Septic Peritonitis

What is the peritoneum and what does it line?

A single layer of mesothelial cells forming a serous membrane that lines the abdominal wall (parietal peritoneum) and is continuous with the visceral peritoneum covering abdominal organs; it absorbs peritoneal fluid based on hydrostatic and oncotic pressures in the abdomen and vasculature.

Define peritonitis.

Inflammation of the peritoneal cavity; can be primary (no intra-abdominal source) or secondary (due to intra-abdominal pathology).

What is primary peritonitis in small animals?

Hematogenous/spontaneous inflammatory peritonitis in the absence of an identifiable intra-abdominal source; uncommon in dogs, more often infectious in cats (e.g. FIP)

What is secondary peritonitis?

Peritonitis secondary to an underlying intra-abdominal problem (GI leakage, organ rupture, post-op dehiscence); this is the most common form in dogs and cats.

Septic vs non-septic peritonitis – what’s the key distinction?

Septic = contamination with GI contents/bacteria.
Non-septic = exposure to usually sterile body fluids (urine, bile, pancreatic fluid) that become inflammatory but not primarily infectious.

What is the most common cause/pathogen in septic peritonitis in dogs?

GI leakage with Escherichia coli as the most common isolate; mixed enteric flora are common.

Give 3 common sources of septic peritonitis.

1) GI foreign body with perforation/leakage, (2) surgical site dehiscence 3–5 days post-GI surgery, (3) cholecystitis with gallbladder rupture / organ abscess.

Why are distal GI perforations usually more severe?

Bacterial load increases aborally: stomach/prox duodenum = low bacterial counts; proximal SI = ↑ gram-negative; distal ileum/colon = dense mixed + anaerobes → worse sepsis.

List the typical flora by GI segment (dog)

Stomach/prox duodenum: few gram-positives, lactobacilli, Candida spp.
Proximal small intestine: more gram-negative bacteria.
Distal ileum/colon: large anaerobic and mixed populations.

Pathophysiology of sepsis from septic peritonitis – what kicks it off?

Bacterial PAMPs bind host toll-like receptors → massive inflammatory mediator release (cytokines, chemokines, vasoactive and coagulation mediators) → vasodilation, endothelial activation, microvascular thrombosis → tissue hypoxia and MODS.

What is septic cardiomyopathy (in sepsis)?

A reversible decrease in cardiac contractility during sepsis, likely due to inflammatory mediators, altered Ca²⁺ handling, and mitochondrial dysfunction; it worsens hypoperfusion.

Name two peri-operative risk factors for septic peritonitis after abdominal surgery.

Pre-op hypoalbuminaemia (<2.5 g/dL) and intra-op hypotension (often with higher PCV).

First 3 diagnostics to stabilize and confirm septic peritonitis.

POCUS/abdominal imaging, abdominocentesis with fluid analysis, and paired serum–effusion measurements (glucose, lactate, creatinine, potassium, bilirubin).

What does a ≥20 mg/dL (1.1 mmol/L) serum–effusion glucose difference mean in dogs?

Highly supportive of septic peritonitis; reported 100% sensitivity and specificity in dogs in early work.

What does the same ≥20 mg/dL serum–effusion glucose difference mean in cats?

Supportive of septic peritonitis; about 86% sensitive and 100% specific.

What does an effusion–serum glucose difference of ≥38 mg/dL (2.1 mmol/L) tell you?

Still highly specific (≈100%); sensitivity reported 82–88% when using effusion supernatant.

How is lactate used in diagnosing septic peritonitis in dogs?

Effusion lactate >2.5 mmol/L or effusion lactate >2 mmol/L higher than serum is consistent with septic peritonitis; effusion lactate >4.2 mmol/L ~72% sensitive and 84% specific.

Is the lactate rule-out as good in cats?

No – the effusion lactate–serum lactate difference did not correlate as well with sepsis in cats

What is the treatment priority order in septic peritonitis?

(1) Early hemodynamic resuscitation, (2) early, appropriate, broad-spectrum IV antibiotics, (3) early source control (usually surgery), (4) ongoing monitoring and organ support.

What is the key timing rule for antibiotics in sepsis?

Every 1-hour delay in appropriate antimicrobial therapy is associated with ~8% ↑ mortality → give broad-spectrum IV antibiotics immediately.

Give 2 reasonable empiric antimicrobial combos for a normotensive dog with no renal disease and no recent Abx.

(1) Unasyn + enrofloxacin
(2) Unasyn + amikacin
(Clindamycin + amikacin is an alternative for anaerobes + gram-negatives.)

Give 2 empiric options for patients with renal insufficiency.

(1) Unasyn + enrofloxacin
(2) Clindamycin + enrofloxacin
(Avoid or minimize aminoglycosides.)

Ampicillin–sulbactam (time-dependent) dose options?

Intermittent: 50 mg/kg IV q6h
CRI: 50 mg/kg IV loading, then 6 mg/kg/h IV CRI.

What is the goal of vasopressor therapy in septic peritonitis?

Maintain organ perfusion, not “perfect” BP; target MAP ~65 mmHg or Doppler 90–100 mmHg.

First-line vasopressor sequence?

Norepinephrine → add vasopressin → then epinephrine → add dobutamine if low CO.

When would you give colloid/albumin?

Severe hypoalbuminaemia (<2 g/dL) with ongoing losses to peritoneal cavity and poor oncotic pressure; albumin often preferred over plasma for predictability.

What is CIRCI and when do you treat it here?

Critical illness–related corticosteroid insufficiency; treat when shock persists despite fluids + vasopressors (after ruling out major metabolic acidosis).

Hydrocortisone dosing for septic dog with suspected CIRCI?

0.5 mg/kg IV q6h (or equivalent low-dose protocol), then taper by ~50% per day once improved.

Why is dexamethasone-SP not preferred in this setting?

Longer HPA-axis suppression; OK if it’s the only drug available, keep to physiologic 0.01–0.05 mg/kg IV q24h for 1–2 doses.

What is the surgical goal in septic peritonitis and when should it be done?

Identify and correct the source of contamination (resect/repair, drain, lavage); ideally within 6 hours of diagnosis, even if the patient hasn’t fully normalized.

How much peritoneal lavage fluid is recommended?

About 200–300 mL/kg warmed fluid, continued until effluent is clear.

Why is TIVA often preferred during surgery in these patients?

Lets you keep inhalant <0.5 MAC, better cardiovascular stability in a septic, vasodilated, sometimes hypotensive patient.

Give a TIVA-style anesthetic plan for a septic peritonitis surgery.

Premed fentanyl → induction alfaxalone + midazolam → maintenance with fentanyl, ketamine, lidocaine, ± alfaxalone infusion; keep inhalant low.

Why place a feeding tube at surgery?

Enables early enteral nutrition within 24 h, supports gut barrier, and can help detect dehiscence (add 1 mL food dye to 200 mL diet and monitor drains).

What indicates possible recurrence on a closed-suction abdominal drain?

Increased drain production or change in character → warrants full reassessment; note that finding intracellular bacteria in the drain is insensitive.

When can you remove an abdominal closed-suction drain?

Clinical improvement, good fluid balance, and drain fluid <2 mL/kg/day or plateaued production.

What monitoring is recommended in the first 24–72 h post-op?

BP and ECG, fluid status q6–12 h (weight, hydration, UOP, drain), PCV/TS/BG/renal panel/electrolytes at least q24h, recumbency care, and repeat abdominal U/S 48–96 h to check the anastomosis/surgical site.

What is the reported recurrence rate of septic peritonitis?

Roughly 10–38%, with GI causes having the highest risk of recurrence.

Overall survival to discharge for dogs and cats with septic peritonitis?

Commonly 60–75%, though literature ranges from 36–88% depending on case mix and source control success.

Name 3 potential complications after septic peritonitis.

Recurrence, AKI (sepsis, hypotension, nephrotoxic drugs), and tension pneumoperitoneum; cats can also develop uveitis.

What is Candida peritonitis and why do we care?

Fungal peritonitis, often after hollow-organ perforation, prior abdominal surgery, immunosuppression, or prolonged antibacterial therapy; associated with worse outcome → treat with systemic antifungals (e.g. IV/PO fluconazole, adjust to C+S).

Why is early nutrition (within 24 h) recommended?

Supports enterocytes, reduces bacterial translocation, and improves overall recovery in critical patients.

Why is albumin often low in these patients?

Capillary leak + peritoneal loss + decreased hepatic production during systemic inflammation → worsens edema and 3rd spacing.

In septic peritonitis, what two opposing processes create organ dysfunction?

Profound vasodilation and endothelial activation (→ maldistribution, hypotension) plus microvascular thrombosis (→ impaired perfusion) → net result is tissue hypoxia and MODS even when systemic BP is “OK.”