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[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)   
 _David Disler_ 
(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. [1] 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. [2] 
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. [2] 
Illustrative Case 
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.  [5] 
Although viral pneumonia is not responsive to  antimicrobial therapy, it is 
not a major cause of mortality, unlike bacterial or  fungal pneumonia. [4] 
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. [3] In  hospitalized patients, 
63 percent of cases result from aerobic infection, 7  percent from anaerobic 
infection and 30 percent from mixed infections. [3] In  the community, most 
cases are caused by aerobic streptococci (80 to 90 percent  of cases). [4] 
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.  [3] 
Necrotizing pneumonia  occurs when simple aspiration pneumonia spreads to 
surrounding parenchyma beyond  the boundaries of the initially involved segments 
or lobes. [3] 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 
percent. [3] 
[1] Fraser RG, Par JA. Synopsis of diseases of the chest.  Philadelphia: 
Saunders, 1983:732-42. 
[2] Reed JC. Chest radiology: plain film patterns and  differential 
diagnoses. 2d ed. Chicago: Year Book Medical Publishers,  1987:293-329. 
[3] Pennza PT. Aspiration pneumonia, necrotizing  pneumonia, and lung 
abscess. Emerg Med Clin North Am  1989;7:279-307. 
[4] 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. 
[5] Robbins SL, Cotran RS, Kumar V. Pathologic basis of  disease. 3d ed. 
Philadelphia: Saunders,  1984:732-42. 
[6] 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 

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