Thursday, June 25, 2009
Student Presentations
Date: July 7th at 8am-9am. You will have 10 minutes to present on a topic of interest to seasoned SLPs like me. Location: TBA.
Search this blog for more information on previous years. Type in "Student Presentations." See what comes up.
Good luck!
Search this blog for more information on previous years. Type in "Student Presentations." See what comes up.
Good luck!
Friday, June 19, 2009
Wednesday, June 10, 2009
VRE, MRSA -- What Else Is New!
Look 'em up! Know why we in healthcare need to be concerned and careful!
Tracheal Stenois and Tracheomalacia - Samantha Conner CSD Graduate Student
Two conditions affecting the trachea include tracheomalacia and tracheal stenosis. Tracheal stenosis is a narrowing or constriction of the tracheal cartilage that can cause shortness of breath, coughing, wheezing, stridor, dyspnea, (and pneumonia - are you sure there is a direct cause-effect relationship?) Tracheal stenosis consists of two types, including congenital and acquired. Congenital stenosis occurs at birth. Acquired stenosis can be secondary to tracheostomy, radiation treatment, surgery, and cancer. Also, stenosis can be caused by bacterial infection, external injury, and autoimmune conditions such as polychondritis and sarcoidosis that cause inflammation. However, the majority of cases are due to prolonged intubation.The most common treatments for tracheal stenosis include endoscopic surgery, open surgery and medical treatment. The treatment varies according to the etiology of the stenosis. For example, if the condition is secondary to an infection, it may be treated using antibiotics or antifungals. Also, if it is secondary to a malignant growth, chemotherapy or corticosteroids may be used for treatment. Although surgery is not necessary in most cases, some stenosis requires surgery. Minimally invasive surgery such as endoscopic surgery can be an effective treatment, as well as open surgery such as a tracheal resection. Tracheal stenosis also can be treated by dilation, either performed by a health care provider or at home by savvy patients.
In contrast to tracheal stenosis, tracheomalacia is a condition characterized by weakness of tracheal cartilage. Symptoms of malacia include stridor, dypnea, upper respiratory infections, and pneumonia. Tracheal malacia can be congenital or acquired. Congenital tracheal malacia occurs when the tracheal cartilage is not properly formed. It is often associated with fistulas. Congenital malacia can be treated with humidified air, physical therapy, careful feeding and monitoring, and antibiotics for infections associated with malacia. Acquired stenosis can occur as type II malacia from pressure on the trachea from an outside force such as a tumor. Another acquired malacia, type III, occurs from prolonged intubation or chronic infections. Acquired tracheomalacia can be treated through CPAP (continuos positive airway pressure), or surgery sometimes followed by the placement of a stint.
In contrast to tracheal stenosis, tracheomalacia is a condition characterized by weakness of tracheal cartilage. Symptoms of malacia include stridor, dypnea, upper respiratory infections, and pneumonia. Tracheal malacia can be congenital or acquired. Congenital tracheal malacia occurs when the tracheal cartilage is not properly formed. It is often associated with fistulas. Congenital malacia can be treated with humidified air, physical therapy, careful feeding and monitoring, and antibiotics for infections associated with malacia. Acquired stenosis can occur as type II malacia from pressure on the trachea from an outside force such as a tumor. Another acquired malacia, type III, occurs from prolonged intubation or chronic infections. Acquired tracheomalacia can be treated through CPAP (continuos positive airway pressure), or surgery sometimes followed by the placement of a stint.
Wednesday, June 3, 2009
June, July Practicum Schedule
No practicum on these dates:
Friday, June 12th
Monday, June 15th
Wednesday, June 24th
Tuesday, June 30th
Thursday, July 9th
Wednesday, July 15th
Monday, July 21st
Friday, July 31st
Friday, June 12th
Monday, June 15th
Wednesday, June 24th
Tuesday, June 30th
Thursday, July 9th
Wednesday, July 15th
Monday, July 21st
Friday, July 31st
Assignment
Look up tracheomalacia and tracheal stenosis, description and etiology. Treatment options.
Tuesday, May 26, 2009
Thursday, May 14, 2009
CHF and Aspiration Pneumonia
The explanation takes a little time to set up so I hope it is worth the wait. This is very condensed from what usually takes a couple of hours to properly describe so I apologize in advance if it is overly simplified. There are some great textbooks that explain this stuff clearly and with good detail.
Congestive heart failure is the inability of the heart to pump blood with adequate pressure to maintain the physiologic demands of organs. It occurs when the myocardium (heart muscle) becomes weak. There are several causes of this progressive weakening of the myocardium. One is disease of the heart muscle itself (cardiomyopathy). Another is arterial hypertension which forces the left ventricle to pump blood against too much resistance for a long period of time, until the muscle itself is overcome by the excessive workload. (The heart muscle first becomes thickened or hypertrophic just as your skeletal muscles get larger when you exercise but heart exercise is good only up to a point.). Likewise, pulmonary hypertension can cause right sided heart failure because the right ventricle is pumping blood through the pulmonary circulation against excessive resistance.
It is this last example that might partially answer your question. Diseases of the lungs such as some forms of COPD (emphysema in particular) can destroy portions of the respiratory membrane which is formed by the alveolar membrane plus the pulmonary capillaries. When the capillaries are destroyed the blood flow into the lungs (to pick up oxygen and get rid of CO2) is blocked so the right ventricle is pumping some blood into a dead end, the pressure in these vessels becomes very high. The result of this pulmonary hypertension is the leakage of material from the blood (that should not leak out of the circulatory system) into the lung. This example is one way that patients develop pulmonary edema (this fluid leakage into the lung is defined as pulmonary edema caused by congestive heart failure). Similarly this heart failure causes fluid to accumulate in the pleural cavity (the space outside of the lungs between the inner and outer pleural membranes that line the lungs and chest cavity).
OK so now we have COPD as a source of CHF. Patients with COPD have reduced mucociliary clearance, reduced expiratory capacity, both of which increase the patient’s resistance to infection (i.e. pneumonia) which are some reasons that COPD patients have a higher risk of any type of pneumonia. These patients also have a different pattern of breathing/swallowing coordination than normals that disrupts the typical “swallow at the onset of exhalation” pattern that predominates in normals, and also increases the respiratory rate above a normal (12-20 or so breaths per minute) further discoordinating (I don’t know if that is a real word) swallow-breathing. Likewise COPD patients exhibit more frequent laryngeal penetration than normals (Mokhlesi, Logemann, Rademaker, Stangl, & Corbridge, 2002; Good-Fratturelli, Curlee, & Holle, 2000)
CHF itself and the associated pulmonary edema and pleural effusions, reduce respiratory surface area by restricting inflation of the lungs (effusions) or by obstructing air from the respiratory membrane (edema). The result of either is the patient has to breathe more times per minute (increased respiratory rate- see above).
There are some good studies that show the association between COPD and dysphagia, and CHF and dysphagia, (see below) but the link between these conditions and dysphagia, as well as the link to subsequent pneumonia risk, is based on the understanding of the pathophysiology of those diseases and mostly based on animal studies, though the inferences are very strong. For example, we know the above processes take place in these diseases, and we know that these patients have increased respiratory rate, swallow-respiratory coordination abnormalities, higher incidence of pneumonia, etc., so we infer that the diseases’ properties explain some if not all of the association between them and dysphagia, increased pneumonia risk, etc. (Langmore, Skarupski, Park, & Fries, 2002).
Cricopharyngeal dysfunction is also seen in some patients with COPD and this can contribute to prandial aspiration and increased likelihood of inoculating thelungs with pathogens ((Good-Fratturelli, Curlee, & Holle, 2000; Langmore, Skarupski, Park, & Fries, 2002; Mokhlesi, 2003; Mokhlesi, Logemann, Rademaker, Stangl, & Corbridge, 2002; Stein, Williams, Grossman, Weinberg, & Zuckerbraun, 1990).
Cheers,
James L. Coyle, Ph.D., CCC-SLP, BRS-S
Assistant Professor, Communication Science and Disorders
University of Pittsburgh
Confidential University of Pittsburgh information. Any unauthorized or improper disclosure, copying, distribution, or use of the contents of this e-mail or attached documents is prohibited. The information contained in this e-mail message is intended only for the personal and confidential use of the recipient(s) named above. If you have received this communication in error, please notify the sender immediately by e-mail and delete the original message.
Good-Fratturelli, M. D., Curlee, R. F., & Holle, J. L. (2000). Prevalence and nature of dysphagia in VA patients with COPD referred for videofluoroscopic swallow examination. Journal of Communication Disorders, 33(2), 93-110.
Langmore, S. E., Skarupski, K. A., Park, P. S., & Fries, B. E. (2002). Predictors of aspiration pneumonia in nursing home residents. Dysphagia, 17(4), 298-307.
Mokhlesi, B. (2003). Clinical implications of gastroesophageal reflux disease and swallowing dysfunction in COPD. American Journal of Respiratory Medicine, 2(2), 117-121.
Mokhlesi, B., Logemann, J. A., Rademaker, A. W., Stangl, C. A., & Corbridge, T. C. (2002). Oropharyngeal deglutition in stable COPD. Chest., 121(2), 361-369.
Stein, M., Williams, A. J., Grossman, F., Weinberg, A. S., & Zuckerbraun, L. (1990). Cricopharyngeal dysfunction in chronic obstructive pulmonary disease. Chest.97(2):347-52.
Congestive heart failure is the inability of the heart to pump blood with adequate pressure to maintain the physiologic demands of organs. It occurs when the myocardium (heart muscle) becomes weak. There are several causes of this progressive weakening of the myocardium. One is disease of the heart muscle itself (cardiomyopathy). Another is arterial hypertension which forces the left ventricle to pump blood against too much resistance for a long period of time, until the muscle itself is overcome by the excessive workload. (The heart muscle first becomes thickened or hypertrophic just as your skeletal muscles get larger when you exercise but heart exercise is good only up to a point.). Likewise, pulmonary hypertension can cause right sided heart failure because the right ventricle is pumping blood through the pulmonary circulation against excessive resistance.
It is this last example that might partially answer your question. Diseases of the lungs such as some forms of COPD (emphysema in particular) can destroy portions of the respiratory membrane which is formed by the alveolar membrane plus the pulmonary capillaries. When the capillaries are destroyed the blood flow into the lungs (to pick up oxygen and get rid of CO2) is blocked so the right ventricle is pumping some blood into a dead end, the pressure in these vessels becomes very high. The result of this pulmonary hypertension is the leakage of material from the blood (that should not leak out of the circulatory system) into the lung. This example is one way that patients develop pulmonary edema (this fluid leakage into the lung is defined as pulmonary edema caused by congestive heart failure). Similarly this heart failure causes fluid to accumulate in the pleural cavity (the space outside of the lungs between the inner and outer pleural membranes that line the lungs and chest cavity).
OK so now we have COPD as a source of CHF. Patients with COPD have reduced mucociliary clearance, reduced expiratory capacity, both of which increase the patient’s resistance to infection (i.e. pneumonia) which are some reasons that COPD patients have a higher risk of any type of pneumonia. These patients also have a different pattern of breathing/swallowing coordination than normals that disrupts the typical “swallow at the onset of exhalation” pattern that predominates in normals, and also increases the respiratory rate above a normal (12-20 or so breaths per minute) further discoordinating (I don’t know if that is a real word) swallow-breathing. Likewise COPD patients exhibit more frequent laryngeal penetration than normals (Mokhlesi, Logemann, Rademaker, Stangl, & Corbridge, 2002; Good-Fratturelli, Curlee, & Holle, 2000)
CHF itself and the associated pulmonary edema and pleural effusions, reduce respiratory surface area by restricting inflation of the lungs (effusions) or by obstructing air from the respiratory membrane (edema). The result of either is the patient has to breathe more times per minute (increased respiratory rate- see above).
There are some good studies that show the association between COPD and dysphagia, and CHF and dysphagia, (see below) but the link between these conditions and dysphagia, as well as the link to subsequent pneumonia risk, is based on the understanding of the pathophysiology of those diseases and mostly based on animal studies, though the inferences are very strong. For example, we know the above processes take place in these diseases, and we know that these patients have increased respiratory rate, swallow-respiratory coordination abnormalities, higher incidence of pneumonia, etc., so we infer that the diseases’ properties explain some if not all of the association between them and dysphagia, increased pneumonia risk, etc. (Langmore, Skarupski, Park, & Fries, 2002).
Cricopharyngeal dysfunction is also seen in some patients with COPD and this can contribute to prandial aspiration and increased likelihood of inoculating thelungs with pathogens ((Good-Fratturelli, Curlee, & Holle, 2000; Langmore, Skarupski, Park, & Fries, 2002; Mokhlesi, 2003; Mokhlesi, Logemann, Rademaker, Stangl, & Corbridge, 2002; Stein, Williams, Grossman, Weinberg, & Zuckerbraun, 1990).
Cheers,
James L. Coyle, Ph.D., CCC-SLP, BRS-S
Assistant Professor, Communication Science and Disorders
University of Pittsburgh
Confidential University of Pittsburgh information. Any unauthorized or improper disclosure, copying, distribution, or use of the contents of this e-mail or attached documents is prohibited. The information contained in this e-mail message is intended only for the personal and confidential use of the recipient(s) named above. If you have received this communication in error, please notify the sender immediately by e-mail and delete the original message.
Good-Fratturelli, M. D., Curlee, R. F., & Holle, J. L. (2000). Prevalence and nature of dysphagia in VA patients with COPD referred for videofluoroscopic swallow examination. Journal of Communication Disorders, 33(2), 93-110.
Langmore, S. E., Skarupski, K. A., Park, P. S., & Fries, B. E. (2002). Predictors of aspiration pneumonia in nursing home residents. Dysphagia, 17(4), 298-307.
Mokhlesi, B. (2003). Clinical implications of gastroesophageal reflux disease and swallowing dysfunction in COPD. American Journal of Respiratory Medicine, 2(2), 117-121.
Mokhlesi, B., Logemann, J. A., Rademaker, A. W., Stangl, C. A., & Corbridge, T. C. (2002). Oropharyngeal deglutition in stable COPD. Chest., 121(2), 361-369.
Stein, M., Williams, A. J., Grossman, F., Weinberg, A. S., & Zuckerbraun, L. (1990). Cricopharyngeal dysfunction in chronic obstructive pulmonary disease. Chest.97(2):347-52.
Subscribe to:
Posts (Atom)
