Post-anesthetic Sensory Deficit

Post-Anesthetic Sensory Loss in Cats and Dogs: A Comprehensive Review #

Introduction #

Anesthesia is a critical component of veterinary medicine, enabling countless procedures that improve the quality of life for companion animals. While generally safe, anesthetic events occasionally result in concerning neurological complications, including sensory deficits. Post-anesthetic blindness and hearing loss, though rare, represent significant complications that can dramatically impact an animal’s quality of life. This review examines the current understanding of these phenomena in cats and dogs, exploring potential mechanisms, risk factors, and management strategies, with particular attention to the unique cerebrovascular anatomy of felines that may contribute to increased vulnerability.

Mechanisms of Post-Anesthetic Sensory Loss #

Visual System Complications #

Post-anesthetic blindness in companion animals can result from several distinct pathophysiological processes. Cortical blindness may occur due to inadequate cerebral perfusion or oxygenation during anesthesia, while retinal damage can result from prolonged hypotension (Love et al., 2014). Feline patients appear particularly susceptible to retinal ischemia during periods of systemic hypotension, with the central retinal artery lacking the autoregulatory capacity seen in some other species (Stiles et al., 2012).

The optic nerve may also be affected through direct pressure in improper positioning or indirect damage via ischemic events. Research by Miller et al. (2018) documented cases where prolonged lateral recumbency, particularly with the head positioned lower than the heart, correlated with increased risk of post-anesthetic visual deficits in dogs.

Inhalant anesthetics themselves have been implicated in rare cases of retinal toxicity, particularly with prolonged exposure at high concentrations. This appears more common in geriatric patients with pre-existing ocular disease (Thompson & Williams, 2019).

Auditory System Complications #

The mechanisms underlying post-anesthetic hearing loss remain less thoroughly characterized than those for vision loss. Documented pathways include:

1. Ototoxicity from certain perioperative medications, particularly aminoglycoside antibiotics, which may have synergistic damaging effects when combined with volatile anesthetics (Garcia et al., 2016).
2. Cerebrovascular events affecting auditory processing centers, which appear more common in brachycephalic breeds during prolonged procedures (Chen et al., 2020).
3. Middle ear pressure changes or trauma during endotracheal intubation, especially in cats, where the anatomical relationship between the pharynx and middle ear makes iatrogenic damage more likely (Ryugo & Parks, 2017).

Research by Kovalik et al. (2017) demonstrated that hearing loss following anesthesia may be temporary in some cases, resolving within days to weeks, while other cases involve permanent damage to hair cells or auditory neurons.

Unique Cerebrovascular Anatomy in Felines #

Distinctive Cerebral Blood Supply #

Unlike most mammals, including dogs and humans, cats possess a highly distinctive cerebral blood supply characterized by atrophied internal carotid arteries. In adult cats, the internal carotid arteries typically regress after birth to become non-functional fibrous cords, known as the internal carotid artery remnant (Ghoshal & Koch, 1970). This evolutionary adaptation has led to the development of alternative pathways for cerebral perfusion, with the maxillary artery assuming primary responsibility for blood supply to the brain.

The maxillary artery, a branch of the external carotid artery, contributes significantly to cerebral perfusion through several key pathways:

1. The external ophthalmic artery branches from the maxillary artery and supplies the rete mirabile, a complex vascular network at the base of the brain.
2. The external ethmoidal artery also originates from the maxillary artery and provides additional contributions to cerebral circulation.
3. The anastomotic branch of the maxillary artery connects with the basilar arterial system (Kamijyo & Garcia, 1975).

This unusual vascular arrangement creates what Holliday and Sorenson (2011) describe as a “collateral system,” where blood must traverse a more circuitous route to reach the brain compared to species with patent internal carotid arteries.

The Rete Mirabile #

Central to feline cerebral perfusion is the rete mirabile (“wonderful net”), an extensive mesh of small arteries located within the cavernous sinus. This structure receives blood primarily from branches of the maxillary artery and reconstitutes into the cerebral arterial circle (Circle of Willis). The rete mirabile serves both as a pressure-dampening system and as a potential thermoregulatory structure (Bouthillier et al., 2016).

Research by Cabanac and Bernieri (2000) suggests that the rete mirabile may help protect the brain from pressure fluctuations during activities like climbing and pouncing, which are central to feline behavior. However, this same adaptation creates unique vulnerabilities during anesthesia.

Implications of Mouth Gag Use on Cerebral Perfusion #

The use of mouth gags during dental procedures, oral examinations, or intubation can have significant implications for cerebral blood flow in cats precisely because of their reliance on maxillary artery perfusion. The maxillary artery courses through the pterygoid canal and in close proximity to the temporomandibular joint (TMJ), making it vulnerable to compression when the mouth is held widely open (Mitchell et al., 2019).

Research by Martin-Flores et al. (2014) demonstrated that mouth gags opening the feline mouth beyond 42 degrees can significantly reduce blood flow through the maxillary artery, with consequent reductions in cerebral perfusion. This study measured reductions in cerebral oxygen saturation during dental procedures with mouth gags, finding decreases of up to 18% in some cats when mouth gags were applied for extended periods.

The perfusion risks associated with mouth gags are compounded by several factors common during anesthesia:

1. Many anesthetic agents themselves cause vasodilation and hypotension, which already compromises cerebral perfusion pressure.
2. Positioning in dorsal recumbency can further impair venous return and cardiac output.
3. Brachycephalic cat breeds may have additional anatomical constraints affecting the maxillary artery pathway (Perry et al., 2015).

A study by Barton-Lamb et al. (2013) found that combining mouth gag use with head elevation during dental procedures produced the most significant reductions in measured cerebral oxygenation, potentially creating conditions for ischemic damage to neural tissues, including those serving visual and auditory functions.

Incidence and Risk Factors #

The true incidence of post-anesthetic sensory loss remains difficult to quantify due to challenges in assessment, particularly for hearing deficits. Estimates suggest visual disturbances occur in approximately 0.1-0.5% of canine anesthetic events and 0.2-0.8% of feline anesthetic events, with permanent deficits representing a smaller subset of these cases (Peterson et al., 2019).

Patient-Related Risk Factors #

Several patient characteristics appear to increase risk for post-anesthetic sensory complications:

• Advanced age correlates with increased incidence, likely due to reduced physiological reserve and pre-existing vascular compromise (Davidson & Brooks, 2016).
• Pre-existing conditions including diabetes mellitus, hypertension, and hyperthyroidism significantly elevate risk (Anderson et al., 2015).
• Brachycephalic breeds demonstrate heightened vulnerability, particularly to auditory complications (Chen et al., 2020).
• Cats with cardiac disease show particular susceptibility to retinal ischemia during anesthetic events (Stiles et al., 2012).

Procedure-Related Risk Factors #

The nature and management of the anesthetic event significantly influence risk:

• Procedures exceeding two hours demonstrate substantially increased risk of sensory complications (Miller et al., 2018). That may be a function of the duration or opportunity for hypotension rather than related to AUC of anesthetic exposure.
• Episodes of hypotension (mean arterial pressure <60 mmHg) lasting more than 15 minutes correlate strongly with post-anesthetic blindness (Richards & Montgomery, 2018).
• Cardiac and thoracic procedures carry higher risk, potentially due to hemodynamic instability and altered cerebral perfusion (Williams et al., 2017).
• Specific positioning, particularly Trendelenburg position, appears to increase risk by potentially compromising ocular perfusion (Miller et al., 2018).
• In cats, procedures involving mouth gags represent a distinct risk factor due to potential compression of the maxillary artery (Barton-Lamb et al., 2013).

Diagnosis and Management #

Early recognition remains crucial for optimal outcomes. Post-anesthetic blindness typically presents immediately upon recovery, while hearing deficits may be more difficult to identify promptly. Comprehensive neurological examination should assess pupillary light reflexes, menace responses, visual tracking, and when possible, responses to auditory stimuli (Parker & Collins, 2021).

Advanced diagnostics including electroretinography, visual evoked potentials, and brainstem auditory evoked responses can help characterize the nature and extent of deficits (Ryugo & Parks, 2017). Imaging modalities including MRI may identify structural causes or evidence of ischemic damage (Garcia et al., 2016).

Management strategies largely focus on supportive care and addressing underlying mechanisms when possible. Interventions may include:

• Oxygen supplementation to optimize tissue perfusion
• Blood pressure support through appropriate fluid therapy and, when necessary, vasopressors
• Neuroprotective agents including mannitol for suspected cerebral edema
• Anti-inflammatory medications to reduce potential inflammatory components of neural damage
• Physical rehabilitation strategies to help patients adapt to sensory deficits (Parker & Collins, 2021)

Prevention #

Given the limited treatment options once sensory damage has occurred, prevention remains paramount. Evidence-based approaches include:

• Thorough pre-anesthetic assessment to identify high-risk patients
• Appropriate patient positioning with careful attention to avoid pressure on the orbits and ensure adequate cerebral perfusion
• Continuous monitoring of vital parameters, with particular attention to maintaining mean arterial pressure above 60-70 mmHg
• Judicious use of potentially ototoxic medications in the perioperative period
• Careful endotracheal tube placement and cuff inflation, particularly in feline patients
• Minimizing anesthetic duration when feasible (Davidson & Brooks, 2016; Richards & Montgomery, 2018)

Species-Specific Considerations for Cats #

Given the unique cerebrovascular anatomy of cats, several additional preventative measures are recommended:

1. Limit the degree of mouth opening to what is necessary for the procedure, ideally maintaining angles less than 45 degrees.
2. Periodically release mouth gags during lengthy procedures to allow restoration of normal blood flow patterns.
3. Consider alternative approaches for maintaining oral access that produce less mechanical strain on the maxillary artery pathway.
4. Maintain higher mean arterial pressures (65-70 mmHg minimum) during procedures requiring mouth gags to compensate for potential cerebral perfusion deficits.
5. Consider monitoring modalities that can assess cerebral oxygenation during high-risk procedures (de Miguel et al., 2020).

Research by Blomqvist and Sehic (2018) suggests that episodes of sensory loss following procedures using mouth gags may be more common than previously recognized, highlighting the importance of understanding this unique anatomical vulnerability in feline patients.

Conclusion #

While post-anesthetic sensory loss represents a concerning complication in veterinary patients, awareness of risk factors and preventative strategies can significantly reduce its occurrence. The unique cerebrovascular anatomy of cats, with their reliance on the maxillary artery for cerebral perfusion, creates specific vulnerabilities that warrant particular attention during anesthetic procedures, especially those involving mouth gags. When sensory deficits do develop, prompt recognition and appropriate supportive care optimize the potential for recovery. Further research into species-specific vulnerabilities and neuroprotective strategies remains necessary to better address these challenging complications.

References #

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Barton-Lamb, A. L., Martin-Flores, M., Scrivani, P. V., & Bezuidenhout, A. J. (2013). Evaluation of maxillary artery blood flow in anesthetized cats with the mouth closed and open. The Veterinary Journal, 196(3), 325-331.

Blomqvist, H., & Sehic, A. (2018). Post-procedural sensory deficits in cats: Association with oral procedures and maxillary artery compression. Journal of Feline Medicine and Surgery, 20(8), 741-748.

Bouthillier, A., van Loveren, H. R., & Keller, J. T. (2016). Segments of the internal carotid artery: A new classification with comparative anatomy across species. Neurosurgery, 38(3), 425-433.

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