Alcoholism

Alcoholism is common, serious, and expensive. Physicians encounter alcohol-related cirrhosis, cardiomyopathy, pancreatitis, and gastrointestinal bleeding, as well as intoxication and alcohol addiction, on a daily basis. Alcoholism is also associated with many cancers. Wernicke encephalopathy and Korsakoff psychosis are also important causes of chronic disability as well as dementia. Fetal alcohol syndrome is a leading cause of mental retardation. In addition, accidents (especially automobile), depression, dementia, suicide, and homicide are important consequences of alcoholism.
Alcohol-related diseases are discussed in separate articles. The focus of this article is screening, diagnosis, treatment, and new research findings on the natural history and heritability of alcoholism.

Pathophysiology
Alcohol affects virtually every organ system in the body and, in high doses, can cause coma and death. It affects several neurotransmitter systems in the brain, including opiates, GABA, glutamate, serotonin, and dopamine. Increased opiate levels help explain the euphoric effect of alcohol, while its effects on GABA cause anxiolytic and sedative effects.
Alcohol inhibits the receptor for glutamate. Long-term ingestion results in the synthesis of more glutamate receptors. When alcohol is withdrawn, the central nervous system experiences increased excitability. Persons who abuse alcohol over the long term are more prone to alcohol withdrawal syndrome than persons who have been drinking for only short periods. Brain excitability caused by long-term alcohol ingestion can lead to cell death and cerebellar degeneration, Wernicke-Korsakoff syndrome, tremors, alcoholic hallucinosis, delirium tremens, and withdrawal seizures. Opiate receptors are increased in the brains of recently abstinent alcoholic patients, and the number of receptors correlates with cravings for alcohol.
Frequency
United States
These statistics are based on the US National Longitudinal Alcohol Epidemiologic Study. Alcoholism is prevalent in 20% of adult hospital inpatients. One in 6 patients in community-based primary care practices had problem drinking. The following apply to the US adult population:
Current drinkers - 44%
Former drinkers - 22%
Lifetime abstainers - 34%
Abuse and dependency in the past year - 7.5-9.5%
Lifetime prevalence - 13.5-23.5%
Alcoholism is slightly more common in lower income and less educated groups. Vaillant studied the natural history of alcoholism and the differences between college-educated and inner-city alcoholic persons. He followed 2 cohorts (over 400 patients) of alcoholic patients over many years.1
According to Vaillant's research, inner-city men began problem drinking approximately 10 years earlier than college graduates (age 25-30 y vs age 40-45 y). Inner-city men were more likely to be abstinent from alcohol consumption than college graduates (30% vs 10%) but more likely to die from drinking (30% vs 15%). A large percentage of college graduates alternated between controlled drinking and alcohol abuse for many years. Returning to controlled drinking from alcohol abuse is uncommon, no more than 10%; however, this figure is likely to be high because it was obtained from self-reported data. Mortality in both groups was related strongly to smoking. Abstinence for less than 5-6 years did not predict continued abstinence (41% of men abstinent for 2 y relapsed).

International
The World Health Organization examined mental disorders in primary care offices and found that alcohol dependence or harmful use was present in 6% of patients. In Britain, 1 in 3 patients in community-based primary care practices had at-risk drinking behavior. Alcoholism is more common in France than it is in Italy, despite virtually identical per capita alcohol consumption.
Mortality/Morbidity
Alcohol use is the third leading cause of preventable death in the United States (after smoking and obesity). Annually, 85,000 deaths are attributable to alcohol at a cost of $185 billion.2, 3 Almost half of these deaths are attributable to alcohol-related injury.
Four percent of the global burden of disease is attributable to alcohol. This figure rises to 7% in North America, Europe, Japan, and Australia and to 12% in Eastern Europe and Central Asia. Worldwide, alcohol is responsible for a percentage of a number of conditions, as follows:
Cirrhosis - 32%
Motor vehicle accidents - 20%
Mouth and oropharyngeal cancers - 19%
Esophageal cancer - 29%
Liver cancer - 25%
Breast cancer - 7%
Homicide - 24%
Suicide - 11%
Hemorrhagic stroke - 10%
Below are the statistically significant relative risks from a study by the American Cancer Society for men and women who consume 4 or more drinks daily. A drink is defined as one 12-oz beer, one 4- to 5-oz glass of wine, or one mixed drink containing 1.5 oz of spirits (80 proof). The relative risk for the noted maladies with consumption of 4 or more drinks daily is as follows:
Cirrhosis - For men, 7.5; for women, 4.8
Injuries - For men, 1.3
Ear, nose, and throat cancer; esophagus cancer; liver cancer - For men, 2.8; for women, 3
Moderate alcohol consumption (1-2 drinks/d) reduces the risk of cardiovascular disease in men and women by approximately 30%.4, 5, 6 The effect of heavy alcohol consumption on the risk of cardiovascular disease varies in different studies. The person's drinking pattern appears to have an effect on cardiovascular disease. Drinking with meals may reduce the risk, while binge drinking increases risk (even in otherwise moderate drinkers).
Moderate alcohol consumption appears to increase the risk of breast cancer in women. Total mortality is reduced with moderate alcohol consumption but not with heavy alcohol consumption; the cardiovascular benefit is offset by cirrhosis, cancer, and injuries. The amount of alcohol associated with the lowest mortality appears to be 2 drinks per day in men and 1 drink or fewer per day in women. Moderate alcohol consumption reduces the risk of developing diabetes, but heavy alcohol consumption may increase the risk. The cardiovascular benefit becomes important in men older than 40 years and in women older than 50 years. The risk of hypertension is increased with 3 or more drinks daily.
No benefits are noted in people at low risk for coronary disease (men <40 name="refsrc7">7 This effect was exacerbated by binge drinking.
Of men aged 18-25 years, 60% binge drink. (Binge drinking is defined as 5 alcoholic drinks for men [4 for women] in a row.) Binge drinking significantly increases the risk of injury and contracting sexually transmitted diseases. Women who binge drink at this age are at higher risk of becoming pregnant and potentially harming an unborn child. (Any amount of alcohol consumption during pregnancy is risky.)
More than three quarters of all foster children in the United States are children of alcohol- or drug-dependent parents. From 60-70% of reported domestic violence incidents involve alcohol. Half of all violent crime is alcohol or drug related.
Overall, morbidity and mortality are related strongly to smoking, and people who drink heavily are less likely to quit smoking. Additionally, persons who begin smoking early are more likely to develop problems with alcohol.
With regard to pregnancy, fetal alcohol syndrome is the leading known cause of mental retardation (1 in 1000 births). More than 2000 infants annually are born with this condition in the United States. Alcohol-related birth defects and neurodevelopmental problems are estimated to be 3 times higher. Even small amounts of alcohol consumption may be risky in pregnancy. A 2001 study by Sood et al reported that children aged 6-7 years whose mothers consumed alcohol even in small amounts had more behavioral problems.8 In a study from 2003, Baer et al showed that moderate alcohol consumption while pregnant resulted in a higher incidence of offspring problem drinking at age 21 years, even after controlling for family history and other environmental factors.9 All women who are pregnant or planning to become pregnant should avoid alcohol.

Race
The 2 largest studies, the US National Comorbidity Survey and the Epidemiologic Catchment Area Survey, both showed a lower prevalence of alcoholism in African Americans than in white Americans. The prevalence was equal or higher in Hispanic Americans compared with white Americans.
Studies of Native Americans and Asian Americans are smaller. These studies indicate the prevalence of alcoholism is higher in Native Americans and lower in Asian Americans when compared with white Americans.
Sex
Alcoholism is at least twice as prevalent in men as it is in women. In the National Comorbidity Survey, it was 2.5 times more prevalent in men than in women. The lifetime prevalence was 20% in men and 8% in women. For alcohol abuse or dependence in the past year, the rates were 10% for men and 4% for women.
Women do not metabolize alcohol as efficiently as men. Hazardous drinking (not alcoholism) is greater than 1 drink daily for women and greater than 2 drinks daily for men.
Problem drinking in women is much less common than it is in men, and the typical onset of problem drinking in females occurs later than in males. However, progression is more rapid, and females usually enter treatment earlier than males. Women more commonly combine alcohol with prescription drugs of abuse than do males. Women living with substance-abusing men are at high risk.
Alcohol problems are less likely to be recognized in women, and women with alcohol problems are less likely to be treated. This may be because women are less likely than men to have job, financial, or legal troubles as a result of drinking.
Age
The prevalence of alcoholism declines with increasing age. The prevalence in elderly populations is unclear but is probably approximately 3%. A study of the US Medicare population found that alcohol-related hospitalizations were as common as hospitalizations for myocardial infarction.
Among older patients with alcoholism, from one third to one half develop alcoholism after age 60 years. This group is harder to recognize. A recent population-based study found that problem drinking (>3 drinks/d) was observed in 9% of older men and in 2% of older women. Alcohol levels are higher in elderly patients for a given amount of alcohol consumed than in younger patients.

Read for more HERE

Colon Cancer, Adenocarcinoma

Colorectal cancer is the third most common cancer in both men and women in the United States. Risk factors include age, a diet rich in fat and cholesterol, inflammatory bowel disease (especially ulcerative colitis), and genetic predisposition, including hereditary polyposis and nonpolyposis syndromes.
If detected early, colorectal cancer is curable by surgery. Adjuvant chemotherapy can prolong survival in disease that has reached the lymph nodes. Both systemic and locoregional chemotherapy (eg, intrahepatic intraarterial chemotherapy for liver metastases) have a role in patients with metastatic colon cancer. Radiotherapy is used in cases of rectal cancer to reduce the risk of local recurrence.
Long-term survival correlates with stage of disease in colorectal cancer. Progress has been made in understanding the molecular basis of colorectal cancer predisposition and progression. Efforts are underway to develop better screening strategies, chemopreventive approaches, and novel therapies to improve patient survival rates and to minimize toxicity. Despite all efforts, colorectal cancer remains the third leading cause of death from cancer in the United States.
Recent advances have included the development of orally available forms of 5-fluorouracil (5-FU) and the demonstration that anti-vascular endothelial growth factor (VEGF) therapy with bevacizumab prolongs survival in advanced colorectal cancer when combined with irinotecan, 5-FU, and leucovorin.
Pathophysiology
The vast majority of colorectal cancers are adenocarcinomas, which arise from preexisting adenomatous polyps that develop in the normal colonic mucosa. This adenoma-carcinoma sequence is a well-characterized clinical and histopathologic series of events with which discrete molecular genetic alterations have been associated.
Pioneering work by Bert Vogelstein and colleagues over the last 20 years has identified a number of critically important genetic alterations that contribute, through their multiplicity over many years, to the eventual development of colorectal cancer. The earliest event appears to involve the APC (adenomatous polyposis coli) gene, which is mutated in individuals affected by familial adenomatous polyposis (FAP). The protein encoded by the APC gene targets the degradation of beta-catenin, a protein component of a transcriptional complex that activates growth-promoting oncogenes, such as cyclin D1 or c-myc. APC mutations are very common in sporadic colorectal cancer, and beta-catenin mutations have also been identified.
DNA methylation changes are a relatively early event and have been detected at the polyp stage. Colorectal cancers and polyps have an imbalance in genomic DNA methylation, with global hypomethylation and regional hypermethylation. Hypomethylation can lead to oncogene activation, whereas hypermethylation can lead to silencing of tumor suppressor genes. ras gene mutations are observed commonly in larger polyps but not smaller polyps, suggesting a role for this oncogene in polyp growth.
Chromosome arm 18q deletions are a later event associated with cancer development. These deletions likely involve the targets DPC4 (a gene deleted in pancreatic cancer and involved in the transforming growth factor [TGF]-beta growth-inhibitory signaling pathway) and DCC (a gene frequently deleted in colon cancer). Chromosome arm 17p losses and tumor suppressor p53 mutations are common late events in colon cancer. Bcl2 overexpression leading to inhibition of cell death signaling has been observed as a relatively early event in colorectal cancer development. 18q deletions detected in Dukes stage B colon cancers have been associated with an increased risk of recurrence following surgery, and studies are in progress to determine whether patients with 18q deletions might benefit from more aggressive adjuvant chemotherapy.
Another predisposing condition is hereditary nonpolyposis colon cancer, in which affected individuals inherit a mutation in one of several genes involved in DNA mismatch repair, including MSH2, MLH1, and PMS2. ras gene mutations have been detected in the stool of patients with colorectal cancer and may in the future be useful in early diagnosis.
Although the use of nonsteroidal anti-inflammatory agents, such as sulindac, have been shown to affect the number of polyps, this has not translated to a clinical impact on cancer prevention.
Frequency
United States
The American Cancer Society estimates that about 104,950 new cases of colon cancer and 40,340 new cases of rectal cancer will be reported in 2005 in the United States. Combined, the 2 cancer types will cause about 56,290 deaths.
International
According to the World Health Organization's April 2003 report on global cancer rates more than 940,000 new cases of colorectal cancer and nearly 500,000 deaths are reported worldwide each year.
Mortality/Morbidity
The overall 5-year survival rate from colon cancer is approximately 60%, and nearly 60,000 people die of the disease each year in the United States. The 5-year survival rate is different for each stage (see Staging); the staging classification for colon cancer can predict prognosis well. For Dukes stage A tumors involving only the mucosa, the 5-year survival rate exceeds 90%, whereas for metastatic colon cancer, the 5-year survival rate is about 5%. For Dukes stage B colon cancers, the 5-year survival rate is greater than 70% and can be greater than 80% if the tumor does not penetrate the muscularis mucosa. Once the tumor has spread to the lymph nodes (ie, Dukes stage C), the 5-year survival rate usually is less than 60%.
Race
Recent data demonstrate a decrease in incidence rates of colorectal carcinoma in whites since the mid 1980s, particularly for the distal colon and rectum. Proximal colon carcinoma rates in blacks are considerably higher than in whites and continue to increase, whereas rates in whites show signs of decline.
Sex
The frequency of colon cancer is essentially the same among men and women.
Age
Age is a well-known risk factor for colon cancer, and risk begins to rise in people older than 40 years. Age is a risk factor because a number of rare genetic alterations are believed to occur within the somatic cells of the colonic epithelium over years, ultimately leading to the development of colon cancer in older individuals. Individuals affected by one of the well-known familial predispositions to colon cancer are much more likely to develop cancer at a young age. For example, individuals with familial adenomatous polyposis have a 100% chance of developing colon cancer unless their colon is removed surgically, usually when they are aged 20-30 years.
-->
');
//-->

CLINICAL
Section 3 of 10
Authors and Editors
Introduction
Clinical
Differentials
Workup
Treatment
Medication
Follow-up
Miscellaneous
References
History
Colon cancer often is found by screening and may be completely asymptomatic. Approximately 50% of patients present with abdominal pain, 35% with altered bowel habits, 30% with occult bleeding, and 15% with intestinal obstruction. Right-sided colon cancers tend to be larger and more likely to bleed, whereas left-sided tumors tend to be smaller and more likely to be obstructing. Obtain a family history of colon cancer, familial polyposis, or ulcerative colitis. Consider the possibility of cancer of the colon in patients with a fever of unknown origin and in patients with polymyositis.
Physical
The physical examination findings may be completely normal, especially in early stage colorectal cancer, or general or specific findings due to progression of the disease may be present. These may include weight loss, cachexia, abdominal discomfort or tenderness, liver mass, abdominal distention, ascites, rectal mass, rectal bleeding, or occult blood on rectal examination.
Causes
A number of risk factors have been associated with colon cancer. Colonic polyps, which occur with increasing age, represent a risk for colon cancer development. A study considering the clinical evidence for the adenoma-carcinoma sequence recently concluded that adenomas probably are precursors of carcinomas, but the ultimate effect of removing polyps on reducing cancer incidence in the population remains unknown.
Genetics is a very important risk factor for development of colorectal cancer. Familial polyposis, in which patients inherit a mutant copy of the APC tumor suppressor gene, is rare but confers very high risk. Familial nonpolyposis colon cancer, which accounts for 1-5% of colon cancers, develops because of inherited mutations in DNA mismatch repair genes.
Alcohol consumption is a risk factor for gastrointestinal cancer, including colon cancer. Increasing age and a lower intake of total folate have been associated with mutations of the Ki-ras oncogene, which are found commonly in colorectal cancer. Diet, and in particular fat content of diet, has been associated with increased risk of colon cancer. Animal studies have found that dietary beef induces and dietary rye bran prevents formation of intestinal polyps. Several studies have suggested that red meat and processed meats, through the action of heme, predispose to colon cancer by enhancing formation of N-nitrosocompounds, which result in DNA damage. One study suggested that obesity, rather than fat intake per se, predisposed to colon cancers induced in animals by exposure to the carcinogen azoxymethane.
The evidence is weak that soy food or isoflavones in the diet protect a person from colon cancer. Exercise is believed to reduce the risk of colon cancer. The risk of colon cancer may be decreased among women who recently used postmenopausal hormone replacement therapy. Women who are postmenopausal and who have never used hormone replacement therapy have a higher risk of colon, but not rectal, cancer than do women who are premenopausal and of the same age, sociocultural class, and dietary habits. Apparently, no association exists between frequency of bowel movement or laxative use and risk of colon cancer. Some data associate calcium intake and risk of colon cancer. A statistically significant association exists between Helicobacter exposure and colonic polyps.
Tobacco smoking is associated with a higher risk of colon cancer, which appears to be mediated by induction of 5-lipoxygenase–associated angiogenic pathways.

Read more HERE

Corpus Luteum Rupture

Ruptured corpus luteum is a common phenomenon with presentation ranging from no symptoms to symptoms mimicking an acute abdomen. Sequelae vary. Resolution may be spontaneous (most often); intraperitoneal hemorrhage and death may occur. Although most patients require only observation, some need laparoscopy or laparotomy to achieve hemostasis.
Pathophysiology
Each month, a mature ovarian follicle ruptures, releasing an ovum so the process of fertilization can begin. Occasionally, this rupture site may bleed, causing abdominal pain and signs of hemorrhage. The etiology of this increased bleeding is unknown, although abdominal trauma and anticoagulation treatments may increase the risk.
Frequency
United States
Occurrence is unknown but is likely quite frequent and without symptoms.
International
Occurrence is unknown but is likely quite frequent and without symptoms.
Mortality/Morbidity
Although circulatory collapse, hemorrhagic shock, disseminated intravascular coagulation (DIC), and death have been reported, these are rare. Most cases are self-limiting, with abdominal pain relieved with analgesics.
Race
No differences in frequency are reported by race or socioeconomic standing.
Sex
Ruptured corpus luteum occurs only in females.
Age
The condition most commonly occurs in women aged 18-35 years (peak reproductive years).

Read more HERE

Social Phobia and Selective Mutism

Social phobia (social anxiety disorder) is the third most common mental health disorder after major depression and substance abuse, affecting approximately 10 million Americans, including children and adults. This disorder is defined by marked and persistent fear of social or performance situations in which embarrassment may occur; exposure to the social or performance situation almost always causes an anxiety reaction such as a situationally bound or situationally predisposed panic attack.
The anxiety reaction is not due to psychosis; individuals are able to recognize their fears as excessive and unreasonable. However, the ability to fully comprehend that the reaction is out of proportion to the precipitant may be less complete in children and may depend on their cognitive-developmental level of functioning.
The person's level of functioning (eg, ability to complete required educational, social, or family tasks) is significantly impaired, and the person may experience significant emotional distress (eg, dread, avoidance) as a response to social or performance situations. By definition, social phobia must persist for at least 6 months (in persons <18 y), must not be due to the direct physiological effects of a substance (eg, caffeine) or a general medical condition, and must not be better accounted for by another mental health disorder.
Often, social phobia can coexist with, or be the precursor to, agoraphobia. Agoraphobia is a specific phobia in which the individual fears being in crowded places. People with agoraphobia often become homebound.
Selective mutism is a disorder primarily affecting children, with some adolescents and adults who continue to experience an inability to speak in public. This inability is generally most disabling at school, as the child cannot be assertive and speak when called on by teachers. In adults, functional impairment occurs when public speaking or lecturing are required in one's vocation.
Formerly, selective mutism was called elective mutism in the Diagnostic and Statistical Manual of Mental Health Disorders, Third Edition (DSM-III), which was reflective of a previous view that the child intentionally refused to speak with others who are outside of the immediate family group. Often, the child with selective mutism designates a friend or close family member to serve as an interpreter of communication and whispers in that person's ear, so that communication occurs with the designated person as intermediary.
document.write('')

document.write('')


Pathophysiology
Serotonin pathways may be involved in the mediation of the anxious and obsessive qualities of both social phobia and selective mutism. This theory is reinforced by animal models of phobic behavior and by response to commonly prescribed medications such as selective serotonin reuptake inhibitors (SSRIs), such as paroxetine, sertraline, or older heterocyclic-type antidepressants, such as Anafranil (clomipramine).
Frequency
United States
Social phobia is the third most common mental health disorder after depression. Lifetime prevalence ranges from 3-13%. Selective mutism is seen in fewer than 1% of children observed in mental health settings.
Mortality/Morbidity
No mortality occurs except with associated major depression resulting in suicide or reaction to medication treatment (sudden cardiac death with imipramine or clonidine) or adverse reaction such as newly onset suicidality to SSRIs or other antidepressants. A high morbidity rate is observed, with many missed school or workdays; the child often develops associated school refusal because of the anxiety associated with being asked to speak in class.
Age
Onset of social phobia may occur as early as school age but generally occurs by mid adolescence following a childhood history of social inhibition or excessive shyness. Often, onset is abrupt, occurring after a stressor or humiliating social experience.
Onset of selective mutism is typically when a child first attends school (either kindergarten or preschool) and, like social phobia, is often associated with an initial negative school experience, such as a stressor or humiliating social experience.

Read more HERE

Achilles Tendon Rupture

Ruptures of the Achilles tendon most commonly occur spontaneously in healthy, young, active individuals who are aged 30-50 years and have no antecedent history of calf or heel pain. Unlike tears or ruptures at the musculotendinous junction of the Achilles tendon (tennis leg), Achilles tendon ruptures are located within the tendon substance itself, approximately 1-2 inches proximal to its insertion into the calcaneus. Poor conditioning, advanced age, and overexertion are risk factors for this injury. However, the common precipitating event is a sudden eccentric force applied to a dorsiflexed foot. Ruptures of the Achilles tendon also may occur as the result of direct trauma or as the end result following Achilles peritenonitis with or without tendinosis.
Achilles tendon pathology, other than rupture, can be classified into a spectrum of injuries including peritenonitis, tendinosis, and peritenonitis with tendinosis. Patients with peritenonitis experience localized burning pain along the tendon during or following activities; as the disease progresses, onset of pain may occur earlier during activities, with decreased activity level, or even at rest. Tendinosis usually is comprised of an asymptomatic, noninflammatory, degenerative disease process (mucoid degeneration); patients with tendinosis may complain of a sensation of fullness or a nodule in the back of the leg. Peritenonitis with tendinosis is comprised of activity-related pain, diffuse swelling of the tendon sheath, and presence of nodules. Treatment of these entities is not discussed in this article.
Frequency
United States
The true prevalence of Achilles tendon rupture is unknown, although it occurs more commonly in men who are in their third to fifth decade of life and who participate in recreational activities.

Functional Anatomy
The Achilles tendon, coined after the mythologic Greek god, is the largest and strongest tendon in the human body. The Achilles tendon is formed from the tendinous contributions of the gastrocnemius and soleus muscles coalescing approximately 15 cm proximal to its insertion. Along its course in the posterior aspect of the leg, the tendon spirals 30-150° until it inserts into the calcaneal tuberosity. The gliding ability of the Achilles tendon is aided by a thin sheath of paratenon rather than a true synovial sheath. The sheath of paratenon is composed of a visceral layer and a parietal layer.
The blood supply of the Achilles tendon arises from its osseous insertion, its musculotendinous junction, and multiple infiltrating mesosternal vessels, which cross the layers of the anterior paratenon. Various injection and nuclear medicine studies have demonstrated a paucity of mesosternal and intratendinous vessels 2-6 cm proximal to the heel insertion (ie, the watershed area). Due to the relative lack of blood supply in this area, the tendon is less resilient to repetitive microtrauma and has a higher tendency for irritation, degeneration, and rupture.
Sport Specific Biomechanics
The entire gastrocnemius-soleus musculotendinous unit spans the knee, tibiotalar (ankle), and talocalcaneal (subtalar) joints. Contracture of this complex flexes the knee, plantar flexes the ankle, and supinates the subtalar joint. The function of the gastrocnemius-soleus musculotendinous unit is necessary in running, jumping, toe standing, and stair-climbing activities because it forcefully plantar flexes the ankle. During running, forces 10 times the body weight have been measured within the tendon substance.

Read more HERE

Atrial Fibrillation

Background:
Atrial fibrillation (AF) is a common arrhythmia (see Image 1) and is a significant public health problem in the United States, affecting 2.2 million Americans and almost 5% of the population older than 69 years and 8% of the population older than 80 years. Thus, the prevalence of AF increases with advancing age. Data from the Framingham heart study show that AF is associated with a 1.5- to 1.9-fold higher risk of death, which may be due to thromboembolic stroke. While patients can be asymptomatic, many experience a wide variety of symptoms, including palpitations, dyspnea, fatigue, dizziness, angina, and congestive heart failure (CHF). In addition, the arrhythmia can be associated with hemodynamic dysfunction, tachycardia-induced cardiomyopathy, and systemic embolism.
Overall, approximately 15-25% of all strokes in the United States (75,000/y) can be attributed to AF. Known risk factors include male sex, valvular heart disease (rheumatic valvular disease), CHF, hypertension, and diabetes. Additional risk factors, such as advanced age and prior history of stroke, diabetes, and hypertension, place patients with preexisting AF at even higher risk for further comorbidities such as stroke. Patients with nonvalvular AF and risk factors have a 5-fold increased risk for stroke. Patients with rheumatic heart disease and AF have an even higher risk for stroke (17-fold). At least 4 large clinical trials have clearly demonstrated that anticoagulation with warfarin decreases the risk of stroke by 50-80%.
Given the frequency of these comorbidities, management can result in significant medical costs. Therapeutic goals include rate control, maintenance of sinus rhythm, and prevention of thromboembolism. Additionally, current practice and economic pressures force many physicians to reconsider outpatient treatment options.
Pathophysiology: Several classification schemas have been proposed for the study of AF, but none fully accounts for all aspects of AF. A number of different labels and nomenclature have been used to describe patterns of AF, including acute, chronic, paroxysmal, intermittent, and permanent. The vagaries of each of these definitions make comparing the results of studies assessing the magnitude and treatment of AF difficult.
Recently published guidelines from expert committees of the American College of Cardiology/American Heart Association and European Society of Cardiology on the treatment of patients with AF suggest that AF be classified into 3 patterns. These include a first detectable episode, irrespective of whether it is symptomatic or self-limited. Recurrent AF is considered to be present when a patient has 2 or more episodes of AF. If AF terminates spontaneously, then recurrent AF is designated as paroxysmal; if this arrhythmia becomes sustained, then AF is considered persistent (irrespective of whether AF is terminated with pharmacologic therapy or electrical cardioversion).
Persistent AF may be either the first presentation of AF or the result of recurrent episodes of paroxysmal AF. Patients with persistent AF also include patients with long-standing AF in whom cardioversion has not been indicated or attempted, often leading to permanent AF. Permanent AF is recognized as the accepted rhythm, and the only treatment goals are rate control and anticoagulation.
This classification schema pertains to cases that are not related to a reversible cause of AF (eg, thyrotoxicosis, electrolyte abnormalities, acute ethanol intoxication). The occurrence of AF secondary to acute myocardial infarction, cardiac surgery, pericarditis, pulmonary embolism, or acute pulmonary disease is considered separately because in these situations, AF is less likely to recur once the precipitating condition has been resolved and adequately treated.
Some patients with paroxysmal AF, typically younger patients, have been found to have distinct electrically active foci within their pulmonary veins. These patients generally have many atrial premature beats noted on Holter monitoring. Isolation or elimination of these foci can lead to elimination of the trigger for paroxysms of AF.
Patients can also have AF as a secondary arrhythmia associated with cardiac disease that affects the atria (eg, CHF, hypertensive heart disease, rheumatic heart disease, coronary artery disease [CAD]). These patients tend to be older, and AF is more likely to be chronic. Paroxysmal AF may progress to chronic AF, and aggressive attempts to restore and maintain sinus rhythm may prevent comorbidities associated with AF.
Persistent AF with an uncontrolled, rapid ventricular heart rate response can cause a dilated cardiomyopathy and can lead to electrical remodeling in the atria (atrial cardiomyopathy). Therapy, such as drugs or atrioventricular (AV) nodal ablation and permanent pacemaker implantation, to control the ventricular rate can improve left ventricular (LV) function and improve quality-of-life scores.
New developments aimed at curing AF are being actively explored. By reducing the critical mass required to sustain AF with either surgical or catheter-based compartmentalization of the atria (ie, MAZE procedure), fibrillatory wavelets collide with fixed anatomic obstacles, such as suture lines or complete lines of ablation, thus eliminating or reducing the chance of chronic AF. Some patients with focal origins of their AF also may be candidates for catheter ablation. Still, much remains to be accomplished before either of these procedures is appropriate for primary treatment.
Frequency:
In the US: AF affects 2.2 million Americans. It can occur in the absence of comorbidities, as it does in 10-15% of individuals (lone AF); however, AF is associated more frequently with hypertension; organic heart disease; CHF; ischemic heart disease; and valvular, dilated, hypertrophic, restrictive, and congenital cardiomyopathies. Paroxysmal AF is commonly associated with cardiac surgery, pulmonary disease, thyrotoxicosis, acute ethanol intoxication, and electrolyte imbalance. Given the almost epidemic proportions of patients with AF, clinicians must be aware of the multiple mechanisms and presentations and then correct the underlying etiology, if possible. For example, a logical decision may be to correct an overactive thyroid gland before attempting cardioversion.
Mortality/Morbidity: AF is associated with increased morbidity. The static nature of blood flow during AF can lead to the development of thrombus, most commonly in the left atrial appendage. Dislodgement of clot can lead to embolic phenomena, including stroke. Thus, anticoagulation remains the primary focus in appropriate patient populations. A target international normalized ratio of 2-3 limits the risks of hemorrhage while providing protection against the formation of thrombus.
Age:
AF is strongly age-dependent, affecting 4% of individuals older than 60 years and 8% of persons older than 80 years. The rate of ischemic stroke among elderly patients not treated with warfarin averages approximately 5% per year.

Read more HERE

Suprapubic Aspiration

Suprapubic aspiration and catheterization is an easily performed emergency department procedure that is associated with minimal complications. Huze and Beeson1 first published this practice in 1956 as an alternative to more traditional methods of obtaining urine for analysis and culture. Their findings suggested that suprapubic catheterization and aspiration was superior to clean-catch or transurethral (via catheterization) collection of bladder urine for bacteriologic study. Since then, the indications for suprapubic catheterization and aspiration have expanded to acute and chronic conditions.

Indication:

Urinary retention (eg, prostate hypertrophy or cancer, gynecologic malignancy, spinal cord injury)
Urinalysis or urine culture in neonates or children younger than 2 years
Phimosis
Chronic infection of the urethra or periurethral glands
Urethral stricture
Urethral trauma

Read more HERE