Diagnosis and treatment of acute pancreatitis in dogs and cats


Pancreatitis in dogs is a disease due to inflammation of the pancreas.. There are many causes that can produce it, and the dogs that suffer from it suffer a lot of abdominal pain. This is a problem that is sometimes incurable and may require lifelong treatment, but other times dogs will have a chance to recover. Achieving or not healing will depend on the involvement of the organ.

If we know the symptoms of the disease we will be able to detect it before and give it faster treatment, improving the prognosis for our best friend.

What is the pancreas and what is it for?

Understanding the function of the pancreas will help us better understand the symptoms we find in animals with pancreatitis. The pancreas is an organ that is found in the abdomen and It is responsible for producing pancreatic juice, a substance that contains digestive enzymes. Enzymes are proteins that allow us to digest and process the proteins and fats of the food we eat.

further It is also responsible for the production of several essential hormones for proper functioning of the entire body, among which is insulin.

Acute pancreatitis

We will talk about acute pancreatitis when the symptoms appear suddenly. It is a serious and very painful disease, so it is important to go to the veterinarian as soon as possible if we detect your symptoms. Many times a rapid detection and action on our part can improve the prognosis of our dog.

Chronic pancreatitis

It usually appears progressively, the symptoms do not appear suddenly as in the previous case. It may be a consequence of acute pancreatitis, and damage to the pancreas will be irreversible in most cases. The state of the animal will get worse over time.

Causes of pancreatitis in dogs

Pancreatitis is a disease that can appear for many causes. Is more common in adult dogs of 4 or 5 years, mainly in females, obese animals and in small breeds like the Yorkshire Terrier, the Miniature Schnauzer and the Dachshund).

The factors that predispose to the onset of the disease are:

    Too fat diets: Before a habitual consumption of a diet with a cant> Symptoms of pancreatitis in dogs

The most common symptom is to see that our dog rejects food. Also in case you eat can throw up food by the end. It is also very common for pancreatitis in dogs to cause high fever, reaching 40 or 41 ° C.

It is a very painful disease, and therefore the dog will give us signs of great abdominal pain. We can see how the muscles of the abdomen are very tense and the animal is stiff, decayed and very apathetic, because each gesture involves a lot of pain.

Another common symptom is a doughy, yellowish, fatty and sometimes sometimes bloody and foamy stools. These characteristics are due to poor digestion of dietary fat. In addition, vomiting and diarrhea can cause dehydration, and the dog may be very thirsty.

In cases of chronic pancreatitis, the symptoms are more varied, and as they appear progressively, they can sometimes go unnoticed. We can find digestive problems that are not solved and reappear over time. Also the dog lose weight despite eating a proper ration because you can't digest food well. Finally we will see feces with a yellowish or grayish coloration, pasty and very pestilent.


In some cases the treatment may allow the cure of pancreatitis in the dog, but in other animals it may be necessary to administer medication throughout its life.

The treatment of pancreatitis should always be prescribed by a veterinarian. It usually consists of a fasting between 24 and 48 hours, since food promotes the production of more enzymes in the pancreas and therefore increases the damage that the organ receives. It is also recommended to avoid any stimulus that the dog relates to food, as it can also increase the production of digestive enzymes.

Can also be applied fluid therapy to rehydrate the animal and compensate for diarrhea and vomiting losses. The lack of fluids can cause problems in other organs such as the liver and kidneys and complicate the situation.

They can also be administered antibiotics to avoid complications from bacterial infections, and to reduce the pain suffered by the dog with pancreatitis can also be used analgesics and anti-inflammatories.

In the event that pancreatitis is caused by a bad diet it will be important correct dog nutrition and move on to a less fatty feed. If the animal is obese, it is highly recommended to start working to lose weightIt is an important risk factor for pancreatitis and can cause relapses. Sometimes it may be necessary to administer pancreatic enzymes with food to facilitate digestion.

Etiology and pathogenesis

The etiology and pathogenesis of spontaneous pancreatitis is poorly understood. Table 1 summarizes the major factors that have been implicated (by association) as causes of acute pancretitis in dogs and cats and experimental evidence to support their commitment.

Table 1. Factors associated with the development of acute pancreatitis in dogs and cats.

Abnormal lipid profiles

High fat diet

IV Free fatty acids

Fat >> Protein diet

Ethionine Supplements

Concomitant biliary disease (cats)

Calcium infusion

Calcium infusion

+ Disc surgery

Increased CCK sensitivity

Hyperplasia of the pancreatic duct

Miniature Schnauzer, Mini Poodle, Terriers, non-sport dogs

Cats: hepatic trematodes, Toxoplasma, PIF

Hypothyroidism, diabetes mellitus

Only recently has acute pancreatitis been considered a significant entity in cats. It is the authors' impression that pancreatitis in cats seems more chronically active and severe than in most dogs. While pancreatitis in cats has been diagnosed as the sole or predominant entity of disease in cats at necropsy, it has also been alternately associated with diseases in other organs, such as in the liver (cholestasis, cholangiohepatitis, hydropic change, lipidosis severe), in the kidney (mild or severe nephritis), in the endocrine pancreas (diabetes mellitus), in the lungs (pulmonary thrombosis) and in the intestines (inflammation, ulceration). Spills in the pleural and peritoneal cavity have also been noted. At this time it is unclear whether these non-pancreatic abnormalities appear as a consequence of pancreatitis, or are associated with or unrelated to the disease processes that cause pancreatitis.

Regardless of the initiating cause of pancreatitis, it is generally believed to occur when digestive enzymes are activated prematurely in the pancreas. Experimental pancreatic hyperstimulation with cholecystokinin (CCK: or its cerulein analogue), dietary supplements with ethionine, and obstruction of the pancreatic duct lead to the formation of large intracellular vacuoles in acinar cells. It is thought that the formation of vacuoles is a consequence of the alteration of cytogen exocytosis and the abnormal intracellular trafficking of digestive and lysosomal enzymes. These subcellular alterations are considered to precipitate intracellular activation of digestive enzymes. Edematous pancreatitis induced by CCK hyperstimulation in dogs is characterized by a burst of rapid but self-limiting trypsinogen activation. It is to emphasize that pancreatic necrosis in humans is associated with the activation of persistent trypsinogen, therefore it may be the ability of the pancreas to limit the activation of trypsinogen which causes edematous pancreatitis not to reach necrotizing pancreatitis. Pancreatic hyperstimulation can also be of direct relevance in pancreatitis that occurs naturally in dogs and cats. CCK is normally released by cells in the duodenum in response to fat and intraluminal amino acids and coordinates and stimulates pancreatic secretion and contraction of the gallbladder during digestion. It is possible that high-fat diets exert their effects through the excessive release of cholecystokinin and that hypercalcemia, organophosphates and high levels of circulating glucocorticoids also facilitate or cause pancreatic hyperstimulation, however, this has not been proven.

Pancreatic inflammation is often a self-limiting process, but in some animals the flow of pancreatic blood and the migration of leukocytes and platelets to the inflamed pancreas can cause a progression to pancreatic necrosis. A secondary infection may appear by bacterial translocation of the intestine. The release of active pancreatic enzymes and inflammatory mediators of the inflamed pancreas, such as Tumor Necrosis Factor a (TNF- a), interleukin-1 (IL-1) and platelet activating factor (PAF), extend the severity of pancreatic inflammation, and adversely affect the function of many organs (systemic inflammatory response), and cause disorders of fluid, electrolyte and acid-base balance. What separates mild pancreatitis from severe and life-threatening is the development of multisystemic abnormalities.

A more extensive study of the cellular mechanisms that govern the secretion and enzymatic activation, the recruitment to the leukocyte and platelet pancreas, the bacterial translocation and the development of a systemic inflammatory response in pancreatitis will provide, it is expected, information that will be useful in the Treatment of acute pancreatitis in patients in the future.


There is currently no single specific test for pancreatitis in dogs and cats and the diagnosis is based on a combination of compatible clinical, clinicopathological and imaging findings. To confirm the diagnosis and to distinguish the inflammation from the neoplasm, surgical biopsy may be necessary.

Physical exam

The physical findings in dogs with acute pancreatitis are highly variable and range from depression to mild dehydration with signs of abdominal pain, to acute abdominal crisis with shock (tachycardia, prolonged capillary filling time, viscous mucous membranes, hypothermia), petechiae, jaundice and ascites. In some dogs an abdominal mass can be palpated.

In cats, dehydration and hypothermia have been commonly observed. Jaundice may also occur. Abdominal pain does not occur frequently. The presence of a palpable cranial abdominal mass or abdominal pain has been reported in a quarter or a third of cats in some clinical series and in cats with experimental and trauma-induced pancreatitis.

Diagnostic approach and differential diagnosis

The differential diagnosis of acute pancreatitis in dogs usually focuses on the problems of vomiting and abdominal pain. In dogs with vomiting, the initial approach is to distinguish causes of self-limiting vomiting from more severe ones based on physical findings and a minimal database (eg hematocrit, total proteins, azotemia, urine tests, sodium and potassium concentrations in plasma ). When vomiting is associated with systemic signs of disease, or it is persistent, the clinician has to differentiate the metabolic, infectious, polysystemic, toxic and neurological causes from intra-abdominal. This is usually achieved on the basis of combined historical and clinical findings coupled with a minimal database and evaluation of the hematological and serum chemical profile, urine analysis and abdominal radiographs. He often requests the measurement of serum amylases and lipases in routine serum chemical profiles. Frequently, additional procedures are performed based on the results of these initial examinations such as ultrasonography, abdominal paracentesis or immunoreactivity tests of a trypsin analogue (TLI) that help distinguish pancreatitis from other causes of intra-abdominal vomiting.

In those in which abdominal pain is the greatest finding, local abnormalities such as abdominal distension can be searched quickly with x-rays, ultrasonography and paracentesis while giving a supportive treatment based on physical findings and a minimum database and the results of the serum chemical profile, hematology and urine analysis are expected. Abdominal pain of any intra-abdominal structure may appear. The distinction between musculoskeletal disorders such as discoespondylitis and disc prolapse and abdominal causes of pain can be hindered.

It is noted that in dogs with experimental acute pancreatitis diarrhea, which in some cases was bloody, was a more frequent sign than vomiting. Acute pancreatitis and its complications (infections, abscess formation and pseudocysts) should also be considered in the differential diagnosis of jaundice and pyrexia. Some dogs with pancreatitis exhibit few local clinical signs. The diagnosis in these animals requires a high index of suspicion and the use of versatile diagnostic tests such as ultrasonography.

The most common complaints that appear in cats are lethargy, anorexia and weight loss. When local signs or findings such as vomiting, jaundice, diarrhea, abdominal pain, abdominal mass are found, polyuria or polydipsia should be sought. Rarely, an antemortem diagnosis of acute pancreatitis is made, so its full significance as a cause of these problems is not clear.

In those in which vomiting occurs, the diagnosis is approximated by localized findings such as pain or masses and eliminating infectious, parasitic, metabolic and gastrointestinal causes. Hyperthyroidism as a cause should be eliminated in older cats by determining the total serum T4 concentration. Elevated liver enzymes, hyperbilirubinemia, hyperglycemia and glycosuria are frequently found in cats with acute pancreatitis, so pancreatitis should be highly considered in these cats.

The diagnostic approach to feline jaundice is, in principle, to eliminate pre-hepatic causes and then to look for hepatic or post-hepatic causes. Some studies have shown the association of acute pancreatitis with high-mortality lipidosis, cholangiohepatitis and inflammatory bowel disease. A high index of suspicion for pancreatitis should be adopted in cats with liver, biliary or intestinal diseases. Cats with a confirmed diagnosis of hepatic lipidosis who have peritoneal effusions are also suspected of having pancreatitis.

In some cats, pancreatitis may be the cause of diabetes mellitus, but the actual association between these diseases is unclear. One study suggests that cats with pancreatitis and diabetes mellitus are insulin sensitive. Transient euglycemia and reduced insulin requirements after removing a pancreatic abscess suggest that inflammation or pancreatic infection may aggravate diabetes mellitus in cats. A case of transient diabetes mellitus was also reported in a cat suspected of suffering from pancreatitis.

When there is a high index of suspicion of pancreatitis, ultrasonography and enzymology should be used initially (feline TLI test, being careful with cats with inflammatory bowel disease - see below) to help detect pancreatic inflammation. To reach a definitive diagnosis, a pancreatic biopsy is required.


It is highly variable, ranging from moderate neutrophilia and slightly elevated hematocrit through leukocytosis with a left turn, thrombocytopenia, anemia and leukopenia with a non-regenerative left turn. If thrombocytopenia is detected, blood coagulation tests (OSPT, APTT, FDP) are performed to determine if the patient has disseminated intravascular coagulopathy (CID). When antithrombin III measurement is available it is useful in the early diagnosis of CID.

The most common findings in cats with pancreatitis are a mild anemia that may be non-regenerative, and a leukocytosis that is not usually accompanied by a left turn.

Serum biochemistry

Serum biochemical abnormalities vary and include azotemia (pre-renal and renal), increased liver enzymes (ALT, AST, AP), hyperbilirubinemia, lipemia, hyperglycemia, hypoproteinemia, hypocalcemia, metabolic acidosis and variable (usually decreased) alterations in sodium, potassium and chloride

Increases in ALT, AP, bilirubin, cholesterol and glucose, hypokalemia and hypocalcemia are common. Azotemia is present with variations.

Urine analysis

It allows azotemia to be characterized as renal or pre-renal. Transient proteinuria occurs in some dogs with acute pancreatitis, possibly as a result of glomerular damage mediated by pancreatic enzymes. The absence of white blood cells and bacteria helps rule out pyelonephritis as a cause of abdominal pain. The presence of glucose or ketonuria should boost the consideration of diabetes mellitus.

Specific pancreatic enzymes

Classically, elevations in serum amylase and lipase activity have been used as indicators of pancreatic inflammation in dogs. However, these tests are not very accurate because dogs with non-pancreatic disorders may have elevated enzyme activities. This can occur because both amylase and lipase are normally present in other organs and their serum activities can be increased with non-pancreatic disorders including intestinal obstruction (amylase), administration of corticosteroids (lipase) and kidney disease (both enzymes). Dogs with confirmed pancreatitis may also have normal amylase and lipase activity. For example, in two recent case series of dogs with histologically confirmed pancreatitis, lipase was normal in 28 and 61% of dogs, and amylase was normal in 31 and 47% of dogs. This may be due to the depletion of enzymes, thrombosis of pancreatic vessels, the presence of inhibitors, alterations in activity and perhaps increased clearance. It seems correct to express that amylase and lipase have no utility in diagnosing pancreatitis in cats.

These limitations have stimulated the development of assays for enzymes considered pancreatic in origin. The TLI (Trypsin-like immunoreactivity) is a candidate. This species-specific immunoassay measures the trypsinogen circulating in healthy individuals and the trypsinogen and trypsin in those with pancreatitis.

In dogs, circulating TLI is suppressed by a pancreotomy, and extremely low concentrations appear in exocrine pancreatic insufficiency (PID). Experimental and clinical studies have documented high levels of TLI in dogs with acute pancreatitis. Therefore, TLI is considered a useful indicator of pancreatic masses and potentially inflammation. Non-pancreatic diseases such as kidney and possibly corticosteroids can increase TLI in circulation. It is important to note that the usefulness of TLI for diagnosing spontaneous pancreatitis in dogs has not been thoroughly evaluated, and the author has observed normal and subnormal concentrations in dogs with pancreatitis.

A TLI test for cats has also been developed. Cats with exocrine pancreatic insufficiency and some cats with spontaneous pancreatitis have abnormal TLI concentrations. An increased use of this test indicates that high levels of TLI may appear in the presence of normal pancreatic histology in cats with inflammatory bowel disease or lymphomas. The reason for this is not clear. Non-pancreatic diseases such as kidney and possibly corticosteroids can also increase TLI circulation in cats.

At present it seems correct to conclude that the TLI test is highly accurate in differentiating PID from minor intestinal diseases. It seems less accurate to detect pancreatitis. This is not surprising since pancreatitis is a very dynamic disease, and it can influence the synthesis, secretion, elimination and activity of circulating marker enzymes such as TLI. The tissue specificity of TLI makes it an attractive alternative to amylase and lipase in dogs, and is currently the only useful indicator in the cat.

Bone scan

Radiographic findings in dogs and cats with acute pancreatitis may include loss of serous detail, increased opacity in the right cranial quadrant of the abdomen, ventral displacement of the duodenum or to the right, dilated duodenum (hypomotility) and caudal displacement of the transverse large intestine Dotted calcification is occasionally identified in dogs with long-standing pancreatitis, this indicates saponification of mesenteric fat around the pancreas. Although radiographic signs are often absent, and not specific, radiography remains a useful diagnostic method for pancreatitis mostly because it allows the detection of other abnormalities that can cause similar signs (eg gastric foreign body or intestinal obstruction). Radiography is a logical first diagnostic imaging option for animals with gastrointestinal signs. Negative or equivocal radiographic findings may be followed by ultrasonography or a gastrointestinal contrast study.

Chest x-rays may allow the detection of pleural fluid, edema or pneumonia that have been associated with pancreatitis in dogs and cats.


The use of ultrasound to detect pancreatic lesions is perhaps one of the most significant advances in the diagnosis of acute pancreatitis in dogs and cats. Ultrasound findings include enlarged and hypoechoic pancreas, cavitary lesions such as abscesses or pseudocysts, dilated pancreatic duct, inflamed duodenum, biliary dilation and peritoneal fluid. A recent study of dogs with acute acute pancreatitis indicated that ultrasound corroborated pancreatitis in 23/34 dogs. The findings in cats are also encouraging, but they emphasize that a normal ultrasound does not eliminate pancreatitis. The clinician should be careful to consider other diagnoses other than pancreatitis, e.g. pancreatic neoplasia, pancreatic edema (associated with hypoproteinemia or portal hypertension) and enlarged peri-pancreatic structures that may have an ultrasonographic appearance identical to pancreatitis. Fine needle aspirations of cavitary lesions may be useful to distinguish abscesses from pseudocysts.

Abdominal paracentesis

A peritoneal fluid test can help detect several causes of acute abdominal signs such as pancreatitis, abdominal perforation or herniated bile duct. The accumulation of fluid in the abdomen or in the pleural cavity in cats with acute pancreatitis has been found in various ways. One study found a spill in the abdomen or chest in 17/40 cats, in another study, in the abdomen in 5/5 cats with liver lipidosis and pancreatitis, and in another in the abdomen in 2/8 cats.

Prognostic Indicators

Stratifying the severity of pancreatitis is useful in deciding the aggressiveness that should be had with medical and nutritional support, and in offering a prognosis. Severe pancreatitis requires aggressive support and includes a cautious prognosis, while mild pancreatitis often responds to short-term symptomatic therapies and has a good prognosis. The presence of shock or abnormalities such as oliguria, azotemia, jaundice, markedly elevated transaminases, hypocalcemia, hypoglycemia, hypoproteinemia, acidosis, leukocytosis, decreased hematocrit, thrombocytopenia and CID should be considered as likely indicators of severe pancreatitis in dogs and cats.

The measurement of components of the systemic inflammatory response such as FNT- a, C-reactive protein, and IL-6 can also give information on the severity of pancreatitis in dogs and cats, and in the future may lead to the administration of specific antagonists. of this answer.

Indicators that are potentially useful in the diagnosis and prognosis of pancreatitis include trypsinogen peptide activation assays (TAP), trypsin compound with inhibitors and phospholipase A2. TAP has been shown to accurately predict severity in humans with pancreatitis. This peptide is released when trypsinogen, as a specific enzyme in the pancreas, becomes its active form and rapidly accumulates in the urine and plasma of dogs and cats with experimental acute pancreatitis. Phospholipase A2 rises in dogs with severe pancreatitis. A wider confirmation of these markers is required before clinical application.

In humans, a morphological evaluation of severity is performed using contrast enhanced computed tomography (EC-CT). In those found lack of pancreatic perfusion, eg. necrosis, fine needle aspiration is used to distinguish septic from sterile necrosis. A substantially reduced mortality has been achieved through the detection and surgical treatment of people with septic necrosis. The lack of availability of CT has restricted veterinary application to date, but the relative accessibility of canine and feline pancreas to ultrasound-guided needle aspiration supports the potential adoption of a similar approach.

Initial handling

The initial medical management of dogs and cats with acute pancreatitis is invariably initiated before the diagnosis is confirmed and is based on the clinical findings present and the results of an initial database. Those who encounter dehydration or hypovolemia are maintained with intravenous fluid therapy. The first common options are Ringer's solution with lactate or 0.9% NaCl. When necessary, potassium and glucose supplements should be given. The type of fluid must be adapted based on electrolyte and pH measurements to restore the normal electrolyte and acid-base balance. For example, crystalloid solutions such as Ringer's with lactate are supplied in an amount that provides maintenance and replaces both deficits and progressive losses over a period greater than 24 hours, to dogs with a history of vomiting that are slightly dehydrated. Dogs with signs of shock require more aggressive help. The volume deficit can be replaced with crystalloid solutions in an initial amount of 60-90ml / kg / h, and then adapted to maintain tissue perfusion and hydration.

In the presence of hypoproteinemia or shock, plasma (20 ml / kg i.v.) or colloids (eg degraded gelatin, Haemaccel®, Hoechst Animal Health, Milton Keynes at 10-20 ml / kg / day i.v.) may be indicated. Colloids such as dextran 70 and hetastarch can also have antithrombotic effects that help maintain microcirculation.

Insulin therapy begins in diabetic patients. In cats, stress hyperglycemia must be differentiated from diabetes mellitus.

When vomiting is a problem, oral intake is restricted, when vomiting is persistent or severe, antiemetics (metoclopramide or chlorpromazine), and antacids (eg famotidine) are prescribed.

In patients with shock, fever, diabetes mellitus or evidence of GI barrier failure, the use of broad-spectrum prophylactic antibiotics (eg amoxicillin ± enrofloxacin, depending on severity) may be justified.

An important aspect in the care of animals with pancreatitis is analgesia. It can be controlled using opioids such as buprenorphine (0.005-0.01 mg / kg SC every 6-12 hours) or oxymorphone (0.05-0.1 mg / kg in cats, 0.1-0.2 mg / kg in dogs IM, SC every 1-3 hours). It may be necessary to administer low-dose sedatives such as acepromazine (0.01 mg / kg IM) to patients who become dysphoric after opioids. It should be borne in mind that buprenorphine is a partial agonist and may antagonize the administration of more potent analgesics in animals with severe pain. A transdermal fentanyl patch (Duragesic, Janssen) applied to an area of ​​bare and clean skin is a good way to provide a longer duration of analgesia in dogs (10-20kg, 50 µg / h patch every 72 hours) and in cats (patch of 25 µg / h every 118hs). Adequate fentanyl levels are not maintained for 6-48 hours after application, so another analgesic should be administered in the short term. The author is careful to use nonsteroidal analgesics in patients with acute pancreatitis due to the relationships with GI ulceration, renal failure and potentially hepatotoxicity.

Specific therapy

Once the diagnosis of pancreatitis is confirmed, a potentially more specific therapy can be used. Most dogs with acute pancreatitis respond to fluid therapy and total fasting for 48 hours. Hence, the specific therapy is usually reserved for dogs that do not respond to fluid therapy or to those with signs of multiorganic or CID epidemic complications. Pancreatitis in cats seems to be more chronically active and severe than in dogs, so cats with a confirmed diagnosis of pancreatitis generally need more help than most dogs.

The specific treatment of pancreatitis has developed along two lines: 1. Stopping a wider pancreatitis from happening. 2. Limitando las consecuencias locales y sistémicas de la pancreatitis. Las terapias para inhibir la secreción pancreática (ej. glucagón, somatostatina) o la activación intracelular de proteasas (ej. gabexato mesilato) que han sido beneficiosas al mejorar la severidad de pancreatitis experimentales, han mostrado pocas ventajas en el tratamiento de pacientes con pancreatitis espontánea. Esta falta de éxito está relacionada probablemente, con la habilidad de escoger el momento oportuno de la terapia en relación al desarrollo de la pancreatitis, la terapia experimental es usualmente iniciada antes o poco después de la inducción de la pancreatitis mientras que la mayoría de los pacientes no se presentan hasta 24-48hrs del comienzo de la pancreatitis. El sustento de esta hipótesis está dado por la eficacia de la somatostatina y el gabexato mesilato en la reducción de la pancreatitis en personas sometidas a procedimientos electivos tales como la colecistopancreatografía endoscópica retrógrada que están asociados a la pancreatitis.

La falta de éxito con la inhibición de la progresión de la pancreatitis espontánea ha llevado a poner mayor énfasis en la limitación del daño, aliviando los efectos de los mediadores inflamatorios o de las enzimas pancreáticas en el paciente y manteniendo la perfusión pancreática.

Se deben monitorear las anormal >a es promisoria para el futuro.

Se ha reportado que los extractos orales de enzima pancreática reducen el dolor en humanos con pancreatitis crónica, aunque esto es controvertido. Son menos probables de ser efectivos en perros ya que parecen no tener un sistema de retroalimentación negativo mediado por proteasas.

Manejo dietario

Las recomendaciones precisas del manejo dietario de la pancreatitis aguda se ven entorpecidas por la ausencia de estudios controlados sobre el mismo.

En los perros sospechosos de padecer pancreatitis aguda usualmente no se administra una ingesta oral durante las primeras 48 hs y luego se reintroduce gradualmente, si la tolera. La razón de no dar nada por boca aún cuando no haya vómito es para "hacer descansar al páncreas" disminuyendo la estimulación pancreática. Como las grasas y los aminoácidos son potentes estimuladores de la secreción de enzimas pancreáticas, sus efectos inicialmente se evitan alimentando con una dieta alta en carbohidratos y luego aumentando gradualmente el contenido de grasa y proteínas durante el período de recuperación (la primera y segunda semana luego del inicio). Una restricción de grasa continuada es usualmente recomendada para perros que han tenido pancreatitis y se basa en observaciones clínicas y experimentales, que sugieren una asociación entre comidas con alto contenido graso, hiperlipidemia y "alto nivel" de nutrición y la pancreatitis. El contenido proteico de la dieta también puede ser importante ya que los perros que se alimentan con una dieta deficiente en colina pero suplementada en etionina, o una dieta con alto contenido graso y restringida en proteínas desarrollan pancreatitis.

Estrategias alternativas para minimizar la estimulación pancreática incluyen nutrición parenteral total y alimentación distal a la zona de liberación de CCK vía un tubo de yeyunostomía, pero estas opciones usualmente se reservan para perros con vómitos persistentes o pancreatitis severa. Estudios recientes en personas indican que la pancreatitis aguda puede ser exacerbada por una administración temprana de nutrición parenteral total (antes de 5 días), y que la nutrición enteral, administrada vía un tubo de naso-yeyunostomía, puede atenuar la respuesta inflamatoria sistémica y puede disminuir las complicaciones.

En contraste con los perros, donde predominan los vómitos y los dolores abdominales, la pancreatitis en los gatos se asocia usualmente con la anorexia y la pérdida de peso. La presencia de anorexia y pérdida de peso en gatos con pancreatitis puede ser un factor significativo que contribuye a su pobre pronóstico. El ayuno prolongado (> 3 días) para evitar la estimulación pancreática puede servir sólo para agravar la desnutrición. El clínico está frente al dilema de tener que proveer ayuda nutricional para prevenir o revertir la desnutrición y la lipidosis hepática, y hacer ayunar al paciente para prevenir la estimulación pancreática. El empleo quirúrgico o endoscópico de un tubo de gastrostomía o esofagostomía puede evitar la anorexia cuando el vómito no es un problema. Un dogma actual sugiere que se debe alimentar con una dieta que limite la estimulación pancreática y provea nutrientes adecuados. Sin embargo este ideal puede ser difícil de alcanzar ya que los gatos están fisiológicamente adaptados a dietas ricas en grasas y proteínas, y la mayoría de los alimentos balanceados para gatos contienen entre 30-60% de grasa sobre una base de energía. El autor ha tenido éxito al alimentar con dietas comerciales de mantenimiento o dietas intestinales a través de un tubo de gastrostomía. El Feline Clinicare, con 30% de proteínas y 45% de grasa sobre una base de energía también ha sido usado exitosamente.

Como se vió más arriba, el empleo quirúrgico o endoscópico de un tubo de yeyunostomía y la alimentación con una dieta líquida distal al duodeno, y la nutrición parenteral total son otras soluciones para proveer una nutrición balanceada y minimizar la secreción pancreática, que probaron ser útiles en casos refractarios.

Monitoreo del paciente

Los pacientes con pancreatitis sospechada o confirmada deben ser monitoreados cuidadosamente para permitir una detección temprana de shock u otras anormalidades sistémicas. El control mínimo para pacientes estables incluye evaluación regular de signos vitales y del balance de fluídos y electrolitos. En aquellos con anormalidades sistémicas, la inspección debería ser más agresiva y podría incluir signos vitales, peso, hematocrito, proteínas totales, ingesta y eliminación de líquido, presión sanguínea (venosa central y arterial), electrolitos y glucosa, estado ácido-base, plaquetas y estado de coagulación. El monitoreo de la amilasa, lipasa o TLI en una base secuenciada, también puede ayudar a confirmar la resolución o la progresión de la inflamación pancreática.

Una aspiración del páncreas con aguja fina guiada por ultrasonido puede permitir la detección de una necrosis pancreática séptica. La ultrasonografía también puede permitir la detección de consecuencias de pancreatitis aguda postergadas, como formación de abscesos y pseudoquistes y obstrucción biliar.

Surgical intervention

La cirugía está potencialmente indicada para remover tejido desvitalizado en pacientes con necrosis pancreática séptica y para investigar y aliviar la obstrucción biliar persistente. Otra indicación para la cirugía es la remoción o el drenaje de abscesos. La resección o el drenaje quirúrgico de pseudoquistes pancreáticos no siempre es necesario ya que éstos se pueden solucionar espontáneamente o siguiendo el drenaje percutáneo. La pancreatitis recurrente o insensible a un tratamiento también puede requerir una cirugía para confirmar un diagnóstico y para descartar cáncer pancreático.

La cirugía a menudo ha sido necesaria para confirmar un diagnóstico antemormem de pancreatitis aguda en gatos. El aumento en la aplicación de la ultrasonografía y medición de TLI, ha llevado a disminuir la dependencia de la cirugía en gatos con alto TLI y anormalidades sonográficas. Sin embargo, se debe enfatizar que los gatos con pancreatitis a menudo tienen anormalidades concomitantes en otros sistemas orgánicos, ej. hígado e intestino, y se puede indicar una biopsia de éstos órganos y del páncreas para optimizar el diagnóstico y el tratamiento. La euglucemia transitoria y los requerimientos reducidos de insulina que se notaron luego de la remoción de un absceso pancreático en un gato, sugieren que la intervención quirúrgica puede ser beneficiosa en estos casos.

¿Qué es la pancreatitis canina?

El término pancreatitis significa de forma literal inflamación del páncreas, pero debido a las importantes funciones de este órgano, esta afección va mucho más allá de un simple estado inflamatorio. Para comprender los daños que se producen en el páncreas conozcamos antes una de sus principales funciones.

El páncreas sintetiza enzimas digestivas que están preparadas para activarse en el estómago y facilitar la digestión de los alimentos, en cambio, cuando existe pancreatitis, estas enzimas se activan en el páncreas y provocan la digestión del mismo, lo que causa una enorme inflamación en este órgano y daños que en ocasiones pueden llegar a ser irreparables. Podemos distinguir dos tipos de pancreatitis canina:

    Pancreatitis aguda: Los síntomas se presentan de forma súbita y son muy defin >

¿Cuáles son las causas de la pancreatitis canina?

No se conoce cuál es la causa exacta de la pancreatitis canina pero si se sabe que la aparición de esta enfermedad está estrechamente vinculada con la nutrición, debido a que los siguientes factores se han identificado muy claramente como factores de riesgo:

  • Perros con obesidad
  • Dietas con exceso de grasas
  • Alimentación con alto porcentaje de proteínas

Además de las causas relacionadas con la alimentación del perro, la pancreatitis también puede ser producida como consecuencia de otras enfermedades como las siguientes: cáncer, diabetes, problemas renales, infecciones o enfermedades cardiovasculares.

Síntomas de la pancreatitis en perros

Los siguientes síntomas nos deben alertar pues si los observamos en nuestra mascota nos pueden estar indicando la presencia de pancreatitis:

  • Vomiting
  • Loss of appetite
  • Weightloss
  • Diarrhea
  • Abdominal swelling
  • Apathy

Será imprescindible acudir al veterinario para que este realice un diagnóstico, si bien no existe un test diagnóstico específico, el veterinario realizará un análisis de sangre y heces así como una ecografía para confirmar el diagnóstico de la pancreatitis y valorar los daños que se han producido sobre el órgano.


El pronóstico para perros con pancreatitis aguda leve es bueno. Se asocia la pancreatitis severa o recurrente con un pronóstico cauteloso.

El pronóstico para la pancreatitis aguda en gatos siempre debe ser considerado cauteloso. Cuando se presenta una lipidosis hepática extensiva o se diagnostica una pancreatitis supurativa el pronóstico es pobre.

Bibliografía complementaria sugerida

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Hess RS, Kass PH, Shofer FS, Van Winkle TJ, Washabau RJ (1999). Evaluation of ri sk factors for fatal acute pancreatitis in dogs. Journal of the American Veterin ary Medical Association 214:46-51.

Hess RS, Saunders HM, Van Winkle TJ, Shofer FS, Washabau RJ (1998). Clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in dogs with fatal acute pancreatitis: 70 cases (1986-1995). Journal of the American Veterinar y Medical Association 213: 665-668.

Hill RC, Van Winkle TJ. Acute necrotizing and acute suppurative pancreatitis in the cat: a retrospective study of 40 cases (1976-1989). J Vet Intern Med 1993, 7 : 25-33.

Johnson, S.E. (1992) Fluid therapy for gastrointestinal, pancreatic, and hepatic disease. In: DiBartola, S.P. (ed) Fluid therapy in small animal practice. Saund ers, Philadelphia, pp507-528.

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Lamb C.R. & Simpson K.W., Boswood A., Matthewman L.A. (1995). Ultrasonography of pancreatic neoplasia in the dog: retrospective review of 16 cases. The Veterina ry Record 137, 65-68.

Lucena R, Ginel PJ, Novales M, Molleda JM. (1999). Effects of dexamethasone administration on serum trypsin-like immunoreactivity in healthy dogs. American Journal of Veterinary Research 60: 1357-1359.

Macintire DK (1988). The acute abdomen - differential diagnosis and management . Seminars in Veterinary Medicine and Surgery Small Animal 3, 302-310.

Murtaugh, RJ. (1987) Acute pancreatitis: diagnostic dilemmas. Seminars in Veterinary Medicine and Surgery (Small Animal) 2, 282-295.

Ruaux CG, Atwell RB.(1998). A severity score for spontaneous canine acute pancreatitis. Australian Veterinary Journal 76: 804-808.

Salisbury SK et al (1988). Pancreatic abscess in dogs: six cases (1978-1986). JAVMA 193,1104

Saunders HM (1991) Ultrasonography of the pancreas. In Problems in Veterinary Medicine Vol 3, Ultrasound. Ed PM Kaplan. Philadelphia, WB Saunders p583.

Simpson K.W., Shiroma J.T., Biller D.S., Wicks J., Johnson S.E., Dimski D., Chew D. (1994). Antemortem diagnosis of pancreatitis in four cats. Journal of Small Animal Practice 35, 93-99.

Steinberg WM, Schlesselman SE (1987). Treatment of acute pancreatitis: Comparison of animal and human studies. Gastroenterlogy 93, 1420-1426.