Hypertensive Intracerebral Hemmorrhage

advertisement
Hypertensive Intracerebral
Hemmorrhage
Gerry Dunlap, MS3
Fall 2005
Patient Presentation
• May have onset after exertion or
intense emotional activity
• More often during routine activity
• May occur during trauma
• As opposed to embolism and
subarachnoid, symptoms
progress to peak gradually over
several hours, instead of
appearing at maximal intensity
Patient Presentation
• ½ of patients present with headache and
vomiting
• Additional symptoms such as decrease in LOC
may occur if hematoma progresses in size
• Seizures in 7 to 9%, more often in lobar
hemorrhages than cerebellar or deep
hemorrhages
• May progress to stupor and coma if the bleed
is severe enough
Pathogenesis
• Hemorrhages occur in the territory of
penetrator arteries branching off major
intracerebral arteries
• Small arteries are more susceptible to effects
of systemic hypertension- abrupt change in
caliber from larger vessels to smaller
• Current theory of hemorrhage similar to
pathogenesis in larger systemic vessels:
chronic HTN- intimal hyperplasia with
hyalinosis- focal necrosis- vessel wall ruptures
– More massive hemorrhage may occur if clotting
cascade unable to compensate for the damage
Signs/ Symptoms
• Neurological signs present depend on
location of hemorrhage
Location
• Putaminal- 50-60%
Hemiplegia
hemisensory loss
homonymous hemianopsia
gaze palsy
Stupor
coma
p: Putamen
c: Caudate
ic: Insular Cortex
al: Ant limb Int Capsule
pl: Post limb Int Capsule
t: Thalamus
hem: Hemorrhage
cav: Post drainage cavity
Location
• Cerebellar
– Inability to walk
– Vomiting
– Headache, possibly
referred to neck or
shoulder
– Neck Stiffness
– Gaze palsy
– Facial weakness
Location
• Thalamic
–
–
–
–
Hemiparesis
Hemisensory loss
Aphasia
Neglect (nondominant
hemisphere)
– “wrong way eyes”eyes deviate toward
the hemiparesis, as
opposed to
hemispheric injury
13 year old boy, acute right sided HA
Numbness on L side of body and face
no motor deficit
Hemorrhage in R posterodorsal thalamus involving
pulvinar nucleus
Location
• Lobar
– Most often in parietal and occipital lobes
– Occipital lobes present with contralateral
homonymous hemianopsia
– High incidence of seizures
– Frontal region- contralateral plegia or
paresis of the leg with arm sparing
Location
• Pontine
– deep coma within
minutes of the
hemorrhage, due to
disruption of the
reticular activating
system
– Total paralysis
– Pinpoint pupils
Pontine hemorrhage in R pons anterior to
fourth ventricle, near facial nerve nuclei
Differential Diagnosis
• Based on risk factors- severely
hypertensive patient with a typical bleed
can be assumed to have ICH
• History of recent trauma
• Underlying bleeding disorder
• Iatrogenic anticoagulant therapy
• Neoplastic bleeding
• Drug abuse, ie cocaine- more likely with
underlying AVM
Differential
• Amyloid Angiopathy
– Usually lobar, occasionally cerebellar
– Posterior portions of brain, including parietal
and occipital lobes
– May have multiple hemorrhages
– Typically older than 65
Differential
• Intracerebral Arteriovenous
Malformation
• 0.14% estimated incidence in
US population (1/5 to 1/7 of
incidence of intracranial
aneurysms)
• Annual risk of an ICH is 2-3%,
with mortality of 10%,
increasing with subsequent
bleeds
• May be present as part of
neurocutaneous symndrome;
ie Sturge-Weber or RenduOsler-Weber
Images from:
MyPacs.com
Treatment
• ICP control
– Maintaining Cerebral Perfusion Pressure (CPP)
above 60 mmHg
– CPP=MAP-ICP
– Goal: To reduce mass effect and hydrocephalus, yet
maintain perfusion pressure
– Can reduce increased ICP by IV mannitol (1g/kg
bolus with .25 to .5 g/kg q 6hr)
– Also with barbiturate anesthesia, hyperventilation
(provides temporary lowering effect)
Treatment
• Ventricular drain or shunt may be
required to obtain ICP control
• Blood pressure control is challengingmaintaining sufficient CPP while
preventing extension of hemorrhage by
increased MAP
• Maintain systolic between 140 to 160
mmHg
Treatment
• Surgery- indications vary depending on site of
bleed
– Cerebellar hemorrhages need to be decompressed
if greater than 3 cm
– Supratentorial ICH hematoma evacuation more
controversial
• 1997 meta-analysis had insufficient data to draw
conclusions of risk/ benefit of surgery
• Now considered to treat refractory increases in ICP in a per
patient basis
– Patients with decreased LOC (obtundation- stupor)
– Also supportive of surgery- recent onset, ongoing
deterioration, involvement of nondominant hemisphere,
accessible hematoma location
Imaging- CT vs. MRI
• HEME study- Hemorrhage and Early MRI
Evaluation
• MRI was much more accurate at detecting
hemorrhage than CT
– Study was stopped early due to clear superiority of
MRI over CT
• High concordance of the two imaging modalities with acute
hemorrhage
• MRI more sensitive (49 patients of 200) at detecting
chronic hemorrhage or microbleeds
– However, MRI does not pick up subarachnoid
hemorrhages as well, so CT remains the imaging
most often performed upon admission into the
hospital
Imaging
• MRI findings depend on the age of the bleed
• Degradation of hemoglobin in the hemorrhage
provides different blood products
(deoxyhemoglobin, methemoglobin) with
different signal enhancement on MRI
• Variable presentation of Hyperacute (1-6
hours) subacute, chronic and microbleeds
Summary
• Presents as an escalating neurological insult,
submaximal at onset
• Signs depend on cerebral location
• Treatment includes medical and surgical
approaches to limit extent of ongoing
hemorrhage while maintaining CPP
• CT in the acute setting to allow for possibility of
visualizing subarachnoid hemorrhage,
otherwise MRI is more sensitive for diagnosis
References
•
•
•
•
•
UptoDate.com- Hypertensive intracerebral hemorrhage
Kidwell CS, Chalela JA, Saver JL, et al; “comparison of MRI and CT for detection of acute intracerebral
hemorrhage,” JAMA, October 2004;292(15):1823
Cotran, Kumar, Collins; Robbins Pathologic Basis of Disease 6th ed., page 1310-14
Goetz; Textbook of Clinical Neurology 2nd ed., page 410-20
Images:
–
–
–
–
–
MyPacs.com- various images for ICH
Sherman SC; “pontine hemorrhage presenting as an isolated facial nerve palsy,” Ann Emerg Med, Jul 2005, 46(1): 64-6
Mijovic-Prelec D, Bentley P, Caviness VS; “selective rotation of egocentric spatial representation following right putaminal
hemorrhage,” Neuropsychologia; 2004; 42(13):1827-37
Kirollos RW, Tyagi AK, Ross SA, et al.; “management of spontaneous cerebellar hematomas: a prospective treatment
protocol,” Neurosurgery; Dec 2001; 49(6):1378-86
Wester K, Irvine DRF, Hugdahl K; “auditory laterality and attentional deficits after thalamic haemorrhage,” Journal of
Neurology; Aug 2001; 248(8):676-83
Download