January 2016www.hkmacme.org
香港醫學會THE HONG KONG
MEDICAL ASSOCIATION
by Dr. LEUNG Wai Ching
by Dr. HUEN Kwai Fun
Dr. YOUNG Hong Ming, Jack
Night Eating Syndrome, Weight Gain and Psychiatry
Stay Alert to Increasing Life-threatening Hyperglycemic Hyperosmolar Syndrome in Obese children and adolescents
持 續 醫 學 進 修 專 訊
B U L L E T I N
HKMA CME Bulletin
Editorial 1
Spotlight 1 2Night Eating Syndrome, Weight Gain and Psychiatry
Spotlight 2 7Stay Alert to Increasing Life-threatening Hyperglycemic Hyperosmolar Syndrome in Obese children and adolescents
Cardiology 15A 27-year-old lady with shortness of breath
Dermatology 17An elderly man with purplish papules on the leg
Complaints & Ethics 18
Answer Sheet 20
CME Notifications 21
Meeting Highlights 23
CME Calendar 26
Contents
持續醫學進修專訊
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Please read the fol lowing art icles and answer the
questions. Participants in the HKMA CME Programme
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(2865 0943) or by mail to the HKMA Secretariat on
or before 15 February 2016. Answers to questions
will be provided in the next issue of the HKMA CME
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www.hkmacme.org)
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Spotlight 1Night Eating Syndrome,
Weight Gain and
Psychiatry
Spotlight 2Stay Alert to Increasing
Life-threatening
Hyperglycemic
Hyperosmolar Syndrome
in Obese children and
adolescents
NOTICEMedical knowledge is constantly changing. Standard safety precautions must be followed, but as new research
and clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary
or appropriate. Readers are advised to check the most current product information provided by the manufacturer
of each drug to be administered to verify the recommended dose, the method and duration of administration, and
contraindications. It is the responsibility of the practitioner, relying on experience and knowledge of the patient, to
determine dosages and best treatment for each individual patient. Neither the Publisher nor the Authors assume any
liability for any injury and/or damage to persons or property arising from this publication.
Although all advertising material is expected to conform to ethical (medical) standards, inclusion in this publication does
not constitute a guarantee or endorsement of the quality or value of such product or of the claims made of it by its
manufacturer.
EDITORIAL
Happy New Year.
This is the first issue of the Bulletin for 2016. Hope
everyone enjoys reading it and learns something on
hyperglycaemia and night eating.
Recently I heard some scattered noise on mandatory
CME for non-specialists from government officials.
Personally, I think CME is important for practicing
doctors, whether specialists or non-specialists. I am not
sure if it is important or practical to “quantify” learning
activities into CME points. I am not convinced by the
red-tape and controls packaged with compulsory CME.
The HKMA has always been against mandatory CME for
non-specialists, particularly linking CME with licensing
certificate. I do not think such noise about CME would
gain much momentum. However, since it is important, we
shall keep an eye on this issue and report to our members
if there is any progress. Just to reassure you, the stance
of HKMA has not changed.
In the mean time, let us continue our efforts in continue
medical education. If you have not registered with us,
please try to do so. We shall keep the records for you
and submit it to the Medical Council. We can show the
public that we do keep ourselves up without any so-called
mandatory measures.
Dr. CHENG Chi Man
Co-Chairman, CME Committee
CME Bulletin & Online Editorial Board
Chief Editor
Dr. WONG Bun Lap, Bernard 黃品立醫生
Executive Committee
Dr. CHAN Yee Shing, Alvin 陳以誠醫生Dr. CHENG Chi Man 鄭志文醫生Dr. CHEUNG Hon Ming 張漢明醫生Dr. CHOI Kin 蔡 堅醫生Dr. CHOW Pak Chin, JP 周伯展醫生Dr. HO Chung Ping, MH, JP 何仲平醫生Dr. HO Hung Kwong, Duncan 何鴻光醫生Dr. LAM Tzit Yuen, David 林哲玄醫生Dr. LI Sum Wo, MH 李深和醫生Dr. SHIH Tai Cho, Louis 史泰祖醫生Dr. TSE Hung Hing, JP 謝鴻興醫生Dr. WONG Bun Lap, Bernard 黃品立醫生
Cardiology
Dr. CHEN Wai Hong 陳偉康醫生Dr. HO Hung Kwong, Duncan 何鴻光醫生Dr. LEE Pui Yin 李沛然醫生Dr. LI Siu Lung, Steven 李少隆醫生Dr. WONG Bun Lap, Bernard 黃品立醫生Dr. WONG Shou Pang, Alexander 王壽鵬醫生Dr. WONG Wai Lun, Warren 黃煒倫醫生
Cardiothoracic Surgery
Dr. CHENG Lik Cheung 鄭力翔醫生Dr. CHIU Shui Wah, Clement 趙瑞華醫生Dr. CHUI Wing Hung 崔永雄醫生Dr. LEUNG Siu Man, John 梁兆文醫生
Colorectal Surgery
Dr. CHAN Cheung Wah 陳長華醫生Dr. LEE Yee Man 李綺雯醫生Dr. TSE Tak Yin, Cyrus 謝得言醫生
Dermatology
Dr. CHAN Hau Ngai, Kingsley 陳厚毅醫生Dr. HAU Kwun Cheung 侯鈞翔醫生Dr. SHIH Tai Cho, Louis 史泰祖醫生
Endocrinology
Dr. LEE Ka Kui 李家駒醫生Dr. LO Kwok Wing, Matthew 盧國榮醫生
ENT
Dr. CHOW Chun Kuen 周振權醫生
Family Medicine
Dr. LAM King Hei, Stanley 林敬熹醫生Dr. LI Kwok Tung, Donald, SBS, JP 李國棟醫生
Gastroenterologist
Dr. NG Fook Hong 吳福康醫生
General Practice
Dr. YAM Chun Yin 任俊彥醫生
General Surgery
Dr. LAM Tzit Yuen, David 林哲玄醫生Dr. Hon. LEUNG Ka Lau 梁家騮醫生
Geriatric Medicine
Dr. KONG Ming Hei, Bernard 江明熙醫生Dr. SHEA Tat Ming, Paul 佘達明醫生
Haematology
Dr. AU Wing Yan 區永仁醫生Dr. MAK Yiu Kwong, Vincent 麥耀光醫生
Hepatobiliary Surgery
Dr. CHIK Hsia Ying, Barbara 戚夏穎醫生Dr. LIU Chi Leung 廖子良醫生
Medical Oncology
Dr. TSANG Wing Hang, Janice 曾詠恆醫生
Nephrology
Dr. CHAN Man Kam 陳文岩醫生Dr. HO Chung Ping, MH, JP 何仲平醫生Dr. HO Kai Leung, Kelvin 何繼良醫生
Neurology
Dr. FONG Chung Yan, Gardian 方頌恩醫生Dr. TSANG Kin Lun, Alan 曾建倫醫生
Neurosurgery
Dr. CHAN Ping Hon, Johnny 陳秉漢醫生
Obstetrics and Gynaecology
Dr. CHAN Kit Sheung 陳潔霜醫生
Ophthalmology
Dr. CHOW Pak Chin, JP 周伯展醫生Dr. LIANG Chan Chung, Benedict 梁展聰醫生Dr. PONG Chiu Fai, Jeffrey 龐朝輝醫生
Orthopaedics and Traumatology
Dr. IP Wing Yuk, Josephine 葉永玉醫生Dr. KONG Kam Fu 江金富醫生Dr. POON Tak Lun 潘德鄰醫生Dr. TANG Yiu Kai 鄧耀楷醫生
Paediatrics
Dr. CHAN Yee Shing, Alvin 陳以誠醫生Dr. FUNG Yee Leung, Wilson 馮宜亮醫生Dr. TSE Hung Hing, JP 謝鴻興醫生Dr. YEUNG Chiu Fat, Henry 楊超發醫生
Plastic Surgeon
Dr. NG Wai Man, Raymond 吳偉民醫生
Psychiatry
Dr. LAI Tai Sum, Tony 黎大森醫生Dr. LEUNG Wai Ching 梁偉正醫生Dr. WONG Yee Him, John 黃以謙醫生
Radiology
Dr. CHAN Ka Fat, John 陳家發醫生Dr. CHAN Yip Fai, Ivan 陳業輝醫生
Respiratory Medicine
Dr. LEUNG Chi Chiu 梁子超醫生Dr. WONG Ka Chun 黃家進醫生Dr. YUNG Wai Ming, Miranda 容慧明醫生
Rheumatology
Dr. CHAN Tak Hin 陳德顯醫生Dr. CHEUNG Tak Cheong 張德昌醫生
Urology
Dr. CHEUNG Man Chiu 張文釗醫生Dr. KWOK Ka Ki 郭家麒醫生Dr. KWOK Tin Fook 郭天福醫生
Vascular Surgery
Dr. TSE Cheuk Wa, Chad 謝卓華醫生Dr. YIEN Ling Chu, Reny 顏令朱醫生
HKMA Secretariat
Ms. Jovi LAM 林偉珊女士Miss Sophia LAU 劉思妃小姐Miss Irene GOT 葛樂詩小姐
2 HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
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Night Eating Syndrome,Weight Gain and Psychiatry
NIGHT EATING SYNDROME
The night eating syndrome (NES) was first described
by S tunka rd i n 1955 as a d i so rde r de f i ned by
morning anorexia, evening hyperphagia (consuming
25% of the daily food intake after the evening meal),
and insomnia. NES was original ly thought to be a
maladaptive response to stress in obese persons who
were unsuccessful in weight loss treatment. Attention
to NES was neglected until late 1990s, when the focus
of eating-related research shifted in response to the
growing prevalence of obesity in the United States.
Across the years, the diagnosis and definition of night
eating syndrome was constantly modified to aid the
better understanding of the syndrome.
In 2008, experts who attended the First International
Night Eating Symposium drafted the first consensus-
driven set of diagnostic criteria for NES (Allison et al.,
2010).
The diagnosis for Night Eating Syndrome include six
criteria.
The essential feature is that the person has significantly
increased food intake in the evening and/or nighttime;
and that is defined as 25% of food consumption after
the evening meal and at least two episodes of nocturnal
eating per week.
The second criteria emphasizes the awareness and
recall of the nocturnal eating episodes (because in
sleep-related eat ing disorder, the person has no
awareness of the nocturnal food intake).
The third criteria requires meeting three of the five core
features of night eating syndrome: lack of desire to eat
in the morning and/or breakfast is omitted on four or
more mornings per week, presence of a strong urge to
eat between dinner and sleep onset and/or during the
night, sleep onset and/or sleep maintenance insomnia
are present four or more mornings per week, presence
of a belief that one must eat in order to initiate or return
to sleep, mood is frequently depressed and/or mood
worsens in the evening.
The other three criteria, as in the DSM style, establish a
threshold for assessing the impact on the person. They
are (1) the disorder must be associated with significant
distress and/or impairment, (2) must be evidence for
at least three months, and (3) cannot be attributable or
secondary to other disorders.
The First International Night Eating Symposium Diagnostic Criteria.
A. The daily pattern of eating demonstrates a significantly increased intake in the evening and/or nighttime, as manifested by one or both of the following:
1. At least 25% of food intake is consumed after the evening meal
2. At least two episodes of nocturnal eating per week
B. Awareness and recall of evening and nocturnal eating episodes are present.
C. The clinical picture is characterized by at least three of the following features:
1. Lack of desire to eat in the morning and/or breakfast is omitted on four or more mornings per week
2. Presence of a strong urge to eat between dinner and sleep onset and/or during the night
3. Sleep onset and/or sleep maintenance insomnia are present four or more mornings per week
4. Presence of a belief that one must eat in order to initiate or return to sleep
5. Mood is frequently depressed and/or mood worsens in the evening
D. The disorder is associated with significant distress or impairment in functioning.
E. The disordered pattern or eating has been maintained for at least 3 months.
F. The disorder is not secondary to substance abuse or dependence, medical disorder, medication, or another psychiatric disorder.
Note. Reproduced from: Allison, K.C. Lundgren, J.D., O’Reardon, J.P., Geliebter, A., Gluck, M.E., Vinai, P., Stunkard, A.J. (2010). Proposed diagnostic criteria for night eating syndrome. International Journal of Eating Disorder, 43(3), 241-247.
Dr. LEUNG Wai Ching
MBBS (HK), FHKAM (Psych), FHKCPsych
Specialist in Psychiatry
3HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
SPOTlight -1
PHYSIOLOGY
With some lifestyle and cultural variation, we eat once
every four to six hours (breakfast, lunch and dinner).
Nighttime, however, is characterized by a prolonged
period of fasting associated with sleep.
Under normal physiological condit ions, there is a
consecutive absence of food intake for approximately
half of every 24 hours. However, energy homeostasis
is maintained through alterations in glucose regulation
and appetite modulation. Despite a lack of food intake,
serum glucose levels are adequately maintained
throughout the sleep period, this is in contrast to fasting
during sedentary wakefulness which demonstrates a fall
in glucose over 12 hours.
The homeostasis during sleep seems to be related to
five reasons.
Firstly, of course, we have reduced motor activity at
sleep and that lead to decreased glucose utilization.
Apart from the decreased motor activity, decreased
cerebral glucose activity is the other cause for the
homeostasis. This effect is particularly noted during
delta non-rapid eye movement (NREM) sleep which
is concentrated in the first half of the sleep period.
Positron emission tomography (PET) of NREM sleep
demonstrates a 40% reduction in glucose metabolism
compared to wakefu lness. Conversely, PET has
demonstrated that glucose utilization in the brain during
REM sleep, primarily in the second half of the sleep
period, is as high as and occasionally higher than during
wakefulness. This correlates with glucose utilization data
in the second half of the sleep period which is closer to
wakefulness.
The third reason for the homeostasis during sleep
is growth hormone secretion at sleep onset. When
we start to sleep, growth hormone is released and it
stimulates hepatic gluconeogenesis and inhibits glucose
uptake; and the glucose level therefore increases. Apart
from that, increased insulin disposal during sleep is the
other reason for the elevated glucose level during sleep.
F ina l l y , Lept in , a pept ide hormone secreted by
adipocytes p lays the ro le of mainta in ing energy
homeostasis during sleep. Leptin level rises at night and
associates with onset of sleep. It inhibits hunger centers
in the hypothalamus during condition of energy surplus.
It is a satiety hormone.
CLINICAL CHARACTERISTICS
Night eat ing syndrome gets a prevalence which
increases along with body mass index. In a study of
106 night eaters (Zwaan, 2006), the mean BMI was in
the obese range (BMI=31); although 1/4 of the subjects
had a BMI <25. Also, when compared to obese control,
NES individuals have more awakening and awakening
involves eating. It tends to occur during non REM sleep.
It more often starts during early adulthood and runs by
period of remission and exacerbation. NES associates
with stress events and tends to have family history.
Var ious studies showed that NES has no gender
preference and has no obvious racial differences.
Common comorbidities include obesity, eating disorder,
depressive disorder, anxiety disorder, primary insomnia
and drugs abuse.
TreatmentPharmacological treatment
Previous researches noticed that central nervous system
serotonin modulation may help the treatment of NES.
A randomized double blinded, placebo controlled trial
on the efficacy of sertraline was conducted. Thirty-
four patients with NES were randomized to either
8-weeks course of sertraline (n=17) or placebo (n=17).
After 8 weeks, it found that 12 of the 17 subjects in
the sertraline group improved while only 3 of the 17
subjects in the placebo group improved. In addition,
the improvement in the primary outcome measure
d id not corre late wi th the per formance on Beck
Depression Inventory. That means the night eating
symptoms improvement was not the result of the mood
improvement.
4 HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
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Apart from sertraline, evidence also suggested that
topiramate, an anti-epileptic drug with anorexic effects,
can be effective in reducing symptoms of NES with
PTSD; 8 months treatment with topiramate improved
the abnormal feeding pattern in a patient and led to 32
kg of weight reduction.
O’Reardon reviewed 23 patients of NES. Among them,
16 took sedating agents (primarily zolpidem). None
of the cases were reported to have improvement. In
addition, zolpidem was found to be associated with
amnestic nocturnal eating.
Cognitive Behavioral Therapy (CBT)
It was found that the core belief in NES is that “If I
don’t eat, I won’t be able to fall asleep.” Therefore,
the essential features of CBT is to shift food intake
earlier and to correct the distorted thinking about the
relationship between eating and sleep onset.
The whole set of CBT includes psychoeducation about
sleep hygiene and healthy eating schedule. For example,
to limit the intake of alcohol, caffeine and water before
sleep and to maintain a regular sleep time.
Eating modification is an important component and
includes using food diary for monitoring, taking a regular
eating habit, establishing control over environmental
factor, gradually increasing morning intake and reducing
night intake, leaving bedroom to eat and using response
prevention for craved foods.
Apart from that, relaxation exercises and cognitive
restructuring are also important parts of CBT.
Going further – Weight Gain (Metabolic Syndrome) in Psychiatric Treatment
From author’s own experience in psychiatry, among
the various reasons for non-compliance and premature
drop out, the side effect of weight gain is one of the
most important reasons. By having more understanding
about weight gain in psychiatric treatment, we can
engage the patients in follow-up; and thus helping
them to keep remission. More importantly, we noticed
a clear association between metabolic syndrome and
psychiatry; and we identified that metabolic syndrome
increased the mortal ity and morbidity because of
cardiovascular risk (heart disease and stroke).
Why do the psychiatric patients get more weight gain and metabolic syndrome?
Up to now, we have evidence and we can postulate a
lot of reasons for the association between weight gain
(metabolic syndrome) and psychiatric patients. The
author summarized the cause as: A) Genetic factors B)
Lifestyle factors C) Medications factors and D) Hormonal
factors.
Genetic factors
An at-risk al lele of type 2 diabetes, rs7903146(T),
has been found in the transcription factor 7-l ike 2
(TCF7L2) gene and this genotype is also associated
with an increased risk of schizophrenia (Hansen, 2011).
Associations between weight gain in patients with
schizophrenia and various genetic polymorphisms have
also been identified.
Lifestyle factors
Psychiatric patients have a higher tendency towards
physical inertia (depressive patients can have more
inactivity and schizophrenia patients can have negative
symptoms) and poor eating habits (higher tendency
towards overeating and consuming unbalanced high
amount of fat and carbohydrate).
Medication factors
Firstly, we have a tendency to use second generation
antipsychotics for the patients because they have less
extrapyramidal side effects when compared with the
first generation ones. However, second generation
antipsychotics lead to more weight gain; that side effect
is more prominent in clozapine and olanzapine. The
following table compares the weight gain side effects
among different second generation antipsychotics.
5HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
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S e c o n d - g e n e r a t i o n a n t i p s y c h o t i c s a n d w e i g h t g a i n (metabolic syndrome)
Ranking on the basis of relative risk for development of metabolic syndrome
1. Clozapine (highest risk)
2. Olanzapine
3. Quetiapine
4. Risperidone
5. Amisulpride
6. Aripiprazole
7. Ziprasidone (lowest risk)
From the table, of course, Ziprasidone is the best choice
when we consider the ‘risk of weight gain and metabolic
syndrome’. The second generation antipsychotics lead
to weight gain because they are 5-HT2c antagonist.
5HT2c antagonist increases insulin resistance and
reduces glucose uptake by skeletal muscles and
therefore increases r isk of diabetes. In addit ion,
antipsychotics compete with histamine for binding sites
on the H1 receptors, therefore lead to sedation and
reduced metabolic rate.
C o n s i d e r i n g t h e a n t i d e p r e s s a n t s , t r i c y c l i c
antidepressants (TCA) and mirtazapine were well known
for the side effects of weight gain. Selective Serotonin
Reuptake Inhibitor (SSRI), although may lead to nausea
and dyspepsia at the beginning, long-term use may lead
to weight gain. From the author’s experience, when
considering the risk of weight gain, Norepinephrine and
Dopamine Reuptake Inhibitor (NDRI) and Serotonin
Norepinephrine Reuptake Inhibitors (SNRI) can be better
choices. SNRI seems to be neutral to weight gain on
average. NDRI may sometimes lead to weight loss.
Antidepressants and weight gain (metabolic syndrome)
Ranking on the basis of relative risk for development of metabolic syndrome
1. Noradrenergic & Specific Serotonergic Antidepressants (NaSSA) (e.g. Mirtazapine) (highest risk)
2. Tricyclic Antidepressants (TCA)
3. Selective Serotonin Reuptake Inhibitor (SSRI)
4. Serotonin Norepinephrine Reuptake Inhibitors (SNRI) (e.g. Venlafaxine, Desvenlafaxine/Duloxetine)
5. Norepinephrine and Dopamine Reuptake Inhibitor (NDRI) (e.g. Bupropion) (lowest risk)
Hormonal factors
I n c a s e o f d e p r e s s i o n , t h e a c t i v a t i o n o f t h e
hypothalamic-pituitary-adrenal (HPA) axis causes
elevation of cortisol level; and the increase in cortisol
level gives rise to pseudo-Cushing’s syndrome which
results in dyslipidaemia, adiposity, hyperinsulinaemia
and insulin resistance. At the same time, depression
leads to chronic increase in leptin. Both the increase
in insu l in and lept in s t imu la te the sympathet ic
nervous system; and this leads to increase in blood
catecholamine level and subsequently faulty glucose
metabolism and finally results in deposition of abdominal
fat.
Summary
Weight gain is one of the commonest challenges among
our psychiatric patients. In this article, we introduced
“Night Eating Syndrome”. The essential feature of night
eating syndrome is that the person has a significantly
increased food intake in the evening and/or nighttime;
and that is defined as 25% of food intake consumed
after the evening meal and at least two episodes
nocturnal eating per week.
About its treatment, evidence tell us that sertraline
and topiramate can help but zolpidem may sometimes
worsen the condition.
Psychiatr ic patients gain more weight because of
various interactive reasons. We can classify them into
genetic factors, lifestyle factors, medication factors and
hormonal factors.
Among the second generation antipsychotics, clozapine
and olanzapine have the highest risk for weight gain and
metabolic syndrome while ziprasidone has the lowest
risk.
Among the antidepressants, NaSSA and TCA have the
highest risk for weight gain. SNRI seems to be neutral to
weight gain on average; and NDRI may sometimes lead
to weight loss.
6 HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
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References
1. Kelly C. Alison, PhD, Ellen P. Traves, MA. Treatment of Night Eating Syndrome. Psychiatr Clin N Am 34 (2011) 785-796.
2. Allison KC, Lundgren JD, O’Reardon, J, et al. Proposed diagnostic criteria for night eating syndrome. Int J Eat Disord 2010;43:241-7.
3. Michael J. Howell, Carlos H. Schenck, et al. A review of nighttime eating disorders. Sleep Medicine Reviews (2009) 13,23-24.
4. Zwaan M, Roeriq DB, Crosby RD, Karaz S, Mitchell JE. Nighttime eating: a descriptive study. Int J Eat Disord 2006; 39:224-32.
5. Jillon S. Vander Wal. Night eating syndrome: A critical review of the literature. Clinical Psychology Review 32 (2012) 49-59.
6. Cyrus S.H. Ho, Melvyn W.B. Zhang, et al. Metabolic syndrome in psychiatry: advances in understanding and management. Advances in psychiatric treatment (2014), vol.20, 101-112.
7. Stunkard AJ Allison KC. Two forms of disordered eating in obesity: binge eating and night eating. Int J Obesity Relat Metab Disord 2003;27:1-12.
8. Hansen T, Ingason A, Djurovic S, et al (2011) At risk variant in TCF7L2 for type 2 diabetes increases risk of schizophrenia. Biological Psychiatry, 70: 59-63.
Answer these on page 20 or make an online submission at: www.
hkmacme.org Please indicate whether the following statements are true or
false.
1. NES is defined as 50% of food intake consumed after evening.
2. Leptin inhibit the hunger centre in hypothalamus during condition of energy surplus.
3. Depressive Disorder and anxiety disorder are common comorbidities in NES.
4. Sertraline may relieve symptoms in NES.
5. Zolpidem was found to be associated with amnestic nocturnal eating.
6. At-risk allele of type 2 diabetes, rs7903146(T) i s assoc ia ted w i th i nc reased i nc idence o f schizophrenia.
7. Clozapine does not lead to weight gain.
8. NDRI lead to severe weight gain.
9. In depressed patients, sometimes increased cortical level are found.
10. Depression lead to chronic reduction in Leptin.
Self-assessment questions:
Complete thiscourse and earn
1 CME PointQ&A
Answers to December 2015
Spotlight – Fat Grafting in Post-mastectomy Patients
1. T 2. F 3. T 4. F 5. T 6. F 7. F 8. F 9. T 10. T
香港醫生網The Hong Kong Doctors Homepage
www.hkdoctors.org
This web site is developed and maintained by the Hong Kong Medical Association
for all registered Hong Kong doctors to house their Internet practice homepage. The
format complies with the Internet Guidelines which was proposed by the Hong Kong
Medical Association and adopted by the Medical Council of Hong Kong.
We consider a practice homepage as a signboard or an entry in the telephone
directory. It contains essential information about the doctor including his specialty and
how to get to him. This facilitates members of the public to communicate with their
doctors.
This website is open to all registered doctors in Hong Kong. For practice page design
and upload, please contact the Hong Kong Medical Association Secretariat.
由香港醫學會成立並管理的《香港醫生網》,是一個收錄本港註冊西醫執業網頁的網站。內容是根據由香港醫學會擬訂並獲香港醫務委員會批准使用的互聯網指引內的規定格式刊載。
醫生的「執業網頁」性質與電話索引內刊載的資料相近。目的是提供與醫生執業有關的基本資料,例如註冊專科及聯絡方法等,方便市民接觸個別醫生。
任何香港註冊西醫都可以參加《香港醫生網》。關於網頁版面安排及上載之詳情,請與香港醫學會秘書處聯絡為荷。
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SPOTlight -2
HKMA CME Bulletin 持續醫學進修專訊 January 2016
Stay Alert to Increasing Life-threatening Hyperglycemic Hyperosmolar Syndrome in Obese children and adolescents
INTRODUCTION
Obesity has become a pandemic health care issue.
The proportion of overweight children has tripled since
19601. Most children diagnosed with Type 2 Diabetes
(T2DM) are overweight or obese2. The incidence of
T2DM has increased 10-fold in the last 20 years3. In
pediatric diabetic clinics, up to 45% of patients have
T2DM. It is estimated that nearly 4% of newly diagnosed
pediatric T2DM will have hyperglycemic hyperosmolar
syndrome4.
HYPERGLYCEMIC HYPEROSMOLAR SYNDROME HHS
This is a l i fe-threatening complicat ion commonly
associated with uncontrolled T2DM in adults. The
syndrome is characterized by severe hyperglycemia,
a marked increase in serum osmolality, and clinical
evidence of dehydration without the accumulation of
β -hydroxybutyric or acetoacetic ketoacids. There is a
variable alteration in sensorium. The syndrome had been
rarely reported in children. However, recent case series
describing HHS in children suggest the incidence of this
disorder is increasing5.
C o n s e n s u s s t a t e m e n t b y A m e r i c a n D i a b e t e s
Association
• Plasma glucose level ≥600mg/dl (33mmol/L)
• Effective serum osmolality ≥ 320mOsm/kg
• Profound dehydration (typically 8 to 12L)
• Small ketonuria, absent to low ketonemia
• Bicarbonate ≥15mmol/L
• Some alteration in consciousness
PATHOPHYSIOLOGY6
In a diabetic patient with pre-existing insulin deficiency
or resistance, a physiologic stress can cause further
net reduct ion in the ef fect iveness of c i rcu lat ing
insulin. Concomitant elevations in counter regulatory
hormones contr ibute to impaired glucose use in
the peripheral tissues. Hypercortisolemia increases
proteolysis which leads to the production of amino
acid precursors for gluconeogenesis and glucagon
induces glycogenolysis. The combination of hepatic
glucose production and decreased peripheral glucose
use is the main pathogenic etiology for hyperglycemia
in HHS. Hyperglycemia leads to glycosuria, osmotic
diuresis, and dehydration. As serum concentrations
of glucose exceed 10mmol/L, the kidney’s capacity
to reabsorb glucose is exceeded. The presence of
glucose in the urine impairs the concentrating capacity
of the kidney and exacerbates water loss. If the patient
is unable to maintain adequate f luid intake, these
water losses further decrease kidney perfusion which
markedly exacerbates the hyperglycemia. It is this renal
insufficiency in HHS that allows for the extremely high
levels of glucose seen with this disorder, resulting in
severe hyperosmolarity and intracellular dehydration.
The alteration in consciousness seen in HHS directly
corresponds to the elevation in effective osmolarity and
may be related to intracellular cerebral dehydration,
Dr. HUEN Kwai Fun
MBBS, FRCPCH, FHKCPaed, FHKAM(Paed)
Consultant Paediatrician, Department of Paediatrics &
Adolescent Medicine, Tseung Kwan O Hospital
Dr. YOUNG Hong Ming, Jack
MBBS, MRCPCH, FHKCPaed, FHKAM(Paed)
Paediatrician, Department of Paediatrics & Adolescent
Medicine, Tseung Kwan O Hospital
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HKMA CME Bulletin 持續醫學進修專訊 January 2016
changes in neurotransmitter levels, and microischemia.
In the osmotic diuresis, free water is lost in excess of
electrolytes, but there is also a large loss of sodium,
potassium, magnesium, and phosphate in the urine.
The full development of HHS occurs over several days,
and the total body water deficit averages 8 to 12 L. The
reason for the absence of ketosis in HHS is not known.
It is proposed that insulin levels may be adequate to
prevent lipolysis and ketogenesis, yet inadequate to
facil itate peripheral glucose uptake and to prevent
hepatic gluconeogensis. Hyperosmolarlty itself may act
to decrease lipolysis and subsequent ketogenesis.
TRIGGERS
There is typically a trigger event. The most common
t r igger is in fect ion. Others are non-compl iance
with insulin, substance abuse, long-term steroid or
L-asparaginase use.
Carbonated carbohydrate fluid intake in large volumes
to relieve polydipsia may precipitate a more severe
presentat ion of DM. A study reported f ive cases
complicated by HHS required intensive therapy. Fluid
intake pr ior to admission in each case consisted
of between 5 and 12L of carbonated carbohydrate
beverages (cola, lemonade) and isotonic sports
drinks. These drinks typically contain approximately
40g of sugar and 15-120mg of sodium per 370ml.
Hyperglycemia is potentiated by ingestion of high
glucose, high sodium-containing drinks. Exacerbation
of hyperg lycemia worsens the osmot ic d iures is
with subsequent increase in loss of free water and
electrolytes and subsequent dehydration. When more
water than sodium is lost, hypernatremia sets in,
especially if ingested fluids are also high in sodium.
These cases reflect the worrying trend in western society
where soft drinks are replacing water.
• Teenagers (13-19y) 78%
• Boy 89%
• African-American 89%
• Family history of T2DM 67%
• Obesity 97%
• Acanthosis nigricans 72%
• Altered mental status 88%
Figure 1: Pathophysiology of HHS6
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HKMA CME Bulletin 持續醫學進修專訊 January 2016
to restore peripheral perfusion. Subsequently, 0.45%
to 0.75% NaCl should be administered to replace
the deficit (8-12L) over 24 to 48 hours, with a goal
of promoting a gradual decline in serum sodium and
osmolality. The specific choice for subsequent fluid
replacement is dependent on serum electrolyte and
glucose concentrations, urinary output, and clinical
hydration status. Serum sodium is recommended to
decline by 0.5mmol/L/hr. With adequate rehydration,
serum glucose concentrations should decline by about
5.0mmol/L/hr. Patient may be more dehydrated than
assumed because of obesity and frequent reassessment
of fluid balance and peripheral perfusion is necessary.
Central venous pressure monitoring may be helpful.
However, the benefit should be balanced against the
risks of thrombosis. Replacement of urinary loss is
recommended. 0.45% saline solution is recommended.
Fluid with higher sodium content may be acceptable for
replacement of urinary losses where there is ongoing
concern over adequate circulatory volume.
Ketosis in HHS is usually minimal and mild acidosis is
typically the result of hypoperfusion (lactic acidosis).
Therefore early insulin administration is unnecessary
in HHS and may increase the risk of death. Fluid
administration alone results in a substantial decline
in serum glucose as a result of di lution, improved
renal perfusion, and increased tissue glucose uptake
with improved circulation. The osmotic pressure that
glucose exerts within the vascular space contributes
to maintenance of blood volume in these profoundly
dehydrated patients. Therefore more rapid declines in
serum glucose concentration and osmolality after insulin
administration might lead to circulatory compromise
and thrombo-embolism unless there is adequate fluid
replacement. Patients with HHS have extreme deficits
of potassium, and the rapid insulin-induced shift of
potassium from the circulation to intracellular space can
result in arrhythmia. Insulin administration should be
considered when serum glucose concentrations are no
longer declining adequately (<2.7mmol/L/hr) with fluid
administration alone. Insulin should be considered earlier
in children with more severe ketosis and acidosis. Insulin
at 0.025 to 0.05 units/kg/hr can be used initially, with
the dosage titrated to achieve a decrease in glucose
concentration of 2.7-4.1mmol/L/hr. Insulin boluses are
Other common symptoms: vomit ing, polydipsia,
polyuria, abdominal pain, weight loss and headache.
Differential diagnosis includes any cause of altered
level of consciousness, including hypoglycemia,
hyponatremia, severe dehydration, sepsis and diabetic
ketoacidosis (DKA).
Table 1: Comparison between HHS and DKA8
HHS DKA
Serum glucose mmol/l ≥34 ≥14
Arterial pH >7.30 ≤7.30
Serum bicarbonate mmol/l >15 ≤15
Serum osmolality mmol/kg >320 ≤320
Anion gap mmol/L variable >12
Serum ketones None or Moderate
trace to high
Urine ketones None or Moderate
trace to high
Serum sodium mmol/L, mean (SD) 149(3.2) 134(1.0)
Serum potassium mmol/L, mean (SD) 3.9(0.2) 4.5 (0.13)
Urea mmol/L, mean(SD) 21.8(3.9) 11.4(1.1)
Creatinine μmol/L, mean(SD) 123.8(8.8) 97.2(8.8)
Lactate mmol/L, mean(SD) 3.9 2.4
Insulin pmmol/L, mean(SD) 270(50) 90(10)
GUIDELINES FOR TREATMENT OF HHS IN CHILDREN
Th is i s suggested by Lawson Wi lk ins Ped ia t r ic
Endocrine Society6. There is no prospective data
to gu ide t reatment of ch i ldren and adolescents
with HHS. Experience with adults and awareness
of the physiological differences between HHS and
DKA suggest a rational approach for children and
adolescents. All patients with HHS should be admitted
to ICU.
The goal of init ial f luid therapy is expansion of the
intravascular and extravascular volume and restoration
of normal renal perfusion. Aggressive fluid therapy is
indicated. A minimum initial bolus of 20ml/kg of isotonic
saline solution (0.9% NaCl) should be administered and
fluid deficits of ~12% to 15% of body weight should
be assumed. Additional fluid boluses should be given
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HKMA CME Bulletin 持續醫學進修專訊 January 2016
not recommended for pediatric patients. Unlike in DKA,
insulin therapy is not usually necessary for resolution of
ketosis in HHS and should be suspended if the glucose
concentration drops more than 5.5mmol/L/hr.
ELECTROLYTES REPLACEMENT
Electrolyte deficits, particularly potassium, phosphate,
and magnesium, are more extreme in HHS than DKA.
Potassium replacement should begin as soon as
potassium concentrations are within the normal range
and adequate renal function has been established.
Potassium replacement should be initiated at 40mmol/
L of replacement fluid, but higher rates of administration
may be needed af ter insu l in in fus ion is star ted.
Phosphate deficits are more severe in HHS. Severe
hypophosphatemia may lead to rhabdomyolysis,
hemolytic anemia or paralysis. Phosphate treatment
may contribute to hypocalcemia. Use of intravenous
solutions containing a 50:50 mixture of potassium
phosphate and potassium chloride permits adequate
phosphate replacement and avoids hypocalcemia.
Pat ients with HHS frequent ly have large def ic i ts
o f magnes ium. The re i s no da ta to de te rm ine
whether replacement of magnesium is beneficial.
Hypomagnesemia may occasional ly contr ibute to
hypocalcemia during therapy. Replacement should be
considered in patients with hypocalcemia and a low
magnesium concentration. The recommended dose for
magnesium replacement is 25 to 50mg/kg/dose for 3
to 4 doses given every 4 to 6 hours, with a maximum
infusion rate of 150mg/min or 2g/hr.
Figure 2: Treatment of HHS in pediatric patients6
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HKMA CME Bulletin 持續醫學進修專訊 January 2016
COMPLICATIONS
Thromboembolic complications occur commonly in
HHS. Central venous catheters appear to be particularly
prone to thrombosis. Prophylaxis with low dose heparin
has been suggested in adult, but there are no data
that indicate benefit. Low dose heparin administration
may cause gastrointestinal bleeding. Heparin treatment
should be reserved for children who require central
venous catheters for monitoring or venous access
and are immobi le for >24 to 48 hours . The use
of compression stockings should be considered.
Rhabdomyolysis is potentially life-threatening. It may
result in acute renal failure, severe hyperkalemia, and
hypocalcemia leading to cardiac arrest, and muscle
swelling causing compartment syndrome. Monitoring of
CK every 2-3 hours is recommended for early detection.
If rhadbomyolysis is suspected, consultation with a
nephrologist should be obtained promptly.
MALIGNANT HYPERTHERMIA-LIKE SYNDROME MHLS9
Malignant hyperthermia occurs when the muscle
calcium flux is disrupted, leading to depleted calcium
in the sarcoplasmic reticulum and increased calcium
in the myoplasm. It is most commonly described as a
condition triggered by anesthetic agents in genetically
susceptible patients. MHLS of unclear cause has been
reported in several children with HHS. Dantrolene may
reduce the release of calcium from the sarcoplasmic
reticulum and stabil ize calcium metabolism within
muscle cells. It should be initiated early for children who
have fever associated with a rise in CK.
CEREBRAL OEDEMA
CE is rare, unlike that of DKA. Declines in mental status
after improvement in the hyperosmolar state are unusual
and such declines should prompt further investigation.
Patient should be monitored closely for headache and
changes in level of consciousness. Severe dehydration,
electrolyte disturbance, and hypertonicity are far more
frequent causes of death in HHS than is CE. Concerns
about possible CE should not deter the clinician from
administering necessary amounts of fluid for adequate
hydration.
Data regarding the mortality of HHS in the pediatric
populat ion are st i l l l imited given the much lower
incidence compared with adults. Current consensus
estimates fatality at 20% to 60%.
POOR PROGNOSTIC FACTORS5
• Delay in diagnosis and treatment
• Failure to aggressively treat HHS
• Elevated creatinine kinase
• Coma
• Hypotension
• Serum osmolarity >350mOsm
CONCLUSION
Paediatric HHS is uncommon but potentially fatal. With
increasing childhood obesity and paediatric T2DM,
incidence of HHS may increase. HHS may be first
presentation of DM.
Family physicians should have a high index of suspicion
for T2DM in sick obese youngsters, especially those
with a family history of T2DM. One should appreciate the
difficulty of assessing hyperosmolar dehydration in the
obese youngsters. Check the urine for glycosuria and
note absence of ketosis – no vomiting or abdominal pain.
Be alert that neurological symptoms may be absent in
cases of severe, gradually developing hyperglycaemia,
symptomatic only if hypernatremia is also present.
Note that they have more gradual onset, longer
metabolic derangement and more dehydrated 15-20%
(vs 10% in DKA). Be aware that just before the acute
decompensation and coma, they typically take in large
amount of high glucose drinks to relieve the thirst and
weakness (paradoxically patient is committing suicide!).
Paediatricians can also make the situation worse
by wrong assessment and diagnosis, giving early
insulin and delaying aggressive fluid therapy! Do note
blood glucose (sky high, can be up to100 mmol/l) and
osmolality results can come back rather late!
本診所將於 至 休息,
並於年初 開診。
This clinic will be closed from
to for Lunar New Year.
如有緊急查詢,請致電
In an emergency, please contact
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HKMA CME Bulletin 持續醫學進修專訊 January 2016
It is essential for us to have high index of suspicion to
include HHS as a DDx in patients with hyperglycemia
and dehydrat ion increased our awareness of the
differences in management strategy between DKA
and HHS so as to improve the outcome in this life-
threatening disorderarly correct diagnosis, aggressive
fluid therapy with NS to reverse hypovolemic shock,
delay institution of insulin therapy, early recognition of
malignant hyperthermia-like syndrome and treatment
with dantrolene, early replacement of potassium and
phosphate and giving means to improve renal perfusion.
References
1. Smith J. The current epidemic of childhood obesity and its
implications for future coronary heart disease. Pediatr Clin North
Am 2004;51:1679-95.
2. American Diabetes Association. Type 2 diabetes in children and
adolescents. Pediatrics 1999; 105:671-80.
3. Ludwig D, Ebbeling C. Type 2 diabetes mellitus in children. JAMA
2001;286:1427-30.
4. Fourtner SH, Weinzimer SA, Levitt Katz LE. Hyperglycemic
hyperosmolar non-ketotic syndrome in children with type 2
diabetes. Pediatr Diabetes Sep2005;6(3):129-35.
5. Cochran JB, Walters S, Losek JD. Pediatric hyperglycemic
hyperosmolar syndrome: diagnostic difficulties and high mortality
rate. Am J Emergency Medicine (2006) 24,297-301.
6. Zeitler P, Haqq A, Rosenbloom A, Glaser N for Drug and
Therapeutics Committee of the Lawson Wilkins Pediatric
Endocrine Society. Hyperglycemic Hyperosmolar Syndrome
in Children: Pathophysiological considerations and suggested
guidelines for treatment. The J of Pediatrics Vol 158, issue 1, Jan
2011, 9-14.e2.
7. McDonnell CM, Pedreira CC, Vadamalyan B, Cameron FJ,
Werther GA. Diabetic ketoacidosis, hyperosmolarity and
hypernatremia: are high-carbohydrate drinks worsening initial
presentation? Pediatr Diabetes Jun 2005;6(2):90-4.
8. Chiasson JL, Nahla AJ, Belanger R, Bertrand S, et al. Diagnosis
and treatment of diabetic ketoacidosis and the hyperglycemic
hyperosmolar state. Canadian Medical Association Journal Apr
1,2003;168(7).
9. Kibane BJ, Mehta S, Backeljauw PF, Shanley TP, Crimmins
NA Approach to management of malignant hyperthermia-like
syndrome in pediatric diabetes mellitus. Pediatr Crit Care Med
Mar 2006;7(2):169-73.
Answer these on page 20 or make an online submission at: www.
hkmacme.org Please indicate whether the following statements are true or
false.
1. Serum glucose, osmolality and sodium are much higher in HHS than DKA.
2. Sporty drinks and coco-cola are good for the patients with HHS to relieve the polydipsia and weakness.
3. Urine for multistix can help to differentiate between HHS and DKA.
4. It is easy to detect dehydration in obese adolescents with HHS because they have severe dehydration.
5. Family doctors can help to make an early diagnosis o f T2DM by a s imple ur ine test in an obese adolescent.
6. Aggressive isotonic fluid therapy is the key for the management of HHS.
7. Early insulin treatment is the key for the management of HHS.
8. Cerebral edema is common in HHS and is the main cause of death in these patients.
9. HHS carr ies a very high mortal i ty rate and is increasing in incidence in Hong Kong.
10. Be a l e r t t o t he comp l i ca t i on o f ma l i gnan t hyperthermia-like syndrome in patients with HHS with fever and rising creatine kinase.
Self-assessment Questions
Complete thiscourse and earn
1 CME PointQ&A
HKMC CME Bulletin
Monthly Self-Study Series
Call for Articles
Since its publication, the HKMA CME Bulletin has become one
of the most popular CME readings for doctors. This monthly
publication has been serving more than 9,000 readers each
month through practical case studies and picture quizzes. To
enrich its content, we are inviting articles from experts of different
specialties. Interested contributors may refer to the General
Guidance below. Other formats are also welcome.
Deadline: All manuscripts for publication of the month should reach
the Editor before the 1st of the previous month.
For further information, please contact
Miss Sophia Lau at 2527 8452 or by email at [email protected].
All articles submitted for publication are subject to review and
editing by the Editorial Board.
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Cardiology
HKMA CME Bulletin 持續醫學進修專訊 January 2016
A 27-year-old lady with shortness of breathMs. X was a 27-year-old lady who enjoyed good past health. She complaint of progressive shortness of breath on
exertion in recent one week, associated with bilateral ankle swelling. On admission, her blood pressure was on low
side 90/60. She was mildly tachypneic in room air. Physical examination was unremarkable except bilateral pitting
oedema up to knees.
Her ECG (Figure 1) and CXR (Figure 2) were shown below.
Blood tests including complete blood picture, liver and renal function test were unremarkable. She had normal
lipid and sugar profile. However, echocardiography showed very poor left ventricular ejection fraction of 20%, all
chambers were dilated, there was moderate mitral and tricuspid regurgitation.
Complete BOTH Cardiology andDermatology courses and earn
0.5 CME POINT
The content of the January Cardiology Series is provided by:
Dr. CHEUNG Ling Ling MBBS(HK), MRCP(UK), FHKCP, FHKAM(Med), Specialist in Cardiology
一月臨床心臟科個案研究之內容承蒙張玲玲醫生提供。
Figure 1 Figure 2
Q&A Please answer ALL questions
Answer these on page 20 or make an online submission at: www.hkmacme.org
1. What is shown in Figure 1? 3. What is shown in Figure 3?
2. What is shown in Figure 2? 4. What is your management?Figure 3
MRI was ordered for workup of congestive heart failure and images were shown below.
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Cardiology
HKMA CME Bulletin 持續醫學進修專訊 January 2016
December Answers
Answers:
1. E 2. C 3. C
This gent leman was admitted for recent infer ior
myocardial infarction (MI) complicated by cardiogenic
shock secondary to rupture papillary muscle. The most
common etiology of cardiogenic shock in such clinical
setting is patient with left ventricular failure, but it can
also be caused by mechanical complications, such
as acute mitral regurgitation (MR), ventricular septal
rupture or free wall rupture.
Delayed hospitalization (≥24 hours), undue in-hospital
physical activity, and post-infarction angina increased
the risk of mechanical complications in predisposed
patients.
The causes of acute MR after acute MI inc lude
ischemic papillary muscle displacement (previously
known as papi l lary muscle dysfunction) with left
ventricular dilatation, and papillary muscle or chordal
rupture.
Pap i l l a r y musc le rup tu re i s a l i f e - th rea ten ing
complication that accounts for approximately 5% of
deaths in acute MI patients. It usually occurs two to
seven days after the infarct. The rupture may be partial
(occurring at one of the muscle heads) or complete.
Because of differences in blood supply, rupture of the
posteromedial papillary muscle occurs more frequently
than rupture of the anterolateral papillary muscle.
The posteromedial papillary muscle is supplied with
blood from the posterior descending artery, while the
anterolateral papillary muscle has a dual blood supply
from the left anterior descending and left circumflex
arteries.
The clinical manifestations of papillary muscle rupture
include acute onset hypotension and pulmonary edema
with a new mid- or pansystolic murmur that may have
widespread radiation.
The diagnosis of papillary muscle disease after MI
is typically confirmed by echocardiography. Two-
dimensional transthoracic echocardiography usually
demonstrates a f lai l segment of the mitral valve,
and a severed papil lary muscle can frequently be
seen moving freely within the left ventricular cavity.
Color flow Doppler can demonstrate the presence of
severe mitral regurgitation. In some cases, however,
transthoracic echocardiography is not informative
and transesophageal echocardiography (with addition
3D images, see Figure a) is required to establish
the diagnosis. Left ventricular function is usually
hyperdynamic as a result of ventricular contraction
against the low impedance left atrium.
Figure a. 3D TEE of mitral valve viewed from left atrial
side. The partially ruptured posteromedial papillary
muscle (red arrow) is seen popping into left atrium
during systole
Prompt diagnosis and initiation of medical therapy
and emergent su rgery a re a l l necessary fo r a
favorab le ou tcome. Med ica l the rapy inc ludes
aggressive afterload reduction with nitrates, sodium
nitroprusside, diuretics, and intraaortic balloon pump
counterpulsation. Afterload reduction decreases the
regurgitant fraction, thereby increasing forward flow.
Emergent surgical intervention remains the treatment of
choice for papillary muscle rupture.
Mortality of patients with papillary muscle rupture
are higher than those with other causes of ischemic
mitral regurgitation, with an operative mortality rate
of about 50%; however, the outcome is worse with
medical therapy with a mortality of 75% at 24 hours
and 95% within two weeks after complete papillary
muscle rupture. Risk factors for worse outcomes after
surgery include older age, female gender, and poor left
ventricular systolic function.
The content of the December Cardiology Series is provided by:
Dr. CHUI Shing Fung
MBChB (CUHK), MRCP (UK), FHKCP, FHKAM (Med), Specialist in Cardiology
Dr. WONG Chi Yuen
MBBS (HK), MRCP (UK), FHKCP, FHKAM (Med), Specialist in Cardiology
十二月臨床心臟科個案研究之內容承蒙徐城烽醫生及黃志遠醫生提供。
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Dermatology
HKMA CME Bulletin 持續醫學進修專訊 January 2016
1. What is the most likely diagnosis?
2. What are the differential diagnoses?
3. What is the underlying cause of these lesions?
4. How do you diagnose the skin disease?
5. What are the treatment options?
Q&A Please answer ALL questions
Answer these on page 20 or make an online submission at: www.hkmacme.org
December AnswersAnswers:
1. The differential diagnoses include scabies,
urticaria, papular eczema, drug eruptions and
insect/arthropod bites.
2. The diagnosis is insect/arthropod bites.
3. The cause is probably due to bedbugs. It is a
parasitic arthropods from the family Cimicidae.
They are less than 1 cm in length and reddish
brown in colour. They can be found in furniture,
f loorboards, peel ing paint or commonly in
areas of clutter. They come out at night with
peak feeding t imes just before dawn. They
are attracted by sweating, body heat, carbon
dioxide or ordour of human body.
4. The classical presentation makes the diagnosis
and no investigation is needed. The typical
bedbugs presentation is erythematous papules
sometimes with urticarial components in a linear
group of 3 – called “breakfast, lunch and dinner”
(see the clinical photo).
5. Treatment of bedbug bites is not usual ly
requ i red. Top ica l s te ro id cream or ora l
antihistamines can be used for symptoms
relief. Topical antibiotic or antiseptic lotion is
used for secondary bacterial infections. The
home environment should be maintained clean
and advice from insect control and elimination
experts may be needed to reduce and finally
eliminate the bedbugs in living environment.
The content of the December Dermatology Series is provided by:
Dr. KWAN Chi Keung, Dr. TANG Yuk Ming, William,
Dr. CHAN Hau Ngai, Kingsley and Dr. LEUNG Wai Yiu
Specialists in Dermatology & Venereology
十二月皮膚科個案研究之內容承蒙關志強醫生、鄧旭明醫生、陳厚毅醫生及梁偉耀醫生提供。
An elderly man with purplish papules on the legA 70-year-old man with background ischemic heart disease and diabetes presented with a few asymptomatic
papules on his lower leg for 6 months. There was no history of trauma or insect bite. He had previous history of
similar lesions which regressed with intralesional injection. He had no systemic symptoms otherwise. (Figure)
Complete BOTH Cardiology andDermatology courses and earn
0.5 CME POINT
Dermatology Series for January 2016 is provided by:
Dr. CHANG Mee, Mimi, Dr. TANG Yuk Ming, William, Dr. CHAN Hau Ngai, Kingsley,
Dr. KWAN Chi Keung and Dr. LEUNG Wai Yiu
Specialists in Dermatology & Venereology
一月皮膚科個案研究之內容承蒙張苗醫生、鄧旭明醫生、陳厚毅醫生、關志強醫生及梁偉耀醫生提供。
Multiple purplish papules with neighbouring
yellowish-brown pigmentation on lower leg.
Complaints & Ethics
18 HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
A physiotherapist sent me a Chr istmas card last
week. He attached a letter with the card which I am
reproducing here:
Dear Dr. Choi,
Not long ago, a representative of a doctor came to
my clinic to see if there is any chance of co-operation.
Immediately I understood what she meant. I told her
that for 30 years of my practice, I had no financial
arrangement or connection with any doctor. She was
stunned and exclaimed, ‘How can you have patients?’ ‘I
was lucky that I survived, and I don’t want to change my
policy’. I said.
Yes, I am lucky that there are some good doctors who
refer patients for physiotherapy solely for the benefits of
the patients, and you are one of them!
May I take this opportunity during the Great Season
to express my greatest gratitude to thank you for all
your support. Your referrals are the most posit ive
confirmation to my treatments for which I am always
trying my best to improve and aim at the highest
standard of healing patients.
Wishing you Merry Christmas and a prosperous Happy
New Year 2016!!!
Again my many thanks!
Best regards,
Physiotherapist
I am trying to persuade the physiotherapist to reveal
the name of the doctor whose representative was trying
to solicit fee-splitting through referrals. This is not only
considered serious professional misconduct by the
Medical Council, but may incur a jail sentence for the
culprit. ICAC and the HKMA collaborated over a decade
ago to produce a booklet on those scenarios which may
not be allowed and which may bring the doctor to court.
This would be one of those scenarios and I am surprised
that some doctors may have forgotten the implication,
even when they are doing the dirty work behind the back
of the administrators they hired.
Over 3 decades ago when I first started private practice,
I received a phone call from a colleague who was not
a local graduate. He asked me how much rebate I
would be paying him for each referral. It was a slow day
and I curtly replied that at $300 per consultation plus
medication, I could not afford to rebate him anything.
Many years later, I still pick up complaints to the PIC
even from foreign medical graduates practicing in Hong
Kong. A specialist complaint that his GP colleagues
asked for kickbacks for the surgical cases they refer to
him. Even then, secret audio recording was made use of
and the complaint went even to ICAC.
Doctors have asked in the past whether i t was
appropriate to surrender their incomes to their landlords
to facilitate rental determination. I have advised that a
clinic’s rental should not be determined by the clinic’s
income, which varies day to day. To base rental on
clinic income may amount to fee-splitting of patient’s
consultation fee which is not permissible according to
our Code of Conduct.
Fee splitting, again MBBS (HK), MFM (Clin)(Monash), LRCP (Lond), MRCS (Eng), MRCP (UK), FRCP (Irel), FHKCP, FRACGP, FHKCFP, DFM (CUHK), FHKAM (Medicine), FHKAM (Family Medicine), DCH (Lond), DOM (CUHK), DPD (Cardiff), PDipID (HK), PDipComPsychMed (HK), PDipCommunityGeriatrics (HK), Dip Ger Med RCPS (Glasg)Specialist in NephrologyDr. CHOI Kin
Complaints & Ethics
19HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
HKMA was recently informed that some members were
asked about their consultation fees before deciding on
their professional indemnity charges. In a recent meeting
with the heads of the MPS, I had openly expressed that
this approach is inappropriate and the doctors’ incomes
should only be the knowledge of the Inland Revenue
Department and no one else.
The HKMA Council met with the Privacy Commissioner
earlier this month. I raised this issue of the landlord
and the MPS trying to obtain knowledge of income
before deciding rental and professional indemnity fees.
According to Ms. Joanna CHAN, Senior Personal Data
Officer, Office of the Privacy Commissioner for Personal
Data (PCPD), data requested in the two examples
seemed excessive. Besides, the collection of data
was not done in a fair way and for personal interest.
Mr. Stephen WONG Kai Yi, Privacy Commissioner for
Personal Data, advised that one could try to bargain to
provide income range, and to review the Memorandum
and Articles of Association of MPS to see if its practices
were within purview. He further suggested that members
forced to divulge the income may complain to the PCPD
for the case to be reviewed.
HKMA can only stand firm to fight on members’ behalf if
members stand firm with the HKMA. Are we ready for a
fight?
20 HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
ANSWER SHEET
Answer Sheet
January 2016
答題紙
Name 姓名 Signature簽名:
HKMA Membership No. or HKMA CME No.香港醫學會會員編號或持續進修號碼:
Contact Tel No.聯絡電話:
HKID No. 香港身份証號碼: - xxx(x)
Dermatology
1
2
3
4
5
Complete BOTH Cardiology & Dermatology cases and earn 0.5 CME point
Please return thecompleted answer sheetto the HKMA Secretariat(Fax: 2865 0943) on orbefore 15 February 2016for documentation.If you completethe exercise online,you are NOT required toreturn the answer sheet byfax.請回答所有問題,並於2016年2月15日前將答題紙傳真或寄回香港醫學會 (傳真號碼:2865 0943)。如果選擇在網上完成練習,便無需將答題紙傳真到秘書處。
SPOTlight - 2Complete Spotlight and earn 1 CME point
1 2 3 4 5 6 7 8 9 10
Cardiology
Please answer ALL questions and write the answers in the space provided.
SPOTlight - 1Complete Spotlight and earn 1 CME point
1 2 3 4 5 6 7 8 9 10
1
2
3
4
21HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
REPLY SLIP
HKMA New Territories West Community Network Fax: 2865 0943Seminar on Management of Common Breastfeeding Problems:What Primary Care Doctors Need to Know and Practice?
I would like to register for the above event. Please “✓” as appropriate
Name: HKMA No.:
Mobile No.*: Fax No.:
*Please fill in your updated mobile number so that you can be notified of your application via SMS. If you do not have a mobile phone,
the Secretariat will still issue a confirmation letter to you.
Practising location: In New Territories West (Please specify *: )
Others (Please specify: )
* Null entry will be treated as non-New Territories West member registration.
Signature: Date:
Data collected will be used and processed for the purposes related to this event only.
Date : Thursday, 18 February 2016
Speaker : Dr. FOK Oi Ling, Annie
Medical & Health Officer, Family Health Service Head Office, Department of Health
Time : 1:00 – 2:00 p.m. Registration & Lunch
2:00 – 2:45 p.m. Lecture
2:45 – 3:00 p.m. Q & A Session
Venue : Plentiful Delight Banquet(元朗喜尚嘉喜酒家),
1/F., Ho Shun Tai Building, 10 Sai Ching Street, Yuen Long
Moderator : Dr. TSUI Fung
Hon. Secretary, HKMA NT West Community Network
Deadline : Monday, 1 February 2016
Fee : Free-of-charge
Capacity : 48. Registration is strictly required on a first come, first served basis.
Priority will be given to doctors practising in NT West district.
Enquiry : Miss Hana YEUNG, Tel: 2527 8285
*Please call and confirm that your facsimile has been successfully transmitted to the HKMA
Secretariat if you do not receive confirmation 14 days before the event.
CME Accreditation : Pending
THE HONG KONGMEDICAL ASSOCIATION
Seminar on Management of Common Breastfeeding Problems:What Primary Care Doctors Need to Know and Practice?
Co-organized by
The HKMA New Territories West Community Network
and Primary Care Office of the Department of Health
CMEnotifications
22 HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
REPLY SLIP
HKMA KW & KE Community Networks Fax: 2865 0943CME Lectures in February 2016
I would like to register for the following lecture(s): Please “✓” as appropriate
16 February 2016 (KW) 18 February 2016 (KE)
Name: HKMA No.:
Mobile No.*: Fax No.:
*Please fill in your updated mobile number so that you can be notified of your application via SMS. If you do not have a mobile phone, the Secretariat will still issue a confirmation letter to you.
Practising location: In Kowloon West (Please specify *: )
In Kowloon East (Please specify *: )
Others (Please specify: )
* Null entry will be treated as non-Kowloon West or non-Kowloon East member registration.
Signature: Date:
Data collected will be used and processed for the purposes related to these events only.
Organizer : HKMA Kowloon West Community Network HKMA Kowloon East Community Network
Date : Tuesday, 16 February 2016 Thursday, 18 February 2016
Topic and Speaker : Common Medical Emergencies in GP SettingDr. LIT Chau Hung, AlbertChief of Service, Accident & Emergency Dept.,Princess Margaret Hospital & North Lantau Hospital
The Changing Scenario of Chronic Ischemic Heart Disease:Focus on Diabetic Coronary PatientsDr. TING Zhao Wei, RoseSpecialist in Endocrinology, Diabetes & Metabolism
Time : 1:00 – 2:00 p.m. Registration & Lunch2:00 – 2:45 p.m. Lecture2:45 – 3:00 p.m. Q&A Session
Venue : Crystal Room IV-V, 3/F., Panda Hotel,3 Tsuen Wah Street, Tsuen Wan, N.T.
V Cuisine, 6/F., Holiday Inn Express Hong Kong Kowloon East, 3 Tong Tak Street, Tseung Kwan O
(將軍澳唐德街3 號香港九龍東智選假日酒店6 樓彩雲軒)Moderator : Dr. WONG Wai Hong, Bruce
Hon. Secretary,HKMA Kowloon West Community Network
Dr. MA Ping Kwan, DannyVice-chairman,HKMA Kowloon East Community Network
Deadline : Monday, 1 February 2016 Monday, 1 February 2016
Fee : Free-of-charge
Capacity : 50 48
Registration is strictly required on a first come, first served basis. Priority will be given to doctors practising in KW districts (for the lecture on 16 Feb)/KE districts (for the lecture on 18 Feb).
Enquiry : Miss Hana YEUNG, Tel: 2527 8285*Please call and confirm that your facsimile has been successfully transmitted to the HKMA Secretariat if you do not receive confirmation 14 days before the event.
Sponsor :
CME Accreditation : Pending
THE HONG KONGMEDICAL ASSOCIATION
CME Lectures in February 2016
CMEnotifications
23HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
Meeting Highlights
HKMA Structured CME Programme with Hong Kong Sanatorium & Hospital 2015
Dr. KWAN Wing Hong, Specialist in Radiology, delivered
a luncheon lecture on “Targeted Therapy for General
Practitioners” on Thursday, 10 December 2015 at the
HKMA Central Premises. Dr. LEE Fook Kay, Aaron, kindly
acted as the moderator for the event.
Dr. LEE Fook Kay, Aaron (right) presenting a souvenir to the speaker, Dr. KWAN Wing Hong, (left).
The HKMA Hong Kong East Community Network (HKECN) ~ Dr. CHAN Nim Tak, Douglas
Dr. MA Pui Shan, Specialist in Endocrinology, Diabetes & Metabolism, delivered a lecture on “A Pathophysiological Approach to
the Treatment of Type 2 Diabetes” on Thursday, 3 December 2015. Dr. CHAN Hoi Yee, Catherine, Specialist in Ophthalmology,
delivered a lecture on “Recent Development in DME Management” on Thursday, 17 December 2015.
Dr. Henry KONG (left, moderator) presenting a souvenir to Dr. Catherine CHAN (speaker) during the lecture on 17 December 2015
Dr. MA Pui Shan (left, speaker) receiving a souvenir from Dr. AU YEUNG Shiu Hing (moderator) during the lecture on 3 December 2015
HKMA CME
Dr. SO Man Kit, Thomas, Specialist in Infections Disease,
delivered a lecture on “Interferon & Infections” on Friday,
18 December 2015 at the HKMA Central Premises. Dr.
CHOI Kin, kindly acted as the moderator for the event.
Dr. CHOI Kin (right) presenting a souvenir to the speaker, Dr. SO Man Kit, Thomas (left).
24 HKMA CME Bulletin 持續醫學進修專訊 January 2016 www.hkmacme.org
Meeting Highlights
From left: Dr. Alvin YS CHAN, Dr. Michael CHAN (speaker) and Dr. Stanley LAM (moderator)
The HKMA Kowloon East Community Network (KECN) ~ Dr. AU Ka Kui, GaryDr. SO Man Kit, Thomas, Specialist in Infectious
Disease, presented on “Shingles Prevention from
Infectious Disease Specialist’s Perspective” on
Thursday, 10 December 2015. The final session
of the “Certificate Course for GPs 2015” titled
“Update on DM Management” was given by
Dr. KAM Yee Wai, Grace, Consultant of the
Department of Medicine and Geriatrics of United
Christian Hospital, on Thursday, 17 December
2015.
The HKMA Kowloon West Community Network (KWCN) ~ Dr. TONG Kai Sing
Group photo taken during the lecture on 17 December 2015 From left: Dr. Gary AU, Dr. Grace KAM (speaker), Dr. Edmund SHA (moderator) and Dr. Danny MA
Dr. Danny MA (right, moderator) presenting a souvenir to Dr. Thomas SO (speaker) during the lecture on 10 December 2015
Group photo taken during the lecture on 1 December 2015 From left: Dr. CHAN Ching Pong, Dr. Bruce WONG (moderator), Dr. Kenneth TSUI (speaker) and Dr. Bernard CHAN
A CME lecture on “Advance in Rheumat ic
Diseases” co-organized by the Network and
Hong Kong Society of Rheumatology was given
by Dr. TSUI Hing Sum, Kenneth, Specialist in
Rheumatology, on Tuesday, 1 December 2015.
Another CME lecture on “Rosacea and Related
Dermatoses” was presented by Dr. LEE Tze Yuen,
Specialist in Dermatology & Venereology, on
Tuesday, 15 December 2015.
Dr. LIT Chau Hung, Albert, Chief of Service of Accident & Emergency Department
of Princess Margaret Hospital & North Lantau Hospital, is invited to give a talk on
“Common Medical Emergencies in GP Setting” on Tuesday, 16 February 2016.
Interested members please refer to the announcement on p.22 for details and
enrolment.
Group photo taken during the lecture on 15 December 2015From left: Dr. LEUNG Gin Pang, Dr. CHAN Ching Pong, Dr. Bruce WONG, Dr. TONG Kai Sing, Dr. LEE Tze Yuen (speaker), Dr. Raymond LAM (moderator) and Dr. Bernard CHAN
Dr. TING Zhao Wei, Rose, Specialist in Endocrinology, Diabetes & Metabolism, will
present on “The Changing Scenario of Chronic Ischemic Heart Disease: Focus on
Diabetic Coronary Patients” on Thursday, 18 February 2016. Interested members please
refer to the announcement on p.22 for details and enrolment.
The HKMA Yau Tsim Mong Community Network (YTMCN) ~ Dr. LAM Tzit Yuen, David
The lecture on “Complementary and Alternative Medicine (CAM) for Childhood
Asthma: An Overview of Evidence” was given by Prof. HON Kam Lun, Ell is,
Professor of Department of Paediatrics of The Chinese University of Hong Kong, on
Tuesday, 8 December 2015.
Prof. Ellis HON (left, speaker) receiving a souvenir from Dr. Thomas CHENG (moderator) during the lecture on 8 December 2015
25HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
Meeting Highlights
The HKMA Shatin Doctors Network (SDN) ~ Dr. FUNG Yee Leung, Wilson and Dr. MAK Wing Kin
Group photo taken during the lecture on 16 December 20152nd from left: Dr. John WONG (speaker)3rd from left: Dr. MAK Wing Kin (moderator)
Group photo taken during the lecture on 4 December 2015From left: Dr. Wilson FUNG, Dr. Daniel CHIU (speaker) and Dr. MAK Wing Kin (moderator)
The HKMA Central, Western and Southern Community Network (CW&SCN) ~ Dr. YIK Ping YinDr. Barbara CC LAM, JP, Specialist in Paediatrics, Honorary Consultant of Queen
Mary Hospital and Honorary Clinical Associate Professor of The University of Hong
Kong, delivered a lecture on “Early Infant Feeding & Allergic Disorders” on Wednesday,
2 December 2015.
Dr. YIK Ping Yin (right, moderator) presenting a souvenir to Dr. Barbara LAM (speaker) during the lecture on 2 December 2015
Dr. CHIU Cheung Shing, Daniel, Specialist in Paediatrics,
presented on “Allergy Management in Primary Care” on
Friday, 4 December 2015.
Dr. WONG Tai Hung, John, Special ist in Cardiology,
delivered a lecture on “Update on the Management of
Hypertension” on Wednesday, 16 December 2015.
The HKMA New Territories West Community Network (NTWCN) ~ Dr. CHEUNG Kwok Wai, Alvin
Dr. CHAN Yung, Specialist in Dermatology & Venereology, gave a talk on “New
Insight for Atopic Eczema Treatment” on Thursday, 17 December 2015.
A CME lecture on “Seminar on Management of Common Breastfeeding Problems:
What Primary Care Doctors Need to Know and Practice?” co-organized by the
Network and Primary Care Office of the Department of Health (DH) will be given
by Dr. FOK Oi Ling, Annie, Medical & Health Officer of Family Health Service Head
Office of DH, on Thursday, 18 February 2016. Interested members please refer to the
announcement on p.21 for details and enrolment.
Group photo taken during the lecture on 17 December 2015From left: Dr. CHAN Yung (speaker), Dr. Ivan CHUNG (moderator) and representative from sponsor
CMECalendar
26 HKMA CME Bulletin 持續醫學進修專訊 January 2016www.hkmacme.org
January 2016
19 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – Kwai Chung HospitalCAC Clinical Module – KCH Level 1 (Jan-Jun 2016) Topic 11: General Adult Psychiatry: Sleep disordersMeeting Room, 1/F, Admin Block, Kwai Chung HospitalMs. Kaman Chan – Tel: 2871 8717
2
19 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – Kwai Chung HospitalCAC Clinical Module – KCH Level 2 (Jan-Jun 2016) Topic 31: Child & Adolescent Psychiatry: Assessment of care support system and carer stressSeminar Room, 1/F, Admin Block, Kwai Chung HospitalMs. Kaman Chan – Tel: 2871 8717
2
19 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – Pamela Youde Nethersole Eastern HospitalHA – Queen Mary HospitalCAC Clinical Module – PYNEH & QMH Level 1 (Jan-Jun 2016) Topic 11: General Adult Psychiatry: Sleep disordersRoom 036, 1/F, East Block, PYNEHMs. Kaman Chan – Tel: 2871 8717
2
19 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – Pamela Youde Nethersole Eastern HospitalHA – Queen Mary HospitalCAC Clinical Module – PYNEH & QMH Level 2 (Jan-Jun 2016) Topic 31: Child & Adolescent Psychiatry: Assessment of care support system and carer stressJ5 Conference Room, QMHMs. Kaman Chan – Tel: 2871 8717
2
19 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – Kowloon HospitalHA – UCH-training centreCAC Clinical Module – KH & UCH Level 1 (Jan-Jun 2016) Topic 11: General Adult Psychiatry: Sleep disordersConference Room 103, 1/F, Block A, Kowloon HospitalMs. Kaman Chan – Tel: 2871 8717
2
19 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – Kowloon HospitalHA – UCH-training centreCAC Clinical Module -KH & UCH Level 2 (Jan-Jun 2016) Topic 31: Child & Adolescent Psychiatry: Assessment of care support system and carer stressMeeting Room, 3/F, Block P, United Christian HospitalMs. Kaman Chan – Tel: 2871 8717
2
20 Jan 2016(Wed)1:00 – 3:00 pm
HKDU – Wan Chai Study GroupCurrent Surgical Strategy in management of lumbar spinal problemLee Garden, Shop 1003, 10/F, Times Square, 1 Matheson Street, Causeway Bay, Hong KongMiss Cheng – Tel: 2388 2728
1
22 Jan 2016(Fri)4:30 – 6:00 pm
Hong Kong College of PsychiatristsHospital Authority – Kwai Chung HospitalCase Based Discussion GroupConference Room, KCHMs. Lucita Chan – Tel: 2871 8777
1
26 Jan 2016(Tue)1:00 – 3:00 pm
Hong Kong Medical Association – Kowloon West Community NetworkHow to Avoid being Brought to the PIC?Crystal Room IV-V, 3/F, Panda Hotel, 3 Tsuen Wah Street, Tsuen Wan, NTMiss. Hana Yeung – Tel: 2527 8285
1
26 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – Castle Peak Hospital-training centreCAC Clinical Module – CPH Level 1 (Jan-Jun 2016) Topic 12: General Adult Psychiatry: Assess suicidal risk after an episode of deliberate self harm, with subsequent verbal report to a consultant (Part I)Kaizen Room, Block D, Castle Peak HospitalMs. Kaman Chan – Tel: 2871 8717
2
26 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – Castle Peak Hospital-training centreCAC Clinical Module – CPH Level 2 (Jan-Jun 2016) Topic 32: Child & Adolescent Psychiatry: Assessment of early psychosisSeminar Room 4, Block F, Castle Peak HospitalMs. Kaman Chan – Tel: 2871 8717
2
26 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – New Territories East Cluster (training centre)CAC Clinical Module – NTEC Level 1 (Jan-Jun 2016) Topic 12: General Adult Psychiatry: Assess suicidal risk after an episode of deliberate self harm, with subsequent verbal report to a consultant (Part I)Multicentre Seminar Room, Tai Po HospitalMs. Kaman Chan – Tel: 2871 8717
2
26 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – New Territories East Cluster (training centre)CAC Clinical Module – NTEC Level 2 (Jan-Jun 2016) Topic 32: Child & Adolescent Psychiatry: Assessment of early psychosisMulticentre Seminar Room, Tai Po HospitalMs. Kaman Chan – Tel: 2871 8717
2
26 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – Kwai Chung HospitalCAC Clinical Module – KCH Level 1 (Jan-Jun 2016) Topic 12: General Adult Psychiatry: Assess suicidal risk after an episode of deliberate self harm, with subsequent verbal report to a consultant (Part I)Meeting Room, 1/F, Admin Block, Kwai Chung HospitalMs. Kaman Chan – Tel: 2871 8717
2
26 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – Kwai Chung HospitalCAC Clinical Module – KCH Level 2 (Jan-Jun 2016) Topic 32: Child & Adolescent Psychiatry: Assessment of early psychosisSeminar Room, 1/F, Admin Block, Kwai Chung HospitalMs. Kaman Chan – Tel: 2871 8717
2
26 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – Kowloon HospitalHA – UCH-training centreCAC Clinical Module – KH & UCH Level 1 (Jan-Jun 2016) Topic 12: General Adult Psychiatry: Assess suicidal risk after an episode of deliberate self harm, with subsequent verbal report to a consultant (Part 1)Conference Room 103, 1/F, Block A, Kowloon HospitalMs. Kaman Chan – Tel: 2871 8717
2
26 Jan 2016(Tue)3:30 – 5:30 pm
HK College of PsychiatristsHA – Kowloon HospitalHA – UCH-training centreCAC Clinical Module – KH & UCH Level 2 (Jan-Jun 2016) Topic 32: Child and Adolescent Psychiatry: Assessment of early psychosisMeeting Room, 3/F, Block P, United Christian HospitalMs. Kaman Chan – Tel: 2871 8717
2
27 Jan 2016(Wed)1:00 – 3:00 pm
Hong Kong Medical Association – Central, Western & Southern Community NetworkManagement of CKD Patients before and while on DialysisHong Kong Medical Association Central Premises, Dr. Li Shu Pui Professional Education Centre, 2/F, Chinese Club Building, 21-22 Connaught Road Central, Hong KongMiss Hana Yeung – Tel: 2527 8285
1
28 Jan 2016(Thu)1:00 – 3:00 pm
Hong Kong Medical Association – Hong Kong East Community NetworkUnicompartmental Knee Arthroplasty – Joint Replacement for The Active PatientsThe HKMA Wanchai Premises, 5/F, 15 Hennessy Road, WanchaiMs. Candice Tong – Tel: 2527 8285
1
28 Jan 2016(Thu)1:00 – 3:00 pm
Hong Kong Medical Association – Kowloon East Community NetworkOA Knee Handling in ElderlyPier 88, Shop 203. 2-3/F, Fung Tak Shopping Centre, Fung Tak Estate, Diamond HillMiss Hana Yeung – Tel: 2527 8285
1
28 Jan 2016(Thu)1:00 – 3:00 pm
Hong Kong Medical Association – New Territories West Community NetworkNew Horizons for Managing Type 2 Diabetes with High CV RiskGarden Room, G/F, Gold Coast Yacht and Country Club, 1 Castle Peak Road, Castle Peak Bay, Hong KongMiss Hana Yeung – Tel: 2527 8285
1
29 Jan 2016(Fri)1:00 – 3:00 pm
Hong Kong Medical Association – Yau Tsim Mong Community NetworkGetting to the Heart of Cardiovascular Risk in People with Type 2 DiabetesPearl Ballroom, Level 2, Eaton, Hong Kong, 380 Nathan Road, KowloonMs. Candice Tong – Tel: 2527 8285
1
29 Jan 2016(Fri)4:45 – 6:00 pm
Hong Kong College of PsychiatristsHospital Authority – Kwai Chung HospitalSeminar on Specific CBT Skill III (Topic: CBT for GAD)Conference Room, KCHMs. Lucita Chan – Tel: 2871 8777
1
5 Feb 2016(Fri)1:00 – 2:00 pm
Hospital Authority-Tuen Mun Hospital-Department of Obstetrics & GynaecologyMortality and Morbidity MeetingRoom SB1034 A&B, Conference Room, 1/F, Special Block, Tuen Mun HospitalMs. Angela Cheung – Tel: 2468 5404
1
13 Feb 2016(Sat)2:15 – 4:15 pm
Hong Kong Medical AssociationHong Kong College of Family PhysiciansHospital Authority – Our Lady of Maryknoll HospitalRefresher Course for Health Care Providers 2015/2016 – Primary Care Knee Problems Through the LifespanTraining Room II, 1/F, OPD Block, Our Lady of Maryknoll Hospital, 118 Shatin Pass Road, Wong Tai Sin, KowloonMs. Clara Tsang – Tel: 2354 2440
2