With some of the latest literature, the recommendation has been to transfer patients with STEMI post resuscitation if they are responsive. This latest article from the Journal of the American College of Cardiology just published this gem that talks about what we do if they are still comatose!

This algorithm starts pre-hospitally. Return of circulation occurs and we transport to the nearest hospital. Within 10 minutes, the physician is to have a 12-lead ECG done and initiate mild therapeutic hypothermia (like the studies suggest, avoiding fever is the goal).

So, now we see the massive STEMI. As the previous literature suggests, we push these guys for emergent angiography and PCI should the patient not have unfavourable conditions. Nothing changes here.

What about those patients  that the physician finds that is non-STEMI?

They introduce the “ACT” abbreviation. Essentially, Assess for unfavourable resuscitation features. Consult with cardiology and intensive care.  Transport to cath lab once the decision has been made for angiography.

What is an unfavourable feature you might ask? Well, they include the following:

• Unwitnessed arrest
• Initial rhythm: Non-VF
• No bystander CPR
• >30 min to ROSC
• Ongoing CPR
• pH <7.2
• Lactate >7
• Age >85
• End stage renal disease
• Noncardiac causes (e.g.,traumatic arrest)

(Rab et al. 2015, p. 64)

With multiple unfavourable features, the patient should be considered for individualised care. Those who are deemed suitable should be sent for early angiogram and PCI.

We may start to see this coming into play within your local ED. What are your local policies and procedures involving this?

As practitioners, remember the value of your history. We can relay important information, such as down time, bystander CPR, initial rhythm and so on.

“Successfully resuscitated comatose patients represent a heterogeneous population with a baseline survival rate of only 25%. With hypothermia and PCI, survival improves to 60%, with favorable neurological outcomes achieved in 86% of survivors” (Rab et al. 2015, p. 63)

Rab, T., Kern, K., Tamis-Holland, J., Henry, T., McDaniel, M., & Dickert, N. et al. (2015). Cardiac Arrest. Journal Of The American College Of Cardiology, 66(1), 62-73. doi:10.1016/j.jacc.2015.05.009

The debate has been happening for a while now! Do we actively cool or not? Well, many guidelines have us pushing our patients for that deep hypothermia to below 33 degrees. Nielson in 2013, found that patient outcomes did not change with the maintaining normothermia when compaired to hypothermia.

So fever is bad, and we ultimately need to avoid it.

While the debate continues with adults, there has been little evidence with pediatrics surrounding this.

Until now!

In an article published in the New England Journal of Medicine, Moler et al (2015) find that “in comatose children who survived out-of-hospital cardiac arrest, therapeutic hypothermia, as compared with therapeutic normothermia, did not confer a significant benefit in survival with a good functional outcome at 1 year”.

Here is a link to the abstract

This study showed there was a difference, however not significant. Perhaps a larger study would be required. Let me know your thoughts in the comment section!

References

Moler, Frank W. et al. ‘Therapeutic Hypothermia After Out-Of-Hospital Cardiac Arrest In Children’.New England Journal of Medicine 372.20 (2015): 1898-1908. Web. 17 June 201

Nielsen et al. Targeted Temperature Management at 33°C versus 36°C after Cardiac Arrest NEJM 2013;epub Nov 17, 2013

University of Oxford – Patients who monitor their own treatment with warfarin or other blood-thinning drugs reduce their risk of developing blood clots by half, an Oxford University study has found.

Taking charge of their own treatment can empower patients, improve the quality of treatment and be more convenient. The researchers say their findings confirm that self-monitoring of warfarin is safe for suitable patients of all ages.

The results are published in the medical journal The Lancet.

‘Warfarin is used for a number of conditions to prevent the blood clotting,’ explains Dr Carl Heneghan, who led the work at the Department of Primary Health Care at Oxford University. ‘These conditions include atrial fibrillation, treatment of deep-vein thrombosis and patients with artificial heart valves.’

In the UK, it is thought that around 1 million people are eligible for blood-thinning drugs, or anticoagulants, with demand set to rise further due to the ageing population.

But the use of anticoagulants needs regular monitoring to make sure the dose remains within the right range.

‘If the dose is too high then individuals can be at substantial risk of a major bleed, whereas if it is too low they run the risk of having a blood clot,’ says Dr Heneghan.

The right dose is affected by a number of factors that make safe and effective management of anticoagulation challenging. For example, increasing age, medications, vitamins, alcohol, diet, and changes in lifestyle can all affect the dose that should be used.

‘Management of oral anticoagulation treatment is often done badly,’ says Dr Heneghan. Up to 40% of cases can be outside the correct dosing level. ‘But it is possible to empower patients not only to self-measure but also to self-adjust their therapy.

Patients use a simple test, much like a blood glucose meter for diabetics, to ‘self-monitor’ their treatment. Some patients also then ‘self-adjust’ their dose as appropriate, while others may see their doctor at this point.

The Oxford team looked at the evidence for any benefits of self-monitoring by pooling individual patient data from 11 previous randomised trials involving over 6,400 patients.
It is possible to empower patients not only to self-measure but also to self-adjust their therapy

The researchers found that self-monitoring reduced by 49% the risk of blood clots – events including deep vein thrombosis, stroke, or a heart attack – compared with usual care. There was no difference in the number of major bleeds or deaths.

‘A wide range of ages was included in the analysis. The youngest was 17 and the oldest was 94 years of age. Across all these ages self-monitoring proved to be a safe intervention,’ says Dr Heneghan.

The group’s results show that patients with artificial heart valves and younger patients benefitted the most. ‘For these two groups we would now expect widespread use of self-monitoring,’ says Dr Heneghan.

For people with artificial heart valves who monitored their own treatment, the risk of blood clots was halved. For every 1000 patients monitoring their warfarin therapy for 5 years, 42 such ‘thromboembolic events’ would be prevented with no extra risk of bleeding.

The risk was reduced by two-thirds for patients under 55 years old, with 48 thromboembolic events prevented per 1000 patients.

Dr Heneghan does say that: ‘Patients vary considerably in their ability to self-monitor. Some are very capable of both self-testing and self-management, whereas others are either unable or unwilling to do either. The challenge then is to identify which individuals are suitable for self-monitoring of oral anticoagulation therapy, and to provide sufficient training to ensure that they can do so safely and effectively.’

‘The concept of self-care and self-monitoring is a growing part of health care,’ adds Dr Heneghan. ‘It is recognized in many chronic conditions as an important part of the overall management strategy. For instance, it use widely in diabetes, asthma and hypertension management.’

He notes that managing chronic disease is an important and costly element of health care which accounts for about 80% of GP consultations.

From University of Oxford

Read Full Article

Giant platelets are shown here on a blood smear. Image: wikipedia/Bobjgalindo

MIT cancer biologists determine how platelets in the bloodstream help cancer cells form new tumors.

Anne Trafton, MIT News Office
November 15, 2011
Repost from MIT News

About 90 percent of cancer deaths are caused by secondary tumors, known as metastases, which spread from the original tumor site.

To become mobile and break free from the original tumor, cancer cells need help from other cells in their environment. Many cells have been implicated in this process, including immune system cells and cells that form connective tissue. Another collaborator in metastasis is platelets, the blood cells whose normal function is to promote blood clotting.

The exact role played by platelets has been unclear, but a new paper from Richard Hynes, the Daniel K. Ludwig Professor for Cancer Research, and colleagues shows that platelets give off chemical signals that induce tumor cells to become more invasive and plant themselves in new locations. The findings, published Nov. 14 in Cancer Cell, may help researchers develop drugs that could prevent cancers from spreading, if they are diagnosed before metastasis occurs.

For many years, cancer biologists believed that platelets helped to promote metastasis by helping the cells to form big clumps, allowing them to get stuck in new locations more easily. However, some suspected they might have a more active role, because they contain many growth factors and cytokines, many of which can stimulate cancerous growth.

Before cancer cells can metastasize, they typically undergo a shift known as the epithelial-mesenchymal transition (EMT). During this shift, cells lose their ability to adhere to each other and begin to migrate away from their original locations.

Myriam Labelle, a postdoc in Hynes’ lab and lead author of the Cancer Cell paper, found that cancer cells would undergo this transition if grown in contact with platelets in a lab dish. She then analyzed which genes were being turned on in the metastatic cells and found that genes activated by transforming growth factor beta (TGF-beta, or TGF-b) were very active. TGF-beta was already known to promote EMT. Labelle then went on to show that depletion of TGF-beta from platelets in vivo blocked metastasis.

“This work shows that platelets are not just a shield for circulating cancer cells, but also a traveling kit of pro-invasive stimuli,” says Joan Massagué, chair of the cancer biology and genetics program at the Sloan-Kettering Institute, who was not part of this study. “For nearly three decades platelets have been known to be the richest source of TGF-b in the body, yet it is only now that someone realized what an important role platelets play as a TGF-b source in tumor dissemination.”

A complex interaction

In further experiments, Labelle found that the cancer cells would not become metastatic if exposed only to TGF-beta, suggesting that they need an additional signal from the platelets.

Platelets release many chemicals other than TGF-beta — they are “little bags of stickiness and growth factors,” designed to promote wound healing, says Hynes, who is a member of the David H. Koch Institute for Integrative Cancer Research at MIT. However, none of those chemicals on its own was enough to promote metastasis. Labelle found that direct physical contact between platelets and tumor cells was necessary for the cells to become metastatic.

Specifically, when platelets come into contact with tumor cells, they somehow activate the NF-kappa-b pathway, which is involved in regulating the immune response to infection. Both of the signals, NF-kappa-b activation and TGF-beta, are necessary for the switch to occur.

While tumor cells receive the initial stimulus to become mobile while still in their original location, Hynes and Labelle suspect that the additional boost they get from platelets once they enter the bloodstream makes it easier for the cells to penetrate the walls of blood vessels into a new tumor site.

White blood cells are also suspected in promoting metastasis, and Labelle is now doing experiments to figure out what their role may be, and how they may work together with platelets. She is also examining how platelets activate the NF-kappa-b pathway in tumor cells.

Better understanding of the signals that tumor cells need to metastasize may help researchers develop drugs that can prevent such metastases from developing. “It’s important to understand exactly what platelets are doing, and eventually this could be an opportunity for drugs that would treat metastasis,” Labelle says.

Such an approach would be useful for stopping primary tumors or metastases from spreading, but would likely not have much effect on secondary tumors that had already formed.

Reprinted with permission of MIT News

The following article, while not Canadian, gives a stark reality to what you may see on the road. The drugs mentioned are ones you should definitely know for their various uses.

November 16, 2011

(AP) — More than 20 percent of American adults took at least one drug for conditions like anxiety and depression in 2010, according to an analysis of prescription data, including more than one in four women.

Read Full Original Article

Image provided by ADHD CENTER

Published: 16 Nov 11 08:19 CET

Scientists in central Germany are working on a method with which they reckon they could diagnose Alzheimer’s disease years before any symptoms are noticed – by looking up patients’ noses.

An early diagnosis would give people the chance to try to slow the development of incurable dementia, said the researchers at the Technical University of Darmstadt.

Until now diagnosis has only been possible using radiological techniques such as computer or magnetic resonance tomography – or memory tests, the scientists said in a statement on Tuesday. But these do not allow for an early diagnosis.

But now chemists and pathologists at the university are developing a new method – having realised that tests of the nasal mucous membrane can show whether the damaging tau protein, which kill brain cells and can lead to dementia, are being deposited in the brain.

Read Full Article

Photo by McBeth April 16, 2005