Introduction

In the pediatric population the prevalence of Helicobacter pylori‐related gastritis is in decline due to changes in overall global socioeconomic status, better diagnostic techniques, and effective treatment. Henc,e the other causes of gastritis and gastropathy have become more relevant and will be discussed in this chapter.

Gastritis and gastropathy are two terms which are inappropriately used interchangeably. The term gastritis should be used if there is an inflammation or gastric mucosal injury. Gastropathy should be used when there is gastric mucosal disorder without any inflammation or with negligible inflammation. The mucosal disorder can further be defined as epithelial cell injury which may be followed by regeneration [1]. Gastritis and gastropathy can be classified according to morphological features or based on etiology (Table 22.1).

Infective gastropathy

Helicobacter pylori has traditionally been the most common cause of gastritis in children [2] but with better socioeconomic conditions, early diagnosis and effective treatment, there has been a steady decline in its prevalence [3]. Hence there is increased reporting of non‐Helicobacter pylori gastritis [4]. Besides H. pylori, H. heilmanii (previously called Gastrospirillium hominis), which is a spiral bacterium, can also cause chronic gastritis [5]. This bacterium is transmitted to humans via cats and dogs [6,7].

Gastric tuberculosis usually develops secondary to other primary lesions but sporadic primary gastric tuberculosis has been reported [8,9]. This can present as pyrexia of unknown origin [10], gastric outlet obstruction [11], benign peptic ulcer [12], stomach perforation [13], and gastric carcinoma [14]. The lesions are primarily present in the antrum and prepyloric region. The endoscopic findings could be solitary or multiple ulcer or hypertrophic nodular lesions or pyloric stenosis.

Cytomegalovirus (CMV) gastritis is primarily but not exclusively seen in immunocompromised children [15]. It is also associated with childhood Menetrier’s disease [16]. The endoscopic findings can include congested mucosa, swollen rugal folds with multiple erosions or ulcerations [17] and primarily it affects the gastric body and fundus. CMV DNA polymerase chain reaction (PCR) from biopsy samples is more sensitive than serology and also aids in disease localization [18,19]. Though spontaneous recovery usually occurs within 1–2 months, early detection and antiviral therapy can reduce morbidity and mortality in high‐risk cases [20].

Other viruses that can cause gastritis are Epstein–Barr virus (EBV), herpes virus, hepatitis C, measles, varicella, and influenza, especially influenza A which can cause hemorrhagic diffuse gastritis.

The two most common gastritides caused by parasites are those ascribed to giardiasis and ascariasis. Giardiasis is associated with conditions causing hypochlorhydria such as biliary reflux, atrophic gastritis, partial gastrectomy or use of proton pump inhibitors (PPI). In such situations, correction of gastric pH, for example by discontinuation of PPI, can lead to decolonization of Giardia without any specific therapy [21].

Cryptosporidium, Toxoplasma, and Leishmania are other parasites causing gastritis, particularly in immunocompromised patients [22–24].

Fungal gastritis is seen in children with faltering growth, burns or those who are immunocompromised. The main pathogens are Candida, Aspergillus, Histoplasma, and mucormycosis.

Phlegmonous or suppurative gastritis is a rare rapidly progressive bacterial infection of the gastric submucosa leading to gangrene/necrosis or emphysema [25] which can occur predominantly in immunocompromised patients [26–28]. The main pathogens are alpha‐ and beta‐hemolytic streptococci, although Pneumococcus, E. coli, Staphylococcus aureus, Proteus, and Clostridium welchii may also be implicated. The treatment includes aggressive use of antibiotics and very occasionally gastrectomy.

Reactive gastropathy

Reactive gastropathy or type C gastritis is the most common histological finding on gastric biopsies in North America [29]. There are no known specific endoscopic findings, but histologically it is characterized by foveolar hyperplasia, edema, smooth muscle hyperplasia and congestion of superficial capillaries in the lamina propria in absence of significant inflammation [30,31]. It occurs in response to long‐term exposure to irritants such as bile, NSAIDs, corrosives, and other drugs.

It is important to highlight here the term acute hemorrhagic erosive gastropathy which develops shortly after exposure of gastric mucosa to various injurious irritants or may be due to significantly diminished gastric mucosal blood flow, leading to disruption of the gastric protective barrier, or occasionally viruses such as influenza A. Endoscopy shows multiple petechial hemorrhages and erosions [32], which are usually confined to the fundus and body in stress‐related lesions (Curling’s ulcers) or could be widespread, as with NSAIDs or ethanol [33].

Stress‐induced gastritis (stress‐related erosive syndrome) is associated with massive burn injury, head injury, sepsis, trauma and multiple system organ failure. A cohort of 1006 consecutive admissions enrolled in a pediatric intensive care unit reported upper GI bleeding in 10.2% admissions with 1.6% having significant upper GI bleed [34]. Although there is a clear guideline on stress‐related prophylaxis for adults admitted to intensive care, unfortunately no such standardized guideline exists for the pediatric population [35].

Duodenogastric reflux (DGR) leading to biliary gastropathy could primarily occur due to motility issues or it could be secondary to surgery of the stomach, duodenum or gallbladder [36]. Therapeutic options are limited. Ursodeoxycholic acid is effective in reducing pain, nausea and vomiting [37]. Ursodeoxycholic acid is not proved to be effective in resolution of endoscopic or histological findings, but sucralfate does improve histological features [38]. Colestyramine can also be helpful by binding bile acids.

Accidental corrosive ingestion leading to gastropathy is a common problem in children worldwide [39]. In a review of 156 children with caustic ingestion, 11% had esophageal and gastric burns and 9% had gastric burns only [40]. Gastric injury is more likely to occur after ingestion of liquid rather than solid alkali [41]. The North American Society for Pediatric Gastroenterology Hepatology and Nutrition (NASPGHAN) has published guidelines for management of corrosive ingestion in the pediatric population [42].

Other causes of gastropathy are summarized in Table 22.1.

Conclusion

The etiology of pediatric gastropathy is different from that seen in adults and thus requires a tailored approach. Endoscopy and histopathology play a pivotal role in defining the etiology, localization, and extent of injury. As the prevalence of H. pylori declines, more emphasis is being placed on other causes of gastropathy. There is a need to develop an acceptable pediatric guideline for prophylaxis of stress‐related gastropathy in an ICU setting and also in stress‐inducing operations such as big orthopedic procedures – PPI prophylaxis is indicated in these situations.