Transcript Morning Report

Jieli Li
12/29/05
Chief Complaint
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Pain and difficulty on swallowing
HPI
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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.
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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
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Langerhans Cell Sarcoma with spinal
compression s/p decadron and palliative
XRT
Syphillis
Htn
Erectile Dysfunction
OSA
Medications
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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.
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All:
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SH:
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Codeine  dizziness
Denies hx of etoh, tobacco and illicit drug use
FH:
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NC
Physical Exam
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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.
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Lungs: cta bilaterally, no wheezes
Abd: soft, mild epigastric tenderness, nondistended, 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)
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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
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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
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Odynophagia = painful swallowing
Suggests disruption of the esophageal mucosa
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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
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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
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Candidiasis
Herpes simplex
CMV
Idiopathic HIV ulcers
GERD
Pill-induced
Differential Dx of Dysphagia
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Extrinsic pressure on the
esophagus
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Thyromegaly, left atrial
enlargement
Aortic arch aneurysm
Zenker’s diverticulum
Cervical
lymphadenopathy
Anomalous right
subclavian artery
Cephalad extension of
gastric cancer
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Intrinsic narrowing of the
esophageal lumen
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Esophageal tumors
Esophageal strictures
Disorders of esophageal
motility
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Achalasia
Esophageal spasm
scleroderma
Infectious Esophagitis
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Bacteria rarely cause primary esophageal
infection, although secondary involvement by
direct extension from the lung is possible
Two most common forms of infectious
esophagitis:
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Candida
HSV
Other viruses and fungi can cause esophagitis, but
usually associated with immunosuppression
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CMV
HIV
Candida Esophagitis
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The most common form of infectious esophagitis
Predisposing conditions:
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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
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Esophagogram
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EGD
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Irregular granular or even cobblestone or “shaggy”
appearance
25% will have a normal barium esophagogram
Required to make the diagnosis
Small raised whitish plaques
Underlying mucosa is erythematous and friable
Biopsy or brush cytology
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Pseudohyphae
Candidiasis on EGD
Complications of Esophageal
Candidiasis
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Ulceration and hemorrhage
Mycetoma (fungus ball)
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Formed by necrotic mucosal debris
Causes obstruction
Strictures
Perforation
Fistulas
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Tracheobronchial
Aortoesophageal
Treatment of Esophageal Candidiasis
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Oral nystatin
Ketoconazole or fluconazole for more
extensive involvement or if pt is
immunocompromized
Amphotericin B if evidence of systemic
spread
Herpes Simplex Esophagitis
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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
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Esophagogram
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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
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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
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Self-limiting disease in immunocompetent
individuals, so symptomatic tx only
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Viscous Xylocaine and PPI
In severely immunocompromised pts
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IV acyclovir
CMV Esophagitis
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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
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Esophagogram
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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
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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
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Antiviral agents
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Ganciclovir
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Bone marrow toxicity
Foscarnet
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Renal toxicity
HIV Esophagitis
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Believed to be caused by HIV
Electron microscopy confirm presence of HIVlike 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.
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Diagnosis
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EGD and biopsy are again required to
distinguish it from CMV esophagitis
Treatment
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Oral steroids
Esophagitis Associated with
Immune-Mediated Disease
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Crohn’s disease
Behçet’s syndrome
Pemphigoid
Pemphigus
Epidermolysis bullosa
Sarcoidosis
Eosinophilic
gastroenteritis
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Chronic graft-versus-host
disease after bone
marrow transplantation
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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
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Acid ingestion
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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
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Tends to be more injurious to the esophageal mucosa
Liquefaction necrosis
Thermal burns
Acid/Alkali Ingestion cont.
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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
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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
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Common culprits
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Antibiotics
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NSAIDS
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Tetracyclines (particularly doxycycline)
Highest number of reported cases is with ASA
Others
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KCl
Quinidine preparations
Iron compounds
alendronate
Pill-Induced Esophagitis cont.
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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
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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