Journal ofNeurology, Neurosurgery, and Psychiatry 1994;57:717-723

Jugular venous desaturation and outcome afterhead injury

S P Gopinath, C S Robertson, C F Contant, C Hayes, Z Feldman, R K Narayan,R G Grossman

Department ofNeurosurgery, BaylorCollege ofMedicine,Houston, Texas USAS P GopinathC S RobertsonC F ContantC HayesZ FeldmanR K NarayanR G GrossmanAddress for correspondence:Dr Shankar P Gopinath,Department ofNeurosurgery, BaylorCollege of Medicine, OneBaylor Plaza, Houston,Texas 77030, USA.Received 20 May 1993and in revised form12 August 1993.Accepted 5 October 1993

AbstractEarly experience with continuous moni-toring of jugular venous oxygen satura-tion (SjvO2) suggested that thistechnology might allow early identifica-tion of global cerebral ischaemia inpatients with severe head injury. Thepurpose of the present study was toexamine the relationship betweenepisodes of jugular venous desaturationand neurological outcome. One hundredand sixteen severely head-injuredpatients had continuous monitoring ofSjvO, during days 1-5 after injury.Episodes of jugular venous desaturation(SjvO, < 50% for more than 10 minutes)were prospectively identified, and theincidence of desaturation was correlatedwith neurological outcome: 77 episodes ofdesaturation occurred in 46 of the 116patients; 27 had one episode and 19 hadmultiple episodes of desaturation. Thecauses of these episodes were systemic(n = 36), cerebral (n = 35), or both(n = 6). Most of the episodes were lessthan 1 hour in duration, and it isprobable that many of them would nothave been detected without continuousmeasurement of SjvO,. Episodes of de-saturation were most common on day 1after injury, and were twice as common

in patients with a reduced cerebral bloodflow as in patients with a normal or

elevated cerebral blood flow. The occur-

rence of jugular venous desaturation was

strongly associated with a poor neurolog-ical outcome. The percentage of patientswith a poor neurological outcome was

90% with multiple episodes of desatura-tion and 74% in patients with one desatu-ration, compared to 55% in patients withno episodes of desaturation. Whenadjusted for all co-variates that were

found to be significant, including age,

Glasgow coma score, pupillary reactivity,type of injury, lowest recorded cerebralperfusion pressure, and highest recordedtemperature, the incidence of desatura-tion remained significantly associatedwith a poor outcome. Although a cause

and effect relationship with outcomecannot be established in this study, thedata suggest that monitoring SjvO, mightallow early identification and thereforetreatment of many types of secondaryinjury to the brain.

(7 Neurol Neurosurg Psychiatry 1994;57:717-723)

A number of physiological factors have beenrelated to outcome after severe head injury.Intracranial hypertension, systemic hypo-tension, arterial hypoxia, and hypocapniahave been implicated as causes of cerebralhypoxia/ischaemia and have been associatedwith a poor neurological outcome.'-6

Early experience with continuous monitor-ing of jugular venous oxygen saturation(SjvO,) using a fibroptic catheter hadsuggested that this technology might allowearly identification of both cerebral ischaemiaresulting from systemic and cerebral causesand transient episodes of ischaemia whichwould otherwise go undetected and un-treated.7-'2 More recent studies have suggest-ed that SjvO2 monitoring might helpdetermine optimal hyperventilation"3 and,combined with transcranial Dopplermeasurements, optimal cerebral perfusionpressure.'4 15 The purpose of the present studywas to examine the relationship betweenepisodes of jugular venous desaturation andneurological outcome in patients who hadsustained a severe head injury.

Patients and methodsPATIENT POPULATION AND MANAGEMENTBetween 15 July 1989 and 30 September1992, 116 patients admitted consecutively toBen Taub General Hospital, Houston, Texas,USA, with a severe head injury (Glasgowcoma scale, GCS < 8) had continuous mea-surements of SjvO2 using a fibroptic oxygensaturation catheter (4 French gauge catheter,Abbott Laboratories, North Chicago IL,United States) positioned in the jugular bulb.The accuracy of the oxygen saturation mea-surements obtained with this catheter hasbeen described in a previous publication. 12The protocol was approved by the BaylorInstitutional Review Board and informed con-sent was obtained from the families of thepatients participating in the study.

Ninety per cent of the patients studied weremale; most were between the ages of 16 and35, with an average age of 31-5 (SD 14-7)years. Eighty-six per cent of the patients stud-ied had a closed head injury, whereas theremaining 14% had a gunshot wound to thehead. Eighty per cent of the patients werecomatose on admission to the hospital. TheGCS after resuscitation was 3-5 in 34% of thepatients and 6-8 in 46%. Twenty per cent ofthe patients had an initial GCS of >8, butdeteriorated to coma within 48 hours ofinjury. The average GCS was 6-9 (SD 3 0) on

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arrival in the emergency room, and 6 8 (SD2-3) on day 1 after injury.

All patients were managed with a protocolthat emphasised prompt evacuation ofintracranial haematomas and prevention ofsecondary insults to the brain. Patients wereintubated and ventilated to maintain a PaO,of at least 100 mmHg and a PaCO, of about35 mmHg. Intracranial pressure (ICP) wasmonitored, usually by ventriculostomy, andpressure >20 mmHg were treated.Intracranial hypertension was treated withcerebrospinal fluid drainage, hyperventilation(PaCO, 25-30 mmHg), sedation, paralysis,and mannitol. Mean arterial blood pressure(MAP) was continuously monitored andmaintained so that cerebral perfusion pressure(CPP) was at least 60 mmHg. Barbituratecoma was used only if intracranial hyperten-sion was refractory to the above regimen.Other routine medications included pheny-toin and antibiotic drugs.

CONTINUOUS PHYSIOLOGICAL MEASUREMENTSTo monitor SjvO2, the fibroptic catheter wasinserted into the internal jugular vein through a4-5 French gauge peel-away introducer (CookCritical Care, Bloomington Ind., UnitedStates), and threaded into the jugular bulb.The catheter for measurement of SjvO2 wasplaced on the right side unless the left jugularvenous circulation was demonstrated to bedominant: 96 (83%) were placed on the rightside and 20 (17%) on the left. A radiographwas obtained to ensure that the catheter wascorrectly positioned in the jugular bulb. Everyeffort was made to start the monitoring asearly after admission as possible. The catheterfor measurement of SjvO, was inserted anaverage of 16-6 (SD 15-0) hours after admis-sion to the neuro-intensive care unit: 93(80%) were inserted within 24 hours ofadmission. Where monitoring was startedmore than 24 hours later, reasons included:inability to obtain informed consent fromfamilies (n = 6), early contraindication forjugular catheter such as coagulopathy or sus-picion of a cervical spine injury (n = 3), andneurological deterioration after 24 hours(n = 14). Patients were monitored for anaverage of 88-2 (SD 75 5) hours.The following physiological parameters

were recorded at an interval of 1-2 minutes,stored in a computerized database, plottedagainst time, and correlated with clinicalevents and intermittent measurements ofcerebral blood flow (CBF) and cerebralmetabolism: ICP, mean arterial bloodpressure (MAP) via a radial artery cannula,CPP, arterial oxygen saturation (SaO,), end-tidal CO,, and SjvO,. The catheter formeasurement of SjvO, was calibrated beforeinsertion using the standard provided by themanufacturer. In addition, an in vivocalibration was performed after insertion, andevery eight hours thereafter, if the differencebetween the catheter value and the SO,measured in a blood sample drawn throughthe catheter was more than 4%.

IDENTIFICATION AND MANAGEMENT OFJUGULAR VENOUS DESATURATIONEpisodes of jugular venous desaturation,defined as an SjvO, <50% for more than 10minutes, were identified prospectively. The firsttask was to verify the accuracy of the catheterat the time of the desaturation, this is because,as discussed in a previous report, the catheter issubject to artefactual readings from move-ment of the catheter within the jugular bulb.'2In the 116 patients, 172 episodes of jugularvenous desaturation were identified initially.On investigation, 95 (55 2%) of the episodescould not be confirmed by measuring SO2 in ablood sample drawn through the catheter.

Once it was confirmed that the SjvO2 was<50% in a blood sample drawn through thecatheter, it was necessary to identify thecause. Systemic causes of reduced oxygendelivery were sought by examining bloodpressure, arterial blood gases, and haemo-globin concentration; ICP and CPP werenoted. If an obvious cause was not found,cerebral blood flow was measured. When aremediable cause for the desaturation wasfound the appropriate treatment was applied.

INTERMITTENT MEASUREMENTS OF CBF ANDMETABOLISMCBF was measured by the nitrous oxide satu-ration method every eight hours.'6 A total of1042 measurements of CBF or an average ofnine measurements per patient (range 1-29per patient) were obtained. Arterial and jugularvenous blood samples were obtained togetherwith measurements of CBF for determinationof PaO,2 PaCO2 pH, oxygen saturation, lac-tate, and haemoglobin concentration. A bloodgas analyser was used to measure PaO,2PaCO2, and pH. Oxygen saturation andhaemoglobin concentration were measured ona co-oximeter (IL-282, InstrumentationLaboratories, Lexington Mass., UnitedStates). Patients were classified as having anormal, elevated, or reduced CBF, throughcomparison of the individual measurementswith the normal range for CBF at the patient'sPaCO2, as described in a previouspublication.'6

DETERMINATION OF NEUROLOGICAL OUTCOMEOutcome was determined three months afterinjury by personnel who were unaware of thedesaturation information. The Glasgow out-come scale (GOS) was used to quantify theseverity of the neurological deficits. Forcomparison of the outcome with the SjvO2data, a favourable outcome was defined as aGOS score of good recovery or moderatedisability, and a poor outcome was defined as aGOS score of severe disability, vegetative, ordead.

STATISTICAL METHODSSummary data are reported as the mean ±standard deviation. Categorical variables wereanalysed using X-square whereas differencesin means were tested using a one-way analysis

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_Jugular venous desaturation and outcome after head injury

of variance. Statistical significance wasdefined as p < 005 for primary effects.

Multiple logistic regression analysis wasused to determine the contribution of morethan one variable to the outcome and to theoccurrence of desaturations. The model wasfitted in a forward selection manner. Co-variates in the multiple logistic regressionswere included when p < 0-20. The finalmodel contains only those additional variablesthat were significantly associated with out-come.

ResultsCONFIRMED EPISODES OF JUGULAR VENOUSDESATURATIONSeventy-seven episodes of jugular venousdesaturation, defined as SjvO2 <50% for morethan 10 minutes, were identified prospectivelyand confirmed in 46 of 1 16 patients. Theepisodes were confirmed by measuring SO2 ina blood sample drawn through the catheter.

12 24Time after admission (h)

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500 12 24 31

Time after admission (h)

Figure 1 Two patients exhibiting different effects of hyperventilation on SjvO2. Thepatient whose data are shown in A had a marked decrease in CBF and SjvO2 when(PCO2 was decreased to 3-3 kPa (25 mmHg). These abnormalities reversed when theventilator was adjusted to normalise PCO2. The patient whose data is shown in B hadacceptable CBF and SjvO2 with similar PC02 values of2-7-3-3 kPa (20-25 mmHg).

The SjvO2 values at the time of the identifica-tion ranged from 17% to 49%, averaging39*3 +11-7%.

Twenty-seven (23-3%) of the patients hadone episode, 11 (9 5%) two episodes, andeight (6 9%) more than two episodes of de-saturation. Demographic characteristics, typeof injury, severity of injury, and presence ofsystemic injuries were not significantly relatedto the incidence of desaturation (table 1).The incidence of jugular venous desatura-

tion was more common early after injury.Twenty-eight (36 8%) of the 77 episodes ofdesaturation occurred within 24 hours ofadmission to the neuro-intensive care unit.There were 13, 10, 12, and seven episodes ondays 2-5 after injury, respectively. Only sevenepisodes occurred after day 5, with a meanonset of the episodes of desaturation of 53 9(SD 47'9) hours after admission to the non-intensive care unit.

Duration of the 77 episodes of desaturationranged from 15 minutes to five hours; 57(75%) were less than one hour. The meanduration of all the episodes was 1 2 (SD 1-6)hours.The causes of the jugular venous oxygen

desaturation could be identified as having acerebral origin in 35 episodes, arising fromintracranial hypertension in 34 and vasospasmin one case. The most common systemiccause was hypocarbia, defined as a PaCO, <3-7 kPa (28 mmHg) (n = 21), followed bysystemic hypotension, defined as systolicblood pressure < 90 mmHg (n = 8), arterialhypoxia, defined as an SaO, < 90% (n = 6),and anaemia (n = 1). Combinations of bothsystemic and cerebral causes were observed insix episodes.

UNIQUE INFORMATION PROVIDED BYMONITORING OF SjvO2An example of hypocarbia producing jugularvenous desaturation is given in figure 1 whichillustrates two patients with very differentresponses to lowering PCO2 to 3-3 kPa (25mmHg). One patient developed a very lowSjvO2 and a low CBF which returned to

Table 1 Demographic and injury related parameters which were examinedfor an effect on the relationship between desaturations and outcome

Number of desaturatioms Three month Glasgow outcome score

None One Multple p value* GRIMD SDIV Dead p value*

Number 70 27 19 40 40 36Age (years) 31-3 (14-9) 28-5 (11-6) 36-2 (16-9) 0-23 28-8 (13-3) 31-2 (14-0) 35-0 (16-5) 0-18Sex (% male) 65 (92 9) 23 (85 2) 16 (84-2) 0 37 37 (92 5) 35 (87 5) 32 (88-9) 0 75

Severity of injuryER GCS (score) 7-2 (3-0) 6-3 (2-5) 7-0 (3-5) 0 45 7-6 (3-1) 6-5 (2 7) 6-6 (3 2) 0-21ERpupils (% normal) 53 (75-7) 16 (59-3) 14 (73 7) 0-25 34 (85 0) 29 (72-5) 20 (55-6) 0 004Day 1 GCS (score) 7-0 (2-1) 6-6 (2-2) 6-4 (3 2) 0-61 8-1 (2 3) 6-7 (1-8) 5-5 (2-2) <0-001Day 1 pupils (% normal) 56 (81-2) 24 (88 9) 15 (78 9) 0-62 39 (97 5) 31 (79-5) 25 (69 4) <0-001

Injury type (%) 0-87 0-001Closed head injury

Diffuse 23 (60 5) 10 (26-3) 5 (13-20) 21 (55 3) 11 (28-9) 6 (15-8)Hematoma 36 (58-1) 14 (22 6) 12 (19-4) 16 (25 8) 19 (30 6) 27(43 5)

Gunshot wounds 11 (68 8) 3 (18-8) 2 (12-5) 3 (18-8) 10 (62-6) 3 (18-8)

Presence of systemic injuriesISS (score) 26 (6) 26 (4) 27 (5) 0-88 26 (7) 26 (5) 27(4) 0 95

*p value is for analysis of variance when mean values were compared and the X squared test used with categorical data. Values in parentheses are standarddeviations.ER = emergency room (post resuscitation); GCS = Glasgow coma score; ISS = injury severity score; GR = good recovery; MD = moderate disability;SD = severe disability; V = vegetative.

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Fluidadministration

41 42 43

Time after admission (h)Figure 2 SjvO2 recordingfrom a patient who developedjugular venous desaturation as

result ofsystemic hypotension after a small dose offrusemide (furosemide) had been givenAs the blood pressure gradually decreasedfrom 100 to 75 mmHg, the SjvO2 alsodecreased. Both the MAP and the SjvO2 normalised when intravenous fluid was given.ETCO2 = end tidal CO2.

normal after normalising PCO2. The otherpatient had acceptable SjvO, and CBF valuesat a PCO2 of 3-3 kPa (25 mmHg). Monitoringof SjvO, allowed identification of thosepatients who might have been adverselyaffected by hyperventilation. Although not allpatients were hyperventilated in the presentseries, 21 episodes of hypocapnia-induceddesaturation were identified in 19 of the 116patients.

Although conventional teaching has beenthat a CPP of 50 mmHg is normal, recent

studies have suggested that a CPP level of 70or even 80 mmHg may be desirable in headinjured patients.14151718 In addition, the opti-mal CPP may vary from patient to patient.Figure 2 illustrates a patient who developeddesaturation when his MAP fell from 95 to

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Figure 3 Patients with a reduced CBF had twice theincidence of one or multiple episodes ofjugulardesaturation, compared to patients with a normal or

elevated CBF.

75 mmHg after a dose of frusemide(furosemide) was given. Although the CPPremained >60 mmHg, the SjvO, dropped tobelow 50%. The MAP and SjvO, values nor-malised with fluid administration.

RELATIONSHIP OF JUGULAR VENOUSDESATURATION AND CEREBRAL BLOOD FLOW

Twenty (17%) of the patients had a reducedCBF, averaging 0-352 (SD 0-083) ml/g perminute; 65 (56%) had an elevated and 31(27%) a normal CBF, averaging 0-606 (SD0-124) ml/g per minute and 0-422 (SD 0 90)ml/g per minute, respectively. As shown infigure 3, patients with a reduced CBF weretwice as likely to have episodes of jugularvenous desaturation as patients with a normalor elevated CBF. Fourteen (70%) of the 20patients in the reduced CBF group had eithersingle or multiple episodes of desaturation,compared with nine (29%) in the normalCBF group, and 22 (34%) in the elevatedCBF group.

RELATIONSHIP OF JUGULAR VENOUSDESATURATION AND NEUROLOGICAL OUTCOMEForty (34 5%) of the patients had afavourable outcome three months after injury(20 = good recovery, 20 = moderate disabil-ity); 40 (34 5%) survived with a severe dis-ability (n = 26) or were vegetative (n = 14),and 36 (31%) died. The incidence of jugularvenous desaturation was strongly associatedwith neurological outcome (fig 4). The mor-tality rate of patients with no episodes ofdesaturation was 17%, compared to 41% inpatients with one desaturation, and 68% inthose with multiple desaturations. Thepercentage of patients with a poor neurologi-cal outcome (GOS of severe disability, vegeta-tive, or dead) was 55% in patients with nodesaturation, 74% in those with one desatura-tion, and 89-5% in those with multipledesaturations.The total duration of time that SjvO, was

less than 50% was significantly longer(p = 0 002) in the patients who died than inthe patients who survived. The total durationof all the episodes of desaturation averaged

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Figure 4 Occurrence ofjugular venous desaturation was

strongly associated with a high mortality rate and a pooroutcome; 3 month Glasgow outcome scale: O good recoverylmoderate disability; X severe disabilitylvegetative; * dead.

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Table 2 Systemic physiological variables that were examinedfor an effect on the relationship between desaturations and outcome

Number of desaturations Three month Glasgow outcome score

None One Multiple p value* GRIMD SDIV Dead p value*

Number of patients 70 27 19 40 40 36BP (mmHg)Mean 93 (7) 91 (10) 85 (11) 0-005 94 (7) 94 (7) 85 (11) <0-001Lowest 68 (9) 63 (14) 60 (13) 0-010 70 (8) 69 (10) 57 (12) <0-001

PaO,(mean) (mmHg) 173 (39) 184 (46) 160 (39) 0-138 174 (44) 170 (36) 177(45) 0-748

PaCO,(mean) (mmHg) 32 (4) 30 (3) 31 (3) 0-046 32 (4) 32 (4) 29 (2) 0-001

Haemoglobin(mean) (g/dl) 10-8 (2-1) 10.1 (1-8) 10-6 (1-8) 0 390 10-6 (2 0) 10-7 (2 0) 10-4 (1 9) 0-802

TemperatureMean (°C) 100-5 (6) 100-2 (0 7) 100-1 (1-0) 0-068 100-4 (0 6) 100-6 (0-5) 100-0 (0 9) <0-001Highest 103-0 (0-1) 102-9 (0-2) 102-7 (0 3) 0-613 102-7 (0-1) 103-1 (0 2) 102-9 (0 2) 0-166

*p value is for analysis of variance. Values in parentheses are standard deviations. BP = mean blood pressure; PaO, = arterial PO2; PaCO, = arterial PCO.

1-3 (SD 1 6) hours in the patients who died,compared to 04 (SD 0-8) hours in patientswith a good recovery or moderate disability,and 0-4 (SD 1 1) hours in patients who had a

severe disability or were vegetative.

RELATIONSHIP OF OTHER FACTORS TONEUROLOGICAL OUTCOMEMany factors have been associated with out-come after severe head injury, including age,severity of injury, type of injury, presence ofsystemic injuries, severity of intracranialhypertension, and level of CBF. The relation-ship of the demographic factors to neurologicaloutcome in the 116 patients are summarisedin table 1. Age was not significantly associatedwith outcome, although there was a trend forthe patients with a favourable outcome to beyounger.The severity of injury was examined in the

emergency room by using the best GCS andpupillary reactivity on day 1 after injury. TheGCS after resuscitation in the emergencyroom was not significantly associated withneurological outcome, but the best GCS on

day 1 after injury had a strong relationship tooutcome, averaging 8-1 (SD 2.3) in patientswith a favourable outcome, compared to 6-5(SD 2.7) in patients with a poor outcome, and5-5 (SD 2-2) in patients who died. Pupillary

size and reactivity in the emergency room andon day 1 were strongly related to outcome.Patients who died of their head injury had a

higher incidence of one or both pupils beingdilated and unreactive.

Sixteen (14%) of the patients had a gun-shot wound to the head and 100 (86%) hadclosed head injuries. The type of closed headinjury was classified as described by theTraumatic Coma Data Bank group.19 Thirty-eight (38%) of the patients with closed headinjuries had one of the four categories of dif-fuse injury (6-I, 19-II, 1 1 -III, and 2-IV).Fifty-four (54%) had evacuated haematomasof at least 25 ml in volume, and eight (8%)had unevacuated haematomas. The neuro-

logical outcome of patients with diffuselesions was significantly better than for thosewith haematomas and gunshot wounds.Twenty-one (55%) of the 38 patients with dif-fuse lesions had a favourable outcome com-

pared to only 16 (26%) of the 62 patients withhaematomas and three (19%) of the 16patients with gunshot wounds. The mortalityrate was 16% in patients with diffuse injuries,43-5% in those with haematomas, and 19% inthose with gunshot wounds.The injury severity score (ISS) was used to

assess whether multiple systemic injuries wereassociated with neurological outcome. An ISS

Table 3 Cerebral physiological variables that were examinedfor an effect on the relationship between desaturations and outcome

Number of desaturations Three month Glasgow outcome score

None One Multiple p value* GR/MD SD/V Dead p value*

Number of patients 70 27 19 40 40 36ICP (mmHg)Mean 17 (6) 22 (9) 21 (12) 0-008 15 (5) 16 (5) 25 (10) <0-001Highest 35 (12) 47 (22) 43 (24) 0-009 33 (11) 34 (11) 53 (23) <0-001

CPP (mmHg)Mean 76 (9) 70 (17) 64 (20) 0-003 78 (7) 78 (9) 60 (17) <0 001Lowest 48 (14) 33 (28) 33 (30) 0-001 53 (10) 49 (15) 22 (26) <0-001

CBF (ml/g per min)Mean 0-523 (0-146) 0-516 (0-147) 0-464 (0-178) 0-314 0 544 (0-163) 0-530 (0-148) 0-456 (0-130) 0-024Lowest 0-459 (0-156) 0 415 (0-140) 0-429 (0-186) 0-421 0-465 (0-163) 0-433 (0-155) 0-434 (0-157) 0 590

SjvO5 (%)Mean 71 (6) 69 (7) 68 (5) 0 059 69 (5) 70 (5) 71 (7) 0-325Lowest 50 43(1) 34 (2) <0-001 51 (7) 50 (9) 45 (13) 0-027No oftimes <50% 0 1 >1 0 3 (0 6) 0 4 (0 7) 1 0 (0 8) <0-001Time <50% (h) 0 1 4 (0 3) 1-9 (0-4) <0-001 0-4 (1 1) 0-4 (0-8) 1-3 (1-6) 0-002

CMRO, (umol/g per min)Mean 1-00 (0 39) 1-09 (0 53) 0-94 (0 30) 0 433 1-12 (0-41) 1-03 (0 43) 0-86 (0 35) 0-017Lowest 0-62 (0-28) 0-69 (0 47) 0-54 (0-29) 0-340 0-73 (0 35) 0-61 (0 32) 0 52(0 30) 0-017

CVR (mmHg/ml per 100 gper min)Mean 1 94 (0 58) 1-57 (0 50) 1-79 (0-75) 0-480 1-65 (0 49) 1-73 (0-67) 1-56 (0-61) 0-491

*p value is for analysis of variance. Values in parentheses are standard deviations. ICP = intracranial pressure; CPP = cerebral perfusion pressure; CBF = cerebralblood flow; SjvO, = jugular venous oxygen saturation; CMRO, = cerebral metabolic rate of oxygen; CVR = cerebral vascular resistance.

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Table 4 Final logistic regression modelfor poorneurological outcome (severe disability, vegetative, or deadthree months after injury) as dependent variable

OddsVanablelCategory ratio p value

Number of desaturations 0-0348 (overall variable)Multiple 14-46 0-012One 2-09 0-289None 1-00

Type of injury 0-0652 (overall variable)Gunshot wound 4-39 0-253Closed head injury-hematoma 4-60 0-021

Closed head injury-diffuse 1-00

Day 1Glasgow coma score 0-0025 (overall variable)

3-5 41-79 0 0006-8 861 00059-15 1-00

Pupillary reactivityOne or both dilated

and unreactive 21-55 0-052Neither unreactive 1-00

Highest temperature(per °F increase) 2-23 0-023

Lowest cerebral perfusionpressure (per mmHg

increase) 0 94 0-004Age (per year increase) 1-06 0-017

of 25 indicates the presence of only a severehead injury. The presence of systemic injuriesincreases the score, depending on their sever-ity. The ISS was not significantly related toneurological outcome.The relationships of the physiological vari-

ables to outcome are listed in tables 2 and 3.The mean and the highest recorded ICP val-ues, the mean and the lowest blood pressurevalues, the mean and the lowest CPP values,the mean PaCO2, and the mean temperaturewere all significantly related to outcome. Themean CBF was lower in patients who died.The mean and the lowest cerebral metabolicrate of oxygen (CMRO2) values were signifi-cantly lower in the patients who died.

Logistic regression analysisTo determine whether the difference in neu-

rological outcome with jugular desaturationreflected the effect of other co-variates, logis-tic regression analysis was used as describedabove. The final best fit model is shown intable 4. When the effect of jugular desatura-tion was adjusted for all other co-variateswhich were found to be significant, includingage, severity of injury (day 1 GCS and pupil-lary reactivity), type of injury (CT category),lowest recorded CPP, and highest recordedtemperature, the incidence of jugular desatu-ration was still significant (p = 0 03). A singleepisode of desaturation resulted in a doublingof the probability of a poor outcome, andmultiple episodes of desaturation were associ-ated with a 14-fold higher probability of a

poor outcome.

DiscussionAlthough the critical level for SjvO2, belowwhich the brain is ischaemic, has not beenestablished definitely, a few studies suggestthat an SjvO2 value of <50% can be related tocerebral ischaemia. Continuous monitoring of

oxygen saturation in the lateral sinus, duringcarotid endarterectomy in 50 patients,revealed that cerebral dysfunction was foundin patients with a venous oxygen saturation(SvO,) <50%, and there were no cases of dys-function when SvO, remained at least 60%.2°EEG slowing appeared when jugular venousPjvO,) fell to <2-5 kPa (19 mmHg) (an SjvO2value of about 40%) in 19 healthy volun-teers.2' Neurological deterioration occurred inhead injured patients when the SjvO2 valuewas <30% for more than 10 minutes.22The critical duration of ischaemia neces-

sary to produce injury is not known, butexperimental studies suggest that briefepisodes of ischaemia can be injurious, partic-ularly if they are repeated. Cerebral oedemaand brain tissue injury were more severe ingerbils sacrificed 24 hours after three separatefive-minute periods of bilateral carotidocclusion at one-hour intervals than in ani-mals which received a single 15-minuteocclusion.2'25

There are several limitations to themethodology of the present study whichmight have underestimated the actual inci-dence of cerebral ischaemia. SjvO2 values area measure of global cerebral oxygenation, andsignificant regional ischaemia can occur in thepresence of a normal SjvO2 value. Systemicinsults on admission to the hospital have beenshown to increase mortality rate approxi-mately twofold.3426 Andrews et al27 found asignificant incidence of secondary insults dur-ing within hospital transfers of head injuredpatients. Insults before admission and duringtransfer were not monitored in the presentstudy. Very low CBF values, suggestingischaemia have been described after a severehead injury, but only commonly within thefirst eight hours.28 29 The average start time ofSjvO2 monitoring in the present study was 17hours after admission.The present study demonstrates that

episodes of jugular venous desaturation arecommon during the first five days after severehead injury, and that these episodes are theresult of both systemic and cerebral causes,some of which are treatable. The occurrenceof jugular venous desaturation is stronglyassociated with a poor neurological outcome.Although a cause and effect relationship withoutcome cannot be established in the presentstudy, it is reasonable to hypothesise thatmonitoring SjvO2 might allow early identifica-tion and therefore treatment of a number ofcauses of secondary injury to the brain.

This work was supported by United States Public HealthService Grant PO1-NS27616.

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