Category Archives: WebNotes in Emergency Medicine

05.01.13
by

The Silent Majority or the Silenced Majority ?


It is a favourite excuse of the powers-that-be in Malaysia, to say that voices of opposition, discontent and dissatisfaction are coming just from a small group of dissidents, of trouble-makers and 'pengacau'. They often claim that the "silent majority" of Malaysians are very happy and satisfied, and that is why they keep silent. Of course, those who support them will often parrot this argument. Even when the opposition won almost half of all votes in 2008, they still insisted that the "silent majority" was with them.

But let me ask you, the common man, the average Malaysian on the street. Are you happy with the way things are going ? Have you tried to voice out your dissatisfaction, only to realize that you can't ? Have you written in complaints to the Press, only to see only "favourable" letters praising the government of the day being printed ? Have you felt that you are not heard, and your point of view not considered ?

Well, you are not wrong. Malaysia has built a large gap in the last few decades; a gap not between the races, not between the common Malaysians. That gap is the gap between the people and its leaders. We, in fact, top the world, in that we have the largest gap between the common man, and their leaders. Our common Malaysians cannot communicate with our leaders; they cannot hear us (or maybe they just don't want to hear us). Malaysia BOLEH!!!

So then, are we now the silent majority, happy satisfied content and silent because we have just nothing to say; or are we the silenced majority, who shout out but are not heard, who tell but are ignored, who suggest but are laughed at, who resist and are labelled trouble-makers ?

I REFUSE to be silenced anymore. I will shout out for me, for my family, for my friends (even those who continue to support BN), for my neighbours and my fellow Malaysians; for our future, and our common path toward that better tomorrow.



I was there, and I will not be silenced anymore


Les Miserables "Do you hear the people sing?"

So shut up about the silent majority already ....

whewww !      
04.25.13
by

You mean there was all that MONEY in the other pocket ?



This election has seen government spending on an unprecedented scale. From free concerts by Psy and Taiwan artists, to big-name events like Michelle Yeoh and Alan Tam. From handouts to all and sunder, to free makan, free beer and free T-shirts. From spending on flags and banners (with enough cloth to clothe all the poor in Malaysia for 5 years at least), to online ads on every social media webpage that you may be on.

In any other democracy, this would have constituted vote-buying, an election offence. It is an election offence here in Malaysia too, but as always, there are two sets of rules; one for the governing, where "we'll close both eyes" is the guiding principle; and the other for the rest of us, the governed, where we learn quickly "do as I say, not do as I do".

The amount of money spent is staggering. Where did all this money come from ? Where is this other pocket, where we had all this extra money to spend ?

I wish we had known about this other pocket full of cash when -
  • we were short of money for specialized medicines
  • we had to treat patients 4 to a room
  • we had not enough beds and had to treat patients on wheelchairs, until ...
  • we ran out of wheelchairs
  • we have not enough ambulances
  • we asked for an allocation of just RM 5 per person in the community to provide additional ambulance services
I wish we had known about this other pocket full of cash when - 
  • we treated that retired school teacher who was getting RM 350 in pension to survive on
  • our staff was so much in debt that his six children were just taking one meal per day; the church group came in to support this Muslim family with daily rations
  • the whole family structure disintegrated when the sole breadwinner suffered a stroke; and they are now all relying to donations from fellow villagers
Free beers and free makan ? I really find it distasteful.
04.24.13
by

Absolutely ….. !!



Rabies is not endemic in Malaysia ie we don't have this. If you have been bitten by a dog in Penang for example (unless there were incredibly suggestive features eg drooling crazy dog who bit you and then died) I would really not think about rabies. 

But rabies is endemic in Thailand. And Westerners, being Westerners, like dogs, and like to pet dogs who don't belong to them. Invariably, some of them get bitten. So, rabies, being endemic in Thailand, it makes sense for them to get an anti-rabies vaccine. This is almost always started in Thailand. But this vaccine requires multiple doses over many days. So this Western tourist decides that they can continue their travels to, Penang !!

Now, when in Penang, they now want to continue their anti-rabies vaccine. Which we don't have. It is not unreasonable for us not to have it, since rabies is not endemic in Malaysia, it is very expensive, and really, should we carry vaccines for something that uncommon ?

Generally, these Western tourists are usually diverted to private hospitals, where apparently they are charged about RM 500 per dose. "What ?? RM 500 ?? Are you trying to rip us off ??" becomes the standard reply because they think we are cheap. 

Bring your sick dog to the vet in UK, and it would easily cost you 100 pounds. Ditto the US. Ditto everywhere in the Western world. But because we are "cheap", these tourists make noise. 

If you make noise at the private hospital, they have one standard option. They tell you to go to the government hospital. 

So, now the already upset tourists appear at your doorstep, expecting something more, and ready to make even more noise. 

Are we wrong not to store anti-rabies vaccine ? 

Remember we are spending the rakyat's money. Each dose costs a couple of hundred bucks; you don't know when you will use it, and it expires in under 2 years. Will you decide to stock up this vaccine ? What say you ?

What next, you may ask ?

Well, let me tell you. We have no King Cobras in Penang. Cobras, yes; vipers, yes. Kraits, probably yes. No King Cobras. So we keep anti-venom for Cobras, Vipers and Kraits. Being good people, we also keep some anti-venom for sea snake just in case, considering that we are an island, and a sea-snake bite is rather deadly. A few thousand RM per vial. We did not keep any antivenom for King Cobra.

Last year, a zoo in Kuantan imported and kept King Cobras without informing anyone. One of their staff got bitten, and of course, everybody was in chaos. A King Cobra anti-venom was sourced finally after many hours, and administered. The blame game then started. Easy to blame. Why no anti-venom stock ? Why govt hospital so lousy ? Interestingly nobody blamed the zoo.

But similarly to rabies, would you stock an anti-venom which costs a thousand RM, and lasts less than 2 years, if you have no King Cobras in your expected area ? Would you ?

I wouldn't. And we didn't. 

Until a couple of weeks ago, and I nearly fainted when I found out; that the Snake temple people have imported King Cobras and are conducting snake shows, where the handler will kiss the head of the snake. 

And now we are hearing the some people like to keep exotic pets including rattlesnakes.

So really, what can I say; I am absolutely ..... !!   [speechless!]
03.26.13
by

How Doctors Die



A magnificent article by Ken Murray. Original link here. Worth reading to the very end.

Years ago, Charlie, a highly respected orthopedist and a mentor of mine, found a lump in his stomach. He had a surgeon explore the area, and the diagnosis was pancreatic cancer. This surgeon was one of the best in the country. He had even invented a new procedure for this exact cancer that could triple a patient’s five-year-survival odds–from 5 percent to 15 percent–albeit with a poor quality of life. Charlie was uninterested. He went home the next day, closed his practice, and never set foot in a hospital again. He focused on spending time with family and feeling as good as possible. Several months later, he died at home. He got no chemotherapy, radiation, or surgical treatment. Medicare didn’t spend much on him.
It’s not a frequent topic of discussion, but doctors die, too. And they don’t die like the rest of us. What’s unusual about them is not how much treatment they get compared to most Americans, but how little. For all the time they spend fending off the deaths of others, they tend to be fairly serene when faced with death themselves. They know exactly what is going to happen, they know the choices, and they generally have access to any sort of medical care they could want. But they go gently.
Of course, doctors don’t want to die; they want to live. But they know enough about modern medicine to know its limits. And they know enough about death to know what all people fear most: dying in pain, and dying alone. They’ve talked about this with their families. They want to be sure, when the time comes, that no heroic measures will happen–that they will never experience, during their last moments on earth, someone breaking their ribs in an attempt to resuscitate them with CPR (that’s what happens if CPR is done right).
Almost all medical professionals have seen what we call “futile care” being performed on people. That’s when doctors bring the cutting edge of technology to bear on a grievously ill person near the end of life. The patient will get cut open, perforated with tubes, hooked up to machines, and assaulted with drugs. All of this occurs in the Intensive Care Unit at a cost of tens of thousands of dollars a day. What it buys is misery we would not inflict on a terrorist. I cannot count the number of times fellow physicians have told me, in words that vary only slightly, “Promise me if you find me like this that you’ll kill me.” They mean it. Some medical personnel wear medallions stamped “NO CODE” to tell physicians not to perform CPR on them. I have even seen it as a tattoo.
To administer medical care that makes people suffer is anguishing. Physicians are trained to gather information without revealing any of their own feelings, but in private, among fellow doctors, they’ll vent. “How can anyone do that to their family members?” they’ll ask. I suspect it’s one reason physicians have higher rates of alcohol abuse and depression than professionals in most other fields. I know it’s one reason I stopped participating in hospital care for the last 10 years of my practice.
How has it come to this–that doctors administer so much care that they wouldn’t want for themselves? The simple, or not-so-simple, answer is this: patients, doctors, and the system.
To see how patients play a role, imagine a scenario in which someone has lost consciousness and been admitted to an emergency room. As is so often the case, no one has made a plan for this situation, and shocked and scared family members find themselves caught up in a maze of choices. They’re overwhelmed. When doctors ask if they want “everything” done, they answer yes. Then the nightmare begins. Sometimes, a family really means “do everything,” but often they just mean “do everything that’s reasonable.” The problem is that they may not know what’s reasonable, nor, in their confusion and sorrow, will they ask about it or hear what a physician may be telling them. For their part, doctors told to do “everything” will do it, whether it is reasonable or not.
The above scenario is a common one. Feeding into the problem are unrealistic expectations of what doctors can accomplish. Many people think of CPR as a reliable lifesaver when, in fact, the results are usually poor. I’ve had hundreds of people brought to me in the emergency room after getting CPR. Exactly one, a healthy man who’d had no heart troubles (for those who want specifics, he had a “tension pneumothorax”), walked out of the hospital. If a patient suffers from severe illness, old age, or a terminal disease, the odds of a good outcome from CPR are infinitesimal, while the odds of suffering are overwhelming. Poor knowledge and misguided expectations lead to a lot of bad decisions.
But of course it’s not just patients making these things happen. Doctors play an enabling role, too. The trouble is that even doctors who hate to administer futile care must find a way to address the wishes of patients and families. Imagine, once again, the emergency room with those grieving, possibly hysterical, family members. They do not know the doctor. Establishing trust and confidence under such circumstances is a very delicate thing. People are prepared to think the doctor is acting out of base motives, trying to save time, or money, or effort, especially if the doctor is advising against further treatment.
Some doctors are stronger communicators than others, and some doctors are more adamant, but the pressures they all face are similar. When I faced circumstances involving end-of-life choices, I adopted the approach of laying out only the options that I thought were reasonable (as I would in any situation) as early in the process as possible. When patients or families brought up unreasonable choices, I would discuss the issue in layman’s terms that portrayed the downsides clearly. If patients or families still insisted on treatments I considered pointless or harmful, I would offer to transfer their care to another doctor or hospital.
Should I have been more forceful at times? I know that some of those transfers still haunt me. One of the patients of whom I was most fond was an attorney from a famous political family. She had severe diabetes and terrible circulation, and, at one point, she developed a painful sore on her foot. Knowing the hazards of hospitals, I did everything I could to keep her from resorting to surgery. Still, she sought out outside experts with whom I had no relationship. Not knowing as much about her as I did, they decided to perform bypass surgery on her chronically clogged blood vessels in both legs. This didn’t restore her circulation, and the surgical wounds wouldn’t heal. Her feet became gangrenous, and she endured bilateral leg amputations. Two weeks later, in the famous medical center in which all this had occurred, she died.
It’s easy to find fault with both doctors and patients in such stories, but in many ways all the parties are simply victims of a larger system that encourages excessive treatment. In some unfortunate cases, doctors use the fee-for-service model to do everything they can, no matter how pointless, to make money. More commonly, though, doctors are fearful of litigation and do whatever they’re asked, with little feedback, to avoid getting in trouble.
Even when the right preparations have been made, the system can still swallow people up. One of my patients was a man named Jack, a 78-year-old who had been ill for years and undergone about 15 major surgical procedures. He explained to me that he never, under any circumstances, wanted to be placed on life support machines again. One Saturday, however, Jack suffered a massive stroke and got admitted to the emergency room unconscious, without his wife. Doctors did everything possible to resuscitate him and put him on life support in the ICU. This was Jack’s worst nightmare. When I arrived at the hospital and took over Jack’s care, I spoke to his wife and to hospital staff, bringing in my office notes with his care preferences. Then I turned off the life support machines and sat with him. He died two hours later.
Even with all his wishes documented, Jack hadn’t died as he’d hoped. The system had intervened. One of the nurses, I later found out, even reported my unplugging of Jack to the authorities as a possible homicide. Nothing came of it, of course; Jack’s wishes had been spelled out explicitly, and he’d left the paperwork to prove it. But the prospect of a police investigation is terrifying for any physician. I could far more easily have left Jack on life support against his stated wishes, prolonging his life, and his suffering, a few more weeks. I would even have made a little more money, and Medicare would have ended up with an additional $500,000 bill. It’s no wonder many doctors err on the side of overtreatment.
But doctors still don’t over-treat themselves. They see the consequences of this constantly. Almost anyone can find a way to die in peace at home, and pain can be managed better than ever. Hospice care, which focuses on providing terminally ill patients with comfort and dignity rather than on futile cures, provides most people with much better final days. Amazingly, studies have found that people placed in hospice care often live longer than people with the same disease who are seeking active cures. I was struck to hear on the radio recently that the famous reporter Tom Wicker had “died peacefully at home, surrounded by his family.” Such stories are, thankfully, increasingly common.
Several years ago, my older cousin Torch (born at home by the light of a flashlight–or torch) had a seizure that turned out to be the result of lung cancer that had gone to his brain. I arranged for him to see various specialists, and we learned that with aggressive treatment of his condition, including three to five hospital visits a week for chemotherapy, he would live perhaps four months. Ultimately, Torch decided against any treatment and simply took pills for brain swelling. He moved in with me.
We spent the next eight months doing a bunch of things that he enjoyed, having fun together like we hadn’t had in decades. We went to Disneyland, his first time. We’d hang out at home. Torch was a sports nut, and he was very happy to watch sports and eat my cooking. He even gained a bit of weight, eating his favorite foods rather than hospital foods. He had no serious pain, and he remained high-spirited. One day, he didn’t wake up. He spent the next three days in a coma-like sleep and then died. The cost of his medical care for those eight months, for the one drug he was taking, was about $20.
Torch was no doctor, but he knew he wanted a life of quality, not just quantity. Don’t most of us? If there is a state of the art of end-of-life care, it is this: death with dignity. As for me, my physician has my choices. They were easy to make, as they are for most physicians. There will be no heroics, and I will go gentle into that good night. Like my mentor Charlie. Like my cousin Torch. Like my fellow doctors.
Ken Murray, MD, is Clinical Assistant Professor of Family Medicine at USC.

10.01.12
by

The Perfect Evidence Based Emergency Doc



Let's just say that there is this PERFECT emergency doctor. Just perfect. Evidence-based references, guidelines, NNTs and all that. We all wish that we worked with someone like that, right ? Or even better, we all wished sometimes we were as good as that, eh ?

Now, one day, whilst managing a patient, he applied a guideline correctly. Performed a score, applied a guideline and made a decision based on that guideline. Something goes wrong. A diagnosis is missed and an adverse outcome occurs.

Until now, everything has been done as would have been done in usual practice. Even more, the guideline applied is well accepted both locally and internationally. But looking deeper at guidelines and evidence, nothing is ever 100%. It is always in the high 90's percentage points but never 100%.

So the real question is, what do you say to the patient or family members, who have suffered the adverse outcome ? Those who were unfortunately in the small percentage points not covered within the guideline ?

How do we answer the allegation that the guideline is not good enough, or that the doctor who we all think is perfect, was negligent and incapable ? Can we actually say that the guideline was good enough, when it had failed in that particular rare occasion ? 

And how do we counter-argue when (invariably) some Googles and finds some loophole or some other obscure guideline which would have picked up this patient ?

Is there a way to win the scientific argument, legal argument, moral argument and at the same time, reconcile that with what the heart says ?

Help. I don't know this one.



09.06.12
by

EMS Asia 2012 – Welcome Address


On behalf of the Organising Committee, I am most honoured to welcome all of you to the inaugural EMS Asia 2012 Conference, to the island of Penang and the country of Malaysia. We are most honoured to be able to present this conference to all of you and to share in an experience which we hope you will find most memorable. If you look around this hall, you will see more than 500 participants - all of them EMS leaders, experts, trainers and providers, from 20 represented countries in Asia and beyond. What an opportunity to make friends or renew friendships, seek collaborators and exchange ideas.

The EMS Asia 2012 Conference was built on this very foundation - To bring together experts; and to learn from best practices in the region. To develop models of good care and to raise the standards of prehospital care. To conjointly develop standards and safety specifications for ambulances. And to develop a road map for the further collaboration between EMS systems in Asia.

This inaugural conference is co-organised by the Asian EMS Council, St John Ambulance of Malaysia in Penang, and the Penang General Hospital. The theme of "Safety and Quality in Pre-Hospital Care" highlights the conjoint effort of us all to develop better safety standards and specifications for our ambulances and to provide better care in our ambulances as we all move toward developing our EMS systems in Asia.

I must thank Assoc Prof Marcus Ong and the Asian EMS Council for giving us the honour of hosting the Inaugural EMS Asia Conference, and for believing our assertion that an EMS Conference here would be able to attract participation from around the region. I would like to thank Dr Sarah Shaik Abd Karim, our Scientific Chair, and her team for her tireless work in bringing together our faculty of more than 60 Malaysian and International experts. I must also thank the team from the Penang General Hospital for their very admirable effort in coordinating and supporting the entire conference. I would also like to express our gratitude to our partners and sponsors from around the world, who have worked with us to make this event a success. 

I must especially thank the St John Ambulance of Malaysia team in Penang, who have yet again, taken up the challenge of working towards improving EMS in Malaysia in bringing together this international congregation. The many months of shared work have resulted in this magnificent conference and this unique opportunity to share and learn. I am very proud of this team.

Do take some time to enjoy the beaches of Batu Ferringhi, the food and shopping that Penang has to offer. Take some time to explore some of the heritage tours or hiking trails. Soak in the sun or try the fun-filled beach activities that are just outside that door. 

We are most happy to welcome you all, and we look forward to an enjoyable conference and a memorable time.

Thank you.
09.06.12
by

EMS Asia 2012 – Welcome Address


On behalf of the Organising Committee, I am most honoured to welcome all of you to the inaugural EMS Asia 2012 Conference, to the island of Penang and the country of Malaysia. We are most honoured to be able to present this conference to all of you and to share in an experience which we hope you will find most memorable. If you look around this hall, you will see more than 500 participants - all of them EMS leaders, experts, trainers and providers, from 20 represented countries in Asia and beyond. What an opportunity to make friends or renew friendships, seek collaborators and exchange ideas.

The EMS Asia 2012 Conference was built on this very foundation - To bring together experts; and to learn from best practices in the region. To develop models of good care and to raise the standards of prehospital care. To conjointly develop standards and safety specifications for ambulances. And to develop a road map for the further collaboration between EMS systems in Asia.

This inaugural conference is co-organised by the Asian EMS Council, St John Ambulance of Malaysia in Penang, and the Penang General Hospital. The theme of "Safety and Quality in Pre-Hospital Care" highlights the conjoint effort of us all to develop better safety standards and specifications for our ambulances and to provide better care in our ambulances as we all move toward developing our EMS systems in Asia.

I must thank Assoc Prof Marcus Ong and the Asian EMS Council for giving us the honour of hosting the Inaugural EMS Asia Conference, and for believing our assertion that an EMS Conference here would be able to attract participation from around the region. I would like to thank Dr Sarah Shaik Abd Karim, our Scientific Chair, and her team for her tireless work in bringing together our faculty of more than 60 Malaysian and International experts. I must also thank the team from the Penang General Hospital for their very admirable effort in coordinating and supporting the entire conference. I would also like to express our gratitude to our partners and sponsors from around the world, who have worked with us to make this event a success. 

I must especially thank the St John Ambulance of Malaysia team in Penang, who have yet again, taken up the challenge of working towards improving EMS in Malaysia in bringing together this international congregation. The many months of shared work have resulted in this magnificent conference and this unique opportunity to share and learn. I am very proud of this team.

Do take some time to enjoy the beaches of Batu Ferringhi, the food and shopping that Penang has to offer. Take some time to explore some of the heritage tours or hiking trails. Soak in the sun or try the fun-filled beach activities that are just outside that door. 

We are most happy to welcome you all, and we look forward to an enjoyable conference and a memorable time.

Thank you.
08.29.12
by

Statutory Rape for Dungooos


Dungoo - Dungu = 'village idiot'

Statutory rape - sex with a minor under the age of maturity to provide consent for the act; in Malaysia, girls under the age of 16 years. 

The law assumes that girls under the age of 16 years are too young to understand the act and consequences of the sexual act; so it is considered as RAPE even if it would seem that the girl had consented to the act.

In many countries, due to the higher incidence of teenage sex, and I suppose the earlier exposure of our teenagers to sex, boyfriend and girlfriend sexual activity takes place before the ages of 16. 

But this needs to be differentiated from SEXUAL PREDATORY behaviour ie sex between a 22 year old man and a 12 year old girl; or between a 19 year old and a 14 year old girl. In these situations, the larger age gaps between both the man and the girl provides ground to believe the the older man should know that sex with a young girl is illegal and she is not old enough to make a reasonable decision.

So, in many countries, an age gap of more than 3 years is considered in convicting of statutory rape.

Malaysia, as usual, must be different. Read here.

But in Malaysia, our courts apparently determine that "first time offenders", people who are "not highly educated", are "young and have a bright future" can be bound over for good behaviour without going to jail !! 

So if you are a bloody young DUNGOO, our courts have said that you can have your way with young girls because your DUNGOO-ness really spells a bright future.

Not sure who is the DUNGOO in this whole matter. Sigh !
08.29.12
by

Statutory Rape for Dungooos


Dungoo - Dungu = 'village idiot'

Statutory rape - sex with a minor under the age of maturity to provide consent for the act; in Malaysia, girls under the age of 16 years. 

The law assumes that girls under the age of 16 years are too young to understand the act and consequences of the sexual act; so it is considered as RAPE even if it would seem that the girl had consented to the act.

In many countries, due to the higher incidence of teenage sex, and I suppose the earlier exposure of our teenagers to sex, boyfriend and girlfriend sexual activity takes place before the ages of 16. 

But this needs to be differentiated from SEXUAL PREDATORY behaviour ie sex between a 22 year old man and a 12 year old girl; or between a 19 year old and a 14 year old girl. In these situations, the larger age gaps between both the man and the girl provides ground to believe the the older man should know that sex with a young girl is illegal and she is not old enough to make a reasonable decision.

So, in many countries, an age gap of more than 3 years is considered in convicting of statutory rape to try to differentiate between early teenage sex and predatory sexual behaviour.

Malaysia, as usual, must be different. Read here.

In Malaysia, our courts apparently determine that "first time offenders", people who are "not highly educated", are "young and have a bright future" can be bound over for good behaviour without going to jail !! 

So if you are a bloody young DUNGOO, our courts have said that you can have your way with young girls because your DUNGOO-ness really spells a bright future.


I am sure there are extenuating circumstances, but the law was made to protect our young girls. Have  our system let down this 12 year old ? Are we at the doorstep of making 12 year olds girls marry their 22 year old boyfriend- rapists ?

Not sure who is the DUNGOO in this whole matter. Sigh !


07.02.12
by

Dear Julia

Dear Julia,


Forgive the lack of honorifics; at least for the length of this blog, I would like to speak to you as a friend, instead of a Prime Minister of a country. I am after all, a nobody in a voiceless country, one where it would seem we have got our priorities totally wrong. 


Our countries are quite similar in many ways; we have about the same population size, our countries flourished at around the same time mainly from large-scale immigration, yours mainly from Western nations, mine from China, India and the surrounding Malay archipelago. And for many many years, our countries have had close ties. Both in good times and in war. Generations of Malaysian have gained from the high standards of university education in your country; in many ways, the entire life earnings of millions of Malaysian families have gone to your country to pay for that education. Many Malaysian having found the way of life there to their liking, have stayed on. Many more Malaysians, having found life in Malaysia lacking fair prospects and opportunities, have left for your shores. 


So in many ways, your country have gained somewhat from this relationship with us. We have worked away so that we can pay for our children's education in your country; our best and brightest have left us for your greener pastures, and now contribute to your country, instead of the land of their birth and early education. As I said, our priorities, totally wrong, was never to retain our Malaysians, nor to create an environment for them to flourish. But that, Julia, is our mistake.


Your mistake, if you should decide to do so, would be to continue to support the Lynas Advanced Materials Plant in Gebeng Malaysia. This project is just wrong. Malaysia has no need for rare earth. We have no special skills, no special environment, no special resources that make us THE ideal place in the world to process rare earth. The only special thing that we may have is a government that is willing to spend our money to make the infrastructure for this plant, offer a 12-year tax holiday for its earnings; a government that is willing to believe that Lynas would like to ship unprocessed materials, a few thousand miles to Gebeng for processing, just because it likes Malaysia. 


This plant, in Gebeng, will produce radioactive byproducts. There are half a million people who live within 30 km of this Gebeng plant. That is 150,000 more people that the entire population of Canberra. Look around you. Imagine. What would you think, if Lynas decided to build one in Kambah, one of your most popular suburbs, about 30 km from the Canberra CBD ? Well, you don't have to worry really, because Australian regulations insist that such plants must be at least 300 km away from the nearest human community. But just imagine one in Kambah, and you may actually understand a bit more about Gebeng.


So the truth of the matter is this. We don't want it. We don't need it. And we definitely do not appreciate being lectured about the adverse impact on businesses and foreign investments. We don't want it because it does not make any sense to us. We are simple people, of simple ways. Our simple minds just tell us that it is wrong. Despite what the powerful people say. Despite all our government says, and what your government may say.


We don't want it because it has happened to us before. Bukit Merah, near Taiping, was also a rare earth plant. It is now abandoned, contaminated and desperately never mentioned in our news. 

This Lynas issue never really hit me until very recently, when a fellow doctor was lamenting the high numbers of leukemia and cancer patients in Taiping Hospital. I wonder if the ones who approved and supported the Bukit Merah plant can sleep well at night.


Julia, we have over the years, given to your country, our best. We even thanked you for it. Must you, and your country, really, give us your worst ?



07.02.12
by

Dear Julia

Dear Julia,


Forgive the lack of honorifics; at least for the length of this blog, I would like to speak to you as a friend, instead of a Prime Minister of a country. I am after all, a nobody in a voiceless country, one where it would seem we have got our priorities totally wrong. 


Our countries are quite similar in many ways; we have about the same population size, our countries flourished at around the same time mainly from large-scale immigration, yours mainly from Western nations, mine from China, India and the surrounding Malay archipelago. And for many many years, our countries have had close ties. Both in good times and in war. Generations of Malaysian have gained from the high standards of university education in your country; in many ways, the entire life earnings of millions of Malaysian families have gone to your country to pay for that education. Many Malaysian having found the way of life there to their liking, have stayed on. Many more Malaysians, having found life in Malaysia lacking fair prospects and opportunities, have left for your shores. 


So in many ways, your country have gained somewhat from this relationship with us. We have worked away so that we can pay for our children's education in your country; our best and brightest have left us for your greener pastures, and now contribute to your country, instead of the land of their birth and early education. As I said, our priorities, totally wrong, was never to retain our Malaysians, nor to create an environment for them to flourish. But that, Julia, is our mistake.


Your mistake, if you should decide to do so, would be to continue to support the Lynas Advanced Materials Plant in Gebeng Malaysia. This project is just wrong. Malaysia has no need for rare earth. We have no special skills, no special environment, no special resources that make us THE ideal place in the world to process rare earth. The only special thing that we may have is a government that is willing to spend our money to make the infrastructure for this plant, offer a 12-year tax holiday for its earnings; a government that is willing to believe that Lynas would like to ship unprocessed materials, a few thousand miles to Gebeng for processing, just because it likes Malaysia. 


This plant, in Gebeng, will produce radioactive byproducts. There are half a million people who live within 30 km of this Gebeng plant. That is 150,000 more people that the entire population of Canberra. Look around you. Imagine. What would you think, if Lynas decided to build one in Kambah, one of your most popular suburbs, about 30 km from the Canberra CBD ? Well, you don't have to worry really, because Australian regulations insist that such plants must be at least 300 km away from the nearest human community. But just imagine one in Kambah, and you may actually understand a bit more about Gebeng.


So the truth of the matter is this. We don't want it. We don't need it. And we definitely do not appreciate being lectured about the adverse impact on businesses and foreign investments. We don't want it because it does not make any sense to us. We are simple people, of simple ways. Our simple minds just tell us that it is wrong. Despite what the powerful people say. Despite all our government says, and what your government may say.


We don't want it because it has happened to us before. Bukit Merah, near Taiping, was also a rare earth plant. It is now abandoned, contaminated and desperately never mentioned in our news. 

This Lynas issue never really hit me until very recently, when a fellow doctor was lamenting the high numbers of leukemia and cancer patients in Taiping Hospital. I wonder if the ones who approved and supported the Bukit Merah plant can sleep well at night.


Julia, we have over the years, given to your country, our best. We even thanked you for it. Must you, and your country, really, give us your worst ?



06.05.12
by

The Physiology of Bleeding to Death

Young man, on his bike. Side-swiped by another vehicle going in the opposite direction. Crash, dragged, rolled and left almost lifeless by the road. Passers-by spot him, load him up into their car, drop him off at the nearest Emergency Department and leave.


The ED doctor on duty there identifies a patient with multiple injuries; very restless, not obeying commands, hypotensive (80/40) and tachycardic (130) with an SpO2 of 80%. Automatic mode kicks in - oxygen is given via non-rebreather high-flow mask at 15 L/min, Normal Saline is started at full flow, bloods are taken for inx, and documentation of injuries ensues. Repeat BP comes back at 130/60, HR 135, SpO2 94% and doctor sighs relief. Would you do the same ? Same sigh of relief as well ?


Patient gets sent to X-ray; spends an hour there with X-rays of just about everything unimportant, when the accompanying staff notices that the patient was gasping and rushed him back to the ED; in time for them to note asystole and commence CPR. The patient succumbs to his injuries (and the doctor's failure to understand physiology of bleeding to death) about 45 minutes later.


What was the doctor thinking about ? I thought I would ask some of the new doctors who were posted to our ED. Scenario presented; and this reply was their COMMON thought process. Initially restless and then obtunded (must be head injury - must do CT scan as priority). Initially hypotensive (must be bleeding - need to look for source of bleeding - but since BP improved with fluids, should be getting better). Very tachycardic (must be due to pain, anxiety). Low SpO2 (something wrong with the breathing - better look for pneumo- or haemothorax - but since improved with oxygen, must be getting better - let's do x-rays to find out more). Yup, that's right. This was their COMMON reply. So it is not merely that particular doctor's failure to understand the physiology of bleeding to death, it is ALL our YOUNGER DOCTORS FAILURE to do so as well.


This is what happened to that patient, in physiological simple speak. This patient did suffer many many injuries; abrasions, lacerations, a few fractures of the limbs. These injuries bled quite a bit, but they were not killers. Nope. He had, instead, suffered a high force impact onto his left torso which broke multiple ribs, resulted in a severely lacerated spleen and severe pulmonary contusions. Which was not recognized, and which continued to bleed until he bled to death. That was the killer.


The reason why he came in very restless was because of hypoxia and hypotension, NOT because of head injury. Being very short of oxygen and deprived of blood supply to the vital organs would make every single one of us become highly agitated and distressed. This is the reason why GCS is not a useful tool for estimation of head injury until the ABCs have been stabilized.


In severe bleeding, the body compensates to try to maintain the blood pressure. The pressure is maintained to try to preserve blood flow to the most vital of organs; the brain, heart and lungs. But this pressure is maintained mainly by squeezing all the main blood vessels (vasoconstriction). Blood is now shunted away from the skin, limbs and intestines to the brain, heart and lungs. The limbs become cold and bluish from the lack of fresh oxygenated blood, and the SpO2 reading drops. 

This entire compensation mechanism maintains pressure, but the total amount of blood flow and oxygen supplied decreases, to the rest of the body. Cells in the body, deprived of enough oxygen, are now forced use their fuel without oxygen; in an inefficient manner that starts producing huge amounts of acids, mainly lactic acid. This leads to worsening acidosis.


So this patient has severe bleeding from his lacerated spleen, and had lost so much blood that his compensation mechanisms were beginning to fail; that was why he came in hypotensive. He was definitely restless from all that lack of oxygen and blood to his brain. His peripheries were cold as no blood was reaching his fingers and toes; his SpO2 was obviously going to be low.

Let's look at what happened next. He was given oxygen, a good thing. What it did, was filled the little blood that was still available with oxygen. Which made the saturation SpO2 of the little blood that was available, 95%. Although 95%, it was still too little blood to really carry the oxygen needs of the patient. NO, the SpO2 of 95% did not mean he was any better.


And he was given fluids. So all those fluids would have rushed into the "squeezed" blood vessels and immediately raised the pressure within those blood vessels. This gave the impression of "improvement" to the doctor. In fact, it probably made things worse. There are two main down-sides to this. Firstly, the sudden increase in the pressure has the tendency to suddenly burst some of the newly formed clots, causing bleeding to resume. Secondly, the fluid now dilutes the clotting factors in the blood making it more inefficient at formed a clot to stem the bleeding. 


So, none of the initial therapy really helped much. What was worse, was the assumption that he was now "better" and could be sent to the X-rays Dept for further xrays. What happened there was this. The bleeding continued, and the compensations were not able to maintain his blood pressure anymore. The decreased blood supply to the brain made the patient obtunded (accompanying staff may have just thought that the patient was now more quiet and easier to handle). He would also have lost his airway control reflexes, and regurgitation of food may have partially blocked his airway, further worsening his overall hypoxia. 

By now, the amount of blood circulating would have been minimal, and acid levels would have skyrocketed. This acidosis would be the final nail. Reaching a particular dangerous level, it would essentially have prevented the heart from working properly. The heart essentially stops and the quick spiral to death ensues.


What was reversible, and when was it reversible ? Could things done right made a difference ? What things, done differently in what ways ?


Firstly, any person in trauma, with tachycardia, is in SHOCK until proven otherwise. SHOCK in a patient presents with various degrees of anxiety and restlessness, tachycardia, cool peripheries, rapid breathing and signs of poor organ perfusion (low urine output, acidosis and altered mental states). SHOCK is almost always due to bleeding from trauma (significant alternatives include only tension pneumothorax, cardiac tamponade and airway obstruction; but always think of bleeding as well). So, the first right thing to do is to recognize the SHOCK state.


Next, look very carefully for the source of bleeding. Search carefully for spilled blood, either on-the-floor (external bleeding) or in only 4 other areas of significant internal bleeding. Massive haemothorax (diagnosed clinically and with the bedside ultrasound), bleeding into the pelvis and retroperitoneal space (almost always related to pelvic fractures, lower spinal injuries and associated vascular injuries), bleeding into the peritoneal space (mainly due to liver and splenic lacerations, as in this case; and diagnosed with a FAST ultrasound scan) and the tissue spaces of the thighs (which are easily seen, and associated with fractures and vascular injuries). That's it. No X-rays other than the bedside trauma X-ray of the chest and pelvis. No other x-rays needed. Search carefully for bleeding, and once you find it, get the surgeon. 


And lastly, this patient needed blood. Lots of blood. Preferably fresh whole blood. If not, packed cells and the freshest plasma you can get. What needs to be done is to replace the lost blood with actual blood. And with it, hopefully some additional coagulation factors to help stop the bleeding. 


The physiological derangements needed to be reversed. To do that, young doctors must must simply must understand the physiology first. That was the only way to save this patients life.


06.05.12
by

The Physiology of Bleeding to Death

Young man, on his bike. Side-swiped by another vehicle going in the opposite direction. Crash, dragged, rolled and left almost lifeless by the road. Passers-by spot him, load him up into their car, drop him off at the nearest Emergency Department and leave.


The ED doctor on duty there identifies a patient with multiple injuries; very restless, not obeying commands, hypotensive (80/40) and tachycardic (130) with an SpO2 of 80%. Automatic mode kicks in - oxygen is given via non-rebreather high-flow mask at 15 L/min, Normal Saline is started at full flow, bloods are taken for inx, and documentation of injuries ensues. Repeat BP comes back at 130/60, HR 135, SpO2 94% and doctor sighs relief. Would you do the same ? Same sigh of relief as well ?


Patient gets sent to X-ray; spends an hour there with X-rays of just about everything unimportant, when the accompanying staff notices that the patient was gasping and rushed him back to the ED; in time for them to note asystole and commence CPR. The patient succumbs to his injuries (and the doctor's failure to understand physiology of bleeding to death) about 45 minutes later.


What was the doctor thinking about ? I thought I would ask some of the new doctors who were posted to our ED. Scenario presented; and this reply was their COMMON thought process. Initially restless and then obtunded (must be head injury - must do CT scan as priority). Initially hypotensive (must be bleeding - need to look for source of bleeding - but since BP improved with fluids, should be getting better). Very tachycardic (must be due to pain, anxiety). Low SpO2 (something wrong with the breathing - better look for pneumo- or haemothorax - but since improved with oxygen, must be getting better - let's do x-rays to find out more). Yup, that's right. This was their COMMON reply. So it is not merely that particular doctor's failure to understand the physiology of bleeding to death, it is ALL our YOUNGER DOCTORS FAILURE to do so as well.


This is what happened to that patient, in physiological simple speak. This patient did suffer many many injuries; abrasions, lacerations, a few fractures of the limbs. These injuries bled quite a bit, but they were not killers. Nope. He had, instead, suffered a high force impact onto his left torso which broke multiple ribs, resulted in a severely lacerated spleen and severe pulmonary contusions. Which was not recognized, and which continued to bleed until he bled to death. That was the killer.


The reason why he came in very restless was because of hypoxia and hypotension, NOT because of head injury. Being very short of oxygen and deprived of blood supply to the vital organs would make every single one of us become highly agitated and distressed. This is the reason why GCS is not a useful tool for estimation of head injury until the ABCs have been stabilized.


In severe bleeding, the body compensates to try to maintain the blood pressure. The pressure is maintained to try to preserve blood flow to the most vital of organs; the brain, heart and lungs. But this pressure is maintained mainly by squeezing all the main blood vessels (vasoconstriction). Blood is now shunted away from the skin, limbs and intestines to the brain, heart and lungs. The limbs become cold and bluish from the lack of fresh oxygenated blood, and the SpO2 reading drops. 

This entire compensation mechanism maintains pressure, but the total amount of blood flow and oxygen supplied decreases, to the rest of the body. Cells in the body, deprived of enough oxygen, are now forced use their fuel without oxygen; in an inefficient manner that starts producing huge amounts of acids, mainly lactic acid. This leads to worsening acidosis.


So this patient has severe bleeding from his lacerated spleen, and had lost so much blood that his compensation mechanisms were beginning to fail; that was why he came in hypotensive. He was definitely restless from all that lack of oxygen and blood to his brain. His peripheries were cold as no blood was reaching his fingers and toes; his SpO2 was obviously going to be low.

Let's look at what happened next. He was given oxygen, a good thing. What it did, was filled the little blood that was still available with oxygen. Which made the saturation SpO2 of the little blood that was available, 95%. Although 95%, it was still too little blood to really carry the oxygen needs of the patient. NO, the SpO2 of 95% did not mean he was any better.


And he was given fluids. So all those fluids would have rushed into the "squeezed" blood vessels and immediately raised the pressure within those blood vessels. This gave the impression of "improvement" to the doctor. In fact, it probably made things worse. There are two main down-sides to this. Firstly, the sudden increase in the pressure has the tendency to suddenly burst some of the newly formed clots, causing bleeding to resume. Secondly, the fluid now dilutes the clotting factors in the blood making it more inefficient at formed a clot to stem the bleeding. 


So, none of the initial therapy really helped much. What was worse, was the assumption that he was now "better" and could be sent to the X-rays Dept for further xrays. What happened there was this. The bleeding continued, and the compensations were not able to maintain his blood pressure anymore. The decreased blood supply to the brain made the patient obtunded (accompanying staff may have just thought that the patient was now more quiet and easier to handle). He would also have lost his airway control reflexes, and regurgitation of food may have partially blocked his airway, further worsening his overall hypoxia. 

By now, the amount of blood circulating would have been minimal, and acid levels would have skyrocketed. This acidosis would be the final nail. Reaching a particular dangerous level, it would essentially have prevented the heart from working properly. The heart essentially stops and the quick spiral to death ensues.


What was reversible, and when was it reversible ? Could things done right made a difference ? What things, done differently in what ways ?


Firstly, any person in trauma, with tachycardia, is in SHOCK until proven otherwise. SHOCK in a patient presents with various degrees of anxiety and restlessness, tachycardia, cool peripheries, rapid breathing and signs of poor organ perfusion (low urine output, acidosis and altered mental states). SHOCK is almost always due to bleeding from trauma (significant alternatives include only tension pneumothorax, cardiac tamponade and airway obstruction; but always think of bleeding as well). So, the first right thing to do is to recognize the SHOCK state.


Next, look very carefully for the source of bleeding. Search carefully for spilled blood, either on-the-floor (external bleeding) or in only 4 other areas of significant internal bleeding. Massive haemothorax (diagnosed clinically and with the bedside ultrasound), bleeding into the pelvis and retroperitoneal space (almost always related to pelvic fractures, lower spinal injuries and associated vascular injuries), bleeding into the peritoneal space (mainly due to liver and splenic lacerations, as in this case; and diagnosed with a FAST ultrasound scan) and the tissue spaces of the thighs (which are easily seen, and associated with fractures and vascular injuries). That's it. No X-rays other than the bedside trauma X-ray of the chest and pelvis. No other x-rays needed. Search carefully for bleeding, and once you find it, get the surgeon. 


And lastly, this patient needed blood. Lots of blood. Preferably fresh whole blood. If not, packed cells and the freshest plasma you can get. What needs to be done is to replace the lost blood with actual blood. And with it, hopefully some additional coagulation factors to help stop the bleeding. 


The physiological derangements needed to be reversed. To do that, young doctors must must simply must understand the physiology first. That was the only way to save this patients life.


04.01.12
by

What happens to bad habits ?



What happens to bad habits ? Well, the nuns just change them for better ones ...

Really, what happens to bad habits ? You know, common ones like
  • the motorcyclist who likes to take a shortcut through pedestrian walkways and park illegally there
  • the motorcyclist who goes the wrong way down a one-way lane 
  • the motorist who habitually cuts the queue on the left; using the emergency lanes
  • the motorist who double parks and leaves
  • the public toilet user who just cannot aim right, both in the bowl and in the rubbish bin
When do those bad habits ever end ? 

How do they end ? Will there come a day, when that motorist / motorcyclist just come to his senses and realize his bad ways ? I just don't see that happening. Or will someone have to die, or get injured as a result of a crash first before they see the folly of their bad habits ? 

Or can someone else, maybe, help change their ways before that something bad happens. Who is that someone ? The police ? When was the last time you saw our police handing out summonses for shortcuts, wrong way motorcyclists, queue-cutting maniacs and double parkers ? No ? Well I haven't. I think our Police are busy hiding in bushes trying to catch you when you go a few km above the speed limits. Easier job for them. That right. The Police isn't all that interested in correcting dangerous bad habits; they are probably more interested in meeting their monthly saman targets. So much easier to sit in bushes and hide.


Or maybe, just maybe, that someone special is you. 


All you need to do is speak up. Say something, to that motorcyclist / motorist with the bad and dangerous habits. Try to avoid profanity, like most of us mere mortals will resort to. Tell them to stop before they kill someone; or someone kills them. Please don't believe that Malaysians are just too polite to say something bad or critical to another. Just speak up, it may save a life.


And if you have that skill to help someone aim right, wowww, that will really help too.



04.01.12
by

What happens to bad habits ?



What happens to bad habits ? Well, the nuns just change them for better ones ...

Really, what happens to bad habits ? You know, common ones like
  • the motorcyclist who likes to take a shortcut through pedestrian walkways and park illegally there
  • the motorcyclist who goes the wrong way down a one-way lane 
  • the motorist who habitually cuts the queue on the left; using the emergency lanes
  • the motorist who double parks and leaves
  • the public toilet user who just cannot aim right, both in the bowl and in the rubbish bin
When do those bad habits ever end ? 

How do they end ? Will there come a day, when that motorist / motorcyclist just come to his senses and realize his bad ways ? I just don't see that happening. Or will someone have to die, or get injured as a result of a crash first before they see the folly of their bad habits ? 

Or can someone else, maybe, help change their ways before that something bad happens. Who is that someone ? The police ? When was the last time you saw our police handing out summonses for shortcuts, wrong way motorcyclists, queue-cutting maniacs and double parkers ? No ? Well I haven't. I think our Police are busy hiding in bushes trying to catch you when you go a few km above the speed limits. Easier job for them. That right. The Police isn't all that interested in correcting dangerous bad habits; they are probably more interested in meeting their monthly saman targets. So much easier to sit in bushes and hide.


Or maybe, just maybe, that someone special is you. 


All you need to do is speak up. Say something, to that motorcyclist / motorist with the bad and dangerous habits. Try to avoid profanity, like most of us mere mortals will resort to. Tell them to stop before they kill someone; or someone kills them. Please don't believe that Malaysians are just too polite to say something bad or critical to another. Just speak up, it may save a life.


And if you have that skill to help someone aim right, wowww, that will really help too.



03.28.12
by

Leptospirosis


a.k.a. Weil's Disease, Icterohaemorrhagic Fever (haemorrhagic jaundice), Swamp fever

Zoonotic disease ie spread from animals to man; probably the most widespread zoonotic disease in the world at the moment. Humans get infected by coming in contact with urine of infected animals esp rodents, cows, pigs and dogs. 

Leptospira sp. is a spirochaete which can enter the body through micro-breaks in the skin or intact mucous membranes. Unlike the other infamous spirochaete (Treponema pallidum causing syphilis), Leptospirosis does not spread from human to human.

Essentially the disease has two forms, a mild disease of fever, headache, chills, rigors and muscle pain lasting for a few days, accounting for more than 90% of all cases; or a severe disease which often starts off in the same way, improves then deteriorates again with severe jaundice, red eyes, abdominal pain, diarrhoea and a rash. This may often deteriorate to Multi-Organ Failure and death; believed mainly due to the severe vasculitis caused by the organism's spread in small vessels of most organs.

Difficult to diagnose in the early stages; the presentation is quite varied, difficult to differentiate from any other infections, and a history of exposure to rivers, streams, swamps and ponds is rarely obtainable. I personally don't think this is a major source of the problem; all the rats running around our sewers could easily be the culprits as well. 

The problem is that infected animals don't die. They often live asymptomatically, shedding the Leptospira with every pee, throughout their lives. Trying to trace these rats would be quite impossible. It is also believed that the global warming phenomenon is playing a huge role in the re-emergence of leptospirosis in tropical areas; especially as a result of floods and contamination of drinking water sources. 

Not worried yet ? There has been recorded in history, instances of epidemics of what is now believed to be leptospirosis, in wars especially. (Napoleon's infectious jaundice, American Civil War's swamp fever) But it is not only in ancient times, that these epidemics occur; it swept through the Andaman islands in the late 80's, Philippines in 2009, Ireland in 2010 with high mortality rates.

It could easily have been us; it still can.

How to treat ? fairly easily really with the right antibiotics. They are still sensitive to Penicillin group drugs and to the old favourite Doxycycline. Erythromycin if pregnant. Amoxicillin is another alternative. Only 3rd gen cephalosporins have any effect on the Leptospira spirochaete.

To my simple mind, we are losing the fight with Leptospirosis; the battle cannot be won if we keep on thinking that it is due to isolated exposure to contaminated water in the wild. Many of the patients we see do not have that history. I think the problem is much closer to home; the infected animals, probably rodents in our urban and sub-urban areas, especially in our longkangs (sewers). 

That rat hiding there may just kill us one day.
 
03.28.12
by

Leptospirosis


a.k.a. Weil's Disease, Icterohaemorrhagic Fever (haemorrhagic jaundice), Swamp fever

Zoonotic disease ie spread from animals to man; probably the most widespread zoonotic disease in the world at the moment. Humans get infected by coming in contact with urine of infected animals esp rodents, cows, pigs and dogs. 

Leptospira sp. is a spirochaete which can enter the body through micro-breaks in the skin or intact mucous membranes. Unlike the other infamous spirochaete (Treponema pallidum causing syphilis), Leptospirosis does not spread from human to human.

Essentially the disease has two forms, a mild disease of fever, headache, chills, rigors and muscle pain lasting for a few days, accounting for more than 90% of all cases; or a severe disease which often starts off in the same way, improves then deteriorates again with severe jaundice, red eyes, abdominal pain, diarrhoea and a rash. This may often deteriorate to Multi-Organ Failure and death; believed mainly due to the severe vasculitis caused by the organism's spread in small vessels of most organs.

Difficult to diagnose in the early stages; the presentation is quite varied, difficult to differentiate from any other infections, and a history of exposure to rivers, streams, swamps and ponds is rarely obtainable. I personally don't think this is a major source of the problem; all the rats running around our sewers could easily be the culprits as well. 

The problem is that infected animals don't die. They often live asymptomatically, shedding the Leptospira with every pee, throughout their lives. Trying to trace these rats would be quite impossible. It is also believed that the global warming phenomenon is playing a huge role in the re-emergence of leptospirosis in tropical areas; especially as a result of floods and contamination of drinking water sources. 

Not worried yet ? There has been recorded in history, instances of epidemics of what is now believed to be leptospirosis, in wars especially. (Napoleon's infectious jaundice, American Civil War's swamp fever) But it is not only in ancient times, that these epidemics occur; it swept through the Andaman islands in the late 80's, Philippines in 2009, Ireland in 2010 with high mortality rates.

It could easily have been us; it still can.

How to treat ? fairly easily really with the right antibiotics. They are still sensitive to Penicillin group drugs and to the old favourite Doxycycline. Erythromycin if pregnant. Amoxicillin is another alternative. Only 3rd gen cephalosporins have any effect on the Leptospira spirochaete.

To my simple mind, we are losing the fight with Leptospirosis; the battle cannot be won if we keep on thinking that it is due to isolated exposure to contaminated water in the wild. Many of the patients we see do not have that history. I think the problem is much closer to home; the infected animals, probably rodents in our urban and sub-urban areas, especially in our longkangs (sewers). 

That rat hiding there may just kill us one day.
 
03.23.12
by

Ahhhh, so that is why ….




Question 1 - Malaysia has huge resources of Rare Earth that will bring economic wealth to the country and its people. True or False ? 

Question 2 - Malaysia has vast acres of available land suitable to make some Rare Earth refinery and loads of space where the waste materials can be thrown away, stored or buried. True or False ?

Question 3 - Malaysia has a high expertise workforce, the only ones in the world capable of running a Rare Earth plant as it should be run. True or False ?


Question 4 - Malaysia needs to products of Rare Earth processing to further develop our economy, our wealth and our people's well-being. True or False ?


Question 5 - Malaysia has something RARE, and that is why the Rare Earth plant needs to be here. True or False ?


We unfortunately have nothing rare in our earth, not in Gebeng, nor anywhere near Malaysia. That rare earth that will need processing and refining will be imported from China on rail or from the US on ships to reach our shores; be processed and then sent out again all over the world especially to Australia. What they will leave behind is the rare waste products and rare waste water; rare mainly because it will be radioactive and will potentially lead to contamination of our land, water and exposure to our people. Question 1 False.


China and the US has Rare Earth, but no processing plants for it. Both these countries have land way way way more than we have in Malaysia. Australia, which is probably a zillion times the size of Malaysia, has existing processing plants for rare earth, hundreds of miles from the nearest human population. Gebeng has 700,000 people living within 35 km of the Rare Earth plant !!! Question 2 bites the dust with a resounding False !


They are employing 400 people. Just find me 400 radiation and rare earth specialists in Gebeng. High expertise ? or administrative staff ? human resource henchmen ? or just employ anyone, who doesn't understand radiation, to handle the dangerous stuff ? The "lucky" chap would probably not live the 10 years to see his hair fall off and his balls wrinkle up. Question 3 just cannot be true. False !


Pahang needs the FDI ? We need the jobs ? Our economy needs this ? Well, so does the US economy, the Euro economy, the African economy. Let's just do it in Portugal or Spain. Or let's just do it in Obama's backyard; surely the FDI and jobs will boost his chances of winning another term. WTF ? Question 4 False.


So then why why why is Gebeng the damn lucky place to be picked as the next Rare Earth plant ? That, my friends, lies in the answer to Question 5. For Malaysia, yes, our Malaysia, is a unique place. We have something rare that nobody else has. RARE ! NOBODY else !! BOLEHHHHHH ! 


We have a parliament, the highest authority in the land, duly elected by its people to take care of the country, that will accept being snubbed and humiliated, by a foreign company. How else can you explain, that when the Parliament summoned the top management of Lynas to answer questions on the project, they duly sent their HR Manager with 2 lawyers, whose only answer to our Parliament, is that they were not authorized to answer any questions !!!! And our towering Parliamentarians in effect said, errrr, okay lah ! Now, that is truly RARE. No where else in the world, will this happen. We BOLEHHHH !!


Our parliament is also the only one where parliamentarians are not allowed to ask questions or raise issues, when cases are still under the courts deliberation. No discussion on NFC allowed because scared the courts will find the parliament in contempt !! Another unique one in the world. Because we BOLEHHHH !!


Our Malaysia, yes, our Malaysia, is also the only place, where we can get Malaysian hooligans, rempits and samsengs, to fight, abuse, assault and intimidate their fellow Malaysians, on behalf of a foreign company. Yes, our towering Malaysians. Damn proud of these fellows laaa.


Ahhhh, so that is why .... we are so lucky to be picked. We are just so rare, so unique, so truly Malaysian to support this cause just because someone says so. So taat, so setia. 


Ahhhhh ....


P.S. I really do wonder how many cancers there are, reported and linked to the Bukit Merah area. To the people of Gebeng and the 700,000 people of Kuantan and its surrounding areas, you are not alone. Vote TAK NAK !!

03.23.12
by

Ahhhh, so that is why ….




Question 1 - Malaysia has huge resources of Rare Earth that will bring economic wealth to the country and its people. True or False ? 

Question 2 - Malaysia has vast acres of available land suitable to make some Rare Earth refinery and loads of space where the waste materials can be thrown away, stored or buried. True or False ?

Question 3 - Malaysia has a high expertise workforce, the only ones in the world capable of running a Rare Earth plant as it should be run. True or False ?


Question 4 - Malaysia needs to products of Rare Earth processing to further develop our economy, our wealth and our people's well-being. True or False ?


Question 5 - Malaysia has something RARE, and that is why the Rare Earth plant needs to be here. True or False ?


We unfortunately have nothing rare in our earth, not in Gebeng, nor anywhere near Malaysia. That rare earth that will need processing and refining will be imported from China on rail or from the US on ships to reach our shores; be processed and then sent out again all over the world especially to Australia. What they will leave behind is the rare waste products and rare waste water; rare mainly because it will be radioactive and will potentially lead to contamination of our land, water and exposure to our people. Question 1 False.


China and the US has Rare Earth, but no processing plants for it. Both these countries have land way way way more than we have in Malaysia. Australia, which is probably a zillion times the size of Malaysia, has existing processing plants for rare earth, hundreds of miles from the nearest human population. Gebeng has 700,000 people living within 35 km of the Rare Earth plant !!! Question 2 bites the dust with a resounding False !


They are employing 400 people. Just find me 400 radiation and rare earth specialists in Gebeng. High expertise ? or administrative staff ? human resource henchmen ? or just employ anyone, who doesn't understand radiation, to handle the dangerous stuff ? The "lucky" chap would probably not live the 10 years to see his hair fall off and his balls wrinkle up. Question 3 just cannot be true. False !


Pahang needs the FDI ? We need the jobs ? Our economy needs this ? Well, so does the US economy, the Euro economy, the African economy. Let's just do it in Portugal or Spain. Or let's just do it in Obama's backyard; surely the FDI and jobs will boost his chances of winning another term. WTF ? Question 4 False.


So then why why why is Gebeng the damn lucky place to be picked as the next Rare Earth plant ? That, my friends, lies in the answer to Question 5. For Malaysia, yes, our Malaysia, is a unique place. We have something rare that nobody else has. RARE ! NOBODY else !! BOLEHHHHHH ! 


We have a parliament, the highest authority in the land, duly elected by its people to take care of the country, that will accept being snubbed and humiliated, by a foreign company. How else can you explain, that when the Parliament summoned the top management of Lynas to answer questions on the project, they duly sent their HR Manager with 2 lawyers, whose only answer to our Parliament, is that they were not authorized to answer any questions !!!! And our towering Parliamentarians in effect said, errrr, okay lah ! Now, that is truly RARE. No where else in the world, will this happen. We BOLEHHHH !!


Our parliament is also the only one where parliamentarians are not allowed to ask questions or raise issues, when cases are still under the courts deliberation. No discussion on NFC allowed because scared the courts will find the parliament in contempt !! Another unique one in the world. Because we BOLEHHHH !!


Our Malaysia, yes, our Malaysia, is also the only place, where we can get Malaysian hooligans, rempits and samsengs, to fight, abuse, assault and intimidate their fellow Malaysians, on behalf of a foreign company. Yes, our towering Malaysians. Damn proud of these fellows laaa.


Ahhhh, so that is why .... we are so lucky to be picked. We are just so rare, so unique, so truly Malaysian to support this cause just because someone says so. So taat, so setia. 


Ahhhhh ....


P.S. I really do wonder how many cancers there are, reported and linked to the Bukit Merah area. To the people of Gebeng and the 700,000 people of Kuantan and its surrounding areas, you are not alone. Vote TAK NAK !!

03.04.12
by

Irrigating Deserts


It has been a while since I blogged. I've been busy, true; distracted and undisciplined all too likely; and maybe I had nothing to write about because I had too much to write about. You know, when no work gets done just because there is too much work to do.

No EM topic unfortunately; Geography will be the flavour for this post. I expect this to be a long rambling post of not much importance, just showing how minds can wander on long flights; just as mine is on this 3 hour flight to Tawau. So you may want to just skip over to the last paragraph. Heh heh heh.

Looking out of the plane, interestingly I noticed rather thick clouds over land; which for some reason suddenly disappeared at the shore line. Weird I thought. Why should the clouds only appear over land, and not over sea ? Trying to dig back to those few memory cells that may still contain info about physical geography learnt at school, I thought of an explanation.

During day, the land heats up much more than the sea. The land of Malaysia, with its high humidity and relatively wet conditions, has high levels of water; which then evaporates and forms those clouds. Which ultimately will condense forming rain bringing all that water back to the land again. The convection rains that we get on many afternoons and evenings  is formed in this way. Nice cycle, right ?

The sea however, although it has much more water than land, heats up much less than land; and thus does not form those dense clouds, but rather lighter clouds which need more monsoonal winds to bring them together and inland for them to condense and form rain. Our seasonal monsoon rains are probably formed this way.

Being rather pleased with myself, [any Form 4 kid learning Geography will probably just say Bahhh!! at this] I thought that was why deserts always remain deserts. For even though they do receive lots and lots of sun, there is precious little water for the sun to evaporate and form rain. And the common direction of the monsoon winds do not favour deserts, that's why they are deserts.

Trying to act smart and think out of the box, I thought, wouldn't it help if we were to irrigate the deserts with huge amounts of sea water; just to increase the humidity levels of land ? Then maybe, just maybe if we can cross some magical humidity level, that cycle of convection rain may actually start, and continue its perpetuating cycle.

Why sea water ? For one, fresh water is super valuable in desert lands. Sea water often is in huge amounts, although the logistics of it may be difficult. Maybe we should try some "irrigating the desert" experiment in a desert that is small, narrow and above all, near the coast. Something like the Kalahari, or that desert in Chile which is supposed to be the driest one of them all.

Waaaaaa imagining Nobel prize for Geography given to some unknown Emergency doc ... waaaaaa !!!!

Okay, okay, okay .... you can stop all that laughing and rolling on the floor.

But anyways, since I am an Emergency doc, and this is an EM blog, maybe I can bring this slightly toward Emergency Medicine.

Honestly I have always felt very very [extremely] strongly that EM should be taught in Medical Schools. I have always felt that doctors should be learning EM content, and EM way of thinking, and EM prioritization and sense of urgency in medical school. After all, almost every single priority situation that a doctor will ever face, in which he or she will make an impact of the patients' outcome, either positively or adversely, is related to their ability to analyze the situation and act rapidly and accurately. This unfortunately is not something learnt in any way in medical schools today.

Instead, our medical students are learning Medicine by rote, emphasizing stuff that used to be important decades ago, or things that are easy to teach and convenient to test. Then, when they are released, totally wet behind the ears on our patients, we struggle to teach them good EM; unfortunately, often too little and just too late.

Surely surely EM is as important to the young doctor that Ophthalmology or ENT or Forensic Medicine or Anaesthesia. Surely like the proverbial desert, it is much better to water our medical students with the EM way of life, so that they do not become deserts, but instead will flourish and continually produce good rain with the nurturing sun. Think about it, and see if you can argue this point with me.

How ? When ? You tell me, in your comments.
03.04.12
by

Irrigating Deserts


It has been a while since I blogged. I've been busy, true; distracted and undisciplined all too likely; and maybe I had nothing to write about because I had too much to write about. You know, when no work gets done just because there is too much work to do.

No EM topic unfortunately; Geography will be the flavour for this post. I expect this to be a long rambling post of not much importance, just showing how minds can wander on long flights; just as mine is on this 3 hour flight to Tawau. So you may want to just skip over to the last paragraph. Heh heh heh.

Looking out of the plane, interestingly I noticed rather thick clouds over land; which for some reason suddenly disappeared at the shore line. Weird I thought. Why should the clouds only appear over land, and not over sea ? Trying to dig back to those few memory cells that may still contain info about physical geography learnt at school, I thought of an explanation.

During day, the land heats up much more than the sea. The land of Malaysia, with its high humidity and relatively wet conditions, has high levels of water; which then evaporates and forms those clouds. Which ultimately will condense forming rain bringing all that water back to the land again. The convection rains that we get on many afternoons and evenings  is formed in this way. Nice cycle, right ?

The sea however, although it has much more water than land, heats up much less than land; and thus does not form those dense clouds, but rather lighter clouds which need more monsoonal winds to bring them together and inland for them to condense and form rain. Our seasonal monsoon rains are probably formed this way.

Being rather pleased with myself, [any Form 4 kid learning Geography will probably just say Bahhh!! at this] I thought that was why deserts always remain deserts. For even though they do receive lots and lots of sun, there is precious little water for the sun to evaporate and form rain. And the common direction of the monsoon winds do not favour deserts, that's why they are deserts.

Trying to act smart and think out of the box, I thought, wouldn't it help if we were to irrigate the deserts with huge amounts of sea water; just to increase the humidity levels of land ? Then maybe, just maybe if we can cross some magical humidity level, that cycle of convection rain may actually start, and continue its perpetuating cycle.

Why sea water ? For one, fresh water is super valuable in desert lands. Sea water often is in huge amounts, although the logistics of it may be difficult. Maybe we should try some "irrigating the desert" experiment in a desert that is small, narrow and above all, near the coast. Something like the Kalahari, or that desert in Chile which is supposed to be the driest one of them all.

Waaaaaa imagining Nobel prize for Geography given to some unknown Emergency doc ... waaaaaa !!!!

Okay, okay, okay .... you can stop all that laughing and rolling on the floor.

But anyways, since I am an Emergency doc, and this is an EM blog, maybe I can bring this slightly toward Emergency Medicine.

Honestly I have always felt very very [extremely] strongly that EM should be taught in Medical Schools. I have always felt that doctors should be learning EM content, and EM way of thinking, and EM prioritization and sense of urgency in medical school. After all, almost every single priority situation that a doctor will ever face, in which he or she will make an impact of the patients' outcome, either positively or adversely, is related to their ability to analyze the situation and act rapidly and accurately. This unfortunately is not something learnt in any way in medical schools today.

Instead, our medical students are learning Medicine by rote, emphasizing stuff that used to be important decades ago, or things that are easy to teach and convenient to test. Then, when they are released, totally wet behind the ears on our patients, we struggle to teach them good EM; unfortunately, often too little and just too late.

Surely surely EM is as important to the young doctor that Ophthalmology or ENT or Forensic Medicine or Anaesthesia. Surely like the proverbial desert, it is much better to water our medical students with the EM way of life, so that they do not become deserts, but instead will flourish and continually produce good rain with the nurturing sun. Think about it, and see if you can argue this point with me.

How ? When ? You tell me, in your comments.
01.28.12
by

ED Management of Pneumonia in Malaysia


Huge topic. Brief notes on few important points only. Information pertinent for ED practice in Malaysia.

Generally, divided into 1) community acquired pneumonia (CAP) has less dangerous and less antibiotic resistant organisms; 2) healthcare associated pneumonia (HCAP) defined as some contact with healthcare facilities (hospitals, nursing homes, dialysis centers, wound care, outpatient clinics or family member in healthcare) in the last 90 days and develops pneumonia, which tends to be associated with a higher incidence of bad bugs and worse outcomes, and 3) hospital acquired pneumonia (HCAP) and its variant ventilator associated pneumonia (VAP) essentially with the worst bugs of the lot.

Outcomes from pneumonia very much depends on type of infection (type of bug, resistance to treatment) and presence of co-morbidities (DM, structural lung disease, underlying heart disease, extremes of age, immune status etc) and if treatment is initiated early and accurately.

Although exact microbial identification is only possible in a small percentage of cases, and antibiotic therapy is often empiric in nature, different bacteria do produce different presentations, and some knowledge of the differences may be helpful.

Strep Pneumoniae remains the most common organism associated with pneumonia; and still the most common cause of death. Gram +ve encapsulated Diplococci. Produces the typical pneumonia presentation of high spiking fever with chills and rigor, rust coloured sputum, raised TWBC, chest x-rays showing lobar consolidation with air bronchograms.

Staph Aureus infection is much more gradual in onset, but it can cause a much more severe disease. Often it is a secondary infection to a primary viral illness or viral bronchitis. Gram +ve cocci that seems to group in clusters. It also causes lobar infiltrates seen on X-ray but is much more likely to cause lung abscesses and pleural effusions. Must think of this in IVDUs and in immuno-compromised patients especially if they have an indwelling catheter somewhere.

Klebsiella sp. is much more common in alcoholics, elderly patients and those with long standing DM. Typically it causes a "currant-jelly sputum". On X-rays, the bulging fissure sign is specifically associated with Klebsiella infection.

Klebsiella Bulging Fissue Sign 


Pseudomonas aeruginosa is much more associated with VAP, HAP and HCAP. (note: although this is commonly quoted, available data from Malaysian hospitals still have other organisms like Klebsiella sp and Strep Pneumoniae ahead in total numbers). Gram -ve bacilli. Much more likely to cause patchy infiltrates on chest x-ray rather than lobar consolidation. Must be considered in patients with structural lung disease esp bronchiectasis.

The "Atypical Pneumonias" were so named because they seemed so different from the Strep Pneumoniae infections. Their onsets were much more gradual, the patients seemed much less sick (leading to the nickname "walking pneumonias"), they never produced anything like the rust coloured sputum and their X-rays were more patchy infiltrates rather than the white-out lobar infiltrates. None of them are seen on Gram staining. And they never responded to traditional penicillin antibiotics ! This group includes Mycoplasma sp., Chlamydophilia pneumonieae, Hemophilus Influenza and Moraxella Catarrhalis.

Hemophilus Influenza and Moraxella Catarrhalis infections are more common in the elderly, and in those patients with underlying lung disease eg COPD and smokers.

Chlamydophilia pneumonieae often causes a dry cough, fever and wheezing. It is much more common in young healthy adults. Another demographic to consider is the few week old infant who develops a staccato like cough; being infection during passage through the birth canal. 

Mycoplasma sp. is the primary atypical pneumonia. Affecting younger patients (it is probably the most common organism causing CAP in the younger below 40 population), usually previously healthy, it's presentation of a persistent and gradually worsening dry cough is very similar to some of the other atypicals; in addition to that, it does often produce a mobiliform rash all over the body, it seems to be associated with erythematous tympanic membranes (or even bullous myringitis, or bubbles on the eardrums), a reddish throat without exudates, triggering off asthmatic episodes and extra-pulmonary auto-immune manifestations eg. Stevens Johnson and Guillian Barre Syndrome. Chest X-rays commonly show a multi-focal bilateral patchy perihilar infiltrates (many have said that the X-rays often look worse than the patient).

Mycoplasma sp. do cause outbreaks especially in army camps and college hostels; but sudden outbreaks should bring to mind Legionella sp. infection. Typically related to infections via air-conditioning systems, these patients present with pneumonia and GI symptoms, often associated with Hypo-Na and LFT abnormalities. Interestingly they often show a relative bradycardia.

Infection from Mycobacterium tuberculosis may present as an apparent CAP and must be considered in Malaysia. Our data show about 5 - 15% of our patients with CAP end up with a diagnosis of TB. Last but not least, in rural areas, Burkholderia pseudomallei must also be considered especially if the patient also has DM.

How should the ED doc treat ? Luckily, it is not nearly as complex.

First question would be whether admission is needed. This is a clinical decision; based on the clinical findings, the presence of co-morbidities, support structure at home, hospital policy and some guesswork about the possible bug. Traditionally quoted statistics that about 20% of CAP would require admission, and about 1% would require ICU care is not particularly useful. These percentages refer to the total number of CAP in the community; at the ED, we tend to see the more serious and we should be wary of this fact. I would suggest putting in extra effort to identify co-morbidities and whether it is a true CAP or a HCAP. [HCAP and especially HAP must be treated with extra caution and a much lower threshold for admission] As a decision tool, the Pneumonia Severity Index (PSI) is quite tedious to complete; I do however find it useful to identify the low-risk patient that can be safely treated on an outpatient basis.

Next question is which antibiotics to start, if discharged. Here, I would like to refer you to Prof CK Liam's paper in the Med Journal of Malaysia in 2005. [click to enlarge] or [click here for the actual paper.]

 

I would say that common mistakes of the young ED doc, is to think that all pneumonias are the same, that all respiratory infections are treated the same, and to prescribe antibiotics blindly and for a too short duration. Atypical pneumonias should be treated with macrolide antibiotics for at least 10 - 14 days !


Hope this "brief" post has been helpful. Whewwwwww !


Credit to Mel Herbert and the EM-RAP team. And the Prof CK Liam.



01.28.12
by

ED Management of Pneumonia in Malaysia


Huge topic. Brief notes on few important points only. Information pertinent for ED practice in Malaysia.

Generally, divided into 1) community acquired pneumonia (CAP) has less dangerous and less antibiotic resistant organisms; 2) healthcare associated pneumonia (HCAP) defined as some contact with healthcare facilities (hospitals, nursing homes, dialysis centers, wound care, outpatient clinics or family member in healthcare) in the last 90 days and develops pneumonia, which tends to be associated with a higher incidence of bad bugs and worse outcomes, and 3) hospital acquired pneumonia (HCAP) and its variant ventilator associated pneumonia (VAP) essentially with the worst bugs of the lot.

Outcomes from pneumonia very much depends on type of infection (type of bug, resistance to treatment) and presence of co-morbidities (DM, structural lung disease, underlying heart disease, extremes of age, immune status etc) and if treatment is initiated early and accurately.

Although exact microbial identification is only possible in a small percentage of cases, and antibiotic therapy is often empiric in nature, different bacteria do produce different presentations, and some knowledge of the differences may be helpful.

Strep Pneumoniae remains the most common organism associated with pneumonia; and still the most common cause of death. Gram +ve encapsulated Diplococci. Produces the typical pneumonia presentation of high spiking fever with chills and rigor, rust coloured sputum, raised TWBC, chest x-rays showing lobar consolidation with air bronchograms.

Staph Aureus infection is much more gradual in onset, but it can cause a much more severe disease. Often it is a secondary infection to a primary viral illness or viral bronchitis. Gram +ve cocci that seems to group in clusters. It also causes lobar infiltrates seen on X-ray but is much more likely to cause lung abscesses and pleural effusions. Must think of this in IVDUs and in immuno-compromised patients especially if they have an indwelling catheter somewhere.

Klebsiella sp. is much more common in alcoholics, elderly patients and those with long standing DM. Typically it causes a "currant-jelly sputum". On X-rays, the bulging fissure sign is specifically associated with Klebsiella infection.

Klebsiella Bulging Fissue Sign 


Pseudomonas aeruginosa is much more associated with VAP, HAP and HCAP. (note: although this is commonly quoted, available data from Malaysian hospitals still have other organisms like Klebsiella sp and Strep Pneumoniae ahead in total numbers). Gram -ve bacilli. Much more likely to cause patchy infiltrates on chest x-ray rather than lobar consolidation. Must be considered in patients with structural lung disease esp bronchiectasis.

The "Atypical Pneumonias" were so named because they seemed so different from the Strep Pneumoniae infections. Their onsets were much more gradual, the patients seemed much less sick (leading to the nickname "walking pneumonias"), they never produced anything like the rust coloured sputum and their X-rays were more patchy infiltrates rather than the white-out lobar infiltrates. None of them are seen on Gram staining. And they never responded to traditional penicillin antibiotics ! This group includes Mycoplasma sp., Chlamydophilia pneumonieae, Hemophilus Influenza and Moraxella Catarrhalis.

Hemophilus Influenza and Moraxella Catarrhalis infections are more common in the elderly, and in those patients with underlying lung disease eg COPD and smokers.

Chlamydophilia pneumonieae often causes a dry cough, fever and wheezing. It is much more common in young healthy adults. Another demographic to consider is the few week old infant who develops a staccato like cough; being infection during passage through the birth canal. 

Mycoplasma sp. is the primary atypical pneumonia. Affecting younger patients (it is probably the most common organism causing CAP in the younger below 40 population), usually previously healthy, it's presentation of a persistent and gradually worsening dry cough is very similar to some of the other atypicals; in addition to that, it does often produce a mobiliform rash all over the body, it seems to be associated with erythematous tympanic membranes (or even bullous myringitis, or bubbles on the eardrums), a reddish throat without exudates, triggering off asthmatic episodes and extra-pulmonary auto-immune manifestations eg. Stevens Johnson and Guillian Barre Syndrome. Chest X-rays commonly show a multi-focal bilateral patchy perihilar infiltrates (many have said that the X-rays often look worse than the patient).

Mycoplasma sp. do cause outbreaks especially in army camps and college hostels; but sudden outbreaks should bring to mind Legionella sp. infection. Typically related to infections via air-conditioning systems, these patients present with pneumonia and GI symptoms, often associated with Hypo-Na and LFT abnormalities. Interestingly they often show a relative bradycardia.

Infection from Mycobacterium tuberculosis may present as an apparent CAP and must be considered in Malaysia. Our data show about 5 - 15% of our patients with CAP end up with a diagnosis of TB. Last but not least, in rural areas, Burkholderia pseudomallei must also be considered especially if the patient also has DM.

How should the ED doc treat ? Luckily, it is not nearly as complex.

First question would be whether admission is needed. This is a clinical decision; based on the clinical findings, the presence of co-morbidities, support structure at home, hospital policy and some guesswork about the possible bug. Traditionally quoted statistics that about 20% of CAP would require admission, and about 1% would require ICU care is not particularly useful. These percentages refer to the total number of CAP in the community; at the ED, we tend to see the more serious and we should be wary of this fact. I would suggest putting in extra effort to identify co-morbidities and whether it is a true CAP or a HCAP. [HCAP and especially HAP must be treated with extra caution and a much lower threshold for admission] As a decision tool, the Pneumonia Severity Index (PSI) is quite tedious to complete; I do however find it useful to identify the low-risk patient that can be safely treated on an outpatient basis.

Next question is which antibiotics to start, if discharged. Here, I would like to refer you to Prof CK Liam's paper in the Med Journal of Malaysia in 2005. [click to enlarge] or [click here for the actual paper.]

 

I would say that common mistakes of the young ED doc, is to think that all pneumonias are the same, that all respiratory infections are treated the same, and to prescribe antibiotics blindly and for a too short duration. Atypical pneumonias should be treated with macrolide antibiotics for at least 10 - 14 days !


Hope this "brief" post has been helpful. Whewwwwww !


Credit to Mel Herbert and the EM-RAP team. And the Prof CK Liam.



01.12.12
by

Life-Saving Information on Hollow Viscous Injury (HVI)












Pictures speak a thousand words, right ?

But only if some of those words are spoken, from the knowing paramedic to the astute emergency doctor, do these words become meaningful information, that may save lives.

Huh ? Words that save lives ? Are we psychiatrist or psychologists ? Nahhh .... let me explain.

In the pictures above, you see common scenes in a bad accident. "Waaaa MVA teruk-lah" would be a probably part of the information given by the paramedic.

There are much more important and specific information that can and should be conveyed instead. The presence of a STARRED WINDSHIELD would give more concern to the treating doctor about traumatic head injury; a SEAT BELT sign would warn about the possibility of intra-abdominal injury of both the solid organs and hollow viscous injury; INTRUSION into the passenger compartment signifies transfer of high force onto the passengers; and the BENT STEERING WHEEL and the failure of the air-bag to deploy (ahahhh! I betcha missed that one) would give much worry about chest and abdominal injury.

Today's blog would like to discuss one component of blunt abdominal injury today. 

Road Traffic Accidents remain the most common cause of blunt intra-abdominal injury; other causes would be non-accidental trauma in children, being punched in assaults or domestic violence esp in pregnant women; and sometimes following Heimlich maneuvers and CPR.

Intra-abdominal injury has 3 basic mechanisms (this is important to know .... so read this part). The external force applied may CRUSH the solid organs caught in between; the solid organs like spleen, liver and kidney are most commonly affected in this way; and is more common in those with lax abdominal walls (elderly, alcoholics). Fatties like myself are "slightly more cushioned". Or a sudden and powerful external force applied locally may suddenly increase the intra-abdominal pressure and BURST a hollow viscous, like the intestines. This is exemplified by the seat-belt injury (seat-belt sign) or the handle-bar injury (handle-bar target sign). Lastly, the extreme acceleration deceleration seen in many road traffic accidents result in varying degrees of deceleration of the internal organs. In short, when parts of the body has stopped, some of the more mobile organs are still moving forward and SHEARS off (usually the vascular pedicles of organs or the large vessels are torn in these situations).

It is not easy to diagnose intra-abdominal injury; and probably the most difficult one to identify (and hence the most commonly missed one) is the Hollow Viscous Injury (HVI). The sudden increased pressure results in varying degrees of injury to the mesentery and intestines from bruising and wall haematomas, to loss of vascular supply, loss of viability or overt rupture. The main problem is that diagnosing this in the first few hours is difficult. Clinical signs are few and unreliable. FAST is often not sensitive enough, and neither is the CT. DPL probably performs better, but tell me honestly, how many of us are going the DPL a fellow purely based on suspicion without some clinical signs ?

Unfortunately many of these patients are not identified early; and sometimes discharged home. What happens next is that the contamination of the peritoneum occurs as the contents of the GI spills out; in younger patients, some natural attempt by the body to contain and compensate results in delayed onset of clinical signs and later presentations. Often these patients are brought back to the hospital in extremis and do very poorly thereafter.

It is really easy to identify it retrospectively; but not at all easy live, in real-time. Needless to say, the medicolegal risk associated with missing these injuries are high.


The only guide to a better pick-up rate is to have a higher index of suspicion. Having information about mechanism of injury, how it happened, was it high force, were some of the situations depicted in the pictures above there, is this a "high-risk" patient, are life-saving information to get. Life-saving for both the patient and the doctor. (lawyers can "kill off" doctors, you know). So, high index of suspicion based on information about mechanism of injury.


Next, in these patients, keep them for a while. Check them again and again and again. If you have seen them several times, and documented your findings, this will serve you well, even if you still end up missing the odd one (or two; hope not too many). Time, repeated clinical examinations and repeated investigations are probably the only way.


And if they are planned for discharge, please please please make sure that they understand that they MUST return to the ED at the first sign of any problems (usually vomiting starts fairly early) or worsening of symptoms (usually pain).


Investigations needed for to rule out the possible HVI is still unclear. Free air on chest X-rays and Chance-type fractures of the lumbar spine are uncommon, but significantly associated with HVI. DPL probably has a role with either visualization of intestinal contents or elevated ALP and WBC counts.


Just remember, don't forget HVI; especially with a significant mechanism of injury. If you do suspect it, please discuss it with someone more senior and experienced; specialists if possible. 


Whewwwww !



01.12.12
by

Life-Saving Information on Hollow Viscous Injury (HVI)












Pictures speak a thousand words, right ?

But only if some of those words are spoken, from the knowing paramedic to the astute emergency doctor, do these words become meaningful information, that may save lives.

Huh ? Words that save lives ? Are we psychiatrist or psychologists ? Nahhh .... let me explain.

In the pictures above, you see common scenes in a bad accident. "Waaaa MVA teruk-lah" would be a probably part of the information given by the paramedic.

There are much more important and specific information that can and should be conveyed instead. The presence of a STARRED WINDSHIELD would give more concern to the treating doctor about traumatic head injury; a SEAT BELT sign would warn about the possibility of intra-abdominal injury of both the solid organs and hollow viscous injury; INTRUSION into the passenger compartment signifies transfer of high force onto the passengers; and the BENT STEERING WHEEL and the failure of the air-bag to deploy (ahahhh! I betcha missed that one) would give much worry about chest and abdominal injury.

Today's blog would like to discuss one component of blunt abdominal injury today. 

Road Traffic Accidents remain the most common cause of blunt intra-abdominal injury; other causes would be non-accidental trauma in children, being punched in assaults or domestic violence esp in pregnant women; and sometimes following Heimlich maneuvers and CPR.

Intra-abdominal injury has 3 basic mechanisms (this is important to know .... so read this part). The external force applied may CRUSH the solid organs caught in between; the solid organs like spleen, liver and kidney are most commonly affected in this way; and is more common in those with lax abdominal walls (elderly, alcoholics). Fatties like myself are "slightly more cushioned". Or a sudden and powerful external force applied locally may suddenly increase the intra-abdominal pressure and BURST a hollow viscous, like the intestines. This is exemplified by the seat-belt injury (seat-belt sign) or the handle-bar injury (handle-bar target sign). Lastly, the extreme acceleration deceleration seen in many road traffic accidents result in varying degrees of deceleration of the internal organs. In short, when parts of the body has stopped, some of the more mobile organs are still moving forward and SHEARS off (usually the vascular pedicles of organs or the large vessels are torn in these situations).

It is not easy to diagnose intra-abdominal injury; and probably the most difficult one to identify (and hence the most commonly missed one) is the Hollow Viscous Injury (HVI). The sudden increased pressure results in varying degrees of injury to the mesentery and intestines from bruising and wall haematomas, to loss of vascular supply, loss of viability or overt rupture. The main problem is that diagnosing this in the first few hours is difficult. Clinical signs are few and unreliable. FAST is often not sensitive enough, and neither is the CT. DPL probably performs better, but tell me honestly, how many of us are going the DPL a fellow purely based on suspicion without some clinical signs ?

Unfortunately many of these patients are not identified early; and sometimes discharged home. What happens next is that the contamination of the peritoneum occurs as the contents of the GI spills out; in younger patients, some natural attempt by the body to contain and compensate results in delayed onset of clinical signs and later presentations. Often these patients are brought back to the hospital in extremis and do very poorly thereafter.

It is really easy to identify it retrospectively; but not at all easy live, in real-time. Needless to say, the medicolegal risk associated with missing these injuries are high.


The only guide to a better pick-up rate is to have a higher index of suspicion. Having information about mechanism of injury, how it happened, was it high force, were some of the situations depicted in the pictures above there, is this a "high-risk" patient, are life-saving information to get. Life-saving for both the patient and the doctor. (lawyers can "kill off" doctors, you know). So, high index of suspicion based on information about mechanism of injury.


Next, in these patients, keep them for a while. Check them again and again and again. If you have seen them several times, and documented your findings, this will serve you well, even if you still end up missing the odd one (or two; hope not too many). Time, repeated clinical examinations and repeated investigations are probably the only way.


And if they are planned for discharge, please please please make sure that they understand that they MUST return to the ED at the first sign of any problems (usually vomiting starts fairly early) or worsening of symptoms (usually pain).


Investigations needed for to rule out the possible HVI is still unclear. Free air on chest X-rays and Chance-type fractures of the lumbar spine are uncommon, but significantly associated with HVI. DPL probably has a role with either visualization of intestinal contents or elevated ALP and WBC counts.


Just remember, don't forget HVI; especially with a significant mechanism of injury. If you do suspect it, please discuss it with someone more senior and experienced; specialists if possible. 


Whewwwww !



01.05.12
by

Do you prescribe Allopurinol ?

I think she was trying to tell me to write this blog. So here it is. Thanks CK.

Allopurinol is a commonly prescribed drug; usually for symptomatic hyperuricaemia (gout) or treatment of uric acid kidney stones. It is pretty standard care in many patients with cancers on treatment to try to prevent the development of hyperuricaemia.


Its indication is not clear in the patient with asymptomatic hyperuricaemia though. And I think, that in view of some of the following, it should not be easily prescribed to all and sunder. 

First No-No is for those who are pregnant or even thinking of getting pregnant. Absolutely no-no for breastfeeding moms.


Next problem is its degree of drug interactions with other very commonly prescribed drugs. Main interaction with the ACE inhibitors. The evidence is not great but reports of hypersensitivity reactions and leucopenia have led to the constant reminder about avoiding prescribing both together. Same goes with many Diuretics, Amoxicillin and Antacids. 


But the biggest worry for Allopurinol is the possibility of ALLOPURINOL HYPERSENSITIVITY SYNDROME; a type-III hypersensitivity reaction that often leads to diffuse vasculitis, multi-organ failure and death. It is not very common (granted!) but genetically linked and (me suspects) more common in the Asian population. 


The standard criteria for diagnosis are a history of recent exposure to Allopurinol, clinical findings of worsening renal impairment or acute hepatocellular damage, and often a skin rash (either toxic epidermal necrolysis, erythema multiforme, or a diffuse maculopapular or exfoliative dermatitis) with at least one of either fever, eosinophilia or leucocytosis. 


In short, a drug that has high levels of drug interactions with other commonly prescribed drugs and potential for severe hypersensitivity reactions, really should not be a drug that is easily prescribed by the youngest doctors for a common asymptomatic condition.

In these asymptomatic hyperuricaemic patients, the much more unpopular medical advice of giving up the beef rendang, the seafood platter and the bak kut teh is much better and much safer!


Whewwwww !


p.s. no professional conflicts of interest declared.
01.05.12
by

Do you prescribe Allopurinol ?

I think she was trying to tell me to write this blog. So here it is. Thanks CK.

Allopurinol is a commonly prescribed drug; usually for symptomatic hyperuricaemia (gout) or treatment of uric acid kidney stones. It is pretty standard care in many patients with cancers on treatment to try to prevent the development of hyperuricaemia.


Its indication is not clear in the patient with asymptomatic hyperuricaemia though. And I think, that in view of some of the following, it should not be easily prescribed to all and sunder. 

First No-No is for those who are pregnant or even thinking of getting pregnant. Absolutely no-no for breastfeeding moms.


Next problem is its degree of drug interactions with other very commonly prescribed drugs. Main interaction with the ACE inhibitors. The evidence is not great but reports of hypersensitivity reactions and leucopenia have led to the constant reminder about avoiding prescribing both together. Same goes with many Diuretics, Amoxicillin and Antacids. 


But the biggest worry for Allopurinol is the possibility of ALLOPURINOL HYPERSENSITIVITY SYNDROME; a type-III hypersensitivity reaction that often leads to diffuse vasculitis, multi-organ failure and death. It is not very common (granted!) but genetically linked and (me suspects) more common in the Asian population. 


The standard criteria for diagnosis are a history of recent exposure to Allopurinol, clinical findings of worsening renal impairment or acute hepatocellular damage, and often a skin rash (either toxic epidermal necrolysis, erythema multiforme, or a diffuse maculopapular or exfoliative dermatitis) with at least one of either fever, eosinophilia or leucocytosis. 


In short, a drug that has high levels of drug interactions with other commonly prescribed drugs and potential for severe hypersensitivity reactions, really should not be a drug that is easily prescribed by the youngest doctors for a common asymptomatic condition.

In these asymptomatic hyperuricaemic patients, the much more unpopular medical advice of giving up the beef rendang, the seafood platter and the bak kut teh is much better and much safer!


Whewwwww !


p.s. no professional conflicts of interest declared.
01.03.12
by

Traumatic Optic Nerve Neuropathy (TON)

This is not particularly common; but is very often missed. When missed, the potential for medicolegal action is high, and often very difficult to defend. So, listen up.


TON refers to injury to the optic nerve as a result of trauma; which may be direct (often a result of orbital fractures and bone ends that sever the nerve) or indirect (usually as a result of blunt force applied on the orbit or malar eminences - a high force impact over the eye or on the cheek). Nobody can really know for sure why the Optic N gets injured indirectly; shear force injuring the axons, or local swelling of the nerve at that area resulting in secondary injury. But regardless, TON must be considered in every patient with local injury over the eye and / or cheek; especially if associated with blunt head injury.


Which is why TON is easily missed. The main symptom is blurring of vision in that eye; not something the patient will readily complain of when their face is smashed, or their eyes are so swollen that they cannot open it to see. Worse still, if it is associated with blunt head injury and a low GCS. It is NOT easily identified on fundoscopic examination in the initial 24 hours, and the main suspicion will come from a Relative Afferent Pupillary Defect (RAPD) detected by the swinging torchlight test. (YouTube) This is often not done in the ED, for many reasons (none of which will convince the Judge in a medical negligence suit). Therefore, this is commonly missed; and the patient will only notice persistent vision blurring or loss after days to weeks; when nothing can be done.


So what can be done, if TON is diagnosed ? Actually, nothing much. In many patients, the visual loss is temporary and will recover to some extent. Surgical decompression was used for some time in some countries, but very little evidence can support its efficacy (probably unless structural defects that require decompressing can be demonstrated). For some time, the use of high dose steroids (esp Methyl Prednisolone) was promoted as the wonder drug, to be given early for better outcomes. Most recent trials have not found conclusive evidence to support this either. 


So what then is the issue, you may ask ? If there is no real treatment, why sue the doctor for missing it in the first place ? The Courts do not work that way, my friend. As long as there is a "potential" for recovery, and that "potential" was not made available to the patient because the diagnosis was missed, it is negligence. Not really how medicine works, but that's why they are lawyers and not doctors. 


How then to stay safe ie how to keep the lawyers at bay ? Examine the eye carefully in every patient with injury around the eye and cheek; esp if they have head injury as well. Check for the RAPD. Check for pupillary response. DOCUMENT IT. If you are unable to check (swollen, uncooperative, priority to head injury etc), make sure you refer to the Ophthalmology team for a complete eye examination. And write that down it. 


Much, much better than having to appear in inquiry and inquiry after inquiry and then in courts. Stay safe.