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Application of Transmission-Based Precautions in ambulatory and home care settings diabetic diet home delivery glucovance 500/5 mg low cost. This document is intended for use by infection control staff diabetic pancakes cheap 500/5 mg glucovance amex, healthcare epidemiologists diabetes insipidus zucker discount 400/2.5 mg glucovance with amex, healthcare administrators diabetes test calgary buy glucovance 500/5mg with visa, nurses, other healthcare providers, and persons responsible for developing, implementing, and evaluating infection control programs for healthcare settings across the continuum of care. Also new is a definition of “epidemiologically important organisms” that was developed to assist in the identification of clusters of infections that require investigation. However, new to this guideline, is important information on healthcare system components that influence transmission risks, including those under the influence of healthcare administrators. The categories of Transmission-Based Precautions are unchanged from those in the 1996 guideline: Contact, Droplet, and Airborne. One important change is the recommendation to don the indicated personal protective equipment (gowns, gloves, mask) upon entry into the patient’s room for patients who are on Contact and/or Droplet Precautions since the nature of the interaction with the patient cannot be predicted with certainty and contaminated environmental surfaces are important sources for transmission of pathogens. New in this guideline is a figure that shows a recommended sequence for donning and removing personal protective equipment used for isolation precautions to optimize safety and prevent self-contamination during removal. Recommendations for each category apply to and are adapted for the various healthcare settings. Summary this updated guideline responds to changes in healthcare delivery and addresses new concerns about transmission of infectious agents to patients and healthcare workers in the United States and infection control. These previous documents are summarized and referenced in Table 1 and in Part I of the 1996 Guideline for 1 Isolation Precautions in Hospitals. This guideline is designed for use by individuals who are charged with administering infection control programs in hospitals and other healthcare settings. This term reflects the inability to determine with certainty where the pathogen is acquired since patients may be colonized with or exposed to potential pathogens outside of the healthcare setting, before receiving health care, or may develop infections caused by those pathogens when exposed to the conditions associated with delivery of healthcare. In combination, these provide comprehensive guidance on the primary infection control measures for ensuring a safe environment for patients and healthcare personnel. Sources of infectious agents Infectious agents transmitted during healthcare derive primarily from human sources but inanimate environmental sources also are implicated in transmission. Some individuals are prone to becoming transiently or permanently colonized but remain asymptomatic. Some infections associated with invasive procedures result from transmission within the 46-50 healthcare facility; others arise from the patient’s endogenous flora. Opportunities for direct contact transmission between patients and healthcare personnel have been summarized in the Guideline for Infection Control in Healthcare Personnel, 1998 17 and include: • blood or other blood-containing body fluids from a patient directly 66 enters a caregiver’s body through contact with a mucous membrane 67 or breaks. However, extensive evidence cited in the Guideline for Hand Hygiene in Health-Care Settings suggests that the contaminated hands of healthcare personnel are important contributors to indirect contact 16 transmission. Examples of opportunities for indirect contact transmission include: • Hands of healthcare personnel may transmit pathogens after touching an infected or colonized body site on one patient or a contaminated inanimate object, if hand hygiene is not performed before touching 72, 73 another patient. Although contaminated clothing has not been 16 implicated directly in transmission, the potential exists for soiled garments to transfer infectious agents to successive patients. Studies have shown that the nasal mucosa, conjunctivae and less frequently the mouth, are susceptible portals of entry for respiratory viruses 106. More studies are needed to improve understanding of droplet transmission under various circumstances. Airborne transmission Airborne transmission occurs by dissemination of either airborne droplet nuclei or small particles in the respirable size range containing infectious agents that remain infective over time and distance. Preventing the spread of pathogens that are transmitted by the airborne route requires the use of special air handling and ventilation systems. Also, aerosolized particles <100 fim can remain suspended in air when room air current velocities exceed the terminal settling 109 velocities of the particles. It is hypothesized that the aerosolized particles are inhaled and subsequently swallowed. Concerns about unknown or possible routes of transmission of agents associated with severe disease and no known treatment often result in more extreme prevention strategies than may be necessary; therefore, recommended precautions could change as the epidemiology of an emerging infection is defined and controversial issues are resolved. For example, anthrax spores present in a finely milled powdered preparation can be aerosolized from contaminated environmental 150, 151 surfaces and inhaled into the respiratory tract. As a rule, neither of these organisms is subsequently transmitted from infected patients. Legionella) transmitted to humans through a common aerosol source is distinct from direct patient-topatient transmission. Other sources of infection Transmission of infection from sources other than infectious individuals include those associated with common environmental sources or vehicles. Vectorborne transmission of infectious agents from mosquitoes, flies, rats, and other vermin also can occur in healthcare settings. Infectious agents of special infection control interest for healthcare settings Several infectious agents with important infection control implications that either were not discussed extensively in previous isolation guidelines or have emerged recently are discussed below. This pathogen is a major cause of healthcare-associated diarrhea and has been responsible for many large outbreaks in healthcare settings that were extremely difficult to control. Standardization of testing methodology and surveillance definitions is needed for accurate comparisons of trends in rates 175 among hospitals. It is hypothesized that the incidence of disease and apparent heightened transmissibility of this new strain may be due, at least in part, to the greater production of toxins A and B, increasing the severity of diarrhea and resulting in more environmental contamination. Prevention of transmission focuses on syndromic application of Contact Precautions for patients with diarrhea, accurate identification of patients, environmental measures. The response is likely to differ for exposures resulting from an intentional release compared with naturally occurring disease because of the large number persons that can be exposed at the same time and possible differences in pathogenicity. Sources of information on specific agents include: anthrax; 204-206 207, 208 209 210 smallpox; plague; botulinum toxin; tularemia; and 211, 212 hemorrhagic fever viruses. There were no cases of eczema vaccinatum, progressive vaccinia, fetal vaccinia, or contact transfer of vaccinia in healthcare 218, 219 settings or in military workplaces. Outside the healthcare setting, there were 53 cases of contact transfer from military vaccinees to close personal contacts. This experience emphasizes the importance of ensuring that newly vaccinated healthcare personnel adhere to recommended vaccination-site care, especially if they are to care for high-risk patients. The risk of transmission associated with such exposures is believed to be extremely low but may vary based on the specific circumstance. The illness is initially difficult to distinguish from other common respiratory infections. The relative contribution of potential modes of transmission is not precisely known. In Hong Kong, the use of Droplet and Contact Precautions, which included use of a mask 113 but not a respirator, was effective in protecting healthcare personnel. Transmission from infected animals and humans is believed to occur primarily through direct contact with lesions and respiratory secretions; airborne transmission from animals to humans is unlikely but cannot be excluded, and may have occurred in veterinary practices. Additional recent literature documents transmission of Congo Basin monkeypox in a hospital compound for an extended number of generations 268. There has been no evidence of airborne or any other person-to-person transmission of monkeypox in the United States, and no new cases of 269 monkeypox have been identified since the outbreak in June 2003. The outbreak strain is a clade of monkeypox distinct from the Congo Basin clade and may have different epidemiologic properties (including human-to-human 270 transmission potential) from monkeypox strains of the Congo Basin; this awaits further study. Noroviruses Noroviruses, formerly referred to as Norwalk-like viruses, are members of the Caliciviridae family. These agents are transmitted via contaminated food or water and from person-to-person, causing explosive 273 outbreaks of gastrointestinal disease. The disease is largely self-limited; rarely, death caused by severe dehydration can occur, particularly among the elderly with debilitating health conditions. Widespread, persistent and inapparent contamination of the environment and fomites can 147, 275, 284 make outbreaks extremely difficult to control. In addition, individuals who are responsible for cleaning the environment may be at increased risk of infection. Development of disease and transmission may be facilitated by the low infectious dose. There are insufficient data to determine the efficacy of alcohol-based hand rubs against noroviruses when the 294 hands are not visibly soiled. Absence of disease in certain individuals during an outbreak may be explained by protection from infection conferred by the B 295 histo-blood group antigen. In resource-limited healthcare settings, transmission of these agents to healthcare personnel, patients and visitors has been described and in some outbreaks has 298-300 accounted for a large proportion of cases.
Conference Comment: this is an interesting For this case conference participants preferred a and complex entity in which pinpointing morphologic diagnosis of epiphyseal and causation to managing diabetes with diet and exercise order glucovance 400/2.5 mg on-line a specific genetic anomaly has not metaphyseal chondrodysplasia to gestational diabetes type 1 or 2 buy discount glucovance 500/5 mg online identify the been successful blood glucose journal template buy glucovance 500/5mg fast delivery. The clinical managing diabetes journal articles glucovance 500/5 mg with amex, radiographic and histologic abnormalities of chondrocytes/cartilage morphologic abnormalities associated with matrix and disruption of normal ossification skeletal dysplasias are heterogeneous with over within both the epiphysis and metaphysis visible 200 described disorders, and can be broadly in most sections. However, the more general term divided into connective tissue disorders that “osteochondrodysplasia” would be appropriate as disrupt formation of bone (osteodysplasia) or well. However, conference participants recognize cartilage and endochondral ossification the difficulty involved in characterizing these (chondrodysplasia). The diversity in causes and presentations of both osseous and chondrous dysplasias reveal the intricate and complex nature of osteogenesis both during development and in repair from injurious stimuli. Contributing Institution: Michigan State University, Diagnostic Center for Population and Animal Health, Skeletal dysplasias caused by a disruption of skeletal patterning and endochondral ossification. Clinical, radiographic, and pathogic abnormalities in dogs with multiple epiphyseal dysplasia: 19 cases (1991-2005). Chondrodysplasia in the Alaskan Malamute: involvement of arteries, as well as bone and blood. At the distal end of the bone fragment, there is a small hematoma Signalment: 12-week-old male Sprague-Dawley composed of erythrocytes admixed with rat, Rattus norvegicus. The hematoma is surrounded by densely packed proliferating History: While under anesthesia, this animal mesenchymal cells (callus) which contain underwent blast over-pressure at 120 kPa, numerous perpendicularly oriented arterioles, traumatic fracture of the right rear limb with a fragments of woven bone, collagen, and few drop weight apparatus, soft tissue crush injury at scattered multinucleate cells (osteoclasts). There 20 psi for 1 minute and a trans-femoral is subperiosteal new woven bone composed of amputation. The animal was maintained on an irregular and random to densely organized appropriate sustained-release pain control collagen fibers which widens from proximal to regimen and humane euthanasia was performed 7 distal as it extends towards the fracture site and days post injury. The right rear limb was forms a small region of hyaline cartilage adjacent disarticulated from the hip joint and submitted for to the fracture. Femur, rat: There is a mid-shaft, angled femoral fracture with removal of the distal fragment. Femur, rat: the distal end of the fragment is surrounded by a thick hematoma with hemorrhage and loosely polymerized fibrin strands. The periosteum (right) (34X) is elevated by proliferating trabeculae of woven bone, and a focal area of cartilage is present at the distal end. Multifocally, myofibers are phase, which may take months or years, involves separated, surrounded and replaced by loose the replacement of woven bone in the callus with connective tissue, fibrin, edema, and hemorrhage. In adults, persistence3 around a pocket of fibrin, hemorrhage, edema, of medullary trabeculae and thickening of the and eosinophilic cellular and karyorrhectic debris periosteal bone surface are likely to persist at the (necrosis). Multifocally, there are clusters of healed fracture site, whereas in younger animals, histiocytes, neutrophils, lymphocytes and plasma the fracture may completely resolve. Multifocally there is scattered golden yellow pigment (hemosiderin) Three critical constituents are required for within the callus and within surrounding formation of bone: (1) the presence of collagen, connective tissues. Contributor’s Comment: Unlike most other tissues, bone is capable of repair by regeneration Signaling Molecules. Parathyroid hormone and calcitonin cells from the medullary cavity, endosteum, and are hormones that function to maintain a stable serum calcium concentration. Femur, rat: the callus transitions into abundant granulation tissue which infiltrates the adjacent atrophic abnormalities. The contributor provided a the most abundant ligand and has been shown to comprehensive overview of the most well known stimulate osteoblast proliferation and enhance 1 signaling molecules which play a prominent role, bone formation. Excessive motion or load results in Platelet-Derived Growth Factor and Vascular delayed healing or non-union. It is the desired end state of surgical fracture repair, as the direct remodeling of lamellar bone, Haversian canals and blood vessels may lead to complete healing within months, while indirect healing often occurs for years before the bone is completely remodeled from a fracture callus to lamellar bone. Biological basis of bone formation, remodeling, and repairpart I: biochemical signaling molecules. Intraoperative measurement of bone electrical potential: a piece in the puzzle of understanding fracture healing. Diffuse and mild fibrosis is in interstitial tissues with mild lymphoplasmacytic Signalment: 8-month-old female thoroughbred infiltration, sometimes along with concentric horse, Equus caballus. Rarely, uremia were continuing and the animal was abnormal large muscular arteries are in euthanized. Pale basophilic myxoid material depositions are rare in Gross Pathology: After formalin fixation, the the interstitium. Variously affected glomeruli with hypercellularity and sclerosing Histopathologic Description: Diffuse and changes suggest that the primary lesions are not global, partially segmental glomerular sclerosis located in glomeruli. However, regenerative and enlarged glomeruli with mild to moderate tubules with juvenile epithelial cells, interstitial proliferation of mesangial cells are remarkable. The present case Immature small tubules with indistinct luminal was negative for leptospires. Further, plant structures and dysplastic tubules with enlarged toxicosis is unlikely because no other case of clear nuclei are frequent. Kidney, foal: Immature renal tubules with atypical epithelial cells of renal architecture with dilstation of tubules and markedly enlarged and incomplete luminal structures. The histopathological changes in the present case are very complicated; however, some of them, including oxalate deposition, appear to be secondary changes following renal failures. The various proposed pathogeneses of renal dysplasia, like abnormal metanephrons or vascular malformation, may be putative but clear mechanisms are still unknown. Kidney, foal: Enlarged glomerulus with proliferation of mesangial cells and adhesion with Bowman’s capsule. The size of the affected metanephric ducts, primitive mesenchyme and kidney shows small and irregular surface with cartilaginous or osseous tissue, are not present in demonstration of immature histological structures this case. Yet the clinical history and glomerular like undifferentiated stromal tissues, immature changes are consistent with the diagnosis. Primitive ductal reports of equine renal dysplasia describe renal structures and cartilage and/or bone formation are cysts, fetal glomeruli, and tubules lined by sometimes found. Pathologic Basis of cortex, and speculated whether these may have Veterinary Disease. Renal these aberrant vascular features have been dysplasia in two adult horses: clinical and reported in human cases of segmental or complete pathological aspects. Unilateral renal hypoplasia vascular anomalies (Ask-Upmark kidney) has also with hypertension (Ask-Upmark kidney). Bilateral renal dysplasia is referred to as progressive juvenile dysplasia with nephron hypoplasia in a foal. These conditions share several features with dysplasia though typical presentation depends on the breed. Often a g l o m e r u l o p a t h y r e s e m b l i n g membranoproliferative glomerulonephritis is present and may progress to glomerulosclerosis. Overall gross and microscopic features are comparable to those of chronic renal disease with renal fibrosis in aging dogs, but this condition affects dogs under 2 years of age. End-stage kidney disease probably due to reflux nephropathy with segmental hypoplasia (AskUpmark kidney) in young Boxer dogs in Norway. No other gross lesions have been observed in the other organs of the deer Signalment: Male white-tailed deer, age examined. No other ancillary tests have been Gross Pathology: the gross pathology of the performed on other organs. Cerebrum, deer: Centrally within the section, there is a focal, well-demarcated cellular infiltrate. Mortality generally occurs from fall (following velvet s h e d d i n g) t h r o u g h spring (shortly after antler casting). Thus, the period when bucks are developing antlers or when antlers have hardened is when they are most susceptible to this disease. Cerebrum, deer: the cellular infiltrate is composed of degenerate neutrophils and abundant cellular debris, consistent with an abscess. The bacterium wide zone of inflammatory cells, mainly Arcanobacterium pyogenes was the primary cause of infection. There is diffuse intravascular the clinical signs include several behavioral lymphocytic cuffing. Encephalitis, locally extensive, necrotizing, Often times, deer can become emaciated, which is subacute with granulation tissue (capsule) characterized by excessive weight loss or having a formation and bacterial colonization.
Differential diagnosis: Fowl cholera for septicemic form diabetes type 1 omega 3 buy discount glucovance 500/5mg online, infectious tenosynovitis or Marek’s disease for the arthritic form and traumatic injury for bumblefoot diabetic kidney pain cheap 400/2.5mg glucovance visa. Cause diabetes prevention 9 easy glucovance 500/5mg mastercard, transmission diabetes test ziekenhuis glucovance 400/2.5 mg overnight delivery, and epidemiology: the causative agent, Staphylococcus aureus, is soil-borne, and outbreaks in flocks often occur after storms when birds on range drink from stagnant rain pools. Diagnosis: A definitive diagnosis is based on the clinical appearance of the disease and the recovery of the causative bacteria. Erythromycin and penicillin can be administered in the water for 3-5 days or in the feed for 5 days. Recovery: After treatment, if the immediate environment of the birds is removed or cleaned, then there will be no residual risk of infection on the premises to new birds. Energy that could have been used in the production of more meat and eggs in these birds ends up being used to respond to stress. Causes of stress: A husbandry system can be stressful if it exerts abnormal or extreme demands on the bird. Family poultry are subjected to mental stress (pain, fear, anxiety) during a variety of common activities including: Catching Being chased by predators Running away from vehicles Tying and wing restraint, Bundling in crates (“tenga”) Being on vehicle roof tops for transportation Not having adequate food or water the mental stress associated with these activities may be caused by visual, auditory, social, and/or physical factors. Birds are subjected to physical stress (environmental: heat, cold, wind, strokes, wounds, etc. Indigenous poultry are particularly susceptible to stress and this may be reflected in their poor responses to vaccination (Newcastle disease, infectious bursal disease). This has been demonstrated by comparing the responses of commercial birds and indigenous chickens and ducks. Immunosuppressed birds succumb more easily to both infectious conditions (viral diseases and bacterial diseases) and non-infectious conditions (such as worm infestations) than non-immunosuppressed birds. Some of these birds become carriers of various diseases for other healthy birds around them. The raising, transportation, marketing, and movement of birds to and from various sites need to be done in a way that minimizes stress for the birds. Vaccination programs need to be appropriately targeted for scavenging poultry, taking into account their interactions with wild birds, other livestock, and humans, but also considering the difficulty and in handling and vaccinating them. Adult chickens have mild respiratory disease followed by some birds having swollen heads. Other signs include disorientation, twisting of the neck, and a significant decrease in egg production (up to 70%). Cause, transmission, and epidemiology: the disease is caused by a virus classified as a pneumovirus. Experimentally, guinea fowl and pheasants are susceptible but pigeons, ducks, and geese are resistant to the infection. The infection spreads by direct contact with infected birds or indirectly by exposure to infectious material. Humans can be infected and will develop flu like symptoms if exposed to sick or ill birds. Diagnosis: A definitive diagnosis can be made through the direct identification or isolation and identification of the disease agent in embryonating chicken or turkey eggs or chicken organ culture from the nasal secretions of clinically ill birds. Recovery: A premises with infected birds can be rid of the organism through cleaning and sanitation of all facilities and equipment in contact with birds and the removal of infectious material on the farm like manure. New introductions must be prevented with strict biosecurity if recovery is to be complete. Other signs included emaciation, watery droppings streaked with urates, and dull ruffled feathers. At necropsy, punctate ulcers are typical and may be visible from the mucosal surface of the gut. The liver will have circumscribed areas of necrosis and hemorrhage that with time, will become depressed. Differential diagnosis: A differential diagnosis of ulcerative enteritis will include coccidiosis, histomoniasis and necrotic enteritis. Complicating the differentiation of ulcerative enteritis is the fact that coccidiosis and necrotic enteritis may be predisposing on concurrent infections in affected birds or flocks. Cause, transmission, and epidemiology: the causative agent is the bacterium Clostridium colinum. Birds become infected by direct contact with carrier birds, infected droppings or contaminated pens, feed and water. Infection can be spread mechanically on shoes, feed bags, equipment, and from contamination by rodents and pets. Diagnosis: A diagnosis of ulcerative enteritis is indicated by the presence of typical button ulcers in the intestine with concurrent target lesions in the liver. However, this can be very difficult because the organism is fastidious and difficult to grow in culture. In these cases, a diagnosis will be based on the presence of typical gross lesions. Other antibiotics and drugs such as tetracyclines, penicillin, Lincomycin, and Virginomycin are also effective. To eradicate, depopulate stock, thoroughly clean and disinfect, and start over with young, clean stock. Recovery: Clostridium colinum is a spore-forming organism and infectious spores will remain in the soil after an outbreak. Controlling predisposing factors, like immunosuppressive diseases and internal parasites will make birds more resistant. In highly susceptible species, like quail, preventative medication may be the only means of recovery. Urolithiasis Clinical signs and lesions: this is primarily observed in laying flocks and characterized by severe atrophy of one or both kidneys, distended ureters with uroliths, and varying degrees of renal and visceral gout. Urolithiasis will generally mimic the appearance of, and also can be caused by management problems like a lack of water or feed. Cause, transmission, and epidemiology: Physiologic impact of urolithiasis on kidney damage is the result of reduced renal mass, rather than inappropriate renal handling of minerals and electrolytes. Uroliths may cause sudden death by plugging ureters, which is probably secondary to kidney damage. It can also be secondary to infectious bronchitis, or due to excess dietary calcium with low phosphorous levels, water deprivation, and some nephrotoxic mycotoxins. However, a diagnosis of the cause of the renal disease will depend on what that cause is. Feed analysis and testing for infectious bronchitis viruses should be standard in cases of urolithiasis. Prevention: Urolithiasis is prevented by feeding a correctly balanced diet, providing adequate water for chickens and preventing infectious bronchitis through a combination of vaccination and biosecurity. Recovery: Affected individuals will not recover but once the cause of the kidney damage is corrected, then no additional individuals will develop the condition. Nodular airsacculitis with involvement of intercostal muscles, multiple nodules in the lungs, ventriculitis, and proventriculitis (ostriches) may be seen. The lesions are pyogranulomatous (with necrotic center) with numerous multinucleated giant cells. Differential diagnosis: the symptoms of zygomycosis may be non-specific depending on the system affected. Lung infections and systemic fungal infections such as aspergillosis, cryptococcosis, histoplasmosis and dactylariosis; mycobacteriosis should be considered. Cause, transmission, and epidemiology: the disease is caused by fungi belonging to genera Mucor, Rhizopus, Absidia, Rhizomucor, and Mortierella. They are acquired from environmental sources (soil, manure, and rotting vegetation), and are not contagious. Diagnosis: Clinical signs of disease, lesions at necropsy and the epidemiology of the case can be indicative of zygomycosis or other fungal disease. Confirmation of the specific disease agent is by microscopic examination of histological lesions or culture. If, however, the cause of the contamination is corrected and/or the source removed, there is no residual risk to flocks. A Laboratory Manual for the Isolation and Identification of Avian Pathogens, Fourth Edition. The chemical disinfectants discussed for patient-care equipment include alcohols, glutaraldehyde, formaldehyde, hydrogen peroxide, iodophors, ortho-phthalaldehyde, peracetic acid, phenolics, quaternary ammonium compounds, and chlorine.
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Available in 2-mg/mL and 4-mg/mL concentrations (1 mL preservative free vial) and 2 mg/mL multidose vial (10 mL) diabetes test york cheap glucovance american express. Some available products contain 2% (20 mg/mL) benzyl alcohol and 18% polyethylene glycol 400 in propylene glycol managing diabetes kits buy glucovance 500/5mg low cost. This will make it easier to blood glucose newborn buy generic glucovance 400/2.5 mg online measure the dose and decrease the benzyl alcohol content to diabetic cake cheap 400/2.5 mg glucovance mastercard 0. Uses Anticonvulsant, acute management of patients with seizures refractory to conventional therapy. Rhythmic myoclonic jerking has occurred in premature neonates receiving lorazepam for sedation. Acyclovir, amikacin, amiodarone, bumetanide, cefepime, cefotaxime, cimetidine, dexamethasone, dobutamine, dopamine, epinephrine, erythromycin lactobionate, famotidine, fentanyl, fluconazole, fosphenytoin, furosemide, gentamicin, heparin, hydrocortisone succinate, labetalol, levetiracetam, linezolid, methadone, metronidazole, midazolam, milrinone, morphine, nicardipine, nitroglycerin, pancuronium bromide, piperacillin, piperacillin-tazobactam, potassium chloride, propofol, ranitidine, remifentanil, trimethoprim-sulfamethoxazole, vancomycin, vecuronium, and zidovudine. Dose Adjustments Renal Impairment: Although there are no dosing recommendations available for neonates or pediatric patients with renal impairment, a reduction in the dose and/or an increase in the dosing interval should be considered [2]. Black Box Warning Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported (in adults). Adverse Effects Adverse effects reported in neonates were increased liver function tests, anemia, diarrhea, electrolyte disturbances, hypoglycemia, jaundice and hepatomegaly, rash, respiratory infections, sepsis, gastroenteritis (with associated convulsions), and transient renal insufficiency associated with dehydration. Deaths (1 from gastroenteritis with acidosis and convulsions, 1 from traumatic injury, and 1 from unknown causes) were reported in 3 neonates. Patients should receive the lamivudine product appropriate to their diagnosis [2] [3]. It is intracellularly converted in several steps to the active compound, and then renally excreted. In 36 infants up to 1 week of age administered lamivudine and zidovudine, lamivudine clearance was substantially reduced in 1-week-old neonates compared with children older than 3 months of age [2]. Deaths (1 from gastroenteritis 464 Micormedex NeoFax Essentials 2014 with acidosis and convulsions, 1 from traumatic injury, and 1 from unknown causes) were reported in 3 neonates. Data for successfully supplying patient-specific, partial doses of lansoprazole through pediatric/neonatal feeding tubes are lacking. In some cases, hypomagnesemia was not reversed with magnesium supplementation and discontinuation of the proton pump inhibitor was necessary. Onset of action is within one hour of administration, maximal effect is at approximately 1. Adverse Effects Hypergastrinemia and mild transaminase elevations are the only adverse effects reported in children who received lansoprazole for extended periods of time. References Franco M, Salvia G, Terrin G, Spadaro R, et al: Lansoprazole in the treatment of gastrooesophageal reflux disease in childhood. In one study attempting to provide a partial dose (orally disintegrating tablet formulation) through a feeding tube, a 7. Tablets may not disintegrate entirely when water is added to form a suspension, and/or the tablets may disintegrate but later form clumps which can adhere to the inside walls of the tubes. In the neonatal period, it has been used as a second line of therapy for seizures refractory to phenobarbital and other anticonvulsants. Pharmacology Rapidly and completely absorbed after oral administration, with the onset of action by 30 minutes and peak concentration within 2 hours. Levetiracetam inhibits burst firing without affecting normal neuronal excitability, suggesting that levetiracetam may selectively prevent hypersynchronization of epileptiform burst firing and propagation of seizure activity. Special Considerations/Preparation Keppra injection for intravenous use is available in single-use 5 mL vials containing 500 mg (100 mg/mL). Administration Intravenous: Dilute to a concentration of 5 to 15 mg/mL and infuse over 15 minutes [1]. Half-life in the immediate neonatal period is approximately 18 hours, decreasing to 6 hours by 6 months of age. Primarily (66%) excreted unchanged in the urine, with some metabolism via enzymatic hydrolysis to inactive metabolites (no cytochrome p450 involvement). When discontinuing therapy, wean the dose gradually to minimize the potential of increased seizure frequency. Monitoring Serum trough concentrations are not routinely monitored, although they may be useful when determining the magnitude of dosing adjustments. Must be further diluted to a concentration of 5 to 15 mg/mL in compatible diluent prior to administration. Adverse Effects Prolonged over-treatment can produce premature craniosynostosis and acceleration of bone age. Assess for signs of hypothyroidism: Lethargy, poor feeding, constipation, intermittent cyanosis, and prolonged neonatal jaundice. Assess for signs of thyrotoxicosis: hyperreactivity, altered sleep pattern, tachycardia, tachypnea, fever, exophthalmos, and goiter. Also available in capsules that contain a viscous liquid ranging from 13 to 150 mcg per capsule. Monitor patient closely when switching brand of drug due to some differences in bioavailability. Injectable form is available as lyophilized powder in vials containing 100 or 500 mcg. Title Levothyroxine Dose Initial oral dose: 10 to 14 mcg/kg/dose orally every 24 hours. Monitoring After 2 weeks of treatment, serum levothyroxine (T4) concentration should be in the high normal range (10 to 16 mcg/dL) and should be maintained in this range for the first year of life. Special Considerations/Preparation 477 Micormedex NeoFax Essentials 2014 Oral suspension is not commercially available. Capsules cannot be crushed, suspended in water, or dissolved by placing in water before use. To prepare a 15-mcg/mL levothyroxine oral suspension: Crush levothyroxine 100-mcg tablets in glycerol and add sterile water up to desired volume. Stability tests demonstrated a 12% decline in levothyroxine concentration in the prepared suspension over 11 days. An oral liquid formulation of levothyroxine sodium 25 mcg/mL in 40% glycerol compounded from crushed tablets and distilled water with no preservatives added was stable for 8 days when stored in amber bottles at 4 degrees C. Product Information: levothyroxine sodium intravenous injection, levothyroxine sodium intravenous injection. Contraindications/Precautions Contraindicated in complete heart block and wide complex tachycardia attributable to accessory conduction pathways [3] [4]. Free drug fraction in both term and premature neonates is approximately twice that found in older children because of significantly reduced protein binding by I±1-acid glycoprotein. Special Considerations/Preparation 480 Micormedex NeoFax Essentials 2014 Use only preservative-free lidocaine without epinephrine. Alteplase, aminophylline, amiodarone, ampicillin, caffeine citrate, calcium chloride, calcium gluconate, cefazolin, cefoxitin, chloramphenicol, cimetidine, dexamethasone, digoxin, dobutamine, dopamine, enalaprilat, erythromycin lactobionate, famotidine, fentanyl, flumazenil, furosemide, glycopyrrolate, heparin, hydrocortisone succinate, insulin, linezolid, methicillin, metoclopramide, micafungin, morphine, nafcillin, nicardipine, nitroglycerin, penicillin G, pentobarbital, potassium chloride, procainamide, ranitidine, sodium bicarbonate, and sodium nitroprusside. Title Lidocaine Antiarrhythmic Dose 481 Micormedex NeoFax Essentials 2014 Initial bolus dose: 0. Transformed in the liver to metabolites with antiarrhythmic activity; approximately 30% is excreted unchanged in neonates. Later signs include seizures, loss of consciousness, respiratory depression, and apnea. Cardiac toxicity is associated with excessive doses and includes bradycardia, hypotension, heart block, and cardiovascular collapse. Pharmacology the mode of action for lidocaine as an anticonvulsant drug is unknown. The clinically effective dose of 6 mg/kg/hr will lead to accumulation of both lidocaine and metabolites within several hours. Measuring blood concentrations is not clinically useful except when accumulation is suspected. References Shany E, Benzaqen O, Watemberg N: Comparison of continuous drip of midazolam or lidocaine in the treatment of intractable neonatal seizures. Caution: Preterm newborns and term newborns undergoing hypothermia treatment are at risk for drug accumulation due to slower drug clearance.