Plasmapheresis therapeutic plasma exchange

Removal and replacement of a patient's plasma in order to remove large molecules such as antibodies and other proteins. The rationale for plasmaphere-sis is simpleā€”if a disease is caused by antibodies, removing them should improve the disease.

Plasmapheresis is performed by drawing blood out of a vein and passing it into a centrifuge that separates cells from plasma. The patient's plasma is removed and replaced with saline and albumin or plasma from the blood bank. The reconstituted blood is infused back into the patient through another vein. Removing the entire plasma volume takes about two hours, and doing this reduces the concentration of large proteins in the circulation by about 60 percent. usually three to five exchanges are performed over seven to 10 days, removing 90 percent of the patient's own antibodies.

Side effects of plasmapheresis The side effects of plasmapheresis are usually temporary and minor. obtain venous access in patients with small veins can sometimes be difficult. unsuccessful attempts to place a needle in a vein can cause local bruising. Removing blood during plasmapheresis can lower the blood pressure to the extent that the person becomes dizzy or faints. This can be treated by infusing more fluid to replace the volume that has been removed from the circulation. if too much fluid is replaced, it can cause shortness of breath due to heart failure. This is treated by slowing down the rate of fluid replacement or treating with a diuretic that increases urine production.

Blood will clot in the plastic tubes used to remove it unless it is mixed with an anticoagulant. The anticoagulant used, citrate, can bind calcium in the patient's blood and cause muscle cramps and numbness or tingling around the mouth and in the hands and feet. calcium supplements will improve these symptoms but are seldom needed.

Allergy to the replacement plasma is rare but can cause a rash or a more severe allergic reaction. Patients taking AcE inhibitors (angiotensin-converting enzyme inhibitors), a class of drug used to treat high blood pressure or heart failure, may flush and have low blood pressure during the procedure. The reason is that AcE inhibitors slow the breakdown of a bradykinin, a chemical produced when the blood is processed during plasmapheresis. Patients are asked to discontinue ACE inhibitors for at least 24 hours before plasmapheresis.

Viral infections such as hepatitis C can be transmitted in the replacement plasma, but this is rare because donors are screened. Plasmapheresis is expensive.

Indications for plasmapheresis Plasmapheresis is used as an emergency treatment for patients who have a serious illness caused by a circulating antibody or protein. The procedure reduces the amount of antibodies, but only temporarily. Therefore treatment with immunosuppressive drugs to decrease production of new antibodies is often started at the same time.

The indications for plasmapheresis are controversial. Generally Goodpasture's syndrome, myasthenia gravis, Guillain-Barre syndrome, and a closely related disease, chronic inflammatory demyelinating polyneuropathy, as well as throm-botic thrombocytopenic purpura (see thrombocytopenia), cryoglobulinemia, and hyperviscosity syndrome are accepted indications.

Controlled trials show that plasmapheresis had no benefit in rheumatoid arthritis, kidney disease due to systemic lupus erythematosus (SLE) and polymyositis. The SLE trial was criticized because plasmapheresis alone was compared with standard immunosuppressive drugs. Plasmaphere-sis, although it temporarily decreases proteins, can cause a rebound increase in antibody production if it is used without immunosuppressive drugs. Plasmapheresis is used empirically in critically ill patients with SLE or vasculitis.

podiatrist A doctor of podiatric medicine (D.P.M. degree), specializing in the treatment of foot and ankle disorders. Podiatrists train for four years at a podiatric school and then spend several years in a residency program.

Podiatrists deal with problems such as bunions, corns, calluses, ingrown toenails, hammertoes, claw toes, foot pain, flat feet, diabetic foot problems, and foot and ankle injuries. Treatment usually involves orthotics, devices designed to correct or improve foot and ankle biomechanics. Examples of orthotics are wedges to correct uneven leg length or adjust the angle of the ankle or forefoot, shoe inserts to provide greater shock absorption and decrease pressure on painful areas, arch supports, braces, and fitted shoes. Podiatrists also perform foot and ankle surgery.

polyarteritis nodosa This was the first form of vasculitis described, in 1866, in Germany. It is uncommon, affecting about five per million persons per year in England, nine per million in Minnesota, but up to 77 per million in Alaskan Eskimos. All ages and races are affected, but it is more common in men than women and usually affects those in middle age.


In most patients with polyarteritis nodosa defining the precise cause is difficult. Circulating immune complexes are often found in the blood system. These are complexes of antibodies or immunoglob-ulins together with sometimes identifiable antigens that can become large enough to lodge in vessel walls. Here they may initiate an immune attack on the vessel wall that is the primary manifestation of the disease. Small- and medium-sized arteries are affected in polyarteritis nodosa. Biopsy specimens show localized destruction of the vessel walls, particularly by neutrophils. These areas are weakened and may bulge as they heal, giving rise to small nodules that could be felt along the course of arteries and the origin of the earlier name, periarteritis nodosa. Feeling these today is unusual because the disease is diagnosed and treated much earlier.

There is a strong association with chronic hepatitis b infection in some parts of the world. Evidence of hepatitis B infection is found in 10-50 percent of polyarteritis patients and probably accounts for the higher incidence in Alaskan Eskimos in whom this infection is very common. Hepatitis B may be the antigen that drives the development of immune complexes. Antibodies directed against the vessel wall have also been found. It is possible that antigens on an infectious agent are similar to those on the endothelium of the vessel wall. The antibodies against the one may therefore cross-react against the other and direct the immune attack against the endothelium. Other infections that have been linked to the development of polyarteritis include hepatitis A, cytomegalovirus, parvovirus, and HTLV1.

At the site of damage in the vessel wall, is often overgrowth of endothelial cells and fibrous tissue, presumably in an attempt to repair the damage. This sometimes leads to blocking off of the artery. in addition, many factors promote coagulation (clotting) during a vasculitic illness. Clots may occur not only in damaged arteries but also in veins, whose slower blood flow makes them susceptible to this.


As with many forms of vasculitis, polyarteritis nodosa can start and progress in many different ways. The most frequently involved organ is in fact the kidney (70 percent), although this is seldom what leads to the diagnosis. More commonly the joint, skin, or nerve manifestations lead to investigation and diagnosis. Most patients will experience a degree of fever, weight loss, loss of energy, and generalized aches. More specific symptoms include the following.

Skin Half of all patients develop skin lesions. The earliest lesions are often small purplish black spots on the feet and legs that can easily be felt to be lumpy (palpable purpura). This may progress to ulceration or even gangrene, usually affecting one or several toes. livedo reticularis is common.

Joints More than 50 percent of patients have joint symptoms. This may be widespread joint pain or arthritis of the lower-limb joints. Occasionally polyarteritis presents with a polymyalgia rheumat-iCA-like syndrome. There is seldom damage to the joints.

Kidney There is commonly a protein leak into the urine, indicating damage to the filtering part of the kidneys (glomeruli). Occasionally this can be severe and cause nephrotic syndrome. Red blood cells in the urine also signal glomerular damage. High blood pressure may be due to glomerular damage or narrowing of the artery taking blood to the kidney and affects 25 percent of patients.

Nerves Most patients, 50-70 percent, develop nerve damage. Classically, this involves one or several peripheral nerves in the arms or legs. it starts with pain and altered sensation in the distribution of the nerve followed by weakness, developing hours or days later. Less commonly there is loss of sensation in both legs in the area short socks would cover. Very occasionally blood vessels in the brain may be affected, leading to seizures or a stroke.

Gut The gallbladder and appendix are most likely to be affected, but blood vessels supplying the intestines (mesenteric arteries) may also become narrowed or clot. if severe these are surgical emergencies. The liver is seldom affected except where there is chronic hepatitis B infection.

Other Virtually any organ may be affected, but apart from the above, this is rare. Myocardial infarction and heart failure have been reported. Lung lesions presumably due to vasculitis may be found. Testicular and eye involvement are also well recognized but uncommon.

Associated diseases A variant of polyarteritis nodosa called microscopic polyarteritis or microscopic polyangiitis affects the kidneys in almost all patients and the lungs in many. unlike classical polyarteritis nodosa, it does not usually affect medium-sized blood vessels in the gut or other parts of the body. Microscopic polyangiitis can also cause eye and ear symptoms and can sometimes be mistaken for Wegener's granulomatosis.

A polyarteritis nodosa-like syndrome can occur in patients with other rheumatic diseases such as

RHEUMATOID ARTHRITIS, SJOGREN'S SYNDROME, CRYOGLOBULINEMIA, hairy cell leukemia, and other blood disorders. Metastatic cancer that is usually highly malignant and septicemia (infection in the bloodstream) can mimic polyarteritis nodosa, although the mechanisms of disease are different.

Was this article helpful?

0 0

Post a comment