Protein catabolism in the critically ill
- Increased blood levels of catabolic hormones (cortisol, catecholamines, glucagon)
- Resistance to endogenous anabolic hormones (insulin, IGF-1) in peripheral tissue
- Muscle wasting and decrease in protein anabolism
Immobilization, neuromuscular blockade - Corticosteroids:
Skeletal muscle degradation
In critical illness, whether the patient has acute or chronic disease, increase in protein breakdown is higher than protein synthesis. So there is always a net protein breakdown.
What are the reasons for this negative nitrogen balance?
Increased blood levels of catabolic hormones and resistance to endogenous anabolic hormones in peripheral tissues are among the main determinants for protein catabolism in the critical ill.
immobilization and neuromuscular blockade also lead to muscle wasting and decrease in protein anabolism.
Even corticosteroids cause skeletal muscle degradation.
In critical illness, whether the patient has acute or chronic disease, increase in protein breakdown is higher than protein synthesis. So there is always a net protein breakdown. What are the reasons for this negative nitrogen balance? Increased blood levels of catabolic hormones and resistance to endogenous anabolic hormones in peripheral tissues are among the main determinants for protein catabolism in the critical ill.
Immobilization and neuromuscular blockade also lead to muscle wasting and decrease in protein anabolism.
Even corticosteroids cause skeletal muscle degradation.
Skeletal muscle catabolism and amino acid degradation is used for energy production through gluconeogenesis and protein synthesis for tissue repaired for immune and inflammatory responses, and for synthesis of acute phase proteins and even in the endogenous antioxidant enzymes.
Whole body protein synthesis and breakdown
Protein synthesis | Protein breakdown | Net protein breakdown | |
---|---|---|---|
Acute disease | ⬆ | ⬆⬆⬆ | ⬆⬆ |
Chronic disease | ⬆ | ⬆⬆ | ⬆ |
Critical illness
Skeletal muscle catabolism
Amino acid degradation for protein synthesis
- Gluconeogenesis and tissue repair
- Immune and inflammatory responses
- Acute phase proteins synthesis
- Endogenous antioxidant enzyme synthesis
Sequential Changes in the Metabolic Response in Critically Injured Patients During the First 25 Days After Blunt Trauma
There is solid data showing protein resting in the critically ill obtained by body composition, ultrasound and Computed Tomography studies. These findings provide valuable insights into skeletal muscle wasting in critical illness. In a case study of body composition, skeletal muscle was measured by DEXA. Over the 21 day study period, there was 16% loss of total body protein, and two thirds of this loss came from skeletal muscle. These losses were greater than had been taught in the past. Measurement of rectus femurs muscle cross sectional area by ultrasound showed muscle resting acute early and rapidly during the first week of critical illness. That was 70% loss in 10 days, it was more severe among those with multi organ failure compared with single organ failure.
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