الأربعاء، 13 فبراير 2013

Week marked by Liga match away to Granada

This week is marked by the Liga match away to Granada at Los Cármenes. The team will train on Wednesday, Thursday and Friday at 11.00 at the Ciutat Esportiva Joan Gamper.

The leaders of the league will close out the week on Saturday at 20.00 with the match in Andalusia. The team will have the day off on Sunday, and start to prepare for the away leg of the Champions League knock out stage away to AC Milan.

Monday, February 11
Day off

Tuesday, February 12
Day off

Wednesday, February 13
11.00 - Training session at the Ciutat Esportiva Joan Gamper (first 15 minutes are open to the press)

Thursday, February 14
11.00 - Training session at the Ciutat Esportiva Joan Gamper

Friday, February 15

11.00 - Training session at the Ciutat Esportiva Joan Gamper

Saturday, February 16

20.00 - Liga match against Granada

Sunday, February 17

Day off

46 new Supporters Clubs make the Club even bigger

The Club’s directors met this Monday, February 11th and one of the items they approved was the incorporation of 46 new penyes.

The Club welcomes the new penyes, who will certainly help Barça continue to be a reference point in the social area around the world.

Below are the names of the new penyes:

Peña Azulgrana de Fuencaliente (Fuencaliente, Ciudad Real)

Penya Blaugrana Nicolau Casaus de Sant Andreu de la Barca (Sant Andreu de la Barca, Barcelona)

Penya Barcelonista Chicho Sibilio (Distrito Federal, Dominican Republic)

Penya Barcelonistas de Gante (Ghent, Belgium)

Asociación Peña Barcelonista de Porriño (O Porriño, Pontevedra)

Peña Barcelonista de Ablitas (Ablitas, Navarra)

Peña Barcelonista Paco Seirul·lo (Salamanca, Salamanca)

Penya Barcelonista de Sineu (Sineu, Balearic Islands)

Penya Blaugrana d'Artesa de Lleida (Artesa de Lleida, Lleida)

Penya Barcelonista Do Barbanza (Boiro, La Coruña)

Peña Barcelonista de Ruecas (Ruecas, Badajoz)

Peña Barcelonista Dilar (Dilar, Granada)

Peña Barcelonista Almadén de la Plata (Almadén de la Plata, Sevilla)

Penya Barcelonista de Monofacio (Tefeli, Crete)

Penya Blaugrana de Llivia (Llivia, Girona)

Penya Blaugrana de Maracay Gent del Barça (Maracay, Venezuela)

Penya Barcelonista de Beneixema (Beneixema, Alicante)

Penya Barcelonista de Campins (Campins, Barcelona)

Peña Castillo Blaugrana (Bercial, Segovia)

Peña Barcelonista de Pedroche (Pedroche, Córdoba)

Penya Blaugrana Aït Nsar (Aït Nsar, Morocco)

Penya Barcelonista di Bergamo - Città dei Mille (Bergamo, Italy)

Peña Barcelonista San Benito (San Benito de la Contienda, Badajoz)

Penya Barcelonista Alcalà-Alcossebre (Alcalà de Xivert, Castelló)

Peña Barcelonista Pasión Culé de Zaragoza (Zaragoza)

Peña Barcelonista de Tauste (Tauste, Zaragoza)

Peña Barcelonista Colloto (Colloto, Asturias)

Penya Blaugrana Gerard Piqué de Talamanca (Talamanaca, Barcelona)

Gent Blaugrana d'Anfa (Casablanca, Morocco)

Penya Barcelonista de Castelldans (Castelldans, Lleida)

Penya Barcelonista de Sils (Sils, Girona)

Peña Barcelonista "El Toboso" (El Toboso, Toledo)

Penya Blaugrana del Conflent (Prades, France)

Penya Barcelonista Ibense "Reyes Magos" (Ibi, Alicante)

Penya Blaugrana Garriguella (Garriguella, Girona)

Barcelona Fan Club Guanzhou (Guanzhou, China)

Penya Barcelonista Vall de Guadalest (Guadalest, Alicante)

Peña Barcelonista Santiago de Calatrava (Santiago de Calatrava, Jaén)

Penya Blaugrana Garraf (Garraf, Barcelona)

Penya Barcelonista Knokke-Heist (Bruges, Belgium)

Peña Barcelonista Nerjeña (Nerja, Málaga)

Bayerische Penya Blaugrana (Munich, Germany)

Penya Blaugrana de Calahonda (Mijas Costa, Málaga)

Penya Blaugrana de Bellaterra (Bellaterra, Barcelona)

Penya Barcelonista Eslovaca dels Altos Tatras (Bratislava, Slovakia)

Peña Barcelonista de Córdoba (Córdoba)

FCB Regal - Valencia Basket: Copa del Rey champions! (85-69)

Barça Regal won the Copa del Rey this Sunday evening, the first big title of the season, after defeating Valencia Basket in the final by 85 to 69. The men managed by Xavi Pascual jumped to an insurmountable lead in the fourth quarter and won the 23rd Cup in Club history.

Equal first half
In a final it’s always important to strike first, this let’s your rival know that you mean business and that you’re on form. This was the attitude that Barça Regal had when they came out onto the Buesa Arena court and in five minutes they already had an eight-point lead (14-6). Víctor Sada led the Blaugrana in the opening minutes - 7 of the team’s 14 points were his - which forced Perasovic to call timeout.

Valencia reacted with a 3-12 run of their own. The teams finished the first quarter with 17 to 18 on the scoreboard. Both sides were evenly matched in the second quarter. Perasovic’s men started knocking down points from beyond the three-point line and jumped to a five-point lead (21-26). That was the biggest lead Valencia enjoyed in the second quarter, but Barça fired back and took a three-point lead thanks to Jawai, Oleson and Wallace (36-33).

Importance difference

At the start of the second half, Barça Regal came out with one idea: break the game. Said and done. An imperious Jawai dominated on both sides of the court and Oleson knocked down four consecutive points. The difference of 52 to 39 seemed to be close to decisive, but Valencia never gives up, and much less in a final. They fought back to come within eight points (61-45) at the end of the third quarter.

Lorbek secures the title

On various occasions Barça could have closed out the game, but they were unable to land the crippling blow. In fact, Valencia came within five points of Barça in the last quarter (63-57), but a 7-0 run led by Oleson and Lorbek saw Barça take a 13-point lead (70-57). In the last four minutes of the game, the Slovenian proved decisive on both sides of the court.

The final score of 85 to 69 secured the third Cup of the Xavi Pascual era and the 23rd Cup in the history of FC Barcelona.

Leo Messi and Andrés Iniesta, face to face

The two players with their respective individual prizes to talk about their origins and the essence of the Masia style

Messi: “The Barça philosophy isn’t about just one coach or another, it’s based on an idea, a line that is laid down and all coaches follow. That has always been the way in which the Club has worked with the academy”

Iniesta: “The Barça way of playing – which we’ve worked on for such a long time –helps create success. The most important thing is to have an idea, but you have to have the right players to put it into practice – the two have to go hand in hand”

Leo Messi and Andrés Iniesta / PHOTO: REVISTA BARÇA.

New 2012 Berlin Definition for ARDS

The new 2012 definition for Acute Respiratory Distress Syndrome (ARDS) (published in JAMA June 2012)


According to the previous definition published in 1994 by the American-European Consensus Conference (AECC), ARDS must have the following 4 criteria:
  • the onset must be acute
  • there must be hypoxemia with PaO2/FIO2 ratio ≤ 200
  • there must be bilateral infiltrates on CXR
  • these findings cannot be attributed to other causes
A separate category for acute lung injury (ALI) is defined with PaO2/FIO2 ≤ 300

However, a number of problems are found with the 1994 definition, including:

  • term 'acute' was not defined (i.e., how "acute" is acute)
  • the category of ratio PaO2/FIO2 between 201-300 is confusing (PaO2/FIO2 ≤ 300 is ALI, PaO2/FIO2  ≤  200 is ARDS, PaO2/FIO2 between 201 - 300 ?ALI/ARDS)
  • CXR interpretation has poor inter-observer reliability

With this, the new Berlin 2012 definition of ARDS is published with the following changes:
  1. the category of acute lung injury (ALI) with PaO2/FIO2 ≤ 300 is REMOVED
  2. instead, ARDS is now divided into three categories based on severity of hypoxemia
    1. PaO2/FIO2 between 200–300 is defined as mild
    2. PaO2/FIO2 between 101 - 199 is defined as moderate
    3. PaO2/FIO2 of less than 100 is defined as severe
  3. The term 'acute' now has a specified time frame of symptoms developing within ONE week of a known clinical insult
  4. Other changes:
    1. the CXR criteria is now more defined with the added phrase "bilateral opacities - not fully explained by effusions, lobar/lung collapse, or nodules"
    2. PCWP reading is no longer required as part of the diagnosis as this is increasingly not used. Instead, this new definition requires that the respiratory failure cannot be explained fully by cardiac failure or volume overload.

Editorial comment in JAMA June 2012 points out that this new definition only improves its predictive value of mortality slightly; however, the clarity of the criteria is significantly improved.

Ref:The ARDS Definition Task Force. Acute respiratory distress syndrome: The Berlin definition. JAMA 2012 Jun 20; 307:2526
Abstract: http://jama.jamanetwork.com/article.aspx?articleid=1160659

A case of recurrent abdominal distension


A 50-year old man with recurrent history of unable to pass stools for 3 days’ duration with abdominal distension. Otherwise he appears comfortable. On examination, abdomen is distended, but soft and non-tender on palpation. Bowel sounds were diminished. He had multiple admissions for similar complaints for the last two years. The abdominal x-ray for the current admission is as below:



And the abdominal x-ray taken 9 months ago when he was admitted similarly is as below:


Further history revealed that when he presented for the first time, the surgical team performed an exploratory laparatomy and found no abnormality. He has history of schizophrenia and is on antipsychotics. 

What diagnosis should you consider in this case?


Ans: recurrent colonic pseudo-obstruction also known as Ogilvie Syndrome.

Pathophysiology:

1. When Ogilvie first described these cases, he hypothesized that the etiology was due to sympathetic deprivation to the colon, leading to unopposed parasympathetic tone, resulting in regional contraction, and thus functional obstruction.

2. However, the current understanding is, unlike the hypothesis Ogilvie proposed, is because of parasympathetic suppression (in this case, sacral parasympathetic outflow), or excessive sympathetic stimulation (Maloney & Vargas, 2005)

RECALL that:
the parasympathetic nervous system increases gut motility and
the sympathetic nervous system decreases gut motility

Thus, in the presence of disruption of the parasympathetic stimulation, results in reduced gut motility or adynamic of distal gut segment, resulting in functional dilatation. This hypothesis is supported by the use of neostigmine in the treatment of this condition.

3. Neostigmine is an acetycholinesterase inhibitor (Ponec et al, 1999).
Acetycholinesterase results in the breakdown of acetylcholine into acetate and choline.
Thus, neostigmine, by inhibiting the action of this acetylcholinesterase, inhibits the breakdown of acetylcholine (by the same token, neostigmine can be used to treat myastenia gravis by increasing the concentration of acetycholine)

4. The cecum is the usual site of the largest dilatation in Ogilvie syndrome and, thus, is more prone to the risk of perforation. This is because cecum has a large diameter. Laplace law states that the intraluminal pressure needed to stretch the wall of a hollow tube is inversely proportional to its diameter.  Thus, because of its large diameter, it is easier to overcome the wall tension of cecum with a small amount of pressure than with other parts of the gut (Click here to access the article in emedicine)

5. Of course, this syndrome has to be a diagnosis of exclusion. Mechanical obstruction has to be ruled out. In this patient, exploratory laparatomy was first performed and the gut was found to be normal.


6. The patient is on anti-psychotic drugs. Many of these anti-psychotics such as phenothiazines have anticholinergic properties; thus aggravate this patient's condition.

Click here for a chapter on Ogilvie Syndrome

One should also differentiate toxic megacolon from Ogilvie syndrome. However, the clinical features in toxic megacolon are quite different from this syndrome. Patient with toxic megacolon is rather sick looking. Jalan criteria for toxic megacolon are:
  • Radiographic evidence of colonic dilatation - The classic finding is more than 6cm in the transverse colon PLUS
  • Any 3 out of 4 of the following
    • Fever (>38.6C)
    • Tachycardia (>120/min)
    • Leukocytosis (>10.5 x 103/µL) or 
    • anemia  PLUS
  • Any 1 of the following - Dehydration, altered mental status, electrolyte abnormality, or hypotension
(Jalan KN, Sircus W, Card WI, Falconer CW, Bruce CB, Crean GP, McManus JP, Small WP, Smith AN. An experience of ulcerative colitis. I. Toxic dilation in 55 cases. Gastroenterology. 1969 Jul;57(1):68-82.)




References:
1. Maloney N, Vargas HD. Acute intestinal pseudo-obstruction (Ogilvie's syndrome). Clin Colon Rectal Surg. 2005 May;18(2):96-101. Click here for free full text in pdf

2. Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute colonic pseudo-obstruction. N Engl J Med. 1999 Jul 15;341(3):137-41. Click here for free full text.

10 things I learned from the 46th Malaysia-Singapore Congress of Medicine



10 things I learned from the 46th Malaysia-Singapore Congress of Medicine

Although this congress has not much relevant topics pertaining to emergency medicine, I learned a number of things on cardiometabolic updates. Below are some of the things I learned:

1. In a patient with STABLE coronary disease, a recent landmark trial called the COURAGE trial shows that the nearly 5-year incidence of death or MI was similar whether the patient undergoes PCI or optimized medical therapy alone, although PCI showed some advantage in relieving angina.

Reference:Boden WE, O'Rourke RA, Teo KK, Hartigan PM, Maron DJ, Kostuk WJ, Knudtson M, Dada M, Casperson P, Harris CL, Chaitman BR, Shaw L, Gosselin G, Nawaz S, Title LM, Gau G, Blaustein AS, Booth DC, Bates ER, Spertus JA, Berman DS, Mancini GB, Weintraub WS. Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med. 2007 Apr 12;356(15):1503-16. Click here to download the FREE FULL TEXT in pdf

2. However, in another on-going study with has to be halted prematurely (the FAME II study), for a specific sub-group of patients with stable coronary disease and documented hemodynamically significant stenosis (detected from fractional flow reserve, FFR), these patients will have a more than 10-times-higher risk of urgent revascularization if they are initially treated with optimal medical therapy (OMT) rather than PCI.

Hence, as the coordinating clinical investigator of this trial, Dr Bernard De Bruyne, said, the findings from FAME II are not "anti-COURAGE", but a complement or an extension of "COURAGE."

In other words, if properly selected, a patient would benefit significantly from PCI.
3. In a patient with left ventricular systolic dysfunction, CABG may reduce the risk for cardiovascular death or revascularization, but it does not appear to prolong life compared with contemporary guideline-based medical therapy (no statistical significant difference in the rate of all-cause mortality in a follow-up of up to nearly 5 years) (STICH trial)

Reference:
Velazquez EJ, Lee KL, Deja MA, Jain A, Sopko G, Marchenko A, Ali IS, Pohost G, Gradinac S, Abraham WT, Yii M, Prabhakaran D, Szwed H, Ferrazzi P, Petrie MC, O'Connor CM, Panchavinnin P, She L, Bonow RO, Rankin GR, Jones RH, Rouleau JL. Coronary-artery bypass surgery in patients with left ventricular dysfunction. N Engl J Med.  Apr 28;364(17):1607-16. Click here to download the FREE FULL TEXT in pdf
4.  In a patient with homozygous familial hypercholesterolemia (FH), with very high cholesterol level and who do not respond well to maximum multiple drug therapy, LDL apheresis may be considered (much like renal dialysis). Meanwhile statins have the adverse effect of elevating the liver enzymes.

Reference:
2011 Malaysian CPG Management of Dyslipidemia (4th ed). Click here to download the FREE FULL TEXT in pdf

5.  Statins, especially in high dose, can cause derangement in liver enzymes but ACC/AHA/NHLBI recommends that statins should be discontinued (or lowered the dose of) if the ALT or AST are above 3 times the upper limit of normal on 2 consecutive occasions. Nonetheless, the exact mechanism of how statins cause elevations of ALT and AST is still unknown.

Reference:
Pasternak RC, Smith SC, Jr., Bairey-Merz CN, Grundy SM, Cleeman JI, Lenfant C. ACC/AHA/NHLBI Clinical Advisory on the Use and Safety of Statins. Circulation. 2002 Aug 20;106(8):1024-8. Click here to download the FREE FULL TEXT in pdf
6. For patient with subclinical hypothyroidism, initiate treatment if the TSH ≥10 mIU/L. TSH levels ≥10 mIU/L associated with increased cardiovascular morbidity and mortality.

Reference:
Weiss IA, Bloomgarden N, Frishman WH. Subclinical hypothyroidism and cardiovascular risk: recommendations for treatment. Cardiol Rev.  Nov-Dec;19(6):291-9.

7. Overt hyperthyroidism which has been shown to be associated with cardiac arrhythmias, hypercoagulopathy, stroke, and pulmonary embolism, is found to be associated with a 20% increased mortality in a recent meta-analysis.

Reference:
Brandt F, Green A, Hegedus L, Brix TH. A critical review and meta-analysis of the association between overt hyperthyroidism and mortality. Eur J Endocrinol.  Oct;165(4):491-7. Click here to download the FREE FULL TEXT in pdf
8. Metformin is the only oral anti-diabetic that has been proven to reduce cardiovascular mortality in trials such as the UKPDS; and as such, it should be continued unless the patient has been shown to have documented a GFR reduction <30%. Metformin does not cause hypoglycemia attack and has been shown to be weight neutral or result in weight reduction. Lactic acidosis is a concern but only in the presence of hepatic failure. There is, however, a question that metformin may lead to Vit B12 deficiency over a long term use.
Thiazolidinediones, like rosiglitazone, has been shown to be associated with an increased risk for myocardial infarction and possibly cardiovascular mortality in a recent meta-analysis.  There are also evidence to suggest that thiazolidinediones may increase risk of bladder cancer (click here for an article).

References:
1. Management of Type 2 Diabetes 2009 - Malaysian CPG. Click here to download the FREE FULL TEXT in pdf.

2. Home PD, Pocock SJ, Beck-Nielsen H, Gomis R, Hanefeld M, Jones NP, Komajda M, McMurray JJ. Rosiglitazone evaluated for cardiovascular outcomes--an interim analysis. N Engl J Med. 2007 Jul 5;357(1):28-38. Click here for full text access.

9. Bariatric surgery is a useful and appropriate treatment for obese people with type 2 diabetes NOT achieving the recommended treatment targets with medical therapies, especially when there are other major co-morbidities.

Diabetic patients with a BMI between 30 and 35 and cannot be adequately controlled by optimal medical regimen and especially in the presence of other major cardiovascular disease risk factors, may also be considered for bariatric surgery.

There are various methods of bariatric surgery, which can be divided into
  • Gastric restrictive procedures (laparoscopic adjustable gastric banding, sleeve gastrectomy, vertical gastroplasty) limit gastric volume and, hence, restrict the intake of calories by inducing satiety. Gastric banding, for example, may limit the volume to only 30 ml or 2 table spoons!
  • Intestinal bypass procedures (Roux-en-Y gastric bypass, biliopancreatic diversion) also restrict caloric intake, the way gastric banding and vertical gastroplasty do. But because the small intestine is shortened, they have an added component of malabsorption of fat and nutrients.
Bariatric surgery as a treatment for Type 2 diabetes is endorsed by the International Diabetes Federation (IDF) in its position statement on bariatric surgery. Click here to download the statement.

However, the  IDF position statement recommends only 2 procedures, namely Roux-en-Y gastric bypass (RYGB) and laparoscopic adjustable gastric banding (LAGB), are currently conventional bariatric surgical procedures for adolescents.




The image is taken from Cleveland Clinic Journal of Medicine at URL http://www.ccjm.org/content/77/7/468/F1.large.jpg for educational purpose only


How does bariatric surgery works? Besides limiting the volume of the "stomach", bariatric surgery induces a number of hormonal or metabolic changes. There are two theories behind:
  • the “hindgut theory” which suggests that accelerated transit of concentrated nutrients (particularly glucose) to the distal intestine results in increased production of insulinotropic and appetite-controlling substances
  • the “foregut theory” which suggests that since nutrient interactions in the duodenum are diabetogenic; through bypassing the duodenum, this would reverse this defect. 
Reference:
Kashyap SR, Gatmaitan P, Brethauer S, Schauer P. Bariatric surgery for type 2 diabetes: weighing the impact for obese patients. Cleve Clin J Med.  Jul;77(7):468-76. Click here to download the FREE FULL TEXT in pdf.
10. Contrary to what many think, an infant's low birth weight and poor nutrition can actually lead to increased prevalence of coronary heart disease, diabetes, hypertension, stroke, etc during adult life.This is known as the Barker hypothesis because it was first described by Barker in an epidemiology study.

Epigenetics is the study of the heritable changes in gene expression or cellular phenotype WITHOUT changes in the underlying DNA sequence – hence the name epi- (over, above, outer) -genetics.

It refers to functionally relevant modifications to the genome by mechanisms such as the histone chain that wraps around the gene. The more tightly "wrapped" the gene is, the more silenced the gene becomes.  The other mechanism is through epigenome tags such as the methyl tag.  The more methylation, the more silenced the gene becomes.

These epigenomes can interact with the environment and can "listen" to signals from the environment. This, early-life metabolic adaptations help in survival of the organism by selecting an appropriate trajectory of growth in response to environmental cues.

Click here to watch a video on epigenetics.

Reference: 
Barker DJ. Fetal origins of coronary heart disease. BMJ. 1995 Jul 15;311(6998):171-4.

The use of morphine in acute pulmonary edema

The use of morphine in acute pulmonary edema: good or bad?

In med schools, we have often been taught that the treatment of acute pulmonary edema is LMNOP where L = Lasix, M = morphine, N = nitrates, O = oxygen, P = position/prop up the patients.

However, many recent studies have shown that the evidence of the use of morphine in acute pulmonary edema is not only weak, but is potentially harmful to the patients.

Here's some notes on the use of morphine in acute pulmonary edema:

1. Why morphine was initially advocated for APO? (a history question)
This is because animal studies suggest that morphine produces a significant peripheral venodilation and moves significant quantities of blood from the central to the peripheral circulation; and thus reduce the workload of the heart.

(Ref: Vasko JS, Henney RP, Oldham HN, Brawley RK, Morrow AG. Mechanisms of action of morphine in the treatment of experimental pulmonary edema. American Journal of Cardiology 1966; 18:876-83.)

2. However, subsequent studies (e.g., Vismara et al, 1976) of venous tone changes in normal subjects vs patients with mild stable APO demonstrate that magnitude of the venodilation induced by morphine is rather minimal, and the amount of blood that could be pooled in the limbs has been calculated to be quite small (70ml in normal subjects vs 116mls in patients with APO).  This in fact is insufficient to cause significant clinical improvement in patients’ with APO.

(Ref: Vismara LA, Leaman DM, Zelis R. The effects of morphine on venous tone in patients with acute pulmonary edema. Circulation 1976; 54:335-7.)

3. Also, some studies show that these effects are indeed mediated via the histamine receptors and has nothing to do with the opiate receptors. In other words, we are depending on the side-effects of morphine to exert the venodilation.

(Ref: Grossmann M, Abiose A, Tangphao O, et al. Morphine-induced venodilation in humans. Clinical Pharmacology and Therapeutics 1996;60:554)

4. As early as 1999, Sacchetti et al (1999) reported increased intubation rates and a longer stay in the ICU if morphine was used.

(Ref: Sacchetti A, Ramoska E, Moakes ME, et al. Effect of ED management on ICU use in acute pulmonary edema .Am J Emerg Med 1999;17:571–4)

5.  In a recent retrospective analysis of the Acute Decompensated Heart Failure National Registry (ADHERE), as compared to patients not on morphine, patients on morphine:
  • were more likely to require mechanical ventilation (15.4% vs 2.8%)
  • had a longer median hospitalisation (5.6 vs 4.2 days)
  • more ICU admissions (38.7% vs 14.4%), and
  • had greater mortality (13.0% vs 2.4%) (all with p<0.001).

Even after risk adjustment and exclusion of ventilated patients, morphine was an independent predictor of mortality (OR 4.84 (95% CI 4.52 to 5.18), p<0.001). 
(Ref: Peacock WF, Hollander JE, Diercks DB, Lopatin M, Fonarow G, Emerman CL. Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis. Emerg Med J. 2008 Apr;25(4):205-9.)

Choice of muscle relaxant in myasthenic crisis

 Image from microsoft.com image gallery, MP900178484. 
Available at: http://office.microsoft.com/en-us/images/results.aspx?ex=2&qu=drug#ai:MP900178484|mt:0|

We encountered a case of 38-year old Malay female with history of myasthenia gravis. She presented this time with the complaint of difficulty of getting up after praying. She also complained of episodes of vomiting and passing out loose stools for one day prior to her presentation. She has past history of hypokalemia and for this current admission, her potassium level from venous blood gas analysis was on the lower end of 3.2 mmol/l. The hypokalemia probably aggravates her proximal myopathy. However, about half an hour later, she complained of progressive breathing difficulty, and at one point she was cyanotic and gasping. We immediately put her through positive pressure ventilation by bag-valve-mask. We almost thought of intubating the patient. What would be the better choice of muscle relaxant in this case?

The more predictable choice would be a non-depolarizing agent although they may slightly slower compared to scoline. The reason being the post-synaptic receptors are now being occupied by the auto-antibodies and therefore, if you use scoline you would probably need a higher than usual dose. And  its duration of action may be last longer because of the higher dose! And that's why, scoline may be rather unpredictable. On the other hand, the non-depolarizing type could be displaced away after its action through competition. Reference: http://emedicine.medscape.com/article/793136-overview#aw2aab6c10

We almost wanted to intubate this patient but fortunately the patient had a rather quick recovery of its respiratory and diaphragm muscles following a dose of neostigmine, and thereby intubation was avoided. We gave her NIPPV too. Literature seems to suggest NIPPV helps.

Chaudhuri and Behan (2009) has written a rather interesting and informative review article on myasthenic crisis and it is worth to download this article which is available free at URL: http://qjmed.oxfordjournals.org/content/102/2/97.full.

According to Chaudhuri and Behan (2009), respiratory failure is a must in definition criteria of myasthenic crisis. Furthermore, in that article, it is also mentioned that the continuous use of anticholinesterase (such as IV pyridostigmine) (which this patient, fortunately, did not require) as a therapy for myasthenic crisis remains controversial, especially because of the risk of cardiac arrhythmias and myocardial infarction. As mentioned in the article, coronary vasospasm from excessive anticholinergic treatment is known to be an iatrogenic cause of myocardial infarction in myasthenia gravis.  Besides the risk of cardiac complication, large doses of anticholinesterases promote excessive salivary and gastric secretions, which may increase the risk of aspiration pneumonia.

In that article, Chaudhuri and Behan (2009) also listed a table with various differentiating features of other common causes that may mimic myasthenic crisis. Click here for the table.

A final thought: in any syndromic case, a syndrome is a syndrome; a clustering of signs and symptoms. It is important to treat the underlying cause(s). One of the common causes in many syndromes is offending drugs. In the case of myasthenic crisis, the various offending drugs include:
the various groups of antimicrobials such as the aminoglycosides, the macrolides, tetracycline group, the quinolones (ciprofloxacin, ofloxacin, norfloxacin); anticonvulsants such as phenytoin and carbamazepine; antipsychotics such as the neuroleptics; beta-blockers, calcium channel blockers, etc.


Reference:
1.    Chaudhuri A, Behan PO. Myasthenic crisis. QJM. 2009 Feb;102(2):97-107.

Estimating the volume of intracranial hematoma on CT

The commonly used formula for estimating the volume of intracranial bleed on CT is


ABC/2 
where

A is the maximal diameter of the hematoma by CT
B is the diameter 90° to A, and
C is the approximate number of CT slices with hemorrhage multiplied by the slice thickness

For a number of years, I could not really grasp why the formula is as such. I thought that the formula is derived from the formula of volume for a cylinder. The part of (C) in the formula I could understand as it involves the height of the cylinder. But what I could not grasp is that, if this formula is derived from the volume of a cylinder, the formula should entail the use of "pi" (π) which is taken to be 3.14 (up to 2 decimal points).  This is because the surface area of a circle is π * r *r; and therefore, the formula for volume of cylinder is π * r *r * h where h is the height of the cylinder.

Until I found this article Kothari et al (1996) which is helpful in explaining how this formula of ABC/2 comes about.

This formula is actually derived from the volume of an ellipsoid object and NOT of cylinder.
Figure 1
Image copyrighted to JoshDif licensed under under the Creative Commons Attribution-Share Alike 3.0 Unported license. Original site: Wikipedia


The volume for an ellipsoid object is

4/3 * π * a *b * c (a, b, and c as of Figure 1 above)

Applying this formula to the hematoma object on CT,
a and b are actually half of the two diameters mentioned on 2 dimension plane; and c is half of the height of the hematoma.

Therefore, the volume of the hematoma is

4/3 * π * (A/2) * (B/2) * (C/2)

where
A is the maximal diameter of the hematoma by CT
B is the diameter 90° to A, and
C is the approximate number of CT slices with hemorrhage multiplied by the slice thickness

assuming π ~ 3, therefore,

the volume of the hematoma is therefore,
4/3 * 3 * (A/2) * (B/2) * (C/2) = ABC/2

In an article by Freeman et al (2008), it is found that the ABC/2 method accurately estimates smaller ellipsoid hematoma volumes but inaccurately measures larger, irregularly shaped hematoma, or multicompartment hemorrhage such as intraventricular hemotoma and subdural hematoma. This article by Freeman et al (2008) has great pictures showing the ellipsoid shape of intracranial hematoma.

The importance of estimating the volume is that if the volume is large (~20 - 30 cc), it may be one of the indications for neurosurgical intervention, depending on the local neurosurgical management protocol of the center.

References:
1. Kothari RU, Brott T, Broderick JP, Barsan WG, Sauerbeck LR, Zuccarello M, Khoury J. The ABCs of measuring intracerebral hemorrhage volumes. Stroke. 1996 Aug;27(8):1304-5. Click here.

2. Freeman WD, Barrett KM, Bestic JM, Meschia JF, Broderick DF, Brott TG. Computer-assisted volumetric analysis compared with ABC/2 method for assessing warfarin-related intracranial hemorrhage volumes. Neurocrit Care. 2008;9(3):307-12. Click here.

The New WHO 2010 Severity Classification

WHO, in its recent dengue guidelines 2009, has alluded to the fact that its existing classification into dengue fever and dengue hemorrhagic fever (further divided into 4 grades) have a number of limitations due to the rigidity of its criteria.  Download also the Malaysian guidelines on dengue management.

For example,  in a number of cases, patients can present with dengue and shock but without fulfilling all the 4 criteria for DHF These patients would have been classified as dengue fever if the WHO criteria were strictly applied.

The requirement of 20% increase in HCT as one of the evidence of plasma leakage is difficult to fulfill due to several issues:
  • Baseline hematocrit may not be easily available unless blood sampling for full blood count has been recently obtained in the same hospital or healthcare center where the patient presents himself to.
  • Early fluid administration in a health clinic may have changed the hematocrit reading prior to referral to hospital.
  • Bleeding itself will lower the HCT level
(* Previously, the following must ALL be present in order to classify the patients as having dengue hemorrhagic fever:
  • Fever, or history of acute fever, lasting 2–7 days, occasionally biphasic.
  • Haemorrhagic tendencies, evidenced by at least one of the following :
  1. a positive tourniquet test
  2. petechiae, ecchymoses or purpura
  3. bleeding from the mucosa, gastrointestinal tract, injection sites or other locations
  4. haematemesis or melaena.
  • Thrombocytopenia (100,000 cells per mm3 or less).
  • Evidence of plasma leakage due to increased vascular permeability, manifested by at least one of the following:
  1. a rise in the HCT equal to or greater than 20% above average for age, sex and population
  2. a drop in the HCT following volume-replacement treatment equal to or greater than 20% or baseline
  3. signs of plasma leakage such as pleural effusion, ascites and hypoproteinaemia.)
As such, since 2009-2010, WHO and Malaysia has adopted a new classification that is more pragmatic. The whole idea is to capture early the group of patients that may potentially deteriorate due to the following pathogenetic processes:
Plasma leakage
Hemorrhage
Organ impairment
Under this classification, the patients would be classified into either
  • Dengue fever (either probable or laboratory-confirmed)
  • Dengue fever WITH warning signs
  • Severe dengue (under which may have manifestations of severe plasma leakage, severe hemorrhage, severe organ impairment

For patients to be classified as dengue fever (probable), the pre-criteria is that any patients living in or travelling ENDEMIC AREA for dengue (including Malaysia) AND with FEVER and with 2 out of the following criteria:
  • Nausea, vomiting
  • Rash
  • Aches and pains 
  • Tourniquet test positive 
  • Leukopenia 
  • Any warning sign

These can be remembered with the following mnemonic:
AEEGYPTI (AEGYPTI)
A = Area endemic
E = Emesis
E = Exanthem (rash)
G = groan and ache
Y = yes to warning signs
P = Positive tourniquet test
T = total white cell low
I = increased temperature
Patients with dengue with warning signs need to be admitted.  These warning signs are:
Abdominal pain or tenderness 
Persistent vomiting
Clinical fluid accumulation 
Mucosal bleed
Lethargy, restlessness 
Liver enlargment >2 cm 
Laboratory: increase in HCT concurrent with rapid decrease in platelet count
The warning signs can be remembered by:
FLLLAVI (“Flavivirus”)
F = fluid accumulation
LLL = Liver, Lab, Lethargy
A = Abd pain
V = vomiting
I = “insignificant” bleed (“insignificant” does not mean “not important” but minor)
Other pointers in the diagnosis and management of dengue and severe dengue fever that should be kept in mind:

1. The earliest abnormality in the full blood count is a progressive decrease in total white cell count; not thrombocytopenia or increased hematocrit.

2. A relative bradycardia may be noted despite the fever, especially in the recovery phase. It is not always tachycardia in dengue.

3. Do not give acetylsalicylic acid (aspirin), ibuprofen or other non-steroidal anti-inflammatory agents (NSAIDs) as these drugs may aggravate the bleeding in dengue due to capillary fragility. Acetylsalicylic acid (aspirin) may be associated with Reye’s Syndrome.

4. Fresh whole blood or fresh red cells should be given whenever possible. This is because oxygen delivery at tissue level is optimal with high levels of 2,3 di-phosphoglycerate (2,3 DPG). Stored blood loses 2,3 DPG, low levels which may impede the oxygen-releasing capacity of hemoglobin.

5. If the haematocrit was low (<40% in children and adult females, <45% in adult males), this indicates bleeding and the need to cross- match and transfuse blood as soon as possible (see treatment for haemorrhagic complications).

The criteria in Surviving Sepsis Campaign Guideline for blood transfusion, i.e., hematocrit of <30% is not applicable to severe dengue. In fact, blood transfusion is life-saving and should be given as soon as severe bleeding is suspected or recognized. Do not wait for the haematocrit to drop too low before deciding on blood transfusion. This is because, in dengue, bleeding usually occurs AFTER a period of prolonged shock that is preceded by plasma leakage. During the plasma leakage the hematocrit IN FACT, increases to relatively high values before the onset of severe bleeding. As a result, when bleeding occurs in the later stage, hematocrit will then drop from this higher level; and therefore, it may not be as low as in the absence of plasma leakage.

6. A patient with normal SBP and normal mentation does not mean that he is not in shock. Patients in dengue shock often remain conscious and lucid. Look for narrowed pulse pressure despite normal SBP.

Once decompensation occurs, the BP may drop abruptly. Such prolonged hypotensive shock and hypoxia may in turn lead to multi-organ failure and an extremely difficult clinical course.
Differentiating chikungunya from dengue.
The key distinguishing feature for chikungunya is JOINT PAIN.

In fact, some clinicians came out with the aphorism “dengue + arthritis = chikungunya”!

The classical triad of clinical features for chikungunya infection are
•    fever,
•    arthralgia and
•    skin rash
(Ref: Robinson, M.C., 1955. An epidemic of virus disease in Southern Province, Tanganyika territory, in 1952-1953. Trans. R. Soc. Trop. Med. Hyg., 49 :28-32)
The arthralgia in chikungunya is usually symmetrical and involved more than one joint. The pain can be excruciating and involved fingers, wrist, elbows, toes, ankles and knees.

On the other hand, dengue presents with myalgia compared to chikungunya. The rash in chikungunya appears earlier (even in day 1 or 2 itself), as compared to dengue (around day 4). Furthermore, the rash in chikungunya starts with face and chest; those in dengue, the legs and trunks.

Legal Definition of a Child in Malaysia and the Definition of Statutory Rape

I made a mistake when discussing on the legal definition of a child in Malaysia and the definition of statutory, and so I thought it would be a good idea to revise on this topic.

I mistakenly thought that a child in Malaysia is defined as one aged 18 years old and below. I was wrong. According to the Malaysian Child Act 2001 or Act 611, a child is defined as

a person under the age of eighteen years or below 18 years old (NOT 18 years and below)
However, as Nadesan and Omar (2002) writes, the consenting age for sexual intercourse in Malaysia is 16 years old. As such, statutory rape is defined as sexual intercourse (regardless of whether WITH or WITHOUT consent) with a girl BELOW 16 years old (AND NOT with ANY child).

This definition is according to Section 376 of the Malaysian Penal Code (or Act 574).

Therefore, there exist a time period where a person under the age of 18 years old AND above the age of 16 years old, CAN consent to sexual intercourse, but cannot give consent to medical procedures and treatment (because she is below 18 years old).

The article written by Nadesan and Omar in 2002 is an excellent treatise of the current rape scenario in the Malaysian context. The article can be downloaded here.

The criteria of rape as per Section 375 of the Penal Code is as below:
  1. Against her will
  2. Without her consent
  3. With her consent, when her consent has been obtained by putting her in fear of death or hurt to herself or any other person, or obtained under a misconception of fact and the man knows or has reason to believe that the consent was given in consequence of such misconception 
  4. With her consent, when the man knows that he is not her husband, and her consent is given because she believes that he is another man to whom she is or believes herself to be lawfully married or to whom she would consent
  5. With her consent, when, at the time of giving such consent, she is unable to understand the nature and consequences of that to which she gives consent
  6. With or without her consent, when she is under sixteen years of age (statutory rape)
The word rape originates from the Latin word "rapere", which means "to snatch".  Often, to snatch something from someone would entail some amount of violence imposed. Furthermore, according to Section 375 of the Penal Code above, rape is defined when the sexual intercourse is done "against her will". As such, this places the burden on the victim and the prosecution team to establish the evidence of violence and "against her will". This can pose serious problems because, as Nadesan and Omar (2002) said:
".....the absence of injuries does not necessarily mean that the woman was a willing partner. Owing to many reasons, a victim may not resist the rapist and in that event the chances of a physical attack by the rapist is reduced. When victims are taken by surprise they may be too scared to resist. More importantly, in many instances the rapist is an immediate family member, a close relative or a friend. Several cases are actually incest and many more are statutory rapes where the victims are under the age of sixteen years."
In many countries, the burden of proof has been shifted to the defendant (alleged perpetrator) to prove that there was consent for sexual intercourse, but in Malaysia, the position still remains unchanged for the prosecution to establish that the woman did not consent.

Another thing I learned from the article by Nadesan and Omar (2002) is that amendment to the 1988 Section 146A of the Evidence Act (Act 56) states that no question in cross-examination shall be adduced or asked concerning the sexual activity of the complainant with any other person other than the accused. Previously, victims during cross-examinations were asked about their sexual encounters with persons other than the suspect in order to discredit their moral behavior.

Doctors and nurses working in the emergency departments should have a general knowledge of this important issue as these victims will be presented to the One Stop Crisis Center (OSCC) in emergency department. It is of utmost importance that such victims be accorded to utter privacy and confidentiality. No gossiping of the nature of the suffering inflicted upon the victim should be discussed among healthcare professionals!

My previous post on OSCC: click here.

Reference:

1. Nadesan K, Omar SZ. Rape--the Malaysian scenario. Malays J Pathol. 2002 Jun;24(1):9-14. [Click here to download the FREE full text in pdf]

Advanced ECG by Amal Mattu in Singapore

Attended the Advanced ECG workshop tomorrow conducted by Prof Amal Mattu in the Society for Emergency Medicine in Singapore 2012 Annual Scientific Conference (SEMS ASC).

A number of good streaming video ECG lectures by him in this website. Click here to assess.

Some highlights from the class:


 


Sgarbossa's criteria

The dictum that "in the presence of LBBB, one cannot diagnose myocardial infarction" is no longer true.

The three Sgarbossa criteria are the two concordances (elevation and depression) and one discordance (elevation). Discordance depression IS NOT part of Sgarbossa's criteria.

Discordance elevation requires an elevation of more than 5 mm as it obeys the rule of appropriate discordance.

Concordance depression is only for V1 - V3, but it is kind of a gestalt pattern recognition thing, because if you see, you should recognize it immediately.

Both concordances are more specific than the discordance elevation.

EMS123lead.com has a nice ECG on concordance elevation in this link (click here).

Sgarbossa's criteria also applies for patient with pacemakers.

Remember RBBB does NOT need special criteria such as Sgarbossa. For RBBB, interpret as straight forward STE as you would for any STEMI.

For Sgarbossa, only one abnormal lead is required.

On the other hand, once there is LBBB (as in Sgarbossa's), the significance of STE in aVR cannot be ascertained anymore.

2. Wellen's Syndrome

The problem is usually not with Wellen's Type 1 - it is rather easy to recognize Wellen's Type 1 with its typical deep symmetrical T inversion.

On the other hand, Wellen's Type 2 can be easily missed if we do not know what we are looking for.



The danger with Wellen's is that at the time of presentation, the patient may seem deceptively stable with a subsiding episode of chest pain. However, in reality, these ECG changes in Wellen's may represent a critical ischemia of LAD; medical therapy most probably may not work. The patient should be sent urgently to the cath lab. Although relatively asymptomatic, the patient should be subjected to a stress test, as the critical ischemia may trigger sudden collapse in these patients.

 Wellen's criteria is not dependent on ST changes, just the T inversion!

Note that young children and especially female up to 40 years, may have normal variant of T inversion (the juvenile pattern).

3. Posterior MI
Isolated posterior MI do occur in up to 5% of cases.
Do a posterior lead if unsure. An STE of even more than 0.5 mm is significant for posterior leads
I have previously written a detailed blog post on posterior MI.

4. STE in AVR
aVR is often called the forgotten lead. It is often ignored, often said to be of no use because of its position facing away from the normal direction of depolarization (rendering it to display negativity as reciprocal changes in most of the waveforms).

IN ACTUAL FACT,  ST ELEVATION IN AVR may SIGNIFY a LEFT MAIN CORONARY ARTERY (LMCA) STENOSIS with mortality up to 70%!!

Numerous articles have been written on this. It is coined as "a mostly ignored but very valuable lead in clinical electrocardiography", a "widow maker", etc.

STE in aVR itself of more than 1.5 mm carries a 75% specificity of LMCA  [in some articles, it is more than 1.0 mm. Check references in this article here.]
STE in aVR + avL -- 90% specificity
STE in aVR + V1 -- suggestive either prox LAD or LMCA occlusion but
STE in aVR > V1 -- more suggestive of LMCA

STE in aVR should be interpreted in conjunction with the symptoms presented; and also, its significance would be rendered dubious in the presence of BBB.

5. Brugada Syndrome
Any physician living in this part of south east Asia (SEA) should have Brugada in mind when its typical coved-shape STE jumps out in right sided leads.  Brugada syndrome is now thought of to be more widespread than just confined to SEA population. It is related to channelopathies (particularly sodium channel) and is associated with sudden cardiac arrest in young population.

Brugada syndrome may be confused with RBBB but RBBB would present with ST dep, NOT STE!

6. AF with underlying WPW
It is often difficult to suspect whether the AF is associated with underlying WPW.

However, WPW should be strongly suspected if the following features are seen in the AF:
  • an irregularly irregular (with wide complexes) [by this virtue, AF should be suspected]
  • a fast ventricular response up to 300 - 600/s
  • a changing, (often bizzare) morphology

Anyway, delta wave in WPW might not be seen. However, short PR interval should be seen in almost all leads.

NEVER give ABCD drugs (Adenosine, B-Blocker, CCB, Dig) AND also should NOT give Amiodarone in WPW (although in many literature, including AHA guidelines, amiodarone is said to be safe in WPW. It is not! See an article on this here).

The drug that should or could be given in WPW is procainamide.
 
7. Prolonged QT interval
Technically prolonged QT interval is more than 400 ms; but for it to be dangerous of degenerating into Torsades, it often has to be more than 500 ms.

Grey-Turner Sign


Grey-Turner’s sign simply refers to the bluish discoloration of the flanks. The interesting thing about this sign is that whenever this sign is found, medical students are alerted to the fact that there is a possible underlying retroperitoneal bleeding going on.  Obviously, this sign could also indicate a possible intraperitoneal bleed besides the possibility of retroperitoneal bleed. The source of bleed could be traumatic or non-traumatic, as in hemorrhagic pancreatitis.

However, when British surgeon George Grey Turner (1877-1951) first described it in 1920, in the British Journal of Surgery, it was described as a sign of hemorrhagic pancreatitis.

Not many know about the pathophysiologic basis of this sign, however.  It is actually due to the action on the abdominal wall and skin of leaking extravasated pancreatic juice from the hemorrhagic or necrotizing pancreatitis tracked subcutaneously. It could also be the blood collection tracked subcutaneously from retroperitoneal organs in the flank region.

In this picture, CT scan was done; showing no evidence of retroperitoneal or intraperitoneal bleed. This patient had an intramuscular bleeding resulting in the bruise. Does this considered as a Grey Turner sign? But how do we know conclusively whether retroperitoneal bleed has actually occurred  without performing a CT scan? Isn't Grey-Turner sign a clinical sign?

Grey-Turner sign can be accompanied by another sign, the Cullen sign; also of similar pathophysiologic basis but at a different location. Grey-Turner refers to bruising at the flank; Cullen sign refers to bruising at the periumbilical region.

Grey-Turner vs Cullen: How to remember which is which?
The way I remember which is Grey-Turner and which is Cullen:

C = Cullen = Central abdomen (periumbilical)

Grey-Turner is the other one, then ("periphery", flank)

Elderly Abuse in Malaysia


The official visit by the undergraduate students and their lecturers from Tzu Chi University from Taiwan ended a week ago.
 
During that visit, I talked about elderly care and abuse, particularly within the Malaysian context because I feel this is one area which is not very much talked about, not easily detected, and in fact, what we know is probably the tip of the iceberg only. This forum would also provide a space for our students to interact with the Taiwanese students as Taiwan has a good legal provision for the elderly, although Professor Hanson Huang (extreme right in front row, pic) from this team of Tzu Chi university said that the problem still remains a concern as the issue is not the law, but the implementation of the law.

In Malaysia, elderly is defined as one who is “60 years and over”  (adapted from: United Nations World Assembly on Ageing, Vienna, 1982). Some would further divide them into the  “young old”, aged 55-75 years old, and the “old old”, aged above 75 years old.

Unfortunately, many of us as healthcare professionals have narrow perception on what health is. We often define health as an “absence of disease” as defined by Sidell (1995).

On the other hand, the World Health Organization (WHO) gives a more wholistic definition of health:


“the state of complete physical, mental and social well-being” (World Health Organization,1995)

The elderly population in Malaysia has increased from 5.9% in 1991 to 6.5% in 2000. And it is expected that the proportion of people age 60 years and above in 2020 would increase further to 9.5% (Sherina et al, 2005). The life expectancy of Malaysian men and women in 1957 was 55.8 years and 58.2 years respectively, but today, it is 71 for men and 74 for women.

Contrary to what many believe, elderly abuse is not only confined to physical abuse, but, may also be sexual, or emotional abuse or neglect

WHO defines elderly abuse as:
"a single or repeated act, or lack of appropriate action, occurring within any relationship where there is an expectation of trust which causes harm or distress to an older person" (World Report on Violence and Health, World Health Organization, 2002)
As mentioned, elderly abuse can be:
  • Physical abuse
  • Sexual abuse
  • Emotional and psychological abuse
  • Financial exploitation
  • Neglect
  • Abandonment
Many believe that elderly abuse only occurs in nursing homes. But the truth is, more often than not, the abuser is a close relative – 80% being spouses and children of the victims or a close relative.
Another common myth is that elderly abuse would not happen in rich families although in actuality, elderly affects all ethnic groups and cuts across all socio-economic and religious lines. Those at risk are most likely to be female, widowed, frail, cognitively impaired, and chronically ill.

According to the 4th Malaysian Population and Family Survey, by the National Population and Family Development Board (LPPKN) 2011, one in three Malaysian elderly (33%) aged 60 and above are abandoned and do not receive financial support from their children. Click here and here to read further.

The main problem is that unlike child abuse (where there is the Malaysia Child Act 2001 to provide a protective legal environment for children), elderly abuse per se is not an offence in Malaysia as there is no law to explicitly deal with this. The only way is to charge any perpetrator under the Penal Code or Domestic Violence Act for physical abuse.

Under the Malaysian Domestic Violence Act 1994 (Act 521), domestic violence means the commission of any of the following acts:
willfully or knowingly placing, or attempting to place, the victim in fear of physical injury;
causing physical injury to the victim by such act which is known or ought to have been known would result in physical injury; 
compelling the victim by force or threat to engage in any conduct or act, sexual or otherwise, from which the victim has a right to abstain; 
confining or detaining the victim against the victim's will; or 
causing mischief or destruction or damage to property with intent to cause or knowing that it is likely to cause distress or annoyance to the victim
by a person against—
    his or her spouse;
    his or her former spouse;
    a child;
    an incapacitated adult
    any other member of the family. 
Under the domestic violence act 1994, the main issue of course is the fact that many of the more subtle forms of abuse such as emotional abuse, neglect and financial exploitation would be difficult to be legally charged.

Questions:
From your experience is elderly abuse? Why or why not?
What steps can you contribute to combat this society ill?


References:
Sidell, M. (1995) Health in Old Age: Myth, Mystery and Management, Buckingham: Open University Press.
Sherina M, Sidik Rampal L, Aini M, Norhidayati MH. The prevalence of depression among elderly in an urban area of Selangor, Malaysia. Int Med J. 2005;4(2):57-63.

Heuristics and Cognitive Biases in Decision Making During Clinical Emergencies

When faced with a potential clinical emergency situation, physicians are often expected to make diagnostic decisions within a limited time frame. A delayed decision, albeit an accurate one, is a futile decision if the patient deteriorates. Therefore, as almost always, such urgent decisions have to be made with some degree of uncertainty. This is especially so in an environment like the emergency department.



Physicians in emergency department make many decisions in the course of a working shift, some of which can have high consequences. Furthermore, emergency departments often have unpredictable and variable patient volume load as well as clinical acuity. Given the unfavorable nature of such environment, emergency department is often a place that is vulnerable to error. Under such circumstances, a physician in emergency situation often employs a compendium of heuristics (Croskerry et al, 2009).

Heuristics are mental shortcuts or “rules of thumb” or “gut-feeling” (Croskerry et al, 2009) used to assist a physician to rapidly make decisions without formal analysis. It is largely a form of gestalt pattern recognition that is intuitive and its accuracy is dependent on the experience of the physician. Two heuristics that are considered essential when faced with an emergency situation are the “rule-out-worst-case-scenario” and the sick/not sick dichotomy (Croskerry et al, 2009).

When properly applied, these heuristics can be beneficial, but they will occasionally spell disaster when a number of cognitive biases are overlooked. Among the important cognitive biases in clinical medicine are:
  1. availability bias – it refers to our tendency to judge things as being more likely, or frequently occurring, if they readily come to mind. Therefore, a recent experience with a disease might inflate our likelihood to diagnose the patient with this disease
  2. anchoring – it refers to out tendency to perceptually fixate on to the salient features in the patient’s initial presentation at an early point of the diagnostic process and failing to adjust our initial impression even in the light of later information. 
  3. confirmation bias - it refers to our tendency to look for confirming evidence to support the diagnosis we are “anchoring” to, while downplaying, or ignoring or not actively seeking evidences that point to the contrary. 
  4. search satisficing – it refers to our tendency to stop looking for alternate or even coexisting diagnoses when we have found one. A classic example of this is the tendency of the physician to call off the search for a second fracture once he thinks he is “sufficiently satisfied” with finding the first fracture (Croskerry et al, 2009).
Actually there is a long list of cognitive biases (but the four listed are the common ones in emergency medicine) taken from a book written by Baron, J. Professor Baron has done significant works in this area of judgment, decision making and cognitive biases (not specifically pertaining to emergency medicine, but in general). Check out his website for more resources.  Also see the list of cognitive biases in wikipedia.


Ultimately however, the application of heuristics in clinical medicine is inevitable, particularly in emergency situations where every minute counts. For example, in a case of witnessed ventricular fibrillation (VF), immediate step of resuscitation and defibrillation is called for. In such cases, the physician must be trained with the ability for gestalt pattern recognition of VF even within the ‘blink’ of an eye. No time should be lost in searching for the underlying causes of the ventricular fibrillation.

The question, therefore, is not whether the use of heuristics can be minimized or not. The question is how we can temper heuristics with de-biasing strategies so that a more calibrated and balanced diagnostic decision could be made. Such de-biasing strategies are often called cognitive forcing strategies. These are deliberate, systematic self-regulatory cognitive mechanisms to provide a check and balance to minimize biases.
One form of cognitive forcing strategy often used is known as the metacognition. It describes an individual’s ability to stand apart from his own thinking in order to be aware of his own preferred learning approaches and ultimately to manipulate his own cognitive processes to his own advantages. In short, metacognition is “thinking about thinking.” It allows one to ask questions like: “How well did I do?” “What could I have done it differently if I am given a chance again?”, etc.

Therefore, making a timely, well-calibrated decision in an emergency situation is a critical thinking skill that should be inculcated in every physician. In fact, critical thinking in emergency medicine is defined as “the intellectually disciplined process of actively and skillfully conceptualizing, applying, analyzing, synthesizing, and/or evaluating information gathered from, or generated by, observation, experience, reflection, reasoning or communication, as a guide to belief or action” (Croskerry et al, 2009).

It is often assumed that every medical student would have developed this critical thinking skill by the time they have graduated from medical schools and would continue to further mature their cognitive process when they start working. After all, university graduates are expected to have a scholarly attitude towards knowledge and university is expected to be more than just a center for knowledge transmission (Biggs & Tang, 2007).

Unfortunately, within the specific context of undergraduate medical curriculum, the expectation that medical students will eventually develop matured critical thinking skill is largely empirical and yet to be explored or formally studied.

Furthermore, studies done in other field of tertiary education show potential cultural influence on critical thinking skill acquisition among undergraduate students. In fact, these differences have led to discussions and debates about the appropriateness of applying Western pedagogy for Asian students.

From some of these studies, it was shown that Asian university students are less likely to engage in critical thinking compared to their Western counterparts. In many Asian countries, the teaching and learning activities are often exam-driven in large-sized classrooms and structured around the goal of succeeding in examinations (Biggs & Watkins, 2001). Furthermore, Asian learners are usually perceived as silent, passive, uncritical and compliant rote-learners who rely on memorization (Biggs and Watkins, 1996); although paradoxically, despite of this rote-based learning strategy, Asian learners have often been found to outperform their Western counterparts (Biggs and Watkins, 2001).

Even within Malaysia, our tertiary students are found to be rather reserved about voicing their own opinions. One of these culturally influenced perceptual learning styles is their preference to be neutral, to “save face” as well as to adopt a conservative rather than confrontational approach (Yong, 2010).


The questions therefore are:

What is the preferred learning style of our medical students – passive rote learning or active engagement in discussion and challenges? And is this preference culturally influenced?

Does this pedagogy preference translate into the way our house officers deal with their seniors with they have a different opinion compared to their seniors? Do they passively comply with following orders or do they actively engage in discussion with them?

How does that affect our house officers when they face with a decision-making situation in clinical emergencies? Do they passively leave the decision to their seniors? What is their risk preference – they do prefer to choose a riskier alternative to “do something for the patient” (much like a gambling paradigm) or do they rather choose a more conservative approach of “wait and see”?

Do our house officers, therefore, perceive a chasm in the acquisition of the decision-making skill in clinical emergencies during their transition from being a student in medical school to being a newly qualified doctor? In other words, do they perceive that their medical schools do not prepare them enough for critical thinking and decision-making skills?
Professor Croskerry has written a substantial number of articles and books on these topics. Click here to download an article by Prof Croskerry.

References:

Biggs, J. B. & Watkins, D. A. (1996) In Asian Contributions to Cross-Cultural Psychology (Eds, Paudey, J., Sinha, D. and Bhawuk, D. P.) Sage Publication, New Delhi.

Biggs, J. B. & Watkins, D. A. (2001) In Teaching the Chinese Learner: Psychological and Pedagogical Perspectives(Eds, Watkins, D. A. and Biggs, J. B.) Comparative Education Research Centre, the University of Hong Kong, Hong Kong, China, pp. 277-300.

Biggs, J. B., & Tang, C. (2007). Teaching for Quality Learning at University: What the Students Does (3rd ed.). New York, NY: Open University Press.

Croskerry, P. (2009). A universal model of diagnostic reasoning. Acad Med, 84(8), 1022-8.

Croskerry, P., Cosby, K., Schenkel, S. M. & Wears, R. L. (2009) Patient Safety in Emergency Medicine, Wolters Kluwer Health/Lippincott Williams & Wilkins, Philadelphia.

Yong, F. L. (2010). A Study on the Cultural Values, Perceptual Learning Styles, and Attitudes Toward Oracy Skills of Malaysian Tertiary Students. Europ. J. Soc. Sci., 13, 478-92.

Severe Sepsis Talk by Emmanuel Rivers (Originally posted in EMCrit Blog)

Early goal directed therapy (EGDT) is a series of targeted treatment measures directed aggressively and as early as possible for the first 6 hours for patients with severe sepsis and septic shock. The EGDT was first conceptualized by Emmanuel Rivers. The EGDT was well known through a landmark paper published in NEJM (looking back, this paper is already 10 years old!):



Rivers E., Nguyen B., Havstad S., et al: Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 345. (19): 1368-1377.2001
EMCrit Blog recently featured Part 1 of a talk by Dr. Rivers on severe sepsis. EMCrit has graciously provided, not just the audio mp3 version of the lecture, but the pdf slide handouts and, best of all, the video mp4 download of the powerpoint slide with lecture. All for FREE download. Please click here for all the FREE downloads.

Embedded below is Part 1 of the talk originally posted in EMCrit.  If you have not subscribed to EMCrit RSS feeds, I would encourage you to do so by clicking on this RSS link. The audio of this Part 1 may be a little soft, but if you connect to a speaker or if you use a headset, that should be clear enough.



Part 2. Original post at http://emcrit.org/podcasts/rivers-sepsis-ii/

Part 3. Original post at http://emcrit.org/podcasts/rivers-sepsis-iii/

Prehospital Care in Malaysia and Kendrick Extrication Device

This talk was the first lecturer that I gave during the Prehospital Care course that I conducted for the Red Crescent volunteers of Penang Branch Malaysia. This slide was prepared based on a commentary journal article that I wrote together with Dr. Hiang Chuan Chan from Kuching Sarawak.
Red Crescent members demonstrating the use of KED. They have a designated Kancil car to be used for their training purposes. One of the fastest way to slip in a spinal board for rapid extrication is through the back bonnet door
These guys and gals from the Penang Red Crescent are really a nice group of people - they are warm and friendly, and I learned much from them even as I shared with them whatever that I know. In fact, they were more "expert", in fixing devices like immobilizing the spine using Kendrick Extrication Device (KED) (picture below).
Image: Wikipedia, filed under Wikimedia Commons
KED is a device designed by Rick Kendrick back in the 1978-79 that allows for total spinal immobilisation during extrication. In fact, Rick Kendrick has invented the latest version known as the KOED (Kendrick Other Extrication Device).
Advantages of KED:
  • Because KED is designed to enclose the torso and cervical spine in a rigid frame, it prevents flexion, extension and rotation movements of the spine.
  • KED can be quickly and easily inserted into the seat of a vehicle by a single rescuer, and thereby, allows access to the airway even in a restrained space such as being trapped in a vehicle.
Disadvantage of KED
  • KED may take time to secure; in my estimation, at least two minutes in order to properly maintain the cervical spine and at the same time to properly tighten up the straps. Therefore, KED should typically be used only on hemodynamically stable victims; unstable victims may need to be extricated using rapid extrication techniques without the prior application of the KED.
One of the issues we were discussing during the Prehospital Care course in Red Crescent Penang is
should you bring the leg straps under the leg, criss-cross to the other side for strapping,
or
should you just strap it around the same side?
When I did a bit of search from the internet, it seems that this issue is a rather debatable issue until now among the community of prehospital care providers (read a forum here).
Well, according to the inventor himself, Rick Kendrick, it really doesn't matter (watch the video below)
The bottom line is:
If you suspect a groin injury, do not criss-cross the straps; just strap them on the same side.
And if you suspect a pelvic injury, it is advisable not to strap at all in case that you exert too much external rotatory movement that may aggravate an open book pelvic injury.
Otherwise, you may wish to cross them if you are comfortable with that. I personally find criss-crossing the straps a rather unnecessary and tedious steps, especially for female victims as you do not want to "accidentally" touch unnecessary regions.
Here is a video clip where the operator did not cross the leg straps:
And here is another clip where the operator criss-crossed the straps:
Hope that shed some light on the KED.
Another thing about the Red Crescent team that impressed me is their rather simple but innovative alternative to commercial splints.
This, I believe, is an effective and economical solution if you have limited fund to buy commercial splints like the Hare traction. After all, if you are only transporting for a short distance of time, what different would that make between self made splints and commercial splints? All you want is a solid enough splint for immobilization, reduce movement and thus reduce pain and swelling (as a temporary measure).