Nasal hemorrhage in the horse – from where and why? (Proceedings)

Horses with evidence of epistaxis can be challenging to diagnose and manage. The volume of visible blood can range from a trace of serosanguinous discharge that is suggestive of a past episode of bleeding, to high volume fresh blood flow from both nares. The occurrence can be sporadic and intermittent or sudden, continuous and fatal in a short period of time. Epistaxis can be secondary to hemorrhage arising from anywhere along the respiratory tract. Unilateral epistaxis tends to arise from somewhere rostral to the caudal extent of the nasal septum, i.e. from the ipsilateral nasal passage/paranasal sinus region. Bilateral nasal epistaxis is typically from a lesion caudal to the end of the nasal septum but occasionally the lesion will be located in the caudal nasal passage on one side and blood tracks down both nasal passages. Successful treatment of the cause of epistaxis depends on an accurate and timely diagnosis. Respiratory tract endoscopy and radiography remain the key imaging modalities to facilitate most diagnoses. Biopsy of masses is also required for definitive diagnosis in many cases. Awareness of the causes of nasal epistaxis and classic history and clinical signs are useful to formulate a differential diagnosis and determine if a case represents an emergency. This paper will describe the causes of nasal hemorrhage moving from the upper to the lower respiratory tract. Iatrogenic causes of nasal hemorrhage are not discussed (for example, nasogastric intubation trauma, and surgical trauma).

Upper Respiratory Tract Origin

Idiopathic Mucosal Bleeding

Rarely, or perhaps more commonly than appreciated, a steady or intermittent low flow nasal bleed will arise from a leaking mucosal vessel in the nasal, paranasal or nasopharyngeal wall. Historically these horses are reported to have spontaneous epistaxis of very small volume, sometimes related to exercise. The bleeding often stops and then recurs intermittently days, weeks or months apart. Veterinary attention is sought when the bleeding persists or is more frequent in occurrence. Diagnosis is completely dependent on endoscopic visualization of the source of bleeding from a mucosal surface. Use of a pediatric endoscope allows thorough examination of the nasal conchal surfaces where access into the recesses of the nasal meati is too tight for a standard 9-10 mm diameter endoscope to pass without traumatizing the tissues. Active bleeding must be present to find the source of this hemorrhage. A single vessel rupture, sometimes with a low pulsatile flow if a small arterial branch is damaged, or a diffuse oozing of blood from a small surface area of the mucosa has been seen. These cases have been successfully treated by cauterizing any accessible bleeding vessel/mucosa with silver nitrate sticks or laser ablation.

Progressive Ethmoid Hematoma (PEH)

This is a slowly expanding, locally destructive mass, considered non-neoplastic, that arises from the submucosa of the ethmoidal labyrinth or less commonly from the paranasal sinus mucosa. The cause is unknown. The tissue is a conglomeration of clotted blood, collagen, hemosiderin-filled macrophages, and multinucleated giant cells, contained by a lining of respiratory mucosa. The space-occupying mass can grow into the nasal passage, paranasal sinuses and nasopharynx. The classic history is an intermittent serosanguinous and sometimes fresh blood discharge from one or both nostrils, not associated with exercise. Excessive bleeding is extremely infrequent and often veterinary examination is delayed because the bleeding is considered very mild and it will spontaneously clear up and not occur again for weeks until the mass develops further and bleeding or serosanguinous discharge becomes more regular. Hemorrhage occurs as the mass expands and ruptures its mucosal lining. The site then clots, seals over and remains subclinical again until another rupture and bleed. Bilateral disease occurs uncommonly. Many horses with bilateral nose bleeds will have an ethmoid hematoma originating from one side that has expanded around the caudal aspect of the nasal septum to enter the contralateral nasal passage too. The median age of affected horses is 10 years, with a predilection for Arabians and Thoroughbreds, and genders are affected equally. Other clinical signs include halitosis, abnormal respiratory noise, dyspnea, coughing, head shaking and facial deformity. Small PEHs may cause no clinical signs, whereas extensive masses can be seen at the nostril. Rhinoscopy is critical for diagnosis, supplemented by radiographs and CT imaging if desired. Endoscopically, PEHs appear glistening, red-green-yellow-purple, depending on recent hemorrhage, with a smooth surface, perhaps multilobulated. White colonies of Aspergillus may partially cover the surface. Careful examination of the ethmoid turbinate region confirms the typical origin for PEHs; however larger masses obscure this area preventing accurate visualization. Histopathology provides a definitive diagnosis. Nasal polyps, fungal masses and tumors can resemble PEH endoscopically. Treatments include transendoscopic laser ablation, transendoscopic intralesional injection of 10% formalin, and surgical removal via a sinus bone flap. Longterm successful resolution of PEH is guarded – recurrence is up to 50% and persistence with regular rechecks and follow up treatments is necessary. Even after a lesion appears to be resolved longterm endoscopic surveillance once or twice a year is recommended, along with sinus radiographs as indicated.

Guttural Pouch Mycosis (GPM)

Of all the upper airway causes and sources of hemorrhage this one is the most critical and immediately life-threatening. Any confirmation or suspicion of bleeding arising from the guttural pouch should result in the recommendation for urgent referral to a surgical facility. Horses show epistaxis ranging from low volume intermittent bleeds through to catastrophic, massive hemorrhage resulting in hypovolemic shock and death of the horse before any medical assistance is possible. Hemorrhage is not associated with exercise or any apparent traumatic event. Blood will exit both nostrils because of the location of the guttural pouch openings caudal to the nasal septum. Prior to bleeding events, there may be development of a mucopurulent nasal discharge. Hemorrhage is a consequence of the causative fungal organism (most commonly Aspergillus spp) invading and compromising vascular walls of vessels associated with the guttural pouches. The lesion often develops in the dorsocaudal region of the guttural pouch, more medial than lateral, and therefore the internal carotid artery is primarily disrupted. The external carotid and maxillary arteries may also be affected. Disease is usually unilateral. However, some lesions expand to the point of destroying the median septum of the guttural pouches and passing into the contralateral side. In these cases, hemorrhage will be apparent from both guttural pouch openings on endoscopy and careful examination is required to determine the primary lesion side. Diagnosis is by endoscopic examination. Cranial nerves and their branches can also be damaged by the fungal infection and endoscopic signs of laryngeal hemiplegia and dysphagia may be noted. In some cases, hemorrhage will be mild and have ceased spontaneously before examination and if blood clots have cleared, a cream-tan-yellow, irregular mass can be seen on the wall of the guttural pouch of variable size. When bleeding is active lack of visualization is a major problem and when a horse is unstable and anxious due to hemorrhagic shock endoscopic examination can be very awkward. Getting into the guttural pouches whose entrances are clogged with blood clots is difficult at best and if both pouches are filled with blood clots, determining which side might be the primary disease could be impossible without angiography. Because the endoscope can dislodge blood clots and activate bleeding again, it is strongly advised to be prepared for emergency surgery before performing guttural pouch endoscopy. The main endoscopic differential for hemorrhage arising from the guttural pouch is rupture of the rectus capitis/longus capitis muscles (discussed later). Treatment of GPM is aimed at stopping and preventing further hemorrhage from compromised arteries and providing resuscitation of horses in hemorrhagic shock. Various surgical techniques exist to stop bleeding (artery ligation, balloon-tipped thrombectomy catheters, transarterial coil or plug embolization) and when performed successfully, the fungal disease invariably resolves over a few months with the rare need for supplemental antifungal therapy. The final prognosis after treatment of GPM is dependent on the degree of cranial nerve dysfunction.

Other Upper Airway Fungal Infections

Mycotic infections of the upper airway can establish in the nasal passages or nasopharynx. Horses in humid environments are more likely to contract these infections. Significant organisms include Rhinosporidium seeberi, Conidiobolus coronatus, Cryptococcus neoformans, and Coccidioides immitis. Generally a chronic, malodorous, unilateral or bilateral nasal discharge of a sanguinolent mucopurulent nature is noted. Headshaking, stertorous breathing, sneezing, epistaxis, and dysphagia may be common signs. Submandibular lymphadenopathy is often present. Disease may be present at the nares. Endoscopic examination reveals ulcerated, red, irregular plaques or granulomas with localized tissue destruction. Pedunculated or sessile nodular lesions are a feature of rhinosporidosis. Diagnosis is dependent on cytology, histopathology and culture of organisms. Interpretation of the pathogenicity of an organism must be made with the knowledge that fungal spores and hyphae are commonly found in the respiratory tract of normal horses. Treatments include surgical debulking or excision of accessible lesions and topical and systemic antifungal agents.

Upper Respiratory Tract Neoplasia

Squamous cell carcinoma is the most common upper airway neoplasm, followed by adenocarcinoma and undifferentiated carcinomas. Definitive diagnosis requires biopsying the mass, and cytology and histopathology. Clinical signs include the slow, insidious development of mucopurulent, sanguinous or serosanguinous nasal discharge, unilateral or bilateral depending on the location of the tumor. Frank blood may be noted on some occasions that is usually a small volume and diminishes to a serosanguinous discharge within a day or two. Hemangiosarcoma of the paranasal sinuses causes persistent dark bloody discharge. Other clinical signs include worsening stertorous respiration, reduced or absent airflow from the affected nasal passage, malodorous breath, facial deformity, enlarged submandibular lymph nodes, and epiphora. Aged horses are more at risk for upper airway tumors. Frequently, by the time of diagnosis, disease is advanced and treatment options are limited with poor prognoses. Radical surgical excision is generally not feasible in the nasal cavity or paranasal sinuses. Radiation therapy has been useful in isolated cases.

Skull Fractures, Rectus Capitis/Longus Capitis Muscle Trauma

Traumatic fractures of the petrous temporal bone that extend to the cribriform plate can result in nasal epistaxis. These horses are likely to have aural bleeding as well. Associated neurologic dysfunction is often immediately apparent, including vestibular disease, facial nerve paralysis, recumbency and coma. Rectus capitis and longus capitis muscle trauma usually occurs when a horse falls over backward and strikes its poll on the ground. The sudden head extension that occurs when the poll hits the ground results in avulsion of the insertions of the capitis muscles and accompanying fracture of the basioccipital and/or basisphenoid bones. The torn muscles can bleed profusely into the guttural pouches and nasal epistaxis can be dramatic with this injury. Signs of concussion, and vestibular and facial nerve damage can be evident. Guttural pouch endoscopic findings and the classic history of falling backwards help determine a diagnosis of capitis muscle trauma. Treatment is supportive medical care. Fractures to the facial bones overlying the paranasal sinuses and the nasal cavity usually result in some degree of nasal bleeding.

Foreign body

Infrequently, foreign bodies (small twigs, brambles, wood splinters from a fence line) may be caught in the upper or lower airway and the tissue trauma sustained during lodgment causes epistaxis. Subsequently if the foreign body is not expelled by coughing or sneezing, local tissue necrosis and inflammation result in further serosanguinous-mucopurulent discharge and possibly evidence of fresh blood. Other clinical signs include chronic coughing or sneezing, head shaking, malodorous breath, and abnormal respiratory noise. Diagnosis is by endoscopic examination and treatment is extraction of the foreign body. Some foreign bodies can migrate into a bronchus and careful examination with a 3 m endoscope, preferably less than 10 mm diameter, is needed to follow the evidence of discharge to the location. To securely grasp and extract foreign bodies from the lower airway, a temporary tracheotomy may be required to get instruments in closer to the location.

Tracheal Lesions

The trachea is a very rare location for the primary origin of epistaxis. External trauma resulting in tracheal lacerations can cause transient bleeding at the nose. Neoplastic conditions are rare but invasion of tissues and irritation from chronic coughing can cause a sanguinolent mucopurulent discharge. A foreign body lodged in the trachea may also cause evidence of bleeding.

Lower Respiratory Tract Origin

Exercise-Induced Pulmonary Hemorrhage (EIPH)

Most breeds of horses have been detected to have blood in the lower airway following strenuous exercise. The caudodorsal lung fields are the common source of hemorrhage. Less than 10% show frank blood at the nostrils. When other causes of nasal epistaxis have been ruled out and bleeding occurs post exercise, EIPH should be high on the differential diagnosis list, even if the bleeding is not consistent after exercise or an endoscopy fails to see obvious blood in the trachea. Ancillary diagnostics including radiographs, transtracheal washes, and bronchoalveolar lavage can be necessary to help support a diagnosis.

Pneumonia, Pulmonary Abscess Or Neoplasia

Bacterial pneumonia follows viral infections and stressful events (competitive showing and racing, long trailer rides with physical prevention of head lowering, general anesthesia, overcrowded and inadequate nutrition, and constant exposure to inclement weather). Aspiration pneumonia can occur secondary to laryngeal surgery (laryngoplasty or arytenoidectomy) and esophageal obstruction (choke). Early clinical signs include increased airway sounds, fever and depression. Respiratory distress, tachypnea, nasal discharge, coughing, inappetence, weight loss and exercise intolerance follow. The nasal discharge is usually mucopurulent but in some cases can be sanguinolent or frank blood, particularly after a coughing episode. Endoscopy will aid in confirming the source of the discharge and blood as being the lower airway. Pulmonary abscesses can develop secondary to a focal pneumonia or as part of a pleuropneumonia complex. Blood that pools in the airways and alveoli following EIPH, provide a favorable environment for bacterial proliferation and abscess development. As the abscesses develop and expand, erosion of vessels can result in epistaxis. Primary lung tumors are rare in horses and bleeding is more likely secondary to metastatic disease (adenocarcinoma, hemangiosarcoma, and lymphoma) eroding through pulmonary vasculature. Clinical signs are similar to those for pneumonia and the prognosis is poor following a diagnosis of pulmonary neoplasia.

References

Hardy J, Leveille R. Disease of the guttural pouches. Vet Clin North Am: Equine Pract, 2003;19:123-158.

Freeman DE. Sinus disease. Vet Clin North Am: Equine Pract, 2003;19:209-243.

Saulez MN. Exercise-induced pulmonary hemorrhage. In, Current Therapy in Equine Medicine, 6th Edition, Robinson NE, Sprayberry KA, editors, Saunders Elsevier, St Louis, Missouri, 2009, pp 320-323.