INTRA-ABDOMINAL INFECTIONS Learning Objectives: 1. Describe patient risk factors, signs and symptoms that may indicate an intra-abdominal infection 2. Identify tests and significant laboratory values used to diagnose intra-abdominal infections and differentiate among the various types of intra-abdominal infections 3. List common causative organisms for intra-abdominal infections 4. Distinguish between antimicrobial treatment options for intra-abdominal infections based on causative organisms 5. Describe supportive care and monitoring that may be needed for intra-abdominal infections Patient Case: Chief Complaint: “My belly hurts so bad I can barely move.” HPI: John Chavez is a 47-year-old Hispanic man who was brought to the ED by his wife. She stated that he has been suffering from nausea, vomiting, and severe abdominal pain for the last 2–3 days. His intake of food and fluids has been minimal over the past several days. Meds: Spironolactone 100 mg PO once daily, Omeprazole 20 mg PO once daily, Maalox 30 mL PO QID PRN PMH: Cirrhosis, diagnosed 2014 with onset of ascites, GERD, Cholecystectomy 15 years ago, Chronic hepatitis C virus infection diagnosed 2014. FH: Mother was alcoholic; died 10 years ago in car accident. Father’s history unknown. SH: Retired construction worker; EtOH abuse with 10–12 cans of beer per day × 25 years, sober for 6 months; however, recently did binge drink after an argument with his wife; denies use of tobacco or illicit drugs; poor adherence to medications and dietary restrictions Background ● Contained within the peritoneum or retroperitoneal space. Two general types: peritonitis and abscess ● Peritonitis- acute, inflammatory response of peritoneal lining to microorganisms, chemicals, irradiation, or foreign body injury ○ Primary - intra-abdominal focus of disease may not be evident ○ Secondary- a focal disease process is evident within the abdomen ● Abscess-purulent collection of fluid separated from surrounding tissue by a wall consisting of inflammatory cells and adjacent organs ○ Usually contains necrotic debris, bacteria, and inflammatory cells. Pathophysiology ● Causes ○ Appendicitis is MOST common ○ Entry into host . From bacterial collections within intra-abdominal organs, peritoneal dialysis (skin surface flora introduced via the peritoneal catheter) . In primary peritonitis → enter abdomen via bloodstream or lymphatic system, transmigration through the bowel wall, through an indwelling peritoneal dialysis catheter, or fallopian tubes in female patients . In secondary peritonitis → enter peritoneum or retroperitoneum as a result of disruption of the integrity of the GI tract caused by diseases or traumatic injuries . Fluid and protein shift into abdomen (called “third spacing”) may decrease circulating blood volume and cause hypotension, shock & death . An abscess begins by the combined action of inflammatory cells, bacteria, fibrin, and other inflammatory component; O2 is low → anaerobic bacteria! Signs/Symptoms ● Primary ○ Loss of appetite ○ Bloating ○ Nausea/ Vomiting (sometimes with diarrhea) ○ Abdominal tenderness ○ Fever - may be only mildly elevated or not elevated in patients undergoing peritoneal dialysis ○ Bowel sounds are hypoactive ○ Cirrhotic patients may have worsening encephalopathy ○ Culture of peritoneal dialysate or ascitic fluid should be positive, particularly if collected prior to initiation of antibiotics ○ Procalcitonin in conjunction with clinical findings is a sensitive test for bacterial peritonitis ● Secondary ○ Generalized abdominal pain ○ Tachypnea ○ Tachycardia ○ Nausea/Vomiting ○ Fever - normal initially, then increases to 37.8–38.9°C (100–102°F) within the first few hours and may continue to rise for the next several hours ○ Hypotension, hypoperfusion, and shock if volume is not restored ○ Decreased urine output due to vascular volume depletion ○ Voluntary abdominal guarding changing to involuntary guarding and a “board-like abdomen” ○ Abdominal tenderness and distension ○ Faint bowel sounds that cease over time Back to our case: What are the signs/symptoms of an intra-abdominal infection in this patient? Which type is most likely? Gen: Thin man who appears older than his stated age, disoriented, and in severe pain VS: BP 154/82, P 102, RR 32, T 38.2°C; current Wt 92 kg, (IBW 68 kg) Skin: Jaundiced, warm, coarse, and very dry. Spider angiomata present on chest, back and arms. HEENT: Yellow sclera; PERRLA; Oropharynges show poor dentition but are otherwise unremarkable Neck/Lymph Nodes: Supple; normal size thyroid; no JVD or palpable lymph nodes Chest: Lungs are CTA; shallow and frequent breathing CV: Tachycardia, normal S1 and S2 with no S3 or S4 Abd: Distended; pain on pressure or movements; pain is sharp and diffuse throughout abdomen; (+) guarding. (+) HSM. Decreased bowel sounds. Genitorectal: Prostate normal size; guaiac (–) stool Extremities: No clubbing or cyanosis; bilateral pitting pedal edema 1+ Neuro: Oriented to place; lethargic and apathetic, slumped posture, slowed movements Testing/Diagnosis ● Primary ○ Cloudy dialysate fluid with peritoneal dialysis ○ WBC count may be only mildly elevated ○ Ascitic fluid usually contains greater than 250 leukocytes/mm3 (0.25 × 109/L), and bacteria may be evident on Gram stain of a centrifuged specimen ○ In 60%–80% of patients with cirrhotic ascites, the Gram stain is negative ● Secondary ○ Leukocytosis (15,000–20,000 WBC/mm3 [15 × 109 to 20 × 109/L]), with neutrophils predominating and an elevated percentage of immature neutrophils (bands) ○ Elevated hematocrit and blood urea nitrogen because of dehydration ○ Patient progresses from early alkalosis because of hyperventilation and vomiting to metabolic acidosis ○ Abdominal radiographs may be useful because free air in the abdomen (indicating intestinal perforation) or distension of the small or large bowel is often evident Back to our case: What lab values indicate an intra-abdominal infection? Abdominal US: Nodular liver consistent with cirrhosis; ascites; splenomegaly Paracentesis: Ascitic fluid: leukocytes 720/mm3, protein 2.8 g/dL, albumin 1.1 g/dL, pH 7.28, lactate 30 mg/dL Causal Organisms ● Primary bacterial peritonitis: ○ Usually a single organism ○ Children . Group A Streptococcus, Escherichia coli, Streptococcus pneumoniae, or Bacteroides species ○ When peritonitis occurs in association with cirrhotic ascites, E. coli is isolated most frequently ● Peritonitis in patients undergoing peritoneal dialysis: ○ Common skin organisms . Coagulase negative staphylococci, Staphylococcus aureus, streptococci and enterococci ○ Gram-negative bacteria . E. coli, Klebsiella, and Pseudomonas ● Secondary intra-abdominal infections: ○ Usually polymicrobial - gram positive and gram negative ○ Combination of aerobic & anaerobic organisms appears to greatly affect the severity of infection . Aerobic bacteria: ● E. coli - responsible for the early mortality from peritonitis . Anaerobic bacteria ● Bacteroides fragilis (think abscesses) Back to our case: What do you think is the most common causative organism for this patient? Blood Cultures: Pending × 2 Paracentesis: Gram stain: numerous PMNs, no organisms. Treatment Options ● 3 Major Modalities ○ Prompt surgical drainage of the infected site . Secondary treated surgically - “source control”!! ● Physical measures to eradicate the focus of infection ● Abdominal laparotomy may be used to correct the cause ○ Hemodynamic resuscitation and support of vital functions . To ensure intravascular volume, CO, tissue perfusion, correct acidosis . The Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock recommend treatment goals during the first 6 hours or resuscitation: ● CVP 8-12 mm Hg ● MAP more than or equal to 65 mm Hg ● UO more than or equal to 0.5 mL/kg/h . In 1st hour- 30 mL/kg bolus of IV fluids (lactated ringers or normal saline) may be needed for intravascular volume, followed by up to 1 L/hr . Significant blood loss (hematocrit ≤25%) → PRBC ○ Early administration of appropriate antimicrobial therapy to treat infection not removed by surgery . Empiric antibiotic regimens (before organism is known) ○ For continuous ambulatory peritoneal dialysis–associated peritonitis: . cefazolin (loading dose 500 mg/L; maintenance dose 125 mg/L) . vancomycin (LD 1000 mg/L; MD 25 mg/L) in cases of high prevalence of methicillin-resistant Staphylococcus aureus (MRSA) or β-lactam allergy, may be utilized for Gram-positive coverage . One of these Gram-positive agents should be combined with a Gram- negative agent such as: ● ceftazidime (LD 500 mg/L; MD 125 mg/L) ● cefepime (LD 500 mg/L; MD 125 mg/L) ● aminoglycoside (gentamicin or tobramycin LD 8 mg/L; MD 4 mg/L) ○ Check peak and trough levels! ● Definitive therapy (once organism is identified) ○ At 24-48 hours, aerobic cultures should return . If pathogen not sensitive to empiric regimen → change . If sensitive and susceptible, improving → can de-escalate therapy . Anaerobic cultures at 4-7 days Duration of therapy ● Patients should start improving in 2-3 days ● Established infections → 4 to 7 days ● At least 1 week after the dialysate fluid is clear and for a total of at least 14 days ○ Treatment failure if re-operation needed, or do not improve until 1-2 weeks ● Adjunctive Therapy ○ Enteral or parenteral nutrition to improve immune function and wound healing to ensure recovery Other considerations ● Superinfection ○ Due to candida usually - treat with an azole antifungal ○ Enterococci, opportunistic gram-negative bacilli (pseudomonas, serratia) may be involved Monitoring ● MAP, CVP ● Urine output, renal function tests ● Weight to ensure proper nutrition ● Wound healing ● Aminoglycoside peaks/troughs (if applicable) ○ See “General ID Knowledge Sheet” References: - Link to Dipiro Textbook - Chapter 114 - https://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=1 46072317 - Link to Dipiro Handbook - Chapter 42 - https://accesspharmacy.mhmedical.com/content.aspx?bookid=2177&sectionid=1 65473051 .