What are the complications of a heart attack?

Heart failure. When a large amount of heart muscle dies the ability of the heart to pump blood to the rest of the body is diminished and this can result in heart failure. The body retains fluid, and organs, for example the kidneys, begin to fail.

Ventricular fibrillation. Injury to heart muscle can also lead to ventricular fibrillation. It occurs when the normal, regular, electrical activation of heart muscle contraction is replaced by chaotic electrical activity that causes the heart to stop beating and pumping blood to the brain and other parts of the body. Permanent brain damage and death can occur unless the flow of blood to the brain is restored within five minutes. Most of the deaths from heart attacks are caused by ventricular fibrillation of the heart that occurs before the victim of the heart attack can reach an emergency room. Those who reach the emergency room have an excellent prognosis; survival from a heart attack with modern treatment should exceed 90%. The 1 to 10% of heart attack victims who later die frequently had suffered major damage to the heart muscle initially or additional damage at a later time.

Death from ventricular fibrillation can be avoided by cardiopulmonary resuscitation (CPR) started within five minutes of the onset of ventricular fibrillation. CPR requires breathing for the victim and applying external compression to the chest to squeeze the heart and force to pump blood. In 2008 The American Heart Association modified the mouth-to mouth instruction of CPR and recommends that chest compressions alone are effective if a bystander is reluctant to do mouth-to-mouth. When paramedics arrive medications and an electrical shock (cardioversion) can be administered to convert ventricular fibrillation back to a normal heart rhythm and allow the heart to pump blood normally. Therefore, prompt CPR and rapid response by paramedics can improve the chances of survival from a heart attack. In addition, many public venues now have automatic external defibrillators (AEDs) that provide the electric shock needed to restore a normal heart rhythm even before the paramedics arrive. This greatly improves the chances for survival.

What are the risk factors for atherosclerosis and heart attack? Factors that increase the risk of developing atherosclerosis and heart attacks include increased blood cholesterol, high blood pressure, use of tobacco, diabetes mellitus, male gender, and a family history of coronary heart disease. While family history and male gender are genetically determined the other risk factors can be modified through changes in lifestyle and medications.

High blood cholesterol (hyperlipidemia). A high level of cholesterol in the blood is associated with an increased risk of heart attack because cholesterol is the major component of plaques deposited in arterial walls. Cholesterol, like oil, cannot dissolve in the blood unless it is combined with special proteins called lipoproteins. Without combining with lipoproteins cholesterol in the blood would turn into a solid substance. Cholesterol in the blood is either combined with lipoproteins as very low-density lipoproteins (VLDL), low-density lipoproteins (LDL), or high-density lipoproteins (HDL).

Cholesterol that is combined with LDL (LDL cholesterol) is the “bad” cholesterol that deposits cholesterol in arterial plaques. Thus, elevated levels of LDL cholesterol are associated with an increased risk of heart attack.

Cholesterol that is combined with HDL (HDL cholesterol) is the “good” cholesterol that removes cholesterol from arterial plaques. Thus, low levels of HDL cholesterol are associated with an increased risk of heart attacks.

Measures that lower LDL cholesterol and increase HDL cholesterol (losing excess weight, diets low in saturated fats, regular exercise, and medications) have been shown to lower the risk of heart attack. One important class of medications for treating elevated cholesterol levels (the statins) have actions in addition to lowering LDL cholesterol which also protect against heart attack. Most patients at high risk for a heart attack should be on a statin no matter what the levels of their cholesterol are.

High blood pressure (hypertension). High blood pressure is a risk factor for developing atherosclerosis and heart attack. Both high systolic pressure (when the heart beats) and high diastolic pressure (when the heart is at rest) increase the risk o heart attack. It has been shown that controlling hypertension with medications can reduce the risk of heart attack.

Tobacco use (smoking). Tobacco and tobacco smoke contain chemicals that cause damage to blood vessel walls, accelerate the development of atherosclerosis, and increase the risk of heart attack.

Diabetes mellitus. Both insulin dependent and non-insulin dependent diabetes mellitus (type 1 and 2 respectively) are associated with accelerated atherosclerosis throughout the body. Therefore, patients with diabetes mellitus are at risk for reduced blood flow to the legs, coronary heart disease, erectile dysfunction, and strokes at an earlier age than non-diabetic subjects. Patients with diabetes can lower their risk through rigorous control of their blood sugar levels, regular exercise, weight control, and proper diets.

Male gender. At all ages men are more likely than women to develop atherosclerosis and coronary heart disease. Some scientists believe that this difference is partly due to the higher blood levels of HDL cholesterol in women than in men. However, this gender difference narrows as men and women grow older.

Family history of heart disease. Individuals with a family history of coronary heart diseases have an increased risk of heart attack. Specifically, the risk is higher if there is a family history of early coronary heart disease including a heart attack or sudden death before the age of 55 in the father or other first-degree male relative or before the age of 65 in the mother or other first-degree female relative.

How is a heart attack diagnosed? When there is a severe chest pain suspicion that a heart attack is occurring is usually high and tests can be performed quickly that will confirm the heart attack. A problem arises, however, when the symptoms of a heart attack may not be suspected and the appropriate tests may not be performed. Therefore, the initial step in diagnosing a heart attack is to be suspicious that one has occurred.

Electrocardiogram. An electrocardiogram (ECG) is a recording of the electrical activity of the heart. Abnormalities in the electrical activity usually occur with heart attacks and can identify the areas of heart muscle that are deprived of oxygen and areas of muscle that have died. In a patient with typical symptoms of heart attack such as crushing chest pain and characteristic changes of heart attack on the ECG a secure diagnosis of heart attack can be made quickly in the emergency room and treatment can be started immediately. If a patient’s symptoms are vague or atypical and if there are pre-existing ECG abnormalities, for example, from old heart attacks or abnormal electrical patterns that make interpretation of the ECG difficult, the diagnosis of a heart attack may be less secure. In these patients the diagnosis can be made only hours later through detection of elevated cardiac enzymes in the blood.

Blood tests. Cardiac enzymes are proteins that are released into the blood by dying heart muscles. These cardiac enzymes are creatine phosphokinase (CPK), special subfractions of CPK and troponin and their levels can be measured in blood. These cardiac enzymes are typically elevated in the blood several hours after the onset of a heart attack. A series of blood tests for enzymes performed over a 24-hour period are useful not only in confirming the diagnosis of heart attack but the changes in their levels over time also correlates with the amount of heart muscle that has died.

The most important factor in diagnosing and treating a heart attack is prompt medical attention. Rapid evaluation allows early treatment of potentially life-threatening abnormal rhythms such as ventricular fibrillation and allows early reperfusion (return of blood flow to the heart muscle) by procedures that unclog the blocked coronary arteries. The more rapidly the blood flow is reestablished, the more heart muscle that is saved.

Large and active medical centers of the have a “chest pain unit” where patients suspected of having heart attacks are rapidly evaluated. If a heart attack is diagnosed prompt therapy is initiated. If the diagnosis of heart attack is initially unclear the patient is placed under continuous monitoring until the results of further testing are available.

 

ARTHRITIS

We all have mornings when we wake up a bit stiff. We all know the achy feeling that comes from working too hard in the garden, sitting too long at the computer or sleeping in an awkward position, And from time to time we have all suffered pain because we’ve lifted a heavy object in a slightly wrong way. Even a particularly ferocious sneeze can cause a twinge of discomfort. But arthritis goes far beyond these occasional aches or pains.

The condition that we commonly refer to as arthritis includes a number of diseases that result in inflammation, pain and stiffness, primarily in the joints and connective tissues. Connective tissues are the supporting structures for joints, such as muscles, cartilage, ligaments and tendons. In many cases, these diseases affect other parts of the body as well. Arthritic disorders may be able chronic, but some such as gout, are intermittent. The conditions that are truly inflammatory (that is with actual joint inflammation present) cause warmth and swelling, whereas others are degenerative in which cartilage lining the joint wears out and the amount of inflammation is minor.

How the joint works.The ends of bones meet at the joint where they are cushioned by cartilage, a layer of smooth tissue. Around many of the larger joints such as the knee, hip and shoulder there is a pad-like sac or cavity called the bursa which is lined with cells similar to those lining the joint. In addition to acting as a buffer to reduce friction between the muscle, tendon tissue and bone, the inner lining produces a fluid, synovial fluid, that keeps the joints lubricated and provides nutrients. Ligaments connect and support bones to keep them in proper alignment whereas tendons connect muscles to bones. Joints move when a muscle on the one side of a joint contracts and pulls on the tendons that attach to a bone on the other side of the joint.

How arthritis affects the joints.The word arthritis means joint inflammation. Inflammation, a natural part of the body’s response to injury and infection, is a complex process that produces swelling, pain, warmth and redness. But inflammation is not only a response to injury, it may perpetuate injury as well. Significant problems arise when inflammation is persistent, intense or recurrent or spreads to other areas of the body.

Joints and the surrounding areas become inflamed for a number of reasons including trauma, disease, infection or merely wear and tear, which naturally occurs over time. Many forms of arthritis are thought to result from the uncontrolled inflammation of an autoimmune disease in which the body’s defense mechanism malfunctions and attacks its own tissues. At other times the joint area becomes inflamed and tender for no apparent reason.

When joints become arthritic, swelling causes stiffness, rigidity and tissue damage. Pain which is the body’s signal that something is wrong occurs as the joint is moved to the brink of its own limits. As mobility decreases the muscles surrounding the joint also weaken allowing for further injury to the joint. Over time, the cartilage breaks down, the bone erodes, and the joints become misshapen. It is this process regardless of the source, that may develop in the worst forms of arthritis.

There are more than 100 different types of arthritis and each has its own characteristic symptoms and its own course. In addition, the way in which the disease progresses varies from individual to individual. If you suffer from an arthritic condition you will most likely experience pain and limited movement at the involved sites. In chronic forms of arthritis there may be times when the disease is active (flares) and times when it is inactive (remission). Depending on the specific condition and how severe it is arthritis can interfere with even the most ordinary activities such as walking, dressing or bathing. In the most inflammatory types of arthritis such as rheumatoid arthritis pain and stiffness are more severe in the morning or on certain days. Sometimes symptoms disappear completely for considerable stretches of time only to flare up again later.

Diagnosing arthritis.Inmost cases, arthritis is diagnosed after an individual contacts with his or her health care professional because pain is significant and has begun to interfere with daily life. If you have that kind of pain your physician will ask you to describe the feeling because he severity and quality of the pain is helpful in figuring out the cause. Is it a throbbing, achy, burning or stabbing sensation? Is it constant or occasionally intense? Do certain activities make the pain worse? Is it worse in the morning or at night? In some cases your doctor may ask you to record your daily experiences in a pain diary.

Your health care professional will review your current symptoms as well as your past medical history, family history, and medication use. A thorough medical examination will follow. The doctor may order blood and urine tests and in select cases X-rays and possibly imaging procedures such as a computed tomography (CT) or magnetic resonance imaging (MRI) may be recommended.

Once arthritis has been detected a treatment plan can be developed to suit you and your lifestyle. With early diagnosis most arthritic conditioned can be managed sufficiently to minimize both the pain and the disruption to your daily life. In many instances early diagnosis and treatment can also work to curtail the actual damage that the condition can cause.

The pain associated with arthritis stems from a number of sources. When, for example, the tissue that lines the joints (synovial membrane), tendons or ligaments swells, you may feel aches and discomfort right at the joint. Muscle strain and fatigue frequently follows as well adding to the intensity and duration of pain. If there is joint damage over time, even the most ordinary activities – getting out of bed in the morning, taking a bath, holding a pencil – can cause pain.

At the same time the level of pain and discomfort that people find tolerable varies from person to person, from situation to situation. Each person’s threshold for pain is different. In addition it is not uncommon for an individual who lives with chronic pain or the possibility of intense, intermittent pain, to experience anxiety and reactive depression as a result. Emotional stress and distress can intensify the sensation of pain.

Recognizing the typical types of pain, the location and the accompanying features helps clarify whether arthritis is present. Once diagnosis is established, the type of arthritis may help direct treatment and provide an idea of what to expect. It should be noted, however, that the specific type of arthritis cannot always be diagnosed early in the course of illness. In addition, many types of arthritis are treated similarly so a specific diagnosis is not always as helpful as it might seem.

In many types of arthritis, the course of the disease is unpredictable. Most chronic diseases involve periods when the symptoms are active and troublesome (flares) and periods when symptoms are negligible (remissions). This unpredictable and variable course can complicate both diagnosis and treatment.

Low back pain. What to do when so much is unknown.If you are one of the millions of people unfortunate enough to suffer from low back pain you may have received advice from your primary care doctor, your family, your friends or others experiencing similar symptoms. Few will suggest the same remedy, but remarkably all of their suggestions may be right. Because there is no single approach that will reliably help everyone numerous treatments (including no treatment at all) may provide relief.

How can this be? The answer reveals a well-kept secret about low back pain: for most people the cause is not known. However, there are many things about low back pain that are well known:

Low back pain is common. About 80 percent of the population will have low back pain at least once in the lifetime. Low back pain is not an inevitable result of aging, strenuous work or injury. It often develops for no apparent reason. Most low back pain is not associated with a dangerous or serious cause. There are reliable ways to detect the rarer and more serious causes. Most patients are not helped much by X-rays, computed tomography (CT) or magnetic resonance imaging (MRI). There is no single best treatment for low back pain. The goal of treatment should be to strike an acceptable balance between pain relief and the possible side effects of treatment, that balance is different for different patients.

Causes.Despite decades of research on thousands of people with thecondition, despite detailed anatomic pictures with CT scans and MRI, and despite major advances in the scientific understanding of disease mechanisms, the cause of pain in most cases remains uncertain. Moreover, many experts – for example, those at “back clinics” and specialty centers – will disagree about why your back hurts.

For the majority of patients with low back pain the cause is not serious. The pain is variable in its onset, quality, location and course. It may be: acute (sudden in onset) or chronic (lasting many weeks, months or years; centered on one or both sides of the lower back or radiating into one or both legs; sharp or dull, burning or aching; improved or worsened by different positions.

The sudden onset of pain increases the likelihood that the cause is a muscle spasm or bulging (herniated) disk. A patient who has pain on one side spreading into the buttock and back of the leg is often considered to have sciatica because the pain follows the path of the sciatic nerve, a common cause of this problem is a bulging disk.

If low back pain moves into both legs and worsens when you stand, spinal stenosis may be considered. In spinal stenosis the lower part of the spinal cord is compressed by a disk, ligaments, degenerative bone changes or some combination of these. Other common causes include back strain, muscle spasm and osteoarthritis (degenerative joint disease), but the symptoms that are associated with these disorders are much more variable. In older patients slippage of one vertebra on another (spondylolisthesis) and compression fractures (often related to osteoporosis) are important to consider after more serious causes have been excluded.

In many cases even when a common cause is suspected the diagnosis is generally difficult or impossible to prove. Even an abnormal MRI that reveals a bulging disk may not explain low back pain. Many patients perhaps one-third or more of the population have abnormalities on the MRI even when they have no pain and patients thought to have a disk problem based on their history and physical examination often have normal findings or irrelevant abnormalities on MRI. Among older individuals abnormalities on MRI are even more common.

Fortunately, among patients with low back pain dangerous causes are very uncommon representing only 1 percent or fewer of cases. These serious causes include infection, a tumor, vascular disease and fracture.

The red flags that alert your health care provider that one of these may be at play are advances age, weight loss, fever, past cancer, trauma, immune system problems, difficulty with bowel or bladder control, or vascular disease elsewhere in the body. The combination of past and current problems along with the physical examination will generally help guide which people with low back pain should be treated without further tests and which people should be evaluated further.

Treatment.If you or somebody close to you has low back pain what should be done? Common treatments include: rest, pain relievers, anti-inflammatory medicines, muscle relaxants, exercise. Other conservative treatments – those that avoid surgery or other invasive procedures – may include physical therapy, massage, chiropractic treatment and acupuncture.

Only when low back pain persists or worsens or when a doctor suspects a more serious cause should a patient consider elaborate testing and more aggressive treatments such as injections or surgery.

The role of imaging tests.When willa doctor recommend X-rays or MRI? A doctor will suggest imaging tests if he or she believes that the results are likely to lead to a change in your treatment or your outcome (how much pain you have, how good your function is, or even how long you live). Despite the development of guidelines by experts in the evaluation and management of low back pain, the approach continues to vary greatly among health care providers.

For example, one study found that a patient who sees a neurologist, rheumatologist andorthopedic surgeon with the same back complaints would receive dramatically different recommendations regarding which diagnostic tests to order, each specialist would tend to order tests that detect diseases in his or her field of expertise. Even when a disk problem is suspected and confirmed by MRI this test is probably unnecessary if no change in treatment or outcome follows.

Conclusion.Low back pain continues to e a big problem. it is common, its cause is frequently uncertain and the available treatments are not uniformly effective. Until we know more about why only some people have low back and which treatments are reliably effective, the answers you get about your back pain will depend largely on whom you ask. The good news is that most of the time low back pain improves, function returns to normal and the overall outcome is excellent regardless of the diagnosis offered or treatments provided.

 

 

DIABETES

Diabetes mellitus often simply called diabetes is a common disorder in which the body cannot properly use the carbohydrates (starches and simple sugars), fats and proteins in foods. All of these nutrients can be processed by the liver into one type of simple sugar, glucose, which then enters the bloodstream. All body cells require glucose for energy. Glucose enters body cells with the help of hormone called insulin which acts somewhat like a gatekeeper. If the body becomes less responsive to insulin or if the body is not producing insulin, glucose cannot pass through the cell wall and the cell “starves”. Because the glucose cannot enter cells it remains in the blood that is why people with diabetes have high blood sugar. As a result of cellular starvation and high blood sugar the body has to work harder to keep functioning, and organs and systems can suffer severe damage,

There are three types of diabetes mellitus.

Type I diabetes sometimes called insulin-dependent diabetes mellitus or juvenile-onset diabetes. Only about 5 to 10% of people with diabetes have type I. It is typically diagnosed before age 35, most often during adolescence. In type I diabetes some or all of the insulin producing cells of the pancreas (called beta cells) are destroyed by the body’s own immune system leaving the patient with little or no naturally produced insulin. What causes the immune system to attack the beta cells is a mystery. Both genetics and environment play a part, with the disease being triggered in genetically susceptible people by some outside factor. Viral infections and drinking cow’s milk early in life are two possible triggers.

Type II diabetes previously called non-insulin-dependent diabetes mellitus or adult-onset diabetes. About 90 to 95% of people with diabetes have type II. Although type II diabetes is diagnosed mostly in people older than 40, it is becoming increasingly common in young adults and children. In type II diabetes the pancreas produces amounts of insulin that would ordinarily be sufficient but the body cells become resistant to insulin, meaning the cells do not respond to insulin unless it is produced in much larger amounts. Insulin then loses its gatekeeper abilities and glucose is not able to enter the cells. Initially, the pancreas increases its output of insulin to try to make up for the cells’ insulin resistance but eventually, insulin production falls as the pancreas tires of producing extra insulin. At this point, blood sugar levels will rise and the person will begin to experience symptoms of diabetes.

Type II diabetes has a genetic component and is associated with obesity, although not everyone with type II diabetes is overweight. Fat accumulation around the waist can lead to a more serious condition known as metabolic syndrome, insulin-resistance syndrome, or syndrome X. Metabolic syndrome includes a cluster of conditions: insulin resistance, increased blood levels of insulin (hyperinsulinemia), high blood pressure, elevated levels of triglycerides, low levels of protective high-density lipoprotein cholesterol, and an increased incidence of atherosclerosis (narrowing of the arteries).

Gestational diabetes, also known as diabetes of pregnancy. This form of diabetes usually disappears after the baby is born.

Symptoms. The initial symptoms of diabetes are related to high blood glucose levels. These symptoms include excessive urination, thirst and hunger, weight loss, and increased susceptibility to infections, especially of the skin and vagina. Extremely high blood sugar levels can lead to a dangerous complication called hyperglycemic hyperosmolar coma. Usually seen in people with type II diabetes, hyperglycemic hyperosmolar coma is a state of mental confusion and disorientation that can progress to loss of consciousness and is associated with extreme dehydration. It can be the first sign of undiagnosed type II diabetes.

People with diabetes who have had high blood sugar levels for long periods of time can develop complications including: damage to the eyes (retinipathy) which can lead to blindness; damage to the nerves (neuropathy) which can lead to numbness, tingling or pain in the legs and arms; damage to the kidneys (nephropathy) which can result in kidney failure.

People with diabetes are also at increased risk of cardiovascular disease caused by atherosclerosis (thickening and hardening of the artery). Atherosclerosis can involve: the heart (coronary heart disease) with symptoms of chest pain or heart attack, the brain (cerebrovascular disease) causing stroke, the arteries supplying the legs (peripheral vascular disease) causing leg pain whi9le walking or exercising that stops quickly with rest. People with diabetes who have peripheral nerve damage and poor circulation associated with peripheral vascular disease eventually can develop foot ulcers and infections which can lead to gangrene (dead tissue and skin) and amputation.

Diagnosis. The main test used to diagnose diabetes is a blood test that measures the amount of glucose in your blood. The test is performed in the morning after you have fasted overnight. The diagnosis of diabetes is made when fasting blood glucose is greater than 126 milligrams per deciliter on more than one blood test.

Another blood test that may be done is called hemoglobin A1C which measures average blood glucose over the preceding two months. Although this test is not used to diagnose diabetes it is helpful for your doctor to measure it when you are first diagnosed. The success of treatment then can be measured by comparing late A1C numbers to your baseline.

When diabetes has been diagnosed your doctor will use your age, body weight, family history, and other medical history to decide what type of diabetes (type I or type II) is most likely. Your doctor will also check for signs of developing complications and other health problems that commonly occur with diabetes. For example, your doctor will check for high blood pressure, signs of retinopathy, decreased sensation and reflexes in the legs, poor pulses in the feet, blisters, ulcers or infections of the feet, and abnormal heart rhythm. Your doctor may also want to measure the level of creatinine in the blood and check for small amounts of protein in the urine (called a microalbumin teat). Both of these tests are used to check for evidence of kidney disease. A blood test called a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein cholesterol) may be done to elevate the risk of atherosclerosis.

Expected duration. Diabetes is a lifelong illness. Some people with type II diabetes are able to reduce their blood sugars to normal levels through diet and exercise but even these people should continue to identify themselves as diabetic and be monitored closely by a physician. In such cases aging or episodic illness typically causes the body’s insulin resistance to increase, so additional treatment may be required over time.

Prevention. There is currently no effective prevention for type I diabetes. However, it is possible to prevent the most common type of diabetes, type II. Because prevention strategies are available it is worthwhile to have your blood sugar tested if you have risk factors for diabetes such as obesity or a family history of diabetes. Mild elevations in blood sugar signify a condition called glucose tolerance or impaired fasting glucose. These blood sugar elevations show that your body is developing insulin resistance which typically leads to diabetes. Without changes in lifestyle or medication you have about a 10 percent chance per year of progressing to diabetes if you have elevated blood sugar. A large three year study that ended in 2002 showed that people with elevated blood sugar could cut their risk of progressing to diabetes by more than a half if they ate a reduced calorie diet, exercised regularly, and lost a modest amount of weight. A medication called metformin also offered some protection.

If you already have diabetes you can delay or prevent late complications (retinopathy, neuropathy, nephropathy) by controlling your blood sugar. You can lower your risk of cardiovascular complications by minimizing any other risk factors for atherosclerosis such as high blood pressure, high blood levels of cholesterol and triglycerides, cigarette smoking, and obesity.

Treatment. Currently, treatment of type I diabetes requires insulin to be injected under the skin to make up for the insulin not produced by the body. Patients can use syringes, injector pens, or an insulin pump. In order to properly regulate insulin intake people with type I diabetes need to monitor their blood sugar levels several times per day by testing a small sample of blood.

People with type I diabetes also need to watch their diets and get regular exercise. A healthy diet for type I diabetics is one that keeps the amount of glucose entering the blood relatively constant which makes it easier to control with insulin. Exercise kelps keep blood vessels healthy, promotes glucose usage by muscles, and keeps body weight down.

For people with type II diabetes treatment begins with weight reduction through diet and exercise. The recommended diet is a reduced-calorie diet that is usually the same as the diet traditionally used to lower cholesterol and prevent cardiovascular disease. Initially most patients with type II diabetes can control their blood sugar with medications taken by mouth. Insulin is often used in small dosed before bed to help prevent release of glucose from the liver during sleep. In advanced type II diabetes insulin may be needed more than once per day in higher doses.

If you take more insulin or diabetes medication than is needed to balance the diet daily calories, blood sugar levels can drop and cause hypoglycemia (low blood sugar). Symptoms of hypoglycemia include sweating, trembling, dizziness, hunger, confusion, seizures, and loss of consciousness.

When to call a professional. Because people with diabetes are at an increased risk of dehydration if you have diabetes you should call your doctor whenever you have nausea and vomiting especially if your fluid intake is poor.

If you have diabetes see your doctor regularly (as your doctor advises) to make sure that you are keeping good control of your blood sugar and to be checked for early signs of complications such as heart disease, eye problems, and skin infections. Your doctor most likely will suggest that you periodically visit other specialists such as a podiatrist to check your feet and an ophthalmologist to check for signs of diabetes complications that affect the eye.

Call your doctor immediately if your blood glucose is extremely high (greater than 500, for example) especially if you also have any of the following problems: an acute illness, extreme thirst with an inability to drink fluids because of nausea, vomiting, confusion, or loss of consciousness.

Prognosis. Because of the dangerous complications that diabetes can cause this disease is a very serious health risk. As a group, diabetics have twice the risk of dying at a premature age and have two to four times the average risk of heart attack and stroke. However, there is a great deal you can do to reduce your personal risk of diabetes complications. A “healthy diabetic” who is able to carefully control blood glucose and who makes every effort to reduce risk factors for cardiovascular disease has a dramatically reduced risk of diabetes complications.

 

 

CLINICAL CIRRHOSIS

Cirrhosis is the end stage of all chronic liver diseases. It kills about 26, 000 people every year in the United States making it the 12^th leading cause of death overall and the 8^th leading cause of death in men. But although cirrhosis is widwspread managing it still posses a challenge to emergency physicians because the disease affects every body system. It not only causes a range of unique diseases but also makes treating common diseases more difficult.

Most cases of cirrhosis are preventable, with alcohol and viral infections causing the majority of them. Nonalcoholic fatty liver disease may develop as a result of obesity, diabetes, hypertriglyceridemia, or profound weight loss after jejunoileal bypass surgery. Mortality rates in alcoholic liver disease are higher than those in other causes causes of cirrhosis in the United States.

How cirrhosis develops. Cirrhosis is a progressive liver fibrosis with nodular regeneration and distortion of hepatic architecture. This distorted architecture causes resistance to portal flow that leads to portal hypertension. As a result, blood is shunted away from the liver. The body’s attempt to compensate this leads to local production of vasodilators, like nitric oxide, that induce splanchnic arterial vasodilation and collateral vein formation, causing blood to be diverted to the systemic circulation and development of a hyperdynamic circulatory system.

Splanchnic vasodilation is the most important factor in the development od ascites. Eventually, visodilation becomes so severe that the effective circulating blood volume decreases and arterial pressure drops. This leads to activation of the sympathetic nervous and retin-angiotestin-aldosterone systems resulting in sodium and fluid retention. Also, the combination of splanchnic arterial vasodilation and portal hypertension alters intestinal capillary permeability and pressure facilitating the accumulation of retained fluid within the abdominal cavity and further increasing fluid retention.

Clinical profile. About 40% of patients with cirrhosis are asymptomatic. This is because 80 to 90% of the liver parenchyma must be destroyed before the clinical manifestations of liver failure and cirrhosis develop. Once ascites or gastrointestinal bleeding develops, cirrhosis is considered decompensated. Half of all patients with cirrhosis and ascites will die within two years if they do not receive an orthotopic liver transplant.

Jaundice, palmar erythema, hepatomegaly, splenomegaly, or ascites may be discovered on abdominal examination depending on how far the disease has progressed. Tremor of the hands may be present in cases of hepatic encephalopathy. Abdominal ultrasonography is the first-line radiographic study for diagnosing cirrhosis. Therapy consists of sodium restriction, diuretics (spironolactone, furosemide), and abstention from alcohol. Fluid restriction is unnecessary unless serum sodium is less than 125 mEq/L, although it may help control ascites and minimize the amount of diuretic required.

Common complications. Cirrhosis is an immunocompromised state. As more and more damage is done to the liver its synthetic function begins to decline. This problem is compounded by increased sympathetic tone causing a decrease in gut motility. This in its turn promotes bacterial stasis and overgrowth which leads to an overpopulation of enteric gram-negative bacteria. Intestinal submucosal edema from portal hypertension increases intestinal capillary permeability and compromises the protective integrity of the mucosal barrier. The above problems combined with the failure of antibacterial defense mechanisms to microorganisms and toxins from the blood often have disastrous results in the body including sepsis.

Another common problem associated with cirrhosis is malnutrition due to anorexia, poor diet, malabsorption, and an altered metabolic state. Malnutrition also decreases the risk of infection. Bleeding can occur secondary to decreased production of clotting factors. In addition, patients with cirrhosis are prone to hypoglycemia due to decreased hepatic glycogen storage.

Special treatment considerations. Because of the unusual physiologic mechanisms of their disease patients with cirrhosis do not respond to traditional therapies for common problems. Early goal-directed therapy, intensive insulin therapy, and other sepsis treatments have been shown to decrease mortality in the general population but have not been tried on patients with cirrhosis.

Hypotension from sepsis or other causes of shock may be refractory to catecholamine administration in patients with cirrhosus because of sympathetic desensitization. Priliminary evidence shows that vasopressin may improve refractory shock in these patients. Terlipressin has been extremely beneficial in treating hepatorenal syndrome and has shown great promise in treating acute liver injury with hypotension and severe lactic acidosis resistant to volume expansion as well as catecholamine-resistant septic shock. This drug is still in phase III clinical trials in the United States.

Marked adrenal insufficiency almost always occurs in patients with cirrhosis and severe sepsis and can lead to circulatory collapse. Steroids should be considered early in the course of therapy. In addition, septic patients with cirrhosis are more prone to developing disseminated intravascular coagulopathy (DIC) than the general population so early vigilant monitoring is suggested. Distinguishing DIS from hepatic coagulopathy can be difficult because fibrinogen levels may be low, high, or normal in cirrhosis. Early monitoring for trends in these laboratory values may help differentiate DIC from hepatic coagulopathy.

Some drugs should be avoided in patients with cirrhosis. Nonsteroidal anti-inflammatory drugs cause a decrease in renal perfusion. In addition, iodinated contrast agents given for computed tomography or other imaging studies may cause renal vasoconstriction when administered intravascularly. Nitrovasodilators or substances inhibiting angiotensin II action may be used to treat portal hypertension but they shunt blood away from the kidneys and may include renal dysfunction in patients with cirrhosis and ascites. They should not ne used by emergency physicians because they may precipitate prerenal failure.

Finally, 33 to 46% of patients with cirrhosis have gallstones, a higher incidence than in the general population. Keep this in mind, especially when patients present with abdominal pain. Traditional laboratory results, such as liver function test, may not be helpful in delineating this diagnosis. If gallstones are strongly suspected, an abdominal ultrasound should be performed.

Variceal bleeding: most feared complication. Variceal bleeding is one of seven unique complications that may occur with cirrhosis. The others are spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal syndrome, cirrhotic cardiomyopathy, hepatopulmonary syndrome, and portopulmonary hepertension.

Patients can lose massive amounts of dlood rapidly with variceal bleeding, making it the cirrhosis complication physicians fear most. The situation is further complicated by impared platelet function and coagulopathy. About 50% of patients with cirrhosis develop varices.

Once varices have been identified, profilaxis with40 mg of oral propranolol twice a day is recommended. If propranolol is contraindicated or not tolerated 20 mg of oral isosorbid mononitrate twice a day may be used, but patients must be monitored closely for renal failure. Beta blockers should never be started during acute bleeding in patients with cirrhosis.

When patients present to the emergency department with variceal bleeding the mainstays of therapy are correcting hypovolemia, achieving hemostasis, and preventing complications. Upper gastrointestinal hemorrhage from esophageal varices may be massive and patients may have trouble protecting their airway. If airway compromise seems likely early intubation is recommended.

There is no mortality benefit in using both medical and endoscopic management for an initial bleeding. Each of these therapies reduces the risk of bleeding by 40-50%. Endoscopy is a reasonable choice for the first rebleeding but surgical placement of a transjugular intrahepatic portosystemic shunt (TIPS) must be strongly considered.

There is a significant decrease in mortality when antibiotics are implemented early in the course of variceal hemorrhage so prophylaxis with norfloxacin should begin as soon as possible.

 

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