Stress erosive gastritis

Miller, Thomas A.; Tornwall, Michael S.; Moody, Frank G.

doi:10.1016/0011-3840(91)90030-s

Cited by 18 publications

(7 citation statements)

References 87 publications

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“…The pathogenesis of stress ulceration remains poorly understood. Various factors and mechanisms, alone or in combination, are probably responsible for the lesions [1,13,14]. Despite the multifactorial mechanisms proposed as contributing to the development of stress‐related gastrointestinal erosions, the presence of luminal gastric acid appears essential.…”

Section: Pathogenesis Of Stress Ulcersmentioning

confidence: 99%

“…Furthermore, patients with achlorhydria have been reported not to develop stress ulceration [16]. However, the majority of patients with stress ulceration have normal acid secretion [1,13,14]. Alterations in mucosal blood flow, the mucus layer, protein synthesis, bicarbonate and prostaglandins secretion, and epithelial cell renewal have been postulated to alter the gastric mucosal barrier leading to the back diffusion of acid and thus leading to mucosal damage [3,13,14,17].…”

Section: Pathogenesis Of Stress Ulcersmentioning

confidence: 99%

“…However, the majority of patients with stress ulceration have normal acid secretion [1,13,14]. Alterations in mucosal blood flow, the mucus layer, protein synthesis, bicarbonate and prostaglandins secretion, and epithelial cell renewal have been postulated to alter the gastric mucosal barrier leading to the back diffusion of acid and thus leading to mucosal damage [3,13,14,17]. In addition, alterations in endothelin‐1 and serotonin production as well as infection with Helicobacter pylori may play a role in the development of stress ulceration [11,18,19].…”

Section: Pathogenesis Of Stress Ulcersmentioning

confidence: 99%

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Stress Ulcer Prophylaxis: A Practical Approach

Marik¹

1999

J Intensive Care Med

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Although the incidence of bleeding from stress ulceration has declined over the last two decades, this condition remains of both clinical and economic importance. Recent studies suggest that stress ulcer prophylaxis is only indicated in high‐risk patients, most notably those patients undergoing mechanical ventilation and patients with a coagulopathy. There is little evidence that antacids, sucralfate, and H2 blockers differ with respect to the prevention of clinically important bleeding. The choice of agents is therefore largely determined by economic factors and the risk of drug‐associated complications.

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Section: Pathogenesis Of Stress Ulcersmentioning

confidence: 99%

Section: Pathogenesis Of Stress Ulcersmentioning

confidence: 99%

Section: Pathogenesis Of Stress Ulcersmentioning

confidence: 99%

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Stress Ulcer Prophylaxis: A Practical Approach

Marik¹

1999

J Intensive Care Med

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“…9 This type of ulcer increases in frequency with an increase in the percentage of body surface area involved in a burn. 8,10 Risk factors for stress ulcers include trauma, hypotension, respiratory and renal failure, sepsis, jaundice, recent surgery, and burns. 7 High-stress conditions that have been documented previously as causing stress ulcers in infants include cyanotic heart disease, gastroenteritis, and pneumonias.…”

mentioning

confidence: 99%

Curling’s Ulcer in Association with Staphylococcal Scalded Skin Syndrome in the Neonate

Orehek

Cook

1999

J Perinatol

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Case ReportThis 24-day-old infant boy was the second born of a 36-week twin gestation delivered at an outlying hospital by spontaneous vaginal delivery after a pregnancy complicated only by mild maternal preeclampsia. His nursery course was unremarkable. Physical examination at 2 weeks of life was within normal limits, and an elective circumcision was then performed without difficulty at his community hospital. Over the 2 days following the circumcision, his mother noted increased redness in the groin area; on day 3, peeling of the skin of the scrotum and penis were evident. On day 4 after circumcision, the patient was febrile and was seen by his primary physician. Rectal temperature at this time measured 38.3°C. Blood and urine cultures were performed. Lumbar puncture was unsuccessful. The infant received intravenous (i.v.) antibiotics and was transferred to the neonatal intensive care unit for further management of suspected staphylococcal scalded skin syndrome (SSSS). His vital signs on admission revealed a rectal temperature of 37°C, a heart rate of 200 beats/min, a respiratory rate of 50 breaths/minute, and blood pressure of 104/69 mm Hg. Physical examination at this time was notable for erythematous and tender skin with sloughing over the entire body but was otherwise unremarkable (Figure 1, A and B). Skin cultures and a skin biopsy of the affected area were performed on admission. Topical therapy with Vaseline and Aquaphor was initiated. Systemic antibiotic therapy included i.v. vancomycin (15 mg/kg i.v. every 12 hours) and gentamicin (2.5 mg/kg i.v. every 12 hours). Blood and urine cultures obtained at the referring hospital showed no growth at 3 days, and many colonies of Staphylococcus aureus were identified on the admission skin culture. Antibiotic therapy was then changed to i.v. nafcillin (50 mg/kg i.v. every 8 hours). Skin biopsy revealed a plane of separation in the region of the granular cell layer of the epidermis consistent with SSSS. Pain was controlled with morphine (0.05 mg/kg i.v.) and subsequently with acetaminophen (20 mg/kg orally every 4 hours). The patient's cardiorespiratory status remained stable, and oral feedings of human milk and/or standard infant formula were continued from admission. By day 3 of hospitalization, the patient was feeding well; however, a 10% weight loss from admission was noted, and supplemental i.v. fluids at 100 ml/kg per day were started to supplement oral feedings. On day 5, the patient became edematous and had several episodes of emesis; blood cultures were redrawn, and the abdominal x-ray was interpreted as normal. On day 7 of hospitalization, the patient developed acute onset of pallor, abdominal distention, and irritability. Hemoglobin measured at 5.3 gm/dl, and the abdominal radiograph revealed evidence of free intraperitoneal air. He was stabilized with red blood cell transfusions and oxygen and emergently taken to the operation room, where a clean, round, 7-to 8-mm isolated perforation of the first part of the duodenum was identified and closed with an...

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“…Other agents that can cause erosive gastritis include Helicobacter (H.) pylori infection, biliary reflux, alcohol, cocaine or ionizing radiation [6,7]. Traumatic injuries, critical illness, severe burns, major surgery or hypothermia can also end up in an acute erosive gastritis called stress gastritis [8]. However, it should be noted that almost one half of the diagnoses do not reveal the pathogenesis of gastritis [9].…”

Section: Introductionmentioning

confidence: 99%

Influence of inhomogeneous static magnetic field-exposure on patients with erosive gastritis: a randomized, self- and placebo-controlled, double-blind, single centre, pilot study

Juhász

Nagy

Székely

et al. 2014

J. R. Soc. Interface.

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This pilot study was devoted to the effect of static magnetic field (SMF)-exposure on erosive gastritis. The randomized, self- and placebo-controlled, double-blind, pilot study included 16 patients of the 2nd Department of Internal Medicine, Semmelweis University diagnosed with erosive gastritis. The instrumental analysis followed a qualitative (pre-intervention) assessment of the symptoms by the patient: lower heartburn (in the ventricle), upper heartburn (in the oesophagus), epigastric pain, regurgitation, bloating and dry cough. Medical diagnosis included a double-line upper panendoscopy followed by 30 min local inhomogeneous SMF-exposure intervention at the lower sternal region over the stomach with peak-to-peak magnetic induction of 3 mT and 30 mT m −1 gradient at the target site. A qualitative (post-intervention) assessment of the same symptoms closed the examination. Sham- or SMF-exposure was used in a double-blind manner. The authors succeeded in justifying the clinically and statistically significant beneficial effect of the SMF- over sham-exposure on the symptoms of erosive gastritis, the average effect of inhibition was 56% by p = 0.001, n = 42 + 96. This pilot study was aimed to encourage gastroenterologists to test local, inhomogeneous SMF-exposure on erosive gastritis patients, so this intervention may become an evidence-based alternative or complementary method in the clinical use especially in cases when conventional therapy options are contraindicated.

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Stress erosive gastritis

Cited by 18 publications

References 87 publications

Stress Ulcer Prophylaxis: A Practical Approach

Stress Ulcer Prophylaxis: A Practical Approach

Curling’s Ulcer in Association with Staphylococcal Scalded Skin Syndrome in the Neonate

Influence of inhomogeneous static magnetic field-exposure on patients with erosive gastritis: a randomized, self- and placebo-controlled, double-blind, single centre, pilot study

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