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Septic Peritonitis

Septic Peritonitis

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Septic Peritonitis

William T. N. Culp, VMD, DACVS University of California-Davis

David E. Holt, BVSc, DACVS University of Pennsylvania

Abstract: Bacterial septic peritonitis is a serious condition that requires immediate treatment. The pathogenesis is complex, and the list of diagnostic differentials is extensive. The keys to successful treatment are early recognition of the condition and elimination of the causative organism. Multiple options for draining the peritoneal cavity exist, and further studies are neces- sary to establish specific, evidence-based guidelines. The prognosis is generally guarded in dogs and cats. Much depends on whether the patient develops concurrent , systemic inflammatory response syndrome, or multiple dysfunction syndrome.

eptic peritonitis is a life-threatening condition that , Macrophages, and Mast Cells occurs secondary to many intraabdominal diseases in Normally, the peritoneal cavity contains a diverse array of Sdogs and cats. This article reviews bacterial peritonitis cells capable of reacting to antigens.10,11 When a peritoneal and sepsis and describes treatment options and prognosis. occurs, vasoactive substances (e.g., ) are released. Histamine from degranulating resident peritoneal Anatomy and Intrinsic Defense Systems of the mast cells stimulates vasodilation and exudation of fluid con- Peritoneal Cavity taining complement and opsonins that are capable of coat- Mesothelium ing , promoting phagocytosis and encouraging an The peritoneal cavity is lined with a serous layer of meso- influx of neutrophils and macrophages into the peritoneal thelial cells.1–3 After peritoneal injury, regeneration begins cavity.7,10,11 Peritoneal mast cells, neutrophils, macrophages, with an influx of round cells that eventually transform into and lymphocytes interact to promote cytokine expression, mesothelial cells. This regeneration can occur as rapidly as chemoattraction, and phagocyte recruitment. Phagocytes 4 hours after injury.2 kill bacteria by generating reactive oxygen species, acidify- ing vacuoles containing phagocytosed bacteria, and releas- Intraperitoneal Fluid ing hydrolytic lysosomal enzymes.11 A small amount of fluid is normally found within the perito- neal cavity. This fluid constantly lubricates organs to prevent Complement System friction. Normal human peritoneal fluid has been shown to Complement system proteins control and have antimicrobial activity against gram-positive and gram- assist in bacterial phagocytosis.10 The complement system negative bacteria.4 can be activated by the presence of antigen–antibody com- Fluid injected into the is dispersed throughout plexes, endotoxin, damaged cells, and other components of the peritoneal cavity within 15 minutes to 2 hours.5 It is likely bacterial cell walls.12 Activated forms of complement com- that peritoneal contaminants are disseminated by a similar ponents 3 and 5 are formed and act as anaphylotoxins. The movement of peritoneal fluid.2,6 Fluid moves toward the dia- secondary effects of these complement proteins are vaso- phragm, where it is absorbed by diaphragmatic lymphat- dilation, chemotaxis of neutrophils, degranulation of mast ics.6–8 Bacteria in contaminated peritoneal fluid penetrate cells and basophils, clearance of immune complexes, and the diaphragm through 8- to 12-μm gaps (stomata) between cytolysis.7,10,11 the peritoneal mesothelial cells and enter specialized lym- phatic collecting vessels (lacunae).7 The bacteria travel from Fibrin and these vessels to the mediastinal lymph node and eventually The fluid exuded into the inflamed peritoneal cavity con- to the thoracic duct system and bloodstream.8,9 tains plasma proteins, including fibrinogen and thrombo-

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FIGURE 1 ity.16 Any major abdominal organ may act as the septic nidus for peritonitis.

Gastrointestinal Leakage of contents from the gastrointestinal (GI) tract is the most common cause of septic peritonitis in dogs and cats. GI diseases account for 38% to 75% of cases of sec- ondary septic peritonitis,20–25 and GI ulceration accounts for 24% to 35% of GI-associated peritonitis cases21,23,25 (FIGURE 1). Conditions that predispose dogs to GI ulceration include underlying hepatic disease (33%) and administration of NSAIDs and corticosteroids.26 Concurrent administration of NSAIDs and corticosteroids or administration of NSAIDs at a higher-than-approved dosage may increase the risk of GI ulceration.27 Many different NSAIDs28–30 have been linked to ulcer-associated peritonitis in dogs. Carprofen was a Perforated gastric ulcer. potential cause of a duodenal ulcer in a feline case report.31 Corticosteroid administration has been associated with plastin.7 Tissue thromboplastin converts prothrombin to colonic perforation and peritonitis in dogs with interverte- thrombin, which activates fibrinogen. Fibrin is generated, bral disk disease.32 polymerizes, and accumulates—in part because fibrinoly- Septic peritonitis can also occur after GI resection and sis is down-regulated.13 Fibrin walls off bacteria, preventing .33,34 In one study of 121 dogs that underwent phagocytosis by neutrophils and macrophages and leading this procedure, the overall dehiscence rate was 15.7%, and to formation.6,7,11 However, fibrin also prevents sys- dehiscence was often fatal (73.7% mortality).33 Dogs that temic bacterial spread. In one study performed in mice, pre- required resection and anastomosis for foreign-body entrap- vention of formation resulted in earlier systemic ment or traumatic injury were significantly more likely to spread of bacteria and higher mortality.14 have anastomotic dehiscence. Risk factors associated with anastomotic leakage in another retrospective study included Etiology preoperative peritonitis, hypoalbuminemia, and the pres- Primary Peritonitis ence of an intestinal .34 The leakage rate for In human medicine, peritonitis is generally categorized as dogs in that study was 14%. None of the 25 cats in the study primary, secondary, or tertiary. Primary peritonitis occurs developed leakage.34 spontaneously, meaning that no obvious intraperitoneal Primary GI neoplasia and non-GI neoplasia (, cause of bacterial contamination is found.8,15,16 This process mast cell tumors)26 can cause GI perforation. Neoplasia is is more common in people than in companion animals and a common cause of GI leakage in cats, accounting for 25% is generally associated with the presence of sec- of septic peritonitis cases in one study.35 Adenocarcinoma ondary to alcoholic .15,16 The presence of bacteria and lymphosarcoma were the most common neoplasms in the peritoneal cavity in primary peritonitis is attributed reported.35 to spread via a hematogenous or lymphogenous route or Other documented causes of GI leakage include gastric to bacterial translocation through an intact intestinal wall.15 necrosis secondary to gastric dilatation– (GDV), Feline infectious peritonitis (FIP) is the most common cause gastropexy site leakage, perforation, postopera- of primary peritonitis in companion animals.8,17 FIP occurs tive GI biopsy site dehiscence, uremic gastropathy, stress- in two major forms: dry (granulomatous) or wet (effusive).18 induced GI lesions, and traumatic wounds.8,17,26,34–36 The wet form is characterized by abdominal effusion and Bite wounds to the abdomen should be explored imme- peritonitis. The pathogenesis of this process is complex and diately to evaluate for viscus rupture that may result in the still not fully elucidated.18 A retrospective study evaluating leakage of bacteria into the peritoneal cavity.37,38 Bacteria peritoneal effusion in 65 cats found only four cases of effu- from the attacking animal’s mouth can contaminate the peri- sive FIP.19 toneal cavity even in the absence of GI perforation. Gunshot can cause extensive damage to the and Secondary Peritonitis intestines. Five dogs in one series of 84 gunshot wounds had Secondary peritonitis is the most common form of perito- peritoneal penetration.39 All five dogs had multiple, severe nitis encountered in companion animals and results from intestinal injuries, emphasizing the need for early surgical leakage of bacteria-containing fluid into the peritoneal cav- intervention in such cases.39

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FIGURE 2 FIGURE 3

Severe with abscessation. Ruptured prostatic abscess (arrow).

Biliary Tract Urogenital leakage often results in septic peritonitis.40,41 Bile leak- Rupture of a is a potential but uncommon cause age can occur from trauma, infarction, necro- of septic peritonitis. This occurs either before tizing , cholelithiasis, and iatrogenic biliary or during surgical manipulation of the friable uterus. damage (e.g., intraoperative manipulation, gallbladder is the bacteria isolated in most cases of pyo- expression, gallbladder aspiration).41–43 A retrospective study metra.53 Although not routinely evaluated in clinical practice, evaluating 17 dogs and two cats with leakage a lower endotoxin concentration is associated with found septic effusion in 10 cases (seven due to necrotiz- a better prognosis in dogs with pyometra.54 A retrospective ing cholecystitis and three due to trauma).41 Although not study of pyometra in 183 cats found that seven cats (3.8%) compared statistically, animals in that study with septic bile developed uterine rupture. Four of these cats died as a result peritonitis seemed to have a lower survival rate than those of septic peritonitis.55 with aseptic peritonitis.41 In another study evaluating extra- Prostatic abscessation can be life-threatening, and rup- hepatic biliary surgery in dogs, septic bile peritonitis was ture of prostatic abscesses (FIGURE 3) resulting in septic significantly associated with mortality.44 peritonitis has been reported to occur relatively frequently in dogs (17 of 92 cases; 18%).56 Seven of these 17 dogs died Pancreatic/Splenic/Hepatic within 1 week due to sepsis. Abscessation of the pancreas, , or spleen is rare in dogs Septic peritonitis secondary to infection from the urinary and cats. Pancreatic abscesses (FIGURE 2) are usually seque- system is rare.57 Documentation of renal abscessation is lim- lae to the development of necrotizing pancreatitis, but they ited to a few case reports and a large retrospective study of can also occur when a becomes 61 dogs that included only three cases.58 Septic peritonitis infected.45 Hepatic abscesses have been documented more may also be associated with trauma to the urinary tract and often than pancreatic or splenic abscesses but are still a very subsequent leakage.58 One retrospective study evaluat- uncommon finding in dogs and cats.46–49 The development ing uroperitoneum in cats found three positive bacteriologic of septic peritonitis secondary to hepatic abscess rupture cultures among the five samples submitted from the peri- was only documented in one case among several retrospec- toneal cavity.59 Enterococcus spp were the most commonly tive studies.47–49 Septic peritonitis has also been documented isolated organisms in that study.59 Four cases of septic peri- secondary to liver lobe torsion in one dog50 and liver lobe tonitis secondary to urinary tract infection were reported necrosis in one cat.35 in another retrospective study.35 Sources of infected urine Splenic abscesses accounted for 0.3% of all splenic dis- included a ruptured urinary bladder (n = 2) and leakage ease in dogs in one large retrospective study51 and 1.7% from a diseased bladder (n = 1); the source was unknown of all splenic disease in cats in another retrospective in a cat with pyelonephritis.35 study.52 However, these studies did not mention whether the abscesses were septic or nonseptic, and the feline ret- Tertiary Peritonitis rospective study included splenic abscessation in a general Tertiary (recurrent) peritonitis has not been documented in category of splenitis.52 dogs and cats. In humans, tertiary peritonitis refers to a

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FIGURE 4 cally important to this cascade, facilitating the intracellular signaling that leads to cytokine release after interacting with MD-2.65,68 The process by which gram-positive bac- teria induce their effects is less well under- stood. Gram-positive bacteria contain many substances—including peptidoglycan, teichoic acid, and polysaccharide–hyaluronic acid capsules—that can act as proinflammatory agents.65,69 Peptidoglycan released by bacteria has demonstrated proinflammatory activities that are mediated via the cell surface molecule CD14. Teichoic acid also seems to use CD14 This figure demonstrates the process by which endotoxin LPS( ) binds receptors to induce proinflammatory actions, to LPS-binding protein (LBP), accelerating further binding between such as the production of cytokines, includ- LPS and CD14 on macrophages. Binding is further promoted by interactions ing interleukin 1 (IL-1), tumor necrosis factor between CD14, TLR, and MD-2. The result of these interactions is the release of (TNF), and nitric oxide (NO). Gram-positive cytokines (IL-1, TNF) from the macrophage. (CD14 = cluster differentiation antigen 14, IL-1 = interleukin 1, LPS = lipopolysaccharide, MD-2 = extracellular adaptor pro- capsules are capable of inducing resistance 69 tein, TLR = Toll-like receptor, TNF = tumor necrosis factor) to phagocytosis. Gram-positive bacteria can also produce superantigenic toxins that can recurrent infection of the peritoneal cavity after an episode lead to T-lymphocyte activation and cytokine release.65,69 of primary or secondary peritonitis.60 This syndrome tends to occur after optimal surgical treatment and manifests as sys- Cytokines temic sepsis without an evident septic focus.61,62 Organisms The major cytokines in the inflammatory process are IL-1 and cultured from the peritoneal cavity in cases of tertiary peri- TNF-α.67,70 Both gram-positive and gram-negative bacteria tonitis tend to come from the GI tract or to be lesser patho- can cause the release of these cytokines.69,70 IL-1 and TNF-α genic organisms such as spp or initiate many events, including activation of the arachidonic epidermidis.15,62 Bacterial translocation is thought to play a acid cascade, production of acute-phase proteins in the liver, role in these cases because humans with severe illness are and induction of and intravascular coagulation.7,11,61 more likely to have intestinal hypoperfusion, altered gut These cytokines also signal peritoneal mesothelial cells to flora, and inadequate gut barrier function.62 Recent studies release interleukin 8 (IL-8),11 which acts as a chemoattractant of tertiary peritonitis have found a possible association with for polymorphonuclear leukocytes (PMNs). endocrine dysfunction and immune paralysis.62 Platelet-activating factor (PAF), high mobility group box-1 (HMGB1), and macrophage migration inhibitory factor (MIF) Pathophysiology are cytokines or cytokine-like substances that are released Bacteria from macrophages secondary to TNF-α activation.61,67 PAF may The presence of a bacterial contaminant within the perito- be produced from the same membrane phospholipid as leukot- neal cavity induces the cascade of events associated with rienes during inflammation.71 Leukotrienes and PAF increase septic peritonitis. In animals, peritonitis is most commonly vascular permeability and PMN activation.71 LPS has been associated with gram-negative bacteria.20,21,23,36 The effects shown to increase levels of HMGB1. Patients with increased of gram-negative bacteria are primarily related to endotoxin levels of HMGB1 during sepsis have higher mortality.67 In mice, (lipopolysaccharide [LPS]). Endotoxin is composed of three MIF has been shown to act as a proinflammatory agent and parts: lipid A and two groupings of polysaccharides, the can alter the antiinflammatory effects of glucocorticoids.67 R-core and the O-polysaccharide.7,63 Most toxic effects are attributed to the lipid A segment64 (FIGURE 4). /Hypoproteinemia Endotoxin binds to LPS-binding protein, thereby acceler- The combined effects of the inflammatory mediators (espe- ating the binding of LPS to the cluster differentiation (CD) cially cytokines) increase vascular permeability and vaso- 14 antigen gene receptor on macrophages.7,14,63 A specific dilation.72 Increased vascular permeability results in fluid interaction between the CD14 receptors, Toll-like receptors and albumin influx into the peritoneal cavity. The resulting (TLRs, which initiate cellular activation), and the lympho- decreased albumin concentration in the intravascular space cyte antigen MD-2 (another cell surface molecule) also pro- and decreased albumin synthesis in the liver during times of motes binding.64–66 This binding stimulates macrophages to stress73 allow more fluid to extravasate as oncotic pressure release multiple cytokines67,68 (FIGURE 4). TLR-4 is specifi- decreases.

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As more fluid enters the peritoneal cavity, hypovolemia worsens. This results in decreased venous return to the Key Facts heart with subsequent decreased cardiac output and poor • Septic peritonitis may not be immediately recognizable tissue perfusion. Cardiac compromise may be worsened by based on . the release of a myocardial depressant factor. • Peritoneal fluid analysis is essential to diagnosing and Arachidonic Acid Cascade treating septic peritonitis. The activation of the arachidonic acid cascade by endotoxin • Severe sequelae such as systemic inflammatory and bacteria-induced cytokine release results in the produc- response syndrome or multiple organ dysfunction 7,11,12,61 tion of leukotrienes, prostacyclins, and prostaglandins. syndrome may still occur after the nidus of infection has These substances recruit leukocytes such as PMNs and been removed. eosinophils to the site of inflammation and can result in vasodilation.7,61,71 fluid has also been shown to lead to increased bacterial Coagulation Abnormalities numbers and decreased bacterial clearance.8 Many studies have documented coagulation abnormalities that accompany sepsis.67,74–76 Both animals and humans have Nitric Oxide been shown to develop a procoagulant state.67,75,76 Endotoxin Endotoxin, interferon γ (IFN-γ), lipoteichoic acid, and pep- initiates coagulation by stimulating expression of tissue tidoglycan stimulate macrophage production of NO.65,69 In factor,67,75 which in turn activates the intrinsic and extrin- addition, IL-1 and TNF can initiate transcription and transla- sic coagulation pathways to produce fibrin. Fibrinolysis is tion of NO synthase.69 NO causes vasodilation, decreasing impaired by high levels of plasminogen activator inhibitor systemic vascular resistance and resulting in hypotension.70 type 1 and down-regulation of tissue factor pathway inhibi- NO can also interact with reactive oxygen molecules (e.g., tor (TFPI), protein C, protein S, and antithrombin III.13,67,76 superoxide) to generate a series of cytotoxic nitrogen radi- The role of sepsis in TFPI system dysfunction is not fully cals, including peroxynitrite.65 understood, but some authors have suggested that TFPI All of these processes culminate in the initiation of sys- may not be able to deactivate the increased levels of tis- temic inflammatory response syndrome (SIRS) and sep- sue factor associated with sepsis.13 In addition, the structure sis. Antiinflammatory cytokines are produced to attenuate of TFPI may be altered by the endothelial injury induced this massive reaction but can be overwhelmed. Eventually, by inflammatory cytokines.13 Higher amounts of protein the effects of vascular compromise, poor tissue perfusion, C are consumed, contributing to a decrease in levels. The thromboembolism, and infarction manifest as multiple organ anticoagulant activity of protein C is also decreased by dysfunction syndrome (MODS), including acute respiratory sepsis-induced increases in levels of protein C inhibitor.13 distress syndrome, pulmonary thromboembolism, pleural Antithrombin III levels fall as liver production decreases and effusion, renal hypoperfusion and infarction, GI hypoperfu- peripheral consumption and inactivation by activated neu- sion and perforation, , , malaise, and neu- trophils increase.13,77 The imbalance associated with a highly rologic infarction. procoagulant state and decreased fibrinolytic activity results in clinical disseminated intravascular coagulation (DIC) and Clinical Signs the formation of microvascular thromboses, further compro- Dogs and cats with septic peritonitis generally present with mising tissue perfusion.13,77 vague signs. Many have a history of lethargy, depression, vomiting, diarrhea, or collapse. These signs are nonspe- Adjuvant Substances cific, and unless the history includes a penetrating perito- Intraperitoneal mucin, bile, foreign bodies, hemoglobin, and neal wound or obvious trauma, the index of suspicion for blood can worsen septic peritonitis. Gastric mucin decreases peritonitis may not be high. Clinical signs of vomiting and the phagocytic activity of intraperitoneal macrophages by diarrhea may be associated with a primary GI problem (e.g., exerting an anticomplement effect.7,8 Bile salts destroy peri- foreign body) or may occur due to the developing peritoni- toneal mesothelial cells, inhibit PMN function,11 and lower tis. Icterus may be encountered in animals with severe pan- surface tension, leading to altered cell adhesion and destruc- creatitis or primary biliary disease. Hematuria, pollakiuria, tion of red blood cells.8 Foreign material in the peritoneal polyuria, and polydipsia are common indications of uro- cavity may induce bacterial translocation.11 Hemoglobin acts genital diseases such as urinary tract infection or pyometra. as an adjuvant substance by interfering with chemotaxis Abdominal discomfort and distention are often noticed on and phagocytic activities.7 Blood can be an excellent growth abdominal palpation. medium for bacteria,11 and the presence of intraperitoneal Many animals with septic peritonitis present in

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FIGURE 5 tion, and cholelithiasis.43 Liver enzyme values may also rise in animals without primary and may be related to alterations in hepatic perfusion.35 Animals with poor perfusion or sepsis may have hyper- lactatemia.81 The plasma lactate level has been shown to be a prognostic indicator in dogs with GDV,82 but its usefulness as a prognostic indicator in septic peritonitis is less clear. Septic patients may demonstrate hyperglycemia or hypo- glycemia.83 Proposed mechanisms for hypoglycemia include in a cat secondary to GI perforation endotoxin-induced hepatic glycogen depletion, increased due to lymphoma. peripheral glucose use, and impaired gluconeogenesis.83

due to hypovolemia from intraperitoneal fluid loss and the Radiography and Ultrasonography effects of SIRS. Animals may present in one of three broad Survey radiography is generally a first-line diagnostic tool stages of shock: compensatory, early decompensatory, and when evaluating a dog or cat with suspected peritonitis. terminal decompensatory. The clinical signs depend on Loss of abdominal serosal detail, , and pneumoperi- when the animal is evaluated.78 In the compensatory stage toneum are radiographic signs suggestive of intraperito- of shock, animals are generally hypermetabolic with tachy- neal disease. Loss of serosal detail can be caused by free cardia, tachypnea, and hypertension and may have injected peritoneal fluid or a mass effect. Ileus can be seen as a mucous membranes with a rapid capillary refill time. In result of secondary to neoplasia or for- early decompensatory shock, tachycardia continues, but eign body ingestion but may also be induced by peritoni- blood pressure decreases. In addition, the animal may have tis.84 Pneumoperitoneum that occurs without any history of depressed mentation, poor pulse quality, pale mucous mem- recent surgery or penetrating wounds is most commonly branes, and a prolonged capillary refill time. Tachycardia is of GI origin85 and warrants immediate surgical explora- not as common in cats as in dogs during this stage. When tion (FIGURE 5). Radiography can also be used to diagnose terminal decompensatory shock is reached, bradycardia, specific diseases, including GDV, GI foreign bodies,86 pyo- hypotension, pale or cyanotic membranes, weak or absent metra,53 cholelithiasis, biliary emphysema,43 and organo- pulses, and severe mental depression develop. Renal failure megaly secondary to intraabdominal abscessation (hepatic, and pulmonary edema may also be encountered.78,79 splenic, renal, prostatic)46,47,49 or neoplasia.86 Ultrasonography can generally localize a tumor or mass Diagnostics to a specific organ and guide sampling of free peritoneal Clinicopathologic Findings fluid. Specific findings on ultrasonography relative to the Anemia and are common abnormalities noted many disease processes that can lead to septic peritonitis on complete blood cell count in animals with septic peri- are beyond the scope of this article. tonitis. Band neutrophils are often present, and if the infection is long-standing, the animal may be leukopenic. Peritoneal Fluid Analysis Coagulation profiles may be normal in the early stages of Sample Collection septic peritonitis, but prothrombin time (PT) and activated Several techniques can be used to obtain a sample of fluid partial thromboplastin time (aPTT) often become pro- from the peritoneal cavity and have been detailed else- longed. In animals with DIC, thrombocytopenia and higher where.87–91 All techniques involve clipping the hair in the levels of fibrin degradation products and D-dimer may be area that will be tapped, preparing the abdomen with ster- encountered. A hypercoagulable state can be detected by ile technique, and sterile introduction of a needle or an thromboelastography. 80 over-the-needle . Ideally, this procedure should Serum biochemistry findings vary widely depend- be performed with ultrasonographic guidance. Although ing on the underlying cause and stage of the peritonitis. definitive studies are lacking, clinical experience with ultra- Extravasation of protein-rich fluid rapidly leads to hypoal- sound-guided fluid aspiration suggests that this technique buminemia. Increases in blood urea nitrogen and creatinine has a much higher yield than blind peritoneal tapping and values may be prerenal (i.e., from decreased kidney perfu- decreases the need for diagnostic peritoneal lavage (DPL). sion) or associated with primary renal disease such as pyelo- DPL is likewise superior to blind needle .92 A nephritis or (rarely) renal abscessation. Uroperitoneum may study comparing needle paracentesis, catheter paracentesis, also result in or alterations in . Liver and DPL found an accuracy rate of less than 50% for needle enzyme levels increase with many primary hepatic and bil- paracentesis compared with 94.6% for DPL. DPL was 100% iary diseases, such as biliary mucocele, gallbladder infarc- accurate in dogs with septic peritonitis.92

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Complications are uncommon with these techniques. FIGURE 6 Needle paracentesis is generally considered safe, but there is some disagreement about whether a syringe should be attached to the needle.92 Some authors believe that the lack of syringe attachment allows for the introduction of air, causing pneumoperitoneum that confounds diagnos- tics.91 Others think that suction with a syringe may increase the risk of obstruction with omentum or abdominal viscera and impede sample collection.91 Overall complication rates for the placement of and DPL have been reported at 4.7%; for significant complications (e.g., splenic laceration, urinary bladder puncture), the rate is 1.6%.91

Cytology Normal cell counts for the peritoneal cavity are <3000 × 106/L in small animals.89 One study93 evaluated the use of Peritoneal fluid cytology shows (1) predominantly neu- DPL preoperatively and postoperatively to assess cell count trophils that are mildly to moderately degenerate in morphology and (2) occasional mononuclear cells. A large and intraabdominal enzyme content. The per- mesothelial cell is present in the center of the image. formed in that study included GI resection and anastomosis, cystotomy, gastrotomy, pyloromyotomy, and repair of a dia- the peritoneal fluid total nucleated cell count was >13,000 phragmatic laceration. Macrophages and segmented neutro- cells/μL.96 Cytology was diagnostic for septic peritoneal effu- phils were the most common cells found in the peritoneal sion in 86% of the cases in the latter study.96 Other reports fluid, and preoperative nucleated cell counts ranged from 71 have found cytology to be accurate in diagnosing septic to 697 cells/μL. White blood cell and nucleated cell counts peritonitis 57%,25 87%,26 and 100%96 of the time. were significantly increased in postoperative fluid compared with preoperative fluid.93 pH Septic effusions generally contain increased numbers of Peritoneal fluid pH as an indicator of septic peritonitis has neutrophils and macrophages, and intracellular or extracel- been evaluated in dogs and cats. In one study,96 the pH of lular bacteria may be present (FIGURE 6). Peritoneal fluid the fluid in septic effusions in cats was significantly lower samples are specifically evaluated for degenerate neutro- than the pH of the fluid in nonseptic effusions. This study phils. Bacterial toxins cause changes in the cell membrane did not find the same to be true in dogs. Comparison of permeability of neutrophils, leading to cell and/or nuclear blood pH to peritoneal fluid pH was not found to be useful swelling, nuclear fragmentation, and eosinophilic nuclear for dogs or cats.96 chromatin.88,90 The lack of degenerate neutrophils does not rule out septic peritonitis,88 and it is important to differen- Glucose tiate degenerate neutrophils from aging and toxic neutro- A study has found that comparing blood glucose levels to phils.94 The presence of intracellular bacteria is diagnostic peritoneal glucose levels is diagnostic for peritonitis in 100% for septic peritonitis.90 of dogs and 92% of cats.96 When the blood glucose concen- Reagent strips that test for the presence of leukocytes in tration exceeded the peritoneal fluid glucose concentration peritoneal fluid have been used to diagnose primary perito- by >20 mg/dL, the sensitivity and specificity were 100% in nitis in humans. A PMN count of ≥250 cells/μL in ascitic fluid dogs and 86% and 100%, respectively, in cats.96 is considered the “gold standard” for diagnosis of primary peritonitis, and in humans, the sensitivity and specificity of Lactate some of these strips have been reported as high as 88.2% Peritoneal fluid lactate concentration has been evaluated in and 99.6%, respectively.95 The use of these strips to diagnose two studies. In the first,96 a blood-to-peritoneal fluid lactate peritonitis in small animals has not been evaluated. concentration of less than −2.0 mmol/L was found to be 100% Results of using total peritoneal fluid leukocyte counts sensitive and specific for the diagnosis of a septic peritoneal and cytology to diagnose septic peritonitis have been vari- effusion in dogs but did not reach statistical significance in able. Peritoneal leukocyte counts ranged from 5,400/μL to cats. The second study97 reported an accuracy of 95% in the 43,100/μL in an experimental peritonitis model.93 One study diagnosis of septic peritonitis in dogs when the peritoneal found an 86% sensitivity and a 100% specificity for peritoni- fluid lactate concentration was >2.5 mmol/L. When using a tis in dogs and 100% sensitivity and specificity in cats when blood-to-peritoneal fluid lactate concentration difference of

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Box 1 less than −1.5 mmol/L, the accuracy was 90% for the diagno- sis of septic peritoneal effusion in dogs. Lactate concentra- Medical Management Checklist for the tion differences were diagnostically inaccurate in cats.97 Treatment of Septic Peritonitisa Culture Fluid therapy Gram-negative bacteria predominate in septic peritonitis. E. • Crystalloids coli is the most commonly isolated organism, being found —Plasmalyte A in 57% to 74% of cultures from the peritoneal cavity. Other —Lactated Ringer’s solution common gram-negative bacteria include Klebsiella and —Normosol-R Bacteroides spp.20,21,25,36 Gram-positive bacteria that have been • Colloids isolated include , Staphylococcus, Enterococcus, —Hetastarch and Clostridia spp.20,21,23,36 Commonly, multiple species of —Dextrans bacteria are isolated from a septic . In one report, multiple organisms were isolated in 15 of 19 (79%) cases.36 Blood products In dogs with cholelithiasis, bile cultures are often positive —Fresh whole blood for aerobic or anaerobic bacteria. One study40 found a posi- —Stored whole blood —Packed red blood cells tive aerobic culture in 14 of 20 dogs and a positive anaerobic —Plasma culture in eight of 18 dogs. Although cholelithiasis with sec- —Albumin ondary biliary tract rupture is uncommon in dogs, it should be considered in the differential diagnosis when a dog has Analgesia septic peritonitis. • Intravenous bolus In 23 cases of necrotizing cholecystitis treated surgically, —Buprenorphine: 0.005–0.02 mg/kg IV, IM, SC q4–6h bacteria were found in 13 of 16 (81%) of gallbladder mucosa • Constant-rate infusion samples submitted for culture. The most common bacterial —Fentanyl: 1–5 μg/kg/h isolate was E. coli (69%). Nine of the 23 dogs died in the —Lidocaine: 30–50 μg/kg/min perioperative period; the deaths were attributed to sepsis, —Ketamine: 0.1 mg/kg/h peritonitis, or debilitation.98 E. coli has also been isolated in 59% to 96% of cases of pyometra52 and approximately 85% Gastrointestinal protectants of cases of prostatic abscessation.55 • Antiemetics —Metoclopramide: 0.1–0.5 mg/kg PO, SC q8h or Medical Management 1–2 mg/kg/d IV CRI Fluids —Dolasetron: 0.6–1 mg/kg/d IV, PO —Chlorpromazine: 0.2–0.5 mg/kg IM, SC q6–8h Fluid resuscitation is essential to the management of dogs • Antisecretory and cats with septic peritonitis. The goal of resuscitation is —Famotidine: 0.5–1 mg/kg IV, IM, PO, SC q12–24h to restore and maintain tissue perfusion. The loss of large —Omeprazole: 0.5–1 mg/kg PO q24h volumes of fluid and protein from the vasculature into the • Cytoprotective peritoneal cavity, combined with vasodilation secondary to —Sucralfate: 0.5–1 g PO q8h (dogs) systemic inflammation, can result in shock. BOX 1 provides 0.25–0.5 g PO q8–12h (cats) a checklist for the treatment of septic peritonitis. —Misoprostol: 1–5 μg/kg PO q6–8h Both crystalloids and colloids are often necessary for adequate resuscitation. Intravenous (IV) crystalloid solutions (empiric) are the initial mainstay of intravascular volume replacement. • Gram-positive coverage Ongoing resuscitation with crystalloids alone may lead to —Ampicillin: 22 mg/kg IV q8h an increased capillary hydrostatic pressure and a decreased —: 10 mg/kg IV, PO q12h plasma oncotic pressure. This decreased oncotic pressure • Gram-negative coverage from dilutional and sepsis-associated hypoalbuminemia, —Enrofloxacin: 10–15 mg/kg IV, PO (dogs) combined with the increased vascular permeability seen in 5 mg/kg IV, PO (cats) sepsis, can result in significant fluid extravasation from the —Cefotaxime: 25–50 mg/kg IV, IM, SC q8h vasculature into the interstitial tissue spaces. • Anaerobic coverage Synthetic colloids such as hetastarch and dextrans —Metronidazole: 10 mg/kg IV, PO q12h decrease the fluid volume requirement for resuscitation.

aAll dosages listed are for dogs and cats unless otherwise indicated. Natural colloids such as fresh whole blood, stored whole blood, and plasma can also be given but do not provide

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FREE Septic Peritonitis CE as significant an increase in colloid osmotic pressure (COP) with biliary obstruction and rupture because fat-soluble as do synthetic colloids. Synthetic and natural colloids are vitamins, including vitamin K, cannot be absorbed without often administered simultaneously because natural colloids bile emulsification of fat. Coagulation abnormalities are also can provide other important substances such as coagulation commonly associated with nonbiliary peritonitis. In one factors and albumin. study, septic dogs were found to have significantly longer PT Several factors should be considered when administering and aPTT and higher levels of fibrin degradation products crystalloids and colloids. In a patient with shock, boluses of and D-dimers than control dogs.74 When the PT and aPTT both fluid types may be necessary. A shock bolus of crys- are prolonged, plasma should be given until these values talloids in dogs (90 mL/kg) and cats (55 mL/kg) should be are within normal limits. given over 10 to 15 minutes.8 The initial bolus of hetastarch An animal receiving a transfusion of blood products in shock patients is 10 to 20 mL/kg given as quickly as should be watched carefully. It is especially important to possible.99 Further boluses of these fluids may be required monitor pulse, temperature, and respiratory rate during the depending on the patient’s status. If further colloidal sup- first 30 minutes of the transfusion. If a patient appears to be port is necessary, synthetic colloids can be continued as experiencing a transfusion reaction, the transfusion should a constant-rate infusion (CRI) at a dose of 1 mL/kg/h.99 be stopped immediately.103 Higher doses may be necessary if the COP remains low. When administering CRIs of crystalloids and colloids simul- Antibiotics taneously, the amount of crystalloid can be decreased by as If septic peritonitis is suspected, use is manda- much as 40% to 60%.99 tory. Ideally, the antibiotic regimen should be based on the Fluid resuscitation goals include maintaining the mean results of culture and susceptibility testing. However, in arterial blood pressure above 80 mm Hg and the heart rate most cases, empirical therapy is instituted while awaiting between 80 and 120 bpm in dogs and 180 and 200 bpm in these test results. Dosing should be based on an under- cats. Other parameters to maintain include central venous standing of the pharmacodynamic properties that predict pressure (6 to 8 cm H2O) and urine output (>1 mL/kg/h). antimicrobial efficacy. New human guidelines focus on arterial lactate levels and Antibiotic pharmacology is reviewed extensively else- mixed venous oxygen saturation as more sensitive and spe- where.104 In general, β-lactam drugs (e.g., penicillins, cific indicators of tissue perfusion.100 When administering ) are classified as time-dependent, meaning synthetic colloids, a COP of 17 mm Hg should be main- that their bactericidal effect corresponds to the amount of tained while avoiding volume overload.99,101 time their plasma and tissue concentrations remain above the minimum inhibitory concentration for the pathogen. Blood Products Therefore, β-lactams should be administered frequently Blood products can be required in animals with septic peri- to enhance efficacy. Conversely, fluoroquinolones and tonitis for a variety of reasons. Animals with bleeding GI aminoglycosides are concentration-dependent drugs with ulcers, peritonitis secondary to trauma, GDV, or avulsion maximum effect when a high peak plasma concentration is of the short gastric blood vessels may need transfusions attained, even if only for a short period of time. Therefore, of whole blood or packed red blood cells. The decision to the entire dose of these drugs is appropriately administered transfuse an anemic patient with whole blood or packed once daily. General recommendations for broad-spectrum red blood cells depends on several factors. In dogs and empiric antibiotic treatment in cases of septic peritonitis cats, transfusions should often be given if the packed cell include either a penicillin or for gram-pos- volume (PCV) drops below 20%.102 Other factors to consider itive coverage combined with either a fluoroquinolone or include a massive loss of blood volume (>30%), ongoing an aminoglycoside for gram-negative coverage until culture hemorrhage, inadequate response to fluid resuscitation, or and susceptibility data become available. severe clinical signs (e.g., collapse). Transfusing 10 mL/kg Anaerobes are a large component of normal GI flora, of packed red blood cells or 20 mL/kg of whole blood can especially in the colon. Not all anaerobes are susceptible increase the PCV by 10%.102 to penicillins, and many are resistant to cephalosporins.105 Whole blood, packed red blood cells, and plasma can The addition of an antibiotic with documented or enhanced be used for colloidal support, but these products can raise antianaerobic activity (e.g., metronidazole) is often justified the oncotic pressure by only a limited amount.101 This and should be considered empirically while awaiting cul- increase is often transient because of the ongoing loss of ture results. albumin into the peritoneal cavity. However, fresh frozen plasma transfusions are often used clinically to treat coagu- lation abnormalities associated with peritonitis and sepsis. has been extensively described elsewhere86 Coagulation abnormalities should be suspected in animals and may be either visceral (dull) or somatic (piercing).

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Analgesia is an important aspect of presurgical and post- dogs and cats with septic peritonitis. In humans, physiologic surgical management. Opioids are a first-line choice for the doses of hydrocortisone and fludrocortisone in a group of treatment of pain in patients with septic peritonitis. Some septic patients with inadequate adrenocorticotropic hor- opioids, such as morphine and hydromorphone, can induce mone stimulation resulted in a significantly reduced risk of GI ileus and vomiting and cause dose-dependent respiratory death at 28 days.110 The incidence and role of adrenal insuf- depression. These drugs should be avoided in patients for ficiency in septic peritonitis is under investigation in com- whom further GI upset is contraindicated. Buprenorphine panion animals. tends to have fewer GI effects and may be a better option The dose of corticosteroids in septic patients varies based for these patients. The usual dose of buprenorphine in dogs on the purpose of administration. High doses of cortico­ and cats is between 0.005 and 0.02 mg/kg. CRIs of analgesics steroids (hydrocortisone, 150 mg/kg, and dexamethasone, 4 may also be required. Common medications that are used in to 10 mg/kg)1,111 have been used in the treatment of shock, CRIs include fentanyl, lidocaine, and ketamine. whereas much lower “stress” doses (hydrocortisone, 1 mg/ kg,112 and dexamethasone, 0.5 to 1 mg/kg) are used to treat Gastrointestinal Protectants relative adrenal insufficiency. Most dogs and cats with septic peritonitis benefit from GI protectants. As these animals often experience vomiting, Insulin antiemetics such as dopamine antagonists, serotonin antago- As with humans, septic companion animals often develop nists, and phenothiazines may be indicated. Metoclopramide, insulin resistance.113,114 A study114 evaluating intensive insulin a dopamine antagonist, has some prokinetic activity and is therapy in 1548 critically ill human patients found a decreased contraindicated in cases of GI obstruction because increases mortality in those whose glucose levels were maintained in may lead to further “bunching” of intestine. with insulin at ≤110 mg/dL. Patients with a septic focus and Phenothiazines have been associated with sedation and secondary MODS had the greatest reduction in mortality.114 hypotension.106 Drugs that decrease secretion may also be Protein C 74 75 used. Commonly employed H2-receptor antagonists include Protein C levels can be decreased in people and dogs famotidine and cimetidine. Proton pump inhibitors (e.g., with sepsis. A multicenter study74 evaluating the administra-

omeprazole) are considered better alternatives to H2-receptor tion of protein C to humans with septic conditions found antagonists in patients with gastric ulcers.106 some promising results. In that study, 840 patients received Sucralfate and misoprostol are commonly used in cases a placebo and 850 patients received activated protein C. The of GI ulceration. Sucralfate binds with ulcers and coats the patients receiving the protein C had a 19.4% reduction in mucosa to prevent acid damage. Misoprostol has both anti- the relative risk of death and a 6.1% reduction in the abso- secretory and cytoprotective properties, directly inducing GI lute risk of death compared with those in the control group. ulcer healing. However, the incidence of bleeding was higher in the group that received activated protein C.74 Other Medical Treatments Corticosteroids Fluconazole The use of corticosteroids in the treatment of septic perito- The antifungal azoles have demonstrated antiinflammatory nitis remains controversial.107 Steroids were previously advo- properties by interfering with leukocyte function.115 It has cated in the treatment of septic shock, based on membrane been suggested that fluconazole may decrease mortality in stabilization and decreased vascular permeability.1 Steroids patients with bacterial sepsis.115 Fluconazole caused no side also exert antiinflammatory effects by modulating cytokines effects (e.g., hepatotoxicosis) in a group of dogs with bacte- (including IL-1 and TNF) and stimulating production of anti- rial peritonitis, but the number of subjects was too small inflammatory factors such as IL-10 and IL-1 receptor antago- to determine whether fluconazole therapy produced any nist.108 However, a lack of efficacy in the treatment of sepsis improvement in outcome.116 and septic shock has been reported,107 and their routine use has fallen out of favor. Surgical Management Recently, much attention has been paid in human medi- Despite the induction of numerous inflammatory cascades cine to the early treatment of adrenal insufficiency in sep- in septic peritonitis, the crucial therapeutic intervention is tic patients.108,109 In humans, sepsis and SIRS are the most surgical removal of the nidus of infection, once the ani- common causes of acute adrenal insufficiency,108 decreasing mal is stabilized. After the patient is anesthetized, the hair production of the glucocorticoids that help to modulate the over the abdomen should be generously clipped and the inflammatory response in sepsis.109 area prepared with sterile technique and draped. The surgi- It may be beneficial to obtain a baseline cortisol level in cal approach involves a large ventral midline incision often

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FREE Septic Peritonitis CE extending from just caudal to the xiphoid cartilage to just Diagnostic positive-contrast imaging of the urinary tract cranial to the pubis. can generally locate the site of urine leakage before surgery. Obvious contamination of the peritoneal cavity should Unilateral ureteral ruptures are treated by primary repair be removed immediately and thorough abdominal explo- or unilateral ureteronephrectomy, provided the contralat- ration performed. When the inciting organ is identified, it eral kidney is functioning normally. Bladder ruptures are should be isolated from the rest of the peritoneal cavity with located and sutured with 3-0 or 4-0 polydioxanone suture in . a simple interrupted pattern. Incomplete urethral tears may Leakage from the GI tract is the most common cause of be managed with an indwelling urethral catheter for several bacterial peritonitis. Perforated gastric ulcers can generally days to weeks; complete urethral transections often require be treated by partial gastrectomy. Duodenal ulcer resection surgical repair. may be performed by a local resection of diseased tissue, Copious peritoneal lavage is an appropriate part of the Y-U antral advancement flap pyloroplasty, or biliary rerout- standard of care for animals with septic peritonitis. The ing, depending on the location and size of the ulcer. It is peritoneal cavity is viewed as a large, contaminated wound, essential that sutured bowel edges be healthy and demon- and lavage with a large volume of warm, balanced electro- strate sufficient blood supply. If a previous GI anastomosis lyte solution is used to remove bacteria and proinflamma- has dehisced, the entire area must be removed and another tory cytokines, GI contents, hemoglobin, , and bile. anastomosis performed. The anastomosis site is reinforced However, peritoneal lavage is not entirely benign and may by omental wrapping or serosal patching.117 Serosal patch- impair normal peritoneal defense mechanisms. Bacteria ing has been used to treat defects in the , adhere to the peritoneal surfaces and may not be removed colon, and urinary bladder.118 This technique involves sutur- by low-pressure lavage. Lavage may disseminate bacteria, ing loops of over an area of questionable viability. remove opsins and complement proteins necessary for As pancreatic abscesses are uncommon and little stud- phagocytes, prevent phagocytes from gaining access to bac- ied, results of various treatment methods should be inter- teria, and damage peritoneal mesothelial cells.122 Detailed, preted with caution. Omentalization of the abscess cavity controlled clinical trials studying the efficacy of lavage in and abdominal closure resulted in better survival (five of companion animals with septic peritonitis are lacking. The eight patients) than treatment by open peritoneal drainage following recommendations are based on experimental and (one of four patients) in one study.119 human clinical studies: Omentalization has also largely replaced Penrose drain- age or partial prostatectomy for the treatment of prostatic • A large volume of lavage fluid should be used (e.g., 500 abscessation.120 Long-term resolution of disease (>12 months) mL to 1 L in a cat, several liters in large dogs). was achieved in 19 of 20 dogs treated with omentalization. • All of the lavage fluid must be aspirated from the perito- One dog had a ruptured prostatic abscess before surgery but neal cavity. was successfully treated by combining prostatic omentaliza- • The addition of antibiotics to the lavage fluid has not tion with open abdominal drainage.120 proved beneficial, provided the animal is receiving appro- Treatment of abscesses in other abdominal organs priate doses of antibiotics parenterally. generally involves removal of the organ in question. • The addition of chlorhexidine to the lavage fluid has not Ovariohysterectomy is recommended in cases of pyometra; proved beneficial. Experimentally, 0.05% chlorhexidine care should be taken to prevent leakage from the uterus reduced bacterial numbers in residual lavage fluid and during its removal. Liver lobe resection, nephrectomy, and improved survival in a mouse peritonitis model,123 but it splenectomy are recommended for abscessation of the liver, is potentially toxic to normal cells. kidneys, and spleen, respectively. One study evaluating per- • Povidone iodine should never be added to lavage fluid, cutaneous drainage and alcoholization of hepatic abscesses as it has been associated with high mortality and scleros- in five dogs and one cat obtained favorable results in all six ing, encapsulating peritonitis.122 animals.121 Uroperitoneum presents a specific and urgent challenge Early postoperative enteral nutrition appears to be bene- because of potential life-threatening hyperkalemia. Every ficial in experimental peritonitis, but a distinct survival ben- effort should be made to reestablish normal renal function efit has not been demonstrated. Potential benefits include and urine flow. In cases of bladder rupture, an indwell- increased anastomotic strength and more rapid healing, pos- ing urinary catheter and a peritoneal dialysis catheter are itive nitrogen balance, and decreased bacterial translocation placed to drain urine from the bladder and peritoneal cavity, through a compromised GI mucosal barrier. respectively. Serum potassium and calcium levels and acid– In a rat peritonitis model, early postoperative enteral base status should be normalized, if possible, before the feeding resulted in a significantly higher nitrogen level, animal is anesthetized for laparotomy. higher anastomotic bursting strength, and lower TNF-α lev-

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els. TNF-α has the ability to decrease the synthesis of col- three cases (two dogs with sump-Penrose drainage and one lagen and up-regulate collagenase activity, contributing to with open peritoneal drainage).130 potential anastomotic breakdown and leakage.124 Several studies have reported results of primary closure In another study,125 mortality in human patients receiv- without the use of abdominal drainage,24,25 open drainage ing early postoperative enteral nutrition via a jejunostomy compared with primary closure,25,128 and open peritoneal tube was similar to that in a control group (19.1% and 18.2%, drainage.20–22,25 It is difficult to compare results between respectively). However, the patients in the study group had studies because of the heterogeneity of the patient popu- a positive nitrogen balance by the third postoperative day, lations, the lack of a single standard for patient care, and whereas those in the control group had a negative nitrogen variability in the surgeons’ preference. None of the three balance until the end of the study. Furthermore, the patients treatment options (primary closure, open peritoneal drain- receiving early enteral nutrition had significantly fewer sep- age, or closed suction drainage) seems to have an obvious tic complications compared with the control group. survival benefit based on the available clinical information In one veterinary study,36 14 of 23 animals with peritoni- in companion animals. The lack of statistically significant tis received nutritional support with either total parenteral survival differences in studies that compare peritoneal drain- nutrition or a feeding tube. Nine of these 14 patients sur- age methods may be associated with small sample sizes but vived. Although nutritional support was not associated with may also reflect the possibility that other factors (e.g., sever- outcome in this study, this may have been due in part to ity of sepsis, preoperative and postoperative management) small group numbers. are more important in determining survival.

Peritoneal Drainage Prognosis Once the underlying disease process has been treated, the Mortality in 50 dogs with septic peritonitis was reported to peritoneal cavity lavaged, and the fluid aspirated, the sur- be 68%, regardless of drainage technique.131 A study of 51 geon must decide whether postoperative peritoneal drain- cats with septic peritonitis35 found a mortality of 30% in 23 age is required and, if so, whether the abdomen should be cats that were treated by surgical exploration. Treatment was left open. There are no clear-cut, objective guidelines for not pursued in the other 28 cats either because the cats died this decision. Prevailing opinion views the peritoneal cavity or were euthanized before treatment could be attempted, in the same manner as any other contaminated wound: if or because the extent of disease found during exploratory substantial contamination remains despite the surgeon’s best surgery was too great.35 efforts, drainage options include open peritoneal drainage Prognostic indicators in dogs and cats with septic perito- and the placement of a closed suction or sump drain.126,127 nitis have been evaluated in two studies.22,36 In one study,22 Advantages of open peritoneal drainage include effec- survivors had significantly lower preoperative values for tive removal of excess amounts of peritoneal fluid, easier alanine aminotransferase and γ-glutamyl transferase than access for reexploration of the peritoneal cavity, and the nonsurvivors. In the other study,36 animals that experienced creation of an environment unfavorable to anaerobic bacte- hypotension that was not correctable with treatment by IV ria.127 Complications associated with open peritoneal drain- fluids and those that developed respiratory dysfunction or age include evisceration of abdominal organs, formation of DIC had a worse prognosis. intestinal fistulae, visceral adhesion to the peritoneal ban- dage, nosocomial infection of the peritoneum, excessive Conclusion fluid loss, and hypoproteinemia with secondary peripheral The clinical syndrome of septic peritonitis presents a thera- edema.21,22,128 In humans, vacuum-assisted suction is com- peutic challenge. Although prognoses vary, the potential for monly employed when open peritoneal drainage is used to sepsis and its sequelae makes timely diagnosis and treat- prevent abdominal compartment syndrome.129 ment essential. More study is needed to identify treatment Closed-suction drainage is being used in patients with modalities that can be directed at specific targets involved in septic peritonitis with increasing frequency. A clinical study the inflammatory cascade, but advances in human medicine found it to be effective for treating generalized peritonitis, are promising. reporting no clinically significant complications.23 Potential concerns with any intraabdominal drain include ineffective References 1. Withrow SJ, Black AP. Generalized peritonitis in small animals. Vet Clin North Am drainage secondary to omental or serosal walling off of the Small Anim Pract 1979;9:363-379. 2. Hosgood GL, Salisbury SK. Pathophysiology and pathogenesis of generalized peri- drain and nosocomial infection. tonitis. Probl Vet Med 1989;1:159-167. Sump-Penrose drainage has been compared with open 3. Swann H, Hughes D. Diagnosis and management of peritonitis. Vet Clin North Am drainage in normal dogs,130 yielding no significant differ- Small Anim Pract 2000;30:603-615. 4. Bercovici B, Michel J, Miller J, Sacks TG. Antimicrobial activity of human perito- ences in blood chemistry, peritoneal fluid analysis, or neal fluid.Surg Gynecol Obstet 1975;141:885-887. necropsy findings. Nosocomial infections were cultured in 5. Hosgood G, Salisbury SK, Cantwell HD, et al. Intraperitoneal circulation and drain-

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1. In dogs and cats, the bacteria that cause b. toxic neutrophils d. treatment of adrenal insufficiency septic peritonitis most commonly origi- c. mesothelial cells e. promotion of wound healing nate from the d. macrophages a. uterus. e. intracellular bacteria 8. The options for surgical management of b. bladder. septic peritonitis do not include c. stomach/intestines. 5. When evaluated in a peritoneal effusion, a. omentalization. d. liver. ______has not been found to be use- b. serosal patching. e. spleen. ful in the diagnosis of septic peritonitis c. copious lavage with a balanced electro- in dogs. lyte solution. 2. Which of the following does not directly a. glucose d. removal of the nidus of infection. contribute to the intrinsic defense sys- b. lactate e. lavage with iodine. tem of the peritoneal cavity? c. total nucleated cell count a. complement d. pH 9. ______is not a disadvantage of open b. neutrophils e. cytology peritoneal drainage. c. macrophages a. Evisceration of abdominal organs d. mast cells 6. The organism most commonly cultured b. Nosocomial infection e. fibrinogen from peritoneal effusions in cases of c. Hypoproteinemia septic peritonitis is d. Increased likelihood of anaerobic 3. What substance is the primary contribu- a. Streptococcus pyogenes. infection tor to the pathophysiology induced by b. Clostridium perfringens. e. Formation of intestinal fistulae gram-negative bacteria? c. Escherichia coli. a. endotoxin d. Enterococcus faecalis. 10. ______has been associated with a b. teichoic acid e. . negative outcome in cases of septic c. peptidoglycan peritonitis. d. polysaccharide/hyaluronic acid capsule 7. Which is not a benefit of corticosteroids a. Respiratory dysfunction e. slime layer in patients with septic peritonitis? b. Open peritoneal drainage a. decreased vascular permeability c. Anemia 4. The presence of ______in a perito- b. decreased negative effects of inflam- d. Hypertension neal effusion is diagnostic for septic matory cytokines such as IL-1 and TNF e. Peritoneal fluid lactate concentration peritonitis. c. promotion of production of antiinflam- >2 mmol/L a. red blood cells matory factors such as IL-10

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