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When a hos- pital laboratory cannot perform the requested test and the specimen is sent to a referral laboratory buy 20 mg celexa mastercard treatment wpw, the hospital laboratory may receive the bill from the referral laboratory directly celexa 20mg free shipping medicine 8 discogs. The hospital laboratory is then responsible for billing and recovering the refer- ral laboratory charges from either the patient’s insur- ance or the patient directly buy cheap celexa 20 mg online medicine engineering. Some reference laboratories will directly bill the patient’s insurance (“third-party billing”) and will take on the fnancial risk if the insurance or patient does not pay buy cheap celexa 20mg on line symptoms 8dpiui. Unfortunately, many outreach clients are physician offces that are closed after hours. These physician offces may have intermit- tent coverage that can present a challenge to laboratories that need to reach the ordering physician after hours. The laboratory must contact a clinician in real time, either the ordering physician or their designee who can take clinical action, to commu- nicate a critical result and verify accurate under- standing of the communication via read-back. Communication is essential between out- reach sales staff who may have little laboratory experience and the laboratory staff and medical directors with extensive clinical and technical experience. Regulations implementing Clinical laboratories improvement Amendments of 1988 (CliA). Laboratory Medicine Practice Guidelines; Evidence-Based Practice for Point-of-Care Testing. H21-A4: Collection, Transport, and Processing of Blood Specimens for Testing Plasma-Based Coagulation Assays: Approved Guideline. Pipeline and hazardous Materials Safety Administration, Department of Transportation. For serological testing, the timing of the serum collection may be an equally critical factor for optimal use. Unfortunately, the clinicians often do not have the tools, interest, training, access to data, or time to determine optimal use of the clinical microbiology laboratory for their patients. This chapter discusses common preanalytic medical errors in the clinical microbiology laboratory. Thus, oncologists and surgeons must be alert and always consider the possibility of infection even when malignancy is their frst concern. This is a very subtle type of medical error and is considered an individual type of error that is not easily rectifed by a systems approach. Bone marrow aspirations and biopsies are often done to rule out malignancy; cultures may not be requested on the aspirate/biopsy as the clinicians are focused on malignancy and not thinking about infection. For example, failure to consider infection may occur when evaluating a patient with neck mass and/ or cervical lymphadenopathy in which lymphoma or metastatic carcinoma is the working diagnosis. Because lymph node biopsy is often reserved for situ- ations in which a malignant process is suspected, the clinician may not think to order cultures. Biopsy for asymptomatic cervical lymphadenopathy of greater than three weeks’ duration is a common situation in which metastatic carcinoma is suspected, particularly in patients over 40 years of age. These enlarged cervi- cal lymph nodes thus are usually excised or biopsied, and the lymphatic tissue is sent to the surgical pathol- ogy laboratory. Failure to send part of the lymphatic tissue to the clinical microbiology labo- ratory for culture is a particular problem in children, in whom nontuberculous cervical lymphadenopa- thy is more commonly seen. Biopsy of indeterminate mediastinal masses, which is often done in order to evaluate the medias- tinal mass/lymph nodes for malignancy, presents another example. When histopathologic examination reveals no malignancy, the opportunity for culture has passed. Tuberculosis is an unusual cause of mediastinal mass in an infant, but in contrast, histoplasmosis as a cause of medias- tinal mass in an infant or in a child has been reported on many occasions. These cases of mediastinal his- toplasmosis in children were sometimes mistakenly diagnosed as lymphoma. There is a signifcant risk for medical errors in cases involving a mediastinal mass in a child if infection is not considered. These fndings, however, are not specifc and can be seen with pulmonary infections. Thus, the clinician must keep in mind the possibility of infection when initiating diagnostic pro- cedures to confrm a presumed pulmonary malignancy. This type of error is best avoided by obtaining consultation (informal or formal) from infectious disease cli nicians and/or the clinical microbiology laboratory director. Consider the example of failure to consider an uncommon infection such as ehrlichiosis/anaplasmosis in the differential diagnosis of a febrile patient with “summer fu. Treatment thus should be initiated based on the clinical presentation and not based on the results of laboratory testing. With rMsF, a potential outcome is rickettsial meningoencephalitis resulting in death. Pitfalls related to the evaluation of the patient with possible rMsF include (a) waiting for the rash to develop, (b) misdiagnosing the febrile ill- ness as another infection such as gastroenteritis, (c) dis- counting the diagnosis in the absence of history of tick bite, (d) using an inappropriate geographic exclusion, (e) using an inappropriate seasonal exclusion, (f) fail- ing to treat on clinical suspicion, (g) failing to elicit an appropriate history, and (h) failing to treat with doxy- cycline. The most widely used diagnostic tool is serologic testing, which is not useful during active infection. The diagnosis and empirical doxycycline therapy of rMsF is particularly diffcult in children as pediatricians, family physicians, and/or emergency room physicians may not appreciate that rMsF is seen in children or be aware that the appropriate treatment strategy requires doxycycline treatment before the rash is seen. Finally, it should be noted that a newly recognized tickborne spotted fever group rickettsiosis has been described. The cause of this tickborne escar-associated spotted fever group rickettsiosis is Rickettsia parkeri, which originally was thought to be nonpathogenic in humans. Clinically, this rickettsiosis presents in a manner that is very similar to rMsF with symptoms of fever, fatigue, myalgia, headache, and a generalized rash; in addi- tion, patients describe a “sore” or “pimple” at the site of a tick bite. Babesiosis is another tickborne infection seen dur- ing summer months that can be particularly diffcult to identify unless it is considered in the differential diagnosis. Patients may require the review of multiple thin and thick blood smears to make a diagnosis. Diagnosis may be made serendipi- tously on a routine blood smear; however, autoana- lyzers or a less observant medical technologist might miss this diagnosis, and multiple blood smears and/ 5: CliniCal MiCroBiology ■ 197 or thick smears may be required. Tickborne infections should be considered in the differential diagnosis for a febrile illness in a patient with thrombocytopenia, especially in a patient presenting in summer. However, levels of West nile virus rna typically peak before symp- toms appear and then rapidly decline as igM antibody production begins. To avoid missing cases of acute West nile infection, both West nile virus rna testing and West nile virus igM testing may be required. However, as there is no current anti- viral therapy for West nile virus encephalitis, a delay in the diagnosis may not present a therapeutic problem. Humans are accidental hosts and become infected through exposure to environmen- tal sources contaminated by the urine of chronically infected mammals. Patients hospitalized with leptospirosis may have mortality rates as high as 25%; this is, in part, related to a delay in diagnosis. The current standard is the microscopic agglutination test, which involves the reaction of antigens in the form of live Leptospira organisms with the antibodies found in the patient’s sera. The igg 200200 ■■ CliniCal DiagnosTiC TesTsCliniCal DiagnosTiC TesTs antibody response to leptospirosis for this test takes about two weeks and can be delayed by antimicro- bial therapy. The need to understand the sensitivity and speci- fcity of specifc microbiology tests was illustrated vividly during the spring and summer of 2009, when a novel infuenza a virus of swine origin, H1n1, emerged in humans in north america.
Angiosarcoma of the heart in an adolescent: a light and electron microscopic and immunohistochemical study purchase celexa 20mg mastercard symptoms 0f brain tumor. Primary right cardiac tumor: detection by echocardiographic and radioisotopic studies order celexa australia medicine balls for sale. Primary left ventricular rhabdomyosarcoma in a child: noninvasive assessment and successful resection of a rare tumor buy cheap celexa 20 mg online 10 medications. Recurrent left-sided heart leiomyosarcoma: should heart transplantation be legitimate? Heart transplantation for cardiac angiosarcoma: should its indication be questioned? Primary cardiac tumors in infants and children: Immediate and long-term operative results order celexa 20mg amex medicine cabinets. Human cardiac explantation and autotransplantation: application in a patient with a large cardiac pheochromocytoma. Two-dimensional echocardiographic findings in a case of massive cardiac involvement by malignant lymphoma. Shaddy Introduction Chronic heart failure is a clinical syndrome with diverse etiologies and broad variation in its clinical manifestations, all of which ultimately result from impaired ventricular filling or ejection of blood (1). Traditionally, chronic heart failure has been viewed as a syndrome of inadequate cardiac output to maintain end-organ perfusion during rest or exercise, and has historically been equated with reduced left ventricular ejection fraction. In this chapter, the various causes of chronic heart failure in children will be described, along with their management and prognosis. Acute heart failure syndromes in the child, fetus, and adolescent, including myocarditis, as well as mechanical circulatory support and heart transplantation, will be discussed in further detail elsewhere within this textbook. The topic of chronic heart failure in adults is of great significance for public health given its substantial incidence and burden on healthcare costs and utilization in developed countries, and is only expected to increase in coming years (4). While the comparative impact of pediatric chronic heart failure is much more limited relative to that of the adult syndrome, it is a resource-intensive disease (5,6) with higher rates of hospital-related mortality compared to adults, in addition to having high rates of hospital-associated morbidity (7). The treatment of chronic heart failure has recently been subject to comprehensive evidence-based review and recommendations by professional societies for both adults and children (1,8,9,10,11). Nomenclature and Classification The term “heart failure” is used in several contexts throughout the medical literature as well as common usage, and can hence be confusing to the novice practitioner. In infants and young children, objective assessment of activity limitation can be difficult, so surrogate measures such as growth failure may be used in this patient population. However, “heart failure” may also be used to describe a constellation of acute signs and symptoms seen in conjunction with systemic ventricular dysfunction: left atrial hypertension, pulmonary edema, hepatomegaly, tachycardia, and gallop rhythm, without consideration given to assessment of cardiac output or ventricular function. Adding another layer of ambiguity to the definition of heart failure is the frequent application of this term to infants with large left-to-right intracardiac shunt lesions, who will often manifest the aforementioned symptom complex but have no evidence of systemic ventricular dysfunction; their symptoms merely resemble that of patients with systemic ventricular dysfunction due the common symptoms of left atrial hypertension, pulmonary vascular congestion, and systemic vascular congestion (hepatomegaly and peripheral edema). Several classification schemes have been proposed to define the clinical severity of chronic heart failure in children and adults, similar to the staging criteria utilized for various malignancies. Etiology An approach to understanding chronic heart failure in children begins with an investigation of the cause (Table 73. For the purposes of this chapter, “structural heart disease” encompasses primary anatomic cardiac abnormalities such as congenital heart disease, valvar stenosis and/or regurgitation independent of a congenital abnormality, and coronary artery disease. This is in distinction to cardiomyopathies and pericardial disease, which primarily affect cardiac muscle and the pericardium, respectively. Broadly speaking, from the standpoint of age, children can be divided into two broad groups: neonates/infants (<1 year of age) and children/adolescents; the etiologies of chronic heart failure in these populations tend to be distinct, although overlap certainly exists. Neonates and Infants The neonate or infant with heart failure typically presents for care after an episode of acute illness in which the diagnosis of heart failure is made, hemodynamic instability and symptoms are stabilized, and medical management is initiated. In some instances, the diagnosis is clear, although in a substantial proportion of cases, the diagnosis remains unclear and the child is left with the diagnosis of “idiopathic dilated cardiomyopathy. The Ross classification for heart failure in children after 25 years: a review and an age-stratified revision. Broadly speaking, potential etiologies of chronic heart failure in neonates and infants can be grouped under infectious, inflammatory, toxic, structural/congenital, metabolic, arrhythmogenic, and idiopathic. The differential diagnosis for the unusual presentation of heart failure at the time of birth includes birth asphyxia with myocardial dysfunction from hypoxemia, hypoglycemia, hypocalcemia, sepsis, anemia or polycythemia, myocarditis, arrhythmias (congenital complete heart block, supraventricular tachyarrhythmias), large arteriovenous malformations, severe atrioventricular valve regurgitation, or Ebstein abnormality of the tricuspid valve (13). Essentially any form of congenital heart disease can precipitate ventricular dysfunction, although ventricular dysfunction with resultant symptoms of low cardiac output are generally restricted to the following physiologic derangements: (a) obstructive lesions (i. Much of what is termed “critical” congenital heart disease consists of defects within the obstructive lesion group, in which severe hypoplasia or atresia of left heart structures and/or the aorta leads to inadequacy of cardiac output upon closure of the ductus arteriosus. Without maintenance of ductal patency with prostaglandin E , affected infants usually present within1 the first 1 to 2 weeks of life with signs and symptoms of low cardiac output, including but not limited to pallor, poor feeding, weak cry, acidosis, shock, and varying degrees of cyanosis due to intracardiac mixing. The advent of pulse oximetry screening has made it possible to identify readily infants with ductal-dependent cyanotic congenital heart disease who may otherwise escape detection before discharge from the newborn nursery (14); the effects on infant outcomes of a nationwide implementation of this practice remain unclear, but at least appear to be cost effective (15,16,17). The clinical presentation of volume overload lesions depends upon the size of the defect and the ratio of pulmonary to systemic vascular resistance. During the neonatal period, the ratio may be nearly equal, leading to a well-balanced circulation and little net left-to-right shunt. However, as pulmonary vascular resistance falls normally with age, the proportion of pulmonary blood flow increases, with a decrease in the ratio of systemic blood flow. This progressive net left-to-right shunt may lead to impaired cardiac output (18), which may be accentuated by periods of increased metabolic demand (fever) or by the physiologic fall in hemoglobin (19). The prototypic regurgitant lesion causing symptoms of a low cardiac output and heart failure in the neonate and/or infant is Ebstein anomaly of the tricuspid valve. The anatomy and physiology of this lesion is described in detail in Chapter 38 of this textbook. When severe, the combination of significant tricuspid regurgitation and functional right ventricular hypoplasia leads to a state in which the right ventricle is unable to generate sufficient forward output. Frequently, however, the pulmonary valve in Ebstein abnormality is incompetent, leading to an inefficient cycle in which deoxygenated blood is recirculated through the heart, leading to worsening cyanosis even in the setting of ductal patency (20). This sets off a vicious cycle, sometimes termed a “circular shunt,” in which cyanosis and low cardiac output are intertwined. Many complex congenital abnormalities are associated with both obstruction and volume overload, which may result in a combination of heart failure and cyanosis. Patients with single ventricle physiology, will frequently fall into this category. The specific manifestations of heart failure and cyanosis, and their severity, depend on the balance of systemic and pulmonary vascular resistance as well as the specific anatomic characteristics of the defect. As an example, in tricuspid atresia with normally related great vessels, a large muscular ventricular septal defect, and no pulmonary stenosis, the patient may require no interventions as a neonate but eventually require an additional source of pulmonary blood flow later in infancy due to progressive cyanosis due to the development of restriction at the ventricular septal defect. The numerous categories and variations of the complex defects capable of causing both pressure and volume overload are discussed in detail in their respective chapters. The anatomy, physiology, and treatment of this lesion are described in detail in Chapter 32. Its clinical presentation is dependent upon the normal fall in pulmonary vascular resistance; as pulmonary vascular resistance and pressure fall, perfusion pressure in the left coronary artery falls in concert.
Mammals have a four- the descending thoracic aorta generic celexa 10 mg without a prescription symptoms right after conception, are present in the embryo by chambered heart (Fig buy celexa online now medicine 54 357. By far the majority of vascular rings consist of a dominant This anomaly represents persistence of the right dorsal aorta right arch purchase cheap celexa on line symptoms 7 days past ovulation. The surgical relevance of this fact order celexa from india medications bad for liver, as will be dis- with incomplete resorption of the left. Note that the right cussed later, is that almost all vascular rings are most safely recurrent laryngeal nerve must pass around the right aortic and conveniently approached through a left thoracotomy. Double Aortic Arch As the name implies, this anomaly consists of two aortic Right Aortic Arch, Aberrant Left Subclavian arches, an anterior and leftward arch and a posterior and Artery, and Left Ligamentum rightward arch (Fig. The right arch is generally dominant and gives rise to common carotid, the right subclavian, and the left subclavian the right common carotid and right subclavian arteries either arteries. The left subclavian passes behind the esophagus and as an innominate artery or as two separate vessels. The left then gives rise to the ligamentum arteriosum, which passes arch gives rise to the left common carotid and left subclavian anteriorly to connect to the left pulmonary artery, thereby arteries. It may be hypoplastic or atretic beyond the origin of completing the vascular ring. This anomaly represents per- either the left common carotid or left subclavian artery, being sistence of the right fourth aortic arch with resorption of the little more than a fbrous cord. A sphincter-like mechanism within the ventricle can preferentially direct blood to the lungs or the systemic circulation. Right Aortic Arch, Mirror-Image Branching, Left Aortic Arch, Right Descending Aorta, and Right- and Retroesophageal Ligamentum Sided Ligamentum Arteriosum to Right Pulmonary Artery With this form of vascular ring there is a right aortic arch that The branching sequence from the left aortic arch is the right gives off, in sequence, the left innominate artery (left com- common carotid, left common carotid, left subclavian, and, mon carotid with left subclavian), the right common carotid, fnally, right subclavian as a fourth branch from the proximal and the right subclavian artery. This anomaly also represents persistence of the Vascular rings, in contrast to a pulmonary artery sling, fourth right aortic arch with resorption of the fourth left aor- encircle both the esophagus and trachea and, therefore, may tic arch. A short segment of the distal end of the left fourth result in obstructive symptoms of both. Nevertheless, the arch persists as an aortic diverticulum, which gives rise to mere presence of a ring does not guarantee that there will be the ligamentum. Note that the aortic diverticulum has been reported as the site of origin of aortic dissection. Also note that when there is mirror-image branching, if the ligamen- tum arteriosum arises from the innominate artery to pass to the origin of the left pulmonary artery rather than from the diverticulum of Kommerell this does not result in a vascular ring (Fig. Dominant Left Aortic Arch A dominant left aortic arch is extremely rare but should be recognized, because the best approach for surgical division is through a right thoracotomy. The ligamentum arteriosum contributes to secondary tracheoesophageal compression and should be divided together with the left anterior arch. Ao a double arch from the retroesophageal subclavian or ligament, based on the angulation of the esophageal impression. However, it is be through a left thoracotomy, which will be true in more an essential part of the workup for congenital tracheal stenosis. If a double aor- tic arch is present, it is important to be aware preoperatively Aortography which of the arches is dominant. In the majority of cases, it Expensive, invasive, and carrying additional risk for the will be the right aortic arch. Nevertheless, in cases of dou- patient, aortography is rarely justifed for the diagnosis of a ble patent arches it is useful to place pulse oximeter probes vascular ring. In addition, if there is an atretic segment, such on both hands and one foot so that temporary occlusion of a study will not be diagnostic. Because the point of division will be the or dysphagic symptoms are present, surgical division of the narrowest segment of the ring, there should be no pressure ring is indicated. Preoperatively the child should be given maxi- eral decubitus position, and a left posterolateral thoracotomy is performed that is more posterior than lateral. The chest is mal nutritional support as well as general respiratory care, entered through the fourth intercostal space, and the left lung including chest physiotherapy and appropriate treatment of is retracted anteriorly. Surgery should not be unduly delayed reveal a taut, ligamentous structure in the case of a ring with because of the presence of a respiratory infection, as division an atretic left arch. If a double arch is present, it is gener- of the ring, which allows more adequate clearing of respira- ally visible to some degree through the mediastinal pleura. The vagus nerve, giving off the left recurrent laryngeal nerve (which then passes around the ligamentum arteriosum), is a inDicAtions for AnD timing of surgEry useful landmark. The segment to be divided, if patent, should be controlled tory infections, dysphagia, refux, and failure to thrive. After division the vessel ends are oversewn with mild symptoms appearing for the frst time in the older infant a continuous Prolene suture. If the segment to be divided is may improve with time as the child grows, in which case clearly atretic, it suffces to doubly ligate the cord and divide it may be possible to defer surgery. After division the ends generally retract briskly, indicat- the risks of surgery are extremely small, the child should ing the tension with which the ring has been surrounding the undergo surgery within a reasonably short time from diagno- esophagus and trachea. The maximal delay until surgery should be determined tant that the ligamentum arteriosum should also be divided. There may be additional fbrous strands passing across the Vascular Rings, Slings, and Tracheal Anomalies 655 esophagus, and these should be divided. Final palpation in rEsults of surgEry the area should reveal complete relief of the taut band that Traditional Thoracotomy Approach was present previously. Between 1947 and 1992, 37 patients underwent traditional surgery for relief of tracheo- together with absorbable suture to the muscle layers, with esophageal obstruction caused by vascular rings. Of the 37 subcutaneous and subcuticular absorbable suture completing patients, 18 had a double aortic arch, 11 had a right aortic arch wound closure. In the rare case requiring approach through a with aberrant left subclavian, 4 had a left aortic arch with right thoracotomy, the same principles are applied. There was one early postop- Video-Assisted Technique of erative death and no late deaths. At long-term follow-up three Management of Vascular Ring patients had residual symptomatic tracheomalacia, one of This has become the method of choice for all vascular rings whom required right middle and lower lobectomy for recur- unless preoperative studies suggest that there is a patent rent pneumonia. A similar conclusion was drawn by Bakker position following single lumen endotracheal intubation. There was no operative mortality after tive feld achieved by retracting the infated left upper lobe 1959. The ring is dissected free from patients had preoperative or intraoperative bronchoscopy. The atretic segment The technique of operation shifted to a muscle-sparing left thoracotomy without routine chest drainage. Clips are patients with right aortic arch and a Kommerell diverticulum, placed and the ring and ligamentum are divided between clips. Of note, there was transferred to the left carotid artery as a primary pro- are limited thorascopic options to plicate the diverticulum of cedure. Primary reimplantation of the left subclavian artery Kommerell as one could in an open approach. Due to the thin- for right aortic arch with Kommerell’s diverticulum is also walled nature of the diverticulum, suture plication via a thora- 22 recommended by Shinkawa et al.
As data are electronically transmit- ted from the laboratory to the hospital and onward to other electronic databases and records in the physi- cian’s offce order celexa online from canada medicine wheel native american, insurance companies order generic celexa line treatment 5th metatarsal fracture, government agen- cies cheap 20mg celexa visa medicine vs medication, and even personal health records cheap celexa 40 mg amex treatment research institute, test names can be confused, decimal points moved, and comments misinterpreted. A new responsibility of the laboratory in the age of paperless records is verifying that the result is correctly displayed for the ordering physician and that it can be appropriately interpreted after it is transferred through the variety of electronic systems. Test names typically convey both the purpose and utility of the laboratory analysis. Test names can also be confus- ing, especially when there are several closely related tests that differ in method limitations, sensitivity, or clinical application. The laboratory has a responsibility to clarify for both ordering physicians and information system programmers which test result is the correct one being reported. Test names can also be confusing in the order and result interfaces between electronic record systems. A phy- sician may want a specifc test and use one name on the requisition, but the reference laboratory perform- ing the test may call the test by a different name or offer several tests with similar names. Mapping test requests in one system to specifc tests on a menu in another system is part of the programmer’s job when developing communication interfaces between dif- ferent electronic systems. The processing staff in the specimen-receiving area of the laboratory must fur- ther determine the appropriate test to select when translating test requests and written requisitions as they arrive in the laboratory. Placing test requests over an liS interface or selection of the wrong test because the correct name is not known to the ordering provider can both be sources of error. An liS can provide inter- nal checks to warn of potential errors and caution the operator to verify the data before continuing. With elec- tronic information systems, many tasks routinely con- ducted by technologists are now automated. Specimen clots and bubbles can be discovered by pres- sure sensors in the instrument probes during analysis. Automated devices centrifuge, aliquot, and label ali- quots based on the specimen barcode. Trends in results can more easily be followed in a tabu- lar display across a row compared to scrolling through multiple pages of chronologically displayed full text results. Clinicians want to review as much data on a single page or computer screen as possible, since this is more effcient than pag- ing through multiple screens in the electronic record. The display of test results for the ordering clinician is cru- cial to the clinical interpretation. The recent push for ultrasensitive or third- generation assays emphasizes the clinical desire for higher sensitivity for disease detection. While an analyzer may be capable of reporting to a hundredth decimal place, the question is whether the method per- formance can achieve precision at that level to make the hundredth decimal point number meaningful. Reporting a result to two signifcant fgures can mis- lead a clinician to assume better performance than can be achieved by the test method. The integrity of data transmission needs to be verifed on an ongoing basis to ensure cor- rect appearance for the ordering physician. Managing access to information systems can be compli- cated and presents a source for potential duplicative analysis and errors. Test results and medical record notes made by one physician should not neces- sarily be accessible to other physicians unless the results and records are released by the ordering physician or access is granted by the patient. Requiring staff to actively seek out specimen comments rather than passively displaying information with the result poses the risk that the staff will miss clinically signifcant details. The occupational Safety and health Administration (oShA) is a federal agency concerned with employee safety and protection of employees from workplace injuries. A clinical laboratory presents particular hazards includ- ing exposure to patient specimens (e. An employee can be injured simply by moving heavy instrumentation or boxes of supplies. Specimen processors that utilize high-speed centrifuges to spin tubes and separate the cellular com- ponents of blood can present a danger of fying metal, tube breakage, and specimen aerosols when operated incorrectly or with equipment failure. Technologists can contact corrosive acids and bases, and be exposed to fumes from volatile solvents when preparing rea- gents. There are a signifcant number of potential safety hazards in a clinical laboratory. Administration also needs to consider the potential for injury to others beyond their laboratory employees. Failuretoclean portable laboratory analyzers between patients when testing at the point-of-care presents a risk of transmitting hepatitis, hiV, or nosocomial infections among patients. Thus, safe laboratory operations consider all sources and effects of potential harm to employees, patients, the general public, and the environment. A frst commandment of today’s labo- ratory safety is prohibiting eating and drinking in the laboratory. When specimens are being processed, the opening and aliquoting of tubes and specimen contain- ers present a risk of aerosols, spills, splashes, and other sources of contamination of food and drink. Specimens that are spilled or splashed on countertops during testing can present a hazard if the countertops are not suffciently cleaned after use. The presence of organ- isms (some of which may be resistant to antibiotics) risks a spread of nosocomial infections unless devices, reagents, and supplies are thoroughly cleaned and dis- infected between patients. Contamination on counter- tops can be picked up on gloves and on the bottoms of reagent vials or meters and carried to other surfaces if adequate disinfection is not conducted after testing. Protective pads and other absorbent materials on labo- ratory benches can help contain specimens, but may not completely prevent contact with surfaces under- neath the pad. Failure to separate items intented for patient or employee use from laboratory specimens and supplies related to testing can cause problems. Consideration should be made for separation of clean linens, medica- tions, and other supplies that could become contami- nated in areas where laboratory testing is taking place. Food and medications that are intended for patient or employee consumption should not be stored in the same refrigerators as patient specimens or with poten- tially biohazardous controls or reagents made from blood products. Separate clean and dirty refrigera- tors are recommended and should be clearly labeled as to their intended purpose. Chemical Hazards Failure to ensure safe handling and storage of chemicals can be extremely dangerous. Such chemicals should be stored in vented cabinets and only utilized in fume hoods or rooms with adequate air exchange. Transportation and Processing Specimen storage and transport can present hazardous situ- ations. Couriers who transport specimens need to be concerned about the potential for container breakage and specimens leaking into cars or vans. The poten- tial for a vehicle accident requires consideration that specimens could be released into the environment and contaminate surroundings.