On Camshafts and Communication

“It’s a really loud rumble as I’m driving along and it sounds like it’s coming from the back axle. I’ve spoken to my mate Dave (he used to rebuild old bikes you know) and he thinks it’s the wheel bearing. Not trying to tell you your job, you understand… You’re the expert…. Have a look and see what you think…”

I trail off into a slightly awkward silence that the mechanic cheerfully fills. I realise that what I’ve done is akin to what my patients frequently do; I’ve come into the car emergency department (well, my local garage) with a preconceived idea of what’s wrong because I’ve “spoken to Dave.” I could equally have “googled it” or “had a friend who had the same problem.” I feel a building empathy for the chap in front of me who has almost certainly stripped down more wheel bearings than I’ve inserted cannulas, yet who manages to indulge my ramblings. He does so because it’s part of his job not to offend the customer, just as much as it is to actually work out why my car is making more noise than an angry swarm of wasps in a bass drum.

As I sit there waiting to find out if Dave was right (he wasn’t), watching anxious customer follow anxious customer, I begin to see frequent parallels between the mechanic’s job and my own. He listens to symptoms (“She’s knockin’ when I go over a bump” or “She’s pulling to the left when I brake”) and he clarifies detail: “Did you hit the curb parking?” I can see him making a differential diagnosis in his mind as he walks off into the workshop to begin the initial investigations. The customer waits nervously, wondering how serious it is (how many columns will be on the final invoice.) The mechanic checks the car for dangerous faults (“…of COURSE your 24-year-old weight-lifter’s pleuritic chest pain is probably musculoskeletal, but you wouldn’t want to miss a P.E. Where’s that link to the Wells score again?”) and then has a look at the more likely stuff. He also humours me by checking out the wheel bearings, not because he thinks they’re the likely source of my noisy ride but because he knows I won’t be happy until he’s allayed my concerns.

Finally he comes to a diagnosis (“the tracking’s out and your rear wheels are wearing unevenly”) and proposes a treatment plan (“New tires and a quick go on the machine that makes sure all 4 wheels are pointing in the same direction, at least until you hit that curb again…”) In my case it’s easy; no complicated jargon, no debate about the cause of my problem, a relatively cheap solution and a high chance of success. But what about the unfortunate chap after me? He had an intermittently illuminating ABS light.

The mechanic patiently explained that unless the light came on whilst he was in the garage, investigating the multitude of possible causes would be drawn out, expensive and potentially fruitless. I couldn’t help but think back to the 24-year-old weight-lifter again. More specifically, I was remembering the inner monologue that occurred whilst I wrote my notes; that wonderful breathing space in any emergency physician’s day where you actually get a chance to think. “Of course it’s ALMOST certainly musculoskeletal, but he IS describing sudden onset pleuritic chest pain… What’s his Wells score? Good, low risk… Oh, bugger, his D-dimer’s up. I KNEW it would be, he said he had a snotty nose. Oh, thank goodness, I can PERC him… Excellent, PERC negative, I can discharge. Wait, what about pneumothorax? Better get a chest x-ray, just in case…” In medicine, and particularly in the emergency department, we’re comfortable balancing probability and risk. However, it took me longer to learn how to explain this to the anxious young lady with the non-specific abdominal pain, the normal observations and the soft belly than I care to admit. I know perfectly well that her pain will almost certainly dissipate as inexplicably as it arrived and if it doesn’t then we’ll have plenty of time to act on her worsening symptoms before anything untoward happens. However, convincing her of this fact at 3am is always a task requiring rapport, finesse and careful safety netting advice.

As I hear my mechanic put yet another anxious patient at ease (“It’s probably just smoking because it’s a diesel. They always run a bit dirty and if it’s your head gasket that’s going then you’ll get plenty of warning. Just keep an eye on the oil and make sure it doesn’t turn milky.”) I wonder where he developed the consultation skills that I’ve worked on my whole career. I’m relatively sure that nowhere in his training was there a session labeled “Simulated Customer Encounter” or “Breaking Bad News”, yet he manages it like a seasoned, kindly, greying physician who appears to have all the time in the world in the middle of a busy medical ward round.

Perhaps if we’d spent less time ensconced amongst the pillars of books with our noses buried in the latest journal and just a little more time chatting to Dave we wouldn’t need lectures to remind us how to talk to people.

Now, if only I knew my camshaft from my timing belt then I might even be ready for a career change.

Guest post by Dr Andrew Tabner. CESR Trainee and Teaching Fellow, Royal Derby Hospital

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Correcting Acidosis or Just adding CO2?: On Sodium Bicarbonate for Metabolic Acidosis

Clinical Scenario:
You are working in the emergency department when an elderly male is brought in by EMS after being found unresponsive at home with an unknown downtime.  The paramedics report a possible seizure.  His finger stick glucose registers as critical high.  Post-intubation for poor GCS,  his initial labs reveal an ABG of  6.8/20/90 and a lactate of 18.   As you are signing out the patient to the ICU the ICU team requests a sodium bicarbonate infusion.  You wonder, will sodium bicarbonate administration improve outcomes or correct acidosis faster when compared to normal saline?

Physiology & Literature Review:
Other than well-defined indications for sodium bicarbonate administration (such as treatment of Na-channel blockade in TCA overdose or to induce alkalinization in salicylate toxicity), one should be skeptical about administering sodium bicarbonate simply for acidosis. On the one hand if a patient is acidotic, it makes intuitive sense that you should try to alkalinize them, which is why sodium bicarbonate has been used so often in the past.  On the other hand, there is evidence to show that administration of sodium bicarbonate shifts the oxygen dissociation curve, increasing hemoglobin affinity to oxygen,  and resulting in paradoxical tissue hypoxia and causes an increase in lactate production. In addition, it causes an intracellular acidosis.  Despite this,  because it tends to be part of the "code cocktail",  it is often administered anyway. 

Rise in EtC02 after bicarb (Dr. Sacchetti video)
The effect of administration of Sodium bicarbonate on the end-tidal CO2 in an intubated patient with severe metabolic acidosis is well demonstrated by  this video by Dr. Alfred Sacchetti. While we disagree in giving a bicarb drip as mentioned in the video, it does demonstrate the acid-base physiology in real time. 

A small randomized-controlled trial published in Critical Care Medicine more than 20 years ago gave either a blinded bolus of saline or sodium bicarbonate to patients with lactic acidosis vasopressor support [1].  They then checked ABGs one hour later.   While sodium bicarbonate did increase the venous bicarb level, improved pH, it did not improve hemodynamics.

Regarding two common metabolic acidosis scenarios seen in the emergency department, Diabetic ketoacidosis, the evidence suggests that sodium bicarbonate has the potential to cause harm:
     1. Diabetic ketoacidosis: A recent retrospective observational cohort study examined the effect of sodium bicarbonate on 86 patients in DKA with a pH less than 7.044 patients received sodium bicarbonate and 42 did not.  There was no difference in time to resolution of acidosis (pH greater than 7.2) or hospital length of stay between the two groups. However, there was a significant increase in insulin and fluid requirements in the sodium bicarbonate group. With regard to pediatrics, the PECARN study examining DKA in the pediatric population found that one of the only risk factors for cerebral edema (once again a retrospective analysis) was administration of sodium bicarbonate [3].

    2. Lactic Acidosis: Regarding lactic acidosis, an article from Korea retrospectively looked at 103 patients with acidosis (CO2 less than 20) and lactate greater than 3.3 mmol and compared those that got bicarb (69) to those that did not (34) [4].  Patients who received sodium bicarbonate had increased mortality, but this was confounded by the fact that these patients had lower initial pH, higher initial lactate, and higher APACHE 2 scoresWhen they ran their regression analysis, the only two things that were independently associated with mortality were Sequential Organ Failure Assessment (SOFA) and bicarb administration (95% CI 1-251).   When the authors did a subgroup analysis by excluding less ill patients (SOFA less than 8), they found again that administration of sodium bicarbonate was  associated with death.  They also found that those that received sodium bicarbonate cleared their lactate more slowly. 

Take home points:
Sodium bicarbonate may increase serum pH, but may worsen rather than improve prognosis.  Other than indications where sodium bicarbonate is the treatment for the acidosis (such as TCA overdose), the treatment for metabolic acidosis is to correct the underlying cause, whatever it may be.

Submitted by Wes Watkins, PGY-4
Edited by Louis Jamtgaard, PGY-3 @Lgaard
Faculty reviewed by Evan Schwarz @TheSchwarziee

1. Mathieu D, Neviere R, Billard V, Fleyfel M, Wattel F (1991) Effects of
bicarbonate therapy on hemodynamics and tissue oxygenation in patients with lactic-acidosis: a prospective, controlled clinical study. Crit Care Med 19: 1352– 1356.
2. Adeva-Andany, M. M., Fernández-Fernández, C., Mouriño-Bayolo, D., Castro-Quintela, E., & Domínguez-Montero, A. (2014). Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis. The Scientific World Journal, 2014.
3. Glaser N, Barnett P, McCaslin I, et al; Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics: Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med 2001; 344:264–269

4. Kim, H. J., Son, Y. K., & An, W. S. (2013). Effect of Sodium Bicarbonate Administration on Mortality in Patients with Lactic Acidosis: A Retrospective Analysis. PloS one, 8(6), e65283.

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New Medical Device to Bring Tears to Your Dry Eyes


Serious dry eye can be quite debilitating and current therapies like eye drops and cyclosporine are either difficult to manage or don’t really fix the problem. Eye drops require refrigeration, so keeping them cold and handy is a challenge. Cyclosporine, on the other hand, only treats the inflammation and has a low rate of patient compliance. A company called Oculeve, which came out of the Stanford Biodesign program, has developed a tiny implant that may help a lot of people suffering from dry eye caused by a variety of underlying conditions.

The device electrically stimulates the lacrimal gland, the organ responsible for tear production. There’s two versions of the device, one that is placed within the nasal cavity and the other is implanted under the skin above the eyelids. The device, which can be controlled using a wireless interface, has already been in clinical trials in Australia, New Zealand, and Mexico toward getting European and Canadian approvals, and trials aimed at the FDA are already being planned.

Stanford: A real tear-jerker: Team creates device to alleviate dry eye…

Oculeve’s ghost homepage…

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Pillole di infermieristica: prelievo venoso e agocannula

Giulio, è da almeno  6 ore in osservazione in Pronto Soccorso per eseguire una curva enzimatica a causa di un dolore toracico. Mentre mi preparo ad eseguire il prelievo venoso mi chiede pensieroso: “Perchè non preleva direttamente dall’agocannula anziché pungermi un’altra volta?” Questa domanda è servita come spunto per scrivere questo post. Premessa: Nonostante l’assistenza […]

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MIT’s Fiber Implants Deliver Light, Electrical, Chemical Stimulation While Monitoring Brain (VIDEO)


Conventional brain implants are typically rigid and use materials that can irritate fragile tissue. Such devices have limited in-vivo lifetime and prevent more complicated functionality to be built into them. They typically do one task, such as drug delivery or neural sensing, and usually can’t deliver therapy while monitoring its effects in real time. Scientists at MIT have now developed a novel type of fibers that can simultaneously transmit electrical and optical stimulation, deliver drugs, and read the brain’s electric signals while causing little irritation to nearby tissue.

The polymer fibers in some ways mimic our own nerves but have electrodes, a tube, and an optical channel built. These are created by first making them relatively large and easy to work with. Once the components are built, positioned, and aligned, the device is heated to soften it up. Carefully sucking it through a narrow straw while still hot squishes it together into a very narrow fiber that maintains the functional components created earlier. Repeating this process makes the implant progressively narrower.

The new implants should help further develop the science of optogenetics, which uses light to stimulate small groups of brain neurons, as well as advance research into all kinds of brain therapies in which multi-modal stimulation and simultaneous monitoring can have a great benefit.


Study in Nature Biotechnology: Multifunctional fibers for simultaneous optical, electrical and chemical interrogation of neural circuits in vivo…

MIT: New fibers can deliver many simultaneous stimuli…

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