Introduction
Currently in New Zealand 21.1% of men and 18.8% of women smoke (Ministry of Health, 2015). The Maori smoking rate is at 41% in New Zealand (Dempsey, Hillege, & Hill, 2014 ). As smoking can effect healing, this means that potentially a lot of the population’s bones may not heal normally if they were to suffer a fracture. This is a big issue in New Zealand and is seen regularly at fracture clinics across the country. Bone healing is a long and complicated process which requires the ideal angle of realignment and an adequate environment for healing to occur. Most of the patients that had fractured bones that were taking a long time to heal and not progressing smoked cigarettes daily. When a fracture occurs, all of the components of the bone including the periosteum, blood vessels, marrow and surrounding soft tissues are disrupted. There is no longer oxygenation around the fracture site so this bone tissue dies which stimulates an inflammatory response that consists of vasodilation, increased permeability, and infiltration by inflammatory leucocytes, mast cells and growth factors that work in unison to decalcify the fractured bone ends (Craft, Gordon, & Tiziani, 2011). After this response, phagocytic cells, fibroblasts, and osteoblasts migrate into the fracture and begin to rebuild the bone into a fibrocartilaginous callus, which will then remodel into spongy bone, then hard bone (Craft et al, 2011). I decided to carry out this literature review on the effects of cigarette smoking on bone healing in order to see the effect smoking has on bone healing and whether the public needs to be better educated about the risks of smoking while they have a fracture. In this literature review I will explore the effects of cigarette smoking on the body as a whole, and in relation to fractures. I will discuss how cigarette smoking affects the ability of fractures to heal, and the effect of nicotine on the healing process, as well as the effect on the surrounding soft tissues.
Literature Review
There is a wide variety of research articles and other literature surrounding fracture healing and the effects of cigarette smoking. A key point in many of these is the adverse effects of cigarette smoking on the body. Cook, Ryaby, McCabe, Frey, Heckman and Kristiansen (1997) said that smoking increases heart rate, total peripheral resistance, blood pressure and raises coronary blood flow. Cook et al., (1997) also said that ‘the risk of fractures is 2 to 6 times higher in patients who smoke because of reduced bone density’ (p. 199). El-Zawawy, Gill, Wright and Sandell (2006) said that there is a relationship between cigarette smoking and a variety of orthopaedic conditions such as delayed fracture healing, and non-union of fractures. Decreased bone mineral density means that the bones are weaker, indicating there are areas of fragility throughout the bones of the body (Marshall, Johnell & Wedel, 1996). It can be argued that cigarette smoking has adverse effects on the healing of a fracture. Other factors may increase the adverse effect of smoking, such as obesity, bone mineral density conditions such as osteoporosis, diabetes, lack of exercise and poor hygiene (Gaston & Simpson, 2007). Although, since the above research was carried out on rodents it could be argued that it is not relevant to humans or the human anatomy. However, the cigarette smoke acts on the same organs within rodents as it does in humans so there could be an assumed similarity in effect. Cigarette smoking is known to have a vast array of adverse effects on the human body and these systemic effects can result in delayed or inadequate healing of fractures. It is important to address these negative effects in the clinical setting as many patients are not educated about the risks of smoking and the effects it has on the body. Smoking cessation should be advised and support offered in achieving this.
One of the main constituents of cigarette smoke is the nicotine, which is a highly addictive alkaloid (Nawful, Sewell, Bhavikatt & Gikas, 2012). Nawfal et al., (2012) stated in their report that ‘nicotine exposed bones to be 26% weaker in three-point bending’ (p. 286). Cesar-Neto, Duarte, Sallum, Barbieri, Moreno & Nociti (2003) said that low bone area and low bone density can be caused by nicotine. Miller (2014) stated that since nicotine is a vasoconstrictor the decreases blood flow to the extremities. Blood flow is essential in fracture healing as the nutrients needed for healing are delivered to the site through the blood. Because of the abundance of nicotine in each cigarette, the effects of this chemical on the body are large and instantaneous. Cigarettes containing nicotine were found to have contributed to a large incidence of non-union and delayed healing of tibial fractures in current smokers (Bender, Jefferson-Keil, Biglari, Swing, Schmidmaier & Moghaddam, 2014). It can be argued that nicotine is the largest contributor to the negative effects of cigarette smoking on the human body, as the evidence has shown that nicotine is playing a large role in hindering effective fracture healing. Because nicotine is highly addictive, it can be extremely difficult for patients to cease smoking completely while their fracture heals and this means that almost all cigarette smokers will continue to smoke, resulting in a larger incidence of complications throughout the fracture healing process. This is an issue in clinical practice as advising and offering support for a patient to cease smoking is very rarely successful and can be hard to follow up on as many fractures are cared for on an outpatient basis.
When a fracture occurs, not only is the bone itself damaged but the surrounding soft tissue can be severely affected. Miller (2014) found that fractures can result in injuries to surrounding soft tissue which leads to infection and increased healing time. El-Zawawy et al., (2006) argued that carbon monoxide inhaled during smoking of cigarettes reduced the oxygen carrying capacity of red blood cells to the site of injury, meaning less oxygen is available to promote healing in the site of soft tissue injury, and within the fracture itself. Nawfall et al., (2012) stated that carbon monoxide has a higher affinity of bonding to haemoglobin than oxygen where it forms carboxyhaemoglobin. Because it bonds to haemoglobin so readily, oxygen is not able to bond, and therefore less oxygen is circulating in the bloodstream resulting in hypoxia. If the tissue surrounding a fracture site does not adequately heal, it can increase the incidence of non-union and other complications within the fracture itself (Adams, Keating, & Court-Brown, 2001). This can contribute to future weakness within the bone and chronic pain or inflammation around the site if scar tissue is present. Karlsson (2011) concluded that patients who ceased smoking and or entered a smoking cessation programme at the beginning of the recovery process from a fracture had fewer complications in and around the fracture site. This could be viewed as conclusive evidence that cigarette smoking has a profound negative effect on fracture healing and healing of the surrounding soft tissue, as when efforts are made to cease smoking, the outcome statistics of the fracture improve dramatically. For a fracture to heal effectively, the surrounding environment must be healthy and have access to red blood cells and nutrients to promote healing. If the surrounding soft tissue is healthy, the fracture itself has a better chance of uniting and remodelling effectively so there is reduced future weakness or other complications. Advising patients to cease smoking or even to decrease the amount they are smoking will have a significant effect on blood flow the oxygen availability to the fracture area and surrounding tissue.
Cigarette smoking can have a lasting effect on the body. Although a person may cease smoking, the damage to body systems such as the pulmonary, cardiac, vascular systems and the connective tissue throughout the body remains present and can have negative impacts on health. In a study by Cook et al., (1997), it was found that patients who had previously smoked 10 years prior to a fracture had similar complications in the fracture healing process to those who still currently smoked, compared with patients who did not smoke at all who had significantly less complications. Kanis, Johnell, Oden, Johansson, De Laet, Eisman et al., (2005) stated that smoking is considered a large risk factor for fractures in the future. This means that although a person may quit smoking and not have any cigarettes for 10 years, they will always have a greater risk of fracture than a person who has never smoked a cigarette. Gaston and Simpson (2007) report that patients that currently or have previously smoked have a fourfold greater risk of fracturing their tibia during low-energy activity than non-smokers, and are at greater risk of complications and non-union during recovery. It is important to consider that people may see these results as an excuse not to quit smoking as they are not a great deal better off than if they did not quit in relation to risk of fracture. However, the other health benefits associated with smoking cessation such as weight loss, total lung capacity and level of physical ability are a great incentive and can also help reduce the risks of fracture and fracture complications (McKee, O’Malley, Salovey, Krishnan-Sarin & Mazure, 2005). Risk of fracture and fracture healing complications is greatly increased by smoking and unfortunately does not disappear when cigarette smoking is ceased. Smoking cessation is very important in improving health outcomes and decreasing other risk factors associated with poor fracture healing, therefore it is worthwhile quitting smoking in relation to improving bone health and healing. Advising and offering support to cease smoking in the clinical environment is extremely important when dealing with fractures. This is because the positive systemic effects for the patient will benefit them in all aspects of their health, improving their general wellbeing and contributing to decreased risk factors for non-union and delayed fracture healing.
Recommendations
The recommendations developed from this literature review for health professionals regarding fracture healing and the effects of cigarette smoking are as follows.
Conclusion
In conclusion, the literature conveys evidence that cigarette smoking does indeed hinder fracture healing. Cigarette smoking is proven to have a vast range of negative and potentially life threatening effects on the human body and this includes the ability of the bone and surrounding soft tissue to heal after a fracture. Bone mineral density is decreased due to cigarette smoking which leads to complications in healing such as non-union and delayed healing, and also increases the risk of future fractures as the bones are weaker. Nicotine is a highly addictive component of cigarette smoking and causes vasoconstriction and therefore reduced blood flow to the extremities, reducing the oxygenation of the tissue around the fracture. Nicotine also makes it very hard to quit because of its addictive properties and so it continues the damage to other body systems. Carbon monoxide reduces the amount of oxygen bonding to haemoglobin to be dispersed around the body causing hypoxia, severely reducing the healing at the fracture site. Vasoconstriction and hypoxia delay healing of surrounding soft tissue at the fracture site, leading to infection and scar tissue. Unfortunately quitting smoking does not undo the damage caused by previous cigarette smoking; however, stopping will still have great health benefits for overall health and wellbeing. The recommendations developed from this literature review will help health professionals increase the incidence of smoking cessation among fracture patients in the clinical setting. Educating the patient, offering support, and being accessible will allow the patient to feel supported and in control of their health outcomes. If smoking cessation occurs, there will be increased positive outcomes for fracture healing and shorter recovery time, meaning the patient can get on with their life and reducing the financial burden on the health sector, as well as overcrowding in local clinical settings. New Zealand as a country aims to be ‘Smokefree’ by the year 2025, and if this goal is achieved, there will be greater positive health outcomes, less complications and better general wellbeing across the country. This is a great outcome for all communities and will lead to a healthier, and more able New Zealand.
References
Adams, C., Keating, J., & Court-Brown, C. (2001). Cigarette smoking and open tibial fractures. Injury, 32(1), 61-65. http://dx.doi.org/10.1016/s0020-1383(00)00121-2
Bender, D., Jefferson-Keil, T., Biglari, B., Swing, T., Schmidmaier, G., & Moghaddam, A. (2013). Cigarette smoking and its impact on fracture healing. Trauma, 16(1), 18-22. http://dx.doi.org/10.1177/1460408613504064
César-Neto, J., Duarte, P., Sallum, E., Barbieri, D., Moreno, H., & Nociti, F. (2003). A Comparative Study on the Effect of Nicotine Administration and Cigarette Smoke Inhalation on Bone Healing Around Titanium Implants. Journal of Periodontology, 74(10), 1454-1459. http://dx.doi.org/10.1902/jop.2003.74.10.1454
Cook, S., Ryaby, J., McCabe, J., Frey, J., Heckman, J., & Kristiansen, T. (1997). Acceleration of Tibia and Distal Radius Fracture Healing in Patients Who Smoke. Clinical Orthopaedics and Related Research, 337, 198-207. http://dx.doi.org/10.1097/00003086-199704000-00022
Craft, J., Gordon, C., & Tiziani, A. (2011). Understanding Pathophysiology. Chatswood: Mosby Elsevier.
Dempsey, J., Hillege, S., & Hill, R. (2014 ). Fundamentals of Nursing and Midwifery: A person-centred approach to care. Sydney: Lippincott Williams & Wilkins.
El-Zawawy, H., Gill, C., Wright, R., & Sandell, L. (2006). Smoking delays chondrogenesis in a mouse model of closed tibial fracture healing. Journal of Orthopaedic Research, 24(12), 2150-2158. http://dx.doi.org/10.1002/jor.20263
Gaston, M. & Simpson, A. (2007). Inhibition of fracture healing. Journal of Bone and Joint Surgery - British Volume, 89-B(12), 1553-1560. http://dx.doi.org/10.1302/0301-620x.89b12.19671
Kanis, J., Johnell, O., Oden, A., Johansson, H., De Laet, C., & Eisman, J. et al. (2004). Smoking and fracture risk: a meta-analysis. Osteoporosis International, 16(2), 155-162. http://dx.doi.org/10.1007/s00198-004-1640-3
Karlsson, J. (2011). Quit smoking and reduce surgical complications. Knee Surgery, Sports Traumatology, Arthroscopy, 19(3), 331-332. http://dx.doi.org/10.1007/s00167-010-1385-9
Marshall, D., Johnell, O., & Wedel, H. (1996). Meta-analysis of how well measures of bone mineral density predict occurrence of osteoporotic fractures. BMJ, 312(7041), 1254-1259. http://dx.doi.org/10.1136/bmj.312.7041.1254
McKee, S., O'Malley, S., Salovey, P., Krishnan-Sarin, S., & Mazure, C. (2005). Perceived risks and benefits of smoking cessation: Gender-specific predictors of motivation and treatment outcome. Addictive Behaviors, 30(3), 423-435. http://dx.doi.org/10.1016/j.addbeh.2004.05.027
Miller, S. (2014). How smoking can hinder fracture healing. Emergency Nurse, 22(4), 28-30. http://dx.doi.org/10.7748/en.22.4.28.e1219
Ministry of Health. (2015). Annual Update of Key Results 2014/15. Wellington: New Zealand Health Survey.
Nawfal, A. H., Sewell, M., Bhavikatt, M., & Gikas, P. (2012). The effect of smoking on fracture healing and on various orthopedic procedures. Acta Orthopaedica Belgica, 285-590.
Quitline. (2016, March 27). Quitline Home Page. Retrieved from Quitline: http://www.quit.org.nz/