Cyanosis confined to the hands and feet is not serious and is usually due to slow blood flow, often as a result of exposure to cold.
A blue tinge to the lips and tongue, however, could be due to a heart or lung disorder such as chronic obstructive pulmonary disease or heart failure.
Cause Asthma runs in families, so that parents with asthma have a strong risk of having children with asthma, or with other atopic (see ATOPY) illnesses such as HAY FEVER or eczema (see DERMATITIS). There is therefore a great deal of interest in the genetic basis of the condition. Several GENES seem to be associated with the condition of atopy, in which subjects have a predisposition to form ANTIBODIES of the IgE class against allergens (see ALLERGEN) they encounter – especially inhaled allergens.
The allergic response in the lining of the airway leads to an in?ammatory reaction. Many cells are involved in this in?ammatory process, including lymphocytes, eosinophils, neutrophils and mast cells. The cells are attracted and controlled by a complex system of in?ammatory mediators. The in?amed airway-wall produced in this process is then sensitive to further allergic stimuli or to non-speci?c challenges such as dust, smoke or drying from the increased respiration during exercise. Recognition of this in?ammation has concentrated attention on anti-in?ammatory aspects of treatment.
Continued in?ammation with poor control of asthma can result in permanent damage to the airway-wall such that reversibility is reduced and airway-narrowing becomes permanent. Appropriate anti-in?ammatory therapy may help to prevent this damage.
Many allergens can be important triggers of asthma. House-dust mite, grass pollen and animal dander are the commonest problems. Occupational factors such as grain dusts, hard-metals fumes and chemicals in the plastic and paint industry are important in some adults. Viral infections are another common trigger, especially in young children.
The prevalence of asthma appears to be on the increase in most countries. Several factors have been linked to this increase; most important may be the vulnerability of the immature immune system (see IMMUNITY) in infants. High exposure to allergens such as house-dust mite early in life may prime the immune system, while reduced exposure to common viral infections may delay the maturation of the immune system. In addition, maternal smoking in pregnancy and infancy increases the risk.
Clinical course The major symptoms of asthma are breathlessness and cough. Occasionally cough may be the only symptom, especially in children, where night-time cough may be mistaken for recurrent infection and treated inappropriately with antibiotics.
The onset of asthma is usually in childhood, but it may begin at any age. In childhood, boys are affected more often than girls but by adulthood the sex incidence is equal. Children who have mild asthma are more likely to grow out of the condition as they go through their teenaged years, although symptoms may recur later.
The degree of airway-narrowing, and its change with time and treatment, can be monitored by measuring the peak expiratory ?ow with a simple monitor at home – a peak-?ow meter. The typical pattern shows the peak ?ow to be lowest in the early morning and this ‘morning dipping’ is often associated with disturbance of sleep.
Acute exacerbations of asthma may be provoked by infections or allergic stimuli. If they do not respond quickly and fully to medication, expert help should be sought urgently since oxygen and higher doses of drugs will be necessary to control the attack. In a severe attack the breathing rate and the pulse rate rise and the chest sounds wheezy. The peak-?ow rate of air into the lungs falls. Patients may be unable to talk in full sentences without catching their breath, and the reduced oxygen in the blood in very severe attacks may produce the blue colour of CYANOSIS in the lips and tongue. Such acute attacks can be very frightening for the patient and family.
Some cases of chronic asthma are included in the internationally agreed description CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) – a chronic, slowly progressive disorder characterised by obstruction of the air?ow persisting over several months.
Treatment The ?rst important consideration in the treatment of asthma is avoidance of precipitating factors. When this is a speci?c animal or occupational exposure, this may be possible; it is however more di?cult for house-dust mite or pollens. Exercise-induced asthma should be treated adequately rather than avoiding exercise.
Desensitisation injections using small quantities of speci?c allergens are used widely in some countries, but rarely in the UK as they are considered to have limited value since most asthma is precipitated by many stimuli and controlled adequately with simple treatment.
There are two groups of main drugs for the treatment of asthma. The ?rst are the bronchodilators which relax the smooth muscle in the wall of the airways, increase their diameter and relieve breathlessness. The most useful agents are the beta adrenergic agonists (see ADRENERGIC RECEPTORS) such as salbutamol and terbutaline. They are best given by inhalation into the airways since this reduces the general side-effects from oral use. These drugs are usually given to reverse airway-narrowing or to prevent its onset on exercise. However, longer-acting inhaled beta agonists such as salmeterol and formoterol or the theophyllines given in tablet form can be used regularly as prevention. The beta agonists can cause TREMOR and PALPITATION in some patients.
The second group of drugs are the antiin?ammatory agents that act to reduce in?ammation of the airway. The main agents in this group are the CORTICOSTEROIDS. They must be taken regularly, even when symptoms are absent. Given by inhalation they have few side-effects. In acute attacks, short courses of oral steroids are used; in very severe disease regular oral steroids may be needed. Other drugs have a role in suppressing in?ammation: sodium cromoglycate has been available for some years and is generally less e?ective than inhaled steroids. Newer agents directed at speci?c steps in the in?ammatory pathway, such as leukotriene receptor-antagonists, are alternative agents.
Treatment guidelines have been produced by various national and international bodies, such as the British Thoracic Society. Most have set out treatment in steps according to severity, with objectives for asthma control based on symptoms and peak ?ow. Patients should have a management plan that sets out their regular treatment and their appropriate response to changes in their condition.
Advice and support for research into asthma is provided by the National Asthma Campaign.
See www.brit-thoracic.org.uk
Prognosis Asthma is diagnosed in 15–20 per cent of all pre-school children in the developed world. Yet by the age of 15 it is estimated that fewer than 5 per cent still have symptoms. A study in 2003 reported on a follow-up of persons born in 1972–3 who developed asthma and still had problems at the age of nine. By the time these persons were aged 26, 27 per cent were still having problems; around half of that number had never been free from the illness and the other half had apparently lost it for a few years but it had returned.... asthma
The exact trigger is unknown, but it is thought that, whatever the stimulus, chemical mediators produced by cells of the immune system or elsewhere in the body spread and sustain an in?ammatory reaction. Cascade mechanisms with multiple interactions are provoked. CYTOTOXIC substances (which damage or kill cells) such as oxygen-free radicals and PROTEASE damage the alveolar capillary membranes (see ALVEOLUS). Once this happens, protein-rich ?uid leaks into the alveoli and interstitial spaces. SURFACTANT is also lost. This impairs the exchange of oxygen and carbon dioxide in the lungs and gives rise to the clinical and pathological picture of acute respiratory failure.
The typical patient with ARDS has rapidly worsening hypoxaemia (lack of oxygen in the blood), often requiring mechanical ventilation. There are all the signs of respiratory failure (see TACHYPNOEA; TACHYCARDIA; CYANOSIS), although the chest may be clear apart from a few crackles. Radiographs show bilateral, patchy, peripheral shadowing. Blood gases will show a low PaO2 (concentration of oxygen in arterial blood) and usually a high PaCO2 (concentration of carbon dioxide in arterial blood). The lungs are ‘sti?’ – they are less e?ective because of the loss of surfactant and the PULMONARY OEDEMA.
Causes The causes of ARDS may be broadly divided into the following:... acute respiratory distress syndrome (ards)
Both HIV-1 and HIV-2 are predominantly sexually transmitted and both are associated with secondary opportunistic infections. However, HIV-2 seems to result in slower damage to the immune system. HIV-1 is known to mutate rapidly and has given rise to other subtypes.
HIV is thought to have occurred in humans in the 1950s, but whether or not it infected humans from another primate species is uncertain. It became widespread in the 1970s but its latency in causing symptoms meant that the epidemic was not noticed until the following decade. Although it is a sexually transmitted disease, it can also be transmitted by intravenous drug use (through sharing an infected needle), blood transfusions with infected blood (hence the importance of e?ective national blood-screening programmes), organ donation, and occupationally (see health-care workers, below). Babies born of HIV-positive mothers can be infected before or during birth, or through breast feeding.
Although HIV is most likely to occur in blood, semen or vaginal ?uid, it has been found in saliva and tears (but not sweat); however, there is no evidence that the virus can be transmitted from these two body ?uids. There is also no evidence that HIV can be transmitted by biting insects (such as mosquitoes). HIV does not survive well in the environment and is rapidly destroyed through drying.
Prevalence At the end of 2003 an estimated 42 million people globally were infected with HIV – up from 40 million two years earlier. About one-third of those with HIV/AIDS are aged 15–24 and most are unaware that they are carrying the virus. During 2003 it is estimated that 5 million adults and children worldwide were newly infected with HIV, and that 3 million adults and children died. In Africa in 2003,
3.4 million people were newly infected and 2.3 million died, with more than 28 million carrying the virus. HIV/AIDS was the leading cause of death in sub-Saharan Africa where over half of the infections were in women and 90 per cent of cases resulted from heterosexual sex. In some southern African countries, one in three pregnant women had HIV.
In Asia and the Paci?c there were 1.2 million new infections and 435,000 deaths. The area with the fastest-growing epidemic is Eastern Europe, especially the Russian Federation where in 2002 around a million people had HIV and there were an estimated 250,000 new infections, with intravenous drug use a key contributor to this ?gure. Seventy-?ve per cent of cases occurred in men, with male-to-male sexual transmission an important cause of infection, though heterosexual activity is a rising cause of infection.
At the end of 2002 the UK had an estimated 55,900 HIV-infected adults aged between 15 and 59. More than 3,600 individuals were newly diagnosed with the infection in 2000, the highest annual ?gure since the epidemic started
– in 1998 the ?gure was 2,817 and in 1999 just over 3,000 (Department of Health and Communicable Disease Surveillance Centre). The incidence of AIDS in the UK has declined sharply since the introduction of highly active antiretroviral therapy (HAART) and HIV-related deaths have also fallen: in 2002 there were 777 reported new AIDS cases and 395 deaths, compared with 1,769 and 1,719 respectively in 1995. (Sources: UNAIDS and WHO, AIDS Epidemic Update, December 2001; Public Health Laboratory Services AIDS and STD Centre Communicable Disease Surveillance and Scottish Centre for Infection and Environmental Health, Quarterly Surveillance Tables.)
Poverty is strongly linked to the spread of AIDS, for various reasons including lack of health education; lack of e?ective public-health awareness; women having little control over sexual behaviour and contraception; and, by comparison with the developed world, little or no access to antiretroviral drugs.
Pathogenesis The cellular target of HIV infection is a subset of white blood cells called T-lymphocytes (see LYMPHOCYTE) which carry the CD4 surface receptor. These so-called ‘helper T-cells’ are vital to the function of cell-mediated immunity. Infection of these cells leads to their destruction (HIV replicates at an enormous rate – 109) and over the course of several years the body is unable to generate suf?cient new cells to keep pace. This leads to progressive destruction of the body’s immune capabilities, evidenced clinically by the development of opportunistic infection and unusual tumours.
Monitoring of clinical progression It is possible to measure the number of viral particles present in the plasma. This gives an accurate guide to the likely progression rate, which will be slow in those individuals with fewer than 10,000 particles per ml of plasma but progressively more rapid above this ?gure. The main clinical monitoring of the immune system is through the numbers of CD4 lymphocytes in the blood. The normal count is around 850 cells per ml and, without treatment, eventual progression to AIDS is likely in those individuals whose CD4 count falls below 500 per ml. Opportunistic infections occur most frequently when the count falls below 200 per ml: most such infections are treatable, and death is only likely when the CD4 count falls below 50 cells per ml when infection is developed with organisms that are di?cult to treat because of their low intrinsic virulence.
Simple, cheap and highly accurate tests are available to detect HIV antibodies in the serum. These normally occur within three months of infection and remain the cornerstone of the diagnosis.
Clinical features Most infected individuals have a viral illness some three weeks after contact with HIV. The clinical features are often non-speci?c and remain undiagnosed but include a ?ne red rash, large lymph nodes, an in?uenza-like illness, cerebral involvement and sometimes the development of opportunistic infections. The antibody test may be negative at this stage but there are usually high levels of virus particles in the blood. The antibody test is virtually always positive within three months of infection. HIV infection is often subsequently asymptomatic for a period of ten years or more, although in most patients progressive immune destruction is occurring during this time and a variety of minor opportunistic infections such as HERPES ZOSTER or oral thrush (see CANDIDA) do occur. In addition, generalised LYMPHADENOPATHY is present in a third of patients and some suffer from severe malaise, weight loss, night sweats, mild fever, ANAEMIA or easy bruising due to THROMBOCYTOPENIA.
The presentation of opportunistic infection is highly variable but usually involves either the CENTRAL NERVOUS SYSTEM, the gastrointestinal tract or the LUNGS. Patients may present with a sudden onset of a neurological de?cit or EPILEPSY due to a sudden onset of a STROKE-like syndrome, or epilepsy due to a space-occupying lesion in the brain – most commonly TOXOPLASMOSIS. In late disease, HIV infection of the central nervous system itself may produce progressive memory loss, impaired concentration and mental slowness called AIDS DEMENTIA. A wide variety of opportunistic PROTOZOA or viruses produces DYSPHAGIA, DIARRHOEA and wasting. In the respiratory system the commonest opportunistic infection associated with AIDS, pneumonia, produces severe shortness of breath and sometimes CYANOSIS, usually with a striking lack of clinical signs in the chest.
In very late HIV infection, when the CD4 count has fallen below 50 cells per ml, infection with CYTOMEGALOVIRUS may produce progressive retinal necrosis (see EYE, DISORDERS OF) which will lead to blindness if untreated, as well as a variety of gastrointestinal symptoms. At this stage, infection with atypical mycobacteria is also common, producing severe anaemia, wasting and fevers. The commonest tumour associated with HIV is Kaposi’s sarcoma which produces purplish skin lesions. This and nonHodgkin’s lymphoma (see LYMPHOMA), which is a hundred times more frequent among HIV-positive individuals than in the general population, are likely to be associated with or caused by opportunistic viral infections.
Prevention There is, as yet, no vaccine to prevent HIV infection. Vaccine development has been hampered
by the large number of new HIV strains generated through frequent mutation and recombination.
because HIV can be transmitted as free virus and in infected cells.
because HIV infects helper T-cells – the very cells involved in the immune response. There are, however, numerous research pro
grammes underway to develop vaccines that are either prophylactic or therapeutic. Vaccine-development strategies have included: recombinant-vector vaccines, in which a live bacterium or virus is genetically modi?ed to carry one or more of the HIV genes; subunit vaccines, consisting of small regions of the HIV genome designed to induce an immune response without infection; modi?ed live HIV, which has had its disease-promoting genes removed; and DNA vaccines – small loops of DNA (plasmids) containing viral genes – that make the host cells produce non-infectious viral proteins which, in turn, trigger an immune response and prime the immune system against future infection with real virus.
In the absence of an e?ective vaccine, preventing exposure remains the chief strategy in reducing the spread of HIV. Used properly, condoms are an extremely e?ective method of preventing exposure to HIV during sexual intercourse and remain the most important public-health approach to countering the further acceleration of the AIDS epidemic. The spermicide nonoxynol-9, which is often included with condoms, is known to kill HIV in vitro; however, its e?ectiveness in preventing HIV infection during intercourse is not known.
Public-health strategies must be focused on avoiding high-risk behaviour and, particularly in developing countries, empowering women to have more control over their lives, both economically and socially. In many of the poorer regions of the world, women are economically dependent on men and refusing sex, or insisting on condom use, even when they know their partners are HIV positive, is not a straightforward option. Poverty also forces many women into the sex industry where they are at greater risk of infection.
Cultural problems in gaining acceptance for universal condom-use by men in some developing countries suggests that other preventive strategies should also be considered. Microbicides used as vaginal sprays or ‘chemical condoms’ have the potential to give women more direct control over their exposure risk, and research is underway to develop suitable products.
Epidemiological studies suggest that male circumcision may o?er some protection against HIV infection, although more research is needed before this can be an established public-health strategy. Globally, about 70 per cent of infected men have acquired the virus through unprotected vaginal sex; in these men, infection is likely to have occurred through the penis with the mucosal epithelia of the inner surface of the foreskin and the frenulum considered the most likely sites for infection. It is suggested that in circumcised men, the glans may become keratinised and thus less likely to facilitate infection. Circumcision may also reduce the risk of lesions caused by other sexually transmitted disease.
Treatment AIDS/HIV treatment can be categorised as speci?c therapies for the individual opportunistic infections – which ultimately cause death – and highly active antiretroviral therapy (HAART) designed to reduce viral load and replication. HAART is also the most e?ective way of preventing opportunistic infections, and has had a signi?cant impact in delaying the onset of AIDS in HIV-positive individuals in developed countries.
Four classes of drugs are currently in use. Nucleoside analogues, including ZIDOVUDINE and DIDANOSINE, interfere with the activity of the unique enzyme of the retrovirus reverse transcriptase which is essential for replication. Nucleotide analogues, such as tenofovir, act in the same way but require no intracellular activation. Non-nucleoside reverse transcriptase inhibitors, such as nevirapine and EFAVIRENZ, act by a di?erent mechanism on the same enzyme. The most potent single agents against HIV are the protease inhibitors, such as lopinavir, which render a unique viral enzyme ineffective. These drugs are used in a variety of combinations in an attempt to reduce the plasma HIV viral load to below detectable limits, which is achieved in approximately 90 per cent of patients who have not previously received therapy. This usually also produces a profound rise in CD4 count. It is likely, however, that such treatments need to be lifelong – and since they are associated with toxicities, long-term adherence is di?cult. Thus the optimum time for treatment intervention remains controversial, with some clinicians believing that this should be governed by the viral load rising above 10,000 copies, and others that it should primarily be designed to prevent the development of opportunistic infections – thus, that initiation of therapy should be guided more by the CD4 count.
It should be noted that the drug regimens have been devised for infection with HIV-1; it is not known how e?ective they are at treating infection with HIV-2.
HIV and pregnancy An HIV-positive woman can transmit the virus to her fetus, with the risk of infection being particularly high during parturition; however, the risk of perinatal HIV transmission can be reduced by antiviral drug therapy. In the UK, HIV testing is available to all women as part of antenatal care. The bene?ts of antenatal HIV testing in countries where antiviral drugs are not available are questionable. An HIV-positive woman might be advised not to breast feed because of the risks of transmitting HIV via breastmilk, but there may be a greater risk associated with not breast feeding at all. Babies in many poor communities are thought to be at high risk of infectious diseases and malnutrition if they are not breast fed and may thus be at greater overall risk of death during infancy.
Counselling Con?dential counselling is an essential part of AIDS management, both in terms of supporting the psychological wellbeing of the individual and in dealing with issues such as family relations, sexual partners and implications for employment (e.g. for health-care workers). Counsellors must be particularly sensitive to culture and lifestyle issues. Counselling is essential both before an HIV test is taken and when the results are revealed.
Health-care workers Health-care workers may be at risk of occupational exposure to HIV, either through undertaking invasive procedures or through accidental exposure to infected blood from a contaminated needle (needlestick injury). Needlestick injuries are frequent in health care – as many as 600,000 to 800,000 are thought to occur annually in the United States. Transmission is much more likely where the worker has been exposed to HIV through a needlestick injury or deep cut with a contaminated instrument than through exposure of mucous membranes to contaminated blood or body ?uids. However, even where exposure occurs through a needlestick injury, the risk of seroconversion is much lower than with a similar exposure to hepatitis C or hepatitis B. A percutaneous exposure to HIV-infected blood in a health-care setting is thought to carry a risk of about one infection per 300 injuries (one in 1,000 for mucous-membrane exposure), compared with one in 30 for hepatitis C, and one in three for hepatitis B (when the source patient is e-antigen positive).
In the event of an injury, health-care workers are advised to report the incident immediately where, depending on a risk assessment, they may be o?ered post-exposure prophylaxis (PEP). They should also wash the contaminated area with soap and water (but without scrubbing) and, if appropriate, encourage bleeding at the site of injury. PEP, using a combination of antiretroviral drugs (in a similar regimen to HAART – see above), is thought to greatly reduce the chances of seroconversion; it should be commenced as soon as possible, preferably within one or two hours of the injury. Although PEP is available, safe systems of work are considered to o?er the greatest protection. Double-gloving (latex gloves remove much of the blood from the surface of the needle during a needlestick), correct use of sharps containers (for used needles and instruments), avoiding the resheathing of used needles, reduction in the number of blood samples taken from a patient, safer-needle devices (such as needles that self-blunt after use) and needleless drug administration are all thought to reduce the risk of exposure to HIV and other blood-borne viruses. Although there have been numerous cases of health-care workers developing HIV through occupational exposure, there is little evidence of health-care workers passing HIV to their patients through normal medical procedures.... aids/hiv
Extrinsic allergic alveolitis is the condition induced by the lungs becoming allergic (see ALLERGY) to various factors or substances. It includes BAGASSOSIS, FARMER’S LUNG and BUDGERIGAR-FANCIER’S LUNG, and is characterised by the onset of shortness of breath, tightness of the chest, cough and fever. The onset may be sudden or gradual. Treatment consists of removal of the affected individual from the o?ending material to which he or she has become allergic. CORTICOSTEROIDS give temporary relief.
Fibrosing alveolitis In this disease there is di?use FIBROSIS of the walls of the alveoli of the lungs. This causes loss of lung volume with both forced expiratory volume and vital capacity affected, but the ratio between them remaining normal. The patient complains of cough and progressive DYSPNOEA. Typically the patient will be cyanosed (blue – see CYANOSIS), clubbed (see CLUBBING), and have crackles in the mid- and lower-lung ?elds. Blood gases will reveal HYPOXIA and, in early disease, hypocapnia (de?ciency of carbon dioxide in the blood due to hyperventilation). There is an association with RHEUMATOID ARTHRITIS (about one-eighth of cases), systemic lupus erythematosus (see under LUPUS), and systemic SCLEROSIS. Certain drugs – for example, bleomycin, busulphan and hexamethonium – may also cause this condition, as may high concentrations of oxygen, and inhalation of CADMIUM fumes.... alveolitis
The most common effects of opioid overdose are vomiting, drowsiness, pinpoint pupils, BRADYCARDIA, CONVULSIONS and COMA. Respiratory depression is common and may lead to CYANOSIS and respiratory arrest. HYPOTENSION occurs occasionally and in severe cases non-cardiogenic pulmonary oedema and cardiovascular collapse may occur. Cardiac ARRHYTHMIA may occur with some opioids. Some opioids have a HISTAMINE-releasing e?ect which may result in an urticarial rash (see URTICARIA), PRURITUS, ?ushing and hypotension. Activated CHARCOAL should be given following overdose and NALOXONE administered to reverse respiratory depression and deep coma.... opioid poisoning
Severe and extensive burns are most frequently produced by the clothes – for example, of a child – catching ?re. This applies especially to cotton garments, which blaze up quickly. It should be remembered that such a ?ame can immediately be extinguished by making the individual lie on the ?oor so that the ?ames are uppermost, and wrapping him or her in a rug, mat or blanket. As prevention is always better than cure, particular care should always be exercised with electric ?res and kettles or pots of boiling water in houses where there are young children or old people. Children’s clothes, and especially night-clothes, should be made of non-in?ammable material: pyjamas are also much safer than nightdresses.
Severe scalds are usually produced by escape of steam in boiler explosions. Cigarettes are a common cause of ?res and therefore of burns; people who have fallen asleep in bed or in a chair while smoking may set ?re to the bed or chair. Discarded, unextinguished cigarettes are another cause.
Degrees of burns Burns are referred to as either super?cial (or partial-thickness) burns, when there is su?cient skin tissue left to ensure regrowth of skin over the burned site; and deep (or full-thickness) burns, when the skin is totally destroyed and grafting will be necessary.
Symptoms Whilst many domestic burns are minor and insigni?cant, more severe burns and scalds can prove to be very dangerous to life. The main danger is due to SHOCK, which arises as a result of loss of ?uid from the circulating blood at the site of a serious burn. This loss of ?uid leads to a fall in the volume of the circulating blood. As the maintenance of an adequate blood volume is essential to life, the body attempts to compensate for this loss by withdrawing ?uid from the uninjured areas of the body into the circulation. If carried too far, however, this in turn begins to affect the viability of the body cells. As a sequel, essential body cells, such as those of the liver and kidneys, begin to suffer, and the liver and kidneys cease to function properly. This will show itself by the development of JAUNDICE and the appearance of albumin in the urine (see PROTEINURIA). In addition, the circulation begins to fail with a resultant lack of oxygen (see ANOXIA) in the tissues, and the victim becomes cyanosed (see CYANOSIS), restless and collapsed: in some cases, death ensues. In addition, there is a strong risk of infection occurring. This is the case with severe burns in particular, which leave a large raw surface exposed and very vulnerable to any micro-organisms. The combination of shock and infection can all too often be life-threatening unless expert treatment is immediately available.
The immediate outcome of a burn is largely determined by its extent. This is of more signi?cance than the depth of the burn. To assess the extent of a burn in relation to the surface of the body, what is known as the Rule of Nine has been evolved. The head and each arm cover 9 per cent of the body surface, whilst the front of the body, the back of the body, and each leg each cover 18 per cent, with the perineum (or crutch) accounting for the remaining 1 per cent. The greater the extent of the burn, the more seriously ill will the victim become from loss of ?uid from his or her circulation, and therefore the more prompt should be his or her removal to hospital for expert treatment. The depth of the burn, unless this is very great, is mainly of import when the question arises as to how much surgical treatment, including skin grafting, will be required.
Treatment This depends upon the severity of the burn. In the case of quite minor burns or scalds, all that may be necessary if they are seen immediately is to hold the part under cold running water until the pain is relieved. Cooling is one of the most e?ective ways of relieving the pain of a burn. If the burn involves the distal part of a limb – for example, the hand and forearm – one of the most e?ective ways of relieving pain is to immerse the burned part in lukewarm water and add cold water until the pain disappears. As the water warms and pain returns, more cold water is added. After some three to four hours, pain will not reappear on warming, and the burn may be dressed in the usual way. Thereafter a simple dressing (e.g. a piece of sterile gauze covered by cotton-wool, and on top of this a bandage or adhesive dressing) should be applied. The part should be kept at rest and the dressing kept quite dry until healing takes place. Blisters should be pierced with a sterile needle, but the skin should not be cut away. No ointment or oil should be applied, and an antiseptic is not usually necessary.
In slightly more severe burns or scalds, it is probably advisable to use some antiseptic dressing. These are the cases which should be taken to a doctor – whether a general practitioner, a factory doctor, or to a hospital Accident & Emergency department. There is still no general consensus of expert opinion as to the best ‘antiseptic’ to use. Among those recommended are CHLORHEXIDINE, and antibiotics such as BACITRACIN, NEOMYCIN and polymixin. An alternative is to use a Tulle Gras dressing which has been impregnated with a suitable antibiotic.
In the case of severe burns and scalds, the only sound rule is immediate removal to hospital. Unless there is any need for immediate resuscitation, such as arti?cial respiration, or attention to other injuries there may be, such as fractures or haemorrhage, nothing should be done on the spot to the patient except to make sure that s/he is as comfortable as possible and to keep them warm, and to cover the burn with a sterile (or clean) cloth such as a sheet, pillowcases, or towels wrung out in cold water. If pain is severe, morphine should be given – usually intravenously. Once the victim is in hospital, the primary decision is as to the extent of the burn, and whether or not a transfusion is necessary. If the burn is more than 9 per cent of the body surface in extent, a transfusion is called for. The precise treatment of the burn varies, but the essential is to prevent infection if this has not already occurred, or, if it has, to bring it under control as quickly as possible. The treatment of severe burns has made great advances, with quick transport to specialised burns units, modern resuscitative measures, the use of skin grafting and other arti?cial covering techniques and active rehabilitation programmes, o?ering victims a good chance of returning to normal life.
CHEMICAL BURNS Phenol or lysol can be washed o? promptly before they do much damage. Acid or alkali burns should be neutralised by washing them repeatedly with sodium bicarbonate or 1 per cent acetic acid, respectively. Alternatively, the following bu?er solution may be used for either acid or alkali burns: monobasic potassium phosphate (70 grams), dibasic sodium phosphate (70 grams) in 850 millilitres of water. (See also PHOSPHORUS BURNS.)... burns and scalds
Chronic bronchitis is typi?ed by chronic productive cough for at least three months in two successive years (provided other causes such as TUBERCULOSIS, lung cancer and chronic heart failure have been excluded). The characteristics of emphysema are abnormal and permanent enlargement of the airspaces (alveoli) at the furthermost parts of the lung tissue. Rupture of alveoli occurs, resulting in the creation of air spaces with a gradual breakdown in the lung’s ability to oxygenate the blood and remove carbon dioxide from it (see LUNGS). Asthma results in in?ammation of the airways with the lining of the BRONCHIOLES becoming hypersensitive, causing them to constrict. The obstruction may spontaneously improve or do so in response to bronchodilator drugs. If an asthmatic patient’s airway-obstruction is characterised by incomplete reversibility, he or she is deemed to have a form of COPD called asthmatic bronchitis; sufferers from this disorder cannot always be readily distinguished from those people who have chronic bronchitis and/ or emphysema. Symptoms and signs of emphysema, chronic bronchitis and asthmatic bronchitis overlap, making it di?cult sometimes to make a precise diagnosis. Patients with completely reversible air?ow obstruction without the features of chronic bronchitis or emphysema, however, are considered to be suffering from asthma but not from COPD.
The incidence of COPD has been increasing, as has the death rate. In the UK around 30,000 people with COPD die annually and the disorder makes up 10 per cent of all admissions to hospital medical wards, making it a serious cause of illness and disability. The prevalence, incidence and mortality rates increase with age, and more men than women have the disorder, which is also more common in those who are socially disadvantaged.
Causes The most important cause of COPD is cigarette smoking, though only 15 per cent of smokers are likely to develop clinically signi?cant symptoms of the disorder. Smoking is believed to cause persistent airway in?ammation and upset the normal metabolic activity in the lung. Exposure to chemical impurities and dust in the atmosphere may also cause COPD.
Signs and symptoms Most patients develop in?ammation of the airways, excessive growth of mucus-secreting glands in the airways, and changes to other cells in the airways. The result is that mucus is transported less e?ectively along the airways to eventual evacuation as sputum. Small airways become obstructed and the alveoli lose their elasticity. COPD usually starts with repeated attacks of productive cough, commonly following winter colds; these attacks progressively worsen and eventually the patient develops a permanent cough. Recurrent respiratory infections, breathlessness on exertion, wheezing and tightness of the chest follow. Bloodstained and/or infected sputum are also indicative of established disease. Among the symptoms and signs of patients with advanced obstruction of air?ow in the lungs are:
RHONCHI (abnormal musical sounds heard through a STETHOSCOPE when the patient breathes out).
marked indrawing of the muscles between the ribs and development of a barrel-shaped chest.
loss of weight.
CYANOSIS in which the skin develops a blue tinge because of reduced oxygenation of blood in the blood vessels in the skin.
bounding pulse with changes in heart rhythm.
OEDEMA of the legs and arms.
decreasing mobility.
Some patients with COPD have increased ventilation of the alveoli in their lungs, but the levels of oxygen and carbon dioxide are normal so their skin colour is normal. They are, however, breathless so are dubbed ‘pink pu?ers’. Other patients have reduced alveolar ventilation which lowers their oxygen levels causing cyanosis; they also develop COR PULMONALE, a form of heart failure, and become oedematous, so are called ‘blue bloaters’.
Investigations include various tests of lung function, including the patient’s response to bronchodilator drugs. Exercise tests may help, but radiological assessment is not usually of great diagnostic value in the early stages of the disorder.
Treatment depends on how far COPD has progressed. Smoking must be stopped – also an essential preventive step in healthy individuals. Early stages are treated with bronchodilator drugs to relieve breathing symptoms. The next stage is to introduce steroids (given by inhalation). If symptoms worsen, physiotherapy – breathing exercises and postural drainage – is valuable and annual vaccination against INFLUENZA is strongly advised. If the patient develops breathlessness on mild exertion, has cyanosis, wheezing and permanent cough and tends to HYPERVENTILATION, then oxygen therapy should be considered. Antibiotic treatment is necessary if overt infection of the lungs develops.
Complications Sometimes rupture of the pulmonary bullae (thin-walled airspaces produced by the breakdown of the walls of the alveoli) may cause PNEUMOTHORAX and also exert pressure on functioning lung tissue. Respiratory failure and failure of the right side of the heart (which controls blood supply to the lungs), known as cor pulmonale, are late complications in patients whose primary problem is emphysema.
Prognosis This is related to age and to the extent of the patient’s response to bronchodilator drugs. Patients with COPD who develop raised pressure in the heart/lung circulation and subsequent heart failure (cor pulmonale) have a bad prognosis.... chronic obstructive pulmonary disease (copd)
Arrhythmias An abnormal rate or rhythm of the heartbeat. The reason is a disturbance in the electrical impulses within the heart. Sometimes a person may have an occasional irregular heartbeat: this is called an ECTOPIC beat (or an extrasystole) and does not necessarily mean that an abnormality exists. There are two main types of arrhythmia: bradycardias, where the rate is slow – fewer than 60 beats a minute and sometimes so slow and unpredictable (heartblock) as to cause blackouts or heart failure; and tachycardia, where the rate is fast – more than 100 beats a minute. A common cause of arrhythmia is coronary artery disease, when vessels carrying blood to the heart are narrowed by fatty deposits (ATHEROMA), thus reducing the blood supply and damaging the heart tissue. This condition often causes myocardial infarction after which arrhythmias are quite common and may need correcting by DEFIBRILLATION (application of a short electric shock to the heart). Some tachycardias result from a defect in the electrical conduction system of the heart that is commonly congenital. Various drugs can be used to treat arrhythmias (see ANTIARRHYTHMIC DRUGS). If attacks constantly recur, the arrhythmia may be corrected by electrical removal of dead or diseased tissue that is the cause of the disorder. Heartblock is most e?ectively treated with an arti?cial CARDIAC PACEMAKER, a battery-activated control unit implanted in the chest.
Cardiomyopathy Any disease of the heart muscle that results in weakening of its contractions. The consequence is a fall in the e?ciency of the circulation of blood through the lungs and remainder of the body structures. The myopathy may be due to infection, disordered metabolism, nutritional excess or de?ciency, toxic agents, autoimmune processes, degeneration, or inheritance. Often, however, the cause is not identi?ed. Cardiomyopathies are less common than other types of heart diseases, and the incidence of di?erent types of myopathy (see below) is not known because patients or doctors are sometimes unaware of the presence of the condition.
The three recognised groups of cardiomyopathies are hypertrophic, dilated and restrictive.
•Hypertrophic myopathy, a familial condition, is characterised by great enlargement of the muscle of the heart ventricles. This reduces the muscle’s e?ciency, the ventricles fail to relax properly and do not ?ll suf?ciently during DIASTOLE.
In the dilated type of cardiomyopathy, both ventricles overdilate, impairing the e?ciency of contraction and causing congestion of the lungs.
In the restrictive variety, proper ?lling of the ventricles does not occur because the muscle walls are less elastic than normal. The result is raised pressure in the two atria (upper cavities) of the heart: these dilate and develop FIBRILLATION. Diagnosis can be di?cult and treatment is symptomatic, with a poor prognosis. In suitable patients, heart TRANSPLANTATION may be considered. Disorders of the heart muscle may also be
caused by poisoning – for example, heavy consumption of alcohol. Symptoms include tiredness, palpitations (quicker and sometimes irregular heartbeat), chest pain, di?culty in breathing, and swelling of the legs and hands due to accumulation of ?uid (OEDEMA). The heart is enlarged (as shown on chest X-ray) and ECHOCARDIOGRAPHY shows thickening of the heart muscle. A BIOPSY of heart muscle will show abnormalities in the cells of the heart muscle.
Where the cause of cardiomyopathy is unknown, as is the case with most patients, treatment is symptomatic using DIURETICS to control heart failure and drugs such as DIGOXIN to return the heart rhythm to normal. Patients should stop drinking alcohol. If, as often happens, the patient’s condition slowly deteriorates, heart transplantation should be considered.
Congenital heart disease accounts for 1–2 per cent of all cases of organic heart disease. It may be genetically determined and so inherited; present at birth for no obvious reason; or, in rare cases, related to RUBELLA in the mother. The most common forms are holes in the heart (atrial septal defect, ventricular septal defect – see SEPTAL DEFECT), a patent DUCTUS ARTERIOSUS, and COARCTATION OF THE AORTA. Many complex forms also exist and can be diagnosed in the womb by fetal echocardiography which can lead to elective termination of pregnancy. Surgery to correct many of these abnormalities is feasible, even for the most severe abnormalities, but may only be palliative giving rise to major diffculties of management as the children become older. Heart transplantation is now increasingly employed for the uncorrectable lesions.
Coronary artery disease Also known as ischaemic heart disease, this is a common cause of symptoms and death in the adult population. It may present for the ?rst time as sudden death, but more usually causes ANGINA PECTORIS, myocardial infarction (heart attack) or heart failure. It can also lead to a disturbance of heart rhythm. Factors associated with an increased risk of developing coronary artery disease include diabetes, cigarette smoking, high blood pressure, obesity, and a raised concentration of cholesterol in the blood. Older males are most affected.
Coronary thrombosis or acute myocardial infarction is the acute, dramatic manifestation of coronary-artery ischaemic heart disease – one of the major killing diseases of western civilisation. In 1999, ischaemic heart disease was responsible for about 115,000 deaths in England and Wales, compared with 153,000 deaths in 1988. In 1999 more than 55,600 people died of coronary thrombosis. The underlying cause is disease of the coronary arteries which carry the blood supply to the heart muscle (or myocardium). This results in narrowing of the arteries until ?nally they are unable to transport su?cient blood for the myocardium to function e?ciently. One of three things may happen. If the narrowing of the coronary arteries occurs gradually, then the individual concerned will develop either angina pectoris or signs of a failing heart: irregular rhythm, breathlessness, CYANOSIS and oedema.
If the narrowing occurs suddenly or leads to complete blockage (occlusion) of a major branch of one of the coronary arteries, then the victim collapses with acute pain and distress. This is the condition commonly referred to as a coronary thrombosis because it is usually due to the affected artery suddenly becoming completely blocked by THROMBOSIS. More correctly, it should be described as coronary occlusion, because the ?nal occluding factor need not necessarily be thrombosis.
Causes The precise cause is not known, but a wide range of factors play a part in inducing coronary artery disease. Heredity is an important factor. The condition is more common in men than in women; it is also more common in those in sedentary occupations than in those who lead a more physically active life, and more likely to occur in those with high blood pressure than in those with normal blood pressure (see HYPERTENSION). Obesity is a contributory factor. The disease is more common among smokers than non-smokers; it is also often associated with a high level of CHOLESTEROL in the blood, which in turn has been linked with an excessive consumption of animal, as opposed to vegetable, fats. In this connection the important factors seem to be the saturated fatty acids (low-density and very low-density lipoproteins [LDLs and VLDLs] – see CHOLESTEROL) of animal fats which would appear to be more likely to lead to a high level of cholesterol in the blood than the unsaturated fatty acids of vegetable fats. As more research on the subject is carried out, the arguments continue about the relative in?uence of the di?erent factors. (For advice on prevention of the disease, see APPENDIX 2: ADDRESSES: SOURCES OF INFORMATION, ADVICE, SUPPORT AND SELFHELP.)
Symptoms The presenting symptom is the sudden onset, often at rest, of acute, agonising pain in the front of the chest. This rapidly radiates all over the front of the chest and often down over the abdomen. The pain is frequently accompanied by nausea and vomiting, so that suspicion may be aroused of some acute abdominal condition such as biliary colic (see GALLBLADDER, DISEASES OF) or a perforated PEPTIC ULCER. The victim soon goes into SHOCK, with a pale, cold, sweating skin, rapid pulse and dif?culty in breathing. There is usually some rise in temperature.
Treatment is immediate relief of the pain by injections of diamorphine. Thrombolytic drugs should be given as soon as possible (‘rapid door to needle time’) and ARRHYTHMIA corrected. OXYGEN is essential and oral ASPIRIN is valuable. Treatment within the ?rst hour makes a great di?erence to recovery. Subsequent treatment includes the continued administration of drugs to relieve the pain; the administration of ANTIARRHYTHMIC DRUGS that may be necessary to deal with the heart failure that commonly develops, and the irregular action of the heart that quite often develops; and the continued administration of oxygen. Patients are usually admitted to coronary care units, where they receive constant supervision. Such units maintain an emergency, skilled, round-the-clock sta? of doctors and nurses, as well as all the necessary resuscitation facilities that may be required.
The outcome varies considerably. The ?rst (golden) hour is when the patient is at greatest risk of death: if he or she is treated, then there is a 50 per cent reduction in mortality compared with waiting until hospital admission. As each day passes the prognosis improves with a ?rst coronary thrombosis, provided that the patient does not have a high blood pressure and is not overweight. Following recovery, there should be a gradual return to work, care being taken to avoid any increase in weight, unnecessary stress and strain, and to observe moderation in all things. Smoking must stop. In uncomplicated cases patients get up and about as soon as possible, most being in hospital for a week to ten days and back at work in three months or sooner.
Valvular heart disease primarily affects the mitral and aortic valves which can become narrowed (stenosis) or leaking (incompetence). Pulmonary valve problems are usually congenital (stenosis) and the tricuspid valve is sometimes involved when rheumatic heart disease primarily affects the mitral or aortic valves. RHEUMATIC FEVER, usually in childhood, remains a common cause of chronic valvular heart disease causing stenosis, incompetence or both of the aortic and mitral valves, but each valve has other separate causes for malfunction.
Aortic valve disease is more common with increasing age. When the valve is narrowed, the heart hypertrophies and may later fail. Symptoms of angina or breathlessness are common and dizziness or blackouts (syncope) also occur. Replacing the valve is a very e?ective treatment, even with advancing age. Aortic stenosis may be caused by degeneration (senile calci?c), by the inheritance of two valvular leaflets instead of the usual three (bicuspid valve), or by rheumatic fever. Aortic incompetence again leads to hypertrophy, but dilatation is more common as blood leaks back into the ventricle. Breathlessness is the more common complaint. The causes are the same as stenosis but also include in?ammatory conditions such as SYPHILIS or ANKYLOSING SPONDYLITIS and other disorders of connective tissue. The valve may also leak if the aorta dilates, stretching the valve ring as with HYPERTENSION, aortic ANEURYSM and MARFAN’S SYNDROME – an inherited disorder of connective tissue that causes heart defects. Infection (endocarditis) can worsen acutely or chronically destroy the valve and sometimes lead to abnormal outgrowths on the valve (vegetations) which may break free and cause devastating damage such as a stroke or blocked circulation to the bowel or leg.
Mitral valve disease leading to stenosis is rheumatic in origin. Mitral incompetence may be rheumatic but in the absence of stenosis can be due to ISCHAEMIA, INFARCTION, in?ammation, infection and a congenital weakness (prolapse). The valve may also leak if stretched by a dilating ventricle (functional incompetence). Infection (endocarditis) may affect the valve in a similar way to aortic disease. Mitral symptoms are predominantly breathlessness which may lead to wheezing or waking at night breathless and needing to sit up or stand for relief. They are made worse when the heart rhythm changes (atrial ?brillation) which is frequent as the disease becomes more severe. This leads to a loss of e?ciency of up to 25 per cent and a predisposition to clot formation as blood stagnates rather than leaves the heart e?ciently. Mitral incompetence may remain mild and be of no trouble for many years, but infection must be guarded against (endocarditis prophylaxis).
Endocarditis is an infection of the heart which may acutely destroy a valve or may lead to chronic destruction. Bacteria settle usually on a mild lesion. Antibiotics taken at vulnerable times can prevent this (antibiotic prophylaxis) – for example, before tooth extraction. If established, lengthy intravenous antibiotic therapy is needed and surgery is often necessary. The mortality is 30 per cent but may be higher if the infection settles on a replaced valve (prosthetic endocarditis). Complications include heart failure, shock, embolisation (generation of small clots in the blood), and cerebral (mental) confusion.
PERICARDITIS is an in?ammation of the sac covering the outside of the heart. The sac becomes roughened and pain occurs as the heart and sac rub together. This is heard by stethoscope as a scratching noise (pericardial rub). Fever is often present and a virus the main cause. It may also occur with rheumatic fever, kidney failure, TUBERCULOSIS or from an adjacent lung problem such as PNEUMONIA or cancer. The in?ammation may cause ?uid to accumulate between the sac and the heart (e?usion) which may compress the heart causing a fall in blood pressure, a weak pulse and circulatory failure (tamponade). This can be relieved by aspirating the ?uid. The treatment is then directed at the underlying cause.... heart, diseases of
Cause The disease is caused by a VIRUS of the in?uenza group. There are at least three types of in?uenza virus, known respectively as A, B and
C. One of their most characteristic features is that infection with one type provides no protection against another. Equally important is the ease with which the in?uenza virus can change its character. It is these two characteristics which explain why one attack of in?uenza provides little, if any, protection against a subsequent attack, and why it is so di?cult to prepare an e?ective vaccine against the disease.
Epidemics of in?uenza due to virus A occur in Britain at two- to four-year intervals, and outbreaks of virus B in?uenza in less frequent cycles. Virus A in?uenza, for instance, was the prevalent infection in 1949, 1951, 1955 and 1956, whilst virus B in?uenza was epidemic in 1946, 1950, 1954 and, along with virus A, in 1958–59. The pandemic of 1957, which swept most of the world, although fortunately not in a severe form, was due to a new variant of virus A
– the so-called Asian virus – and it has been suggested that it was this variant that was responsible for the pandemics of 1889 and 1918. Since 1957, variants of virus A have been the predominating causes of in?uenza, accompanied on occasions by virus B.
In 1997 and 2004, outbreaks of Chinese avian in?uenza caused alarm. The in?uenza virus had apparently jumped species from birds
– probably chickens – to infect some people. Because no vaccine is available, there was a risk that this might start an epidemic.
Symptoms The incubation period of in?uenza A and B is 2–3 three days, and the disease is characterised by a sudden onset. In most cases this is followed by a short, sharp febrile illness of 2–4 days’ duration, associated with headache, prostration, generalised aching, and respiratory symptoms. In many cases the respiratory symptoms are restricted to the upper respiratory tract, and consist of signs of irritation of the nose, pharynx and larynx. There may be nosebleeds, and a dry, hacking cough is often a prominent and troublesome symptom. The fever is usually remittent and the temperature seldom exceeds 39·4 °C (103 °F), tending to ?uctuate between 38·3 and 39·4 °C (101 and 103 °F).
The most serious complication is infection of the lungs. This infection is usually due to organisms other than the in?uenza virus, and is a complication which can have serious results in elderly people.
The very severe form of ’?u which tends to occur during pandemics – and which was so common during the 1918–19 pandemic – is characterised by the rapid onset of bronchopneumonia and severe prostration. Because of the toxic e?ect on the heart, there is a particularly marked form of CYANOSIS, known as heliotrope cyanosis.
Convalescence following in?uenza tends to be prolonged. Even after an attack of average severity there tends to be a period of weakness and depression.
Treatment Expert opinion is still divided as to the real value of in?uenza vaccine in preventing the disease. Part of the trouble is that there is little value in giving any vaccine until it is known which particular virus is causing the infection. As this varies from winter to winter, and as the protection given by vaccine does not exceed one year, it is obviously not worthwhile attempting to vaccinate the whole community. The general rule therefore is that, unless there is any evidence that a particularly virulent type of virus is responsible, only the most vulnerable should be immunised – such as children in boarding schools, elderly people, and people who suffer from chronic bronchitis or asthma, chronic heart disease, renal failure, diabetes mellitus or immunosuppression (see under separate entries). In the face of an epidemic, people in key positions, such as doctors, nurses and those concerned with public safety, transport and other public utilities, should be vaccinated.
For an uncomplicated attack of in?uenza, treatment is symptomatic: that is, rest in bed, ANALGESICS to relieve the pain, sedatives, and a light diet. A linctus is useful to sooth a troublesome cough. The best analgesics are ASPIRIN or PARACETAMOL. None of the sulphonamides or the known antibiotics has any e?ect on the in?uenza virus; on the other hand, should the lungs become infected, antibiotics should be given immediately, because such an infection is usually due to other organisms. If possible, a sample of sputum should be examined to determine which organisms are responsible for the lung infection. The choice of antibiotic then depends upon which antibiotic the organism is most sensitive to.... influenza
Shock may result from loss of blood or plasma volume. This may occur as a result of haemorrhage or severe diarrhoea and vomiting. It may also result from peripheral pooling of blood due to such causes as TOXAEMIA or ANAPHYLAXIS. The toxaemia is commonly the result of a SEPTICAEMIA in which leakage through capillaries reduces circulating blood volume. Another form is called cardogenic shock, and is due to failure of the heart as a pump. It is most commonly seen as a result of myocardial infarction (see under HEART, DISEASES OF).
If failure of adequate blood ?ow to vital organs is prolonged, the effects can be disastrous. The ischaemic intestine permits the transfer of toxic bacterial products and proteins across its wall into the blood; renal ISCHAEMIA prevents the maintenance of a normal electrolyte and acid-base balance.
Treatment If the shock is a result of haemorrhage or diarrhoea or vomiting, replacement of blood, lost ?uid and electrolytes is of prime importance. If it is due to septicaemia, treatment of the infection is of paramount importance, and in addition, intravenous ?uids and vasopressor drugs will be required. Cardiogenic shock is treated by attention to the underlying cause. Full intensive care is likely to be required, and arti?cial ventilation and DIALYSIS may both be needed.... shock
In an atomic age the collapse of medical services provided by governments is not far removed from the bounds of possibility. Wars come and go, medical fashions change, what is regarded as scientific today, may be neglected to tomorrow’s superstition. It is possible this book may be consulted long after 20th century medicine has had its day.
The preventative remedy of history is Garlic. It was given to workers on the Great Pyramid of Cheops as a known antiseptic and prophylactic against infection. A riot ensued when supplies ran out. During the Great Plague under Charles II a colony of people escaped death, living to reveal their secret – all were in the habit of eating Garlic. It was later confirmed that the plague was not found in houses in which Garlic had been consumed.
The disease is spread by fleas from the black rat by the organism: bacillus pestis. Incubation period is two to five days, followed by severe headache, shivering, dizziness, fever and rapid pulse. Before delirium, the patient may have the ‘staggers’ and confused speech.
Glands of the body enlarge and may suppurate. Suppuration is a welcome sign indicating speedy elimination of pus. Haemorrhagic spots break out on the skin.
The most dangerous type is that which affects the lungs, known as ‘pneumonic’ and which is highly infectious; characterised by cyanosis (blueness of the face).
Occasionally there are human cases of Bubonic Plague in California and the West but today they seldom prove fatal. Public health officials point out that the incidence of the disease in China and Vietnam is lower than for centuries because of vaccine therapy. Wild animals still spread sporadic cases of the Plague.
Treatment: Health Authorities to be notified immediately and patient isolated. All bedding and personal effects to be destroyed or disinfected. Specialised nursing necessary. If hospital care is not available, the patient should receive treatment for collapse (Capsicum, Ginger or other circulatory stimulants).
In the absence of streptomycin and tetracycline, to which the organism yersinia is sensitive, powerful alternatives may assist: Echinacea, Wild Indigo, Poke root, Queen’s Delight, Sarsaparilla, Yellow Parilla, Goldenseal, Prickly Ash.
Topical. Poultice of Slippery Elm, Marshmallow, or both combined to promote suppuration. History records pulped fresh Plantain leaves.
To be treated by general medical practitioner or Infectious Diseases consultant. ... bubonic plague
It is spread by polluted water as in the case of the composer, Tchaikovsky, who died imprudently drinking unboiled water during a cholera epidemic, despite warnings of his friends. It is transmitted also by milk, shellfish and by the faeces of infected people.
Symptoms. Profuse rice-water diarrhoea, vomiting and shock from severe loss of body fluids. Muscle cramps, cyanosis, stupor.
Alternatives. Powders. Formula: Tormentil root 2; Ginger 8; Poplar bark 2; Ipecacuanha half; Gum Myrrh quarter; Cloves; Cayenne quarter; Slippery Elm 5. (Reformed School of Medicine, W. Beach MD, USA) No dosage recorded. Suggested hourly dose: Liquid Extract: 1 teaspoon. Tinctures: 2 teaspoons. Powders: 500mg.
Tinctures. Formula No 1. Turkey Rhubarb 3; Hops 2; Peppermint 1. Dose: 1-2 teaspoons in water hourly, as tolerated.
Tinctures. Formula No 2. Turkey Rhubarb 2; Camphor (spirits) 1; Capsicum quarter; Peppermint quarter. Dose: 1-2 teaspoons hourly, as tolerated.
Orange berries. (Maeso lanceolata) Tea drunk by natives before visiting cholera epidemic areas. (Dr Isno Kufo, University of California, Berkeley)
Barberry. Berberine alkaloid. (Indian Journal of Medical Research, 50. 732, 1962)
Camphor. In the Cholera epidemic of 1831, a Russian Consol-General reported 70 cases in two places, all were cured. Elsewhere, of 1270 cases only 108 died. Practitioner use: Spirits of Camphor (10 per cent Camphor in 90 per cent brandy, gin or Vodka). 0.3 to 2ml (5 to 30 drops). Effective in the early stages. Also, rub into soles of feet and use as an inhalant.
Calamint. Old European remedy.
Enema. Bring 2 pints (1 litre) water to boiling point. Allow to cool. Add 20 drops Goldenseal and 20 drops Tincture Myrrh; for soothing and healing injection.
Diet. During an outbreak of cholera: avoid unboiled or unbottled water, uncooked seafood, vegetables and fruit unless fruit can be peeled.
Strict sanitary hygiene. Wash hands frequently.
Recovery period. Replacement of body fluids: glasses of boiled water to which 2-3 teaspoons cider vinegar has been added. Make up potassium loss with 3-4 bananas daily. Calcium, Magnesium and Potassium. Multivitamins.
Alternative rehydration therapy: spring or bottled water with sugar and salt; salt to replace water in the blood, sugar to promote absorption. Glass of water to contain 1 teaspoon salt and 2 teaspoons sugar.
To be treated by a general medical practitioner or hospital specialist.
CHOLERETIC. An agent which reduces cholesterol levels by excreting cholesterol. It also causes bile to flow freely. Differs from a cholagogue in that the latter increases the flow of bile (Artichoke). ... cholera
Symptoms: low grade fever, malaise, sore throat, massive swelling of cervical lymph glands, thick white exudate from tonsils, false membrane forms from soft palate to larynx with brassy cough and difficult breathing leading to cyanosis and coma. Toxaemia, prostration, thin rapid pulse. Throat swabs taken for laboratory examination. See: NOTIFIABLE DISEASES.
Treatment. Bedrest. Encourage sweating.
Recommendations are for those parts of the world where medical help is not readily available and may save lives. Alternatives:–
1. Combine: Tincture Echinacea 3; Tincture Goldenseal 2; Tincture Myrrh 1. Dose: 30-60 drops in water, two-hourly.
2. Combine equal parts: Tincture Lobelia; Tincture Echinacea. Dose: 30-60 drops in water, two-hourly.
3. Combine Tincture Poke root 2; Tincture Echinacea 3. Dose: 30-60 drops in water, two hourly.
4. G.L.B. Rounseville, MD, Ill., USA. I have treated diphtheria since 1883. I have treated diphtheria until I am sure the number of cases treated run into four digits. I have never given a hypodermic of antitoxin on my own initiative, nor have I ever lost a case early enough to inhibit conditions. I have depended upon Echinacea not only prophylactic but also as an antiseptic . . . In the line of medication the remedies are: Aconite, Belladonna, Poke root and Cactus grand, according to indications. But remember, if you are to have success, Echinacea must be given internally, externally and eternally! Do not fear any case of diphtheria with properly selected remedies as the symptoms occur. Echinacea will also be your stimulant, diaphoretic, diuretic, sialogogue, cathartic and antipyretic. (Ellingwood’s Physiomedicalist, Vol 13, No 6, June, 1919, 202)
5. Alexander M. Stern MD, Palatka, Florida, USA. Combine: tinctures Echinacea 1oz, Belladonna 10 drops, Aconite 10 drops. Water to 4oz. 1 teaspoon 2-hourly.
6. F.H. Williams, MD, Bristol, Conn., USA. I took a case which had been given up to die with tracheal diphtheritic croup. I gave him old-fashioned Lobelia (2) seed and Capsicum (1) internally and externally and secured expulsion of a perfect cast of the trachea without a tracheotomy.
7. Gargle, and frequent drink. To loosen false membrane. Raw lemon juice 1, water 2. Pineapple juice. Teas: Red Sage, fresh Poke root. Cold packs – saturated with Echinacea (Tincture, Liquid Extract or decoction) to throat.
Note: Capsicum and Lobelia open up the surface blood flow of the body thus releasing congestion on the inner mucous membranes.
Diet. Complete lemon-juice and herb tea fast with no solid foods as long as crisis lasts.
To be treated by a general medical practitioner or hospital specialist. ... diphtheria
Failure of the left ventricle may occur in cases of pericarditis, disease of the aortic valve, nephritis or high blood pressure.
Left ventricular failure is often of sudden onset, urgent, and may manifest as “cardiac asthma”.
Causes: blood clot, anaemia, thyroid disorder, coronary disease, congenital effects, drug therapy (beta blockers, etc), and to fevers that make heavy demands on the left ventricle.
Symptoms: breathlessness, wheezing, sweating, unproductive cough, faintness, bleeding from the lungs, palpitation. Cardiac asthma at night: feels he needs air; better upright than lying flat. Exertion soon tires. Sensation as if heart would stop. Blueness of lips and ears from hold-up in circulation of the blood through the lungs. Frequent chest colds. Awakes gasping for breath. Always tired. Cold hands and feet. Symptoms abate as compensation takes place. ‘Cream and roses’ complexion. The failure of left ventricle soon drags into failure of the right ventricle.
Right ventricular failure leads to congestive heart failure, with raised venous pressure in neck veins and body generally, causing oedema, ascites and liver engorgement.
Treatment. Agents to strengthen, support, and eliminate excess fluids from the body. BHP (1983) advises four main remedies: Hawthorn, Motherwort, Broom and Lily of the Valley. The latter works in a digitaloid manner, strengthening the heart, contracting the vessels, and lessening congestion in the lungs. Tinctures. Hawthorn 2; Stone root 1. Lily of the Valley 1. Dose: 15-45 drops thrice daily.
Broom tea. 2 teaspoons flowers, or 2-3 teaspoons tops and flowers, in cup water brought to boil and simmered one minute. 1 cup freely.
To remove fluid retention in the lungs, diuretics are indicated; chief among which is Dandelion root because of its high potassium content to prevent hypokalaemia. Dandelion coffee. As urinary excretion increases, patient improves.
Vitamin E. Not to be taken in left ventricular disorders.
Diet. See entry: DIET – HEART AND CIRCULATION.
UK Research. Researchers found that left ventricular failure was reduced by a quarter when patients were given magnesium intravenously for the first 24 hours after admission to the coronary care unit. They conclude that it should be given before any other heart therapy is commenced, and that patients should receive regular infusions if no other drug treatment is used. (The Lancet, 2.4.1994). This supports the use of magnesium sulphate (Epsom’s salts) by a past generation of herbal practitioners for the condition. ... heart – left ventricular failure (lvf)
The diagnosis is confirmed by cardiac catheterization.
Once Eisenmenger complex has developed, surgical correction of the original defect will not help.
Drug treatment may control symptoms.... eisenmenger complex
Developmental errors leading to defects arise early in the life of the embryo. In most cases, there is no known cause. Rubella in the mother is the most common known cause.
The onset and severity of symptoms depend on the defect. Some anomalies cause cyanosis and breathlessness but others may go undetected. Possible complications of an untreated heart defect include impaired growth, pneumonia as a result of mild respiratory infections, rapid tiring during exercise, and Eisenmenger complex.
Antenatal diagnosis, using specialized ultrasound scanning, is possible for most defects. After birth, any suspected defect is investigated using chest Xrays, ECG, or echocardiography.
Oxygen and various drug treatments may improve the symptoms of heart block. Some conditions, such as small septal defects or patent ductus arteriosus, may get smaller or disappear of their own accord. Other defects will require surgical correction. Narrowed heart valves can often be treated by balloon valvuloplasty. In other cases, open heart surgery or a heart transplant may be required.
Children with heart defects are at an increased risk of bacterial endocarditis; to prevent this, they are given antibiotic drugs before all surgical procedures including dental treatments.... heart disease, congenital
An ECG, echocardiogram (see echocardiography), and sometimes cardiac catheterization are performed to confirm the diagnosis and assess the severity of the condition. The disorder is corrected by open heart surgery.... tetralogy of fallot
brief resolved unexplained episode (BRUE) a sudden, brief (less than 30 to 60 seconds), and resolved episode in an infant that includes one or more of the following: decreased or irregular breathing; change in muscle tone; pallor or cyanosis or altered responsiveness. The episode is frightening for the person caring for the infant. BRUE is a description rather than a diagnosis and the term is used only when there is no explanation for the event after a thorough history and examination.... bridge
In partial (or focal) seizures, the nature of the seizure depends upon the location of the damage in the brain. For example, a simple partial motor seizure consists of convulsive movements that might spread from the thumb to the hand, arm, and face (this spread of symptoms is called the Jacksonian march); there is no loss of awareness. Complex partial seizures are commonly caused by damage to the cortex of the temporal lobe or the adjacent parietal lobe of the brain: this form of epilepsy is often called temporal lobe (or psychomotor) epilepsy. Symptoms may include *hallucinations of smell, taste, sight, and hearing, paroxysmal disorders of memory, and *automatism. Throughout an attack the patient is in a state of clouded awareness and afterwards may have no recollection of the event (see also déjà vu; jamais vu). A number of these symptoms are due to scarring and atrophy (mesial temporal sclerosis) affecting the temporal lobe.
The different forms of epilepsy can be controlled by the use of antiepileptic drugs (see anticonvulsant). Surgical resection of focal epileptogenic lesions in the brain is appropriate in a strictly limited number of cases. See also aura; postictal phase. —epileptic adj., n.... epilepsy
A variety of side-effects may occur with sulphonamide treatment, including nausea, vomiting, headache, and loss of appetite; more severe effects include *cyanosis, blood disorders, skin rashes, and fever. Because of increasing bacterial resistance to sulphonamides, and with the development of more effective less toxic antibiotics, the clinical use of these drugs has declined. Those still used include *sulfadiazine, *sulfasalazine, and sulfamethoxazole (combined with trimethoprim in *co-trimoxazole).... sulphonamide
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