PERITONITIS

Nicole Spurlock DVM, DACVECCEmergency and Critical Care Medicine

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Peritoneum

• Fenestrated basement membrane

• Semi-permeable– Passive diffusion of electrolytes, urea, H20, certain

drugs/toxins– Equilibration of concentration and osmotic gradients

between peritoneal cavity and intravascular space (peritoneal dialysis)

• Large exudative and absorptive area when inflamed

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Primary Peritonitis

• Spontaneous inflammation of the peritoneum in the absence of underlying intra-abdominal pathology– <1% of cases– Hematogenous spread

• FIP– Other routes of entry

• Across lumbosacral arches from pleural cavity• From uterus via ovarian bursae• Across GIT (bacterial translocaiton)

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Primary – Small AnimalsJAVMA 2009; 234(7): 906

• 24 cases (1990-2006)

• Primary vs. secondary– Less exudative fluid– More likely Gram+ infection– Surgery may do harm to patients with primary peritonitis

• Surgery is typically not indicated for humans with primary peritonitis

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Secondary Peritonitis

• Inflammation of the peritoneum associated with pre-existing abdominal pathology

• More common

• Infectious

• Noninfectious (sterile/aseptic/chemical/traumatic)

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Secondary Peritonitis: Infectious

Gastrointestinal tract• Necrosis, rupture,

perforation• Surgical wound dehiscence• Pancreatic abscess

Urogenital tract• Pyometra/uterine rupture• Prostatic abscess• Ruptured urinary bladder

with UTI• Renal abscess• Vaginal rupture

Hepatobiliary• Necrotizing cholecystitis• Liver lobe torsion• Hepatic abscess

Other• Penetrating wounds• Surgical contamination• Evisceration• Splenic abscess• Peritoneal dialysis

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Secondary Peritonitis:Compromise of the GIT

• 50-60% cases of bacterial peritonitis

– Gastric/intestinal perforations secondary to GDV– Surgical wound dehiscence– Perforated small intestinal ulcers– Foreign body– Tumor rupture

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Secondary Peritonitis: Sterile

• Neoplasia

• Pancreatitis

• Sterile bile peritonitis

• Uroabdomen

• Sterile foreign bodies (sponge, talcum powder, suture material)

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Pathogenesis

• Bacterial/chemical irritants vascular dilatationincreased capillary permeability– Facilitates phagocytosis of bacteria and foreign material

• Local deposition of fibrin and plastering of adjacent bowel mesentery (omentum!) to inflamed areas

• Walling-off inflammation

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Potential Outcomes

• Successful walling-off, host defenses resolve infection

• Confined suppuration and abscess formation

• Diffuse peritonitis

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Diffuse Peritonitis: Pathophysiology

• Large protein-rich fluid losses (tremendous surface area) hypovolemic shock

• Exacerbated by vomiting, diarrhea

• Vasodilation relative hypovolemia

• Splanchnic edema or vasoconstricton stress ulceration/ischemic damage bacterial translocation

• Increased absorption across inflamed peritoneum septicemia, bacteremia, SIRS, sepsis

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Course Determination

• Virulence of contaminating microorganisms ± presence of certain enhancing substances (bile salts, talc, hemoglobin)

• Extent of contamination (volume, rate, duration)

• Immunocompetence of host

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History & Clinical Signs

• Lethargy/depression, • Inappetance, • Vomiting• Diarrhea• ± Acute collapse• Intact female?• Trauma?• Recent surgery?• Abdominal pain ± distention

– “Praying position”

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Physical Exam: Nebulopathy

• Evidence of perfusion impairment– Severe dehydration– Dull mentation– Pallor/injected mucous membranes– +/-Weak femoral/distal pulse quality with BP

• Symptoms of SIRS/sepsis:– Hypo/hyperthermia– Brady/tachycardia– Tachypnea– Leukocytosis or leukopenia

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Primary Peritonitis – CatsJAAHA 2009; 45: 268-76

• 13 cases

• Mortality 31%

• Common presentation: Tachypnea, bradycardia, ascites, hypoalbuminemia, anemia

• All cats surgically explored

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Laboratory Abnormalities

• Hemoconcentration/anemia

• Hypoglycemia/hyperglycemia

• Decreased sodium/potassium ratio

• Azotemia

• Elevated transaminases

• Hyperbilirubinemia

• Hypoalbuminemia/panhypoproteinemia

• Hypochloremic metabolic alkalosis with hypokalemia

• High anion gap metabolic acidosis:– Lactic– Urinary tract

• Leukocytosis with a shift to the immature forms on the differential cell count

• Absence of leukocytosis or leukopenia

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Abdominal Radiography

• Loss of intra-abdominal contrast

• Ileus with distended loops of bowel

• Isolated distended loop bowel or two distinct populations of small intestines

• Foreign body

• Mass effect

• GDV

• Free fluid (> 8 ml/kg)

• pneumoperitoneum

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When to cut: PneumoperitoneumJAVMA (223)4, Aug 15 2003JAVMA (225)2, July 15, 2004

Secondary to:– Ruptured hollow viscus– Gas-forming bacteria (abscess)– Penetrating injuries

But also secondary to:– Abdominocentesis– Recent abdominal surgery (18 d)

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Ultrasound Examination

• Free fluid• Abscesses in parenchymal organs• Pyometra• Pancreatitis• Abdominal masses• Abnormalities in organ blood flow

– Organ torsion

• Intestinal obstruction

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FASTJAVMA 225(8), Oct. 15, 2004

• Focused Abdominal Sonogram Trauma

• Adapted from human medical field to identify abdominal fluid in dogs following trauma

• 4 Views, named for landmarks in R recumbency– DH: diaphragmatico-hepatic– SR: spleno-renal– CC: cysto-colic– HR: hepato-renal

• Sensitive, not specific

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Abdominal Paracentesis

• Patient in L lateral recumbency (spleen!)

• Ventral abdomen at the level of the umbilicus clipped and prepared aseptically

• Urinary bladder evacuated

• Local infiltration with lidocaine?

• 4-quadrant centesis– 23 ga needles (4-6)– 1 ml syringe– Slides & sample collection tubes

• Closed or open-needle techniques described

• Contraindications: coagulopathy; organomegaly; distension of abdominal viscus

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Abdominal Paracentesis

Bloody fluid that clots:• r/o vessel or organ

Effective? • Canines: 5.2-6.6 ml/kg

abdominal fluid required for positive results

Alternative:• Diagnostic peritoneal lavage?

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Evaluation of Peritoneal Fluid

• Cytology/culture: Crystals? Microbes? Pigments?

• Total protein• Lactate• Glucose• Creatinine• Bilirubin• PCV

• Surgical Intervention:– Septic abdomen– Bile peritonitis– Uroabdomen (+/-)– Persistent hemoabdomen

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Normal Peritoneal Fluid

• < 1mL/kg non-clotting, clear, yellow fluid (straw-colored)

• Transudate:– < 3000 nucleated cells/L– 50% macrophages, 50% lymphocytes– < 2.5 g/dL protein (albumin)

• Functions– Decreases friction between opposing surfaces– Dissemination of localized inflammation/infection

• Drainage– Diaphragmatic lymphatics and thoracic duct to sternal lymph nodes

(80%)

Abdominal effusion

Total protein count, total nucleated cell

count

< 2.5 g/dl protein

<1500 nucleated cells/L

2.5-7.5 g/dl protein

1000-7000 nucleated cells/L

> 3 g/dl protein

> 7000 nucleated cells/L

Transudate

Modified transudate

Exudate

Algorithm to Classify Effusions

Transudate

Low serum albumin

YesNo

Proteinuria

YesNo

Diarrhea Consider PLN

No Yes

Consider hepaticinsufficiency Consider PLE

Abdominal fluid [creatinine]greater than serum

creatinine

No Yes

Consider leakagefrom intestinal

lymphatics

Uroabdomen

Modified Transudate

Fluid bile-stained, with phagocytized bile pigments

NoYes

Fluid is red, with phagocytized RBCs

NoYes

Bile peritonitis

Intracavitary hemorrhage

Fluid is milky white

Yes No

Chylous/pseudo-chylous

Small lymphocytes predominate

Yes No

Chylous/pseudo-chylous Lymphoblasts, mast cells, cells w/nuclear

criterea for malignancy

No

Neutrophils predominate

YesNo

Nonexfoliating neoplasia, FIP, chronic inflammation,

Diaphragmatic Hernia, Liver Lobe Torsion, other

Abdominal fluid [creat] > serum [creat]

Yes No

Uroperitoneum Organsims present (mycotic, rickettsial, protozoal)

Yes No

Yes No

Neoplasia

Heart failure?

Yes

Infectious pleuritis/peritonitis

FIP, tissue inflammation, nonexfoliating

neoplasia, other

Mostly degenerate

Yes

Bacteria present

YesNo

Culture

Bacterial peritonitis

No

Bacterial, mycotic, protozoal or rickettsial organisms

Yes

Infectious peritonitis

No

Yes

Nuclear criterea malignancy

No

Possible neoplasiaFluid very bloody

YesNo

Erythrophagocytosis

YesNo

Intracavitary hemorrhageBloody tap, organ tap,

acute hemorrhage

Bile-stained with phagocytized bile pigments

Exudate where Neutrophil

predominates

Neutrophils

Yes

Bile peritonitis

No

Abd. fluid [creat] > serum [creat]

Uroperitoneum

YesNo

Infectious, inflammatory, neoplastic

Exudate where Neutrophil does not

predominate

No

Primarily mast cells

Primarily small lymphocytes

NoYes

Mast cell tumor

Chylous/pseudo- chylous

Primarily lymphoblasts

Yes NoLymphosarcoma

Primarily macrophages

Yes NoFluid is bile-stained with phagocytized bile pigment

Cells with nuclear criterea for malignancy

Yes

Yes

Bile peritonitis

NoLow-grade chronic inflammation, FIP

Yes No

Neoplasia? Refer

Exudate

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When to Cut: Septic Effusions

• Non-septic effusions: cut?

• Hepatic disease, GI neoplasia, multicentric lymphoma, splenic leiomyosarcoma, pancreatitis, right-congestive heart failure, intact pyometra

• Septic effusions: cut!

– GI – intestinal neoplasia, foreign body, postoperative enterotomy dehiscence, duodenal feeding tube leakage

Other – hepatic abscess, pancreatic abscess, mesenteric lymph node abscess, contamination from urinary bladder

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Septic Effusion: Lactate and GlucoseBonzynski et al. JAVMA 2003

• Blood-to-fluid (BFG) glucose difference > 20 mg/dl (1.1 mmol/L) – 100% sensitive and specific for dx septic peritonitis in dogs – 86% sensitive and 100% specific in cats

• Blood to fluid lactate difference < 2mmol/L – 100% sensitive and specific for dx of septic peritonitis

(dogs)

• IV administration of glucose or presence of hemoabdomen may decrease accuracy

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Evaluation of post-celiotomy peritoneal drain fluid volume, cytology, and blood-to-peritoneal fluid lactate and glucose differences in normal dogs Vet Surg 2011 40(4)

• JP drain placed after abdominal explore in 10 healthy dogs

• Peritoneal fluid analyzed q6 x 7 days

• Results after day 4:– blood-to-peritoneal glucose concentration differences were consistent with septic

effusion based on previously reported values (all dogs)

– Blood-to-peritoneal lactate concentration consistent with septic peritonitis (70% of dogs)

• Conclusion: post-operative blood to peritoneal fluid glucose & lactate may not be reliable indicators of septic peritonitis when evaluating fluid collected from closed suction drains

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When to Cut: Bile Peritonitis

• Abdominal fluid – Presence of bilirubin = 100% effective in diagnosis bile

peritonitis

– Effusion [bilirubin] > serum [bilirubin]

– Cytology: bile pigments & crystals may also be seen microscopically

– If secondary to ruptured mucocele, these changes may not be present

• Gelatinous bile may not disperse intra-abdominally

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When to Cut: Uroabdomen

• Abdominal fluid [creatinine] to peripheral blood [creatinine] ratio of >2:1

• Abdominal fluid [potassium] to peripheral blood [potassium] ratio of >1.4:1

• Remember:– Bladder palpable in majority (>50%)– Ascites can occur subsequent to severe UO– Some animals with urinary compromise will still urinate & have urine

collecting in the abdomen

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Pre-op Stabilization

• Fluid resuscitation • Blood products (peri-op)• Correction acid/base, electrolyte abnormalities• Euglycemia• Vasopressors for refractory hypotension• Inotropes for documented myocardial failure• 4-quandrant bacteriocidal systemic antibiotics• Pain management• Source control

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When to Cut: a Summary

• Septic peritonitis– Abdominal abscess– GI obstruction– Ischemic/perforated/ruptured GI

• Persistent abdominal hemorrhage– Trauma– Neoplasia

• Uroperitoneum (+/-)• Free abdominal gas (non-iatrogenic or associated with

pneumomediastinum)• Bile peritonitis

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How to know: a Summary

– Septic peritonitis:• Intracellular microbes• Blood-to-fluid glucose

concentration difference > 1.1 mmol/L

• Blood –to-fluid lactate difference < 2 mmol/L

– Bile peritonitis:• Effusion [bilirubin] > blood

[bilirubin] (usually x2)• Presence of bile pigments or

crystals

– Uroperitoneum• Fluid creatinine > 2:1 of

serum creatinine• Fluid potassium > 1.4:1

serum potassium

– Hemoperitoneum• PCV of fluid near peripheral

blood (or increasing)• Evaluate with TP: decreasing

protein levels indicate hemorrhage

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Phone - (02) 9889 0289 Fax - (02) 9889 0431

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www.sashvets.com.au twitter: @SASHvets

Phone - (02) 9889 0289 Fax - (02) 9889 0431

Level 1, 1 Richardson Place, North Ryde 2113, Sydney, NSW