Janet A. Englund, M.D.
During weeks 3 and 4 pulse pressure guidelines generic 0.25mg digoxin with amex, a dose of 25 mg once a day may be given instead of the 25 mg twice daily dose (total daily dose of 50 mg) wireless blood pressure monitor generic 0.25 mg digoxin free shipping. Dose increases should not exceed this rate hypertension warning signs buy cheapest digoxin, unless the clinical response supports larger increases blood pressure up 0.25 mg digoxin for sale. Stopping Oral Contraceptives: For women not taking inducers of lamotrigine glucuronidation. Pediatrics Safety and efficacy in patients below the age of 16 years, other than those with LennoxGastaut Syndrome, have not been established. The starting doses and dose escalations listed below are different than those used in clinical trials, however the maintenance doses are the same as those used in clinical trials. Smaller starting doses and slower dose escalations than those used in clinical trials are recommended because of concern that the risk of serious rash may be greater with higher initial doses and more rapid dose escalation. Consequently, it may take several weeks to months to achieve an individualized maintenance dose. To ensure a therapeutic dose is maintained, the weight of a child must be monitored and the dose reviewed as weight changes occur. Only whole tablets should be administered (scoreline on the 5 mg tablet is not intended for tablet splitting). Caution should be exercised in dose selection for patients with impaired renal function. Hepatic Impairment Mild and Moderate Hepatic Impairment: It is recommended that initial, escalation and maintenance doses be reduced by approximately 50% in patients with either mild or moderate (Child-Pugh Grade A or B) hepatic impairment; dosage schedules based on pharmacokinetic data are summarized in Table 9. It is recommended that initial, escalation and maintenance doses be reduced by approximately 75% in severe (Child-Pugh Grade C) hepatic impairment; dosage schedules based on pharmacokinetic data are summarized in Table 10. The patient should be instructed to not make up for a missed dose by taking a double dose next time. If the tablets are chewed, consume a small amount of water or diluted fruit juice to aid in swallowing. To disperse the tablets, add the tablets to a small amount of liquid (1 teaspoon, or enough to cover the medication). Approximately 1 minute later, when the tablets are completely dispersed, swirl the solution and consume the entire quantity immediately. No attempt should be made to administer partial quantities of the dispersed tablets. He was given supportive therapy, and his condition improved rapidly with full recovery in 3 days. Following a suspected overdose, immediate hospitalization of the patient is advised. In the event of a very recent overdose/ingestion of a potentially life-threatening amount of the drug, emesis may be induced if indicated. General supportive care is indicated, including frequent monitoring of vital signs and close observation of the patient. It is uncertain whether hemodialysis is an effective means of removing lamotrigine from the blood. In six renal failure patients, about 20% of the amount of lamotrigine in the body was removed during 4 hours of hemodialysis. Lamotrigine is thought to act at voltage-sensitive sodium channels to stabilize neuronal membranes and inhibit the release of excitatory amino acid neurotransmitters. When administered with food, the rate of absorption is slightly reduced, but the extent remains unchanged. The time-to-peak concentration, elimination half-life (tfi) and volume of distribution (Vd/F) are independent of dose. Following repeated dosing in healthy volunteers for 14 days, the tfi decreased by an average of 26% (mean steady state tfi of 26. In a single-dose study where healthy volunteers were administered both oral and intravenous doses of lamotrigine, the absolute bioavailability of oral lamotrigine was 98%. This binding is unaffected by therapeutic concentrations of phenytoin, phenobarbital or valproic acid. Lamotrigine does not displace other antiepileptic drugs (carbamazepine, phenytoin, phenobarbital) from protein binding sites. Metabolism: Lamotrigine is metabolized predominantly in the liver by glucuronic acid conjugation. The major metabolite is an inactive 2-N-glucuronide conjugate that can be hydrolyzed by fi-glucuronidase. Special Populations and Conditions Pediatrics: Lamotrigine was rapidly absorbed in children, with a Tmax ranging from 1 to 6 hours. Population analysis results showed that the estimated apparent plasma clearances in patients aged 13 to 18 years were similar to those found in adult patients. Geriatrics: Results of a population pharmacokinetic analysis, based on individual trials in which both adult (n = 138) and elderly (n = 13) patients with epilepsy were enrolled, indicated that the clearance of lamotrigine in elderly patients did not change to a clinically relevant extent. After single doses, apparent clearance was lower in the elderly by 12% (31 mL/min at age 70 vs 35 mL/min at age 20). After 48 weeks of treatment, the difference in clearance was 10% (37 mL/min at age 70 vs 41 mL/min at age 20). In addition, the pharmacokinetics of lamotrigine were studied in 12 healthy elderly volunteers who each received a single oral dose of 150 mg. Hemodialysis: In six hemodialysis patients, the elimination half-life of unchanged lamotrigine was doubled off dialysis, and reduced by 50% on dialysis, relative to individuals with normal renal function. Hepatic Impairment: A single dose pharmacokinetic study was performed in 24 subjects with hepatic impairment (n = 12 mild/Grade A; n = 5 moderate/Grade B and n = 7 severe/Grade C), versus 12 healthy controls. The key lamotrigine parameters for adult patients and healthy volunteers are summarized in Table 11, and for pediatric patients in Table 12. Other Drug Interactions Chronic administration of acetaminophen was shown to slightly decrease the tfi and increase the clearance of a single dose of lamotrigine. The effectiveness of lamotrigine adjunctive therapy has also been shown in pediatric and adult patients with Lennox-Gastaut syndrome. A significant reduction in major motor seizures, drop Page 42 of 55 attacks, and tonic-clonic seizures were seen following lamotrigine treatment compared with placebo treated patients. Improvements in cognitive skills (speech, nonverbal communication, alertness, attention, intellectual capacity), behaviour, and fine co-ordination have been seen with lamotrigine treatment in these patients. Studies have also been conducted using lamotrigine monotherapy in adult patients (n = 443) newly diagnosed with epilepsy (partial seizures, with or without secondary generalization or primary generalized tonic clonic). Results have shown comparable efficacy (time to first seizure, seizure frequency, percentage of patients seizure-free) with fewer side effects than currently approved therapies. Clinical trials have also demonstrated that adult patients (any seizure type) can be converted to lamotrigine monotherapy from polytherapy with significant numbers of patients maintaining or improving seizure control. A 24 week monotherapy trial was conducted in elderly newly diagnosed patients (102 patients received lamotrigine and 48 received carbamazepine). The findings indicate comparable efficacy, and demonstrate that lamotrigine was well tolerated in the elderly. However, the small and unbalanced number of patients in the study precludes any firm conclusions on the relative safety of the two drugs. In mice and rats, lamotrigine has a longer duration of action than phenytoin, carbamazepine, diazepam or valproate. In rats, convulsions possibly related to drug administration were rarely observed (in no more than 1 of 46 to 49 animals per dose group) and did not occur until week 24 of chronic oral dosing with 15 mg/kg/day. Preclinical Pharmacokinetics Lamotrigine was found to accumulate in the kidney of the male rat, bind to melanin-containing ocular tissue of the pigmented rat and cynomolgus monkey, and prolong gastric emptying time in rats. Clinical studies showed no evidence in humans for manifestations of these preclinical observations regarding accumulation in the kidney, melanin binding, gastric emptying, or cardiac effects. In vitro Studies In vitro pharmacological studies suggest that lamotrigine acts at voltage-sensitive sodium channels to stabilize neuronal membranes and inhibit the release of excitatory amino acid neurotransmitters. In clinical studies, lamotrigine did not affect blood folate concentrations or associated hematologic parameters. Other signs, including tremors, ataxia, hypoactivity, decreased respiration, and hypothermia were also observed. Survivors generally recovered within 24 hours, but hypoactivity lasted for several days in some animals. Long-Term Toxicity Subacute to subchronic (14 fi 30 days) studies were conducted in rats (oral and intravenous), marmosets (oral) and cynomolgus monkeys (intravenous). Effects seen in rats which were considered to be consistently associated with oral lamotrigine administration included specific nephropathy (males, 1 mg/kg/day), increased weight of stomach contents (6. Toxoplasmosis has also been observed in rabbits heart attack risk factors order digoxin line, guinea pigs blood pressure chart images generic digoxin 0.25 mg online, and other laboratory animals hypertension jama order cheap digoxin line, sometimes with fatal outcome prehypertension occurs when buy discount digoxin 0.25 mg on-line. Because toxoplasmosis is a strong trigger for helper lymphocyte type 2 immune reactions (cell-mediated immunity), the infection may interfere with experimental results. In acute cases, necrotic foci have been observed in the liver, spleen, lungs, and lymph nodes. Source of Infection and Mode of Transmission: the human infection can be acquired in utero or postnatally. Presumably, infection acquired from infected earth or food played an important role, because the rate was higher in rural areas (16. This result may be due to the fact that the populations studied were mainly infected through the consumption of contaminated meat, or else because cats shed oocysts for only 1 or 2 weeks; hence, the infection correlates more with the existence of a contaminated environment that with the presence of these animals. Cats and other felines are very important links in the epidemiology of toxoplasmosis. Unlike man, other omnivores and carnivores can become infected by ingesting food, especially meat, contaminated with oocysts. Sheep, which are one of the main sources of human infection, become infected only by ingesting oocysts. It appears that cats are a significant factor in the contamination of pastures, because a single infected cat produces millions of oocysts, which survive in the ground for almost a year as long as they are protected from the sun and from drying out. The results of studies conducted on islands near Australia lend credence to this idea: only 2% of the sheep raised on the islands without cats had antibodies to T. Apparently, the main sources of infection for cats are rodents or birds infected with bradyzoite cysts: some experiments have shown that oocysts infect a smaller proportion of cats than do cysts and that most cats develop antibodies against the parasite at around the age when they begin to hunt. Although there have been reports of cats infected with tachyzoites, these forms cannot be very efficient because they are destroyed by gastric acid. At some point between 3 and 21 days after the initial infection, the cat begins to shed oocysts in its feces for a period of 1 or 2 weeks, thus contaminating the environment. However, the oocysts can remain viable for about a year in environments that are cool, humid, and shady. Even though it is difficult to diagnose clinical infection in a cat, positive serology indicates that the animal has already had an infection, and in that case it poses no risk of contamination because it will no longer shed any oocysts. It has been pointed out that there is a correlation between meat handling and the prevalence of seropositivity. In a serologic survey of 144 employees and workers at a slaughterhouse in Belo Horizonte, Brazil, the prevalence of positive reactors was 72%, with the highest rate among meat inspectors (92%) and the lowest rate among workers in the corrals (60%) (Riemann et al. Higher reactor rates have also been found in housewives who handle meat in the kitchen compared with the general population. Presumably, their hands become contaminated by infected meat and transmission occurs via the oral route. Recent studies have suggested that coprophilic flies and cockroaches may act as transport hosts carrying cat fecal oocysts to human food, which would account for infections in vegetarians. The literature also cites a few cases of transmission to man through raw milk (Riemann et al. Congenital transmission in humans, despite its clinical significance, is also unimportant epidemiologically, both because it is relatively rare and also because the infected person is a source of infection only for the fetus during the acute phase. Because the latter are a source of infection for man, they are the only species that are epidemiologically significant. Diagnosis: Specific diagnosis can be made in acute-phase patients by directly visualizing the parasite in fluid or tissue, but this is a difficult and low-yield process. The parasite can also be isolated from organic fluid or tissue by intraperitoneal inoculation in mice. In chronic cases, samples of muscle or brain tissue may be subjected to peptic digestion before inoculation (this procedure is not recommended in acute cases because the tachyzoites are destroyed by gastric acid). During the first week after inoculation, tachyzoites may appear in the peritoneal exudate of the mice. At 6 weeks, serologic diagnosis is performed on the surviving animals, and, if the result is positive, the mice are sacrificed to confirm the presence of cysts in the brain. The S-F dye test is based on the fact that live tachyzoites do not ordinarily stain with methylene blue but they do stain if they have been subjected to the lethal action of antibodies and complement; if the patient is infected, the serum to be studied provides the antiToxoplasma antibodies. Clinicians are especially interested in developing a test that can distinguish between the acute and chronic forms of the infection, given the importance of the former in congenital transmission. In the case of acute infection, it is believed that the study of IgG antibody avidity (the total combined power of an antibody molecule and its antigen, which depends on the number of binding sites and the affinity of each) and the presence of IgA antibodies give better results than merely verifying the presence of IgM antibodies (Rodriguez et al. Because IgM does not cross the placenta, the presence of these antibodies in the serum of newborns is reliable evidence that the fetus developed them in utero and that the infant was born with the infection. It has also been proposed to investigate the presence of IgE antibodies for Toxoplasma as an indicator of acute infection, even though they appear after the infection and persist for only three to five months. Unfortunately, the specificity of the antibodies is high (98%), but their sensitivity is low (76%); hence, the absence of IgE antibodies does not rule out acute infection (Gross et al. Another procedure used for determining the presence of acute infection is the evolution of IgG antibody titers, for which purpose a quantitative serologic test is used and is repeated after two to four weeks. The toxoplasmin skin test reveals past infections and is mainly useful in epidemiologic studies. The positive response appears several months after the initial infection and may last for life. The intestinal infection in cats is diagnosed by feces flotation procedures, which permit observation of the small immature oocysts that are characteristic of the parasite. However, it is difficult to find positive cats with this test because they shed oocysts for only 1 to 2 weeks starting 3 to 21 days after primary infection. Since feline toxoplasmosis leaves strong immunity against reinfection, the animal will not contaminate the environment by shedding oocysts in the future. Control: Two circumstances facilitate human postnatal Toxoplasma infection: the ingestion of bradyzoites in infected undercooked meat, and the ingestion of oocysts via hands or food contaminated with the feces of infected cats. Hence, the control of human toxoplasmosis consists of avoiding these circumstances. Although the measures apply to everyone, pregnant women and immunodeficient individuals merit special attention, the former because of the possibility of congenital infection and the latter because of the risk of developing a severe case. Meat, particularly pork and lamb, should be cooked until there is no reddish color left. Just as it is not recommended to use microwave ovens to kill Trichinella, the same is true for Toxoplasma, because these ovens do not cook meat evenly. Food handlers should avoid tasting raw meat, and they should wash their hands carefully after touching it because water destroys the tachyzoites. These cats should be kept indoors and fed canned, cooked, or previously frozen food to keep them from hunting and catching infected rodents and birds and thus becoming infected. A serologically negative cat in the home of a pregnant woman should be removed from the household because it could acquire a primary infection and contaminate the environment with oocysts. It has been shown in the laboratory that the addition of monensin (a carboxylic ionophore produced by Streptomyces cinnamonensis) to dry cat food can suppress the excretion of oocysts in feces (Frenkel and Smith, 1982). Pregnant women and immunodeficient individuals should not perform tasks that expose them to potentially contaminated soil (for example, gardening) unless they use waterproof gloves and wash their hands carefully afterward. Fruit and vegetables that grow near the ground should be washed or cooked, since they might be contaminated. Flies and cockroaches should be controlled to prevent them from serving as transport hosts for the fecal oocysts of cats. It would appear that an effective means of controlling infection in newborns is to identify pregnant women with acute infection and treat them. In Switzerland, 10 of 17 mothers treated during pregnancy had babies with antibodies to T. Preventing infection in sheep and swine requires eliminating cats and wild felines from stables and pastures, which would be a major challenge. Veterinary inspection of slaughterhouses, which has been effective in controlling trichinosis and teniasis, is not being done for toxoplasmosis. For some years, work has been under way to develop vaccines against toxoplasmosis for cats (Freyre et al. Order digoxin online now. Lower Your Blood Pressure Naturally with These 6 Herbs and Plants.
In addition to depending on the type of Brucella strain blood pressure good range purchase digoxin with paypal, the severity of the illness depends on host factors and dose blood pressure medication without hair loss buy digoxin 0.25mg visa. Patients have the intermittent fevers and sweating that are the hallmarks of brucellosis prehypertension chart cheap 0.25mg digoxin otc, along with other potential symptoms (described in Symptoms section blood pressure medication used for anxiety buy 0.25mg digoxin mastercard, below). If the diagnosis of brucellosis is delayed or the disease is left untreated, the disease may become chronic, and focalizations of brucellosis in bones. Other potential complications include bacterial endocarditis, meningioencephalitis, and myocarditis. Allergic hypersensitivity (dermal) is not uncommon and should be a consideration for laboratory workers or others with repeated exposures to the organism or antigens. The antibiotics most commonly used to treat human brucellosis include tetracycline, rifampicin, and the aminoglycosides. However, due to a high likelihood of relapse, health officials recommend the administration of more than one antibiotic for up to 6 weeks. Common combinations include doxycycline plus rifampicin or doxycycline plus streptomycin. For approximately 90% of patients, such aggressive therapy is enough to treat the infection and prevent relapse. Patients who develop complications may show symptoms of endocarditis or myocarditis, such as shortness of breath, arrhythmia, edema, or chest pain; meningoencephalitis, such as severe headache, stiff neck, confusion, or seizures; or spondylitis, such as back pain. How Brucella, an intracellular parasite, survives intracellularly and its pathogenesis pathway in humans are not well understood. Once inside the macrophage, some bacteria are killed; however, a subpopulation can be transported into the intracellular spaces. When moved to the lymph nodes, macrophages die and can release large amounts of bacteria. In humans, the infection is primarily focused within the reticuloendothelial system, but, in other animal hosts, the organism targets the placental trophoblast cells of pregnant animals, causing fetuses to be aborted. Human cases of spontaneous abortion have been noted following infections with Brucella, similar to occurrences associated with another intracellular pathogen, Listeria monocytogenes, that likewise affects dairy products. Study of human neutrophils found in the bloodstream demonstrated different responses for different species of Brucella. For example, the bacteria were killed more readily in neutrophils infected with B. Effects of Brucella on animal hosts: Brucella species generally do not cause illness in their primary (animal) hosts. In many cases, the only evidence of infection appears when a pregnant host suffers an abortion. Male animals can asymptomatically harbor the organism in their reproductive organs. Although Brucella strains have a strong preference for their host animals, interspecies transmission does occur through close physical contact with the bacterium. Sources Brucellosis in humans is usually associated with consumption of unpasteurized milk and soft cheeses made from the milk of infected animals. Diagnosis Most often, the diagnosis of brucellosis relies on the isolation of the organism from blood or bone marrow. In addition, a number of immunologic techniques exist for detection of antiBrucella antibodies. The organism may also be isolated from the liver, spleen, bone marrow, or cerebrospinal fluid. The growth of Brucella from blood culture is notoriously slow, contributing to difficulties in diagnosis. In the case of disease progression to focalizations or chronic infections, histologic changes and radiologic evidence of erosion of lumbar vertebrae are useful for diagnosis. Localization of infection in the spinal column, brucellar spondylitis, is not uncommon with chronic infection. Target Populations Veterinarians and farm workers are at particular risk of infection, due to occupational exposure to tissues of aborted animal fetuses, which may contain millions of organisms. Human cases of brucellosis are found primarily in developing countries with animal cases and a high level of consumption of unpasteurized milk products. This is in contrast to countries such as Mexico, where both human and animal infection of B. Food Analysis Currently no method is available for routine analysis of foods for Brucella spp. Bad Bug Book Foodborne Pathogenic Microorganisms and Natural Toxins Vibrio cholerae Serogroups O1 and O139 1. Organism For Consumers: A Snapshot Vibrio cholerae serogroups O1 and O139 There are different kinds (species) of Vibrio, a bacterium. This kind of Vibrio can live in both saltwater (for example, coastal ocean water) and freshwater, bacteria that occur naturally in aquatic such as rivers. After the 2010 earthquake in confused with other Vibrio species Haiti, when many people had only unsanitary water for addressed in other chapters of this book; bathing and drinking, a large cholera outbreak killed more i. This bacterium makes a toxic substance, Vibrio parahaemolyticus, and Vibrio in the bowel, that causes watery diarrhea. Symptoms start a few hours to 3 days after contaminated food or water is taken in. But susceptible to disinfectants, cold preventing the illness in the first place is a better idea. You temperatures (especially freezing), and can help protect yourself by cooking seafood until the inside acidic environments. Cooked resistance to common disinfectants, such as foods should always be kept from touching raw foods, to prevent contamination. Approximately 20% of those infected have watery diarrhea, and 10% to 20% of those develop severe watery diarrhea (characteristic rice-water stools) and vomiting. Cholera gravis, the most severe form of cholera infection, is characterized by severe fluid and electrolyte loss from vomiting and profuse, watery diarrhea. Doxycycline and/or tetracycline are the antibiotics of choice; however, some resistance to tetracycline has been reported. Cases requiring medical intervention via rehydration therapy or antibiotic treatment can persist longer, depending on severity of illness when treatment is initiated. Frequency No major outbreaks of cholera have occurred in the United States since 1911. However, sporadic cases and small outbreaks have been reported since 1973, suggesting an environmental reservoir in the U. This organism causes an estimated 11 million cases per year worldwide, excluding outbreaks. Illness generally results from consumption of these seafoods raw, improperly cooked, or cross contaminated by a raw product. Although cooking kills these bacteria, serogroups O1 and O139 can grow in shellfish that have been contaminated after cooking, and prompt refrigeration of food remnants is important for prevention of this illness. Diagnosis Cholera can be confirmed only by isolation of the causative organism from the diarrheic stools of infected people.
Double phototherapy can produce a fall of begins hypertension pulmonary discount digoxin 0.25 mg with amex, converting bilirubin molecules into more as much as 29% in the first 24 hours arteria thoracoacromialis purchase 0.25mg digoxin overnight delivery,28 and intensive polar photoisomers blood pressure chart symptoms purchase digoxin online from canada, that are unable to cross the phototherapy can lower the bilirubin level by as blood-brain barrier independently to gain access to much as 5 mg/dL/h (85 mol/L/h) In infants with the neurons arteria jugularis purchase digoxin visa. Fundamentals of Phototherapy for Neonatal Jaundice S21 impairs immune system function through alterations 14. Which pholinked to the development of abnormal melanocytic totherapy system is most effective in lowering serum bilirubin in very preterm infantsfi Open crib phototherapy: using for this association is not definitive and has been evidence to change practice. Use of eye patches in phototherapy: effects on debated, but at this time, this possible effect cannot be conjunctival bacterial pathogens and conjunctivitis. Changes in skin temperature of hyperbilirubinemic newborns under phototherapy: conventional versus fiberoptic device. Effect of different phototherapy lights on incubator characteristics and dynamics under three modes of servocontrol. Transepidermal water loss standard of care for the treatment of hyperbilirubineand skin hydration in preterm infants during phototherapy. Transepidermal water have prevented nearly as much morbidity and morloss during halogen spotlight phototherapy in preterm infants. A randomized controlled trial of fluid supplemencertainly done so with fewer complications. Mist and water condensation inside incutherapy, however, we must guard against becoming bators reduce the efficacy of phototherapy. Comparison of the efficacy of fiberoptic and conventional phototherapy for neonatal hyperbilirubinemia. Transcutaneous bilirubinombut not always benign problem of neonatal hyperetry in preterm infants receiving phototherapy. Prevention of hyperbilirubinemia of prematurity by jaundice is increased by the use of low-cost white reflecting curtains. The pattern of bilirubin response to phototherapy for neonatal hyperprint April 1, 2011]. The importance of irradiance and area in neonatal phophototherapy: retrospective cohort study. Jaundice is the most common cause of readmission after discharge from birth 1 hospitalization. High serum bilirubin levels carry a potential to cause neurological impairment with serious consequences in a small fraction of jaundiced babies. Approximately 5-10% of them have clinically significant jaundice that require treatment to lower serum bilirubin levels in order to prevent neurotoxicity. Presence of one or more of following conditions would qualify a neonate to 2 have pathological jaundice: 1. However slight jaundice on face at the end of first day (say 18 to 24 hr) is common and can be considered physiological. Clinical jaundice persisting beyond 2 weeks in term and 3 weeks in preterm neonates Causes of pathological jaundice Common causes of pathological jaundice include: 1. Extravasated blood: cephalhematoma, extensive bruising etc Clinical assessment of jaundice fi the parents should be counselled regarding benign nature of jaundice in most neonates, and for the need to be watchful and seek help if baby appears too yellow. The parents should be explained about how to see for jaundice in babies (in natural light and without any yellow background). The babies being discharged from the hospital at 48 to 72 hours should be seen again after 48 to 72 hours of discharge. Breastfeeding problems such as improper positioning and attachment, cracked or sore nipple, engorgement, perceived inadequacy of milk production are very common and require intense and sustained support from health professionals caring mothers and babies. Breastfeeding support must include, in addition to providing adequate information, actual helping the mothers to learn proper positioning and attachment, and adequate measures to address breastfeeding problems. However, current devices are costly and has a significant recurring cost of consumables such as disposable tips etc. TcB is unreliable in infants less than 35 weeks gestation and during initial 24 hr of age. TcB th value below 50 centile for age would rule out the risk of subsequent 7 hyperbilirubinemia with high probability (high negative predictive value) d. Trends in TcB values by measuring 12 hr apart would have a better predictive value than 8 a single value. We routinely perform TcB measurement in infants of 35 wk or more gestation to screen for hyperbilirubinemia. During phototherapy, for monitoring progress and after phototherapy to check for rebound in select cases (such as those with hemolytic jaundice) b. Approach to a jaundiced neonate: A step wise approach should be employed for managing jaundice in neonates (Figure 1). All the neonates should be visually inspected for jaundice every 12 hr during initial 3 to 5 days of life. Visual assessment (when performed properly) and TcB have reasonable sensitivity for initial assessment of jaundice. Phototherapy should be initiated if the infant meets the criteria for serious jaundice. TcB value more than 95 centile as per age specific nomogram Management of jaundice 1. The nomograms have lines for three different risk categories of neonates (Figure 2 and 3). These lines include one each for for lower risk babies (38 wk or more and no risk factors), medium risk babies (38 wk or more with risk factors, or 35 wk to 37 wk and without any risk factors) and higher risk (35 wk to 37 wk and with risk factors). The babies at lower and higher risk have their cut-offs at approximately 2 mg/dL higher or 2 mg/dL lower than that for medium risk babies, respectively. Figure 3 depicts nomogram for exchange transfusion in three risk categories of babies. Any baby showing signs of bilirubin encephalopathy such as hypertonia, retrocollis, convulsion, fever etc should receive exchange transfusion without any delay. Preterm babies There are no consensus guidelines to employ phototherapy or exchange transfusion in preterm babies. It acts by converting insoluble bilirubin (unconjugated) into soluble isomers that can be excreted in urine and feces. Many review articles have provided detailed discussion on phototherapy related issues. The bilirubin molecule isomerizes to harmless forms under blue-green light (460 to 490 nm); and the light sources having high irradiance in this particular wavelength range are more effective than the others. It is important that a plastic cover or shield be placed before phototherapy lamps to avoid accidental injury to the baby in case a lamp breaks. As the irradiance varies at different points on the footprint of a unit, it should be measured at several points. The lamps should be changed if the lamps are flickering or ends are blackened, if irradiance falls below the specified level or as per the recommendation of manufacturers. Avoid blocking the lights by any equipment (say radiant warmer), a large diaper or eye patch, a cap or hat, tape, dressing or electrode etc. Make sure that light falls on the baby perpendicularly if the baby is in incubator. |
