thediagnosis ofsubarachnoid haemorrhagenoid haemorrhage (sah). at present, com-puted tomography (ct)...

Journal of Neurology, Neurosurgery, and Psychiatry 1990;53:365-372

OCCASIONAL REVIEW

The diagnosis of subarachnoid haemorrhage

M Vermeulen, J van Gijn

Lumbar puncture (LP) has for a long time beenthe mainstay of diagnosis in patients whopresented with symptoms or signs of subarach-noid haemorrhage (SAH). At present, com-puted tomography (CT) has replaced LP forthis indication. In this review we shall outlinethe reasons for this change in diagnosticapproach. In the first place, there are draw-backs in starting with an LP. One of these isthat patients with SAH may harbour anintracerebral haematoma, even if they are fullyconscious, and that withdrawal of cerebro-spinal fluid (CSF) may occasionally precipitatebrain shift and herniation. Another disadvan-tage of LP is the difficulty in distinguishingbetween a traumatic tap and true subarachnoidhaemorrhage. Secondly, the use of CT withinthe first two or three days offers a wealth ofinformation about the origin and extent of thehaemorrhage, and about the presence of earlycomplications requiring urgent treatment. Anearly brain scan also serves as a baseline againstwhich future changes can be measured. Theinformation about the location of the haemor-rhage is especially valuable in patients withSAH and a negative angiogram. This is aheterogeneous group of patients which will bediscussed separately. The review continueswith guidelines about the interpretation of theCSF in patients with a negative CT scan, whichis the only remaining indication for LP in thediagnosis of SAH. The final paragraph pointsout the many pitfalls in the diagnosis ofrebleeding by analysis of CSF samples, whichmakes serial CT scanning by far the preferredmethod.

Department ofNeurology, UniversityHospital Dijkzigt,RotterdamM VermeulenUniversityDepartment ofNeurology, Utrecht,The NetherlandsJ van Gijn

The dangers of lumbar punctureThe possibility of a haematoma being presentin patients who present with the clinicalfeatures of SAH should be considered. In aseries of 100 consecutive patients who weresuspected of aneurysmal rupture, fifteen had anon-aneurysmal haematoma and eight of thesewere located in the cerebellum.' It is obviousthat an LP could have done harm in thesepatients. In addition, a third of patients with aruptured aneurysm harbour an intracerebralhaematoma,`'' and even in patients withoutneurological signs other than neck stifEfess 10per cent may have a haematoma of at least30 mm.4

Deterioration after LP is not only a theor-etical possibility as shown by Duffy, whodescribed severe clinical deterioration in seven

of 55 patients with SAH who had LP, beforeCT scanning and within 12 hours of the bleed.Intracranial haematomas with brain shift wasproven by operation or subsequent CT scan-ning in six of the seven patients, and it wassuspected in the remaining patient who stop-ped breathing at the end of the procedure.5Rebleeding may have occurred in some ofthesepatients.We therefore agree with Hillman that it is

advisable to perform a CT scan first in allpatients who present within 72 hours of asuspected SAH, even if this requires referral toanother centre.4

It could be argued that by first performingCT the diagnosis may be delayed and that thismay be dangerous if the patient has bacterialmeningitis. However, the likelihood of menin-gitis is extremely small in patients with anadequate history of headache or unconscious-ness coming on within seconds and only rarelyis the distinction more difficult, for instance, inpatients who have been found in a- confusedstate, with marked neck stiffness and moderatefever.

Ideally, patients with suspected SAH shouldnot be admitted to a hospital without CTscanning facilities (and patients with confirmedSAH not to hospitals without a neurosurgicalunit).

Traumatic tap or intracranial bleeding?Neck stiffness following SAH takes three to 12hours to develop-it is an unreliable test toperform on domiciliary calls. Patients arrivingin casualty with a history of "thunderclapheadache" a few hours earlier and with equi-vocal neck stiffness may either have a true SAHor a more usual type of headache with anunusual onset.' If an LP is performed andblood-stained CSF is found it is difficult todistinguish between a traumatic tap and intra-cranial bleeding. It is a widely held belief thatthis distinction can be made by collecting theCSF in three test tubes and by counting the redcells in the consecutive tubes. A decrease in redcells would indicate a traumatic tap. Indeed, adecrease in red cells occurs more often intraumatic punctures than in intracranial bleed-ing, but it also occurs in patients with aprevious bleed.9 Conversely, a constant num-ber of cells can be seen with traumatic taps. Inthe individual case therefore no firm diagnosiscan be made with this "three tube method".The opinion of the doctor who carried out

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the LP also appears unreliable. In a study byBuruma et al doctors were often unable todecide for themselves whether the blood-stained CSF had resulted from the procedureor not.9 The form of the red cells changes in theCSF, and this so-called crenation of red cellshas been advocated as a means of differentiat-ing a traumatic tap from a true haemorrhage.However, crenation of red cells occurs verysoon after red cells have entered the CSF andmay therefore be seen in many traumatic taps.'0Cytology of the CSF is also of limited value.The presence of erythrophages indicatesintracranial haemorrhage if an LP was notcarried out earlier, but it takes some time beforesiderophages are demonstrable. Moreover,negative cytology does not exclude a haemor-rhage.9The most reliable method for distinguishing

a traumatic tap from a genuine bleed is to spindown the CSF and to examine the supernatantfluid for the presence of xanthochromia.Examination of the supernatant should be dohewith spectrophotometry and not with thenaked eye, since direct vision is a rather in-sensitive method. In a series of32 CSF samplesin which spectrophotometry had detected xan-thochromia, this was visible with the naked eyein only half the samples." The pigments thatare responsible for the yellow colour ofthe CSFafter a haemorrhage result from lysis of redcells. The average survival of red cells in theCSF is much shorter than in the circulation.This rapid haemolysis has not been fully ex-plained. Recently, it has been suggested thatred cells in the subarachnoid space lose theiridentity as autologous cells and this results inimmune mediated haemolysis.'2

In the classic study by Barrows et al thedevelopment of xanthochromia was studied bymeans of spectrophotometry.'3 This techniquemeasures the light intensity in different regionsof the visible spectrum (400-700 nm), aftertransmission of light through the colouredCSF. Three different pigments can be distin-guished by their characteristic absorptionbands in the spectrum: oxyhaemoglobin,methaemoglobin, and bilirubin. The wave-length where absorption occurs permits quali-tative determination, whereas the height of thepeak makes quantification possible.The rate at which the pigments appear in the

CSF is of great practical importance, as theirpresence excludes a traumatic puncture. Oxy-haemoglobin has been detected as early as twohours after the bleeding,'3 but usually it takes afew hours or more for red cells to lyse and forxanthochromia to develop. In two large seriesofpatients with SAH it was shown that xantho-chromia could be detected in all patients inwhom the CSF was examined at least 12 hoursafter the haemorrhage. 4 15

Extra information by CT scanningComputed tomography not only obviates theneed for a potentially hazardous LP, it offersimportant information other than the merepresence or absence of intracranial blood. Thisapplies particularly if the scan is made as early

as possible. On the day of SAH, intracranialblood is detected in about 95% of patients.This proportion declines to 90% after one day,80% after five days, and 50% after one week.316

In the first place, if intracranial blood isdetected, the site of the haemorrhage oftenindicates the likely source. In case of anintracerebral haematoma, it is often possible todistinguish primary intraparenchymal bleed-ing from SAH extending into the brain tissue(fig 1).1' It is not always easy to determinewhether a haematoma associated withaneurysm rupture is in fact intraparenchymalor whether it has only distended the subarach-noid space, usually the frontal interhemis-pheric or sylvian fissure.'8 However, this dis-tinction is of limited importance for practicalmanagement, and follow up scans will usuallyresolve the issue. In case the extravasated bloodis confined to the basal cisterns, a rupturedaneurysm can be diagnosed if the subarachnoidclots are most dense at one of the classicalaneurysm sites (fig 2): the frontal interhemis-pheric fissure (aneurysm of the anterior com-municating artery), the chiasmatic cistern onone side (aneurysm of the internal carotidartery, usually at the origin of the posteriorcommunicating artery), or the most lateral partof the sylvian fissure (aneurysm of the middlecerebral artery).' '9

Bleeding from aneurysms at more unusualsites may be more difficult to recognise;aneurysmal bleeding from a posterior inferiorcerebellar artery, for instance, may be easilymissed by CT.202' Predicting the site of aruptured aneurysm from the CT scan is morethan an intellectual game. This information ishelpful in planning angiography, in particularthe order and the extent of selective catheter-isation, and it is vital ifmore than one aneurysmis found.' 21-23 Even the uncommon event oftwoaneurysms rupturing at the same time can becorrectly documented by CT.24 Visualisation ofthe aneurysm itself, after injection of contrast,used to be the exception with CT, indicatingthat the aneurysm is very large, with or withoutcalcification.' High-resolution CT scanning,with 1-5 mm slices, is more sensitive but notinfallible.25 Magnetic resonance imaging(MRI) is not well suited for imaging subarach-noid haemorrhage in the acute stage.26 Afterseveral days or weeks, however, when the CTscan has become normal, MRI may detectsubpial deposition of haemosiderin near thesource of the haemorrhage.2'26 In addition,MRI allows visualisation of the aneurysmitself. In two studies, a T2-weighted 2000/80spin echo sequence, identified an aneurysm inabout half the cases, by means of a signal-voidarea.27 28

Not all haemorrhage in the basal cisterns isof aneurysmal origin. A recently recognisedform is the perimesencephalic haemorrhage,29with extravasated blood mainly or only in theinterpeduncular, ambient, or quadrigeminalcisterns (fig 3a). Not only is the pattern ofhaemorrhage on CT different from that withaneurysmal haemorrhage, the clinical featuresmay also differ; loss of consciousness occursless often and a gradual onset of headache

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Figure I (a) Bifrontalhaematoma,from rupturedaneurysm of the anteriorcommunicating artery; (b)haematoma in the medialpart of the temporal lobe,from ruptured aneurysm ofthe internal carotid artery,at thejunction with theposterior communicatingartery; (c) haematoma inthe lateral part of thetemporal lobe,fromruptured aneurysm of themiddle cerebral artery (theaneurysm itself is visible asa less dense area within thehaematoma).

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& ~ ~~~~~~~~~ ~ ~~~~~~~~:.4.

(minutes rather than seconds) occurs more

often than with aneurysms. Together with theexcellent prognosis this suggests a venous or

capillary source of bleeding.29 This type ofhaemorrhage is not rare, occurring in about1000 of all subarachnoid haemorrhages, and inhalf the patients with a negative angiogram(table). It is also rather specific. Basilaraneurysms may also produce an isolated clotin the interpeduncular cistern, but theseaneurysms constitute only one out of 10 rup-

tured aneurysms, and in turn only one in eighthaemorrhages from basilar aneurysms do notextend into the chiasmatic and other basalcisterns (fig 3b).29 For every 100 SAHs 80 are

aneurysmal. After the exclusion by CT ofintracerebral haemorrhages and arteriovenousmalformations the remaining 10 are of non-

aneurysmal perimesencephalic type and abouthalf of these occur mainly in the interpedun-cular cistern. Thus, the chance of a rupturedbasilar aneurysm with such a type of haemorr-hage is about one in six (fig 4). This is of coursereason enough to perform a vertebral angio-gram if the patient is fit for operation, but if thisis negative repeated angiography does not seem

warranted.A similar calculation applies to patients

without blood in the basal cisterns or even

without any evidence of extravasated blood on

CT scanning, despite an interval of less thanthree days from the onset of symptoms, and yetwith true SAH demonstrated by xantho-chromia of the CSF. With third or fourthgeneration CT scanners, and with adequateexperience in the detection of subarachnoidblood, evidence of blood in the basal cisterns islacking on the first day in about 5 %// of rupturedaneurysms,3 16 29 and in about a quarter ofpatients with SAH and a normal angiogram.29Given that 800/ of patients with SAH have an

aneurysm, the chance of an aneurysm in

Table Patterns of bleeding on CT and results ofangiography in 120 consecutive patients withsubarachnoid haemorrhage. Patients with primaryintracerebral haemorrhage have been excluded.24 CT wasperformed within five days in all patients, and withinthree days in most

Angiography

NoAneurysm aneurysm(n = 92) (n = 28)

Pattern of haemorrhage on CT:Basal cisterns, compatible withaneurysm 85 7

Predominantly around midbrain 1 13Aspecific or no evidence ofhaemorrhage 6 8

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Figure 2 (a)Subarachnoidhaemorrhage,predominantly in thefrontal part of theinterhemispheric fissure,from a ruptured aneurysmof the anteriorcommunicating aneurysm;(b) subarachnoidhaemorrhage, with centrein the right suprasellarcisterns (to reader's left),from a ruptured aneurysmof the internal carotidartery, at thejunction withthe posteriorcommunicating artery;(c) subarachnoidhaemorrhage,predominantly in thesylvianfissure,from aruptured aneurysm of themiddle cerebral artery. |~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

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patients with true SAH but without cisternalblood on an early CT scan is about one in two.

Early CT scanning not only gives importantdiagnostic information on the source ofhaemorrhage, it also demonstrates complica-tions that may require urgent treatment,especially acute hydrocephalus"0 or a life-threatening haematoma." Finally, the initialCT scan provides an important baseline for thediagnosis of future complications, particularlyrebleeding, infarction or hydrocephalus.

"Angiogram-negative SAH": a mixedbagThe fate of patients with the diagnosis ofsubarachnoid haemorrhage but a negativeangiogram has been the subject of a spate ofpublications that have reported follow up

studies. We shall abstain from listing thesestudies, as it is abundantly clear from thepreceding paragraphs that these patients are

not all of one kind. The distinction betweenthese groups is difficult from the perspective ofthe neurosurgeon whose patients are referredafter five days or more, without a CT scan, thediagnosis being based on a lumbar puncture ofwhich there are no details. The relative propor-tions of the different categories of patients with

. a negative angiogram may differ betweencentres, which makes it even more pointless tolump all these patients under one heading. Itmay be useful therefore to remember that thereare, at present, at least four subgroups ofpatients with "angio-negative SAH".The first and most unfortunate category is

that of patients who are brought to the emer-gency room with what in fact is nothing morethan "crash migraine" or a sudden exacerba-tion of tension headache, 8 and who undergoan ill-timed and traumatic lumbar puncture byyoung and eager physicians. They are thenconfined to bed with a diagnosis of SAH,subsequently transferred to a specialised unitfor angiography, and they are finally told thatthe weak spot in one of their brain vessels hasprobably healed but that they would be wise totake things a bit easier in the future.The remaining groups of patients all have

a true SAH, but without a demonstrableaneurysm. Again, it is assumed that on the basisof the CT scan primary intracerebral haemor-rhages consistent with either the "hyper-tensive" type or with arteriovenous malforma-tions, cryptic or overt, have been ruled outbefore. About half of these patients show bloodon CT around the midbrain, unlikely to becompatible with aneurysmal rupture (fig 3a).The localised nature of the extravasated blood,the less explosive onset of the symptoms insome cases, and the excellent prognosis allmake it improbable that an occult arterialaneurysm underlies these haemorrhages."9 Thethird group of patients, making up about one

quarter ofpatients with true SAH and a normalangiogramj shows no evidence of blood in the

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Figure 3 (a) Non-aneurysmalperimesencephalichaemorrhage, withextravasated bloodpredominantly in theinterpeduncularfossa, andto a lesser extent in theambient cisterns; (b)subarachnoid haemorrhagefrom ruptured aneurysm ofthe basilar artery, withextravasated bloodpredominantly in theinterpeduncularfossa, butalso more anteriorly, in thechiasmatic cistern, theSylvian fissures, and thefrontal part of theinterhemispheric fissure.

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basal cisterns on CT, or no blood at all.29 Inthese patients the cause of bleeding is evenmore elusive than in the perimesencephalicgroup, but it may be the same. The fate of thesepatients has not been separately investigated,but the impression is that they do well.The fourth and last category are patients

with a pattern of bleeding on CT, that is typicalof ruptured aneurysm but in whom angio-graphy fails to demonstrate the expectedaneurysm. This group constitutes the lastquarter of patients with SAH and normalangiography, and about 5%/ of all patients withcisternal haemorrhage (table). It may be thatoccasional observations of local thrombosis,32vasospasm33 or rebleeding34 apply only to thesepatients, and that these harbour "occult"aneurysms, despite a normal angiogram. It isthis category of patients in which repeatedangiography seems most indicated.

Lumbar puncture after a negative CTscanExamination ofthe CSF is still important ifCTscanning provides no evidence of subarachnoid

100patients withisubarachnoid

haemorrhage

Aneurysm Other(80) aneurysm (72) Blood also in

anterior cisternsL Basilar (7)

aneurysm (8)-(1)

Blood mainily in 1 in 6

interpedu ncu larcistern

(5)Peri -

mesencephalic -

(10) _I-Blood elsewhere

-No aneurysm Other (10) around midbrain

(20) (5)

Figure 4 The chance of a ruptured aneurysm in patients with an isolated clot in theinterpeduncular cistern on CT is 1 in 6.

or other intracranial haemorrhage. Yet, if thepatient is seen soon after the headache, we wishto emphasise again that it is vital to defer lumbarpuncture to at least 12 hours after the onset ofsymptoms and that xanthochromia should beexamined not with the naked eye but withspectrophotometry. If LP is carried out tooearly, xanthochromia may not have had enoughtime to develop and it is then impossible todistinguish between a traumatic lumbar punc-ture and a genuine SAH. Blood artificiallyintroduced into the CSF will later lead to theappearance of pigments, and repeated CSFstudies can never solve the problem that hasbeen created by an LP that has been performedtoo soon.CSF examination in the diagnosis of SAH is

also important when the patient presents lateafter a suspected SAH. The 90% probability3 16ofdetecting blood in the basal cisterns on CT inthe first two days after an SAH decreasesrapidly thereafter. In contrast, all patients witha true SAH have CSF xanthochromia between12 hours and two weeks after the bleeding.'4 15Xanthochromia is still present in over 700,, ofpatients after three weeks, and even after fourweeks this proportion is still over 40%." Thesefindings contrast with another study35 wherexanthochromia was investigated with the nakedeye, which explains the high proportion ofpatients with SAH who had no xanthochromia.Could an SAH have occurred in patients

with symptoms suspected of SAH who haveblood-stained CSF but no xanthochromia?Although one study suggested that this mayoccur,35 this is extremely unlikely. In a centrewith approximately 80 patients with a provenSAH admitted each year, only 12 patients in asix year period had bloodstained CSF but noxanthochromia. In three of these 12 patientsangiography was performed; all three werenegative. All 12 patients survived withoutdisability and were not admitted again for an

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SAH during a mean follow up period of fouryears.'5 Again, the most probable explanationfor bloodstained CSF without xanthochromiain patients suspected of SAH is that thesepatients had a non-haemorrhagic "thunderclapheadache" and a traumatic LP.

It has been suggested that angiographyshould be carried out in patients with a suspec-

ted SAH but with bloodless CT or LP. Thissuggestion is based on two reports of singlepatients suspected of SAH, who had a normalCT and normal CSF but in whom subsequentangiography showed an aneurysm with vaso-

spasm.36 37

In contrast, a study of 71 patients withsudden, severe and unusual headache but withnormal CT and CSF showed that none of thesepatients had complications related to SAH andnone later had a documented SAH, during a

mean follow up period of 3-3 years.6 It is likelythat these patients have had benign "thunder-clap headaches", without bleeding. In bothreported cases with aneurysms, vasospasm dn

the angiogram was the feature believed to havea causal relation with the headache. We thinkthat migraine is a more probable explanationfor both the headache and the vasospasm.38 Asmall proportion of adults harbour asympto-matic aneurysms,39 and indiscriminate angio-graphy is bound to uncover some of these. Weagree that angiography should be done inpatients without blood on CT and even withoutCSF xanthochromia if these patients presentafter more than two weeks of the suspectedbleeding, since not only the blood on CT butalso xanthochromia of the CSF may havedisappeared by that time.'5

The diagnosis of rebleedingIf a patient with a recently ruptured aneurysmcomplains of a sudden increase ofheadache andthen abruptly becomes deeply unconscious,with wide, non-reacting pupils and apnoea,there is no diagnostic problem. However, othercomplications may mimick rebleeding.YDeterioration of consciousness and focalneurological signs may have various causes,particularly delayed cerebral ischaemia.Furthermore, the clinical picture is oftenclouded by the previous haemorrhage. Coma-tose patients do not report an increase ofheadache, and "increased neck stiffness" isoften equivocal. Finally, close observation ofthe patient around the clock for several weeksis not always practicable, with the result thatthe onset of any deterioration is not alwaysdocumented. Even if a sudden loss of con-sciousness (within minutes) is witnessed in a

patient with SAH, only two out of three turnout to have a rebleed on CT. If the fatal casesare excluded an even larger proportion ofabrupt episodes, nearly 50%, was not causedby rebleeding.4l Other causes of acute

deterioration were epilepsy, ventricularfibrillation (in only one of 62 episodes ofdeterioration) and, surprisingly, cerebralischaemia. Cerebral ischaemia after SAHusually presents with a gradual onset ofdeterioration. In contrast three patients in this

series of 62 episodes mimicking a rebleed had asudden impairment of consciousness, followedby a period of a fe hours in which there was nochange, and then had further gradual deter-ioration while evidence of infarction developedon CT.4' Therefore, rebleeding cannot be diag-nosed on purely clinical grounds. Theseproblems used to be often dismissed with thestatement that rebleeding "was confirmed bylumbar puncture or autopsy".The diagnosis of rebleeding by analysis of

CSF samples is, in fact, extremely difficult.Just as the diagnosis of a first haemorrhage byCSF analysis requires the demonstration ofxanthochromia, the diagnosis of rebleedingrequires the demonstration of "fresh" pig-ments. This raises the question of whetherblood pigments appear in and disappear fromthe CSF in a predictable fashion. Oxyhaemo-globin may be detected in the CSF a few hoursafter the bleed.'3 In the early study by Barrowset al it remained the predominant pigment onlyfor the first few days, after which it wasconverted to bilirubin, the iron-free derivativeof haemoglobin.'3 This conversion does nottake place in test tubes, as it is dependent uponthe enzyme haem oxygenase, which is presentin macrophages, the arachnoid membrane, andthe choroid plexus.42 In a later study, however,the relative concentration of oxyhaemoglobinwas found to increase spontaneously after aninitial decrease, and oxyhaemoglobin couldstill be the predominant pigment as late asthree weeks after the initial haemorrhage.43 Thesame fluctuating pattern was observed whenthe haemoglobin concentration was seriallymeasured.43 Therefore, measurement ofneither the proportion of oxyhaemoglobin northe haemoglobin concentration can help in thediagnosis of rebleeding. It has also been sug-gested that the total amount of pigments fromred cell lysis, the xanthochromic index,decreases after the first few days following thehaemorrhage.44 Rebleeding would becomeapparent by the interruption of this normalresolution pattern. However, the xantho-chromic index may continue to rise up to thesixteenth day after SAH.43 The marked dif-ferences in the velocity of pigment clearancefrom the CSF have been attributed to advancedage, diabetes, and atherosclerosis.45 Since mostrebleeds occur within this period' a suspectedrebleed cannot be confirmed merely by demon-strating an increase in xanthochromia.These findings make the often reported

statement that rebleeding was confirmed by LPbarely tenable. If rebleeding is suspected andLP is repeated, the demonstration of blood-stained CSF does not prove rebleeding, as theCSF may remain blood-stained for as long asfour weeks after the initial bleed.'2 The blood-staining may also have resulted from a trau-matic tap, and the distinction between atraumatic tap and recurrent bleeding is impos-sible to make since the CSF supernatant wasalready xanthochromic before the suspectedrebleed. In summary, examination of the CSFcan only be of help in the diagnosis of rebleed-ing if two earlier LPs had demonstrated adecrease of the xanthochromic index, which is

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The diagnosis of subarachnoid haemorrhage 371

then followed by an increase.43 It is clear that inpractice this method can seldom be applied.Apart from the unpredictable clearance of

pigments the diagnosis of rebleeding by CSFanalysis is also difficult because LP cannotalways be performed after a rebleed. Since"fresh" xanthochromia needs time to develop,the LP has to be postponed to at least 12 hoursafter the rebleed. Meanwhile the patient mayhave died. In addition, the risk of LP inpatients with an unsuspected haematoma maybe even greater than after a first bleed. In aconsecutive series of 17 patients with CTevidence of rebleeding, it was possible in onlysix patients to carry out an LP and compare theresults ofspectrophotometry with two previoussamples (the diagnosis was confirmed in five).43In short, the diagnosis of rebleeding by LP ishardly possible.

Necropsy, if feasible, does not settle thematter either. The pathologist can confidentlydiagnose rebleeding only if the interval be-tween the first haemorrhage and rebleedingwas not too short, and that between rebleedingand death was not too long.A' The presentaccepted standard in the diagnosis of rebleed-ing consists of the demonstration of a freshhaemorrhage on CT scanning or at necropsy,not previously demonstrated on CT scan. Suchcomparisons are quite sensitive, as even threeor more successive haemorrhages can be relia-bly distinguished.4' Nevertheless, earlyrebleeds cannot be diagnosed if these occurbefore the admission CT scan.'Conclusions1 Lumbar puncture after SAH may pre-

cipitate brain shift and herniation from anunsuspected haematoma, even in patientswho are fully conscious.

2 Subarachnoid haemorrhage can be reliablydiagnosed by analysis of the CSF only afterexamination of the supernatant fluid with aspectrophotometer. This implies that lum-bar puncture should be postponed until atleast 12 hours after the onset of symptoms.If lumbar puncture is performed earlier, atraumatic tap may unnecessarily stigmatisepatients with benign forms of "thunderclapheadache".

3 Computed tomography (CT) scanning isa safe and sensitive method for demon-strating subarachnoid blood, but shouldpreferably be performed within threedays. Important additional informationprovided by CT is: firstly, the demonstra-tion of non-aneurysmal sources of haemor-rhage ("hypertensive" haemorrhages,arteriovenous malformations, cryptichaemorrhages around the midbrain);secondly, the demonstration of early com-plications requiring urgent treatment;thirdly, evidence about the probable site ofruptured aneurysms, and fourthly, estab-lishment of a baseline for future changes.

4 Patients with negative angiograms are nota single category. This group consists ofpatients without SAH but with a traumaticlumbar puncture, patients with varioustypes of non-aneurysmal subarachnoid

haemorrhage, and finally a few patientswith "occult" aneurysms.

5 Lumbar puncture is indicated in SAH onlyif CT scanning is negative. If LP is carriedout between 12 hours and two weeks afterthe haemorrhage, xanthochromia of theCSF can be demonstrated in all patientswith SAH, provided xanthochromia isinvestigated by spectrophotometry. Evenafter three weeks xanthochromia is stillpresent in over 70%0 of patients, and afterfour weeks in over 40%.

6 Rebleeding is the cause of acute deteriora-tion in only two out of three cases withsudden loss of consciousness; the diagnosiscannot be confirmed by CSF analysis,except under exceptional circumstances.Necropsy is also fallible in this respect.Serial CT scanning is mandatory for aconfident diagnosis of rebleeding.

We received helpful comments from Dr E FM Wijdicksand D Hasan and we are grateful to Mrs Betty Mast andMrs Ellen Budelman for secretarial assistance.

1 Van Gijn J, Van Dongen KJ. Computed tomography in thediagnosis of subarachnoid haemorrhage and rupturedaneurysms. Clin Neurol Neurosurg 1980;82:11-24.2 Pasqualin A, Bazzan A, Cavazzani P, Scienza R, Licata C,Da Pian R. Intracranial hematomas following aneurysmalrupture: experience with 309 cases. Surgical Neurology1986;25:6-17.

3 Van Gijn J, Van Dongen KJ. The time course ofaneurysmalhaemorrhage on computed tomograms. Neuroradiol 1982;23:153-6.

4 Hillman J. Should computed tomography scanning replacelumbar puncture in the diagnostic process in suspectedsubarachnoid haemorrhage? Surg Neurol 1986;26:547-50.5 Duffy GP. Lumbar puncture in spontaneous subarachnoidhaemorrhage. Br Med J 1982;285:1 163-4.

6 Wijdicks EFM, Kerkhoff H, Van Gijn J. Long-term followup of 71 patients with thunderclap headache mimickingsubarachnoid haemorrhage. Lancet 1988;ii:68-9.

7 Salloum A, Lebel M, Reiher J. Acces cephalalgiquessimulant une hemorrhagic meningee. Rev Neurol 1977;133:131-8.8 Pearce JMS, Pearce SHS. Benign paroxysmal cranial

neuralgia or cephalgia fugax. Br Med J 1986;292:1015.9 Buruma OJS, Janson HLF, Den Bergh FAJTM, BotsGTHAM. Blood-stained cerebrospinal fluid: traumaticpuncture or haemorrhage? J Neurol Neurosurg Psychiatry1981;44:144-7.

10 Matthews WF, Frommeyer WB. The in vitro behaviourof erythrocytes in human cerebrospinal fluid. J Lab ClinMed 1955;45:508-15.

11 Soderstrom CE. Diagnostic significance of CSF spectro-photometry and computer tomography in cerebrovasculardisease. A comparative study in 231 cases. Stroke 1977;5:606-12.

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