Not infrequently, tortoise and reptile enthusiasts are confronted
by acutely dehydrated specimens. Many leave dealers premises in this
condition, and others are the result of poor husbandry on the part
of previous keepers. Spontaneous dehydration may also occur as a
result of illness, particularly protozoan infections of the G.I
tract or pneumonia, both of which can cause acute dehydration to occur
within a surprisingly short period of time. It is extremely
important that persons who encounter dehydrated reptiles recognise
the symptoms, metabolic implications and support therapy required
to overcome the condition.
Symptoms: Dehydrated tortoises are usually underweight compared to
a healthy specimen of similar proportions, although an obese animal
may not be so. The eyes are almost always sunken, and in very acute
cases, the centres of the cornea may be depressed. On manual
examination, muscular tissue will lack resilience and the skin may also
be unusually dry and the surface powdery. With the possible
exception of cases of pneumonia, the oral mucous may be unusually
viscous and turgid.
Metabolic implications: Terrestrial chelonians, lizards and snakes
excrete nitrogenous waste products including ammonia (which is produced
as a result of the protein metabolism) in the form of uric acid. Urates
are transported from the liver in the blood to the renal glomeruli for
filtration and then to the linings of the tubules where the water
required for transportation is re-absorbed. In animals adapted to arid
habitats such water being of far too much importance to waste. The
concentrated uric acid, in the form of a crystaline deposit of low
water content is then excreted via the cloaca. Should the animal
suffer dehydration, the process of transporting nitrogenous waste
products is the first major metabolic function to suffer. Blood urea
levels rise and excess uric acid precipitates within the renal tubules
and elsewhere throughout the body. The filtration function of the
kidneys ceases, and necrotic degeneration of the renal system
eventually follows. Post mortem, the kidneys are usually enlarged and
infiltrated by yellowish-brown deposits of uric acid.
Prevention and supportive therapy: For practical purposes it can be
useful to divide dehydrated reptiles into two groups. Group A animals
may have acute dehydration but blood urea levels and uric acid
precipitation has not yet reached a critical level. Renal function has
not been impaired. Such dehydration is often encountered following a
protozoan or similar G.I tract infection which has resulted in
diarrhoea and excessive cloacal voiding. Animals of this group are
also encountered following short-medium term failures of husbandry. The
problem can usually be corrected by oral dosing with a compound sodium
chloride, potassium chloride and glucose oral rehydration combination
(e.g, 'Dioralyte' or ' Lectade').
Group B animals are much more problematic. Here, in addition to the
usual external signs of dehydration, blood urea is elevated and renal
function is impaired to a greater or lesser degree. Victims of long
term neglect, inanition and dehydration or animals which have been on
an excessively high protein diet for their species are those most
likely to fall into this group. The first objective, even before
inanition is dealt with, must be to restore renal function as quickly
as possible. In herbivorous chelonia, oral dosing with Hartmann's
Solution (compound sodium lactate) at up to 5% bodyweight daily has
been highly successful. Where renal function is severely impaired and
following fluid support therapy severe oedema manifests the use of a
diuretic such as Frusemide may be warranted. Only when renal function
and uric acid excretion has been restored should additional support
therapy be administered in the form firstly of an oral rehydration
compound followed within a week or two by 'Duphalyte' or similar
combination electrolyte and amino-acid preparation.
It is a common mistake upon confronting an animal suffering from
inanition and dehydration to overlook the dehydration and concentrate
upon the inanition. In chelonians, large quantities of high protein
force feeds are often administered. This is in fact extremely
dangerous and can result in mortality. If renal function or
nitrogenous waste excretion is impaired additional protein input can
only exacerbate the problem. For the same reason, the protein content
of the general and post-recovery diet should also be carefully
monitored, and steps should be taken to ensure that animals adapted to
ultra low dietary protein inputs such as herbivorous chelonians are not
placed upon artificially high protein diets, e.g animal proteins or
foodstuffs of vegetable origin which are similarly high in protein
content such as legumes. The nitrate content of processed animal
protein sources is particularly lethal in this context.
Prevention obviously is better than cure, and much can be achieved by
ensuring that all captive reptiles are provided with adequate access to
fresh drinking water. The fluid and protein contents of food items
should also be considered relative to the specific requirements of the
species. Where dehydration is suspected, early detection, prompt
intervention and veterinary treatment can do much to prevent serious
secondary renal damage from occurring.
NB: Hartmann's solution, Duphalyte and Frusemide mentioned above are
prescription only medicines which must only be used under veterinary
supervision.