Background:

Natalie is a 2 year-old Jersey cow from a mid-sized dairy farm. She was brought to the hospital because she went off feed last night and had a dramatic drop in milk production this morning. She also has not been passing any feces. The referring veterinarian suspected intestinal torsion.

Clinical Findings:

Physical Exam:

-Temperature: 97.6 (low)

-No pinging could be elicited on auscultation

-Heart and lungs ausculted normally

-No rumen contractions heard

-Withers pinch resulted in no reaction

-On rectal palpation, small intestines felt normal

Ultrasound:

Several loops of small intestine were distended with fluid and appeared static. The abomasum was empty and also static. All other abdominal organs appeared normal, was not able to visualize the cranial abdomen. No abdominal free fluid was appreciated.

CBC:

-Increased RBC, hemoglobin, hematocrit, platelet, WBC, band cells, lymphocytes

-Decreased Mean cell volume

-Aniscocytosis

Biochemistries:

-Increased globulin, glucose, GGT, CPK (CK), cholesterol total, GLDH

-Decreased calcium, potassium

Top clinical problems:

Abdominal pain
Static gastrointestinal tract
High CPK levels

The clinical problems that are of greatest concern are all related to the gastrointestinal tract not functioning normally with abdominal pain and bloodwork showing high CPK levels. The abdominal pain was determined by the negative withers test. A withers test in a normal animal should result in a twitch or some movement, but if an animal is in pain, they will not twitch because the twitching would make their pain worse. Since animals will try to hide their pain as long as possible, this is a top concern. The abdominal pain most likely comes from the static gastrointestinal tract. There are multiple abnormalities from the history that point to a static gastrointestinal tract. Evidence of a static gastrointestinal tract include the lack of rumen contractions, the static abomasum and small intestine on ultrasound, and not passing any feces. The elevated CPK level is also of top concern. CPK levels over 1000 U/L indicate severe muscle damage that is usually associated with a down cow (3). A question for the owner that I would ask would be if Natalie was down prior to deciding to bring her in. My suspicion is that she most likely had been down for quite a few hours since her problems began, damaging muscles and increasing the CPK levels.

There were numerous abnormalities found in the exam and diagnostic tests. To rule some of the problems out from making the top problems list I used a study of 97 dairy cows and heifers that examined specific blood chemistry components. In this study concentrations of cholesterol, glucose, and progesterone were compared at certain times post-partum. Cholesterol was found to increase 88 days post-partum and was also increased in winter-calving cows post-partum. Glucose was elevated in first-lactation heifers and was also found to be inversely proportional to milk production. Since this is Natalie’s first calf and it’s during winter, the dramatic decrease in milk production at approximately the same amount of time post-partum as in the study, is consistent with the results from this study. The study also found results that are consistent with Natalie’s elevated glucose and cholesterol levels in winter-calving and first-lactating heifers. (1)

Differentials:

Milk fever
Intestinal torsion
Traumatic Reticuloperitonitis

Milk Fever

During lactation, the cow requires more calcium to produce milk and still meet her normal requirements. When the cow does not have enough calcium, this causes hypocalcemia, or milk fever. Typically, hypocalcemia is more common to occur closer to parturition due to the great amount of calcium in colostrum (3). However, if feed rations with inadequate calcium amounts or excessive levels other cations, like potassium, were changed to recently, this could also cause a lactating cow to become hypokalemic (3). This mistake in changing feedstuffs could have been made without considering the time of peak lactation. Milk fever could also be a secondary problem that arose due to a primary problem causing a metabolic issue. The symptoms of milk fever are broken into three stages.

Stage 1 Symptoms: “loss of appetite, excitability, nervousness, hypersensitivity, weakness, weight shifting, and shuffling of the hind feet” (3)
Stage 2 Symptoms: “turning head towards flank, extending neck, dull or listless, cold ears, incoordination when walking, muscles trembling, inactive digestive tract and constipation, decreased body temperature ranging from 96-100 F, increased heart rate” (3)
Stage 3 Symptoms: “inability to stand, progressive loss of consciousness, heart beats nearly inaudible, heart rate increases to 120 bpm” (3)

Intestinal Torsion

There are many different types of intestinal obstructions that lead to intestinal torsion. Signs and symptoms that are common with intestinal obstructions include anorexia, depression, abdominal pain, absence of feces, drop in milk production, decreased calcium, and decreased potassium (6). If feces are passed with an intestinal obstruction, it may be covered with mucus or coated with blood (6). To determine which type of obstruction may be present, rectal palpation, auscultation, abdominal distension in specific areas, and ultrasound can be used. Cecocolic volvulus can be identified with a ping on percussion and auscultation in the upper right caudal abdominal quadrant along with rumen hypomotility. On rectal palpation, “one or more large, distended loops of large intestine are identified” to rule in cecocolic volvulus (6). Small intestine distension that would indicate an obstruction caudal to that point can be identified by ballottement and auscultation of the right side of the abdomen or on rectal palpation the small intestines can be palpated to determine if they are of normal (6). Once the small intestine becomes obstructed, hypocalcemia can occur because the duodenum may not be able to absorb as much calcium (6).

Traumatic Reticuloperitonitis-Hardware Disease

Hardware disease occurs when cattle ingest foreign objects that get stuck in their rumen or reticulum. Common signs and symptoms of hardware disease include decreased milk production, constipation, anorexia, fever, reluctance to move, tachypnea, increased fibrinogen, increased total protein with an increase in globulin, neutrophilia with a left shift, and decreased potassium (5). When hardware disease is suspected an abdominocentesis of the peritoneal fluid is checked to rule peritonitis in or out (4). “Normal peritoneal fluid of an adult cow is straw-colored, clear, and odorless” (5). On ultrasound of the abdomen, foreign objects are rarely seen, so ultrasound is often not a definitive test for hardware disease. However, ultrasound of the thorax can rule out a pleuritis or pericarditis that could be caused by traumatic reticuloperitonitis.

Interpretations:

As would be expected of a cow that is off feed, the CBC shows that Natalie is dehydrated. An increase in RBC’s, hemoglobin, and hematocrit supports dehydration. An increase in hematocrit shows an increase in the solid portion, or blood cells, compared to the liquid portion, or plasma. The image below compares a normal hematocrit to a dehydrated hematocrit that has an increased ratio RBC’s to plasma. Since hemoglobin is carried on RBC’s it would be expected that as the level of RBC’s increases, that hemoglobin would be increased as well.

Image source (7)

Evidence from Case Observations:

Most likely the traumatic reticuloperitonitis occurred, causing a suppressed immune function, and the milk fever was secondary or only began to show signs after the onset of the traumatic reticuloperitonitis . “Increased risk of diseases observed in cows that develop SCH in early lactation might, in part, be caused by suppressed function of immune cells mediated by reduced cytosolic iCa2+concentrations.” (8) SCH, subclinical hypocalcemia, could have been present before the traumatic reticuloperitonitis, and it only started to show symptoms after it’s onset. Intestinal obstruction and torsion are supported by the ultrasound findings of distended small intestines with fluid that appeared to be static, as well as the abomasum being static, but this could as be an additional secondary complication to traumatic reticuloperitonitis. Each of the conditions results in a down cow that explains the extremely elevated CPK levels that are indicative of severe muscle damage.

In the chart below, milk production is plotted along a time of the months after calving. As seen in the chart below, peak lactation occurs 60-80 days after calving which fits in the time frame of Natalie’s symptoms occurring (2). The matching of occurrence of peak lactation to the onset of Natalie’s issues leads to milk fever being considered as a part of her diagnosis. The main support of milk fever being present in this case is because on the biochemistry, hypocalcemia is present. Other symptoms that are present that supports milk fever are the decreased temperature, loss of appetite, lack of passing feces, and inactive digestive tract. These symptoms can be matched from the information found in the differentials section to support that stage 2 milk fever is present. Milk fever also can explain the hypokalemia that was found on the blood chemistry. Hypokalemia would be expected to be found in a cow that is off feed, has a static gastrointestinal tract, and not passing any feces. Therefore, since hypokalemia and hypocalcemia are present, the anion gap that is present in Natalie’s biochemistry would also be expected to be found.

Image source (2)

Traumatic reticuloperitonitis is supported by Natalie having all the common signs and symptoms of traumatic reticuloperitonitis that were listed above except for having a fever. A fever may have been present early in the onset of traumatic reticuloperitonitis, but once the milk fever set in as a secondary issue, it most likely lowered the temperature. The symptoms that Natalie has that support traumatic reticuloperitonitis include: decreased milk production, lack of passing feces, anorexia, fever, reluctance to move, tachypnea, increased fibrinogen, increased total protein with an increase in globulin, neutrophilia with a left shift, and decreased potassium (5).

How to proceed:

The CBC was performed to confirm that there is a peritonitis present. It supports peritonitis because it shows that there is a neutrophilia with a left shift. In the image below, varying degrees of neutrophilia are depicted. The left shift means that immature neutrophils are circulating to fight an infection. The neutrophils are immature because neutrophils are recruited to fight infection, and if the infection is acute, then the body is requiring as many neutrophils as possible. Once the body has had more time to fight the infection, the neutrophils should return to a normal level when the body has caught up with the high demand. (9)

Image source (9)

At this point an abdominocentesis would be the next step to help determine if a peritonitis is present. Normal peritoneal fluid does not rule out traumatic reticuloperitonitis because cattle often “wall off inflammation in the peritoneal cavity, making it more difficult to diagnose local peritonitis” (5). Purulent peritonitis is confirmed by immature, degenerative, or toxic neutrophils. Degenerative neutrophils can be seen in the image below, as well as phagocytosed bacteria. Intracellular bacteria and/or degenerative neutrophils is indicative of septic peritonitis (5). Since there is a left shift neutrophilia present, it is suspected that bacterial purulent peritonitis present.

Degenerative Neutrophils

Image Source (5)

If nothing was done to treat Natalie, she would most likely go down. Once a cow is down, they are not likely to get back up without some medical management. With her not being able to stand to eat or drink, her condition would continue to worsen, ultimately leading to death.

The most common treatment of milk fever is intravenous calcium administration (8). IV fluids should also be given to correct her dehydration. To correct traumatic reticuloperitonitis, a decision must be made as to if this case can be corrected medically or if it requires surgery. Whether medical management or surgery are chosen, antimicrobials should be administered to correct any peritonitis present. Oxytetracycline and penicillin have both shown to be effective (4). In surgery, “rumenotomy with manual removal of the object(s) from the reticulum” (4). Preventative measures can also be taken to prevent the onset of milk fever and traumatic reticuloperitonitis. Working with a feed nutritionist to ensure that a proper ration is being fed is often the first step to prevent milk fever. A magnet be placed to help prevent future traumatic reticuloperitonitis.

Learning issues:

One issue that I had with this case was deciding what clinical problems could be related to each other to be causing one problem and which others could be related to be causing another problem. This is why I eventually decided to say that there was most likely a secondary problem occurring simultaneously to the primary problem. Once I started to work on explaining the case with the thought of there being two issues occurring, the case started to make a lot more sense. I also had trouble finding supporting information in journals about these differentials. I would have thought that there would have been more research done on issues that are common in dairy cattle. It also could have been that I just was not searching in the right places or with the right search phrases to find the information I was hoping to. Not being able to find exactly what I was looking for in the sources that I have is why I ended up having so many sources. Between all the sources I found, I eventually was able to gather enough information to pull my paper together.

Clinical Case Analysis

Project Overview

Project Description

Cow-Natalie

Background:

Clinical Findings

Differentials

Interpretations

Evidence from Case Observations

How to proceed

Learning issues

References