Dok ,hidung anak saya bauSTEP 11. Rinoscopi : pemeriksaan rongga hidung , anterior dari depan menggunakan spekulum hidung , posterior untuk melihat nasofaring .

2. Epitaksis : Merupakan perdarahan dari hidung yang banyak dijumpai pada anak dan usia lnjut , manifestasi dari penyakit lain Tipe anterior : berasal dari sinus dan mata dan perdarahan masuk ke saluran pencernaan sehingga keluhan muntah .Berasal dari plexus kiselbachTipe posterior : Lokal dan sistemik , lokal penyebab nya trauma KLL , benda asing , fraktur tulang hidung , Sistemik berasal dari demam berdarah , hipertensi , chikungunya , hemofili . Tipe anteriorTipe posterior

Plexus KiesselbachA.Ethmoidalis posterior

Gejala lebih ringanLebih berat

Dari trauma mengorek hidungLokal dan sistemik

Dapat berhenti sendiri perdarahannyaJarang bisa berhenti sendiri

Sumber: Buku ajar THT FK UI

3. Hidung bau pada satu sisi :Benda asing terjebak di daerah rongga hidung sehingga menimbulkan mekanisme peradangan sel sel radang berkumpul peradangan, sehingga didapatkan sekret mukoserous yang menyebabkan bau. Bau ditimbulkan dari sekret mukoserous yang berasal dari debris sel-sel peradangan dari mukosa rongga hidung karena adanya benda asing.

Benda asing yg menimbulkan peradangan menimbulkan sel radang yg hasilkan sekret yang menyebabkan hidung bau

Hidung bau (foeter et nose) yg baunya dlm skenario terjadi karena pembusukan biji jagung

Mekanisme peradangan karena benda asing transudasi awalnya sekretnya serous, jika menetap beberapa hari akan menjadi media yg baik sbg perkembangan bakteri sekret mukopurulen

Benda asing peradangan tetapi karena ada biji jagung tsb, sekret tersumbat sekret mukopurulen bauDiberi obat antipilek, bau hilang namun setelah obat dihentikan jd bau lagi

Benda asing luka rongga hidung luka, dijadikan untuk perkembangan bakteri dilawan oleh sel-sel pertahanan tubuh sekret bau dari bakteri dan sel-sel tubuh sendiri

Inflamasi pembengkakan mukosa hidung sekret tdk bisa keluar ulser, sekret tdk bisa keluar bau busuk

Biasanya ditemukan di anterior vestibulum / meatus inferior sepanjang dasar hidung

Benda asing jg bisa sebabkan epistaksis inflamasi pembengkakan pd hidung spina septum tajam terjadi pd spina itu sendiri maupun pd concha

Awalnya anak pilek, karena ada biji jagung, sekret tdk bisa keluar bercampur dengan sel-sel peradangan bau

Keluhan pilek, berawal karena sekret mukoserous tdk ada perlakuan ekstraksi sekret mukopurulen. Diberi obat pilek tdk sembuh karena tdk mengobati etiologinya

Bau karena sumbatan bisa dari benda asing, tumor partikel bau tdk mencapai daerah mukosa

Terapi: pasien nostrilnya ditekan, dgn mggunakan head lamp dilakukan ekstraksi tampon bisa dicampur dengan BIPP nasal packing jika tdk bisa, kontrol THT.

STEP 21. Anatomi dan fisiologi dari hidung ?

Fisiologi

Fungsi hidung adalah :1. Jalan napas2. alat pengatur kondisi udara (air conditioning)3. penyaring udara4. sebagai indra penghidu5. untuk resonansi suara6. turut membantu proses bicara7. refleks nasalSebagai Jalan Napas ;Inspirasi udara masuk melalui nares anterior naik ke atas setinggi konka media turun ke bawah (nasofaring) aliran udara berbentuk lengkungan atau arkus.Ekspirasi udara masuk melalui koana mengikuti jalan yang sama dengan inspirasi tetapi bagian depan aliran udara memecah sebagian melalui nares anterior da sebagian lain kembali ke belakang membentuk pusaran dan bergabung dengan aliran dari nasofaring.Pengatur Kondisi Udara ;Untuk mempersiapkan udara yang akan masuk ke alveolus paru.Cara: a. Mengatur kelembaban udara . fungsi ini dilakukan oleh palut lender(mucous blanket). Pada musim panas, udara hamper jenuh oleh uap air, penguapan dari lapisan ini sedikit, sedangkan pada musim dingin akan terjadi keadaan sebaliknya.b. Mengatur suhu. Karena banyak pembuluh darah di bawah epitel dan adanya permukaan konka dan septum yang luas, sehingga radiasi dapat berlangsung secara optimal. Dengan demikian suhu udara setelah melalui hidung kurang lebih 37 derajat celcius.Sebagai Penyaring dan Pelindung.Berguna untuk membersihkan udara inspirasi dari debu dan bakteri dan dilakukan oleh : a. rambut padavestibulum nasi, b.silia , c.palut lender (mucous blanket). Debu dan bakteri akan melekat pada palut lender dan partikel besar akan dikeluarkan oleh refleks bersin. Faktor lain : enzim yang dapat menghancurkan beberapa jenis bakteri, yang disebut lysozyme.Indra PenghiduYaitu dengan adanya mukosa olfaktorius pada atap rongga hidung, konka superior, dan sepertiga bagian atas septum. Partikel bau dapat mencapai daerah ini dengan cara difusi dengan palut lender atau bila menarik napas dengan kuat.Resonansi Suara.Penting untuk kualitas suara ketika berbicara dan menyanyi. Sumbatan hidungakan menyebabkan resonansi berkurang atauhilang, sehingga terdengar suara sengau.Proses BerbicaraHidung membantu pembentukan kata-kata. Kata dibentuk olh lida, bibir, dan palatum molle. Pada pembentukan konsonen nasal (m, n, ng) rongga mulut tertutup dan hidung terbuka, palatum mole turununtuk aliran udara.Refleks NasalContoh :iritasi mukosahidungmenyebabkan refleks bersin dan nafas terhenti. Rangsang bau tertentu menyebabkan sekresi kelenjar liur, lambung dan pancreas Buku Ajar Ilmu Kesehatan THT, FK UI

FisiologiCHAPTER 41Physiology of Olfaction Donald A.Leopold,Eric H.Holbrook The olfactory epithelium is a pseudostratified columnar neuroepithelium containing supporting cells, bipolar olfactory receptor neurons, and dividing basal cells located in the superior cleft between the middle and superior turbinates and the septum.

The axons extending from the receptor neurons coalesce into bundles (cranial nerve I) that travel through the cribriform plate to make primary synapses with the olfactory bulb.

As identified in rodents, an olfactory map exists in which individual odorant receptor types that are randomly distributed among zones within the olfactory mucosa converge to form synapses in specific glomeruli. This receptor map formation appears to extend to higher processing centers.

Multiple testing mechanisms for olfactory ability exist and are commercially available and accessible for all physicians. Testing allows for an assessment of extent of olfactory loss and measures change in ability over time.

The most common reasons for olfactory loss include chronic rhinosinusitis and polyps, upper respiratory infections, head trauma, and aging. Patient history is extremely important in determining etiology of olfactory disorders.

Patchy replacement of olfactory mucosa with respiratory epithelium appears to be common with aging. Alzheimer's disease is closely correlated with olfactory loss independent of aging.

Chronic rhinosinusitis can cause both a conductive loss of olfaction and a sensorineural loss. Nasal endoscopy is extremely useful in assessing obstruction of the olfactory cleft.

Computed tomography scans are helpful in assessing conductive losses and chronic rhinosinusitis. Magnetic resonance imaging can be helpful if there are neurologic signs suggesting mass lesion or neurodegenerative disease.

Available therapies for olfactory disorders continue to be limited. Patient support and counseling of hazards associated with the loss of smell are an important part of the patient visit.

The perception of odors adds a quality to life that is difficult to express. Odors are part of our everyday life, from the pleasures of perfume, to the satisfactions of toast and coffee, to the warnings of skunks and fire. As the molecules of substances are transported through the nose, the possibility of their being perceived occurs. The quality and intensity of that perception depend on the anatomic state of the nasal epithelium and the status of the peripheral and central nervous systems.This chapter explores the physiology of olfaction, noting pertinent research data. The initial discussion focuses on the pathways and obstacles that odorant molecules must negotiate as they come in contact with the olfactory receptor cells. A consideration of the neural processing of odorant stimulation and the pathways projecting to the brain gives some insight into the mechanisms underlying olfactory perception. Olfactory testing explores the assessment and method of this perception. The chapter ends with a section on clinical olfactory problems in humans and includes suggestions for their diagnosis and management.The study of olfaction poses many tantalizing questions. For example, do humans, like many animal species, communicate through odorant signals (pheromones)? Why are primary olfactory receptor cells able to regenerate entirely but other special sensory primary neurons are not? Can olfactory tissue be transplanted in humans as demonstrated in rodents? The study of olfaction has attracted the attention of researchers in the fields of endocrinology, anatomy, biochemistry, neurophysiology, and others. Through these efforts, the ability to diagnose and help individuals with chemosensory problems is improving.Anatomy of Olfactory Stimulation Nasal Passageways Experiencing an odor is a result of input from the olfactory, trigeminal, glossopharyngeal, and vagus nerves. Apparently, the properties of any given odorant determine the particular mix of these various inputs. Olfactory nerve (cranial nerve I) stimulation, which is necessary for identification of most odorants, depends on the odorant molecules reaching the olfactory mucosa at the top of the nasal cavity. Although molecules can reach the olfactory cleft by diffusion, essentially olfaction requires some type of nasal airflow, usually as part of inhalation (orthonasal flow). During eating, there is a retronasal flow of odorant molecules that stimulate the olfactory receptors at the top of the nose and contribute greatly to the flavor of the food.[1,2] This airflow can be very small, such as that generated by the mouth and pharyngeal motion.[3-5] Additional data from a large-scale model indicate that at physiologic airflow rates, approximately 50% of the total airflow passes through the middle meatus, with approximately 35% flowing through the inferior meatus (Fig. 41-1). About 15% flows through the olfactory region.[6]

Figure 41-1. Streamline patterns for resting inspiratory flow (250mL/sec) through an expanded (20? normal size) scale model of a healthy human adult male nasal cavity (sagittal view). Lines show the paths taken by small dust particles entering at the external nares.(From Scherer PW, Scherer PW, Hahn II, Mozell MM. The biophysics of nasal airflow. Otolaryngol Clin North Am. 1989;22:265.)

Mathematical models of the nose, created from digitized computed tomography (CT) anatomy slices and predicted mass transport functions, can predict odor intensity for varying amounts of olfactory epithelium, the character of the carrier gas, and the solubility of the odorant molecules.[7-9] These theoretical results show agreement with human and animal experimental data.The effect of a rapid change in flow velocity, such as with a sniff, on the in vivo airflow pattern remains unknown. Scherer and colleagues[6] have found in their large-scale model studies that the percentage and velocity of airflow to the olfactory region are similar for various steady-state airflow rates in the physiologic range. The fact remains, however, that sniffing is an almost universally performed maneuver when a person is presented with an olfactory stimulus. It is possible that its purpose is to momentarily increase the number of olfactory molecules in the olfactory cleft by means of a transient change in the airflow pattern of the nose. A sniff also may allow the trigeminal nerve to alert the central olfactory neurons that an odorant is coming. Sniffing duration, flow velocity, and volume are quite different among subjects but remain remarkably constant for any one subject.[10] Furthermore, Laing[11] has shown that different sniffing paradigms do not improve a subject's olfactory perception. The naturally chosen sniff seems to be optimal for that subject's nasal anatomy.For molecules to reach the olfactory area, they must pass through the tall but narrow nasal passageways. The epithelium lining the walls of these passageways is wet, has variable thickness, and is aerodynamically rough. Schneider and Wolf[12] have observed that olfactory ability is best when this epithelium is moderately congested, wet, and red, such as during an upper respiratory infection. Furthermore, olfactory ability seems to improve with narrowed nasal chambers,[13,14] but the changes in nasal patency that occur during the natural rhythmic engorgement and thinning of the nasal epithelium (nasal cycle)[15] do not have any effect on olfactory ability.[16-18]The sorption of molecules to these mucus-lined walls extracts some of them from the air stream and increases their travel time. This process could influence the spectrum of chemicals reaching the olfactory cleft or spread their arrival over time. Moncrieff[19] described this phenomenon in the variable times required for odorants to traverse the nasal passageways of sheep. The sorption of molecules may separate or sort the odorants before they reach the olfactory mucosa. Highly sorbable chemicals may have minimal or no odor simply because they sorb to the nasal walls before they reach the olfactory cleft, thereby accentuating the trigeminal component. Could it be that our world would smell different if we had no external nose to lengthen the path of the olfactory region? Does an animal with a long snout, such as the dog, smell the world differently as a result of these sorptive effects?Olfactory Mucus After the odorant molecules reach the olfactory region, they must interact with the mucus overlying the receptor cells. The mucus apparently comes from both Bowman's glands deep in the lamina propria (only of serous type in humans)[20,21] and the adjacent respiratory mucosa (goblet cells). Researchers have observed that the supporting (sustentacular) cells of the human olfactory epithelium are not histologically equipped to secrete mucus.[21-23] The supporting cells of most other species, however, do secrete mucus, often in response to odorants.[20,24-26]The partitioning of an odorant's molecules between the air phase and the mucus phase is most certainly another determinant of its being perceived. To reach the olfactory receptors, the odorant molecules must be soluble in the mucus but, as Laffort and associates[27] argue, not so strongly captured that they are unable to interact with the receptors. In addition, changes in the thickness or composition of the mucus can influence the diffusion time required for odorant molecules to reach the receptor sites.[28] Adrenergic, cholinergic, and peptidergic agents have caused these changes in the mucus overlying the olfactory receptors through their effects on the secretory activities of the mucosal glands. Moreover, these same agents have influenced the sensitivity of the olfactory receptor cells themselves.[29-31]Once in the olfactory mucus-epithelial system, the rate at which the odorant is cleared also is important. Hornung and Mozell[32] showed that 79% of a radioactively labeled odorant (butanol) remained trapped in the mucus 30 minutes after inspiratory exposure, whereas radioactively labeled octane cleared rapidly. The mucus may exert a differential role in deactivating, removing, or desorbing odorants from the olfactory area.Olfactory Epithelium Located 7cm inside the nasal cavity, the olfactory sensory neurons are protected in a 1-mm-wide crevice of the posterosuperior nose. At the epithelial surface, these bipolar neurons are exposed to the outside world through their dendrites and cilia. Proximally, axons of these same neurons synapse at the base of the brain (olfactory bulb). Although the olfactory receptor region is a solid sheet of olfactory mucosa housed in a protected environment in human fetuses and laboratory animals, a number of research groups have shown that there is mixing of olfactory and respiratory epithelial tissues in adult humans (Fig. 41-2).[22,33-36] The number of these clumps of respiratory epithelium, which are found in the olfactory area, increases with age, suggesting that a loss of primary olfactory neurons at least partially explains the decreased olfactory ability associated with aging.[37]

Figure 41-2. Low magnification of the surface of the nasal cavity taken from a transition region. Patches of respiratory (R) epithelium (dark areas) can be seen within the olfactory (O) region (?28).(From Morrison EE, Costanzo RM. Morphology of the human olfactory epithelium. J Comp Neurol. 1990;297:1,

The human olfactory epithelium covers an area of roughly 1cm2 on each side. The epithelium is pseudostratified columnar, and it rests on a vascular lamina propria with no submucosa (Fig. 41-3). In most mammals studied, four main cell types have been identified (Figs. 41-4 and 41-5): ciliated olfactory receptors, microvillar cells, supporting (sustentacular) cells, and basal cells.[22,23,35,38] Research that uses immunohistochemical staining of olfactory elements continues to provide information on growth, maturation, function of specific cellular elements, and similarities with other neural tissue.[39-45] One possible use for this technique may be to clarify the etiology of the patient's olfactory dysfunction and possibly offer a prognosis regarding improvement of olfactory ability.[18,46] Equally important to analysis of the epithelium is the evaluation of the olfactory axon bundles that travel within the lamina propria of the mucosa. Given that these bundles arise from receptor neurons distributed along a region of the epithelium, the identification of mature olfactory axons in comparison with the abundance of immature axons or collagen replacement within these bundles suggests a healthy functional olfactory mucosa. This may be a truer representation of the status of the epithelium as a whole than what can be deduced from analysis of the epithelial surface alone in a small biopsy specimen.[47]

Figure 41-3. Low-power three-dimensional scanning view of the olfactory epithelium and lamina propria. The olfactory epithelium (E) overlies a thick connective tissue lamina propria that contains olfactory axon fascicles (A x) and blood vessels (V) (?248).(From Morrison EE, Costanzo RM. Morphology of the human olfactory epithelium. J Comp Neurol. 1990;297:1.

Figure 41-4. Cross-sectional view of the olfactory epithelium showing the columnar supporting cells (S) that extend the full length of the epithelium. An olfactory neuron (O) with its dendrite and basal cell (B) can be seen among supporting cells (?1241).(From Morrison EE, Costanzo RM. Morphology of the human olfactory epithelium. J Comp Neurol. 1990;297:1.

Figure 41-5. Low-power magnification of fractured olfactory epithelium illustrating the axon-like processes (arrows) from microvillar cells (M), which extend basally between supporting cells (?3060).(From Morrison EE, Costanzo RM. Morphology of the human olfactory epithelium. J Comp Neurol. 1990;297:1.

The olfactory receptor neuron is bipolar and has a club-shaped peripheral knob that bears the cilia (Fig. 41-6). The surface of human olfactory epithelium is covered with cilia extending from the dendritic knobs of olfactory receptor neurons, but two electron microscopic studies show that there are no dynein arms on these cilia.[21,23] The researchers in these studies conclude from this observation that neither dynein arms nor motility is essential for human olfaction. After widening for the nucleus, the olfactory receptor neuron tapers to a long, thin, nonmyelinated axon that can travel several centimeters to the olfactory bulb. Bundles of these fibers form in the lamina propria and become surrounded as a group by the plasma membranes of the Schwann-type ensheathing cells, forming the olfactory nerve (cranial nerve I), which traverses the 15 to 20 foramina in the cribriform plate to synapse in the bulb. Allison and Warwick[48] estimate the rabbit to have approximately 50 million olfactory axons, whereas Jafek[21] estimates humans to have only 6 million bilaterally.

Figure 41-6. High-power magnification of an olfactory knob with long cilia gradually tapering as they extend over the epithelial surface. At the base of individual cilia, a necklace-like structure (arrow) can be seen on the surface of the olfactory knob (?14,220).(From Morrison EE, Costanzo RM. Morphology of the human olfactory epithelium. J Comp Neurol. 1990;297:1.

The olfactory ensheathing cells are unique in that they share characteristics that are common with Schwann cells and central glial cells. Because olfactory neurons have the ability to regenerate and make functional synapses with the olfactory bulb, there has been interest in the role of the ensheathing cells in this process and its possible therapeutic potential for repair of peripheral neuronal injury. The glial-type cells that ensheathe olfactory neurons support axonal growth of both olfactory and nonolfactory neurons.[49] Because of their ability to promote long-distance growth of regenerating axons in vivo and their ability to remyelinate axons of the adult mammalian spinal cord, these cells have received great interest as potential agents for reversing spinal cord injuries and demyelinating diseases.[50] Guntinas-Lichius and others[51] compared transplants of olfactory mucosa with buccal mucosa laid over a primary reanastomosis of the facial nerve in rats. Use of the olfactory mucosa resulted in better vibrissal movements, less branching of motor neurons, and greater accuracy of reinnervation.The microvillar cell occurs about one tenth as often as the ciliated olfactory neurons.[21,22] The cell body is flask-shaped, is located near the epithelial surface, and has an apical membrane containing microvilli that project into the mucus overlying the epithelium (see Fig. 41-5).[23,52] The deep end of the cell tapers to a thin, axon-like cytoplasmic projection that proceeds into the lamina propria. Although there is no electrophysiologic evidence that these cells respond to chemical stimuli, Rowley and others[38] have hypothesized that the cells are a morphologically distinct class of sensory receptors. The evidence for this hypothesis is the backfilling of a cytochemical tracer macromolecule (horseradish peroxidase) into the ciliated olfactory receptors and the microvillar cells when it is injected into the olfactory bulb.In among these two receptor-type cells are the supporting or sustentacular cells. These tall cells have an apical membrane that joins tightly with the surface of the receptor cells and the microvillar cells. They seem positioned to separate the receptor cells from each other; however, intimate apposition between receptor cells does occur.[21-23] Whether this proximity allows some receptor cells to influence each other's firing patterns is unknown. Sustentacular cells do not generate action potentials, nor are they electrically coupled to each other[53,54]; thus, they do not seem to contribute directly to the olfactory transduction process and the elicitation of generator potentials by odorant stimuli. However, they do appear to play a role in ion and water regulation[55] and, along with Bowman's gland duct cells, contain xenobiotic enzymes such as cytochrome P-450 that likely contribute to odorant metabolism.[56]Deep to all of these cells, the basal cells sit along the basal lamina. The basal cells are divided into two groups of replicating cells. The horizontal basal cells are just above the basal lamina, and the globose basal cells are positioned between the horizontal basal cells and immature neurons. The globose basal cells seem to be responsible for the continuous replacement of olfactory receptor neurons; however, during severe insult, they may repopulate the nonneuronal components of the epithelium as well.[57-60] This function identifies the globose basal cell as the bona fide stem cell located within the olfactory mucosa, but new evidence for the horizontal basal cell as the neural stem cell has also been presented.[61] The ongoing renewal of these special sensory neurons is not known to occur in other sensory systems. The replication cycle is between 3 and 7 weeks.[62,63] When the new receptor cell forms, it also projects its axon to the olfactory bulb, where it synapses with second-order neurons, thereby ensuring continual olfactory function and continual olfactory neuron replacement.Vomeronasal Organ Many mammals have an identifiable pit or groove in the anteroinferior part of the nasal septum that contains chemosensitive cells.[64] In most of these animals, a nerve can be identified connecting these cells to the central nervous system, often to an accessory olfactory bulb. In some situations, this system has been receptive to pheromones.[65] There have been investigations into the possibility that humans have some type of vomeronasal system.[66] Biopsy studies of the nasal mucosa in the small pit often seen along the anteroinferior nasal septum (Jacobson's organ) show olfactory-like histology but no central connection (Fig. 41-7). Electrophysiologic studies have shown negative action potentials from this vomeronasal area in response to specific chemical stimuli but without a subjective response from individuals tested.[67] These same stimuli did not cause negative potentials in the olfactory system. Similar electrical activity elicited by certain compounds directly delivered to the vomeronasal area has been shown to cause changes in blood pressure, heart rate, and hormonal levels.[68] Because no identified central brain connection seems to exist, and an accessory olfactory bulb seen in other mammals has never been identified in humans, it is possible that this system functions as a neuroendocrine system, emitting a substance in response to a specific chemical stimulus. Positron emission tomography (PET) scanning after presentation of a putative pheromone show detection of the compound executed in higher cortical regions different from those usually activated in the perception of odors, and in contrast to PET scanning results in the olfactory system, responses to the putative pheromone show gender differences.[69] V2R genes encoding for vomeronasal receptors have been found in mammals; however, in humans putative vomeronasal receptors are nonfunctioning pseudogenes.[70] It may be that human vomeronasal receptors are unrelated to olfaction and that other mammalian receptors have yet to be identified. Genetic, biochemical, and electrophysiologic data now suggest that some pheromone-based behaviors in vertebrates are mediated through the main olfactory epithelium.[71,72] At present, no good evidence for symptom-related importance of the human vomeronasal organ exists, but prudence suggests that this anatomic area should not be disturbed during surgery unless it is necessary.[73]

Figure 41-7. Photograph from the right nasal cavity demonstrating the vomeronasal organ pit in the right central part of the image; it is on the anterior septum. Note the inferior turbinate and floor of the nose to the left.

Olfactory Bulb The olfactory bulb lies at the base of the frontal cortex in the anterior fossa (Fig. 41-8). It serves as the first relay station in the olfactory pathway, where the primary olfactory neurons synapse with secondary neurons. These synapses and their postsynaptic partners form dense aggregates of neuropil called glomeruli. In humans, projections of mature olfactory axons into the bulb end in glomeruli as well, but misrouted projections commonly occur, usually into the external plexiform layer.[74] In the adult rabbit, approximately 26,000 olfactory axons enter each glomerulus, where they contact roughly 100 second-order neurons.[75] This relationship indicates a considerable convergence of information, because these neurons pass from the periphery onto this first central station. (The interconnections among the various glomeruli in one bulb, the interconnections between bulbs, and the afferent and efferent connections with the brain indicate that considerable processing also occurs at the bulb level.)

Figure 41-8. Structure of olfactory bulbs and their neural connections to one another, the olfactory mucosa, and the brain.

The neuronal projection of the olfactory mucosa onto the bulb displays some anatomic restrictions but is not strictly point-to-point. In other words, a given region of the bulb receives its most dense input from a particular region of the mucosa,[76] but inputs to a particular region of the bulb converge from many receptor cells distributed throughout a certain zone of the mucosa.[77] Conversely, a small focus in the epithelium projects widely, but within a restrictive region of the bulb.[78] These dense and diffuse inputs possibly represent excitatory and inhibitory influences, which, as in other sensory systems, narrow the neural stimulus representation as the processing moves centrally. Alternatively, the convergence and divergence of projections from neurons in the epithelium may serve to coalesce inputs from receptor cells of sensitivity to odorants. Evidence to support this notion emerges from the coherent activation of single glomeruli or sets of glomeruli by specified odorants.[79,80] Therefore, it is clear that the microcircuitry of the bulb is specialized to narrow the spatial pattern of the glomerular activation elicited by an odorant or mixture of odorants.In line with the regenerative capacity of the olfactory epithelium, there is a mechanism for neuronal replacement in the olfactory bulb. In mammals, the olfactory bulb is closely associated with dividing cells in the lateral ventricles that migrate via the rostral migratory stream (RMS) into the bulb and become mature neurons. In humans, the rostral migratory stream appears to be located around an extension of the lateral ventricle into the olfactory bulb, and at least some of the cells derived from the stream relocate to the periglomerular region.[81]Olfactory Connections in the Brain The more central olfactory connections include the olfactory tubercle, the prepiriform cortex, part of the amygdaloid nuclei, and the nucleus of the terminal stria, with further projections to a number of structures, including the hypothalamus. Although these structures receive olfactory input, they also serve other functions, such as food intake, temperature regulation, sleeping cycles, vision, memory, hearing, and taste. These connections may explain the strong memories and emotional context of various odors. It also is possible that these structures influence the olfactory process by efferent connections.[82,83]The organization of like olfactory receptors projecting into the olfactory bulb with the formation of an olfactory map (described later) appears to also occur to some degree in higher cortical areas. In mice, single odorants activate distinct patterns in the anterior piriform cortex. Exposure to different odorants results in different but overlapping maps of activity in the piriform cortex that are similar in individual mice. Odors that are related in structure also stimulate similar patterns of activity within the piriform cortex. These findings suggest an organization of axonal projection and stimulation in response to odorant stimulation within the cortex.[84]Common Chemical Sense Free nerve endings of three cranial nervestrigeminal (the most important), glossopharyngeal, and vagusprovide added chemoreceptivity in the mucosa of the respiratory tract.[85,86] The trigeminal nerves are sensitive to the burn of ammonia and the bite of hot pepper. In the nose, virtually all odorants stimulate olfactory and trigeminal nerves, even when no apparent pungency can be perceived. The peripheral anatomic pathways for these cranial nerves have long been known; however, the central connections that allow their interaction and how they interrelate with other senses are just beginning to be determined.[85,87,88] Cometto-Muniz and Cain[89] have shown that when tested with ammonia, the common chemical sense behaves more like a total-mass detector than a concentration detector (i.e., at a given concentration, the perceived magnitude increases with the time of presentation). It is even possible that the trigeminal nerve interprets pungent or chemically irritative stimuli as being painful or nociceptive in nature.

2. Kenapa sudah berobat ke dokter obat habis , hidung berbau lagi ?masuknya benda asing dalam rongga hidung kemudian terjadi pemadatan, peradangan akut atau kronis, obstruksi terjadi akibat terhalangnya dan stagnasi mukus, serta pengendapan garam-garam mineral. Sekret hidung menjadi bau karena memiliki kandungan kalsium dan / atau magnesium yang tinggi. Sekresi tersebut harus terpapar dengan aliran udara dalam hidung untuk memusatkan pus dan mukus yang menyebabkan terbentuknya endapan garam-garam mineral. Perkembangan dan progresifitasnya terjadi bertahun-tahun.Pada umumnya rinolit terdiri dari 90% bahan anorganik, dengan sisa 10% yang terbuat dari bahan organik dimasukkan ke dalam lesi dari sekret hidung. Garam-garam yang tidak larut dalam sekret hidung membentuk suatu kalsifikasi sebesar benda asing atau bekuan darah yang tertahan lama. Sekret pada sinusitis kronik dapat mengawali terbentuknya massa kalsifikasi dalam rongga hidung. Rinolit ini terutama terbuat dari fosfat dan kalsium karbonat. Kadang-kadang juga dibentuk oleh magnesium fosfat, natrium klorida dan magnesium karbonat. Garam ini juga dapat berasal dari sekresi mukosa hidung, air mata, dan eksudat inflamasi

3. Bagaimana mekanisme hidung sebagai organ pembau ?4. Mengapa anak nya mengalami epitaksis ?TraumaEpistaksis dapat terjadi setelah trauma ringan, misalnya waktu mengeluarkan ingus dengan kuat, bersin, mengorek hidung atau sebagai akibat trauma yang hebat, seperti terpukul, jatuh dan sebagainya. Selain dari itu iritasi oleh gas yang merangsang, benda asing di hidung dan trauma pembedahan, dapat juga menyebabkan epistaksis.Buku Ajar Ilmu Kesehatan THT, FK UI

CHAPTER 45Epistaxis Daniel B.Simmen,Nick S.Jones Epistaxis is the most common otolaryngologic emergency.

The most common etiology of epistaxis is idiopathic, followed by primary neoplasms and traumatic or iatrogenic causes.

The management ranges from resuscitation, through visualization, and cautery, nasal packing, and surgery (either endoscopic or external), to embolization.

Terminal branches of the external and internal carotid arteries supply the mucosa of the nasal cavity, with frequent anastomosis between these systems.

Various anastomoses on the ipsilateral side between the internal and external carotid systems exist as well as crossover to the contralateral side.

The philosophy of management for epistaxis is: (1) establish the site of bleeding, (2) stop the bleeding, and (3) treat the cause.

The majority of posterior idiopathic bleeds are from the septum, usually from the septal branch of the sphenopalatine artery.

Endoscopic bipolar diathermy treats most cases of epistaxis.

If a bleeding point cannot be found, ideally the nose is packed with an absorbable hemostatic agent that produces minimal mucosal trauma.

Endoscopic sphenopalatine artery ligation (ESPAL) has replaced the need for posterior nasal packs, other than in an emergency situation to control profuse bleeding.

The branching pattern of the sphenopalatine artery is complexmost commonly there are two or three branches medial to the crista ethmoidalis, sometimes even more.

Persistent posterior epistaxis can be controlled by percutaneous embolization of bleeding arteries.

Epistaxis is the commonest otolaryngologic emergency, affecting up to 60% of the population in their lifetimes, with 6% of cases requiring medical attention.[1] It has been estimated that nosebleeds affect 108 per 100,000 population per year.[2] In England and Wales an average of 10.2 per 100,000 patients with nosebleed are admitted, for an average stay of 2.9 days, in a 3-month period[3]; and in the United States 17 per 100,000 or 6% of patients with nosebleed are admitted.[4] There are peaks in incidence for patients both younger than 10 years old and older than 40 years.[4-6] The etiology of epistaxis in the majority of patients is idiopathic,[7] followed in frequency by primary neoplasms and traumatic or iatrogenic causes.Decisions about the optimum therapeutic intervention and timing are often made on an ad hoc basis, and most units do not have a protocol (systematic algorithm) for the management of epistaxis,[8] despite a 2005 published protocol aimed at junior doctors.[9] However, this protocol does not contain the timing of surgical intervention. The management of a patient with epistaxis ranges from resuscitation, through direct visualization and cautery, nasal packing, and surgery (both endoscopic and external) to embolization.Vascular Anatomy The nasal cavity is extremely vascular. Terminal branches of the external and internal carotid arteries supply the mucosa of the nasal cavity with frequent anastomoses between these systems (Fig. 45-1). The anterior nasal septum is the site of a plexus of vessels called Little's or Kiesselbach's area, which is supplied by both systems.

Figure 45-1. Latex-injected human skull showing the functional vascular anatomy of the nasal mucosainternal and external artery supplies with rich anastomoses in between and also crossover anastomoses.(Courtesy of the Institute of Anatomy, University of Z?rich, Switzerland.)

The terminal branches of the external carotid artery that supply the nasal cavity are the facial artery and the internal maxillary artery. The facial artery supplies the superior labial artery, which enters the nose and supplies the anterior nasal septum. The internal maxillary artery courses within the pterygopalatine fossa and terminates in the sphenopalatine, descending palatine, pharyngeal, infraorbital, and posterior superior alveolar arteries. The branching of the sphenopalatine artery when it enters the nasal cavity is a key point in the understanding of the management of posterior nosebleeds. The sphenopalatine artery enters the nasal cavity through the sphenopalatine foramen and then divides into conchal (posterior-lateral) and septal (posterior-medial) branches.[10,11] The descending palatine artery courses through the greater palatine canal and becomes the greater palatine artery, entering the nose through the incisive foramen, where it supplies the anterior inferior septum and anastomoses with medial branches of the sphenopalatine artery. Importantly, the vidian artery has a significant anastomosis between the internal carotid artery and a branch of the sphenopalatine artery and therefore with the external carotid system (Fig. 45-2).

Figure 45-2. Endoscopic view of an anatomic, injected specimen showing the vidian artery along the floor of the right sphenoid with the ball probe anastomosing the internal carotid (asterisk) with the sphenopalatine artery system (plus sign).

The internal carotid artery supplies the nasal mucosa via the ethmoidal branches of the ophthalmic artery. The ophthalmic artery is the first branch of the internal carotid artery. The posterior ethmoidal artery passes through the posterior ethmoidal canal into the anterior cranial fossa and divides into lateral and medial branches, supplying the superior part of the posterior septum and lateral nasal wall. The anterior ethmoidal artery enters the nasal cavity through the anterior ethmoidal canal and passes anteromedially to the area of the anterior skull base (Fig. 45-3). Where it crosses the anterior ethmoid roof to reach the fovea ethmoidalis and cribriform plate, a nasal branch supplies the anterior superior part of the septum (Fig. 45-4) and its other branchthe anterior meningeal arteryenters intracranially.

Figure 45-3. Internal and external artery supply with rich anastomoses in between and also crossover anastomoses: lateral nasal wall (A), external nose (B), and septum (C).(Adapted from Zuckerkandl: Anatomie der Nasenh?hle, Taf. XIII, 1892.)

Figure 45-4. Endoscopic view of the left skull base in a injected specimen, showing the course of the anterior ethmoid artery. A, Z?rich microscissors dividing the artery close to the orbit. B, Endoscopic view to the left skull base area after a median drainage procedure, showing the anterior nasal branch coming off the ethmoidal artery and the first olfactory fiber just behind (arrows).

A fundamental aspect of the understanding of the vascular anatomy and its importance to epistaxis is the fact that various anastomoses on the ipsilateral side between the internal and external carotid systems exist as well as crossover to the contralateral side. The rich anastomoses underlie the importance of a strategy to address the most distal site of any bleeding (Figure 45-5).

Figure 45-5. Endoscopic view (A) and computed tomography scan (B) of a cavernous hemangioma arising from the olfactory cleft on the right side that has caused a severe epistaxis.

The maxillary sinus ostium serves as the dividing line between anterior and posterior epistaxis. Anterior bleeding is usually easier to access and is therefore less dangerous. Posterior epistaxis is more difficult to treat because visualization is more difficult and blood is often swallowed, making it more difficult to gauge the amount of blood loss.The term posterior bleeding is all too often used incorrectly to label bleeding that cannot be visualized with a head lamp. It transpires in many cases that endoscopic examination shows the bleeding to be located high on the septum.

5. Mengapa dokter melakukan pemeriksaan rinoscopi anterior pada hidung pasien dengan menggunakan lampu kepala dan spekulum hidung ?

6. Bagaimana mekanisme pertahanan di dalam hidung ?7. Mengapa ditemukan konka hiperemis? Pilek : Adanya sumbatan diakibatkan adanya benda asing yang masuk ke cavitas nasi ( ada kelenjar dan serosa ) jika ada sumbatan mukus yang lairan normal akan terhambat stagnansi mukus akan mengendap obstuksi dan sekret hidung ( kandungan magnesium dan kalsium yang tinggi ) akan menyebabkan bau yang tidak enak.

Juga disekret terdapat carbonat, fosfat, dan berakumulasi dan menepempel ke flora normal patogen

Jika benda asing masuk jika dianterior masih mudah dikeluarkan namun jika sudah masuk ke dalam lebih sulit dikeluarkn akan menyebabkan gangguan mukosa bengkak nekrosis ulserasi erosi mukosa epistaksisAdanya partikel sumbatan mengeluarkan sekret bercampur dengan benda asing dan bercampur dengan produk bau

Rinolit ( bendabenda eksogen ) terjadi inflmasi abnormalitas di cavum nasal menghambat aliran udara udem venul-venul menjadi rapuh epistaksisRinolit ( muatan muatan garam yang akan membentuk rinolit )

Benda asing hidung ada mukosa dan epitel yang perang epitel terjadi reaksi imun jika alergi terjadi hipersensitivitas tipe I dan IV ( tipe I = IgE bekerja kontak dengan alergen akan ditangkap oleh APC APC akan menghantarkan ke MHC di persentasikan oleh ThO akan memanggil Th2 ( mengahasikan sitokin iL13 , il4, il5 akan mengikat limfosit B aktif menghasilkan IgE, IgE masuk jaringan, diikat oleh IgE reseptor yang berada pada sel mastoid atau basofil sel akan aktif sitokin) histamin gatal hipersekresi mukus.Mediator yang menyebabkan keluarnya ingus sendiriTerjadi vasodiltasi mukosa edem hidung tersumbat ingus jadi kental ( diakibatkan sel-sel darah yang berakumulasi )

8. Bagaimana penatalaksanaan dari skenario?

9. DD Benda asing di hidung tersering ditemukan di antara septum dan bagian bawah konka nasalis inferior, dapat dilihat pada gambar di bawah.6

Gambar 2. Predileksi benda asing di hidung

2.2. DefinisiBenda asing di hidung adalah benda yang berasal dari luar atau dalam tubuh yang dalam keadaan normal tidak ada pada hidung.7

2.3. EpidemiologiKasus benda asing di hidung paling sering terjadi pada anak, terutama pada usia 1 - 4 tahun. Pada usia ini anak cenderung mengeksplorasi tubuhnya, terutama daerah yang berlubang, termasuk hidung. Mereka dapat pula memasukkan benda asing sebagai upaya mengeluarkan sekret atau benda asing yang sebelumnya ada di hidung, atau untuk mengurangi rasa gatal atau perih akibat iritasi yang sebelumnya sudah terjadi. Benda asing yang tersering ditemukan yaitu sisa makanan, permen, manik-manik dan kertas. Benda asing seperti plastik dapat pula bertahan lama karena sukar didiagnosis akibat sifatnya yang noniritatif dan radiolusen sehingga tidak tampak dari pemeriksaan radiologik.3,4,5Benda asing, meskipun tampak sebagai masalah yang tidak serius, juga dapat menimbulkan morbiditas bahkan mortalitas bila masuk ke saluran nafas bawah. Pada usia dibawah 1 tahun, aspirasi benda asing merupakan penyebab utama kematian.3

2.4. Faktor PredisposisiFaktor yang mempermudah terjadinya aspirasi benda asing di hidung antara lain faktor personal (umur, jenis kelamin, pekerjaan, kondisi sosial dan tempat tinggal), kegagalan mekanisme proteksi normal (keadaan tidur, kesadaran menurun, alkoholisme dan epilepsi), ukuran, bentuk serta sifat benda asing serta faktor kecerobohan.32.5.Klasifikasi Benda AsingBerdasarkan asalnya, benda asing digolongkan menjadi dua golongan :1. Benda asing eksogen, yaitu yang berasal dari luar tubuh, biasanya masuk melalui hidung atau mulut. Benda asing eksogen terdiri dari benda padat, cair atau gas. Benda asing eksogen padat terdiri dari zat organik seperti kacang-kacangan (yang berasal dari tumbuhan-tumbuhan), tulang (yang berasal dari kerangka binatang) dan zat anorganik seperti paku, jarum, peniti, batu, kapur barus (naftalen) dan lain-lain. Benda asing eksogen cair dibagi dalam benda cair yang bersifat iritatif, seperti zat kimia, dan benda cair noniritatif, yaitu cairan dengan pH 7,4. 2. Benda asing endogen, yaitu yang berasal dari dalam tubuh. Benda asing endogen dapat berupa sekret kental, darah atau bekuan darah, nanah, krusta, perkijuan, membran difteri. Cairan amnion, mekonium dapat masuk ke dalam saluran napas bayi pada saat proses persalinan.3Berdasarkan konsistensinya benda asing dapat juga digolongkan menjadi benda asing yang lunak seperti kertas, kain, penghapus, sayuran, dan yang keras seperti kancing baju, manik-manik, baterai dan lain-lain.3Pembagian yang lain yaitu :1. Benda asing hidup, yang pernah ditemukan yaitu larva lalat, lintah, dan cacing.a. Larva lalatBeberapa kasus miasis hidung yang pernah ditemukan di hidung manusia dan hewan di Indonesia disebabkan oleh larva lalat dari spesies Chryssomya bezziana.Chrysomya bezziana adalah serangga yang termasuk dalam famili Calliphoridae, ordo diptera, subordo Cyclorrapha, kelas Insecta. Lalat dewasa berukuran sedang berwarna biru atau biru kehijauan dan berukuran 8-10 mm, bergaris gelap pada toraks dan pada abdomen bergaris melintang. Larva mempunyai kait-kait di bagian mulutnya berwarna coklat tua atau coklat orange. Lalat dewasa meletakkan telurnya pada jaringan hidup dan hewan berdarah panas yang hidup liar dan juga pada manusia misalnya pada luka, lubang-lubang pada tubuh seperti mata, telinga, hidung, mulut dan traktus urogenital.3,8b. LintahLintah (Hirudinaria javanica) merupakan spesies dari kelas hirudinae. Hirudineaadalahkelasdari anggotahewan tak bertulang belakangyang termasuk dalamfilumannelida. Anggota jenis cacing ini tidak mempunyai rambut, parapodia, dan seta.Tempat hidup hewan ini ada yang berada di air tawar, air laut, dan di darat. Lintah merupakan hewan pengisap darah. Pada tubuhnya terdapat alat pengisap di kedua ujungnya yang digunakan untuk menempel pada tubuh inangnya. Pada saat mengisap, lintah ini mengeluarkan zat penghilang rasa sakit dan mengeluarkan zat anti pembekuan darah sehingga darah korban tidak akan membeku. Setelah kenyang mengisap darah, lintah itu akan menjatuhkan dirinya ke dalam air. Bentuk tubuh lintah ini pipih, bersegmen, mempunyai warna kecokelatan, dan bersifat hemaprodit.9

Gambar 3. Lintah hidup di hidung c. CacingAscaris lumbricoides merupakan nematoda usus yang masih menjadi masalah di negara berkembang seperti Indonesia. Hidung dapat menjadi Port dentry atau tempat cacing tersebut bermigrasi dari usus untuk mendapatkan oksigen yang lebih banyak.102. Benda asing mati, yang tersering yaitu manik-manik, baterai logam, kancing baju. Kapur barus merupakan kasus yang jarang namun mengandung naftalen yang bersifat sangat mengiritasi. Kasus baterai logam di hidung juga harus diperlakukan sebagai kasus gawat darurat yang harus dikeluarkan segera, karena kandungan zat kimianya yang dapat bereaksi terhadap mukosa hidung.3

Gambar 4. Manik-manik di bawah konka inferior2.6. PatofisiologiBenda asing hidung lebih sering terjadi pada anak-anak, karena anak yang berumur 2-4 tahun cenderung memasukkan benda-benda yang ditemukan dan dapat dijangkaunya ke dalam lubang hidung, mulut atau dimasukkan oleh anak lain.3 Benda yang dimasukkan ke dalam hidung anak biasanya benda yang lembut. Benda tersebut masuk ke hidung saat anak mencoba untuk mencium sesuatu. Anak sering menaruh benda ke dalam hidung karena perasaan bosan, ingin tahu atau meniru anak lain.11Benda asing hidung dapat ditemukan di setiap bagian rongga hidung, sebagian besar ditemukan di dasar hidung tepat dibawah konka inferior. Lokasi lainnya ada di depan dari konka media. Benda-benda kecil yang masuk kebagian anterior rongga hidung dapat dengan mudah dikeluarkan dari hidung. Benda asing yang berada di rongga hidung dalam waktu yang cukup lama serta benda hidup dapat menimbulkan berbagai kesulitan dalam mengeluarkan benda asing.12

Gambar 5. Lokasi benda asing yang masuk ke rongga hidung (IT= inferior turbinate, MT= middle turbinate, SS= sphenoid sinus, ST= superior turbinate).

Benda asing yang masuk ke rongga postnasal dapat teraspirasi dan terdorong ke belakang saat usaha pengeluaran sehingga menimbulkan obstruksi jalan nafas akut. Benda asing di hidung juga berpengaruh dalam membawa organisme penyebab penyakit difteri dan penyakit infeksi lainnya. Oleh karena itu, benda asing hidung dapat menyebabkan masalah yang nyata dan jangan dianggap remeh.12Beberapa benda asing yang masuk kedalam rongga hidung dapat bertahan bertahun-tahun tanpa adanya perubahan mukosa, namun sebagian besar benda mati yang masuk ke hidung dapat menimbulkan pembengkakan mukosa hidung dengan kemungkinan menjadi nekrosis, ulserasi, erosi mukosa, dan epistaksis. Tertahannya sekresi mukus, benda asing yang membusuk serta ulserasi dapat menyebabkan sekret berbau busuk.12Sebuah benda asing dapat menjadi inti peradangan yang nyata bila terbenam di jaringan granulasi dengan menerima lapisan kalsium, magnesium fosfat dan karbonat yang demikian akan menjadi sebuah rhinolith.12 Terkadang proses ini dapat terjadi di area mukopus bahkan bekuan darah yang sering disebut nidus. Rhinolith endogen yang terbentuk dari inti darah atau mukus jarang terjadi pasa usia dibawah 4 tahun, sedangkan rhinolith eksogen yang terbentuk dari benda asing yang diselimuti oleh garam dapat terjadi pada usia berapapun.11 Rhinolith umumnya terletak di dasar hidung bersifat radioopak, single, sferis ireguler namun dapat menunjukkan pemanjangan sesuai dengan arah tumbuh di rongga hidung.11 Benda-benda erosif seperti baterai dapat mengakibatkan kerusakan parah dari septum hidung. Hal ini dapat terjadi karena benda erosif ini mengandung berbagai jenis logam berat seperti merkuri, seng, perak, nikel, kadmium, dan lithium. Pembebasan zat ini menyebabkan berbagai jenis lesi tergantung pada lokalisasi dengan reaksi jaringan lokal serta nekrosis. Sebagai hasilnya terbentuk perforasi septum, sinekia, penyempitan dan stenosis dari rongga hidung.12Benda asing hidup dapat menginisiasi proses inflamasi dari infeksi lokal ringan sampai kerusakan tulang hidung.12

2.7. Manifestasi klinisBenda asing di hidung pada anak sering luput dari perhatian orang tua karena tidak ada gejala dan bertahan untuk waktu yang lama. Dapat timbul rinolit di sekitar benda asing. Gangguan umumnya terjadi pada sisi rongga hidung yang terdapat benda asing. Gejala yang paling sering adalah hidung tersumbat, rinore unilateral dengan cairan kental dan berbau. Kadang-kadang terdapat rasa nyeri, demam, epistaksis dan bersin. Pada pemeriksaan, tampak edema dengan inflamasi mukosa hidung unilateral dan dapat terjadi ulserasi. Benda asing biasanya tertutup oleh mukopus, sehingga sering disangka sinusitis. Benda asing seperti karet busa, sangat cepat menimbulkan sekret yang berbau busuk.3,12

Gambar 6. Vestibulitis unilateral akibat bendaasing hidung.

Benda asing hidup dapat menimbulkan gejala bilateral seperti hidung tersumbat, sakit kepala, sekret serosanguinous, demam. Rhinolith umumnya bergejala dan menimbulkan obstruksi nasal bila rhinolith membesar. Pemeriksaan didaptkan massa ireguler keabuan, terletak di sepanjang dasar hidung.122.8. Diagnosis bandingDiagnosis banding untuk obstruksi hidung unilateral antara lain:1. Sinusitis2. Polip3. Tumor4. Upper respiratory infection (URI)5. Atresia koana unilateral6. Tumor hidung7. Abses 8. Hematoma septumKeluhan hidung bau dapat ditemukan juga pada rhinitis atrofi, sinusitis dan tumor. Perlu juga dipertimbangkan adanya masalah psikis bila ternyata tidak ditemukan kelainan pada hidung pasien.10

2.9. Penegakkan DiagnosisDiagnosis klinis benda asing di saluran napas ditegakkan berdasarkan anamnesis adanya riwayat tersedak sesuatu, tiba-tiba timbul "choking" (rasa tercekik), gejala, tanda, pemeriksaan fisik dengan auskultasi, palpasi dan pemeriksaan radiologik sebagai pemeriksaan penunjang. Diagnosis pasti benda asing di saluran napas ditegakkan setelah dilakukan tindakan endoskopi atas indikasi diagnostik dan terapi.3Anamnesis yang cermat perlu ditegakkan, katena kasus aspirasi ditegakkan karena kasus aspirasi benda asing sering tidak segera dibawa ke dokter pada saat kejadian. Perlu diketahui macam benda atau bahan yang teraspirasi dan telah beberapa lama tersedak benda asing itu.3Pemeriksaan fisik merupakan hal terpenting untuk mendiagnosis serta dibutuhkan kerjasama yang baik dengan pasien maupun orangtua pasien. Pasien harus dalam keadaan imobilisasi agar memudahkan pemeriksaan, oleh karena itu terkadang dibutuhkan obat-obat sedatif pada pasien pediatrik.Hampir seluruh kasus benda asing pada hidung tidak memerlukan pemeriksaan penunjang. Namun terdapat pengecualian pada kasus benda asing berjenis metal yang memberikan gambaran radiolusen pada foto X-Ray.13Selain itu, rinolith dapat dilihat dari pemeriksaan rhinoskopi anterior, CT scan maupun endoskopi.13

Gambar 7. Rinolith pada pemeriksaan CT scan

Gambar 8. Rinolith yang tampak pada pemeriksaan endoskopi

2.10. PenatalaksanaanUntuk dapat menanggulangi kasus aspirasi benda asing dengan cepat dan tepat perlu diketahui dengan sebaik-baiknya gejala di tiap lokasi tersangkutnya benda asing tersebut. Secara prinsip benda asing di saluran napas diatasi dengan pengangkatan segera secara endoskopik dalam kondisi yang apling aman, dengan trauma yang minimum. Kebanyakan pasien dengan aspirasi benda asing yang datang ke ahli THT telah melalui fase akut, sehingga pengangkatan secara endoskopik harus dipersiapkan seoptimal mungkin, baik dari segi alat maupun personal yang telah terlatih.3Penatalaksanaan benda asing di hidung pada anak-anak cukup sulit karena biasanya pasien anak-anak sulit untuk koopertif. Hal ini disebabkan oleh ketakutan anak-anak yang berlebihan serta diperparah dengan ketakutan mereka akibat nyeri yang ditimbulkan saat mengeluarkan benda asing di hidung sebelumnya baik oleh orang tua maupun tenaga kesehatan. Terdapat beberapa metode dalam mengeluarkan benda asing di hidung, seperti metode wax hook, menggunakan forgarty catheter, suction, metode tekanan positif, maupun dengan metodeParentsKiss.14 Gambar 9. Pengunaan Forgarty Catheter

Cara mengeluarkan benda asing dari dalam hidung ialah dengan memakai pengait (haak) yang dimasukkan ke dalam hidung dib again atas, menyusuri atap kavum nasi sampai menyentuh nasofaring. Setelah itu pengait diturunkan sedikit dan ditarik ke depan. Dengan cara ini benda asing itu akan ikut terbawa ke luar. Dapat pula menggunakan forsep aligator, cunam Nortman atau wire loop. Bila benda asing berbentuk bulat, maka sebaiknya digunakan pengait yang ujungnya tumpul.3

Gambar 10. Mengeluarkan benda asing dengan forsep aligator

Tidaklah bijaksana bila mendorong benda asing dari hidung kearah nasofaring dengan maksud supaya masuk ke dalam mulut. Dengan cara itu benda asing dapat terus masuk ke laring dan saluran napas bagian bawah, yang menyebabkan sesak napas, sehingga menimbulkan keadan yang gawat.3Pemberian antibiotika sistemik selama 5-7 hari hanya diberikan pada kasus benda asing hidung yang telah menimbulkan infeksi hidung maupun sinus.3

2.11. KomplikasiPerdarahan merupakan komplikasi yang paling sering terjadi, meskipun hal ini hanya bersifat minimal dan hilang dengan tampon sederhana. Selain itu benda asing pada hidung juga dapat menyebabkan iritasi dan reaksi inflamasi.12 Beberapa komplikasi benda asing pada hidung yang telah dilaporkan, antara lain: Sinusitis Otitis Media Akut Perforasi septum nasi Selulitis periorbital Meningitis, Epiglotitis akut Difteria Tetanus

Gambar 11. Komplikasi Akibat Benda Asing di Hidung

1. Apa penatalaksanaan pada benda asing ?Prinsip : jika benda asing dilakukan nasoendoskopi dengan trauma minimum1. Metode waxhook2. For garty cateter3. Suction4. Metode tekanan positif5. Menggunakan pengkait atau haak6. Juga memberikan antibiotik sistemik jika sudah menyebabkan infeksi pada hidung ataupun sinus

2. Apa penatalaksanaan perdarahan hidung ?3. Jelaskan mekanisme hidung sebagai jalan nafas dan 4. Jelaskan mekanisme hidung sebagai fungsi proteksi5. Jelaskan mekanisme hidung sebagai fungsi fonasi6. Jelaskan mekanisme patogenesis perdarahan pada hidung7. Jelaskan mekanisme patogenesis benda asing pada hidungPatofisiologiBenda asing hidung lebih sering terjadi pada anak-anak, karena anak yang berumur 2-4 tahun cenderung memasukkan benda-benda yang ditemukan dan dapat dijangkaunya ke dalam lubang hidung, mulut atau dimasukkan oleh anak lain.3 Benda yang dimasukkan ke dalam hidung anak biasanya benda yang lembut. Benda tersebut masuk ke hidung saat anak mencoba untuk mencium sesuatu. Anak sering menaruh benda ke dalam hidung karena perasaan bosan, ingin tahu atau meniru anak lain.11Benda asing hidung dapat ditemukan di setiap bagian rongga hidung, sebagian besar ditemukan di dasar hidung tepat dibawah konka inferior. Lokasi lainnya ada di depan dari konka media. Benda-benda kecil yang masuk kebagian anterior rongga hidung dapat dengan mudah dikeluarkan dari hidung. Benda asing yang berada di rongga hidung dalam waktu yang cukup lama serta benda hidup dapat menimbulkan berbagai kesulitan dalam mengeluarkan benda asing.12

Gambar 5. Lokasi benda asing yang masuk ke rongga hidung (IT= inferior turbinate, MT= middle turbinate, SS= sphenoid sinus, ST= superior turbinate).

Benda asing yang masuk ke rongga postnasal dapat teraspirasi dan terdorong ke belakang saat usaha pengeluaran sehingga menimbulkan obstruksi jalan nafas akut. Benda asing di hidung juga berpengaruh dalam membawa organisme penyebab penyakit difteri dan penyakit infeksi lainnya. Oleh karena itu, benda asing hidung dapat menyebabkan masalah yang nyata dan jangan dianggap remeh.12Beberapa benda asing yang masuk kedalam rongga hidung dapat bertahan bertahun-tahun tanpa adanya perubahan mukosa, namun sebagian besar benda mati yang masuk ke hidung dapat menimbulkan pembengkakan mukosa hidung dengan kemungkinan menjadi nekrosis, ulserasi, erosi mukosa, dan epistaksis. Tertahannya sekresi mukus, benda asing yang membusuk serta ulserasi dapat menyebabkan sekret berbau busuk.12Sebuah benda asing dapat menjadi inti peradangan yang nyata bila terbenam di jaringan granulasi dengan menerima lapisan kalsium, magnesium fosfat dan karbonat yang demikian akan menjadi sebuah rhinolith.12 Terkadang proses ini dapat terjadi di area mukopus bahkan bekuan darah yang sering disebut nidus. Rhinolith endogen yang terbentuk dari inti darah atau mukus jarang terjadi pasa usia dibawah 4 tahun, sedangkan rhinolith eksogen yang terbentuk dari benda asing yang diselimuti oleh garam dapat terjadi pada usia berapapun.11 Rhinolith umumnya terletak di dasar hidung bersifat radioopak, single, sferis ireguler namun dapat menunjukkan pemanjangan sesuai dengan arah tumbuh di rongga hidung.11 Benda-benda erosif seperti baterai dapat mengakibatkan kerusakan parah dari septum hidung. Hal ini dapat terjadi karena benda erosif ini mengandung berbagai jenis logam berat seperti merkuri, seng, perak, nikel, kadmium, dan lithium. Pembebasan zat ini menyebabkan berbagai jenis lesi tergantung pada lokalisasi dengan reaksi jaringan lokal serta nekrosis. Sebagai hasilnya terbentuk perforasi septum, sinekia, penyempitan dan stenosis dari rongga hidung.12Benda asing hidup dapat menginisiasi proses inflamasi dari infeksi lokal ringan sampai kerusakan tulang hidung.12