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Chest Pain of Gastrointestinal Origin Arch Dis Child: first published as 10.1136/adc.63.12.1457 on 1 December 1988. Downloaded from Archives of Disease in Childhood, 1988, 63, 1457-1460 Chest pain of gastrointestinal origin S BEREZIN, M S MEDOW, M S GLASSMAN, AND L J NEWMAN Department of Pediatrics, New York Medical College, Valhalla, New York, USA SUMMARY Twenty seven children who had been diagnosed as having idiopathic chest pain were investigated to find out if the pain was of gastrointestinal origin. The symptoms had lasted from two weeks to eight months. In 21 of the 27 children (78%) the chest pain had a gastrointestinal cause: 16 had oesophagitis, four had gastritis, and one had diffuse oesophageal spasm. All patients responded to medical treatment of their gastrointestinal symptoms, resulting in disappearance of the chest pain. Although chest pain is not usually associated with the central or retrosternal areas, or both, and serious disease in children, if it occurs it is a cause of episodes of pain lasted from less than a minute to great anxiety for the patient and family. In one study several hours (table 1). 16% of children with chest pain made more than one In order to determine the cause of the pain, each visit to the accident and emergency department.' patient was investigated by oesophagogastroduode- Gastrointestinal disorders have not been de- noscopy, oesophageal manometry, and a Bernstein copyright. scribed as being important causes of chest pain in acid perfusion test. In addition, eight patients had children.1-3 To further our understanding of the extended ambulatory pH monitoring. association between gastrointestinal dysfunction and Oesophageal manometry was carried out with a chest pain in children, we carried out oesophageal triple lumen polyvinyl catheter assembly (individual manometry, oesophagogastroduodenoscopy, and outside diameter 1*2 mm) with three pressure Bernstein acid perfusion tests on 27 children with sensing orifices separated by 5 mm. The catheter idiopathic chest pain, and extended ambulatory oesophageal pH monitoring on eight of the 27 patients. Table 1 Details ofpatients with chestpain of http://adc.bmj.com/ gastrointestinal origin Patients and methods No (%) of Fifty one patients between 8 and 20 years of age who patients complained of chest pain were investigated. All Age at onset (years): patients were initially examined by general paediat- 0-7 O (0) ricians and the diagnoses were: idiopathic chest pain 8-12 6 (28) 13-17 11 (52) on September 30, 2021 by guest. Protected (n=27), musculoskeletal disorders (n= 12), cos- 17-20 4 (19) tochrondritis (n=9), and oesophagitis (n=3). Pre- Duration of symptoms (months): viously established criteria were used to make these <1 3 (14) diagnoses.2 1-6 15 (72) >6 3 (14) The 27 children in whom a diagnosis of idiopathic Site of pain: chest pain had been made were further investigated Left praecordium 4 (19) by the division of paediatric gastroenterology at Central or retrosternal 4 (19) New York Medical College. The three patients with Right praecordium 1 (4) Combination (left praecordium and central or symptoms of oesophagitis were not included in the retrosternal 12 (57) study. None of the patients had the characteristic Duration of attacks (minutes): symptoms of gastro-oesophageal reflux such as <1 4 (19) heartburn, regurgitation, pain on swallowing, dys- 1-5 8 (38) 6-60 6 (28) phagia, haemorrhage, or 'water brash'. The chest >60 3 (14) pain was usually localised to the left praecordium, 1457 Arch Dis Child: first published as 10.1136/adc.63.12.1457 on 1 December 1988. Downloaded from 1458 Berezin, Medow, Glassman, and Newman was perfused with sterile water at 0-5 ml/minute by a vascular pattern and there was spontaneous friabil- low compliance pneumatic hydraulic capillary infu- ity, ulceration, or erythema. Gastritis was diagnosed sion system with a pressure response of >106-8 when there was erythema, erosions, or bleeding. kPa/second. Pressures were transmitted through the Oesophagitis8 9 and gastritisl° were graded histolo- fluid filled catheters to transducers connected to a gically according to established criteria. three channel polygraph recording system. The The protocol was approved by the office of station pullthrough technique was used to determine research administration of New York Medical Col- lower oesophageal sphincter location and pressure. lege. Informed consent was obtained from the legal The normal range of lower oesophageal sphincter guardian of each patient. pressure in our laboratory is 2-0 to 4-0 kPa. To measure oesophageal peristalsis, 10 swallows of 5 ml Results water were given at 30 second intervals. Abnormal oesophageal contractions were defined as: non-peristaltic contractions including simul- In 21 of the 27 patients a gastrointestinal cause was taneous onset or the peaks of waves recorded at found for the chest pain. Sixteen of the 21 (76%) adjacent recording sites, and non-conducted swal- had oesophagitis and four (19%) had gastritis lows that caused no oesophageal pressure wave, or a diagnosed both macroscopically and histologically. wave too weak to be transmitted to the three In one patient endoscopy was normal but there was recording sites; or repetitive contractions with the diffuse oesophageal spasm on oesophageal man- second and third peaks of more than 10% of the ometry (table 2). Five patients with oesophagitis primary wave amplitude; or spontaneous contrac- (31%) had abnormalities of oesophageal motility. tions of more than 4-00 kPa that were not generated Nine of the 16 with oesophagitis (56%) had lower by swallows.4 Wave amplitude expressed in kPa was oesophageal sphincter pressure that were signifi- measured from the mean intraoesophageal baseline cantly less (mean 9-44, SEM 0-75) than the mean of pressure to the peak of the wave. Individual wave the group of patients with gastrointestinal chest pain duration in seconds was measured from the onset of (mean (SEM) 16*43 (1-54), p<0001). The four copyright. the principal upstroke to the end of the wave. patients with gastritis had a mean lower oesophageal The Bernstein acid perfusion test was carried out sphincter pressure significantly higher (25-00 (1.41), by positioning the catheter in the upper third of the p<0.01) than the group of patients with gastrointes- oesophagus. An infusion of 0*9% sodium chloride tinal chest pain. Eight patients with oesophagitis was given at a rate of 100 drops/minute for 10 underwent prolonged oesophageal pH monitoring minutes. This was followed by infusion of 0.1 mol/l and all had appreciable gastro-oesophageal reflux. hydrochloric acid for up to 10 minutes. The test was Nine patients with oesophagitis had positive Bern- negative if the patient remained asymptomatic. If stein acid perfusion tests (table 3). severe discomfort was produced in the chest, the The patients with oesophagitis and gastritis had http://adc.bmj.com/ acid perfusion was stopped and saline reinstilled. marked decreases in the severity of their chest pain Repeated elicitation of chest pain by acid perfusion within three weeks of starting activated dimethicone followed by relief of symptoms on perfusion with 0*5 mg/kg (maximum 30 ml/dose) one and three saline indicated that the symptoms were due to the hours after meals, or ranitidine (150 mg twice daily) acid challenge. (table 4). Follow up endoscopies after two months Oesophageal pH monitoring was carried out by of treatment showed that the oesophagitis and with diffuse placing a pH monitoring probe in the mid- gastritis had resolved. The patient on September 30, 2021 by guest. Protected oesophagus after localisation of the lower oesophageal spasm had appreciably less chest pain oesophageal sphincter by oesophageal manometry.5 after treatment with dicyclomine hydrochloride; Ambulatory pH monitoring was usually continued permission to carry out repeat manometry, how- for 18 hours after placement of the probe. ever, was refused (table 4). Appreciable gastro-oesophageal reflux was di- agnosed if there was a pH of less than 4 for 10% or more of the first two postprandial hours,6 or if the Table 2 Aetiology ofchestpain ofgastrointestinal origin mean duration of reflux during sleep was greater than four minutes more than two hours after No (%) feeding.7 of patients Oesophagogastroduodenoscopy was carried out Oesophagitis 16 (76) with an Olympus GIFXP1O gastroscope after seda- Gastritis 4 (19) tion with meperidine and diazepam. Oesophagitis Diffuse oesophageal spasm 1 (5) was diagnosed when the mucosa lost its normal Arch Dis Child: first published as 10.1136/adc.63.12.1457 on 1 December 1988. Downloaded from Chest pain of gastrointestinal origin 1459 Table 3 Results in 21 patients with chestpain ofgastrointestinal origin Case Appearance Lower Oesophageal Bernstein acid Prolonged No at endoscopy oesophageal motility perfusion test oesophageal sphincter pH monitoring pressure (kPa) 1 Gastritis 2-93 Normal Negetive No 2 Oesophagitis 1-33 Normal Negative No 3 Oesophagitis 1-20 Normal Negative No 4 Oesophagitis 2-40 Normal Negative No 5 Oesophagitis 3-47 Normal Positive Yes 6 Oesophagitis 0-933 Normal Positive Yes 7 Gastritis 3-33 Normal Negative No 8 Gastritis 3-73 Normal Negative No 9 Oesophagitis 1-60 Simultaneous Negative No contractions 10 Gastritis 3.33 Normal Negative No 11 Oesophagitis 2-93 Normal Negative Yes 12 Oesophagitis 2-67 Normal Positive Yes 13 Oesophagitis 1-07 Repetitive Positive Yes contractions 14 Normal 2-13 Diffuse oesophageal Negative No spasm 15 Oesophagitis 0-800 Simultaneous Positive Yes contractions 16 Oesophagitis 1-33 Normal Positive Yes 17 Oesophagitis 1-47 Normal Negative Yes 18 Oesophagitis 2-53 Normal Positive No 19 Oesophagitis 2-40 Simultaneous Positive No contractions 20 Oesophagitis 2-80 Simultaneous Positive No contractions copyright. 21 Oesophagitis 1-60 Normal Negative No Table 4 Treatment ofchestpain ofgastrointestinal origin trunks.11 We therefore performed gastrointestinal investigations in 27 children with 'idiopathic' chest Activated Ranitidine Dicyclomine pain.
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