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Gallbladder Mucocele



AUTHOR: FRED S. PIKE



EDITOR: KEITH. RICHTER



BASIC INFORMATION image



DEFINITION


An abnormal accumulation of bile-laden mucus within the gallbladder (GB) lumen; the mucosa of the GB wall is characterized histologically by glandular hyperplasia. Once a rare condition, GB mucocele has recently been reported as the most common cause of canine extrahepatic biliary obstruction (EHBO).



SYNONYMS


Kiwi GB, cystic mucinous hyperplasia of the GB



EPIDEMIOLOGY


SPECIES, AGE, SEX: Older small or medium-size dogs usually affected, with no sex predilection reported. GB mucocele formation in humans is the result of cystic duct obstruction and not cystic mucinous hyperplasia.


GENETICS & BREED PREDISPOSITION: Cocker spaniels and Shetland sheepdogs are predisposed. In recent reports, miniature schnauzers are overrepresented.


ASSOCIATED CONDITIONS & DISORDERS: A weak association exists between hyperadrenocorticism and GB mucocele.



CLINICAL PRESENTATION



DISEASE FORMS/SUBTYPES



• GB mucocele can be an incidental finding or it can be responsible for the presenting complaint (approximately 75% of patients diagnosed with GB mucocele show overt signs of illness).

• Inflammation and necrosis of the GB wall can lead to rupture and peritonitis (focal or diffuse).

HISTORY, CHIEF COMPLIANT: Vomiting, inappetence, and lethargy are the most common presenting complaints. Other complaints include weight loss, diarrhea, ptyalism, and polyuria/polydipsia.


PHYSICAL EXAM FINDINGS: Abdominal pain, ascites, tachypnea, tachycardia, fever, hepatomegaly, and icterus



ETIOLOGY AND PATHOPHYSIOLOGY



• Abnormal accumulation of intraluminal mucus and inspissated bile

• Potential mechanisms for mucocele formation include progressive biliary sludging and alterations in water absorption across the GB mucosa.

• Histologic evidence of GB wall inflammation is not present in the majority of cases.


DIAGNOSIS image



DIAGNOSTIC OVERVIEW


GB mucocele diagnosis requires abdominal ultrasound. The stellate intraluminal pattern and non–gravity-dependent GB contents are considered pathognomonic. Less organized mucoceles can be more challenging to confirm.



DIFFERENTIAL DIAGNOSIS



• Cholecystitis (acute, chronic or necrotizing)

• Cholelithiasis

• Biliary sludge


INITIAL DATABASE



• CBC: most common abnormalities reported are leukocytosis characterized by a mature neutrophilia and monocytosis. In dogs, leukocytosis is significantly higher (21,200 cells/μL) with GB rupture than when the GB is intact (12,500 cells/μL).

• Serum biochemistry profile: common abnormalities include elevated serum alanine transaminase (ALT), alkaline phosphatase (ALP), aspartate transaminase (AST), and gammaglutamyl transpeptidase (GGT) activities. Increasing serum GGT activity may be associated with increased risk for mortality. Total bilirubin concentration is elevated in 63%-77% of cases. Hypercholesterolemia, hyperglobulinemia, and hypoalbuminemia are less common findings.

• Urinalysis: generally unremarkable; bilirubinuria may be noted.

• Abdominal radiography: generally unremarkable. In cases with GB rupture, decreased serosal detail may be noted if ascites is present.

• Abdominal ultrasonography: characteristic stellate/striated intraluminal GB contents. Increased GB volume/subjective distension can be noted. Other potential findings include common bile duct (BD) distension and ascites. The pancreas should be evaluated for ultrasonographic evidence of pancreatitis.


TREATMENT image



TREATMENT OVERVIEW


Surgical intervention is indicated, with cholecystectomy generally considered the treatment of choice.



ACUTE GENERAL TREATMENT



• Emergency surgery is indicated for cases of suspected GB rupture. If present, ascitic fluid should be evaluated to determine whether the effusion is septic.

• GB rupture is suspected if (1) GB wall continuity can not be confirmed, (2) hyperechoic cranial abdominal fat is noted, (3) free abdominal fluid is present, and/or (4) stellate echogenic material is present within the peritoneal cavity.

• Patients with GB rupture are often hemodynamically unstable and require aggressive perioperative supportive care.

• Initial presurgical therapy generally includes fluid therapy, intravenous antibiotics (gram-negative anaerobes are the most common isolate), antiemetics, and analgesics.

• Cholecystectomy, cholecystoenterostomy, and cholecystotomy have been described for the treatment of GB mucoceles. Given that GB wall dysfunction appears to be associated with the etiopathogenesis of mucocele formation, the author believes that cholecystectomy is the treatment of choice.

• During surgery, confirmation of patency of the common BD is imperative. Gastrointestinal and hepatic biopsies should be considered.

• Samples of the GB wall and/or intraluminal contents should be collected for aerobic and anaerobic culture.

• Laparoscopic cholecystectomy has been reported for the treatment of uncomplicated cases of GB mucocele.


CHRONIC TREATMENT



• The nonsurgical resolution of GB mucocele has been reported in two dogs; however, the current literature is lacking adequate numbers to validate medical treatment.

• Patients with biliary sludge without mucocele formation generally do not require therapy unless clinical findings suggest GB disease. In these rare cases, medical management with antibiotic therapy, choleretics, and hepatoprotectants may prove helpful.


NUTRITION/DIET



• Esophagostomy, gastrostomy, or nasogastric tube placement should be encouraged, as postoperative inappetence is common in the author’s experience (see pp. 1267, 1269, 1270).


POSSIBLE COMPLICATIONS



• The most commonly reported postoperative complications include pancreatitis and bile peritonitis. Aspiration pneumonia has also been reported.

• Postoperative common BD obstruction has been reported, emphasizing the need to confirm patency of the common BD at the time of cholecystectomy.


PROGNOSIS AND OUTCOME image



• Perioperative mortality ranges from 21.7%-32%.

• The long-term prognosis for patients surviving to release from hospital is excellent.

• Mortality rates do not differ significantly between ruptured or intact mucoceles.

• If GB rupture results in diffuse bile peritonitis, mortality rates are as high as 68%-100%.


PEARLS & CONSIDERATIONS image



COMMENTS



• Mucocele rupture does not preclude a successful outcome.

• Diffuse bile peritonitis with mucocele rupture is unlikely, owing to containment of bile salts within a solid mucinous matrix that limits exposure of bile salts to the peritoneal surface.

• To prevent reobstruction with mucocele material within the common BD and hepatic ducts, confirmation of patency of the common BD is imperative following cholecystectomy.

• Intestinal biopsies should be considered in patients with a history of chronic gastrointestinal disease.


SUGGESTED READING



Aguirre AL, Center SA, Randolph JF, et al. Gallbladder disease in Shetland sheepdogs: 38 cases (1995-2005). J Am Vet Med Assoc. 2007;231(1):79-88.


Pike FS, Berg RJ, King NW, et al. Gallbladder mucocele in dogs: 30 cases (2000-2002). J Am Vet Med Assoc. 2004;224(10):1615-1622.



Gallbladder Rupture



AUTHOR: DAVID. HOLT



EDITOR: RICHARD. WALSHAW



BASIC INFORMATION image



DEFINITION


Loss of gallbladder wall integrity



EPIDEMIOLOGY



SPECIES, AGE, SEX


Dogs:


• Associated with trauma: younger dogs (mean 2.8 years)

• Associated with intrinsic gallbladder disease: middle-aged dogs (mean 8.1 years)


GENETICS & BREED PREDISPOSITION



• Shetland sheepdogs and possibly cocker spaniels are overrepresented.


ASSOCIATED CONDITIONS & DISORDERS


Dogs:


• Cholelithiasis, cholecystitis, bile peritonitis, sepsis

• Associated with gallbladder mucocele

• Gallbladder infarction

• Hypothyroidism and hyperadrenocorticism may predispose a subset of dogs to gallbladder infarction/rupture.


CLINICAL PRESENTATION



DISEASE FORMS/SUBTYPES



• Gallbladder infarction/necrotizing cholecystitis:
○ Without rupture

○ With hepatic and omental adhesions and possibly fistulae to other abdominal structures

○ With gallbladder perforation and diffuse peritonitis

• Gallbladder perforation associated with penetrating trauma and subsequent bile peritonitis


HISTORY, CHIEF COMPLAINT



• Nonspecific signs: vomiting, anorexia, weakness, polydipsia, polyuria, weight loss. Often chronic (duration from onset of signs to presentation: up to 1 month; mean = 12 days)

• Some owners may notice icterus, discolored urine (bilirubinuria).


PHYSICAL EXAM FINDINGS



• Icterus: very common (77% of bile peritonitis cases)

• Abdominal distension: common (65% of bile peritonitis cases), may be subtle

• Signs of abdominal pain

• Pyrexia

• Shock


ETIOLOGY AND PATHOPHYSIOLOGY



• Causes of gallbladder rupture:
○ Necrotizing cholecystitis

○ Gallbladder infarction

○ Penetrating trauma

○ Inadequate choleresis due to excessively thick bile, defective gallbladder contractility, and/or altered outflow

• Gallbladder rupture may result in the development of septic or nonseptic peritonitis (see p. 865).

• Lack of bile secretion into the intestine results in:
○ Lack of digestion and absorption of fat and fat-soluble vitamins, most importantly vitamin K (coagulopathy)


DIAGNOSIS image



DIAGNOSTIC OVERVIEW


The diagnosis is suspected based on nonspecific history and physical examination finding of icterus +/− abdominal signs. Confirmation requires abdominal ultrasound examination and peritoneal fluid analysis.



DIFFERENTIAL DIAGNOSIS



• Icterus:
○ Hyperbilirubinemia due to hemolysis: immune-mediated hemolytic anemia and other diseases causing severe intravascular hemolysis

○ Hepatic diseases: cholangiohepatitis, cirrhotic/fibrosing liver disease, neoplasia, copper and other toxins

○ Extrahepatic biliary obstruction: choleliths, pancreatitis, cholangitis, neoplasia, stricture

○ Biliary leakage from other parts of the biliary system:
▪ Traumatic rupture of the common or hepatic ducts

• Abdominal distension (if icterus not apparent):
○ Septic peritonitis: gastrointestinal perforation, penetrating trauma

○ Uroabdomen

○ Hemoabdomen: ruptured mass/viscus, bleeding disorder

○ Abdominal organ dilation/enlargement: gastric dilation/volvulus, mesenteric volvulus, splenic torsion, overeating, hyperadrenocorticism

○ Intraabdominal abscess: severe pancreatitis, hepatic abscess, ruptured prostatic abscess, ruptured pyometra

○ Portal hypertension

○ Congestive heart failure (right-sided)


INITIAL DATABASE



• CBC:
○ Inflammatory leukogram

○ Degenerative left shift with toxic changes:
▪ Septic bile peritonitis

• Serum biochemistry profile:
○ Elevated bilirubin concentration (virtually all cases)

○ Elevated liver enzymes concentration (virtually all cases)

○ Hypokalemia

• Survey abdominal radiographs:
○ Increased opacity/loss of detail in anterior abdomen

○ Cholelithiasis (in dogs, 14%-48% are radiopaque)

○ Generalized loss of abdominal detail/fluid:
▪ Bile peritonitis


ADVANCED OR CONFIRMATORY TESTING



• Abdominal ultrasound examination:
○ Evaluate gallbladder wall thickness and integrity (cholecystitis); contents (choleliths, mucocele), presence of attached omentum, and surrounding fluid, suggesting either bile peritonitis or unrelated (e.g., other differential diagnoses)

• Peritoneal fluid analysis (obtained during abdominal ultrasound examination):
○ Bilirubin concentration: > twice that of serum bilirubin is diagnostic of bile peritonitis

○ Cytologic evaluation and bacterial culture and sensitivity testing (aerobic and anaerobic): septic peritonitis

• Coagulation profile (prothrombin time is first to be abnormal with vitamin K deficiency/malabsorption)


TREATMENT image



TREATMENT OVERVIEW


Treatment consists of patient stabilization followed by surgical exploration of the abdomen, with removal of the ruptured gallbladder and treatment of associated bile peritonitis; adjunctive pain control is important.



ACUTE GENERAL TREATMENT



• Rehydration: intravenous administration of balanced electrolyte solution
○ Normalization of serum electrolyte concentrations

• Parenteral antibiotics effective against gram-negative bacteria and anaerobes
○ Empirical therapy:
▪ Cefoxitin, 22 mg/kg IV q 2 h peri-operatively, then q 6 h; or

▪ Metronidazole, 10-15 mg/kg IV q 12 h with:

▪ Enrofloxacin, 2.5-5 mg/kg IV q 12 h (maximum 5 mg/kg q 24 h in cats)

○ Specific long-term therapy based on culture and sensitivity test results

• Possible administration of fresh frozen plasma: (see p. 1347)
○ Hypoproteinemia

○ Possible coagulopathy

• Vitamin K administration: 2.5 mg/kg SQ q 12 h × 3 days, then weekly

• Exploratory laparotomy once animal is stabilized:
○ Cholecystectomy

○ Ensure patency of biliary system

○ Aerobic and anaerobic microbiologic culture of peritoneal fluid

○ Treatment of bile peritonitis: consider open peritoneal drainage


CHRONIC TREATMENT


Maintenance of bile flow: ursodeoxycholic acid 10-15 mg/kg/day PO—only after biliary obstruction is definitively ruled out/corrected, because stimulates gallbladder contraction



NUTRITION/DIET


Nutritional support via placement of feeding tube if indicated (see pp. 1322 and 1267)



POSSIBLE COMPLICATIONS



• Ongoing/recurrent bile leakage

• Failure to resolve septic bile peritonitis:
○ Endotoxemia

○ Sepsis

• Biliary obstruction:
○ Recurrence of cholelithiasis

• Pancreatitis


RECOMMENDED MONITORING



• Clinical and laboratory parameters assessing perfusion, including capillary refill time, pulse rate and quality, blood pressure, urine output, arterial pH, and lactate concentrations

• Respiratory function

• Serum liver enzymes and bilirubin concentrations

• Coagulation profile


PROGNOSIS AND OUTCOME image



• Guarded to fair in animals with aseptic bile peritonitis

• Poor to guarded in animals with septic bile peritonitis


PEARLS & CONSIDERATIONS image



COMMENTS


In dogs and cats with bile peritonitis:


• Peripheral white blood cell count is significantly lower in survivors (mean = 20,608/μL) compared with nonsurvivors (mean = 35,715/μL).

• The immature neutrophil count is significantly lower in survivors (mean = 686/μL) than in nonsurvivors (mean = 4852/μL).


SUGGESTED READING



Aguirre AL, Center SA, Randolph JF, et al. Gallbladder disease in Shetland sheepdogs: 38 cases (1995-2005). J Am Vet Med Assoc. 2007;231(1):79-88.


Holt DE, et al. Canine gallbladder infarction. Vet Pathol. 2004;41:416.


Ludwig LL, et al. Surgical treatment of bile peritonitis in 24 dogs and 2 cats: a retrospective study (1987-1994). Vet Surg. 1997;26:90.



Gallops and Other Extra Heart Sounds



AUTHOR: STEPHEN J. ETTINGER



EDITOR: ETIENNE. CÔTÉ



BASIC INFORMATION image



DEFINITION


Extra heart sounds are classified as sounds or vibrations other than the normally ausculted first and second heart sounds. They alter the sound of a heartbeat but not the rhythm of the heartbeat. Gallops and extra heart sounds are different from premature cardiac beats and arrhythmias.



SYNONYMS


Third heart sound, fourth heart sound, diastolic heart sound, protodiastolic heart sound, presystolic heart sound, summation diastolic heart sound



EPIDEMIOLOGY



SPECIES, AGE, SEX


Dogs and cats of any age and either sex, in the presence of heart disease/failure (gallop sounds)



RISK FACTORS



• Gallop sounds: congestive heart failure, systolic and diastolic ventricular dysfunction

• Systolic clicks: early mitral valvular insufficiency or flail leaflet

• Split heart sounds: increased ventricular pressures (causing splitting sounds due to delayed aortic or pulmonic valve closure under specific circumstances)

• Pericardial friction rubs: pericarditis, inflammation of the external pericardial lining


CLINICAL PRESENTATION


HISTORY, CHIEF COMPLAINT: Clinical signs relating to heart failure of virtually any etiology (see p. 468) are associated with gallop sounds. Splitting sounds may be normal or an indication of delay in valvular closure due to increased pressures on one or both sides of the heart or due to high pressure delaying valvular opening. Systolic clicks are not associated with clinical signs. Pericardial rubs are associated with pericardial diseases and their associated clinical signs.


PHYSICAL EXAM FINDINGS: A triple heart sound sequence with accentuated low-frequency sounds mimicking a cantering horse best describes a gallop sound. This sound is of low frequency, heard best with the bell of the stethoscope and usually over the mitral and or tricuspid valve area. The sound is likely to be associated with other signs of heart failure such as dyspnea, tachypnea, heart murmurs, and an increase in the heart rate.



ETIOLOGY AND PATHOPHYSIOLOGY



• Normally, only the S1 and S2 sounds are heard when auscultating the heart of the dog or cat.

• When the usually inaudible third or fourth sounds are so loud that they can be heard (gallops), they are an indication of the presence of ventricular systolic and/or diastolic dysfunction and are usually an indication of heart failure. By definition they occur during diastole and are generated by the vibration of ventricular walls during active ventricular filling (S3) or final ventricular filling by atrial contraction (S4) in a poorly compliant ventricle.

• Other additional sounds within the normal cardiac cycle can include:
○ Splitting of the normal heart sounds: either split S1, due to the asynchronous closure of AV valves, or split S2, due to asynchronous closure of aortic and pulmonic (semilunar) valves; caused by alterations in pressures within the heart and great vessels causing early or delayed valve closure

○ Extracardiac rubbing sounds

○ Systolic clicks: etiology unidentified, possibly caused by the warping/snapping of a diseased, prolapsed mitral valve. They are usually heard best with the diaphragm of the stethoscope, in contrast to the gallop sound which is a lower frequency sound heard better with the bell. The systolic click may be single or multiple. It also may come and go between consecutive cardiac cycles.

○ Opening snaps: heard in diastole and indicative of a calcified or hardened valve leaflet making a snapping sound when the valve opens during that phase of the cardiac cycle. These are unusually heard in dogs and cats, and they may be demonstrated by phonocardiography.

○ Friction rubs: due to rubbing of a diseased pericardium against portions of the thorax


DIAGNOSIS image



DIFFERENTIAL DIAGNOSIS


Triple heart sounds occurring at a slow rate are not likely to be gallop rhythms and must be differentiated from extra beats, heart block, systolic clicks, split heart sounds, and opening snaps. Systolic clicks are higher-frequency sounds heard with the diaphragm of the stethoscope and usually are heard at the point of maximal intensity on the thorax. The sound may be consistent or variable and may be single or multiple. It can easily mimic a gallop sound except in the frequency of the ausculted sound. Split heart sounds are usually heard cranially and left over the aortic and pulmonic valve regions. They tend to be higher-frequency sounds heard best with the diaphragm of the stethoscope.



INITIAL DATABASE


Cardiac evaluation in the form of auscultation, radiography of the thorax, laboratory analyses, and echocardiographic examination usually are sufficient to identify the specific abnormality present.



TREATMENT image



TREATMENT OVERVIEW


Extra heart sounds in and of themselves are NOT treated. Attention is directed to identifying the underlying cause and determining whether treatment is required for the primary etiology.



PROGNOSIS AND OUTCOME image


Variable, depending on cause



PEARLS & CONSIDERATIONS image



COMMENTS


The bell of the stethoscope is useful for differentiating low-frequency sounds such as gallop sounds (bell disproportionately enhances the third heart sound) from other heart sounds of higher frequency such as split heart sounds and systolic clicks (heard more clearly with the diaphram of the stethoscope).



SUGGESTED READING



Prosek R. Abnormal heart sounds and murmurs. In: Ettinger SJ, Feldman EC, editors. Textbook of veterinary internal medicine. ed 7. St Louis: Elsevier; 2010:259.



Garbage Toxicosis



AUTHOR: SHARON. GWALTNEY-BRANT



EDITOR: SAFDAR A. KHAN



1ST EDITION AUTHOR: CHARLOTTE. MEANS



BASIC INFORMATION image



DEFINITION


Gastroenteritis or hemorrhagic gastroenteritis caused by ingestion of food or garbage contaminated with bacteria or preformed bacterial toxins. Tremors or seizures can occur secondary to presence of tremorgenic mycotoxins. Garbage toxicosis is a common occurrence in dogs but less commonly seen in cats, owing to their more discriminating dietary habits.



SYNONYMS


Bacterial food poisoning, carrion toxicosis, garbage gut, songbird fever



EPIDEMIOLOGY



SPECIES, AGE, SEX



• Potentially all animals; dogs are more likely to ingest spoiled foods.

• Cats that hunt and consume birds may develop this disorder.


RISK FACTORS



• Roaming animals

• Dogs fed food considered unfit for human consumption

• Raw food diets


CONTAGION & ZOONOSIS



• Disease is transmissible between animals because of habits of licking and sniffing.

• Dogs also might eat vomitus or feces containing bacteria or bacterial toxins.

• Zoonotic transmission possible, especially in young children or people with compromised immune systems.

GEOGRAPHY AND SEASONALITY: Disease common during warmer months, or year round in tropical and subtropical regions.



ASSOCIATED CONDITIONS & DISORDERS



• Botulism

• Tremorgenic mycotoxicosis


CLINICAL PRESENTATION



HISTORY, CHIEF COMPLAINT



• History of exposure to carrion or garbage or raw food diets

• Clinical signs within 15 minutes to 6 hours post ingestion; diarrhea can be delayed for 48 hours

• Severe vomiting, diarrhea, lethargy, anorexia


PHYSICAL EXAM FINDINGS



• Signs of abdominal pain

• Abdominal distension from gas

• Foul smelling feces; watery or bloody diarrhea

• Fever

• Ataxia

• Weak pulse, muddy mucous membranes, increased capillary refill time, hypovolemic shock

• Hypothermia as the shock state progresses


ETIOLOGY AND PATHOPHYSIOLOGY


Source:


• Streptococcus spp., Salmonella spp., Bacillus spp., Escherichia coli, and Clostridium perfringens are the most common bacteria involved.

• Endotoxemia and enterotoxemia are possible.

Mechanism of Toxicosis


• Via different mechanisms; endotoxins produce hypovolemic shock, collapse, and death.

• Tremors, seizures, hyperthermia may occur from tremorgenic mycotoxins.

• Gastrointestinal (GI) epithelial cells irritated/eroded:
○ Permeability disturbed, initiating vomiting, GI hemorrhage, fluid and electrolyte loss

○ Normal absorptive capabilities of the GI tract may be disrupted.

○ Stasis and GI dilation with gas accumulation follows.

○ GI stasis encourages growth of gram-negative bacteria which liberate endotoxin.


DIAGNOSIS image



DIAGNOSTIC OVERVIEW


Diagnosis is based on a history of ingesting garbage, spoiled food, carrion, songbirds (cats), and the like and typical clinical signs of gastroenteritis or tremors/seizures (with tremorgenic mycotoxins). The disorder is different from benign self-resolving gastroenteritis in the following ways: known ingestion of contaminated substances and/or presence of systemic signs (endotoxemia, neurologic dysfunction, other). In the absence of historical evidence of ingestion, other causes of gastroenteritis must be ruled out with appropriate testing.



DIFFERENTIAL DIAGNOSIS


Toxicologic:


• Plants: castor beans, sago palm, ornamental bulbs, autumn crocus, etc.

• Metals: arsenic, antimony, iron, etc.

• Others: disulfoton (an organophosphate pesticide), gastrointestinal-irritant mushrooms

Nontoxicologic, Spontaneous:


• Viral gastroenteritis

• Hemorrhagic gastroenteritis

• Acute pancreatitis

• Acute hepatopathies

• “Salmon poisoning”


INITIAL DATABASE



• CBC and serum biochemistry profile: nonspecific changes

• Abdominal radiographs: to identify abnormal ingesta or rule in/rule out other disorders

• Monitor blood glucose (hypoglycemia associated with endotoxemia)


ADVANCED OR CONFIRMATORY TESTING



• Bacterial fecal culture is of mixed value (healthy animals often have cultures that are positive for “pathogenic” bacteria).

• Blood culture if sepsis is suspected

• Serologic identification of staphylococcal or clostridial toxins

• Penitrem A or roquefortine (tremorgenic mycotoxins) can be analyzed in the contaminated food or stomach contents (through a diagnostic laboratory).


TREATMENT image



TREATMENT OVERVIEW


Treatment is aimed at limiting absorption of bacterial toxins by inducing emesis and administering activated charcoal, controlling vomiting, correcting fluid and electrolyte disorders, and other supportive measures (preventing shock and preventing secondary infection). Initial approach is similar to any general intoxication, and specific treatments are indicated if systemic signs arise.



ACUTE GENERAL TREATMENT



• In animals with a known recent exposure but no clinical signs, induction of vomiting is indicated: hydrogen peroxide 3%: 1-2 mL/kg (maximum 45 mL total) PO once; or apomorphine, 0.04 mg/kg IV or instilled in conjunctival sac and rinsed out when vomiting begins (dogs); or xylazine, 0.44 mg/kg IM (cats).

• Activated charcoal, 1-3 g/kg PO (dose according to packaging label of product; e.g., 10 mL/kg of activated charcoal suspension PO made from 2 g/kg activated charcoal suspended in 10 mL/kg tap water)

• Appropriate fluid and electrolyte therapy

• Antibiotics
○ Injectable aminoglycosides generally contraindicated because of synergistic action with endotoxins in depressing the myocardium and risk of nephrotoxicosis in hypovolemia.

○ Oral aminoglycosides (streptomycin, 5-10 mg/kg PO q 12 h; or neomycin 10-20 mg/kg PO q 8-12 h) work well.

○ Metronidazole, 25 mg/kg PO q 12 h (for a maximum of 5 days at this dosage) can also be used.

○ If a cat has known songbird fever, routine antibiotics are not recommended, as this tends to alter normal GI flora, allowing colonization by Salmonella.

• Gastrointestinal protectants such as sucralfate ¼ to a whole 1-gram tablet PO q 8 h

• Treatment for shock as needed (see p. 585)

• Appropriate treatment if disseminated intravascular coagulation occurs (e.g., including heparin 75 IU SQ q 8 h (see p. 315)

• Control tremors and seizures with methocarbamol (55-220 mg/kg IV, repeat as needed; max dose 330 mg/kg/day) or diazepam (0.5-2 mg/kg IV, repeat as needed) in cases involving tremorgenic mycotoxins.
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