Kyle Restle, DVM, is a small animal surgery resident at the University of Tennessee’s small animal teaching hospital. He is a 2016 graduate of Auburn University’s College of Veterinary Medicine. His primary interests are veterinary surgery, 3-dimensional printing, and medical technology/instrumentation.Read Articles Written by Kyle Restle
DVM, PhD, DACVIM (SAIM)
Jacqueline Whittemore, DVM, PhD, DACVIM (SAIM), is an associate professor at the University of Tennessee College of Veterinary Medicine, where she also serves as the minimally invasive procedures service chief and the Acree Research Chair in Small Animal Medicine. She received her DVM from the University of California, Davis, and completed her residency and PhD at Colorado State University. Her major research foci are identification and amelioration of adverse effects of exogenous therapies (particularly antiplatelet, immunosuppressive, and antibiotic) on the gastrointestinal tract, development of simulators for veterinary training, and validation of minimally invasive diagnostic techniques to decrease patient morbidity and improve patient outcome.Read Articles Written by Jacqueline Whittemore
Chronic vomiting is a common presenting sign for cats, and evaluation can be frustrating for both owners and veterinarians because of the long differential list. Chronic vomiting has previously been defined as vomiting 3 or more times per month for at least 3 months.1 Vomiting of trichobezoars (hairballs) should not be dismissed, particularly in cats without long hair, because their development could reflect altered gastrointestinal (GI) motility due to underlying disease.2
Endoscopy can be a valuable tool in achieving a final diagnosis, but it is not inexpensive or completely without risk. Additionally, premature performance of endoscopy can result in misdiagnosis because histologic findings do not differentiate among types of chronic enteropathy, such as food responsive disease (FRD) and inflammatory bowel disease (IBD).3,4 Thus, when evaluating a cat for chronic vomiting, clinicians must follow a systematic approach.
Vomiting should first be differentiated from regurgitation. Vomiting is an active process with retching or heaving, and it is often preceded by nausea or hypersalivation. Vomitus may contain partially digested food and be discolored because of the presence of bile. In contrast, regurgitation is a passive process; regurgitated food is typically undigested, might have a mucus coating, and lacks bile.
After confirmation of chronic vomiting, the next step is crafting an appropriate differential list based on the patient’s signalment, environment and husbandry, history, and physical examination findings because this can drastically alter the diagnostic approach. For example, although metabolic evaluation is generally warranted in older cats before abdominal imaging, immediate performance of abdominal radiography might be more appropriate in a young cat because of increased risk for linear foreign body ingestion.5
Tables 1 and 2 present the systemic and GI diseases most commonly associated with chronic vomiting in cats. An exhaustive review of causes of vomiting in cats, along with a ranking of the level of evidence supporting each association, has been published by Batchelor et al.8
Table 1. Extragastrointestinal or Systemic Diseases Associated With Chronic Vomiting in Cats:
|CAUSE||SIGNALMENT AND CLINICAL SIGNS||PHYSICAL EXAMINATION FINDINGS||POSSIBLE RELEVANT DIAGNOSTIC TEST RESULTS|
|Parasitic (eg, heartworm, hepatic and pancreatic flukes, Toxoplasma)||Young cat that hunts Outdoor exposure Exposure to raw meat||Potbelly Underweight||? Albumin ? Globulins ? Liver enzymes + Heartworm test, echocardiogram|
|Viral (FeLV, FIV, FIP)||Young to adult, geriatric Outdoor exposure Multicat environment History of cat fights||Anterior uveitis or chorioretinitis Fever Peritoneal effusion Thickened intestines Underweight||? Hct ? WBC ? Globulins without ? albumin ? Liver enzymes and bilirubin Positive viral test results|
|Chronic kidney disease||PUPD Hyporexia/food aversion Weight loss||Hypothermia (without shock) Hypertension, retinal hemorrhages Poor hair coat Irregular, small kidneys||? Hct ? BUN, creatinine ? tCa, PO4, ?/? K+ Isosthenuria/minimally concentrated urine ? UPC|
|Diabetes mellitus||Burmese Polyphagia PUPD||Ill-kempt coat Obese Plantigrade stance||? Glucose, fructosamine Glucosuria|
|Hepatobiliary disease (eg, lymphocytic cholangitis, suppurative cholangitis)||Middle-aged Weight loss (lymphocytic)||Dehydration and fever (suppurative) Jaundice Peritoneal effusion Underweight (lymphocytic)||? Hct (lymphocytic) ? Albumin ? Globulins ? Liver enzymes, bilirubin|
|Hyperthyroidism||Behavioral changes Polyphagia PUPD Weight loss||Heart murmur Hypertension Palpable goiter Thickened intestines6||Heart murmur Hypertension Palpable goiter Thickened intestines6 n/? Hct ? Liver enzymes n/? BUN, creatinine Isosthenuria/minimally concentrated urine ? UPC7 ? T4/fT4 GI thickening|
|Pancreatitis||Middle-aged Hyporexia/food aversion Weight loss||Ill-kempt coat Cranial abdominal pain Peritoneal effusion Thickened intestines||? Liver enzymes ? fPL/DGGR lipase Widened gastroduodenal angle, loss of serosal detail Hypoechoic or heterogenous pancreas, hyperechoic mesentery, duodenal corrugation|
|Hepatic and pancreatic||Adult Hyporexia/food aversion Weight loss||Cranial abdominal organomegaly Underweight||? Hct ? Liver enzymes Organomegaly on radiography Mass on ultrasonography|
|Round cell tumors (lymphoma, mast cell tumor)||Any age Hyporexia Weight loss||Cranial abdominal organomegaly (uncommon)||Variable Gastric ulceration (mast cell)|
|BUN, blood urea nitrogen; DGGR, 1,2-o-dilauryl-rac-glycero glutaric acid-(6'-methylresorufin) ester; fPL, feline pancreas-specific lipase; fT4, free thyroxine; GI, gastrointestinal; Hct, hematocrit; n, normal; PUPD, polyuria and polydipsia; T4, thyroxine; tCa, total calcium; UPC, urine protein-to-creatinine ratio; WBC, white blood cell.|
Table 2. Gastrointestinal Diseases Associated With Chronic Vomiting in Cats
|DISEASE||SIGNALMENT AND CLINICAL SIGNS||PHYSICAL EXAMINATION FINDINGS||POSSIBLE RELEVANT DIAGNOSTIC TEST RESULTS|
|Obstruction (gastric or linear foreign body, trichobezoars, neoplasia)||History of foreign-body ingestion Long-hair coat Vomiting associated with food ingestion||Mass effect Intestinal plication String under tongue||Mass effect Intestinal plication|
|Pseudoobstruction (hypomotility||Large, fluid-filled stomach on imaging|
|Bacterial (spiral bacteria)||Hyporexia, food aversion||Generally normal||Demonstration of organisms on biopsy (with lack of gross or histologic abnormalities in the small intestine)|
|Fungal (Histoplasma species)||Geographic location Outdoor/bird exposure Lameness Respiratory signs Weight loss||Anterior uveitis or chorioretinitis Bone pain Fever, jaundice Abnormal lung sounds Thickened intestines Splenomegaly||? Hct/WBC/platelets ? Globulins, ? albumin ? Liver enzymes Pulmonary infiltrates Thickened intestines, lymphadenomegaly FeLV positivity|
|Parasitic (Physaloptera, Ollulanus, Ancylostoma, Toxocara, Toxascaris, and Dipylidium species)||Hunter Outdoor exposure New cat or dog introduced into home Cattery History of fleas||Generally normal Thickened intestines||? Eosinophils Positive fecal test result Microscopic visualization in vomitus or gastric lavage samples Direct visualization|
|Viral (dry form FIP)||Outdoor exposure Multicat environment||Anterior uveitis or chorioretinitis Fever Thickened intestines Underweight||? Hct ? Liver enzymes and bilirubin ? Globulins without ? albumin Positive viral test results GI thickening, scant perinephric effusion|
|FRD||Behavioral changes Diarrhea Hyporexia, food aversion Polyphagia Weight loss||Dermatologic abnormalities Ill-kempt coat Thickened intestines Underweight||? BUN with normal creatinine ? Albumin ? Eosinophils GI thickening, muscularis thickening Response to diet trial|
|IBD (including ESF)||Behavioral changes Diarrhea Hyporexia, food aversion Polyphagia Weight loss||Ill-kempt coat Thickened intestines Underweight||? Eosinophils GI thickening ± muscularis thickening (primarily duodenal), loss of wall layering Mass effect (ESF)|
|Carcinoma||Older animals Hyporexia, food aversion Polyphagia Weight loss||Mass effect Thickened intestines||Focal mass effect Gastric ulceration GI thickening/mass effect ± loss of wall layering|
|Lymphoma||FeLV positivity Diarrhea Hyporexia, food aversion Polyphagia Weight loss||Abdominal pain Nausea Mesenteric lymphadenomegaly Thickened intestines||Gastric ulceration GI thickening ± muscularis thickening (primarily jejunal), loss of wall layering, mass effect, mesenteric lymphadenomegaly|
|BUN, blood urea nitrogen; ESF, eosinophilic sclerosing fibroplasia; FeLV, feline leukemia virus; FIP, feline infectious peritonitis; FIV, feline immunodeficiency virus; FRD, food responsive disease; GI, gastrointestinal; Hct, hematocrit; IBD, inflammatory bowel disease; WBC, white blood cell.|
Signalment and Clinical History
Retrospective analysis suggests that the prevalence of urinary, neoplastic, cardiovascular, and GI diseases increases with age, whereas the prevalence of infectious and traumatic diseases decreases.9 Cats with outdoor access often have greater exposure to parasites and retroviruses, although all cats should be considered at risk. Although these trends can help guide the formation of an appropriate initial diagnostic plan, atypical presentation is possible.
Cats with chronic vomiting should be assessed for the changes listed in Box 1. Polydipsia with polyuria should be differentiated from polydipsia in the absence of polyuria. The latter can result from increased GI water loss, which is not always accompanied by diarrhea. Fecal scoring charts should be reviewed with clients to determine fecal consistency. If present, diarrhea should be categorized (small, large, or mixed bowel) and the presence of blood determined. Weight loss should be subdivided into changes to fat stores, muscle mass, or both.
If GI disease is diagnosed, the feline chronic enteropathy activity index should be calculated to quantitate the severity of disease,10 thereby facilitating more accurate evaluation of the patient’s response to therapy.
Although physical examination is often unremarkable in cats with chronic vomiting, abnormalities can aid in winnowing the differential list.
Cats with chronic GI disease are typically euvolemic but can have decreased skin turgor due to dermal aging changes or depletion of fat stores. Conversely, oral mucous membranes can be moist in dehydrated cats because of ptyalism. The nictitans, sclera, and mucous membranes should be carefully assessed for jaundice. The base of the tongue should be elevated to check for linear foreign bodies, particularly in younger cats and cats with a history of pica. The breath should be checked for uremic halitosis and the mouth surveyed for periodontal disease, calculus, ulcers, and masses. Complete ophthalmic evaluation might reveal anterior uveitis, chorioretinitis, vascular tortuosity, or retinal hemorrhage. The ventral neck should be carefully palpated for thyroid nodules.
Abnormalities on thoracic auscultation or abdominal palpation might alter initial testing. The thorax should be auscultated for cardiac murmurs, rhythm disturbances, and abnormal bronchovesicular sounds. Gentle but thorough abdominal palpation might reveal nausea (licking of lips, excessive swallowing, resistance to palpation), hepatomegaly, cranial abdominal pain, irregularity or asymmetry of the kidneys, an enlarged urinary bladder, or peritoneal effusion, increasing prioritization of abdominal imaging. Careful attention should be paid to GI abnormalities, such as diffuse thickening or mass effects.
Rectal temperature should be determined regardless of patient temperament; alterations such as hypothermia and fever generally suggest systemic disease. Hematochezia or melena might be identified on inspection of the thermometer or sedated rectal examination.
Initial Diagnostic Tests
As noted above, the diagnostic approach for each case should be customized after assessment of the patient’s history, physical examination findings (including metabolic stability), and differential diagnosis. The typical baseline diagnostics are discussed below. Although a second-tier test for most cases of chronic vomiting, abdominal radiography might be the initial diagnostic test performed when obstruction or an abdominal mass effect is suspected.
Fecal Flotation/Empirical Deworming
Fecal flotation and empirical deworming should be performed in all cases, regardless of outdoor exposure. A minimum of 2 g of feces, a solution with a specific gravity greater than 1.240, and centrifugation should be used for fecal flotation to decrease the likelihood of false-negative results (by up to 10-fold for some parasites).11 A broad-spectrum parasiticide, such as fenbendazole (generally given for 3 days, repeated at 3 weeks and 3 months), should be administered in cases with negative fecal flotation results because of the poor sensitivity of this test.12 In cases with direct or indirect flea exposure, treatment for Dipylidium species should also be administered. When Physaloptera species are suspected, multiple pyrantel treatments are recommended.13
Half of cats in a study of chronic enteropathy experienced clinical cure after diet change, with almost immediate cessation of vomiting.3 Other GI signs, if present, resolved in most cats within 3 days. Because serial diet trials often do not need to exceed 7 to 14 days each, it is reasonable to perform them before pursuing the remaining first-tier diagnostic tests in cats without evidence of systemic disease.
Although the phrase “diet trial” is often used interchangeably with the term “novel protein trial”—suggesting that FRD is uniformly triggered by protein sources—grains, feed additives, and nonspecified changes associated with commercial processing can trigger clinical signs in some cats.3 Thus, over-the-counter and highly digestible diets can be used in addition to novel or hydrolyzed protein diets.
During each dietary trial, cats should not receive treats, human food, flavored medications, or vitamins or feast on prey. If clinical cure is noted, rechallenge with the cat’s initial diet is important to determine whether long-term dietary modification is necessary to prevent recrudescence. In 1 trial, 40% of cats with FRD remained in clinical remission in the face of rechallenge with their initial diet, while the rest experienced recurrence of signs within 3 to 4 days.3
Noninvasive Blood Pressure Measurement
Hypertension may indicate the presence of systemic disease, such as chronic kidney disease or hyperthyroidism. To avoid misdiagnosis, blood pressure should be measured in a relaxed environment after a 10-minute acclimation period to the environment and personnel. Use of Doppler method is recommended because it has better accuracy and precision in awake cats compared with oscillometry.14 Additionally, the coccygeal artery should be used in cats with low muscle condition scores because of a confounding influence of sarcopenia on radial artery measurements.15
Complete Blood Count
Normocytic, normochromic, nonregenerative anemia is a nonspecific finding. In contrast, regenerative anemia and microcytic, hypochromic anemia occur secondary to chronic GI bleeding, often without hematochezia or melena. Erythrocytosis in apparently euvolemic patients can result from hyperthyroidism,16 although subclinical dehydration should be considered. Eosinophilia and basophilia are common in cats with GI disease and/or parasitism, but they are nonspecific findings.
Serum or Plasma Biochemical Profile
Abnormalities should be considered in light of magnitude, proportionality of change, and physical examination findings. For example, discordant increases in blood urea nitrogen and creatinine generally suggest GI bleeding but can also occur in cats with cachexia due to chronic kidney disease.
Discordant elevation of globulin over albumin might indicate systemic disease, while proportional elevation is more consistent with total body water losses and dehydration. Hypochloremia, hyponatremia, hypokalemia, and hypophosphatemia might occur as sequelae of vomiting, while hypercalcemia and hyperphosphatemia generally reflect underlying systemic disease. Ionized calcium measurement is occasionally necessary to differentiate between hemoconcentration-associated increases in total calcium and true hypercalcemia.
Liver enzyme activity increases are more significant in cats than in dogs because of shorter enzyme half-lives and the lack of a glucocorticoid-induced alkaline phosphatase isoform in this species. Discrimination between hepatocellular and cholestatic liver enzyme patterns is a crucial step to guide clinical reasoning. Additional information regarding liver enzyme assessment can be found in McAtee and Lidbury.17
Urine concentration should be interpreted in light of the water content of the patient’s diet, as well as the patient’s hydration status. Minimally concentrated urine in a cat eating a dry commercial diet suggests extragastrointestinal disease. Proteinuria should be quantified by urine protein:creatinine ratio in patients with negative urine sediment and culture results, with values 0.2 to 0.4 considered borderline proteinuria and >0.4 considered significant proteinuria. If proteinuria is present, thorough evaluation for systemic disease is generally warranted before pursuing primary GI disease.
Heartworm and Retroviral Testing
Geographic location dictates prioritization of heartworm testing, although it should be considered a first-tier test in areas where heartworms are endemic. Serum antigen testing is generally considered more specific but less sensitive than antibody testing18 because it assesses the presence of worm antigen versus historical exposure. However, a recent study found serum antigen testing to be more sensitive and specific than serum antibody testing.19 Combination testing has the highest sensitivity, although false-negative results still occur.20
Retroviral status should be confirmed as part of initial diagnostic screening, even for indoor-only cats.21 Confirmatory testing is recommended for cats that are positive on initial screening. Care should be taken to ascertain FIV vaccination status because not all point-of-care antibody tests can accurately differentiate between prior vaccination and infection.22 A positive FIV result from an antibody test with unknown differentiation ability should be confirmed via Western blot or polymerase chain reaction (PCR).
Thyroid Hormone Quantitation
Screening for hyperthyroidism is warranted regardless of age, given reports of clinical hyperthyroidism in cats as young as 8 months.23 Measurement of total thyroxine (T4) concentration is diagnostic for hyperthyroidism in approximately 95% of cases. Free T4 concentration determination is recommended for cats suspected of hyperthyroidism that have total T4 concentrations in the upper half of the reference range. Elevated free T4 in the presence of total T4 measurements in the upper half of the reference range suggests hyperthyroidism.24
Second-Tier Diagnostic Tests
If the cause of vomiting remains unknown after completion of the preceding tests, second-tier diagnostics are warranted.
To optimize diagnostic accuracy, abdominal radiography and ultrasonography should be performed after a routine fast. Inadequate fasting particularly complicates assessment for motility disorders.
Radiographs are evaluated for alterations in organ size, the presence of mass effects and foreign bodies, GI abnormalities suggestive of obstruction or motility disorders, and peritoneal effusion. Such findings are generally specific, although their absence does not rule out significant disease.
Advantages of ultrasonography in evaluation of patients with GI signs include the ability to detect homogenous and heterogenous changes to the parenchyma of various viscera; visualize the biliary tree and its path through the pancreas; differentiate between the GI lumen and various layers of the wall, as well as localize and quantitate any thickening present; assess intestinal motility, corrugation, and plication; identify mesenteric lymphadenomegaly, foreign bodies, and masses; and guide noninvasive tissue and fluid sampling. Care should be taken in differentiating between dilatation and simple dilation of the common bile duct (an aging-related change in cats).
Assuming hyperthyroidism has been ruled out, changes in GI wall layering or thickness suggest primary GI disease (eg, FRD, IBD, neoplasia, histoplasmosis). It is generally accepted that small intestinal wall thickening of 0.28 cm or greater is clinically significant; such thickening has been associated with both lymphoma and IBD.1,2,25,26 Wall thickening can be focal, diffuse, or segmental. Although focal thickening can suggest neoplasia, ulceration and IBD also can be associated with focal defects and warrant consideration. Segmental thickening has been found with multiple abnormalities, such as concurrent IBD and lymphoma.26 Thickening can affect all wall layers or specific layers (Figure 1). Thickening of the muscularis propria (greater than half the thickness of the submucosa) is more likely in cats with lymphocytic lymphoma, although it also can be seen in normal cats or those with IBD.27 Additionally, loss of intestinal wall layering, mass-like lesions, and/or reduced wall echogenicity have been associated with lymphoblastic lymphoma.27
Markers of Dysbiosis, Vitamin Deficiency, and Pancreatic Inflammation
Hypocobalaminemia is present in 61% of cats with primary GI disease,28 and vomiting has been reported as the only clinical sign in some cats with hypocobalaminemia.29 Hypocobalaminemia also has been reported in cats with extragastrointestinal disease, such as hepatitis and hyperthyroidism.27,30,31 It is important that cobalamin deficiency be detected and addressed because failure to do so can result in persistence of clinical signs despite treatment of the primary disease.27 Some cats have been diagnosed with clinical cobalamin deficiency based on the presence of increased methylmalonic acid concentrations without hypocobalaminemia.28 Consequently, supplementation should be considered for cats with values in the low end of the reference range.
Folate is absorbed in the proximal small intestine only. Elevated serum folate concentrations can be secondary to small intestinal bacterial overgrowth (resulting from GI disease or dysbiosis) or coprophagia (feces have high folate concentrations).32 Decreased serum folate concentrations can be secondary to focal proximal or diffuse small intestinal disease, but they also have been noted in cases of pancreatitis or cholangiohepatitis.27 Low serum folate concentrations also can be seen in clinically healthy cats.27
Concurrent low cobalamin and folate concentrations have been associated with severe diffuse GI disease.33 Some patients with high serum folate and low cobalamin concentrations experience normalization of folate concentrations after cobalamin supplementation.29 Reevaluation of folate concentration after correction of hypocobalaminemia might, therefore, be prudent in some cases.
Exocrine pancreatic disease can be divided into exocrine pancreatic insufficiency (EPI) and pancreatitis. EPI is diagnosed based on decreased serum trypsin-like immunoreactivity concentration. Although feline EPI historically has been considered rare, the apparently low prevalence could reflect inadequate surveillance for the disease, according to a recent report.34 Clinical signs in cats with EPI in that report included poor body condition, weight loss, loose stools or diarrhea, and polyphagia, but also lethargy, anorexia, and vomiting. The study found a high frequency of low cobalamin and high folate concentrations.
Elevated trypsin-like immunoreactivity also can be seen in cats with small intestinal disease, pancreatitis, and kidney failure. Sensitivities (42% to 80%) and specificities (63% to 100%) of the validated lipase assays for pancreatitis vary dramatically, depending on the criteria for diagnosis (histologic inflammation, clinical signs and ultrasonographic changes, or some combination thereof).35–38 A semiquantitative point-of-care feline pancreatic-specific lipase test is available, but its sensitivity, specificity, and accuracy have not been independently validated. None of the biomarkers for pancreatic inflammation are a substitute for clinical judgment, and clinical signs and other diagnostic test results should be integrated into the diagnosis of feline pancreatitis.
Urine Histoplasma Antigen
Histoplasma urine antigen concentration (miravistalabs.com) should be quantitated in cases with appropriate clinical history and exposure, laboratory findings, and abdominal imaging changes. Histoplasma infections primarily occur in the Ohio River Valley and southeastern United States. The assay has good sensitivity (94.4%), although negative test results do not rule out infection.39 Cross-reactivity with other systemic infectious agents is possible.39
Helicobacter Species Testing
Helicobacter species have been identified in biopsy specimens from both clinically ill and healthy cats.40–44 Prevalence increases with age,43 although the organisms have been noted in animals as young as 6 weeks.45 Because of the high prevalence of Helicobacter species within healthy populations, treatment is generally withheld unless concurrent histopathologic abnormalities have been identified and other causes of gastritis have been ruled out.45 Treatment consists of multimodal antibiotics with or without gastric acid suppression.45–47
When to Recommend Endoscopy
Direct evaluation of the GI tract should be considered when the preceding testing does not reveal a systemic cause for vomiting and diet trials have failed or the cat has evidence of focal disease that warrants focused investigation. This can be accomplished via endoscopy, laparoscopy, or laparotomy. The decision to perform endoscopy over laparotomy is multifactorial, and advantages of each approach are listed in Box 2.
Investigating Imaging Finding
Endoscopy is generally preferable as an initial sampling technique for patients without abnormalities on imaging because it is less invasive and might reveal focal mucosal lesions that would be missed by laparotomy.
Endoscopy should be considered for cases with diffuse or accessible focal GI changes, whereas laparotomy is prioritized for patients with ultrasonographic abnormalities limited to the jejunum. Although the muscularis is inaccessible endoscopically, thickening on ultrasonography does not necessarily dictate use of more invasive sampling techniques, such as laparotomy. Diffuse ultrasonographic thickening is often associated with IBD and lymphoma (Figure 2),49,50 which are regularly diagnosed via endoscopic biopsy.
Focal thickening of the muscularis propria has been associated with mast cell tumor,51 which might be amenable to endoscopic sampling depending on location. Because muscularis thickening can occur in cats without GI disease, sampling is not warranted in the absence of clinical signs.52 Similarly, although focal mass effects on examination or diagnostic imaging are most suggestive of neoplasia, disorders such as GI eosinophilic sclerosing fibroplasia and (rarely) fungal infection should not be overlooked. Because the location of lesions can substantially complicate surgical removal and positive, long-term responses can be achieved by using a combination of diet and medical therapies,53 it is reasonable to rule out GI eosinophilic sclerosing fibroplasia via endoscopy before proceeding to laparotomy.
Identifying Lesions for Surgery
Endoscopy can be useful for localizing and targeting mucosal lesions for surgical intervention, although it is very reasonable to proceed directly to laparotomy in cases with concurrent abnormalities in the liver, pancreas, or other organs. If financial limitations are present, laparotomy with biopsies of all possibly affected organs is generally recommended to avoid missing the primary disease process or a chance to achieve surgical cure.
Collecting Samples for Biopsy
Endoscopically collected biopsy samples can be both highly sensitive and specific for GI disease, depending on the histologic quality of the samples.48 To be considered histologically adequate, samples must contain 3 or more villi and lamina propria extending to the mucosa–muscularis mucosa border. A 99% likelihood of detecting cellular infiltrates and villus blunting in the stomach and duodenum can be achieved with as few as 6 adequate samples;54 if samples are histologically inadequate, 18 to 26 specimens are required for this level of confidence. Histologic quality cannot be determined on the basis of gross appearance; therefore the endoscopist should collect a reasonable number of biopsy samples and follow best practices for sample alignment to avoid overlooking a subtle lesion.48
Sensitivity of endoscopic biopsy for detection of lymphoma does not vary according to sample quality,54 although distinguishing between lymphoma and lymphoplasmacytic enteritis can be difficult regardless of sample quality.55 The use of immunohistochemistry and PCR for antigen receptor rearrangements can help differentiate between the two differentials.56–59 Simultaneous collection of ileal biopsy specimens increases the chance of detecting regional disease, particularly with regard to ileal lymphoma.60 Because this necessitates colonoscopy, clinical judgment should be used in deciding whether the increase in patient preparation, anesthesia time, costs, and potential complications is warranted.
Chronic vomiting in cats is a frustrating condition, and accurate diagnosis hinges on use of a systematic approach. Endoscopy is warranted after systemic diseases have been ruled out, particularly in cases without solitary jejunal disease. In the absence of other findings, the presence of muscularis thickening does not indicate a need for laparotomy. As technology advances and endoscopy becomes more sophisticated, it may become more useful or reliable in obtaining samples and performing interventional techniques.
- Norsworthy GD, Estep JS, Hollinger C, et al. Prevalence and underlying causes of histologic abnormalities in cats suspected to have chronic small bowel disease: 300 cases (2008-2013). JAVMA 2015;247(6):629-635.
- Norsworthy GD, Scot Estep J, Kiupel M, et al. Diagnosis of chronic small bowel disease in cats: 100 cases (2008-2012). JAVMA 2013;243(10):1455-1461.
- Guilford WG, Jones BR, Markwell PJ, et al. Food sensitivity in cats with chronic idiopathic gastrointestinal problems. J Vet Intern Med 2001;15(1):7-13.
- Washabau RJ, Day MJ, Willard MD, et al. Endoscopic, biopsy, and histopathologic guidelines for the evaluation of gastrointestinal inflammation in companion animals. J Vet Intern Med 2010;24(1):10-26.
- Felts JF, Fox PR, Burk RL. Thread and sewing needles as gastrointestinal foreign bodies in the cat: a review of 64 cases. JAVMA 1984;184(1):56-59.
- Nussbaum LK, Scavelli TD, Scavelli DM, et al. Abdominal ultrasound examination findings in 534 hyperthyroid cats referred for radioiodine treatment between 2007-2010. J Vet Intern Med 2015;29(4):1069-1073.
- Williams TL, Peak KJ, Brodbelt D, et al. Survival and the development of azotemia after treatment of hyperthyroid cats. J Vet Intern Med 2010;24(4):863-689.
- Batchelor DJ, Devauchelle P, Elliott J, et al. Mechanisms, causes, investigation and management of vomiting disorders in cats: a literature review. J Feline Med Surg 2013;15(4):237-265.
- Egenvall A, Nødtvedt A, Häggström J, et al. Mortality of life-insured Swedish cats during 1999–2006: age, breed, sex, and diagnosis. J Vet Intern Med 2009;23(6):1175-1183.
- Jergens AE, Crandell JM, Evans R, et al. A clinical index for disease activity in cats with chronic enteropathy. J Vet Intern Med 2010;24(5):1027-1033.
- Dryden MW, Payne PA, Ridley R, et al. Comparison of common fecal flotation techniques for the recovery of parasite eggs and oocysts. Vet Ther 2005;6(1):15-28.
- Little S, Adolph C, Downie K, et al. High prevalence of covert infection with gastrointestinal helminths in cats. JAAHA 2015;51(6):359-364.
- Companion Animal Parasite Council. Phylasoptera spp. Available at: capcvet.org/guidelines/physaloptera-spp/. Accessed September 2017.
- Binns SH, Sisson DD, Buoscio DA, et al. Doppler ultrasonographic, oscillometric sphygmomanometric, and photoplethysmographic techniques for noninvasive blood pressure measurement in anesthetized cats. J Vet Intern Med 1995;9(6):405-414.
- Whittemore JC, Nystrom MR, Mawby DI. Effects of various factors on Doppler ultrasonographic measurements of radial and coccygeal arterial blood pressure in privately owned, conscious cats. JAVMA 2017;250(7):763-769.
- Broussard JD, Peterson ME, Fox PR. Changes in clinical and laboratory findings in cats with hyperthyroidism from 1983 to 1993. JAVMA 1995;206(3):302-305.
- McAtee B, Lidbury J. Continuing education: liver enzyme interpretation and liver function tests. Today Vet Pract 2017;7(3):28-38.
- Snyder PS, Levy JK, Salute ME, et al. Performance of serologic tests used to detect heartworm infection in cats. JAVMA 2000;216(5):693-700.
- Berdoulay P, Levy JK, Snyder PS, et al. Comparison of serological tests for the detection of natural heartworm infection in cats. JAAHA 2004;40(5):376-384.
- Jones S, Graham W, von Simson C, et al. Current feline guidelines for the prevention, diagnosis, and management of heartworm (Dirofilaria immitis) infection in cats. Batavia, IL: American Heartworm Society; 2014.
- Levy J, Crawford C, Hartmann K, et al. 2008 American Association of Feline Practitioners’ feline retrovirus management guidelines. J Feline Med Surg 2008;10(3):300-316.
- Westman ME, Malik R, Hall E, et al. Determining the feline immunodeficiency virus (FIV) status of FIV-vaccinated cats using point-of-care antibody kits. Comp Immunol Microbiol Infect Dis 2015;42:43-52.
- Gordon JM, Ehrhart EJ, Sisson DD, et al. Juvenile hyperthyroidism in a cat. JAAHA 2003;39(1):67-71.
- Peterson ME, Melian C, Nichols R. Measurement of serum concentrations of free thyroxine, total thyroxine, and total triiodothyronine in cats with hyperthyroidism and cats with nonthyroidal disease. JAVMA 2001;218(4):529-536.
- Goggin JM, Biller DS, Debey BM, et al. Ultrasonographic measurement of gastrointestinal wall thickness and the ultrasonographic appearance of the ileocolic region in healthy cats. JAAHA 2000;36(3):224-228.
- Lingard AE, Briscoe K, Beatty JA, et al. Low-grade alimentary lymphoma: clinicopathological findings and response to treatment in 17 cases. J Feline Med Surg 2009;11(8):692-700.
- Reed N, Gunn-Moore D, Simpson K. Cobalamin, folate and inorganic phosphate abnormalities in ill cats. J Feline Med Surg 2007;9(4):278-288.
- Dossin O. Laboratory tests for diagnosis of gastrointestinal and pancreatic diseases. Topics Compan Animal Med 2011;26(2):86-97.
- Ruaux CG, Steiner JM, Williams DA. Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia. J Vet Intern Med 2005;19(2):155-160.
- Cook AK, Suchodolski JS, Steiner JM, et al. The prevalence of hypocobalaminaemia in cats with spontaneous hyperthyroidism. J Small Animal Pract 2011;52(2):101-106.
- Geesaman BM, Whitehouse WH, Viviano KR. Serum cobalamin and methylmalonic acid concentrations in hyperthyroid cats before and after radioiodine treatment. J Vet Intern Med 2016;30(2):560-565.
- Suchodolski JS, Steiner JM. Laboratory assessment of gastrointestinal function. Clin Tech Small Animal Pract 2003;18(4):203-210.
- Simpson KW, Fyfe J, Cornetta A, et al. Subnormal concentrations of serum cobalamin (vitamin B12) in cats with gastrointestinal disease. J Vet Intern Med 2001;15(1):26-32.
- Xenoulis PG, Zoran DL, Fosgate GT, et al. Feline exocrine pancreatic insufficiency: a retrospective study of 150 cases. J Vet Intern Med 2016;30(6):1790-1797.
- Oppliger S, Hilbe M, Hartnack S, et al. Comparison of serum spec fPL() and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester assay in 60 cats using standardized assessment of pancreatic histology. J Vet Intern Med 2016;30(3):764-770.
- Oishi M, Ohno K, Sato T, et al. Measurement of feline lipase activity using a dry-chemistry assay with a triolein substrate and comparison with pancreas-specific lipase (Spec fPL(TM)). J Vet Med Sci 2015;77(11):1495-1497.
- Oppliger S, Hartnack S, Riond B, et al. Agreement of the serum spec fPL and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester lipase assay for the determination of serum lipase in cats with suspicion of pancreatitis. J Vet Intern Med 2013;27(5):1077-1082.
- Oppliger S, Hartnack S, Reusch CE, et al. Agreement of serum feline pancreas-specific lipase and colorimetric lipase assays with pancreatic ultrasonographic findings in cats with suspicion of pancreatitis: 161 cases (2008-2012). JAVMA 2014;244(9):1060-1065.
- Cook AK, Cunningham LY, Cowell AK, et al. Clinical evaluation of urine Histoplasma capsulatum antigen measurement in cats with suspected disseminated histoplasmosis. J Feline Med Surg 2012;14(8):512-515.
- Neiger R, Dieterich C, Burnens A, et al. Detection and prevalence of Helicobacter infection in pet cats. J Clin Microbiol 1998;36(3):634-637.
- Jalava K, Hielm S, Hirvi U, et al. Evaluation of a molecular identification scheme based on 23S rRNA gene polymorphisms for differentiating canine and feline gastric Helicobacter spp. Lett Appl Microbiol 1999;28(4):269-274.
- Norris CR, Marks SL, Eaton KA, et al. Healthy cats are commonly colonized with “Helicobacter heilmannii” that is associated with minimal gastritis. J Clin Microbiol 1999;37(1):189-194.
- Otto G, Hazell SH, Fox JG, et al. Animal and public health implications of gastric colonization of cats by Helicobacter-like organisms. J Clin Microbiol 1994;32(4):1043-1049.
- Papasouliotis K, Gruffydd-Jones TJ, Werrett G, et al. Occurrence of ‘gastric Helicobacter-like organisms’ in cats. Vet Rec 1997;140(14):369-370.
- Neiger R, Simpson KW. Helicobacter infection in dogs and cats: facts and fiction. J Vet Intern Med 2000;14(2):125-133.
- DeNovo R, Magne M, eds. Current concepts in the management of Helicobacter-associated gastritis. In: Proceedings of the 13th Annual Veterinary Medical Forum-American College of Veterinary Internal Medicine; 1995 Lake Buena Vista, Florida, USA.
- Khoshnegah J, Jamshidi S, Mohammadi M, et al. The efficacy and safety of long-term Helicobacter species quadruple therapy in asymptomatic cats with naturally acquired infection. J Feline Med Surg 2011;13(2):88-93.
- Jergens AE, Willard MD, Allenspach K. Maximizing the diagnostic utility of endoscopic biopsy in dogs and cats with gastrointestinal disease. Vet J 2016;214:50-60.
- Daniaux LA, Laurenson MP, Marks SL, et al. Ultrasonographic thickening of the muscularis propria in feline small intestinal small cell T-cell lymphoma and inflammatory bowel disease. J Feline Med Surg 2014;16(2):89-98.
- Zwingenberger AL, Marks SL, Baker TW, et al. Ultrasonographic evaluation of the muscularis propria in cats with diffuse small intestinal lymphoma or inflammatory bowel disease. J Vet Intern Med 2010;24(2):289-292.
- Laurenson MP, Skorupski KA, Moore PF, et al. Ultrasonography of intestinal mast cell tumors in the cat. Vet Radiol Ultrasound 2011;52(3):330-334.
- Winter MD, Londono L, Berry CR, et al. Ultrasonographic evaluation of relative gastrointestinal layer thickness in cats without clinical evidence of gastrointestinal tract disease. J Feline Med Surg 2014;16(2):118-124.
- Linton M, Nimmo JS, Norris JM, et al. Feline gastrointestinal eosinophilic sclerosing fibroplasia: 13 cases and review of an emerging clinical entity. J Feline Med Surg 2015;17(5):392-404.
- Willard MD, Mansell J, Fosgate GT, et al. Effect of sample quality on the sensitivity of endoscopic biopsy for detecting gastric and duodenal lesions in dogs and cats. J Vet Intern Med 2008;22(5):1084-1089.
- Willard MD, Jergens AE, Duncan RB, et al. Interobserver variation among histopathologic evaluations of intestinal tissues from dogs and cats. JAVMA 2002;220(8):1177-1182.
- Kiupel M, Smedley RC, Pfent C, et al. Diagnostic algorithm to differentiate lymphoma from inflammation in feline small intestinal biopsy samples. Vet Pathol 2011;48(1):212-222.
- Moore PF, Rodriguez-Bertos A, Kass PH. Feline gastrointestinal lymphoma: mucosal architecture, immunophenotype, and molecular clonality. Vet Pathol 2012;49(4):658-668.
- Pohlman LM, Higginbotham ML, Welles EG, et al. Immunophenotypic and histologic classification of 50 cases of feline gastrointestinal lymphoma. Vet Pathol 2009;46(2):259-268.
- Gabor LJ, Canfield PJ, Malik R. Immunophenotypic and histological characterisation of 109 cases of feline lymphosarcoma. Austral Vet J 1999;77(7):436-441.
- Scott KD, Zoran DL, Mansell J, et al. Utility of endoscopic biopsies of the duodenum and ileum for diagnosis of inflammatory bowel disease and small cell lymphoma in cats. J Vet Intern Med 2011;25(6):1253-1257.