Loobani AcademyAbstract
Pancreatitis is an inflammation of the pancreas. A female,pomeranian dog was presentd with sign of depression and vomiting of 3 days duration following episode of dietary indiscretion.Clinical signs,previous medical history, and diagnostic test supported diagnosis acute pancreatitis. Specific and supportive treatment was instituted,and clinical signs resolved 3 days after presentation.
Key words:Vomiting,Pain management,shock
1. Bases information
Name: BAI BAI
Breed: Pomeranian dog
Sex: Female (castrated)
Age: 3 years old
Body weight: 3.7kg
History: Dietary habit with meat and mankind food for a long tern
2. Before therapy
At the first visit, the dog began to show symptoms of lethargy and weakness, especially weakness in the pelvis and limbs, and would not fall over after walking more than a few steps. The owner noticed it was vomiting and it has gotten worse recently. The day before the examination, Bai Bai had no appetite at all and took her to the hospital. Completed a vaccine history check and found it was not dewormed this year.
3. Physical examination
On physical examination, it showed increased mouth-breathing, forceful injection, and injection into the oral mucosa. The surface was cold when the limbs were in contact, and the oral mucosa was injected at the same time, the capillary refill time (CRT) was prolonged (>2s), and white foam appeared on the tongue. Tachycardia (heart rate 170 beats/min) and mild hypothermia (37.2°C). The abdomen was slightly distended and painful on palpation, and upon examination, there appeared to be no evidence of a foreign body.
4. Laboratory examination
4.1 Complete Blood Count（CBC）result
Project | Unit | Result | Reference Range |
RBC（Red blood count） | 109/ L | 7.35 | 5.65~8.87 |
HCT | 0.411 | 0.37~0.55 | |
HGB | 109/ L | 136 | 120~180 |
MCV | fL | 55.9 | 61.6~73.5 |
MCH | pg | 18.5 | 21.2~25.9 |
MCHC | g/L | 331 | 320~360 |
WBC(Whiteblood count) | 109/ L | 14.9 | 6~17 |
LYM | % | 0.083 | 0.6~0.77 |
EOS | % | 0.01 | 0.06~1.23 |
OTHR | % | 0.93 | 0.6~0.77 |
PLT | 109/ L | 45 | 200~500 |
4.2 Idexx Catalyst biochemistry CHEM15
Project | Unit | Result | Reference Range |
GLU(Glucose) | mmol/L | 7.5 | 4.11~7.95 |
CREA（Creatinine） | mg/dL | 65 | 44~159 |
BUN/CREA | 2.1 | ||
TP(Total protein) | g/L | 71 | 52~82 |
ALB(ALBUMIN) | g/L | 22 | 23~40 |
GLOB(Globulin) | g/L | 49 | 25~45 |
ALB/GLOB | 0.45 | ||
ALT(Alanine transaminase) | U/L | 49 | 10~125 |
ALKP(Alkaline phosphatase) | U/L | 11 | 23~212 |
GGT | U/L | 0 | 0~11 |
TBIL | umol/L | 1 | 0~15 |
CHOL | mmol/L | 1.44 | 2.84~8.26 |
PHOS | mmol/L | 0.57 | 0.81~2.20 |
Ca | mmol/L | 2.05 | 1.98~3.00 |
AMYL | U/L | 554 | 500~1500 |
LIPA | U/L | 441 | 200~1800 |
4.3 EDXX cPL test
Project | Result |
CPL | Positive（+） |
4.4 CRP test
Project | Result | Reference Range |
CRP | 39.78 mg/L | ≤20 |
4.5 X-ray examination
Picture 1-2:Gas accumulate in abdomen seen on radiographs from a dog. Ultrasound showed pancreatitis.
Picture 3 :In this image we can see the enlarged pancreas with hypoechoic and hypoechoic areas within it.
Diagnosis: Acute pancreatitis
Differential diagnosis based on clinical symptoms, physical examination: acute pancreatitis, foreign body or toxin ingestion. Liver or kidney disease cannot be ignored. Gastric dilatation torsion (GDV) is found in animals in pain, leptospirosis is usually found, and initial diagnostic tests include abdominal X-ray, complete blood (cell) count (CBC), complete biochemical profile, and canine pancreatic lipase SNAP test (Canine SNAP cPL; IDEXX Laboratories, Westbrook, Maine, USA). There was no obvious foreign body in the abdominal dorsal and right abdominal X-ray films except for abdominal gas, which may cause vomiting and blood circulation disorders due to pain. CBC, CRP, and biochemical studies show a Acute inflammation;Hypoglobulinemia; Hypophosphatemia; and e Hypochloremia. Canine SNAP cPL test was positive. The numerical results of these experiments are summarized in Tables 1-2.
The blood smear showed no toxic changes, and the CRP results were presumed to be inflammation. Decreased albumin presumably may be due to nutritional deficiencies and their manifestations were found.Hypochloremia and hypophosphatemia are most likely due to loss of chloride and phosphorus in vomit. In many cases acute pancreatitis we see hypercholesterolemia, but it is normal in this case. The Canine SNAP cPL test returned a positive result, and a combination of the dog’s medical history, physical examination, radiology results, and blood and biochemical features led to an initial diagnosis of acute pancreatitis.
Treatment
Rx:
1. Lactated Ringer + CoB ivggt
2. 0.9% Nacl + Omeprazole ivggt,bid
3. Maropitant s.c sid
4. Lidocanine CRI for 24h
Initial supportive treatments consisted of Lactated Ringer(crystalloid intravenous fluids)at a rate of 300mL/h for 3h to supply the dehydration, lidocanine CRI at a rate of 0.05mg/kg/h for 24h, and provide warm-water bag to recovery the temperature.After 6 hour, the dog could wake up by himself. And we treated with Synulox(amoxicillin clavulanic acidt), 20mg/kg,IV, q24h to prevent the secondary to bacteria infection from the damaged pancreas, omeprazole ,1mg/kg, mixed with 30mL 0.9% NaCl liquid, IVGTT in 30min q12h, Maropitant at 1mg/kg s.c q24h as an antiemetic therapy. When the dehydration was no longer clinically detectable, the LRS fluid rate was reduced to 50mL/h.
24 hours after the dog was sent to the hospital, he was more alert, his body temperature, breathing, and pain began to stabilize. He did not vomit after being admitted to the hospital, and he could drink a small amount of water. This time, the treatment with canned rice powder lasted for 2 days. The dog can walk and control the pace without collapsing, indicating that the weakness of the pelvis and limbs has recovered. Instruct the owner to feed the dog a tablespoon amount, and offer a small meal if the dog does not vomit. After 5 days of cessation of antiemetic treatment, the clinical symptoms did not reappear and the client requested to bring the dog back.
Summary
Pathophysiology of Pancreatitis
Pancreatitis is inflammation of the pancreas, which can be acute or chronic.
The major digestive enzymes are present in pancreatic acinar cells in an inactive form called zymogens. Packaging inactive enzymes into proenzymes helps prevent premature activation prior to release into the duodenum. 9 Enzyme inhibitors are also present in the pancreas (eg, alpha-antitrypsin) and circulate in plasma (eg, alpha-macroglobulin, antichymotrypsin, alpha-antitrypsin). Once zymogens are released into the intestinal lumen, they are broken down by enterokinase peptides secreted by duodenal mucosal cells. This breakdown activates pancreatic enzymes and allows them to begin digesting nutrients. If the inhibitory substances are blocked, or the enzymes are activated while they are still in the pancreas, the pancreas begins to digest itself inappropriately. For example, the conversion of trypsinogen (inactive) to trypsin (active form) can be triggered by enterokinase, bile, lysosomal enzymes, or other stimuli. The result is pancreatic membrane destruction, dilation of arterioles, increased vascular permeability, edema, and hemorrhage, followed by pain, leukocyte infiltration, and peripancreatic fat necrosis. Decreased blood flow to the pancreas and leukocyte infiltration can lead to pancreatic necrosis. Secondary infection may be due to arterial hypotension, portal hydrops, and hypovolemia that may lead to shock.
Peripheral venous constriction and leakage of pancreatic enzymes into the abdominal cavity and vascular compartment exacerbate the injury. Local tissue invasion and destruction caused by pancreatic enzyme release can be extensive. Possible end results include damage to the liver, kidneys, lungs, heart, and abdominal lymphatic vessels. Pancreatitis can lead to obstruction of the extrahepatic bile ducts. The feline pancreas is also prone to ascending biliary infection and bile reflux because the pancreas and bile ducts merge with the papilla before reaching the duodenum.
Types of Pancreatitis
Pancreatitis in dogs can be classified as acute or chronic. Acute pancreatitis is characterized by neutrophil infiltration, moderate to severe pancreatic necrosis, edema, and/or hemorrhage. Acinar tissue and ducts remain intact. Chronic pancreatitis is a long-term inflammation associated with low-grade, mononuclear inflammation and fibrosis. Chronic pancreatitis may be a sequela of recurrent acute pancreatitis. Chronic pancreatitis can eventually lead to diabetes and/or pancreatic exocrine insufficiency. There is no clinical distinction between acute pancreatitis and chronic pancreatitis. Although acute and chronic cases may have mild or severe clinical symptoms, chronic cases are more likely to have mild symptoms, while acute cases usually have severe symptoms.
Etiology and Risk Factors of acute pancreatitis
The cause of acute pancreatitis is usually unknown. Risk factors associated with fatal acute pancreatitis include being overweight, so we’ll discuss some nutritional therapy later; the presence of diabetes, hyperadrenocorticism, hypothyroidism, or epilepsy; and pre-existing gastrointestinal (GI) tract disease history. A study suggests that increasing age and certain breed types are risk factors for pancreatitis. 11 Breeds with a reported higher risk of pancreatitis include Miniature Schnauzers, Dachshunds, Miniature Poodles, Cavalier King Charles Spaniels, Cocker Spaniels, Collies, Boxers, as well as Yorkshire Terriers, Foxes and others. Terrier. In one study, neutered females and castrated males had an increased risk compared with males who did not have sex. Affected dogs are mostly middle-aged dogs. In one study, eating unusual or human foods was shown to increase the chance of developing pancreatitis, similar to this case. Other potential risk factors include high-fat diet, malnutrition, hypertriglyceridemia, exposure toxins(eg,zinc,organophosphates), hypercalcemia, pancreatic duct obstruction, and reflux of duodenal contents into the pancreas. ducts, pancreatic trauma (eg,surgery,blunt instruments), parasites(eg, flukes), hepatobiliary disease, small bowel disease, and pancreatic ischemia/reperfusion injury. Infection with Babesia rosei has been associated with pancreatitis, however, Babesia gibbetii infection is less likely to cause pancreatitis.
Nutritional Therapy
An important risk of acute pancreatitis is being overweight, so we will discuss nutritional management of the pancreas in this section. Traditionally, fasting is done for the first 24-48 hours, as food stimulates the pancreas. However, there is currently debate over when to feed affected dogs. Prolonged fasting can lead to hypoalbuminemia; loss of intestinal motility; increased intestinal permeability; decreased intestinal blood flow; Feed small amounts. One study showed that dogs fed within 48 hours of hospitalization had reduced time intake to resume voluntary food intake and maximal food intake, as well as fewer gastrointestinal symptoms. The length of hospital stay was not affected. Enteral nutrition is preferred over parenteral nutrition in patients with acute pancreatitis.
The ideal diet for dogs with pancreatitis is unclear. However, feeding an easily digestible, low-fat diet is usually the initial choice. A diet of ≤8% fat on a dry matter basis is generally recommended. Diets designed for obesity management or fibro-responsive disease are less digestible and may not be suitable. Once recovered, some patients need to be on a high-digestive, fat-restricted diet long-term, especially those at risk of relapse or with hyperlipidemia. Other patients may be able to transition to a moderate-fat diet, i.e. up to 15% fat on a dry matter basis.
Monitoring and prognosis
Patients with acute pancreatitis may have mild to severe clinical symptoms. On the other hand, patients with chronic pancreatitis tend to have mild intermittent signs. Vomiting occurs in approximately 90% of dogs with pancreatitis and abdominal pain in 58%. Other possible signs include lethargy, anorexia, diarrhea, cranio-abdominal pain, irritability, blood in the stool, and hematemesis. Severe acute pancreatitis may present with fever, collapse, and vomiting. Evidence of concurrent coagulopathy (eg, petechiae), hepatobiliary disease (eg, jaundice), diabetes (eg, polyuria, polydipsia), and AKI (eg, oliguria) may be present. 9,62 Diabetes mellitus is the most common co-morbidity.
Monitoring requirements vary depending on the severity of pancreatitis and the presence of other systemic abnormalities. Vital parameters, body weight, pain scores, and fluid intake and output were assessed multiple times daily in hospitalized patients. Some tests, such as CBC, biochemical tests, electrolytes, blood pressure, and coagulation status, require repeated evaluation. Monitoring of clinical improvement in patients treated in outpatient setting. Repeat cPLI, ultrasonography, and CRP testing can be done to determine if pancreatic inflammation is receding.
Patients with mild acute pancreatitis usually have a good prognosis. The prognosis for patients with severe acute pancreatitis is more cautious. Patients with chronic pancreatitis may eventually develop pancreatic exocrine insufficiency. In a study of 138 dogs with acute pancreatitis, 33% died within 30 days of diagnosis. Bilirubin concentrations ≥18.7 mg/L, elevated creatinine, hypocalcemia, metabolic acidosis, and AKI grade 4 or 5 in IRIS were associated with increased short-term mortality. In a study of 50 dogs with acute pancreatitis, serum sodium <139 mmol/L was associated with poor prognosis. In another study, high ALT at diagnosis was associated with longer hospital stay, and lower CRP levels were associated with recovery.
