Anterior Cutaneous Nerve Entrapment Syndrome Triggered by Thoracic Compression Fracture and Weight Loss

Abstract

Anterior cutaneous nerve entrapment syndrome (ACNES) and thoracic radiculopathy are rare forms of abdominal pain. Therefore, we herein report an older man with chronic right lower abdominal pain from coexisting ACNES and thoracic radiculopathy, probably triggered by asymptomatic thoracic compression fractures and significant weight loss. The diagnosis was confirmed based on a positive Carnett's sign and immediate pain relief after the diagnostic lidocaine injection. Imaging revealed a T12 compression fracture with narrowing of the right T11/12 intervertebral foramen. This case highlights the need to consider ACNES and spinal pathology in older patients with unexplained abdominal pain in the context of frailty and postural changes.

Introduction

Anterior cutaneous nerve entrapment syndrome (ACNES) is characterized by chronic, localized abdominal pain resulting from entrapment of the anterior cutaneous branch of the intercostal nerve at the level of the rectus abdominis muscle fascia (1). Imaging and laboratory findings are frequently unremarkable, making the diagnosis of ACNES challenging (2). In older adults, vertebral compression fractures, weight loss, and postural changes may contribute to the development (3). In addition, the nerve root symptoms resulting from compression fractures may present as abdominal pain (4).

We herein report an older man with ACNES and spinal nerve root symptoms presumably triggered by an asymptomatic thoracic compression fracture and significant weight loss.

Case Report

An 89-year-old man with a medical history of hypertension presented with progressive kyphosis that had developed over the past year. He reported a decreased oral intake and 3 kg weight loss over the preceding 6 months, without associated back pain. He began experiencing persistent localized pain in the right lateral abdomen approximately four months before presentation. He visited the emergency department of another hospital multiple times. While small gallstones were identified, no signs of cholecystitis, common bile duct dilation, or other abnormalities that could explain the pain were observed. Laboratory tests yielded unremarkable results. He was managed conservatively with oral acetaminophen; however, the treatment was ineffective, and abdominal pain persisted. The ongoing pain further worsened the patient's appetite and oral intake.

Abdominal computed tomography (CT) performed eight months before the symptom onset revealed preserved subcutaneous and visceral fat (Fig. 1A). The dull right lower abdominal pain was aggravated by specific movements, including raising the right arm, eye drop instillation, and adopting a supine position (Fig. 1B, dashed-line area). Pain was not associated with food intake. A physical examination revealed persistent dull pain localized to the right T11/12 region, with a 2-cm area of pinpoint tenderness located approximately 5 cm inferior to the umbilicus on the right side (Fig. 1B, solid circle). While Murphy's sign was negative, Carnett's sign and pinch test were positive at that site. Pain worsened with spinal extension, raising suspicion of T11/12 nerve root involvement. Due to the localized tenderness, ACNES was suspected. Subcutaneous injection of 5 mL of 1% lidocaine at the tender point resulted in immediate pain relief, confirming the diagnosis of ACNES.

Figure 1.

Changes in abdominal and subcutaneous fat over time and localization of abdominal pain. A: Upper: Superficial CT image of the abdominal wall obtained eight months before the symptom onset, showing thick subcutaneous fat. Lower: Axial abdominal CT image at the same time point, confirming sufficient subcutaneous and visceral fat. B: Upper: Superficial CT image obtained four months after the symptom onset, revealing two distinct pain regions: dull pain in the right lower abdomen corresponding to the T11/12 dermatome (dashed-line area) and a localized tender point below the right umbilicus (solid circle). Lower: Axial CT at the time point reveals significant reduction in subcutaneous and visceral fat and relaxation of the rectus abdominis muscle. A pinpoint site of tenderness is observed in the right lower abdomen (arrow). CT: computed tomography

CT conducted before the symptom onset revealed no compression fractures at T12 or L1 and no evidence of fat loss or intervertebral foramen narrowing at T11/12 (Fig. 2A). Conversely, CT images obtained at presentation revealed a significant reduction in subcutaneous and visceral fat, with relaxation of the rectus abdominis muscle (Fig. 1B, 2B, lower and upper, respectively). In addition, new compression fractures at T12/L1 were observed, exhibiting burst-like protrusions anteriorly and posteriorly. This resulted in narrowing of the right T11/12 intervertebral foramen, suggesting corresponding nerve root compression, thereby resulting in abdominal pain in the T11/12 (Fig. 2B).

Figure 2.

Vertebral and foraminal changes before and after the symptom onset. A: Upper: Sagittal CT image recorded eight months before the symptom onset shows no evidence of compression fractures (arrowhead) with thick subcutaneous abdominal fat (black arrow). Lower: Sagittal CT at the same time shows no narrowing of the right T11/12 right intervertebral foramen (arrows). B: Upper: Sagittal CT image obtained four months after the symptom onset shows the region of pin-point lower abdominal pain (arrow) and new compression fractures at T12 (arrowhead) and L1, with anterior and posterior bony protrusion. Significant reduction in visceral and subcutaneous fat is also observed. The pinpoint site of localized pain is marked using a white arrow. Lower: Concurrent sagittal CT shows narrowing of right T11/12 intervertebral foramen (arrows), indicating possible nerve root compression. CT: computed tomography

A laboratory evaluation revealed a white blood cell count of 3,900 cells/μL, a C-reactive protein level of 0.5 mg/dL, and a serum creatinine of 3.2 mg/dL, with an estimated glomerular filtration rate of 15 mL/min/1.73 m², indicating significant renal dysfunction.

The patient was treated with 10 mg of mirogabalin to manage the pain. His symptoms improved; however, he died a month later because of an unrelated episode of pneumonia.

Discussion

ACNES causes chronic, localized abdominal pain and has a multifactorial etiology, with musculature and posture being the key contributors (1). In patients with rapid weight loss or low body fat, decreased visceral and subcutaneous fat weakens the structural support of the abdominal wall, increasing the risk of anterior cutaneous nerve compression (5). Furthermore, vertebral compression fractures may cause persistent kyphosis, resulting in chronic mechanical stress on the abdominal wall and an increased risk of nerve entrapment (4).

ACNES is often misdiagnosed as a gastrointestinal disorder, with patients (approximately 50%) experiencing pseudo-visceral symptoms such as anorexia, nausea, and bloating, thereby contributing to further weight loss (3). A study reported the frequencies of bloating (78%), nausea (66%), and bowel irregularities (50%) as common symptoms, attributing them to shared afferent pathways between the somatic and visceral structures (6). In our patient, the initial presentation of right-sided abdominal pain raised suspicion of gallbladder disease. However, a physical examination and imaging revealed no abnormalities, making the early diagnosis challenging. In the present case, Carnett's sign was instrumental in identifying the cause of abdominal pain (7). This physical examination maneuver involves persistent or worsened tenderness when the abdominal muscles are tensed, suggesting a somatic source, such as myofascial pain, nerve entrapment, or rectus sheath hematoma. Reduced tenderness indicates a visceral source, such as appendicitis, cholecystitis, or intestinal ischemia, and is useful when imaging reveals no clear abnormalities or when tenderness is localized. Carnett's sign, a simple noninvasive bedside test, should be actively utilized in the differential diagnosis of abdominal pain.

In older individuals, reduced food intake due to aging or frailty often leads to weight and fat loss. These changes can promote the development or exacerbation of ACNES (8). Cases of ACNES following rapid weight loss or bariatric surgery have been reported, suggesting that loss of protective fat layers increases friction and compression of the anterior cutaneous nerves (9). A study indicated that 7.4% of patients developed unexplained abdominal pain following laparoscopic bariatric surgery (10), supporting fat loss as a risk factor for ACNES. In the present case, visceral and subcutaneous fat reduction probably contributed to the nerve entrapment.

Osteoporotic compression fractures at the thoracolumbar junction are common and often asymptomatic in older adults (11,12). However, in some cases, they can cause abdominal pain due to nerve involvement (13). The intercostal and subcostal nerves originate from the thoracic and upper lumbar spine, making vertebral injury an anatomically plausible source of abdominal pain (6). In a previous study, 20% of patients with thoracolumbar fractures exhibited abdominal pain, and 27% reported gastrointestinal symptoms, such as nausea. These findings highlight that the lower thoracic spine is a frequent site of neurological involvement (14). A previous study showed that approximately 72% of compression fractures are associated with neurological symptoms, consistent with the T12 and L1 fractures observed in our case (15). Other reports have shown that patients initially diagnosed with ACNES or lateral cutaneous nerve entrapment syndrome were later found to have underlying compression fractures (16). These findings highlight the need to carefully differentiate between or recognize the coexistence of these conditions. Approximately two-thirds of compression fractures remain asymptomatic and are often incidentally detected (12). Pain aggravated by trunk or abdominal wall movement, especially right-arm elevation, often reflects spinal extension. In our patient, this pattern suggests T11-T12 nerve root involvement, whereas posture and load changes associated with compression fractures may have increased the risk of ACNES (4).

In conclusion, this case highlights a rare cause of chronic abdominal pain in an older patient resulting from coexisting asymptomatic thoracolumbar compression fractures with nerve root symptoms and ACNES, probably triggered by weight loss and postural changes. In older patients with unexplained abdominal pain, clinicians should evaluate focal abdominal tenderness and consider vertebral compression fractures, including ACNES, in the differential diagnosis.

The authors state that they have no Conflict of Interest (COI).