by dr. leung wai ching - hkma.org · dr. chen wai hong 陳偉康醫生 dr. ho hung kwong, duncan

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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Tel: 2527 8452 / 2861 1979

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Programme, a CME registration process has been created to document the CME

efforts of doctors and to provide special CME avenues. The Association strives to

foster a vibrant environment of CME throughout the medical profession. Both members

as well as non-members of the Association are welcome to join us. You may contact

the HKMA Secretariat for details of the programme.

Please read the fol lowing art icles and answer the

questions. Participants in the HKMA CME Programme

will be awarded credit points under the Programme

for returning the completed answer sheet v ia fax

(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

Bulletin. (Questions may also be answered online at

www.hkmacme.org)

HKMA CME Bulletin – MONTHLY SELF-STUDY

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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

SPOTlight -1

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.


SPOTlight -1

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.


SPOTlight -1

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.


SPOTlight -1

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.

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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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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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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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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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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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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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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.

15www.hkmacme.org

Cardiology


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.

16 www.hkmacme.org

Cardiology


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。

17www.hkmacme.org

Dermatology


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


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


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?


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


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


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


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


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


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

by dr. leung wai ching - hkma.org · dr. chen wai hong 陳偉康醫生 dr. ho hung kwong, duncan

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