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For tortoise, terrapin and turtle care and conservation


Stuart McArthur, BVetMed, MRCVS, Holly House Veterinary Surgery, 468 Street Lane, Moortown, Leeds, LS17 6HA
Tel: 0113 2369030
Presented to the BCG Symposium at Bristol University on 29th March 2003.

Excessively lengthy hibernation

In the wild, most Testudo sp. specimens will have a long period of warm weather to prepare for a short hibernation period. In captivity, these animals may be exposed to a short period of warm weather to prepare for a notably long period of dormancy, inactivity and hibernation. It may not be possible for Testudo sp. metabolism to adapt to this. I advise restricting Testudo sp. hibernation in captivity to a maximum of 3 months regardless of size. Juvenile Testudo sp. may be hibernated for as little as a month.


Leucopaenia is common following long periods of hibernation. If a tortoise was poorly maintained during the previous season, its white blood cell count may have been very low before hibernation was even begun. The life expectancy of white blood cells is limited, and where hibernation is prolonged, numbers may decline to extremely low levels. Such leucopaenic animals awake with compromised immune systems.

When leucopaenic tortoises are warmed (naturally or artificially) bacterial, mycotic and viral agents within them appear to replicate quickly, potentially before rebound and replication of white blood cell stem cells has been possible. In such circumstances stomatitis, rhinitis and systemic infections are common. This scenario appears to be exacerbated by failing to allow a tortoise to reach its preferred body temperature during hibernation recovery and allowing it to chill below its ATR (appropriate temperature range) at night, compromising the immune system but favouring the pathogens.

Inadequate post-hibernation husbandry

Inadequate care and lack of understanding of the physiological needs of chelonians are the main reasons for illness in the post-hibernation period in animals presented to me.

Common factors include:

  • Failure to observe that a confined animal is no longer in hibernation - sometimes for several weeks
  • Failure to hydrate the animal - most animals will have been recycling bladder fluid without taking fresh fluid on board for about six months
  • Failure to feed the animal. If a chelonian is maintained without suitable food or without the light and heat conditions necessary to allow it to eat, it will become catabolic. Many chelonians will have gathered inadequate energy reserves pre-hibernation, and warming the animal moderately without allowing food or fluid intake will result in muscle wastage and hypertonic dehydration
  • Failure to provide suitable heat and light.

Disease or trauma during hibernation

Protection and observation are sometimes inadequate, resulting in:

  • Frost damage - the result of exposure to subzero temperatures. Thermal trauma to the central nervous system, eyes and frostbite to the distal limbs are the usual consequences
  • Rat bites - common where tortoises are hibernated in cardboard boxes in outhouses and are too cold to escape from their predators.

Undetected Chronic Disease

Often disease will have been present but asymptomatic for a long period prior to hibernation. All animals exhibiting inactivity or anorexia in the post-hibernation period should undergo a comprehensive examination. The history should be thoroughly reviewed for predisposing adverse husbandry practices. Examples of such chronic disease conditions are:

  • bacterial and mycotic infections
  • viral infections
  • lower respiratory tract disease
  • nutritional disease
  • dehydration
  • renal failure
  • follicular stasis
  • gastrointestinal disease
  • hepatic disease
  • sight impairment
  • central nervous system disease
  • inappropriate environmental provision
  • inappropriate food provision
  • pain
  • maladaptation
  • social disruption


History data (hibernation preparations, duration, monitoring, frequency of urination/defecation, post-hibernation vivarium conditions, appetite, food offered) are an essential part of the evaluation of the ill patient after hibernation. Most healthy animals eat, drink and urinate within one week of emerging from hibernation. The reader is encouraged to consider underlying dehydration (presented in most Testudo spp as hyperuricaemia, hyperkalaemia and anuria) in parallel with the management of other conditions and lesions.

Some simple information should always be requested from the client, and the following are examples:

  • What progress would this tortoise have made in previous years at this time of year?
  • What are the animal's environment and climatic conditions? Does the client have a vivarium? How do they provide heat and light?
  • What are the tortoise's day and night temperatures?
  • Is the tortoise displaying abnormal behaviour e.g. respiratory movements?
  • Is the tortoise displaying any specific clinical signs associated with disease, such as a nasal discharge?
  • What is the condition of other tortoises owned by the client? How many are there? Have there been any recent introductions to the group, and were these quarantined?
  • What is the quality of the client's normal husbandry?
  • What nutrition is usually provided by the client?
  • What provision has been made to ensure effective calcium metabolism?
  • What health checks are performed by the client and how frequent are they throughout the year?


An initial pre-treatment biochemistry assessment is an essential part of evaluating the PHA patient. A general tortoise profile at my surgery includes haematology (including differential white cell count), and examination for haemoparasites, total protein, potassium, uric acid, albumin, alkaline phosphatase, urea, calcium (ionised and total), GLDH, LDH, ß-hydroxybutyrate, phosphate, AST, sodium, CK, and glucose. A base-line profile on admission allows sequential blood monitoring during hospitalisation and recovery. Following the results of a general profile, it is normal to monitor critical parameters such as PCV, albumin, uric acid, urea, and potassium throughout the stabilisation period. Through these parameters the response to fluids, nutrition and medication, such as allopurinol, can be assessed.

Urine acidity, urine specific gravity and blood ß-hydroxybutyrate (BHB) appear to be additional parameters worth monitoring when stabilising a dehydrated terrestrial chelonian. In the immediate post-hibernation period of herbivorous chelonians it was found that pH was 5.0 and 6.0 but this rose to 8.0 and 8.5 after one month of normal feeding (Innis 1997). Acidic urine (< pH 7) is suggestive of catabolism and is a consistent feature of herbivorous chelonians suffering from prolonged anorexia (Innis 1997; personal observation).

Urine specific gravity is likely to provide a sensitive indication of hydration status (Gibbons 2000), especially in uricotelic species, and particularly when uraemic, although this deserves further investigation. ß-hydroxybutyrate (BHB) is thought to be a good indicator of ketogenesis in reptiles (Christopher et al. 1994). These authors found that, in desert tortoises (Gopherus agassizii), plasma levels varied from 0.4 - 0.75 mmol/l in times of significant rainfall (and food availability) but increased to 2.0 mmol/l after two months of drought. In contrast, ketogenesis did not appear to be important during hibernation.


In animals where blood uric acid and potassium levels and historical urine output following hibernation encourage the clinician to feel that further treatment can be attempted, and euthanasia considerations postponed, the primary aims of treatment should be:

  • To correct dehydration
  • To achieve diuresis and consequently decrease the elevated blood uric acid, potassium and urea levels. This generally involves fluid administration in combination with medication, such as with allopurinol
  • To elevate the blood glucose levels temporarily once diuresis and dehydration have been achieved. This will help reduce further catabolism adding to the azotaemia, and is normally achieved by adding appropriate nutritional products to the oral fluids administered
  • To provide optimal environmental conditions - we suggest hospitalisation in a vivarium
  • To provide appropriate nutrition, initially by hand feeding or via stomach-tube/oesophagostomy feeding, and then by reverting to the normal diet and withdrawing supportive feeding as self-feeding commences
  • To treat all concurrent disease or nutritional disorders effectively
  • To continue active fluid therapy and management of hyperuricaemia and gout for several weeks beyond recovery, as determined by observation
  • To improve the long term care and management of the affected animal following initial recovery.

Fluid therapy

In hyperuricaemic, hyperkalaemic, hypoglycaemic post-hibernation Testudo spp, urgent fluid therapy (possibly in conjunction with drugs inhibiting further uric acid production) is essential to preserve life. This will help preserve renal function, maintain plasma osmolarity, prevent hyperuricaemia and gout, and increase the renal excretion and general metabolism of toxins, anaesthetics and medications. Fluid therapy may involve the use of orogastric tubes, oesophagostomy tubes and intracoelomic, intraosseous, intravenous, intracystic (bladder) or epicoelomic routes.

In hospitalised terrestrial chelonians treated at my surgery over the past three years, fluid therapy protocols aim to restore urine output in anuric post-hibernation patients. In hyperuricaemic, hyperkalaemic cases presented to the author, it would appear safe to give fluids by the intraosseous, oral or epicoelomic routes at up to 4 ml/100g/day, until multiple urination is achieved. Following this, fluid levels are generally reduced to 2 ml/100g/day by oesophagostomy or stomach tube, as uric acid and blood potassium levels fall. Maintenance is continued for several weeks at least at about 0.5 - 1 ml/100g/day.

The intraosseous and epicoelomic routes are of help during early management, especially where uric acid levels are above 16.81 mg/dl (1000 µmol/l), but they must be used with caution, as it is impossible to quantify how much fluid is required. Excessive hydration by these routes, especially in the absence of renal output, may cause pulmonary or cerebral oedema. Generally, the author's routes of choice are oral fluids over time, soaks, and cloacal/bladder lavage and irrigation. In my opinion, intravenous fluid therapy is really an emergency life-saving measure and of limited benefit to a chronically-ill hyperuricaemic patient. Other clinicians, however, anecdotally report intravenous fluid therapy to be of use.


Hospitalisation protocol and record keeping are an essential part of the evaluation of recovery. Without admission into a therapeutic hospitalisation environment, it is hard to gauge the impact of any treatment.

With respect to dehydration, I would advocate the hospitalisation of Testudo species with the following signs or biochemistry markers:

  • hyperuricaemia (uric acid >11.76 mg/dl, >500 µmol/l)
  • hyperkalaemia (k+ >19.5 mg/dl, > 5mmol/l)
  • anuria (no urine within the previous 10 days).

These animals are generally hospitalised on a fluid therapy protocol as described below until repeated urination, decreasing uric acid levels and decreasing potassium levels are achieved. I have found that many dehydrated terrestrial Testudo spp can be stabilised satisfactorily providing that severe renal pathology does not exist.


Animals with uric acid levels above 33.61 mg/dl (2000 µmol/l) and potassium levels above ~35 mg/dl (9 mmol/l) often demonstrate no urine output despite active fluid therapy. Death in such animals appears to be the result of hyperkalaemic cardioplegia (heart failure) unless animals are euthanased. Histopathology in five recent terminal hyperuricaemic cases suggests that renal failure is due to loss of functional renal tubules because of active urate excretion in the proximal tubes, without sufficient glomerular filtrate to carry this urate sludge away. Glomeruli are often ruptured and contain excessive crystalline urate precipitates (SM: personal observation).

Lawrence (1987) suggests that it is unrewarding to treat post-hibernation anorexia in Testudo cases demonstrating a blood urea of more than 560 mg/dl (200 mmol/l), but that tortoises with a post-hibernation urea level of 420 mg/dl (150 mmol/l) often respond well to treatment. As he did not assess potassium or uric acid values it is possible that his figures reflect a combination of catabolism and dehydration. I would advocate the assessment of uric acid and potassium values wherever possible.

Continued supportive care

Following initial urination, nutritional support should be offered. Donoghue (1996) proposes that the treatment of energy deficiency in chelonians should first involve fluid and electrolyte replacement and then small but increasing levels of calories and nutrients in order to reduce the possibility of re-feeding syndrome. However, in hyperkalaemic patients, it is advantageous to give glucose to drive potassium ions into the cells. I use Critical Care Formula® (Vetark, UK), initially double diluted. This means half the recommended feeding amount is given in order to counter re-feeding syndrome. It is wise to monitor blood potassium levels, urine output, uric acid levels, and activity throughout this period. Alternatively, the normal diet is liquidised and blended with dilute Critical Care Formula and powdered fibre.


Allopurinol (Allopurinol BP, Generics UK, Potters Bar) is a standard medication given by this author to all chronically-ill chelonians with uric acid levels above 16.81 mg/dl (1000 µmol/l). Generally, allopurinol is given at 20 mg/kg/day by dissolving a 100 mg tablet in 5 ml of water and then offering 1 ml/kg/day PO, or by stomach/oesophagostomy tube. In most cases, treatment is continued for about three months, with further therapy dictated by regular blood biochemistry assessment. Correction of husbandry problems, especially those associated with possible nutritional hyperparathyroidism, may reduce the long-term need for allopurinol, which, however, seems to be very well tolerated.

I have not found probenecid (Benemid®, MSD) to be of major use in these cases. All animals treated with probenecid by the author have died, and histopathology of cases has suggested that increased active excretion in the absence of a glomerular filtrate has resulted in irreparable glomerular and tubular damage.

Bladder lavage

Bladder lavage, involving the cloacal insertion of a Foley catheter into the bladder and lavage of its contents (Dantzler & Schmidt-Nielson 1966) offers exciting possibilities for the future stabilisation of hyperuricaemic, hyperkalaemic patients. Bearing in mind the function of the lower urinary tract, it should be possible to remove excess potassium and uric acid, and to administer fluids (and possibly even medications such as allopurinol) by this route. Initial trials at my surgery using water have been interesting, but it is too early to draw any firm conclusions.


Euthanasia is the treatment of choice for post-hibernation anorexia cases that are considered to be beyond recovery. However, identification of these cases is generally based upon a failure to respond to stabilising fluid therapy. We have successfully treated cases where uric acid had risen to 30.25 mg/dl (1800 µmol/l), but never a case exceeding 33.61 mg/dl (2000 µmol/l). Similarly, blood potassium of 26.92 mg/dl (7 mmol/l) or less might be stabilised whereas potassium of 34.62 mg/dl (9 mmol/l) or more has been consistently fatal.

In my experience, renal biopsy does result in an understanding of renal pathology, but has not yet been able to differentiate cases capable of recovery from those that are beyond help. Cases that fail to urinate, but where appropriate hospitalisation and fluid therapy is given as described above (i.e. greater than 2 ml/100g/day by any combination of routes) over a period of ten days, are candidates for humane euthanasia.


Christopher, M.M, Brigmon, R. & Jacobson, E. (1994). Seasonal alterations in plasma beta-hydroxy-butyrate and related biochemical parameters in the Desert Tortoise Gopherus agassizii. Comparative Biochemistry and Physiology 108A, pp. 303-310.

Donoghue, S. (1996). Nutrition of the tortoise. Proceedings of the Association of Reptilian and Amphibian Veterinarians pp. 21-30.

Dantzler, W. H. & Schmidt-Nielson, B. (1966). Excretion in the fresh-water turtle (Pseudemys scripta) and desert tortoise (Gopherus agassizii). American Journal of Physiology pp. 198-210.

Gibbons, P.M. (2000). Urinalysis in box turtles. Proceedings of the Association of Reptilian and Amphibian Veterinarians, Reno, NV, pp. 161-165.

Innis, C.J. (1997). Observations on urinalyses of clinically normal captive tortoises. Proceedings of the Association of Reptilian and Amphibian Veterinarians 1997, pp. 109-112

Lawrence, K. (1987). Post hibernational anorexia in captive Mediterranean tortoises. Veterinary Record 120, pp. 87-90.

Adapted from Medicine and Surgery of Tortoises and Turtles (2004), McArthur, Wilkinson and Meyer (eds), Blackwell Publishing, Oxford , UK; with kind permission.

Glossary of scientific terms

AzotaemiaHigh blood level of nitrogenous products such as urea
CatabolicType of metabolism that breaks down body tissues
DiuresisIncrease in urine production
Epi/intracoelomicOutside/into the body cavity
HyperkalaemiaHigh blood level of potassium
HypertonicMore concentrated
HyperuricaemiaHigh blood level of uric acid
HypoglycaemiaLow blood sugar level
IntraosseousInto the bone
KetogenesisMetabolism of body tissues to produce ketones
LeucopaeniaLow white blood cell count
OedemaSwelling due to fluid retention
OesophagostomySurgical placement of stomach tube down the oesophagus via the neck
OrogastricVia the mouth into the stomach
OsmolarityChemical concentration affecting fluid balance
UraemicHigh blood level of urea
UricotelicProducing uric acid and urates as waste products

Testudo Volume Six Number One 2004