Baby's Necropsy Report-Death Caused By Acute Pancreatitis Attack

Baby's necropsy report shows she died of complications from an acute pancreatitis episode. She did NOT HAVE TRUE HEART DISEASE although she had mild changes to her heart due to age. Her liver had signs of decrease function due to the overall decline in her body function. The kidneys were STABLE despite CKD, and she was not in end stage CKD. She DID NOT HAVE CANCER. We finally got a copy of her initial test results-the reason she had the biopsy in the first place-and she did NOT have lymphoma. She did NOT die of any of her known illnesses. She did NOT have any complications from her known illnesses that led to her demise. (Except pancreatitis which was diagnosed as IBD even in January.) She did NOT have any clots in her legs and no skeletal signs of damage so the pathologist does not know why she was lame unless it was due to severe dehydration that caused weakness. 

Pancreatitis can kill our pets? Yes, and humans. A severe flareup can lead to shock, blood loss, enzymes released basically can eat away at the fat in the pancreas causing severe damage; as the body shuts down, all other organs are affected. This is why keeping track of pets' vomiting and diarrhea, getting a PLI blood test, keeping up the weight by eating on a consistent basis (normal weight), and giving necessary medications (antibiotics for example) is key to avoiding or decreasing pancreatic or even IBD flareups in order to maintain a healthy GI tract, and avoid deadly acute attacks. Here's one study that showed many of the same signs that were exhibited in Baby:

 "...Dehydration (127/157 cats; 84.7%), lethargy (114/157; 72.6%), and anorexia (97/157; 61.8%) were commonly observed. Other signs, in decreasing order of frequency included vomiting, owner‐reported weight loss, hypothermia, tachypnea, icterus, inappetence, abdominal pain, diarrhea, and fever (rectal temperature, >39.5°C; Table 1). Lethargy was more frequent (P = .003) in nonsurvivors compared to survivors. Fever (P = .042) and weight loss (P = .034) )...Putative etiologies of pancreatitis (21 cats; 13.4%) included recent general anesthesia (10 cats; 6.4%), trauma (6; 3.8%), hemodynamic compromise secondary to heart failure, urinary obstruction or gastrointestinal foreign body (4; 2.5%), and organophosphate intoxication (1)...weight loss was negatively associated with outcome.32 Lower BCS at presentation and occurrence of weight loss are frequent findings in FP,11, 13, 24, 28 possibly representing a protracted disease course...Duration of clinical signs before presentation plays a role in development of a negative energy balance, and results of the multivariable logistic regression analysis suggest the longer the duration, the higher the risk of death...increased frequency of azotemia in nonsurvivors, which previously has been associated with hypothermia in cats...withholding food is no longer recommended, and PN alone has been shown to compromise intestinal barrier integrity, increasing the risk of bacterial translocation and promoting mucosal atrophy and proinflammatory responses...failure to eat voluntarily during hospitalization was a significant risk factor for death...intrahepatic bacteria were noted in 41% of cats with inflammatory liver disease,59 which is clinically relevant, because hepatic and pancreatic inflammations are common comorbidities in cats, because their collecting ducts join anatomically before entering the duodenum..."

Something happened at the vet hospital to cause pancreatitis, and then they ignored her decline and that she was weak when they released her. They continue to say that she was too sick and that's why she declined (I want to point out that their initial exam said she was 8/9 body condition, and that the ultrasound found nothing seriously wrong.) It's their way of ignoring what they failed to do-to follow proper protocol, if they have any-to keep track of all patients' conditions at all times. They also excuse themselves by saying that I told them she often doesn't like to eat when away from home-which is true. BUT how does that absolve them of all medical care and responsibility for her care and condition? It does not. She got an acute attack of pancreatitis which they triggered, ignored, didn't notice and therefore, didn't treat nor did they alert me to her condition. 

I spoke to the pathologist and here is the explanation from the report listed below: 

Her body declined because it was not able to compensate for all that was happening due to the acute attack of pancreatitis. She was possibly going into DIC-"...can lead to massive bleeding in other places." Many illnesses or issues can lead to DIC and pancreatitis can cause DIC. She would have needed blood transfusions (which the ER tried to find for her-they tried to find a donor-and couldn't; it turned out a local vet hospital near us actually carries blood.I didn't find out until after she died. The pathologist said she would have likely needed more than one and that she may have been too far gone for it to work.) She was leaking internally as she declined, leading to organ failure and some fluid in the abdomen cavity and the lungs and pericardial sac: "whole body tricavitary effusion". The thickened heart seen grossly was not apparent histologically, meaning she did not have HCM nor any heart disease. She had necrosis of the pancreas abdomen fat because the pancreatic enzymes eat the fat, break it down, damaging the pancreas further. The body's systemic response to pancreatitis, can lead to shock which she may have been or had begun to experience. The duodenum can release bacteria into the pancreas and that could have caused the early onset of inflammation. Fluids, pain meds and a feeding tube are the only and best methods for support and treatment for pancreatitis. But Baby wasn't responding. She had mild heart changes due to age or CKD but did not have HCM. She had liver changes due to either the heart, or as her body failed, or if she had been hypotensive for too long, or if she her body lacked oxygen to the liver. The pulmonary edema was not CHF or heart failure. Could have been from fluid therapy that the body couldn't handle as it declined, leading to the "tricavitary effusion".

From the actual necropsy report:

"...

Microscopic Description

Representative routinely stained sections of brain, heart, lung, trachea, kidney, liver, spleen, adrenal gland, thyroid, pancreas, stomach, small and large intestine are examined. Autolysis (destruction) was at least mild in all tissues and moderate in sections of intestine.

In sections of pancreas, there is regionally extensive necrosis of pancreatic acini (dead cells of digestive enzymes.)  There are low numbers of inflammatory cells infiltrating the supporting stroma between acini, primarily neutrophils, lymphocytes, and plasma cells. The supporting stroma is moderately expanded by edema. Within the pancreas, there are multifocal expansile nodules composed of proliferative pancreatic acini. Peripancreatic fat is infiltrated by large numbers of variably degenerate neutrophils. Extensive regions of peripancreatic and mesenteric adipose are replaced by pools of variably mineralized necrotic material and degenerate inflammatory cells (fat cells were dying and they release calcium.)

In the sections of left ventricle, there are occasional regions where there is variation in myofiber size, with a small number of cardiomyocytes appearing shrunken, with loss of cross striations and pyknotic nuclei. The interstitium in these regions is expanded by variably loose fibrous connective tissue. In sections of liver, there is moderate to severe centrilobular hepatic cord atrophy and sinusoidal congestion. Central veins are often dilated. In both kidneys, there are aggregates of lymphocytes and plasma cells infiltrating the interstitium. The interstitium is multifocally replaced by fibrous connective tissue. A small portion of glomeruli are shrunken and sclerotic. All other examined tissues are histologically unremarkable.

Morphologic Diagnosis(es)

Pancreas: Severe acute necrotizing pancreatitis, steatitis and saponification of fat; Exocrine nodular hyperplasia Heart, left myocardium: Mild multifocal interstitial fibrosis and cardiomyocyte degeneration
Liver: Centrilobular congestion and hepatic cord atrophy
Kidney: Moderate multifocal lymphoplasmacytic interstitial nephritis, fibrosis and occasional glomerulosclerosis

Final Diagnosis(es)

1. Severe acute necrotizing pancreatitis, steatitis, and saponification of fat
2. Mild degenerative heart disease and secondary hepatic chronic passive congestion  3. Chronic kidney disease

Comments

The most significant findings histologically was the severe necrotizing pancreatitis. The most common cause for necrotizing pancreatitis in cats is ascending bacteria from the duodenum. While no bacteria were observed in the examined sections, once the pancreas becomes inflamed, release of digestive enzymes can drastically exacerbate the condition. The changes in the heart were overall mild, however, there was evidence of decreased cardiac function in the liver (chronic passive congestion). The findings in both kidney are supportive of chronic kidney disease. The There was no evidence of a neoplastic process in any of the examined tissues.

..."