1

CHAPTER I INTRODUCTION

Vomiting is defined as the forceful, coordinated act of expelling gastric contents through the mouth. Vomiting may becaused by number of problems in diverse organ systems. Although it often represents a transient response to a selflimited infectious, chemical, or psychologic insult, it also may portend serious infections, metabolic disturbances, or diseases in gastrointestinal (GI), neurologic, or other major organ systems. Thus, an orderly approach to diagnosis is crucial. 1 Vomiting is a common self-limiting symptom in children, but occasionally heralds serious surgical or life threatening disease.2 Vomiting involves the forceful expulsion of the contents of the stomach and is a highly coordinated, reflexive process. It is a feature of many acute and chronic disorders, including those causing increased intracranial pressure, metabolic diseases, and anatomic and mucosal GI abnormalities. Descent of the diaphragm and constriction of the abdominal musculature on relaxation of the gastric cardia force gastric contents back up the esophagus. The process is coordinated by the *vomiting center" in the central nervous system. The vomiting center receives sensor input from the vestibular nucleus (cranial nerve VIII), thc GI tract via vagal afferents (cranial nerve X), and the bloodstream via the area postrema, also known as the chemoreceptor (or chemoreceptive) trigger zone. The stereotypic behaviors associated with emesis are a result of output from the vomiting center through vagal, phrenic, and sympathetic nerves.3 A related complaint, also often heard in the emergency department, is that of young infants who spit up. This refers to the nonforceful reflux of milk into the mouth, which often accompanies eructation. Such nonforceful regurgitation of gastric

or esophageal contents is most often physiologic and of little consequence, although it occasionally represents a significant disturbance in esophageal function.2 Therapy to alleviate vomiting should be directed at the specific cause, when possible. Gastrointestinal obstructions should be corrected, as deemed appropriate by the pediatric surgery team. Management of nonsurgical causes of vomiting include steps to correct fluid and electrolyte imbalances that result from prolonged or excessive vomiting and to identify and treat the underlying disorder causing the symptom.4

CHAPTER II

LITERATURE REVIEW

2.1. Definition of Vomiting The reflex action of ejecting the content of stomach trough the mouth. Vomiting is controlled by a special centre in the brain that may be stimulated by drugs(e.g. apomorphine) acting directly on it; or by impulses transmitted through nervous pathways either from the stomach(e.g. after ingesting irritating substances or in stomach diseases such as peptic ulceration or pyloric stenosis), the intestine(e.g. in intestinal obstruction), or from the inner ear(in motion sickness). The stimulated vomiting centre sets off a chain nerve impulses producing coordinated contractions of diaphragm and abdominal muscle at the entrance os stomach, etc., causing the stomach to be expelled. Medical name : emesis3 2.2. Physiology of Vomiting Vomiting is a coordinated autonomic response involving neural, hormonal, and muscular responses generated by the reticular formation of the medulla that consists of several scattered groups of neurons. The vomiting response may be triggered by peripheral and central stimuli (see picture 1). In particular, the area postrema in the medulla (unprotected by the blood brain barrier) samples peripheral blood and cerebrospinal fluid and likely causes vomiting associated with metabolic disorders and hormones. Once the vomiting response is triggered, a pattern of somatic muscle action occurs with abdominal, thoracic, and diaphragm muscles contracting against a closed glottis. The resulting increased intra-abdominal pressure reverses the negative pressure of the esophagus and forces gastric contents upwards. The vomiting response also alters intestinal motility by generating a retroperistaltic contractile complex that moves intestinal contents towards the esophagus1. Picture 1 :

2.3. Types of Vomiting Vomiting can be classified according to its nature and cause as well as by the character of the vomitus. The nature of the vomiting may be projectile or nonprojectile. Projectile vomiting refers to forceful vomiting and may indicate increased intracranial pressure, especially if it occurs early in the morning. Projectile vomiting also is a classic feature of pyloric stenosis. Nonprojectile vomiting is seen more commonly in gastroesophageal reflux. These somewhat arbitrary descriptions are not definitive in establishing a diagnosis. Emesis often is classified based on its quality. The vomitus may be bilious, bloody, or nonbloody and nonbilious. Emesis originating from the stomach usually is characterized as being clear or yellow and often contains remnants of previously ingested food. Emesis that is dark green is referred to as bilious because it indicates the presence of bile. Bilious vomiting frequently is pathologic because it may be a sign of an underlying abdominal problem such as intestinal obstruction beyond the duodenal ampulla of Vater, where the common bile duct empties. The presence of blood in the emesis, also known as hematemesis, indicates acute bleeding from the upper portion of the GI tract, as canoccur with gastritis, Mallory-Weiss tears, or peptic ulcer disease. Coffee ground-like material often is representative of an old GI hemorrhage because blood darkens to a black or dark-brown color when exposed to the acidity of the gastric secretions. The more massive or proximal the bleeding, the more likely it is to be bright red. 1 Another classification is according to : Central Vestibular - motion-sickness and vertigo Infectious - gastroenteritis, septicemia, non-GI infections Cortical - pain, strong emotions, smell, taste Drugs - chemotherapy, opiates Hormonal - pregnancy Metabolic - acidosis, uremia, hyperthyroidism, hypercalcemia, adrenal disorders

Peripheral Pharyngeal stimulation Gastric mucosal irritation Gastric and intestinal distension2 2.4. Diagnosis History History of presenting illness : Characteristics of vomitus Smell, Quantity, Colour, Blood (bright red/dark red/coffee-ground/bilious) Timing Onset, Duration, Frequency, Time of day, Triggers Associated symptoms Diarrhea, Fever, Abdominal pain/distension, Anorexia, Stool frequency, Urinary output, Headache, Vertigo, Lethargy, Stiff neck, Cough, Sore throat Past medical history Chronic illnesses (diabetes) Travel history (infectious gastroenteritis) Sexual history (pregnancy) Ineffective use of birth control, Last menstrual period Recent head trauma Toxin exposure

Medications Allergies2

Physical exam findings Vitals Fever sign of infection Hypotension, tachycardia volume loss Consciousness - intracranial hypertension, meningitis, metabolic disorders, toxic ingestion Weight loss eating disorders, obstruction Red, bulging tympanic membrane ear infection Bulging anterior fontanelle and nuchal rigidity meningitis Erythematous tonsils upper respiratory tract infection Tachycardia infection, dehydration Abdominal distention obstruction, mass, congenital abnormality, Head and Neck

Inspection

Cardiovascular system Abdominal exam organomegaly Bowel sounds high pitched tinkle (obstruction), absent (ileus) Guarding, rigidity, rebound tenderness appendicitis, peritoneal inflammation Petechiae or purpura serious infection Skin turgor, capillary refill dehydration Jaundice metabolic disorder Rashes food intolerance, viral infection Lethargy and listlessness Inconsolability and bulging fontanelle in an infant

Skin and extremities

Red flags: The following findings are of particular concern:

Nuchal rigidity, photophobia, and fever in an older child Peritoneal signs or abdominal distention (surgical abdomen) Persistent vomiting with poor growth or development2

2.5. Differential Diagnosis A variety of organic and nonorganic disorders can be associated with vomiting. Organic causes are those related to specific medical conditions. The primary care practitioner needs to remember that vomiting does not localize the problem to the GI system in young infants but can be a nonspecific manifestation of an underlying systemic illness such as a urinary tract infection, sepsis, or an inborn error of metabolism. Nonorganic causes are much more difficult to identify and often are viewed as diagnoses of exclusion. Examples of nonorganic causes of vomiting are psychogenic vomiting, cyclic vomiting syndrome, abdominal migraine, and bulimia. Table 1 lists the differential diagnosis of vomiting based on organ systems.1 However, from a clinical perspective, it often is useful to consider causes from an age-related perspective1 (table 2)2 Table 1 : Differential Diagnosis of Vomiting by Systems Gastrointestinal

Esophagus: Stricture, web, ring, atresia, tracheoesophageal fistula, achalasia, foreign body Stomach: pyloric stenosis, web, duplication, peptic ulcer, gastroesophageal reflux Intestine: duodenal atresia, malrotation, duplication, intussusception, volvulus, foreign body, bezoar, pseudo-obstruction, necrotizing enterocolitis Colon: Hirschsprung disease, imperforate anus, foreign body, benzoar Acute gastroenteritis Helicobacter pylori infection

Renal

Parasitic infections : ascariasis, giardiasis Appendicitis Celiac disease Milk/soy protein allergy Inflammatory bowel disease Pancreatitis Cholecystitis or cholelithiasis Infectious and noninfectious hepatitis Peritonitis Trauma : Duodenal hematoma Tumor Cyst Hematoma Cerebral edema Hydrocephalus Pseudotumor cerebri Migraine headache Abdominal migraine Seizure Meningitis Obstructive uropathy: Ureteropelvic junction obstruction, hydronephrosis, nephrolithiasis Renal insufficiency Glomerulonephritis Urinary tract infection

Neurologic

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Renal tubular acidosis

Metabolic Galactosemia Hereditary fructosemia Amino acidopathy Organic acidopathy Urea cycle defects Fatty acid oxidation disorders Lactic acidosis Lysosomal storage disorders Peroxisomal disorders Diabetic ketoacidosis Adrenal insufficiency Pneumonia Sinusitis Pharyngitis Sepsis syndromes Pregnancy Rumination Bulimia Psychogenic Cyclic vomiting syndrome Overfeeding

Endocrine

Respiratory

Miscellaneous

11

Age Infant year

Medications/vitamin/drug toxicity Superior mesenteric artery syndrome Child abuse Acute Gastroenteritis Hirschsprungs disease Acutely evolving surgical abdomen Congenital atresias and stenosis Malrotation Intussusception Chronic Gastroesophageal reflux disease Food intolerance Congenital atresias and stenosis Malrotation Intussusception

Table 2 : Differential Diagnosis: Common causes of vomiting by age group

1 month to 1 Pyloric stenosis

Sepsis and non-GI infection Children and adolescents Metabolic disorders Gastroenteritis Appendicitis Sepsis and non-GI infection Metabolic disorders Pregnancy Toxic ingestion Gastroesophageal reflux disease Gastritis Food intolerance Cyclic vomiting Intracranial hypertension Inborn errors of metabolism Eating disorders

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Common causes of vomiting by age group : Vomiting in Infancy Vomiting in the first few days after birth may be a sign of serious pathology. Bilious emesis is suggestive of congenital obstructive GI malformations,such as duodenal/jejunal atresias, malrotation with midgut volvulus, meconium ileus or plugs, and Hirschsprung disease. Published reports of neonates evaluated in neonatal intensive care units with a principal diagnosis of bilious emesis revealed that 38% to 69% had an intestinal obstruction. Nonsurgical causes of bilious emesis include necrotizing enterocolitis and gastroesophageal reflux (GER).When caring for a neonate who has persistent bilious vomiting, the clinician should place a nasogastric ororogastric catheter to decompress the stomach and prevent any additional vomiting or aspiration before initiating any diagnostic or therapeutic maneuvers. Plain radiographs of the abdomen can demonstrate dilated bowel loops and air-fluid levels, which strongly suggest bowel obstruction. Contrast imaging studies are more specific and can help pinpoint a precise diagnosis. Surgical and neonatal consultations should be obtained urgently when the diagnosis of bowel obstruction is considered. Intestinal Atresias Intestinal atresias are surgical emergencies and typically present within a few hours after birth. Duodenal atresia is a congenital obstruction of the second portion of the duodenum that occurs in 1 per 5,000 to 10,000 live births and is associated with trisomy 21 in approximately 25% of cases. It is believed to be due to a failure of recanalization of the bowel during early gestation. Infants present with clinical features of failure to tolerate feedings and bilious emesis shortly after birth. Due to the proximal nature of the obstruction, abdominal distention usually is not present. Plain abdominal radiographs may show a double bubble sign, which represents air in the stomach and proximal duodenum (Fig. 1). More distal obstructions, such as jejunoileal atresias,

13

typically present with bilious vomiting along with abdominal distention within the first 24 hours after birth. The cause of these atresias is believed to be a mesenteric vascular accident at some point during the course of gestation. The frequency of their occurrence is approximately 1 per 3,000 live births. Anatomically, jejunoileal atresias can be classified into four types: membranous, interrupted, apple-peel, and multiple. Abdominal radiography may show dilated loops of small bowel with air-fluid levels (Fig. 2). Urgent surgical correction is necessary for all types of intestinal atresias. Malrotation With Midgut Volvulus Understanding malrotation requires a review of the organogenesis of the gut. During the third week of fetal development, the primitive gut is divided into three regions: the foregut, midgut, and hindgut, based on vascular supply. The first stage of intestinal development involves rapid growth of the midgut outside the abdominal cavity through a herniation of the umbilical orifice. During the second stage, the midgut returns to the abdominal cavity, rotating 180 degrees and pushing the hindgut to the left. The last stage of intestinal development involves the retroperitonealization of portions of the right colon, left colon, duodenum, and intestinal mesentery, helping them serve as anchors for the bowel. Disruption of this process during the second or third stage can result in an aberrant return or anchoring of the midgut within the abdominal cavity. Although most infants who have intestinal malrotation present within the first week after birth due to the accompanying volvulus, the malrotation itself does not cause any notable symptoms and may be undetected for years. Bowel strangulation can occur at any age and any time because affected patients are at increased risk of volvulus due to a lack of proper mesenteric anchoring to the retroperitoneum. The midgut twists in a clockwise direction around the superior mesenteric vessels, leading to obstruction of vascular supply to most of the small and large intestine. Once bowel ischemia occurs, metabolic acidosis, unstable hemodynamics, and intestinal necrosis with perforation may ensue if the condition is not diagnosed and rapidly corrected surgically. A spiral configuration of the jejunum or demonstration of failure of contrast to pass beyond the

14

second portion of the duodenum on upper GI radiographic series is diagnostic (Fig. 3). Abdominal ultrasonography also may reveal a malposition of the superior mesenteric vessels. Timely surgical correction with the Ladd procedure is critical. If bowel ischemia is prolonged, loss of bowel and resultant short gut syndrome may occur.

Figure 1. Double bubble sign on plain radiograph, which represents air in the stomach and proximal duodenum and indicates duodenal atresia.

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Figure 2. Dilated loops of small bowel with air-fluid levels, indicative of jejunoileal atresia.

Figure 3. Failure of contrast to pass beyond the second portion of the duodenum, which is characteristic of malrotation with midgut volvulus.

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Vomiting in Infancy Beyond the Neonatal Period The differential diagnosis of vomiting in infants beyondthe neonatal period is more extensive. Common causes are acute gastroenteritis, GER, and nutrient intolerances such as milk or soy protein allergies. Metabolic diseases and inborn errors of metabolism also should be considered for infants who have persistent progressive vomiting. Acquired or milder intestinal obstructive lesions, such as infantile hypertrophic pyloric stenosis (IHPS), also are possible and should be ruled out when clinically indicated. Common entities such as GER, dietary protein intolerance, and IHPS are discussed in greater detail in this section. Intussusception is another important cause of vomiting in the young infant that is discussed in the next section because it also may present beyond infancy. The management of acute gastroenteritis is discussed in the section on management. Gastroesophageal Reflux GER is the most common cause of recurrent nonbilious emesis in infancy. It involves the retrograde movement of gastric contents into the esophagus as a result of an abnormally functioning lower esophageal sphincter (LES). Under normal circumstances, the LES relaxes after swallowing to allow passage of ingested food into the stomach. Patients who have GER have transient relaxations of the LES that are not precipitated by a swallow, allowing gastric contents to move freely back into the esophagus from an area of higher to lower pressure. In young infants, such relaxation often results from developmental immaturity of the LES, which may improve over time. Infants who have GER present with recurrent postprandial regurgitation of ingested food or milk, most often within 30 minutes of a feeding. Affected children may appear irritable during or after feedings, and stereotypic opisthotonic movements with extension and stiffening of arms and legs and extension of the head (Sandifer syndrome) occasionally may be observed. Infants who have severe GER can have recurrent microaspiration into their lungs, resulting in chronic wheezing, respiratory symptoms, and even failure to thrive. Infants who have the classic history of recurrent

17

emesis but who are thriving and have normal physical examination findings do not need specific treatment. Thickening the formula or human milk by adding cereal may help reduce vomiting in such infants, but elevating the head in the supine position has no proven beneficial effect. Infants who are irritable during feedings and those who have respiratory or growth problems mayneed pharmacologic intervention. Acid blockade with histamine2 receptor antagonists or proton-pump inhibitors may help lessen the burning sensation caused by the gastric refluxant. Prokinetic agents such as metoclopramide and erythromycin may help decrease the physical process of GER by targeting the LES. A Cochrane meta-analysis reviewing seven randomized control trials showed that metoclopramide was superior to placebo in reducing daily symptoms of GER. However, its use must be weighed against the potential adverse effects of extrapyramidal symptoms, headache, and drowsiness. Recent studies have suggested that baclofen, a GABA receptor agonist, may lessen the number of transient LES relaxations via vagal-mediatedmechanisms and, thus, improve the pathophysiologic process associated with GER. Additional investigation into this agents overall efficacy for the treatment of GER is necessary. Dietary Protein Intolerance Dietary protein intolerance is a non-immunoglobulin E-mediated type of food hypersensitivity that typically presents in infants in the first postnatal year, shortly after exposure to the offending allergen. Commonly implicated proteins include cow milk protein, soy protein, and egg protein. Among the clinical symptoms are irritability, feeding intolerance, recurrent vomiting and diarrhea, and in severe cases, failure to thrive. Occasionally, patients may present with Heiner syndrome, manifesting as pulmonary hemosiderosis (due to recurrent microhemorrhages into the lungs), iron deficiency anemia, and failure to thrive. Examination of stools in patients who have protein intolerance may reveal occult blood, with polymorphonuclear cells, lymphocytes, and eosinophils. Stool-reducing substances may be positive due to carbohydrate malabsorption. Intestinal biopsies may reveal flattened villi and colitis

18

with infiltration of lymphocytes, eosinophils, and mast cells. Treatment of dietary protein intolerance involves removal of the allergen from the diet. In the case of cow milk protein allergy, 80% of patients respond to hydrolyzed casein formula; the remaining 20% require L-amino acid-based formulas or intravenous nutrition. Once elimination has occurred, symptoms usually resolve in 3 to 10 days. The dietary protein intolerancetypically subsides by 18 to 24 months of age. Infantile Hypertrophic Pyloric Stenosis Infants who have pyloric stenosis typically present to medical attention with persistent projectile nonbilious emesis between 2 and 6 weeks of age. Males, especially those who are firstborn, are affected approximately four times as often as females. The incidence is approximately 3 per 1,000 live births. The exact cause of pyloric stenosis remains unclear. The relaxation mechanism of the pyloric smooth muscle depends on nonadrenergic noncholinergic inhibitory innervation, mediated by vasoactive intestinal peptide and nitric oxide (NO). Deficiencies in neuropeptidergic innervation and NO have been implicated in cases of pyloric stenosis, but neither has been substantiated as etiologic. Very early exposure to erythromycin (within the first 2 weeks after birth) also has been associated with an eightfold increased risk of pyloric stenosis. It is hypothesized that erythromycin interacts with intestinal motilin receptors, causing strong gastric and pyloric contractions and subsequent pyloric muscle hypertrophy. Pyloric stenosis usually is diagnosed by a typical history and physical findings. Inspection of the abdomen shortly after an infant feeding may reveal a peristaltic wave because the stomach muscles contract in an attempt to pass ingested milk past the pylorus. A palpable olive in the mid-epigastric region represents the hypertrophic pyloric muscle and strongly supports the diagnosis of pyloric stenosis. Repeated episodes of vomiting of the gastric contents due to pyloric stenosis may result in characteristic electrolyte abnormalities, although serum electrolyte values may be normal if the patient is diagnosed in the early stages. The classic electrolyte abnormality is a hypochloremic hypokalemic metabolic alkalosis. Normal acid

19

production in the stomach is accompanied by the release of bicarbonate ions into the blood as a result of the action of carbonic anhydrase. Because of the loss of the hydrogen ions, this bicarbonate is unbuffered, resulting in an ensuing metabolic alkalosis. Under normal conditions, the excess bicarbonate is excreted in the urine. However, affected infants also lose significant amounts of fluid in addition to the electrolytes. The subsequent volume contraction triggers a renal response of enhanced proximal tubular reabsorption of bicarbonate and activation of the renin-angiotensinaldosterone mechanisms. In addition, the lack of chloride ion in the proximal tubule results in increased local production and reabsorption of bicarbonate, thus worsening the existing metabolic alkalosis. Under the influence of high concentrations of aldosterone, the distal tubule excretes large amounts of potassium and hydrogen ions in exchange of sodium. Lack of hydrogen ions results in enhanced excretion of potassium, leading to significant hypokalemia. When the diagnosis of pyloric stenosis is being considered, ultrasonography of the pyloric muscle can confirm the clinical suspicion, with sensitivity rates rangingfrom 85% to 100%. Pyloric muscle thickness of 4 mm or more and muscle length of 14 mm or more are diagnostic of pyloric stenosis. If ultrasonographic examination findings are normal, an upper GI radiographic series can be performed. The radiographic series has a slightly higher sensitivity for pyloric stenosis (89% to 100%) and can aid in the diagnosis of other causes of progressive emesis in this age group, such as antral web and other structural abnormalities. Surgical pyloromyotomy is the definitive treatment of pyloric stenosis and is being performed laparoscopically at many centers. Vomiting in Older Children Vomiting occurs most commonly in older children in the setting of an acute gastroenteritis accompanied by fever and diarrhea. Vomiting also can be a nonspecific manifestation of a systemic illness, although much less commonly than in the young infant. Both viral and bacterial meningitis can present with vomiting, usually accompanied by complaints of headache, fever, and neck stiffness. Elevation of

20

intracranial pressure from entities such as a brain tumor or an intracranial hemorrhage also may present with a chief complaint of vomiting in association with a severe, progressive headache. Vomiting in such patients often occurs shortly after waking in the morning because of a gradual rise in intracranial pressure as the child sleeps in the supine position. Inadvertent toxic ingestions also should be considered, especially in toddlers. Intussusception Acquired bowel obstructions such as intussusceptions may present in the older infant and young child, with the peak incidence occurring between 3 months and 3 years of age. Intussusception is the telescoping of one portion of the bowel into its distal segment. Most commonly, the terminal ileum invaginates into the cecum, often as a result of lymphatic hypertrophy in the Peyer patches from a recent viral infection. A history of intermittent episodes of severe and crampy abdominal pain with bilious emesis is classic. Parents often report that their child is lethargic in between episodes of pain and may describe blood-tinged, currant jelly stools. Physical examination may reveal intestinal obstruction with a sausageshape mass palpable in the right lower quadrant. Rapid consultation with a pediatric surgeon is warranted. Contrast or air enemas can be diagnostic, with the contrast outlining the lead portion of the intussusception, giving the typical coiled spring appearance (Fig. 4). In addition, the hydrostatic pressure from the contrast enema may reduce telescoping of the intestine. Surgical reduction of the intussusception is indicated when the contrast enema is not successful.

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Figure 4. Contrast outlining the lead portion of the intussusception, giving the typical coiled spring appearance. Cyclic Vomiting Syndrome Cyclic vomiting syndrome (CVS) is characterized by stereotypic recurrent episodes of nausea and vomiting without an identifiable organic cause. It is an idiopathic disorder that usually begins in early childhood; relatively little is known about its pathogenesis or cause. The diagnosis is based on several characteristic features: 1) three or more episodes of recurrent vomiting, 2) intervals of normal health between episodes, 3) episodes that are stereotypic with regard to symptom onset and duration, and 4) lack of laboratory or radiographic evidence to support an alternative diagnosis. Vomiting episodes are of rapid onset and persist for hours to days, separated by symptom-free intervals that can range from weeks to years. Treatment is supportive, focused on fluid management in cases where dehydration and electrolyte imbalance occur. Amitriptyline and propranolol have been described as effective for prophylactic therapy (antiemetics may be of benefit during an acute episode).

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Abdominal Migraine Abdominal migraines involve episodic attacks of epigastric or periumbilical abdominal pain and are believed to share pathophysiologic mechanisms with CVS. Abdominal migraines are more common in females than in males, with a ratio of 3:2, and the onset is primarily between 7 and 12 years. A family history of migraine headaches may be present. Episodes of abdominal pain are acute in onset and last for 1 hour or more. The pain is so intense that it interferes with the performance of normal activities and is associated with anorexia, nausea, vomiting, headache, photophobia, and pallor. Much like those who have CVS, patients who have abdominal migraines report intervals of completely normal health between the episodes of pain. Diagnostic evaluation looking for alternative organic conditions yields negative results. The diagnosis of abdominal migraine is supported by a favorable response to medications used for treatment of migraine headaches. Patients should be advised about trigger avoidance, specifically caffeinecontaining foods, altered sleep patterns, prolonged fasting, emotional stress, and exposure to flickering lights. Rumination Rumination is the repeated and painless regurgitation of ingested food into the mouth beginning soon after food intake. The food is re-chewed and swallowed or spit out. Symptoms do not occur during sleep and do not respond to the standard treatment of GER. To qualify for the diagnosis, symptoms must be present for longer than 8 weeks. Rumination is not associated with retching and often is viewed as a behavioral entity, typically seen in mentally retarded children, neonates during prolonged hospitalization, and children and infants who have GER. Rumination also has been described in cases of child neglect and in older children and adolescents who have bulimia or are depressed. Most commonly, rumination is seen among female adolescents or male infants. One third of affected individuals have underlying psychological disturbances. The management of rumination involves a multidisciplinary approach, with a primary

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focus on behavioral therapy and biofeedback. Occasionally, tricyclic antidepressants and nutritional support may be necessary. Superior Mesenteric Artery Syndrome Superior mesenteric artery (SMA) syndrome, otherwise known as Wilkie syndrome or cast syndrome, is a functional upper intestinal obstructive condition. Normally, the SMA forms a 45-degree angle, with the abdominal aorta at its origin and the third portion of the duodenum crossing between the two structures. When the angle between the SMA and the aorta is narrowed to less than 25 degrees, the duodenum may become entrapped and compressed. This condition most commonly is described in patients who have experienced rapid weight loss, immobilization in a body cast, or surgical correction of spinal deformities. SMA syndrome typically presents with epigastric abdominal pain, early satiety, nausea, and bilious vomiting. Patients experience worsening pain in the supine position, which may be relieved in the prone or kneechest position. Diagnosis usually is confirmed by upper GI radiographic series (Fig. 5) or computed tomography scan (Fig. 7) with failure of contrast to pass beyond the third portion of the duodenum. Conservative initial management of SMA syndrome focuses on gastric decompression, followed by the establishment of adequate nutrition and proper positioning after meals. Placement of an enteral feeding tube distal to the obstruction or parenteral nutrition may be needed in severe cases. Surgical correction with a duodenojejunostomy is a last resort.1

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Figure 6. Severely dilated stomach and proximal duodenum indicative of high obstruction consistent with superior mesenteric artery syndrome.

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Procedure for Investigation (this will be based on the differential diagnosis)2,4 Condition Gastroenteritis History and Physical Diarrhea (usually), history of infectious contact, fever (sometimes) GERD Fussiness after feeding, poor weight gain Pyloric stenosis Recurrent projectile vomiting in neonates aged 3-6 weeks, emaciated and dehydrated Congenital atresia Abdominal distension, bilious or stenosis emesis in first 24-48 hours of life Malrotation Bilious emesis, abdominal distention, abdominal pain, bloody stool Sepsis Fever, lethargy, tachycardia, tachypnea, widening pulse pressure, hypotension Food intolerance Abdominal pain, urticarial, eczematous rash Metabolic disorder Poor feeding, failure to thrive, hepatosplenomegaly, jaundice, dysmorphic features, developmental delays, unusual odors Diagnostic approach Clinical evaluation

Empiric trial suppression Ultrasound

of

acid

Abdominal X ray Contrast enema Abdominal X ray Upper GI series with contrast under fluoroscopy CBC Cultures (blood,urine,CSF) Elimination diet

Non-GI infection

Serious infection

Cyclic vomiting

Electrolytes, ammonia, liver function tests, BUN, creatinine, serum glucose, total and direct bilirubin, CBC, PT/PTT Further specific tests based on findings Fever, localized findings (sore Clinical evaluation throat, dysuria, flank pain) Further tests if needed depending on source Meningitis CBC, Cultures (CSF, photophobia, nuchal blood, urine) rigidity, headaches gram stains Pyelonephritis CBC, Cultures (urine, fever, back pain, dysuria blood) At least 3 self-limited episodes of Diagnosis of exclusion

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Intracranial hypertension

Eating disorder

Pregnancy

Toxic ingestion

vomiting lasting 12 h, 7 days between episodes, no organic cause of vomiting Nocturnal wakening, progressive recurrent headache made worse by coughing or Valsalva maneuver, nuchal rigidity, visual changes, weight loss, photofobia Body dysmorphism, teeth erosions, skin lesions on hand (Russells sign), binge eating behaviour Amenorrhea, morning sickness, breast tenderness, bloating, history of sexual activity and improper contraception use History of ingestion, findings vary depending on substance and pattern of ingestion

Brain CT (without contrast)

Clinical evaluation

Urine pregnancy test

Varies depending substance

on

2.6. General Principles in the Management of Vomiting Therapy to alleviate vomiting should be directed at the specific cause, when possible. Gastrointestinal obstructions should be corrected, as deemed appropriate by the pediatric surgery team. Management of nonsurgical causes of vomiting include steps to correct fluid and electrolyte imbalances that result from prolonged or excessive vomiting and to identify and treat the underlying disorder causing the symptom. The 2003 Centers for Disease Control and Prevention practice guidelines for the management of acute gastroenteritis in children, endorsed by the American Academy of Pediatrics, recommend oral rehydration therapy (ORT) in cases of mild-to-moderate dehydration from acute gastroenteritis. Using an appropriate glucose-electrolyte solution, 50 to 100 mL/kg of fluid should be administered to the child over the course of 4 hours, along with replacement of continuing losses from stool and emesis. This is

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most effective when the ORT is administered in small, 5-mL increments every 1 to 2 minutes. In cases of severe dehydration, ileus, or persistent vomiting despite adequate attempts at ORT, parenteral fluids must be administered. Although the previously cited guidelines do not recommend the routine use of antiemetic drugs in the management of patients who have acute gastroenteritis, unique situations may warrant their use. If the cause of the vomiting is unclear, antiemetics are contraindicated. Phenothiazines such as prochlorperazine, promethazine, and chlorpromazine are antiemetics that act as D2receptor antagonists at the chemoreceptor trigger zone.Such drugs rarely are used in pediatric patients because of their extrapyramidal and sedative adverse effects. Antihistamines such as diphenhydramine, hydroxyzine, and dimenhydrinate also may help alleviate nausea and vomiting but have a sedative effect that makes clinical reevaluation difficult. A newer class of antiemetics is the 5HT3-receptor antagonists, ondansetron and granisetron. The 5HT3 blockade occurs both at the enteric level and at the chemoreceptor trigger zone. These drugs, unlike the phenothiazines and antihistamines, do not have central nervous system adverse effects, making them more attractive options. The 5HT3-receptor antagonists have been approved for the management of chemotherapy-induced nausea and vomiting and for pregnancyassociated and postoperative vomiting in adults. For children, however, there is no substantive scientific evidence supporting their efficacy in treating acute gastroenteritis. Therefore, these agents have not been endorsed officially for routine use.1

CHAPTER III CASE REPORT Objective

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The aim of this paper is to report a case of vomitting in a 2 years 2 months old girl. Case RF, 2 years 2 months old girl, was admitted to Haji Adam Malik Hospital at July 27th 2012 with the chief complaint of vomiting. Vomiting has been experienced by the patient 3 days ago with the frecuency of more than 3 times a day, volume of 1/2 aqua glass, content of the vomit was what has been eaten and drank. Diarrhea was not found. Fever was not found. The patient is a patient of the Paediatric Surgery Department where she has been operated with the diagnosed of Wilms tumor on March 2012. History of immunization History of previous illness History of previous medication : Complete : Post operation Wilms tumour : Not clear.

Physical Examination Presence Status : Consciousness : Alert , Temperature: 37,0C, anaemic (-), dyspnoea (-), cyanotic (-), edema (-), icteric (-). Weight: 9 kg Length: 82cm BW/BL: 69,3% Head : Eye : Light reflexes (+/+), sunken eyes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (+/+) Ear and Nose : within normal limit; Mouth : dry oral mucosa (+) Neck Thorax : Lymph node enlargement (-) : Symmetrical fusiform, retraction (-) HR: 110 bpm, regular, murmur (-) RR : 30 tpm, regular, ronchi (-/-)

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Abdomen Genitalia Extremities

: Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, poor turgor, scar (+) : Female, within normal limit : Pulse : 110 bpm, regular, adequate pressure/volume, CRT<3, warm, oedem (-)

Photo Rontgen

Conclusion of the radiological 1. KV enough 2. The size of heart is normal with CTR <50%

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3. Trakea at the midline

4.

Lung is normal Conclusion : Normal

5. Bones and soft tissue is normal

Conclusion of the radiological 1. Preperitoneal fat line normal 2. Psoas line not clear

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3. Both kidney conture not clear 4. There is no sign of bowel distention. 5. There is a few layer of air fluid level.

Conclusion : Sub ileus, there is no sign of perforation.

Laboratory Result (July 26th 2012) : Test Complete Blood Count Hemoglobin (Hb) Erytrocyte (RBC) Leukocyte (WBC) Hematocrite Trombocyte (PLT) MCV MCH MCHC RDW MPV PCT PDW Neutrofil Limfosit Monosit Eosinophil Basophil Neutrophil absolute Limfosit absolute Monosit absolute Eosinophil absolute Basophil absolute Results 13.40 g % 5.06 x 106/mm3 15.70 x 103/mm3 40.00 % 622 x 103/mm3 79.20 fL 26.60 pg 33.60 g % 14.70 % 6.66 fL 0.414 % 16.9 fL 57.70 % 31.50 % 7.88 % 2.16 % 0.781 % 9.04x103/L 4.93x103/L 1.23x103/L 0.339x103/L 0.122x103/L Normal Value 11.3 14.1 g % 4.40 4.48x106/mm3 4.5 11.0 x103/mm3 37 - 41 % 217 497 x103/mm3 81 - 95 fL 25 - 29 pg 29 31 g % 11.6 14.8 % 7.0 10.0 fL 37 80 % 20 40 % 28% 16% 01% 2.4 7.3 x103/L 1.7 5.1 x103/L 0.2 0.6 x103/L 0.10 0.30 x103/L 0 0.1 x103/L

Parameters Carbohydrate Metabolism Blood Glucose ad Random Renal Ureum

Value 131.80 67.10

Normal Value < 200 <50

32

Creatinin Electrolite Sodium Pottasium Chloride Differential Diagnosis : - Observation of vomiting ec GERD
-

0.56 116 5.2 78

0.24-0.41 135-155 3.6-5.5 96-106

Observation of vomiting ec cyclic vomiting syndrome

Working Diagnosis :
-

Observation of vomiting + post operation Wilms tumor

Treatment : - Rehydration
-

IVFD NaCl 0,9% 75ml/kgBW in 4 hours 168 microdrips/minute

Planning: - Recheck Electrolyte, RFT - Abdominal X-ray - Chest X-ray - Urinalysis

-

Consult to Nephrology and GE

33

Date 26/8/2012

S Vomit (+)

27/8/2012

Vomit (+)

28/8/2012

Vomit (-), Defecate (-) in 3

O GFR = 80,5 (102.5-150.5) Correction for Hyponatremia = (135-116)x0.6x9 = 102.6 mEQ Na maintenance = 3-4 mEQ/kg BW = 27-36 mEQ Rapid correction = (125-116) x0.6x9 =48.6 mEQ NaCl 0.9% = (48.6/154)x1000=315.58 in 4 hours 78 micro drips per minute Slow hyponatremia correction = (135-116)x0.6x9 = 102.6 mEQ NaCl 0.9%=(102.5/154)x1000=666.23ml in 20 hours 30 micro drips in a minute Consciousness: Alert, T: 37,0C, BW: 9kg Head : Eye: Sunken eyes (+/+), pale conjunctiva palpebra inferior (+/+), Light reflexes (+/+), isochoric pupil Ear and Nose : within normal limit Mouth : dry oral mucosa (+) Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 116bpm,reg, murmur (-) RR : 28tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 116bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-) Consciousness: Alert, T: 37,0C, BW: 9kg Head : Eye: Sunken eyes (-/-), pale conjunctiva palpebra inferior (-/-), Light reflexes (+/+), isochoric

Observation of vomitting ec DD/GERD + post operation Wilms tumor

- IVFD NaCl 0,9% 30gtt/i - Zinc 1x20mg - Oralit 50cc/x diarrhea - Inj Ceftriaxon 450mg/12 hours/IV R/ Urinalysis Dipstick Consult to Nephrology Consult to GE - IVFD NaCl 0,9% 30gtt/i - Zinc 1x20mg

Observation of vomitting ec DD/GERD +

34

days

29/8/2012

Vomit (-), Defecate (-)

pupil Ear and Nose : within normal limit Mouth : dry oral mucosa (-) Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 116bpm,reg, murmur (-) RR : 28tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 116bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-) Consciousness: Alert, T: 37,0C, BW: 9kg Head : Eye: Sunken eyes (-/-), pale conjunctiva palpebra inferior (-/-), Light reflexes (+/+), isochoric pupil Ear and Nose : within normal limit Mouth : dry oral mucosa (-) Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 116bpm,reg, murmur (-) RR : 28tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 116bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-) Laboratory Results Ca/Na/K/Phospor/Cl/Mg: 8.4/131/3.0/3.9/96/2.35 Urinalysis Colour : clowdy yellow

post operation Wilms tumor

- Oralit 50cc/x diarrhea - Inj Ceftriaxon 450mg/12 hours/IV R/ Consult to Nephrology Consult to GE

Observation of vomitting ec DD/GERD + post operation Wilms tumor

- IVFD NaCl 0,9% 30gtt/i - Zinc 1x20mg - Oralit 50cc/x diarrhea - Inj Ceftriaxon 450mg/12 hours/IV - Inj Ranitindin 10mg/12hours IV

35

30/8/2012

31

Glu/Bil/Ket/ SG /pH/Pro/Uro/Nit/Blo - / - / - /1.010/8.0/ + / - / - / + Sediment Eri /Leu/Epi /Casts/Cristal 4-10/3-7 / 0-2/ - / Vomit (+), Consciousness: Alert, T: 37,0C, BW: 9kg Defecate Head : Eye: Sunken eyes (-/-), pale conjunctiva (-) palpebra inferior (-/-), Light reflexes (+/+), isochoric pupil Ear and Nose : within normal limit Mouth : dry oral mucosa (-) Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 116bpm,reg, murmur (-) RR : 28tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 116bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-) Vomit (+), Consciousness: Alert, T: 37,0C, BW: 9kg Diarrhea Head : Eye: Sunken eyes (-/-), pale conjunctiva (-) palpebra inferior (-/-), Light reflexes (+/+), isochoric pupil Ear and Nose : within normal limit Mouth : dry oral mucosa (-) Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 116bpm,reg, murmur (-) RR : 28tpm, reg, ronchi (-)

Observation of vomitting ec DD/GERD + post operation Wilms tumor

- IVFD NaCl 0,9% 30gtt/i - Zinc 1x20mg - Oralit 50cc/x diarrhea - Inj Ceftriaxon 450mg/12 hours/IV - Inj Ranitindin 10mg/12hours IV - Dulcolax

Observation of vomitting ec DD/GERD + post operation Wilms tumor

- IVFD NaCl 0,9% 30gtt/i - Inj Ranitidin 10mg/12hours - Inj Ceftriaxon 450mg/12hours - Eas primer 10gtt/i micro in 1 hour/12 hours - Zinc 1x20mg

36

Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 116bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-) Laboratorium Results Renal Ur/Cre/Uric Acid: 16.90/0.39/5.8 GFR: = 114,2 (Normal) 1/8/2012 Vomit (+) 5 times Consciousness: Alert, T: 37,0C, BW: 9kg Head : Eye: Sunken eyes (-/-), pale conjunctiva palpebra inferior (-/-), Light reflexes (+/+), isochoric pupil Ear and Nose : within normal limit Mouth : dry oral mucosa (-) Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 116bpm,reg, murmur (-) RR : 28tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 116bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-) Observation of vomitting ec DD/GERD + post operation Wilms tumor

- Oralit 50ml/x diarrhea - Diet MII 900kkal and 18g protein R/ Check RFT

2/8/2012

Vomit (+) twice, Fever (-)

Consciousness: Alert, T: 37,0C, BW: 9kg Head : Eye: Pale conjunctiva palpebra inferior (-/-), Light reflexes (+/+), isochoric pupil Ear and Nose : within normal limit Mouth : dry oral mucosa (-)

- IVFD NaCl 0,9% 30gtt/i - Inj Ranitidin 10mg/12hours - Inj Ceftriaxon 450mg/12hours - Eas primer 10gtt/i micro in 1 hour/12 hours - Zinc 1x20mg - Oralit 50ml/x diarrhea - Diet MII 900kkal and 18g protein R/ NGT Abdominal X-Ray Observation of - IVFD NaCl 0,9% vomitting ec 30gtt/i DD/GERD, Susp - Inj Ranitidin ileus + post 10mg/12hours operation Wilms - Inj Ceftriaxon

37

Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 116bpm,reg, murmur (-) RR : 28tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 116bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-)

tumor

450mg/12hours - Eas primer 10gtt/i micro in 1 hour/12 hours - Zinc 1x20mg - Oralit 50ml/x diarrhea - Diet MII 900kkal and 18g protein

3/8/2012

4/8/2012

Vomit (+), Consciousness: Alert, T: 37,0C, BW: 9kg Fever (-) Head : Eye: Pale conjunctiva palpebra inferior (-/-), Light reflexes (+/+), isochoric pupil Ear and Nose : within normal limit Mouth : dry oral mucosa (-) Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 116bpm,reg, murmur (-) RR : 28tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 116bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-) Vomit (+) Consciousness: Alert, T: 37,0C, BW: 9kg 3 times, Head : Eye: Pale conjunctiva palpebra inferior (-/-), Bloody Light reflexes (+/+), isochoric pupil vomit (+) Ear and Nose : within normal limit once Mouth : dry oral mucosa (-)

Observation of - IVFD NaCl 0,9% vomitting ec 30gtt/i DD/GERD, Susp - Inj Ranitidin ileus + post 10mg/12hours operation Wilms - Inj Ceftriaxon tumor 450mg/12hours - Zinc 1x20mg - Diet MII 900kkal and 18g protein

Observation of - IVFD NaCl 0,9% vomitting ec 30gtt/i DD/GERD, Susp - Inj Ranitidin ileus + post 10mg/12hours operation Wilms - Inj Ceftriaxon

38

5/8/2012

Vomit (+)

6/8/2012

Vomit (-), Greenish and blackened NGT (+)

Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 116bpm,reg, murmur (-) RR : 28tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 116bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-) Consciousness: Alert, T: 37,0C, BW: 9kg Head : Eye: Pale conjunctiva palpebra inferior (-/-), Light reflexes (+/+), isochoric pupil Ear and Nose : within normal limit Mouth : dry oral mucosa (-) Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 116bpm,reg, murmur (-) RR : 28tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 116bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-) Consciousness: Alert, T: 37,0C, BW: 9kg Head : Eye: Pale conjunctiva palpebra inferior (-/-), Light reflexes (+/+), isochoric pupil Ear and Nose : within normal limit Mouth : dry oral mucosa (-), Greenish NGT (+) Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 116bpm,reg, murmur (-)

tumor

450mg/12hours - Zinc 1x20mg - Diet MII 900kkal and 18g protein

Observation of - IVFD NaCl 0,9% vomitting ec 30gtt/i DD/GERD, Susp - Inj Ranitidin ileus + post 10mg/12hours operation Wilms - Inj Ceftriaxon tumor 450mg/12hours - Zinc 1x20mg - Diet MII 900kkal and 18g protein

Observation of - IVFD NaCl 0,9% vomitting ec 30gtt/i DD/GERD , - Inj Ranitidin Susp Ileus + post 10mg/12hours operation Wilms - Inj Ceftriaxon tumor 450mg/12hours - Zinc 1x20mg - Diet MII 900kkal

39

7/8/2012

8/8/2012

RR : 28tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 116bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-) Laboratory Results Hb/RBC/WBC/Ht/Plt: 9.60/3.53/8.84/29.90/391 MCV/MCH/MCHC/RDW/MPV/PCT/PDW 84.70/27.20/32.10/16.00/9.20/0.36/9.9 N/L/M/E/B: 40.00/42.80/6.00/11.10/0.100 PT/INR/APTT/TT: 1.04/1.07/0.54/1.13 Blackened Consciousness: Alert, T: 37,0C, BW: 9kg NGT (-), Head : Eye: Pale conjunctiva palpebra inferior (-/-), Greenish Light reflexes (+/+), isochoric pupil NGT (+) Ear and Nose : within normal limit Mouth : dry oral mucosa (-), Greenish fluid flow from NGT Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 108bpm,reg, murmur (-) RR : 20tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 108bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-) Laboratory Results Ca/Na/K/Phospor/Cl/Mg: 8.4/136/3.3/3.5/110/2.32 Greenish Consciousness: Alert, T: 37,0C, BW: 9kg NGT (-) Head : Eye: Sunken eyes (-/-), pale conjunctiva

and 18g protein R/ Check CBC, electrolyte, HST Re-consult with paediatric surgery

Observation of - IVFD NaCl 0,9% vomitting ec 30gtt/i DD/GERD, Susp - Inj Ranitidin ileus + post 10mg/12hours operation Wilms - Inj Ceftriaxon tumor 450mg/12hours - Zinc 1x20mg - Diet MII 900kkal and 18g protein

Observation of vomitting ec

- IVFD NaCl 0,9% 30gtt/i

40

9/8/2012

Vomit (-), Greenish NGT (-)

palpebra inferior (-/-), Light reflexes (+/+), isochoric pupil Ear and Nose : within normal limit Mouth : dry oral mucosa (-), greenish NGT (-) Neck : lymph node enlargement (-) Thorax : SF, retraction (-) HR : 100bpm,reg, murmur (-) RR : 24tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 100bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-) Consciousness: Alert, T: 37,0C, BW: 9kg Head : Eye: Sunken eyes (-/-), pale conjunctiva palpebra inferior (-/-), Light reflexes (+/+), isochoric pupil Ear and Nose : within normal limit Mouth : dry oral mucosa (-), greenish NGT (-) Neck : lymph node enlargement (-) Thorax : SF, retraction (-), HR : 100bpm,reg, murmur (-) RR : 26tpm, reg, ronchi (-) Abdomen : Soepel, peristaltic (+) N, Hepar/Spleen : not palpable, scar (+) Extremities : Pulse 100bpm, reg, adequate pressure/volume, CRT<3, warm, oedem (-)

DD/GERD , - Inj Ranitidin Susp ileus + post 10mg/12hours operation Wilms - Inj Ceftriaxon tumor 450mg/12hours - Zinc 1x20mg - Diet MII 900kkal and 18g protein

Observation of - IVFD NaCl 0,9% vomitting ec 30gtt/i DD/GERD , - Inj Ranitidin Susp ileus + post 10mg/12hours operation Wilms - Inj Ceftriaxon tumor 450mg/12hours - Zinc 1x20mg - Diet MII 900kkal and 18g protein

41

DISSCUSSION RF, 2 years 2 months old girl, was admitted to Haji Adam Malik Hospital at July 27th 2012 with the chief complaint of vomiting. Vomiting has been experienced by the patient 3 days ago with the frecuency of more than 3 times a day, volume of 1/2 aqua glass, content of the vomit was what has been eaten and drank. Diarrhea was not found. Fever was not found. The patient is a patient of the Paediatric Surgery Department where she has been operated with the diagnosed of Wilms tumor on March 2012. The cause of this patients vomiting is still unknown but its differential diagnose is observation of vomiting cause by either gastroesophageal reflux disease or cyclic vomiting syndrome. This is because the symptoms found in this patient is closest to both disease. These includes vomiting was experienced by this patient after eating, in the morning and having projectile vomit. First, the differential diagnose is gastroesophageal reflux. GER is the most common cause of recurrent nonbilious emesis in infancy. It involves the retrograde movement of gastric contents into the esophagus as a result of an abnormally functioning lower esophageal sphincter (LES). Under normal circumstances, the LES relaxes after swallowing to allow passage of ingested food into the stomach. Patients who have GER have transient relaxations of the LES that are not precipitated by a swallow, allowing gastric contents to move freely back into the esophagus from an area of higher to lower pressure. In young infants, such relaxation often results from developmental immaturity of the LES, which may improve over time. Infants who have GER present with recurrent postprandial regurgitation of ingested food or milk, most often within 30 minutes of a feeding. Infants who have the classic history of recurrent emesis but who are thriving and have normal physical examination findings do not need specific treatment. Then the second is cyclic vomiting syndrome. The estimated prevalence of CVS in children is in the range of 0.3%2.2 %. This disorder is primarily recognized in

42

children, primarily Caucasians (mean age of onset at five years), with increasing recognition in adults (mean age of onset at 35 years). There have been case reports of symptoms starting as early as the sixth day of life and as late as 73 years. In children, females appear to be more affected than males, compared to a male predominance in adults. Cyclic vomiting syndrome (CVS) is characterized by stereotypic recurrent episodes of nausea and vomiting without an identifiable organic cause. It is an idiopathic disorder that usually begins in early childhood, relatively little is known about its pathogenesis or cause. The diagnosis is based on several characteristic features to support an alternative diagnosis such as: 1) three or more episodes of recurrent vomiting, 2) intervals of normal health between episodes, 3) episodes that are stereotypic with regard to symptom onset and duration, 4) lack of laboratory or radiographic evidence Vomiting episodes are of rapid onset and persist for hours to days, separated by symptom-free intervals that can range from weeks to years. Treatment is supportive, focused on fluid management in cases where dehydration and electrolyte imbalance occur. Amitriptyline and propranolol have been described as effective for prophylactic therapy (antiemetics may be of benefit during an acute episode). Conclusion Patient RF, 2 years and 2 months old, is diagnosed with observation of vomiting cause by cyclic vomiting syndrome and the therapy for this patient is fluid management and electrolyte correction.

43

References:
1.

Stevens, M.W., Henretig,F.M., Vomiting In Fleisher, G.R., Ludwig,S., Textbook of Pediatric Emergency 4th edition. Lippincot, William & Wilkins. 2000. Pages 555-567.

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Chandran, L., Chitkara, M., Vomiting in Children: Reassurance, Red Flag, or Referral? Pediatr. Rev. 2008 :29 :l 83 - 192 DOI: I 0. 1 5 42lpir.29-6-183 Wang, B.W., Definition of Age Group Terminology Pediatric Care Online Infants and Children: Merck Manual Professional

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4. Nausea and Vomiting Infants and Children: Approach to the Care of Normal 5. Scorza K, Williams A, Phillips JD, Shaw J. Evaluation of nausea and vomiting, Am.Fam.Physician 2007 Jul 1;76(1):76-84. 6. Burton, J.L., et al, Owford Concise Medical Dictionary, seventh edition, 2007, Oxford University Press
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Maclennan, A.C., Investigation in Vomiting Children 2003 Elsevier Inc. Glasgow, Scotand, UK McAlister, W.H., Kronemer, K.A.,: Emergency gastrointestinal radiology of the newborn. Radiol Clin North Am 34:819-844, 1996 Carty, H., Brereton, R.J.,: The distended neonate. Clin Radiol 34:367-380, 1983 Berrocal, T., Lamas, M., Gutieerrez, J., et al: Congenital anomalies of the small intestine, colon, and rectum. Radiographics 19:1219-1236,1999

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9. 10.