Middle meningeal hemorrhage

Middle meningeal hemorrhage

MIDDLE MENINGEAL HENRY A. SHENKIN, M.D. AND FRANCIS C. Philadelphia, E CONSIDERATIONS Our group of tweIve patients were a11 maIes, ranging in ag...

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MIDDLE MENINGEAL HENRY

A. SHENKIN, M.D.

AND FRANCIS C.

Philadelphia,

E

CONSIDERATIONS

Our group of tweIve patients were a11 maIes, ranging in age from seven to fiftythree years, with the surprisingIy Iow age average of twenty-six. The rapidity of deveIopment and the character of the cIinica1 picture was reIated not onIy to the severity of the trauma but aIso to that part of the middIe meningea1 artery from which the hemorrhage arose. Thus six of our patients suffered reIativeIy minor injuries such as a faI1 down the stairs, sIipping upon an icy pavement, etc., and yet four of these had an extraordinariIy expIosive clinica course and a high mortality resuIted in spite of what we considered prompt surgica1 attention. Our criteria of reIativeIy minor crania1 trauma are that the patients promptIy and more or Iess compIeteIy recovered consciousness folIowing the injury and there was Iittle evidence of severe associated brain damage. NevertheIess when the main stem or a very Iarge branch of the middIe meningea1 vesse1 was severed, the patient’s Iife was threatened in a matter of hours. ConverseIy six of our patients suffered what couId be cIassified as severe crania1 trauma : auto accidents, tree faIIing on head, etc., and in three of these the deveIopment of evidence of increasing tension * From the Department

GRANT,

M.D.

Pennsylvania

XTRADURAL hemorrhage of surgicaI proportions aImost aIways resu1t.s from injury to the middIe meningea1 artery. According to Munro it is present in 3 per cent of a11 cranial trauma. This important subject has been frequentIy and adequateIy discussed. However, in reviewing a recent series of our cases (TabIe I) added data were found which we beIieve worthy of emphasis. ETIOLOGIC

HEMORRHAGE*

was reIativeIy sIow. In each of these instances a reIativeIy smaI1 branch of the middIe meningeal vesse1 was invoIved. The severity of the associated cerebra1 trauma aIso served to mask, for a time at Ieast, the evidences of increasing cerebra1 compression. In a11 instances in which the point of trauma to the head couId accurateIy be determined, the hemorrhage was found beneath this area. In most instances a horizonta1 Iinear fracture of the skuI1 was recognized and proved to be the cause of the rupture of the artery. SYMPTOMATj3LOGY

The majority of our patients presented the cIassica1 picture of this disorder: an initia1 period of unconsciousness foIIowing the injury, succeeded by a Iucid interval and a subsequent period of impairment of consciousness with foca1 evidence of cerebra1 compression such as a contraIatera1 hemiparesis and homoIatera1 diIatation of the pupi1. EIeven of the tweIve patients were unconscious folIowing the trauma. The tweIfth patient was struck in the forehead by a back-firing crank handIe without immediate Ioss of consciousness. The initia1 period of unconsciousness Iasted from a few moments to as Iong as one to two hours. The more severe the injury, the Ionger the period of immediate unconsciousness. The severity of the syndrome of extradura1 hemorrhage was in no way reIated to the duration of the initia1 unconsciousness. AI1 patients had a Iucid interval, the Iength of which in two instances was obscured by severe aIcohoIic intoxication. In the six patients whose course was very rapid and in whom a middIe meningea1

of Neurosurgery, University of Pennsylvania, Philadelphia, delphia Academy of Surgery, ApriI 7, 1947. 704

Pa. Read before The PhiIa-

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Grant-MeningeaI

main stem vessel was found to be the bIeeding point the Iucid interva1 was consistently about one hour and the coma which folIowed was rapidly progressive being complete at two to two and one-half hours

Onset

of

Coma

4C” tc altoholism

IpSCht.

of Surgery

Onset 01 Decerehrx tion

?

?

T

Journal

I

-

Lucid lntcrvnl

Acute alto. holism

A m&can

Not <,pcrated

-I

2 hr.

dilated

Prir8cipal \‘C’iSicI

3b.J hr.

pupil and contralat hcmipnrcsi: -1 I hr

I

-~ hr.

Principal vvssel

Ip0ht. dilstcd pupil and L!ontralat hcmiparcsi, _--

5 hr.

Marked B1 X), 5% hr.

hr.

Principal veswl

30 min.

Ipsolat. dilated pupil and COntrUlilt hemiparesi:

zsy

0

0

hr

Ipsolat. dilated pupil nnd contralilt hemiparesi>

Few

sec.

_

Minor

Principal \ cssrl

R hr.

at

3’2

I

(alcoholism)

17, M

hlarked 6 hr.

Bilateral Babinski nt 3 hr.

sec.

_/

M Severe

hr.

2 hr.

Few

9.

2

dilated pupil and Confral;Lt hemiparesi,

-__

33. M 1 Minor

pwlar

maxi rn,l 111

hr.

-I-

_

hr

3



-2

hr.

50

hr.

Small itnterior branch

_5

min.

Contralat

38 hr.

hemiparesia

I

hr.

z hr.

,

_

Ips&t. dilated pupil and contralat hemiparesis _____

~__ 3 hr.

___ I hr.

-

I-

Ipsolat. dilated pupil and contralilt hemiparesi5

hr.

30 hr.

22

Not

xted

___~

Dilated ipsilat. pupil

hr

Small posterior branch

_

Dilated ipsolat. pupil ~-

705

after the injury. In the six patients whose course was reIativeIy sIow and in whom a smaller branch of the middIe meningea1 vessel was found to be the origin of hemorrhage the lucid interval was generaIIy

TABLE

T

Hemorrhage

Semicomat. at 6 hr.

-__ 8 hr.

~__

BiIateral Babinski nt 5s; hr

_!_

-

opcr-

Small posterior br:lnCh

____~

Moderate sized posterior branch --

706

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~~~~~~~~~~~~~~~~ Shenkin,

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Ionger, one, two, three, three, twenty-four Both were instances of main trunk middIe and thirty-eight hours, respectiveIy. The meningea1 arteria1 bIeeding and both died two patients with proIonged intervaIs of in spite of successfu1 evacuation of the Iucidity were both instances of extradura1 hemorrhage at eight and eight and one-haIf hemorrhage from a reIativeIy smaII anhours, respectively, after injury. Three terior (fronta1) branch of the middIe other patients had biIatera1 Babinski remeningea1 vessel. AI1 four patients in this flexes but no rigidity of the ipsiIatera1 group with more sIowIy progressive extraextremities. One was a deepIy comatose dura1 hemorrhage but who had Iucid interchiId of seven, operated upon successfuIIy vaIs of onIy one to three hours had the three hours after injury and the main hemoirhage occurring from a smaI1 postrunk of the middIe meningea1 vesse1 terior branch. However, in these patients identified as the bIeeding point. A second the succeeding period of aItered consciouswas a patient with hemorrhage from a Iarge ness was onIy sIowIy progressive and comsize posterior branch of the middIe meninpIete coma never induced even as long as gea1 vesse1 in coma at the end of eight hours severa days after the injury. but nevertheIess saved by operation. The We do not wish to overstress the imthird was a severeIy injured chiId in whom portance of the Iucid interva1 by its presa Iarge hemorrhage from the main middIe ence in eIeven of our tweIve cases. We fuIIy meningea1 vesse1 was evacuated three hours beIieve, as has been stated by Gurdjian after injury. UnfortunateIy, death occurred and Webster,’ that in severeIy injured in- abruptIy forty-eight hours Iater from individuaIs the deepening of an aIready unconcreased intracrania1 pressure and meduIIary scious state wouId be even more commonIy compression foIIowing a Iumbar puncture. observed than the Iucid interva1. However, The cause of decerebrate symptoms is in instances of reIativeIy minor injuries the herniation of the uncus of the tempora1 as was the situation in many of our paIobe through the incisura of the tentorium tients, one wouId expect the presence of a with pressure upon the mid-brain. Severe Iucid interva1 to be invariabIe. compression of the mid-brain undoubtedly AI1 of our patients with bIeeding from causes hemorrhage into this vita1 area and the principa1 middIe meningea1 vesse1 had the damage is now irreversibIe. That this evidences of a contraIatera1 hemiparesis occurs most prominentIy in tempora1 Iobe and an ipsiIatera1 dilated pupi when first &ass Iesions has been frequentIy and reseen by the surgeon. Neither of the two centIy emphasized,2 Extradural hemorpatients with hemorrhage from a fronta rhage, particuIarIy when resuIting from branch of the middIe meningea1 vesse1 had rupture of the main vesse1 near its point of pupiIIary changes. On the other hand a11 entrance into the cranium, exerts pressure four patients with a posterior branch midprincipaIIy upon the tempora1 Iobe. The die meningea1 hemorrhage had an ipsihomoIatera1 dilated pupi apparentIy reIateraI diIated pupi and onIy two of these suits from this same mechanism, the third had a contraIatera1 hemiparesis. crania1 nerve being exposed to pressure We wish to emphasize an interesting from the tempora1 uncus as it passes forgroup of signs noted in some of our paward through the incisura of the tentorium. tients. These were in our opinion evidences The vita1 signs reffected the increasing of decerebrate rigidity: rigidity of a11 four cerebra1 compression. This was particuIarIy Iimbs and neck with evidence of biIatera1 true of the puIse which in the rapidIy propyramida tract invoIvement as indicated gressing cases invariabIy was beIow 60 per by the Babinski reflex and the presence of minute and frequently beIow 30. The ankIe cIonus. Two patients definitely prerespirations were not as consistentIy aIsented ‘these signs and one of these even tered as the puIse and earIy were increased had “tonic fits” just prior to operation. as often as sIowed; aIthough in those pa-

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tients who died, the respirations were always rapid, deep and stertorous. The pulse pressure was generaIIy increased due to an increase in systolic pressure. The increase in pulse pressure was generally of the magnitude of 20 to 40 mm. of mercury. The temperature earIy in the clinical course was elevated possibIy one or two degrees, but terminahy all moribund patients had a hyperthermia. The hyperthermia accompanied or soon folIowed the appearance of decerebration. TREATMENT

AND

RESULTS

The only treatment is prompt evacuation of the hemorrhage. A subtemporal decompression is generally agreed to be the approach of choice: (I ) It affords adequate exposure for evacuation of the clot and for contro1 of the bleeding point. (2) It is a procedure rapidIy accomplished with minimal operating room preparation. (3) It provides a decompression for postoperative cerebra1 edema and increased intracranial pressure. The dura should be opened and the underlying cortex inspected. The presence of a subdural collection of spinal fluid, either clear or blood-tinged, beneath the area of extradural hemorrhage is not unusual. This was noted in four of our twelve cases and has been remarked upon by other observers.’ Though the origin and significance of this subdural coIIection is not cIear, it is often large enough to require evacuation. Other points in favor of opening the dura are that it provides better decompression for postoperative cerebra1 edema and makes possible direct observation of any cerebra1 contusion. Extensive cortical damage has therapeutic as well as prognostic significance. On rare occasions a subdural coIIection of blood may accompany an extradural hemorrhage. Our series has led us to revise our opinions as to the rapidity with which the syndrome of extradural hemorrhage can progress and how truly prompt surgical intervention must be. In instances of rupture of the main stem or principal branch

Hemorrhage

A mericnn Journal

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of the middle meningeal artery surgical intervention cannot hope to be successful unless instituted within three to six hours after the injury. Shortly after the third hour foIlowing the rupture of the principal middle meningeal vessel decerebration occurs. Thereafter it is probable the neurologic damage caused by the pressure of the hemorrhage is irreversibIe. We have had six patients in this category and only two survived. Both patients that survived were operated upon within less than three and one-haIf hours after their injury. When only a small branch is the source of the hemorrhage, the surgeon is afforded considerably more time in which operation can be successfu1. In our series we had two patients the source of whose bleeding was a smnIl anterior branch. In both the lucid interval had been prolonged (twenty-four and forty-eight hours) and operation was successful fifty and seventy-two hours after injury. In four patients the small vessel that had been opened lay posteriorly in the cranium. The lucid interval was short (one to three hours) but the succeeding period of altered consciousness was only slowly progressive and coma never occurred. Three were operated upon successfulIy eight to thirty hours after injury. The fourth of this group died unoperated upon owing to an error in diagnosis. The patient had never really become more than stuporous and his exodus occurred abruptly ten days after the injury. In the entire series the operative mortality was 30 per cent, two deaths being instances of late operation upon main stem middle meningea1 bIeeding and the third operative fatality occurred as a result of severe associated brain damage. The case mortaIity was 42 per cent, there being two additiona patients dying without operation. One of the nonoperative deaths has been discussed above as being due to an error in diagnosis and the other was an instance of bleeding from the principal middle meningeal vesse1 in a patient who was dead upon arrival at the hospital seventeen hours after injury. This mortal-

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ity is in the range reported in recent years: Munro3 reports an overa mortaIity of 55 per cent, Kennedy and Wortis4 72 per cent, McKenzie5 45 per cent and Gurdjian and Webster’ 27 per cent. SUMMARY

AND

CONCLUSIONS

I. The urgency for surgical treatment in cases of intracrania1 extradura1 hemorrhage is dependent upon the portion of the middIe meningea1 compIex that is the origin of the bIeeding and independent of the severity of the initia1 trauma. 2. When the origin of the bIeeding is the principa1 middIe meningea1 vesse1, the Iucid interva1 is aImost invariabIy one hour or Iess and the succeeding coma compIete at two hours foIIowing the injury. ShortIy after the third hour foIIowing trauma evidences of decerebration become manifest, which when fuI1 bIown indicate that the neuroIogic damage to the patient is irreversible. Therefore, in instances of hemorrhage from the principa1 middIe meningea1 vesse1 operation must be undertaken within three to six hours of the injury if the patient is to be saved. 3. BIeeding from an anterior branch of the middIe meningea1 vesse1 is associated with a proIonged Iucid interva1 of one to two days. The succeeding aIteration of consciousness is not severe and onIy sIowIy

Hemorrhage

MAY. 1948

progressive. PupiIIary changes are not the ruIe though a contraIatera1 hemiparesis may., be present. 4. In instances of extradura1 hemorrhage from a posterior branch of the middIe meningea1 artery the Iucid interva1 is generaIIy of-one to t-hree hours’ duration,-but th‘k succeeding state of aIteration of consciousnesris not profound and onIy sIowIy progressive. IpsiIateraI diIatation of the pupil appears to be constant. A contraIateraI hemiparesis was present in onIy haIf of our cases of extrad;raI hemorrhage originating from a posterior middle meningeal branch. 1

REFERENCES

E. S. and WEBSTEK, J. E. ExtraduraI hemorrhage-a coIIective review of the Iiterature and a report of 30 cases of middle meningeal hemorrhage and 4 cases of dura1 sinus hemorrhage treated surgicaIIy. Inter. Abstr. Surg., 75: 206220, 1942. 2. (a) JEFFERSON, -G. The tentoria1 pressure cone. Arch. Neurol. Ed Pqxbiat., 40: 857-876, 1938. (b) WOODHALL, B., DEVINE, J; W. and HART, D. HomoIateraI dilatation of the m&I. homoIatera1 paresis and bilateral muscuI& *rigidity in the diagnosis of extradural hemorrhage. Surg., Gynec. CYObst., 72: 391-398, 1941. 3. MUNRO, D. and MALTBY, G. L. ExtraduraI hemorrhage-a study of 44 cases. Ann. Surg., I 13: 192I. GURDIJIAN,

203, 1941. d. KENNEDY. F. and WORTIS. H. Acute subdura1 hema-

toma and acute epidura1 hemorrhage. Surg., Gynec. CTObst., 63: 732-742, 1936. 5. MCKENZIE, K. G. ExtraduraI hemorrhage. Brit. J. Surg., 26: 346-365, 1938.