This page intentionally left blank 287 Chapter 12 Neurological disorders Brain cancer 288 Acute narcosis 290 Parkinsonism 292 Compression neuropathies 294 Periphera l neuropathy 296 Organophosphate poisoning 298 Hand \200\223arm vibration syndrome 300 Nois e-induced hearing loss 302 12_Smedley_Chap12.indd 287 1/2/2013 12:13:51 PM CHAPTER 12 Neurological disorders 288 Brain cancer Epidemiology Primary brain cancers are relatively rare with an annual incidenc e in UK adults of 7/100,000 population. \200 Although relatively rare, p brain tumor is t he eighth most common tumor in people of working age Most adult p brain tumors are supratentorial and are gliomas (85%) \200 The incidence of p brain tumor increases with increasing age \200 Epidemiological \201 ndings regarding possible risk factors for primary brain tumor have been inconsistent Several occupations (e.g. \201 re \201 ghters) and chemical exposures (e.g. pesticides) have been associated with i risk of p brain tumor, but studies are inconclusive Metastatic brain tumor is much more common than p brain tumor: \200 up to 40% of adult ca ncer sufferers develop brain metastases. Clinical features Patients with a primary brain tumor may present with: \200 Headache \200 Seizure \200 Focal neurological de \201 cits: diplopia \200 dysphasia \200 hemiparesis \200 hemisensory de \201 cits Non-focal neurological de \201 cits: \200 confusion/memory problems \200 visual sympto ms \200 ataxia \200 personality change. Causal exposures/industries \200 Few occupational risk factors for primary brain tumor ha ve been identi \201 ed Some studies suggest an increased risk in the petroleum industry. Clinical assessment and diagnosis \200 CT scan with contrast or an MRI scan \200 Tumor excision or biopsy will permit histological diagnosis. Prognosis Survival for those adults with malignant brain tumor remains poor with 64% mortal ity in 12mths and 85% mortality by 5yrs. Medical management \200 Surgical excision or biopsy, with/without subsequent local radiot herapy \200 Corticosteroids to reduce brain swelling \200 Chemotherapy such as vincrist ine, lomustine, and procarbazine 12_Smedley_Chap12.indd 288 1/2/2013 12:13:51 PM BRAIN CANCER 289 During the immediate phase of diagnosis and management most patients will not be \201 t for work. Legislation/guidance DVLA. At a glance guide to the current medical standards of \201 tne ss to drive . Available at: M http://www.dft.gov.uk/dvla/medical/ataglance.aspx 12_Smedley_Chap12.indd 289 1/2/2013 12:13:51 PM CHAPTER 12 Neurological disorders 290 Acute narcosis Acute narcosis occurs in those workers exposed to solvent vapor or to gasses with narcotic action. Epidemiology There is little information regarding the incidence of acute narcosis in the w orkplace in the UK. Clinical features The features of acute narcosis are those of anesthesia. If suf \201 cien tly heav- ily exposed, workers will go through the four stages of anesthesia unless exposur e ceases. Signs and symptoms of narcosis include: \200 Euphoria \200 Disinhibition \200 Aggression \200 Dizziness \200 Ataxia \200 Loss of consciousness \200 Apnoea \200 Death. Causal exposures Exposure to narcotic agents may occur during normal work, or following spi lls or accidents. Rarely, volatile substance abuse may present in the workplace with narcos is. \200 Organic solvents : glues and adhesives \200 polishes \200 paint or varnish \200 degreasants (e.g. trichl oroethylene) \200 printing inks \200 dry cleaning \202 uids (e.g. perchloroethylene) Nitrogen dioxide \200 Nitrogen (air divers below 30m) \200 VCM. Clinical assessment and diagnosis The diagnosis may be made by workmates or the emergency s ervices responding to a reported collapse. History of exposure to narcotic agents such as o rganic solvents (especially in con \201 ned spaces) should alert you to the diagnosis. Prognosis Most make a full recovery. Those workers who suffer hypoxia may sustain long-term damage (e.g. cognitive impairment). 12_Smedley_Chap12.indd 290 1/2/2013 12:13:51 PM ACUTE NARCOSIS 291 Emergency medical management See b p. 792, General principles and contact details for speci alist advice, Immediate management of poisoning in the workplace) \200 The affected worke r, if conscious, may appear drunk \200 If it is safe to do so: withdraw from exposure \200 remove contaminated clothing If respiratory depression is present, administer oxygen. Relevant legislation Acute narcosis leading to unconsciousness is reportable under RIDDOR 1 995. 1 A serious incident, such as acute narcosis, demands that the risk assess- ment for t hat work activity be reviewed; it is likely that further controls are necessary. 12_Smedley_Chap12.indd 291 1/2/2013 12:13:51 PM CHAPTER 12 Neurological disorders 292 Parkinsonism Parkinsonism is the term for a group of movement disorders, the best known of which is Parkinson \200\231s disease (PD). Degeneration of the dopa- minergic neurons of th e substantia nigra occurs in PD. The neuropatho- logical hallmark of PD is the presence of Lewy bodies, although this is not unique to PD. PD epidemiology \200 Peak age at disease onset 65yrs \200 Incidence 17/100,000 populati on/year \200 Prevalence 1 in 1000 of population \200 Prevalence 1 in 100 of population aged >65yrs \200 No \201 gures exist regarding the number of cases of PD that may be du e to occupational exposures. PD clinical features \200 Tremor \200 Rigidity \200 Bradykinesia (slow movements) \200 Postural instability \200 Half of patients show unilateral onset \200 Expressionl ess face \200 Shuf \202 ing gait \200 Cognitive impairment later in illness \200 Spe ech becomes soft and indistinct as disease progresses \200 Drooling \200 Sleep problems \200 \200\230On \200\223off \200\231 phenomenon. Causal exposures \200 Repeated head trauma \200 Pesticides: no single agent identi \201 ed as causal \200 Manganese: parkinsonism, not PD \200 Carbon disulphide (CS 2 ) \200 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), very rare. Industries at risk \200 Boxing \200 Farming \200 Manganese mining, smelting \200 In dustrial chemistry. Individual susceptibility \200 Tobacco smoking halves the risk of PD \200 Familial form s of PD are recognized. Clinical assessment and diagnosis \200 On clinical features and response to L-dopa-contai ning drugs \200 Exclude vascular parkinsonism (stepwise progression) or drug-induced parkinsonism. 12_Smedley_Chap12.indd 292 1/2/2013 12:13:51 PM PARKINSONISM 293 Prognosis Progressive deterioration in neurological and cognitive function occurs over seve ral years. Working life may be curtailed by disease progression. The main functional conseq uences are reduced mobility, dexterity, and stamina. Medical management \200 Optimize drug regime \200 Patients do best when cared for by a neurologist with an interest in movement disorders Support from a specialist PD nurse is helpful for patients \200 Depression is common and may go unrecognized. Compensation Central nervous system toxicity characterized by parkinsonism is pre- scribed (C2) for Industrial Injuries Disablement Bene \201 t in those who are exposed to the fumes , dust, or vapor of manganese, or a compound of manganese, or a substance containing mangan ese. Relevant legislation Parkinsonism due to occupational poisoning by manganese (or one of its compounds) or CS 2 is reportable under RIDDOR. 12_Smedley_Chap12.indd 293 1/2/2013 12:13:51 PM CHAPTER 12 Neurological disorders 294 Compression neuropathies Compression neuropathies may occur in jobs where local pressure, h igh force, or repetition leads to peripheral nerve entrapment. They include the following: \200 Carpal tunnel syndrome (CTS): compression of the median nerve within the carpal tunnel at the wrist Cubital tunnel syndrome: compression of the ulnar nerve at the medial humeral epicondyle or more distally as it goes between the two heads of \202 exor carpi ulnaris in the forearm Guyon \200\231s canal syndrome: compression of the ulnar nerve at the wrist \200 Radial t unnel syndrome: compression of the posterior interosseous branch of the radial nerve in the forearm without motor symptoms. Where motor weakness occu rs, it is termed posterior interosseous nerve syndrome. Epidemiology \200 CTS is the most common entrapment neuropathy in the upper limb; cubital tunnel syndrome is the second most common Radial tunnel syndrome is uncommon \200 Twin studies suggest that genetic factors may exp lain up to half of CTS cases among women Prevalence estimates of CTS vary widely, re \202 ecting differing case de \201 nitions between studies Occupational exposures are only one among a number of risk factors for these conditions. Clinical features Carpal tunnel syndrome \200 Tingling or burning of the thumb, index, mi ddle \201 ngers, and lateral border of the ring \201 nger Pain in the hand and wrist, sometimes spreading up the forearm \200 Symptoms often worse at night \200 Symptomatic relief by shaking the affected limb in the air \200\224 \200 \230 \202 ick sign \200\231 \200 Thenar wasting \200 d Grip strength. Cubital tunnel syndrome/Guyon \200\231s canal syndrome \200 Tingling of the little and ri ng \201 ngers and medial border of the hand \200 d Grip strength. Radial tunnel syndrome \200 May be confused with lateral epicondylitis (tennis elbow) \200 Maximal tenderness approximately 4cm below the lateral epicondyle \200 Forearm pain without objective weakness \200 Pain i by extending the middle \201 nger against resis tance. Causal exposures \200 Awkward posture \200 High force Frequent repetition \200 Hand-transmitted vibration. 12_Smedley_Chap12.indd 294 1/2/2013 12:13:51 PM COMPRESSION NEUROPATHIES 295 Individual susceptibility for CTS \200 Female gender \200 Pregnancy \200 Diabetes mel litus \200 Obesity Hypothyroidism \200 Rheumatoid arthritis \200 Acromegaly. Clinical assessment and diagnosis \200 A good history is central to the diagnosis of CTS \200 Tinel \200\231s test: pain on percussing the median nerve in the carpal tunnel \200 Phalen \200\231s test: pain reproduced by holding the forearm upright and \202 exing the wrist for 1min Nerve conduction studies may be helpful in con \201 rming the diagnosis \200 Neither a n egative Tinel \200\231s test nor normal nerve conduction studies excludes CTS. Prognosis \200 Following surgery to divide the \202 exor retinaculum the majority of CT S sufferers will make an excellent recovery Time to return to normal work following open or endoscopic CTS surgery is about 7 \200\2231 4 days for sedentary work and 42 \200\22370 days for heavy work. Where workplace modi \201 cations are available, return to work can be earlier Dependent on underlying cause, CTS may develop in the other wrist \200 An important diffe rential diagnosis of CTS is hand \200\223arm vibration syndrome (HAVS). Surgery for CTS in a worker with HAVS and symptoms consistent with CTS is unlikely to give complete resolution of CTS symptoms because of digital nerve damage. Health surveillance None appropriate. Medical management \200 Clinical care includes physiotherapy, splinting, and surgical decompression Workplace interventions should focus on occupational risk factors \200 Task redesign may be required because of d grip strength and dexterity; the advice of an ergonomist may be required. Prevention \200 Task rotation and i automation may be indicated \200 Consider tool rede sign. Compensation CTS is prescribed (A12) for Industrial Injuries Disablement Bene \201 t in th ose who are exposed to hand-transmitted vibration. Relevant legislation CTS that is reliably attributable to work is reportable under RIDDOR. 12_Smedley_Chap12.indd 295 1/2/2013 12:13:51 PM CHAPTER 12 Neurological disorders 296 Peripheral neuropathy Peripheral neuropathies may occur because of occupational exposure to physical agents, neurotoxic chemicals, or zoonoses (e.g. Lyme disease). Physical factors i nclude local pressure leading to compression of a periph- eral nerve. Peripheral neuropathy may affect the sensory, motor, or auto- nomic nerves. A mixed sensory \200\223motor neurop athy is usual, but some agents such as inorganic lead may cause a pure motor neuropathy. Epidemiology Most peripheral neuropathy is not due to occupation \200\224common causes of p eripheral neuropathy include diabetes mellitus and connective tissue diseases. Clinical features Sensory neuropathy \200 Altered sensation (paraesthesia) or anesthesia \200 Patient may describe a glove and stocking pattern of altered sensation \200\224as if wearing gloves and stockings Typically, the feet are affected \201 rst; with continued exposure the neuropathy may ascend the legs before affecting the hands and arms d Vibration perception \200 d Thermal sensation \200 d Proprioception \200 Loss of re \202 exes \200 Neuropathic pain: burning pain (worse at night) \200 Allodynia: non-pa inful stimuli (e.g. light touch) are perceived as painful \200 Altered skin appearance: s kin becomes shiny, with loss of hair. Motor neuropathy \200 Muscle wasting \200 Paralysis \200 Fasciculation \200 Cramps. Autonomic neuropathy Symptoms depend on affected organ: \200 Postural hypotension \200 Loss of sweating \200 Diarrhea or constipation \200 Incontinence (fecal or urinary). Causal exposures \200 Radiation \200 Lead \200 Mercury \200 Arsenic \200 Thallium \200 Tellurium (rare) \200 Methyl bromide (CH 3 Br) 12_Smedley_Chap12.indd 296 1/2/2013 12:13:51 PM PERIPHERAL NEUROPATHY 297 Acrylamide monomer \200 Organic solvents: \200 n-hexane \200 methyl n-butyl ketone Organophosphates: tri-orthocresyl phosphate (TOCP) \200 organophosphate insecticides (see b p. 90, Pesticid es; b p. 298, Organophosphate poisoning). Clinical assessment and diagnosis \200 A good history is important in the diagnosis of oc cupationally acquired peripheral neuropathy \200 Neurological examination \200 Nerve conduction studies to co n \201 rm the diagnosis \200 Electromyography (EMG) to distinguish between muscle and ne rve disease Nerve biopsy, if taken, may show demyelination, but an axonopathy is more usual in occupati onal toxic neuropathy. Some agents may cause axonopathy and demyelination. Prognosis \200 After withdrawal from exposure some patients continue to deteriorate for several months Over many months recovery generally occurs (assuming the neurons have survived), but may be incomplete. Health surveillance Depends on the agent implicated. For lead, see b p. 434, Inorganic lead . Medical management \200 Substitute a less hazardous agent in the workplace \200 Withdra w the worker from further exposure to the neurotoxin. Compensation Peripheral neuropathy is a prescribed disease (C29) for Industrial Injuries Di sablement Bene \201 t in those exposed to n-hexane or methyl n -butyl ketone. Relevant legislation \200 Peripheral neuropathy reliably attributable to work is reportab le under RIDDOR in work with n-hexane or methyl n-butyl ketone Lyme disease in work involving tick exposure is reportable under RIDDOR Poisoning by acrylamide monomer, arsenic, lead, or methyl bromide is reportable under RIDDOR. 12_Smedley_Chap12.indd 297 1/2/2013 12:13:51 PM CHAPTER 12 Neurological disorders 298 Organophosphate poisoning Organophosphates (OPs) are used widely as insecticides. Epidemiology \200 Most cases of acute OP poisoning occur in developing countries \200 A systematic review in 2007 1 estimated that there were 260 000 deaths/year from pesticide self-poisoning worldwide with OPs accounting for 2/3 of cases in Asia. Clinical features Three patterns of illness are associated with OP poisoning. Acute OP poisoning Acute poisoning presents with the symptoms of cholinergic toxicity due t o inhibition of acetylcholinesterase (AChE), leading to a failure to break down acetylcholi ne post-synaptically. \200\230Ageing \200\231 of the enzyme may occur, resulting in irreve rsible inhibition. Main clinical features of OP poisoning; \200 Bronchospasm \200 Diarr hea \200 Meiosis (constricted pupils) \200 Nausea and vomiting \200 Lacrimation \200 Profuse salivation \200 Urinary incontinence. Other effects include: \200 Psychomotor effects: increasing confusion, anxiety, sleep problems \200 Cardiac arrhythmia: bradycar dia (dizziness, fainting) or tachycardia \200 Tremor, muscle fasciculation \200 Sweatin g \200 Seizures \200 Coma \200 Death may occur because of respiratory paralysis or ca rdiac arrhythmias. Intermediate syndrome \200 Develops 712 \200\22396h after exposure \200 Proximal muscle weakness \200 Cranial nerve palsies \200 Respiratory muscle paralysis \200 Death due to respiratory paralysis. OP-induced delayed neuropathy (OPIDN) \200 OPIDN occurs with OPs that inhibit neuropathy target esterase (NTE), e.g. TOCP. Nowadays this is only seen following severe OP poisoning Gradual onset over several days after acute OP poisoning \200 Paraesthesia \200 Distal muscle wasting: feet > hands \200 Ataxia \200 Spasticity. 12_Smedley_Chap12.indd 298 1/2/2013 12:13:51 PM ORGANOPHOSPHATE POISONING 299 X Chronic OP poisoning in the absence of previous acute poisoning is a condition that some attribute to exposure to OPs, e.g. in sheep dipping or aviation. The symptoms reported are similar to chronic fatigue syndrome. However, a causal association with OPs remains unprove n. Causal exposures/industries The main route of exposure is dermal. \200 Agriculture: pesticide applicators \200 cotton growers \200 market gardening \200 sheep dippers \200 crop-dusting pilots, pesticide loaders Agrochemical manufacture \200 Terrorism, chemical warfare (sarin, tabun, VX) (see b p. 82 9, Chemical weapons). Clinical assessment and diagnosis \200 5mL of blood in EDTA tube for measurement of both red cell and plasma cholinesterase in suspected poisoning \200 Nerve conduction tests in suspected OPI DN. 2 AChE level within the normal range does not exclude poisoning. 2 The emergency treatm ent of OP poisoning is covered in b p. 802, Organophosphate poisoning. Prognosis \200 Acute poisoning: resolves over 3 \200\2234 days \200 Intermediate syndro me: resolves over 14 days \200 OPIDN: depends on severity. Recovery takes place over 6 \200\22312mths, but de \201 cits are lifelong if severe. Health surveillance \200 \200 \200 \200 Pre-exposure red cell and plasma AChE level Monthly AChE testing during use of OPs Absolute level of AChE is less important than change in level Multiple exposures may lead to cumula tive depression of cholinesterase levels and presentation with acute poisoning after appare ntly low-level exposure If AChE suspension from OP exposure. d 30% from pre-exposure level, examine worker and consider Relevant legislation/guidance \200 \200 OP poisoning is reportable under RIDDOR HSE Biological monitoring of workers exposed to org ano-phosphorus pesticides. MS 17. Health and Safety Executive, Sudbury. HSE (1999). Reporting incidents of exposure to pesticides and veterinary medicines M http://www.hse.gov.uk/pubns/indg141.pdf 1 Gunnell D, Eddleston M, Phillips MR, Konradsen F (2007). The global distribution of fatal pesti- cide self-poisoning: Systematic review. BMC Public Health 7 , 357. 12_Smedley_Chap12.indd 299 1/2/2013 12:13:52 PM CHAPTER 12 Neurological disorders 300 Hand \200\223arm vibration syndrome The term \200\230hand \200\223arm vibration syndrome \200\231 has been used to collec- tively de \201 ne the disorders thought to be associated with exposure to hand-transmitted vibration. Clinical features \200 Vibration white \201 nger (VWF): episodic \201 nger blanching, usually marble-white (but occasionally cyanotic) and cold-induced. Classically: is sharply demarcat ed and distal in initial development (only rarely \200 affecting the thumbs) affects the areas most in contact with vibrating parts is associated (during the attack) with numbness/ coldness and (in recovery) with parasthesiae and a reactive hyperaemia \200 Vibration-induced sensorineural disease (peripheral neuropathy and carpal tunnel syndrome) Effects on hand function (weakness of grip, poor manual dexterity) that may have a neuropat hic or myopathic origin Hand-arm pains, osteoarthritis of the wrist or elbow, speci \201 c musculoskeletal disorders of the upper limb and Dupuytren \200\231s contracture may also b e commoner in workers exposed to hand-transmitted vibration Dysfunction of the autonomic ne rvous system (with protean non- speci \201 c symptoms) is a proposed but not a well accept ed effect. Epidemiology HAVS is common. According to one population survey there are more than 220,000 cases in the UK; while claims assessed among ex-miners from British Coal exceeded 90,000. Causal exposures and industries See b p. 10, hand-transmitted vibration. Clinical assessment and diagnosis Diagnosis usually rests on a careful clinical history in a worker with symp- toms post-dating substantial exposure. Episodic attacks of VWF are sel- dom witnessed, while crude cold challenge tests lack sensitivity. \200 More complicated procedures exist for specialist legal assessment of HAVS, including: measurement of \201 nger systolic blood pressure during cooling, skin temperature and skin re-warming rates after cold challenge, thermal aesthesiometry, vibrot actile thresholds and tests of dexterity Vascular and sensory effects are normally graded s eparately, according to two three-point scales proposed in 1986 by an expert Stockholm Work shop (see b p. 768, clinical assessment of HAVS). Some assessors now combine these clinical features with the output from objective tests. Medical management There is no well-established and really satisfactory treatment. Most eff orts are directed against blanching attacks. 12_Smedley_Chap12.indd 300 1/2/2013 12:13:52 PM HAND \200\223ARM VIBRATION SYNDROME 301 Conservative measures are often advocated (e.g. the wearing of thermal gloves and warm clot hing, avoidance of drafts and exposure to cold, wet, windy conditions), but such advice can not always be followed in the work situation Evidence on ef \201 cacy of other forms of tr eatment is relatively weak; bene \201 ts have been claimed from: \200 physical therapy (exercises, compresses, hot packs, paraf \201 n baths, massage, traction, infrared treatment) adrenergic receptor blockers antiplatelet and antithrombotic agents \200 \200 calcium-channel blockers \200\224oral nifedipine and diltiazem may offer some promise. Prognosis \200 Until the 1960s VWF was considered irreversible, but more recent studies show vascular symp toms can improve on withdrawal from exposure, albeit slowly, over several years. Workers wi th advanced disease are less likely to recover The neurological effects do not improve with time; stage 3SN disease can be seriously disabling, in terms of impaired hand function, an d is the most important avoidable morbidity (the aim should be to prevent progression from early- to late-stage 2SN). Prevention See b p. 10, Hand-transmitted vibration. Health surveillance \200 This is required for workers who remain regularly exposed above the EAV A(8) of 2.5m/s 2 de spite controls The aims are: \200 \200 The main element is periodic symptom inquiries. Health records need to be maintained. to aid early detection and counseling/job modi \201 cation to provide a check of workplace control measures Compensation \200 In the UK, HAVS (A11) is prescribed for Industrial Injuries Bene \201 t in employed earner s, provided that it occurs the year round, is extensive, and occurs in a scheduled occupati on 1 Many other European countries compensate VWF on a similar basis. Relevant legislation Employers are required to notify cases to the appropriate enforcing au thority (HSE or local authority) under the RIDDOR Regulations. 1 Social Security (Industrial Injuries) (Prescribed Diseases) Regulations 1985, Schedule 1: http:// www.dwp.gov.uk/docs/a4-3851.pdf 12_Smedley_Chap12.indd 301 1/2/2013 12:13:52 PM CHAPTER 12 Neurological disorders 302 Noise-induced hearing loss Hearing loss due to occupational noise exposure is, in theory, p reventable, but noise-induced hearing loss (NIHL) remains common. Epidemiology \200 \200 Hearing loss affects 2% of adults of working age in Britain Prevalence aged 55 \200\22364yr s British estimates deafness due to occupational noise exposure. i from 1% among 4 aged 16 \200\22324yrs to 8% among those 1 suggest that 153,000 men and 26,000 women have Clinical features \200 \200 \200 Reduced auditory acuity Tinnitus Increasing social isolation as hearing decreases. Causal industries \200 \200 \200 \200 \200 \200 \200 \200 Quarrying and mining Food industry Agriculture Entertainment industry (pubs, clubs, discos) Armed forces and security services Construction industry Metal working Aviation. Individual susceptibility Some individuals with \200\230tender ears \200\231 appear to be especially sensitive to the adverse effects of noise exposure. Others, despite signi \201 cant noise expo- sure, have apparently normal hearing. Clinical assessment and diagnosis Noise exposure history: both occupational and hobby expos ures \200 \200 \200 \200 DIY Music Motor sport Hunting/target shooting. Medical history seeking risk factors for hearing loss \200 \200 \200 \200 \200 Meningitis Congenital infections: rubella, CMV Head injury (fracture of base of skull) Otot oxic medication including Aminoglycosides (e.g. gentamicin): \200 \200 \200 M ni re \200\231s disease (tinnitus, deafness, vertigo) Family history of deafness Otitis media quinine salicylates furosemide \200 \200 12_Smedley_Chap12.indd 302 1/2/2013 12:13:52 PM NOISE-INDUCED HEARING LOSS 303 \200 Otosclerosis Perforated tympanic membrane. Examination \200 Examine external ear: scars (previous surgery) \200 Otoscopy: \200 \200 \200 Tuning fork testing (512 Hz tuning fork): \200 \200\223 a ir conduction > bone conduction (Rinne positive) in sensorineural tympanic scars tympanic perforation mastoid surgery Rinne \200\231s test \200\224 loss or normal hearing \200\223 bone conduction > air conduction (Rinne negative) in conductive hearing loss (e.g. otosclerosis) Weber \200\231s test \200\224lateralizes to affected ear in conductive loss Pure tone audiometry: classical pattern in NIHL is a 4kHz dip with recovery although peak l oss can be anywhere between 3 and 6kHz ( b p. 430, Classi \201 cation of hearing loss and b p. 432, Patterns of hearing loss) Auditory evoked response (AER). Prognosis NIHL does not progress after withdrawal from exposure. However, the combination o f established NIHL and age-related hearing loss (presbyacu- sis) means that even after with drawal from exposure the affected worker \200\231s hearing will continue to decline. Health surveillance \200 Pre-employment audiometry (identi \201 es existing losses) (see b p. 764, Screening audiom etry) Annual testing for \201 rst 2yrs of employment Three-yearly testing after \201 rs t 2yrs. \200 Medical management NIHL suggests that the hearing conservation program has not pro- tected worker \200\231s hearing. Exclude other causes of hearing loss. Compensation NIHL is prescribed (A10) for Industrial Injuries Disablement Bene \201 t for those involved in speci \201 ed activities. Hearing loss must be at least 50dB in each ear to qualify. Relevant legislation/guidance HMSO (2005). The Control of Noise at Work Regulations . Stati onery Of \201 ce, London. Available at: M http://www.legislation.gov.uk/uksi/2005/1643/ co ntents/made 1 Palmer KT et al. (2002). Occupational exposure to noise and the attributable burden of he aring dif \201 culties in Great Britain. Occup Environ Med 59 , 634 \200\2239. 12_Smedley_Chap12.indd 303 1/2/2013 12:13:52 PM This page intentionally left blank 305 Chapter 13 Psychiatric disorders Psychoses due to occupational exposures 306 Stress 1: recognition and assessment 308 Stress 2: interventions/risk controls 311 Post-traumatic stress disorder 1: diagnosis and risk fa ctors 313 Post-traumatic stress disorder 2: management 314 13_Smedley_Chap13.indd 305 1/2/2013 1:34:25 PM CHAPTER 13 Psychiatric disorders 306 Psychoses due to occupational exposures Epidemiology Organic psychosis due to occupational exposures is thankfully unusual, but its very rarity means that the diagnosis may be missed . Historically, exposures in certain industries put workers at risk of organic psychoses or psychiatric effects: \200 Mirror silvering (mercury) \200 Manganese mining \200 Cold vulcanization of rubber (CS 2 ) \200 Manufacture of organoleads for leaded gasoline. Clinical features Manganese madness A syndrome of hallucinations, nervousness, insomnia, em otional lability, (especially inappropriate laughter), compulsive behavior, and altered lib ido. Organolead Insomnia, anxiety, emotional lability, delusions and mania. If exposure is sever e, death due to encephalopathy may occur. Methylmercury Depression, emotional lability (including inappropriate laughter), and increa sed response to stimuli (erethism). Neurological de \201 cits, including coarse tremor, dy sarthria, ataxia, visual \201 eld losses, and peripheral neu- ropathy, may co-exist. Carbon disulphide Irritability, agitation, hallucinations, and bipolar illness. Causal exposures/industries \200 Organolead (tetraethyl lead, triethyl lead) \200 Methy lmercury \200 Manganese: chronic exposure in manganese mining \200 Aluminum? \200 Tin (triethyl tin, trimethyl tin) \200 Organic solvents: e.g. in glues, paints, degreasants carbon disulphide (CS 2 ) \200 styrene \200\224boat building \200 lacquers, varnishes \200\224furniture making \200 microelectronics industry. Individual susceptibility Manganese: adverse effects generally present in susceptible indiv iduals after 6mths exposure. The young appear more susceptible. 13_Smedley_Chap13.indd 306 1/2/2013 1:34:25 PM PSYCHOSES DUE TO OCCUPATIONAL EXPOSURES 307 Clinical assessment and diagnosis A history of exposure to any of these agents should alert the treating doctor to the possibility of an organic cause for the patient \200\231s illne ss. Manganese intoxication may present with both psychiatric symptoms and parkinsonian feat ures (see b p. 292, Parkinsonism). Prognosis The psychiatric effects of manganese may be reversible if identi \201 ed early a nd exposure ceases. Health surveillance See b p. 436, Organic lead for details of organic lead surveillance. Medical management Withdraw from exposure. Compensation CNS toxicity characterized by tremor and neuropsychiatric disease is pre- scri bed (C5(a)) for Industrial Injuries Disablement Bene \201 t in those who have been exposed to mercury for >10yrs. Relevant legislation Control of Lead at Work Regulations 2002 Approved Code of Practice. 13_Smedley_Chap13.indd 307 1/2/2013 1:34:25 PM CHAPTER 13 Psychiatric disorders 308 Stress 1: recognition and assessment De \201 nition The emotional and physiological state of disequilibrium that pertains when the perceived demands of life exceed one \200\231s per ceived ability to cope. It is: \200 Not a mental illness \200 Not listed in the Interna tional Classi \201 cation of Diseases (ICD) or the Diagnostic and Statistical Manual of Me ntal Disorders, 4th edition (DSM IV) Natural response to range of challenges or life events \200 Not necessarily harmful; can improve performance in some situations \200 In some individuals may be a risk factor for poor mental ill health. Epidemiology \200 435,000 people in the UK reported work related stress, anxiety, or depr ession in 2006/7. See M http://www.hse.gov.uk/statistics/overall/ hssh0910.pdf 20% of the UK working population \200\230very \200\231 or \200\230extremely \200\231 stre ssed \200 More than 9.3 million working days are lost each year in the UK from work-related mental ill health or \200\230stress \200\231 Individual, local, organizational, and cultural factors affect the level of reported stress The sharp rise in cases of reported stress contrasts with the relatively minor secular changes in prevalence of mental illness. Clinical features Individual symptoms \200 \200 Behavioral changes \200 Increased irritability \200 Impulsive behavior \200 Social wi thdrawal \200 Less able to relax at home \200 Working more than usual \200 Increased use of caffeine, cigarettes or alcohol, addictive drugs or other substances 1 Remember stre ss is not an ill- ness and all these symptoms are non-speci \201 c Reduced self-con \201 dence Feelings of tension and nervousness Self-doubt Indecisiveness Increased irritability Fluctuations of mood Sleep dif \201 culties Poor concentration \200\230Burn-out \200\231 \200 \200 \200 \200 \200 \200 Adjustment disorders \200 Mainly anxiety \200 Temporal association with an apparent str essor \200 Signi \201 cant impairment of social and occupational functioning is required to establish the diagnosis depressive symptoms 13_Smedley_Chap13.indd 308 1/2/2013 1:34:25 PM STRESS 1: RECOGNITION AND ASSESSMENT 309 Causal exposures/industries The Management Standards HSE describes a system to identify risk factors at work (see b p. 134, Organizational psychosocial factors) \200 \200 \200 \200 \200 Demand Change Relationships Control Role Support Workers in several sectors report higher levels of stress, but that does not mean these sec tors are more stressful: \200 Secondary school teachers \200 HCWs \200 Call center op eratives \200 Emergency service workers (police in particular). Sector-speci \201 c guidance on risk management is available on the HSE website. M http://www.hse.gov.uk/stress/information.htm Individual susceptibility \200 Previous history of work-related stress \200 Co-existing non-work-related stress (e.g. domestic upheavals) \200 Previous history of mental health problems \200 High alcohol intake \200 Excessive personal expectations, Type A persona lity. Diagnostic assessment \200 Exclusion of psychiatric disorder: e.g. major depressive illne ss, generalized anxiety disorder, obsessive \200\223compulsive disorder (OCD) Identi \201 cation of potential occupational stressors: including interpersonal con \202 ict, bullying, harassment, or grievances, by risk assessment Identi \201 cation of non-work stressors \200 Identify current coping strategies: are th ey helpful, can they be in \202 uenced by individual mentors or training? \200\230Post-traumatic stress disorder \200\231 has very speci \201 c diagnostic criteria and the term should not be used if these are not met. Prognosis \200 In general, excellent \200 Early intervention critical to successful out come (see b p. 311, Stress 2: interventions/risk controls). 13_Smedley_Chap13.indd 309 1/2/2013 1:34:25 PM CHAPTER 13 Psychiatric disorders 310 Time off work \200 Can be detrimental to recovery of the employee unless the condition in terferes signi \201 cantly with performance at work. As far as possible, with adequate sup port and adjustments, it is advisable to keep the employee at work If time off work is needed, there should be clarity about reason for absence, return to work process, and how progress will be monitored. Relevant legislation and guidance \200 Protection from Harassment Act 1997 \200 Tacklin g stress: The Management Standards Approach (1997). M http://www.hse.gov.uk/stress/standards/ 13_Smedley_Chap13.indd 310 1/2/2013 1:34:25 PM STRESS 2: INTERVENTIONS/RISK CONTROLS 311 Stress 2: interventions/risk controls Primary (preventing stress in the workforce) See b p. 134, Organizational psychosocial factors, Risk controls. \200 Stressor identi \201 cati on and risk assessment \200 Attention to job design \200 Skills and leadership training at all levels in the organization \200 Flexible working as part of work \200\223life bal ance program. Secondary (preventing recurrence or exacerbation in an individual with work-related stress) \200 Attentive and compassionate management \200 Cognitive behavioral therapy (CBT) \200 Change management \200 Assertiveness training \200 Time management \200 Interpe rsonal skills training. Interventions for the individual with work-related stress Psychological support through occ upational health (OH) and employee support program: \200 Con \201 dential self-referral service available to all employees \200 Access to clinical psychology \200 Therapy tech niques aimed at problem-solving \200 Highly focused individualized approach \200 Emphas is on therapeutic bene \201 ts of work. Including round-table discussions \200 Involving employee, OH +/ \200\223 treating psychologist, patient \200\231s manager, and HR taking a shared problem-solving approach to deal with stress issues Particularly useful if patient is off work and where interpersonal con \202 ict has complicated the situation Enabling early agreement on a graduated rehabilitation program back to work, establishing job de \201 nition, hours and days of work, etc. Educating managers on nature of stress-related dif \201 culties and ensuring their commitment to the rehabilitation program, including preparation of the rest of the team for the employee \200\231s return from sickness absence. Further information and guidance Health and Safety Executive. (1999). Managing Stress at Wo rk . HSE, Sudbury. Health and Safety Executive. (2001). Tackling work-related stress: a man ager \200\231s guide to improving and maintaining employee health and wellbeing . HSE, Sudbury. Health and Safety Executive. (2004). Stress Management Standards . HSE, Sudbury. Calnan M, Wainwright D (2002) Work stress: the making of a modern epidemic . Open University Press, London. Available at: M http://www.hse.gov.uk/stress/index.htm 13_Smedley_Chap13.indd 311 1/2/2013 1:34:25 PM CHAPTER 13 Psychiatric disorders 312 Post-traumatic stress disorder 1: diagnosis and risk factors Effects of severe stress Extre mely disturbing events can have marked and sustained emotional effects. Warfare has provide d most evidence and it has generated many diagnoses, including Da Costa \200\231s syndrome, soldier \200\231s heart, and shell shock. The Vietnam War led to post-traumatic stress dis order (PTSD) enter- ing the Diagnostic and Statistical Manual of Mental Disorders (DSM III) (American Psychiatric Association, 1980). The current revision is the DSM-IV (1994 America n Psychiatric Association, 1994). The nosology used most frequently in the UK is the ICD-10 (WHO, 1992). 1 Epidemiology \200 Community samples: no community-based survey of PTSD has been conducted in the UK and most data derive from the USA. Note the obvious sociocultural differences, i ncluding availability of \201 rearms. \200 lifetime prevalence for adult exposure to tr auma 3.9 \200\22389.6% \200 lifetime PTSD prevalence rates 1.0 \200\22311.2% \200 risk of PTSD is greater for 5 than 4 (20.4% vs. 8.1%) \200 younger urban populations report hi gher incidence (up to 30.2% for 5 and 13% for 4 ) Selected samples: