Necrosis of the femoral head is one of the most common causes of secondary coxarthrosis in middle-aged adults.
It frequently affects active middle-aged adults, mostly men between the ages of 30 and 50. The peak age is 36 years. In around 30% to 70% of cases, both sides of the hip are affected consecutively.
The early stage of the disease is characterized by sudden, pulling pain in the deep groin area.
The mobility of the hip joint is restricted as a result, particularly with internal rotation. Often no trigger, such as sporting overload, is necessary. The affected person limps and can no longer put any weight on the leg.
As the condition progresses, the joint surface often collapses. The pain now becomes load-dependent and secondary coxarthrosis manifests itself. The restriction of hip joint mobility becomes more and more pronounced. The joint can feel "walled in".
The success of treatment depends largely on an early diagnosis and therefore an early start to treatment. A hip specialist should therefore be consulted even if there is a slight suspicion.
The structure of the pelvis © Henrie | AdobeStock
Necrosis of the femoral head is caused by a lack of blood supply .
As a result, not enough
- oxygen,
- minerals and
- other nutrients
reach the bone cells via the blood vessels. The bone cells that continuously ensure bone formation and resorption die off.
As a result, the bone balls inside the bone are no longer formed. They are responsible for the stability of the femoral head. The affected parts of the bone lose strength and collapse.
The bone tissue under the hip cartilage now has a hole that can damage the overlying hip joint cartilage. This leads to hip arthrosis (coxarthrosis).
The lack of blood supply is often caused by trauma. However, other risk factors can also promote the manifestation of femoral head necrosis.
(Post-)traumatic necrosis of the femoral head
In the case of trauma-related femoral head necrosis, the blood vessels are acutely interrupted as a result of an accident. This also interrupts the blood supply. This leads to an undersupply of oxygen (ischemia) to the femoral head.
Typical injuries for (post-)traumatic necrosis of the femoral head are in particular
Non-traumatic necrosis of the femoral head
The cause of non-traumatic or idiopathic femoral head necrosis has not yet been conclusively clarified. Doctors identify certain risk factors in 80% of cases of this form. A coagulation disorder combined with the reduced activity of the fibrinolysis system and thus an increased tendency to thrombosis leads to an impairment of the microcirculation.
The following risk factors or underlying diseases can cause non-traumatic femoral head necrosis:
- Nicotine and alcohol abuse and excessive blood lipid levels. Alcoholism in particular increases the risk. Alcohol abuse causes the development of a fatty liver and lipid metabolism disorders, which in turn promote femoral head necrosis.
- Taking certain medications: These include cytostatics (chemotherapeutic agents) with bone-damaging effects as well as long-term corticosteroid use as part of drug treatment (for example chronic inflammatory diseases) or long-term steroid doping with resulting hypercortisonism. In addition, damage to the femoral head can occur due to radiation, especially ionizing radiation.
Certain diseases are associated with an increased risk of femoral head necrosis. These include, for example
- decompression sickness in divers and tunnel workers due to lack of decompression
- metabolic circulatory disorders in the area of the femoral head, including
- Thrombophilia (tendency to thrombosis) and hypofibrinolysis (reduced fibrinolysis) with
- Antithrombin III deficiency,
- protein C or protein S deficiency,
- a factor V mutation,
- a nephrotic syndrome,
- hypertriglyceridemia
- Endotoxins released by gram-negative bacteria (including meningococcal sepsis)
- Gaucher's disease (lipometabolic disease) after splenectomy (removal of spleen)
- Hemoglobinopathy (hemoglobin disorder) in sickle cell anemia
- Perthes' disease(necrosis of the femoral head in children)
- Systemic lupus erythematosus (autoimmune disease, hypersensitivity reaction)
- Pregnancy due to suppression of the fibrinolytic system with hypercoagulability and hyperlipidemia
- Malignancies (malignant tumors)
Not all risk factors for femoral head necrosis have yet been clarified. For this reason, femoral head necrosis can also occur independently of the risk factors mentioned.
The course of femoral head necrosis is divided into five stages. However, the timing and natural course are subject to wide individual fluctuations.
Depending on
- on the respective stage and
- the severity and localization of the disease
different therapeutic approaches are recommended.
In the early stages, the femoral head necrosis is drilled to relieve the intraosseous pressure and to refresh the area of necrosis. The necrosis zone is opened several times in a minimally invasive procedure using small drill diameters. This serves to stimulate the body's own regeneration. This procedure is particularly suitable for small and medium-sized defects.
Hyperbaric oxygen therapy can improve the oxygen supply to the cell tissue of the femoral head. Cartilage cell transplantation or osteotomy may also be indicated to limit necrosis.
The affected joint should also be relieved by means of physiotherapeutic measures and immobilization (including orthoses, crutches). Pain-relieving medication and medication that interferes with the coagulation cascade can be used as support.
At an advanced stage, the hip joint is usually destroyed to such an extent that the use of an artificial joint(hip endoprosthesis) is necessary.
