Vocal cord polyp (VCP) and vocal cord nodule (VCN) are fairly common benign reactive lesions, causally related to phonotrauma and vocal abuse [85, 175, 177, 181, 194, 308]. The distinction between a VCP and VCN is
probably only a matter of terminology, since both exhibit similar aetiology, pathogenesis , and to a certain degree, similar histologic characteristics.
A VCP is a pedunculated or sessile, mono- or mul-tilobulated lesion, measuring up to 10 mm in diameter, and located between the anterior and middle thirds of the vocal cord . Bilateral polyps are found in only 15% of cases . They affect primarily adults between 20 and 50 years of age, although they may also occur in other age groups. Men are affected at least twice as frequently as women [177, 181, 194].
Vocal chord nodules are smaller, often bilateral, sessile, fusiform swellings of the vocal cords, positioned symmetrically, and rarely exceed 2 mm in diameter. They usually occur in children, more frequently in boys with the peak between the ages of 5 and 10 years . In adults, the highest incidence of these lesions is in young to middle-aged women. VCNs are considered to be the most common benign lesions of the vocal cords [177, 386].
In addition to phonotrauma and vocal abuse, cigarette smoking, unfavourable occupational exposure, infections and endocrine dysfunction, are also considered to be possible aetiologic factors of VCPs [175, 177, 181, 194, 308]. VCNs are mainly caused by chronic misuse and overuse of the voice, as well as by emotional disturbances in children, and hormonal disorders and smoking in adults [4, 177, 308].
Damage of the subepithelial blood vessels is the initial event in the evolution of a VCP or VCN. However, the morphology of the two exudative lesions depends on the severity of the initial damage and repeated injuries [123, 138, 177, 181, 194, 308].
The gross appearance of a VCP varies from a glassy translucent gelatinous formation, to congested and purple red in teleangiectatic variants, and finally, to whitish, firm and opalescent in the predominant fibrous forms at the end stage of the lesions (Fig. 7.6a). VCNs start as a soft reddish swelling. Gradually, when the fibrous tissue proliferates, the VCNs become firmer, whitish in colour, and conical in shape.
Hoarseness is the predominant clinical symptom in both lesions. A great variety of voice changes, ranging from mild hoarseness to complete aphonia, is found, depending on the location and size of the lesions [21, 94, 177, 181, 352].
Histologically, different stages of VCP development are noted. Initially, the subepithelial stroma is diffusely oedematous with dilated vessels. After severe or repeated injuries, massive leakage of oedema, mainly fibrin as amorphous hyaline pink material, and erythro-cytes, are the predominant features in the vicinity of the angiectatic vessels, which may also be thrombotic (hyaline forms of the VCP). Evidently dilated vessels, haemorrhages with consequent haemosiderosis and conspicuous ingrowths of new blood vessels create the angiectatic or vascular stage of the VCP (Fig. 7.6b). Finally, the lesions may be transformed into a fibrous variant containing an increased amount of fibrous tissue and blood vessels. Not infrequently, mixed type VCPs are seen, composed of two or more different histologic patterns [21, 123, 177, 194, 308].
Rarely, scattered atypical stromal cells, not associated with increased mitotic activity, may be found within the core of the VCP. This finding must not incorrectly lead to a diagnosis of malignancy .
In the initial stage, VCNs show diffusely oedematous tissue with distended capillaries and venules and tiny perivascular haemorrhages surrounded by a minimal or moderate inflammatory reaction. In time, the loose connective stroma is replaced by a mild to moderate cellular fibrous tissue changing in varying stages of evolution.
As previously mentioned, the covering squamous epithelium in both lesions shows predominantly benign reactive changes. In 4 (0.8%) patients, potentially malignant changes (atypical hyperplasia) were noted in the covering epithelium, but there were no data on malignant alteration [177, 226].
The treatment of choice for VCPs is microlaryngo-scopic surgical removal. Childhood VCNs may disappear in puberty. Small incipient VCNs in adults may also vanish spontaneously or after voice rehabilitation. Surgical intervention is indicated when there is no improvement after conservative treatment.
Contact ulcer (CU), granuloma (CG) and intubation granuloma (IG) are benign, inflammatory, exophytic or ulcerative lesions, usually located in the posterior third of the glottic area. Aetiologically, the lesions arise in response to various mechanical and chemical injuries, such as voice abuse or protracted forceful coughing, acid regurgitation and intubation injuries. They display similar symptomatology and clinical appearance, and more or less identical histopathological features and prognosis [16, 28, 77, 177, 180, 374, 383, 384].
Excessive shouting or coughing cause repeated microtraumas of the thin mucosa of the vocal cord processes. They strike each other in phonatory adduction of the arytenoids, which leads to the development of ulcerative or exophytic lesions of one or both vocal cords . Additionally, acid regurgitation due to hiatal hernia or gastritis may cause the same type of lesions in the posterior glottic area.
Intubation granuloma is an undesired sequel of intubation tube pressure during anaesthesia or intensive care treatment.
Intubation granulomas are more common in females, while hyperacidic granulomas and CU/CGs are predominant in males [104, 177, 180, 383].
Clinically, ulceration or exophytic lesions can be found, mono- or multilobular, frequently bilateral, measuring up to 15 mm in diameter, that range from pale grey to dark red, sometimes with an ulcerated surface (Fig. 7.7a) . Hoarseness . the sensation of a foreign body. coughing, a sticking sensation, pain in the throat, and the feeling of acidity, are the prevailing symptoms in all three types of lesions.
Histologically, an ulceration of the posterior mucosa, covered by necrotic tissue and fibrin, is initially seen.
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