Subdural hematoma

SUBDURAL HEMATOMA W.

D. ABBOTT,

M.D.

AND

D.

H.

KAUMP,

M.D.

Attending Neurosurgeon, Mercy, Iowa Lutheran and Iowa Methodist HospitaIs

Attending PathoIogist, Providence HospitaI

DES MOINES, IOWA

DETROIT, MICHIGAN

T

HE purpose of this paper is to emphasize the frequency of dura1 hematoma as a seque1 to cerebra1 trauma and to discuss some of the sahent pathoIogic and clinical features. Recent pubhcations by other author9 and ourseIves1s3 have reviewed the historica and etioIogic phases of the subject so that a repetition is not deemed advisabIe. In the past few years, many papers on this subject have appeared in the Iiterature. Those of Putnam and Cushing, as we11 as those of Leary, have been particuIarIy descriptive. According to these authors, hematomas may be divided into two groups, spontaneous and traumatic. The so-caIIed spontaneous or vascuIar type of hematoma is found particuIarIy in chronic wasting diseases, such as paresis, as we11 as in chronic and acute aIcohoIism. The traumatic or reactive form is found chiefIy foIIowing trauma, but it overlaps the first group somewhat as it may be found associated with certain of the conditions just mentioned. AIthough by no means the first to describe subdura1 hematoma, Virchow in 1857 brought this particuIar entity to the attention of physicians. He proposed the theory that in certain cases where there was chronic infIammation of the dura, an exudation of fibrin took pIace. Into this thin fiIm capiharies grew, which under the inffuence of continued inffammation and hyperemia, ruptured and produced smaI1 hematomata which in turn became organized. This theory has profoundly iniluenced subsequent workers aIthough much other work has been done and numerous other theories have been advanced. Anatomy. The dura is thick, dense, ineIastic fibrous membrane which lines the interior of the skuI1 where it forms an

interna periosteum. The dura has a rich bIood suppIy and receives numerous arteries. In the anterior fossa there are branches from the anterior ethmoidal, posterior ethmoidal, interna carotid, and middle meningea1 arteries. In the middle fossa, branches enter from the ascending pharyngea1, interna carotid, and lacrimal arteries and the posterior fossa receives branches from the occipita1, vertebral, ascending pharyngea1 and middIe meningea1 arteries. The veins, with the exception of the middIe meningea1 vein, anastomose with the dipIoic veins and empty into the sinuses. According to Kaump and Love, as we11 as Hannah, the dura consists microscopicahy of three Iayers. The outer layer which Iines the skuI1 is composed largely of dense fibrous connective tissue, and it is in this Iayer that the Iarge vesseIs course. The inner Iayer consists of fibrous connective tissue but in a somewhat Iooser arrangement than the outer. This Iayer apparentIy has a scanty blood suppIy and it is Iined by a thin ffattened Iayer of frbrobIastic ceIIs. The middle Iayer, with which we are most concerned, is composed IargeIy of loose fibrous connective tissue in which there are many smaII vesseIs and numerous endotheIia1 Iined spaces which may be empty or which may contain bIood ceIIs. Histopathology. Kaump and Love have reported a series of thirty post-mortem specimens of so-caIIed subduraI hematoma. Thirteen of the hematomata were of the traumatic type and the remaining seventeen were considered to be of the spontaneous type. The hematomata described in this series of cases were a11 of a similar character. There was no change in the outer or periostea1 layer of the dura mater except in the case of older lesions where 64

NC,+

SE.HLES VOL.

MAX,

No.

I

Abbott,

Kaump-Subdural

phagocytes Iaden with pigment were usually- seen. This pigment was Iargely in the form of hemosiderin and was seen in

Hematoma

.lourn.~l of Surgcr.v

6,s

occasiona sma11 coIIections of lymphocytes were noted, but it must be remembered that this reaction might be readily due to

FIG. I. Roentgenogram revealing multiple linear fracture the Ieft temporal and parietnl bones.

sections stained for iron. There frequentIy was some hyalinization of the connective tissue. The middIe Iayer in which the hematoma formed was fiIIed with blood in various stages of degeneration, the more advanced degeneration appeared in oIder Iesions. The inner lining of the hematoma was composed of new connective tissue cells. This organization was best seen at the angle where the separation in the dura had occurred. At this pIace bands of newly formed fibroblasts projected into the degenerating blood cIot. In this new tissue and externa1 to it were seen the dilated endotheIia1 Iined spaces which occasionaIly contained erythrocytes. These spaces were irregular and varied greatIy in size. The inner or meningeal layer was thickened, edematous and contained many fibrobIasts in the process of organizing the cIot. In a few of the cases sections were taken from positions remote to the site of the hemorrhage. Th ese were examined for evidence of chronic infiammation particularly, and so far as couId be determined they appeared to be normal. This does not, however, eliminate the possibility of a localized area of inflammation predisposing to hematoma formation. In examining the sections taken through the hematomata,

American

in

destruction of blood as to any chronic inflammation. In the one case in which there was clinicaI and seroIogicaI evidence of syphilis, and in which the Iesions resembIed miliary gummas, the Iesions were undoubtedly due to syphilis and in this case may conceivably have played a part in the production of the hematoma. In all three cases in which there was an associated bIood dyscrasia, coIIections of lymphocytes were noted. Here again as in the presence of syphilis, one must definiteIy consider the possibiIity of a Iocal accumulation of lymphocytes playing a causative role in the formation of the hematoma. Contradictory reports have been published as to the fate of bIood subdurally injected, and Putnam and Putnam said in a true progressive part that, “Apparently chronic hematoma of the dura has never been produced experimentally. The lesions seen after the subdura1 injection of bIood, and in patients after operation resembled a progressive Iesion in appearance, but not in theoretical behavior.” From a purely standpoint, it wouId seem pIausible that bIood set free in this potentia1 space would flow to the dependent portions and fail to become encapsuIated, simply because

66

American Journal of Surgery

Abbott,

Kaump-Subdural

of the diffuse distribution of the bIood. In this regard, it might be said that in our experience at Ieast, bIood subdurally located

Hematoma

JULY, 1940

patients in the earlier stages, are not fuIIy aware of the condition itseIf, its insidious deveIopments and the methods whereby

FIG. 2. .EncephaIogram reveaIing slight diIatation of the ventricular system with no evidence of air over cerebra1 hemispheres.

at the site of trephine wounds organizes from the dura1 side onIy and shows no evidence of membranous formation. No evidence couId be deduced from this series of cases which woufd put a11 cases of so-called subdura1 hematoma into one etioIogic cIassification, that is, traumatic or spontaneous. It shouId be kept in mind that onIy reIativeIy sIight trauma may produce these hematomata and aIso that in the group of cases in which spontaneous hematomata appeared the history was often unreIiabIe and mishaps of a sIight nature couId have readiIy been overlooked. These considerations together with the known etioIogic r8Ie pIayed by trauma in many cases tend to make one fee1 that they may we11 have a11 been of a traumatic nature. Diagnosis. So-caIIed subdura1 hematoma stiI1 goes unrecognized in a Iarge percentage of cases. NeuroIogists and neurosurgeons who are constantIy seeing cases of increased intracrania1 pressure and of cerebra1 compression usuaIIy consider the lesion in the differentia1 diagnosis of many intracrania1 Iesions, particuIarIy if there has been a history of crania1 trauma. The genera1 surgeon and the genera1 practitioner, however, who see most of these

FIG. 3. Posterior-anterior gram, reveaIing absence hemispheres.

view of encephaIoof air over cerebral

diagnosis can be made during the optimal time for successfui treatment. The cIinica1 picture presented by patients with subdura1 hematoma is quite confusing and any evidence of a pathoIogic nature which might aid in the identification of this condition is to be sought for. The Iatent period is perhaps the most characteristic of a11 the cIinica1 features of so-caIIed subdura1 hematoma and perhaps the most diffIcuIt to expIain. The period preceding the onset of the neuroIogic signs may apparentIy be uneventful or in the cases in which there is a definite history of trauma, symptoms may be initiated by a period of unconsciousness immediateIy foIIowing the injury. The patient appears to recover from this in the space of a few minutes and then after a varying period of time, often severa months, he begins to show definite neuroIogic signs. It is possible that the cessation of bIeeding is brought about by an increased intracrania1 pressure due partIy to the hemorrhage. Into this cIot grow newIy formed vessels which are fragile and can

Nti.\r SERIES

VOL.

SL.IX,

No.

I

Abbott,

Kaump-Subdural

easiIy be damaged and Iead to further bleeding. This theory of successive bIeeding seems most logical, aIthough Monroe and

Hematoma

A mcricanJ0urn.d of Surgery

67

the endotheiiai lined tissue spaces mentioned previousIy. Perhaps the most confusing of the clini-

FIG. 4. Incision in superior temporat bone (small inset). Trephine opening and method of aspirating contents of hematoma ilarger djagram).

Merritt have also postulated a very ingenious theory to explain the growth of these expanding Iesions. They maintain that every subdura1 hematoma starts as a mixture of blood and cerebrospinal fluid. With the dissoIution of the blood there is an increased protein content and with diffusion of fluid across the pia aiachnoid there resuIts an increasing volume of solution. This dissolution of bIood with the consequent increased protein content covers a period of about sixteen days foIIowing which rapid diIution takes pIace for the two succeeding weeks. Slower diIution then takes pIace for at least two months. This explanation may be a IogicaI one if we grant the admixture of bIood and cerebrospina1 fluid. This could occur only in case the arachnoid was torn and such an admixture obviousIy couId not occur in hemorrhages which are truIy intradural. Furthermore, the cerebrospinai fIuid wouId, in cases of intradura1 hemorrhage, of necessity diffuse through the arachnoid as we11 as the inner Iayer of the dura. It might be just as IogicaI to suppose that, if dilution actuaIIy does take place, the fluid added is derived directly from the blood stream by means of

cal signs presented Iies in the bizarre nature of the neuroIogic signs. It must be remembered that a Iarge uniIatera1 tumor or hematoma may cause sufficient pressure to compress the opposite cerebra1 peduncle on to the cerebeIIar tentorium. This, of course, produces damage to the pyramidal tract and results cIinicaIIy in paradoxical homoIateraIity of the pyramida tract signs such as the Babinski reflex, spasticity, cIonus and increased reffexes. The sensory reIations remain undisturbed, as a rule, because of their deep seated location in the Iemnisci. The other group of clinical signs which might occur is genera1 and is due to the increase in intracrania1 pressure. It is thus seen that this apparent confusion of clinical signs can best be interpreted in the knowledge of the pathorogic change which may be present. Furthermore, in addition to the evidence gained by history and neuroIogic examination, diagnosis may be quite readiIy confirmed by the presence of choked discs and various changes in the reffexes, station and gait. In a few instances roentgenograms of the skuII reveal caIcification in a subdural hematoma, but these

68

Abbott,

American Journal of Surgery

Kaump-SubduraI

usuaIIy are in patients in whom the Iesions are more chronic in nature. More often it is necessary to utilize Iaboratory tests such as

Hematoma

dura1

hematoma

JULY. rp.lo

are

included

in TabIes

I to v. SUMMARY

TABLE 111 OF SIGNS AND SYMPTOMS IN FIFTY-ONE PATIENTS WITH DURAL HEMATOMAS

T

7-

Number ,F ‘er Cent _ Headaches ..................... Personality changes ............. Vomiting. .......................

21

41.

17 16

ConvuIsion ...................... Paralysis. .......................

'3 8 8

33.3 30.9 25.7 15.7 ‘5.7 ‘3.7 II.7

Coma ........................... UniIateraI diIatation of pupil. ..... Choked d’iscs.................... Latent period (5 days to I I months -average 5x months)

:,

I

TABLE IV Age: IO months to 67 years Sex:MaIes 38-FemaIes 13

FIG. 5. Method

of removing adherent from surface of brain.

TABLE v TECHNICAL MEASURES

hematoma

USED Per Cent

cerebrospina1 Auid studies to prove the existence of increased spina ffuid pressure and xanthochromic fluid. In many instances ventricuIar and encephaIographic studies must be carried out. TABLE

Encephalography. VentricuIography Trephine and drainage., Osteoplastic flap.

IO

19.2

3 35 16

5.7 67.3 30.7

I

525 CONSECUTIVE HEAD INJURIES

Type of Injury

Number

Dural hematoma. IntraduraI.. Subdural BiIateraI. Unilateral.

CASE

Per Cent

31

9.7 76-4 23.6

39

1,”

45.1 54.9

28

TABLE II RESULTS IN FIFTY-ONE CASES OF DURAL HEMATOMA

Number

I Recovery................... Death......................

Per Cent

I 84.6

44 7

1

If.4

~

Clinical Material. A summary of the findings and resuks in fifty-one cases of

REPORTS

In order to demonstrate more graphically certain of the diagnostic diffrcuIties which are encountered, we have summarized the saIient features in six cases from this group of fifty-one. CASE I. FemaIe, aged 17, was in an auto accident September 5, 1933, which resuIted in coma, paralysis of the right face, arm and leg, and Iaceration of the right arm. Gas gangrene deveIoped September 17, 1933. BIood transfusion and gas baciIIus serum were administered intravenousIy. On October 6 the patient was stiI1 in coma. The Ieft frontoparieta1 flap was turned and the dura1 hematoma removed. The patient regained consciousness on October

13, moved on

her

November

This

case

right legoctober IO. CompIete

iIIustrates the

the rather rare complication

14,andtaIked recovery

ensued.

accompaniment

of

of gas gangrene.

Nvw

SI.KIFS

VW..X1.,1X,No I

Abbott,

Kaump--Subdural

FortunateJy the patient survived both the hematoma and the gas gangrene. CASE II. Male, 38, a known alcoholic, feII in a cement driveway January 21, 1934. He was thought to be drunk, and remained comatose. He was taken to the hospital seventy-two hours Iater. The right pupi was diIated and there was paraIysis of the left extremities with a positive Ieft Babinski. Roentgenograms re\.,eaIed a linear fracture of the right temporal bone. (Fig. I.) The spinal Auid was under increased pressure and xanthochromic. A dural hematoma was removed on February I, 1934 ancl complete recovery folIowed. This case illustrates the role of alcohol. The confusion of an accident in a known aIcohoIic is obvious; a severe cranial injury may be present and be masked by symptoms of alcoholism. CASE III. Male, 7, was struck by a car ApriI 30, 1937. He remained semi-comatose for three days with headaches on exertion. Later there was a personality change, with failure in schoo1 and extreme irritability. Physical examination was essentially negative. Encephalography on May 26, 1937 revealed a biIatera1 cIefect over the cerebra1 hemispheres. (Figs. 2 and 3_) On June IO the biIatera1 dural hematoma was removed and recovery foIlowed. This iIIustrates the insidious progress of hematomata which are often first evidenced by headaches on exertion and marked change in personality. CASE IV. Female, 39, was kicked in the face t\vo days prior to admission conscious.

She

was a history injury.

and rendered

was acImittecI

in coma.

of heavy drinking

Examination

un-

There

just prior to the

was negative

except

for

the obvious moribund condition. The patient expired thirty minutes after admission. Necropsy revealed a large dural hematoma compressing the right cerebral hemisphere. Here the role of alcohol had confused a possibility of the organic

lesion which caused

CASE v. Male, 45, on suffered a severe head injury

death.

August IS, 1935 and was comatose

for four days. SubsequentIy he developed graduaI 10~s of memory and was pIaced in a psychopathic hospita1 for two months. Examination reveaIed an emotionaIIy unstabIe male who cried readily and complained of vomiting. There was a right hemiparesis. On March 20, 1936, remova of biIatera1 dural resulted in complete recovery.

hematomata

JwII-~.I~ 01S,ir~rv A,,,urici,,>

Hematoma

49

CASE VI. Female, 32, a known alcoholic, feII off a couch in an alcoholic stupor in February, 1938. She suffered from severe headaches and a right hemipIegia for three weeks. The spina fluid revealed increased pressure and cIear fluid. On examination she was dull and disoriented, with divergent strabismus of the right eye and a right hemiplegia. A dural hematoma was removed on the right. Exploration of the left cerebral hemisphere disclosed no abnormaIity. This illustrates a cast of paradoxical homolaterality. SURGICAL In of

most instances

such

chronicity

TECHNIQUE these that

hematomas removal

may

are be

done through a small opening in the posterior tempora1 region. Evacuation is accompIished by irrigating the subdural or intradura1 space with saIine soIution followed by the application of a suction apparatus. (Fig. 4.) OccasionaIIy the hematoma is so densely adherent to the pia that a Iarger opening must be made. This is done by turning an osteopIastic flap after which the cIot can usuaIIy be satisfactoriIy evacuated. (Fig. 3.) It is our custom to make an incision and smaI1 trephine opening in the posterior tempora1 region on each side so that a biIateral dura1 hematoma will not be overIooked. The postoperative care differs somewhat from the routine care foIIowing remova of the usua1 cerebral tumor. Coleman has shown that foIIowing Iong compression, the brain does not return to its norma proportions and these patients frequently die from continued cerebra1 compression. Therefore, it is our custom to administer ffuids generousIy to these patients for severa days. If signs of cerebra1 edema develop they may be combated by the use of hypertonic fluids intravenousIy or by bowe1 and by judicious cerebrospina1 fIuid drainage. SUMMARY

In this article are reviewed the salient cIinica1 and pathoiogic aspects of dural hematoma. The intradural character of the ciot, the pathologic picture and the paradoxica1 homoIateraIity of pyramida signs

70

American

Journal

of Surgery

Abbott,

Kaump-Subdural

which may occur are stressed. IncIuded is a review of the information gained from a study of fifty-one cases of dura1 hematoma as we11 as a summary of signs, symptoms and operative procedures used. FinaIIy, we have incIuded a summary of the Iindings on six patients in order to better demonstrate the diagnostic diffIcuIties often encountered. REFERENCES I.ABBOTT, W. D. Traumatic

subdural hematoma. Am. J. Surg., 63: 32-35 (JuIy) 1936. 2. COLEMAN, C. C. Chronic subdura1 hematoma. Am. J. Surg., 28: 341 (May) 1935.

Hematoma

JULY,

,940

3. HANNAH, J. A. The etioIogy of subdurat hematoma. An anatomical and pathoIogica1 study. J. Nerv. em Ment. Dis., 84: 169-186, 1936. 4. KAUMP, D. H., and LOVE, J. G. Subdural bematoma. Surg., Gynec. @ Obst., 67: 87-93 (JuIy) 1938. 5. LEARY, T. Subdural hemorrhages. J. A. M. A., 103:

897-903, 1934. 6. MUNRO, D., and MERRITT, H. H. Surgical pathoIogy of subdura1 hematoma based on a studv of one hundred five cases. Arch. Neurol. EdPsych., 35: 64-78, 1936. 7. PUTNAM, T. J., and CUSHING, HARVEY. Chronic subdura1 hematoma. Arch. Surg., I I: 379-393, 1925. 8. PUTNAM, T. J., and PUTNAM, I. K. The experimental study of pachymeningitis hemorrhagica. J. Nerv. CYMent. Dis., 65: 260-272, 1927. g. VIRCHOW, R. Haematoma durae matris. Verbandl. d. pbys.-med. Geseilscb. z. Wuerzb., 7: 134-142. 1857.

A SATISFACTORY program for convaIescing psychiatric patients includes an environment in which wholesome and attractive ways of Iiving are maintained, an intehigent and we&trained nursing service, occupational therapy, physica education, and physiotherapy, al1 under medical supervision with opportunity for frequent interviews of patient by physician. From-“Convalescent Care” (New York Academy of Medicine).