The continuous growth in patient numbers and needs poses several challenges for medical professionals and support staff within the National Health Service (NHS).1 Health care services are under financial strain in the light of the changing demographic structure of the UK population that requires improved access to health services. Managing patient satisfaction represents another major challenge. Evidence from a recent national survey in the UK shoes that dissatisfaction with the NHS has increased by seven percentage points in 2017, reaching 29 percent, its highest level since 2007.2 Staff shortages, long waiting times for surgical operations and access to care, inadequate funding, and slow-paced government reforms are among the reasons for dissatisfaction. For hospitals, long waiting times at the A&E department, and delays for patients in need of critical care represent major concerns.3
Unsatisfactory health care service experiences generate negative outcomes for health service providers in terms of managing patients’ experience of care, and meeting performance targets. As patients are ultimately the receivers of health care provision, understanding their experiences of care is pivotal.4 The psychological processes underlying patients’ perceptions and evaluations of service provided by the health care professionals, play a crucial role in patient satisfaction. The cognitive processes of patients and their support network, such as friends and relatives, influence perceptions and attitudes towards health care treatment and service. Research underpinned by knowledge from social psychology can shed light on such cognitive processes and generate insights for effective management of patient satisfaction.
The concept of psychological threat in health care service experiences can be explained through the notion of ‘lock-in situations’5 perceived by the patients. For instance, when visiting a hospital or a GP surgery, patients often undertake externally-imposed activities, such as long waiting time for a doctor’s appointment, ease of self-service check-in, lack of acuity in self-care and monitoring, and/or unsatisfactory interactions with support staff – all parts of the service provision. Such situations can be perceived as a threat to the self-determination needs, such as the need for autonomy. Patients who regularly use health care services in the UK associate four main types of threat to health care service experiences, in response to which coping strategies are activated. We discuss these below.
Perceived threats associated with health care services
Patients who use health care services in the UK often report situations they find threatening or questioning their astuteness and sense of control. Interactions with health care staff can make patients feel unintelligent and/or incompetent and restricted in personal control. This is typical of encounters where healthcare support staff are unable to address patients’ queries accurately, and their attempt at resolving the issue is perceived subconsciously as unnecessary and inappropriate by the patients. The above seems to be due to a general lack of trust in the competence of health care personnel, and more conspicuously the perception that they were not willing to act in the interest of patients. Poor health status at the time of accessing health care services might also hinder patients’ willingness to accept advice from health care professionals. Such experiences of threat to self-competence are often associated with negative or even vengeful behavior towards the health service provider, which is the party perceived as threatening. The psychological mechanism behind such behavior is that retaliation alleviates the emotional discomfort caused by threat perceptions6.
Threats to personal control are often reported when processes in the health care service provision are perceived as inadequate and lead to, for instance, long waiting times for appointment booking and/or rescheduling. Our qualitative research show that patients perceive the process of booking a doctor’s appointment as ‘a nightmare’, ‘particularly time-consuming’ and ‘complicated’. They perceive a loss of control when seeking to book or reschedule an appointment. When appointments are not scheduled around their commitments, patients perceive that they are not being heard.
Furthermore, health care service experiences are perceived as threatening to the individual’s self-esteem; especially in situations where patients feel ignored by the health care personnel, and their own self-esteem and social identity are being undermined. A key reason is the perceived lack of empathy and concern of health care personnel during interactions with patients.
How patients activate coping strategies
The lock-in situations discussed above can affect satisfaction and well-being, despite patients’ general compliance with requests from health care personnel.5 Social psychology research shows that perceived threats, such as those reported in health care service experiences, increase feelings of anxiety, averseness, lack of control, and aggressiveness.6 Crucially, in response to threats and consequent negative feelings, patients activate coping strategyas a mechanism of self-defense. We postulate that coping strategies, in turn, influence their behavior, aimed at compensating for the unsatisfactory experience7. Such behaviour can be negative, and at times even vindictive towards the health care service provider.
Social psychology research distinguishes between individual’s coping strategies8 aimed at addressing the source of the threat (i.e. problem-focused coping), and those focused on re-establishing positive emotions, for instance through the act of venting dissatisfaction caused by the threat (i.e. emotion-focused coping). In health care services, patients often seek to proactively react to threats, thereby engaging in problem-solving. This is especially the case when unsatisfactory health care service experiences are aggravated by a serious illness. Severity of the illness markedly influences patients’ willingness to take actions in response to threats. Crucially, the decision to act seems to benefit patients, as they report feeling ‘back in control of the situation’ – a form of compensatory behaviour9. Cerebral activities, such as rational and positive thinking, influence the extent to which patients confront threats. Rational thinkingcan induce patients to take a step back from the experience, reconsider the factors at play, and plan their next actions.
Crucially, in the process of coping with threats imposed by health service experiences, patients often feel overwhelmed. Negative emotions in such threatening circumstances are heightened, and the support from their network of friends and family appears to be fundamental. Intriguingly, for some patients, social media is increasingly seen as a useful source of emotional support, which appears to be gradually replacing conventional forms of verbal, face-to-face support.
Final remarks
We offer an overview on how insights from social science research can be valuable for informing decision-making of health care service providers. This is especially the case in decisions related to staff hiring, training and development, service process improvement and supporting systems design. Lack of empathy and concern from frontline health care staff, outdated service processes and systems represent threats to patients. An implication is that innovative training of frontline staff is necessary for the development of soft skills, which are highly valued by patients. Developing caring and supportive relationships between health care personnel and patients is necessary, as these have considerable bearing on the outcome of healthcare service experiences. Similarly, introducing the practice of simulating patients’ care experience can help to identify threats whilst introducing service improvements and innovations. There is also need for health care service providers to be aware of the fact that patients’ health status at the time of seeking access to and experiencing health services influences their evaluations of the quality of care and of the service experience. It follows that the service provision needs to be adapted to account for patients’ health status and vary according to different patients’ groups. Insights from social science research can inform practice for enhanced provision of health care services. Further survey-based research focusing on the causal links between psychological threat, coping and patient well-being10 is on hand.
The recent increase in the number of patients presenting with a borderline personality disorder (BPD) in general adult psychiatry and primary care is creating pressure within the National Health Service (NHS)1.Currently, BPD is perceived to be like an ‘epidemic’ entity, particularly in areas with a high incidence of socioeconomic deprivation. Similarly, there is a parallel increase in the human and medical resources needed to manage this disorder efficiently. In fact, the authors have found that BPD tends to be comorbid with factitious disorders and depression (Tripolar syndrome) with a tendency to overuse hospital and medical facilities, inclusive of Accident and Emergency (A&E) departments, family doctors and General Practitioner (GP) surgeries2.
Consequently, patients with BPD require a constant and unlimited allocation of medical and psychiatric resources, together with targeted care plans. In fact, they might be prone to frequent self-referrals to A&E, seek hospital admissions and augment all their psychotropic medications in order to deal with their on-going crises not solvable in their homes. Also, the skills needed by healthcare personnel to reduce chronic self-harming and suicidal ideation in this vulnerable population are complex and need to be updated on an on-going basis also due to the tendency of these patients to raise allegations towards their healthcarers3. Nonetheless, the provision of treatment is often hindered by various healthcare system limitations, such as the lack of beds on medical and psychiatric units, forced reduction in the length of stay in a hospital and insufficient human resources. This scenario has mostly affected female patients with BPD who seek admission to psychiatric hospitals often for respite from chronic suicidal ideation4.Moments of amplified suicidal ideas become evident when internal voices, perceived as auditory hallucinations commanding to self-harm or to commit suicide, become more intense5.
As observed by the authors of the current editorial, increased suicidal ideation in persons with BPD also occurs during minor crises in life, when experiencing intensified flashbacks about past abuses, during minor losses, after significant conflicts with others and after the separation from influential people in their social network. Besides, admissions in psychiatric wards, very commonly, occur when there is an intensification of internal voices commanding BPD patients to take overdoses of the prescribed medication or to jump in front of a train, a car or off a pier to commit suicide. Police is often involved to stop these dramatic plans. At the same time, healthcare professionals are discouraged by the complex management of patients with BPD, which, in combination with their tendency to challenge or make unwarranted allegations against their health carers, results in feelings of sadness, rejection and alarm in the latter. Kanin reported that the reason to produce a false allegation is to create a defence or to get compassion6. Nonetheless, it is also likely that some healthcare professionals might have some preconceived ideas about people with Borderline Personality Disorder, which might reduce the depth of health carers’ empathy towards these patients and lead to burnout after prolonged treatment of BPD in hospital or community. Attempts to treat and to reduce suicidal ideation and self-harm in this group of patients are often thwarted as they challenge medical decisions and endeavour to sabotage the proposed care plans. The strain on the doctor-patient relationship is determined by the underlying ‘Mistrust/Abuse’ scheme of patients with BPD who expect from others, and are thus sensitive to, signals of relational wound, treachery and abuse7.
Consequently, a chronic feeling of inadequacy in patients with BPD translates itself in enduring dissatisfaction with any therapy and healthcare professionals. Hence, in the authors’ experience, any attempt to establish a long-term therapeutic relationship with BPD patients might have limited outcomes. Frustration in healthcare professionals aiming to create an enduring therapeutic alliance with patients with BPD happens as these patients tend to interpersonal biases and to ascribe undesirable experiences to people (hence to healthcare professionals) as opposed to circumstances8. Therefore, social interactions with primary carers result in dissatisfaction of people with BPD about any medical or psychiatric plan is set up for them. Consequently, community teams, general practitioners and hospital staff feel hopeless due to recurrent readmissions of people with BPD and the lack of definitive treatment for such pathology. Stress caused by difficulties encountered in ensuring that BPD patients comply with the therapy regularly places doctors and nurses at crisis point.
Once in the hospital, discharging patients with BPD can be difficult as they are frequently reluctant to return to the community, leading to recurrent readmissions within a short period. In fact, the period before discharge from a psychiatric hospital is complicated by mounting anxiety and distress in patients with BPD. The authors observed a regular escalation of self-harming behaviours and increased suicidal ideation in these patients just before discharge, possibly indicating their underlying anxiety in going back to the home environment. Many BPD patients suggest that they would rather stay in the hospital instead of returning to the community that is considered by them as unsafe or unstructured. Furthermore, as these patients have an intense vulnerability to social rejection, they rarely feel adequate during social interactions thus developing an enduring sense of solitude9. Therefore, any hospital discharge or a visit to the GP will be interpreted by them as disappointing and will lead patients with BPD to confirm their sense of rejection. As a reaction, the authors observed that BPD patients demand endless and unconditional attention from their primary carers. Attempts by patients with BPD to self-harm or commit suicide intensify over weekends or public holidays as their sense of solitude increases during these periods, especially when there is also a shortage of healthcare professionals available for immediate support.
The authors of the current editorial propose possible strategies of intervention both on the psychopharmacological and managerial side. The challenge is that patients with BPD often use overdoses of oral medication in a suicide attempt10. Hence, the authors recommend the use of long-lasting depot antipsychotic injections (e.g., Zuclopenthixol Decanoate) to stabilise their mood and reduce impulsivity, the risk of overdoses, pseudo-psychotic symptoms and command hallucinations leading to deliberate self-harm. The use of oral lithium to treat mood swings poses an ethical dilemma for doctors as it could be lethal when used as an overdose. Healthcare management is another way of intervention. One point of difficulty is the tendency of patients with BPD to split their teams and to create niches of protectors and opposers within staff with possible conflicts within the team that is treating them. In this case, inter-professional coordination, integrated care and constant information sharing are required11. Furthermore, several healthcare services treating patients with BPD are trying to find an integrated approach for their hospital and community treatment. The authors speculate that the increased number of admissions of patients with BPD is reducing the total capabilities of physical and mental wards to treat patients with other pathologies. Besides, the dramatic presentation of patients with BPD who tend to overuse the healthcare services poses ethical dilemmas in their management. This scenario has created discrepancies in health care policies about treatments and hospital (re)admissions of patients with BPD reaching an epidemic magnitude in many healthcare trusts. Hence, a new culture is required for the management and treatment of patients with BPD in the community.
Culture is defined as the character of an institution that affects employee gratification and organisational accomplishments12.What is needed is a frank and constructive dialogue between healthcare managers, leaders and medical staff in the hospital and in the community. Furthermore, clear and regional guidelines should exist to improve the efficacy of care which is offered to BPD patients at home and to reduce the constant risks which patients pose to themselves, their sense of solitude and their tendency to seek hospital admission in order to solve chronic existential difficulties. A model of integrated care comes from Max Weber who differentiated between ‘formal rationality’, the endorsement by healthcare managers of the most efficient ways of achieving organisational goals (e.g., ensuring more hospital beds by quick discharges of ‘bed blockers’), and ‘substantive rationality’, the expectation by healthcare professionals that values and morals should instead be based on tradition, compassion and dedication13;pertinent to the care of BPD patients in our case. The collaboration of all those involved parties is also important to reduce the risk of ‘silo management’ where confined and regional policies do not embrace a wider perspective for the management of specific problems while responding only within the confines of the own guidelines and procedures14.In these cases, integrated care in communities can halt self-harming and suicidal attempts of patients with BPD. The organigram sees inter-professional actions, targeted psychopharmacological policies and psychiatric crisis teams in A&E that can reduce the need to hospitalise patients with BPD at any ensuing crisis.
Medicine is a dynamic science and discipline, which arise from the human need to face the suffering, pain and give hopes for better life. Since its inception, medicine has entered a career development that has brought great advances in science. Part of this momentum observed in medicine is defined as its reason for being, or rather, its primary goal, maintaining the health status in different populations1. This simple statement but becomes an object of great complexity which has received attention by many physicians and researchers from ancient times to the present, and in the tenth century, Ibn Hazm, a father of modern medicine enunciated the truth in this science was going to be impossible, since its dynamism is always present and the truth became a clear misrepresentation or significantly modified in the future2.
The goal of keeping adequate health status and prevent diseases has kept biomedical research in an alarming race in which the speedometer registering increases day by day. Today medical science is one of the most important sources of scientific innovation around the world; hundreds of manuscripts on health issues are published every day in multiple languages, in addition to numerous books and other non-official publications2-3. The increase in the medical literature during the last decade, led to think that the development of medicine has become a breakneck ratio, both the magnitude of the information obtained and its complexity.
However, the real reason for this phenomenon in biomedical sciences should be as a result of the new funding sources available for biomedical research either from the biomedical industry and government agencies. Each year new sources of money are offered to scientists to encourage innovation and the development of new ideas; and the resources existing to perform this goal increase. The OECD (Organization for Economic Co-operation and Development) suggests that countries spend about 500 billion dollars a year on research in biomedical sciences, including private laboratories and research institutes4. Medicine has become one of the most promising businesses in the economic field, and up today, and it is considered one of the greatest science future with wide range of prospects5.
Despite this encouraging situation, the concerning of development of modern medicine could be measured as a fundamental problem: the doctors and other scientists in charge of biomedical innovation are not trained in the administrative field. The above problem is clearly seen in different situation in the current medical and research practice, weak reflected on wasteful resource allocation processes6.
Each organization facilitating biomedical research resources requires that its resources are managed and used in an appropriate manner. Institutions demand to distribute funding for various interests not only in biomedical sciences. On the other hand, institutions have to verify the novelty and the ethical viability of the proposals, with the main idea of support ethical-approved studies, avoiding catastrophes in non-well-designed trials. Nowadays, as a result of better “quality control processes”, grant submissions involve a great number of administrative steps in order to be ready to submit any proposal. In this verification process, no only questions have to be addressed in term of sciences; a lot of administrative issues have to be explained in detail, including budget utilization and personnel management1, 4, 7.
Academics and scientists in universities are trained mostly in the technical aspects of their daily work, for this reason the horizon shows that the physician (M.D.) receives their training focus for the clinical management of patients, a doctor of science (Ph.D.) receive their training in the handling the samples to obtain the best results in the tests planned. In both cases, scientists are plainly educated out of the business and administrative field, leading important limitations with resources (personnel and funding) management3, 5.
Nowadays, the easiest application to obtain resources requires the approval of at least 5 different offices responsible for reviewing ethical, financial, legal, logistical, and scientific issues. Now back to the main problem in this discussion, the fact that medical researchers are not trained as integrated researchers (sciences and business), we are in the position to deduct that this condition may generate a bottleneck, specifically in this time where biomedical research are gaining a lot of power and interest in the industry8.
A potential alternative for this dilemma is to offer manager and administration training to researchers in order to be able to efficiently manage the resources requested. Masters degree programs are now available in health sciences management and administration, gaining popularity in the last five years. Researchers are more committed to show better profiles in their grant applications. Modern scientists must be people with a proven knowledge on costs and productivity that allows performing biomedical research with scientific quality combined with attractive financial management in terms of production2, 5, 8.
In the last few decades, the practice of medicine has seen swift changes, as well as its visualisation in the near future. It was designed and focused on serving the community and helping people in need. However, it is not a secret that there is a huge business around this labour and the economic interest of a diverse industry in the field. 1,2
Not intending to generalise, many have observed in daily practice a comparable trend with modern society. A phenomenon including both patients and health personnel, where there is a demand for health services, a growing supply, and a considerable revenue. Basic market economics, right? 3
Not that simple.
It would be the triumph of basic sciences to explain each disease under a biological substrate, minimising the involvement of other factors. A definitive targeting of biological research would be the key to unlocking knowledge. What is certain is that this approach has transformed pharmacotherapy, treatment alternatives and prognosis.2, 3, 4
Early physicians had little to nil information on what today we call aetiology, pathophysiology and therefore treatment. Patients were rarely relieved due to human intervention. Trepanations were frequently performed in the Classical and Renaissance periods and although having modern indications (decompressive craniotomy), its uses and technique were at best questionable. Belief and verbally transmitted understanding of a handful of medicinal plants whose effect were known empirically were standards of care.5
These times have changed, the pharmaceutical industry is a pillar of the economies in many countries, and the number of transactions and cash flow that they move are beyond the wildest dreams of the first physicians. Born each year, thousands of new pharmaceutical companies develop and market new drugs and medical supplies. 1, 6
As advocated by experts, pharmaceutical and medical supply companies are considered one the safest businesses nowadays, with everyone being a potential consumer/patient. It is the race for continuous development of new drugs to its current rate that guarantees soon we will have more drugs and procedures available. The drug industry may be easily overloaded by an oversupply of organic compounds and procedures to patients. 2, 4, 6
This pharmaceutical industry thriving is widening its horizon. Personalised medicine, the study of the influence of a patient’s genetic makeup on their disease susceptibility, prognosis, or treatment response (efficacy and safety), is actually in the spotlight. This can be assessed in different ways, being preventive and/or therapeutic. 7
In the preventive field, preconception screening studies have been unravelling genetic disorders, as recommended by different guidelines such as those of the American College of Medical Genetics, which are designed for individuals with known genetic conditions or high-risk patients who wish to become pregnant. 8
In the therapeutic filed, pharmacogenomics can aid in the identification of alterations of Single Nucleotide Polymorphism (SNPs) that affect the function or expression of proteins associated with pharmacokinetics or pharmacodynamics of different drugs. In recent years the research community has doubled efforts in personalising certain therapies. Hormonal therapy in breast cancer has been from the beginning a receptor-guided therapy, especially with ER (Oestrogen Receptor) therapy. Initial clinical results of trials conducted so far have allowed to establish single therapies regimens with Tamoxifen or combined with Arimidex. 9
Another model of the advances in this arena is reflected in the new alternatives for prostate cancer. This hormone-dependent tumour has demonstrated recurrent alterations in the androgen receptor and its pathway. In specific patients the disease can be found in Castration-Resistant Prostate Cancer (CRPC), a lethal clinical state in which the tumour has developed resistance to androgen deprivation therapy. This clinical scenario is commonly established in advanced or metastatic prostate cancer patients. The genomic landscape of localised prostate cancer has been well defined, describing putative pathogenic BRCA2 germ line mutations as well as somatic and germ line DNA repair alterations found such as BRCA1, CDK12, FANCA, and RAD51B. Furthermore, the research advances described above can allow clinicians to determine treatment, therefore achieving better outcomes. 10
It is unquestionable that personalising treatment will improve clinical outcomes for patients in the near future and help achieve a more effective use of available health care resources. The next challenge for scientists and researchers is to demonstrate with strong evidence the clinical and cost-effectiveness to support the use of personalised medicine and its implementation in different health care systems around the world. 2, 3, 5
In conclusion, individual patient variability currently studied in drug efficacy and drug safety has represented a major objective in current clinical practices. Years of research results have converged in progresses in pharmacogenetics and human genomics that have dramatically accelerated the discovery of genetic variations that potentially determine variability in drug response, providing better clinical outcomes for patients. The future in this field is expected to allow us to have effective and safe medications to targeted patients with appropriate genotypes.
Effectiveness of homeopathic remedies continues to be a question of concern for public, policy makers and the other involved stakeholders. A recent systematic review of studies by Australian National Health and Medical Research Council (NHMRC) 1 heightened further the concerns about the perception of effectiveness of homeopathic treatments in general. After an exhaustive review, the authors found no good quality, or well-designed studies with adequate sample size to support claims made by homeopathic practitioners. They concluded that the homeopathic remedies are no better than a placebo. Authors of the report cited concerns about the designs of the most of the studies especially the ones that showed any beneficial effect. Authors noted that such studies either had smaller sample sizes, were conducted poorly and/or were insufficiently powered to detect a statistically significant outcome. NHMRC concluded that there is no evidence from systematic reviews regarding the effectiveness of homeopathy as a treatment for any clinical condition in humans. The NHMRC identified “claiming benefits for human health not based on evidence”1 as a major health issue in Australia.
NHRMC’s report comes as no surprise as many other exhaustive reviews had failed to show any objective benefits of such remedies. Authors of a 2009-10 UK report titled as Evidence Check 2: Homeopathy2, reached to a similar conclusion. They questioned the lack of homeopathic treatment trials and cited that there is plenty of evidence showing that it is not efficacious. Their conclusion was no different from NHRMC’s and proposed that “systematic reviews and meta-analyses conclusively demonstrate that homeopathic products perform no better than placebo”2. They further recommended stopping any public funding of Homeopathic remedies in UK. Although a Swiss report3 argued otherwise claiming that homeopathy is a “valuable addition to the conventional medical landscape”3; however its methodology was considered to be flawed, biased, misinterpreting and discrediting the current science based study methodologies4.
The homeopathic notion of successive dilution of its products in water increasing the potency of the final product and “like cures like” doesn’t only defy any science based medicine logic, it is also in contrast to other alternative systems of medicine. The paucity of good-quality studies of sufficient size that examine the effectiveness of homeopathy as a treatment for any clinical condition in humans does no favors to this notion either. As cited by many reports referenced above, the available evidence is not compelling and fails to demonstrate that homeopathy is an effective treatment for any of the reported clinical conditions in humans. In spite of these significant concerns about the legitimacy and efficacy of homeopathy, the industry continues to benefit from public’s increasingly favorable attitudes toward homeopathy. The National Institutes of Health5 in the United States, reports that there is little evidence to support homeopathy as an effective treatment for any specific condition however millions of American adults and thousands of children use homeopathy. Even in UK6 where there is no legal regulation of homeopathic practitioners, The National Institute of Health and Care Excellence (NICE)-that advises the NHS on proper use of treatments, doesn’t recommend that homeopathy should be used in the treatment of any health condition. However homeopathy has seen a significant increase in its market share not only in UK but many other European countries too7.
With its market share in USA and rest of the world markets reaching in billions of dollars with yearly incremental increase, its claims for its remedial effects albeit lacking any generally acceptable evidence, raises concern that a vulnerable person may choose an ineffective remedy that may actually worsen their clinical status. There is a clash between patient autonomy and informed consent in decision making by a vulnerable patient about the appropriateness of homeopathic remedies. The ethical and policy debate on the appropriate balance between public’s access to different remedies (autonomy) and government institutional duty of public’s protection from potentially harmful or ineffective medicines is a delicate balance. An objective and thorough evaluation of homeopathic remedies is needed however how to decide what is an objective and accurate way to assess homeopathic research continues to be the bone of contention. Although from a science based medicine perspective, homeopathic remedies have no scientific explanation, its advocates3, 4 don’t agree that it has to fall or go through same process of research methodology for its effectiveness as do allopathic remedies. Though it is a valid logic that reasoning directly from data that is gathered by controlled structure, as is true of science based trials in allopathy, is not always accurate as it’s with many biases and confounders, however the statistical testing helps to get beyond mere correlation to cause-and-effect and eliminate most of these concerns. These trials also help to formulate conclusions that can be further validated or refuted by gathering real world data. The mainstream science considers the homeopathic notion of ultra-dilutions, particle leaving imprint of itself on water, and “likes cures like” to be scientifically implausible. Even though this notion of scientists may be considered as a bias towards evaluating any homeopathic remedy, the public health institutions have an ethical obligation to educate public especially the vulnerable ones, not to substitute a proven and effective treatment for the ones whose effectiveness has not been scientifically proven.
As the saying goes, “change the rule and you will get a new number”, the onus is on homeopathic advocates not only to design trials, gather data, and publish papers but also to collect real world data to further study the impact of treatments on outcomes. The real world data can further help to understand the effects of treatments on patient outcomes that was not generated from a clinical trial. It is also an obligation of the homeopathic practitioners and organizations to seek to create standards of medical treatment, that are objective, replicable, and that will be made broadly available to physicians, researchers, parents, policy makers, and others who want to improve the care of individuals. As recommended by many exhaustive reviews1,2, these studies should recruit larger samples of patients, utilize methodologies that eliminate the bias, better discoverable record keeping for proper reporting and follow up, an objective analysis of outcomes data and how they were measured, and better discussion of potential confounders or biases. Besides they have to adequately and accurately report study details including treatment regimens, length of follow up, outcomes studied and the clinical and statistical significance of results.
Going by the logic of famous words attributed to the noted statistician and management scientist, W Edwards Deming, “In God we trust; all others must bring data,” the ball is in their court.
Global Health can be defined as “an area for study, research, and practice that places a priority on improving health and achieving health equity for all people worldwide”. 1 Article 25 of the 1948 Universal Declaration of Human Rights declares that, “everyone has the right to a standard of living adequate for the health of himself and of his family”. 2 Unfortunately, the health disparity between high-income and low-income countries, as well as between individuals within a country, often makes this impossible, leaving many people living in unhealthy settings without sufficient access to care.
The field of global health is concerned with the health of populations worldwide, focusing on issues that typically have global, political, and economic significance. These health issues usually transcend national boundaries and are best solved through international collaboration. 3 Global health initiatives aim to improve the health and wellbeing of impoverished, vulnerable, and underserved people worldwide. 1 These initiatives include poverty reduction strategies, disease prevention measures (for HIV/AIDS, malaria, and tuberculosis, for instance), efforts to improve nutrition and food security, policy to raise environmental standards and living conditions, and the promotion of gender equality.
In 2001, the Commission of the World Health Organization (WHO) recommended to fund global health with 0.1% of GDP. 4
The average expenditure per capita for health in low-income countries is estimated at $ 20 per year while that of Western countries is estimated at $ 947. The target to be reached to help out the most disadvantaged countries is $ 44-60 per capita, which would ensure the populations of the poorest countries with the access to essential health services. Directing the 0.1% of the GDP of developed Western countries to the aids for global health would mean closing the gap to reach the target base of $ 44-60 that would allow the saving of 8 million lives a year. 4
Despite the good intentions, there is still a marked disparity between the current spending levels and the commitments made by developed countries in a context in which, among other things, the percentage of aid for global health has been in decline for almost all donor countries.
Activists claim that only 10 per cent of global health research is devoted to conditions that account for 90 per cent of the global disease burden – the so-called ‘10/90 Gap’. 5 They argue that virtually all diseases prevalent in low income countries are ‘neglected’ and that the pharmaceutical industry has invested almost nothing in research and development for these diseases.
In fact, the WHO acknowledges that there are only three diseases that are genuinely ‘neglected’: African trypanosomiasis, leishmaniosis and Chagas disease. 6
A large proportion of illnesses in low-income countries are entirely avoidable or treatable with existing medicines or interventions. Most of the disease burden in low-income countries finds its roots in the consequences of poverty, such as poor nutrition, indoor air pollution and lack of access to proper sanitation and health education. The WHO estimates that diseases associated with poverty account for 45 per cent of the disease burden in the poorest countries. 7 However, nearly all of these deaths are either treatable with existing medicines or preventable in the first place.
If treatments exist for the majority of poor countries’ health problems, why then do mortality rates remain so high? Any discussion of this question must address the problem of access to essential medicines, which remains an intractable political and economic problem. According to the WHO, an estimated 30 per cent of the world population lacks regular access to existing drugs, with this figure rising to over 50 per cent in the poorest parts of Africa and Asia. 8 And even if drugs are available, weak drug regulation may mean that they are substandard or counterfeit.
Within these populations, it is the poorest socioeconomic groups that disproportionately suffer from a lack of access to existing medicines. 9 The implications of this failure of public health policy on global mortality are profound – according to one study, over 10 million children die unnecessarily each year, almost all in low-income or poor areas of middle income countries, mostly from a short list of preventable diseases such as diarrhoea, measles, malaria and causes related to malnutrition. 10
Many governments fail their populations in this respect by imposing punitive tariffs and taxes on medicines, and by skewing their spending priorities in favour of defence over health. The governments of poor countries hinder the creation of wealth, imposing obstacles in the way of owning and transferring property, imposing unnecessary regulatory barriers on entrepreneurs and businesses, and restricting trade through extortionate tariffs. It is these and other political failures that have left poor populations without the necessary resources to access the medicines that could so easily transform their quality of life.
In conclusion, it appears more and more urgent and necessary to decide where to direct our efforts and investment in research, without prejudice, analyzing all the possible strategies for tackling global health issues, including those standing beyond the current economic paradigm based on the market.
Nearly 30% of seniors have chronic musculoskeletal pain. The most common cause of pain in seniors is related to the degenerative changes of the spine and joints9. Conventional treatments are often restricted to the management of symptoms. Use of chronic anti-inflammatory medications in seniors may bear serious risks in gastrointestinal and renal systems. Physical therapy has limited value. Epidural steroid injection(s) may provide up to three months of pain relief. However, there are some risks involved. Spine surgery for degenerative spine diseases has a limited success rate. Up to 30% or 40% of patients may continue to have pain after back surgery. Surgical repair of a knee injury and knee replacement surgeries are popular. However, the costs are relatively high. Many senior patients may not be ideal candidates for surgery due to cardiovascular conditions. Furthermore, all these treatments do not address the key cause of spine and joint pain due to degeneration of cells and subsequent tissue damage9. Recent development in stem cells therapy (SCT) has provided a new hope for seniors.
Back Pain
The major cause of back pain is the degeneration of the cells in the intervertebral discs. Over the last few years molecular, cell-based therapies and tissue-engineering strategies with SCT for disc regeneration have significantly increased. A recent report showed that injection of mesenchymal stem cells (MSC) into bovine intervertebral discs can increase the expression of extracellular type II collagen and maximize extracellular matrix production7. Chun et al 1injected human adipose-derived stem cells (ADSCs) into 20 mature male New Zealand white rabbits. The proliferation of ADSCs at the L4-5 disc was found at 10 weeks after cell injection. Histologically, the ADSC-injected discs exhibited elevated extracellular matrix secretion and little ossification of damaged cartilage in the nucleus pulposus compared with degenerative control discs.
In addition to the promising results from animal research, preliminary human studies showed mixed results. In 2006, Haufe et al3 reported 10 patients who underwent intradiscal injection of hematopoietic precursor stem cells (HSCs) obtained from their pelvic bone marrow. Of the 10 patients, none achieved any improvement of their discogenic low back pain after one year follow-up. More recently Orozco et al 8 reported a study of ten patients with chronic back pain treated with intradiscal injection of autologous expanded bone marrow MSC. Patients were followed for 1 year. Rapid improvements of pain and disability were reported (85% of maximum in 3 months). Although disc height was not recovered, water content was significantly elevated at 12 months. Advantages of intradiscal MSC therapy include simpler and preservation of normal biomechanics without surgery. However, long term survival of the transplanted MSCs in the harsh environment of the discs is still a major challenge. To the date, no double-blind, controlled studies have been published to confirm the clinical efficacy of SCT for the pain due to degenerative disc diseases.
Knee Pain
It is estimated there will be seven-fold increase in knee replacements in the United States between 2005 and 2030. However, SCT may reduce the future need for knee replacement5. Autologous MSC and ex vivo expanded skeletal SC all have shown promising results in the treatment of knee pain caused by osteoarthritis (OA).
In an experimental animal meniscus injury model, it has been reported 10 that transplantation of human meniscus stem/progenitor cells (hMeSPCs) effectively protected articular cartilage, promoted neo-tissue formation with better-defined shape and more matured extracellular matrix and smother surface cartilage, and maintained joint space at 12 weeks postsurgery11. MSC therapy may also reduce animal pain behavior14.
In human studies, Turajane et al13 conducted a case-series study with five patients that failed conservative treatment. It was reported that the combination of intra-articular autologous activated peripheral blood stem cells with growth factor addition/preservation along with hyaluronic acid in conjunction with arthroscopic microdrilling MCS resulted in Quality of Life improvements and succeeded in regenerating articular cartilage in early osteoarthritic knee disease. Skowronski12 reported 52 patients treated with autologous blood MSC for knee pain due to cartilage lesions. Scores improved across all scales with an average improvement of 23 points in the Knee Injury and Osteoarthritis Outcome Score scale and 35 points in the Lysholm knee scale at one year.
Koh et al4 treated eighteen patients with injection of autologous fat pad-derived MSC for knee pain due to OA. Patients were followed for 24 to 26 months after therapy. Western Ontario and McMaster Universities Osteoarthritis Index, Lyholm scores as well as VAS scores all significantly improved. Radiographic study showed the whole-organ MRI score had significantly improved from 60.0 points to 48.3 points at the final follow-up point. Particularly notable was the change in cartilage whole-organ MRI score, which improved from 28.3 points to 21.7 points. More recently, Vangsness et al reported15a randomized, double-blind, controlled study on adult human MSC delivered via intra-articular injection to the knee following partial medial meniscectomy. A single superolateral knee injection was given to 55 patients within seven to ten days after the meniscectomy. It was found that there was significantly increased meniscal volume determined by quantitative MRI in groups that received SCT. No patients in the control group had significant increase in meniscal volume. Patients with osteoarthritic changes who received MSC experienced a significant reduction in pain compared with those who received the control. This randomized, double-blind, controlled study confirmed that MSC could be a promising treatment for knee pain due to osteoarthritis and meniscus tear.
Challenges for SCT
The advantage of SCT is that stem cells can regenerate healthy and functionally specialized cells and tissues to replace the destroyed or degenerative tissues. Though it is promising, it is still facing a variety of challenges. Firstly, there are many studies reporting the clinical efficacy, most studies are open label. Only few, if any, double-blind, controlled studies have supported the efficacy of SCT for knee pain due to osteoarthritis. To the date, there are no controlled studies confirming the clinical efficacy of SCT for degenerative spine diseases. Thus more clinical studies are needed. Secondly, biological techniques for stem cell transplantation are waiting to be enhanced. For example, the stem cells transplanted into degenerated intervertebral discs will face a harsh environment, which has very high pressure, low nutrition and low oxygen. To enhance the cell survival rate and ensure the transplanted cells differentiating toward chondrocyte-like cells, which can produce proteoglycans and type II collagen, more basic science studies are needed2. The third challenge for SCT is iatrogenic cancerogenesis. Embryonic stem cells, including totipotent stem cells (produced from fusion of egg and sperm), and pluripotent stem cells (5-14 day old blastocytes) have a strong potency of cell reproducing and potentially highly teratogenic. Novel strategies such as using transgenic expression of the genetically engineered human recombinant DNases in proliferating and directed differentiation resisting stem cells are being developed to inhibit or prevent the iatrogenic cancerogenesis6. Adult SCs (Adipose, peripheral and bone marrow derived SCs) have the ability to differentiate and form a variety of tissues. These adult SCs have been used in researches to treat variety of human diseases. So far no iatrogenic carcinomas have been reported as the results of the treatment. The fourth major issue related to SCT is the legal challenge. Worldwide, different countries have different laws on SC research and use. Even President Barack Obama signed an executive order on March 9, 2009 to lift the restrictions on federally funded human embryonic stem cells (hESC) research, currently only adult stem cells (adipose, peripheral and bone marrow derived stem cells) are allowed to be used in most clinical settings. These cells should be minimally manipulated. Use of hESC from fetus, umbilical cord and amniotic fluid are all limited for research purposes. Researchers and clinicians must be familiar with the laws of their respective countries and states before becoming involved in SC therapy or research.
Conclusion
The treatment of chronic pain conditions is constantly evolving. Recent advancements in SCT for pain due to degenerative diseases in the spine and joints are promising and indicative that SCT will undoubtedly play a major role in the future. However, more studies are needed to enhance the biological techniques, confirm the clinical efficacy, reduce the risk of iatrogenic carcinoma and address the legal issues related to this exciting treatment. It is likely that SCT will be utilized more extensively in the future for replacing diseased tissues as an alternative to open back surgery or joint replacement.
Hospital acquired infections (HAI) are one of the most common complications involving hospital care and are the leading cause of death in U.S. Central line associated Blood stream Infection (CLABSI), Ventilator Associated Pneumonia (VAP), Surgical site infection (SSI) and Catheter associated urinary tract infection (CAUTI) represent 75% of all HAI1 . HAI prevention is one of the 20 ‘priority areas’ identified in the Institute of Medicine (IOM) 2003 report ‘transforming health care quality’2. Certain HAI are preventable, but as the prevention efforts become more defined, there remains a lack of evidence of a strong return of investment for hospitals and health care payers in preventing these infections. This lack of evidence presents potential obstacles in advancing efforts to prevent infections.
Central Line Associated Blood Stream Infection (CLABSI)
CLABSI is a primary blood stream infection that develops in a patient with a central line in place within the 48 hour period before the onset of blood stream infection, which is not related to infection at another site. Central line associated blood stream infection occurs up to 80,000 times per year resulting in 28,000 deaths among patients in the Intensive Care unit (ICU). Average cost of CLABSI is approximately $ 45,000 per incidence3. CLABSI reduction is also one of the success story of how inexpensive interventions, grouped as a checklist could reduce the rate of nosocomial infections to a median rate of zero. Although quality control interventions in many areas of ICU have been studied, the idea of integrating quality indicators with group of interventions known as bundles has been validated in the ICU most successfully in CLABSI. The landmark study on reduction of CLABSI was the ‘Keystone ICU’ project funded by the Agency for Health care Research and Quality (AHRQ) 4. One hundred and three ICUs in Michigan participated in this state wide safety initiative. The study intervention recommended five evidence based procedures that were identified as having the greatest effect on the rate of catheter related BSI and the lowest barriers to implementation. The interventions were remarkably successful, nearly eliminating CLABSI entirely in most ICUs over an 18 month follow up period.
Although in short term intensive training and monitoring can lead to improved outcomes, in long term the biggest impact on decreasing HAI, is of the safety climate of the unit. Studies have linked safety climate to clinical and patient outcomes in addition to showing that the safety climate is responsive to interventions. A large study targeting the culture of safety was a follow up of the Michigan Keystone study. The study was a prospective cohort study to improve quality of care and safety culture by implementing and evaluating patient safety interventions in participating ICUs and showed large scale improvements in safety climate among diverse organizations5. As part of the national effort to reduce the HAI, the Department of Health and Human Services (HHS) launched the HHS action plan to reduce the health care associated infections in 2009. The project was titled ‘On the cusp: Stop BSI’, designed to apply the principles of comprehensive unit based safety program (CUSP) to improve the culture of patient safety and implement evidence based best practices to reduce the risk of infection. The initiative ultimately reduced mean rates of CLABSI in participating units by an average of 40%, preventing more than 2000 CLABSI, saving more than 500 lives and avoiding more than $34 million in excess health care costs6.
Ventilator Associated Pneumonia
Optimizing the care of mechanically ventilated patients is an important goal of health care providers and hospital administrators. An easily acquired and reliable marker for medical quality has been elusive for this patient population. VAP has historically been used as a marker of the quality of care associated with mechanically ventilated patient and is associated with worse outcomes7. However the diagnosis of VAP is non-specific, the clinical diagnosis by the widely used American College of Chest Physicians (ACCP) criteria includes a new progressive consolidation on chest radiography plus at least two of the following clinical criteria: fever > 38, leucocytosis or leucopenia and purulent secretions. Unfortunately, all these findings alone or in combination can occur in other non-infectious conditions, making the diagnosis of VAP subjective and prone to bias. In fact, for the last many years, the surveillance rates of VAP are decreasing, whereas the clinical diagnosis of VAP and tracheobronchitis as well as antibiotic prescribing remains prevalent. External reporting pressures may be encouraging stricter interpretation of the subjective signs that can cause artifactual lowering of the VAP rates. The result is that, it is almost impossible to detangle the relative contribution of quality improvement efforts in the ICU versus surveillance efforts as explanation for the currently observed lower rates of VAP8.
To eliminate the subjectivity and inaccuracy and to create an objective , streamlined and potentially automatable criteria, Center of Disease Control (CDC) now recommends surveillance of ventilator associated events (VAE) as a more general marker and defines it as sustained increase in patient’s ventilator settings after a period of stable or decreasing support . There are three definition tiers within the VAE algorithm; 1) Ventilator Associated Condition (VAC); 2) Infection Related Ventilator Associated Complication (IVAC); and 3) Possible and probable VAP. The screening for VAC captures a similar set of complications to traditional VAP surveillance, but it is faster, more objective and potentially a superior predictor of clinical outcomes9. In a CDC funded study of 597 mechanically ventilated patients on use of VAC as an outcome predictor, it was noted that 9.3% of the study population had a VAP, whereas 23% had VAC. VAC was associated with increased mortality (odds ratio of 2.0) but VAP was not. VAC assessment was also faster (mean 1.8 minutes vs 3.9 minute per patient) 10.
Similar to the CLABSI bundles, prevention of VAP by utilization of evidence-based bundles of care has proved to be a very successful. Heimes and colleagues recently conducted a study examining 696 consecutive ventilated patients in a level 1 trauma center to evaluate a VAP prevention bundle with 7 elements. They found a VAP rate of 5.2/1000 days of ventilator support in the pre intervention phase, while a 2.4 /1000 and 1.2/1000 days (p= 0.085) in the implementation and enforcement periods respectively11.
Health care associated UTI account for up to 40% of infections in hospitals and 23% of the infections in the ICU. The vast majority of UTIs are related to indwelling urinary catheters. CAUTI result in as much as $ 131million excess direct medical costs nationwide annually12. Since October 2008, Center of Medicare Services (CMS) no longer reimburses hospitals for the extra costs of managing a patient with hospital acquired CAUTI.
There are certain factors like Diabetes mellitus, old age or severe underlying illness that places patients at a greater risk of CAUTI, but there also are modifiable factors like non adherence to aseptic catheter care recommendations and duration of catheterization that can be targeted by quality improvement efforts, to decrease the risk13. The key strategies for prevention of CAUTI include avoiding insertion if possible, early removal by implementation of checklists, nurse based interventions or daily electronic reminders, utilization of proper techniques for insertion and maintenance and considering alternatives to indwelling catheters like intermittent catheterization, condom catheters and portable bladder ultrasound scanner. Most of these strategies have been utilized in quality improvement efforts to decrease CAUTI. Assessment of the need is essential as Munasinghe et al have found urinary catheter placed in 21 to 50% of patients for inappropriate reasons14. A nurse based reminder to physician to remove unnecessary urinary catheters in a Taiwanese hospital resulted in reduction of CAUTI from 11.5 to 8.3 /1000 catheter days15. Similarly utilization of electronic urinary catheter reminders system and stop orders have been shown to reduce the mean duration of catheters by 37% and CAUTI by 2%16. Utilization of condom catheter has also been shown to be effective in reducing bacteriuria, symptomatic UT and mortality as compared to indwelling catheter17.
Final word
Health care is often compared with airline industry with six sigma efficiency. This would translate to 0.002 defective parts or errors/million, obviously we are not close to that and may not be realistic. However this also cannot be an excuse to rationalize poor practice culture. As in any industry, in health care to establish change it is essential to regulate interpersonal interactions. With behaviors change leading to changes in processes of care, change is not only possible, it is sustainable.
It cannot be denied that healthcare services have become an attractive business for any party involved, whether it be government, insurance companies, hospitals and doctors, to look out for their own interest and leave aside the real priority of this system – the patients’ healthcare and welfare.1
Recent proposed changes in the health system (i.e. healthcare reform) have commanded the attention of all people involved. If nothing else, it has provided an avenue in which each detail can be scrutinized and assessed. And, ultimately, it can be used to optimize the balance of clinical outcomes with resource requirements.
As expected, each guild has its own theories and proposals for improving the delivery of care. However, coming to a consensus will be a difficult task given the economic interests at stake. It should be obvious that the most important guild affected by the changes is the guild formed by patients.2
From the physician’s point of view, achieving optimal patient care has become more difficult. In part, this is due to how the government has chosen to assess and improve the delivery of healthcare services, which is by implementing patient surveys to assess the quality of care and level of satisfaction. Basically, the government has hired private companies to prepare and distribute these assessments. Based on the results of these surveys, the government will allocate various economic resources. As a strategy to face these measures, hospitals have established annual incentive plans to motivate doctors to get good scores in patient satisfaction surveys, including offering higher salaries and compensations.2-3
This impasse pushes the system to operate in an inappropriate manner. For example, hospitals and physicians have increased the number of diagnostic tests, surgical interventions, use of medications, and number of hospitalizations with the sole purpose of making their patients happier. By showing more interest in their patients’ diseases, the hospital and physicians expect to get better scores on the surveys. However, this excess of interventions and expenses does not always ensure the best clinical outcomes. Instead, increased monetary investments can directly affect the finances of the health system.3-4
Currently, 66% of physicians are sheltered under an annual incentive plan; this leads to the idea that "more satisfaction of patients = higher salary.” Many authors consider this to be the silent murderer of the healthcare system since it does not guarantee increased patient satisfaction but it surely guarantees high monetary investment strategies.5
There are two key questions to address as a result of the problems generated by the survey results: How reliable are these surveys? Must we, as healthcare providers, modify our daily clinical practice based on these results? To start, I should mention that from my perspective as a physician, I do not agree that wage benefits and salaries of medical staff should be defined based on these results. More importantly, it should not determine the amount of money provided by the government to the health system and as aid to hospitals.5
Up to today, many scientific studies have been conducted to determine the impact of these assessments on the quality of the service in terms of clinical outcomes and patient satisfaction. The findings are controversial because some studies support the hypothesis that there is direct relationship between the scores of the surveys and the quality of healthcare services provided to patients. However, other studies have shown opposite results. There are some key points to be considered to reach a more objective conclusion regarding the implementation of these evaluation systems for medical staff and hospitals.2-4
There are many factors involved in each patient's experience that can affect the general opinion on the quality of his or her medical treatment and how satisfied he or she was with the treatment. Many observers argue that the number of treatments directly correlates with a better perception of the quality of patient care, regardless of the final outcome of the disease. On the other hand, some authors argue that there is a direct relationship between the expected and actual results achieved, thus fulfilling levels of patient expectations.
Based on this relationship, patients judge the effectiveness of physicians and medical staff according to their levels of satisfaction. However, it should be noted that patients receiving a greater number of interventions and treatments do not always get maximum level of satisfaction in spite of all the effort from the physicians and their teams. In fact, better results have been found on surveys when patients are encouraged to take the leadership of their medical treatment. This leads to better clinical outcomes and a reduction of resources used.
Other factors that may influence the assessment outcomes are: the number of events evaluated per patient (since many of them are chronic patients and have different experiences to be evaluated), the number of physicians involved in the patient care (i.e. different specialties working together), the time between medical care, and the evaluation of that care.3
Despite the variety of studies available in this particular area of knowledge, there is no clear definition of patient satisfaction in healthcare. In turn, many authors are concerned with the patients’ lack of medical knowledge. Therefore, if they receive negative patient comments, they cannot adequately judge and modify their medical practice.
In conclusion, the government must design healthcare reform strategies with all parties in mind. The ultimate goal of these strategies should be to safeguard the healthcare and welfare of patients, not to implement controversial evaluation systems that create conflicts within the system and ultimately lead to detrimental changes in physicians’ clinical practices.
Resource allocation in medicine applies to two complementary levels of care. One pertains to the organisation of public health and the provision of general rules informing the management of the system (macro-allocation). On the other hand, there is the need to specify decision criteria for the daily practice of health care providers who have to decide on the utilisation of their allocated resources, while dealing with a demand that often exceeds supply (micro-allocation).1
Beneficence, i.e. acting for the good of the patient, is one of the founding value of traditional ethics in medicine. However, the picture has changed when the core value of medicine shifted toward the centrality of the human person and the ideal of self-determination. The patient is now a 'health care user' who consults a professional whose knowledge and expertise is used in order to arrive at options. Good medical practice seems the result of a 'contract bargaining', which must take into account different criteria: clinical indication, patient preferences and subjective values, and appropriateness within the social context. Controlling how these three elements interact with each other requires a constant commitment and synchronised interventions.2
For cultural reasons, physicians consider, quite rightly, the costs of their interventions to be incommensurable with the life and the restoration to health of the diseased person. The most difficult problem in the distribution of resources remains the finding of convincing criteria to provide guidance, when often painful choices have to be made in the face of inadequacies in the availability of resources.3
Intensive care is one of the most expensive specialities of medicine and intensive care beds nowadays represent a limited resource.4, 5 The lack of beds is a daily problem in many ICU6, 7 and bed allocation has been considered one of the thorniest and stressful aspects of the intensivist's job.8 Studies have shown that resource use is often inefficient in European ICU. One of the main reasons for this inefficiency has been identified as nursing force “waste”.9
Monitoring and support of deficient vital functions are the main aims of intensive care. Usually, intensivists carry out the adequate diagnostic procedures and necessary medical and surgical treatments required to improve patient outcomes. There has been a considerable international effort to define the ethical, clinical and economical criteria for admission to ICU and to draft the relevant guidelines. The fundamental point is that resources should be utilised appropriately, i.e. that the patient be of the right category, in the right place and at the right time. Furthermore, ethics dictates that resources be allocated where they are more likely to make an impact.10-13
ICU admission and discharge can be ruled by means of a priority scale which classifies patients based on the expected benefit to result from intensive treatment.14 However, while it may be relatively easy to create “on-paper” scenarios affirming that patients who are too critical or not critical enough to benefit should not be admitted to intensive care, identifying these patients in everyday practice is far from simple.
As far as a reasonable doubt may be considered regarding the irreversibility of the clinical status, it is appropriate to initiate or continue intensive treatment. On the contrary, if the irreversibility of the clinical setting is deemed to be reasonably certain, it is appropriate not to initiate or to withdraw intensive measures to spare the patient the undue prolongation of the dying process. Excessive treatment is ethically unfair and should be strongly condemned, because it determines an inappropriate use of the means of treatment; it is likely to cause harm and pain to the patient and fails to respect the patient's dignity in death. Excessive treatment also increases the suffering of family members, is frustrating for care providers and generates an inequitable distribution of resources by curtailing them for other patients. The withdrawal of an intensive treatment, which was previously initiated because deemed to be indicated and accepted, or because the patient's clinical status and relevant prognosis were not clear enough at the time, should be considered whenever the clinical picture counter-indicates treatment continuation, the patient withdraws consent, or a previously defined therapeutic limit is reached.15
Immortality has always been an ambition for human beings. Today's medicine appears to be instrumental in dealing with this type of issues by making promises that will be hard not to break. The most urgent form of action to be undertaken regards these unwarranted expectations that society holds about the efficacy of medicine. The message to put across ought to be that death is inescapable and that the most severe diseases are incurable.
Once the inevitability of resorting to often dramatic measures in today's health care system is postulated, we are confronted with the problem of finding an ethical justification to subsequent decisions. On the basis of the choices made necessary by the paucity of available resources, medical treatment would be “apportioned”, i.e., distributed according to commitments and rules, with the inevitable exclusion of some from the utilization of the services themselves.
Rationalisation, intended as best utilisation and fair limitation, is an economic necessity, juridically and ethically legitimate. The ultimate objective must remain that of equitable apportionment.
Evidence has consistently shown that patients with mental illness have greater physical health morbidity and mortality compared to the general population.1 Many factors have been implicated and include a generally unhealthy lifestyle, side effects of medication, and inadequate physical healthcare.2, 3 Higher rates of suicide and accidents are other known risks. Psychiatric patients are more likely to smoke, have less inclination to exercise, and are prone to poor dietary habits and obesity, the latter through general inertia, the result of the adverse effects of neuroleptic medication, or increased alcohol use. Psychotropic medication is associated with impaired glucose tolerance and diabetes, metabolic syndrome, dyslipidemia, cardiovascular complications, extrapyramidal side effects and sexual dysfunction. A broad range of clinician and organisational factors prevent access to adequate physical healthcare that in turn compounds the above problems.
Scale of physical morbidity and mortality in mental illness
Patients suffering from depression are twice as likely to develop type 2 diabetes mellitus, and the prevalence of stroke and myocardial infarction is three- and five-fold respectively higher than people without depression.4 A mortality rate ratio (MRR) of 2 to 3 in patients with schizophrenia or bipolar disorder is a general finding.5 Schizophrenia is associated with higher rates of diabetes mellitus (side effects of medication partly to blame), osteoporosis (lifestyle risk factors play a role), obesity, and cardiovascular problems. 2, 6, 7, 8 It has been estimated that life expectancy is reduced by at least ten years. 9, 10 People with learning disabilities, particularly those with concurrent epilepsy, dementia and polypharmacy, are at greater risk of developing added complications.11 Eating disorders are associated with a high mortality because of physical disorders caused by anorexia/bulimia nervosa affecting other organ systems.12 Mental illness in general is associated with an increased risk of hepatitis, human immunodeficiency virus (HIV), tuberculosis, and poor dental health. 9, 10
Causes of raised physical health morbidity and mortality in psychiatric patients
Explanations for the higher morbidity and mortality in mental illness include cardiovascular and respiratory problems in addition to the increased suicide risk. Aetiological factors include adverse effects of medication (weight gain, diabetes, and dyslipidemia), lifestyle (smoking and the cost of smoking, poor diet and nutrition, lack of exercise, and obesity) and inability to access physical healthcare. Obesity, smoking and physical inactivity contribute to hypertension. Poor physical healthcare outcomes in mental illness are related to a combination of factors generally considered under the headings of patient/illness, psychiatrist/physician, and service provider/system issues.
De Hert and colleagues 9, 10 have outlined the factors that account for the raised physical health problems.For instance the patient/illness factors comprised difficulty in understanding health care advice combined with the motivation required to adopt new changes in lifestyle, poor compliance with treatment, cognitive deficits, reduced pain sensitivity (induced by antipsychotic medication), poor communication and deficient social skills (seen in many cases of schizophrenia, for example) which all accounted for the shortened life-span of patients with severe mental illness (SMI).
An additional patient/illness factor is that psychiatric symptoms may render patients less inclined to discuss physical problems. Some doctors are uncomfortable dealing with psychiatric patients because the latter may be cognitively compromised which may impair or impede a doctor’s clinical assessment. The stigma of mental illness, often the result of disparaging media coverage and negative stereotypes surrounding psychiatric patients, are other hurdles that prevent people from seeking treatment. Furthermore, psychiatric patients are less likely to see a primary care physician and therefore to receive other interventions such as screening for cancer.
Psychiatrist-related factors are characterised by an overemphasis on mental health to the exclusion of physical health, infrequent screening rates for metabolic abnormalities, omission of medical examination of patients because physical complaints frequently are part of the psychiatric presentation, poor communication with the patient and the primary care teams, a lack of awareness and perhaps adherence to treatment guidelines, insufficient medical knowledge, and erroneous, sometimes misguided beliefs about patients’ capability to change their lifestyle.9, 10 Even when risk factors are documented in the patient's clinical file, very little is done by way of further investigations or prevention.
Factors common to the psychiatrist and other physicians include a tendency to dismiss or interpret physical symptoms as psychosomatic, lack of good quality care, unequipped teams, insufficient assessment, and difficulties providing consistent monitoring and continuity of care. Other physician-related factors relate to problems coordinating psychiatric and medical care.9, 10
Service-provision factors included a lack of clarity and consensus as to where the responsibility of physical health lies.9, 10 Should general practitioners (GPs) supervise the majority of patients who do not suffer from severe, enduring mental illness? Should patients with acute alcohol withdrawal symptoms be managed at home by the GP, treated in a general hospital, or admitted to a psychiatric unit? The fragmentation of medical and mental health care systems, lack of integration of services (poor or absent liaison links) and insufficient funds to resource the mental health service, limit the ability of most psychiatrists to focus beyond their own speciality.
Service and system changes are prevalent in industrialised countries because reforms in mental health have led to reduced inpatient resources leading to shorter and infrequent hospital admissions with less time available to focus or investigate physical health problems. In the United Kingdom (UK) there is intense emphasis on community care and talking therapies, yet the management of physical health issues by community mental health teams may be poor because of inadequate training and learning.
Recommendations to improve physical health care in psychiatric patients
Health care professionals need to be more aware of these findings in order to improve medical screening and treatment of psychiatric patients. Currently there is no evidence this is happening, with increasing concerns regarding inequalities between those with and without mental illnesses.13
We propose the following recommendations to promote integration between mental and physical health care:
1.A greater effort to increase awareness of the problem among primary care and mental health care providers. The Royal College of Psychiatrists has launched a campaign called Fair Deal to highlight the importance of physical health of people with mental illness.1 Patients still feel stigmatised and therefore psychiatrists need to boost their efforts to reduce this discrimination. The excess mortality associated with this discrimination needs to be recognised as a human rights issue.13
2.Primary care providers need to change the culture of undertreating physical health in mental health patients. The National Institute for Health and Clinical Excellence (NICE) guidelines for schizophrenia and bipolar disorder highlight the importance of monitoring antipsychotics and mood stabilizers.14 The Royal College of Psychiatrists should lead by implementing the NICE guidelines for mental and behavioural conditions.
3.Education and training of doctors who pursue a career in psychiatry needs to be improved with mandatory trainee placements in acute medicine or neurology, regular personal development plan (PDP) courses, and training to update knowledge of recognising physical illness and the performance of basic medical tasks. The Royal College of Psychiatrists should develop a diploma in clinical psychiatry for GPs and clinicians with a specialist interest in psychiatry. The curriculum needs to be widened to include electrocardiogram (ECG) interpretation, basic endocrinology, and neurological investigations (magnetic resonance imaging and so forth). This would allow psychiatrists to develop better liaison with their fellow professionals and share responsibility with them, which undoubtedly would encourage good medical practice.
4.The Royal College Scoping Group’s report15 sets key standards for the physical healthcare of patients in a range of psychiatric services. It outlines the responsibilities of psychiatrists monitoring the physical health of patients, such as problems associated with adverse effects of medication. The report recommends that psychiatrists are trained and kept up to date in relevant physical health matters. These recommendationsneed to be followed.
5.Mental health professionals should encourage patients to monitor simple measures such as weight, dietary plans, and exercise programs, with the involvement of the voluntary sector (MIND, Mental Health Foundation) where possible. Patients and carers need to be educated about the health risks associated with unhealthy lifestyles: for example, smoking and alcohol misuse may interfere with the metabolism of neuroleptic medications. Smoking cessation clinics and alcohol treatment programmes may help. Advice from dieticians about patients' nutritional requirements to offset changes in metabolism caused by neuroleptics is important.
6.Because of the large-scale reduction of inpatient psychiatric beds and service redesign the majority of psychiatric care provision now exists in the community. Therefore community mental health teams and psychiatric outpatient clinics need to be appropriately designed and equipped to enable proper assessment of physical health monitoring. Annual health checks from the GP would benefit patients who require long-term monitoring in the community. Screening for deleterious effects of medication for example, hypothyroidism and renal dysfunction caused by lithium, at regular intervals would be appropriate.16 It should also be made clear to psychiatrists that they should resist working in clinical settings that compromise patient care and inhibit good medical practice.
7.Financial initiatives such as Commissioning for Quality and Innovation (CQUIN)17 may be used by commissioners to improve physical health monitoring.As part of this process, primary care commissioners could mutually agree with mental health providers to fulfil measured targets related to such monitoring.
8.In order to better understand the interplay between psychiatric conditions and medical complications contributing to the high physical morbidity and mortality, further studies are essential. To cite one example, we now know that psychotropic medications contribute to many physical problems (abnormal ECGs, weight gain, changes in plasma glucose) and lead to higher morbidity rates. The 'newer' generation of antidepressants and neuroleptics have not lived up to expectations and have as many untoward effects as the older drugs. Developments of newer drugs with different mechanisms of action are required, though this will take time.
9.The discrimination faced by people with mental illness and learning disabilities, with the accompanying excess mortality, represents a human rights issue13 that requires legislative changes. The Disability Right’s Commission18 has already recommended appropriate physical health care screening, for example, annual physical health checks. The government’s health inequality agenda should incorporate these conditions into its indicators of disadvantage and include mental illnesses and learning disability in the framework.
Conclusion
Traditionally the field of psychiatry involves a holistic approach in the management of patients. Unfortunately, over the decades psychiatry appears to have lost its way and therefore it is important to re-establish a more comprehensive system of treating mental illness that encompasses regular physical health monitoring. Physical morbidity and mortality in patients with mental illness is on the rise and is associated with a complex interplay of factors outlined above. The overall health care of psychiatric patients can be improved through the changes in education and training of clinicians, close liaison between primary and secondary care, implementation of recommendations by NICE and the Royal College of Psychiatrists, improved research through better funding, public health education of patients and carers, and legislative changes.
It is well documented that many HBsAg-positive / HBeAg-negative patients show normal alanine aminotransferase (ALT) levels. However, two different scenarios have been proven to exist: inactive Hepatitis B Virus (HBV) carriers (previously defined as “healthy” HBV carriers) and patients with chronic hepatitis B (CHB) with transient virological and biochemical remission. These subsets of patients share HBsAg positivity and normal ALT levels; however, progression of disease, outcome, HBV DNA levels, severity of liver damage, requirement for liver biopsy and antiviral treatment significantly differ between the two patient populations.
Thus, among HBsAg-positive / HBeAg-negative subjects with normal liver biochemistry, it is important and sometimes difficult to distinguish the ‘true inactiveHBV carriers’ from patients with ‘activeCHB’ in whom phases of spontaneous remission have occurred. The former have a good prognosis with a low risk of complications, while the latter patient population have active liver disease with a high risk of progression to liver cirrhosis and/or hepatocellular carcinoma (HCC). Therefore, prolonged biochemical and virological follow-up are mandatory for diagnosis and decision to treat.
The term ‘chronic hepatitis B’ refers to a chronic necroinflammatory disease of the liver caused by persistent HBV infection 1. The term ‘necroinflammatory’ describes the presence of death of periportal hepatocytes (periportal necrosis) with or without disruption of the limiting plate by inflammatory cells, intralobular necrosis, portal or intralobular inflammation, and formation of bridges between vascular structures (the so-called bridging necrosis). Chronic hepatitis B can be subdivided into HbeAg positive and HBeAg-negative chronic hepatitis B 1,2. These two forms may have different natural histories and different response rates to antiviral treatment, although both may progress to more severe liver damage 3, such as, liver cirrhosis 4 or HCC 5.
The second subset is called the ‘inactive HBsAg carrier state’. It means a persistent HBV infection of the liver but without continual significant necroinflammatory disease. It is characterized by very low or undetectable serum HBV DNA levels and normal serum aminotransferases 1. It has been shown that histologically significant liver damage is rare in these patients, particularly when HBV DNA is lower than 2000 IU/ml, and thus a liver biopsy is not indicated in these subjects 4. Even among HBeAg-negative carriers with serum HBV DNA between 2000 and 20,000 IU/ml, histologically significant liver disease is also rare 6. Thus, these subjects should be followed up closely, but biopsy and treatment are not currently indicated.
As mentioned above, it is sometimes difficult to distinguish true inactive HBV carriers from patients with active HBeAg-negative CHB in whom phases of spontaneous remission may have occurred 1. The former patients have a good prognosis with a very low risk of complications, while the latter have active liver disease with a high risk of progression to advanced hepatic fibrosis, cirrhosis and subsequent complications such as decompensated cirrhosis and HCC 3-6. Thus, a minimum follow-up of 1 year with ALT levels every 3–4 months and periodical measurements of serum HBV DNA levels are required before classifying a patient as an inactive HBV carrier 1. ALT levels should remain consistently within the normal range, and HBV DNA should be below 2000 IU/ml 7. Thereafter, the inactive HBV carrier with undetectable or very low HBV DNA levels should be followed up with ALT determinations every 6 months after the first year and periodical measurement of HBV DNA levels 6 for the rest of their lifetime. This follow-up policy usually allows detection of fluctuations of activity in patients with true HBeAg-negative CHB 8.
It is important to underline that some inactive carriers may have HBV DNA levels greater than 2000 IU/ml (usually below 20,000 IU/ml), despite their persistently normal ALT levels 1,6,9. In these carriers the follow-up should be much more condensed, with ALT determinations every 3 months and HBV DNA measurements every 6–12 months for at least 3 years 1. After these 3 years, these patients should be followed up for life like all inactive chronic HBV carriers 6. After all, the inactive HBV carrier state confers a favourable long-term outcome with a very low risk of cirrhosis or HCC in the majority of patients 1,10,11. Patients with high baseline viremia levels have higher risk of subsequent reactivation. A liver biopsy should be recommended if ALT levels become abnormal and HBV DNA increases above 20,000 IU/ml. Non-invasive evaluation of liver fibrosis 12 may be useful, although these non-invasive tools, such as transient elastography, need further evaluation 6.
HBsAg clearance and seroconversion to anti-HBs antibody may occur spontaneously only in 1–3% of cases per year, usually after several years with persistently undetectable HBV DNA 7. On the other hand, progression to HBeAg-negative CHB may also occur 10.
Although the optimal definition of persistently normal ALT (PNALT) levels has not been established, the fluctuating nature of chronic HBV infection reasonably justifies serial ALT determinations. These should be done with a minimum of four to five tests 3–4 months apart within the first year of presentation, before determining whether an HBeAg-negative patient truly has PNALT. An initial follow-up of at least 1 year is supported by the finding of mild histological lesions in HBeAg-negative patients with true PNALT during the first year 6. The risk of developing abnormal ALT levels in HBeAg-negative patients with a normal baseline ALT have been reported to be higher during the first year (15–20%) and decline after 3 years of follow-up, therefore frequent monitoring during the first 1–3 years is critical 6,10.
Antiviral treatment of inactive HBsAg subjects is not indicated 1. Patients should be considered for treatment only when they have HBV DNA levels above 2000 IU/ml, serum ALT levels above the upper limit of normal and severity of liver damage assessed by liver biopsy showing moderate to severe active necroinflammation and/or at least moderate fibrosis 1,2.
Claiming historic triumph, that has defined his presidency ever since, President Barak Obama signed the $ 1 trillion Patient Protection and Affordable Care Act (in short called as ACA) in a highly visible white house ceremony on Tuesday March 23, 2010 (using 20 different pens) thereby establishing health care as a ‘right’ of every American for the first time. It took all the legislative and political skills from him to get the bill passed through both houses of Congress as was suggested on these pages previously.1
Soon after President Obama signed the landmark legislation, 26 States filed law suit contesting that the health care legislation, which earned the nickname of “Obamacare” from its opponents, was unconstitutional for several reasons. The legal challenge created significant uncertainty about the viability and future implementation of the legislation. There was also growing concern about the law’s impact on the national debt that became, and continues to be, an extremely divisive issue between the Democrats and the Republicans in the US Congress.
The law suit finally, as expected, made its way to the Supreme Court of the United States. The Court was looking at the legislation from three angles. First, at the core of the legislation, was the requirement that nearly all Americans obtain health insurance by 2014 or face a financial penalty- a provision that came to be known as the ‘individual mandate’ . The penalty would be recycled into “health exchanges” providing alternate options to low income Americans and small businesses for purchase of health care. The ‘individual mandate’ was the backbone of the legislation that wouldcover millions of uninsured Americans, majority of whom would be healthy young individuals. And, if this ‘individual mandate’ were to be struck down by the Court (as was expected by many), then the second question would be what happens to the rest of the ACA as insurance industry was supporting the legislation since it would provide them with tens of millions of new healthy ‘customers’. If such healthy individuals were left out, the pool would have mostly sicker individuals compromising the profitability, and perhaps the very viability, of the insurance industry. The third issue related to the mandate for the states to accept a large number of individuals into Medicaid program that provides health care for the poor and those with income of up to 133 % of the federal poverty level.2
The Supreme Court, mercifully for President Obama, upheld virtually the entire legislation in its historic decision on June 28, 2012. The four ‘liberal justices’ ( Justices Stephen Breyer, Ruth Ginsburg, Elena Kagan and Sonia Sotomayor) were joined by the conservative Chief Justice John Roberts in upholding the ‘individual mandate’. In what many observers of the court called a surprising twist, the justices held that the mandate was not constitutional under the ‘interstate commerce clause’, as argued by the administration, but was constitutional under Congress’ power of taxation. The other four dissenting conservative justices (Justices Samuel Alito, Anthony Kennedy, Antonin Scalia and Clarence Thomas) held that the Congress had exceeded its authority on several levels.
The reaction to the ruling was prompt and mixed. Dr. Jeremy A. Lazarus, President American Medical Association said “The AMA has long supported health insurance coverage for all, and we are pleased that this decision means millions of Americans can look forward to the coverage they need to get healthy and stay healthy”. The President and CEO of American Hospital Association, Mr Rich Umbdenstock, said “The decision means that hospitals now have much-needed clarity to continue on their path toward transformation”Perhaps the President of the American College of Physicians stated it best “We hope that a day will come when the debate will no longer be polarized between repeal on one hand, or keeping the law exactly as it is on the other, but on preserving all of the good things that it does while making needed improvements.”
The President of the U.S. Chamber of Commerce, Thomas J. Donohue, lamented that “While we respect the court’s decision, today’s Supreme Court ruling does not change the reality that the health care law is fundamentally flawed. It will cost many Americans their employer-based health insurance, undermine job creation and raise health care costs for all.” And in a scathing statement, the President of National Federation of Independent Business, Dan Danner, echoing the sentiments of a growing number of small businesses said “Under [the ACA], small-business owners are going to face an onslaught of taxes and mandates, resulting in job loss and closed businesses. We will continue to fight for the repeal of [the ACA] in the halls of Congress; only with [the ACA’s] full repeal will Congress have the ability to go back to the drawing board to craft real reform that makes reducing costs a No. 1 priority.” 3
This line of argument, apart from bringing some uncertainly, provided politicians fodder as they move closer to the Presidential elections. And as expected, the Republicans (who control the House of Representatives) passed legislation repealing the law but the bill died in the US Senate (controlled by Democrats). And the Republican Presidential candidate, Gov. Mitt Romney, framed the decision as a political call to arms. “What the Court did not do on its last day in session, I will do on my first day if elected President of the United States. And that is I will act to repeal Obamacare.” While both President Obama and Gov. Romney agree that Medicare costs have to be reined in but there is fundamental difference in their approach to cost cutting. President Obama’s plan relies on a powerful board to reduce payments to service providers and gradually changing how hospital and doctors are paid in order to eliminate fee for service and establish pay for performance (pay for the quality, not quantity). Gov. Romney would limit the amount future retirees would receive from the federal government to approximately $ 7000 (also called as Voucher System) and relying on the private industry to find an efficient solution.
It is clear that Gov. Romney, who previously implemented ‘Obamacare’ type of legislation as the governor of Massachusetts, flipped his position to appease extreme right wing of the Republican Party. As usual politics trumps policy. This drama continues to play out as we get closer to the election on November 6, 2012.
As identified by an independent nonpartisan educational institute based in Washington, The Centre for American Progress (CAP), some of the popular provisions of the law are 4:
The law provides for young adults to stay on their parents’ insurance to age 26 enabling 2.5 millionyoung Americans toenrol on their parents policies (73 % of young adults now have coverage as a result of this provision);
For seniors living on fixed income (Medicare patient population), one of the immediate benefits of the ACA was the closure of prescription drug coverage gap (known as the ‘donut hole’) saving 4 million seniors about$ 2 billion on prescription drugs or approximately $604 per person, in 2011 alone;
The law provides $11 billion to support and expand community health centres nationwide. More than 350 new community health centres were established in 2011 serving 50 million Americans in medically underserved areas;
Starting in 2014, the law prohibits health insurance carriers from excluding and/or denying coverage or charging higher premiums and limiting benefits to those with pre-existing medical conditions (as happens currently in too many cases);
50,000 Americans have already enrolled in the Pre-existing Condition Insurance Plan (PCIP) that ensures medical services including prescription drugs for those with pre-existing conditions as soon as possible ;
Provision of $200 million to expand school-based health centres for primary care, dental care, behavioural health services and substance abuse counselling;
In 2011 alone, 85 million Americans benefitted from preventive services included in the legislation. Many more will benefit since a major provision of the preventive services for women took effect in August 2012;
However, several components of the legislation remain unclear and their impact rather unknown. As an example the Obama administration fought hard for formation of the Independent Payment Advisory Board (IPAB) to address the inordinate influence of stakeholders in Congressional decisions over Medicare. This group of 15 nonpartisan experts is responsible for developing payment and related Medicare policy changes to assure that Medicare spending does not exceed budget targets tied to economic growth. Although now the law, the IPAB may never be formed because the Senate is unlikely to find 60 votes required to confirm IPAB members (unless the election brings unforeseen changes in the makeup of the Senate). Politics may again triumph policy. The payment approaches that need to evolve from “volume” to “value,” remain vexing. The Centre for Medicare & Medicaid Innovation charged with developing the pilot programs that may result in a reformed delivery system, have no pilots that focus on developing alternative models to reimburse physicianservices.5, 6
And the “invisible problem” of physician shortage! While there is growing bipartisan appreciation that the primary care workforce is insufficient to handle increasing demand for primary care services, the problem has not been fully addressed. The Association of American Medical Colleges estimates that in 2015 the country will have 62,900 fewer doctors than needed and those numbers will more than double by 2025. 7, 8
In coming months the States may become the battleground for implementing the “health exchanges”. By 2014 States are required to establish American Health Benefits exchanges and small business health operations program (SHOP) exchanges. These exchanges called in short, “health exchanges”, are basically subsidized market places with tax credits for consumers to shop for their health insurance at very competitive rates. Individuals who will not be eligible for Medicaid and with income of up to 400% of the Federal poverty level will have access to these health exchanges to purchase insurance. Such subsidies and tax credits will also be available to businesses with less than 100 employees. 9
It is also becoming apparent that the financial burden of the legislation will be significantly higher than initially estimated.For example the non-partisan Congressional Budget Office (CBO) estimates that 80 % of Americans who will face penalty for lack of health insurance under the ‘individual mandate’ would be those with yearly income of $ 55, 250 (for individuals) and $ 115, 250 (for couples). This is in contrast to the statements of President Obama who continues to pledge that he will not raise taxes on individuals making less than $ 200,000 and couples making less than $ 250, 000. And the Republican side of the Senate Budget Committee estimates that Obamacare will cost $2.6 trillion dollars in its first real decade since the bill does not fully go into effect until 2014. 10
Fortunately for President Obama, the prestigious Institute of Medicine released a report,last month on September 6, confirming what has been suggested by him and others, that the US health care system wastes almost 30 % ($750 Billion) each year on unnecessary procedures, fraud and waste. Therefore, the administration has redoubled its efforts to check the waste and fraud in order to pay for the cost of ACA. However, the real battle will begin as soon as the Congress reconvenes in January 2013. They are immediately faced with dealing with “Sequestration”. Originally a legal term referring to the act of valuable property being locked away for safe keeping by an agent of the court, the term has been adapted by Congress in 1985 for fiscal discipline. Under this rule, an amount of money equal to the difference between the cap set in the Budget Resolution and the amount actually appropriated is "sequestered" by the department of Treasury and not handed over to the departments it may have been appropriated originally by the Congress. The balanced budget act of 2011established a Congressional task force (called ‘Super Committee’) that was charged to make recommendations to cut the US Budget deficit by $ 1.5 trillion by November 23, 2011. Failure to do so would automatically trigger “Sequestration”. On November 21, 2011, the committee issued a statement that it had failed to reach agreement. This failure is viewed by most as a triumph of political ideology over genuine leadership. But the prospect of ‘sequestration’ has come to be seen so catastrophic that key members of Congress and the Presidentare expected to abandon brinkmanship and come to an agreement in early 2012.
So, as the drama and the debate continue vigorously in the days leading up to the November 6 elections, it is clear that “Obamacare” will continue to divide the US congress and the country. Irrespective of the party that will control the Congress and who becomes the next President of the US, “Obamacare” is here to stay. And, no matter how hard the Republican Party may try, they will face a monumental task in reversing the course of the history. There will be bickering, name calling, finger pointing and horse trading. But, the warring factions will realize that the escalating costs and complexities of the health care system demand that the legislators and the President come together to find real solutions to keep the American health care system as the best in the world. The real challenges will remain the same no matter who is elected as President: to stem the unsustainable tide of national health expenditure as percentage of the gross national product (rising from 7.2 % in 1970 to over 17 % in 2010), rapidly increasing number of Americans without health insurance (approaching almost 50 million), exploding national debt and, more immediately, the looming threats from sequestration.
In rheumatology clinics chronic painful conditions are the norm. Although many pain syndromes are associated with low mood and sometimes clinical depression, the mood disorder often goes unrecognised. Fibromyalgia is one such chronic pain syndrome, 'chronic' arbitrarily defined as lasting longer than six months. It is a common, poorly understood, musculoskeletal disorder which more often affects women between the ages of 25-50 years generally.
In nearly all patients three symptoms predominate, namely, neuropathic pain (nerve injury pain), fatigue and non-restorative sleep disturbance. The chronic neuropathic diffuse pain, described as whole body pain, is felt particularly in deep tissues such as ligaments, joints, and muscles of the axial skeleton in mainly the lower cervical and lumbar spine. The pain is often characterised by an exaggerated and prolonged response to a noxious stimulus (hyperalgesia). Patients may be considered to be malingering because there is no obvious explanation for the symptoms. Anxiety, stress and depression caused by fibromyalgia add insult to injury, with personality and cognitive factors coming into play in addition.1 Paraesthesiae (abnormal sensory sensations) or dysaesthesiae (painful sensations) of the extremities may also occur. There is no objective muscular weakness or neurological disorder to account for the symptoms, which adds to the diagnostic dilemma. For example, fibromyalgia affecting the supraspinatus muscle of the shoulder would limit initial abduction of the arm because of pain, not because of any muscle weakness. Cognitive function is sometimes described as 'fibrofog' or 'conscious confusion' and may be a primary symptom of fibromyalgia, reflecting impairments in working memory (a form of short-term memory), episodic (memory for events), and semantic memory (memory for words, rules, language).
Nociception refers to the process of information about harmful stimuli conveyed by neuronal activity up to the point of perception in the dorsal horn of the spinal cord where primary afferents synapse.2 Evidence is accumulating which shows that atypical sensory processing in the central nervous system (CNS) and dysfunction of skeletal muscle nociception are important in the understanding of fibromyalgia and other chronic pain syndromes.3The concept of 'central pain sensitization' or 'central sensitivity syndrome' considers fibromyalgia to be a disturbance of nociceptive processing which causes a heightened experience of pain or pain amplification.4 Because pain signals are subject to variation in amplitude, the modulation of sensory processing may be the key to understanding the pain response not only in fibromyalgia but also in other conditions, such as irritable bowel syndrome. Descending spinal noradrenergic and serotonergic neurons inhibit the neurotransmitters noradrenaline and serotonin, released from primary afferent neurons and dorsal horn neurons. Therefore, when descending inhibition is decreased, irrelevant nociceptive stimuli are more readily felt. Put another way, in patients with chronic pain syndromes descending inhibition may not be functioning adequately to prevent or mask irrelevant pain stimuli. When appropriate medication is used this normal descending inhibition is enhanced and pain is no longer troublesome.
The release of neurotransmitters (ligands) also requires a mechanism that involves voltage-sensitive calcium and sodium channels. Repetitive action potentials cause the calcium channels to open with the ensuing release of neurotransmitters into the synaptic cleft. The postsynaptic neurons are thus stimulated leading to molecular and structural changes (sprouting) which cause neuropathic pain. Drugs such as Pregabalin and Gabapentin bind to voltage-sensitive calcium channels and reduce calcium influx, which in turn diminishes pain. The concept of central pain sensitization now incorporates affective spectrum disorders and functional somatic syndromes. It seems that the more painful symptoms one has which are difficult to explain, the more likely the patient is suffering from a mood disorder. Dopamine may be involved in the regulation of cognition in the dorsolateral prefrontal cortex and could account for the cognitive deficits.5Because cingulate and prefrontal cortices are particularly implicated in pain modulation (inhibition and facilitation of pain), structural changes in these systems could contribute to the chronic pain associated with fibromyalgia.6
Many patients with fibromyalgia have an increased sensitivity to sensory stimuli that are not normally or previously painful (allodynia). In other words, minor sensory stimuli that ordinarily would not cause pain in most individuals induce disabling, sometimes severe pain in patients with fibromyalgia.7 In normal individuals 4 kg/square cm2pressure (approximately the pressure needed to blanch the skin at the top of one’s thumb) causes patients with fibromyalgia to wince with pain or suddenly withdraw when the tender point is palpated. This indicates that pain occurs at a lower pain threshold in fibromyalgia sufferers when this pressure is applied.
The pain of fibromyalgia may be aggravated by emotional stress though the latter is difficult to quantify and evaluate. For instance, corticosteroid hormones are released in high amounts after stress yet fibromyalgia is associated in some patients with a decreased cortisol response to stress. Stress may therefore initiate, inhibit or perpetuate alterations in the corticotrophin-releasing hormone (CRH) neuron, with associated effects on the hypothalamic pituitary axis (HPA) and other neuroendocrine axes.8
There are many other possible explanations for fibromyalgia pain. One of the major neurotransmitters involved in nociception is substance P, found in high concentrations in the spinal cord, limbic system, hypothalamus, and nigrostriatal system. It is involved in the transmission of pain impulses from peripheral afferent receptors to the central nervous system. Nerve growth factor (NGF), a cytokine-like mediator may indirectly exert its effect through enhancing glutaminergic transmission and could account for sustained central sensitization in fibromyalgia. 9, 10 Another neuropeptide, calcitonin gene-related peptide, a potent vasodilator, present in non-myelinated afferent neurons, may also play a role in pain pathology.5
Levels of the neurotransmitter serotonin have been found to be low in some studies in fibromyalgia patients. Although serum levels of serotonin are lower than in some patients with rheumatoid arthritis and healthy controls, the variation is too broad and therefore measurement of serotonin has not proved useful tool in determining a diagnosis of fibromyalgia. 11
Logically, pharmacologic agents used to treat pain in fibromyalgia would act by either increasing levels of inhibitory neurotransmitters or decreasing levels of excitatory neurotransmitter. In the United States of America (USA), Pregabalin was the first drug to be approved by the Food and Drug Administration (FDA) for the treatment of fibromyalgia and has been shown to improve pain, sleep and quality of life. It is ineffective against depression. The main inhibitory mediator in the brain, gamma amino butyric Acid (GABA), is formed from glutamate (excitatory) by the enzyme glutamate decarboxylase (GAD). It is particularly plentiful in the nigrostriatal pathways. About 20% of CNS neurons are GABAergic and it serves as a neurotransmitter at some 30% of all CNS synapses.12 Pregabalin increases neuronal GABA levels by producing a dose-dependent increase in glutamate decarboxylase activity. In a meta-analysis of 21 clinical trials to estimate treatment differences vs. placebo, statistically significant improvement was observed with Duloxetine, Milnacipran 200 mg/day, Pregabalin 300 or 450 mg/day, and Tramadol plus Paracetamol. The meta-analysis showed a statistically increased risk of discontinuation because of adverse events related to Milnacipran and Pregabalin.13
Antidepressants may improve fibromyalgia symptoms by reducing pain, stabilizing mood and improving sleep, though the effect seems to be modest. If abnormal sleep, and hence subsequent tiredness, precedes the development of fibromyalgia the effect of antidepressants may be primarily associated with improved sleep. However, the efficacy of tricyclic antidepressants is difficult to quantify and their limited superiority over placebo lasts no more than a few months. A meta-analysis of ten randomized double-blinded, placebo-controlled studies revealed only poor to moderate evidence for a beneficial effect at low doses of Amitriptyline (25mg daily) over 6-8 weeks. Even when given in higher doses or prescribed for a longer duration, Amitriptyline did not make a great deal of difference. 14
The efficacy of Selective Serotonin Reuptake Inhibitors (SSRIs) is also inconclusive. More promising results have been demonstrated with Serotonin and Noradrenaline Reuptake Inhibitors (SNRIs) such as Duloxetine. Both serotonin (5-HT) and noradrenaline (NA) exert analgesic effects via descending pain pathways. Pain is a prominent feature of depression and vice versa and the alleviation of one modifies the other. 15, 16 The reduction in pain reduces fatigue and Duloxetine improves mood.
Other drugs used in this condition include Milnacipran and Cyclobenzaprine (a muscle relaxant structurally related to tricyclic antidepressants). Milnacipran and Cyclobenzaprine are not available in the United Kingdom (UK). Tramadol (a serotonin and noradrenaline reuptake inhibitor) is a weak mu-receptor opioid agonist used to control pain but its adverse effects are those of opiates in general, mainly nausea and dependence.
Although other adjunctive non-pharmacological treatments have been advocated the results are disappointing. Assessments of non-drug treatments are generally mediocre. Aerobic exercises benefit some patients, especially when combined with biofeedback, patient education and cognitive therapy. A whole gamut of treatments such as graded exercises, yoga, dietary advice, balneotherapy (heated pool bathing), homeopathy, massage, acupuncture, patient education, group therapy and cognitive behaviour therapy, have been suggested and tried, but few of them demonstrated clear-cut benefits in randomized controlled trials.Support groups may help some patients. 17, 18, 19
Fibromyalgia is now considered to be, in part, a disorder of central pain processing. Central sensitization manifests as pain hypersensitivity, particularly allodynia, and hyperalgesia. It is believed that central sensitization occurs in part through the action of glutamate on the N-methyl-D-aspartate (NMDA) receptor, resulting in an increase in intracellular calcium and kinase activation, leading to hyperalgesia and allodynia.20
Response to standard analgesics is erratic and more promising results have emerged with drugs such as the SNRIs Duloxetine and Milnacipran, the anticonvulsants Gabapentin and Pregabalin, either used alone or in combination, or with other agents such as Amitriptyline. There is only modest evidence to support SSRIs and Tramadol. Treatment needs to be holistic and multidisciplinary, focussing on both physical pain management and psychological dysfunction. The multidisciplinary approach, though difficult to measure, may help by imparting a sense of empathy and support for patients. Overall, most patients with fibromyalgia continue to have chronic pain and fatigue with symptoms persisting for many years, but it is not necessarily a progressive disorder and some patients may show moderate improvement.
In recent years, increasing attention has focused on the treatment of chronic pain with a considerable number of research and publications about it. At the same time, opioid prescription, use, abuse and death related to the inappropriate use of opioids have significantly increased over the last 10 years. Some reports indicated that there were more than 100 ‘pain clinics’ within a one-mile radius in South Florida, between 2009 and 2010, which led to the birth of new opioid prescription laws in Florida and many other states to restrict the use of opioids. In the face of clinical and social turmoil related to opioid use and abuse, a fundamental question facing each clinician is: are opioids effective and necessary for chronic non-malignant pain?
Chronic low back pain (LBP) is the most common pain condition in pain clinics and most family physician offices, which ‘requires’ chronic use of opioids. Nampiaparampil et al conducted a literature review in 20121 and found only one high-quality study on oral opioid therapy for LBP, which showed significant efficacy in pain relief and patient function. Current consensus believes that there is weak evidence demonstrating favourable effectiveness of opioids compared to placebo in chronic LBP.2Opioids may be considered in the treatment of chronic LBP if a patient fails other treatment modalities such as non-steroidal anti-inflammatory drugs (NSAIDs), antidepressants, physical therapy or steroid injections. Opioids should be avoided if possible, especially in adolescents who are at high risk of opioid overdose, misuse, and addiction. It has been demonstrated that the majority of the population with degenerative disc disease, including a disc herniation have no back pain. A Magnetic Resonance Imaging (MRI) report or film with a disc herniation should not be an automatic ‘passport’ for access to narcotics.
Failed back surgery syndrome (FBSS) is often refractory to most treatment modalities and sometimes very debilitating. There are no well-controlled clinical studies to approve or disapprove the use of opioids in FBSS. Clinical experience suggests oral opioids may be beneficial and necessary to many patients suffering from severe back pain due to FBSS. Intraspinal opioids delivered via implanted pumps may be indicated in those individuals who cannot tolerate oral medications. For elderly patients with severe pain due to spinal stenosis, there is no clinical study to approve or disprove the use of opioids. However, due to the fact that NSAIDs may cause serious side effects in gastrointestinal, hepatic and renal systems, opioid therapy may still be a choice in carefully selected patients.
Most studies for pharmacological treatment of neuropathic pain are conducted with diabetic peripheral neuropathy (DPN) patients. Several randomized clinical controlled studies have demonstrated evidence that some opioids, such as morphine sulphate, tramadol,3 and oxycodone controlled-release,4 are probably effective in reducing pain and should be considered as a treatment of choice (Level B evidence), even though anti-epileptics such as pregabalin should still be used as the first line medication.5
Some studies indicate opioids may be superior to placebo in relieving pain due to acute migraine attacks and Fiorinal with codeine may be effective for tension headache. However there is lack of clinical evidence supporting long-term use of opioids for chronic headaches such as migraine, chronic daily headache, medication overuse headache, or cervicogenic headache. Currently there are large amounts of opioids being prescribed for headaches because of patients' demands. Neuroscience data on the effects of opioids on the brain has raised serious concerns for long-term safety and has provided the basis for the mechanism by which chronic opioid use may induce progression of headache frequency and severity.6 A recent study found chronic opioid use for migraine associated with more severe headache-related disability, symptomology, comorbidities (depression, anxiety, and cardiovascular disease and events), and greater healthcare resource utilization.7
Many patients with fibromyalgia (FM) come into pain clinics to ask for, or even demand, prescriptions for opioids. There is insufficient evidence to support the routine use of opioids in fibromyalgia.8 Recent studies have suggested that central sensitization may play for role in the aetiology of FM. Three central nervous system (CNS) agents (pregabalin, duloxetine and milnacipran) have been approved by United States Food and Drug Administration (US FDA) for treatment of FM. However, opioids are still commonly prescribed by many physicians for FM patients by ‘tradition’, sometimes even with the combination of a benzodiazapine and muscles relaxant - Soma. We have observed negative health and psychosocial status in patients using opioids and labeled with FM. Opioids should be avoided whenever possible in FM patients in face of widespread abuse and lack of clinical evidence.9
Adolescents with mild non-malignant chronic pain rarely require long-term opioid therapy.10 Opioids should be avoided if possible in adolescents, who are at high risk of opioid overdose, misuse, and addiction. Patients with adolescents living at home should store their opioid medication safely.
In conclusion, opioids are effective and necessary in certain cases. However, currently no single drug stands out as the best therapy for managing chronic non-malignant pain, and current opioid treatment is not sufficiently evidence-based. More well-designed clinical studies are needed to confirm the clinical efficacy and necessity for using opioids in the treatment of chronic non-malignant pain. Before more evidence becomes available, and in the face of widespread abuse of opioids in society and possible serious behavioural consequences to individual patients, a careful history and physical examination, assessment of aberrant behavior, controlled substance agreement, routine urine drug tests, checking of state drug monitoring system (if available), trials of other treatment modalities, and continuous monitoring of opioid compliance should be the prerequisites before any opioids are prescribed.
Opioid prescriptions should be given as indicated, not as ‘demanded’.
The use of dietary supplements has grown rapidly over the past several decades, and are now used by more than half of the adult population in the United States (US).1 In 1994, the Dietary Supplements Health and Education Act (DSHEA) significantly changed the Food and Drug Administration’s (FDA) role in regulating supplement labelling. According to the DSHEA dietary supplements may contain products taken by mouth including vitamins, minerals, herbs or other botanicals, amino acids, other dietary substances, or combinations or extracts of any of these ‘dietary ingredients.’ The DSHEA reaffirmed that dietary supplements are to be regulated as foods and not as drugs. Annual sales of supplements to Americans are now reported at about $23 billion, a substantial share of which is spent on vitamins and minerals.
The purpose of this review is to present the discussion from available research to internists and other clinicians to help guide their decisions behind the efficacy and safety of dietary supplement use in primary prevention of chronic disease in the general non-pregnant adult population.
Profile of a dietary supplement user
In general dietary supplements are used by individuals who practise healthier lifestyles. Its use is higher among women and the children of women who use supplements; in elderly persons; among people with more education, higher income, healthier diets, and lower body mass indices; and among residents of the western US.2 Individuals with chronic illnesses, or those who are seeking to prevent recurrence of a serious disease (for example, cancer) also tend to be more frequent supplement users.3 Many dietary supplement users perceive their health as better.
Why use dietary supplements?
The growth in supplement use has accelerated rapidly with marketing spurred by claims that chronic conditions could be prevented or treated by supplement use. The commonly used over-the-counter multivitamin and mineral supplements contain at least 10 vitamins and 10 minerals. On a daily basis consumers receive advertising and promotional material of unproven claims made about dietary supplements or other products and the medical wonders they can achieve. Some of the promotional material makes a consumer feel guilty if he or she is not using one. Many users feel so strongly about the potential health benefits of some of these products that they reported that they would continue to take them even if they were shown to be ineffective in scientifically conducted clinical studies.4 More than half of American adults take dietary supplements in the belief that they will make them feel better, give them greater energy, improve their health, and prevent and treat disease.
Is there clinical evidence for use of dietary supplements?
Most studies do not provide strong evidence for beneficial health-related effects of supplements taken singly, in pairs, or in combinations of 3 or more.5 In some studies, or subgroups of the study populations, there is encouraging evidence of health benefits such as increased bone mineral density and decreased fractures in postmenopausal women who use calcium and vitamin D supplements.
Huang et al 5 performed a systematic review to synthesize the published literature on the efficacy of multivitamin and mineral supplements and certain commonly used single vitamin or mineral supplements in the primary prevention of cancer and chronic disease in the general adult population. The authors concluded that the strength of evidence for the efficacy of multivitamin/mineral supplementation in the general adult US population was very low for primary prevention of cancer, cardiovascular disease, and hypertension; and low for cataract and age-related macular degeneration.
The National Institutes of Health (NIH) consensus panel statement2 on ‘multivitamin/mineral supplements and chronic disease prevention’ did not find any strong evidence for beneficial health-related effects of supplements taken singly, in pairs, or in combinations of 3 or more. The panel concluded that the present evidence is insufficient to recommend either for or against the use of dietary supplements by the American public to prevent chronic disease. It also concluded that the current level of public assurance of the safety and quality of dietary supplements is inadequate, given the fact that manufacturers of these products are not required to report adverse events and the FDA has no regulatory authority to require labeling changes or to help inform the public of these issues and concerns.
A recent study published in Archives of Internal Medicine6 raised some disturbing concerns. In this large prospective study, 38,772 older women in the Iowa Women's Health Study were followed up for a mean time of 19.0 years. The authors found that most of the supplements studied were not associated with a reduced total mortality rate in older women. In contrast, they found that several commonly used dietary vitamin and mineral supplements, including multivitamins, vitamins B6, and folic acid, as well as the minerals iron, magnesium, zinc, and copper, were associated with a higher risk of total mortality. Of particular concern, supplemental iron was strongly and dose dependently associated with increased total mortality risk. The association was consistent across shorter intervals, strengthened with multiple use reports and with increasing age at reported use. Supplemental calcium was consistently inversely related to total mortality rate; however, no clear dose-response relationship was observed. The strengths of this study include the large sample size and longitudinal design. In addition, the use of dietary supplements was queried three times: at baseline in 1986, in 1997, and in 2004. The use of repeated measures enabled evaluation of the consistency of the findings and decreased the risk that the exposure was misclassified.
Summary
The use of dietary supplements has grown rapidly over the past several decades even though clinical deficiency of vitamins or minerals, other than iron, is now uncommon in the US.2 Fortification of foods has led to the remediation of vitamin and mineral deficits. The cumulative effects of supplementation and fortification have also raised safety concerns about exceeding upper levels besides interactions of dietary supplements with the prescriptions drugs taken by a consumer. There is no evidence-based data about what the optimal compositions and dose of a multivitamin and mineral supplement should be. Though dietary supplements are perceived to be safe, that should not be sufficient reason for using them without a valid medical need. Providers should take into consideration their efficacy and cost-effectiveness. There are also no outcomes data or data about quality adjusted life years gained by using dietary supplements taken singly, in pairs, or in combinations. The current data available on the efficacy and safety of dietary supplements is conflicting. Clinicians considering the use of dietary supplements should be aware of their risks, consider the likelihood of the adverse effects, interaction with prescription medications, safety, efficacy, costs, and possibility of unintended effectsof dietary supplements.
Conclusion
The conclusion from the available data (new and old) is that consumption of dietary supplements for prolonged periods appears not to be safe and is not cost-effective in primary prevention of chronic disease in the general non-pregnant adult US population. Practitioners should evaluate each case individually and take a decision based on available evidence-based data when considering dietary supplements in this population. Given the potential for widespread use of dietary supplements, there is a need for robust study methods in the future.
Many subjects with chronic Hepatitis C Virus (HCV) infection show persistently normal alanine aminotransferase (ALT) levels (PNALT),1-4 and thus formerly defined as ‘healthy’ or ‘asymptomatic’ HCV carriers.1 However, it is now clear that only a minority of these people show normal liver (15-20%).5-7 Therefore, ‘normal ALT’ does not always mean ‘healthy liver.’4
It is known that during the course of HCV infection ALT levels could fluctuate widely, with long periods of biochemical remission.1-4Thus, at least two different subsets of HCV-PNALT carriers exist: patients with temporal ALT fluctuations, that could be within the normal range for several months, and true ‘biochemically silent’ carriers showing persistently normal ALT values.4It means that the observation period should not be shorter than 12 - 18 months, and ALT determinations should be performed every 2 - 3 months.4, 6
Although liver damage is usually mild, 1, 2the presence of more severe chronic hepatitis (CH) or cirrhosis has been reported despite consistently normal liver biochemistry.8Although some studies showed that HCV carriers with normal ALT have mild and rather stable disease, others reported a significant progression of fibrosis in approximately 20-30% of the patients with ALT normality.9The development of hepatocellular carcinoma (HCC) has been also described.10Sudden worsening of disease with ALT increase and histological deterioration has been reported after many years of follow-up.11
Finally, HCV carriers with PNALT may suffer from extra-hepatic manifestations, sometimes more severe than the underlying liver disease: lymphoproliferative disorders, mixed cryoglobulinaemia, thyroid disorders, sicca syndrome, porphyria cutanea tarda, lichen planus, diabetes, chronic polyarthritis, etc.1, 2, 12
Therefore, the possibility of progression to more severe liver damage despite persistently normal biochemistry, the risk of HCC, the possibility of extra-hepatic diseases, and economic considerations, suggest that HCV-infected persons with PNALT should not be excluded a priori from antiviral treatment.1, 2
The earliest guidelines discouraged interferon (IFN) treatment in patients with PNALT because of the cost and side effects of therapy,1, 2 and of the low response rates to IFN monotherapy (<10-15%) with a risk of ALT flares in up to 50% of patients during treatment.9
The introduction of the combination of weekly subcutaneous pegylated-IFN (PEG-IFN) plus daily oral ribavirin (RBV) has led to response rates >50%, with a favourable risk-benefit ratio even in patients with slowly progressing disease.1, 2, 9 The first trial of PEG-IFN plus RBV found a sustained virological response (SVR) in 40% of HCV-1 carriers with PNALT treated for 48 weeks, and in 72% of HCV-2 and HCV-3 treated for 24 weeks.13The efficacy of antiviral treatment with PEG-IFN plus RBVwas subsequently confirmed in clinical practice.14, 15
However, in everyday practice, management of carriers with PNALT may be paradoxically more difficult than that of patients with abnormal ALT levels. Indeed, it is not always so easy to ascertain in the single case whether it should be considered as healthy subject or true patient. Several topics to date remain unresolved: Should these ‘seemingly healthy’ people undergo routine liver biopsy? Is antiviral treatment justified in ‘asymptomatic’ subjects with persistently normal liver biochemistry? Is long-term follow-up needed in this setting, and how long it should last?2
Liver biopsy provides helpful information on liver damage, as it may reveal the presence of advanced fibrosis or cirrhosis. Without a biopsy, it is impossible to clinically distinguish true ‘healthy’ carriers from those with CH.4 On the other hand, it is difficult to recommend routine biopsy for all HCV-PNALT .4 The decision to perform a biopsy should be based on whether treatment is being considered, taking into account the estimated duration of infection, probability of disease progression, willingness to undergo a biopsy, motivation to be treated, and availability of non-invasive tools to assess liver fibrosis.12 The recently developed transient elastography has improved our ability to non-invasively define the extent of fibrosis in HCV persons.5
Careful evaluation of parameters associated with disease progression is mandatory to assess the actual need for antiviral treatment.4 Indeed, it is really impossible to suggest antiviral therapy in all HCV carriers, as the costs would be exceedingly high, due to the high number of HCV patients with PNALT. Data from the literature indicate that the main factors of progression are male gender, advanced age, severe fibrosis, ALT flares, and steatosis.1-2
Cost/benefit might be particularly favourable in:
Young patients, having high rate of SVR (e.g. females, low viral load, HCV genotype non-1, etc).
Middle age patients with ‘significant’ liver disease and/or co-factors of progression of liver damage, thus at risk of developing more severe liver disease.12
The age issue has a critical role for decision making. Younger patients have a higher chance of achieving SVR and tolerating therapy better; they a have longer life expectancy, are often well motivated, usually have minimal disease and fewer contraindications. Thus, in this group decision to treat should be based more on expected response and motivation than on the severity of liver disease.
On the contrary, older patients respond less well to therapy, are more likely to have significant liver disease and/or co-factors, could experience more side effects and may be less motivated. Thus, in this group decision to treat should be based on the severity of liver disease and on the possibility of SVR.
A recent Italian Expert Opinion Meeting suggested the following recommendations:12
HCV carriers with PNALT may receive antiviral treatment with PEG-IFN plus RBV using the same algorithms recommended for HCV patients with abnormal ALT.
Decision making should rely on individual characteristics such as HCV genotype, histology, age, potential disease progression, probability of eradication, patient motivation, desire for pregnancy, co-morbidities, co-factors, etc.
Treatment might be offered without liver biopsy in patients with a high likelihood of SVR (e.g. age <50 years + non-1 HCV genotype + low viral load), in the absence of co-factors of poor responsiveness.
Inpatients aged 50–65 years, and in those with a reduced likelihood of achieving a response, biopsy may be used to evaluate the need for therapy, with treatment being recommended only for patients with more severe fibrosis and higher possibility of SVR. Biopsy and therapy are not recommended in the elderly (>65-70 years).
In patients who are not candidates for antiviral treatment, follow-up may be continued, and ALT should be monitored every 4-6 months. Avoidance of alcohol and obesity may be strongly recommended.12 It is not clear whether these subjects should be routinely offered anti-HBV vaccine, given the risk of disease progression in the case of HBV infection.12 Antiviral treatment should be re-considered in the case of ALT flares, US abnormalities or platelet count decrease. Repeated measurements of serum HCV RNA to evaluate disease progression is not recommended.1, 9, 11, 12.
Warfarin is the most commonly used oral anticoagulant and has established efficacy for more than 50 years for the prevention of thromboembolic events, but its use is limited by fear of bleeding, drug-drug and drug-food interactions, and routine monitoring of international normalized ratio (INR). In patients with atrial fibrillation (AF), warfarin prevents 64% of strokes in research studies but the real-world effectiveness drops to 35% because of various factors leading to its suboptimal use.1 In October 2010 the United States (US) Food and Drug Administration (FDA) approved Pradaxa capsules (dabigatran etexilate) as the first new agent to prevent stroke and systemic emboli in patients with non-valvular AF. In this article we will discuss some of the evidence for and against the use of dabigatran.
In the RE-LY study2 (Randomized Evaluation of Long-term Anticoagulant Therapy), high-dose dabigatran (150mg twice a day) was found to be superior to warfarin for the prevention of stroke and systemic emboli, required no routine INR monitoring, and had few food and drug interactions. James Freeman and colleagues,3 using data from the RE-LY trial, found that high-dose dabigatran (150mg twice a day) was the most efficacious and cost-effective strategy compared with adjusted-dose warfarin among adults older than 65 with AF.
Dabigatran has been shown to specifically and reversibly inhibit thrombin, the key enzyme in the coagulation cascade. Studies in healthy volunteers4 and in patients undergoing orthopaedic surgery have indicated that dabigatran has a predictable pharmacokinetic/pharmacodynamic profile, allowing for a fixed-dose regimen. Peak plasma concentrations of dabigatran are reached approximately two hours after oral administration in healthy volunteers, with no unexpected accumulation of drug concentrations upon multiple dosing. Excretion is predominantly via the renal route as unchanged drug. Dabigatran is not metabolized by cytochrome P450 isoenzymes. Though use of dabigatran for non-valvular AF and venous thromboembolism (VTE) is gaining practice,5 it remains far from being the standard of care.
What are the concerns with use of dabigatran? In the RE-LY study the INR control was relatively poor (64% TTR (time in the therapeutic range)) but, probably more importantly, the relationship between events and individual’s INR control was not reported. The use of centre’s time in therapeutic range (cTTR) in the RE-LY study as a surrogate for INR control may not truly reflect TTRs for individual patients. Also in RE-LY study, randomization was stratified for centre and by the centre-based analyses, and the quality of oral anticoagulant services was the basis for the comparisons in this report. A subgroup analysis6 concluded that relative effectiveness of dabigatran versus warfarin was mainly seen at centres with poorer INR control. For example, Swedish centres had good TTR and the relative effectiveness and safety of dabigatran was virtually the same as with warfarin; thus, it is only the price difference that counts. It also highlights how local standards of care affect the benefits of use of new treatment alternatives and hence further limits the generalizability of any ‘overall average’ cost-effectiveness of dabigatran, raising the question that if an intervention does not do more, why should a payer pay more for it? There are several other factors that could impact on the cost-effectiveness7 of dabigatran such as patient medication adherence, dosing frequency, and the potential effect of new efficient methods of warfarin management improving INR control by patient self-testing.
The other shortcomings of dabigatran include lack of antidotes when patients do bleed and lack of any alert to physicians that patients are not compliant with dabigatran (INR serves this purpose for warfarin). Additionally, in the RE-LY trial, dabigatran was used twice daily thus raising compliance issues compared to once daily warfarin (the rates of discontinuation of dabigatran were higher at 15% and 21% at one and two years, respectively); 11.3% reported dyspepsia (twice the rate of warfarin group); high rate of gastrointestinal bleed compared with warfarin; patients in the dabigatran cohort were at slightly higher risk of myocardial infarction (not sure how it will translate in real world practice); and contraindication of dabigatran in severe renal dysfunction raises some more questions about its use and cost effectiveness. In addition, the RE-LY trial excluded patients who had: contraindications to anticoagulation, severe heart-valve disorder, stroke within 14 days or severe stroke within six months before screening, a condition that increased risk of haemorrhage, creatinine clearance of less than 30ml per minute, active liver disease, and pregnancy. Clinicians will need to use their judgement to weigh and balance the risk for bleeding with this new agent in a setting of an acute stroke versus the risk of having another ischaemic stroke in someone with AF if not given anti-coagulation therapy immediately. Safety and efficacy at extremes of body weight is not well established with current FDA approved doses of dabigatran either.
In summary dabigatran is a very exciting new agent with significant advantages over warfarin. However, in view of dabigatran’s higher non-adherence rate and greater risk of non-haemorrhagic side effects, patients already taking warfarin with excellent INR control have little to gain by switching to dabigatran.1 Until more studies and post-marketing data become widely available, we should advocate tight INR control for which there is a wealth of evidence for benefits, and promote strategies to improve the management of therapy with warfarin.
Chronic pain, arbitrarily defined as that lasting longer than six months, is a clinical, social, and economic problem. It is often accompanied by feelings of low mood and despondency.
Whether chronic pain induces clinical depression or depression initiates psychosomatic pain (through physiological mechanisms) is difficult to prove. The burden of illness increases when patients suffer from both. Financial hardship and medical costs affect the quality of life which leads to difficulties in coping and further decreased functioning, making the treatment of both conditions more complicated. Therefore, better recognition, assessment, and treatment of comorbid pain and depression should, at least in theory, lead to better outcomes.
Pain is broadly categorized into three groups: nociceptive (any painful stimulus), neuropathic (for example, diabetes), and psychogenic. Nociceptive pain occurs with direct noxious stimuli. Neuropathic pain is a result of disease or injury to the nervous system or spinal cord. Psychogenic pain has no discernible physical origin. Although the precise physiological mechanisms are not entirely understood, there are two basic categories of sensory neurones. The first type is myelinated and fast conducting; the second is unmyelinated and slow conducting.
Acute pain which follows damage to tissue (an ankle sprain, for example) is usually correlated with hyperalgesia (an increase in the pain elicited by a noxious stimulus and felt as a sharp, burning sensation) and allodynia (‘other’ pain evoked by a normally innocuous stimulus) and serves to protect the injury from further trauma while allowing the damage to be repaired.
Depression is often a chronic disorder and though its symptoms may be alleviated by appropriate medication and other therapies, physical complaints tend to be more intractable. For example, fibromyalgia (FM), a syndrome characterized by widespread muscle pain and generalized tender points, is often associated with major depressive disorder.1 However, although the vast majority of patients with fibromyalgia do not meet criteria for a psychiatric disorder, psychological symptoms are common. In a randomized controlled trial of primary care patients with musculoskeletal problems and depression, antidepressant medication followed by a self-management pain programme led to improvement in both.2 The tricyclic antidepressant amitriptyline was traditionally used usually in small doses, to treat pain, with moderate success. In addition to its own intrinsic analgesic effect amitriptyline appears to enhance the effects of opioid analgesia. Other antidepressants are now in vogue; for example, duloxetine, a serotonin (5-HT)/noradrenaline (NA) reuptake inhibitor, is sometimes used for diabetic neuropathic pain.
Of the numerous neurotransmitters at least two, namely 5-HT and NA, may prove to be one common link between depression and pain. Both serotoninergic and noradrenergic pathways ascend from subcortical areas (brainstem, hypothalamus and thalamus) to the whole neocortex and mediate emotional and physiological responses.3 Their pathways descend the spinal cord and suppress nociceptive inputs. Serotoninergic cell bodies located in the raphe nucleus in the brainstem, and noradrenergic neurones located in the locus coeruleus (also in the brainstem) send projections to various parts of the brain involved in the control of mood, appetite, sexual activity, attention and concentration. Theoretically at least, a dysfunction at the level of the serotoninergic and noradrenergic neurons could affect both ascending and descending pathways resulting in the psychological and physically painful symptoms of depression. Neurotransmitters may open or close the ‘gate’ on perception of painful stimuli. Therefore adrenergic and serotoninergic pathways from the brainstem to the spinal cord will inhibit incoming painful stimuli. This is perhaps an oversimplification as some sensory fibres enter via the ventral spinal roots.
The hypothalamic pituitary axis (HPA) is probably also involved. The hypothalamus, which synthesises and secretes neurohormones, has a wide range of physiological functions including regulation of thirst and hunger, sexual behaviour, defence reactions such as fear and rage, and circadian rhythm: disturbances of all these functions are frequently seen in depressed or anxious patients. The HPA is also affected in patients with physical stress as well as major depression, as shown by increased levels of adrenocorticotropic hormone and cortisol in the plasma. Stimulation of the lateral areas of the hypothalamus produces a diffuse sympathetic discharge possibly because some areas of the hypothalamus control adrenaline and NA secretion. Prolonged stress associated with pain leads to depletion of central 5-HT and malfunction of other associated receptors.4
The hypothalamus and limbic system (whose boundaries are difficult to define) with its associated structures – the amygdala, hippocampus and septal nuclei, are involved in the mental and affective aspects of emotions. The amygdala, a cluster of nuclei in the medial temporal lobe, may have a role in the reciprocal relationship between pain and depression. The amygdala controls not only emotional behaviour but also memory. However, mixed results have been reported regarding the level of activity of the amygdala in response to pain.
Nociceptor afferents terminate within distinct regions of the dorsal horn and within the spinal cord, synapses are sites of considerable modification, hence the term ‘gate’ for the dorsal horn cells. The neurotransmitter for slow pain is believed to be substance P, and glutamate is the putative transmitter secreted by primary afferent fibres subserving fast pain.5
5-HT and NA neurotransmitter systems influence neuroplasticity in the brain. Most currently available antidepressants act through reuptake inhibition of either or both. Therefore, it would seem feasible to prescribe dual-action antidepressants when pain symptoms are associated with depression. However depressed patients with pain comorbidity are less likely to take antidepressant medications compared to those with depression alone. Also, individuals who develop pain or depression are at risk for developing the other, thus escalating the clinical management. Furthermore, when pain is refractory to treatment, it is associated with more depressive symptoms and worse depression outcomes, and vice versa. Depressive symptoms are very common in physically ill patients. Unfortunately, depression is often overlooked in pain patients because pain symptoms take priority or worse still, comorbid depression is not considered.
It is difficult to state with certainty whether or not unexplained pain is ‘psychological’. Such an assumption might be perceived as demeaning and patronizing to patients and the suggestion of providing cognitive therapy misinterpreted as him/her overplaying their reaction to pain or that the pain is ‘psychological’. Others do not like being labelled ‘psychiatric’, and are therefore reluctant to take antidepressants even when a physiological explanation is given. Pain perception involves physical and emotional factors and its primary function is to protect the organism from harm. It follows therefore, that pain thresholds and pain tolerance vary from individual to individual, and especially among patients with depression.
Antidepressants are frequently used in the treatment of depression and generalized anxiety disorders. Their use extends beyond these areas, however, and it is now accepted that antidepressants are efficacious in treating chronic pain syndromes in addition to their effects on psychological features such as low mood, inordinate guilt, or feelings of worthlessness. Because physical symptoms are often the main complaint in many depressed patients and pain is common as a presenting symptom, clinicians need to know about the dual use of antidepressants for both. Future antidepressants may involve neurotransmitters, other than 5-HT and NA, which could include dopaminergic pathways, opioid (antagonists of morphine-type drugs) receptors and the pentapeptides (enkephalins) which bind to these receptors.
In anticipation of new recommendations from the Institute of Medicine and others, it behooves physicians and healthcare providers to review their knowledge base concerning adequate vitamin D intake for fall and fracture prevention in the elderly. There is enough new data for the Institute of Medicine to consider a new Dietary Reference Intake, or DRI, for vitamin D.1 A recent review by Bischoff-Ferrari et al, of numerous randomized controlled trials of vitamin D supplementation in older persons, concluded that both falls and fractures could be prevented. In addition, a dose-response relationship suggested that the optimal supplementation dose is 700 IU to 1000 IU per day.2 Epidemiologic associations between low vitamin D status and various cancers has led some to recommend balancing risk and benefit of moderate ultraviolet light (UV) exposure against complete UV protection for prevention of skin cancer.3 Others have reviewed the epidemiologic evidence for vitamin D supplementation in treatment of hypertension and prevention of cardiovascular disease.4 These epidemiologic studies are tantalizing, yet the evidence is not sufficient to support a causal relationship in making decisions about vitamin D supplementation for the prevention of cancer and cardiovascular disease. I will limit my editorial comments to preventing falls and fractures.
I would suggest looking at potential short- and long-term risks as well as the benefits of any intervention. What evidence do we have for the risks of vitamin D use for prevention? One recent study using a single dose of 500,000 IU of vitamin D daily showed an increased relative risk of fractures,5 but the dose of vitamin D in that study was far higher than other randomized controlled trials. Bischoff-Ferrari et al reviewed documented cases of hypercalcaemia in the randomized controlled trials;2 those authors add that only one trial reported nephrolithiasis, the Women’s Health Initiative.6 It is noteworthy that only the self-reported vitamin D and calcium dose was determined in that study, not the vitamin D status of the subjects. My opinion is that hypercalcaemia is uncommon and its complications are rare.
Many interventions that are routinely recommended for the older person probably have higher risks than the 700 IU to 1000 IU of vitamin D per day suggested by the evidence. Medications for hyperlipidaemia are one case in point; antihypertensives are another. Both are considered relatively safe and effective in primary and secondary prevention of cardiovascular disease. The long-term risks of the supplementation of 700 IU to 1000 IU of vitamin D are not well known compared to those long-term risks associated with lipid-lowering drugs or antihypertensives. On the other hand, some older persons at increased fall risk have more immediate threats to their health from a fall or fracture than any long-term risks of vitamin D supplementation. Given the detrimental consequences of falls and fractures in the elderly, the risks of vitamin D supplementation may be worth it.
Cervicogenic headache (CH) refers to head pain originating from the pathology in the neck.1 However, the diagnosis of CH is still controversial 2,3 and it is often misdiagnosed. The author was called to consult a patient in a university hospital not so long ago. The patient was a 28-year-old female with a history of headache for six months. Her headache was described as continuous, dull and achy. It was mainly in the right side occipital and parietal areas. Sometimes she felt a headache behind the eyes. Her headache got worse periodically, several times a month, with nausea, photophobia, and phonophobia. She had no previous history of headache until a whiplash injury six months before. She had been diagnosed as having ‘migraine’ and ‘post-traumatic headache.’ She had used all anti-migraine medications. ‘Nothing was working.’ The patient was admitted into hospital because of ‘intractable headache.’
On the day when the author saw the patient, she was lying on the bed, with the room light turned off and a bed sheet covering her head and eyes. She was given Dilaudid, 2mg/h continuous intravenous (IV) drip, for the headache. The patient had normal results from magnetic resonance imaging (MRI) of the brain and lumbar puncture. According to the patient, no doctors had touched the back of her head and upper neck since admission. The author examined the patient and found a jumping tenderness over the right greater occipital nerve. The patient was given 2ml of 2% lidocaine with 40mg of Kenalog for the right greater occipital nerve (GON) block. Her headache was gone within five minutes and the Dilaudid drip was immediately discontinued. At follow-up four weeks later, the patient was headache-free. This was a typical missed case of CH (occipital neuralgia).
The concept of CH was first introduced by Sjaastad and colleagues in 1983.4 The International Headache Society published its first diagnostic criteria in 1998 which was revised in 2004.5 Patients with CH may have histories of head and neck trauma. Pain is often unilateral. Headache is frequently localized in the occipital area. However, pain may also be referred to the frontal, temporal or orbital regions. Headaches may be triggered by neck movement or sustained neck postures.6 Headache is constant with episodic throbbing attacks, like a migraine. Patients may have other symptoms mimicking a migraine such as nausea, vomiting, photophobia, phonophobia, and blurred vision. Due to the fact that there is a significant overlap of symptoms between CH and migraine without aura, CH is often misdiagnosed as migraine. CH is commonly found in patients after whiplash injuries, especially in the chronic phase.7
Anatomical studies have provided a basis for the pathogenesis of CH. The suboccipital nerve (dorsal ramus of C1) innervates the atlanto-occipital (AO)joint and dura matter over in the posterior fossa. Therefore, a pathologic condition of AO joint is a potential source for occipital headache. It has been reported that pain from the C2-3 and C3-4 cervical facet joints can radiate to the occipital area, frontotemporal and even periorbital regions. Even pathology in C5 or C6 nerve roots have been reported to cause headache.8 The trigeminocervical nucleus is a region of the upper cervical spinal cord where sensory nerve fibres in the descending tract of the trigeminal nerve (trigeminal nucleus caudalis) are believed to interact with sensory fibres from the upper cervical roots. This functional convergence of upper cervical and trigeminal sensory pathway sallows the bidirectional referral of painful sensations between the neck and trigeminal sensory receptive fields of the face and head.
Clinicians should always put CH in the list of differential diagnoses when they work up a headache patient. A history of head/neck injury, and detailed examination of the occipital and upper cervical area, should be part of the evaluation. Patients with CH may have tenderness over the greater or lesser occipital nerve, cervical facet joints and muscles in the upper or middle cervical region. Diagnostic imaging such as X-ray, computerized tomography (CT) and MRI cannot confirm CH, but can lend support to its diagnosis.
Treatment of CH is empirical. This headache does not respond well to migraine medications. Treatment should be focused on the removal of the pain source from the occipital-cervical junction. Initial therapy should be directed to non-steroidal anti-inflammatory drugs (NSAIDs) and physical therapy modalities.9 GON block is easy and safe to perform in office.10 It is effective for the treatment for occipital neuralgia and CH.11 The author followed a group of patients after GON block. The pain relief effects of GON block lasted an average of 31 days (unpublished data). If patients do not respond to GON block, diagnostic medial branch block and radiofrequency (RF) denervation of the upper cervical facet joints can be considered. Early studies have reported positive results.12 A subsequent randomized study found no benefit of RF. However, there were only six cases in each group,13 which significantly limited the power and validity of the conclusion from that study. Surgical treatment of cervical degenerative disc disease may offer effective pain relief for CH. Jansen14 reported 60 cases of CH patients treated mainly with C4/5, C5/6 and C6/7 nerve root decompression. More than 63% patients reported long lasting pain freedom or improvement (> 50%).
CH is common, with a prevalence of 0.4% and 2.5% in the general population. However, compared with other common pain conditions, CH is less studied. A Medline search found 6818 abstracts for migraine in 2009, whereas only 86 abstracts on CH were found. CH has not been well studied and it is often misdiagnosed. It is time to call for more attention.
Initial reports of Obesity Hypoventilation Syndrome (OHS) date back as early as 18891, but it was not until 1955 that Auchincloss2 and colleagues described a case of obesity and hypersomnolence paired with alveolar hypoventilation. Burwell3 coined the term Pickwickian syndrome describing the constellation of morbid obesity, plethora, oedema and hypersomnolence. Hypercapnia, hypoxaemia and polycythemia were described on laboratory testing. Obstructive Sleep Apnea (OSA) had not been described at that time and came to be recognized for the first time in the mid 1970s. With attention shifting to upper airway obstruction, hypercapnia began to get lesser emphasis and confusion began to emerge in describing OSA and OHS. The term ‘Pickwickian’ began to be used for OSA-related hypersomnolence in the obese patient regardless of the presence of hypercapnia. This confusion was finally settled by the American Academy of Sleep Medicine (AASM) in its published guidelines in 1999.4 The AASM statement identified that awake hypercapnia may be due to a predominant upper airway obstruction (OSA) or predominant hypoventilation (Sleep Hypoventilation Syndrome) easily distinguished by nocturnal polysomnography (PSG) and response to treatment. Both disorders are invariably associated with obesity and share a common clinical presentation profile.
Salient features of OHS consist of obesity as defined by a BMI > 30kg/m2, sleep disordered breathing, and chronic daytime alveolar hypoventilation (PaCO2 ≥ 45 mmHg and PaO2 < 70 mmHg). 4 Sleep disordered breathing, as characterized by polysomnography in OHS, reveals OSA (Apnea-hypopnea index [AHI]>5) in up to 90% of patients and sleep hypoventilation (AHI<5) in up to 10%.5 Daytime hypercapnia and hypoxaemia are the hallmark signs of OHS and distinguish obesity hypoventilation from OSA. Severe obstructive or restrictive lung disease, chest wall deformities and hypoventilation from severe hypothyroidism, and neuromuscular disease need to be excluded before a diagnosis of OHS is established. As obesity is becoming more prevalent in western society, this disorder has gained more recognition in recent years. However, patients with this syndrome may still go undetected and untreated. No population-based prevalence studies of OHS exist till date but, at present, can be estimated from the relatively well known prevalence of OHS among patients with OSA. Recent meta-analysis with the largest cohort of patients (n=4250) reported a 19% prevalence of OHS among the OSA population, confirming an overall prevalence of about 3 per 1000.6
Whilst transient rectifiable nocturnal hypercapnia is common in patients with OSA, awake hypercapnia in OHS appears to be a final expression of multiple factors. There has been a debate about BMI and AHI not being the most important independent predictors of hypercapnia in obese patients with OSA. More definitive evidence for the role of OSA, however, is suggested by resolution of hypercapnia in the majority of patients with hypercapnic OSA or OHS with treatment, with either PAP or tracheostomy, without any significant changes in body weight or respiratory system mechanics. Yet some recent studies have shown that nocturnal hypoxaemia and diurnal hypercapnia, persist in about 50% of such individuals even after complete resolution of OSA with CPAP or tracheostomy. This raises questions such as how good is AHI as a measure of severity of OSA?
It is intuitive to argue that obesity may exert its effect through mass loading of CO2 due to (increased production via) higher basal metabolic rate or reduced functional residual capacity on lung function. But why do only some severely obese patients with OSA go onto develop OHS? Is the pathophysiology driven by the severity of BMI? Whilst weight loss, particularly surgically-induced, clearly shows resolution of both OSA and hypercapnia7, the role of BMI as an independent factor for hypercapnia has been challenged by the fact that only a small fraction of severely obese patients do in fact develop chronic diurnal hypercapnia. More importantly, not only can PaCO2 be normalized in a majority of patients without weight loss and with positive airway pressure therapy (PAP), but awake hypercapnia can develop even at lower BMIs among the Asian population. Some investigators have tried to explain the incremental role of BMI as follows. In situations where AHI is not a presumed independent predictor of nocturnal hypercapnia, potential pathophysiologic contributors can include pre-event (apnea or hypopnea) amplitude in relation to the post-event amplitude.8 Such inciting events for nocturnal hypercapnia may then be perpetuated in the daytime by factors such as AHI, functional vital capacity (FVC), FVC/FEV1, or BMI as shown in the largest pooled data to date.6 It has been shown that, for a given apnea/interapnea duration ratio, a greater degree of obesity is associated with higher values of PaCO2.9 However the same group of investigators, in another study, did not find any of these factors to be related to the post-event ventilatory response.8
Looking further at the breath by breath cycle, the post-event ventilatory response in chronic hypercapnia may relate to eventual adaptation of chemoreceptors perhaps in consequence to elevated serum bicarbonate known to blunt the ventilatory drive.10 Or it may relate to whole body CO2 storage capacity which is known to exceed the capacity for storing O2.11 With definite evolution in our understanding of hypercapnia among obese patients, these questions continue to dominate. Some of the more pressing ones include: are the predictors of daytime hypercapnia different from those of nocturnal hypercapnia in obese patients with OSA? An understanding of these facts can help us with the more important understanding of the associated morbidity and mortality from OHS and its correct management. In addition, what is the true effect of untreated OHS on mortality independent of the co-morbidities related to obesity and OSA? Can morbidities like cor pulmonale and pulmonary hypertension be reversed with treatment of OHS? How do we treat patients with OHS who fail CPAP/ BiPAP short of tracheostomy?
Bisphosphonates, which have been on the market for roughly a decade, have raised safety concerns in the past. Several case series and multiple individual case reports suggest that some subtrochanteric and femoral shaft fractures may occur in patients who have been treated with long-term bisphosphonates. Several unique clinical and radiographic features are emerging. Recent media spotlight in the United States (US), implying that long-term use of alendronate could cause spontaneous femur fractures in some women, has reignited the debate about the safety of bisphosphonates. The question posed: is the risk of bisphosphonate-associated fractures so great that treatment should be stopped?
Postmenopausal women with osteoporosis are commonly treated with the bisphosphonate class of medications, one of the most frequently prescribed medications in the US. While alendronate therapy has been shown to decrease the risk of vertebral and femoral neck fractures in postmenopausal osteoporotic patients, recent reports have associated long-term alendronate therapy with low-energy subtrochanteric and diaphyseal femoral fractures in a number of patients. In the past four years reports have been published implying that long-term bisphosphonate therapy could be linked to atraumatic femoral diaphyseal fractures.1, 2 According to two studies reported recently at the American Association of Orthopedic Surgeons 2010 Annual Meeting, an unusual type of bone fracture has been reported in women who have taken bisphosphonates for osteopenia and osteoporosis for more than four years.3, 4 The first report was published in 2005. Odvina et al5 reported on nine patients who sustained atypical fractures, including some with delayed healing, while receiving alendronate therapy. These authors raised the concern that long-term bisphosphonate therapy may lead to over-suppression of bone remodelling, an impaired ability to repair skeletal microfractures, and increased skeletal fragility. There have been other reports of "peculiar" fractures - i.e. low-energy femur fractures that are typically transverse or slightly oblique, diaphyseal, or subtrochanteric, with thickened cortices and a unicortical beak - in patients who have been on long-term bisphosphonate treatment.1-4, 6
In a small prospective study, Lane et al3 obtained bone biopsies from the lateral femurs of 21 postmenopausal women with femoral fractures. Twelve of the women had been on bisphosphonate therapy for an average duration of 8.5 years, and nine had no history of bisphosphonate use. They found that the heterogeneities of the mineral/matrix ratio were significantly reduced in the bisphosphonate group by 28%, and the crystallinity of the bone was significantly reduced by 33% (p < 0.05). The authors concluded that this suggested suppression of bone turnover, resulting in a loss of heterogeneity of the tissue properties, which may be a contributing factor to the risk of atypical fractures that we are starting to see. It is believed that long-term alendronate administration may inhibit normal repair of microdamage arising from severe suppression of bone turnover (SSBT), which, in turn, results in accumulation of microdamage. This process would lead to brittle bone and the occurrence of unexpected stress fractures, characteristically at the subtrochanter of femur. The typical presentation of these fractures consist of prodromal pain in the affected leg and/or a discrete cortical thickening on the lateral side of the femur in conventional radiological examination or the presentation with a spontaneous transverse subtrochanteric femur with typical features. The morbidity of atypical femoral fractures, particularly when bilateral, is high. Surgical intervention is generally required and healing may not be achieved for several years. Despite the lack of conclusive evidence of a causal relationship with bisphosphonate therapy, the current consensus is that treatment should be discontinued in patients who develop these fractures. In view of the high frequency of bilateral involvement, imaging of the contralateral femoral shaft with X-rays, MRI, or an isotope bone scan should be performed. MRI and bone scanning havegreater sensitivity than radiography for an incipient stressfracture. If lateral cortical thickening and/or an incipient stress fracture is seen, prophylactic surgical fixation should be considered. Suppressed bone formation in these patients provides a possible rationale for the use of anabolic skeletal agents, such as parathyroid hormone peptides, but at the present time the efficacy of this approach remains to be established. Parathyroid hormone not only has activated bone-formation markersin trials in humans but has also enhanced the healing of fracturesin studies in animals.
The question of whether these fractures are causally linked to bisphosphonate therapy is widely debated but as yet unresolved. Consequences of long-term suppression of bone turnover include increased mineralization of bone, alterations in the composition of its mineral/matrix composite and increased micro damage, all of which may reduce bone strength. Whilst these lend biological plausibility to a causal association, however, they do not constitute direct evidence. The bilateral fractures seen in many patients corroborate the suspicion that patients with bisphosphonate-associated stress fractures carry some other risk factor in addition to taking the drug. Microfractures,inadequate mineralization, and outdated collagen are some of the candidate causes. However, until further studies can provide definitive evidenceof bisphosphonate-associated fractures, it is premature to attributeatypical fractures to over-suppression of bone turnover alone,while disregarding secondary and patient-related factors. Many experts believe that prolonged suppression of bone remodelling with alendronate may be associated with a new form of insufficiency fracture of the femur. Studies have not shown if the entire class of medications produce a similar result, but patients who have been treated with any bisphosphonate for an extended period of time should be considered at risk.
A wealth of information from well-designed clinical trials clearly shows that, as a class, bisphosphonates are highly effective at limiting the loss of bone mass, deterioration of bone micro architecture, and increased fracture risk that occur with aging. The benefit/risk ratio of bisphosphonate therapy in patients at high risk of fracture remains overwhelmingly positive because of the very low incidence of atypical femoral fractures. Current estimates suggest that alendronate prevents 200 clinical fractures if 4000 women are treated over three years and will cause one femur fracture over the same course of time.7 A study by Schilcher et al8 found that the incidence density of a stress fracture for a patient on bisphosphonate was 1/1000 per year (95% CI: 0.3-2), which is acceptable considering that bisphosphonate treatment is likely to reduce the incidence density of any fracture by 15/1000.9 Nevertheless, limitation of treatment duration to five years in the first instance, with evaluation of the need to continue therapy thereafter, may be appropriate in clinical practice. The Fracture Intervention Trial Long-term Extension (FLEX), in which postmenopausal women who had received alendronate therapy for five years were randomised to continue receiving alendronate for five additional years or switched to placebo, provided clinical evidence that the effect of bisphosphonate therapy was maintained after discontinuation of therapy.7, 10 Women who are being treated with bisphosphonates should take a drug holiday if they have been on them for five years. Patients in whom bisphosphonate therapy is discontinued should typically follow up with bone mineral density measurements at 1- to 2-year intervals, with some experts advocating periodic measurement of biochemical markers of bone turnover to detect loss of the antiresorptive effect. Additional research is necessary to determine the exact correlation between the use of bisphosphonates and spontaneous or low-energy trauma fractures.
Contrary to the period in 1993, when the United States (US) President Bill Clinton failed to gain any traction on his healthcare reform, the current President, Barack H Obama, has been able to embark on historic healthcare reform. This is because major stakeholders agree that US healthcare is in crisis and requires major reform. Businesses and consumer groups have joined the insurance industry, pharmaceutical industry, and physician groups in asking for this healthcare reform that would blunt the rapidly escalating costs and provide healthcare for all Americans. While the number of uninsured Americans increased from 39.8 million in 2001 to 46.3 million in 2008, the National Health Expenditure (NHE) grew from 7.2% of the gross domestic product (GDP) in 1970 to 16% in 2005 1. This growth is projected to climb further to 19.5% in 2016. To put these figures into perspective, the US is projected to spend almost $13 trillion on healthcare over the ten years from 2010 to 2019 if the current trend continues2. Add to that the number of bankruptcies filed in the US due to healthcare expenses. Himmelstein and colleagues have recently demonstrated that of all the bankruptcies filed in the US in 2007, 62.1% were due to medical reasons as opposed to 46.2% in 2001 and only 8% in 19813 .
Hence, there is no longer any debate about ‘whether there is a problem’ but rather ‘what can be done to fix this problem’. How to fix it has been, and will continue to be, a highly contentious issue that will pitch Democrats against Republicans even after the passage of the pending legislation. Some of the key elements President Obama had identified as his basic objectives in healthcare legislation, that he is expected to sign into law by the end of 2009, include:
Providing universal coverage to all Americans and requiring employers to provide health insurance to their employees.
Barring insurance companies from providing policies that would exclude patients with ‘pre-existing conditions’ thereby ensuring uniform health insurance premiums for all Americans irrespective of their health status.
Providing a one-stop marketplace for national health insurance exchange to allow consumers to compare and shop for different insurance plans.
Promoting the use of electronic medical records and the practice of evidence-based medicine.
Introducing a government-run health insurance option providing low cost, affordable health insurance that would directly compete with the private insurance industry.
This last provision, often called the ‘Public Option’, has been regarded by its opponents as an indication of how the federal government would grab political power and control the lives of all Americans. Some have gone as far as to say that the Administration is trying to introduce a ‘socialist system’ and set up ‘death panels’ to decide the fate of terminally ill Americans.
The raging debate in both Houses of Congress (House of Representatives and US Senate), since the introduction of the legislation early this year, has been highly partisan and, at times, acrimonious. The primary debate will continue to target accessibility and the ‘Public Option’ on one hand and affordability and deficit reduction on the other. Additionally, fundamental ideological issues of the rights of women to their health (read right for abortion) and accusations of ‘socialist medicine’ (read demand for free market healthcare with little or no government oversight) will continue to fuel this debate well after the legislation has been enacted into law. At the time of writing it is clear that President Obama’s deadline of this year will not be met.
On 7th November 2009, President Obama won a major battle in this war when the House of Representatives passed the ‘Affordable Healthcare for America Act’. The vote was 220-215 and essentially along party lines with the Democrats and only one Republican voting for this legislation. According to Representative John Dingle, the 83-year-old Michigan lawmaker who had introduced national health insurance in every congress since 1955, this 1990-page bill provides coverage for ‘96% of Americans and offers everyone, regardless of health or income, the peace of mind that comes from knowing that they will have access to affordable healthcare when they need it’. However, in the run-up to the final vote, conservatives from both political parties joined hands to impose tough restrictions on abortion coverage that will continue to be a divisive issue throughout the legislative process 4 .
President Obama won the second major victory on 21st November 2009 when the Democrats (with the help of two independents) in the US Senate pushed the legislation past a key hurdle, despite vocal Republican opposition, with 60-39 votes. Sixty votes are needed in the US Senate to prevent ‘filibuster’ or an indefinite discussion on any bill 5 . With this vote the bill will now be debated in the Senate. Table 1 highlights some of the important features of the two bills:
Table 1: Important features of the Senate Bill and House Bill.
Senate Bill
House Bill
Cost*
$848 billion
$1.02 trillion
Projected deficit savings*
$127 billion
$104 billion
New patients*
31 million
36 million
Protection against generic drugs**
12 years
12 years
Government sponsored program
New plan to compete with private plans; government to negotiate payment rates.
New public plan through insurance exchanges; government to negotiate payment rates.
Projected reduction in Medicare growth***
$400 billion
$400 billion
How is it paid for?
Fees on insurance companies, pharmaceutical and medical devices industries. A new payroll tax and 5% tax on elective cosmetic surgery.
$460 billion over the next decade from income tax on individuals making over $500,000 and couples making over $1 million per year.
* These are the estimates for the 10-year-period (2009-2019) from the Congressional Budget Office 6 .
** Both bills would protect biological drugs (made from living organisms rather than chemical
compounds) from competition from generic drugs.
*** The reduction in Medicare spending is non-binding and future Congress can restore these cuts.
In this national debate, two well-known medical centres in the US, the Mayo Clinic of Minnesota and the Cleveland Clinic in Ohio, have frequently been cited as examples that could perhaps be emulated to deliver quality care in an efficient and cost-effective fashion. Both centres practise a ‘medical home’ concept based on a coordinated team approach that was introduced by the American Academy of Paediatrics in 1967. This has been further refined into the ‘patient-centred medical home’ by the American College of Physicians (ACP), American Academy of Family Physicians, and the American Academy of Paediatrics in 2007. This concept is exceedingly important for the management of chronic illnesses because the cost associated with unmanaged chronic conditions is astronomically high. It is estimated that 45% of the US population has a chronic medical condition. Amongst Medicare recipients aged 65 and above, 83% have at least one chronic health problem and almost 25% have at least five co-morbidities. Whereas the current system rewards acute care, it generally does not reimburse preventative care, chronic care management or active integrated inter-specialty management 7. A medical home provides expanded primary care that is personalized, focuses on prevention, actively involves patients in making decisions about their care and helps coordinates all of their care.
One of the deficiencies of the proposed reform is the absence of any tort reform. For physicians in the US the threat of a malpractice lawsuit is real. Without legislative relief, ‘defensive medicine’ will take a significant chunk out of healthcare dollars. Estimates suggest that savings accrued from such legislation could account for 20-25% of the NHE and may be prudently used to reduce the healthcare costs. President Obama’s outright rejection to consider tort reform in his address to the American Medical Association in June is very unfortunate and runs counter to his passionate plea to help reduce medical waste. Some of the important discussions that will take place relate to the need to revamp the physician reimbursement schedules and empower the Medicare Payment Advisory Commission to enhance primary care reimbursement, establish incentives to implement health information technology (including electronic medical records), and mandate the use of evidence based medicine and established protocols to stem the tide of escalating costs with ‘pay for performance’ and other quality measurements 8.
Healthcare reform must also address the physician shortage issue. Several studies, including those from the Institute of Medicine and the American Association of Medical Colleges (AAMC), have indicated a growing physician shortage particularly in Primary Care. In order to address this rising tide of physician shortages the Balanced Budget Act of 1996, that froze the number of reimbursable training positions at the 1996 level, needs to be revisited. As a preliminary target ACP and AAMC have recommended that the availability of Medicare-funded training positions in adult primary care specialties be increased by 3000 each year for the next 15 years 9-11.
From here on I suspect a bruising legislative debate (and drama) will continue with passion and, undoubtedly, some acrimony. Since mid-term elections are coming up in 2010, both the parties are jockeying their position as best as they can. To end the ‘filibuster’ the Democrats will need, yet again, 60 votes to pass the bill in the Senate. However that is not guaranteed at this time since many Democratic senators continue to have concerns and Republicans have made it clear that they will do whatever they can to derail this initiative. Hence further deliberation, particularly in the Senate, will entail significant manoeuvring and arm-twisting, passionate appealing, horse-trading, and perhaps additional funding for select senators to achieve 60 votes. However, in the end there will be a bill from the Senate, perhaps in mid to late January 2010. Subsequently, a conference committee will hammer out the differences in the two bills that can be presented to both houses for final passage and submitted to the President for signature. I believe the President will have the bill on his desk for signature at the end of January or early February 2010.
The huge disease burden and vast health inequalities and given that one in six person in the world is an Indian on the one hand, and the country’s recent economic rise and its intellectual capital in-country and also overseas on the other hand, has created the Indian conundrum for global health challenges. India is now both: the problem – as it contributes to the challenges, and the solution – if it can mobilise its resources. This short paper will expand on the theme and especially explore how the Indian Diaspora in the UK can help to ensure good health and affordable health care to the needy.
The problem: Global health challenges
The World Health Organisation (WHO) has established the ten facts on the global disease burden (Table) (1) and its 2008 report: Primary Care: Now More than Ever (2) has identified the five global challenges in ensuring health care (Box).
TABLE : FACTS ON THE GLOBAL BURDEN OF DISEASE (Source: www.who.int)
1. Around 10 million children under the age of one year die each year
2. Cardiovascular diseases are the leading cause of death worldwide
3. HIV/AIDS is the leading cause of adult deaths in Africa
4. Population ageing is contributing to rise in cancer and heart disease
5. Lung cancer is most common cause of deaths from cancer in the world
6. Complications of pregnancy account for 15% of deaths in women of reproductive age worldwide
7. Mental disorders such as depression are among the leading causes of disability worldwide
8. Hearing loss, vision problems and mental disorders are the most common causes of disability worldwide
9. Road traffic injuries are projected to rise from the ninth leading cause of death worldwide in 2004 to fifth in 2030
10. Under-nutrition is the underlying cause of death for at least 30% of children under five years of age
BOX: FIVE COMMON SHORTCOMINGS OF HEALTH-CARE DELIVERY (Source: WHO Report 2008)
1. Inverse care. People with the most means – whose needs for health care are often less – consume the most care, whereas those with the least means and greatest health problems consume the least. Public spending on health services most often benefits the rich more than the poor in high- and low income countries alike.
2. Impoverishing care. Wherever people lack social protection and payment for care is largely out-of-pocket at the point of service, they can be confronted with catastrophic expenses.Over 100 million people annually fall into poverty because they have to pay for health care.
3. Fragmented and fragmenting care. The excessive specialization of health-care providers and the narrow focus of many disease control programmes discourage a holistic approach to the individuals and the families they deal with and do not appreciate the need for continuity in care. Health services for poor and marginalized groups are often highly fragmented and severely under-resourced, while development aid often adds to the fragmentation.
4. Unsafe care. Poor system design that is unable to ensure safety and hygiene standards leads to high rates of hospital-acquired infections, along with medication errors and other avoidable adverse effects that are an underestimated cause of death and ill-health.
5. Misdirected care. Resource allocation clusters around curative services at great cost, neglecting the potential of primary prevention and health promotion to prevent up to 70% of the disease burden. At the same time, the health sector lacks the expertise to mitigate the adverse effects on health from other sectors and make the most of what these other sectors can contribute to health.
As would be expected the situation in India confirms these facts and challenges. There is a lot of health information for India in the public domain (1,3) although the nature and detail could be improved. Like in many other developing countries the life expectancy has increased and although improved health has led to further economic welfare in India, the country is currently experiencing the triple whammy of the disease burden due to communicable (CD) and non-communicable (NCD) diseases and injuries. Communicable diseases account for about 38% of the disease burden – not only are the ‘traditional’ CDs like malaria rife, the country has seen a big increase in new infections like HIV/AIDS. NCDs including diabetes, heart disease and cancers account for 53% percent of all deaths in the age group 30-59 years in 2005. It is projected that by 2015, 59% of the total deaths in India would be due to NCDs. With 47% of men and 15% of women being regular consumers, tobacco remains the single biggest preventable risk factor. Whilst the developed world is seeing a reduction in deaths due to road traffic accidents, these injuries are projects to rise by nearly 150% in SE Asia region including India. This health picture is compounded by the lower human development, largely due to poverty – a situation that has not been addressed despite recent economic successes, as bemoaned by Amartya Sen (4):
“Yet even a hundred Bangalores and Hyderabads will not on their own solve India’s tenacious poverty and deep seated inequality. The very poor in India get a small- and basically indirect- share of the cake that information technology and related developments generate. The removal of poverty, particularly of existing poverty, calls for more participatory growth on a wide basis, which is not easy to achieve across the barriers of illiteracy, ill-health, uncompleted land reforms and other sources of severe societal inequality. The process of economic advancement cannot be divorced from the cultivation and enhancement of social opportunities over a broad front. “
India’s health sector is diverse and includes not just modern medicine but also a range of traditional systems like Homeopathy, Ayurveda and Unani. The overall governmental expenditure on health has been rather low (0.9% of GDP, whilst the total expenditure is about 5%), with 75% of it being borne by patients and, over 90% of the latter being out of pocket due to a lack of organized insurance. Being sick has meant being bankrupt for a substantial number of rural poor Indians. There is a burgeoning private sector that is driving the specialist end of the provision, with rather poor and often outdated primary care services. The cost of health care keeps going up with little or no assurance that services are appropriate or safe, and the regulatory mechanisms are few. The bottom line in India is that good health happens by chance and good quality health care is a privilege and not a right.
The solution: Add value to planned developments in India
Although it may not seem like it, there is a comprehensive plan to develop national health policy and address some of the fundamental challenges, the following are some of the highlights stated by the Government (1,5):
1. “Commitment of the Government to increase public health share to at least 2% of GDP
2. Efforts to develop regulatory frameworks and options for alternative financing mechanisms including insurance
3. National Rural Health Mission and Reproductive & Child Health Programme. Integrated Management of Newborn and Childhood Illnesses (IMNCI) pre-service and home-based newborn care activities initiated. Multi-skilling of health providers for Emergency Medical Obstetric Care. Introduction of Accredited Social Health Activists (ASHAs). Increased attention to women’s health in national Schemes
4.Increased commitment to health system strengthening, use of capacities in other sectors, and effective partnerships. Enhanced nursing profile and increasing nursing autonomy in practice.
5.Public health education, job descriptions and career paths under review; expanding efforts for multi-disciplinary and multi-sectoral approaches; establishment of the Public Health Foundation.
6.Ongoing capacity building to deal with international agreements and strengthening of the World Trade Organization (WTO) cell in the Union Ministry of Health.
7.Increased commitment and investments, and significant progress in the control and/or elimination of communicable diseases like yaws, leprosy, tuberculosis and several vaccine preventable diseases.”
Overall, there is action at all levels: national, state, institutional and individual and across the range of necessary issues: policy, regulation, resourcing, provision and capacity building by both, public and private sectors. The two key questions for the Indian Diaspora, however, are:
Can we help accelerate these developments?
How can we ensure that these become sustainable?
There is no denying that many individuals from the UK have been, and continue to be, involved in various efforts back in India; be it fundraising, community development, school education or direct clinical provision. In addition, there are various organisations like BIDA, IMA and BAPIO who have potentially the infrastructure albeit their focus has largely been on activities within the UK. The UK Government has recognised its responsibility in supporting international efforts as part of the recent Health is Global Strategy (6), and this provides another timely opportunity. From both, philanthropic and business angles, it makes sense to create a robust Indo: UK collaboration around health and education given common heritage and needs and opportunities on both sides. In addition to working on discrete areas like patient safety (7) or public health capacity building (8) an important first step would be to create a mechanism for regular dialogue in order to identify and progress priority projects of mutual interest.
Conclusions
India has come a long way since its independence and given its size and complexity continues to have ongoing challenges (9, 10,11). It is essential to recognise that health is not a consumptive sector, but by creating healthy people, free from illnesses, can be a productive sector. The basic message of this paper is that being a physician in India in the 21st century is both, a privilege – given the ancient history and traditions and recent economic successes, and a responsibility- given that despite being the world’s largest democracy and an economic superpower there are vast health inequalities and lack of safe, affordable basic health care to a large proportion of the citizens in India.
At the time of writing this paper, there is intense debate about the NHS in the American press triggered by President Obama’s attempts to reform US health care. No doubt whilst things could be better in the NHS, there is still a lot that the world, both developed and developing nations, can learn from the NHS (12, 13) . Indeed best practices, regardless of whether they come from US, UK or anywhere else could, and should, be adapted to support ongoing efforts in India.
Severe pulmonary
hypertension (PH) is a rare disorder characterized by multifactorial
etiology and shared pathophysiology. The belief that primary pulmonary
hypertension (PPH) is an idiopathic variety mostly affecting younger
women may still be held by some. However, PH has often been reported
in overweight and obese individuals and postmenopausal women.1
Earlier studies have also suggested that combination of obesity and
higher altitude favors the development of pulmonary arterial hypertension.
Hypercapnic acidemia and increased total blood volume have been implicated
in this group of patients. Pulmonary artery systolic pressures (PASP)
greater than 40 mmHg is found in 6% of otherwise normal individuals
age 50 years or older and in 5% of individuals with a BMI greater than
30kg/m2 . 2
Overall,
the widely held view has been that alveolar hypoxia is the main pathophysiologic
cause of vasoconstriction in obese patients living at sea level or higher
altitudes. In 1947, Motley et al demonstrated that breathing a gas mixture
containing 10% oxygen induced a rise in pulmonary artery pressure (PAP).3Papers
dating back more than three decades have documented increases in PAP
associated with hypoxemia related to sleep disordered breathing (SDB).
It is well known that apneic episodes during sleep are associated with
transient elevations in PAP, which return to baseline when breathing
resumes after relief of obstruction. Earlier studies suggested
that daytime hypoxemia attributable to abnormal lung function was the
main cause of pulmonary hypertension in patients with sleep apnea. Whether
transient hypoxemias and associated elevations in PAP with obstructive
events during sleep are adequate to produce daytime resting “fixed”
pulmonary vascular disease, or whether daytime hypoxemia is required
remains unclear. It is also less certain whether daytime pulmonary
arterial hypertension also occurs in OSA patients without underlying
pulmonary or cardiac disease. Additionally, studies have shown
that the severity of SDB as measured by apnea-hypopnea index (AHI) and
the PAP elevations often fail to correlate.
Sajkov et
al 4 were amongst the first to demonstrate that hypoxemia
in PH patients with obstructive sleep apnea syndrome (OSAS) could not
be explained by impairment of lung or cardiac function, BMI and smoking
history. However, most of the studies that have tackled this question
(including the one done by Sajkov) have used echocardiography based
pulmonary artery pressures and the few that have used the gold standard
Right heart catheterization (RHC) used a definition of mean pulmonary
artery pressure (mPAP) >20 mmHg. At present, pulmonary arterial hypertension
is defined as a mean PAP greater than 25mmHg at rest or 30 mmHg with
exercise, as measured by RHC. The largest such study found PAH in 17%
patients but it also included some patients with chronic obstructive
pulmonary disease (COPD).5
Smaller series of patients with OSA but no clinical history of COPD
have reported daytime PAH as measured by RHC in 20-42% patients.
6, 7
Thus, despite
acute nocturnal increases in PAP associated with obstructive apneas,
proof that OSA causes PH has been limited by other co-morbidities related
to obesity. The three biggest confounders making this issue difficult
to be explored are associated COPD in OSAS patients (overlap syndrome),
Obesity Hypoventilation Syndrome (OHS) and underlying concomitant left
ventricular dysfunction in patients with OSA. OHS as defined at present
is characterized by combination of obesity (BMI ≥30kg/m2)
and chronic daytime hypercapnia (PaCo2 >45 mmHg); and sleep disordered
breathing in the absence of other known causes of hypercapnia.8
PH has been shown to be more frequent and mean PAP higher in patients
with OHS or the overlap syndrome when compared to patients with pure
OSAS only. 9 Elevated mPAP associated with higher pulmonary
capillary wedge pressure (PCWP) from underlying elevated left
ventricular end-diastolic pressure and in some studies apnea associated
have been other potential confounders.10 Other difficulties
related to exploring this issue are technical concerns regarding non-invasive
measurement of pulmonary artery pressure in obese OSA patients and difficulties
in identifying suitable controls i.e, obese patients with PH and without
OSA. Studies are also needed to investigate the role of humoral vasoactive
factors like natriuretic peptides, nitric oxide or norepinephrine and
individual genetic predisposition to account for different remodeling
responses to hypoxia in the pulmonary circulation. In OSAS patients
no neutrally mediated effect of apneas on PAP has been demonstrated.
PH seen
in association with OSA is generally regarded as mild and can be attributed
to elevated pulmonary vascular resistance (PVR) because cardiac output
and PCWP are normal atleast at rest. Although the association between
left sided-heart disease and OSA is widely accepted, most studies of
OSA patients with PH do not differentiate between pre-capillary (PAH)
and post-capillary pulmonary hypertension (PVH). Additionally a good
proportion of the studies do not even report PCWP.6, 9 while
some explain higher PAP on the basis of PCWP alone.
Elevations in both PCWP and PVR have been reported to contribute to
PH in patients with OHS. A recent study of referred patients who met
the WHO criteria for PAH from Duke University reported PCWP> 15 mmHg
in 25% of the patients. These patients were predominantly obese (58%)
and all had normal LVEF%. 11
In ourretrospective analysis of 8254 patients who underwent
RHC for suspected PH, mean Right atrial pressure, mean PA diastolic
pressure, mean PCWP and mean cardiac output increased proportionately
with increase in BMI regardless of the underlying contributory disease
process. 12
The debate
about whether OSA alone can be a cause of sustained pulmonary arterial
hypertension continues, but based on the above literature, the latest
revision of the Clinical Classification of Pulmonary Hypertension identifies
SDB as a part of the category of respiratory disorders associated with
PH.13 The most direct evidence comes from observations that
treatment of OSA with continious positive airway pressure (CPAP)
may lower daytime PAP. OSA patients with PH seem to have increased pulmonary
vascular reactivity to hypoxia compared to patients without PH and CPAP
has been reported to decrease pulmonary vascular reactivity to hypoxia.14
In studies from Stanford as early as 1978, 50% reduction in PAP
was noted in six selected patients with OSA after tracheostomy. In a
recent randomized placebo-controlled cross-over trial of effective versus
sham CPAP in 23 patients with OSA, effective CPAP was associated with
decreases in echocardiographic measurements of PASP especially in patients
with PH or left ventricular diastolic dysfunction at baseline.
15 This trial was limited by baseline differences in obesity and
lung function between the two groups. Larger randomized studies are
needed to identify more definitively any sustained effects of CPAP therapy
on PH and right heart function and to better establish any role for
CPAP as one of the rapidly evolving therapeutic options for PH.
COMPETING INTERESTS
None Declared
AUTHOR DETAILS
ROOP KAW, MD, Assistant Professor of Medicine, USA
CORRESPONDENCE: DR ROOP KAW,
Cleveland Clinic Main Campus, A12, 9500 Euclid Avenue, Cleveland, USA. OH44197
Email: KAWR@ccf.org
References
Taraseviciute
A, Voelkel NF et al. Severe pulmonary hypertension in postmenopausal
obese women. Eur J Med Res.2006 May 5; 11(5): 198-202.
McQuillan BM,
Picard MH, Leavitt et al. Clinical correlates and reference intervals
for pulmonary artery systolic pressure among echocardiographically normal
subjects. Circulation 2001; 104: 2797-2802.
Motley HL, Cournand
A, Werko et al. The influence of short periods of induced acute anoxia
upon pulmonary artery pressures in man. Am J Physiol 1947; 150: 315-320.
Sajkov D, Crowie
RJ, Thronton TH et al. Pulmonary hypertension and hypoxemia in obstructive
sleep apnea syndrome. Am J Respir. Crit. Care Med. 1994; 149: 416- 422.
Chaouat A, Weitzenblum
E, Krieger J et al. Pulmonary Hemodynamics in the Obstructive Sleep
Apnea Syndrome: Results in 220 Consecutive patients. Chest 1996; 109;380-386.
Laks L, Lehrhaft
B, Grunstein R et al. Pulmonary hypertension in obstructive sleep apnea.
Eur Respir J 1995 (8): 537-541.
Sanner BM, Doberauer
C, Konermann M et al. Pulmonary hypertension in patients with obstructive
sleep apnea syndrome. Arch Int Med 1997; 157: 2483-2487.
Olson AL, Zwillich
C. The Obesity hypoventilation syndrome. Am J Med 2005(118): 948-56.
Kessler R, Chaouat
A, Schinkewitch P et al. The Obesity-Hypoventilation Syndrome revisited.
A prospective Study of 34 cases. Chest 2001; 120(2): 369-376.
Buda AJ,
Schroeder JS, Guilleminault C et al. Abnormalities of pulmonary
artery wedge pressures in sleep-induced apneas. Int J Cardiol 1981;
I: 67-74.
Fortin TA, Krichman
A, Hargett CW et al. Characteristics of pulmonary arterial hypertension
associated with elevated pulmonary capillary wedge pressure. Chest 2005
Abstracts, Monday October 31.
Kaw R, Thota
A, Minai O. Pulmonary hypertension in Obese patients: An analysis of
hemodynamic data. Chest 2008; 134: p 134003.
Simmonneau G,
Galie N, Rubin LJ et al. Clinical classification of pulmonary hypertension.
J Am Coll of Cardiol. 2004; 43;5S-12S
Sajkov D, Wang
T, Saunders NA et al. Continous positive airway pressure treatment improves
pulmonary hemodynamics in patients with obstructive sleep apnea. Am
J Resp Crit Care Med. 2002; 165: 152-158.
Arias MA, Garcia-Rio
F, Alonso Fernandez A et al. Pulmonary hypertension in obstructive sleep
apnoea: effects of continous positive airway pressure: a randomized,
controlled cross-over study. Eur Heart J 2006; 27: 1106-1113.
Treatment of low back pain remains a dilemma. In the USA more than 300 thousand back surgeries are performed each year. For about 10% to 39% patients, pain may continue or even get worse after back surgeries1. This condition is called failed back surgery syndrome. In the USA, about 80,000 new cases of failed back surgery syndrome are accumulated each year2. Pathological changes such as recurrent disc herniation, arachnoiditis, scar tissue formation, poor surgical indication, misdiagnosis, and surgical technique failure can all contribute to the failure of surgery. Pain after back surgery is difficult to treat. Many patients have to live with pain for the rest of their lives with severe disability.
Over the last several decades, our understanding of the causes of low back pain has been challenged. With a sensitivity up to 95%3, MRI has been used a gold standard for the diagnosis of spine disease such as lumbar disc herniation. With the MRI evidence of a disc herniation and nerve root compression, patients are more easily convinced surgery is their best and only option. However, the reliability of MRI as the evidence for surgical decision has been questioned. An early study found that in a group of asymptomatic volunteers at age of 60 years or older, about 57% had abnormal MRI findings including disc herniation and spinal stenosis4. Follow up studies have yielded similar results. Now it is widely accepted that degenerative disc disease, such as disc herniation is a common finding in asymptomatic adults. Even though at the age of 60 years or older, 57% or more may have abnormal MRI findings in the lumbar spine, however, only less than 20% of this group of people have chronic low back pain. A recent study also suggested a lack of correlation between imaging findings of spine degenerative change and back pain5. Simply, degenerative change in the lumbar spine, such as a herniated disc, is not necessary painful.
The results of these studies have changed our belief in the relationship between lumbar disc herniation and back pain. It is believed that back and leg pain in the presence of acute disc herniation is not merely the result of a pinched nerve root, rather it is more related to the inflammation of the nerve roots and nerve endings around the herniated disc or it may be the combined results of chemical inflammation and mechanical compression6. A herniated disc is not a sole indication for back surgery and up to 70% to 95% of patients may be pain free after 12 months without major intervention7. The primary goal of treatment of lumbar radicular pain should be the suppression of inflammation, relieving the pain and restoring function rather than removal of the herniated disc. Before one chooses an open back surgery the following options should be considered:
Diagnosis: Low back pain can be related to a herniated disc, nerve root irritation, annular tear, facet joint arthritis, muscle spasm, injuries to the ligament, sacroiliac joint arthritis and referred pain from visceral organs. An MRI finding of a herniated disc, no matter how large, is not enough to justify surgery. A thorough history and physical examination is tantamount to judge whether the herniated disc is the real source for the ongoing pain.
Medications: Non-steroid anti-inflammatory medications should be offered as the first line medication to patients with mild back pain. Early administration of oral steroid medication in patients with acute sciatica may lead to slightly more rapid improvement in pain, mental well-being, and disability scores8. Anti-depressants, especially tricyclic antidepressants, are often used to treat patients with chronic back pain.
Physical therapy, massage therapy and chiropractic management have been widely used for treatment of back pain and lumbar radicular pain, even though the value of these treatment modalities have yet to be proven.
Spine injections: Multiple double blind, clinical controlled studies have confirmed the clinical efficacy of lumbar epidural steroid injection (LESI) in relieving the acute radicular pain due to herniated nucleus pulposus, speeding the rate of recovery and return to function9. The pain relieving effect of LESI may last up to three months. Inflammatory mediators, such as phospholipase A2, have been implicated in lumbar radiculopathy and disc herniation and have been the focus of recent research. Lumbar epidural steroid injections can decrease pain by suppressing the function of inflammatory mediators. As long as the patient is pain free and is without any neurological deficits, a herniated disc should not be a clinical concern. Even though LESI alone may not decrease the necessity of back surgery, it will be intriguing to investigate whether a combination of LESI and other treatment such as physical therapy and life style modification will decrease the need for surgery.
Minimally invasive surgery: Minimally invasive surgery offers another alternative in the treatment of back pain. These treatments include chymopapaine, percutaneous nucleotome, automated percutaneous lumbar discectomy, laser discectomy, neucleoplasty and disc deKompressor. The advantage of the minimally invasive techniques is that it leaves no or minimal scar after the surgery. Among the minimal invasive techniques, laser discectomy has a reported success rate of 80% to 90%10. Neucleoplasty and disc deKompressor have been recently introduced with early non-controlled studies showing success rates up to 78%11. These procedures are still not widely accepted and more studies are needed to confirm their clinical efficacy.
Life style modification: Low back pain can often be the result of improper lifestyle choices. Smoking can increase the risk of low back pain12. Obesity can worsen back pain and contribute to disk degeneration13. Heavy lifting, sport related injuries and motor vehicle accidents can cause back pain. Education to patients with low back pain is critical to help them recover from back pain and prevent future back pain. Smoking cessation and weight control should be strongly recommended to back pain patients. Proper exercise techniques should be taught. Patients, especially those with spinal stenosis often have difficulty walking due to neurological claudication. Treadmills and long distance walking exercise may exacerbate back pain. Some studies suggested therapeutic aquatic exercise is potentially beneficial to patients suffering from chronic low back pain14.
Conclusion: Lumbar spine surgery can potentially provide quick pain relief and functional recovery. There are many downsides to surgery however that would include post laminectomy surgery syndrome and a lack of proven long term benefit. Because of these risks one should be very careful in determining surgical candidacy. A preliminary study15 has provided the evidence that the rate of back surgery can potentially be decreased through appropriate education and application of evidence-based medicine for patients, general practitioners and spine surgeons. Conservative treatment with the combination of medications, physical therapy, spinal injections and life style modification should be tried before surgery is considered.
COMPETING INTERESTS
None Declared
AUTHOR DETAILS
YILI ZHOU, MD, PH.D, Comprehensive Pain Management of North Florida, USA
STEPHEN IRWIN, MD, Comprehensive Pain Management of North Florida, USA
CORRESPONDENCE: YILI ZHOU, MD, PH.D, Medical Director, Comprehensive Pain Management of North Florida, Gainesville, USA, FL32608
Email: Yilizhoumd@yahoo.com
References:
Graz B, Wietlisbach V, Porchet F, et al. Prognosis or "curabo effect?": physician prediction and patient outcome of surgery for low back pain and sciatica. Spine 2005 June 15;30(12):1448-52.
Ragab A, Deshazo RD. Management of back pain in patients with previous back surgery. Am J Med 2008 April;121(4):272-8.
Mullin WJ, Heithoff KB, Gilbert TJ, Jr., et al. Magnetic resonance evaluation of recurrent disc herniation: is gadolinium necessary? Spine 2000 June 15;25(12):1493-9.
Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am 1990 March;72(3):403-8.
Kalichman L, Kim DH, Li L, Guermazi A, et al. Spondylolysis and spondylolisthesis: prevalence and association with low back pain in the adult community-based population. Spine 2009 January 15;34(2):199-205.
Roberts S, Butler RC. Inflammatory mediators as potential therapeutic targets in the spine. Curr Drug Targets Inflamm Allergy 2005 April;4(2):257-66.
Legrand E, Bouvard B, Audran M, et al. Sciatica from disk herniation: Medical treatment or surgery? Joint Bone Spine 2007 December;74(6):530-5.
Holve RL, Barkan H. Oral steroids in initial treatment of acute sciatica. J Am Board Fam Med 2008 September;21(5):469-74.
Sethee J, Rathmell JP. Epidural steroid injections are useful for the treatment of low back pain and radicular symptoms: pro. Curr Pain Headache Rep 2009 February;13(1):31-4.
Goupille P, Mulleman D, Mammou S, et al. Percutaneous laser disc decompression for the treatment of lumbar disc herniation: a review. Semin Arthritis Rheum 2007 August;37(1):20-30.
Al-Zain F, Lemcke J, Killeen T, et al. Minimally invasive spinal surgery using nucleoplasty: a 1-year follow-up study. Acta Neurochir (Wien ) 2008 December;150(12):1257-62.
Mikkonen P, Leino-Arjas P, Remes J, et al. Is smoking a risk factor for low back pain in adolescents? A prospective cohort study. Spine 2008 March 1;33(5):527-32.
Hangai M, Kaneoka K, Kuno S, et al. Factors associated with lumbar intervertebral disc degeneration in the elderly. Spine J 2008 September;8(5):732-40.
Waller B, Lambeck J, Daly D. Therapeutic aquatic exercise in the treatment of low back pain: a systematic review. Clin Rehabil 2009 January;23(1):3-14.
Goldberg HI, Deyo RA, Taylor VM, et al. Can evidence change the rate of back surgery? A randomized trial of community-based education. Eff Clin Pract 2001 May;4(3):95-104.
The prevalence of behavioural symptoms in dementia is well known. Patients may exhibit outright psychotic features (delusions, hallucinations) and commonly experience a host of symptoms such as screaming, hitting, agitation, and wandering. The patient often appears to be upset and suffering, and whether the symptom is the cause of that distress, or a result of some inner discord, is unknown. Clearly, these behaviours are upsetting to the patient’s family, loved ones, and their caregivers. Physicians are driven to attempt to reduce the suffering of patients and support the family and other professional caregivers. Hence, medications are often the first approach to dealing with such problems. Given the similarity between these symptoms and those seen in patients with schizophrenia, antipsychotics are often the first choice. As a result, nearly 1 in 4 elderly nursing home residents in the United States are given antipsychotic drugs1.
Unfortunately, they are not very effective. Schneider, in an extensive review of the efficacy of antipsychotics found an effect size of only 18% favouring these drugs over placebo2. But much more worrisome are the potentially lethal, or permanently disabling, side-effects. A meta-analysis of 15 randomized controlled trials evaluating dementia patients with behavioural and psychological symptoms concluded that there was an overall increase in the risk of death (odds ratio 1.54, 95% CI 1.06–2.23; p = 0.02) when atypical antipsychotics were compared to placebo3. This means that for every 9 to 25 persons helped in these trials, therepossibly will be 1 death due to the treatment itself. Older “typical” antipsychotics may not be any less risky. A comedian once commented, “I don’t consider ‘death’ a side-effect, I think it’s a primary effect!” In addition, the risk of the patient acquiring the permanent though not lethal side-effect of tardive dyskinesia is higher in older patients than younger ones. Finally there are other serious potential adverse affects such as falls, confusion, and weight gain or increased risk of diabetes.
Some have written that using antipsychotics in dementia is “off label” prescribing, a term which is usually reserved for the use of a drug for which there has been little study but presumed efficacy based on clinical experience. However, the “Black Box Warning” on the use of antipsychotics in dementia is non-ambiguous: these drugs are “not approved for dementia-related psychosis.” Yet one company, Eli Lilly, incurred a $1.4 billion fine from the FDA for marketing Zyprexa (Olanzapine) in the use of dementia related psychosis.
Clinical guidelines by both Canadian and American interests have clearly described these risks and suggest that antipsychotics be used only as a last resort4,5. Searching for a treatable medical problem, ranging from a serious condition such as pneumonia, to a painful irritation like an ingrown toenail, is the first step. But perhaps most importantly, providing a caring, nurturing and non-stressful environment is likely to be most helpful6. The work of Tom Kitwood in defining the problematic behaviours of caregivers which may increase dementia-related agitation is refreshing7. Unfortunately, few long term care programs have provided for this type of caregiver training. Other interventions, such as music therapy, caregiver support, and caregiver stress reduction may be helpful but have not been extensively studied8. So what’s the clinician to do if an antipsychotic medication is to be used “as a last resort?”
For the patient’s protection and to reduce medical-legal risks, I believe that a formal informed consent process should be initiated. Such a process should entail adequate description of the risks of the treatment, the potential benefits, and the plan for further monitoring and adjustments to the treatment course. As in any informed discussion, it should include the alternatives available, along with the risks and benefits of each alternative. Finally, it should include a discussion of what is likely to happen if no pharmacologic treatment is provided. In most cases, these discussions will necessarily be conducted with the surrogate decision-maker (usually a family member), given the occurrence of psychotic symptoms later in the course of dementia when decision-making capacity is usually severely impaired.
The key elements of the discussion, including open and specific disclosure of the risks, should be documented in written form and entered into the patient’s medical record. An example of such documentation is in Appendix 1. Some clinicians with whom I have discussed this idea have responded that the caregivers would not be likely to approve the use of medications if these risks were so openly discussed. My response is simple – the ethical thing to do is always to inform the patient (or his or her surrogate) before initiating treatment. If that leads to a reduction in the use of these drugs, I would not be unhappy.
CORRESPONDENCE: KENNETH BRUMMEL-SMITH .M.D. Charlotte Edwards Maguire Professor and Chair, Department of Geriatrics, Florida State University College of Medicine, 1115 West Call St, Suite 3140-D, Tallahassee, FL 32306-4300, 850-644-2291
REFERENCES
Kamble P, Chen H, Sherer J, et al. Antipsychotic Drug Use Among Elderly Nursing Home Residents in the United States, Am J Geriatr Pharmacother 2008;6:187–197.
2 Schneider LS, Pollock V, Lyness S. Further analysis of meta-analysis. J Am Geriatr Soc. 1991;39:441-442.
3 Schneider LS, Dagerman KS, Insel P. Risk of death with atypical antipsychotic drug treatment for dementia: meta-analysis of randomized placebo-controlled trials. JAMA 2005;294:1934-43.
4 Gauthier S, Herrmann N, Diagnosis and treatment of dementia: 6. Management of severe Alzheimer disease. CMAJ 2008;179(12):1279-87
5 American Psychiatric Association (APA). Practice guideline for the treatment of patients with Alzheimer's disease and other dementias of late life. Am J Psychiatry 1997 May;154(5 Suppl):1-39.Updated Oct. 2007.
6 Verkaik R, van Weert JC, Francke AL. The effects of psychosocial methods on depressed, aggressive and apathetic behaviors of people with dementia: a systematic review. Int J Geriatr Psychiatry 2005;20:301-14.
7 Kitwood T. Dementia Reconsidered, Philadelphia, Open University Press.1997
8 Brummel-Smith K, Alzheimer’s disease and the promise of music and culture as a healing process, in The Oxford handbook of Medical Ethnomusicology, Koen BD, Lloyd J, Barz G, Brummel-Smith KL (eds), Oxford University Press, 2008, Oxford, pp.185-200.
Appendix 1
Consent for Use of Antipsychotic Medication
Indications: Antipsychotic medications are sometimes used to treat behavioral symptoms in patients with dementia. These symptoms include delusions (fixed beliefs that are not real), hallucinations (seeing or hearing things that are not real), and others. The Federal Drug Administration (FDA) has approved the use of antipsychotic medications in the treatment of schizophrenia and other mental conditions. While the FDA has not approved these medications in treatment of behavioral symptoms of dementia, physicians may use them for “off-label” purposes if it is believed they well help the patient.
These medications should be used as a last resort to help patients with dementia who are suffering behavioral symptoms. Other “treatments” include changing the person’s environment, getting them more involved in activities, making sure there are no medical problems causing the symptoms (like pain), and making sure other medications the patient is taking have not caused the symptoms. If the patient is not suffering from the symptoms (that is, they are not bothered by them) and they do not prevent the caregivers from giving good and safe care, then it is best not to give them medications for the symptoms.
These types of medications have two very serious potential side-effects, which is why it is important that you know both the risks and the benefits of using them.
Anticipated duration of use: ______________________________
Alternatives: Sometimes other medications, like sedatives, are used if the patient is anxious. But they also have side-effects and may not help the severe behavior problems and usually do not help delusions and hallucinations. Another alternative is to keep trying the non-medicine interventions described above. The final alternative is to give no treatment and just live with the symptoms. As the person’s dementia gets worse over time, the symptoms do usually go away. But that may take some time.
Expectations of Treatment: If the medication is used, we expect the person with dementia to have less suffering. The patient should be calmer and feel less distressed. The hallucinations and/or delusions may not go completely away, but they should be less bothersome to the patient. Caregiving should be more accepted by the patient. Hopefully, the patient will not experience any side effects but many patients do have some side effects so it is important to report any change that may be due to the medication.
Side effects and complications include but are not limited to:
The most serious concern is that older patients with dementia who are given these medications have an increased risk of death compared to patients given placebos (sugar-pills). That risk is about 1.7 times the risk of using the placebo. Most of the deaths were due to heart problems or pneumonia.
The second most serious concern is the development of a permanent side-effect called “tardive dyskinesia.” It is an uncontrolled movement of the face and mouth. This occurs in about 25% of patients who take the medication for a long time. Rarely, it can occur even in patients who only take a few doses of the medication.
Neuroleptic malignant syndrome – a rare but potentially fatal side effect with fever, blood pressure problems, and irregular pulse.
Contraindications: These medications should not be used if you or your loved-one has an allergy to them. A history of having bad reactions to this medication (or ones similar to this medication) is also a concern and should be discussed with the doctor.
*******************************************
I understand the above, and have had the risks, benefits, and alternatives explained to me. I have had an opportunity to ask questions about the recommended treatment. I understand that no guarantees about results have been made. I give my informed consent for the use of:
______________________________.
_______________________________
Patient Signature
_________________________
Date
_______________________________
Witness
_________________________
Surrogate Signature (if the patient does not have decision-making capacity)
“Schizophrenia’ is written and spoken about as if the language used simply reflected a reality already discovered or about to be discovered. Such a representational view of language has been strongly questioned in a range of theoretical ideas whose common assumption is that what we think of as reality or truth is not discovered or reported but is constructed, primarily through the strategic use of language” (Boyle 2002).
INTRODUCTION
It is not a revelation, that practising psychiatry or psychotherapy and pursuing psychological research, rely heavily on phenomenology, which may be descriptive (Jasper, Husserl), or dynamic (Freudian), and influences that which may have on several diagnostic categories. The question of how our use of terms correlates with whatever it is trying to describe, requires serious consideration. The aim of this editorial is to sketch some significant developments in psychological, biological, physical and philosophical studies, with specific reference to the role of language in these evolving scientific endeavours.
EARLIER PERSPECTIVES
As early as 1921, Wittgenstein (1889 – 1951) proposed two major ideas that revolutionised philosophical thinking. The first was the principle of verification (that statements are meaningful, only when they can be verified by experiment), which has since been adopted as the manifesto of logical positivism, and the basis of new scientific thinking. His second central thesis was to deny that logical or linguistic concepts represent reality. Furthermore, he suggested that the apparent harmony between language and reality is merely the shadow cast upon the world by grammar. In his major work “The Concept of Mind” (1949), Gilbert Ryle (1900-1976), suggested that the Cartesians (followers of Descartes) have been misled, in picturing the mind as a “ghostly” counterpart of the brain; simply due to our way of expression, when handling “one category as if it belonged to another” (Category Error).
It is undeniable that logical positivism (sentences are meaningful if they can be assessed either by an appeal to sense data or by an appeal to the meaning of the wards and the grammatical structure that constitute them) has lived up to expectations in ridding scientific methodology of metaphysical arbitrance. It also brought a range of new issues under the spotlight, which were previously unrecognised. First, the verification condition for a given Empirical statement presupposes a massive background of default auxiliary assumptions (Duhem, 1954), i.e. all experiments will presume the truth of some theories to help judge that the set-up is adequate and the instruments are reading what they are meant to read. But these presupposed theories need not be identical to the theory under test. Second, the long held dichotomy between Priori statements (true by virtue of meaning), and Contingent statements (true by empirical evidence) is no longer tenable, and that neither is shown to be immune to revision at some point in time (Quine, 1961). Furthermore, single terms in scientific theories are meaningful only on their place in the theory.
DOES REDUCTIONISM HELP?
Although a reductionist approach (describing a phenomenon in relation to its constituent parts) has been traditional in biology, there has been some reluctance to apply reductionism to the study of human behaviour. However, it was precisely the assumption that elementary forms of learning are common to humans and simple animals, that consequently led to the discovery of the cellular and molecular basis of memory and learning (Kandel, 2000).
On the other hand, the common misconception, even in textbooks of genetics is to speak of genes determining traits of the whole organism, as if identifying a gene will mean the trait of the organism is known. If one examines the more general relation between gene, environment and organism, it is apparent that the situation is more complex. First, there is no unique phenotype corresponding to a genotype; the phenotype depends on both genotype and environment. Second, the form and direction of the environment’s effect upon development differs from genotype to genotype. Third, and reciprocally, there is no unique ordering of genotype such that one can always be characterized as “superior” or “inferior” to another. (Levins and Lewontin, 1985).
Even with reductionist sciences like physics, the view held is “that physics is not about how nature is. Physics concerns what we can say about nature” (Bohr, in Peterson, 1963). This view recently echoed by Hawking (New Scientist, 2003), where he suggested that our deepest theories rely on our language of logics, which is self-referential, and cannot be complete and consistent at the same time. In simple terms, there is an eternally unbridgeable gap between what is true within a given logical framework or system and what we can actually prove by logical means using that same system. Obviously, this may open the way to confusion and paradoxes, as causality within the system cannot be determined.
PSYCHOANALYSIS BEING ANALYSED
Wittgenstein makes serious criticism of determinism in psychodynamic theories. When Freud says, “he could not believe that an idea produced by the patient could be an arbitrary one and unrelated to the idea we were in search of”. He is apparently making a category error by mixing two different statements: “Everything has a meaning” (can be interpreted) is not “Everything has a cause” (Bouveresse, J 1995). The person who agrees with us about the way things had to happen “suddenly sees the cause”. This, however, neither constitutes causality, nor can be empirically tested.
There is also the unjustifiable assumption that if meaning can be given to some mental events, it must be possible to assign meaning to all such events, even if it hasn’t yet been found. The latter might explain the common characterization of Freudian theories as pseudoscientific.
Curiously, one may well reasonably argue (due to lack of clear causality) that both patient and therapist, having reached different explanation of the same behaviour, are entirely justified, within the context of their own paradigm of thinking.
LANGUAGE ACQUISITION AND PERCEPTION
An influential framework of language acquisition, where knowledge of language is mentally represented as “grammar” (a finite system of rules) and the fundamental properties of these grammars are part of innate endowment was first proposed by Chomsky (1965). Chomsky’s ideas provide some explanation for our tendency to formulate premature theories (including scientific ones) on weak and limited evidence. Furthermore, when one considers both the evidence of how young children use language, and of how they understand it, there is often a lack of accord between the two (Huttenlocker, 1974). Interestingly, the interpretation of terms (language) is significantly dependent on the context of occurrence (the situations that it is used in) (Macnamara, 1972).
Studies of models of colour vision, support a wealth of evidence that what people treat as the same or as different depends on what language they speak. Furthermore, in the perception of space, language categories significantly mould thought and behaviour in a striking way (Scientist American, April 2004).
One may conclude from the above that our emotions, perceptions and theorizing are constrained by the limits of our own language. It is worth noting that the Epistemological limitations imposed by our language is not fixed in time but rather continuously change as we endlessly renegotiate our notion of reality as our language and our life develops (Putnam, 1994). Others went further to suggest that assigning diagnostic labels to human behaviour may even be more dramatic because people classified in a certain way, change in response to being classified (Hacking, 1999). Hence, it may be fair to say that diagnostic labels do not register the value of some passive attribute but of an attribute that is determined in part by our own actions in the process of ascribing labels to these attributes.
IN CONCLUSION
Francis Crick’s (1979) remark that “we are deceived at every level by our introspection” may well be more appropriately applied to our capacity to use language. This is especially relevant when language is employed in describing human behaviour, psychiatric diagnostic categories and neurophysiological studies. By virtue of its logical incompleteness, self referentiality and the context in which it is employed, language may lead to erroneous interpretations, would that be a therapeutic session, a psychiatric diagnosis, or even describing the microscopical functions of a nerve cell.
One is not suggesting how these issues could be remedied (that would require another editorial). However, it cannot even be overestimated that, although diagnostic categories assist our every day clinical work, a detailed analysis of the limitations and complexity of our language would facilitate understanding of our patients, and lead to fruitful scientific research.
