aka Postcards from the Edge 004

This ‘postcard from the edge’ is by Swedish Emergency doctor Katrin Hruska (@akutdoktorn), who writes a predominantly Swedish language blog called akutdoktorn.

I am a born optimist, which is why I have taken on the struggle to establish emergency medicine as a specialty in Sweden. Since EM is a supraspecialty I had to take the long way through an internal medicine residency, but now I am at least seeing the end of my EM training. I am also mildly adventurous. Not in the crazy, head-first, emergency physician way, but in a safe, Swedish way. Somehow I managed to convince my program director that a rotation abroad would make a great contribution to my education, so me and my family moved to Botswana in southern Africa for four months.

I came to Botswana for an ED rotation, hoping to do some good and learn something from it. Four months later I am ready to leave and I look back at my experience with a sense of relief. At least I didn’t kill anybody. I think.

Primum non nocere. First, do no harm. A principle that, hopefully, is more sacred to us doctors than the traditional medicine men here, whose remedies worsen the metabolic acidosis of babies with diarrhea and cause hematuria and acute renal failure in adults. Of course we know better than those quacks. We are highly educated medical doctors who practice evidenced-based medicine. Right?

Only I have learned evidenced-based in a kind of EM rule-in/rule out or good/bad way. Intubation for traumatic brain injury with GCS less than 8 is good. Intubation without proper skills and equipment is bad. But what do you do when that is all you have to work with? What is the threshold for intubation if your only airway adjunct is an ET tube size 7,5 or 9 and there is no endtidal CO2? And you are out of oral airways, except the infant sized? And there is only one ventilator, which does not work with assist-control settings, so you have to sedate the patient. And getting blood gases is a hassle since you have to rely on the benevolence of the ICU staff to analyze them? And you are lucky to even get the help of inexperienced A&E nurses?

I have no idea if intubating these patients saves more brain than it kills. And four months of experience in this setting has not made it any clearer to me. It has just made me care less. Because even if I try me very best to minimize the risks and optimize the care for a patient, I will later find them alone in the resuscitate room, with no one there to hear the alarms, while waiting for paperwork to be filled out, transport to arrive or just other doctors to make up their minds. That is when I start to blame the system. And when the system is at fault, you sort of resign from responsibility. Irresponsible doctors are lousy caregivers, so I struggle to feel responsible for every single one of my patients. I never thought it would be so hard and I doubt that I could do it for much longer.

I must admit that I had a somewhat naive perception of doctors in resource limited settings before coming to Botswana. I had heard stories about great clinicians who made accurate diagnoses based on clinical findings, auscultating and percussing the patients all over. But the only ones I see assessing chest expansion and vocal fremitus are the medical students. The medical officers have all trained abroad in hospitals with better resources, where you just order a chest x-ray. They are well trained with the same theoretical education as myself. When it comes to experience they are in some ways way ahead of me. After a year of internship they are supposed to work independently and with the patient clientele here, they quickly learn procedures and gain experience of treating very sick patients. They learn and seem to accept that they have to work with what they have got. And since x-rays are readily avalable, they are ordered in the same just-in-case fashion as back home. It is as if whatever resources are available are not limited. Another example of this is the iv fluids. During my stay we were sometimes out of normal saline and sometimes out of Ringers lactate and a few times we were out of both. You can be an expert on fluid resuscitation, but if their are no other fluids available than Dextrose when you are treating a severely dehydrated, septic child you are just as helpless as everybody else. It is an awful experience.

But when the next load of fluids arrives everything is back to normal. Almost anyone who hits the door gets an infusion. If it is there, it will be used until it runs out. In fact the iv fluids are used to clean wounds, since it is the only sterile solution available. If fluids were truly a limited resource and you knew that you only got a certain supply per month, it would not be hard to rationalize their use. The problem is not that fluids and other basic supplies are unaffordable, but that the stocks are not replenished on a regular basis and that running out of fluids, gloves or other necessities is somehow acceptable and seen as something uncontrollable. The most limited resource is structure.

CT scans, on the other hand, are indeed limited. The CT scanner in the hospital cannot do contrast enhanced exams, which means that abdominal and thoracic scans have to be ordered from outside. It is still financed by the government but the costs are much higher and the use is restricted, which means that those scans are hardly ever ordered from the emergency department. We mainly use the CT for brain scans. By some order, the cervical spine cannot be included in such a scan, even if there is a clear clinical indication and the result might actually influence the outcome. At the same time, surgery can demand a CT brain for a patient slightly confused patient with GCS 15 who needs admission for observation after a road traffic accident and refuse to admit without it. We see 85 year olds with hemiparesis, who are transferred from other hospitals for CT scans, only to confirm their strokes. This practice seems reasonable in the rich world, but if resources are limited, is this really where you want to spend your money?

To prioritize is ethically challenging and I don’t think that I, as a visiting doctor and a foreigner in this cultural context, is the right person to tell the local doctors how to use their resources, just because I have been trained to know what is possible in my own setting. And by bringing our way of practicing here, we are indeed prioritizing emergency care over other aspects of health care. If we are guided by patient-oriented outcomes, such as mortality and morbidity, we are probably doing good. But if we use surrogate markers, such as adherence to what is regarded as evidenced-based principles in the rich world, we are diverting resources away from other areas, without knowing with reasonable certainty that we are saving lives. If we successfully resuscitate a patient in cardiac arrest, that patient will need one of the very scarce ICU beds. The return of spontaneous circulation might seem like a victory, but considering how few people actually leave the hospital neurologically intact even with high quality intensive care, we have to ask ourselves if we don’t have more to gain from preventing cardiac arrest than treating it once it has occurred.

The unique dimension of Emergency medicine is time. Sometimes seconds matter and sometimes even days don’t count. Our job is to see the difference. But it is also to plan ahead and lead a team. When you are working in a well organized ED, you don’t realize how much work is done by others than yourself. You just expect carts and trays to be complete and the medicine cabinet to contain the same things today that you used yesterday. You certainly don’t expect the bag-valve mask to be assembled in a way that can give your younger patients bilateral pneumothoraces. Knowing how to work all the equipment yourself is important everywhere, but here it is indispensable.

In some ways emergency medicine here is similar to what I learned as a medical student in the mid-nineties. A myocardial infarction is chest pain with ECG-changes and STEMIs are treated with streptokinase, unless there is a contraindication. A few patients can be admitted or referred to cardiology, but that is more an exception than a rule. What happens with all the MIs that are missed this way? I have no idea. I do know, however, that the step to the current practice, where every tiny increase in troponins is an NSTEMI, is huge. Should the development here follow the same path or is it acceptable to keep missing those MIs, because other areas are more important to improve on first? What about pulmonary embolism? If we did get a CT scanner that could scan for PE, who should we scan? And what would we do with the results? There is not great evidence for anticoagulation to begin with. Who do you start on warfarin if INR monitoring is only done at the main hospital, if you cannot get even plasma to reverse the effect and to get packed red cells for a transfusion can take four hours. If more patients bleed to death, than are saved from dying of PE, we are no better than the traditional medicine men, harming people with toxic remedies.

I am convinced that a well functioning emergency department saves lives. But I think that development has to focus on getting the basics right and minimizing the adverse effects of our interventions. To secure impeccable hygiene and barrier care limits the spread of nosocomial infections at a low cost. To organize the ED in a way that allows good monitoring and an overview of all patients makes it possible to intervene before the patient deteriorates. Excellent on the floor management that stresses team work and communication reduces the unnecessary errors and speeds up processes. Documentation that makes it possible to measure quality and follow-up can help us identify problem areas. It also tells us how our patient population compares to study populations and if the evidence that is available is at all applicable in our setting. Because to use even excellent evidence from a completely different setting is not to practice evidenced-based medicine. If there is no evidence you just have to rely on your clinical judgement and common sense. And keep doing your absolute best for every single patient. In a dysfunctional organization that feels like banging your head against the wall, again and again.

But what else can you do?

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

Beware the foreign traveler!

Today we explore the evolving ‘furuncle‘ or boil. A simple enough beast to deal with under normal circumstances – but in the returning traveler…myriad possibilities raise their ugly heads…

The common or garden furuncle is usually associated with infection (commonly staphylococcus aureus) at the base of a hair follicle where purulent material extends through the dermis into the subcutaneous tissue, and is evident by a small abscess.

However, in the returning traveler furuncular myiasis caused by Dermatobia hominis must be on the differential diagnosis. Furuncular myiasis is endemic throughout Central and South America and produces boil-like lesions commonly misdiagnosed as a furuncle.

The furuncle has a central pore that intermittently exudes a serosanguinous discharge (the feces of the larva), and protrusion of the breathing tube of the larva frequently can be observed

The larvae are transmitted to vertebrate animals by hematophagous insects, most commonly mosquitoes, on whose abdomens the female botfly has deposited her eggs. When the blood-feeding vector encounters a warm-blooded animal, the change in temperature causes the botfly eggs to hatch. The larvae enter the vertebrate host either through a hair follicle, the bite site, or by directly burrowing in the skin. Over the next 4–18 weeks, the larva grows by eating the flesh of its host. At maturity it emerges from the wound, falls to the soil, and pupates.

Treatment

Although the botfly will, when mature, exit the site by itself, this is not usually acceptable to the patient…

Botflies, when properly diagnosed, either are surgically removed or asphyxiated and then manually removed. Many methods for extracting the larvae have been described for the treatment of furuncular myiasis.

http://www.youtube.com/watch?v=eMbPFr72S7k

Bacon Therapy

I think using bacon fat is a good idea. It doesn’t take too long (about three hours), doesn’t leave dead larvae under the skin (as oil occlusion, lignocaine infiltration or larvacide treatment may), it’s non-invasive (avoids the need for incision and drainage) and is cheap. However, it may not be suitable for extreme cases of Tumbu larva infestation as the female fly lays 100-300 eggs in several batches – that would need a lot of bacon.

Procedure: The furuncles are left covered with bacon fat. This encourages the larvae to exit the skin, either due to suffocation or an attraction to bacon. After about 3 hours the bacon fat is carefully removed with forceps at the ready to help fully extricate the larvae.

What you do with the bacon and the larvae afterward is your business. And if you’ve got myiasis, try to look on the bright side, things could always be worse…

Ocular myiasis - don't use bacon for this, it needs surgery. It is usually caused by a Screwworm rather than Tumbu fly or Bot fly larvae (although the larvum bottom right does look like Dermatobia hominis).

Asphyxiants

Duct Tape: Covering the location with adhesive tape results in partial asphyxiation and weakening of the larva, but is not recommended because the larva’s breathing tube is fragile and would be broken during the removal of the tape, leaving most of the larva behind.

Petroleum jelly or vaseline can also be applied over the location, which prevents air from reaching the larva, suffocating it. It can then be squeezed out.

Nail Polish: A larva has been successfully removed by first applying several coats of nail polish to the area of the larva’s entrance, weakening it by partial asphyxiation.

Procedure: Apply nail polish to the central pore of the nodule. This leads to partial asphyxiation of the larva causing it to retract its spines and attempt to reposition its breathing tube to reach air. Although the larva may succeed in penetrating the first few applications of nail polish, eventually it is trapped and asphyxiated. This facilitates subsequent manual extraction of the entire larva provided that it is grasped well down its length. The breathing tube is fragile and breaks easily, contraindicating the use of duct tape which some use for larva removal

References:

• Bringing home the bacon
• Bhandari, Ramanath; David P. Janos and Photini Sinnis (March 2007). “Furuncular myiasis caused by Dermatobia hominis in a returning traveler“. The American journal of tropical medicine and hygiene 76 (3): 598–9. PMC 1853312. PMID 17360891.
• Boggild, Andrea K.; Jay S. Keystone and Kevin C. Kain (August 2002). “Furuncular myiasis: a simple and rapid method for extraction of intact Dermatobia hominis larvae“. Clinical Infectious Diseases 35 (3): 336–338. doi:10.1086/341493. PMID 12115102

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

It’s not every day that a new emergency medicine journal is born. Especially one as sorely needed as The African Journal of Emergency Medicine (AfJEM),  the official journal of the African Federation for Emergency Medicine.

This international, peer-reviewed journal aims to support emergency care across Africa. It intends to publish manuscripts of international quality and to facilitate this has a unique Author Assist program involving a team of experienced volunteers to help authors with their submissions. I have no doubt that this journal, headed by Editors-In-Chief Lee Wallis and Stevan Bruijns, will achieve its stated aim of becoming the international voice of quality emergency medical care in Africa.

Check out the first issue here. My top 3 picks are:

• Africa should be taking responsibility for emergency medicine in Africa — the Editors-in-Chief explain why this journal is so necessary.
• The development of emergency medicine systems in Africa — the full scope of the task at hand for emergency medicine in Africa.
• Ujuzi (Practical Pearl): The Double Tube in technique for difficult laryngoscopy — I love this pearl, first taught to me by an anesthetist in the NT (who had been around a while) as: “during intubation, if the first tube doesn’t go into the trachea, leave it in the esophagus, and keep putting more tubes in until one goes where you want it to…”

Also, if you haven’t heard it yet, check out the recent special edition of Rob Rogers’ EMRAP: Educator’s Edition podcast featuring Lee Wallis talking about Emergency Medicine in South Africa.

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

aka Postcards from the Edge 001

Postcards from the Edge is series of LITFL posts on International Emergency Medicine. Also, remember to join the International Emergency Medicine (Australasia) group if you’re on Facebook!

The first of our “Postcards from the Edge” comes from Perth, Western Australia but spans from the southern tip of the globe, through Papua New Guinea and Asia to Nepal! Associate Professor Chris Curry has ventured the globe doing things as adventurous as Antarctic expedition medicine since becoming an Emergency Physician. Currently working at Fremantle Hospital, Chris maintains a strong interest in International Emergency Medicine dedicating significant portions of his professional life towards helping support the development of Emergency Medicine overseas. He has done much work in Papua New Guinea, helping set up an Emergency Medicine training program, and he has ongoing involvement in the development of the specialty in several other countries in the Asian region. He is also the foundation chair of the Australasian College for Emergency Medicine‘s special interest group in International Emergency Medicine (IEMSIG), and the editor behind the newsletter that is published electronically through this group (the newsletters can also be accessed on LITFL here for wider dissemination).

“Brolly – Ladakh, Indian Tibet, 2010”

Chris was kind enough to answer a few questions from the LITFL team..

Q1. Chris, do you mind telling us a little background about your Emergency Medicine career and what inspired you to do international work?

As a student I organised elective time in several hospitals in the country of my birth, Kenya, with a view towards rural hospital generalist practice in developing environments.  On graduating from UWA I initially joined the then infant Family Medicine Training Program.  I tried to get to South Africa for developing world experience but settled for the NHS in the UK.  There I signed up for a Diploma in Tropical Medicine and Public Health, amongst other things, but got side-tracked by mountaineering.  I eventually returned to my initial objective 23 years later.

“Skiing snow - Alaska – that's gear on a sled, not a corpse... 1986”

Q2. At what stage of your career did your interest in international Emergency Medicine start?

I was interested in international  hospital generalism as a student.  I turned to EM when I went to New Zealand to climb mountains and found the delivery of emergency care there even more dysfunctional than in the NHS and at the same time found ACEM through an introduction by Bryan Walpole, a foundation fellow.  I pursued EM training to try to improve delivery of care in New Zealand.  More than a decade later an association with Antarctica led me to discovering a PNG proposal to AusAID to develop an EM training program there.  I became involved with that in 2001.  So I moved from high altitudes to high latitudes, high temperatures and high humidities.

Q3. Can you tell us what the International Emergency Special Interest Group (IEMSIG) is all about? How did it start? What is it’s vision and what has the association already achieved?

I was approached by Paul Gaudry, a foundation fellow and then Honorary Secretary of the Council of ACEM, to chair an IEMSIG to be launched at the 2004 International Conference on Emergency Medicine (ICEM) which was being hosted by ACEM in Cairns.

Essentially it is a loose collection of people with an interest in IEM who are prepared to share what they are doing in the hope of encouraging others.  The main vehicle of what it is about and what it is doing is the IEMSIG Newsletter.  This is accessible on the ACEM website, go Infocentre, go International Emergency Medicine (or click here for the direct link!).  There is now a Noticeboard carrying notices of opportunities that might be of interest.

IEMSIG now numbers more than 250 people who have connections of various shapes and sizes in more than forty countries, many of these being LDCs (Least Developed Countries).  ACEM is establishing an International Development Fund to expand the college contribution to IEM.

UN's Least developed countries map (click image for source)

Q4. Have you been on any IEM missions recently? If so could you briefly tell us what the trip was about, and share with us a few highlights and low points or challenges?

Now that the EM program in PNG is established and the country is producing its own emergency physicians I have been returning to former haunts.  I have recently (May 2011) returned from Nepal where, after several visits, the leading postgraduate medical training facility, the Institute of Medicine at Tribhuvan University in Kathmandu, is progressing towards launching an EM training program in November 2011.  A highlight is that progress is being made.  The challenges are many, as they are in all LDCs, and include matters of governance, resources, understanding, culture and will.

“In the ED at Port Moresby General Hospital, Papua New Guinea 2003”

Q5. From your experience of work in the field of International EM, are there any words of advice you would like to give either medical students, junior doctors or registrars about getting involved in International Emergency Medicine?

There are many opportunities for those prepared to make the effort and to cope with the sacrifices involved.  IEM is an area for those who not only say they would ‘love to do that’, but also have the initiative to get up and do things for themselves.  It is an area that can be hugely rewarding in arrays of intangible ways that can vastly surpass the more tangible rewards of income, career and status that seem to pre-occupy so many in our wealthy corner of the world.  But those rewards you have to discover for yourself — by going there and doing it.

“life in the slow lane, in Kathmandu, 2011”... Editor's note: apparently this was taken during the Great Nepali Helmet Shortage of 2011...

Further reading

Check out the IEMSIG newsletters and this selection of papers authored by Chris Curry:

• Aitken P, Annerud C, Galvin M, Symmons D, Curry C. Emergency medicine in Papua New Guinea: beginning of a specialty in a true area of need. Emerg Med (Fremantle). 2003 Apr;15(2):183-7. PMID: 12675629
• Curry C, Annerud C, Jensen S, Symmons D, Lee M, Sapuri M. The first year of a formal emergency medicine training programme in Papua New Guinea. Emerg Med Australas. 2004 Aug;16(4):343-7.  PMID: 15283722.
• Curry C. The ACEM training programme: flexibility and diversity are important. Emerg Med Australas. 2005 Feb;17(1):92. PMID: 15675918.
• Curry C. Taking emergency medicine international: what can we learn and teach? Emerg Med Australas. 2006 Aug;18(4):313-6. PMID: 16842297.
• Curry C. A perspective on developing emergency medicine as a specialty. Int J Emerg Med. 2008 Sep;1(3):163-7. Epub 2008 Sep 25. PMID: 19384509;  PMCID: PMC2657278.
• O’Reilly GM, Curry C. International emergency medicine: building on a strong information-sharing foundation. Emerg Med Australas. 2010 Dec;22(6):488-92. doi: 10.1111/j.1742-6723.2010.01343.x. PMID: 21143396.
• Pearce A, Mark P, Gray N, Curry C. Responding to the Boxing Day tsunami disaster in Aceh, Indonesia: Western and South Australian contributions. EmergMed Australas. 2006 Feb;18(1):86-92. PMID: 16454781.

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

What if someone told you this:

“Fluid boluses significantly increased 48-hour mortality in critically ill children with impaired perfusion”

I think most emergency and critical care doctors wouldn’t believe it, unless it was the conclusion of a well designed randomised controlled trial. Which it is:

Maitland K, et al and the FEAST Trial Group. Mortality after Fluid Bolus in African Children with Severe Infection. N Engl J Med. 2011 May 26. [Epub ahead of print] PMID: 21615299.

There have already been excellent discussions of this study in the EM/ ICU blogosphere courtesy of Dr G’s blog and Resus.ME, but this video summary featuring the investigators illustrates the nature and findings of the study better than anything in writing.

http://www.youtube.com/watch?v=hK9VUkL-DqU

Like any important study, it raises as many questions as answers. How do these findings from resource-poor developing countries in Africa — with large numbers of anemic malaria-infected children — relate to the rest of the world? Was the choice of fluid important (perhaps contributing to hyperchloremic acidosis)? What if smaller boluses were used? Would intensive monitoring have altered the outcome?

Background
The role of fluid resuscitation in the treatment of children with shock and life-threatening infections who live in resource-limited settings is not established.

Methods
We randomly assigned children with severe febrile illness and impaired perfusion to receive boluses of 20 to 40 ml of 5% albumin solution (albumin-bolus group) or 0.9% saline solution (saline-bolus group) per kilogram of body weight or no bolus (control group) at the time of admission to a hospital in Uganda, Kenya, or Tanzania (stratum A); children with severe hypotension were randomly assigned to one of the bolus groups only (stratum B). Children with malnutrition or gastroenteritis were excluded. The primary end point was 48-hour mortality; secondary end points included pulmonary edema, increased intracranial pressure, and mortality or neurologic sequelae at 4 weeks.

Results
The data and safety monitoring committee recommended halting recruitment after 3141 of the projected 3600 children in stratum A were enrolled. Malaria status (57% overall) and clinical severity were similar across groups. The 48-hour mortality was 10.6% (111 of 1050 children), 10.5% (110 of 1047 children), and 7.3% (76 of 1044 children) in the albumin-bolus, saline-bolus, and control groups, respectively (relative risk for saline bolus vs. control, 1.44; 95% confidence interval [CI], 1.09 to 1.90; P=0.01; relative risk for albumin bolus vs. saline bolus, 1.01; 95% CI, 0.78 to 1.29; P=0.96; and relative risk for any bolus vs. control, 1.45; 95% CI, 1.13 to 1.86; P=0.003). The 4-week mortality was 12.2%, 12.0%, and 8.7% in the three groups, respectively (P=0.004 for the comparison of bolus with control). Neurologic sequelae occurred in 2.2%, 1.9%, and 2.0% of the children in the respective groups (P=0.92), and pulmonary edema or increased intracranial pressure occurred in 2.6%, 2.2%, and 1.7% (P=0.17), respectively. In stratum B, 69% of the children (9 of 13) in the albumin-bolus group and 56% (9 of 16) in the saline-bolus group died (P=0.45). The results were consistent across centers and across subgroups according to the severity of shock and status with respect to malaria, coma, sepsis, acidosis, and severe anemia.

Conclusions
Fluid boluses significantly increased 48-hour mortality in critically ill children with impaired perfusion in these resource-limited settings in Africa.

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

In the mid-1980s Alastair Coutts was the surgeon for the Solomon Islands. In 1999 he described one of his more interesting cases in an article published in the BMJ.

The story starts with a telegram he received from Dr Bob Eason (who if I remember correctly, taught me clinical physiology back in medical school):

Fifty five year old lady. Acute extradural haemorrhage. Ipsilateral pupil up. Unconscious flexor pain responses. Boggey haematoma over left middle meningeal area. Any chance you can come plus equipment to evacuate clot. Helena Goldie Hospital would refund fares.
Dr Bob Eason

An adventurous 400 mile trip from Honiara to Munda, and its landing strip with no lights, ended with Alastair jumping on the back of Bob’s moped as they sped to the hospital. This is what he found when he got there:

The patient was deeply unconscious and both pupils were dilated; she made extensor movements to pain with only her left arm and had a large swelling over the left side of her head as a result of being hit by a falling coconut. Her Glasgow coma score was about 4, but at least she had a clear airway and was breathing.

Scan or no scan, it didn’t take a brain surgeon to figure out what was going on: an extradural hemorrhage and a coning patient. First Bob got the consent:

No operation—100% chance of dying, operation—99% chance of dying.

The family deliberated for ages, then agreed to proceed with a craniectomy. The operation was swift.

As soon as the clot had been evacuated the patient woke up, tried to get off the table, and promptly hit her head on the lamp, exclaiming, “The Lord be praised.” She lay back and the previously quiescent middle meningeal artery started spurting everywhere.

The patient was no longer coning — she was bleeding to death. Bob grabbed four bystanders and bled them, assuring Alastair that everyone in Munda was O positive.

Under the flickering lamp with minimal equipment in a small wooden hut, Alastair simply could not stop the bleeding. His patient was going to die. Then he looked up and saw Jesus.

Opposite me was a large Roviana male nurse who was chewing gum… he announced his name was Jesus.

Coutts had to think fast:

“Jesus, please could I have some of your chewing gum?” “Of course,” he said reaching into his shorts pocket for a fresh stick. “No, not that stuff, the stuff in your mouth,” I retorted. Incredulously, he opened wide and handed me his gum. With thumb and forefinger I skilfully rammed it into the left foramen spinosum. The bleeding stopped.”

Bob administered the new antibiotics that had been recently donated from New Zealand. Six months later Alastair reviewed his patient:

“She had a minor right sided hand weakness but wanted the bone back in her head.”

Reference

Coutts A. Chewing gum for extradural haemorrhage. BMJ. 1998 Dec 19-26;317(7174):1687. PMID: 9857127;   PMCID: PMC28750.

Hat tip to Trevor Jackson F.UCEM HTFU for directing us to the original paper.

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

Wednesday, December 1st is World AIDS Day — a day to raise awareness for the ongoing AIDS pandemic around the world and to remember the past. As a trainee intern I spent 3 months in Zambia (see ‘A Change in Condition’), a time that really opened my eyes up to what AIDS was doing to the world.  Much has changed since then, antivirals have arrived in Zambia for instance, yet the disaster continues: 1 in 8 Zambians are HIV positive and the burden of AIDS has now persisted for 3 decades.

This is what I wrote about my experience and views on the AIDS crisis in Zambia back in 2002.

The AIDS Crisis and Zambia

Before my time in Zambia, I knew that the AIDS crisis was a serious global problem. However, until my arrival at SFH I never fully realised what that meant. When personally confronted by it, the horror of AIDS defies expression.

In Zambia 1 in 5 adults are HIV positive (1). The life expectancy of a baby born in Zambia today is now thought to average as low as 37 years. Of 15 year olds in Zambia, 60% will die of AIDS (2).  When seeing Zambian children I often find myself wondering which of them number among the country’s plague of orphans (1). It is hard to imagine that children can have AIDS, that they can have a life of sickness ahead of them – a Hobbesian life: “nasty, brutish, and short”.

The italicised paragraphs below are excerpted from a letter published in the British Medical Journal (3). This letter was written by Dr A. W. Logie, who contracted HIV while working at SFH and later died of AIDS. The paragraphs describe the impact and some of the causes of the AIDS epidemic in Zambia and in Africa as a whole:

“… AIDS in Africa is not merely a medical problem: it is having major socioeconomic effects. Industrial output is falling as a result of the premature death of many skilled workers. The traditional extended family care system has broken down. In Zambia, there are almost half a million AIDS orphans, of a total population of 10 million, and many of these are on the streets, easy prey to exploitation, especially sexual abuse.

More teachers are dying every day than are being replaced. Education is suffering, and many children, especially girls, are being withdrawn from school because of unaffordable fees. Poverty or abandonment or both is forcing many women to sell sex in return for food for their families. Lack of respect for female sexual rights, dry sex, poor facilities for the affordable treatment of sexually transmitted disease, unpopularity of the male condom, unavailability of male and female condoms, insufficient research, and development of safe, effective, and acceptable vaginal virucides and vaccines: these and many other factors are contributing to the inexorable progression of the pandemic throughout the Third World.”

The Stigma of HIV

It is hard to know how many patients on the wards at SFH are infected with HIV. On St. Augustine I would estimate three out of every four or five patients.  Before working at SFH I think I must have naively imagined that everyone passing through the hospital doors would have a sticker placed on them stating their status. In my experience, very few people will agree to have an HIV test performed, even after special counselling. A study found that “only 7% of couples invited for counselling and testing in Lusaka decided to have a test”(4). One of the reasons must be that there is very little to gain from having the test done. In Lusaka the most common reason cited for declining a test was that “no medical intervention was available”(4) – it seems that as long as a person’s status is uncertain there is still hope. Of those infected with HIV in sub-Saharan Africa, 90% are thought to be unaware of their infection (4).

All that can be gained by an HIV test is stigmatisation. At SFH, if a patient is to be counselled about having an HIV test the identity of their bed-side attendants is always checked first. If the patient is a man and HIV is mentioned while his mother is present, the man’s wife may be held to blame. It seems that the mention of HIV has the capacity to wreck someone’s life, just as the virus itself can cripple a whole nation.

Abuse of Authority

Stories of the abuse of authority abound in Africa. A commonly cited form of abuse is a male authority figure extracting sexual favours from females. Male secondary school teachers are often a threat to female students for this reason. A graphic example of this is the suspicion that a male teacher is responsible for HIV prevalence rates of 30% at a school in one of Katete’s neighbouring districts. The average prevalence rate in secondary schools is thought to be less than 5%. Africa seems to be overflowing with horror stories like this.

Infertility and Polygamy

Another aspect of sexually transmitted disease I had never fully appreciated before is the importance of infertility associated with pelvic inflammatory disease. At an infertility clinic I was stunned to see the vast numbers of women unable to get pregnant. The consequences of this are extreme. It seems that infertile women are considered next to useless, and their husbands often resort to polygamy (5). Ironically, almost all the semen analysis results that I saw at the infertility clinic seemed to contain pus cells, suggestive of infection. Thus, it is often the husband’s sexual indiscretions that have actually led to the infection of his wife and her subsequent infertility.

AIDS Education

I was overwhelmed by the prevalence of sexually transmitted infections when I started working at SFH. However, measures to fight the pandemic are in operation. SFH has an AIDS outreach programme that sends a group of trained health worker-come-actors on  tours of the local villages. They perform plays and encourage discussion to educate people about AIDS. Billboards carrying anti-AIDS information line Zambia’s streets, and men roam Lusaka dishing out handouts on “genital leakage”. However, there appears to have been little real impact in terms of changing sexual behaviours (2) despite apparently widespread public awareness and health education. For instance, I found that many male patients seem to agree that the use of condoms is a good idea. However, their view is usually that it’s a good idea for someone else – in other words, “the someone else who is HIV positive… not me”.

Denial and Hope

AIDS in Zambia has been called “the silent killer – because people are too afraid to admit they have the disease” . On the wards the letters “H-I-V” are spoken only in hushed tones, if at all. Generally, euphemisms like “immune suppression” or “the virus” are used. It took me a while before I clicked onto to what “?RVD”  written at the bottom of an admission note meant – “possible retroviral disease”. I’ve considered trying to establish my own euphemism in readiness for when the others take on unwanted connotations. Perhaps “an RNA-based life-form associated illness” would do, it could have a nice acronym like “ARNALAI”.

Seriously though, such denial can only be damaging. In 1999 the Zambian government initially denied the UN estimates of 20% adult HIV prevalence rates (1). Furthermore, as stated by Dr A W Logie, “The Zambian government has largely abandoned responsibility for HIV/AIDS and tuberculosis to the non-governmental organisations. Now local supervision programmes for tuberculosis treatment do exist, but they are mainly organised by non-governmental organisations” (3). Also damaging in recent times has been the opposition of the Catholic church in Zambia to the use of condoms (6). Health workers need to face up as well, it has been reported that “HIV is rarely entered in African death certificates, yet treatment decisions are made on the assumption that a patient is infected” (4).

Progress in the fight against AIDS will only be made when those on the battlefield face up to the disease. This can only happen when the stigma is taken away and local leaders rather than “meddling mzungus” lead the way. Benefits such as access to medical care and tuberculosis prophylactics need to be offered to HIV positive people to promote testing. The denial and stigma of HIV must be eroded away. I think there is some hope – not much, I admit, but perhaps enough.

Footnotes

(1) Moszynski  P. United Nations estimates of HIV prevalence in Zambia under attack. BMJ 1999;319:338.
2) Logie D. AIDS cuts life expectancy in sub-Saharan Africa by a quarter. BMJ 1999;319:806.
(3) Logie A W. Africa revisited: a distressing experience. BMJ 2001;322:59.
(4) Godfrey-Faussett P, Baggaley R. Exceptionalism in HIV – challenge for Africa too. BMJ 1998;316:1826.
(5) I will always remember the time I asked the identity of the two women at a male patient’s bedside and the nurse matter-of-factly responded, “they are his wives – he is a polygamist”.
(6) Jackson T. No news is bad news. BMJ 2000;321:14194.

Another St. Francis’ Hospital/ AIDS related BMJ article was written by a former physician at the hospital: Elphick D. Memorable patients – Zambia needs basic medicines and HIV education. BMJ 2002;324:895.

Other related LITFL posts based on my experience in Zambia include:

• A Change in Condition
• The Shrinking Feet of the Man from Malawi
• A Midsummer Night’s Dream
• World AIDS Day and the Crisis in Zambia

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

My recent talk on marine envenoming is now alive in blog-post form thanks to the MicroGnome. It gives a brief overview of the clinical aspects of marine envenoming from an Australian perspective. Go here for the show notes.

Otherwise just look at the pretty pictures…

Marine Envenoming

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

Can contemporary medical economics combat the growing threat of microbes?

Have we created sufficient evolutionary pressures that the microbe diseases of yesteryear and the neglected pathogens of today become a threat for us tomorrow? Whilst I don’t yet have the answers I intend to test my hypotheses and opinions expressed below as part of a review, which I also intend on making  into a science communication presentation, (I will share if it’s of sufficient quality). I aim to tie in a few ideas below, to prevent my introducing any biases of my own, or false preconceptions I hope this will generate discussion from those with relevant experience and knowledge.

Sulphonamides may have been the first antibiotic agents, but the golden age of antibiotics starts with the mass production of penicillin. Gram positive infections of Staphylococcus and Streptococcus as well as what is believed to be the first human pathogen Treponaema pallidum are optimistically believed to be treatable and diseases of the past. Whilst we were successfully defeating the life shortening infections of old from septicaemia to rheumatic fever, we weren’t aware yet of the optimal treatment protocols. With limited knowledge comes great irresponsibility, and what some of us may regard as poor use today was standard practise in eras past. Without complete knowledge of dosage efficacy, or clearing time, the push to gain return on investment from pharmaceutical companies with limited regulation or guidelines for prescription meant antibiotics were prescribed for inappropriate illnesses. In part the placebo effect that the average person receives from being given what is believed to be an effective treatment further reinforced the overprescribing tradition in our community’s culture, and in our human fallibility some will succumb to the pressure to prescribe.

Once the prescription is filled, we entrust the patient with the responsibility to properly administer the remedies recommended. With limited knowledge, therapies are often discontinued when the patient “feels” normal. Before the understanding of clearing time, it was assumed that once a patient regained healthy features, the treatment could be ceased. The first attempt to treat a Staphylococcal septicaemia with penicillin unfortunately failed as the subject soon relapsed and insufficient antibiotic had been produced to properly resolve the infection, resulting in the rapid decline and death of the patient. Whilst we are now more than aware of the persistence of infection, in minor illness patients are liable to discontinue full dose upon feeling they have benefited from therapy. The patient may feel they are healthy, depending on the pathogen, the host-pathogen relationship will determine whether the organism is overcome, or returns to commensal status. Whilst the host immune system may return to sufficient functionality to balance out pathogenicity from commensal flora, commensal organisms may not be fully eradicated, the selection pressures exerted by antibiotics may be sufficient to produce, or select for resistant strains. Currently, 10-15% of S. aureus infections in the community are resistant. Given what we know of the immune suppression that comes with age, and the demographic forecasts of the future, could our aged population die earlier as a result of opportunistic infections for which we have no treatments? Whilst host factors will determine matters of adhesion and virulence (as was found with Neisseria meningitidis B there are a series of host genes that if present determine colonisation or invasion) unfortunately with many opportunistic infections our mainline of adaption extends only so far as our immune system, and once this line of defence is sub-optimal, disease is a likely outcome. Further, given the age of onset for these diseases it is highly unlikely that the human species will have any significant change in gene frequency that will confer any form of protection from these ailments.

Parallel to aging population are lifestyle factors of the as yet not geriatrics. An increasingly sedentary lifestyle coupled with increased calorie consumption has seen an obesity epidemic. With obesity comes problems including cardiovascular disease, diabetes and some increased cancer risks. These conditions should they increase in frequency will place increased pressure on hospitals to provide surgical services as the population continues to age. With increased average population age comes a decline in the average income, paradoxically health infrastructure requires more funds to cope with the aged (this may be exacerbated by the above neglecting of health), whilst the lack of funds means cuts are an inevitability. According to a presentation given by Andy Simor, hospitals typically react in two ways when cuts are forced, decrease in cleaning or attempt to cut back on chemotherapeutics (including antibiotics). Unfortunately, the money saved is usually quickly lost as infection control stringency goes south. Cuts to antibiotic treatment could again result in adequate resolution of infection and therefore resistance. Perhaps longer or more combination therapies should be deployed to act as a series of changed host factors which are too great for the infection to overcome, and hope we make a return on investment in the future from a long term savings dividend? Those with diabetes, cancer and CVD suffer from a decreased immune status, which again adds more gravity to the situation of resistant opportunistic infections, particularly the already difficult gram negative anaerobes.

Alcohol and smoking also contribute to the host susceptibility. According to Australian Bureau of Statistics data, indicates that many young Australians are engaging in binge drinking. Drinking heavily is associated with immuno-suppression and therefore leaves a host open to numerous pathogens including Klebsiella pneumoniae and other aspiration pneumonias. In Western Australia 1.3% of jobs are in the mining sector. With fly in fly out workers from remote areas potentially in a less than healthy state, could diseases like rheumatic faver and Acinetobactor pneumonias become more common, and possibly endemic in hospitals? Further, will we see more cases of melliodosis?

Preventable childhood illnesses are again on the rise. This trend is mirrored across the developed world, cases in point being California where a whooping cough epidemic and England where a measles epidemic are already claiming the lives of children. For the main, complacency on the behalf of parents who no longer believe these diseases are circulating in their particular region of the world is to blame. However, the concept of an isolated region is one now confined to the annals of history.  Another contributing factor is the fictional representation of these ailments as harmless childhood illnesses with limited adverse outcomes. Whooping cough may cause an epiglottitis and measles an aseptic encephalitis both of which are rapidly fatal in children. Anti-vaccination groups dangerously deny these facts, dangerous and evident untruths that place communities at risk (as has lately been highlighted by NSW health tribunal decision to have the AVN state that their content does not constitute medical advice). Adverse sequalea (chicken pox and measles in particular) of some of these childhood diseases are much worse in adults who contract these ailments. For measles to remain in a population it is estimated that 500,000 unprotected individuals must be present. Might we see increased mortality from childhood diseases in more adults as the unvaccinated children enter adulthood, and these diseases enter endemicity?

Additionally, the continued lack of regulation of pharmaceuticals in underdeveloped countries combined with a lack of sanitation, population growth, and increased population density in urban areas are a dangerous combination, providing evolutionary opportunities for the selection and propagation of highly resistant mutant strains. The problem of third world health is further compounded by a lack of return on investment for the creation of new treatments and vaccines for some of the most deadly pathogens. The resurgence of nationalism has and always will pose a barrier to adequate funding of foreign aid programmes. Measles, malaria, dengue, Yersinnia pestis, HIV, yellow fever, Mycobacterium tuberculosis and various waterborne diseases will ever find a reservoir in the third world for a long time yet, and diseases have a very cosmopolitan outlook. One only needs to look at the spread of West Nile virus to the USA, and the case of the South American raspberries that infected consumers with Ballintidium hominis in non-endemic areas to realise that with an increasingly internationalised world (travel, trade, etc) we should never believe that a disease will remain exclusive to one region of the world.

Climate change and environmental degradation are factors that are set to broaden the distribution of several pathogens and associated vectors. Whilst not a human pathogen, it is believed that the disruption of many microrhiza opened up an ecological niche for the jarrah dieback disease. Could other environmental pathogens like Burkholderia psuedomallei move into such a vacant spot in a depleted ecosystem? With climate’s change, some of the environmental barriers will cease to exist for diseases and vectors to become endemic in an area. It is predicted that dengue fever and the Aedes egypti mosquito will move further south in Australia over the coming decades. Likewise, malaria and its Anopheles vectors will continue to become endemic in more regions of the world. As we never invested in vaccines or new treatments, first world countries still be just as vulnerable to these diseases (pending vector control attempts, however as with West Nile virus in the US there may be little that can be done to prevent spread once they are at detectable levels). In the case of bacteria, with increased geographic distribution comes new environmental pressures to direct the evolution of new traits. Traits such as adhesion to chitin in Vibrio cholerae are the very genes that determine virulence in the human small intestine (ironic example as it was this organism that struck down the daughter of Charles Darwin). Other examples would include the ability to survive inside amoeba (Legionella, Burkholderia) conferring them with the ability to survive in macrophages, and environmental iron chelating proteins overcoming anaemia of inflammation. What niches are we selecting for through climate change, and how could these affect pathogenicity? The human side of climate change can be seen in Pakistan. Increased frequency of adverse weather related disasters in concentrated foci of dense human populations (like a Hurricane Katrina scenario) would have devastating implications for the spread of infectious diseases (melliodosis being one in our region). Additionally could disaster relief teams act as unwitting carriers of diseases from one region to another? However with clean water and sanitation in the Western World the threat of a reemergence of water borne disease remains unlikely. As sanitation is estimated to have led to 25 years of the 30 year increase in human life expectancy since 1850, perhaps the decrease in future life expectancy will be modest (factoring out lifestyle factors)?

Evolving alongside to the antibiotic resistant commensals, livestock and aquaculture’s use of antibiotics have produced antibiotic resistant strains of many bacteria including E.coli, Vibrio spp. Vegetables may not be much safer as night soil remains in use in some countries as increasingly, Australia consumes food entering from the third world, are we at the mercy of the lowest common denominator of food safety? Are we liable to more E. coli O157-H7 and other food borne pathogens (see B. hominis entering US on South American raspberries)? People living with their livestock in rural areas of the South East Asian region also open the door to many new zoonoses like SARS and H1N1. Fish sources becoming exhausted and the rise of aquaculture too may change the nature of infectious diseases. Fish lack lymph nodes and therefore receptor revision making vaccinology of fish a challenge. Being an intensive industry, Vibrio spp being a common pathogen for which there are few effective fish vaccines, could future fish consumption be associated with increased risk of haemolytic food poisoning, and Streptococcus iniae infections especially as oceans warm?

So, what does the future hold in store?

I would like to acknowledge Dr. Tim Inglis for his inspiring lectures and conversations which fostered my interest in this topic.

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

The popularity of the Kokoda Trail has increased dramatically over the last decade.  More and more Australians are making the arduous trek through the muddy, steep terrain of the Owen Stanley Range in Papua New Guinea.

This fantastic adventure serves as a moving military history shrine and, for some, the ultimate mental and physical challenge.

The first case of severe exercise-associated hyponatraemia in Kokoda occurred in 2006, with a second case in 2008.  In addition, six apparently healthy trekkers have died on the track since 2006, their causes of death unknown.

In April this year, Dr Sean Rothwell and Dr David Rosengren led a research expedition to investigate the prevalence of exercise-associated hyponatremia (EAH) on the Kokoda Trail.

Funded by the Kokoda Track Authority and expertly guided by Executive Excellence, the team collected blood from nearly 200 people over a four day period in trying conditions in the Papua New Guinean jungle. They were joined by Michael Usher and his crew from 60 Minutes who compiled this great story first aired on 60 minutes June 6th 2010. Read the full transcript of ‘tracking a killer’ or watch the full 60 minutes video of the research expedition

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Double-Click Image to play movie

Most of the trekkers had normal blood tests results.  However a small number of them demonstrated mild hyponatraemia.  These trekkers had consumed a large amount of fluids.  They were observed for a few hours of fluid restriction, and their sodium returned to normal.

EAH is caused by excessive fluid intake in the setting of exercise-induced ADH release.  This causes a dilutional hyponatraemia which manifests as headache, nausea, confusion, ataxia, seizures, coma and ultimately death

The Kokoda Track is a safe and fantastic experience for nearly all trekkers .  This study has confirmed that a small number of trekkers are susceptible to the potentially fatal EAH.

The best way to avoid EAH is to only drink when you are thirsty.

Obviously drink enough fluids to prevent dehydration…but don’t overdo it

References:

• Tracking a Killer – 60 Minutes June 6th 2010 [Video Interview] [Transcript] [Slideshow] [Blog]
• Kokoda Track Research – Adventure Medicine
• Rothwell SP, Rosengren DJ. Severe exercise-associated hyponatremia on the Kokoda Trail, Papua New Guinea. Wilderness Environ Med. 2008 Spring;19(1):42-4. PMID 18333641
• Exercise-associated hyponatremia – clinical quiz
• Hyponatraemia – the basics
• Hyponatremia – Wikipedia
• O’Connor RE. Exercise-induced hyponatremia: causes, risks, prevention, and management. Cleve Clin J Med. 2006 Sep;73 Suppl 3:S13-8. Review. PubMed PMID: 16970148. (fulltext)
• Rogers IR, Hew-Butler T. Exercise-associated hyponatremia: overzealous fluid consumption. Wilderness Environ Med. 2009 Summer;20(2):139-43. PMID: 19594207 (fulltext)
• Rosner MH, Kirven J.  Exercise-associated hyponatremia. 2007 Jan;2(1):151-61. PMID:17699400 (fulltext)

Life in the Fast Lane Medical Blog - Emergency Medicine education blog