ESOPHAGUS / SWALLOWINGDANIEL TODD, MDESOPHAGEAL ANATOMY Outer longitudinal layer=ADVENTITIA – no serosa MUSCULARIS EXTERNA Upper 1/3 skeletal—- MID 1/3 MIXED Lower 1/3 smooth muscle Myenteric plexus of Auerbach- parasympathetic ganglion SUBMUCOSA Submucosa – myenteric plexus of Meissner MUSCULARIS MUCOSA=Inner circular layer LAMINA PROPRIA–(DERMAL EQUIVELENT) Mucosa – muscularis mucosa, stratified squamous epithelium 40 cm in length (teeth to cardia of the stomach)—-DO MEASUREMENTS FROM THE SUP INCISORS LA left vagus is anterior—LARP Angle of His- oblique angle at GE junction – in babies this angle is non existent (ie reflux) LES -lower esophageal sphincter extends 1-2cm above and below the diaphragm—PURELY FUNCTIONAL—ABOUT 3 CM TOTAL interplay of acetylcholine and gastrin STRUCTURES WHICH CONTRIBUTE TO NATURAL NARROWINGS—-UES (CP MUSCLE), AORTIC ARCH WHERE L MAINSTEM CROSSES ESOPHAGUS (TEF LEADS TO A LEFT PNEUMONIA), LEFT ATRIUM, AND LES UES = CP MUSCLE—THI INF MOST OF THE INF CONSTRICTORS—RETAINS A COSTANT TONE—-HAS DUAL INNERVATION FROM THE VAGUS (PHARYNGEAL BR.) AND THE RLN—-IS THE CULPRIT FOR ZENKERS, GLOBUS PHARYNGEUS, AND POST TEP APHONIA. ESOPHAGEAL PHYSIOLOGY SWALLOWING SWALLOW 10-15 TIMES/HOUR W.A.——1000-1500 TIMES/DAY W.A AND 50-100 TIMES WHILE ASLEEP PRIDUCE 1 L NASAL SECRETIONS AND 1.5 L OF SALIVA PER DAY Normal swallowing stages – oral, pharyngeal and esophageal Oral – voluntary Pharyngeal – involuntary NP closure, bolus advancment by BOT, sup, middle, and inf constrictors, laryngeal elevation by suprahyoid muscles, and closure of laryngeal aperature by vocal cords and synchronized CP relaxation—-LARYNGEAL ELEVATION VIA THE SUPRAHYOID MUSCLES IS VERY IMPORTANT IN DEGLUTITION TO PROTECT THE AIRWAY—-IS ALSO THE PRIMARY MECHANISM FOR DILATING THE UES TAKES 25 CM OF H2O PRESSURE IN THE HP TO OPEN THE UES TAKES 100 CM OF H2O PRESSURE IN THE MID ESOPHAGUS TO OPEN THE UES——BOTH THE UES AND LES OPEN MUCH EASIER FROM ABOVE Esophageal – involuntary Abnormalities either structrural or neurologic CN 9, 10,11, 12 Treatment: correction of stenosis, self boulenage, CP myotomy, intracordal injection or thyroplasty for laryngeal penetration, laryngectomy

SYMPTOMS AND SIGNS Odynophagia – painful swallowing “heart burn”—PYROSIS—–10% OF AMERICANS EXPERIENCE THIS DAILY—40% MONTHLY Chest pain Aerophagia- belching Rumination – regurgitates food and swallows it again Hypersalivation, PTYALISM, SIALORHEA—ACTUALLY AN UNDERESTIMATED DEFENSE MECHANISM Globus – “lump in throat”-PHARYNGEUS—-FORMERLY TERMED HYSTERICUS VOICE CHANGES OSA CHRONIC COUGH ASTHMA (REACTIVE AIRWAYS) 50% OF PEOPLE WITH THESE SYMPTOMS HAVE LPR ADENOCA IS INCREASING DRAMATICALLY IN INCIDENCE IN THE US IN WHITE MALES—NOW MAKES UP 2.2% OF ALL CANCERS—PEPSIN IS THE CULPRIT AND RELATIVE XEROSTOMIA IS EXPONENTIALLY EXASERBATING

GERD—THE DIAGNOSIS OF THE NINETIES OFTEN POST PRANDIAL OR NOCTURNAL NON PRODUCTIVE COUGH–GLOBUS PHARYNGEUS, STRESS, HORSENESS, CHRONIC THROAT CLEARING–SX WORSE IN THE AM–OTALGIA, CERVICAL ODYNOPHAGIA, NUT CRACKER ESOPHAGUS—MOST DO NOT HAVE PYROSIS HORSENESS, THROAT CLEARING, PND, DYSPHAGIA, CHOKING EPISODES, COUGH, TICKLE, GLOBUS, PYROSIS PE—-OVERWEIGHT, SMOKERS/DRINKER–ANTIDEPRESSANTS, CAFFEINE, ETOH, B BLOCKERS CISAPRIDE/REGLAN, H-2 BLOCKER, PROTON PUMP INHIBITOR ROUTINE PRECAUTIONS (HOB UP 6-8 INCHES), WT LOSS, D/C CAFFFEINE, D/C ETOH, D/C NICOTINE DO NOT EAT OR DRINK AFTER 1900 Dx—-Hx—ENDOSCOPY—COBBLESTONING–Bx THE ESOPHAGUS FOR INFLAMMATORY OR METAPLASTIC CHANGES—BRONCHOALVEOLAR LAVAGE–LIPID LAYDEN MACROPHAGES (3 DAY 2 LIFE)—-PH PROBE, BARIUM STUDY, MANOMETRY DL—POST GLOTTIC LARYNGITIS, DIFFUSE NONEYTHEMATOUS LARYNGEAL EDEMA, DIFFUSE ERYTHEMA, OR DISCRETE GRANULOMA FLEXIBLE EXAM:SUBGLOTTIC EDEMA, VENTRICULAR OBLITERATION, ERYTHEMA/HYPEREMIA, VOCAL CORD EDEMA,, DIFFUSE LARYNGEAL EDEMA, POST COMMISURE HYPERTROPHY, GRANULOMA/GRANULATION, THICK ENDOLARYNGEAL MUCOUS “STRING SIGN” ASSOC WITH SIDS, LARYNGOMALACIA,GLOBOUS, LARYNGOSPASM, REACTIVE AIRWAY Dz, ASPIRATION PNEUMONIA, LARYNGOTRACHEAL STENOSIS, ECT….

HOARSENESS—MAY NEED TO TREAT MONTHS TO OVER COME THIS!, COUGH, GLOBUS PHARYNGEUS, THROAT CLEARING, DYSPHAGIA, PYROSIS (43%) SUPINE, NOCTERNAL REFLUXERS—USUALLY HEAVY AND OLDER. PROMOTERS: EATING QHS. ETOH, TOBACCO, MINTS, CHOCOLATE, FAT, HIATAL HERNIA HIATAL HERNIA REDUCES LES COMPETENCE BY 33 % MENDELSOHN=S SYNDROME—-ASPIRATION DUE SECONDARY TO GERD—70% RIGHT SIDED PNEUMONITIS DELAHANTY=S SYNDROME—LARYNGITIS SECONDARY TO GERD Rx: BEHAVIOR, PHARMICOLOGIC—OMEPRAZOLE (PRILOSEC) 20-40MG Q D—LANSOPRAZOLE (PREVICID) 30 MG PO Q D, CISAPRIDE(PROPULSID) 20 MG P.O Q D(REGLAN (METACLOPROPAMIDE) CAN INDUCE PARKINSONISM), SURGERY (NISSEN)—COST EFFECTIVE IF YOU ARE GIONG TO REQUIRE 10 YEARS OF PPI’S

LPR (LARYNGOPHARYNGEAL REFLUX)—THE DIAGNOSIS OF THE NEW MILLENIUM A TOTALLY DIFFERENT DIAGNOSIS THAN GERD UPRIGHT DAYTIME REFLUXERS—USUALLY THINNER AND YOUNGER PEPSIN IS THE CULPRIT—-AN ENZYME WHICH IS ACTIVATED BELOW PH OF 4 (ACIDIC) AND DOES TISSUE DAMAGE MUCH MORE PREDISPOSED TO XEROSTOMIA—BICARB (HCO) IN SALIVA NEUTRALIZES AND CLEARS THE ACIDAND PEPSIN IN THE PHARYNX. RX: CONSERVATIVE MEASURES—-DIET, EXERCISE, SUGARLESS GUM, MMW(WITH CARAFATE), HOB UP, HYDRATION, GUIFENESIN, PPI’S BID

EXAMINATION

OTOLARYNGOLOGISTS ARE REALLY INTERESTED IN TRANSFER DYSPHAGIA—GETTING THE BOLUS TO THE ESOPHAGUS MBS—MOD BARIUM SWALLOW A VIDEOFLUROGRAPHIC STUDY = GOLD STANDARD—-REALLY STUDIES THE OROPHARYGEAL ASPECT OF SWALLOWING FEES -FEESST functional endoscopic evaluation of swallowing (TEMPLER TEST) +(SENSORY TESTING) MAY BE BETTER THAN A MBS–(VESS–VIDEO ENDOSCOPIC SWALLOWING STUDY)—TOUCH AROUND TO TEST THE AFFERENTS–OR USE PREMEASURED PUFFS OF AIR, ASSSSSS@ AND WATCH FROM THE NC FOR VPI, MODIFIED VALSALVA TO VISUALIZE HP, SALTINE CRACKERS SWALLOW, VANILLA PUDDING SWALLOW, H2O SWALLOW (START SOLID TO LIQUID) WHILE WATCHING FROM ABOVE—–@EEEEEEE@ ELEVATES THE LARYNX INTO VIEW

GLUCOSE OXIDASE STRIP TEST DL ESOPHAGOSCOPY

CT,MRI

TN99 NUC SCAN

Barium swallow—REALLY FOCUSES ON THE ESOPHAGUS, cine study, cytologic, Berstein’s test (acid perfusion test), 24 hour pH monitoring, balloon distention, motility (manometrics – LES, body of esophagus, cricopharyngeus), esophagoscopy (flexible or rigid) FUNCTIONAL MOTOR DISORDERS Esophageal spasm— DIFFUSE ESOPHAGEAL SPASM=CORKSCREW ESOPHAGUS-“CORKSCREW SIGN”–NON-PERISTALTIC SIMULTANEOUS CONTRACTIONS OF PRIMARILY SMOOTH MUSCLE PERISTALTIC ESOPHAGEAL SPASM=NUTCRACKER ESOPHAGUS—-MOST COMMON DISORDER OF PTS WITH NON CARDIAC CP—ACID REFLUX STIMULATES GE JUNCTION—UES SPASM—-MAY TRY CA CHANNEL BLOCKERS, NITRATES, ANTICHOLINERGICS, DILATION, LONG MYOTOMY Presbyesophagus – incoordination of sphincter, reduced peristaltic function Ganglion degeneration – elderly achalasia, chagas disease Irritant – GER, corrosive Obstruction – tumor or stricture Neuromuscular disorder – DM alcoholism, ALS Idiopathic Spasm Cricopharyngeal dysphagia Analogous to achalasia – failure of sphincter to relax Diseases – idio, polio, thyrotoxic myophathy, L or R RLN paralysis, post surgical, CVA, ALS——MAY TRY A CP MYOTOMY OR BOTOX PRIOR TO A SEPARATION PROCEDURE Achalasia (megaesophagus) Disorder of motility, aperistalsis, eso dilation and failure of LES to relax Degeneration of Auerbach’s plexus IN LES GET “BIRD BEAK SIGN” ON BARIUM STUDY Etiology – CA, chaga disease—IN BRAZIL, post vagotomy, CVA, DM, AGE Rx: HELLER’S MYOTOMY, CALCIUM CHANNEL BLOCKERS, BOTOX, NITRATES.

DIVERTICULUM Killian’s dehiscence Btwn cricopharyngeus inf and the INF CONSTRICTORS superiorly Laimer-Haeckerman space btwn CP sup and circular fiber of eso inferiorly Killian – Jamieson space lateral dehiscence btwn CP and eso muscle through which the RLN and artery pass HYPOPHARYNGEAL (PHARYNGOESOPHAGEAL) AZENKER=S@ PSUEDO PULSION DIVERTICULUM FIRST DESCRIBED BY LUDLOW 1769, CLARIFIED BY ZENKER 1874 JUST SUP TO TRANSVERSE FIBERS OF THE CRICOPHARYNGEUS (CP)—IN INF ASPECT OF KILLIAN=S DEHISSANCE (DEHISSANCE IN INF CONSTRICTORS)—DESCRIBED BY BELL OFTEN COINCIDE WITH REFLUX—-HIATAL HERNIA—LEADS TO CP SPASM AND PULSION DIVERTICULUM USUALLY LEFT OF MIDLINE ON POST HYPOPHARYNGEAL WALL –LESS FASCIAL SUPPORT AND MORE ROOM TO THE CAROTID SHEATH A PULSION DIVERTICULUM A PSEUDO DIVERTICULUM—-ONLY THE MUCOSA VS A TRUE (ALL LAYERS) DIVERTICULUM —TRACTIONS ARE TRUE ( VS LATERAL HYPOPHARYNGEAL DIVERTICULUM [CAN BE B], EPIPHRENIC PULSION DIVERTICULUM USUALLY RIGHT OF MIDLINE JUST OVER LES, MIDTHORACIC ATRACTION@ DIVERTICULUM IS USUALLY LEFT OF MIDLINE AND ASSOC. WITH HILAR ADENOPATHY[BRONCHOGENIC CA, SARCOID, TB]) 60% PTS > 60 HAVE SOME DEGREE OF IT GRADUAL ONSET OF ATRANSFER@ DYSPHAGIA—-MAY BE YEARS GLOBUS SENSATION AT SUPRASTERNAL NOTCH REGURGITATION AFTER MEALS—RUMINATION ASPIRATION—POST PRANDIAL COUGH, PNEUMONIA HALITOSIS Dx: MOD BARIUM SWALLOW, FLEX FIBEROPTIC NASOPHARYNGOSCOPY WITH REVERSE MUELLER MANUEVER Rx: OBSERVATION, DIETARY MODIFICATION, EXTERNAL APPROACH: EXCISION, PEXY, CP MYOTOMY (HIGH RISK TO RLN), ENDOSCOPIC CP MYOTOMY ADOHLMAN PROCEDURE@ WITH KTP LASER OR ENDOSCOPIC STAPLING WITH US SURGICAL ENDOSCOPIC IGA STAPLER—MAY HAVE TO DEAL WITH APEX OF WOUND WITH SUTURES COMPLICATIONS INCLUDE—RLN PARALYSIS, DENTAL, PERF—MEDIASTINITIS DOHLMAN PROCEDURE—GUSTA DOHLMAN (1960)

HAVE PRE-OP CXR AND EKG KEFZOL OCOR? LASER WRAP TUBE—-EYEWEAR GET KTP LASER UP—–CONTINUOUS MODE AT 6 WATTS START WITH DL—-WEERDA OR DIVERTICULOSCOPE STEROIDS AND ABX MAY MASK AN EARLY MEDIASTINITIS—–PROBABLY AVOID HAVE KTP OR CO2 LASER UP CONSIDER ENDO IGA 30 –3.5 STAPLER—-WORKS WELL HAVE PT IN CLINIC OPEN MOUTH AND EXTEND THEIR NECK PUT IN NG TUBE INTRA-OP—MAY DO INITIALLY OR CONFIRM WITH ESOPHAGOSCOPE—CONSIDER LUMEN FINDERS KEEP NPO OVER NIGHT DON’T FORGET TEETH GUARD PUT IN DIVERTICULOSCOPE, LIFT UP CRICOID, FIND ESOPHAGUS WITH LUMEN FINDER GET POST OP CXR (NEED NOT BE ACUTE)—LOOKING FOR PNEUMOMEDIASTINIM ECT.. WATCH POST OP VS CAREFULLY (TEMP, HR, RR) PLEURODYNIA, ECT…. Mid esophageal diverticuli Level of pulmonar hilum–TRACTION 7% of diverticuli Epiphrenic Often on right, above the cardio eso junction 13% Intra luminal dilated excretory ducts, middle aged seen in common with stricture or candidiasis hiatal hernia – stomach passes through the normal eso hiatus above diaphragm sliding and paraesophageal (sliding more common) sandifer syndrome – contorsions of neck to alleviate pain, seen in children DYSPHAGIA Oral, pharyngeal, or esophageal dysfunction Diseases with dysphagia INFLAMMATORY ETIOLOGY: ie viral infection (EBV), tonsillitis, thrush, retropharyngeal abscess, Vincent’s angina CMV, HSV, NSAIDS—-GIANT ULCERS IN THE ESOPAGUS LYMPHOMA, KAPOSIS, THRUSH ACTINOMYCOSIS, TB AND CROHNS PRESENT WITH MUCOSAL SINUS TRACTS AND FISTULAE BULLOUS LESIONS WITH PEMPHIGUS, PEMPHIGOID, AND EPIDERMAL BULLOSA RA—PROBLEMS WITH THE ODONTOID—C1, C2—CAN HAVE SLOW PERISTALSIS AND REFLUX AND RHEUMATOID NODULES IN THE AERODIGESTIVE TRACT CELIAC Dz = GLUTEN SENSITIVE ENTEROPATHY GERD/REFLUX–20%–@THE Dx OF THE 90’S@ NON-INFLAMMATORY: MEDS: TETRACYCLINE, VIT C , DOXYCYCLINE ANTIDEPRESSANTS—GLOBUS DM—-HYPOMOTILITY, REFLUX AND DELAYED GASTRIC EMPTYING HYPOTHYROIDISM, AMYLOID—-GLOSSOMEGALLY Plummer vincent syndrome Polio CVA MS, Myasthenia gravis MD Dermatomyositis, scleroderma, reynauds, SLE Tumors benign and malignant Diverticulum, rings, webs Psycological ETOH
FAMILIAL DYSAUTONOMIA PRESBYESOPHAGUS ALS (AMYOTROPIC LATERAL SCLEROSIS)—(LOU GHERRIG=S Dz) ALS —–MAY BENEFIT FROM CP BOTOX OR MYOTOMY AN IDIOPATHIC MOTOR SYSTEMS Dz—THE MOST COMMON PROGRESSIVE MOTOR NEURON Dz MAINLY (90%) SPORATIC, 10% AUTO D (HEREDITARY) UPPER MOTOR NEURON FINDINGS IN THE LE=S LOWER MOTOR NEURON FINDINGS IN THE UE=S—–SYMMETRIC WEAKNESS OF HANDS AND ARMS INITIALLY FATIGUE—-THEN WEAKNESS—–FINALLY ATROPHY CAN OFTEN PRESENT INITIALLY WITH BULBAR TYPE SYMPTOMS—-PND AND ILL DESCRIBED DYSPHAGIA
OCULAR MOTILITY IS SPARRED TONGUE FASCICULATIONS DYSPHAGIA (MAY BE HELPED BY BOTOX OR CP MYOTOMY) VPI, HOARSENESS, DYSARTHRIA EMOTIONAL LABILITY 50% DIE WITHIN 3-5 YEARS DEMISE IS USUALLY DUE TO PULM INFXNS DUE TO LACK OF ADEQUATE PULM TOILET TRAGIC AS DEMENTIA IS NOT ASSOC AND INTELLECT AND AWARENESS REMIAN INTACT Dx: Hx, PE, EMG Rx: SUPPORTIVE (TRH HAS BEEN TOUTED IN THE PAST AS HELPFUL)–BOTOX OR CP MYOTOMY POLYMOSITIS—-1/3—DERMATOMYOSITIS(ASSOC. SKIN RASH) CHRONIC IDIOPATHIC AUTOIMMUNE INFLAMMATORY MYOPATHY WITH PROXIMAL MUSCLE WEAKNESS, TIREDNESS, AND WASTING OTHER INFLAMMATORY MYOPATHIES CAN BE INFECTIOUS(TRICHINOSIS) ATIRED CLIMBING THE STAIRS@–MYOGENIC (STRIATED MUSCLE) USUALLY LEADS TO PROX LIMB WEAKNESS AARMS TIRED DOING HAIR@–FIBRILLATION POTENTIALS ON EMG BIMODAL (5-15) AND (40-60) FEMALE 2:1 GOTTRON=S PAPULES = PATHOGNEUMONIC ERYTHEMATOUS PLAQUES ON DORSAL KNUCKLES VIOLACEOUS HELIOTROPE RASH UNDER THE EYES 1/3 OF PTS HAVE UPPER ESOPHAGEAL AND PHARYNGEAL DYSMOTILITY–UPPER 1/3 OF THE ESOPHAGUS (VS LOWER 2/3 IN SCLERODERMA) DYSARTHRIA, DYSPHAGIA, NASAL REGURGE, ASPIRATION, HOARSENESS, SOB, TONGUE WEAKNESS –NOT FASCICULATIONS ANTI JO-1 Ag Ab (IgG) HIGH CPK, LDH-5, AND ALDOLASE (MUSCLE ENZYMES) FIBRILLATION POTENTIALS ON EMG ASSOC WITH ANOTHER MALIGNANCY 9-14%—LUNG, PROSTATE, OVARY, UTERUS, BREAST ASSOC WITH OTHER AUTOIMMUNE Dz–SLE, SCLERODERM Rx: SYMPTOMATIC, STEROIDS, MTX, CLOSE OBSERVATION Polymyositis Striated muscle Proximal muscle weakness Skin rash – dermatomyositis Manometric – decreased upper eso sphincter pressure, skeletal muscle involved SCLERODERMA = PSS (PROGRESSIVE SYSTEMIC SCLEROSIS) AN IDIOPATHIC SYSTEMIC AUTOIMMUNE Dz WITH A VARIABLE COARSE FEMALE 3:1 ONSET 30-50 (USUALLY < 40) WORSE Px IN BLACKS AND MALES BILAT SYMMETRICAL STIFFNESS AND THICKNESS IN THE SKIN BASICALLY PT DIES BACK FROM A PERIPHERAL VASCULAR INSUFFICIENCY (VASCULITIS) ABNL RATE OF SYNTHESIS AND DEPOSITION OF NL COLLAGEN—PRIMARILY AFFECTS CT AND BV=S—LOSS OF 80% OF CAPILLARIES IN INVOLVED SKIN ANDORGANS—-FIND FIBROSIS AND CONTRACTURE ON ESOPHAGOSCOPY —-SMOOTH MUSCLE REPLACED FIBROSIS “STOVE PIPE” APPEARANCE OF STIFF ESOPHAGUS ON BARIUM STUDY NAIL FOLD CAPILLARY CHANGES—FINGER TIP ULCERS INTESTINAL STASIS AND BACTERIAL OVERGROWTH (BLIND LOOP SYNDROME)—STEATORHEA (>6MG FAT / DAY IN THE STOOL) RAYNAUD=S PHENOM NEPHROCALCINOSIS HTN—ARTERITIS 50% ABNL EKG=S TELANGIECTASIA ON THE HARD PALATE—RARE EPISTAXIS -TIGHT FACIAL SKIN–TIGHT SKIN –THIN LIPS–INABILITY TO OPEN THE MOUTH IS THE INITIAL COMPLAINT IN 20%–VERTICLE PERIORAL FURROWS– DRY SKIN—RESORBTION OF MANDIBULAR ANGLES TRISMUS—DYSPHAGIA PROGRESSIVE DYSPHAGIA—WT LOSS (52%)—-LOSS OF CONTRACTION OF DISTAL 2/3 OF ESOPHAGUS(VS DERMATOMYOSITIS-POLYMOSITIS = UPPER 1/3)—DILATED AND PATULOUS LES—LEADS TO REFLUX AND SUBSEQUENT BREAK DOWN—–BLEEDING, STRICURE FORMATION (HOARSENESS AND PYROSIS)—INCREASED INCIDENCE OF BARRETT=S—-ADENOCA LES INCOMPETENCE—AEROPHAGIA (BURPING) = ASCLERODERMA BARK@ OTHER CAUSES OF ESOPHAGEAL DYSMOTILITY = ETOH/DM–NEUROPATHY, SLE, RAYNAUD=S, CHAGAS DZ, PRESBYESOPHAGUS LAB: HIGH ESR, MILD ANEMIA, ANA, HYPERGAMMAGLOBULINEMIA, POS RF, EKG CHANGES, POS, ANTI-SCL-70 DNA TOPOISOMERASE I, ANTI-CENTROMERE AB VARIANTS: CREST VARIANT CALCINOSIS RAYNAUD=S (TONGUE BLANCHING WITH DYSARTHRIA)
ESOPHAGEAL DYSMOTILITY SCLERODACTALY TELANGIECTASIA THIBIERGE-WEISSENBACH SYNDROME EXTENSIVE SUB-Q CALCINOSIS MORPHEA OR LINEAR SCLERODERMA(LIMITED TO SKIN) LOCALIZED/DISCRETE WELL DEMARKATED IVORY PLAQUES WITH VIOLACEOUS BORDERS ON THE SKIN Rx: PRIMARILY SUPPORTIVE MANAGE HTN AGGRESSIVELY, OBSTAIN FROM TOBACCO, ELEVATE HOB(REFLUX PRECAUTIONS), ABX (TETRACYLCLINE) TO COMBAT BACTERIAL OVERGROWTH AND MALABSORBTION, D-PENICILLAMINE TO PREVENT COLLAGEN CROSS-LINKING, INTRA-ARTERIAL RESERINE TO COMBAT PERIPHERAL VASOCONSTRICION, AND OTHER SYMPTOMATIC TREATMENTS STEROIDS ARE LARGELY UNEFFECTIVE Scleroderma 60% symptomatic dysphagia Raynauds Reflux – 40% may develop stricture because of GER Aperistalsis of lower 2/3 is smooth / normal upper skeletal function Decrease in LES pressure PLUMMER-VINSON SYNDROME—JAMA (PVS)—PATTERSON-KELLY-BROWN SYNDROME (LANCET)—SIDEROBLASTIC DYSPHAGIA—SIDEROPENIC DYSPHAGIA DYSPHAGIA—IDA—UPPER ESOPH WEBS ALONG WITH THE PREDISPOSIITON FOR MALIGNANCY HIGH INCIDENCE WITH SCANDINAVIAN DESCENT PRIMARILY NORTHERN HEMISPHERE FEMALE 9:1 COMMONLY ASSOC. WITH HYPOTHYROIDISM USUALLY AGE 20-50 90% OF PTS EDENTULOUS 50% INCIDENCE OF MULT CIRCULATING ANTIBODIES HIGH INCIDENCE (UP TO 50%) OF POST CRICOID (PARTY WALL) AND CERVICAL ESOPHAGEAL CARCINOMAS (ALSO OP/OC) DYSPHAGIA (86% UPPER ESOPHAGEAL/PHARYNGEAL WEBS)—ATROPHIC DEGENERATION OF PHARYNGEAL AND ESOPHAGEAL MUSCULATURE BLUE SCLERA ACHLORHYDRIA (35%) ATROPHIC GASTRITIS (40%) PERLECHE = ANGULAR CHELITIS/CHEILOSIS = FISSURES AT THE CORNERS OF THE MOUTH ATROPHIC GLOSSITIS–ASH GRAY ORAL MUCOSA SPLENOMEGALLY (IDA) IRON DEFICEINCY ANEMIA MICROCYTIC, HYPOCHROMIC, ANISOCYTOSIS (RDW>14) PICA (COMPULSIVE CONSUMPTION OF NON-NUTRITIVE SUBSTANCES)—PAGOPHAGIA (ICE) KIOLONYCHIA (SPOON NAILS)–FURROWED FINGER AND TOE NAILS PALLOR, TACHY Dx = MODIFIED BARIUM SWALLOW, CBC WITH PBS Plummer Vincent syndrome 90% women Fe def anemia Upper eso web Hypothyroidism Glossitis, dysphagia Tx – fe replacement, dilation Malignancy risk – post cricoid SCCA 15% Esophagitis Barrett’s esophagus -gastic mucosa in lower eso instead of squamous – adenoca Barrett’s ulcer RINGS AND WEBS Rings Schatzki’s ring —CONCENTRIC WEBLIKE NARROWING AT THE G-E JUNCTION IN 6-14% OF BARIUM SWALLOWS—-IF LUMEN LESS THAN 13 MM–DYSPHAGIA TO SOLIDS GE JUNCTION lower eso ring COVERED WITH SQUAMOUS EP SUP AND GASTRIC MUCOSA INF Incidence is 6-14% only 1/3 symptomatic Webs Web – aberrant structure of squamous mucosa anywhere in eso—-TOTALLY SQUAMOUS COVERED
Cervical web – iron defiency Webs and hypopharyngeal CA – Usu ant eso MAY DILATE EITHER—MALONEY = TAPERED——-HURST = BLUNT TIP C RENNER TEP SYNDROMES Boerhaave syndrome–A YOUNG PRINCE WHO PERFED OUT DURING A PURGE AFTER A FREQUENT BINGE Tear through 3 layers of eso just above diaphragm, L 90% Mallory – weiss – prolonged forceful vomiting – bleeding—VOMIT THEN BLEED dysphagia lusora (Bayford syndrome) – anomolous R subclavian artery which originates from the decending aorta instead of the inominate artery – TRAVELS BEHIND THE TRACHEA—USUALLY FOLLOWING A retropharyngeal course into right arm right RLN goes directly into the larynx not around subclavian–ASSOC. WITH NONRECURRENT LARYNGEAL NERVE—INTERMITTENT DYSPHAGIA AND WT LOSS NL SCA TAKES OFF BCT AND TRAVELS ANT TO THE TRACHEA CERVICAL SPONDYLOSIS—DEGENERATIVE DZ OF THE C SPINE—CAN PREDISPOSE TO CERVICAL OSTEOPHYTES AND RESULTANT DYSPHAGIA DIFFICULT TO PROVE CAUSE AND EFFECT FORESTIER=S DISEASE—DISH–DIFFUSE IDIOPATHIC SKELETAL HYPEROSTOSIS (ANKYOSING HYPEROSTOSIS) AN OSTEOPHYTIC HYPEROSTOSIS OF THE ANT CERVICAL VERTEBRAE SWOOPING INCISION—–DISSECT DOWN ANT BORDER OF THE SCM—PULL CAROTID SHEATH CONTENTS POST—-PULL VISCERAL STRUCTURES ANT—BOVIE LONG LIG— PERIOSTEAL ELEVATOR—DRILL OFF OSTEOPHYTE—PUT IN AN ESOPHAGEAL DILATOR—-DO A CP MYOTOMY—-CLOSE OVER A #10 JP—–PUT A HARD C-COLLAR ON — KEEP NPO FOR SOME TIME—PROBABLY NO ABX.—-GREAT CASE MENDELSOHN=S SYNDROME—-ASPIRATION DUE SECONDARY TO GERD—70% RIGHT SIDED PNEUMONITIS DELAHANTY=S SYNDROME—LARYNGITIS SECONDARY TO GERD IATROGENIC Iatrogenic perforation Sx: sore throat, tachycardia, temp, subcut emphysema Esophageal Foreign body Commonly AT THE UES (CP)–95%—–AORTIC KNOB, LES CEA ANT CERVICLE FUSION POST LARYNGEAL SURGERY ASPIRATION—SUPER SUPRAGLOTTIC SWALLOW (VOLUNTARY BREATH HOLDING) REGULAR SUPRAGLOTTIC SWALLOW MENDELSSOHN MANEUVER=MANUALLY ELVATING THE LARYNX NEOPLASM Leiomyomata – benign most common—(INTRAMURAL!) GET MRI FOR THE DIAGNOSIS Carcinoma – adeno and squamous—PRESENT USUALLY WITH PAINLESS DYSPHAGIA 4% of CA deaths males 5/1 no genetic Pre disposing – plummer vincent syn, lye ingestion, esophagitis Location – lower 50%, mid 30%, upper 10-30% CONGENTIAL Tracheoesophageal fistula—-GET L PNEUMONIA (WITH L MAINSTEM) 1/3000 87% – dilated upper pouch ends blindly with lower segment attached to trachea 8% – blind upper and lower pouch – no connection to trachea 4% – H type – true fistula with out atresia <1% – upper and lower eso segmetns open independently into trachea 16% have hydramnios Diagnosis – catheter unable to pass > 9-13cm, GET CXR— Right upper lobe pneumonia, marked air filling the stomach on film 60 -80% survive and do well VATER SYNDROME VERTEBRAL ANOMALIES, VSD ANAL ATRESIA CARDIAC TEF ESOPH ATRESIA RENAL DEFECTS
RADIAL LIMB DYSPLASIA dysphagia lusora (Bayford syndrome) – anomolous R subclavian artery which originates from the decending aorta instead of the inominate artery – retropharyngeal course into right arm right RLN goes directly into the larynx not around subclavian Chalasia – reflux in infants PLC Duplication Rings Webs diaphragmatic hernias Pleuroperitoneal (Bochdalek’s) – posterior Retrosternal (Maorgagni’s) – anterior BURNS/CAUSTIC INGESTION REALLY 2 TYPES OF INSULTS—-KIDS (SMALL QUANTITY) MUCH LESS OF AN ENTITY SINCE CHEVALEIR JACKSON FAMILIARIZED THE NATION WITH SAFETY RECS—AND ADULTS (MASSIVE SUICIDAL QUANTITY) 2 GOALS OF THE PRACTITIONER—DONT GET BLAMED FOR THE SHORT TERM DISASTERS AND MINIMIZE THE LONG TERM COMPLICATIONS Hx EXACT TYPE AND QUANTITY OF THE INGESTION -SEND PARENTS HOME TO GET THE PACKAGING CALL POISON CONTROL BASE (WORSE)–LIQUIFACTION NECROSIS (BLEECH, LYE(95% SODIUM HYDROXIDE)—DRANO, AMONIA, ELECTRIC DISHWASHER SOAP, HAIR RELAXER)—-ALSO DISK BATTERIES—BEGIN TO EVOKE DAMAGE IN HOURS ACID—-COAGULATION NECROSIS PE ALWAYS EXAMINE THE PT THOUROUGHLY—–NOTE APPEARANC OF OC AND OP—AND SKIN OF FACE MAY HAVE MAX SWELLING AND REQUIRE INTUBATION FROM 1-5 HOURS NOTE DROOLING, ODYNOPOHAGIA, CHEST PAIN, ACUTE ABDOMEN (PERF) MAY TRY FLEXIBLE EXAM OF AIRWAY AND HP 20% WITH NO OC BURN WILL HAVE ESOPHAGEAL BURNS BARIUM STUDY WILL SHOW ATONIC DILATED ESOPHAGUS—NOT INDICATED EARLY esophagoscopy within 24-48 hours (TODAYS BLEACHES NOT MORE THAN 6% SODIUM HYPOCHLORITE—–PROBABLY DO NOT REQUIRE ENDOSCOPY)) Rx: ADMIT, NPO, CXR, IVF, steroids, IV ABX, IV ANTACIDS MANAGE EXPECTANTLY IF INSULT MORE THAN 48 HOURS AGO IRRIGATE OC AND OP WITH LARGE AMOUNTS OF WATER —MAY DRINK MILK OF WATER FREELY—DO NOT INDUCE VOMITING USING AN ACID SUCH AS CITRUS JUICE TO NEUTRALIZE A BASE CREATES AN EXOTHERMIC RXN—-PROBABLY NOT DANGEROUS BUT NOT ADVOCATED REMOVE ALL CLOTHES WHICH ARE CONTAMINATED ESOPHAGOSCOPY—-@ALL CAUSTIC INGESTIONS GET SCOPED@—-UNLESS—LESS THAN 1 HOUR POST INGESTION, MORE THAN 48 HOURS POST INGESTION, KNOWN AGENT WHICH ISN=T SO CAUSTIC (BLEACH), PTS WHO HAVE BEEN ON HIGH DOSES OF STEROIDS, AND SEVERE HP OR SUPRAGLOTTIC BURNS FLEXIBLE VS RIDGID? IF LESS THAN 1 HOUR—ERYTHEMA—-NOT VERY TELLING Ø 1 HOUR—SEE SHAGGY AREA–BURN—-STOP WHEN YOU SEE THE 1ST BURN—IMMEDIATELY PLACE NG TUBE?—-PROBABLY A GOOD IDEA SUCRULFATE DRIP THROUGH A SECOND SUP PLACED NG TUBE MAY BE A GOOD IDEA P.O AMOX ELIXIR TREATS TOPICALLY ABX (CLEOCIN 25 MG/KG/DAY), STEROIDS(PREDNISONE 2MG/KG/DAY)—PROBABLY HELP PREVENT STRICTURE FORMATION—ALSO MAY MASK PERFERATION CLINICALLY (HPD AND TEMP), ANTACIDS(PROTON PUMP INHIBITOR) AND NPO—-PRAY—-PROBABLY–USE TPN–AVOID ANY ENTERAL STIMULATION (REST THE GUT)—FREELY CONSULT MANY EXPERTS—SHARE THE BLAME ALL VERY CONTROVERSIAL—-SOME LITERATURE ADVOCATES ENDOSCOPY ON ONLY SYMPTOMATIC INDIVIDUALS AIRWAY IS YOUR BIGGEST CONCERN RESULTS: Negative – FU in 2 weeks if asymptomatic Barium swallow if symptomatic Positive—-PHOTODOCUMENT TO SHOW CONSULTANTS Do not proceed past point of burn, IMMEDIATELY INSTITUTE abx, steroids
NG controversial < 24 hours /direct visualization Weakest point IS at 5 – 8 days Scar at 6 weeks REPEAT ESOPHOGRAM Q 3 WEEKS IF PRESENT AFTER 48 HOURS—CXR AND BARIUM ESOPHAGRAM MAY NEED DILATIONS—-NO STEROIDS AS A RULE TEMPLER WOULD ADMIT—-CONSULT, NPO, TPN, NG TUBE, STEROIDS, IV ANTACIDS, SCHEDULE FOR ENDOSCOPY IN 24-36 HOURS—DON=T BE A COWBOY AND DISCHARGE THEM UNTIL YOU ARE SURE THEY ARE OUT OF THE WOODS! GERD—THE DIAGNOSIS OF THE NINETIES FB—95% FB FOUND AT THE CP (UES) COINS AND DISKS WILL BE IN THE CORONAL PLANE ALWAYS GET A PA AND LAT CXR——-5% INCIDENCE OF A SECOND FOREIGN BODY
MAY PRESENT AS CROUP LIKE Sx AS THEY AGREVATE THE POST MEMBRANOUS TRACHEAL WALL REMOVE ALL DEBRIS—PHOTO DOCUMENT—–NOTE STATUS OF THE MUCOSA DO A BRONCH TO EVAL MEMBRANOUS TRACHEA ANTACIDS MAY BE HELPFUL—-KEEP NPO FOR SOME TIME—-THEN ADVANCE TO LIQUIDS PROBABLY HOLD ON STEROIDS AND ABX TO FOLLOW HPD AND TEMP AND CLINICAL STATUS OF PT