CASE REPORT

FROM LABUANG BAJI HOSPITAL

Thusrday, March 22nd 2007

By :: Jeane
Jeane Novita
Novita I.Abbas
I.Abbas
By

Supervised by
by ::
Supervised
Dr.Hj.Misnah D.
D. Basir
Basir Sp.S
Sp.S (K)
(K)
Dr.Hj.Misnah

REGISTRATION
Name

: Mrs.M

Reg.Number

: 105824
: 29 year old

Age
Admission

date : Feb 16 th2007

HYSTORY/ANAMNESIS
A 29th year old woman consulted from Ob-Gin
department 24 th days post partum +anemia+puerpuralis
septic shock +decrease of consciousness
Alloanamnesis :
Decrease of conciousness gradually when she was
lying on the bed ( in Bantaeng Hospital),3 days before
admission
12 hours before admitted to Labuang baji hospital, patient
had no contact with other people

 No

history of : seizure , fever, vomiting, headache and

head trauma.
hypertension before and during pregnancy (-)
history of labour assisted by Dukun 24 days before
admission to Labuang Baji Hospital ( on 22nd January
2007).
The placenta couldnt be drawn Puskesmas the
placenta was completely drawn by midwife

history

of intrauterine bleeding a week after labour

volume of the blood about 3 sarung
Patient had been treated in Bantaeng Hospital 3
days (13-15 February) complain of dizziness and
lower abdominal pain.
patient was transfused with 4 bag of blood (her Hb
was 2 gr/dl)

transferred

to Labuang Baji Hospital with post

placenta retention, accompanied by anemia and septic
shock.
The patient hadnt defecated since 3 days ago
Micturation was with inserted catheter.

PHYSICAL EXAMINATION
Internal

status :
BP: 100/60 mmHg RR: 24/min,thoraco abdominal type
HR : 88/min-regular.
Body temperature : 36,5 0 C
Head : Conjungtiva : anemis +/+, Icterus : -/ Chest : heart and lung : within normal limits
Abdomen : Liver and spleen were not palpable
Uterus fundus : 2 finger above symphisis.
Genitalia : Blood Fluxus (+), pus (+), foetor (+)

Neurological status :
GCS E2M4V1
Higher

cortical function : diffcult to evaluated

Meningeal signs : Neck stiffness (-), Kernig sign (-)
Cranial nerves : Pupil were isocore, 2,5mm, reactive to
light
Funduscophy on right and left eyes: within normal limits.
Corneal Reflexes : +/+
Dolls eye movement (+)
Other cranial nerves difficult to be evaluated

Motoric examination :
Movement and muscle strength were difficult to evaluated
( Right lateralization)
Muscle tone

Physiological Reflexes

Pathological Reflexes +

Sensoric

function

Autonomic

: difficult to evaluated

Function : Uninhibitted bladder

LABORATORY FINDINGS :

16 Feb 2007
WBC : 18.3.103 Hb : 5,3 gr/dl RBC : 2.09.10 6
HCT : 18,5 % PLT : 175.103
Creatinin : 0,33 mg/dl Glucosa at random : 124mg/dl
BT : 115 CT : 6.45

DIAGNOSIS
Clinical

: Decrease of consiusness with right

lateralization
Topical
: Left Hemisphere
Etiological : Non Hemorrhagic Stroke
DD/ Hemorrhagic Stroke

THERAPY
5B :
Breathing : O2 3- 4 l/min
Blood
:
- Blood transfusion
- IVFD RL 20 drops/min
Brain
: - Head elevation 20 - 300
- Anti oedema : Dexamethason 2 amp
bolus, continued with 1 amp/6hours/IV
Bowel
: - Inserted NGT
- Ranitidin 1 amp/12hours/IV
- Bisacodyl Supp
Bladder
: - Insert catheter
- Fluid balance

Neuroprotector : Piracetam 3 gr/ 8 hours/IV

Metronidazole 500mg/8hours/IV
Cefotaxime 1 gr/12hours/IV

ECG : Within Normal Limit

Head CT Scan
Hypodens

and hyperdens lesions in right parietal

region and hypodens lesion in left corona radiata with
density 21-59 HU.
Normal gyri, Sylvii fissure and cortical sulcus.
No midline shift.
Slight widening of ventricle system and cysterna.
No abnormalities were seen in pons, cerebellum and
CPA.
Impression : Cerebral infarct with hemorrhagic in right
parietal and cerebral infarct in left corona radiata.

FOLLOW UP
Feb,

17th 2007
BP: 110/60 mmHg RR: 24/min,thoraco abdominal type
HR : 80/min-regular Body temperature : 380C.
GCS E3M5V1
Movement and muscle strength were difficult to
evaluated ( Right lateralization)
Muscle tone Physiological Reflexes


Pathological Reflexes +
Hb : 6,3gr/dl

Therapy :
5B
Neuroprotector : Piracetam 3 gr/ 8 hours/IV
Metronidazole 500mg/8hours/IV
Cefotaxime 1 gr/12hours/IV
Metamizole 1amp/8hours/IV

 Feb,

19th 2007
BP: 100/60 mmHg RR: 24/min,thoraco abdominal type
HR : 72/min-regular Body temperature : 370C.
GCS E3M5V3
Movement and muscle strength were difficult to
evaluated ( Right lateralization)
Muscle tone
Physiological Reflexes

Pathological Reflexes +

Hb

: 8,7 WBC : 14.9.103

 Therapy

:
IVFD RL 20 drops/min
Neuroprotector : Piracetam 3gr/8hours/IV
Dexamethason 1 amp/ 8 hours/IV
Cefotaxime 1gr/12 hours/IV
Metronidazole 500mg/8hours/IV
Ranitidin 1 amp/12hours/IV
Metamizole 1 amp/8hours/IV
Sulfous Ferrosus 2X1 tab

 Feb,

22nd 2007
BP: 110/60 mmHg RR: 24/min,thoraco abdominal type
HR : 80/min-regular Body temperature : 36,80C.
GCS E4M6V5
Movement

Muscle tone

Pathological Reflexes

Muscle strength 0
3
0
3
Physiological Refelexes

+

 Therapy

IVFD RL 20 drops/min
Neuroprotector : Piracetam 3gr/8hours/IV
Cefotaxime 1gr/12 hours/IV
Metronidazole 500mg/8 hours/IV
Sulfous Ferrosus 2 X 1
FT

 Feb,

24th 2007
BP: 110/70 mmHg RR: 24/min HR : 72/min-regular Body
temperature : 380C
GCS E4M6V5
Movement

Muscle

tone

Muscle strength 0
0

Physiological Refelexes

Pathological Reflexes +
+
Hb : 8,1gr/dl WBC : 18.0.103

3
3

 Therapy

IVFD RL 20 drops/min
Neuroprotector : Piracetam 2x1200mg
Cefotaxime 1gr/12 hours/IV
Metronidazole 500mg/8 hours/IV
Sulfous Ferrosus 2 X 1
Metamizole 1amp/8hours/IV
FT

 March,

1st2007
BP: 120/70 mmHg RR: 24/min,thoraco abdominal type
HR : 80/min-regular Body temperature : 36,8 0C
GCS E4M6V5
Movement
Muscle strength 0
3

0
3
Muscle

tone

Physiological Reflexes

Pathological Reflexes +

Hb : 8,5 gr/dl WBC : 13.0.103

 Therapy

:
Piracetam 2 x1200mg
Cefadroxyl 3 x 500mg
Metronidazole 3 x 500mg
Sulfous Ferrosus 2 X 1
FT

On March 5th 2007, the patient

discharges from
hospital

DIAGNOSIS
Clinical

: Double hemiparesis
Topical
: Right and Left Hemispher (Middle
cerebral artery)
Etiological : Hemorrhagic Infarction due to
Systemic Hypoperfusion

DISCUSSION
Systemic

hypoperfusion (watershed stroke) reduction of

blood flow to all of the body
most commonly due to cardiac pump failure from cardiac
arrest or arrhytmias or from reduced cardiac output as result of
myocardial infarction, pulmonary embolism, pericardial
effusion or bleeding.
Hypoxemia (low blood oxygen content) may precipitate the
hypoperfusion.

Because

the reduction in blood flow is global, all part

of the brain may be affected especially watershed
areas border zone regions supplied by the major
cerebral arteries.
this patient had decrease of consiousness that
occured during admission in Bantaeng Hospital with
history of intra uterine bleeding as much as 3 sarung.
On examination, the bleeding still persisted.

 Neurological

examination lateralization to the right

and bilateral Babinski sign
Laboratory findings : Hb : 5,3 gr/dl, RBC : 209 .10 6 after
4 bags of blood transfusion .
Head CT Scan showed cerebral infarct with hemorrhagic
in right parietal and cerebral infarct in left corona
radiata.

on anamnesis, neurological examination,

laboratory findings and head CT Scan Dx double
hemiparesis due to hemorrhagic infarction due to
systemic hypoperfusion.

Based

 reduced

blood flow to the cerebral hemisphere a

tendency for focal infarction to occur in the regions of
lowest watershed infarction
Blood supply disturbance on that area can rapidly
destruct brain tissue, including neuron, glia and
vasculature

 Colateral

vascularization on that area can be

improved but with a risk that blood supplied to
the area of destruction would accumulate
extravascularly because of hypoxemic
degeneration of the blood vessel wall
there was mix area of infarct with hemorrhage
hemorrhagic infarction

The main syndromes after the patient awakens are :

1. Visual agnosia including Balint Syndrome and cortical
blindness, representing infarction of the watershed
between the middle and posterior cerebtral artery.
2. Proximal arms and shoulder weakness, sometime
accompanied by hip weaknes, reflecting infarction in
the territory between the middle and anterior cerebral
arteries. These patients are able to walk but their arms
dangle and their hip is may be weak

 Treatment

prevention of further hypoxic injury.

Oxyen may be of value during the first hours but
probably of little user after the blood becomes well
oxygenated.
Corticosteroid allay brain possibly celluler swelling,
but again their therapeutic benefit has not been
corroborated by clinical trials

 Prognosis

All of them incorporate several simple

clinical features involving loss of motor, verbal and
pupillary function in various combinations.
Anoxic patients intact brain stem function as indicated
normal pupillary light and dolls head eye movements
and oculovestibular reflexes more favorable out look
to recovery of consiousness and perhaps all their
faculties.

 Conversely, the

absence of these brainstem

reflexes even after circulation and oxygenation
have been restored, particularly pupil that
unchanged to light, implies a grave on most
circumstances.

This

patient has excellent prognosis eventhough

during admission the patient was unconscious
neurological examination positive sign of light
reflex, corneal reflexes and positive Dolls eye
movement indicate that the brainstem still
intact.