AZCEP Posted July 6, 2006 Posted July 6, 2006 On to the "blue baby" syndromes, eh? Fallot was the doctor that got the honor of having it named after him, but it was recognized long before his time. The tetrology is: A ventricular septal defect Pulmonary stenosis An overriding aorta Right ventricular hypertrophy These defects create a situation that allows for de-oxygenated blood from the right side of the heart to mix with oxygenated blood in the left, and also reduce the amount of oxygenated blood that is available. Usually corrected with open-heart surgery in the first few months, depending on severity of presentation. These children have "blue periods", when exposed to increased oxygen demand they will become cyanotic. Removal of the stimulation, and placement of the child in a knee-chest position will help mitigate the effects.
Ridryder 911 Posted July 7, 2006 Posted July 7, 2006 You know it is a shame this thread is not lighting fires... if it was a discussion of red lights, or how many star of life's it takes to cover your windshield, or maybe how many times can I fail the National Registry before I should call it quits..... we be hitting triple digits by now...but alas it is over something silly like medicine and medical care! Okay next Honk Case.. even the basics should have an understanding: Cor Pulmonale R/r 911
medic429 Posted July 7, 2006 Posted July 7, 2006 I'll take a stab at Fifth Disease, since both kids had it...my oldest while I was pregnant with my youngest :shock: Fifth disease is a virus and usually starts with a fever and general ill feeling. After a few days a bright red rash appears on the body and usually on the face. Fifth disease is usually seen and spread among young children. Once a child gets it, they usually build immunity and do not contract it again. Pregnant women need to be very careful with exposure to Fifth Disease. The virus can cause severe anemia in the fetus. Handwashing is of utmost importance. Called fifth because it's one of the five rash causing diseases...and the only one I can think of at one a.m. is measels! That's what I can remember. We'll stick with Rid's question: Cor Pulmonale
Ridryder 911 Posted July 7, 2006 Posted July 7, 2006 Your right, as well a common symptom is the "slapped face" appearance of the rash on the cheek, sometimes also the "butterfly" rash that spreads around eyes and down nose... The Fifth Disease was not named after a Dr. named Fifth etc... " but rather to the fifth of six classic exanthems, or rash-associated diseases, of childhood. The numbering was of medical historic interest only: the other rashes, in order are first: measles; second: scarlet fever; third: rubella; fourth: "Dukes' disease", which was never clearly understood or able to distinguish from other rashes. Which is now thought to have been either the measles, rubella, scarlet fever, a Staphylococcal infection, or one of several enteroviral infections; and sixth: was Rosella. ... Now don't we feel smarter! Now someone can discuss cor pulmonale.... R/r 911
medic001918 Posted July 7, 2006 Posted July 7, 2006 Cor Pulmonale is also commonly referred to as pulmonary hypertension. One of the more common causes is left sided heart failure causing a fluid backup in the pulmonary vasculature. This can potentitally lead to pulmonary edema and can require emergent management, as well as being a contributing factor to congestive heart failure. That's the quick, simple off the top of my head at 0240 hrs version. Below is the version from emedicine.com that offers a rather interesting read on the condition. Background: Cor pulmonale is defined as an alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system. Pulmonary hypertension is the common link between lung dysfunction and the heart in cor pulmonale. Right-sided ventricular disease caused by a primary abnormality of the left side of the heart or congenital heart disease is not considered cor pulmonale, but cor pulmonale can develop secondary to a wide variety of cardiopulmonary disease processes. Although cor pulmonale commonly has a chronic and slowly progressive course, acute onset or worsening cor pulmonale with life-threatening complications can occur. Pathophysiology: Several different pathophysiologic mechanisms can lead to pulmonary hypertension and, subsequently, to cor pulmonale. These pathogenetic mechanisms include (1) pulmonary vasoconstriction due to alveolar hypoxia or blood acidemia; (2) anatomic compromise of the pulmonary vascular bed secondary to lung disorders, eg, emphysema, pulmonary thromboembolism, interstitial lung disease; (3) increased blood viscosity secondary to blood disorders, eg, polycythemia vera, sickle cell disease, macroglobulinemia; and (4) idiopathic primary pulmonary hypertension. The result is increased pulmonary arterial pressure. The right ventricle (RV) is a thin-walled chamber that is more a volume pump than a pressure pump. It adapts better to changing preloads than afterloads. With an increase in afterload, the RV increases systolic pressure to keep the gradient. At a point, further increase in the degree of pulmonary arterial pressure brings significant RV dilation, an increase in RV end-diastolic pressure, and circulatory collapse. A decrease in RV output with a decrease in diastolic left ventricle (LV) volume results in decreased LV output. Since the right coronary artery, which supplies the RV free wall, originates from the aorta, decreased LV output diminishes blood pressure in the aorta and decreases right coronary blood flow. This is a vicious cycle between decreases in LV and RV output. Right ventricular overload is associated with septal displacement toward the left ventricle. Septal displacement, which is seen in echocardiography, can be another factor that decreases LV volume and output in the setting of cor pulmonale and right ventricular enlargement. Several pulmonary diseases cause cor pulmonale, which may involve interstitial and alveolar tissues with a secondary effect on pulmonary vasculature or may primarily involve pulmonary vasculature. Chronic obstructive pulmonary disease (COPD) is the most common cause of cor pulmonale in the United States. Cor pulmonale usually presents chronically, but 2 main conditions can cause acute cor pulmonale: massive pulmonary embolism (more common) and acute respiratory distress syndrome (ARDS). The underlying pathophysiology in massive pulmonary embolism causing cor pulmonale is the sudden increase in pulmonary resistance. In ARDS, 2 factors cause RV overload: the pathologic featuresof the syndrome itself and mechanical ventilation. Mechanical ventilation, especially higher tidal volume, requires a higher transpulmonary pressure. In chronic cor pulmonale, right ventricular hypertrophy (RVH) generally predominates. In acute cor pulmonale, right ventricular dilatation mainly occurs. History: Clinical manifestations of cor pulmonale generally are nonspecific. The symptoms may be subtle, especially in early stages of the disease, and mistakenly may be attributed to the underlying pulmonary pathology. * The patient may complain of fatigue, tachypnea, exertional dyspnea, and cough. * Anginal chest pain also can occur and may be due to right ventricular ischemia (it usually does not respond to nitrates) or pulmonary artery stretching. * Hemoptysis may occur because of rupture of a dilated or atherosclerotic pulmonary artery. Other conditions, such as tumors, bronchiectasis, and pulmonary infarction, should be excluded before attributing hemoptysis to pulmonary hypertension. Rarely, the patient may complain of hoarseness due to compression of the left recurrent laryngeal nerve by a dilated pulmonary artery. * Variety of neurologic symptoms may be seen due to decreased cardiac output and hypoxemia. * In advanced stages, passive hepatic congestion secondary to severe right ventricular failure may lead to anorexia, right upper quadrant abdominal discomfort, and jaundice. * Syncope with exertion, which may be seen in severe disease, reflects a relative inability to increase cardiac output during exercise with a subsequent drop in the systemic arterial pressure. * Elevated pulmonary artery pressure can lead to elevated right atrial pressure, peripheral venous pressure, and then capillary pressure and by increasing the hydrostatic gradient, it leads to transudation of fluid, which appears as peripheral edema. Although this is the simplest explanation for peripheral edema in cor pulmonale, other hypotheses explain this symptom, especially in a fraction of patients with COPD who do not show increase in right atrial pressure. A decrease in GFR and filtration of sodium and stimulation of arginine vasopressin (which decreases free water excretion) due to hypoxemia play important pathophysiologic roles in this setting and may even have a role for peripheral edema in patients with cor pulmonale who have elevated right atrial pressure. Physical: Physical findings may reflect the underlying lung disease or pulmonary hypertension, RVH, and RV failure. * On inspection, an increase in chest diameter, labored respiratory efforts with retractions of chest wall, distended neck veins with prominent a or v waves, and cyanosis may be seen. * On auscultation of the lungs, wheezes and crackles may be heard as signs of underlying lung disease. Turbulent flow through recanalized vessels in chronic thromboembolic pulmonary hypertension may be heard as systolic bruits in the lungs. Splitting of the second heart sound with accentuation of the pulmonic component can be heard in early stages. A systolic ejection murmur with sharp ejection click over the region of the pulmonary artery may be heard in advanced disease, along with a diastolic pulmonary regurgitation murmur. Other findings upon auscultation of the cardiovascular system may be third and fourth sounds of the heart and systolic murmur of tricuspid regurgitation. * RVH is characterized by a left parasternal or subxiphoid heave. Hepatojugular reflex and pulsatile liver are signs of RV failure with systemic venous congestion. * On percussion, hyperresonance of the lungs may be a sign of underlying COPD; ascites can be seen in severe disease. Medical Care: Medical therapy for chronic cor pulmonale is generally focused on treatment of the underlying pulmonary disease and improving oxygenation and RV function by increasing RV contractility and decreasing pulmonary vasoconstriction. However, the approach might be different to some degree in an acute setting with priority given to stabilizing the patient. Cardiopulmonary support for patients experiencing acute cor pulmonale with resultant acute RV failure includes fluid loading and vasoconstrictor (eg, epinephrin) administration to maintain adequate blood pressure. Of course, the primary problem should be corrected, if possible. For example, for massive pulmonary embolism, consider administration of anticoagulation, thrombolytic agents or surgical embolectomy, especially if circulatory collapse is impending, consider bronchodilation and infection treatment in patients with COPD and consider steroid and immunosuppressive agents in infiltrative and fibrotic lung diseases. Oxygen therapy, diuretics, vasodilators, digitalis, theophylline, and anticoagulation therapy are all different modalities used in the long-term management of chronic cor pulmonale. * Oxygen therapy is of great importance in patients with underlying COPD, particularly when administered on a continuous basis. With cor pulmonale, the partial pressure of oxygen (PO2) is likely to be below 55 mm Hg and decreases further with exercise and during sleep. Oxygen therapy relieves hypoxemic pulmonary vasoconstriction, which then improves cardiac output, lessens sympathetic vasoconstriction, alleviates tissue hypoxemia, and improves renal perfusion. The Nocturnal Oxygen Therapy Trial (NOTT), a multicenter randomized trial, showed that continuous low-flow oxygen therapy for patients with severe COPD resulted in significant reduction in the mortality rate. In general, in patients with COPD, long-term oxygen therapy is recommended when PaO2 is less than 55 mm Hg or O2 saturation is less than 88%. However, in the presence of cor pulmonale or impaired mental or cognitive function, long-term oxygen therapy can be considered even if PaO2 is greater than 55 mm Hgor O2 saturation is greater than 88%. Although it is not clear whether oxygen therapy has a mortality rate benefit in patients with cor pulmonale due to pulmonary disorders other than COPD, it may provide some degree of symptomatic relief and improvement in functional status. Therefore, oxygen therapy plays an important role in both the immediate setting and long-term management, especially in patients who are hypoxic and have COPD. * Diuretics are used in the management of chronic cor pulmonale, particularly when the right ventricular filling volume is markedly elevated and in the management of associated peripheral edema. Diuretics may result in improvement of the function of both the right and left ventricles; however, diuretics may produce hemodynamic adverse effects if they are not used cautiously. Excessive volume depletion can lead to a decline in cardiac output. Another potential complication of diuresis is the production of a hypokalemic metabolic alkalosis, which diminishes the effectiveness of carbon dioxide stimulation on the respiratory centers and lessens ventilatory drive. The adverse electrolyte and acid-base effect of diuretic use can also lead to cardiac arrhythmia, which can diminish cardiac output. Therefore, diuresis, while recommended in the management of chronic cor pulmonale, needs to be used with great caution. * Vasodilator drugs have been advocated in the long-term management of chronic cor pulmonale with modest results. Calcium channel blockers, particularly oral sustained-release nifedipine and diltiazem, can lower pulmonary pressures, although they appear more effective in primary rather than secondary pulmonary hypertension. Other classes of vasodilators, such as beta agonists, nitrates, and angiotensin-converting enzyme (ACE) inhibitors have been tried but, in general, vasodilators have failed to show sustained benefit in patients with COPD and they are not routinely used. A trial of vasodilator therapy may be considered only in patients with COPD with disproportionately high pulmonary blood pressure. Beta-selective agonists have an additional advantage of bronchodilator and mucociliary clearance effect. Right heart catheterization has been recommended during initial administration of vasodilators to objectively assess the efficacy and detect the possible adverse hemodynamic consequences of vasodilators. The Food and DrugAdministration (FDA) has approved epoprostenol, treprostinil, bosentan, and iloprost for treatment of primary pulmonary hypertension. Epoprostenol, treprostinil, and iloprost are prostacyclin PGI2 analogues and have potent vasodilatory properties. Epoprostenol and treprostinil are administered intravenously and iloprost is an inhaler. Bosentan is a mixed endothelin-A and endothelin-B receptor antagonist indicated for PAH, including PPH. In clinical trials, it improved exercise capacity, decreased rate of clinical deterioration, and improved hemodynamics. PDE5 inhibitor sildenafil has also been intensively studied and recently approved by the FDA for treatment of pulmonary hypertensionbased on a large randomized study. Sildenafil promotes selective smooth muscle relaxation in lung vasculature. Not enough data are available regarding the efficacy of these drugs in patients with secondary pulmonary hypertension such as in patients with COPD. * The use of cardiac glycosides, such as digitalis, in patients with cor pulmonale has been controversial, and the beneficial effect of these drugs is not as obvious as in the setting of left heart failure. Nevertheless, studies have confirmed a modest effect of digitalis on the failing right ventricle in patients with chronic cor pulmonale. It must be used cautiously, however, and should not be used during the acute phases of respiratory insufficiency when large fluctuations in levels of hypoxia and acidosis may occur. Patients with hypoxemia or acidosis are at increased risk of developing arrhythmias due to digitalis through different mechanisms including sympathoadrenal stimulation. * In addition to bronchodilatory effect, theophylline has been reported to reduce pulmonary vascular resistance and pulmonary arterial pressures acutely in patients with chronic cor pulmonale secondary to COPD. Theophylline has a weak inotropic effect and thus may improve right and left ventricular ejection. As a result, considering the use of theophylline as adjunctive therapy in the management of chronic or decompensated cor pulmonale is reasonable in patients with underlying COPD. * Anticoagulation with warfarin is recommended in patients at high risk for thromboembolism. The beneficial role of anticoagulation in improving the symptoms and mortality in patients with primary pulmonary arterial hypertension clearly was demonstrated in a variety of clinical trials. The evidence of benefit, however, has not been established in patients with secondary pulmonary arterial hypertension. Therefore, anticoagulation therapy may be used in patients with cor pulmonale secondary to thromboembolic phenomena and with underlying primary pulmonary arterial hypertension. Surgical Care: * Phlebotomy is indicated in patients with chronic cor pulmonale and chronic hypoxia causing severe polycythemia, defined as hematocrit of 65 or more. Phlebotomy results in a decrease in mean pulmonary artery pressure, a decrease in mean pulmonary vascular resistance, and an improvement in exercise performance in such patients. There is, however, no evidence of improvement in survival. Generally, phlebotomy should be reserved as an adjunctive therapy for patients with acute decompensation of cor pulmonale and patients who remain significantly polycythemic despite appropriate long-term oxygen therapy. Replacement of the acute volume loss with a saline infusion may be necessary to avoid important decreases in systemic blood pressure. * No surgical treatment exists for most diseases that cause chronic cor pulmonale. Pulmonary embolectomy is efficacious for unresolved pulmonary emboli, which contribute to pulmonary hypertension. Uvulopalatopharyngoplasty in selected patients with sleep apnea and hypoventilation may relieve cor pulmonale. Single-lung, double-lung, and heart-lung transplantation are all used to salvage the terminal phases of several diseases (eg, primary pulmonary hypertension, emphysema, idiopathic pulmonary fibrosis, cystic fibrosis) complicated by cor pulmonale. Apparently, lung transplantation will lead to a reversal of right ventricular dysfunction from the chronic stress of pulmonary hypertension. Strict selection criteria for lung transplant recipients must be met, however, because of the limited availability of organ donors. And now one that we should all be familiar with...Munchausen Syndrome and also Munchausen by proxy. Shane NREMT-P
mediccjh Posted July 7, 2006 Posted July 7, 2006 From The Cleveland Clinic: What is Munchausen syndrome? Munchausen syndrome is a type of factitious disorder, or mental illness, in which a person repeatedly acts as if he or she has a physical or mental disorder when, in truth, they have caused the symptoms. People with factitious disorders act this way because of an inner need to be seen as ill or injured, not to achieve a concrete benefit, such as financial gain. They are even willing to undergo painful or risky tests and operations in order to get the sympathy and special attention given to people who are truly ill. Munchausen syndrome is a mental illness associated with severe emotional difficulties. Munchausen syndrome—named for Baron von Munchausen, an 18th century German officer who was known for embellishing the stories of his life and experiences—is the most severe type of factitious disorder. Most symptoms in people with Munchausen syndrome are related to physical illness—symptoms such as chest pain, stomach problems, or fever—rather than those of a mental disorder. Note: Although Munchausen syndrome most properly refers to a factitious disorder with primarily physical symptoms, the term is sometimes used to refer to factitious disorders in general. In this article, Munchausen syndrome refers to factitious disorder with physical symptoms. What are the symptoms of Munchausen syndrome? People with this syndrome deliberately produce or exaggerate symptoms in several ways. They might lie about or fake symptoms, hurt themselves to bring on symptoms, or alter diagnostic tests (such as contaminating a urine sample). Possible warning signs of Munchausen syndrome include the following: Dramatic but inconsistent medical history Unclear symptoms that are not controllable and that become more severe or change once treatment has begun Predictable relapses following improvement in the condition Extensive knowledge of hospitals and/or medical terminology, as well the textbook descriptions of illnesses Presence of multiple surgical scars Appearance of new or additional symptoms following negative test results Presence of symptoms only when the patient is alone or not being observed Willingness or eagerness to have medical tests, operations, or other procedures History of seeking treatment at numerous hospitals, clinics, and doctors offices, possibly even in different cities Reluctance by the patient to allow health care professionals to meet with or talk to family, friends, or prior health care providers Problems with identity and self-esteem What are LeForte fractures?
Rezq304 Posted July 7, 2006 Posted July 7, 2006 Basically, LeForte Fx's are three different Fx's within the head/facial area. The below linked info goes further in depth. From eMedicine.com Rene Le Fort described the classic patterns of fracture in his 1901 work. Le Fort's experiments consisted of dropping cadaver skulls from several stories or striking them with a wooden club. He found 3 distinct fracture patterns, which he termed the linea minoros resistentiae. Simply stated, the Le Fort I fracture separates the palate from the maxilla, the Le Fort II separates the maxilla from the face, and the Le Fort III results in craniofacial dysjunction. The Le Fort I fracture is a low transverse fracture that crosses the floor of the nose, pyriform aperture, canine fossa, and lateral wall from the maxilla, resulting in separation of the palate from the maxilla. The Le Fort II fracture crosses the nasal bones on the ascending process of the maxilla and lacrimal bone and crosses the orbital rim. Only the Le Fort II fracture violates the orbital rim. This proximity to the infraorbital foramen causes type II fractures to have the highest incidence of infraorbital nerve hypesthesias. The Le Fort II fracture extends posteriorly to the pterygoid plates at the base of the skull. Whereas a Le Fort I fracture causes a low septal fracture, a Le Fort II fracture results in a high septal fracture. Finally, the Le Fort III fracture traverses the frontal process of the maxilla, lacrimal bone, lamina papyracea, and orbital floor. This fracture often involves the posterior plate of the ethmoid. Because of their location, Le Fort III fractures are associated with the highest rate of cerebrospinal fluid (CSF) leaks. Pathophysiology: The maxilla has 4 processes: zygomatic, frontal, palatine, and alveolar. The maxillary sinus is housed within the maxilla and varies in size depending on the degree of pneumatization. The midface can be thought of as a grid of horizontal and vertical buttresses that provide support for the face. The 3 paired vertical buttresses of the midface are the nasomaxillary, zygomaticomaxillary, and pterygomaxillary structures. The nasomaxillary buttress is formed by the lower maxilla, the frontal process of the maxilla, the lacrimal bone, and the nasal process of the frontal bone. The zygomaticomaxillary buttress is formed form the lateral portion of the maxilla, zygoma, and lateral portion of the frontal bone. The final buttress extends along the pterygoid plates to the skull base. The lone unpaired, vertical support mechanism is the nasal septum/ethmoid complex. The horizontal buttresses are comprised of the alveolus, hard palate, inferior orbital rim, and frontal bar. Horizontal buttresses have coronal and sagittal components. The sagittal buttresses are vital for facial projection. The midface is relatively deficient in sagittal buttresses. The skull base is at a 45° angle relative to the occlusal plane of the maxilla and can act as an axial buttress as well. Nahum revealed that low forces can create a fracture in the midface. This is partly due to the large air-filled sinus cavities. Therefore, the midface acts as a shock absorber. The midface is relatively resistant to vertically oriented forces (anteroposterior [AP] direction). The lateral oriented forces may fracture the obliquely directed force vectors. The fractures can be of significant functional and aesthetic importance. Functional problems can lead to disorders of occlusion, nasal obstruction, and trigeminal-nerve sensation. Aesthetic losses include decreased midface height, facial width, facial projection, and malar eminence. These losses can lead to a dish-face deformity. Clinical Details: Because of the accompanying injuries to the entire body, the standard trauma protocol of ABCs must be strictly followed prior to any intervention. Often, the midface fracture assumes a less important role because of the severity of intracranial injury and associated body injuries. Since about one half of midface fractures are associated with significant cerebral edema, a low Glasgow Coma Scale score (<5), and a poor prognosis, it is important to understand the goals of the family and the other medical teams involved in the care of the trauma patient. First of all, it is important to evaluate the airway early to rule out intraoral hemorrhage, edema, loose teeth, and posteroinferior displacement of the maxilla. Establishment of a safe airway is a priority, and a tracheostomy may be needed if intubation proves to be not possible or unsafe for the patient. Bleeding may complicate midface fractures. If the bleeding is severe enough, packing of the midface vessels and temporary reduction of the fracture may be necessary. Angiography may be necessary to locate arterial bleeding from the internal maxillary prior to embolization. Obvious clinical signs of facial skeleton compromise include malocclusion, subcutaneous emphysema, abnormally mobile skeletal structures, and palpable step-offs. Crepitus can be a result of paranasal sinus air leaking into the soft tissues of the face. Palpable step-offs are especially seen with zygomatic fractures. Associated facial fractures must be evaluated and ruled out. The patient's visual status, before and after traumatic insult, is vital in the treatment algorithm of midface fracture. There is a high incidence of visual problems associated with midface fractures, including enophthalmos, diplopia, entrapment, and epiphora. Epiphora occurs in 4% of Le Fort II or III fractures. CSF leakage is also seen, especially in Le Fort III fractures. Any persistent clear rhinorrhea should be tested appropriately for CSF fluid leak (see Skull Base, CSF Otorrhea). Patients may complain of paresthesias of the upper jaw due to damage to the superior alveolar nerve. As in all facial fractures, malocclusion is important to assess. Patients may present with trismus and mouth pain. Palatal fractures often include a lip laceration and/or lacerations of the gingival and palatal mucosa. Patients with a palatal fracture may have an anterior open-bite deformity. Facial edema may obscure the facial examination, and step-offs may not be palpable. It is important to assess fracture mobility by palpating the anterior maxilla between thumb and forefinger. Motion at the level of anterior nasal spine without simultaneous motion is a sign of a Le Fort I fracture. Le Fort I fractures may be associated with gingival crepitation. Le Fort II fractures result in motion of nasal pyramid along medial orbit rims. The patient may have midface flattening and elongation. Le Fort II fractures often are associated with infraorbital paresthesias. Le Fort III fractures have motion at the zygomaticofrontal suture (craniofacial dysjunction). The patient may have anosmia due to fracture at the cribriform plate, severe edema, or lengthening; this is known as a dish-face deformity. Midface fractures are usually not confused with other phenomena. The main concern is whether associated fractures are present. Examples include nasoethmoidal and orbitozygomatic fractures. These associated fractures are typically evident on examination or CT scanning. A history of trauma to the face and proper suspicion of imaging results should lead to the proper diagnosis. I'll be the fun killer and leave a commonly known one for my predecessor. Tell me about Tuberculosis.
Ridryder 911 Posted July 7, 2006 Posted July 7, 2006 For those that need visually to see what one looks like, here is what a La Forte Fxr. is .....
Ace844 Posted July 7, 2006 Posted July 7, 2006 Tuberculosis (commonly abbreviated as TB) is an infection caused by the bacterium Mycobacterium tuberculosis, which most commonly affects the lungs (pulmonary TB) but can also affect the central nervous system (meningitis), lymphatic system, circulatory system (Miliary tuberculosis), genitourinary system, bones and joints. Tuberculosis is one of the most deadly and common major infectious diseases today. As of 2004, 14.6 million people have active TB disease with nine million new cases of the disease and nearly two million deaths, [1] mostly in developing countries. However, developing countries are not the only places with tuberculosis. There is a rising number of people in the developed world who contract tuberculosis because they have compromised immune systems, typically as a result of immunosupressive drugs or HIV/AIDS. These people are at particular risk of tuberculosis infection and active tuberculosis disease. Most of those infected (90%) have asymptomatic latent TB infection (LTBI). There is a 10% lifetime chance that LTBI will progress to TB disease which, if left untreated, will kill more than 50% of its victims. TB is one of the top four infectious killing diseases in the world: TB kills 1.7 million, and malaria kills 2-3 million. HIV/AIDS, the neglect of TB control programs, and immigration have caused a resurgence of tuberculosis. Multidrug-resistant strains of TB (MDR-TB) and Extreme Drug-Resistance in Tuberculosis (XDR-TB) are emerging. The World Health Organization declared TB a global health emergency in 1993, and the Stop TB Partnership proposed a Global Plan to Stop Tuberculosis which aims to save an additional 14 million lives between 2006 and 2015. The bacterium Acid-fast bacilli (AFB) (shown in red) are tubercle bacilli Mycobacterium tuberculosis. The cause of tuberculosis, Mycobacterium tuberculosis (MTB), is a slow-growing aerobic bacterium that divides every 16 to 20 hours. This is extremely slow compared to other bacteria (although not the slowest), which tend to have division times measured in minutes (among the fastest growing bacteria is a strain of E. coli that can divide roughly every 20 minutes; by contrast, Mycobacterium leprae divides every 20 days). MTB is not classified as either Gram-positive or Gram-negative because it does not have the chemical characteristics of either. If a Gram stain is performed, it stains very weakly Gram-positive or not at all (ghost cells). It is a small rod-like bacillus which can withstand weak disinfectants and can survive in a dry state for weeks but, spontaneously, can only grow within a host organism (in vitro culture of M. tuberculosis took a long time to be achieved, but is nowadays a routine laboratory procedure). MTB is identified microscopically by its staining characteristics: it retains certain stains after being treated with acidic solution, and is thus classified as an "acid-fast bacillus" or AFB. In the most common staining technique, the Ziehl-Neelsen stain, AFB are stained a bright red which stands out clearly against a blue background. Acid-fast bacilli can also be visualized by fluorescent microscopy, and by an auramine-rhodamine stain. The M. tuberculosis complex includes 3 other mycobacteria which can cause tuberculosis: M. bovis, M. africanum and M. microti. The first two are very rare causes of disease and the last one does not cause human disease. Nontuberculous mycobacteria (NTM) are other mycobacteria (besides M. leprae which causes leprosy) which may cause pulmonary disease resembling TB, lymphadenitis, skin disease, or disseminated disease. These include Mycobacterium avium, M. kansasii, and others. The disease Epidemiology One-third of the world population (2 billion people) have latent TB infection; in 2004, around 14.6 million people have active TB disease with 9 million new cases. The annual incidence rate varies enormously, from 356 per 100,000 in Africa to 41 per 100,000 in the Americas.[1] In the UK, incidence ranges from 90 per 100,000 in the centre of Birmingham to less than 5 per 100,000 in rural Hertfordshire. Approximately 1.7 million people died from TB in 2004. Transmission TB is spread by aerosol droplets expelled by people with active TB disease of the lungs when they cough, sneeze, speak, or spit. Each droplet is 5 µm in diameter and contains 1 to 3 bacilli. Close contacts (people with prolonged, frequent, or intense contact) are at highest risk of becoming infected (typically a 22% infection rate). A person with untreated, active tuberculosis can infect an estimated 20 other people per year. Others at risk include foreign-born from areas where TB is common, immunocompromised patients (eg. HIV/AIDS), residents and employees of high-risk congregate settings, health care workers who serve high-risk clients, medically underserved, low-income populations, high-risk racial or ethnic minority populations, children exposed to adults in high-risk categories, and people who inject illicit drugs. Transmission can only occur from people with active TB disease (not latent TB infection). The probability of transmission depends upon infectiousness of the person with TB (quantity expelled), environment of exposure, duration of exposure, and virulence of the organism. The chain of transmission can be stopped by isolating patients with active disease and starting effective anti-tuberculous therapy. Pathogenesis While only 10% of TB infection progresses to TB disease, if untreated the death rate is 51%. TB infection begins when MTB bacilli reach the pulmonary alveoli, infecting alveolar macrophages, where the mycobacteria replicate exponentially. The primary site of infection in the lungs is called the Ghon focus. Bacteria are picked up by dendritic cells, which can transport the bacilli to local (mediastinal) lymph nodes, and then through the bloodstream to the more distant tissues and organs where TB disease could potentially develop: lung apices, peripheral lymph nodes, kidneys, brain, and bone. Tuberculosis is classed as one of the granulomatous inflammatory conditions. Macrophages, T lymphocytes, B lymphocytes and fibroblasts are among the cells that aggregate to form a granuloma, with lymphocytes surrounding infected macrophages. The granuloma functions not only to prevent dissemination of the mycobacteria, but also provides a local environment for communication of cells of the immune system. Within the granuloma, T lymphocytes (CD4+) secrete a cytokine such as interferon gamma, which activates macrophages to destroy the bacteria with which they are infected, making them better able to fight infection. T lymphocytes (CD8+) can also directly kill infected cells. Importantly, bacteria are not eliminated with the granuloma, but can become dormant, resulting in a latent infection. Latent infection can be diagnosed only by tuberculin skin test, which yields a delayed hypersensitivity type response to purified protein derivatives of M. tuberculosis in an infected person. Another feature of the granulomas of human tuberculosis is the development of cell death, also called necrosis, in the center of tubercles. To the naked eye this has the texture of soft white cheese and was termed caseous necrosis. If TB bacteria gain entry to the blood stream from an area of tissue damage they spread through the body and set up myriad foci of infection, all appearing as tiny white tubercles in the tissues. This is called miliary tuberculosis and has a high case fatality. In many patients the infection waxes and wanes. Tissue destruction and necrosis are balanced by healing and fibrosis. Affected tissue is replaced by scarring and cavities filled with cheese-like white necrotic material. During active disease, some of these cavities are in continuity with the air passages bronchi. This material may therefore be coughed up. It contains living bacteria and can pass on infection. Treatment with appropriate antibiotics kills bacteria and allows healing to take place. Affected areas are eventually replaced by scar tissue. Progression In those people in whom TB bacilli overcome the immune system defenses and begin to multiply, there is progression from TB infection to TB disease. This may occur soon after infection (primary TB disease – 1 to 5%) or many years after infection (post primary TB, secondary TB, reactivation TB disease of dormant bacilli – 5 to 9%). The risk of reactivation increases with immune compromise, such as that caused by infection with HIV. In patients co-infected with M. tuberculosis and HIV, the risk of reactivation increases to 10% per year, while in immune competent individuals, the risk is between 5 and 10% in a lifetime. About five percent of infected persons will develop TB disease in the first two years, and another five percent will develop disease later in life. In other words, about 10% of infected persons with normal immune systems will develop TB disease in their lifetime. Some medical conditions increase the risk of progression to TB disease. In HIV infected persons with TB infection, the risk increases to 10% each year instead of 10% over a lifetime. Other such conditions include drug injection (mainly because of the life style of IV Drug users), substance abuse, recent TB infection (within two years) or history of inadequately treated TB, chest X-ray suggestive of previous TB (fibrotic lesions and nodules), diabetes mellitus, silicosis, prolonged corticosteroid therapy and other immunosuppressive therapy, head and neck cancers, hematologic and reticuloendothelial diseases (leukemia and Hodgkin's disease), end-stage renal disease, intestinal bypass or gastrectomy, chronic malabsorption syndromes, or low body weight (10% or more below the ideal). Some drugs, including rheumatoid arthritis drugs that work by blocking tumor necrosis factor-alpha (an inflammation-causing cytokine), raise the risk of causing a latent infection to become active due to the importance of this cytokine in the immune defense against TB. Symptoms TB most commonly affects the lungs (75% or more), where it is called pulmonary TB. Symptoms may include a productive, prolonged cough of more than three weeks duration, chest pain, and hemoptysis. Systemic symptoms include fever, chills, night sweats, appetite loss, weight loss, and easy fatigability. The term consumption arose because sufferers appeared as if they were "consumed" from within by the disease. People from Asian and African descent may have lymph node TB more often than Caucasians. Lymph node TB is not contagious. Extrapulmonary sites include the pleura, central nervous system (meningitis), lymphatic system (scrofula of the neck), genitourinary system, and bones and joints (Pott's disease of the spine). An especially serious form is disseminated, or miliary TB, so named because the lung lesions so-formed resemble millet seeds on x-ray. These are more common in immunosuppressed persons and in young children. Pulmonary TB may co-exist with extrapulmonary TB. Drug resistance Drug-resistant Tuberculosis is transmitted in the same way as regular TB. Primary resistance develops in persons initially infected with resistant organisms. Secondary resistance (acquired resistance) may develop during TB therapy due to inadequate treatment regimen, i.e. not taking the prescribed regimen appropriately or using low quality medication. Drug-resistant TB is an important public health issue in many developing countries, as treatment of drug-resistant TB requires the use of more expensive drugs and treatment is longer. Multidrug-resistant TB is defined as resistance to the two most effective first line TB drugs - Rifampicin and Isoniazid (INH). Diagnosis A complete medical evaluation for TB includes a medical history, a physical examination, a tuberculin skin test, a serological test, a chest X-ray, and microbiologic smears and cultures. The measurement of a positive skin test depends upon the person's risk factors for progression of TB infection to TB disease. Bacteriophage-based assays are among a few new testing procedures that offer the hope of cheap, fast and accurate TB testing for the impoverished countries that need it most. See: tuberculosis diagnosis, tuberculosis radiology Treatment For all practical purposes, only patients with tuberculosis of the lungs can spread TB to other people. People may become infected with TB but not have active disease: such people are said to have latent TB infection (LTBI) and are not capable of passing the infection on to other people. The reason for treating people with LTBI is to prevent them from progressing to active TB disease later in life (approximately 10% lifetime risk). The distinction is important because treatment options are different for the two groups. See: tuberculosis treatment Prevention of Tuberculosis Prevention and control efforts include three priority strategies: · identifying and treating all people who have TB · finding and evaluating persons who have been in contact with TB patients to determine whether they have TB infection or disease, and treating them appropriately, and · testing high-risk groups for TB infection to identify candidates for treatment of latent infection and to ensure the completion of treatment. In tropical areas where the incidence of atypical mycobacteria is high, exposure to nontuberculous mycobacteria gives some protection against TB. BCG vaccine Many countries use BCG vaccine as part of their TB control programs, especially for infants. The protective efficacy of BCG for preventing serious forms of TB (e.g. meningitis) in children is high (greater than 80%). However, the protective efficacy for preventing pulmonary TB in adolescents and adults is variable, from 0 to 80%. In the United Kingdom, children aged 10-14 were typically immunized during school until 2005. (Routine BCG vaccination was stopped as it was no longer cost-effective. The incidence of TB in people born in the UK, and with parents and grandparents who were born in the UK, was at an all time low, and falling. Others continue to be offered BCG vaccination.) The effectiveness of BCG is much lower in areas where mycobacteria are less prevalent. In the USA, BCG vaccine is not routinely recommended except for selected persons who meet specific criteria: · Infants or children with negative skin-test result who are continually exposed to untreated or ineffectively treated patients or will be continually exposed to multidrug-resistant TB. · Healthcare workers considered on individual basis in settings in which high percentage of MDR-TB patients has been found, transmission of MDR-TB is likely, and TB control precautions have been implemented and not successful. Tuberculosis vaccine The first recombinant Tuberculosis vaccine entered clinical trials in the United States in 2004 sponsored by the National Institute of Allergy and Infectious Diseases (NIAID).[2] A 2005 study showed that a DNA TB vaccine given with conventional chemotherapy can accelerate the disappearance of bacteria as well as protecting against re-infection in mice; it may take four to five years to be available in humans.[3] Because of the limitations of current vaccines, researchers and policymakers are promoting new economic models of vaccine development including prizes, tax incentives and advance market commitments. Animals Tuberculosis can be carried by many mammals. Domesticated species, such as cats and dogs, are generally free of tuberculosis, but wild animals may be carriers. As a result, many places have regulations restricting the ownership of novelty pets, possibly including such partially domesticated species as pet skunks; for example, the American state of California forbids the ownership of pet gerbils. The strictness of such restrictions generally depends on the public health policies adopted for fighting tuberculosis. An effort to eradicate bovine tuberculosis from the cattle and deer herds of New Zealand is underway. It has been found that herd infection is more likely in areas where infected vector species such as Australian brush-tailed possums come into contact with domestic livestock at farm/bush borders. Controlling the vectors through possum eradication and monitoring the level of disease in livestock herds through regular surveillance are seen as a "two-pronged" approach to ridding New Zealand of the disease. In both the Republic of Ireland and Northern Ireland, badgers have been identified as a vector species for the transmission of bovine tuberculosis. As a result, the government in both regions has mounted an active campaign of eradication of the species in an effort to reduce the incidence of the disease. Badgers have been culled primarily by snaring and gassing. It remains a contentious issue, with proponents and opponents of the scheme citing their own studies to support their position.[4][5][6] History Tuberculosis has been present in humans since antiquity. The origins of the disease are in the first domestication of cattle (which also gave humanity viral poxes). Skeletal remains show prehistoric humans (4000 BCE) had TB, and tubercular decay has been found in the spines of Egyptian mummies from 3000-2400 BCE. There were references to TB in India around 2000 BCE, and indications of lung scarring identical to that of modern-day TB sufferers in preserved bodies (such as mummies) suggests that TB was present in The Americas from about 2000 BCE. Phthisis is a Greek term for consumption. Around 460 BCE, Hippocrates identified phthisis as the most widespread disease of the times which was almost always fatal. During the Industrial Revolution, tuberculosis was more commonly thought of as vampirism. When one member of a family died from it, the other members that were infected would lose their health slowly. People believed that the cause of this was the original victim draining the life from the other family members. To cure this, people would dig up the body of what they thought was the vampire, open the chest and burn the heart, sometimes with the rest of the body. Furthermore, people who had TB exhibited symptoms similar to what people considered to be vampire traits. People with TB often had symptoms such as red, swollen eyes (which also creates a sensitivity to bright light), pale skin and coughing blood (which people often thought needed to be replenished, so they figured the only way for the afflicted to get blood back was by sucking blood). This may be how much of the common mythology of the vampire originated. Although it was established that the pulmonary form was associated with 'tubercles' by Dr Richard Morton in 1689,[7][8] due to the variety of its symptoms, TB was not identified as a single disease until the 1820s and was not named 'tuberculosis' until 1839 by J. L. Schönlein. During the years 1838-1845, Dr. John Croghan, the owner of Mammoth Cave, brought a number of tuberculosis sufferers into the cave in the hope of curing the disease with the constant temperature and purity of the cave air. The first TB sanatorium opened in 1859 in Poland, with another opening in the United States in 1885. The bacillus-causing tuberculosis, Mycobacterium tuberculosis, was identified and described on March 24, 1882 by Robert Koch. He received the Nobel Prize in physiology or medicine in 1905 for this discovery. Koch did not believe that bovine (cattle) and human tuberculosis were similar, which held back the recognition of infected milk as a source of infection. Later, this source was eliminated by the pasteurization process. Koch announced a glycerine extract of the tubercle bacilli as a "remedy" for tuberculosis in 1890, calling it 'tuberculin'. It was not effective, but was later adapted by von Pirquet in a test for pre-symptomatic tuberculosis. The first genuine success in immunizing against tuberculosis developed from attenuated bovine-strain tuberculosis by Albert Calmette and Camille Guerin in 1906. It was called 'BCG' (Bacillus of Calmette and Guerin). The BCG vaccine was first used on humans on July 18, 1921 in France. It wasn't until after World War II until BCG received widespread acceptance in the USA, Great Britain, and Germany. Tuberculosis caused the most widespread public concern in the 19th and early 20th centuries as the endemic disease of the urban poor. In 1815, one in four deaths in England was of consumption; by 1918 one in six deaths in France were still caused by TB. After the establishment in the 1880s that the disease was contagious, TB was made a notifiable disease in Britain; there were campaigns to stop spitting in public places, and the infected poor were "encouraged" to enter sanatoria that rather resembled prisons. Whatever the purported benefits of the fresh air and labor in the sanatoria, 75% of those who entered were dead within five years (1908). The promotion of Christmas Seals was started in 1904 in Denmark as a way to raise money for tuberculosis programs. It expanded to the United States and Canada in 1907-08 to help the National Tuberculosis Association (later called the American Lung Association). In the United States, concern about the spread of tuberculosis played a role in the movement to prohibit public spitting except into spittoons. In Europe, deaths from TB fell from 500 out of 100,000 in 1850 to 50 out of 100,000 by 1950. Improvements in public health were reducing tuberculosis even before the arrival of antibiotics, although the disease's significance was still such that when the Medical Research Council was formed in Britain in 1913 its first project was tuberculosis. It was not until 1946 with the development of the antibiotic streptomycin that treatment rather than prevention became a possibility. Prior to then only surgical intervention was possible as supposed treatment (other than sanatoria), including the pneumothorax technique: collapsing an infected lung to "rest" it and allow lesions to heal, which was an accomplished technique but was of little benefit and was discontinued after 1946. Hopes that the disease could be completely eliminated have been dashed since the rise of drug-resistant strains in the 1980s. For example, Tuberculosis cases in Britain, numbering around 50,000 in 1955, had fallen to around 5,500 in 1987, but in 2000 there were over 7,000 confirmed cases. Due to the elimination of public health facilities in New York in the 1970s, there was a resurgence in the 1980s. The number of those failing to complete their course of drugs was very high. NY had to cope with more than 20,000 "unnecessary" TB-patients with many multidrug-resistant strains (i.e., resistant to, at least, both Rifampin and Isoniazid). The resurgence of tuberculosis resulted in the declaration of a global health emergency by the World Health Organization in 1993. Incidence According to the World Health Organization (WHO), nearly 2 billion people, one-third of the world's population, have tuberculosis. [1] In the United Kingdom, the rate of tuberculosis in London is 40 per 100,000 - three times the national average of 13 per 100,000, according to the Public Health Laboratory Service and WHO. The highest rates in Western Europe are in Portugal (42 per 100,000) and Spain (20 per 100,000). These rates compare with 113 per 100,000 in China and 64 per 100,000 in Brazil. Tuberculosis is the world's greatest infectious killer of women of reproductive age and the leading cause of death among people with HIV/AIDS. Globally more than 23 000 people develop active TB and almost 5 000 die from the disease every day. [2]. The city of Porto in northern Portugal, is placed among the European Union's largest cities with over 250,000 inhabitants having the highest rates of tuberculosis positive cases - 53 per 100,000 (in 2004). General Features Mycobacterium tuberculosis is the organism that is the causative agent for tuberculosis (TB). There are other "atypical" mycobacteria such as M. kansasii that may produced a similar clincal and pathologic appearance of disease. M. avium-intracellulare (MAI) seen in immunocompromised hosts (particularly in persons with AIDS) is not primarily a pulmonary infection in terms of its organ distribution (mostly in organs of the mononuclear phagocyte system). Tuberculosis is becoming a world-wide problem. War, famine, homelessness, and a lack of medical care all contribute to the increasing incidence of tuberculosis among disadvantaged persons. Since TB is easily transmissible between persons, then the increase in TB in any segment of the population represents a threat to all segments of the population. This means that it is important to institute and maintain appropriate public health measures, including screening, vaccination (where deemed of value), and treatment. A laxity of public health measures will contribute to an increase in cases. Failure of adequate treatment promotes the development of resistant strains of tuberculosis. Patterns of Infection There are two major patterns of disease with TB: Primary tuberculosis: seen as an initial infection, usually in children. The initial focus of infection is a small subpleural granuloma accompanied by granulomatous hilar lymph node infection. Together, these make up the Ghon complex. In nearly all cases, these granulomas resolve and there is no further spread of the infection. Secondary tuberculosis: seen mostly in adults as a reactivation of previous infection (or reinfection), particularly when health status declines. The granulomatous inflammation is much more florid and widespread. Typically, the upper lung lobes are most affected, and cavitation can occur. When resistance to infection is particularly poor, a "miliary" pattern of spread can occur in which there are a myriad of small millet seed (1-3 mm) sized granulomas, either in lung or in other organs. Dissemination of tuberculosis outside of lungs can lead to the appearance of a number of uncommon findings with characteristic patterns: Skeletal Tuberculosis: Tuberculous osteomyelitis involves mainly the thoracic and lumbar vertebrae (known as Pott's disease) followed by knee and hip. There is extensive necrosis and bony destruction with compressed fractures (with kyphosis) and extension to soft tissues, including psoas "cold" abscess. Genital Tract Tuberculosis: Tuberculous salpingitis and endometritis result from dissemination of tuberculosis to the fallopian tube that leads to granulomatous salpingitis, which can drain into the endometrial cavity and cause a granulomatous endometritis with irregular menstrual bleeding and infertility. In the male, tuberculosis involves prostate and epididymis most often with non-tender induration and infertility. Urinary Tract Tuberculosis: A "sterile pyuria" with WBC's present in urine but a negative routine bacterial culture may suggest the diagnosis of renal tuberculosis. Progressive destruction of renal parenchyma occurs if not treated. Drainage to the ureters can lead to inflammation with ureteral stricture. CNS Tuberculosis: A meningeal pattern of spread can occur, and the cerebrospinal fluid typically shows a high protein, low glucose, and lymphocytosis. The base of the brain is often involved, so that various cranial nerve signs may be present. Rarely, a solitary granuloma, or "tuberculoma", may form and manifest with seizures. Gastrointestinal Tuberculosis: This is uncommon today because routine pasteurization of milk has eliminated Mycobacterium bovis infections. However, M. tuberculosis organisms coughed up in sputum may be swallowed into the GI tract. The classic lesions are circumferential ulcerations with stricture of the small intestine. There is a predilection for ileocecal involvement because of the abundant lymphoid tissue and slower rate of passage of lumenal contents. Adrenal Tuberculosis: Spread of tuberculosis to adrenals is usually bilateral, so that both adrenals are markedly enlarged. Destruction of cortex leads to Addison's disease. Scrofula: Tuberculous lymphadenitis of the cervical nodes may produce a mass of firm, matted nodes just under the mandible. There can be chronic draining fistulous tracts to overlying skin. This complication may appear in children, and Mycobacterium scrofulaceum may be cultured. Cardiac Tuberculosis: The pericardium is the usual site for tuberculous infection of heart. The result is a granulomatous pericarditis that can be hemorrhagic. If extensive and chronic, there can be fibrosis with calcification, leading to a constrictive pericarditis. The following images illustrate gross pathologic findings with tuberculosis: Ghon complex in lung, gross. Ghon complex in lung, closer view, gross. Cavitary tuberculosis in lung, gross. Cavitary tuberculosis in lung, closer view, gross. Cavitary tuberculosis in lung, florid, gross. Miliary tuberculosis in lung, gross. Miliary tuberculosis in lung, closer view, gross. Microscopic Findings Microscopically, the inflammation produced with TB infection is granulomatous, with epithelioid macrophages and Langhans giant cells along with lymphocytes, plasma cells, maybe a few PMN's, fibroblasts with collagen, and characteristic caseous necrosis in the center. The inflammatory response is mediated by a type IV hypersensitivity reaction. This can be utilized as a basis for diagnosis by a TB skin test. An acid fast stain (Ziehl-Neelsen or Kinyoun's acid fast stains) will show the organisms as slender red rods. An auramine stain of the organisms as viewed under fluorescence microscopy will be easier to screen and more organisms will be apparent. The most common specimen screened is sputum, but the histologic stains can also be performed on tissues or other body fluids. Culture of sputum or tissues or other body fluids can be done to determine drug sensitivities. Granulomas in lung, low power microscopic. Granuloma with caseous necrosis, high power microscopic. Granuloma with epithelioid macrophages and a Langhans giant cell, high power microscopic. Granulomatous endometritis, high power microscopic. Ziehl-Neelsen acid fast stain, microscopic, AFB stain. Auramine stain, M. tuberculosis, fluorescence microscopy. Tuberculin Skin Testing Skin testing for tuberculosis is useful in countries where the incidence of tuberculosis is low, and the health care system works well to detect and treat new cases. In countries where BCG vaccination has been widely used, the TB skin test is not useful, because persons vaccinated with BCG will have a positive skin test. The TB skin test is based upon the type 4 hypersensitivity reaction. If a previous TB infection has occurred, then there are sensitized lymphocytes that can react to another encounter with antigens from TB organisms. For the TB skin test, a measured amount (the intermediate strength of 5 tuberculin units, used in North America) of tuberculin purified protein derivative (PPD) is injected intracutaneously to form a small wheal, typically on the forearm. In 48 to 72 hours, a positive reaction is marked by an area of red induration that can be measured by gentle palpation (redness from itching and scratching doesn't count). Reactions over 10 mm in size are considered positive in non-immunocompromised persons. Repeated testing may increase the size of the reaction (induration), but repeated TB skin testing will not lead to a positive test in a person not infected by TB. Anergy, or absence of PPD reactivity in persons infected with TB, can occur in immunocompromised persons, or it may even occur in persons newly infected with TB, or in persons with miliary TB. Hypertensive Urgency, Emergency, Crisis, and Treatment??
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