Neonatal diarrhea is a significant economic loss to the cattle industry and continues to be the most common cause of mortality in calves. Recognition of proper use and application of oral and intravenous (IV) fluid therapy is essential to decreasing calf mortality. Additionally, use of ancillary treatments is also important in complete therapy for neonatal diarrhea.
First and foremost, a clinician must be able to appropriately estimate the degree of dehydration of an ill calf during the physical examination. The most accurate estimations of hydration status based on physical exam parameters are eyeball recession into the orbit (degree of enophthalmos) and skin tent duration, summarized in Table 1. Ancillary diagnostics such as measurement of packed cell volume and plasma protein concentration are also useful for estimation of hydration status, but this isn’t always possible in field situations. Eyeball recession is estimated by inverting the lower eyelid and assessing the degree of recession of the globe into the orbit. Positioning of the eyeball is also dependent on body fat stores and may be inaccurate in cases of chronic cachexia. Therefore, estimation of hydration status using skin tent may be more accurate. Skin tent is best measured on the lateral aspect of the cervical region by pinching the skin and measuring the amount of time it takes for the skinfold to return to normal position.
Development of metabolic acidosis is very common in calves with diarrhea. Therefore, it is also important to determine if metabolic acidosis exists and to assess the degree of severity based on clinical signs. In the past, severity of metabolic acidosis was correlated with the degree of dehydration. However, it has now been proven that degree of acidosis is correlated with suckle presence and vigor, degree of weakness and age of calf. Signs of central nervous system (CNS) depression, decreased suckle response, weakness and ability to stand are all strongly correlated with acidosis. Additionally, calves with diarrhea that are less than 8 days of age have less severe metabolic acidosis. Calves that are greater than 8 days of age will have a more severe acidosis (almost double the base deficit of calves less than 8 days of age). It is also important to mention that calves can have diarrhea and normal hydration status with clinical signs of metabolic acidosis (weakness, ataxia and decreased suckle, menance and panniculus reflex). This CNS depression is likely a result of D-lactate acidosis and will need to be treated with IV bicarbonate therapy. Estimations of severity of metabolic acidosis with base deficits are summarized in Table 2.
Once the degrees of dehydration and acidosis have been estimated, an appropriate fluid therapy plan can be created for the individual calf. Calves with a hydration status less than 8 percent dehydrated and normal CNS can be treated with oral fluid therapy. Calves with a hydration status of 8 percent or more dehydrated and/or CNS depression (weakness, recumbency, no suckle) need IV fluid therapy.
Oral fluid therapy
Not all oral electrolyte products are the same! I will attempt to summarize the aspect of oral electrolyte products that are important and what you should consider when choosing an electrolyte product and recommending electrolyte products for your clients. Goals of oral electrolyte fluid therapy include: supply sufficient sodium to normalize the extracellular fluid volume, provide agents that facilitate absorption of sodium and water from the intestines, provide an alkalinizing agent and provide energy.
Recommended sodium concentration should be between 90 and 130 mmol/L. Sodium is an important component of extracellular fluid and vital to restoring hydration status. Use caution with electrolyte products high in sodium because excessive use can result in hypernatremia. While not as significant as sodium, chloride is also lost with diarrhea. Recommended electrolyte concentration ranges between 40 to 80 mmol/L. Despite often having normal to elevated serum potassium levels, diarrheic calves are usually hypokalemic through fecal loss. The hyperkalemia is due to an extracellular shift secondary to the metabolic acidosis. Therefore, inclusion of potassium in oral electrolytes is important and the recommended concentration is between 10 and 30 mmol/L.
In order for sodium to be systemically absorbed from the lumen of the small intestines it must be coupled with glucose or amino acids. It is not essential to include both glucose and amino acids for transport. However, it is important to maintain a glucose-to-sodium ratio between 1:1 and 1:3 to facilitate sodium transport. An additional benefit of glucose in oral electrolytes is an immediate energy source for the calf.
It is also important to maintain an osmolality of 600 mOsm/L because hypertonic solutions provide greater nutritional support in comparison to isotonic solutions (milk replacer is best at maintaining normal glucose). I would also caution against using extremely hypertonic oral solutions (more than 700 mOsm/L) as they can worsen GI secretions thus worsening diarrhea and the risk of causing abomasal ileus and subsequent bloat.
An alkalinizing agent is essential for diarrheic calves as most are in an acidotic state. The most common alkalinizing agents are acetate, propionate and bicarbonate. Keep in mind a severely acidotic calf will require IV therapy to restore normal blood pH. Acetate and propionate are considered far superior alkalinizing agents than bicarbonate for several reasons. Acetate and propionate facilitate sodium and water absorption and are both metabolized into energy. Additionally, acetate and propionate do not alkalinize the abomasums, thus not interfering with mechanisms preventing bacterial proliferations, and they do not interfere with milk clotting. Oral electrolytes are recommended to include 50 to 80 mmol/L of an alkalinizing agent.
Oral electrolytes are not intended to replace milk replacer and are intended to be administered as an extra meal between feedings. If the additional electrolyte feeding is not possible, then the electrolytes can be added to the milk replacer (ideally use a solution with acetate or low concentrations of bicarbonate).
IV fluid therapy
As mentioned previously, IV therapy is indicated in calves that are 8 percent or more dehydrated or are showing signs of CNS depression or weakness, are comatose or absent suckle, and/or calves that have rapidly progressive diarrhea or fail to respond to oral therapy. Goals of IV fluid therapy include: restoring the calf to normovolemia, correcting metabolic acidosis, correcting mental depression, restoring suckle reflex, correcting electrolyte abnormalities and correcting energy deficit.
Initial approach to IV fluid therapy for any species begins with calculation of fluid deficit using the following formula: replacement fluid (L) = dehydration (%) X bodyweight (kg).
Additionally, one must estimate ongoing losses through diarrhea (up to 7 L/day) and maintenance fluid rate (80-100 ml/kg).
Next, the clinician must decide what type of fluids for therapy. Potential fluid choices for diarrheic calves include: isotonic and hypertonic saline (NaCl), isotonic and hypertonic sodium bicarbonate (NaHCO3), lactated Ringer’s solution, and dextrose. All of these solutions can be commercially purchased or be prepared very inexpensively with supplies in your clinic or truck (see Table 3). Saline solutions are good choices for rehydration but fail to address metabolic acidosis likely occurring in diarrheic calves. Use caution with hypertonic saline; many calves with chronic diarrhea may have pre-existing hypernatremia due to severe dehydration or due to excessive administration of oral electrolyte solutions. Lactated Ringer’s produces an alkalinizing effect but does not alkalinize as quickly as sodium bicarbonate. Additionally, lactated Ringer’s should be avoided in extremely acidemic calves because D-lactate concentrations are likely already elevated and lactated Ringer’s is composed of L-lactate and D-lactate. extrose is indicated in calves with prolonged anorexia or calves diagnosed with hypoglycemia via glucometer.
In general, calves with diarrhea likely have metabolic acidosis, and isotonic bicarbonate solutions are generally a good first-choice fluid replacement therapy for their ability to rapidly correct dehydration and acidosis. Base deficits can be estimated from clinical signs, as previously mentioned in Table 2, or through measurement of base excess from blood gas analysis or plasma total carbon dioxide concentration. Once this is determined, bicarbonate requirements can be calculated using the following formula: bicarbonate requirement (mEq) = bodyweight (kg) X base deficit (mEq/L) X 0.6.
Bicarbonate requirements can be administered as isotonic bicarbonate in conjunction with fluid expansion, or bicarbonate can be administered via hypertonic sodium bicarbonate preparations. Hypertonic sodium bicarbonate preparations include 4.2 percent, 5 percent and 8.4 percent. Solutions of 4.2 percent and 5 percent can be rapidly administered undiluted to comatose calves prior to volume expansion therapy. Or 8.4 percent (1 mEq/ml) can be diluted in isotonic saline for resuscitation or can be administered undiluted slowly intravenously. Generally, I administer 8.4 percent undiluted sodium bicarbonate when an animal is in a severely acidemic state with normal sodium levels. Administration of undiluted 8.4 percent hypertonic sodium bicarbonate can result in potential side effects such as: hyperosmolality of extracellular fluid, hypokalemia, hypernatremia, hypocalcemia, and paradoxic intracellular and CSF acidosis. Hypertonic bicarbonate should not be used in calves with respiratory disease due to inability to appropriately exhale excessive CO2.
It is also important to consider potassium concentrations once bicarbonate therapy has been administered. Potassium will shift intracellularlly once the body returns to a physiologic pH. I typically add approximately 20 mEq/L of potassium chloride to the next bag of isotonic fluids. We use potassium chloride salt which equals approximately 18 mEq of potassium per milliliter of salt.
Ancillary therapies for diarrheic calves are going to be aimed at treating or preventing septicemia/bacteremia and decreased numbers of coliform. In general, most calves with diarrhea have a small intestinal bacterial overgrowth of E. coli with a percentage of those calves having bacteremia from E. coli. Therefore, antimicrobials should be administered to any calf exhibiting systemic signs of illness or calves showing a breakdown in the blood mucosal barrier. Antibiotics should not be administered to calves with a normal hydration status, activity, appetite and temperature, and no evidence of concurrent disease. Antimicrobial should be aimed at treating E. coli, being mostly Gram-negative in spectrum and bactericidal.
Analgesia and anti-inflammatories are also important components of treating calf diarrhea. Antiinflammatory administration will aid with intestinal cramping and discomfort, as well as decreasing inflammation in the gastrointestinal cramp and decreasing effects of endotoxemia and septicemia. NSAIDs will also have an anti-pyrexia and anti-secretory effect that assist in treatment. We usually administer flunixinmeglumine (1.1-2.2 mg/kg IV) once, not to exceed three doses.
Lastly, nutrition is always important to consider with diarrheic calves. Obviously, calves that are comatose or extremely weak will not receive enteral feeding. Ideally, missed enteral feedings should not exceed over 12 hours. If the dam/cow’s milk is not available, milk replacer is recommended to be fed at 12 percent of the calf’s bodyweight. At a bare minimum, 10 percent of the calf’s bodyweight should be fed daily to a diarrheic calf. If the calf is unwilling to suckle despite therapy, then esophageal intubation should be performed to ensure adequate intestinal nutrition is obtained.