Category Archives: Pediatrics

Lack of motivation affects and effects children

For every growing child motivation plays a significant role in his development as an individual. Recent studies done by various universities show that lack of motivation prevent physical activities in children. This can be solved by conducting physical training program every day after school. According to the census very less number of students does exercise daily. Most of the children prefer playing play station and computer games.

Watching TV for long hours is also another young age hobby. These activities act as barriers to the physical development of boys. There are also environmental barriers. Lack of facilities such as playground in schools also affects the physical activities. Boys tend to be more active during this age. But the modern life and inadequate caring of parents to their children due to immense work are all degrading the physical and mental health of the children. Due to the above, children are becoming more obese these days. Fast food along with lack of exercise can lead to serious diseases. These diseases tend to appear only at an older age but we must understand that it comes as a result of the habits during the childhood. This age boys are more obese than girls. We, parents must take care of our children. So, how can we do this? We must spend more time with our children.

We must encourage them and allow them to entertain in activities like playing football or other outdoor games. Playing in door and video games must be reduced. Fast food must be minimized. Send your child to schools which give good importance to games and activities. Make walking as a habit. Try to walk at least 1km daily. Make sure that teachers also provide enough encouragement to your children. In this way you can develop your child physically and mentally.

Pediatrics

Depression Syndrome in children

Jaundice in Children-Different types and Symptoms

Jaundice means yellow discoloration of the skin, mucous membrane and sclera due to elevation of bilirubin level in the blood. Intensity of jaundice depends on the amount of free bilirubin circulating in the blood which can easily diffuse into the tissues. Jaundice should be distinguished from yellow coloration of the skin due to hypercarotenemia. In the latter condition sclera does not become yellow.


Regurgitant jaundice (conjugated hyperbilirubinemia)
1.  Hepatocellular jaundice.
(a)   Viral hepatitis A and B
(b)   Toxic injury to the liver-antibiotics, drugs, poisons.
(c)    Infestations: malaria, bilharzia.
(d)   Cirrhosis of the liver
(e)   Infections:  Infectious mononucleosis.
2.   Cholestatic jaundice.
(a)   Due to drug reaction to chlorpromazine, methyl testosterone, isoniazid and rifampicin.
(b)   Dubin Johnson syndrome (chronic benign conjugated hyperbilirubinemia with deposition of melanin like pigment in the liver; autosomal recessive inheritance, no mechanical obstruction of duct); Rotor syndrome (Like Dubin Johnson; no pigment in the liver).

Aemolytic jaundice
(a)   Hereditary spherocytosis.
(b)   Sickle cell anemia.
(c)   Thalassemia.
(d)   Drug induced hemolytic anemia in patients with G 6-PD deficiency.
(e)   Acute acquired hemolytic anemia.
Hepatocellular jaundice
Unconjugated bilirubin level in the blood is elevated due to impaired uptake, defective transport and diminished glucuronation of the bile by the damaged hepatic cell. Conjugated bilirubin level also rises due to the blockage of canaliculi by the thick bile and obstruction due to the inflammatory cells around the cholangioles. Altered permeability of the liver cells and rupture of the canaliculi also contribute to the elevation of the level of conjugated bilirubin.
Thus in hepatocellular jaundice, serum levels of both the conjugated and unconjugated bilirubin are elevated and bilirubin is excreted in the urine. The excretion of urobilinogen in the feces is reduced because less bile passes into the gut. A part of the urobilinogen (or stercobilinogen) is absorbed in the portal circulation but liver is unable to excrete it and therefore it is excreted mostly in the urine. As the illness becomes severe and the obstruction becomes almost complete, the bilirubin cannot be excreted into the gut. Consequently no urobilinogen is formed and absorbed from the gut. Therefore at this stage urobilinogen disappears from the urine in complete obstruction or at the peak of the disease process.

Cholestatic jaundice
Cholestatic jaundice occurs following drug reaction to chlorpromazine, methyl testosterone and isonicotinic acid hydrazide and rifampicin. The jaundice in Dubin Johnson and Rotor syndromes is also cholestatic. The defect is due to the functional disturbances in the transport of bilirubin across the liver cells.
Obstructive jaundice
Following obstruction of the bile duct, the conjugated bilirubin escapes into the circulation. This may be due to (1) rupture of the distended canaliculi into the hepatic sinusoids or lymph spaces, (2) through leaks in the canals of Hering which connect the bile canaliculi with the terminal bile ducts and (3) in the blood through the parenchymal cells. Later, hepatocellular damage may occur as a result of marked increase in the level of unconjugated bilirubin.
Complete obstruction of the extrahepatic biliary system is uncommon in children. Cholecystitis and gall bladder calculi rarely present in childhood. Partial intermittent obstruction due to cystic dilatation of a part or whole of the common bile duct may occur due to partial obstruction or neuromuscular incoordination of the ampulla of Vater.
Large cyst of the bile duct is called choledochal cyst.
Patient presents with a mass in the right upper quadrant of

Hepatomegaly-Liver enlargement- Symptoms ,Causes and different types

Palpability of liver does not always indicate enlargement.It only reflects the relation of the liver to adjacent structures.In normal children,liver is palpable 1 cm below the costal margin and in Infants it may be felt up to 2 cm below the rib margin.

Besides the size and shape of the liver, consistency and character of the surface and palpable margin should be evaluated for the assessment of hepatomegaly. Liver should be examined for tenderness and also auscultated for any murmurs. The upper border of the liver should be defined by percussion. Abdomen should be palpated for other masses or enlargement of the spleen.
Pathogenesis of liver enlargement. The liver may be enlarged due to any of the following causes:
(a) Inflammation
(b) Fatty infiltration
(c) Kupffer’s cell hyperplasia
(d) Congestion
(e) Cellular infiltration and
(f) Storage of metabolites

CAUSES OF LARGE LIVER

Newborn
Infections, (a) Intrauterine infection e.g., toxoplasmosis, cytomegalic inclusion disease, congenital syphilis., (b) septicemia, and (c) neonatal hepatitis including viral hepatitis.
Cellular infiltration. Erythroblastosis fetalis.
Hepatobiliary obstruction.   Biliary atresia.
Congestive cardiac failure.
Alpha-1-anti trypsin deficiency.
Infants and children
1.  Benign hypertrophy. Periportal round cell infiltration following viral infections of upper respiratory tract. The liver regresses in 6 to 8 weeks.
2.  Fatty infiltration. Kwashiorkor, Reye’s syndrome, tetracycline toxicity, tuberculosis, diabetes mellitus, cystic fibrosis and galactosemia.
3.   Inflammatory processes. (i) Intrauterine and intrapartum infection, (ii) hepatitis, (iii) infectious mononucleosis, (iv) parasitic infestations (visceral larva migrans, amebic hepatitis), (v) pyogenic or amebic abscess of liver, cholangitis (vi) toxins and (vii) drugs.
4.   Cellular infiltration. (i) Leukemia and lymphomas (ii) neoplasms-primary (hepatoblastoma, hemangioendothelioma), (iii) secondaries to Wilms’ tumor and neuroblastoma and (iv) histiocytosis (Letterer-Siwe disease).
5.   Storage disorders (Metabolic). (i) Glycogen storage disease, (ii) galactosemia, (iii) mucopolysaccharidoses, (iv) lipidosis (Gaucher, Niemann Pick, gangliosidosis M). (v) amyloidosis, (vi) alpha-1-anritrypsin deficiency, (vii) hepatic porphyria, (viii) cystinosis and (ix) hemosiderosis, Wilson disease, cystinosis and tyrosinosis.
6.    Congestion. (i) Congestive cardiac failure, (ii) pericarditis, (iii) Budd Chiari syndrome (thrombosis of hepatic vein) and (iv) veno-occlusive disease of the liver.
7.   Kupffer’s cell hyperplasia. Granulomatous hepatitis as in tuberculosis and sarcoidosis.
8.  Miscellaneous. Cirrhosis of liver—Indian Childhood cirrhosis, congenital cysts and hydatid cyst.

EVALUATION OF THE HEPATIC ENLARGEMENT

Assess if the liver is just palpable or is actually enlarged. Determine if the enlargement is due to organic causes and also the nature and severity of the illness responsible for it.
A good medical history, intelligent interpretation of the associated clinical manifestation and judicious use of laboratory investigations and ultrasonography are helpful in arriving at a correct diagnosis in most cases of hepatic enlargement. The following points may help in diagnosis.
Age of the patient. Age of onset of the illness limits the etiological possibilities.
Geographic factors. Indian childhood cirrhosis is common in children of Indian extraction. Thalassemia is more frequent in North West India, Bengal, Indochina, Sri Lanka and persons of Mediterranean extraction. Veno-occlusive disease is observed in Jamaica and West Indies. It has been recently reported from Afghanistan and some parts of central India.
Associated clinical manifestations which aid in diagnosis of hepatomegaly
Protein-energy malnutrition. There is fatty infiltration of the liver.
Jaundice. Intrauterine infections, septicemia, neonatal hepatitis, viral hepatitis, biliary atresia and Indian childhood cirrhosis in terminal stages present with jaundice.
Engorged neck veins and raised jugular venous pressure.

Constrictive Pericarditis
Skin rash. Histiocytosis.
Microcephaly or hydrocephaly. Intrauterine infections like toxoplasmosis and cytomegalic inclusion disease.
Eyes. Cataract and mental retardation with hepatosplenomegaly suggest galactosemia.
Presence of Kayser-Fleischer ring over the cornea indicates Wilson     disease.         Hazy     cornea     is     seen     in
Mucopolysaccharidosis type 1.
Neurological manifestations. Wilson disease may present with neurological manifestations.
Skeletal changes of rickets may be observed in cystinosis and tyrosinosis.
Mental retardation. Patients with galactosemia may show gross mental retardation.

Prolonged Fever in children-Treatment and Details

Prolonged fever among children is hard to diagnose ,some time only specialists can diagnose the problem.Some common reasons for prolonged fever are given below which may help its 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 especially , Hodgkin disease,lymphoma and leukemia.
Not that common cases
1.   Immune deficiency disorders.
2.   Hematologic disorders like agranulocytosis.
3.   Neurologic  disorders   e.g.,  familial  dysautonomia, hypothalamic and third ventricle lesions.
4.   Genetic disorders  like anhidrotic ectodermal dysplasia.

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.
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.