Camelidae and Cervidae Colic Study Guide

Overview and Clinical Importance

Colic in camelids (llamas, alpacas) and cervids (deer, elk) represents a significant clinical challenge due to their unique gastrointestinal anatomy. South American camelids (SAC) possess a three-compartment stomach system (C1, C2, C3) that differs substantially from true ruminants. Understanding these anatomical differences is essential for diagnosis and treatment of gastrointestinal disorders. Colic accounts for approximately 5% of camelid hospital admissions and can be responsible for up to 19% of camelid deaths.

The three major causes of colic covered in this guide include: C1 (first compartment) impaction, C3 (third compartment) ulcers, and phytobezoar obstruction. Each has distinct pathophysiology, clinical presentations, and treatment approaches that are commonly tested on the NAVLE examination.

Camelid Gastrointestinal Anatomy

Unlike true ruminants with four stomach compartments (rumen, reticulum, omasum, abomasum), camelids possess three gastric compartments designated C1, C2, and C3. Importantly, there is no omasum equivalent in camelids. Fermentative digestion occurs in C1, C2, and the cranial 80% of C3, while the distal 20% of C3 secretes hydrochloric acid (analogous to the abomasum).

First Compartment (C1)

C1 is the largest compartment, comprising approximately 83% of total gastric volume and 50% of abdominal volume. It occupies most of the left side of the abdomen and consists of large cranial and caudal sacs divided by a prominent transverse pillar. Key anatomical features include:

• Glandular saccules: Located ventrally, these secrete bicarbonate to buffer pH (unlike ruminant papillae)
• No papillae: Unlike the rumen, C1 has stratified squamous epithelium dorsally without papillae
• Ventricular groove: Located near esophageal entry, leads toward C2 (similar to reticular groove in cattle)
• Motility pattern: 2-4 contractions per minute, traveling caudal to cranial

Second and Third Compartments (C2 and C3)

C2 (Second Compartment): Small, reniform (kidney-shaped) structure comprising only 6% of gastric volume. Located atop C3 medial to C1. Contains sacculations with small papillae and functions similarly to the reticulum.

C3 (Third Compartment): Elongated, tubular structure with two distinct functional regions:

• Cranial 80% (Gastric tube): Lined with glandular epithelium similar to C1 saccules; highly absorptive for water and volatile fatty acids
• Distal 20% (True stomach): Contains gastric glands secreting hydrochloric acid; functionally equivalent to the abomasum

Anatomical Comparison: Camelids vs. Ruminants

C1 Impaction

Etiology and Pathophysiology

C1 impaction occurs when the first compartment becomes overloaded with poorly digestible material. Unlike cattle where rumen impaction is common, true C1 impaction in camelids is relatively uncommon. However, C1-otomy may be necessary for:

• Gastric indiscretion: Ingestion of foreign material or excessive roughage
• Dietary factors: Poor-quality, highly fibrous feed with inadequate water intake
• Secondary to ileus: Vagal-type indigestion or functional obstruction
• Forestomach acidosis: Grain overload causing microbial population changes

Clinical Signs

Clinical signs of C1 impaction are often subtle in camelids compared to horses. Characteristic findings include:

• Decreased or absent fecal output (present for greater than 24 hours suggests obstruction)
• Abdominal distension, particularly on the left flank
• Decreased C1 motility on auscultation (normal: 2-4 contractions per minute)
• Anorexia and depression
• Mild colic signs: abnormal recumbency, kicking at abdomen, frequent position changes

Diagnosis

C1 Fluid Analysis

C1 fluid can be obtained via orogastric tube or percutaneous paracentesis. Key parameters include:

Treatment

C3 (Third Compartment) Ulcers

Prevalence and Significance

C3 ulcers are a common finding in camelids, with studies reporting prevalence of 23-34% in necropsy examinations. C3 is most frequently affected (61% of cases), followed by C1 (16%) and C2 (9%). Ulcers appear more common in animals kept outside South America than in their native habitat, suggesting management and dietary factors play important roles.

Gastric ulcers are responsible for approximately 5-6% of fatal casualties in alpacas. Perforated ulcers lead to peritonitis and carry a grave prognosis. Animals 1 year of age and older are more frequently affected than juveniles, with no sex predilection.

Etiology

The pathogenesis of C3 ulcers is multifactorial. Proposed mechanisms include:

• Stress: Increases cortisol, gastric acid, and pepsin while decreasing prostaglandin E synthesis
• NSAIDs: Inhibit cyclooxygenase and reduce protective prostaglandin production
• Dietary factors: Forestomach acidosis, reduced feed intake, grain overload
• Anatomical predisposition: No separation between fermentative and acid-secreting regions; acid reflux with ileus
• Concurrent disease: Debilitating conditions, uremia, vitamin D toxicosis, neoplasia
• Bile reflux: Duodenal contents refluxing into C3

Clinical Signs

Clinical signs are often non-specific and many ulcers may be subclinical. When present, signs include:

• Mild to severe colic (present in approximately 1/3 of cases)
• Depression and anorexia (most common presenting signs)
• Bruxism (teeth grinding)
• Decreased fecal output
• Weight loss and poor body condition
• Recumbency
• Melena: Rare in camelids (unlike ruminants) due to differences in ulcer characteristics

Signs of Perforated Ulcer: Acute deterioration, severe colic, fever progressing to hypothermia, tachycardia, tachypnea, evidence of peritonitis on abdominocentesis (elevated WBC, bacteria), and septicemia. Abdominocentesis is usually unremarkable if perforation has NOT occurred.

Diagnosis

Diagnosis of C3 ulcers in living animals is largely one of exclusion. No definitive antemortem diagnostic test exists.

Diagnostic Approaches

• Fecal occult blood: Questionable value; positive results in animals without ulcers and negative results in animals with overt hemorrhage have been reported
• Hematology: Non-specific changes; leukopenia with left shift may indicate perforation/sepsis
• Serum biochemistry: Hypochloremic metabolic alkalosis suggests obstruction; hyponatremia and hypoalbuminemia suggest enteritis
• Abdominocentesis: Usually unremarkable unless perforation has occurred; peritonitis findings indicate full-thickness ulceration
• Gastroscopy: Anatomically difficult in camelids; limited by narrow nasal passages (6mm in neonates, 1cm in adults)
• Exploratory surgery: Right paracostal approach allows inspection of terminal C3; ventral midline or right paralumbar fossa for other areas

Treatment

Acid Suppression Therapy

Phytobezoars and Intestinal Obstruction

Types of Bezoars

Bezoars are concretions that form in the gastrointestinal tract. Three types occur in camelids:

• Phytobezoars: Compacted plant fiber balls; most common cause of intestinal obstruction
• Trichophytobezoars: Combination of hair and plant material; common in weanling crias
• Gastroliths (Enteroliths): Mineral concretions (phosphates) around a plant fiber nucleus; common in C1 saccules

Pathophysiology

Despite being selective feeders that thoroughly chew food, phytobezoar obstruction is common in camelids of all ages. Contributing factors include:

• Inadequate chewing: Incisor malocclusion, poor molar grinding, hurried eating
• Dietary factors: Long-stem spring pasture, highly fibrous feed, poorly digestible fiber
• Wider C2-C3 opening: Unlike the narrow reticulo-omasal orifice in ruminants, large particles can pass into intestine
• Hair ingestion: Crias may chew fiber from dams after weaning; especially Suri alpacas

Location and Species Predilection

Clinical Signs

Clinical signs vary based on obstruction location and completeness:

Small Intestinal (Duodenal) Obstruction

• Often SUBTLE colic signs that may abate after a few days (due to progressive dehydration/depression)
• Abdominal distension
• Regurgitation
• Fluid sequestration with rapid dehydration
• Hypochloremic metabolic alkalosis

Colonic Obstruction

• More obvious pain signs
• Minimal dehydration (most absorptive epithelium remains functional)
• Absent fecal output

Diagnosis

• Serum biochemistry: Hypochloremic metabolic alkalosis with elevated bicarbonate strongly suggests obstruction
• C1 chloride: Elevated (greater than 50 mEq/L) due to reflux
• Abdominal radiography: Most useful in neonates; may visualize gastric distension or obstruction. Mineralized bezoars may be visible in adults.
• Ultrasonography: Distended intestinal loops, fluid accumulation; has largely supplanted rectal palpation
• Rectal palpation: Possible in llamas (similar to cattle); bladder, reproductive tract, left kidney, caudal C1 palpable. Use caution - rectal injuries reported.

Treatment

Surgical options for bezoar removal: Duodenotomy (direct incision into duodenum) or retropulsion of bezoar combined with C3 gastrotomy. Camelids tolerate intestinal surgery well when performed early. Ileus is generally not a limiting factor postoperatively.

Cervid Gastrointestinal Disorders

Cervids (deer, elk, moose) are true ruminants with four-compartment stomachs, making their GI physiology more similar to cattle than to camelids. Key NAVLE-relevant conditions include:

Rumen Acidosis (Grain Overload)

This is the most important GI emergency in cervids, occurring when animals gain sudden access to high-carbohydrate feeds (especially corn). Wild and captive deer and elk are highly susceptible.

Pathophysiology

• Sudden dietary change from high-fiber browse to low-fiber, high-carbohydrate grain
• Within 2-6 hours: Streptococcus species proliferate, producing large amounts of lactic acid
• Rumen pH drops to 5 or below, destroying protozoa and cellulolytic organisms
• Reduced rumen motility traps ingesta
• Osmotic fluid shifts into rumen cause systemic dehydration
• Lactic acid absorption causes metabolic acidosis
• Chemical rumenitis and abomasal ulceration may occur

Clinical Signs

• Animals found dead acutely in good body condition
• If alive: recumbency, staggering, standing quietly
• Rumen stasis, diarrhea
• Normal temperature initially
• Death within 24-72 hours of grain ingestion

Necropsy Findings

• Large quantities of corn/grain in rumen
• Dark red to maroon erosions on abomasal folds (most common lesion)
• Rumenitis with damaged mucosa

Enterotoxemia

Often occurs concurrently with rumen acidosis. Clostridium perfringens proliferates when undigested carbohydrates reach the lower GI tract.

• Acute indigestion, CNS signs (convulsions), incoordination, depression
• Diarrhea, colic
• Rapid death
• Prevention: Vaccinate captive cervids with multivalent clostridial bacterins

Differential Diagnosis of Colic in Camelids