Pathophysiology of Osteomyelitis

 

Introduction

            Osteomyelitis is a severe pyogenic infection that affects the bones and their surrounding tissues. It results in inflammation, necrosis, and inflammation and formation of a new bone. The condition is in two categories, which is; according to severity (acute, subacute, and chronic) and according to the route of entry (hematogenous and exogenous) (Murillo et al., 2014). The most common cause of the condition is Staphylococcus aureus. Other causes include Coliform organisms, Pseudomonas, Hemophilus influenza, and salmonella. The risk factors for the disease are diabetes, prior spleen removal, intravenous drug administration, and trauma

Normal anatomy and physiology of the bones

            The skeleton of adult human being has a total of 213 bones, with sesamoid bones not included. All of the bones undergo constant modeling as the individual grows to adapt to the changes in the biochemical forces and also changes to remove old and damaged bones and replace it with new and stronger ones (Tortora & Derrickson, 2017). Bones are generally in four categories, which are short bones, flat bones, long bones, and irregular bones.

            The human skeleton serves several functions such as providing structural support to the body, protection of the internal structures and organs, permission of movement and locomotions through the provision of levers for the muscles. The bones also work to ensure the maintenance of homeostasis and acid-base balance as well as serving as a reservoir of growth factors and cytokines. The bones also provide the environment for hematopoiesis, which occurs within the bone marrow (Tortora & Derrickson, 2017).

Mechanism of Pathophysiology

Bacteria enter the bone through metaphyseal capillaries and are contained by the epiphyseal growth plate — an acute pyogenic inflammatory response results. There is increased capillary permeability that allow plasma protein and cells of acute inflammation to the bone tissue. A combination of leukocyte migration, edema with microvascular obstruction leads to increased pressure in the bone. These combine with the bacterial growth causes necrosis of bone, and secondary infection follows (Roy et al., 2012). As the disease proceeds to the chronic stage, Organisms start spreading through Haversian and Volkmann canals. The infection extends laterally and, as pressure builds, perforates the bony cortex, lifts the periosteum, and spreads subperiosteally, Ischemic necrosis of the underlying bone and secondary infection of the damaged bone result. The periosteum itself responds by laying down new bone—the involucrum. Pus that is sub-periosteal is under pressure, this perforates through the involucrum forming holes called cloacae, then through soft tissue to the skin (Roy et al., 2012). Part of the cortex without the periosteum which becomes necrotic is the sequestrum. In the hip and the shoulder; the synovial capsule reaches beyond the epiphyseal plate. Infection no longer limited by the growth plate may spread to the joint (Zardo & Kutschka, 2016). In infants younger than one year of age, metaphyseal capillaries perforate the epiphyseal growth plate, and infection may spread to the epiphysis. Consequently, septic arthritis and the destruction of epiphyseal growth are common in this age group, however, treatment with antibiotics or surgical procedure in the early course of the condition, will resolve the situation and prevent the development of complications.

Therefore, the condition undergoes five stages, which include, inflammation, suppuration, sequestrum, involucrum, and finally, resolution or progression to complications. This condition interferes with the normal functions of the body because it results in pain, malaise, chills, and inflammation (Zardo & Kutschka, 2016). The functioning of the human skeleton to provide support and also aid in locomotion and movement are greatly affected, thus interfering with the individual life.

 

Prevention

            It involves primary and secondary prevention, and this is mainly focused on minimizing the risk factors for the condition. Individuals at risk, for example, those with diabetes mellitus are advised to mitigate foot trauma and prevent the development of foot ulcers (Griffon, 2016). They should be monitored for the development of ischemia with the involvement of the multidisciplinary team to improve the outcomes. Education on foot care such as daily cleaning and moisturizing to prevent skin breakage is vital because it may provide a route of entry to microorganisms.  Secondary prevention involves the preventable physician measures, for example, surgical debridement, reducing the bacterial load, muscle-flap, wound irrigation, avoiding the internal fixing of contaminated bone, and provision of antibiotics (Griffon, 2016).

Treatment

Medical management

            The main aim is to control or to stop the spread of the infection. Prescription of antibiotics with general supportive measures such as the provision of a diet high in proteins and proteins, hydration, and correction of anemia is provided (Griffon, 2016). Pharmacologic therapy can be an administration of penicillins, tetracyclines, cephalosporins, or aminoglycosides.

Surgical management

            Surgical debridement is indicated for infections which do not respond to antibiotic treatment. The infected bone is surgically exposed, and the purulent and necrotic material is removed, and then the area is removed with sterile saline then intravenous antibiotic therapy is continued (Griffon, 2016).

 

 

Clinical relevance

            Infection of the long bones with acute pain and signs of sepsis. It results in localized pain and drainage that might be described by the patients as pulsating that intensifies with movement (Griffon, 2016). Those with chronic osteomyelitis present with a non-healing ulcer that overlies the affected bone, with a sinus that drains pus.

Conclusion

            Osteomyelitis is an infection of the bones that affect both infants and adults. It is mainly associated with bacteria which can spread from one point to another through the bloodstream. It is predisposed by trauma and also diabetes mellitus however, it can be prevented through proper foot care and avoidance of injury. Treatment can be through surgical intervention or administration of antibiotics.

 

 

 

References

Griffon, D. (2016). Osteomyelitis. Complications in Small Animal Surgery, 28-33.

Roy, M., Somerson, J. S., Kerr, K. G., & Conroy, J. L. (2012). Pathophysiology and pathogenesis of osteomyelitis. In Osteomyelitis. IntechOpen.

Tortora, G. J., & Derrickson, B. (2017). Principles of anatomy & physiology. John Wiley & Sons, Incorporated.

Zardo, P., & Kutschka, I. (2016). Pathophysiology of sternal osteomyelitis. In Deep Sternal Wound Infections (pp. 13-16). Springer, Berlin, Heidelberg.