Cancer Patients


70
Cancer Patients


Timothy M. Fan and Stephanie Keating


Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois at Urbana–Champaign, Urbana, Illinois, USA


Prevalence of cancer pain


The true prevalence of cancer pain in dogs and cats is unknown; however, given the conserved biology and malignant transformation processes shared between companion animals and people, it is plausible that the occurrence of cancer pain is comparable across these species. Pain is a common ailment in human cancer patients; the incidence of cancer pain at initial diagnosis approaches 30% and, upon disease progression, up to 65–85% of human cancer patients will experience pain at some point [1]. Importantly, the clinical impact of cancer pain is significant with moderate to severe pain reported in 38% of all patients undergoing cancer treatment [2], and pain being the most common physical symptom reported in people diagnosed with terminal cancer [3].


Cancer pain negatively affects quality of life as well as many important physiological functions and pain alleviation in patients should be an utmost clinical and humane priority. No cures exist for many patients suffering from advanced cancer; however, effective analgesic strategies can ameliorate the discomfort and suffering associated with terminal disease. Estimates indicate that more than 70% of human cancer patients suffering from pain can find relief with opioid‐based regimens [4]. It is justifiable to believe that equally effective cancer pain management may be achievable for companion animals too; however, alternative analgesic strategies must be employed due to pharmacokinetic differences and decreased analgesic efficacy of oral opioids in companion animals compared with humans [5]. In order for cancer pain to be adequately managed, it must be recognized early and frequently reassessed by veterinary caregivers and pet owners. Many barriers obstruct the optimal management of cancer‐related pain in animals, including poor recognition associated with many cancers, difficulty in response assessment, limited knowledge regarding the efficacy and usage of analgesics in veterinary outpatients, and suboptimal communication between veterinary caregivers and pet owners [6].


Recognition and assessment of cancer pain


One essential component of pain recognition is adequate communication with the pet owner [6]. Observant pet owners know their pet’s personality well and can recognize subtle changes in behavior that might represent pain or discomfort [7,8]. As such, it is imperative that veterinary caregivers make conscious efforts to believe the perceptions of pet owners who think their pet is experiencing pain. Common behaviors noted by pet owners that might represent pain include changes in movement, posture, grooming, appetite and thirst, respiration rate, or defecation and urination patterns. Development of new behaviors such as focal licking, drooling, dysphagia, or vocalization, as well as changes in their interactions with people, other animals, or the environment may also be noted [9].


To facilitate the recognition of pain and its assessment through behavioral observations, several validated observer pain scales have been developed [10–13]. However, the majority of conventional pain scales have been validated in the context of acute, postoperative pain, or chronic osteoarthritic pain, and hence their suitability for cancer pain assessment might be limited and they may require interpretative modifications to maximize their utility in assessing pain in cancer patients. Unidimensional pain scales are conceptually simplistic, and hence user‐friendly, and include the visual analog scale (VAS), the numerical rating scale (NRS), and the simple descriptive scale (SDS). These scales involve subjective, unguided assessment by the observer, where pain is (1) assigned an integer score from 0 (absent) to 10 (worst possible pain) (NRS); (2) indicated on a continuous 10‐cm line to indicate the severity of pain (VAS); or (3) assigned a designation such as absent, mild, moderate, severe, very severe, or worst possible pain (SDS). There are many weaknesses with these assessment tools, including interobserver variability, number bias, and baseline drift, among others; however, these scales may be helpful when used consistently by the same observer in conjunction with more objective and quantifiable metrics.


Species‐specific multidimensional composite pain scales have been developed to reduce the subjective nature of pain assessment and attempt to capture the sensory‐discriminative as well as affective and cognitive components of pain [13,14]. These scales have been validated and some offer analgesic intervention points in postoperative veterinary patients. Despite the simplicity of unidimensional scales and validity of postoperative multidimensional pain scales, their utilization by pet owners and veterinary caregivers might not be completely applicable to the assessment of tumor‐bearing animals, given the distinct pathophysiology of cancer pain. To address these limitations, alternative assessment schemes have been validated for pets that include either behavioral scales or health‐related quality‐of‐life questionnaires specific to cancer pain [15–20]. Through the use of cancer‐pain‐specific behavior scales or questionnaires, the objective assessment of pain and its alleviation can be more uniformly standardized in tumor‐bearing pets.


In addition to cancer‐pain‐specific scales, it would be ideal to have complementary and orthogonal methodologies for objectively characterizing cancer pain. Some objective and subjective veterinary cancer pain assessment tools have been developed, which correlate well with behavioral changes and perceived pain reported by pet owners [21]. Additionally, some methodologies for quantifying cancer pain that directly affects bodily movement or ambulation can be objectively quantified by activity monitors or computerized force plate and gait analysis systems [22,23].


Types of pain associated with cancer


Cancer pain arises from the direct invasion of tumor cells into nerves, bones, soft tissue, ligaments, and fascia. Pain also can be elicited through the distention and obstruction of internal organs secondary to tumor infiltration. Erosive or inflammatory processes induced by cancer cells within the microenvironment can generate pain too. Mechanistically, cancer pain can be categorized as nociceptive (somatic and visceral) or neuropathic in origin.


Nociceptive pain is associated with direct tissue injury from tumor infiltration and peritumoral inflammation. Perception of pain is caused by the stimulation of peripheral nociceptors residing in cutaneous and deeper musculoskeletal structures.



  • Somatic pain arises from direct injury due to cancer cell invasion into the skeleton, soft tissues, or tendons/ligaments; often manifests as focal and stabbing in nature.

    Table 70.1 Common painful cancers in companion animals.
















































    Type of cancer pain Example
    Nociceptive
     Somatic Primary bone sarcomas (e.g., osteosarcoma, fibrosarcoma, and chondrosarcoma)
    Joint sarcomas (e.g., histiocytic and synovial cell)
    Skeletal metastases (e.g., carcinoma of mammary, prostate, anal sac apocrine gland, lung, and transitional cell)
    Multiple myeloma or solitary osseous plasmacytoma
    Oral cavity tumors (e.g., melanoma, fibrosarcoma, and squamous cell carcinoma)
    Nasal cavity tumors (e.g., adenocarcinoma, chondrosarcoma, and squamous cell carcinoma)
    Skull and orbital tumors (e.g., multilobular osteochondrosarcoma)
    Ear tumors (e.g., ceruminous gland carcinoma)
    Cutaneous and subcutaneous tumors (e.g., mast cell tumor, basal cell carcinoma, apocrine gland carcinoma, and injection‐site sarcoma)
    Mammary tumors (e.g., inflammatory mammary carcinoma)
     Visceral Urogenital tumors (e.g., transitional cell carcinoma, prostate carcinoma, and renal carcinoma)
    Reproductive tumors (e.g., uterine leiomyosarcoma)
    Carcinomatosis (e.g., serosal surface‐involving malignancy)
    Liver and splenic tumors (e.g., hepatocellular carcinoma and hemangiosarcoma)
    Pancreatic carcinoma
    Neuropathic Central nervous system (e.g., meningioma and astrocytoma)
    Brachial plexus tumor
    Vertebral body tumor with compression of spinal cord (e.g., osteosarcoma or other axillary bone sarcoma)

  • Visceral pain arises from cancer cell infiltration, compression, or distortion of internal organs within the abdominal, thoracic, or pelvic cavities; often manifests as diffuse and squeezing in character.

Neuropathic pain is directly related to cancer cell infiltration of peripheral nerves, nerve plexi and roots, or spinal cord; often associated with paresthesia or numbness and described as burning or shooting in nature.


Although cancer‐associated pain can be discretely categorized as either nociceptive or neuropathic, a single tumor type can elicit pain that has blended characteristics of both nociceptive and neuropathic origins. Notably, pain characteristics can be dynamic and change over the course of disease progression. This is a result of surrounding structures becoming increasingly affected, and from structural and neurochemical changes in the peripheral and central nervous systems leading to ongoing pain signals and release of molecular mediators from neoplastic cells. The evolving nature of pain generation has important implications for pain management, and often requires a multimodal analgesic approach. A non‐exhaustive list of common cancers arising in companion animals and the type of pain that they might elicit is summarized in Table 70.1.


Specific underlying causes of cancer pain


Bone cancer pain


Bone is a living organ, rich in blood supply and nerves. Painful sensations arising from the skeleton can decrease quality‐of‐life scores in pets. Given its principal anatomic function for bearing weight and withstanding cyclic compressive forces, compromise of the structural integrity of bone poses risk for pain and pathologic fracture. Neoplasms involving the skeleton can arise primarily from the bone, or secondarily invade or metastasize to involve the skeleton. In dogs, osteosarcoma (OS) is the most common cancer to cause focal skeletal pain. However, other frequently diagnosed tumor types can involve bone too, including metastatic carcinoma and hematopoietic neoplasms such as multiple myeloma. In cats, primary bone tumors occur less frequently than in dogs; however, involvement of bone from local invasion is common for oral squamous cell carcinoma [24]. Despite the diverse tumor histologies that can affect bone, the mechanisms for how tumor cells invade and generate skeletal pain are likely conserved across companion animals.


Mechanisms of bone cancer pain


Bone cancer pain is attributed to specific host responses occurring within the bone microenvironment. First, the presence of cancer cells results in the release of chemical mediators by neoplastic and non‐neoplastic stromal cells, which in turn stimulate sensory afferent nociceptors and cause painful sensations [25]. Specific ligands secreted by both cancer and stromal cells capable of nociceptor activation include endothelin‐1, nerve growth factor (NGF), and prostaglandin‐E2 [26]. Additionally, trafficking immune cells within the tumor microenvironment secrete proinflammatory cytokines, including IL‐1β, TNFα, and bradykinin that also stimulate nociceptors [26]. Second, preclinical evidence indicates that the generation and maintenance of bone cancer pain is directly attributed to pathologic osteoclastic bone resorption [27,28]. Mechanistically, osteoclastic bone resorption is mediated by the coordinated secretion of protons and cathepsin K, a cysteine protease. The localized acidic environment created by osteoclasts stimulates afferent nociceptors through transient receptor potential vanilloid receptor 1 (TRPV1) and acid‐sensing ion channels 2/3 (ASIC 2/3) [26,29]. Third, bone cancer pain can be generated as a consequence of bone erosion and subsequent mechanical instability, which allows for distortion of putative mechanotransducers belonging to the TRPV receptor family [30].


Neuroplastic changes are central to the propagation of nociceptive signals and the development of neuropathic and chronic pain states with bone cancer. The destruction, compression, or stretching of peripheral sensory fibers from the neoplastic process can directly generate aberrant nerve impulses and result in neuropathic pain. Additionally, chemical mediators within the tumor microenvironment, notably NGF, promote ongoing disorganized sprouting of both sensory and sympathetic nerve fibers as has been described in canine OS [31]. These fibers form neuroma‐like structures and have been linked to background, breakthrough, and movement‐induced bone cancer pain, as well as sympathetically mediated pain, all of which contribute to central sensitization and the development of chronic pain states [32,33]. Based on these unifying pathologic mechanisms, effective management of bone cancer pain requires a multi‐pronged therapeutic approach, which addresses the fundamental drivers that contribute to pain generation.


Radiotherapy‐induced pain


Ionizing radiation is effective for managing localized forms of cancer. Mechanistically, ionizing radiation exerts cytotoxic effects by damaging deoxyribonucleic acid (DNA), either directly or indirectly. Following irreparable DNA damage, cancer cells undergo apoptosis. When applied therapeutically, ionizing radiation can be focally conformed to the shape of tumor masses through the use of linear accelerators equipped with three‐dimensional planning software and sophisticated, multi‐leaf collimators. However, even with advanced equipment, small volumes of normal tissue might be irradiated, potentially resulting in painful radiation‐induced toxicity. Although the majority of caregivers who pursue radiation therapy for their pets consider the side effects acceptable [34], some animals might experience considerable morbidity secondary to acute radiation burns. Depending upon the radiation field, acute moist dermatitis, mucositis, and colitis can be early radiation side effects encountered with curative protocols (Fig. 70.1) [35]. Common anatomic sites for the development of painful radiation‐induced mucositis are the mouth when oral or nasal tumors are irradiated, and the large colon/rectum (colitis and proctitis) when pelvic irradiation is performed [36]. Infrequently, late radiation side effects might result in painful and unacceptable toxicity, including the development of osteoradionecrosis (Fig. 70.2), anatomic stricture, and peripheral neuropathies [37].

Two photographs of two dogs affected with acute moist dermatitis.

Figure 70.1 Resolving painful acute moist dermatitis in two different canine patients undergoing palliative or curative‐intent radiation therapy for the treatment of cancer involving the oral or nasal cavities, respectively.

A photograph of a dog affected with late radiation toxicity and nasal squamous cell carcinoma.

Figure 70.2 Irreparable late radiation toxicity in the form of osteoradionecrosis in a dog with nasal squamous cell carcinoma treated with high cumulative doses of radiation therapy.


Chemotherapy‐induced pain


The administration of systemic chemotherapy is not typically uncomfortable; however, it can infrequently result in painful local and systemic side effects. Perivascular extravasation of certain chemotherapeutics, including vincristine, doxorubicin, vinblastine, mechlorethamine, dactinomycin, and pamidronate might result in painful tissue irritation (Fig. 70.3), at times severe enough to necessitate surgical debridement [38]. Additionally, some chemotherapeutic agents have greater tendencies to perturb intestinal transit times and resident microflora, resulting in colitis (e.g., doxorubicin) or constipation (e.g., vinca alkaloids), which have the potential to generate visceral pain [39]. Bioconversion of some chemotherapeutic agents, such as cyclophosphamide, can lead to the production of irritating metabolites (e.g., acrolein) and the subsequent development of painful syndromes, including sterile hemorrhagic cystitis [40]. Certain chemotherapeutic agents, such as dacarbazine, which have low pH (~3) can elicit burning sensations at the catheter site during intravenous infusion. Other chemotherapeutic agents, such as paclitaxel and docetaxel, require Cremophor EL and polysorbate 80, respectively, for solubilization and these solvents can directly activate complement and elicit systemic inflammatory cytokine release, resulting in diffuse pain sensations and systemic hypersensitivity reactions [41,42]. Finally, painful peripheral neuropathies can be associated with the administration of certain drugs such as vincristine, cisplatin, and the taxanes in people [43], and similar side effects have been infrequently documented in companion animals [44,45].

Two photographs of soft tissue inflammation and dermal ulceration in the limb of a cat and a dog.

Figure 70.3 Painful soft tissue inflammation and dermal ulceration secondary to extravasation of vinblastine in a cat (left) and vincristine in a dog (right).


Surgery‐induced pain


Invasive diagnostic or therapeutic procedures can cause acute nociceptive and possibly neuropathic pain in veterinary cancer patients. Staging procedures such as tissue biopsies, bone marrow aspiration, and bone biopsies should be expected to cause mild to moderate pain that can be preemptively treated with analgesics. More aggressive surgeries such as amputation, hemipelvectomy, thoracotomy, radical mastectomy, and large en bloc tumor resection, including orbitectomy, mandibulectomy, or maxillectomy, will generate severe postoperative pain and should be treated with a preventive analgesic strategy, including regional blocks such as epidural or interpleural analgesia or specific peripheral nerve blocks. Longer‐lasting local anesthetic formulations, such as liposomal bupivacaine, can also be administered peri‐incisionally to extend the duration of local analgesia further into the postoperative period. The use of postoperative full μ‐opioid receptor agonists should be a standard analgesic regimen for companion animals undergoing removal of painful invasive tumors through radical surgeries. Opioid analgesics should be combined with an anti‐inflammatory agent whenever possible, as well as adjunctive analgesics as needed, such as lidocaine and ketamine infusions, to address sensitization and prevent the development of persistent postoperative pain states.


Table 70.2 Analgesic drug and oral dosages for dogs.











































































Class Drug Dosage
NSAIDs Robenacoxib 1–2 mg/kg PO q24 h
Deracoxib 1–2 mg/kg PO q24 h
Carprofen 2 mg/kg PO q12 h or
4 mg/kg PO q24 h
Etodolac 5–15 mg/kg PO q24 h
Meloxicam 0.1 mg/kg PO q24 h
Tepoxalin 10 mg/kg PO q24 h
Piroxicam 0.3 mg/kg PO q24 h
Ketoprofen 1 mg/kg PO q24 h
Aspirin 10–30 mg/kg PO q12 h
Acetaminophen 10–33 mg/kg PO q8 h
Grapiprant 2 mg/kg PO q24 h
Opioid Fentanyl patch 2–5 μg/kg/h transdermally
NMDA antagonist Amantadine 3–5 mg/kg PO q24 h
Combination analgesic Tramadol 4–5 mg/kg PO q6–12 h
Anticonvulsants Gabapentin 10–20 mg/kg PO q8 h
Pregabalin 3–4 mg/kg PO q8–12 h
Tricyclic antidepressants Amitriptyline 1–2 mg/kg PO q12–24 h
Clomipramine 1–2 mg/kg PO q12 h
Corticosteroids Prednisone 0.25–1.0 mg/kg PO q24 h
Dexamethasone 0.1–0.2 mg/kg PO q24 h

Pharmacologic treatment strategies


For most pets diagnosed with cancer, pain becomes established early in the course of disease and rapidly intensifies during cancer progression. As such, pharmacologic strategies are often used in the setting of chronic pain management, where the primary intent of intervention is to minimize the clinical consequences of peripheral and central sensitization, as well as maintain quality of life. Tables 70.2 and 70.3 provide general guidelines for common analgesics that are easily administered by pet owners for the management of cancer pain in companion animals. For more detailed pharmacology and dosing regimens, please refer to Chapters 23, 24, and 25.


Table 70.3 Analgesic drug and oral dosages for cats.




























































Class Drug Dosage
NSAIDsa Robenacoxib 1 mg/kg PO q24 h
maximum 3 days (US), 6 days (EU)
Ketoprofen 1 mg/kg PO q24 h
maximum 5 days
Meloxicam 0.05 mg/kg PO q24 h
Tolfenamic acid 4 mg/kg PO q24 h
maximum 3 days
Piroxicam 0.3 mg/kg PO q48 h
Opioids Buprenorphine 0.02 mg/kg PO sublingual q6–8 h
Fentanyl patch 2–5 μg/kg/h transdermally
NMDA antagonist Amantadine 3 mg/kg PO q24 h
Combination analgesic Tramadol 1–2 mg/kg PO q12–24 h
Anticonvulsants Gabapentin 5–10 mg/kg PO q8–12 h
Pregabalin 1–2 mg/kg PO q12 h
Tricyclic antidepressants Amitriptyline 1–2 mg/kg PO q24 h
Clomipramine 0.5–1 mg/kg PO q24 h
Corticosteroidsa Prednisone 1–1.5 mg/kg PO q24 h
Dexamethasone 0.1–0.2 mg/kg PO q24 h

a Long‐term NSAID or corticosteroid administration should be undertaken following informed client consent with regular patient monitoring and administration of the lowest effective dose.


Non‐steroidal anti‐inflammatory drugs


Non‐steroidal anti‐inflammatory drugs (NSAIDs) are used to control nociceptive and inflammatory pain in companion animals. The mechanism of action of most NSAIDs is the inhibition of cyclo‐oxygenases (COXs). For cancer pain, prostaglandin synthase‐2 (COX‐2) is the preferential target of inhibition given its role in inflammatory pain arising as a consequence of prostaglandin‐E2 production. Prostaglandins play an important role in peripheral sensitization leading to hyperalgesia and allodynia. Specifically, prostaglandins regulate the sensitivity of polymodal nociceptors, which typically cannot be easily activated by physiological stimuli. However, following tissue injury and inflammation, the release of prostaglandins facilitates responsiveness of “silent” polymodal nociceptors [46]. Prostaglandins can also activate sodium channels in the dorsal horn of the spinal cord, resulting in central sensitization and the establishment of chronic cancer pain [47]. The NSAID, grapiprant, does not inhibit the production of prostaglandin‐E2 but antagonizes the EP4 receptor, preventing PGE2 from binding, and reducing pain and inflammation without preventing the production of constitutive prostaglandins [48]. The use of NSAIDs for managing cancer pain might be particularly relevant in companion animals given the multiple tumor histologies which overexpress COX‐2 [49], and therefore have the potential for nociceptive sensitization through tumor‐derived prostaglandin generation. Additionally, the anticancer effects of some NSAIDs, notably piroxicam, may have indirect analgesic benefits secondary to possible reductions in tumor burden [50,51].


Opioids


Three conventional opioid receptor subtypes have been cloned and isolated, known as μ‐, κ‐, and δ‐opioid receptors. Opioid receptors are distributed widely, being located in peripheral tissues, immune cells, sensory nerve terminals, and within the central nervous system at spinal and supraspinal sites. Spinally, they are localized primarily in the superficial dorsal horn within laminae I, II, and V. Within the dorsal horn, most opioid receptors are located on presynaptic terminals of afferent fibers; however, lower densities of opioid receptors are also found on postsynaptic sites and interneurons. The mechanism of analgesia is through reduced neurotransmitter release from nociceptive C fibers and postsynaptic inhibition of neurons conveying information from the spinal cord to higher centers of the brain. Binding of opioids to their presynaptic inhibitory receptor blocks the release of glutamate, substance P, and other neurotransmitters, while binding to the postsynaptic receptor further inhibits neuronal depolarization. Opioids further suppress nociception by enhancing activity in descending inhibitory pain pathways, which project down from supraspinal sites to modulate signals in the dorsal horn. Opioids are readily available, can be titrated easily to the desired effect, and demonstrate predictable adverse effects that can be minimized with preventive interventions. Side effects in companion animals include diarrhea, vomiting, constipation, and excessive sedation.


Parenteral opioid administration is highly effective for treating pain in companion animals. Unfortunately, there is considerable evidence that orally administered opioids are unlikely to offer the same analgesic benefits in these species. Many orally administered opioids demonstrate very low oral bioavailability, highly variable absorption, and absent to low plasma concentrations of the parent compound or active metabolite, with short elimination half‐lives [52–56]. These findings, combined with the lack of positive antinociceptive and clinical studies, along with the risk of misuse and drug diversion, do not currently support the routine prescription of orally administered opioids to treat pain in companion animals. However, there is evidence to support alternative routes of opioid administration for outpatients. Analgesic plasma concentrations and evidence of analgesic efficacy have been demonstrated with transmucosal administration of buprenorphine and transdermal patch administration of fentanyl in cats and dogs [57–62].


N‐methyl‐D‐aspartate antagonists


N‐methyl‐D‐aspartate (NMDA) receptors play a key role in central sensitization within the dorsal horn of the spinal cord following the release of excitatory neurotransmitters from nociceptor terminals. Sustained glutamate release leads to perturbations in synaptic receptor density, threshold, kinetics, and activation, with subsequent increases in pain transmission. During central sensitization, glutamate‐activated NMDA receptors undergo post‐translational phosphorylation, increasing their synaptic distribution and responsiveness to glutamate, with resultant hyperexcitability to normally subthreshold noxious stimuli. As such, NMDA antagonists including ketamine, tiletamine, amantadine, and dextromethorphan have a role in the management of chronic cancer pain when central sensitization has been established.


Combination analgesics


Tramadol is a centrally acting analgesic, classified as an opioidergic/monoaminergic drug based on its shared properties with both opioids and tricyclic antidepressants. Tramadol weakly binds to the μ‐opioid receptor, inhibits the reuptake of serotonin and norepinephrine, and promotes neuronal serotonin release. An active metabolite of tramadol, O‐desmethyltramadol, has greater affinity for the μ‐opioid receptor than the parent molecule and is responsible for much of the opioid‐induced analgesia. Based on these properties, tramadol is theoretically a suitable analgesic for the management of both nociceptive and neuropathic pain. Unfortunately, oral administration in dogs has failed to demonstrate any significant analgesia for either postoperative or osteoarthritis pain [63,64]; however, studies in cats have yielded more promising results, likely due to pharmacokinetic and possibly pharmacodynamic differences [65,66]. Additionally, tramadol exerts antihyperalgesic effects, possibly due to the monoaminergic properties of the drug [65] and may offer antinociceptive effects and improve comfort in animals with central sensitization from cancer when used as an adjunctive analgesic. Specifically, tramadol administered in combination with metamizole (dipyrone), with or without NSAIDs, demonstrated clinical efficacy for management of moderate to severe cancer pain in dogs and improved quality‐of‐life scores [16].


Anticonvulsants


Anticonvulsants are useful adjuvant analgesics in patients with neuropathic pain, as well as chronic pain with central sensitization. In companion animals, gabapentin, a structural analog of γ‐aminobutyric acid (GABA), acts on presynaptic axonal terminal voltage‐gated calcium channels to reduce neurotransmitter release. Additionally, gabapentin also induces postsynaptic inhibition by evoking hyperpolarization inhibitory potentials in dorsal horn neurons through the opening of potassium or chloride channels. Gabapentin is well‐tolerated, highly bioavailable, and rapidly metabolized in dogs [67]. Recent studies suggest the adjuvant use of gabapentin does not improve analgesia for the management of acute nociceptive pain in dogs [68,69]; however, other studies suggest gabapentin is effective in the management of neuropathic pain [70]. Pregabalin is a gabapentinoid with similarities to gabapentin; however, the longer elimination half‐life creates a more favorable dosing interval while still demonstrating analgesic efficacy [71,72].


Antidepressants

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May 1, 2025 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on Cancer Patients

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