The nose has four main functions: (1) to provide a portal through which air can flow to reach the alveoli, (2) to modify or regulate the flow of air, (3) to facilitate water and heat exchange (e.g. to condition the inspired air), and (4) to pass inspired air over the olfactory epithelium — the sheet of neurons and supporting cells that lines the nasal cavities. Speculation exists regarding the functions of the nasal sinuses. It seems plausible that the frontal sinuses protect the rostral portions of the brain from frontal trauma.
The apical portion of the nose, consisting of hairless integument and the nostrils, is called the nasal plane. It is supported by cartilage, which also supports the portion of the nose between the nasal plane and the bony portion.The levator nasolabial and levator labii superior muscles can move the cartilaginous parts. Dilation of the nostrils changes the pattern of flow of inspired air. The nostrils are dilated when increased airflow is needed, as in dyspnea, and to aid sampling of interesting odors.
The bony case of the nose is the facial portion of the respiratory passageway. The nasal cavity, comprised of bony and cartilaginous parts, extends from the nostrils to the choanae, being divided into right and left halves by the nasal septum. Each half of the nasal cavity has a respiratory and an olfactory region. The nasal conchae — slighdy ossified scrolls covered by nasal mucosa — fill the nasal cavities. Together with the nasal glands, the nasal mucosa has a role in conditioning the inspired air. During normal inspiration, the respiratory and olfactory air currents are concurrent. When the dog or cat wants to sample environmental odors, the nostrils are dilated and forced inspiration occurs in which a greater volume of inspired air takes a more dorsal course around the ethmoturbinates, where the olfactory receptors are most numerous.
Regulation and Conditioning of the Inspiratory and Expiratory Airflow
The respiratory airflow through the nasal cavity is regulated by the ventilatory control systems. The nose represents an important part of the resistance of the airway and thereby influences gas exchange in the alveoli. The resistance has to be overcome by greater negative pressure in the thorax during inspiration, which leads to better expanding and filling of the alveoli by the inspired air and a greater venous blood flow in the lungs. In humans, a prolonged increase in nasal resistance due to severe obstruction can lead to cor pulmonale, cardiomegaly, and pulmonary edema. In dogs, pulmonary edema is known to develop in laryngeal obstruction. Pulmonary edema may occur by a similar mechanism when severe obstruction of nasal airflow exists. The most common consequence of increased resistance is, however, mouth breathing.
Heating, or cooling of inspired and expired air as it passes through the nose is largely accomplished by radiation from the mucosal blood vessels. The flow of blood is from posterior to anterior, opposite to the flow of the inspired air. Humidification occurs by evaporation from the blanket of mucus covering the mucosa and the serous fluid from the nasal glands. Trie nasal blood flow and the activity of the nasal glands are regulated by the autonomic nervous system. The autonomic innerva-tion of the nose consists of parasympathetic and sympathetic nerve fibers, joined together in the vidian nerve. The conditioning of the inspired air by the nose is an important function for protection of the alveoli. Even under extremely dry or cold conditions, the bronchi receive air warmed to body temperature with a humidity of around 98%.
The pseudostratified respiratory mucosa in the nose consists of ciliated, intermediate, basal, and goblet cells. They rest on a well-defined basement membrane supported by a deep, loose lamina propria containing small blood vessels, venous plexus, and ducts of mucous and serous glands, sensory nerves, and blood cells. The tall ciliated cell is the predominant type, and it extends from the basement membrane to the luminal surface, where cilia admixed with microvilli are found. The cilia actively move the overlying blanket of mucus by a to-and-fro movement, called the ciliary beat. A more forceful forward movement and a less forceful recovery beat occurs. The forward movement transports the mucus blanket toward the pharyngeal end of the esophagus. The two-layer mucous blanket is sticky, tenacious, and adhesive. The outer layer is more viscid than the deeper, periciliary layer. Insoluble particles, allergens, and bacteria caught on the outer layer are thus carried to the esophagus. Soluble material reaches the periciliary layer and is absorbed. Sneezing starts with a rapid inspiration followed by an involuntary, sudden, violent, and audible expulsion of air through the nose and mouth. The reflex occurs after stimulation of sensory receptors in the nasal mucosa. It is the ultimate cleaning procedure for the nasal cavity in dogs and cats.
Three sensory systems are dedicated to the detection of chemicals in the environment: (1) olfaction, (2) taste, and (3) the trigeminal chemosensory system. Olfactory information can influence feeding behavior, social interaction, and reproduction. A dog’s sense of smell, together with its personality and intelligence, functions as a nose for humans in many circumstances.
The transduction of olfactory information occurs in the nasal olfactory epithelium, the sheet of neurons and supporting cells that lines the caudolateral wall, the ethmoidal conchae, and the dorsal part of the nasal septum. The olfactory receptor neuron is a bipolar neuron that gives rise on its basal surface to an unmyelinated axon that carries the olfactory information to the brain. At its apex the receptor neuron has a single process that expands into a knoblike protrusion from which several microvilli, or olfactory cilia, extend into the thick layer of mucus that lines the nasal cavity and controls the ionic milieu of the olfactory cilia.
Generation of receptor potentials in response to odors takes place in the cilia of receptor neurons. The axons of the olfactory receptor cells form the olfactory nerves that pass through the cribriform plate directiy to the olfactory bulb, on the anteroventral aspect of the ipsilateral forebrain. Olfactory informatiori is passed to the amygdala and primary olfactory cortex. Further pathways for processing olfactory information include the thalamus, hypothalamus, entorhinal cortex, and hippocampus.
History, Clinical Signs, And Physical Examination
History and Clinical Signs
The medical history in nasal disease often includes clear statements of specific problems, because the signs of nasal disease — discharge, sneezing, bleeding — are obvious to the owner. Additional questions should be asked about the animal’s general condition, appetite, drinking, activity, and endurance, and about changes in its habits. These questions and a general clinical examination are indicated because some systemic diseases cause nasal discharge (distemper, viral rhinotracheitis) or epistaxis (bleeding disorders), whereas some nasal diseases (such as advanced aspergillosis) can cause general malaise, and dyspnea can occur in obstructive nasal disease.
If nasal discharge is the predominant sign, the following questions should help determine whether it is from the left, the right, or both nostrils. If a nasal discharge is present, it should be characterized (watery, mucoid, pus, blood) and its frequency noted. Discharge occurring only during sneezing indicates a less productive mucosal disease than does continuous discharge. Occasional nasal bleeding is less alarming than frequent and profuse nasal bleeding, which can be fatal.
Sneezing, like coughing, is a reflex associated with protection of the mucosa. Particles, foreign bodies, inflammation of the mucosa, or abnormal turbulence in the nasal cavity associated with local drying of the mucosa can stimulate the sensory receptors in the mucosa. Continuous sneezing can cause irritation of the mucosa, leading to more sneezing and sometimes epistaxis.
Pain in the nose may only become obvious when the animal begins to react adversely to the owner’s customary petting. A dog with pain in the nose may object to having a collar or the loop of a leash drawn over its head, even though this is usually associated with the pleasure of a walk. Questions to obtain information about nasal pain should be adapted to the living conditions of the dog or cat.
A nasal stridor is a soft, rustling or sniffing sound that is synchronous with inspiration, expiration, or both. Narrowing of the nasal passageway, which increases the velocity of the airflow, causes the sound.
Dyspnea may be caused by nasal obstruction in cats and dogs, both of which tend to avoid mouth breathing even in this situation, almost to the point of suffocation. Apparently, avoiding the consequent bypassing of the nasal function of air cleansing and conditioning has a high priority.
After the shape of the nose as a whole is evaluated, the clinician should listen to the animal’s respiration for nasal stridor. Under quiet conditions, the clinician should listen close to the dog’s (and especially the cat’s) nose while gently closing its mouth. If stridor is noted and the clinician suspects it is caused by nostrils that are too narrow, moving the nasal alae laterally can change the tone of the stridor. Symmetry of the airstream can be examined by watching the movement of a small fluff of cotton held in front of each nostril. At the same time, the odor of the expired air can be noted. The area around the nostrils should be inspected for nasal discharge or crusts and the nasal plane for epithelial crusts (which could be caused by pathologic dryness), epithelial lesions, and depigmentation. The ventral wall of the nasal passages, which also forms the roof of the mouth, should be inspected through the opened mouth. The teeth, especially the canine teeth, should be inspected at the same time, because dental abnormalities can cause disorders of the nose. More in-depth inspections belong to special diagnostic procedures and require anesthesia.
Congenital malformation of the nasal plane is a common finding in brachycephalic breeds. The cartilage supporting the nasal plane is soft; thus the alae collapse, closing the nares. Corrective surgery is a simple procedure and consists of removing a cone-shaped piece of the ala and suturing the sides of the incision together in such a way that the nasal opening is enlarged.
In dogs and cats, variable congenital lesions of the nasal plane or more extensive clefts can be repaired surgically. The success of surgery is largely dependant on the available tissue around the cleft. Oronasal and oropharyngeal clefts cause rhinitis and should be considered for surgical repair. Euthanasia may be justified if repair is not possible and nasal discharge and dysphagia are causing recurrent fever and pain. Nasal dermoid sinus cysts have been reported in dogs. This cyst is recognized as a fistula in the midline of the bridge of the nose, producing intermittent discharge. Exploration of the fistula may reveal skin and hair as far down as the nasal septum. This abnormally located tissue must be completely removed before the skin incision is closed. A congenital cerebrospinal fluid (CSF) fistula, causing rhinorrhea, was reported in a cat. It was closed successfully.
The frontal sinuses are variable in size and sometimes even absent. Their absence is not associated with clinical signs. Congenital ciliary dysfunction has been documented in dogs of various breeds. Primary ciliary dyskinesia is a disorder in which ciliary function is ineffective and uncoordinated, resulting in rhinitis, bronchitis, bronchiectasis, and bronchopneumonia. When associated with situs inversus, the clinical syndrome is known as Kartagener’s syndrome. The initial signs (nasal discharge and coughing) usually begin at an early age, from days to 5 weeks of age. However, some dogs have remained asymptomatic for months. Complications are caused by colonization of the mucosa and the conchae by Pasteurella tnultocida and Bordetella bronchiseptica, which can cause hypoplastic conchae via bone resorption.
Mucociliary clearance in the dog’s nasal cavity can be measured by placing a small drop of BBTc macroaggregated albumin deep in the cavity, via a catheter, beyond the non-ciliated rostral half. The velocity of mucus clearance ranges from 7 to 20 mm/min. The test is not affected by anesthesia. However, not all normal dogs have a clearance rate within the reference range, and inflammation can change the velocity of the ciliary beat. To avoid spurious values, the test should be repeated and performed bilaterally.
Functional analysis of cilia in vitro is performed by examining transverse sections in electron micrographs after glutaraldehyde-osmium fixation. Major ultrastructural lesions in cilia of dogs with primary ciliary dyskinesia include lack of outer dynein arms, an abnormal microtubular pattern, and an electron-dense core in the basal body. The prognosis is guarded.
Affected dogs that develop severe recurrent bronchopneumo-nia usually die of sepsis. Continuous treatment with broad-spectrum antibiotics may enable such dogs to survive longer. Therefore cultures should be repeated to maintain correct antibiotic treatment based on sensitivity testing. A worthwhile review of treatment and long-term survival in dogs is available.
Trauma To The Frontal Sinus And The Nose
Trauma to the Frontal Sinus
Blunt or sharp objects can cause traumatic injury to the frontal sinus. The frontal bone in dogs and cats is relatively thick and provides good protection, so a fracture of it implies that a heavy blow to the head has occurred. The pet should therefore be given a thorough clinical examination for (1) signs of shock such as tachycardia, hypotension (prolonged capillary refill time, weak pulse), rapid respiration, dilation of the pupils, hypothermia, muscle weakness, restlessness, and depression or even coma and (2) other fractures or wounds. Frontal bone fractures do not require immediate attention unless brain damage is suspected. In the absence of signs of brain damage, and when other traumatic injuries have been attended to, the nature and extent of the frontal bone fracture should be examined by radiography, CT, or both. Prolonged anesthesia is needed; thus these procedures are usually delayed for 24 hours or more.
When bone fragments are seen to be present in the frontal sinus they should be removed. Like any foreign body, small bone fragments are likely to become sequestered. Surgery should be performed with full attention to aseptic procedures. Before attempting reconstruction of the frontal bone, it is important to examine the patency of the nasofrontal duct and to relieve any obstruction. Airtight suturing of the sub-cutis, including periosteum, followed by routine skin closure prevents the development of subcutaneous emphysema. Administration of broad-spectrum antibiotics for 3 weeks and strict limitation of activity during this period (keeping a cat confined to the house) will prevent complications.
Trauma to the Nose
Trauma to the nose is characterized by massive bleeding, which adds to the other effects of the impact in promoting shock. A thorough examination for signs of this is indicated (see Trauma to the Frontal Sinus). Fractures and wounds should be noted, but priority must usually be given to the treatment of hypovolemic shock.
When the dog or cat is sufficiendy stable, the larger vessels should be ligated and skin sutures should be placed as needed. Skin sutures, sometimes supported by subcutaneous sutures, may be sufficient to remodel the outer form of the nose. Fractures of the choanae are best left alone, because they are unlikely to ever result in obstruction. Severe traumatic damage to the nose almost always causes temporary obstruction, making tracheotomy necessary. Adequate oxygenation aids in avoiding general malaise and loss of appetite. Liquid or soft food facilitates eating. In dogs the tracheal cannula is often left in place for 10 days or longer. In cats that have difficulties with long-term tracheostomy, a small intranasal catheter may be placed and connected to the oxygen supply. Use of this method, however, depends on the pathway through the wounded nose. In the author’s experience, the nose is functionally adequate in 2 to 3 weeks. If needed, more corrective surgery could be attempted after 6 weeks.
Epistaxis (i.e. nasal bleeding) is often spontaneous and transient, and it is apparendy due to a local cause. When it is recurrent or profuse, with considerable loss of blood, diagnostic investigation is indicated. The several causes of epistaxis should be considered in planning diagnostic procedures. Recurring epistaxis occurs in both dogs and cats, but profuse nasal bleeding occurs mosdy in dogs. Recurring epistaxis in dogs and cats can be caused by ulcerative rhinitis, mycotic rhinitis, and tumor in the nasal cavity. Profuse nasal bleeding in dogs is most often caused by aspergillosis in the nasal cavity or frontal sinus, or it is caused by tumor in the nasal cavity and frontal sinus. Epistaxis can also be the sole sign of defects in primary hemostasis (platelet plug formation) or secondary hemostasis (coagulation cascade). Lesions in the nasal mucosa leading to epistaxis can also occur with systemic diseases such as leishmaniasis and amyloidosis.
Epistaxis caused by local disease in the nasal cavity or frontal sinus is approached (as are all nasal diseases) by a general and specific examination for nasal disease, as described earlier in this post. When the bleeding has occurred recendy, radiographic examination should preferably be delayed for at least 48 hours because clotted blood can be misinterpreted as a mass in the nasal cavity. Rhinoscopy should also be delayed for at least 48 hours after the bleeding has stopped, because the presence of blood clots hinders inspection and could lead to misinterpretation of findings.
In the meantime, profuse nasal bleeding should be stopped. It is best to sedate the animal (phenobarbital (2 mg/kg] is advised, because it does not affect blood pressure). After considerable blood loss, sedation that causes hypotension could lead to shock in association with hypovolemia and should therefore be avoided. Sedation will help stop bleeding.
Nasal tamponade is only acceptable for a short period and under anesthesia. For less profuse bleeding, nasal drops of 0.1% adrenaline are helpful. The use of adrenaline should, however, be restricted. Overdose could cause death due to vasoconstric-tion of the arteries supplying the brain. The administration of three drops in one of the nasal cavities in dogs and one drop in cats, repeated up to three times per 24 hours, is acceptable and effective when used during the bleeding. It should not be used in an attempt to prevent nasal bleeding. When examination of the nasal cavity and the frontal sinus reveals no cause for the bleeding, further investigation of primary diseases causing hemostasis is indicated.