Reptiles encompass a vast array of animals, at this time over 10,000 species, with about 96% of those being lizards and snakes. Much like trying to give a one-hour lecture on mammalian (including humans) gastrointestinal (GI) medicine, it will not be possible to cover all aspects of this component of veterinary medicine in all reptile species. This lecture will not cover reptilian oral medicine, as that will be covered in a separate lecture. There are some unique components of anatomy that are important to be aware of in reptiles. It is also important to recognize many of the current limitations in both diagnosing and treating reptile gastrointestinal disease.
Anatomy and Physiology
Many clinicians are surprised by the dilation ability of the esophagus in reptiles, and they may misdiagnose megaesophagus based on this. Most reptiles have skeletal muscle in the first two-thirds of their esophagus, making regurgitation of critical care diets and oral medications a possibility if a feeding tube is not placed far enough down the esophagus. Sea turtles and some tortoises have strong esophageal muscles that assist in crushing food before it enters the stomach. Generally the stomach pH is very acidic in carnivores and only mildly acidic in herbivores. As in mammals, the intestines are longer and more complex in herbivores versus carnivores or omnivores. In herbivores, oxyurids are common and generally considered commensal. Boas and pythons do have a small cecum. The liver/tubular portion of the GI of many reptiles can be pigmented due to the presence of melanomacrophages. High numbers of those may indicate chronic disease; however, black intestines are common in many chameleon species. Some reptiles, such as snakes, have a structure called the splenopancreas, combining those two organs as the name indicates. The snake gall bladder often completes the triad in close proximity to the splenopancreas. Some lizards such as iguanas, Uromastyx, and chuckwallas have a sacculated colon. At the end of the GI, as in birds, the reproductive, urinary, and GI tracts come together to form the cloaca, which is subdivided into the coprodeum, urodeum, and proctodeum. Interestingly, the urinary bladder (in chelonians, some lizards, and crocodilians) is actually a storage container for urinary waste and more importantly water as a pouching off of the colon/cloaca. Urine retrofluxes from the cloaca up into this structure, and water can likewise retroflux from there to the colonic mucosa for fluid and electrolyte absorption. Removal of this structure is not as "problematic" in captive reptiles as it might be in a mammal. There is no rectum or anus. When cloacal/oviductal/intestinal prolapses occur, as in birds, it is best to place side stay sutures versus a purse-string pattern. In severe cases, the author has withheld food and placed a simple cruciate pattern and left it for 3–4 days with moderate success.
Crocodilians have a velum palate or gular valve that can completely seal the mouth from the glottis and esophagus. This allows the crocodilian to sit in the water with its mouth open; however, for the veterinarian, there is a challenge to intubate and to visualize down the esophagus. Crocodilians also have a pseudodiaphragm that functionally acts as a true diaphragm. However, the liver is on the "thoracic" side, while a round structure called the fat body sits in the location a mammalian liver would be found. The fundic portion of the stomach is thickened and contains gastroliths; this structure is considered analogous to the ventriculus of birds. Crocodilians also will naturally become anorectic if the water/air temperature goes below 25°C or above 35°C.
The GI transit time in Greek tortoises, Testudo graeca, was reported as 3–8 days on a lettuce diet, 16–28 days on dog food. At this time, there has been no evidence that metoclopramide or cisapride has any effect on reptilian GI transit time; however, only a few species have been assessed.
The typical rule-out list of possible GI diseases in reptiles does not often deviate from those of a mammal or bird. It is generally prudent to avoid jumping to conclusions on the diagnosis and instead utilize your DAMMNIT list. Most of us tend to gravitate towards an infection of some kind, especially bacterial. However, this default is often because of it being low hanging fruit for both diagnosing - fecal/cloacal/oral bacterial culture will always grow something, +/- a CBC with high/low/normal WBC that one can twist the interpretation however one wants. And then there is the silver bullet of antibiotics to send them out the door with! I challenge practitioners to not follow this default, or if bacteria seem to be an issue, to look deeper into the root cause whether it is husbandry, diet, or another etiologic mechanism.
Virology awareness in reptiles has grown by leaps and bounds in the past few decades, with so much further to go. But once again, one needs to proceed with caution that a positive virus isolation or PCR positive result matches clinical signs and that there is actual pathology occurring in the tissue the sample is from. Koch's postulate has rarely been fulfilled to confirm viral etiology in reptiles, the gold standard for confirming etiology. But viruses do seem to be becoming more and more prevalent and identifiable in reptiles as researchers look for and recognize them. Three well-known ones seen in private practice shall be briefly mentioned. These include inclusion body disease (IBD) in boid snakes, adenovirus in bearded dragons, and herpesvirus in chelonians.
Fungal diseases are becoming more and more of a factor, as well. Important concepts to remember are that many pathogenic fungi need to be cultured at cooler (reptile) temperatures compared to the standard mammalian-based fungal cultures which are run. Systemic mycotic diseases are often diagnosed postmortem, unfortunately. Dermatological infections can quickly become systemic. Parasitic diseases seem to be one of the more commonly implicated infectious causes of disease, from coccidiosis to strongyloidiasis to cryptosporidiosis to amoebiasis. Most ciliates and many flagellates are considered commensal, as previously mentioned for some oxyurids. Also watch for "parasites" that are actually parasites of the food items fed.
Toxins are a challenging etiology to ferret out in reptiles. If in fact the true etiology, it may be days to months after exposure before the condition is appreciated and brought to the attention of the veterinarian. Neoplasia, whether focal or systemic, may be being appreciated with greater frequency in cases presenting with GI signs. Along that same vein, many female reptiles (and even some males) have a physiologic anorexia during reproductive activity. This is completely understandable when for the female, their reproductive tract expands 100 fold in size and there is no room for ingesta to pass. This also explains the greater prevalence of fat stores within the body of reproductively active females. Another atypical, but common "cause" of anorexia, is dysecdysis in snakes, which seems to affect their sense of smell/use of vomeronasal organs to scent and attack their food. Seasonal anorexia may be seen as well; ball pythons often have a period reflecting their natural brumation period in the wild. The social stress, particularly among juvenile lizards and chelonians, whereby one is doing great while the other is a poor doer. Separating the two visually and in some cases even with greater distance to avoid pheromone exposure can correct some anorectic cases in juveniles. Foreign bodies are culprits in many cases of GI disease, but are usually suspected more often than truly an issue.
How to work up GI disease in a reptile? I generally spend a huge amount of time getting a thorough history of the home environment, parsing through the diet offered and actually eaten, looking at the social structure of the enclosure, and assessing weight and body condition. The physical examination may be helpful, but often does not provide me an "Aha!" moment. A fresh fecal can be a useful diagnostic, and in a well-trained clinic, the receptionist encourages the client to bring one in (tell them what is "feces") and to keep it cool and moist. As constipation or anorexia are often the presenting complaint, this sample is often either scant, rock hard, or forgotten. I do not find cloacal washes or enemas provide me useful samples in most cases. My next diagnostic is radiographs, often morphing into a barium series. I have become fairly phobic of automatic enemas; especially in sand cases, the damaged mucosa can rupture and many times the fluids go into the urinary bladder or come right back out. My experience with bloodwork in reptiles tends to make me ambivalent when I am limited by finances. As metabolic bone diseases and renomegaly can sometimes be at the root of the issue, running a total calcium, phosphorus, plus an ionized calcium if I have an i- STAT® may be of value. There does not seem to be go to "liver values" in my book and most of the rest of chemistry can be ambiguous at best. A CBC may have some value, but again I tend to find it rarely gets me further than I am. In boas, the presence of inclusions on the CBC can be used to diagnose IBD. If indicated, Cryptosporidium testing (depending on the test) may have value; however, pass through rodent Cryptosporidium can confound the findings in carnivorous species. If the patient is stable, then an endoscopic biopsy or coeliotomy may be a further step.
One can perform either rigid or flexible endoscopy (depending on patient size and equipment) to collect some foreign bodies and perhaps collect certain tissue biopsies. However, coeliotomy is often the approach most practitioners will perform. For the chelonian patient, there is the whole shell aspect. I generally prefer to cut the plastron using either a surgical saw or sterilized Dremel® parts. In either case, copious cooling with sterile fluids during the cutting can help minimize bone necrosis. Also cutting on a slant can help manage "sinkage" of the cut piece when replaced, along with holes for suture. Topping off usually incorporates an epoxy seal, though some surgeons do not do so.
When a midline coeliotomy is performed in lizards, be aware of a large midline subcutaneous vein. Since it can flop to either side and still be cut, I prefer a true midline approach, albeit it cautiously. The vein originates usually near the pubis in abdominal adipose (fat pad) deep in the coelom, runs the midline surface to the umbilicus where it dives deep to the liver. However, even damaging this vein is not deadly, it can be ligated and other vessels provide collateral supply. Surgeons also need to be aware and careful of the urinary bladder in many lizards and some chelonians. As the coelomic lining is often tissue-paper thin, the thin wall of a full urinary bladder can be mistaken for a part of that lining. However, this mistake can also be remedied easily by flushing any urinary waste from the coelom and closing the bladder before moving on to the primary purpose of the surgery. For snakes, it is best to go between the 2nd and 3rd lateral scutes/scales on either side to encourage more rapid healing.
Generally from this point, surgical concepts follow those of GI surgery in mammals, with a few "howevers." Vessel ligation in most small reptiles can be challenging without extremely good microsurgical techniques and small Hemoclips® or LigaSureTM may be a better option to avoid suture failure. One also needs to coordinate with anyone providing intermittent positive pressure ventilation, as the airsac portion of the lungs often will expand into the surgical field. Finally for closure, remember that the skin is the actual holding layer, though many times putting a suture pattern into the coelomic lining/coelomic muscle/subcutaneous tissue makes everyone feel a little better, if you can find it and actually appose it. Much of the old literature states that closure must be done with an everting pattern. More recent anecdotal and studies have found that tissue can be closed as in mammals. An everting pattern is preferred by the author as he likes to use surgical sutures for speed. This does create greater scar tissue. In any event, suture removal should be done 4–6 weeks after placement.
Another GI "surgery" that is done with some frequency is the placement of an esophageal feeding tube. Reptiles with anorexia and hepatic lipidosis can benefit from this technique as much as domestic cats do. For chelonians, there can be challenges in placement due to the S-curve of their neck and the spurs on the forelegs pulling the tube out. For chelonians and Uromastyx this is often necessary to even give any oral medications if there is anorexia or finicky nature of their appetite.
Treatment ideally aims at the root of the problem, so husbandry and diet changes may be at the forefront. General supportive care with fluids and nutrition are just as critical as in mammals; however, their slower metabolism requires a more conservative approach in dosing and frequency. Gastrointestinal motility agents seem to not have measureable effect in most reptiles at this time. The author has been trying maropitant at mammalian doses to see if it helps with nausea and has not seen definitive adverse effects so far. A broad- spectrum oral antibiotic may be indicated. Generally, prognosis in idiopathic or chronic disease cases should be considered guarded. Many reptiles, in the author's experience, can undergo the "ICU bump," whereupon they improve with treatment then crash and burn. For many of those cases, the prognosis should remain guarded until a few weeks out and upon showing continued improvement.