Mechanical hemolytic anemia

Last updated
Mechanical hemolytic anemia
Specialty Hematology

Mechanical hemolytic anemia is a form of hemolytic anemia due to mechanically induced damage to red blood cells. Red blood cells, while flexible, may in some circumstances succumb to physical shear and compression. [1] This may result in hemoglobinuria. The damage is induced through repetitive mechanical motions such as prolonged marching (march hemoglobinuria) and marathon running. [2] [3] Mechanical damage can also be induced through the chronic condition microangiopathic hemolytic anemia or due to prosthetic heart valves. [1]

Contents

Cause

Repetitive impacts to the body may cause mechanical trauma and bursting (hemolysis) of red blood cells. This has been documented to have occurred in the feet during running [4] and hands from Conga or Candombe drumming. [5] Defects in red blood cell membrane proteins have been identified in some of these patients. [6] Free haemoglobin is released from lysed red blood cells and filtered into the urine.

Hemolytic phenomena

March haemoglobinuria

March hemoglobinuria, occurs when hemoglobin is seen in the urine after repetitive impacts on the body, particularly affecting the feet. The word "march" is in reference to the condition arising in soldiers who have been marching for long periods; the condition was first documented in 1881. [7]

Runner’s macrocytosis

Runner's macrocytosis is a phenomenon of increased red blood cell size as a compensatory mechanism for increased red blood cell turnover. The impact forces from running can lead to red blood cell hemolysis and accelerate red blood cell production. This can shift the ratio of red blood cells towards younger, larger cells. This shift may be reflected in higher than normal mean corpuscular volume (MCV) values, an indicator of red blood cell size. [4]

This is not a pathological condition but may indicate a propensity toward iron deficiency anemia due to high red blood cell turnover.

Related Research Articles

<span class="mw-page-title-main">Hemolysis</span> Rupturing of red blood cells and release of their contents

Hemolysis or haemolysis, also known by several other names, is the rupturing (lysis) of red blood cells (erythrocytes) and the release of their contents (cytoplasm) into surrounding fluid. Hemolysis may occur in vivo or in vitro.

<span class="mw-page-title-main">Spherocytosis</span> Medical condition

Spherocytosis is the presence of spherocytes in the blood, i.e. erythrocytes that are sphere-shaped rather than bi-concave disk shaped as normal. Spherocytes are found in all hemolytic anemias to some degree. Hereditary spherocytosis and autoimmune hemolytic anemia are characterized by having only spherocytes.

Microangiopathic hemolytic anemia (MAHA) is a microangiopathic subgroup of hemolytic anemia caused by factors in the small blood vessels. It is identified by the finding of anemia and schistocytes on microscopy of the blood film.

<span class="mw-page-title-main">Paroxysmal nocturnal hemoglobinuria</span> Medical condition

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired, life-threatening disease of the blood characterized by destruction of red blood cells by the complement system, a part of the body's innate immune system. This destructive process occurs due to deficiency of the red blood cell surface protein DAF, which normally inhibits such immune reactions. Since the complement cascade attacks the red blood cells within the blood vessels of the circulatory system, the red blood cell destruction (hemolysis) is considered an intravascular hemolytic anemia. Other key features of the disease, such as the high incidence of venous blood clot formation, are incompletely understood.

<span class="mw-page-title-main">Hemolytic anemia</span> Medical condition

Hemolytic anemia or haemolytic anaemia is a form of anemia due to hemolysis, the abnormal breakdown of red blood cells (RBCs), either in the blood vessels or elsewhere in the human body (extravascular). This most commonly occurs within the spleen, but also can occur in the reticuloendothelial system or mechanically. Hemolytic anemia accounts for 5% of all existing anemias. It has numerous possible consequences, ranging from general symptoms to life-threatening systemic effects. The general classification of hemolytic anemia is either intrinsic or extrinsic. Treatment depends on the type and cause of the hemolytic anemia.

<span class="mw-page-title-main">Hemoglobinuria</span> Abnormally increased hemoglobin in urine

Hemoglobinuria is a condition in which the oxygen transport protein hemoglobin is found in abnormally high concentrations in the urine. The condition is caused by excessive intravascular hemolysis, in which large numbers of red blood cells (RBCs) are destroyed, thereby releasing free hemoglobin into the plasma. Excess hemoglobin is filtered by the kidneys, which excrete it into the urine, giving urine a purple color. Hemoglobinuria can lead to acute tubular necrosis which is an uncommon cause of a death of uni-traumatic patients recovering in the ICU.

<span class="mw-page-title-main">Schistocyte</span> Fragmented portion of a red blood cell

A schistocyte or schizocyte is a fragmented part of a red blood cell. Schistocytes are typically irregularly shaped, jagged, and have two pointed ends.

<span class="mw-page-title-main">Acanthocyte</span> Abnormal red blood cell with a spiked cell membrane

Acanthocyte, in biology and medicine, refers to an abnormal form of red blood cell that has a spiked cell membrane, due to thorny projections. A similar term is spur cells. Often they may be confused with echinocytes or schistocytes.

Warm antibody autoimmune hemolytic anemia (WAIHA) is the most common form of autoimmune haemolytic anemia. About half of the cases are of unknown cause, with the other half attributable to a predisposing condition or medications being taken. Contrary to cold autoimmune hemolytic anemia which happens in cold temperature (28–31 °C), WAIHA happens at body temperature.

<span class="mw-page-title-main">Hereditary stomatocytosis</span> Medical condition

Hereditary stomatocytosis describes a number of inherited, mostly autosomal dominant human conditions which affect the red blood cell and create the appearance of a slit-like area of central pallor (stomatocyte) among erythrocytes on peripheral blood smear. The erythrocytes' cell membranes may abnormally 'leak' sodium and/or potassium ions, causing abnormalities in cell volume. Hereditary stomatocytosis should be distinguished from acquired causes of stomatocytosis, including dilantin toxicity and alcoholism, as well as artifact from the process of preparing peripheral blood smears.

Autoimmune hemolytic anemia (AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to an insufficient number of oxygen-carrying red blood cells in the circulation. The lifetime of the RBCs is reduced from the normal 100–120 days to just a few days in serious cases. The intracellular components of the RBCs are released into the circulating blood and into tissues, leading to some of the characteristic symptoms of this condition. The antibodies are usually directed against high-incidence antigens, therefore they also commonly act on allogenic RBCs. AIHA is a relatively rare condition, with an incidence of 5–10 cases per 1 million persons per year in the warm-antibody type and 0.45 to 1.9 cases per 1 million persons per year in the cold antibody type. Autoimmune hemolysis might be a precursor of later onset systemic lupus erythematosus.

Paroxysmal cold hemoglobinuria (PCH) is an autoimmune hemolytic anemia featured by complement-mediated intravascular hemolysis after cold exposure. It can present as an acute non-recurrent postinfectious event in children, or chronic relapsing episodes in adults with hematological malignancies or tertiary syphilis. Described by Julius Donath (1870–1950) and Karl Landsteiner (1868–1943) in 1904, PCH is one of the first clinical entities recognized as an autoimmune disorder.

Cold agglutinin disease (CAD) is a rare autoimmune disease characterized by the presence of high concentrations of circulating cold sensitive antibodies, usually IgM and autoantibodies that are also active at temperatures below 30 °C (86 °F), directed against red blood cells, causing them to agglutinate and undergo lysis. It is a form of autoimmune hemolytic anemia, specifically one in which antibodies bind red blood cells only at low body temperatures, typically 28–31 °C.

Acquired hemolytic anemia can be divided into immune and non-immune mediated forms of hemolytic anemia.

Drug-induced autoimmune hemolytic anemia is a form of hemolytic anemia.

Intravascular hemolysis describes hemolysis that happens mainly inside the vasculature. As a result, the contents of the red blood cell are released into the general circulation, leading to hemoglobinemia and increasing the risk of ensuing hyperbilirubinemia.

Donath–Landsteiner hemolytic anemia (DLHA) is a result of cold-reacting antibody immunoglobulin (Ig) induced hemolytic response inside vessels leading to anemia and, thus, a cold antibody autoimmune hemolytic anemias (CAAHA).

Cold sensitive antibodies (CSA) are antibodies sensitive to cold temperature. Some cold sensitive antibodies are pathological and can lead to blood disorder. These pathological cold sensitive antibodies include cold agglutinins, Donath–Landsteiner antibodies, and cryoglobulins which are the culprits of cold agglutinin disease, paroxysmal cold hemoglobinuria in the process of Donath–Landsteiner hemolytic anemia, and vasculitis, respectively.

Hemolytic jaundice, also known as prehepatic jaundice, is a type of jaundice arising from hemolysis or excessive destruction of red blood cells, when the byproduct bilirubin is not excreted by the hepatic cells quickly enough. Unless the patient is concurrently affected by hepatic dysfunctions or is experiencing hepatocellular damage, the liver does not contribute to this type of jaundice.

<span class="mw-page-title-main">Sucrose lysis test</span>

The sucrose lysis test is a diagnostic laboratory test used for diagnosing paroxysmal nocturnal hemoglobinuria (PNH), as well as for hypoplastic anemias and any hemolytic anemia with an unclear cause. The test works by using sucrose, which creates a low ionic strength environment that allows complement to bind to red blood cells. In individuals with PNH, some red blood cells are especially vulnerable to lysis caused by complement. The test may also produce suspicious results in other hematologic conditions, including megaloblastic anemia and autoimmune hemolytic anemia. False-negative results can occur when complement activity is absent in the serum. A simpler alternative called the sugar water test also involves mixing blood with sugar and observing for hemolysis, using the same principle as the sucrose lysis test.

References

  1. 1 2 Dan L. Longo, Harrison's Hematology and Oncology, 2010, ISBN   0-07-166335-5; page 121.
  2. ↑ Reinhold Munker, Erhard Hiller, Jonathan Glass, Ronald Paquette, Modern Hematology: Biology and Clinical Management, 2007, page 126, ISBN   1-58829-557-5.
  3. ↑ Anthony S. Fauci, Eugene Braunwald, Dennis Kasper, Stephen Hauser, Dan L. Longo, Harrison's Manual of Medicine, page 328, 2009, ISBN   0-07-147743-8.
  4. 1 2 Eichner, ER (February 1985). "Runner's macrocytosis: a clue to footstrike hemolysis. Runner's anemia as a benefit versus runner's hemolysis as a detriment". The American Journal of Medicine. 78 (2): 321–5. doi:10.1016/0002-9343(85)90443-7. PMID   3970055.
  5. ↑ Tobal D, Olascoaga A, Moreira G, Kurdian M, Sanchez F, Rosello M, Alallon W, Martinez FG, Noboa O (2008). "Rust Urine after Intense Hand Drumming Is Caused by Extracorpuscular Hemolysis". Clinical Journal of the American Society of Nephrology. 3 (4): 1022–1027. doi:10.2215/cjn.04491007. PMC   2440284 . PMID   18434617.
  6. ↑ Banga JP, Pinder JC, Gratzer WB, Linch DC, Huehns ER (November 1979). "An erythrocyte membrane-protein anomaly in march haemoglobinuria". Lancet. 2 (8151): 1048–9. doi:10.1016/S0140-6736(79)92444-9. PMID   91785. S2CID   28804215.
  7. ↑ Gilligan DR, Blumgart HL (September 1941). "MARCH HEMOGLOBINURIA: Studies of the Clinical Characteristics, Blood Metabolism and Mechanism: with Observations on Three New Cases, and Review of Literature". Medicine. 20 (3): 341–395. doi: 10.1097/00005792-194109000-00002 . S2CID   72767922.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.