Pyloric stenosis as a manifestation of isolated gastric Crohn's disease responding to intralesional steroid injection and balloon dilation: a case report.

BACKGROUND: Crohn's disease is a chronic inflammatory condition that can affect the gut from mouth to anus. Gastroduodenal involvement is seen in less than 5% of all patients with Crohn's disease. Among those cases, isolated gastric Crohn's disease is even rarer. Although most patients with isolated gastric involvement have nonspecific complaints, very few of them do develop features of pyloric obstruction. There is a paucity of data on specific management of gastric Crohn's disease owing to its rarity and its frequent coexistence with colonic or ileal disease. We report a case of a patient who had pyloric stenosis as a manifestation of isolated gastric Crohn's disease responding to intralesional steroid injection and balloon dilation. CASE PRESENTATION: A previously healthy woman presented with recurrent postprandial vomiting, epigastric discomfort, and unintentional weight loss over 6 months. She had no diarrhea or extraintestinal manifestations. Clinically, she was pale and dehydrated. Examination of systems was unremarkable except for mild epigastric tenderness. Her initial laboratory findings were normocytic normochromic anemia, high inflammatory markers, and hypokalemia. Esophagogastroduodenoscopy revealed an inflamed pyloric mucosa with features of pyloric obstruction. Furthermore, magnetic resonance enterography confirmed the pyloric stenosis. Histopathological examination of a biopsy from the pylorus revealed noncaseating granuloma with superficial ulceration. Tuberculosis and sarcoidosis were excluded by appropriate investigations, and a diagnosis of gastric Crohn's disease was made. Following the initial resuscitation, intralesional steroid injection and controlled radial expansion balloon dilation of the pylorus were carried out. The patient was commenced on azathioprine as a maintenance treatment, which led to a successful dilation and remarkable symptom improvement. CONCLUSION: Symptoms of pyloric obstruction as a manifestation of isolated gastric Crohn's disease are extremely unusual in clinical practice, awareness of which would facilitate early appropriate investigations and treatment.

Atropine sulphate: rescue therapy for pyloric stenosis.

Infantile hypertrophic pyloric stenosis (IHPS) is a common condition which presents with non-bilious vomiting and failure to thrive secondary to gastric outlet obstruction. In the UK, management is by fluid resuscitation followed by pyloromyotomy. Incomplete myotomy complicates 0.3% of cases necessitating further surgery and exposing the patient to further risk. Medical management of IHPS with antimuscarinics to promote pyloric relaxation is a well-described treatment modality that is used as first-line therapy in some countries. The use of this technique is limited by the need for extended hospital admission with parenteral nutrition administration. We describe a case of IHPS complicated by incomplete pyloromyotomy and subsequently managed successfully by atropine sulphate therapy.

An adult case of eosinophilic pyloric stenosis maintained on remission with oral budesonide.

We describe an isolated eosinophilic pyloric stenosis in a young female. She was referred for abdominal pain, fever, weight loss and eosinophilia. A sonographic examination revealed a concentric pyloric stenosis, with antral palsy and ascites. The endoscopy confirmed the diagnosis of eosinophilic infiltration of the pylorum. After a short course of systemic steroids, the patient was switched to oral budesonide, which effectively maintained a long-term remission. Eosinophilic gastroenteritis limited to pylorum is exceptional in adults, and in our patient it was not associated with allergic other disorders. This case emphasizes the usefulness of sonografy for diagnosis and monitoring, and the clinical efficacy of oral budesonide.

Treatment of Wernicke's encephalopathy with high dose of thiamine in a patient with pyloric sub-stenosis: description of a case.

Wernicke's encephalopathy (WE) is an acute or subacute syndrome that results from a deficiency in vitamin B1 (thiamine). The syndrome is characterised by a classical triad of symptoms: nystagmus and ophthalmoplegia,mental-status changes, and unsteadiness of stance and gait. When patients with WE are inappropriately treated with low doses of thiamine, mortality rates average out at 20% and Korsakoff's Psychosis develops in about 85% of survivors(Sechi and Serra in Lancet Neurol 6(5):442­455,2007). We report the case of a patient with a pyloric substenosis that developed a WE, and was treated with high doses of thiamine showing after few days of treatment a great improvement of neurological and neuroradiological assessment, even though cognitive impairment was still severe at discharge and at 6 months follow-up.

Feasibility of self-expandable metallic stent plus chemotherapy for metastatic gastric cancer with pyloric stenosis.

BACKGROUND AND AIM: Self-expandable metallic stent placement is accepted as palliative therapy for advanced gastric cancer with gastric outlet obstruction, but data are lacking for chemotherapy after self-expandable metallic stent insertion. This study retrospectively compared results between surgery plus chemotherapy and stenting plus chemotherapy for metastatic gastric cancer with pyloric stenosis. METHODS: Subjects comprised 26 patients who received chemotherapy after surgery or endoscopic stenting for metastatic gastric cancer with pyloric stenosis between April 2000 and December 2007 in four Japanese hospitals. Patients were categorized into two groups: 15 patients who received chemotherapy after surgery for pyloric stenosis (Surgery group); and 11 patients who received chemotherapy after self-expandable metallic stent placement for pyloric stenosis (Stent group). RESULTS: Median survival time and median time to treatment failure were 284 days and 226 days in the Surgery group and 337 days and 247 days in the Stent group, respectively. No significant differences were noted between survival and time to treatment failure. No significant differences were found in median oral intake rate (Surgery, 93.1%; Stent, 93.2%) or median hospital stay rate (Surgery, 24.6%; Stent, 23.7%) during survival. Response rate was 45.5% in the Surgery group and 50% in the Stent group, with no significant difference. Likewise, no significant differences were noted between groups for frequencies of toxicity or complications. CONCLUSIONS: The present results suggest that chemotherapy after stenting is as effective and safe as chemotherapy after surgery. Stents may replace surgery in combination therapy with chemotherapy for metastatic gastric cancer with gastric outlet obstruction.

[Administration of S-1 after gastrojejunostomy for unresectable gastric cancer with pyloric stenosis].

We evaluated the efficacy of chemotherapy using S-1 after gastrojejunostomy for unresectable gastric cancer with pyloric stenosis. We performed gastrojejunostomy to relieve obstruction in 40 patients from 1993 to 2007. After gastrojejunostomy, 15 patients were treated with S-1(S-1 group), 12 patients were treated with another anticancer drug(non S-1 group)and the other 13 patients received no chemotherapy. After informed consent was obtained, S-1(80 mg/m(2)day)and another anticancer drug was administered. The mean period of administered was 16(range 2-56)weeks in the S-1 group. In the non S-1 group, 5-FU was used in 1 patient, 5'-DFUR in 2, UFT in 3, FP chemotherapy in 3, CPT- 11/CDDP chemotherapy in 1, and 5-FU/PTX chemotherapy was conducted in 2 patients. The one-year survival rate was 63% and the median survival time was 394 days in the S-1 group, against 33% and 169 days, respectively, in the non S-1 group. Appetite loss of grade 3 was observed in one(7%)patient with nonhematological toxicity, but no patient suffered grade 3 hematological toxicity. We observed the course of all patients on an outpatient basis. In conclusion, S- 1 administration after gastrojejunostomy appears to be an effective treatment modality for far advanced gastric cancer patients with pyloric stenosis in view of toxicities, antitumor effects and QOL of the patients.

[Gastrojejunostomy for irresectable gastric cancer with pyloric stenosis-new role of surgery in the era of S-1].

We report a patient with an advanced gastric cancer complicated by pyloric stenosis who was effectively treated by S-1 mono-therapy after gastrojejunostomy. A 62-year-old man consulted a general practitioner for abdominal pain and anorexia. Gastric roentgenography and upper gastrointestinal endoscopy showed gastric cancer(Borrmann Type 3) with pyloric stenosis. He was referred to our department. He underwent laparotomy, which revealed a T4 tumor invading the pancreas head, but neither liver nor peritoneal metastasis. A gastrojejunostomy was made. After the operation, chemotherapy of S-1(120 mg/day, day 1-21)+cisplatin(100 mg/day, day 8)was administered. After 2 courses, level of tumor marker decreased remarkably and abdominal enhanced computed tomography showed a significant size reduction of lymph nodes and that direct invasion to the pancreas was not clear any more. Second laparotomy was carried out and curative surgery was performed. After 4 courses of S-1(120 mg/day, day 1 approximately 28)mono-therapy as adjuvant chemotherapy, bone metastasis was confirmed by scintigram. Then methotrexate+5-FU, irinotecan+cisplatin and cisplatin+paclitaxel were chosen as second-, third-and fourth-line chemotherapy, which were not effective for long. He died 572 a days after the initial surgery. In the past, gastrojejunostomy was regarded as useful palliative treatment for those with gastric outlet stenosis to ameliorate the QOL. As S-1 is taking major role in the chemotherapy for advanced gastric cancer recently, usefulness of bypass surgery for such patients is highlighted even for longer survival time.

[A case of advanced gastric cancer with pyloric stenosis and obstructive jaundice responding to s-1/paclitaxel combination therapy after endoscopic balloon dilatation and endoscopic biliary drainage].

A 65-year-old female who complained of appetite loss and upper abdominal pain was diagnosed as unresectable advanced gastric cancer with pyloric stenosis and obstructive jaundice by peritoneal and lymph node metastases. After endoscopic balloon dilatation and endoscopic biliary drainage, S-1(80 mg/m(2)/day, days 1-14 with 1 week rest)/pacli- taxel(PTX)(50 mg/m(2)/day, day 1, day 8)combination therapy was done. After one course of the chemotherapy, subjective symptoms were relieved and oral intake was increased. Computed tomography showed that the volume of gastric wall, the size of paraaortic lymph node, and the amount of pleural effusion and ascites were decreased. Grade 1 alopecia, vasculitis and grade 2 neutropenia were observed as adverse reactions to the treatment. S-1/PTX combination therapy after endoscopic intervention was effective in this case of advanced gastric cancer with pyloric stenosis and obstructive jaundice.

Proton pump inhibition is a feasible primary alternative to surgery and balloon dilatation in adult peptic pyloric stenosis (APS): report of six consecutive cases.

INTRODUCTION: Surgery has been the gold standard in the treatment of adult pyloric stenosis (APS). The introduction of proton pump inhibitors (PPIs) in 1989 revolutionised the treatment of peptic ulcer disease and its complications. PATIENTS AND METHODS: We carried out a prospective study to evaluate the effectiveness of PPIs as an alternative to surgery for treatment of APS. Six consecutive patients admitted with a diagnosis of adult peptic pyloric stenosis between November 1999 and August 2002 were studied. The diagnosis was confirmed with endoscopy. All patients were commenced on a twice-daily dose of intravenous PPI. This was changed to oral treatment after 2 days. Main outcome measures evaluated were resolution of symptoms on PPIs and failure of medical therapy. RESULTS: There were five females and one male. Median age at diagnosis was 72 years (range, 30-90 years). Median duration of symptoms was 2 weeks (range, 1-5 weeks). Of the patients, five had a history of peptic ulcer disease. Complete resolution was achieved in 5 patients (83%). Median duration for resolution of symptoms was 9 days (range, 5-14 days). All patients were changed to oral PPIs after 2 days. One patient did not respond to oral therapy and required surgical intervention (pyloroplasty). Median follow-up was 26 months (range, 6-48 months). There was no recurrence of symptoms. All patients were discharged on low-dose PPI. CONCLUSIONS: This study supports the view that proton pump inhibitors are a safe and feasible alternative to surgery in adult pyloric stenosis secondary to peptic ulcer disease.

The true cause of pyloric stenosis is hyperacidity.

UNLABELLED: Pyloric stenosis (PS) has no known cause. A testable theory of cause is proposed, based on the inheritance of a parietal cell mass (PCM) at the upper end of the normal range. It is proposed that, until 3-4 wk of age, the obligatory high fasting gastrins are at maximal levels and not able to be diminished by increasing antral acidity. Hence, rising acidity is not reduced by a lowered gastrin during this time, and very high acidity occurs. CONCLUSION: Persisting duodenal hyperacidity is created by an inherited high PCM and loss of gastrin control. These two factors produce pyloric stenosis through work hypertrophy from repeated pyloric contraction in response to hyperacidity.

Medical treatment with atropine sulfate for hypertrophic pyloric stenosis.

We investigated whether atropine sulfate was an effective, non-surgical method for treating hypertrophic pyloric stenosis (HPS). The study group consisted of 5 patients, all of the patients presented with projectile vomiting. Hypertrophic pyloric stenosis was diagnosed based on abdominal sonographic findings. The age when symptom arose was 30.8 +/- 15.5 (mean +/- SD) days, the age upon admission was 43.2 +/- 9.6 days. The frequency of vomiting was 5.8 +/- 2.3 times per day. After admission, all patients received 10% atropine sulfate 0.01 mg/kg intravenous (i.v.) for 5 minutes q4H (every four hours) before each feeding. Formular milk was started and increased by 10 ml every feeding until full feeding (120 ml/kg/day) was achieved. When vomiting had ceased for a period of one day, i.v. atropine was changed to 0.02 mg/kg oral q4H before each feeding. The patient was hospitalized until full feeding was maintained for more than 2 days. Then oral atropine was tapered by half a dose every 2 weeks. Oral atropine was continued until the thickness of the pyloric muscle had normalized (< 3.5 mm). All five patients were successfully treated with atropine sulfate. The frequency of vomiting was reduced to less than two times per day (1.8 +/- 1.3 days). i.v. atropine was used for 6.4 +/- 3.4 days, and the oral form was used for 30 +/- 9 days. The total number of days of atropine sulfate treatment was 36.4 +/- 9.58 days. Full feeding was achieved at 8 +/- 5.3 days. The hospitalization was 14.6 +/- 6.2 days. The body weight when admitted was 4000 +/- 760.8 gm and the body weight when discharged was 4282 +/- 901 gm. The body weight one month after treatment was 5210 +/- 772.5 gm. The body weight gain one month after atropine treatment was 1262 +/- 441.4 gm. Body weigh range on admission was from <3rd to 25th percentile, and after one month of atropine treatment, the body weight range was from 10th to 75th percentile. Complications included transiently elevated heart rates (180-200 times/min) in two patients and facial flushing after the first dose of IV atropine in one patient. In conclusion, conservative treatment with initially IV atropine in the initial stages instead of oral atropine sulfate is an effective alternative to pyloromyotomy, particularly in infants with major concurrent disease or when parents are unwilling to let their infants undergo surgery. Surgical intervention is not always necessary.

Congenital hypertrophic pyloric stenosis.

Congenital hypertrophic pyloric stenosis, an important cause of intractable vomiting in infants is diagnosed clinically and confirmed ultrasonographically. Other useful interventions are plain radiography and barium study. Differential diagnosis includes pylorospasm and gastroesophageal reflux. Management protocol includes correction of dehydration and electrolyte imbalance and either Fredet Ramstedt pyloromyotomy or medical treatment with atropine sulphate. Atropine is initially given intravenously till vomiting is controlled and then orally at double the effective i.v. done for another 3 weeks. Atropine sulphate is generally well tolerated and side effects are few like tachycardia, raised SGPT and hyperthermia. Atropine sulphate is very effective, cheap, safe and perhaps more acceptable treatment option for CHPS.

Subacute atropine toxicity in a pygmy sperm whale, Kogia breviceps.

Atropine, an anticholinergic agent commonly used in human and veterinary medicine, is reported to cause toxicity associated with its antimuscarinic action. A juvenile pygmy sperm whale, Kogia breviceps, was treated with atropine in an attempt to relieve symptoms similar to pyloric stenosis, as has been used in humans. Two doses of 0.01 mg/kg were given i.m., 12 hr apart, followed by three doses of 0.005 mg/kg i.m. s.i.d. over the next 3 days. Symptoms associated with atropine toxicity developed gradually and included hyperexcitability, a generalized ascending paralysis of body musculature, shallow, rapid respiration, vomiting, aspiration of seawater, and pulmonary edema. Treatment with physostigmine salicylate (two doses of 2 mg i.m., I hr apart) was effective in counteracting the paralysis, as well as other symptoms, beginning in as little as 17 min after the first dose, and the whale was back to swimming on its own after 8 hr. All overt symptoms of atropine toxicity were gone in about 24 hr, but there were other possible sequella that lasted much longer.

Caudal block with 4 mg x kg-1 (1.6 ml x kg-1) of bupivacaine 0.25% in children undergoing surgical correction of congenital pyloric stenosis.

BACKGROUND: Since 1970, bupivacaine 0.25% in a dose of 4 mg x kg-1 (1.6 ml x kg-1) has been used at the Hospital Infantil de México for caudal block in children undergoing surgical correction of congenital pyloric stenosis (CPS). Although this dose is considered unsafe, in our experience, it has been associated with a high success rate and a low incidence of adverse events. This experience has not been previously documented. METHODS: A retrospective cohort of patients undergoing surgical correction of CPS was studied. Nineteen patients received general anaesthesia while 223 received caudal block. The latter were then grouped according to the sedation technique. The rate of successful caudal blocks and complications were considered the major outcomes of the study, whereas the postsurgical fasting period and hospital stay were considered secondary outcomes. RESULTS: The rate of success of caudal block was 96%. Anaesthetic complications related to bupivacaine were present in 1.3%. Mortality occurred in the postoperatory period in one septic patient who also was suffering from gastroschisis that required general anaesthesia. Postoperatory fasting period and hospital stay tended to be higher with general anaesthesia than caudal block. However, of the 19 patients receiving general anaesthesia, five suffered serious comorbidity and nine were failed caudal blocks. CONCLUSIONS: Caudal block with bupivacaine 0.25% (4 mg x kg-1) was associated with a low rate of anaesthetic complications. Further prospective studies to clarify the risks and benefits are required.

Intravenous atropine treatment in infantile hypertrophic pyloric stenosis.

AIMS: To assess the efficacy of a new regimen of intravenous atropine treatment for infantile hypertrophic pyloric stenosis (IHPS) with special reference to regression of pyloric hypertrophy. METHODS: Atropine was given intravenously at a dose of 0.01 mg/kg six times a day before feeding in 19 patients with IHPS diagnosed from radiographic and ultrasonographic findings. When vomiting ceased and the infants were able to ingest 150 ml/kg/day formula after stepwise increases in feeding volume, they were given 0.02 mg/kg atropine six times a day orally and the dose was decreased stepwise. RESULTS: Of the 19 infants, 17 (89%) ceased projectile vomiting after treatment with intravenous (median seven days) and subsequent oral (median 44 days) atropine administration. The remaining two infants required surgery. No significant complications were encountered. Ultrasonography showed a significant (p < 0.05) decrease in pyloric muscle thickness, but no significant shortening of the pyloric canal after completion of the atropine treatment. The patients exhibited failure to thrive at presentation, but were thriving at 6 months of age (p < 0.01). CONCLUSIONS: This atropine therapy resulted in satisfactory clinical recovery. Pyloric muscle thickness was significantly reduced.