ROAD ACCIDENTS – General Considerations, Injuries Caused by Road Accident and Management At the Site of Accident

General Considerations

In modern times mortality and morbidity caused by road accidents is on the rise. This is common in all countries of the world where fast traffic on the road is increasing.

The accidents may involve the vehicles or the pedestrians using the road. The major types of accidents are collision between vehicles, loss of control of the vehicle and collision with hard objects or overturning. The other type of accidents involves knocking down pedestrians or occupants of lighter vehicles such as two wheelers and light motor vehicles. In general the major damage and passenger injury occurs to the lighter vehicle.

The major factors contributing to road accidents can be classified as given below:

A. Causes attributable to the vehicles

1. Speed of the vehicle- The rate and severity of the accident increases with increasing speed of either vehicle. With the introduction of modern highways speed-related injuries have become much more common

2. Mechanical defects in the vehicle, which lead to failure of the controls.

3. Exceeding the safety limits prescribed for the vehicle in terms of speed, loading and maintenance.

B. Causes attributable to the driver

1. Fatigue and sleep- long driving exceeding 6 hours of continuous driving leads to driver fatigue, delay in the reflexes and tendency to sleep.

2. Drunkenness: Consumption of alcohol and less commonly other narcotic drugs impairs the efficiency of the driver

3. Inattention, non-compliance with signals and rash driving

4. Inexperience of the driver

Most of the major collision accidents occur on highways, especially in the early hours of the morning when driver fatigue and somnolence are maximal. Rarely accidents may occur due to organic disease in the driver such as epilepsy, cardiovascular disease, strokes and others.

Injuries to Pedestrians

Walking on highways and fast traffic roads is associated with injury to the pedestrians. Elderly people, obese individuals, persons with movement disorders, alcoholics and children are involved more.

INJURIES CAUSED BY ROAD ACCIDENTS

Vehicular Accidents

Trauma to the driver and passengers due to the impact and damage and deformation to the vehicle are usually serious. This leads to injuries which may be instantaneously fatal. In motor car accidents, the luggage kept unsecured in the passenger compartment fly out and cause further missile- like injuries to the passengers. Trauma to vital parts such as head, chest cage, spine, bones, abdomen and major blood vessels, intracranial injuries, intracranial bleeding, tension pneumothorax, rupture of major blood vessels like aorta, injuries to the heart, rupture of solid organs and hollow viscera in the abdomen and pelvis and exsanguinating bleeding ( both external and internal ) are the causes of death at the site of accident or within a few hours. Pedestrian injuries cause death due to damage to vital structures, especially intracranial bleeding, chest injuries, intra abdominal injuries and exsanguination.

MANAGEMENT AT THE SITE OF ACCIDENT

Effective first aid helps to save life and reduce morbidity and delayed mortality. Mainly this consists of maintenance of the airway and attention to ventilation, tourniquets to arrest external hemorrhage, immobilization of parts of the body such as the neck and spine to avoid further damage to the vital neural structures, covering open chest injuries which interfere with ventilation and rapid transport to the nearest hospital with adequate facilities. It is the duty of all medical men to give first aid in such a situation. It is to be remembered that an obvious injury may distract the attention of the doctor from other invisible injuries such as internal bleeding or rupture of viscera which can cause death.

When major accidents involving buses occur, a large member of persons will be simultaneously affected and this may cause a heavy strain on the medical facilities. In this situation, a senior medical officer has to inspect the victims and using the principles of ‘triage’, arrange for appropriate management. In such an emergency all medical personnel have to participate in the emergency management.

All road traffic accidents invite legal procedures which have to be complied with. General guidelines to reduce road traffic accidents and their consequences

1. Education of the public on the safe use of roads and motor vehicles

2. Strict compliance with road traffic rules

3. Avoidance of alcohol and drugs before driving

4. Avoid driver fatigue and somnolence

5. Avoid the presence of unsecured luggage in the passenger compartment

6. Use the seat belts as prescribed.

7. Enforcement of traffic regulations by the appropriate authorities

RIBOFLAVIN (VITAMIN – B2)

Riboflavin is essentially required in all oxidation reduction reactions involving the coenzymes flavin mononucleotide and flavin adenine dinucleotide which take part in tissue oxidation and respiration. It is moderately heat resistant, but boiling in alkaline media or exposure to sunlight destroys this vitamin.

Good dietary sources include liver, meat, eggs, kidney, milk, other dairy products, green leafy vegetables, and sprouted cereals and pulses. Daily requirement is 0.60 mg/1000 kcal, i.e. a total of 1.5-2 mg.

1. Signs of deficiency Angulostomatitis, cheilosis, nasolabial seborrhea, and possibly vascularization of the cornea are the characteristic features. Angulostomatitis may also occur in deficiencies of niacin and folic acid. Mucosa of the lips appears red and denuded in cheilosis. On taking hot and spicy food there may be soreness. Vascularization of the cornea has been described in some surveys. In glossitis the mucosa over the tongue is red, swollen and painful. This responds to riboflavin therapy. Some cases show lesions in the oral mucosa, eyes, and genitals (oculooro-genital syndrome). The oculo-orogenital syndrome presents as blepharo-conjunctivitis, angular stomatitis, bright red atrophic tongue and dermatitis of the pubic region. This syndrome may occur in pyridoxine deficiency as well.

2. Treatment Riboflavin in a dose of 2-5 mg thrice a day cures the condition in a few days. The drug can be given orally as tablets or syrup or by injections. Treatment of oculo-orogenital syndrome is to give riboflavin up to 100 mg/day and pyridoxine 150 mg/day. The lesions clear within 7-10 days.

Q FEVER – Forms, Acute Q fever, Chronic Q Fever, Diagnosis, Treatment and Prevention

It is a zoonosis caused by coxicella burnetii- It is a gram negative pleomorphic coccobacillus which is having homology with Legionella pneumophilia

Two forms exist

1. A small cell variant (SCV) and

2. A large cell variant (LCV)

The SCV exists in nature and it is resistant to environmental factors. The LCV develops in the host’s monocytes and multiplies. It is the pathogenic form. The disease exists an Australia, India, USA and other areas. Animal reservoirs include cows, goats, sheep, dogs, cats and others. Organisms are shed in milk, feces, urine and products of conception. Humans become infected by ingestion of infective material or droplet infection through the respiratory tract. Incubation period is 12 to 30 days.

Acute Q Fever

This resembles influenza clinically, with varying degrees of pneumonia and hepatitis. Fever lasts for an average of 10 days (range 10-57 days).

Chronic Q Fever

This occurs in 60-70% of infected persons. It leads to endocarditis which supervenes on pre-existing valvular lesions. Untreated, the condition is fatal. Q fever may recrudesce during pregnancy and lead to abortion. Other manifestations include osteo-articular infections and hepatitis.

Diagnosis

Antibodies can be detected by indirect immunofluorescence.

Treatment

Acute Q fever —doxycycline 100 mg bid po for 14 days. Chronic Q fever—life long doxycycline therapy may be necessary. Addition of hydroxycloroquine 200 mg tds po given for 18 months favours recovery. It acts synergistically with doxycycline.

Prevention

Pasteurization of milk is partly protective. Occupational risk can be reduced by vaccination in persons exposed to the risk.

PYRIDOXINE – Normal Daily Requirement, Clinical Features

The active form of this vitamin is pyridoxal. Pyridoxal phosphate acts as a coenzyme in several reactions, especially in the metabolism of amino acids and biological amines such as catecholamines and 5-hydroxytryptamine. It takes part in the biosynthesis of gamma-amino-butyric acid in the brain. Yeast, liver, meat, whole grain cereals, peanuts, bananas and legumes are good dietary sources.

Normal daily requirement is 1.25 mg and it is present in the ordinary Indian diets and hence nutritional deficiency is rare. Drugs like INH, oral contraceptives and hydralazine may interfere with the metabolism of this vitamin and produce conditioned deficiencies.

Clinical features include dermatitis, cheilosis, angulostomatitis, glossitis, dizziness, vomiting and peripheral neuropathy. Infantile convulsions have been attributed to nutritional pyridoxine deficiency. Pyridoxine deficiency is known to produce one form of sideroblastic anemia which responds to high doses of this vitamin.

Concurrent administration of 6 mg of pyridoxine prevents the development of neuritis in subjects treated with INH.

PROTEIN ENERGY MALNUTRITION – General Characteristics, Etiology and Pathogenesis, Clinical Features (Kwashiorkor and Marasmus)

GENERAL CHARACTERISTICS

Protein-energy malnutrition (PEM) has been defined by WHO and FAO (1973) as “a range of pathological conditions arises from coincident lack of protein and calories in varying proportions occurring most frequently in infants and young children and commonly associated with infections”.

The clinical spectrum includes a variety of clinical syndromes, with ‘marasmus’ and ‘kwashiorkor’ at the two extremes and the intermediate forms (marasmic kwashiorkor) and nutritional dwarfism in between. Mild cases may present only with apathy and retardation of growth. Childhood malnutrition has been graded taking the weight for age as the criteria.

Etiology and pathogenesis:

Protein-energy malnutrition is an environmental disease, caused by deficient intake of protein and calories. It results from the combined influences of low food availability, poverty, ignorance, illiteracy and cultural taboos, frequent infections and poor environmental sanitation.

CLINICAL FEATURES

Marasmus

Severe restriction of food in an infant, as in cases of gross inadequacy of breast milk, leads to arrest of growth. Due to starvation the subcutaneous fat and muscles are used up as energy sources. The baby becomes emaciated. Unlike as in kwashiorkor, there is no edema. Loss of the buccal pads of fat give the infant a withered and ‘old man’s’ look. The weight is below the sixtieth percentile. The height depends upon the onset and duration of undernutrition. In the early stages the infant eats well but appetite is lost as the condition progresses. Initially, inadequacy of food leads to constipation, but later on diarrhea sets in with green stools containing mucus. In the well-established form the baby is apathetic.

Moderate anemia may develop. The skin and hair are usually normal.

KWASHIORKOR

This name was coined by Dr Cicely Williams in 1933, to denote ‘disease of the child deposed from the breast by the conception of a new fetus’. Children between the ages of 1 and 3 years are affected more. The disease starts when the baby is weaned from the breast.

Pathology

Main changes are seen in the small intestines, liver, pancreas and thymus. Small intestinal mucosa shows blunting of villi and atrophy of brush border, so that the columnar epithelium appears to become cuboidal. The total absorbing surface is reduced. Lactose intolerance is common because of disaccharidase deficiency. Liver shows fatty infiltration of the parenchymal cells. The pancreatic acini are atrophic and enzyme activity is reduced. Thymus is markedly atrophied and this may contribute to deficiency of cell mediated immunity.

Clinical features

This child is stunted and skeletal muscles are wasted. The presence of fairly normal amounts of subcutaneous fat and edema give a deceptively plump appearance. Pitting edema is a prominent feature.

The child is apathetic, irritable and drowsy. Characteristic skin changes occur in many and when present; these are diagnostic. These include flaky paint dermatosis seen over areas of pressure and trauma, fissuring and ulceration at the flexures and a mosaic like appearance (crazy pavement appearance). The hair becomes thin, sparse, brownish and lusterless. They may fall off. Regrowth of normal pigmented hair heralds nutritional recovery. Since periods of nutritional deprivation and partial correction of nutrition alternate in many cases, the hair shows alternate bands of pigmentation and depigmentation (flag sign). The appetite is poor. Diarrhea is a frequent feature. There may be concomitant deficiencies of iron, folate, fat soluble vitamins and B complex factors. Hepatomegaly occurs in a third of the cases. This is due to fatty infiltration. With recovery the liver reverts to normal without sequelae.

MARASMIC KWASHIORKOR

In this condition, features of marasmus and kwashiorkor are present simultaneously. The body weight is less than 60% of the normal. Dependent edema is present. Mental changes, skin and hair changes and hepatomegaly are evident.

Secondary infection is very common in protein energy malnutrition. This is due to the fact that both humoral and cellular immunity are defective. The intestinal flora is altered and this may account for the diarrhea. Episodes of infection further jeopardize the nutritional status.

Laboratory investigations

The total protein content of the body is reduced, and this is reflected most prominently as hypoalbuminemia. The plasma levels of essential aminoacids are low, but the non-essential amino acids remain normal or even elevated. Basal metabolic rate is reduced. Hypoglycemia occurs commonly. Total body water is increased and all the compartments show increase of fluid. The plasma osmolality is reduced. Renal plasma flow is diminished and this results in impairment of renal function. Plasma sodium is increased with reduction in potassium and magnesium. Gross reduction of serum sodium is associated with a poor prognosis.

Prognosis depends on the severity of the disease at diagnosis and promptness of treatment. Marked weight loss, severe infections, fluid and electrolyte imbalance, hypoglycemia, hypothermia, cardiac failure, elevation of serum bilirubin and liver enzymes, drowsiness and xerophthalmia indicate poor prognosis. In severe cases mortality goes up to 20%. The disease is entirely preventable by ensuring adequate caloric and protein intake to the growing child in the first three years of life. Proper management in the established case gives rise to full recovery, catch up growth and restoration of normal parameters. Recurrence is likely if the adverse environment is not corrected.

Treatment

Treatment is aimed to supply a diet rich in calories, proteins and other essential nutrients. For success of treatment supplementation should be with natural foods available locally. 150 Kcal/kg of energy and 3.3 g/kg of proteins are optimally required for catch-up growth. Fats are administered to supply adequate calories without increasing the bulk. Children with lactose intolerance do not tolerate carbohydrates, but they tolerate fats. As the child gains appetite the frequency of feeding is increased. If there is severe anorexia, forced feeding has to be

resorted to. Salt should be restricted to avoid congestive cardiac failure. The National Institute of Nutrition, Hyderabad has formulated an energy-protein rich mixture to treat PEM at home. It consists of whole wheat 40 g, Bengal gram 16 g, groundnut 10 g, Jaggery 20 g (total 86 g). This supplies 330 calories and 11.3 g proteins. Skimmed milk, eggs and cereals are added as the condition improves. In addition to nutritional correction, intercurrent infections have to be controlled simultaneously. Initial recovery is heralded by the disappearance of edema. The major biochemical abnormalities are corrected within 2-3 weeks. Complete correction of all reversible changes, referred to as ‘clinical recovery’ occurs only in 2-3 months.

Prevention and Rehabilitation

PEM is a preventable disease. Three levels of prevention have been formulated. Primary prevention is achieved by nutrition education to prevent occurrence of PEM. Secondary prevention is aimed at early detection and proper treatment. Tertiary prevention consists of nutritional rehabilitation of an established case. The importance of breast feeding as a prophylactic against protein calorie malnutrition cannot be overemphasized. Correct feeding practices, both during health and disease, proper sanitation, deworming and family planning methods have to be employed simultaneously to achieve lasting benefit. Nutrition rehabilitation is employed to prevent residual nutritional handicap and prevent recurrence of protein energy malnutrition. Even at the initial stages of treatment the mother should be made to participate in the selection, preparation and administration of food. This measure helps to impart nutritional education to her, prevent recurrence and detect relapse early.

PELLAGRA – General Features, Pathology, Clinical Features, Skin Changes, Course and Prognosis, Treatment and Prevention

General Features

This disease was widely prevalent in India among the maize eating communities in all states, especially Andhra Pradesh, Tamil Nadu and Rajasthan. Consumption of sorghum or jowar also predisposes to this tendency. Newer varieties of maize and sorghum with better nutritive value have helped to reduce the incidence of pellagra.

Alcoholism and malabsorption states precipitate pellagra. Inborn disorders of metabolism such as Hartnup disease in which the absorption of tryptophan is impaired lead to pellagra in rare cases.

Pathology

Dermatitis, changes in the oral and intestinal mucosa and degenerative changes in the central nervous system are seen. Ulcers may develop in the intestines. Chromatolysis of ganglion cells occurs in the central nervous system. Patchy demyelination occurs in the spinal cord.

Clinical features

Generalized malnutrition is evident in most cases. The most well-known features are the three Ds—dermatitis, diarrhea and dementia, but these characterize the very advanced stage of the disease. Pellagra should be diagnosed much before this classical picture develops, since the advanced stage is associated with high mortality.

Skin changes

These are seen over areas exposed to sunlight. These start with erythema which may resemble sunburn. This progresses to vesiculation, ulceration, secondary infection, and crusting. In chronic pellagra the skin becomes rough, thickened, scaly and pigmented. In

home-bound patients not exposed to the sun, pellagra may develop without the skin changes—“Pellagra sine pellagra”.

Mucous membrane changes are evident in the mouth and vulva. Skin of the perianal region shows degenerative and inflammatory lesions. The tongue is raw and beefy in appearance. Angulostomatitis may be present.

Alimentary symptoms

Vague alimentary symptoms like anorexia, nausea, vomiting, and dyspepsia are invariably seen. Diarrhea is common but not always present. The stools may be watery or rarely dysenteric.

Neurological features

Anxiety, depression, irritability and failure to concentrate are early symptoms. Advanced cases show delirium, dementia and psychiatric manifestation. Mental symptoms may be mistaken for primary psychiatric disorders.

Course and prognosis

Advanced cases are fatal due to diarrhea, secondary infections, or other associated nutritional disorders. Early treatment reverses the symptoms completely.

Treatment

Well-balanced diet containing adequate supply of proteins should be instituted. Nicotinamide is well absorbed if given orally. It is given in a dose of 100 mg every 6 h for 2-3 weeks. In the advanced cases 50-100 mg may be given intramuscularly or intravenously.

Supplements such as the other B complex vitamins and iron should be concurrently administered. Local application of antihistamine creams and protective clothing gives relief to the skin lesions.

Prevention

In maize eating communities other sources of niacin should be provided along with. In non-endemic areas pellagra may develop in the elderly, inmates of mental homes, etc. Such groups require vitamin supplementation.

PANTOTHENIC ACID AND BIOTIN

PANTOTHENIC ACID

Pantothenic acid is converted to coenzyme A in the body. This vitamin is widely distributed in animal and vegetable foods and hence dietary deficiency is very rare. Though the exact requirement is not clearly known, 10 mg may represent an adequate daily intake. Deficiency in experimental animals leads to dermal and hair changes, neuromuscular degeneration and fatal adrenal hemorrhage.

Calcium pantothenate has been used for other conditions like paralytic ileus, and streptomycin toxicity based on empirical findings. There is no conclusive proof to support these claims.

BIOTIN

This is an organic acid functioning as a coenzyme in several carboxylation reactions. It is present in several articles of food and is also synthesized by intestinal bacteria. Daily requirement is about 100 mcg. Naturally occurring deficiency is rare, but conditioned deficiency may develop by overfeeding exclusively with white of egg. This is due to the presence of avidin which antagonizes biotin. Infants who are on parenteral feeding with biotin deficient diets may develop symptoms such as lassitude, irritability, paresthesiae, anorexia, rashes, and hair loss. All these improve with the administration of biotin.

Inherited disorders of biotin metabolism occur rarely. Two types are known. One type may present in the first few weeks of life with metabolic acidosis and a rash. The other presents in the first few months of life with rash, keratocojunctivitis, alopecia, ataxia, hypotonia, and metabolic and lactic acidosis. Both groups respond dramatically to large doses of biotin.

OSTEOMALACIA – Definition, Etiology, Clinical Features and Treatment

Definition

Osteomalacia denotes those disorders where mineralization of newly formed bone matrix (osteoid) is defective.

Etiology

Osteomalacia may be of two different types:

1. Nutritional inadequacy of vitamin D, calcium or both.

2. Vitamin D-resistant osteomalacia. The latter occurs in the following conditions.

a. In renal tubular defects which produce hypophosphatemia

and chronic metabolic acidosis.

b. Chronic administration of diphenylhydantoin which leads to excessive metabolism of vitamin D.

c. Osteoporosis.

d. After parathyroidectomy for osteitis fibrosa or hyperthyroidism in which rapid formation of new bone outstrips bone resorption.

Clinical features

Osteomalacia presents with vague pain which starts as aches and pains insidiously, in the lumbar spine and thighs and spreading later to the arms and ribs.

The pain is frequently felt over the bones themselves, and

not at the joints. The pain is usually symmetrical and nonradiating

and is accompanied by tenderness of involved bones. Proximal muscles are weak and there is difficulty in climbing up stairs and getting up from squatting position. Occasionally, localized acute bone pain develops rapidly. These sites correspond to the development of pseudofractures. Classical radicular pain may develop due to compression fracture of the vertebra.

Physical signs include deformities, which may be missed if not specifically looked for. The usual deformities are triradiate pelvis and spinal kyphosis (due to action of gravity). Pathologic fractures due to weight bearing and avulsion of tendinous attachments may develop. Biochemical features resemble those of rickets.

Characteristic radiological features are the appearance of “pseudofractures” (Milkman’s lines and Loser’s zones). These are linear zones of decalcification which tend to be symmetrical and extend perpendicular to the cortex. The common sites are the pubic rami, ischium, the neck of the femur, the outer edge of the scapula, ribs and vertebrae. Occasionally, Loser’s zones may extend right across a long bone simulating complete fractures. They are called pseudofractures because the gap is bridged by uncalcified osteoid tissue. They do not reveal any discontinuity of bone clinically. The pseudofractures are caused by the decalcification along the course of the major arteries entering the bones especially in areas of muscular attachment, namely the adductor insertion in the pubic ramus and attachment of gluteal muscles to the trochanters of the femur.

Vertebral bodies show compression and widening of intervertebral spaces to produce biconcave or “cod-fish” vertebrae.

However, in patients who develop osteomalacia secondary to renal tubular disorders or chronic renal failure, there is marked cortical thickening and increased density of trabeculae in spongy bone. The reason for this hyperosteosis is not clear. Despite the radiological appearances the bone is abnormally brittle and prone to develop fractures.

Treatment

Nutritional osteomalacia responds well to daily administration of 2000-4000 IU of vitamin D (0.05-0.1 mg) for 6-12 weeks followed by maintenance doses of 400-600 IU daily.

Dietary supplementation of calcium in the form of milk 500 mL per day hastens recovery. Medicinal calcium in the form of calcium gluconate, lactate or carbonate can be given as tablets or suspensions orally in doses of 250 to 500 mg daily. Supplementation has to be continued as long as the diet is deficient in calcium. Adequate supplements of calcium are provided in the form of milk 500-750 mL per day or calcium lactate tablets 1 g along with food.

ORGANOPHOSPHORUS COMPOUNDS – General Features, Clinical Features, Diagnosis and Treatment

General Features

These are the most widely used toxic agents for suicidal poisoning. Accidental poisoning occurs in workmen engaged in spraying operations. Contamination of food materials during storage or transportation has led to dramatic outbreaks of food poisoning. A dose of 40-100 mg proves fatal.

The commonly available products are methyl parathion (Folidol, Paramar, Metacid, Paramet), malathion (Malathion, Cythion) and phalone (Zolone, Sumithion, Faithion, Timidan, Ektakin). Organophosphorus compounds irreversibly phosphorylate acetyle cholinesterase (AChE) leading to the accumulation of acetyl choline at the cholinergic nerve endings such as autonomic ganglia, parasympathetic nerve endings and motor end plates.

CLINICAL FEATURES

Symptoms start within 15-30 minutes after ingestion of the toxin. Consumption on an empty stomach and along with alcohol favours rapid absorption.

Gastrointestinal or neurological symptoms may predominate. Nausea, vomiting, diarrhea, involuntary defecation, blurring of vision, miosis, excessive sweating, lacrimation, salivation, and pulmonary edema constitute the muscarinic effects. Effects on central nervous system include drowsiness, coma, convulsions, and respiratory depression. Stimulation of pre-ganglionic fibres leads to sympathetic overaction and later paralysis, muscle twitching, fasciculation, weakness, and flaccid paralysis (nicotinic effects).

Diagnosis

In almost all cases, history, circumstances and the smell of the poison help to confirm the diagnosis. The chemical compound can be identified by examination of gastric contains and blood.

Diagnosis is clinical, supported by evidence of consumption of the poison. Estimation of serum levels of pseudocholinesterase is helpful. Normal level of pseudocholine esterase in serum is 1750-3500 μU/mL. Serum levels of the enzyme correlate inversely with the severity.

TREATMENT

The general measures for oral poisons should be instituted without delay.

Atropine

Atropine is the pharmacological antidote, and it is the sheet anchor of treatment since it antagonizes the peripheral effects of acetylcholine. It is freely available in all hospitals and cheap. This drug prevents pulmonary edema and excessive secretions. The dose requirement varies widely. In general, large doses have to be used. The ideal way to administer the drug is through an intravenous 5% glucose drip. A dose of 2 mg is given initially and 1 mg or more is repeated every 10 minutes (or even at shorter intervals) till the pupils are dilated to normal size and pulmonary edema and bronchorrhea is cleared. In many cases heroic doses, often several hundred ampoules of atropine may be required within a few hours to tide over the crises. The patient has to be observed very closely to prevent deterioration and death.

Maintenance dose is continued to keep the pupils in mid-dilation. It is usually possible to withdraw atropine after 24-48 hours but in some cases it may have to be continued for up to 5 days. Release of the toxin from lipid tissues after an interval of 2-3 days may result in return of symptoms and death after a period of apparent recovery. Hence, all patients have to be closely watched for at least 7 days after onset of the symptoms. In such cases, repetition of massive doses of atropine and supportive measures are to be undertaken.

Pralidoxime Hydrochloride

Pralidoxime hydrochloride is the specific antidote. It is given IV in a dose of 1-2 g initially and repeated 2-3 hrs later. It is available as 500 mg in 20 mL vials. Pralidoxime hydrochloride reactivates cholinesterase enzyme at the neuromuscular junctions by removing the phosphate group bound to the cholinesterase. It also binds to free organophosphate. The toxic effects of pralidoxime include tachycardia, cardiac arrhythmias, tachypnea, hypertension and relaxation of sphincters. The commercial preparation is 2 pyridine aldoxime (“aldopam”). Pralidoxime methane sulphate is also available.

In addition to pralidoxime, atropine has to be continued for symptomatic therapy in the required doses till the enzyme levels reach normal.

A high dose regimen of pralidoxime consisting of a continuous infusion of 1g/h for 48 hours after a 2 g loading dose reduces morbidity and mortality in moderally severe cases of acute organophosphorus pesticide toxicity. This reduces the need for atropine, as well as duration of ventilatory support.

Complications

Fatal bronchopneumonia may develop during convalescence. The neurological complications may take the form of intermediate syndrome occurring within 1-4 days of poisoning, characterized by bulbar, nuchal and proximal muscle weakness including respiratory paralysis or a distal sensorimotor polyneuropathy occurring 2-3 weeks later. The onset of intermediate syndrome usually coincides with the time of atropine withdrawal. Therefore oximes and atropine should be withdrawn carefully and gradually.

Prevention and first aid

Accidental poisoning can be prevented by taking adequate precautions detailed on the commercial packing. Persons spraying insecticides should wear protective clothing and masks, and wash their bodies with soap and water thoroughly after the work, and before taking food or drink. Immediate first aid after accidental poisoning includes induction of emesis and removal of contaminated clothing and washing the body thoroughly with soap and water. The subject should be transported to a hospital without delay.

OBESITY – TREATMENT (Dietary Regulation and Drugs)

TREATMENT OF OBESITY

Dietary Regulation

Strong motivation of the patient is absolutely essential for successful management. Dietary regulation is the basis of modern therapy. Calorie intake should be reduced below the basal requirements and the patient has to be kept on negative energy balance over prolonged periods of time. The excess fat is catabolized and weight is lost.

The therapeutic diet should contain 500-1000 Cals less than the energy expenditure of the individual. An ideal weight reducing diet should be:

1. Deficient in calories

2. Otherwise nutritionally adequate, and

3. Acceptable socio-culturally.

4. The diet should be suitably timed to avoid long intervals between eating.

Since dietary fats account for the palatability of food and they provide the maximum amount of calories the first step should be to cut fat intake to the maximum. This is the most effective single step to bring down weight rapidly in the initial stages. Young and tall subjects lose weight more efficiently than older and shorter people. On an average, daily intake has to be limited to 800-1000 calories. More drastic cuts on foods are frequently resented and result in non-compliance. For optimal results the diet should be acceptable, sufficient in volume and conforming to the general eating habits of the individual.

Bulk is provided by adding moderate amounts of fresh vegetables (not curried) and low-calorie fruits. Vegetables when made into curries with coconut, oil, dhal and condiments become very rich in calories. Clear instructions on the exact quantity of food and its timing are very essential. Regular follow-up is necessary for proper motivation and assessment. Patients put on the subcalorie diets lose weight steadily after an initial latent period ranging from days to weeks. It is ideal to reduce the weight by 1 kg a week. Vitamin and mineral supplementation is advisable, since the restricted diet may fail to meet these requirements.

Obese persons do not generally comply with diets. The low caloric diet should be maintained indefinitely since the tendency to regain weight persists. Strong motivation of the patient is needed to achieve good results. Initial motivation to reduce weight may be easy, but persistent efforts to maintain the ideal weight are generally slackened and so a major proportion of patients regain their weight and may even overshoot the original levels. Even moderate reduction in weight such as 6-10% of the body weight is accompanied by reduction in metabolic risks and blood pressure.

Exercise Moderate exercise augments the beneficial effect of dieting. Walking slowly up to 4-5 km, day, swimming, or games are ideal, depending upon individual preferences. Prescription of the exercise regime should take into account the cardiovascular status and exercise tolerance of the patient. Preferably it should be supervised by trained staff.

Drugs

Several drugs are available which reduce appetite. These anorectic drugs have been employed on short-term basis when the patient is not able to resist the desire to eat. Drugs may be needed when the BMI exceeds 30. Sympathomimetic drugs with amphetamine-like action reduce appetite and increase energy expenditure. These are contraindicated in persons with cardiovascular disease. Serotonin reuptake inhibitors are good appetite suppressants. Fenfluramine and fenoxetine can be given on a shortterm basis over weeks to a few months. When given over prolonged periods they may lead to the development of primary pulmonary hypertension. Acquired defects of the mitral and aortic valves may also develop. Dose Fenfluramine 20-120 mg twice a day given orally one hour before meals. Since these drugs cause dependence, they should preferably be withdrawn after 3 months of administration. Side effects include dryness of the mouth, abdominal pain, drowsiness, alopecia, mental depression, confusion and impotence. These drugs are contraindicated in patients with psychiatric illness.

Sibutramine is an appetite suppressant which can be given in doses of 5-15 mg once a day. It produces loss of weight by reducing appetite and increasing energy expenditure. Side effects include dryness of mouth insomnia and constipation. Sibutramine should not be given to patients with ischemic heart disease heart failure, arrhythmia and stroke. Sibutramine leads to a mean weight loss of 4-5 kg.

Orlistat: It is a lipase inhibitor which prevents absorption of dietary fat. The dose is 120 mg t.i.d. Side effects include flatulence, fecal urgency, and malabsorption of fat soluble vitamins. Orlistat leads to a mean weight loss of 3 kg.

Rimonabant is an endocannabinoid receptor antagonist. The dose is 20 mg given orally daily. It reduces body weight on an average of 4-5 kg. It improves the metabolic syndrome as well. Adverse effects include nausea dizziness, diarrhea and depression. When obesity is extreme and rapid weight reduction is desired, more drastic measures are employed. These include total starvation programmes and surgical procedures.

Total starvation

This can be undertaken under strict medical supervision for 2-3 weeks. Only water, salts and vitamins are allowed during this period. Complications include starvation ketosis, ventricular arrhythmias and sudden death. Due to these risks, total starvation should be undertaken only under exceptional circumstances. Wiring of the jaw to prevent ingestion of solid foods has been practised on persons unable to undertake starvation. Rapid weight loss is achieved by total starvation. Follow-up treatment consists of sub-caloric feeding.

Surgical measures

Surgical measures done to produce short-circuiting of digestive and absorptive portions of the intestines may be required for severe cases. The procedures include jejuno-ileal bypass and gastric bypass. Gastric plication may be done with a view to reduce the capacity of the stomach. Extirpation of excessive fat and plastic surgical procedures to remove redundant skin folds remaining after achieving weight loss help to correct cosmetic disability and also to augment the effects of dietary treatment. Liposuction is a surgical technique which removes large amounts of fat from localized areas such as the abdomen, gluteal regions, breasts, arms and face. This procedure is gaining popularity, being safe and cosmetically rewarding. The surgical management of obesity, as a part of cosmetic surgery is known as bariatric surgery.

In general, loss of weight up to 5-10 kg is easy but further reduction and maintenance of the optimal weight demand great motivation on the part of the patient and skill on the part of the physician. Once the optimum weight is reached, the patient should slowly increase the diet to prevent further weight loss, and try to adhere to the optimum weight. Even an occasional dietary excess results in rapid weight gain. All the complications of obesity can be arrested and may even regress if normal weight is maintained for long periods. Secondary obesity should be treated by adopting dietary measures and giving due attention to the primary cause.