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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
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