One of the 2 means of dialysis used to treat kidney failure.
Dialysis is available as either haemodialysis or peritoneal dialysis.
Haemodialysis Blood is removed from the circulation either through an arti?cial arteriovenous ?stula (junction) or a temporary or permanent internal catheter in the jugular vein (see CATHETERS). It then passes through an arti?cial kidney (‘dialyser’) to remove toxins (e.g. potassium and urea) by di?usion and excess salt and water by ultra?ltration from the blood into dialysis ?uid prepared in a ‘proportionator’ (often referred to as a ‘kidney machine’). Dialysers vary in design and performance but all work on the principle of a semi-permeable membrane separating blood from dialysis ?uid. Haemodialysis is undertaken two to three times a week for 4–6 hours a session.
Peritoneal dialysis uses the peritoneal lining (see PERITONEUM) as a semi-permeable membrane. Approximately 2 litres of sterile ?uid is run into the peritoneum through the permanent indwelling catheter; the ?uid is left for 3–4 hours; and the cycle is repeated 3–4 times per day. Most patients undertake continuous ambulatory peritoneal dialysis (CAPD), although a few use a machine overnight (continuous cycling peritoneal dialysis, CCPD) which allows greater clearance of toxins.
Disadvantages of haemodialysis include cardiovascular instability, HYPERTENSION, bone disease, ANAEMIA and development of periarticular AMYLOIDOSIS. Disadvantages of peritoneal dialysis include peritonitis, poor drainage of ?uid, and gradual loss of overall e?ciency as endogenous renal function declines. Haemodialysis is usually done in outpatient dialysis clinics by skilled nurses, but some patients can carry out the procedure at home. Both haemodialysis and peritoneal dialysis carry a relatively high morbidity and the ideal treatment for patients with end-stage renal failure is successful renal TRANSPLANTATION.... dialysis
The drugs are much more e?ective in the treatment and prevention of venous clotting – for example, deep vein thrombosis (DVT), see under VEINS, DISEASES OF – than in preventing thrombosis formation in arteries with their fast-?owing blood in which thrombi contain little ?brin (against which the anticoagulants work) and many PLATELETS.
The main anticoagulants now in use are the natural agent HEPARIN (a quick-acting variety and a low-molecular-weight long-acting type); synthetic oral anticoagulants such as WARFARIN and the less-often-used acenocoumarol and PHENINDIONE; and antiplatelet compounds such as ASPIRIN, clopidogrel dipyridamole and ticlopidines. Fondaparinux is an extract of heparin which can be given once daily by injection; ximelagatran, an inhibitor of thrombin, is being trialled as the ?rst new oral anticoagulant since heparin.
Patients taking anticoagulants need careful medical monitoring and they should carry an Anticoagulant Card with instructions about the use of whatever drug they may be receiving – essential information should the individual require treatment for other medical conditions as well as for thrombosis.... anticoagulants
Excessive doses of anticoagulant drugs increase the risk of unwanted bleeding, and regular monitoring is needed.... anticoagulant drugs
Severe poisoning from ingestion of fungi is very rare, since relatively few species are highly toxic and most species do not contain toxic compounds. The most toxic species are those containing amatoxins such as death cap (Amanita phalloides); this species alone is responsible for about 90 per cent of all mushroom-related deaths. There is a latent period of six hours or more between ingestion and the onset of clinical effects with these more toxic species. The small intestine, LIVER and KIDNEYS may be damaged – therefore, any patient with gastrointestinal effects thought to be due to ingestion of a mushroom should be referred immediately to hospital where GASTRIC LAVAGE and treatment with activated charcoal can be carried out, along with parenteral ?uids and haemodialysis if the victim is severely ill. In most cases where effects occur, these are early-onset gastrointestinal effects due to ingestion of mushrooms containing gastrointestinal irritants.
Muscarine is the poisonous constituent of some species. Within two hours of ingestion, the victim starts salivating and sweating, has visual disturbances, vomiting, stomach cramps, diarrhoea, vertigo, confusion, hallucinations and coma, the severity of symptoms depending on the amount eaten and type of mushroom. Most people recover in 24 hours, with treatment.
‘Magic’ mushrooms are a variety that contains psilocybin, a hallucinogenic substance. Children who take such mushrooms may develop a high fever and need medical care. In adults the symptoms usually disappear within six hours.
Treatment If possible, early gastric lavage should be carried out in all cases of suspected poisoning. Identi?cation of the mushroom species is a valuable guide to treatment. For muscarine poisoning, ATROPINE is a speci?c antidote. As stated above, hospital referral is advisable for people who have ingested poisonous fungi.... fungus poisoning
After entering the body, mercury accumulates in organs, principally the brain and kidneys. Mercury deposits in the brain cause tiredness, incoordination, excitability, tremors, and numbness in the limbs. In severe cases, there may be impaired vision and dementia. Deposits of mercury in the kidneys may lead to kidney failure.
Treatment may involve chelating agents, which help the body to excrete the mercury quickly; haemodialysis (see dialysis); and induced vomiting or pumping out the stomach, if mercury has been swallowed within the previous few hours.... mercury poisoning
Viral infections by any of hepatitis A, B, C, D, or E viruses and also CYTOMEGALOVIRUS (CMV), EPSTEIN BARR VIRUS, and HERPES SIMPLEX.
Autoimmune disorders such as autoimmune chronic hepatitis, toxins, alcohol and certain drugs – ISONIAZID, RIFAMPICIN, HALOTHANE and CHLORPROMAZINE.
WILSON’S DISEASE.
Acute viral hepatitis causes damage throughout the liver and in severe infections may destroy whole lobules (see below).
Chronic hepatitis is typi?ed by an invasion of the portal tract by white blood cells (mild hepatitis). If these mononuclear in?ammatory cells invade the body (parenchyma) of the liver tissue, ?brosis and then chronic disease or cirrhosis can develop. Cirrhosis may develop at any age and commonly results in prolonged ill health. It is an important cause of premature death, with excessive alcohol consumption commonly the triggering factor. Sometimes, cirrhosis may be asymptomatic, but common symptoms are weakness, tiredness, poor appetite, weight loss, nausea, vomiting, abdominal discomfort and production of abnormal amounts of wind. Initially, the liver may enlarge, but later it becomes hard and shrunken, though rarely causing pain. Skin pigmentation may occur along with jaundice, the result of failure to excrete the liver product BILIRUBIN. Routine liver-function tests on blood are used to help diagnose the disease and to monitor its progress. Spider telangiectasia (caused by damage to blood vessels – see TELANGIECTASIS) usually develop, and these are a signi?cant pointer to liver disease. ENDOCRINE changes occur, especially in men, who lose their typical hair distribution and suffer from atrophy of their testicles. Bruising and nosebleeds occur increasingly as the cirrhosis worsens, and portal hypertension (high pressure of venous blood circulation through the liver) develops due to abnormal vascular resistance. ASCITES and HEPATIC ENCEPHALOPATHY are indications of advanced cirrhosis.
Treatment of cirrhosis is to tackle the underlying cause, to maintain the patient’s nutrition (advising him or her to avoid alcohol), and to treat any complications. The disorder can also be treated by liver transplantation; indeed, 75 per cent of liver transplants are done for cirrhosis. The overall prognosis of cirrhosis, however, is not good, especially as many patients attend for medical care late in the course of the disease. Overall, only 25 per cent of patients live for ?ve years after diagnosis, though patients who have a liver transplant and survive for a year (80 per cent do) have a good prognosis.
Autoimmune hepatitis is a type that most commonly occurs in women between 20 and 40 years of age. The cause is unknown and it has been suggested that the disease has several immunological subtypes. Symptoms are similar to other viral hepatitis infections, with painful joints and AMENORRHOEA as additional symptoms. Jaundice and signs of chronic liver disease usually occur. Treatment with CORTICOSTEROIDS is life-saving in autoimmune hepatitis, and maintenance treatment may be needed for two years or more. Remissions and exacerbations are typical, and most patients eventually develop cirrhosis, with 50 per cent of victims dying of liver failure if not treated. This ?gure falls to 10 per cent in treated patients.
Viral hepatitis The ?ve hepatic viruses (A to E) all cause acute primary liver disease, though each belongs to a separate group of viruses.
•Hepatitis A virus (HAV) is an ENTEROVIRUS
which is very infectious, spreading by faecal contamination from patients suffering from (or incubating) the infection; victims excrete viruses into the faeces for around ?ve weeks during incubation and development of the disease. Overcrowding and poor sanitation help to spread hepatitis A, which fortunately usually causes only mild disease.
Hepatitis B (HBV) is caused by a hepadna virus, and humans are the only reservoir of infection, with blood the main agent for transferring it. Transfusions of infected blood or blood products, and injections using contaminated needles (common among habitual drug abusers), are common modes of transfer. Tattooing and ACUPUNCTURE may spread hepatitis B unless high standards of sterilisation are maintained. Sexual intercourse, particularly between male homosexuals, is a signi?cant infection route.
Hepatitis C (HCV) is a ?avivirus whose source of infection is usually via blood contacts. E?ective screening of blood donors and heat treatment of blood factors should prevent the spread of this infection, which becomes chronic in about 75 per cent of those infected, lasting for life. Although most carriers do not suffer an acute illness, they must practise life-long preventive measures.
Hepatitis D (HDV) cannot survive independently, needing HBV to replicate, so its sources and methods of spread are similar to the B virus. HDV can infect people at the same time as HBV, but it is capable of superinfecting those who are already chronic carriers of the B virus. Acute and chronic infection of HDV can occur, depending on individual circumstances, and parenteral drug abuse spreads the infection. The disease occurs worldwide, being endemic in Africa, South America and the Mediterranean littoral.
Hepatitis E virus (HEV) is excreted in the stools, spreading via the faeco-oral route. It causes large epidemics of water-borne hepatitis and ?ourishes wherever there is poor sanitation. It resembles acute HAV infection and the patient usually recovers. HEV does not cause chronic infection. The clinical characteristics of the ?ve hepatic
viruses are broadly similar. The initial symptoms last for up to two weeks (comprising temperature, headache and malaise), and JAUNDICE then develops, with anorexia, nausea, vomiting and diarrhoea common manifestations. Upper abdominal pain and a tender enlarged liver margin, accompanied by enlarged cervical lymph glands, are usual.
As well as blood tests to assess liver function, there are speci?c virological tests to identify the ?ve infective agents, and these are important contributions to diagnosis. However, there is no speci?c treatment of any of these infections. The more seriously ill patients may require hospital care, mainly to enable doctors to spot at an early stage those developing acute liver failure. If vomiting is a problem, intravenous ?uid and glucose can be given. Therapeutic drugs – especially sedatives and hypnotics – should be avoided, and alcohol must not be taken during the acute phase. Interferon is the only licensed drug for the treatment of chronic hepatitis B, but this is used with care.
Otherwise-?t patients under 40 with acute viral hepatitis have a mortality rate of around
0.5 per cent; for those over 60, this ?gure is around 3 per cent. Up to 95 per cent of adults with acute HBV infection recover fully but the rest may develop life-long chronic hepatitis, particularly those who are immunode?cient (see IMMUNODEFICIENCY).
Infection is best prevented by good living conditions. HVA and HVB can be prevented by active immunisation with vaccines. There is no vaccine available for viruses C, D and E, although HDV is e?ectively prevented by immunisation against HBV. At-risk groups who should be vaccinated against HBV include:
Parenteral drug abusers.
Close contacts of infected individuals such as regular sexual partners and infants of infected mothers.
Men who have sex with men.
Patients undergoing regular haemodialysis.
Selected health professionals, including laboratory sta? dealing with blood samples and products.... hepatitis
During a bite by the female mosquito, one or more sporozoites – a stage in the life-cycle of the parasite – are injected into the human circulation; these are taken up by the hepatocytes (liver cells). Following division, merozoites (minute particles resulting from the division) are liberated into the bloodstream where they invade red blood cells. These in turn divide, releasing further merozoites. As merozoites are periodically liberated into the bloodstream, they cause the characteristic fevers, rigors, etc.
Malaria occurs in many tropical and subtropical countries; P. falciparum is, however, con?ned very largely to Africa, Asia and South America. Malaria is present in increasingly large areas; in addition, the parasites are developing resistance to various preventative and treatment drugs. The disease constitutes a signi?cant problem for travellers, who must obtain sound advice on chemoprophylaxis before embarking on tropical trips – especially to a rural area where intense transmission can occur. Transmission has also been recorded at airports, and following blood transfusion.
The World Health Organisation (WHO) has listed malaria as one of Europe’s top ten infectious diseases. In 1992, 20,000 cases were reported: this had risen to more than 200,000 by the late 1990s. The resurgence of malaria has been worldwide, in part the result of the development of resistant strains of the disease, and in part because many countries have failed (or been unable) to implement environmental measures to eliminate mosquitoes. Nearly 40 years ago the WHO forecast that by 1980 only four million people would be affected worldwide; now, at the beginning of the 21st century, around 500 million people a year are contracting malaria with about 3,000 people a day dying from the infection – as many as 70 per cent of them children under the age of ?ve, according to WHO ?gures. The apparently steady advance of global warming means that countries with temperate climates may well warm up su?ciently to enable malaria to become established as an ENDEMIC disease. In any case, the great increase in international air travel has exposed many more people to the risk of malaria, and infected individuals may not exhibit symptoms until they are back home. Doctors seeing a recent traveller with unexplained pyrexia and illness should consider the possibility of malarial infection.
Diagnosis is by demonstration of trophozoites – a stage in the parasite’s life-cycle that takes place in red blood cells – in thick/thin blood-?lms of peripheral blood. Serological tests are of value in deciding whether an individual has had a past infection, but are of no value in acute disease.
P. vivax and P. ovale infections cause less severe disease than P. falciparum (see below), although overall there are many clinical similarities; acute complications are unusual, but chronic ANAEMIA is often present. Primaquine is necessary to eliminate the exoerythrocytic cycle in the hepatocyte (liver cell).
P. falciparum Complications of P. falciparum infection include cerebral involvement (see BRAIN – Cerebrum), due to adhesion of immature trophozoites on to the cerebral vascular endothelium; these lead to a high death rate when inadequately treated. Renal involvement (frequently resulting from HAEMOGLOBINURIA), PULMONARY OEDEMA, HYPOTENSION, HYPOGLYCAEMIA, and complications in pregnancy are also important. In complicated disease, HAEMODIALYSIS and exchange TRANSFUSION have been used. No adequate controlled trial using the latter regimen has been carried out, however, and possible bene?ts must be weighed against numerous potential side-effects – for instance, the introduction of a wide range of infections, overload of the circulatory system with infused ?uids, and other complications.
P. malariae usually produces a chronic infection, and chronic renal disease (nephrotic syndrome) is an occasional sequel, especially in tropical Africa.
Gross SPLENOMEGALY (hyper-reactive malarious splenomegaly, or tropical splenomegaly syndrome) can complicate all four human Plasmodium spp. infections. The syndrome responds to long-term malarial chemoprophylaxis. BURKITT’S LYMPHOMA is found in geographical areas where malaria infection is endemic; the EPSTEIN BARR VIRUS is aetiologically involved.
Prophylaxis Malaria specialists in the United Kingdom have produced guidance for residents travelling to endemic areas for short stays. Drug choice takes account of:
risk of exposure to malaria;
extent of drug resistance;
e?cacy of recommended drugs and their side-effects;
criteria relevant to the individual (e.g. age, pregnancy, kidney or liver impairment). Personal protection against being bitten by
mosquitoes is essential. Permethrinimpregnated nets are an e?ective barrier, while skin barrier protection and vaporised insecticides are helpful. Lotions, sprays or roll-on applicators all containing diethyltoluamide (DEET) are safe and work when put on the skin. Their e?ect, however, lasts only for a few hours. Long sleeves and trousers should be worn after dark.
Drug prophylaxis should be started at least a week before travelling into countries where malaria is endemic (two or three weeks in the case of me?oquine). Drug treatment should be continued for at least four weeks after leaving endemic areas. Even if all recommended antimalarial programmes are followed, it is possible that malaria may occur any time up to three months afterwards. Medical advice should be sought if any illness develops. Chloroquine can be used as a prophylactic drug where the risk of resistant falciparum malaria is low; otherwise, me?oquine or proguanil hydrochloride should be used. Travellers to malaria-infested areas should seek expert advice on appropriate prophylactic treatment well before departing.
Treatment Various chemoprophylactic regimes are widely used. Those commmonly prescribed include: chloroquine + paludrine, me?oquine, and Maloprim (trimethoprim + dapsone); Fansidar (trimethoprim + sulphamethoxazole) has been shown to have signi?cant side-effects, especially when used in conjunction with chloroquine, and is now rarely used. No chemotherapeutic regimen is totally e?ective, so other preventive measures are again being used. These include people avoiding mosquito bites, covering exposed areas of the body between dusk and dawn, and using mosquito repellents.
Chemotherapy was for many years dominated by the synthetic agent chloroquine. However, with the widespread emergence of chloroquine-resistance, quinine is again being widely used. It is given intravenously in severe infections; the oral route is used subsequently and in minor cases. Other agents currently in use include me?oquine, halofantrine, doxycycline, and the artemesinin alkaloids (‘qinghaosu’).
Researchers are working on vaccines against malaria.... malaria
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