[Date Prev][Date Next]
[Dysphagia] vocal cord paralysis and dysphagia
- Subject: [Dysphagia] vocal cord paralysis and dysphagia
- From: Drirenect at aol.com (Drirenect@aol.com)
- Date: Fri Feb 10 20:26:27 2006
Pt is a 48 year old man with a history of alcohol and abuse. Came to
hospital with a Dx of necrotizing pneumonia.
*** Necrotizing pneumonia is usually pneumonitis from aspiration of reflux
or vomitis ? given his Hx of alcoholism, most likely. Also see article below.
He was found to have a paralyzed right vocal cord, which was injected with
Perlane and is now back in medial position.
*** Why was it paralyzed? Right sided paralysis is unusual ? so the
etiology is most important.
Following the Perlane injection he penetrated every consistency (head turn
and chin tuck did not change this)
*** Head turn rarely works and only when it?s to the side of relatively
closed vallecula. Chin tuck ? if you mean neck flexion ? would be exactly the
wrong thing in this ? and most- patients as it interferes with anterior
movement of the hyoid.
The epiglottis doesn't move as well as it should
*** On the AP view, is it symmetrical or not? Also the UES is innervated
anteriorly by the recurrent laryngeal so may be impaired on the right also. This
is the usual problem with paralyzed VC.
Necrotizing aspiration pneumonia
_American Family Physician_
(http://www.findarticles.com/p/articles/mi_m3225) , _Nov, 1991_ (http://www.findarticles.com/p/articles/mi_m3225/is_n5_v44)
(http://www.findarticles.com/p/search?tb=art&qt="David+Disler") , _Salvatore A. Deluca_
A lung cavity is a focus of increased density, with the central portion
replaced by air.  Cavitation occurs when there is tissue necrosis and
secondary expulsion of necrotic material into the tracheobronchial tree. [1,2] A
cavity can also form when a fluid-filled cyst communicates with the airways or
when a preexisting space such as a bulla becomes secondarily infected. 
As implied, air-fluid levels are typically, although not necessarily, seen
on radiographs. [1,3] Cavitation is most commonly the result of infectious
disease, [1-4] such as acute pyogenic or granulomatous infection, but can also
be seen in collagen vascular diseases such as Wegener's granulomatosis and
rheumatoid arthritis, in infarction by pulmonary emboli or in tumor necrosis.
[2,3] Qualitative features of cavities, such as internal contours or wall
thickness, are not accurate predictors of the etiology. However, the clinical
history and the number of cavities provide some diagnostic information. Cavities
associated with primary tumors and lung abscesses are typically solitary,
whereas those associated with septic emboli, metastases and rheumatoid nodules
are multiple. 
A 55-year-old alcoholic man had recently undergone a hemiglossectomy and
radical neck dissection for squamous cell carcinoma of the tongue. He also was
treated with chemotherapy consisting of 5-fluorouracil and cisplatin.
The patient presented with a two-day history of fever, cough and the
production of yellow sputum. A chest film taken one month before admission was
normal; the current admission chest film demonstrated patchy right upper lobe
consolidation with areas of cavitation (Figures 1 and 2). A computed tomographic
scan of the chest showed extensive bilateral thick-walled cavitations, most
prominent in the right upper lobe (Figure 3). Sputum cultures revealed
abundant growth of Staphylococcus aureus and Serratia marcescens.
The differential diagnosis of lung cavitation includes cavitary infectious
processes from bacteria (S. aureus, Klebsiella pneumoniae, Serratia and
Nocardia species, and anaerobes), fungi and tuberculosis. [2,3] Clinical and
radiologic findings make vasculitides or cavitary infarction resulting from
pulmonary emboli possible, but less likely, diagnoses.
Aspiration is the most common route of entry for both community- and
hospital-acquired pneumonia. [3,4] Normally, microaspirates are cleared by several
mechanisms, with lines of defense occurring at two levels. [3-5] The first
level consists of physical entrapment and removal of foreign particles by
filtration in the nose or sequestration in the mucous layer of the tracheobronchial
tree, followed by removal of mucus, either by coughing or by the action of
the cilia in the respiratory epithelium. The second line of defense occurs at
the cellular level throughout the immune system, including inactivation by
IgA antibodies of opsonization and subsequent ingestion by phagocytic cells.
Absence or loss of any of these defense mechanisms can result in colonization
and infection by pathogenic organisms. 
Although viral pneumonia is not responsive to antimicrobial therapy, it is
not a major cause of mortality, unlike bacterial or fungal pneumonia. 
Viral pneumonia is, however, the cause of considerable morbidity and economic
loss. Viral infection predisposes the patient to subsequent bacterial
superinfection, presumably as a result of mucosal damage by the virus, with subsequent
impairment of mucociliary clearance. [3-5]
Bacterial pneumonia may occur in a normal host secondary to overwhelming
inoculum or in an abnormal host who has impaired resistance. [3,5,6] Factors
that place patients at risk for aspiration include impaired cough reflex, coma
or sedation. Dehydration and drugs can impair mucociliary clearance.
Congenital or acquired immunosuppression decreases the effectiveness of the humoral or
cellular host response, which increases the risk of opportunistic infection.
Aspiration of a large quantity of secretions results in lower respiratory
tract infection, with consolidation in the dependent areas of the lung. If the
infection is not treated, it can progress to necrotizing pneumonia or lung
abscess. [3,5] The areas most susceptible to aspiration in supine patients are
the superior segments of the lower lobes, the apicoposterior segment of the
left upper lobe and the posterior segment of the right upper lobe. In the
upright position, the basal segments of the lower lobes are the greatest risk.
The organism responsible for the infection typically reflects the setting in
which aspiration occurs. In the nursing home population, approximately 80
percent of cases are the result of mixed aerobic and anaerobic infection, and 5
percent are due to strict anaerobic infection.  In hospitalized patients,
63 percent of cases result from aerobic infection, 7 percent from anaerobic
infection and 30 percent from mixed infections.  In the community, most
cases are caused by aerobic streptococci (80 to 90 percent of cases). 
Despite their high rate of occurrence, anaerobes are rarely cultured from
sputum aspirates. [3,5] The culture yield is poor because anaerobes tend to be
obscured by aerobic mouth flora. Careful sampling techniques, such as
transtracheal aspiration or bronchoscopic brushing, are often required to make a
specific diagnosis. 
Necrotizing pneumonia occurs when simple aspiration pneumonia spreads to
surrounding parenchyma beyond the boundaries of the initially involved segments
or lobes.  Multiple small cavities form and eventually coalesce. If the
pleural space is breached, empyema results. [3-5]
Anaerobic infection tends to be delayed in presentation, whereas infections
caused by highly aggressive organisms, such as S. aureus and Klebsiella
species, progress quite rapidly. Patients with anaerobic infection typically have
symptoms for up to two weeks prior to presentation, whereas patients with
staphylococcal or other aggressive pneumonias usually have symptoms for only
three to four days before presentation. [2,3]
In addition to antibiotic therapy, chest tube drainage or decortication may
be required, particularly when the infectious process extends to the pleural
space. Resolution can take several weeks, and mortality is as high as 20
 Fraser RG, Par JA. Synopsis of diseases of the chest. Philadelphia:
 Reed JC. Chest radiology: plain film patterns and differential
diagnoses. 2d ed. Chicago: Year Book Medical Publishers, 1987:293-329.
 Pennza PT. Aspiration pneumonia, necrotizing pneumonia, and lung
abscess. Emerg Med Clin North Am 1989;7:279-307.
 Miller WT. Pulmonary infections. In: Taveras JM, Ferrucci JT, Elliott
LP, eds. Radiology: diagnosis, imaging, intervention. Vol 1. Philadelphia: J.B.
Lippincott Co., 1988:1-29.
 Robbins SL, Cotran RS, Kumar V. Pathologic basis of disease. 3d ed.
Philadelphia: Saunders, 1984:732-42.
 Liu YC, Tomashefski JF Jr, Tomford JW, Green H. Necrotizing Pneumocystis
carinii vasculitis associated with lung necrosis and cavitation in a patient
with acquired immunodeficiency syndrome. Arch Pathol Lab Med 1989;
COPYRIGHT 1991 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group