Sydney Trains v Brookes

DETERMINATION OF REVIEW PANEL
CITATION:	Sydney Trains v Brookes [2023] NSWPICMP 32
CLAIMANT:	Colin Allan Brookes
INSURER:	Sydney Trains
REVIEW Panel
MEMBER:	Susan McTegg
MEDICAL ASSESSOR:	Tai Tak Wan
MEDICAL ASSESSOR:	Wing Chan
DATE OF DECISION:	3 February 2023
CATCHWORDS:	MOTOR ACCIDENTS – On 22 January 2018 the claimant was on a train waiting at the door to alight when the train hit the buffer at the end of the line; the accident constitutes a ‘public transport accident’ for the purposes of the Transport Administration Act 1988; damages assessed under chapter 5 of the Motor Accidents Compensation Act 1999; the claimant suffered fractured ribs, fractured nasal bones, a laceration to the forehead and an abrasion to the left patella; on 14 May 2018 the claimant diagnosed with thrombosis in the left popliteal artery which led to amputation; injuries referred for assessment of permanent impairment were fractured ribs and Guillain-Barre syndrome (GBS); question of causation of the thrombosis of the right popliteal artery and resulting amputation; question of diagnosis; question of causation of GBS; Held – fractured 4^th, 6^th, 7^th and 8^th ribs caused by accident; rib fractures resolved and do not result in permanent impairment; Review Panel accepts diagnosis of GBS; the claimant’s hospitalisation associated with the amputation either caused or contributed to infection, in all likelihood, clostridium difficile caused or contributed to the development of the GBS; injury to the patella remote from anatomical location of the popliteal artery; claimant predisposed to thrombosis; no evidence of vascular insufficiency until three months post-accident; thrombosis in the popliteal artery was not causally related to the accident; subsequent below knee amputation and ensuing period of hospitalisation not causally related to the accident; GBS not caused by accident and no assessable permanent impairment.
DETERMINATIONS MADE:	Review Panel Certificate issued under Part 3.4 of the Motor Accidents Compensation Act, 1999 following a review under s 63 as to WHETHER THE DEGREE OF PERMANENT IMPAIRMENT OF THE CLAIMANT AS A RESULT OF THE INJURY CAUSED BY THE ACCIDENT IS GREATER THAN 10% The Panel revokes the certificate of Medical Assessor O’Neill dated 19 May 2021 and issues a new certificate determining that the following injuries were caused by the motor accident but do not give rise to permanent impairment: · ribs – rib fractured 4th, 6th, 7th and 8th ribs. The Panel determines that the Guillian Barre syndrome was not caused by the motor accident.

REASONS FOR DECISION

BACKGROUND

On 22 January 2018 Mr Colin Allan Brookes (the claimant) was working as a cleaner on the trains. On that day Mr Brookes was on the train on his way to work and was waiting at the door to alight when the train came into the station too quickly and hit the buffers. Mr Brookes was thrown about in the carriage sustaining injury (the accident).
Mr Brookes sustained a chest injury with fractured ribs, fractured nasal bones and a laceration to his forehead. Whilst he was a patient at Nepean Hospital it was noted he had a painful left knee on the medial aspect. On 14 May 2018 Mr Brookes was again admitted to Nepean Hospital where he ultimately underwent a left below knee amputation after he developed a thrombosis in the left popliteal artery aneurysm. Whilst in hospital he developed Guillian Barre syndrome (GBS). The cause of the aneurysm, the subsequent amputation and the development of GBS is the subject of dispute between the parties.
Sydney Trains is liable to pay damages to Mr Brookes for injuries sustained in the accident under the Motor Accidents Compensation Act, 1999 (the MAC Act).
The accident constitutes a ‘public transport accident’ for the purposes of s 121(3) of the Transport Administration Act, 1988 (NSW) (TA Act). Section 121(1) of the TA Act provides that a claim for damages arising from an accident within the meaning of ‘public transport accident’ is to be assessed in accordance with Chapter 5 of the MAC Act.
Pursuant to s 132 of the MAC Act the dispute about whether the degree of permanent impairment is sufficient for an award of damages for non-economic loss is to be assessed by a medical assessor under Part 3.4 of the MAC Act.
This dispute is in relation to whether the degree of permanent impairment of Mr Brookes as a result of the injury caused by the accident is greater than 10%. This constitutes a medical dispute within the meaning of the MAC Act.[1]
[1] Sections 57 and 58 of the MAC Act.

REVIEW PROCEDURE

The present application is a review of a medical assessment pursuant to s 63 of the MAC Act. The relevant medical assessment was conducted by Medical Assessor John O’Neill. He issued a certificate dated 19 May 2021.
Sydney Trains filed an application for review of that medical assessment within 28 days after the parties were issued with the combined certificate of Medical Assessor Curtin dated 1 December 2021.
On 20 December 2022, the Delegate of the President being satisfied there was reasonable cause to suspect that the medical assessment was incorrect in a material respect having regard to the particulars set out in the application referred the medical assessment to the Review Panel (the Panel).[2]
[2] Section 63(2B) of the MAC Act.
The Personal Injury Commission (Commission) commenced operation on 1 March 2021 and the Dispute Resolution Service (DRS) was abolished by cl 3 of Part 2, Division 2, Schedule 1 to the Personal Injury Commission Act 2020 (the PIC Act).
Clause 14F of Schedule 1 of the PIC Act provides that the new review provisions apply in relation to a decision of a new decision-maker. A ‘new decision-maker’ is defined in cl 14A of Schedule 1 of the PIC Act and includes Medical Assessor Haber where the medical assessment the subject of this review occurred after 1 March 2021.
The new review provisions provide that a review panel consists of two medical assessors and a member assigned to the Motor Accidents Division of the PIC. The President’s Delegate referred this application for review to the panel.
The assessment of the degree of permanent impairment is to be made in accordance with the Motor Accident Permanent Impairment Guidelines (the Guidelines). The Guidelines are issued pursuant to s 44(1)(c) of the MAC Act and are based on the American Medical Association’s Guides to the Evaluation of Permanent Impairment, Fourth Edition (AMA 4 Guides). The Guidelines are definitive with regard to the matters they address but where they are silent on an issue, the AMA 4 Guides should be followed.[3]
[3] Clause 1.2 of the Guidelines.
Part 5 of the PIC Act enables the Commission to make rules with respect to the practice and procedure before the Commission including proceedings before a panel reviewing a decision of a medical assessor.[4]
[4] Section 41(2) of the PIC Act.
Rules 127 to 130 of the Personal Injury Commission Rules 2021 (PIC Rules) are made pursuant to Part 5 of the PIC Act. A Review Panel determines how it conducts and determines the proceedings and may determine the proceedings solely based on the written application.[5]
[5] Rule 128 of the PIC Rules.
The review is by way of a new assessment of all matters with which the medical assessment is concerned.[6]
[6] Section 63(3A) of the MAC Act.
The Panel issued a Direction to the parties on 10 November 2022 (the first Direction) which required each party to file an indexed, paginated bundles of documents. In response to this direction the insurer filed a bundle of documents paginated from pages 1 to 1,685 and marked AD2. The claimant filed a bundle of documents paginated from pages 1 to 1,544 and marked AD3.

MEDICAL ASSESSMENT UNDER REVIEW

The following injuries were referred to Medical Assessor O’Neill for assessment:
· ribs – rib fractured 4th, 6th, 7th and 8th ribs, and
· leg – neurological – Guillain-Barre syndrome.
In his certificate dated 19 May 2021[7] Medical Assessor O’Neill found the following injuries were caused by the accident and gave rise to a permanent impairment of 20%:
· Guillain-Barre syndrome (GBS) – persisting facial diplegia.
[7] AD2 page 20.
Medical Assessor O’Neill found that the rib fractures were outside his area of expertise.
Medical Assessor O’Neill noted Mr Brookes had persisting bilateral facial weakness with associated slurring of speech and mild impairment of taste.
In relation to causation, he stated:
“There is absolutely no doubt that Mr Brookes sustained a fracture of the nose, fracture of the right fourth to seventh ribs (inclusive) and an apparent ‘soft tissue injury’ to the left knee in the accident of 22 January 2018.
The question of causation is difficult in terms of subsequent events.
It is outside my area of expertise to state whether or not the development of a thrombosed left popliteal artery aneurysm could have arisen from the knee injury which took place in the accident of 22 January 2018. It was during rehabilitation for complications arising from management of the left popliteal artery aneurysm that Mr Brookes developed GBS. GBS can arise in the setting of recent surgery and so if it was deemed that the popliteal artery aneurysm arose from the accident then it would be reasonable to say that the GBS was a further remote complication of the accident”.

OTHER MEDICAL ASSESSMENTS

Medical Assessor Richard Haber

The following injuries were referred to Medical Assessor Haber for assessment:
·        pulmonary embolism;
·        left knee – thrombosed left popliteal artery aneurysm secondary to trauma, and
·        rib – fractured 4th, 6th, 7th and 8th ribs.
In his certificate dated 28 June 2021 Medical Assessor Haber found the following injuries were caused by the accident but had resolved and did not result in permanent impairment:[8]
·        fractures of the ribs;
·        pulmonary emboli, and
·        thrombosis in the left thigh.
[8] AD2 p 129.
Medical Assessor Haber found that the amputation of the left leg was outside his area of expertise.

Medical Assessor Geoffrey (Paul) Curtin

Medical Assessor Curtin provided a certificate dated 26 November 2021.[9] He concluded the following injuries were caused by the accident and gave rise to a permanent impairment of 39%:
·        left knee-soft tissue injury, amputation secondary to thrombosed left popliteal artery aneurysm;
·        nose-fractured nose with deformity, and
·        skin-left thigh scarring.
[9] AD2 p 133.
Medical Assessor Curtin noted there were three opinions provided by vascular surgeons as to whether the soft tissue issue to the left knee could have resulted in the thrombosis of the femoral artery which ultimately resulted in the amputation of the left leg. He noted Dr Myers concluded there was no evidence to link the thrombosis with the earlier accident. Dr Peter Tomlinson opined that the soft tissue injury to the knee resulted in damage to a pre-existing aneurysm in the femoral artery which went on to be occluded by thrombosis. Dr Neische did not address the question of causation but found there was no history or evidence of pre-existing vascular disease prior to the accident and that the diagnosis was “thrombosis of a traumatic left popliteal artery aneurysm”.
Medical Assessor Curtin agreed with the opinion of Medical Assessor Haber who considered the left femoral artery thrombosis which resulted in the below knee amputation had developed as a result of the accident.

Combined certificate of Medical Assessor Curtin

Medical Assessor Curtin issued a Combined Certificate dated 1 December 2021[10] in which he found that that the following injuries caused by the accident gave rise to a permanent impairment greater than 10%:
·        knee – left knee – thrombosed left popliteal artery aneurysm secondary to trauma;
·        lung – lungs – pulmonary embolic;
·        nose and air passage – nose – fractured nose with external deformity;
·        ribs – rib fractures 4th, 6th, 7th and 8th ribs;
·        leg – neurological – Guillain Barre syndrome, and
·        skin – scaring – left thigh scarring.
[10] AD2 p 141.

Medical Review Panel (review of certificate of Medical Assessor Haber)

A Medical Review Panel revoked the certificate of Medical Assessor Richard Haber dated 28 June 2021 and issued a new certificate dated 29 September 2022 followed by a replacement certificate dated 22 November 2022, determining that the following injuries were caused by the motor accident and do not give rise to permanent impairment:
· fractured right 4th, 6th, 7th and 8th ribs.
The Medical Review Panel determined that the following injuries were not caused by the accident:
· pulmonary embolism, and
· left knee – thrombosed left popliteal artery aneurysm.

Medical Review Panel (review of certificate of Medical Assessor Curtin)

A Medical Review Panel revoked the certificate of Medical Assessor Curtin dated 17 November 2021 and issued a new certificate dated 29 September 2022 followed by a replacement certificate dated 22 November 2022, determining that the following injury was caused by the motor accident and does not give rise to a whole person impairment (WPI) which is greater than 10%:
· fractured nose with deformity, and
· left knee-soft tissue injury.
The Medical Review Panel determined that the following injuries were not caused by the motor accident:
· amputation secondary to thrombosed left popliteal artery aneurysm, and
· skin-left thigh scarring.

MATERIAL BEFORE THE REVIEW PANEL
Hawkesbury District Health Service, 22 January 2018

The triage note records Mr Brookes was brought in by ambulance. He was standing on a train when he fell forward, hit his head and sustained a laceration to his forehead and pain to his nose.[11]
[11] AD2 page 640.
The clinical record reports Mr Brookes was thrown against the wall, hit his face and chest. He was complaining of nasal, right chest and left knee pain, with no loss of consciousness. Mr Brookes was diagnosed with four right sided rib fractures without displacement and a nasal bone fracture (x2) with a nasal septum fracture. He was also noted to have a laceration to the forehead and left knee tenderness at the patella and medially.
Mr Brookes underwent an X-ray of his left knee on 22 January 2018 having regard to the history of left knee pain.[12] The findings were recorded as follows:
“There is good preservation of the joint space in the medial, lateral and patellofemoral articulations with no evidence of degenerative change or a synovial arthropathy. The skyline view suggests satisfactory patellar tracking. There is no evidence of a joint effusion or loose body. No fracture seen.”
[12] AD2 page 288.

Nepean Hospital

Mr Brookes was transferred by ambulance to Nepean Hospital where he was admitted until 23 January 2018.[13] The Emergency Department notes list the injuries as follows:
-       Multiple rib fractures;
-      laceration to forehead – sutured;
-      L knee pain with abrasion, and
-      nasal fracture – displaced.

Sydney Street Medical Practice[14]
[13] AD3 page 322.
[14] AD2 page 1,582.

Mr Brookes consulted his general practitioner (GP) Dr Selim at Sydney Street Medical Practice. The first relevant consultation was on 5 February 2018 when Dr Selim noted Mr Brookes had been involved in a train accident on 22 January 2018 sustaining a fractured nose, fractured ribs and a lacerated forehead.[15]
[15] AD3 p 153.
On 9 February 2018 Dr Selim recorded a history of intermittent right elbow pain and left knee pain when flexed for an extended period of time. On examination of the knee, he recorded: “L knee-prepatellar effusion+.no tenderness. Full RON all movements” [sic].
On 16 February 2018 (approximately four weeks after the accident) Dr Selim noted continuous left knee pain and on 23 February 2018 he recorded the left knee pain was stable. On 2 March 2018 Dr Selim reported the left knee pain was 4/10 and on 7 March 2018 he reported persistent left knee pain, localised around the patella. On examination he reported “localised tenderness and central patella/ bruising”.
On 19 April 2018 Mr Brookes underwent nose surgery, namely nasal bone osteotomies and septal reconstruction at Minchinbury Community Hospital under the care of Dr Michael Hunter.
The next relevant complaint is on 3 May 2018 when Dr Selim records left foot and calf pain for the past three days. However, on examination Dr Selim records “L calf – no swelling, localised tenderness”. Dr Selim referred Mr Brookes for a leg venous doppler.
An ultrasound venous doppler of the left leg performed on 3 May 2018 concluded there was no evidence of deep vein thrombosis in the left lower limb.

On 7 May 2018 Dr Selim notes no abnormality disclosed on the left venous doppler and records “pain now localised to L ankle”. He noted mild tenderness of the left ankle with a full range of motion.
On 9 May 2018 Dr Selim reported “L knee pain persists since accident. Mild but became severe after slight trauma”.
On 14 May 2018 (nearly four months after the accident) Dr Selim reported the left foot was worse and was turning bluish. On observation he recorded “L foot appear cyanotic, nailbed capillary return sluggish [sic]”. Dr Selim concluded Mr Brookes required an urgent arterial doppler and intervention.

Minchinbury Community Hospital

On 19 April 2018 Mr Brookes underwent surgery, namely reconstruction of the septum at Minchinbury Community Hospital under the care of Dr Michael Hunter.[16]

Nepean Hospital admission 14 May 2018
[16] AD2 p 1,569.

Mr Brookes was an inpatient at Nepean Hospital from 14 May 2018 to 27 August 2018.[17] The discharge summary states:
“…Colin Brookes a 54-year-old male who was admitted to Nepean Hospital on the 14.05.18 with pain and paraesthesia of the left leg. He was admitted under Dr Nguyen (Vascular Surgeon) and diagnosed with an occluded popliteal aneurysm. He underwent a femoral - popliteal bypass which unfortunately was unsuccessful and required a left below knee amputation. Mr Brookes had a complex and complicated recovery suffering from post-operative DVT, Guillain Barre Syndrome, Stump dehiscence and suffering from a UTI and urinary retention”.
[17] AD 2 p 194.
The clinical summary of the left occluded popliteal artery states:[18]
“-      Presented to Nepean hospital on the 14/5/18 with a 2 week history of pain in the left calf and limited in mobility. Left foot cool to palpate with monophasic flow on ultrasound of posterior tibial artery, unable to elicit DP
-       CTA 12 mm left popliteal artery aneurysm with near complete occlusion
-       Femoral popliteal bypass on the 15/05/18
-       Day 1 post op had pain crisis which required a femoral nerve block
-       Required a left BKA (below knee amputation) on the 24/05/18 due to occluded bypass graft”.
[18] AD2 P 202.
In relation to the GBS (Pharyngeal Cervical Brachial Variant) the discharge summary records:[19]
[19] AD2 P 805.
“- On the 06.06.18 whilst in rehab patient complained of bilateral finger paraesthesia. Isolated to the fingers, nil dermatomal pattern found, nil headache, nil speech disturbance, nil visual disturbance. Cranial nerve exam deemed to be normal. Reduced power in finger abduction and adduction, no other abnormalities detected on peripheral nerve exam. However, 24 hours later paraesthesia and weakness ascending to the level of the wrist.
- Consult to Neurology who took over care under Dr Hague
- completed stroke work up with nil positive results
- impression of GBS
- LP completed and patient commenced IVIG (intravenous immunoglobulin) for 5 days
- Patient began expressing central weakness, unable to close eyes, difficulty in speech and swallow, nil issues with breathing
- NGT inserted and x-ray confirmed correct placement for feeds
- Slow improvement whilst under Neurology and subsequently under Rehab
- Will follow up with Dr Hague on Discharge 24.09.18”
In relation to infection the discharge summary also includes the following:
“Clostridium Difficile
-on the 25/06/18 began having loose stools
-stool sample revealed C. diff infection
-treatment with Metronidazole”.

Mr Brookes underwent a CT lower limb with spiral angiography on 14 May 2018. The report concludes:
“There is abrupt cut off of the left superficial femoral artery in the mid thigh …. There is good opacification and calibre of the profunda femoris artery. There is no contrast in the popliteal artery. Some of the collaterals in the anterior compartment of the thigh are supplying the proximal posterior compartment of the leg. There is minimal to no opacification of the anterior and posterior tibia and peroneal artery. Hyperdensity within the posterior tibia is likely due to calcified atherosclerosis.
Calcified atherosclerosis is present in the right posterior tibial. There is reduced opacification from ankle joint onwards. There is good calibre and opacification of the right femoral, profunda femoral, popliteal and proximal arteries of the leg.
There is mild calcified atherosclerosis of the right common iliac artery. The abdominal para and major branches show good opacification otherwise. There is early branching of the right renal artery. No dissection or aneurysm identified…”.

Dr Sameen Haque, neurologist

On 9 June 2018 nurse Leonie Martin made the following entry in the progress notes:[20]
“Patient was requesting pain relief, same given, awaiting effect
Patient was experiencing difficulty holding the cup and stated, ‘its getting worse, I can’t even lift this plastic bag up [sic]’.
Patient attempted to lift plastic bag onto bed table and couldn’t
Patient stated both arms were the same
Asked patient had this been like this for long, stated ‘for a couple of days’
Asked patient if his leg felt heavy or odd, did it feel any different, he stated no it felt the same
Patient did say that his swallow and throat felt difference, he was finding it difficult to swallow
Asked patient if he felt he was having difficulty breathing, stated no.”
[20] AD3 p 1,141.
Mr Brookes subsequently came under the care of Dr Haque, Department of Neurology Nepean Hospital.
Mr Brookes underwent an MRI of the cervical spine on 10 June 2018 having regard to the following clinical history:
“Left below knee amputation for acute limb ischaemia - On Clexane + Aspirin. Right upper limb pyramidal weakness, treated as CVA. MRl Head normal (08/06/2018). Worsening left upper limb weakness on 09/06/2018. Areflexic, dysarthria, dysphagia. Lower limbs showed no weakness. Concern re: cervical pathology, Gullian Barre Syndrome”.
The findings were reported as follows:
“The cranio-cervical junction is normal. The spinal cord demonstrates normal morphology and signal intensity.
No spinal cord lesion is identified.
There is no evidence of cord or cauda equina compression. The spinal cord terminates at the superior margin of the L1 vertebral body.
There is no evidence of epidural collection in the cervical spine. There is no enhancing lesion in the spinal cord.
There is normal alignment of the vertebral bodies and demonstrate normal signal intensity. There is no dislocation or subluxation.
There is straightening of the normal cervical lordosis.
Mild diffuse posterior disc bulges from C3-C7 with mild indentation of the anterior dural theca and mild encroachment into the adjacent neural exit foramina. No definite nerve root compression is identified.
There is no evidence of significant disc herniation, spinal canal stenosis or neural exit foramina narrowing in the lumbar spine. There is no thickening of the cauda equina nerve roots.
Bilateral vertebral arteries demonstrate normal signal intensity”.
Mr Brookes also underwent additional investigations, as a process of elimination to determine the appropriate diagnosis including an MRI of the brain and an MRI of the head on 8 June 2018, and a CT of the brain on 10 June 2018 with no apparent abnormality detected.
Mr Brookes underwent a lumbar puncture on 13 June 2018 and nerve conduction studies (NCS) and IVIG on 21 June 2018.
Mr Brookes underwent NCS on 21 June 2018.
Dr Haque reported to Dr Selim on 24 September 2018.[21] In respect of the diagnosis of pharyngeal-cervical-brachial onset-weakness variant of Guillian-Barre syndrome he reported:
(a)     noted during rehabilitation syndrome to have developed right upper limb weakness, facial diplegia with successive weakness of the other three limbs;
(b)     administered IVIG for five days;
(c)     NCS/EMG showed neurophysiological evidence of a predominantly sensory motor neuropathy with axonal loss (26 June 2018), and
(d)     GQ1B antibodies negative.
[21] AD2 p 1,579.
Dr Haque reported persistent facial weakness, especially on the right side and complaints of dribbling of tea and coffee from the right corner of his mouth. He also noted excessive tearing or pooling of the tears in the context of lower eyelid ptosis on the right side, and an element of facial synkinesis causing hyperlacrimation on the right side. Mr Brookes still felt weak in his lower limbs.
Dr Haque reviewed Mr Brookes on 19 November 2018.[22] He reported a progress neurophysiological study on 8 November 2018 was consistent with large fibre sensorimotor neuropathy of mixed type. Compared to the study of 21 June 2018 he noted overall improvement in the sensory and motor potentials.
[22] AD2 p 1,581.
Dr Haque reported:
“Colin's persistent problem is the right sided facial synkinesis due to aberrant reinnervation of the seventh cranial nerve. He has the so-called ‘crocodile tear syndrome’ (hyperlacrimation). This results from aberrant neural interaction between the salivary and the lacrimal glands. Colin classically describes ‘shedding tears involuntarily’ at the sight of meals or while having his meals. He is not too distressed with the symptoms. MRI of the brain on 11 November 2018 showed no abnormality associated with the seventh cranial nerve or along its course on either side”.

Dr Madelaine Max, rehabilitation registrar for Dr Laurence Chu

Mr Brookes was reviewed by Dr Max on 20 September 2018.[23] In relation to the Guillain Barre syndrome she reported he was suffering from right sided weakness and speech disturbance.

Dr John Taper
[23] AD3 p 186.

Dr Taper, a staff specialist in the Haematology Clinic, Nepean Hospital reviewed Mr Brookes on 7 November 2018.[24] He noted Mr Brookes was involved in a train related accident with significant trauma to his thorax and left lower limb, requiring admission to Nepean Hospital. He reported after discharge the limb was never entirely normal and in May an arterial thrombotic event occurred which eventually results in an amputation.
[24] AD3 p 177.
He reported during the hospital stay it was noted that Mr Brookes had a proximal left lower limb venous thrombosis. He also noted Mr Brookes was well with no medical issues prior to the accident, was a non-smoker and did not drink alcohol (it is clear from other records that Mr Brookes did drink alcohol – the clinical notes of Nepean Hospital refer to a carton a week). He also reported there was no significant family history of a thrombotic disorder and extensive procoagulant and vasculitic investigations in the hospital were unremarkable. He concluded the arterial event was related to the trauma and the venous thrombotic event attributable to his hospital stay and surgery.

Nepean Hospital admission 8 January 2019

Mr Brookes was readmitted to Nepean Hospital on 8 January 2019 and discharged the following day.[25] He was admitted for a pulmonary embolism demonstrated on an outpatient CT-Pulmonary Angiogram.
[25] AD2 page 183.

The Discharge Summary includes the following:
“Further Review of his CTPA in hospital revealed left upper and lower lobe pulmonary embolism, with suspicion of consolidation. Colin was further investigated with a Doppler ultrasound of both lower limbs with findings of persistent DVT (previous DVT from distal external iliac vein extending into femoral and popliteal veins) and no other significant findings in the proximal external iliac vein. The right limb showed no pathology. Colin was further investigated with an ECG which showed sinus tachycardia, however he remained hemodynamically stable”.
In a report dated 3 April 2019 Dr Monica Comsa, respiratory specialist, Nepean Hospital, noted Dr Brookes had been referred back to her following his pulmonary embolism in January 2019 which she thought was likely provoked by his immobility in the wheelchair following the left leg amputation in 2018.[26]
[26] AD2 page 181.

Nepean Hospital, 24 March 2021

Mr Brookes presented to Nepean Hospital on 24 March 2021 with Rutherford Type 1a acute right limb ischemia under the care of Dr Daniel Nguyen.[27]
[27] AD1 page 221 and AD2 page 916.
On 24 March 2021 Mr Brookes underwent a CT angiogram of the lower limb.[28] The reason for examination was right side ischemic leg. The report concluded:
“There is contiguous soft plaque extending from the distal right common lilac artery to the origin of the right superficial femoral artery causing up to severe stenosis as described above”.

Dr Daniel Minh Le Nguyen[29]
[28] AD2 page 1,679.
[29] AD2 page 1,682.

Dr Nguyen, vascular surgeon, provided a report to Dr Selim dated 6 May 2021. He reported two months earlier Mr Brookes was admitted under his care to Nepean Hospital in respect of an acute thrombosis in the right leg. He reported a recent ultrasound demonstrated improvement in the thrombus burden with residual EIA (internal iliac artery) stenosis 50 to 75%, non-occlusive thrombus in the popliteal artery with 75% stenosis and occlusion of the PTA from the midcalf.

Medico-legal evidence
Dr Peter Tomlinson

Dr Tomlinson, a vascular surgeon, assessed Mr Brookes at the request of his solicitors on 15 October 2018 and provided a report dated 24 October 2018.[30]
[30] AD3 p 116.
Whilst he did not address the Guillain Barre syndrome Dr Tomlinson expressed the following opinion as to causation of the left popliteal artery aneurysm and the subsequent amputation:
“It is my opinion that this gentleman has had a left popliteal artery aneurysm and has developed trauma to the medial aspect of his left knee resulting in some damage to the aneurysm itself. This has resulted in a degree of thrombosis of the aneurysm with total occlusion of the aneurysm and popliteal artery at the time of surgery to his fractures of the nose which were necessary as a result of the accidents sustained on 22 January 2018.”
He concluded further:
“I do believe that the surgery performed on 23 May 2018 for left below knee amputation was reasonably necessary due to ischaemia of the left leg. I believe that this surgery is directly related to the injury of 22 January 2018. I believe there has been a history of direct trauma to the left knee and there has most likely been some damage to the popliteal artery aneurysm resulting in thrombosis. Complete occlusion of the aneurysm has taken place in association with surgery for fractures to the nose, which were again sustained on 22 January 2018”.

Dr Kenneth Howison

Dr Howison, ear, nose and throat specialist assessed Mr Brookes at the request of his solicitor and provided a report dated 17 May 2019.[31] He noted the obvious deformity of the nasal pyramid and assessed a 10% WPI as a result of the external deformity of the nose.
[31] AD3 p 36.

Dr Uthum Dias

Dr Dias, occupational physician assessed Mr Brookes at the request of his solicitor and provided a report dated 23 July 2019.[32] He concluded as a result of the accident Mr Brookes sustained an acute traumatic impaction injury to his head resulting the nasal fractures as well as an acute soft tissue injury to the left knee which resulted in a posttraumatic popliteal aneurysm and consequentially the left below knee amputation in late May 2018. He found the causal chain from the accident to the current condition was unbroken.
[32] AD3 p 76.
He also concluded that the Guillain Barre syndrome diagnosed in June 2018 and the pulmonary emboli diagnosed in January 2019 were consequential to the accident of 22 January 2018. He reported Mr Brookes felt generally weak and fatigued as a consequence of the Guillain Barre syndrome.

Associate Professor Paul Myers

Associate Professor Myers provided a report on the papers dated 16 January 2020.[33] He noted that aneurysms of the peripheral vasculature are very common. He described the vast majority as atherosclerotic where the wall of the artery becomes damaged and inherently weak, and the outward radial pressure of the blood flow and the pulse caused the artery to dilate over time. He stated the normal diameter of a popliteal artery is 6-8mm in adults and Mr Brooks has said to have an aneurysm of 12mm in diameter, twice the normal diameter of the vessel. Associate Professor Myers noted when an aneurysm forms the blood flood in that artery becomes turbulent and because of the turbulence of the blood flow at the periphery of the aneurysm, thrombus forms on the wall of the aneurysm.
[33] AD2 p 73.
Associate Professor Myers said aneurysm can also occur due to infection but noted there was no evidence of infection in Mr Brooks.
He also noted that there can be false aneurysms where the artery wall is broached and blood escapes from the artery into the surrounding tissues where it is contained. False aneurysms do not include dilation of the actual vessel itself. Again, he noted there was no evidence of this occurring in Mr Brookes.
Associate Professor Myers stated there are other genetic causes of aneurysms, but he is not aware of such causes in Mr Brookes.
He stated the most common presentation of popliteal artery aneurysm is thrombosis of the vessel which can occur due to bending and straightening of the knee pressing on the artery which is already weakened and dilated and containing mural thrombus and therefore vessel thromboses. He said this usually happens without warning or any symptoms. When this happens the distal vessels past the knee rapidly thrombose and occlude.
Associate Professor Myers stated the most common outcome of a spontaneous thrombosis of a popliteal aneurysm is amputation. He stated the pre-patellar effusion experienced by Mr Brookes is an indication of soft tissue issues in the bursa around the kneecap but was not associated with the aneurysm. He concluded the popliteal aneurysm was not made worse by the incident in the train and the thrombosis was not caused by the incident in the train. Indeed, he stated it was not sustainable to argue that an existent popliteal aneurysm would thrombose four months down the track from a blunt soft tissue trauma.

Dr John Niesche

Dr Niesche, vascular surgeon, assessed Mr Brookes at the request of the insurer and provided a report dated 20 January 2021.[34]
[34] AD3 page 107.
He diagnosed thrombosis of a traumatic left popliteal artery aneurysm. He noted Mr Brookes developed Guillain Barre syndrome, during his hospital stay following amputation, mainly affecting the left side with gradual but incomplete recovery. Other than noting there was no history of pre-existing vascular disease he did not otherwise express an opinion as to causation.

Dr Henley Harrison

Dr Harrison, ear, nose and throat specialist assessed Mr Brookes at the request of the insurer and provided a report dated 12 February 2021.[35] He diagnosed a nasal fracture with resulting nasal deformity and facial laceration and assessed a 7% WPI.
[35] AD3 page 112.
Dr Harrison stated he could not find any connection between the Guillain Barre syndrome and the accident.

Dr Brian Stephenson

Dr Stephenson, orthopaedic surgeon, assessed the claimant and provided a report dated 5 January 2021.[36] He indicated he agreed with the opinion of Dr Tomlinson as to causation of the thrombosis of the aneurysm and subsequent amputation but did not otherwise address the question of causation.
[36] AD3 p 93.

RELEVANT LEGAL AUTHORITY

Causation

Causation of injury is addressed in the Guidelines as follows:
“1.5   An assessment of the degree of permanent impairment is a medical assessment matter under clause 2(a) of Schedule 2 of the Act. The assessment must determine the degree of permanent impairment of the injured person as a result of the injury caused by the motor accident. A determination as to whether the injured person’s impairment is related to the accident in question is therefore implied in all such assessments. Medical assessors must be aware of the relevant provisions of the AMA4 Guides, as well as the common law principles that would be applied by a court (or claims assessor) in considering such issues.
1.6    Causation is defined in the Glossary at page 316 of the AMA4 Guides as follows: ‘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:
1. The alleged factor could have caused or contributed to worsening of the impairment, which is a medical determination.
2.The alleged factor did cause or contribute to worsening of the impairment, which is a non-medical determination.’
This, therefore, involves a medical decision and a non-medical informed judgement.
1.7    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.”

SUBMISSIONS
Insurer’s submissions

The insurer provided submissions dated 28 February 2022. Those submissions address the test to be considered by the Delegate in determining whether the assessment of Medical Assessor Haber was incorrect in a material review. The insurer relies upon the opinion of Associate Professor Myers as to causation.

Claimant’s submissions

The claimant provided submissions dated 18 March 2022.[37] Those submission address the test to be considered by the Delegate in determining whether the assessment was incorrect in a material respect.
[37] AD2 p 22.

DETERMINATION

The following issues arise for consideration:
·        whether Guillain Barre syndrome (GBS) is the correct diagnosis;
·        causation of the GBS;
·        if the GBS was caused by either the amputation or the hospitalisation associated with the amputation, whether the thrombosis in the left popliteal artery which led to amputation was casually related to the injury sustained by the claimant on 22 January 2018, and
·        depending on causation the assessment of permanent impairment.
The Panel considered it was appropriate to determine the matter on the papers in accordance with Rule 128(2) of the Personal Injury Commission Rules in circumstances where the Panel concluded the GBS was not caused by the accident. The Panel would have undertaken a re-examination of Mr Brookes if the Panel concluded the GBS was caused by the accident but determined not only was a medical examination not required but it would inconvenience Mr Brooks unnecessarily.

Diagnosis

The first issue to be determined is the accuracy of the diagnosis of GBS. GBS is an autoimmune disease which affects the peripheral nervous system causing demyelination of the nerves (the destructions of the myelin sheath). The syndrome can be triggered by a bacterial or viral illness, although on rare occasions surgical procedures have been known to cause GBS.
GBS is difficult to diagnose and diagnostic techniques include lumbar puncture, electromyography (EMG) and nerve conduction studies (NCS). Mr Brookes underwent a lumbar puncture on 13 June 2018 and nerve conduction studies on 21 June 2018. Whilst the Panel was unable to locate the results amongst the clinical notes of Nepean Hospital the Panel notes Dr Haque informed Dr Selim on 24 September 2018 that the NCS/EMG of 26 June 2018 showed neurophysiological evidence of a predominately sensory motor neuropathy with axonal loss.

Further Dr Haque reported a progress neurophysiological study on 8 November 2018 was consistent with large fibre sensorimotor neuropathy of mixed type. He also noted overall improvement in the motor and sensory potentials.
Treatment options include gammaglobulin (IVIG) infusion. This treatment was provided to Mr Brookes, initially on 10 June 2018 in respect of GBS.[38] In his report to Dr Selim of 24 September 2018 Dr Haque reported IVIG was administered for five days.
[38] AD2 p 210.
Dr Haque also reported symptoms consistent with GBS, namely, right upper limb weakness, facial diplegia with successive weakness of the other three limbs and dysphagia due to pharyngeal weakness;
The Panel accepts the opinion of Dr Haque as to diagnosis where he noted symptoms consistent with GBS, supported by the neurophysiological evidence apparent on the NCS/EMG of 26 June 2018, and having regard to the overall improvement shown following IVIG infusion.

Causation of the GBS

The discharge transfer documents from Nepean Hospital of 27 August 2019 confirm the presence of clostridium difficile diarrhoea, a common bacterial infection which can be related to GBS.[39]
[39] AD2 p 803.
It is widely accepted that clostridium difficile diarrhoea is a leading cause of infectious diarrhea acquired in hospitals. The Panel notes Mr Brookes had been hospitalised since 14 May 2018, a period of four weeks at the time he first displayed symptoms of GBS on 10 June 2018.
On the balance of probabilities, the Panel is satisfied the claimant’s period of hospitalisation associated with the amputation either caused or contributed to Mr Brookes contracting an infection, in all likelihood, by clostridium difficile which caused or contributed to the development of the GBS.

Causation of the thrombosis in the left popliteal artery

The next issue is whether the thrombosis in the left popliteal artery was causally related to the left knee injury Mr Brookes suffered in the accident.
Atherosclerosis is the process where fat, cholesterol, calcium and inflammatory cells build up inside the innermost lining (endothelium) of the wall of the body’s arteries to form an atherosclerotic plaque over a period of time.
With time, the atherosclerotic plaque builds up and it gets larger and hardens. The larger plaques bulge into the lumen (the hollow tube) of the artery, narrowing the passage where the blood flows.
The atherosclerotic plaque weakens the wall of the artery resulting in the wall of the artery bulging outwards to form an aneurysm.
The atherosclerotic plaque can break down and render the surface of the endothelium highly thrombogenic increasing the likelihood of a thrombus (blood clot) being formed on the endothelium, the inside wall of the artery. If the thrombus is large enough, it can completely block the flow of oxygen-rich blood to vital organs.
When the atherosclerotic plaque becomes unstable bits break off and become impacted resulting in the blockage of a smaller artery downstream.
The popliteal artery is situated in the posterior aspect of the knee joint (the popliteal fossa). After the accident Mr Brookes complained of pain in the medial side and the front of the knee, that is, to the patella. If the force to his left knee had been significant and had resulted in the fracture of his left patella, or the distal femur and/or the tibia tuberosity/head it may have caused injury to the popliteal artery which lies just behind the knee joint.
However, the left knee X-ray report of 22 January 2018 stated there was no bony injury or fracture to the distal femur or to the tibia tuberosity/head to which the popliteal artery lies in close proximity. There was no fracture of the patella, and the patellofemoral joint space was normal (“good preservation”). There was no effusion or loose body in the knee joint.
On 9 February 2018, the clinical notes of Dr Selim documented that Mr Brookes had complained of pain in the patella and the medial aspect of the left knee after the accident reporting there was “L knee prepatellar effusion +, no tenderness. Full RON [sic] all movements”. Whilst there was no effusion in the knee joint shown on the 22 January 2018

X-ray of the left knee, Dr Selim noted that he had a prepatellar effusion which was situated in front of the patella. However, this effusion was not connected with the left knee joint and would not affect the movement of the left knee. Hence, Dr Selim recorded “Full RON all movement [sic].”
The Panel believes if Mr Brooke had injured his left popliteal artery in the accident, the circulation to his left leg would have been immediately compromised, and he would have developed some symptoms in his left calf and or left leg by 9 February 2018.This was not the case.
On 16 February 2018 Dr Selim noted continuous left knee pain and on 23 February 2018 he recorded the left knee pain was stable. On 2 March 2018 Dr Selim reported the left knee pain was 4/10 and on 7 March 2018 he reported persistent left knee pain, localised around the patella. On examination he reported “localised tenderness and central patella/ bruising”. Again, the left knee pain was in the patella, not in the knee joint and it was remote from the anatomical location of the popliteal artery.
On 19 April 2018 Mr Brookes underwent nose surgery, namely nasal bone osteotomies and septal reconstruction at Minchinbury Community Hospital under the care of Dr Michael Hunter.
On 3 May 2018, Dr Selim recorded left foot and calf pain for the past three days. However, in the examination record, Dr Selim recorded “L calf – no swelling, localised tenderness”. Dr Selim referred Mr Brookes for a leg venous doppler.
An ultrasound venous doppler of the left leg performed on 3 May 2018 concluded there was no evidence of deep vein thrombosis in the left lower limb.
On 7 May 2018 Dr Selim recorded there was no abnormality disclosed on the left venous doppler and Mr Brooke’s lower limb pain was “now localised to L ankle”. He noted mild tenderness of the left ankle with a full range of motion.
On 14 May 2018 Dr Selim reported the left foot was worse and was turning bluish. On observation he recorded “L foot appear cyanotic, nailbed capillary return sluggish [sic]”. Dr Selim concluded that Mr Brookes required an urgent arterial doppler and intervention.
The CT lower limb angiography of 14 May 2018 revealed that the left popliteal artery was occluded, and calcification was reported in the atherosclerotic plaques in the left posterior tibial artery, the right common iliac artery and the right posterior tibial artery. The presence of calcification in these atherosclerosis plaques in both lower limbs indicates that Mr Brookes had atherosclerosis in both lower limbs which predisposed him to the development of the thrombus forming in the artery.
The Panel finds the blood flow in the aneurysm artery became turbulent and because of the turbulence of the blood flow at the periphery of the aneurysm, a thrombus formed on the wall of the aneurysm. Hence Mr Brooke’s left popliteal artery aneurysm was predisposed to the formation of the thrombus although the formation of the thrombus was asymptomatic until the artery became occluded.
Nearly three years after the left popliteal artery thrombosis, Mr Brookes presented to Nepean Hospital on 24 March 2021 with a Rutherford Type 1a acute right limb ischemia under the care of Dr Daniel Nguyen. He had a CT angiogram of the lower limb. The findings of this angiogram were:
“Right lower limb
There is soft (atherosclerotic) plaque within the distal right common iliac artery, the right internal iliac artery is occluded.
There is soft (atherosclerotic) plaque seen within the right external iliac artery causing severe stenosis.
There is a continuous soft plaque seen within the common femoral artery causing moderate to severe stenosis.
The proximal profundus femoris is occluded with distal reconstitution. There is popliteal artery involvement.
Left lower limb
There is complete occlusion seen of the left superficial femoral artery at the level of the mid-thigh”.
The Panel finds the 24 March 2021 angiogram showed that Mr Brookes had extensive atherosclerotic plaques in his lower limbs. The plaques narrowed the lumen, known as stenosis of the arteries, blocking the flow of blood. The angiogram findings demonstrate that Mr Brooke had a predisposition to the development of atherosclerotic plaque deposition in his arteries.
The presence of atherosclerotic plaques in his right common iliac artery was apparent in 2018. The CT lower limb with Spiral Angiography performed on 14 May 2018 referred to mild calcified atherosclerosis of the right common iliac artery.
Mr Brooke’s predisposition to atherosclerotic plaque formation supports the contention that the thrombosis in his left popliteal artery aneurysm occurring nearly four months after the accident was due to his predisposition to thrombosis. The Panel finds the temporal separation in excess of three months supports the conclusion that the thrombosis was too remote in time to be causally connected to the accident.

In summary the Panel finds the thrombosis in the popliteal artery was not causally related to the accident where:
(a)     Mr Brookes was predisposed to thrombosis;
(b)     the clinical notes record Mr Brookes complained of pain in the patella with pre-patella effusion which the Panel finds was a minor soft tissue injury and unlikely to cause injury to the popliteal artery on the opposite side of the knee joint;
(c)     the injury to the patella or the anterior aspect of the knee was remote from the anatomical location of the popliteal artery;
(d)     there was no bony injury, no fracture of the distal femur and no fracture of the tibial tuberosity;
(e)     Mr Brookes had full range of movement when examined by Dr Selim on 9 February 2018;
(f)    there was no complaint of compromised circulation or symptoms in the left calf or leg as of 9 February 2018;
(g)   an injury to the popliteal artery at the time of the accident would more likely than not produce symptoms of vascular insufficiency shortly after the accident whilst the arterial thrombosis of the left popliteal artery did not occur until three months post-accident;
(h)   there was no evidence of deep vein thrombosis in the left lower limb disclosed on the left venous doppler on 3 May 2018;
(i)    on 7 May 2018 Dr Selim reported Mr Brooks’ pain was localised to the left ankle;
(k)   calcification was reported in the atherosclerotic plaques, the left posterior tibial artery, the right posterior tibial artery and the right common iliac artery on 14 May 2018, and
(k)   the 24 March 2021 angiogram showed that Mr Brookes had extensive atherosclerotic plaques in both lower limbs.

The assessment of permanent impairment

Fractured 4th, 6th, 7th and 8th ribs

The Panel finds that the fractured right 4^th, 6^th, 7^th and 8^th ribs were caused by the accident.
Under cl 1.23 of the Guidelines uncomplicated healed rib fractures do not result in any assessable impairment.
The Panel finds the rib fractures have resolved and do not result in permanent impairment.

Leg – neurological – Guillain-Barre syndrome.

The Panel finds the thrombosis in the left popliteal artery, the subsequent below knee amputation of the left leg and the ensuing period of the claimant’s hospitalisation not causally related to the accident.
Hence, the Panel finds the Guillain Barre syndrome was not caused by the accident and therefore, there is no assessable permanent impairment in relation to the claimant’s GBS

The Panel assesses 0% WPI.

[2023] NSWPICMP 32

3 February 2023