Jieli Li

12/29/05

Chief Complaint

Pain and difficulty on swallowing

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

History cont. All:

Codeine dizziness SH:

Denies hx of etoh, tobacco and illicit drug use FH:

NC

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

Candidiasis on EGD

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

Herpes Esophagitis on EGD

Cowdry A Intranuclear Inclusion Body in a herpetic ulcer

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

CMV Esophagitis under Microscopy

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