Subdural hematoma after lumbar puncture: two case reports and review of the literature

Subdural hematoma after lumbar puncture: two case reports and review of the literature

Subdural hematoma after lumbar puncture: two case reports and review of the literature P.E. Vos* * * * *, W.A. de Boer* *, J.A.L. Wurzer* * *, and J. ...

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Subdural hematoma after lumbar puncture: two case reports and review of the literature P.E. Vos* * * * *, W.A. de Boer* *, J.A.L. Wurzer* * *, and J. van Gijn* * * *

Introduction Summary

Post lumbar puncture headache (PLPH) is a common problem (30-40%) following lumbar puncture (LP), myelography or spinal anesthesia. PLPH may be accompanied by several other symptoms: nausea and vomiting, stiff neck, vertigo, tinnitus or even hearing loss, diplopia, and blurred visior&*. These symptoms are caused by cerebrospinal fluid (CSF) hypotension and characteristically are posture dependent. They arise when the patient is upright and immediately disappear when the patient lies down. Intracranial subdural hematoma (SDH) is a rare complication of lumbar puncture (see table 1 & 2), but it should be considered in all patients who complain of persistent headache after lumbar puncture. SDH has been described after inadvertent dural puncture in epidural anesthesia, after lumbar myelography, and after spinal anesthesia. The following two case reports describe the occurrence of SDH after cervical myelography, via the lumbar route and after lumbar puncture performed for laboratory analysis only. Case reports

Case l- A 54-year old man underwent myelography * ** *** ****

for evaluation

of a recurrent

cervical cervi-

Two cases of intracranial subdural hematoma following lumbar puncture are presented. A review of all previously reported cases shows that subdural hematoma after lumbar puncture is a rare but serious complication. The pathogenesis of subdural hematoma after lumbar puncture is probably related to that of post lumbar puncture headache. Application of an epidural blood patch may therefore be a safe way not only to treat typical post lumbar puncture headache but also to prevent subdural hematoma after lumbar puncture. Key words: myelography; subdural hematoma; epidural blood patch; lumbar puncture; spinal anesthesia.

cal root syndrome.

Four years before he had been operated upon for removal of a C5-C6 intervertebral prolapse on the left side. Fifteen ml Iopamiro@ 300 fluid was injected through a single lumbar puncture at the L4-L5 level. A 22 Gauge needle was used. During myelography the patient was tilted in prone, head down posi-

tion. Apart from a small ventral indentation of the contrast column no abnormalities were seen. After the puncture he complained of postural headache for several days, which was treated with bed rest. The symptoms gradually disap-

Rudolf Magnus Institute for Pharmacology, Utrecht, The Netherlands. Department of Internal Medicine, Academic Medical Centre, Amsterdam, The Netherlands Department of Neurosurgery, Westeinde Hospital, Den Haag, The Netherlands. University Department of Neurology, Utrecht, The Netherlands.

Address for correspondence and reprint requests: Pieter E. Vos, University Department of Neurology, 3584 CX Utrecht, The Netherlands

Heidelberglaan

100,

Accepted 12.10.90 Clin Nemo1 Neurosurg 1991. Vol. 93-2

127

peared and he was discharged 3 days later. Twenty days after cervical myelography the patient still suffered from headache, an EEG was made which was normal. Thirty-five days after cervical myelography he was readmitted to another hospital because of intractable headaches. There was no history of trauma or of alcohol abuse. The headache was initially attributed to persistent leakage of CSF through the puncture hole, and he was treated with bed rest. Because the symptoms persisted, he was treated with an epidural blood patch (EBP) 38 days after cervical myelography. Despite this treatment, no improvement occurred. From the 44th day onwards, the headache was located unilaterally, on the left side, instead of bifrontally, and it did not disappear on lying down. He became more severely ill, with dizziness, nausea and vomiting. There were no focal neurological signs. Haematologic screening and coagulation tests were normal. The EEG showed slow activity over the left hemisphere. CT-scanning finally showed a left-sided isodense subdural hematoma. On the 46th day after cervical myelography, burr hole exploration was carried out and a chronic subdural hematoma was evacuated. Following surgery the patient made a gradual and complete recovery and he was discharged 10 days postoperatively.

ing showed no biochemical or coagulation disorders. CT scanning showed a border zone infarct between the territories of the left middle and posterior cerebra1 arteries. A diagnostic lumbar puncture, one day after CT-scanning. gave a normal pressure, and analysis of the cerebrospinal fluid showed no abnormalities. An ECG showed evidence of an apical infarct which was not present on an ECG performed several months before. It was assumed that the cerebral infarct had developed as a result of hypotension after myocardial infarction. Five hours after the LP the patient started complaining of throbbing headache with a postural character. This headache persisted on the first and second day after LP. On the second day he suddenly became more unwell, with increased headache, nausea and vomiting. A right-sided central facial palsy and a right hemiplegia were diagnosed. A CT scan showed a subdural hematoma over the left hemisphere. Burr hole exploration was performed, and the SDH was evacuated. Postoperatively the signs and symptoms disappeared within two months. Eight months after operation, neurological examination showed only the minimal left sided weakness that existed before the LP.

Case 2- A 61-year old man was admitted to the hospital because of memory disorders and loss of dexterity. He had been well until 3 months earlier when he suffered one evening from dyspnoea, sweating and chest pain. From that time on he had difficulties in writing and in remembering phone numbers. He experienced no weakness but was yet unable to open and close doors and to manipulate faucets. His past medical history included essential hypertension for which he was treated with labetalol and dipyridamol. General physical examination was normal. On neurological examination, speech was fluent and speech comprehension was normal. On reading, however, he showed perseveration, and on writing there were disphasic errors of spelling. There was also constructional apraxia and a disturbance of visual orientation, but no finger agnosia. In the limbs, a minima1 left-sided hemiparesis was found. Haematological screen-

After LP the spinal needle leaves a small hole in the dura mater, through which CSF can leak to the epidural space. If leakage of CSF exceeds the production of CSF, the CSF volume will decrease. PLPH is caused by CSF hypotension. The volume depletion is partially compensated by (painful) venous dilatation and by an increase of brain vo1ume2. The brain, normally kept afloat by the CSF, will be displaced downwards when the patient assumes a vertical position, with stretching of the pain-sensitive veins and meninges. This explains the typical postural character of PLPH’x*,“. The same pathogenesis as that for PLPH can be invoked to explain the occurrence of SDH after LP. Congestion of bridging veins, in combination with traction by downward displacement of the brain, may cause tearing of these veins in the subdural space, and unilateral or bilateral SDH will develop. Other causes of SDH associated with reduced counter pressure

128

Discussion

Table

1. Review

Study

of cases of SDH following

lumbar

puncture

for anesthetic

Age --

Procedure

Sex

Indication

0

spinal anesthesia

Gerlach

purposes

Diagnosis

PLPH

Therapy

Outcome

? 10d

RSDH

+

none

CR

Interval

Welch

69/M 421F

spinal anesthesia spinal anesthesia

22 7w ? 5m

Bil. SDH LSDH

+ f

surgery surgery

: CR

Arseni

2.7130 46/49 58162 M 42/F

spinal anesthesia

?

LSDH

?

surgery

CR

IF

accidental LP Iabour accidental LP labour accidental LP labour spinal anesthesia rectal abcess accidental LP labour spinal anesthesia

Ganz McDonald Jack

29/F

Pavlin

23iF 37/M

Edelman

22lF

Reinhold

36/F

Reynolds

22/F

Mantia

27iF

l-4m

ref

PI

(4) Bil. SDH accidental

LP

?

llw

(2) SDH

+

surgery

CR

?

?

RSDH

+

surgery

CR

?

28d

Bil. SDH

+

surgery

CR

18 8d

Bil. SDH

+

surgery

CR

22 6d

RSDH

+

surgery

PR

16 4od

Bil. SDH

i-

non

t

1171

18 18d

LSDH

+

surgery

CR

1231

25 35h

LSDH

-

surgery

PR

1241

26 Sd

RSDH

+

CR

1251

25 Ild

RSDH

+

?

1261

18 4w

Bil. SDH

-

conservative conservative surgery

PR

1271

22 13d

LSDH

-

surgery

-t

21 26d

LSDH

+

surgery

CR

I91

22 2Od

RSDH

+

surgery

CR

1281

24 13d

LSDH

-

surgery

CR

1291

22 21d

Bil. SDH

+

surgery

CR

I301

22 Jm

LSDH

+

surgery

CR

1311

?

3od

LSDH

+

surgery

CR

1321

?

16d

SDH

-

surgery

CR

I331

25 21d

LSDH

-

surgery

CR

1341

?

Bil. SDH

?

surgery

CR

1351

Jonsson

63/M

Personne

70/M

Kiersz

79/M

Giamundo

SO/M

Ruutiainen

69/M

Blake

67/M

Lam-My

3.5/M

accidental LP labour spinal anesthesia labour spinal anesthesia urological operation accidental LP labour spinal anesthesia inguinal hernio~haphy spinal anesthesia cesarean section spinal anesthesia inguinal hemiorrhaphy spinal anesthesia inguinal hemiorrhaphy spinal anesthesia hydrocele spinal anesthesia spermatocele spinal anesthesia inguinal terniorrhaphy spinal anesthesia urological operation spinal anesthesia urotogical operation accidental LP

Kunz

70/M

spinal anesthesia

25 43d

LSDH

?

surgery

CR

[361

Brinquin

47/M

spinat anesthesia

?

3w

RSDH

+

surgery

CR

1371

Degiaire

70/M

accidentai

17 30h

RSDH

?

surgery

*

I381

BCal

67/M

spinal anesthesia

22 6d

I.. SDH

+

surgery

PR

1391

61/M

diagnostic

?

LSDH

+

surgery

CR

Eernla Newrick

29/F 67iM

Miyazaki

33/F

Rudehi

LP

LP

6Od

12d

Abbreviations: M = mate; F = female; LP = lumbar puncture; 8 = needle diameter (Gauge); h = hours; d = days; w = weeks; m = months; L = left; R = right; Bil. = bilateral; SDH = subdural hematoma; PLPH = post lumbar puncture headache; CR = complete recovery; PR = partial recovery; : = died; ref = reference.

129

Table 2. Review of cases of SDH following

lumbar

puncture

for lumbar

myelopraphy

_-_ ..- -_.. ._ Age

Iel

Study

SCX

Indication

0

Interval

Diagnosis

PLPH

Therapy

Gabriele

58/M

low back pain



id

RSDH

+

none

Alemohammed

40/M

low back pain

IX hw

Bil. SDH

t

surgery

CR

Von E. Heiss

60/M

low back pain

‘!

Sd

LSDH

+

surgery

CR

Dohrmann

65/M

low back pain

9

Zld

RSDH

surgery

CR

50/M

low back pain

?

Xd

RSDH

-

surgery

:

Benzon

58/F

sciatica

?

5d

LSDH

-

none

t

1161

Gupta

62/M

lumbar stenosis

‘?

2w

LSDH

?

none

CR

1441

Dan

31/F

sciatica

7

26d

R SDH

‘?

surgery

CR

1451

Megele

50/F

low back pain

20 16d

RSDH

?

surgery

CR

1461

Lam-My

52/F

low back pain

?

RSDH

surgery

CR

I351

Llewellyn

40/M

low back pain

20 4d

LSDH

+

surgery

CR

I471

vos

54/M

cervical root syndrome

22 44d

LSDH

+

surgery

CR

60d

Gutcomc

Abbreviations: M = male; F = female; LP = lumbar puncture; 0 = needle diameter (Gauge); h = hours; d = days; w = weeks; m = months; L = left; R = right; BiI. = bilateral; SDH = subdural hematoma; PLPH = post lumbar puncture headache; CR = complete recovery; PR = partial recovery; t = died; ref = reference.

of the brain, are cerebral atrophy, brain shrinkage from alcoholism and operative shunting of the ventricular system4s5*6.SDH also complicated an operation on a tumor of the cauda equina with withdrawal of large amounts of CSF7. Another theory for the development of acute or chronic SDH was proposed by ArakiB and later by Miyazaki et aP. They hypothesized that acute SDH results from laceration of the superior sagittal sinus. If only the arachnoid granulation in the parasagittal subdural region ruptures and the sinus itself remains intact, leakage of CSF will only cause a chronic hygroma. The incidence of SDI-I after LP is not known. We expect that a patient with severe PLPH, and therefore probably with a greater displacement of the brain, is at more risk of developing SDH than a patient with minor PLPH complaints. All 35 reported cases of SDH in relation to spinal or epidural anesthesia have been summa130

rized in table 1. In table 2 we listed all 12 reported cases of SDH after LP for myelographic procedures. All cases were clearly related to the lumbar puncture, without a history of trauma or other predisposing factors. In 25 of the 47 reviewed cases a clear history of PLPH preceded the demonstration of SDH, in 10 cases it was recorded absent and in 12 cases it could not be distilled from the text. This association gives support to the role of CSF hypotension in the development of SDH. The tables make clear that the use of a small bore needle does not absolutely protect against SDH. Use of a 26G needle, however, diminishes the incidence of PLPH’O and therefore will probably also diminish the chance of developing SDH after LP. Only one case has been reported with this needle size. In the elderly patient, cerebral atrophy and vulnerability of the venous wall may increase the risk of SDH”.

Our review also shows that SDH is a potentially serious complication; of the 47 reported patients 8 died and 4 were left with serious neurological deficits. PLPH can be easily differentiated from other forms of headache by its postural character. Other rare causes of headache are lumbar puncture induced meningitis and, in case of a preexistent brain shift, tentorial or tonsillar herniation. SDH should be suspected if PLPH lasts for longer than a week, if it loses its typical postural character, or when it returns after an initial disappearance. Cases with small SDH’s may be missed, if these spontaneously resolve’2*13. Treatment of PLPH may also prevent development of SDH. A safe and successful therapy for PLPH is E13P1~*2~‘4. By means of an epidural needle 10 cc autologous blood is introduced in the epidural space. A clot will form over and in the dural rent, thus stopping further leakage of CSFi2. In patients with chronic PLPH, the success rate of this procedure is very high (859.5%)s*‘4.1*.In the cases reviewed by us SDH developed as early as 30 hours and as late as 5 months after LP. The average interval was 25 days. Apparently, intracranial hypotension usually exists for a long time before SDH develops. If patients with severe and prolonged postural headache would be treated with EBP not only the symptoms would disappear, but so might the risk of SDH16.“. References DE BOER WA. Hoofdpijn na lumbale punctie. Ned Tijdschr Geneeskd 1987; 131:2(X%12. HILTON JONES D. What is post lumbar puncture headache and is it avoidable? In Wharlow C, Garfield T, eds. Dilemmas in the management of the neurological patient. Edinburgh: Churchill Livingstone, 1984; 144-57. ARSENI C,IONESCUS,L~NU M. Intracranialhypotension, an etiologic factor of subdural hematoma (chronic subdural hematoma following spinal subarachnoid block anesthesia). Rev Roum de Nemo1 1970; 7~283-6. MARKWALDER T-M. Chronic subdural hematomas: a review. J Neurosurgery 1981; 54637-45. SAMUELSON S,LONGDM,SHOU SN. Subduralhematoma as a complication of shunting procedures for normal pressure hydrocephalus. J Neurosurg 1972; 37548-51. WHITTIER JR. Deaths related to pneumoencephalography during a six year period. Arch Neural Psychiat 1951; 65:463-71. COONEY JF,BAKER GS. Subdural hematoma following an operation on the spinal cord Report of acase. Proc. Staff Meet. Mayo Clin. 1953; 28~364-7. ARAKI C. Pathology of chronic subdural hematoma and

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