Here's a slide show with some great ECG pearls which also illustrates the effectiveness of Prezi.
Saturday, January 30, 2016
Friday, January 29, 2016
Thursday, January 28, 2016
We have previously shown that a single dose of ketamine, a glutamate N-methyl-d-aspartate (NMDA) receptor antagonist, is associated with a rapid reduction in depressive symptom severity and SI in patients with treatment-resistant depression.
Method. We conducted a randomized, controlled trial of ketamine in patients with mood and anxiety spectrum disorders who presented with clinically significant SI (n = 24). Patients received a single infusion of ketamine or midazolam (as an active placebo) in addition to standard of care. SI measured using the Beck Scale for Suicidal Ideation (BSI) 24 h post-treatment represented the primary outcome. Secondary outcomes included the Montgomery–Asberg Depression Rating Scale – Suicidal Ideation (MADRS-SI) score at 24 h and additional measures beyond the 24-h time-point.
Results. The intervention was well tolerated and no dropouts occurred during the primary 7-day assessment period. BSI score was not different between the treatment groups at 24 h (p = 0.32); however, a significant difference emerged at 48 h (p = 0.047). MADRS-SI score was lower in the ketamine group compared to midazolam group at 24 h (p = 0.05). The treatment effect was no longer significant at the end of the 7-day assessment period.
Conclusions. The current findings provide initial support for the safety and tolerability of ketamine as an intervention for SI in patients who are at elevated risk for suicidal behavior. Larger, well-powered studies are warranted.
Well, this is intriguing but I am a little concerned about the use of midazolam for the comparison group. How do we know it didn't make the depression worse? Apparently though, according to the abstract above, there are previous data suggesting a beneficial effect of ketamine so this warrants further investigation.
Wednesday, January 27, 2016
Here is a case report and brief review. From the article:
Amyloidosis is a rare, multisystem disease characterized by deposition of fibrils in extracellular tissue that involves the kidney, liver, heart, autonomic nervous system, and several other organs.1 Based on the type of amyloid protein, cardiac involvement in amyloidosis can be seen in the following five types: (1) amyloid light chain (AL) or primary amyloidosis, (2) transthyretin (TTR) or familial/hereditary amyloidosis, (3) systemic senile amyloidosis, (4) isolated atrial amyloidosis, and (5) serum amyloid A (AA) or secondary amyloidosis.2 The diagnostic evaluation in suspected cardiac amyloidosis includes electrocardiography, echocardiography, and CMR and in certain cases requires a myocardial biopsy.
Tuesday, January 26, 2016
Monday, January 25, 2016
Sunday, January 24, 2016
Saturday, January 23, 2016
Just about every line in this free full text review is relevant and I would not do it justice by trying to distill it down to any key points here. It is worth the read in the original.
Friday, January 22, 2016
From a recent review:
IgG4-related disease (IgG4-RD) is a systemic disease characterized by the infiltration of IgG4-bearing plasma cells and, more importantly, distinctive histopathological features: storiform fibrosis, obliterative phlebitis, a lymphoplasmacytic infiltrate, and mild-to-moderate tissue eosinophilia. The diagnostic approach is complex and relies on the coexistence of various clinical, laboratory, and histopathological findings, none of which is pathognomonic in and of itself. IgG4-related disease should be suspected in patients presenting with unexplained enlargement or swelling of 1 or more organs or tissue organs. Four laboratory abnormalities often provide initial clues to the diagnosis of IgG4-RD: peripheral eosinophilia, hypergammaglobulinemia, elevated serum IgE levels, and hypocomplementemia. Elevated serum IgG4 levels provided critical information in identifying the first cases of IgG4-RD, but recent studies have reported substantial limitations to the measurement of serum IgG4 concentrations, precluding reliance on serum IgG4 concentrations for diagnostic purposes. In contrast, new studies have suggested a promising role of flow cytometry studies in the diagnosis and longitudinal management of IgG4-RD. Demonstration of the classic histopathological features of IgG4-RD remains crucial to diagnosis in most cases, and biopsy proof is preferred strongly by most disease experts before the initiation of treatment. Of note, the multiorgan nature of IgG4-RD was first established in 2003. This review intends to provide most recent knowledge about the clinical, laboratory, radiological, and pathological characteristics of IgG4-RD that may guide the physician to establish an early diagnosis.
Thursday, January 21, 2016
From a recent review:
A substantial number of patients admitted to the ICU because of an acute illness, complicated surgery, severe trauma, or burn injury will develop a de novo form of muscle weakness during the ICU stay that is referred to as “intensive care unit acquired weakness” (ICUAW). This ICUAW evoked by critical illness can be due to axonal neuropathy, primary myopathy, or both..The main risk factors for ICUAW include high severity of illness upon admission, sepsis, multiple organ failure, prolonged immobilization, and hyperglycemia, and also older patients have a higher risk. The role of corticosteroids and neuromuscular blocking agents remains unclear..The cornerstones of prevention are aggressive treatment of sepsis, early mobilization, preventing hyperglycemia with insulin, and avoiding the use parenteral nutrition during the first week of critical illness.
Though aggressive blood glucose control seems to reduce this problem, the article points out that it is associated with worse outcomes overall, and therefore no strong recommendation for glycemic control is made. The role of corticosteroids and neuromuscular blocking agents in this syndrome is not as clear as was once thought.
Wednesday, January 20, 2016
We conducted a longitudinal, single-center, retrospective cohort study of adult patients who underwent echocardiography during a medical or surgical ICU admission at the Beth Israel Deaconess Medical Center using the Multiparameter Intelligent Monitoring in Intensive Care II database. The final cohort had 2867 patients, of whom 324 had HDLVEF, defined as an ejection fraction greater than 70 %. Patients with an ejection fraction less than 55 % were excluded.
Compared with critically ill patients with normal left ventricular ejection fraction, the finding of HDLVEF in critically ill patients was associated with female sex, increased age, and the diagnoses of hypertension and cancer. Patients with HDLVEF had increased 28-day mortality compared with those with normal ejection fraction in multivariate logistic regression analysis adjusted for age, sex, Sequential Organ Failure Assessment score, Elixhauser score for comorbidities, vasopressor use, and mechanical ventilation use (odds ratio 1.38, 95 % confidence interval 1.039–1.842, p =0.02).
The presence of HDLVEF portended increased 28-day mortality, and may be helpful as a gravity marker for prognosis in patients admitted to the ICU. Further research is warranted to gain a better understanding of how these patients respond to common interventions in the ICU and to determine if pharmacologic modulation of HDLVEF improves outcomes.
Tuesday, January 19, 2016
Monday, January 18, 2016
Sunday, January 17, 2016
Saturday, January 16, 2016
Friday, January 15, 2016
We retrospectively analyzed the clinical data of 541 patients who were diagnosed with GBS from 2003 to 2014. Independent predictors for MV and short-term prognosis in mechanically ventilated patients were identified via multivariate logistic regression analysis.
The mean age was 41.6 years with a male predilection (61.2 %). Eighty patients (14.8 %) required MV. Multivariate analysis revealed that shorter interval from onset to admission (p less than 0.05), facial nerve palsy (p less than 0.01), glossopharyngeal and vagal nerve deficits (p less than 0.01) and lower Medical Research Council (MRC) sum score at nadir (p less than 0.01) were risk factors for MV; disease occurrence in summer (p less than 0.01) was a protective factor. As to prognostic factors, absence of antecedent infections (p less than 0.01) and lower MRC sum score at nadir (p less than 0.01) were predictors of poor short-term prognosis in mechanically ventilated patients regardless of treatment modality. We further investigated the predictors of poor short-term prognosis in patients requiring MV with different nadir MRC sum scores. Combined use of intravenous corticosteroids with intravenous immunoglobulin (odds ratio 10.200, 95 % confidence interval 1.068–97.407, p less than 0.05) was an independent predictor of poor short-term prognosis in mechanically ventilated patients with a nadir MRC sum score from 0 to 12 points, regardless of existence of antecedent infection.
Clinical predictors of MV and poor short-term prognosis in mechanically ventilated GBS patients were distinct. Add-on use of intravenous corticosteroids was a risk factor for poor short-term prognosis in mechanically ventilated patients with a nadir MRC sum score from 0 to 12 points.
Thursday, January 14, 2016
This has already been the subject of numerous social media posts since the guidelines were released in November. Here I'll just comment on what I believe to be the most important changes since 2010.
The full text of the guideline issue of Circulation is here.
A new and different format for future updates.
Instead of continuing with a single update release every 5 years ACLS guidelines will now transition to a continuously updating web based format. The link to that web site is here.
Scientific advances influence ethical decision making.
The loftiest ethical principles are next to useless if not supported by appropriate scientific understanding. Put another way, many bad decisions are made not because of fundamentally bad ethics but because of a lack of understanding about what available technology will and won't do. Examples relevant to ACLS 2015 include therapeutic hypothermia and ECMO.
New upper limits of compression rate and depth.
This became necessary to deal with a manifestation of the law of unintended consequences. When word got out that we should fall on top of the chest and push hard and fast people at times got carried away. Accumulating evidence suggested that excessive rate and depth were associated with lower ROSC rates and more injury, respectively. Here's what the new guidelines have to say about it:
In adult victims of cardiac arrest, it is reasonable for rescuers to perform chest compressions at a rate of 100 to 120/min (Class IIa, LOE C-LD). The addition of an upper limit of compression rate is the result of 1 large registry study associating extremely rapid compression rates with inadequate compression depth.
During manual CPR, rescuers should perform chest compressions at a depth of at least 2 inches or 5 cm for an average adult, while avoiding excessive chest compression depths (greater than 2.4 inches [6 cm]) (Class I, LOE C-LD).
But how do you gauge your own compression depth down to tenths of an inch?
New recommendations for patients with respiratory arrest and suspected opioid abuse.
From the executive summary:
For patients with known or suspected opioid addiction who have a definite pulse but no normal breathing or only gasping (ie, a respiratory arrest), in addition to providing standard BLS care, it is reasonable for appropriately trained BLS providers to administer intramuscular or intranasal naloxone (Class IIa, LOE C-LD).
At long last the guidelines acknowledge the Arizona protocol for cardiocerebral resuscitation (CCR) but don't go far enough.
Again from the executive summary:
For witnessed OHCA with a shockable rhythm, it may be reasonable for emergency medical service (EMS) systems with priority-based, multi-tiered response to delay positive-pressure ventilation by using a strategy of up to 3 cycles of 200 continuous compressions with passive oxygen insufflation and airway adjuncts (Class IIb, LOE C-LD).
We do not recommend the routine use of passive ventilation techniques during conventional CPR for adults, because the usefulness/effectiveness of these techniques is unknown (Class IIb, LOE C-EO). However, in EMS systems that use bundles of care involving continuous chest compressions, the use of passive ventilation techniques may be considered as part of that bundle (Class IIb, LOE C-LD).
For some background on CCR read here. The first sentence of the second paragraph above is misleading. Although data in support of CCR might be considered low level by some EBM purists the evidence in the aggregate is convincing, as cited in the link above. Despite evidence of better neurologically intact survival attributable to CCR it only gets a IIb recommendation. In this particular area the guideline, in my opinion, is about a decade out of date.
Despite an emerging body of evidence for point of care ultrasound it is given only brief mention in the guidelines.
From part 7 of the guideline:
Bedside cardiac and noncardiac ultrasound are frequently used as diagnostic and prognostic tools for critically ill patients.44 Ultrasound may be applied to patients receiving CPR to help assess myocardial contractility and to help identify potentially treatable causes of cardiac arrest such as hypovolemia, pneumothorax, pulmonary thromboembolism, or pericardial tamponade.45 However, it is unclear whether important clinical outcomes are affected by the routine use of ultrasound among patients experiencing cardiac arrest.
Changes in the recommendations for vasopressin.
It has been removed from the routine algorithms but inserted in a new bundle that has a low level recommendation. Again from the executive summary:
Vasopressin was removed from the ACLS Cardiac Arrest Algorithm as a vasopressor therapy in recognition of equivalence of effect with other available interventions (eg, epinephrine). This modification valued the simplicity of approach toward cardiac arrest when 2 therapies were found to be equivalent.
A IIb recommendation for vasopressin as part of a bundle was given for in hospital cardiac arrest. From the executive summary:
The use of steroids in cardiac arrest is controversial. In OHCA, administration of steroids did not improve survival to hospital discharge in 2 studies, and routine use is of uncertain benefit. The data regarding the use of steroids for IHCA were more vexing. In 2 randomized controlled trials led by the same investigators, a pharmacologic bundle that included methylprednisolone, vasopressin, and epinephrine administered during cardiac arrest followed by hydrocortisone given after ROSC improved survival. Whether the improved survival was a result of the bundle or of the steroid therapy alone could not be assessed. As a result of this study, in IHCA, the combination of intra-arrest vasopressin, epinephrine, and methylprednisolone and postarrest hydrocortisone as described by Mentzelopoulos et al16 may be considered; however, further studies are needed before the routine use of this therapeutic strategy can be recommended (Class IIb, LOE C-LD).
The study in question is linked here.
ECMO (ECPR) is given a IIb recommendation in limited situations when expertise is available.
From part 6:
There is insufficient evidence to recommend the routine use of ECPR for patients with cardiac arrest. In settings where it can be rapidly implemented, ECPR may be considered for select patients for whom the suspected etiology of the cardiac arrest is potentially reversible during a limited period of mechanical cardiorespiratory support (Class IIb, LOE C-LD). Published series have used rigorous inclusion and exclusion criteria to select patients for ECPR. Although these inclusion criteria are highly variable, most included only patients aged 18 to 75 years, with arrest of cardiac origin, after conventional CPR for more than 10 minutes without ROSC. Such inclusion criteria should be considered in a provider’s selection of potential candidates for ECPR.
Lipid rescue (ILE) is given a IIb recommendation.
From part 10:
It may be reasonable to administer ILE, concomitant with standard resuscitative care, to patients with local anesthetic systemic toxicity and particularly to patients who have premonitory neurotoxicity or cardiac arrest due to bupivacaine toxicity (Class IIb, LOE C-EO). It may be reasonable to administer ILE to patients with other forms of drug toxicity who are failing standard resuscitative measures (Class IIb, LOE C-EO).
A multimodal approach to estimation of prognosis.
There are detailed updated recommendations for combining neuro exam findings, imaging findings, EEG findings and biomarkers in the guideline. Of interest, for intubated patients, failure to achieve an ETCO2 of greater than 10 is a negative indicator that can be combined with other findings in the estimation of prognosis.
Techniques to promote negative intrathoracic pressure and mechanical CPR devices were reviewed.
These were all either given a IIb recommendation or not recommend at all.
When PE is the cause of the arrest
From part 10:
In patients with confirmed PE as the precipitant of cardiac arrest, thrombolysis, surgical embolectomy, and mechanical embolectomy are reasonable emergency treatment options (Class IIa, LOE C-LD). Comparative data are not available to recommend one strategy over another. Patient location, local intervention options, and patient factors (including thrombolysis contraindications) are recognized elements to be considered. Thrombolysis can be beneficial even when chest compressions have been provided (Class IIa, LOE C-LD). Given the poor outcomes associated with fulminant PE in the absence of clot-directed therapy, standard contraindications to thrombolysis may be superseded by the need for potentially lifesaving intervention.
This, unfortunately, is not very helpful. In the peri-arrest situation the best opportunity for benefit with thrombolytic therapy usually comes when PE is only suspected, not confirmed. But for merely suspected PE the authors give no recommendation one way or the other, citing a lack of evidence.
Updated recommendations for post arrest evaluation and care.
An EEG is recommend for all comatose post arrest patients to diagnose possible seizure, whether or not motor activity is manifested. The guideline cites evidence that epileptiform activity, including non convulsive seizures, may have a prevalence as high as 22%. This is a class I recommendation. The recommendation for antiepileptic drugs is similar to that for status epilepticus in general.
A post arrest oxygen saturation target of 94% is recommended.
There being insufficient evidence, no blood glucose targets are recommended.
No special hemodynamic goals were recommended other than the avoidance of hypotension, meaning SBP below 90 or MAP below 65. This is a IIb recommendation.
Early cardiac catheterization is recommended for all patients in whom an acute coronary event is merely suspected, with or without ST elevation and regardless of neurologic status.
Therapeutic hypothermia is recommend for 24 hours for all post arrest patients not following commands, regardless of presenting rhythm or location of the arrest. No absolute contraindications were given. The new target is 32 to 36 C inclusive.
Defer estimation of neurologic prognosis until: 72 hours post ROSC in those not treated with hypothermia (add estimated time for sedatives and paralytics to wear off) and 72 hours post return to normothermia plus similarly added time in those treated with hypothermia. This often amounts to 4 or 5 days in hypothermia patients.
From the paper:
Methods. We identified all cases of invasive fusariosis between January 2002 and December 2014. We recorded patient characteristics including clinical presentation, treatment, and outcomes at 6 and 12 weeks after diagnosis, as well as species identification and antifungal drug susceptibilities.
Results. Fifteen patients were diagnosed with proven (12, 80%) or probable (3, 20%) fusariosis. Median age was 60 years (range, 26–78), and 10 patients were male. Underlying conditions included hematological malignancies (13, 87%), juvenile idiopathic arthritis (1, 7%), and third-degree burns (1, 7%). Five patients underwent hematopoietic stem-cell transplantation before diagnosis. Six patients (40%) received systemic glucocorticoids, and 11 patients (73%) had prolonged neutropenia at the time of diagnosis. Clinical presentations included the following: skin/soft tissue infection (8, 53%), febrile neutropenia (4, 27%), respiratory tract infection (2, 13%), and septic arthritis (1, 7%). Twelve patients were treated with voriconazole: 6 (40%) with voriconazole alone, 4 (27%) with voriconazole and terbinafine, and 2 (13%) with voriconazole, terbinafine, and amphotericin. One patient (7%) was treated with terbinafine alone, and another with micafungin alone. Four patients underwent surgical debridement (4, 27%). Susceptibility testing was performed on 9 isolates; 8 demonstrated voriconazole minimum inhibitory concentrations greater then or equal to 4 µg/mL. The cumulative probability of survival was 66.7% and 53.3% at 6 and 12 weeks after diagnosis.
Conclusions. Mortality associated with invasive fusariosis remains high. Cumulative mortality at our center was lower than previous reports despite elevated voriconazole minimum inhibitory concentrations. Combination therapy should be studied systematically for fusariosis.
Wednesday, January 13, 2016
Tuesday, January 12, 2016
Published here. The guideline opens with this disclaimer, which acknowledges the first principles of EBM:
It is important to realize that guidelines cannot always account for individual variation among patients. They are not intended to supplant physician judgment with respect to particular patients or special clinical situations. IDSA considers adherence to these guidelines to be voluntary, with the ultimate determination regarding their application to be made by the physician in the light of each patient's individual circumstances.
Candidemia in nonneutropenic patients
An echinocandin is first choice. Fluconazole is considered an alternative in selected patients, not critically ill and considered unlikely to have resistance. (Note that in candidemia the blood cultures initially come back as showing “yeast” rather than “candida.” Although the guideline doesn't specifically address this real world issue treatment needs to be started without delay at that point).
Concerning susceptibility testing in these patients:
Testing for azole susceptibility is recommended for all bloodstream and other clinically relevant Candida isolates. Testing for echinocandin susceptibility should be considered in patients who have had prior treatment with an echinocandin and among those who have infection with C. glabrata or C. parapsilosis..
Transition to fluconazole from an ecinocandin is recommended if all the following conditions are met: the patient is clinically stable; the isolates are sensitive to fluconazole on susceptibility testing; repeat blood cultures after initiation of treatment are negative.
Such patients are recommended to have an ophthalmology exam, preferably by an ophthalmologist, within the first week of diagnosis. (This recommended timing for the exam differs from that of neutropenic patients as will be mentioned below. Different types of occular involvement have specific treatment indications including intraoccular injections in some).
Follow up blood cultures are recommend at least every other day until clearance. The duration of treatment, absent metastatic complications, is two weeks post documented blood culture clearance and symptom resolution.
Regarding central venous catheters, form the paper:
Central venous catheters (CVCs) should be removed as early as possible in the course of candidemia when the source is presumed to be the CVC and the catheter can be removed safely; this decision should be individualized for each patient
Candidemia in neutropenic patients
An ecinocandin is recommend as first choice. Lipid based amphotericin, fluconazole and voriconazole are discussed for certain situations as alternatives.
Duration of therapy is essentially the same as in nonneutropenic patients provided the neutropenia has resolved.
The ophthalmologic exam, in contrast to nonneutropenic patients, is deferred until within one week of recovery from neutropenia, since manifestations are minimal during neutropenia.
The recommendation for central venous catheter removal is similar to that for nonneutropenic patients: clinical judgment, with the understanding that non-CVC sources such as the GI tract figure prominently in neutropenic candidemia.
Ecinocandins and lipid based amphotericin are recommend with equal strength. Treatment is continued until lesions resolve on imaging, often a matter of several months.
Empiric treatment in critically ill patients when candida is suspected but not confirmed
From the paper:
28. Empiric antifungal therapy should be considered in critically ill patients with risk factors for invasive candidiasis and no other known cause of fever and should be based on clinical assessment of risk factors, surrogate markers for invasive candidiasis, and/or culture data from nonsterile sites (strong recommendation; moderate-quality evidence). Empiric antifungal therapy should be started as soon as possible in patients who have the above risk factors and who have clinical signs of septic shock (strong recommendation; moderate-quality evidence).
29. Preferred empiric therapy for suspected candidiasis in nonneutropenic patients in the intensive care unit (ICU) is an echinocandin (caspofungin: loading dose of 70 mg, then 50 mg daily; micafungin: 100 mg daily; anidulafungin: loading dose of 200 mg, then 100 mg daily) (strong recommendation; moderate-quality evidence).
This seems to me like a low threshold for adding antifungal agents and this is in reference to nonneutropenic patients. Oddly enough neutropenia is not mentioned in this portion of the guideline but I would think an even lower threshold might apply.
Prophylaxis against invasive candidiasis in critically ill patients
Here a low level and somewhat vague recommendation is given:
34. Fluconazole, 800-mg (12 mg/kg) loading dose, then 400 mg (6 mg/kg) daily, could be used in high-risk patients in adult ICUs with a high rate (greater than 5%) of invasive candidiasis (weak recommendation; moderate-quality evidence).
35. An alternative is to give an echinocandin (caspofungin: 70-mg loading dose, then 50 mg daily; anidulafungin: 200-mg loading dose and then 100 mg daily; or micafungin: 100 mg daily) (weak recommendation; low-quality evidence).
From the paper:
Empiric antifungal therapy should be considered for patients with clinical evidence of intra-abdominal infection and significant risk factors for candidiasis, including recent abdominal surgery, anastomotic leaks, or necrotizing pancreatitis (strong recommendation; moderate-quality evidence).
Concerning necrotizing pancreatitis most general recommendations are against antimicrobial treatment unless there is evidence of infected necrosis.
From the paper:
122. For mild disease, clotrimazole troches, 10 mg 5 times daily, OR miconazole mucoadhesive buccal 50-mg tablet applied to the mucosal surface over the canine fossa once daily for 7–14 days are recommended (strong recommendation; high-quality evidence).
123. Alternatives for mild disease include nystatin suspension (100 000 U/mL) 4–6 mL 4 times daily, OR 1–2 nystatin pastilles (200 000 U each) 4 times daily, for 7–14 days (strong recommendation; moderate-quality evidence).
124. For moderate to severe disease, oral fluconazole, 100–200 mg daily, for 7–14 days is recommended (strong recommendation; high-quality evidence).
From the document:
131. Systemic antifungal therapy is always required. A diagnostic trial of antifungal therapy is appropriate before performing an endoscopic examination (strong recommendation; high-quality evidence).
132. Oral fluconazole, 200–400 mg (3–6 mg/kg) daily, for 14–21 days is recommended (strong recommendation; high-quality evidence).
133. For patients who cannot tolerate oral therapy, intravenous fluconazole, 400 mg (6 mg/kg) daily, OR an echinocandin (micafungin, 150 mg daily, caspofungin, 70-mg loading dose, then 50 mg daily, or anidulafungin, 200 mg daily) is recommended (strong recommendation; high-quality evidence).
There is much more in the body of the paper. I have only provided highlights of things I think hospitalists might need for quick reference.
Here is the transcript of a wonderful talk by Faith Fitzgerald.
Over the past decade there has been a call to increase the emphasis on the humanities in the pre medical curriculum. Dr. Fitzgerald seems to take a contrarian view:
A number of months ago, a second-year medical student e-mailed me to ask about the value of humanities courses in our preclinical curriculum. A humanities major in college, he questioned the overwhelming dominance of medical sciences in his first 2 years of classes.
Science is, and must be, the mind of medicine: It is what differentiates us from quacks, and what patients depend on for their future well-being. Yet some say we should, in addition, teach humanities in medical schools because the applicants preferentially selected for admission are science-techno-geeks.
But that's not true! Among our medical students are musicians, poets, historians, dancers, and artists. They come from many and diverse backgrounds in culture, religion, and language. These humanities aren't extinguished in medical school, although some may be temporarily sidelined.
Still, shouldn't we have required classes in the humanities to emphasize to our students that study of the humanities makes people better doctors?
Sadly, there's not much evidence that it does. In the first half of the 20th century, Germany was a highly educated nation in literature, philosophy, and music. And what this allowed Nazi doctors to do in the death camps was to march their victims to the ovens with prisoner orchestras playing Handel and Bach to quiet them on their way to a cruel death.
The real education in the humanities, she maintains, comes from spending time with patients and getting to know them as persons.
There is a lot to unpack in her talk and I highly recommend reading it in full.