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LBD is not a rare disease. It affects an estimated 1.4 million individuals and their families in the United States. Because LBD symptoms can closely resemble other more commonly known diseases like Alzheimer’s and Parkinson’s, it is currently widely underdiagnosed. Many doctors or other medical professionals still are not familiar with LBD. LBD is an umbrella term for two related diagnoses. LBD refers to both Parkinson’s disease dementia and dementia with Lewy bodies. The earliest symptoms of these two diseases differ, but reflect the same underlying biological changes in the brain. Over time, people with both diagnoses will develop very similar cognitive, physical, sleep, and behavioral symptoms. While it may take more than a year or two for enough symptoms to develop for a doctor to diagnose LBD, it is critical to pursue a formal diagnosis. Early diagnosis allows for important early treatment that may extend quality of life and independence. LBD is a multisystem disease and typically requires a comprehensive treatment approach. This approach involves a team of physicians from different specialties who collaborate to provide optimum treatment of each symptom without worsening other LBD symptoms. Many people with LBD enjoy significant improvement of their symptoms with a comprehensive approach to treatment, and some can have remarkably little change from year to year. Some people with LBD are extremely sensitive or may react negatively to certain medications used to treat Alzheimer’s or Parkinson’s in addition to certain over-the-counter medications.

What causes rheumatic fever? Rheumatic fever is not an infection itself, but rather the result of an untreated strep infection. When your body senses the strep infection, it sends antibodies to fight it. Sometimes, these antibodies attack the tissues of your joints or heart instead. If the antibodies attack your heart, they can cause your heart valves to swell, which can lead to scarring of the valve "doors" (called leaflets or cusps). Who is at risk for rheumatic fever? Fewer than 0.3% of people who have strep throat also get rheumatic fever. Rheumatic fever is most common among children aged 5 to 15, but adults may have the condition as well. Doctors think that a weakened immune system may make some people more likely to get rheumatic fever. And, although antibiotic medicines have reduced the number of cases of rheumatic fever in developed countries, there are still thousands of reported cases. What are the symptoms of rheumatic fever and how is it diagnosed? Symptoms of rheumatic fever usually begin 1 to 6 weeks after you have had a strep infection. They are Fever Joint pain or swelling in your wrists, elbows, knees, or ankles Small bumps under the skin over your elbows or knees (called nodules) A raised, red rash on your chest, back, or stomach Stomach pain or feeling less hungry Weakness, shortness of breath, or feeling very tired Your doctor will begin by doing a throat culture to find out if you have a strep infection. Then, your doctor will use a stethoscope to listen to your heart. He or she will also look for nodules on your joints. Sometimes, blood tests, chest x-rays, or an electrocardiogram (ECG or EKG) may be needed for a more definite diagnosis. How is rheumatic fever treated? Rheumatic fever must be treated right away. If you have a sore throat that lasts longer than 3 days, or if you have a fever and headache along with your sore throat, you should see your doctor for a throat culture. Even if you do not have a sore throat but have a fever and a skin rash, this could also mean a strep infection, and you should get tested. Remember rheumatic fever can result from an untreated strep infection, so it is very important to treat the infection before it leads to a worse condition.

Hyperkalemia is defined as a serum potassium concentration higher than the upper limit of the normal range; the range in infants and children is age-dependent, whereas the range for adults is approximately 3.5-5.5 mEq/L. The upper limit may be considerably higher in young or premature infants, as high as 6.5 mEq/L.[5] Degrees of hyperkalemia are defined as follows[6] : 5.5-6.0 mEq/L – Mild 6.1-7.0 mEq/L – Moderate ≥7.0 mEq/L – Severe levels higher than 7 mEq/L can lead to significant hemodynamic and neurologic consequences. levels exceeding 8.5 mEq/L can cause respiratory paralysis or cardiac arrest and can quickly be fatal. Because of a paucity of distinctive signs and symptoms, hyperkalemia can be difficult to diagnose. Indeed, it is frequently discovered as an incidental laboratory finding. The physician must be quick to consider hyperkalemia in patients who are at risk for this disease process. (See Etiology.) However, any single laboratory study demonstrating hyperkalemia must be repeated to confirm the diagnosis, especially if the patient has no changes on electrocardiography (ECG). Because hyperkalemia can lead to sudden death from cardiac arrhythmias, any suggestion of hyperkalemia requires an immediate ECG to ascertain whether ECG signs of electrolyte imbalance are present (see Workup). Continuous ECG monitoring is essential if hyperkalemia is confirmed. Other testing is directed toward uncovering the condition or conditions that led to the hyperkalemia (see Workup). The aggressiveness of therapy for hyperkalemia is directly related to the rapidity with which the condition has developed, the absolute level of serum potassium, and the evidence of toxicity. The faster the rise of the potassium level, the higher it has reached, and the greater the evidence of cardiotoxicity, the more aggressive therapy should be. In severe cases, treatment focuses on immediate stabilization of the myocardial cell membrane, rapid shifting of potassium to the intracellular space, and total body potassium elimination. In addition, all sources of exogenous potassium should be immediately discontinued. (See Treatment.)

The incidence of digitalis toxicity has declined in recent years, due to decreased use of this drug along with improved technology for monitoring of drug levels and increased awareness of drug interactions. Nevertheless, cardiac glycoside toxicity continues to be a problem in the United States because of the wide use of digoxin (a preparation of digitalis) and its narrow therapeutic window. Digitalis is a plant-derived cardiac glycoside commonly used in the treatment of chronic heart failure (CHF), atrial fibrillation, and reentrant supraventricular tachycardia.[1, 2] Digoxin is the only available preparation of digitalis in the United States. (See Etiology and Epidemiology.) Cardiac glycosides are found in certain flowering plants, such as oleander and lily-of-the-valley. Indigenous people in various parts of the world have used many plant extracts containing cardiac glycosides as arrow and ordeal poisons. The ancient Egyptians used squill (Urginea maritime) as a medicine. The Romans employed it as a diuretic, heart tonic, emetic, and rat poison. Digitalis, or foxglove, was mentioned in the year 1250 in the writings of Welsh physicians. Fuchsius described it botanically 300 years later and named it Digitalis purpurea. William Withering published his classic account of foxglove and some of its medical uses in 1785, remarking upon his experience with digitalis. He recognized many of the signs of digitalis toxicity, noting, "The foxglove, when given in very large and quickly repeated doses, occasions sickness, vomiting, purging, giddiness, confused vision, objects appearing green or yellow; increased secretion of urine, slow pulses, even as low as 35 in a minute, cold sweats, convulsions, syncope, death." (See Presentation and Workup.) During the early 20th century, as a result of the work of Cushny, Mackenzie, Lewis, and others, the drug was gradually recognized as specific for treatment of atrial fibrillation. Only subsequently was the value of digitalis for treatment of CHF established. Cardiac glycosides enhance cardiac contractility and slow conduction through the atrioventricular (AV) junction by increasing vagal tone.[3] (See Etiology.) Cardiac glycoside toxicity has been known to result from ingestion of some plants, including yellow oleander (Thevetia peruviana) and foxglove, and a similar toxidrome has been associated with the use of herbal dietary supplements that contain cardiac glycosides. Digoxin is among the top 50 prescribed drugs in the United States.[4] In 2011, the American Association of Poison Control Centers reported 1601 single exposures to cardiac glycoside drugs.[5] Cardiac glycosides account for 2.6% of toxic plant exposures in the United States.[6, 7] Most of these exposures are in children.[7] (See Epidemiology.) Digoxin-specific fragment antigen-binding (Fab) antibody fragments have contributed significantly to the improved morbidity and mortality of toxic patients since their approval in 1986 by the US Food and Drug Administration (FDA). (See Prognosis, Treatment, and Medication.)