Saturday, 26 November 2016
Tuesday, 8 November 2016
Web wisdom this edition comes from the climes of mostly trauma this time but also from philosophers in our field from around the globe.
- Amal Mattu to the graduating resident - Advice from a sage
- Liver lacs explained - Are you enzyme addicted?
- Motorbike accident with a rare complication - Pneumo - what?
- Out of Africa - Could you take one night in the Cape?
- 10 resus orders - Fire fighting in EM
- Pressure in trauma? - Probably the best explanation in managing hypotense trauma patients
The last link and its sequel is a must hear audio cast. It is a simplistic yet deep dive into management of the critically injured trauma patient.
Wednesday, 26 October 2016
Sometimes you just have to introspect and surmise that you have been doing silly things in your craft. This is undoubtedly one of those times.
Superb myth busting by Medscape. Original article with references is here.
Superb myth busting by Medscape. Original article with references is here.
Myths Surrounding Antibiotics
After 80 years of experience, much is known about antibacterial agents. Unfortunately, some of what is "known" is incorrect. To paraphrase Osler, half of everything we're taught is wrong—the problem is, which half?
Here, we seek to debunk five widely believed myths about antibiotics and resistance.
Myth 1: Humans Invented Antibiotics in the 20th Century
The first clinically useful antibacterial agent that was safe and effective was prontosil rubrum, a sulfa drug synthesized in 1931. However, prontosil was not the first antibacterial agent to be invented, and humans were not the initial inventors.
Genetic analysis indicates that bacteria invented antibiotics and an antibiotic-resistance mechanism somewhere between 2 and 2.5 billion years ago.[2-4] Bacteria have been killing each other with these weapons, and using resistance mechanisms to protect themselves against these weapons, for 20 million times longer than we have even known that antibiotics exist.
To underscore the point, in 2011, a study was published in which investigators explored a deep cave in the Carlsbad Caverns system in New Mexico, a geological formation that has been isolated from the surface of the planet for 4 million years. The section of the cave that they explored had never before been accessed by humans.
The investigators cultured many different types of bacteria from the walls of the caves. Every strain of bacteria was resistant to at least one modern antibiotic; most were multidrug-resistant. Not only was resistance found to naturally occurring antibiotics, it was also found to synthetic drugs that were not created until the 1960s-1980s (including fluoroquinolones, daptomycin, and linezolid).
Implications of busting this myth. After 2 billion years of microbial evolutionary warfare, microbes have already invented antibiotics to poison every possible biochemical pathway, and resistance mechanisms to protect every one of those pathways. Thus, resistance mechanisms to antibiotics that have not yet been invented are already widespread in nature. Resistance is inevitable.
Myth 2: Inappropriate Antibiotic Use Causes the Development of Resistance
This myth is often repeated, with the implication that if we could eliminate inappropriate antibiotic use, resistance would no longer develop. However, all antibiotic use causes selective pressure by killing off bacteria. Appropriate use applies the same selective pressure as does inappropriate use. The difference is that we can and should stop inappropriate use because it offers no benefit. In contrast, appropriate antibiotic use is necessary to reduce mortality and morbidity from bacterial infections.
Implications of busting this myth. We accept that there will always be emergence of resistance from appropriate antibiotic use, but the benefit of appropriate antibiotic use to patients and society outweighs the collective harm. In contrast, without a benefit attached to inappropriate use, there is no "pro" to offset the "con" of selective pressure for antibiotic resistance.
In essence, we must seek to eliminate inappropriate antibiotic use not because this will end emergence of resistance, but because it will slow it down without forgoing any meaningful benefit of antibiotic use.
Myth 3: To Prevent Resistance, Patients Must Complete Every Dose of Antibiotics Prescribed, Even After They Feel Better
The origins of this myth are slightly obscure, but appear to date back to the 1940s.[6,7] Despite how widespread and deeply this belief is held, there are no data to support the idea that continuing antibiotics past resolution of signs and symptoms of infection reduces the emergence of antibiotic resistance.
To the contrary, studies have repeatedly found that shorter-course therapies are less likely to select out for antibiotic resistance, which is consistent with fundamental principles of natural selection. Every randomized clinical trial that has ever compared short-course therapy with longer-course therapy, across multiple types of acute bacterial infections (including cellulitis, acute bacterial sinusitis, community-acquired pneumonia, nosocomial pneumonia/ventilator-associated pneumonia, complicated urinary tract infections, and complicated intra-abdominal infections), has found that shorter-course therapies are just as effective. When evaluated, shorter-course therapies have resulted in less emergence of resistance.
Implications of busting this myth. This myth needs to be replaced by a new antibiotic mantra: "Shorter is better!" Patients should be told that if they feel substantially better, with resolution of symptoms of infection, they should call the clinician to determine whether antibiotics can be stopped early. Clinicians should be receptive to this concept, and not fear customizing the duration of therapy.
Continuing antibiotics past resolution of symptoms for acute bacterial infections (not chronic infections, such as osteomyelitis, tuberculosis [TB], or actinomycosis) does not afford patient benefit and probably selects for antibiotic resistance.
Myth 4: When Antibiotic Resistance Emerges, It Is Usually a Consequence of New Mutations at the Site of Infection
This myth possibly stems from the correct recognition that resistance in TB occurs at the site of infection, owing to spontaneous mutations targeting TB therapy. However, TB has unique features distinct from those of most acute bacterial infections.
There is no environmental reservoir for TB, and TB is not part of our normal flora. Therefore, TB resistance can only occur at the site of infection in the body. TB cavities also contain very high densities of bacilli (ie, > 1012 per gram), which predispose to the emergence of resistance on monotherapy, on the basis of the statistical frequency of spontaneous mutations to such drugs as isoniazid and rifampin.
In contrast, when we use typical antibiotics (different from isoniazid, which is specific for TB), they inevitably cause selective pressure among a person's normal bacterial flora. In most cases, resistance emerges not at the site of infection during a course of therapy, but rather among bacteria in the gut or on the skin as a result of genetic sharing of preexisting resistance mechanisms (eg, plasmids, transposons, phages, naked DNA).
Enrichment for resistant normal flora can result in future infections caused by the resistant pathogens, and spread of the resistant pathogens through contact with other people or fomites.
Implications of busting this myth. In most cases, we are not aware when resistance emerges in patients. The fact that the patient's infection resolves with prolonged or unnecessarily broad antibiotic therapy does not mean that you have escaped inducing resistance. To the contrary, it is very likely that after exposure to antibiotics, somewhere in the patient's body, strains of normal flora that are resistant to the antibiotics used have been enriched. Those strains can cause future infections, or spread to others in communities or hospitals.
Myth 5: Cidal Antibiotics Result in Superior Clinical Outcomes and Less Risk for Emergence of Resistance Than Do Static Antibiotics
This is another widespread clinical belief that is based on no evidence. First, contrary to common belief, bacteriostatic ("static") antibiotics do kill bacteria; they just require a higher concentration to achieve specific thresholds of bacterial reduction. The formal definition of a bactericidal ("cidal") antibiotic is one for which the minimum bactericidal concentration (MBC) of the drug is fourfold or more above the minimum inhibitory concentration (MIC) of the drug.
The MBC is the concentration of the drug that results in a 1000-fold reduction in bacterial density at 24 hours of growth. The MIC is the concentration that inhibits visible growth at 24 hours of growth. These definitions are arbitrary: Why should it be that MBC requires a 1000-fold reduction in bacterial density as opposed to a 100-, 500-, 5000-, or 10,000-fold reduction? Why 24 hours? Why must the MBC not be more than fourfold above the MIC, as opposed to twofold, or 16-fold, or 23-fold?
Finally, an antibiotic that achieves a > 1000-fold reduction in bacterial density but does so at a concentration that is eightfold above the MIC of the drug is considered static, even though it clearly kills the bacteria.
Given that these terms have been defined by accepted convention and are not based on specific scientific principles, perhaps it is not surprising that there is no clinical evidence of benefit of cidal agents over static agents. A systematic literature review identified 28 randomized controlled trials that compared the efficacy of static vs cidal antibiotics, head to head, for patients with invasive bacterial infection.
In contrast, only one trial found a cidal antibiotic to be superior in efficacy to a static agent. That trial compared tigecycline vs imipenem for the treatment of ventilator-associated pneumonia, and found that tigecycline was inferior. However, pharmacologic analysis determined that the tigecycline dose used in the trial was too low, resulting in inadequate drug levels compared with the susceptibility of bacteria causing the infections; when a subsequent trial was done with double the dose of tigecycline, tigecycline was similar in efficacy to imipenem for the same disease.
Thus, there is no evidence that cidal antibiotics are more clinically effective than static antibiotics. To the contrary, more studies have found a static agent to be superior in efficacy to a cidal agent than the reverse!
Implications of busting this myth. Although clinicians continue to prefer cidal antibiotics, there is no evidence that these result in superior clinical outcomes than static agents, nor that cidal drugs more effectively prevent the emergence of resistance. Whether an antibiotic is static or cidal should not be a factor in determining antibiotic therapy for patients.
What Are the Take-Home Messages for Clinicians?
There is no end to our struggle with bacteria; we will never "win a war" against them, and no "gorilla-cillin" will ever come along to save us from emergence of antibiotic resistance. Resistance is inevitable.
Thus, it is critical that we not waste antibiotics. They must not be prescribed to patients who do not have bacterial infections. When appropriate, prescribe the narrowest-spectrum agent and the shortest duration possible to treat bacterial infections.
Do not instruct patients to take every dose prescribed even after they feel better. Rather, focus on evidenced-based, short-course regimens, and if the patient's symptoms resolve before completing the course of therapy, ask that they call you to discuss whether they should stop the antibiotic course early. Encourage them to stop early when their symptoms resolve.
Do not be falsely reassured by the lack of emergence of resistance at the site of infection. When you prescribe an antibiotic, you are selecting for resistance in the patient's microbiome. The resistant bacteria colonize the patient and can cause future antibiotic-resistant infections.
When choosing an antibiotic regimen, cidal vs static is largely irrelevant.
Tuesday, 27 September 2016
Friday, 9 September 2016
Another post from our senior residents in EM - Dr Koh Shao Hui.0830H:
It is a quiet Monday morning in the resus room. Suddenly the VHF radio crackles to life: “48, yr old, Indian male. Standby for AMI. ETA 10 mins”
A 12 lead ECG is faxed over by the paramedics
What does the pre-hospital ECG show? The team prepares for the arrival of the patient.
Patient arrives with rhythm strip on board ambulance. (Together with strip done at OPS)
Additional history: Chest pain radiating to left arm since last night. Worse this morning occurring even at rest. A/w diaphoresis. Went to OPS, conveyed here by SCDF. PO aspirin 300mg loaded en route.
O/e: Alert, Diaphoretic, cold and clammy peripheries. L: clear. H: dual heart sounds, no murmurs. Pulses equal. Calves supple. No pedal oedema
Vitals: BP 160/74 HR 70 spo2 98% on RA
Defib pads put on stat with continuous cardiac monitoring.
Standard and right-sided ECG leads
What do the above ECGs show?
Diagnosis: Inferior-right sided STEMI
Consent taken. Cath Lab activated. Patient loaded with PO ticagrelor. IV cannulation performed and bloods sent off. Given IV morphine and maxolon.
Cath lab calls for patient. Ready to move out.
Change in cardiac rhythm noted on monitoring and patient becomes unresponsive.
1 x DC shock 150J delivered stat. Rhythm changes to NSR transiently and patient transiently regains consciousness. Goes back into VF shortly after. 2nd shock delivered. Goes back into NSR transiently but goes back into VF shortly after. Still spontaneously (agonally) breathing. Decision made to secure away via RSI. (Etomidate and Sux) Intubation performed. CPR commenced with manual bagging. Patient remains in VF. Further shock given. Given IV adrenaline 1mg. CPR continued. Further 4 shocks given. Further bolus doses of adrenaline given. IV boluses of amiodarone, lignocaine and MgSo4 given (As patient noted to have runs of polymorphic VT in between).
First semblance of a perfusing rhythm seen
Pulse present! BP 150/80. Total downtime (Time from collapse to first sustained ROSC) - 19 mins.
Patient connected to ventilator and started on IV fentanyl infusion 50mg/H. Maintained on amiodarone infusion.
Leaves ED for cath lab. Reaches cath lab. (Door to balloon time approx 1Hr)
Cardiac catheterisation performed with angioplasty done.
100% stenosis noted in p-mRCA (accounting for ST elevation in Right sided leads)
85% stenosis noted in dRCA extending into RPAV (accounting for ST elevation in inferior leads)
Thrombectomy performed and Drug eluting stents put into RCA and RPAV.
Patient is subsequently transferred to MICU (under cardiology) for further monitoring
He is extubated the next day with neurology fully intact.
2 days after:
Friday, 2 September 2016
Saturday, 20 August 2016
Troponins have been with us from the 90's and the more refined they are, the more wide your "catch" will be from the high sensitivity "net" we cast. But you may wonder what the outcome is from all the high sensitivity. Here's a short viewpoint from an Aus study.
Original article from Medscape:
Original article from Medscape:
High-Sensitivity Troponin Test Yields Only Modest Benefit in Assessing Chest Pain in ER
Larry HandAugust 12, 2016
BEDFORD PARK, AUSTRALIA — Use of high-sensitivity troponin T (hs-TnT) assays, compared with standard TnT assays, may result in only modest improvement in evaluating emergency-department patients with chest pain, according to a new study.
For the high-sensitivity assays to be clinically effective, it may require closely joining them with protocols that can help guide interpretation and care, researchers conclude.
"The adoption of new technologies such as high-sensitivity TnT assays requires commensurate adaptions in the health service. Just releasing the assays provides very modest improvements in care and outcome since practice, appropriately, needs to remain conservative," Dr Derek P Chew (Flinders Medical Center, South Australia), told heartwire from Medscape by email.
Chew and colleagues conducted a prospective trial involving 1937 emergency-department patients without ST-segment elevation presenting at five hospitals in Adelaide, Australia, between July 2011 and March 2013.
The results were published online August 9, 2016 in Circulation: Cardiovascular Quality and Outcomes.
The patients were randomized to troponin testing reported to standard TnT levels (>30 ng/L n=964) or high-sensitivity TnT levels (>3 ng/L, n=973) to assess for the cumulative composite end point of all-cause mortality and new or recurrent acute coronary syndrome (ACS) within 12 months. Median patient age was 61, and just over half were men.
The researchers found no significant between-group differences for the primary end point. At 12 months, deaths or new or recurrent ACS occurred in 57 (9.7%) of patients in the high-sensitivity group and in 69 (7.2%) of patients in the standard group (hazard ratio 0.83, P=0.362).
Although the researchers found no between-group differences overall in discharge to home directly from the emergency department, they did observe a higher rate of discharge from the emergency department among low- or no-risk patients in the high-sensitivity group compared with the standard group (168 vs 148, P=0.010).
Researchers observed a significant interaction between use of hs-TnT and the prescription of aspirin among patients with peak troponin of 14 to 29 mg/L within 24 hours (55.4% vs 34.0%, P=0.006).
During the index hospitalization, 1466 patients (75.7%) reached maximal troponin of <30 ng/L within 24 hours.
The researchers found no between-group difference in performance of angiography, and high-sensitivity reporting did not lead to a reduction in 12-month death or new or recurrent ACS overall. But they did observe a modest reduction in death or new or recurrent ACS among patients with troponin levels <30 ng/L (2.6% vs 4.4%, HR 0.58, P=0.050).
The authors say that this study is the first to evaluate unguided troponin T reporting at levels that are possible with a high-sensitivity troponin T assay "on clinical care and outcome within a randomized clinical trial embedded within routine emergency-department care.
"Reporting of the troponin T level without integration with clinical protocols had relatively little impact on admission and cardiac investigations, with modest differences in discharge rates among patients at low and intermediate risk based on other clinical criteria," they conclude.
"To that end, I am a little surprised that the difference is very small, given the numerous voices demanding access to new tests," Chew said. "Clearly, better access will require validated protocols. The further research that is needed is validation of some of the emerging protocols that have been promoted without randomized evidence of safety and efficacy. We have commenced a randomized study with a 1-hour protocol."
The National Health & Medical Research Council of Australia and the South Australian Department of Health supported this research. The authors reported no relevant financial relationships.