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Peritonitis is an umbrella term for any inflammatory or infectious disease of the visceral lining (peritoneum) of the abdomen.
Regardless of cause, peritonitis in dogs usually involves the majority of the abdominal organs including the liver, stomach, intestines, spleen, kidney, reproductive organs and urinary bladder. In early stages, peritonitis is limited to regional inflammation of the serosal lining of affected organs (e.g. the uterus in pyometra), but as the condition worsens, multi-organ dysfunction occurs due to deteriorating hemodynamic changes caused by liberation of bacterial endotoxins.
Academically, peritonitis can be defined as either primary in origin or secondary to perforation of and leakage from gastrointestinal organs. It may also be classified as septic (bacterial, fungal, protozoal) or aseptic (inflammatory, e.g., encapsulating peritoneal sclerosis).
Causes of peritonitis include:
- Perforating wounds of the abdominal wall (e.g., dog bites, motor vehicle accidents, gunshot wounds, migrating grass awns)
- Perforating ulcers due to gastritis or duodenitis - usually associated with meloxicam, lornoxicam or deracoxib
- Intraoperative spillage, wound dehiscence, or perforations
- Foreign body perforations of intestines - linear foreign bodies, ingested wooden foreign bodies, magnets, lithium batteries
- Gastrointestinal accidents - intussusception, gastric dilatation/volvulus, retroperitoneal rectal diverticulum
- Pancreatitis with secondary pancreatic abscess formation
- Cholecystitis and cholelithiasis resulting in bile peritonitis
- Pyometra with secondary leakage of pus from the uterus
- Prostatic abscess due to fulminating prostatitis
- Dystocia with secondary uterine rupture or fetal decomposition
- Urolithiasis with secondary urinary bladder rupture (uroabdomen)
- Metastatic necrotizing tumors
- Primary viral peritonitis
- Primary bacterial peritonitis
- Secondary bacterial peritonitis - often secondary to gastrointestinal perforation
- Secondary fungal peritonitis - commonly seen as post-operative infections
- - Nocardia spp - granulomatous peritonitis
- - Candida albicans
- - Ochroconis gallopavum
- - Blastomyces spp
- - Neospora spp (usually pups)
- - Leishmania spp
- - Mesocestoides spp
- - Echinococcus alveolaris
- - Spirometra spp
Clinically affected dogs typically present with nonspecific symptoms which, depending on the cause, include depression, anorexia, tachycardia, tachpnea, vomiting and pain upon palpation of the abdomen. Fever is an inconsistent feature of this condition, as some patients with septic peritonitis may have progressed to hypothermia due to overwhelming sepsis. Mucous membranes are invariably pale and hypotension may be apparent in advanced cases.
Blood tests usually revealed a marked leucocytosis, neutrophilia (with a left shift or, if very severe, a degenerative right shift), hypoglycemia, hypomagnesemia, hypoalbuminemia and delayed clotting time, characterized by reduced platelet count, prothrombin time and activated partial thromboplastin time.
Radiography is usually unreliable, but may reveal evidence of pneumoperitoneum or free abdominal effusion. Thoracic radiography may be indicated to rule out concurrent conditions (e.g., metastatic disease, aspiration pneumonia) as complicating factors.
Percutaneous fluid aspiration (abdominocentesis) of the abdomen or diagnostic peritoneal lavage is frequently diagnostic. Serosanguinous fluid is commonly removed in inflammatory diseases, with an increased in nucleated cells (> 1 X 109 cells/L), presence of intracellular bacteria and elevated protein concentrations (> 25 g/L). The presence of amylase or lipase suggests pancreatitis, and the presence of bile is usually indicative of cholelithiasis or biliary tract rupture. The presence of elevated levels of creatinine and potassium in abdominal fluid may suggest a uroabdomen due to urolithiasis.
The use of serum markers such as C-type natriuretic peptide (serum NT-pCNP) have been shown to be poor indicators of septic peritonitis, but lactate concentrations in abdominocentesis fluid >2.5 mmol/L (and higher than the blood lactate concentration) is suggestive of septic peritonitis.
A presumptive diagnosis can be established on presenting clinical signs, blood tests, imaging studies (radiography, ultrasoography and CT) and abdominal fluid content. Peritoneal lavage is considered a rapid diagnostic tool in most cases.
In most cases of septic peritonitis, surgery is required. If surgery is not feasible, euthanasia is the most humane option.
Prior to surgical intervention, supportive treatment is critical for long-term survival, and includes nutritional support, intravenous fluids (with crystalloid and colloids at 90 mL/kg/hr), aggressive intravenous antimicrobial therapy (e.g. enrofloxacin and metronidazole), oxygen support, analgesia (e.g. buprenorphine at 0.005 - 0.02 mg/kg three times daily), intravenous canine-specific albumin and peritoneal lavage.
In severe cases open abdominal drainage and closed suction drainage are required.
In certain breeds such as the Collie, Shetland Sheepdog, Australian Shepherd and Old English Sheepdog, a relative adrenal insufficiency may be a complication of septic peritonitis. This may require the administration of physiological levels of glucocorticoids, avoiding large doses which would compromise immunocompetency against bacteremia.
In hypotensive patients, the use of vasopressor agents such as dobutamine (2 - 20 µg/kg/min), dopamine (5 - 20 µg/kg/min) or vasopressin (0.01 - 0.1 U/kg as a bolus, followed by 0.001 - 0.1 U/kg/hr intravenously as constant rate infusion) should be considered. If hypotension persists, norepinephrine should be given at 0.05 - 3.3 µg/kg/min intravenously.
To guard against DIC, use of intravenous plasma (10 mL/kg intravenously over 3 - 4 hours), or low dose heparin may be warranted to replace spent clotting factors. Plasma is less effective than hetastarch for colloidal support alone.
Reliable indicators of survival include marked hyperkalemia, hypoalbuminemia, lymphopenia and intraoperative hypotension tend to have a poorer response due to development endotoxemic shock and DIC.
The prognosis is generally guarded to poor in septic cases with systemic signs of secondary toxic shock.
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