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		<title>Anaphylactic Shock, A Life-Threatening Condition</title>
		<link>https://www.mark8ng.com/anaphylactic-shock/</link>
		
		<dc:creator><![CDATA[Mary Anne]]></dc:creator>
		<pubDate>Wed, 07 Jul 2021 21:28:31 +0000</pubDate>
				<category><![CDATA[Health & Fitness]]></category>
		<category><![CDATA[Research]]></category>
		<category><![CDATA[Anaphylactic Shock]]></category>
		<category><![CDATA[Medical]]></category>
		<category><![CDATA[Pathophysiology]]></category>
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					<description><![CDATA[<p>Anaphylactic Shock, A Life-Threatening Condition Introduction Anaphylactic shock is a life-threatening condition that can be fatal if treatment is delayed. Anaphylactic shock is defined as “an acute, life-threatening hypersensitivity reaction</p>
<p>The post <a href="https://www.mark8ng.com/anaphylactic-shock/">Anaphylactic Shock, A Life-Threatening Condition</a> appeared first on <a href="https://www.mark8ng.com">Mark8ng.com</a>.</p>
]]></description>
										<content:encoded><![CDATA[<h1>Anaphylactic Shock, A Life-Threatening Condition</h1>
<h2>Introduction</h2>
<p>Anaphylactic shock is a life-threatening condition that can be fatal if treatment is delayed. Anaphylactic shock is defined as <strong>“an acute, life-threatening hypersensitivity reaction to a sensitizing substance”</strong> (Lewis, Bucher, Heitkemper, &amp; Harding, 2017, p. 1590). When a patient is exposed to a sensitized allergen, the reaction escalates rapidly due to the release of inflammatory mediators ultimately causing vasodilation, circulatory failure, and respiratory distress (Lewis, Bucher, Heitkemper, &amp; Harding, 2017). Due to the rapid progression of the condition, nursing students need to accurately identify clinical manifestations and provide immediate interventions. Otherwise, it can be a matter of life and death. Interestingly, anaphylactic shock is not being treated effectively according to a study in 2014. In a survey, out of 410 pediatrician participants with anaphylaxis scenarios, <strong>“just 11.3% of respondents answered all of the questions about management of mild anaphylaxis correctly, while 3.2% correctly answered all of the questions about management of severe anaphylaxis”</strong> (Kornusky &amp; Ashley, 2017, p. 3).</p>
<p>According to CINAHL, <strong>“Anaphylactic shock is fatal in 0.65-2% of cases; 500-1,000 people die from the condition in the U.S. each year”</strong> (Kornusky &amp; Ashley, 2017, p. 2). The purpose of this paper is to educate nursing students on the medical diagnosis of anaphylactic shock as an attempt to decrease the mortality rate of this condition. It encompasses the pathophysiology, signs, symptoms, assessments, diagnostic tests, complications, and interventions.</p>
<h2><strong>Pathophysiology</strong></h2>
<p>Anaphylactic shock is a severe reaction that is experienced by people when exposed to an allergen. Some of the most common allergens that can cause an anaphylactic reaction can be remembered by the mnemonic: MBLF (Many Boys Love Food) referring to medications, beestings, latex, and food. The antibody principally responsible for these reactions is immunoglobulin E (IgE) (Kemp, 2018). This paper will delve into the two categories that cause anaphylactic shock; immunologic and non-immunologic.</p>
<h2><strong>Immunologic</strong></h2>
<p>In immunologic anaphylactic shock, IgE is the main culprit. When exposed to the allergen in the lymphoid tissue, B cells start producing IgE cells with the help of T cells. These specially-formulated IgE cells only respond to the specific allergen it was created for. IgE cells then travel through the body’s circulatory system and tissues to attach to mast cells and basophils and continue to circulate throughout the body. Until the allergen is exposed near to the mast cell or basophil, the attached IgE interacts with the allergen. When multiple IgE antibodies are activated with the same allergen, it causes the cell to become activated thus initiating the inflammatory response by intracellular signaling by releasing mediators such as histamines and tryptase. The released cells either directly cause the inflammatory response to surrounding tissues or activate other inflammatory cells such as eosinophils. This process causes even more intracellular signaling and releases even more histamines and tryptase (Kemp, 2018). Histamines directly respond to surrounding tissue by causing vasodilation and encouraging the vessels to leak intracellular fluid from the vascular system. As a result, the blood pressure (BP) drops causing low oxygen perfusion to tissues and swelling. Consequently, shock is caused (Mannarino, 2014). In simpler terms, the allergen must have been sensitized in order for the reaction to develop. Therefore, the patient would have been exposed to the substance beforehand which may or may not have caused an allergic reaction at that time. During the first exposure, the immune system creates an antibody to detect and fight off the allergen to prepare for the next exposure.</p>
<h2><strong>Non-immunologic</strong></h2>
<p>In the less common non-immunologic anaphylactic shock, specific medications are the primary cause. These types of medications directly activate mast cells and basophils by the receptors without the involvement of IgE. This activation of mast cells and basophils act the same way as the immunologic anaphylactic shock with the production of inflammatory mediators such as histamine. Medications that can cause this type of anaphylactic shock include vancomycin and opiates (Kemp, 2018). It is important for health care providers to consider and observe any allergic reactions when providing such types of medications.</p>
<h2><strong>Clinical Manifestations</strong></h2>
<p>The two chemical mediators in response to IgE activation that cause clinical manifestations are histamine and tryptase. Low level of histamine can cause tachycardia. However, symptoms of hypotension, itching, bronchospasm, and headache are apparent when the levels are increased. Tryptase is a protease (enzyme that breaks down proteins) produced from mast cells specifically. It acts as a coagulant which facilitates hypotension and increases risk for clots. In rare cases, it can also cause disseminated intravascular coagulation (DIC) (Kemp, 2018).</p>
<p>Researchers from BioMed Research International, Tang et al. conducted a study in 2015 on inpatients’ clinical characteristics of anaphylactic shock. The study indicated that the most common clinical presentation of anaphylactic shock is on the skin (observed in up to 90% of studied cases). Integumentary presentations include hives, erythema, itching, and swelling (Tang et al., 2015). It happens due to the inflammatory response of histamine and other cell mediators released from IgE activation. Most common clinical manifestations shown in participants include, <strong>“Rash (62%), Dyspnea (46.3%), Loss of consciousness (38%), Nausea/ Vomiting (27.8%), Pallor (25%), excessive sweating (21.3%), palpitations (18.5%), abdominal pain (13%), facial swelling (12%), Rales heard in the lungs (10.2%), and dizziness (10.2%)”</strong> (Tang et al., 2015, p. 3). Hypotension is another expected symptom with anaphylactic shock due to histamine effects on the vascular permeability. Tang et al. (2015) studied the extent the BP drops during anaphylactic shock and found that, <strong>“the systolic pressure decreased from 117.4 ± 13.8 mmHg during baseline conditions to 54.3 ± 31.9 mmHg during episodes and the diastolic pressure decreased from 71.6 ± 13.6 mmHg during baseline conditions to 33.9 ± 21.4 mmHg during episodes”</strong> (p. 2). This study thus revealed how much the BP can drop during an episode of anaphylactic shock and some clinical presentations to assess while providing early treatment.</p>
<h2><strong>Assessments</strong></h2>
<p>If the patient is not active in anaphylactic shock, prevention is the key. A thorough health history is important to identify allergies and eliminate those allergens from the patient’s care. If a patient mentions an allergy, it is important to ask questions to explore the type of reactions they get from exposure, how they were exposed in the past, progression of condition, and if they have an EpiPen or use other treatments (Lewis, Bucher, Heitkemper, &amp; Harding, 2017).</p>
<p>While in active anaphylactic shock, the primary assessment is airway, breathing, circulation (ABC’s) and management of life-threatening problems. Assessment should also include mental status to ensure adequate oxygenation to the brain tissue. Signs of angioedema should also be assessed with intubation equipment nearby in case of respiratory failure. Management of these will be discussed in the interventions. Secondary assessment is to determine patient’s history of allergies, allergen exposed to, how they were exposed, how long ago they were exposed, progression of symptoms, and interventions the patient has done (such as medications they took). Finally, it is imperative to assess vital signs and obtain remaining information concerning health history (Campbell &amp; Kelso, 2018).</p>
<p>In general, it is important to assess patients for signs and symptoms of anaphylaxis. As mentioned earlier, one of the first manifestations shown is integumentary signs. Other signs that can indicate anaphylaxis are dyspnea, adventitious lung sounds, hives, pallor, swelling, tachycardia, and hypotension (Tang et al., 2015).</p>
<h2><strong>Diagnostic Tests</strong></h2>
<p>During the episode of anaphylactic shock, there is no test that specifically diagnoses the condition. It is purely based on the clinical presentation and history of exposure to allergens. However, laboratory tests, electrocardiogram (EKG), and chest x-rays are used to rule out other conditions and aide in the diagnosis of anaphylactic shock. Laboratory tests that simplify the anaphylactic shock diagnosis are a total tryptase serum and histamine in the plasma. Elevation in these levels indicates anaphylactic shock due to the mass production during the inflammatory process when exposed to a sensitized allergen. These tests are more accurate if there are baseline values to compare to after the anaphylactic shock episode. Total tryptase will have a maximum elevation above baseline values (up to 60 minutes) after onset of anaphylaxis and declines to baseline (approximately 2 hours after). Histamine will elevate 10 min after onset of anaphylaxis and declines to baseline by approximately 30 minutes. Therefore, blood should be drawn as soon as possible after the onset of symptoms to be the most accurate for histamine test and approximately 30-60 min after for the tryptase test (Schwartz, 2018).</p>
<p>Other tests should be considered to rule out additional conditions. Due to manifestations on the lungs and respiratory system, a chest x-ray should be done and evaluated to rule out other respiratory conditions, such as sepsis or pneumonia. It is also recommended to evaluate an EKG to assess for myocardial infarction (MI) (Schwartz, 2018). MI can develop due to the Kounis syndrome’s effect on coronary arteries &#8211; a complication of anaphylactic shock.</p>
<h2><strong>Complications</strong></h2>
<p>Complications that result from anaphylactic shock can be tragic. This section will explore some complications of anaphylactic shock to include cardiac and neurological conditions. One of the most tragic cardiac complications of anaphylaxis is sudden death. This occurs as a manifestation of the Kounis syndrome &#8211; an acute coronary syndrome that causes the coronary arteries to spasm due to mast cell activation and inflammatory mediators that are released in the inflammatory process during an anaphylactic shock episode. In addition to the pathophysiology of anaphylactic shock, coronary arteries are not being perfused adequately. Contributors of coronary deterioration include <strong>“systemic vasodilation, reduced venous return, leakage of plasma and volume loss due to increase vascular permeability, and diminished cardiac output”</strong> (Kounis, Soufras, &amp; Hahalis, 2014, p. 228). The coronary arteries that are affected by Kounis syndrome, in addition to anaphylactic shock progression, can progress into a MI and ultimately sudden death (Kounis, Soufras, &amp; Hahalis, 2014). Therefore, assessing an EKG for MI manifestations can lead to early detection and prompt treatment.</p>
<p>In 2018, Michelle Mangold and Mahboob Qureshi, physicians for Touro University Nevada College of Osteopathic Medicine, studied two aspects of anaphylactic shock complications; long-term effects and neurological manifestations. In this study, a patient had an extreme case of anaphylactic shock that resulted in loss of consciousness and four consecutive seizures induced by hypotension. The patient was later intubated and found with a Glasgow Coma Scale (GCS) score of 3. Fortunately, the patient recovered the following day with intact neurological function as evidenced by results from a computed tomography (CT) and magnetic resonance imagining (MRI). However, 8 months later, the patient indicated her vision changed by decrease in distance and depth perception and noticed halos while night driving. She also noticed short-term memory problems and a difference in hand writing. It is said that this may be due to long lasting effects as <strong>“the lasting sequela of visual and fine motor skill deficits may very well be a result of hypoxic injury to the brain… It is important to note that the patient had no pre-existing neurologic conditions nor symptoms of such”</strong> (Mangold &amp; Qureshi, 2018, p. 4). This case is important to consider when treating patients with anaphylactic shock to make neurological assessments due to hypoxic effects on the brain. It is also significant to consider the increase of time in observation after anaphylactic shock treatment alongside more frequent follow-up appointments to check for long-lasting neurological effects.</p>
<h2><strong>Nursing Diagnoses</strong></h2>
<p>Nursing diagnoses that are relevant for anaphylactic shock indicate the priority of respiratory and cardiac problems including Ineffective Airway Clearance, Impaired Gas Exchange, and Decreased Cardiac Output (Ackley &amp; Ladwig, 2014).</p>
<p><strong><u>Ineffective Airway Clearance</u></strong> is relevant due to anaphylactic shock characteristics of bronchospasm, diminished lung sounds, dyspnea, and adventitious lung sounds. Goals should include airway patency. For example, the patient will always maintain a patent airway. This is accurate because if the patient is unable to have airway patency, intubation and other measures may be required. In addition to an accurate time frame, a patient should always have a patent airway even after discharge (Ackley &amp; Ladwig, 2014, p. 129).</p>
<p><strong><u>Impaired Gas Exchange</u></strong> is pertinent for anaphylactic shock due to the lack of tissue perfusion of oxygen caused by vascular permeability and vasodilation from histamine. Some manifestations are pallor, confusion, and tachycardia. Goals should include improvement of tissue perfusion. For example, the patient will have adequate oxygenation as evidenced by peripheral capillary saturation above 95% until discharge. In other cases, the patient will not show respiratory distress until discharge (Ackley &amp; Ladwig, 2014, p. 375).</p>
<p><strong><u>Decreased Cardiac Output</u></strong> is germane to anaphylactic shock because it describes the effects of histamine on the body with decreased tissue perfusion, edema, decreased central venous pressure, and dyspnea. Goals should include improvement of tissue perfusion as similar to improved gas exchange. For example, the patient will demonstrate adequate cardiac output as evidenced by blood pressure and heart rate within normal parameters until discharge (Ackley &amp; Ladwig, 2014, p. 179).</p>
<h2><strong>Nursing Interventions</strong></h2>
<p>The nursing interventions for anaphylactic shock should be immediate once the onset of symptoms occurs. The first step is to remove the allergen causing the problem such as an intravenous (IV) medication. The cornerstone intervention for anaphylactic shock is the administration of an intramuscular injection of epinephrine as soon as possible. To prevent poking yourself with the EpiPen, remember the saying, <em>“Blue to the sky, orange to the thigh.”</em> Unless contraindicated, the patient should be placed in shock position by laying him/her supine with their feet passively elevated. Contraindications would be present if the patient is having respiratory complications of the upper airway (as they should be in high fowler’s position). If the patient is unable to keep a patent airway, as evidenced by stridor or respiratory arrest, intubation should be performed immediately upon assessment. If this is not the case, the patient should still be given supplemental oxygen with 15L/min via nonrebreather mask. The patient should then have two IV catheters inserted; one for emergency medications and the other for volume resuscitation with normal saline (NS) at a rate of 125 mL/hour. Epinephrine is usually infused slowly on the IV after the initial injected dose (Campbell &amp; Kelso, 2018). The nurse should continue monitoring the patient’s vital signs including BP, heart rate, respiratory status, and peripheral capillary saturation. The patient should also be monitored for manifestations of fluid volume overload due to the large quantity of fluids that are being infused.</p>
<p>Epinephrine is an effective treatment for anaphylactic shock for its mechanism of action and preventing histamine and tryptase release from mast cells and basophils. It stops inflammation from progressing. Other beneficial mechanisms are vasoconstriction, bronchodilation, and decreased edema. Other pharmacological treatments that supplement epinephrine, but not used alone, are antihistamine and albuterol. Antihistamines are often administered to help relieve integumentary symptoms such as itching, redness, and hives (mostly caused by histamine). Albuterol is a bronchodilator that is administered to help relieve symptoms of dyspnea due to bronchospasm (caused by cell mediators) (Campbell &amp; Kelso, 2018). Antihistamines and albuterol neither relieve symptoms of shock nor prevent the release of cell mediators from mast cells and basophils. For the same reason, it is paramount to administer epinephrine as priority and only use a supplement.</p>
<p>After treatment and observation period of anaphylactic shock, the nurse should provide comprehensive discharge education to prevent recurrence in the future. It is recommended for patients to schedule a follow up appointment with their immunologist for further evaluation of suspected allergens (Campbell &amp; Kelso, 2018). In addition to an anaphylaxis emergency plan that outlines information about anaphylaxis and self-administering epinephrine, a prescription for an emergency EpiPen must also be given. Overall, it is important to educate the patient on how to avoid the allergen to prevent recurrence.</p>
<h4><strong>Conclusion</strong></h4>
<p>Anaphylactic shock is a life-threatening condition that can progress rapidly. Delay in epinephrine administration often results in death. To help combat the mortality rate of anaphylactic shock, this paper reviewed the diagnosis of the condition for nursing students. Therefore, nursing students could be more prepared for the rapid assessment and management for this life-threatening condition. To support this, this paper reviewed anaphylactic shock’s clinical manifestations, assessments, complications, and interventions.</p>
<h5>References</h5>
<p>Ackley, B. J., &amp; Ladwig, G. B. (2014). <em>Nursing diagnosis handbook: An evidence-based guide to </em></p>
<p><em>planning care </em>(10th ed.). Maryland Heights, MS: Mosby Elsevier.</p>
<p>Campbell, R. L., &amp; Kelso, J. M. (2018). Anaphylaxis: Emergency treatment. <em>UpToDate.</em></p>
<p>Retrieved from https://www.uptodate.com/contents/anaphylaxis-emergency-treatment?csi=45f3d755-dd9c-4a11-9fdd-9a052fbcea55&amp;source=contentShare</p>
<p>Kemp, S. F. (2018). Pathophysiology of anaphylaxis. <em>UpToDate. </em>Retrieved from https://</p>
<p>www.uptodate.com/contents/pathophysiology-of-anaphylaxis?csi=5020749f-23c7-4005-8304-bfd36032cfa5&amp;source=contentShare</p>
<p>Kornusky, J., &amp; Ashley, T. J. (2017). Shock, Anaphylactic. <em>CINAHL Nursing Guide.</em> Retrieved</p>
<p>from https://ceu.cinahl.com</p>
<p>Kounis, N. G., Soufras, G. D., &amp; Hahalis, G. (2014). Anaphylactic cardiac collapse, sudden</p>
<p>death and the Kounis syndrome. <em>Journal of Postgraduate Medicine, </em>60(3), 227–229. https://doi.org/10.4103/0022-3859.138704</p>
<p>Lewis, S., Bucher, L., Heitkemper, M., &amp; Harding, M. (2017). Shock, Sepsis, and Multiple</p>
<p>Organ Dysfunction Syndrome. In<em> Medical-Surgical Nursing: Assessment and Management of Clinical Problems</em> (10th ed., pp. 1590-1591). St. Louis, MO: Elsevier.</p>
<p>Mangold, M., &amp; Qureshi, M. (2018). Neurologic manifestations in anaphylaxis due to</p>
<p>subcutaneous allergy immunotherapy: A case report.<em> Medicine</em>, 97(18), 1–5. http://</p>
<p>dx.doi.org/10.1097/MD.0000000000010578</p>
<p>Mannarino, I. (2014). Anaphylactic shock. <em>Kahn Academy. </em>Retrieved from https://</p>
<p>www.khanacademy.org/science/health-and-medicine/circulatory-system-diseases/shock/v/anaphylactic-shock</p>
<p>Schwartz, L. B. (2018). Laboratory tests to support the clinical diagnosis of anaphylaxis.</p>
<p><em>UpToDate.</em> Retrieved from https://www.uptodate.com/contents/laboratory-tests-to-support-the-clinical-diagnosis-of-anaphylaxis?csi=fe986a82-12f4-4463-b6dd-3afa044b2c3f&amp;source=contentShare</p>
<p>Tang, R., Xu, H., Cao, J., Chen, S., Sun, J., Hu, H., … Li, Z. (2015). Clinical</p>
<p>characteristics of inpatients with anaphylaxis in China. <em>BioMed Research International</em>, <em>2015, </em>1–6. https://doi.org/10.1155/2015/429534</p>
<p>The post <a href="https://www.mark8ng.com/anaphylactic-shock/">Anaphylactic Shock, A Life-Threatening Condition</a> appeared first on <a href="https://www.mark8ng.com">Mark8ng.com</a>.</p>
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		<post-id xmlns="com-wordpress:feed-additions:1">1009</post-id>	</item>
		<item>
		<title>Folliculitis Barbae</title>
		<link>https://www.mark8ng.com/folliculitis-barbae/</link>
		
		<dc:creator><![CDATA[Mary Anne]]></dc:creator>
		<pubDate>Sun, 14 Mar 2021 17:16:14 +0000</pubDate>
				<category><![CDATA[Health & Fitness]]></category>
		<category><![CDATA[Research]]></category>
		<category><![CDATA[Folliculitis Barbae]]></category>
		<category><![CDATA[Medical]]></category>
		<category><![CDATA[Perifolliculitis barbae]]></category>
		<category><![CDATA[treatment]]></category>
		<guid isPermaLink="false">https://www.mark8ng.com/?p=634</guid>

					<description><![CDATA[<p>Folliculitis Barbae Introduction According to histological definitions, folliculitis barbae can be described as the “presence of inflammatory cells within the wall and ostia of the hair follicle, creating a follicular-based</p>
<p>The post <a href="https://www.mark8ng.com/folliculitis-barbae/">Folliculitis Barbae</a> appeared first on <a href="https://www.mark8ng.com">Mark8ng.com</a>.</p>
]]></description>
										<content:encoded><![CDATA[<h1>Folliculitis Barbae</h1>
<h2>Introduction</h2>
<p>According to histological definitions, folliculitis barbae can be described as the <strong>“presence of inflammatory cells within the wall and ostia of the hair follicle, creating a follicular-based pustule”</strong> (Satter, 2012). There is a variation in the tangible kind of inflammatory cells as their nature is mainly dependent on folliculitis’ etiology. The inflammation has different effects. It may limit itself to the external phase of the follicle with the involvement of the infundibulum at a primary level. On the other hand, there may be an inflammatory effect on both aspects of the follicle i.e. external and internal (Satter, 2012).</p>
<p>In contrast, Perifolliculitis barbae is <strong>“the presence of inflammatory cells in the perifollicular tissues and can involve the adjacent reticular dermis”</strong> (Satter, 2012). Both the mentioned types of folliculitis have independent manifestations. However, they may also occur together as a consequence of follicular disorder, disturbance and irritation (Satter, 2012).</p>
<h2>Folliculitis Barbae</h2>
<p>Folliculitis Barbae is the condition in which the formation of hair occurs within the skin as hair follicles that are minute hairy structures. The word folliculitis is used to depict the inflammation of these tiny hairy structures. Even though such kind of inflammation can affect any part of the skin, folliculitis barbae is the term that specifically refers to the inflammation of the hair follicles that affect the area where beard grows.</p>
<h3>Causes</h3>
<p>In general, Staphylococcus aureus infection is the major cause of this condition. The mentioned infection is recognized as mainly affecting the skin of a person. Though folliculitis barbae may transpire in a bearded area that is not shaved; men who shave are mostly affected by this condition. These bacteria unnoticeably line inside the nasal area due to which there are higher chances of reinfection. In addition, shaving equipment containing contaminations also have these bacteria and when an individual uses improper and unclean equipment for shaving, reinfection may take place. In some cases, there is no involvement of S.aureus and the involvement of harmless skin bacteria results in folliculitis barbae.</p>
<p>More often than not, the upper part of the hair follicle is affected by the infection on the external surface of the skin. In a number of cases, on the other hand, the infection is more deep-rooted. The follicles may appear red and feel itchy due to the setting up of a constant inflammatory reaction by the immune system. Such a condition has been given the name of sycosis barbae. At seldom occasions, scarring is caused by such a condition. It is exceedingly important to note here that the infections that are caused by fungi or herpes virus cannot be considered as folliculitis barbae. It is also imperative to note that folliculitis barbae is not hereditary.</p>
<h3>Symptoms</h3>
<p>Folliculitis barbae is characterized by itchiness and tenderness of the beard area. The use of razor may cut the spots that have a severe effect on the beard area. Bleeding may result as a consequence. Folliculitis barbae may infect the hair follicles in the beard area by causing a small red inflammation and enlargement to appear at the root of the skin from where the hair grows up.This swelling is frequently observed to come together with a septic spot with a yellow-head. Thus, folliculitis barbae usually affects a lot of hair follicles. In case of the development of an inflammatory reaction, an extension can be seen from where the follicles appear red. These follicles are joined up often that cause itchiness and irritation.</p>
<h3>Diagnosis</h3>
<p>For diagnosis of folliculitis barbae, the doctors take a pus sample and then test it for infection. The sample results then makes it easier for them to recommend the antibiotics that may help the individual. In case when there is no quick clearance of the folliculitis, swabs and scrubbing down of the infected area is done and sometimes noses of the patient and family members are also checked to check whether any bacteria is the real cause of the infection. The skin is also closely examined to find out whether the spots indicate the occurrence of folliculitis barbae or pseudofolliculitis. This close examination of the skin is important as both conditions can affect the skin at the same time.</p>
<h3>Treatment</h3>
<p>Every now and then, this condition can be cured. However, the curing varies from person to person as every individual has a distinctive skin type. In some individuals, curing shows less response. But treatment in a timely and appropriate manner can help this condition to go away. One of the most important things to mention here is that the scars which develop as a result of this condition are life-long. The skin appearance improves usually over a period of time but the scars do not vanish. In many cases where there is a straightforward infection, a proper antibiotic course is enough for the skin to response quickly. Such antibiotics are available in the form of creams and oral medications. In case of a reinfection due to nasal bacteria, physicians usually recommend the application of an antibiotic ointment inside the nostrils. When there is a development of chronic inflammation, the patient is recommended to use a mild steroid cream. In cases that are more difficult to treat, the suggestions given by the doctors include the use of an antibiotic that may help to get rid away of both anti-inflammatory and antibacterial effects.</p>
<p>If an individual is persistently affected by the folliculitis barbae, he/she is advised to take necessary steps to lessen the contamination from equipment used for shaving. It is suggested that metal parts of the shaving equipment must be scalded on a regular basis with boiling water. If a person uses razor or electric shaver, the plastic parts that may infect the skin must be cleaned in a careful manner after every time they are used. Alcoholic antiseptic solutions must also be used to soak the shaving equipment. Sometimes, it is better to use an antiseptic lotion instead of using shaving soap or foams to avoid any infection of the skin.</p>
<h3>Pseudofolliculitis barbae</h3>
<p>Pseudofolliculitis barbae is an irritating and irking chronic condition that can develop as a result of attempts to get rid of hair from the bearded area (Quarles, Brody, Johnson, Badreshia, Vause, Brauner &amp; Callendar, 2007). It is quite difficult to determine the occurrence of this disorder. However, studies regarding the disorder have reported that this disfiguring condition affects more or less one individual out of every five Caucasian individuals. It is also revealed from the studies that it occurs very commonly in black persons. It is not only a condition that affects men but women can also get this disorder no matter from which race they belong. The inflammatory papules and pustules appearance is the main clinical characteristic of this disorder. This condition is a direct result of the inappropriate shaving techniques causing <strong>“ingrown hairs through both transfollicular and extrafollicular mechanisms”</strong> (Halder, 1988). Same treatment as that of acne is adopted, once the pseudofolliculitis barbae is established. It can also be treated by avoiding shaving along with the medication and in extreme cases, diode lasers can be used (Yamauchi, Kelly &amp; Lask, 1999). The long-term result is dependent entirely on prevention through a correct shaving technique. In severe cases of pseudofolliculitis, when definitive solution is sought, the choice of treatment is photodepilation (Ribera, Fernández-Chico &amp; Casals, 2010). As the main factor that is responsible in the condition’s pathogenesis is hair, a definite treatment is the elimination of hair.</p>
<h3>Epidemiology</h3>
<p>In general, men with curly, coarse hair are affected by Pseudofolliculitis barbae. It is reported that 45-83% African-American men suffer from this condition and it has turned out to be a leading concern in black US army recruits. A survey carried out at the Skin of Color Center concerning 71 patients with PFB (41 females and 30 males) confirmed an average age of beginning to be 22 years (Coley &amp; Alexis, 2009).</p>
<h3>Pathogenesis</h3>
<p>An ingrown hair shaft results in this chronic-body reaction that is called Pseudofolliculitis barbae. It is thought that a curved hair follicle which is present in African descent individuals, predispose cut hair and reenter the dermis which leads to this reaction. There are two mechanisms which are so far described i.e. extrafollicular penetration and transfollicular penetration. In the extrafollicular penetration, the very sharp edge of the hair that was shaved follows its natural curvature to the surface of the skin and re-penetrates in a retrograde fashion. Transfollicular penetration is the piercing of the follicular wall by the shaft of the hair recently cut, which as a consequence enters the dermis without ever exiting the epidermis (Coley &amp; Alexis, 2009).</p>
<p>Pulling of the skin rigidly while shaving boosts the danger of transfollicular penetration by allowing recently cut hair to retract underneath the skin&#8217;s exterior. Transfollicular penetration can also result for ingrown hair seen with waxing or plucking, which leaves hair fragments inside the skin. In both of the types of re-entry, the shaft of the hair penetrates the dermis thus triggering the foreign-body inflammatory response that may result in the formation of pustules and papules. A single nucleotide polymorphism has been identified by medical scientists which imparts the partial genetic risk of the development of the PFB (Coley &amp; Alexis, 2009).</p>
<h3>Clinical Features</h3>
<p>The hallmarks of PFB are follicular and perifollicular papules and pustules in the beard area. Post-inflammatory hyper-pigmentation (PIH) is also a commonly linked feature which is reported in a majority of cases. Commonly affected area is the bearded area of the face, which may or may not include the anterior neckline, mandibular areas, chin and cheeks. In some severe cases, hypertrophic scars are also seen. Embedded hair can also be seen with the papules in severe cases. After growing approximately 1cm in length, this hair will spontaneously release through the loop mechanism. Depressed patterns can be present due to the parallel hair growth. Some patients may feel itching and pain. In the secondary infection cases, cultures of pustules are generally sterile (Coley &amp; Alexis, 2009).</p>
<p>The presence of PFB lesions can be distressing to patients. Considerable anxiety in appearance can also be present. PFB majorly contributed to racial tension among African-American soldiers in the US army due to the military grooming code which requires a clean-shaven face. For majority of these men, compliance with the code means suffering with PFB (Coley &amp; Alexis, 2009). The Folliculitis Barbae inflammatory response is dependent on <strong>“the shape of the hair follicle, hair cuticle, and the direction of hair growth</strong>” (Perry, Cook-Bolden, Rahman, Jones &amp; Taylor, 2002) as every one of them has a certain role. People with this condition tend to suffer emotional distress as it causes as unattractive and ugly cosmetic appearance.</p>
<h3>Treatment</h3>
<h4>Hair Removal</h4>
<p>This condition can be prevented by allowing the beard to grow for a month which can result in spontaneous resolution of most PFB papules cases in Folliculitis Barbae. However, in some cases, the growth of the beard for a full month is not possible. Personal preferences and clean-shaven face appearance may act as the limiting factors. In such cases, alternative hair removal and counseling about proper shaving techniques become mandatory in order to control and reduce the flares (Coley &amp; Alexis, 2009).</p>
<p>Most men can easily control the condition with maintaining an optimal beard length of 0.5 to 1 mm. The hair can be cut through the electronic clippers as they allow the user to set the length of the hair and cut the rest. By tradition, most of the authorities suggest the use of a single blade razor to avoid the PFB. A recommended razor is Bump Fighter (American Safety Razor Company, VA, USA) as its blade is coated with the polymer and a foil guard that keeps the edge of the blade slightly off the skin and it prevents the trimming of the hair too close from the skin. In a study, this razor has been shown to reduce the number of PFB lesions. According to a recent study in this field, no increase was observed in the number of PFB lesions in men who used Gillette five blade razor daily for 8 weeks.  Random, blinded clinical research comparing the use of single-edged and multi-edged razors, shaving techniques and frequencies are needed in order to explain optimal shaving recommendations for PFB (Coley &amp; Alexis, 2009).</p>
<h4>Medical Management</h4>
<p>Medical Management is another treatment option that includes a combination of therapies that are used to treat PFB, topical antibiotics, low-potency corticosteroids and use of topical retinoid. Topical retinoid helps to alleviate the hyperkeratosis associated with the repetition of the follicular epithelium as well as PIH.  In place of commercial aftershave products, low to mid potency topical corticosteroids can be used. Prior to shaving, benzoyl peroxide wash can also be helpful. Antimicrobials such as Benzoyl peroxide and erythromycin can be used to reduce the colonization of bacteria which can result inflammation and result to secondary infections. PFB-associated PIH can be treated successfully with bleaching agents such as hydroquinone and kojic acid etc (Coley &amp; Alexis, 2009).</p>
<h4>Chemical Depilatories</h4>
<p>Chemical Depilatories can be used as an alternative too by men who are burdened with this condition as it is a useful hair-removal option. Chemical depilatories are an alternative to shaving that has been used from several years as an alternate for shaving. Barium sulfide or calcium thioglycolate are the substances that are present in cream and lotion forms and they work well in weakening the disulfide bonds in keratin. By the use of these substances in Folliculitis Barbae, the hair can be easily removed from the skin surface with a blunt instrument for the removal of hair (Bridgeman-Shah, 2004). It makes the transfollicular and extrafollicular penetration very less likely to happen. Irritant and allergic reactions may appear with the use of these chemicals resulting in PIH in case of prolonged exposure. A test patch to determine irritation potential is recommended before taking the treatment (Coley &amp; Alexis, 2009).</p>
<h4>Eflornithine Hydrochloride</h4>
<p>US FDA approved a cream named as Eflornithine hydrochloride for the treatment of unwanted facial hair in women (Coquilla &amp; Lewis, 1995). This cream irreversibly slows down the enzyme in hair cell division, which ultimately results in less hair growth rate in the area applied. Although, this cream is not indicated for the use of PFB, it has been found to be used for the purpose of decreasing the hair growth in men suffering from PFB. All the considerations need to be discussed with the patient prior to adoption to avoid the unrealistic expectations from the treatment (Coley &amp; Alexis, 2009).</p>
<h4>Epilating</h4>
<p>Epilating in the form of electrolysis is one of the forms of permanent hair removals which can be considered for limited areas. This process is potentially painful and costly. This process is not of more success in African-American people as it is difficult to ablate the curved and distorted hair follicle. A merged technique of electrolysis by means of galvanic and thermolysis currents have been effective. In fact, electrolysis can actually exacerbate PFB and promotes transfollicular penetration and therefore is generally not recommended as a cure treatment (Coley &amp; Alexis, 2009).</p>
<h4>Chemical peels</h4>
<p>Chemical peels is an another option to treat Folliculitis barbae as superficial chemical peels are safe and effective in addition to therapy for PFB. It has been proposed that glycolic acid have properties to reduce sulfhydryl bonds and in addition to that its exfoliating effects are good. The reduced bonds of sulfhydryl in the hair shaft can result in the growth of straighter hair and can potentially reduce the possibility for re-entry of the hair shaft in the epidermis. The peels of salicylic acid offer exfoliation and lightening in the cases complicated with PIH. Research showed reduced number of PFB lesions with both salicylic acid and glycolic acid peels (Coley &amp; Alexis, 2009).</p>
<h5>References</h5>
<p>Bridgeman-Shah, S. (2004). The Medical and Surgical Therapy of Pseudofolliculitis Barbae. <em>Dermatologic Therapy</em>, 17(2), 158-163.</p>
<p>Coley, M. K., &amp; Alexis, A. F. (2009). Dermatologic Conditions in Men of African Ancestry. <em>Medscape Today</em>. Retrieved August 12, 2013, from <a href="http://www.medscape.com/viewarticle/715199_2">http://www.medscape.com/viewarticle/715199_2</a></p>
<p>Coquilla, B., &amp; Lewis, C. (1995). Management of Pseudofolliculitis Barbae. <em>Military Medicine</em>, 160(5), 263-269.</p>
<p>Halder, R. (1988). Pseudofolliculitis Barbae and Related Disorders. <em>Dermatologic Clinics</em>, 6(3), 407-412.</p>
<p>Quarles, F., Brody, H., Johnson, B., Badreshia, S., Vause, S., Brauner, G., &amp; Callendar, V. (2007). Pseudofolliculitis Barbae. <em>Dermatologic Therapy</em>, 20(3), 133-136.</p>
<p>Perry, P., Cook-Bolden, F., Rahman, Z., Jones, E., &amp; Taylor, S. (2002). Defining Pseudofolliculitis Barbae in 2001: A Review of the Literature and Current Trends. <em>I</em>, 46(2 Suppl Understanding), S113-S119.</p>
<p>Ribera, M., Fernández-Chico, N., &amp; Casals, M. (2010). [Pseudofolliculitis barbae]. <em>Actas Dermo-Sifiliográficas</em>, 101(9), 749-757.</p>
<p>Satter, E. K. (2012, July 10). Folliculitis .<em>Medscape Reference: Drugs, Diseases and Procedures</em>. Retrieved August 12, 2013, from emedicine.medscape.com/article/1070456-overview</p>
<p>Yamauchi, P., Kelly, A., &amp; Lask, G. (1999). Treatment of Pseudofolliculitis Barbae with the Diode Laser. <em>Journal Of Cutaneous Laser Therapy</em>, 1(2), 109-111.</p>
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