Gastrocnemius Strain Flashcards
What, aetiology, epidemiology, predisposing factirs if strains, clinical features, types, pathophysiology
What is a gastrocnemius strain?
A muscle is stretched to far resulting in a tear ir multiple tears of a muscle.
Aetiology of gastocnemius strain.
Eccentric force being applied to the muscle when the knee is extended and the ankle is dorsiflexed.
Epidemiology of gastrocnemius strain.
Commonly seen in sporting injuries- running, tennis
Younger people
Predisposing factors of strains.
- 2 joint muscles
- Eccentric contraction
- Inadequate warm up
- Insufficient joint ROM
- Excessive muscle tightness
- Muscle tightness
- Fatigue
- Overuse/inadewuate recovery
- Previous injury
- Faulty technique
What are the types of gastrocnemius strain?
Acute- result of a single traumatic injury, causes a macro-trauma to the muscle
Overuse- chronic or exercises induced injuries are subtler and usually occur over a long period of time. Repetitive micro-trauma.
What are the grades?
Grades 1, 2 and 3.
What is grade 1?
Mild Pain/tenderness are delayed till next day Small tear/overstretched fibres No loss of function/strength/ROM 10-12 days
What is grade 2?
Moderate >10-15% of fibres torn Moderate pain and swelling Incomplete tear but some loss of function/strength/ROM-pain Pain reproduced on muscle contraction 16-21 days
What is grade 3?
Severe Complete tear Severe pain initially Complete loss of function/strength/ROM Tendon separated from muscle belly or muscle belly is torn in 2 Severe swelling 6 months after surgery
What is the pathophysiology of gastrocnemous strain?
A strain occurs when muscle fibres cannot cope with the tension placed on them by exercise overload and leads to tearing of the muscle fibres.
What is the healing process of a ruptured gastrocnemius?
Hemostatsis- bleeding. Platelets in contact eith collagen results in activation. Prothrombin is converted to thrombin and fibrrinogen is converted to fibrin. Form fibrin cross-linking to strengthen the platelet clumps into a stable clot coagulation. 4-6hrs.
Inflammation- focuses on destroying bacteria/removing debris. White blood cells (neutrophils) enter the wound and destroy bacteria. An inflammatory response releases inflammatory cytokines e.g serotonin , bradykinin, histamine. Onve neutophils leaves macrophages enter clear debris. Secrete growth factors/proteins to facilitate repair. 5 cardinal signs of inflammation.
Proliferation- distinct stages with stage.
1. Filling wound - shiny, deel, red granulation tissue fills the wound bed with connective tissueand new blood vessels are formed
2. Contraction of wound margins- wound margins pull towards the centre if wound.
3. Covering the wound (epithelialisation)-> epithelial cells arise from the wound bed it margins and migrate across the wound until completely covered
4 - 24 days
Remodeling- new tissue slowly gains strength/flexibility. Collagen fibres reorganise the tissue remodels/matures. Increase in tensile strength (max strength limited to 80% of preinjured strength) 21 days - 2 years.
