A Baker cyst is swelling caused by fluid from the knee joint protruding to the back of the knee. The back of the knee is also referred to as the popliteal area of the knee. A Baker cyst is sometimes referred to as a popliteal cyst. When an excess of knee joint fluid is compressed by the body weight between the bones of the knee joint, it can become trapped and separate from the joint to form the fluid-filled sac of a Baker cyst. The name of the cyst is in memory of the physician who originally described the condition, the British surgeon William Morrant Baker (1839-1896).

• A Baker cyst is swelling caused by fluid from the knee joint protruding to the back of the knee.
• Baker cysts are common and can be caused by virtually any cause of joint swelling (arthritis).
• A Baker cyst may not cause symptoms or be associated with knee pain and/or tightness behind the knee, especially when the knee is extended or fully flexed.
• Baker cysts can rupture and become complicated by spread of fluid down the leg between the muscles of the calf (dissection).
• Baker cysts can be treated with medications, joint aspiration and cortisone injection, and surgical operation, usually arthroscopic surgery.SIGNS & SYMPTOMS OF BAKER CYSTS:Baker cysts can become complicated by spread of fluid down the leg between the muscles of the calf (dissection). The cyst can rupture, leaking fluid down the inner leg to sometimes cause the appearance of a painless bruise under the inner ankle. Baker cyst dissection and rupture are frequently associated with swelling of the leg and can mimic phlebitis of the leg. A ruptured Baker cyst typically causes rapid-onset swelling of the leg.How is a Baker cyst treated? Baker cysts often resolve with aspiration (removal) of excess knee fluid in conjunction with cortisone injection. Medications are sometimes given to relieve pain and inflammation.
• DIAGNOSING BAKER CYSTS: Baker cysts can be diagnosed by the doctor’s examination and confirmed by imaging tests (either ultrasound, injection of contrast dye into the knee followed by imaging, called an arthrogram, or MRI scan) if necessary.
• A Baker cyst may cause no symptoms or be associated with knee pain and/or tightness behind the knee, especially when the knee is extended or fully flexed. Baker cysts are usually visible as a bulge behind the knee that is particularly noticeable on standing and when compared to the opposite uninvolved knee. They are generally soft and minimally tender.
• Baker cysts are not uncommon and can be caused by virtually any cause of joint swelling (arthritis). The excess joint fluid (synovial fluid) bulges to the back of the knee to form the Baker cyst. The most common type of arthritis associated with Baker cysts is osteoarthritis, also called degenerative arthritis. Baker cysts can occur in children with juvenile arthritis of the knee. Baker cysts also can result from cartilage tears (such as a torn meniscus), rheumatoid arthritis, and other knee problems.

When cartilage tears or other internal knee problems are associated, physical therapy or surgery can be the best treatment option. During a surgical operation, the surgeon can remove the swollen tissue (synovium) that leads to the cyst formation. This is most commonly done with arthroscopic surgery.

The aorta is the large artery that exits in the heart and delivers blood to the body. It begins at the aortic valve that separates the left ventricle of the heart from the aorta and prevents blood from leaking back into the left ventricle after a contraction, which is actually when the heart pumps blood. The various sections of the aorta are named based upon “arch-like” initial design and the location of the aorta in the body. Thus, the beginning of the aorta is referred to as the ascending aorta (basically meaning the blood going against resistance due to the vessel being a hill for the blood to go up), followed by the arch of the aorta, then the descending aorta (which is the blood going downward via gravity with the help of the heart pumping the blood of course). The portion of the aorta that is located in the chest (called thorax) is referred to as the thoracic aorta, while the abdominal aorta (the part of the aorta below the thorax region) is located in the abdomen. The abdominal aorta extends from the diaphragm (at the bottom of the lungs like a floor to divide the lungs from the organs in the abdomen) to the mid-abdomen where it splits into the iliac arteries and when it reaches the legs the femoral arteries now start which supplies to the legs oxygenated blood. This is why commonly a cardiac catheterization to visualize the aorta and sometimes the left side of the heart is done starting in the femoral artery since in time it diverts into starting the abdominal aorta.

An aneurysm is an area of a localized widening (dilation) of a blood vessel. The word “aneurysm” is borrowed from the Greek “aneurysma” meaning “a widening”.

An aortic aneurysm involves the aorta, the major artery that leaves the heart to supply blood to the body. An aortic aneurysm is a dilation or bulging of the aorta..

Most aortic aneurysms are fusiform. They are shaped like a spindle (“fusus” means spindle in Latin) with widening all around the circumference of the aorta. (Saccular aneurysms just involve a portion of the aortic wall with a localized out pocketing).

What is inside an aortic aneurysm?

The inside walls of aneurysms are often lined with a blood clot that forms because there is stagnant blood. The wall of an aneurysm is layered, like a piece of plywood.

Who is most likely to have an abdominal aortic aneurysm?

Abdominal aortic aneurysms tend to occur in white males over the age of 60. In the United States, these aneurysms occur in up to 3.0% of the population. Aneurysms start to form at about age 50 and peak at age 80. Women are less likely to have aneurysms than men and African Americans are less likely to have aneurysms than Caucasians.

There is a genetic component that predisposes one to developing an aneurysm; the prevalence in someone who has a first-degree relative with the condition can be as high as 25%.

Collagen vascular diseases that can weaken the tissues of the aortic walls are also associated with aortic aneurysms. These diseases include Marfan syndrome and Ehlers-Danlos syndrome

Aortic aneurysms can develop anywhere along the length of the aorta but the majority are located in the abdominal aorta. Most of these abdominal aneurysms are located below the level of the renal arteries, the vessels that provide blood to the kidneys. Abdominal aortic aneurysms can extend into the iliac arteries.

What shape are most aortic aneurysms?

Most aortic aneurysms are fusiform. They are shaped like a spindle (“fusus” means spindle in Latin) with widening all around the circumference of the aorta. (Saccular aneurysms just involve a portion of the aortic wall with a localized out pocketing).

What is inside an aortic aneurysm?

The inside walls of aneurysms are often lined with a blood clot that forms because there is stagnant blood. The wall of an aneurysm is layered, like a piece of plywood.

Who is most likely to have an abdominal aortic aneurysm?

Abdominal aortic aneurysms tend to occur in white males over the age of 60. In the United States, these aneurysms occur in up to 3.0% of the population. Aneurysms start to form at about age 50 and peak at age 80. Women are less likely to have aneurysms than men and African Americans are less likely to have aneurysms than Caucasians.

There is a genetic component that predisposes one to developing an aneurysm; the prevalence in someone who has a first-degree relative with the condition can be as high as 25%.

Collagen vascular diseases that can weaken the tissues of the aortic walls are also associated with aortic aneurysms. These diseases include Marfan syndrome and Ehlers-Danlos syndrome.

What are risk factors for aortic aneurysms?

The risk factors for aortic aneurysm are the same as those for atherosclerotic heart disease, stroke, and peripheral artery disease and include:

• Cigarette smoking: This not only increases the risk of developing an abdominal aortic aneurysm, but also increases the risk of aneurysm rupture. Aortic rupture is a life-threatening event where blood escapes the aorta and the patient can quickly bleed to death.

• High blood pressure

• Elevated blood cholesterol levels

• Diabetes mellitus The most common cause of aortic aneurysms is “hardening of the arteries” called arteriosclerosis. At a majority of aortic aneurysms are from arteriosclerosis. The arteriosclerosis can weaken the aortic wall and the increased pressure of the blood being pumped through the aorta causes weakness of the inner layer of the aortic wall.Smoking is a major cause of aortic aneurysm. Studies have shown that the rate of aortic aneurysm has fallen at the same rate as population smoking rates.

• The aortic wall has three layers, the tunica adventitia, tunica media, and tunica intima. The layers add strength to the aorta as well as elasticity to tolerate changes in blood pressure. Chronically increased blood pressure causes the media layer to break down and leads to the continuous, slow dilation of the aorta.
• What is the most common cause of aortic aneurysms?

“It is easier to find men who will volunteer to die, than to find those who are willing to endure pain with patience.”

Julius Caesar

‘This is potentially a very important discovery which may go a long way to explain the marked differences in pain sensitivity and chronicity between women and men.”

says James McRoberts, a pain researcher at the University of California-Los Angeles

“When a loved one dies, you might be faced with grief over your loss again and again — sometimes even years later. Feelings of grief might return on the anniversary of your loved one’s death, birthday or other special days throughout the year. This is called anniversary reaction, its not a set back. You’re reflecting memories and that this loved one was important to you. To continue on the path toward healing, know what to expect — and how to cope with reminders of your loss.”

MAYO CLINIC

“Sepsis is the systemic response to infection and is defined as the presence of SIRS (systemic inflammatory response syndrome) in addition to a documented or presumed infection.”

Lewis J Kaplan, MD-author SIRS  Medscape.com

Part 3 talks to you about the multi-hit theory of SIRS with Inflammatory Cascade of SIRS and lastly the coagulation process in SIRS.   It also tells you an extensive amount of infectious and non-infectious causes of SIRS. Lastly the key antidote to SIRS.

Multi-hit theory

A multi hit theory behind the progression of SIRS to organ dysfunction and possibly multiple organ dysfunction syndrome (MODS). In this theory, the event that initiates the SIRS cascade primes the pump. With each additional event, an altered or exaggerated response occurs, leading to progressive illness. The key to preventing the multiple hits is adequate identification of the ETIOLOGY or CAUSE of SIRS and appropriate resuscitation and therapy.

Inflammatory cascade

Trauma, inflammation, or infection leads to the activation of the inflammatory cascade. Initially, a pro-inflammatory activation occurs, but almost immediately thereafter a reactive suppressing anti-inflammatory response occurs. This SIRS usually manifests itself as increased systemic expression of both pro-inflammatory and anti-inflammatory species. When SIRS is mediated by an infectious insult, the inflammatory cascade is often initiated by endotoxin or exotoxin. Tissue macrophages, monocytes, mast cells, platelets, and endothelial cells are able to produce a multitude of cytokines. The cytokines tissue necrosis factor–alpha (TNF-α) and interleukin-1 (IL-1) are released first and initiate several cascades.

The release of certain factors without getting into medical specific terms they ending line induces the production of other pro-inflammatory cytokines, worsening the condition.

Some of these factors are the primary pro-inflammatory mediators. In research it suggests that glucocorticoids may function by inhibit-ing certain factors that have been shown to be released in large quantities within 1 hour of an insult and have both local and systemic effects. In studies they have shown that certain cytokines given individually produce no significant hemodynamic response but that they cause severe lung injury and hypotension. Others responsible for fever and the release of stress hormones (norepinephrine, vasopressin, activation of the renin-angiotensin-aldosterone system).

Other cytokines, stimulate the release of acute-phase reactants such as C-reactive protein (CRP) and pro-calcitonin.

The pro-inflammatory interleukins either function directly on tissue or work via secondary mediators to activate the coagulation cascade and the complement cascade and the release of nitric oxide, platelet-activating factor, prostaglandins, and leukotrienes.

High mobility group box 1 (HMGB1) is a protein present in the cytoplasm and nuclei in a majority of cell types. In response to infection or injury, as is seen with SIRS, HMGB1 is secreted by innate immune cells and/or released passively by damaged cells. Thus, elevated serum and tissue levels of HMGB1 would result from many of the causes of SIRS.

HMGB1 acts as a potent pro-inflammatory cytokine and is involved in delayed endotoxin lethality and sepsis.

Numerous pro-inflammatory polypeptides are found within the complement cascade. It is thought they are felt to contribute directly to the release of additional cytokines and to cause vasodilatation and increasing vascular permeability. Prostaglandins and leukotrienes incite endothelial damage, leading to multi-organ failure.

Polymorphonuclear cells (PMNs) from critically ill patients with SIRS have been shown to be more resistant to activation than PMNs from healthy donors, but, when stimulated, demonstrate an exaggerated micro-bicidal response (agents that kill microbes). This may represent an auto-protective mechanism in which the PMNs in the already inflamed host may avoid excessive inflammation, thus reducing the risk of further host cell injury and death.^[4]

Coagulation

The correlation between inflammation and coagulation is critical to understanding the potential progression of SIRS. IL-1 and TNF-α directly affect endothelial surfaces, leading to the expression of tissue factor. Tissue factor initiates the production of thrombin, thereby promoting coagulation, and is a proinflammatory mediator itself. Fibrinolysis is impaired by IL-1 and TNF-α via production of plasminogen activator inhibitor-1. Pro-inflammatory cytokines also disrupt the naturally occurring anti-inflammatory mediators anti-thrombin and activated protein-C (APC).

If unchecked, this coagulation cascade leads to complications of micro-vascular thrombosis, including organ dysfunction. The complement system also plays a role in the coagulation cascade. Infection-related pro-coagulant activity is generally more severe than that produced by trauma.

What the causes of SIRS can be:

The etiology of systemic inflammatory response syndrome (SIRS) is broad and includes infectious and noninfectious conditions, surgical procedures, trauma, medications, and therapies.

The following is partial list of the infectious causes of SIRS:

• Bacterial sepsis
• Burn wound infections
• Candidiasis
• Cellulitis
• Cholecystitis
• Community-acquired pneumonia ^[5]
• Diabetic foot infection
• Erysipelas
• Infective endocarditis
• Influenza
• Intra-abdominal infections (eg, diverticulitis, appendicitis)
• Gas gangrene
• Meningitis
• Nosocomial pneumonia
• Pseudomembranous colitis
• Pyelonephritis
• Septic arthritis
• Toxic shock syndrome
• Urinary tract infections (male and female)
• The following is a partial list of the noninfectious causes of SIRS:

• Acute mesenteric ischemia
• Adrenal insufficiency
• Autoimmune disorders
• Burns
• Chemical aspiration
• Cirrhosis
• Cutaneous vasculitis
• Dehydration
• Drug reaction
• Electrical injuries
• Erythema multiforme
• Hemorrhagic shock
• Hematologic malignancy
• Intestinal perforation
• Medication side effect (eg, from theophylline)
• Myocardial infarction
• Pancreatitis ^[6]
• Seizure
• Substance abuse – Stimulants such as cocaine and amphetamines
• Surgical procedures
• Toxic epidermal necrolysis
• Transfusion reactions
• Upper gastrointestinal bleeding
• VasculitisThe treatment is don’t get it since it is hard to get rid of especially for people over 65 and in hospitals.  There is no one Rx for it.  If you’re unfortunate enough to be diagnosed with SIRS the sooner you get diagnosed with it including being in stage one as opposed to three the higher the odds the turn out will be for you.  Again the key is prevention; don’t get it. There is no one antidote to this SIRS.
• QUOTE FOR THIS ARTICLE:
• PREVENTION IS THE KEY ANTIDOTE!   So stay healthy and out of  hospitals!

“SIRS can be incited by ischemia, inflammation, trauma, infection or a combination of several “insults”. SIRS is not always associated with infection. While not universally accepted, some have proposed the terms “severe SIRS” and “SIRS shock” to describe serious clinical syndromes that are not infectious in nature and thus cannot be labeled according to the various sepsis definitions”

Steven D. Burdette M.D. (Infectious Disease Medicine M.D.– Wright State Physicians in Dayton, Ohio – http://www.healthgrades.com/physician/dr-steven-burdette-yhfgy)

“The idea behind defining SIRS was to define a clinical response to a nonspecific insult of either infectious or noninfectious origin. In 1992, the American College of Chest Physicians (ACCP) and the Society of Critical Care Medicine (SCCM) introduced definitions for systemic inflammatory response syndrome (SIRS), sepsis, severe sepsis, septic shock, and multiple organ dysfunction syndrome MODS).”

^{Lewis J Kaplan, MD FACS, FCCM, FCCP, Director, SICU and Surgical Critical Care Fellowship, Associate Professor, Department of Surgery, Section of Trauma, Surgical Critical Care, and Surgical Emergencies, Yale University School of Medicine.}