Superior Mesenteric Artery Syndrome Complicating Severe Acute Malnutrition Secondary to Pulmonary Tuberculosis in an Adolescent: A Case Report

Technical Summary: Superior Mesenteric Artery Syndrome Complicating Severe Acute Malnutrition Secondary to Pulmonary Tuberculosis

Problem Statement
Superior Mesenteric Artery (SMA) syndrome, also known as Wilkie's syndrome, is a rare cause of upper gastrointestinal obstruction characterized by the extrinsic compression of the third portion of the duodenum between the superior mesenteric artery and the abdominal aorta. This compression results from the depletion of the retroperitoneal fat pad, leading to a reduction in the aortomesenteric angle and distance. While the condition predominantly affects adolescents and young adults, its etiology is often multifactorial, frequently precipitated by rapid or severe weight loss from catabolic states such as malignancy, HIV/AIDS, or tuberculosis.

The clinical challenge lies in the nonspecific nature of symptoms (epigastric pain, bilious vomiting, early satiety), which often overlap with common gastrointestinal conditions or the underlying wasting disease, leading to diagnostic delays. In resource-limited, tuberculosis-endemic settings, the interplay between severe acute malnutrition (SAM) driven by pulmonary TB and the subsequent development of SMA syndrome is under-recognized. Furthermore, the bidirectional relationship—where malnutrition precipitates the syndrome, and the resulting obstruction perpetuates malnutrition—complicates management. Delayed diagnosis carries a reported mortality of up to 33%.

Methodology
This paper presents a single-case report of a 16-year-old male from Ethiopia. The methodology involved a comprehensive clinical evaluation, anthropometric assessment, and radiological imaging to diagnose and manage the patient.

• Patient Presentation: The patient presented with a three-month history of progressive weight loss, anorexia, productive cough, night sweats, abdominal pain, and bilious vomiting. He had a confirmed household contact with pulmonary tuberculosis.
• Diagnostic Workup:
  • Anthropometry: Admission measurements revealed a Body Mass Index (BMI) of 12 kg/m² and a Mid-Upper Arm Circumference (MUAC) of 13 cm, confirming Severe Acute Malnutrition (SAM).
  • Microbiology: Sputum GeneXpert testing was positive for Mycobacterium tuberculosis.
  • Imaging: An abdominal CT scan was the definitive diagnostic tool. It measured the aortomesenteric angle at 22° and the aortomesenteric distance at 6 mm. These values fell below the diagnostic thresholds of 25° and 8 mm, respectively, confirming SMA syndrome. Upper GI endoscopy was used to rule out intraluminal lesions, revealing only gastric and duodenal dilatation.
• Management Protocol: The patient was managed conservatively without immediate surgical intervention. The protocol included:
  • Rehydration and Electrolyte Correction: ReSoMal via nasogastric tube (NGT).
  • Nutritional Rehabilitation: A phased enteral feeding approach was employed, starting with F-75 formula and advancing to F-100 upon stabilization to mitigate the risk of refeeding syndrome.
  • Pharmacotherapy: Intravenous antibiotics (ampicillin and gentamicin) were administered initially. Anti-tuberculosis therapy (isoniazid, rifampicin, ethambutol, pyrazinamide) was initiated after a two-week period of nutritional stabilization to reduce drug-related adverse risks.
  • Symptom Management: Ondansetron for vomiting and omeprazole for acid suppression.
  • Monitoring: Close monitoring for refeeding syndrome (electrolyte shifts) and clinical response.

Key Results

• Clinical Resolution: The patient's bilious vomiting and abdominal pain resolved over a four-month period.
• Nutritional Recovery: By seven months post-presentation, the patient achieved significant weight gain, was tolerating a full family diet, and had completed the anti-tuberculosis regimen.
• Surgical Outcome: The initially planned surgical intervention (duodenojejunostomy) was successfully deferred due to the efficacy of conservative nutritional rehabilitation.
• Diagnostic Confirmation: The case confirmed that the aortomesenteric angle (22°) and distance (6 mm) were consistent with SMA syndrome, directly linked to the fat pad depletion caused by TB-driven SAM.

Significance and Claims
The authors claim this case report highlights three critical clinical lessons:

1. Bidirectional Relationship: There is a compounding, bidirectional relationship between SAM and SMA syndrome, where each condition can obscure and delay the diagnosis of the other.
2. Etiological Driver: Pulmonary tuberculosis should be recognized as a primary driver of malnutrition severe enough to precipitate SMA syndrome, particularly in adolescents where pubertal growth spurts may further deplete adipose tissue.
3. Conservative Management Efficacy: Systematic conservative nutritional rehabilitation, including a deliberate step-up feeding protocol to prevent refeeding syndrome, can achieve full resolution and obviate the need for surgery, even in resource-limited settings.

The paper posits that clinicians in TB-endemic regions should maintain a high index of suspicion for SMA syndrome when standard malnutrition management fails to produce improvement. It recommends that SAM management guidelines in these settings explicitly acknowledge SMA syndrome as a potential mechanical complication requiring early CT evaluation when clinical responses are unexpectedly poor. The authors note that while this represents a novel etiological dimension for SMA syndrome in a sub-Saharan African adolescent, the management principles align with established conservative strategies that achieve remission in approximately 83% of cases.