Transcript Document
So you think you know everything about Occupational Lung Disease? David Fishwick Consultant Respiratory Physician Centre for Workplace Health STH NHS Foundation Trust and University of Sheffield 01142713631 [email protected] Q1; what lung disease can be caused by manufacturing these products? Q1; answer Aluminosis Stannosis Berylliosis Siderosis Q1; answer Aluminosis Stannosis Berylliosis Siderosis Q2; what is this lung disease? Q2; answer Speedo lung Hot tub lung Lifeguard lung Sarcoidosis Q2; answer Speedo lung Hot tub lung Lifeguard lung Sarcoidosis Case 1; history • • • • 35 year old man Translated history from his wife No childhood problems, living in the UK for 9 years 6 year history of asthma, seen in 2009 • Shortness of breath, wheeze and chest tightness • Good 2 response • Worsening control despite escalating Rx • Noted work related effect with weekend working, better through the week when not at work Case 1; history • 2000-2003; fast food retailer • 2003; Bakery • First 6 months in bakery using flour • 18 months in the sushi department • Subsequent work in the sandwich department • Raw vegetables, salads, chicken and bacon • Tuna, prawn • Chemical and cleaning agents • Cold storage Q3; what is the best initial assessment of whether his symptoms relate to asthma at work FEV1 and FVC Exhaled NO Immunology tests Serial PEF Q3; what is the best initial assessment of whether his symptoms relate to asthma at work FEV1 and FVC Exhaled NO Immunology tests Serial PEF Q3; what is the best initial assessment of whether his symptoms relate to asthma at work • “There is a considerable evidence base for the use of serial PEF measurements to investigate workers when OA is suspected. • With appropriate training and explanation, it is possible to achieve high quality recordings in workers suspected of OA. • Whilst they may be susceptible to falsification and transcription errors, they offer the best and easiest first-line approach to assessing physiological response to asthmagens at work. • High quality recordings can be obtained from over 70% of patients” Fishwick et al. Thorax 2011. SOC for occupational asthma. An update. Case 1; investigations FEV1 54% predicted, FEV1/FVC 0.70 OASYS 2 chart; WEI 4.00 FENO 22.8ppb Q4; tests of immunology in this case will be; Useful Useless Q4; tests of immunology in this case will be; Useful Useless Total IgE 853 (0-81) KU/L Value Units Salmon 48.8 KUA/L Shrimp / prawn >100.0 KUA/L Tuna >100.0 KUA/L Q4; tests of immunology in this case will be; • “New evidence supports both skin prick and serological tests as sensitive tests for detecting specific IgE caused by most high molecular weight agents, but they are not specific for diagnosing asthma or OA” • Classic animal and plant allergens are high molecular weight • E.g. proteins from pets, seafood, lab animals, horses, grains • Certain low molecular weight agents also exhibit IgE responses • Acid anhydrides, reactive dyes Fishwick et al. Thorax 2011. SOC for occupational asthma. An update. Q5; persistent airway hyper reactivity is seen in what proportion of all cases of occupational asthma 1/4 2/4 3/4 4/4 Q5; persistent airway hyper reactivity is seen in what proportion of all cases of occupational asthma 1/4 2/4 3/4 4/4 Case 1; persistent airway hyper reactivity is seen in what proportion of all cases of occupational asthma • “Generally, occupational asthma has a poor prognosis, with about 1/3 of workers achieving symptomatic recovery and about 3/4 having persistent non-specific bronchial hyper-responsiveness. • Workers who remain in the same job and continue to be exposed to the same agent after diagnosis are unlikely to improve and may worsen. • There is consistent evidence that about 1/3 of workers with occupational asthma are unemployed after diagnosis and that loss of employment following a diagnosis of occupational asthma is associated with loss of income” Fishwick et al. Thorax 2011. SOC for occupational asthma. An update. Case 1; progress • Initial redeployment was associated with worsening asthma symptoms • Heavier work tasks in packing area • Reviewed 9 months following diagnosis • Not at work for 2 months • Much improved • Claiming IIDB • Prospect for further employment not yet determined by workplace Case 2; history • 48 years old male welder, workmate called ambulance • A+E admission with severe acute asthma • Unable to complete sentences, haemoptysis • PEF 210 (38% predicted) • RR 32, pulse 128 • Widespread wheeze, oro pharynx ulcerated • Settled with nebuliser and oxygen Case 2; history • • • • • • • • • • Normally fit and well (recreational diver) Never smoked Childhood asthma Lifelong welder Current job for one month, refitting a ship Symptoms came on over 4 days at work Paper mask, welding shield Welding brackets on to the ships bulkhead Bubbling grey paint Associated flu-like symptoms like “galvi poisoning” Case 2; history • Gradually improved over 5 days with steroids, nebulised bronchodilators • Allowed home • Remained wheezy, regular ICS/SABA • Waking at night, breathless on exertion • Variable (DV>20%) low PEF measures • Nasal ulceration healed over 2-3 weeks Q5; what do you think is the most likely diagnosis? Acute bronchitis Acute irritant induced asthma Acute alveolitis Acute rhinitis Q5; what do you think is the most likely diagnosis? Acute bronchitis Acute irritant induced asthma Acute alveolitis Acute rhinitis Reactive airway dysfunction syndrome (RADS) Brooks et al 1985 Case 2; occupational asthma terminology • 90%; asthma induced by sensitisation to an agent inhaled at work (allergic aetiology) OR • 10%; asthma induced by accidental high level irritant exposure at work (AIIA or RADS) Case 2; occupational asthma terminology From Francis, Prys-Picard, Fishwick et al Occupational and Environmental Medicine 2007;64:361-365 Copyright ©2007 BMJ Publishing Group Ltd. Case 2; exposure • Welding zinc chromate paint • Flu like symptoms from zinc (MFF) • Ulceration from hexavalent chromium Q6; the prognosis, or outcome, of acute irritant induced asthma is generally; Excellent Good Moderate Poor Q6; the prognosis, or outcome, of acute irritant induced asthma is generally; Excellent Good Moderate Poor Environ Health Perspect 115:1584–1590 (2007). doi:10.1289/ehp.10248 Environ Health Perspect 115:1584–1590 (2007). doi:10.1289/ehp.10248 Case 3; history • • • • 44 year old male Persistent cough, 18 months, clear phlegm, no blood Worsening, mostly daytime, little nocturnal cough only Aggravated by talking, taking deep breaths, exercise and changes in ambient temperature • Worse exercise tolerance over 6 months (keen walker) • No nasal symptoms, never smoked, no atopic history • No childhood problems, no birds, no other pets, no significant hobbies, no relevant drugs, heterosexual • Previously kept Zebra Finches Examination 27.11.08 • • • • • Well, not breathless No clubbing or lymphadenopathy Globally reduced breath sounds No crackles No wheeze • Cardiac and other examination findings normal • No skin problems, no ocular problems and no sign of connective tissue disorder • SpO2 on air; 97% at rest Lung Function Very difficult technically due to cough, transfer estimate not possible FEV1 Measured Predicted % predicted 3.52 4.09 86 3.94 4.99 79 0.89 0.80 111.3 Litres FVC Litres FEV1/FVC HRCT 1 23.12.08 Q7; the most likely diagnosis is; Extrinsic allergic alveolitis Sarcoidosis Pneumonia Not yet possible to determine Q7; the most likely diagnosis is; Extrinsic allergic alveolitis Sarcoidosis Pneumonia Not yet possible to determine Case 3; Occupational history • EMPLOYED 23 years, until 2003, in the textile industry as mechanic • Cotton, wool dust exposure • SELF EMPLOYED 2004 – Jan 2008 Mechanic, tool grinding shop • Lubricant oils, metals • EMPLOYED Jan 2008 – Jan 2009 Saw and Tool manufacturer • Little coolant inhaled • No masks Q8; what else do you need to know now most importantly? Family history Smoking history More occupational details Drug Allergies Q8; what else do you need to know now most importantly? Family history Smoking history More occupational details Drug Allergies Case 3; Occupational history • 2004 • Bought a company owned by a father and son • Grinding hard metals • Dry grinding process • No MWF or grinding fluids • No lubricant oils • Grinding wheel with “natural” ventilation, no specific LEV • Multiple metal exposure including tungsten and cobalt • [2005/6] cough • January 2008 to January 2009 • Saw and tool manufacturer; similar exposures, ventilation “slightly” better Case 3; Biopsy Open Biopsy; Normal pleura. Established fibrosis, grade 2-3. Established collagenous deposition, some oedema and a mild chronic inflammatory reaction. Scattered fibroblastic foci with bronchiolar metaplasia. Also evidence of DIP and scattered macrophanges on the alveolar surface in close proximity to black pigment. Scanty giant cells are present. ICP-MS full mass spectrum Elevated tungsten Elevated cobalt Q9; what is the best treatment for this patient Prednisolone Prednisolone and NAC Remove exposures Oxygen Q9; what is the best treatment for this patient Prednisolone Prednisolone and NAC Remove exposures Oxygen Lung Function Sequential estimates FEV1 Measured 27.11.08 Measured 18.03.09 Measured 27.08.09 Measured 3.11.09 Measured 5.2.10 3.52 - - - 3.83 3.94 - - - 4.57 - 8.58 1.35 8.43 1.54 8.67 1.55 9.43 1.65 Litres FVC Litres TLco Kco HRCT 23.12.08 and 07.04.09 HRCT 23.12.08 and 27.08.09 Summary • • • • Asthma caused by work is common Early identification and removal improves outlook Serial PEF measures are the first best assessment Immunology may assist • Asthma caused by accidental workplace exposures to irritants develops rapidly, and has a poor outlook • Unusual or “idiopathic” lung diseases may have an occupational cause • Removing the cause may improve physiology and the overall outlook