SAUD VSD Konklin

Clinical
Conference
Monday, September
12 th, 2011
By saud Parulian
Number of cases
September 09th - 11th, 2011
Physiological delivery
Pathological delivery
Spontaneous
VE
0 case
5 case
4 cases
Major operation room
Caesarean section
4 cases
Gynecology
9 case
Oncology
0 case
Hysteroscopy-Laparoscopy
3 cases
Minor operation room

Curettage
Sterilization
1 case
1 case
Cases to discuss
1. Mrs. M, G1P0A0, 20 yo, 38 Weeks+ 3 days GA
DX:Post elective caesarean section o/I CPD,CHF fc I-II, PDA,VSD P1A0
(MFM case)
2.
Mrs. S,P2A0, 35yo

Dx: Irreversible shock due to early postpartum haemorrhage due to
uterine atony,post spontaneously delivery,P2A0 ( Obstetric caseMortality case)
3. Mrs. H, G3P2A0, 35 yo, 36 wga

Dx: Hepatic encephalopathy, with acute hepatitis B dd acute fatty liver
Post partum gemelli,spontaneously baby1, post manual aid (MullerMauriceau) baby 2,P3A0 (MFM case-mortality case)
4.
Mrs. S, P1A0,35 yo
Dx: Post laparatomy exploration,colostomy and resection, on indication
peritonitis,caecum perforation d-7,post caresarean section ,P1A0 d-12
3
FIRST CASE
Mrs. M, G1P0A0, 20 yo, 38

Weeks+3 days
07/09/11
13.00
G1P0A0
38+3 wga
BP: 120/60
mmHg
P: 80x/m
RR: 22 x/m
T: 36,8 C
Heihgt:145
cm
BW:38,5 kg
Patient felt 9 months pregnancy, uterine

contraction (-), bloody show (-), amniotic
fluid (-)
ANC at Sadrjito Hospital
Obstetric Hystory:
1. This pregnancy
Patient felt dyspnea when she walk about
500 meters.
She felt dyspnea since her first pregnancy
control at public health regularly
At 7 month control to Obgyn at Kota gede
and then refer to cardiologyst
Perfomed Echoresult multiple non
cyanotic heart defect
Get digoxin 2x1,furosemide 2x1,KSR

1x1
Cardiologyst suggest to ANC at
Sardjito hospital
After get therapy from cardiologyst
she felt better
Physical examination
General Condition: good,conscious, not
anemic
Palp:singelton baby,head presentation,UC(-),
head palpable 5/5 part,FHR 136 x/m,EFW
2550 gr
Bimanual Examination:v/u smooth,servix
soft,middle,head presentation,head
floating,blody show(-),amniotic fluid(-)
Pelvic examonation:promontorium felt,linea
terminalis felt >2/3 part, pubic arc <90
EFW 2252 gr
11/1/16
Free PowerPoint Template from www.brainybetty.com
11/1/16
Laboratory findings
Haematology
HGB 13,5
WBC 9,26
RBC 4,66
PLT 253
Ureum 10,1
Crea 0,46
SGOT 24
SGPT 12
Prot 6,29
Albumin 2,89
Globulin 3,02
Na 140
K 4,4
Cl 100
PPT 10,7
APTT 27,3
Echocardiography
VSD perimembrane diameter 0,5cm L-R
shunt,Qp/Qs 0,91
PDA with diameter 2.1 cm
Suspect AP widow with diameter 1,1 cm
EF 65 %
Diagnosis
CPD,Primigravida,fullterm pregnancy
not yet in labour,CHF fc I-II,VSD,PDA
Management
Elective caesarean section
Consult to cardiology
departement
Cardiology
Thorax:Minimum rales at basis of lung
Cardiomegaly:
S2 harden at pulmonal,minimum
holosistole LPSS III-IV,cont mur SII
LPSS
Diagnosis: CHF fc II,PDA,VSD,AP widow
with Pulmonar hypertension
severe,CHD,
Ass:Elective caesarean section
Cronology
7/9/2011
13.00
Consult to
cardiology
dept
Plan for
electif CS
8/9/2011
Performed
electif
caesarean
section
08/09/2011
12.45
Female,2430
gr,47 cm AS
4/8
Chronology
ICU
Department,
Day-0
DX:Post elektif
caesarean section
o/I CPD,CHF fc I-II,
PDA,VSD P1A0,d-0
Therapy:
Inj Ampicilin 3x1 gr
Inj. Ketorolac
3x30mg
Inj. Vit c 2x1 A
Inj. Alinamin F 2x1
sept 8th
2011
Vital Sign
Sense:sedation
BP 100/60 mmHg
P 88 x/m
Rr 16 x/m
SIMV FiO2 50%
Blood gas
analysis:
pH 7.308
pCO2 41.5
pO2 199.7
HCO3 21
BE -4,4
Hgb 13.5
Fluid balance
Wbc 9.26
Rbc 4.66
Plt 253
APTT 27.3
PPT 10.7
ALB 2.89
Chronology
ICU
Department,
Day-1
Sep 8th 2011

Vital Sign
BP 108/478 mmHg
P 88 x/m
Rr 24 x/m
Na 139
K 3.7
Cl 98
06.00
04.00 extubation
11.30 go to dds ward
Hgb 11.3
Thorax x ray
Broncopneumonia
cardiomegaly
Wbc 12.4
Rbc 4.66
Hct 32.6
Plt 198
APTT 27.3
PPT 10.7
ALB 2.15
Analysis
1.What is the best mode of
delivery patient with
diagnosis PDA?
2.Next plan for this patient?
Labour and Delivery

In women with small PDA no special precautions are necessary.
In women with high-risk characteristics, labour and delivery should be planned carefully
with a multidisciplinary team well in advance. It is important to communicate the
delivery plan to the woman as well as other physicians involved in her care. The best
delivery plan is not useful if information is not readily available when needed.
Vaginal delivery is preferred. Women with large PDA with ventricular systolic dysfunction
or pulmonary hypertension are at high risk for complications. In these women,
decreased maternal expulsive efforts during the second stage of labour and forceps or
vacuum delivery is often utilized. To decrease potential harmful complications from
difficult mid cavity-assisted delivery, uterine contractions are often utilized to facilitate
the initial descent of the presenting part.
Most women with PDA do not require special monitoring. The need for maternal
monitoring is dictated by and the functional status of woman, the systolic function of
the left ventricle, the degree of pulmonary artery hypertension and the oxygen
saturations.
In general, endocarditis prophylaxis at the time of labour and delivery is not
recommended in women with PDA.
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A ventricular septal defect (VSD) is present in 1.5

to 2.5 of
1000 women with a pregnancy resulting in a live
birth.
Many of these defects close spontaneously.
Some patients with a larger uncorrected defect
may develop congestive heart failure, arrhythmias,
or pulmonary hypertension.
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Although most patients with patent ductus arteriosus (PDA)

undergo repair during infancy or childhood, some patients
may
present
with
uncorrected
lesions
during
pregnancy.Those with uncorrected PDA with a small or
moderate-sized duct and normal pulmonary arterial pressure
can also expect an uncomplicated pregnancy.In patients with
a significant left-to-right shunt, secondary pulmonary
hypertension may occur and result in the increased morbidity
and mortality of Eisenmenger syndrome. Patients who have
corrected PDA generally have an uncomplicated course in
pregnancy.8 Whittemore et al. report the outcome of 105
pregnancies in 42 women with PDA, all of which had been
surgically corrected. The liveborn infant rate was 79%, and
Gregory A.L. Davies, MD, FRCSC, FACOG,1 William N.P. Herbert, MD,
there were no maternal complications.
FACOG2
1Professor and Chair, Division of Maternal-Fetal Medicine, Department of
Obstetrics and Gynaecology, Queens University, Kingston ON
2William Norman Thornton Professor and Chair, Department of Obstetrics and
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What Causes Patent Ductus

Arteriosus?
The cause of patent ductus arteriosus isn't
known. Genetics may play a role. A
defect in one or more genes could
prevent the ductus arteriosus from
closing normally after birth.
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Next management
Surgery
Surgery is planned for treatment of
related congenital heart defects
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Mortality risk associated with pregnancy

Group 1: Mortality less than 1%
Atrial septal defect, uncomplicated
Ventricular septal defect, uncomplicated
Patent ductus arteriosus, uncomplicated
Pulmonic and tricuspid disease
Corrected tetralogy of Fallot
Porcine valve
Mitral stenosis, NYHA classes I and II
Group 2: Mortality 5% to 15%
Mitral stenosis with atrial fibrillation
Artificial valve
Mitral stenosis, NYHA classes III and IV
Aortic stenosis
Coarctation of aorta, uncomplicated
Uncorrected tetralogy of Fallot
Previous myocardial infarction
Marfan syndrome with normal aorta
Group 3: Mortality 25% to 50%
Pulmonary hypertension
Coarctation of aorta, complicated
Marfan syndrome with aortic involvement
Reprinted from Clark SL, Cotton DB, Hankins GDV,
Phelan JP. Handbook of critical care obstetrics.
Boston: Blackwell Scientific Publications; 1994: 58, with
permission from Elsevier
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Mrs.S, P2A0, 35 yo.

P2A0
06/09/2011
18.30
BP:60/palpatio
n
N: not
palpable
RR: 20 x/m
Patient was referred from Midwife with notes

hypovolemic shock, early post partum
hemorrhage due to uterine atony, post
spontaneous delivery, P2A0, Day 0
Patient was delivered by midwife at 15.00 pm,at
laten fase,
At 16.00 with second stage,
At 16.20 baby delivered male,3300 gr,AS 5/9
placenta was delivered spontaneously not
completly and then she performed exploration
not complete,uterine contraction not good
massive bleedingreferred
At 17.45.pm arrived at Emergency BP 60/40room
and get two line IFVDBP 80/60.
History of obstetric
1. 19 yo,spontaneously,healthy
2. , 3000 gr,AS 5/9
History of DM, astma, hipertension, hearth disease
were denied.
Physical Examination
GC: weak,conscious, anemic
Conjunctiva : pale,isokor
Thorax:simetris,vesiculer
Palp : abdomen supple,fh at level of
navel,contraction weak
BE:v/u smooth,servix dilatation 1 cm,
vaginal bleeding,no
laceration,sutured of perineum
ruptured
Exploration of cavum uterine:
no retain placenta
Laboratory
findings
WBC 24,21
RBC 3,35
HB 10,1
HCT 27,1
PLT 222
Diagnosis: Hypovolemic shock, early post partum

hemorrhage due to uterine atony, post
spontaneous delivery, P2A0, Day 0
Management :
- Hemodinamyc stabilization
- IV 2 line
- O2 5 liter/mnt
- Massage of fundal
-Internal bimanual compression
-Uterotonics :-metergin IV 1 amp
-metergin:oxytocin 1:1
-misoprostol 3 tab rectal,2 tab
Management :
- prepare of WB transfusion
Consult to obgynacc dx/tx
Chronology
18.45
Bleeding 1000 ml
Inserted Condom
catheter 500 ml
19.00
Consult for Histerectomy
+Haes
not agree, advis:
- IVFD RL + Nacl
- No more oxcytocin
Chronology
19.15
Patient
decreased of
consciousness
BP not
measured,
Pulse not
palpable
RR:cusmaull
Consult to
obgyn to
ICUacc
ICUfull
19.20
Consult to
obgynadvise
Consult to
anestesia dept
19.25
Anestesia
advise
Intubation
Bagging
CPR
Inj Adrenalin
1mp
Patient was
passed away
Chronology (06 -09- 2011)
19.35
Apnea
BP:unmeasurab
le
Pulse:not
palpable
Performed CPR
19.45
Passed away
Total bleeding 3000 ml

Total of IFVD 6 flsh= 3000 ml
Whole blood 50 ml
Uterotonics:-oxytocin 5 amp
-misoprostol
5 tabs
-methergin 3
amp
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Analysis
1. What is the cause of mortality in this
patient?
2.Is the management of this patient
appropriate?
3. Is it avoidable or unavoidable?
DISCUSSION
The cause of mortality is
irreversible shock hypovolemic
due to uterine atony.
Atony is the most common cause of

postpartum hemorrhage (50% of
cases).
Failure of the uterus to contract properly

following delivery is the most common
cause of obstetrical hemorrhage.
In many women, uterine atony can at
least be anticipated well in advance of
delivery.
Although risk factors are well known,
the ability to identify which individual
woman will experience atony is limited.
Williams Obstetrics, 2010
The risk factors of uterine

atony
Overdistended uterus
Large fetus
Multiple fetuses
Hydramnios
Distension with clots
Labor induction
Anesthesia or analgesia
Halogenated agents
Conduction analgesia with hypotension
Exhausted myometrium
Rapid labor
Prolonged labor
Oxytocin or prostaglandin stimulation
Chorioamnionitis
Previous uterine atony
Williams Obstetrics, 2010
Babinszki and colleagues

(1999), Reported the incidence of
postpartum hemorrhage to be 0.3
percent in women of low parity.
Is the management
appropriate?
Patient referred only with IV
line
In Muntilan Hospital
management inappropriate
-fluid resucitation not
adequat
-blood transfusion not
enough
Condom had inserted but

bleeding still on going and no
improvement uterine
contraction
Management of Hypovolemic
Shock
Estimation of blood loss
Renal blood flow is especially sensitive to change in blood
volume
Resuscitation and acute management

Fluid Replacement
Crystalloid solution typically are used for initial volume
resuscitation
Blood Replacement
Cardiac output does not substantively decrease until Hb
Concentration falls to approximately 7 g/dL or Hematocrit
of 20 volume %.
Blood Replacement
Compatible Whole blood is ideal for treatment of
hypovolemia from catastrophic acute hemorrage
Management
Management shock
Haemorrhage
Blood transfusion should be considered in any

woman with postpartum hemorrhage in whom
abdominal uterine massage and oxytocic
agents fail to control bleeding.
With transfusion and simultaneous manual
uterine compression and intravenous oxytocin,
additional measures are rarely required
Williams
Obstetrics,23e
Obstetrical
Gowri Ramanathan, Postpartum Hemorrhage,

JOGC , 2006
The mortality
precipitat
us
delivery
Uterine
atony
irreversibl
e shock
Avoidable
THIRD CASE
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49
3. Mrs. H, G3P2A0, 35 yo, 36 wga

23/08/2011
18.30
G3P2A0
LMP:
10/12/2010
EDD :
17/09/2011
GA : 36 wga
BP 100/60 mmhg
P 80 x/m
T 36.5
Patient referred from midwife with

notes,G3P2A0 with twin pregnancy.
Patient felt 8 month pregnancy, no
uterine contraction,no bloody show,and
no amniotic fluid. No history of hepatitis.
There are no history of asthma, DM, HT,
cadiac disease . ANC at midwife
Obs history:
male, 3800 gr,spontaneously at midwife ,10
yo
male 3400 gr,spontaneously,at midwife ,8
yo
This pregnancy
GC: good,conscious, not anemic
Sclera : icteric,conjunctiva not anemic
Thorax: within normal limit
Palp: twin pregnancy(cephalic
breech presentation),FHR I
132x/m,FHR II 122x/m,UC (-)
BE:v/u smooth,sevix thick,soft,at
posterior,dilatation 1 finger,head
presentation,heads-2,bloody
show(-),AF(-)
Diagnosis
Twin pregnancy (cephalic-breech
presentation) preterm pregnancy,not
yet in labour,with acute hepatitis B dd
acute fatty liver
management:
curcuma 3x1
Consult to internal
departement
Laboratory findings
WBC 12.34
RBC 3,81
HGB 11,9
HCT 34,2
PLT 179
RBG 79
TP 5,3
ALB 2,4
SGOT 287
SGPT 142
UR 21,8
CRE 0,88
NA 140
K 4,6
CL 109
HBSAG (+)
USG resident: twin pregnancy

(cephalic-breech presentation)
EFW I: 3000 gr
EFW II: 2700 gr
GA: 37 wga
Plan for Staff sonografi
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USG radiology:twin pregnancy

(cephalic-transverse lie
presentation)
EFW I: 2700 gr
EFW II: 2700 gr
GA: 37 wga
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25/8/2011
04.30
Aminiotic membrane
broken
1 jari
second stge
11.00
11.15 Baby I
deliverrspontaneously,
female, 2810 gr, 47 cm,
AS 7/9
11.50 Baby 2 deliver
,Manual
Aid
(MullerMauriceau), female, 2690
gr, 47 cm, AS 7/9
26/8/2011
07.00
WBC 7,54
HgB 2,8
HCT 8,8
PLT 49
Dx: Post partum
Gemeli,
jspontaneously baby1,
post manual aid
(Muller-Mauriceau)
jbaby 2 a, P3A0, d-1
with acute hepatitis B
dd acute fatty liver
Tx:
- Amoxycilin 3x 500
mg
- Mefenamic acid 3x
500 mg
- SF 1X1
- Curcuma 3x1
- Check lab check
for blood
- Consult to internal
dept
Check lab
AL 12,53
AE 8,7
HB 7.5
HCT 27
PLT 149
27/8/2011
07.00
Lab (08.42)
WBC 27,32
HgB 13,8
HCT 37,8
PLT 206
Internal dept
Dx: Hepatitis B
Tx:
Inf D5 20 tpm
Curcuma 3x1
Inj Amoxycilin 3x1 gr
~
28/2011
06.00
BP 130/80
P 82
R 18
T 36,8
Urine analysis
color:yellow
PH 6,0
BJ 1.30
PROT GLU
KET
BIL +3
UROBIL
DRH +2
LEUKOSIT
TEST
Sedimen t
Leuko 10-15
Eritro 20-35
Epitel 2-3
TBIL 20,36
DBIL 9,7
Bil ind 10,66
SGOT 141
SGPT 91
28/8/11
09.00
BP
100/60
N 60x/m
R 32x/m
T afeb
GC: ,delirium
sclera icteric, not anemic,
lateralisasi (-)
Thorax:
Cor: S1-S2 regular, murmur
(-)
Pulmo: Vesicular, wh (-),
rh(-)
Abdomen: Hepatomegaly, 2
j fingers under of right
arcus costae spleen normal
Ekst: RF +/+ (normal),
Dx: decreased of level
conciousness due to hepatic
encephalopaty,
acute hepatitis B dd acute
fatty liver , Post partum
Gemeli
Tx:
Airway clear
Oksigenisasi NRM 10 lpm
ICU dan consult to amesthetic
consult to internal dept and
10.15
BP
130/80
p 120x/m
R 28x/m
T afeb
Internal Dept
Dx:
Hepatitis B
Obs of decreased
level of consc due to
neurogenic dd
vasculer
Post partum Gemeli
SIRS
Tx:
NRM 9 lpm
Inf D5 20 tpm
Inj Cefotaxim 1gr/12
jam
Curcuma 3x1
Urdafak 3x1
11.00Consult
GLU 30 87
(check after
resucitation D40
2 flash)
AST 143
ALT 91
UREA 83,3
CRE 1,63
UA 7,81
NA 139
K 5,0
CL 104
AL 3,33
AE 4,79
HB 15,0
HCT 42,1
PLT 113
neurolgy
dept vby phone
Advise : - CT Scan
Citicholin 2x250 mg
(iv)
Anestetic
Dx: Obs decreased
level of consc due
to ?
Hipoglikemia
Leukopenia
Tx:
NRM 02 10 lpm
Inj D40% 3 flash
(75cc)
IIVFD 10%
Pro CT scan +
thorax
28/8/2011
13.00
GC:
Somnolen
BP
130/palp
P 112x/m
R 32x/m
T 35,6
Tx:
IVFD 2line
Airway clear
Oksigenisasi NRM 10
lpm
Consult anesthesi a
not agree to ICU
14.00
GC Sopor
BP 80/60
P120x/m
R 36
T 35,6
15.00
GC: coma,
GCS 3
BD 50/palp
N 146 x/m
R 40 x/m
T 36,0
Dx: ccma hepatikum

suspect
ensefalopatthy
hepatikum due to
acute hepatitis B dd
acute fatty liver, Post
partum gemelli
15.15
GC:ApneaCPR
15 mnts
15.30
Passed away
CT scan
Cerebral edema
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59
Analysis
1. What is cause of death
2. Is management appropriate for this patient
3.Avoidable or anavoidable
Possibilty of cause of
death
Hepatic encephalopathy
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61
Pathogenesis
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62
Probably cause by
AFLP
Acute fatty liver of pregnancy
(AFLP)
Association with obesity, multiple
pregnancies and male fetus
Women aged 16-39 (mean age
29)
Incidence is 1 in 7,000 to 1 in
Journal of Gynecology
and Obstetrics ISSN: 1528-8439
15,000
pregnancies
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63
The most common symptoms are:

Nausea and vomiting
Abdominal pain
Malaise, headache, tiredness and confusion.
Anorexia, jaundice (usually appears within 2
weeks of the onset of the symptoms)
Renal impairment.
Fulminant liver failure with hepatic
encephalopathy.
Journal of Gynecology and Obstetrics ISSN: 1528-8439

11/1/16
64
Exactly pathogenesis in
unknown
Differential diagnosis is HELLP
syndrome, cholestasis of
pregnancy and viral hepatitis
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65
Common complications are :

Renal failure
Hypoglycemia
Infection
Gastrointestinal hemorrhage
Coagulopathy
Severe postpartum hemorrhage
Fulminate hepatic failure
Stillbirth
Journal of Gynecology and Obstetrics ISSN: 1528-8439
11/1/16
66
Management
Prompt delivery and supportive
care of the mother
Delay in delivery may result in
adverse maternal outcome
Journal of Gynecology and Obstetrics ISSN: 15288439
11/1/16
67
ManagementAppropriate
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68
Conclussion
Unavoidable
FOURTH CASE
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4. Mrs. S, G1P0A0, 35 yo,41 WGA

30/08/11
23.30
G1P0A0
41 wga
BP: 100/70
mmHg
P: 76x/m
RR: 22 x/m
T: 36,8 C
Patient felt 9 months pregnancy,

uterine contraction (-), bloody show
(-), amniotic membrane broken 23.00
ANC at midwife
Obstetric Hystory:
1. This pregnancy
History of ht,asthma,dm,cardiac
disease denied
GC: good,concious,not anemic
Palp:singelton baby,longitudinal
lie,cephalic presentation,palpable 5/5
part,UC(-),FHR 141x/m FH 29 cm
LAB
HGB 11,8
WBC 7.7
RBC 3.78
HCT 33.9
PLT 213
PPT 11.8
APTT 26.6
BE: v/u normal,servix thick, at

posterior,no
dilatation,cephalic
presentation,head s-2,nitrazin
test (+)
Dx:Primigravida,postdate,not yet in
labor,IP 3 years
Tx: Plan for induction misoprostol
25ug/oral/6 hrs,if NST reactive
Consult to obgynCaesarean section
USG:Efw 3613 GR
NST: Reactive
04.45Performed esarean
section
Baby :male,4020 gr,50 cm AS
6/9
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Cronology:
31-08-2011
Dx:Post caesarean section o/I
Premature ruptured of
membrane,IP 3 years,P1A0
02-09-11: Patien felt
distended,pain
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74
Palp:abdomen distended,pain
Auscultation:Peristaltic weak
Tx: Alinamin F 3x1A
Consult to surgery dept:
Rectal xamination:
conclusioncolaps
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Management from surgery

dept:
-NGT
-X ray abdomen
X ray abdomen results:
obstructive ileus
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04/9/2011 10.00
Digestif surgery dept:
-flatus
(+),feces(+),peristaltic(+)
Ass:no action from digestif
surgery
04/9/2011 20.00
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77
Consult to digestif surgery

dept:
There is no emergency sign
Advis: Abdominal x-ray
Abd x-ray result: High
obstructive ileus suspect
adhesion
Plan for laparatomy
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Abdominal x-ray
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Abdominal x-ray
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80
During operation 5-0911

After peritoneum parietale was
open,exploration, pus about 100
ml,distended of intestines from treitz
ligament to caecum
Laceration about 30 cm form treitz lig
Caeum perforation size 0.5 x 0.5 cm
Performed ileum terminal resection,caecum
until colon ascendens
Hartman procedure
Abdominal cavity washing with Nacl
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Diagnosis post
operation
Generalisata peritonitis due to
caecum perforation
Tx: - IVFD Rl 28 dpm
- Inj ceftriaxon 2x1 gr
- Inf Metronidazole 3x500
mg
- Inj Ketorolac 3x30 mg
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NGT: 400 ml/24 hours

8-09-2011 : - Anal dilatation 2x1
day
- Colostomy routine
care
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83
This morning
condition
Dx.Generalisata peritonitis due to caecum
perforation, post LE-Hartman procedures,
d7
Tx: - IVFD Rl 28 dpm
- Inj Ceftriaxon 2x1 gr
- Inf Metronidazole 3x500 mg
- Inj Ketorolac 3x30 mg
- Inj Ranitidin 2x1 A
- Zinc zalf around the stoma k/p
-GV once a day
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84
Laboratory
examination
7/9/11
BUN 42
Crea 1,67
GDS 114
11/1/16
9/9/11
WBC 13,94
RBC 4,37
HGB 12,8
HCT 38,9
PLT 195
Alb 2,49
Na 152
K3
CL 105
85
Analysis
What is cause of caecum
perforation?
How to diagnosis of caecum
perforation?
11/1/16
86
Discussion
Although uncommon after a
Caesarean section, caecal
perforation should be suspected if
a patient presents with symptoms
of a prolonged bowel obstruction
Matthew D. Laskin, MD, Karen Tessler, MD, Sari Kives,
MD
Department of Obstetrics and Gynaecology, St. Michaels
Hospital, University of Toronto ON
11/1/16
87
The first clinical sign of colonic obstruction is usually

abdominal distension without the passage of flatus. If there is
a perforation present, the patient may begin to exhibit signs
of intra-abdominal sepsis such as fever, hypotension,or
tachycardia.
An X-ray with erect and supine views of the abdomen is the
single most reliable diagnostic study. If there is simply a
mechanical obstruction, then there will be grossly dilated
loops of large bowel, which may also lead to mild dilatation of
small bowel loops. However, if a perforationis present, a
significant amount of free air will be visible inferior to the
diaphragm.
11/1/16
88
Colonic obstruction is characterized by a clinical picture

suggestive of a mechanical bowel obstruction. Its
incidence during pregnancy varies from 0.001% to
0.2%.17 Some patients with colonic obstruction may be
asymptomatic before Caesarean section, but most of
these cases will present after Caesarean section even if
there was no evidence of pre-operative symptoms.
During pregnancy, diagnosing colonic obstruction
clinically can be especially difficult due to the gravid
uterus distending the abdomen. Constipation, nausea, and
vomiting occur relatively frequently in pregnancy and
confound the diagnosis.
11/1/16
89
The mortality rate from a postCaesarean section caecal

perforation in our review was
1/21 cases (4.8%)
The mortality rate in the nonobstetrical population ranges
from
5.9%1 to 71%
11/1/16
90
Thank You

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Clinical

Major operation room

Minor operation room

Mrs. S,P2A0, 35yo

3. Mrs. H, G3P2A0, 35 yo, 36 wga

Mrs. M, G1P0A0, 20 yo, 38

Patient felt 9 months pregnancy, uterine

Get digoxin 2x1,furosemide 2x1,KSR

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Sep 8th 2011

Labour and Delivery

A ventricular septal defect (VSD) is present in 1.5

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Although most patients with patent ductus arteriosus (PDA)

What Causes Patent Ductus

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Mortality risk associated with pregnancy

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Mrs.S, P2A0, 35 yo.

Patient was referred from Midwife with notes

Diagnosis: Hypovolemic shock, early post partum

Consult to obgynacc dx/tx

Chronology (06 -09- 2011)

Total bleeding 3000 ml

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Atony is the most common cause of

Failure of the uterus to contract properly

The risk factors of uterine

Williams Obstetrics, 2010

Babinszki and colleagues

Condom had inserted but

Resuscitation and acute management

Blood transfusion should be considered in any

Gowri Ramanathan, Postpartum Hemorrhage,

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3. Mrs. H, G3P2A0, 35 yo, 36 wga

Patient referred from midwife with

USG resident: twin pregnancy

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USG radiology:twin pregnancy

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Dx: ccma hepatikum

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The most common symptoms are:

Journal of Gynecology and Obstetrics ISSN: 1528-8439

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Common complications are :

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4. Mrs. S, G1P0A0, 35 yo,41 WGA

Patient felt 9 months pregnancy,

BE: v/u normal,servix thick, at

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Management from surgery