Allianz Australia Insurance Limited v Marks
[2022] NSWPICMP 244
•8 June 2022
| DETERMINATION OF REVIEW PANEL | |
| CITATION: | Allianz Australia Insurance Limited v Marks [2022] NSWPICMP 244 |
| CLAIMANT: | Glen Marks |
INSURER: | Allianz Australia Insurance Limited |
| REVIEW PANEL: | Member Susan McTegg Dr Christopher Grainge Dr Wing Chan |
| DATE OF DECISION: | 8 June 2022 |
| CATCHWORDS: | MOTOR ACCIDENTS- The claimant suffered serious injury in a motor bike accident; the dispute related to the assessment of permanent impairment; whether accident caused atrial fibrillation or the development of chronic thromboembolic pulmonary hypertension; pre-existing history of atrial fibrillation; pre-existing history of pulmonary embolic disease; assessment of whole person impairment; Motor Accident Compensation Act 1999; question of causation of condition; Held– pre-existing atrial fibrillation temporarily affected by accident; injury to chest and immobilisation in hospital led to development of thrombi which travelled to the right atrium of the heard and via the pulmonary artery into the lungs to result in pulmonary embolism; acute left sided pulmonary embolism and pulmonary arterial hypertension causally related to the accident; assessment of whole person impairment under Respiratory System chapter 5 of American Medical Association AMA 4 Guides using pulmonary function tests; Whole Person Impairment (WPI) assessed at 40%; pre-existing condition assessed at 15%; allowance of 3% for the effects of treatment; total WPI 27%; combined certificate issued for 30% WPI. |
| DETERMINATIONS MADE: | THE ASSESSMENT MADE BY THE REVIEW PANEL UNDER SECTION 63(4) IS AS FOLLOWS: The Panel revokes the Combined Certificate of Medical Assessor Haber dated 17 March 2021 and issues a new Combined Certificate determining that the following injuries were caused by the motor accident and give rise to a whole person impairment (WPI) which, in total, is greater than 10%. · Acute left sided pulmonary embolism and pulmonary arterial hypertension; · Fractured ribs; · Right thumb –soft tissue injury; · Left shoulder–soft tissue injury; · Left knee –patellofemoral crepitus and tenderness; and · Scarring –left elbow, left and right knees. The Panel revokes the certificate of Medical Assessor Richard Haber dated 12 March 2021 and issues a new certificate determining that the following injury was caused by the accident and gives rise to a WPI of 27%: · acute left sided pulmonary embolism and pulmonary arterial hypertension. REASONS This is to certify that permanent impairment was assessed by a Medical Review Panel comprising Medical Assessor Wing Chan, Medical Assessor Christopher Grainge, Details of the assessments and full reasons are given in the following certificates: Assessment 1 Certificate of the Medical Review Panel dated 7 June 2022 The permanent impairment in relation to the following injuries is 27%: · acute left sided pulmonary embolism and pulmonary arterial hypertension. Assessment 2 Certificate of Medical Assessor Mark Burns dated 5 May 2017 The permanent impairment in relation to the following injuries is 4%: · right thumb –soft tissue injury; · left shoulder–soft tissue injury; · left knee –patellofemoral crepitus and tenderness; and · scarring –left elbow, left and right knees. Using the Combined Values Chart at page 322 of American Medical Association Guides to the Evaluation of Permanent Impairment, 4th edition, the combined permanent impairment is 30%. |
MOTOR ACCIDENTS COMPENSATION ACT 1999
WHETHER THE DEGREE OF PERMANENT IMPAIRMENT OF THE INJURED PERSON AS A RESULT OF THE INJURY CAUSED BY THE MOTOR ACCIDENT IS GREATER THAN 10%
STATEMENT OF REASONS
INTRODUCTION
Mr Glen Marks (the claimant) suffered injury in a motor vehicle collision on 23 February 2014 (the accident).
Allianz Australia Insurance Limited (the insurer) is the relevant insurer with liability to pay any damages to Mr Marks under the Motor Accident Compensation Act 1999 (MAC Act).
This dispute is in relation to whether the degree of permanent impairment sustained by Mr Marks 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] Section 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 Richard Haber. He issued a certificate dated 12 March 2021[2] and he subsequently issued a combined certificate dated 17 March 2021.[3][2] AD4 p 66.
[3] AD4 p 71.
Clause 16.3.3 of the Medical Assessment Guidelines requires an application for review of an assessment by a single Medical Assessor in a permanent impairment dispute assessed by more than one Medical Assessor to be lodged within 30 days after the date on which the combined certificate was sent to the parties.
The insurer lodged an application for review of the medical assessment of Assessor Haber on 15 April 2021 within 28 days of the date on which the combined certificate of Assessor Haber was made available to the parties.[4]
[4] Section 63(7) of the MAC Act.
On 15 July 2021, 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).[5]
[5] Section 63(2B) of the MAC Act.
The Personal Injury Commission (the Commission) commenced operation on 1 March 2021 and the Claims Assessment and Resolution Service was abolished by cl 3 of Part 2, Division 2, schedule 1 to the Personal Injury Commission Act 2020 (the PIC Act).
Under cl 14A(1)(vii) Schedule 1 of the PIC Act pre-establishment proceedings include proceedings that before the establishment of the Commission were required or permitted to be dealt with by a review panel for a medical assessment constituted under the MAC Act.
Clause 14F of Schedule 1 of the PIC Act states 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(1) of Schedule 1 of the PIC Act. As the medical assessment the subject of the review was made after 1 March 2021 the new review provisions apply.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 Commission.[6] The President’s delegate referred this application for review to the panel.
[6] Section 63(3) of the MAC Act.
The Motor Accident Permanent Impairment Guidelines (the Guidelines) were issued pursuant to s 44(1)(c) for the assessment of permanent impairment. The Guidelines are based on the American Medical Association’s Guides to the Evaluation of Permanent Impairment (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.[7]
[7] 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.[8]
[8] 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.[9]
[9] 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.[10]
[10] Section 63(3A) of the MAC Act.
The initial Panel comprising Medical Assessor Wing Chan, Medical Assessor Nigel Ackroyd and Member Susan McTegg issued a Direction to the parties on 27 October 2021 (the first Direction) requiring each party to file an indexed, paginated bundle of documents.
In response to this Direction the solicitor for the insurer filed a bundle of documents paginated from pages 1 to 465 and marked AD4.
The solicitor for the claimant filed a bundle of documents paginated from pages 1 to 28 and marked AD6.
Following an objection raised by the insurer as to the expertise of the Medical Assessors, Assessor Nigel Ackroyd recused himself and he was replaced by Medical Assessor Grainge. The decision of the Panel was the subject of a report dated 21 December 2021.
The Panel also informed the parties that absent any objection, the Panel proposed to rely upon the bundle of documents uploaded to the portal by the insurer on 29 November 2021 (AD4) and upon the bundle of documents uploaded to the Portal by the claimant on 14 December 2021 (AD6).
At the request of the Panel the report of Professor Michael O’Rourke dated 21 July 2016 (AD10) and the report of Dr Tanous addressed to Associate Professor Eugene Kotlyar dated 7 August 2014 (AD11) were both uploaded to the portal.
At the request of the Panel the following additional records were uploaded to the portal:
· AD13 – letter from Slater & Gordon dated 25 February 2022;
· AD14 – Pulmonary Function Test Reports for the period 1 January 2020 to the present;
· AD15 – Echocardiogram results for the period 1 January 2020 to the present;
· AD16 – Kariong Medical Centre notes for the period 12 April 2013 to February 2014; and
· AD20 - letter from Dr David Tanous to Dr David Michail dated 7 August 2014 referred to in the letter from Dr Tannous addressed to Associate Professor Eugene Kotlyar dated 7 August 2014.
On 11 February 2022 the Panel agreed an examination was not required.
In the Second Review Panel Report dated 8 March 2022 the Panel informed the parties it did not consider a re-examination of the claimant was required because:
(a) the pulmonary function tests show stability since late 2019 allowing an assessment of permanent impairment;
(b) the echocardiograms are inherently variable due to dependence on image quality. This was commented on by the technicians as ‘difficult’ or ‘very difficult’. Despite this the echocardiogram estimates of pulmonary artery pressure are within expected variation for stability over the repeated studies, allowing an assessment to be made of permanent impairment;
(c) causation of the claimant’s condition can be determined on the available records; and
(d) a medical examination will not contribute meaningfully to either an assessment of causation or the question of permanent impairment which can be assessed based on the pulmonary function tests and echocardiograms.
On 17 March 2022 the claimant’s lawyer advised the claimant had no objection to the matter proceeding without a re-examination of the claimant.
The insurer’s response was set out in a letter dated 28 March 2022 and was in the following terms:
“If the Review Panel intends to apply Table 8 of AMA IV (page 162) for respiratory impairment as Medical Assessor Herman did in his Certificate dated 11 September 2019, the insurer is content for the Review Panel to proceed without re-examination of the claimant.
If the Review Panel intends to assess impairment by analogy and apply Table 12 of AMA IV (page 194) for cardiac arrhythmias as Medical Assessor Haber did in his Certificate dated 12 March 2021, the insurer submits that the claimant will need to be re-examined.”
On 30 March 2022 the Panel informed the parties the Panel proposed to assess the claimant’s impairment using the methodology set out in The Respiratory System, Chapter 5 of the AMA 4 Guides.
Accordingly, the Panel has proceeded to determine the dispute without a medical examination.
BACKGROUND
The claimant was 53 years of age at the date of accident and is now 61 years of age.
On 5 October 2007 Mr Marks was admitted to Gosford Hospital in severe heart failure and was found to be in rapid atrial fibrillation (AF) possibly provoked by a viral infection. He was found to have a dilated left ventricle with a poor ejection fraction (EF) of 20% (N>55%) and was in class 3-4 heart failure. He underwent an electrical cardioversion with successful reversion to sinus rhythm and was commenced on anti-failure therapy in addition to anticoagulation with Warfarin. His ventricle returned to normal, and he was diagnosed as having a "tachycardia related cardiomyopathy".
He was readmitted to Gosford Hospital in July 2010 with a similar problem of rapid AF and left ventricular dysfunction in association with heart failure. His ejection fraction fell to 25% on this occasion and he underwent a transoesophageal echocardiogram (TOE), then cardioversion back to sinus rhythm with re-initiation of his anti-failure and anticoagulant therapy.
By October 2010, his heart size had returned to normal with a low normal function (EF 50-55%) and anticoagulation therapy was ceased.
In September 2011, he was in sinus rhythm, had an ejection fraction of >55% (normal) and was placed on a "watch and wait approach" to assess for further arrhythmia.
Mr Marks was admitted to Royal North Shore Hospital (RNSH) between 29 March 2013 and 15 April 2013. A CT pulmonary angiogram showed a large nonocclusive pulmonary embolus in the main right pulmonary artery and on the left side. He underwent anticoagulant therapy.
A perfusion scan on 27 June 2013 showed bilateral pulmonary emboli.
Apparently, 2 subsequent CT pulmonary angiograms indicated that the emboli were improving but he remained on Warfarin until the accident on 23 February 2014.
On 23 February 2014 Mr Marks was riding his motorcycle wearing a helmet, leather jacket, gloves, jeans, and biker boots. He was riding his motor bike on Pennant Hills Road in the middle lane at 60 kmph. A vehicle in the right-hand turning lane suddenly merged into his lane. He braked heavily and laid the bike down on its side and pushed it away from him to avoid the accident. He reported that he hit the ground heavily and rolled along the road. When he stopped, he felt pain in his left chest and shoulder.
Mr Marks was admitted to Westmead Hospital with pain in the left hemithorax with a trauma CT revealing eight fractured ribs on the left side, a left haemothorax, bilateral aspiration and bilateral small pleural effusions.
He required non-invasive ventilation and patient controlled analgesia but on 24 February, developed acute hypoxia and required intubation for hypoxic respiratory failure and treatment of pneumonia.
On 6 March 2014, he developed recurrent hypoxia and transient left sided weakness and was transferred back to the Intensive Care Unit (ICU). He was shown to have acute left sided pulmonary emboli with chronic right sided pulmonary embolus and signs of pulmonary arterial hypertension.
A CT brain revealed a right parietal lobe infarct and a transoesophageal echo showed evidence of thrombus passing from the inferior vena cava through the right atrium and via a patent foramen ovale into the left atrium.
A lower limb ultrasound on 21 March 2014 revealed a non-occlusive thrombus at the right proximal posterior tibial vein with a transoesophageal echo performed on 26 March 2014 revealing complete resolution of his thrombus crossing the patent foramen ovale.
Further problems in hospital included obstructive sleep apnoea requiring CPAP, aspiration pneumonia, a left pneumothorax, hypomagnesaemia, AF and brittle type 2 diabetic control.
Mr Marks was diagnosed with chronic thromboembolic pulmonary hypertension (CTEPH).
On 7 April 2016 he had pulmonary endarterectomy with removal of clots from his lungs. He was an inpatient at St Vincent’s Hospital for about 5 ½ weeks.
A personal injury claim form dated 8 August 2014 was lodged by the claimant with the insurer.
A dispute arose between the parties as to permanent impairment and the claimant filed an application for assessment of a permanent impairment dispute.
Medical Assessor Mark Burns issued a certificate dated 5 May 2017 in which he assessed a 4% whole person impairment (WPI) arising out of the following injuries caused by the accident:
(a)right thumb - soft tissue injury;
(b)left shoulder-soft tissue injury;
(c)left knee - patellofemoral crepitus and tenderness; and
(d)scarring - left elbow, left and right knees.[11]
[11] AD4 P 38.
Medical Assessor Mark Burns issued a certificate dated 4 December 2017. He concluded the following injuries were caused by the accident:
(a) fractured left ribs with bilateral pneumotharaces; and
(b) cardiorespiratory injury with atrial thrombus, pulmonary emboli and cerebrovascular emboli.
Assessor Burns expressed the following opinion as to diagnosis and causation:
“Mr Marks fractured multiple left sided ribs in the motor vehicle accident and also sustained bilateral pneumothoraces. Due to the presence of previously undiagnosed congenital condition, patent foramen ovale he developed clotting in the heart, which resulted in pulmonary emboli as well as the clot crossing over through the patent foramen ovale to give him cerebrovascular emboli.”
Assessor Burns concluded the claimant’s condition had not stabilised, noting it was recommended that he undergo the insertion of several stents. Assessor Burns also recommended further records be obtained and that the assessment be carried out by either a cardiologist or a cardiothoracic surgeon given the complex nature of the claimant’s medical condition.
The claimant was subsequently assessed by Medical Assessor Herman who issued a certificate dated 11 September 2019. He certified a 27% WPI as a result of the following injuries caused by the accident:
(a) CTEPH;
(b) fractured ribs with left lung injury;
(c) cardiorespiratory injury with clot formation; and
(d) pulmonary emboli and cerebrovascular emboli.
The insurer sought a review of the certificate of Medical Assessor Herman on the basis that Assessor Herman did not offer reasons as to how or why the post-accident emboli were attributable to the accident having identified a cardio-vascular history back to 2007. [12]
[12] AD4 p 21.
The Proper Officer dismissed the application for review on 17 December 2019.
On 16 September 2019 Medical Assessor Nathan Eddy issued a combined certificate certifying a combined permanent impairment of 30%.
The insurer filed an application for a further assessment of permanent impairment having obtained the following additional records relating to the claimant’s pre-accident treatment:
· medical records produced by RNSH pertaining to the claimant's admissions there on 29 March 2013 and treatment on 27 June 2013;
· a report of a lung CT scan performed on 27 June 2013; and
· a report of Professor Michael O’Rourke dated 21 February 2020.
The Proper Officer accepted the insurer’s application for further assessment and the matter was referred to Medical Assessor Haber.
MEDICAL ASSESSMENT UNDER REVIEW
The following injuries were referred for assessment:
(a) CTEPH;
(b) fractured ribs with left lung injury; and
(c) cardiorespiratory injury with clot formation and pulmonary emboli and cerebrovascular emboli.
Medical Assessor Haber issued a certificate dated 12 March 2021 in which he certified the injures referred for assessment gave rise to a permanent impairment of 25%.[13]
[13] AD4 p 66.
Medical Assessor Haber obtained the following history from Mr Marks:
“In October 2007 he had high BP 255/160 and had severe cardiac failure and AF for which he had successful cardioversion LVEF was 20%.
In 2009 he had a similar episode of heart failure and AF, which again responded to cardioversion. Treatment was stopped after one year.
In March/April 2013, while at work he did not feel well and did not look well He was inpatient at RNSH for two weeks treated with heparin and warfarin for clot in the right lung coming from clot in the right leg. He also had two small clots in the left lung. He claims that after this he played golf at least once a month.”
Assessor Haber determined:
“As result of the accident, he had recurrence of atrial fibrillation with clots travelling through foramen ovale and causing cerebral infarct from which he has recovered. However, he also developed new pulmonary emboli increasing his pulmonary hypertension.
Based on AMA4 Guide he can be assessed by analogy, considering especially as he has atrial fibrillation, by a table 12 for assessment of cardiac arrhythmias in class 3 on page 194 as he has symptoms in spite of use of drugs. I consider that he has currently 40% WPI.
Prior to the accident he had symptoms affecting his respiration by his morbid obesity, sleep apnoea as well previous pulmonary emboli and atrial fibrillation. Based on similar analogy his pre-accident WPI can be assessed by class 2 page 194 in AMA4 Guide at 15%.”
EVIDENCE BEFORE THE REVIEW PANEL
Pre-accident medical history
Mr Marks had problems with deep vein thrombosis and pulmonary emboli prior to the accident.
In a report dated 5 November 2007 Dr Fraser Bates, cardiologist stated he reviewed
Mr Marks following his discharge from hospital with peptic ulcer disease, renal calculi, and paroxysmal AF and cardiomyopathy.[14] He noted Mr Marks had remained well following discharge, had lost all his breathlessness and remained at a dry weight of106 kg. His Warfarin dosage was still being adjusted. On examination he was in sinus rhythm and there was no evidence of cardiac failure.[14] AD4 P 88.
An echocardiography report dated 5 October 2007 reported:
“Mildly dilated LV. Severe global impairment of LV systolic function. Mild mitral regurgitation. Moderate to severe pulmonary hypertension.”[15]
[15] AD 4 p 90.
An echocardiogram report from Central Coast Cardiac Services Pty Ltd dated 8 November 2007 reported as follows:
“1. Borderline dilated left ventricle with normal systolic function now in sinus rhythm.
2. No significant valvular abnormalities.[16]
[16] AD4 p 89.
In a report dated 5 December 2007 Dr Bates reported the claimant was back in sinus rhythm, things had almost normalised, and he did not think it necessary to further evaluate the claimant for coronary disease.[17]
[17] AD4 p 91.
A 2D echocardiogram on 22 April 2008 reported no significant valve disease, normal biventricular size and function and mildly dilated left atrium.[18]
[18] AD4 p 92.
On 6 May 2008 Dr Bates reported Mr Marks was asymptomatic from a cardiac point of view, and he had returned to all normal activities even Rugby Union whilst still taking Warfarin 14 mg daily.[19] Dr Bates noted the cardiomyopathy had resolved and concluded it was “related to the atrial fibrillation with rapid ventricular rates and possibly initially precipitated by a viral respiratory tract infection”.
[19] AD4 p 93.
On 26 July 2010 Mr Marks was admitted to Gosford Hospital with AF and recurrent heart failure. Dr Bates provided a report dated 2 August 2010 in which he referred to the claimant’s admission to hospital with shortness of breath.[20] He was cardioverted back to sinus rhythm and with no clinical or radiological evidence for heart failure, his cardiac medication was left unchanged, although following review by the diabetic team he was commenced on insulin.
[20] AD4 p 95.
Mr Marks was reviewed by Dr Bates on 13 September 2011 when it was noted he had not experienced AF since the last review in November 2010.[21] On examination he was in sinus rhythm and his weight was reported to be around 147 kg.
[21] AD4 p 99.
Mr Marks was hospitalised at RNSH between 29 March 2013 and 12 April 2013 after presenting with shortness of breath. It was also noted that his chronic right lower limb ulcer appeared cellulitic. At the time of his discharge from the ICU the impression was of “a large pulmonary embolism, with concomitant infection either from a chest source or due to his right leg cellulitis, with rapid AF precipitated by the infection”.[22]
[22] AD4 p 395.
He was treated with Clexane and Warfarin and was discharged after his Warfarin was considered to be therapeutic.[23]
[23] AD4 p 272.
Mr Marks underwent a CT Pulmonary Angiogram on 29 March 2013 at RNSH.[24] The clinical history included severe shortness of breath and saturation 88% on room air. The conclusion was as follows:
“Large, non-occlusive PE in the right main pulmonary artery with complete occlusion of posterobasal and medial basal segmental arteries. Tiny nonocclusive PE in the right middle lobe artery.
Right posterobasal "mass" like consolidation is likely secondary to the posterobasal PE, ie. Pulmonary infarction.”
[24] AD4 p 236.
A Venous Duplex Scan for DVT conducted on 30 March 2013 found no evidence of major axial or deep calf vein thrombosis.[25]
[25] AD p 268.
A transthoracic echocardiography report dated 30 March 2013 concluded as follows:
“Technically difficult study due to body habitus.
Atrial fibrillation.
Normal left ventricular size. Mild diffuse hypokinesis. Normal wall thickness.
Mildly dilated right ventricle. Moderate hypokinesis.
Moderate left atrial dilation.
Mild right atrial dilation.
Mildly thickened posterior mitral leaflet with trivia regurgitation.
Trivial tricuspid regurgitation within normal limits. Tricuspid regurgitant Jet velocity not analysable for calculation of pulmonary artery systolic pressure.”[26]
[26] AD4 p 271.
On 27 June 2013 Mr Marks underwent a ventilation and perfusion (Technegas) CT scan.[27] It was reported there were multiple pulmonary emboli present throughout both lung fields.
[27] AD4 p 73.
Mr Marks continued taking Warfarin until the accident on 23 February 2014.
Post-accident medical history
The Ambulance report recorded:[28]
"On examination, alert and orientated, pupils equal and react to light. Denies any neck discomfort at rest/palpation, denies any sensory loss, good strength in upper limbs."
"Speaking full sentences, rapid breathing, equal/adequate air entry all lung fields, saturation approximately 90% on oxygen, essentially regular pulses. Pain increases on deep inspiration/chest movement/position/left arm movement."
"Abrasion to right lateral stomach, nil pelvis or lower limb pain.
Patient declined neck collar..."
[28] AD4 p77.
Mr Marks was admitted to Westmead Hospital between 23 February 2014 and 2 April 2014. The Respiratory Med Discharge Referral provides the following summary of treatment at the hospital:[29]
“After arrival in ED on 23/2/14, Mr Marks had a CT - trauma series demonstrating his injuries as detailed above (rib fractures, small left pneumothorax, bilateral aspirations, bilateral pleural effusions and small pneumomediastinum. He was admitted to the high dependency unit on non-invasive ventilation (NIV) and patient controlled analgesia (PCA).
On 24/2/14 Mr Marks had two ALS calls for hypoxia and was transferred to ICU for hypoxic respiratory failure where he was intubated and also received a thoracic epidural for pain management. Treatment for pneumonia was also started in ICU. After extubation and removal of his epidural he was stepped back down to HDU on 4/3/14 on NIV and HFNP (high flow nasal prongs).
On 6/3/14 (within 24 hours of step down) he had another ALS call for hypoxia and transient left sided weakness and was transferred back to ICU where he was again intubated. A subsequent CTPA showed an acute left sided pulmonary embolus (PE) with chronic right sided PE with signs of pulmonary arterial hypertension. A CT Brain showed right parietal lobe infarct. A transoesophageal echo (TOE) showed a thrombus starting in the IVC passing through the right atrium, through a patent foramen ovale into the left atrium. A lower limb ultrasound also showed a right posterior tibial vein (below knee) deep vein thrombosis. After consultation with the cardiothoracic and haematology teams, the thrombi were treated conservatively with anticoagulation and insertion of an IVC filter on 7/3/14. He was extubated on the 9/3/14 but remained on nocte CPAP due to newly diagnosed OSA. He was stable throughout the rest of his stay in ICU. He was stepped out of ICU to high dependency on 18/3/14.
Mr Marks had a Lower limb ultrasound on 21/3/14 demonstrating interval extension of non-occlusive thrombus at the right proximal posterior tibial vein into the popliteal vein since previous US.
Mr Marks had a follow up TOE on 26/3/14 that showed complete resolution of his thrombus. His IVC filter was removed on the 31/3/14 without complication.
Mr Marks remained stable on the wards until discharge on 2/4/14.”
[29] AD4 p 108.
Mr Marks underwent a CT pulmonary angiogram on 14 July 2014 which demonstrated residual thrombus and a probably right lower lobe pulmonary infarct.[30]
[30] AD4 p 153.
Mr Marks was reviewed by cardiologist Dr Tanous on 7 August 2014[31]. In a report to Associate Professor Eugene Kotlyar, he stated:
“He has extensive thromboembolic changes in the right lung and echocardiographic changes of pulmonary hypertension. Whilst other factors such as obesity, sleep apnoea and diastolic dysfunction may be playing a role, it is likely that the previous pulmonary emboli are the major player. Glen also has a patent foramen ovale which may be contributing to some hypoxia but is allowing a blow off for the right ventricle”.
[31] AD 11.
Dr Tanous opined that CTEPH was the result of a combination of pre-existing conditions and injuries sustained in the accident.
Mr Marks was reviewed by Dr Bates on 14 April 2014.[32] His weight was 158.8 kg. He noted the history of admission to Westmead Hospital following the accident. He stated from a cardiac point of view Mr Marks had AF which was well rate controlled and symptomatic.
[32] AD4 p 100.
A CT chest on 24 October 2014 reported:[33]
“Round atelectasis, Chronic right lower lobe pulmonary embolus, right pleural effusion and adjacent soft tissue mass? unchanged from the previous study.”
Medico-legal reports
[33] AD4 p 155.
Dr Richard Sekel
Dr Sekel, consultant in occupational medicine, reviewed the claimant at the request of the insurer and provided a report dated 17 November 2015.[34]
[34] AD4 p 438.
After outlining Mr Marks pre-accident medical history Mr Sekel reported he had returned to all normal hours of all normal operational police duties by 10 May 2013 and continued to work normal hours until the accident. He also reported Mr Marks had played his last game of the competition rugby season in late August or early September 2013 and by late January 2014 he had resumed rugby union training.
Dr Sekel reported Mr Marks had worked as a Police Officer since April 1984 having attained the rank of sergeant. At the time of the accident the claimant weighed 183 kg but “was still active, but slower”. In addition to playing Rugby Union Mr Marks also played golf once or twice a fortnight before the accident. Mr Marks informed Dr Sekel that he continued to experience breathlessness with mild exertion and intermittent AF.
Dr Sekel noted Mr Marks had experienced intermittent AF for several years before the accident. He concluded beyond the initial post-accident deep vein thrombosis and pulmonary emboli, the current intermittent cardiac condition was unrelated to the accident.
Dr Sekel noted Mr Marks had significant problems with deep vein thrombosis and pulmonary emboli before the accident. He noted the condition had clearly continued with Mr Marks continuing to take Warfarin at the time of the accident. Dr Sekel further commented:
“However, based on the available evidence, it appears that his protracted time in hospital resulted in formation of further deep vein thrombosis in his right calf, with multiple pulmonary emboli. However, it is again outside of my area of expertise to comment further on the apportionment of causation of his post-MVA respiratory conditions (possible aspiration pneumonia, possible pulmonary hypertension and pulmonary emboli), between (a) conditions before the accident and (b) conditions after the subject accident.”
Professor O’Rourke
The insurer obtained an expert opinion from Professor Michael O’Rourke who undertook a file review and provided a report dated 21 July 2016 (AD10).
Professor O’Rourke recognised the claimant’s pre-existing condition, stating at page 4 of his report:
“Mr Marks current complaints and disabilities are of breathlessness and chest pain. These complaints are largely due to previous cardiac problems of cardiomyopathy and cardiac failure precipitated by episodes of atrial fibrillation. He also had predisposition to pulmonary embolic disease with first manifestations one year prior to his MVA in February 2014. Mr Marks predisposition to cardiovascular disease and its symptoms are exaggerated by his morbid obesity (BMI >44) and diabetes mellitus which preceded the MVA by many years.”
In response to the question “If you consider the claimant suffers from a recognised condition or injury, do you consider that there is a causal link between the claimant’s condition and the subject motor accident?” he stated:
“Yes. Mr Marks suffered significant trauma to the left side of his chest, with flail segments from multiple rib fractures, followed by impaired ventilation, infection, hypoxia and hypercarbia with need for artificial ventilation for prolonged periods – up to 5 weeks in all. Enforced immobility predisposed to thromboembolic disease, as did pre-existing conditions which include cardiomyopathy, atrial fibrillation and morbid obesity.”
Professor Michael O’Rourke provided a further report dated 21 February 2020.[35]
[35] AD4 p 460.
Professor O’Rourke commenting on the claimant’s hospitalisation in 2007 stated:
“Initial cause of left ventricular failure was considered to be the rapid heart contraction of circa 150 beats/minute, since no other cause was apparent, and heart failure improved and soon became quite normal when the atrial fibrillation was terminated by cardioversion and appropriate drug therapy. A viral cause of cardiomyopathy was considered but excluded. He was anticoagulated with Warfarin to prevent thrombo-embolism, and this was continued until 2010 when he remained in normal sinus rhythm with no heart failure. Warfarin was considered undesirable because he wanted to continue rugby, with risk of trauma and haemorrhage in “contact” sporting activity. At this time other problems were identified. His blood pressure was high and warranted lowering, he was morbidly obese, and he showed kidney insufficiency, had sleep apnoea and developed diabetes mellitus which proved difficult to control. His weight remained in the morbidly obese range. While he remained in sinus rhythm, left ventricular ejection fraction improved but he did show evidence of pulmonary hypertension, with right ventricular systolic pressure calculated as 58mmHg (normal 25mmHg) at echocardiography in 2007. There was no evidence of thrombo-embolic events, he had to be considered at risk.”
And as to events of 2010 he reported:
“A second episode of atrial fibrillation required cardioversion in 2010. Anticoagulant was recommenced but ceased in 2010 because of his participation in rugby as a competitive athlete at age 50, was considered risky.”
And as to events in 2013 he reported:
“Pulmonary embolism from deep vein thrombosis was suspected and confirmed by angiography. There was extensive involvement of the right lung and a large area of pulmonary infarction at the right base. He was treated with Warfarin and antibiotic and improved. He remained morbidly obese however with obstructive sleep apnoea and poorly controlled diabetes. Warfarin was continued. Mr Marks returned to football training.”
Professor O’Rourke noted Mr Marks had evidence of pulmonary hypertension and right heart failure from thrombo embolic disease in 2013, and he noted pulmonary hypertension had been in evidence in 2007. In considering the assessment of Medical Assessor Herman, Professor O’Rourke noted he had failed to factor in the contribution of diabetes mellitus, morbid obesity, and obstructive sleep apnoea in his calculation of WPI.
Professor O’Rourke was sceptical about the claimant’s participation in football, having regard to the severity of his disease, his age, his morbid obesity, and his treatment with Warfarin. He expressed the view that CTEPH is a chronic condition and once it has occurred, it is likely to recur. Professor O’Rourke also noted that the lung scan report of June 2013 indicated widespread pulmonary emboli to both lungs from deep vein thrombosis in one or both legs, confirmed by blood oxygen saturation.
Associate Professor Richards
The claimant relies upon a report of Associate Professor David Richards, cardiologist dated 21 October 2020.[36]
[36] AD6 p 1.
He noted the history of obesity and possibly of sleep apnoea, which in his opinion predisposed Mr Marks to AF. He noted his history of AF and cardiac failure in 2007 and in 2010. He noted in March 2013 Mr Marks was admitted to hospital because of deep venous thrombosis and bilateral pulmonary emboli. Specifically, he reported the ventilation perfusion scan of 27 June 2013 showed emboli in both the right and left lungs, although he also reported Mr Marks apparently improved following that admission and may have been able to resume competitive football.
Associate Professor Richards noted the details of the accident on 23 February 2014. He stated:
“It was not until 5 March 2014 that Mr Marks experienced transient left sided weakness and slurred speech due to right parietal lobe thromboembolism. A transoesophageal echocardiogram the following day revealed thrombus straddling the interatrial septum, likely associated with paradoxical systemic embolization. It is my view that it was only likely that the atrial septal defect was present from birth….”
He concluded the claimant had recovered from the pulmonary embolism in 2013 and had sustained new pulmonary embolism as a consequence of relative immobilisation after the accident leading to new deep venous thrombosis. He stated:
“Systemic arterial thromboembolism after the motorcycle accident 23 February 2014 likely occurred because of a systemic venous clot crossing the atrial septum (atrial septal defect present since birth).”
On the basis Mr Marks had no WPI immediately prior to the accident he concluded the WPI was due to the accident and assessed a 25% WPI.
SUBMISSIONS
Insurer’s submissions
The insurer provided submissions dated 25 October 2019 in support of the application for review of the certificate of Medical Assessor Herman dated 11 September 2019.[37]
[37] AD4 p 21.
The insurer submitted Assessor Herman failed to consider whether the pre-accident emboli were present and contributed to the injuries sustained by the claimant and failed to make an apportionment in respect of any pre-existing condition. The insurer submitted that CTEPH was the result of a combination of pre-existing pulmonary embolus in the right lung and non-accident-related factors including obesity, type II diabetes, sleep apnoea, hypertension, hypercholesterolaemia, family history and diastolic dysfunction.
The insurer submitted Assessor Herman failed to properly apply the Guidelines or the AMA4 Guides. Assessor Herman used an “analogy method” to assess permanent impairment but failed to provide any “rationale” for his choice of this methodology in accordance with clause 124 of the Guidelines.
Whilst Assessor Herman used Table 8 at page 162 of the AMA4 Guides to assess permanent impairment the insurer submitted he failed to either apply or explain the measurements he used to assess the claimant or to place him in Class 2.
The insurer provided submissions dated 26 February 2020 in support of the insurer’s application for a further assessment of permanent impairment. Those submissions hinge on the report of the lung CT scan performed on 27 June 2013 and the report of Professor O’Rourke addressing that evidence. The insurer submits the scan report provides evidence of pulmonary emboli to both lungs in 2013 as well as in 2014. Indeed, the insurer submits there is clear evidence that CTEPH was present since 2007.
The insurer provided submissions dated 15 April 2021 in support of the application for review of the certificate of Medical Assessor Haber. Insofar as the submissions address the task to be undertaken by the Review Panel the insurer submits:
(a) the assessment should address pulmonary function rather than AFs;
(b) if the assessment is to be undertaken by analogy to cardiac arrhythmias (as per Assessor Haber) as opposed to the assessment of respiratory impairment via Table 8 (as per Assessor Herman) the Assessor is required in accordance with Clause 1.24 of the Guidelines to explain the reason assessment by analogy is appropriate and the rationale for the methodology chosen for assessment; and
(c) in undertaking the assessment, a Medical Assessor must consider whether the post-accident embolic were part of a pre-existing and unbroken clinical trajectory, noting the CT scan of the lung dated 27 June 2013 evidenced widespread pulmonary emboli to both lungs prior to the accident.
Claimant’s submissions
The claimant provided submissions in reply to the application by the insurer for a review of the certificate of Medical Assessor Herman.[38]
[38] AD6 p 8.
The claimant submitted that Assessor Herman correctly applied the New York Heart Association criteria in the absence of relevant criteria under AMA4. For instance, Assessor Herman stated on page 6 of his certificate:
“Mr Marks is currently functionally Class 2 by the NYHA classification system i.e. he reports mild dyspnoea on moderate activity and would be able to achieve 5.7 – 7.1 METS of energy expenditure.”
Assessor Herman further explained:
“He does have moderate residual pulmonary hypertension. I have therefore used the high end of the WPI range given his multiple surgeries and moderate residual pulmonary hypertension. Utilising Table 8 of the AMA 4 Guide on page 5/162 The respiratory system, he falls in Class 2, 10 – 25%, mild impairment of the whole person.”
The claimant submitted that Assessor Herman considered the claimant’s “historical cardiovascular disease” having regard to the following comment which appeared on page 3 of his certificate:
“Importantly, Mr Marks was asymptomatic from his pulmonary embolis prior to the motor vehicle accident and had returned to playing competition rugby until September 2013. He had, in fact, returned to rugby training in late 2014, shortly before his motorcycle accident.”
The claimant provided submissions dated 25 March 2020 in response to the insurer’s application for further medical assessment.[39] It was that application which led to the assessment by Medical Assessor Haber.
[39] AD6 p 16.
The claimant points out that he was not admitted to hospital on two separate occasions in 2013 as suggested by the insurer. The CT lung scan performed on 27 June 2013 was an investigation carried out on an outpatient, follow-up visit by Mr Marks, at the request of the treating specialist, Dr Christopher Dennis.
The claimant refers to the report of Professor O’Rourke dated 21 July 2016 where he causally linked the claimant’s condition to the accident.
The claimant points out that there is no suggestion from his 2020 report that
Professor O’Rourke had changed his opinion as to causation. The claimant also highlights the lack of evidentiary support for the doubts expressed by
Professor O’Rourke about the claimant’s return to training for rugby prior to the accident.The claimant’s submissions dated 13 May 2021 respond to the insurer’s application for review addressing each of the grounds of review but do not otherwise add to the submissions set out above.[40]
[40] AD6 p 20.
RELEVANT LEGAL AUTHORITY
Causation of injury is addressed in the Guidelines:
“1.5 An assessment of the degree of permanent impairment is a medical assessment matter under Section 58 (1)(d) 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.”
In Wingfoot Australia Partners Pty Ltd v Kocak Harrison AsJ at [57] confirmed that a Review Panel has “an obligation to set out its actual path of reasoning so as to enable a reader to determine whether it fell into error”. [41]
[41] [2013] HCA 43; (2013) 252 CLR 480, Wingfoot.
DETERMINATION
The fractured ribs themselves do not result in any assessable impairment in accordance with clause 1.23 of the Guidelines.
Regarding Mr Marks’ AF, the Panel noted the following:
(a) Mr Marks had rapid AF as far back as October 2007 when he was admitted to Gosford Hospital under Dr Bates[42]. He had AF and heart failure. He was treated with cardioversion which reverted his rapid heart rate and abnormal heart rhythm back to normal (sinus rhythm);
(b) he had other medical conditions - high blood pressure, he was very overweight, and he had Type 2 diabetes which could affect the management of AF;
(c) with AF, the contraction of the heart muscles became erratic and unco-ordinated. Blood not completely pumped out of the atria can remain and may pool in the atria to clot. Hence, he was treated with Warfarin, an anticoagulant. The Warfarin makes the blood less likely to form clots and keeps clots from getting bigger. However, Warfarin does not break up a clot that has already formed, clot degradation occurs as a result of natural body function over time;
(d) three years later, Mr Marks was readmitted to Gosford Hospital in July 2010 with a similar problem of rapid AF and left ventricular dysfunction in association with heart failure. He underwent a cardioversion and his heart’s rhythm was back to sinus rhythm. He was treated with anticoagulant therapy and medications for his heart failure;
(e) when Dr Bates reviewed him on the 13 September 2013[43] Mr Marks did not have AF, his ECG showed sinus rhythm with normal left ventricle function on echo. Dr Bates discussed with him the use of “Trambocor to try to prevent AF or simply watch and wait until the next episode”. He chose the “watch and wait” option;
(f) on 29 March 2013 Mr Marks was brought to RNSH “Emergency by ambulance with sudden onset of shortness of breath and rigors whilst at work. He was noted to be febrile to 38.9 degrees, dyspnoeic with respiratory rate of 40/min and in rapid AF at a rate of 137. The chronic right lower limb ulcer appeared cellulitic”.[44] A CT pulmonary angiogram showed a large nonocclusive pulmonary embolus in the main right pulmonary artery.[45] The Panel noted that on admission to RNSH, he had medications to treat his hypertension, diabetes and lipidaemia. However, he was not on any anticoagulant;
(g) he was anticoagulated with Warfarin and was discharged from RNSH on 12 April 2013 when the International Normalised Ratio (INR) used to monitor Warfarin treatment was satisfactory.[46] In addition, he was prescribed Metoprolol to treat his AF;
(h) on 27 June 2013 Mr Marks had a Ventilation and Perfusion CT scan which reported that there were pulmonary emboli in his left lung in addition to the right lung.[47] There was no evidence of left sided pulmonary emboli in the CT Pulmonary Angiogram (CTPA) performed at RNSH in March 2013. The Panel noted the following comment in the report: “The patient states he was sub-therapeutic for some time following this and perhaps the left sided emboli occurred during this time period.” (12 April 2013 to 27 June 2013). The ‘sub-therapeutic’ refers to the Warfarin dose being sub-therapeutic with respect to anticoagulation of his blood; and
(i) the Panel received the requested Kariong Medical Centre’s clinical notes.[48] The clinical notes confirm that Mr Marks had been prescribed Metoprolol by his GP to manage his AF and he had regular INR done to monitor his Warfarin treatment after his discharge from the RNSH, up until 18 February 2014, a few days before the accident. Hence, before the accident,
Mr Marks had AF which was treated with Metoprolol, and he was also taking Warfarin.[42] AD4 p 88.
[43] AD4 p 99.
[44] AD4 p 395.
[45] AD4 p 236.
[46] AD4 p 272.
[47] AD4 p 73.
[48] AD16.
Based on the preceding documented medical evidence, Mr Marks had pre-existing AF (a cardiac arrhythmia) and was on medication before the accident to treat the AF. The accident did not cause the AF. The AF could have temporarily been affected by the accident and required some time to stabilise after the accident.
As the AF was not causally related to the accident, it is not appropriate to assess the degree of permanent impairment of his injuries due to the accident using AF. The Panel disagreed with Assessor Haber’s assessment by analogy using AF and Table 12 on page 195 of the AMA 4 Guides for the assessment of cardiac arrhythmias.
Regarding the pulmonary emboli and the development of CTEPH, the Panel considered the following:
(a) in the ‘Personal Injury Claim Form’ Mr Marks described the accident: “I skidded onto my Left side I fell off my bike causing my bike to skid & impact with vehicle (1). Vehicle (1) at fault & infringed by police. As a rider I was severely injured”;[49]
(b) Mr Marks had fractured numerous left ribs and had a left haemothorax with bilateral aspirations[50] after the accident in addition to the other injuries detailed in the medical certificate.[51] He was admitted to Westmead Hospital’s High Dependency Unit (HDU) for non-invasive ventilation (NIV) and patient controlled analgesia (PCA);
(c) on 24 February 2014 Mr Marks had two alarms for hypoxia and was transferred to the ICU for hypoxic respiratory failure where he was intubated and also received a thoracic epidural for pain management. Treatment for pneumonia was also started in ICU. After extubation and removal of his epidural he was stepped back down to HDU on 4 March 2014;
(d) on 6 March 2014 (within 24 hours of step down) he had another alarm call for hypoxia and transient left sided weakness and was transferred back to ICU where he was again intubated;
(e) a CTPA performed on 6 March 2014 showed an acute left sided pulmonary embolus (PE) with chronic right sided PE with signs of pulmonary arterial hypertension.[52] A Transoesophageal echo (TOE) showed a thrombus starting in the IVC passing through the right atrium, through a patent foramen ovale into the left atrium of the heart;
(f) a lower limb ultrasound (venous doppler) performed on 7 March 2014 also showed a right posterior tibial vein (below knee) deep vein thrombosis;[53]
(g) the blood clots (thrombi) were treated conservatively with anticoagulation and insertion of an IVC filter on 7 March 2014;[54]
(h) he was extubated on 9 March 2014 and was stepped out of ICU to HDU on the 18 March 2014;
(i) a follow up TOE on 26 March 2014 showed complete resolution of his thrombus. His IVC filter was removed on 31 March 2014 without complication; and
(j) Mr Marks had nearly two weeks of immobilization in the HDU and ICU ward. The immobilisation had contributed substantially to the formation of thrombi in the IVC and in his right posterior tibial vein.
[49] AD4 p 5.
[50] AD4 p 108.
[51] AD4 p 14.
[52] AD4 p 140.
[53] AD4 p 142.
[54] AD4 p143.
Based on the above contemporaneous medical evidence, Mr Marks had injuries to his chest sustained in the accident. In the course of treatment of his chest injuries, the nearly two weeks of immobilisation in the HDU and ICU at Westmead Hospital contributed substantially to the development of blood clots (thrombi) in his IVC and right posterior tibial vein. The thrombi had travelled to the right atrium of the heart and via the pulmonary artery into the lungs to result in pulmonary embolism. The Panel is of the opinion that Mr Marks had acute left sided PE and pulmonary arterial hypertension causally related to the accident.
As such it is appropriate to assess the degree of permanent impairment due to ‘chronic thromboembolic pulmonary hypertension’. The Panel considers the use of the Respiratory System, Chapter 5, of the AMA 4 Guides as the correct methodology to adopt to assess Mr Mark's CTEPH.
Mr Mark’s pulmonary function tests performed at Westmead Private Hospital from 2014 until 2021 are given in the table below:
Date Performed
FVC(L)
FEV1(L)
DLCO (ml/min/mmHg)
16/6/2014
3.77
2.93
27.58
24/10/2018
3.74
2.95
25.56
6/2/2019
3.89
3.09
21.20
6/8/2019
3.59
2.82
20.22
19/2/2020
3.58
2.80
19.13
28/7/20
3.12
2.35
16.73
18/1/21
3.59
2.82
17.58
19/4/2021
3.55
2.79
17.99
Mr Mark’s pulmonary function testing has been stable within the expected variance of testing from mid-2019. As such he has reached maximum medical improvement and can be assessed for permanent impairment.
Using Respiratory System, Chapter 5, of the AMA 4 Guides to assess Mr Mark’s CTEPH in conjunction with the pulmonary function tests undergone by Mr Marks on 19 April 2021 his WPI can be calculated based on his age of 60 years and his height of 182cm.
Mr Mark’s FEV1 is 2.79L, predicted being 3.88L and the lower limit of normal (LLN) being 3.038L. The FEV1 is below the LLN and is 72% of predicted. Mr Mark’s FVC is 3.55L, predicted being 4.99L and the LLN being 3.875L. The FVC is below the LLN and is 71% of predicted. Mr Mark’s DLCO is 17.99, predicted being 35.7 and LLN being 27.5. The DCLO is below the LLN and 50% of predicted.
Using Table 8 in Respiratory System, Chapter 5, of the AMA 4 Guides, the DLCO measurement places Mr Marks in Class 3 impairment of the whole person, giving a range of impairment of between 26% and 50%.
Given the description of Mr Marks’ symptoms and taking reference to other investigations such as repeated cardiac echocardiograms, CT scans of the chest and ventilation perfusion scanning we place Mr Marks’ WPI in the middle of the range given, at 40%.
Pre-existing/subsequent impairment
When considering pre-existing impairment, prior to February 2014, note was taken of the CT scan dated 27 June 2013 showing widespread pulmonary emboli, echocardiograms showing pulmonary hypertension and the history of some functional impairment.
The best way to determine a pre-existing deduction would be a set of pulmonary function tests including DLCO taken between 2013 (the episode of pulmonary embolus) and the date of the accident in 2014. It appears that such testing was not performed. As such, there is no objective evidence of a reduction in DLCO prior to 2014, although there most certainly would have been one.
The Panel proposes to use the DLCO measurement taken on 16 June 2014, the first since the accident, as a baseline. Where Mr Marks’ DLCO prior to February 2014 would not have been worse than this, an assessment of permanent impairment at that time, and hence a pre-existing impairment can be calculated. Using Table 8 in the Respiratory System, Chapter 5, of the AMA 4 Guides, the DLCO measurement from 16 June 2014 of 27.58 places Mr Marks in class 2 impairment which has a range of impairment of between 10% and 25%.
As this data is actually from after the accident of February 2014, and considering his functional impairment at the time, we place Mr Marks at the lower point of Class 2 impairment and assess a 15% WPI. It is recognised that this method of calculation is imperfect, but there is no better data available to assess the pre-existing impairment.
Adjustment for the effects of treatment
Mr Marks will require lifelong treatment; withdrawal of such treatment will result in substantial risk of deterioration in his condition. Lifelong therapy comes with lifelong risk of side effects and complications of treatment. As such the Panel determines there to be an additional 3% WPI for the effects of treatment.
Calculation of whole person impairment
Calculation of WPI:
(a) pre-existing impairment prior to 23 February 2014 15%;
(b) current whole person impairment 40%; and
(c) adjustment for the effects of treatment 3%.
Applying the Combined values chart the current WPI taking into account the effect of treatment is 27%.
The panel finds that the accident caused the claimant to suffer injuries, namely acute left sided pulmonary embolism and pulmonary arterial hypertension which has resulted in a WPI of 27%.
0
2
2