Sequelae Health Dictionary

Sequelae: From 1 Different Sources


The term applied to symptoms or effects which are liable to follow certain diseases. For example, BRONCHITIS and other chest complaints may be sequelae of MEASLES; heart disease is often a sequelae of RHEUMATIC FEVER; PARALYSIS may follow DIPHTHERIA.
Health Source: Medical Dictionary
Author: Health Dictionary

Sequela

A condition that results from or follows a disease, disorder, or injury.

The term is usually used in plural (sequelae) to refer to the complications of a disease.... sequela

Carbon Monoxide (co)

This is a colourless, odourless, tasteless, nonirritating gas formed on incomplete combustion of organic fuels. Exposure to CO is frequently due to defective gas, oil or solid-fuel heating appliances. CO is a component of car exhaust fumes and deliberate exposure to these is a common method of suicide. Victims of ?res often suffer from CO poisoning. CO combines reversibly with oxygen-carrying sites of HAEMOGLOBIN (Hb) molecules with an a?nity 200 to 300 times greater than oxygen itself. The carboxyhaemoglobin (COHb) formed becomes unavailable for oxygen transportation. In addition the partial saturation of the Hb molecule results in tighter oxygen binding, impairing delivery to the tissues. CO also binds to MYOGLOBIN and respiratory cytochrome enzymes. Exposure to CO at levels of 500 parts per million (ppm) would be expected to cause mild symptoms only and exposure to levels of 4,000 ppm would be rapidly fatal.

Each year around 50 people in the United Kingdom are reported as dying from carbon monoxide poisoning, and experts have suggested that as many as 25,000 people a year are exposed to its effects within the home, but most cases are unrecognised, unreported and untreated, even though victims may suffer from long-term effects. This is regrettable, given that Napoleon’s surgeon, Larrey, recognised in the 18th century that soldiers were being poisoned by carbon monoxide when billeted in huts heated by woodburning stoves. In the USA it is estimated that 40,000 people a year attend emergency departments suffering from carbon monoxide poisoning. So prevention is clearly an important element in dealing with what is sometimes termed the ‘silent killer’. Safer designs of houses and heating systems, as well as wider public education on the dangers of carbon monoxide and its sources, are important.

Clinical effects of acute exposure resemble those of atmospheric HYPOXIA. Tissues and organs with high oxygen consumption are affected to a great extent. Common effects include headaches, weakness, fatigue, ?ushing, nausea, vomiting, irritability, dizziness, drowsiness, disorientation, incoordination, visual disturbances, TACHYCARDIA and HYPERVENTILATION. In severe cases drowsiness may progress rapidly to COMA. There may also be metabolic ACIDOSIS, HYPOKALAEMIA, CONVULSIONS, HYPOTENSION, respiratory depression, ECG changes and cardiovascular collapse. Cerebral OEDEMA is common and will lead to severe brain damage and focal neurological signs. Signi?cant abnormalities on physical examination include impaired short-term memory, abnormal Rhomberg’s test (standing unsupported with eyes closed) and unsteadiness of gait including heel-toe walking. Any one of these signs would classify the episode as severe. Victims’ skin may be coloured pink, though this is very rarely seen even in severe incidents. The venous blood may look ‘arterial’. Patients recovering from acute CO poisoning may suffer neurological sequelae including TREMOR, personality changes, memory impairment, visual loss, inability to concentrate and PARKINSONISM. Chronic low-level exposures may result in nausea, fatigue, headache, confusion, VOMITING, DIARRHOEA, abdominal pain and general malaise. They are often misdiagnosed as in?uenza or food poisoning.

First-aid treatment is to remove the victim from the source of exposure, ensure an e?ective airway and give 100-per-cent oxygen by tight-?tting mask. In hospital, management is largely suppportive, with oxygen administration. A blood sample for COHb level determination should be taken as soon as practicable and, if possible, before oxygen is given. Ideally, oxygen therapy should continue until the COHb level falls below 5 per cent. Patients with any history of unconsciousness, a COHb level greater than 20 per cent on arrival, any neurological signs, any cardiac arrhythmias or anyone who is pregnant should be referred for an expert opinion about possible treatment with hyperbaric oxygen, though this remains a controversial therapy. Hyperbaric oxygen therapy shortens the half-life of COHb, increases plasma oxygen transport and reverses the clinical effects resulting from acute exposures. Carbon monoxide is also an environmental poison and a component of cigarette smoke. Normal body COHb levels due to ENDOGENOUS CO production are 0.4 to

0.7 per cent. Non-smokers in urban areas may have level of 1–2 per cent as a result of environmental exposure. Smokers may have a COHb level of 5 to 6 per cent.... carbon monoxide (co)

Japanese Encephalitis

A flavivirus, related to Murray Valley virus (see Australian Encephalitis). Rice paddybreeding Culicine mosquitoes, Culex tritaeniorhyehus, often transmit the disease. Mosquitoes are largely zoophilic. Occasionally Aedes spp and Anopholines implicated in transmission. Disease consists of prodrome, encephalitis and recovery (or death on average in 7%). Affects mostly children less than five years of age and leaves sequelae. A vaccination is available.... japanese encephalitis

Occupational Health, Medicine And Diseases

Occupational health The e?ect of work on human health, and the impact of workers’ health on their work. Although the term encompasses the identi?cation and treatment of speci?c occupational diseases, occupational health is also an applied and multidisciplinary subject concerned with the prevention of occupational ill-health caused by chemical, biological, physical and psychosocial factors, and the promotion of a healthy and productive workforce.

Occupational health includes both mental and physical health. It is about compliance with health-and-safety-at-work legislation (and common law duties) and about best practice in providing work environments that reduce risks to health and safety to lowest practicable levels. It includes workers’ ?tness to work, as well as the management of the work environment to accommodate people with disabilities, and procedures to facilitate the return to work of those absent with long-term illness. Occupational health incorporates several professional groups, including occupational physicians, occupational health nurses, occupational hygienists, ergonomists, disability managers, workplace counsellors, health-and-safety practitioners, and workplace physiotherapists.

In the UK, two key statutes provide a framework for occupational health: the Health and Safety at Work, etc. Act 1974 (HSW Act); and the Disability Discrimination Act 1995 (DDA). The HSW Act states that employers have a duty to protect the health, safety and welfare of their employees and to conduct their business in a way that does not expose others to risks to their health and safety. Employees and self-employed people also have duties under the Act. Modern health-and-safety legislation focuses on assessing and controlling risk rather than prescribing speci?c actions in di?erent industrial settings. Various regulations made under the HSW Act, such as the Control of Substances Hazardous to Health Regulations, the Manual Handling Operations Regulations and the Noise at Work Regulations, set out duties with regard to di?erent risks, but apply to all employers and follow the general principles of risk assessment and control. Risks should be controlled principally by removing or reducing the hazard at source (for example, by substituting chemicals with safer alternatives, replacing noisy machinery, or automating tasks to avoid heavy lifting). Personal protective equipment, such as gloves and ear defenders, should be seen as a last line of defence after other control measures have been put in place.

The employment provisions of the DDA require employers to avoid discriminatory practice towards disabled people and to make reasonable adjustments to working arrangements where a disabled person is placed at a substantial disadvantage to a non-disabled person. Although the DDA does not require employers to provide access to rehabilitation services – even for those injured or made ill at work – occupational-health practitioners may become involved in programmes to help people get back to work after injury or long-term illness, and many businesses see the retention of valuable sta? as an attractive alternative to medical retirement or dismissal on health grounds.

Although a major part of occupational-health practice is concerned with statutory compliance, the workplace is also an important venue for health promotion. Many working people rarely see their general practitioner and, even when they do, there is little time to discuss wider health issues. Occupational-health advisers can ?ll in this gap by providing, for example, workplace initiatives on stopping smoking, cardiovascular health, diet and self-examination for breast and testicular cancers. Such initiatives are encouraged because of the perceived bene?ts to sta?, to the employing organisation and to the wider public-health agenda. Occupational psychologists recognise the need for the working population to achieve a ‘work-life balance’ and the promotion of this is an increasing part of occupational health strategies.

The law requires employers to consult with their sta? on health-and-safety matters. However, there is also a growing understanding that successful occupational-health management involves workers directly in the identi?cation of risks and in developing solutions in the workplace. Trade unions play an active role in promoting occupational health through local and national campaigns and by training and advising elected workplace safety representatives.

Occupational medicine The branch of medicine that deals with the control, prevention, diagnosis, treatment and management of ill-health and injuries caused or made worse by work, and with ensuring that workers are ?t for the work they do.

Occupational medicine includes: statutory surveillance of workers’ exposure to hazardous agents; advice to employers and employees on eliminating or reducing risks to health and safety at work; diagnosis and treatment/management of occupational illness; advice on adapting the working environment to suit the worker, particularly those with disabilities or long-term health problems; and advice on the return to work and, if necessary, rehabilitation of workers absent through illness. Occupational physicians may play a wider role in monitoring the health of workplace populations and in advising employers on controlling health hazards where ill-health trends are observed. They may also conduct epidemiological research (see EPIDEMIOLOGY) on workplace diseases.

Because of the occupational physician’s dual role as adviser to both employer and employee, he or she is required to be particularly diligent with regards to the individual worker’s medical CONFIDENTIALITY. Occupational physicians need to recognise in any given situation the context they are working in, and to make sure that all parties are aware of this.

Occupational medicine is a medical discipline and thus is only part of the broader ?eld of occupational health. Although there are some speci?c clinical duties associated with occupational medicine, such as diagnosis of occupational disease and medical screening, occupational physicians are frequently part of a multidisciplinary team that might include, for example, occupational-health nurses, healthand-safety advisers, ergonomists, counsellors and hygienists. Occupational physicians are medical practitioners with a post-registration quali?cation in occupational medicine. They will have completed a period of supervised in-post training. In the UK, the Faculty of Occupational Medicine of the Royal College of Physicians has three categories of membership, depending on quali?cations and experience: associateship (AFOM); membership (MFOM); and fellowship (FFOM).

Occupational diseases Occupational diseases are illnesses that are caused or made worse by work. In their widest sense, they include physical and mental ill-health conditions.

In diagnosing an occupational disease, the clinician will need to examine not just the signs and symptoms of ill-health, but also the occupational history of the patient. This is important not only in discovering the cause, or causes, of the disease (work may be one of a number of factors), but also in making recommendations on how the work should be modi?ed to prevent a recurrence – or, if necessary, in deciding whether or not the worker is able to return to that type of work. The occupational history will help in deciding whether or not other workers are also at risk of developing the condition. It will include information on:

the nature of the work.

how the tasks are performed in practice.

the likelihood of exposure to hazardous agents (physical, chemical, biological and psychosocial).

what control measures are in place and the extent to which these are adhered to.

previous occupational and non-occupational exposures.

whether or not others have reported similar symptoms in relation to the work. Some conditions – certain skin conditions,

for example – may show a close relationship to work, with symptoms appearing directly only after exposure to particular agents or possibly disappearing at weekends or with time away from work. Others, however, may be chronic and can have serious long-term implications for a person’s future health and employment.

Statistical information on the prevalence of occupational disease in the UK comes from a variety of sources, including o?cial ?gures from the Industrial Injuries Scheme (see below) and statutory reporting of occupational disease (also below). Neither of these o?cial schemes provides a representative picture, because the former is restricted to certain prescribed conditions and occupations, and the latter suffers from gross under-reporting. More useful are data from the various schemes that make up the Occupational Diseases Intelligence Network (ODIN) and from the Labour Force Survey (LFS). ODIN data is generated by the systematic reporting of work-related conditions by clinicians and includes several schemes. Under one scheme, more than 80 per cent of all reported diseases by occupational-health physicians fall into just six of the 42 clinical disease categories: upper-limb disorders; anxiety, depression and stress disorders; contact DERMATITIS; lower-back problems; hearing loss (see DEAFNESS); and ASTHMA. Information from the LFS yields a similar pattern in terms of disease frequency. Its most recent survey found that over 2 million people believed that, in the previous 12 months, they had suffered from an illness caused or made worse by work and that

19.5 million working days were lost as a result. The ten most frequently reported disease categories were:

stress and mental ill-health (see MENTAL ILLNESS): 515,000 cases.

back injuries: 508,000.

upper-limb and neck disorders: 375,000.

lower respiratory disease: 202,000.

deafness, TINNITUS or other ear conditions: 170,000.

lower-limb musculoskeletal conditions: 100,000.

skin disease: 66,000.

headache or ‘eyestrain’: 50,000.

traumatic injury (includes wounds and fractures from violent attacks at work): 34,000.

vibration white ?nger (hand-arm vibration syndrome): 36,000. A person who develops a chronic occu

pational disease may be able to sue his or her employer for damages if it can be shown that the employer was negligent in failing to take reasonable care of its employees, or had failed to provide a system of work that would have prevented harmful exposure to a known health hazard. There have been numerous successful claims (either awarded in court, or settled out of court) for damages for back and other musculoskeletal injuries, hand-arm vibration syndrome, noise-induced deafness, asthma, dermatitis, MESOTHELIOMA and ASBESTOSIS. Employers’ liability (workers’ compensation) insurers are predicting that the biggest future rise in damages claims will be for stress-related illness. In a recent study, funded by the Health and Safety Executive, about 20 per cent of all workers – more than 5 million people in the UK – claimed to be ‘very’ or ‘extremely’ stressed at work – a statistic that is likely to have a major impact on the long-term health of the working population.

While victims of occupational disease have the right to sue their employers for damages, many countries also operate a system of no-fault compensation for the victims of prescribed occupational diseases. In the UK, more than 60 diseases are prescribed under the Industrial Injuries Scheme and a person will automatically be entitled to state compensation for disability connected to one of these conditions, provided that he or she works in one of the occupations for which they are prescribed. The following short list gives an indication of the types of diseases and occupations prescribed under the scheme:

CARPAL TUNNEL SYNDROME connected to the use of hand-held vibrating tools.

hearing loss from (amongst others) use of pneumatic percussive tools and chainsaws, working in the vicinity of textile manufacturing or woodworking machines, and work in ships’ engine rooms.

LEPTOSPIROSIS – infection with Leptospira (various listed occupations).

viral HEPATITIS from contact with human blood, blood products or other sources of viral hepatitis.

LEAD POISONING, from any occupation causing exposure to fumes, dust and vapour from lead or lead products.

asthma caused by exposure to, among other listed substances, isocyanates, curing agents, solder ?ux fumes and insects reared for research.

mesothelioma from exposure to asbestos.

In the UK, employers and the self-employed have a duty to report all occupational injuries (if the employee is o? work for three days or more as a result), diseases or dangerous incidents to the relevant enforcing authority (the Health and Safety Executive or local-authority environmental-health department) under the Reporting of Injuries, Diseases and Dangerous Occurrences Regulations 1995 (RIDDOR). Despite this statutory duty, comparatively few diseases are reported so that ?gures generated from RIDDOR reports do not give a useful indication of the scale of occupational diseases in the UK. The statutory reporting of injuries is much better, presumably because of the clear and acute relationship between a workplace accident and the resultant injury. More than 160,000 injuries are reported under RIDDOR every year compared with just 2,500 or so occupational diseases, a gross underestimate of the true ?gure.

There are no precise ?gures for the number of people who die prematurely because of work-related ill-health, and it would be impossible to gauge the exact contribution that work has on, for example, cardiovascular disease and cancers where the causes are multifactorial. The toll would, however, dwarf the number of deaths caused by accidents at work. Around 250 people are killed by accidents at work in the UK each year – mesothelioma, from exposure to asbestos at work, alone kills more than 1,300 people annually.

The following is a sample list of occupational diseases, with brief descriptions of their aetiologies.

Inhaled materials

PNEUMOCONIOSIS covers a group of diseases which cause ?brotic lung disease following the inhalation of dust. Around 250–300 new cases receive bene?t each year – mostly due to coal dust with or without silica contamination. SILICOSIS is the more severe disease. The contraction in the size of the coal-mining industry as well as improved dust suppression in the mines have diminished the importance of this disease, whereas asbestos-related diseases now exceed 1,000 per year. Asbestos ?bres cause a restrictive lung disease but also are responsible for certain malignant conditions such as pleural and peritoneal mesothelioma and lung cancer. The lung-cancer risk is exacerbated by cigarette-smoking.

Even though the use of asbestos is virtually banned in the UK, many workers remain at risk of exposure because of the vast quantities present in buildings (much of which is not listed in building plans). Carpenters, electricians, plumbers, builders and demolition workers are all liable to exposure from work that disturbs existing asbestos. OCCUPATIONAL ASTHMA is of increasing importance – not only because of the recognition of new allergic agents (see ALLERGY), but also in the number of reported cases. The following eight substances are most frequently linked to occupational asthma (key occupations in brackets): isocyanates (spray painters, electrical processors); ?our and grain (bakers and farmers); wood dust (wood workers); glutaraldehyde (nurses, darkroom technicians); solder/colophony (welders, electronic assembly workers); laboratory animals (technicians, scientists); resins and glues (metal and electrical workers, construction, chemical processors); and latex (nurses, auxiliaries, laboratory technicians).

The disease develops after a short, symptomless period of exposure; symptoms are temporally related to work exposures and relieved by absences from work. Removal of the worker from exposure does not necessarily lead to complete cessation of symptoms. For many agents, there is no relationship with a previous history of ATOPY. Occupational asthma accounts for about 10 per cent of all asthma cases. DERMATITIS The risk of dermatitis caused by an allergic or irritant reaction to substances used or handled at work is present in a wide variety of jobs. About three-quarters of cases are irritant contact dermatitis due to such agents as acids, alkalis and solvents. Allergic contact dermatitis is a more speci?c response by susceptible individuals to a range of allergens (see ALLERGEN). The main occupational contact allergens include chromates, nickel, epoxy resins, rubber additives, germicidal agents, dyes, topical anaesthetics and antibiotics as well as certain plants and woods. Latex gloves are a particular cause of occupational dermatitis among health-care and laboratory sta? and have resulted in many workers being forced to leave their profession through ill-health. (See also SKIN, DISEASES OF.)

Musculoskeletal disorders Musculoskeletal injuries are by far the most common conditions related to work (see LFS ?gures, above) and the biggest cause of disability. Although not all work-related, musculoskeletal disorders account for 36.5 per cent of all disabilities among working-age people (compared with less than 4 per cent for sight and hearing impairment). Back pain (all causes – see BACKACHE) has been estimated to cause more than 50 million days lost every year in sickness absence and costs the UK economy up to £5 billion annually as a result of incapacity or disability. Back pain is a particular problem in the health-care sector because of the risk of injury from lifting and moving patients. While the emphasis should be on preventing injuries from occurring, it is now well established that the best way to manage most lower-back injuries is to encourage the patient to continue as normally as possible and to remain at work, or to return as soon as possible even if the patient has some residual back pain. Those who remain o? work on long-term sick leave are far less likely ever to return to work.

Aside from back injuries, there are a whole range of conditions affecting the upper limbs, neck and lower limbs. Some have clear aetiologies and clinical signs, while others are less well de?ned and have multiple causation. Some conditions, such as carpal tunnel syndrome, are prescribed diseases in certain occupations; however, they are not always caused by work (pregnant and older women are more likely to report carpal tunnel syndrome irrespective of work) and clinicians need to be careful when assigning work as the cause without ?rst considering the evidence. Other conditions may be revealed or made worse by work – such as OSTEOARTHRITIS in the hand. Much attention has focused on injuries caused by repeated movement, excessive force, and awkward postures and these include tenosynovitis (in?ammation of a tendon) and epicondylitis. The greatest controversy surrounds upper-limb disorders that do not present obvious tissue or nerve damage but nevertheless give signi?cant pain and discomfort to the individual. These are sometimes referred to as ‘repetitive strain injury’ or ‘di?use RSI’. The diagnosis of such conditions is controversial, making it di?cult for sufferers to pursue claims for compensation through the courts. Psychosocial factors, such as high demands of the job, lack of control and poor social support at work, have been implicated in the development of many upper-limb disorders, and in prevention and management it is important to deal with the psychological as well as the physical risk factors. Occupations known to be at particular risk of work-related upper-limb disorders include poultry processors, packers, electronic assembly workers, data processors, supermarket check-out operators and telephonists. These jobs often contain a number of the relevant exposures of dynamic load, static load, a full or excessive range of movements and awkward postures. (See UPPER LIMB DISORDERS.)

Physical agents A number of physical agents cause occupational ill-health of which the most important is occupational deafness. Workplace noise exposures in excess of 85 decibels for a working day are likely to cause damage to hearing which is initially restricted to the vital frequencies associated with speech – around 3–4 kHz. Protection from such noise is imperative as hearing aids do nothing to ameliorate the neural damage once it has occurred.

Hand-arm vibration syndrome is a disorder of the vascular and/or neural endings in the hands leading to episodic blanching (‘white ?nger’) and numbness which is exacerbated by low temperature. The condition, which is caused by vibrating tools such as chain saws and pneumatic hammers, is akin to RAYNAUD’S DISEASE and can be disabling.

Decompression sickness is caused by a rapid change in ambient pressure and is a disease associated with deep-sea divers, tunnel workers and high-?ying aviators. Apart from the direct effects of pressure change such as ruptured tympanic membrane or sinus pain, the more serious damage is indirectly due to nitrogen bubbles appearing in the blood and blocking small vessels. Central and peripheral nervous-system damage and bone necrosis are the most dangerous sequelae.

Radiation Non-ionising radiation from lasers or microwaves can cause severe localised heating leading to tissue damage of which cataracts (see under EYE, DISORDERS OF) are a particular variety. Ionising radiation from radioactive sources can cause similar acute tissue damage to the eyes as well as cell damage to rapidly dividing cells in the gut and bone marrow. Longer-term effects include genetic damage and various malignant disorders of which LEUKAEMIA and aplastic ANAEMIA are notable. Particular radioactive isotopes may destroy or induce malignant change in target organs, for example, 131I (thyroid), 90Sr (bone). Outdoor workers may also be at risk of sunburn and skin cancers. OTHER OCCUPATIONAL CANCERS Occupation is directly responsible for about 5 per cent of all cancers and contributes to a further 5 per cent. Apart from the cancers caused by asbestos and ionising radiation, a number of other occupational exposures can cause human cancer. The International Agency for Research on Cancer regularly reviews the evidence for carcinogenicity of compounds and industrial processes, and its published list of carcinogens is widely accepted as the current state of knowledge. More than 50 agents and processes are listed as class 1 carcinogens. Important occupational carcinogens include asbestos (mesothelioma, lung cancer); polynuclear aromatic hydrocarbons such as mineral oils, soots, tars (skin and lung cancer); the aromatic amines in dyestu?s (bladder cancer); certain hexavalent chromates, arsenic and nickel re?ning (lung cancer); wood and leather dust (nasal sinus cancer); benzene (leukaemia); and vinyl chloride monomer (angiosarcoma of the liver). It has been estimated that elimination of all known occupational carcinogens, if possible, would lead to an annual saving of 5,000 premature deaths in Britain.

Infections Two broad categories of job carry an occupational risk. These are workers in contact with animals (farmers, veterinary surgeons and slaughtermen) and those in contact with human sources of infection (health-care sta? and sewage workers).

Occupational infections include various zoonoses (pathogens transmissible from animals to humans), such as ANTHRAX, Borrelia burgdorferi (LYME DISEASE), bovine TUBERCULOSIS, BRUCELLOSIS, Chlamydia psittaci, leptospirosis, ORF virus, Q fever, RINGWORM and Streptococcus suis. Human pathogens that may be transmissible at work include tuberculosis, and blood-borne pathogens such as viral hepatitis (B and C) and HIV (see AIDS/HIV). Health-care workers at risk of exposure to infected blood and body ?uids should be immunised against hapatitis B.

Poisoning The incidence of occupational poisonings has diminished with the substitution of noxious chemicals with safer alternatives, and with the advent of improved containment. However, poisonings owing to accidents at work are still reported, sometimes with fatal consequences. Workers involved in the application of pesticides are particularly at risk if safe procedures are not followed or if equipment is faulty. Exposure to organophosphate pesticides, for example, can lead to breathing diffculties, vomiting, diarrhoea and abdominal cramps, and to other neurological effects including confusion and dizziness. Severe poisonings can lead to death. Exposure can be through ingestion, inhalation and dermal (skin) contact.

Stress and mental health Stress is an adverse reaction to excessive pressures or demands and, in occupational-health terms, is di?erent from the motivational impact often associated with challenging work (some refer to this as ‘positive stress’). Stress at work is often linked to increasing demands on workers, although coping can often prevent the development of stress. The causes of occupational stress are multivariate and encompass job characteristics (e.g. long or unsocial working hours, high work demands, imbalance between e?ort and reward, poorly managed organisational change, lack of control over work, poor social support at work, fear of redundancy and bullying), as well as individual factors (such as personality type, personal circumstances, coping strategies, and availability of psychosocial support outside work). Stress may in?uence behaviours such as smoking, alcohol consumption, sleep and diet, which may in turn affect people’s health. Stress may also have direct effects on the immune system (see IMMUNITY) and lead to a decline in health. Stress may also alter the course and response to treatment of conditions such as cardiovascular disease. As well as these general effects of stress, speci?c types of disorder may be observed.

Exposure to extremely traumatic incidents at work – such as dealing with a major accident involving multiple loss of life and serious injury

(e.g. paramedics at the scene of an explosion or rail crash) – may result in a chronic condition known as post-traumatic stress disorder (PTSD). PTSD is an abnormal psychological reaction to a traumatic event and is characterised by extreme psychological discomfort, such as anxiety or panic when reminded of the causative event; sufferers may be plagued with uncontrollable memories and can feel as if they are going through the trauma again. PTSD is a clinically de?ned condition in terms of its symptoms and causes and should not be used to include normal short-term reactions to trauma.... occupational health, medicine and diseases

Orthoptic Treatment

The examination and treatment by exercises of squints and their sequelae (see EYE, DISORDERS OF).... orthoptic treatment

Endodontics

n. the study, treatment, and prevention of diseases of the pulp of teeth and their sequelae. A major part of treatment is *root canal treatment.... endodontics

Leprosy

Also known as Hansen’s disease, this is a chronic bacterial infection caused by Mycobacterium leprae affecting the skin, mucous membranes, and nerves. Infection is now almost con?ned to tropical and subtropical countries – mostly in Africa and India. There are two distinct (polarised) clinical forms: tuberculoid and lepromatous. The former usually takes a benign course and frequently burns out, whereas the latter is relentlessly progressive; between these two polar forms lies an intermediate/dimorphous group. Susceptibility may be increased by malnutrition. Nasal secretions (especially in lepromatous disease) are teeming with M. leprae and constitute the main source of infection; however, living in close proximity to an infected individual seems necessary for someone to contract the disease. M. leprae can also be transmitted in breast milk from an infected mother.

Only a small minority of those exposed to M. leprae develop the disease. The incubation period is 3–5 years or longer. The major clinical manifestations involve skin and nerves: the former range from depigmented, often anaesthetic areas, to massive nodules; nerve involvement ranges from localised nerve swelling(s) to extensive areas of anaesthesia. Advanced nerve destruction gives rise to severe deformities: foot-drop, wrist-drop, claw-foot, extensive ulceration of the extremities with loss of ?ngers and toes, and bone changes. Eye involvement can produce blindness. Laryngeal lesions produce hoarseness and more serious sequelae. The diagnosis is essentially a clinical one; however, skin-smears, histological features and the lepromin skin-test help to con?rm the diagnosis and enable the form of disease to be graded.

Although the World Health Organisation had originally hoped to eliminate leprosy worldwide by 2000, that has proved an unrealistic target. The reason is an absence of basic information. Doctors are unable to diagnose the disorder before a patient starts to show symptoms; meanwhile he or she may have already passed on the infection. Doctors do not know exactly how transmission occurs or how it infects humans – nor do they know at what point a carrier of the bacterium may infect others. The incidence of new infections is still more than 650,000 cases a year or about 4.5 cases per 10,000 people in those countries worst affected by the disease.

Treatment Introduction of the sulphone compound, dapsone, revolutionised management of the disease. More recently, rifampicin and clofazimine have been added as ?rst-line drugs for treatment. Second-line drugs include minocycline, o?oxacin and clarithromycin; a number of regimens incorporating several of these compounds (multi-drug regimens – introduced in 1982) are now widely used. A three-drug regime is recommended for multi-bacillary leprosy and a two-drug one for parcibacillary leprosy. Dapsone resistance is a major problem worldwide, but occurs less commonly when multi-drug regimens are used. Older compounds – ethionamide and prothionamide

– are no longer used because they are severely toxic to the liver. Corticosteroids are sometimes required in patients with ‘reversal reaction’. Supportive therapy includes physiotherapy; both plastic and orthopaedic surgery may be necessary in advanced stages of the disease. Improvement in socio-economic conditions, and widespread use of BCG vaccination are of value as preventive strategies. Early diagnosis and prompt institution of chemotherapy should prevent long-term complications.... leprosy

Schistosomiasis

Also known as BILHARZIASIS. This infection results from one of the human Schistosoma species. It is common in Africa, South America, the Far East, Middle East, and, to a limited extent, the Caribbean. The life-cycle is dependent on fresh-water snails which act as the intermediate host for the ?uke; the cercarial stage of the ?uke enters via intact human skin and matures in the portal circulation. Clinically, ‘swimmers’ itch’ may occur at the site of cercarial skin penetration. Acute schistosomiasis (Katayama fever) can result in fever, an urticarial rash (see URTICARIA), and enlargement of LIVER and SPLEEN. The adult male is about 12 mm and the female 24 mm in length.

S. haematobium causes CYSTITIS and haematuria – passage of blood in the urine; bladder cancer and ureteric obstruction, giving rise to hydronephrosis and kidney failure, are long-term sequelae in a severe case. S. mansoni can cause colonic symptoms and in a severe case, POLYPOSIS of the COLON; diarrhoea, which may be bloody, can be a presenting feature. In a heavy infection, eggs surrounded by granulomas are deposited in the liver, giving rise to extensive damage (pipe-stem ?brosis) associated with PORTAL HYPERTENSION, oesophageal varices, etc. However, unlike in CIRRHOSIS, hepatocellular function is preserved until late in the disease. S. japonicum (which is con?ned to the Far East, especially Indonesia) behaves similarly to S. mansoni infection; liver involvement is often more severe.

Diagnosis can be made by microscopic examination of URINE or FAECES. The characteristic eggs are usually detectable. Alternatively, rectal or liver BIOPSY are of value. Serological tests, including an ELISA (see ENZYME-LINKED IMMUNOSORBENT ASSAY (ELISA)), have now largely replaced invasive procedures used in making a parasitological diagnosis.

Treatment CHEMOTHERAPY has been revolutionised by the introduction of praziquantel (administered orally); this compound has no serious side-effects, although its cost may limit its use in developing countries. Oxamniquine is cheaper and e?ective in S. mansoni infection, although evidence of resistance has been recorded in several countries. Metriphonate is also relatively cheap and is of value in S. haematobium infection. Prevention is by complete avoidance of exposure to contaminated water; all travellers to infected areas should know about this disease. It is increasing in frequency as new expanses of fresh water appear as a result of irrigation schemes and dam projects. Molluscicides can be employed for snail-control.... schistosomiasis

Liver Disease In The Tropics

ACUTE LIVER DISEASE The hepatitis viruses (A– F) are of paramount importance. Hepatitis E (HEV) often produces acute hepatic failure in pregnant women; extensive epidemics – transmitted by contaminated drinking-water supplies – have been documented. HBV, especially in association with HDV, also causes acute liver failure in infected patients in several tropical countries: however, the major importance of HBV is that the infection leads to chronic liver disease (see below). Other hepatotoxic viruses include the EPSTEIN BARR VIRUS, CYTOMEGALOVIRUS (CMV), the ?avivirus causing YELLOW FEVER, Marburg/Ebola viruses, etc. Acute liver disease also occurs in the presence of several acute bacterial infections, including Salmonella typhi, brucellosis, leptospirosis, syphilis, etc. The complex type of jaundice associated with acute systemic bacterial infection – especially pneumococcal PNEUMONIA and pyomiositis – assumes a major importance in many tropical countries, especially those in Africa and in Papua New Guinea. Of protozoan infections, plasmodium falciparum malaria, LEISHMANIASIS, and TOXOPLASMOSIS should be considered. Ascaris lumbricoides (the roundworm) can produce obstruction to the biliary system. CHRONIC LIVER DISEASE Long-term disease is dominated by sequelae of HBV and HCV infections (often acquired during the neonatal period), both of which can cause chronic active hepatitis, cirrhosis, and hepatocellular carcinoma (‘hepatoma’) – one of the world’s most common malignancies. Chronic liver disease is also caused by SCHISTOSOMIASIS (usually Schistosoma mansoni and S. japonicum), and acute and chronic alcohol ingestion. Furthermore, many local herbal remedies and also orthodox chemotherapeutic compounds (e.g. those used in tuberculosis and leprosy) can result in chronic liver disease. HAEMOSIDEROSIS is a major problem in southern Africa. Hepatocytes contain excessive iron – derived primarily from an excessive intake, often present in locally brewed beer; however, a genetic predisposition seems likely. Indian childhood cirrhosis – associated with an excess of copper – is a major problem in India and surrounding countries. Epidemiological evidence shows that much of the copper is derived from copper vessels used to store milk after weaning. Veno-occlusive disease was ?rst described in Jamaica and is caused by pyrrolyzidine alkaloids (present in bush-tea). Several HIV-associated ‘opportunistic’ infections can give rise to hepatic disease (see AIDS/HIV).

A localised (focal) form of liver disease in all tropical/subtropical countries results from invasive Entamoeba histolytica infection (amoebic liver ‘abscess’); serology and imaging techniques assist in diagnosis. Hydatidosis also causes localised liver disease; one or more cysts usually involve the right lobe of the liver. Serological tests and imaging techniques are of value in diagnosis. Whilst surgery formerly constituted the sole method of management, prolonged courses of albendazole and/or praziquantel have now been shown to be e?ective; however, surgical intervention is still required in some cases.

Hepato-biliary disease is also a problem in many tropical/subtropical countries. In southeast Asia, Clonorchis sinensis and Opisthorchis viverini infections cause chronic biliary-tract infection, complicated by adenocarcinoma of the biliary system. Praziquantel is e?ective chemotherapy before advanced disease ensues. Fasciola hepatica (the liver ?uke) is a further hepato-biliary helminthic infection; treatment is with bithionol or triclabendazole, praziquantel being relatively ine?ective.... liver disease in the tropics

Sleeping Sickness

There are two major forms of the disease: Trypanosoma brucei gambiense is con?ned to west and central Africa, and T.b. rhodesiense to central, east, and south-east Africa. The infection is caused by the bite of tsetse ?y (Glossina spp.). Clinically, a trypanosomal CHANCRE may develop at the site of the tsetse-?y bite. After introduction into the bloodstream, the parasite develops in blood and lymphatic glands. After the blood stage, it enters the central nervous system, causing characteristic neurological sequelae (see below). Infection may be followed by a generalised macular papular reaction. In

T.b. gambiense infection, enlarged glands in the neck (Winterbottom’s sign) may be striking. Onset of disease is accompanied by fever, progressive ANAEMIA, and enlarged glands; these signs and symptoms are followed by increasing lethargy, slowing of mentality, and physical weakness, and give way to headache and an increasing tendency to sleep. These symptoms are caused by proliferation of parasites in the patient’s cerebral blood vessels; this is accompanied by in?ammatory changes and disorganisation of nervous tissue. Patients become emaciated and develop bed sores. Death ?nally takes place either as a result of gross emaciation or of an intercurrent infection.

Diagnosis is by detection of trypanosomes in a blood specimen or, alternatively, a sample of cerebrospinal ?uid. Serological tests are of great value in diagnosis.

Treatment is with suramine or pentamidine; when cerebral involvement has ensued, melarsoprol – which penetrates the blood-brain barrier – is of value. In T.b. gambiense infection, e?ornithine has recently given encouraging results; however, this form of CHEMOTHERAPY is not e?ective in a T.b. rhodesiense infection. From the point of view of prevention, control of the tsetse-?y population is crucial; even so, only a very small percentage of these vectors is infected with Trypanosoma spp.... sleeping sickness




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