Fractures of the acetabulum

                   Fractures of Acetabulum

                                      Dr KS Dhillon

Anatomy

The acetabulum is a deep, cup-shaped, hemispherical depression, directed downward, lateralward, and forward.Three bones of the pelvis, namely the ilium, ischium and the pubic bone contribute to the formation of the acetabulum. A little less than two-fifths is contributed by the ilium, a little more than two-fifths by the ischium, and the remaining fifth by the pubic bone. The pubic bone lies anteriorly, the ilium superiorly and the ischium posteroinferiorly. It has six principal components, the  anterior column, posterior column, anterior wall,   posterior wall, acetabular dome or roof and the medial wall.

The posterior column is composed of the quadrilateral surface, posterior wall, dome, ischial tuberosity and the greater/lesser sciatic notches. The anterior column is composed of anterior ilium, anterior wall, dome, iliopectineal eminence and the lateral superior pubic ramus.

The roof of the acetabulum is the thick, weight bearing portion and forms a separate fragment in bicolumnar fractures. The thin quadrilateral plate forms the medial wall or the floor of the acetabulum.

The acetabulum is bounded by an uneven rim, which is thick and strong above, and to it is attached the glenoid labrum which deepens the surface for articulation. Below it, there is a deep notch, the acetabular notch, which is continuous with a circular non-articular depression, the acetabular fossa, at the bottom of the cavity. This depression contains a mass of fat. The notch is converted into a foramen by the transverse ligament; through which nutrient vessels and nerves enter the joint. The margins of the notch give attachment to the ligamentum teres. The rest of the acetabulum is covered with a curved articular surface, the lunate surface, for articulation with the head of the femur.
The mean lateral inclination of the acetabulum is between 40 to 48 degrees and the mean anteversion is between 18 to 21 degrees.

Classification of acetabular fractures

The most widely used classification of acetabular fractures is that by Judet and Letournel. According to this classification fractures of the acetabulum are broadly divided into 2 categories: elementary fractures and associated fractures. There are 5 elementary and 5 associated fracture patterns. The associated fractures are composed of a combination of at least two of the elementary fracture patterns.

Elementary fractures involve a single wall, involve a single column, or are purely transverse. The simplest elementary fractures are two-part fractures.

Associated fracture patterns have at least three major fracture fragments and include a posterior column fracture with a posterior wall fracture, a transverse fracture with a posterior wall fracture, an anterior column fracture with a posterior hemitransverse fracture, a T-type transverse fracture, and associated both-column fractures.

The wall fractures can be divided into two types: the anterior wall fractures and the posterior wall fractures. The transverse fractures can be divided into three types: the transverse fracture, the T- shaped fracture and the transverse with posterior wall fracture. The column fractures can be divided into five types: posterior column, anterior column, posterior column with posterior wall, both columns and anterior column with posterior hemitransverse fractures [1].

Out of the 10 fracture patterns, 90% of acetabular fractures that occur are one of following five types: associated both-column, T-type, transverse, transverse with posterior wall, and elementary posterior wall fractures [2,3]. Often the acetabular fractures do not fit perfectly into one of the fracture patterns in the classification scheme [4].

Radiography

An anteroposterior view and left and right Judet views are required for evaluation of acetabular fractures. Judet views are the obturator oblique view (fig 1) which shows profile of obturator foramen and also shows the anterior column and posterior wall, and the iliac oblique view (fig 2) shows profile of involved iliac wing and it shows the posterior column and anterior wall.

The radiographic landmarks of the acetabulum include the iliopectineal line (anterior column), ilioischial line (posterior column), anterior wall, posterior wall, teardrop, weight bearing roof and the Shenton's line.

CT scan 

A CT scan is now considered a gold standard in management of patients with acetabular fractures. It helps in identification of the fracture pattern orientation, and definition of fragment size and orientation. Marginal impaction, articular gaps and step offs can be identified with a CT scan.
Loose bodies in the joint can be seen with CT scan.

Treatment of acetabular fractures

Nonoperative treatment

Indications for nonoperative treatment include:

• Undisplaced fractures and minimally displaced fractures (<2mm displacement).
• Displaced fractures where a large portion of the acetabulum remains intact and the femoral head remains congruent with the acetabulum.
• Moderate displacement of a both-column fracture and the patient presents late (>3 weeks after injury).
• Small posterosuperior-wall fractures with a stable hip joint and a congruent reduction.
• A posterior-wall injury that is minimally displaced or nondisplaced.
• If surgery is contraindicated

Surgery would be contraindicated in patients with:

• Severe systemic illness or secondary multiorgan failure due to polytrauma
• Systemic infections or sepsis
• Local infection
• Extreme  osteoporosis
• Severe comminution with preexisting arthrosis would be a relative contraindication.

Nonoperative treatment includes:

• Resuscitation of the patient - Basic or advanced life support where necessary.
• Diagnosis - After patient has been stabilized a clinical and radiologic diagnosis is established.
• Treatment of other life-threatening injuries such as head, chest, abdominal, or other injuries.
• Urgent reduction of associated dislocation is carried out. Posterior dislocations are managed by gentle close reduction on an emergency basis. Central fracture-dislocations are treated by skeletal traction applied to an upper tibial or lower femoral pin. 

For patients with undisplaced and minimally displaced fractures, protected weight bearing for 6-8 weeks is usually recommended.  DVT prophylaxis is usually recommended in patients who are immobilized or are slow to slow to mobilize.

Indications for open reduction and internal fixation include [5,6] :

• Injury less than 3 weeks old
• Patient physiologically stable
• Good soft-tissue coverage
• no local infection
• More than 2 mm displacement of roof 
• Unstable fracture pattern 
• Marginal impaction
• Intra-articular loose bodies
• Irreducible fracture-dislocation
• Intact roof-arc angle less than 30°
• Fractures that have a medial roof-arc angle of 45° or less
• Anterior roof-arc angle of 25° or less
• Posterior roof-arc angle of 70° or less across the weight bearing part of the acetabulum. 
• Vascular injury or sciatic palsy after a closed reduction

The fractures can be approach anteriorly by the ilioinguinal, iliofemoral or the modified stoppa approach. The Kocher-Langenbeck approach can be used for posterior fractures and an extended iliofemoral combined approach for both anterior and posterior fractures.

Outcome of management of acetabular fracture

The outcome after undisplaced and minimally displaced fractures treated conservatively is invariably good. The outcome of treatment of significantly displaced fractures which require open reduction and internal fixation can vary widely. There is a strong correlation between the accuracy of reduction
and the clinical outcome. Accurate reduction with restoration of articular congruence is associated with good clinical outcome [7]. Incongruent reduction correlates strongly with a poor outcome [8]. Excellent results can be achieved even when the reduction is poor, provided that the step or gap is outside the weight-bearing region [9].

A significant negative impact on outcome is seen in patients with simple posterior column fractures and T-shaped fractures. Patients with a combined posterior wall traumatic dislocation and sciatic nerve palsy also fare badly. The outcome is also poor when the acetabular fracture are associated with injury to the femoral head  [10-13].

Deo et al [14] reported good to excellent results in 74% of 79 patients they treated who had acetabular fractures. Early operation and an anatomical reduction was associated with good outcome and poor outcome was seen in patients who had delayed surgery, and in patients where there was failure to achieve or maintain reduction, and in patients who had femoral head damage at the time of injury.

Matta JM [15] published the outcome of treatment of 262 displaced acetabular fractures in 259 patients. The patients were treated with open reduction and internal fixation (ORIF) within 3 weeks after injury. This review was carried out at a mean follow-up of 6 years. Anatomical reduction was achieved in 71% of cases. Greater fracture complexity, age > 40 years, and a longer interval between injury and surgical reduction were  bad prognostic factors which were significantly associated with a decreased rate of anatomical reduction and poorer outcome. The results were excellent in 40%, good in 36%, fair in 8%, and poor in 16% of the patients.The overall clinical results were excellent / good for 76% of patients.

There was neurological injury (2 sciatic nerve injury and 1 femoral nerve injury and 6 peroneal nerve injury) in 3% of the cases. Wound infection occurred in 13 hips (5%), extraarticular in 5 hips and intraarticular in 8 hips. Progressive femoral head wear was seen 13 cases (5%). Osteonecrosis of the femoral head occurred in 8 hips (3%). Subsequent operations included a total hip replacement in 6% of the cases and an arthrodesis in 2% of the patients.

Gänsslen et al [16] in a study 135 patients with both column fractures of the acetabulum found that 69.8% of those with anatomically reconstructed hip joints had no or mild postoperative pain and a good or excellent result at a mean follow up of 54.6 months. Arthritic changes were seen in 17.5% of the patients and joint failure in a further 25.4% of the patients. Joint failure was usually seen in patients with concomitant femoral head lesion and significant preoperative articular fragment displacement.

Briffa et al [7] reported the outcome of treatment of 161 of the 257 patients who had surgical fixation of acetabular fractures at a minimum of 10 years follow up. The result were excellent in 47%, good in 25%, fair in 7% and poor in 20% of the patients.

They had a high infection rate of 11%, of which 6% were deep infection, despite the use of prophylactic antibiotics. They had a 12.5% incidence of sciatic nerve palsy, a 1.8% obturator and a 14.3% incidence of lateral femoral cutaneous nerve palsy.

There were no cases with pulmonary embolism and no cases with deep vein thrombosis. There was a 10.5% incidence of heterotopic ossification. The incidence of posttraumatic osteoarthritis was 38% in this series, which is higher than the  26.6% reported by Giannoudis et al [17] in their 2005 meta analysis.

The incidence of AVN of the femoral head was 11.8% and the incidence of total hip replacement was 16% in the Briffa et al series.

The 10 years survivorship of total hip replacement (THR) in patients with prior acetabular fracture is markedly inferior and is more frequently associated with serious complications when compared with patients undergoing THR for primary osteoarthritis or AVN. Morison et al [18] carried out a retrospective case-control study which compared the outcome of THR in patients with previous acetabular fractures, with the outcome in patients who received a THR for primary osteoarthritis or AVN. They found that the average time to revision of the THR in patients with previous acetabular fractures was 8 years as compared to 13 years in patients without acetabular fracture who had THR. The primary cause for revision in both cohorts was loosening of the acetabular component. There was no difference in revision rates in patients who had conservative or surgical treatment for the acetabular fractures. The primary cause for revision in both cohorts was loosening of the acetabular component.

Patients undergoing THR who had previous acetabular fractures were more likely to develop serious complications such as infection, dislocation, and acetabular loosening and heterotopic ossification. The infection rates were 7% in patients with previous acetabular fractures as compared to 0% in the cohort without previous acetabular fractures. The dislocation rates were 11% in patients with previous acetabular fracture as compared to 3% in the other cohort and heterotopic ossification was seen in 43% and 16% of the patients respectively, in the two cohorts.

Romness and Lewallen [19] did a retrospective study of 55 primary total hip arthroplasties, in 53 patients with a history of previous acetabular fracture, with a mean follow up of 7.5 years and they found radiographic loosening of the acetabular component in 52.9% of the patients and symptomatic loosening in 27.5% of the patients. The revision rates at a mean follow up of 7.5 years was 13.7%.
Weber et al [20] reported revision rates of 22% for aseptic loosening at 10 years follow up, in patients who had a THR for arthrosis from previous acetabular fractures.

Conclusion

Standard AP and oblique obturator and iliac views of the acetabulum are necessary when an acetabular fracture is suspected. CT scan is now gold standard for a workup in the management of acetabular fractures.

Good long term results can be expected for undisplaced and minimally displaced acetabular fractures treated nonoperatively.

The clinical outcome for operatively treated patients are generally good, with acceptable complication rates. Good to excellent results have been reported in about 76% of the patient.
Loss of joint congruency with an intraarticular step-off of more than 2mm leads to increased rates of secondary osteoarthritis. Post traumatic osteoarthritis has been reported in 26% to 38% of the patients. The reported incidence of AVN of the femoral head is about 11.8% and the incidence of total hip replacement in patients with acetabular fractures is about 16%. The survivorship of THR in patients with acetabular fractures is lower than in patients who have THR for primary OA or AVN by about 5 years at 10 years follow up. Revision rates of 22% for aseptic loosening at 10 years follow up have been reported in patients who had a THR following acetabular fractures.

 References

1. Saterbak AM, Marsh JL, Turbett T, et al. Acetabular fractures classification of Letournel and Judet—a systematic approach. Iowa Orthop J  1995; 15: 184–96.
2. Brandser E, Marsh JL. Acetabular fractures: easier classification with a systematic approach. AJR 1998; 171:1217–1228.
3. Durkee NJ, Jacobson J, Jamadar D, Karunakar MA, Morag Y, Hayes C. Classification of common acetabular fractures: radiographic and CT appearances. AJR 2006; 187:915–925.
4. Lawrence DA, Menn K, Baumgaertner M and Haims AH. Acetabular Fractures: Anatomic and Clinical Considerations. American Journal of Roentgenology. 2013;201: W425-W436. 10.2214/AJR.12.10470.
5. Matta JM, Mehne DK, Roffi R. Fractures of the acetabulum. Early results of a prospective study. Clin Orthop Relat Res. 1986 Apr. (205):241-50. 
6. Olson SA, Bay BK, Chapman MW, Sharkey NA. Biomechanical consequences of fracture and repair of the posterior wall of the acetabulum. J Bone Joint Surg Am. 1995 Aug. 77 (8):1184-92.
7. Briffa N, Pearce R, Hill AM, Bircher M. Outcomes of acetabular fracture fixation with ten years' follow-up. J Bone Joint Surg Br. 2011 Feb;93(2):229-36. doi: 10.1302/0301-620X.93B2.24056.
8. Murray MM, Zurakowski D, Vrahas MS. The death of articular chondrocytes after intra-articular fracture in humans. J Trauma 2004;56:128-31.
9. Starr AJ, Watson JT, Reinert CM, et al. Complications following the “T extensile” approach: a modified extensile approach for acetabular fracture surgery: report of forty-three patients. J Orthop Trauma 2002; 16:535-42.
10. Matta JM, Mehne DK, Raffi R. Fractures of the acetabulum: early results of a prospective study. Clin Orthop 1996;205:241-50.
11. Moed BR, Yu PH, Gruson KI. Functional outcomes of acetabular fractures. J Bone Joint Surg [Am] 2003;85-A:1879-83.
12. Murphy D, Kaliszer M, Rice J, McElwain JP. Outcome after acetabular fracture: prognostic factors and their inter-relationships. Injury 2003;34:512-17.
13. Mears DC, Velyvis JH, Chang CP. Displaced acetabular fractures managed operatively: indicators of outcome. Clin Orthop 2003; 407:173-86.
14. Deo SD, Tavares SP, Pandey RK, El-Saied G, Willett KM, Worlock PH. Operative management of acetabular fractures in Oxford. Injury. 2001 Sep;32(7):581-6.
15. Matta JM. Fracture of the acetabulum: accuracy of reduction and clinical results in patients managed operatively within three weeks after the injury. J Bone Joint Surg Am. 1996; 78 (11): 1632 – 1645.
16. Gänsslen A, Frink M, Hildebrand F, Krettek C. Both column fractures of the acetabulum: epidemiology, operative management and long-term-results. Acta Chir Orthop Traumatol Cech. 2012; 79(2):107-13.
17. Giannoudis PV, Grotz MR, Papakostidis C, Dinopoulos H. Operative treatment of displaced fractures of the acetabulum: a meta-analysis. J Bone Joint Surg [Br] 2005;87-B:2-9.
18. Morison Z, Moojen DJ, Nauth A, Hall J, McKee MD, Waddell JP, Schemitsch EH. Total Hip Arthroplasty After Acetabular Fracture Is Associated With Lower Survivorship and More Complications. Clin Orthop Relat Res. 2016 Feb;474(2):392-8. doi: 10.1007/s11999- 015-4509-1.
19. Romness DW, Lewallen DG. Total hip arthroplasty after fracture of the acetabulum. Long-term results. J Bone Joint Surg Br. 1990 Sep; 72(5):761-4.
20. Weber M, Berry DJ, Harmsen WS. Total hip arthroplasty after operative treatment of an acetabular fracture. J Bone Joint Surg Am. 1998 Sep;80(9):1295-305.

Racism in Malaysia

                        Racism in Malaysia

                                      Dr KS Dhillon

“All human beings are born free and equal in dignity and rights…”
         (Universal Declaration of Human Rights, 1948)

What is racism?

The Cambridge English Dictionary defines racism as “the belief that people's qualities are influenced by their race and that the members of other races are not as good as the members of your own, or the resulting unfair treatment of members of other races” [1].

Without doubt racism is a global reality. It is a global hierarchy of human superiority and inferiority which has been politically, culturally and economically produced and reproduced for centuries by certain sections of society. People belonging to the superior race enjoy access to, human rights, civil rights, women rights and/or labor rights as well as to material resources, and social recognition. Those belonging to the inferior race are considered subhuman or non-human and their humanity is questioned and negated. Those of the inferior race are denied their human and other rights, as well as material resources and social recognition [2].

Colonial histories in different parts of the world at different times have constructed racism along racial markers such as color, ethnicity, language, culture and/or religion. Since colonial times, color racism, the so called white supremacy, has been the dominant marker of racism in most parts of the world including the USA.

When the skin color is the same and cannot be used as a marker then the religious marker is often used to claim superiority. The British did this in Ireland where there was a racial conflict between Protestants and Catholics.

Even to present day there is Islamophobia in Europe and in the United States. In North America and Europe, muslim religious identity constitutes one of the most prominent markers of human superiority and inferiority. In these regions of the world islamophobia has led the white supremacist to label muslims with many unsavoury labels with reference to civility, violence, abuse of rights of children, women and gay/lesbians [2]. In these two regions of the world color racism and religious racism continues to be of great importance and entangles itself in complex ways.

In other parts of the world ethnic, linguistic, religious and or cultural identity is used to define racial dominance. Malaysia is a shining example of such racism.

Concept of race in Malaysia

In social sciences the concept of race to analyze and classify groups of people has no scientific foundation and analytical concept of race has been rejected [3]. The main concern of race studies has been the construction of race as a social reality and the survival of race as a concept.

In Malaysia, the term race is widely used as an accepted scientific concept to discuss ethnic relations.
Syed Husin Ali [4], a Malaysian anthropologist, argues that population groups such as Malays, ethnic Chinese, ethnic Indian and so on should be referred to as ethnic groups rather than racial groups. The reason being, all these so called racial groups in Malaysia belong to the same racial stock, namely Mongoloid.

Johann Friedrich Blumenbach’s classification of human race in the 18th century divided the various population groups into three races, namely the Mongoloid, Caucasoid and Negroid [5].
Others have used race for class relationship in Malaysia. Sundram [6] used the term race to discuss social stratification of the three major ethnic groups in Malaysia. He believed that race is a social construction and racial categorization has taken a particular configuration within Malaysian society
on an everyday level and it has become a reality.

The concept of race was introduced into Malaya by the British who popularized it among the people of British Malaya through the education system, mass media and law. They categorised the local population into three major races, namely the malays, ethnic chinese and ethnic indians. The indigenous people of Sabah and Sarawak, and non malay indigenous people the orang asli were labeled as others.

The race concept inherited from the British was retained to give legitimacy to Malay dominated government to sustain and protect the malay power and privileges provided for by the Malaysian Federal Constitution.  Ethnic bargaining and accommodation among the three major ethnic groups resulted in the special privileges for the malays in the Malaysian federal constitution. The bargaining resulted in Non-Malays obtaining citizenship and protection of their culture and language while Malays were guaranteed their special position [7]. Article 153 of the Federal Constitution makes the  monarch responsible for safeguarding the special position of Malays and other indigenous groups [8]. Article 153 provides for the special treatment of Malays and natives of Sabah and Sarawak in federal public service, education, scholarships, training privileges, permits, licenses for trade and business [7].

Article 160 of Malaysian Constitution defines Malay as a person who professes Islam, habitually speaks the Malay language and practices Malay customs. Malays and other indigenous people are known as bumiputras or the son of the soil. Their special position has been achieved through a series of policies know as bumiputera policies which were introduced after the May 13 riots in 1969 [8]. The New Economic Policies (NEP) was introduced to eradicate poverty from Malaysia to improve the economic standing of the bumiputera. In education and employment malays were given priority.

Racism in Malaysia

The Malaysian Federal Constitution has provisions which prohibit racial discrimination in the country, and this is spelt out in Article 8 (1, 2) and Article 12.

Article 8 (1 & 2) states that:
(1) All persons are equal before the law and entitled to the equal protection of the law.
(2) Except as expressly authorized by this Constitution, there shall be no discrimination against citizens on the ground only of religion, race, descent or place of birth or gender in any law or in the appointment to any office or employment under a public authority or in the administration of any law relating to the acquisition, holding or disposition of properly or the establishing on carrying on of any trade, business, profession, vocation or employment.

Article 12 (1) state that:
Without prejudice to the generality of Article 8, there shall be no discrimination against any citizen on the grounds only of religion, race, descent or place of birth.
Although the principles of equality in the protection of rights of every Malaysian exits, exceptions have been made by Article 153 on the Malaysian Constitution.

Article 153 (1) states that:
It shall be the responsibility of the Yang di-Pertuan Agong to safeguard the special position of the Malays and natives of any of the States of Sabah and Sarawak and the legitimate interests of other communities in accordance with the provisions of this Article.

Reservations of quotas for public service positions, scholarships, educational or training privileges, business permits and licenses are also spelled out in this Article. Points (7) and (8) of Article 153 has provisions to ensure the protection of legitimate interests of other communities.

Article 153 (7):
Nothing in this Article shall operate to deprive or authorize the deprivation of any person of any right, privilege, permit or license accrued to or enjoyed or held by him or to authorize a refusal to renew to any person any such permit or license or refusal to grant to the heirs, successors or assigns of a person any permit or license when the renewal or grant might reasonably be expected in the ordinary course of events.

The pro-bumiputera Malays claim that The Federation of Malaya Agreement signed on 21 January 1948 at King House by the Malay rulers, and by the British government representative Sir Edward Gent granted the malays leadership among the three races. This claim however, is apparently not accurate. Upon independence from the British all 3 races were supposed to be given equal rights. Dato' Onn Jaafar - then heading UMNO, agreed to abide by the above original terms of The Federation of Malaya Agreement. After 1951, UMNO, however, gradually  meandered a different course, enshrining the rights of Malays over all other races in law. Today, the Malays dominate in politics at both national and state levels, the civil service, military and security forces [9,10].

The malay dominated government ensures that Bumiputras of Malay origin are given preferential treatment when it comes to admission to public universities and colleges [11]. Many of the Chinese and Indians chose private universities to pursue their studies because of a lack of places for them in public institutions [12]. The private housing developers are forced to give discounts for new houses to the Malays. They also receive cheaper burial plots in most urban areas. All key government positions are held by the malays including the top posts of most sporting associations. Listed companies are expected to have a minimum of a 30% Malay Bumiputera.  Full funding for mosques and Islamic places of worship is provided by the government. Special trust funds which provide high interest rates are set up for the Bumiputera Malays. Special share allocations for new share applications are provided to the Bumiputera Malays. The Malay language has been made a compulsory examination paper to pass in national schools [13,14,15,16,17].

After the 1969 riots the National Economy Policy (NEP) was introduced with two major objectives: “to eradicate poverty irrespective of race” and “to restructure society to abolish the identification of race with economic function” [18]. Prior to 1969 the colonial capitalism had created an ethnic division of labour which emerged from uneven development and socioeconomic disparities. Crudely the three major ethnic groups were labelled as  the Malay farmers, the Chinese traders and the Indian estate labourers.

The NEP aimed to reduce poverty by reducing the incidence of poverty from 49 per cent of all households in 1970 to 16 per cent in 1990 and to restructure society, the NEP planned to raise the bumiputera share of corporate equity from 2.5 per cent in 1970 to 30 per cent in 1990. The NEP also planned to create a Bumiputera Commercial and Industrial Community (BCIC).

Though the aim of the NEP was to eradicate poverty irrespective of race, in reality the poverty eradication programmes rarely reached the non-Malay poor, including the urban poor and the Chinese New Villagers [18].

The NEP allowed and justified the public sector taking on multiple new roles. The public sector emerged as the main provider of opportunities for the Malays. It enlarged the existing numbers of Malay entrepreneurs, graduates and professionals. The aspiring Malay entrepreneurs were given financial assistance, credit facilities, contracts, preferential share allocations, subsidies as well as training. New public universities and all-Malay residential schools and colleges were established. Tens of thousands of young malay students and mid-career officers were sent to universities abroad. The social engineering resulted in an increase numbers of Malay entrepreneurs and capitalists [19] and a sizeable Malay middle-class [20]. The bumiputera participation rate in all professions increased [21].

The public sector became a stringent regulator of both local and foreign businesses. The Industrial Coordination Act (ICA) was introduced in 1975 which enforced compliance with the NEP’s restructuring. A Foreign Investment Committee was set up to introduce bureaucratic procedures, which met the needs of the NEP. A 30% bumiputera (malay) equity participation and employment in companies was introduced and this was enforced through the ICA. The ICA gave the minister of trade and industry power over licensing, ownership structure and employment targets. Product distribution quotas, local content and product pricing were controlled by the ministry of trade and industry [22]. Strict bureaucratic regulations were introduced even at state and local government level which regulated non Malay businesses. NEP requirements were imposed by land offices, town and country planning departments, municipal councils and state economic development corporations for real estate development. NEP requirements were imposed on land-use conversions and on various planning guidelines.

The public sector also became a major investor so that malay ownership of corporate equity could be increased. State resources were used to expand malay ownership of assets via “restructuring” exercises. Public sector started setting up its own companies as well as buying local and foreign companies. This foray into corporate sector allowed the public sector to control large portions of the Malaysian economy in areas such as plantations, mining, banking and finance, property and real estate [23].

With the introduction of NEP the public sector became the trustee of malay economic interests. State-owned agencies such as Bank Bumiputera, Urban Development Authority, Perbadanan Nasional (National Corporation), Permodalan Nasional Berhad (National Equity Corporation), Amanah Saham Nasional (National Unit Trust Scheme) and the state economic development corporations, held equity “in trust” for the bumiputera (malays) [24,25]. 

After 1970, many new public enterprises proliferated and their numbers grew rapidly to perform their new and expanded roles to fulfil the requirements of the NEP [25]. Federal Off-Budget Agencies and companies formed by state economic development corporations came into existence and grew significantly in all sectors of the economy. Their financial allocations steadily rose after 1971. Though the aim of these increase in allocations at federal and state levels was for development, with the aim of eradicating poverty among all ethnic groups, the direction in which public sectors concerns took became  increasingly ethnicized [18].

The expansion of the public sector under the NEP’s restructuring objective served two purposes. The first was to increase employment of the malays in the civil service via a massive civil service recruitment drive. The proportion of malay Division 1 officers in the civil service in 1968 was 37.4% and in 1987 the proportion became 65%. In year 2000 the number of civil servants were 979,464 and in 2013 the sized was 1.42 million. The proportion of malays in the civil service before implementation of the NEP in 1969-70 was 64.5% and in 2009 it was 76.2%. In 1969-70 the proportion of chinese and indians was 18.8% and 15.7%, respectively, and in 2009 it was in 6.0% and 4.3% [27]. Probably the numbers of non malay civil servants is much less now in 2018.

The second objective of the NEP was elimination of identification of race with economic function and malay domination of the civil service clearly contradicts this 2nd objective of the NEP.
The Malay special rights were to be applied only to recruitment, and not to promotion in civil service. In practice, however, malays have been getting promoted because of their race. The highest policy-making positions are  filled by Malays without regard to objective performance standards and these promotion are carried out at rapid rate [28].

As early as 1975, ethnic discrimination in tertiary education which favoured the malays was obvious at all levels of tertiary education in local public universities. Affirmative action favouring malays involved student enrolment in public institutions of tertiary education, disbursement of scholarships, as well as the recruitment of academic staff. Many qualified non-Malay students were denied admission to local public institutions [29].

The Bumiputera ownership of share capital of public listed companies rose from 2.4 per cent in 1970 to 20.6 per cent in 1995.

Quotas and targets were set and were modified as and when necessary in all areas of economic and social life to provide preferences and discrimination favouring the bumiputeras. Price subsidies and discounts were given by the public sector to overcome the bumiputera’s lack of competitiveness.
The NEP had set a 20-year target to achieve a 30% share of corporate assets for bumiputeras. This was interpreted as a minimum of 30 per cent bumiputera participation, in employment in private companies, in allocation of new shares in public listed companies; in sale or transfer of corporate or other assets in selected sectors; in award of government contracts and projects; in admission of students in tertiary education, in awarding of scholarships and financial assistance; and in the development and sale of urban housing and commercial space [18].

With the interpretation of a minimum of 30% bumiputera participation, the bumiputera quotas frequently exceeded 30 percent of whatever was believed to fall within the ambit of restructuring and redistribution. This restructuring and redistribution exercise led to malay versus non-Malay polarity and public-private dichotomy. The public services, public enterprises and statutory bodies became increasingly Malay domains while the private sector remained as a Chinese domain [30].

The borders between Malay social enterprise and Malay private business became blurred as NEP’s multidimensional state economic interventions took the form of statist capitalism. There was a continuous support by the state for malays to accumulate private wealth. Joint ventures between the malays and non-malay partners (socalled “Ali Baba” arrangements) became common.

Expansion of malay private enterprise continued with appointment of malays to company directorships and the politically well connected malays  could obtain government contracts. State capitalism allowed too much power to be put in the hands of a few leaders which in turn led to the corrosion of democratic culture and institutions.

UMNO being the party of the Malays, it made the NEP as its national agenda, which allowed it to enter into business on a large scale and in the process built itself a corporate empire [31]. The technocrats and administrators of this rapidly enlarged Malay-dominated bureaucracy ended up controling vast economic resources in the name of Malay trusteeship via the state-owned enterprises [32].

Lack of business experience and capability among the public bureaucrates  prevented many public enterprises from meeting the criteria of efficiency and profitability. This weaknesses in public sector governance led to large-scale deficits and losses. The public sector deficit rose from RM400 million to RM15.2 billion between 1970 and 1982. In 1982, the statutory bodies, public enterprises and the state governments, collectively owed the federal government as much as RM8.743 billion [32].

Some state managers became entrepreneurs themselves by acquiring the very enterprises they were managing earlier. The malay entrepreneurs complained of unfair state competition and pushed the states to transfer the assets to them directly. UMNO’s entry into business to generate funds for the party saw the establishment of Fleet Holding. In the 1980s and 1990s, Umno’s assets were mostly held through privately held Hatibudi Sdn Bhd and Fleet Group Sdn Bhd. Tan Sri Halim Saad, a businessman and one of Umno’s well-known proxies controlled Hatibudi Sdn Bhd. Hatibudi held substantial stakes in United Engineers (M) Bhd (UEM) and Hume Industries (M) Bhd as well as a 60% stake in Seri Pacific Corp. UEM, which was awarded contracts to build two mega infrastructure projects namely the North-South Expressway and the Malaysia-Singapore Second Link, became one of the biggest conglomerates in Southeast Asia.

Through the Fleet Group, Umno held substantial stakes in several Bursa Malaysia-listed companies, including the New Straits Times Press (M) Bhd, Time Engineering Bhd, Bank of Commerce Bhd, Commerce International Merchant Bankers Bhd (both banks later subsumed into CIMB Group) and Faber Group Bhd. UMNO thus built up an economic empire that penetrated most economic sectors in the name of protecting the rights of the malays and fulfilling the aims of the NEP [19,31]. UMNO managers themselves became big capitatlist themselves by securing enormous lucrative state projects, contracts and assets [19]. Gradually intramalay competition  became more obvious within the party bureaucracy and class axis.  Standard expectations of public sector governance such as transparency, accountability and impartial oversight gradually became diminished due to lack of executive discretion, intervention by the party, corporate rent-seeking, cronyism as well as outright corruption [18].

Conclusion

Racism and racial discrimination has become entrenched in Malaysia. There is not and there will not be a full stop to this issue of racism in Malaysia in the future. It is present in every aspect of our lives. It is seen in business, education and even sports. The politics of hate and instigation of racial tension is a norm in our everyday life. Politicians in Malaysia spew racial hatred on a regular basis to garner support from their majority races.

Malicious and racially provocative statements that are meant to offend a certain ethnic group are a norm on social media nowadays.

No policies and practices to address the issue of racism and racial discrimination exist in Malaysia. There is no engagement by the government with civil society organisations, academicians, media and other sectors of Malaysian society to address this phenomenon. A collective effort by multi-stakeholders is desperately needed to combat the rising incidences of religious and racial discrimination in Malaysia.

References

1. The Cambridge English Dicitionary at https://dictionary.cambridge.org/dictionary/english/racism.
2. Grosfoguel R. What is Racism? Journal of World-System Research. 2016; Vol. 22 (1) : 9-15.
3. Farish A.Noor. What your teacher didn’t tell you; the Annexe Lectures (Vol.1). Petaling Jaya: Matahari Books, 2009.
4. Syed Husin Ali. Ethnic relations in malaysia: Harmony & Conflict, Petaling Jaya: Strategic Information and Research Development Centre, 2009.
5. Barkan E. The retreat of scientific racism: Changing concepts of race in Britain and the United States between the world wars. New York and Melbourne: Cambridge University Press, 1992.
6. Sundram, Jeyaratnam M. A.. “Race, class and uneven development in Malaysia”. MA thesis. Department of Sociology at Michigan State University, 1983.
7. Shad Saleem Faruqi. 2005. “Affirmative action policies and the constitution”. In The 'Bumiputera policy': dynamics and dilemmas Kajian Malaysia Journal of Malaysian Studies special issue, edited by Richard Mason and Ariffin Omar, 21( 1 & 2), 2005.
8. Mason R and Omar A. “The Bumiputera policy:Dynamics and dilemmas”. In The Bumiputera policy: Dynamics and dilemmas Kajian Malaysia Journal of Malaysian Studies special issue, edited by Richard Mason and Ariffin Omar, 21( 1 & 2), 2005.
9. Hong-Hai Lim (2007). "Ethnic Representation in the Malaysian Bureaucracy: The Development and Effects of Malay Domination". International Journal of Public Administration. 30 (12-14: Comparative Asian Public Administration): 1503–1524. doi:10.1080/01900690701229731.
10. Muthiah Alagappa (1 September 2002). Coercion and Governance: The Declining Political Role of the Military in Asia. Stanford University Press. p. 259. ISBN 978-0804742276.
11. Jennifer Pak (2 September 2013). "Is Malaysia university entry a level playing field?". BBC.
12. "Malaysia's system of racial preferences should be scrapped". The Economist. 18 May 2017.
13. Dimitrina Petrova (22 November 2012). "Affirmative Action versus Equality in Malaysia". Oxford Human Rights Hub.
14. Boo Su-Lyn (11 April 2014). "Even in death, no escape from rising prices". The Malay Mail. http://iphira.tripod.com/smih/spm.htm
15.  "Race-based affirmative action is failing poor Malaysians". The Economist. 18 May 2017.
16. "The Malay Language and its role in nation building"- Summary of Saturday Night Lecture 14th September 2013". UTM. 24 September 2013.
17. Khoo Boo Teik. Ethnic Structure, Inequality and Governance in the Public Sector Malaysian Experiences. Democracy, Governance and Human Rights Programme Paper Number 20 December 2005. United Nations Research Institute for Social Development.
18. Searle, Peter. 1999. The Riddle of Malaysian Capitalism: Rent-Seekers or Real Capitalists? Allen and Unwin, St. Leonards, New South Wales.
19. Abdul Rahman Embong. 1995. State-Led Modernization and the New Middle Class in Malaysia. Palgrave Macmillan, Houndmills.
20. Jomo, K.S. 1999. “A Malaysian middle class?” In K.S. Jomo (ed.), Rethinking Malaysia: Malaysian Studies I. Malaysian Social Science Association, Kuala Lumpur.
21. Jesudason, James V. 1989. Ethnicity and the Economy: The State, Chinese Business and Multinationals in Malaysia. Oxford University Press, Singapore.
22. Heng Pek Koon and Sieh Lee Mei Ling. 2000. “The Chinese business community in Peninsular Malaysia, 1957–1999.” In Lee Kam Hing and Tan Chee Beng (eds.), The Chinese in Malaysia. Oxford University Press, Kuala Lumpur.
23. Searle, Peter. 1999. The Riddle of Malaysian Capitalism: Rent-Seekers or Real Capitalists? Allen and Unwin, St. Leonards, New South Wales.
24. Gomez, Terence Edmund and K.S. Jomo. 1997. Malaysia’s Political Economy: Politics, Patronage and Profits. Cambridge University Press, Cambridge.
25. Lim Hong Hai. 2003. The Representativeness of the Bureaucracy in Malaysia: The Problems of Public Administration in a Plural Society. Paper presented at the International Conference on Reform in Public Administration and Social Services in Asia, Macao Polytechnic Institute, Macao, China, 8–9 November 2003.
26. Lim, H. H. (2013). The public service ethnic restructuring under the New Economic Policy: The new challenge of correcting selectivity and excess. In .T. Gomez & J. Saravanamuttu (Eds.), The New
27. Economic Policy in Malaysia: Affirmative action, ethnic inequalities and social justice. Singapore: NUS Press.
28. Means. 1972. “‘Special rights’ as a strategy for development.” Comparative Politics, Vol. V, October, pp. 46–48.
29. Lee, Molly N.N. 2004. Restructuring Higher Education in Malaysia. School of Educational Studies, Monograph Series No. 4/2004. Universiti Sains Malaysia, Penang.
30. Jomo KS. 1990. Growth and Structural Change in the Malaysian Economy. Palgrave Macmillan, London.
31. Gomez TE. 1990. Politics in Business: UMNO’s Corporate Investments. Forum, Kuala Lumpur.
32. Mehmet, Ozay. 1986. Development in Malaysia. Poverty, Wealth and Trusteeship. Croom Helm, London.

Coccydynia-Treatment

                           Coccydynia-Treatment

                                                      Dr KS Dhillon

Anatomy of the coccyx

The coccyx, also known as the tailbone is the terminal end of the spine, just distal to the sacrum. It is about one inch in length and is curved like a hawk’s beak.The human coccyx is considered as a vestigial remnant of a tail. It is composed of 3-5 coccygeal vertebrae. In 80% of individuals, the coccyx is made up of 4 coccygeal vertebrae. The individual bones fuse together to form a single coccygeal bone throughout adulthood. In some individuals, however, the bones only partially fuse, resulting in two separate coccygeal bones.

Anteriorly the coccyx is concave and posteriorly it is convex in shape. The coccyx has an apex, base, anterior surface, posterior surface and two lateral surfaces. The base located proximally contains a facet for articulation with the sacrum. The apex is situated distally at the inferior tip of the coccyx. The lateral surfaces of the coccyx are marked by a small transverse processes, which project from 1st coccygeal vertebra.

The 1st coccygeal vertebra has two small articular processes called coccygeal cornua which articulates with the sacral cornua to form the  sacrococcygeal symphysis. It is a fibrocartilaginous joint which allows limited flexion and extension movements. The intercoccygeal joints also
contain fibrocartilaginous discs.

There are four configurations of the coccyx which were described by Postacchini and Massobrio [1]

Type I: Coccyx is slightly curved forward, with the apex directed downward and caudally.
Type II: Forward curvature is more marked, and the apex extends straight forward.
Type III: Coccyx angulates more sharply forward.
 Type IV: Coccyx is subluxated at sacrococcygeal joint or at intercoccygeal joint.


The sacrococcygeal symphysis is supported by five ligaments:

• Anterior sacrococcygeal ligament which is a continuation of the anterior longitudinal ligament of the spine, and it connects the anterior aspects of the vertebral bodies.
• Deep posterior sacrococcygeal ligament which connects the posterior surface of the 5th sacral body to the posterior surface of the coccyx.
• Superficial posterior sacrococcygeal ligament which attaches the median sacral crest to the dorsal surface of the coccyx.
• Lateral sacrococcygeal ligaments which run from the lateral aspect of the sacrum to the transverse processes of 1st coccygeal vertebra.
• Intra articular ligaments which stretch from the cornua of the sacrum to the cornua of the coccyx. 

The coccyx has an attachment for the gluteus maximus muscle which is a major extensor of the thigh at the hip. The levator ani muscle which consists of the coccygeus, iliococcygeus, and pubococcygeus, also arise from the coccyx. This muscle group supports the pelvic floor (preventing inferior sagging of the intrapelvic contents) and also plays a role in maintaining fecal continence. A midline component of the muscle is the anococcygeal raphe which supports the position of the anus. The coccyx via the anococcygeal ligament helps to support the anus by holding the external anal sphincter in place.

Function of the coccyx

The coccyx and the ischial tuberosities forms a tripod on which an individual sits.The coccyx bears more weight when the seated person is leaning backward and less weight when a person leans forward.

Besides the weight bearing function it also provides support for the pelvic floor and the anus as well as plays a role maintaining fecal continence. 

Coccydynia

Coccydynia (also referred to as coccygodynia, coccalgia, coccygalgia, or coccygeal pain) is a painful syndrome affecting the coccygeal region. It is a rare condition. The patient presents with pain in the coccygeal region which occurs while sitting on hard surfaces and sometimes on getting up from sitting position.

Epidemiology

Frequency

Coccydynia is the cause of back pain in less than 1% of all back pain conditions [2, 3, 4]. It is five times more common in women as compared to men [5]. The mean age of onset is usually around 40 years of age [5].

Etiology of Coccydynia

The most common cause of coccydynia is external or internal trauma. External trauma usually results from a fall on the buttocks or a fall backwards which leads to a bruised, dislocated, or broken coccyx [6]. The  coccyx may also be injured during childbirth especially with instrumented and difficult deliveries. Prolonged sitting on hard narrow and uncomfortable surfaces can lead to minor trauma to the coccyx leading to coccydynia [2]. Non-traumatic coccydynia can result from degenerative joint or disc disease, hypermobility of the coccyx, hypomobility of the sacrococcygeal joint, infections,and malignancies. The pain in the coccygeal region can also be referred pain from other sites. Less commonly coccydynia can be associated with non-organic causes, such as somatization disorder and other psychological disorders [7].

The configuration of the coccyx can predispose a patient to coccydynia and influence the type of pain the patient has. Types II, III, and IV are usually  more painful than type I [1]. Obesity can also a predisposing factor for coccydynia.

Clinical presentation and diagnosis

Most patients present with a history of a fall or an antecedent childbirth. The incidence of posttraumatic coccydynia is about 69.2% [8]. Some patients will present with no preceding incidence of trauma and the onset of pain can be insidious.

Patients usually present with tailbone pain which is worse on prolonged sitting, leaning back while sitting, on getting up from sitting and sometimes on prolonged standing. Sexual intercourse and defecation may also be associated with tailbone pain in some patients.

Physical examination usually reveals tenderness over the coccyx. A rectal examination allows manipulation of the coccyx and it will elicit pain and may reveal hypermobility or hypomobility of the sacrococcygeal joint.

X rays of the coccyx can reveal fractures, subluxations and dislocations of the coccyx. A comparison of lateral radiographs which are taken in the standing and in the most painful sitting position can reveal posterior subluxation of the coccyx and hypermobility of the coccyx [8]. Further evaluations can be carried out using CT scan images. When infection, tumours or other sources of pain are sought, an MRI can be useful.

Treatment of coccydynia

Non-surgical treatment

Non-surgical management remains the gold standard treatment for coccydynia. In many patients the pain resolves without treatment and conservative treatment is usually successful in 90% of cases [3,9,10]. Wedge-shaped cushions (coccygeal cushions) can be used to relieve pressure on the coccyx when  the patient is seated and these are usually available over the counter. Circular cushions (donut cushions) can increase pressure on the coccyx and are not suitable for treatment of coccydynia. Sitting bent forward helps to take pressure off the coccyx and its helps reduce the pain. Application of heat and cold sometimes helps too. Nonsteroidal antiinflammatory drugs (NSAIDs) are most commonly given for pain relief. Opioids are generally not prescribed for pain relief.

Maigne and Chattelier [11] studied the usefulness of levator ani massage, levator ani stretching, and sacrococcygeal joint mobilization in the treatment of coccydynia. They found that at 6-month the success rates for message were 29.2%, for stretching 32% and for joint mobilization 16%. The overall success rate with these conservative approaches was 25.7%.

Local injections of steroids with long acting anesthetics have been used for treatment of coccydynia where conservative treatment has failed. Wray et al [12] recommended a mixture of 40 mg methylprednisolone and 10 ml 0.25% bupivacaine. In some patients where symptoms persisted a third injection was performed in conjunction with coccygeal manipulation under general anesthetic. They reported a success rates of 59% with injections alone and 85% for the injections with manipulation. Twenty one percent patients receiving injections and 28% of those undergoing injections with concurrent manipulation developed recurrence of symptoms.

Although injections into the pericoccygeal tissues have been used in the treatment of coccydynia, there appears to be no clear consensus in the literature regarding the exact site of injection.
Plancarte et al [13] were the first to describe the use of radiofrequency to block the ganglion impar for pericoccygeal pain due to carcinoma. Others have used the same technique to relieve pain in patients with severe coccydynia [14]. Evidence-based literature supporting the effectiveness of these interventional procedures remains lacking.

The published literature on the use of various modes of treatment for coccydynia described above consists of case series which is especially vulnerable to selection bias. Unfortunately there are no cohort studies comparing different interventions and their outcomes.

Surgical treatment

Surgery for the treatment of coccydynia is used only as a last resort when all other treatment options have not been successful. The commonly used surgical procedure used for the treatment of chronic coccydynia not responding to other forms of treatment is coccygectomy. It involves surgical removal of the coccyx just proximal to the sacrococcygeal junction. There is scarcity of literature to support the use of this surgical procedure. As with other modes of treatment of coccydynia most of the available literature consists of case reports and retrospective case series with no cohort studies. The available literature suggests that a coccygectomy may provide relief in some subset of patients who have failed all other forms of treatment [8,10,12,15].

Infection is the most serious complication of coccygectomy because of  proximity of the coccyx to the rectum and anal canal. Rates as high as 16.6% [16] and 14.75% [17] have been reported in literature. Partial skin necrosis and superficial wound infection causing delay in wound healing has been reported in about 50% of the patients [1]. Besides the high complication rates, the procedure can be associated with failure to achieve pain relief. Therefore, ‘based on current available information, this procedure generally is not recommended’[18].

Conclusion

The etiology of the coccydynia can be complex and may often be multifactorial. It is a relatively rare condition with no universally accepted treatment protocol. The symptoms are often mild and the condition can sometimes be self limiting. Though most patients respond to conservative treatment, some may require more aggressive treatment.
A multidisciplinary approach using physical therapy, workplace adaptations, medications (NSAIDs), injections and psychotherapy where necessary, will provide the best opportunity for success in the treatment of these patients. Surgical coccygectomy is generally not recommended for the treatment of patients with coccydynia. More research is needed to establish which is the best mode of treatment of patients with coccydynia. Randomized control trials to study the outcome of treatment of patients with coccydynia are needed.

References

1. Postacchini F, Massobrio M. Idiopathic coccygodynia. Analysis of fifty-one operative cases and a radiographic study of the normal coccyx. J Bone Joint Surg Am. 1983 Oct. 65(8):1116-24.
2. Pennekamp PH, Kraft CN, Stütz A, Wallny T, Schmitt O, Diedrich O. Coccygectomy for coccygodynia: does pathogenesis matter?. J Trauma. 2005 Dec. 59(6):1414­9. 
3.  Thiele GH. Coccygodynia: Cause and treatment. Dis Colon Rectum. 1963 Nov­Dec. 6:422­-36.
4. Peyton FW. Coccygodynia in women. Indiana Med. 1988 Aug. 81(8):697­8. 
5. Fogel GR, Cunningham PY 3rd, Esses SI. Coccygodynia: evaluation and management. J Am Acad Orthop Surg. 2004 Jan­-Feb. 12(1):49­54.
6. Schapiro S. Low back and rectal pain from an orthopedic and proctologic viewpoint; with a review of 180 cases. Am J Surg. 1950 Jan;79(1):117-128.
7. Nathan ST, Fisher BE, Roberts CS. Coccydynia: a review of pathoanatomy, aetiology, treatment and outcome. J Bone Joint Surg Br. 2010 Dec;92(12):1622-1627.
8. Maigne JY, Doursounian L, Chatellier G. Causes and mechanisms of common coccydynia: role of body mass index and coccygeal trauma. Spine (Phila Pa 1976). 2000 Dec 1. 25(23):3072­9.
9. Capar B, Akpinar N, Kutluay E, Müjde S, Turan A. Coccygectomy in patients with coccydynia [in Turkish] Acta Orthop Traumatol Turc. 2007 Aug-Oct;41(4):277–280. 
10. Trollegaard AM, Aarby NS, Hellberg S. Coccygectomy: an effective treatment option for chronic coccydynia: retrospective results in 41 consecutive patients. J Bone Joint Surg Br. 2010 Feb;92(2):242–245. 
11. Maigne J, Chattelier G. Comparison of three manual coccydynia treatments: a pilot study. Spine. 2001;26:E479–84.
12. Wray C, Easom S, Hoskinson J. Coccydynia: aetiology and treatment. J Bone Joint Surg. 1991;73:335–8.
13. Plancarte R, Amescua C, Patt RB, Allende S. Presacral blockade of the ganglion of Walther (ganglion impar) Anesthesiology. 1990; 73(3A):A751.
14. Toshniwal GR, Dureja GP, Prashanth SM. Transsacroccygeal approach to ganglion impar block for management of chronic perineal pain: a prospective observational study. Pain Physician 2007;10:661–6.
15. Perkins R, Schofferman J, Reynolds J. Coccygectomy for severe refractory sacrococcygeal joint pain. J Spinal Disord Tech. 2003 Feb;16(1):100–103.
16. Bayne O, Bateman JE, Cameron HU. The influence of etiology on the results of coccygectomy. Clin Orthop 1984;190:266–72.
17. Doursounian L, Maigne JY, Faure F, Chatellier G. Coccygectomy for instability of the coccyx. Int Orthop 2004;28:176–9.
18. Lirette LS, Chaiban G, Tolba R, Eissa H. Coccydynia: an overview of the anatomy, etiology, and treatment of coccyx pain. Ochsner J. 2014;14(1):84-7.

Elbow Dislocations

                              Elbow Dislocations  

                                             Dr. KS Dhillon

     

Anatomy and biomechanics of the elbow

There are three joints at the elbow:

• Ulnohumeral joint
• Radiocapitellar joint
• Proximal radioulnar joint

Ulnohumeral joint

The ulnohumeral joint is formed by the articulation between the spool shaped distal medial flare of the humerus called the trochlear and the trochlear notch of the proximal ulna formed by the olecranon and coronoid parts of the ulna. It is a hinge type of joint. Forty percent of the axial load in an extended elbow goes through this joint.

Radiocapitellar joint

The radiocapitellar joint is formed by the the capitellum which is situated on the distal lateral flare of the humerus and the head of the radius. It is a pivot type of joint. Sixty percent of the axial load, with elbow in extension, passes through this joint. The radial head is covered by cartilage for about 240 degrees. The lateral 120 degrees contains no cartilage and this information  useful when internal fixation needs to be carried out.

Proximal radioulnar joint

The proximal/superior radioulnar joint is formed by the head of the radius which articulates with the radial notch of the proximal ulna and the joint shares the capsule of the elbow joint. The two bones are held together by the annular ligament which is attached to the anterior and posterior margins of the radial notch of the ulna. The annular ligament circles round the head and neck of the radius and is devoid of ligamentous attachments which enables the radius to rotate freely inside the annular ligament. It is a pivot type of joint and it allows supination and pronation movements of the forearm.

The elbow joint consists of two types of articulation, and it allows two types of motion. The  ulnohumeral articulation is a hinge joint and it allows flexion and extension, whereas the radiohumeral and proximal radioulnar joint are pivot joints which allows axial rotation. Stability of the elbow joint is provided by the bony articulations and the medial and lateral collateral ligaments.

The primary static stabilizer of the elbow is the ulnohumeral joint (coronoid), medial (ulnar) collateral ligament (MCL) and the lateral collateral ligament complex (LCL).
The ulnohumeral stability is provided its bony counters and the coronoid process. A 50% or more loss of coronoid height results in elbow instability. The MCL is composed of the anterior, posterior and transverse bundles. It arises from the posterior medial epicondyle and inserts on the sublime tubercle of medial coronoid process.

The LCL consists of the radial collateral ligament (RCL), lateral ulnar collateral ligament (LUCL), accessory collateral ligament and the annular ligament. The radial collateral ligament (RCL) extends from the lateral epicondyle to the annular ligament deep to the common extensor tendon. The lateral ulnar collateral ligament (LUCL) extends from the lateral epicondyle to the supinator crest on the ulna. The annular ligament (AL), extends from the posterior to the anterior margins of radial notch on the ulna. It encircles the head of radius and holds it against the radial notch of ulna. The accessory lateral collateral ligament (ALCL) extends from the inferior margin of the annular ligament to the supinator crest.

The secondary static stabilizers are the radiocapitellar joint, the capsule and the attachment of the flexor and extensor tendons (biceps, brachialis, brachioradialis and triceps).
The dynamic stabilizers (muscles crossing the joint) of the elbow includes the anconeus, brachialis, triceps and the biceps.

Classification of elbow dislocation

Dislocations of the elbow can be anatomically classified according to the position of the radius and ulna in relation to the humerus after injury. Based on this there are five types of elbow dislocations :

• Posterior (most common)
• Anterior
• Medial
• Lateral
• Divergent (radius and ulna are dislocated in different directions in relation to humerus)

Complex or simple

Depending on the complexity of the dislocation, the dislocations can be class as simple or complex. Simple dislocations are those where a dislocation occurs without associated fractures and complex dislocations are those where an associated fracture or fractures occur. About 50-60% of  dislocations are simple without associated fractures.

There are three common patterns of complex elbow fracture-dislocations, the trans-olecranon fracture-dislocation, the terrible triad injury, and anteromedial coronoid fractures associated with varus posteromedial instability.

Complex elbow dislocation

Initially evaluation

Clinical examination is carried out to rule out open fractures, neurovascular compromise, and associated injuries. Plain X rays are usually sufficient to diagnose complex elbow fracture-dislocations. A closed reduction is carried out if the elbow is dislocated or the limb is grossly deformed. A CT scan of the elbow is than done to assess the fractures and to guide preoperative planning and treatment.

1.Trans-olecranon fracture-dislocations

Trans-olecranon fracture-dislocations, which result from an axial loading injury, are characterized by the disruption of the ulnohumeral joint with  anterior displacement of the radial head relative to the capitellum. Usually there is a complex, comminuted fracture of the proximal ulna, though a simple or an oblique fracture can also occur [1]. Fractures of the coronoid are also commonly associated with these type of injuries and often the fracture  involves more than 50% of the coronoid height [2]. The radial head can also be fractured [1,3,4]. Coronoid fractures can occur concomitantly as well [5, 7, 8]. The collateral ligaments usually remain intact [1,5].

The fractures are treated by internal fixation via the posterior approach. The coronoid or radial head fracture can approached through the exposure afforded by the olecranon fracture. The olecranon fracture can be stabilized with a plate or a tension band wire. The tension band wire fixation has a higher failure rates [3,4]. Occasional additional medial or lateral incision may be required.

2.Terrible triad injury

In the terrible triad injury the elbow dislocates posterolaterally with an associated fracture of the radial head/neck with a fracture of the coronoid. There is usually an injury to the LCL.
Occasionally these injuries can be treated nonoperatively by close reduction of the elbow and immobilization in 90 degree of flexion for 7-10 days. Nonoperative treatment is carried out when the ulnohumeral and radiocapitellar joints can be concentrically reduced, the radial head fracture is minimally displaced and does not prevent rotation and the coronoid fracture is small. Post reduction the elbow must be sufficiently stable to allow early elbow mobilization.

Surgical treatment is indicated for dislocations with an unstable radial head fracture and a type III coronoid fracture (fractures involving more than 50% of the height).
Stability is restored from inside out and lateral to medial [6,7].
The coronoid is stabilized first with internal fixation or anterior capsular repair, followed by internal fixation or replacement of the radial head. Lateral and medial instability is restored by repair of  LCL and MCL [6,7].

3.Anteromedial coronoid fractures

About 58% (26-82%) of the anteromedial facet of the coronoid is unsupported by the proximal ulnar metaphysis and diaphysis and this makes it vulnerable to injury [8]. Anteromedial coronoid fractures are usually associated with disruption of LCL while the radial head and MCL remain intact [9].

O’Driscoll has classified coronoid fracture into 3 types:

• Fractures of the tip of coronoid
• Anteromedial fractures
• Fractures of the base (body) of the coronoid

The anteromedial fractures are further subdivided into subtype 1 (rim), subtype 2 (rim and tip), and subtype 3 (rim and sublime tubercle) [2].

X rays of the elbow can show these fractures but a CT scan is more useful in the identification of these fractures.

Most of the patients with this type of injury will require surgical fixation
because the elbow lacks stability as a result of the LCL injury and the loss of the medial buttressing effect of coronoid. Subtype 1 fractures can be treated with  LCL repair alone, and subtypes 2 and 3 fractures can be treated with internal fixation using cannulated screws, tension band, or a buttress plate.

Coronoid fractures which are minimally displaced (≤5 mm), or undisplaced with a concentric elbow joint, and a stable range of motion to a minimum of 30° of extension can be treated nonoperatively [10].

Simple elbow dislocation

In patients with simple elbow dislocation a closed reduction is carried out and the elbow is splinted in 90 degrees of flexion for 5-10 days. After about a week mobilization of the elbow is started. An extension block brace is used for 3-4 weeks. Recurrent instability after simple dislocations is rare (<1-2% of dislocations).

Complications of elbow dislocation

Some of the complications of elbow include:

• Failure of internal fixation --Most often seen after repair of radial neck fractures. Poor vascularity can lead to osteonecrosis and nonunion.
• Loss of terminal extension of the elbow--This is a common complication after closed treatment of a simple elbow dislocation. This can be prevent by early, active mobilization of the elbow.
• Varus Posteromedial instability--Injury to the LCL and fracture of the anteromedial facet of the coronoid can lead to varus posteromedial instability. This can be prevented by LCL repair and solid fixation of the anteromedial facet.
• Neurovascular injuries--Open elbow dislocations can be associated (rarely) with brachial artery injuries. Median nerve injuries can be associated with brachial artery injuries. Ulna nerve injuries can result from stretch injuries. 
• Compartment syndrome
• Post traumatic osteoarthritis
• Due to chondral damage and residual instability
• Recurrent instability
• Heterotopic ossification
• Contracture/stiffness
• Post traumatic stiffness --Common after complex dislocation. Early mobilization useful for prevention

Outcome of treatment

Simple dislocations

Generally the outcome of treatment of simple elbow dislocations is good with residual stiffness as a possible complication [11,12]. Recurrent instability can be a concern in patients where early mobilization is opted for whereas in patients where the elbow is immobilized for longer periods, elbow stiffness and contractures may be a problem [13]. Recurrent instability is usually not a problem in patients with simple dislocation. The incidence is low at about 0.3% [14]. There is some low quality evidence to show that the outcome at 2 years follow up in terms of pain and range of movements, favours early mobilization [14].

When the outcome is measure by MEPI score, quick DASH score and weeks off work, functional treatment appears to show significantly better outcomes.
There is no difference between surgical treatment of the collateral ligaments and plaster immobilisation of the elbow joint. Overall, functional treatment with early mobilization appears to provide better movements, less pain, better functional scores, shorter disability and shorter treatment time as compared to plaster immobilisation [14].

The is scarcity of good quality evidence, in literature, on the outcome of treatment of simple dislocations of the elbow.

Complex dislocations

The outcome of treatment of complex dislocations of the elbow have traditionally been poor due to the complexity of injury. Long term complications with such injuries include stiffness, pain, arthritis, and joint instability [15].

Chen et al [16] performed a systematic review of the literature to evaluate the the functional outcome and complications associated with the treatment of terrible triad injuries of the elbow (TTIE).
The review included a total of 16 studies all of which were retrospective in design, involving more than 300 patients. The overall, functional outcomes were satisfactory, but complications (including both those requiring reoperation and those not requiring reoperation) were common. The functional outcomes, as determined by Mayo elbow performance, Broberg-Murray, and/or DASH scores were consistently satisfactory.

Though a high proportion of patients had satisfactory functional outcomes, many patients developed complications, which included ulnar neuropathy, elbow joint stiffness, heterotopic ossification, and arthrosis. About a third of the patients required reoperation due to complications such as instability and/or elbow stiffness.

Rodriguez-Martin et al [17] did a review where they analysed the outcome of treatment of 137 elbow triad injuries in five published studies. The average follow up of the patients was 31 months. The overall outcome was satisfactory with an average flexion arc of 111.4 degrees, and average flexion of 132.5 degrees with forearm rotation of 135.5 degrees. The average Mayo elbow performance score was 85.6 points, and Broberg-Morrey score was 85 points. Complications related to ulnar nerve symptoms, post-traumatic arthritis, elbow stiffness and heterotopic ossification were not uncommon. The symptoms of post traumatic arthritis were mild to moderate in most of the patients who developed joint degeneration. Repeat surgical procedures included capsular release, hardware removal and secondary ulnar nerve transposition [17].

Conclusion

The elbow joint consists of three articulation, the ulnohumeral joint, radiocapitellar joint and the proximal radioulnar joint. It is one of the most inherently stable articulations of the skeleton. Static stability is provided the bony counters, capsule and the ligaments. The muscles crossing the joint provide dynamic stability.

Dislocations can be classified anatomically or based on the complexity of the dislocation. Usually the dislocations are classified as simple or complex. Simple dislocations which are not associated with fractures are easy to treat and the outcome of treatment is generally good with minimal complications.

Treatment of complex dislocations which are associated with fractures is much more difficult. The outcome of treatment of complex dislocations is less predictable and is often associated with more complications.

References

1. Ring D, Jupiter JB, Sanders RW, Mast J, Simpson NS. Transolecranon fracture-dislocation of the elbow. J Orthop Trauma. 1997;11(8):545–50.
2. O’Driscoll SW, Jupiter JB, Cohen MS, Ring D, McKee MD. Difficult elbow fractures: pearls and pitfalls. Instr Course Lect. 2003;52:113–34.
3. Mortazavi SM, Asadollahi S, Tahririan MA. Functional outcome following treatment of transolecranon fracture-dislocation of the elbow. Injury. 2006;37(3):284–8.
4. Mouhsine E, Akiki A, Castagna A, Cikes A, Wettstein M, Borens O, et al. Transolecranon anterior fracture dislocation. J Shoulder Elbow Surg. 2007;16(3):352–7. 
5. Wyrick JD, Dailey SK, Gunzenhaeuser JM, Casstevens EC. Management of complex elbow dislocations: a mechanistic approach. J Am Acad Orthop Surg. 2015;23(5):297–306.
6. Mathew PK, Athwal GS, King GJ. Terrible triad injury of the elbow: current concepts. J Am Acad Orthop Surg. 2009;17(3):137–51.
7. McKee MD, Pugh DM, Wild LM, Schemitsch EH, King GJ. Standard surgical protocol to treat elbow dislocations with radial head and coronoid fractures. Surgical technique. J Bone Joint Surg Am. 2005;87(1):22–32.
8. Doornberg JN, De Jong IM, Lindenhovius AL, Ring D, et al. The anteromedial facet of the coronoid process of the ulna. J Shoulder Elbow Surg. 2007;16(5):667–70.
9. Doornberg JN, Ring DC. Fracture of the anteromedial facet of the coronoid process. J Bone Joint Surg Am. 2006;88(10):2216–24.
10. Chan K, King GJ, Faber KJ. Treatment of complex elbow fracture-dislocations. Curr Rev Musculoskelet Med. 2016;9(2):185-9.
11. Morrey BF, An KN. Articular and ligamentous contributions to the stability of the elbow joint. Am J Sports Med 1983; 11: 315-9.
12. de Haan J, Schep NWL, Zengerink I, van Buijtenen J, Tuinebreijer WE, den Hartog D. Dislocation of the elbow: a retrospective multicentre study of 86 patients. Open Orthop J 2010; 4: 76-9. 
13. Schippinger G, Seibert FJ, Steinböck J, Kucharczyk M. Management of simple elbow dislocations. Does the period of immobilization affect the eventual results? Langenbecks Arch Surg 1999; 384: 294-7.
14. de Haan J, Schep NW, Tuinebreijer WE, Patka P, den Hartog D. Simple elbow dislocations: a systematic review of the literature. Arch Orthop Trauma Surg. 2009;130(2):241-9.
15. Rockwood CA, Green DP (1996) Rockwood and Green's fractures in adults. Philadelphia: Lippincott-Raven.
16. Chen HW. Liu GD and Wu LJ (2014). Complications of treating terrible triad injury of the elbow: a systematic review. PloS one. 2014, 9(5), e97476. doi:10.1371/journal.pone.0097476.
17. Rodriguez-Martin J, Pretell-Mazzini J, Andres-Esteban EM, Larrainzar-Garijo R. Outcomes after terrible triads of the elbow treated with the current surgical protocols. A review. Int Orthop. 2010;35(6):851-60.

Drug -- Alcohol Interaction: Medical Myth or Fact

           Drug -- Alcohol Interaction: Medical Myth or Fact

                   

                                             Dr. KS Dhillon

The mythconception that alcohol should never be taken with antibiotics dates back to the 1950’s. According to Karl S. Kruszelnicki [1], the venereal disease (VD) clinics of the 1950s and 1960s gave advice that alcohol should absolutely not be consumed while a patient was taking penicillin although there was no chemical interaction between penicillin and alcohol. Apparently, the advice was given for moral reasons. The doctors of the day were concerned about alcohol reducing the inhibitions of those having VD, while under the influence of alcohol, and they getting "frisky" and passing on the infection to other people before the penicillin could cure the sexually transmitted disease.

Alcohol and drug interaction

Some medications can interact with alcohol and alter the metabolism or effects of alcohol and/or the medication. There are two types of medication--alcohol interactions:
Pharmacokinetic interactions where the alcohol interferes
with the metabolism of the medication. 
Pharmacodynamic interactions where the alcohol enhances the effects of the medication, particularly in the central nervous system (e.g., sedation).

1.Pharmacokinetic interactions

Pharmacokinetics studies of the movement of the drug into, within and out of the body which essentially means what the body does to the drug.
About 10% of the alcohol consumed undergoes first-pass metabolism in the stomach, intestines, and liver. The major enzyme involved in alcohol metabolism is alcohol dehydrogenase (ADH), which converts the alcohol into acetaldehyde (a toxic compound) which is subsequently metabolized by aldehyde dehydrogenase (ALDH) to acetate. After the first-pass metabolism, alcohol goes to various parts of the body where it exerts its effect. Alcohol then goes back to the liver for metabolism and elimination. Beside ADH, CYP450 enzymes, mainly CYP2E1 are also involved in the metabolization of alcohol in the liver [2,3,4]. Alcohol consumption can alter the pharmacokinetics of certain medications by altering gastric emptying, affecting their absorption and metabolism. Similarly, certain medications can alter the pharmacokinetics of alcohol by altering gastric emptying and inhibiting gastric alcohol dehydrogenase. 

2.Pharmacodynamic interactions

Pharmacodynamics studies the effect and mechanism of action of drugs on the body which essentially means what the drug does to the body. Besides the effect of the alcohol on the central nervous system which produces impairment of performance and behavior, alcohol may contribute to the disease state which is being treated. An example would be impairment of gluconeogenesis which can lead to hypoglycemia in diabetic patients who are on treatment with oral hypoglycemic agents. A combination of nonsteroidal anti-inflammatory drugs and alcohol consumption can increase the risk of gastrointestinal hemorrhage.
Pharmacodynamic interactions involving alcohol and medications can increase the risk of adverse drug events and also increase susceptibility to the medications’ effect.

Therapeutic drug classes and drug-alcohol interactions 

There is a dearth of reliable studies on drug-interaction. Most of the evidence for drug-alcohol interactions is based on case reports and not on clinical trials [5].
There are three common therapeutic classes of drugs which interact with alcohol and these include antibiotics, cardiovascular drugs, and analgesics.

Antibiotics

Concomitant use of alcohol and certain type of antibiotics can cause or exacerbate the adverse effects. Disulfiram-like reactions have been reported in patients who consume alcohol while on the following antibiotics [6]:

• Cefamandole (Mandol)
• Cefoperazone (Cefobid)
• Cefotetan (Cefotan)
• Ceftriaxone (extremely rare)
• Chloramphenicol 
• Griseofulvin 
• Isoniazid 
• Metronidazole (Flagyl)
• Nitrofurantoin 
• Sulfamethoxazole (Bactrim)
• Sulfisoxazole

The disulfiram-like effect with cephalosporins is mediated by the inhibition of ADH, which in turn irreversibly inhibits the oxidation of acetaldehyde. The elevated concentrations of acetaldehyde produces facial flushing, nausea, vomiting, headache, tachycardia, hypotension, or a combination of all these effects. 
Metronidazole is also a known cause of disulfiram-like reactions when coadministered with alcohol. This reaction may involve ADH inhibition in the gastrointestinal (GI) tract, instead of in the liver as previously believed [7].  Disulfiram-like reaction has also been reported with the combined use of sulfamethoxazole/trimethoprim and alcohol [8].
Antitubercular drug, Isoniazid, is metabolized more quickly in chronic heavy alcohol users, and this can reduce the effectiveness of the drug [9]. Furthermore, the alcohol-isoniazid combination has been associated with an increased risk of hepatotoxicity and of disulfiram-like reactions [10]. Rifampin (Rifadin) and pyrazinamide which are also used in the treatment of tuberculosis are also known to increase liver toxicity when consumed with alcohol.
Ketoconazole (Nizoral), when combined with alcohol, may increase the risk of liver toxicity and disulfiram-like reaction.
Combination of cyclosporine and alcohol may increase the risk of central nervous system toxicity with possible seizures.
It is therefore imperative to advise patients to avoid alcohol intake for several days after consumption of antibiotic regimens known to interact with alcohol.
There is no scientific evidence to show that moderate alcohol consumption interferes with antibiotic effectiveness.

Cardiovascular Medications

Some medications for hypertension and angina are known to interact with alcohol. Nitrates such as hydralazine and nitroglycerin when taken with alcohol can increase the risk of orthostatic hypotension which may put the patient at risk of falls [3,4]. The metabolism of propranolol can be increased with chronic alcohol consumption, thereby decreasing the effectiveness of this beta-adrenergic blocking agent. Verapamil delays the elimination of alcohol and this can prolong alcohol intoxication [3,11]. Alcohol intake can also aggravate hypertension or heart failure [12,13].

Anticoagulants

Alcohol can interact with warfarin leading to an increase or decrease in its anticoagulation effect. Acute alcohol consumption can decrease the metabolism of warfarin leading to increased risk of hemorrhage. Chronic alcohol consumption increases the metabolism of warfarin leading to a decrease in the drug’s effect which can increase the risk of clot formation [3,4]. The exact mechanism of this alcohol and warfarin interaction is not known. History of alcohol consumption must be obtained from patients who are taking warfarin so that a close monitoring of the international normalized ratio (INR) can be carried out [14,15].

Antidiabetics

Diabetic patients who consume alcohol run the risk of hypoglycemia because alcohol suppresses gluconeogenesis. The risk of hypoglycemia is further increased if the patient is taking insulin or oral hypoglycemics [3,4].
Sulfonylureas such as tolbutamide and chlorpropamide when taken with alcohol are known to increase the risk of hypoglycemia. Excessive consumption of alcohol also increases the risk of diabetic complications such as diabetic neuropathy and retinopathy [3]. Heavy consumption of alcohol along with metformin intake can increase the risk of lactic acidosis [4]. Chlorpropamide, when taken with alcohol, can produce disulfiram-like reactions.

Non-Narcotic Analgesics

Nonsteroidal Anti-inflammatory Drugs (NSAIDs) and Aspirin

Case-control studies show that the use of NSAID or aspirin along with alcohol can increase the risk for an upper GI bleed. There is a three to fivefold increase in the risk of GI ulceration or major GI bleed when NSAIDs are used along with alcohol [16]. Alcohol consumption can cause gastritis by increasing gastric secretion and irritating the gastric mucosa.

Acetaminophen

Acetaminophen is an over the counter drug which is often used for pain relief. It is also found in combination with several narcotic medications. There have been several case reports which have reported severe liver injury in patients who use therapeutic doses of acetaminophen in conjunction with chronic alcohol use. Well-designed clinical studies to verify the validity of this interaction are, however lacking [11].
Acetaminophen is mainly metabolized through glucuronidation or sulfation (90%-96%) and also via CYP2E1 (4%-10%). CYP2E1 is the same enzyme involved in alcohol metabolism. Metabolization of acetaminophen through CYP2E1 produces a hepatotoxic metabolite called  N-acetyl-para-benzoquinoneimine (NAPQI). NAPQI is rapidly deactivated through hepatic stores of glutathione. When acute overdoses of acetaminophen are consumed, the stores of glutathione become exhausted and NAPQI accumulation can lead to fulminant liver failure [11].
In patients taking therapeutic doses of acetaminophen (<4 g/day) there is no increased risk of hepatotoxicity in alcoholic patients unless there are other risk factors [17].
The FDA advises patients that they should consult their doctor before taking over the counter pain medication if they take more 3 alcoholic drinks a day [18].

Narcotic Analgesics 

Opioid analgesics such as methadone and codeine derivatives can act on the central nervous system (CNS) to produce sedation and respiratory depression [19]. Alcohol also acts on the brain and can increase the risk of sedation and CNS depression in patients taking opioid analgesics [19]. There is a lack of studies on the interaction of alcohol and narcotic analgesics.

Besides these three common therapeutic classes of drugs which can interact with alcohol, there are other classes of drugs which can also interact with alcohol.

Antidepressants

Tricyclic antidepressants (TCAs) such as amitriptyline, doxepin, maprotiline, and trimipramine cause sedation and alcohol can increase the sedation caused by TCAs’ through pharmacodynamic interaction. Alcohol also interferes with the metabolism of amitriptyline in the liver thereby increasing the levels of amitriptyline in the blood. Furthermore, alcohol induced liver disease also impairs amitriptyline breakdown leading to significantly increased levels of active medication in the body. These high levels of amitriptyline lead to convulsions and disturbances in heart rhythm.
Selective serotonin reuptake inhibitors (SSRIs) such as fluvoxamine, fluoxetine, paroxetine, and sertraline which are now widely used as antidepressants, however, have much less sedating effect and no serious interactions occur when these are consumed with moderate amounts of alcohol [20].
Monoamine oxidase (MAO) inhibitors such as phenelzine and tranylcypromine can induce severe high blood pressure if consumed with tyramine, a substance which is present in red wine. Hence people taking MAO inhibitors should be warned against consuming red wine.

Antihistamines

Antihistamines, which are often used for the treatment of allergies and colds, are known to cause drowsiness, sedation, and hypotension, especially in elderly patients [21]. Alcohol through pharmacodynamic interactions, can enhance the sedating effects of these antihistamines and increase the patients risk of falling and affect one's ability to drive and operate machinery. Patients taking antihistamines should be warned against
consuming alcohol.

Barbiturates and Benzodiazepines

Sedative-hypnotic agents such as barbiturates (phenobarbital) and benzodiazepines (Valium, Xanax, Ativan) have a sedative effect and when consumed with moderate amounts of alcohol, synergistic sedative effects occurs leading to substantial CNS impairment.
These sedative-hypnotic agents can impair memory, just as alcohol can. Combination of these drugs with alcohol can exacerbate this memory-impairing effect.
Alcohol can inhibit the breakdown of barbiturates in the liver thereby increasing the blood of phenobarbital.

Conclusion

Though the alcohol and medication interaction has been reasonably well studied in chronic heavy alcohol consumers, the effect of moderate alcohol consumption has not been studied as thoroughly. Risks of oversedation in patients combining benzodiazepines and alcohol and the effects of warfarin and alcohol combination can be clinically very significant. The commonly held belief that patients taking antibiotic should not take alcohol is a myth since only a small number of antibiotics produce disulfiram-like side effect. Generally, alcohol does not reduce the efficacy of antibiotics. It is imperative that people taking either prescription or OTC medications, read product warning labels to determine whether possible interactions exist. Similarly, doctors prescribing medications should be alert to the possible interaction between alcohol and the medications been prescribed.

References

1. Kruszelnicki KS. Alcohol and Antibiotics. News in Science, 2 June 2005 at http://www.abc.net.au/science/articles/2005/06/02/1380836.htm accessed on 12/11/18.
2. Jang GR, Harris RZ. Drug interactions involving ethanol and alcoholic beverages. Expert Opin Drug Metab Toxicol. 2007;3:719-731.
3. Moore AA, Whiteman EJ, Ward KT. Risks of combined alcohol/medication use in older adults. Am J Geriatr Pharmacother. 2007;5:64-74. 
4. Fraser AG. Pharmacokinetic interactions between alcohol and other drugs. Clin Pharmacokinet.
5. Noureldin M, Krause J, Jin L, Ng V, Tran M. Drug-Alcohol Interactions: A Review of Three Therapeutic Classes. US Pharm. 2010;35(11):29-40. 
6. Weathermon R, and Crabb DW. Alcohol and Medication Interactions. Alcohol Research & Health. 1999; 23 (1): 40-51.
7. Tillonen J, Vakevainen S, Salaspuro V, et al. Metronidazole increases intracolonic but not peripheral blood acetaldehyde in chronic ethanol-treated rats. Alcohol Clin Exp Res. 2000;24:570-575. 
8. Heelon MW, White M. Disulfiram-cotrimoxazole reaction. Pharmacotherapy. 1998;869-870.
9. Baciewicz AM, Self TH. Isoniazid interactions. South Med J. 1985;78:714-718.
10. Isoniazid package insert. Eatontown, NJ: West-Ward Pharmaceutical Corp; March 2008.
11. Jang GR, Harris RZ. Drug interactions involving ethanol and alcoholic beverages. Expert Opin Drug Metab Toxicol. 2007;3:719-731.
12. Zilkens RR, Burke V, Hodgson JM, et al. Red wine and beer elevate blood pressure in normotensive men. Hypertension. 2005;45:874-879. 
13. Bau PF, Bau CH, Naujorks AA, Rosito GA. Early and late effects of alcohol ingestion on blood pressure and endothelial function. Alcohol. 2005;37:53-58.
14. Hylek EM, Heiman H, Skates SJ, et al. Acetaminophen and other risk factors for excessive warfarin anticoagulation. JAMA. 1998;279:657-662. 
15. Havrda DE, Mai T, Chonlahan J. Enhanced antithrombotic effect of warfarin associated with low-dose alcohol consumption. Pharmacotherapy. 2005;25:303-307.
16. Pfau PR, Lichtenstein GR. NSAIDS and alcohol: never the twain shall mix? Am J Gastroenterol.
17. Kuffner EK, Green JL, Bogdan GM, et al. The effect of acetaminophen (four grams a day for three consecutive days) on hepatic tests in alcoholic patients—a multicenter randomized study. BMC Med.
18. FDA proposes alcohol warning for all OTC pain relievers. U.S. Department of Health and Human Services. November 14, 1997. http://archive.hhs.gov/news/. 
19. Drug interactions. Thomson Micromedex. Greenwood Village, CO. www.thomsonhc.com. 
20. Matilla M.J. Alcohol and drug interactions. Annals of Medicine 22:363–369, 1990.
21. Dufour MC, Archer L and Gordis E. Alcohol and the elderly. Clinical Geriatric Medicine 8:127–141, 1992.

Surgery for removal of metallic implants after fracture union: Is it necessary?

Surgery for removal of metallic implants after fracture union: Is it necessary?

                                   Dr. KS Dhillon, MBBS, FRCS, LLM

Introduction

After fracture union metallic implants used for stabilization of the fracture serves no purpose, hence in the past, it was advocated that all such implants should be removed. This was partly due to fears of corrosion associated with the commonly used stainless steel alloy implants. However, subsequent research found such claims to be unfounded.

There are two broad class of fixation devices used in orthopaedic surgery for fixation of limb bones. The first group consists of wire or pins and the other includes screws, plates, and nails. In the past, most of the implants were made of stainless steel alloy. Now, however, titanium alloy implants are becoming more popular.

There are no clear guidelines in the medical literature on indications for removal of metallic internal fixation devices after fracture union. Surgeons have been making decisions about implant removal arbitrarily because of lack of evidence-based literature to guide them. The general rule has been that all wires should be removed while plates, nails, and screws may or may not be removed depending on prevailing circumstances.

The presence of metallic implants in the body usually does not produce any symptoms. However, under some circumstance, they can be a source of pain and or limitation of movement of the joints. In such circumstances, doctors are often compelled to remove the implants although not all such patients will be relieved of their symptoms after the surgery. Surgery for removal implants is not as innocuous as we often assume.

This review will probe what the current state of knowledge is regarding the need for implant removal after fracture union.

Types of implants used for internal fixation of limb fractures

Kirschner wires

 These are non-malleable stainless steel wires which come in different sizes and usually vary in diameter from between 0.7 mm to about 1.6 mm and in lengths of between 4 to 12 inches. There are usually used to fix small bone fragments which are not suitable for fixation with other devices such as screws, plates, and nails. Wires are frequently used to fix peri-articular fractures in children and also in adults, where non-invasive close reduction of the fracture can be carried out and the fracture stabilized with percutaneous wires. The frequent sites where wires are used for fixation of fractures include the elbow, wrist, hand, fingers, foot and the toes.

Cerclage wires

 These are malleable stainless steel wires which can be twisted around bones and tied in a knot. They are often used to fix fractures of the patella and the olecranon. They can also be used at other sites to complement fixation of bones with other devices.

Plates, screws, and nails

Various designs of plates, screws, and nails are available for internal fixation of fractures. These are usually made of stainless steel alloy or titanium alloy. The stainless steel implants are iron-carbon alloys with some element of chromium, molybdenum, and manganese. The titanium implants are alloys of titanium, aluminum and niobium.

Indications of implant removal

There is usually no disagreement among surgeons that K-wires that are used for temporary fixation of fractures should be removed after fracture union. K-wires protruding under the skin can cause skin irritation and pain. They can also migrate, if they are not securely fixed across two bone cortices, causing damage to other body structures. Cerclage wires can also cause skin irritation and pain if they are not buried in deep tissues and under such circumstance they should be removed. Screws that are subcutaneous and causing skin irritation should be removed.

Deep implants such as plates, nails, and screws may or may not be symptomatic and the removal such implants has been an area of debate and controversy. The questions that arise are whether the implants will cause harm if left in the body and do they cause any functional disability.

Do implants cause harm?

Biocompatibility of metallic implants has always been a concern because of the release of biologically active small particles due to oxidation of metal and the possibility of toxicity of these particles to the human body. Stainless steel alloys do corrode in the body but the implants become covered with a layer of fibrous tissue often as thick as 2 mm depending on the amount of corrosive material released and the amount of movement between the implant and the surrounding tissues.

Titanium alloys, on the other hand, do not corrode but they release ions which diffuse into the surrounding tissues [1]. It was believed in the 1970’s and 1980’s that these corrosive materials and metallic ions may be carcinogenic and predispose patients to cancers. However, experimental studies have not revealed any association between metallic implants and the development of any cancers [2]. Presently the possibility of corrosion and cancer are no longer considered to be an indication for removal of the implant [2]. Allergic reactions to metals in the body are rare and data substantiating implant related allergic reactions is scarce [2].

Another reason why plate removal was recommended in the past was due to the widely held belief that the presence of plates on the bone leads to bone atrophy. However, more recent studies have shown that if the plates are left in the body long enough the density of the bone returns to normal. Rosson et al studied the bone density in patients with forearm fractures and found that the bone density returns to normal after 21 months [3]. Similarly, studies of the tibia after plate removal have failed to show significant bone atrophy [4]. Hence plates can be left in the body without fear of plates causing bone atrophy or stress protection.

Essentially implants, left in the body after fracture union, do not cause any bodily harm. The next question that needs to be answered is whether implant produces symptoms or functional disability.

Do implants cause symptoms and when should they be removed?

There are very few circumstances under which implants would definitely need to be removed (absolute indications). K-wires can migrate and cause harm to other body structures and K-wires that are under the skin can produce pain, hence removal of K-wire would be indicated. Screws that perforate the joint should be removed because they can damage the joint when the joint is mobilized. Cerclage wires whose sharp ends are not properly buried under deep tissues can protrude under the skin leading to pain. Such wires obviously need to be removed. Implants such as plates adjacent to joints which are imperfectly positioned can obstruct joint motion and it would be necessary to remove them to improve joint function. Implants that are loose can migrate or produce irritation of adjoining soft tissues and such implants would also need to be removed.

Indication for removal of implants under most other circumstances is controversial and debateable. Some patients complain of pain or discomfort in the limb even when the implants are securely fixed and well positioned. The cause of such pain remains unclear and it is difficult to determine whether the implant is the cause of the pain or it is due to the injury itself [2]. In patients with such pain, the results of implant removal are ‘unpredictable and depend on both the implant type and its anatomic location’ [5].

Minkowitz in a study of 57 patients who had implant removal because of complaints of pain found that only 53% of the patients had complete resolution of pain at one year follow up [6].

Brown et al studied 126 patients who complained of lateral ankle pain in the region of the implants. Only 50% (11 out of 22 patients) had improvement of pain after implant removal. The functional scores were no different in patients who had and did not have implant removal [7]. The unpredictability of outcome has to be kept in mind when removal of implants for pain is contemplated.

Removal of implants involves another surgery which is accompanied with the risk of anesthesia-related complications as well as complications associated with the surgery itself. Cost of the surgery and hospitalization, as well as time off work, has to be borne in mind. Not only is the results of the surgery unpredictable, but the surgery itself can also sometimes be difficult and frustrating, resulting in broken implants and retrieval instruments. Surgical complications include bleeding, wound infections, neurovascular injury, refractures, recurrence of deformity, incomplete removal of hardware and sometimes poor cosmetic results because incisions for removal of the minimally invasive plate and nails are not so ‘minimal’.

Sanderson et al in a study of 188 patients who had implant removal found an overall complication rate of 20% and for forearm implant removal the complication rate was 42%. The nerve injuries that occurred were all permanent and were produced by junior doctors [8].

Richards et al in a smaller series of 86 adult patients who had a routine removal of implants in both symptomatic and asymptomatic patients reported a much lower rate of complications (3%) which included a nerve injury, a refracture, and a hematoma. However, the authors recommended that it would be appropriate to leave asymptomatic implants in situ [9].

Removals of implants from forearm bones are associated with higher complication rates. Langkamer et al [10] reported a 40% complication rate after forearm implant removal. Chia et al [11] reported a 27% and Bednar et al [12] reported a 10% complication rate following removal implants from the forearm.

Brown et al reported a 19% rate of significant complications in patients who had implant removal. They also found that patients who did not have their implants removed had no ‘appreciable problems’ and the authors recommended that implants should only be removed if there is a clear indication for the removal [13].

Karladani et al in a study of 71 patients who had removal of the tibial nail for pain found that only 39 of the 71 patients had improvement of pain and they were not totally pain-free after the surgery. In 14 patients the pain was the same and in 18 patients the pain was worse after the removal of the nail. Four of the 6 patients who had a previous fasciotomy were unhappy with the outcome of the surgery to remove the nail. The authors concluded that the outcome of tibial nail removal for pain is poor and that the nail should not be removed unless there are convincing reasons to do so [14].

There have been concerns that athletes with implants in situ, who participate in contact sports run the risk of a refracture because the implant can act as a ‘stress riser’. Evans and Evans did a retrospective study of 15 elite rugby players who returned to competitive sports while having implants in situ. Two of the players’ sustained implant related complications and the other 13 continued playing for up to 6 years without any symptoms. One of the players needed removal of wires which produced pain after the tension band wiring for a fracture of the patella while another player sustained an undisplaced fracture of the radius and had to be treated in a cast for one month. The authors concluded that an early return to sports after fracture union is feasible and it is not necessary to remove the implants which would further delay return to sports [15].

Routine removal of implants in pediatric patients is a common practice among many orthopaedic surgeons [16]. Kahle in arguing against routine removal of implants in children did a retrospective survey of 138 patients who had removal of implants and found a complication rate of 13%. Seven percent of the patients had an incomplete removal of the implant and 1.4% had a refracture. The study showed no evidence to support the policy of routine removal of implants [17].

Davids et al in a retrospective survey of 801 children with 1223 implants removed over a 17 years period reported a 12.5% complication rate of which 6% were major and 6.5% minor complications [18].

There appears to be no compelling reason to remove implants in children as is the case in adults after fracture union when the patient is asymptomatic.

Routine implant removal after fracture surgery consumes a remarkable portion of resources allocated for elective orthopedic surgery and is a potentially reducible consumer of hospital resources in trauma units [19].

The medical literature provides only level IV or level V evidence regarding removal of implants after fracture healing. Vos DI et al [20] have carried out a prospective multicentre clinical cohort study to evaluate the outcome of implant removal after fracture healing. The study included 288 adult patients, 146 patients had removal of upper limb implants and 142 patients had removal of lower limb implants. Removal of implants of the clavicle, humerus, radius/ulna, tibia, and femur was included.
The most frequent indication for implant removal was pain (63%) and limitation of joint motion (56%).

For removal of femoral nails, an extension of the scar was necessary in 62% of the patients and for tibial nails in 35% of the patients. For removal of upper limb implants, the estimated blood loss was between 0 to 300 ml and the operating time varied between 3 mins to 90 mins. For removal of lower limb implants, the blood loss was between 0 ml to 500 ml and the operating time was between 13 mins to 120 mins.

Thirty percent of the patients had one or more surgery-related complications. The complications included post-operative bleeding (11%), refractures (1%), nerve injuries (6) other complication in 9% of the patients. The complication rate for upper limb procedures was 22% while for the lower limbs it was 37%.

The number of patients with pre-operative complaints who had complete follow up was 214 (88%) and 6 months after the surgery the number of patients with complaints was reduced to 49% (P<0.0005). Despite the significant number of patients (39%) who had improved after implant removal there were 8 patients, who had no pre-operative complaints but developed 25 new post-operative complaints such as paraesthesia, pain, loss of strength and limited joint motion.

There appears to be no indication for removal of implants in patients, both adults, and children when there are no symptoms. In symptomatic patients the outcome of implant removal is unpredictable and the patient should be advised accordingly if implant removable is contemplated. In about half the patients the symptoms will not improve after the surgery. Furthermore, the surgery is not innocuous and between 3% to over 40% of the patients can develop complications depending on the type and location of the implant.

Conclusion

In the past routine removal of implants after fracture union was a common practice. This was because the metallic implants used for stabilization of the fracture served no purpose after the fracture had united and there were fears of carcinogenic toxicity of ions release form oxidative corrosion of the stainless steel alloy implants that were commonly used for fracture stabilization. However subsequent research has found that such claims are unfounded. Fears of bone atrophy and stress shielding related to the implants have also been found to be unfounded provided the implants are left in situ long enough. Hence implants need not be removed for these reasons.

However, under some circumstances, there are definite indications for removal of implants. There is no controversy or debate about removing K-wires, Cerclage wires, implants that penetrate joints and those that are imperfectly position and obstruct joint motion.

 In most other situations the indications for removal of implants are relative. Even stable infected implants, before fracture union occurs, are often left in situ but infected implants after fracture union should be removed to control infection. Implants that are loose which can sometimes migrate and cause symptom may have to be removed.

Deep-seated stable implants are usually asymptomatic and most authors recommend that they should be left in situ even in children. Removal of implants is not as innocuous as is often believed. Besides anesthesia-related complications, there are surgery-related complications in 3% to over 40% of the patients. Implant removal is also associated with increased cost and time off work.

In many patients who complain of pain around the site of the implant, the actual cause of the pain is often not known and it could be due to the effect of the injury rather than the implant itself. In symptomatic patients removal of implants resolve the symptoms in only about 50 % of the patients.

Before undertaking surgery to remove implants, it is imperative that the surgeon informs the patient about complications that can arise from the surgery. The patient also needs to be made aware of the unpredictability of the outcome of such surgery. Most authors are of the opinion that asymptomatic implants should not be removed and in other situations, the implants should only be removed if there is a definite compelling reason to do so.

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