Managing Acute Abdominal Pain in Children

Abdominal pain is one of the most common reasons for a parent to bring his or her child to medical attention. Evaluation of a “stomach ache” can challenge both parents and the physician.

Possible causes for a child’s abdominal pain range from trivial to life-threatening, with little difference in the child’s complaints. Fortunately, abdominal pain in a child usually improves quickly. Each parent or caregiver faces the difficulty deciding whether a complaint needs emergency care or not.

Abdominal pain is a common problem in children. Although most children with acute abdominal pain have self-limited conditions, the pain may herald a surgical or medical emergency.

Causes to be kept in MindAlthough many cases of acute abdominal pain are benign, some require rapid diagnosis and treatment to minimize morbidity. Numerous disorders can cause abdominal pain. The most common medical cause is gastroenteritis, and the most common surgical cause is appendicitis.

In the acute surgical abdomen, pain generally precedes vomiting, while the reverse is true in medical conditions. Diarrhea often is associated with gastroenteritis or food poisoning. Appendicitis should be suspected in any child with pain in the right lower quadrant. Signs that suggest an acute surgical abdomen include involuntary guarding or rigidity, marked abdominal distention, marked abdominal tenderness, and rebound abdominal tenderness.

The list that should be in mind while evaluating a child with abdominal is is as follows:

Medical causes

• Diabetic ketoacidosis
• Inflammatory bowel disease
• Acute adrenal failure
• Gastroenteritis
• Food Poisioning
• Urinary tract infection
• Hepatitis
• Sickle cell crisis
• Henoch-Schönlein purpura

Surgical Causes

• Acute appendicitis
• Bowel obstruction
• Intussusception/ volvulus
• Testicular torsion
• Meckel’s diverticulum

Others

• Infantile colic
• Functional pain

History and Physical Examination
In a child presenting with acute abdominal pain a complete history and detailed physical examination is important to reach a proper diagnosis and then appropriate management

An Overview of Nephrotic Syndrome

Pediatric Nephrotic syndrome is defined by the presence of:

• nephrotic proteinuria > 1 g/m2/day,
• hypoproteinemia – albumin usually < 25 g/l, based on protein loss to urine,
• hypercholesterolemia – based on increased lipoprotein synthesis (caused by hypoproteinemia),
• edema – based on increased naturism resorption in tubules.

Nephrotic syndrome is a constellation of clinical findings that is the result of massive renal losses of protein. Thus, nephrotic syndrome is not a disease itself, but the manifestation of many different glomerular diseases.

Minimal Change DiseaseMinimal Change Disease (also known as lipoid nephrosis) is a disease of the kidney that causes nephrotic syndrome and usually affects children (peak incidence at 2–3 years of age).

Pathophysiology
Nephrotic syndrome is a nonspecific disorder in which thekidneys are damaged, causing them to leak large amounts of protein from the blood into the urine.

Kidneys affected by nephrotic syndrome have small pores in the podocytes, large enough to permit proteinuria (and subsequently hypoalbuminemia, because some of the protein albumin has gone from the blood to the urine.

NS is believed to have an immune pathogenesis. Evidence of the immune-mediated nature of NS is demonstrated by the fact that immunosuppressive agents, such as corticosteroids and alkylating agents, can result in remission of nephrotic syndrome.

Pathology of Edema in Nephrotic Syndrome
The classical explanation for edema formation is a decrease in plasma oncotic pressure, as a consequence of low serum albumin levels, causing an extravasation of plasma water into the interstitial space. The resulting contraction in plasma volume (PV) leads to stimulation of the renin-angiotensin-aldosterone axis and antidiuretic hormone. The resultant retention of sodium and water by the renal tubules contributes to the extension and maintenance of edema.

A more recent theory of edema formation posits that massive proteinuria leads to tubulointerstitial inflammation and release of local vasoconstrictors and inhibition of vasodilation. This leads to a reduction in single-nephron glomerular filtration rate and sodium and water retention.

Introduction to Hypocalcemia

Hypocalcemia is a laboratory and clinical abnormality that is observed with relative frequency, especially in neonatal pediatric patients.

Definition
Hypocalcemia is defined as a total serum calcium concentration of less than 2.1 mmol/L (8.5 mg/dL) in children, less than 2 mmol/L (8 mg/dL) in term neonates, and less than 1.75 mmol/L (7 mg/dL) in preterm neonates.

Hypocalcaemia is one of the commonest disorders of mineral metabolism seen in children and can be a consequence of several different aetiologies. These include a failure of secretion or action of parathyroid hormone, disorders of vitamin D metabolism and abnormal function of the calcium sensing receptor.

Normal Calcium Metabolism
Calcium is the most abundant mineral in the body. Of the body’s total calcium, 99% is in bone, and serum levels constitute less than 1%.Various factors regulate the homeostasis of calcium and maintain serum calcium within a narrow range. These include parathormone (PTH), vitamin D, hepatic and renal function (for conversion of vitamin D to active metabolites), and serum phosphate and magnesium levels.

Although total serum calcium levels are often measured and reported, ionized calcium is the active and physiologically important component.

The concentration of calcium in the serum is critical to many important biologic functions, including the following:

• Calcium messenger system by which extracellular messengers regulate cell function
• Activation of several cellular enzyme cascades
• Smooth muscle and myocardial contraction
• Nerve impulse conduction
• Secretory activity of exocrine glands.

Effects of Hypocalcemia on the Bodily Functions
Hypocalcemia manifests as central nervous system (CNS) irritability and poor muscular contractility. Low calcium levels decrease the threshold of excitation of neurons, causing them to have repetitive responses to a single stimulus. Because neuronal excitability occurs in sensory and motor nerves, hypocalcemia produces a wide range of peripheral and CNS effects, including paresthesias, tetany (ie, contraction of hands, arms, feet, larynx, bronchioles), seizures, and even psychiatric changes in children.

Approach to a Child with Cyclic Vomiting Syndrome

Cyclic vomiting syndrome (CVS) is a rare disorder characterized by recurrent episodes of severe nausea and vomiting. An episode may last for a few hours to several days and then is followed by a period of time during which affected individuals are free of severe nausea and vomiting. This alternating pattern of disease and disease-free periods distinguishes cyclic vomiting syndrome from other similar disorders.

Etiology

Cyclic vomiting syndrome (CVS) is a chronic functional disorder of unknown etiology that is characterized by paroxysmal, recurrent episodes of vomiting. The pathophysiology is unknown, but data suggest a strong genetic component.

Cyclic vomiting usually develops during childhood usually ages 3–7; although it often remits during adolescence, it can persist into adult life.

Epidemiology
Cyclic vomiting syndrome occurs in all races but seems to disproportionately affect whites.
Females show a slight predominance over males.

Causes and Risk Factors
The cause of cyclic vomiting syndrome is unknown, but the bouts of vomiting that characterize the condition can be triggered by:

• Colds, allergies or sinus problems
• Emotional stress or excitement
• Foods such as chocolate or cheese
• Overeating or eating right before going to bed
• Hot weather
• Physical exhaustion

Many children who have cyclic vomiting syndrome have a family history of migraines or begin having migraines themselves when they get older. 

Abdominal migraine — a type of migraine more common in children — causes abdominal pain but not the severe vomiting associated with cyclic vomiting syndrome.

Brief Summary of Tetralogy of Fallot- A Congenital Heart Disorder

Tetralogy of Fallot is a cyanotic congenital heart disorder which is defined by the following four defects

1. Ventricular septal defect (hole between the right and left ventricles)
2. Narrowing of the pulmonary outflow tract (the valve and artery that connect the heart with the lungs)
3. Overriding aorta (the artery that carries oxygen-rich blood to the body) that is shifted over the right ventricle and ventricular septal defect, instead of coming out only from the left ventricle
4. Thickened wall of the right ventricle (right ventricular hypertrophy)

Tetralogy of Fallot is rare, but it is the most common form of cyanotic congenital heart disease. Patients with tetraology of Fallot are more likely to also have other congenital defects.

Historical Information
Louis Arthur Fallot, after whom the name tetralogy of Fallot is derived, was not the first person to recognize the condition. Stensen first described it in 1672; however, it was Fallot who first accurately described the clinical and complete pathologic features of the defects.

Etiology
The cause(s) of most congenital heart diseases (CHDs) are unknown, although genetic studies suggest a multifactorial etiology.

Prenatal factors associated with a higher incidence of tetralogy of Fallot (TOF) include maternal rubella (or other viral illnesses) during pregnancy, poor prenatal nutrition, maternal alcohol use, maternal age older than 40 years, maternal phenylketonuria (PKU) birth defects, and diabetes. Children with Down syndrome also have a higher incidence of tetralogy of Fallot, as do infants with fetal hydantoin syndrome or fetal carbamazepine syndrome.

Introduction to Rickets

Introduction

Rickets is a disease of growing bone that is unique to children and adolescents. It is caused by a deficiency or impaired metabolism of vitamin D, magnesium, phosphorus or calcium. It leads to softening and weakening of the bones.

Rickets is among the most frequent childhood diseases in many developing countries. The predominant cause is a vitamin D deficiency, but lack of adequate calcium in the diet may also lead to rickets .

Types of Rickets
Different types have been described and may include:

• Nutritional Rickets
• Vitamin D Resistant Rickets
• Vitamin D Dependent Rickets
•  - Type I
•  - Type II
• Congenital Rickets

Pathophysiology
Vitamin D deficiency rickets occurs when the metabolites of vitamin D are deficient. Less commonly, a dietary deficiency of calcium or phosphorus may also produce rickets. Vitamin D-3 (cholecalciferol) is formed in the skin from a derivative of cholesterol under the stimulus of ultraviolet-B light. It is converted into the active metabolite calcitriol after final hydroxylation in the kidney. Calcitriol acts to regulate the body’s calcium metabolism by the following mechanisms:

(1) it promotes absorption of calcium and phosphorus from the intestine; 

(2) it increases reabsorption of phosphate in the kidney; and, 

(3) it acts on bone to release calcium and phosphate. Calcitriol may also directly facilitate calcification. These actions result in an increase in the concentrations of calcium and phosphorus in extracellular fluid.

Wilm’s Tumor- A Childhood Malignancy

Wilms tumor, or nephroblastoma, is the most common childhood abdominal malignancy.

Wilms’ tumor most often affects children ages 3 to 4 and becomes much less common after age 5. This tumor most often occurs in just one kidney, though it can sometimes be found in both kidneys at the same time.

Improvements in the diagnosis and treatment of Wilms’ tumor have improved the prognosis for children with this disease.

Pathology
Wilm’s tumor tends to be encapsulated and vascularized that do not cross the midline of the abdomen. In cases of metastasis it is usually to the lung. A rupture of Wilms’ tumor puts the patient at risk of hemorrhage and peritoneal dissemination of the tumor. In such cases, surgical intervention by a surgeon who is experienced in the removal of such a fragile tumor is imperative.

Pathologically, a triphasic nephroblastoma comprises three elements:

1. blastema
2. mesenchyme
3. epithelium

Wilms’ tumor is a malignant tumor containing metanephric blastema, stromal and epithelial derivatives. Characteristic is the presence of abortive tubules and glomeruli surrounded by a spindled cell stroma. The stroma may include striated muscle, cartilage, bone, fat tissue, fibrous tissue. The tumor is compressing the normal kidney parenchyma.

The mesenchymal component may include cells showing rhabdomyoid differentiation. The rhabdomyoid component may itself show features of malignancy.

Wilms’ tumors may be separated into 2 prognostic groups based on pathologic characteristics:

1. Favorable – Contains well developed components mentioned above
2. Anaplastic – Contains diffuse anaplasia (poorly developed cells)