Uncommon Causes of Appendicitis: Beyond the Obvious

Brief Overview of Common Appendicitis Causes

Appendicitis represents one of the most common surgical emergencies worldwide, with lifetime incidence rates ranging from 7-9% in developed countries. In Hong Kong, approximately 6,000 appendectomy procedures are performed annually according to Hospital Authority statistics. The classic understanding of appendicitis pathogenesis centers on luminal obstruction, typically by fecaliths (hardened stool particles) or lymphoid hyperplasia. When the narrow appendiceal lumen becomes blocked, mucus accumulation creates ideal conditions for bacterial overgrowth, primarily involving Escherichia coli, Bacteroides fragilis, and Pseudomonas species. This leads to distension, compromised blood flow, and eventual inflammation that can progress to ischemia, perforation, and peritonitis if untreated. The standard diagnostic approach combines clinical examination (including rebound tenderness and McBurney's point sensitivity), laboratory findings (leukocytosis, elevated C-reactive protein), and imaging confirmation through ultrasound or computed tomography. However, this conventional understanding fails to explain approximately 15-20% of cases where no obvious obstruction is identified, highlighting the importance of investigating alternative causes of appendicitis.

Recent epidemiological studies from Hong Kong's tertiary care centers reveal that atypical presentations account for nearly 25% of appendicitis cases in patients over 50 years old. These unusual etiologies often present diagnostic challenges, as they may lack the characteristic migratory right lower quadrant pain or exhibit modified inflammatory responses in immunocompromised patients. The clinical course may be indolent or manifest with unusual symptom complexes that deviate from the classic appendicitis presentation. Understanding these less common pathways to inflammation is crucial for accurate diagnosis and appropriate management, particularly when standard treatment protocols might need modification based on the underlying cause of appendicitis.

Types of Parasites: Ascaris, Enterobius vermicularis

Parasitic infections represent a significant but often overlooked cause of appendicitis, particularly in regions with endemic parasitic diseases or among populations with recent travel history. In Hong Kong, despite its advanced sanitation infrastructure, parasitic appendicitis still accounts for approximately 1-2% of cases according to a 2022 review of pathology specimens from Queen Mary Hospital. The most frequently implicated parasites include Ascaris lumbricoides (roundworm) and Enterobius vermicularis (pinworm), though Schistosoma species and Strongyloides stercoralis have also been documented. Ascaris lumbricoides, which can grow up to 35 centimeters in length, may physically obstruct the appendiceal lumen either directly or by inducing spasm of the intestinal wall. The mechanical blockage creates conditions identical to fecalith-induced appendicitis, with subsequent bacterial proliferation and inflammatory cascade.

Enterobius vermicularis presents a different mechanism of appendiceal inflammation. These small nematodes (2-13 mm in length) typically inhabit the cecum and adjacent bowel, with female worms migrating to the perianal region to deposit eggs. When large numbers of pinworms invade the appendix, they cause mucosal irritation and trigger local hypersensitivity reactions. Histopathological examination often reveals eosinophilic infiltration in the appendiceal wall, a finding that should raise suspicion for parasitic etiology. A retrospective analysis of appendectomy specimens at Prince of Wales Hospital identified parasitic involvement in 1.8% of cases, with Enterobius being the predominant species (68%), followed by Ascaris (22%) and mixed infections (10%). The seasonal variation observed—with higher incidence during humid summer months—suggests environmental factors influence parasite transmission patterns.

How Parasites Cause Appendiceal Inflammation

The pathophysiology of parasitic appendicitis involves multiple interconnected mechanisms beyond simple mechanical obstruction. Parasites can directly damage the appendiceal mucosa through attachment and feeding activities, creating portals of entry for secondary bacterial invaders. Additionally, parasites secrete various enzymes and metabolic products that trigger local inflammatory responses. For instance, Ascaris lumbricoides produces ascaronase and other proteolytic enzymes that degrade mucosal barriers and stimulate intense immune reactions. The resulting edema further narrows the appendiceal lumen, establishing a vicious cycle of obstruction and inflammation.

Immunological mechanisms play a crucial role in parasite-induced appendicitis. Helminths typically stimulate a Th2-polarized immune response characterized by eosinophilia and IgE production. While this response helps control parasitic burdens, it can also cause significant tissue damage when occurring within the confined space of the appendix. Eosinophils release major basic protein, eosinophil cationic protein, and other cytotoxic substances that damage epithelial cells and nerve endings. This explains why parasitic appendicitis may present with more pronounced pruritus ani or urticarial reactions compared to conventional bacterial appendicitis. Furthermore, some parasites can induce granuloma formation or cause vasculitis of appendiceal vessels, leading to ischemic changes that compound the inflammatory process.

Diagnosis and Treatment

Diagnosing parasitic appendicitis preoperatively remains challenging, as clinical features often overlap with conventional appendicitis. However, certain elements in the patient history should raise suspicion, including:

• Recent travel to endemic areas
• Household contacts with similar symptoms
• Perianal itching, especially nocturnal
• Visible worms in stool
• Peripheral eosinophilia (>500 cells/μL)

Imaging studies may occasionally reveal the parasites themselves, particularly with Ascaris infections where the worms' tubular appearance might be visible on ultrasound. However, definitive diagnosis usually occurs postoperatively through histopathological examination of the resected appendix. Microscopic analysis typically shows cross-sections of parasites within the lumen, accompanied by eosinophilic infiltration of the mucosal and submucosal layers. In some cases, parasite eggs may be identified in tissue sections or luminal contents.

Treatment requires a dual approach: surgical management of the acute inflammation followed by appropriate antihelminthic therapy. Appendectomy addresses the immediate surgical emergency, while medications such as albendazole (400mg single dose) or mebendazole (100mg twice daily for 3 days) eradicate residual parasitic infection. For complicated cases with disseminated strongyloidiasis, ivermectin may be preferred due to its broader spectrum. Postoperative stool examinations and treatment of household contacts are recommended to prevent recurrence. The table below summarizes the diagnostic and therapeutic approach to parasitic appendicitis:

Parasite	Diagnostic Clues	First-line Treatment	Additional Considerations
Ascaris lumbricoides	Visible worms in stool, biliary symptoms	Albendazole 400mg single dose	May cause intestinal obstruction
Enterobius vermicularis	Nocturnal perianal itching, Scotch tape test	Mebendazole 100mg, repeat in 2 weeks	Treat all household contacts simultaneously
Schistosoma species	Travel history, freshwater exposure, eosinophilia	Praziquantel 40mg/kg single dose	Granulomatous inflammation may mimic Crohn's disease

Carcinoid Tumors: Location and Impact

Neoplastic processes represent another important category among unusual causes of appendicitis, with carcinoid tumors being the most common primary appendiceal malignancy. These neuroendocrine tumors typically arise from enterochromaffin cells in the submucosa and most frequently occur at the tip of the appendix (75-85% of cases). According to data from Hong Kong Cancer Registry, appendiceal carcinoids account for approximately 0.5-0.7% of all gastrointestinal neoplasms, with an estimated incidence of 0.15-0.6 cases per 100,000 population annually. Most appendiceal carcinoids are discovered incidentally during histopathological examination of appendectomy specimens, as they rarely produce the carcinoid syndrome unless metastatic to the liver. The relationship between carcinoid tumors and appendicitis is multifactorial: the tumor may directly obstruct the appendiceal lumen, cause kinking of the appendix due to mass effect, or induce ischemia through vascular compromise.

The clinical significance of carcinoid-induced appendicitis extends beyond the acute inflammatory episode. Tumor size remains the most important prognostic factor, with lesions smaller than 1cm having virtually no metastatic potential, while those larger than 2cm carry a 20-40% risk of metastasis. Location within the appendix also influences management; tumors at the base may require right hemicolectomy due to concerns about margin status, while distal tumors are typically adequately treated with appendectomy alone. A comprehensive review of 48 appendiceal carcinoids treated at Hong Kong Adventist Hospital between 2015-2021 revealed that 62% presented as acute appendicitis, highlighting how this neoplastic process can masquerade as a common surgical emergency while representing a more complex underlying cause of appendicitis.

Other Rare Tumors (e.g., Mucinous Cystadenoma)

Beyond carcinoids, several other rare neoplasms can initiate the inflammatory cascade leading to appendicitis. Mucinous cystadenoma represents an important entity characterized by cystic dilation of the appendix filled with mucin. These tumors cause appendicitis through gradual luminal distension that compromises blood flow or through rupture that incites chemical peritonitis. The distinction between benign mucinous cystadenoma and malignant mucinous cystadenocarcinoma has profound implications for management, as the latter requires right hemicolectomy and carries risk of pseudomyxoma peritonei—a condition where mucinous tumor cells disseminate throughout the peritoneal cavity.

Adenocarcinomas of the appendix, while rare (accounting for only 0.08-0.2% of gastrointestinal malignancies), represent another neoplastic cause of appendicitis. These tumors often present at more advanced stages than carcinoids, with a higher propensity for lymphatic and peritoneal spread. Other unusual tumor types include gastrointestinal stromal tumors (GISTs), lymphomas, and metastatic deposits from distant primaries such as breast, lung, or melanoma. The mechanism of inflammation varies with tumor type: lymphomas may cause appendicitis through diffuse wall infiltration and luminal compromise, while GISTs typically grow extraluminally and cause symptoms through mass effect or ulceration. The diverse presentations underscore the importance of histopathological examination in all appendectomy specimens, particularly in older patients where neoplastic causes of appendicitis become more prevalent.

Implications for Surgical Management

The discovery of an underlying neoplasm significantly alters the surgical approach to appendicitis. For carcinoid tumors, the extent of resection depends on multiple factors:

• Tumor size: Lesions 2cm warrant right hemicolectomy
• Location: Base involvement may necessitate more extensive resection to achieve clear margins
• Histological features: Mesoappendiceal invasion >3mm, lymphovascular invasion, or high mitotic rate may indicate need for hemicolectomy
• Patient factors: Age, comorbidities, and preference influence decision-making

For mucinous neoplasms, surgical strategy must balance complete tumor removal against the risk of iatrogenic rupture. An intact specimen removal is paramount, as rupture can seed the peritoneal cavity with malignant cells. In cases where preoperative imaging suggests mucinous neoplasm, some surgeons advocate for initial laparoscopic evaluation followed by conversion to open procedure if needed to minimize rupture risk. The management of appendiceal adenocarcinoma generally follows colorectal cancer principles, with right hemicolectomy and lymph node dissection representing the standard of care. These considerations highlight how identifying a neoplastic cause of appendicitis transforms what might otherwise be a straightforward appendectomy into a potentially cancer-directed operation with significant implications for staging, adjuvant therapy, and long-term surveillance.

Crohn's Disease and Ulcerative Colitis

Inflammatory Bowel Disease (IBD) represents a well-established but infrequent cause of appendicitis, with distinct pathological mechanisms that differentiate it from conventional acute appendicitis. Both Crohn's disease and ulcerative colitis can involve the appendix, though the patterns and implications differ substantially. Crohn's disease may affect any part of the gastrointestinal tract, including the appendix, either in isolation or as part of more extensive disease. Isolated appendiceal Crohn's is rare, representing only 0.2-1.8% of all Crohn's cases according to data from Hong Kong IBD registry. The inflammation in Crohn's-associated appendicitis is typically transmural, with characteristic non-caseating granulomas found in approximately 15-25% of cases. Patients often present with subacute symptoms that may mimic recurrent appendicitis or have atypical features such as perianal disease concurrent with right lower quadrant pain.

Ulcerative colitis traditionally spares the appendix due to its skip pattern, but recent evidence challenges this dogma. Appendiceal involvement in ulcerative colitis may occur in 20-40% of cases when systematically evaluated, though it rarely causes isolated symptoms. Interestingly, epidemiological studies have identified an inverse relationship between appendectomy and subsequent development of ulcerative colitis, suggesting the appendix may play a role in disease pathogenesis. The inflammation in ulcerative colitis is typically limited to the mucosa and submucosa, contrasting with the transmural involvement characteristic of Crohn's disease. When IBD involves the appendix, the clinical presentation may be indistinguishable from conventional appendicitis, though certain features such as chronic diarrhea, weight loss, extraintestinal manifestations, or family history of IBD should raise suspicion for this alternative cause of appendicitis.

Appendiceal Involvement in IBD

The pathophysiology of appendiceal inflammation in IBD reflects the underlying immunologic dysregulation characteristic of these conditions. In Crohn's disease, the appendix may serve as an initial manifestation or represent skip lesion in established disease. The inflammation typically begins in the mucosa but rapidly becomes transmural, with fissuring ulcers, lymphoid aggregates, and fibrosis. This pattern explains why Crohn's-related appendicitis has higher rates of fistula formation (8-12% versus

In ulcerative colitis, appendiceal involvement typically mirrors the inflammation seen in the adjacent cecum and represents continuity of disease rather than skip inflammation. Histological examination reveals crypt abscesses, basal plasmacytosis, and diffuse mucosal inflammation identical to that seen in colonic disease. An intriguing phenomenon termed "cecal patch" describes ulcerative colitis limited to the cecum and appendix in patients with otherwise left-sided disease. The clinical significance of appendiceal involvement in ulcerative colitis remains debated, with some studies suggesting it predicts more aggressive disease course while others find no association. What is clear is that recognizing IBD as the underlying cause of appendicitis fundamentally alters management, as simple appendectomy may be insufficient and could potentially exacerbate intestinal inflammation in some cases.

Management Considerations

The management of IBD-related appendicitis requires careful consideration of the underlying disease state and extent. Key principles include:

• Preoperative differentiation: When possible, distinguishing IBD-related appendicitis from conventional appendicitis allows for optimized medical management and surgical planning
• Intraoperative assessment: Careful examination of the entire bowel for skip lesions, creeping fat, or other signs of Crohn's disease
• Surgical technique: In established Crohn's disease, stapled rather than ligated appendiceal stump closure may reduce fistula risk
• Medical therapy: Corticosteroids, immunomodulators, or biologics may be needed postoperatively to control underlying IBD

For patients with known IBD presenting with right lower quadrant pain, the decision to operate requires careful judgment. In flare situations, surgery may be avoided with aggressive medical therapy, while true appendiceal obstruction necessitates intervention. When Crohn's disease is first diagnosed at appendectomy, approximately 30-40% of patients will develop recurrent disease elsewhere in the gastrointestinal tract within 5 years, underscoring the need for ongoing gastroenterological follow-up. The table below contrasts key features of IBD-related appendicitis versus conventional appendicitis:

Feature	Conventional Appendicitis	Crohn's-related Appendicitis	Ulcerative Colitis-related Appendicitis
Onset	Acute (24-48 hours)	Subacute or recurrent	May coincide with colonic flare
Histology	Acute inflammation, neutrophils predominant	Transmural inflammation, granulomas	Mucosal inflammation, crypt abscesses
Complications	Perforation, abscess	Fistula, stricture	Typically uncomplicated
Management	Appendectomy	Appendectomy + medical therapy	Medical therapy often primary

Swallowed Objects (e.g., Seeds, Pins)

Foreign body ingestion represents an unusual but important cause of appendicitis, particularly in pediatric populations and individuals with certain behavioral or psychiatric conditions. The most commonly implicated objects include fruit seeds (especially watermelon, orange, or sunflower seeds), fish bones, toothpicks, and metallic objects such as pins or nails. In Hong Kong, a review of emergency department records from 2018-2022 identified 37 cases of appendicitis secondary to foreign bodies, representing approximately 0.3% of all appendicitis cases during that period. The mechanism typically involves the object passing through the gastrointestinal tract until it reaches the narrow appendiceal orifice, where it may become lodged due to size, shape, or surface characteristics. Sharp objects pose additional risk by penetrating the appendiceal wall, leading to localized perforation or facilitating bacterial translocation.

The clinical presentation of foreign body appendicitis often differs from conventional appendicitis in several key aspects. The onset may be more insidious, with symptoms persisting for several days before acute exacerbation. Pain localization might be less precise, and migration patterns may be absent. Certain foreign bodies produce characteristic imaging findings: fruit seeds may be radiolucent but sometimes visible on ultrasound as hyperechoic foci with acoustic shadowing; metallic objects are readily apparent on plain radiographs; fish bones may be visualized on CT scans due to their slight mineralization. A high index of suspicion is necessary, particularly when patients report recent ingestion of potentially problematic items or belong to high-risk groups such as children, denture wearers, or individuals with pica.

Migration Through the Gastrointestinal Tract

The journey of a foreign object from ingestion to appendiceal impaction follows a predictable pathway through the gastrointestinal system. After swallowing, objects traverse the esophagus (narrowest at cricopharyngeus), pass through the stomach (where acidic environment may modify certain materials), and enter the small intestine. Most foreign bodies that reach the small intestine will eventually pass spontaneously, with transit times varying from 12 hours to 10 days depending on size, shape, and composition. The critical point occurs at the ileocecal valve, where objects must navigate the transition from mobile small bowel to relatively fixed colon.

The appendix presents a particular hazard due to its blind-ending structure and small orifice (typically 2-3mm in diameter). Objects that approximate this size or have pointed ends may become entrapped, with subsequent inflammation developing through several mechanisms. Direct mucosal irritation triggers local edema that further narrows the lumen, creating a cycle of worsening obstruction. Bacterial proliferation behind the obstruction leads to conventional acute appendicitis. Sharp objects may cause focal perforation with contained abscess formation. Interestingly, some objects such as fruit seeds may not cause immediate symptoms but can serve as nidi for fecalith formation over time, creating a delayed presentation of appendicitis weeks or months after ingestion. This variable timeline contributes to the diagnostic challenge of foreign body appendicitis.

Diagnostic Challenges

Foreign body appendicitis presents substantial diagnostic difficulties due to its rarity and variable presentation. Key challenges include:

• History limitations: Patients often don't recall or report ingestion, particularly with small objects like seeds
• Radiologic detection: Many problematic foreign bodies (plastic, wood, thin fish bones) have poor radiopacity
• Atypical course: Symptoms may be chronic or recurrent rather than acutely progressive
• Age factors: Children may be unable to provide accurate history, while elderly patients may have cognitive impairment

Advanced imaging plays a crucial role in diagnosis. Computed tomography (CT) with thin slices and multiplanar reconstruction offers the highest sensitivity, capable of detecting approximately 85-90% of radiographically apparent foreign bodies. Characteristic findings include an intraluminal object with surrounding inflammatory changes or an appendicolith with atypical density or morphology. Ultrasound may reveal shadowing echogenic foci within a dilated appendix, though operator dependence limits its reliability. When foreign body appendicitis is suspected but not confirmed preoperatively, intraoperative findings may provide the diagnosis. Surgeons should carefully inspect the resected specimen, as palpation may reveal the foreign object within the inflamed appendix. Pathological examination should include sectioning of the entire appendix to identify radiolucent objects that escaped radiographic detection.

Appendiceal Ischemia

Vascular compromise represents one of the least common but most diagnostically challenging causes of appendicitis. Appendiceal ischemia can result from systemic hypoperfusion, localized vascular obstruction, or vasculitic processes affecting the appendiceal arteries. The appendix receives its blood supply primarily from the appendicular artery, a branch of the ileocolic artery that represents an end-artery with limited collateral circulation. This anatomical arrangement makes the organ particularly vulnerable to ischemic injury when perfusion is compromised. In systemic hypotension states—such as septic shock, profound dehydration, or cardiac failure—the appendix may suffer ischemic damage that progresses to inflammation and necrosis. This mechanism explains why critically ill patients sometimes develop "secondary" appendicitis despite no intrinsic luminal obstruction.

Localized vascular obstruction can occur through several mechanisms. Embolic phenomena, though rare, may involve the appendicular artery in patients with atrial fibrillation, endocarditis, or paradoxical embolism through patent foramen ovale. Thrombosis represents another pathway, potentially associated with hypercoagulable states such as antiphospholipid syndrome, malignancy, or inherited thrombophilias. Vascular compression by tumors, adhesions, or volvulus can also compromise appendiceal perfusion. The clinical presentation of ischemic appendicitis often differs from conventional forms, with more rapid progression to gangrene and perforation due to the combined effects of inflammation and tissue hypoxia. Pain may be disproportionately severe relative to physical findings initially, creating a potential diagnostic pitfall.

Vasculitis

Systemic vasculitides represent another vascular cause of appendicitis, though this manifestation is uncommon. Polyarteritis nodosa (PAN) classically involves small and medium-sized arteries throughout the body, including those supplying the gastrointestinal tract. When the appendicular artery is affected, inflammation, thrombosis, or aneurysm formation may lead to appendiceal ischemia. Similarly, Henoch-Schönlein purpura (HSP), characterized by IgA-dominant immune complex deposition, can cause gastrointestinal involvement in approximately 50-75% of cases, with the appendix affected in 2-6% of abdominal presentations. The vasculitic process damages vessel walls, leading to hemorrhage, edema, and compromised blood flow that culminates in inflammatory changes indistinguishable from conventional appendicitis.

Other vasculitides with potential appendiceal involvement include eosinophilic granulomatosis with polyangiitis (EGPA), microscopic polyangiitis, and Behçet's disease. The diagnosis of vasculitis-related appendicitis should be considered when appendiceal inflammation occurs in the context of systemic symptoms such as fever, weight loss, rash, arthralgias, or renal abnormalities. Laboratory findings may include elevated acute phase reactants, eosinophilia (in EGPA), elevated ANCA titers, or abnormal urinalysis suggesting renal involvement. Histopathological examination of the resected appendix typically reveals transmural inflammation with fibrinoid necrosis of vessel walls, leukocytoclasis, or eosinophilic infiltration depending on the specific vasculitis. Recognizing this unusual cause of appendicitis is crucial, as it necessitates systemic immunosuppressive therapy in addition to surgical management of the acute abdominal condition.

Impact on Appendiceal Integrity

The vascular supply to the appendix plays a fundamental role in maintaining tissue integrity, and compromise through ischemic or vasculitic mechanisms has profound implications for disease progression and complications. Unlike luminal obstruction which typically begins with mucosal inflammation that progresses outward, vascular compromise often causes transmural injury from onset. This explains the accelerated clinical course observed in ischemic appendicitis, with higher rates of gangrene (35-50% versus 15-25% in conventional appendicitis) and earlier perforation. The pattern of necrosis also differs, often involving longer segments of the appendix rather than the focal tip involvement common in obstructive etiologies.

The healing capacity of the appendix following vascular insult is limited by its end-artery supply. While mild ischemia may resolve if perfusion is restored, moderate to severe damage typically progresses to necrosis without the possibility of collateral circulation rescue. This has implications for non-operative management of appendicitis, which may be less successful in vascular causes compared to obstructive etiologies. Additionally, the inflammatory response in ischemic appendicitis involves different cytokine profiles, with greater representation of markers associated with hypoxia-inducible factors and cellular stress pathways. From a surgical perspective, ischemic appendicitis may present technical challenges due to friable tissues that hold sutures poorly and increased risk of stump dehiscence. These factors underscore the importance of considering vascular mechanisms when evaluating atypical presentations of appendicitis, particularly in patients with risk factors for vascular disease or systemic inflammatory conditions.

Recap of Less Common Appendicitis Causes

The landscape of appendicitis etiology extends far beyond the conventional understanding of luminal obstruction by fecaliths or lymphoid hyperplasia. Parasitic infections, though uncommon in developed regions like Hong Kong, remain relevant considerations particularly in specific patient populations or those with travel history. The mechanical obstruction and immunologic responses triggered by parasites such as Ascaris lumbricoides and Enterobius vermicularis create distinctive inflammatory patterns that may modify both presentation and management. Neoplasms, while rare overall, represent an important category of underlying pathology that transforms appendicitis from a simple inflammatory process to a potential malignancy presentation. The discovery of carcinoid tumors, mucinous neoplasms, or adenocarcinomas during appendectomy necessitates tailored surgical approaches and often additional oncological management.

Inflammatory bowel disease demonstrates how systemic conditions can manifest with focal appendiceal involvement, creating diagnostic challenges and altering therapeutic strategies. The recognition of Crohn's disease or ulcerative colitis as the fundamental cause of appendicitis shifts management from purely surgical to predominantly medical in many cases. Foreign bodies illustrate how extrinsic materials can initiate the inflammatory cascade through mechanical, obstructive, or perforating mechanisms. The diagnostic difficulties posed by radiolucent objects and unreliable ingestion histories make this an often-overlooked category. Finally, vascular causes including ischemia and vasculitis highlight how perfusion compromise can generate appendiceal inflammation independent of luminal factors. This diverse array of unusual pathways to a common clinical endpoint underscores the complexity of appendiceal pathology and the importance of maintaining broad diagnostic consideration.

Importance of Considering Atypical Etiologies in Diagnosis

Recognizing unusual causes of appendicitis carries significant implications for patient care, surgical outcomes, and long-term management. When standard treatment protocols based on conventional appendicitis pathophysiology are applied to patients with atypical underlying causes, suboptimal outcomes may result. For instance, simple appendectomy without antiparasitic therapy in parasitic appendicitis risks recurrence if household contacts remain untreated. Similarly, failing to recognize IBD as the fundamental process may lead to inappropriate surgical management or missed opportunities for medical intervention. The discovery of neoplasms during appendectomy necessitates consideration of additional resection, staging procedures, and oncological follow-up that would not be required for conventional appendicitis.

From a diagnostic perspective, maintaining awareness of unusual etiologies prompts more thorough history-taking, targeted physical examination, and selective use of advanced imaging or laboratory studies. Certain red flags should raise suspicion for atypical causes of appendicitis:

• Age >50 years with first presentation of appendicitis
• Recurrent or chronic right lower quadrant pain
• Systemic symptoms (fever, weight loss, rash) accompanying abdominal pain
• History of IBD, vasculitis, or malignancy
• Recent travel to endemic parasitic regions
• Known foreign body ingestion
• Atypical laboratory findings (eosinophilia, markedly elevated inflammatory markers)

The comprehensive approach to appendicitis should balance efficient diagnosis of the common condition with appropriate consideration of unusual etiologies when clinical features deviate from expected patterns. This dual perspective ensures that patients receive timely intervention for their acute condition while also addressing any underlying pathological processes that might have broader health implications. As our understanding of appendiceal pathology continues to evolve, maintaining diagnostic openness to unusual causes of appendicitis remains fundamental to providing optimal patient care across the spectrum of this common yet complex surgical condition.

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