Choke chain collar in a German shepherd dog

Resume of article by Kristina Grohmann et al.


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Severe brain damage after punitive training technique with a choke chain collar in a German shepherd dog

Kristina Grohmann ^a,^*, Mark J. Dickomeit ^b, Martin J. Schmidt ^a, Martin Kramer ^a

^a Department of Veterinary Clinical Sciences, Small Animal Clinic, Justus Liebig-University, Frankfurter Straße, Giessen, Germanyb Tierärztliche Klinik Stommeln, Nettegasse, Pulheim, Germany
^b Tierärztliche Klinik Stommeln, Nettegasse, Pulheim, Germany


Discussion

Swinging or lifting a dog off the ground by the collar (helicoptering or hanging) is a highly controversial form of punitive training technique occasionally applied by dog handlers or trainers (Miller, 2008). Dog handlers in favor of this technique still believe that its correct application “takes the drive and fight out of the dog” and does not cause any pain (Leerburg, 2010). It has been widely recognized by most veterinary behavior specialists that this form of punishment should be avoided as it causes fear and brings about an escalation of defensive aggression and increasing intraocular pressure (Hetts, 2000; Pauli et al., 2006; AVSAB, 2012). Furthermore, choke chains and collars can cause mechanical or ischemical damage to the larynx, esophagus, thyroid, or trachea (Brammeier et al., 2006). Cerebral ischemia may also occur after general anesthesia (Jurk et al., 2001; Stiles et al., 2012) during birth (Levene et al., 1986; Dickey et al., 2011), vascular thrombosis, asphyxia, and cardiac arrest (Püttgen and Geocadin, 2007; Choi et al., 2010). It is reported in humans and animals such as cats or dogs (Panarello et al., 2004; Timm et al., 2008; Choi et al., 2010). To the author’s knowledge, there has been no description of ischemic brain damage as a result of strangulation in animals so far.

The neurological deficits in this case were circling, blindness, and ataxia. Blindness is a well-known risk of hypoxic brain damage and has been described in cats (Palmer andWalker, 1970; Jurk et al., 2001; Panarello et al., 2004; Stiles et al., 2012), humans (Siesjö, 1992; Grover and Jangra, 2012), and dogs (Palmer and Walker, 1970; Timm et al., 2008) especially after anesthesia. Because in this case no severe lesions were displayed in the occipital cortex, the blindness may have been a result of damage to the visual pathway before the cortex. Comparable Figure 1. (A) Sagittal T2-weighted image. There is a hyperintense lesion (white arrows) in the dorsal and ventral aspect of the thalamus, both hippocampi, the lamina tecti of the midbrain. A mild rostrotentorial herniation of the lamina tecti was noticed (white arrowhead). (B) and (C) Dorsal T2-weighted images at the level of the interthalamic adhesion. There is a severe hyperintense ill-defined lesion in the thalamus (white arrow) at the level of the dorsal surface of the cortex. Both marginal gyri and left-sided parts of the ectomarginal gyrus present ill-defined hyperintense lesions (white arrows).

Neurological deficits have been described in cats and horses (Jurk et al., 2001; McKay et al., 2002; Stiles et al., 2012), and deterioration of clinical signs as in our case is a common risk in hypoxic brain damage (Jurk et al., 2001). The pathophysiology of strangulation has been described in human medicine. Pressure on the neck of a victim causes pain followed by anxiety from the subjective sensation of breathing trouble. The rapid loss of consciousness within 10-15 seconds is because of apnea as well as arterial obstruction, venous obstruction, and response of autonomic nervous system reflexes (Kiani and Simes, 2000). Forces applied to the carotid artery impair the flow through the artery by mechanical obstruction or the induction of spasm, leading to a loss of consciousness as observed in our patient. Damage to the vessel walls and intima may induce thrombosis and produce clinical signs occurring over 12-24 hours (Kaki et al., 1997; Clarot et al., 2005; Chokyu et al., 2006). Furthermore, the thrombosis caused by the traumatized internal carotid artery can embolize to the cerebrovascular circulation (Cothren and Moore, 2005). Venous outflow obstruction causing stagnant ischemia is a significant factor that produces loss of consciousness (Khokhlov, 2001). In humans, loss of consciousness because of manual strangulation isconsidered one of the most significant signs of danger to life (Christe et al., 2010).

Brain tissue has a high oxygen and energy demand, yet little reserve. Under normothermic conditions, the oxygen reserves are exhausted within 20 seconds, and glucose required for the production of adenosine triphosphate is consumed within 5 minutes without perfusion (Safar and Kochanek, 2000). The lack of oxygen results in a switch to anaerobic metabolism, followed by a depletion of high-energy phosphate reserves, lactate accumulation, and instability to maintain cellular homeostasis. The consequential disease pattern is described as hypoxic brain damage or rather as postanoxic encephalopathy (Safar and Kochanek, 2000). The return of normal perfusion does not resolve the cell damage and instead may lead to a reperfusion injury, characterized by the release of free radicals, nitric oxide, and further glutamate release (Hallenbeck and Dutka, 1990; Ikeda and Long, 1990). This finding might explain the progressive neurological worsening observed in the present patient.

Hypoxic cell damage is possible throughout the entire brain, yet not all regions of the brain are equally sensitive. Especially vulnerable are the basal ganglia, cerebellum (especially the Purkinje cells), hippocampus, and the layers3, 5, and 6 of the cortex (Püttgen and Geocadin, 2007; Choi et al., 2010). The regions of occipital and parietal cortexes showed changes after reduced perfusion (Choi et al., 2010).

Human patients after a cardiovascular standstill showed an unfavorable outcome when defects in the basal ganglia and cortex occurred (Choi et al., 2010). Panarello et al. (2004) reported a dog and a cat that recovered to almost normal except for a persistent blindness. Therefore, the outcome in pets appears to be favorable compared with humans. The MRI changes presented in this patient relate to those found in humans and dogs (Safar and Kochanek, 2000; Timm et al., 2008) with hypoxia. As in humans and dogs, the areas affected in this German shepherd were principally the hippocampus, mesencephalon, as well as occipital and parietal cortexes. In contrast to veterinary cases where the occipital cortical area is also considered a vulnerable region, it does not apply to the German shepherd dog presented in this case (Safar and Kochanek, 2000; Jurk et al., 2001).

For the diagnosis of hypoxic brain damage, conventional MR is often inadequate during the early phase, as the brain morphology at this point in time appears normal or with only slight changes (Arbelaez et al., 1999; Choi et al., 2008). In contrast to this, diffusion-weighted MR (DWI) is capable of depicting acute and subacute changes after a global cerebral hypoxia (Arbelaez et al., 1999; González et al., 1999). DWI uses the movement of protons within the tissue. During hypoxia, the membrane-bound Na-K pump malfunctions leading to an influx of water from the extracellular into the intracellular space, inhibiting the intracellular proton movement. Areas with limited diffusion appear markedly hyperintense in the DWI (Lövblad and Bassetti, 2000; Schaefer et al., 2000). DWI and the corresponding ADC can show the restricted diffusion associated with acute ischemia about 30 minutes after the ictus in patients with acute stroke (Choi et al., 2010). Furthermore, the degree of the changes of the DWI signal intensity correlates with the severity of neuronal injury (Rojas et al., 2006). Although the MR was performed only a few hours after the strangulation in this case, the T2 images were of diagnostic quality. In human strangulation cases, MRI frequently includes the neck area to evaluate the integrity of the soft tissue structures.

Hemorrhage into the lymph nodes is a specific diagnostic sign indicating strangulation as the pathomechanism (Yen et al., 2005). Further findings may be subcutaneous or glandular hemorrhage and fractures of the larynx, thyroid, and hyoid cartilage (Yen et al., 2005).

Because of the clinical history and unremarkable clinical examination, strangulation by the owner is considered the most probable cause. Furthermore, up to this point in time, the dog had not shown any neurological abnormalities. The main limitation of this study is the lack of necropsy and histopathological examination of the damaged brain tissue, but the owners declined further investigations.

To the author’s knowledge, this is the first case description of a dog with suspected hypoxia after strangulation by the owner. Considering that disciplining a dog by holding it off the ground by its collar appears to be frequently applied practice, it is important to recognize that even a short period is sufficient to produce life-threatening damage to the brain. Because this technique of punishmentis not uncommon, further cases of ischemic brain damage resulting in the death of the dog may have gone unreported.

It is therefore important to inform veterinary personnel, dog trainers and owners that hanging or “helicoptering” dogs as a form of discipline is a severe health risk that can be fatal.