hemolysis

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hemolysis

 [he-mol´ĭ-sis]
rupture of erythrocytes with release of hemoglobin into the plasma. Some microbes form substances called hemolysins that have the specific action of destroying red blood cells; the beta-hemolytic streptococcus is an example. Intravenous administration of a hypotonic solution or plain distilled water will also destroy red blood cells by causing them to fill with fluid until their membranes rupture.

In a transfusion reaction or in erythroblastosis fetalis, incompatibility causes the red blood cells to clump together. The agglutinated cells become trapped in the smaller vessels and eventually disintegrate, releasing hemoglobin into the plasma. Kidney damage may result as the hemoglobin crystallizes and obstructs the renal tubules, producing renal shutdown and uremia.

Snake venoms and vegetable poisons such as mushrooms may also 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 arsenic, lead, benzene, acetanilid, nitrites, and potassium chlorate.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

he·mol·y·sis

(hē-mol'i-sis),
Alteration, dissolution, or destruction of red blood cells in such a manner that hemoglobin is liberated into the medium in which the cells are suspended, for example, by specific complement-fixing antibodies, toxins, various chemical agents, tonicity, alteration of temperature.
[hemo- + G. lysis, destruction]
Farlex Partner Medical Dictionary © Farlex 2012

hemolysis

(hĭ-mŏl′ĭ-sĭs, hē′mə-lī′sĭs)
n.
The destruction or dissolution of red blood cells, with subsequent release of hemoglobin.

he′mo·lyt′ic (hē′mə-lĭt′ĭk) adj.
The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.

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

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, ↓ T1/2 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
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

he·mol·y·sis

(hē-mol'i-sis)
Alteration, dissolution, or destruction of red blood cells in such a manner that hemoglobin is liberated into the medium in which the cells are suspended.
Synonym(s): erythrocytolysis, erythrolysis, hematolysis, haemolysis.
[hemo- + G. lysis, destruction]
Medical Dictionary for the Health Professions and Nursing © Farlex 2012

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.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.

he·mol·y·sis

(hē-mol'i-sis)
Alteration, dissolution, or destruction of red blood cells in such a manner that hemoglobin is liberated into the medium in which the cells are suspended.
Synonym(s): haemolysis.
[hemo- + G. lysis, destruction]
Medical Dictionary for the Dental Professions © Farlex 2012
References in periodicals archive ?
Hair et al., "Complement inhibition significantly decreases red blood cell lysis in a rat model of acute intravascular hemolysis," Transfusion, vol.
With intravascular hemolysis, free hemoglobin becomes bound to haptoglobin forming a hemoglobin-haptoglobin complex which inhibits hemoglobin filtration and prevents the toxic effects on the tubular epithelium [14].
We describe refractory intravascular hemolysis due to a turbulent effect of intra PDA vegetation, a rare complication of PDA endocarditis.
The child is experiencing a painful "sickle cell crisis", or a recurrent episode of vascular occlusion and intravascular hemolysis, due to the crystallization of the abnormal hemoglobin variant forming sickled cells.
The major components of honeybee venom are Mellitin, (a direct hemolysin, cytotoxic and cardiotoxic; is a protein that hydrolyzes cell membranes, alters cellular permeability and causes histamine release and also responsible for local pain), Phospholipase [A.sub.2] (the major allergenic component and causes intravascular hemolysis), Peptide 401 (or mast cell degranulating peptide-causes mast cells to degranulate, releasing histamine and vasoactive amines), Apamin (a neurotoxin that acts on spinal cord), Adolapin (inhibits prostaglandin synthetase and Hyaluronidase (causes changes in cell permeability by altering cell membranes and disrupts collagen, allowing other venom components to penetrate into victim's tissues).
A diagnosis of artesunate-associated hemolysis was made in this case based on the temporal relationship with therapy and the absence of other identified causes of intravascular hemolysis. His time course of hemolysis after treatment corresponds with recent case series in Europe (1-4): his hemoglobin level reached a nadir at approximately day 15.
This disorder is a disease, like sickle cell anemia and thalassemia, in which chronic blood loss requires frequent blood transfusions (though beta minor thalassemia has been associated with hemosiderin deposits in the liver in patients with non-alcoholic fatty liver disease independent of any transfusions).[sup.7,8] Also, renal hemosiderosis is a complication of chronic intravascular hemolytic states, such as hemolytic anemia, paroxysmal nocturnal hemoglobinuria (PNH) and mechanical hemolysis after inserting a prosthetic cardiac valve[sup.9,10] or black-water fever as well.[sup.3] Renal hemosiderosis (blue kidney) is the anatomic indicator of severe intravascular hemolysis.[sup.3]
Massive intravascular hemolysis with the release of thromboplastic substances is a well-known trigger mechanism for diffuse intravascular coagulation (DIC) (3).
Thrombotic microangiopathic syndromes include thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), and hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome; these disorders are characterized by platelet consumption, intravascular hemolysis with schistocytes due to red cell fragmentation, and clinical/laboratory findings of organ dysfunction; histologically they are all marked by small vessel occlusion with hyaline thrombi and fibrin deposition.
Clostridium perfringens sepsis with intravascular hemolysis following laparoscopic cholecystectomy: a newly reported complication.
The rationale for this form of therapy is based on (1) rapid reduction in the parasite load by direct removal (2) decreased risk of severe intravascular hemolysis and its conse- quences (disseminated intravascular coagulation and renal dysfunction) (3) improved rheology with transfused blood and reduced microcirculatory sludging and (4) improved oxygen-carrying capac- ity with transfused erythrocytes.

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