Hypertriglyceridemic Acute Pancreatitis With Concomitant Retrocecal Appendicitis: A Case Report

ABSTRACT

Hypertriglyceridemia‐induced acute pancreatitis and acute appendicitis are distinct clinical conditions rarely reported to occur concurrently. We present a case of hypertriglyceridemia‐induced pancreatitis characterized by clinical deterioration despite a decline in serum triglyceride levels. While initial imaging demonstrated pancreatic inflammatory signatures, emergent exploratory laparotomy revealed a concomitant retrocecal appendicitis complicated by a pelvic abscess.

Key Clinical Message

Concurrent acute abdominal pathologies can mask one another. This case highlights the coexistence of hypertriglyceridemia‐induced acute pancreatitis and retrocecal appendicitis. Clinicians should reassess the patient and maintain a broad differential diagnosis when the clinical course does not follow the expected trajectory.

1. Introduction

Acute abdominal pain is one of the most frequent and diagnostically challenging presentations in emergency settings [1].

Acute pancreatitis (AP) is a potentially life‐threatening inflammatory condition with a rising global incidence and significant morbidity and mortality [2].

Most cases follow a mild course, with mortality reaching up to 30% in severe episodes [3].

Hypertriglyceridemia (HTG) is a well‐established etiology of AP, accounting for 1%–10% of all cases and is associated with higher rates of severe pancreatitis and mortality compared to other etiologies [4].

Acute appendicitis (AA) is one of the most common surgical emergencies worldwide [5]. This pathological process is typically caused by luminal obstruction or infections, although its exact origin largely remains unknown [6].

Establishing a timely diagnosis of AA can be particularly difficult when it manifests atypically, as seen in retrocecal appendicitis that often lacks classical clinical signs [7].

Both AP and AA are common causes of acute abdominal pain; however, their concurrence is exceedingly rare [8]. The diagnostic complexity is further compounded when both conditions present with overlapping or unclear symptoms, leading to potential delays in critical intervention [9]. Herein, we report a unique case of HTG‐induced AP occurring simultaneously with retrocecal AA and a subsequent pelvic abscess.

2. Case History and Examination

In late September 2025, a 43‐year‐old man with a history of HTG and Type 2 diabetes mellitus presented to the emergency department of Khorshid Hospital, Isfahan, Iran with severe diffuse abdominal pain. The pain was predominantly epigastric, developed gradually over the preceding 24 h, and remained continuous with an intensity score of 7/10. It was non‐radiating, non‐positional, and notably exacerbated by deep inspiration. He reported no nausea, vomiting, or respiratory symptoms but had no bowel movements or flatus since the previous day. History revealed a similar episode of abdominal pain 1 month earlier, which had resolved without comprehensive evaluation. His medication regimen had included fenofibrate, rosuvastatin, and a metformin/sitagliptin combination; however, all therapies had been discontinued approximately 4 months prior to presentation, as he perceived his condition to have improved. Upon admission, vital signs were as follows: axillary temperature 36.5°C, blood pressure 126/78 mmHg, marked tachycardia of 136 bpm, respiratory rate 20 breaths/min, and oxygen saturation (SpO2) 94% on room air. He appeared ill and diaphoretic. Abdominal examination revealed a distended, rigid abdomen and marked epigastric tenderness without rebound and guarding. The remainder of the physical examination, including cardiovascular and neurological assessments, was unremarkable.

3. Investigation and Treatment

Initial laboratory results were notable for: WBC 16,800/μL (absolute neutrophil count 15,000/μL), TG 5540 mg/dL, Amylase 383 U/L, Lipase 1075 U/L, Blood Sugar (BS) 412 mg/dL, lactate dehydrogenase (LDH) 527 U/L and urinalysis showing ketones 2+. Arterial blood gas (ABG) analysis indicated pH 7.34, PCO2 28 mmHg, and bicarbonate (HCO3): 15.9 mEq/L compatible with metabolic acidosis. Other objective parameters including the liver function test, renal function test, and coagulation profile were within normal limits. Electrocardiography showed sinus tachycardia.

The patient was managed for diabetic ketoacidosis (DKA) and severe HTG. Given the patient's clinical condition and inability to tolerate oral feeding, initial NPO status was maintained.

Fluid resuscitation with Ringer's lactate (1 L every 8 h) was initiated, along with strict monitoring of intake/output and blood glucose levels.

A continuous intravenous regular insulin infusion was initiated to simultaneously treat DKA and reduce serum triglycerides. Analgesia and general supportive care were provided.

As the metabolic status began to stabilize, the regimen was transitioned to include NPH insulin.

Plain abdominal radiographs were unremarkable. Abdominopelvic ultrasonography showed peripancreatic fluid collections (15 × 75 mm) anterior to the pancreas and a hypoechoic area (68 × 50 mm) in the right lateral aspect of the pancreas, dilated and hyper‐aerated bowel loops, and Grade 2 fatty liver. No gallstones or biliary duct dilation were identified.

A surgical consultation was obtained to evaluate the presence of acute abdomen in the setting of severe AP. At this stage, the absence of bowel movements and diffuse abdominal pain were primarily attributed to AP‐induced paralytic ileus.

The treatment regimen was adjusted to add normal saline 500 mL every 8 h, icosapent ethyl 500 mg twice daily, rosuvastatin nightly, and subcutaneous unfractionated heparin 5000 IU twice daily for deep vein thrombosis (DVT) prophylaxis.

The patient was transferred to the intensive care unit (ICU) for close monitoring and advanced supportive care. Over the following 48 h, BS levels were stabilized, and oral fluid intake was initiated. Notably, the serum TG decreased from 5540 mg/dL to 2110 mg/dL, reflecting a significant biochemical response to insulin‐based therapy.

On hospital Day 4, despite the initial stabilization, he developed severe diffuse abdominal tenderness refractory to conventional analgesics, necessitating opioid administration. This was accompanied by a high‐grade (39°C) fever and progressive respiratory distress, with an oxygen saturation drop to 60% that required supplemental oxygen. The heart rate increased to 130 beats per minute and blood pressure rose to 150/90 mmHg.

On examination, diminished breath sounds were noted at both lung bases with coarse crackles, whereas the chest radiograph revealed no specific changes. Serum TG and WBC had declined to 1400 mg/dL and 13,700/μL respectively, the CRP remained persistently elevated at 58 mg/L. NPO status was re‐established and subcutaneous heparin and oral lipid‐lowering agents were withheld.

Contrast‐enhanced computed tomography (CT) of the chest showed aspiration pneumonia and right‐sided pleural effusion, with no evidence of pulmonary thromboembolism. Abdominopelvic contrast‐enhanced CT scan demonstrated pancreatic swelling, peripancreatic fat stranding, and fluid collections consistent with AP, and diffuse small bowel dilation with a transition point in the distal ileum, suggesting mechanical obstruction (Figure 1). Given the patient's clinical deterioration and concern for acute respiratory distress syndrome (ARDS), intravenous fluids were restricted and empiric broad‐spectrum antibiotics (Meropenem, Levofloxacin, Vancomycin) were administered due to suspected severe intra‐abdominal sepsis. Despite these measures, the patient developed bilious vomiting (approximately 400 mL), prompting the medical and surgical teams to opt for emergent laparotomy. Intraoperative findings were significant for an inflamed retrocecal appendix with a sizeable pelvic abscess, causing extensive entrapment of the small bowel and colon. The appendiceal base was uninvolved, and the pancreas showed no evidence of infection or necrosis. The pathological analysis of the exudate and the resected specimen confirmed the diagnosis (Figure 2). Following appendectomy and adhesiolysis, with abdominal drain placement, the patient was transferred back to the ICU.

FIGURE 1.

Contrast‐enhanced abdominopelvic CT scan demonstrating pancreatic edema and enlargement with extensive peripancreatic stranding and fluid collections extending into the mesentery, compatible with AP.

FIGURE 2.

Muscularis propria layer showing moderate‐to‐dense neutrophilic infiltration (H&E stain).

4. Outcome and Follow‐Up

The patient's postoperative recovery was favorable, allowing for successful extubation on hospital Day 5. Oral nutrition and fenofibrate were resumed on Day 6 as abdominal pain resolved and bowel function returned.

On hospital Day 9, a low‐grade fever prompted an escalation of the antibiotic regimen to meropenem and linezolid following an infectious disease consultation. Subsequent imaging confirmed stable peripancreatic collections with no evidence of secondary infection.

By hospital Day 14, the patient remained afebrile and hemodynamically stable, with a significant reduction in serum triglycerides to 195 mg/dL (Figure 3). He was discharged on hospital Day 15 in good clinical condition, with a strong emphasis on adherence to lipid‐lowering therapy (including fenofibrate), strict glycemic control, dietary modification, and regular outpatient follow‐up. A comprehensive timeline of the clinical course and therapeutic interventions is summarized in (Figure 4).

FIGURE 3.

The graphical trend of serum triglyceride level during hospitalization.

FIGURE 4.

Timeline illustrating the clinical history, interventions, and course of treatment for the presented case. BS, blood sugar; CT, computed tomography; D, day; DKA, diabetic ketoacidosis; DVT, deep vein thrombosis; I&O, intake and output; ICU, intensive care unit; NPO, nil per os (nothing by mouth); PO, per os (by mouth); VS, vital signs.

5. Discussion

Despite being common entities individually, the coexistence of AP and AA poses a significant diagnostic challenge in clinical practice, particularly when one condition obscures the clinical features of the other.

In the present case, the patient exhibited severe epigastric pain, markedly elevated triglyceride levels, and increased pancreatic enzyme levels, fulfilling the diagnostic criteria for HTG‐induced AP. According to the Revised Atlanta Classification, disease severity is determined by the presence and duration of organ failure as well as local and systemic complications. Contrast‐enhanced CT was performed at the appropriate time interval to further support the diagnosis and to assess disease severity and complications [10, 11].

The initial management was therefore primarily directed toward AP and associated metabolic derangements. Although early oral feeding is recommended in acute pancreatitis when clinically tolerated, it was not feasible in this patient [12].

Intravenous insulin infusion was administered as the mainstay of therapy for HTG, consistent with current standards of care [13].

Although earlier studies suggested the use of heparin infusion to enhance lipoprotein lipase activity, it was not incorporated into our treatment strategy, as current evidence discourages its routine use due to transient effects and potential adverse outcomes [14]. In our case, heparin was limited to prophylactic dosing for venous thromboembolism prevention and was withheld upon clinical deterioration.

Despite biochemical improvement and the steady downward trend in serum triglycerides, the patient's clinical condition continued to deteriorate, eventually progressing to signs of an acute surgical abdomen. The emergence of atypical clinical features, including respiratory dysfunction, necessitated a reassessment of the initial diagnosis, repeated imaging, and ultimately prompted exploratory laparotomy.

This approach may further reduce the risk of complications in such patients and allow the initiation of early aggressive management as both severe AP and AA are associated with multi‐organ dysfunction, resulting in a higher rate of morbidity and mortality [15, 16].

The subsequent intraoperative finding of retrocecal appendicitis with a pelvic abscess indicates a concealed pathology.

Retrocecal appendicitis is well known for its atypical presentation and may lack classic right lower quadrant findings.

This diagnostic challenge is particularly compounded by overlapping symptoms with AP, including abdominal pain, leukocytosis, elevated amylase/lipase, and systemic inflammatory response [17].

In this patient, radiological studies failed to identify the inflamed appendix. This diagnostic pitfall is largely attributable to the retrocecal anatomical variant, where the appendix is sequestered by the cecum. Furthermore, its inflammatory signature is masked by the extensive peripancreatic fat stranding and fluid collections associated with severe AP, highlighting the limitations of imaging in complex intra‐abdominal inflammatory states.

These findings are best interpreted as coexistence; however, a potential bidirectional relationship between these conditions cannot be entirely excluded.

Previous reports have described different relationships between AP and appendiceal pathology.

AP may induce periappendiceal inflammation or even secondary appendicitis through the spread of inflammatory exudates within the retroperitoneum [18, 19].

Conversely, AA may rarely trigger AP via systemic inflammation, bacterial translocation, or impaired pancreaticobiliary flow [20].

A limitation of this case report was the absence of intraoperative photographic documentation.

6. Conclusion

Hypertriglyceridemic acute pancreatitis can mask or coexist with other intra‐abdominal emergencies such as retrocecal appendicitis.

This case highlights key clinical considerations in the evaluation of complex abdominal presentations. The diagnosis of acute pancreatitis should not preclude ongoing reassessment, particularly when the clinical course deviates from the expected trajectory. Persistent ileus, unexplained fever, or worsening abdominal findings should raise suspicion for additional intra‐abdominal pathology. Furthermore, retrocecal appendicitis may be missed on imaging and should remain an important differential diagnosis in patients with atypical clinical patterns, especially in the setting of overlapping inflammatory conditions.

Author Contributions

Mansoureh Shekarchizadeh Esfahani: conceptualization, investigation, writing – original draft, writing – review and editing. Masood Shekarchizadeh: writing – original draft, supervision. Seyed Amirhossein Dormiani Tabatabaei: writing – review and editing, writing – original draft, investigation, software, data curation. Mehrnazsadat Dormiani Tabatabaei: writing – original draft.

Funding

The authors have nothing to report.

Ethics Statement

This study was approved by the Ethics Committee of Isfahan University of Medical Sciences.

Consent

Written informed consent was obtained from the patient for publication of the de‐identified data in this case report.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.