NAVLE Multisystemic

Equine Peritonitis Study Guide

📅 March 28, 2026 ⏱ 25 min read

Overview and Clinical Importance

Peritonitis is defined as inflammation of the serous membranes lining the peritoneal cavity. In horses, this condition represents a life-threatening emergency that requires rapid diagnosis and aggressive treatment. The peritoneum serves as a lubricating membrane covering abdominal organs, and its inflammation leads to significant systemic consequences including endotoxemia, sepsis, and potentially death. Understanding peritonitis is essential for NAVLE success as it integrates knowledge of anatomy, pathophysiology, diagnostics, and emergency medicine.

Survival rates for horses with peritonitis vary widely (50-70%) depending on the underlying cause, with gastrointestinal rupture carrying a grave prognosis, while idiopathic peritonitis and Actinobacillus equuli peritonitis generally respond favorably to medical treatment.

Classification	Description and Examples
Primary vs. Secondary	Primary (Idiopathic): No identifiable source; may involve immunodeficiency Secondary: Results from GI disease, trauma, surgery, or spread from other organs
Septic vs. Non-septic	Septic: Bacterial, fungal, or parasitic infection present Non-septic: Chemical (uroperitoneum), neoplastic, or sterile inflammatory
Localized vs. Diffuse	Localized: Contained to specific area (abscess, focal adhesions) Diffuse: Widespread inflammation throughout peritoneal cavity
Acute vs. Chronic	Acute: Rapid onset, severe systemic signs, hours to days Chronic: Insidious onset, weight loss, recurrent colic over weeks to months

Classification of Peritonitis

Peritonitis is classified according to multiple parameters including etiology, infectious status, distribution, and chronicity. Understanding these classifications helps guide diagnostic and therapeutic decisions.

High-YieldMost cases of peritonitis in horses are secondary, acute, diffuse, and septic OR primary, acute, diffuse, and non-septic. GI disease is the most common underlying cause of secondary peritonitis.

Category	Specific Causes
Gastrointestinal	Intestinal ischemia/strangulation, GI rupture, enteritis, colitis, foreign body perforation, post-surgical complications, non-strangulating infarction (Strongylus vulgaris)
Iatrogenic	Rectal tears (Grade 3-4), enterocentesis during abdominocentesis, liver biopsy, castration complications, laparotomy contamination
Infectious	Actinobacillus equuli (most common bacterial isolate), Streptococcus spp., E. coli, Bacteroides spp., parasitic larval migration
Urogenital	Bladder rupture (uroperitoneum), uterine tears, dystocia complications, post-partum hemorrhage
Trauma	Blunt abdominal trauma, penetrating wounds, ingested wire foreign bodies
Other	Abdominal abscess extension, neoplasia, viral diseases (EIA, EVA, influenza - rare)

Etiology and Causes

Common Causes of Equine Peritonitis

Actinobacillus equuli Peritonitis

Actinobacillus equuli is a small, non-motile, gram-negative rod that is a normal inhabitant of the equine oral cavity and intestinal tract. It is the most commonly isolated bacterium in equine peritonitis cases, particularly in idiopathic peritonitis. Two subspecies exist: A. equuli subsp. equuli (non-hemolytic, primarily causes neonatal septicemia) and A. equuli subsp. haemolyticus (hemolytic, associated with respiratory and abdominal infections in adults).

NAVLE TipA. equuli peritonitis carries an EXCELLENT prognosis with appropriate antimicrobial therapy. Most isolates are sensitive to penicillin, trimethoprim-sulfonamide, and aminoglycosides. Horses typically show marked improvement within 24-48 hours of starting treatment. This is in stark contrast to peritonitis from GI rupture, which carries a grave prognosis.

Rectal Tear Grading and Peritonitis Risk

Rectal tears are a critical iatrogenic cause of peritonitis. Understanding the grading system is essential for predicting peritonitis risk and determining appropriate management.

Grade	Layers Involved	Prognosis
Grade I	Mucosa and/or submucosa only	Excellent (93-100% survival); conservative treatment
Grade II	Muscular layers only (mucosa intact)	100% survival; no bleeding on glove
Grade IIIa	Mucosa, submucosa, muscularis; only serosa intact	74% survival; surgical repair often needed
Grade IIIb	Dorsal tear into mesorectum	44% survival; retroperitoneal abscessation risk
Grade IV	Full thickness with peritoneal communication	GRAVE prognosis; septic peritonitis within hours; euthanasia often indicated

Clinical Signs

Clinical signs of peritonitis are often non-specific and variable depending on the underlying cause, severity, and duration. Recognition of these signs is critical for early diagnosis and intervention.

Acute Peritonitis

Abdominal pain: Mild to severe colic, splinted abdomen, reluctance to move, abdominal guarding
Cardiovascular: Tachycardia (greater than 48-60 bpm), increased CRT, injected or toxic mucous membranes
Fever: Pyrexia common (greater than 38.5C/101.5F), though may be masked by prior NSAID administration
Gastrointestinal: Ileus, reduced gut sounds, scant diarrhea, nasogastric reflux in severe cases
Systemic: Depression, anorexia, lethargy, sweating, tachypnea/hyperpnea
Endotoxemia signs: Dark red/purple gum line (toxic line), prolonged CRT, cold extremities, weak pulses

Chronic Peritonitis

Weight loss and poor body condition
Recurrent, low-grade colic episodes
Chronic ill-thrift despite adequate nutrition
Ventral edema (hypoproteinemia from protein-losing enteropathy)

High-YieldIn idiopathic peritonitis, clinical signs are often acute in onset without previous history of illness. The mean duration of signs before presentation is typically 1-3 days. Colic is the most common presenting complaint (approximately 48% of cases).

Parameter	Normal Values	Peritonitis Values
Color/Appearance	Clear to pale yellow, transparent	Turbid, yellow-white, serosanguinous, or green/brown (GI rupture)
Total Protein	Less than 2.5 g/dL (less than 25 g/L)	Greater than 2.5-3.0 g/dL; often greater than 4.0 g/dL
TNCC (Nucleated Cell Count)	Less than 5,000-10,000 cells/uL	Greater than 10,000 cells/uL; often greater than 25,000 cells/uL (diagnostic criterion)
Neutrophil Percentage	40-50% (neutrophil:mononuclear ratio approximately 2:1)	Greater than 80-90%; degenerate neutrophils suggest sepsis
Lactate	Less than 2.0 mmol/L (equal to or less than blood lactate)	Greater than 2.0 mmol/L; elevated above blood lactate suggests strangulation/ischemia
Glucose	Similar to blood glucose	Less than 30 mg/dL suggests septic peritonitis (bacteria consuming glucose)
pH	7.3-7.4	Less than 7.3 suggests septic peritonitis

Diagnosis

Definitive diagnosis of peritonitis relies on peritoneal fluid analysis. A systematic diagnostic approach combines physical examination, laboratory testing, and imaging.

Abdominocentesis Technique

Abdominocentesis is the cornerstone of peritonitis diagnosis. The procedure should be performed aseptically with the horse appropriately restrained.

Site selection: Ventral midline, slightly right of center (to avoid spleen); ultrasound guidance recommended
Preparation: Clip and aseptically prepare a 10x10cm area; sedate if necessary
Technique options: 18-gauge, 1.5-inch needle OR teat cannula (reduces enterocentesis risk)
Collection: Collect 3-5 mL into EDTA (cytology/cell count), plain (chemistry/culture), and blood culture tubes
Normal yield: Less than 10 mL typically obtained; total peritoneal fluid volume is 100-300 mL

Peritoneal Fluid Analysis

NAVLE TipALWAYS compare peritoneal fluid lactate to blood lactate. Peritoneal lactate GREATER than blood lactate strongly suggests intestinal ischemia or strangulation requiring surgical intervention. This is one of the most clinically useful measurements in colic workup!

Cytological Evaluation

Cytology provides critical information for differentiating septic from non-septic peritonitis. Key findings include: degenerate neutrophils (karyolytic changes, swollen nuclei), intracellular bacteria (definitive for septic peritonitis), and extracellular bacteria or plant material (indicates GI rupture).

Hematology and Biochemistry

Complete blood count and serum chemistry support the diagnosis but may be normal in early or localized peritonitis.

CBC findings: Leukopenia with neutropenia and degenerative left shift (acute, severe); leukocytosis with regenerative left shift (less severe or chronic); toxic changes in neutrophils
Fibrinogen: Often elevated (greater than 400 mg/dL); may be normal early in course
SAA (Serum Amyloid A): More sensitive early marker of inflammation; useful for monitoring treatment response
Chemistry: Hypoalbuminemia, hyperglobulinemia, hyperbilirubinemia; azotemia if dehydrated or prerenal failure

Diagnostic Imaging

Transabdominal Ultrasonography

Ultrasound is invaluable for detecting peritoneal effusion and guiding abdominocentesis. A 2.5-5 MHz curvilinear transducer is typically used.

Effusion: Anechoic (normal) to echogenic (cellular/septic) fluid; common locations include ventral abdomen, gastrosplenic space, renosplenic window
Echogenicity: Increased echogenicity and swirling suggests high cellularity (hemorrhage or sepsis)
GI rupture: Heterogeneous echogenicity with foreign material (ingesta), dorsally located free gas
Small intestine: Evaluate wall thickness (normal less than 3-4mm), diameter, and motility
Peritoneal surface: Hyperechoic, irregular fat suggests reactive peritonitis

Treatment Category	Drug/Intervention	Dose/Details
Antimicrobial Therapy	Potassium/Sodium Penicillin	22,000-44,000 IU/kg IV q6h
Antimicrobial Therapy	Gentamicin	6.6 mg/kg IV q24h (monitor renal function)
Antimicrobial Therapy	Metronidazole (anaerobes)	15-25 mg/kg PO q6-8h or 10 mg/kg IV q8h
Anti-inflammatory	Flunixin meglumine	1.1 mg/kg IV q12h (full dose) or 0.25-0.5 mg/kg IV q8h (anti-endotoxic dose)
Anti-inflammatory	Polymyxin B (anti-endotoxin)	1,000-6,000 IU/kg IV q12h (avoid with azotemia)
Fluid Therapy	Crystalloids (LRS, 0.9% NaCl)	Maintenance + deficit replacement; 2-4 mL/kg/hr maintenance
Fluid Therapy	Colloids/Plasma	For severe hypoproteinemia (TP less than 4 g/dL)
GI Protection	Omeprazole	4 mg/kg PO q24h (gastric ulcer prophylaxis)
Abdominal Lavage	Warmed sterile LRS	10-20 L via indwelling drain; removes bacteria, toxins, fibrin; indicated in severe/diffuse cases

Treatment

Treatment of peritonitis must address the underlying cause, combat infection, control inflammation, and provide supportive care. The aggressiveness of treatment depends on the severity and etiology.

High-YieldFor A. equuli peritonitis specifically, penicillin monotherapy may be sufficient as first-line treatment, with marked improvement expected within 24-48 hours. Idiopathic peritonitis in Sweden showed 97% survival rate with medical management. Duration of antibiotic treatment typically ranges from 5-21 days depending on response.

Surgical Considerations

Surgery may be required to address the underlying cause of peritonitis or for abdominal lavage/drainage in refractory cases.

Indications: Strangulating lesions, intestinal rupture (may warrant euthanasia), abscess drainage, foreign body removal, rectal tear repair
Post-surgical peritonitis: Reported mortality of 56%; aggressive treatment essential
Abdominal lavage: Can be performed standing (laparoscopic) or via ventral midline approach; helps remove debris and bacteria

Condition	Prognosis
GI Rupture	GRAVE - euthanasia usually indicated
Grade IV Rectal Tear	GRAVE - septic peritonitis within hours
Post-surgical Peritonitis	Guarded - 44-56% mortality reported
General Peritonitis (mixed)	Guarded to Fair - 50-70% survival; 59.7% in one study
Idiopathic Peritonitis	GOOD to EXCELLENT - responds well to medical treatment
A. equuli Peritonitis	EXCELLENT - 100% survival with treatment in some studies

Prognosis

Prognosis varies dramatically based on the underlying cause and is one of the most important factors in case management and client communication.

NAVLE TipHorses that survive peritonitis may suffer long-term complications including chronic ill-thrift, recurrent colic due to adhesions, and reduced athletic performance. Return to equestrian sport is often guarded.

P - Pain (abdominal, splinting, reluctance to move) E - Effusion (peritoneal fluid accumulation on ultrasound) R - Rectal tear risk (Grade III-IV = grave) I - Infection (A. equuli most common, good prognosis) T - TNCC elevated (greater than 10,000-25,000 cells/uL) O - Output (monitor peritoneal fluid response to treatment) N - Neutrophils degenerate = septic I - IV antibiotics (penicillin + gentamicin +/- metronidazole) T - Tap (abdominocentesis is the key diagnostic test!) I - Ileus (reduced gut sounds common) S - Supportive care (fluids, NSAIDs, gastric protection)

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