The Diagnostic Pitfalls of Subarachnoid Hemorrhage from Intracranial Aneurysms by iasiatube


									Refer to: DeLong WB: The diagnostic pitfalls of subarachnold
          hemorrhage from intracranial aneurysms. West J Med
          123:92-100, Aug 1975

The Diagnostic Pitfalls of
Subarachnoid Hemorrhage from
Intracranial Aneurysms
W. BRADFORD DeLONG, MD, San Francisco

The subtle manner in which subarachnoid hemorrhage frequently presents may
delay appropriate treatment. The patient may deteriorate and die from aneu-
rysmal rebleeding or from cerebral ischemia associated with vasospasm be-
fore the true nature of the disease is recognized. Five patients are described
in whom subarachnoid hemorrhage was initially not recognized. Pitfalls in di-
agnosis are discussed, and an outline is presented for the evaluation of patients
suspected of harboring ruptured intracranial aneurysms.

THE OUTLOOK for patients with ruptured intra-                       Slosberg champions an aggressive nonsurgical
cranial aneurysms is improving. Yasargil, using                  hypotensive regimen in the treatment of intra-
microsurgical techniques, has achieved the re-                   cranial aneurysms.4 Though many neurosurgeons
markably low operative mortality of 1.9 percent                  are skeptical of the safety of Slosberg's approach,
in the 373 patients he operated upon from January                his work has certainly emphasized the importance
1970 through July 1974.1 The use of antifibrino-                 of careful monitoring of blood pressure and con-
lytic agents is being investigated.2 3 These agents              trol of hypertension in the acute and chronic
inhibit clot lysis, and theoretically encourage the              management of the patient who harbors an intra-
formation and preservation of a firm blood clot                  cranial aneurysm.
within and around a ruptured aneurysm, thus re-                     Stereotactic methods under development allow
ducing the risk of rebleeding. This may prove to                 the obliteration of aneurysms without open crani-
be a valuable form of therapy, used either alone                 otomy,5'6 and Serbinenko has been successful in
or as an adjunct to surgical obliteration of the                 catheterizing specific intracranial arteries selec-
aneurysm.                                                        tively.7 Refinement of his methods may make pos-
  From the Saint Francis Memorial Hospital, San Francisco, and   sible the obliteration of aneurysms with little more
the Department of Neurosurgery, University of California, San
                                                                 risk than that of cerebral angiography.
  Submitted, revised, March 21, 1975.                               As the treatment of ruptured intracranial aneu-
  Reprint requests to: W. Bradford DeLong, MD, 4141 Geary
Boulevard, Suite 425, San Francisco, CA 94118.                   rysms improves, it becomes more and more im-

      92      AUGUST 1975 * 123 * 2
                                           SUBARACHNOID HEMORRHAGE

portant to institute appropriate therapy as soon as       of the headache. In a hospital emergency room, a
possible, but it is surprising how often subarach-        history of migraine headaches was given, though
noid hemorrhage is misdiagnosed.8 Inappropriate           there had been no significant headaches during the
measures which may actually harm the patient are          five years preceding the present illness. There was
instituted, and appropriate measures are inad-            no history of hypertension. The patient was neuro-
vertently withheld. It is relatively easy to recog-       logically normal. It is not known if there was
nize subarachnoid hemorrhage in a young or               nuchal rigidity. The patient was told that blood
middle-aged patient presenting with a history of         pressure was elevated, and a diagnosis of hyper-
sudden headache followed by stiff neck, lethargy,        tensive headache was made. Consideration was
hemiparesis or seizures. However, subarachnoid           also given to a diagnosis of acute gastroenteritis
hemorrhage frequently presents in a more subtle          secondary to the ingestion of contaminated shell-
form. It is exceedingly important that these subtle      fish. Two injections (presumably of antihyper-
variations be recognized and therapy instituted          tensive medication) were given and the patient
before the patient deteriorates from rebleeding or       was sent home with an antiemetic. The symptoms
cerebral ischemia associated with vasospasm.             persisted and four days later an internist was con-
   This author has seen a number of patients with        sulted and he admitted the patient to hospital. At
subarachnoid hemorrhage and in whom clinical             that time, there was nuchal rigidity and the patient
features were at first confusing. The following pa-      was somewhat lethargic but oriented. Deep tendon
tients are examples. They were all first seen by         reflexes were hyperactive on the left. Blood pres-
well trained, experienced, conscientious physi-          sure varied between 140/80 and 170/90 mm of
cians. The diagnostic pitfalls these doctors en-         mercury.
countered illustrate that in order to avoid misdiag-        On lumbar puncture, bloody cerebrospinal fluid
nosing subarachnoid hemorrhage, a physician's            was found with a supernatant that was notably
index of suspicion must frequently be very high.         xanthochromic. On transfemoral catheter cerebral
                                                         angiography, a right internal carotid artery aneu-
Reports of Cases                                         rysm was noted at the origin of the posterior com-
   CASE 1. A 50-year-old woman reported that             municating artery (Figure 1, left). There also was
an "exploding" headache had suddenly developed           a small (3 mm) aneurysm on the trunk of the
one evening after she ate a lobster dinner. The pa-      left middle cerebral artery (Figure 1, right). The
tient induced vomiting to relieve severe nausea          patient at first declined surgical operation, but
which developed immediately following the onset          later consented, and the right internal carotid




                                    V-7                                                        gP1

                                                                                     I    At

Figure 1.--(Case 1) In a 50-year-old woman, a right posterior communicating artery aneurysm (arrow, left) which
had ruptured was noted on angiography. This lesion was successfully obliterated, but an aneurysm of the left
middle cerebral artery (arrow, right) remains.

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                                     SUBARACHNOID HEMORRHAGE

artery aneurysm was obliterated by an intracranial     the result of the head trauma. The patient was
microsurgical approach 11 days after the suba-         neurologically normal. It is not known whether or
rachnoid hemorrhage.                                   not nuchal rigidity was present at that time. The
   The patient recovered without neurological          patient was observed in the emergency room for
deficit and returned to work. Over the four years      several hours, then released. However, the symp-
since the procedure, the patient has continued to      toms persisted, and an internist was seen two days
do well, though antihypertensive medication has        later. The patient was admitted to hospital, at
been required for persistently elevated blood          which time the blood pressure was 120/60 mm
pressure. A mild seizure disorder may be present       of mercury. The orbital ecchymosis was again
and diphenylhydantoin is being taken. So far, the      noted. Results of funduscopic and neurological
patient has declined the recommendation that           examinations were normal except for a suggestion
repeat angiography be done to rule out progressive     of impaired graphesthesia in the left upper ex-
enlargement of the left middle cerebral artery         tremity. Nuchal rigidity was present.
aneurysm.                                                 Delayed venous drainage of the right cerebral
                                                       hemisphere was noted on brain scan, though find-
Comment                                                ings on blood brain barrier scintiphotos were
   When this patient presented to a hospital emer-     normal. A lumbar puncture produced bloody
gency room immediately following subarachnoid          cerebrospinal fluid with a pressure of 270 mm.
hemorrhage, a diagnosis of hypertensive headache       The supernatant was moderately xanthochromic.
was made because the blood pressure was ele-           On transfemoral cerebral angiography, an aneu-
vated. However, elevation of the blood pressure        rysm of the right middle cerebral artery was seen.
is common following subarachnoid hemorrhage.           Craniotomy was carried out four days after the
Even if a patient has a history of hypertension, the   subarachnoid hemorrhage and the aneurysm was
development of headache cannot be ascribed             obliterated microsurgically. The patient did well
with certainty to the hypertension alone, and the      postoperatively, though a minor seizure disorder
physician must keep in mind the increased inci-        subsequently developed and administration of
dence of subarachnoid hemorrhage in hypertensive       anticonvulsants was required.
    It is not uncommon for subarachnoid hemor-         Comment
rhage to be misdiagnosed as some sort of ab-              The subarachnoid hemorrhage caused the pa-
dominal disorder (see also Cases 3 and 5). The         tient to lose consciousness and fall. The case was
nausea and vomiting which frequently accompany         originally misinterpreted as one of straightforward
subarachnoid hemorrhage may mask the impor-            cranial trauma. Since cranial trauma is a common
tance of the headache, and the patient may have        cause of secondary subarachnoid hemorrhage, it
abdominal tenderness because of the persistent         may at times be difficult to distinguish between
vomiting.                                              subarachnoid hemorrhage due to a ruptured aneu-
    This patient is at considerable risk from the      rysm and that due to trauma. A careful history
remaining left middle cerebral artery aneurysm         will help, but angiography may be necessary to
and the hypertension increases this risk further.      investigate the possibility that a ruptured aneu-
This author would recommend prophylactic micro-        rysm led to the event responsible for the cranial
surgical obliteration of the aneurysm if progressive   trauma.
enlargement was seen on serial angiography.               CASE 3. A 55-year-old man was awakened
    CASE 2. A 41-year-old woman fell at home,          from sleep one night by headache and severe neck
 striking her head on a television set. Further his-   pain. When admitted to hospital shortly thereafter,
 tory, obtained subsequently, indicated that while     the patient was nauseated, vomited and had com-
 watching television a severe headache developed.      plaint of anterior chest pain and epigastric dis-
 The patient arose from her chair, lost conscious-     tress. A diagnosis of anterior myocardial infarc-
 ness and then fell. This sequence of events was       tion was considered. Peptic ulcer disease 12 years
 not recognized when the patient was seen in a         before the present illness had required gastric
 hospital emergency room the morning following         surgical operation, and recrudescence of this
 the event. Since ecchymosis was present around        problem was also considered as a diagnostic pos-
 the left eye, it was assumed that the headache was    sibility. Morphine was given and the patient soon
      94    AUGUST 1975 * 123 * 2
                                        SUBARACHNOID HEMORRHAGE

became lethargic to a degree out of proportion             hemorrhages in the right fundus as well. Blood
to the dose administered. Pronounced confusion             pressure was 110/70 mm of mercury, and nuchal
was also noted, and the possibility of excessive           rigidity was present. The patient was lethargic,
self-medication at home was considered, as was             but otherwise neurologically intact.
the possibility of a psychotic reaction of some               On lumbar puncture five days after the recur-
sort. Blood pressure was 120/60 mm of mercury.             rence of the headache, xanthochromic cerebro-
Findings on funduscopic and neurologic examina-            spinal fluid was noted. A large anterior communi-
tions were normal except for the lethargy and              cating artery aneurysm (Figure 2, right) was seen
confusion.                                                 on cerebral angiography. The patient initially re-
   It is not known if objective nuchal rigidity was        fused surgical operation, and 21 days following
present at the time of admission to hospital, but          the recurrence of headache, still another sudden
three days later an orthopedic consultant, called          headache developed with nuchal rigidity. Lumbar
because of the patient's continuing neck pain,             puncture was not felt to be necessary. The patient
noted a stiff neck. A diagnosis of acute cervical          agreed to surgical operation, and five days later
strain was made, and the patient was placed in             craniotomy was carried out and the aneurysm
cervical traction.                                         obliterated with microsurgical techniques. A low-
   Five days after admission neurological consul-          grade wound infection from the Providence group
tation was obtained and bloody cerebrospinal               of Gram-negative organisms developed, but this
fluid with xanthochromic supernatant was found             responded well to gentamicin. The patient did well
on lumbar puncture. Transfemoral cerebral angi-            and returned to work. Vision in the left eye subse-
ography was carried out with the left vertebral            quently improved.
and both carotid arteries being injected. The
source of the subarachnoid hemorrhage could not            Comment
be found, though in retrospect mild vasospasm                 The presentation of the initial subarachnoid
was present in the left internal carotid artery            hemorrhage in this patient was confusing. Several
(Figure 2, left). The lethargy and confusion re-           diagnoses were initially considered, including
solved and the patient was discharged from the             anterior myocardial infarction, recrudescence of
hospital 11 days following the subarachnoid hem-           peptic ulcer disease, drug overdose, acute psy-
orrhage.                                                   chotic reaction and cervical strain.
   One month after the initial hemorrhage, there              The large anterior communicating artery aneu-
was recurrence of severe headache and effective            rysm did not fill at the time of initial cerebral
vision in the left eye was lost. Upon admission            angiography, though in retrospect there was in-
to hospital a large preretinal hemorrhage covering         ternal carotid arterial vasospasm which was a
the left macula was noted. There were preretinal           clue to the presence of the lesion. The aneurysm


                                                                                       t..:    14,   v



Figure 2.-(Case 3) In a 55-year-old man, a left cerebral angiogram (above,                    left) showed no aneurysm, though
there was vasospasm of the left internal carotid artery (arrow). Left cerebral                angiogram one month later (above,
right) showed a large anterior communicating artery aneurysm (arrow).

                                                            THE WESTERN JOURNAL OF MEDICINE                            95
                                        SUBARACHNOID HEMORRHAGE

filled well on a subsequent angiogram. This case         paresis was present. The blood pressure then was
well demonstrates the point that cerebral angiog-        100/60 mm of mercury. On funduscopic exami-
raphy should be repeated if the initial study does       nation, preretinal hemorrhages in the left eye
not show the source of an unexplained subarach-          were noted. Lumbar puncture was not done, since
noid hemorrhage. The possibility that the source         the diagnosis of subarachnoid hemorrhage seemed
of the hemorrhage may be occult spinal pathology         secure without it.
should be kept in mind. Intracranial subarachnoid           Two days after admission, a left infraclinoid
hemorrhage can be mimicked by hemorrhage from            carotid aneurysm (Figure 3) was noted on
a spinal cord vascular malformation, especially          transfemoral cerebral angiography. The patient
if the lesion lies in the cervical spinal cord. Intra-   became fully awake and the right hemiparesis
dural spinal tumors, particularly ependymomas,           resolved, though there was some remaining con-
can also present initially with subarachnoid hem-        fusion and''a memory deficit. Five days after ad-
orrhage. If the source of the hemorrhage cannot          mission, a left frontotemporal craniotomy was
be shown by cerebral angiography, then myelog-           carried out and the aneurysm successfully oblit-
raphy and spinal angiography should be con-              erated.
sidered.                                                    Following the craniotomy the patient was neu-
   CASE 4. In a 40-year-old woman, a stiff neck          rologically intact and mental status continued to
and'occipital headache suddenly developed while          improve until the fifth postoperative day when
she was playing tennis. An orthopedist, who was          lethargy and aphasia with hemiparesis on the right
consulted, found no neurological abnormality. It is      developed. Cerebral angiography was repeated and
not known whether or not objective nuchal rigidity       severe spasm of the internal carotid, middle cere-
was present at that time. The headache persisted         bral and anterior cerebral arteries was noted. In-
for two weeks, then subsided. One month later,           travenously administered phenylephrine was-used
again while she was playing tennis, severe head-         to increase the blood pressure. When the blood
ache developed and the patient temporarily lost          pressure dropped below 120 systolic, the patient
consciousness. Upon admission to hospital, blood         became totally unresponsive and decerebrate
pressure was 140/80 mm of mercury. The patient           posturing of all extremities developed. Gradually
was awake though confused, but shortly thereafter        tolerance to the phenylephrine developed. Lev'ar-
suddenly lost consciousness again and became             terenol was substituted, but the blood pressure
apneic. After intubation, the patient regained           become unresponsive to that medication as well.
consciousness but was combative. Right hemi-                On a third cerebral angiogram three'days after


Figure 3.-(Case 4) In a 40-year-old woman, the infraclinoid internal carotid aneurysm (arrows) was clipped
five days after the subarachnoid hemorrhage.

      96    AUGUST 1975 * 123 * 2
                                        SUBARACHNOID HEMORRHAGE

the -onset of neurological deterioration, further        proximately one, week following hemorrhage.9
increase in the spasm was noted. A left superficial      Delayed vasospasm is in some cases associated
temporal-middle cerebral artery microsurgical by-        with severe cerebral ischemia leading to infarc-
pass was done, in the hope that this procedure           tion,"3 and accounts for a number of the deaths
would increase cerebral perfusion enough to re-          resulting from subarachnoid hemorrhage. This
verse the deterioration. Immediately following the       type of vasospasm has proven resistant to direct
procedure the blood pressure was allowed to drift        treatment by any vasodilating drug now available,
toward lower levels. Decerebrate posturing was           but if the ruptured aneurysm has been obliterated
no longer present. The next morning the vasopres-        before the patient develops cerebral ischemia, then
sors were discontinued, and the systolic blood           the ischemia can in some cases be reversed by
pressure stabilized at 90. The neurological status       the use of induced hypertension.'4"15 Induced hy-
began to improve, and 72 hours after the micro-          pertension presumably increases perfusion of the
vascular procedure the patient was fully respon-         compromised cerebral tissue by taking advantage
sive, was taking oral fluids and had returning           of the fact that circulatory autoregulation is im-
function of the right arm. Neurological improve-         paired in the ischemic regions. Perfusion in these
ment continued, and at present-one year and a            areas is directly proportional to the blood pres-
half after the episode-speech is normal and there        sure. However, induced hypertension cannot be
is full use of all extremities. The patient is com-      used safely if the patient still harbors a patent
pletely independent in the activities of daily living,   aneurysm, as Ailcock and Drake have empha-
but still lacks initiative and has some deficit in       sized.'6
recent memory. As improvement continued, the                The author has successfully used a regimen of
superficial temporal arterial pulse gradually di-        induced hypertension in two other aneurysm pa-
minished, finally becoming imperceptible. On             tients severely threatened by cerebral ischemia
cerebral angiography two months after the micro-         which developed several days after craniotomy.
vascular procedure, it was noted that the micro-         In the patient reported above (Case 4), however,
vascular bypass was no longer patent. Presum-            induced hypertension alone did not reverse the
ably it closed as normal cerebral circulation            deterioration, and a microvascular shunt was
became reestablished.                                    carried out in an attempt to increase cerebral per-
                                                         fusion. It cannot be determined with certainty
                                                         whether or not the microvascular bypass contrib-
   In this patient, there almost certainly was           uted to the patient's survival and neurological
minor subarachnoid hemorrhage one month be-              improvement, but the postoperative course sug-
fore the major hemorrhagic episode-reflected by          gests that it did.
the sudden development of a stiff neck and occi-            Early diagnosis of a ruptured aneurysm and
pital headache while playing tennis. Hemorrhage          prompt obliteration of the aneurysm allow vigor-
presenting in this form is extremely subtle and          ous treatment of cerebral ischemia should it occur
confusing, but the severity and persistence of the       several days after the hemorrhage in association
headache and the absence of a specific precipitat-       with delayed vasospasm.
ing traumatic event might have been clues that the
symptoms represented more than a simple cervical            CASE 5. A 37-year-old woman awakened early
strain.                                                  one morning with a severe headache. Nausea,
   The major hemorrhage which precipitated ad-           vomiting and diarrhea followed shortly, and the
mission to hospital almost resulted in immediate         patient came to a hospital emergency room. She
death. The patient did well immediately follow-          stated that she had eaten ham the day before, and
ing the craniotomy, only to be placed at great risk      in the past had had a "reaction" to this food. A
again by the development of vasospasm associated         history of recurrent headaches was given, and the
with severe cerebral ischemia. The author feels          patient reported a recent diagnosis of hypertension.
that cerebral vasospasm in this patient represents       Findings on neurological examination were nor-
the delayed phase of vasospasm which develops            mal, including results of funduscopic examination,
in approximately two thirds of patients following        though the presence or absence of nuchal rigidity
subarachnoid hemorrhage with or without inter-           was not recorded. Blood pressure ranged from
vening craniotomy.9-'2 (See also Case 5.) In hu-         170/1 00 to 210/120 mm of mercury. Antiemetics
mans, delayed vasospasm becomes maximal ap-              and mild analgesics were given and the patient

                                                         THE WESTERN JOURNAL OF MEDICINE            97
                                         SUBARACHNOID HEMORRHAGE

was sent home with a diagnosis of acute gastro-            blood pressure are liable to cause massive hemor-
enteritis.                                                 rhage from the aneurysm.
   Four days later the patient was admitted to                Diagnosis of the subarachnoid hemorrhage at
hospital after presenting to another physician with        the time of the patient's first presentation to the
left hemiparesis and mild confusion. Blood pres-           emergency room would have provided the only
sure at that time was 160/108 mm of mercury.               chance for survival. Obliteration of the aneurysm
Results of funduscopic examination were normal             a day or two after the hemorrhage would have
and there was no nuchal rigidity.                          allowed treatment of the vasospasm when its
   On lumbar puncture, bloody cerebrospinal                effects became severe by attempting to increase
fluid with xanthochromic supernatant was noted.            cerebral perfusion either by further elevating the
By the next day, lethargy and hemiplegia with a            blood pressure with vasopressors or by carrying
tendency toward decerebrate posturing on the left          out a microsurgical vascular bypass.
were present.                                              Discussion
   Findings on cerebral angiography indicated a               Pakarinen has shown that 32 percent of patients
large right internal carotid aneurysm, along with          with ruptured intracranial aneurysms die within
severe vasospasm of the internal carotid, middle           24 hours of the major initial hemorrhage, and 35
cerebral and anterior cerebral arteries (Figure 4).        percent die within three days.'7 However, in many
At that point, the patient was not a candidate for         patients before a major hemorrhage there are
surgical operation. Large doses of dexamethasone           warning signs indicating expansion of the aneu-
were given, but the patient continued to deterio-          rysm or minor leakage from it.8,18,19 Patients can
rate and died 24 hours later.                              be protected from the high initial mortality of a
Comment                                                    major hemorrhage if these warning signs are
                                                           recognized and the aneurysm treated while the
   This patient's case represents an extremely dif-        patient is still neurologically intact.
ficult problem in the management of subarachnoid              Okawara analyzed 112 patients with ruptured
hemorrhage. Cerebral vasospasm and progressive             aneurysms and showed that in 48.2 percent there
neurological deterioration following subarachnoid          were warning signs before the major hemor-
hemorrhage in a hypertensive patient is very fre-          rhage.'8 The incidence of warning signs in patients
quently a lethal chain of events. Attempts to treat        harboring internal carotid artery aneurysms at the
the hypertension by lowering the blood pressure            origin of the posterior communicating artery was
may accentuate the cerebral ischemia. Attempts             69.2 percent; The average interval between the
to increase cerebral perfusion by elevating the            onset of warning signs indicating minor leakage
                                                           of blood into the subarachnoid space and a major
                                                           subarachnoid hemorrhage was 10.4 days.
                                                              Waga, Ohtsubo and Handa analyzed the clini-
                                                           cal histories of 192 patients with intradural intra-
                                                           cranial aneurysms.'9 In 49 percent of the 98 men
                                                           and in 69.1 percent of the 94 women there were
                                                           warning signs before a major hemorrhage. Warn-
                                                           ing signs occurred in 56.5 percent of patients with
                                                           anterior cerebral aneurysms, in 48.8 percent of
                                                           those with middle cerebral aneurysms and in 68.8
                                                           percent of those with intradural internal carotid
                                                              King and Saba found that in 106 (64 percent)
                                                           of 165 patients with ruptured berry aneurysms,
                                                           there were symptoms and signs forewarning a
Figure 4.-(Case 5) Headache, nausea and vomiting           major subarachnoid -hemorrhage, and a third of
in a 37-year-old woman was initially diagnosed as
gastroenteritis. On angiography five days after onset of   these patients had been treated for erroneously
the symptoms, a large right internal carotid artery        diagnosed illness for more than a week before
aneurysm (arrow) was seen. Severe vasospasm had            subarachnoid hemorxhage was considered as a
developed by that time and no effective therapy was
available. The patient died.                               diagnostic possibility.8
     98     AUGUST 1975 * 123 * 2
                                              SUBARACHNOID HEMORRHAGE

   In these studies, warning signs included sudden          motor nerve paralysis, resulting in various degrees
unusual headache, nausea and vomiting, transient            of pupillary dilatation, ptosis and turning of the
loss of consciousness and transient visual dis-             eye to the characteristic "down and out" position
turbances. Expansion of an unruptured posterior             of third cranial nerve palsy.
communicating artery aneurysm can cause oculo-                 The initial symptoms in Case 4, above, fall
                                                            into the category of warning signs. The initial
                                                            symptoms in the other four patients reflect what
TABLE 1.-Misinterpretation of Signs and Symptoms            this author would term major subarachnoid hem-
           in Subarachnoid Hemorrhage
                                                            orrhage. As the case reports show, the symptoms
Headache                                                    and signs of subarachnoid hemorrhage can be
  Migraine                                                  misinterpreted in many ways (Table 1). The
  Sinusitis                                                 headache can suggest the presence of migraine,
  Tension headache
  Hypertensive headache                                     sinusitis, tension headaches, hypertensive head-
  Subdural hematoma                                         ache (see Case 1) or subdural hematoma (see
Nuichal rigidity                                            Case 2). The precipitous nature of the headache
  Cervical strain                                           associated with subarachnoid hemorrhage is
  Ruptured cervical disc                                    usually characteristic. Migraine usually has its
                                                            onset before the age of 30 years and is not an
Nautsea anzd vomiting                                       isolated event. A single headache occurring sud-
  Acute gastroenteritis or food poisoning
  Peptic ulcer disease                                      denly in a middle-aged person is not very likely
  Acute appendicitis (with tenderness of the abdominal      migraine. If there is any question concerning the
     wall)                                                  diagnosis of migraine headache, a lumbar punc-
  Anterior myocardial infarct (with epigastric or an-
     terior thoracic discomfort)                            ture should be done to rule out subarachnoid
Conzfutsion, lethargy   or personality   change             hemorrhage.
  Drug overdose                                                The nuchal rigidity of subarachnoid hemor-
  Alcoholic intoxication                                    rhage can suggest cervical strain (see Cases 3 and
  Acute psychosis                                           4) or ruptured cervical disc. The sudden onset,
Hemiparesis or other focal neurological deficit             the absence of a specific precipitating traumatic
  Cerebral infarction from thrombosis or embolism           event and the usual association of the rigidity with
  Spontaneous intracerebral hemorrhage                      occipital or generalized headache should make
      TABLE 2.-Initial Evaluation of Suspected              the examiner suspect that he is not dealing with a
            Subarachnoid Hemorrhage                         cervical syndrome. The precipitous onset should
                                                            also differentiate the syndrome from meningitis,
History and general physical examination                    though a misdiagnosis of meningitis will at least
  Look for nuchal rigidity and elevated blood pressure.     lead to a lumbar puncture and the true nature
Neurological examination                                    of the disease process will be defined.
  Look for signs of oculomotor nerve palsy, hemiparesis        The nausea and vomiting associated with sub-
  or other focal neurological signs.
Fuinduscopic examination                                    arachnoid hemorrhage may mask the importance
  Look for retinal or preretinal hemorrhage.                of the accompanying headache, and be misinter-
X-ray studies of the skull
                                                            peted as gastroenteritis (see Cases 1, 3 and 5).
  Look for intracranial calcification, an enlarged sella    Prolonged vomiting may result in tenderness of
  turcica, thinning of the dorsum sellae, or other signs    the abdominal wall, thus leading to the diagnosis
  of an intracranial mass lesion or elevated intracranial   of an acute abdomen. If epigastric discomfort is
  pressure.                                                 prominent, occult anterior myocardial infarction
Lumbar puncture                                             may be considered (see Case 3).
   (Withhold lumbar puncture if retinal hemorrhages,           Subarachnoid hemorrhage at times leads to
  papilledema or other signs of increased intracranial
  pressure are present.)                                    lethargy, confusion or personality change misin-
  Look for blood or xanthochromia in the cerebrospinal      terpreted as drug or alcoholic intoxication or as
  fluid (CSF). A traumatic tap is distinguished by clear-   psychiatric disease (see Case 3). The absence of
   ing of blood by the third tube and by the absence of     a history of drug overdose or alcoholic indiscre-
  xanthochromia in the centrifuged CSF.
Cerebral angiography                                        tion along with the presence of a headache should
   This should be done if subarachnoid hemorrhage is        help in narrowing the differential diagnosis.
  confirmed.                                                   Subarachnoid hemorrhage may be associated
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                                          SUBARACHNOID HEMORRHAGE

with hemiparesis or other focal neurological deficit    by nothing more than bedrest and hopeful waiting
as the result of cerebral vasospasm or as the result    is becoming passe. Whether an aneurysm is
of hemorrhage from the aneurysm into the cere-          treated by microsurgical obliteration, antifibrino-
bral substance or into the subdural space. Since        lytic therapy, stereotactic obliteration, a nonsurgi-
both cerebral infarction from thrombosis or em-         cal hypotensive regimen or endovascular oblitera-
bolism and spontaneous intracerebral hemorrhage         tion by selective catheterization of the intracranial
are often associated with blood in the subarach-        arteries, therapy must be planned and instituted
noid space, angiography may at times be the only        as soon as possible-preferably before a major
way in which to rule out a ruptured intracranial        subarachnoid hemorrhage has occurred.
aneurysm as the cause of the patient's neurological        Our diagnostic goals should be prompt recogni-
compromise.                                             tion of patients in whom there are symptoms and
   A patient in whom cranial, occipital or cervical     signs which reflect impending aneurysmal rupture
pain has developed suddenly, especially if asso-        and immediate recognition of patients in whom
ciated with stiff neck, syncope, confusion, person-     major subarachnoid hemorrhage has occurred. It
ality change, hemiparesis, sensory changes, visual      appears that in a significant percentage of patients
disturbances or seizures, should have careful           these goals are not being attained because sub-
neurological and funduscopic examinations, along        arachnoid hemorrhage is often an insidious pro-
with a lumbar puncture (Table 2). The lumbar            cess and may initially masquerade in many guises.
puncture should be withheld in favor of angiog-         The physician may be lulled into a false sense of
raphy or computerized tomographic studies ("EMI"        diagnostic security until the patient deteriorates
scanning) if the patient has retinal hemorrhages,       precipitously and passes beyond therapeutic reach.
papilledema or other signs of increased intra-                                     REFERENCES
cranial pressure. In all other patients in whom            1. Yasargil MG, Fox JL: The microsurgical approach to intra-
subarachnoid hemorrhage seems a diagnostic pos-         cranial aneurysms. Surg Neurol 3:7-14, 1975
                                                          2. Mullan S: Conservative management of the recently ruptured
sibility, lumbar puncture should be done without        aneurysm. Surg Neurol 3:27-32, 1975
                                                          3. Nibbelink DW: The role of fluid restriction in treatment of
hesitation. The indications for lumbar puncture         acute subarachnoid hemorrhage following ruptured intracranial
and the techniques of the tap have been thoroughly      aneurysm (Abstract). Neurology 24:372-373, 1974
                                                          4. Slosberg PS: Treatment of ruptured intracranial aneurysms
reviewed recently.2Y The tap can be done in the         by induced hypotension. Mt Sinai J Med NY 40:82-90, 1973
                                                          5. Mullan S: Experiences with surgical thrombosis cf intra-
office or emergency room with a No. 22 spinal           cranial berry aneurysms and carotid cavernous fistulas. J Neuro-
                                                        surg 41:657-670, 1974
needle. If there is no blood in the cerebrospinal         6. Alksne JF, Rand RW: Current status of metallic thrombosis
fluid, and if there is no other evidence of a dis-      of intracranial aneurysms, In Krayenbiihl H, Maspes PE, Sweet
                                                        WH (Eds): Progr Neurol Surg, Vol 3, Basel, Karge; and Chicago,
order requiring admission to hospital, the patient      Year Book, 1969, pp 212-229
                                                          7. Serbinenko FA: Balloon catheterization and occlusion of
can be released after an hour or two of rest and        major cerebral vessels. J Neurosurg 41:125-145, 1974
                                                          8. King RB, Saba Ml: Forewarnings of major subarachnoid
observation.                                            hemorrhage due to congenital berry aneurysm. NY State J Med
                                                        74:638-639, 1974
   If blood is present in the cerebrospinal fluid, a      9. Bergvall U, Steiner L, Forster DMC: Early pattern of
traumatic tap is usually distinguished by clearing      cerebral circulatory disturbances following subarachnoid hemcr-
                                                        rhage. Neuroradiology 5:24-32, 1973
of the fluid by the time the third tube is collected.      10. Brawley BW, Strandness Jr DE, Kelly WA: The biphasic
                                                        response of cerebral vasospasm in experimental subarachnoid
The supernatant of the centrifuged specimen will        hemorrhage. J Neurosurg 28:1-8, 1968
                                                           11. Marshall Jr WH: Delayed arterial spasm following sub-
usually, but not always, be xanthochromic if true       arachnoid hemorrhage. Radiology 106:325-327, 1973
subarachnoid hemorrhage is present.                        12. Wilkins RH, Alexander JA, Odom GL: Intracranial arterial
                                                        spasm: A clinical analysis. J Neurosurg 29:121-134, 1968
   If subarachnoid hemorrhage is confirmed, then           13. Wilkins RH, Wilkinson RH, Odom GL: Abncrmal brain
                                                        scans in patients with cerebral arterial spasm. J Neurosurg 36:
cerebral angiography should be carried out              133-140, 1972
                                                           14. Farhat SM, Sclmeider RC: Observations on the effect of
promptly, preferably within 24 hours of the pa-         systemic blood pressure on, intracranial circulation in patients
                                                        with cerebrovascular insufficiency. J Neurosurg 27:441-445, 1967
tient's admission, so that operative intervention         15. Wise G, Sutter R, Burkholder J: The treatment of brain
or other appropriate therapy can be planned and         ischemia with vasopressor drugs. Stroke 3:135-140, 1972
                                                          16. Allcock JM, Drake CG: Ruptured intracranial aneurysms-
instituted at the optimal time. If the patient is       the role of arterial spasm. J Neurosurg 22:21-29, 1965
comatose or deteriorating, then angiography                17. Pakarinen S: Incidence, aetiology, and prognosis of primary
                                                        subarachnoid hemorrhage. Acta Neurol Scand 43 (Suppl 29) :1-
should be done as an emergency procedure to rule        127, 1967
                                                          18. Okawara SH: Warning signs prior to rupture of an intra-
out an intracerebral or subdural hematoma pos-          cranial aneurysm. J Neurosurg 38:575-580, 1973
                                                           19. Waga S, Ohtsubo K, Handa H: Warning signs in intra-
sibly amenable to immediate evacuation.                 cranial aneuryms. Surg Neurol 3:15-20, 1975
                                                          20. Petito F, Plum F: The lumbar puncture. N Engl J Med
   Treatment of ruptured intracranial aneurysms         290:225-227, 1974

   100      AUGUST 1975     *   123   *   2

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