Hematome

Subdural in
Neonates
CASE REPORT
Dr. Irma
Yenni

Subdural Hematome
(SDH)
is the accumulation of blood in the subdural cavity
that occur due to tearing of small veins connecting link
between duramater and pia arachnoid
Incidence of SDH in newborn at developing country are
18.2% -46 %, and In developed countries the
incidence of SDH are 12.8 / 100,000 children / year
Subdural hematoma has a poor prognosis, as many as
75% of cases die or live with severe neurological
sequelae

Subdural Hematome
(SDH)
SDH in infants can be caused by various causes and most
are asymptomatic occurring after spontaneous labor

The general symptoms convulsions, pallor, and

decreased of consciousness

The primary diagnostic tool is CT scan, and MRI was use

to determine brain parenchymal damage associated with
trauma that can not be seen with a CT-scan.

Purpose of
this case
presentatio
n

to provide knowledge to us about

the SDH in neonates, clinical
symptoms, and treatment. Which
is expected to provide additional
knowledge and provide better
results in patients

CASE
Identification

A 23 days old boy, weight 3,6 kg,

body length 53 cm, live outside
Palembang, came to the NICU
RSMH on February 16, 2016
Main complaint

Seizures

Additional
Complaint

loss of consciousness

Present illness history

23 days
before
admission

22 days
before
admission

1 days before
admission

23 days before
The baby boy was born spontaneously of
admission
G2P1A0
pregnant mother at home, aterm, and helped
by a midwife.
unknown Apgar scores, birth weight 2400 gr,
body length is unknown.
Mother history of fever during pregnancy : No
History of the premature rupture of
membranes : No
The Amniotic is normal

Present illness history

23 days
before
admission

22 days
before
admission

1 days before
admission

22 days before
admission
the patient suddenly had a seizures, eyes
bulging upward, longer than 5 minutes, postictal: child is unconscious, no fever, and no
vomiting. Patients also look pale and did not
want to suckle.
Patients were taken to RSUD and treated one
day, and had bood transfusion.
7

Present illness history

23 days
before
admission

22 days
before
admission

1 days before
admission

1 days before
admission
The parents complained that the baby do not
cry, and do not wake up despite being in touch
and stimulate.
because there is no improvement and for further
examination the patient was referred to RSMH
Palembang.
8

PAST MEDICAL
HISTORY

History of Traumatic delivery denied

History of Vitamin K injection at birth (-)
History of swung of the child denied

FAMILY HISTORY

Parents or family history with the same

complaint denied
Family history who died at birth or age of the
children
denied
MATERNAL
& BIRTH
HISTORY

Normal

IMUNIZATION

Incomplete basic PPI immunization

NUTRITION HISTORY

Patients were given breast milk

only from birth until now
GROWTH AND
DEVELOPMENT
Normal
SOSIO-ECONOMIC
HISTORY

Low

PHYSICAL
EXAMINATION
General Appearance
General Appearance

GCS : E2M5V5
hypoactive, suction reflect and weak cries
Pulse : 136 times/min
RR : 40 times/min (reguler)
Axillary temp: 37C
Anemic (+)
Head circumference: 34 cm

PHYSICAL EXAMINATION
Spesific finding
Head
Normocephaly, bulging of the head crown (+), the
pupil round, isokor 2mm / 2mm, light reflex + / +
decreased
Thorax, Abdomen and
Extrimities
Normal finding

Initial Problems

Pale history
Seizures
Loss of consciousness

Working Diagnosis

ntracranial Hemorrhag

Problems
Planning
Seizures and loss of
consciousness

Pale

Diagnostic Plan
Routine blood test,
ESR, CRP, hemostasis
physiology
Treatment

Electrolytes test,
BSS,
CT scan of the head
Plan

Blood transfusion

Phenobarbital
Vit K inj 3x1
Education Plan

Provides counseling, information and education (the causes,

examination plan to be
performed, management and prognosis).
Monitoring the complications and side effects of drugs
Provide an explanation of the importance of monitoring

Progress Note
M

Intacranial Hemorrhage

Loss of consciousness

February 17,
2016

Bulging of The head crown

O

Lab: Hb 13 g/dL leukosit 10.800/mm3 Ht 39% Plat

558.000/l PT 12,4 APTT 40,4 INR 0,95 Ca 9.1 Na 135
K 4,9
CT Scan: SDH of the left temporooccipital lobe
Neurosurgery consul: loss of consciousness and
seizures ec left temporooccipital lobe SDH

left temporooccipital lobe SDH

Elective craniotomy

Progress Note

February 20,
2016

Loss of consciousness (-)

Bulging of The head crown

left temporooccipital lobe SDH

Elective craniotomy Waited for schedule

Plans to move to the neonatal ward

Progress Note

February 28,
2016

Loss of consciousness (-)

Bulging of The head crown

Preparation for craniotomy tommorow

Crossmatch
Fasting

Progress Note

February 29,
2016

SDH evacuation Craniotomy is completed

Lab: Hb 13 g/dL leukosit 13.600/mm3 Ht 41%

Plat 460.000/l PT 17,8 APTT 46,3 INR 1,47

Post SDH evacuation craniotomy

Ceftazidim injection 3x160 mg

Progress Note
S

March 3,
2016

Fever (-)

Post SDH evacuation craniotomy 3rd day

Plans to move to the neonate ward

Progress Note
S

March 7,
2016

Fever (-)

Post SDH evacuation craniotomy 8th day

discharge and controls to neurosurgery

polyclinic

Progress Note

AprilA 8, 2016
(neurosurgery
polyclinic)

Fever (-)

Composmentis, HR 136x/min, T 36,70 C, RR

42x/min
CT scan : left hemisfer subarachnoid kist

Post SDH evacuation craniotomy day 40

controls to growth and development

polyclinic

LITERATURE REVIEW

ubdural Hematom
(SDH)

DEFINITION
SDH is a blood accumulation in the subdural
cavity (between the dura and arachnoid), its can
be caused by head trauma or may occur
spontaneously
SDH occurs most frequently on the lateral surface
of hemisferium and partly in the temporal region,
in accordance with the distribution of bridging
veins.

ETIOLOGY
Birth trauma
Regular delivery :
excessive withdrawal of the head
cephalopelvic disproportion
Artificial
2
delivery
vacuum extraction
forceps
1

Precipitate delivery

Non birth trauma commonly in preterm infants

Bleeding disease/Blood clotting disorders

CLASSIFICATION
1

Acute SDH

Sub Acute SDH

Chronic SDH

Acute SDH
occur in severe head trauma, symptoms develop quickly
until hours after the trauma.
1

Bleeding can be less than 5 mm in thickness but wide

area. This condition has a poor prognosis, not only
because of the blood in the subdural alone, but because it
is so often associated with injury to the surrounding
parenchyma
The mortality can reach about 50%.
The Ct-scan hiperdens lesions.

Sub Acute SDH

Usually develops within a few days about 4-21 days after

trauma. symptoms occur a few days up to 10 days after
the trauma.Bleeding may be thicker but no capsule
formation around it.
CT Scan isodens or hipodens lesion

Chronic SDH

usually occurs after 21 days after the trauma or more.

Symptoms appear after some weeks to a few months
after the trauma.
the hematoma surrounded by connective tissue capsule
The capsule is containing blood vessels with thin walls,
especially on the side of the duramater.
Hematoma will enlarge and cause symptoms such as
cerebral tumor
CT Scan Low density lesions

PATHOPHYSIOLOGY
SDH is an intracranial hemorrhage that often found in
term infant caused by rupture of cortical veins that
connect the subdural cavity with the sinuses of the
duramaters .
Bleeding happens between the dura and arakhnoidea. It
may occur as a result of tearing of bridging veins which
connects the brain surface veins and dural venous sinuses
in or due to araknoidea rupture.

In children, SDH in the posterior and tentorium

interhemisferik fissures are often found as a great
shock to the child's body shaken baby
syndrome

CLINICAL
MANIFESTATIONS
signs and symptoms may appear within
minutes or otherwise appear to be up to
2 weeks.
Symptoms seen in neonates is loss of
consciousness, letargy, vomiting,
accompanied by neurological disorders
such as hemiparesis, eye movement
disorders and papill edema

CLINICAL
MANIFESTATIONS
The clinical features is determined by two factors:
1

the severity of a brain injury that occurs when

the collision trauma

The speed of SDH volume increase

CLINICAL
MANIFESTATIONS
Acute SDH
Acute SDH causing neurologic symptoms in 24 to 48
hours after the injury, is closely related to severe
brain trauma.
Progressive neurologic disorder caused by the
pressure on the brain tissue and brain stem herniation
into the foramen magnum pressure on the brain
stem.
This situation quickly lead to cessation of breathing
and loss of control over the pulse and blood pressure.

CLINICAL
MANIFESTATIONS
Sub acute SDH
This hematoma causing neurologic deficit in more
than 48 hours but less than 2 weeks after the injury
Anamnesis shows that is the head trauma that causes
unconsciousness, followed by improvement of
neurologic status slowly. But in certain period of time,
the patient shows signs of worsening neurologic
status.

CLINICAL
MANIFESTATIONS
Chronic SDH
The onset of symptoms is generally delayed several
weeks, months and even years after the first injury.
The first trauma tearing one of the veins that pass
through the subdural space
Within 7 to 10 days after the bleeding occurs, blood
surrounded by a fibrous membrane. the difference in
osmotic pressure attracted fluid into the hematoma
and damaged blood cells in the hematoma tearing
the membrane or the blood vessels around it,
increase the size and pressure of the hematoma

DIAGNOSIS
1

Anamnesis

Physical
examination

Supporting
investigation

DIAGNOSIS
1

Anamnesis

head trauma history (with or without injury)

loss of consciousness or fainting vomitting, seizures
headache or nausea, weakness of limbs
diseases, drugs and alcohol hystory

DIAGNOSIS
2

Physical
Examination

Clinical examination:
Primary survey: airway, breathing, circulation
resuscitation
Neurologic examination
GCS
the examination of the second diameter of the pupil,
and
signs of neurological deficit

DIAGNOSIS
Supporting
3
Investigation
a. Laboratorium:

b.

c.

routine blood tests, electrolytes, hemostasis /

coagulation profile
CT Scan
A CT scan is the primary modality of choice
because the process is fast, able to see the whole
brain tissue and accurately distinguish the nature
and existence of intra-axial lesions and extra-axial.
MRI
use to determine brain parenchymal damage
associated with trauma that can not be seen with a
CT-scan.

SDH on Head CT

MANAGEMENT
1.Operative Treatment

Surgery on SDH should

perform as soon as
possible.

2. Non Operative
Treatment
is an option
for patients
without neurological
disorders.
Its consist:
inpatient observation
steroids or mannitol
experiment
serial CT scans.

1. Operative
Treatment
Operation
indication for SDH:
1. SDH patients without seeing the GCS, with a
thickness of> 10 mm or shift of midline > 5 mm
on CT-scan
2. All SDH patients with GCS <9 that should
monitoring the ICT
3. SDH patients with GCS <9, with a thickness of
bleeding <10 mm and midline structure shift.If
GCS decreased > 2 points between the time of the
incident until the time of admission
4. SDH patients with GCS <9, and / or the pupil
dilation asymmetric / fixed
5. SDH patients with GCS <9, and / or ICT> 20
mmHg

1. Operative
Treatment

Purpose of
the surgery

a.Evacuation of all SDH

b.Treat the source of
bleeding
c.Resection of the nonviable
brain parenchyma
d. Existing of ICH

1. Operative
Treatment

burr-hole
craniotomy

twist drill
craniotomy

subdural drain

Post Operative
Treatment
Monitor the patient's general and neurological condition
Cranioplasty performed 6-8 weeks after the operative
stiches is open
Serial CT Scan to assess whether there occur more
hematoma later

2. Non Operative
Treatment
Performed in:
Minor bleeding case (bleeding volume 30 cc or less)
A coma patients with acute SDH but did not show an
increase of intracranial pressure
An acute SDH Patients with negative brainstem reflexes
and depression of the respiratory center

COMPLICATION
1

Medical
complications

Seizures, Pneumonia, Empiema, and another infections

Operative
complications
Subdural mass, Intraparenchym hematome, tension
pneumocephalus, Brain abcess, Meningitis, etc
2

PROGNOSIS
Not all SDH is lethal.In some cases, bleeding does
not continue reached a size that can cause
compression of the brain, so it only causes mild
symptoms.
Surgery on chronic SDH had a good prognosis,
because about 90% of cases will be cured completely

In patients with mild acute SDH (diameter <1 cm),

the prognosis is good

PROGNOSIS
simple SDH has a mortality rate of approximately
20% good prognosis

Complicated SDH has a mortality rate of

approximately 50% bad prognosis
the most important thing to predict the prognosis is
the presence or absence of brain parenchymal
contusions

CASE ANALYSIS

SUBDURAL HEMATOME
Literature

Case

EPIDEMIOLOGY

All age, often found in

term infant

Baby boy, 23 days old

(aterm baby)

58

SUBDURAL HEMATOME
Literature

Case

CLINICAL MANIFESTATION
loss of consciousness
vomitting, seizures
headache or nausea,
weakness of limbs
pupil anisokor and
deficit of motor function
papilledema and other
neurological deficits

Seizures
loss of consciousness
pale
bulging of the head
crown

59

SUBDURAL HEMATOME
Literature

Case

ETIOLOGY
Birth trauma: excessive
withdrawal of the head
and CPD
Artificial delivery:
Vacuum and forceps
Precipitate delivery:
Bleeding disease/Blood
clotting disorders

Normal and
spontaneous delivery,
CPD (-)
Birth trauma: unknown
Bleeding disease: (-)

60

SUBDURAL HEMATOME
Literature

Case

SUPPORTING INVESTIGATION

Lab: RBT, electrolytes

dan hemostatic profile
CT scan or MRI

RBT : Normal
electrolytes :
Hemostatic/koagulation
profile : Normal
CT Scan: left
temporooccipitale lobe
SDH (hiperdensity
lesions) acute SDH
61

SUBDURAL HEMATOME
Literature

Case

THERAPY
Operative treatment:
1. burr hole
craniotomy
2. Twist drill
craniotomy
3. Subdural drain
Non Operative
treatment

Craniotomy
oral antibiotic :
ceftazidime

62

Thank you