intracerebral hemorrhage medical treatment

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  • 7/28/2019 Intracerebral Hemorrhage Medical Treatment

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    Abstract Intracerebral hemorrhage (ICH) accounts for

    between 10% to 30% of first-ever strokes; outcomes are

    significantly worse than with ischemic stroke with a

    30-day mortality rate up to 50%, furthermore, half of the

    deaths occur in the acute phase. Intracerebral hemorrhage

    (ICH) is classified as primary or secondary according to

    the underlying etiology. Primary ICH (about 80%) comes

    from the spontaneous rupture of small vessels more often

    in relation to long-standing or uncontrolled arterial hyper-

    tension and is generally located in the basal ganglia and

    internal capsula. Secondary ICH (about 20%) is often

    associated with vascular abnormalities, tumors, and anti-coagulant therapy or coagulation disorders, more fre-

    quently located in cerebral lobes or subtentorial (cerebel-

    lum or pons). Rapid recognition and diagnosis of ICH as

    well as identification of early prognostic indicators are

    essential for planning the level of care and avoiding acute

    rapid progression during the first hours. Hematoma size

    has been identified as one of the most important predic-

    tors of 30-day mortality and its expansion is highly pre-

    dictive of neurological deterioration [1]. Blood pressure

    management remains, although controversial, the first-

    line medical approach along with possible new and effec-

    tive treatments coming from the numerous between pilot

    and larger randomized medical trials for ICH completed

    in the past decade.

    Keywords Intracerebral hemorrhage Medical management

    Medical treatment of acute ICH

    General treatment of ICH includes an overall supportive

    medical approach through the management of airways

    and ventilatory measures, circulation stabilization, fever

    and glucose level control, nutrition as well as prophylax-

    is for seizure and deep vein thrombosis [2].

    A standardized medical approach begins with simple

    measures, such as head positioning [head elevation to 30

    improves jugular venous outflow and lowers intracranial

    pressure (ICP)] and appropriate sedation to more aggres-

    sive clinical strategies as indicated.

    Increase of ICP and consequent possible mass effect

    result in neurological deterioration.Specific treatments for increased ICP secondary to

    head trauma may not necessarily apply to ICH patients;

    cerebral perfusion pressure (CPP) should be kept as much

    as possible >70 mmHg where ICP is monitored.

    Hyperventilation is one of the most effective method

    available for rapid reduction of ICP through the physio-

    logical mechanism of cerebral blood flow (CBF) regula-

    tion. However its use is limited due to its transient effect

    and its simultaneous lowering of PCO2 level and CBF.

    Osmotic therapy, despite little evidence of its efficacy,

    is commonly used in patients with large ICH and

    increased ICP; the agent most often used is mannitol,

    Neurol Sci (2008) 29:S271S273

    DOI 10.1007/s10072-008-0961-y

    A N N U A L M E E T I N G O F S I N / S N O L O M B A R D I A

    Intracerebral hemorrhage: medical treatment

    Paola Santalucia

    Springer-Verlag 2008

    Paola Santalucia ()

    Istituto Auxologico Italiano, IRCCS

    U.O. Cardiologia

    Ospedale San Luca

    Via Spagnoletto 3, 20149 Milano, Italy

    e-mail: [email protected]

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    S272 Neurol Sci (2008) 29:S271S273

    which acts as an intravascular osmotic agent thus

    decreasing ICP through cerebral autoregulation; its use

    should however be limited to a few days mostly due to

    electrolyte imbalance and renal function alteration.

    Invasive monitoring of ICP with intraventricular

    catheter positioning, in selected critical cases, allowsCSF drainage that in turn is effective for lowering ICP

    especially in case of hydrocephalus.

    Acute blood pressure management and treatment

    remain controversial and the association of a hyperten-

    sive status to hematoma enlargement is unclear.

    Persistent marked elevation of blood pressure can predis-

    pose to hematoma expansion; however, it may also repre-

    sent a protective response to preserve cerebral perfusion

    mainly in the areas of focal ischemia around the

    hematoma where reduction of blood pressure could pro-

    mote further ischemia.

    It is, therefore, difficult to indicate what is the limit

    for aggressive blood pressure treatment. An acceptable

    target blood pressure value should be tailored on the indi-

    vidual patients factors such as history of hypertension

    and baseline blood pressure, age, and the presumed cause

    of bleeding, as well as correlated with intracranial pres-

    sure. The main goal for lowering blood pressure is avoid-

    ing hematoma enlargement; this is especially true for

    bleeding resulting from a ruptured aneurysm or arteri-

    ovenous malformation. However, in primary ICH, in

    which a specific large vessel rupture is not evident, the

    risk of hematoma enlargement that is blood pressure

    related may be lower and must be balanced with the the-

    oretical risks of inducing cerebral ischemia in the areasurrounding the hematoma.

    Despite the weak evidence to support a specific blood

    pressure threshold, the recommendation from the

    AHA/ASA Guidelines is to maintain a systolic blood

    pressure

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    3. Broderick J, Connolly S, Feldmann E et al (2007) Guidelines for

    the management of spontaneous intracerebral hemorrhage in

    adults. 2007 Update. Stroke 38:20012023

    4. Qureshi AI (2007) Antihypertensive treatment of acute cerebral

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    5. Mayer SA, Brun NC, Broderick J et al (2005) Safety and feasibi-

    lity of recombinant factor VIIa for acute intracerebral hemorrha-

    ge. Stroke 36:7479

    6. Mayer S, Brun NC, Begtrup K et al (2005) Recombinant activa-

    ted factor VII for acute intracerebral hemorrhage. N Engl J Med

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    7. Mayer S (2007) Recombinant activated factor VII for acute intra-

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    S273Neurol Sci (2008) 29:S271S273