Cardiac Arrest Resuscitation

foot cast used in Toe Fractures

Amyotrophic lateral sclerosis The disorder causes muscle weakness and atrophy throughout the body caused by degeneration of the upper and lower motor neurons. Unable to function, the muscles weaken and atrophy. Affected individuals may ultimately lose the ability to initiate and control all voluntary movement, although bladder and bowel sphincters and the muscles responsible for eye movement are usually, but not always, spared. Cognitive function is generally spared for most patients although some (~5%) also have frontotemporal dementia.A higher proportion of patients (~30-50%) also have more subtle cognitive changes which may go unnoticed but are revealed by detailed neuropsychological testing. Sensory nerves and the autonomic nervous system, which controls functions like sweating, are generally unaffected but may be involved for some patients. The earliest symptoms of ALS are typically obvious weakness and/or muscle atrophy. Other presenting symptoms include muscle fasciculation (twitching), cramping, or stiffness of affected muscles; muscle weakness affecting an arm or a leg; and/or slurred and nasal speech. The parts of the body affected by early symptoms of ALS depend on which motor neurons in the body are damaged first. About 75% of people contracting the disease experience "limb onset" ALS i.e. first symptoms in the arms ("upper limb", not to be confused with "upper motor neuron") or legs ("lower limb", not to be confused with "lower motor neuron"). Patients with the leg onset form may experience awkwardness when walking or running or notice that they are tripping or stumbling, often with a "dropped foot" which drags along the ground. Arm-onset patients may experience difficulty with tasks requiring manual dexterity such as buttoning a shirt, writing, or turning a key in a lock. Occasionally, the symptoms remain confined to one limb for a long period of time or for the whole course of the illness; this is known as monomelic amyotrophy. About 25% of cases are "bulbar onset" ALS. These patients first notice difficulty speaking clearly or swallowing. Speech may become slurred, nasal in character, or quieter. Other symptoms include difficulty swallowing, and loss of tongue mobility. A smaller proportion of patients experience "respiratory onset" ALS where the intercostal muscles that support breathing are affected first. Regardless of the part of the body first affected by the disease, muscle weakness and atrophy spread to other parts of the body as the disease progresses. Patients experience increasing difficulty moving, swallowing (dysphagia), and speaking or forming words (dysarthria). Symptoms of upper motor neuron involvement include tight and stiff muscles (spasticity) and exaggerated reflexes (hyperreflexia) including an overactive gag reflex. An abnormal reflex commonly called Babinski's sign (the big toe extends upward and other toes spread out) also indicates upper motor neuron damage. Symptoms of lower motor neuron degeneration include muscle weakness and atrophy, muscle cramps, and fleeting twitches of muscles that can be seen under the skin (fasciculations). Around 15–45% of patients experience pseudobulbar affect, also known as "emotional lability", which consists of uncontrollable laughter, crying or smiling, attributable to degeneration of bulbar upper motor neurons resulting in exaggeration of motor expressions of emotion.

This video goes through a case study of a 40 year old patient getting breast reduction surgery in NYC by board certified plastic surgeon Carlin Vickery of 5th Avenue Surgery located in New York, NY. For more information on this procedure please call our office at (212) 288-9800. This content is intended for general information only and does not replace the need for personal advice from a qualified health professional.

A very funny song made by the staff of the Ob/Gyn Gangnam style

Inserting main port in laparoscopy

http://tratamiento-autismo.plus101.com
---Sintomas Del Autismo Cura Autismo. Más de la mitad de los niños del país que padecen autismo tienen sobrepeso, lo que los pone además en riesgo de sufrir diabetes, enfermedades cardiovasculares y problemas en los huesos y articulaciones. Esta estadística alarmante motivó a la experta en fitness Suzanne M. Gray a desarrollar una rutina de ejercicios que los padres pueden hacer con los pequeños con autismo. Gray ha pasado alrededor de 30 años desarrollando diferentes programas de acondicionamiento físico para niños con necesidades especiales y nos ofrece algunos valiosos consejos.

http://www.youtube.com/watch?v=RprDE2jxLeE
Sintomas Del Autismo Cura Autismo

http://www.youtube.com/user/ParaNinosAutistas
http://www.youtube.com/user/TerapiaParaAutismo
http://www.youtube.com/user/NinosConAutismo
http://www.youtube.com/user/AyudarUnNinoAutista
Sintomas Del Autismo Cura Autismo
Sintomas Del Autismo Autismo Cura
Sintomas Del Cura Autismo Autismo
Sintomas Del Cura Autismo Autismo
Sintomas Del Autismo Autismo Cura
Sintomas Del Autismo Cura Autismo
metodo aba autismo,
metodo aba para autistas,
metodo pecs autismo,
metodo teacch autismo,
metodo teacch para niños autistas,
mi hermano tiene autismo,
mi hijo autista,
mi hijo es autista,
mi hijo tiene autismo,
mms autismo,
musica para niños autistas,
musicoterapia autismo,
musicoterapia en el tratamiento del autismo,
musicoterapia y autismo,
nino autista,
nino con autismo,
ninos autista,
ninos autistas,
ninos con autismo,
ninos con hiperactividad,
niveles de autismo infantil

Perleche, Boqueras Remedios Caseros, Estomatitis Bucal, Comisura Labios, Para Labios Partidos
http://Queilitis-Angular.Good-Info.Co

¿Qué Es Y Cómo Se Trata La Queilitis Angular?

Perleche, queilosis, estomatitis, boqueras, son otras denominaciones con las que se conoce a la queilitis angular. Las comisuras de los labios presentan lesiones inflamatorias. Las grietas verticales a nivel de la piel pueden profundizarse y provocar ulceraciones, llagas, sangrados, infecciones, descamaciones, costras. Con ello, sobrevendrán las dificultades para hablar, para sonreír, para ingerir los alimentos y las bebidas.

http://Queilitis-Angular.Good-Info.Co

Para Más Información

http://queilitis-angular.good-info.co


Visita Nuestro Blog


http://labios-partidos.blogspot.com/


Subscribete A Nuestro Canal

https://www.youtube.com/watch?v=HHVdPoHdn0c


Perleche, Boqueras Remedios Caseros, Estomatitis Bucal, Comisura Labios, Para Labios Partidos, arrugas comisuras labios, remedios para llagas en la boca, llagas en la boca curar, labios partidos, estomatitis definicion, cómo curar llagas en la boca, ulceras bucales causas, estomatitis aftosa recidivante, tratamiento queilitis angular, como se curan las ulceras bucales, labios partidos en niños, remedios caseros para boqueras, infecciones labiales,

Causas De La Diabetes, Signos De La Diabetes, Complicaciones Agudas De La Diabetes, Diabetico

http://todo-sobre-la-diabetes.good-info.co

Remedios Naturales Para Controlar La Diabetes

No es un hecho desconocido que en la actualidad los casos de diabetes se hayan incrementado considerablemente debido a la alimentación de la vida moderna y al estilo de vida que llevan las personas.

La diabetes tipo 2 es una enfermedad que se relaciona profundamente con la alimentación y se caracteriza por un elevado nivel de azúcar en sangre.

Este tipo de diabetes se puede controlar perfectamente llevando un estilo de vida saludable y una alimentación apropiada.

Existen muchos remedios naturales por los que puedes optar para luchar contra la diabetes:

Se trata de un remedio natural muy sencillo de realizar y que te resultará de gran utilidad para combatir la diabetes.


como eliminar la diabetes en pocos dias de manera natural y para siempre haciendo click aqui:
http://todo-sobre-la-diabetes.good-info.co


Haga Clic En El Enlace De Abajo Para Comprobar Que Funciona
http://todo-sobre-la-diabetes.good-info.co


Suscríbete A Nuestro Canal


https://www.youtube.com/user/VivirConSalud1


https://www.youtube.com/watch?v=i89z59Oi7Bg

Causas De La Diabetes, Signos De La Diabetes, Complicaciones Agudas De La Diabetes, Diabetico,
tipos de diabetes que existen,
Causa De La Diabetes,
que provoca la diabetes,
que ocasiona la diabetes,
historia natural de la diabetes mellitus,
fisiopatologia del pie diabetico,
cuales son las causas de la diabetes,
como se detecta la diabetes,
como detectar la diabetes,
clasificacion de la diabetes,
federacion internacional de diabetes

Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills, and eventually the ability to carry out the simplest tasks. In most people with Alzheimer’s, symptoms first appear in their mid-60s. Estimates vary, but experts suggest that more than 5 million Americans may have Alzheimer’s. Alzheimer's disease is currently ranked as the sixth leading cause of death in the United States, but recent estimates indicate that the disorder may rank third, just behind heart disease and cancer, as a cause of death for older people. Alzheimer’s is the most common cause of dementia among older adults. Dementia is the loss of cognitive functioning—thinking, remembering, and reasoning—and behavioral abilities to such an extent that it interferes with a person’s daily life and activities. Dementia ranges in severity from the mildest stage, when it is just beginning to affect a person’s functioning, to the most severe stage, when the person must depend completely on others for basic activities of daily living. The causes of dementia can vary, depending on the types of brain changes that may be taking place. Other dementias include Lewy body dementia, frontotemporal disorders, and vascular dementia. It is common for people to have mixed dementia—a combination of two or more disorders, at least one of which is dementia. For example, some people have both Alzheimer's disease and vascular dementia. Alzheimer’s disease is named after Dr. Alois Alzheimer. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. Her symptoms included memory loss, language problems, and unpredictable behavior. After she died, he examined her brain and found many abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary, or tau, tangles). These plaques and tangles in the brain are still considered some of the main features of Alzheimer’s disease. Another feature is the loss of connections between nerve cells (neurons) in the brain. Neurons transmit messages between different parts of the brain, and from the brain to muscles and organs in the body.

The hepatitis E virus, responsible for major epidemics of viral hepatitis in subtropical and tropical countries, was cloned only 7 years ago.1 Hepatitis E was found to belong to the family of Caliciviridae, which includes the Norwalk virus—a common cause of gastroenteritis in humans—and consists of a single, plus-strand RNA genome of approximately 7.2 kb without an envelope (Fig. 1). The virus contains at least three open reading frames encoding viral proteins against which antibodies are made on exposure. These antibodies, especially those against the capsid protein derived from the second open reading frame2 and a protein of unknown function derived from the third open reading frame, are detected by currently available serologic assays. Retrospective studies on stored sera of past epidemics of viral hepatitis in Mexico, Africa, Afghanistan, Pakistan, India, Bangladesh, Burma, Nepal, and Borneo have revealed that all were caused by strains of hepatitis E. In addition, hepatitis E was found to be responsible for the hepatitis epidemic in the southern part of Xinjiang, China, in which 120,000 persons became infected between September 1986 and April 1988.3 Hepatitis E predominantly affects young adults (15 to 40 years old). The symptoms of hepatitis E are similar to those of hepatitis A. Frequently, a prodrome consisting of anorexia, nausea, low-grade fever, and right upper abdominal pain is present 3 to 7 days before jaundice develops. Aminotransferase levels peak (usually between 1,000 and 2,000 U/L) near the onset of symptoms; bilirubin levels (10 to 20 mg/dL) peak later. Jaundice usually resolves after 1 to 2 weeks. In about 10% of cases, the disease is fulminant—especially in pregnant women, among whom mortality rates as high as 20% due to hemorrhagic and thrombotic complications have been reported. No evidence has suggested that hepatitis E can cause chronic infection. Transmission is by the fecal-oral route, predominantly through fecally contaminated drinking water supplies. In addition, however, preliminary reports have suggested transmission of the hepatitis E virus through blood transfusions. Volunteer studies confirmed the presence of the virus in serum and feces before and during clinical disease.4 The virus is shed into feces approximately 1 week before symptoms develop. The incubation period varies from 2 to 9 weeks (mean duration, approximately 45 days). Until now, a few reports had described symptomatic hepatitis E acquired in Europe;5, 6 all patients with symptomatic hepatitis E in the United States were travelers returning from Mexico, Africa, or the Far East, in whom hepatitis E developed after their return home.7 In this issue of the Mayo Clinic Proceedings (pages 1133 to 1136), Kwo and associates describe a case of hepatitis E in a man who had not left the United States during the previous 10 years. Specific serologic tests for hepatitis E virus IgG (enzyme immunoassays and a fluorescent antibody blocking assay) and IgM8 (US strain-specific enzyme-linked immunosorbent assay with use of synthetic polypeptides deduced from the viral genome, as shown in Figure 1), developed at Abbott Laboratories (IgG and IgM) as well as at the Centers for Disease Control and Prevention (IgG), were used to prove that the patient indeed had acute hepatitis E. Researchers at Abbott Laboratories have prepared a report that describes most of the viral genome in this patient (Fig. I).8 Their results are interesting because this strain from the United States differs considerably from hepatitis E strains isolated in Mexico, Burma, Pakistan, or China. Furthermore, the sequence of the US strain is highly homologous (98% and 94% homology at the amino acid level to the second and third open reading frames, respectively) to a recently isolated hepatitis E strain from American swine.9 This finding suggests that, in the United States, hepatitis E is a zoonosis with the swine population as one of its hosts. This relationship would confirm earlier studies in Asia, where swine were also found to carry variants of the hepatitis E virus.10 Why are these two recent discoveries important for medicine in the United States? First, other sporadic, locally acquired cases of acute hepatitis may be caused by hepatitis E. Second, these back-to-back discoveries strongly suggest that a common natural host for hepatitis E is present in countries with more moderate climates. Because swine do not seem to experience any symptoms associated with infection and because symptoms in humans can be minor or absent, we now may also have an explanation for the 1 to 2% of positive hepatitis E serologic results in blood donors in the United States,11 Netherlands,12 and Italy,6 countries with large swine staples. Clearly, more research needs to be done to confirm this hypothesis. Third, in countries with more moderate climates, hepatitis E may often result in a subclinical infection. Is this variation in manifestation due to less virulent strains, and do sequence variations determine virulence? Fourth, swine may be used as an animal model for study of the disease as well as vaccine development.

http://hidradenitis-suppurativa-cure.good-info.co/ Hidradenitis Suppurativa Cure, How To Treat Hidradenitis Suppurativa, Axillary Hidradenitis Suppurat Free From Hidradenitis Suppurativa Today If you are frustrated and embarrassed by constant Hidradenitis Suppurativa, no matter what you've tried, and if you’re fed up with Drugs, Creams, And Herbs, then you need to see this. You are about to discover the most effective 100% natural and safe solution that has been proven to make you live a free life. This is not like anything you've seen before. This is the same effective formula that helped me end my Hidradenitis Suppurativa in just few days. Too many health products have existed – and still do – and although many sound sweet, they end up wasting your precious time. And the result? About 95% of people who tried to put an end to their Hidradenitis Suppurativa crashed and burned big time! They either experience dangerous side effects, or they don’t actually achieve their desired results. But because you are ready to take action now and try this method, you’re on your way to saying goodbye to Hidradenitis Suppurativa which has only made your life nothing but miserable! reserve the right to take away this incredible secret at any moment. So you need to act fast now if you don’t want to be left out. click here. http://hidradenitis-suppurativa-cure.good-info.co/

In neonates, hypocalcemia is more likely to occur in infants born of diabetic or preeclamptic mothers. Hypocalcemia also may occur in infants born to mothers with hyperparathyroidism. Clinically evident hypocalcemia generally presents in milder forms and is usually the result of a chronic disease state. In emergency department patients, chronic or subacute complaints secondary to mild or moderate hypocalcemia are more likely to be a chief complaint than severe symptomatic hypocalcemia. Once laboratory results demonstrate hypocalcemia, the first question is whether the hypocalcemia is true—that is, whether it is representative of a decrease in ionized calcium. The presence of chronic diarrhea or intestinal disease (eg, Crohn disease, sprue, chronic pancreatitis) suggests the possibility of hypocalcemia due to malabsorption of calcium and/or vitamin D. The patient's past medical history should be explored for pancreatitis, anxiety disorders, renal or liver failure, gastrointestinal disorders, and hyperthyroidism or hyperparathyroidism. Previous neck surgery suggests hypoparathyroidism; a history of seizures suggests hypocalcemia secondary to anticonvulsants. The patient may have a recent history of thyroid, parathyroid, or bowel surgeries or recent neck trauma. The length of time that a disorder is present is an important clue. Hypoparathyroidism and pseudohypoparathyroidism are lifelong disorders. Instead, acute transient hypocalcemia may be associated with acute gastrointestinal illness, nutritional deficiency, or acute or chronic renal failure. In an elderly patient, a nutritional deficiency may be associated with a low intake of vitamin D. A history of alcoholism can help diagnose hypocalcemia due to magnesium deficiency, malabsorption, or chronic pancreatitis. Inquire about recent use of drugs associated with hypocalcemia, including the following: Radiocontrast Estrogen Loop diuretics Bisphosphonates Calcium supplements Antibiotics Antiepileptic drugs Cinacalcet Other considerations in the history include the following: Family history of hypocalcemia Low-calcium diet Lack of sun exposure

The increased risk of thrombosis in patients with active cancer has multiple causes. Acute thrombosis of the aorta is an exceedingly rare but potentially devastating complication in patients with cancer receiving cisplatin-based chemotherapy. Prompt diagnosis and definitive treatment are imperative to decrease morbidity and mortality. Early diagnosis is difficult because initial presentation is often nonspecific, requiring a high degree of clinical suspicion. We report 4 cases of acute thrombosis of the abdominal aorta in patients with cancer receiving cisplatin-based chemotherapy. We review the clinical aspects, recommended investigation, and treatment of this potentially fatal complication.

A traumatic brain injury (TBI) is defined as a blow or jolt to the head, or a penetrating head injury that disrupts the normal function of the brain. TBI can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue. Symptoms of a TBI can be mild, moderate or severe, depending on the extent of damage to the brain. Mild cases (mild traumatic brain injury, or mTBI) may result in a brief change in mental state or consciousness, while severe cases may result in extended periods of unconsciousness, coma or even death. The 4th International Conference on Concussion in Sport held in Zurich, Switzerland in 2012 defined concussion, a subset of mTBI, as the following: Concussion is the historical term representing low velocity injuries that cause brain ‘shaking’ resulting in clinical symptoms and that are not necessarily related to a pathological injury. Concussion is a subset of TBI and will be the term used in this document. It was also noted that the term commotio cerebri is often used in European and other countries. Minor revisions were made to the definition of concussion, which is defined as follows: Concussion is a brain injury and is defined as a complex pathophysiological process affecting the brain, induced by biomechanical forces. Several common features that incorporate clinical, pathologic and biomechanical injury constructs that may be utilised in defining the nature of a concussive head injury include: 1. Concussion may be caused either by a direct blow to the head, face, neck or elsewhere on the body with an "impulsive" force transmitted to the head. 2. Concussion typically results in the rapid onset of short-lived impairment of neurological function that resolves spontaneously. However, in some cases, symptoms and signs may evolve over a number of minutes to hours. 3. Concussion may result in neuropathological changes, but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury and, as such, no abnormality is seen on standard structural neuroimaging studies. 4. Concussion results in a graded set of clinical symptoms that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course. However, it is important to note that in some cases symptoms may be prolonged. To view peer reviewed literature related to sports concussions, the Sports Concussion Library can be found here. Incidence The U.S. Consumer Product Safety Commission (CPSC) tracks product-related injuries through its National Electronic Injury Surveillance System (NEISS). According to CPSC data, there were an estimated 446,788 sports-related head injuries treated at U.S. hospital emergency rooms in 2009. This number represents an increase of nearly 95,000 sports-related injuries from the prior year. All of the 20 sports noted below posted increases in the number of injuries treated in 2009, except for trampolines, which posted 52 fewer injuries in 2009. Sports that exhibited substantial increases from 2008 to 2009 included water sports (11,239 to 28,716*), cycling (70,802 to 85,389), baseball and softball (26,964 to 38,394) and basketball (27,583 to 34,692). *Four categories were tabulated by the AANS in the current analysis that were not reflected in the 2008 injury data analysis, but together, these account for only 1,397 injuries. The actual incidence of head injuries may potentially be much higher for two primary reasons. 1). In the 2009 report, the CPSC excluded estimates for product categories that yielded 1,200 injuries or less, those that had very small sample counts and those that were limited to a small geographic area of the country; 2). Many less severe head injuries are treated at physician's offices or immediate care centers, or are self-treated. Included in these statistics are not only the sports/recreational activities, but the equipment and apparel used in these activities. For example, swimming-related injuries include the activity as well as diving boards, equipment, flotation devices, pools and water slides. The following 20 sports/recreational activities represent the categories contributing to the highest number of estimated head injuries treated in U.S. hospital emergency rooms in 2009.

The preferred route of access for temporary transvenous pacing is the internal jugular vein followed by subclavian and femoral veins. However, all the major venous access sites (internal and external jugular, subclavian, brachial, femoral) have been used and each is associated with particular problems.

Pyogenic granuloma (lobular capillary hemangioma[1] ) is a relatively common benign vascular lesion of the skin and mucosa whose exact cause is unknown. Also see the Medscape Reference article Oral Pyogenic Granuloma. Pyogenic granulomas are misnamed; they are neither infectious nor granulomatous. The lesion usually occurs in children and young adults as a solitary, glistening red papule or nodule that is prone to bleeding and ulceration. Pyogenic granulomas typically evolve rapidly over a period of a few weeks, most often on the head, neck, extremities, and upper trunk. Pyogenic granuloma often arises in pregnancy (or rarely with oral contraceptive usage), particularly on the gingiva or elsewhere in the oral mucosa, and then is termed the "pregnancy tumor." Other pyogenic granuloma variants that have been well documented include the disseminated, subcutaneous, intravenous, and medication-induced (for example, retinoid, antiretroviral, and oncologic agent) subtypes. Removal of pyogenic granuloma is indicated to alleviate any bleeding, discomfort, cosmetic distress, and diagnostic uncertainty. A number of malignant tumors may clinically mimic pyogenic granuloma, making histopathologic confirmation important if the presentation is atypical. Aside from cutaneous and oral lesions, pyogenic granuloma has been reported throughout the gastrointestinal tract and upper airway, at various ocular locations, the central nervous system, the bladder, and the internal vasculature. This article discusses only cutaneous and oral involvement.

Fibroadenomas (fy-broe-ad-uh-NO-muhz) are solid, noncancerous breast tumors that occur most often in adolescent girls and women under the age of 30. You might describe a fibroadenoma as firm, smooth, rubbery or hard with a well-defined shape. Usually painless, a fibroadenoma might feel like a marble in your breast, moving easily under your skin when touched. Fibroadenomas vary in size, and they can get bigger or even shrink on their own. Fibroadenomas are among the most common breast lumps in young women. Treatment may include monitoring to detect changes in the size or feel of the fibroadenoma, a biopsy to evaluate the lump, or surgery to remove it.

Transjugular intrahepatic portosystemic shunt or transjugular intrahepatic portosystemic stent shunting (commonly abbreviated as TIPS or TIPSS) is an artificial channel within the liver that establishes communication between the inflow portal vein and the outflow hepatic vein.

The accumulation of ascitic fluid represents a state of total-body sodium and water excess, but the event that initiates the unbalance is unclear. Although many pathogenic processes have been implicated in the development of abdominal ascites, about 75% likely occur as a result of portal hypertension in the setting of liver cirrhosis, with the remainder due to infective, inflammatory, and infiltrative conditions. Three theories of ascites formation have been proposed: underfilling, overflow, and peripheral arterial vasodilation. The underfilling theory suggests that the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to portal hypertension and a consequent decrease in effective circulating blood volume. This activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention. The overflow theory suggests that the primary abnormality is inappropriate renal retention of sodium and water in the absence of volume depletion. This theory was developed in accordance with the observation that patients with cirrhosis have intravascular hypervolemia rather than hypovolemia. The most recent theory, the peripheral arterial vasodilation hypothesis, includes components of both of the other theories. It suggests that portal hypertension leads to vasodilation, which causes decreased effective arterial blood volume. As the natural history of the disease progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma volume expands. This leads to overflow of fluid into the peritoneal cavity. The vasodilation theory proposes that underfilling is operative early and overflow is operative late in the natural history of cirrhosis. Although the sequence of events that occurs between the development of portal hypertension and renal sodium retention is not entirely clear, portal hypertension apparently leads to an increase in nitric oxide levels. Nitric oxide mediates splanchnic and peripheral vasodilation. Hepatic artery nitric oxide synthase activity is greater in patients with ascites than in those without ascites. Regardless of the initiating event, a number of factors contribute to the accumulation of fluid in the abdominal cavity. Elevated levels of epinephrine and norepinephrine are well-documented factors. Hypoalbuminemia and reduced plasma oncotic pressure favor the extravasation of fluid from the plasma to the peritoneal fluid, and, thus, ascites is infrequent in patients with cirrhosis unless both portal hypertension and hypoalbuminemia are present.