NAVLE Respiratory

Equine Guttural Pouch Diseases Study Guide

The guttural pouches are paired diverticula of the auditory (Eustachian) tubes unique to equids. Each pouch has a capacity of approximately 300-500 mL and is lined with pseudostratified ciliated epithelium containing goblet cells.

Overview and Clinical Importance

The guttural pouches are paired diverticula of the auditory (Eustachian) tubes unique to equids. Each pouch has a capacity of approximately 300-500 mL and is lined with pseudostratified ciliated epithelium containing goblet cells. The stylohyoid bone divides each pouch into a larger medial compartment and smaller lateral compartment. The intimate association of the guttural pouches with major vascular structures and cranial nerves makes diseases of these structures clinically significant and potentially life-threatening.

Structure Location Clinical Significance
Internal Carotid Artery Medial compartment, caudodorsal aspect Primary site of mycotic plaque; erosion causes fatal epistaxis
External Carotid Artery Lateral compartment Secondary site of mycosis (approximately 30% of cases)
CN IX (Glossopharyngeal) Medial compartment Damage causes dysphagia
CN X (Vagus) Medial compartment, along ICA Pharyngeal branch damage causes dysphagia; recurrent laryngeal branch causes laryngeal hemiplegia
CN XII (Hypoglossal) Medial compartment Damage causes tongue paralysis and dysphagia
Sympathetic Trunk Medial compartment Damage causes Horner syndrome (ptosis, miosis, enophthalmos)
Retropharyngeal Lymph Nodes Floor of guttural pouch Rupture into pouch causes empyema; strangles carrier site

Guttural Pouch Anatomy

Understanding the complex anatomy of the guttural pouch is essential for interpreting clinical signs and avoiding iatrogenic injury during treatment. The guttural pouches are located behind the cranial cavity, caudal to the skull, and below the wings of the atlas (C1).

Key Anatomical Structures

High-YieldThe type of nasal discharge helps differentiate guttural pouch diseases: PURULENT discharge suggests empyema (think strangles); HEMORRHAGIC discharge suggests mycosis (think fatal epistaxis) or trauma; AIR accumulation without discharge suggests tympany (think Arabian filly foal).
Treatment Indications Details
Guttural Pouch Lavage All cases of empyema; essential for treatment Daily lavage with saline or polyionic solution via endoscope or catheter; antibiotics alone are NOT sufficient
Systemic Antibiotics Adjunct to lavage; severely ill horses Penicillin is drug of choice for S. equi; trimethoprim-sulfa as alternative
Endoscopic Chondroid Removal Small numbers of chondroids Memory-helical polyp retrieval basket through endoscope biopsy channel
Surgical Drainage Large chondroid accumulations; retropharyngeal abscess Access via Viborg triangle; hyovertebrotomy; risk of nerve damage
Tracheotomy Severe pharyngeal compression causing respiratory distress Temporary alternative airway; addresses the strangling effect

Guttural Pouch Empyema

Etiology and Pathophysiology

Guttural pouch empyema is the accumulation of purulent material within one or both guttural pouches. The most common cause is Streptococcus equi subspecies equi (strangles), which accounts for the majority of cases. The infection typically develops when retropharyngeal lymph nodes abscess and rupture into the ipsilateral guttural pouch, or through direct extension from upper respiratory tract infections.

Approximately 10% of horses in strangles outbreaks develop persistent guttural pouch empyema due to failure of the normal drainage mechanism. In chronic cases, the purulent material inspissates (dries out) and forms discrete, ovoid, smooth concretions called chondroids. These chondroids harbor viable S. equi on their surface and within their core, creating persistent carrier animals that can shed bacteria for months to years.

Clinical Signs

  • Intermittent bilateral purulent nasal discharge
  • Painful swelling in the parotid region (throatlatch area)
  • Lymphadenopathy of submandibular and retropharyngeal lymph nodes
  • Fever, depression, and anorexia (variable)
  • Stiff head carriage and stertorous breathing in severe cases
  • Dysphagia or cranial nerve deficits (uncommon, suggests nerve involvement)

Diagnosis

Endoscopy is the gold standard for diagnosis, allowing direct visualization of both guttural pouches, assessment of purulent material or chondroids, and collection of samples for culture and PCR. Radiography reveals a characteristic fluid line within the guttural pouch and can identify retropharyngeal masses or chondroids as radio-opaque nodules.

Treatment Options

NAVLE TipAlways consider guttural pouch empyema as Streptococcus equi infection until proven otherwise. Implement isolation procedures immediately. Remember: Antibiotics ALONE will NOT resolve empyema - lavage is ESSENTIAL. Horses must have 3 negative PCR/culture tests before being cleared as non-carriers.
Clinical Sign Structure Affected Notes
Epistaxis (MOST COMMON) Internal carotid, external carotid, or maxillary artery Bright red blood; may be intermittent then sudden massive hemorrhage; EMERGENCY
Dysphagia CN IX (glossopharyngeal), CN X (vagus), CN XII (hypoglossal) Second most common sign; causes quidding, coughing, feed-containing nasal discharge
Laryngeal Hemiplegia Recurrent laryngeal nerve (branch of CN X) Causes roaring; usually permanent even after resolution
Horner Syndrome Sympathetic trunk/cranial cervical ganglion Ptosis, miosis, enophthalmos, patchy cervical sweating
Facial Paralysis CN VII (facial nerve) Ear, eyelid, and lip droop

Guttural Pouch Mycosis

Etiology and Pathophysiology

Guttural pouch mycosis (GPM) is a rare but potentially fatal fungal infection, primarily affecting adult stabled horses. Aspergillus fumigatus is the most common causative organism. The fungus is angiotropic (attracted to blood vessels), attaching to arteries within the guttural pouch for nutrition. Fungal plaques form diphtheritic membranes consisting of fungal mycelia, bacteria, necrotic tissue, and cell debris.

The fungal plaques are most commonly located on the caudodorsal aspect of the medial compartment over the internal carotid artery (ICA). In approximately 30% of cases, plaques also involve the lateral compartment over the external carotid or maxillary arteries. The pathogenesis remains unknown, and no predisposing factors have been definitively identified.

High-YieldGuttural pouch mycosis results in FATAL HEMORRHAGE in approximately 50% of untreated cases. The condition is clinically silent until arterial erosion or cranial nerve damage occurs. Any horse with unexplained epistaxis should have guttural pouch endoscopy performed urgently.

Clinical Signs

Clinical signs relate to the structures damaged by the fungal plaque:

Diagnosis

Endoscopy is diagnostic, revealing characteristic fungal plaques as gray-black diphtheritic membranes, typically located over arteries. The examination also allows assessment of which vessels are involved and evaluation of cranial nerve function (larynx, pharynx). Radiography and CT can provide additional information about extent of disease and involvement of adjacent structures.

Treatment: Three-Step Approach

Step 1 - Emergency Field Management: Temporary ligation of the common carotid artery can be performed at the barn as emergency aid to reduce hemorrhage while arranging transfer to a surgical facility. Keep the horse calm and minimize stress.

Step 2 - Definitive Arterial Occlusion: The primary surgical goal is to prevent fatal hemorrhage by occluding affected arteries both proximal (cardiac side) and distal (cerebral side) to the fungal plaque. This is necessary because of the Circle of Willis, which provides collateral blood flow.

Step 3 - Supportive Care and Resolution: Once arterial blood supply is eliminated, the fungal plaque typically regresses spontaneously over 30-180 days WITHOUT additional antifungal therapy. Antifungal treatment (topical enilconazole, systemic voriconazole) may be used as adjunct but is not essential after successful arterial occlusion.

NAVLE TipFor NAVLE: Remember that arterial occlusion must be BOTH proximal AND distal to the lesion because of the Circle of Willis (retrograde flow). Once blood supply is eliminated, the fungus dies without additional antifungal treatment. Horses with dysphagia have a WORSE prognosis than those with epistaxis alone - nerve damage may be permanent.

G = Gray-black fungal plaque on endoscopy

P = Primary location: Internal Carotid Artery (medial compartment)

M = Mortality 50% without treatment; Must occlude artery Both sides of lesion

Technique Advantages Considerations
Transarterial Coil Embolization (TACE) Gold standard; fluoroscopic guidance ensures precise placement; approximately 80% success rate Requires specialized equipment; higher cost; limited availability
Balloon Catheter Occlusion More widely available; approximately 80% success rate Less precise placement; anatomic variation may complicate
Direct Arterial Ligation Can be performed in the field May increase ICA blood flow; best for ECA hemorrhage

Guttural Pouch Tympany

Etiology and Pathophysiology

Guttural pouch tympany is a congenital or acquired condition in which air becomes trapped within one or both guttural pouches, causing abnormal distension. The condition primarily affects foals from birth to 1 year of age and is more common in fillies than colts (ratio 2:1 to 4:1). A breed predisposition exists for Arabian and German Warmblood horses, with genetic components identified in both breeds.

The pathophysiology involves dysfunction or malformation of the plica salpingopharyngea (the mucosal fold at the pharyngeal orifice of the guttural pouch). This creates a one-way valve effect, allowing air to enter the pouch during deglutition but preventing its escape. The condition may also develop secondary to upper respiratory tract inflammation affecting the mucosal flap.

Clinical Signs

  • Nonpainful, fluctuant swelling in the parotid region ("bullfrog" appearance)
  • Usually unilateral, but may appear bilateral due to displacement of median septum
  • Stertorous breathing, especially during nursing
  • Dyspnea in severe cases (compression of nasopharynx)
  • Dysphagia and aspiration pneumonia may develop
  • Secondary empyema can occur if untreated

Diagnosis

Radiography reveals severely enlarged, air-filled guttural pouch(es) extending caudally to the atlas with an excessively rounded caudal border. Endoscopy confirms the diagnosis, rules out other guttural pouch disorders, and helps distinguish between unilateral and bilateral disease. An abnormal guttural pouch opening (redundant plica) is often visible.

Treatment

High-YieldTympany must be treated promptly to prevent secondary empyema. Prognosis is GOOD for unilateral cases treated surgically (recurrence rate 15-33%). Prognosis is GUARDED for bilateral cases. Remember the classic presentation: Arabian FILLY FOAL with nonpainful parotid swelling and stertorous breathing.

Arab breed predisposition

Respiratory stertor while nursing

Air trapped (one-way valve)

Bullfrog appearance

Females more affected

Infection risk if untreated

Laser fenestration for treatment

Less than 1 year of age

Yields good prognosis with surgery

Treatment Indications Details
Medical Management Mild cases with upper respiratory inflammation NSAIDs and broad-spectrum antimicrobials; may resolve if inflammation-related
Temporary Decompression Emergency relief; diagnosis Percutaneous needle or catheter; provides temporary relief only
Foley Catheter Placement Non-surgical option for remodeling Transnasal placement for 2-6 weeks; induces remodeling of plica; permanent resolution possible
Median Septum Fenestration Unilateral tympany Laser creates opening in septum; air exits via normal contralateral pouch; unsuccessful for bilateral cases
Salpingopharyngostomy Bilateral tympany; recurrent cases Laser creates permanent fistula into pharynx; plica salpingopharyngeus resection

Differential Diagnosis Summary

Disease Nasal Discharge Age Swelling Key Feature
Empyema Purulent, bilateral Any age Painful parotid Associated with strangles; chondroids in chronic cases
Mycosis Hemorrhagic (epistaxis) Adults None 50% fatal; cranial nerve deficits; stabled horses
Tympany None initially Foals less than 1 yr Nonpainful, fluctuant Arab/Warmblood fillies; stertor

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