MEDICAL PROVIDERS: Hobson’s Choice in Medicine




TUCSON, Ariz., Dec. 06, 2022 (GLOBE NEWSWIRE) — Sheila Page, D.O., a family physician in Aledo, Texas, and president of the Association of American Physicians and Surgeons (AAPS), is featured in the winter issue of the of the Journal of American Physicians and Surgeons. She writes:  “Today physicians often feel constrained to pick from among options that are not in the best interest of patients but are ‘covered’ by insurance or approved by officials.”

“An apparently free choice when there is no real alternative is a Hobson’s Choice, and physicians must understand the political structure in which this type of ‘choice’ is embedded,” Dr. Page explains.

“During the COVID pandemic, people often faced a Hobson’s Choice of taking a shot that they believed put their life, health, or fertility at risk, or be barred from their education or career,” she noted.

“Voters generally believe that they have two choices, Republican or Democrat, and that they represent extremes of political ideology. However, when they are in office, politicians behave as if they belong to the same club,” she writes.

“Physicians have accepted the Hobson’s Choice of either abiding by ridiculous regulatory burdens or refusing to treat the senior population,” she explains. They “accept the Hobson’s Choice of either standing against the oppression or keeping their ‘place at the table.'” 

“The phrase ‘we need to keep our place at the table to avoid being on the menu’ entirely misses the point,” she states. “The profession is on the table already being carved up. How many times have we been told we must choose the lesser of two evils? Either choice is still evil!”

“We must identify the enemy within,” Dr. Page writes. “The medical profession must grasp the extent to which it has been manipulated by pharmaceutical, insurance, and other systems tied to medicine. We have been burdened with regulations and threats to our licenses by the same people who are selling us the solutions.”

“There is tremendous profit in the existing system, but we must nevertheless offer healing and hope, learn how to fight back effectively, and reject the Hobson’s Choice,” she concludes.

CITE: The Journal of American Physicians and Surgeons is published by the Association of American Physicians and Surgeons (AAPS), a national organization representing physicians in all specialties since 1943.


Contact Information:
Jane Orient
Executive Director


Thank You


2 Responses

  1. HCM

    Many years ago, when the phrases market-based reform and consumer-driven healthcare first surfaced, I couldn’t help but envision people flipping frantically through the Yellow Pages™ of healthcare while being wheeled into an ambulance. I just couldn’t see how patients were going to “drive healthcare,” and I still can’t.

    How can consumers shop around and compare the quality of the care they receive? What do you look for when flipping through the Yellow Pages of healthcare? Friendly clinicians? A nice receptionist? New carpets in the waiting room? Have you ever wondered why hospital food is such a favorite topic of discussion among patients? It’s one of the few things they can judge!

    We like choices. That’s why the phrase, or perhaps more accurately, the slogan, consumer-driven healthcare, caught on. Choices provide a sense of control and freedom. But how can consumers choose and drive healthcare when they have no idea how to judge the quality of their care or the accuracy of a diagnosis or test result? How many choices does one have when there is one hospital in town and the next one is 500 miles away? How can patients reform the market when the number of insurance companies that will accept them totals one, or worse, none? How can providers reform the market and choose when their patient’s carrier reduces payments? What are your options when you have but one liability insurance provider in a geographical area because the “market has contracted?” How free-to-choose are you when, according to The Wall Street Journal, health insurance companies are surreptitiously hiking the rates of the chronically ill?

    In the real world, choices in healthcare are truly Hobson’s choices. In the 17th and 18th centuries, Hobson was in the business of renting horses to Cambridge students. Although he may have had 40 horses available at any given time, when a student wanted to rent one, there were two choices: take the one nearest the stable door or take none at all. If you really needed a horse, you just had to hope for the best. Patients do the same thing every day.

    Have you ever heard someone tell you that his/her procedure would be performed by the second-best surgeon because the top-doc was busy or that he/she was going to the second-best hospital? Of course not. In the real world, there is no choice, only trust – trust that the care provided will be optimal, that the diagnosis is correct, and that the laboratory results are accurate. In the real world, most patients cannot comparison shop for the best chance of a good outcome. There are no Yellow Pages of healthcare or Michelin guides to practitioners and hospitals. In a true market-based system, there could be… and would be. In this market-based system of consumer-driven care, neither the patients nor the providers are in the driver’s seat. They have Hobson’s choices and hope for the best. Perhaps it is time to select another livery.

    Dr. Chia


  2. TH

    Thomas Hobson was a livery stable owner in Cambridge, England, in the 17th century who had an extensive stable of over 40 horses and ran a thriving horse rental business. His customers believed that, on entry, they would be given their choice of mounts, when in fact he offered them no choice: Hobson required that all his customers choose the horse in the stall closest to the door or have no horse at all. Literally, they had no choice but Hobson’s choice.

    Similarly, in percutaneous coronary intervention (PCI), adjunctive pharmacotherapy with platelet inhibitors and anticoagulant regimes have improved clinical outcomes through a reduction in ischemic events, including stent thrombosis,1–3 albeit at the expense of increased bleeding complications.4 Although the delivery of antiplatelet agents and anticoagulant regimes can be personalized at an individual patient level in an attempt to balance the reduction in ischemic risk while minimizing the increased risk of major bleeding, like Hobson’s choice in the 17th century, there is currently no option to avoid these agents altogether in PCI in patients with high bleeding risk. Thus, in general, it is either antiplatelet inhibition or no PCI—a 21st century interventional cardiologist’s manifestation of Hobson’s choice.

    Thrombocytopenia is not uncommon in patients undergoing PCI with a reported prevalence of around 6% in a pooled analysis of the ACUITY trial (Acute Catheterization and Urgent Intervention Triage Strategy) and HORIZONS-AMI trial (The Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction),5 with ≤7% of elective patients6 and 13% of patients with acute coronary syndrome (ACS) developing new thrombocytopenia during their hospitalization.7 Patients with thrombocytopenia tend to be older,5,7,8 have more extensive coronary disease,5 and a greater prevalence of adverse clinical characteristics, including renal failure,9 diabetes mellitus,5,7,8 and prior PCI or coronary artery bypass grafts.5,8 Furthermore, thrombocytopenia is a recognized side effect of treatment with GP IIb/IIIA (glycoprotein IIb/IIIa) inhibitors10 or heparin11 through immune-mediated mechanisms.8,12

    In this issue of Circulation: Cardiovascular Interventions, using a pooled, patient-level analysis derived from >23 000 participants from the CHAMPION trials (Cangrelor Versus Standard Therapy to Achieve Optimal Management of Platelet Inhibition), Groves et al13 report that 0.8% of patients undergoing PCI develop thrombocytopenia. GP IIb/IIIa use, age, diabetes mellitus, hyperlipidemia, and prior coronary artery bypass grafts were all independently associated with acquired thrombocytopenia, with GP IIb/IIIa use as the strongest predictor (odds ratio, 2.85; 95% confidence interval, 2.07–3.94; P<0.001). Importantly, Cangrelor treatment itself had no effect on the incidence of thrombocytopenia irrespective of whether a GP IIb/IIIa was used.

    In line with previous work that has reported adverse clinical outcomes associated with acquired thrombocytopenia after PCI,6,8,14,15 the current study reports that patients who developed thrombocytopenia after PCI had a 13-fold independent increased risk of GUSTO (The Global Use of Strategies to Open Occluded Arteries) severe bleeding and a 3-fold increased risk of stent thrombosis at 48 hours. Further, there was a 3- and 5-fold increased adjusted risk of 30-day major adverse cardiovascular events and mortality, respectively, in the thrombocytopenia group. Even in the patients who did not sustain a major bleeding complication within 48 hours, thrombocytopenia remained independently associated with increased risk of major adverse cardiovascular events at 30 days. The latter is almost certainly underappreciated and of considerable clinical relevance.

    While such increased risks associated with thrombocytopenia are, in general, well known, less is known about the optimal management of patients who either have prevalent thrombocytopenia or develop it after treatment. Patients with thrombocytopenia are routinely excluded from landmark antiplatelet trials, such as TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel Thrombolysis In Myocardial Infarction 38),16 PLATO (Platelet Inhibition and Patient Outcomes),17 and consequently, the safety of contemporary antiplatelet therapies used in patients with ACS is not well defined. Specifically, there are currently no guideline recommendations or consensus reports to guide interventionists on the management of patients with PCI with thrombocytopenia.

    The authors have previously published an opinion piece about the management of patients with PCI with thrombocytopenia and have included management recommendations made according to the clinical setting (elective and ACS) and the severity of thrombocytopenia.18 These recommendations include identification and correction of any reversible causes of thrombocytopenia and minimization of bleeding risk, including avoidance of non-steroidal anti-inflammatory drugs, GP IIb/IIIa inhibitors, and utilization of proton pump inhibitors.

    In patients with ACS who are not undergoing PCI, the authors recommend that clopidogrel monotherapy should be considered if platelet count is 50×109 per liter, in the absence of bleeding. In contrast, in those patients with a platelet count 50×109 per liter undergoing PCI, recommendations include adopting a transradial approach, restricting DAPT therapy to 1 month post-stent, and using second-generation DES rather than BMS. Finally, in patients with stable coronary artery disease, the authors suggest stopping antiplatelet therapy and avoiding PCI in patients with a platelet count 50×109 and <100×109 per liter, clopidogrel monotherapy and a proton pump inhibitor is recommended. If a patient’s symptoms persist, despite optimal medical therapy, the risks should be weighed against the benefits of proceeding with an invasive strategy on an individual basis.

    The data presented remind operators regarding the importance of the challenge we face, on behalf of our patients, in the management of thrombocytopenia. Specifically, we face 2 different clinical scenarios: first, the thrombocytopenic patient in front of us in whom PCI is otherwise the optimal revascularization strategy; and second, the post-PCI patient who develops thrombocytopenia. In the first scenario, our choices include avoiding PCI altogether and modification of the intensity and duration of antiplatelet therapy, although it is common to ignore a degree of thrombocytopenia completely. In post-PCI–acquired thrombocytopenia, our management depends on the level of the drop, whether the low platelet count is accompanied by dysfunction of those platelets that are present, and, of course, the actual or theoretical bleeding risk. Little, above and beyond common sense and experience-based judgment, helps to inform our management decisions in such circumstances, although modification of the intensity and duration of antiplatelet therapy is foremost in our armory. There are currently no risk scores to predict the development of thrombocytopenia post-PCI, and the non-modifiable independent predictors of developing thrombocytopenia identified in the current study such as age, prior coronary artery bypass grafts and diabetes mellitus are non-specific and feature in most risk scores for adverse outcomes for both ischemic and bleeding risk. As such, they offer little value as the basis for thrombocytopenia avoidance strategies.

    There is one exception. In the current study, use of GP IIb/IIIa inhibitors was reported to be the strongest predictor of post-PCI thrombocytopenia, and this represents an important modifiable risk factor. The use of GP IIb/IIIa inhibitors in PCI has fallen dramatically since peak period in the 1990s and early 2000s following randomized trials, such as EPILOG (The Evaluation in PTCA to Improve Long-Term Outcome With Abciximab GP IIb/IIIa Blockade) and EPISTENT (Evaluation of Platelet IIb/IIIa Inhibitor for Stenting), in which such agents were routinely used for large patient subgroups. Their use in contemporary practice has declined because of several factors, including improved PCI technique, stent technology, and more potent oral P2Y12 inhibitors. Nevertheless, they are still used in cases where there is perceived to be high ischemic risk, significant thrombotic burden, or in bailout for cases of slow flow/no reflow. Data derived from the CHAMPION trials have shown that cangrelor reduces the requirement for bailout GP IIb/IIIa inhibitors in PCI19 and so may reduce the requirement for GP IIb/IIIa inhibitors further in contemporary practice.

    Groves et al have provided interventionalists with a timely reminder of the outcome risks associated with the acquisition of thrombocytopenia after PCI. The important observation that this risk of adverse outcome extends beyond the index admission is particularly valuable. Avoiding GP IIb/IIIa inhibitors wherever possible emerges as a clear-cut message. Our response to the development of thrombocytopenia post-PCI in our patients should be based on common sense and experience. Specifically, we should seek factors that may be causing or exacerbating the low platelet count, detect evidence of actual bleeding and estimate theoretical bleeding risk, and then make a bespoke and considered judgment about the need to compromise on the intensity and duration of our proposed ongoing dual antiplatelet therapy.

    Our management plan should be informed by discussion with hematology specialists, who have an important role in helping to diagnose some potential causes, such as heparin-induced thrombocytopenia. Prophylactic platelet transfusions should be avoided because they rarely raise platelet counts and can precipitate thrombosis20 although may be necessary in cases where significant bleeding complications occur. However, it is important for the experienced interventionalist to understand that their clinical experience of post-PCI thrombocytopenia will be greater than that of a clinical hematologist in most circumstances, so a high-level approach that takes into account all factors remains important.

    How patients who develop thrombocytopenia with no immediate bleeding complications should be managed remains unclear. The current study shows that these patients are at significantly increased risk of both bleeding and thrombotic complications, and discontinuing antiplatelet therapy to a single antiplatelet in such cases would further increase the already elevated risk of thrombotic complications. Alternatively, continuing potent newer antiplatelet agents may potentiate the already elevated bleeding risk in this cohort, although the safety and clinical outcomes associated with switching to clopidogrel in such situations is unclear. In patients who have no active bleeding, watchful waiting is often the dominant management strategy, and any theoretical choices related to modifying antiplatelet therapy in these circumstances are not informed by any hard data. It is clear, however, that we should reject the choice apparently offered to us by Hobson in these patients and manage them in a personalized fashion that includes several options regarding the modification of their dual antiplatelet therapy intensity and duration.


    The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
    Correspondence to Mamas A. Mamas, MA, BM BCh, DPhil, Keele Cardiovascular Research Group, Keele University, Stoke-on-Trent ST4 7QB, United Kingdom. E-mail

    Dr. Chia


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