Aortic Aneurysm and Subsequent Cardiopulmonary Arrest in a Burmese Python (Python molurus bivittatus)
American Association of Zoo Veterinarians Conference 1999
Elizabeth Marie Rush, DVM; Thomas M. Donnelly, BVSc, DACLAM; James Walberg, DVM, DACVP
The E. & M. Bobst Hospital of The Animal Medical Center, New York, NY, USA


An approximately 27-kg, 5-m-long, 8-year-old, female Burmese python (Python molurus bivittatus) was presented with acute onset of respiratory arrest after prey strangulation. The owner had observed normal approach, attack, and constriction of a live rabbit (Oryctolagus cuniculus) recently obtained from a local pet store. The rabbit was smaller than other rabbits previously fed to the python. The snake began to swallow the carcass, but after drawing back half of the rabbit, it suddenly backed away from its prey, open-mouthed. The snake gasped, then collapsed in its cage. The owner brought the snake immediately to the Animal Medical Center, which took approximately 35 minutes. During the commute, the owner witnessed 3–4 exaggerated inspirations by the snake.

Upon arrival, a brief physical exam was conducted. The snake was comatose, pale, and hydrated. Respiration was absent, and heart activity was not detected on palpation, observation, auscultation or using a Doppler probe. The initial oral exam was unremarkable, eyes and nasal chambers were clean, and the abdomen was benign. There was no history of egg laying or binding. The snake was in good external physical condition, with clear and smooth scales and no obvious scars. There were no ventral petechiae or other evidence of sepsis.

The snake was intubated with a 3.5-mm endotracheal tube, attached to a medium-size Ambu bag, and provided manual intermittent positive-pressure ventilation (IPPV) with 100% oxygen. Estimating the requirements for full lung field inflation, approximately 15 breaths/minute were delivered. Simultaneous manual cardiac compression was performed. Epinephrine (0.4 ml of a 1:1000 dilution) was administered by intracardiac injection, followed in 5 minutes by 1.0 ml (0.54 mg/ml) atropine sulfate intracardiac. Exploration of the upper airway and esophagus for injuries or possible foreign bodies was unremarkable. A 20-ga Teflon catheter was placed in the right palatine vein and secured. A blood sample was taken from the catheter and collected with a blood gas syringe (Marquest™, Englewood, CO). Electrolytes, glucose, hematocrit, and total solids were determined from the blood sample. Blood gas parameters and electrolytes were determined using a Ciba-Corning 850 Blood Gas Analyzer. Results are as follows (with normal values in parentheses).7 There was a metabolic acidosis; pH was 6.855 and actual bicarbonate was 6.9 mEq/L. The chloride level was 120 mEq/L (100–150), potassium was 3.71 mEq/L (2–8), sodium was 147.4 mEq/L (120–170), and ionized calcium was 5.6 mg/dl (2–5, 8–20). Anion gap was 24.2 mEq/L (10–27). The blood glucose level was measured using a blood glucose monitor (Accu-Check III, Boehringer Mannheim, Indianapolis, IN) and was 123 mg/dl (60–100). The PCV was measured in a microhematocrit tube and was 25% (20–40); total plasma solids (using a refractometer) were 6.1 g/dl. Intravenous lactated Ringer’s solution (LRS) was started as a 500-ml bolus and 250-mg prednisolone sodium succinate (Solu-Delta-Cortef, Pharmacia & Upjohn, Kalamazoo, MI) was added to an additional 250-ml LRS as a slow drip for shock. Heating pads were placed lengthwise on the snake to increase metabolic activity by elevating core body temperature. The ambient temperature was approximately 75°F. Three minutes after administration of the IV LRS bolus, a heart rate of 12 beats/minute (BPM) was detected. A dose of 0.5 ml (50 mg/ml) diphenhydramine hydrochloride was given intramuscularly considering that the cardiopulmonary arrest may have been an anaphylactic response to a topical substance on the rabbit. Manual ventilations were stopped intermittently, for 1-minute periods, to allow for spontaneous breathing by the snake. After approximately 40 minutes, the snake attempted to breathe. The total respiratory rate was 10 breaths/hour. The respiratory attempts appeared exaggerated and were accompanied by craniocaudal peristaltic movements of the thoracic and abdominal muscles.

At 1.5 hours post resuscitation, the snake’s heart rate fell to 2–3 BPM, at which time a second dose of 1.0 ml (0.54 mg/ml) atropine sulfate was given intravenously. Heart rate again increased to 12 BPM. Petechiation became noticeable on the ventral scales. Manual IPPV was continued for an additional 30 minutes, replacing the 100% oxygen with room air. Two hours after beginning cardiopulmonary resuscitation, the manual IPPV was stopped. The snake did not breathe spontaneously, and after 5 minutes of apnea, 1.0 ml (20 mg/ml) doxapram hydrochloride (Dopram-V, Fort Dodge, Cherry Hill, NJ) was given intravenously. This was followed by two respiratory efforts. The ventral petechiation began to resolve at this time. The snake was given 150 mg (22.7 mg/ml) enrofloxacin (Baytril, Bayer, Shawnee Mission, KS) by IM injection prophylactically, then re-dosed with 1.0 ml (20 mg/ml) doxapram hydrochloride before being placed in a heated oxygen cage overnight. The palatine catheter was removed at this time. The snake was not observed to breathe overnight and was pronounced dead the following morning, 12 hours after placement in the oxygen cage.

Complete necropsy was performed at the Animal Medical Center. Gross findings were bruising of the heart muscle and skeletal muscle secondary to injection administration and increased fat deposits. Incidental findings were abdominal adipose tissue cysts and small ovarian follicles. There were no other significant gross findings. Microscopic evaluation of the tissues revealed a dissecting organizing aortic aneurysm with separation of the intima and media. This was located in one aortic arch proximal to the first aortic branching, and it was approximately 2 cm in length. Other microscopic lesions included steatitis of abdominal fat deposits and a focal ulcerative enteritis. No cholesterol deposits or areas of mineralization were seen. Necropsy of the constricted rabbit revealed no gross abnormalities.

Cause of death was assumed to be due to cardiopulmonary arrest and shock secondary to sudden rupture of the aortic aneurysm. It is not certain what caused the initial insult to the cardiovascular system.


To the best of the authors’ knowledge, aortic aneurysm and subsequent shock and death have not been reported in snakes. It is likely that this aneurysm occurred at a pre-existing weakened focus in the aortic intima secondary to a hypertensive episode at the time of prey constriction and swallowing. While reptiles are considered to have relatively low resting blood pressures, hypertension must be considered. Although it is not clear why the aneurysm presented as a dissection and not as a complete rupture, hypovolemic shock likely occurred at this time, resulting in clinical signs. Dissecting organizing aneurysm of the aorta allows blood loss into the defect formed between the intima and media of the aorta. The blood pooling in the defect causes increased vascular resistance by impinging on the normal lumen. This results in increased stasis of blood, leading to hypercoagulability and impedance of blood flow to systemic tissues. The combination of prolonged cardiopulmonary compromise leads to shock and volume depletion, all of which contributed to the snake’s death.

In mammals, cardiovascular dysfunction is due to one of the following:2,9

1.  Disruption of the continuity of the circulatory system permitting blood escape. This prevents cardiac filling and resistance that the normal heart pumps against.

2.  Cardiac conduction disorders or arrhythmias.

3.  Any lesion preventing valvular function or obstruction leading to pressure abnormalities and/or regurgitant flow of blood.

4.  Generalized failure of the cardiac pump.

In general, poikilotherms have few primary cardiovascular disorders; these few include heart enlargement and congenital cardiovascular abnormalities. Heart failure in conjunction with liver abnormalities has been reported.3 Congenital abnormalities are most often associated with juvenile death. Most of the cardiovascular disorders reported in reptiles are secondary and are associated with infection, parasitism, nutritional imbalances (calcification of vessels, obesity, cholesterol deposits) and poor husbandry practices.7 Arteriosclerosis has been documented in iguanas (Iguana iguana),10 although no evidence of this condition existed in the snake presented in this paper. Thrombogenesis is reported to be of lower incidence in reptiles than in mammals, but it could occur in the presence of endothelial damage or altered blood flow.8 One human study indicates that obesity may decrease the clearance of procoagulants and cause fatty necrosis. If plausible in reptiles, this could predispose an animal to vascular stasis, endothelial damage, hypercoagulability, and intravascular coagulation, as it does in humans.4 Hypertension associated with increased activity (15 minutes) has been found to decrease the circulating volume approximately 21% in some snakes, therefore increasing heart rate and PCV.6 This could also contribute to hypercoagulability and turbulence of blood flow.


Although various cardiovascular disorders have been reported in snakes, there are many disorders that have not been observed. Thorough diagnostics and necropsies of diseased and dead snakes will certainly assist in the discovery and better understanding of these diseases.

Overall, for thorough cardiovascular evaluation and resuscitative efforts, the following should be recognized.

1.  Reptile respiratory stimulus is the decrease in oxygen levels,7 and manual ventilation efforts should include periods of pure oxygen with weaning off to room air. Care should be taken that animals are not overventilated, as this will not allow proper stimulus for the animal to attempt spontaneous respiration. The clinician should remember that some reptiles can survive periods of prolonged apnea when compared to mammals.12

2.  Care should be taken with cardiovascular stimulating drugs, as reptiles may respond differently than mammals. One study found that reptiles respond to acetylcholine by vasoconstriction, where in mammals this causes vasodilatation.5 There is much work yet to be done to determine the effectiveness and activities of cardiac glycosides, vasodilators, and sympatholytics in reptiles.

3.  Proper use of ultrasound may aid in diagnosis of certain disorders.11

4.  Doppler is usually effective for evaluation of cardiac rate and rhythm in reptiles.7

5.  If the reptile is in shock, IV access is critical and can be obtained through catheterization of the palatine vein.

6.  Fluid therapy is likely to be indicated, especially in shock, but care must be taken not to overload the cardiovascular system.

7.  Electrolyte panels may or may not be assistive individually, but they could be helpful if taken serially.

Improvement of husbandry practices for reptiles and longevity can be expected to contribute to increased incidence and recognition of cardiovascular disorders. Cardiovascular pathology should be considered as a differential diagnosis if appropriate, and the predisposing factors should be included in history and diagnosis of these patients. If pertinent, these issues (husbandry, congenital, parasitism, and infection) should be addressed and the patient monitored for response to therapy given.

Literature Cited

1.  Avolio, A.P., M.F. O’Rourke, B.T. Billiman, M.E. Webster, and K. Mang. 1982. Systemic arterial hemodynamics in the diamond python Morelia spilotes. Am. J. Physiol. 243: R205–12.

2.  Braunwald, E. 1992. Heart Disease: A Textbook of Cardiovascular Medicine. 4th ed. W.B. Saunders Company, Philadelphia, PA. Pp 393–464.

3.  Jacobson, E.R., J.C. Seely, M.N. Novilla, and J.P. Davidson. 1979. Heart failure associated with unusual hepatic inclusions in a Deckert’s rat snake. J. Wildl. Dis. 15:75–81.

4.  Jones, J.P. 1992. Intravascular coagulation and osteonecrosis. Clin. Orthop. 277:41–53.

5.  Kalsner, S. 1989. Cholinergic constriction in the general circulation and its role in coronary artery spasm. Circ. Res. 65: 237–257.

6.  Lillywhite, H.B. and A.W. Smits. 1984. Liability of blood volume in snakes and its relation to activity and hypertension. J. Exp. Biol. 110: 267–274.

7.  Mader, D.R. 1996. Reptile Medicine and Surgery. W.B. Saunders Company, Philadelphia, PA. Pp 39–46, 95–104.

8.  Petrishchev N.N. and I.A. Mikhailova. 1995. The thrombogenic properties and thromboresistance of the vessels in amphibians and reptiles. Fiziol Zh Im I M Sechenova 81: 105–108.

9.  Robbins, S.L., R.S. Cotran, and V. Kumar. 1994. Robbins Pathologic Basis of Disease. W.B. Saunders Company, Philadelphia, PA. Pp 467–583.

10.  Schuchman, S.M. and D.O. Taylor. 1970. Arteriosclerosis in an iguana (Iguana iguana). J. Am. Vet. Med. Assoc. 157: 614–616.

11.  Silverman, S. 1993. Diagnostic imaging of exotic pets. Vet. Clin. North Am. Small Anim. Pract. 23:1287–1299.

12.  Wasser, J.S., S.S. Guthrie, and M. Chari. 1997. In vitro tolerance to anoxia and ischemia in isolated hearts from hypoxia sensitive and hypoxia tolerant turtles. Comp. Biochem. Physiol. A. Physiol. 118: 1359–1370.


Speaker Information
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Elizabeth Marie Rush, DVM
The E. & M. Bobst Hospital
The Animal Medical Center
New York, NY, USA

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