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ubdural hematoma in olderpatients raises diagnostic and

therapeutic difficulties.Acute subduralhematomas, which are clinically evi-dent (ie, symptomatic) within 72hours, usually occur in younger adults.Chronic subdural hematomas, whichusually occur in older individuals witha peak incidence in the sixth and sev-enth decades of life, are defined ashematomas of more than 20 days ofage (typically determined by patienthistory).1 The incidence of chronicsubdural hematoma is approximately1 in 100,000 population per year; in-cidence increases to approximately 7

cases per 100,000 population per yearin the age 70 to 79 group.2 Significantly,subdural hematoma is a reversiblecause of dementia.3

Case #1A 64-year-old man presents with a one-month history of gait ataxia, urinaryincontinence, and altered mental sta-tus. His past medical history is unre-markable with the exception of chronicalcohol abuse.Vital signs on presenta-tion are blood pressure 110/80mmHg,

pulse 86 bpm, temperature 36.8oC, andrespirations 18/minute. Physical examis remarkable for a fluctuating mentalstatus, consistent with a delirium. Heis somewhat lethargic during exami-nation but cooperative.At other times,he is oriented to place and time. He isnormocephalic and without evidenceof trauma.Pupils and extraocular mus-cles are intact. Funduscopic exam isdifficult secondary to bilateral cataracts.Cranial nerves II through XII are in-tact. The patient’s gait is unsteady. Hismotor exam reveals 4/5 strength in theleft upper and left lower extremity.Computed tomographic (CT) imag-ing of the brain is shown in figure 1.

Case #2A 68-year-old woman with chronic atrialfibrillation (AF),congestive heart failure,and hypertension presents with a one-week history of worsening headaches.The patient has been on warfarin 5 mg/dfor the past 5 years with the internationalnormalized ratio (INR) maintained be-tween 2 and 3.The patient states that shefell on her buttocks two weeks prior topresentation but denies any head trauma.Vital signs on presentation are blood pres-sure 145/90 mmHg,pulse 86 bpm, tem-perature 37.6oC, and respirations16/minute.The patient was alert and ori-ented to time,place,and person.Cranialnerves II through XII are intact. Fun-duscopic exam is difficult due to bilateralcataracts. The patient’s gait is not im-paired. Her strength is 5/5 throughout

NeurologyNeurology

Subdural hematomas pose diagnostic and therapeutic difficulties inolder adults. Presenting signs and symptoms of subduralhematomas—headache, confusion, ataxia, and hemiparesis—canmimic other diseases such as dementia, stroke, transient ischemicattacks, neoplasm, and normal pressure hydrocephalus. Patients withsubdural hematomas and focal neurologic signs should be consideredfor surgical intervention, whereas asymptomatic patients or patientswith only complaints of a headache can be managed medically orfollowed with serial neuroimaging by computed tomography. Patientswho have been chronically anticoagulated pose a dilemma when theypresent with a subdural hematoma.

Karnath B. Subdural hematoma: Presentation and management in older adults. Geriatrics2004; 58(July):18-23.

Key words: Chronic subdural hematoma • anticoagulation • fallsatrial fibrillation

S

Dr. Karnath is assistant profes-sor of medicine, University of TexasMedical Branch at Galveston, Tx.

Disclosure: The author has no realor apparent conflicts of interest relat-ed to the content presented here.

Bernard Karnath, MD

Subdural hematomaPresentation and management in older adults

18 Geriatrics July 2004 Volume 59, Number 7

Figure 1 CT scan of subdural hematoma(A) involving right hemisphere. Note themidline shift (B), blunting of sulci (C), andedema (D). (Visit www.geri.com for alarger image.) Source: Scan supplied by author.

A B

C D


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with equal deep tendon reflexes. Heartexam reveals irregularly irregular rhythmwithout murmurs. CT head reveals anisodense right subdural hematoma with-out midline brain shift.

EtiologyOlder adults are at increased risk forsubdural hematomas due to fragilityof bridging cerebral veins. As cerebralatrophy develops, the brain shrinksaway from the dura and bridging veinsare predisposed to tearing due to in-creased stress.

A history of trauma is elicited in 75%of cases.Men have a higher incidence ofsubdural hematoma due to a higher riskof trauma.Although trauma is the mostcommon cause of subdural hematoma,the actual event may be so trivial thatsome older patients do not rememberit.The etiology is undetermined in 25%of cases; these are sometimes termed“spontaneous.”4,5 Anticoagulant and an-tiplatelet therapy are associated with anincreased risk for spontaneous subduralhematomas.A retrospective study of 123patients (mean age 74, +/-5) who pre-sented with a spontaneous subduralhematoma found that 76% (93 total pa-tients) were on aspirin (78 patients) andwarfarin (15 patients) therapy.6 Otherrisk factors for developing subduralhematomas include age, male gender,coagulopathy, thrombocytopenia, andalcoholism.2 Alcoholics are at particu-lar risk due to a propensity to fall, in ad-dition to the likely presence of underly-ing liver disease with secondary coagu-lopathy and thrombocytopenia.

Many subdural hematomas resolvespontaneously before the onset of signsand symptoms.2 A subset of hematomasdoes progressively enlarge.Whereas sev-eral mechanisms have been proposedfor the enlargement of subduralhematomas in the chronic state, onlyone has gained widespread acceptance.This proposed mechanism includes re-current hemorrhage and fibrinolysis.2

The outer membrane of the hematomacontains a fine network of capillaries.There is an ongoing process of bleed-ing into the hematoma due to activation

of the coagulation–fibrinolytic systemthat results in defective hemostasis andclot formation.As a result, there is slowaccumulation of hemorrhage withinthe subdural space causing compres-sion of the cortex and blunting of sulci(figure 2).

PresentationThe most common presenting symp-toms in patients age 60 and older areheadache, altered mental status, hemi-paresis, gait disturbance, and aphasia.5

In one retrospective study,68% (30/44)of patients presented with headache,

July 2004 Volume 59, Number 7 Geriatrics 19

Subdural hematoma is a reversible cause of dementia. Older adults are at increasedrisk for subdural hematomas due to fragility of bridging cerebral veins. Presentingsymptoms can be subtle and the condition may be overlooked.

Illustration for Geriatrics by Sally Cummings


39% (17/44) with confusion, 32%(14/44) with ataxia, and 30% (13/44)with hemiparesis.Two neurologic grad-ing systems (table 1) have been pro-posed to assess the severity of neuro-logical deficits.4,7,8

DiagnosisThe diagnosis of subdural hematomais definitively established with neu-roimaging of the brain—either withcomputed tomography (CT) or mag-netic resonance imaging (MRI).Chronicsubdural hematomas appear as hypo-dense (ie, similar density as brain) ar-eas on CT images of the brain after threeweeks duration.2 (Tissue density as seenon CT scan is described in “Hounsfieldunits”with air being the least dense andbone being the most dense. Density ofblood in the subdural hematoma varieswith the age of the hematoma.) Sub-dural hematomas are hyperdense in theacute phase (ie,1 week), isodense in thesubacute phase (ie, 2 to 3 weeks), andhypodense in the chronic phase (ie,3 to4 weeks).9 According to one study, thedensity of subdural hematomas mayvary after one month.10 Isodensehematomas are difficult to detect on CTscanning and can be detected by evi-dence of mass effect either by midlineshift or blunting of sulci. MRI is a bet-ter imaging study for detecting isodensehematomas. MRI would show the iso-dense hematoma as a hyperintense le-sion.11 MRI has the disadvantage of be-

ing less readily available than CT scan-ners and restless patients cannot be ex-amined unless sedation is used. Neu-roimaging with CT scanning as the ini-tial diagnostic test should be consideredin the presence of rapid unexplaineddeterioration in mental status,focal neu-rologic signs, gait disturbance, recenthead trauma, and new onset headache.

Potentially reversible causes of de-mentia, such as subdural hematomas,normal pressure hydrocephalus, andtumors, can be detected with CT scanor MRI of the brain. Whereas currentclinical practice guidelines for demen-tia do not recommend routine neu-roimaging, expert groups have identi-fied prediction rules for neuroimag-ing.12 These prediction rules includethe following clinical variables in ad-dition to dementia: rapid unexplaineddecline in cognitive function, focal neu-rologic signs, gait disorder or ataxia,

recent head trauma, anticoagulation,bleeding disorder, new onset headache,and seizures. The presence of any oneof these clinical variables might in-crease the likelihood of finding a sub-dural hematoma.

Differential diagnosisThe symptoms associated with chronicsubdural hematomas can mimic otherdisorders such as Alzheimer’s demen-tia, stroke, transient ischemic attacks,normal pressure hydrocephalus, andintracranial neoplasm. A careful clin-ical history is mandatory, as the pat-tern of onset and time course of symp-toms will help to differentiate chronic

subdural hematomas from other causesof mental status changes and focal neu-rologic deficits.13

Alzheimer’s dementia.Chronic subduralhematomas can be differentiated fromAlzheimer’s dementia based on the on-set and progression of memory deficits.Memory impairment in Alzheimer’sdisease develops over several monthsto years, whereas in chronic subduralhematomas,changes in cognitive func-tion develop over several (approxi-mately 2 to 6) weeks. Some patientswith chronic subdural hematomas willshow focal neurologic signs whereaspatients with Alzheimer’s dementia willnot.

Cerebrovascular insults. Cerebrovas-cular insults can lead to cognitive im-pairment and focal neurologic signs.However, patients with cerebrovascu-lar insults are more likely to show acutefocal neurologic signs and acute men-tal status impairment (ie, within hoursor days) whereas in patients withchronic subdural hematomas focalneurological signs and mental statusimpairment develop progressively overweeks.

Neoplasms. Intracranial neoplasmsare difficult to differentiate fromchronic subdural hematomas withoutneuroimaging. Patients with intracra-nial neoplasms often present with signsof increased intracranial pressure thatinclude headaches, altered mental sta-tus, and focal neurologic signs, a sim-ilar presentation to chronic subduralhematoma. Neuroimaging would bediagnostic. (Whereas MRI would bethe study of choice, it does take longerto obtain and is less readily availablethan CT scanning.)

Normal-pressure hydrocephalus. Symp-toms of normal pressure hydrocephalusare similar to those of chronic subduralhematoma with the exception of uri-nary incontinence. The clinical triadof gait ataxia, altered mental status, andurinary incontinence is considered clas-sic for normal pressure hydrocephalusor other subcortical dementia.14

Whereas urinary incontinence is a latemanifestation of normal-pressure hy-

Subdural hematoma


Figure 2. Subdural hematoma causingmidline shift.

Source: Illustration supplied by author

In chronic subduralhematomas, changesin focal neurologicsigns and mentalstatus progressivelydevelop over weeks


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drocephalus, it is usually not encoun-tered in chronic subdural hematomas.Differentiating normal-pressure hy-drocephalus from chronic subduralhematoma based on clinical exam alonecan be difficult; neuroimaging wouldbe diagnostic.

ManagementSurgical. Smely and colleagues foundtwist-drill trephination (TDT) with aCORDIS catheter to be a superior treat-ment to burr-hole craniotomy (BHC)with closed-system drainage.15 In theirstudy, 18% (6/33) of patients who un-derwent TDT required repeat surgicalintervention as compared with 33%(11/33) of patients who underwentBHC; another 6% of these BHC pa-tients had to operated on a third time.Total mortality rate was 6% for patientundergoing TDT versus 9% for patientsundergoing BHC. Craniotomy is re-served for patients with re-accumulat-ing hematoma or residual hematomamembrane that prevents re-expansionof the brain.

Medical. Medical management is anoption for patients with minimal neu-rologic signs, ie, headache only withno other neurologic signs,no focal neu-rologic deficits or memory impairment.Conservative therapy consists of inpa-tient observation, a trial of steroids ormannitol and serial CT scans. Inpa-tient medical management of chronicsubdural hematomas can result in ahospital stay of 4 to 22 weeks.16 Med-ical management has not been widelyused because patients generally do wellafter surgical treatment and requireconsiderably shorter hospital stays (eg,4 weeks).

Inzelberg and colleagues reportedsuccessful non-surgical treatment of asubdural hematoma in a hemodialysispatient in whom surgery was con-traindicated.17 The patient,who was onmaintenance anticoagulation treatmentbecause of recurrent clotting of her he-modialysis access,presented with hemi-paresis and aphasia.CT scan of the brainrevealed a subdural hematoma with-out midline shift. This patient was

started on 16 mg/d of dexamethasoneparenterally for two weeks. The steroidtreatment was tapered over the subse-quent month and a follow-up CT scanrevealed no evidence of subdural fluid.

Observation. A subset of patients withacute subdural hematomas will resolvespontaneously. Factors favoring spon-taneous resolution of hematomas arelow-density fluid on CT scan, chronicsubdural hematomas of small size, andventricular dilation as opposed to com-pression. Asymptomatic patients withsmall chronic subdural hematomas canbe followed with serial CT scans. Par-lato and colleagues reported a series of5 patients who were diagnosed withchronic subdural hematomas and wereobserved with serial CT scans.18 All pa-tients had spontaneous resolution oftheir hematomas without medical orsurgical intervention.These patients,av-erage age 73, presented with headacheand mild cognitive impairment. CTscans showed subdural hematoma with-out a midline brain shift. All 5 patientshad hematoma resolution within a 6-week follow-up period.

PrognosisMortality rates for subdural hematomascan approach 30%.19 Predictors for hos-

pital mortality in older patients withsubdural hematoma include present-ing level of consciousness with Glas-gow coma scale <7 (table 2), age >80,acute duration of hematoma forma-tion, and craniotomy.19 The presenceof focal neurologic signs and a midlineshift on neuroimaging is not associatedwith increased hospital mortality. Iso-density of the subdural hematoma onCT scan is considered a positive prog-nostic factor whereas hypodensity ofthe subdural hematoma on CT scan isconsidered a negative prognostic fac-tor.20 Isodensity indicates that the sub-dural hematoma is of short duration.Therefore the brain should re-expandmore readily upon drainage of thehematoma.

Chronic AnticoagulationThe risks and benefits of chronic anti-coagulation, especially in chronic atrialfibrillation, must be considered. In-tracranial hemorrhage is the most con-cerning of complications. The twomost common conditions requiringchronic anticoagulation are prostheticheart valves and chronic atrial fibril-lation (AF). Adjusted-dose warfarinhas been shown to reduce stroke in-cidence by 62% in patients with


Table 1 Neurologic grading systems for subdural hematomasBender Markwalder

Group 1 Normal mental function; Grade 0 No neurologic signsno focal signs

Grade 1 Headache;reflex asymmetry

Group 2 Lethargic; Grade 2 Altered mental statusfocal neurologic signs hemiparesis

Group 3 Stuporous; Grade 3 Stupor but responsive;marked focal hemiplegianeurologic signs

Group 4 Coma; Grade 4 Coma;signs of hibernation decerebrate or(pupillary dilation, decorticate posturingdecerebrate or decorticate posturing,respiratory arrest)

Source: Created for Geriatrics by Bernard Karnath, MD, with information from references 8 and 9.


chronic AF.20 This benefit was not off-set by the occurrence of major hem-orrhage. The rate of intracranial he-morrhage is approximately 0.3% peryear for patients receiving warfarinwith a maintained INR of 2.0 to 3.0.The rate of stroke among patients withchronic AF who are not receiving an-ticoagulation ranges from 5% to 12%per year.21,22 There is a dramatic in-crease in the risk for intracranial he-morrhage with increasing INR, espe-cially with INRs greater than 4.0.19

Should the risk of falling influencethe decision to place a patient withchronic AF on anticoagulation? A meta-analysis of studies involving older pa-tients with chronic AF who received notherapy,aspirin,or warfarin, found thatwarfarin provided a 68% relative risk re-duction of stroke.23 Patients on chronic

warfarin who were at risk for falls had arelative risk of 1.4 for developing a sub-dural hematoma (ie, patients on war-farin with risk for falls are 40% morelikely to develop a subdural hematoma).This increased risk of developing a sub-dural hematoma was overshadowed bythe 68% relative risk reduction in strokefor patients on chronic warfarin.

Anticoagulation should be reversedwith fresh frozen plasma and vitaminK in patients who develop a subduralhematoma. Evidence supports thesafety of temporary interruption ofanticoagulation therapy in patientswith intracranial hemorrhage and me-chanical heart valves or AF.24,25 The es-timated risk of having an ischemicstroke after discontinuation of war-farin therapy within 30 days was 3%for patients with metallic valves or AF.Phan and colleagues found no recur-rences of intracranial hemorrhage inpatients who resumed anticoagulationtherapy.24 Anticoagulation therapy canbe restarted 1 to 2 weeks after evacu-ation of a subdural hematoma.23-25

Three separate studies involving 83cases of subdural hematomas in pa-tients receiving chronic anticoagula-tion reported only one recurrence ofhematoma after recommencing war-farin after a mean duration of 7 to10days of discontinuation.24-26 Some au-thors recommend CT before and af-ter surgical drain removal to evaluatethe possibility of bleeding caused bydrain removal.27

No study has evaluated the optimaltime to recommence anticoagulationtherapy in a patient with a subduralhematoma who was medically man-aged, ie, no evacuation performed. Ifevacuation is not performed then arepeat CT should be performed in 1 to2 weeks. Serial CT scans should be per-formed during a 4- to 6-week periodto confirm resolution of hematoma, atwhich time anticoagulation can berestarted.

DiscussionCase #1. The patient in case # 1 presentswith signs and symptoms that were ac-

tually consistent with the classic triadof normal pressure hydrocephalus.Thiscase underscores the importance of neu-roimaging in making the correct diag-nosis. Urinary incontinence is an un-likely finding in chronic subduralhematoma.The patient’s main risk fac-

tor for developing a subdural hematomawas alcohol abuse.Alcoholism has beenreported to be a predisposing factor inthe development of chronic subduralhematoma in up to 35% of patients.20

The chronic use of alcohol leads to liverdisease with secondary coagulopathyand thrombocytopenia. Alcoholism isalso a risk factor for all categories oftrauma.Neuroimaging revealed a largeright subdural hematoma with midlineshift.The patient had altered mental sta-tus with focal neurologic signs (grade 2Markwalder signs or group 2 Bendersigns) and a midline shift was seen onCT scan,providing clear indications forsurgical intervention. The patient un-derwent burr-hole evacuation withclosed-system drainage without com-plications.

Conservative management is ac-ceptable in cases where there are min-imal signs and symptoms.For example,in a patient who presents with aheadache and without focal neurologicsigns and the CT scan does not reveala midline shift, conservative manage-ment is appropriate.

Case #2. This patient represents acommon dilemma for the physiciantreating a patient with chronic AF.

Subdural hematoma


Table 2 Glasgow coma scaleEye opening E

spontaneous 4to speech 3to pain 2no response 1

Best motor response M

To verbal commandobeys 6

To painful stimuluslocalizes pain 5flexion-withdrawal 4flexion-abnormal 3

extension 2no response 1

Best verbal response V

Oriented and converses 5disoriented and converses 4inappropriate words 3incomprehensible sounds 2no response 1

Scores must be broken down intocomponents, ie, E3V3M5 = GCS 11* 90% ≥8 are in coma* ≥8 at 6 hours, 50% die* ≤9 note in coma* 9-11 = moderate severity* 8 is critical score* ≤12 = minor injury

Source: Created for Geriatrics by BernardKarnath, MD.

Evidence supportssafety of temporaryinterruption ofanticoagulation inpatients withintracranialhemorrhage


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Older patients with chronic AF are atrisk for embolic stroke. The annualstroke incidence in patients withchronic AF is 6% if they are not onchronic anticoagulation. However, anolder patient on chronic anticoagula-tion is at risk for intracranial bleeds.This patient presented with headache(grade 1 Markwalder signs) and wasplaced under inpatient observation andreceived serial neuroimaging with CTscanning. Her warfarin was discontin-ued. The subdural hematoma resolvedin 6 weeks. Considering the risk-to-benefit ratio of chronic anticoagula-tion in patients with chronic AF, war-farin should be restarted once thehematoma has resolved. The risk of de-veloping another subdural hematomais overshadowed by the risk reductionin stroke prevention.

ConclusionChronic subdural hematoma is one ofthe reversible causes of dementia. Pre-senting symptoms can be subtle andsubdural hematomas are often over-looked.Whereas current clinical prac-tice guidelines for dementia do not rec-ommend routine neuroimaging, thepresence of clinical variables, such asfocal neurologic signs in the presenceof dementia of brief duration, shouldprompt the use of neuroimaging. Sur-gical intervention should be used incases where there are signs of increasedintracranial pressure.

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