Treatment of AC joint dislocation

                   Treatment of AC joint dislocation

                                           Dr KS Dhillon

Introduction

The true incidence acromioclavicular (AC) injuries is not known because many with such injuries do not seek medical treatment. About 12% of shoulder dislocations involve the AC joint. The treatment of AC joint injury remains controversial although good long term results can be seen in patients treated conservatively. There is an increasing tendency to treat higher grade injuries surgically.

Anatomy of AC joint

The acromioclavicular (AC) joint is a synovial arthrodial joint with an intra-articular disc, where the oval lateral end of the clavicle articulates with an imperfect incongruent facet of the acromion. Although it is a small joint it supports the shoulder girdle and the upper limb [1].

The joint stability is provided superiorly by reinforcement of the capsule with a strong acromioclavicular ligament and inferiorly the capsule and a weak inferior acromioclavicular ligament. These ligaments provide about 68% of joint stability to superior translation of the clavicle. Additional stability is provided by the coracoacromial and the coracoclavicular (conoid and trapezoid) ligaments [1].

The clavicle rotates about 45 degrees on its own axis. Most of this motion occurs at the sternoclavicular joint and only about 5 to 8 degrees of motion occurs at the sternoclavicular joint [2].

Imaging anatomy of the AC joint

The AC joint is best viewed in an AP projection with a 10-15 degree cephalic angulation (Zanca view). In this view, the clavicle is projected off the spine of the scapula [3].

The AC joint space is measured as an average of the cranial and caudal joint space measurements. It is usually less than 5mm. In males the average is about 3.3 plus minus 0.8 and in females the average is about 2.9 plus minus 0.8. In both males and females, the joint space reduces with age and space of less than 0.5 mm can be found. A joint space of more than 7 mm in males and more than 6 mm in females is pathological irrespective of age. There is no significant difference between the left and the right [4].

The coracoclavicular distance is usually less than 11-13mm and the right and left difference is usually less than 5mm [5].

Classification of AC joint injuries

The most commonly used classification for AC joint injuries is the one by Rockwood et al [6]:

Type I. Partial tear of acromioclavicular ligaments. X-rays are usually normal. Pain, swelling and local tenderness at the AC joint often present. Cross arm test is positive.

Type II. Complete tear of the acromioclavicular ligaments. Plain X-rays are usually normal. Some widening of the AC joint space may be present. The inferior border of the clavicle is not elevated beyond the superior border of the acromion.  Pain, swelling, tenderness, and deformity at the AC joint is usually present.

Type III. Clinically obvious deformity is seen. X-rays show vertical translation with the inferior border of the clavicle elevated beyond the superior border of the acromion.

Type IV. Posterior displacement of the lateral end of the clavicle into or through the trapezius muscle occurs. An axial view will show the posterior displacement of the lateral end of the clavicle.

Type V. Disruption of the deltotrapezius fascia occurs which allows the lateral end of the clavicle to lie under the skin. X-rays show marked displacement of the clavicle beyond the medial end of the acromion.

Type VI. A very rare injury. The lateral end of the clavicle is displaced inferiorly and lies below the acromion and the coracoid (as well as the conjoint tendon).

Treatment of AC joint injuries

The treatment of AC joint injuries remains controversial. Although in recent years more surgeons are opting for surgical treatment of severe AC joint injuries, the outcome of conservative treatment is good on long term follow up. Nonoperative treatment of complete AC joint dislocations have generally yielded reasonable results, although there are some patients who have reported dissatisfaction with the outcomes [7,8,9,10]. Rawes and Dias [11] reviewed 30 patients, who were treated conservatively for dislocation of the AC joint, at an average of 12.5 years after the injury. They found good outcomes in all except one patient. X-rays showed persistent dislocation in 17 patients and in 13 the dislocation improved to a subluxation. Atrophy of lateral end of clavicle (similar to resection of lateral end of clavicle) was seen in completely dislocated joints.
Randomized prospective controlled trials also show good outcomes of conservative treatment for dislocation of the AC joint [10,12]. However, the current trend for the treatment of type I and type II injuries is conservative with symptomatic relief provided by ice, arm sling, and analgesics. Heavy lifting and sports are usually avoided for 8 to 12 weeks [13].

The current consensus on the treatment of type III injuries remains that of a conservative approach because the prognosis after conservative treatment is excellent [14,15,16]. However, patients with type III injuries who continue to have symptoms after 3 months may be considered for surgical treatment [13]. Some surgeons prefer surgical treatment in patients with type III injury who are heavy laborers and overhead athletes [17].

Type VI injuries are very rare and most of the reported cases are case reports where the patients have been treated surgically [18,19,20]. In medically fit patients who have type IV and V injuries the treatment is usually surgical [13].

Murray et al [21] published in 1918 the outcome of The ACORN Prospective, Randomized Controlled Trial comparing open reduction and tunneled suspensory device (ORTSD) fixation with nonoperative treatment for type-III and type-IV AC joint dislocations. The study included sixty patients aged 16 to 35 years with an acute type-III or IV disruption of the AC joint who were randomized to receive ORTSD fixation or nonoperative treatment. They assessed functional outcomes with use of the Disabilities of the Arm, Shoulder and Hand (DASH) as the primary outcome measure.  The Oxford Shoulder Scores (OSS) and Short Form (SF-12) were used as secondary outcome measures at 6 weeks, 3 months, 6 months, and 1 year after treatment.
They found that ORTSD fixation confers no functional benefit over nonoperative treatment at 1 year follow up in patients with type-III or IV disruptions of the AC joint. The patients managed nonoperatively generally recovered faster. There were some patients in the nonoperative treatment group who remained dissatisfied and required delayed surgical reconstruction. The principal reason for dissatisfaction was persistent discomfort, with 1 individual making a specific request for a surgical procedure for cosmetic reasons. The cost of surgical treatment was significantly higher than nonoperative treatment.
The authors concluded that routine surgical treatment for displaced AC joint injuries is not justified.

Chang et al [22] carried out a systematic review and meta-analysis to compare the outcome of operative versus nonoperative management of acute high-grade AC joint dislocation. They found that there was no clinical difference in functional outcome scores between the two groups. Patients in the nonoperative group returned to work earlier. Surgery can be associated with implant complications and postoperative infections.

Many surgical procedures have been described for the treatment of AC joint injuries and no one procedure has been shown to be superior to the other. Procedures for acute injuries include reduction and stabilization of the joint with reconstruction of the ligaments. For delayed surgery, an excision of lateral end of the clavicle is usually carried out in addition to the reduction, stabilization and ligament reconstruction [13].

Conclusion

Although there are some controversies regarding the treatment of AC joint dislocations, there is, however, consensus that type I and type II dislocations should be treated nonsurgically. There is also consensus that type III injuries should be treated conservatively. Occasionally type III injuries may need to be treated surgically when there are persistent symptoms after 3 months and in patients who are heavy manual laborers and overhead athletes.

Type IV and Type V injuries are often treated surgically. Type VI injuries are very rare. There are more and more studies being published which show that surgical treatment offers no functional benefits over nonsurgical treatment. Surgery is more expensive and can be associated with complications. Patients treated conservatively return to work faster. In patients with high-grade dislocations who are treated nonoperatively cosmesis is sometimes a cause for dissatisfaction.

References

1. Shaffer B S. Painful conditions of the Acromioclavicular joint.  J Am Acad Orthop Surg. 1999; 7: 176-188.
2. Rockwood CA Jr, Williams GR, Young DC: Injuries to the acromioclavicular joint, in Rockwood CA Jr, Bucholz RW, Green DP, Heckman JD (eds): Fractures in Adults, 4th ed. Philadelphia: Lippincott-Raven, 1996, vol 2, pp 1341-1413.
3. Ursula Nemec, Gerhard Oberleitner, Stefan F. Nemec, Michael Gruber, Michael Weber, Christian Czerny and Christian R. Krestan. MRI Versus Radiography of Acromioclavicular Joint Dislocation. American Journal of Roentgenology. 2011; 197:968-973.
4. Peter CJ and Redlund-John I. Radiographic joint space in normal Acromioclavicular joints. Acta Orthop. Scand. 54, 431-433, 1983.
5. Alyas F, Curtis M, Speed C, Saifuddin A, Connell D. MR imaging appearances of acromioclavicular joint dislocation. RadioGraphics 2008; 28:463–479.
6. Rockwood CA, Williams G, Young D.  Disorders of the acromioclavicular joint. In: Rockwood CA, Matsen FA, eds. The shoulder. Second Ed. Vol. 1. Philadelphia: WB Saunders, 1998:483-553.
7. Canadian Orthopaedic Trauma Society. Multicenter randomized clinical trial of nonoperative versus operative treatment of acute acromioclavicular joint dislocation. J Orthop Trauma. 2015 Nov;29(11):479-87.
8. Phillips AM, Smart C, Groom AF. Acromioclavicular dislocation. Conservative or surgical therapy. Clin Orthop Relat Res. 1998 Aug;(353):10-7.
9. Taft TN, Wilson FC, Oglesby JW. Dislocation of the acromioclavicular joint. An end result study. J Bone Joint Surg Am. 1987 Sep;69(7): 1045-51.
10. Galpin RD, Hawkins RJ, Grainger RW. A comparative analysis of operative versus nonoperative treatment of grade III acromioclavicular separations. Clin Orthop Relat Res. 1985 Mar;(193):150-5.
11. Rawes ML, Dias JJ. Long-term results of conservative treatment for acromioclavicular dislocation. J Bone Joint Surg Br. 1996 May;78(3):410-2.
12. Larsen E, Bjerg-Nielsen A, Christensen P. Conservative or surgical treatment of acromioclavicular dislocation: a prospective, controlled, randomized study. J Bone Joint Surg [Am] 1986:68-A;552-5.
13. Fraser-Moodie JA, Shortt NL, Robinson CM. Injuries to the acromioclavicular joint. J Bone Joint Surg [Br] 2008;90-B:697-707.
14. Bjerneld H, Hovelius L, Thorling J. Acromio-clavicular separations treated conservatively: a 5-year follow-up study. Acta Orthop Scand 1983;54:743-5.
15. Schlegel TF, Burks RT, Marcus RL, Dunn HK. A prospective evaluation of untreated acute grade III acromioclavicular separations. Am J Sports Med 2001;29:699-703.
16. Spencer EE Jr. Treatment of grade III acromioclavicular joint injuries: a systematic review. Clin Orthop 2007;455:38-44.
17. Epstein D, Day M, Rokito A. Current concepts in the surgical management of acromioclavicular joint injuries. Bull NYU Hosp Jt Dis. 2012;70(1):11-24.
18. Gerber C, Rockwood CA Jr. Subcoracoid dislocation of the lateral end of the clavicle: a report of three cases. J Bone Joint Surg [Am] 1987;69-A:924-7.
19. McPhee IB. Inferior dislocation of the outer end of the clavicle. J Trauma 1980;20:709-10.
20. Torrens C, Mestre C, Pérez P, Marin M. Subcoracoid dislocation of the distal end of the clavicle. A case report. Clin Orthop Relat Res 1998;(348):121-3.
21. Murray IR, Robinson PG, Goudie EB, Duckworth AD, Clark K, Robinson CM. Open Reduction and Tunneled Suspensory Device Fixation Compared with Nonoperative Treatment for Type-III and Type-IV Acromioclavicular Joint Dislocations: The ACORN Prospective, Randomized Controlled Trial. J Bone Joint Surg Am. 2018;100(22):1912–1918. 
22. Chang N, Furey A, Kurdin A. Operative Versus Nonoperative Management of Acute High-Grade Acromioclavicular Dislocations: A Systematic Review and Meta-Analysis. J Orthop Trauma. 2018;32(1):1–9. 

The Disruptive Orthopaedic Surgeon and the Consequences of Disruptive Behavior

The Disruptive Orthopaedic Surgeon and the Consequences of Disruptive  Behavior

                                                DR KS Dhillon

What is disruptive behavior?

The American Medical Association’s, Code of Medical Ethics defines disruptive physician behavior as ‘‘personal conduct, whether verbal or physical, that negatively affects or that potentially may negatively affect patient care’’ [1]. Behaviors that can be considered as disruptive include the use of inappropriate language, yelling, gossip, facial expressions, and other mannerisms, as well as physical violations. Disruptive physicians can also affect learning [2] and other work such as research [3].

In the USA, since the publication of the Institute of Medicine report ‘To Err Is Human’, there has been a substantial concerted effort to reduce the number of negative patient outcomes resulting from disruptive physician behavior [4,5]. Apparently, although substantial improvements have occurred in this area in the field of medicine, the same cannot be said for the orthopaedic surgical field regarding disruptive physician behavior [6].

Disruptive Behavior and Orthopaedic Surgery

The working environment in the operating theatre (OT) is very complex. The number of surgical procedures in the OT increases year after year. This combination of complex environment and a high volume of cases creates a very stressful working atmosphere. The surgeons will be under even more stress in the future, when they will have to cope with increasing patient load and advancing technology, reductions in physician reimbursement, and higher costs of medical liability insurance [7].

Private hospitals in some countries have been steadily increasing the number of doctors that they are recruiting to improve their business revenue. The numbers of patients coming to the hospitals is not increasing proportionally resulting in lower incomes for the doctors. This leads to increased stress and a tendency for the doctors to perform more surgeries where the indications may be somewhat doubtful. This can also affect patient outcomes and increase in litigation which in turn leads to higher medical insurance premiums.

Authoritative focused behavior is common among surgeons in the OT and words like please and thank you are not common. The focus is usually on efficiency. This makes some ancillary medical staff perceive surgeons as demanding and unfriendly although surgeons’ behavior may be appropriate in the given circumstance [6].

In most individuals, the specific reason for unprofessional or disruptive behavior is difficult to establish. It is most likely multifactorial, with stress and dissatisfaction with work playing an integral role in the physician’s behavior [8].

Orthopaedic surgeons play a very active role in health care delivery in most countries. With the aging population, musculoskeletal disorders are becoming more common. The numbers of orthopaedic operations are proportional increasing.

A survey by Rosenstein and O’Daniel [9] showed that orthopaedic surgery ranks fourth-highest behind general surgery, neurosurgery, and cardiovascular surgery, with regard to the prevalence of disruptive events. Orthopaedic surgery also ranks fourth-lowest (behind the same above three fields) with regard to patients’ ratings of satisfaction with their doctors [6]. Optimal patient care can only be provided by having proper communication with the patients and other members of the health care delivery team. Doctors must ensure that disruptive events and distractions are minimized at all costs [10].

Rising health care costs and reduction in reimbursements places increasing demands on orthopaedic surgeons. They will have to see more patients and their increase in hours of work will lead to increases in stress  [11]. This increase in stress can lead to a negative attitude toward patients as well as other members of the medical delivery team and also towards the overall job responsibilities [11].

Understanding Disruptive Behavior

What constitutes disruptive behavior remains unclear. The leadership of the Grand Rapids (Michigan, USA) 7 hospital health care system’s perioperative services department led an initiative to evaluate and reduce the incidence of intimidation in the department. They surveyed 110 physicians to ascertain their beliefs about behaviors that constitute intimidation. They found that a majority of physicians in the perioperative services agree that behaviors that were identified as intimidating by national organizations actually constitute intimidation in only 4 of 9 instances. Even for the most egregious behaviors, there was a lack of complete agreement that the behavior constitutes intimidation. These findings suggest why traditional means of addressing intimidating behavior may not be effective [12].

Generally, patients identify thoroughness, empathy, respect, candor, and confidence as ideal physician behaviors. Such behaviors, along with professionalism, have been found to be associated with higher patient satisfaction, trust, compliance, and recommendations of the doctor to others, as well as with fewer patient complaints and patient litigation [6]. Often physicians are more likely to know what is expected of them by patients than what constitutes disruptive or unprofessional behavior [13].

Prevalence of Disruptive Physician Behaviors

A survey by the American College of  Physician Executives [14] of 1627 physician executives, showed that 95.7% of the physicians encountered disruptive physician behavior on a regular basis, and 70.3% of the physicians reported disruptive behaviors nearly always involved the same physician(s). Some of the common disruptive behaviors encountered included disrespect, yelling, insults, physical abuse, refusal to complete tasks and carry out duties and throwing items. A majority (56.5%) of the physicians reported that disruptive physician behaviors very often involved conflict with a nurse or other paramedical staff. The survey also found that disruptive behaviors also involved other physicians (14.7%), administrators (14.5%), as well as patients (14.2%). Eighty percent of the respondents said disruptive physician behavior is often under-reported because of the victim’s fear of reprisal or is only reported when a serious violation occurs.

A survey [15] at 50 Veteran's Administration hospitals in the US was done which found that 86% of nurses surveyed had witnessed disruptive physician behavior. There have been other surveys [16,17] that have found that more than 90% of nurses experienced verbal abuse within the previous year. Physician abuse of pharmacists [18] and students have also been reported to be common [13].
Disruptive physician behavior is often not reported. Most patient complaints to disciplinary boards are usually due to disruptive physician behaviors. Most often the complaints are due to rudeness, poor communication, and unethical or improper behavior [20].

Consequences of Disruptive Physician Behavior

Safety of patients

When there are episodes of disruptive behavior by the surgeon, there is diminished communication, collaboration, and information exchange between the patient and the paramedical staff which adversely affects team dynamics and patient outcomes.

A survey was conducted by VHA West Coast in the US to assess the significance of disruptive behaviors and their impact on patient care. A survey of staff at 102 hospitals was carried out. The staff included physicians, nurses and administrative executives. Seventy-seven percent of the respondents admitted to witnessing disruptive physician behavior [4].

Sixty-seven percent of those who witnessed such behavior indicated that at least one of the episodes of disruptive physician behavior was associated with an adverse event. Seventy-one percent indicated that the episode was associated with a medical error, and 27% indicated that it was associated with patient mortality [4].

The rate at which incidents of disruptive behavior are acknowledged by physicians and by other paramedical staff varies widely.

Jones and McCullough [21] carried out a survey in which they found that 74% of the nurses and doctors but only 43% of the surgeons who responded to the survey reported having witnessed disruptive behavior. Though the incidence of disruptive behavior is prevalent, the percentage of physicians and surgeons who have been reported for disruptive behavior in the US is low at about 3% to 5% [22].

In the survey by Rosenstein and O'Daniel [15], most nurses believed that physician disruptive behavior produced frustration, stress, impaired concentration, reduced collaboration and communication, and led to negative patient outcomes.

Disruptive surgeon behavior in the OT can adversely affect the team dynamics and promote negative patient outcomes. Communication among all members of the surgical team becomes impaired due to frustration, stress, and diminished relationship produced by the disruptive surgeon. One of the leading causes of avoidable surgical errors is poor communication between the surgeon and the surgical staff [23].

According to the Joint Commission guide to improving staff communication, 60% of avoidable adverse medical events are due to communication errors [24].

Malpractice and Punitive Damages

Without any doubt, there is a link between disruptive physician behavior and the risk of malpractice litigation [25,26,27,28]. The public is aware that effective teamwork, good communication, and a collaborative work environment is required for safe and high-quality patient care. They are also aware that a hostile workplace can put the patients safety at risk. Patients lose confidence and trust in the healthcare system when they witness or are subjected to intimidating and disruptive behavior [6].
This lapse in professionalism often transforms a patient into a litigant.

Most iatrogenic injuries do not lead to litigation provided that the patient-physician relationship is good. Poor communication and loss of trust can harm the physician-patient relationship and lead to litigation and malpractice claims [25].

When doctors respond to adverse outcomes with lack of empathy the risk of a malpractice claim becomes very high [26]. Not taking the patient’s concerns seriously, not valuing their perspective, not providing appropriate access to care, and not effectively communicating with the patients leads to litigation and malpractice claims [27].

The most common reason why patients file malpractice claims is when the doctor is perceived by the patient to be insensitive and lacking in integrity or compassion. On the other hand, when patients feel valued and they feel that their opinion matters to the medical care team, they are less likely to seek legal remedy [25,28,29].

An increasing number of lawsuits, legal fees, and compensation expenses have led several states in the US to introduce mandatory disclosure of serious events laws [26].

A serious event has been defined in the law as "an event, occurrence or situation involving the clinical care of a patient in a medical facility that results in death or compromises patient safety and results in an unanticipated injury requiring the delivery of additional health care services to the patient," [30]. Reforms in the US have led many hospitals and insurers to adopt disclosure policies [31,32].

Successful outcome of disclosure of medical error policy was first noticed in the Veterans Affairs (VA) hospital in Lexington, Kentucky. They introduced the policy following two malpractice cases which cost them over $1.5 million. About twenty years after the introduction of the policy the average settlement was $15,000 per claim as compared to over $98,000 at other VA institutions [33]. Such a policy also reduces the duration of legal cases and reduces the legal expenses.

A comprehensive claims management program which involved full disclosure and compensation for medical errors was introduced by the University of Michigan Health System in 2001 [34]. Between 2001 and 2005, their annual litigation costs decreased from $3 million to $1 million. The average time for resolution of a claim also decreased from 20.7 months to 9.5 months and their annual number of claims also fell from 262 to 114 [33,34]. They then began to reinvest the savings in patient-safety reporting systems which resulted in an additional improvement in patient safety [34].
Providing an apology and fair compensation following an adverse event appears to reduce the possibility of punitive damage awards [35,36].

How to Manage Disruptive Behavior

The US Joint Commission has established leadership standards for all accredited programs which addresses inappropriate and disruptive behaviors [37]. From January 1, 2009, The Joint Commission in the US set up a new leadership standard for all accreditation programs, to address disruptive and inappropriate behaviors in two of its elements of performance [37]:

• EP 4: The hospital/organization has a code of conduct that defines acceptable and disruptive and inappropriate behaviors.
• EP 5: Leaders create and implement a process for managing disruptive and inappropriate behaviors.

The Joint Commission has no universal guidelines which can specifically help health care organizations to deal with disruptive physician behavior.  They do, however, recommend that senior management should work with the governing bodies in the organization to develop a process that would be easy to implement when any problem crops up [38]. The Joint Commission has put forward several strategies for dealing with disruptive behaviors which include [39]:

•  Establishing methods to review credentials
•  Regulating clinical privileges
•  Ensuring the participation of medical staff in the improvement process

Rosenstein and O’Daniel have come up with ten recommendations to help identify and address disruptive physician behavior [9]. These include:

• Recognition and Awareness.                                                                                                      The first step is to assess the frequency and significance of disruptive behaviors. This can be accomplished by distributing survey forms in which the respondents are requested to report on behaviors and events that affect job performance and/or patient care. These surveys are carried out confidentially to ensure privacy and potential fears about retaliation.
• Cultural commitment/leadership/champions                                                                             The organization needs to have a top-down, bottom-up approach where all staff and employees are responsible for their behaviors and they are expected to strictly adhere to a well-defined professional standard of behavior. The board, administration and clinical leaders have to be committed and they have to endorse the required standard of behavior at all levels of the organization. Support from the physicians, nurses, and other staff will help to move the initiative along.
• Policies and procedures                                                                                                              The organization needs to introduce a clear definition of acceptable behavioral standards and criteria to reinforce appropriate behaviors. There also has to be a zero-tolerance policy for those who are not in compliance. The policies need to be standardized and consistently applied throughout the organization. Disruptive behavior policies need to be developed which outline the process for dealing with disruptive persons. In many organizations, the staff have to sign a code of conduct agreement or a code of behavior agreement.   Appropriate action has to be taken when dealing with disruptive individuals regardless of their position in the organization. The development and implementation of an effective disruptive behavior program will be inhibited if there is a reluctance to confront and address behavioral problems; there is inadequate executive training, management skills and experience; and also if there is a lack of a formalized program or systematic approach to addressing the behavioral problem. 
• Incident reporting                                                                                                                          A uniform approach to incident reporting is essential to avoid pitfalls and inconsistencies in the reporting process. The reporting process has to be safe and acceptable for employees. Once the incident has been reported the incident has to be addressed in a timely fashion.                    There has to be confidentiality in the entire process. Feedback should be given to those who do the reporting. Many organizations have designated task force or committees, to which all incidents are directed. These committees take responsibility for directing the issue to the correct authority.
• Structure and process                                                                                                              There is a need for consistent, uniform methodology for addressing the issues once the policies are in place and the reporting mechanism has been well established. A team of trained, capable individuals with a multidisciplinary representation ( administrators, human resource personnel, physicians, and nurses) is needed. This team will follow a standardized process for the incident assessment, make an appropriate, unbiased decision and come up with recommendations.
• Initiating factors                                                                                                                            In order to prevent the occurrence of disruptive episodes, the background as to why these events occur has to be understood. Some of the reasons include stressful situations, individual perceptions, deep-seated values. Outbursts can also result due to factors such as culture and ethnicity, age, gender, personality, training, as well as life experiences. Interaction of these factors affect staff values, perceptions, interactions, and relationships. Hence, having a better understanding of these factors will help in education and training programs which are designed to improve communication efficiency. 
• Education and training                                                                                                      Education and training is very important in addressing the issue of disruptive behavior. For starters, the focus should be on raising awareness of disruptive behavior and its effect on patient care. The education and training should involve stress management, anger management, conflict management, sensitivity training, diversity training, and assertiveness training. Sometimes behavioral or psychological counseling may be required. Often there will be resistance to implementing an education and training program for offending physicians because these programs are time-consuming and most surgeons do not have spare time in their busy schedules. In such situations, disruptive behavior can be discussed under umbrella topics such as patient safety, team dynamics, and staff satisfaction. 
• Communication tools                                                                                                Miscommunication has been linked to 60% of preventable adverse events. Hence improving the communication skills of the 3% to 5% of physicians with reported disruptive behavior would go a long way in decreasing disruptive behavior and improving patient outcomes [23,40]. Teaching basic communication skills through training courses and role play is an excellent way to improve team dynamics and decrease misunderstandings. Leaders in an organization should foster an environment where respect, situational awareness, open communication, accountability, feedback, and education, as well as shared decision making, is of paramount importance [23,39].
• Discussion forums                                                                                                                Having discussion forums is one good way to improve communication. People should be brought together. Staff interaction can be promoted during patient rounds and at joint conferences. More formally it can be done by placing nurses, physicians, and other staff on task forces or committees where relationships of nurses, doctors, and other staff are discussed. 
• Intervention strategies                                                                                                            Direct steps must be taken, whenever a disruptive event occurs, to minimize its impact. A “code-white” policy exists in some organizations where selected individuals respond to a call for assistance and help to mediate during a disruptive event [41]. In other organizations, immediate debriefing is carried out to discuss the  reasons for the disruptive event and to come up with constructive suggestions on how to handle the situation better in the future. Staff have to be encouraged to speak up when they come across situations that can adversely affect patient care.

Conclusion

Disruptive behavior is a very sensitive subject and it must be handled with a lot of care especially when it involves prominent physicians and senior employee staff. The issue cannot be swept under the carpet since it involves patient care. There has to be educational and training programs to improve communication and collaboration among the doctors and the staff.

There should be zero tolerance for disruptive behavior. All disruptive events must be identified and investigated to improve patient care and prevent negative patient outcomes. Disruptive behavior affects patient safety and is also known to increase the risk of malpractice litigation.
Reforms are needed in all healthcare organizations to overcome the scourge of disruptive behavior.

References

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8. Quick JC, Saleh KJ, Sime WE, Martin W, Cooper CL, Quick JD, Mont MA. Symposium. Stress management skills for strong leadership: is it worth dying for? J Bone Joint Surg Am. 2006;88:217-25.
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11. Saleh KJ, Quick JC, Conaway M, Sime WE, Martin W, Hurwitz S, Einhorn TA. The prevalence and severity of burnout among academic orthopaedic departmental leaders. J Bone Joint Surg Am. 2007; 89:896-903.
12. Dull DL and Fox L. Perception of intimidation in a perioperative setting. Am J Med Qual. 2010;25:87-94.
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Complications of tourniquet use

                     Complications of tourniquet use

                                        DR KS DHILLON

Introduction

Pneumatic tourniquet was first introduced in 1904 by Harvey Cushing. Pneumatic tourniquets are widely used in orthopaedic surgery for upper and lower limb surgery as well as for Bier block anesthesia. There are five basic components of pneumatic tourniquets which include:
• An inflatable cuff
• A compressed gas source
• A pressure display
• A pressure regulator
• Connection tubing.
There should at least be 3 inches overlap of the tourniquet cuff but the overlap should not exceed 6 inches [1]. Excessive overlap can cause an increase in pressure leading to injury to the underlying skin. Too little overlap can compromise effective tourniquet inflation resulting in  unexpected release or inadequate constriction. It is recommended that the width of the cuff should be wider than half of the limb’s diameter. Wider cuffs reduce the risk of injury to underlying soft tissues [1]. Wider cuffs occlude blood flow at a lower pressure [1]. Tourniquets are usually positioned on the limb at the point of the maximum circumference such as the upper thigh and upper arm. Despite the fact that tourniquets have been used for many years, the optimal inflation pressure has not been established by any study. Most surgical texts recommend a cuff pressure of between 200-300 mmHg for adults. For the upper limb the recommended inflation pressure is obtained by adding 50-75 mm Hg to the systolic blood pressure and for the lower limb by adding 100-150 mm Hg to the systolic blood pressure [2]. Typically orthopaedic surgeons use inflation pressure of 250 mm Hg for upper arm and 300 mm Hg for the thigh. Use of lowest effective inflation pressure is recommended to minimize risk of tourniquet related nerve injury.

No strict guidelines exist for duration of tourniquet inflation. Generally the safe time limit is between 1 to 3 hours. The situation should be reassessed at 2 hours and if the anticipated duration is more then 2.5 hours then a 10-min deflation interval is recommended. In pediatric patients, inflation time should not exceed 75 min for lower extremities [3].

Pathophysiological effects of tourniquet use

When a tourniquet is inflated there is interruption of blood supply which leads to tissue hypoxia, hyperkalemia and acidosis [4]. Tissue ischemia leads to functional changes in the cell and cell membrane. The transport across the membranes is affected with sodium entering the cell and potassium leaving the cell.  Adenosine triphosphatase is activated, adenosine triphosphate (ATP) is used up and mitochondria are stimulated as increased lactate produces acidosis [5]. The calcium regulation is affected and nuclear function and protein synthesis become depressed. The cell begins to swell, and further membrane changes follow with altered hormonal effects and mitochondrial uncoupling. Finally, leakage of  lysosomes occurs with intracellular and mitochondria disruption and the cell becomes destroyed [5].

According to experimental data the severity of tourniquet ischemia is time, tissue and species dependant [6]. Human trials have demonstrated time-dependent hypoxia and acidosis in the venous blood taken from distal to the cuff [7,8]. Venous pH falls to 7 at 2 hours with resultant muscle fatigue, structural changes and muscle damage. If the ischemia time exceeds 1.5 hours the serum creatine phosphokinase (CPK) concentration is elevated [9,10]. Metabolic recovery of muscle is impaired if intracellular adenosine triphosphate (ATP) is depleted after three hours of ischemia [11].

Deflation of the tourniquet leads to reperfusion which allows replenishment of energy supplies as well as elimination of toxic metabolites. At this stage, pulmonary embolization is most likely to occur  [12,13,14]. Echocardiography during surgery has shown that embolization of echogenic material is common following deflation of the tourniquet. The   composition and clinical relevance of these emboli however is uncertain [14]. Peak embolization usually occurs about fifty seconds after deflation of the tourniquet [15]. This may be inversely proportional to the duration of tourniquet time [12].

Although the risk for postoperative deep venous thrombosis in orthopedic extremity surgery is significant, the tourniquet does not appear to be an independent risk factor [16,17,18,19,20].
Tourniquet use, however, adds a significant risk to the release of large venous emboli in patients undergoing intramedullary instrumentation, cementing or insertion of a prosthesis in the lower limb [21].

Avoidance of tourniquets in high-risk cases may be useful to prevent unnecessary embolization [21].
Inflation of the tourniquet can cause hypercoagulability and fibrinolysis. Tissue trauma causes release of catecholamines, which leads to platelet aggregation and a hypercoagulable state [22,23]. Tourniquet deflation on the other hand is associated with thrombolytic activity. Tissue anoxia leads to activation of the antithrombin III and protein C pathways which can lead to post tourniquet bleeding [24,25].

Tourniquet related complications

Tourniquets can cause complications that range from minor and self-limiting to severe and sometimes even fatal. The complications can be local or systemic. The local effects are due to compression and systemic effects are usually related to inflation and deflation of the tourniquet and the resulting ischemia and reperfusion phases.

Local complications

Skin injury

Skin injuries are uncommon. Excessive tourniquet time and poorly placed tourniquets can lead to cutaneous abrasions, blisters and even pressure necrosis [26]. Alcohol-based skin preparations can cause chemical burns beneath the tourniquet [27,28]. Friction burns can result if the tourniquet is unpadded, or if the tourniquet telescopes away from its padding during the surgery [29]. The risk of skin injury is higher in children, the obese, the elderly, and patients with peripheral vascular disease [30].

Vascular injury

The incidence of vascular injury is low with use of the tourniquet. The incidence of direct vascular injury with tourniquet use in patients undergoing knee arthroplasty is between 0.03% to 0.14% [32]. It is usually seen in patients with peripheral vascular disease who are having lower limb surgery [33,34]. The vascular injury is most likely due to fracture of an atheromatous plaque or by thrombosis of a severely atheromatous blood vessels [35]. Tourniquet use is a relative contraindication in patients with peripheral arterial disease [36]. Such at-risk patients should be identified preoperatively. In up to 44% of the patients acute arterial injury may not be detected on the day of the surgery [37]. Hence it is important to carry out neurovascular examination at intervals following surgery. Arteriography and aggressive revascularization are critical to achieving salvage of the limb. Outcomes of treatment following correction of direct injury are excellent, but for thrombotic injury, the results are not so good even if corrected early [38].

Nerve injury

Nerve injuries from tourniquet use can range from paresthesias to paralysis. The estimated incidence of upper limb nerve injury is about 1:6200 and for lower limb nerve injury is about 1:3700. The overall incidence of permanent nerve injury with tourniquet use is 0.032% [39].
Mechanical pressure rather then distal ischemia appears to be the main cause of the nerve injury [40].

Compression of the nerve leads to microvascular congestion and oedema, which leads to inadequate tissue perfusion and degeneration of the axons [41]. High tourniquet pressures and faulty pressure gauges have been implicated in several reports [42]. Excessive continuous compression times increase the risk of neuropathy and delayed recovery of function [43]. Axonal injury leads to muscle weakness, loss of sensation and neuropathic pain. Nerve regeneration following injury occurs at about 3-4 mm per day [44].

The most commonly injured upper limb nerve is the radial nerve followed by ulna and median nerves. In the lower limbs the most commonly injured nerve is the common peroneal nerve.

Muscle injury

Tissue ischemia occurs beneath the cuff as well as distal to the cuff when tourniquet is inflated. Functional and microscopic changes occur in the tissues which are directly proportional to the duration and the pressure applied. Reversal of these changes is significantly prolonged after three hours of ischemia [45,46]. Two hours after tourniquet inflation at pressures of 200 mmHg to 350 mmHg ischaemic necrosis sets in below the cuff. Histological changes distal to the cuff are seen after four hours [47]. The muscle ischemia, oedema, and microvascular congestion leads to the post-tourniquet syndrome which is characterized by stiffness, paresis, pallor, and paraesthesia [48,49]. Unusually high pressures and prolonged tourniquet time leads to rhabdomyolysis [50,51].
Compartment syndrome is an uncommon complication of tourniquet use, and it results from a combination of anoxic edema, reperfusion hyperemia and hematoma formation [52,53,54].

Systematic complications

Cardiovascular effects

Cardiovascular changes occur during exsanguination of the limb and inflation of the tourniquet and on deflation of the tourniquet. With exsanguination of the limb, there is an increase in blood volume and systemic vascular resistance which leads to a transient increase in central venous pressure. Exsanguination of both lower limbs can add about 700-800 ml to the circulation which is about 15% of the blood volume [55]. This leads to an augmentation of the central venous pressure. Heart rate, systolic and diastolic pressures also increase after 30-60 min of tourniquet inflation due to ischemia and tourniquet pain. The syndrome of tachycardia and hypertension which occurs is referred to as ‘tourniquet pain’, and it is believed to be driven by a cutaneous neural feedback mechanism [56]. For about 30 mins it is well-tolerated without analgesia [57] but for longer periods sedation is required [58].

This transient rise in central venous pressure and systolic blood pressure occurs in two-thirds of patients having tourniquets applied under general anesthesia, but only in about 2.7% of patients undergoing spinal anesthesia [59].

The effects of these hemodynamic changes are minimal in healthy patients, but patients who have poor cardiac function may not be able to tolerate these changes. These changes will usually persist until tourniquet deflation and the response to analgesic drugs and increasing the depth of anesthesia is generally poor. Some of the interventions to reduce cardiovascular stress include, ketamine, dexmedetomidine, magnesium sulfate, clonidine, and remifentanil infusion [30].

Tourniquet deflation is a critical stage. During deflation sudden drop in central venous pressure and mean arterial pressures can occur. Cardiac arrests have also been reported following cuff deflation [30]. The reasons for these hemodynamic changes are a combination of a shift in blood volume back into the limb and the shift of metabolites from the ischemic limb into the systemic circulation. These hemodynamic changes are more pronounced with the simultaneous use of tourniquets on both lower limbs. Tourniquet release is associated with a rise in the pCO2. The pCO2 rise increases the blood flow to the middle cerebral artery by about 50% which usually lasts less than ten minutes [60,61]. This may lead to secondary brain injury in patients who have increased intracranial pressure [62,63].
Cerebral blood flow velocity changes can be prevented by maintaining normocapnia after tourniquet deflation [64].

Metabolic effects

Inflation and deflation of tourniquet results in several metabolic changes. The Arterial pH, PaCO2, PaO2, lactic acid, and potassium levels change significantly after release of the tourniquet and the degree of change is dictated largely by the duration of ischemia time. These changes are usually well tolerated by the fit patients. However, in the elderly patients, and in those undergoing mechanical ventilation who are usually unable to compensate for the metabolic load, as well as in patients with poor cardiorespiratory reserve, these changes may become clinically significant [65,66,67].

Potassium leakage leads to hyperkalemia in the early reperfusion stage [68] and this hyperkalemia has been implicated in sudden mortality [69]. This risk can be mitigated ensuring that agents to reduce acidosis and hyperkalemia are available. There should also be a high index of suspicion for such problems.

Metabolic changes are usually fully reversed within 30 min of tourniquet deflation. The metabolic changes are more pronounced with bilateral tourniquet use.

Temperature changes

The core body temperature gradually increases with tourniquet inflation, and decreases when the tourniquet is released [70]. The reason for an increase in temperature is because the available surface area for heat loss decreases after tourniquet application resulting in less heat transfer from the central to the peripheral compartment. Deflation on the other hand leads to a transient fall in core temperature due to the redistribution of body heat and hypothermic blood from the ischemic limb. Maintenance of core body temperature during surgery reduces this decline in temperature [71,72]. High surface area to volume ratio (body habitus) in children causes
a greater increase in core temperature, and hence children should not be actively warmed during surgery [73,74].

Reperfusion syndrome

Deflation of tourniquet re-establishes the circulation to the limb which allows for restoration of energy and removal of toxic metabolites. Paradoxically, however, reperfusion can induce an extension of ischaemic damage [75] and it can lead to several complications which are known as the ‘Reperfusion Syndrome’. The reperfusion can lethally injure cells that had sublethal ischemic damage. This is mediated in part by oxygen free radicals. Research in a feline model showed that three hours of ischemia followed by one hour of reperfusion was worse than four hours of ischemia [76]. Research also shows that gradual return of circulation to ischemic tissues results in less tissue injury [77].

In the pathogenesis of reperfusion syndrome, one of the key components is upregulation of surface adhesion molecules on the vascular endothelium  [78] and their subsequent interaction with the activated neutrophils [79,80].  Further damage to injured tissue occurs with transendothelial migration of neutrophils, with the release of reactive oxygen species and cytokines [81]. The reperfusion syndrome has two main components, the local component which causes an exacerbation of the regional ischaemic damage, and the systemic component which can cause secondary organ failure remote from the site of ischemia.

The systemic sequelae can result in increased pulmonary microvascular permeability which can lead to ARDS and both renal and cardiac injuries can occur which can lead to other severe and often fatal complications [82,83].

Hematological effects

Tourniquet inflation during surgery creates a hypercoagulable state. This is due to increased platelet aggregation as well as stimulation of coagulation factors. Stimulation of coagulation factors is caused by tissue damage and catecholamines release in response to pain from surgery as well as pain from tourniquet application [84,85,86].

There is a short period of increased fibrinolytic activity after deflation of the tourniquet. This is due to the release of tissue plasminogen activator, activating the anti-thrombin III and thrombomodulin- protein C anticoagulant system. This results in increased post tourniquet bleeding. The increase in fibrinolysis is maximal at 15 min after tourniquet deflation and returns to preoperative levels within 30 min of tourniquet deflation [87,88].

Zahavi et al. [89] reported that ischemia from tourniquet use increases levels of plasma beta-thromboglobulin and plasma thromboxane-B2 and this increases the risk of thrombosis in patients undergoing knee replacement. Katsumata et al. [90] reported that during knee replacement, the use of a tourniquet can promote the local release of neutrophil elastase from the neutrophils which together with reactive-oxygen derivatives, can contribute to the development of venous thrombosis and pulmonary embolism.

Respiratory effects

Respiratory changes are rare with the use of a tourniquet and they are mainly seen during the deflation of the tourniquet. On deflation of tourniquet, there is a transient increase in end-tidal carbon dioxide (EtCO2) tension because of efflux of hypercapnic venous blood and metabolites into the systemic circulation from the limb [91,92]. The increase in EtCO2 is related to the duration of ischemia in the limb. EtCO2 increase is greater with the lower limb tourniquet and is greater in men as compared to women. The EtCO2 peaks at 1–3 min after deflation of tourniquet and returns to baseline at about 10–13 min in a spontaneously breathing patient. It will, however, take longer in mechanically ventilated patients unless the minute volume is increased [92,93,94].

Cerebral circulatory effects

Cerebral circulatory changes are due to the increase in EtCO2 after tourniquet deflation. Increased EtCO2 increases the cerebral blood flow in 2 min but it, however, returns to baseline within 10 min. Patients with reduced intracranial compliance are at higher risk for complications related to the increase in cerebral blood flow. Hence all attempts to maintain normocapnia must be made to prevent this increase in cerebral blood flow during deflation [92,95,96].

Besir and Tugcugil [97] reported an increase in intracranial pressure in the early period after tourniquet deflation (after 5 min). The increase was related to the tourniquet time and not to the tourniquet pressure.

Contraindications

There are no absolute contraindications to the use of a tourniquet. Several relative contraindications to tourniquet use have been described in the literature [98].

These include:
• Severe atherosclerotic disease
• Severe crush injuries
• Head injury
• Peripheral neuropathy
• Severe infection in the limb
• Localized tumors
• Arteriovenous (AV) fistula
• DVT in the limb
• Rheumatoid arthritis, and other collagen vascular
          diseases with vasculitis
• Calcified vessels
• Poor skin condition of the limb
• Sickle cell disease.

Conclusion

Tourniquets are useful for upper and lower limb surgery. Tourniquets reduce blood loss and provide a bloodless field during surgery. They are also widely used for Bier block anesthesia. Proper padding under the cuff is important to prevent soft tissue injury. Safe limits of cuff pressure and safe duration of the cuff inflation must be carefully observed.

Improper use of tourniquets can result in serious local and systemic complications including mortality. The use of tourniquets should be avoided in patients with severe atherosclerotic disease, severe crush injuries, head injury, peripheral neuropathy, severe infection in the limb, localized tumors, arteriovenous (AV) fistula, DVT in the limb, rheumatoid arthritis, and other collagen vascular diseases with vasculitis, calcified vessels, poor skin condition of the limb and in patients with Sickle cell disease. There is a need for careful patient monitoring and care after deflation of the tourniquet and a careful search for postoperatively neurological deficit.

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