The subject of abdominal pain in camelids has been addressed a number of times over the years, with the discussion becoming
progressively more detailed as we gain experience with these species. We were truly learning from scratch, as the South American
approach (hands off and deal with the consequences) was generally unsuitable to North American tastes. The tone has varied
over the years, from extremes such as "we had better cut it, because it's worth so much," to, "why cut it, because they all
die." The bases for these extreme views were the high proportion of underlying lesions that were a major morphologic defect,
such as a ruptured ulcer, and they general uncertainty on how to proper assess the likely severity and nature of the disease
in a sick camelid. As we have become more knowledgeable about disease states and more proficient and comfortable in dealing
with them, we have improved in both those regards.
CAUSES OF COLIC
Camelids develop abdominal pain for the same reasons as other animals. The major mechanisms are activation of stretch-pain
receptors in the mesentery, various ligaments, or organ capsules, muscle spasms, inflammation, and ischemia. Similar to cattle,
the capacity and location of the gastric compartments combined with the ability to regurgitate excess fluid decrease the likelihood
of gastric distention or is tug on the mesentery contributing to pain signs. Additionally, relatively complete forestomach
fermentation in adult camelids decreases the likelihood of aberrant intestinal fermentation, and hence gas colics are uncommon.
However, aberrant fermentation can occur in younger camelids, or adults with depletion of their normal gastric microbial population.
In crias, this "milk colic" may be severe, but usually only lasts a few hours. As in other species, poorly digestible milk
replacers or viral damage to the intestinal brush border may contribute to aberrant fermentation. In adults, it is downright
rare. In all ages, infection by gas-producing bacteria may contribute to signs with some forms of enteritis.
Capsular stretch is a more important source of pain when it involves non-digestive abdominal organs. Colic signs may be severe
with distention of the kidney, ureters, or to a lesser degree, bladder. Milder signs are evident with enlargement of the liver
due to lipidosis, hepatitis, or fluke infection.
Anatomically, the camelid stomach and intestines bear more similarity to cattle than horses. Aside from thrombosis due to
systemic events, ischemia is most likely in regions with long mesenteric attachments and relative mobility. In camelids, this
includes the distal phlange of the small intestine and the whole of the ascending colon, including its spiral loop. Rotation
or displacement of the third compartment have not been described. Described ischemic events occur as a results of strangulation
involving the epiploic foramen (rare), body wall defects (intermediate frequency), diaphragmatic defects (rare), mesenteric
defects (rare), rotation around the mesenteric root (most common), intraabdominal adhesions (intermediate), or intussusception
(rare). Non-strangulating entrapments can occur with less severe involvement of most of these structures as well. Intussusception
has been described involving the jejunum, cecum, or ascending colon. Uterine torsion is among the more common causes of colic.
Liver lobe or splenic torsion is extremely rare. Risk factors for entrapments obviously include the presences of body wall,
mesenteric, or diaphragmatic defects. Enteritis or coccidial infection may promote mesenteric volvulus or intussusception,
particularly when they involve the colon.
Intraluminal obstruction is usually caused by hair or plant fiber balls. In most cases, these appear to form in the gastric
compartment, where multiple may be found. Some, smaller balls may form in the proximal loop of the ascending colon. Hairballs
are most common in animals less than one year old. Ectoparasites, boredom, and post-weaning suckling behavior are thought
to be risk factors. Phytobezoars may develop in animals with poor chewing or on excessively fibrous feed. Long-stem spring
pasture appears to increase risk in the Pacific Northwest. Obstruction tends to occur near the pylorus or in the beginning
of the duodenum in alpacas and smaller llamas, and in the centrifugal loops of the spiral colon in adult llamas. With time,
bezoars lodged in the duodenum may migrate further along the intestine, but it is rare for them to make it into the colon
or pass entirely. Tapeworm impaction with ulceration throughout the jejunum has been described in one alpaca. Foreign body
obstruction is very rare.