Grand case report

SECONDARY CHEPALGIA CAUSED BY SUBARACHNOID

HEMORRHAGE

By:
Saleh Nur Azhari
1808437034

Supervisor:
Sucipto, MD, Neurologist

CLINICAL CLERKSHIP DEPARTMENT OF NEUROLOGY

RSUD ARIFIN ACHMAD
FACULTY OF MEDICINE UNIVERSITY OF RIAU
PEKANBARU
2020
 KEMENTRIAN PENDIDIKAN DAN KEBUDAYAAN
FAKULTAS KEDOKTERAN UNIVERSITAS RIAU
SMF/ BAGIAN SARAF
Sekretariat : Gedung Kelas 03, RSUD Arifin Achmad Lantai 04
Jl. Mustika, Telp. 0761-7894000
E-mail : saraffkur@gmail.com
PEKANBARU

I. Patient’s identity

Name Ms. A
Age 18 years old
Gender Female
Address Jl.suhada, Pekanbaru
Religion Moeslim
Marital’s Status Single
Occupation Student
Day of admission July, 16th 2020
Medical Record 01044698

II.ANAMNESIS :
Autoanamnesis and alloanamnesis with patient’s sister (Sept, 12st 2020 on
16.30 AM)
Chief complain
Headache since three weeks ago
Present illness history
Three weeks ago, the patient complained of severe headaches, pain felt in the
back of the head and spread to all parts of the head. Patient felt pain everytime.
Pain was associated with fluctuated fever, nausea and vomiting. Patient vomited
more than 3 times a day and it contained eat. Patient said that pain more
worsening if her eyes are exposed to light so that caused blurred vision especially
her right eye. Patient also bleeding gums.

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 Two weeks ago, the patient had a seizure. The seizure occurs once throughout
the patient's body and flexed his arms and legs. It happened along 20 minutes.
After seizure, the patient had low consciousness. history of trauma was refuse.
Urination and defecate normal limits.

The patient has been treated with a diagnosis of AML and got regular platelet
transfusions but the platelets are still low.

Past illness history

 Trauma history (-)
 History of diabetes mellitus (-)
 Stroke history (-)
 History of heart disease (-)
 High blood pressure history (-)

The family disease history

 No family complained about the same thing.
 History of high blood pressure (-)
 History of diabetes militus (-)
 History of heart disease (-)

SUMMARY
Ms. A, 18 years old, was admitted to Arifin Achmad’s General Hospital with
severe headache since 3 weeks ago. Pain felt in the back of the head that
spread to all parts of the head. Pain felt every time. Pain was following with
fever, nausea, vomit, and seizure. The patient said that the pain more
worsening if the patient’s eyes are exposed to light and caused blurred vision
especially her right eye. The patient has been treated with a diagnosis of
AML and got regular platelet transfusions but the platelets are still low.

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III. Physical examination
Blood Pressure : 117/60 mmHg
Heart Rate : 70 dpm
Respiratory rate : 20 dpm
Temperature : 37,8°C
Weight : 45 kg
Height : 160 cm
Body Mass Index (BMI) : 17,5 kg/m2 (underweight)
Eyes : Pale conjunctiva (+/+), isocoria 2mm/2mm,
direct light reflex (+/+), indirect light reflex (+/
+)
Cardiovascular : HR : 70 bpm, regular, murmur (-), gallop (-)
Respiratory : Vesicular (+/+), Rhonchi (-/-), Wheezing (-/-),
symmetrical lung expansion
Abdomen : Normal skin turgor, bowel sounds : 8x/minutes.
Hepatosplenomegaly (+)
Lymph nodes : Swollen lymph nodes (-)

A. NEUROLOGICAL STATUS (Sept, 12th2020 on 16.30 am)

1) Consciousness : Composmentis Cooperative
GCS : E(4)V(5)M(6)
2) Cognitive Function : Normal
3) Nuchal rigidity : positive
4) Cranial Nerves

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1. Cranial nerve I (Olfactory)
Right Left Interpretation
Sense of Smell Normal Normal Normal

2. Cranial nerve II (Optic)

Right Left Interpretation
Visual Acity >3/60 >3/60
Visual Fields
Normal Normal Normal
Colour Recognition
+ +

3. Cranial nerve III (Oculomotor)

Right Left Interpretation
Ptosis (-) (-)
Pupil
Shape Round Round
Size Φ2mm Φ2mm
Normal
Pupillary reactions to light
Direct (+) (+)
Indirect (+) (+)

4. Cranial nerve IV (Trochlear)

Right Left Interpretation
Extraocular
(+) (+) Normal
Movements

5. Cranial nerve V (Trigeminal)

Right Left Interpretation
Motoric Normal Normal
Sensory Normal Normal Normal
Corneal reflex (+) (+)

6. Cranial nerve VI (Abducens)

Right Left Interpretation
Eyes movement Normal Normal Normal

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 Strabismus (-) (-)
Deviation (-) (-)

7. Cranial nerve VII (Facial)

Right Left Interpretation
Tic (-) (-)
Motoric:
- Frowning Normal Normal
- Raised eye brow Normal Normal
- Closed eyes Normal Normal
- Corners of the Normal
mouth Normal Normal

- Nasolabial fold Normal Normal

Sense of Taste Normal Normal
Chvostek Sign (-) (-)

8. Cranial nerve VIII (Acoustic)

Right Left Interpretation
Hearing sense Normal Normal Normal

9. Cranial nerve IX (Glossopharyngeal)

Right Left Interpretation
Pharyngeal Arch Normal Normal
Sense of Taste Normal Normal Normal
Gag Reflex + +

10.Cranial nerve X (Vagus)

Right Left Interpretation
Pharyngeal Arch Normal Normal
Normal
Dysphonia - -

11.Cranial nerve XI (Accessory)

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 Right Left Interpretation
Motoric Normal Normal
Normal
Trophy Eutrophy Eutrophy

12.Cranial nerve XII (Hypoglossal)

Right Left Interpretation
Motoric Normal Normal
Trophy Eutrophy Eutrophy Normal
Tremor - -
Disartria - -

IV. MOTORIC SYSTEM

Right Left Interpretation
Upper Extremity
Strength
Distal 5 5
Medial 5 5
Proximal 5 5
Tone Normal Normal
Trophy Eutrophy Eutrophy
Involuntary movements - -
Clonus - -
Lower Extremity Normal
Strength
Distal 5 5
Medial 5 5
Proximal 5 5
Tone Normal Normal
Trophy Eutrophy Eutrophy
Involuntary movements - -
Clonus - -
Body
Trophy Eutrophy Eutrophy
Normal
Involuntary movements - -

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V. SENSORY SYSTEM
Right Left Interpretation
Touch Normal Normal
Pain Normal Normal
Temperature Normal Normal Normal
Propioseptive Normal Normal

VI. REFLEX
Right Left Interpretation
Physiologic
Biceps (+) (+)
Triceps (+) (+) Physiologic reflex (+)
Knee (+) (+)
Ankle (+) (+)
Pathologic
Babinsky (-) (-)
Chaddock (-) (-)
HoffmanTromer (-) (-) Pathological reflex(-)
Openheim (-) (-)
Schaefer (-) (-)

VII. COORDINATION
Right Left Interpretation
Point to point movement Normal Normal
Walk heel to toe Difficult to Difficult to
Gait asses asses Normal
Tandem
Romberg

VIII. AUTONOM
Urination : Normal
Defecation : Normal

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IX. OTHERS EXAMINATION
a. Laseque : Unlimited (>70)
b. Kernig : Unlimited (>130)
c. Patrick : -/-
d. Kontrapatrick : -/-
e. Valsava test : -
f. Brudzinski : -

X. EXAMINATION RESUME
Generalized condition
Blood Pressure : 117/60 mmHg
Heart Rate : 70 dpm
Respiratory rate : 20 dpm
Temperature : 37,0 °C
Weight : 45 kg
Height : 160 cm
Body Mass Index(BMI) : 17,5 kg/m2 (Underweight)
Cognitive Function : Normal
Meningeal sign : Positif
Cranial Nerves : Normal
Motoric : Normal
Sensory : Normal
Coordination : Normal
Autonomy : Normal
Reflex : Physiologic (+) normal , Pathologic (-)

XI. WORKING DIAGNOSIS :

CLINICAL DIAGNOSIS : SECONDARY CHEPALGIA
TOPICALDIAGNOSIS : CISTERNA MAGNA ACCORDING TO THE
TERRITORY OF THE VERTEBROBASILARIS ARTERY
ETIOLOGIC DIAGNOSIS : SUBARACHNOID HEMORRHAGE

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ADDITIONAL DIAGNOSA : ACUTE MIELOBLASTIC LEUKIMIA
DIFFERENTIAL DIAGNOSIS : INTRACEREBRAL HEMORRHAGE

SUGESSTION EXAMINATION :
o Blood routine test
o Blood chemistry test
o Peripheal blood profil
o Head CT Scan

MANAGEMENT :
1) O2 3 lpm
2) IVFD Aminofluid /24 hours
3) Metilprednisolon 2x8 mg
4) MST 2x20 mg
5) Durogesic patch 25 ug/h
6) Ketorolac 3x30 mg IV
7) Sandimun 2x50 mg
8) Ondansentron 3x 8mg
9) Lansoprazole 2x30 mg IV
10) Paracetamol 3x500 mg tab
11) Domperidone 3x10 mg

LABORATORY WORK UP:

1. Blood Routine (Sept, 8th 2020)
Hemoglobin :11,1 gr/dl
Hematocrit : 33,9%
Leucocytes : 2.620/mm3
Platelets : 46.000/mm3

2. Peripheal blood profil ( July, 14th 2020 )

Eritrosit : normositic normochrome, eritrosit polichromation +
Leukocyt : increase, morphplogy is normal, blast >20%

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3. Bone Marrow punction ( July, 22nd 2020 )
Blast cell : 95%
Megakarioblast : 94
Conclusion : AML tipe M7

4. Blood Chemistry
Creatinin :-

5. Elektrolyte
Na+ :-
K+ :-
Cl- :-

6. Hematologi
ICT Malaria : Non reaktif
Malaria : Negatif

7. Urinalisa :
Makroskopis
Color : Yellow
Clarity : Clear
Urine Chemistry
Protein : Negative
Glukosa : Negative
Bilirubin : Negative
Urobilinogen : 0,2 Eu/dl
Blood : Negative
Keton : Negative

8. HEAD CT SCAN ( Agust, 28th 2020 )

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 Interpretation :
- There is pathologic hiperdense lesion
in the conchavity temporal dextra,
tentorium cerebeli bilateral, plexus
choroideus bilateral
- Sulci, gyrus and fissura sylvii are not
prominent
- The boundaries of the white matter
and gray matter
- The ventricular system and cysterna
do not narrowed or widened
- Midline shift (-)
- The cerebellum and brainstem are
normal
- There is no SOL
- Paranasal sinuses and mastoidal air
visualized normodens

Conclusion :suggestif sub arachonid

hemorrhage in conchavity temporal
dextra, tentorium cerebeli bilateral,
plexus choroideus bilateral

HEAD CT SCAN (Juli , 15th 2020)

Interpretation :
- There is pathologic hiperdense lesion
in the subarachnoid and intra
ventricular spaces
- Sulci, gyrus and fissura sylvii are not
prominent
- The boundaries of the white matter
and gray matter
- The ventricular system and cysterna
do not narrowed or widened
- Midline shift (-)
- The cerebellum and brainstem are
normal
- There is no SOL
- Paranasal sinuses and mastoidal air
visualized normodens

Conclusion : Subarachnoid
Hemarrhage , intra ventricular
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hemorrhage.
FINAL DIAGNOSIS
Secondary Headache caused by Sub Arachnoid Hemorrhage + AML

FOLLOW UP

Date Subjective Assessment

Objective
Sept 12, Subjective:
2020 headache, Nausea, vomit
Objective:
GCS : E4V5M6
Blood pressure : 115/60 mmHg
Pulse : 90 bpm, reguler
Respiratory rate : 20 times per
minute
Temperature : 37,2 celcius
Cognitive function : Normal
Meningeal sign : (+)
Cranial nerve : Normal
Sensory : Normal
Motoric :
Muscle strength : 555 555
555 555
Autonom : Normal
Reflex : Physiology (+), normal,
Pathologic (-)
Sept 13, Subjective:
2020 Headache, nausea, vomit, fever
Objective:
GCS : E4V5M6
Blood pressure : 120/70 mmHg
Pulse : 80 bpm, reguler
Respiratory rate : 20 times per
minute
Temperature : 38,2 celcius
Cognitive function : Normal
Meningeal sign : (+)
Cranial nerve : Normal
Assessment :
Secondary headache et causa
SAH + AML
Plan :
1) O2 3 lpm
2) IVFD Aminofluid /24
hours
3) Paracetamol 3x500 mg
tab
4) Mst 2x20 mg
5) Ondansentron 3x 8mg k/p
6) Lansoprazole 2x30 mg IV
7) Lactulac Syr 3x15 cc
8) Metilprednisolon 2x8 mg
9) Sandimun 2x50 mg
10) Ketorolac 3x30 mg IV
11) Donperidone 3x10 mg
12) Durogesic patch 25 ug/h
Assessment :
Secondary headache et causa
SAH + AML
Plan :
1) O2 3 lpm
2) IVFD Aminofluid /24
hours
3) Paracetamol 3x500 mg
tab
4) Mst 2x20 mg
5) Ondansentron 3x 8mg k/f
6) Lansoprazole 2x30 mg IV

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 Sensory : Normal 7) Metilprednisolon 2x8 mg
Motoric : 8) Sandimun 2x50 mg
Muscle strength : 555 555 9) Ketorolac 3x30 mg IV
555 555 10) Donperidone 3x10 mg
11) Durogesic patch 25 ug/h
Autonom : Normal
Reflex : Physiology (+), normal,
Pathologic (-)
Sep 14, 2020 Subjective: Secondary headache et causa SAH
Headache, nausea, vomit + AML
Objective:
GCS : E4V5M6 Plan :
Blood pressure : 120/70 mmHg 1) O2 3 lpm
Pulse : 80 bpm, reguler 2) IVFD Aminofluid /24
Respiratory rate : 20 times per minute hours
Temperature : 37,3 celcius 3) Paracetamol 3x500 mg
Cognitive function : Normal tab
Meningeal sign : (+) 4) Mst 2x20 mg
Cranial nerve : Normal 5) Ondansentron 3x 8mg k/f
Sensory : Normal 6) Lansoprazole 2x30 mg IV
Motoric : 7) Metilprednisolon 2x8 mg
Muscle strength : 555 555 8) Sandimun 2x50 mg
555 555 9) Ketorolac 3x30 mg IV
10) Donperidone 3x10 mg
Autonom : Normal 11) Durogesic patch 25 ug/h
Reflex : Physiology (+), normal,
Pathologic (-)

Sep 15, 2020 Subjective: Secondary headache et causa

headache SAH + AML
Objective:
GCS : E4V5M6 Plan :
Blood pressure : 120/70 mmHg 1) O2 3 lpm
Pulse : 80 bpm, reguler 2) IVFD Aminofluid /24
Respiratory rate : 20 times per hours
minute 3) Paracetamol 3x500 mg
tab
Temperature : 36,5 celcius
4) Mst 2x20 mg
Cognitive function : Normal 5) Ondansentron 3x 8mg k/f
Meningeal sign : (+) 6) Lansoprazole 2x30 mg IV
Cranial nerve : Normal 7) Metilprednisolon 2x8 mg
Sensory : Normal 8) Sandimun 2x50 mg
Motoric : 9) Ketorolac 3x30 mg IV
Muscle strength : 555 555 10) Donperidone 3x10 mg
555 555 11) Durogesic patch 25 ug/h
12) Pasient may to go home
Autonom : Normal

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 Reflex : Physiology (+), normal,
Pathologic (-)

LITERATURE REVIEW
1. Headache

1.2 Definition

Headache is pain or discomfort on whole area of the head. Headache is

most commonly subjective chief complaints as reported.1.2 Headache is an

extremely common symptom and collectively headache disorders are among the

most common of the nervous system disorders, with a prevalence of 48.9% in the

general population.1 Headache disorders are divided intoprimary headache

syndromes (in which the headache and associated features comprise the disorder

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itself) and secondary headache syndromes (in which the headache results of

another etiologies).

1.3 Classification

The first step in the diagnosis of a patient presenting with headache is to

differentiate between a benign headache disorder (usually a primary

headachesyndrome) and a serious underlying condition (causing a secondary

headache).

Table 1 . the classification of headache based on etiology

Based on international headache classification 2rd edition from the

International Headache Society (IHS), Primary headache is headache with no

underlying disease. The primary headache, such as:2

 Migraine

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 Periodic disorder with unilateral or bilateral headache and can be

following with vomiting and visual disturbances. This condition occurs

frequently, more than 10% of the population are experiencing at least one

migraine attack in her life. Migraine can occur at all of ages, but generally the

onset occurs on teenage or twenties and female more often than male. There is

family history of migraines on commonly patient.

 Tension-type headache (TTH) 2

This headache is frequenly occurs with unknown etiology, although had

been accepted that the contraction of the head and neck muscles is a mechanism

causes pain. Muscle contraction can be triggered by psychogenic factors such as

anxiety or depression or by local disease on head and neck.

Patients commonly experienced headache that can be settled for a few

days, months or years. headache can worsen in the afternoon and generally not

responsive with analgesic drugs. This headache had a variative pain. Headache

starts from the blunt pain in various places until a thorough pressure sensation to

the feeling of the head tight-tied/tense.

 Cluster Headache2

This syndrome are different from migraine, both marked by unilateral

headache, both can occur at the same time, but the very distinct of the two is red

eye. Histaminergic and humoral mechanisms underlying the autonomous

symptoms is estimated to occur in conjunction with this head pain.

Patients usually are men, aged 20 to 60 years. Patients feel great pain

around one eye (always on the same side) for 20 to 120 minutes, can be repeated

several times a day, and patient often woke up more than one time in the middle

16
of the night. Alcohol can also trigger an attack. This pattern lasted for days, weeks

and even for months.

The secondary headache :

 Headache attributed to head and/or neck trauma and cranial or cervical

vascular disorder

 Headache attributed to non-vascular intracranial disorder

 Headache attributed to a substance or its withdrawal and infection

 Headache attributed to disorder of homeoeostasis

 Headache or facial pain attributed to disorder of cranium, neck, eyes, ears,

nose, sinuses, teeth,mouth, or other facial or cranial structures.

 Headache attributed to psychiatric disorder

 Cranial neuralgias and facial pains

 Cranial neuralgias and central causes of facial pain

 Other headache, cranial neuralgia central, or primary facial pain.

2.0 Epidemiology And Pathophysiology SAH

The incidence of subarachnoid hemorrhage is about 6-7 cases out of

100,000 per year, often increasing with increasing age but half of the patients are

17
under 55 years of age; he was more likely to be women with a ratio of 1.6 to men.
The mortality rate is about 50%; many deaths occurred within 2 weeks; 10% of
patients die before arriving at the hospital.

Gambar (1). Subarachnoid hemorrhage (a) subarachnoid hemorrhage masif

dengan invasi ventricular (b).

Rupture of intracranial aneurysm is responsible for 85% of cases of SAH,

10% due to non-aneurysmal conditions and 5% due to other medical conditions
such as inflammatory or non-inflammatory lesions of the cerebral arteries,
coagulopathy, neoplasms and drug abuse.

Cerebral aneurysms are present in 2-3% of the population. Usually found

in Willis bifurcation polygon vessels or branches. The risk of rupture is somewhat
low, about 0.05% per year, but the risk may increase if the diameter is> 10 mm or
its location in the posterior cerebral circulation. International studies report that
the cumulative risk for rupture after 5 years is zero for aneurysms less than 7 mm,
2.6% for dimensions between 7 and 12 mm, 14.5% for dimensions between 13
and 24 mm and 40% for aneurysms greater than 25 mm. The levels of risk
increased by 2.5%, 14.5%, 18.4% and 50% for aneurysms in the posterior
circulation.

Modifiable risk factors for preventing aneurysm rupture include arterial

hypertension, smoking, alcoholism and cocaine use. Genetic factors are a
determinant of the high risk in the first-generation family line. Connective
inherited diseases such as polycystic DICney, Ehlers Danlos Syndrome (Type
IV), pseudoxantoma elasticum and fibromuscular dysplasia are conditions
associated with intracranial aneurysms and SAH.

Non-aneurysmal perimesencephalic subarachnoid hemorrhage is

categorized as blood extravasated into the cistems around the midbrain, pons or in
the quadrigeminal cistern surface without passing through the Sylvi fissures or the
interhemispheric fissures and the ventricular system. Perimesencephalic SAH is
usually not due to aneurysmic malformation and is usually good. Normal

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angiography results support the origin of bleeding veins due to rupture in the
prepontin or interpeduncular veins. In these patients the perimensephalic venous
flow always flows directly into the dural sinus, not into the Galen vein,
predisposing to venous congestion.

Clinical symptoms

The clinical manifestations of SAH can vary from asymptomatic to sudden

death. This is believed to be due to the misdiagnosis of 12% with potentially
severe consequences in delayedo treatment cases.
Headache is the main symptom and the only symptom in one third of
patients. Usually the pain in the occipital region to the neck is of severe intensity
and has been described by patients as the most painful headache with rapid onset.
The speed reaches the maximum intensity, in seconds indicates the intensity itself.
Nausea, vomiting and photophobia may occur but are nonspecific because they
are often associated with primary or secondary headaches. As many as 75% of
patients with "thunderclap headache" have subarachnoid hemorrhage.
Two thirds of treated patients showed a decrease in consciousness; half of
them are in a coma. Agitation and confusion can also be seen. Stiff neck,
increased resistance to passive flexion / extension in the neck are clinical signs of
meningeal irritation due to extravasation of blood within the subarachnoid space.
Other signs of meningeal excitability include positive Laseque, Kernig and
Brudzinski signs. Meningeal stimulation signs can take 3-12 hours to be obtained
and may not be seen in cases of coma or minimal blood expasation. Thus, the
absence of signs of nuchal rigidity should not rule out the diagnosis of
subarachnoid hemorrhage.
Seizures may occur in 7% of patients. Young age (<40 years), bleeding
entity, hydrocephalus and premature bleeding are major risk factors for early
onset seizures while vasospasm with cortical ischemia, intraparenchyma
hemorrhage and neurosurgery in place of endovascular therapy are risk factors for
late onset seizures.
Approximately 14% of patients can have intraocular hemorrhage: a sudden
increase in intracranial pressure can cause retinal central vein occlusion with

19
subsequent pre-retinal (subhyaloidal) extravasation bleeding. In cases of severe
bleeding, emovitreous may occur (Tearson's Syndrome).
Focal neurologic deficit is not a typical sign seen in the acute phase of
SAH but may appear in cases of intraparenchymal hemorrhage of cranile nerve
extensions or ischoled lesions due to early vasospasm.
Cardiovascular changes, usually hypertension and tachycardia due to
adrenergic tone, may be seen in the acute phase; Sudden cardiac arrest can occur
at onset in 3% of cases.

2.1 Subarachnoid Hemorrhage

The physical findings in patients with ruptured aneurysms depend in large
measure on the mount and location of the hemorrhage. Aneurysmal rupture can
result in hemorrhage into the subarachnoid spase alone or in combination with
intracerebral hemorrhage, intraventrikular hemorrhage or, more rarely, subdural
hematoma. Thus, the immediate physical findings can vary from slight
meningismus to profiund neurological deficits with coma or death. Because
treatment and prognosis depend to a great extent to the clinical status of the
patient, a grading scale based on the neurological presentation of the patient in
utilized routinely. These grading scales are simple to use and should be noted for
all patients presenting with SAH. The two systems that are in most common use
are the hunt and hess scale and the world federation of neurological suregeons
grading scale. (Tables 55C-1)

Tables 55C-1

Hunt and Hess Scale and World Federation Of Neurological Surgeon Scale.

HUNT AND HESS SCALE

Grade 0 Asymptomatic
Grade I Slight headache, no neurological deficit
Grade II Severe headache but no neurological deficit other than perhaps a
cranial nerve palsy
Grade III Drowsiness and mild deficit
Grade IV Stupor, moderate to severe hemipareses, and possible early rigidity

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 and vegetative disturbances
Grade V Deep coma, decerebrate rigidity, and moribund appearance

WORLD FEDERATION OF NEUROLOGICAL SURGEON SCALE

Grade I GCS 15; Motor deficit absent

Grade II GCS 13 or 14 ; motor deficit absent
Grade III GCS 13 or 14 ; motor deficit present
Grade IV GCS 7- 14 ; motor deficit absent or present
Grade V GCS 3-6 ; motor deficit absent or present
GCS ; Glasgow Coma Scale

2.2 DIAGNOSTIC STUDIES

The evaluation of patients suspected of having an intracranial aneurysm

depends on the type of presentation and may include invasive or noninvasive

studies.

Subarachnoid Hemorrhage

The conventional CT scan is indispensable for delineating the amount and

location of blood in the subarachnoid spase that appropriate therapeutic measures

can be undertaken. Imaging needs to include all the vessels, because multiple

aneurysms occur in approximately 20% of patients. The goals of imaging are to

identify the cause of the hemorrhage and, if an aneurysm is present, to delineate

its neck and the relationship to surrounding vessels. Although conventional

catheter based digital subtraction angiography (DSA) with 3-dimensional

rotational imaging remains the mainstay for workup of rup- tured intracranial

aneurysm, CT angiography (CTA) has been used with promising results as the

21
primary diagnostic imaging modality with or without DSA confirmation (Hoh et

al., 2004; Jayaraman et a., 2004).

Aneurysms are named according to their vessels of origin. Approximately

80% to 85% of aneurysms arise from arteries located in the anterior circulation,

the majority of which occur on the anterior communicating artery, the posterior

communi- cating artery, or the middle cerebral artery. Between 15% and 20% of

aneurysms arise from the posterior circulation, the majority of which occur at the

bifurcation of the basilar artery or at the origin of the posterior inferior cerebellar

artery on the vertebral artery.

2.3 Treatments for SAH 5

Subarachnoid hemorrhage is a clinical emergency with high mortality from

onset. First, respiratory and cardiovascular stability should be evaluated and
treated if necessary. Once the vital signs have stabilized, the second step is to
prevent re-bleeding and possible complications that could affect the patient's
prognosis.5
Hypertension should be treated with endovenous hypertension drugs such as
labetalol or urapidil if necessary. Recommended systolic blood pressure values
are between 140 and 90 mmHg; after aneurysm exclusion blood pressure therapy
can be less intensive. If the risk of hypoperfusion is estimated, hypotension should
be avoided even if the definitive targets have not been achieved.5
The headache needs medical treatment. NSAIDs should be avoided because
they can increase the risk of bleeding while opioids also need to be avoided
because they can affect the level of consciousness. The drug of first choice is
paracetamol per os or intravenously. Hyperprexia should be treated
(recommended body temperature 37.2oc).5
Hyperglycemia should be corrected (recommended blood sugar values
around 80-120 mg / dl) because it can give bad results. Proton pump inhibitors are

22
indicated for preventing peptic ulcers. Deep vain thrombosis prophylaxis with low
molecular weight heparin can be used after aneurysm therapy.5
Giving nimodipine 60 mg orally every 4 hours for 21 days can reduce the
risk of delayed cerebral ischemia due to vasospasm. A Cochrane revision reported
an 18% reduction in relative risk with a 5.1% reduction in absolute risk.5
Magnesium sulfate has been studied and used in the prevention of
vasospasm because hypomagnesia can occur in 50% of patients with SAH and is
closely related to delayed cerebral ischemia. Phase II studies have yielded positive
results but the results of phase III trials do not support the clinical benefit of
intravenous magnesium sulfate infusion versus placebo in patients with acute
auerysme of subarachnoid hemorrhage.5
Antifibrinolytic agents can reduce the rate of rebleeding although they
increase the risk of cerebral ischemia or systemic thrombosis. Tranexamic acid
reduced the rebleeding rate from 11 to 2.4% but this benefit was affected by
ischemic complications.5
Aneurysm exclusion is an effective therapy to prevent re-bleeding. Over the
last decade, endovascular coiling has been the first choice of therapy along with
neurosurgical clipping. Endovascular coiling is performed by placing a
superselective catheterism and platinum compacting with a detachable coil of
sufficient length and diameter to reach the aneurysm sac in the neck of the
aneurysm. After that, blood clots form around the coil blocking blood flow into
the bulge and preventing the blood vessels from rupturing or leaking.5
A randomized clinical trial was conducted of 2,272 patients to compare the
use of endovascular therapy with traditional neuroseurgery. Endovascular coling
showed a 24% reduction in relative risk versus an outcome that was less favorable
to a 7% reduction in absolute risk. However, this technique is not suitable for all
types of aneurysms: a wide neck and close contact with a vascular branch that
requires neurosurgery. Regarding the timing of the procedure, in the past it was
chosen to avoid the lag time in vasospasm with the greatest risk - from day 4 to 15
- presumably delayed therapy, evidence suggests initial therapy is the best option
for preventing re-bleeding.5

23
 In conclusion, subarachnoid hemorrhage should be considered as a clinical
emergency even in mild symptoms. A complete diagnostic process is
recommended although few clinical symptoms are present. Prompt and precise
management and medical intervention can reduce mortality and disability.5

III.1 Acute Mielobalstic Leukimia

III.2 Definition AML
CNS leukemia is the invasion of leukemic cells on leptomeninges with or
without infiltration of adjacent nerve tissue. From various studies, the invasion of
leukemia cells in the CNS follows a certain predictable anatomic pattern, both in
lesions and in clinical manifestations. Leukemia cell invasion can occur when the
diagnosis of leukemia is confirmed or afterward (relapse).

3.2 Anatomi
Leptomeninges consists of arachnoid and piamater. The arachnoid consists
of two parts, namely: the surface membrane and trabecular connective tissue, in
which there are blood vessels and nerve fibers, and a layered mesothelial canal as
the flow of CSS.
The arachnoid membrane has two parts, namely: Superficial portion, that
covers the surface of the brain, and the deep portion, which surrounds cerebral
blood vessels and form the perivascular space (Virchow-Robin). Most of the CSS
channels, including large sisterna, are located in superficial portions. These
channels are not visible in the deep portion. Anatomical differences between the
two sections need to be understood in relation to CNS leukemia therapy, where
the CSF canals in the superficial portion are the main route of passage of
intrathecal drugs.
The CNS tissue is tightly enclosed by a wattle-glial membrane separating
the arachnoid from the nervous tissue. This membrane extends inward to the brain
parenchyma and joins the adventitia (outer portion of the blood vessels) of the
precapillary arterioles and postcapillary venules. In these capillaries there is a
blood-brain barrier (BBB).

24
3.3 Patofisiologi
The discovery of leukemic cells in the walls of the leptomeningeal blood
vessels by Dr. Fried in 1926 led to the hypothesis that circulating cells flow in
blood vessels and invade surrounding brain tissue. Leukemic cells residing in the
vein wall in superficial leptomeninges are the first histologic findings in CNS
leukemia. From the clinical features associated with the autopsy findings, it was
concluded that it was invasion Superficial leptomeninges may occur at the time of
diagnosis of leukemia enforced, or shortly thereafter.
During the early infiltration phase, only the superficial portion of the
leptomeninges is affected, whereas the deep portion along the blood vessels in the
gray matter and white matter is still free of leukemic cells. The arachnoid
trabeculae are still intact and CSF is still clean from malignant cells. (Mastrangelo
et al., 2012).
Leukemic cell infiltration will eventually cause destruction of the trabeculae
followed by the release of leukemic cells into CSF. In these circumstances, a
cytologic diagnosis of CNS leukemia is possible.
Schwab and Weiss in 1935 concluded that CSF examination can diagnose
meningeal leukemia even though the clinical symptoms of CNS disease are not
yet visible. Currently, CSS cytology examination is a routine procedure and must
be performed in the management of ALL in children (Mastrangelo et al., 2012).
With the increasing number of invading leukemic cells, arachnoid becomes
denser by the cells which will then reach deepportion, to the farthest part, namely
precapillary arterioles and venules postcapiler. This process is an advanced stage
of meningeal leukemia,
wherein infiltration of leukemic cells has occurred extraneurally, separated from
the parenchyma by the pial-glial membrane. In this situation, attempts to
administer fat-insoluble drugs through the BBB to the brain tissue are likely
ineffective because in most cases, the leukemic cells are more in the meninges
than in the neural network itself (Mastrangelo et al., 2012).
The final stage of CNS leukemia occurs when a large cell mass has been
established destroys the pial-glial membrane so that it eventually infiltratesbrain
parenchyma. From post mortem studies, this figure only occurs in less than 15%

25
of children with leukemia who die at the time of relapse (Mastrangelo et al.,
2012).

THE BASIC OF DIAGNOSIS

1. Basic clinical diagnosis
Miss A, 18 years old, came to the hospital Arifin Achmad was first
diagnosed with acute myeloblastic leukemia. 3 weeks ago the patient had a
very severe headache. the headache is persistent. the patient says his head
feels about to burst. nausea and vomiting and the patient also feels
photophobia. the headache disappeared after being given the analgesic drug
morphine and ketorolac. when the physical examination was performed, the
patient's face was pale, conjunctival anemic, sclera not icteric, nuchal
rigidity was positive in this patient. motor movements after headache are
normal. normal autonomic function, normal physiological reflexes and no
pathological reflexes. and there is no parasis and paresthesia. After a Head
CT scan was performed, it was found that the sub arachnoid hemorage had
an impression.

Secondary cephalgia is cephalgia that is triggered by a cause, such as

coagulopathy, tumors, bleeding in the brain. in this patient based on
anamnesis, physical examination and laboratory examination, it was found
that the patient's severe headache was triggered by sub arachnoid hemorage.
sub arachnoid hemorrhage causes compression of the meningens membrane.
If the meninges are stimulated it will cause a very severe headache, and in
this patient there is a stiff neck which is evidence that the meninges are
stimulated by sub arachnoid hemorrhage. This very intense headache can
cause nausea and vomiting
2. Basic topic diagnosis
Two-thirds of the anterior cerebral area vascularized the branches of
the internal carotid artery while one third of the area posterior to the
vertebrobasilaris artery branches. Carotid artery interna will branch into the
anterior cerebral artery and the media cerebral artery. While the

26
vertebrobasilaris artery will continue to become the posterior cerebral artery.
The anterior cerebro artery (ACA) supplies the medial portion of the frontal
and parietal lobes and the anterior portion of the basal ganglia and the
anterior portion of the interma capsule. ArteryMedia cerebral (MCA)
supplies the lateral portions of the frontal and parietal lobes, as well as
parts12 anterior and lateral to the temporal lobe, and gives perforating
branches to the globus palidus, putamen, and the internal capsule. The
posterior cerebral artery (PCA) provides the perforating branch which
supplies the thalamus and brainstem and cortical ramus to the posterior and
medial temporal and occipital lobes. The inferior cerebellar hemisphere is
supplied by arteries inferior posterior cerebeli (PICA) originating from the
vertebral artery, while part superiorly vascularized by the superior cerebellar
artery. The anterior part of the cerebellum vascularized by the anterior
inferior cerebellar artery (AICA) originating from the basilar artery.
3. Basic etiological diagnosis
based on the anamnesis. the patient has severe headache, nausea and
vomiting and develops photophobia. on physical examination, he found
positive nuchal rigidity and no neurological deficit. On the head CT scan, it
was concluded that there was bleeding in the sub arachnoid. The presence of
bleeding in the sub arachnoid causes blood to press the lining of the
meninges in the brain. due to the stimulation of the meninges in the brain,
will cause a very severe headache. This was also proven in one of the
physical examinations found in this patient where there was a positive
Nuchal rigidity. The nausea and vomiting found in this patient were due to
increased content (blood), while the cranial volume was limited as a result,
according to law monro kelly . there was an increase in intra cranial
pressure. one of the signs of an intra cranial increase is the nausea and
vomiting. neurological deficits do not occur because the sub arachnoid
hemorrhage does not compress the motor areas in the brain parenchyma. so
that neurological deficits do not occur.

4. Basic differential diagnosis

27
 Based on the anamnesis, physical examination and investigation of the
patient, this patient's secondary cephalgia was caused by bleeding in the sub
arachnoid. the differential diagnosis was intracerebral hemorage. in this
patient there is headache. in ICH there is also headache. things that
distinguish between SAH and ICH. at SAH the headache is very intense and
the pain exceeds ICH. in these patients there is decreased consciousness and
seizures. this is a sign of bleeding in the subrachnoid and bleeding in the
intra cerebral. the thing that distinguishes between SAH and ICH. On the
intra cerebral. there is usually a neurological deficit and motor weakness. in
this patient there was no neurological deficit and motor weakness. After
doing physical examination, this patient found . This is one strong evidence
that the meninges membrane is stimulated. in SAH, the bleeding will press
and stimulate the meninges membrane in the brain. in ICH, nuchal rigidity
was not found.
5. Basic workup
 Blood routine test (to find any change that show )
 Peripheal blood profil (to find whether there is blast cell (leukimia)
 Bone Marrow punction (to detect type of leukimia)
 Hematologi ( to find malaria because pasien lie on endemic area)
 Head CT Scan (to find intracranial cause of the altered level of
consciousness)
 Urine chemistry (to find renal disease caused leukimia)

6. Additional diagnosa :
Based on data from the anamnesis, physical examination and adjunct
examination that have been done, this patient was diagnosed as acute myeloblastic
leukemia. Diagnosis of acute myeloblastic leukemia in this patient is based on
anamnesis, physical examination, and adjunct examination.
Based on the anamnesis, it was found with fever, and weakness. On
physical examination, the temperature was febrile, conjunctival anemic. Patients
with AML often exhibit non-specific symptoms that begin with anemia,
leucocytosis, leucopenia or leukocyte dysfunction, or thrombocytopenia either

28
gradually or suddenly. Most of them showed these symptoms for + 3 months
before being diagnosed with leukemia.
In the patient's supporting examination, the results of blood tests were
obtained: Hb: 11.1 g / dl Leukocytes: 2620 / uL, Ht: 33.9%, Trombocytes:
46,000 / uL. Reduced platelet counts in acute leukemia are usually the result of
bone marrow infiltration or chemotherapy, but it can also be caused by several
other factors such as disseminated intravascular coagulation (DIC),
immunological processes and hypersplenism secondary to spleen enlargement.
Platelet transfusions should be given to maintain a platelet count> 10,000-20,000 /
SL. Platelet counts should remain high in febrile patients and during episodes of
active bleeding or DIC. Red blood cell transfusions should be given to maintain
hemoglobin levels> 8g / dL if there is no active bleeding, DIC or congestive heart
failure.
In the Bone Marrow Punction examination, it was found that Blast Cells:
95%, Megakarioblast: 94 with the impression of acute myeloblastic leukemia type
M7. In LMA patients, maturity block occurs due to genetic disorders caused by
gene mutations. Gene mutations in AML, besides causing an increase in cell
proliferation and a decrease in cell life span, also causes disruption of the cell
differentiation process. The disruption of the differentiation process of myelocyte
cells will cause the development to stop in young cells (blast) resulting in the
accumulation of blasts in the bone marrow. These young cells can migrate out of
the bone marrow to the peripheral blood and can infiltrate other organs such as
skin and soft tissue.

7. Basic treatment
 Ketorolac is an non steroidal anti inflamatory drug (NSAID) as an
analgetik for headache.
 Ondansentron is an anti emetic for nausea. Its inhibit the action of
serotonin, a chemical messenger that can trigger nausea and vomiting.
 lansoprazole is an proton pump inhibitor, it works by reducing the amount
of acid in the stomach which help in the relief of acid in the stomatch
which help in the relief of acid-related indingetion and heartburn.

29
 Metil Prednisolon at 8 mg three times a day tapering over a few days is
often administered in the presence of cerebral oedema or mass effect. 34
Corticosteroids should be used in the treatment of Corticosteroids are also
recommended perioperatively for reducing intracranial pressure and
avoiding acute brain herniation, but only in those patients that demonstrate
signs of meningitis or disproportionate cytotoxic edema posing a life-
threatening problem.24
 Paracetamol has been given as antipiretic for treating the fever.
 Sandimun is one of imunosupressan which given for AML
 Domperidon is one of antiemetic which given to patient had nause and
vomiting
 Aminofluids are used to supply various nutrients body who have difficulty
carrying out or chewing food. Apart from that, Aminofluid can also
increase nutrients such as electrolytes, protein, amino acids and also
glucose.
 Morphine is a drug used to relieve mild to severe pain. This medicine
changes how the body feels pain. This class of drugs is opioid analgetics.
 Durogesic patch has been given as analgetic.

30
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