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Peptic Ulcer Clinical Case

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Peptic Ulcer Disease A Case Study Approach.

Published by Monica Goodman Modified over 6 years ago

Presentation on theme: "Peptic Ulcer Disease A Case Study Approach."— Presentation transcript:

Nursing Care of Patients WithUpper GI Disturbances

Josh v.d. Kroft, Gabby Arancio, Taylor Hopwood, Stevi Juall

Peptic ulcer disease.

Peptic Ulcer Disease Biol E /11/06. From: Current Diagnosis & Treatment in Gastroenterology - 2nd Ed. (2003)

Peptic Ulcer By: Allicia Kwakye Miss Tran TPJ-3MO.

PEPTIC ULCER DISEASE NRS452 Norhaini Majid.

Made by: Belal Doudin Alaa Almor To: Dr. Adham Abu taha

Peptic Ulcer Disease. Peptic ulcer  refers to erosion of the mucosa lining any portion of the G.I. tract.  It is defined as : A circumscribed ulceration.

Gastrointestinal Disorders Chapter 6 Medical Considerations.

Stomach Ulcer(Peptic Ulcer) Stomach ulcer or peptic ulcer is the damage of the protective layer (lining) of stomach or gastrointestinal tract It may be.

Digestive System Diseases/Complications

Hepatitis By: Mst Tabassum. History Early case in the 18 th century By 1885, it was showed to be transmittable through blood transfusion and syringes.

MNA M osby ’ s Long Term Care Assistant Chapter 41 Digestive and Endocrine Disorders.

Gastric Acid Secretion 1. Acid synthesis – regulated by 3 transporters Lumen Plasma Parietal cell.

Pharmacology B Lin, I-Yao. A 43y/o male CEO of a multinational company experienced severe burning pain one and a half hour after a sumptuous lunch. This.

Raneen Omary. Contents Definition Pathogenesis Epidemiology Acute Radiation Enteritis Chronic Radiation Enteritis Risk Factors Diagnosis DD Medical Management.

Digestive Disorders. Crohn’s Disease Chronic inflammatory bowel disease. Most common in small/large intestine. Causes: –Possible hereditary link to autoimmune.

Surgical Treatment of Ulcers. Anatomy Introduction  Number of admissions for uncomplicated disease is falling  Incidence of complications related to.

Digestive Disorders Lesson 2. Constipation Infrequent bowel movements Stools are dry, small and difficult to eliminate Can be caused by –inadequate water.

Peptic Ulcer Disease Dr. Wael H. Mansy, MD Assistant Professor College of Pharmacy King Saud University.

About project

Peptic Ulcer Disease Case Study (60 min)

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Mrs. Baker is a 54 year old female who presented to the ED complaining of nausea and severe epigastric pain x 3 days. She reports a history of osteoarthritis and reports taking ibuprofen 400 mg 3-4 times a day regularly for the last few months since her “arthritis has gotten really bad”.

What initial nursing assessments should be performed?

Put the patient on a monitor to assess EKG. A 12-lead EKG should be done to rule out cardiac involvement, request order for cardiac enzymes from provider
Auscultate heart and lung sounds
Full abdominal assessment – inspect, auscultate, palpate and percuss. Assess for tenderness over specific areas, feel for masses, and look for guarding.
Get more detailed history questions – vomiting? Bloody stools? Has this happened before?

Patient demonstrates guarding when palpating epigastric region, no tenderness to palpation over RLQ, LLQ, or LUQ. Some tenderness over RUQ. Bowel sounds are hyperactive, lungs are clear to auscultation, S1 and S2 heard clearly with no murmurs. As you finish your assessment, Mrs. Baker reports she is going to be sick and vomits approximately 300 mL of coffee-ground emesis.

Explain the significance of coffee-ground emesis.

Coffee-ground emesis is vomit that looks like it has coffee-grounds in it.
These black specs are actually hemolyzed blood cells/clots.
Coffee-ground emesis is indicative of a slow source of bleeding within the stomach or refluxing from the duodenum.

You notify the provider of the coffee-ground emesis, administer Ondansetron 4 mg IV per provider orders, and assist Mrs. Baker with oral care.

What further diagnostic testing do you expect to be performed for this patient?

Complete Blood Count
Occult blood testing of stool and emesis
Patient may need an EGD (esophagogastroduodenoscopy) to check for bleeding ulcers

Mrs. Baker is now weak and drowsy. Her fecal occult test is positive and her CBC shows a Hemoglobin of 10 g/dL and a Hematocrit of 31%. Per provider orders, you insert an NG tube to evaluate stomach contents and decompress the stomach. You connect the NG tube to intermittent low wall suction.

What is likely going on with Mrs. Baker physiologically?

Mrs. Bakers chronic heavy use of NSAID’s may have caused ulcers to form in the lining of her stomach and/or duodenum
It is possible that these ulcers are now bleeding

What is the benefit to decompressing the stomach via NG tube?

Decompressing the stomach removes the majority of stomach acid, thereby decreasing the irritation on the stomach lining
The hope is to prevent further irritation to any bleeding ulcers

The UAP notifies you that Mrs. Baker’s blood pressure has dropped to 96/60. You enter the room and see that the suction canister is over halfway full of bright red blood.

What is your priority assessment at this time?

Assess Mrs. Baker – LOC, heart and lung sounds, confirm the accuracy of vital signs
Protect airway – suction if needed, minimize risk for aspiration

What may be happening to Mrs. Baker?

She may have an ulcer that is bleeding more actively than before. With that amount of blood, it could possibly be an arterial bleed.

Mrs. Baker is pale, diaphoretic, and drowsy. Her heart rate is up to 122. You notify the provider who orders to transfuse 2 units of PRBC’s and calls the Gastroenterology team for a STAT EGD. Within 30 minutes the patient is taken to the GI lab for an EGD, where they find two slow-bleeding gastric ulcers, which they cauterize, and 1 arterial bleed which they repair as well. Mrs. Baker returns to the unit post-procedure for observation.

What are nursing priorities for Mrs. Baker after this procedure?

Keep NPO until gag reflex returns
Assess and monitor output from NG tube
Monitor vital signs closely
Monitor LOC as she awakens from sedatives used during the procedure
Ensure the full 2 units of PRBC’s were administered. If not, continue transfusion.

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Nursing Case Studies

This nursing case study course is designed to help nursing students build critical thinking. Each case study was written by experienced nurses with first hand knowledge of the “real-world” disease process. To help you increase your nursing clinical judgement (critical thinking), each unfolding nursing case study includes answers laid out by Blooms Taxonomy to help you see that you are progressing to clinical analysis.We encourage you to read the case study and really through the “critical thinking checks” as this is where the real learning occurs. If you get tripped up by a specific question, no worries, just dig into an associated lesson on the topic and reinforce your understanding. In the end, that is what nursing case studies are all about – growing in your clinical judgement.

Nursing Case Studies Introduction

Cardiac nursing case studies.

6 Questions
7 Questions
5 Questions
4 Questions

GI/GU Nursing Case Studies

2 Questions
8 Questions

Obstetrics Nursing Case Studies

Respiratory nursing case studies.

10 Questions

Pediatrics Nursing Case Studies

3 Questions
12 Questions

Neuro Nursing Case Studies

Mental health nursing case studies.

9 Questions

Metabolic/Endocrine Nursing Case Studies

Other nursing case studies.

Peptic ulcer disease

Raika Jamali M.D.

Gastroenterologist and hepatologist

Sina Hospital

Tehran University of Medical Sciences

Ulcers : breaks in the mucosal surface >5 mm, with depth to the submucosa
Health care costs of ~$10 billion / year in the US
Despite the constant attack on the gastroduodenal mucosa by noxious agents (acid, pepsin, bile acids, pancreatic enzymes, drugs, and bacteria), integrity is maintained by a system that provides mucosal defense and repair

Oxyntic Gastric �Gland

Gastric parietal cell � undergoing transformation after stimulation

Gastroduodenal Mucosal Defense

Physiology of Gastric Secretion

Epidemiology

DUs occur in 6–15% of the Western population.
The incidence of DUs declined from 1960 to 1980 and has remained stable since then.
The death rates , need for surgery , and physician visits have decreased over the past 30 years.
This is likely related to the decreasing frequency of Helicobacter pylori
Eradication of H. pylori has greatly reduced the recurrence rates.
Peak incidence : sixth decade.
More than half of GUs occur in males
GUs are less common than DUs, perhaps due to the higher likelihood of GUs being silent
DUs occur most often in the first portion of duodenum (>95%) (~90% located within 3 cm of the pylorus).
They are usually 1 cm in diameter
Giant ulcer: >3 cm
Ulcers depth at times reaching the muscularis propria.
The base of the ulcer often consists of a zone of eosinophilic necrosis with surrounding fibrosis.
Malignant DUs are extremely rare .
GUs can represent a malignancy.
Benign GUs are most often found distal to the junction between the antrum and the acid secretory mucosa (rare in fundus).
Benign GUs associated with H. pylori antral gastritis
NSAID-related GUs are not accompanied by chronic active gastritis (but have evidence of a chemical gastropathy)

Duodenal Ulcer

H. pylori & NSAID-induced injury account for the majority of DUs
Basal and nocturnal gastric acid secretion is increased
Bicarbonate secretion is decreased ( H. pylori ?)
Accelerated gastric emptying of liquids ?

Gastric Ulcer

Majority can be attributed to either H. pylori or NSAID-induced mucosal damage
GUs that occur in the prepyloric area are similar in pathogenesis to DUs
Acid output (basal and stimulated) tends to be normal or decreased in GU
Impairment of mucosal defense
Abnormalities in resting and stimulated pyloric sphincter pressure ?
bile acids, lysolecithin, and pancreatic enzymes (duodenal gastric reflux) ?
Delayed gastric emptying of solids ?

H. pylori & PUD

Gastric infection with the bacterium H. pylori accounts for the majority of PUD
Development of gastric MALT lymphoma and gastric adenocarcinoma
Gram-negative microaerophilic rod
Does not invade cells
Contains multiple sheathed flagella
Migrates toward the more proximal segments of the stomach
Outer membrane protein (Hop proteins)
Vacuolating cytotoxin (Vac A)
Cag pathogenicity island (cag-PAI).
Cag A activates a series of cellular events in cell growth and cytokine production
Urease produces ammonia from urea, an essential step in alkalinizing the surrounding pH
Multiple strains of H. pylori exist and are characterized by their ability to express several of these factors
Different diseases related to H. pylori infection can be attributed to different strains of the organism with distinct pathogenic features.
In developing parts of the world, 80% of the population may be infected by the age of 20,
prevalence is 20–50% in industrialized countries
Risk factors:
Poor socioeconomic status
less education
Birth or residence in a developing country,
Domestic crowding,
Unsanitary living conditions,
Unclean food or water,
Exposure to gastric contents of an infected individual
Transmission of H. pylori occurs from person to person , following an oral-oral or fecal-oral route
risk of H. pylori infection is declining in developing countries
Pathophysiology
associated with a chronic active gastritis
H. pylori is present in only 30–60% of GUs and 50–70% of DUs

H. pylori may lead to gastric secretory abnormalities

Natural history of H. pylori

Development of Non-cardia cancer is a multistage and multifactorial process

Atrophic gastritis + IM
hypochlorhydria

Host Genetic - IL-1B genotype

Dietary - Low antioxidant high salt

Environmental - Smoking

Bacterial - Colonisation of

achlorhydric stomach by nitrosating species

Superficial gastritis

Dysplasia & Cancer

H pylori infection

NSAID-Induced Disease

prescriptions written for NSAIDs was >111 million at a cost of $4.8 billion.
The most common drug-related toxicities in the US: NSAIDs
The spectrum of NSAID-induced morbidity ranges from:
Nausea and dyspepsia (50–60%)
Peptic ulceration (15–30% of individuals taking NSAIDs regularly)
Bleeding or perforation (1.5% of users per year)
> 80% of patients with serious NSAID-related complications did not have preceding dyspepsia
No dose of NSAID is completely safe
Enteric-coated are also associated with PUD
Established risk factors include:
Advanced age,
History of ulcer,
Glucocorticoids,
High-dose NSAIDs,
Multiple NSAIDs,
Anticoagulants,
Serious or multisystem disease.
Possible risk factors include :

NSAIDs may induce mucosal injury

Pathogenetic Factors Unrelated to� H. pylori and NSAIDs in PUD

Smokers have ulcers more frequently
Decrease healing rates,
Impair response to therapy
Increase ulcer-related complications (perforation)
Mechanisms:
Altered gastric emptying,
Decreased duodenal bicarbonate production,
Increased risk for H. pylori infection,
Generation of noxious mucosal free radicals
Genetic predisposition
First-degree relatives of DU patients are three times as likely to develop an ulcer
Increased frequency in blood group O
Psychological stress has been thought to contribute to PUD
Diet has also been thought to play a role in peptic diseases
Strong association are :
1) Systemic mastocytosis,
2) Chronic pulmonary disease,
3) Chronic renal failure,
4) Cirrhosis,
5) Nephrolithiasis,
6) A1-antitrypsin deficiency.
Possible association are:
1) Hyperparathyroidism,
2) Coronary artery disease,
3) Polycythemia vera,
4) Chronic pancreatitis

Clinical Features

Abdominal pain is common, but has a poor predictive value for the presence of PUD
10% of patients with NSAID-induced mucosal disease can present with a complication without antecedent symptoms
Typical pain pattern in DU occurs 90 min to 3 h after a meal and is frequently relieved by antacids or food.
Pain that awakes the patient from sleep (between midnight and 3 A.M.) is the most discriminating symptom, in two-thirds
This symptom is also present in 1/3 of patients with NUD
In GU, discomfort may actually be precipitated by food
Nausea and weight loss occur more commonly in GU
possible explanations for pain include:
Acid-induced activation of chemical receptors in the duodenum,
Enhanced duodenal sensitivity to bile acids and pepsin,
Altered gastroduodenal motility
Dyspepsia that becomes constant, is no longer relieved by food or antacids, or radiates to the back may indicate a penetrating ulcer (to the pancreas).
Sudden onset of severe, generalized abdominal pain may indicate perforation .
Pain worsening with meals, nausea, and vomiting of undigested food suggest gastric outlet obstruction .
Tarry stools or coffee-ground emesis indicate bleeding .

Physical Examination

Epigastric tenderness is the most frequent finding ( predictive value of this finding is rather low )
Tachycardia and orthostasis suggest dehydration secondary to vomiting or active gastrointestinal blood loss.
A severely tender, board like abdomen suggests a perforation.
Presence of a succession splash indicates retained fluid in the stomach, suggesting gastric outlet obstruction.

PUD-Related Complications

Gastrointestinal Bleeding
The most common complication
In ~15% of PUD patients
More often in individuals >60 y (likely due to the increased use of NSAIDs)
Perforation
The second most common complication
In 6–7% of PUD patients
Penetration is a form of perforation in which the ulcer bed tunnels into an adjacent organ.
DUs penetrate posteriorly into the pancreas , leading to pancreatitis,
Whereas GUs tend to penetrate into the left hepatic lobe

Gastric Outlet Obstruction

The least common complication
In 1–2% of patients
Obstruction secondary to inflammation and edema often resolves with ulcer healing.
A fixed, mechanical obstruction secondary to scar formation in the peripyloric areas requires endoscopic (balloon dilation) or surgical intervention

Differential Diagnosis

NUD, also known as functional dyspepsia is typified by upper abdominal pain without the presence of an ulcer
Proximal gastrointestinal tumors,
Gastroesophageal reflux,
Vascular disease,
Pancreaticobiliary disease (biliary colic, chronic pancreatitis),
Gastroduodenal Crohn's disease

Diagnostic Evaluation

In view of the poor predictive value of abdominal pain for the presence of an ulcer, documentation of an ulcer requires either a radiographic (barium study) or an endoscopic procedure
Double-contrast study
Detection rates as high as 90%
Sensitivity for detection is decreased in small ulcers (<0.5 cm), presence of previous scarring , or in postoperative patients
Ulcers >3 cm in size or those associated with a mass are more often malignant.
Up to 8% of GUs that appear to be benign by radiographic appearance are malignant by endoscopy or surgery.
Radiographic studies that show a GU must be followed by endoscopy and biopsy

A benign duodenal ulcer A benign gastric ulcer

The most sensitive and specific approach for examining the upper gastrointestinal tract
Facilitates tissue biopsy to rule out malignancy (GU) or H. pylori
Identifies lesions too small to detect by radiography
Evaluates atypical radiographic abnormalities
Determines if an ulcer is a source of blood loss

a benign duodenal ulcer a benign gastric ulcer

______________________________________________________________

Serum gastrin and gastric acid analysis (sham feeding) may be needed in individuals with complicated or refractory PUD (Zollinger-Ellison Syndrome).
Screening for aspirin or NSAIDs (blood or urine) may also be necessary in refractory H. pylori–negative PUD patients.
Acid suppression
Eradication of H. pylori
Therapy/prevention of NSAID-induced disease

Acid Neutralizing/Inhibitory Drugs

They are now rarely, used as the primary therapeutic agent
Mixtures of aluminum hydroxide and magnesium hydroxide
Should not be used in CRF, because of possible hypermagnesemia, and chronic neurotoxicity
Calcium carbonate can lead to milk-alkali syndrome (hypercalcemia, hyperphosphatemia with possible renal calcinosis and progression to renal insufficiency).

H2 Receptor Antagonists

Cimetidine, ranitidine, famotidine, and nizatidine have different potency,
Inhibit basal and stimulated acid secretion
May have weak antiandrogenic side effects (reversible gynecomastia & impotence)
Inhibit cytochrome P450 , (warfarin, phenytoin, and theophylline)
Confusion and elevated levels of serum aminotransferases, creatinine, and prolactin
Tolerance to H2 blockers
Pancytopenia

Proton Pump (H+,K+-ATPase) Inhibitors

Omeprazole, esomeprazole, lansoprazole, rabeprazole, and pantoprazole are benzimidazole derivatives that covalently bind and irreversibly inhibit H+,K+-ATPase
The most potent acid inhibitory agents
Maximum acid inhibitory effect between 2 and 6 h after administration
Duration of inhibition lasting up to 72–96 h
It can take 2 and 5 days for gastric acid secretion to return to normal levels once these drugs have been discontinued
Before a meal
No carcinoid tumor development in humans
Gastrin levels return to normal levels within 1–2 weeks after drug cessation
IF production is also inhibited, but vitamin B12-deficiency anemia is uncommon
Interfere with absorption of drugs such as ketoconazole, ampicillin, iron, and digoxin
Hepatic cytochrome P450 can be inhibited by omeprazole & lansoprazole
Warfarin, diazepam, atazanavir, and phenytoin concomitantly with PPIs
Associated with a higher incidence of community-acquired pneumonia
Tenatoprazole : longer half-life and inhibits nocturnal acid secretion
Potassium-competitive acid pump antagonists (P-CABs), inhibit gastric acid secretion via potassium competitive binding of the H+,K+-ATPase.

Cytoprotective Agents

Binding primarily to sites of active ulceration
Physicochemical barrier
Promoting a trophic action by binding growth factors such as EGF
Enhancing prostaglandin synthesis
Stimulating mucous and bicarbonate secretion
Enhancing mucosal defense and repair
Avoid in CRF to prevent aluminum-induced neurotoxicity.
Hypophosphatemia
Gastric bezoar formation
Ulcer coating;
Prevention of further pepsin/HCl-induced damage;
Binding of pepsin;
Stimulation of prostaglandins, bicarbonate, and mucous secretion
Black stools,
Constipation,
Darkening of the tongue
Neurotoxicity

Prostaglandin Analogues

Enhance mucous bicarbonate secretion,
Stimulate mucosal blood flow
Decrease mucosal cell turnover.
The most common toxicity noted with this drug is diarrhea (10–30%).
Uterine bleeding and contractions
Contraindicated in pregnancy

Therapy of H. pylori

PUD who are found to be H. pylori –positive by serology or breath testing.
Gastric MALT lymphoma
Patients with NUD, to prevent gastric cancer?
Patients with GERD requiring long-term acid suppression?
14 days provides the greatest efficacy
Promote ulcer healing,
Prevent ulcer recurrence and complications
Diminished recurrent ulcer bleeding
The most complication with amoxicillin is pseudomembranous colitis (<2%)
Tetracycline has been reported to cause rashes,hepatotoxicity and anaphylaxis
Resistant to amoxicillin, and tetracycline is uncommon
Quadruple therapy
Antibiotic-resistant strains are the most common cause for treatment failure in compliant patients
Second-line therapy include:
(levofloxin, amoxicillin, PPI) for 10 days
(furazolidone, amoxicillin an PPI)
Then culture and sensitivity of the organism
Cigarette smoking
Sequential therapy:5 days of amoxicillin + PPI, followed by an additional 5 days of PPI + tinidazole + clarithromycin
If H. pylori present, eradication is recommended for 14 days, followed by continued acid-suppressing drugs for 4–6 week
Test of choice for documenting eradication is the urea breath test (UBT).
Stool antigen assay (off PPI)
Multiple biopsies of a GU should be taken initially; even if these are negative for neoplasm, repeat endoscopy to document healing at 8–12 weeks should be performed, with biopsy if the ulcer is still present.
~ 70% of GUs eventually found to be malignant undergo significant (usually incomplete) healing.
A GU that fails to heal after 12 weeks and a DU that does not heal after 8 weeks of therapy should be considered refractory
Poor compliance
Persistent H. pylori infection
Malignancy ( For a GU)
Hypersecretory state such as ZES, (fasting gastrin or secretin stimulation test )
Crohn's disease
Amyloidosis
Sarcoidosis
Eosinophilic gastroenteritis
Infection [CMV, tuberculosis, or syphilis].
Higher dose is also effective in maintaining remission.
Surgical intervention

Surgical Therapy

Elective, for medically refractory disease,
Or as urgent/emergent, for an ulcer-related complication
GIB unresponsive or refractory to endoscopic intervention + IV PPI, will require surgery (~5% of transfusion-requiring patients)

Specific Operations for Duodenal Ulcers

Surgical treatment is designed to decrease gastric acid secretion by Vagotomy
1) vagotomy and drainage (by pyloroplasty, gastroduodenostomy, or gastrojejunostomy to compensate for the vagotomy-induced gastric motility disorder)
2) highly selective vagotomy (which does not require a drainage procedure)
3) vagotomy with antrectomy in prepyloric ulcers and refractory to medical therapy (lowest rates of ulcer recurrence but the highest complication rate)

Operations for Gastric Ulcers

Antrectomy (including the ulcer) with a Billroth I anastomosis is the treatment of choice for an antral ulcer.
Vagotomy is performed only if a DU is present
Ulcers located near the esophagogastric junction require subtotal gastrectomy with a Roux-en-Y esophagogastrojejunostomy (Csende's procedure).
A less aggressive approach, including antrectomy, intraoperative ulcer biopsy, and vagotomy (Kelling-Madlener procedure

Surgery-Related Complications

More aggressive surgical procedures have a lower rate of ulcer recurrence but a greater incidence of gastrointestinal dysfunction
Recurrent Ulceration
Afferent Loop Syndromes
Dumping Syndrome
Postvagotomy Diarrhea
Bile Reflux Gastropathy
Maldigestion and Malabsorption
Gastric Adenocarcinoma

Case Report: Peptic ulcer disease following short-term use of nonsteroidal anti-inflammatory drugs in a 3-year-old child

Alin Dumitru Ciubotaru Roles: Conceptualization, Project Administration, Resources, Supervision, Writing – Original Draft Preparation Carmen-Ecaterina Leferman Roles: Conceptualization, Writing – Original Draft Preparation, Writing – Review & Editing

peptic ulcer disease, upper gastrointestinal bleeding, nonsteroidal anti-inflammatory drugs, proton pump inhibitors, children

Revised Amendments from Version 1

In the new version, revisions in various sections have been made following the reviewers recommendations. Introduction – As suggested by the reviewers, regarding clarity of information related to epidemiology, we elaborated more about the indications for endoscopies mentioned in the two studies to which we referred in the second paragraph of the first version. Case presentation – Following the reviewers recommendation, we added hemodynamic parameters at admission (first paragraph), we gave more details of drugs administration (first and second paragraphs), family history and relevant medical history (second paragraph) and nutritional status of the patient (third paragraph). Discussion- We expanded on the accumulation of risk factors (third and fourth paragraphs), including family history, NSAIDs and paracetamol administration in the presented case, referring to the data found in published literature.

See the authors' detailed response to the review by Vera L. Sdepanian See the authors' detailed response to the review by Parijat Ram Tripathi

Introduction

Peptic ulcer disease (PUD) affects 1–2/1000 people annually in the USA, UK and Europe and has been gradually decreasing 1 . An explanation could be the declining prevalence of Helicobacter pylori infection. While the rate of infections is decreasing, the rate of complications remains static, likely due to an aging population which has an elevated usage of ulcerogenic medication 1 .

PUD occurs less frequently in children than adults. Epidemiological data are limited due to the rareness of the disease. A prospective European multicenter study aimed at determining frequency and risk factors of gastric and duodenal ulcers in children who underwent upper gastrointestinal endoscopies for different indications (epigastric or abdominal pain, gastroesophageal reflux disease) 2 . The study showed a frequency of 8.1% of ulcers and/or erosions, occurring mainly during the second decade of development 2 . In the USA, another study reported 17.4% of insured pediatric patients diagnosed as having any upper gastrointestinal ulcer developed peptic ulcer bleeding 3 .

PUD is a heterogenous disease defined by an imbalance between mucosa-protective and aggressive factors in the presence of risk factors including: H. pylori infection, chronic disease (inflammatory bowel disease, rheumatic diseases) and drug use, particularly nonsteroidal anti-inflammatory drugs (NSAIDs) 2 . In practice, NSAIDs are commonly used to manage acute febrile illness or pain in healthy children. One adverse reaction is acute gastrointestinal bleeding associated with short-term NSAIDs use, with a high rate of hospitalization and mortality in developed countries 4 . The adverse effect of short-term utilization of NSAIDs among children and their association with PUD are less clear.

We present a rare case of upper gastrointestinal bleeding following a low dose of ibuprofen in a 3-year-old to underline potentially severe side-effects of short-term NSAIDs use at appropriate doses in children.

Case presentation

A 3-year-old-female, with a family history of peptic ulcers, was admitted with fever, coffee-ground vomiting and abdominal pain, hemodynamically stable (heart rate 128 beats per minute, blood pressure 108/71 mmHg, respiratory rate 28 breaths per minute). The mother stated the patient received two weight-appropriate doses of ibuprofen (two doses of 100 mg -6.66 mg/kg- by mouth, 8 hours apart) and a dose of paracetamol (250 mg - 16.66 mg/kg- by mouth), both administered within an appropriate time interval in the previous 24 hours for fever control.

The patient had a positive medical history of upper respiratory tract infections with febrile seizures and interstitial pneumonia treated with antypiretics and clarithromycin, respectively. In the first days of the upper respiratory infection (5 weeks prior to the bleeding episode) ibuprofen 100 mg -6.66 mg/kg- was administered by mouth every 8 hours for three days and in the next two days two doses a day within an appropriate time interval. For the convulsion episode no antiseizure medication was needed. Also, clarithromycin 7.5 mg/kg/day was administered by mouth for 10 days. The duration of the symptoms was 2 weeks.

The patient is allergic to cephalosporin and amoxicillin/clavulanic acid. No immune deficiency disease was documented.

Clinical examination revealed general malaise, pallor, fever, pharyngotonsillar congestion and productive cough, normal breath sound, a distended and mildly tender abdomen moving normally with respiration and normal stool. The patient weighed 15 Kg (z-score 0.65) at the 72nd percentile and measured 88 cm tall (z-score -1.63) at the 5th percentile for stature. She has a body mass index (BMI) of 19.4 (z-score 2.15), placing the BMI-for-age at the 98th percentile.

Initial laboratory tests indicated anemia with reticulocytosis (Hematocrit 29.7%, Hemoglobin 9.6 g/dl, reticulocytes 3.6%, corrected reticulocyte count 3.24) and lower total protein (5.52 g/dL). Remaining laboratory results were normal, including coagulation tests.

Soon after hospitalization, the patient had a second episode of coffee-ground vomiting.

An upper digestive endoscopy with biopsy was performed revealing a non-bleeding gastric ulcer at 2 cm from pylorus ( Figure 1 ). H. pylori gastric biopsy testing was negative.

Figure 1. Endoscopic imaging.

This shows a non-bleeding gastric ulceration measuring 2.5 × 2 cm with edematous rim located 2 cm from the pyloric ring; pale gastric mucosa, fluid stasis and food debris; snake skin appearance of gastric mucosa in the fundus.

Based on this data, a diagnosis was made of NSAID-induced gastric ulcer, causing upper gastrointestinal bleeding.

During hospitalization, perfusion with glucose and electrolytes was administered in order to compensate for fluid loss. The patient was treated with a proton pump inhibitor (esomeprazole 10 mg/day - 0.66 mg/kg/day) for 2 months.

There were no further gastrointestinal symptoms. Hemoglobin values returned to normal, indicating resolution of gastrointestinal bleeding and the report of the endoscopy performed at the end of the treatment period confirmed the healing of the gastric ulceration area.

Upper gastrointestinal bleeding in a 3-year-old following short-term NSAIDs use is an uncommon presentation. Similar cases 5 have been reported in literature, but the adverse effects of short-term NSAIDs use among children and their association with PUD is not completely understood. However, some studies offer compelling data indicating certain risk factors, primarily: the child’s age 2 , NSAIDs consumption 2 , 4 , 6 , 7 and H. pylori infection 2 , 6 – 8 .

PUD seems to primarily affect patients between 10–20 years old 2 . A retrospective cohort study reported a lower median age for those with gastric ulcers, than those with duodenal ulcers 8 .

The second important factor is NSAIDs consumption. The probability of PUD increases with the duration of therapy, dose and presence of risk factors, including positive familial history or drugs coadministration 7 , 9 . Thus, despite a low dose of ibuprofen, the gastric ulcer (GU) in this case can be explained in part by a positive family history and association with a dose of paracetamol. A joint effect of paracetamol (a dosage higher than 2g) combined with NSAIDs was reported in adults that had both compounds prescribed together 10 . Conversely, the risk for gastrointestinal ulcers and ulcer complications due to normal paracetamol intake has not been yet supported by available biological and clinical data.

The accumulation of more risk factors, like positive family history, NSAID administration or H. Pylori infection in pediatric population affected by PUD, has been well documented. The father of the patient was diagnosed with PUD, but was unable to confirm whether he was H. Pylori positive.

Moreover, some studies conclude that short-term NSAIDs use is highly correlated with GU 6 . The association between short-term NSAIDs use and proton pump inhibitors (PPIs) can theoretically reduce the risk of upper gastrointestinal bleeding in children. Although coadministration of NSAIDs and PPIs is considered safe to reduce adverse gastrointestinal effects in adults 11 , there is not sufficient data about this drugs association in the prevention of short-term NSAIDs-PUDs in children.

The third important risk factor in PUD, H. pylori infection, was negative in our case. Some studies suggest a weaker association between H. pylori and PUD in children as compared with adults 2 , 12 . However, this infection is a well-recognized cause of chronic gastritis and plays an important role in the pathogenesis of PUD in children 13 .

Patients who develop gastrointestinal bleeding caused by NSAIDs-associated ulcers should discontinue use. Therapeutic strategies in these cases depend on the severity of presentation. Pharmacologic, endoscopic and surgical techniques have been developed to achieve hemostasis. In cases of massive bleeding, immediate endoscopic or surgical intervention is required. Scoring systems for upper gastrointestinal bleeding in children, laboratory tests and blood transfusion requirements are still under development 14 – 16 . In the present case, clinical presentation with two episodes of isolated hematemesis (coffee-ground vomiting) and endoscopic examination findings (non-bleeding gastric ulcer) correlated with laboratory tests indicated pharmacologic management.

Short term NSAIDs use in appropriate doses, commonly prescribed to control fever in children, can lead to PUD. Before administration, risk factors such as other antipyretic medication use, or a suggestive familial history must be considered. Doctors should inform caregivers of the risks involved and encouraging limited NSAIDs use.

Data availability

All data underlying the results are available as part of the article and no additional source data are required.

Written informed consent for the publication of this case report was obtained from the parents of the patient.

1. Sverdén E, Agréus L, Dunn JM, et al. : Peptic ulcer disease. BMJ. 2019; 367 : l5495. PubMed Abstract | Publisher Full Text
2. Kalach N, Bontems P, Koletzko S, et al. : Frequency and risk factors of gastric and duodenal ulcers or erosions in children: a prospective 1-month European multicenter study. Eur J Gastroenterol Hepatol. 2010; 22 (10): 1174–1181. PubMed Abstract | Publisher Full Text
3. Brown K, Lundborg P, Levinson J, et al. : Incidence of peptic ulcer bleeding in the US pediatric population. J Pediatr Gastroenterol Nutr. 2012; 54 (6): 733–736. PubMed Abstract | Publisher Full Text
4. Grimaldi-Bensouda L, Abenhaim L, Michaud L, et al. : Clinical features and risk factors for upper gastrointestinal bleeding in children: a case-crossover study. Eur J Clin Pharmacol. 2010; 66 (8): 831–837. PubMed Abstract | Publisher Full Text
5. Berezin SH, Bostwick HE, Halata MS, et al. : Gastrointestinal bleeding in children following ingestion of low-dose ibuprofen. J Pediatr Gastroenterol Nutr. 2007; 44 (4): 506–508. PubMed Abstract | Publisher Full Text
6. Huang SC, Sheu BS, Lee SC, et al. : Etiology and treatment of childhood peptic ulcer disease in taiwan: a single center 9-year experience. J Formos Med Assoc. 2010; 109 (1): 75–81. PubMed Abstract | Publisher Full Text
7. Cardile S, Martinelli M, Barabino A, et al. : Italian survey on non-steroidal anti-inflammatory drugs and gastrointestinal bleeding in children. World J Gastroenterol. 2016; 22 (5): 1877–1883. PubMed Abstract | Publisher Full Text | Free Full Text
8. Roma E, Kafritsa Y, Panayiotou J, et al. : Is peptic ulcer a common cause of upper gastrointestinal symptoms? Eur J Pediatr. 2001; 160 (8): 497–500. PubMed Abstract | Publisher Full Text
9. Autret-Leca E, Bensouda-Grimaldi L, Maurage C, et al. : Upper gastrointestinal complications associated with NSAIDs in children. Therapie. 2007; 62 (2): 173–176. PubMed Abstract | Publisher Full Text
10. García Rodríguez LA, Hernández-Díaz S: Relative Risk of Upper Gastrointestinal Complications among Users of Acetaminophen and Nonsteroidal Anti-Inflammatory Drugs. Epidemiology. 2001; 12 (5): 570–6. PubMed Abstract | Publisher Full Text
11. Gwee KA, Goh V, Lima G, et al. : Coprescribing proton-pump inhibitors with nonsteroidal anti-inflammatory drugs: risks versus benefits. J Pain Res. 2018; 11 : 361–374. PubMed Abstract | Publisher Full Text | Free Full Text
12. Elitsur Y, Lawrence Z: Non- Helicobacter pylori related duodenal ulcer disease in children. Helicobacter. 2001; 6 (3): 239–243. PubMed Abstract | Publisher Full Text
13. Blecker U, Gold BD: Gastritis and peptic ulcer disease in childhood. Eur J Pediatr. 1999; 158 (7): 541–546. PubMed Abstract | Publisher Full Text
14. Nasher O, Devadason D, Stewart RJ: Upper Gastrointestinal Bleeding in Children: A Tertiary United Kingdom Children’s Hospital Experience. Children (Basel). 2017; 4 (11): 95. PubMed Abstract | Publisher Full Text | Free Full Text
15. Thomson MA, Leton N, Belsha D: Acute upper gastrointestinal bleeding in childhood: development of the Sheffield scoring system to predict need for endoscopic therapy. J Pediatr Gastroenterol Nutr. 2015; 60 (5): 632–636. PubMed Abstract | Publisher Full Text
16. Garber A, Jang S: Novel Therapeutic Strategies in the Management of Non-Variceal Upper Gastrointestinal Bleeding. Clin Endosc. 2016; 49 (5): 421–424. PubMed Abstract | Publisher Full Text | Free Full Text

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In paragraph 3 of the Discussion section, the authors pointed out that positive family history of peptic ulcer and association with a dose of paracetamol could explain the gastric ulcer. First of all, the positive family history should be clarified, and secondly what should be the importance of using one dose of paracetamol.
The authors should emphasize all drugs used during at least in the last month because the patient “had a positive medical history of upper respiratory tract infections with febrile seizures and interstitial pneumonia treated with antipyretics and clarithromycin, respectively”.
The patient was treated with a proton pump inhibitor (esomeprazole 10 mg/day) for two months. Although there were no further gastrointestinal symptoms, and hemoglobin values returned to normal, there is no assurance that the ulcer improved. Therefore, the authors have to explain if another upper endoscopy was done and justify the reason do not perform it.

Is the background of the case’s history and progression described in sufficient detail?

Are enough details provided of any physical examination and diagnostic tests, treatment given and outcomes?

Is sufficient discussion included of the importance of the findings and their relevance to future understanding of disease processes, diagnosis or treatment?

Is the case presented with sufficient detail to be useful for other practitioners?

Competing Interests: No competing interests were disclosed.

Reviewer Expertise: Pediatric Gastroenterologist

In paragraph 3 of the Discussion section, the authors pointed out that positive family history of peptic ulcer and association with a dose of paracetamol could explain the gastric ulcer. First of all, the positive family history should be clarified, and secondly what should be the importance of using one dose of paracetamol.
The authors should emphasize all drugs used during at least in the last month because the patient “had a positive medical history of upper respiratory tract infections with febrile seizures and interstitial pneumonia treated with antipyretics and clarithromycin, respectively”.
The patient was treated with a proton pump inhibitor (esomeprazole 10 mg/day) for two months. Although there were no further gastrointestinal symptoms, and hemoglobin values returned to normal, there is no assurance that the ulcer improved. Therefore, the authors have to explain if another upper endoscopy was done and justify the reason do not perform it.
Respond or Comment
COMMENT ON THIS REPORT
In the introduction, the second paragraph, “An extensive study estimated the prevalence of ulcers and/or erosions in European children at 8.1%, occurring mainly during the second decade of development. In the USA, 17.4% of pediatric patients are diagnosed with upper gastrointestinal ulcers each year.” In both the studies endoscopies were performed for specific indications rather than in the general pediatric population. Please mention the indications for better clarity of information.
What were the hemodynamic parameters of the patient at admission?
What tests were performed for H. pylori in the patient?
Please give details of family history of peptic ulcer disease (PUD) and how was it diagnosed? Was that person H. pylori -positive?
In the discussion, the second paragraph, “A retrospective cohort study reported a lower median age for those with gastric ulcers, than those with duodenal ulcers. Our patient confirms this ratio.” This is not right to say that this case report confirms this ratio. Please change or remove it.
How do authors think that the presence of positive family history (in absence of H. pylori ) and paracetamol intake can explain the presence of gastric ulcer even with a low dose of NSAID? Please explain in more detail.
Why a repeat endoscopy was not performed to confirm the healing of gastric ulcer?
Please mention doses (in per kg) and interval of ibuprofen used in the patient.
Please do not write the brand name until significant or important (e.g. Augmentin).
Duration and severity of respiratory tract infection are not mentioned. Please give details.
The patient’s weight and height interpretation should be mentioned as per Z score.
Mention corrected reticulocyte count.
How laboratory reports (hemoglobin, hematocrit, total protein, and reticulocyte count) are suggesting bleeding characteristics? Please explain.
Please mention the dose of esomeprazole in mg/kg/day along with the dose written in case details.

Reviewer Expertise: Pediatric gastroenterology and hepatology

In the introduction, the second paragraph, “An extensive study estimated the prevalence of ulcers and/or erosions in European children at 8.1%, occurring mainly during the second decade of development. In the USA, 17.4% of pediatric patients are diagnosed with upper gastrointestinal ulcers each year.” In both the studies endoscopies were performed for specific indications rather than in the general pediatric population. Please mention the indications for better clarity of information.
What were the hemodynamic parameters of the patient at admission?
What tests were performed for H. pylori in the patient?
Please give details of family history of peptic ulcer disease (PUD) and how was it diagnosed? Was that person H. pylori positive?
In the discussion, the second paragraph, “A retrospective cohort study reported a lower median age for those with gastric ulcers, than those with duodenal ulcers. Our patient confirms this ratio.” This is not right to say that this case report confirms this ratio. Please change or remove it.
How do authors think that the presence of positive family history in absence of H. pylori ) and paracetamol intake can explain the presence of gastric ulcer even with a low dose of NSAID? Please explain in more detail.
Please mention doses (in per kg) and interval of ibuprofen used in the patient.
Please do not write the brand name until significant or important (e.g. Augmentin).
Duration and severity of respiratory tract infection are not mentioned. Please give details.
The patient’s weight and height interpretation should be mentioned as per Z score.
Mention corrected reticulocyte count.
How laboratory reports (hemoglobin, hematocrit, total protein, and reticulocyte count) are suggesting bleeding characteristics? Please explain.
Please mention the dose of esomeprazole in mg/kg/day along with the dose written in case details.

Reviewer Status

Alongside their report, reviewers assign a status to the article:

Reviewer Reports


	1	2
(revision) 09 Jun 21
22 May 20	read	read

Parijat Ram Tripathi , Ankura Hospital for Women and Children, Hyderabad, India
Vera L. Sdepanian , Universidade Federal de São Paulo, São Paulo, Brazil

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Case Presentation

Harold, a fifty-eight year old grocery store manager, had recently been waking up in the middle of the night with abdominal pain. This was happening several nights a week. He was also experiencing occasional discomfort in the middle of the afternoon. Harold decided to schedule an appointment with his physician.

The doctor listened as Harold described his symptoms and then asked Harold some questions. He noted that Harold's appetite had suffered as a result of the pain he was experiencing and as a result of the fear that what he was eating may be responsible for the pain. Otherwise, Harold seemed fine.

The doctor referred Harold to a physician that specialized in internal medicine and had Harold make an appointment for a procedure called an endoscopy. The endoscopy was performed at a hospital later that week. During the procedure, a long, thin tube was inserted into Harold's mouth and directed into his digestive tract. The end of the tube was equipped with a light source and a small camera which allowed the doctor to observe the interior of Harold's stomach. The endoscope was also equipped with a small claw-like structure that the doctor could use in order to obtain a small tissue sample from the lining of Harold's stomach, if required.

The endoscopy revealed that Harold had a peptic ulcer. Analysis of a tissue sample taken from the site showed that Harold also had an infection that was caused by bacteria. The doctor who performed the endoscopy gave Harold prescriptions for two different antibiotics and a medication that would decrease the secretion of stomach acid. The doctor also instructed Harold to schedule an appointment for another endoscopy procedure in 6 months.

Case Background

A peptic ulcer is a sore that occurs in the lining of a part of the gastrointestinal tract that is exposed to pepsin and acid secretions. Most peptic ulcers occur in the lining of the stomach or duodenum. 90% of all duodenal ulcers and 80% of all gastric ulcers are caused by H. pylori infection. Most of the remaining peptic ulcers are caused by long-term usage of certain anti-inflammatory medications like aspirin.

There is still some question as to how is spread. However, has been identified in the saliva of infected individuals and may be spread via this fluid. bacteria have the ability to survive the acid environment in the stomach because they produce enzymes that neutralize stomach acids. They also have the ability to move through the mucous membrane lining the stomach or duodenum and take up residence in the underlying connective tissue. The damage to the mucous membrane that results from a infection allows pepsin and hydrochloric acid to further damage the wall of the stomach or duodenum. The sore that results is the peptic ulcer.

Describe the functions of the following components of gastric juice.

		infection?

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Pathophysiology and clinical presentation – correct diagnosis

Normal physiology of the peptic tissues and mechanisms

The peptic tissue includes two major layers (mucous barrier & surface mucous cells) and utilizes numerous gastric mucosal mechanisms to safely contain the digestive gastric acid.

secrete a protective, gel-like mucus layer to protects gastric mucosa against autodigestion from pepsin and erosion by acids and other caustic materials from ingestion.
secrete bicarbonate ions to neutralize acids from the lumen
form tight junctions to repel harsh fluid that may injure the stomach lining
retrieves excess hydrogen ions back-diffused into the mucosa from the lumen and transport bicarbonate to mucosa
sustains high cellular metabolic and regenerative activity
promotes secretion of bicarbonate
promote production of gel mucous barrier
maintain mucosal blood flow (vasodilator)

Figure 1. Cross section of peptic tissue (Glyn, 2018)

Pathophysiology

Breakage or ulceration of the protective mucosal lining in the lower esophagus, stomach (i.e., gastric ulcers), and duodenum (i.e., duodenal ulcers; most common).

Figure 2. (A) Endoscopic and (B) histologic cross section views of peptic ulcer (Pathology for health Professionals 4th. edition, 2013)

Underlying causes

Inhibition of prostaglandin synthesis by aspirin and NSAIDs — decrease in protective mucus production, decrease in bicarbonate secretion (decrease in buffering capacity).

Stress-Related factors secondary to serious illness or ischemic conditions, such as multiple system organ failure, head trauma, and severe burn, resulting in multiple ulceration or ischemia in the stomach and/or duodenum.

Risk factors

H. pylori , habitual use of aspirin and/or NSAIDs, alcohol, smoking, chronic obstructive pulmonary disease, and acute pancreatitis.

Key criteria for diagnosis

Epigastric pain – burning sensation occurs after meals (gastric ulcers), 2-3 hours after meal or in the middle of night (duodenal ulcers) due to sensorineural stimulation by acid or muscle spasm. Duodenal pain could be immediately relieved by ingestion of food or NSAIDs.
Habitual use of aspirin and/or NSAIDs.
Presence of pylori.
Bleeding — more often seen in stress-related mucosal diseases with coagulopathy or mechanical ventilation.

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