Abdominal Masses – IMAGING

Abdominal masses in a child are source of concern to the parent, as well as the paediatrician, and present a diagnostic challenge. A radiologist plays a pivotal role in the diagnostic workup. Enlarged organs constitute 57% of abdominal masses in the infants and children, but the main thrust of imaging studies in childhood abdominal masses is directed towards pathological masses other than diffuse organomegaly. In general, 90% of such abdominal masses in infants and children are retroperitoneal of pelvic and half of these are related to urinary tract.
Irrespective of anatomical location of the abdominal masses and age of the child, the plain film radiography forms the primary imaging modality. Dilated bowel loops, which may simulate a mass, can be easily detected on plain film. The underlying cause may also be evident either on the plain film itself or a directed contrast examination. Other findings on the plain film which may aid in the diagnosis of an abdominal mass are displacement of adjacent bowel loops due to a soft tissue density, presence of calcification and its nature, associated bony abnormalities like congenital defects, metastasis, or direct invasion by a tumour mass.
Abdominal sonography forms the next important imaging modality, speciality if a gastrointestinal origin is not suspected. Sonography helps differentiate retroperitoneal form intraperitoneal masses and solid from cystic masses. Further diagnostic work is based on the information, obtained at plain film and ultrasonography. However, a selective and caring approach is mandatory, in order to limit the radiation hazards and for cost effectiveness.
Intravenous urography was a routine and essential part of diagnostic armamentarium in the work-up of a child with abdominal masses until recent past. With the advent of cross-sectional imaging techniques, the use of IVU has become more judicious, being needed only when a mass in renal region is suspected at plain film and/or ultrasonography needs further evaluation. IVU provides information regarding the functional status of the kidneys, and the effect of the mass on its position, outline and pelvicalyceal system.
Computerized Tomography (CT) is an excellent cross-sectional imaging technique in abdominal masses due to the explicit anatomical details. It helps assess the exact size and extent of the mass, thereby allowing accurate staging, which is a prerequisite to a successful management in childhood malignancies. Involvement of major blood vessels by dynamic CT following intravenous contrast administration is an added advantage. However, it has limitation in children, in addition to the radiation involved, the relative paucity of fat in children may result in images which may be difficult to interpret.
MRI, especially with the advent of short scan time and open type magnets, is a very promising modality although long-term results are still awaited in imaging of paediatric abdominal masses. Use of angiography is now limited to providing a road map prior to surgery for the hepatic tumours or when a partial nephrectomy is being contemplated. Radioisotope scans have limited role. It may be diagnostic in haemangioendothelioma, choledochal cyst, biliary atresia and helps distinguishing between a UPJ obstruction and a congenital multi-cystic dysplastic kidney.
Abdominal masses can be divided into three major groups in paediatric age:
Retroperitoneal (which may be renal, or extrarenal), Hepatobiliary and Gastrointestinal. Retroperitoneal masses constitute the great majority of abdominal masses in children and most are renal in origin e.g., hydronephrotic kidney, multicystic dysplastic kidney, polycystic kidney, nephroblastoma, mesoblastic nephroma, renal vein thrombosis etc. Characteristic findings of some of the important and commonly met childhood masses are as follows:

Staging is done at CT
• Stage I – Tumour limited to kidney; capsule intact.
• Stage II – Tumour extends beyond the kidney into perineal soft tissues; vessels outside kidney substance infiltrated or contain tumour thrombus.
• Stage III – Non-haematogenous tumour confined to abdomen: (i) Lymph nodes in renal hilum, periaortic or beyond, (ii) implants on peritoneal surfaces.
• Stage IV – Haematogenous metastases e.g., lung, liver, bone and brain.
• Stage V – Bilateral renal involvement at diagnosis.
Retroperitoneal tumours of non-renal origin are neuroblastoma, teratoma, adrenal haemorrhage, etc.

Hepatobiliary masses constitute approx 6% of all childhood abdominal masses.

• Choledochal Cyst: About 40-60% present before 10 years of age. Most commonly present with obstructive jaundice. Can develop complications like stones in up to 70% cases, pancreatitis, rupture or neoplasia. USG is the imaging modality of choice. It shows focal dilatation of CBD with sparing of IHBR.
CT helps to differentiate from intrahepatic cysts:
• Infantile Haemangioendothelioma: Usually well-defined but has varying picture on USG.
• Hepatoblastoma: It was seen most commonly in boys < 3 years. Plain film shows hepatomegaly ± calcification ± infiltration or compression of hepatic vasculature. CT scan further helps.
• Hamartoma: Hamartoma accounts for 22% of benign liver tumours in childhood. A multi-septated cystic mass is seen at USG or CT.
• Hepatic Abscess: These can be hematogenous, biliary, post-traumatic or post-surgical in origin. At USG these are seen as hypoechoic masses. At CT, these are seen as hypoattennuating rim enhancing lesions.
Among the masses of GI origin, duplication cysts, pancreatic masses and lymphomatous masses are of great importance.

• Duplication Cyst of Intestinal Tract: Frequent location is terminal ileum and ileocaecal valve. Others are oesophagus, stomach and duodenum.
Plain film shows mass effect with calcification in wall. Ultrasound shows an anechoic cystic mass. Barium study may demonstrate lumen of communicating duplications and mass effect.
• Omental and Mesenteric Cysts: 50% are located in mesentery of small bowel. USG shows a cystic mass. CT reveals a low attenuation mass.
• Ovarian Masses: Mature teratoma: Most common benign lesion (40-50%). At USG it is cystic/solid/complex in appearance. Malignant ovarian lesions are rare and appear as solid lesion on USG/CT.
• Hydrocolpos: USG shows a large midline cystic structure consistent with distended vagina and uterus, with scattered internal echoes.

Although the imaging investigations have to be tailored according to the individual cases, but a strategy has to be formulated by each paediatric radiology centre, based on the facilities available and their health care policies.

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ABDOMINAL PAIN

Abdominal pain is a very common symptom in the childhood. It can be present in acute, or chronic or recurrent manner. In acute abdominal pain, it is important to distinguish between medical and surgical causes. On the other hand, in recurrent abdominal pain, the distinction has to be made between organic and in-organic (psychogenic) pain abdomen.

PATHOLOGY
Abdominal pain may arise because of inflammatory lesions of different intra-abdominal structures. It may also be because of the distension of the hollow viscus, where the discomfort caused by the distension is often felt as pain. Increased peristaltic activity of the hollow organs may be felt as acute or recurrent colicky abdominal pain. The pain is usually felt in the same dermatome, which shares the neurological supply of the underlying organ. Thus pain arising from the stomach is often felt in the epigastric region (T8), from urinary bladder in the supra-pubic region
(S2). Intestinal pain is usually felt in the umbilical region (T 10).
Abdominal pain can also be referred from structures like pleura, spine, etc. which are outside, but whose dermatomes are represented in the abdominal region. Basal pneumonia and caries of the thoracic vertebrae are frequent causes of pain abdomen, which may be missed, if the phenomenon of referred pain is not kept in mind.

ACUTE PAIN
When the child is brought with the complaints of acute pain in abdomen, which is occurring for the first time, a careful evaluation is required for an underlying surgical cause. Age of the child and attendant circumstances are helpful in making a diagnosis.
Whenever pain is the first symptom in the triad of pain, vomiting and fever, underlying surgical causes should be strongly considered. On the other hand, whenever fever and vomiting are preceding symptoms, the underlying cause is more likely to be medical in nature.
Severity of pain is not helpful in determining the cause of the disease. Some of the important causes of acute abdominal pain are as following:

1. Surgical Causes

Acute Intussusception
This is caused by the sliding of the proximal part of intestine into the distal part, causing acute obstruction. Ileocolic intussusception is the most common. Diarrhoeal illness may be a precipitating cause. Usual age group is 6-36 months. It is characterised by the episode of sudden colicky pain abdomen, during which the infant cries severely and draws up his/her limbs over the abdomen. In the between the attacks the infant may appear to be quite normal. It may be accompanied with passage of red currant jelly (mucus with blood) type of stools. Abdominal examination may reveal a saucer shaped mass usually away from the right iliac fossa. Diagnosis can be confirmed by barium enema, which may also help to reverse the intussusception failing which, urgent surgery would be required.

Acute Appendicitis
It can occur in any age, but comparatively less common in childhood. Usual triad of pain, vomiting and fever is seen but the site of pain may be typical in children as the caecum (and the appendix) is quite often in right lumbar or right hypochondria areas due to incomplete descent. Abdominal examination shows rebound tenderness and rigidity. Ultrasound of the abdomen could be diagnostically helpful. Urgent surgery is required for relief.

Acute Intestinal Obstruction
It is often caused by congenital stenosis and strictures of the different parts of the intestines. These usually present in the neonatal period. In older infants and children, acute obstruction may be due to volvulus, round worms, or tuberculosis.
Acute colicky abdominal pain, bilious vomiting, abdominal distension and varying degrees of constipation are the important clinical features. A combined medical and surgical approach is required for the diagnosis and management.

Acute cholecystitis, acute renal colic, and acute pancreatitis are the other causes of the acute abdominal pain in children. Presentations are similar to that of adults, but overall occurrence is less common in children.

2. Medical Causes

Acute Infective Colitis
This is clinically characterized by the passage of the small frequent stools, with mucus and blood, and feeling of the tenesmus. It is very common in childhood. Often colicky abdominal pain may be first symptom, causing confusion in the diagnosis. Fever is often present. The most common cause id shigella infection.

Acute Mesenteric Lymphadenitis
This condition is also characterized by t he presence of pain, vomiting, and fever, and may closely mimic acute appendicitis. However, rebound tenderness is almost never present. Brief period of observation would normally clarify the situation. The usual cause of this otherwise self-limiting condition is viral infection.

Basal Pneumonia
This is very frequent cause of abdominal pain. This is accompanied by upper abdominal distension. There may be rapid breathing and careful examination of the chest would reveal the correct diagnosis.

Acute hepatitis, Congestive heart failure causing sudden enlargement of liver and Acute pyelonephritis are the other medical causes of acute abdominal pain in children.


RECUURENT ABDOMINAL PAIN
The syndrome of recurrent abdominal pain (RAP) is very common in school age children. . Apley defined RAP occurrence of more than 2 episodes over a period of 3 months.
Recurrent abdominal pain in children can be due to variety of causes (mentioned in the table below). Although a very large number of organic causes (as illustrated below) can lead to RAP, they together do not cause more than 5-10 percent episodes of RAP. The clinical features, which suggest organic causes of RAP, are given below.
Whenever anyone or more of these features are present, the child should be completely evaluated using various diagnostic tests. However, if none of these features are present, then only baseline investigations like routine stool, urine examination, and a tuberculin test should be obtained. If anyone of these tests is positive, then appropriate further workup (X-ray chest, barium meal, ultrasound, tuberculin test) may be required. If all these investigations are also negative, it is very unlikely that there is any underlying organic cause of RAP. In such cases, these children are probably having psychogenic pain in abdomen.

Causes of Recurrent Abdominal Pain

1.Organic

A. Gastrointestinal : Gastroesophageal reflex, Peptic Ulcer Disease, Non-ulcer duspepsia, intestinal worms, intestinal tuberculosis.
B. Renal : Urolithiasis, Urinary tract infection
C. Hepatic : Recurrent Cholecystitis
D. Pancreatic : Recurrent Chronic Pancreatitis
E. Extra-Abdominal: Spinal caries, Root pain.

Features suggesting Organic Cause:
• Age < 3 years
• Pain well-localized,consistent, away from umbilicus
• Tenderness/ rigidity on local examination
• Accompanying symptoms like fever, rash, joint pain
• Jaundice
• Raised Blood Pressure

2.Psychogenic
Role model, attention-seeking behaviour

However, for a definitive diagnosis of the psychogenic pain in abdomen, it is very important to establish “Secondary Gain Pattern”, i.e. what is that which the child may be achieving school Absenteeism, attention-seeking from parents, etc. are important secondary gain. Help of specialist would be required to evaluate such children. Most of such type children, usually grown out of this symptom.

3. Uncommon Causes

Abdominal Epilepsy
It is believed to be due to epileptic discharges from the temporal lobe. It manifests as brief episode of pain, accompanied by sudden pallor and may be brief episode of loss of sensorium. EEG is helpful in diagnosis, and the management is on the lines of temporal lobe epilepsy (complex partial seizures).



Acute Hepatic Porphyria
The abdominal pain is severe and colicky in nature, accompanied by passage of dark coloured urine; or urine, which becomes dark on standing. Drugs like Phenobarbitone may be the precipitating cause. Diagnosis is confirmed by demonstrating presence of porphobilinogen in the urine. Management is usually symptomatic and avoidance of drugs which may precipitate the acute attack.


Management of RAP
If the organic cause, like dyspepsia, gastroesophageal reflux disease, peptic ulcer disease, urinary tract infection, chronic colitis, constipation etc. are found, they would need appropriate management.
For psychogenic pain in abdomen, it must be realized that the pain is real as far as the child is concerned. It should never be suggested that the child is only feigning symptom or the pain is the ‘head’. This will only worsen the situation. Brief period of observation and assurance, that there is nothing seriously wrong with the child, helps to manage the child. Most children usually overcome their problem, if less attention is given to their symptom (of pain) and more attention is given to the child himself. In difficult cases, a specialist would be required.


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IRON DEFICIENCY ANAEMIA

By: Dr. Deepak Seth, Deptt. Of Paediatrics, Himalayan Institute of Medical Sciences

Guest Editor: Dr Neeraj Jain, Dept. of Paediatrics, HIMS

Editors: Surya Aggarwal and Katyayni Seth

Anaemia (or Pallor in layman’s term) is a condition to all in which our blood is not able to carry oxygen to all our body parts, efficiently. In paediatric age group, the most common cause is nutritional deficiency. Nutritional anaemia is a state where in normal levels of haemoglobin cannot be maintained by red blood cells. And among deficiencies, iron deficiency is most common in India.

Normally iron levels in the blood vary from person to person depending upon his/her age, sex and even geographical altitude. At birth it is highest; levels fall by the age of 3 months and then gradually increases to adulthood.

Our body has its own iron stores, which are balanced between iron absorption, utilization, and iron excretion.

Iron absorption in our body depends upon factors:

(i) Form of iron salt- ferrous salts and haeme are better absorbed

(ii) Iron absorption is also regulated by duodenal mucosa

(iii) Iron absorption is inversely proportional to iron stores and directly proportional to erythropoiesis.

Iron stores: iron released during the first 8-12 weeks of life is stored in the body and it helps to maintain erythropoiesis up to 4-6months of age in a normal term infant and up to 3 months in a low birth weight baby or pre-term baby.

Iron deficiency causes can be divided as:

1. Decreased intake-
   Milk is a poor source of iron, although breast milk iron is better absorbed so compensates for its low concentration. Delayed introduction of iron rich food supplements is the major cause for the pathogenesis. Iron in vegetarian diets is predominantly in Non- Haeme form, haeme form is found in non-vegetarian diet. Haeme form is readily absorbed and its absorption is less affected by other components such as phylates, tannates, calcium, fibre and phosphates. These factors reduce the absorption of non- haeme iron.
2. Increased losses:
   Iron losses in the faeces are insignificant in normal conditions, but in the presence of parasitic infestation, diarrhoea and dysentery it may increase manifolds.
3. Reduced absorption:
   absorption of iron is inversely proportional to the amount present in the diet. Ascorbic acid, citrate, alcohol, sugars, aminoacids ( hystidine and cystine) enhance iron absorption. While iron is poor absorbed from wheat and rice as they are rich in phylates. Iron absorption from meat and fish is up to 30%.
4. Increased demands:
   Rapid growth during infancy, and childhood results in increased demands of iron. During pregnancy also mother should take good amount of iron in diets and even supplements to avoid deficiency in the growing fetus in her womb.

Clinical features of Iron Deficiency Anaemia:
Fatigue, headache, dyspnoea, apathy, behavioural problems together with the symptoms secondary to abnormalities of the epithelial surfaces such as koilonychias (i.e. thin spoon shaped nails), glossitits (inflammation of the tongue), papiilay atrophy, dysphagia (difficulty in swallowing), diarrhoea and malabsorption. Koilonychia is characteristic of of iron deficiency anaemia.

Congestive heart failure is produced in severe anaemia even in the absence of pre-existing heart disease. Examination of lips, nails, tongue, and conjunctiva enables to assess the presence and degree of anaemia (pallor). Severe chronic deficiency, may, in addition lead to (i) retardation of physical growth, (ii) delay in language and cognitive development, (iii) clumsiness and poor performance in school, (iv) Attention Deficit Disorder, (v) repeated infections.

Investigations

• Blood picture will show presence of microcytic, hypochromic anaemia. With progressive increase in the severity of anaemia anisocytosis and poikilocytosis (various and abnormal shape red blood cells) may appear.
• Haemogram will show blood hemoglobin levels, packed cell volume and condition of RBCs and WBCs.
• Serum iron, total iron binding capacity and transferrin saturation: These parameters get affected only after a decrease in the ferritin level but before a fall in the haemoglobin level or peripheral smear changes.
  Serum iron is variable but fasting levels of less than <75ug/dl>
• Serum ferritin: It’s an indirect measure of iron stores and most sensitive indicator of body iron stores. Level less than <15mg/>
• Marrow stainable iron: Prussian blue staining of a marrow aspirate is a measure of iron stores and an absence of stainable iron is the earliest abnormality detected in iron deficient states.

The commonest differential diagnosis of the condition includes thalassemia trait, anaemia of chronic disease sideroblastic anaemia. These conditions should be suspected if a patient fails to respond to adequate iron therapy. It is most important to differentiate IDA from b- thalassemia trait. In thalassemia microcytosis is more marked than hypochromia. Moreover the red cells distribution is more uniform than in IDA and target cells and basophilic slipping is indicative of thalassemia. The diagnosis of thalassemia trait can be made by detecting the elevated levels of HbA2 and diagnosis of thalassemia major is dependant upon fetal haemoglobin levels of

greater than 10 percent. Anaemias secondary to chronic disease frequently have normocytic, normochromic picture on peripheral smear, however a few patients may have a microcytic hypochromic picture. A therapeutic trial with iron is helpful to differentiate between these conditions.

Sideroblastic anaemia can be reliably diagnosed by demonstrating ringed sideroblasts in a bone marrow aspirate.

Management of IDA:

A thrapeutic response of iron therapy is probably the only definitive evidence of IDA. Treatment of a patient with IDA involves two aspects, the first being the iron supplementation and the second aimed at correcting the underlying cause. Important points to keep in mind regarding iron therapy are:

Oral Therapy is the best form of treatment.

Dose of elemental iron for the treatment is 6mg/kg body weight in two or three divided doses on an empty stomach. Ferrous sulphate is the best and cheapest form of therapy. However, since a large number of iron preparations are available, it is important that the paediatricians should be aware of the amount and concentration of elemental iron of products. Iron preparations containing haemoglobin or enteric-coated preparations do no offer any advantage.

Treatment should be continued for at least 6-8 weeks for correction of the haemoglobin levels and to replenish the stores.

Parenteral iron therapy is indicated only when oral iron is either not tolerated or compliance is poor, or in presence of malabsorptive states. The requirement for iron is calculated by the formula:

Elemental iron required (mg) = weight in kg ´ haemoglobin deficit ´ 4 ( as iron dextran) should be given deep intramuscularly.

Prevention of Iron Deficiency: Nutritional Counselling: Milk is poor source of iron and solids such as green vegetables, pulses, and peas should be introduced by 6 months of age. Hookworm infestation should be prevented by footwear or by periodically de-worming. The children health education and hygienic habits should be improved to prevent parasitic infestation. WHO has recommended additional iron and folic acid supplementation during infancy and childhood.

Fortification: Supplementation of biologically active and acceptable form of iron in food is an accepted method of prevention of iron deficiency. Salt, which is produced only in a few centres, but is consumed by all, was considered to be the most suitable vehicle for fortification. The National Institute of Nutrition, Hyderabad has developed a successful method for fortification of common table salt. The formula for fortified table salt is : Ferrous sulphate- 3.2gms, Sodium Acid Sulphate- 5.0gms and Orthophosphoric acid- 3.2gms in one kg of common salt to provide an iron content of one mg/gm of salt in the preparation. The average per capita daily consumption of salt is 5 gms which will provide 5mg of elemental iron which is sufficient to prevent iron deficiency.

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