Friday, September 17, 2010

How to infuse a local anesthetic into a wound

Wound Healing Phases

Picture of Congenital Subglottic Stenosis

Congenital subglottic stenosis is defined as subglottic stenosis in the absence of a history of intubation, other laryngeal trauma, or extrinsic compression, such as a vascular malformation like a double aortic arch. The child may present at birth, in the neonatal period, or in the first few weeks or months of life. It is caused by failure to recanalize the lumen of the larynx and trachea in embryonic life, thus resulting in atresia, webs, or stenosis. Not unexpectedly, there is an increased incidence of other lesions in the airway if one area is already affected.

Symptoms :The children appear reasonably well with normal growth and development, but they come to the physician's attention because of stridor. The stridor may have an expiratory component as well as the normal inspiratory component , ie, biphasic. The child may also present with dyspnea, a brassy or barky cough, hoarseness, and/or weak or unusual cry. A prolonged episode or unusual course of croup may also bring the child to attention.

The physical examination findings depend on the amount of obstruction in the airway. The child may have only a minimal amount of obstruction, and normally may be without symptoms. But obstruction of the airway may rapidly increase when the edema caused by an URI is superimposed on the already compromised airway. For example, 1 mm of edema in the subglottic region will decrease the cross-sectional area of the airway by over 50%.

Obviously, if the original obstruction is severe, the child will present early and with more severe symptoms, including presentation of stridor in the delivery room.

Evaluation of the child with possible congenital subglottic stenosis may include the use of endolateral neck x-rays to look for narrowing in the subglottic region. Bronchoscopy, or the more correct term laryngoscopy if only the laryngeal structures are visualized, is needed for complete evaluation of the airway, to rule out other anomalies, and for definitive diagnosis.
Bronchoscopy shows marked soft tissue swelling 2-3 mm below the vocal cords. Occasionally, the lumen is eccentric with greater involvement of one area of the wall. Click Here

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Lecture of Amino Acids II


Lecture of Amino Acids I


ttt of Paralysis by Injection of Vocal Cords

The most common causes of true vocal cord paralysis are lung carcinoma, surgical injury, and idiopathic causes "which will often resolve in the course of six to nine months" .
If the left true vocal cord is paralyzed, the presence of a lung carcinoma or other chest disease is likely. The left recurrent laryngeal nerve extends deep into the neck and loops around the aortic arch. It is in the chest that the lung cancer injures the nerve. The two most common surgical causes of true vocal cord paralysis are thyroid surgery, with injury to the recurrent laryngeal nerve; and carotid endarterectomy, with injury to the vagus nerve.

There are 2 basic methods of treating true vocal cord paralysis:

*Number 1: is external larynogplasty with the placement of a lateral laryngeal implant. This method was pioneered by James Netterville from Vanderbilt University in Nashville, TN. It can be done under local anesthesia, has a high success rate and is reversible. An external neck incision is required to do the procedure.

*Number 2: is injection laryngoplasty (as seen in the photo above ), which consists of of injecting the true vocal cord with gel-foam or with a variety of permanent substances. Teflon was used in the past but fell into disfavor because of tissue compatibility problems. All permanent injectable substances can be very difficult to remove if injected in the wrong place. Permanent substances include hydroxy-appetite, silicone, hyluronic acid derivatives, autologist fascia and others. One needs to be careful to match the implant with the patient. Tissue compatibility and safety are of primary concerns. Patients with a long longevity need to be injected with a well tested highly tissue compatible substance.

Gel-foam is absorbed and can be used to temporize. This method can be performed under local anesthesia, has about a 80% success rate. However it is temporary with relief lasting only for 2 to 3 months. An external incision is not required and if injected in the wrong place, it will absorb and the procedure can be repeated. The surgery is preformed with a long needle through and laryngoscope.

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Real Thyroid Cartilage

The thyroid cartilage has been exposed for a vertical hemilaryngectomy.

This cartilage is the largest of the laryngeal cartilages. It consists of two roughly quadrilateral laminae (alae) of hyaline cartilage. These fuse anteriorly in their inferior two thirds, but are separated superiorly by the deep thyroid notch where they extend furthest anteriorly to form the laryngeal prominence. The thyroid cartilage is more prominent in males.

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McMinn’s Clinical Atlas of Human Anatomy

Map out all of the key structures of the human body with examples of real human dissections…and easily place them in a clinical context! This popular atlas incorporates an unrivalled collection of cadaveric, osteological, and clinical images with surface anatomy models, interpretive drawings, orientational diagrams, and diagnostic images – emphasizing a well-rounded visual perspective of a real human body as seen by modern doctors. The 6th Edition offers new endoscopic images, 250 new dissection photos (including eight pages of new dissections on lymphatics), and 300 new clinical thumbnails. A bonus DVD – new to this edition – includes 1,000 additional photos not found in the text, as well as questions and answers that accompany each section from the book.
* Displays X-ray, MR, and CT images next to corresponding dissections, showing how to recognize anatomic structures in diagnostic images.
* Presents interpretive drawings to help you differentiate between structures with a similar appearance (i.e., veins, arteries, and nerves).
* Offers orientational diagrams that make it easier to relate the dissections in the text to real experiences in the lab.
* Provides an unobstructed view of the artwork by using a numbered labeling system, which also allows you to self-test by covering up the key and identifying each numbered structure yourself.
* Presents 300 new clinical thumbnails – with relevant clinical notes and additional images on the DVD – that emphasize the clinical relevance of images depicted and demonstrate their clinical relevance.
* Offers 250 new dissection photos that enhance the overall quality and scope of the images shown · eight pages of new dissections on lymphatics · 50 new illustrations reflecting the increasing use ofdiagnostic imaging in anatomy teaching · and 20 new endoscopic images to reinforce memorization of structures.
* Features a bonus DVD with 1,000 clinical photos not found in the text…more information on clinical correlations…and questions and answers that accompany each section of the book.

PART 1 - PART 2 - PART 3 - PART 4

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Chronic (total) renal infarction X-ray

Renal infarction due to acute renal artery occlusion. (A) An initial nephrotomogram demonstrates a thin cortical rim surrounding the right kidney (arrows), reflecting viable renal cortex perfused by perforating collateral vessels from the renal capsule. (B) Four months later, a repeat nephrotomogram shows a marked decrease in the size of the atrophic right kidney (arrowheads).

Imaging Findings :
Global shrinkage of the kidney with absent opacification. There may be a peripheral rim of opacified cortex during the nephrogram phase (probably reflects viable renal cortex perfused by perforating collateral vessels from the renal capsule).

NOTE : Renal occlusion is most commonly secondary to an embolism from the heart. A decrease in renal size is detectable within 2 weeks and reaches its maximum extent by 5 weeks. Compensatory enlargement of the contralateral kidney (in individuals young enough to provide this reserve).

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