Management of equine emergencies can often be distilled to the basics of resuscitation: establishing an airway when necessary and maintaining adequate circulatory volume by providing timely and appropriate fluid resuscitation.
Colic is one of the most common problems presented to equine veterinarians. Diagnosis is aided by nasogastric intubation, transrectal palpation, and ultrasonographic evaluation, which can be used to guide treatment recommendations.
Emergency Fluid Therapy for Horses
In emergency situations, resuscitation fluids are often indicated to replace blood volume and fluid deficits. Lack of adequate circulating volume can lead to multiorgan dysfunction and greater likelihood of death in horses with hypovolemic shock.
Conditions that can require emergency fluid replacement include the following:
injuries with concurrent blood loss
physical exhaustion
acute rhabdomyolysis
hyperthermia
circulatory shock secondary to systemic illness
There are two main types of clinical fluid deficit: hypovolemia and dehydration.
Hypovolemia is a decrease in the effective circulating blood volume that results in circulatory shock. The loss of vascular fluid volume causes decreased venous return to the heart, resulting in decreased stroke volume, decreased cardiac output, and ultimately decreased tissue delivery of oxygen.
Hypovolemic shock is an emergency, requiring rapid replacement of the extracellular fluid volume to improve tissue perfusion and prevent organ failure.
The simplest clinical parameter for determining hypovolemia is warmth of the extremities, which decreases as perfusion is decreased. Other clinical signs that can indicate the need for fluid administration include increased heart rate, increased respiratory rate, increased concentrations of blood lactate, and decreased blood pressure.
The cause of fluid loss from the circulation that results in hypovolemia can be absolute or relative.
Absolute causes of hypovolemia remove fluids directly from circulation or from the lumen of the GI tract. These losses can be external in the form of hemorrhage, reflux, or diarrhea, or they can be due to internal shifts between compartments, including losses into the interstitial space by capillary leakage or third-space losses of fluids (eg, the pleural or peritoneal space).
Relative hypovolemia results from vasodilation that increases venous capacitance, allowing blood to pool in vessels and decreasing perfusion pressure. Relative hypovolemia occurs in sepsis and in systemic inflammatory response syndrome (SIRS), and it can be iatrogenic, resulting from the administration of anesthetic agents or vasodilators.
Dehydration is defined as a decrease in total body water. Compared with hypovolemia, it is a more chronic cause of fluid loss, and the body has time to compensate for the loss by shifting fluid from the intracellular and interstitial spaces to the vascular system.
In dehydration, blood pressure is typically preserved, and vital signs are relatively normal until dehydration is severe (> 8%).
In contrast to hypovolemia, dehydration cannot be corrected rapidly. If a patient is dehydrated but has an adequate circulatory volume, a rapid bolus of IV fluids will simply activate mechanisms to increase urine production. The fluid bolus will be excreted and will not replace the fluid lost from the intracellular and interstitial spaces. Dehydration should therefore be addressed more slowly than hypovolemia would be—ie, over a period 12–36 hours.
Design of a fluid therapy regimen requires consideration of the volume required, the types of fluids needed, and the rate and route of administration.
Fluid Volume
The first step in fluid therapy is to identify whether fluid losses are due to hypovolemia, dehydration, or a combination of the two. The next step is to determine the volume of fluids or deficit to calculate the dose of fluids required.
For acute losses resulting in signs of hypovolemia, fluids to replace the deficit should be administered quickly, in shock doses (see Rate of Fluid Administration), to improve perfusion. Shock doses are subtracted from the calculated fluid plan. When fluid losses are suspected to be the result of dehydration, the estimated extent of dehydration is used to calculate the fluid deficit, which is then added to the maintenance fluid rate along with estimates of ongoing losses (eg, reflux, diarrhea, or hemorrhage) for the next 24 hours. The volume to be administered over 24 hours can be estimated with the following formula:
Volume to Administer (L) = Maintenance Rate (approximately 40–60 mL/kg/day) + Estimated Fluid Deficit (body weight [kg] × Estimate of Dehydration) + Estimate of Ongoing Losses
Maintenance fluid requirements are approximately 1 L/hour for adult horses (approximately 450 kg). The fluid deficit due to dehydration is usually calculated by percentage of dehydration multiplied by body weight in kilograms, which gives the volume needed in liters. Percentage of dehydration can be estimated from clinical and laboratory parameters (see the table Physical and Laboratory Parameters to Estimate Dehydration in Adult Horses).
Physical and Laboratory Parameters to Estimate Dehydration in Adult Horses
Parameter | Estimated Dehydration | |||
|---|---|---|---|---|
6% | 8% | 10% | 12% | |
Heart rate, bpm | 40–60 | 61–80 | 81–100 | > 100 |
Capillary refill time, s | 2 | 3 | 4 | > 4 |
PCV, % | 40 | 45 | 50 | > 50 |
Total protein concentration, g/dL | 7 | 7.5 | 8 | > 8 |
Plasma creatinine concentration, mg/dL | 1.5–2 | 2–3 | 3–4 | > 4 |
Skin tent (seconds to return to normal) | 2 | 2–3 | 3–4 | > 4 |
Sunken eyes | +/– | +/– | Apparent | Obvious |
Membrane moisture | Moist | Tacky | Dry | Dry |
Mucous membrane color | Pink | Pink | Red/white | Cyanotic/white |
The horse’s age and clinical condition can affect these estimated deficits. For example, a nervous horse can have a transiently high heart rate in response to excitement and a falsely increased PCV because of splenic contraction. Clinically, dehydration < 5% is undetectable on physical examination, whereas dehydration > 15% is incompatible with life.
Ongoing fluid losses from the GI tract can be hard to measure. If the large intestine is not reabsorbing water (eg, the patient has diarrhea), fluid losses can be appreciable but difficult to quantify; horses with severe diarrhea can lose approximately 50% of their extracellular fluid volume daily. In contrast, when small intestinal ileus or obstruction is present, the amount of gastric reflux obtained by nasogastric intubation can be easily quantified.
The formula to calculate the volume of fluid to administer provides only a crude estimate of needs. Fluid volumes administered should be adjusted according to the response to treatment, including measurement of the following parameters:
heart rate
pulse quality and capillary refill time
urine production
PCV and serum total protein concentration
serum creatinine concentration
peripheral blood lactate concentration
Reassessment is required to adjust the daily fluid requirements for any horse receiving supplemental fluids, and the timing of the assessment should be dictated by the horse’s clinical condition. In horses in severe shock, cardiovascular parameters might need to be monitored continually (eg, every 15 minutes) until improvement is noted. In horses with severe ongoing fluid losses (eg, due to diarrhea or proximal enteritis), cardiovascular parameters should be reassessed every 4 hours and laboratory parameters measured as frequently as every 6 hours until the horse stabilizes.
Fluid Type
After the required volume of fluid to administer has been determined, the type of fluid should be selected. Fluid choices include crystalloids (fluids containing substances that freely cross the capillary membrane) and colloids (fluids retained in the vascular space for a certain number of hours because of their larger molecular size). Crystalloids are usually used for replacement fluid therapy; colloids are generally reserved for resuscitation or severe hypoproteinemia.
Two general types of crystalloids are available: balanced electrolyte solutions, which contain electrolytes in concentrations similar to those in plasma; and saline solutions, which contain only sodium chloride. The choice of balanced electrolyte solution or saline solution can be based on the results of a serum chemical profile. In most emergency cases, a balanced electrolyte solution is administered.
Dextrose solutions are also considered to be crystalloids, but they are rarely administered alone. Dextrose is usually added as a supplement to a balanced electrolyte solution when indicated by the needs of the individual horse.
Isotonic crystalloid fluids are believed to distribute mainly to the extracellular fluid compartment, thereby rapidly expanding the circulating volume. However, these fluids also redistribute to the interstitial space, and only approximately 25% of the fluids administered remain in the vasculature 1 hour after infusion in healthy patients. Because of this rapid redistribution, it is better to titrate fluids to the patient’s needs over time than to deliver calculated losses via bolus.
Colloid solutions contain large, branched, charged molecules (either proteins or synthetic components) that maintain oncotic pressure by remaining in the vascular space, thereby retaining fluid in the vascular space as well. The addition of colloids to a fluid therapy regimen serves two purposes: 1) better maintenance of the intravascular fluid volume than can be provided by crystalloids, and 2) in cases with current or anticipated hypoproteinemia, mitigation ofedema.
Colloid solutions are available in natural or synthetic forms.
Natural colloids used in horses are plasma products. In general, fresh or fresh frozen plasma is selected when an increase in colloid oncotic pressure is needed and coagulation factors or specific anticoagulants such as antithrombin III are required.
Synthetic colloids used in horses include hydroxyethyl starch and dextrans. The synthetic colloid usually administered to horses is hydroxyethyl starch (hetastarch), because dextrans have higher risk of adverse effects. Hetastarch increases plasma oncotic pressure, and its effect is best evaluated by clinical response (decreased edema) or increased oncotic pressure (measured by colloid osmometry). A refractometer that measures total protein concentration cannot be used to monitor the effect of synthetic colloid administration, because of the low refractive index of synthetic colloids.
Rate of Fluid Administration
The rate of fluid administration depends on the needs of the horse. For horses in hypovolemic shock, the primary goal is to quickly restore the circulating volume and blood pressure to reestablish adequate tissue perfusion.
Assessing the absolute volume of fluid loss of horses in shock is often difficult because of the effects of relative hypovolemia due to vasodilation. The simplest method is to rapidly provide a shock dose of isotonic replacement crystalloid solution and then reassess the patient.
Typical doses for a shock bolus range from 6 to 20 mL/kg administered over 15–30 minutes. The dosage is based on clinical signs and the severity of hypovolemic shock.
Parameters that should be monitored during and after each dose include heart rate, extremity temperature, capillary refill time, pulse quality, jugular refill rate, mentation, blood lactate concentration, PCV, total protein concentration, and urine production (1–2 mL/kg/hour). Fluid boluses are repeated until these parameters plateau and are closer to normal.
Most horses with hypovolemia require two or three shock bolus doses, and no more than four.
Because of the large volumes of balanced electrolyte solutions required, small-volume resuscitation with hypertonic fluids or colloids can be provided first to immediately support the circulation until the shock dose of crystalloids can be administered. A 2- to 4-mL/kg dose of hypertonic saline solution (7.5% NaCl) can rapidly expand the circulating volume by redistributing extravascular fluids into the vascular space.
Because of redistribution and equilibration, the effect of hypertonic solutions lasts only approximately 45 minutes in horses. Colloid solutions can be administered for a more sustained effect. Hydroxyethyl starch (5–10 mL/kg) has been reported to increase oncotic pressure for up to 36 hours. However, it is important to note that dosages of colloids > 10 mL/kg every 24 hours can cause coagulopathies by diluting or inhibiting coagulation factors. For resuscitation, a combination of hypertonic saline solution (4 mL/kg) and hetastarch (4 mL/kg) might have the most beneficial and sustained effects.
The goals of fluid replacement are to normalize acid-base derangements, electrolyte abnormalities, and clinical perfusion parameters, including heart rate, extremity temperature, pulse quality, mucous membrane color, capillary refill time, and urine output. Laboratory parameters for monitoring can include blood lactate concentration, urine specific gravity, PCV, and total protein concentration.
Route of Fluid Administration
The IV route is the fastest method to restore circulating volume because fluids are provided directly to the intravascular compartment. Administration rates can be precisely controlled, and both nutrition (eg, dextrose, lipids) and specific concentrations of electrolytes can be provided. IV fluids are recommended for cases of hypovolemic shock or severe dehydration.
Disadvantages of IV administration are that the fluids provided must be sterile, venous access is needed, and continuous monitoring is required. These requirements increase the cost to the client.
A rate of 7 L/hour can be achieved when fluids are > 2 feet above the jugular vein using a large-bore administration set, and faster rates can be achieved through gravity flow if fluid bags are raised even higher. Polytetrafluoroethylene or polyurethane 14-gauge catheters are routinely used in full-size, adult horses. For more rapid flow, 10- or 12-gauge catheters with large-bore connection sets can be used; however, large-gauge catheters are more thrombogenic. Other ways to increase fluid administration rates include catheterizing both jugular veins or using a pressure bag system or peristaltic pump.
An alternative route of fluid administration is via an intermittent or indwelling nasogastric tube. Enteric fluids might be preferable in some cases because the enteric route is a natural route for fluid intake and absorption, and it is economical, easy, and relatively safe. For these reasons, the enteric route should be the first choice if the patient can tolerate nasogastric administration. However, case selection is key when administering enteral fluids: horses that are in shock, are > 8% dehydrated, or have positive net gastric reflux are not candidates for enteral fluid administration.
Fluids delivered via nasogastric tube do not need to be sterile, larger quantities can be administered at one time, and the exact composition is less important than with parenteral fluids, because the slower absorption time gives the body time to adjust. The solution can include water, electrolytes, and nutrients. Equine electrolyte solutions are preferred, or a homemade mixture of 5.27 g sodium chloride, 0.37 g potassium chloride, and 3.78 g bicarbonate per liter of water can be formulated. Disadvantages of nasogastric fluid administration include the lack of precise control over administration rate and the slower restoration of fluid balance.
For nasogastric fluid administration, the daily fluid rate is divided into boluses and delivered via bilge pump or gravity infusion with a funnel. The horse should be checked for positive net reflux (> 2 L) before administration. Rates < 8 L every 2–4 hours for a 450-kg horse are typically well accepted. If a smaller-gauge feeding tube is in place, a continuous delivery system from a nonsterile IV set and fluid bags or a carboy can be used, and the rate should be determined in a manner similar to that of an IV infusion.
Fluids can also be administered rectally, with indications similar to those for oral fluids. Large boluses of fluids are not tolerated or safe when given rectally. Administration of rectal fluids at 5 ml/kg/hr as a constant rate infusion can provide hydration similar to IV or enteral fluid administration. Some fluids will be excreted during defecation before absorption, and therefore wasted if administered in this manner. Water may be better tolerated and less irritating than electrolyte solutions given per rectum.
Nasogastric Intubation in Horses
Nasogastric intubation is an essential procedure performed routinely in horses with GI disease to decompress the stomach and provide fluid therapy. In extreme cases, gastric decompression can save the life of the horse by preventing rupture of the stomach.
After the horse is adequately restrained, the clinician passes the nasogastric tube into the ventral meatus, using a thumb to keep the tube directed correctly. If a hard structure is encountered (eg, the ethmoid or nasal turbinates) and the tube is difficult to pass, the tube should be retracted and redirected more ventrally, or a smaller tube should be selected.
After the pharynx is reached, a soft resistance is felt when the tube contacts the larynx or esophageal opening. Ideally, the horse’s head should be flexed at the poll to aid passage into the esophagus.
Swallowing is stimulated by applying gentle pressure against the esophageal opening or blowing small puffs of air into the tube, and the tube is then passed into the esophagus as the horse swallows.
The presence of the nasogastric tube in the esophagus is confirmed by one of the following methods:
detection of negative pressure when suction is applied to the tube by mouth
palpation of the nasogastric tube above the left jugular vein
visual identification of the tube passing down the esophagus in the cranial third of the neck
identification of feed material in collected reflux (see reflux secondary to mechanical obstruction image)
Courtesy of Dr. Amelia Munsterman.
If the tube is passed into the trachea, shaking the trachea will result in a rattle. If air is noted when suction is applied by mouth (indicating that the tube is in the trachea), the tube should be withdrawn into the pharynx and the procedure gently repeated until the tube is correctly positioned. A cough is not a reliable signal that the tube is in the trachea; horses do not always cough when the tube is in the trachea, and sometimes they cough when the tube is not in the trachea.
Once the tube is confirmed to be in the esophagus, intermittently blowing into the tube will help to dilate the esophagus and facilitate passage into the stomach. The tube is advanced into the stomach until it is level with the 12th rib (measured externally before the tube is passed).
If spontaneous reflux is not obtained after the tube is confirmed to be in the esophagus, the stomach should be lavaged to check for positive net reflux. It should not be assumed that any excess fluid in the stomach will drain spontaneously.
Before administering medications or fluids via nasogastric tube, the clinician should check for net reflux by filling the tube with approximately 1–2 L of water via a pump or funnel with gravity flow, then removing the pump or funnel and directing the end of the tube downward to create a siphon effect. Subtracting the total amount of water instilled from the total amount of fluid obtained determines the amount of net reflux.
Horses should be lavaged with 6–8 L of water to confirm lack of net nasogastric reflux before treatment is administered. While being removed, the tube should be kinked off to prevent leakage of its contents and possible aspiration.
Positive net nasogastric reflux of more than 2 L is abnormal. Occasionally, a small amount of reflux (< 1 L) is obtained if a horse has had an indwelling nasogastric tube.
When reflux is obtained, the amount, character, and timing in relation to the onset of colic should be noted, as well as any clinical response to gastric decompression.
Common causes of positive net nasogastric reflux include the following:
small intestinal ileus (functional, mechanical)
obstruction of the small intestine or pylorus
compression of the outflow tract by a distended large colon or cecum
anterior enteritis
grain overload
Lesions of the proximal small intestine or pylorus produce large amounts of nasogastric reflux quickly. With lesions of the distal jejunum and ileum, there is initially no net reflux; however, nasogastric reflux usually becomes productive as the disease progresses.
Foul-smelling, fermented, or copious bloody reflux is associated with anterior enteritis (see hemorrhagic reflux image), and all gastric reflux should be treated as a biohazard because of the association of this disease with clostridial and Salmonella spp organisms.
Courtesy of Dr. Amelia Munsterman.
With mechanical obstructions, including strangulating lesions and ileal impactions, reflux is usually composed of feed material and intestinal secretions. However, nasogastric reflux can become hemorrhagic with loss of intestinal viability.
Response to gastric decompression should be noted. Horses with functional ileus or anterior enteritis show clinical improvement as the stomach distention is relieved, and the heart rate can decrease in response to decompression. Horses with a mechanical obstruction usually continue to show discomfort.
The remainder of the physical examination of horses with nasogastric reflux should focus on determining whether functional or mechanical ileus is present. The amount of net reflux obtained should be noted after each gastric decompression, and the volume of fluids administered intravenously should be adjusted accordingly.
Horses with functional ileus generally need gastric decompression every 2–4 hours. The nasogastric tube should be left in place only as long as required, or passed intermittently, because indwelling tubes can cause pharyngeal and laryngeal irritation. Esophageal rupture has been described as a complication of nasogastric intubation.
Epistaxis is a common complication after or during nasogastric intubation, and though rarely life-threatening, it can be impressive and is often alarming to owners. Draping a towel over the noseband of the halter helps prevent blood splattering on the walls and decreases the amount of blood pooling on the floor. Elevation of the head can help to slow and stop epistaxis.
Abdominocentesis in Horses
Abdominocentesis is important in the evaluation of abdominal disease (eg, weight loss, colic, peritoneal effusions, or postoperative complications). It is commonly performed to identify the cause of small intestinal distention and net nasogastric reflux, because large intestinal diseases often do not cause changes in peritoneal fluid in the peracute stage.
Ultrasonography can show the best location to obtain a fluid sample, which can be collected via an 18-gauge needle, a canine bitch catheter, or a teat cannula. A lack of free abdominal fluid on ultrasonographic examination is not a contraindication for this procedure, because fluid is always present in the peritoneal space.
Usually, the sample is obtained just to the right of midline, caudal to the ascending pectoral muscle at the most dependent aspect of the abdomen (see teat cannula placement image). This site will not interfere with a surgical incision if exploratory laparotomy is needed, and it helps avoid trauma to the spleen.
Courtesy of Dr. Amelia Munsterman.
The body wall is much thicker off midline, and the length of the instrument used to sample the fluid should be considered. A needle tap should be avoided whenever severe small intestinal distention is known to exist, to minimize the risk of bowel puncture and iatrogenic peritonitis.
Peritoneal fluid is aseptically collected by free catch into one tube with anticoagulant for cytological analysis (see abdominocentesis sample image) and into a second, plain sterile tube for culture if peritonitis is suspected. It is useful to shake out most of the anticoagulant from the tube before sampling, because excess EDTA will falsely increase the total protein concentration measurement.
Courtesy of Dr. Amelia Munsterman.
Normal peritoneal fluid should be straw-colored and clear on gross assessment.
Normal values for abdominocentesis samples from horses with abdominal disease include a total protein concentration < 2.0–2.5 g/dL and a WBC count of < 5,000 cells/mcL. Repeated abdominocentesis does not appreciably alter these values. On cytological examination, most of the cells are neutrophils; the remainder are lymphocytes and macrophages.
With intestinal strangulation, protein concentration increases in the first 1–2 hours. After 3–4 hours of strangulation, RBCs are present, and after ≥ 6 hours, WBCs continue to increase gradually as intestinal necrosis progresses. Degenerate neutrophils will be noted on cytological examination, and the gross appearance is serosanguinous when strangulation is present (see serosanguinous abdominocentesis sample image).
Courtesy of Dr. Amelia Munsterman.
Peritoneal lactate concentration is often increased with intestinal ischemia and increases over time if serial abdominocenteses are performed.
Enterocentesis sometimes occurs, especially in cases of sand colic, and should be differentiated from intestinal rupture. With enterocentesis, cytological examination reveals plant material, free bacteria, and debris, but few cells.
Clinical signs of enterocentesis are not consistent with spontaneous intestinal rupture. However, in cases of peracute rupture (approximately 2–4 hours), clinical signs of endotoxemia (eg, lethargy, tachycardia, congested mucous membranes, signs of shock) might not be evident.
Cytological examination of abdominal fluid compatible with intestinal rupture shows a large number of toxic and degenerate neutrophils, in addition to bacterial organisms, plant material, and neutrophils containing phagocytosed bacteria.
Both enterocentesis and intestinal rupture can demonstrate evidence of plant material characteristic of luminal contents when examined grossly (see gastric rupture abdominocentesis sample image).
Courtesy of Dr. Amelia Munsterman.
Blood contamination that occurs during abdominocentesis should be differentiated from hemoabdomen or severely devitalized bowel. Blood from vessels in the skin or body wall usually swirls in the sample and sediments when centrifuged, leaving a clear supernatant. Fresh blood contamination shows platelets on cytological examination, which are not present in blood accumulations > 12 hours old. If the spleen is accidentally punctured, centrifugation of the sample reveals a PCV the same or higher than the peripheral PCV. In cases of internal hemorrhage, blood in the sample is usually hemolyzed, platelets are clumped or absent, and erythrophagocytosis can be evident. When centrifuged, the supernatant remains serosanguinous. If vascular compromise of the bowel has occurred, hemolysis of RBCs that leak from damaged capillaries also results in serosanguinous peritoneal fluid that may produce a red supernatant after centrifugation.
Abdominal ultrasonographic examination of hemoabdomen reveals fluid swirling, termed a "smoke sign."
Abdominal surgery or primary peritonitis can also produce abnormal abdominocentesis results, as follows:
With sterile peritonitis, the WBC count remains elevated for up to 2 weeks, and cell counts of 40,000 cells/dL have been reported 6 days after surgery. Neutrophils appear nondegenerate on cytological examination, and bacteria are not observed. Total protein concentration peaks 6 days after surgery and can remain increased for 1 month.
After enterotomy, or resection and anastomosis, degenerate neutrophils and occasional bacteria can be evident in the first 12–24 hours, but they should resolve over time.
With septic peritonitis, clinical signs are consistent with bacterial infection (eg, fever, lethargy, anorexia, ileus, colic, endotoxemia). The WBC count and total protein concentration in the abdominocentesis sample are markedly increased. On cytological examination, > 90% of cells are degenerate neutrophils. Free and phagocytosed bacteria are evident.
A serum–peritoneal glucose difference > 50 mg/dL, or peritoneal fluid pH < 7.2 with peritoneal glucose < 30 mg/dL, supports the diagnosis of peritonitis.
Ultrasonographic Examination of the Acute Abdomen in Horses
Transabdominal ultrasonography is indicated in horses with acute and chronic abdominal pain, fever of unknown origin, anorexia, colitis, and weight loss. An abbreviated ultrasonographic examination, in conjunction with the results of other diagnostics, is commonly performed in horses to help determine the cause of colic.
The ultrasonographic method known as fast localized abdominal sonography of horses, or FLASH, focuses on seven regions of the abdomen and the cranial thorax (see FLASH sites image) and can be completed in ≤ 10 minutes (1). The structures typically identified or located in specific regions of the abdominal cavity for horses with acute abdominal pain are the stomach, spleen, and left liver lobe; left kidney and base of the spleen; left dorsal and ventral colon; jejunum; right liver lobe, right dorsal colon, and duodenum; right kidney, cecum, and duodenum; and right ventral colon. The cranial ventral lung is also imaged to rule out thoracic disease.
Courtesy of Dr. Amelia Munsterman.
Stomach, Spleen, and Left Liver Lobe
In an ultrasonographic image, the caudal aspect of the stomach can be identified on the left side between the 8th and 13th ribs at the level of and ventral to the point of the shoulder. The greater curvature is normally observed as a hyperechoic, curved line caudal to the diaphragm to the 12th-13th intercostal space (ICS; see stomach and spleen ultrasonographic image).
Courtesy of Dr. Amelia Munsterman.
The spleen and splenic vein are evident adjacent to the stomach wall.
A gas-fluid interface or extension of the greater curvature past the 14th ICS can indicate gastric distention with fluid, ingesta, and gas.
In younger horses, the left liver lobe (7th-9th ICS) and spleen might be noted adjacent to each other, cranial and dorsal to the stomach and caudal to the diaphragm (see left liver lobe and spleen ultrasonographic image). The liver (with portal and hepatic vessels visualized within the parenchyma) will be dorsal and lateral to the spleen (which has a homogenous, "ground glass" appearance). However, the lung often obscures this view.
Courtesy of Dr. Amelia Munsterman.
Left Kidney and Base of the Spleen
The left kidney should be visible adjacent to the spleen in the dorsal left flank (see left kidney and spleen ultrasonographic image). If a hyperechoic shadow is noted deep to the spleen and the kidney is not visible, a nephrosplenic entrapment of the large colon is suspected. If both left kidney and spleen are obscured by gas-filled intestine, a left dorsal displacement of the large colon is suggested.
Courtesy of Dr. Amelia Munsterman.
Large colon displacements and nephrosplenic entrapment (see spleen and colon displacement image) should be confirmed by transrectal palpation. The left kidney should also be evaluated for nephrolithiasis, hydronephrosis, or abnormal architecture.
Courtesy of Dr. Amelia Munsterman.
The spleen occupies most of the left flank and extends cranially to lie at or just across midline. It is diffusely echogenic with a hyperechoic capsule.
The descending (small) colon can be visible as a hyperechoic, undulating structure deep to the spleen (see descending colon and spleen and small intestine and spleen ultrasonographic images).
Courtesy of Dr. Amelia Munsterman.
Courtesy of Dr. Amelia Munsterman.
Left Dorsal and Ventral Colon
The left ventral abdomen should allow visualization of the left ventral colon, with sacculations and acoustic shadowing consistent with gas in the lumen (see left ventral colon ultrasonographic image). The left dorsal colon does not have sacculations and should appear as a smooth, hyperechoic line.
Courtesy of Dr. Amelia Munsterman.
Horses with colitis can demonstrate hypoechoic fluid within the colon, which can appear to swirl on ultrasonography. Fluid in the lumen provides contrast, enabling measurement of the colon wall, which can be thickened with inflammation (up to 9 mm). Normal colon wall thickness is < 3–4 mm but is difficult to measure because of gas present in the colon.
In cases of large colon displacement or volvulus, the colon wall can be thickened, and nonsacculated colon can be visible on the ventral body wall. Increased free abdominal fluid is hypoechoic and observed on both the left and right, as well as on ventral midline.
Jejunum and Ileum
Typically, the small intestine is not visible on ultrasonography as a distinct structure. Diseases that cause ileus, intraluminal obstruction, or inflammation can result in distention and thickened walls, making it possible to identify and measure loops of small intestine.
The lumen of the small intestine normally contains fluid ingesta, which appears hypoechoic. Normal small intestine should have a wall thickness < 4 mm and a diameter < 3 cm.
The contractility of the small intestine should also be assessed during examination. If hyperechoic gas shadows are present in the wall of the small intestine, an anaerobic infection or necrosis should be suspected.
A horse with a small intestinal strangulating lesion might have two differing ultrasonographic appearances of small intestine: small intestine oral to the strangulated intestine will be distended and hypomotile, with normal wall thickness, whereas the strangulated section will be maximally dilated, with thickened walls.
Abnormalities of the small intestine are most often identified ultrasonographically by scanning ventrally in the inguinal region, adjacent to the udder or prepuce. These abnormalities can also be seen in the cranial ventral abdomen at midline. In severe disease, small intestine can be observed throughout the abdominal cavity in multiple acoustic windows (see distended small intestine ultrasonographic image); however this finding is not indicative of a specific diagnosis.
Courtesy of Dr. Amelia Munsterman.
If distended small intestine is noted between the stomach and spleen, a gastrosplenic incarceration should be suspected. Alternatively, distended small intestine in the dorsal and cranial abdomen, caudal to the diaphragm on the right side of the abdomen, can be consistent with an epiploic foramen entrapment.
The presence of linear foreign bodies in the lumen of distended small intestine can indicate ascarid infestation in foals.
Right Liver Lobe, Right Dorsal Colon, and Duodenum
The liver in a horse is more commonly observed on the right side of the abdomen and is ultrasonographically visible between the right 6th-15th ICS. It should not extend past the costochondral junction. The duodenum courses between the liver and right dorsal colon (10th-14th ICS; see right dorsal colon, right liver, and duodenum ultrasonographic image).
Courtesy of Dr. Amelia Munsterman.
The duodenum should contract and empty completely; hypomotility or a static and distended duodenum is consistent with obstructive or inflammatory disease that causes ileus. In these cases, the stomach can be distended as well.
Only a single loop of duodenum should be visible in this acoustic window. Additional loops of abnormal small intestine can be consistent with an epiploic foramen entrapment. The right dorsal colon is represented by a hyperechoic curvilinear line because of gas in the lumen.
Ultrasonographic examination of the right dorsal colon can show a hypoechoic, fluid-filled lumen in horses with colitis, and the wall of the colon can appear thickened (> 4 mm).
Right Kidney, Cecum, Right Dorsal Colon, and Duodenum
Moving caudally in the right dorsal abdomen, the descending duodenum is evident caudal and ventral to the right kidney, which lies dorsally in the 14th-16th ICS (see right dorsal colon, kidney, and duodenum ultrasonographic image).
Courtesy of Dr. Amelia Munsterman.
The right kidney is easier to visualize than the left, and the ultrasonographic image should demonstrate a hypoechoic cortex with a less echogenic renal medulla. The renal pelvis is hyperechoic because of fat and fibrous tissue. The right kidney should also be evaluated for nephrolithiasis, hydronephrosis, and abnormal architecture.
The duodenum should be assessed for motility and distention as it courses caudally over the cecal base. The cecum lies caudal and ventral to the right kidney (13th-16th ICS) and, with a gas-filled lumen, should appear similar to the left ventral colon.
Horses with typhlocolitis demonstrate a hypoechoic, fluid-filled cecal lumen, and the wall of the cecum can be thickened with decreased motility.
Right Ventral Colon
The right ventral colon is visible in the ventral abdomen and has haustra and sacculations similar to those of the left ventral colon. Changes consistent with colitis, described above, can also be noted in this acoustic window.
With large colon displacements or volvulus, mesenteric vessels can sometimes be observed coursing along the right body wall (see mesenteric vessels image). The colon wall can be thickened as a result of inflammation or vascular occlusion (up to 9 mm), and nonsacculated dorsal colon is visible on the ventral body wall with displacements.
Courtesy of Dr. Amelia Munsterman.
Free abdominal fluid might be increased in horses with inflammation or peritonitis and observable throughout the ventral abdomen.
Trocarization in Horses
Percutaneous trocarization can be performed to decompress the cecum or large intestine in cases of severe gas distention. Pathological increases in intraluminal pressure can result in severe abdominal distention, pain, dyspnea, and perfusion abnormalities.
Before the procedure, the segment of intestine involved must be identified. In adult horses, the affected intestinal segment is localized by transrectal palpation combined with transabdominal ultrasonography. Abdominal auscultation can produce a “ping” after percussion that is indicative of a gas-filled organ.
The distended segment of the cecum or large intestine must be against the body wall so that it can be safely reached by trocarization. The position of the organ targeted for trocarization is confirmed by ultrasonography, to minimize risk of inadvertent organ or vascular damage. The most common trocarization site is the upper right flank in the general location of the cecal base (see cecal trocarization image).
Courtesy of Dr. Amelia Munsterman.
Trocarization is performed as follows:
The area around the insertion site is clipped and aseptically prepared, and then a local anesthetic is infiltrated into the subcutaneous tissues.
The catheter is inserted aseptically and attached to an extension set that is placed in a nonsterile cup of water to monitor progress through the appearance of gas bubbles released into the water. In adult horses, a 14-gauge, 12.5-cm, over-the-needle catheter is typically used. In neonates, an 18-gauge, 5-cm needle could be adequate.
Release of gas produces bubbles; to maintain flow, the catheter can be repositioned as the bowel decompresses.
An antimicrobial (usually approximately 5 mL of gentamicin) is infused subcutaneously as the catheter is withdrawn.
Trocarization can be accompanied by any of the following complications:
peritonitis
hemorrhage
local subcutaneous abscess
The horse should be observed for 48 hours for clinical signs of infection, including abdominal pain and fever. Peritonitis is confirmed by evaluation of abdominal fluid and treated with systemic broad-spectrum antimicrobials until it is resolved. Hemorrhage is typically self-limiting, and local abscesses can be drained percutaneously.
Tracheotomy in Horses
Tracheotomy is an emergency procedure for conditions resulting in acute upper airway obstruction (eg, arytenoid chondritis, snakebite, foreign body).
The tracheotomy incision site is selected at the junction of the proximal and middle third of the neck, above the V formed by the paired sternothyroid and sternohyoid muscles (see tracheotomy incision image). If possible, the skin should be clipped, aseptically prepared, and infiltrated with a local anesthetic. With severe, life-threatening respiratory distress from an obstruction, this procedure needs to be performed without aseptic preparation of the surgical site.
Courtesy of Dr. Amelia Munsterman.
The initial incision (6–10 cm), made on midline with a scalpel through the skin and cutaneous colli muscle, is then extended between the paired sternothyroid and sternohyoid muscles. Alternatively, the muscles can be divided on midline by blunt dissection with Metzenbaum scissors.
The trachea is exposed by this incision and digital dissection, and a sharp transverse incision is made through the mucosa between two tracheal rings, taking care to avoid tracheal cartilages. The incision will extend to approximately 30–40% of the circumference of the trachea. If the horse's head is elevated or extended, the tracheal incision should be centered slightly distal relative to the skin incision, to avoid covering the tracheotomy site when the head is lowered.
A J-shaped silicone tracheostomy tube can be inserted and secured in place by attachment to the mane with gauze. The cuff should not be inflated, unless the horse is to be ventilated, to prevent intraluminal tracheal necrosis. Alternatively, a metal, self-retaining tracheostomy tube might be preferred (see tracheostomy tube image) because of the tendency of J tubes to fall out.
Courtesy of Dr. Amelia Munsterman.
The tracheostomy tube should be removed, cleaned, and replaced twice a day (or more often, if secretions occlude the lumen of the tube). Local inflammation and superficial infections are common because of the contaminated nature of the procedure. Attention to postoperative nursing care (cleaning the wound) decreases the amount of contamination. Petroleum jelly applied to the surrounding skin also helps to decrease skin scalding.
It is important to prevent water from entering the tracheotomy site. Baths should be avoided, and the horse should not be turned out in a pasture with access to a pond.
Complications of tracheotomy (eg, cartilage deformity, intraluminal granulation tissue, mucosal stricture) are rare and can be minimized by removal of the tube as soon as possible. One method to determine when the tube can be removed is to temporarily occlude the lumen by hand and observe whether the horse can breathe without it.
After removal of the tracheostomy tube (see tracheotomy incision after tube removal image), the site should be cleaned with saline solution twice daily and allowed to heal by second intention. The trachea generally closes in 10–14 days and heals completely in 3 weeks.
Courtesy of Dr. Amelia Munsterman.
Thoracostomy Tube Placement in Horses
Thoracostomy tubes are indicated for evacuation of fluid or air in the pleural cavity. Causes of pleural effusion or pneumothorax include hemothorax, pleuropneumonia, and trauma.
The site for insertion of the thoracostomy tube depends on whether air or fluid is to be evacuated.
For pneumothorax, the incision is placed caudal and dorsal in the thoracic cavity, ventral to the epaxial muscles, at the level of the 12th-15th ICS.
For fluid effusions, the incision is cranial and ventral, above the point of the olecranon, in the 7th-8th ICS.
The site and depth of thoracostomy tube placement can further be localized by thoracic ultrasonography to prevent inadvertent trauma to the lungs or heart.
Thoracostomy is performed as follows:
The insertion site is aseptically prepared, and anesthesia is provided by infusion of a local anesthetic solution in the skin, subcutaneous tissues, and intercostal muscles.
An incision is made over the cranial aspect of the rib, immediately caudal to the selected intercostal space, and extended to the costal surface (see thoracostomy tube incision image).
The thoracostomy tube with its trocar is introduced perpendicular to the skin until it reaches the rib surface, and then bluntly inserted cranial to the rib through the intercostal muscles and pleura into the thorax (see thoracostomy tube insertion image).
Once the pleura is penetrated, the tube is pushed off the trocar in a cranial and ventral direction, and secured with a purse-string and finger-trap suture.
A one-way valve is placed at the end of the tube to prevent the entrance of air.
Fluid in the thorax is drained slowly by gravity flow to prevent hypovolemic shock.
Courtesy of Dr. Amelia Munsterman.
Courtesy of Dr. Amelia Munsterman.
For pneumothorax, a large-gauge catheter is often adequate. Air can be removed with a 60-mL syringe and three-way stopcock valve. Slow removal of air can prevent barotrauma. If air is removed too rapidly, reexpansion trauma can result with increased capillary permeability in the lungs that leads to pulmonary edema, hypoxemia, decreased cardiac output, hypotension, and death.
Thoracostomy tube placement can be accompanied by any of the following complications:
local subcutaneous abscess
hemorrhage
hypovolemic shock
Common complications of thoracostomy can include localized infection, swelling, and edema at the site of insertion. Strict asepsis and good surgical technique can lower the risk.
Occasionally, large volumes of fluid can be present in horses with pleuritis. Rapid removal of this third-space fluid can result in cardiovascular decompensation. Therefore, these patients should be preloaded with IV fluids before drainage. Gradual removal of fluid is also recommended.
Some horses have bilateral thoracic disease because the mediastinum is incomplete in horses. However, horses with long-standing lung disease often lose the normal communication between both sides of the thorax as a result of fibrin accumulation. Ultrasonography is used to confirm whether drainage of one hemithorax has removed fluid in the contralateral hemithorax.
Key Points
To stabilize a hypovolemic patient, shock fluid boluses can be repeated up to 4 times until clinical signs improve or plateau.
Nasogastric intubation should be performed in all horses presenting with clinical signs of GI disease. Volumes of net reflux > 2 L warrant further investigation.
Abdominocentesis is most useful for identifying small intestinal disease or peritonitis.
Trocarization is useful for decompressing the large intestine and cecum in severely distended, painful patients.
Tracheotomy should be urgently performed in horses with upper airway obstruction.
Thoracostomy tubes can be placed for drainage of effusion or air from the pleural cavity.
For More Information
Fielding CL, Magdesian KG, eds. Equine Fluid Therapy. John Wiley & Sons; 2015.
Cook VL, Hassel DM. Evaluation of the colic in horses: decision for referral. Vet Clin North Am Equine Pract. 2014;30(2):383-398, viii.
Busoni V, De Busscher V, Lopez D, Verwilghen D, Cassart D. Evaluation of a protocol for fast localised abdominal sonography of horses (FLASH) admitted for colic. Vet J. 2011;188(1):77-82.
Radcliffe RM, Hill JA, Liu SY, Cook VL, Hurcombe SDA, Divers TJ. Abdominocentesis techniques in horses. J Vet Emerg Crit Care (San Antonio). 2022;32(S1):72-80.
Schroeder EL, Gardner AK, Mudge MC. How to perform a percutaneous cecal or colonic trocarization in horses with severe abdominal tympany. J Vet Emerg Crit Care (San Antonio). 2022;32(S1):57-62.
Also see pet owner content regarding common emergency procedures in horses.
References
Busoni V, De Busscher V, Lopez D, Verwilghen D, Cassart D. Evaluation of a protocol for fast localised abdominal sonography of horses (FLASH) admitted for colic. Vet J. 2011;188(1):77-82. doi:10.1016/j.tvjl.2010.02.017
