Abcès Hépatique

Préparé par : Dr. Our kimlaing

Dr. Chim Prohos
Hospital Oreang Ov

2
 Abcès Hépatique
1 . Définition : suppurations collectées dans le
parenchyme hépatique causée
par :
- Bactérienne ( a pyogène)
- parasitaire ( amibienne)
- Fungique rare

3
A pyogène

4
 Physiopatologies
Etiologies des abcès hépatique a pyogène
+ porte d’entrée :
- Causes biliaire: lithiases , angiocholite…..
- Causes veins portales : diverticulite ,
appendicite , cancer colique ……
- Causes artérielle : abcès dentaire ,
infection voie ORL , infection
urinaire …..
5
 Physiopatologies
+ Germes responsables des abcès à pyogène
- Bactéries aérobies gram négatifs : E- coli ,
klebsiella pneumoniae , pseudomonas …..
- Bactéries aérobies gram positifs :
streptocoque , staphylocoque ….
- Batéries anaérobies : batériodes ,
fusobactérium …..

6
 Diagnostiques positif
• Clinique
- symptômes généraux: fièvre (39c) , frisson
asthénie , anorexie , amaigrissement
- symptômes locaux :douleurs HCD
- Examen : Hépatomégalie douleur
douleur à la palpation du foie

Triade de fontan: Douleur de l’HCD ,

HMG , Fièvre
7
 Paracliniques
• Biologie : NFS
- Hyperleucocytose>10000/mm3 à
prédominan polynucléaire neutrophile ,
CRP élevé
- Hémocultures: Systèmatique+++
Perturbation du bilan hépatique

8
 Paraclinique
- Echographie : - Image variable selon le stade évolutif de l’abcès
- Phase pré-suppurative : lésions hétérogène de contours irrégulier
- Phase suppurative : contenu hypo ou anéchogène contours arrondis a
parois nettes

9
 Paraclinique
- TDM abdomen : Image en cible

- Ponction: échoguidée pour comfirmé le

diagnostique. (antibiogramme)

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 Traitements
1 . Antibiothérapie

2 . Antibiothérapies + Traitement per cutané

-Ponction aspiration
-Drainage per cutané

3 . Drainage chirurgical

11
 Traitement
1 . Antibiothérapie
- Utilisation de Céphalosporine 3ème
géneration par voie intraveinense (01 à 2
semaines ) puis relais per os 4 à 6 semaines

12
 Traitement
2 . Antibiothérapie + Traitement per cutané
- Ponction aspiration sous échoguidée de
la phase de collection ( si taille < 5cm )
- Ponction drainage per cutané sous
échoguidée de la phase de collection
( si taille > 5cm)

13
 Traitement
3 . Drainage chirurgical
- En cas d’eçhec du traitement per cutané
- Abcès rompu ou fisulisé
- Abcès très cloisonné

14
Amibienne

15
 Indroduction
- Amibienne hépatque: protozoaire
( Entamoeba histolytica)
- Cause importante de mortalité d’origine
parasitaire
- diagnostique: imagerie + sérologies amibienne

16
 Epidémiologies
• Etiologies des abcès hépatique amibienne
- porte d’entrée :
- veins porte
- Voies biliaire
- Zones d’endémie : payes tropicaux
- Réservoir principal : homme
- intubation : anné selon immunitaire

17
 Diagnostiques positifs
• Cliniques:
- Forme aiguë typique : triade de Fontan
douleur d’HCD , HMG , Fièvre et Douleur
a la palpation en masse du foie
<< sigue de Blanc>>

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 Paraclinques
1. Biologies:
- NFS : Hyperleucocytose>10000mm3 à (PNN)
- CRP élevée
- Sérologie de l’amibiase (+++)
2. Imagerie :
- Echo : zones hypoéchogène
- TDM : Zones hypodense
3. Ponction écho-guidée <pus chocolat>

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 Traitements
1 . Anti-amibienne
- Métronidazole ( 500mg ) 1fl x 3 par jours
2 . Antibiothérapie : en cas surinfection
bactérienne.

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MERCI DE VOTRE
ATTENTION!

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OBSERVATION CLINIQUE MÉDICALE

Abcès du foie
Préparé Dr. OUR KIMLAING

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I-MOTIF D’ENTRÉE

Mas.. AAAAA âgé de 55 ans sex M venant de Phomi

Korng Chey, Khum Korng Chey, O reang Ov distrite
TBONG KHMOM Provint ,Il est entrée dans hôspital O
Reang Ov ; le 20 . 6 . 2022 à 9 h.00 mn pour la fièvre et
douleur de l’HCD

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 II.HISTOIRE DE LA MALADIE
• La maladie a rémonté depuis 4jours , Il est caractérisée au
début par la fièvre élevé s’accompagnée de frison et de
céphalée avec de douleur au niveau de l’ HCD à type
pésanteur à irradiatoin en arrière et en haut de l’omoplate
avec inspiration profond . A domicile il a été traitée par des
médicaments de types inconnue pendant 3 jours mais les signe
au dessus est augmenté . C’est motif d’entrée son
hospitalisation Oreang Ov.

24
III-ANTÉCÉDENT
o Médical
+ Personnel
- épisode dysenterie chronique
+ Familiales
- bonne santé
o Chirurgical
-Pas d’intervention chirurgicale auparavant.

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IV-EXAMEN CLINIQUE:Fait le 20 - 6 - 2022 à 9:00mn
A-Signes généraux et fonctionnels
- Etat général est peu altéré
- Conscience conservée
- Conjonctif et tégument peu pâleur
- Asthénie , anorexie ,insomnie , amaigrissement
- Fièvre , frison , céphalée
- Douleur de l’HCD
- TA : 100/70mmHg , Pouls : 110/mn , RR: 22/mn
- SpO2 97% , T o : 39,5 c
- poide : 60 kg

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IV-EXAMEN CLINIQUE( suite)
B-Examen physique
1- Appareil digestif

- Nausé et vomissement

- Douleur de l’HCD

- Hépatomégalie

-Ventre souple , Rate non palpable

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IV-EXAMEN CLINIQUE( suite)
2- Appareil respiratoire
- Cage thoracique: symétrique, respiration régulier
- RR : 22 /mn
- SpO2 : 97 %
- MV et VV : normaux
3- Appareil génito-urinaire
- Urine de coloration jaune
- Pas de contact lombaire ni de ballottement rénal

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IV-EXAMEN CLINIQUE( suite)
4- Système nerveux Central :

- Pas de signes :neurologique

29
 IV-EXAMEN CLINIQUE( suite)

5- Appareil cardio-vasculaire
- TA:100/70mmHg
- poul:110/min
- BDC : bien battants pas de souffle pathologique
- Rythme cardiaque est régulier
6- System cutanée muqueux
- Conjonctive et tégument sont légèrement pâles
- Pas d’ictère
7- Autres appareils
-Normaux

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 V-BILAN CLINIQUE
Il s’agit âgé de 55ans, ayant présenté dans son:
1. Histoire
- Fièvre brutale avec frison
- Douleur à type pesanteur au niveau de l’HCD à irradiation en arrière
et en haut vers l’omoplate
- Asthénie , nausée , anorexie ,insomnie , amaigrissement
2. ATCD :
- Episode dysenterie chronique
3. A l’examen
- Fièvre brutal
- Hépatomégalie
- Douleur de l’HCD
- Donc Je pense à une abcès du foie .

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VI- DIAGNOSTIC DIFFÉRENTIEL

1 - Cholécystite
2 - Lithiasique

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 VII- EXAMEN PARACLINQIUE

Pour confirmer le diagnostic et aider le traitement, on demande les

examens para cliniques suivantes:
- Hg
- Sérologie Amibias
- HBS : ( Ac , Ag ) , HCV
- Transamina , CRP ,
- Echo abdomen

33
VII- Echographie
Echographie: Une masse hypoéchogène , Bord irrégulier
D (4 x 5 cm )
Conclusion : Abcèse du foie stade pré-suppuratif

34
VII- EXAMEN PARACLINQIUE(suite)
Résultat 20. 6 . 2022 `a 10 h 00 mn
o Hg
NUMERATION GLOBULAIRE VALEURS NORMALS

LEUCOCYTES : 16.0 x109/l ( 4.00 - 10.0 )

HEMATIES : 4,6 x1012/l ( 4.50 - 5.50 )

Hématocrite : 41 % ( 37.0 - 47.0 )

Hémoglobine : 12,9 g/dl ( 12.0 - 15.0 )

V.G.M : 85.7 fl ( 85.0 – 95.0)

T.C.M.H : 33.0 pg ( 28.0 - 33.0 )

C.C.M.H : 33.3 % ( 32.0 - 35.0 )

Plaquettes : 250 x106/l ( 150 - 400 )

FORMULE LEUCOCYTAIRE
Polynucléaires neutrophiles : 75 % ( 40-65 )

Polynucléaires éosinophiles : 03 % ( 00-03 )

Polynucléaires basophiles \: 00 % ( 0 - 05 )

Lymphocytes : 20 % ( 20-40 )

Monocytes : 02 % ( 02-07 )

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 VII- EXAMEN PARACLINQIUE(suite)

• SEROLOGIE
Ag HBs : NEGATIVE
Ac HBs : NEGATIVE
HCV : NEGATIVE
• BIOCHIMIE

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VIII- BILAN GÉNÉRAL
Il s’agit âgé de 55ans, ayant présenté dans son:
1. Histoire
- Fièvre brutale avec frison
- Douleur à type pesanteur au niveau de l’HCD à irradiation en arrière
et en haut vers l’omoplate
- Asthénie , nausée , anorexie ,insomnie , amaigrissement
2. ATCD :
- Episode dysenterie chronique
3. A l’examen
- Fièvre brutal
- Hépatomégalie
- Douleur de l’HCD
- Donc le diagnostique positif : Abcès du foie stade pré - suppuratif

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IX- TRAITEMENT
- PIV = NSS =1000mL 20goutte/min
- Ceftri 1000mg 1fl x 2 / j ( IVL )
- Métronidazole 500mg 1fl x 3 / j ( PIV ) 8h
- paracétamol ( 1000 mg) 1Fl x 3 /j ( PIV )
- Cimétidine 400mg 1c x 2 / j ( PO )
- Multivitamine 1c x 2 / j (PO)

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 TRAITEMENT J2

• Evolution • TRAITEMENT
- Etat général conserve - PIV = NSS =1000mL 20goutte/min
-TA =110/75mmHg ,T= 37,8c - Ceftri 1000mg 1fl x 2 / j ( IVL )
- P = 85/min - Métronidazole 500mg 1fl x 3 / j
( PIV ) 8h
- Asthénie
- paracétamol 1000 mg 1fl x 3 /j
- Hépatalgie
( PIV) condition
- Hépatomégalie
- Cimétidine 400mg 1c x 2 / j ( PO )
- Ventre Souple - Multi 1c x 2 / j ( PO )
- urine (+) , selles ( - )

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 TRAITEMENT J3
• Evolution • TRAITEMENT
- Etat général bon - PIV = NSS = 1000ml 10goutte/min
- TA=120/70mmHg ,T= 37,5c - Ceftri 1000mg 1fl x 2 / j ( IVL )
P = 78/min - Métronidazole 500mg 1fl x 3 /J
- Appetite (+) (PIV) 8h
-Hépatalgie diminuée - paracétamol 500 mg 1c x 3 /j ( PO)
- Cimétidine 400mg 1c x 2 / j ( PO )
-Ventre Souple
- Multi 1c x 2 / j ( PO )
- Selles (+)
-urine ( + )

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 TRAITEMENT J4-J7
• Evolution • TRAITEMENT
- Etat général bon - PIV = NSS = 1000ml 10 goutte/min
-TA=120/70mmHg T= 37c - Ceftri 1000mg 1fl x 2 / j ( IVL )
- Métronidazole 500mg 1fl x 3 / j
- P = 72/min
- paracétamol 500 mg 1c x 3 /j ( PO )
- Appetite (+)
condition
- Hépatalgie diminué
- Cimétidine 400mg 1c x 2 / j ( PO )
- Ventre souple - Multivitamines 1c x 2 / j ( PO )
- urine ( +)
- selles ( - )

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XII-CONSEIL AU MALADE

- Alimentation : protéine , hygiène

- Activité physique

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XI-EVOLUTION ET PRONOSTICE

- Septicémie
- Choc septique
- Perforation

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MERCI DE VOTRE ATTENTION!

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 Breast Cancer Surgical Treatments

Asst. Preap Ley, M.D.

1
2
 INTRODUCTION
 In Cambodia, breast cancer
is the second most
common cancer among
women.
 In March 2004: National
breast cancer guidelines for
diagnostic and treatment of
breast cancer.

3
 Result of Cancer registry in SHCH during 15
months (01/03/2005- 30/06/2006)

LEADING DIFFERENT CANCER

69

43
30
23 21 20
15 12 15
9 9 9 8 8 6 6 5
4 1 1 1 1 1
Pancreas

Bone

Cervix
Thyroid

Liver
Stomach

ENT

Tongue
Oesoph
Lymphoma

Penis

Kidney
Colon

Duodenum
Appendix

Unknown
Breast

Neuro
Lung

Parotid
Ovary
Soft tissue

Biliary

4
 RESULTS study at SHCH from March 1, 2008 till March
31, 2011 recording 215 breast cancer women.
Age distribution
50 47
44
45
39
40
Patient Number

35
29
30
25 22
20
15 12
9
10 6
5
5 2
0
<31 31-35 36-40 41-45 46-50 51-55 56-60 61-65 66-70 >70
Patient Age

5
 RESULTS study at SHCH from March 1, 2008 till March
31, 2011 recording 215 breast cancer women.
Geographic distribution

Others Prey Veng

20% 19%

Kg. Speu
6%
Kg. Cham
Battambang 17%
7%

Takeo
8% Kandal P.Penh
10% 13%

6
 Kinds of Breast Cancer treatment
 Treatment plan is usually base on
cancer types, stage, TNM classification,
and grade.

 Treatment of the breast: The breast and

axillar L/N are treated by surgery, and
often in combination with radiation.

 Treatment for cancer cells that may

have spread to other parts of the body:
 The treatment for cancer cell that may
have spread beyond the breast and
lymph nodes in the axilla is a hormone
therapy or chemotherapy or
combination of both.

7
 Kinds of Breast Cancer treatment
 Surgery will usually be the first treatment for operable
primary breast cancer.
 Some neo-adjuvant endocrine or chemo or radiotherapy may
be appropriate in some instances to downstage bulky disease
to facilitate breast conserving surgery.
 The two comments types of surgery:
 Breast- conserving surgery (started in 1981)
 Mastectomy.

8
 Breast-conserving surgery (BCT)
 Lumpectomy, partial or segmental mastectomy or
quadrantectomy.
 Must understand:
 further surgery may be necessary if not complete excision (with rim of
normal tissue less than 1 or 2cm), and
 expect that adjuvant radiation therapy will be required.
 Assessment of regional lymph node status to stage disease and
to aid in planning of adjuvant systemic therapy.

9
 Breast-conserving surgery (BCT)
 Indications:
 Small tumor stage 0 (CIS),
 I and IIa breast carcinoma with availability of radiotherapy facility
 Patient preference
 Contraindications:
 Tumor>4cm
 Multicentricity
 Centrally located tumors
 Poor tumor differentiation
 Node positive disease
 Positive margin after re-excision
 Hx of previous radiotherapy
 Pregnancy.

10
 Mastectomy
 Removal of the entire breast, including the nipple.
 Indicated when
 breast conserving treatment is not advisable (Large tumor
related to size of the breast) or has failed (No free margin or
local recurrence).
 Central tumor beneath the areola or involving nipple
 Multifocal disease
 Patient preference.

11
 Mastectomy
 There are different mastectomies
depending on the extent of the
surgery in the axilla and the
muscles under the breast.
 Simple mastectomy:
 Removal of the whole of breast tissue
superficial to the pectoral fascia .
That means superficial fascia is left
behind.
 Indication:
 Stage I and IIa carcinoma,
multicentric and multifocal CIS
 For Metastatic Breast Disease.
 It is also called Toilet
Mastectomy. The purpose of
doing Simple Mastectomy in
Carcinoma Breast with metastasis
is to prevent fungation and local
ulceration of the tumor.

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 Mastectomy
 Total mastectomy:
 Removal of the whole of breast tissue including the pectoral fascia.
 Indication:
 The same as for simple mastectomy.
 Paget Disease of the breast with no palpable lump.
 (Paget Disease of the Breast with a palpable lump should be done by
Modified Radical Mastectomy).

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 Mastectomy
 Modified radical mastectomy (MRM):
 The entire breast and some axillary lymph nodes are removed.
 Indication:
 Early Breast Carcinoma (Stages 0, I and II with residual cancer cell
after conservative surgery and persist after adjuvant therapy, or
multifocal or multicentric disease)
 Paget Disease of the breast with a palpable lump
 Local advanced breast cancer (LABC) (Stage III).

14
 Mastectomy
 Radical mastectomy:
 Halstead’s Radical
Mastectomy in 1882 both
Pectoralis major and
Pectoralis minor muscles are
removed along with the
whole breast and the axillary
lymph nodes. (William
Stewart Halsted, U.S Surgeon
1852-1922).
 Radical mastectomy is rarely
used today, and for most
women, this surgery is not
more effective than more
limited forms of mastectomy.

15
 RESULTS study at SHCH from March 1, 2008 till March
31, 2011 recording 215 breast cancer women.

Preoperative diagnostic

Histology
FNA
2%
10%

Clinically
Biopsy 55%
33%

16
 RESULTS study at SHCH from March 1, 2008 till March 31,
2011 recording 215 breast cancer women.
Histology
No %
LCIS 0 0
Histological diagnosis DCIS 1 0.4
DIC 173 80.4
LIC 11 5.3
Medullary Carcinoma 1 0.4
Others 29 13.5
G1 5 2.4
Grade G2 36 16.7
G3 87 40.4
Gx 87 40.5
ER-/PR- 51 23.7
Hormone receptor ER+/PR+ 54 25.2
ER+/PR- 4 1.8
ER-/PR+ 11 5.1
17
Unknown 95 44.2
 RESULTS study at SHCH from March 1, 2008 till March 31,
2011 recording 215 breast cancer women.
Staging No %
T0 0 0
T-stage T1 4 1.8
T2 25 11.6
T3 61 28.3
T4 65 30.2
Tx 60 28.1
N0 30 14.0
N-stage N1 31 14.5
N2 56 26.0
N3 16 7.4
Nx 82 38.1
M0 164 76.2
M-stage M1 27 12.5
Mx 24 11.3
I 3 1.4
Stage II (A,B) 40 18.6
III (A,B,C) 104 48.5
IV 47 21.8
18 Unknown 21 9.7
 RESULTS study at SHCH from March 1, 2008 till March
31, 2011 recording 215 breast cancer women.
Comparing with Western literature
≥ T3 or 5cm Axillary lymph nodes Distance metastasis
(N1, N2, N3) (M1)

SHCH
58.5% 47.9% 12.5%
Western literature (Gills
and Thursfield)
3.8% ≈25% <10%

19
 RESULTS study at SHCH from March 1, 2008 till March
31, 2011 recording 215 breast cancer women.
Treatment

No %

No surgery
46 21.3
Surgery Mastectomy/ax clearance (MRM)
121 56.2
Palliative simple Mastectomy
48 22.3
Neo-adjuvant CT+
3 1.39
Treatment adopted Adjuvant anti-hormone+
67 31.1
Adjuvant RT+ and CT+
1 0.4
Adjuvant CT+
2 0.9
20
 Mastectomy
 Most our patients:
 Too late and cannot be treated with curative attempt anymore.
 Often can not follow the national guidelines.
 Almost of cases are classified as Local Advanced Breast Cancer (LABC).
 All effort is made to offer the best possible palliative treatment, surgery in
this setting is to achieve loco-regional control only.
 MRM is the routine choice for almost our patients and then we
provide hormone therapy for ER or PR positive patients for 5
years.
 Because of SHCH is a low resource setting place of Low Income country, we
follow a Breast Health Global Initiative (BHGI) Pioneered by Prof. Ben
Anderson, Seattle USA .

21
 Surgical Treatments

 Because of SHCH is a low resource

setting place of Low Income
country, we follow a Breast
Health Global Initiative
(BHGI) Pioneered by Prof.
Ben Anderson, Seattle USA .

 BHGI- Study, develop &

implement evidence based,
economically feasible, and
culturally appropriate guidelines
for Breast Health care LMIC .

22
 MRM techniques
 The entire breast and some axillary lymph
nodes are removed.
 3 types of MRM
1. Patey’s MRM in 1943:– Pectoralis
major muscle is preserved and
Pectoralis minor removed. (David
Howard Patey, English surgeon, 1899-
1977)
2. Scanlon’s MRM:– Pectoralis minor
muscle is divided but not removed.
(Edward F. Scanlon, U.S surgeon, 1918-
2008).
3. Auchincloss’ MRM:– Pectoralis minor is
retraced but not divided. (Hugh
Auchincloss, U.S surgeon, 1915-1998).
 Auchincloss’ Modified Radical
Mastectomy is widely practiced
nowadays of level 1 to 2 axillary dissection
to remove 10 or more nodes, being
sufficient for staging and the degree of
morbidity is less than with level 3 dissection.

23
 MRM techniques
Patient position
 The patient is placed in
supine position with the
arm abducted <90o
 Sandbag or folded sheet is
placed under thorax and
shoulder of affected side
 Skin prepped and draped.

24
 Auchincloss’ MRM procedure
Skin incision
 Incision depends on the location of
the primary tumor.
 Usually oblique elliptical incision
angled towards axilla encompassed
nipple, areola or previous scar.
 Should be 2 to 3cm away from
tumor margins.
 Two skin edges should be of
equivalent length.

25
 Auchincloss’ MRM procedure
Extent of dissection and flaps
 Superiorly till the clavicle,
 Inferiorly till the level of the
insertion of rectus abdominis
muscle,
 Medially to the sternal border,
 Laterally till anterior border of the
latissimus dorsi muscle.
 Ideally skin flap thickness should be
7 to 10mm. So that blood perfusion
to the skin is not compromised.

26
 Auchincloss’ MRM procedure
Remove breast
 Once the anterior surface of the
breast is dissected free from the
overlying subcutaneous tissue, then
its posterior surface should be
dissected free from the underlying
pectoralis major muscle.
 The specimen is retracted upward
and laterally to expose pectoralis
minor.

27
 Auchincloss’ MRM procedure
Axillary clearance
 The interpectoralis (Rotter) group
lymph nodes are removed. Care should
be taken to preserve the medial and
lateralpectoral nerves.
 Then we identified lateral border of
Pectoralis minor well. It is medial
marker line of axilla to dissect.
 The loose lateral areolar in axillar space
is dissected to expose axillary vein. It
should be superior marker line to
dissect.
 The latissimus dorsi muscle forms the
lateral border of the axilla to dissect,
and it should be dissected along its
lateral and anterior aspect so that the
surgeon can visualize the entire axilla.

28
 Auchincloss’ MRM procedure
Axillary clearance
 Then dissection can be
done either from medial to
lateral or vise versa.
 The pectoralis minor
muscle is retracted
medially, and the axillary
tissue with group II lymph
nodes that runs posterior
to the muscle is visualized
and dissected.

29
 Auchincloss’ MRM procedure
Axillary clearance
 The investing layers of axillar
vessels is cut, the tributaries
are ligated.
 Dissection is carried out
laterally including lateral
group I nodes. This dissection
have to deeply from
Latissimus dorsi muscle with
very take care of Long
thoracic and Thoracodorsalis
vessels and nerves.
30
 Auchincloss’ MRM procedure
 Wound irrigated with sterile
water to shrink/crenate
cancerous cells.
 1 or 2 suction drains are put
and fixed.
 Subcutaneous tissue is closed
using 0/0 absorbable
interrupted sutures.
 Skin closed using non-
absorbable sutures or staples
 Elastic bandage dressing is
applied.

31
32
 Post-op care
 Wound examined on D3, if there is not infection clinical
signs.
 Drain can be removed when it is less than 30cc.
 Skin sutures or staples can be removed after D10.
 Shoulder have to keep in 90o
 Arm movements started in the 1st week
 Active shoulder and arm exercises are started from 2 weeks.

33
34
Type 2 Diabetes in Cambodia
Epidemiology, Morphotype and
Management

SUM Satha, MD, FACE

Faculty of Medicine, UHS
Calmette Hospital, Phnom Penh, Cambodia
INTRODUCTION
• Cambodia is a tropical country in Southeast Asia with a population of
16 million.

• During the last years of the 20th century, Cambodia returned to

political stability after many years of war and deprivation, and it is
now enjoying an economic recovery.

• Diabetes is a major health problem that has reached significant

proportions.

2
 1

The diabetes challenge in Cambodia

430.6 THOUSAND 893.2 THOUSAND 854 THOUSAND

ADULTS HAVE DIABETES1, ADULTS COULD HAVE adults were living with
which equals 6.3% of the DIABETES BY 20451 PREDIABETES, which equals
adult population 10% of the adult
population1.
606 309 764
107% $ 103M
1 OUT OF 16 INCREASE was spent treating
ADULTS in Cambodia diabetes in 20191. This
had diabetes in 20191. number is expected to
increase 83% by 2045.
2019 2045

An estimated 62% of all patients with diabetes were undiagnosed1. 7,919 adults were estimated to have died
from diabetes-related complications during the year, averaging 22 deaths every day1.

Note: Adults ages 20-79. For the prevalence of Diabetes and Prediabetes the age-adjusted comparative prevalence has been used. Diabetes includes both T1D & T2D.
References: 1 IDF. Diabetes Atlas, Ninth Edition, 2019.

3
Prevalence of cardiovascular risk factors in population
aged 25-64 in Cambodia
Risk factors Value (%)

Diabetes 3.1

Current smoking 29.4

Physically underactive 9.0

Overweight 15.5

Hypertension 12.3

Hypercholesterolemia 3.2

Otgontuya D et al. BMD Public Health 2012

4
• Younger adults (23-34 years old) have a lower prevalence rate (1.1%).
Older age groups (55-64 years) a higher rate (6%). Women (3.3%) are
more affected than men (2.5%).
Otgontuya D et al. BMD Public Health 2012

• The prevalence of the urban population is twice as high as that of the

rural population.

Hilary King et al. Lancet 2005

Otgontuya D et al. BMD Public Health 2012

5
• About half of the total diabetic population is undiagnosed.

• Rates of previously undiagnosed diabetes are increasing in semi-

urban (55%) and rural (67%) areas.

Hilary King et al. Lancet 2005

Otgontuya D et al. BMD Public Health 2012
Julie Wagner et al. J Diabetes 2018

6
The trend of overweight and obesity among people
aged 18 and over from 2000 to 2020

Ritchie H and Roser M. Obesity 2019

7
• Among Cambodians, the increased
risk of hypertension, diabetes mellitus
and hypercholesterolemia was
statistically significant in both sexes
with a BMI ≥23kg/m2 and WC >80cm.

• These results are similar to the results

of some studies in Asian populations.

8
 Type 2 diabetes epidemic in Cambodia
• In addition to economic growth and lifestyle changes, an association
between diabetes in later life and nutritional deprivation in fetal life
and early childhood has been proposed.

• The hardships of the Cambodian people during the second half of the
20th century, particularly under the Khmer Rouge regime (1975-
1979), may have left a dark legacy (The Epigenetics of Hunger).

DECODE Study BMJ 1998

Hilary King, Keuky Lim et al. Lancet 2005
Keuky Lim The Epigenetics of Hunger 2014

9
 Early life undernutrition and the development of T2D

10
Calvin Ke et al. Nature Reviews Endocrinology, 2022
 From patient side: major
challenges
Low awareness of the disease

Low rate of diagnosis/late

diagnosis

Low level of adherence

Low glycemia control

Sum Satha et al. Journal of Diabetes Investigation. 2018 (s1)
Jacobs B et al. BMJ Glob Health. 2017
Raguenaud ME et al. BMC Med. 2009
Janssens B et al. Bull World Health Organ. 2007
King H et al. Lancet. 2005

11
PLOS ONE 2014

12
 Pathophysiology of T2D

Impaired Increased
insulin secretion glucagon secretion

Increased hepatic glucose Decreased

production incretin effect

Impaired
Increased lipolysis
appetite regulation

Decreased Increased glucose

glucose uptake reabsorption

T2D, type 2 diabetes

Adapted from DeFronzo RA. Diabetes 2009;58:773–95 13
Etiology of β-cell Dysfunction
Genetic predisposition

Lean phenotype Obese phenotype

IGT, IFG Elevated FFA

Initial glucolipoadaptation (increased

FFA usage)
Hyperglycemia
Oxidative stress and Cellular lipid synthesis and
glucotoxicity glucolipotoxicity

Glucolipotoxicity and glucotoxicity

Progressive -cell failure and type 2 diabetes

Poitout V, Robertson RP. Endocrine Rev. 2008;29:351-366. 14

Progression to Type 2 Diabetes: “Falling Off the
Curve”
500

400

Nonprogressors
300 NGT
NGT
NGT
NGT
200
IGT
Progressors
100
DIA
0
0 1 2 3 4 5
Glucose disposal (insulin sensitivity)
(mg/kg EMBS/min)

EMBS, estimated metabolic body size; IGT, impaired glucose tolerance; NGT, normal glucose tolerance.
Weyer C et al. J Clin Invest. 1999;104:787-794. 15
Pathophysiology of
Type 2 Diabetes
Organ System Defect
Major Role
Pancreatic beta cells Decreased insulin secretion
Muscle Inefficient glucose uptake
Liver Increased endogenous glucose secretion
Contributing Role
Adipose tissue Increased FFA production
Digestive tract Decreased incretin effect
Pancreatic alpha cells Increased glucagon secretion
Kidney Increased glucose reabsorption
Nervous system Neurotransmitter dysfunction

DeFronzo RA. Diabetes. 2009;58:773-795 16

Tissues Involved in T2D Pathophysiology
Organ System Normal Metabolic Function Defect in T2D
Major Role
Pancreatic beta cells Secrete insulin Decreased insulin secretion
Muscle Metabolizes glucose for energy Inefficient glucose uptake
Secretes glucose during fasting periods to maintain brain
Increased endogenous glucose
Liver function; main site of gluconeogenesis (glucose production in
secretion
the body)
Contributing Role
Stores small amounts of glucose for its own use. When fat is
Adipose tissue (fat) broken down, glycerol is released, which is used by the liver to Increased FFA production
produce glucose
Digests and absorbs carbohydrates and secretes incretin
Digestive tract Decreased incretin effect
hormones
Secrete glucagon, which stimulates hepatic glucose production
Pancreatic alpha cells between meals and also helps suppress insulin secretion during Increased glucagon secretion
fasting periods
Reabsorbs glucose from renal filtrate to maintain glucose at
Kidney steady-state levels; also an important site for gluconeogenesis Increased glucose reabsorption
(glucose production)
Utilizes glucose for brain and nerve function
Brain Neurotransmitter dysfunction
Regulates appetite
T2D, type 2 diabetes.
DeFronzo RA. Diabetes. 2009;58:773-795 17
Natural History of Type 2 Diabetes
Years from –10 –5 0 5 10 15
diagnosis
Onset Diagnosis

-Cell function

Insulin resistance
Insulin secretion

Postprandial glucose
Fasting glucose
Microvascular complications
Macrovascular complications
Prediabetes Type 2 diabetes

Figure courtesy of CADRE.

Adapted from Holman RR. Diabetes Res Clin Pract. 1998;40(suppl):S21-S25;
Ramlo-Halsted BA, Edelman SV. Prim Care. 1999;26:771-789; Nathan DM. N Engl J Med. 2002;347:1342-1349; UKPDS Group.
Diabetes. 1995;44:1249-1258 18
-cell Loss Over Time
100 – UKPDS

75 –
-Cell Function (%)

50 –

25 –
Impaired
Postprandial
Glucose Type 2 Diabetes
Hyperglycemia
Tolerance
0 –l l l l l l l l l
-12 -10 -6 -2 0 2 6 10 14
Years from Diagnosis

Dashed line = extrapolation based on Homeostasis Model Assessment (HOMA) data.

Data points from obese UKPDS population, determined by HOMA model.
Holman RR. Diabetes Res Clin Pract. 1998;40(suppl):S21-S25. 19
Normal Glucose Homeostasis and Pre- and Postmeal Insulin and Glucagon
Dynamics
Normal (n=11)
120 Premeal Postmeal
Meal
90
Insulin 60
(µU/mL)  Insulin  Insulin
30
0

140
130
120  Glucagon  Glucagon
Glucagon
(pg/mL) 110
 HGP  HGP
100
90

360
330 Modest
300 Just enough
postprandial
Glucose 270 glucose to meet
increase with
(mg %) metabolic needs
240 prompt return to
between meals
110
fasting levels
80
-60 0 60 120 180 240
Time (min)
Müller WA, et al. N Engl J Med. 1970;283:109-115. 20
Hyperglycemia in Type 2 Diabetes Results from Abnormal Insulin and
Glucagon Dynamics
Normal (n=11)
120
Meal Premeal Postmeal
90 T2D (n=12)
Insulin
60
(µU/mL)
30  Insulin  Insulin
0

140
130

Glucagon
120  Glucagon  Glucagon
(pg/mL) 110
100  HGP  HGP
90

360
330
300
Glucose 270
(mg %)  FPG  PPG
240

110
80
-60 0 60 120 180 240

T2D, type 2 diabetes. Time (min)

Müller WA, et al. N Engl J Med. 1970;283:109-115. 21
 Acute Insulin Response Is Reduced in Type 2
Diabetes

1st 2nd phase

20 g glucose infusion
120
Normal (n=85)
100 Type 2 diabetes (n=160)

Plasma IRI 80
(µU/ml)
60

40

20

0
-30 0 30 60 90 120
Time (minutes)

IRI, immunoreactive insulin.

22
Pfeifer MA, et al. Am J Med. 1981;70:579-588.
Defective Insulin Action
in Type 2 Diabetes
7 12

6
Total Body Glucose Uptake

(mg/kg leg wt per min)

Leg Glucose Uptake
8
(mg/kg • min)

3
4
2
P<0.01
1

0 0
Normal T2D 0 20 60 100 140 180
Time (minutes)

T2D, type 2 diabetes.

DeFronzo RA. Diabetes. 2009;58:773-795; DeFronzo RA, et al. J Clin Invest. 1985;76:149-155. 23
Elevated Fasting Glucose in Type 2 Diabetes
Results From Increased HGP
4.0

3.5
r=0.85
P<0.001
(mg/kg • min) 3.0
Basal HGP

2.5

2.0 Control
T2D

0
100 200 300
FPG (mg/dL)
FPG, fasting plasma glucose; HGP, hepatic glucose production; T2D, type 2 diabetes.
DeFronzo RA, et al. Metabolism. 1989;38:387-395. 24
The Incretin Effect Is Diminished
in Type 2 Diabetes Type 2 Diabetes
Normal Glucose Tolerance
(n=8) (n=14)
240
Plasma Glucose (mg/dL)
240 IV Glucose

Plasma Glucose (mg/dL)

Oral Glucose
180 180

90 90

0 0
0 60 120 180 0 60 120 180
30 30
C-Peptide (nmol/L)

C-peptide (nmol/L)
20 20
*
* * * *
10 * * 10
*

0 0
0 60 120 180 0 60 120 180
Time (min) Time (min)
*P≤.05.
Nauck M, et al. Diabetologia. 1986;29:46-52. 25
Actions of GLP-1 and GIP
GLP-1
• Released from L cells in ileum and
colon
• Stimulates insulin release from -cell
in a glucose-dependent manner
• Potent inhibition of gastric emptying
• Potent inhibition of glucagon
secretion
• Reduction of food intake and body
weight
• Significant effects on -cell growth
and survival
Drucker DJ. Diabetes Care 2003;26:2929-2940.
GIP
• Released from K cells in duodenum
• Stimulates insulin release from -cell
in a glucose dependent manner
• Minimal effects on gastric emptying
• No significant inhibition of glucagon
secretion
• No significant effects on satiety or
body weight
• Potential effects on -cell growth and
survival
26
Renal Glucose Reabsorption
in Type 2 Diabetes
• Sodium-glucose cotransporters 1 and 2 (SGLT1 and SGLT2) reabsorb
glucose in the proximal tubule of kidney
• Ensures glucose availability during fasting periods
• Renal glucose reabsorption is increased in type 2 diabetes
• Contributes to fasting and postprandial hyperglycemia
• Hyperglycemia leads to increased SGLT2 levels, which raises the blood glucose
threshold for urinary glucose excretion

Wright EM, et al. J Intern Med. 2007;261:32-43.

27
Normal Renal Handling of Glucose
(180 L/day) (90 mg/dL) = 162 g glucose per day

Glucose
SGLT2

S1

SGLT1

90% of S3
glucose

10% of
glucose

No Glucose

Abdul-Ghani MA, et al. Endocr Pract. 2008;14:782-790. 28

Increased SGLT2 Protein Levels Change Glucose
Reabsorption and Excretion Thresholds
Reabsorption Excretion
TmG
Reabsorption
Renal Glucose Reabsorption

TmG

Renal Glucose Excretion

increases

Excretion
threshold
increases

90 180 270 90 180 270

Blood Glucose Concentration Blood Glucose Concentration
(mg/dL) (mg/dL)
TmG, glucose transport maximum.
Abdul-Ghani MA, DeFronzo RA. Endocr Pract. 2008;14:782-790.
29
Hypothalamic Dopaminergic Tone and
Autonomic Imbalance
In diabetes:
Low dopaminergic tone in
hypothalamus in early
morning

Sympathetic tone
HPA axis tone
 Hepatic gluconeogenesis
 FFA and TG
 Insulin resistance
 Inflammation/hypercoagulation

Impaired glucose metabolism

Hyperglycemia
Insulin resistance
Adverse cardiovascular pathology
Fonseca V. Dopamine Agonists in Type 2 Diabetes. New York, NY: Oxford University Press; 2010.
Cincotta AH. In: Hansen B, Shafrir E, eds. Insulin Resistance and Insulin Resistance
30 Syndrome. New York, NY: Taylor
& Francis; 2002:271-312.
30
Mechanism of Action of Antihyperglycemic
Agents
Pancreas

Muscle Decreased insulin Liver

secretion from
Increase glucose uptake Increased endogenous
-cells
TZD glucose production
GLP1 RA, DPP4i, SU, GLN Metformin, TZD,
GLP1 RA, DPP4i
Adipose (fat)
Increased FFA production The Ominous Octet Digestive tract
Decreased incretin effect
TZD GLP1 RA, AGis,
Colesevelam
GLP1 RA, DPP4i

Brain Increased glucagon Kidney

Neurotransmitter dysfunction secretion from Increased glucose reabsorption
-cells
GLP1 RA SGLT2i
Bromocriptine Pancreas
31
DeFronzo RA. Diabetes. 2009;58:773-795
 Novel and complementary mechanisms to reduce
hyperglycemia in T2D

Insulin-dependent mechanisms Insulin-independent mechanism

• Insulin action
• TZD
• Metformin
• Insulin secretion
• SU • SGLT2-I (Gliflozins)
• Glinide
• DPP4-I
• GLP1-RA
• Insulin replacement
• Insulin

32
 Anti Diabetic Agents in Cambodia
Anti Diabetic agents Availability Price

Metformin Yes $

Sulfonylurea Yes $

Thiazolidinedione Yes $

DPP-4 Inhibitor Yes $$$

SGLT-2 Inhibitor Yes $$$

GLP-1 receptor agonist (Glucagon-Like-peptide Yes $$$$

receptor agonist)
Insulin Yes $

33
 T2D Management
Glycemic
Control

Insulin therapy
Bi-therapy (Met+SFU)
Monotherapy (Metformin)
Life style management
MoH Guidelines-Cambodia 2015
34
Framework for Diabetes Care
Role of clinician: Usually at referral hospital
• Clinical care based on guidelines but individualized
• Risk factor management
• Empowering patients in self-management
• Coordination with other health professionals, peers and community-
based organizations
• From part of the provincial working group on Non-Communicable
Disease

MoH Guidelines-Cambodia 2015

35
Screening for T2D
• BMI > 23, Waist circumference ≥85cm (men) ≥80cm (women)
• Family history of diabetes
• HTA, dyslipidemia
• History of stroke or ischemic heart disease
• Women with history of gestational diabetes
• Women who have given birth to a large baby (>3500g)
• Age over 35

MoH Guidelines-Cambodia 2015

36
DIABETES AND TECHNOLOGY
Digital health is growing…

Satha SUM and al. DMJ 2019 37

DIABETES AND TECHNOLOGY
• 2021: 1st Pump Center at Calmette
Hospital

• Indications
• DT1 > DT2
• Diabetes and pregnancy
• Motivated patients
• Unstable diabetes despite muptiple daily
injections
• Hypoglycemia (Severe >1/an, moderate
>4/week)
• Inpatients with uncontrol diabetes

38
 2022 ADA: Pharmacologic treatment of hyperglycemia in adults with T2D
FIRST-LINE THERAPY DEPENDS ON COMORBIDITIES, PATIENT-CENTERED TREATMENT FACTORS, INCLUDING COST AND ACCESS CONSIDERATIONS, AND
MANAGEMENT NEEDS AND GENERALLY INCLUDES METFORMIN AND COMPREHENSIVE LIFESTYLE MODIFICATION^ TO AVOID THERAPEUTIC
INERTIA REASSESS
AND MODIFY TREATMENT
REGULARLY
(3-6 MONTHS)
ASCVD/INDICATORS OF HIGH-RISK, HF,CKD† None

RECOMMEND INDEPENDENTLY OF BASELINE A1C, INDIVIDUALIZED A1C TARGET, OR METFORMIN USE † †

Incorporate agents that provide adequate EFFICACY to achieve and maintain glycemic goals
Higher glycemic efficacy therapy: GLP-1RA; insulin; combination approaches (Table 9.2)
+ASCVD/lndicators +HF* +CKD** • Consider additional comorbidities , patient centered treatment factors and management needs in choice of therapy, as below:
of High Risk*
CKD and CKD without
Albuminuria Albuminuria
Either/ (e.g., ≥200mg/g (e.g., eGFR<60
GLP-1 RA OR SGLT2i SGLT2i with proven creatinine) mL/min/ MINIMIZE HYPOGLYCEMIA MINIMIZE WEIGHT GAIN OR PROMOTE CONSIDER COST AND ACCESS
with with benefit in this 1.73m2 ) WEIGHT LOSS
proven CVD proven CVD population1
benefit1 benefit1 No/low inherent risk of hypoglycemia: PREFERABLY Available in generic form at lower cost
PREFERABLY
DPP-4i, GLP-1 RA, SGLT2i, TZD GLP-1 RA with good efficacy for weight loss • Certain insulins; consider insulin available at
For SU or basal insulin, consider agents with lower OR the lowest acquisition cost
If A1C above target SGLT2i with primary evidence
risk of hypoglycemia 3,4 SGLT2i • SU
of reducing CKD progression
OR • TZD
• For patients on a GLP-1 RA, SGLT2i with evidence of If A1C above target
consider incorporating SGLT2i reducing CKD progression in CVOTs If A1C above target
with proven CVD benefit and vice OR If A1C above target
versa1 GLP-1 RA with proven CVD benefit1 if For patients on a GLP-1 RA, consider
• TZD2 SGLT2i not tolerated or contraindicated incorporating SGLT2i and vice versa
Incorporate additional agents based on
• If GLP-1 RA not tolerated or indicated, Incorporate additional agents based on
comorbidities, patient-centered treatment
consider DPP-4i (weight neutral) comorbidities, patient-centered treatment
factors, and management needs
For patients with CKD (e.g., eGFR<60 factors, and management needs
mL/min/1.73m2) without albuminuria,
recommend the following to decrease CV risk Incorporate additional agents based on
comorbidities, patient-centered treatment
factors, and management needs

GLP-1 RA with SGLT2i with 1. Proven CVD benefit refers to label indication (see Table 9.2) 5. Consider county and region-specific cost of drugs
proven CVD benefit1 Either/ proven CVD benefit1 2. Low dose may be better tolerated though less well studied for CVD effects
OR 3. Choose later generation SU to lower risk of hypoglycemia
4. Risk of hypoglycemia: degludec / glargine U-300 < glargine U-100 / detemir <
NPH insulin
^ For adults with overweight or obesity lifestyle modification to achieve and maintain ≥5% weight loss and ≥150 min/week moderate to vigorous intensity physical activity is recommended
† Actioned whenever these become new clinical considerations regardless of background glucose-lowering medications.
If A1C above target, for patients on SGLT2i, consider
† † Most patients enrolled in the relevant trials were on metformin at baseline as glucose-lowering therapy.
incorporating a GLP-1RA and vice versa
If A1C remains above target, consider treatment *Refer to section 10: Cardiovascular disease and risk management
intensification based on comorbidities, patient-centered ** Refer to section 11: Chronic Kidney Disease and risk management and specific medication label for eGFR criteria
treatment factors, and management needs

A1C, glycated hemoglobin; ASCVD, atherosclerotic cardiovascular disease; CKD, chronic kidney disease; CVD, cardiovascular disease; CVOTs, cardiovascular outcomes trials; DPP-4i, dipeptidyl peptidase 4 inhibitor; eGFR, estimated glomerular filtration rate; GLP-1 RA, glucagon-like peptide 1
receptor agonist; HF, heart failure; NPH, Neutral Protamine Hagedorn; SGLT2i, sodium–glucose cotransporter 2 inhibitor; SU, sulfonylurea; T2D, type 2 diabetes; TZD, thiazolidinedione
American Diabetes Association (ADA). Diabetes Care 2022 Jan; 45(Supplement 1):S125-S143, https://diabetesjournals.org/care/article/45/Supplement_1/S125/138908/9-Pharmacologic-Approaches-to-Glycemic-Treatment
40
41
42
43
Therapeutic Inertia
Failure to initiate or intensify
the therapy regimen when a
patient’s therapeutic goals are
not met.

44
Therapeutic
Inertia
HCPs are unfamiliar with new
drugs

Possible HCPs has inadequate knowledge

of guidelines
Causes

HCPs are uncertain about clinical

objectives

Adreozzi F et al. Diabetol Metab Syndr 2020

45
 Therapeutic Inertia: Adopting
Guidelines
Current practice guidelines

Lifestyle and Addition of

dietary other
modifications therapies
Metformin
monotherapy T
Treatment algorithm recommends delay of
three months before treatment intensification
Reach G et al. Diabetes Metab J 2017 46
Summary
Diabetes is a multifactorial
disease
We can prevent progression of
diabetes complications
Many T2D patients have ASCVD, Multidiciplinary team
renal disease and/or HF approaches
MoH-Cambodia guideline provides
International guidelines provide
appropriate and affordable needs
modern managements and
for the patients according to our
strategies
limited resources
47
 សូមអរគុណចំព ោះការយកចិត្តទុកដាក់
THANK YOU VERY MUCH FOR YOUR ATTENTION

48
 ព្រះរាជាណាចព្ររម្ពជា
ុ
ជាតិ សាសនា ព្រះម្ហារសព្រ

Diabetic Foot 6
Dr. HUON Layheak, Surgical Department,
Memot Referral Hospital, Tbuong Khmum, Cambodia

CME TBOUNG KHMUM

25-August-2022
ប្រវត្តស
ិ ង្ខេរ
• ង្្មោះ​​​ ហួន​ឡៃហ៊ាក

• ទក
ី ន្នែខកំង្ ើ ត្ ង្េត្តរន្ទាយមានជ័យ

• រញ្ច រ់ថ្នាក់ង្វជជរ ឌិ ត្ ២០១៥​ពស

ី កលវទាល័
ិ យអនតរជាត្ិ

• ចូលរង្ប្រកា
ើ រងាររដ្ឋ ០១​រថ
ិ ុន្ទ​២០១៥​ង្ៅរនារី ង្ពទយរន្ខែក​ង្ររត្់
• ត្ួន្ទទរ
ី ចចុរបនា ប្រូង្ពទយពាបាលន្នាកររួសរោះទខគច
ិ ​នខ
ិ វោះកាត្់

• វរគរ ុ ត ោះរណ្ត
ត ល

២០១៦​ រ ុ ត ោះរណ្តត លរយៈង្ពល៦ន្េ​

ន្នាកវោះកាត្់ទូង្ៅ​ង្ៅរនារី ង្ពទយង្េត្តកំពខ់ចារ​
២០១៧-២០១៨​ រ ុ ត ោះរណ្តត លរយៈង្ពល១ឆ្ា​ំ
ន្នាកវោះកាត្់ររួសរោះទខគច
ិ ​នខ
ិ ​បាក់ន្រកឆ្ែខ
ឹ ​ង្ៅរនារី ង្ពទយប្ពោះកុសុរៈ
Objectives

I. Diabetes Complication
II. Risks of DFU
III. Essential of early diagnosis and
Prevention of DFU
IV. Principle of treatment
I. Diabetes Complications
1. Progressive micro-angiopathy
2. Diabetic retinopathy
3. Diabetic nephropathy (glomerular nephrosclerosis)
4. Diabetic Peripheral Neuropathy
5. Peripheral Arterial Disease (Atherosclerosis)
6. Gangrene
Diabetic Peripheral Neuropathy (DPN)
• ranges from 16% to as high as 66%
• definition of neuropathy is nerve disease or damage
• An internationally recognized definition of DPN is “the presence of
symptoms and/or signs of peripheral nerve dysfunction in people
with diabetes after exclusion of other causes”
Peripheral Arterial Disease
• Atherosclerosis In DM
• More diffuse
• More distal (smaller a.)
• More risk of plaque rupture
• More risk of Amputation
(Multiple Vx)
• Alter vv (calcification)
• Glycemic vx injury
 II. Risks of DFU
• General
• Uncontrolled Hyperglycemia
• Duration of DM
• PAD
• Visual loss
• Chronic Renal Disease
• Older age
 II. Risks of DFU
• Local
• Peripheral neuropathy
• Foot deformity
• Trauma or improper fitted shoes
• Callus
• Hx of prior ulcer or amputation
• Prolonged elevated pressure
• Limited joint mobility
III. Diagnosis and Prevention
• Clinical Exam
• Check for skin breaks, discoloration, numbness, pain or
swelling
• Forefoot Valgus
• Increase pressure under 1st metatarsal head
• Callus tissue development
• Tissue breakdown
• Identify Risks of DFU
• Early treatment to reduce rate of disability (Amputation)
What is diabetic foot? • Neuropathic
• Purely ischemic
• Neuroischemic
Mix of pathologies:
• Diabetic neuropathy
• Ischemia
• Charcot Neuroarthropathy
• Foot ulceration
• Osteomyelitis
• Limb amputation
Ulcer Classification of Diabetic Foot
Grade Lesion
1 Superficial diabetic ulcer
2 Ulcer extension involving
ligament, tendon, joint
capsule, or fascia with no abscess
or osteomyelitis
3 Deep ulcer with abscess or
osteomyelitis
4 Gangrene to potion of forefoot
5 Extensive gangrene of foot
Gangrene
• Death of body tissue due to infection and a loss of blood supply.
• The common signs of gangrene include:
• Sores or blisters
• The affected area turns red, which then turns brown or black
• Severe pain followed by numbness
• Cold, thin, shiny skin
• Foul-smelling discharge leaking
There are several types of gangrene with diabetes
Wet Gangrene
• bacterial infection develop after a minor injury due to neuropathies produces pus fluid
leak "wet“
Dry Gangrene
• lack of blood flow, common in extremities , no wound or bacterial infection, develops
slowly
Gas Gangrene
• internal infection usually caused by Clostridium perfringens, damage skin, blood vessels
and tissues
• reddish, purple or gray, bubbly or make a cracking sound when pressed
Fournier's Gangrene
• genital gangrene, quickly spread, leading to necrosis
• symptoms include intense pain in the genital area, fatigue, fever, blisters and a foul odor
Prevention
• Regular Health check
• Quit smoking
• Lipid lowering
• Exercising regularly
• Categories the risk of
DFU
IV. Treatment
• Off-loading
• Mechanical off-loading
• Total contact casting, especially in plantar ulcers
• Temporary footwear
• Individually moulded insoles and fitted shoes
IV. Treatment

• Restoration of skin perfusion

• Vascular intervention (e.g. stenting) to improve
distal blood flow
• Cardiovascular risk reduction to stabilize and
regress macrovascular disease
IV. Treatment

• Treat infection
• Treat superficial ulcers with
debridement and oral antibiotics
• Deeper, limb threatening infection may
need IV antibiotics, drainage and
removal of necrotic tissue
IV. Treatment

• Local wound care

• Frequent inspection
• Frequent debridement
• Wound drainage
IV. Treatment
Anti-microbial agents
• Mild:
• Flucloxacillin
• Clarithromycin, Erythromycin or Doxycycline
• Moderate or severe:
• Flucloxacillin with or without Gentamicin and/or Metronidazole
• Co-amoxyclav with or without Gentamicin
• Co-trimoxazole with or without Gentamicin and/or Metronidazole
• Ceftriaxone with Metronidazole
• Others:
• Piperacillin with Tazobactam
• Clindamycin with Ciprofloxacin and/or Gentamicin
• Vancomycin
• Teicoplanin
• Linezolid
Case Discussion 1
• 48 year-old male
• DM 5years
• Pain, numbness, edema
• DPN
• Ischemia due to PAD
• Infection and Gangrene
• Emergency
Case Discussion 2
• 58 y/o Female
• Hx of DM 6years
• 1yr unhealed ulcer with
mild pain and swelling
after a small puncture
wound
• Present due to a new
Burn on her big toe
• Uncontrolled Blood sugar
• Normal biochemistry Test
• Bone expose and chronic
osteomyelitis ( with deformity)
• After cleaning patient was referred
to DM center for further management
Case Discussion 3
• 63 y/o Female
• T2DM several years
• No medication
• BS 175 fasting
• Acute foot inflammation
• Hx of planta puncture wound 10d ago
• Mild pain
• Moderate pus drained
• D2
• Minimal pus drain
• Reduces edema

• D3
• Serofibrinoeus drain
• No sign of inflammation
• No Dorsal edema
Reference
• ររគុង្ទាសក៍​ សតីពីការរងាារ​និខការប្ររ់ប្រខជរងឺង្ជើខទឹកង្ន្ទរន្នែរ​ឡនការយា
ិ ល័យប្រយុទធនឹខជរងឺរិនឆ្ែខ​ន្ទយលដ្ឋឋនការពារសុ េ
ភាព​ន្េសីហ​ឆ្ា​ំ ២០២១
• IDF Clinical Practice Recommendations on the Diabetic Foot – 2017
• Handbook of Diabetes 5th edition © 2021 John Wiley & Sons Ltd
• Netter’s Illustrated Human Pathology
• Documents and Images from Memot Hospital and Medica Clinic 2022
MCQ
1. ង្ត្រ
ើ ូលង្ហត្ុអរ
វី ខាឲ្យមាន​DFU?
A. ង្ដ្ឋយសារ​Microangiopathy
B. Infection and Trauma
C. Peripheral Neuropathy (DPN) and Ischemia (PAD)
D. Prolonged uncontrolled Hyperglycemia

Answer C
MCQ
2. ការង្្វង្ើ ោរវន
ិ ច
ិ យ
ឆ័ បានង្លឿន​មានប្រង្យាជន៍អវី?
A. ពាបាលទាន់ង្ពល​ង្ជៀសនុត្ការកាត្់អវៈយវៈ
B. កាត្់រនថយង្ប្រោះថ្នាក់ដ្ល់ជីវត្
ិ
C. កាត្់រនថយចំណ្តយកាុខការពាបាល
D. ទាំខអស់ខាខង្លើ

Answer D
MCQ
3. រូលង្ហត្ុអេ
ីវ ោះែ ង្្វឲ្
ើ យ​Atherosclerosis ង្ៅង្លើអក
ា ជរងទ
ឺ ឹកង្ន្ទរន្នែរ​ប្រឈរ
នខ
ឹ ការកាត្់ង្ជខ
ើ ង្ប្ចន
ើ ជាខអាករន
ិ មានជរងទ
ឺ ក
ឹ ង្ន្ទរន្នែរ​?
A. Glycemic vascular injury

B. ង្ត្បៀត្សរឡស្រន្នាកចុខៗ​នខ
ិ ង្ប្ចន
ើ កន្នែខ​ពបា
ិ កកាុខការង្្វើ Bypass ឬ​Stent
C. មាន Atherosclerosis ង្ៅង្លើសរឡស្រ្ំៗ

D. អាកជរងទ
ឺ ក
ឹ ង្ន្ទរន្នែរ​ប្រឈរខាែខ
ំ ជារួយ​Plaque Rupture

Answer B
Thank You!
 PATIENT ID
• 007-858-792-1 : Female 34 ans
• Adresse : Soksan Rumchek Memot TBK
• Came in GM unit : at 09H45 on 30 Nov 2021
• With symptoms and signs :
– Burn sensation and
– Pain full
– Ecchymosis coloration in left hand
 History of present illness
• The disease has been on the rise for 3 months with
symptoms and signs :
– Burning sensation and
– Changing skin color and
– Pain full in the left hand and
– Does not respond to home treatments
• Past Medical History :
– Marriage 5 years with 03 infants
– No: DM. HBP. CHR. Alcohol . Tobacco. Abuse .
 Clinical Exam on 30 Nov 2021 @09H45
• VS:
– BP : 129/80 mmHg . Pulse : 90/min . T : 36.5oC
– RR : 20/min. SatO2 : 98%. H : 155cm. W : 58 Kg
• PS:
– Consciences : Normal
– Glasgow : 4-5-4 = 13 points
– Pain score : 03/10 sometime 05/10 ( EVA )
– ORL : Normal
– Urine Stool and gas : normal
 Clinical Exam on 30 Nov 2021 @09H45
• PS:
– Cutaneous mucosal system :
• Ecchymosis on left hand
• Burning sensation
• Pain score: 03/10 sometime 05/10 ( EVA )
• Coolness sensation and heavy weight
• CRT long time superior from 3-5mn
– CNS :
• Normal alert
• Glasgow scale : 4-5-4 = 13
 Clinical Exam on 30 Nov 2021 @09H45
• PS:
– Cardio Vascular:
• Regular tachycardia
• No murmurs
• BP : 129/80 mm Hg
• Pulse : 90 /min
– Digestive system:
• Abdominal soft no tenderness
• No Hepato-plenomegaly
• No mass palpable
• No rebound, no guarding
• Bowel sound +. Gas +. Stool +
 Clinical Exam on 30 Nov 2021 @09H45
• PS:
– Other system: Normal
• Conclusions:
– RAYNAUD DESEASE ?
– Palmar erythema?
– Acute Lymphangitis ?
– Gangrene ?
– Hemangioma ?
– Plantar palmar erythrodysesthesia ?
 Laboratory Exam
• Complete blood count
• Ionongam . Electrolyte
• Renal function test
• CRP
• Peripheral Vessels ultrasound
Laboratory Result

creatinine clearance = 51.84 ml/min

**Male: 97 to 137 ml/min (1.65 to 2.33 ml/s)
**Female: 88 to 128 ml/min (14.96 to 2.18 ml/s)

Peripheral Vessels ultrasound : No Act

Clinical Diagnosis
 Management and Plant
HYGIENE and Kinesis MEDICAMENTS

• Protection from cool • Calcium channel blockers

• And humidity ( by lotion ) • Tone vasomotor; Vasodilator ;

• Kinesis every day: • Anti-platelet; Statine

(Light massage shower the area) • Antalgic ( Nociceptive / Neurogenic /Mix )

• Vitamin D / Omega 3
 Evolution of the patient form
01-05 Dec 2021
• VS:
▪ BP:112/70, P:70/min, T: 36.8oC
▪ RR: 18/min, SatO2: 97%,
▪ Urine/ Stool/ Gas : Normal
• GS : Normal
• Asthenia; Insomnia
• Pain and Burn Sensation (+)
• Pain score 03/10 ( EVA )
• Left hand Cyanosis ( + )
• Stool . Urine : Normal
• IV Fluid Nss 1000ml
• Amlodipin (5) : 01Tab bid OR
• Aspirin ( 81 ) : 01Tab qd OR
• Clopidogrel (75) : 01Tab bid OR
• Amitriptyline (25) : ½ Tab bid OR
• Fenofibrat (100) : 01Cap qd OR
• Daily shower massage
• Drink warm water 03L
 Evolution of the patient form
06-10 Dec 2021
• VS:
▪ BP:100/65, P:90/min, T: 36.1oC • IV Fluid Nss 1000ml
▪ RR: 18/min, SatO2: 98% • Amlodipin (5) : 01Tab bid OR
▪ Urine/ Stool/ Gas : Normal • Sildonafil : 01 Tab qd PO
• Aspirine ( 81 ) : 01Tab qd PO

• GS : Normal • Clopidogrel (75) : 01Tab bid PO

• Asthenia; Insomnia • Amitriptylin(25) : 01 Tab bid PO
• Pain and Burn Sensation decrease • Fénofibrat (100) : 01Cap bid PO

• Pain score : 03/10 ( EVA ) • Multivitamin : 01 Tab bid PO

• Left hand Cyanosis ( light ) • Daily shower massage
• Drink warm water 03L
 Evolution of the patient form
11-16 Dec 2021
• VS:
▪ BP:123/85, P:85/min, T: 36.3oC • IV Fluid Nss 1000ml
▪ RR: 20/min, SatO2: 96% • Amlodipin (5) : 01Tab bid OR
▪ Urine/ Stool/ Gas : Normal • Sildonafil : 01 Tab qd PO
• Aspirine ( 81 ) : 01Tab qd PO

• GS : Normal • Clopidogrel (75) : 01Tab bid PO

• Asthenia little ; Sleepy well • Amitriptylin(25) : 01 Tab bid PO
• Pain and Burn sensation decrease • Fénofibrat (100) : 01Cap bid PO
( little and sometime )
• Multivitamin : 01 Tab bid PO
• Pain score : 01/10 ( EVA )
• Daily shower massage
• Left hand no Cyanosis
• Drink warm water 03L
 17 Dec 2021

• Avoid exposure to cold, and

• Take vitamin D/H3 in winter, which
sudden changes in temperature
promotes healing
• Warm up hands and feet, as well
• Stop caffeine, tobacco
as all other extremities. "We cover
• Do not use over-the-counter
ourselves well, we put on a hat,
medications
scarf, etc."
 Overview
• Raynaud's (ray-NOSE) disease causes some areas of the body :
– Such as your fingers and toes
– To feel numb and cold in response to cold temperatures or
stress.
– In Raynaud's disease, smaller arteries that supply blood to your
skin become narrow, limiting blood flow to affected areas
(vasospasm).
• Women are more likely than men to have Raynaud's disease
or syndrome.
• It appears to be more common in people who live in colder
climates.
• Treatment of Raynaud's disease depends on its severity and
whether you have other health conditions.
• For most people, Raynaud's disease isn't disabling, but it can
affect your quality of life.
 Symptoms
• Signs and symptoms of Raynaud's disease include:
– Cold fingers or toes
– Color changes in your skin in response to cold or stress
– Numb, prickly feeling or stinging pain upon warming or stress relief
• During an attack of Raynaud's, affected areas of skin usually :
– First turn white
– Then, they often turn blue and feel cold and numb
– As you warm and your circulation improves, the affected areas may
turn red, tingle or swell
• Although Raynaud's most commonly affects the fingers and toes,
• It can also affect other areas of your body, such as your nose,
lips, ears and even nipples.
• After you warm up, the return of normal blood flow to the area
can take 15 minutes.
 Causes
• Doctors don't completely understand the cause of Raynaud's
attacks, but blood vessels in the hands and feet appear to
overreact to cold temperatures or stress.
• Blood vessels in spasm
– With Raynaud's, arteries of fingers and toes become narrow and
briefly limit blood supply when exposed to cold or stress.
– Over time, these small arteries can thicken slightly, further
limiting blood flow.
– Cold temperatures are most likely to trigger an attack.
– Exposure to cold : such as putting your hands in cold water,
taking something from a freezer or being in cold air, is the most
likely trigger.
– For some people, emotional stress can trigger an episode.
 Causes
• There are two main types of the condition:
– Primary Raynaud's ( Raynaud's disease )
• This most common symmetric
• Primary Raynaud's don't seek treatment
• And it can resolve on its own
– Secondary Raynaud's ( Raynaud's phenomenon )
• This form is caused by an underlying problem
• Secondary Raynaud's is less common than the primary form
• it tends to be more serious
• Signs and symptoms of secondary Raynaud's usually appear
around age 35, later than they do for primary Raynaud's.
 Causes
• Causes of secondary Raynaud's include:
– Connective tissue diseases :
• Most people who have a rare disease that leads to hardening and
scarring of the skin (scleroderma) have Raynaud's.
• Other diseases that increase the risk of Raynaud's include lupus,
• Rheumatoid arthritis and Sjogren's syndrome.
– Diseases of the arteries :
• These include a buildup of plaques in blood vessels that feed the
heart,
• Disorder in which the blood vessels of the hands and feet become
inflamed,
• Type of high blood pressure that affects the arteries of the lungs.
– Carpal tunnel syndrome :
• This condition involves pressure on a major nerve to hand,
• producing numbness and pain in the hand that can make the hand
more susceptible to cold temperatures.
 Causes
• Causes of secondary Raynaud's include:
– Repetitive action or vibration. Typing, playing piano or doing
similar movements for long periods and operating vibrating
tools, such as jackhammers, can lead to overuse injuries.
– Smoking : constricts blood vessels.
– Injuries to the hands or feet. Examples include a wrist fracture,
surgery or frostbite.
– Certain medications :
• Beta blockers for high blood pressure,
• Migraine medications that contain ergotamine and sumatriptan,
• Attention-deficit/hyperactivity disorder medications,
• Chemotherapy agents, and drugs that cause blood vessels to
narrow, such as some over-the-counter cold medications.
 Risk factors
• Risk factors for primary Raynaud's include:
– Sex : More women than men are affected.
– Age : Although anyone can develop the condition, primary
Raynaud's often begins between the ages of 15 and 30.
– Climate : The disorder is also more common in people who live
in colder climates.
– Family history :
• A first-degree relative a parent,
• Sibling or child having the disease appears to increase your
risk of primary Raynaud's.
 Risk factors
• Risk factors for secondary Raynaud's include:
– Associated diseases :
• These include conditions such as scleroderma and lupus.
– Certain occupations :
• These include jobs that cause repetitive trauma, such as operating
tools that vibrate.
– Exposure to certain substances :
• This includes smoking,
• Taking medications that affect the blood vessels
• Exposed to certain chemicals ( such as vinyl chloride )
 Diagnosis
• Sorting out primary or secondary Raynaud's
– The difference between primary and secondary Raynaud's
• Do a test called nailfold capillaroscopy during the test, looks at the
skin at the base on fingernail under a microscope or magnifier to
look for deformities or swelling of the tiny blood vessels.
– No one blood test can diagnose Raynaud's
– But the doctor might order other tests, for rule out diseases of
the arteries, to help pinpoint a condition that can be associated
with Raynaud's.
 Treatment
• Dressing for the cold in layers and wearing gloves or heavy
socks usually are effective in dealing with mild symptoms of
Raynaud's.
• Medications are available to treat more-severe forms of the
condition.
• The goals of treatment are to:
– Reduce the number and severity of attacks
– Prevent tissue damage
– Treat the underlying disease or condition
 Treatment
• Depending on the cause of your symptoms, medications
might help. To widen blood vessels and increase blood flow :
– Calcium channel blockers. These drugs relax and open small blood
vessels in your hands and feet, reducing the severity and number of
attacks in most people with Raynaud's. These drugs can also help heal
skin ulcers on your fingers or toes.
– Vasodilators. These drugs, which relax blood vessels, include
nitroglycerin cream (Nitro-Dur) applied to the base of your fingers to
help heal skin ulcers.
– Other vasodilators include the high blood pressure drug losartan
– The erectile dysfunction medication ( sildenafil )
– The antidepressant : ( fluoxetine )
 Complications
• If secondary Raynaud's is severe : is rare — reduced blood
flow of the fingers or toes could cause tissue damage.
• A completely blocked artery :
– Lead to sores (skin ulcers) or dead tissue, both of which can be
difficult to treat.
– Rarely, extreme untreated cases might require removing the
affected part of your body.
 Prevention
• To help prevent Raynaud's attacks:
– Bundle up outdoors. When it's cold, don a hat, scarf, socks and
boots, and two layers of mittens or gloves before you go
outside. Wear a coat with snug cuffs to go around your mittens
or gloves,
– To prevent cold air from reaching your hands.
– Also use chemical hand warmers.
– Wear earmuffs and a face mask if the tip of your nose and your
earlobes are sensitive to cold.
 Prevention
• To help prevent Raynaud's attacks:
– Warm your car : Run your car heater for a few minutes before
driving in cold weather.
– Take precautions indoors : Wear socks. When taking food out of
the refrigerator or freezer, wear gloves, mittens or oven mitts.
wear mittens and socks to bed during winter.
– The air conditioning can trigger attacks : set your air conditioner
to a warmer temperature.
– Use insulated drinking glasses.
 Lifestyle and home remedies
• Avoid smoke
• Exercise
• Control stress
• Avoid rapidly changing temperatures :
– Get indoors or to a warmer area
– Wiggle your fingers and toes
– Place hands under armpits
– Make wide circles ( windmills ) with your arms
– Massage your hands and feet
 Lifestyle and home remedies
• Lifestyle changes and supplements that encourage better
blood flow might help you manage Raynaud's. However, it's
unclear how well these measures may work for Raynaud's.
More study is needed. If you're interested, talk to your doctor
about:
– Fish oil : taking fish oil supplements could help improve your
tolerance to cold and could help decrease the number of
Raynaud's attacks.
– Acupuncture : This practice appears to improve blood flow, so it
may be helpful in relieving Raynaud's attacks.
• References :
– ESVM guidelines – the diagnosis and management of Raynaud’s phenomenon
– https://www.hopkinsmedicine.org/health/conditions-and-diseases/raynauds-phenomenon
 Images similar to Raynaud disease

Prim RAYNAUD DISEASE 2nd RAYNAUD DISEASE Hemangioma

Acute Lymphangitis Gangrene Palmar erythema

Plantar palmar erythrodysesthesia
https://www.cancer.net/coping-with-cancer/physical-emotional-and-social-effects-cancer/managing-physical-side-effects/hand-foot-syndrome-or-palmar-plantar-erythrodysesthesia