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Canine and Feline Mega Esophagus

Canine and Feline Mega Esophagus

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Vol. 19, No. 3March 1997SmallAnimalGastroenterologyContinuing Education Article
Refereed Peer Review
FOCAL POINTKEY FACTS
s
Disruption of the afferentpathway has been implicatedin the pathophysiology ofboth congenital and adult-onset idiopathic caninemegaesophagus.
s
Definitive diagnosis of eithergeneralized or focal myastheniagravis requires identification ofcirculating antibodies againstacetylcholine receptors.
s
The most common endocrinediseases associated withmegaesophagus arehypoadrenocorticism and,possibly, hypothyroidism.
s
Advanced techniques,including manometry andnuclear scintigraphy, areuseful in evaluating esophagealmotility.
5
Acquired megaesophaguscan result from numerousneuromuscular, endocrine,or inflammatory disorders aswell as from obstructive lesionsin the esophagus.
Canine and FelineMegaesophagus
University of Tennessee
Erick A. Mears, DVMChristine C. Jenkins, DVM
M
egaesophagus refers to a diffusely dilated esophagus with decreasedor absent motor function. Canine megaesophagus can occur as acongenital disorder (with signs first appearing before or soon after weaning), as an acquired disorder (secondary to an underlying primary condi-tion), or as an adult-onset idiopathic disease. Feline megaesophagus is rare andoccurs as a congenital or secondary acquired disorder.
1
Congenital megaesophagus is recognized at weaning and is believed to becaused by a lack of innervation of the esophagus.
2,3
The mode of transmissionin most breeds of cats and dogs has not been well defined.
4,5
However, congeni-tal megaesophagus is known to be inherited in wirehaired fox terriers andminiature schnauzers.
6,7
It is transmitted in wirehaired fox terriers as a simpleautosomal-recessive trait, whereas in miniature schnauzers, it is transmitted as asimple autosomal-dominant or a 60% penetrance autosomal-recessive trait.
6–8
 A predisposition may exist in other canine breeds, including Great Danes, Ger-man shepherds, Irish setters, Labrador retrievers, Newfoundlands, and Chineseshar-peis.
8
Feline breeds that may have a hereditary predisposition include theSiamese and Siamese-related breeds.
9
 Acquired megaesophagus can result from numerous neuromuscular, en-docrine, or inflammatory disorders as well as from obstructive lesions in theesophagus.
4,5
Early diagnosis and elimination of predisposing diseases are essen-tial for successful management because prolonged dysfunction can cause irre-versible distention. Adult-onset idiopathic megaesophagus is associated with a poor to graveprognosis. A high percentage of patients are euthanatized because of the pro-gression of clinical signs and recurrent aspiration pneumonia.
ANATOMY
The esophagus consists of the upper esophageal sphincter proximally, theesophageal body, and the lower esophageal sphincter distally. The upperesophageal sphincter separates the pharynx from the body of the esophagusand indirectly prevents aspiration of ingesta into the respiratory tract. Thissphincter is composed of striated muscle and is innervated by the somaticbranches (glossopharyngeal, pharyngeal, and recurrent laryngeal) of the vagusnerve, which originates from the brain stem nucleus ambiguus.
10
V
 
tone of the lower esophagealsphincter, the interdigitatingesophageal and gastric rugalfolds, the diaphragmatic crus(which serves as a muscularsling), the oblique angle of thedistal esophagus as it enters thestomach, and the compressionexerted on the short intraabdom-inal esophageal segment by posi-tive intraabdominal pressure.
13
In dogs, the lower esophagealsphincter contains fibers of bothstriated and smooth muscle, whereas in cats, it contains only fibers of smooth muscle.Esophageal contraction, orperistalsis, follows swallowingand the movement of food fromthe pharyngeal area into theesophagus. Sensory, or afferent,receptors in the pharynx andproximal esophagus are stimulat-ed by the presence of food. Solidboluses are more effective thanliquid in stimulating a swallow-ing reflex.
12
The afferent recep-tors stimulate the afferent nerve fibers of the vagus. Theorigin of the vagus nerve (i.e., the nucleus ambiguus forstriated muscle and the dorsal motor nucleus for smoothmuscle) initiates an efferent response via the somaticand parasympathetic nerve fibers of the vagus. This neu-ronal pathway ends at the myoneural junction with acoordinated contraction of the upper esophageal sphinc-ter.
12
This peristaltic wave propagates caudally throughthe body of the esophagus, passes through the loweresophageal sphincter, and then moves into the stomach.The initial wave that begins at the pharynx is called
 pri- mary peristalsis 
. Any remaining intraluminal ingesta within the esophagus stimulates esophageal afferent re-ceptors and initiates
secondary peristalsis 
, which clearsthe lumen of the esophagus
12
(Figure 1).
PATHOGENESISCongenital
The neural pathway of esophageal innervation hasbeen identified.
12
 Any lesion along this neural pathway could alter the normal motility of the esophagus.
4,5
 A study that evaluated the efferent pathway found thatdogs with congenital idiopathic megaesophagus hadnormal vagal efferent innervation and decreasedesophageal motor function, possibly secondary to al-tered biomechanical or viscoelastic properties of the
Presence of food Afferent receptors (sensory)in the proximalesophagusVagus/glossopharyngeal nervesNucleus solitarius
The esophageal body consists of two muscle layersthat propel food via coordinated contractions from theoral cavity to the stomach. The entire length of the ca-nine esophageal body is composed of two oblique layersof skeletal muscle, which contains predominantly typeIIA fibers and is innervated by the somatic branches of the vagus nerve.
11
The two layers of skeletal muscle of the esophagus in the cat are in an oblique orientationin the proximal portion of the esophagus and becomespiral in the distal portion, thus forming a longitudinaland circular pattern.
12
Unlike the dog, the cat has anincreased quantity of smooth muscle in the distal thirdof the esophageal body. The striated muscle of theesophagus of the cat is also innervated by the vagusnerve; however, the smooth muscle is innervated by theautonomic branches of the vagus nerve, which origi-nates from the dorsal motor nucleus.The lower esophageal sphincter is considered a physi-ologic sphincter and not a true anatomic sphincter be-cause of the absence of muscle mass at the sphinctersite.
12
This sphincter separates the esophagus and thecardia of the stomach and allows ingesta to pass into thestomach while preventing reflux of most stomach con-tents into the esophagus. Esophageal reflux is preventedby various contributing factors at the site of the loweresophageal sphincter. These factors include the resting
Small Animal
The Compendium 
March 1997
ANATOMY
s
ESOPHAGEAL MOTILITY
s
NEURAL PATHWAYS
Figure 1—
Neural pathway for esophageal motility.
Nucleus ambiguusVagus nerve (motor)Neuromuscular junctionStriated muscleEsophageal contractionDorsal motor nucleusVagus nerve (motor)Neuromuscular junctionStriated and smooth muscle
 
esophagus.
14,15
Two other studies confirmed anormal efferent limb and implicated a disrup-tion of the afferent limb of the neural pathway as the cause of congenital canine megaesopha-gus.
16,17
Adult-Onset Idiopathic
In an evaluation of the afferent nerve pathway in adult dogs with acquired idiopathic mega-esophagus, pressure measurements were takenfrom the upper esophageal sphincter, theesophageal body, and the lower esophagealsphincter after both swallowing and intraluminaldistention.
18
Pressure measurements of the loweresophageal sphincter after swallowing were nor-mal and indicated appropriate relaxation of thesphincter,
18,19
thus suggesting a normal efferentpathway. However, measurements taken after in-traluminal distention of the esophagus revealedfailure of the lower esophageal sphincter to relax.
18
Therefore, a defect probably exists in the afferentpathway of dogs with both congenital and adult-onset idiopathic megaesophagus. Similar studieshave not been done in cats.
Secondary Acquired
Megaesophagus can be caused by any diseasethat inhibits esophageal body peristalsis by dis-rupting central, efferent, or afferent neuralpathways or esophageal musculature.
8
The vari-ous causes and their proposed mechanisms willbe discussed in the following section.
CAUSESCongenital
The neurologic dysfunction that results indiffuse megaesophagus is unclear. It has beenhypothesized that the innervation of the esophagus isincomplete in congenital megaesophagus and that in-nervation may improve with maturity.
2,3
Secondary Acquired
The list of specific diseases that cause megaesophagusis extensive. Broad disease categories include centraland peripheral neuropathies, diseases of the neuromus-cular junction, myopathies, and obstructive lesions of the esophagus (see Disorders that Cause Megaesopha-gus
20
44
). The following discussion focuses on several of the most common specific diseases
myasthenia gravis,a disorder of the neuromuscular junction; hypoadreno-corticism (and possibly hypothyroidism), which alterthe function of the esophageal musculature; and alltypes of obstructive lesions, which cause focal mechani-cal obstruction and possibly generalized esophageal dis-tention.
Myasthenia Gravis 
Myasthenia gravis is a common cause of secondary megaesophagus in dogs and, although rare in cats, hasbeen reported to cause proximal esophageal dilatation.
45
Myasthenia gravis can be either congenital or acquired,and both can result in megaesophagus.
31
Because con-genital myasthenia gravis is less common, it will not beaddressed in this article. Acquired myasthenia gravis is a disorder of neuro-muscular transmission in which autoantibodies againstnicotinic acetylcholine receptors at the neuromuscular junction result in a reduction of acetylcholine receptorsand subsequent muscle weakness.
46
Two forms of ac-
The Compendium 
March 1997Small Animal
AFFERENT PATHWAY DEFECT
s
SECONDARY DISORDERS
s
MYASTHENIA GRAVIS
Central Nervous System
s
Distemper
7,20
s
Cervical vertebralinstability withleukomalacia
20
s
Brain stem lesions
20
s
Neoplasia
20
s
Trauma
20
Peripheral Neuropathies
s
Polyradiculoneuritis
20
s
Dysautonomia
,21,22
s
Ganglioradiculitis
23
s
Giant cell axonalneuropathy
24
s
Spinal muscular atrophy
25
s
Polyneuritis
26
s
Thallium toxicity
27
s
Lead toxicity
,28
s
Acrylamide toxicity
29
s
Mediastinitis
30
s
Bronchoesophagealfistula
30
s
Bilateral vagal damage
Neuromuscular Junction
s
Myasthenia gravis
,20,31–33
s
Botulism
34,35
s
Tetanus
5
s
Anticholinesterasetoxicity
36
Diagnosed in cats.
Esophageal Musculature
s
Systemic lupuserythematosus
20,37
s
Glycogen storagedisease
38
s
Polymyositis
20,39
s
Dermatomyositis
40
s
Cachexia
26
s
Trypanosomiasis
41
s
Hypoadrenocorticism
20
s
Hypothyroidism (?)
Obstructive Lesions
s
Neoplasia
s
Granulomas
s
Vascular ringanomalies
s
Strictures
s
Foreign body
Miscellaneous
s
Pyloric stenosis
,42
s
Gastric dilatation volvulus
s
Gastric heterotopia
,43
s
Pituitary dwarfism
s
Thymoma
s
Familial reflex clonus
s
Dystrophin deficiency
,44
Disorders that Cause Megaesophagus

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