Photo by Ellen Bonacarti.
The benefits of necropsy.
by John Dillberger, DVM, PhD
Reprinted from the September/October 2015 issue of The Claymore.
A necropsy for an animal is the equivalent of an autopsy for a human being. Simply put, a necropsy is an examination of an animal’s body after death for the purpose of discovering what might have caused it to be sick or to die. Ideally the examination is conducted by a veterinary pathologist who has the training and experience to use various diagnostic tools and to recognize and describe abnormalities. An important part of the necropsy examination is to collect fluid and tissue samples for microscopic examination and, if appropriate, other analyses. The information gained at necropsy can not only answer questions about the cause of illness and death, but also reveal unsuspected health problems that may influence breeding decisions.
Lyn Robb recently lost her 7-year-old male Deerhound, Ioan, and asked me to help her interpret his necropsy report. She also gave me permission to use her experience to illustrate the benefits of necropsy. This month’s column is Ioan’s story.
Ioan’s Last Days
In early May 2015, while Lyn was away from home, Ioan’s caretaker noticed that he had lost his appetite. She knew Ioan had experienced several episodes of pneumonia in the past, and so she took him to an emergency clinic immediately, at 8:00 p.m. on May 4th. The medical records from that visit reveal that Ioan had a normal respiratory rate (18 breaths/minute) and body temperature (101.9 degrees F), but his attitude was described as “dull.” It is hard to know if Ioan was feeling unwell or if instead the examining veterinarian was just unfamiliar with the phlegmatic Deerhound personality, which can come across as dull if one is using another breed as a reference point. Ioan also had a very fast heart rate of 150 beats/minute. I expect an adult male Deerhound to have a resting heart rate of about 30 to 40 bpm and an “excited/anxious” rate of up to 100 bpm. Ioan also was mildly dehydrated (estimated at 6% to 7%) and had fluid in his scrotum.
The examining veterinarian summarized Ioan’s condition as “very serious.” Blood was drawn for laboratory tests, radiographs were taken, and an ultrasound examination of the abdomen was done. X-rays and ultrasound both showed excess fluid in Ioan’s abdomen. Many things can cause this, but in Ioan’s case, microscopic examination of a fluid sample revealed that it had diffused out of the blood. The ultrasound examination also revealed a blood clot in the splenic vein and a small liver. The blood test results were mostly normal, with the following exceptions:
- Slightly high concentrations of urea and phosphorus. Both are kept in normal limits by the kidneys, so the high concentrations could reflect kidney disease; however, reduced blood flow to the kidneys can produce the same elevations, and the slight dehydration and fluid build-up in the abdomen both suggest that Ioan’s circulation wasn’t the best at this point.
- Low concentration of albumin, which is the primary protein in blood. Albumin concentration normally is about 3 to 4 grams/deciliter in Deerhounds, but Ioan had only 2.3 grams/deciliter. Albumin can be low because of chronic liver disease (the liver makes albumin) or chronic kidney disease (which can cause albumin to leak into the urine). If albumin concentration gets low enough, then that in itself can result in fluid build-up.
- Slightly high red blood cell count, probably reflecting the mild dehydration. The red blood cell count is the ratio of cells to plasma. With dehydration, plasma volume goes down, so RBC count goes up. Deerhounds normally have as many as 9 million red blood cells/microliter of blood, but Ioan had 9.15 million cells.
Ioan was hospitalized and given intravenous fluids. By 1:40 a.m. (now May 5th) his heart rate was down to 100 beats/minute, he was described as quiet and resting, and he ate; however, by 1:56 a.m., his heart rate was back up to 150 bpm. By 6:15 a.m., Ioan was described as “dull but responsive.” His temperature was down to 98.5 degrees F, his heart rate was 128 bpm, and his mucous membranes were “tacky” (despite intravenous fluids), all of which makes me think that he had gotten sicker overnight.
At 8:40 a.m., Ioan was transferred to his regular veterinarian for the day. When he returned to the emergency clinic at 5:35 p.m, he still had a fast heart rate (150 bpm) and low body temperature (99 degrees F), but now he also was breathing rapidly (40 breaths/minute) and with some effort. He was not dehydrated and was described as quiet, alert, responsive, and comfortable; however, his abdomen was distended and taught, and he seemed mildly uncomfortable when it was pressed. He also had gained six pounds in the past 24 hours, which represented water retention. During the examination, Ioan regurgitated some partially digested food. Given his worsening condition and multiple health issues, Lynn decided to euthanize him.
Ioan’s Necropsy Results
Ioan’s body was taken to the Oregon State University Veterinary Diagnostic Laboratory. During necropsy, the pathologist noted that there was three liters of fluid in the abdomen and blood clots in both the portal vein and splenic vein. The portal vein carries blood to the liver from the spleen and gastrointestinal tract. The splenic vein carries blood to the portal vein from the spleen.
Microscopic examination of tissue samples taken at necropsy revealed:
- Severe amyloid accumulation in the kidneys. The word amyloid means “starch-like stuff,” and it refers to the microscopic appearance of amyloid, which looks and stains like starch. But amyloid isn’t starch—it’s protein. Most often (some would say always), the protein is antibodies—lots and lots of antibodies. They become trapped when the blood is filtered in the kidneys and accumulate in the filters themselves, which are called glomeruli. As a result, the glomeruli either get blocked completely or distorted so they become leaky.
- An acute pneumonia with visible bacteria in one area of the lungs. The word acute means that this infection had developed only shortly before Ioan’s death.
- A chronic pneumonia in another area of the lungs that had been present for a long time.
- Fluid build-up (edema) in the pancreas.
- Severe congestion (back-up of blood) in the spleen, omentum (tissue that cradles the intestines), mesenteric blood vessels (that supply the intestines), and pancreas.
Putting It All Together
The information provided by a necropsy must be integrated with the results of tests and examinations that were done in life. If one is lucky, then all of this information will tell a story about what happened before death. Here is the story I would write about Ioan’s illness.
The immediate cause of Ioan’s ill health was the portal vein blood clot that totally blocked the vessel. To understand what this meant, one needs to know that the liver is unique in having two different blood supplies. Most (75%) of the liver’s blood supply comes from the portal vein, which drains the gastrointestinal tract and spleen. The advantage of this arrangement is that anything absorbed from the gut will pass first through the liver before it reaches the rest of the body. Thus, the liver gets first crack at nutrients and can filter and remove anything undesirable before it reaches the rest of the body. The downside of this arrangement is that the blood in the portal vein already has delivered oxygen to other organs, and so there isn’t much oxygen left for the liver. That’s why the liver has a second supply of oxygen-rich blood, which comes directly from the aorta via the hepatic artery.
If the portal vein is blocked, as Ioan’s was, then blood will back up into the spleen and gastrointestinal tract. That’s what is meant by the severe congestion seen microscopically in various abdominal organs. As you can imagine, even if the portal vein is blocked, the heart continues to pump blood into those organs. As a result, the blood pressure in the vessels supplying those organs will go up—way up! Without getting into the physiology involved, the net result is that fluid will leak out of the vessels and accumulate in abdominal organs and the abdominal cavity. Ioan had this in the pancreas (edema) and in the abdomen.
Ioan’s acute bacterial pneumonia was most likely due to aspiration of water, food, or regurgitated stomach contents. Those who have had a Deerhound with pneumonia know that it can develop very fast (in a matter of hours). It seems likely that this acute pneumonia began after Ioan first went to the emergency clinic. If the acute pneumonia had been present when Ioan first went to the emergency clinic, then it would have been visible on the chest X‑rays taken at that time.
Ioan also had a chronic interstitial pneumonia. This was reflected in the “multifocal areas of interstitial expansion by fibrous tissue” seen microscopically. Fibrous tissue is basically scar tissue. In Ioan’s case, it represented healing from past episodes of pneumonia. There also were “occasional perivascular accumulation[s] of lymphocytes and plasma cells.” The lymphocytes are normal and found in healthy lungs. Not so, the plasma cells—they are lymphocytes that have morphed into specialized antibody-making factories. Their presence means that there was some ongoing need to make antibodies. By far the most likely reason would be a chronic infection in the lungs. Possibly the antibiotics used to treat previous episodes of pneumonia had suppressed but not eliminated the infection, which was kept under control by a constant immune response.
Unfortunately, one potential consequence of chronic infection and antibody production is amyloid accumulation in the kidneys. This does not always happen, but it is a real problem when it does. The end result of amyloid accumulation is gradual kidney failure. As this happens, various proteins that normally are retained in the blood can “escape” into the urine. One such protein is albumin, and the loss of albumin in the urine can lead to low albumin concentration in the blood. Proteins that regulate blood coagulation also can be lost in the urine. As a result, the blood becomes more prone to clotting.
Here is one way to put Ioan’s story together, although it is not the only way. Ioan had a chronic pneumonia that was “silent” because he was able to mount an immune response that kept the infection under control but didn’t eliminate it. The ongoing immune response included making lots of antibodies, and these began to accumulate in his kidneys as amyloid. The amyloid caused loss of some blood proteins that keep blood coagulation in balance, shifting that balance slightly toward clotting, making Ioan more susceptible to clot formation. It is impossible to say what caused a massive clot to form in Ioan’s portal vein when it did. Maybe it was the acute pneumonia, since an acute infection also tends to make the blood more likely to clot. But this doesn’t “feel” right to me, because the splenic vein blood clot was present before any acute pneumonia was visible on X-rays. I think instead that the acute pneumonia was something that happened after the clot formed and Ioan already was sick.
Ioan’s case is a good example of how information gained at necropsy can help explain why a dog was sick. But this requires that someone integrate all of the in-life and necropsy findings. Unfortunately, the person best trained and experienced to do this usually is the pathologist who did the necropsy, but the person who has all of the information usually is the veterinarian who treated the dog in life. Too often, owners are left at the end of necropsy with medical records, lab test results, and a necropsy report, all full of medical jargon, instead of what they really wanted: a simple explanation of what happened to their dog.
If you find yourself in that situation, ask the treating veterinarian to share the dog’s medical records and lab test results with the pathologist and then to talk with the pathologist how s/he would “put it all together.” If the treating veterinarian is reluctant, then get the records and contact the pathologist yourself to get the answers.