub-segmental ventilation and perfusion defects in the left lower lobe and left and right lower lobe. It was believed that he may have had further episodes of pulmonary emboli, and this was associated with pulmonary hypertension. I note that a further CT Angiogram at the time did not demonstrate any visible thrombus within the pulmonary system.

Mr Georgiadis agreed that he had been seeing Dr Freiberg over a prolonged period and that further respiratory testing was done in 2007 and 2009. I noted that within the documentation there was respiratory testing dated 5 June 2007 and 19 June 2009. The only abnormality noted in these findings was a degree of mild to moderate obstruction. This in fact is in keeping with his asthma. With respect to his FVC this was in the low normal range as was his single breath diffusion for carbon monoxide (DLCO).

I questioned Mr Georgiadis about a medical report of Dr Freiberg, which was dated 5 August 2009. This report stated that Mr Georgiadis had a long history of recurrent thromboembolic disease and was on Warfarin for 2 decades until recently switching to Pradaxa. A decade ago, his pulmonary artery pressures were around 50 and now they are around 61 on recent echocardiogram. A decade ago, his DLCO, an indirect marker of pulmonary vascular function was 70% of predicted normal. Today it is 48% of predicted normal. In the last paragraph on Page 1, Dr Freiberg stated, therefore in summary this man’s pulmonary hypertension has progressed and he is now in borderline respiratory failure.

Mr Georgiadis stated that he has no memory of seeing Dr Freiberg around that time and he did not believe that the facts in the report were correct. He did not believe that around the period of 2009 that he had any shortness of breath and that he could have had borderline respiratory failure. Following my re-examination of Mr Georgiadis I again reviewed the documentation going through Dr Chan’s clinical notes from 2000 up until 2024. I noted that in May 2009 he was referred to Dr Freiberg. What I did not find was the correspondence from Dr Freiberg back to Dr Chan and in subsequent medical consultations Dr Chan made no mention at all of shortness of breath or respiratory problems. I was therefore not able to confirm the date in the report of Dr Freiberg. This was discussed and resolved in paragraph 60 herein, of these reasons.

PHYSICAL ACTIVITY
Mr Georgiadis again stated that prior to his accident in 2020 he would play 18 holes of golf regularly and would cycle for recreation. He reported that he was also walking up to 10kms a day as part of his work with no breathlessness. This was the same information he gave Assessor Grainge.

INVESTIGATIONS
I noted multiple investigations reports within the documentation. In chronological order the following were noted.
§A lung scan, which was performed on 17 June 2005 was reported as showing a partially mismatched perfusion defect involving the postero-basal segment of the left lower lobe. Perfusion elsewhere matches the ventilation study. This was reported as being consistent with a pulmonary emboli.
§A CT coronary artery calcium score dated 19 April 2013 was reported as showing, there are some linear capacities in the medial segment of the right middle lobe and in the right lower lobe with some associated ground glass opacities. Some small linear opacities are also visualised in the lingula and to a lesser extent the left lower lobe. These appearances are non-specific as only a short segment of the lung has been imaged. This may represent some underlying fibrotic change. Further assessment of the lungs is suggested with a lung CT scan. Ground glass opacities are consistent with Interstitial Pneumonitis. It is not possible to define the exact type (Usual interstitial pneumonitis (UIP) of Non specific interstitial pneumonitis (NSIP)) This can only be done by a lung biopsy. It appears though that no further lung scan CT scan was carried out immediately after the coronary artery calcium score.
§A CT scan of the chest was carried out on 30 May 2017. This revealed the following:
No pulmonary emboli were appreciated. Interstitial disease with sub-pleural thickening and parenchymal reticulation with mild traction bronchiectasis. Scattered non-specific ground glass opacities, a finding that may be seen with air trapping, interstitial pneumonitis (i.e. UIP) and infection. It was also noted that there were sub-centimeter right apical pulmonary nodules. It was recommended that a follow-up exam be carried out in 3 months. I note from Dr Chan’s clinical notes that no subsequent examination was carried out.
§I noted a CT pulmonary angiogram report dated 4 June 2020. This report states that diffuse ground glass appearance and pulmonary fibrosis in both lungs. Sub-centimeter lymph nodes in the mediastinum hilum are likely reactive.
§A CT of the chest dated 7 August 2020 reported the following.
The findings within the lungs remain unchanged from a previous CT performed on 4 June 2020. There is persistent mediastinal and hilum lymphadenopathy. Findings suggest a non-specific interstitial pneumonitis and are not typical for a UIP pattern of interstitial lung disease. Review by Respiratory Physician is recommended.
§A CT chest high resolution scan was carried out on 17 August 2020. This was reported as follows.
There is interstitial lung disease that is not consistent with UIP pattern of pulmonary fibrosis. Alternative diagnoses should be considered. These include fibrosing NSP and less likely chronic hypersensitivity pneumonitis. There are non-calcified pleural plaques, indeterminate but not felt to represent evidence of asbestosis exposure.
§Finally, a high resolution CT scan of the chest dated 7 January 2023 reported increased reticular markings within the lungs with ground glass change appearing similar to the previous CT from 2021.

DISCUSSION
Reviewing Mr Georgiadis’s history and the possible cause of his Interstitial Pneumonitis, the following is noted.
·Episodes of Pulmonary Emboli may lead to pulmonary hypertension but are not known to cause interstitial pneumonitis. His pulmonary hypertension was casually related to his pulmonary emboli but improved significantly after his emboli were treated.
·Pulmonary hypertension is not known to cause interstitial pneumonitis.
·His pre-existing asthma and chronic obstructive airways disease is not known as a cause of interstitial pneumonitis.
·It is known that surgery and anaesthesia can aggravate pulmonary interstitial pneumonitis. This is the case with Mr Georgiadis. It is thus a causative factor in the severe deterioration of his interstitial pneumonitis.

From my re-examination of Mr Georgiadis, I believe that interstitial pulmonary disease did exist prior to his motor accident and surgery in 2020. This is supported by his CT scans showing a ground glass appearance in 2013 and 2017. I was unable from the current documents to confirm that his DLCO had dropped to 48% in 2009 (as listed in Dr Freiberg’s report).
Finally, I note that there is no objective evidence within the documentation to assess the level of impairment which existed from NSIP prior to his motor vehicle accident and subsequent surgery. From para 6.31 of the guidelines, it states ‘If there is no objective evidence of the pre-existing symptomatic permanent impairment then it’s possible presence should be ignored’.
Permanent Impairment Table

Body Part or System

AMA4 Guides/ Guidelines References

(chapter/ page/table)

Permanent (YES/NO)

Current

%WPI*

%WPI* from pre-existing OR

subsequent causes

%WPI* due to motor accident

Lung – Non- specific interstitial pneumonitis

Chapter 5,

Tables 6 & 8

Yes

44%

44%

Assessor Grainge assessed respiratory permanent impairment from the lung function test on 16 February 2023. He compared FVC (forced vital capacity), FEV1 (forced expiratory volume in 1 second) and TLCO (total lung single breath carbon monoxide diffusion capacity) values against the normal values for a man of the claimants age and height from Tables 2, 4 and 6 of Chapter 5 of AMA 4. The FVC and FEV1 results were above the LLN (lower limit of normal). The TLCO figure was 42.2% of the normal level and from Table 8 of Chapter 5 of AMA 4 places the claimant into Class 3 (26 – 50% WPI). Assessor Grainge assessed 44% WPI and I agree with this figure.
Previous lung function tests carried out by Dr Freiberg (Respiratory Physician) in 2005, 2007 and 2009 revealed FVC and TLCO results above the lower limit of normal with FEV1 just below the normal range. This is consistent with his reported history of Asthma. There is no evidence of an assessable impairment due to Interstitial Pneumonitis (UIP or NSIP) at that time. I could find no lung function testing between 2009 and 2020 within the documents. The tests in 2020 on 7 September and 2 December were both after his surgery and did display a significant drop in TLCO to 51% and 55% of normal.
In conclusion, whilst I believe that the claimant had interstitial pneumonitis before the aggravation in 2020, there is no evidence to support a percentage respiratory impairment due to any pre-existing interstitial pneumonitis.

The Panel adopts the findings of Medical Assessor Burns.
The Panel notes that the table applied by Medical Assessor Grainge in his certificate was not appropriate and was from the American Medical Association Guides 5th edition although the WPI assessment was the same.

Causation

To the Medical Assessor, the claimant said that he smoked cigarettes from age 20 until age 50, eight years before the accident (This would mean that he stopped in 2012). He said that he smoked approximately five cigarettes per day. To Dr Freiburg, the claimant said that he smoked for 19 years (that would be to age 38 from age 19 and that would be until 1989) and smoking half a packet a day and stopped two weeks prior to his examination on 27 October 2020. In his letter of 28 June 2005, Dr Freiberg referred to the claimant smoking 15 cigarettes a day between the ages of 22 and 39. This is an inconsistent factual recollection.
In 2000, the claimant had surgery and following this a pulmonary embolus was diagnosed.
On 13 March 2000, Dr Hannan noted in his medical history that the claimant had an asymptomatic lifelong cardiac murmur.
Dr Freiburg in his report of 27 October 2000 said that, at that time, showed moderately severe airway obstruction with reversibility post bronchodilator indicating an asthmatic component. He said that of concern, there was also a reduction in his diffusing capacity for carbon monoxide (DLCO). ( is this significant).
In 2002, after a long-haul flight, another pulmonary embolus was diagnosed.
The claimant also had asthma as a child. Dr Freiberg referred to claimant suffering mild asthma as an adult and noted medications of Ventolin, Seretide and Atacand. As at
3 October 2000, Dr Hopkins noted the claimant continuing to have difficulties with asthma.
The claimant had a lung scan on 17 June 2005. It was reported that there was a partially mismatched perfusion defect involving the posterobasal segment of the left lower low. A chest X-ray of 16 June 2005 showed bi-basal linear shadowing. Following the lung scan it was reported that in light of the chest X-ray findings there was an intermediate (40%) likelihood for a recent pulmonary embolism at this site. It was said that this demonstrated abnormality may be chronic.
Dr Janjis said in his report of 6 July 2005 that he had explained to the claimant that he needed to continue on long-term coagulation to prevent further thromboembolic disease
Dr Hsu from the Pulmonary Hypertension Clinic said on 6 February 2009 that the claimant had pulmonary hypertension likely secondary to chronic recurrent pulmonary embolic disease.
The claimant had a left rotator cuff repair (subscapularis tear) in 2013. Presumably this would have involved surgery and an anaesthetic.
Dr Freiburg in his incorrectly dated report of 5 August 2009, and which should be dated in 2020, said “the tipping point was an anaesthetic with sedation for orthopaedic surgery and he was noted to be hypoxic post operatively and has not fully recovered from this. A CT pulmonary angiogram showed no acute pulmonary emboli”. The Panel notes that the claimant’s solicitors have recently informed the Panel there was an error in the clinical notes of Dr Freiberg. The report of 5 August 2009 is actually a report referring to surgery on
19 May 2020. Taken at face value, the report of 5 August 2009 makes it difficult to know what orthopaedic surgery Dr Freiberg was discussing. The Panel is satisfied that the report has been incorrectly dated and reference to the claimant’s oxygen saturation is not a reference to something a decade ago. As the claimant’s solicitors have also noted, the report incorrectly dated 5 August 2009 in the claimants bundle of documents also has page 3 of that document missing. See again, paragraph 60 herein.
The claimant also had a left rotator cuff repair in 2013 (presumably involving surgery and anaesthetic).
Medical Assessor Grainge said that the claimant had no pre-existing respiratory illness or disease prior to the accident and that the claimant was an active individual who did not experience any shortness of breath. This is not correct noting that three years before the accident, clinical notes of Dr Chan of 31 May 2017 note that the claimant had a follow-up CT scan of his lung and had interstitial disease with subpleural thickening and parenchymal reticulation and bronchiectasis interstitial pneumonia and infection. There was also a considerable symptomatology and treatment, pre-accident, referred to elsewhere in these reasons.
The claimant had been treated, long-term, on Warfarin since about 2002.
While the claimant said that pre-accident, he could ride his bike for 30 km and walk, at work, 10 km a day, it should be noted that at the time of examination by the Medical Assessor he weighed 94 kg and was 169 cm in height which gives him a BMI of 32.9 which is considered obese. His pushbike was an e-bike and would possibly have meant he was self-propelled or partially self-propelled, which might assist the claimant not being short of breath.
A CT of the chest on 30 May 2017 reported:
“No pulmonary emboli appreciated.
Interstitial disease with subpleural thickening and parenchymal reticulation and mild traction bronchiectasis. Scattered non specific ground glass opacities a finding that may be seen with air trapping. interstitial pneumonias (i.e., UIP) and infection”.
The claimant’s general practitioner (GP), Dr Chan recorded on 31 May 2017:
“Surgery consultation: follow-up CT scan lung: interstitial disease with some pleural thickening and parenchymal reticulation and bronchiectasis interstitial pneumonias infection”.
Kogarah hospital discharge notes 19 May 2020 reported:
“Andrew was admitted with hypoxia post left shoulder reconstruction, likely as a result of infective exacerbation of asthma worsened with exercise induced bronchosparn. He is advised to continue augmentin df Hab bd, prednisolone 25mg od for total of 5 days, and use regular ventolin (4-6 puffs qid) and atrovent (2-4puffs qid) prior to mobilisation.”
He is currently on clexane-warfarin bridging for recurrent pulmonary embolism”.
Professor Barnes reported on 26 August 2021:
“The Claimant's diagnosis of NSIP, is based on his CT scan findings. A specific diagnosis would (i.e. idiopathic [a disease of unknown cause that does not occur spontaneously]). It is sometimes due to connective tissue or autoimmune conditions like lupus, rheumatoid arthritis and scleroderma. You are asking whether it arose as a result of his MVA or his shoulder surgery. Both of those events are not known to cause NSIP but having said this most cases are idiopathic and therefore one cannot absolutely exclude the possibility of an association between either of these events and his subsequent NSIP. We do know that interstitial lung disease can be aggravated by surgery and general anaesthetic, and if he did have preexisting NSIP then that surgical intervention may have increased the severity of his NSIP. This is not able to be proven as he was not known to have any lung condition prior to the MVA or surgery.”
The insurer submitted that it did not appear that Professor Barnes was aware of the claimant's history of lung disease, including interstitial pneumonitis. However, this is not correct as in his report of 17 August 2020, Professor Barnes noted that the claimant had a background of hypertension, pulmonary emboli, pulmonary hypertension, asthma, and COPD. Professor Barnes provided a diagnosis of NSIP. He said that the claimant’s symptoms commenced following day surgery on 19 May 2020.
Professor Barnes' opinion was that “interstitial lung disease can be aggravated by surgery and general anaesthetic, and if he did have pre-existing NSIP then that surgical intervention may have increased the severity of his NSIP.”
The insurer submitted that any such aggravation would have been temporary. The insurer that this is consistent with the claimant having ongoing symptoms since, at least, 22 years from 2000. The Insurer submits the accident and subsequent surgery did not cause the claimant's non- specific interstitial pneumonitis. The surgery may have aggravated it.
An ultrasound of the left shoulder was performed on 20 April 2020 which showed a completely torn subscapularis tendon and a full thickness tear of the supraspinatus tendon. This would appear to be causally related to the accident. When the claimant attended Bankstown Hospital immediately following the accident he complained of pain to the left shoulder. This investigation, two days post-accident, clearly arose as a consequence of the accident on 18 April 2020. The question for consideration by the Panel, however, is whether the surgery caused NSIP.
Letter from associate Professor McGrady to Dr Chan dated 31 August 2023:
“… he was not sounding great on the phone. He has seen Professor Lau and is trying some new treatments for his pulmonary fibrosis.”
The claimant, in his statement of 18 November 2021 said that he had absolutely no symptoms of NSIP before the accident and surgery. He said the symptoms manifested immediately after the surgery.

The Motor Accident Guidelines

The Guidelines identify the test for causation in cls 6.6 and 6.7.[1]
[1] Causation is defined in the Glossary at page 316 of the American Medical Association Guides 4th edition (AMA 4 Guides). It is in the same terms as Clause 6.6 of the Guidelines.
Clause 6.6 provides:
“Causation means that a physical, chemical or biologic factor contributed to the occurrence of a medical condition. To decide that a factor alleged to have caused or contributed to the occurrence or worsening of a medical condition has, in fact, done so, it is necessary to verify both of the following:
(a) The alleged factor could have caused or contributed to worsening of the impairment, which is a medical determination.
(b) The alleged factor did cause or contribute to worsening of the impairment, which is a non-medical determination.”
Clause 6.7 provides:
“6.7 There is no simple common test of causation that is applicable to all cases, but the accepted approach involves determining whether the injury (and the associated impairment) was caused or materially contributed to by the motor accident. The motor accident does not have to be a sole cause as long as it is a contributing cause, which is more than negligible. Considering the question 'Would this injury (or impairment) have occurred if not for the accident?' may be useful in some cases, although this is not a definitive test and may be inapplicable in circumstances where there are multiple contributing causes.”

The authorities

In Ackling v QBE Insurance (Aust) Ltd,[2] Johnson J indicated that the task of a review panel in assessing whether an injury was caused by the relevant accident is "a practical one". His Honour also observed that a review panel will derive practical assistance from the Guidelines when undertaking the task of assessing causation.[3]
[2] [2009] 75 NSWLR 482; [2009] NSWSC 881.
[3] At [87]. Justice Johnson was then referring to the predecessors to clauses 6.5-6.7 of the Motor Accident Guidelines, being clauses 1.7-1.9 of the Permanent Impairment Guidelines.
Section 5D of the Civil Liability Act 2002 (CLA) also needs to be considered when assessing causation.
Section 5D of the CLA provides:
"General principles
(1) A determination that negligence caused particular harm comprises the following elements:
(a) that the negligence was a necessary condition of the occurrence of the harm ('factual causation), and
(b) that it is appropriate for the scope of the negligent person's liability to extend to the harm so caused ('scope of liability')."
There are two elements to address when assessing causation under s 5D(1):
"factual causation";[4] and
"scope of liability".[5]
[4] See s 5D(1)(a) of the CLA - this is the statutory restatement of the “but for” test (see Adeels Palace Pty Ltd v Moubarak [2009] 239 CLR 420; [2009] HCA 48 at [45]) i.e. but for the negligent act or omission, would the harm have occurred?
[5] See s 5D(1)(b) of the CLA. See Adeels Palace at 42; Wallace v Kam [2013] 250 CLR 375; [2013] HCA 19 at [12].
Assessing "factual causation" and "scope of liability" involves making value judgments.[6]
[6] There is a conflict between s 5D and the Guidelines. Section 5D requires the use of the “but for” test and the Guidelines state that while the “but for” test may be useful in some cases, it “is not a definitive test and may be inapplicable in circumstances where there are multiple contributing causes”..
In the accident involving the claimant, he was riding his bicycle when the insured car collided into him. He was completely exposed to injury in those circumstances without any physical protection. The collision was sudden and might have been with some degree of force. Following impact, the claimant fell from his bicycle to the ground. The claimant injured his left shoulder and knee. The claimant then had surgery to his left shoulder which the Panel considers was consequent of the accident. Thereafter the claimant developed NSIP.

Campbell J in Owen v Motor Accidents Authority (NSW),[7] adopted Justice Johnson's approach with a caution touching upon the CLA:
"Given that the task of the Medical Review Panel in determining the causation question is not solely a medical determination within the expertise of the assessor's constituting the Panel, the position has, with respect, been aptly put by Johnson J in Ackling at p 500 [87] that the Assessors will derive practical assistance from this part of the Permanent Impairment Guidelines. But it is well to emphasise that the question to be assessed is one of legal causation involving mixed questions of fact and law arising principally from the law of negligence as modified by Civil Liability Act 2002, s 5D. (See s 3B(2)) of the Civil Liability Act (the CLA)."[8]
[7] [2012] 61 MVR 245; [2012] NSWSC 650.
[8] At [27].
In Kinchela v Insurance Australia Group Ltd t/as NRMA Insurance [2021] NSWSC 804 (Kinchela) Justice Walton set aside the decision of a Medical Review Panel. The issues determined in Kinchela involved applying the definition of “minor injury” (now referred to as threshold injury”) and involved a question of causation in respect of an amputated toe.
The correct principles to apply relating to causation were discussed in Kinchela and follow:
“[38] The second defendant’s task was not to answer the question of whether there was any contemporaneous evidence, or corroborative evidence, to support an injury to the right 2nd toe, but whether the accident contributed to the right 2nd toe infection, avulsion of the nail and ultimate right 2nd toe amputation. By focussing only on whether there was a contemporaneous record of complaint in the clinical notes or the ambulance notes, the actual question it was required to consider was overlooked – did the motor vehicle accident materially contribute to the right 2nd toe amputation?
[39] The second defendant fell, therefore, into the type of error identified in Owen v Motor Accidents Authority of NSW (2012) 61 MVR 245; [2012] NSWSC 650 at [51]- [52]; Bugat v Fox (2014) 67 MVR 150; [2014] NSWSC 888 (“Bugat”); AAI Ltd t/as GIO v McGiffen (2016) 77 MVR 348; [2016] NSWCA 229 (“McGiffen”). The error identified is in treating the absence of a contemporaneous complaint or report of injury as determinative of the issue of causation. Associate Justice Harrison cited the decision in Bugat with approval in Briggs. Her Honour said at [64]-[65]:
[64] In Bugat, RS Hulme AJ held that the lack of contemporaneous evidence cannot be determinative of causation. His Honour stated at [31]-[32]:
‘[31] One of the pivotal questions for the panel was whether the injuries of which the plaintiff complained had been caused (or materially contributed to) by the motor accident she alleged. To that question the presence or absence of contemporaneous evidence of injury was relevant but not determinative in circumstances where there was other evidence, in particular the plaintiff’s claim form made but 15 days later, the remarks of Dr Hor in his report of 13 July 2011, and the plaintiff’s statements which the certificate discloses were made to the panel to the effect that at the time of the accident she suffered ‘pain in her neck going out to both shoulders’.
[32] While I accept that, as an administrative decision-maker, the panel’s reasons should not be subjected to ‘minute and detailed textual criticism in the hope of finding something on which to base an argument’ [Allianz Australia Insurance Ltd v Motor Accidents Authority (NSW) (2006) 47 MVR 46, [2006] NSWSC 1096 at [36]] in expressing themselves the way they have, the panel have clearly shown that they have regarded what they perceived as the absence of contemporaneous evidence as determinative on the issue of causation. In doing so they erred, the error being one apparent on the face of the record.’
[65] In McGiffen, the Court of Appeal held at [64] – [65]:
“[64] The question that the review panel was required to address was not simply whether there was any contemporaneous evidence of complaint about an injury to the lumbar thoracic spine. It included whether Mr McGiffen’s lumbar thoracic spinal injury was causally related to the ‘gait derangement’, itself caused by the accident. That is, was the accident a contributing cause of a lumbar thoracic spinal injury by reason of the gait derangement caused by the accident.
[65] In deciding causation solely on the basis of the existence or otherwise of contemporaneous evidence of complaint of injury to the thoracic spine the review panel only partially addressed the question posed by s 58(1)(d)(of the Motor Accidents Compensation Act). For that reason, the decision recorded in the panel’s certificate must be treated as a purported and not real exercise of its statutory function under s 58(1)(d), leaving that function unexercised, and the Authority and the panel liable to the relief granted by the primary judge for jurisdictional error.”
[40] The second defendant failed to apply the correct test of causation as set out in the relevant Guidelines informed by s 5D of the Civil Liability Act 2002 (NSW) and the common law. As result, the second defendant failed to apply the appropriate legal test in order to discharge its jurisdictional function.”
Issues for consideration of causation were discussed at length in Briggs v IAG Limited trading as NRMA Insurance [2022] NSWSC 372. Because of the detail with which Wright J considered these issues, the Panel repeats the relevant comments in full. Wright J said;
“67 The second ground of review concerned the second review panel’s approach to the issue of causation. It was submitted that the panel applied an erroneous test in relation to causation and thus failed to exercise its jurisdiction.
68 As to whether the motor vehicle accident trauma was a cause of a “left posterolateral annular tear” with “mild disc desiccation” shown on Mr Brigg’s MRI test results, the second review panel concluded that causation had not been established because:
(1) “[a]t present, causation cannot be determined by medical imaging, unless there are sequential studies, either side of a motor vehicle accident and within a short time period”, and Mr Briggs only had post-accident MRI results;

(2) “a delamination may not fall within the definition of a tear”; and

(3) “the defect may not be the source of his pain and disability”.
69 The substance of the reasoning was that since there could be no scientific certainty that the L4/5 left posterolateral annular tear with mild disc desiccation was caused by the accident based on medical imaging and there was a possibility that the injury was not a tear and may not have been what led to Mr Brigg’s pain and disability, causation had not been established.
70 This reasoning does not accord with the relevant legal test in relation to causation, which does not require scientific certainty. In Metro North Hospital and Health Service v Pierce [2018] NSWCA 11, the Court of Appeal said, in relation to causation in a similar context, as follows at [138] (White JA, Macfarlan and Payne JJA agreeing):
“138 Whether the Hospital’s negligence in not responding to the induced seizures in a timely manner materially contributed to Ms Pierce’s worsened condition is not to be determined on the basis of scientific certainty, but on the balance of probabilities. As Spigelman CJ said in Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262; [2000] NSWCA 29 at [143]:
‘An inference of causation for purposes of the tort of negligence may well be drawn when a scientist, including an epidemiologist, would not draw such an inference.’”
71 The relevant principles were stated by Herron CJ, with whom Asprey and Holmes JJA agreed, in EMI (Australia) Ltd v Bes [1970] 2 NSWR 238 as follows, at 242:
“... it is not incumbent upon the applicant, upon whom the onus rests, to produce evidence from medical witnesses which proves to demonstrate that the applicant’s contention is correct. Medical science may say in individual cases that there is no possible connexion between the events and the death, in which case, of course, if the facts stand outside an area in which common experience can be the touchstone, then the judge cannot act as if there were a connexion. But if medical science is prepared to say that it is a possible view, then, in my opinion, the judge after examining the lay evidence may decide that it is probable. It is only when medical science denies that there is any such connexion that the judge is not entitled in such a case to act on his own intuitive reasoning. It may be, and probably is, the case that medical science will find a possibility not good enough on which to base a scientific deduction, but courts are always concerned to reach a decision on probability and it is no answer, it seems to me that no medical witness states with certainty the very issue which the judge himself has to try.”
72 Furthermore, a finding of causal connection may be open without any medical evidence at all to support it, or when the expert evidence does not rise above the opinion that a causal connection is possible: Fernandez v Tubemakers of Australia Ltd [1975] 2 NSWLR 190 at 197 (Glass JA); Metro North Hospital at [140].
73 The second review panel did not address the question of whether on the balance of probabilities the motor vehicle accident caused the annular tear even though there might be no scientific certainty. Furthermore, the second review panel’s reasoning did not reflect the approach to determining causation in cll 6.6 and 6.7 of the Guidelines, which in my view is consistent with the legal principles I have outlined.
74 The present case is not one where medical science established that there was no possible connexion between the motor accident and Mr Brigg’s relevant injuries. From the material available, the second review panel accepted that the motor accident in this case could have caused or contributed to Mr Brigg’s L4/5 left posterolateral annular tear. Indeed, the panel expressly accepted that:
“the plaintiff was involved in relatively severe front-end collision. The medical and biomechanical literature supports the conclusion that spinal injuries with resulting pain and disability can arise from this type of trauma.”
75 This being so, it was necessary for the panel to consider whether the motor accident did cause or contribute to Mr Brigg’s condition. This required, not a consideration of material derived as a result of an internet search for “all past and recent high-quality research articles pertaining to MRI imaging of the lumbar spine, with a focus on injury, degeneration and pain”, but rather a consideration of the material referred to in cl 5.6 of the Guidelines, namely all the evidence available to the panel including all relevant findings derived from:
(1) a comprehensive, accurate history, including pre-accident history and pre-existing conditions;
(2) a review of all relevant records available at the assessment;
(3) a comprehensive description of the injured person’s current symptoms;
(4) a careful and thorough physical examination; and
(5) diagnostic tests available at the assessment, noting that imaging findings that are used to support the assessment should correspond with symptoms and findings on examination.
76 In Mr Briggs’s case that would include, without attempting to be exhaustive:
(1) Mr Briggs’s age, circumstances and relevant medical history at the time of the motor accident, including whether there was any previous history of lumbar spine pain;
(2) the particular nature and extent of the accident and the forces that would have been operative on Mr Briggs as a result of the accident; and
(3) Mr Briggs’s circumstances and relevant medical history including the MRI results and results of other medical examinations and testing, after the motor accident.
77 In light of all that material and in accordance with cll 6.6 and 6.7 of the Guidelines, the panel should then have made “a non-medical informed judgment” as to whether it was likely that the motor accident caused or contributed to Mr Briggs’s injury in question”.

The Panel must consider whether, with the claimants NSIP, the disability is causally related consequent upon shoulder surgery which took place shortly after the accident and possibly leading to the claimant suffering respiratory distress.
The Panel is mindful that a lack of immediate reported complaint of NSIP should not preclude a conclusion that this condition arose from the accident.
Scientifically, there is a possibility that the accident could have caused NSIP. The Panel considers, did the accident contribute to the claimant suffering NSIP when surgery was required to the claimant’s shoulder and thereafter symptoms of NSIP occurred? Medical Assessor Grainge drew the conclusion that NSIP was caused by the accident. Therefore, scientifically, it might be considered possible although the Medical Assessor provided no clear justification for this.
Did the accident contribute to the claimant’s physical injuries and did the claimant’s NSIP condition arise because of contribution by the accident. More succinctly, did the accident materially contribute to that condition?
On the balance of probabilities, can it be said that the NSIP suffered by the claimant was caused by the accident? The claimant, at the time of the accident, was 58 years of age. He had been treated for symptoms of NSIP before the accident but apparently at the time of the accident. He had a long-standing condition of lung disease since at least 2000 and involving hypertension, pulmonary emboli, pulmonary hypertension, asthma, and COPD. The claimant is currently awaiting a double lung transplant. NSIP usually occurs idiopathically. When the claimant last had symptoms of NSIP before the accident the subject of this claim, it followed surgery and, in the opinion of the Panel, on the balance of probabilities, it is likely that NSIP following surgery for his shoulder injury after coming off his bike, was causally related to the accident.
Would the impairment have occurred, if not for the accident? The Panel notes that the NSIP had occurred previously, before the accident. The claimant had a demonstrated predisposition to NSIP, however, the Panel is satisfied that on the balance of probabilities, the accident was a contributing cause to the need for shoulder surgery which in turn gave rise to the exacerbation of NSIP, an outcome caused by the accident which was more than negligible.

Threshold injury

In the claimant’s case the respiratory injury involves the lung parenchyma which is not a supporting structure but part of the lung which is an organ. There has not been a soft tissue injury. The claimant has suffered a non-threshold injury.

CONCLUSION

This is a dispute between the claimant and the insurer about whether the injury caused by the accident is a threshold injury under Schedule 2 section 2(e) of the Act.
The Panel is satisfied that the accident and impact has had a more than negligible effect on the NSIP condition suffered by the claimant. That condition has been caused by the accident.
The claimant has an assessment of WPI of 44%

DETERMINATION

The Panel revokes the certificate of Medical Assessor Grainge dated 4 May 2023.
The Panel is satisfied that the condition of NSIP arises because of the accident and that this is a non-threshold injury.
The Panel assesses the claimant’s whole person impairment at 44%.

[2024] NSWPICMP 695

4 October 2024