Prolonged Fever in children-Treatment and Details

The prolonged fever in children is a difficult diagnostic problem requiring astute clinical judgment and skill. Some causes of prolonged fever in children are enumerated below to help in the discussion of clinical approaches in differential diagnosis.

Common causes of the prolonged fever.
Relatively common causes
1.   Infections.
2.   Diseases of hypersensitization e.g., rheumatoid arthritis and systemic lupus erythematosus
3.   Neoplastic disorders e.g., lymphoma, Hodgkin disease, leukemia.
Less common causes
1.   Immune deficiency disorders.
2.   Hematologic disorders e.g., spherocytosis, agranulocytosis.
3.   Neurologic  disorders   e.g.,  familial  dysautonomia, hypothalamic and third ventricle lesions.
4.   Genetic disorders e.g., anhidrotic ectodermal dysplasia.
5.   Miscellaneous causes e.g., drug fever, periodic fever.
Infections

In all cases of prolonged fever, infections especially those which are epidemiologically more relevant must be considered in differential diagnosis. Pulmonary or extra pulmonary tuberculosis, typhoid and paratyphoid fevers, malaria and Kala azar; amoebic hepatitis and amebic liver abscess; and subacute bacterial endocarditis should always be excluded by “appropriate clinical, laboratory and radiological evaluation.
Liver, urinary tract, pelvic viscera, ovaries, retroperitoneum, lungs, pleural cavity, mechastinum, subdiaphragmatic region, bones, and brain should always be considered as possibiliites of chronic pyogenic infections. Rickettsial infections (e.g., typhus, psittacosis, Q fever); brucellosis; leptolpirosis and relapsing fever are rare but should be considered in differential diagnosis if epidemiologically relevant. Infectious mononucleosis is common in the subtropical and temperate zones. Nosocomial infections with unusual organisms e.g., anaerobic bacilli should be considered in differential diagnosis of patient who had received various antibiotics especially aminoglycosides for several days in the hospital.
The onset, type and character of fever and the course of illness should be evaluated clinically to arrive at the possible diagnosis. Appropriate laboratory investigations such as total leucocyte count, differential leucocyte count; blood smear examination for malaria and filaria (night blood); serological test for typhoid, brucellosis, leishmaniasis, toxoplasmosis, amebiasis; bacteriological culture of blood for salmonella and brucella should be undertaken. Erythrocyte sedimentation rate is non-specific and is elevated in several inflammatory disorders.
Diseases of hypersensitization (Collagen vascular disorders)
(i) Rheumatic fever in childhood may occur without arthritis or arthralgia. The diagnosis of rheumatic fever should never be considered unless there is evidence of recent streptococcal infection prior to illness with  elevated titer of ASLO and acute phase reactants.
(ii) Rheumatoid disease. History of prolonged hectic fever without localizing signs, continuing for weeks, without the evidence of arthritis is not unusual in the early phase of rheumatoid arthritis. Erythrocyte sedimentation rate is elevated and there may be leucocytosis with high neutrophil count. A careful history and physical examination may reveal history of evanescent maculopapular rashes, which should arouse suspicion of a collagen vascular disorder.
(iii) Systemic lupus erythematous.
Leukemia and other malignancies
(Refer chapter on malignancies)
THE MANAGEMENT OF FEVERS
1. Evaluate the medical history, physical examination and laboratory investigations to develop a working diagnosis for the etiology of fever.

2.   Specific treatment of the infections, if present, should be undertaken.
3.   The general treatment of pyrexia is symptomatic and supportive.
(a)   Most children appear quite comfortable until their temperature reaches 38.5°C, and therefore no antipyretic measures are indicated in children with temperature below 38.5°C.
(b)   If the temperature exceeds 38.5°C, drugs such as acetaminophen (paracetamol) may be used in, a small dose at more frequent intervals, just to lower the temperature to around 38°C.
(c)   Environment. The child’s environment should be cool and airy.
(d)   The clothing should be loose and absorbent.
(e)   The body should be massaged gently so that the cutaneous vessels dilate and body heat is dissipated.
(f) Hydrotherapy. An absorbent towel should be soaked in cold water, rinsed and placed on the legs, trunk and forehead in order to reduce the body temperature. Hydrotherapy should be continued till the body temperature comes down to 38°C.
(g)   A close watch should be kept on the vital signs.
4.   Hyperpyrexia. When the temperature exceeds 41°C the body of the child below the neck should be immersed in the cold water without further delay to prevent irreversible brain damage. The parents should be reassured that this seemingly drastic measures will not induce shock. Ice cold bath does not cause significant vaso constriction. The rectal temperature should be recorded continuously and the hydrotherapy should be discontinued as the temperature falls below 38°C.
While hydrotherapy is being given, a lytic cocktail consisting of very small doses of chlorpromazine, promethazine and pethidine may be given intravenously at intervals of 30 minutes to reduce shivering and rebound rise of temperature after hydrotherapy.
5.   Hydration. Dehydration should be treated by intravenous administration of fluids.
6.   Other supportive measures for associated complications should be adopted. Patient with unexplained bleeding should be investigated for disseminated intravascular coagulation. In these cases fibrinogen degradation products in the serum are elevated, prothrombin time is increased and platelets are reduced. Such patients are treated with fresh blood transfusion if the bleeding is significant.

What is Enuresis in Children,Enuresis Prevention

The children with nocturnal enuresis usually sleep very deeply at night and it may be difficult to arouse them. The signals from the digtended bladder indicating the need to empty the bladder do not reach the conscious level of their mind during sleep and this may cause involuntary emptying of the bladder.
Management. Organic causes such as juvenile diabetes mellitus, anomalies of the urinary tract, nephropathies and neurological illnesses should be excluded by suitable physical examination and investigations. Since the condition is generally harmless and self-limiting, the child and parents should be reassured. About 15 percent of children between the ages of 5 and 10 years are known to be enuretic. About 1 percent of normal children may continue to wet the bed till the age of 15 years. Every attempt should therefore, be made to minimize the emotional impact of enuresis on the child. The sympathetic over activity, which is associated with emotional disturbances and fear aggravate the condition. The parents are advised not to nag, criticize or reprimand the child for wetting the bed at night. The bed sheet, should be quietly changed next morning, without making the child conscious of it. The child should refrain from taking beverages such as tea, milk or sherbet after 5 o’clock in the evening. He should be habitually made to pass urine before retiring to bed. The parents should arouse him fully again after two or three hours of sleep and persuade him to walk unaided to the toilet to empty his bladder.
The bladder should be trained to retain urine for a longer time. This may be done by making the child drink large quantity of water during the day and persuading him to delay emptying of the bladder as long as possible.

Different Fevers in Childhood

Fever is a common problem in clinical practice. Most fevers are self-limiting and the illness usually lasts for less than two weeks. If there is no lead in the medical history or when there are no significant localizing signs, fevers pose a difficult diagnostic challenge.

SHORT DURATION FEVERS

Most cases of short duration fevers (less than(2 weeks}) are attributed to infections due to viruses, bacteria, or protozoa.Many of these patients recover completely even before a precise diagnosis is made or treatment is given.
Malaise, headache, nausea, vomiting and impaired appetite are non-specific symptoms. These are associated with most infective fevers in childhood and therefore are not helpful in arriving at definitive diagnosis. Diagnostic aspects of some common infections causing short fevers are considered below.
1.Respiratory system: Common cold, pharyngitis, acute otitis media, mastoiditis and pneumonia are the usual acute respiratory illnesses. These are often viral in etiology. Ordinarily, in viral infections a number ofmucosal surfaces are involved simultaneously or in quick succession. In bacterial infections, The inflammatory process is usually localized. Regional lymph nodes are involved. The rate of spread of infection is slower. The throat should always be examined to exclude follicular tonsillitis and diphtheria (suspected if the fever is moderate and the patient appears toxic). The otoscopic examination of the tympanic membrane is an essential part of examination in children with fever. In cases of acute otitis media, the drum membrane appears dull red and the cone of light disappears. The drum membrane may bulge slightly.
Flaring of the alae nasi and working of accessory muscles of respiration indicate pneumonia.

2.Urinary tract infections: Infections of urinary tract are equally common in infancy among both sexes. After infancy, girls are more vulnerable to suffer from urinary tract infections. Symptoms and signs referable to urinary tract may be minimal or absent. The fever may be hectic and intermittent, at times associated with chills. Some patients may present with fever, vomiting, diarrhea abdominal pain. This may mislead the physician to focus attention on the gastrointestinal system. Urinalysis must be carried out for the diagnosis of unexplained short fevers especially in girls.

3.Exanthematous disorders: Careful search should be made for exanthem or enanthem in all cases of fever. Sudaminal rash (often described by parents of the patients in North India as moti-jhera) should not be confused with true enanthems. Sudamen is a non-inflammatory eruption from sweat glands. It appears as pearly white vesicles caused by retention of sweat in the corneous layer of skin. These appear after profuse sweating or in certain febrile disease. Sudamens disappear by absorption in a few days. Sudaminal rash is not diagnostic.

4. Meningitis: Marked irritability and photo phobia  with headache and persistent vomiting should arouse the suspicion of meningitis. The patient may show neck rigidity, positive Kernig’s sign, neurological deficits,convulsions, apathy, stupor or coma. The diagnosis should be confirmed by himbajjjuncture and examination of the cerebrospinal fluid.
Meningitis and septicemia in the first 4-6 months of life usually have an atypical presentation.

5. Pyogenic infections: A meticulous search should be made for the foci of infections in the liver, perinephric and subdiaphragmatic regions,bones and joints. Long bones should be palpated for tenderness over metaphyses. X-ray films of bones should be obtained on suspicion  of acute osteomylitis .radiological manifestations such as raising of periosteum may not be apparent for several days after the onset of illness.
6. Malaria: With the resurgence of malaria in most developing countries of Asia, Africa and South America, it should always be considered in differential diagnosis. Although fever in malaria is classically intermittent and relapsing,, it may present in an atypical manner especially in children in endemic areas.
7.Typhoid fever: Typhoid fever is endemic in most tropical and subtropical countries, with poor standards of sanitation and personal hygiene. Exanthems of typhoid fever (rose spots) are usually evanescent and may be missed in dark skinned individuals. Classical step ladder pattern onset, with sustained character of temperature are not always present. Most patients have distended tympanitic abdomen.
Other causes of short duration fever. JTeat hyperpyrexia, . dehydration jgver,   allergy   to   drug   (drug   fever), thromboembolic phenomena and hemolytic crisis are other less common causes of short fevers.
8. Heat hyperpyrexia: Heat hyperpyrexia is not an unusual cause of fever in tropical countries where ambient temperature may go as high as 45°C. Heat hyperpyrexia may occur even without exposure of the child to the direct sunlight. The predisposing factors include high temperature and humidity  in the  environment,  unsuitable clothing,dehydration and debilitating illness, such as malaria, pneumonia, measles and renal disorders. Invariably, heat hyperpyrexia is associated with cessation of sweating. Children with ectodermal dysplasia and absence of sweat glands are more prone to develop episodes of heat Tvyperpyrexia.
The onset of high fever may be quite sudden. The rectal temperature may exceed 42°C to 43°C. The skin appears hot and dry (without sweating). Tachycardia and tachypnea are present. The loss of consciousness occurs early. The patient may develop peripheral circulatory failure and hemorrhages. Headache, faintness, abdominal discomfort and delirium are usually complained of. The liver and kidney failure may complicate heat hyperpyrexia?
Fever in young infants below 3 months of age.

Fever in young infants may be trivial, self limited due to a viral illness or may be due to severe bacterial sepsis. Young infants are potentially immuno compromised and thus more predisposed to invasive bacteremia. It is difficult to accurately assess them neurologically because of neurologic immaturity.
Infants with diminished spontaneous activity, lethargy, respiratory compromise (tachypnea, retraction and grunting), diminished muscle tone, mottled cool extremities, irritability, weak sucking are at high risk. They must be evaluated for sepsis by complete blood count, lumbar puncture, blood culture, and chest radiograph. Apart from pneumococcus, Hemophilus influenzae, enterococci and Neisseria meningitidis, group B streptococcal infections are a major cause of bacterial infections at this age period.

Child’s Pre school Bad habits and their Solutions|Pica Disorder

Head banging or rocking in bed
A toddler who is fatigued or is under stress may bang his head against the bed or rock it in rhythmic movements. Apparently this gives him a pleasurable diversion. In these cases, the bed should be padded to prevent injury.
Thumb-sucking and nail-biting
Thumb-sucking or nail-biting also indicate that a pleasurable sensation is derived by the child from this self-stimulation. These are manifestations of a feeling of insecurity. Thumb-sucking has little effect on the dental alignment. The parents should be advised not to show excessive anxiety about thumb-shucking until at least the child is 4 years old.
Masturbation
The child may obtain pleasure by genital stimulation, rubbing of thighs against each other or by rhythmic swaying movement. Mother’s anxiety should be allayed as this is generally harmless. In severe cases psychiatric treatment may be necessary.
Unclear speech
Clarity of speech normally improves gradually during the first few years of life. It becomes completely intelligible by 4 years of age. Unclear speech often signifies that child may have a major disorder of language, cognitive development or hearing. Such children may develop language based learning disabilities later in school years.
Stuttering
Stuttering is a defect in speech characterized by hesitation or stumbling and spasmodic repetition of some syllables with pauses. There is difficulty in pronouncing the initial consonants and it is caused by the spasm of lingual and palatal muscles.
Most children show some degree of repetition and hesitation in their speech at some period of early life. However, there are individual variations in the extent of such difficulties with speech. Whereas some children can speak very fluently, others are severely handicapped. It is probable that the children who cannot cope with the environmental and emotional stresses are more likely to stutter. Stuttering usually begins between the ages of 2 and 5 years, a period in which there is non-fluency of speech. The parents and playmates, who remind the child of his stumbling speech or ridicule him, aggravate his emotional stress. As a result of this, he loses his self-confidence and becomes more and more hesitant in speech. The stress caused by conflict between the parental expectations and the child’s achievements may precipitate stuttering in some children.

PICA DISORDER

The child may develop habit of eating non-edible substances such as wall plaster, clay, paint and earth, etc. Pica is a disorder seen in children.Children with pica usually have a history of neonatal insults. They are slow in motor and mental development and show more neurologic defects and deviant behavior. Tasting or mouthing of strange objects is normal in infant and children up to age of 2 years. Persistence of this habit beyond the age of 2 years may be a manifestation of parental neglect, poor supervision or lack of affection. It is commoner in children from lower socioeconomic strata and at times in the malnourished and mentally subnormal children. These children are prone to lead poisoning and often complain of chronic abdominal pain and pallor. There is no specific treatment. Iron is often prescribed, without any definite evidence of benefit.

Sleep Disturbances

The child may suddenly awaken after a frightening nightmare. Manifestation may include fear of the dark, difficulty in falling asleep, night walking (somnambulism), sleep talking or night terror.

Thalassemia Minor Causes,Symptoms and Treatment

Thalassemia Minor is the mildest form of the illness. The individuals may be heterozygous and inheriting only one mutant or p-thal gene, which limits the synthesis of beta-peptide chains. Or they may have inherited a genetically distinct abnormality of p-globin chain which produces a milder disease. The gene for alpha chain synthesis is normal. There is usually compensatory increase in delta chain synthesis, leading to levels of Hb A2 being higher than normal. Hemoglobin A2 may be markedly reduced with co-existing iron-deficiency anemia.
Increase in the level of hemoglobin F is inconstant. Production of hemoglobin A is only slightly reduced.
Thalassemia Minor patients have only a very mild anemia, sometimes with abdominal pain and mild icteric, tinge. Thalassemia minor is often confused with iron deficiency anemia and is treated as such, till the correct diagnosis is suspected. Serum iron concentration is on the higher side and iron binding capacity is reduced. Free erythrocyte porphyrin is normal in thalassemia minor (30 microgram/dL of whole blood). This is moderately raised in iron deficiency anemia (30 to 190 ug/ dL of whole blood). This is a useful diagnostic test to differentiate iron deficiency states from thalassemia minor and lead poisoning.
ALPHA-THALASSEMIA-HEMOGLOBIN H DISEASE
The synthesis of alpha-peptide chains is suppressed. Defective alpha chain synthesis effects the production of all the normal hemoglobin viz., A, A2 and F. Four beta-peptide chains polymerise to a tetrameric form giving rise to hemoglobin H. Heterozygous alpha thalassemia is usually very mild and is often not associated with any regular alteration in the hemoglobin pattern in the adult life.
There are possibly two alleles for alpha-thalassemia gene viz., alpha-thalassemia1 causing complete inhibition of alpha chain synthesis and alpha-thai2 causing only impaired synthesis of alpha chains.
Alpha-thalassemia is most prevalent in the countries of South East Asia. The infant is usually normal at birth.

TREATMENT OF THALASSEMIA
Blood transfusion

The mainstay of managing these cases is repeated blood transfusions. An attempt should be made to maintain hemoglobin level above 10-12 g/dL (by hyper transfusion) to ensure active life and adequate growth. Group and type specific, fresh, triple saline washed, packed red cell transfusions are the most desired form of component therapy. These are to be transfused at the rate of 10-15 ml/kg every 2 to 3 weeks. Blood transfusions may result in hemolytic or febrile reactions, transmission of viral infections (HIV1 & 2, Hepatitis B and C, Cytomegalovirus) and iron overload. Routine donor screening for these viral infections is a must. All thalassemics should be vaccinated with Hepatitis B vaccine before starting transfusions. Iron overload results in multiple organ dysfunction due to hemosiderosis and hemochromatosis. Chronic anemia itself is a potent stimulator of iron absorption from the gut. Iron overload can be reduced by regular chelation therapy and reducing iron absorption by keeping the hemoglobin levels high.
Neocyte transfusion

Special cell separators are available for obtaining younger cells with longer life span (neocytes). Infusion of these cells instead of the whole blood increases interval between two transfusions and decreases the transfusion requirement and hence the iron load. Simultaneous removal of older cells (gerocytes) from patient’s circulation by pheresis technique reduces iron load considerably. However, these procedurs are cumbersome, costly and need a lot of expertise.
Chelation therapy

At present only desferrioxamine is available as iron chelating agent in parenteral form. It should be given as continuous subcutaneous infusion in the dose of 25-50 mg/kg/day over a period of 8-12 hours, during the night, by specially designed microinfusion pumps, (at least 5-6 nights per week). The chelation should start by 12-14th transfusion. 100 mg of vitamin C daily should be concurrently administered. Overdose of desferrioxamine results in growth retardation, visual and auditory toxicity. Cataracts have been noted in some children on long term desferrioxamine therapy. Deferiprone (DFP) is an effective oral iron chelating agent with minimal toxicity. It is given in a dose of 75 mg/kg/day in 2-4 divided doses. The most common side-effect is arthropathy. Other oral chelators include pyridoxine hydrazine, HBED and desferrothiocine. These are still under trials.

Splenectomy

Splenectomy is recommended in cases when the transfusion requirement exceeds 250 ml/kg/year of packed red cells. The decision should be deferred as far as possible and if required delayed beyond the age of five years.

Eye disorders in Children

Problems of Conjunctiva

Conjunctiva is best examined with a torch. Note the color. Look for any edema (chemosis), hemorrhages, pigmentation. It may also occur in scurvy, thrombocytopenia, injury or even in malaria.

Chemosis. Edema of conjunctiva may be due to orbital cellulitis, nephritis, urticaria, angioneurotic edema or cavernous sinus thrombosis.

Pigmentation. Vitamin A deficiency causes conjunctival xerosis (manifesting as dryness and wrinkling) and triangular white dry patches on the outer and inner sides of the cornea (Bitot’s spots). Wedge shaped brownish lesions are seen in chronic non-neuronopathic form of Gaucher’s disease while Pingueculae (whitish yellow elevated lesion on bulbar conjunctiva) are characteristic of the adult type of the disease.

Deposits. Deposits of cystine crystals in the conjunctiva are seen in the infantile variety of cystinosis. Surface nodules over conjunctiva may be seen in tuberculosis, leprosy and syphilis. Conjunctival neurofibromas are found in neurofibromatosis.

Inflammation (conjunctivitis)

Conjunctivitis may be observed as a part of generalized viral (measles, adenovirus) or bacterial (membranous conjunctivitis of diphtheria) infections. It may at times be an allergic manifestation such as (i) endogenous i.e., phlyctenular conjunctivitis of tuberculosis and streptococcal infection and (ii) exogenous i.e., vernal (allergic) conjunctivitis associated with eosinophilia. Conjunctivitis may be a component of Reiter’s disease (arthritis, urethritis, conjunctivitis). Pseudomembranous conjunctivitis occurs characteristically in Steven-Johnson syndrome.

Problems of Cornea

Cornea should be examined with a focussed light and not a diffuse one (such as a pen torch). Measure the size. Cornea has a diameter of 10 mm at birth and achieves the adult size of 12 mm by the end of second year of life. Corneal diameter of more than 13 mm is known as megalocornea. It is observed in Marfan’s syndrome and osteogenesis imperfecta.

Note down any corneal haze, opacities, pigmentations, scarring or ulceration. Kayser Fleischer rings, colored gray green or golden brown are located round the periphery of cornea in Wilson’s disease.

Conical cornea (keratoconus) in which cornea is thin near the center and progressively bulges forwards is a feature ©f Down’s syndrome, Marfan’s syndrome and osteogenesis imperfecta.

Opacities and pigmentation

Haze. Corneal haze at birth or early infancy may be due to congenital anomalies, birth injury or metabolic disorders including mucopolysaccharidosis, glycogen storage disease and lipidosis. Full fledged opacities are observed in mucopolysaccharidosis and glycogen storage disease.

This type of keratitis may also develop in Riley-Day syndrome.

Phlyctenular keratitis. Corneal phlycten may be a manifestation of an allergic reaction to tubercular protein. In phlycten, a leash of capillaries is seen leading from the scleral conjunctiva towards the limbus or over the cornea.

Interstitial keratitis. Congenital syphilis causes inflammation of corneal stroma producing interstitial keratitis. Corneal opacities develop and generally remain as permanent stigmata of the disease. Interstitial keratitis may also follow lesions due to tuberculosis or leprosy.

Problems of Scleria

Color
Sclera becomes yellow in jaundice. Blue sclera is observed in Marfan’s syndrome, osteogenesis imperfecta and cutis hyperelastica. Blackish discoloration of sclera is due to accumulation of homogentisic acid in alcaptonuria (ochronosis).
Look for any infection. Superficial infection (episcleritis) presents as raised congested nodules at the sclera around the cornea while deep infection (scleritis) is characterized by dusky ciliary congestion and opacification of cornea at the periphery.
Episcleritis occurs as an allergic reaction to tuberculosis or streptococcal infection. Scleritis is associated with connective tissue disorders such as polyarteritis nodosa, SLE and rheumatoid arthritis.

Disorders of Eye in Childhood

Diseases of the eye should not be considered in isolation from the rest of the body as the eye can be involved in a variety of systemic disorders. Ocular symptoms in children may often be the first clue to systemic disorder. Many neurological, developmental, metabolic, allergic, infective, collagen, vascular and deficiency disorders can be diagnosed with careful examination of eyes. Though the management of eye problems is the domain of the ophthalmologist, it is necessary for a pediatrician to conduct examination of the eye with a torch and an ophthalmoscope for proper diagnosis and management of the child as a whole.

The following account describes in brief the principles of ocular examination in a child. It is followed by description of those manifestations of the eye which are associations, reflections or extension of a systemic disease.

Disorders of Orbit

Look for abnormal protrusion of the eyeball (proptosis), retraction of the eye back into its orbit (enophthalmos), wide separation of the eyes (hypertelorism) and small palpebral fissures (microphthalmos). Palpate for any bony defects or swellings.

In a proptosed eye, a rim of sclera can be seen between lower limbus and lower eyelid and the amount of exposed sclera indicates the degree of proptosis.

Proptosis may occur due to diminished orbital volume as in craniostenosis or increase in the orbital tissue mass such as with malignant deposits, cavernous sinus thrombosis, orbital hemorrhage and cellulitis. Proptosis caused by thyrotoxicosis is multifactorial.

Enophthalmos occurs as a feature of Horner’s syndrome which is associated with ptosis, absent ciliospinal reflex, anhidrosis and miosis. It is caused by lesion of lower cervical and upper thoracic sympathetic nerve fibers, which supply the eyes.

Hypertelorism can be determined by calculating :

Inner-canthal distance

Canthal index =—————————-x 100

Outer canthal distance

which is normally 38 in males and 38.5 in females (SD ± 2.4). This index is increased in hypertelorism.

Microphthalmos and hypertelorism are frequently encountered in Down’s syndrome and intrauterine infections (CMV, rubella and toxoplasmosis).

Disorders of Eyelids

Keep one hand firmly on the forehead to prevent action of the frontalis muscle and ask the patient to lift the upper eyelid. Normally the upper eyelid should cover about 2 mm of cornea below the upper limbus. Drooping of upper eyelid below this level is known as ptosis. An upper lid that rests above the upper limbus is referred to as lid retraction. Inability to completely close the palpebral fissure (lagophthalmos) should also be looked for. Inspect for any lid inflammation (blepharitis), vascular anomalies (nevus or telangiectasias) and swelling of lid. Notice the placement of the palpebral fissure. It is oblique, short and wide with the highest point at the centre of the lid in Down’s syndrome (mongoloid slant). Also note any skinfolds above the inner canthus (epicanthic folds) which are characteristic of many chromosomal disorders.

Ptosis may be congenital or acquired due to hemangioma (Sturge-Weber syndrome), plexiform neuroma (neurofibromatosis), myasthenia gravis, Horner’s syndrome, lesions affecting the third nerve, lid tumors and following drugs such as vincristine.

Lagophthalmos and Lid retraction may occur as part of thyrotoxicosis.

Disorders of Lacrimal System

Conjunctival irritation of one eye only or watering are clues to lacrimal involvement. Look for any signs of inflammation and production of tears. The lacrimal gland is undeveloped at birth and tears are produced only after first month of life. Non canalization of lacrimal passages lead to apparent increase in tears (epiphora).

Acute and bilateral inflammation of lacrimal gland (dacryoadenitis) occurs with influenza, mumps and infectious mononucleosis. Chronic dacryoadenitis is associated with syphilis, tuberculosis and sarcoidosis.

Alacrima (Dry eye) occurs in Riley-Day syndrome and ectodermal dysplasia. Deficiency of conjunctival mucus following Steven-Johnson syndrome is another cause of alacrima. Formation of tears is reduced in dehydration.

How to manage bronchial asthma in children

Avoidance of exposure to allergens and non-specific irritants

1.  The bedroom of the child should be kept clean and as free from dust as possible. Wet mopping of the floor should be done because dry dusting increases exposure of the child to house dust.

2.  Heavy tapestry attracts dust and therefore light plain cloth sheets should be used as curtains in the child’s room.

3.   Carpets, stuffed furniture, loose clothing, wall hangings, calendars and books attract lot of dust and should be regularly cleaned at periodic intervals.

4.  The bed of the child should be made of light material and should be aired regularly.

5.   Caressing of animal pets should be discouraged, as the child may be sensitive to their fur.

6.  Generally, it is not necessary to restrict the diet of the child because bronchial asthma due to food allergy is unusual.

7.  Adolescent patients should be advised to refrain from smoking.

8.  Exposure to strong or pungent odors such as wet paint, disinfectants and smoke should be minimized.

9.   The child should not go to attics or basements, especially if these were unoccupied and kept closed for some days.

How to remove poison from child’s body

1. Copious irrigation of the external surface of the body should be done to remove the poisons like insecticides which can be absorbed from the skin.

2. Emesis. Many poisons induce vomiting and are largely eliminated. If vomiting has not occurred spontaneously, it should be induced unless contraindicated as in corrosive or kerosene poisoning and in comatose patients.

In children this is best done by having them drink a glass of water or milk. They should then be gagged by stroking the posterior pharynx with the finger or a blunt object. To prevent aspiration in small children, the head should be kept low. The use of warm saline and mustard is impracticable as children don’t take these and valuable time is lost in coaxing them. Syrup of ipecac is given in dose of 10-15 ml and is repeated in 15 to 30 minutes.

Apomorphine does not appear to be superior to syrup of ipecac.  Apomorphine causes respiratory depression:

3.  Gastric lavage. If the vomiting does not occur quickly, gastric lavage should be done promptly to remove the poison. Gastric lavage is contraindicated in corrosive poisoning. In kerosene poisoning, lavage may done very cautiously if the child has consumed a large gulp of kerosene and is brought quickly to the hospital. Otherwise it is better to avoid stomach wash. Technique of stomach wash is given below.

Size 8-12 F catheter is used. The distance between the tip of the nose and xiphisternum is measured and marked on the catheter. A restraint is required for most children and mouth gag is placed in the mouth before the procedure. The child is kept in the left lateral position with the head hanging over edge of the table and the face down. The catheter is immersed in cold water or ice to facilitate insertion through the nose or oral cavity. Oil is not used to lubricate the tip to prevent aspiration of oil. The catheter is passed gently and free end is dipped under water to make sure that the catheter is not in the airway. Generally tap water is used for lavage and four or five washes are done. Catheter is pinched before it is withdrawn or suction is maintained during withdrawal to prevent aspiration especially in kerosene poisoning. Kerosene has low surface tension and unlike water it spreads rapidly on the surface around and thus may easily be aspirated in the air passages.

4. Antidotes. The antidotes may be physiological, chemical or physical. Chemical antidotes combine with the poison and render it innocuous. Physiological antidotes counteract the effects of the poison on the metabolism and physiological functions of the body and thus prevent its harmful effects. Physical antidotes prevent the contact of the poisonous substance with the target organ or adsorb the toxic

When the nature of poison is not known, it is useful to administer a universal antidote which can be easily prepared as follows:

Activated charcoal 2 parts (adsorbs toxins).

Magnesium hydroxide 1 part (neutralises acids).

Tannic acid 1 part (precipitates alkaloids).

If these are not easily available, burnt toast, milk of magnesia and strong tea may be used as a substitute for the universal antidote.

Milk and egg white are used as demulcents especially when the offending substance is copper sulphate, croton oil or chlorate.

Promotion of excretion

1.  Laxative and purgative. May be given in poisoning with substances which do not cause corrosive action on gastrointestinal mucosa. Increased motility of the gut may reduce absorption. Do not give magnesium salt cathartics in cases with renal failure.

2.  Fluid intake. The fluid intake is increased to promote glomerular filtration and excretion of poison through the urine.

How to prevent child poisoning

1. Protection of the child from the poisonous substances.

The poisonous substances should be kept in secure places out of reach of the child. The poisonous substances should be replaced in their proper place. Potential household poisons should not be transferred to empty containers otherwise used for innocuous food or beverages. Drugs should be dispensed in the original container. The word poison should be exhibited prominently on the containers of potential poisonous substances. Kerosene oil and caustic soda should not be stored in tumblers or beverage bottles. The containers should not be left on the ground. Kerosene bottles and stoves should be kept out of reach of the children in the kitchen.

2.  Education of parents about the potential household poisons.

3.  Need for parental supervision of toddler’s behavior should be emphasized.

4. Safety regulations by the State should be enforced.

5.  Establishment of poison control centers to collect, compile and disseminate information on poisons and their management. These should promote research on prevention and treatment.