hemolysis (redirected from fragmentation hemolysis)

hemolysis /he·mol·y·sis/ (he-mol´ĭ-sis) the liberation of hemoglobin, consisting of separation of the hemoglobin from the red cells and its appearance in the plasma.hemolyt´ic

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immune hemolysis  lysis by complement of erythrocytes sensitized as a consequence of interaction with specific antibody to the erythrocytes.

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he·mol·y·sis (h-ml-ss, hm-lss) or he·ma·tol·y·sis (hm-tl-ss)

n.

The destruction or dissolution of red blood cells, with release of hemoglobin. Also called erythrocytolysis, erythrolysis.

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Hemolysis

The process of breaking down of red blood cells. As the cells are destroyed, hemoglobin, the component of red blood cells which carries the oxygen, is liberated.

Mentioned in: Coombs' Tests, Glucose-6-Phosphate Dehydrogenase Deficiency, Hemolytic Anemia, Hepatitis, Alcoholic, Jaundice, Physical Allergy

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hemolysis

[himol′isis]

Etymology: Gk, haima + lysis, loosening

the breakdown of red blood cells and the release of hemoglobin that occur normally at the end of the life span of a red cell. Hemolysis may occur in antigen-antibody reactions, metabolic abnormalities of the red cell that significantly shorten red cell life span, and mechanical trauma, such as cardiac prosthesis. Dilution of the blood by IV administration of excessive amounts of hypotonic solutions, which causes progressive swelling and eventual rupture of the erythrocyte, also results in hemolysis. Also spelled hematolysis. See also hemolysin, hemolytic anemia, transfusion reaction. -hemolytic">haemolysis. Also called hematolysis. See also hemolysin, hemolytic anemia, transfusion reaction. -hemolytic, adj.

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hemolysis (himol´isis),

n the breakdown of red blood cells and the release of hemoglobin that occurs normally at the end of the life span of a red blood cell.

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hemolysis

rupture of erythrocytes with release of hemoglobin.

In a transfusion reaction or in alloimmune hemolytic anemia antibody mediated lysis of red blood cells involves triggering of the complement cascade. Red blood cells also clump together. The agglutinated cells become trapped in the smaller vessels or are phagocytosed and eventually disintegrate.

Some microbes form substances called hemolysins that have the specific action of destroying red blood cells; beta-hemolytic streptococci are an example.

Intravenous administration of a hypotonic solution or plain distilled water will cause the red cells to fill with fluid until their membranes rupture and the cells are destroyed.

Wherever either in vitro or in vivo IgG or IgM antibodies are bound to red blood cell antigens in the presence of complement, the complement cascade is triggered the final products of which include enzymes that result in holes being 'punched' in the wall of the red blood cell, allowing hemoglobin to escape and which is observed as lysis.

Snake venoms and certain plant substances may cause hemolysis. A great variety of chemical agents can lead to destruction of erythrocytes if there is exposure to a sufficiently high concentration of the substance. These chemical hemolytics include copper.

A disorder of the immune response in which antibodies are made to 'self' red blood cell antigens resulting in the lysis of the cells. See also autoimmune hemolytic anemia.

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alpha (α) hemolysis

a characteristic of some bacteria, especially streptococci, manifested by a zone of greenish coloration of cleared agar around a colony of the bacteria on a blood-agar plate. Note that α-hemolysis of staphylococci causes complete lysis. See also streptococcus.

beta (β) hemolysis

complete hemolysis of sheep and ox erythrocytes by bacteria in culture media. Note that β-hemolysin of staphylococci causes incomplete hemolysis.

blood transfusion hemolysis

see transfusion reaction.

differential hemolysis

a technique for identification of chimerism, e.g. freemartin calves. Antisera against a single blood group causes only partial hemolysis of the blood composed of two cell populations with different blood cell antigens.

double hemolysis

two types of hemolysis produced on blood agar by alpha and beta lysins found in Staphylococcus aureus and S. intermedius.

extravascular hemolysis

the hemolysis which occurs when fragments of erythrocytes and the majority of aged erythrocytes are phagocytosed directly by the cells of the mononuclear phagocytic system.

hemolysis fever

the rise in body temperature which accompanies each hemolytic incidence of significant size.

fragmentation hemolysis

see microangiopathic anemia.

hemolysis inhibition test

a serological test used in the diagnosis of Corynebacterium pseudotuberculosis infection.

intravascular hemolysis

disruption of red blood cells occurs while they are within blood vessels.

microangiopathic hemolysis

fragmentation hemolysis often associated with microvascular injury, as in disseminated intravascular coagulation, and resulting from a primary disease.

target hemolysis

see double hemolysis (above).

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transfusion reaction

Blood transfusion reaction, incompatibility reaction Transfusion medicine Any untoward response to the transfusion of non-self blood products, in particular RBCs, which evokes febrile reactions that are either minor–occurring in 1:40 transfusions and attributed to nonspecific leukocyte-derived pyrogens, or major–occurring in 1:3000 transfusions and caused by a true immune reaction, which is graded according to the presence of urticaria, itching, chills, fever and, if the reaction is intense, collapse, cyanosis, chest and/or back pain and diffuse hemorrhage Note: If any of above signs appear in a transfusion reaction, or if the temperature rises 1ºC, the transfusion must be stopped; most Pts survive if < 200 ml has been transfused in cases of red cell incompatibility-induced transfusion reaction; over 50% die when 500 ml or more has been transfused; TF mortality is ± 1.13/105 transfusions Clinical Flank pain, fever, chills, bloody urine, rash, hypotension, vertigo, fainting

Transfusion reactions

Immune, non-infectious transfusion reactions  

• Allergic Urticaria with immediate hypersensitivity

• Anaphylaxis Spontaneous anti-IgA antibody formation, occurs in ± 1:30 of Pts with immunoglobulin A deficiency, which affects 1:600 of the general population–total frequency: 1/30 X 1/600 = 1/18,000

• Antibodies to red cell antigens, eg antibodies to ABH, Ii, MNSs, P1, HLA

• Serum sickness Antibodies to donor's immunoglobulins and proteins

Non-immune, non-infectious transfusion reactions  

• Air embolism A problem of historic interest that occurred when air vents were included in transfusion sets

• Anticoagulant Citrate anticoagulant may cause tremors and EKG changes

• Coagulation defects Depletion of factors VIII and V; this 'dilutional' effect requires massive transfusion of 10 + units before becoming significant

• Cold blood In ultra-emergent situations, blood stored at 4º C may be tranfused prior to reaching body temperature at 37º C; warming a unit of blood from 4 to 37º C requires 30 kcal/L of energy, consumed as glucose; cold blood slows metabolism, exacerbates lactic acidosis, ↓ available calcium, ↑ hemoglobin's affinity for O₂ and causes K⁺ leakage, a major concern in cold hemoglobinuria

• Hemolysis A phenomenon due to blood collection trauma, a clinically insignificant problem

• Hyperammonemia and lactic acid Both molecules accumulate during packed red cell storage and when transfused, require hepatorenal clearance, of concern in Pts with hepatic or renal dysfunction, who should receive the freshest units possible

• Hyperkalemia Hemolysis causes an ↑ of 1 mmol/L/day of potassium in a unit of stored blood, of concern in Pts with poor renal function, potentially causing arrhythmia

• Iron overload Each unit of packed RBCs has 250 mg iron, potentially causing hemosiderosis in multi-transfused Pts

Microaggregates Sludged debris in the pulmonary vasculature causing ARDS may be removed with micropore filters

Pseudoreaction Transfusion reaction mimics, eg anxiety, anaphylaxis related to a drug being administered at the same time as the transfusion

Infections transmitted by blood transfusion

• Viruses B19, CMV, EBV, HAV, HBV, HCV, HDV, HEV, Creutzfeldt-Jakob disease, Colorado tick fever, tropical viruses–eg Rift Valley fever, Ebola, Lassa, dengue, HHV 6, HIV-1, HIV-2, HTLV-I, HTLV-II

• Bacteria Transmission of bacterial infections from an infected donor is uncommon and includes brucellosis and syphilis in older reports; more recent reports include Lyme disease and Yersinia enterocolitica  Note: Although virtually any bacteria could in theory be transmitted in blood, the usual cause is contamination during processing rather than transmission from an infected donor

• Parasites Babesiosis, Leishmania donovani, L tropica, malaria, microfilariasis–Brugia malayi, Loa loa, Mansonella perstans, Mansonella ozzardi, Toxoplasma gondii, Trypanosoma cruzi

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hemoglobinuria

Hematology The presence of Hb in the urine which, if of sufficient quantity, colors urine, the intensity of which directly correlates with the quantity of Hb. See Paroxysmal cold hemoglobinuria, Paroxysmal nocturnal hemoglobinuria.

hemolysis Destruction or lysis of RBCs

Hemolysis

Intracorpuscular hemolysis

•  Membrane defects, eg hereditary elliptocytosis, spherocytosis, stomatocytosis and paroxysmal nocturnal hemoglobinuria

•  Metabolic defects, eg G6PD, pyruvate kinase deficiency

•  Abnormal Hbs see Hemoglobin

Extracorpuscular hemolysis

1º immune reactions, eg autoimmune hemolytic anemia

2º immune reactions, due to

• Infections, eg Bartonella, Clostridia, malaria, sepsis

• Neoplasia, eg lymphoma, leukemias

• Drug reactions due to the 'Innocent bystander' phenomenon (drug-antibody complex activates complement, causing intravascular hemolysis, eg quinidine), hapten-mediated —a protein-bound drug attaches to the red cell membrane, eliciting an immune response when the hapten-protein complex is recognized as foreign, evoking an immune response, eg penicillin acting as a hapten

• Induction of autoimmunity by RBC antigen alterations, eg Rh antigen

Physical, eg thermal, concentrated glycerol due to inadequate washing of frozen blood, bladder irrigation, cardiac valves

Extravascular Less severe, IgG-mediated and does not activate complement, eg Rh, Kell, Duffy Laboratory ↓ haptoglobin, ↓ T_1/2 of circulating RBCs, ↑ indirect BR as liver capacity to conjugate BR–ergo direct BR is overwhelmed by massive hemolysis, ↑ LDH, Hb in blood and urine, hemosiderinuria, MetHb and metalbumin, ↑ urobilinogen in urine and feces, ↑ in acid phosphatase, K+, and prostatic acid phosphatase Clin Chem 1992; 38:575; peripheral smears demonstrate anisocytosis, polychromatophilia, nucleated RBCs, basophilic stippling; immune hemolysis is suggested by spherocytes NEJM 2000; 342:722cpc

Intravascular More severe, IgM-mediated and requires complement activation, eg ABO blood groups Laboratory ↑ free Hb  Note: Clinically significant hemolysis is usually detected by hemagglutination, less commonly by hemolysis per se, which detects anti-P,
-P₁, -PP₁Pk, -Jka, -Lea, occasionally also anti-Leb and -Vel