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MEDICAL REPORT ON

MR. THEODORE BELL


DATE OF BIRTH: 17.06.1938
188 FABIAN ROAD, ESTON, MIDDLESBROUGH. TS6 9RN
SOLICITORS’ REFERENCE: GS/JAC/BEL126/1 (Macks)

1. Dr. Stephen Anthony Murphy. Qualifications: MD, FRCP, Consultant


Physician General and Respiratory Medicine, James Cook University
Hospital.

2. I have been instructed to prepare a medical report on Theodore Bell. This


concerns his assertion that he has developed an asbestos-related condition as a
consequence of occupational exposure to asbestos. Materials included in the
preparation of this report:
1. Mr. Bell’s statement
2. Mr. Bell’s hospital and general practice records
3. X-rays and scans on a CD rom
4. Articles that I have made reference to in my report

3. Date of examination: 25th November 2009


Mr. Bell is 71 years old. He says that he has been breathless for
approximately two and a half years with recurrent pleural effusions. His
symptoms first began a few months after he had a coronary artery by-pass
operation in Warwick. Initially he had a left-sided pleural effusion that was
drained on a number of occasions. Over the past six months he has developed
right sided pleural effusions which have also been drained at James Cook
University Hospital, Middlesbrough. He is now breathless on walking
approximately 100 metres and has difficulty climbing the stairs. He lives in a
bungalow. He has an occasional cough and has had symptoms of bronchitis
for approximately one year.

4. He has had an inhaler for six months but he is not sure if it makes any
difference. He has been expectorating small quantities of sputum which
occasionally has spots of blood in it. He required a bronchoscopy to
investigate the blood in his sputum and this was apparently negative. He is
often wheezy and has to sleep with six pillows because of breathlessness
which wakes him up from sleep when he is lying flat. He has also had central
chest discomfort since he had his coronary artery by-pass graft.

5. His past medical history includes myocardial infarction, coronary artery by-
pass graft, duodenal ulcer and hiatus hernia. He denies any chest problems as
a child. On systematic review he says that he has lost approximately three
stones in weight in association with his recent chest problems. Mr. Bell says
that he has never smoked cigarettes. He previously worked as a Fitter’s Mate
and was exposed to asbestos over many years.

6. On examination Mr. Bell is of slim stature. He had finger clubbing and a


resting tremor. His weight was 55 kg, height 1.64m, BMI 20.4 kg/m2. On
examination of the cardiovascular system his heart rate was 60-sinus rhythm,
heart sounds were normal and blood pressure 137/79. Jugular venous pressure
was not elevated and he had no ankle oedema. On examination of the chest
there was a left thoracotomy scar and on percussion both lung bases were dull.
Breath sounds were reduced bilaterally. I exercised Mr. Bell to a distance of
approximately 50 metres, during which he was tachypnoeic. Oxygen
saturations were 97% and did not fall on exercise.

7. Occupational History
Mr. Bell states that he left school aged 15 in 1953 and started work at
Donaldson’s delivering milk. He was there for three years then joined the
Army in 1956 until 1958. On leaving the Army he joined Dorman Long
where he was employed for three to four years as a Jigger, this involved
pouring molten steel into ingot moulds. There was no exposure to asbestos
during this job. He then joined Cargo Fleet Road Materials based at Dorman
Long, South Bank Coke Ovens. This involved him cleaning coke debris from
the floor around the ovens. Again there was no recollection of exposure to
asbestos during this job.
8. Mr. Bell then went to work at Smith’s Dock and the Furness Shipyard at
Haverton Hill. He worked at both locations, off and on for a month at a time.
He was at Furness Shipyard until the early 1970’s and Smith’s Dock until the
early 1980’s. He was employed as a Fitter’s Mate. Most of the work was on
newly commissioned ships and re-fitting of older ships. The work involved
handling copper piping lagged with asbestos. He often worked alongside
Laggers. Much of the work was conducted in confined spaces below decks.
Laggers would mix asbestos in the open and the air was often thick with dust.
Mr. Bell doesn’t recall being provided with a mask or informed of the hazards
of asbestos. When working on the older ships he would have to rip off old
asbestos lagging from around the pipework by hand, this generated a large
amount of dust, and Laggers would be on hand to re-insulate the pipework.

9. During this period of employment Mr. Bell worked intermittently for other
companies: This included Stillite Products, fitting Rockwool insulation. There
was no exposure to asbestos during this work. He also had some brief periods
of employment at ICI Wilton as an Electrician’s Mate and has no recollection
of exposure to asbestos in this job. In the early 1980’s he was employed at the
Immingham Power Plant near Grimsby as a Labourer. He was involved in
cleaning pipework but there was no lagging.

10. In summary Mr. Bell was experienced exposure to asbestos at a moderately


high intensity over a cumulative period of approximately three to four years
whilst employed at Smith’s Dock and Furness Shipyards.

11. Review of General Practice Records


In November 2008 Mr. Bell relocated back to Teesside from Warwickshire;
there are no GP records prior to this. He was seen as a new patient in March
2009. He was noted to be a lifelong non-smoker. Height was 1.64 metres,
weight 58 kg and blood pressure 149/84. It was noted that he had been an
inpatient in Coventry with congestive cardiac failure and that he had had a
pleural biopsy. Investigations had revealed an elevated plasma viscosity.
12. On 6th April 2009 he was complaining of shortness of breath and cough
thought to be due to a chest infection. He was treated with Furosemide 40mg
and Co-Amoxiclav. He was seen by his GP again on 3rd June 2009. He was
still complaining of shortness of breath but no chest pain. He had a cough,
often with specks of blood. On examination chest expansion and percussion
was normal but there were fine crepitations. He was given further antibiotics.
On 12th June 2009 he was still coughing thick sputum and was short of breath
and wheezy and was prescribed steroids.

13. He was reviewed again on 14th July 2009 and continued to complain of
breathlessness and cough. On 13th August 2009 a diagnosis of chronic
obstructive pulmonary disease was made. He was started on Tiotropium and
Salmeterol inhalers and also Salbutamol inhalers. He was reviewed again on
2nd September 2009. He was still coughing flecks of blood. On examination
there were fine crepitations in his chest; blood pressure was normal (125/85)
and pulse rate 70/min. He had also been passing blood per rectum. Recent
investigations revealed a low vitamin B12. He was started on vitamin B12
injections and was referred for a gastroenterology opinion. A diagnosis of
gastritis and duodenitis was made and a colonoscopy that showed diverticular
disease.

14. On 7th October 2009 he was reviewed by his GP. It was noted that exercise
was “physically impossible”. A diagnosis of COPD was noted. He had a
blood pressure of 122/70. It was noted that he had never smoked tobacco. He
was breathless with an MRC score of 3. Lung function was assessed with an
FEV1 of 1.57, FVC 1.8, FEV1/FVC 87%.

15. On 23rd September 2009 Mr. Bell was seen by Dr. Dallal, Consultant
Gastroenterologist at James Cook University Hospital. He was complaining
of epigastric pain, vomiting and altered bowel habit with rectal bleeding.
There had been significant weight loss although he was now regaining weight.
Subsequent investigations showed pleural effusion and spiculated lesion in the
right upper lobe was noted. Upper and lower GIT endoscopy were arranged,
these showed oesophagitis, possibly Barrett’s oesophagus, and extensive
diverticulosis.

16. 7th May 2009 letter from Dr. Muir, Consultant Cardiologist, James Cook
University Hospital. There was a history of previous by-pass surgery in 2007,
angiogram in 2008 showed three patent grafts and no obvious ischaemic
problems. Mr. Bell had chest discomfort 24 hours per day, in Dr. Muir’s
opinion it was “certainly not angina.” His breathlessness had not improved
since drainage of the pleural fluid. His history of pleural plaques was noted
and recurrent pleural aspirations. It was noted that he had never smoked and
was an ex-dock worker.

17. On examination he was cachectic. There was superficial chest tenderness. He


had no signs of cardiac failure. He had bilateral carotid bruits and evidence of
bilateral pleural effusions. Echocardiograph showed moderate left ventricular
dysfunction. It was Dr. Muir’s opinion that the pleural effusion was not
cardiac in origin and the chest pain was not angina.

18. Discharge summary James Cook University Hospital: Date of admission


01.03.2009 and date of discharge 02.03.2009. A diagnosis of congestive
cardiac failure was made. Mr. Bell had been admitted following episodes of
pre-syncope, shortness of breath and chest pain. Chest x-ray showed
pulmonary congestion and bilateral pleural effusions, greater on the right than
the left. He was treated with diuretics and antibiotics.

19. Discharge summary from James Cook University Hospital: He was admitted
on 12.04.2009 and discharged 23.04.2009. Mr. Bell was admitted under the
care of Dr. Krishnaraj (Chest Physician). A diagnosis of asbestos-related
pleural effusion and possible pneumonia was made. He complained of a three
day history of shortness of breath with central chest pain and a productive
cough. On examination he had bilateral crackles. Chest x-ray showed a right
pleural effusion and consolidation on the left. His history of asbestos
exposure was noted.
20. Pleural biopsy and aspiration of pleural fluid was performed. No malignant
cells were identified. A CT scan showed bilateral pleural thickening, greater
on the left with loss of volume in the left hemithorax. There was moderate
right pleural effusion. There was evidence of asbestos exposure. There was
also opacification in the left upper and lower lobes suggesting a possible chest
infection. There was borderline mediastinal lymphadenopathy. Medication
included Aspirin, Clopidogrel, Isosorbide Mononitirate, Thiamine,
Omeprazole, Levetiracetam, Simvastatin and Bisoprolol.

21. Letter 21st July 2009 for a clinic on 25th June 2009 by Dr. Guhan. Mr. Bell
was short of breath. His chest x-ray showed a right upper lobe nodule and a
pleural effusion. Biopsies on 14th May and 22nd April showed no evidence of
malignancy. The suggestion that the nodule may be cancer was discussed and
CT scan was arranged. He was re-admitted to hospital on 23.07.2009 with
shortness of breath and recurrent haemoptysis. Bronchoscopy was arranged.
There is a letter from Dr. Guhan on 13th August which reported that the
bronchoscopy was normal and there had been no change in the size of the right
pleural effusion. The CT scan report suggested that the right upper lobe
nodule was loculated fluid. On the 13th August Dr. Guhan made a diagnosis of
COPD and right pleural effusion and prescribed Tiotropium, Salmeterol and
Salbutamol inhalers.

22. Chest x-ray report 12th June 2009: “Comparison made with previous chest
radiograph 13th May 2009. Left lateral chest wall pleural thickening and right
sided pleural effusion have remained unchanged. There is a new 8 mm
diameter focal nodule with irregular margins in the right upper zone.
Evidence of previous thoracic surgery.” Reported by Dr. Saha, Consultant
Radiologist.

23. 17th May 1991 letter from Dr. Moss, Consultant Gastroenterologist at Grimsby
District General Hospital; Mr. Bell was diagnosed with a hiatus hernia. In May
1992 he was admitted to South Cleveland Hospital in Middlesbrough with a
vague history of haemoptysis. It was noted that he had recently been
diagnosed with a gastric ulcer and diverticulitis. Examination was
unremarkable. Chest x-ray was normal. He was treated with Zantac and
Gaviscon and discharged.

24. In May 1997 he was referred to see Dr. Bain, Consultant Physician at Grimsby
Hospital, with recurrent episodes of collapse. A CT scan of brain showed
cerebral cortical atrophy but was otherwise normal. ECG was normal. He
was subsequently started on Sodium Valproate for presumed epilepsy. Shortly
after this he was found to have paroxysmal atrial fibrillation although no
treatment seems to have been initiated. In 1998 he was admitted to Grimsby
Hospital with recurrent seizures. At the time he was taking Sodium Valproate
and Lamotrigine. By March 1999 his seizure control had improved. But he
was admitted to hospital again in 1999 with a further seizure, followed by an
upper GI bleed from a peptic ulcer.

25. In October 2003 he was referred to see Dr. Buckley, Senior Registrar to Dr.
Pallas, Consultant Neurologist at the Horton Hospital, Oxford. A diagnosis of
epilepsy had been made in 1997. At the time he had a normal CT scan of
brain and EEG. He had been drinking up to eight pints of beer per day but
recently reduced this to two pints. He was having early nocturnal seizures
about twice per month and had not had a day time seizure for three years. He
had had significant injury following a fall from an oil rig onto a deck 15 to 20
years previously. Medication was Epilim, Lamotrigine and Omeprazole.

26. In February 2004 he saw Mr. Hasnie, Consultant ENT Surgeon, with recurrent
ear infections. He was diagnosed with sensory neural hearing loss. In July
2004 he was seen by Mr. O’Driscoll, Consultant Ophthalmic Surgeon,
Warwick Hospital because of cataracts that required surgery. In September
2004 he had a gastroscopy. This showed Barrett’s oesophagus, hiatus hernia,
gastritis and duodenitis. There was also evidence of Helicobacter infection that
required treatment.

27. In May 2006 he was admitted to Warwick Hospital with an anterior


myocardial infarction. During admission angiography showed triple vessel
disease. He had a seizure whilst in Coronary Care. Doppler ultrasound scan
showed severe 80 – 99% stenosis of the right internal carotid artery. He was
given thrombolysis with TPA but had a frank GIT bleed.

28. In July 2006 he was seen by Mr. Loubani, Specialist Registrar in


Cardiothoracic Surgery, University Hospital, Walsgrave. He was continuing
to have angina once or twice per week, occasionally at rest. He was breathless
on exertion. A previous myocardial infarction in 1984 with no subsequent
angina was noted. He was found to have hypercholesterolaemia, and
hypertensive but not diabetic. Medication included Sodium Valproate,
Lamotrigine, Metoprolol, Perindopril, Ascorbic Acid, GTN spray, Vitamin B
compound, Aspirin, Lansoprazole, Simvastatin and Thiamine.

29. He also complained of claudication in the right leg at 100 yards. His history
of heavy alcohol consumption was noted. He had never smoked. On
examination he had a carotid bruit, normal heart sounds and no murmurs. He
had palpable femoral pulses but no pulses from the popliteal down on the
right. Angiography in May 2006 had shown an ejection fraction of 45% with
disease in four vessels. Opinions regarding carotid artery surgery and surgery
for peripheral vascular disease were to be considered before coronary artery
by-pass grafting.

30. In August 2006 Mr. Bell was seen by Tracy Jones, Community Psychiatric
Nurse. He had a history of recent onset of confusion and was experiencing
auditory hallucinations. A history of previous heavy alcohol consumption was
noted. On testing he scored 17/30 in the mini mental state examination. It
was also noted that he was incontinent of urine. He was reviewed by Dr. Arif,
Consultant in Elderly Psychiatry. A diagnosis of vascular dementia was made.

31. On 27th September 2006 Mr. Bell was seen by Dr. Allroggen, Consultant
Neurologist. Diagnoses included epilepsy, cerebrovascular disease with
critical right ICA stenosis and ischaemic heart disease awaiting a CABG.
Neurological signs included a resting tremor and brisk reflexes in the right leg.
It was thought the neurological signs were due to cerebrovascular disease.
Some changes were made to his anticonvulsant therapy. The vascular surgeons
did not think that his carotid arteries required surgical intervention.

32. Mr. Bell was admitted to hospital in January 2007 for coronary artery by-pass
graft. The Cardiac Surgeon was Mr. Parmar. It was noted that angiography
had show compromised left ventricular function. Carotid doppler studies
showed almost complete occlusion of the right internal carotid and moderate
57% stenosis of the left internal carotid artery. Thoracotomy showed
moderate left ventricular hypertrophy and patchy anterior and inferior
scarring. There was evidence of more generalised atherosclerosis. He had
two saphenous vein grafts and a left internal mammary artery anastamosis was
performed. He made an uneventful recovery.

33. He was discharged home on 11th January 2007. He was reviewed in the
cardiothoracic clinic on 26th February 2007 and had no angina or
breathlessness. He did complain of a persistent dry cough. Respiratory
system examination was clinically normal.

34. He was seen in the neurology clinic again on 16th March 2007 and was well.
On 31st July 2007 he was seen in the cardiology clinic. He had no chest pain
or breathlessness. On examination there was reduced air entry in the left base
which was interpreted as being a post-operative finding.

35. On 12th December 2007 Mr. Bell was admitted to Warwick Hospital with
increasing breathlessness. He was found to have a left sided pleural effusion.
His CT scan confirmed a pleural effusion and mediastinal lymphadenopathy.
It also showed bilateral diaphragmatic calcification due to previous asbestos
exposure. There was pleural thickening on the left. A diagnostic pleural
aspiration was performed. He was reviewed by Dr. Mukherjee, Consultant
Respiratory Physician at Warwick Hospital, who thought that the effusion may
be related to the previous cardiac surgery.

36. Mr. Bell was readmitted to hospital on 11th February 2008 and discharged on
26th February 2008. He was complaining of left sided chest pain an
unproductive cough and breathlessness. He was treated with antibiotics for a
presumed lower respiratory tract infection. Chest x-ray showed persistent left
pleural effusion
.
37. Letter March 2008 from Dr. Ricky Jones, Consultant Chest Physician,
Warwick Medical School and Warwick Hospital. He confirmed that Mr. Bell
had a coronary by-pass graft a year ago and some time after this developed a
pleural effusion. It was thought that the pleural effusion was secondary to
this. He was breathless on two occasions, requiring admission to hospital and
had also lost between one and two stones in weight.

38. He was referred to Mr. Siaw, Specialist Registrar in Cardiothoracic Surgery.


It was noted that Mr. Bell had had a coronary by-pass graft in January 2007
and developed a cough in October 2007. Chest x-ray demonstrated a
significant left sided pleural effusion which was aspirated. Cytology was
negative. He had been admitted five times for aspiration, currently he is short
of breath on exertion and has anterior chest pain.

39. A history of exposure to asbestos whilst working in shipyards was noted and
that he was a non-smoker. A further chest x-ray showed a left sided pleural
effusion but also blunting of the right costophrenic angle. A VAT’s pleural
biopsy and talc pleurodesis was arranged. Mr. Bell was admitted to the
University Hospital, Walsgrave in April 2008 for a left thoracotomy and
decortication. Pathology of the pleura showed features of chronic pleuritis.

40. He was reviewed by the Cardiothoracic Surgeons in June 2008 and appeared
to be improving. Mr. Bell was seen in the cardiology clinic, Warwick
Hospital, in August 2008. He was experiencing persistent pleuritic chest pain
but was otherwise well. He was admitted with Warwickshire General Hospital
in September 2008 with an episode of acute coronary syndrome. His ECG
showed no new features and troponins were normal.

41. A further angiogram was arranged in November 2008. This showed occlusion
of the left anterior descending coronary and mild stenosis of the circumflex
coronary. The right coronary artery had severe proximal disease and distal
occlusion. Two of the three previous grafts were patent but one showed poor
run-off. Left ventricular function was well preserved.

42. Review of medical notes from James Cook University Hospital


12th April 2009 Mr. Bell was admitted to hospital with increasing
breathlessness and a productive cough. On examination he was febrile
(Temperature 38.7oC). On examination of the chest there were bilateral
crackles with reduced air entry. A chest x-ray showed a right pleural effusion
and some asbestos-related changes. Further investigations included an
elevated C reactive protein and haemoglobin of 13.6. A diagnosis of
pneumonia was made and he was started on antibiotics.

43. On 14th April 2009 a right pleural aspiration was performed. This showed
haemorrhagic fluid. On 22nd April 2009 he was seen by Dr. Guhan who
carried out a pleural biopsy. Histology reported: "This is dense fibrous tissue,
probably arising from a pleural plaque and some skeletal muscle. There is no
evidence of tumour”. Pleural cytology showed lymphocytes and red blood
cells only.

44. CT scan report 15th April 2009, reported by Joanne Fletcher, Consultant
Radiologist. “There is a moderate right-sided pleural effusion with associated
pleural thickening mostly on the diaphragmatic surface. There is multi-focal
coarse pleural calcification. Loss of volume in the left hemithorax in
association with extensive circumferential pleural thickening and sparing of
the mediastinal surface. Small volume left lower lobe containing patchy
consolidation and atelectasis. Cluster of pre-vascular mediastinal nodes up to
11 mm in short axis. Conclusion: Bilateral pleural thickening left greater than
right associated with loss of volume in the left. Moderate right sided pleural
effusion; exudate (pleural fluid greater than 33 g/L) and haemorrhagic.”

45. Echocardiogram report 2nd March 2009: This shows overall moderate left
ventricular systolic dysfunction. Normal left ventricular cavity size. No
significant valvular abnormality.
46. Review of x-rays and CT scan.
1st March 2009: AP chest x-ray. Sternal wires visible. The heart size appears to
be increased but it is an AP film. There is bilateral pleural shadowing
including a probable right pleural effusion. There is a ground glass appearance
to the lung fields particularly the left. The left heart border is indistinct.
12th April 2009: AP chest x-ray. Similar appearances to previous film although
left lung field is more opaque. The patient has an oxygen mask on.

47. 22nd April, 13th May, 12th June 2009, 12thAugust 2009, 23rd September: PA
chest x-rays. These films show similar appearances. There are sternal wires
and borderline cardiomegaly but left heart border is indistinct. There is a
small-moderate right effusion and pleural thickening bilaterally most marked
on the left. None-specific increased opacification of the left lower lobe. Left
thoracotomy clips visible. In the film from 12th June there is a small opacity in
the periphery of right upper lobe, which is less pronounced in later films. The
changing opacification of the lung fields suggests that this is in part due to
pulmonary oedema.

48. 2nd July 2009. CT scan of Thorax: There is circumferential pleural thickening
most marked on the left with partial calcification. On the right there are two
irregularly shaped opacities one 27x14 mm and the other 17x17 mm. There is
a small right pleural effusion.

49. 15th April 2009: CT scan of Thorax. Bilateral pleural thickening most marked
on the left with patchy calcification. There is a moderate right pleural effusion.
There is patchy left basal consolidation and marked distortion of the normal
architecture with fibrotic scarring of the lower lobe

50. In summary the chest x-rays and CT scans show diffuse bilateral pleural
thickening and a right pleural effusion. There is fibrotic scarring of the left
lower lobe although the appearances are not typical of interstitial fibrosis
(asbestosis).There is also evidence of pulmonary oedema.
51. Lung Function Tests.
Lung function was assessed using a micromedical digital spirometer. Mr Bell
made three attempts two of which were satisfactory. The results show
moderate restriction of lung function.

FEV1 FVC PEF VAR Quality Time Date


1st 1.67 1.95 261 +0 % Good Blow 15:29
25/11/2009
nd
2 1.54 1.86 222 -6 % Good Blow 15:29
25/11/2009
3rd 1.48 1.74 204 -11 % Poor Effort 15:29
25/11/2009 (-)

Index Base %Pred Predicted (Litres/s)


FEV1 1.67 72 2.33 (1.49-3.17)
FVC 1.95 64 3.03 (2.03 -4.03)
PEF 261 63 415 (296- 535)
FEV1/FVC 86 %

52. Summary of Medical History


Mr Bell is a life-long none-smoker but has moderately severe generalised
atherosclerosis. He was hypertensive and had hypercholesterolaemia. He has 2
MI’s and a 3 vessel coronary bypass graft. However he has evidence of re-
occlusion of one graft. He has left ventricular failure. He has cerebrovascular
disease and significant carotid disease, and has evidence of early vascular
dementia. He has epilepsy possibly due to a previous head injury. He has a
hiatus hernia with Barrett’s oesophagus and also diverticulosis.

53. Mr Bell has been breathless on moderate exertion for approximately 12


months. This initially appeared to be due to recurrent left sided pleural
effusions presumed to be related to his previous CABG surgery; however he
has since developed recurrent effusions on the opposite side and a diagnosis of
asbestos related effusions has been suggested. Mr Bell has also been
diagnosed (by Dr Guhan) with COPD. I disagree with this diagnoses as Mr
Bell’s lung function tests show no airflow obstruction, furthermore he is a
lifelong non-smoker.

54. Asbestos Related Diagnosis.


Mr Bell is suffering from asbestos related chronic pleuritis. He experienced
intense exposure to asbestos over a period of 3 years approximately 30 years
ago. The symptoms of benign asbestos pleuritis typically occur 20-30 years
after exposure. Mr Bell’s symptoms are typical of the condition which usually
presents initially with pleural effusions followed by the development of
diffuse pleural thickening. His CT scan showed bilateral diffuse pleural
thickening with calcification and pleural biopsy (left) confirmed chronic
pleuritis.

55. An alternative explanation for Mr Bell’s pleural effusions would be that they
are related to his CABG surgery. However post CABG pleural effusions are
typically unilateral (left side), develop within 7 days of surgery and diminish
over time. They may persist for a few months usually in association with a
pericardial effusion. However Mr Bell’s left pleural effusion initially
manifested 9 months after his CABG operation. The right pleural effusion did
not develop until 2 years after his surgery; furthermore he did not have a
concurrent pericardial effusion.

56. Disability and Prognosis


Mr Bell is breathless on mild-moderate exertion such as walking at his own
pace or climbing the stairs. I estimate that he has 40% cardio respiratory
disability half of which (20%) is attributable to his cardiac disease and the
remainder (20%) is due to restriction of lung function because of his asbestos
related chronic pleuritis. There is a 30% risk of progression of his pleuritis
resulting in further disability at a rate of approximately 5% additional
disability per year leading to a maximum 40% disability due to his asbestos
related condition.
57. The average life expectancy of a 71year old man is 15.9 years (UK
actuarial table 2007). This requires an adjustment of 8 years to allow
for Mr Bell’s considerable co-morbidity; including coronary artery
disease, cerebrovascular disease and generalised atherosclerosis. His
diffuse pleural thickening will not shorten is life expectancy. However
he is at increased risk of malignancy because of exposure to asbestos.
The risk of him developing malignant mesothelioma of the pleura or
lung cancer is approximately 6%. This requires a further 5-month
reduction in projected life expectancy to allow for this risk.

58. Summary
Theodore Bell is a 71-year-old man with asbestos related benign chronic
pleuritis. He has developed this condition as a consequence of occupational
exposure to asbestos. He has moderate restriction of lung function with 20%
cardio-respiratory disability due to his asbestos related condition. He is at
increased risk of malignancy because of his exposure to asbestos.

59. Statement of Truth


I understand that my duty is to the Court, I have complied with that duty. I
confirm that insofar as the facts stated in my report are within my knowledge
they are made clear which they are and I believe them to be true and that the
opinions I have expressed represent my true and complete professional
opinion.

Dr. S. Murphy MD FRCP


5th December 2009
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