Therapy consists of sun protection, IPL or Q-switched alexandrite laser treatment [ 61 , 62 ]. The recent WHO classification of cutaneous vascular tumors differentiates between benign vascular tumors, intermediate vascular tumors, tumors of lymph vessels and tumors of perivascular cells.
However, 53 different cutaneous vascular tumors have been described in this classification [ 63 ]. Because the face and scalp are common locations, the nose is also often affected by vascular tumors of different origins. The most frequent are described below. Caucasians, females and premature infants with low birth weight show a higher prevalence [ 64 ].
In facial hemangiomas, A careful history and examination is the basis for the diagnosis of hemangiomas. Because the lesion is usually absent at birth, it proliferates starting from an erythematous macule or telangiectasia during the first days or weeks of life.
The growth phase, which can either be gradual or rapid, is usually six months long and is followed by a longer involution phase of months [ 67 , 68 ]. According to Waner et al. The diffuse lesions are more likely to be complicated by ulceration or airway obstruction and show a strikingly segmental distribution pattern compared with focal hemangiomas [ 66 ].
Ninety percent of all hemangiomas spontaneously involute prior to the age of Despite this high percentage of spontaneous self-healing, there are still a variety of situations where therapy is indicated. In nasal hemangiomas on the upper third of the nose, the periorbital area is often additionally affected, which can result in impairment of the field of sight.
In cases of intraorbital progression, bulbar deviation and amblyopia are dangerous side effects [ 70 ]. Nasal involvement can result in nasal deformity Cyrano nose deformity or the impairment of nasal breathing [ 71 ]. Therefore, treatment of hemangiomas of the nose should be started early to prevent possible complications. Infantile hemangioma. Well-circumscribed red, violet, exophytic vascular tumor on the nose of a one-year-old child.
Different therapies such as topical, systemic or intra-lesional applications of steroid, alpha 2a and 2b interferon injections, cytotoxic medications, angiogenesis inhibitors, embolization, cryosurgery, laser therapy and conventional surgery have all been described [ 72 , 73 ]. Imiquimod has also recently been described for the treatment of severe complicated hemangiomas. However, side effects and the small study size make further studies necessary in order to assess this therapeutic option [ 74 ].
Recently, Leaute-Labreze and colleagues have achieved impressive results by treating severe fetal hemangiomas of the face with systemic application of the beta-blocker propranolol [ 75 ]. Telangiectasias on the nose are extremely common vascular lesions consisting of dilated blood vessels with a linear appearance. They measure between 0. When they appear in abundance, telangiectasias on the nose can hint toward heavy liver illnesses or carcinoid syndrome.
Although very rare, there are also a group of hereditary telangiectatic syndromes that should be considered when telangiectasias appear in large numbers and during early childhood. These include Rothmund-Thomson syndrome, Bloom syndrome, Cockayne syndrome, ataxia-telangiectasia and hereditary hemorrhagic telangiectasia [ 79 — 85 ]. Former therapy options included needle diathermy occlusion and polidocanol sclerotherapy.
However, modern laser treatment has emerged as the first-line therapy for telangiectasias on the face. Spider nevi show a spider-like growth pattern with a pin head-sized central arterial vascular nodule and small vascular radiations in a starburst-like pattern Fig. When they appear in abundance, spider nevi can be a clinical sign of heavy liver illness or carcinoid syndrome.
The most frequent localization is the face and upper body. Under light compression with a glass spatula, arterial pulsations can be recognized in the center, fading toward the periphery. Nevus araneus spider nevus. In the center of the red lesion a small 1 mm red papule is visible, surrounded by several distinct radiating vessels. Pressure on the lesion causes it to disappear. Blanching is replaced by rapid refill from the central arteriole when pressure is released.
Osler-Weber-Rendu disease is an autosomal dominant disorder that induces the formation of multiple punctate telangiectasias and hemangiomas Fig. Accompanying epistaxis and mucocutaneous visceral arteriovenous malformations with melena are common.
The prevalence is per , Notably, estrogen therapy has been effective in severe cases of Osler-Weber-Rendu disease [ 89 ]. Electrocautery or argon beam ablation is described as a possible treatment option for cases of spontaneous recurrent epistaxis [ 90 ]. Hereditary hemorrhagic telangiectasia Osler-Weber-Rendu syndrome. Flat, star-shaped skin lesions mm in diameter on the entire face.
Some non-pulsating telangiectasias appear similar to araneus nevi. A papule the size of a match head is visible at the alar. Rosacea is a multiphasic inflammatory condition that typically affects the skin of the face and nose. Clinically, rosacea has been classified in four different stages. Stage I, also called rosacea erythematosa telangiectasia pre-rosacea , shows facial flushing and telangiectasia.
Stage II, rosacea papulopustulosa vascular rosacea , is characterized by persistent facial erythema, telangiectasia, thickened skin, papules and pustules Fig 9. Stage III, glandular-hypertrophic or inflammatory rosacea, shows erythematous papules and pustules, telangiectasias, edema, connective tissue and sebaceous gland hyperplasia.
Stage IV, or rhinophyma, shows dermal and sebaceous gland hyperplasia, and dilated and cystic sebaceous glands. Most individuals affected by rosacea are of northern European origin, and up to one-third have a family history of the disorder [ 91 ]. Clinical signs include facial flushing, erythema, telangiectasia and papulopustular efflorescence similar to acne as described previously.
Women are three times more likely to be affected than men, with the reported prevalence between 0. The pathophysiology has been poorly understood, and there have been only limited descriptions of factors that exacerbate or improve this disease [ 94 ]. Recent molecular studies suggest that an altered innate immune response is involved in the pathogenesis of vascular and inflammatory disease and is responsible for the observed clinical findings in patients with rosacea [ 95 ].
Erythema and telangiectasia are seen over the cheeks, nasolabial area and nose. Inflammatory papules and pustules can be observed over the nose. The absence of comedos is a helpful tool to distinguish rosacea from acne. A variety of topical, systemic and physical treatment options are available that have been adjusted to the stage and severity of the disease [ 96 ].
Standard topical therapy includes metronidazole 0. Systemic therapy with doxycycline, minocycline, clarithromycin, and moderately high doses of prednisolone or oral isotretinoin has also been described. Persistent erythema and telangiectasia might respond to pulsed dye laser PDL and intense pulsed light IPL treatments [ 98 ]. The main symptom is conjunctival injection, which is sometimes accompanied by chalazion or episcleritis.
Rosacea patients should therefore be seen by an ophthalmologist early in the disease course [ ]. First described by Wigley in , this condition is a chronic inflammation of the skin that generally occurs on the nose Fig. Clinically, round or oval brown-red macular and popular lesions with large follicular pores giving the lesion an orange peel-like appearance can be observed. Histologically, eosinophilia and patterns of leukocytoclastic vasculitis are characteristic. Therapy consists of dapsone p.
Dapsone therapy should be evaluated critically as the results are moderate, and the course of the disease is benign. Recently, the topical preparation of tacrolimus, a macrolide immunosuppressant, has been described as successful [ ]. In cases of resistance to conservative therapy, the surgical excision of solitary lesions, cryotherapy, dermabrasion or ablative laser therapy CO 2 , argon or erbium: YAG laser should be considered.
Facial eosinophilic granuloma. Red-brown nodule on the nose. Clearly visible follicular structures "peau d'orange". Sarcoidosis is a multisystem granulomatous inflammatory disease that can affect any organ. Cutaneous sarcoidosis is characterized by non-caseating granulomatas that consist of mononuclear phagocytes, epithelioid macrophages and multinucleate giant cells [ ].
The macronodular type involving the nose and cheek is called lupus pernio and was first described by Besnier in [ ]. The etiology of this disease is still unknown. Clinically, dark red, purple or violaceous plaques and nodules can be seen [Fig. The serum concentration of angiotensin-converting enzyme ACE is increased, and measurements have been used as an index of disease activity. Aside from topical and intra-lesional steroids, multiple forms of internal therapy immunosuppressants such as steroids, interleukin-2 inhibitors or anti-tumor necrosis factor alpha treatment have been described [ ].
Pulsed dye or CO 2 laser ablation is available for the debulking of granulomatous lesions; however, there are no evidence-based recommendations because of the limited number of patients treated [ ]. Cutaneous lesions of sarcoidosis lupus pernio.
Red-to-purple indurated plaques and nodules affecting the nose and cheeks. Located on the nose, face, scalp, forearms and back of the hand, this very common pre-malignant lesion consists of crusty, scaly patches of skin. Size ranges from 2 - 10 mm, and colors such as pink, red or the same degree of pigmentation as the surrounding skin are observed. Actinic keratoses are associated with UV light exposure and therefore accompanied by solar damage to the surrounding skin.
Patients are in or past middle age, very often with fair complexion. Histologically, five types can be distinguished: hypertrophic, atrophic, bowenoid, acantholytic and pigmented [ ]. Left untreated this lesion can potentially result in squamous cell carcinoma. In case of surgical excision, histologic examination should be performed to exclude squamous cell carcinoma. First described in by Hutchinson as a "crateriform ulcer of the face", keratoacanthoma is a fast-growing, epithelial tumor that develops from hair follicles or the surface epithelium of the skin.
It can occur solitarily frequent or with multiple lesions rare. The lesion consists of a firm, cone-shaped nodule cm in diameter with a central horn-filled crater. It shows rapid growth within weeks or months followed by spontaneous resolution over months in most cases. Histologically and clinically it often resembles SCC. Nevertheless, as SCC can masquerade as keratoacanthoma, surgical excision with an excision margin of mm is recommended [ ].
Because the histologic changes at the base of the lesion are important for histologic differentiation, a shave biopsy should be avoided and an excision of the lesion in its entirety should be performed [ ]. Immunocompromised patients and those with Muir-Torre syndrome the combined occurrence of at least one sebaceous skin tumor and one internal malignancy in the same patient show an increased incidence of keratoacanthoma [ , ].
The skin of the nose is a very common location for malignant tumors. UV-light exposure is a potent carcinogen of the skin, which results in frequent tumor involvement of the skin of the nose. In the following paragraph we present the most frequent malignant skin tumors of the nose.
Melanoma is the most devastating skin cancer with the highest increase in incidence in recent years, according to the World Health Organization WHO. It has been estimated that incidences of melanoma will double every years [ , ]. Melanoma originates from a malignant degenerated melanocyte, which is a highly aggressive tumor cell with poor rates of survival once it has metastasized.
Congenital melanocytic nevus. Brown papule on the nose, which developed shortly after birth. The brownish exophytic lesion is well circumscribed. Unfortunately, there are only a few studies dealing specifically with melanoma on the nose.
Jahn et al. In their group of 45 patients, they showed a female predisposition of In another study by Fisher et al. Forty-five percent of these cases were observed in female patients. Therapy involves surgical excision by cold steel, similar to the procedure performed for cutaneous melanomas at other locations on the body. However, according to the ADO's guideline, in special localizations such as the facial, acral or anogenital regions a reduction of these margins is possible on the condition that micrographic controlled surgery is performed.
However, current randomized trial evidence has recently shown to be insufficient in addressing optimal excision margins for primary cutaneous melanomas [ ]. Although the nose has a distinct concave and convex anatomy, pre-operative tumor thickness can be assessed by ultrasound of the skin, depending on the localization of the melanoma [ , ]. In cases of LMM, different techniques of 3D histology have been described. Some authors prefer the Tuebingen cake technique, whereas other authors prefer classic Mohs surgery [ — ].
Micrographic surgery according to the Tuebingen cake technique has been studied by Jahn and colleagues [ ]. It ideally utilizes a cylindrical piece of tissue where the base and the margin of the tumor are assessed separately Fig.
Micrographic surgery according to the Tuebingen cake technique. The base and the margin of the tumor are assessed separately. Breuninger Mohs surgery allows complete circumferential peripheral and deep margin assessment using frozen section histology. In classic Mohs surgery, the tissue is excised in a cone-shaped pattern with a very small surgical margin 1 to 1. Specimen preparation consists of cutting the specimen on the cryostat, placing sections on slides, followed by staining and evaluation by the Mohs surgeon Fig.
The special method of tissue processing and staining in Mohs surgery has been compared with peeling an orange, where the peel is the surgical margin that is removed and flattened out for further examination [ ]. Actually there are no equivalent data to compare both methods.
Mohs surgery allowing the complete circumferential peripheral and deep margin assessment, using frozen section histology. The authors report recurrence rates of 6. The prognoses with stage I and II melanoma of the nose were good, with a survival rate of Unfortunately, there were no data available for patients with stage III melanoma. To date all available studies on elective lymph node dissection ELND have failed to demonstrate a beneficial effect on patients with cutaneous melanoma of the trunk and extremities; therefore, there is limited evidence to support application of this technique in patients with melanoma of the nose [ , — ].
In contrast to the relatively good prognosis for stage I and II melanomas of the skin of the nose, melanoma with sinonasal involvement arising from the nasal cavity and paranasal sinuses is associated with generally poor survival rates [ ]. Because UV light associated with chronic sun exposure is the main risk factor, BCC commonly occurs on the face, with the nose being the most frequently affected location and the alae, dorsum and tip being the parts most frequently affected [ ].
Although it rarely metastasizes, untreated BCC can cause considerable disfigurement and is potentially life threatening when eroding vital structures. Five BCC subtypes with different clinical behavior can be distinguished: pigmented, cystic, superficial multicentric, morphea-like and nodular-ulcerative types with the last being the most common, Fig. Pigmented BCC can mimic melanoma upon clinical examination and usually occurs in sun-exposed areas [Fig.
Morphea-like BCC shows a lingular growth pattern and varies in size [Fig. BCC Nodular type. Red, waxy nodule on the tip of the nose. Visible telangiectasias over the surface. Pigmented BCC. Dark nodule resulting from melanin deposition at the alar of the nose. Small ulceration at the center.
A variety of different treatment options such as cryotherapy, photodynamic therapy, application of imiquimod or 5-fluourouracil, electrodessication and radiation therapy have been described. However, micrographic-controlled surgery is the gold standard with the lowest rate of recurrence 1. The nose, which is part of the so called H-zone of the face, shows the highest rate of recurrence compared with other localizations [ ]. Embryonic fusion planes such as the nasolabial fold or the medial canthus can be affected by large BCCs of the nose, possibly contributing to tumor recurrence.
It is related to chronic sun exposure and immunosuppression and rarely arises from normal-appearing skin. SCC typically develops on sun-damaged skin or actinic keratoses and less frequently on scars from burns [ , ].
In patients having undergone renal transplants and immunosuppression, the incidence has been 18 times greater than in healthy individuals [ ]. Clinically, SCC presents as an erythematous crusting, sometimes ulcerated, lesion with a red granular base. It shows a tendency to bleed with minimal trauma. The diagnosis and extent of the lesion sometimes necessitate multiple biopsies. When SCC arises in sun-damaged skin, a minority of patients develop metastases 0.
The likelihood of metastasis increases with tumors with a diameter of at least 15 mm and a Breslow tumor thickness vertical of at least 2 mm [ ]. Death occurs in three-quarters of patients with metastasis [ , ]. The parotid gland is the "metastatic basin" for cutaneous SCC of the head and neck because it drains via lymphatic vessels on the nose, cheek and forehead [ ].
In cases of parotid involvement, a parotidectomy with or without a simultaneous neck dissection is the procedure of choice. Micrographic-controlled surgery is the treatment of choice. Excision margins of 4 mm and 6 mm have been suggested for lesions less than and greater than 2 cm, respectively [ ]. Because there are no large randomized studies regarding excision margins for cutaneous SCCs, these are rough guidelines.
The surgeon's experience and judgment in planning surgical treatment is therefore significant for successful treatment [ ]. In cases where patients are unable to undergo surgery radiation, therapy has been described as successful with cure rates similar to those obtained with standard surgical excision. Although chemotherapy has not been effective, some studies report that epidermal growth factor receptor EGFR inhibitors might be useful adjuncts to surgical treatment [ , ].
KS was first described in by the Hungarian dermatologist Moritz Kaposi and is a carcinoma arising from the endothelial lining of lymphatic tissue [ ]. The histology is characteristic and shows an excessive proliferation of spindle cells, slit-like vascular spaces and extravasated erythrocytes. Principally, KS can arise anywhere on the skin or mucosa of the body, including internal organs. The lower extremities of the skin especially the soles of the feet and the head and neck are typically involved.
Masih et al. Fifteen of these patients also had oral-facial KS and 13 showed a prominent tip-of-the-nose KS lesion. The authors concluded that tip-of-the-nose KS lesions are commonly associated with pulmonary KS and should be noticed as a sentinel sign for pulmonary KS, suggesting that bronchoscopy should be considered for these patients. On clinical examination the vascular pattern results in a dark red to blue or violaceous appearance, as the vascular spaces within the lesions fill with blood.
The lesions are non-pruritic and appear as macular Fig. Four different types have been distinguished in the literature. The classic type mainly occurs in Mediterranean men male-to-female ratio of of years of age [ , ]. The endemic African type occurs in HIV-negative individuals and shows a tendency for lymph node involvement.
The immunocompromised type can occur in individuals just after organ transplantation [ , ]. Finally, the AIDS-related type is now the most commonly presented. It is the most common malignancy seen in HIV-infected patients [ , ].
Kaposi's sarcoma. Characteristic violaceous plaques on the alar and tip of the nose in an HIV-positive female patient. Concerning therapy, a variety of modalities have been described. Therapeutic options include systemic therapy in HIV-positive patients HAART , systemic chemotherapy with doxorubicin, conventional radiation therapy, electron beam radiation therapy EBRT , surgical excision, topical retinoids, cryotherapy, laser therapy and intra-lesional therapy with vincristin, vinblastin or bleomycin [ , ].
The most important skin diseases of the nose, which might require surgical consultation or laser therapy, have been described briefly in this review. In conclusion, the authors suggest that all disciplines that offer conservative or surgical treatment must be familiar with the special morphology and characteristics of skin diseases of the nose. In the case of complex lesions an interdisciplinary approach that combines dermatology, otolaryngology and surgery can provide optimal care for the patient.
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Clin Dermatol. Br J Dermatol. J Dermatol Surg Oncol. Grimalt R, Ferrando J, Mascaro JM: Premature familial sebaceous hyperplasia: successful response to oral isotretinoin in three patients. A prospective study. Kilty S, Brownrigg P: Surgical treatment of rhinophyma. J Otolaryngol Head Neck Surg. Being located just posterior to the frontal sinus, these supraorbital cells may be easily overlooked on the coronal plane; the axial and sagittal planes are far more accurate in the detection of these cells, which drain through an ostium located inferior and lateral to the frontal recess [ 5 ] Fig.
Concha bullosa , i. Both the variants may restrict the ostiomeatal complex, however no statistically significant correlation was found between the presence of these variants and any sinus disease [ 7 ]. Bulla frontalis is a group of variants basically indicating air cells located cranial to agger nasi cells and extending towards the frontal sinus: they can be isolated and protruding type III or not type I Fig.
The uncinate process itself may exhibit variants such as pneumatisation or medial bending of the tip. The most relevant variant of the uncinate process is hypoplasia, which results in occlusion of the ethmoid infundibulum; this is associated with hypoplasia of the maxillary sinus, and commonly also chronic maxillary inflammation [ 8 ] Fig. In the posterior compartment, the Onodi cell is by far the most dreaded variant for the surgeon; this is generally a rather huge posterior ethmoid cell, which expands on top or lateral to the sphenoid sinus.
If overlooked on a presurgical image, it can increase the hazard of middle cranial fossa penetration during endoscopic surgery Fig. Similarly, the risk of iatrogenic damage may be amplified by other variants such as dehiscences and protrusions Fig. Dehiscences are more crucial when seen at the level of the ethmoid roof and medial orbital wall; their classification as either of post-traumatic or of congenital origin is debated as the apparently congenital ones might also be the result of a neglected trauma [ 9 ].
Protrusions relate to bulging of the carotid canal, foramen rotundum, vidian canal, optic canal within an hyperpneumatised sphenoid sinus [ 10 ]. MSCT coronal a , b and sagittal reformations obtained on the right c and left d sides.
Bilateral agger nasi cells asterisks are visible on the coronal images, but sagittal reformations better display their relationships with the frontal recesses arrows. A type I bulla frontalis arrowhead in b can be seen on top of the left agger nasi cell. Inflammatory material with focal calcifications is retained within the right sphenoid sinus whose walls are densely sclerotic arrowheads in c : chronic inflammation, possibly a fungus ball see below.
Anterior a and posterior p infraorbital cells seen in two different patients; the former is strictly adjacent to the ethmoid infundibulum, the latter minimally displaces the orbital wall. The anterior one is also called a Haller cell. Coronal and sagittal MSCT reformations showing type I bulla frontalis bf , on top of an agger nasali cell asterisk , and its relationships with the frontal recess arrows , posteriorly.
Axial MSCT and coronal reconstructions of a patient suffering silent sinus syndrome. The left uncinate process u is hypoplastic and tightly attached to the medial orbital wall compare with the contralateral side , hindering maxillary sinus drainage. The sinus cavity is shrunk and the orbital floor is slightly depressed because of chronic hypopressure.
A huge Onodi cell extends above and lateral to the right sphenoid sinus arrowhead points to the sphenoethmoid recess , the arrow points to the protrusion of the optic canal within the air cell. Two focal bone dehiscences are seen along the medial orbital wall, through which a small amount of orbital fat tissue herniates. This condition increases the risks of endoscopic sinus surgery, particularly if extrinsic ocular muscles are entrapped in the bone gap.
The rationale for imaging of patients affected with chronic rhinosinusitis, simplified to the extreme, consists in demonstrating any impairment of mucus clearance through the aforementioned pathways, along with any anatomical variant that may either incite rhinosinusitis or raise the risks of endoscopic surgery.
Given its superb detail in depicting the thinnest bone structures, MSCT is the most suitable technique for the task [ 3 ]; the inherent contrast displayed on bone algorithm reconstructions among bone, air and soft tissues allows the radiation dose to be decreased to a minimum, thus allowing all information to be obtained with limited biological invasiveness.
MSCT reporting of the paranasal sinuses should be done in a centripetal fashion, thus moving from the centre, i. Both soft-tissue and bone changes should be reported. Five patterns of rhinosinusitis, namely the infundibular, sphenoethmoidal, ostiomeatal and sporadic patterns as well as nasal polyposis are described [ 11 , 12 ]. Sometimes several patterns are combined in the same patient.
Similarly, obstruction of the sphenoethmoid recess will impair the drainage of the posterior ethmoid and sphenoid sinus, producing what is referred to as a sphenoethmoid pattern Fig. The ostiomeatal pattern is a more complex one, reflecting the higher complexity of this anatomical subunit, which, when blocked, simultaneously impairs mucus drainage from the anterior ethmoid cells and the maxillary and frontal sinus Fig. Nasal polyposis is the most extensive pattern, and nearly always occurs bilaterally.
The mucosa investing the middle turbinate, the uncinate process and the ethmoid infundibulum are the most usual sites of origin of polyps. The hypertrophied, polypoid soft-tissue thickening tends to distort the adjacent bone structures and enlarge the ethmoid infundibulum, quite often invading the maxillary sinus. Such a growth pattern almost invariably produces ostiomeatal pattern rhinosinusitis; pansinusitis due to extension to the posterior ethmoid and thus impairment of the sphenoethmoid recess is similarly frequent Fig.
Sinusitis with infundibular pattern: the most proximal part of the ethmoid infundibulum asterisks is obstructed by thickened mucosa, the maxillary sinus is completely opacified by inflammatory material. Although large, the infraorbital cell ioc does not narrow the drainage pathway. Sinusitis with a sphenoethmoid pattern: the sphenoethmoid recess is obstructed by thickened mucosa asterisks , both the small left sphenoid sinus and the posterior ethmoid cells are opacified.
Note the basal lamella arrows clearly demarcating the anterior ethmoid from the inflamed posterior ethmoid cells. Secretions are also retained within the pneumatised vertical lamella of the middle turbinate arrowhead. Ostiomeatal complex pattern: the middle meatus asterisk and anterior ethmoid cells are occupied by tissue, the medial orbital wall appears slightly displaced arrows.
Mucus drainage from the ethmoid infundibulum and frontal recess is simultaneously hindered producing frontal and maxillary sinusitis io infraorbital cell. Nasal polyposis: diffuse bilateral thickening of the mucosa investing the middle meati, the middle turbinate, and the anterior and posterior ethmoid cells. The turbinates and ethmoid labyrinth are distorted and partially decalcified.
Retained secretion can be seen within the blocked maxillary and sphenoid sinuses. The sporadic pattern is a large box in which several different conditions are stored, such as isolated mucosal thickenings, retention cysts, antrochoanal polyp, silent sinus syndrome, odontogenic sinusitis and mucocele. Isolated mucosal thickenings are incidentally found in a large number of MSCT performed for non-sinonasal pathological conditions.
As a general rule, such mucosal thickening is unrelated to clinical symptoms, and when seen in the maxillary sinus and ethmoid cells, it does not need to be reported unless the mucosal thickness exceeds 4 mm and 2 mm, respectively. On the other hand, the mucosal lining of the frontal and sphenoid sinuses should not be visible on MSCT under normal conditions [ 13 ].
Retention cysts are submucosal pseudo- cystic lesions that may have serous fluid accumulation in the submucosa or may be of a mucous nature blockage of a submucosal mucus gland. They have little clinical relevance unless large enough to hinder mucus drainage Fig. A retention cyst, displaying typical smooth and convex borders, partially fills the maxillary sinus cavity. Antrochoanal polyp is a relatively easy diagnosis, based on the pattern of growth from the maxillary sinus to the nasal fossa and farther to the choana and nature cystic appearance of this generally isolated polypoid lesion.
Though much rarer, spheno- and ethmoidochoanal variants are also reported [ 14 , 15 ] Fig. Antrochoanal polyp: the polypoid lesion arises from the right maxillary sinus, and extends through an accessory ostium arrows into the nasal fossa, reaching posteriorly the nasopharynx through the choana. Silent sinus syndrome refers to an obstructed maxillary sinus, occupied by inflamed mucosa and secretions, which is shrunken with depression of the orbital floor causing exophthalmia.
It is called silent sinus syndrome when clinically there is no clue as to the maxillary sinus disease, only being discovered on an imaging study. Differentiation of this entity from a congenitally hypoplastic maxillary sinus may be difficult. Interestingly, antrochoanal polyp and silent sinus syndrome share the same pathophysiological mechanism, i.
In antrochoanal polyp, an increased intrasinusal pressure due to partial ostial obstruction with unidirectional flow of air through the ostium into the sinus is the trigger to force the expulsion of an intramural cyst through an accessory ostium [ 16 ]. In silent sinus syndrome, conversely, complete sinus blockage and progressive resorption of air within the cavity leads to a pressure drop, orbital floor depression and sinus contraction [ 8 ] Fig.
Odontogenic sinusitis Fig. Intrasinus dental filling material may cause fungal surinfection. The differential diagnosis between dentogenic sinusitis and fungal infection see below may be difficult on imaging studies. Odontogenic sinusitis. A large area of bone resorption is seen in the alveolar ridge, around the root of a molar tooth; the floor of the maxillary sinus is interrupted, the sinus filled by inflammatory material.
The small calcifications found along the ethmoid infundibulum and in the anterior ethmoid arrows were proven to be bone fragments, possibly transported by mucociliary clearance. Finally, chronic sinus drainage obstruction may end up in mucocele formation: a mucocele is an epithelium-lined mucus collection completely filling a sinus cavity; while the secretions accumulate, pressure within the cavity increases, inducing sinus expansion and bone remodelling.
Mucoceles Fig. The right middle turbinate is swollen by a sharply defined lesion exhibiting spontaneously high density on MSCT, and showing different fluid components on MRI. Absence of solid, enhancing areas confirms mucocele within a pneumatised middle turbinate.
Bone remodelling is a broad definition that encompasses the whole spectrum of alterations that may accompany the aforementioned mucosal changes in chronic rhinosinusitis and nasal polyposis. As described by Giacchi et al.
The prevalence of osteoclastic activity provokes bone resorption and demineralisation; this is mostly seen in thin bone structures subject to chronic pressure. Thinning and displacement of ethmoid septa or the medial wall, as well as truncation of the middle turbinate are, for example, frequent findings in nasal polyposis; similarly, the expanded sinus walls of mucoceles are often thinned if not totally demineralised.
On the other hand, osteoblastic activity manifests itself as thickening and sclerosis of bone osteitis [ 13 ], more typically encountered in thicker bone structures, such as the walls of the maxillary sinus and sphenoid sinus. As expected, all the described bone changes can be present simultaneously in the same patient, particularly if affected by nasal polyposis and fungal infections see below Fig. Demineralisation and distortion of thin bony laminae middle turbinates and ethmoid labyrinth and sclerosis of thicker bone structures sphenoid sinus are present simultaneously in a patient with diffuse nasal polyposis.
Some of the imaging patterns of chronic rhinosinusitis already described such as the ostiomeatal pattern and mucocele can also be encountered as indirect signs of the presence of a neoplasm—either benign or malignant. Furthermore, extensive nasal polyposis may completely obstruct sinonasal cavities, severely distorting the normal anatomy. Patients examined for rhinosinusitis undergo imaging applying a standard MSCT protocol, without contrast agent injection, and using bone algorithm reconstructions alone.
As a consequence, the major concern for radiologists particularly those not routinely involved in sinonasal imaging is how to safely rule out a neoplasm harboured amid inflammatory changes. Some landmarks may be of help: chronic rhinosinusitis and nasal polyposis are much more commonly bilateral. Whenever a ostiomeatal pattern is seen as unilateral disease, the presence of a neoplasm in the middle meatus should be considered, and endoscopic assessment of the region should be prompted.
Neoplastic lesions, even when benign, tend to behave more aggressively towards bone, causing more pronounced displacement, erosion and destruction [ 18 ]. In chronic rhinosinutis and nasal polyposis bone is remodelled, distorted, demineralised but, as a general rule, not fragmented. Mucocele is emblematic: frequently the line of demarcation between demineralised and normal bone is represented by a blunt but sharp border, whereas in neoplasms the border is ill-defined and spiculated.
Density measurements are not of great help, neither for the differentiation between tumour and polyp both are within the solid range of densities nor to discriminate tumour from mucocele which may exhibit high density if secretions are desiccated. In some cases, MRI may add information polyps are generally more T2 hyperintense than most malignant tumours; inverted papilloma, the most common benign nasosinusal tumour, may display the almost pathognomonic cerebriform pattern.
However, the bottom line is that in any unclear case an endoscopic examination should be performed, and a biopsy obtained Fig. The left ostiomeatal complex is occupied by solid tissue, the anterior ethmoid cells, the maxillary and frontal sinus are completely opacified.
The absence of inflammatory changes on the right side as well as the displacement and destruction of the anterior arrowheads s and the posterior arrows maxillary sinus wall suggests the presence of a neoplasm. Actually, MRI shows a mass arising from the maxillary sinus and protruding into the nasal fossa, histologically proven as ameloblastoma. Fungal infection is rather common, given the ubiquitous presence of fungal agents in the environment and the high frequency of colonisation of sinonasal mucosa [ 19 ]; the role of fungi in promoting chronic rhinosinusitis has been suggested.
Fungal infections may be classified as either non-invasive or invasive forms, according to the absence or presence of invasion of mucosa, submucosa, bone and vessels by hyphae [ 20 ]. Eosinophilic rhinosinusitis is also called allergic fungal rhinosinusitis. On MSCT, non-invasive fungal infection is suspected whenever spontaneously hyperdense material is detected within the sinus cavities.
In the case of a fungus ball, such hyperdensity is due to a high content of heavy metals in the hyphae, but small calcifications can also be seen. Maxillary fungal sinusitis may also be caused by the presence of intrasinusal dental filling material, which appears extremely hyperdense. In eosinophilic rhinosinusitis, besides fungal hyphae, the accumulation of dense eosinophilic mucin may account for the detection of sinus hyperdensities, which are scattered in multiple sinus cavities, uni- or bilaterally.
MRI can be misleading in both conditions, because heavy metal and calcium, on the one hand, and the tight packing of fungal material within sinuses, on the other hand, produce very hypointense signal which, particularly on T2 sequences, can be as low as the signal void of air Fig.
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Here we will examine the connection between eye and nose, the specific anatomy linking the two, and some of the ways this connection can. 1 Tumours of the frontal and sphenoid sinuses are rare.1 Despite the anatomical proximity of the nasopharynx to the sino- nasal cavities (behind the nasal. The complex regional anatomy of the nose and paranasal sinuses makes The mucosa investing the middle turbinate, the uncinate process and.