Shock in Kudu Antelope During Capture and Chemical Immobilization
The kudu is considered to be one of the most striking and majestic of the African antelopes, largely due to the male’s large, spiraling horns. There are two species of kudu: The lesser kudu (Tragelaphus imberbis) and the greater kudu (Tragelaphus strepsiceros). The greater kudu is comprised of three subspecies: Tragelaphus strepsiceros, Tragelaphus chora Tragelaphus cottoni.1 Female kudu have short horns, while the horns of the males grow up to 1.8 meters, the longest of any antelope. The greater kudu has a larger body size, with a height ranging between 1.3 and 1.5 meters (greater kudu males being the tallest antelope after the eland).1,2 Lesser kudus are lighter in weight and shorter in stature.
The kudu’s skin coloration ranges from reddish-brown to blue-gray with white markings. They also carry 6 to10 vertical white stripes on their torsos and nose chevrons. The greater kudus have white forelegs. Greater kudus are common in Eastern and Southern Africa. They are widely distributed in Southern Africa, especially in the bushveld lowlands.1 The more elusive lesser kudu is common in the arid lowland thornbush of northeast and East Africa.2
The Dynamics of Shock in Antelope
Even under the best circumstances, chemical immobilization is a risky proposition. Almost all of the drugs that produce anesthesia endanger cardiovascular stability by producing dose-dependent impairment of cardiac function, vascular reactivity and autoregulatory responses.3 Hemoglobin is found within red blood cells and carries oxygen to tissues. Normally, the amount of oxygen delivered to the cell is 2 to 4 times the amount required, depending on the tissue, which ensures an adequate supply.4 However, if tissues are not adequately perfused with blood, the oxygen fails to get to the cells, regardless of the oxygen content in the blood.5
Venous circulation represents approximately 70% of a kudu’s total blood volume, and is a chief contributor to stroke volume and cardiac output.5 Vasodilation is the primary cause of hypovolemia produced by anesthetic drugs. It is often associated with increased venous compliance, decreased venous return, and reduced response to vasoactive substances.1Depending on things like patient status and monitoring, a state of relative hypovolemia can remain clinically undetected for protracted periods of time.3-5
Shock is a critical condition that is brought on by a sudden drop in blood flow throughout an animal’s body. Shock can be the result of a wide variety of conditions or circumstances, including extreme physical stress, trauma, disease, heatstroke, blood loss, allergic reactions or severe infection. When an animal is in shock, its organs are not receiving an adequate amount of blood or oxygen. If untreated, this can lead to permanent organ damage or death.
Unfortunately, the processes surrounding capture and/or chemical immobilization can include extreme physical stress and/or trauma sufficient to induce shock in kudu. The degree of risk is contingent upon factors such as species, sex, age, overall health, environmental factors, length of immobilization, the degree of stress involved in the capture/immobilization event itself, the specific chemical agents involved in immobilizing the animal and others.
The three main categories of shock are:
Circulatory Shock. This occurs when there is a decrease in effective circulating blood volume. This category is further divided into the three subcategories of cardiogenic, hypovolemic and distributive shock. Cardiogenic shock occurs when the circulating volume of blood decreases despite normal or increased blood volume. Hypovolemic shock occurs when blood volume is decreased through hemorrhage, third space fluid distribution, or dehydration. Distributive shock occurs when the body is unable to maintain the vasoconstriction of blood vessels.3
The remaining two categories of shock are hypoxic shock and metabolic shock. Hypoxic shock results from impaired oxygen delivery to cells, while metabolic shock involves cells that have become unable to utilize oxygen for energy production.3,4 For the purposes of this discussion, the types of shock being discussed are the subcategories of circulatory shock and hypoxic shock, which are the most likely to be brought on due to capture and/or immobilization events.
Diagnosis and Treatment of Shock in Kudu Antelope
Clinical signs of shock in kudu can include any combination of the following:
- Unresponsiveness
- Hypothermia
- Tachycardia
- Bradycardia
- Tachypnea
- Bradypnea
- Marked hypotension
- Cyanosis
- Orthopnea
Treatment of shock must focus on increasing oxygen delivery to the tissues. This can be accomplished by providing supplemental oxygen, increasing effective circulating volume, increasing hemoglobin concentration and increasing cardiac output with stimulants.4,6 If possible, an intravenous catheter should be placed for vascular access. If venous access cannot be established, an intraosseous catheter can be placed. Oxygen supplementation, when available, will also provide benefits to the animal experiencing shock. This can be accomplished via flow-by oxygen, mask, nasal cannulas or an oxygen cage.7
Regarding fluid therapy, lactated Ringer’s solution, Normosol-R, and Plasma-Lyte are the preferred choices for resuscitation, as these have been shown to cause fewer complications as well as decrease the risk of mortality3 as compared to other options.
Hypertonic saline is also a popular option for fluid therapy (increasing vascular volume). Hypertonic saline increases plasma osmolarity, pulling water into the vascular space from the interstitial space, thereby expanding plasma volume. It should be noted that hypertonic saline has unwanted side effects, such as a transient, dose-dependent increase in sodium and chloride will occur.3,4
Finally, blood products are an important adjunct for the treatment of shock. In normal patients, anemia can be well-tolerated with oxygen delivery being maintained. In animals with trauma and acute loss of blood volume however, the associated stressors can contribute to decreased oxygen delivery.4
4Noel-Morgan, J., Muir, W. (2018) Anesthesia-Associated Relative Hypovolemia: Mechanisms, Monitoring, and Treatment Considerations. Frontiers in Veterinary Science, Vol. 5 (53).
5Haller G, Laroche T, Clergue F. Morbidity in anaesthesia: today and tomorrow. Best Pract Res Clin Anaesthesiology (2011) 25(2):123–32.
6Steadman J, Catalani B, Sharp CR, Cooper L. Life-threatening perioperative anesthetic complications: major issues surrounding perioperative morbidity and mortality. Trauma Surg Acute Care Open (2017).
7Ball, L. Antelope Anesthesia. Wiley Online Library, 25 July 2014,
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