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MOTILITY

DISORDERS OF
ESOPHAGUS
PROF DR OLCAY ALVER
Cerrahpaşa Medical Faculty,
Department of General Surgery
MOTILITY
DISORDERS OF
ESOPHAGUS
PROF DR OLCAY ALVER
Cerrahpaşa Medical Faculty,
Department of General Surgery
MANOMETRIC FEATURES OF
ACHALASIA
 1) APERISTALSIS or
HYPOPERISTALTISM
(incoordinated,feeble,simultaneous,and
repetetive peristaltic pattern within the 2/3 of
esophageal body)
 2)BASAL HYPERTONICITY OF LES
(pressure>45mmHg)
 3)INCOMPLETE RELAXATION OF LES
IN RESPONSE TO SWALLOWING
(<70%)
NEUROPATHOLOGY OF ACHALASIA

 Denervation of PRE-GANGLIONIC
CHOLINERGIC NERVE supply to esophagus
 Denervation of INHIBITORY( relaxing NON-
ADRENERGIC,NON-CHOLINERGIC) nerves
to LES
 Absence or degeneration of GANGLION
CELLS OF AUERBACH’S MYENTERIC
PLEXUS
 Ultrastructural alterations of VAGUS
NERVE(WALLERIAN DEGENERATION)
 Decreased and distorted motor cells of
VAGAL DORSAL NUCLEUS in brainstem
FUNCTIONAL NEUROPHARMACOLOGY OF
ACHALASIA

 Supersensitivity (excessive motor response)of LES to


CHOLINERGIC drugs-CANNON’S LAW of DENERVATION
SUPERSENSITIVITY
 Supersensitivity of LES to GASTRIN
 EDROPHONIUM (anti-cholinesterase)↑ LES pressure(=post-
gn. Cholinergic nerves to LES are intact)
 CHOLECYSTOKININ invokes a paradoxal excitatory response
of LES (=dysfunction of post-gn. inhibitory /non-adr +non-
Ch nerves)
 Marked ↓ in VIP nergic nerve fibers and NEUROPEPTID-Y
(neurotransmitters of LES relaxation)
 Marked ↓ in NITRINERGIC NEURONS(=↓ NO
concentration=inhibitory neurotransmitter)
 ACHALASIA=NİTRİNERGİC NEURONITIS,AUTO-İMMUNE DIS.?
SYMPTOMS OF
ACHALASIA
 1)DYSPHAGIA:80-100% paradoxal
dysphagia; adoption of certain manoevres to facilitate
swallowing; odynophagia
 2)REGURGITATION : 70% undigested
food,foamy mucoid saliva ; nocturnal regurgitation,and
aspiration into the respiratory tract; halitosis, foul
eructation
 3)WEIGHT LOSS : 40% sitophobia;
odynophagia; anemia ; avitaminosis ;cachexia
 4)CHEST PAIN : 30% early stage;vigorous
achalasia :odynophagia
DIAGNOSIS OF
ACHALASIA
 RADIOLOGICAL FEATURES
 Proximal esophageal dilatation
 Smoothly tapered distal end
 Fluid level in post mediastinum
 Absence of gastric air bubble
 ENDOSCOPIC FEATURES
 Esophageal dilatation+retained food
 Retention esophagitis
 Passage of scope through resistant LES
produces characteristic “pop” sensation
 Endoscopic biopsy excludes esophageal ca
 MANOMETRIC FEATURES
ACHALASIA
DIFFERENTIAL DIAGNOSIS OF ACHALASIA
achalasıa Diffuse Vigorous
SYMPTOM spasm achalasia
+ SIGN
Pain Uncommo Almost Frequent
n always
obstruction Sometime Nearly
Always s always
Regurgitat. Frequent
Retention Common Rare Frequent
Frequent Never
Dilatation Common Never Occasiona
Spasm Uncommo Frequent l
TREATMENT OF SPASTIC MOTOR
DISORDERS OF ESOPHAGUS

 PHARMACOTHERAPY
 SMOOTH MUSCLE RELAXANTS
 NITRATES ( ISOSORBIDE DINITRATE)
 CALCIUM-CHANNEL BLOCKERS
(NIFEDIPINE,VERAPAMIL)
 ANTICHOLINERGICS , SILDENAFİL
 HYDRALAZINE(ARTERİAL MUSCLE RELAXANT)
 PSYCHOTROPIC AGENTS
 BOTULİNUM TOXİN
 NON-PHARMACOLOGIC MEASURES
 REASSURANCE, BEHAVIOR MODIFICATION/BIOFEEDBACK
 ESOPHAGEAL DILATATION
 OPEN OR LAPAROSCOPIC MYOTOMY ± PARTIAL
FUNDOPLICATION ( H E L L E R + D O R procedure)
DIFFUSE ESOPHAGEAL
SPASM
 Hypertrophy and spasms of smooth musle layers of the
esophageal body,Wallerian degeneration of the vagal
fibers,denervation supursensitivity to cholinergic
compounds
 MAJOR CLINICAL SYMPTOMS
 INTERMITTENT SUBSTERNAL PAIN-varies from
slight discomfort to severe spasmodic pain mimicking
ANGINA PECTORIS with radiation to back,jaws,arms
aggravated by emotional upsets,very hot,cold,carbonated
drinks
 DYSPHAGIA / HEARTBURN /ODYNDPHAGIA /
no weight loss
MANOMETRIC FEATURES OF
DIFFUSE ESOPHAGEAL SPASM
 Synchronous,non-spesific , repetetive(at
least three peaks) peristaltic contractions
with prolonged duration (>6 sec),high-
amplitude (>120mm)
 Failure of hypertensive LES to relax
completely in 30% of the cases
 Denervation supersensitivity to
cholinergic,anticholinesterase,ergonovine
compounds
DIAGNOSIS OF DIFFUSE ESOPHAGEAL
SPASM
 RADIOLOGICAL FEATURES
 Delayed esophageal transit due to segmental
spasms, areas of narrowing , irregular
uncoordinated peristalsis described as
 “ C U R L I N G “ , “ C O R K S C R E W “ or
 “ R O S A R Y B E A D ESOPHAGUS “ and
 “PSEUDODİVERTICULOSIS“
involving the two-thirds of the esophageal body
 with coexisting small sliding hiatal hernia,
epiphrenic diverticula
 ENDOSCOPY- Normal unless reflux esophagitis or
other lesion is associated
 MANOMETRY
TREATMENT OF DIFFUSE
ESOPHAGEAL SPASM
 MEDICAL-
 Long-acting nitrates,isosorbide,ca-channel
blockers(nifedipine,verapamil)
 Bougienage,pneumatic dilatation
 SURGICAL- long esophageal
myotomy(Long HELLER operation)
 Extending from LES to aortic arch +
anterior hemifundoplication(DOR
procedure )
HYPERCONTRACTING
ESOPHAGUS
 “NUTCRACKER” / HYPERTENSIVE
ESOPHAGUS
 Hıgh-amplitude contractions(>180 mmHg)
 Prolonged duration contraction (>6 sec)
 Normal peristalsis
 HYPERTENSIVE LES
 Hıgh resting LES pressure (>45mmHg)
 Normal or incomplete LES relaxation
 Normal peristalsis
HYPOCONTRACTING
ESOPHAGUS
 INEFFECTIVE ESOPHAGEAL MOTILITY
 NONSPECIFIC ESOPHAGEAL MOTOR DYSFUNCTION
 FREQUENT NON-PROPULSIVE OR RETROGRADE
CONTRACTIONS (30% or more)
 LOW-AMPLITUDE CONTRACTIONS (< 30mmHg)
 PROLONGED DURATION CONTRACTION(>6 Sec)
 BODY PERISTALSIS WITH NORMAL LES

LOW RESTING LES PRESSURE (< 10mmHg )
PATHO PHYS IOLO GY OF
SCLE RODERMA
 NEURAL DYSFUNCTION OF ESOPHAGUS
 Normal sphincteric response to cholinergic drugs but
not to gastrin or a cholinesterase inhibitor/ loss of
intrinsic Ach mechanism(?)
 RAYNAUD’s phenomenon usually present
 Functional abnormalities precede morphologic
changes by light microscopy
 OTHER POSSIBLE PATHOGENIC MECHANISMS-
abnormal fibrotic process ; marked smooth musle
atrophy with fibrous replacement / primary muscle
disease:smooth muscle atrophy with aperistalsis /
evidence lacking vascular abnormality / Raynaud’s
phenomenon /prolonged warming time after swallow of
cold bolus
CLINICAL FEATURES OF
SCLERODERMA
 SYMPTOMS: DYSPHAGIA / HEARTBURN /
REGURGITATION / SKIN + SYSTEMIC CHANGES OF
SCLERODERMA / RAYNAUD’S PHENOMENON
 SIGNS: SKIN CHANGES / RAYNAUD’S
PHENOMENON , C R E S T SYNDROME
 Calcinosis cutis Raynaud Esophageal
involvement Sclerodactyly Telangiectasia
DIAGNOSIS OF
SCLERODERMA
 RADIOGRAPHY: aperistalsis of distal 2/3
esophagus/mild dilatation / gastroesophageal
reflux / possible peptic stricture + shortening of
distal esophagus/impaired esophageal clearence
 MANOMETRY:Upper sphincter+ 1/3 esophagus-
NORMAL / feeble or no peristalsis
(<30mmHg)in distal 2/3 esophagus / feeble or
sphincter(LES absent lower esophageal p-<10
mmHg )
 ENDOSCOPY:mildly dilated,tubular esophagus
/distal esophagus and LES remains open/ free
reflux /peptic esophagitis with possible stricture
formation(60%)
ESOPHAGEAL SCLERODERMA
(LONG TUBULER STRICTURE)
TREATMENT OF
SCLERODERMA
 MEDICAL TREATMENT
 Proton pump inhibitors/ prokinetic
drugs (metoclopramide,domperidon)
 SURGICAL TREATMENT
 Combined gastroplasty+antireflux
procedure(COLLIS-NISSEN ± BELSEY MARK IV ) /
DISTAL ESOPHAGECTOMY
replacement with a colonic or an
isoperistaltic jejunal segment
ESOPHAGECTOMY + COLONIC
INTERPOSITION

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