Portal Venous Gas

 

What is portal venous gas?

• Definition: Portal venous gas is the accumulation of gas in the portal vein and its branches, distinct from pneumobilia (gas in the biliary system).
• Radiographic Appearance:
  • Portal Venous Gas: Gas is typically peripheral within the liver.
  • Pneumobilia: Gas is centrally located, often closer to the liver hilum.

What is the pathology and etiology?

• Traditional View: Once considered a sign of severe illness with high mortality, portal venous gas is now recognized in a broader range of conditions, not all of which carry a high mortality risk.
• Causes by Age:
  • In Children:
    • Umbilical vein catheterization.
    • Necrotizing enterocolitis (NEC).
    • Neonatal gastroenteritis.
    • Erythroblastosis fetalis.
    • Postoperative outcome in corrective bowel surgeries.
  • In Adults:
    • Bowel Wall Alterations:
      • Ischemic bowel (associated with high mortality but not an independent predictor).
      • Necrotic or ulcerated colorectal carcinoma.
      • Inflammatory bowel disease (IBD).
      • Perforated peptic ulcer.
    • Bowel Luminal Distention:
      • Iatrogenic causes like gastric/bowel dilation from endoscopic procedures or enemas.
      • Paralytic ileus or mechanical bowel obstruction.
      • Acute gastric dilation.
    • Infections and Intra-abdominal Sepsis:
      • Diverticulitis, infectious colitis, pelvic abscess, cholecystitis, cholangitis, appendicitis, hemorrhagic pancreatitis.
    • Unknown Mechanism:
      • Pneumatosis intestinalis, COPD, corticosteroid usage, diabetes mellitus, diarrhea, cardiopulmonary resuscitation.

What are the radiographic features of portal venous gas?

• Plain Radiographs: Shows branching lucencies within the liver or in the vessels extending toward the liver.
• Ultrasound: Manifests as echogenic mobile foci within the portal vein lumen, with Doppler showing sharp spectral spikes.
• CT: Branching gas patterns of low density in the liver and portal veins; gas is seen peripherally, helping differentiate it from central pneumobilia.

Historical Background

• First Description: Documented in 1955 by Wolfe and Evens, noting its presence on radiological imaging.

What is HPVG and why is it significant?

• Definition: HPVG is the presence of gas within the portal venous system, often considered a serious radiologic sign due to its association with potentially severe underlying conditions.
• Historical Perspective: Initially described in infants with necrotizing enterocolitis (NEC), HPVG is seen in a range of conditions, both benign and severe.

Physiopathology and Etiology

• Mechanism:
  • Gas can enter the portal venous system due to gas-forming bacteria either within the bowel lumen or an abscess.
  • Alternatively, gas-forming organisms may be present directly in the portal venous system, introducing gas into circulation.
• Common Causes:
  • Bowel Ischemia/Necrosis: The most common etiology, with ischemia leading to gas production within the bowel wall that subsequently enters the portal circulation.
  • Inflammatory Bowel Disease: Mucosal damage in conditions like ulcerative colitis or Crohn's disease can lead to HPVG, especially after endoscopic procedures.
  • Infections and Intra-abdominal Conditions: Diverticulitis, appendicitis, and cholecystitis are frequently associated.
  • Post-Surgical/Procedural: Endoscopic procedures, bowel surgeries, or liver transplant operations can lead to HPVG as a temporary finding.
  • Rare Causes: Severe pancreatitis, gastric pathologies, and trauma have also been linked.

Diagnosis and Imaging

• Radiographic Modalities:
  • CT Scan: Preferred due to high sensitivity, showing peripheral branching gas within the liver.
  • Ultrasound: Reveals echogenic particles within the portal vein; color Doppler imaging can show characteristic bidirectional spikes.
  • Plain Radiography: Less sensitive but can show branching lucencies in the liver extending toward the capsule.
• Differentiation from Pneumobilia: HPVG typically shows peripheral distribution in the liver, while pneumobilia appears centrally due to bile flow.

Prognosis

• Mortality Risk: HPVG alone is not an independent predictor of mortality, but the underlying cause (such as bowel ischemia) greatly influences prognosis.
• Clinical Outcome:
  • HPVG due to benign causes (like post-procedural cases) often resolves with conservative management.
  • For severe cases such as ischemic bowel, mortality rates remain high (up to 90%) if transmural necrosis is present.

Treatment

• Management Strategy:
  • HPVG itself does not necessitate surgery. Treatment focuses on addressing the underlying pathology.
  • Ischemic Bowel: Surgical intervention is often required, especially with signs of necrosis.
  • Diverticulitis: Management typically includes antibiotics and may involve surgery if complications arise.
  • Conservative Management: For benign causes, supportive care, gastric decompression, and close monitoring are generally sufficient.
  • Hyperbaric Oxygen Therapy: Considered for cases involving gas embolization with systemic symptoms.

Key Takeaways

• HPVG is a critical radiologic finding often associated with severe underlying abdominal pathology. Its presence alone does not dictate treatment; rather, management should focus on the causative condition.
• Prognosis and Intervention are dependent on the specific diagnosis; while some cases necessitate urgent surgery, others may only require conservative measures

Summary and Recommendations for Intestinal Ischemia:

Intestinal Ischemia Overview

• Definition: Reduced blood flow to the intestine, either in the small (mesenteric ischemia) or large intestine (colonic ischemia).
• Types:
  • Acute: Commonly affects the small intestine and accounts for 60-70% of cases of mesenteric ischemia. Associated with high mortality (>60%).
  • Chronic: Less common and generally associated with recurrent symptoms.

Risk Factors

• Perfusion-related: Conditions that reduce systemic perfusion or lead to vasoconstriction.
• Thrombosis-related: Risks for mesenteric arterial embolism, arterial or venous thrombosis.
• Outcome Factors: The extent and duration of ischemia depend on systemic perfusion adequacy, vessel involvement, and collateral circulation.

Clinical Features

• Acute Ischemia: Characterized by severe abdominal pain that is often "out of proportion" to physical findings.
• Chronic Ischemia: Typically involves recurrent postprandial abdominal pain (pain after eating).
• Distinguishing Features: Specific pain characteristics can help differentiate between small and large intestine ischemia.

Diagnosis

• High Clinical Suspicion: Especially important in patients with known risk factors and severe symptoms.
• Imaging:
  • CT Angiography: Initial test of choice, without oral contrast. It is accurate for diagnosing mesenteric ischemia and excluding other causes of acute abdominal pain.
  • Arteriography: May be needed if CT angiography does not confirm the diagnosis.
  • Colonoscopy/Sigmoidoscopy: Useful for diagnosing colonic ischemia.

Treatment

• Primary Goal: Rapid restoration of blood flow to the intestines.
• Supportive Management: Includes anticoagulation if not contraindicated, to prevent new or worsening thrombus.
• Interventions:
  • For Arterial Causes: Options include embolectomy, bypass, stenting, thrombolysis, and intra-arterial vasodilators.
  • For Venous Causes: Thrombolysis and other supportive treatments.
  • Nonocclusive Mesenteric Ischemia: Managed with vasodilators and addressing the underlying causes.

Key Takeaway: Timely diagnosis and intervention are crucial in managing intestinal ischemia, especially the acute form, to prevent progression to infarction and improve patient outcomes. Treatment is tailored based on the specific cause, with surgical and interventional options aimed at re-establishing blood flow.

Types of Intestinal Ischemia

1. Acute Mesenteric Ischemia (AMI)

   • Pathophysiology: Caused by a sudden reduction in blood flow to the small intestine, often due to:
     • Arterial embolism (most common in SMA).
     • Arterial thrombosis due to atherosclerosis.
     • Nonocclusive mesenteric ischemia, especially in critically ill patients.
     • Mesenteric venous thrombosis in hypercoagulable states.
   • Clinical Features:
     • Severe periumbilical pain disproportionate to physical findings.
     • Nausea, vomiting, and diarrhea (may become bloody in advanced stages).
     • Signs of sepsis, peritonitis, and hemodynamic instability in late stages.
   • Diagnosis:
     • CT Angiography: Preferred for identifying vessel occlusion, bowel wall changes, and pneumatosis intestinalis.
     • Laboratory: Leukocytosis, elevated lactate, metabolic acidosis.
   • Treatment:
     • Supportive: IV fluids, antibiotics, anticoagulation.
     • Definitive: Endovascular revascularization (embolectomy, stenting, thrombolysis) or urgent surgery if there are signs of peritonitis or infarction.
     • High mortality rate (>50%), so early intervention is critical.

2. Chronic Mesenteric Ischemia (CMI)

   • Pathophysiology: Gradual stenosis of mesenteric arteries, typically due to atherosclerosis, leads to recurrent hypoperfusion episodes.
   • Clinical Features:
     • Postprandial abdominal pain starting 10-30 minutes after eating and lasting for 1-2 hours.
     • Food aversion and weight loss due to pain.
     • Abdominal bruit may be present.
   • Diagnosis:
     • Duplex Ultrasound: Initial screening.
     • CT Angiography: Confirms >70% stenosis of the SMA, IMA, or celiac artery.
   • Treatment:
     • Definitive: Endovascular revascularization (angioplasty, stenting).
     • Supportive: Frequent small meals and a low-fat diet. Total parenteral nutrition if necessary.
     • Prognosis is better than AMI but still requires timely revascularization to prevent progression.

3. Colon Ischemia (Ischemic Colitis)

   • Pathophysiology: Hypoperfusion of the colon, commonly at watershed areas (splenic flexure, rectosigmoid junction).
   • Etiology:
     • Nonocclusive ischemia due to systemic hypotension, dehydration, or vasoconstriction (∼95%).
     • Occlusive causes such as thromboembolism are less common.
   • Clinical Features:
     • Cramping left lower quadrant pain.
     • Bloody diarrhea within 24 hours of symptom onset.
     • Symptoms are typically self-limited, but severe cases can lead to bowel infarction and peritonitis.
   • Diagnosis:
     • CT with Contrast: Shows bowel wall thickening, edema, and pneumatosis intestinalis.
     • Colonoscopy: For mild to moderate cases, reveals segmental ischemic changes in the mucosa.
   • Treatment:
     • Mild to Moderate: Supportive care (IV fluids, bowel rest, and antibiotics).
     • Severe: Surgical resection for gangrenous colitis, with laparotomy if there are signs of peritonitis or massive bleeding.
     • Most cases resolve with conservative management; however, severe cases have a poorer prognosis.

---

Summary Recommendations

• Early Recognition: Rapid diagnosis is essential, especially for AMI, due to the high mortality rate.
• Imaging:
  • CT Angiography is the test of choice for both AMI and severe cases of colonic ischemia.
  • Duplex Ultrasound is useful for CMI screening.
• Management:
  • Acute Mesenteric Ischemia: Requires urgent revascularization (endovascular or surgical) and supportive care.
  • Chronic Mesenteric Ischemia: Revascularization is recommended to prevent progression, along with dietary modifications.
  • Colon Ischemia: Managed conservatively in mild cases; severe cases need surgical intervention.
• Prognosis:
  • AMI has a high mortality rate, particularly if diagnosis and treatment are delayed.
  • CMI and colonic ischemia have better outcomes, though complications like bowel necrosis or perforation are associated with increased morbidity and mortality.