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By: H. Roy, M.B. B.A.O., M.B.B.Ch., Ph.D.

Professor, Pacific Northwest University of Health Sciences

Severe ventricular arrhythmias associated with digoxin toxicity may be managed with phenytoin medications 73 cheap curcumin generic, 2 to 4 mg/kg over 5 minutes symptoms gestational diabetes safe 500mg curcumin, or lidocaine treatments purchase curcumin overnight delivery, 1 mg/kg loading dose medications 126 curcumin 500mg free shipping, followed by an infusion at 1 to 2 mg/kg per hour. Severe bradycardia may be refractory to these therapies and require temporary cardiac pacing. The use of digoxin-specific antibody Fab (antigen-binding fragments) preparation (Digibind; Burroughs Wellcome) is reserved for those patients with evidence of severe digoxin intoxication and clinical symptoms of refractory arrhythmia and/or atrioventricular block; in these patients, it is quite effective. Calculation of the Digibind dose in milligrams is as follows: (serum digoxin concentration in nanograms per milliliter 5. A second dose of Digibind may be given to those patients who continue to have clinical evidence of residual toxicity. Furosemide, 1 to 2 mg/kg per dose, usually results in a brisk diuresis within an hour of administration. If no response is noted in an hour, a second dose (double the first dose) may be given. Chronic use of furosemide may produce urinary tract stones as a result of its calciuric effects. A more potent diuretic effect may be achieved using a combination of a thiazide and a "loop" diuretic such as furosemide. It is important to carefully monitor serum potassium and sodium levels when beginning or changing the dose of diuretic medications. When changing from an effective parenteral to oral dose of furosemide, the dose should be increased by 50% to 80%. Furosemide may increase the nephro toxicity and ototoxicity of concurrently used aminoglycoside antibiotics. When evaluating any infant with an arrhythmia, it is essential to simultaneously assess the electrophysiology and hemodynamic status. If the baby is poorly perfused and/or hypotensive, reliable intravenous access should be secured and a level of resuscitation should be employed appropriately for the degree of illness. These arrhythmias frequently require immediate defibrillation but are extremely rare arrhythmias in neonates and young infants. In nearly all circumstances, appropriate therapy (short term and long term) depends on an accurate electrophysiologic diagnosis. Although rhythm strips generated from a cardiac monitor can be helpful supportive evidence of the final diagnosis, they are typically not diagnostic and should not be the only documentation of arrhythmia if at all possible. The three broad categories for arrhythmias in neonates are (i) tachyarrhythmias, (ii) bradyarrhythmias, and (iii) irregular rhythms. An algorithm for approaching the differential diagnosis of tachyarrhythmias can be consulted. Differential diagnosis and initial management in the hemodynamically stable patient 1. Algorithm for bedside differential diagnosis of narrow complex tachycardias, the most common type of arrhythmia in neonates. Note that, regardless of the mechanism of tachycardia, if the patient is hemodynamically unstable, immediate measures to resuscitate the infant including cardioversion are required. In addition, treatment with adenosine is helpful therapeutically as well as diagnostically. In general, tachycardias that terminate (even briefly) after adenosine are of the reentry type. The infant may initially be asymptomatic but later may become irritable, fussy, and may refuse feedings. Vagal maneuvers (facial/malar ice wrapped in a towel to elicit the "diving reflex") may be tried in stable neonates. If digoxin successfully maintains the patient in sinus rhythm, it is typically continued for 6 to 12 months. Treatment with propranolol may be associated with apnea and hypoglycemia; therefore, neonates started on propranolol, especially premature infants, should be observed on a continuous cardiac monitor and have serial serum glucose checks for 1 to 2 days. The addition or substitution of other antiarrhythmic drugs such as amiodarone, alone or in combination, may be necessary and should be done only in consultation with a pediatric cardiologist. In neonates, verapamil should only rarely be used because it has been associated with sudden death in babies.

Women with uncontrolled hypertension treatment 0f gout order curcumin 500 mg on-line, thrombocytopenia shakira medicine buy generic curcumin, hepatocellular dysfunction medicine escitalopram purchase cheap curcumin online, pulmonary edema symptoms iron deficiency curcumin 500 mg with visa, compromised renal function, or persistent headache or visual changes are not candidates for conservative management of severe preeclampsia. Although a trial of labor induction is not contraindicated in patients with severe preeclampsia, the success rate is low. The managing team must balance the risks of progression of the disease against the time required to induce labor. Conservative management of mild preeclampsia generally includes hospitalization with bed rest and close maternal and fetal observation. Outpatient management is an option only for a few carefully selected, well-supported and reliable patients after a period of initial observation to assess maternal and fetal status. Betamethasone should be administered to accelerate fetal maturity if the fetus is 34 weeks of gestation and no maternal contraindications exist. If the fetus is appropriately grown with reassuring fetal testing, testing should be at regular intervals. If the estimated fetal weight is 10th percentile or there is oligohydramnios (amniotic fluid index of 5 cm or less), then testing should be performed at frequent regular intervals (consider daily) after consideration of delivery. Fetal indications for delivery include severe fetal growth restriction, nonreassuring fetal testing, and oligohydramnios. Women should be evaluated for signs and symptoms of preeclampsia and severe preeclampsia. Laboratory evaluation includes hematocrit, platelet count, and quantification of protein excretion in the urine, serum creatinine, transaminases, and uric acid level in addition to prothrombin time/partial thromboplastin time. If criteria for mild preeclampsia are met, laboratory studies should be performed at frequent intervals. Maternal indications for delivery include a gestational age 37 weeks, thrombocytopenia (100,000), progressive deterioration in hepatic or renal Prenatal Assessment and Conditions 43 function, abruptio placentae, and persistent severe headaches, visual changes, or epigastric pain. Antihypertensive agents are not routinely given because they have not been shown to improve the outcome in cases of mild preeclampsia. When early delivery is indicated, it is our practice that vaginal delivery is preferred. Cesarean delivery should be reserved for cases when fetal decompensation is suspected, when further fetal evaluation is not possible, or when a rapidly deteriorating maternal condition mandates expeditious delivery. Magnesium sulfate has been shown to be the agent of choice for seizure prophylaxis in randomized double-blind comparisons against both placebo and conventional antiepileptics. Because the kidneys clear magnesium sulfate, urine output should be carefully monitored. Signs and symptoms of maternal toxicity include loss of deep tendon reflexes, somnolence, respiratory depression, cardiac arrhythmia, and, in extreme cases, cardiovascular collapse. Careful monitoring of fluid balance is critical because preeclampsia is associated with endothelial dysfunction leading to decreased intravascular volume, pulmonary edema, and oliguria. A serum magnesium level should be considered if reduced renal function is suspected while magnesium sulfate is being administered. Severe hypertension may be controlled with agents including hydralazine, labetalol, or nifedipine. Sodium nitroprusside should be avoided before delivery because of potential fetal cyanide toxicity. It is important to avoid large or abrupt reductions in blood pressure because decreased intravascular volume and poor uteroplacental perfusion can lead to acute placental insufficiency and a resulting loss of reassurance regarding fetal well-being. Continuous electronic fetal monitoring is recommended given the potential for placental dysfunction in the preeclamptic setting. Monitoring should be established during the initial evaluation, induction of labor, and labor itself. Continuous monitoring is less likely to be useful during intervals of prolonged expectant management. Patterns that suggest fetal compromise include persistent tachycardia, minimal or absent variability, and recurrent late decelerations not responsive to standard resuscitative measures.

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Initial laboratory evaluation should include serum creatinine and assessment of acid-base status symptoms ulcer stomach order 500mg curcumin amex. Many causes of hyperkalemia medicine you can overdose on purchase 500mg curcumin with mastercard, such as renal insufficiency and aldosterone insufficiency or resistance medications heart failure buy discount curcumin 500 mg on line, cause a metabolic acidosis symptoms 1974 cheapest generic curcumin uk. Cell destruction, as seen in rhabdomyolysis or tumor lysis syndrome, can cause concomitant hyperphosphatemia, hyperuricemia, and an elevated serum lactate dehydrogenase. Chronic, mild derangements in acid-base status may interfere with normal growth and development, whereas acute, severe changes in pH can be fatal. Control of acid-base balance depends on the kidneys, the lungs, and intracellular and extracellular buffers. An adult normally produces about 1 to 2 mEq/kg/day of hydrogen ions, whereas a child produces 2 to 3 mEq/kg/day. The hydrogen ions from endogenous acid production are neutralized by bicarbonate, potentially causing the bicarbonate concentration to fall. The kidneys regenerate this bicarbonate by secreting hydrogen ions, maintaining the serum bicarbonate concentration in the normal range (20 to 28 mEq/L). An additional source of concern is a patient with increasing plasma potassium despite minimal intake. This situation can occur if there is cellular release of potassium (tumor lysis syndrome), especially in the setting of diminished excretion (renal failure). Acidosis is a pathologic process that causes an increase in the hydrogen ion concentration, and alkalosis is a pathologic process that causes a decrease in the hydrogen ion concentration. During a simple metabolic disorder, there 120 Section 7 u Fluids and Electrolytes an unknown medical problem, the presence of a metabolic acidosis is often helpful diagnostically because it suggests a relatively narrow differential diagnosis (Table 37-2). With metabolic acidosis, the decrease in the pH increases the ventilatory drive, causing a decrease in the Pco2. This appropriate respiratory compensation for a metabolic process happens quickly and is complete within 12 to 24 hours. During a primary respiratory process, there is metabolic compensation mediated by the kidneys. The kidneys respond to a respiratory acidosis by increasing hydrogen ion excretion, increasing bicarbonate generation, and raising the serum bicarbonate concentration. The kidneys increase bicarbonate excretion to compensate for a respiratory alkalosis; the serum bicarbonate concentration decreases. In contrast to a rapid respiratory compensation, it takes 3 to 4 days for the kidneys to complete appropriate metabolic compensation. However, there is a small and rapid compensatory change in the bicarbonate concentration during a primary respiratory process. The expected appropriate metabolic compensation for a respiratory disorder depends on whether the process is acute or chronic. A mixed acid-base disorder is present when there is more than one primary acid-base disturbance. An infant with bronchopulmonary dysplasia may have a respiratory acidosis from chronic lung disease and a metabolic alkalosis from a diuretic used to treat the chronic lung disease. Formulas are available for calculating the appropriate metabolic or respiratory compensation for the six primary simple acid-base disorders (Table 37-1). If a patient does not have appropriate compensation, a mixed acid-base disorder is present. The amount of bicarbonate lost in the stool depends on the volume of diarrhea and the bicarbonate concentration of the stool, which tends to increase with more severe diarrhea. Diarrhea often causes volume depletion because of losses of sodium and water, potentially exacerbating the acidosis by causing hypoperfusion (shock) and a lactic acidosis. Failure to thrive, resulting from chronic metabolic acidosis, is the most common presenting complaint. Along with renal wasting of bicarbonate, Fanconi syndrome causes glycosuria, aminoaciduria, and excessive urinary losses of phosphate and uric acid. The chronic hypophosphatemia is more clinically significant because it ultimately leads to rickets in children. Fanconi syndrome is rarely an isolated genetic disorder, with pediatric cases usually secondary to an underlying genetic disorder, most commonly cystinosis. However, bicarbonate therapy increases bicarbonate losses in the urine, and the urine pH increases.

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Early encephalitis probably is caused by direct viral infection of brain tissue symptoms quitting tobacco order curcumin pills in toronto, whereas later onset encephalitis is a demyelinating and probably an immunopathologic phenomenon symptoms of ms curcumin 500mg with mastercard. Subacute sclerosing panencephalitis is a late neurologic complication of slow measles infection that is characterized by progressive behavioral and intellectual deterioration and eventual death symptoms celiac disease 500 mg curcumin. It occurs in approximately 1 in every 1 million cases of measles symptoms 0f ms buy cheapest curcumin, an average of 8 to 10 years after measles. Late deaths in adolescents and adults usually result from subacute sclerosing panencephalitis. Other forms of measles encephalitis in immunocompetent persons are associated with a mortality rate of approximately 15%, with 20% to 30% of survivors having serious neurologic sequelae. Rubella virus invades the respiratory epithelium and disseminates via a primary viremia. After replication in the reticuloendothelial system, a secondary viremia ensues, and the virus can be isolated from peripheral blood monocytes, cerebrospinal fluid, and urine. Rubella virus is most contagious through direct or droplet contact with nasopharyngeal secretions from 2 days before until 5 to 7 days after rash onset, although virus may be present in nasopharyngeal secretions from 7 days before until 14 days after the rash. Maternal infection during the first trimester results in fetal infection with generalized vasculitis in more than 90% of cases. Infants with congenital rubella may shed the virus in nasopharyngeal secretions and urine for longer than 12 months after birth and may transmit the virus to susceptible contacts. Epidemiology In unvaccinated populations, rubella usually occurs in the spring, with epidemics occurring in cycles of every 6 to 9 years. Outbreaks of rubella occasionally occur in nonvaccinated groups from internationally imported cases. Contraindications to measles vaccine include immunocompromised states or an immunosuppressive course of corticosteroids (>2 mg/kg/day for >14 days); pregnancy; or recent administration of immunoglobulin (3 to 11 months, depending on dose). Susceptible household contacts with a chronic disease or who are immunocompromised should receive postexposure prophylaxis with measles vaccine within 72 hours of measles exposure or immunoglobulin within 6 days of exposure. The characteristic signs of rubella are retroauricular, posterior cervical, and posterior occipital lymphadenopathy accompanied by an erythematous, maculopapular, discrete rash. The rash begins on the face and spreads to the body, lasting for 3 days and less prominent than that of measles. Rose-colored spots on the soft palate, known as Forchheimer spots, develop in 20% of patients and may appear before the rash. Other manifestations of rubella include mild pharyngitis, conjunctivitis, anorexia, headache, malaise, and low-grade fever. Polyarthritis, usually of the hands, may occur, especially among adult females, but usually resolves without sequelae. The white blood cell count usually is normal or low, and thrombocytopenia rarely occurs. Diagnosis is confirmed by serologic testing for IgM antibodies (typically positive 5 days after symptom onset) or by a fourfold or greater increase in specific IgG antibodies in paired acute and convalescent sera. They infect mature mononuclear cells and cause a relatively prolonged (3 to 5 day) viremia during primary infection. They can be detected in the saliva of healthy adults, which suggests, as with other herpesviruses, the development of lifelong latent infection and intermittent viral shedding. Cases of suspected congenital rubella syndrome and postnatal rubella infection should be reported to the local and state health department. Differential Diagnosis the rash must be differentiated from measles, roseola, enteroviral or adenoviral infection, infectious mononucleosis, toxoplasmosis, scarlet fever, rickettsial disease, Kawasaki disease, serum sickness, and drug rash. The incidence of infection increases as maternally derived antibody levels decline. The virus is likely acquired from asymptomatic adults who periodically shed these viruses. Complications and Prognosis Other than congenital rubella syndrome (see Chapter 66) arising from rubella infection during pregnancy, complications are rare. After vaccination, rubella virus is shed from the nasopharynx for several weeks, but it is not communicable. In children, rubella vaccine rarely is associated with adverse effects, but in postpubertal females, it causes arthralgias in 25% of vaccinated individuals and acute arthritis-like symptoms in 10% of vaccinated individuals. These symptoms typically develop 1 to 3 weeks after vaccination and last 1 to 3 days. Contraindications to rubella vaccine include immunocompromised states or an immunosuppressive course of corticosteroids (>2 mg/kg/day for >14 days); pregnancy; or recent administration of immunoglobulin (3 to 11 months, depending on dose).

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