Vomiting in Pediatrics

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AbstractAbstract

Vomiting is a common complaint in any healthcare facility that deals with children. A child recently presented to ouremergency department with an occult cause of vomiting, which led to the development of the following differentialdiagnosis of vomiting in children. Although usually of gastrointestinal origin, vomiting can be caused by the dysfunctionof many different organ systems, the results of which may range from benign to life threatening. The differentialdiagnosis is presented in order of frequency, in order to make it as clinically relevant as possible, and then eachsection is further broken down to the pathophysiology, the historical facts, the pertinent physical examination findings,and the therapeutics of each diagnosis is discussed in variable detail.

Case Report

Chief complaint: fall from 3 feet and vomiting.

History of Present Illness

Patient 'DF' is a 6-month-old healthy male with no significant past medical, surgical or birth history who is brought tothe emergency department (ED) by ambulance after an unwitnessed fall from bed (approximately 3 feet off the ground)onto a carpeted floor at 16:30. The child's mother reported that she heard the fall, which was immediately followed bycrying, and that the child was fully alert from when she entered the room several seconds later. A total of 2 h after theincident, the patient had one episode of nonbloody, nonbilious vomiting, at which point the emergency services werecalled. The child's mother reported that changes in the child's behavior consisted of increased tiredness and fussybehavior since receiving the 6-month immunizations on the day prior to the incident, but no noticeable behavioralchanges since the fall. The child was otherwise without complaint.

Review of Condition (As per Mother):

General: generally healthy;

Dermatological: no rashes;

Head/ears/eyes/nose/throat: no rhinorrhea, hears normally;

Pulmonary: no cough or audible wheezing. No difficulty breathing;

Gastrointestinal (GI): vomiting (see history of present illness). Feeding normally up to the time of the incident;

Genitourinary: normal urine output;

Past medical history: full-term product of an uncomplicated pregnancy and delivery;

Past surgical history: none;

Medications: none;

Allergies: none.

Physical Examination Findings

Vomiting in the Pediatric Age GroupNeil MullenPediatr Health. 2009;3(5):479-503.

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Vitals: blood pressure: 96/56 mm Hg; heart rate: 134 bpm; respiratory rate: 22 bpm; SaO2: 100%; temperature(rectal): 99.4°F; weight: 6 kg;

General: patient is sitting up on gurney (unassisted), holding a bottle, dressed only in a diaper with no obvioussigns of trauma. Patient tracks the physician around the room with both eye and head movement. Patient is wellnourished, well appearing and in no acute distress;

Skin: pink, warm and dry with no rashes or petechiae;

Head: normocephalic/atraumatic. No hematomas, bruises or abrasions;

Eyes: pupils equal, round, reactive to light, extraocular movements normal with normal sclera and conjunctiva;

Ears: tympanic membranes clear bilaterally with no blood or cerebral spinal fluid (CSF) noted;

Nose: no nasal discharge;

Mouth: moist mucus membranes. Appropriate dentition for 6 months. Stable jaw and midface with no signs oftrauma;

Neck: supple with no palpable nodes and no apparent tenderness to palpation over spinous processes;

Cardiovascular: regular rate and rhythm;

Lungs: clear to auscultation;

Abdomen: scaphoid, soft, nontender with normal bowel sounds;

Back: normal spinal alignment with no step-off or apparent bony tenderness;

Genitourinary system: normal circumcised male. A large lymph node could be palpated in the left inguinalcrease;

Neurologic: normal motor, sensory and cerebellar function for age.

ED Course

Patient had another episode of nonbloody, nonbilious emesis in the ED. A noncontrast CT scan of the head wasordered; this was read as normal by radiology. Patient was observed for several hours. The patient had three morevomiting episodes. At that time, an intravenous drip was placed with 120 cc normal saline (NS) infused (20 cc/kg) andblood drawn; x-rays of the abdomen were ordered.

Laboratory Statistics

Complete blood count: white blood cell: 6.700/µl, with 54% PMNs. Hemoglobin: 12.4; hematocrit: 39%;

Electrolytes: Na+: 134; Cl−: 109; K+: 4.3; HCO3 −: 21; Cr: 0.6; BUN: 8; Glu: 111;

Liver function test: alanine aminotransferase: 92; aspartate aminotransferase: 73; alk phos: 357;

Lipase: 28;

Acute abdominal series: nonspecific bowel gas pattern with air in colon. No free air on left lateral decubitus x-rays.

At this time, the patient had one episode of bilious vomiting and it was decided to admit the child for intravenoushydration and bowel rest. He was re-examined. He was less attentive and the mother reported poor feeding sincepresentation to ED. His diaper was removed and a tender, 2 cm left inguinal mass was noted, which now extended into

the upper scrotum. The right testes was descended and normal - the left testicle could not be palpated. An attemptwas made to reduce inguinal mass without success and surgery was consulted. An ultrasound of the inguinal area wascarried out, which confirmed a left inguinal hernia and showed good blood flow to the left testicle. The hernia wasreduced under sedation. Patient was then admitted to surgery for observation with elective left inguinal hernia repair tofollow in the morning.

Diagnosis Left inguinal hernia.

Differential Diagnosis of Vomiting in the Pediatric Age Group

Differential diagnosis of vomiting in the pediatric age group may be a result of a range of causes, including GI (i.e.,obstructive and inflammatory) etiologies, CNS disease, pulmonary problems, renal disease, endocrine/metabolicdisorders, drugs (either as side effects or in overdosages), psychiatric disorders, strep throat, pregnancy or stress.

Gastrointestinal

The most common cause for vomiting is often GI. It can be helpful to think of the GI tract as a long tube, stretchingfrom the mouth to the anus, with four buds sticking out in the middle: the liver, the gall bladder, the pancreas and theappendix. When faced with a patient who may have a GI cause to their vomiting, it is helpful to simply start at the topand work down. Anything that either obstructs or inflames the tube or any of its buds may cause vomiting.

Obstruction

Anything that obstructs the GI tract or any of its buds, including foreign bodies, idiopathic hypertrophic pyloric stenosis,intussusception, indirect inguinal hernias, appendicitis, volvulus and gastroesophageal reflux, may cause vomiting.

Foreign Bodies Foreign bodies (FBs) in the esophagus may be occult.

Pathophysiology The most common foreign bodies in children are coins.[1] The two places where coins mostcommonly lodge are at the cricopharyngeous and the lower esophageal sphincter (LES; see Figures 1). The LES hasthe smallest diameter of the GI tract, and if a FB can pass into the stomach it can generally pass through the anus.

Figure 1.

Obstruction of the gastrointestinal tract by a foreign body.

(A) Foreign body at the cricopharyngeous. (B) Foreign body at the lower esophageal sphincter.

Reproduced with permission from Madigan Army Medical Center Department of Radiology, WA, USA.

Historical Facts Children are often witnessed swallowing the coins or tell their parents soon after. Some will developabrupt respiratory distress with partial (or complete) airway obstruction. Most will have vomiting.

Pertinent Physical Examination Findings Coins at the cricopharyngeous are rarely a diagnostic dilemma: thesechildren drool and may be stridorous and dyspneac. The coin should be removed at the time of presentation, usually inthe operating room by an otorhinolaryngologist. Coins at the level of the LES may be occult. A metal detector has beensuccessfully used in the past to determine the presence of coins.[1]

Therapeutics If the child is not drooling or vomiting, coins at the LES can be watched for 24 h to see if the coin passesinto the stomach spontaneously; if not, the child should be referred to a gastroenterologist for removal.[2] Removal witha Foley catheter[2] and bougienage[3] has been described. Sharp FBs and button batteries should have immediate GIreferral.

Infantile Hypertrophic Pyloric Stenosis Infantile hypertrophic pyloric stenosis (PS) is a relatively common cause ofvomiting in young infants.[4]

Pathophysiology The etiology is hypertrophy of the circular musculature of the pylorus, which then obstructs the lumen.

Historical Facts The typical patient first develops symptoms at 3 weeks of age and is typically diagnosed at 5 weeks.Children with PS have nonbilious projectile vomiting. The child with PS is always hungry; children with vomiting fromgastroenteritis or a metabolic cause are usually anorexic. There is no history of diarrhea or fever. PS often runs infamilies, and is frequently observed in first-born males. The use of erythromycin in this age group is associated withthe development of infantile hypertrophic PS.[5]

Pertinent Physical Examination Findings Classically, these children are dehydrated and malnourished, and have ahypovolemic, hypochloremic metabolic alkalosis (a 'contraction' alkalosis) with hypoglycemia and hypokalemia, butrecent studies demonstrate that the majority of infants with PS have normal electrolytes and only mild dehydration.[6]

In order to determine whether the child has PS, the primary-care provider (PCP) should flex their hips and knees, andgive them a bottle to drink, which they will take avidly. With patience, an 'olive' is often palpable deep just to the right ofthe spinal column. Ultrasound is the diagnostic imaging of choice if the pylorus is not palpated (Figure 2).

Figure 2.

Pylorus with hypertrophic musculature surrounding outlet.

Musculature larger than 4.0 mm is considered abnormal, as is a pyloric canal larger than 16 mm.


Therapeutics All patients with PS should be given electrolytes and an Accucheck should be performed, and the childshould be rehydrated with D5NS with K+.[7] Treatment is surgical (after the child achieves metabolic balance).[4]

Intussusception Intussusception is usually observed in patients aged 3-18 months.[8-10]

Pathophysiology These children suffer from telescoping of a portion of their proximal intestine into a portion moredistal, with obstruction and eventual mucosal ischemia. Ileocolic intussusception is most common. Intussusceptionafter 2 years of age may be due to a lead point: a polyp or tumor on the intestinal wall. Henoch Schoenlien Purpuramay also present with intussusception (see Figures 3 & 4).[11]

Figure 3.

Ultrasound of patient with intussusception.


Figure 4.

Air-contrast enema of patient with intussusception.


Historical Facts Vomiting, abdominal pain and bloody, mucoid stools (that look like 'currant jelly') are classic, althoughit is rare that all three present in the same patient. The symptoms are episodic, in time with the peristaltic waves, andin between the child is left exhausted, sometimes to the point of coma.

Pertinent Physical Examination Findings The child is intermittently fussy and typically has guaiac-positive stool(bloody). An allantoid-shaped mass is sometimes palpable in the right upper quadrant (RUQ).

Therapeutics Diagnosis is most commonly made by ultrasound, although this is technician dependant. An air-contrastenema is both diagnostic and is curative in approximately 80% of patients if carried out within the first 48 h after onsetof symptoms. Perforation with an enema occurs with 2.5% of enemas; therefore, surgical physicians should beconsulted prior to sending the child to the radiology suite. Intussusception recurs in 10% of patients within 24 h and soall patients should be hospitalized overnight.

Indirect Inguinal Hernia Indirect inguinal hernia is rare in females.

Pathophysiology Embryologically, a loop of peritoneum extends through the inner and outer inguinal rings down intothe scrotum to form the tunica vaginalis. If this does not properly involute, a loop of bowel may follow this tract into the

groin or all the way into the scrotum. A hernia may slide in and out (reducible) or become trapped (incarcerated).Premature infants have an increased incidence of inguinal hernias.[12]

Historical Facts Some patients with reducible hernias present with a history of a mass, but nothing upon examination.The PCP should slide their finger up into the external inguinal ring and have the patient cough or bear down: a loop ofbowel may be palpable as it bounces against the examiner's fingertip. Incarcerated hernias most commonly present asa painful mass noted in the groin, extending into the upper part of the scrotum, but may present with simple vomiting,as did the patient described in the case report of this article.

Pertinent Physical Examination Findings The child is usually in pain, fussy and a mass is noted in the inguinal creaseor scrotum (Figures 5 & 6).

Figure 5.

Inguinal hernia.

Left sided small inguinal hernia (A), which enlarged with crying, forcing a loop bowel into the scrotum (B).


Figure 6.

X-ray of child with inguinal hernia showing loops of bowel in the scrotum.

Reproduced with permission from Aukland District Health Board, Aukland, NZ.

Therapeutics Patients with a history compatible with an inguinal hernia (but nothing present upon examination) shouldbe referred to a surgeon for elective repair. The parents should be asked to take a picture of the mass the next time itis present. Children with incarcerated hernias should have an attempt at reduction, but surgical physicians shouldmake the final decision as to which hernias are reducible and which are truly incarcerated. A hernia that remainsincarcerated for a prolonged period of time may become ischemic and 'strangulated', and, if reduced, can lead toperforation and sepsis.[13,14]

Appendicitis

Pathophysiology Appendicitis starts with an obstruction of the lumen, usually by a fecalith. This causes swelling andsubsequent ischemia of the antimesenteric surface, which becomes inflamed and then progresses over 36-48 h toperforation. Appendicitis is the most common surgical emergency in childhood, and vomiting is the most commonsymptom, followed by fever and abdominal pain. The rate of perforation is much higher in the pediatric population.[15-

17] It is especially difficult to diagnose in children over 4 years of age.[18]

Historical Facts Classically, the child presents with anorexia, periumbilical pain, low-grade fever and vomiting. Over thecourse of 24-36 h, the pain radiates to the right lower quadrant. If not diagnosed, perforation and peritonitis occurs. A'classic' presentation is rare.

Pertinent Physical Examination Findings The child with appendicitis will lie quietly in the bed; he/she may resist yourexamination, but screaming and thrashing does not occur. The child starts out with a low-grade fever, and althoughhe/she points to their belly-button the child will have right lower quadrant tenderness from the beginning. Then, afterperforation, the child develops generalized peritonitis, with diffuse peritonitis upon examination, and the vomitingdiminishes.

Therapeutics The work-up and management of appendicitis alone can fill chapters of literature. For the purposes ofthis review, let it be said that abdominal pain and vomiting, without diarrhea, must have appendicitis in the differential,and the clinician should be fairly certain that appendicitis is not the cause of the child's symptoms prior to lettinghim/her go home, or else additional work-up (ultrasound, CT scan of the abdomen and pelvis or surgery consult)should be entertained (see Figures 7-9). Ultrasound is sensitive and specific, but is technician dependent. A CT scanis even more accurate (and less dependent on operator experience) but entails significant radiation exposure to ayoung child.[19] A protocol using ultrasound and CT scans has increased sensitivity of preoperative diagnosis and hasdecreased the negative laparotomy rate from 17% to less than 5% over a 3-year period.[20]

Figure 7.

CT scan of acute appendicitis with fecalith.

Reproduced with permission from [102].

Figure 8.

CT scan of acute appendicitis with fecalith.

Reproduced with permission from [77].

Figure 9.

Ultrasound of acute appendicitis.


Volvulus Volvulus can occur in any age group but is most common in neonates.[21-23]

Pathophysiology Volvulus is the sequelae to a malrotation of the intestine. When malrotation occurs, the mesenterydoes not adhere to the retroperitoneum along a line from the ligament of Trietz to the cecum, but instead adheresalong a slender base surrounding the celiac axis. This makes twisting of the bowel possible, with subsequentischemia.

Historical Facts The infant presents with bilious vomiting, abdominal pain (if old enough to complain) and somnolence.Older children may have intermittent symptoms, as the intestine twists back and forth.

Pertinent Physical Examination Findings Upon examination, the child may be critically ill, in hypotensive shock. Thechild will have a taut, tender abdomen, high pitched (or no) bowel sounds and distended loops of bowel with air/fluidlevels can be observed on x-ray (Figures 10 & 11).

Figure 10.

Infant with volvulus.


Figure 11.

Infant with volvulus showing air/fluid levels and no air in the rectum.


Therapeutics This is a medical and surgical emergency. Resuscitation, repeated boluses of NS (20 cc/kg), antibioticsand often pressors are needed, along with an immediate surgical consult. Although many references suggest going

straight to CT scan or an upper GI series, the PCP should hesitate before filling the stomach of a neonate who isvomiting. A barium enema will determine whether malrotation is present, and essentially diagnose volvulus.

Gastroesophageal Reflux Gastroesophageal reflux (GER) is included in this report because GER is so oftenmistaken for true vomiting and is the exact opposite of an obstruction. These are the classic 'wet burps', observed inalmost 100% of infants.

Pathophysiology Almost all infants have GER: retrograde flow of formula or breast milk up through the loweresophageal sphincter and out of the mouth (re-flux). Exactly why this occurs is unclear, but infants do have poorlycoordinated swallowing and delayed gastric emptying. This, plus the fact that children are on an all-liquid diet and theyspend so little time in the upright position, all probably contributes to reflux, especially after a large feeding whenintragastric pressures are high. All of the above mechanisms tend to diminish with time, and it is rare to see a patientwith significant reflux after 12 months of age. GER disease (GERD) occurs when the child develops aspiration andrecurrent pneumonias, failure to thrive or esophagitis (which will present as true vomiting and fussiness - see below).GERD can also present in young infants as an apparent life-threatening event.

Historical Facts The PCP should ask the parents about feedings. Typically, these patients are infants who have'vomiting' that is not forceful but drools down their front, is bottle fed and routinely takes in large volumes, gulping itdown avidly (also developing aerophagia) and then 'vomits 15-times a day' but has no diarrhea or fever. The PCPshould ask the parents about fussiness and true vomiting, and any cough or previous pneumonias.

Pertinent Physical Examination Findings Upon examination, the child looks entirely well, happy, well fed and wellhydrated. The PCP should check the child's growth over time, listen for evidence of respiratory symptoms and look forsymptoms of esophagitis (see below).

Therapeutics The PCP should try to persuade the mother to reduce the volume of each feed and increase the numberof feeds per day so that total intake per day does not change. A time-honored trick is to add one teaspoon of ricecereal to each ounce of formula, which works for some children but not others. The use of playtex nursers (formula-filled bags that collapse down as the infant suckles) will also decrease aerophagia. Many PCPs will call this a foodallergy and switch formulas; however, formula allergies rarely present with reflux, and as long as the child is growingand does not have recurrent pulmonary symptoms the PCP should wait until the child is older and sitting up. Diet andhydrostatic pressures will make everything all better, no matter what formula the child is having.[24]

Inflammation

Anything that inflames the tube of the GI tract or any of its buds, including esophagitis, gastroenteritis, peptic ulcerdisease, hepatitis, pancreatitis, cholecystitis or appendicitis, may cause vomiting.

Esophagitis In pediatrics, esophagitis is rarely observed, except in the infant with GERD.

Pathophysiology Most of these patients will be infants who have always had 'wet burps' but are now fussy and havetrue, forceful vomiting.

Historical Facts The parent will provide the PCP with a history of frequent 'wet burps' that, similar to all GER, involvesdrooling down the front of the bib, but lately, the child has become fussy and has developed true, nonbilious vomiting.The fussiness appears to improve slightly during feeds, but then quickly recurs. There may be a positional component:"We can't lay him down or he/she cries," or "every time we lay him down he/she cries and arches his back."

Pertinent Physical Examination Findings Most of these children present to PCPs because of their fussiness and thevomiting is discovered in the review of systems, although some children will vomit to the point of a Mallory-Weiss tear,and have blood streaks in their vomitus. The child's stomach is not tender. The PCP should check for guaiac-positivestool, and if this is positive then the PCP should check the child's hematocrit. The child's examination will be otherwisenormal.

Therapeutics A 5 cc dose of Maalox will quiet the child for the first time in days. The PCP should try the patient onranitidine (75 mg/5 cc, 10 mg/kg/day, divided in two doses). All patients need follow-up with their PCP after 3-4

days.[25,26]

Acute Gastroenteritis Acute gastroenteritis (AGE) is the most common cause of vomiting in the pediatric agegroup.[27,28]

Pathophysiology Most cases of gastroenteritis are associated with some degree of vomiting. Rotavirus, the mostcommon known etiology of gastroenteritis, causes vomiting in almost all cases. Bacterial causes of AGE, on the otherhand, are associated with vomiting in less than 50% of cases.

Historical Facts Whatever the etiology, the signs and symptoms of gastroenteritis usually follow a fairly set pattern. Thechild will develop fever, vomiting and (in older children) vague bouts of periumbilical abdominal pain that may be quitesevere. This is followed by diarrhea after a few hours. The fever is usually low-grade, but in shigellosis may reach104°F. The fever peaks within 24 h and then fades over 48 h. The vomiting also peaks quickly and is much improvedwithin 24 h after onset, and is essentially gone within 48 h. Significant vomiting lasting longer than 48 h needs to beevaluated for something other than AGE. Stomach pain is typically worst before the diarrhea begins, and thenbecomes paroxysmal, occurring just before the child has a stool. Diarrhea is worst over the first 2 days, and will last insome diminished form for 4-7 days, depending on severity and etiology.[29,30] The parent should be asked about timecourse, and the physician should try to fit the child into the pattern seen in Figure 12.

Figure 12.

Typical pattern observed in patients with acute gastroenteritis (especially viral illness).

The PCP should also ask the parent about the number of episodes of vomiting and diarrhea over the last 24 h. It is notadvisable to ask the parent about how much is vomited - parents are notoriously unable to quantitate volume of stoolor vomitus. The PCP should also ask about the presence of blood or mucous in the diarrhea, two fairly reliablemarkers of bacterial disease. The PCP should ask about the 'three great signs of dehydration': tears, drool and urineproduction. The three great signs are so named because they are common findings that anyone can use to determinewhether or not a child is dehydrated. Tears and drool and a wet diaper are almost always signs of a well-hydratedbaby. Unfortunately, these signs are not infallible. Infants less than 2 or 3 months of age often do not have tears ordrool, no matter what their fluid status. A dehydrated child sucking on a bottle may have a wet mouth and a well-

hydrated child with fever and excessive mouth breathing may have a dry mouth. However, overall, the three greatsigns are the most accurate indicators of fluid status that parents are capable of using.

Pertinent Physical Examination Findings Upon examination, the most important consideration is the degree ofdehydration; this is often quite difficult. The PCP should look for dry lips: most children drool or suck on a pacifier andtheir lips are glistening with saliva. Dry lips are worrisome. Significant dehydration is observed when the child hassunken eyes: the retro-orbital fat pad shrinks and the eyes retract. Parents may say the eyes 'look dark' because theoverlying orbit casts shadows over the eyes. Poor capillary refill and diminished pulses are observed in children whoare more than 10% dry, but it is often very difficult to decide. Dehydration can be accurately assessed only if a recentweight is available. The findings of increased heart rate, sunken eyes and fontanel, decreased skin turgor, poorcapillary refill and the three signs noted above all vary with fever, age, nutritional status and the experience of theobserver. Assigning numbers - 'percentage dehydration' - is subjective at best. The following calculations work as wellas any:

Less than 5%: lots of diarrhea and vomiting but the child looks well;

More than 10%: quite ill, usually in shock;

7%: everything else.

Many older children will complain of abdominal pain and have some tenderness on examination, all of which resolveswith hydration and an antiemetic (see below). No laboratory tests are needed in the vast majority of cases, except anAccucheck (infants and young children have limited glycogen stores and can quickly become hypoglycemic withprolonged vomiting and starvation) or a set of electrolytes in cases of moderate or severe dehydration. Hypoglycemicchildren are commonly fussy and refuse to drink and, therefore, will often need intravenous fluids and admission to ahospital. Children who refuse repeated attempts of oral fluids, those who appear to be clinically moderately/severelydehydrated, those with a serum Na+ of more than 150 mEq/l or a bicarb of less than 14 mEq/l should be admitted tohospital.

Therapeutics Owing to the self-limited nature of vomiting associated with gastroenteritis, no therapy is usually needed.Worldwide, children with gastroenteritis and dehydration are rehydrated with oral solutions, except in the USA wherethe average child is administered NS after vomiting six times.

The use of antiemetics is in a state of flux. For years they were thought to be contraindicated owing to the frequency ofdystonic reactions, but with the advent of the newer 5HT3 antagonists (especially ondansetron oral dissolving tablets)this has become much less of an issue.[24] Ondansetron oral dissolving tablets can be used at a dose of 2 mg (<5years of age), 4 mg (5-10 years of age) or 8 mg (10 years of age to adulthood), and is very helpful in avoidingintravenous hydration, getting children out of the ED and avoiding hospitalization. Metoclopramide (0.1 mg/kgintravenous, maximum 20 mg), dolasetron (0.35 mg/kg intravenous/intramuscular, maximum 12.5 mg) orpromethazine (as a suppository only, and only in children >2 years of age, at a dose of 0.5 mg/kg/dose) are also usedoccasionally.[31]

With the onset of oral antiemetics for all age groups, a simple protocol of oral rehydration in the outpatient settingmight be to administer the appropriate dose of ondansetron, and then a trial of small volumes of any rehydrationsolution: although Pedialyte is most popular, it contains only 50 mEq/l of sodium, compared to the 90 mEq/l in theWHO formulation (and in the dehydrated state, sodium is absorbed and water passively follows) making Pedialyte lessof a rehydration formula and more of a maintenance solution. Nonetheless, Pedialyte is better than juice or sportsdrinks and more appropriate solutions (WHO formula or Rehydralyte) are not universally available. Pedialyte (andother brands) is the oral solution of choice (by default) in infants and young children. Sport drinks are appropriate forchildren over 4 years of age. The child should be given a dose of ondansetron, wait 30 min, and then 1-2 oz ofPedialyte. If the child tolerates an oz every 15-30 min for 1-2 h, the child should be sent home with one more dose ofondansetron to use if the child has more than three episodes of vomiting at home. Small, frequent volumes ofPedialyte should be continued for the next 24 h, and then the child's diet should be built back up to a full diet in 2-3days. The PCP should try to ensure that the child is on clear liquids for no more than 24 h: a common complication isthat the infant stays on clear liquids for days and continues to have diarrhea (because of the lack of solids in their diet)

and failure to thrive ensues.[25,26]

It is noteworthy that the vomiting associated with the vast majority of patients with gastroenteritis lasts less than 48 h;therefore, if the PCP sends the patient home on antiemetics, the PCP should only administer one or two doses. Again,the natural history of most cases of AGE is that the vomiting should improve within 48 h, and if the child continues toneed antiemetics after this then another cause for their vomiting should be entertained.

It is also healthy to culture stools that are bloody or mucoid. If the child goes to day-care, and if anyone in the familyworks as a food handler, the importance of good hand washing should also be stressed.

Intravenous Rehydration If the child requires hospitalization and intravenous fluids, calculations to replace fluid lossesshould be made (if the child's Na+ level is <160 mEq/l, fluid deficit should be replaced in 24 h) using D5NS with 20mEq KCl/l (giving half the dose over the first 8 h and half of the dose over the next 16 h), as well as to replace on-going losses and give maintenance fluids. All children admitted for dehydration need strict recording of intake andoutputs, and losses are replaced every shift, one-to-one with NS. Usual maintenance fluids are given (4 cc/kg/h for thefirst 10 kg, 2 cc/kg/h for the second 10 kg, and 1 cc/kg/h for every kg beyond 20 kg). If the child is hyperosmolar(usually hypernatremic) replace 1/48th of the deficit hourly over 48 h. Maintenance and on-going losses areunchanged.[32]

Hepatitis

Pathophysiology The most common cause of hepatitis in children is hepatitis A. The exact incidence of the disease isunknown, because hepatitis A often presents in an anicteric form and is misdiagnosed as a case of simplegastroenteritis (i.e., typical symptoms of fever, vomiting, abdominal pain and occasionally diarrhea).[33] Hepatitis A isfound only in humans, and the development of a vaccine in 1978 led to the belief that the disease could be eradicated.Routine hepatitis A vaccination has been instituted over the last few years, and will make this a rare event in the nearfuture. Other pathogens causing hepatitis include hepatitis B, cytomegalovirus, Epstein-Barr virus and many drugs(e.g., valproic acid, acetaminophen, isoniazide and oral contraceptives). If there is any question of an intentionalingestion, the PCP should check acetaminophen levels and ask about suicidal ideation.

Historical Facts Parents should be asked about sick contacts and the color of the child's stool: if the stools are acholicthe PCP should be sure to check liver enzymes. The PCP should also ask the parents about medication uses,especially acetaminophen.

Pertinent Physical Examination Findings Look for icterus (which, again, may not be present) and RUQ tenderness. Apositive Murphy's sign (increased pain with palpation of the RUQ while the patient takes a deep breath) is oftenpresent.

Therapeutics Unless the diagnosis is obvious, vomiting with abdominal pain should lead the PCP to check liverenzymes and perform a lipase test as part of their work-up. The classic 'liver function tests' are actually 'liver damagetests', and will rise with hepatocyte lysis. The PCP should check for liver function, including a serum ammonia andprothrombin time. A hepatitis panel should be checked for the etiology. γ-globulin should be given to contacts, but onlyafter the PCP knows exactly which pathogen is involved.[33] The importance of good hand washing should be stressedto the family (which should be done in any case of diarrhea).

Peptic Ulcer Disease Peptic ulcer disease (PUD) is occasionally observed in older children (preteens and teenagers).PUD is a catch-all diagnosis, and includes GERD, gastritis, a true ulcer and a perforated ulcer.[34]

Pathophysiology For various reasons there is a breakdown of the protective mucous barrier of the stomach, whichallows gastric acid to erode into the muscularis layer. The excess acid lowers LES tone and can cause irritation of thegastric wall and of the duodenum. In children, PUD may present with little prodromal. Steroid or NSAID use arecommon precipitants. Concomitant infection with Helicobacter Pylori is uncommon in children younger than 10 years ofage.[35]

Historical Facts Peptic ulcer disease in pediatrics usually presents with abdominal pain (which may be quite severe)

that awakens the child from sleep. Vomiting is universal. The child may complain of water 'brash': burping gastric acidinto the back of the mouth. Many patients will have had similar symptoms in the past, and will have been successfullytreated with antacids. Others, however, simply have poorly defined upper abdominal pain, which may have no relationto food.

Pertinent Physical Examination Findings Upon examination, the patient typically has isolated epigastric tenderness. Allsuch patients should have a rectal examination (to prove that there is no GI bleed).

Therapeutics The patient will typically improve with a GI cocktail (1 cc/kg Maalox [maximum of 30 cc] and 0.3 cc/kg 2%viscous xylocaine [maximum 10 cc]). If their symptoms improve, no additional work-up is needed. PUD is not usuallystress related in the pediatric age group, as it is in adult. As long as the child is not a runaway, involved with drugs,failing at school or seeing a therapist, among other issues, the PCP should reassure the family that their child is not'stressed out' and start him/her on an H2 blocker - ranitidine (Zantac 4 mg/kg/day given twice daily, maximum of 300mg/day).

The patient should continue follow-up with their PCP for a more detailed work-up if their condition does not improve in2-3 days, sooner if worse. Children with persistent or recurrent symptoms need referral to a gastroenterologist.

Gall Bladder Disease Gall bladder disease is rare in pediatrics.[36]

Pathophysiology Gall bladder disease most commonly occurs in children with an underlying precipitant, such as sicklecell disease, previous intravenous hyperalimentation or pregnancy. There are no risk factors in approximately 30% ofcases. Although it can be observed in all age groups, in children without some sort of predisposition it is most commonin obese adolescent girls. Cholecystitis is defined as 'inflammation of the gall bladder', as evidenced by elevated whiteblood cell count and inflammatory markers (C-reactive protein and erythrocyte sedimentation rate) and a thickened gallbladder wall, with pericholic fluid on ultrasound. This is an indication for hospitalization on antibiotics and a surgicalconsult and emergent or urgent cholecystectomy. Biliary colic occurs when the patient has gall stones and one passesthrough the common bile duct and into the duodenum. This causes severe pain with abrupt onset, which resolvesspontaneously within 3-4 h. Gall stones will be observed on the ultrasound but inflammatory markers are negative. Ifthe pain resolves, this is an indication for elective cholecystectomy.[37]

Historical Facts In pediatric patients, cholecystitis is much more common. The child typically presents withperiumbilical or RUQ abdominal pain and vomiting, and sometimes complains of pain in the right shoulder.Occasionally, a child will have symptoms consistent with passage of a gall stone: abrupt, excruciating RUQ pain andvomiting.

Pertinent Physical Examination Findings On examination, the child will have RUQ tenderness and a low-grade fever iscommon. There may be a positive Murphy's sign: the child has increased pain with inspiration when the fingers arewrapped around the right costal margin.

Therapeutics Laboratory tests and physical examination have poor sensitivity and specificity for gall bladder disease,and if the clinical presentation is worrisome, examination should proceed quickly to an ultrasound. If the ultrasound isnormal, the patient should be placed on an H2 blocker and the PCP should arrange for outpatient follow-up - aradionucleotide scan (HIDA scan) may be indicated.

Pancreatitis Pancreatitis is very rare in pediatrics.

Pathophysiology In the pediatric age group, pancreatitis is most commonly idiopathic, but can be caused by trauma,drugs (e.g., diuretics, trimethoprim-sulfa or H2 blockers), gall stones or infections (e.g., mumps or varicella).

Historical Facts These children will present with epigastric pain and vomiting, and often a history as noted above.

Pertinent Physical Examination Findings Upon examination, these are miserable, dehydrated patients, with significantpain and protracted vomiting, who have a very tender epigastrium and decreased bowel sounds. Diabetes maycoexist.

Therapeutics Again, patients with abdominal pain and vomiting without an obvious etiology should have liver functiontests and a serum lipase. Lipase is usually three-times that of normal. These children are usually dehydrated and needvolume resuscitation, control of their pain and nausea and a CT scan of the abdomen. All such patients needhospitalization. A RUQ ultrasound and endoscopy are part of the work-up. Management involves bowel rest and case-specific therapy.[38,39]

Appendicitis Appendicitis begins as an obstructive lesion that causes an inflammatory state. Details can be found inprevious sections of this review.

CNS Disease

There are four relatively common CNS causes for vomiting in pediatrics: concussion/postconcussion syndrome,increased intracranial pressure (ICP), migraine headache and viral meningitis.

Concussion/Postconcussion Syndrome

Pathophysiology Concussion is defined as "a trauma-induced alteration in mental status that may or may not involveloss of consciousness. Confusion and amnesia are hallmarks of concussion".[40] A concussion occurs when anacceleration/deceleration mechanism causes a shearing stress applied to the brain between the brain stem and thecerebral cortices. With a mild injury, axons become dysfunctional but are not damaged. Some change in mentationoccurs, which is termed as concussion. When the shearing force is severe, axons are lysed and do not heal, and thepatient is then said to be suffering from a diffuse axonal injury.[41] Patients with a concussion have symptoms that last,by definition, less than 6 h; longer than this the patient is assumed to have had a diffuse axonal injury. Diffuse axonalinjury may be mild, moderate or severe, with a variable degree of morbidity and mortality.

Historical Facts Memory loss and the inability to form new memories are the hallmarks of a concussion. The child willnot remember being struck or the few moments leading to the injury (retrograde amnesia) or the period of timeimmediately after the blow (anterograde amnesia). Occasionally, the child will have problems forming memories andwill repeatedly ask: "What happened to me?" and appear to be quite agitated, only to calm down when reassured, untilthe process starts again 5 min later. A younger child will simply cry uncontrollably for an excessive length of time,inconsistent with the injury. Vomiting is very common.

In all cases of head trauma, PCPs should ask the parent: "Did the child cry immediately after he/she was sick, or wasthe child unresponsive for a period?" and, "Did the child act normally after the injury or did the child cry excessively;were you unable to console him/her?" The PCP should ask the child: "Do you remember falling? Hitting the ground?Who was the first person to talk with you? What did he/she say? Did you get up by yourself or did somebody helpyou?"

Pertinent Physical Examination Findings A Glasgow Coma Scale (GCS) score should be assigned () and a completeneurological examination preformed. PCPs should check for blood behind the auricle, or blood and/or CSF behind thetympanic membrane or dripping from the external auditory canal. PCPs should also check for anisochoria and look fora hematoma of the scalp.

Table 1. Glasgow Coma Score/Pediatric Glasgow Coma Score.

Scale Infant aged <1 year Child aged 1-4 years Age 4 years to adulthood

Eyes

4 Open Open Open

3 Open to voice Open to voice Open to voice

2 Open to pain Open to pain Open to pain

1 No response No response No response

Verbal

5 Coos, babbles Oriented, speaks, interacts and social Oriented and alert

4 Irritable cry, consolable Confused speech, disoriented and consolable Disoriented

3 Cries persistently to pain Inappropriate words and inconsolable Nonsensical speech

2 Moans to pain Incomprehensible and agitated Moans and unintelligible


Motor

6 Normal, spontaneous movement Normal, spontaneous movement Follows commands

5 Withdraws to touch Localizes pain Localizes pain

4 Withdraws to pain Withdraws to pain Withdraws to pain

3 Decorticate flexion Decorticate flexion Decorticate flexion

2 Decerebrate extension Decerebrate extension Decerebrate extension


Therapeutics Generally, children with a history consistent with a concussion should have a CT scan of the head. If thisis normal, the majority of patients can be managed as outpatients. There are a number of recommendations as towhen the pediatric athlete can return to sports after a concussion.[42]

Postconcussion Syndrome

Pathophysiology Although a concussion, by definition, lasts less than 6 h, approximately 15% of children will sufferfrom a postconcussion syndrome, which consists of persistent headache, 'cloudy' mentation, nausea with occasionalvomiting and personality changes that can run from 'being moody' to school failure, to (in adults) losing one's job ordivorce.[43]

Historical Facts The PCP should ask the parents about recent head trauma, as well as the psychosocial issues listedpreviously.

Pertinent Physical Examination Findings There should be little in the way of physical examination findings.

Therapeutics The parents should be warned about postconcussion syndrome when the diagnosis of concussion ismade, and should be told to seek help from their PCP if symptoms are persistent.

Increased Intracranial Pressure There are four basic types of increased ICP: hydrocephalous (Figure 13), cerebraledema, intracranial bleeding and tumors. All are associated with vomiting, especially at night (when hydrostaticpressures come into play).

Figure 13.

Hydrocephalous.

Reproduced with permission from Kenneth Ott, MD: Neurosurgical Medical clinic, Inc., San Diego, CA, USA.

Pathophysiology Since the skull functions as a rigid container, increases in the volume of any of the brain's threecompartments - blood, CSF or parenchyma - will result in increased ICP. In addition to this, any mass effect - tumor orblood - within the skull will increase ICP. Hydrocephalus may be due to obstruction of the flow of CSF from theventricles or an inability to absorb it in the arachnoid granulations. The ventricles swell and ICP increases. The majorityof these children were premature and had intraventricular bleeding and now have ventricular-peritoneal shunts inplace.[44] Cerebral edema develops after some asphyxic or anoxic event (Figure 14). Approximately four of the fivemost common pediatric brain tumors are cerebellar and, therefore, typically present with headache and vomiting,especially at night or early in the morning (Figure 15). Ataxia may be present.

Figure 14.

Cerebral edema.


Figure 15.

Epidural hematoma.


Head trauma with vomiting should always raise the possibility of intracranial hemorrhage. Increased blood volumewithin the skull can be broken down into four types: epidural, subdural, subarachnoid and intraparenchymal (Figures15-18).[45,46] They may be indistinguishable in their presentation: a severe blow to the head followed by an abruptchange in mentation. The vast majority of children that present will be obviously sick. The clinical presentation of thefour injuries listed above are interchangeble except for some children with epidural bleeds. Approximately 20% ofchildren with an epidural hematoma will present with a lucent period: a blow occurs that causes a concussion and aninjury to the middle meningeal artery. The child wakes up from their concussion, only to later slip into unconsciousnessfrom their enlarging epidural hematoma and subsequent increase in ICP.

Figure 16.

Subdural hemorrhage.


Figure 17.

Subarachnoid hemorrhage.


Figure 18.

Intracerebral contusion.


Historical Facts Although there are some questions that are similar to all of the diagnoses above (vomiting, headacheand change in mentation), many historical points are specific to the pathophysiology involved. The longer a ventricular-peritoneal shunt has been in place, the less likely it is to become dysfunctional or become infected. Cerebral edema iscommon in patients with near-drowning or strangulation, and is rarely observed in diabetic ketoacidosis (DKA). Tumorsclassically present in the early morning, after the child has been lying flat during the night, and their tumor swells andobstructs the fourth ventricle, causing headache and vomiting. The child may have developed 'clumsiness', or trueataxia. The different types of intracranial hemorrhage are usually only determined after the CT scan is carried out.

Pertinent Physical Examination Findings Similar to concussion, this is specific to the mechanism of the problem. ThePCP should check the head circumference (if the patient is younger than 2 years of age), and try to catch a glimpse ofthe fundus and disc, which is not easy in any pediatric patient. The PCP should then watch the child walk and look forataxia.

Therapeutics Primary-care providers are advised to have a low threshold for getting a CT scan of the head. Although

much better resolution of the cerebellum is achieved with MRI, evidence of acute bleeding, increased ICP and/orhydrocephalous is usually evident on a noncontrast CT scan. Management follows accordingly. Some children withshunts have a normal CT scan and a normal shunt series. In other words, when worried about shunt malfunction, thePCP should always call a neurosurgeon prior to discharge.[47]

Migraine Headaches Migraine headaches (MHAs) are so often associated with vomiting, and the lay populationsometimes refer to them as 'sick' headaches. PCPs should be advised to be careful when obtaining a history ofmigraine headaches in a patient: many people consider any severe headache a 'migraine'.

Pathophysiology The exact etiology of MHA is in evolution. At one time it was thought that vasoconstriction occurs,which leads to distal ischemia (with the subsequent 'aura'), which then led to an area of vasodilatation and aconcomitant 'throbbing' headache. Now it is thought to have more to do with serotonin release from the brainstem andspread to other parts of the brain.[48] Nonmigraine headaches are not uncommon in children as young as 3 years ofage, and are usually associated with viral illness or fever.[49] There appears to be an increase in the incidence ofheadaches that occur at approximately 10 years of age, which is thought to be due to complete aeration of thesinuses, and the child's first 'sinus' headache. Strep throat commonly causes headache.

Historical Facts Pediatric MHAs must have three of the following seven criteria: abdominal pain, nausea or vomiting,throbbing headache, unilateral location, associated aura (usually preceding the headache), relief following sleep or apositive family history.[50]

Migraine headaches are divided into 'classic' (those associated with an aura, which is usually visual but may besensory or motor) and 'common' (those without an aura). There are also many pediatric 'migraine variants', includingcyclic vomiting: recurrent, prolonged bouts of vomiting lasting 72 h or less, without any diagnostic markers or historicalfacts, pertinent physical examination findings or laboratory tests. The first few episodes are commonly misdiagnosed,but then the pattern becomes clear and management with intravenous fluids and antiemetics (and sometimeshospitalization) falls into place. Cyclic vomiting, 'abdominal migraine' and episodes of ataxia can all be atypicalmigraine, and present with little headache, but, as the child ages, typical MHA commonly develops.[51] Patients withmigraine typically get better with sleep; headache that awakens the child from sleep is unusual.

Pertinent Physical Examination Findings These findings may be entirely normal, unless there is an aura present. Thepatient may be extremely sensitive to light and/or sound. The PCP should be sure that they are not missing a case ofviral meningitis: there is no nuchal rigidity in MHA, and fever is rare. The PCP should look for evidence of strep throat.

Therapeutics A CT scan of the head is indicated at some time in anyone with MHAs; PCPs should have a lowthreshold for carrying out CT scans at the time of presentation. There are more than a dozen drugs used for MHA, butthe vast majority of children do well with simple analgesic NSAIDs for mild attacks, or, if the headache is severe,intravenous prochlorperazine (0.1-0.15 mg/kg intravenous over 15 min, maximum of 10 mg). It is noteworthy that theuse of intravenous antiemetics is sometimes associated with a dystonic reaction, and many clinicians also routinelyadminister diphenhydramine (1-2 mg/kg slow intravenous).[52] All children should have a referral to a pediatricneurologist in follow-up.

Viral Meningitis

Pathophysiology Viral meningitis is typically a summertime disease, caused by arboviruses (mosquito borne) orenteroviruses (fecal-oral transmission). It may occur in epidemics: 456 cases were documented in 3 months onesummer in Cincinnati, OH, USA in 1978.[53] There is something about viral meningitis itself that makes the child vomit,because it occurs even if the ICP is normal, and children with bacterial meningitis usually do not have much in the wayof emesis.

Historical Facts The child typically presents with fever, headache, photophobia and vomiting.

Pertinent Physical Examination Findings The child usually has fever and light hurts their eyes. The child may beslightly dehydrated due to protracted vomiting. Meningismus is common, but may be missing. A viral exanthem may bepresent. Change in sensorium is uncommon.

Therapeutics All children with symptoms consistent with meningitis need a lumbar puncture (even those presentingduring an epidemic of viral disease) to rule out the possibility of a bacterial infection. Although white cell counts of morethan 1000 cells/high-power field and CSF glucose values less than 30 mg/dl can be observed in viral meningitis, anyequivocal results (cells: >250; glucose: <50; protein: >70) should be assumed to be bacterial, and treated withantibiotics until cultures are negative for 72 h.[54] More typical cases may be managed as an outpatient, with paincontrol and antiemetics.

Pulmonary Problems

Pathophysiology Pulmonary problems are classically observed in pertussis (which is rare) and in asthma (which iscommon). Some children with asthma have no wheezing, just a cough (cough-variant asthma).[55] Children will coughup a fleck of sputum that initiates a gag response, and the child will have an episode of post-tussive emesis. Inaddition, children do not expectorate: they swallow whatever they cough up. This leads to nausea, decreased appetiteand occasional vomiting. The vomitus in both situations is thick, mucoid and stringy. Adults with waning immunity arethe reservoir of pertussis: as much as 15% of adults with a cough for longer than 2 weeks have grown outpertussis.[56]

Historical Facts The PCP should ask if the child has asthma. Some may have a cough without wheezing and neverbeen diagnosed as having asthma. The PCP should ask about any coughing, whether the night is worse than the dayand any associated wheezing. Many children with mild asthma will have a prolonged, nagging cough for a week or twoafter viral illnesses, while their classmates cough for just 2-3 days. The PCP should also ask if the infant has ever hadcolor change or syncope with these spells (more typical of pertussis), and ask if there has been any adult contact witha recent persistent cough.

Pertinent Physical Examination Findings The PCP should check for wheezing and ronchi on examination, and aprolonged inspiratory:expiratory ratio. The child may have a significant cough during the examination. Sometimes theexamination is entirely normal, and the diagnosis is made by history alone.

Therapeutics The PCP should try a peak flow before and after an albuterol nebulizer (physicians should note to usean appropriate dose of albuterol: 2.5 mg if the child is younger than 5 years of age, and 5 mg if the child is older than 5years). If this appears to help, the PCP should send the patient home on an albuterol metered dose inhaler and aspacer. If symptoms are severe, or continues for more than a week, add prednisone (2 mg/kg/day for 5 days) ordexamethasone 0.6 mg/kg (maximum of 18 mg) immediately;[57] administer another dose in 24 h if necessary.

It is noteworthy that asthmatics are commonly underdosed on their albuterol. The PCP should always use a spacer.The patient should puff twice, breathe for a few minutes, wait for a few minutes, then repeat. This is one treatment;repeat this four- to six-times per day for 5 days. PCPs should never prescribe albuterol on an every 4-6 h basis. It isessentially impossible to overdose on albuterol, and the one thing that should be avoided is having a child who is shortof breath but the mother thinks she cannot give another treatment because "it has not been 4 h yet".[101]

Renal Disease

Pathophysiology There are three renal problems that may present with vomiting: acute or chronic renal failure,urinary tract infections in neonates and pyelonephritis in older children and adults, and kidney stones.

Renal Failure

Pathophysiology Vomiting is due to the metabolic derangements typical with renal failure. Uremia and acidosis willboth cause vomiting. Acute renal failure is usually difficult to miss, with elevated blood pressure and tea-colored urine,and is typically caused by poststreptococcal acute glomerulonephritis, hemolytic uremic syndrome or Henoch-Schoenlien Purpura. Chronic renal failure may be much more occult, presenting with growth failure or hypertension, ora number of nonspecific complaints, including back pain, fatigue and weight loss (or gain from edema).[58]

Historical Facts The PCP should ask the parents about vomiting, weight gain, headache, urine output (volume andcolor), recent strep infections and a family history of renal disease, as well as about medications.

Pertinent Physical Examination Findings The PCP should check blood pressure, fundi, edema and growth curves. Anelectrocardiogram (ECG) should be ordered and the PCP should look for evidence of hypertension and hyperkalemia.A set of electrolytes and a urinalysis (UA) should be obtained, looking for proteinuria plus hematuria, and red cell/whitecell casts. A throat culture should be carried out, and an acute antistreptolysin 'O' titer should be drawn. Completeblood count should be checked for evidence of microangiopathic hemolytic anemia, and a complete examination(including guaiac stool) should be carried out to check for Henoch-Schoenlien Purpura.

Therapeutics Acutely, the PCP should make sure the patient has a normal potassium and ECG. Most of the time thehypertension need not be treated, but if there is a true hypertensive emergency (with end-organ damage, such aschange in mentation or ECG changes), hypertension should be treated with nitroprusside or labetolol, and anephrologist should be involved early on.

Pyelonephritis

Pathogenesis This is an infection of the parenchyma of the kidney itself, usually caused by coliforms (Escherichia coliis most common). Infants with fever and an infected urine may have cystitis or pyelonephritis - it is impossible todetermine at the time of presentation: PCPs should assume that all patients have pyelonephritis.[59] For unclearreasons, neonates with urinary tract infections often develop a direct hyperbilirubinemia.[60]

Historical Facts The PCP should ask about back pain, which develops slowly. Vomiting and fever are common. Theremay or may not be symptoms of cystitis, so the PCP should ask about dysuria and frequency.

Pertinent Physical Examination Findings These patients look miserable, febrile and clutch their back. They havemarked costovertebral angle tenderness to fist percussion. The PCP should look for jaundice in infants.

Therapeutics Pyelonephritis in children can be treated orally (either with cefixime or amoxicillin clavulanate),[61] but thevomiting child will need to be hospitalized. Blood cultures are rarely positive. The PCP should give a dose ofceftriaxone (50 mg/kg, maximum of 1 g) prior to transferring to the floor.

It is noteworthy that clean-catch UA is considered accurate in continent children. In other words, a child who is nottoilet trained should have a catheterized (or suprapubic) UA.

Kidney Stones Kidney stones are uncommon in children, and any child with a kidney stones needs to be worked-upfor metabolic disorder, especially cystinuria.

Historical Facts Kidneys stones are another in a list of relatively unsubtle causes of vomiting. Excruciating, colickyflank pain develops abruptly, supposedly worse than anything normal people can imagine, associated with blood in theurine (in 85% of the time) and vomiting. The pain usually starts at the costovertebral junction, but may radiate anteriortoward the lower quadrants of the abdomen and into the testes/labia. A positive family history is common.

Pertinent Physical Examination Findings Upon examination, these patients are writhing about on the bed or walkingaround looking for a comfortable position. Palpation does not reproduce the pain of their chief complaint.

Therapeutics Pain control with a narcotic is paramount, and an NSAID will relax the ureter and facilitate passage of thestone. Antiemetics and intravenous fluid are sometimes needed, but there is no need to 'flush' the stone out. Unlessthis is typical of previous stones, all patients need a noncontrast CT scan of the abdomen in order to confirm thediagnosis and help the urologist. A stone high up near the uretero-pelvic junction may need lithotripsy or a stent; thoseat the uretero-vesicular junction rarely do. The same applies to size: a stone 4 mm in size or smaller almost alwayspasses, and those larger than 6 mm rarely pass. The PCP should make sure there is no concomitant infection; suchpatients should be hospitalized. If the pain can be controlled, the patient can be sent home with narcotics and anNSAID. The patient should strain their urine and try to catch the stone; urologists will need it in order to determineetiology and long-term management. All these children should also see a pediatric nephrologist.[62]

Endocrine/Metabolic Disorders

There are three endocrine problems that commonly cause vomiting: DKA[63,64] and congenital adrenal hyperplasia

and inborn errors of metabolism. The last two are rarely observed, as they are now part of the newborn metabolicscreen.

Diabetic Ketoacidosis

Pathophysiology Diabetic ketoacidosis is typically observed in new-onset diabetes, in adolescents who arenoncompliant with their insulin or children who are sick whose parents do not give them their insulin "because they arenot eating much". The details of DKA is beyond the scope of this article, but, simplistically, it revolves around lack ofinsulin and the build-up of glucose and ketone bodies, which function as osmotic diuretics, leading to a child whopresents with vomiting, both shock and dehydration, acidosis and a hyperosmolar state. This hyperosmolarity isthought to be the cause of the cerebral edema observed in some children with DKA.[65,66]

Historical Facts The PCP should ask about usual insulin needs, diet and recent blood sugars, and try to seek out anetiology for their DKA: infection is not as common as it is in adults (most common is noncompliance).

Pertinent Physical Examination Findings The PCP should assess the degree of dehydration, look for signs of infectionand check mental status. A GCS score should be assigned at the time of presentation.

Therapeutics The mantra for the fluid management of DKA: 'correct their hypovolemia and shock now, correct theirdehydration later'.

These children are in a hyperosmolar state, both intracellularly and extracellularly. Correction of the extracellulardehydration and hyperosmolarity is easy. While correcting the dehydrated, extracellular state, fluid will cross the blood-brain barrier quickly and the brain may absorb free fluid and cerebral edema sets in, which can be fatal. Therefore, inthe acute-care setting, sufficient NS should be provided to correct the child's hypovolemia and shock, 10 cc/kg at atime, and then the child should be given fluids to correct their dehydration over 48 h in the intensive care unit, replacing1/48th of the deficit each hour. Assessing the degree of hypovolemia is difficult: anti-insulin hormones, such asadrenaline, are high so it is difficult to rely on heart rate, and they often have a metabolic encephalopathy so theirmentation may not improve after their intravascular volume improves. The PCP should ensure that the child hasperipheral pulses, adequate capillary refill and an appropriate blood pressure (for age) and then get the child into theintensive care unit. At the time of arrival, an Accucheck blood glucose, blood chemistries, complete blood count and avenous blood gas (as accurate a measurement of serum pH as anarterial gas) should be obtained. The child should beresuscitated (i.e., get out of shock) with NS. A total of 20 mEq KCL/l intravenous fluids should be added if the blood K+

level is less than 5.0 mEq/l. Most clinicians also test serum ketones, but these can be misleading. If the blood sugar ishigher than 250 mg/dl and pH is less than 7.30, a drip of insulin at 0.1 u/k/h should be started. The PCP should besure to check the child's glucose again before starting insulin, because the dilutional effect of the intravenous bolus(es)is sometimes enough to bring the blood sugar down to approximately 250 mg/dl. If blood glucose is lower than 300mg/dl, glucose should be added to the intravenous fluids (typically D5NS). While on a drip, Accucheck should beobtained every 30 min. If the blood glucose is lower than 250 mg/dl, the drip should be cut in half until the child gets tothe intensive care unit. Generally speaking, a child should never be given bicarb.

Drugs

There are many drugs with some degree of GI side effects, but vomiting is relatively rare.

Pathophysiology Only a few commonly used drugs cause vomiting when given in appropriate doses - codeine,erythromycin, some birth control pills, theophylline and, for some unknown reason, some of the proton pump inhibitors.These symptoms are always worse when taken on an empty stomach. Many other drugs will make the patient vomitwhen overdosed - digoxin, aspirin, iron and acetaminophen to name a few.[67]

Historical Facts The PCP should always ask if any drugs were taken and what drugs are in the house (even if thefamily is 'certain' that the child could not have become involved with drugs).

Pertinent Physical Examination Findings There are toxidromes that point to specific ingestions, such as narcotics(miosis, somnolence and respiratory depression), sympathomimetic (mydriasis, tachycardia and diaphoresis) andanticholenergic, but many present with vomiting and somnolence and little else.

Therapeutics The PCP should decide if the injestion is potentially significant. Poison Control should be called in 100%of patients. In general, any significant ingestion should be treated the same way: all patients should have a urine drugscreen, acetaminophen level, aspirin level, ECG and electrolytes tests (and a pregnancy test if applicable). Lavage isindicated if the ingestion occurred less than 60 min prior to arrival, is potentially dangerous and the child is awake andalert. Activated charcoal (with sorbitol) should be given (1 gm/kg, maximum of 50 g) to these patients if the child iscompliant. In general, if the PCP needs to place an nasogastric tube, then the charcoal should be omitted entirely.Somnolent patients are different; they will need to be intubated and their airway controlled prior to lavage oradministration of charcoal.[68]

Psychological

There are two well-defined clinical psychological entities that are associated with vomiting: anorexia nervosa andbulimia.[69,70]

Pathophysiology Both anorexia nervosa and bulimia have a very similar psychological basis, which revolves aroundproblems with dependence and individuation. Often the parents are excessively attached and dependent upon theiroffspring (women more common than men in a ratio of 10:1) than is appropriate. This functions to increase the child'sdependence on his/her parents, and retard their efforts at individuation. The parents often lack confidence in theirparenting skills, which is compounded by their child's hyperemesis. Anorexics are very thin; bulimics may be almostchubby.

Historical Facts Most of these patients are adolescent females. The PCP should ask about body image (mostpatients, however thin they might be, think they are fat and want to be thinner). PCPs should ask about diet: many areon very restricted diets. Excessive exercise is common: 300 sit-ups at a time. The patient should also be questionedabout 'purging' and use of laxative.

Pertinent Physical Examination Findings Most of these patients are very thin and many have delayed menarche.The PCP should check for evidence of bruxism, a side effect of regurgitation of stomach acid. Carotinemia is common.

Therapeutics Electrolytes and liver function tests should be checked. All such patients should be managed inconjunction with a psychotherapist: anorexia nervosa has a 1-10% mortality.[71]

Streptococcal Pharyngitis

For unclear reasons, strep throat may cause significant vomiting.[72]

Historical Facts The PCP should ask the following questions:

What is the child's age? Streptococcal pharyngitis (caused by group A b-hemolytic streptococci [GABHS]) rarelyoccurs in children younger than 2 years of age, and is not observed in children younger than 1 year of age;

Does the child have a fever? Almost all children with a strep throat will have had a fever higher than 101°F atsome time during the illness, although the child might be afebrile at the time of examination;

Does the child have a rash? Scarlet fever occurs only in GABHS infections;

Is the child suffering from headache, abdominal pain and vomiting? All are very common;

Is the child sick during the months of November through to May? Strep infections occur during the school year,and the incidence will vary on a weekly basis: six this week, two next week, none for 3 weeks, then three thenext week and five the following week;

What symptoms does the child present? No viral symptoms, typically cough, conjunctivitis, a viral rash ordiarrhea are common;

Does the child have classic presentation? Streptococcal infection causes sore throat, fever, anterior cervicaladenitis and a bright red pharyngeal mucosa, but exudates are rare in children younger than 8 years of age.

Pertinent Physical Examination Findings Again, exudates are uncommon in children younger than 8 years of age,and so small exudates lying on the crypts of the tonsils in younger children are almost always a marker for viraldisease. Oral ulcers or gingivitis also indicate viral disease. In patients with strep throat, the oral mucosa is bright red,and petechiae on the palate are common. The patient has a muffled voice. It is noteworthy that the use of clinicalcriteria to diagnose strep throat has been debated for decades, but the fact is that there has never been any study thatdemonstrated that clinical criteria alone is much better than flipping a coin. The most commonly used clinical criteria inadults are the 'Centor Criteria',[73] republished by the Centers for Disease Control (CDC) in 2001: fever, exudativetonsillitis, anterior cervical adenitis and lack of cough means the patient has GABHS pharyngitis.[74] However, thisscale is not applicable to patients younger than 12 years of age. The CDC recommends treating with four points,getting a rapid strep test or throat culture for those with two to three points, and diagnosing the patients with one orzero points as having viral disease and doing no testing.

Although clinical diagnosis is difficult, diagnosing GABHS pharyngitis with laboratory tests also has its problems.Technique is very important: a good swab commonly causes gagging of the child. PCPs should recognize that rapiddiagnostic tests are highly specific but sensitivity is (on average) approximately 75%; all negative tests should have athroat culture carried out as a back-up. Culture is sensitive and specific, but takes 24-48 h, and neither proves aninfection: infection can only be proven by antibody titers, which are of little use in the acute-care setting. Both tests willbe positive in streptococcal carriers and, because as many as 20% of children are carriers during the winter, there is ahigh risk of infection. Finally, there are few rheumatogenic strains prevalent now, and so missing a case of GABHSinfection in not the potential catastrophe it used to be. However, the Red Book[75] says that the diagnosis of strepthroat in children should be confirmed by either throat culture or rapid diagnostic test prior to treatment. However, onthe other hand, diagnostic tests should not be carried out without screening for viral disease, for fear of treating astreptococcal carrier.

There is a high risk of confusion, but the diagnosis of GABHS can be summarized as follows: a diagnostic test shouldbe carried out if the patient appears to have strep throat on clinical grounds, but if the preponderance of the history andphysical examination points to viral disease, this should be diagnosed but not acted upon.

Therapeutics If the PCP decides to treat the infection, phenoxymethyl penicillin 250 mg twice daily (in children) or 500mg twice daily (in teens and adults) should be used. Amoxicillin in the same dose can be given once per day. Theparent should always be offered benzathine penicillin: the dose is 600,000 units intramuscularly (for children <30 kg)and 1.2 million units intramuscularly (for patients >30 kg). Single dosing is very convenient.

Pregnancy

Pathophysiology Women who are pregnant often vomit, for unclear reasons, but morning sickness is very common.Its incidence usually decreases markedly by the end of the first trimester, but hyperemesis graviderum is occasionallydiagnosed at any time.[76]

Historical Facts First, the PCP should decide if this is due to the pregnancy. Vomiting may be the presentingsymptom of a pregnancy; therefore, the PCP should be quick to check a urine pregnancy test in any female of child-bearing age who presents with vomiting, and vomiting in the pregnant woman is not always due to hormonalimbalance: PCPs should consider the differential diagnosis and look for the diabetic or the woman with AGE orpyelonephritis. Stomach pain is not usually observed with morning sickness or hyperemesis graviderum, and suchpatients need a work-up.

Pertinent Physical Examination Findings These patients can be miserable and dehydrated. Again, PCPs should notassume hyperemesis: they should look for other etiologies.

Therapeutics Any of the usual antiemetics are commonly used, but metoclopramide (10 mg intravenous) andondansetron (4-8 mg intravenous) are the only 'category B' drugs. UAs should be repeated and follow the patient'sketonuria; if the patient is tolerating oral fluids and their urinary ketones are improving they can be discharged on anoral antiemetic with 24-h follow-up.

Stress

Many children will vomit following stress of any sort. This may be quite severe (children with sepsis or shock of anycause may vomit because of an ileus) but, much more commonly, it is relatively minor: children with otitis media mayvomit once or twice, as might a child who is crying for any reason. This is sometimes quite confusing: children whobump their heads, without a concussion or intracranial injury, will often vomit a couple times. But how can you be surethe vomiting is due to stress? Vomiting associated with minor stress is never prolonged or protracted - rarely is theremore than two separate episodes - and has no other associated symptoms: diarrhea and abdominal pain, amongothers. However, unless the diagnosis is obvious, the clinician is forced to go through the differential of vomiting aslisted above and see if anything fits. It always makes the PCP worry, sometimes to the point of a CT scan. The PCPshould never stop worrying, but should recognize that this is common and usually benign.

Conclusion: Case Report

The patient in the case report had a small inguinal hernia that was mistaken for a lymph node until the child hadrepeated episodes of vomiting, which increased intra-abdominal pressure, increasing the size of the mass and makingthe diagnosis of inguinal hernia obvious. Management proceeded accordingly.

Future Perspective

Vomiting will be with us forever. It is up to the clinician who is face-to-face with the child to determine a diagnosis andtherapeutic plan. The use of the 5HT3 antagonists, especially the dissolving forms, have made antiemetic treatment inchildren safer and more effective. As these drugs are replaced by cheaper, generic forms, more children will bemanaged as outpatients, to the benefit of all.

Sidebar: Executive SummaryExecutive Summary

The most common causes of vomiting are gastrointestinal in origin, and these can be easily arranged bythinking of the gastrointestinal tract as a tube with four buds: anything that inflames or obstructs the tube or anyof its buds will cause vomiting.

However, there are also nine other categories of vomiting, and it may be useful to remember that some childrenwill vomit suddenly with no obvious reason.

Vomiting in the first month of life should always to be taken seriously, especially bilious vomiting.

References

1. Waltzman ML: Management of esophageal coins. Curr. Opin. Pediatric 18, 571-574 (2006).

2. Uyemura MC: Foreign body ingestion in children. Am. Fam. Physician 72, 287-291 (2005).

3. Arms JL, Mackenberg-Mohn MD, Bowen MV et al.: Safety and efficacy of a protocol using bougienage orendoscopy for the management of coins acutely lodged in the esophagus: a large case study. Ann. Emerg.Med. 51, 367-372 (2008).

4. Schwartz MZ: Hypertrophic pyloric stenosis. In: Pediatric Surgery 6th Edition. Grosfeld JL, O'Neill JA, CoranAG, Fonkalsrud EW (Eds). Mosby Elsevier, PA, USA 1215-1224 (2006).

5. Honein MA, Paulozzi LJ, Himelright IM et al.: Infantile hypertrophic pyloric stenosis after pertussis prophylaxiswith erythromycin: a case review and cohort study. Lancet 354, 2101-2105 (1999).

6. Papadakis K, Chen EA, Luks FI, Lesin MS, Wesselhoett CW Jr, DeLuca FW: The changing presentation ofpyloric stenosis. Am. J. Emerg. Med. 17, 67-69 (1999).

• Study demonstrating how the presentation of pyloric stenosis is changing over the years.

7. Steven IM, Allen TH, Sweney DB: Congenital hypertrophic pyloric stenosis: the anaethetist's view. Anaesth.Intensive Care 1, 544 (1973).

8. Ein SH, Dane A: Intussusception. In: Pediatric Surgery 6th Edition. Grosfeld JL, O'Neill JA, Coran AG,Fonkalsrud EW (Eds). Mosby Elsevier, PA, USA 1313-1341 (2006).

9. Wyllie R: Intussusception. In: Nelson's Textbook of Pediatrics, 17th Edition. Berhman RE, Kliegman RM,Jenson HB (Eds). Saunders, PA, USA 1242-1243 (2004).

10. McCollough M, Sharieff GQ: Abdominal pain in children. Pediatr. Clin. North Am. 53, 118-121 (2006).

• Good review of abdominal pain in children.

11. Blakelock RT, Beasley SW: The Clinical implications of non-idiopathic intussusception. Pediatr. Surg. Int. 14,163-167 (1998).

12. Aiken JJ: Inguinal hernias. In: Nelson's Textbook of Pediatrics, 17th Edition. Berhman RE, Kliegman RM,Jenson HB (Eds). Saunders, PA, USA 1293-1297 (2004).


14. Glick PL, Boulanger SC: Inguinal hernias and hydrocoeles. In: Pediatric Surgery 6th Edition. Grosfeld JL, O'NeillJA, Coran AG, Fonkalsrud EW (Eds). Mosby Elsevier, PA, USA 1173-1192 (2006).

15. Dunn JC: Appendicitis. In: Pediatric Surgery 6th Edition. Grosfeld JL, O'Neill JA, Coran AG, Fonkalsrud EW(Eds). Mosby Elsevier, PA, USA 1501-1513 (2006).


17. D'Agostino J: Common abdominal emergencies in children. Emer. Med. Clinic North Am. 20, 139-53 (2002).

18. Alloo J, Gerstle T, Ein SH: Appendicitis in children less than 3 years of age: a 28 year review. Pediatric Surg.Int. 19, 777 (2004).

19. Brener DJ: Estimating cancer risks from pediatrics CT: going from the qualitative to the quantitative. Pediatr.Radiol. 32, 228 (2002).

• One of the first articles that discussed cancer risk following x-ray exposure associated with CT scans.

20. Jones K, Peña AA, Dunn EL, Nadalo L, Mangram AJ: Are negative appendectomies still acceptable. Am. J.Surg. 188, 748-755 (2004).

21. Smith DS: Disorders of intestinal rotation and fixation. In: Pediatric Surgery 6th Edition. Grosfeld JL, O'Neill JA,Coran AG, Fonkalsrud EW (Eds). Mosby Elsevier, PA, USA 1347-1348, 1352 (2006).

22. Okada PJ, Hicks B: Neonatal surgical emergencies. Clin. Pediatr. Emerg. Med. 3, 3-13 (2002).

23. Kimura K: Bilious vomiting in the newborn: rapid diagnosis of intestinal obstruction. Am. Fam. Phys. 61, 2791-2798 (2000).

24. Vandenplas Y: Gastroesophageal reflux. In: Pediatric Gastrointestinal and Liver Disease 3rd Edition. Wyllie R,Hyams JS (Eds). Saunders Elsevier, PA, USA 305-310 (2006).

25. Orenstein S, Peters J, Khan S, Youseff N, Hussain SZ: The esophagus. In: Nelson's Textbook of Pediatrics,17th Edition. Berhman RE, Kliegman RM, Jenson HB (Eds). Saunders, PA, USA 1222-1224 (2004).

26. Vandenplas Y: Gastroesophageal reflux. In: Pediatric Gastrointestinal and Liver Disease 3rd Edition. Wyllie R,

Hyams JS (Eds). Saunders Elsevier, PA, USA 311-325 (2006).

27. Pickering LK, Snyder JD: Gastroenteritis. In: Nelson's Textbook of Pediatrics, 17th Edition. Berhman RE,Kliegman RM, Jenson HB (Eds). Saunders, PA, USA 1272-76 (2004).


29. Guerrant RL, van Gilden T, Stiener TS: Practical guidelines for the management of infectious diarrhea. Clin. Inf.Dis. 32, 331-351 (2001).

• Excellent review of the management of diarrhea.

30. Sandhu B, Devadason D: Management of diarrhea. In: Pediatric Gastrointestinal and Liver Disease 3rd Edition.Wyllie R, Hyams JS (Eds). Saunders Elsevier, PA, USA 1165-1176 (2006).

31. Freedman SB, Adler M, Seshadri R, Powell EC: Oral ondansetron for gastroenteritis in a pediatric emergencydepartment. N. Engl. J. Med. 354, 1698-1705 (2006).

• First review of ondansetron use in children in the outpatient setting.

32. Stone B: Fluids and electrolytes. In: Nelson's Textbook of Pediatrics, 17th Edition. Berhman RE, Kliegman RM,Jenson HB (Eds). Saunders, PA, USA 283-294 (2004).

33. Pall H, Jonas M: Acute and chronic Hepatitis: In: Pediatric Gastrointestinal and Liver Disease 3rd Edition. WyllieR, Hyams JS (Eds). Saunders Elsevier, PA, USA 925-929 (2006).

34. Sylvester FA: Peptic ulcer disease. In: Nelson's Textbook of Pediatrics, 17th Edition. Berhman RE, KliegmanRM, Jenson HB (Eds). Saunders, PA, USA 1244-1247 (2004).

35. Sherman P, Czinn S, Drumm B et al.: Helicobacter pylori infection in childhood and adolescence: WorkingGroup of the First World Congress of Pediatric Gastroenterology, Hepatology and Nutrition. J. Pediatr.Gastroenterol. Nutr.35(Suppl. 2),S128-S133 (2002).

36. Gilger MA: Diseases of the gallbladder. In: Pediatric Gastrointestinal and Liver Disease 3rd Edition. Wyllie R,Hyams JS (Eds). Saunders Elsevier, PA, USA 987-1001 (2006).

37. Brady WJ, Auklerheide TP, Tintinelli J: Cholecystitis and biliary colic. In: Emergency Medicine: AComprehensive Study Guide, 6th Edition. Tintinelli JE, Kelen GD, Stapczynski JS (Eds). McGraw Hill, NY, USA561-566 (2006).

38. Werlin SL: Pancreatitis. In: Nelson's Textbook of Pediatrics, 17th Edition. Berhman RE, Kliegman RM, JensonHB (Eds). Saunders, PA, USA 1300-1303 (2004).

39. Werlin SL: Acute pancreatitis in children. Curr. Treat. Option. Gastroenterol. 4, 403-408 (2001).

40. Quality Standards Subcommittee, American Academy of Neurology: Practice Paramenter: the mangement ofconcussion in sports (summary statement). Neurology 48, 581-585 (1997).

41. Heegaard WG, Biros MH: Diffuse axonal injury. In: Rosen's Emergency Medicine: Concepts and ClinicalPractice, 6th Edition. Marx JA, Hockberger RS, Walls RM (Eds). Mosbym, PA, USA 374 (2006).

42. Poirier M: Concussions: assessment, management and recommendations for return to activity. Clin. Ped.Emerg. Med. 4, 179 (2003).

43. Ganesalingam K, Yeates KO, Ginn MS et al.: Family burden and parental distress following mild traumatic braininjury in children and its relationship to post-concussive symptoms. J. Pediatric Psychol.33(6),621-629 (2008).

44. Han CY, Backous DD: Basic principles of cerebral spinal fluid metabolism and intracranial pressurehomeostasis. Otolaryngol. Clin. North Am. 38, 569-576 (2005).

45. Vincent JL, Berre J: Primer on medical management of severe brain injury. Crit. Care Med. 33, 1392-1399(2005).

46. Adelson PD, Bratton SL, Carney NA et al.: Guidelines for the acute medical management of severe traumaticbrain injury in infants, children, and adolescents. Pediatric Crit. Care Med.4,S2-S75 (2003).

47. Pitetti R: Emergency department evaluation of ventricular shunt malfunction? Is the shunt series reallynecessary? Pediatr. Emerg. Care 23, 137-141 (2007).

48. Goodsby PJ, Lipton RB, Ferrari MD: Migraine - current understanding and treatment. N. Engl. J. Med. 346, 257-270 (2002).

49. Anttila P: Tension-type headache in childhood and adolescence. Lancet Neurol. 5, 268-274 (2006).

50. Maytal J, Young M, Shechter A, Lipton RB: Pediatric migraine and the International Headache Society criteria.Neurology 48, 602-607 (1997).

51. Al-Twaijri WA: Pediatric migraine equivalents: occurrence and clinical features in practice. Pediatr. Neurol. 26,365-368 (2002).

52. Kabbouche MA: Acute treatment of pediatric headache in the emergency department and inpatient settings.Pediatr. Ann. 34, 466-471 (2005).

• Good review of the management of headache in children.

53. Singer JI, Maur PR, Riley JP, Burger-Smith P: Management of central nervous system infections during anepidemic of enteroviral aseptic meningitis. J. Peditr. 96, 559-563 (1980).

54. Rothbart HA: Viral meningitis. Sem. Neurol. 20, 277-292 (2000).

55. de Jonste JC, Shields MD: Cough 2: chronic cough in children. Thorax 58, 998-1003 (2003).

56. Tejpratap T, Murphy TV, Moran J: Recommended antimicrobial agents for the treatment and postexposureprophylaxis of pertussis, 2005 Guidelines. MMWR54(RR14),1-16 (2005).

57. Altamimi S, Robertson G, Jastaniah W et al.: Single-dose oral dexamethasone in the emergency managementof children with exacerbations of mild to moderate asthma. Pediatr. Emerg. Care 22, 786-793 (2006).

58. Vogt BA, Avner ED: Renal failure (acute and chronic). In: Nelson's Textbook of Pediatrics, 17th Edition.Berhman RE, Kliegman RM, Jenson HB (Eds). Saunders, PA, USA 1764-1777 (2004).

59. Santan SA, Alteri MF: Pediatric urinary tract infection. Emerg. Med. Clin. North Am. 19, 675-690 (2001).

60. Seeler RA, Hahn K: Jaundice in urinary tract infections in infancy. Am. J. Dis. Child. 18, 553-558 (1969).

61. Wald ER: Oral antibiotics are effective in pyelonephritis in children. J. Pediatr. 152, 141-142 (2008).

• Good review of the management of pyelonephritis with oral medications.

62. Srivastava T, Alon US: Urolithiasis in adolescent children. Adolesc. Med. Clin. 16, 87-109 (2005).

63. Orlowski JP, Cramer CL, Fiallos MR: Diabetic ketoacidosis in the pediatric ICU. Pediatr. Clin. North Am. 55,577-587 (2008).

64. Wolfsdork J, Craing ME, Danemane D et al.: Diabetic ketoacidosis. Pediatr. Diabetes 8, 28-42 (2007).

65. Hom J, Sinert R: Is fluid therapy associated with cerebral edema in children with diabetic ketoacidosis. Ann.Emerg. Med. 52, 69-75 (2008).

66. Rosenbloom AL: Treatment of diabetic ketoacidosis and the risk of cerebral edema. J. Pediatr. 152, 146-147(reply 147-149) (2008).

67. Davis CO, Max PM: Focused physical examination/toxidromes. In: Clinical Toxicology, 1st Edition. Ford MD,Delaney KD, Ling LJ, Erickson T (Eds). Saunders, St. Louis, MO, USA 31 (2001).

68. Erickson TB, Thompson TM, Lu JJ: The approach to the patient with an unknown overdose. Emerg. Med. Clin.North Am. 25, 249-281 (2007).

• Good overview to the management of the patient with a toxic ingestion.

69. American Academy of Pediatrics Committee on Adolescence Policy Statement: Identification and treatment ofeating disorders. Pediatrics111204-11 (2003).

70. Litt IF: Anorexia nervosa and bulimia. In: Nelson's Textbook of Pediatrics, 17th Edition. Berhman RE, KliegmanRM, Jenson HB (Eds). Saunders, PA, USA 652-653 (2004).

71. Sullivan PF: Mortality in anorexia nervosa. Am. J. Psych. 152, 1073-1074 (1995).

72. Powers GF, Boisvert PL: Age as a factor in streptococcosis. J. Pediatr. 25, 481-504 (1944).

• Classic article detailing the multiple presentations of streptococcal infections in children.

73. Centor RM, Witherspoon JM, Dalton HP et al.: The diagnosis of strep throat in adults in the emergency room.Med. Decis. Making 1, 239-246 (1981).

74. Snow V, Mottur-Pilson C, Cooper RJ, Hoffman JR: Principles of appropriate antibiotic use of acute pharyngitisin adults. Ann. Intern. Med. 134, 506-508 (2001).

75. American Academy of Pediatrics: Group A streptococcal illness. In: Red Book: Report of the Committee onInfectious Disease, 27th Edition. Pickering LK, Baker CJ, Long SS, McMillan JA (Eds). American Academy ofPediatrics, IL, USA 610-620 (2006).

76. Kuhn GJ: Emergencies during pregnancy and the post-partum period. In: Emergency Medicine: AComprehensive Study Guide, 6th Edition. Tintinelli JE, Kelen GD, Stapczynski JS (Eds). McGraw Hill, NY, USAp677-678 (2006).

77. Massachusetts General Hospital. Radiology Rounds 4, 1 (2006).

Websites

101. National Asthma Education and Prevention Program: Expert panel report III: guidelines for the diagnosisand management of asthma. Bethesda, MD: National Heart, Lung and Blood Institute, (2007).www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm

102. Madison Radiologists http://www.madisonradiologists.com/

Financial & competing interests disclosure

The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest inor financial conflict with the subject matter or materials discussed in the manuscript. This includes employment,consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, orroyalties.

No writing assistance was utilized in the production of this manuscript.

Pediatr Health. 2009;3(5):479-503. © 2009 Future Medicine Ltd.

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Vomiting in Pediatrics

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