Treatment In severely affected fetuses, a fetal blood transfusion may be required and/or the baby may be delivered early for further treatment. Mild cases may need observation only, or the reduction of jaundice by phototherapy alone (treatment with light, involving the use of sunlight, non-visible ULTRAVIOLET light, visible blue light, or LASER).
Whatever the case, the infant’s serum BILIRUBIN – the bilirubin present in the blood – and its HAEMOGLOBIN concentration are plotted regularly so that treatment can be given before levels likely to cause brain damage occur. Safe bilirubin concentrations depend on the maturity and age of the baby, so reference charts are used.
High bilirubin concentrations may be treated with phototherapy; extra ?uid is given to prevent dehydration and to improve bilirubin excretion by shortening the gut transit time. Severe jaundice and anaemia may require exchange TRANSFUSION by removing the baby’s blood (usually 10 millilitres at a time) and replacing it with rhesus-negative fresh bank blood. Haemolytic disease of the newborn secondary to rhesus incompatibility has become less common since the introduction of anti-D (Rho) immunoglobulin. This antibody should be given to all rhesus-negative women at any risk of a fetomaternal transfusion, to prevent them from mounting an antibody response. Anti-D is given routinely to rhesus-negative mothers after the birth of a rhesus-positive baby, but doctors should also give it after threatened abortions, antepartum haemorrhages, miscarriages, and terminations of pregnancy.
Occasionally haemolytic disease is caused by ABO incompatibility or that of rarer blood groups.... haemolytic disease of the newborn
The death rate is 2–10 per cent and the majority of patients survive without renal failure. The longer the period of OLIGURIA, the greater the risk of chronic renal failure.
Treatment is supportive, with replacement of blood and clotting factors, control of HYPERTENSION, and careful observation of ?uid balance.... haemolytic uraemic syndrome
Bilirubin is formed from haemoglobin when old red cells are broken down, mainly by the spleen. It is absorbed by the liver, where it is made soluble in water and excreted in bile.
There are 3 main types of jaundice: haemolytic, hepatocellular, and obstructive. In haemolytic jaundice, too much bilirubin is produced for the liver to process. This is caused by excessive haemolysis of red cells, which can have many causes (see anaemia, haemolytic).
In hepatocellular jaundice, bilirubin accumulates because its transfer from liver cells into the bile is prevented, usually due to acute hepatitis (see hepatitis, acute) or liver failure.In obstructive jaundice, also known as cholestatic jaundice, bile cannot leave the liver because of bile duct obstruction.
Obstructive jaundice can also occur if the bile ducts are not present (as in biliary atresia) or if they have been destroyed by disease.
Cholestasis then occurs and bilirubin is forced back into the blood.
For all types of jaundice, treatment is for the underlying cause.... jaundice
Habitat: Throughout the country, ascending to an altitude of about 1,050 m in the outer Himalayas.
English: Indian Wild Liquorice, Jequirity, Crab's Eye, Precatory Bean.Ayurvedic: Gunjaa, Gunjaka, Chirihintikaa, Raktikaa, Chirmi- ti, Kakanti, Kabjaka, Tiktikaa, Kaakananti, Kaakchinchi. (Not to be used as a substitute for liquorice.)Unani: Ghunghchi, Ghamchi.Siddha/Tamil: Kunri.Folk: Chirmiti, Ratti.Action: Uterine stimulant, abortifa- cient, toxic. Seeds—teratogenic. A paste of seeds is applied on vitiligo patches.
Along with other therapeutic applications, The Ayurvedic Pharmacopoeia of India has indicated the use of seeds in baldness.Seeds contain abrin, a toxalbumin, indole derivatives, anthocyanins, ste- rols, terpenes. Abrin causes agglutination of erythrocytes, haemolysis and enlargement of lymph glands. A non- toxic dose of abrin (1.25 mcg/kg body weight), isolated from the seeds of red var., exhibited a noticeable increase in antibody-forming cells, bone marrow cellularity and alpha-esterase-positive bone marrow cells.Oral administration of agglutinins, isolated from the seeds, is useful in the treatment of hepatitis and AIDS.The seed extract exhibited antischis- tosomal activity in male hamsters.The methanolic extract of seeds inhibited the motility of human spermatozoa.The roots contain precol, abrol, gly- cyrrhizin (1.5%) and alkaloids—abra- sine and precasine. The roots also contain triterpenoids—abruslactone A, methyl abrusgenate and abrusgenic acid.Alkaloids/bases present in the roots are also present in leaves and stems.A. fruticulosus Wall. Ex Wight and Arn. synonym A. pulchellus Wall., A. laevigatus E. May. (Shveta Gunjaa) is also used for the same medicinal purposes as A. precatorius.Dosage: Detoxified seed—1-3 g powder. Root powder—3-6 g. (API Vols. I, II.)... abrus precatoriusThe complication is frequently fatal, being associated with HAEMOGLOBINURIA, JAUNDICE, fever, vomiting and severe ANAEMIA. In an extreme case the patient’s urine appears black. Tender enlarged liver and spleen are usually present. The disease is triggered by quinine usage at subtherapeutic dosage in the presence of P. falciparum infection, especially in the non-immune individual. Now that quinine is rarely used for prevention of this infection (it is reserved for treatment), blackwater fever has become very unusual. Treatment is as for severe complicated P. falciparum infection with renal impairment; dialysis and blood transfusion are usually indicated. When inadequately treated, the mortality rate may be over 40 per cent but, with satisfactory intensive therapy, this should be reduced substantially.... blackwater fever
Habitat: Mishmi Hills in Arunachal Pradesh. Cultivated commercially in China.
Ayurvedic: Mamira, Maamiraa, Tiktamuulaa. (Pita-muulikaa and Hem-tantu are provisional synonyms.)Unani: Maamisaa, Maamiraa.Folk: Titaa (Bengal and Assam).Action: Stomachic, antiperiodic, antibacterial, antifungal. Prescribed in debility, convalescence, intermittent fevers, dyspepsia, dysentery and intestinal catarrh. Used as a local application in thrush.
The rhizomes contains berberine (9%) as the major alkaloid; other alkaloids present are: coptin (0.08%), cop- tisin 0.02%) and jatrorrhizine (0.01%). Samples from China contained 9.2612.23% berberine, 2.39-3.25% coptisin and 3.20-4.46% jatrorrhizine. In China, the herb is used as an antidiabetic; the ethanolic (50%) extract exhibited hypoglycaemic and hypotensive activity.The drug due to berberine and its related alkaloids promoted reticuloen- dothelium to increased phagocytosis of leucocytes in dog blood in vitro and in vivo.Coptis chinensis (Huang Lian) inhibited erythrocyte haemolysis, decreased lipid peroxidation in brain and kidney, decreased generation of superoxide peroxidation and decreased hy- droxyl radicals in rats. (Life Sci, 2000, 66(8), 725-735.)Dosage: Root—1-3 g powder. (CCRAS.)... coptis teetaHabitat: Native to China and Japan; cultivated in Indian gardens as an ornamental.
English: Maidenhair tree called Living Fossils (in India), Kew tree.Action: Antagonizes bronchospasm, used as a circulatory stimulant, peripheral vasodilator.
Key application: Standardized dry extract—for symptomatic treatment of disturbed performance in organic brain syndrome within the regimen ofa therapeutic concept in cases of dementia syndromes— memory deficits, disturbance in concentration, depressive emotional conditions, dizziness, tinnitus and headache. (German Commission E, ESCOP, WHO.) As vasoactive and platelet aggregation inhibitor.(The British Herbal Pharmacopoeia.) (For pharmocological studies in humans and clinical studies, see ESCOP.)The majority of pharmacological studies and clinical trials have been conduced using a standardized extract which contains 24% flavonoid glyco- sides (Ginko flavone glycosides) and 6% terpenoids (ginkgolides and bilob- alide).The extract increases tolerance to hypoxia and exhibits anti-ischaemic effect. It simultaneously improves the fluidity of blood, decreases platelet adhesion, decreases platelet and erythro- cyte aggregation and reduces plasma and blood viscosity. The extract protects erythrocytes from haemolysis. The extract also decreases the permeability of capillaries and protects the cell membrane by trapping deleterious free radicals.The extract also increased cerebral blood flow in about 70% patients evaluated (patients between 30-50 year age had 20% increase from the base line, compared with 70% in those 50- to 70- year-olds).A reversal of sexual dysfunction with concurrent use of ginkgo with antidepressant drugs has been reported. (Am J Psychiatry, 2000 157(5), 836837.)The National Centre for Complementary and Alternative Medicine, USA, is conducting a 5-year study of 3000 people aged 75 and older to determine if ginkgo, 240 mg daily, prevents dementia or Alzheimer's disease.... ginkgo biloba– is conjugated or unconjugated. If conjugated, this indicates that HAEMOLYSIS is causing the jaundice; if unconjugated, disease of the LIVER or BILE DUCT is the likely diagnosis.... van den bergh test
Symptoms These depend upon whether the anaemia is sudden in onset, as in severe haemorrhage, or gradual. In all cases, however, the striking sign is pallor, the depth of which depends upon the severity of the anaemia. The colour of the skin may be misleading, except in cases due to severe haemorrhage, as the skin of many Caucasian people is normally pale. The best guide is the colour of the internal lining of the eyelid. When the onset of the anaemia is sudden, the patient complains of weakness and giddiness, and loses consciousness if he or she tries to stand or sit up. The breathing is rapid and distressed, the pulse is rapid and the blood pressure is low. In chronic cases the tongue is often sore (GLOSSITIS), and the nails of the ?ngers may be brittle and concave instead of convex (koilonychia). In some cases, particularly in women, the Plummer-Vinson syndrome is present: this consists of di?culty in swallowing and may be accompanied by huskiness; in these cases glossitis is also present. There may be slight enlargement of the SPLEEN, and there is usually some diminution in gastric acidity.
CHANGES IN THE BLOOD The characteristic change is a diminution in both the haemoglobin and the red cell content of the blood. There is a relatively greater fall in the haemoglobin than in the red cell count. If the blood is examined under a microscope, the red cells are seen to be paler and smaller than normal. These small red cells are known as microcytes.
Treatment consists primarily of giving suf?cient iron by mouth to restore, and then maintain, a normal blood picture. The main iron preparation now used is ferrous sulphate, 200 mg, thrice daily after meals. When the blood picture has become normal, the dosage is gradually reduced. A preparation of iron is available which can be given intravenously, but this is only used in cases which do not respond to iron given by mouth, or in cases in which it is essential to obtain a quick response.
If, of course, there is haemorrhage, this must be arrested, and if the loss of blood has been severe it may be necessary to give a blood transfusion (see TRANSFUSION – Transfusion of blood). Care must be taken to ensure that the patient is having an adequate diet. If there is any underlying metabolic, oncological, toxic or infective condition, this, of course, must be adequately treated after appropriate investigations.
Megaloblastic hyperchromic anaemia There are various forms of anaemia of this type, such as those due to nutritional de?ciencies, but the most important is that known as pernicious anaemia.
PERNICIOUS ANAEMIA An autoimmune disease in which sensitised lymphocytes (see LYMPHOCYTE) destroy the PARIETAL cells of the stomach. These cells normally produce INTRINSIC FACTOR, the carrier protein for vitamin B12 (see APPENDIX 5: VITAMINS) that permits its absorption in the terminal part of the ILEUM. Lack of the factor prevents vitamin B12 absorption and this causes macrocytic (or megaloblastic) anaemia. The disorder can affect men and women, usually those over the age of 40; onset is insidious so it may be well advanced before medical advice is sought. The skin and MUCOSA become pale, the tongue is smooth and atrophic and is accompanied by CHEILOSIS. Peripheral NEUROPATHY is often present, resulting in PARAESTHESIA and numbness and sometimes ATAXIA. A rare complication is subacute combined degeneration of the SPINAL CORD.
In 1926 two Americans, G R Minot and W P Murphy, discovered that pernicious anaemia, a previously fatal condition, responded to treatment with liver which provides the absent intrinsic factor. Normal development requires a substance known as extrinsic factor, and this depends on the presence of intrinsic factor for its absorption from the gut. The disease is characterised in the blood by abnormally large red cells (macrocytes) which vary in shape and size, while the number of white cells (LEUCOCYTES) diminishes. A key diagnostic ?nd is the presence of cells in the BONE MARROW.
Treatment consists of injections of vitamin B12 in the form of hydroxocobalamin which must be continued for life.
Aplastic anaemia is a disease in which the red blood corpuscles are very greatly reduced, and in which no attempt appears to be made in the bone marrow towards their regeneration. It is more accurately called hypoplastic anaemia as the degree of impairment of bone-marrow function is rarely complete. The cause in many cases is not known, but in rather less than half the cases the condition is due to some toxic substance, such as benzol or certain drugs, or ionising radiations. The patient becomes very pale, with a tendency to haemorrhages under the skin and mucous membranes, and the temperature may at times be raised. The red blood corpuscles diminish steadily in numbers. Treatment consists primarily of regular blood transfusions. Although the disease is often fatal, the outlook has improved in recent years: around 25 per cent of patients recover when adequately treated, and others survive for several years. In severe cases promising results are being reported from the use of bone-marrow transplantation.
Haemolytic anaemia results from the excessive destruction, or HAEMOLYSIS, of the red blood cells. This may be the result of undue fragility of the red blood cells, when the condition is known as congenital haemolytic anaemia, or of acholuric JAUNDICE.
Sickle-cell anaemia A form of anaemia characteristically found in people of African descent, so-called because of the sickle shape of the red blood cells. It is caused by the presence of the abnormal HAEMOGLOBIN, haemoglobin S, due to AMINO ACID substitutions in their polypeptide chains, re?ecting a genetic mutation. Deoxygenation of haemoglobin S leads to sickling, which increases the blood viscosity and tends to obstruct ?ow, thereby increasing the sickling of other cells. THROMBOSIS and areas of tissue INFARCTION may follow, causing severe pain, swelling and tenderness. The resulting sickle cells are more fragile than normal red blood cells, and have a shorter life span, hence the anaemia. Advice is obtainable from the Sickle Cell Society.... inadequate intake of iron
Habitat: Assam, Naga and Khasi Hills, Travancore and the Andamans.
English: Common Emetic Nut.Ayurvedic: Madana, Chhardana, Pindi, Shalayaka, Vishapushpaka.Unani: Mainphal, Jauz-ul-Qai.Siddha/Tamil: Marukkaaraikai, Madkarai.Folk: Mainphal.Action: Fruit—nervine, calmative, antispasmodic, emetic, anthelmintic, abortifacient. Used as a substitute for ipecacuanha.
The Ayurvedic Pharmacopoeia ofIn- dia recommends the dried fruit in chlorosis, common cold, rhinitis and obstinate skin diseases.The activity of the drug is attributed to the presence of saponins which occur to the extent of 2-3% in fresh fruits and about 10% in dried whole fruit. The saponins are concentrated mostly in the pulp. A mixture of two saponins, viz. randialic or neutral saponin and randialic acid or acid saponin has been isolated from the pulp. On complete hydrolysis both the saponins yield oleanolic acid as sapogenin. Ursosaponin, isolated from the ethanolic extract of the dried whole fruit, gave ursolic acid and glucose. Randianin, isolated from the fruit, gave a haemolytic triterpe- noid saponin.In experimental animals, the drug caused haemolysis both in vitro and in vivo. Crude saponin fraction showed haemolytic, molluscidal and immuno- stimulating activities.Oleanolic acid 3-glucoside, isolated from the seed, exhibited anti-arthritic activity in exudative and proliferative phases of inflammation in rats.Dosage: Fruit—0.5-1.0 g powder for decoction, 3-6 g for induction vomiting. (API, Vol. I.)... randia dumetorumHabitat: Native to tropical Asia; grown in Assam, Bengal, Punjab, Vadodara, Andhra Pradesh and Tamil Nadu.
English: Agati Sesban, Swamp Pea.Ayurvedic: Agastya, Agasti, Munidrum, Munitaru, Muni, Vangasena, Vakrapushpa, Kumbha.Siddha/Tamil: Agatti.Action: Plant—astringent, antihistamine, febrifuge. Used for intermittent fevers, catarrh, cough, consumption, glandular enlargement.
The aqueous extract of flowers has been found to produce haemolysis of human and sheet erythrocytes even at low concentration due to methyl ester of oleanolic acid. Flowers also gave nonacosan-6-one and kaempferol-3- rutinoside.The seed gave kaempferol-3,7-diglu- coside, (+)-leucocyanidin and cyani- din-3-glucoside. Seed also contains galactomannan.A saponin present in the leaves on hydrolysis gave an acid sapogenin oleanoic acid, galactose, rhamnose and glucuronic acid. Besides saponin, the leaves contain an aliphatic alcohol, grandiflorol.The bark contains gum and tannin. The red gum is used as a substitute for Gum arabic. An infusion of the bark is given in first stages of smallpox and other eruptive fevers (emetic in large doses).Dosage: Whole plant—10- 20 ml juice; 50-100 ml decoction. (CCRAS.)... sesbania grandifloraWhen haemolysis is due to a defect inside the red cells, the underlying problem is abnormal rigidity of the cell membrane. This causes the cells to become trapped, at an early stage of their life-span, in the small blood vessels of the spleen, where they are destroyed by macrophages (cells that ingest foreign particles). Abnormal rigidity may result from an inherited defect of the cell membrane (as in hereditary spherocytosis), a defect of the haemoglobin in the cell (as in sickle-cell anaemia), or a defect of one of the cell’s enzymes. An inherited deficiency of the glucose-6phosphate dehydrogenase enzyme (see G6PD deficiency) may result in episodes of haemolytic anaemia since the red cells are prone to damage by infectious illness or certain drugs or foods.
Haemolytic anaemias due to defects outside the red cells fall into 3 main groups. First are disorders in which red cells are destroyed by buffeting (by artificial surfaces such as replacement heart valves, abnormal blood-vessel linings, or a blood clot in a vessel, for example). In the 2nd group, the red cells are destroyed by the immune system. Immune haemolytic anaemias may occur if foreign blood cells enter the bloodstream, as occurs in an incompatible blood transfusion, or they may be due to an autoimmune disorder. In haemolytic disease of the newborn, the baby’s red cells are destroyed by the mother’s antibodies crossing the placenta. Thirdly, the red cells may be destroyed by microorganisms; the most common cause is malaria. People with haemolytic anaemia may have symptoms common to all types of anaemia, such as fatigue and breathlessness, or symptoms specifically due to haemolysis, such as jaundice.
Diagnosis is made by examination of the blood (see blood film). Some inherited anaemias can be controlled by removing the spleen (see splenectomy). Others, such as G6PD deficiency, can be prevented by avoiding the drugs or foods that precipitate haemolysis. Anaemias due to immune processes can often be controlled by immunosuppressant drugs. Transfusions of red cells are sometimes needed for emergency treatment of life-threatening anaemia.... anaemia, haemolytic
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