Chapter 28 - Grafting Flashcards
1
Q
What is the predominant type of skin disease in horses requiring surgical consultation?
A
sarcoids, which are neoplastic in origin
2
Q
What are the clinical subtypes of sarcoids based on their appearance?
A
- Occult,
- verrucous,
- nodular fibroblastic,
- ulcerative fibroblastic,
- mixed tumors, and
- malevolent.
3
Q
Which subtype of sarcoid is considered the most aggressive?
A
Malevolent sarcoids.
4
Q
Where on the horse’s body do sarcoids commonly occur?
A
Common sites include the face, distal limbs, neck, ventral abdomen, and areas of previous injury
5
Q
Which breed of horse is statistically more likely to develop sarcoids?
A
Quarter Horses and related stock breeds.
6
Q
What genetic component is associated with the risk of developing equine sarcoids?
A
Equine leukocyte antigens (ELA) alleles, particularly A3 and W13.
7
Q
How does age correlate with the development of sarcoids in horses?
A
Sarcoids generally develop in younger individuals, suggesting a genetic predisposition or exogenous factor.
8
Q
What virus is closely associated with the presence of sarcoids in horses?
A
Bovine papillomavirus (BPV).
9
Q
Do papillomaviruses trigger transformation alone in horses?
A
No, viral infection alone is not sufficient for transformation; other factors are involved.
10
Q
What role do the viral proteins E5 and E6 play in the context of sarcoids?
A
They have the capability to transform cells into a malignancy.
11
Q
What clinical outcome was observed in 48% of affected Franches-Montagnes horses over a study period of 2 to 5 years?
A
Spontaneous regression of sarcoids.
12
Q
Which subtype of sarcoids is more likely to undergo spontaneous regression?
A
Occult sarcoids.
13
Q
Why Standardbred are resistant to sarcoids?
A
The absence of the W13 allele in the Standardbred population may confer relative resistance to sarcoid.
14
Q
What impact does incomplete or unsuccessful treatment of sarcoids have on future treatments?
A
It can transform the tumors into a more aggressive phenotype, making them harder to resolve.
15
Q
What factors complicate the assessment of treatment efficacy for sarcoids?
A
The variability in treatment success and the lack of controlled early studies.
16
Q
What is a potential triggering event that may activate a latent viral state in sarcoids?
A
Previous injury or trauma.
17
Q
What does the evidence suggest about the relationship between environmental factors and sarcoid occurrence?
A
Sarcoid occurrence is likely due to a combination of host, viral, and environmental factors.
18
Q
Why is it challenging to assess the efficacy of treatment options for sarcoids?
A
Most early studies were not controlled and based on a subset of cases.
19
Q
What type of sarcoids are commonly referred for treatment?
A
More aggressive variants or tumors that have recurred after treatment.
20
Q
What can incomplete or unsuccessful treatment of sarcoids lead to?
A
Transformation into a more aggressive phenotype.
21
Q
How successful is surgical excision alone for treating sarcoids, based on reported recurrence rates?
A
Recurrence rates range from 15.8% to 82%.
22
Q
What factor may contribute to the low success rates of surgical excision?
A
The presence of malignant cell projections into surrounding tissue.
23
Q
What treatment method showed the best success rate in a recent retrospective study?
A
Electrosurgical excision.
24
Q
What success rate was reported for laser ablation of sarcoids?
A
An overall success rate of 83%.
25
What is a significant benefit of laser ablation compared to traditional excision methods?
t causes less damage to surrounding tissues and reduces malignant cell spread.
26
What challenge is associated with cryotherapy for periorbital sarcoids?
A high recurrence rate of 91%.
27
How can cryotherapy achieve better outcomes?
With experienced practitioners and multiple treatment sessions.
28
What treatment method involves the use of thermal energy to treat sarcoids?
Hyperthermia.
29
What does radiotherapy using iridium-192 reportedly achieve in treating sarcoids?
Low recurrence rates, with some studies showing up to 100% initial success.
30
What are some potential complications of radiotherapy in equine sarcoid treatment?
Hair loss, pigmentation changes, fibrosis, cataract formation, and corneal ulceration.
31
What role does immunotherapy play in treating equine sarcoids?
It enhances immune recognition and can lead to tumor resolution.
32
Which immunotherapeutic agent has been used successfully against equine sarcoids?
Bacille Calmette-Guérin (BCG) vaccine.
33
What outcome is associated with the use of autogenous tumor vaccines in treating sarcoids?
Clinical resolution was achieved in 68.8% of cases.
34
What aspect of intralesional cisplatin treatment is critical for success?
The concentration and administration in an oily emulsion.
35
How effective was imiquimod found to be in pilot studies for treating sarcoids?
It resulted in over 75% size reduction in 80% of treated sarcoids.
36
What is the mechanism of action of aciclovir in treating equine sarcoids?
It inhibits viral DNA synthesis.
37
What treatment option had a resolution rate of 66% for small tumors?
5-fluorouracil (5-FU).
38
What is the preferred protocol for administering imiquimod?
Every-other-day application.
39
What does electrochemotherapy (ECT) combine to improve treatment outcomes?
Chemotherapeutic drugs and high-voltage electric pulses.
40
What reported resolution rate exists for sarcoids treated with electrochemotherapy in retrospective studies?
Between 92.3% to 100%.
41
Why might combined treatment modalities be necessary in managing equine sarcoids?
They are often larger, more aggressive, or occur in multiple locations.
42
What potential benefit does cryotherapy provide beyond direct treatment?
It may initiate an immune response against distant untreated sarcoids.
43
What systemic effects can be mitigated by using cisplatin in an oily emulsion?
It prevents significant systemic levels and maintains effective tissue levels for prolonged periods.
44
What is electrochemotherapy (ECT) and what are its reported resolution rates for sarcoids?
ECT combines chemotherapeutics and electric pulses to enhance drug efficacy, with reported resolution rates of 92.3% to 100%.
45
Marteens study mentions surgical excision of sarcoid of minimum ______ mm
12 mm and gloove changes
success rate 86.8%
46
How effective was aciclovir in decreasing tumor mass according to reported findings?
Complete regression occurred in 32 out of 47 tumors (68%).
47
What successful treatment method for sarcoids was highlighted in recent studies?
Electrosurgical excision with an overall success rate of 86.8%.
48
What factor contributes to the low success rate of surgical excision of sarcoids?
The presence of malignant cell projections into surrounding normal tissue that may be missed during histopathology.
49
What percentage of ocular SCC cases occur in horses with no periocular pigmentation?
69%
50
What is the reported nonrecurrence rate for β-irradiation in treating small corneal lesions?
89%
51
What is the proposed cause of SCC in poorly pigmented horses?
Ultraviolet light-induced damage
52
Squamous cell carcinoma is what type of neoplasia?
a malignant, locally invasive neoplasia of squamous epithelial cells
53
What is the second most common neoplasia in horses?
SCC
54
What are the predilected areas for SCC?
areas lacking pigmentation, poorly haired regions, and skin near mucocutaneous junctions
eye, conjunctiva, ocular adnexal structures, and external genitalia
55
It should be considered in horses with chronic refractory foot abcesses?
Yes
56
Proposed irritants include topically
applied chemicals, smegma, and flies.
57
What breeds are predisposed to SCC?
Breeds with poorly pigmented, pink-skinned areas, including Appaloosas and paint-colored horses, draft horses are more prone to develop SCC
58
What virus has been detected in a subset of genital SCC?
equus caballus papillomavirus 2 (EcPV2)
59
SCC can be classified in 2 types name them
ulcerative - mistaken for nonhealing wounds
proliferative -
60
SCC has also been reported in the nasal cavity, paranasal sinuses, pharynx, larynx, and hoof capsule TRUE or FALSE
TRUE
61
How are caractherized teh ocular lesion?
can begin as small ulcerative lesions on lid margins, or as keratitic plaques on the cornea
62
Proliferative pedunculated lesions on the penis often have a _____________(1w) appearance
Proliferative pedunculated lesions on the penis often have a cauliflower-like appearance
63
SCC typically spreads to surrounding tissues and local lymph nodes, but distant metastasis is rare - TRUE or FALSE
TRUE
64
Name the tx
1. Surgical excision
2. Radiation therapy
3. Topical application
4. Antimitotics
5. Intralesional chemotherapy
6. Cryotherapy
7. Laser excision
8. Hyperthermia
9. immunotherapy
10. Photodynamic
65
Why is β-irradiation considered effective for small corneal SCC lesions?
It has a very short penetration depth, making it useful for small lesions.
66
What are the limitations of radiation therapy for treating SCC in horses?
It requires specialized equipment, licensure, and special housing, limiting its use to referral practices.
67
How does intralesional chemotherapy work in the treatment of SCC?
It involves injecting chemotherapy directly into the tumor, often after surgical cytoreduction.
68
What is the advantage of using intralesional cisplatin in treating SCC?
t is effective in achieving local control, particularly in genital SCC cases.
69
What are some side effects or drawbacks of intralesional chemotherapy for SCC?
Multiple treatments, high cost, and potential exposure of staff to chemotherapy agents.
70
In what cases is topical 5-FU recommended for SCC treatment?
For small, superficial tumors of the external genitalia.
71
What are some adverse effects associated with the use of topical 5-FU?
Local inflammation and swelling.
72
How is mitomycin C used in treating ocular SCC in horses?
It can be used alone or in combination with surgical excision to treat SCC.
73
What are the comparative cure rates for mitomycin C and CO2 photoablation in treating ocular SCC?
Both treatments have similar cure rates, according to a retrospective study.
74
How does the nonsteroidal anti-inflammatory drug piroxicam treat SCC?
By inhibiting COX enzymes, which are overexpressed in some neoplastic tissues.
75
What was the outcome of using piroxicam to treat recurrent SCC of the lower lip in horses?
Both lower lip and metastatic lesions resolved with no recurrence after 5 years.
76
What is photodynamic therapy and how is it used in treating SCC in horses?
It involves using a photoactive agent and light to generate reactive oxygen species, causing local tissue necrosis.
77
What was the result of using photodynamic therapy as an adjunct treatment for periocular SCC?
Horses remained tumor-free for the duration of the follow-up period.
78
What was the recurrence rate of SCC when photodynamic therapy was compared to cryotherapy?
Photodynamic therapy showed a significantly lower recurrence rate than cryotherapy.
79
What types of SCC lesions might benefit from β-irradiation treatment?
Small corneal lesions.
80
Why is SCC often more challenging to treat when it affects the periorbital region?
Periorbital SCC is less responsive to treatment than genital SCC.
81
What is the benefit of combination therapy over single-modality treatment for ocular SCC?
Combination therapy has a higher success rate.
82
What role does cyclooxygenase-2 (COX-2) overexpression play in SCC?
It is overexpressed in some SCC tissues and is targeted by drugs like piroxicam.
83
How effective is the combination of mitomycin C and surgical excision for treating ocular SCC?
It has a high cure rate.
84
What challenges are associated with the use of radiation implants in SCC treatment?
Hospitalization and special housing are required, along with specialized equipment.
85
In which anatomical locations other than the eye and genitalia can SCC develop in horses?
Nasal cavity, paranasal sinuses, pharynx, larynx, and hoof capsule.
86
What factors were found to influence survival in cases of ocular/adnexal SCC?
Tumor location and size.
87
How does the use of CO2 photoablation as adjunct therapy for SCC compare to mitomycin C?
They have similar cure rates according to retrospective studies.
88
What are some common sites where ulcerative SCC lesions may appear in horses?
Lid margins, cornea, sclera, or conjunctiva.
89
What is the reported nonrecurrence rate for β-irradiation in treating small corneal lesions?
89%
90
What is the 2-year local control rate for SCC treated with intralesional cisplatin?
89%
91
What was the success rate of topical 5-FU in treating SCC of the external genitalia
90%
92
What percentage of recurrence was reported with cryotherapy as an adjunctive treatment for SCC?
78%
93
What percentage of horses treated with radiation therapy had a nonrecurrence of ocular SCC?
75%
94
What percentage of horses treated with cryotherapy alone experienced nonrecurrence?
33.4%
95
What is the success rate of topical 5-FU treatment for small superficial SCC?
90%
96
What percentage of surgical excisions resulted in nonrecurrence for ocular SCC?
55.6%
97
What was the success rate for using radiation therapy on ocular SCC in a retrospective study?
75%
98
What percentage of horses showed tumor-free status after photodynamic therapy compared to cryotherapy?
Photodynamic therapy: 0% recurrence; Cryotherapy: 78% recurrence
99
Which percentage of horses with genital SCC responded better to intralesional cisplatin?
Greater success in genital SCC compared to periorbital SCC (no specific percentage mentioned)
100
How many horses were treated successfully with a combination of mitomycin C and CO2 photoablation?
82.4% with mitomycin C, 85.7% with CO2 photoablation
101
How long did piroxicam treatment prevent SCC recurrence in the reported case?
5 years
102
What percentage of all skin tumors in horses are melanomas?
4% to 15%.
103
Which type of horses is most commonly affected by melanoma?
Gray horses.
104
What is the primary cause of breed predisposition to melanoma in horses?
he incidence of the color gray within a breed.
105
What is believed to cause melanocytic tumors in gray horses?
Disturbance in melanin transfer from dermal melanocytes to follicular cells.
106
What percentage of Lipizzaner horses 16 years and older are free of melanoma?
Fewer than 6%.
107
What are the four types of equine melanomas?
Melanocytic nevi, dermal melanomas, dermal melanomatosis, and malignant melanomas.
108
Which type of equine melanoma has the highest risk of metastasis?
Dermal melanomatosis.
109
What histopathologic features characterize malignant melanomas in horses?
Invasive growth and poor prognosis for complete resolution.
110
In which anatomical locations do most equine melanomas occur?
Around the perineum and base of the tail, with less frequent occurrence on the head and other sites.
111
What is the typical prognosis for malignant melanoma in horses?
Poor, with a high recurrence rate.
112
What treatment is curative for most melanocytic nevi and dermal melanomas?
Surgical excision margins of >1cm
113
What benefit does CO2 laser excision provide for melanoma treatment?
It cauterizes the wound bed and controls hemorrhage.
114
How does cimetidine function in treating equine melanoma?
As a histamine receptor antagonist with antitumor activity.
115
Why might frequent dosing of cimetidine be important in melanoma treatment?
It may be the most critical factor in predicting clinical response.
116
What types of therapies are used for smaller equine melanoma nodules besides surgery?
Intralesional chemotherapy and cryotherapy.
117
What type of vaccine has shown promise in treating equine melanoma?
DNA vector vaccines encoding interleukin genes.
118
What cytokine has been used in successful intratumoral treatment for melanoma?
Human interleukin-12 (IL-12).
119
Which enzyme targeted by a canine vaccine might be useful in treating equine melanoma?
Tyrosinase.
120
What is the risk of progression in horses with melanoma as they age?
Increased risk of dermal melanomatosis and metastasis.
121
How common are external lipomas in horses compared to mesenteric lipomas?
External lipomas are relatively rare.
122
In which age group of horses are external lipomas principally found?
Young horses.
123
What are the typical sites where subcutaneous lipomas occur in horses?
Limbs, thorax, abdominal wall, and eyelids.
124
What organisms cause cutaneous habronemiasis in horses?
Habronema muscae, Habronema microstoma, and Draschia megastoma.
125
Which flies transmit the larvae of habronemiasis to horses?
House fly (Musca domestica) and stable fly (Stomoxys calcitrans).
126
In what percentage of cases are Arabian horses overrepresented in cutaneous habronemiasis?
This is not provided as a specific percentage but Arabian horses are overrepresented.
127
In which seasons does the highest incidence of cutaneous habronemiasis occur?
Late summer or early fall.
128
What percentage of horses with ophthalmic habronemiasis show epiphora and chemosis?
No specific percentage, but these are common symptoms.
129
Which horses are at greater risk for habronemiasis due to poor manure collection and fly populations?
Horses living in areas with increased fly populations and poor manure management.
130
What treatment kills migrating larvae in habronemiasis?
Systemic ivermectin.
131
How often does self-trauma occur after oral ivermectin treatment for habronemiasis?
Occasionally, due to an increase in pruritus.
132
What is a common adjunctive treatment to systemic ivermectin for large habronemiasis lesions?
Intralesional corticosteroid injection.
133
In how many cases do lesions resolve with the onset of cooler weather?
The exact percentage is not mentioned, but it is noted that this occurs frequently.
134
What is the recommended treatment for ophthalmic habronemiasis?
Oral ivermectin, topical corticosteroid eye drops, and débridement.
135
What organism causes pythiosis in horses?
Pythium insidiosum.
136
In which geographical regions is pythiosis most commonly found?
Warm, tropical regions, particularly in the southern United States.
137
During which seasons is pythiosis most commonly seen?
Late summer and early fall.
138
What percentage of pythiosis lesions contain "kunker"?
Not specified as a percentage, but kunker is commonly found in pythiosis lesions.
139
What are "kunker" made of in pythiosis lesions?
Necrotic vessels, inflammatory cells, and Pythium hyphae.
140
What percentage of untreated pythiosis infections invade deeper tissues?
No percentage given, but deeper invasion occurs in chronic, untreated cases.
141
What is the preferred treatment for pythiosis in horses?
Surgical excision.
142
How successful is surgical excision in resolving pythiosis lesions?
Success is possible, but recurrence is common without excision.
143
What is the maximum daily dosage of amphotericin B used in pythiosis treatment?
0.8 to 0.9 mg/kg.
144
How long is amphotericin B treatment continued for pythiosis?
Daily for 30 days, then every other day until cured.
145
What are common side effects of amphotericin B in horses?
Depression, anorexia, pyrexia, and urticaria.
146
What percentage of horses were cured of pythiosis using vaccination alone in one study?
53%.
147
What is the prognosis for pythiosis if surgical excision is impossible?
Poor.
148
Which antifungal agent is used in combination with terbinafine to improve treatment success for pythiosis?
Azole antifungals like itraconazole.
149
How should nephrotoxicity be monitored during amphotericin B treatment?
Monitor serum creatinine, urea nitrogen, hydration, water consumption, and urine output.
150
What percentage of horses experienced disseminated pythiosis even after treatment?
One horse in the study died, but no percentage is specified.
151
In which anatomical locations does pythiosis most commonly occur in horses?
Distal extremities and ventral body wall.
152
What percentage of success was seen when surgical cytoreduction was combined with vaccination within 2 weeks?
The exact percentage is not provided, but success rates improved.
153
What is the standard dosage of amphotericin B given intravenously for pythiosis treatment?
0.3 mg/kg diluted in 1 L of 5% dextrose, increasing every third day.
154
What other treatments are used if surgical excision is not possible in pythiosis cases?
Systemic, topical, and intralesional antifungals.
155
What is the primary reason for poor prognosis in untreated pythiosis?
Rapid lesion enlargement and potential invasion of deeper tissues.
156
What is a major risk factor for horses developing pythiosis?
Exposure to lakes, swamps, or flooded lands where zoospores are present.
157
Figure 28-4. Typical appearance of aural plaques in the pinna.
VetBooks
158
What size range do typical nodular necrobiosis lesions fall within?
0.5 to 1.0 cm in size.
159
What percentage of juvenile warts regress spontaneously?
The majority of cases (not quantified, but implied to be >50%).
160
For systemic corticosteroids used in treating nodular necrobiosis, what is the daily prednisolone dosage for the first 14 days?
1 mg/kg orally.
161
After the first 14 days of prednisolone treatment for nodular necrobiosis, what is the reduced dosage?
0.5 mg/kg orally for the following 14 days.
162
What percentage of horses showed resolution of aural plaques after using topical imiquimod 5% cream?
87.5%.
163
Over what duration can the topical imiquimod 5% cream therapy for aural plaques last?
1.5 to 8 months.
164
What dosage of triamcinolone acetonide is typically used for intralesional injection in nodular necrobiosis lesions?
3–5 mg per lesion.
165
What dosage of methylprednisolone acetate is typically used for intralesional injection in nodular necrobiosis lesions?
5–10 mg per lesion.
166
What is the average size of juvenile papillomas?
5 mm.
167
At what age are horses typically affected by juvenile papillomatosis?
6 months to 4 years of age.
168
What is the differential diagnosis list for nodular necrobiosis?
Equine amyloidosis, foreign body granuloma, dermoid cysts, habronemiasis, equine sarcoid, and other neoplasia.
169
What diagnostic method is required for confirming dentigerous cysts?
Surgical excision and histopathologic examination.
170
What type of cells are found in histopathologic findings of nodular necrobiosis?
Eosinophils, lymphocytes, and histiocytes.
171
What treatment is required for congenital papillomas in most cases?
None, as they typically regress spontaneously.
172
What surgical complication can occur from opening a dentigerous cyst during surgery?
Contamination of the incision site, infection, dehiscence, and scarring.
173
What percentage of vaccination success is reported when combined with surgical cytoreduction for pythiosis?
The success rate improves but is not quantified precisely.
174
What is the histopathologic hallmark of nodular necrobiosis?
Collagen degeneration.
175
What alternative treatments are suggested for juvenile papillomas aside from surgery?
Cryotherapy, intralesional chemotherapy, and radiofrequency hyperthermia.
176
What is the risk of recurrent dentigerous cysts if the cyst lining is not completely excised?
Recurrence is likely.
177
How large are typical lesions in nodular necrobiosis?
0.5-1.0 cm.
178
How often is dentigerous cyst removal successful without complications?
Success depends on careful excision without opening the cyst, but no percentage is given.
179
What proportion of horses with dentigerous cysts require preoperative imaging?
Ideally all horses undergoing surgery.
180
What role does trauma play in the development of nodular necrobiosis lesions?
It may be a contributing factor, especially at pressure points like under the saddle.
181
What size is a large ectopic tooth found in dentigerous cysts?
Varies from small teeth to large enamel-covered bone.
182
What immune compromise can lead to in papillomas?
Failure to regress.
183
What substance exacerbates aural plaques due to irritation?
Fly irritation.
184
How long can systemic corticosteroid treatment last for nodular necrobiosis?
At least 28 days (14 days at 1 mg/kg, then 14 days at 0.5 mg/kg).
185
What is the likely reason for the high incidence of nodular necrobiosis in certain horses?
Potential insect hypersensitivity or trauma.
186
What histopathological features are common in dentigerous cysts?
The presence of dental elements such as enamel, dentin, and cementum.
187
What is the percentage of spontaneous resolution in aural plaques treated with imiquimod 5% cream?
1.5 to 8 months.
188
In what region of the horse are nodular necrobiosis lesions most commonly found?
The withers and dorsum.
189
What clinical signs are associated with aural plaques?
Raised, white or tan smooth masses inside the pinnae.
190
What is the differential diagnosis of papillomatosis in horses?
Various viral-induced growths and papillomavirus infection.
191
What is the common size of lesions seen with juvenile papillomatosis?
About 5 mm.
192
How does fly irritation exacerbate aural plaques in horses?
It causes cracking and discomfort in affected horses.
193
What is the primary causative agent of papillomatosis in horses?
Equine papillomaviruses (EqPV).
194
Figure 28-5. Dentigerous cyst. (A) Identification of the sinus tract is made easier with a malleable probe inserted into the cloaca until it touches the dental material. (B) After closure of the sinus tract, the cyst is removed intact. The dental material may need to be loosened with an elevator or an osteotome to complete cyst removal.
195
FIGURE 10.9-1 Masses on the pinna of a 6-year-old Shire mare (white arrows). (A) Cranial view. (B) Dorsolateral view. Compatible with sarcoid
196
197
Blood supply to the external ear is provided primarily by th
rostral auricular artery (from the superficial temporal
artery) and the caudal auricular artery (Fig. 10.9-3) (from the external carotid artery). A rostral branch from
the occipital artery also contributes
198
Venous drainage from ear
rostral auricular vein to the superficial
temporal vein, and via the caudal auricular vein. The latter 2 veins drain to the maxillary vein
199
Lymphatic drainage from ear
Lymph from
the external ear drains primarily to the parotid lymph nodes. Afferents also flow to the lateral retropharyngeal,
superficial cervical, and cranial deep cervical lymph node centers
200
In case of facial nerve paralysis the ear can movE?
The fact that the cervicoauricularis superficialis
muscle is innervated by the great auricular nerve—not a
branch of the facial nerve—has clinical implications. This
means the ear may still exhibit some movement in cases of
facial nerve paralysis.
201
The inner and ouer surfaces of pinna may be blocked by injecting 2 nerves, name them
by blocking the internal auricular branch
and the great auricular nerve
202
Placement of needles for the great auricular nerve block (A) and internal auricular branch block (B) in a standing, unsedated horse.
203
Mucoid fluid draining from a sinus tract at the rostrolateral base of a horse’s right ear, characteristic of discharge from a dentigerous
cyst. There is crusty dried discharge coating the skin and hair around the tract opening.
204
Dentigerous cysts are congenital defects caused by a failure of
closure of the 1st branchial cleft during
embryonic development
205
What structures must be avoided when removing the dentigerous cyst?
Meticulous excision
of the mass and draining track is required to preserve the auricular muscles, rostral auricular artery, and
auriculopalpebral nerve. risk of injury to deeper structures in the area, including the parotid salivary gland, the base of the auricular cartilage, and associated vascular and nerve structures, is avoidable.
206
FIGURE 10.9-9 Oblique radiograph of the right ear base and associated skull region of a horse showing a discrete circular radio-opaque structure
(white arrow) consistent with the appearance of a dental body within a dentigerous cyst.
207
Innervation of innear ear
vestibulocochlear nerve (CN VIII) provides innervation to the inner ear
208
Vascularization of innear ear
labyrinthine artery (which has a variable origin off the basilar or caudal cerebellar artery) provides vestibular
and cochlear branches to the inner ear, entering via the internal acoustic meatus.
209
Venous drainage of inner ear
Labyrinthine veins return blood
to the basilar sinus. Lymphatic drainage of the inner ear is not well described for t
210
Which nerves would you block to check this eye suspected of SCC?
Sedate
zygomatic branch of the auriculopalpebral nerve (commonly referred to as the
“palpebral branch”) and the supraorbital nerve were locally anesthetized with 2% lidocaine to allow for a complete
ophthalmic examination. Additionally, the surrounding orbital bones and the eyelids were palpated for irregularities
and the globe was retropulsed to evaluate for any extension of disease into the retrobulbar space. Palpation and
retropulsion were normal
CT under GA
211
Common locations for ocular squamous cell
carcinoma i
include the eyelids, nictitating membrane
(3rd eyelid), and lateral limbus (corneoscleral junction).
