Colic

K. Gary Magdesian • Bradford P. Smith

Colic is defined as the manifestation of visceral abdominal pain. Colic may be the result of nongastrointestinal pain such as urinary tract obstruction (Boxes 7.6 and 7.7).

• Distention of gut with fluid, gas, or ingesta

• Pulling on the root of the mesentery (mesenteric tension)

• Ischemia or infarction

• Deep ulcers in the stomach or bowel

• Peritoneal pain (peritonitis)

Signs of colic in the horse include restlessness, lying down and getting up, groaning, grunting, rolling, sweating, kicking at the abdomen, or suddenly dropping to the ground in pain. Anorexia and depression often accompany these signs. Horses may develop hypovolemic or endotoxic shock characterized by tachycardia with weak pulse quality and prolonged capillary refill time, cold extremities, and bright red (vasodilatory phase) followed by dark or pale (vasoconstrictive phase or low cardiac output state) mucous membranes if the problem is severe and affects cardiovascular integrity.

Evidence of shock is usually present only when the disease condition is severe and involves ischemic or infarctive disease (volvulus, torsion, thromboembolism) or advanced visceral distention (extreme flatulence, impaction, or dilation). Foreign bodies such as sand or enteroliths in the large colon may result in low-grade recurrent colic. When an enterolith is passed into the transverse colon where it obstructs the bowel, signs of complete obstruction and acute colic ensue. These signs are manifestations of visceral pain, mediated by the sympathetic nervous system.

In contrast, parietal pain associated with peritonitis is sometimes responsive to external palpation. Whereas the animal with visceral pain shows active signs of colic, the animal with parietal pain is usually reluctant to move and has a splinted abdomen. Acute peritonitis occurs within minutes after rupture of the stomach or perforation of an ulcer as a result of immediate irritation of serosal surfaces by the acid contents, whereas with rupture of the colon or rectum it may take several hours or more before peritonitis is clinically apparent.

Ruminants exhibit colic less frequently than horses, probably because of a higher threshold for pain and because dietary shifts principally affect the rumen; thus intestinal gas pains occur less frequently. Colic with visceral pain (including urinary tract) is manifested by grinding the teeth (odontoprisis or bruxism), grunting or groaning, treading with the hind feet, kicking at the abdomen, restlessness, repeatedly lying down and getting up, anorexia, and depression. With parietal pain caused by peritonitis, ruminants demonstrate abdominal pain by arching the back, splinting, and exhibiting pain on deep palpation of the area. These signs are seen most commonly with traumatic reticuloperitonitis and perforating abomasal ulcers; rarely are these diseases associated with the colic signs described previously.

■ BOX 7.6

Gastrointestinal Causes of Colic in Horses^a

Common Causes

Accumulation of intestinal, cecal, or colonic gas Hypermotility and intestinal spasms

Feed impaction, constipation

Meconium impaction (newborn)

Gastric ulcers (foal)

Less Common Causes

Thromboembolism

Intestinal foreign body (sand; enterolith; phytobezoar) Volvulus of small intestine

Pedunculated lipoma with bowel strangulation Hernia, inguinal, epiploic, umbilical, diaphragmatic Nephrosplenic ligament bowel entrapment

Ascarid impaction

Massive strongyle infection

Gastric dilation

Anterior enteritis (duodenitis or proximal jejunitis)

Enteritis, impending or active

Peritonitis

Parasympathomimetic drugs

Irritant cathartics

Necrotizing enterocolitis

Psychogenic colic

Rectal tear

Volvulus or displacement of large bowel

Rupture of stomach or intestine

Ileus

Intussusception

Uncommon Causes

Abdominal adhesions

Intramural hematomas of stomach or intestine

Stenosis or stricture of bowel lumen

Botulism

Tetanus

Potomac fever

Exhaustion

Anaphylaxis

Rhodococcus equi, gut abscesses

Cribbing or wind sucking

Abdominal fibroma

Segmental ischemic necrosis following mesocolic tearing Equine viral arteritis

Anthrax with bleeding

Malignant edema (Clostridium species)

Malignant mesothelioma

Gastric or intestinal tumor

Atropine

Vitamin K3 deficiency (moldy sweet clover)

Toxins

(See also toxins listed under Diarrhea)

Cantharidin toxicity

Dioxin

Trichloroethylene-extracted feed toxicity

Warfarin (dicumarol)

Herbicides

Lead

Nitrophenyl urea (vacor)

Phenylbutazone or other nonsteroidal antiinflammatory drugs

Poison plants (many of those that produce diarrhea also produce colic; see plant toxins listed under Diarrhea)

African horse sickness (exotic)

Grass sickness (exotic)

^aSee additional lists at www.vet.cornell.edu/consultant.

■ BOX 7.7

■ BOX 7.8

Causes of Colic in Ruminants^a

Common Causes

Increased intestinal gas

Intussusception

Torsion or volvulus of the mesenteric root

Peritonitis

Intestinal foreign body or obstruction

Urolithiasis

Ruptured bladder

Acute pyelonephritis

Abomasal torsion

Abomasal ulcer

Cecal dilation or volvulus

Severe bloat

Less Common Causes

Cystitis or urinary tract disease

Abomasal bloat (neonates)

Uterine torsion or rupture

Hernia

Parturition, impending

Hypermotility and spasms of gut

Feed impaction

Right displaced abomasum

Acute traumatic reticulitis, abomasitis, or duodenitis

Acute liver disease

Vagal indigestion

Hemorrhagic bowel syndrome

Atresia coli (neonates)

Uncommon Causes

Rabies

Rectal tear

Rectal prolapse

Diaphragmatic hernia

Grain overload

Water intoxication

Winter dysentery

Ovarian abscess

Fat necrosis

Cholelithiasis

Intestinal adhesions

Enterotoxemia

Ileus

Intestinal strangulation

Inversion of uterine horn

Malignant edema

Malignant mesothelioma

Ruptured uterine artery

Intestinal neoplasia

Aortic, iliac, or femoral thrombosis

Anaphylaxis

Renal cysts

Ruptured prepubic tendon

Vaginal laceration

Torsion of descending colon

Rinderpest (exotic)^b

Toxins

Plant poisonings (many of those that cause diarrhea also produce colic; see plant toxins listed under Diarrhea)

^aSee additional lists at www.vet.cornell.edu/consultant.

^bRinderpest was a cause of colic in ruminants until 2011, when it was eradicated worldwide.

Extraintestinal Causes of Colic in Horses

Common Causes

Mesenteric abscess

Ovarian tumor, abscess, or hematoma Parturition

Acute hepatitis (massive necrosis) or hepatic lipidosis Diaphragmatic hernia

Ruptured bladder (foal) Uterine torsion

Less Common Causes

Urinary tract or renal disease, including urolithiasis Pleuritis or pericarditis (referred pain)

Retained placenta

Uterine rupture or retroflexion Spermatic cord thrombosis or torsion Hypocalcemia

Uncommon Causes

Perirectal abscess Pheochromocytoma Purpura hemorrhagica

Biliary atresia Vaginal or vulvar tear

Cholelithiasis

White muscle disease

Atypical myopathy

Rabies

Rupture of prepubic tendon Splenitis, splenic abscess, splenomegaly

Cauda equina neuritis with retention of feces or urine

Diagnosis and Management of Colic in the Horse (for Neonates, See Chapter 17)

1. Take history. Because colic is a common problem in horses, mild to moderate degrees of abdominal pain are often initially treated symptomatically with analgesics and/or laxatives before major diagnostic efforts are undertaken. Most colic of mild to moderate severity responds favorably to symptomatic treat­ment. In general, severe pain or pain that is unresponsive to analgesics indicates a more serious condition for which more aggressive medical management or surgical correction may be indicated. Recurrent mild-to-moderate colic may be an indica­tion of a more serious problem such as bowel entrapment or displacement, thromboembolism, internal abscess, enterolith, sand or other foreign body, tumor, gastric ulcers, hypobiotic cyathostomiasis, Strongylus vulgaris larval migration, heavy burden of ascarids, abdominal adhesions, cholangiohepatitis, biliary stones, strictured bowel, or urinary tract disease.

2. Perform physical examination. Intestinal causes of colic can often be differentiated from colic associated with other organ systems (Box 7.8) by physical examination findings and laboratory data.

3. Ultrasound and radiology. Ultrasound may help in locating masses, adhesions, or enlarged liver (see Abdominal Ultra­sonography, Chapter 32). It may also be helpful in the diagnosis of gastrointestinal disease including nephrosplenic entrapment of the large colon, right dorsal displacement, and small intestinal distention. Detection of sand from the ventral abdomen may be possible. Ultrasound can be particularly useful in foals and small ruminants because of their size. Radiology can also be useful in detecting entero­liths or sand in adult horses and in some gastrointestinal conditions of foals, such as meconium impaction or sand enteropathy, provided powerful units are available. Rarely is radiology useful in diagnosing the cause of colic in ruminants, except for urethrographs in sheep and goats to locate a urethral stone.

4. Examine feces. Gross examination of feces should be performed. The presence of sand can often be detected by mixing feces with water in a bucket, then pouring off the water and looking for sediment.

5. Use laboratory aids. Laboratory aids of immediate benefit in diagnosis and management include measurement of PCV and plasma protein concentration to aid in assessing hydration and vascular integrity, as well as an abdominal paracentesis to evaluate abdominal fluid grossly and microscopically. Pain and excitement alone can increase the PCV in horses, but some studies indicate that there is a correlation of increased PCV (>55%) and nonsurvival in colic cases. Plasma proteins are not increased acutely unless blood volume is decreased through shifts in compartmental distribution of body fluids. In colic cases these fluid shifts usually mean that an increased and abnormal amount of extracellular fluid is in the gut lumen, a “third space” where it is not available for maintaining blood volume. Blood lactate concentration measurement has become routine in evaluation of horses with acute abdominal disease. It is useful in monitoring as an end point to fluid therapy, as well as of systemic inflammation and cell metabolic health. Some studies have suggested a prognostic role of lactate in horses with colic, although there is marked overlap between survivors and nonsurvivors. An increase in peritoneal lactate concentration over time has been predictive of strangulating lesions in horses with colic.³³

6. Abdominal fluid is normally present in small volume (a few drops to 50 mL); is clear and colorless to yellow; and has a total protein concentration below 2.5 g/dL, specific gravity less than 1.015, little or no fibrinogen (50 mg/dL difference is abnormal) and evaluation of abdominal fluid pH, lactate (as compared with blood lactate), and lactate dehydrogenase (LDH) concentrations can aid in the diagnosis of septic peritonitis.³⁴ Grossly, fluid changes to cloudy yellow, then to blood-tinged with fibrin clots, and finally to black in color as bowel necrosis and hemolysis of extravasated red blood cells (RBCs) occur.

7. Plasma fibrinogen, as well as peripheral leukocyte counts, can aid in the differentiation of enterocolitis or anterior enteritis from strangulating lesions. Serum electrolyte concentrations and acid-base status are important from a therapeutic standpoint. Serum biochemistries including liver enzymes, creatinine, and BUN are important in evaluating for liver and renal compromise. Hyperglobulinemia may be indicative of chronic disease.

8. Evaluate response to treatment. The approach to diagnosis of colic signs is often tied in with management because if the animal's pain cannot be alleviated, surgical intervention and specific diagnosis of displacements, torsions or volvulus, internal hernias, masses, and adhesions are the next steps. The initial diagnosis considers the history of deworming and feeding. The findings of the physical examination including rectal examination and evaluation of the degree of pain determine whether additional laboratory workup is indicated. In many cases with mild to moderate pain and no evidence of shock, standard treatment includes parenteral administration of an analgesic agent such as flunixin meglumine (as long as the patient is hydrated) or butylscopolamine (see Chapter 3) and oral administration of a mild laxative such as mineral oil (4 to 8 mL/kg). When a nasogastric tube is passed, the stomach should be checked for reflux and decompressed as needed. The pH of the gastric reflux may indicate primary gastric dilation if acidic, or small intestinal blockage or ileus if alkaline. Dark brown, foul-smelling, and alkaline reflux is often associated with anterior enteritis (duodenitis and proximal jejunitis). If a significant amount of reflux is present, oral medications should be withheld. If cardiovas­cular function is impaired (poor mucous membrane color and capillary refill, weak pulse, cold extremities, impending shock), balanced, polyionic, and isotonic crystalloid fluids should be given intravenously at a rate of 10 to 20 mL/kg boluses until signs of shock abate or plateau. In addition, 4 mL/kg hypertonic saline can be administered as a rapid but transient treatment of shock. Large amounts of apparently painful gas that is auscultable in the right flank can be tapped and drawn off with cecal trocharization, although the risk for peritonitis should be considered and this technique should be reserved for when surgical exploration is not an option or is delayed. The principles of colic management include 1) control of pain, 2) relief of distention, 3) relief of obstruction, and 4) treatment of shock.

9. Perform exploratory surgery. In making a decision concerning management of colic, it is important to separate impending enteritis and peritonitis from bowel disease requiring surgical intervention. Anterior or proximal enteritis can result in prolonged moderate pain and requires constant or frequently repeated analgesic administration and gastric decompression of the foul-smelling, dark reddish-to-brownish stomach contents. However, pain often subsides and is replaced with depression after gastric decompression in horses with anterior enteritis, whereas horses with strangulating lesions often remain in pain. The presence of fever or decreased total WBC count (with neutropenia) may be an indication of impending or ongoing enteritis, in which case surgery may not be indicated.

Surgery is indicated in the following situations:

a. Pain is severe and intractable or nonresponsive/poorly responsive to analgesics.

b. Pulse is weak and rate is over 70 beats/min, and oleander or other cardiotoxicity and acute enterocolitis are ruled out.

c. Perfusion is poor, as evidenced by cold extremities, off-color mucous membranes, and poor capillary refill, and enterocolitis or toxicities are ruled out.

d. No gut sounds are auscultated (a lack of fecal production).

e. Bowel is markedly distended on rectal palpation or abdominal ultrasound.

f. Large volumes of yellowish alkaline gastric reflux are present.

g. Abdominocentesis indicates damaged bowel (blood tinged, increased protein, increased WBCs). When proximal enteritis remains a possibility, surgery should be avoided unless it is indicated to decompress bowel.

Surgery may be contraindicated in the following situations:

a. Fever

b. Neutropenia or marked neutrophilia

c. Severe icterus or marked enzyme abnormalities indicating primary liver disease

d. Foul-smelling, brownish-red gastric reflux characteristic of proximal enteritis (duodenitis/jejunitis), especially when removal of reflux results in discontinuation of signs of pain

e. Evidence of an extraintestinal cause not amenable to surgical correction (such as severe pyelonephritis) or hyperammonemia

f. Colitis, enterocolitis, or diarrhea

g. Abnormal behavior or neurologic signs (look for neu­rologic diseases and recent fluphenazine administration, and check blood ammonia concentrations)

Diagnosis and Management of Colic in Ruminants

1. Take history. Colic in neonates is most often associated with increased abomasal or intestinal gas and is discussed in Chapter 20. Perforating ulcers are not uncommon as a cause of colic in calves 1 to 6 months of age. It should be determined whether the onset of colic was acute or whether the colic is chronically recurrent. Few diseases cause recur­rent colic in ruminants. Urolithiasis is the most common cause of colic in male or neutered male goats and sheep and occurs under varied dietary and environmental condi­tions. Urolithiasis in cattle occurs most frequently in bulls or steers eating high-grain diets, but silicate stones can occur in very young animals and animals on pasture diet.

2. Perform a physical examination. Take vital signs; with torsion or severe peritonitis, shock signs such as rapid heart rate (>90 beats/min), cold extremities, and weakness may be seen. Tympany can be detected by simultaneous auscultation and percussion. Such causes of colic as cecal dilation, bloat, free gas in the peritoneal cavity, and severe abomasal dilation can be diagnosed in this way (see Figs. 1.3 to 1.5). Rectal examination detects such abnormalities as gas in the cecum, uterine abnormalities, urinary tract disease, and intussuscep­tion. Observe animal urinating to rule out obstructive urolithiasis. Ultrasound examination of the abdomen is also useful (see Abdominal Ultrasonography, Chapter 32).

3. Examine feces. Observe grossly; intussusception usually has scant dark red (almost black) feces. Black tarry feces may also be seen with bleeding abomasal ulcer of some duration. Scant feces are seen with cecal dilation or displacement.

4. Check preputial hairs and urethral process for sediment and stones. Grit on the preputial hairs is often associated with urolithiasis. Observe animal urinating and check urine for abnormalities. Rule out pyelonephritis. Radiology and ultrasound can be useful in sheep and goats when urolithiasis is a consideration. Ultrasound can detect a distended bladder, and stones may sometimes be detected. Radiology (lateral view) may detect a stone in the urethra or stones in the bladder. A contrast urethrogram may also be diagnostic.

5. Perform paracentesis to look for peritonitis caused by perforated abomasal ulcer, serosal devitalization, intussuscep­tion, or ruptured bladder. Interpret as earlier for horses, except that normal peritoneal fluid protein concentration can go as high as 5 g/dL in ruminants.

6. Other laboratory aids such as CBC and clinical chemistries are seldom diagnostic in ruminant colic. If grossly abnormal, they may be grounds for formulating a poor prognosis. Intussusception may be associated with neutrophilia (as well as dark feces and colic) in cases where peritonitis is occurring.

7. Symptomatic treatment of colic includes analgesics and, if heart rate is over 90 beats/min, intravenous fluid therapy with a sodium-containing fluid. Take a blood sample for electrolytes and acid-base status before initiating fluid therapy.

8. Surgical exploration is indicated if colic is persistent, abdominal distention occurs, the heart rate is over 100 beats/ min, feces are scant (especially those that are dark red and indicative of intussusception), there are pings indicating abomasal or cecal displacement or torsion, or the peritoneal fluid indicates bowel devitalization (blood-tinged fluid with elevated protein and WBCs). If surgical exploration is indicated, an important consideration is whether the animal will remain standing under local anesthesia during surgery. It is often best to perform abdominal surgery on animals with colic in left lateral or dorsal recumbency, aided by sedation and restraint, to avoid sudden collapse when painful surgical manipulations are performed. If the left lateral position is selected, use padding to raise the hip and shoulder so that the abdominal viscera can sit in a depression.