Spontaneous Bacterial Peritonitis

Written By Danial Mirza

Definition

Spontaneous Bacterial Peritonitis (SBP) is formally defined as a bacterial infection of pre-existing ascitic fluid in a patient, most commonly with liver cirrhosis, that occurs in the absence of any evident, contiguous, surgically-treatable source of infection within the abdomen (1, 21). The term "spontaneous" is key; it underscores that the infection does not arise from a ruptured organ like the appendix or colon. This definition is of paramount clinical importance because it establishes a critical divergence in management: SBP is a medical condition treated with antibiotics and supportive care, whereas secondary bacterial peritonitis is a surgical emergency. Misdiagnosing the latter as SBP and delaying surgery is associated with a mortality rate that approaches 100% (1). Therefore, the very definition serves as a clinical directive for the house officer: in every patient with suspected SBP, one must actively exclude a surgical cause.

Epidemiology

In Malaysia, SBP stands as a frequent and severe complication of decompensated cirrhosis. While large-scale national registries are limited, local hospital-based studies have reported a prevalence of approximately 13% among patients with chronic liver disease who undergo diagnostic paracentesis (37). The etiological landscape of liver disease in Malaysia's multi-ethnic population is diverse, with major contributors being chronic Hepatitis B (HBV) infection and alcohol-related liver disease (37). The high prevalence of HBV is a key feature of hepatology throughout Southeast Asia and has direct relevance to SBP. A significant meta-analysis, co-authored by Malaysian researchers from Universiti Sains Malaysia, highlighted this by finding a higher pooled global prevalence of SBP in patients with HBV-related cirrhosis (8.0%) compared to those with HCV-related cirrhosis (4.0%) (39, 41). This underscores the need for integrated management, including antiviral therapy for HBV, in the local patient population.

Globally, SBP affects a substantial portion—10% to 30%—of hospitalized patients with cirrhosis and ascites (14). The onset of SBP is a grim prognostic watershed, signaling the transition to end-stage liver disease. Despite modern therapies, in-hospital mortality rates remain stubbornly high at 10-30%, and the long-term outlook is even more sobering, with a 1-year mortality rate that can reach as high as 70% (14, 23). This statistic means that for many patients, an episode of SBP is a terminal event, and survival should immediately trigger conversations about liver transplantation and palliative care.

Etiology

SBP is characteristically a monomicrobial infection, a feature that helps distinguish it from the typically polymicrobial nature of secondary peritonitis. The causative organisms are of enteric origin, reflecting their translocation from the gut lumen. However, the microbiological landscape has been shifting, a trend with critical implications for empiric antibiotic selection (4, 45).

  • Classic Pathogens (Gram-Negative Aerobes): These have historically been the predominant isolates, accounting for up to 70% of infections.

    • Escherichia coli remains the single most frequently isolated pathogen, responsible for a large proportion of all culture-positive episodes (4, 45).

    • Klebsiella pneumoniae is consistently the second most common Gram-negative isolate (4).

  • Emerging Pathogens & The Rise of Resistance: A significant epidemiological shift has occurred over the past two decades, driven by invasive procedures and the widespread use of prophylactic antibiotics.

    • Gram-Positive Cocci: These now cause a substantial number of SBP cases, with some series reporting rates as high as 48-62% (15). The most common isolates include Streptococcus species (especially S. pneumoniae) and Enterococcus species.

    • Multidrug-Resistant (MDR) Organisms: The emergence of MDR pathogens is a major global threat, particularly in healthcare-associated SBP. These include extended-spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae, methicillin-resistant Staphylococcus aureus (MRSA), and vancomycin-resistant Enterococcus (VRE). The high rates of MDR organisms in Asian healthcare settings (up to 50% in some studies) make this a critical consideration for any Malaysian clinician when choosing initial antibiotics for a patient who develops SBP in the hospital (40, 44).

Pathophysiology

The development of SBP is not a random event but the culmination of a "perfect storm" of pathological changes in advanced liver disease. The central mechanism is bacterial translocation, a process enabled by a triad of intestinal dysbiosis, increased gut permeability, and profound immune dysfunction (2, 3).

  1. Portal Hypertension & Gut Permeability: Chronically elevated pressure in the portal venous system is the initial driver. It causes splanchnic arterial vasodilation, leading to vascular stasis and congestion within the gut wall. This impairs the physical integrity of the intestinal mucosal barrier, increasing its permeability and making it "leaky," which allows bacteria and their products to escape the gut lumen (2).

  2. Intestinal Dysbiosis & Bacterial Overgrowth: In cirrhosis, several factors disrupt the normal gut microbiome. Impaired intestinal motility slows transit time, allowing bacteria to proliferate. Furthermore, reduced secretion of bile acids, which have natural antimicrobial properties, contributes to an overgrowth of pathogenic bacteria. The widespread use of Proton Pump Inhibitors (PPIs) in this population can exacerbate this issue by reducing gastric acid, a crucial chemical barrier to bacterial colonization of the upper gastrointestinal tract. This creates an environment where pathogenic bacteria can flourish (2, 46).

  3. Profound Immune Dysfunction (Cirrhosis-Associated Immune Dysfunction - CAID): The cirrhotic state is one of systemic immunosuppression.

    • Systemic Immunity: The reticuloendothelial system, particularly the Kupffer cells in the liver, normally acts as a filter to clear bacteria from the portal blood. In cirrhosis, this system's phagocytic activity is depressed, allowing translocated bacteria to bypass the liver and enter the systemic circulation, causing bacteremia (2).

    • Local Immunity (in Ascitic Fluid): The ascitic fluid itself is an immunologically vulnerable space. A low total protein concentration (<1.5 g/dL) is a major independent risk factor for SBP because it directly correlates with deficient levels of opsonins (like complement and immunoglobulins). These molecules "tag" bacteria for destruction. Their deficiency turns the protein-poor ascitic fluid into a nutrient-rich, undefended growth medium, often described as a "Petri dish" for bacteria (30, 46).

Once bacteria or their endotoxins (like lipopolysaccharide, LPS) establish a foothold, they trigger a massive, dysregulated systemic inflammatory response. This "cytokine storm" exacerbates the underlying circulatory dysfunction, leading to the life-threatening complications of septic shock and hepatorenal syndrome (HRS), which are the primary drivers of mortality in SBP (3).

Clinical Presentation

The clinical presentation of SBP is notoriously subtle and non-specific, demanding a high index of suspicion. A crucial teaching point is that up to 30% of patients may be entirely asymptomatic, with the infection only discovered through a routine screening paracentesis performed upon hospital admission (5, 9).

  • Diagnostic Clues: There is no single pathognomonic sign for SBP. The clinical maxim for any house officer must be: Any fever or new/worsening hepatic encephalopathy in a patient with cirrhosis and ascites is SBP until proven otherwise (9, 11). The brain and the kidneys are often the first organs to show signs of trouble.

  • Common Symptoms (>50%):

    • Fever (>37.8°C) (~70%): The most common sign, though its absence does not rule out SBP (5).

    • Worsening or new-onset Hepatic Encephalopathy (~55%): A very common presentation. SBP is a key precipitant and must be excluded in any patient with unexplained altered mental status (5).

    • Diffuse, constant abdominal pain or tenderness (~50%): The pain is typically mild to moderate and constant. Sharp, localized pain or peritoneal signs (rebound, rigidity) are atypical and should raise suspicion for secondary peritonitis (5).

  • Less Common Symptoms (10-50%):

    • General malaise or unexplained clinical deterioration (11).

    • Nausea, vomiting, or paralytic ileus, reflecting peritoneal inflammation (11).

  • ⚠️ Red Flag Signs & Symptoms: These indicate severe sepsis and require immediate, aggressive resuscitation.

    • Hypotension / Shock: A sign of advanced infection and carries a very poor prognosis.

    • Unexplained worsening renal function (Acute Kidney Injury): Often the first sign of impending hepatorenal syndrome.

    • Hypothermia: A paradoxical but ominous sign of severe sepsis, particularly in immunocompromised cirrhotic patients.

Complications

  • Renal: Acute Kidney Injury (AKI) and Hepatorenal Syndrome (HRS) are the most feared complications. HRS is a form of functional renal failure caused by intense renal vasoconstriction in the setting of severe systemic and splanchnic vasodilation, precipitated by the infection (3, 49).

  • Systemic: Sepsis and septic shock, leading to multi-organ failure (9).

  • Neurological: Worsening or irreversible hepatic encephalopathy, driven by the systemic inflammatory state and impaired toxin clearance (5).

Prognosis

The prognosis following an episode of SBP is extremely poor, marking the patient's transition to the terminal phase of their liver disease. Even with successful treatment, in-hospital mortality remains high at 10-30% (14). The risk of recurrence is nearly 70% within one year if long-term antibiotic prophylaxis is not administered (22). Consequently, any patient who survives an episode of SBP has a very limited life expectancy from liver failure and must be considered for liver transplantation evaluation as it is the only curative option (21).

Differential Diagnosis

  • Secondary Bacterial Peritonitis: This is the most critical differential to exclude. It is suggested by focal abdominal signs (rebound, rigidity), a polymicrobial Gram stain, or ascitic fluid meeting at least two of Runyon's criteria: total protein >1 g/dL, glucose <50 mg/dL, and LDH above the upper limit of normal for serum (13, 21). This is a surgical emergency requiring an urgent CT scan and surgical consultation.

  • Fungal Peritonitis: While rare, consider this in severely ill patients, those on long-term antibiotics, or those who fail to respond to standard therapy. It carries a very high mortality rate (4).

  • Tuberculous Peritonitis: This should be considered in the Malaysian context. It typically has a more insidious onset with a lymphocytic predominance in the ascitic fluid. Diagnosis is challenging and may require ascitic fluid adenosine deaminase (ADA) levels or peritoneal biopsy.

Investigations

Immediate & Bedside Tests

  • Diagnostic Paracentesis: This is the mandatory, cornerstone investigation for any cirrhotic patient admitted with ascites or any form of clinical deterioration (fever, pain, encephalopathy, AKI) (58). An urgent tap is essential to obtain fluid for analysis before starting antibiotics (the action), as this provides the definitive diagnostic information that guides all subsequent therapy (the rationale).

    • Crucial Technique: Inoculate 10 mL of ascitic fluid directly into an aerobic and an anaerobic blood culture bottle at the patient's bedside. This simple procedure is non-negotiable as it dramatically increases the sensitivity of the culture from approximately 50% to over 80% compared to sending fluid to the lab in a sterile container (11, 21).

  • Leukocyte Esterase Reagent Strips: Using a standard urine dipstick on ascitic fluid can serve as a rapid bedside screening tool. A negative result has a high negative predictive value, making SBP unlikely (the action), but it is not sensitive or specific enough to replace formal cell counting for diagnosis (the rationale) (17).

Diagnostic Workup

  • First-Line Investigations:

    • Ascitic Fluid Analysis: Send samples for an absolute polymorphonuclear (PMN) cell count, culture, Gram stain, albumin, protein, glucose, and LDH.

    • Blood Tests: A Full Blood Count (FBC), Renal Profile, Liver Function Tests (LFTs), INR, and two sets of blood cultures are essential to assess for systemic inflammation and baseline organ function (the action), which are critical for prognostication and guiding therapy like albumin administration (the rationale) (21).

  • Gold Standard: The definitive diagnosis is established by an ascitic fluid absolute PMN count ≥250 cells/mm³ (0.25 x 10⁹/L) (21, 55). Treatment must be initiated based on this cell count alone, without waiting for culture results.

  • Imaging: An Abdominal CT scan with contrast is not routine for SBP. It becomes mandatory and urgent if secondary bacterial peritonitis is suspected (e.g., focal signs, polymicrobial culture, failure to improve) to search for a surgical source like a perforated viscus or abscess (21).

Monitoring & Staging

  • Repeat Paracentesis at 48 Hours: This is strongly recommended for patients with an atypical course, severe infection, or an inadequate clinical response. It is the key investigation to objectively assess treatment efficacy (the action). A decrease in the PMN count by at least 25% from the baseline value indicates an adequate response. Failure to achieve this decrease defines treatment failure and is a critical event that mandates an immediate change in management: broadening antibiotic coverage and urgently re-evaluating for a missed secondary cause of peritonitis (the rationale) (21, 55).

Management

Management Principles

The management of SBP is a time-critical emergency. It focuses on three immediate goals: prompt eradication of the infection with appropriate antibiotics, prevention of hepatorenal syndrome with intravenous albumin, and comprehensive supportive care to stabilize the patient (21, 55).

Acute Stabilisation (The First Hour)

  • Circulation:

    • Secure two large-bore IV cannulas and begin fluid resuscitation if the patient is in shock.

    • Administer intravenous albumin. This is a critical, evidence-based intervention that has been proven to significantly reduce the incidence of hepatorenal syndrome (from 33% to 10%) and decrease in-hospital mortality (from 29% to 10%) (21, 49). It works by acting as a plasma expander to improve circulatory dysfunction and by binding inflammatory endotoxins (the rationale).

      • Dose: 1.5 g of albumin per kg of body weight administered on Day 1 (at the time of diagnosis), followed by a second dose of 1.0 g of albumin per kg on Day 3. This is especially crucial if baseline serum creatinine is >88 µmol/L or total bilirubin is >68 µmol/L (21, 55). Forgetting to prescribe albumin is a common and potentially fatal omission.

Definitive Therapy

Empiric antibiotic therapy must be started immediately after the diagnostic paracentesis is performed in any patient with a PMN count ≥250 cells/mm³. Treatment should never be delayed while awaiting culture results.

  • First-Line Treatment (Guided by Setting):

    • Community-Acquired SBP: IV Ceftriaxone 2g once daily is the drug of choice. It provides excellent coverage against common enteric Gram-negative pathogens and streptococci (the rationale) and is the international standard of care for uncomplicated cases (the action) (21, 55).

    • Healthcare-Associated / Nosocomial SBP: IV Piperacillin-tazobactam 4.5g every 6 hours. This is essential to provide broader coverage that includes Pseudomonas and anaerobes, and has better activity against potential MDR organisms (the rationale) which are common in hospital settings, especially in Asia (the action) (40, 52).

  • Second-Line/Escalation: For patients with septic shock, known colonization with MDR organisms, or who fail first-line therapy (based on the 48-hour tap), escalate to a carbapenem (e.g., Meropenem 1g IV every 8 hours) and consult with an Infectious Diseases specialist (52). The typical duration of therapy for uncomplicated SBP is 5 days.

Supportive & Symptomatic Care

  • Temporarily discontinue non-selective beta-blockers, ACE inhibitors/ARBs, and diuretics during the acute episode to improve renal perfusion.

  • Strictly avoid all nephrotoxic agents, particularly NSAIDs and aminoglycoside antibiotics.

  • Manage hepatic encephalopathy with lactulose and rifaximin as indicated.

  • Ensure adequate nutrition and manage pain with caution, avoiding sedating opiates.

Key Nursing & Monitoring Instructions

  • Strict hourly input/output chart monitoring to assess for oliguria.

  • Hourly monitoring of vital signs (BP, HR, RR, Temp) and neurological status (GCS) for the first 6 hours, then 4-hourly if stable.

  • Inform medical staff immediately if systolic BP drops below 90 mmHg, urine output is <0.5mL/kg/hr for more than 2 hours, or there is any decline in mental status.

Long-Term Plan & Patient Education

  • Secondary Prophylaxis: After a patient survives their first episode of SBP, the one-year recurrence rate is nearly 70%. Therefore, lifelong secondary antibiotic prophylaxis is the standard of care to prevent another episode (the action) by suppressing the growth of enteric Gram-negative bacteria (the rationale) (21).

    • Regimen: Oral Ciprofloxacin 500mg daily or Norfloxacin 400mg daily (36).

  • Primary Prophylaxis: This is indicated for high-risk patients who have not yet had SBP. This includes all cirrhotic patients admitted with an acute gastrointestinal bleed (who should receive short-term IV ceftriaxone) and outpatients with low ascitic fluid protein (<1.5 g/dL) combined with advanced liver failure (Child-Pugh score ≥9) or renal dysfunction (21, 36).

  • Patient Education: Educate the patient and family on the importance of lifelong medication adherence and to seek immediate medical attention for fever, increasing abdominal distension, abdominal pain, or confusion.

When to Escalate

Clear, objective triggers for escalation are crucial for patient safety.

  • Call Your Senior (MO/Specialist) if:

    • The patient develops signs of septic shock (e.g., hypotension requiring vasopressors, lactate > 2 mmol/L).

    • There is no clinical improvement (persistent fever, pain, or encephalopathy) after 48 hours of appropriate antibiotics.

    • The 48-hour repeat paracentesis shows treatment failure (PMN count has not decreased by ≥25%).

    • The initial culture results reveal a resistant organism (e.g., ESBL, MRSA) or multiple organisms (polymicrobial), suggesting secondary peritonitis.

  • Referral Criteria:

    • Surgical Team: Refer urgently if secondary bacterial peritonitis is suspected at any point.

    • Liver Transplant Team: Refer all survivors of an SBP episode for transplant evaluation.

    • Palliative Care Team: Introduce early for holistic symptom management (refractory ascites, pain, encephalopathy) and to facilitate advance care planning, acknowledging the patient's end-stage disease trajectory (60).

References

(Note: While Malaysia does not have a dedicated national CPG for SBP, the Malaysian Consensus on Hepatorenal Syndrome provides relevant guidance (31). Practice should be guided by major international guidelines and local data.)

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  17. Tandon, P., & Garcia-Tsao, G. (2008). Prophylaxis for Spontaneous Bacterial Peritonitis. Gastroenterology & Hepatology, 4(6), 423-424. https://www.gastroenterologyandhepatology.net/archives/june-2008/prophylaxis-for-spontaneous-bacterial-peritonitis/

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  19. Othman, H., et al. (2023). Prevalence of Spontaneous Bacterial Peritonitis (SBP) in Hepatitis B (HBV), and Hepatitis C (HCV) Liver Cirrhosis: A Systematic Review and Meta-Analysis. Journal of Clinical Medicine, 12(2), 275. https://doi.org/10.3390/jcm12020275

  20. Wong, F. (2009). Ascites and spontaneous bacterial peritonitis: an Asian perspective. Journal of Gastroenterology and Hepatology, 24(9), 1486-1494. https://pubmed.ncbi.nlm.nih.gov/19743995/

  21. Othman, H., et al. (2023). Prevalence of Spontaneous Bacterial Peritonitis (SBP) in Hepatitis B (HBV), and Hepatitis C (HCV) Liver Cirrhosis: A Systematic Review and Meta-Analysis. PubMed. https://pubmed.ncbi.nlm.nih.gov/36673643/

  22. Cheong, H. S., et al. (2009). Epidemiology of Spontaneous Bacterial Peritonitis, Bacterial Species and Resistances. Harvard DASH. https://dash.harvard.edu/handle/1/27901306

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  24. Dr. Oracle AI. (n.d.). What are the risk factors for Spontaneous Bacterial Peritonitis (SBP)? https://www.droracle.ai/articles/69281/what-are-the-risk-factors-for-sbp

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  26. UCSF IDMP. (n.d.). VASF Spontaneous Bacterial Peritonitis (SBP) Treatment Guidelines. https://idmp.ucsf.edu/content/vasf-spontaneous-bacterial-peritonitis-sbp-treatment-guidelines

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  28. Hospital Procedures Consultants. (2021). Summary of AASLD Practice Guidelines on Cirrhotic Ascites – Paracentesis Indicated for all Hospitalized Patients. https://hospitalprocedures.org/summary-of-aasld-practice-guidelines-on-cirrhotic-ascites-paracentesis-indicated-for-all-hospitalized-patients/

  29. Low, J., & Vickerstaff, V. (2020). Palliative care in liver disease: what does good look like? Frontline Gastroenterology, 11(3), 218-225. https://fg.bmj.com/content/11/3/218

Danial Mirza
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