Monday, May 30, 2011
Once upon a time, when the world was young, I had a ranch practice in northern Montana. It was a wonderful time and place for a young man. Streams were filled with trout, pheasants were in every field, ducks in all the ponds, and every rancher had lovely daughters. But delivering calves was my livelihood. Laboring cows taught me a lesson germane to today’s small animal practice. If a fetus is not positioned in the birth canal it will not be born, nor will the dam strain to deliver it. The problem is uterine inertia for the uterus will not constrict and start the fetus into the pelvis. In most cases intravenous administration of calcium will correct the problem. The uterus can then constrict placing the fetus where it can be expelled normally. But not always!
Jessica, a four pound Maltese female had delivered one pup. Then everything stopped! For an hour she did not deliver any more pups. Didn’t even try! And yet her belly was still distended. She remained pregnant. I could palpate a pup out of position in the anterior abdomen. This seemed to be typical uterine interia so I injected calcium and sent her home. Often these cases will deliver a pup during the car ride home but not this time, nor during the ensuing hour. She had to be returned for a caesarian section. One has to get fetuses out of the abdomen or they will die, start to decompose in the abdomen, and the rotten material will kill the dam. On reexamination the pup had not been moved. It was no nearer to the pelvis then when the dog was initially examined. During surgery I found the wall of the uterus surrounding the remaining pup had ruptured spilling the pup into the abdominal cavity and making it impossible for the pup to be properly positioned. Why the rupture occurred I don’t know. Perhaps it was due to incoordination of uterine contractions. Both pup and mom survived surgery.
Rarely did I find a cow with uterine rupture and the calf lying free in the abdominal cavity. If one did surgery in time the cow might live but usually the calf was dead.
"Photo Attributed to S. Fulljames via flickr.com
Thursday, May 26, 2011
Jack was in last week. He needed vaccinations and his teeth cleaned. I hadn’t seen him for a while, but for an old cat, he’s 18 now, he was sleek and vigorous.
He wasn’t always this way. One cold winter evening five years ago his owner brought him to me. She thought he was dead but wanted to be certain. At the time he was an indoor-outdoor cat and had been missing for several days. When he came home his owner found his lifeless body on her back porch. As she gently laid him on the exam table a quick glance convinced me it was time for condolences. As the comforting words formed in my mind I saw just the slightest hint of a movement of his chest. Could it be he was still alive? If so, there surely wasn’t any time so spare. The examination was hasty. His heart was beating slowly and the pulse was so weak I could barely feel it. There were no eye reflexes. Body temperature was so low the mercury didn’t budge from the bulb. His belly held a clue; the bladder was grossly distended with urine. Quickly I performed a cystocentesis and drained the bladder of thick brownish urine. He had feline urologic syndrome. The urethra was plugged with exudates and crystals so he couldn’t void. Metabolic waste products had backed up and accumulated in his blood and he had gone into a coma. A blood sample showed an extremely high level of urea, confirming that he had uremic poisoning, complicating his condition.Jack was catheterized so urine would flow freely. Intravenous fluids were given to flush the poisons from his system and we put him on a heating pad to warm him. Amazingly, in an hour he was stirring, six hours later he sat up on his sternum and in two days he went home. Now in his waning years, he lives the good life indoors. Perhaps, because it is so easy to become the caretaker of a cat some people view them as expendable. But not his owner, he has been her valued friend for many years. A relationship that has grown over time, especially since his close encounter with death.
Saturday, May 14, 2011
Wilbur is a 7-years-old French bull dog whose vomiting started a week ago. He cried when his abdomen was pressed and he had refused to eat for the past several days. Also, water consumption had declined.
He was a very sick dog when brought to the hospital. Several abnormalities of his serum chemistry profile suggested he might have acute pancreatitis, for the blood study showed dehydration, inflammation, and stress. He was started on intravenous fluids to rehydrate him and sustain kidney function. An overnight blood test confirmed the diagnosis of acute pancreatitis. Next morning all food and water consumption was stopped and drugs were administered to depress stomach-acid production. Acidic stomach contents passing into the small intestine can aggravate pancreatitis so it must be controlled. Also, he was given a low dose of antibiotics as insurance against infection in the region of the pancreas. Intravenous fluid therapy was altered to provide essential energy and protein building blocks to help with healing. He was maintained on this program for two days. Then, drugs were dispensed to prevent vomiting and continue reduced gastric acidity and he was sent home. Such treatment would permit him to eat and drink without aggravating the pancreatitis and still facilitate continued healing.
Tuesday, May 10, 2011
“Doctor Howard,” Robin called from the intensive care ward, “he ate, the kitty ate, a little.”
Mrs. Andrews had found a dying kitten in the alley behind her home the previous day. When she brought him to the hospital he was so weak he could not stand. About four weeks old, he was mostly bones, frizzy fur, and fleas. A Siamese, and quite handsome we thought, in spite of his wretchedness, with black outline of his eyes, nose, and mouth. On closer examination we found the black markings were flea dirt. There was no outward sign of infection other than the parasites, but the membranes of the mouth and eyes were almost white because he was so anemic. I supposed the anemia was due to fleas draining his blood as they fed, which was partially correct.
Our first order of care was to rid him of the fleas. JoAnn, knowing the little fellow might be killed by routine flea treatment, dampened a piece of cotton with flea spray and gently rubbed the hair against the lay getting the chemical to the fleas but not on the kitten’s skin. Then, with a flea comb she and Phyllis removed the poisoned pests. This took more than an hour.
In the meantime, John found the kitten’s blood cells had hemoplasma organisms on them. These bacteria, spread by fleas, sensitize blood cells which are then destroyed by the spleen faster than the bone marrow can replace them. We had our diagnosis, but what to do? While JoAnn bathed, dried and warmed the little tyke, we caught Tazz, the clinic cat, varmint control officer, and donor of blood for ailing kittens. We transferred six milliliters of his blood into the kitten’s abdominal cavity so it would flow into his circulation giving him essential blood cells, protein and immune factors. Then, just a tiny bit of antibiotic was injected to start controlling the hemoplamas.
By this time it was getting late in the day so Robin fed him milk replacer with a dropper and put him to rest in a small cage with an insulated heating pad to warm him. The next day he was able to stand and, as mentioned earlier, eat. The day following he was released to Mrs. Andrews’ care with two more weeks of antibiotic treatment. He recovered and grew to be a handsome cat. Never cross or arrogant, he seemed to understand that he was in debt for his life.
When you consider adding a new pet from any source to your household, you should realize that the new animal may be carrying a disease that can spread to resident animals. To help avoid trouble be sure your existing pets are current on vaccinations, and regardless of how healthy it seems, have the new pet examined by your veterinarian before it is introduced to its new home as Mrs. Andrews did.