Guttural pouch empyema is defined as the accumulation of purulent, septic exudate in the guttural pouch. The infection usually develops subsequent to a bacterial (primarily Streptococcus spp) infection of the upper respiratory tract. Clinical signs include intermittent purulent nasal discharge, painful swelling in the parotid area, and in severe cases, stiff head carriage and stertorous breathing. Fever, depression, and anorexia may or may not be seen. Diagnosis is determined by endoscopic examination of the guttural pouch. Radiographs of the pharynx demonstrate a fluid line in the guttural pouch and may allow identification of an associated retropharyngeal mass.
Systemic antimicrobial therapy alone rarely resolves the infection; guttural pouch lavage is necessary. Penicillin gel (prepared using sodium penicillin) can be administered directly into the guttural pouch and may enhance bacterial clearance. Retropharyngeal abscesses can be resolved by rupturing the abscess into the guttural pouch using an endoscopic blade. If endoscopic rupture into the guttural pouch is unsuccessful, surgical drainage is necessary for retropharyngeal abscessation. Guttural pouch empyema may compress the dorsal pharynx and produce upper airway obstruction. Tracheotomy may be necessary to provide a temporary alternative airway in these cases. If guttural pouch empyema is not treated, chondroid material may form in the guttural pouch and serve as a source of chronic infectious exudate. A small number of chondroids can be removed endoscopically, but accumulations of exudate, chondroid material, or unresolved retropharyngeal abscesses require surgical drainage.
Mycotic plaques in the guttural pouch are typically located on the caudodorsal aspect of the medial guttural pouch, over the internal carotid artery. In some instances, fungal plaques may be multiple or diffuse. The most common fungal organism associated with guttural pouch mycosis is Aspergillus spp (see Aspergillosis Aspergillosis Aspergillosis is caused by several Aspergillus spp, especially A fumigatus and A terreus. A niger, A nidulans, A viridinutans, A flavus, and A felis are being recognized more commonly with increasing... read more ). Clinical signs arise from damage to the cranial nerves and the arteries within the mucosal lining of the guttural pouch. The most common sign is epistaxis, due to fungal erosion of the wall of either the internal carotid artery (most cases) or branches of the external carotid artery. Hemorrhage is spontaneous and severe, and repeated bouts may precede a fatal hemorrhagic episode. Dysphagia, Horner syndrome, and dorsal displacement of the soft palate may develop in response to fungal damage to cranial nerves and the sympathetic nerve that superficially traverse the guttural pouch. Dysphagia is a poor prognostic indicator and is highly correlated with nonsurvival. Diagnosis is determined by endoscopic examination of the guttural pouch. Treatment consists of topical and systemic antifungal therapy, based on sensitivity testing. Topical antifungal therapy is administered directly on the lesion via infusion through the biopsy channel of an endoscope. A fatal hemorrhagic event can be prevented by occluding the affected arteries along their course through the guttural pouch by means of a balloon-tipped catheter or a coil embolus. It is necessary to occlude the arteries proximal and distal to the lesion to prevent retrograde bleeding from the circle of Willis.
Guttural pouch tympany is seen in horses ranging from birth to 1 yr of age and is more common in fillies than in colts. A genetic basis of disease has been identified in Arabian and German warmblood breeds. In some cases, the condition is acquired due to inflammation of the upper respiratory tract. The affected guttural pouch is distended with air and forms a characteristic nonpainful swelling in the parotid region. Breathing may become stertorous in severely affected animals. Tympany may result from inflammation or malformation of the pharyngeal orifice of the eustachian tube, which then acts as a one-way valve by allowing air to enter the pouch but preventing its return into the pharynx. Diagnosis is based on clinical signs and radiographic examination of the skull. Severely affected animals may develop a secondary empyema. Tympany is usually unilateral, but bilateral cases have been reported. Medical management with NSAIDs and antimicrobial therapy resolves most cases due to upper respiratory tract inflammation. Surgical intervention is warranted in horses with malformation of the guttural pouch opening and involves fenestration of the membrane that separates the affected guttural pouch from the normal one. This provides a route for air in the abnormal guttural pouch to pass to the normal side and be expelled into the pharynx. The postoperative prognosis is good.
Traumatic rupture of the longus capitis is the second most common cause (after mycosis) of severe hemorrhage from the guttural pouch. The longus capitis muscle is one of the ventral straight muscles of the head. It inserts on the basisphenoid bone at the base of the skull. The point of rupture occurs at the insertion of the muscle dorsal to the guttural pouch. Rupture results from traumatic poll injury (rearing over backward) and produces profuse hemorrhage. Hemorrhage into the retropharyngeal space can cause asphyxia and death. On endoscopic examination, swelling and hemorrhage can be seen in the most rostral and medial aspects of the guttural pouch by retroflexion of the endoscope. On lateral radiographic examination, an avulsion fracture of the basisphenoid bone may be seen overlying the guttural pouch region. Significant neurologic deficits are often seen with this fracture. Treatment involves stall rest for 4–6 wk; broad-spectrum antibiotics are given for 5–7 days for any infection at the site of muscle rupture. Prognosis for full recovery is good, but persistent neurologic signs or recurrent hemorrhage worsens the prognosis.