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HPI 54 y/o AAM with hx of syphillis, htn, OSA and
Langerhans Cell Sarcoma with spinal cord compression s/p steroids and XRT now c/o pain and difficulty upon swallowing. Pt was originally admitted on 11/18 to MICU for spinal chord compression, treated with decadron (11/18 to 12/05) and transferred to GMED on 11/22, now has completed 2 full wks of palliative XRT (11/23-12/7) to the area of T9-12 on TCU.
HPI cont. Pt noticed that “food was getting stuck”, soon
after that he developed a burning/spasm-like pain in his throat when swallowing. Liquid or solid food makes no difference to him. Pt was started on viscous lidocaine without much improvement. + constipation, denies diarrhea, hematochezia, melena, hematemesis, SOB.
Per pt he was tested at outside facility for HIV within the last 6 months and was negative. He reports hx of syphillis > 10 yrs ago s/p treatment.
PMH Langerhans Cell Sarcoma with spinal
compression s/p decadron and palliative XRT
Syphillis Htn Erectile Dysfunction OSA
Medications Omeprazole 20 po bid Lidocaine viscous 20 q3 prn swish and spit Dilaudid 2mg q3 prn Cyclobenzaprine 10 tid prn back spasms Albuterol 2 puffs qid Es-Maalox prn Docusate Senna 2 tabs qhs prn
Physical Exam VS: 97.6, 109/61, 83, 18, 7/10 pain Gen: NAD, AAO x 4, slim AAM sitting in bed,
speaks with a faint voice Skin: no rash HEENT: PERRLA, o/p clear, no oral
ulcers/lesions, no thrush, no erythema of posterior pharynx or uvula
Neck: supple, no LAD Heart: rrr, s1s2, no murmurs
Physical Exam cont. Lungs: cta bilaterally, no wheezes Abd: soft, mild epigastric tenderness, non-
distended, na bs, no HSM Ext: no edema/cellulitis/clubbing Neuro: CN II-XII grossly intact, sensory
and motor function intact, DTR 2/2
Laboratory 12.5
2.3 116
36.2
MCV 92
69% neutrophils, 15% lymphs, 14% monos, 1% eosinophils
Anion gap panel normal, Cr 1.0
EGD (12/14/05)
There are multiple ulcers in the distal esophagus with a large linear line of ulcers tracking up the mid esophagus. Bx and brushing done.
The stomach and duodenum were normal.
Follow up ID was consulted to decide whether emperic antiviral tx is
advisable while awaiting bx/viral cx results to return Ddx included XRT-induced esophagitis, HSV and CMV.
Time course and location of the ulcers were suspicious for radiation induced ulcers. Since pt’s pain symptoms were already improving on its own without any specific tx by the time of the ID consultation, no empiric antiviral tx was recommended.
Pt’s symptoms resolved on its own 1.5 wks later. Bx results came back negative for HSV and CMV.
Overview Odynophagia = painful swallowing Suggests disruption of the esophageal mucosa
Any inflammatory process involving the mucosa of the oropharynx or esophagus or its muscle may cause odynophagia
Odynophagia is a common symptom of pill-induced esophagitis or infection of the esophagus
A muscle spasm may also lead to muscle pain odynophagia
Differential Dx of Odynophagia Pill esophagitis Infection Crohn’s involvement of the esophagus
(uncommon) Reflux esophagitis (usually not acute) Caustic ingestion Radiation esophagitis Ulcerated neoplasm (usually not acute)
Differential Dx of Odynophagia in AIDS patients Candidiasis Herpes simplex CMV Idiopathic HIV ulcers GERD Pill-induced
Differential Dx of Dysphagia Extrinsic pressure on the
esophagus Thyromegaly, left atrial
enlargement Aortic arch aneurysm Zenker’s diverticulum Cervical
lymphadenopathy Anomalous right
subclavian artery Cephalad extension of
gastric cancer
Intrinsic narrowing of the esophageal lumen Esophageal tumors Esophageal strictures
Disorders of esophageal motility Achalasia Esophageal spasm scleroderma
Infectious Esophagitis Bacteria rarely cause primary esophageal infection,
although secondary involvement by direct extension from the lung is possible
Two most common forms of infectious esophagitis: Candida HSV
Other viruses and fungi can cause esophagitis, but usually associated with immunosuppression CMV HIV
Candida Esophagitis The most common form of infectious esophagitis Predisposing conditions:
DM Abx therapy Immunocompromise Alcoholism Malnutrition Advanced age
Occasionally seen in otherwise healthy individuals Presentation usually involves odynophagia, dysphagia,
chest pain or upper GI bleeding
Diagnosis of Candida Esophagitis Esophagogram
Irregular granular or even cobblestone or “shaggy” appearance
25% will have a normal barium esophagogram EGD
Required to make the diagnosis Small raised whitish plaques Underlying mucosa is erythematous and friable
Biopsy or brush cytology Pseudohyphae
Complications of Esophageal Candidiasis Ulceration and hemorrhage Mycetoma (fungus ball)
Formed by necrotic mucosal debris Causes obstruction
Strictures Perforation Fistulas
Tracheobronchial Aortoesophageal
Treatment of Esophageal Candidiasis Oral nystatin Ketoconazole or fluconazole for more
extensive involvement or if pt is immunocompromized
Amphotericin B if evidence of systemic spread
Herpes Simplex Esophagitis Second most common form of infectious
esophagitis Presentation is similar to candida esophagitis Esophageal symptoms may be preceded by viral
URI type symptoms Herpetic mouth or skin lesions may also develop Usually found in immunocompromized pts, but
also sporadically seen in healthy young adults
Diagnosis of Herpes Esophagitis Esophagogram
Multiple, small, superficial ulcers in the upper or mid esophagus
Severe herpes esophagitis may produce extensive ulceration and plaque formation, mimicking the appearance of Candida esophagitis
EGD with biopsy and brush cytology are required to confirm the diagnosis
Brush cytology Epithelial cells at the edge of the ulcers are characterized by
multinucleation, ground-glass nuclei and pathognomonic eosinophilic “Cowdry’s Type A” intranuclear inclusion bodies
Treatment of Herpes Esophagitis
Self-limiting disease in immunocompetent individuals, so symptomatic tx only Viscous Xylocaine and PPI
In severely immunocompromised pts IV acyclovir
CMV Esophagitis Asymptomatic CMV infection is common worldwide The first clinical case of CMV esophagitis was reported in
1985 Unlike herpes esophagitis, CMV esophagitis almost never
occurs in immunocompetent patients Vast majority of affected individuals are found to have
AIDS Evidence of CMV infection may be present in other
organs such as the retina, liver, and colon Occasionally, odynophagia may become so severe pt
develop sitophobia (fear of eating) and require TPN
Diagnosisof CMV Esophagitis Esophagogram
Typically shows 1 or more giant and relatively flat ulcers, sometimes with associated satellite ulcers
EGD with biopsy and brush cytology are required to confirm the diagnosis
Brush Biopsy Infected cells contain eccentrically placed
intranuclear inclusion bodies with surrounding halos mainly found near the base of the ulcers
Treatment of CMV Esophagitis
Antiviral agents Ganciclovir
Bone marrow toxicity
Foscarnet Renal toxicity
HIV Esophagitis Believed to be caused by HIV Electron microscopy confirm presence of HIV-
like viral particles in these lesions Most pts are found to have chronic AIDS with
CD4 counts < 100 HIV esophagitis can form giant esophaageal
ulcers indistinguishable from CMV esophagitis Account for 40% of all esophageal ulcers in
AIDS pts
HIV Esophagitis continued.
Diagnosis EGD and biopsy are again required to
distinguish it from CMV esophagitis Treatment
Oral steroids
Esophagitis Associated with Immune-Mediated Disease Crohn’s disease Behçet’s syndrome Pemphigoid Pemphigus Epidermolysis bullosa Sarcoidosis Eosinophilic
gastroenteritis
Chronic graft-versus-host disease after bone marrow transplantation Generalized epithelial
desquamation of the upper and middle esophagus, sometimes with ring-like narrowings
A nonspecific esophageal motor disorder may also develop resulting in superimposed reflux esophagitis
Acid/Alkali Ingestion Acid ingestion
Superficial coagulation necrosis and eschar formation immediate chest pain and odynophagia Oral burns may produce local pain and drooling Respiratory symptoms (stridor, dyspnea and
hoarseness) if the airway is contaminated Alkali ingestion
Tends to be more injurious to the esophageal mucosa Liquefaction necrosis Thermal burns
Acid/Alkali Ingestion cont. Symptoms alone do not permit accurate prediction of the
presence or absence of esophageal injury Early diagnostic endoscopy should be considered (but not
if there is evidence of esophageal perforation) Adequate airway is imperitive NPO and IVF Empiric tx involves abx and corticosteroids, but no good
evidence documenting the efficacy Survivors tend to develop strictures because of collagen
deposition during healing. Often requires repeated esophgeal dilation
Lye-Induced Injury Lye-induced injury increases the risk of
squamous cell cancer of esophagus Typically there is a 30- to 50-year lag time Any pt with previous lye inury and new
esophageal symptoms should be promptly investigated
However periodic endoscopic surveillance is not indicated
Pill-Induced Esophagitis Common culprits
Antibiotics Tetracyclines (particularly doxycycline)
NSAIDS Highest number of reported cases is with ASA
Others KCl Quinidine preparations Iron compounds alendronate
Pill-Induced Esophagitis cont. Pts typically take meds with small amount of water and
then immediately go to bed, then wake up hrs later with severe retrosternal CP and odynophagia
Typical lesion shows a small punched out ulcer in a limited area that was conceivably in contact with a high concentration of medication released from a dissolving pill
Usually ulceration is superficial and heals in weeks; Rarely, can see deep esophageal ulcer with perforation
Late stricture formation may occur Pts with esophageal motility disorders are particularly
prone
Radiation-Induced Esophagitis Seen in up to 80% of pts receiving XRT to the
chest Use of cytotoxic chemo has an additive effect Typically chest pain, dysphagia and odynophagia
occur shortly after the initiation of therapy Late stricture formation is a common
complication Usually self-limited, treatment is symptomatic
Recommended