CASE PRESENTATION

HEMORRHAGIC STROKE

Supervised by:
dr. H. Oscar Djauhari, Sp. THT-KL
Presented by:
Adrienne Trinovia Sulistyo
Daniela Angeline

2011.061.020
2012.061.001

Clinical Rotation
Otolaryngology, Head and Neck Surgery Department
Medical Faculty of Unika Atma Jaya
Syamsudin, S.H. Regional General Hospital, Sukabumi
July 8th, 2013 August 3rd, 2013

A. PATIENTS IDENTITY
Name
: Mr. W
Age
: 70 years old
Occupation : Driver
Address
: Sukaraja
B. HISTORY OF ILLNESS
Chief complaint
Additional complaint

: Decreased level of consciousness

: Difficulty of breathing, unable to move the left side of

the body, dropping of the left corner of lips, hoarseness, and talks unclearly.
History of present illness :
The patient is brought to the ER by his family with complaint of decreased
level of consciousness since 6 hours before admitting to the hospital.
Approximately 1 hour before that the family complains about difficulty of
breathing, unable to move the left side of the body, dropping of left corner of the
lips, hoarseness, and talks unclearly.
This is the first time the patient experiencing a condition like this. No

history of trauma before. No history of consumption of certain drugs.

History of past illness
:
o History of uncontrolled hypertension since 20 years ago.
o History of diabetes mellitus was denied.
History of Family Illness
o Family history with the same complaints was denied.

C. PHYSICAL EXAMINATION
General appearance : severely ill
Awakeness
: somnolen (GCS 12, E3M6V3)
Blood Pressure
: 180/100 mmHg
Pulse rate
: 88 beat per minute
Respiration rate
: 29 beat per minute
Temperature
: 36,8 oC
ENT Examination
Ear
Auris dextra
- Auricle
: with in normal range
- External auditory canal:
hyperemic (-), edema (-), mass (-), laceration (-), secretion (-), cerumen (-)
- Tymphanic membrane:
Intact, bulging (-), retraction (-), light reflex (+)
Auris sinistra
- Auricle
: normal, no deformities
- External auditory canal:
hyperemic (-), edema (-), mass (-), laceration (-), secretion (-), cerumen (-)
- Tymphanic membrane:

Intact, bulging (-), retraction (-), light reflex (+)

Nose
Right nose
- Mucous membrane:
hyperemic (-), edema (-), discharge (-), mass (-), laceration (-) , crust (-)
- Inferior conchae : eutrophy
- Septum
: no deviation
- Air passage : normal
Left nose
- Mucous membrane:
hyperemic (-), edema (-), discharge (-), mass (-), laceration (-) , crust (-)
- Inferior conchae : eutrophy
- Septum
: no deviation
Air passage
: normal
Oropharynx
- Posterior pharynx
- Palatine tonsils
- Uvula
-

: hyperemic (-)
: T1 / T1, hyperemic (-), detritus (-)
: deviation to the right
Pharynx
: dropping of right anterior and posterior

pharyngeal arc, hyperemia (-)

Dental
: no abnormatlities
Maxillofacial
asyimmetric , a dropping of left corner of lip
Neck
unpalpable lymphe node / unpalpable lymphe node

Neurologic Examination
Cooperation
: cooperative
Cranial nerve examination:
N. I : normosmia/normosmia
N. II :
Asies visus
: not did
Color perception
: not did
N. III-IV-VI
Diplopia
: -/Eve movement
: normal/normal
Pupil
: round, 3mm/3mm, isocor
Light reflex
: +/+
N.V
: hemihipestesi facies dextra
N. VII
Face
: asymmetric, dropping of the left corner of lips
Elevation of eyebrow : +/+
Closed eye tightly
: +/+
N.VIII
N.vestibularis

Vertigo
Nistagmus

::-

N.cochlearis
Tinitus
: -/Schwabach test: same with the examiner / same with the examiner
Rinne test
Weber test
N.IX-X
Voice
Swallow

: +/+
: no lateralitation
: hoarseness
: difficult

N.XI
Elevation of shoulder : +/difficult
N.XII
Disartria
:+
Tongue position
: deviation to the right
Motoric
- Arms
- Legs

: 5/3
: 5/2

D. WORKING DIAGNOSIS
Suspect of hemorrhagic stroke in brainstem with impairment of N. VII, X, XI, XII et
causa emergency hypertension
E. DIFFERENTIAL DIAGNOSIS
Non-hemorrhagic stroke in brainstem with impairment of N. VII, X, XI, XII and
emergency hypertension
F. WORK-UP
Complete blood count : Hb, Ht, Leucocyte, Trombocyte, Ureum, Creatinine,
SGOT, SGPT, Blood Glucose, HDL, LDL, Total Cholesterol, Triglyceride, Uric

Acid, Electrolyte
Electrocardiography
Rontgen thorax
Brain CT Scan
Laryngoscopy

G. THERAPY
Hospitalized the patient
Nutrition : 2000 calories per day via nasogastric tube
IVFD Ringer Laktat + Neurobion 5000 1 amp, 20 drops per minute
Amlodipine tablet 2 x 5 mg po
Citicholine caps 2 x 250 mg po
Ranitidine amp 2 x 50 mg IV

Monitoring level of consciousness and vital sign (blood pressure, pulse rate,
respiratory rate, tempetarure) every 4 hours

INTRACRANIAL HEMORRHAGE
Hemorrhages are classified by their location and the underlying vascular pathology.
Bleeding into subdural and epidural spaces is principally produced by trauma. SAHs are
produced by trauma and rupture of intracranial aneurysms. Intraparenchymal and
intraventricular hemorrhage will be considered here.
DIAGNOSIS
Intracranial hemorrhage is often discovered on noncontrast CT imaging of the brain
during the acute evaluation of stroke. Since CT is more sensitive than routine MRI for acute
blood, CT imaging is the preferred method for acute stroke evaluation. The location of the
hemorrhage narrows the differential diagnosis to a few entities.
EMERGENCY MANAGEMENT
Close attention should be paid to airway management since a reduction in the level of
consciousness is common and often progressive. The initial blood pressure should be
maintained until the results of the CT scan are reviewed. There is growing evidence that
intraparenchymal hemorrhage may be exacerbated by acutely elevated blood pressure, and
current recommendations are to lower mean arterial blood pressure to <130 mmHg. Blood
pressure should be lowered with nonvasodilating IV drugs such as nicardipine, labetalol, or
esmolol. Patients with cerebellar hemorrhages or with depressed mental status and
radiographic evidence of hydrocephalus should undergo urgent neurosurgical evaluation.
Based on the clinical examination and CT findings, further imaging studies may be necessary,
including MRI or conventional x-ray angiography. Stuporous or comatose patients generally
are treated presumptively for elevated ICP, with tracheal intubation and hyperventilation,
mannitol administration, and elevation of the head of the bed while surgical consultation is
obtained.
INTRAPARENCHYMAL HEMORRHAGE
Intraparenchymal hemorrhage is the most common type of intracranial hemorrhage. It
accounts for ~10% of all strokes and is associated with a 50% case fatality rate. Incidence
rates are particularly high in Asians and African Americans. Hypertension, trauma, and
cerebral amyloid angiopathy cause the majority of these hemorrhages. Advanced age and

heavy alcohol consumption increase the risk, and cocaine use is one of the most important
causes in the young.
Pathphysiology of Hypertensive Intraparenchymal Hemorrhage
Hypertensive

intraparenchymal

hemorrhage

(hypertensive

hemorrhage

or

hypertensive intracerebral hemorrhage) usually results from spontaneous rupture of a small

penetrating artery deep in the brain. The most common sites are the basal ganglia (especially
the putamen), thalamus, cerebellum, and pons. When hemorrhages occur in other brain areas
or in nonhypertensive patients, greater consideration should be given to hemorrhagic
disorders, neoplasms, vascular malformations, and other causes. The small arteries in these
areas seem most prone to hypertension-induced vascular injury. The hemorrhage may be
small or a large clot may form and compress adjacent tissue, causing herniation and death.
Blood may dissect into the ventricular space, which substantially increases morbidity and
may cause hydrocephalus. Most hypertensive intraparenchymal hemorrhages develop over
3090 min, whereas those associated with anticoagulant therapy may evolve for as long as
2448 h. Within 48 h macrophages begin to phagocytize the hemorrhage at its outer surface.
After 16 months, the hemorrhage is generally resolved to a slitlike orange cavity lined with
glial scar and hemosiderin-laden macrophages.
CLINICAL MANIFESTATIONS
Although not particularly associated with exertion, intracerebral hemorrhages almost
always occur while the patient is awake and sometimes when stressed. The hemorrhage
generally presents as the abrupt onset of focal neurologic deficit. Seizures are uncommon.
The focal deficit typically worsens steadily over 3090 min and is associated with a
diminishing level of consciousness and signs of increased ICP, such as headache and
vomiting.
The putamen is the most common site for hypertensive hemorrhage, and the adjacent
internal capsule is usually damaged. Contralateral hemiparesis is therefore the sentinel sign.
When mild, the face sags on one side over 530 min, speech becomes slurred, the arm and
leg gradually weaken, and the eyes deviate away from the side of the hemiparesis. The
paralysis may worsen until the affected limbs become flaccid or extend rigidly. When
hemorrhages are large, drowsiness gives way to stupor as signs of upper brainstem
compression appear. Coma ensues, accompanied by deep, irregular, or intermittent
respiration, a dilated and fixed ipsilateral pupil, and decerebrate rigidity. In milder cases,
edema in adjacent brain tissue may cause progressive deterioration over 1272 h.

Thalamic hemorrhages also produce a contralateral hemiplegia or hemiparesis from

pressure on, or dissection into, the adjacent internal capsule. A prominent sensory deficit
involving all modalities is usually present. Aphasia, often with preserved verbal repetition,
may occur after hemorrhage into the dominant thalamus, and constructional apraxia or
mutism occurs in some cases of nondominant hemorrhage. There may also be a homonymous
visual field defect. Thalamic hemorrhages cause several typical ocular disturbances by virtue
of extension inferiorly into the upper midbrain. These include deviation of the eyes
downward and inward so that they appear to be looking at the nose, unequal pupils with
absence of light reaction, skew deviation with the eye opposite the hemorrhage displaced
downward and medially, ipsilateral Horners syndrome, absence of convergence, paralysis of
vertical gaze, and retraction nystagmus. Patients may later develop a chronic, contralateral
pain syndrome (Djerine-Roussy syndrome).
In pontine hemorrhages, deep coma with quadriplegia usually occurs over a few
minutes. There is often prominent decerebrate rigidity and pin-point (1 mm) pupils that
react to light. There is impairment of reflex horizontal eye movements evoked by head
turning (dolls-head or oculocephalic maneuver) or by irrigation of the ears with ice water.
Hyperpnea, severe hypertension, and hyperhidrosis are common. Death often occurs within a
few hours, but small hemorrhages are compatible with survival.
Cerebellar hemorrhages usually develop over several hours and are characterized by
occipital headache, repeated vomiting, and ataxia of gait. In mild cases there may be no other
neurologic signs other than gait ataxia. Dizziness or vertigo may be prominent. There is often
paresis of conjugate lateral gaze toward the side of the hemorrhage, forced deviation of the
eyes to the opposite side, or an ipsilateral sixth nerve palsy. Less frequent ocular signs
include blepharospasm, involuntary closure of one eye, ocular bobbing, and skew deviation.
Dysarthria and dysphagia may occur. As the hours pass, the patient often becomes stuporous
and then comatose from brainstem compression or obstructive hydrocephalus; immediate
surgical evacuation before brainstem compression occurs may be lifesaving. Hydrocephalus
from fourth ventricle compression can be relieved by external ventricular drainage, but
definitive hematoma evacuation is essential for survival. If the deep cerebellar nuclei are
spared, full recovery is common.
ACUTE MANAGEMENT
Nearly 50% of patients with a hypertensive intracerebral hemorrhage die, but others
may have a good to complete recovery if they survive the initial hemorrhage. The volume and
location of the hematoma determine the prognosis. In general, supratentorial hematomas with

volumes <30 mL have a good prognosis; 3060 mL, an intermediate prognosis; and >60 mL,
a poor prognosis during initial hospitalization. Extension into the ventricular system worsens
the prognosis, as does advanced age, location within the posterior fossa, and depressed level
of consciousness at initial presentation. Any identified coagulopathy should be reversed as
soon as possible. For patients taking warfarin sodium, more rapid reversal of coagulopathy
can be achieved by infusing prothrombin complex concentrates followed by freshfrozen
plasma and vitamin K. When intracerebral hemorrhage is associated with thrombocytopenia
(platelet count < 50,000/L), transfusion of fresh platelets is indicated. At present, little can
be done about the hemorrhage itself. Hematomas may expand for several hours following the
initial hemorrhage, so treating severe hypertension seems reasonable to prevent hematoma
progression. Preliminary data suggest that treatment with recombinant factor VIIa, even in
patients without coagulopathy, may decrease risk of hematoma expansion and improve
clinical outcome; a multicenter randomized trial of this approach was recently completed.
Evacuation of supratentorial hematomas does not appear to improve outcome. The
International Surgical Trial in Intracerebral Haemorrhage (STICH) randomized 1033 patients
with supratentorial intracerebral hemorrhage to either early surgical evacuation or initial
medical management. No benefit was found in the early surgery arm, though analysis was
complicated by the fact that 26% of patients in the initial medical management group
ultimately had surgery for neurologic deterioration. Overall, these data do not support routine
surgical evacuation of supratentorial hemorrhages; however, many centers operate on patients
with progressive neurologic deterioration. Surgical techniques continue to evolve, and
minimally invasive endoscopic hematoma evacuation may prove beneficial in future trials.
For cerebellar hemorrhages, a neurosurgeon should be consulted immediately to assist
with the evaluation; most cerebellar hematomas >3 cm in diameter will require surgical
evacuation. If the patient is alert without focal brainstem signs and if the hematoma is <1 cm
in diameter, surgical removal is usually unnecessary. Patients with hematomas between 1 and
3 cm require careful observation for signs of impaired consciousness and precipitous
respiratory failure.
Tissue surrounding hematomas is displaced and compressed but not necessarily
infarcted. Hence, in survivors, major improvement commonly occurs as the hematoma is
reabsorbed and the adjacent tissue regains its function. Careful management of the patient
during the acute phase of the hemorrhage can lead to considerable recovery.
Surprisingly, ICP is often normal even with large intraparenchymal hemorrhages.
However, if the hematoma causes marked midline shift of structures with consequent

obtundation, coma, or hydrocephalus, osmotic agents coupled with induced hyperventilation

can be instituted to lower ICP. These maneuvers will provide enough time to place a
ventriculostomy or ICP monitor. Once ICP is recorded, further hyperventilation and osmotic
therapy can be tailored to the individual patient. For example, if ICP is found to be high, CSF
can be drained from the ventricular space and osmotic therapy continued; persistent or
progressive elevation in ICP may prompt surgical evacuation of the clot or withdrawal of
support. Alternately, if ICP is normal or only mildly elevated, induced hyperventilation can
be reversed and osmotic therapy tapered. Since hyperventilation may actually produce
ischemia by cerebral vasoconstriction, induced hyperventilation should be limited to acute
resuscitation of the patient with presumptive high ICP and eliminated once other treatments
(osmotic therapy or surgical treatments) have been instituted. Glucocorticoids are not helpful
for the edema from intracerebral hematoma.
PREVENTION
Hypertension is the leading cause of primary intracerebral hemorrhage. Prevention is
aimed at reducing hypertension, excessive alcohol use, and use of illicit drugs such as cocaine
and amphetamines.