Hemolysis

Hemolysis is the release of intracellular components of blood cells (primarily erythrocytes) into the extracellular space (Hofmann 2014). This can be physiological or pathological (Hoffbrand 2003). The release of these intracellular components can occur due to degradation or destruction of the erythrocytes (Michl 2019).

- Site of erythrocyte degradation:

Hemolysis can occur in- vivo both intravasally (usually pathologically [Hoffbrand 2003]) and extravasally (Herold 2022 / Müller 2023). In addition, hemolysis is possible in- vitro during e.g. blood collection (Gressner 2013). For more details see "Etiology".

- Type of injury:

The damage can be intrinsic (corpuscular) or extrinsic (extracorpuscular) (Michl 2019).

Hemolysis can also be compensated or uncompensated:

- Compensated hemolysis:

If hemolysis results in increased erythropoiesis and the Hb- content in the blood remains within the normal range, it is called compensated hemolysis (Herold 2022).

- Non-compensated hemolysis:

If the hemolysis is not compensated and thus both erythrocytes and the hemoglobin content of the blood drop, it is called hemolytic anemia (Herold 2022).

A further distinction is made between acute and chronic hemolysis (Berger 2010).

Erythrocytes have a lifespan of approximately 120 days. After this period, they are degraded by extravascular in vivo hemolysis (Müller 2023).

However, in vivo hemolysis can also occur intravasally and is then usually pathological (Müller 2023).

Hemolysis is visible to the naked eye in serum or plasma from an Hb concentration of approx. 20 mg / dl (Herold 2022).

In -vivo hemolysis can be caused by:

- physiologically at the end of the erythrocyte's life (Müller 2023)

- thermally induced by e.g. burns

- traumatic after e.g. march hemoglobinuria or heart valve replacement

- chemically by e.g. snake venom

- drug-induced as so-called immune hemolysis (theoretically possible by any drug, especially by nonsteroidal anti-inflammatory drugs, cephalosporins, tuberculostatics [Kiefel 2010])

- parasitically caused by e.g. malaria (Berger 2010)

- bacterial caused by streptococci in particular (Müller 2023)

- hypersplenism (Aulbert 2008)

- blood group incompatibilities due to antigen-antibody reaction (Emminger 2005)

- Osmotic damage (Müller 2023)

In vitro hemolysis in the course of blood sampling can occur, for example, due to:

- too narrow puncture cannulas

- too long venous stasis

- poor transport conditions (Müller 2023)

The main symptoms of hemolysis are hemoglobinuria and icterus (Aulbert 2008).

Acute hemolysis may be accompanied by:

- Tachycardia

- palpitations

- exertional dyspnea (Berger 2010).

In chronic hemolysis , there are usually hardly any symptoms. Even hemoglobin levels up to 6 - 8 mg / dl are tolerated. Otherwise there may be:

- low grade icterus

- often bilirubin-containing gallstones

- splenomegaly (Berger 2010)

In a hemolytic crisis may additionally occur:

- chills

- fever

- pain in the back, abdomen, head (Berger 2010)

The destruction of the erythrocytes releases hemoglobin and other cell components such as LDH, GOT, potassium. Hemoglobin is bound to haptoglobin, so that free haptoglobin decreases (Müller 2023).

Typical laboratory changes in hemolysis are therefore:

There is a decrease in:

- Haptoglobin (most sensitive parameter).

- AP

- gamma- GT

- hemoglobin

- hematocrit

- erythrocytes

- Survival time of erythrocytes (Berger 2010)

and to an increase in :

- total bilirubin

- GPT

- reticulocytes

- Serum iron

- Free Hb

- hemopexin

- LDH (Berger 2010)

It should be noted that hemolysis in a blood sample causes the following values to increase artificially:

- LDH

- AST (GOT)

- ALT (GPT)

- Potassium (Herold 2022)

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