Gastroenterology · Vascular Disorders
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Most commonly caused by cardioembolic disease (e.g., atrial fibrillation) or hypercoagulable states like sickle cell disease.
Classically presents with sudden severe LUQ pain radiating to the left shoulder (Kehr sign) and fever.
Contrast-enhanced CT of the abdomen is the gold standard, showing a peripheral wedge-shaped hypodense lesion.
Underlying mechanism is coagulation necrosis from occlusion of the splenic artery or its branches.
Labs are nonspecific but often show leukocytosis and a markedly elevated LDH from tissue necrosis.
Management is mostly supportive with hydration and analgesics plus treatment of the underlying cause.
Splenectomy is reserved for complications such as splenic rupture or splenic abscess.
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A 62-year-old man with atrial fibrillation who is not taking anticoagulation presents with sudden, severe left upper quadrant pain radiating to the left shoulder. He is febrile with localized LUQ tenderness. Laboratory studies show leukocytosis and a markedly elevated lactate dehydrogenase. Contrast-enhanced CT of the abdomen reveals a peripheral, wedge-shaped, non-enhancing hypodense lesion in the spleen.
Which of the following is the most likely diagnosis?
Splenic infarction.
A wedge-shaped, peripheral non-enhancing splenic lesion on contrast CT in a patient with untreated atrial fibrillation is classic for cardioembolic splenic infarction. Kehr sign (referred left shoulder pain) and elevated LDH support the diagnosis, and management is supportive plus anticoagulation for the embolic source.
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Etiology / Epidemiology
Usually caused by arterial occlusion, most commonly from cardioembolic disease (e.g., atrial fibrillation) or hypercoagulable states like Sickle cell disease.
Clinical Manifestations
Classically presents with sudden, severe left upper quadrant (LUQ) pain radiating to the left shoulder (Kehr sign) and fever.
Diagnosis
Contrast-enhanced CT of the abdomen is the gold standard, demonstrating a classic wedge-shaped hypodense lesion.
Treatment
Primarily supportive with hydration and analgesics, alongside targeted therapy for the underlying cause (e.g., anticoagulation).
Prognosis
Usually self-limiting, but requires monitoring for splenic rupture or abscess formation which mandate surgical intervention.
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Epidemiology & Etiology
The most frequent etiologies are cardioembolic events (e.g., atrial fibrillation, valvular disease) and hematologic disorders, particularly Sickle cell disease and myeloproliferative neoplasms. Other high-risk triggers include systemic hypercoagulable states and infective endocarditis, which carries a high risk of seeding septic emboli.
Pertinent Anatomy
The splenic artery is a tortuous end-artery branching directly from the celiac trunk. The spleen lacks a robust collateral blood supply, making its parenchyma highly susceptible to ischemia when the main artery or its segmental branches become occluded.
Pathophysiology
Occlusion of the splenic artery or its branches halts perfusion, leading directly to focal coagulation necrosis. Embolic showers typically produce localized, peripheral wedge-shaped infarcts, whereas massive in-situ thrombosis can result in global splenic infarction. The infarcted tissue eventually undergoes fibrosis and scarring, but is highly vulnerable to secondary bacterial infection if the source was a septic embolus.
Clinical Manifestations
Patients acutely develop severe, tearing left upper quadrant (LUQ) pain that frequently radiates to the left shoulder, a referred pain phenomenon known as Kehr sign. Associated symptoms include fever, nausea, vomiting, and localized LUQ tenderness with guarding. The sudden onset of hemodynamic instability or a rapidly dropping hemoglobin is a red flag for the dreaded complication of splenic rupture.
Diagnosis
Contrast-enhanced CT of the abdomen is the gold-standard imaging modality, classically revealing a peripheral, wedge-shaped, non-enhancing hypodense lesion with its base resting on the splenic capsule. Laboratory studies are generally nonspecific but frequently demonstrate leukocytosis and a markedly elevated lactate dehydrogenase (LDH) due to tissue necrosis.
Treatment
Uncomplicated cases are managed conservatively with intravenous hydration, antiemetics, and analgesics. Management must also address the underlying etiology, such as initiating anticoagulation for atrial fibrillation or performing exchange transfusion for a severe sickle cell crisis. Splenectomy is strictly reserved for life-threatening complications, including splenic rupture, intractable hemorrhage, or splenic abscess.
Prognosis
The majority of patients recover fully with conservative management as the infarcted area undergoes sterile fibrosis and atrophy. However, patients must be closely monitored for splenic abscess (indicated by persistent fever and leukocytosis) and pseudocyst formation, which may necessitate percutaneous drainage or surgical excision.
Differential Diagnosis
1. Splenic abscess: Presents with similar LUQ pain but features swinging fevers, positive blood cultures, and requires prompt drainage.
2. Left lower lobe pneumonia: Presents with pleuritic chest pain and fever, but is distinguished by focal crackles and consolidation on chest X-ray.
3. Acute pancreatitis: Characterized by severe epigastric pain radiating straight to the back, diagnosed by a serum lipase >3x upper limit of normal.
4. Nephrolithiasis: Presents with colicky flank pain radiating to the groin and hematuria, lacking the classic Kehr sign.