Skin and Musculoskeletal Diseases

Skin and Musculoskeletal Diseases

Paulo V. M. Steagall

Faculté de Médecine Vétérinaire, Université de Montréal, Saint-Hyacinthe, Québec, J2S 2M2, Canada


This chapter presents a concise description of the pathophysiology, diagnosis, and treatment of the most relevant canine and feline skin and musculoskeletal diseases. An emphasis is given to the impact of these diseases on anesthetic and analgesic management of patients. In some instances, skin and musculoskeletal disease is presented as a secondary complication rather than the main clinical concern. Adequate preanesthetic patient assessment and monitoring are essential for the successful outcome of any case.


Skin burns are a result of thermal, chemical, electrical, or radiation injury [14]. In dogs, exposure to high ambient temperatures has been associated with severe burns with concomitant heatstroke; a condition known as dorsal thermal necrosis [5]. Patients with burns may constitute a life‐threatening condition that requires intensive care and aggressive pain management. Burns have been classified as follows:

  • Superficial partial‐thickness (e.g., first‐degree) burns involve only the epidermis and healing generally occurs within 5 days. Lesions are bright red, nonblistered, and painful.
  • Deep partial‐thickness (e.g., second‐degree) burns involve all epidermal layers and variable depths of the dermis. They may appear dry or blistered and moist, usually resulting in the formation of scar tissue after a prolonged healing period (Figure 15.1).
  • Full‐thickness (e.g., third‐degree) burns involve destruction of the entire dermis and may extend into the subcutaneous tissues. They are dry, leathery, and appear white or charred. These burns are expected to be insensate, and loss of function may result.

Characterization of injury severity is warranted for appropriate prognosis and treatment planning. The criterion has been adapted from the human literature and is described elsewhere [5]. Full‐thickness burns can be initially numb; however, late nerve regeneration can be a significant cause of neuropathic pain in humans. It is also important to recognize that all burn stages can be present in the same patient, making pain assessment and treatment more challenging. For example, dogs with “garden hose scalding syndrome” can present with thermal scald burns of different degrees after exposure to hot water from hoses lying in the sun in the Southern and Western regions of the United States [1].

Photo depicts dorsal aspect of a dog with thermal scald, deep partial-thickness burns.

Figure 15.1 Dorsal aspect of a dog with thermal scald, deep partial‐thickness burns.

Knowledge about burns in veterinary medicine is limited and is mostly related to personal experience, case reports, and review articles [1, 3, 4, 6, 7]. However, the prevalence of burns and associated injuries can be relatively high, especially after large fires (i.e., flame burns) in specific geographic regions. Radiation burns associated with radiation therapy treatment may also present a problem in veterinary oncology. Iatrogenic burns may occur in the perianesthetic period and may be associated with inappropriate monitoring in the magnetic resonance imaging (MRI) unit (Figure 15.2) or with the use of supplemental heat to treat or prevent hypothermia during general anesthesia (Figure 15.3). In the latter cases, occult burns are commonly overlooked until the injury is evident days later.

Metabolic Derangements and Systemic Effects

Euthanasia may be advisable if lesions extend to >50% of total body surface area (TBSA). After a burn injury affecting >20% of the patient’s TBSA or if the wounds are of deep, partial, or full thickness, a systemic inflammatory response syndrome (SIRS) may develop within minutes of the injury, resulting in cardiovascular collapse and multiorgan system failure (Figure 15.4) [8]. Sepsis is another important consideration in burn patients and one major cause of death [9]. Wound‐, respiratory‐, and catheter‐related infections may occur secondary to the compromised integrity of the natural barriers and subsequent free passage of bacteria and endotoxins through the skin, contributing to the development of multiorgan failure. Humoral immunity and cell‐mediated immunity are altered resulting in immunosuppression, which may further increase the prevalence of sepsis. Other signs may be present in sepsis, such as fever or hypothermia, tachycardia, bradycardia (more commonly in cats), tachypnea, altered mental status, hypoglycemia or hyperglycemia, edema, leukopenia or leukocytosis, hemodynamic instability, thrombocytopenia, ileus, hypocoagulability or hypercoagulability, and hyperlactatemia, among others [9]. A hypermetabolic response is typically observed until final resolution of the wounds and long after. This consists of a variety of disorders such as increased sympathetic stimulation, gluconeogenesis, protein catabolism, insulin resistance, and weight loss.

Photo depicts accidental multifocal burns associated with the use of magnetic-resonance-imaging-compatible electrocardiogram patches in a dog. These burns were not noted until days later and are often called occult or heating pad burns.

Figure 15.2 Accidental multifocal burns associated with the use of magnetic‐resonance‐imaging‐compatible electrocardiogram patches in a dog. These burns were not noted until days later and are often called occult or heating pad burns.

Photo depicts accidental burns related with the use of polymer fiber resistive warming devices or adaptations to prevent or treat hypothermia such as beverage plastic bottles with hot water during anesthesia.

Figure 15.3 Accidental burns related with the use of polymer fiber resistive warming devices or adaptations to prevent or treat hypothermia such as beverage plastic bottles with hot water during anesthesia. These burns may happen due to faulty equipment, the use of high temperatures, equipment misuse, and direct contact between the conductive material and skin with pressure points creating “hot spots.” Burns during general anesthesia are usually less common with forced‐air warming devices.

Source: Photo courtesy of Dr. Javier de Benito.

Schematic illustration of algorithm of burn injury.

Figure 15.4 Algorithm of burn injury.

Smoke inhalation injury is of concern and constitutes an important aspect of increased morbidity. Direct thermal damage to respiratory epithelium leads to sloughing and edema of the upper airways that, in addition to the formation of cellular casts, may obstruct the airways [10]. The systemic inflammatory response, with the release of thromboxane, causes pulmonary vasoconstriction, hypertension, and hypercoagulability. Carbon monoxide (CO) poisoning frequently occurs in conjunction with inhalation injury, further contributing to tissue hypoxia. Carbon monoxide interferes with the oxygen transport function of blood by combining with hemoglobin to form carboxyhemoglobin; the latter has about 240 times the affinity of oxygen for hemoglobin leading to hypoxemia and high morbidity.

Treatment and Anesthetic Management

Wound care is paramount in the management of burn patients and has been described elsewhere [4]. Emergency treatment is often required with burns, since patients may be at high risk for metabolic derangements. However, many individuals are not presented to the veterinarian immediately after injury, especially in occult burns. The risk of hypoxemia should be minimized with 100% inspired oxygen administration via face mask or nasal cannula; gentle manipulation should minimize patient’s fear and anxiety during oxygenation. Immediately following injury (within 2–4 h of burns), cool compresses aid in alleviating pain and stopping any ongoing burning trauma due to high skin temperatures. Careful attention to catheter‐related infection must be made and aseptic technique should be practiced. Intraosseous catheterization is an alternative if intravenous (IV) access is limited. Antibiotic administration may be required in the presence of sepsis. Considerations for fluid therapy are presented in Figure 15.5 [11].

Direct myocardial depression leading to hypotension can be treated with infusion rates of dopamine (5–15 μg kg−1 min−1 IV) or dobutamine (1–5 μg kg−1 min−1 IV). If inhalation injury has occurred, systemic administration of beta‐adrenergic receptor agonists such as terbutaline or inhaled albuterol can be used to treat bronchospasm. Supplemental oxygen should be provided for as long as deemed necessary according to blood gas analysis. However, long‐term use (i.e., days) of high concentrations of oxygen (i.e., patients under ventilation in the intensive care unit) can lead to oxygen toxicity. Nutritional support may be required depending on the severity and location of skin burns. Hypothermia is usually observed in patients with burns due to rapid and excessive heat loss and should be prevented and treated accordingly. Individuals with burns are typically expected to develop excruciating pain and to have exceedingly high opioid requirements [12]. The prevalence of acute neuropathic pain in humans with burns can be up to 52% for years after the injury and is associated with an increased extent/percentage of body surface burns at presentation [1315]. These patients are at high risk of developing chronic pain syndromes following healing [16]. An association between acute pain severity during hospitalization and the prevalence of persistent burn pain may exist and the same issue could exist in veterinary patients. Therefore, analgesic administration is imperative, and agents (Table 15.1) should be given in the emergency setting, especially if one considers that pain increases morbidity and the extent of protein catabolism, and delays healing. Analgesics can be administered as a constant rate infusion (CRI) to maintain long‐term therapeutic plasma concentrations. For example, ultra‐short‐acting mu‐opioid receptor agonists such as remifentanil or fentanyl in combination with ketamine, an N‐methyl D‐aspartate (NMDA) receptor antagonist, are recommended in the treatment of central sensitization [17]. In dogs, lidocaine may also provide additional analgesia administered either using an infusion or transdermal patch. The lidocaine patch is 10 × 14 cm2 and contains 700 mg of lidocaine in an aqueous base with other inactive ingredients. This formulation of lidocaine produces analgesia without blocking all the sensory and motor inputs [18] and can be used in cats as well [18]. However, it is not known if changes in skin permeability would change the safety and efficacy of lidocaine patches in burn patients. Lidocaine has also been shown to have free‐radical scavenging and anti‐inflammatory properties when administered systemically [19, 20]. Nonsteroidal anti‐inflammatory drugs (NSAIDs) should be withheld until renal function is reestablished and should not be administered in combination with corticosteroids. Gabapentin has been used in cats with neuropathic injury due to burns [2]. The drug can be easily incorporated into the multimodal analgesic approach, although evidence‐based information is lacking for patients with burns. It is not clear what dosages are effective for these cases, but gabapentin has been shown to produce perioperative pain relief in combination with opioids in dogs and cats [21, 22]. Amantadine is an orally administered NMDA antagonist that can be given as long as pain persists. Constant nursing and care contribute to the pain assessment and treatment and can improve animal welfare.

Schematic illustration of considerations for fluid therapy in the burn patient.

Figure 15.5 Considerations for fluid therapy in the burn patient.

Table 15.1 Suggested analgesics for the management of pain in patients with burns.

Drug Dosage Comments
Remifentanil 2–8 μg kg−1 h−1 IV infusion Can be combined with ketamine
Fentanyl 1–4 μg kg−1 h−1 IV infusion Can be combined with ketamine
Ketamine 2–10 μg kg−1 min−1 IV infusion Can be combined with remifentanil or fentanyl
Lidocaine 1–2 mg kg−1 bolus followed by 25–50 μg kg−1 min−1 IV infusion


Patch of 10 × 14 cm2 containing 700 mg of lidocaine (50 mg of lidocaine per gram of adhesive patch)
IV use in dogs only
Gabapentin 10–20 mg kg−1 every 8 h PO
Amantadine 3–5 mg kg−1 every 24 h PO
Nonsteroidal anti‐inflammatory drugs Follow label recommendations Should be withheld until renal function is reestablished. Should not be administered in combination with corticosteroids

IV, intravenously; CRI, constant rate infusion; PO, orally.

General anesthesia may be required for daily wound management or for escharotomies with skin graft coverage to attenuate the postburn hypermetabolic response. This is usually the case for full‐thickness burns. Inhalant anesthetics should be reserved for cases where smoke inhalation injury is not present; sevoflurane is preferred for suppressing upper airway reactivity while being the least irritating/pungent anesthetic agent for inhalation [23]. Otherwise, total intravenous anesthesia (TIVA) with propofol (0.2–0.4 mg kg−1 min−1) is recommended. Alfaxalone infusion (0.2–0.4 mg kg−1 min−1) is also a potential alternative for TIVA; however, anesthetic recoveries can be protracted and of poor quality [24]. Ventilatory support can be provided with positive end‐expiratory pressure (PEEP), but barotrauma is best avoided with the use of low peak airway pressures. Sterile endotracheal tubes (high‐volume, low‐pressure cuff) and lubricants should be used for patient intubation to decrease the risk of secondary infection. In humans, there is no conclusive evidence about the use of steroids for the management of severe upper airway edema [25, 26]. Overall, the patient should be evaluated on a case‐by‐case basis because shock, hyperdynamic circulation, decreased serum albumin concentration, increased alpha‐1 acid glycoprotein concentration, and altered receptor sensitivity alter the response to various drugs. Anesthetic induction can be performed with any of the classic IV anesthetic agents such as propofol, alfaxalone, or ketamine combined with a benzodiazepine. The dosages and choice of anesthetic will depend on the physical status and preoperative evaluation of the patient and the use of other drugs with anesthetic‐sparing effects. Etomidate or opioid/benzodiazepine (e.g., fentanyl with midazolam) induction can be used if cardiovascular collapse is present, especially in dogs. If serial anesthetic events for wound debridement are required, repeated use of etomidate should be avoided due to adrenocortical suppression. Overall, balanced anesthetic techniques are preferred; doses can be given “to effect.”

Chronic Pain Syndrome after Feline Onychectomy

Onychectomy (“declawing” or phalangectomy) is the amputation of the third phalanx of each digit of cats [27]. This still occurs in the United States and parts of Canada, even considering that most owners are against this practice or think onychectomy is a painful procedure [2831]. It involves surgical trauma and nerve damage. The surgical procedure is aggressive with many postoperative complications. Owners sometimes choose to declaw their cats to prevent property damage or personal injury from scratching. The discussion of the ethical issues involved with feline onychectomy is ongoing, but several state/province legislations have banned the procedure in North America.

Laser onychectomy should be the preferred over scalpel surgical approach due to significantly decreased hemorrhage and postoperative complications including pain [32]. Complications after feline onychectomy can be as high as 50% and include persistent postsurgical pain [33, 34]. Radiographic and clinical signs include lameness, back pain, protrusion of the second phalanx, muscle loss, flexor tendon contracture, reluctance to jump, inappropriate eliminating habits, licking and chewing at the digits, aversion to the feet being touched, bleeding, swelling, changes in weight‐bearing, infection, neuropathies, chronic draining tracts, and regrowth of claws [32, 33,3539]. There is also a possible link between onychectomy and late onset osteosarcoma [40], hypothesized to result from chronic inflammation inducing neoplastic changes, as has been reported in cats with injection‐site sarcomas [41]. Chronic pain syndrome after feline onychectomy is characterized by behavioral changes that may develop within the immediate postoperative period or years after the procedure. These changes can lead to suffering, reduced quality of life, and disability. Central sensitization after severe peripheral nociceptive input can result in allodynia and chronic pain, which involves the activation of NMDA receptors. Secondary hyperalgesia is expected due to the amplification of postoperative pain. The diagnosis of the syndrome is mostly based on clinical signs and behavioral changes after ruling out degenerative joint disease or other complications that could be surgically corrected.

Anesthesia and Perioperative Analgesia

Judicious perioperative anesthetic and analgesic management may avoid chronic pain development after feline onychectomy. The following analgesic principles and techniques should be used in these cases:

  • Multimodal analgesia is characterized by the simultaneous use of two or more different classes of analgesics, where each class of analgesic acts at different levels of the nociceptive input pathway and has different onsets and durations of action.
  • Analgesic doses may be reduced while minimizing the incidence of adverse effects.
  • Postoperative pain attenuation usually occurs with preventive analgesic administration. Opioid and local anesthetic use is recommended to prevent central sensitization and reduce intraoperative analgesic requirements and anesthetic‐induced cardiopulmonary depression due to their inhalant anesthetic‐sparing effects [4244].
  • Preoperative NSAID administration improves postoperative analgesia in cats undergoing onychectomy [44]. For example, cats receiving meloxicam for 5 days had better outcomes than those receiving for only 3 days [45]. Additionally, long‐term administration of NSAIDs might be required in some cases (see the section titled “Chronic Pain Syndrome Treatment”).

Cats undergoing onychectomy are generally young and healthy at presentation and, therefore, minimal preoperative diagnostics are required before general anesthesia unless otherwise indicated. The patient’s history and physical examination will guide the anesthetic plan. Table 15.2 shows the perioperative anesthetic management for cats undergoing onychectomy. The veterinarian should be aware of NSAID label recommendations in cats, which can vary among countries. For example, in Europe, meloxicam is licensed for long‐term use at 0.05 mg kg−1 day−1. Treatment of acute and chronic pain after feline onychectomy may require off‐label administration of NSAIDs such as robenacoxib and meloxicam, unless contraindicated (see the section titled “Chronic Pain Syndrome Treatment”).

Table 15.2 Perioperative analgesic management for cats undergoing onychectomy.

  • Premedication: dexmedetomidine (5–10 μg kg−1) or acepromazine (0.03–0.05 mg kg−1) + hydromorphone (0.05–0.1 mg kg−1) or methadone (0.3–0.5 mg kg−1) IM. The addition of ketamine (2–3 mg kg−1) might be required in cats requiring chemical restraint.
  • Induction: ketamine (5 mg kg−1) + diazepam or midazolam (0.25 mg kg−1), propofol (3–8 mg kg−1), or alfaxalone (1–3 mg kg−1) IV considering that these cats are usually healthy. Doses should be given to effect depending on the protocol and effects of premedication.
  • NSAIDs: meloxicam (0.2 mg kg−1 SC after induction; then 0.05 mg kg−1 PO every 24 h for 3 days; this is “off‐label use” in the United States, but not in Canada) or robenacoxib (1–2.4 mg kg−1 SC followed by PO for 3–5 days).
  • Local blocks: 0.5% bupivacaine hydrochloride (2 mg kg−1 as a maximum dose). Therefore, the total volume should be divided depending on the number of limbs undergoing surgery. Dilution may be required when used in kittens (1:1 with saline). Doses for liposomal bupivacaine preparations are described in the text.
  • Postoperative: buprenorphine at 0.24 mg kg−1 SC if veterinarians are using a high‐concentrated formulation of buprenorphine (1.8 mg ml−1) every 24 h for up to 3 days in the United States shortly after extubation. Otherwise, buprenorphine at 0.02 mg kg−1 can be administered IV every 4 h after hydromorphone administration, and then 0.02 mg kg−1 buccally every 8 h for 2–3 days as “home‐medication.” A second dose of hydromorphone or methadone can be administered IV or IM until therapy is switched to buprenorphine.

In the perioperative setting and under general anesthesia, blockade of the distal branches of the radial, ulnar, median, common peroneal, and tibial nerves can be performed with bupivacaine (Figure 15.6) [46]. An alternative four‐point local anesthetic block has been also described in cats with precise anatomical landmarks and high success of nerve staining in cat cadavers [47]. Bupivacaine hydrochloride is preferred over lidocaine due to its long‐acting anesthetic effects. In the United States, an injection of liposomal bupivacaine injectable suspension is approved for use in a peripheral nerve block to provide up to 72 h of regional postoperative pain after single administration in cats following onychectomy. The dose of liposomal bupivacaine injectable solution is 5.3 mg kg−1 (0.4 ml kg−1) per forelimb. The administration technique and further details on handling of the suspension can be found on the manufacturer’s website [48].

Image described by caption.

Figure 15.6 (a) In the thoracic distal limbs, on the dorsomedial aspect and proximal to the carpal joint, the superficial branches of the radial nerve are desensitized with local anesthetics. Proximal and lateral to the accessory carpal bone, the palmar and dorsal cutaneous branches of the ulnar nerve are desensitized with local anesthetics. The median nerve is blocked proximal to the median carpal pad. Alternatively, a four‐point digital block or a ring block can be performed by injecting bupivacaine into the subcutaneous tissues distal to the carpal joints [46]. (b) In the pelvic distal limb, on the dorsomedial aspect and distal to the tarsus, the superficial branches of the common peroneal nerve are desensitized. Ventromedially and distal to the tarsal joints, the superficial branches of the tibial nerve are blocked. For these procedures, local anesthetics are administered at each site in the subcutaneous tissues using a 22‐gauge 1‐in. needle [46].

Source: Adapted from reference 46, with permission.

Local anesthetics are safe when appropriate doses and techniques are used. For this reason, toxic doses must be calculated, especially in kittens. Nonflammable antiseptic should be used around the local block sites if laser surgery is to be performed. Safety glasses must be used for protection of the eyes from any reflected beam during laser surgery [27].

Chronic Pain Syndrome Treatment

Cats must be examined for any other source of pain when chronic pain after feline onychectomy is suspected; the feet must be evaluated for residual inflammation or underlying infection. Diagnostic imaging can determine the presence of any remaining bony fragments and claw regrowth. If the syndrome is confirmed, analgesia and treatment of central sensitization are therapeutic goals. A multimodal analgesic approach for long‐term treatment with the combination of NMDA receptor antagonists, opioids, and NSAIDs is proposed in Table 15.3 [49]. Therapy is usually constituted by off‐label administration of analgesics.

Ketamine is a dissociative anesthetic with NMDA receptor antagonistic properties that is commonly used in cats. Activation of NMDA receptors is involved with the transmission and exacerbation of nociceptive stimuli in the dorsal horn of the spinal cord, which plays a key role in neuropathic and chronic pain. Ketamine may prevent central sensitization and the development of chronic pain and is normally administered as a bolus (0.3–0.5 mg kg−1) followed by an infusion (2–10 μg kg−1 min−1) during hospitalization [17]. Amantadine (3–5 mg kg−1 PO every 12 or 24 h) is also an NMDA receptor antagonist that has been administered to cats as part of chronic pain treatment after feline onychectomy.

Table 15.3 Suggested treatments for feline chronic pain syndrome after onychectomy using off‐label medications: an attempt to reverse central sensitization and allodynia.

  • Amantadine: 3 mg kg−1 PO every 24 h for 21 days.
  • Meloxicam: 0.05 mg kg−1 PO every 24 h for 4 days; then 0.025 mg kg−1 PO every 24 h for 4 days, then 0.05 mg per cat PO every 24 h for 4 days, and finally 0.05 mg per cat PO every 48 h for 5 days.
  • Buprenorphine: 0.01–0.02 mg kg−1 every 8 h buccally for up to 5 days (2–3 days) or 0.24 mg kg−1 SC for up to 3 days of a high‐concentration formulation of buprenorphine (1.8 mg kg−1; in the United States).
  • Gabapentin: 10–20 mg kg−1 PO every 8 h until resolution of clinical signs. Gabapentin should be tapered down over a 3‐week period to avoid breakthrough pain.

Analgesic therapy involves opioid administration, such as buprenorphine, especially during breakthrough pain. A sustained‐release formulation of buprenorphine has been advocated to provide analgesia for up to 5 days in cats [50]. Alternatively, a high‐concentration buprenorphine formulation (1.8 mg ml−1) can be administered at 0.24 mg kg−1 SC every 24 h. NSAID administration has been recommended at a progressively decreasing dosing schedule for up to 12 days. A full biochemical profile is mandatory before NSAID therapy is initiated. Cats must be carefully observed for the development of NSAID‐induced adverse effects; immediate cessation of NSAID should occur if adverse effects arise.

Gabapentin is a calcium channel antagonist that can be used as an adjuvant in the treatment of hyperalgesia and allodynia. This drug has been widely used for neuropathic pain treatment in humans and rodents, although its mechanism of action is not fully elucidated. Gabapentin (10–20 mg kg−1 every 8–12 h PO) may be useful as part of a multimodal analgesic approach in the treatment of feline onychectomy pain syndrome. Shredded paper or compressed paper pallets should be used in the litter box until effective therapy becomes evident.

The advent of anti‐nerve growth factor (NGF) monoclonal antibodies could represent a significant advantage in the treatment of persistent postsurgical pain such as chronic pain syndrome after feline onychectomy. In brief, NGF is pro‐nociceptive and can contribute to peripheral and central sensitization. Species‐specific antibodies that target NGF have been used in the treatment of feline osteoarthritis with promising results. Studies indicated adequate safety and efficacy for up to 6 weeks after a single subcutaneous injection in cats [51, 52].

Auricular Disease

The ear is a specialized extension of the integumentary system. Auricular diseases can be particularly painful, especially in the presence of chronic inflammation and neoplasia (Figure 15.7). Sedation and general anesthesia are occasionally required to perform an otic examination, diagnosis, and/or treatment. Ear infection or inflammation can induce neurological deficits due to the proximity of the facial nerve and sympathetic innervations of the eyes and ears. The classification of otitis is described in the following text:

  • Otitis externa describes any inflammatory condition of the external ear canal. Clinical signs consist of head shaking, scratching, otic pain, variable accumulation of cerumen or exudates, and malodor.
    Photo depicts an invasive adenocarcinoma and chronic inflammation of the auricular canal in a dog. A secondary infection with Pseudomonas was diagnosed. Auricular disease can produce severe pain and impair the patient's quality of life.

    Figure 15.7 An invasive adenocarcinoma and chronic inflammation of the auricular canal in a dog. A secondary infection with Pseudomonas was diagnosed. Auricular disease can produce severe pain and impair the patient’s quality of life.

    Source: Photo courtesy of Dr. Lucilene Bernardi de Souza.

  • Otitis media may result from extension of otitis externa through the tympanic membrane, aspiration of pharyngeal contents up the auditory tube, or from hematogenous spread, neoplasia, trauma, and inflammatory polyps. However, otitis media may be a perpetuating factor for otitis externa.
  • Otitis interna is usually an extension of otitis media or neoplasia of the middle ear. A careful neurological examination is required to locate the vestibular signs, as animals with otitis interna will present with nystagmus, circling, or falling toward the side of the lesion. If there is involvement of the labyrinth, animals may become nauseated and vomit. Horner’s syndrome or deficits in cranial nerves may be observed with otitis media and/or interna [53].


Skull radiography, computed tomography (CT), and MRI are commonly indicated for otic evaluation. These procedures normally involve general anesthesia and are employed to evaluate the integrity of the tympanic bulla and reveal the presence of underlying otitis media, neoplasia, polyps, foreign bodies, otitis interna, and central vestibular disease [54]. Advanced imaging helps in distinguishing the anatomic location of the disease process. CT is considered superior to MRI for bony changes, whereas MRI is better for detection of soft tissue abnormalities in both dogs and cats [55]. Cytologic and culture examinations are performed to detect endoparasite/ectoparasite infection, inflammatory processes, or neoplastic lesions. Auricular tumors are more common in cats than dogs and include squamous cell carcinoma, mast cell tumor, basal cell tumor, and fibrosarcoma. General anesthesia is also performed for a complete otoscopic examination in cases of severe otitis in which thorough cleaning of the ear is necessary for therapy and diagnosis [53].

If the tympanic membrane is intact in a dog with otitis media, a myringotomy is performed to obtain samples for culture and susceptibility testing and cytologic examination. Briefly, a spinal needle penetrates the tympanic membrane through the caudoventral aspect of the pars tensa. Suction is applied and samples collected. Ear flushing of external ear canal is usually required under the same anesthetic episode [54].

Brainstem auditory evoked response (BAER) is an objective hearing test that detects the presence or absence of hearing or progression of changes in hearing. Electrodes placed on standard head sites record responses to an auditory stimulus generated. The waves generated are evaluated, and each wave corresponds to a specific cranial nerve or portion of it, or an area of the central nervous system. Since there is conduction of impulses through the brainstem, the test is also valuable for diagnosis of brainstem lesions. Sedation is often required for uncooperative patients. Both sedation and anesthesia cause changes in wave latency [53].


In addition to medical therapy, surgery is commonly performed in dogs and cats for the treatment of ear diseases. Aural hematoma repair due to self‐induced trauma of head shaking or scratching is an example. In this case, blood accumulates within the fractured cartilage of the pinna, and swelling is most visible on the concave aspect. Treatment of otitis externa or other underlying cause is required to avoid recurrence of aural hematoma. Surgical incision, drainage, curettage, and closure with mattress sutures provide apposition of the cartilage edges.

The two most common surgical procedures for the treatment of otitis externa are lateral ear resection and total ear canal ablation (TECA) [56]. Opening the vertical ear canal with lateral ear resection in dogs improves aeration, decreases humidity, facilitates removal of cerumen or exudate, and improves the distribution of topical medication in the ear canal. TECA is the mainstay treatment of end‐stage otitis and malignant otic neoplasia. The technique is always combined with bulla osteotomy to allow complete removal of all secretory epithelium and exudate associated with the external and middle ear. Severe secondary changes and proliferative disease are surgically removed with the ear canal. Finally, a lateral bulla osteotomy of the tympanic bulla allows complete exploration of the middle ear for the removal of secretory epithelium, exudates, and/or tumor. Surgical complications include facial nerve paralysis, hemorrhage, severe pain, and hearing loss [57]. Secondary complications may occur due to compressive bandage placement, especially in cats, causing obstruction of the airways with further hypoxemia, collapse, and death.

Anesthetic Management

Health status and differentiation of ear disease (i.e., primary or secondary disorder) are important for the anesthetic management. Endocrinopathies are a common cause of ear disease. Systemic glucocorticoid administration is usually the elective therapy for acute inflammation of the ear canal, chronic proliferative changes of the ear canal, and allergic otitis. Special attention should be paid to antibiotic therapy that could potentially involve drug‐induced toxicity. Nephrotoxicity induced by aminoglycosides manifests clinically as nonoliguric renal failure, with a slow rise in serum creatinine and a hypo‐osmolar urinary output developing days after initiation of therapy. Systemic aminoglycoside administration is nephrotoxic because a small but sizable proportion of the drug accumulates in the proximal tubules after glomerular filtration [58]. Therefore, the veterinarian should be aware of this potential nephrotoxic effect in animals treated with aminoglycosides.

If a ruptured eardrum is present, manipulation or flushing can cause material to drain through the Eustachian tube into the nasopharynx, resulting in aspiration. An appropriately sized, cuffed endotracheal tube is always required for these procedures.

Chronic ear conditions are associated with pain on palpation and may be exacerbated during the otoscopic examination (Figure 15.7). Pain on opening the mouth may be related to middle ear involvement because of inflammation, swelling, and pain within the bulla, located adjacent to the temporomandibular joint. The ears can be extremely sensitive and painful; anesthetic depth must be rapidly adjusted if head shaking is observed during surgery or otoscopy; a bolus of injectable anesthetic is usually preferred over increases in the concentration of inhalant anesthetics in these cases. Perioperative analgesia is imperative in the management of TECA and bulla osteotomy, as these surgical interventions are highly invasive and painful procedures. Multimodal analgesia with local anesthetic blocks, opioid, and anti‐inflammatory drug administration should be the cornerstone in the treatment of perioperative pain associated with TECA. Premedication with a sedative combined with a mu‐opioid receptor agonist (e.g., methadone [0.2–0.3 mg kg−1 in the cat or 0.5–1.0 mg kg−1 in the dog] or hydromorphone [0.025–0.05 mg kg−1 in the cat or 0.1–0.2 mg kg−1 in the dog]) is recommended. In the intraoperative and postoperative periods, fentanyl reduces inhalant anesthetic requirements, often resulting in less cardiopulmonary depression while providing reliable analgesia. Doses up to 42 μg kg−1 h−1 have produced maximum reductions in the minimum alveolar concentrations of inhalant (approximately 63%) in dogs [59]. However, the use of lower doses will lessen the likelihood of opioid‐induced dysphoria in the anesthetic recovery period. Lower doses of fentanyl (10–15 μg kg−1 h−1 IV) may be combined with lidocaine (50 μg kg−1 min−1 IV; in dogs only) and/or ketamine (10 μg kg−1 min−1 IV) as part of a balanced anesthetic technique. In cats undergoing ovariohysterectomy, a combination of remifentanil (20 μg kg−1 h−1 IV) and ketamine (30 μg kg−1 min−1 IV) reduced isoflurane concentrations by approximately 48% when compared with saline infusions [60]. Remifentanil infusion alone reduced these requirements by only approximately 15% when compared with saline infusions. Therefore, the infusions of a mu‐opioid receptor agonist and ketamine could potentially reduce inhalant anesthetic‐induced adverse effects and provide smooth short‐term anesthetic protocols in cats. Anesthetic recoveries were not protracted due to ketamine infusions [60].

Local and regional techniques can be utilized in addition to systemic analgesic agents. This approach usually minimizes the development of breakthrough pain and a high incidence of opioid‐induced side effects (e.g., dysphoria, respiratory depression, or drug‐induced hyperalgesia). A local anesthetic block has been described in dogs undergoing TECA. Under general anesthesia, bupivacaine is injected in a line from the wing of the atlas to the caudal aspect of the vertical ear canal to block the greater auricular nerve. The drug is administered between the caudodorsal aspect of the masseter muscle and rostral aspect of the vertical ear canal to desensitize the auriculotemporal nerve [61, 62]. Another method of analgesic administration has been described with the use of a local anesthetic delivery system that allows continuous delivery of local anesthetics via a fenestrated catheter (Figure 15.8) [63, 64]. An elastomeric bulb or syringe pump device is filled with drug to deliver a constant volume directly to the surgical site. However, results of these studies could not demonstrate a significant benefit in using local anesthetic blocks in dogs that underwent TECA when other multimodal analgesic techniques were employed. Despite the lack of significant differences among treatment groups, a benefit may exist, and failing to detect an advantage could be attributable to an inadequate dosage of the drug, technique error, inconsistent analgesia of all nerves, adequate effect of other systemic analgesics, and/or poor study design, including inappropriate methods for the recognition and evaluation of pain in animals.

Schematic illustration of application of a pain booster local anesthetic infusion system in a total ear canal ablation.

Figure 15.8 Application of a pain booster local anesthetic infusion system in a total ear canal ablation.

Source: Adapted from reference 63, with permission.

Laryngeal Paralysis

Laryngeal paralysis (LP) is a well‐recognized cause of upper respiratory stridor and dyspnea in dogs and more rarely in cats [65, 66]. The disease is characterized by laryngeal malfunction during abduction of the arytenoid cartilages, thus creating an inspiratory partial or full upper airway obstruction. Hereditary and acquired forms have been recognized in dogs and cats [67]. The hereditary form, less frequent than the acquired form, affects young dogs of many breeds such as Bouvier, Bull Terrier, Dalmatian, Rottweiler, and Siberian Husky. Mixed‐breed dogs can be affected by both forms of the disease. The acquired form is most reported in middle‐aged to older dogs; Labrador Retrievers are overrepresented [68, 69], but other breeds such as Golden Retrievers, Afghan Hounds, Irish Setters, Standard Poodles, and Saint Bernards have been affected [70].

Unilateral or bilateral LP can be a result of trauma or an intrathoracic or extrathoracic mass that could compress or stretch the recurrent laryngeal nerve [65, 67]. In addition, neuropathy of the recurrent laryngeal nerve, myopathy of the intrinsic laryngeal muscles, as well as neuromuscular disorders such as myasthenia gravis (MG), megaesophagus, or idiopathic myositis have been associated with LP. In addition, LP may be a manifestation of a generalized neuromuscular disorder from a peripheral neuropathy [67]. LP can be linked to esophageal dysfunction and generalized weakness [68], as well as to other clinical neurological deficits, electrodiagnostic, and/or pathologic abnormalities [69, 71]. In cats, LP is an uncommon cause of upper airway obstruction, although both forms have been observed. The acquired form has been reported after bilateral thyroidectomy, but no breed or sex predisposition has been identified in this species [66].

Clinical Signs

Clinical sign severity is dependent on the severity of LP and can manifest from altered barking, gagging, coughing, and mild exercise intolerance to severe respiratory distress. Inspiratory stridor or increased lung sounds cranially may be noted during thoracic auscultation. Dyspnea, collapse, cyanosis, and hyperthermia may occur in the emergency setting, possibly requiring general anesthesia and ventilatory support [67]. Vomiting, regurgitation, and inhalation of gastrointestinal contents into the respiratory tract (i.e., aspiration pneumonia) may occur. Clinical signs are usually progressive, and patients are presented for investigation late in the course of the disease. Other clinical signs include concurrent pelvic limb weakness with bilateral cranial tibial muscle atrophy, generalized weakness, and neurological deficits.


Physical examination and laboratory findings may be unremarkable. The most used method for diagnosing LP is laryngoscopy (Figure 15.9). Failure of one or both of the arytenoid cartilages to abduct during inspiration may confirm the diagnosis.

Photo depicts laryngoscopy is the preferred method for the diagnosis of laryngeal paralysis. The procedure is performed via direct examination of the laryngeal function under sedation and a light depth of general anesthesia. Oxygen insufflation should be provided to prevent hypoxemia.

Figure 15.9 Laryngoscopy is the preferred method for the diagnosis of laryngeal paralysis. The procedure is performed via direct examination of the laryngeal function under sedation and a light depth of general anesthesia. Oxygen insufflation should be provided to prevent hypoxemia.

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Oct 18, 2022 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on Skin and Musculoskeletal Diseases

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