طبيبك الخاص

Myomectomy, Vagina Fibroid Surgery,

2011-04-20T10:11:00.000-07:00

Gallbladder Removal Surgery

2011-04-20T09:25:00.001-07:00

Gallbladder Surgery for Gallstones

2011-04-19T13:33:00.000-07:00

B-Lynch surgery technique septate uterus

2011-04-19T12:19:00.000-07:00

Hysterectomy

2011-04-19T12:08:00.000-07:00

Liver Transplants and Hepatitis C

2011-04-19T10:47:00.000-07:00

Quick Linker - 3 - (Liver) Donor Operation

2011-04-19T10:20:00.001-07:00

Breast Anatomy

2011-04-18T15:52:00.000-07:00

Anatomy of the Breast

As with all surgical procedures, understanding the anatomy is crucial prior to performing an operative procedure. Comprehension of breast anatomy enhances the surgeon's ability to perform surgery safely and effectively. For information on various breast surgery procedures, please see the Breast section of eMedicine's Plastic Surgery journal.

Vascular Anatomy

The blood supply to the breast skin depends on the subdermal plexus, which is in communication with underlying deeper vessels supplying the breast parenchyma. The blood supply is derived from (1) the internal mammary perforators (most notably the second to fifth perforators), (2) the thoracoacromial artery, (3) the vessels to serratus anterior, (4) the lateral thoracic artery, and (5) the terminal branches of the third to eighth intercostal perforators. The superomedial perforator supply from the internal mammary vessels is particularly robust and accounts for some 60% of the total breast blood supply. This rich blood supply allows for various reduction techniques, ensuring the viability of the skin flaps after surgery.

Innervation of the Breast

Sensory innervation of the breast is dermatomal in nature. It is mainly derived from the anterolateral and anteromedial branches of thoracic intercostal nerves T3-T5. Supraclavicular nerves from the lower fibers of the cervical plexus also provide innervation to the upper and lateral portions of the breast. Researchers believe sensation to the nipple derives largely from the lateral cutaneous branch of T4.

Breast Parenchyma and Support Structures

The breast is made up of both fatty tissue and glandular milk-producing tissues. The ratio of fatty tissue to glandular tissue varies among individuals. In addition, with the onset of menopause (ie, decrease in estrogen levels), the relative amount of fatty tissue increases as the glandular tissue diminishes.

The base of the breast overlies the pectoralis major muscle between the second and sixth ribs in the nonptotic state. The gland is anchored to the pectoralis major fascia by the suspensory ligaments first described by Astley Cooper in 1840. These ligaments run throughout the breast tissue parenchyma from the deep fascia beneath the breast and attach to the dermis of the skin. Since they are not taut, they allow for the natural motion of the breast. These ligaments relax with age and time, eventually resulting in breast ptosis. The lower pole of the breast is fuller than the upper pole. The tail of Spence extends obliquely up into the medial wall of the axilla.[1]

The breast overlies the pectoralis major muscle as well as the uppermost portion of the rectus abdominis muscle inferomedially. The nipple should lie above the inframammary crease and is usually level with the fourth rib and just lateral to the midclavicular line. The average nipple – to – sternal notch measurement in a youthful, well-developed breast is 21-22 cm; an equilateral triangle formed between the nipples and sternal notch measures an average of 21 cm per side.

Musculature Related to the Breast

The breast lies over the musculature that encases the chest wall. The muscles involved include the pectoralis major, serratus anterior, external oblique, and rectus abdominus fascia. The blood supply that provides circulation to these muscles then perforates through to the breast parenchyma, thus also supplying blood to the breast. By maintaining continuity with the underlying musculature, the breast tissue remains richly perfused, thus preventing complications arising from aesthetic or reconstructive surgery that requires the placement of a breast implant. (For more information, see the Breast section of eMedicine's Plastic Surgery journal.)

Pectoralis major
The pectoralis major muscle is a broad muscle that extends from its origin on the medial clavicle and lateral sternum to its insertion on the humerus. The thoracoacromial artery provides its major blood supply, while the intercostal perforators arising from the internal mammary artery provide a segmental blood supply. The medial and lateral anterior thoracic nerves provide innervation for the muscle, entering posteriorly and laterally. The action of the pectoralis major is to flex, adduct, and rotate the arm medially.

The pectoralis major is extremely important in both aesthetic and reconstructive breast surgery, since it provides muscle coverage for the breast implant. In reconstructive surgery, the pectoralis major muscle covers the implant, providing a decreased risk of exposure of the implant since the skin and underlying subcutaneous tissues are often thin following mastectomy. The muscle also provides additional tissue between implant and skin, thus decreasing palpability of the implant. Often, placement of the implant beneath the muscle causes it to be noticeable when the pectoralis is contracted. In these instances, it may be helpful to release the pectoralis muscle from its inferior and medial attachments to decrease the incidence of noticeable contractions. In addition, with inferior release of the pectoralis muscle, lower positioning of the implant can be achieved, resulting in a more aesthetically pleasing appearance.

Serratus anterior
The serratus anterior muscle is a broad muscle that runs along the anterolateral chest wall. Its origin is the outer surface of the upper borders of the first through eighth ribs, and its insertion is on the deep surface of the scapula. Its vascular supply is derived equally from the lateral thoracic artery and branches from the thoracodorsal artery. The long thoracic nerve serves to innervate the serratus anterior, which acts to rotate the scapula, raising the point of the shoulder and drawing the scapula forward toward the body. Transection of the long thoracic nerve is carefully avoided during an axillary lymph node dissection, since its loss results in "winging" as the scapula is released from the chest wall and moves upward and outward.

Because the serratus anterior underlies the lateral aspect of the breast, in aesthetic surgery, blunt elevation of the pectoralis major laterally inadvertently elevates a small portion of the serratus muscle. To completely cover the implant with muscle in reconstructive surgery, often the serratus anterior must be elevated sharply to obtain a sufficient muscle layer to provide coverage.

Rectus abdominus
The rectus abdominus muscle demarcates the inferior border of the breast. It is an elongated muscle that runs from its origin at the crest of the pubis and interpubic ligament to its insertion at the xiphoid process and cartilages of the fifth through seventh ribs. It acts to compress the abdomen and flex the spine. The 7th through 12th intercostal nerves provide sensation to overlying skin and innervate the muscle. Vascularity of the muscle is maintained through a network between the superior and inferior deep epigastric arteries.

When placing an implant for breast reconstruction, in attempting to achieve complete coverage with muscle, the rectus fascia must often be elevated to place the implant sufficiently caudal. This dense thick fascia is often intimately adherent to the ribs below it. Once it is elevated and released, proper positioning and expansion of the implant can proceed.

External oblique
The external oblique muscle is a broad muscle that runs along the anterolateral abdomen and chest wall. Its origin is from the lower 8 ribs, and its insertion is along the anterior half of the iliac crest and the aponeurosis of the linea alba from the xiphoid to the pubis. It acts to compress the abdomen, flex and laterally rotate the spine, and depress the ribs. The 7th through 12th intercostal nerves serve to innervate the external oblique. A segmental blood supply is maintained through the inferior 8 posterior intercostal arteries.

The external oblique muscle abuts the breast on the inferior lateral aspect. Elevated along with the rectus abdominus fascia to provide inferior coverage of the breast implant during reconstructive surgery, its fascia, like the fascia of the rectus abdominus muscle, must be released adequately to provide for proper placement and expansion of the implant. In aesthetic surgery, placement of the implant inferiorly is usually not below these fascial attachments. If the implant is placed behind the fascia, the implant often "rides too high" and may result in a "double bubble" effect, wherein the breast parenchyma slides over and off the implant.

Conclusion
Breast shape varies among patients, but knowing and understanding the anatomy of the breast ensures safe surgical planning. When the breasts are carefully examined, significant asymmetries are revealed in most patients. Any preexisting asymmetries, spinal curvature, or chest wall deformities must be recognized and demonstrated to the patient, as these may be difficult to correct and can become noticeable in the postoperative period. Preoperative photographs with multiple views are obtained on all patients and maintained as part of the office record.

Labour and Birth

2011-04-18T15:04:00.000-07:00

acetaminophen/guaifenesin

2011-04-18T14:39:00.000-07:00

Adult Dosing & Uses

Dosing Forms & Strengths

acetaminophen/guaifenesintablet
325mg/200mg

capsule
325mg/200mg

oral solution
(500mg/200mg)/15mL

packet
1000mg/400mg

Cough, Fever, Headache, Minor Aches & Pains

Theraflu Flu & Chest Congestion: 1 packet dissolved in 8 oz of hot water q6hr; not to exceed 4 packets/day; consume entire drink within 10-15 minutes

Tylenol Chest Congestion: 2 capsules PO q4–6hr; not to exceed 12 capsules/day

Pediatric Dosing & Uses

Dosing Forms & Strengths

acetaminophen/guaifenesin

tablet
325mg/200mg

capsule
325mg/200mg

oral solution
(500mg/200mg)/15mL

packet
1000mg/400mg

Cough, Fever, Headache, Minor Aches & Pains

Theraflu Flu & Chest Congestion
<12 years old: Ask a pediatrician
>12 years old: 1 packet dissolved in 8 oz of hot water q6hr; not to exceed 4 packets/day; consume entire drink within 10-15 minutes

Tylenol Chest Congestion
<12 years old: Ask a pediatrician
>12 years old: 2 capsules PO q4–6hr; not to exceed 12 capsules/day

Pharmacology

Mechanism of Action

Acetaminophen: blocks pain impulse generation peripherally & may inhibit the generation of prostaglandin in the CNS; reduces fever by inhibiting the hypothalamic heat-regulating center

Guaifenesin: increases respiratory tract fluid secretions & helps to loosen phlegm & bronchial secretions

Adverse Effects

Dizziness

Drowsiness

Headache

Dermatologic rash

Nausea

Vomiting

Anemia blood dyscrasias (neutropenia, pancytopenia, leukopenia)

Bilirubin and alkaline phosphatase may increase

Drug Interactions

eltrombopag

exenatide

isoniazid
clonazepam

colestipol
carbamazepine

diazepam
ethanol

ethosuximide
felbamate

Contraindications & Cautions

Contraindications

Hypersensitivity

G-6-PD deficiency

Severe hepatic impairment

Cautions

Acetaminophen hepatotoxicity possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; contained in many OTC products and combined use with these products may result in toxicity due to cumulative doses exceeding recommended maximum dose

Guaifenesin is not for administration in persistent cough associated with chronic bronchitis, smoking, asthma, or accompanied with excessive secretions

Patient Handout

Patient Education
acetaminophen-guaifenesin Oral

IMPORTANT: HOW TO USE THIS INFORMATION: This is a summary and does NOT have all possible information about this product. This information does not assure that this product is safe, effective, or appropriate for you. This information is not individual medical advice and does not substitute for the advice of your health care professional. Always ask your health care professional for complete information about this product and your specific health needs.

EXPECTORANT/ACETAMINOPHEN - ORAL

USES:
This combination medication is used to temporarily treat symptoms caused by the common cold, flu, allergies, or other breathing illnesses (such as sinusitis, bronchitis). The expectorant helps thin and loosen mucus in the lungs, making it easier to cough up the mucus. Acetaminophen (APAP) is a non-aspirin pain reliever and fever reducer.

This medication is not usually used for ongoing coughs from smoking, asthma, other long-term breathing problems (such as emphysema), or coughs with a lot of mucus unless directed by your doctor.

Cough-and-cold products have not been shown to be safe or effective in children younger than 6 years. Therefore, do not use this product to treat cold symptoms in children younger than 6 years unless specifically directed by the doctor. Some products (such as long-acting tablets/capsules) are not recommended for use in children younger than 12 years. Ask your doctor or pharmacist for more details about using your product safely.

These products do not cure or shorten the length of the common cold and may cause serious side effects. To decrease the risk for serious side effects, carefully follow all dosage directions. Do not use this product to make a child sleepy. Do not give other cough-and-cold medication that might contain the same or similar ingredients (see also Drug Interactions section). Ask the doctor or pharmacist about other ways to relieve cough and cold symptoms (such as drinking enough fluids, using a humidifier or saline nose drops/spray).

HOW TO USE:
Read and follow all directions on the package label. If you have any questions, consult your pharmacist.

Take this medication by mouth with or without food, usually every 4 to 6 hours as needed, or as directed by your doctor. Drink plenty of fluids when you use this medication unless otherwise directed by your doctor. The fluid will help loosen the mucus in your lungs.

If you are using the liquid form of this medication, carefully measure the dose using a special measuring device/spoon. Do not use a household spoon because you may not get the correct dose. If your liquid form is a suspension, shake the bottle well before each dose.

The dosage is based on your age, medical condition, and response to treatment. Do not increase your dose, take it more frequently, or use it for a longer time than directed. Do not give children medicines labeled only for adults.

One ingredient in this product is acetaminophen. Taking too much acetaminophen may cause serious (possibly fatal) liver disease. Adults should not take more than 4 grams (4000 milligrams) of acetaminophen a day. A smaller dose should be used in children and in people with liver disease. Read the product package or consult your doctor. Carefully check the labels of all your medicines (such as pain/fever drugs or cough-and-cold products) to make sure they do not also contain acetaminophen. (See also Side Effects section.)

Tell your doctor if your condition persists for more than 1 week, if it worsens, or if it occurs with rash, persistent headache, or fever lasting more than 3 days. These may be symptoms of a serious medical problem and should be checked by a doctor.

SIDE EFFECTS:
Upset stomach or nausea may occur. If any of these effects persist or worsen, tell your doctor or pharmacist promptly.

Taking more than the recommended dose of acetaminophen may cause serious (possibly fatal) liver disease. Seek immediate medical attention if you have any of the following symptoms of liver damage: dark urine, persistent nausea/vomiting, stomach/abdominal pain, yellowing eyes/skin.

A very serious allergic reaction to this drug is rare. However, seek immediate medical attention if you notice any symptoms of a serious allergic reaction, including: rash, itching/swelling (especially of the face/tongue/throat), severe dizziness, trouble breathing.

This is not a complete list of possible side effects. If you notice other effects not listed above, contact your doctor or pharmacist.

In the US -

Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.

In Canada - Call your doctor for medical advice about side effects. You may report side effects to Health Canada at 1-866-234-2345.

PRECAUTIONS:
Before taking this product, tell your doctor or pharmacist if you are allergic to any of its ingredients; or if you have any other allergies. This product may contain inactive ingredients, which can cause allergic reactions or other problems. Talk to your pharmacist for more details.

If you have any of the following health problems, consult your doctor or pharmacist before using this medication: breathing problems (such as asthma, emphysema), liver disease.

Acetaminophen may cause liver damage. Daily use of alcohol and acetaminophen may increase your risk. Avoid alcoholic beverages.

Some brands of this product may contain sugar, alcohol, or aspartame. Caution is advised if you have diabetes, alcohol dependence, liver disease, phenylketonuria (PKU), or any other condition that requires you to limit/avoid these substances in your diet. Ask your doctor or pharmacist about using this product safely.

During pregnancy, this medication should be used only when clearly needed. Discuss the risks and benefits with your doctor.

This medication may pass into breast milk. Consult your doctor before breast-feeding.

DRUG INTERACTIONS:
If you are taking this product under your doctor's direction, your doctor or pharmacist may already be aware of any possible drug interactions and may be monitoring you for them. Do not start, stop, or change the dosage of any medicine before checking with your doctor or pharmacist first.

The ingredients in this product are available in many prescription and nonprescription products. Check the labels on all your medicines (such as pain/fever drugs or cold/allergy products) because they may contain the same or similar ingredients. Ask your pharmacist about using those products safely. (See also How to Use section.)

This medication may interfere with certain laboratory tests (including urine 5-HIAA), possibly causing false test results. Make sure laboratory personnel and all your doctors know you use this drug.

This document does not contain all possible interactions. Therefore, before using this product, tell your doctor or pharmacist of all the products you use. Keep a list of all your medications with you, and share the list with your doctor and pharmacist.

OVERDOSE:
If overdose is suspected, contact your local poison control center or emergency room immediately. US residents can call the US National Poison Hotline at 1-800-222-1222. Canada residents can call a provincial poison control center. Symptoms of overdose may include: persistent nausea/vomiting, dark urine, stomach/abdominal pain.

NOTES:
Keep all regular medical and laboratory appointments.

MISSED DOSE:
If you are taking this product on a regular schedule and miss a dose, take it as soon as you remember. If it is near the time of the next dose, skip the missed dose and resume your usual dosing schedule. Do not double the dose to catch up.

STORAGE:
Store in a tightly closed container at room temperature between 59-86 degrees F (15-30 degrees C) away from light and moisture. Do not store in the bathroom. Do not freeze liquid forms of this medication. Keep all medicines away from children and pets.

Do not flush medications down the toilet or pour them into a drain unless instructed to do so. Properly discard this product when it is expired or no longer needed. Consult your pharmacist or local waste disposal company for more details about how to safely discard your product.

Information last revised January 2011 Copyright(c) 2011 First DataBank, Inc.

Anatomy of Olfactory System

2011-04-18T12:25:00.000-07:00

Overview

The olfactory system represents one of the oldest sensory modalities in the phylogenetic history of mammals. Olfaction is less developed in humans than in other mammals such as rodents. As a chemical sensor, the olfactory system detects food and influences social and sexual behavior. The specialized olfactory epithelial cells characterize the only group of neurons capable of regeneration. Activation occurs when odiferous molecules come in contact with specialized processes known as the olfactory vesicles. Within the nasal cavity, the turbinates or nasal conchae serve to direct the inspired air toward the olfactory epithelium in the upper posterior region. This area (only a few centimeters wide) contains more than 100 million olfactory receptor cells. These specialized epithelial cells give rise to the olfactory vesicles containing kinocilia, which serve as sites of stimulus transduction.

The image below depicts olfactory anatomy.

Olfactory Epithelium

The olfactory epithelium consists of 3 cell types, basal, supporting, and olfactory receptor cells. Basal cells are stem cells that give rise to the olfactory receptor cells. The continuous turnover and new supply of these neurons are unique to the olfactory system. In no other location in the mature nervous system do less differentiated stem cells replace neurons. Supporting cells are scattered among the receptor cells and have numerous microvilli and secretory granules, which empty their contents onto the mucosal surface. The receptor cells are actually bipolar neurons, each possessing a thin dendritic rod that contains specialized cilia extending from the olfactory vesicle and a long central process that forms the fila olfactoria. The cilia provide the transduction surface for odorous stimuli.

The vomeronasal organ is a specialized bilateral membranous structure located in the base of the anterior nasal septum, at the junction of the septal cartilage and the bony septum. It is believed to detect external chemical signals called pheromones. These signals, which are not detected consciously as odors by the olfactory system, mediate human autonomic, psychological, and endocrine responses.

The trigeminal nerve innervates the posterior nasal cavity to detect noxious stimuli.

Olfactory Nerve and the Cribriform Plate

The small unmyelinated axons of the olfactory receptor cells form the fine fibers of the first cranial nerve and travel centrally toward the ipsilateral olfactory bulb to make contact with the second-order neurons. Conduction velocities are extremely slow, and support is provided in bundles by a single Schwann cell. As previously mentioned, the trigeminal nerve (cranial nerve V) sends fibers to the olfactory epithelium to detect caustic chemicals such as ammonia. The cribriform plate of the ethmoid bone, separated at the midline by the crista galli, contains multiple small foramina through which the olfactory nerve fibers, or fila olfactoria, traverse. Fracture of the cribriform plate in traumatic settings can disrupt these fine fibers and lead to olfactory dysfunction.

Olfactory Bulb

The olfactory bulb lies inferior to the basal frontal lobe. The olfactory bulb is a highly organized structure composed of several distinct layers and synaptic specializations. The layers (from outside toward the center of the bulb) are differentiated as follows:
Glomerular layer
External plexiform layer
Mitral cell layer
Internal plexiform layer
Granule cell layer

Mitral cells are second-order neurons contacted by the olfactory nerve fibers at the glomerular layer of the bulb. The glomerular layer is the most superficial layer, consisting of mitral cell dendritic arborizations (glomeruli), olfactory nerve fibers, and periglomerular cells. Periglomerular cells contact multiple mitral cell dendrites within the glomeruli and provide lateral inhibition of neighboring glomeruli while allowing excitation of a specific mitral cell dendritic tree. Each mitral cell is contacted by at least 1000 olfactory nerve fibers.

The external plexiform layer contains the passing dendrites of mitral cells and a few tufted cells, which are similar in size to mitral cells. Some of the granule cell dendrites in the plexiform layer contact mitral cell dendrites through a specialized dendrodendritic synapse, which also is termed a reciprocal synapse (vesicles seen within both presynaptic and postsynaptic membranes).

Tufted cells also receive granule cell input through dendrodendritic and dendrosomatic contact. Pyramidal mitral cells are the largest neurons in the bulb and are located in a narrow band between the external and internal plexiform layers. The granule cell layer contains multiple small round neurons that lack axons. Long dendritic processes of the neurons reach the more superficial layers and inhibit mitral cells and tufted cells. Small distal processes make contacts with the exiting mitral cell axons.

Olfactory Tract and Central Pathways

Mitral cell axons project to the olfactory cortex via the olfactory tract. Medial fibers of the tract contact the anterior olfactory nucleus and the septal area. Some fibers project to the contralateral olfactory bulb via the anterior commissure. Lateral fibers contact third-order neurons in the primary olfactory cortex (prepyriform and entorhinal areas) directly. Third-order neurons send projections to the dorsomedial nucleus of the thalamus, the basal forebrain, and the limbic system.

The thalamic connections are thought to serve as a conscious mechanism for odor perception, while the amygdala and the entorhinal area are limbic system components and may be involved in the affective components of olfaction. Investigations of regional cerebral blood flow have demonstrated a significant increase in the amygdaloid nucleus with the introduction of a highly aversive odorant stimulus, and this has been associated with subjective perceived aversiveness.

Central Projections

The pyriform lobe includes the olfactory tract, the uncus, and the anterior part of the parahippocampal gyrus. The prepyriform and the periamygdaloid areas of the temporal lobe represent the primary olfactory cortex. The entorhinal area is known as the secondary olfactory cortex and is included in the pyriform lobe. The olfactory system is the only sensory system that has direct cortical projections without a thalamic relay nucleus. The dorsomedial nucleus of the thalamus receives some olfactory fibers that ultimately reach the orbitofrontal cortex.

The anterior olfactory nucleus receives collateral fibers from the olfactory tract and projects to the contralateral olfactory bulb and anterior olfactory nucleus via the anterior commissure.

The region of anterior perforated substance contains cells that receive direct mitral cell collaterals and input from the anterior olfactory nucleus, amygdaloid nucleus, and temporal cortex. This area ultimately projects to the stria medullaris and the medial forebrain bundle.

Using the uncinate fasciculus, the entorhinal area sends projections to the hippocampal formation, anterior insula, and frontal cortex.

Clinical Correlation

As many as 2 million people in the United States experience some type of olfactory dysfunction, causes of which include head trauma, upper respiratory infections, tumors of the anterior cranial fossa, and exposure to toxic chemicals or infections. The following terms are used to describe the degree of smell aberration:
Anosmia - Absence of smell sensation
Hyposmia - Decreased sensation
Dysosmia - Distortion of smell sensation
Cacosmia - Sensation of a bad or foul smell
Parosmia - Sensation of smell in the absence of appropriate stimulus

Olfactory dysfunction is a hallmark of certain syndromes such as Kallmann syndrome (ie, hypogonadism with anosmia) and Foster Kennedy syndrome (ie, papilledema, unilateral anosmia, and optic atrophy usually associated with an olfactory groove meningioma).

The classic description of partial complex epilepsy with a mesial temporal focus includes an aura of foul-smelling odors (termed uncinate fits) that occur before seizure onset, emphasizing presumed origination at the uncus.

Olfactory dysfunction is associated with early Parkinson disease and with other neurodegenerative disorders such as Alzheimer disease and Huntington chorea.[1] An association also exists between abnormal olfactory identification and obsessive-compulsive disorder.[2]

Head trauma leading to fracture of the cribriform plate may cause cerebrospinal fluid (CSF) rhinorrhea and a potential for meningitis. Paranasal sinus endoscopy may lead to violation of the cribriform plate and potential infectious complications. Olfactory structures also can be injured during craniotomies involving the anterior cranial base or from subarachnoid hemorrhage, which may disrupt the fine fibers of the olfactory nerve.

Clinical Evaluation

Detection of olfactory dysfunction begins with sampling of a series of common odors, which can be performed at the bedside with odiferous substances such as coffee, lemon, and peppermint. Tests, including those developed at the Connecticut Chemosensory Clinical Research Center (CCCRC), have aided examiners in identification of abnormalities in odor detection and discrimination. The University of Pennsylvania Smell Identification Test (UPSIT) is another useful tool; it consists of 40 items for evaluation of olfactory and trigeminal nerve function in the nasal cavity.

Central hyposmia may manifest as abnormalities in odor recognition rather than odor detection. Thorough evaluation of patients who have anosmia includes imaging of anterior cranial structures. The clinician should always counsel patients with anosmia regarding sensory loss, including potential risks associated with the lack of smell sensation (eg, inability to detect dangers such as smoke, spoiled foods, toxins).

Promptly complete evaluation and treatment of clear rhinorrhea in the patient in whom leakage of CSF is suspected. Initial testing of fluid for glucose suggests CSF but is not confirmatory. Presence of beta-transferrin is a more sensitive indicator of CSF rhinorrhea. Computed tomography with cisternography or radionuclide scans can be used to detect the site of CSF leakage from the anterior cranial fossa. Repair of leaks at the level of the cribriform plate may be achieved from the intracranial approach, intranasal (endoscopic) approach, or both, depending on the nature of the defect.

Positron emission tomography (PET) and functional MRI are promising modalities to assist in making the diagnosis of different types of hyposmia (central vs peripheral), as well as in delineation of the role of limbic structures as sites of odor recognition, memory, and integration of multisensory inputs.

Brachial Plexus

2011-04-18T11:41:00.000-07:00

Overview

The brachial plexus (plexus brachialis) is a somatic nerve plexus formed by intercommunications among the ventral rami (roots) of the lower 4 cervical nerves (C5-C8) and the first thoracic nerve (T1).

The plexus is responsible for the motor innervation to all of the muscles of the upper extremity with the exception of the trapezius and levator scapula. The image below depicts the brachial plexus (BP).


The basic anatomical relationships of the brachial plexus (BP). The BP is subdivided into roots, trunks, divisions, cords, and branches. LC stands for lateral cord, PC stands for the posterior cord, and MC stands for the medial cord

The BP supplies all of the cutaneous innervation of the upper limb, except for the area of the axilla (which is supplied by the supraclavicular nerve) and the dorsal scapula area, which is supplied by cutaneous branches of the dorsal rami.

The BP communicates with the sympathetic trunk via gray rami communicantes, which join the roots of the plexus. They are derived from the middle and inferior cervical sympathetic ganglia and the first thoracic sympathetic ganglion.

Gross Anatomy

Brachial plexus architecture

The brachial plexus (BP) is subdivided into roots, trunks, divisions, cords, and branches. Several mnemonics can be used to remember this architecture (eg, Really Tired Drink Coffee Black). Typically, the brachial plexus is composed of 5 roots, 3 trunks, 6 divisions, 3 cords, and terminal branches, as seen in the image below


Brachial plexus with terminal branches labeled. MC is musculocutaneous (nerve), AXI is axillary, RAD is radial, MED is median, and ULN is ulnar.

Roots

The ventral rami of spinal nerves C5 to T1 are referred to as the "roots" of the plexus. The typical spinal nerve root results from the confluence of the ventral nerve rootlets originating in the anterior horn cells of the spinal cord and the dorsal nerve rootlets that join the spinal ganglion in the region of the intervertebral foramen.

The roots emerge from the transverse processes of the cervical vertebrae immediately posterior to the vertebral artery, which travels in a cephalocaudad direction through the transverse foramina. Each transverse process consists of a posterior and anterior tubercle, which meet laterally to form a costotransverse bar. The transverse foramen lies medial to the costotransverse bar and between the posterior and anterior tubercles. The spinal nerves that form the brachial plexus run in an inferior and anterior direction within the sulci formed by these structures.

Trunks

Shortly after emerging from the intervertebral foramina, the 5 roots (C5-T1) unite to form 3 trunks. The trunks of the BP pass between the anterior and middle scalene muscles.

The ventral rami of C5 and C6 unite to form the upper trunk. The suprascapular nerve and the nerve to the subclavius arise from the upper trunk. The suprascapular nerve contributes sensory fibers to the shoulder joint and provides motor innervation to the supraspinatus and infraspinatus muscles.

The ventral ramus of C7 continues as the middle trunk. The ventral rami of C8 and T1 unite to form the lower trunk .

Divisions

Each trunk splits into an anterior division and a posterior division. These separate the innervation of the ventral and dorsal aspect of the upper limb. The anterior divisions usually supply flexor muscles. The posterior divisions usually supply extensor muscles.

Cords

The cords are referred to as the lateral, posterior, and medial cord, according to their relationship with the axillary artery, as seen in the image below.

The cords pass over the first rib close to the dome of the lung and continue under the clavicle immediately posterior to the subclavian artery.

The anterior divisions of the upper and middle trunks unite to form the lateral cord, which is the origin of the lateral pectoral nerve (C5, C6, C7).

The anterior division of the lower trunk forms the medial cord, which gives off the medial pectoral nerve (C8, T1), the medial brachial cutaneous nerve (T1), and the medial antebrachial cutaneous nerve (C8, T1).

The posterior divisions from each of the 3 trunks unite to form the posterior cord.

The upper and lower subscapular nerves (C7, C8 and C5, C6, respectively) leave the posterior cord and descend behind the axillary artery to supply the subscapularis and teres major muscles. The thoracodorsal nerve to the latissimus dorsi (also known as the middle subscapular nerve, C6, C7, C8) also arises from the posterior cord, as seen in the image below.

Musculocutaneous nerve branch

These are mixed nerves containing both sensory and motor axons (as seen in the image below). The musculocutaneous nerve is derived from the lateral cord. The musculocutaneous nerve leaves the BP sheath high in the axilla at the level of the lower border of the teres major muscle and passes into the coracobrachialis muscle. It innervates the muscles in the flexor compartment of the arm. It carries sensation from the lateral (radial) side of the forearm.

Ulnar nerve branch

The ulnar nerve is derived from the medial cord. Motor innervation is mainly to intrinsic muscles of the hand (as seen in the image below). Sensory innervation is from the medial (ulnar) 1.5 digits (little finger and one-half of the ring finger).

Median nerve branch

The median nerve is derived from both the lateral and medial cords. Motor innervation is to most flexor muscles in the forearm and intrinsic muscles of the thumb (thenar muscles), as seen in the image below. Sensory innervation is to the lateral (radial) 3.5 digits (thumb, index, middle, and half of the ring finger).

Axillary nerve branch

The axillary nerve is derived from the posterior cord. The axillary nerve leaves the BP at the lower border of the subscapularis muscle and continues along the inferior and posterior surface of the axillary artery as the radial nerve. The axillary nerve serves as motor innervation to the deltoid and teres minor muscles, as seen in the image below. These act at the glenohumeral joint. Sensory innervation is from the skin just below the point of the shoulder. The axillary nerve continues as the superior lateral brachial cutaneous nerve of the arm.

Radial nerve branch

The radial nerve is also derived from the posterior cord. The radial nerve continues along the posterior and inferior surface of the axillary artery. The radial nerve innervates the extensor muscles of the elbow, wrist, and fingers, as seen in the image above. Sensory innervation is from the skin on the dorsum of the hand on the radial side.

Terminal Branches

Five "terminal" branches and numerous other "pre-terminal" or "collateral" branches leave the plexus at various points along its length.

Dorsal scapular nerve

The dorsal scapular nerve is derived from the C5 root just after its exit from the intervertebral foramen. It serves as the motor nerve to the rhomboids major and minor muscles

Long thoracic nerve

The long thoracic nerve is derived from C5, C6, and C7 roots immediately after their emergence from the intervertebral foramina. The long thoracic nerve crosses the first rib and then descends through the axilla behind the major branches of the plexus. It innervates the serratus anterior muscle.

Phrenic nerve

The phrenic nerve arises from C3, C4, and C5 root levels, chiefly from the C4 nerve root. It crosses the anterior scalene from lateral to medial and extends into the thorax between the subclavian vein and artery.

Subclavius muscle nerve

The nerve to the subclavius muscle is a small filament, which arises from the upper trunk. It descends to the subclavius muscle in front of the subclavian artery and the lower trunk of the plexus.

Suprascapular nerve

The suprascapular nerve arises from the upper trunk formed by the union of the fifth and sixth cervical nerves. It innervates the supraspinatus muscles and infraspinatus muscles. It runs laterally beneath the trapezius and the omohyoideus and enters the supraspinatus fossa through the suprascapular notch, below the superior transverse scapular ligament; it then passes beneath the supraspinatus and curves around the lateral border of the spine of the scapula to the infraspinatus fossa.

Lateral pectoral nerve

The lateral pectoral nerve arises from the lateral cord of the brachial plexus, from the fifth, sixth, and seventh cervical nerves. It passes across the axillary artery and vein, pierces the coracoclavicular fascia, and is distributed to the deep surface of the pectoralis major. It sends a filament to join the medial anterior thoracic and forms with it a loop in front of the first part of the axillary artery. This nerve innervates the clavicular head of the pectoralis major muscle.

Medial pectoral nerve

The medial pectoral nerve arises from the medial cord from the eighth cervical and first thoracic nerve. It passes behind the first part of the axillary artery, curves forward between the axillary artery and vein, and unites in front of the artery with a filament from the lateral nerve. It then enters the deep surface of the pectoralis minor, where it divides into a number of branches, which supply the muscle. Several branches of the medial pectoral nerve pierce the muscle and end in the pectoralis major, which supply the muscle.

The medial and lateral pectoral nerve often join together to act as a single nerve innervating both the pectoralis major and minor muscles.

Medial brachial cutaneous nerve

The medial brachial cutaneous nerve is the smallest branch of the brachial plexus and, arising from the medial cord, receives its fibers from the eighth cervical and first thoracic nerves. It passes through the axilla, at first lying behind and then medial to the axillary vein, and communicates with the intercostobrachial nerve. It descends along the medial side of the brachial artery to the middle of the arm, where it pierces the deep fascia, and is distributed to the skin of the back of the lower third of the arm, extending as far as the elbow, where some filaments are lost in the skin in front of the medial epicondyle, and others over the olecranon. It communicates with the ulnar branch of the medial antebrachial cutaneous nerve. It carries sensation from the lower medial portion of the arm.

Medial antebrachial cutaneous nerve

The medial antebrachial cutaneous arises from the medial cord of the brachial plexus. It derives its fibers from the eighth cervical and first thoracic nerves, and at its commencement is medial to the axillary artery. It gives off, near the axilla, a filament, which pierces the fascia and supplies the integument covering the biceps brachii, nearly as far as the elbow. The nerve then runs down the ulnar side of the arm medial to the brachial artery, pierces the deep fascia with the basilic vein, about the middle of the arm, and divides into a volar and an ulnar branch.

Microscopic Anatomy

Blood supply of the brachial plexus

The blood supply of the brachial plexus is based largely on the subclavian (which becomes the axillary) artery and its branches, and variations exist. Generally, the vessels involved are the vertebral, the ascending and deep cervical, and the superior intercostal arteries. The cord and rootlets of the cervical nerves are supplied by the anterior and posterior spinal branches of the vertebral artery. The trunks of the plexus are supplied by muscular branches of the ascending and deep cervical arteries and superior intercostals, and occasionally from the subclavian itself.

Natural Variants

Many variant forms of the brachial plexus exist, with none representing most patients. Kerr catalogued 29 forms of the brachial plexus among some 175 cadaver specimens dissected between 1895 and 1910.[2] In the early part of the last century, one author described a total of 38 variations of the plexus. Up to 53.5% of plexuses in cadaver studies possess significant anatomic variation from the "classic" description of the brachial plexus. A study published in September 2003 found variants in 107 of 200 fetuses examined. The authors pointed out that morphological variations were more common in female fetuses and right sides.[3]

Prefixed brachial plexus (cephalic or high)

This occurs when the C4 ventral ramus contributes to the brachial plexus. Contributions to the plexus usually come from the C4-C8.

Postfixed brachial plexus (caudal or low)

This occurs when the T2 ventral ramus contributes to the brachial plexus. Contributions to the plexus usually come from C6-T2.

Other Considerations

Lesions of the Brachial Plexus

Knowledge of the muscles innervated by branches of the brachial plexus and the actions of these muscles and areas of anesthesia and/or paraesthesia allows the physician to determine the localization of a given lesion.

Brachial plexus injuries have numerous causes, such as labor and delivery. A plexus injury at birth is likely caused by a stretch or tear of the child's brachial plexus during the delivery process. The abducted arm of the infant can get pinned against the child's head. This injury results in incomplete sensory and/or motor function of the injured nerve. Traumatic brachial plexus injuries may occur due to motor vehicle accidents, bike accidents, ATV accidents, or sports.

Nerve injuries vary in severity from a mild stretch to the nerve root tearing away from the spinal cord.

Avulsion

The nerve is torn away from its attachment at the spinal cord; this is the most severe type of injury.

Rupture

The nerve is torn, but not at the spinal cord attachment.

Neuroma

Scar tissue has grown around the injury site, putting pressure on the injured nerve and preventing the nerve from sending signals to the muscles.

Neurapraxia

The nerve has been stretched and damaged but not torn.

Diagnoses Related to Brachial Plexus Injuries

Diagnoses related to brachial plexus injuries include Erb palsy, Klumpke palsy, thoracic outlet syndrome, Burner syndrome, and Parsonage-Turner syndrome.

Erb palsy

This condition involves the upper root nerves of C5, C6.
The patient often presents with the arm extended and wrist fully flexed (waiter's tip).
Motor deficits are loss of abduction, flexion, and rotation at the shoulder (axillary, suprascapular, upper, and lower subscapular nerve); weak shoulder extension; and weak elbow flexion and supination of the radioulnar joint (musculocutaneous and radial nerve).
The patient is susceptible to shoulder dislocation due to loss of rotator cuff muscles .
Sensory deficits are to the posterior and lateral aspect of arm (axillary nerve ), radial side of the forearm (musculocutaneous nerve), and thumb and first finger (superficial branch of radial nerve; digital branches of the median nerve ).

Klumpke palsy
This condition involves the lower root nerves of C8 and T1.
This is caused by a rare injury of the lower brachial plexus, usually following breech delivery.
Motor deficits are opposite the thumb (thenar branch of the median nerve), loss of adduction of the thumb (ulnar nerve), loss of abduction and adduction of metatarsophalangeal joints; flexion at the metatarsophalangeal and extension of the interphalangeal joints (deep branch of ulnar and median), and weak flexion of proximal interphalangeal joints and distal interphalangeal joints (ulnar and median nerve).
Sensory deficit is to the ulnar side of the forearm, hand, and ulnar one and a half digits (ulnar and medial antebrachial cutaneous nerve).

Thoracic outlet syndrome
This condition is caused by compression of the neurovascular structures (subclavian vessels, brachial plexus, cervical ganglia, and vertebral artery) in the cervicoaxillary region. It may be congenital or acquired.
Bony causes include the following: long transverse process of the seventh cervical vertebra, cervical rib, anomalous first rib, clavicle fracture, and first rib fracture.
Soft tissue causes include the following: congenital bands, poor posture, mass lesions, cervical strain, hypertrophy, and/or injury of the anterior and middle scalene muscles or the pectoralis minor muscle.

Burner syndrome
This condition is thought to be related to brachial plexus stretch and/or nerve root compression. It generally involves the upper trunk of the brachial plexus, particularly C5-C6.
This condition is usually a result of traction injury with axial distraction or downward force on the shoulder combined with lateral bend of the neck away from the shoulder.
Brachial plexus stretch injuries are found in young athletes, with neck pain being less common.
Nerve root compression is found in older athletes (college), generally associated with cervical disc disease or cervical stenosis. Neck pain is more common.

Parsonage-Turner syndrome (brachial neuritis)
This condition is generally associated with a viral prodrome, immunizations, and significant pain.
Acute excruciating unilateral shoulder pain is present, followed by flaccid paralysis of shoulder and parascapular muscles several days later.
This condition varies greatly in manifestation and nerve involvement. Due to the extreme pain involved, patients usually present acutely. Often, the affected arm is supported by the uninvolved arm and is held in adduction and internal rotation.
The patient may have atrophy of the affected muscles.
Pain may occur with palpation and active and passive range of motion.
Reflexes may be reduced/absent, depending on the nerves involved.
Sensory loss is usually not prominent, although it may be detectable.
This condition may cause scapular winging.

H1N1 Influenza A Virus (Swine Flu)

2011-04-18T11:12:00.000-07:00

The H1N1 influenza A virus (swine flu) is a novel influenza A virus, more properly termed a new subtype of influenza A (H1N1) that was not previously detected in swine or humans. The H1N1 designation refers to hemagglutinin and neuraminidase -- proteins on the surface of the influenza virus that enable the virus to enter and leave host cells. The conformation of these proteins determines the ability of the virus to infect humans; antibodies to these proteins determine humans' ability to resist the infection. Image courtesy of eMedicine.

Influenza A strains that can infect mammals (eg, pigs and humans) may undergo genetic reassortment through contact with avian strains. The reassortment of an avian strain with a mammalian strain may produce a chimeric virus that is transmissible between mammals; such mutation products may contain hemagglutinin and/or neuraminidase proteins that are unrecognizable to the immune systems of mammals. This antigenic shift results in a much greater population of susceptible individuals in whom more severe disease is possible. Image courtesy of the CDC/Dr. E. Palmer; R. E. Bates.

Such antigenic shifts as described on the previous slide can cause a pandemic -- only 3 pandemics have occurred in recorded history. The most striking of these pandemics was the 1918 Spanish influenza, which infected one third of the world's population (an estimated 500 million people) and caused approximately 50 million deaths. Despite its name, this pandemic may well have originated in the United States; the first known outbreak occurred at an Army base in Kansas. Image courtesy of the National Library of Medicine.

There was a significant difference in age-related mortality distributions between the 1918 pandemic and normal influenza epidemics. This graph shows the deaths per 100,000 persons in each age group in the United States from 1911 to 1917 (dashed line) and in the pandemic year, 1918 (solid line). Image courtesy of the United States Federal Government.

A 1976 outbreak of swine influenza in Fort Dix, New Jersey, involved more than 200 cases, some of them severe, including 1 death. The fear of an influenza pandemic led to a national campaign in the United States designed to immunize nearly the entire population. Approximately 40 million people received the A/NewJersey/1976/H1N1 vaccine before the initiative was halted because of the strong association between the vaccine and Guillain-Barré syndrome. About 500 cases of Guillain-Barré syndrome were reported, with 25 deaths due to associated pulmonary complications. Subsequent influenza vaccines did not have this strong association. Image courtesy of the United States Federal Government.

In the current outbreak in the United States, preliminary testing has shown the same genetic pattern in all cases of the virus. The virus is being described as a new subtype of influenza A/H1N1, one that has not previously been detected in either swine or humans. On April 26, 2009, the US Department of Health and Human Services declared a national public health emergency involving swine influenza A, citing its significant potential to affect national security. Image courtesy of the CDC/Dr. Erskine L. Palmer; Dr. M. L. Martin.

In response to the spread of the virus, the World Health Organization raised its pandemic alert level for H1N1 influenza to phase 6 on June 11. Phase 6 is characterized by sustained community-level transmission of the virus in more than 1 World Health Organization region of the world. As of September 30, laboratory-confirmed cases of pandemic influenza H1N1 had been reported in 191 countries and territories worldwide. Image courtesy of the World Health Organization.

Rapid influenza diagnostic tests are commercially available. These tests can provide results within 30 minutes or less for point-of-care decisions. However, they cannot distinguish between seasonal influenza A and H1N1 influenza, nor can they provide information about antiviral drug susceptibility. In addition, a negative result does not rule out H1N1 infection. Confirmation of H1N1 influenza infection requires laboratory testing of a respiratory specimen. Image courtesy of CDC/Greg Sykes, ATCC.

Personnel providing direct patient care for suspected or confirmed cases of H1N1 influenza should wear a fit-tested disposable N95 respirator when entering the patient's room. Healthcare personnel should wash their hands with soap and water or use hand sanitizer immediately after any contact with respiratory secretions. Isolation precautions should be continued for 7 days from symptom onset or until the resolution of symptoms, whichever is longer. Image courtesy of CDC/C. S. Goldsmith and A. Balish.

For confirmed, probable, or suspected cases of influenza A (H1N1) virus infection, healthcare providers should consider antiviral treatment with oseltamivir or zanamivir for 5 days. Hospitalized patients and patients at higher risk for influenza complications should be prioritized. Antiviral treatment is recommended as soon as possible after symptom onset. Antiviral medications should be used during pregnancy only if the potential benefit outweighs the potential risk to the embryo or fetus. Infants younger than 1 year of age who typically have high rates of morbidity and mortality from influenza may benefit from treatment with oseltamivir. Image included with permission and copyrighted by First DataBank, Inc.

In addition to empiric antiviral treatment for confirmed, probable, or suspected cases of influenza A (H1N1), basic supportive therapy, as used in previous pandemics, should be provided and include bed rest, increased fluid consumption, cough suppressants, and antipyretics and analgesics (eg, acetaminophen, nonsteroidal anti-inflammatory drugs) for fever and myalgias. Severe cases may require intravenous hydration and other supportive measures. Image included with permission and copyrighted by First DataBank, Inc.

On September 15, the Food and Drug Administration approved four vaccines for use against the 2009 H1N1 influenza virus. National distribution is expected in October. The vaccine can be given at the same time as seasonal influenza vaccine. Image courtesy of CDC/Judy Schmidt.

Atelectasis

2011-04-18T10:44:00.000-07:00

Background

The term atelectasis is derived from the Greek words ateles and ektasis, which mean incomplete expansion. Atelectasis is defined as diminished volume affecting all or part of a lung. Pulmonary atelectasis is one of the most commonly encountered abnormalities in chest radiology findings. Recognizing an abnormality due to atelectasis on chest x-ray films can be crucial to understanding the underlying pathology. Several types of atelectasis exist; each has a characteristic radiographic pattern and etiology. Atelectasis is divided physiologically into obstructive and nonobstructive causes.

Obstructive atelectasis

Obstructive atelectasis is the most common type and results from reabsorption of gas from the alveoli when communication between the alveoli and the trachea is obstructed. The obstruction can occur at the level of the larger or smaller bronchus. Causes of obstructive atelectasis include foreign body, tumor, and mucous plugging. The rate at which atelectasis develops and the extent of atelectasis depend on several factors, including the extent of collateral ventilation that is present and the composition of inspired gas. Obstruction of a lobar bronchus is likely to produce lobar atelectasis; obstruction of a segmental bronchus is likely to produce segmental atelectasis. Because of the collateral ventilation without a lobe or between segments, the pattern of atelectasis often depends on collateral ventilation, which is provided by the pores of Kohn and the canals of Lambert.

Nonobstructive atelectasis

Nonobstructive atelectasis can be caused by loss of contact between the parietal and visceral pleurae, compression, loss of surfactant, and replacement of parenchymal tissue by scarring or infiltrative disease. Examples of nonobstructive atelectasis are described below.

Relaxation or passive atelectasis results when a pleural effusion or a pneumothorax eliminates contact between the parietal and visceral pleurae. Generally, the uniform elasticity of a normal lung leads to preservation of shape even when volume is decreased. The different lobes also function differently, eg, the middle and lower lobes collapse more than the upper lobe in the presence of pleural effusion, while the upper lobe may be affected more by pneumothorax.

Compression atelectasis occurs from any space-occupying lesion of the thorax compressing the lung and forcing air out of the alveoli. The mechanism is similar to relaxation atelectasis.

Adhesive atelectasis results from surfactant deficiency. Surfactant normally reduces the surface tension of the alveoli, thereby decreasing the tendency of these structures to collapse. Decreased production or inactivation of surfactant leads to alveolar instability and collapse. This is observed particularly in acute respiratory distress syndrome (ARDS) and similar disorders.

Cicatrization atelectasis results from diminution of volume as a sequela of severe parenchymal scarring and is usually caused by granulomatous disease or necrotizing pneumonia. Replacement atelectasis occurs when the alveoli of an entire lobe are filled by tumor (eg, bronchioalveolar cell carcinoma), resulting in loss of volume.

Right middle lobe syndrome

Right middle lobe syndrome is a disorder of recurrent or fixed atelectasis involving the right middle lobe and/or lingula. It can result from either extraluminal (bronchial compression by surrounding lymph nodes) or by intraluminal bronchial obstruction. It may develop in the presence of a patent lobar bronchus without identifiable obstruction. Inflammatory processes and defects in the bronchial anatomy and collateral ventilation have been designated as the nonobstructive causes of middle lobe syndrome.[1] Timely medical intervention in patients

(especially children) with middle lung syndrome, including fiberoptic bronchoscopy with bronchoalveolar lavage, prevents bronchiectasis that may be responsible for recurrent infections and an ultimately unfavorable outcome of chronic atelectasis.[2]

Middle lobe syndrome has been reported as a pulmonary manifestation of primary Sjögren syndrome. Transbronchial biopsies performed in such patients revealed lymphocytic bronchiolitis in the atelectatic lobes. Atelectasis responds well to glucocorticoid treatment, suggesting that the peribronchiolar lymphocytic infiltrates may play an important role in the development of middle lobe syndrome in these patients

Rounded atelectasis

Rounded atelectasis represents folded atelectatic lung tissue with fibrous bands and adhesions to the visceral pleura. Incidence is high in asbestos workers (65-70% of cases), most likely due to a high degree of pleural disease. Affected patients typically are asymptomatic, and the mean age at presentation is 60 years.

Pathophysiology

The mechanism of obstructive and nonobstructive atelectasis is quite different and is determined by several factors

Obstructive atelectasis

Following obstruction of a bronchus, the circulating blood absorbs the gas in the peripheral alveoli, leading to retraction of the lung and an airless state within a few hours. In the early stages, blood perfuses the airless lung; this results in ventilation-perfusion mismatch and arterial hypoxemia. A filling of the alveolar spaces with secretions and cells may occur, thereby preventing complete collapse of the atelectatic lung. The uninvolved surrounding lung tissue distends, displacing the surrounding structures. The heart and mediastinum shift toward the atelectatic area, the diaphragm is elevated, and the chest wall flattens.

If the obstruction is removed, any complicating postobstructive infection subsides and the lung returns to its normal state. If the obstruction is persistent and infection continues to be present, fibrosis develops and the lung becomes bronchiectatic.

Nonobstructive atelectasis

The loss of contact between the visceral and parietal pleurae is the primary cause of nonobstructive atelectasis. A pleural effusion or pneumothorax causes relaxation or passive atelectasis. Pleural effusions affect the lower lobes more commonly than pneumothorax, which affects the upper lobes. A large pleural-based lung mass may cause compression atelectasis by decreasing lung volumes.

Adhesive atelectasis is caused by a lack of surfactant. The surfactant has phospholipid dipalmitoyl phosphatidylcholine, which prevents lung collapse by reducing the surface tension of the alveoli. Lack of production or inactivation of surfactant, which may occur in ARDS, radiation pneumonitis, and blunt trauma to the lung, cause alveolar instability and collapse.

Middle lobe syndrome (recurrent atelectasis and/or bronchiectasis involving the right middle lobe and/or lingula) has recently been reported as the pulmonary manifestation of primary Sjögren syndrome.

Scarring of the lung parenchyma leads to cicatrization atelectasis.

Replacement atelectasis is caused by filling of the entire lobe by a tumor such as bronchoalveolar carcinoma.

Platelike atelectasis

Also called discoid or subsegmental atelectasis, this type is seen most commonly on chest radiographs. Platelike atelectasis probably occurs because of obstruction of a small bronchus and is observed in states of hypoventilation, pulmonary embolism, or lower respiratory tract infection. Small areas of atelectasis occur because of inadequate regional ventilation and abnormalities in surfactant formation from hypoxia, ischemia, hyperoxia, and exposure to various toxins. A mild-to-severe gas exchange abnormality may occur because of ventilation-perfusion mismatch and intrapulmonary shunt.

Postoperative atelectasis

Atelectasis is a common pulmonary complication in patients following thoracic and upper abdominal procedures. General anesthesia and surgical manipulation lead to atelectasis by causing diaphragmatic dysfunction and diminished surfactant activity. The atelectasis is typically basilar and segmental in distribution. After induction of anesthesia, atelectasis increases from 1 to 11% of total lung volume. End-expiratory lung volume is also found to be decreased.

In 2009 study, a recruitment maneuver plus positive end-expiratory pressure (PEEP) reduced atelectasis to 3 ±4%, increased end-expiratory lung volume, and increased the PaO2/FiO2 ratio from 266 ±70 mm Hg to 412 ±99 mm Hg. It was found that the PEEP alone did not reduce the amount of atelectasis or improve oxygenation, but a recruitment maneuver followed by PEEP reduced atelectasis and improved oxygenation.

Epidemiology

Frequency

United States

Postoperative atelectasis is extremely common. Lobar atelectasis is also common. The incidence and prevalence of this disorder are not well documented.

Mortality/Morbidity

Patient mortality depends on the underlying cause of atelectasis. In postoperative atelectasis, the condition generally improves. The prognosis of lobar atelectasis secondary to endobronchial obstruction depends on treatment of the underlying malignancy.

Race

Atelectasis has no racial predilection.

Sex

Atelectasis has no sexual predilection

Age

The mean age at presentation for rounded atelectasis is 60 years.

Cellulitis

2011-04-16T10:15:00.000-07:00

Background

The term cellulitis is commonly used to indicate a nonnecrotizing inflammation of the skin and subcutaneous tissues, a process related to acute infection that does not involve the fascia or muscles and that is characterized by localized pain, swelling, tenderness, erythema, and warmth.

Cellulitis was classically considered to be an infection without formation of abscess and without purulent drainage or ulceration. In clinical practice, the division between cellulitis and abscess is not distinct. Frequently, the macular erythema of cellulitis coexists with nodules, areas of ulceration, and frank abscess formation (see Clinical Presentation). The following images illustrate some of these presentations.

Media file 1: Mild cellulitis with a fine lacelike pattern of erythema. This lesion was only slightly warm and caused minimal pain, which is typical for the initial presentation of mild cellulitis.

Media file 2: Cellulitis involving the hand.

Media file 3: Severe cellulitis of the leg in a woman aged 80 years. The cellulitis developed beneath a cast and was painful and warm to the touch. Significant erythema is evident. The margins are irregular but not raised. An ulcerated area is visible in the center of the photograph.

Pathophysiology

Cellulitis usually follows a break in the skin, such as a fissure, cut, laceration, insect bite, or puncture wound. Organisms on the skin and its appendages gain entrance to the dermis and multiply to cause cellulitis. Facial cellulitis of odontogenic origin may also occur. However, cellulitis frequently occurs in areas where no apparent injury exists. This is common in dry and irritated skin where microscopic breaks allow penetration of bacteria. Patients with toe web intertrigo and/or tinea pedis and those with lymphatic obstruction, venous insufficiency, pressure ulcers, and obesity are particularly vulnerable to recurrent episodes of cellulitis.[1, 2, 3, 4]

The vast majority of cases are caused by Streptococcus pyogenes or Staphylococcus aureus. Occasionally, cellulitis may be caused by the emergence of subjacent osteomyelitis. Cellulitis may rarely result from the metastatic seeding of an organism from a distant focus of infection, especially in immunocompromised individuals. This is particularly common in cellulitis due to S pneumoniae (pneumococcus) and marine vibrios. Neisseria meningitidis, Pseudomonas aeruginosa, Brucella species, and Legionella species have also been reported as rare causes of cellulitis resulting from hematogenous spread.[5]

Etiology

Host factors

Certain host factors predispose to severe infection. Individuals with comorbid conditions such as diabetes mellitus (frequently polymicrobial), immunodeficiency, cancer, venous stasis, chronic liver disease, peripheral arterial disease, chronic kidney disease, and other systemic disease appear to be at a higher risk for both recurrent and more severe infection, owing to an altered host immune response. Other factors that affect host immunity and predispose to cellulitis include concurrent intravenous (IV) or subcutaneous (SC) “skin popping” drug use; infections in this setting are most often polymicrobial, but community-associated methicillin-resistant S aureus (CA-MRSA) is also a common pathogen.

In individuals with normal host defenses, the most common causative organisms are group A streptococci (GAS) and S aureus. Group B Streptococcus cellulitis occurs in infants younger than 6 months, as their immune responses are not fully developed. The cellulitis may present as sepsis[6] ; underlying osteomyelitis or septic arthritis must be excluded in these infants. (See the image below.)

Media file 6. A case of cellulitis without associated purulence in an infant. Note the presence of lymphedema, a risk factor for cellulitis (Photo courtesy of Amy Williams).

In children, facial cellulitis is frequently associated with H influenzae type B and S pneumoniae; prophylactic pneumococcal vaccine may be effective in the latter cases. A study of one-half million pediatric hospitalizations demonstrated that, although bacterial meningitis and epiglottitis diminished as a result of immunization for H influenzae type B and S pneumoniae, the incidence of facial cellulitis was unaffected.[7] However, another study noted that 96% of the serotypes that cause facial cellulitis are included in the heptavalent-conjugated pneumococcal vaccine that is licensed in the United States.

Immunocompromised hosts typically become infected from opportunistic organisms, including gram-negative rods (eg, Pseudomonas, Proteus, Serratia, Enterobacter, Citrobacter), anaerobes, and others (eg, Helicobacter cinaedi, Fusarium species). Although fungi (eg, Cryptococcus) may also cause cellulitis, this is rare.

Pneumococci may cause a particularly malignant form of cellulitis that is frequently associated with tissue necrosis, suppuration, and bloodstream invasion. Two distinct syndromes are recognized: the first is marked by involvement of the extremities in patients with diabetes or substance abuse, and the second is marked by involvement of the head, neck, and upper torso in patients with systemic lupus erythematosus, nephrotic syndrome, or hematologic disorders.[8]

Mycobacterial infections may present as cellulitis. Typically, the lack of response to antibiotics prompts further investigation. The diagnosis is made based on the presence of granulomas, multinucleated giant cells, and acid-fast bacilli (AFB) from biopsy specimens.[9, 10, 11]

S aureus is the leading cause of soft-tissue infections in injection drug users,[12] followed by Streptococcus species.[13]

Gram-negative bacteria may cause bullous cellulitis in patients with cirrhosis.[14] Early recognition is vital, as the course of the disease is rapid, typically progressing to septic shock and death. Gram stain and culture of fluid aspirated from the bullae may aid in management.

Recurrent staphylococcal cellulitis may occur in patients with nasal carriage of staphylococci and those with Job syndrome.

Hospital-acquired infections

Various hospital-acquired infections following soft-tissue trauma may lead to cellulitis, such as those around surgical wounds less than 24 hours postoperatively (group A beta-hemolytic Streptococcus [GABHS] or Clostridium perfringens, which produces gas that may be appreciated as crepitus on examination) or from gunshot wounds or invasive devices (Acinetobacter baumannii is an emerging multidrug-resistant pathogen in these scenarios.)[15]

Cellulitis due to lymphatic obstruction or venectomy is generally caused by non–group A streptococci (ie, groups B, C, and G).[16, 17] Postvenectomy status following saphenous vein stripping can also result in cellulitis[16] and is associated with tinea pedis; culture of toe web spaces may assist in identifying a bacterial pathogen.[18] Lymphadenectomy following tumor excision, such as mastectomy, is also a predisposing factor for cellulitis.

Varicella

Cellulitis can complicate varicella and may be identified by a margin of erythema surrounding the vesicles. In one study, patients with invasive GAS cellulitis complicating varicella were identified.[19] The median onset of GAS infection was day 4 of varicella, with fever, vomiting, and localized swelling reported.[19] This condition mandates antibiotic treatment and careful clinical follow-up. Untreated cellulitis in association with varicella may progress to severe necrotizing soft-tissue infections requiring surgical intervention.[20]

MRSA

Cellulitis can be complicated by abscess formation. A maxim in microbiology states, "The hallmark of staph infection is abscess formation." This has become a significant concern due to changing patterns of antibiotic resistance in S aureus, particularly MRSA.[21]

MRSA was first reported in 1968[22] ; for years, MRSA infections were identified only in patients with recent hospitalization, surgery, renal dialysis, residence in long-term-care facilities, or IV drug use. However, in recent years, isolates of S aureus have been found in patients without risk factors for nosocomial disease.[23] These isolates have been termed CA-MRSA to distinguish them from the previously identified hospital or healthcare-associated MRSA (HA-MRSA). (See the images below.)

Although reports have indicated that MRSA causes the majority of skin and soft-tissue infections (SSTIs), these studies are plagued by variability in case-finding methodologies.[24] Furthermore, in the context of cellulitis, the finding is misleading in that these reports come from analysis of wound cultures in cases in which abscess formation occurred. Cultures in cellulitis are difficult to perform and are infrequently done. Therefore, the results of these studies cannot be generalized to cellulitis without abscess formation. Studies are under way to determine the incidence of S aureus —in particular, CA-MRSA in soft-tissue infection in which there is no identifiable abscess. However, until results of those studies are available, treatment decisions must be made on clinical grounds.

Media file 7. Patient with cellulitis of the left ankle. Note the area of drainage. This cellulitis was caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. of Public Health)

Media file 8. Abscess and associated cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. of Public Health)

Bite wounds, lacerations, and puncture wounds

Mammalian bite wounds represent a specific subset of cellulitis with unique pathogens. The infections are usually polymicrobial.[25] Human, dog, cat, and wild-animal bites all predispose to cellulitis with unique pathogens, but dogs are the most commonly encountered bite wound in both the primary care and emergency setting.[26] Several organisms are of particular interest in animal bites, including the following[25] :
Capnocytophaga canimorsus (dog)
Eikenella corrodens (human)
Pasteurella multocida (dog or cat)
Streptobacillus moniliformis (rat)

Puncture wounds, especially through the bottom of athletic shoes, may cause Pseudomonas osteomyelitis and/or cellulitis. However, lacerations and puncture wounds sustained in an aquatic environment (eg, oceans, lakes, streams) may be contaminated with bacteria not typically found in land-based injuries, including Aeromonas hydrophila, Pseudomonas and Plesiomonas species, Vibrio species, Erysipelothrix rhusiopathiae, Mycobacterium marinum, and others.[27] Individuals with chronic liver disease are particularly susceptible to V vulnificus infections (see the image below).[28]

Media file 5. Cellulitis due to documented Vibrio vulnificus infection. Image courtesy of Kepler Davis.

Epidemiology

Because cellulitis is not a reportable disease, the exact prevalence is uncertain; however, it is a relatively common infection, affecting all racial and ethnic groups. There is no statistically significant difference in the incidence of cellulitis in men and women,[29] and no age predilection is usually described. However, studies have found a higher incidence of cellulitis in general among individuals older than 45 years.[2, 30, 31] Cellulitis was found to be more common in geriatric patients in a retrospective study of international travelers by the GeoSentinel Surveillance Network.[32]

Certain age groups are at a higher risk in some unique scenarios, such as the following:
Historically, buccal cellulitis caused by H influenzae type B was more common in children younger than age 3 years. Vaccination against this organism may have decreased the incidence of buccal cellulitis, but recent data suggest that this source remains a consideration, even in vaccinated cohorts.[7]
Facial cellulitis is more common in adults older than 50 years. However, pneumococcal facial cellulitis occurs primarily in young children who are at risk for pneumococcal bacteremia.[8, 33]
Perianal cellulitis, usually with GABHS, occurs in children younger than 3 years.[34]
Elderly patients with cellulitis are predisposed to thrombophlebitis.

A 2006 study of an insurance database in Utah found an incidence rate of 24.6 cases per 1000 person-years. The incidence was noted to be higher in males and in those individuals aged 45-64 years.[30] In a large epidemiologic hospital-based study on skin, soft-tissue, bone, and joint infections, 37.3% patients were identified as having cellulitis.[35]

Overall rates of visits increased for skin and soft-tissue infections (SSTIs) from 32.1 to 48.1 visits per 1000 population and reached 14.2 million by 2005, and visits for abscess and cellulitis increased from 17.3 to 32.5 visits per 1000 population and accounted for more than 95% of the increase, according to the National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey. The study provided data regarding visits by patients with SSTIs to physician offices, hospital outpatient departments, and emergency departments in the United States.[36]

Cellulitis was found to account for approximately 3% of emergency medical consultations at one United Kingdom district general hospital.

Prognosis

The vast majority of cellulitis and soft-tissue infections can be treated on an outpatient basis with oral antibiotics and do not result in lasting sequelae. Most patients’ conditions respond well to standard oral antibiotics. When outpatient therapy is unsuccessful and for patients who require admission initially, IV antibiotics are usually effective.

Because cellulitis may progress to serious illness by uncontrolled contiguous spread or via the lymphatic or circulatory systems, complications include lymphangitis, abscess formation, gangrenous cellulitis, and necrotizing fasciitis.[37] Certain strains of bacteria, most notably group A beta-hemolytic Streptococcus (GABHS) and S aureus, produce toxins that may mediate a more severe systemic infection, leading to septic shock and death.

Patient Education

Depending on the location of the affected area, the patient may want to decrease physical activity and elevate the extremity, if possible. They may take over-the-counter (OTC) pain medication such as acetaminophen (Tylenol) or ibuprofen (Advil, Motrin) for pain, if approved by their physician.

Patients should call their doctor's office immediately if they have any of the following features:
Fever (>100.5°F), especially when associated with chills
Cellulitis with soft, fluctuant areas suggestive of abscess formation
A red streak from an area of cellulitis or a fast-spreading area of redness, which indicates that the infection may need a different antibiotic or an IV antibiotic
Significant pain not relieved by acetaminophen or ibuprofen
Inability to move an extremity or joint because of pain

Patients with diabetes, cancer, or immunosuppression should be made aware that localized cellulitis may become serious.

For additional patient education resources, visit eMedicine's Diabetes Center. Also, see eMedicine's patient education article Cellulitis

Nasal polyp surgery

2011-04-16T05:18:00.000-07:00

Background

Polyp formation in the nasal cavity is due to chronic allergic rhinitis, chronic sinusitis, and, less commonly, underlying disease such as cystic fibrosis. Patients usually present with nasal obstruction, persistent nasal discharge (rhinorrhea), sinus infection, and loss of the sense of smell (anosmia) of prolonged duration.

History of the Procedure

Knowledge of nasal polyposis extends to medical antiquity. The disease process was mentioned in Egyptian and Indian medical treatises 2500-3000 years ago.

Through the ages, several treatments have been advocated, including cautery with hot irons, application of caustic chemical substances, abrasion by drawing rags through the choanae and out the nose, and snaring.

Today, the standard surgical therapy is endoscopically guided removal of diseased tissues with preservation of maximal amount of normal nasal mucosa.

Problem

Patients usually have chronic nasal symptoms prior to detection of nasal polyps.

Epidemiology

Frequency

The frequency of nasal polyps is uncertain. Only 0.5% of individuals with atopic symptoms manifest nasal polyposis, and most patients with diffuse nasal polyposis do not demonstrate an immunoglobulin E (IgE)–mediated type 1 hypersensitivity reaction. Patients with cystic fibrosis have a higher prevalence of nasal polyposis (up to 40%).

Etiology

Polyp development within nasal and sinus regions implicates an IgE-type hypersensitivity and an immunologic or possibly inflammatory basis for such formation.

The exact etiology of polyp formation is unknown. Research is demonstrating an eosinophil-mediated mechanism with damage to the mucosa by major basic protein, but the complicated interplay of secondary messengers and chemical mediators is not clear.

Nasal polyposis in association with cystic fibrosis, sinobronchial syndrome, aspirin sensitivity, and Samter triad (asthma, aspirin allergy, nasal polyposis) indicates manifestation of nasal mucosal damage by many different possible disease processes.

Pathophysiology

The polyp surface consists of pseudostratified respiratory epithelium and is subject to metaplasia due to local pressure and trauma. Polyps can undergo fibrosis and neovascularization.

Presentation

Patients present with nasal airway obstruction, chronic rhinosinusitis, exacerbation of asthma, and nasal and facial deformity (rarely).[1, 2] Patients may also present with bleeding and anosmia. Not insignificantly, these patients may have undergone recurrent surgery and costly medical therapy.

Indications

The patient may require surgical intervention if severe symptoms of obstruction and infection prove refractory to medical treatment.

Medical therapies include treatment for underlying chronic allergic rhinitis using antihistamines and topical nasal steroid sprays. For severe nasal polyposis causing severe nasal obstruction, treatment with short-term steroids may be beneficial. Topical use of cromolyn spray has also been found to be helpful to some patients in reducing the severity and size of the nasal polyps.

Within the nasal and sinus region, polyps originate from the middle meatus/ostiomeatal complex. With surgical removal of diseased tissues (polyps), future recurrence of polyp formation is still possible. In endoscopic sinus surgery, the goal is to remove diseased tissue and provide adequate sinus aeration in order to prevent recurrence.

Relevant Anatomy

Nasal polyps can develop in all the paranasal sinuses, but the region of middle meatus/osteomeatal complex lateral to the middle turbinate is of great importance.

Contraindications

Severe pulmonary or cardiac problems may be contraindications to surgical treatment. Relative contraindications to surgical treatment include bleeding diathesis (which can be medically treated before surgery), acute asthma exacerbation, and the patient's inability or unwillingness to obtain appropriate postoperative follow-up care and treatment.

open heart surgery at the wellcome institute

2011-04-16T04:51:00.000-07:00

Treatment of Atherosclerosis

2011-04-16T03:21:00.000-07:00

The prevention and treatment of atherosclerosis require risk factor control, including the medical treatment of hypertension, hyperlipidemia, diabetes mellitus, and cigarette habituation.

Some studies have claimed reversal of atherosclerosis with pharmacologic agents such as statins and cilostazol, but these need to be further tested before it can be determined whether they offer any significant benefit in reducing clinical events.[7]

Advances in the understanding of the vascular biology of atherosclerosis have raised the possibility of using novel therapies to address more directly the various aspects of endothelial dysfunction and the role of endothelial dysfunction in atherogenesis. Potential cellular targets include vascular smooth muscle cells, monocyte/macrophage cell lines, platelets, and endothelial cells. Evidence exists that antiplatelet agents, antioxidant therapies, amino acid supplementation, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin receptor blockers may prove to prevent or slow the progression of the disease.

Treatment of hypertension

The dietary and pharmacologic treatment of hypertension is associated with a decreased incidence of stroke.

Management of hyperlipidemia and dyslipidemia

The 3-hydroxy-3-methyl Co-A (HMG-CoA) reductase inhibitors inhibit the rate-limiting step of cholesterol synthesis in the liver. They are effective in lowering the serum total cholesterol, LDL cholesterol, and triglyceride levels and in raising the serum HDL cholesterol level. HMG-CoA reductase inhibitors also have a low incidence of adverse effects, the most common being hepatotoxicity and myopathy.

The success of the HMG-CoA reductase inhibitors in reducing circulating lipid levels and improving the clinical and anatomic course of atherosclerosis has focused attention on the management of hyperlipidemia.

In addition, an important role remains for other hypolipidemic agents that may be of particular benefit for patients with refractory LDL hypercholesterolemia, hypertriglyceridemia, low HDL cholesterol, and elevated lipoprotein(a).

Management of diabetes mellitus

For patients with diabetes mellitus, strict control of comorbid risk factors is especially important. Ample evidence exists that such control reduces the incidence of the clinical complications of microvascular and macrovascular disease.

The benefit of strict glycemic control in the prevention of macrovascular disease has been difficult to confirm, although this intuitively is beneficial and is known to retard the progression of microvascular disease.

Treatment of familial hypercholesterolemia

Treatment options for familial hypercholesterolemia include combination drug therapy, although drug therapy alone often is inadequate because of the relative or absolute deficiency of hepatic LDL receptors.

Lipid apheresis is an effective means of reducing circulating lipid levels. Liver transplantation has been performed on young patients with severe disease.

Drug Agents

HMG-CoA reductase inhibitors

These agents are competitive inhibitors of 3-hydroxy-3-methyl Co-A reductase, an enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis, resulting in up-regulation of LDL receptors in response to the decrease in intracellular cholesterol. The HMG-CoA reductase inhibitors are indicated for the secondary prevention of cardiovascular events and for the treatment of hypercholesterolemia and mixed dyslipidemia.

A number of HMG-CoA reductase inhibitors are indicated for patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments. However, these agents may be less effective in patients with rare homozygous familial hypercholesterolemia, possibly because these patients are lacking functional LDL receptors, making it more likely to raise serum transaminases.

HMG-CoA reductase inhibitors include the following:
Pravastatin (Pravachol)
Simvastatin (Zocor)
Lovastatin (Mevacor, Altocor)
Fluvastatin (Lescol)
Atorvastatin (Lipitor)
Rosuvastatin (Crestor)
Pitavastatin (Livalo)

Vitamin E (Vita-Plus E, Softgels, Aquasol E)

This antioxidant protects polyunsaturated fatty acids in membranes from attack by free radicals.

Bile acid sequestrants

The bile acid sequestrants block enterohepatic circulation of bile acids and increase the fecal loss of cholesterol. This results in a decrease in intrahepatic levels of cholesterol. The liver compensates by up-regulating hepatocyte LDL-receptor activity. The net effect is a 10-25% reduction in LDL cholesterol, but no consistent effect on triglycerides or HDL cholesterol exists.

Bile acid sequestrants include cholestyramine (Questran, LoCholest, Prevalite) and colestipol (Colestid).

Atherosclerosis &its risk factors

2011-04-15T11:53:00.000-07:00

Overview of Atherosclerosis
Atherosclerosis is a disease of large and medium-sized muscular arteries and is characterized by endothelial dysfunction, vascular inflammation, and the buildup of lipids, cholesterol, calcium, and cellular debris within the intima of the vessel wall. This buildup results in plaque formation, vascular remodeling, acute and chronic luminal obstruction, abnormalities of blood flow, and diminished oxygen supply to target organs.

Etiology of Atherosclerosis
The mechanisms of atherogenesis remain uncertain. An incompletely understood interaction exists between the critical cellular elements—endothelial cells, smooth muscle cells, platelets, and leucocytes—of the atherosclerotic lesion. Vasomotor function, the thrombogenicity of the blood vessel wall, the state of activation of the coagulation cascade, the fibrinolytic system, smooth muscle cell migration and proliferation, and cellular inflammation are complex and interrelated biologic processes that contribute to atherogenesis and the clinical manifestations of atherosclerosis.

The "response-to-injury" theory is most widely accepted explanation for atherogenesis. Endothelial injury causes vascular inflammation and a fibroproliferative response ensues. Probable causes of endothelial injury include oxidized low-density lipoprotein (LDL) cholesterol; infectious agents; toxins, including the byproducts of cigarette smoking; hyperglycemia; and hyperhomocystinemia.

Circulating monocytes infiltrate the intima of the vessel wall, and these tissue macrophages act as scavenger cells, taking up LDL cholesterol and forming the characteristic foam cell of early atherosclerosis. These activated macrophages produce numerous factors that are injurious to the endothelium.

Elevated serum levels of LDL cholesterol overwhelm the antioxidant properties of the healthy endothelium and result in abnormal endothelial metabolism of this lipid moiety. Oxidized LDL is capable of a wide range of toxic effects and cell/vessel wall dysfunctions that are characteristically and consistently associated with the development of atherosclerosis. These dysfunctions include impaired endothelium-dependent dilation and paradoxical vasoconstriction. These dysfunctions are the result of direct inactivation of nitric oxide by the excess production of free radicals, reduced transcription of nitric oxide synthase messenger ribonucleic acid (mRNA), and posttranscriptional destabilization of mRNA.

The decrease in the availability of nitric oxide also is associated with increased platelet adhesion, increased plasminogen activator inhibitor, decreased plasminogen activator, increased tissue factor, decreased thrombomodulin, and alterations in heparin sulfate proteoglycans. The consequences include a procoagulant milieu and enhanced platelet thrombus formation. Furthermore, oxidized LDL activates inflammatory processes at the level of gene transcription by up-regulation of nuclear factor kappa-B, expression of adhesion molecules, and recruitment of monocytes/macrophages.

The lesions of atherosclerosis do not occur in a random fashion. Hemodynamic factors interact with the activated vascular endothelium. Fluid shear stresses generated by blood flow influence the phenotype of the endothelial cells by modulation of gene expression and regulation of the activity of flow-sensitive proteins. Atherosclerotic plaques characteristically occur in regions of branching and marked curvature at areas of geometric irregularity and where blood undergoes sudden changes in velocity and direction of flow. Decreased shear stress and turbulence may promote atherogenesis at these important sites within the coronary arteries, the major branches of the thoracic and abdominal aorta, and the large conduit vessels of the lower extremities. (This article will focus on noncoronary sites of atherogenesis.)

One study suggested that hypercholesterolemia-induced neutrophilia develops in arteries primarily during early stages of atherosclerotic lesion formation.[1]

The earliest pathologic lesion of atherosclerosis is the fatty streak, which is the result of focal accumulation of serum lipoproteins within the intima of the vessel wall. Microscopy reveals lipid-laden macrophages, T lymphocytes, and smooth muscle cells in varying proportions.

The fatty streak may progress to form a fibrous plaque, the result of progressive lipid accumulation and the migration and proliferation of smooth muscle cells.

Platelet-derived growth factor, insulinlike growth factor, transforming growth factors alpha and beta, thrombin, and angiotensin II are potent mitogens that are produced by the activated platelets, macrophages, and dysfunctional endothelial cells that characterize early atherogenesis, vascular inflammation, and platelet-rich thrombosis at sites of endothelial disruption. The relative deficiency of endothelium-derived nitric oxide further potentiates this proliferative stage of plaque maturation.

The proliferating smooth muscle cells are responsible for the deposition of extracellular connective tissue matrix and form a fibrous cap that overlies a core of lipid-laden foam cells, extracellular lipid, and necrotic cellular debris. Growth of the fibrous plaque results in vascular remodeling, progressive luminal narrowing, blood-flow abnormalities, and compromised oxygen supply to the target organ.

Progressive luminal narrowing of an artery due to expansion of a fibrous plaque results in impairment of flow once more than 50-70% of the lumen diameter is obstructed. Flow impairment causes symptoms of inadequate blood supply to the target organ in the event of increased metabolic activity and oxygen demand.

Developing atherosclerotic plaques acquire their own microvascular network, which consists of a collection of vessels known as the vasa vasorum. These vessels are prone to hemorrhage and contribute to the progression of atherosclerosis.[2]

Denudation of the overlying endothelium or rupture of the protective fibrous cap may result in exposure of the thrombogenic contents of the core of the plaque to the circulating blood. This exposure constitutes an advanced or complicated lesion.

The plaque rupture occurs due to weakening of the fibrous cap. Inflammatory cells localize to the shoulder region of the vulnerable plaque. T lymphocytes elaborate interferon gamma, an important cytokine that impairs vascular smooth muscle cell proliferation and collagen synthesis. In addition, activated macrophages produce matrix metalloproteinases that degrade collagen. These mechanisms explain the predisposition to plaque rupture and highlight the role of inflammation in the genesis of the complications of the fibrous atheromatous plaque.

A plaque rupture may result in thrombus formation, partial or complete occlusion of the blood vessel, and progression of the atherosclerotic lesion due to organization of the thrombus and incorporation within the plaque.

Development of atherosclerosis from childhood through adulthood

The process of atherosclerosis begins in childhood with the development of fatty streaks. These lesions can be found in the aorta shortly after birth and appear in increasing numbers in persons aged 8-18 years. More advanced lesions begin to develop when individuals are aged approximately 25 years. Subsequently, an increasing prevalence of the advanced complicated lesions of atherosclerosis exists, and the organ-specific clinical manifestations of the disease increase with age through the fifth and sixth decades of life.

Risk Factors for Atherosclerosis

A number of large epidemiologic studies in North America and Europe have identified numerous risk factors for the development and progression of atherosclerosis.

The risk factors can be divided into modifiable and nonmodifiable types and include hyperlipidemia, hypertension, cigarette habituation, diabetes mellitus, age, sex, physical inactivity, and obesity. In addition, a number of novel risk factors have been identified that add to the predictive value of the established risk factors and may prove to be a target for future medical interventions.

Hypertension

Hypertension has been shown, in epidemiologic and experimental studies, to accelerate atherosclerotic vascular disease and increase the incidence of clinical complications.

The mechanism by which hypertension causes these effects is not known, and some uncertainty exists as to what the primary and secondary factors are in a typically multifactorial syndrome. These factors may include the above-mentioned hyperlipidemia, hypertension, diabetes mellitus, obesity, and physical inactivity.

Hypertension is associated with morphologic alterations of the arterial intima and functional alterations of the endothelium that are similar to the changes observed in hypercholesterolemia and established atherosclerosis. Endothelial dysfunction is a feature of hypertension, hyperlipidemia, and atherosclerosis and is known to represent and contribute to the procoagulant, proinflammatory, and proliferative components of atherogenesis.

Diabetes mellitus

This is an important risk factor for hyperlipidemia and atherosclerosis and is commonly associated with hypertension, abnormalities of coagulation, platelet adhesion and aggregation, increased oxidative stress, and functional and anatomic abnormalities of the endothelium, and endothelial vasomotion.

Cigarette smoking

Cigarette smokers have double the risk for stroke compared with nonsmokers.

Familial hypercholesterolemia

Familial hypercholesterolemia is an autosomal dominant disorder caused by a defect in the gene for the hepatic LDL receptor. In the United States, heterozygous familial hypercholesterolemia occurs in approximately 1 in 500 individuals. Homozygous familial hypercholesterolemia occurs in approximately 1 in 1 million individuals in the United States, and total cholesterol may exceed 1000 mg/dL.

cardiac surgery 2

2011-04-15T11:36:00.000-07:00

cardiac surgery

2011-04-15T11:02:00.000-07:00