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Relationship between intracranial pressure monitoring and outcomes in severe traumatic brain injury patients.

Traumatic brain injury (TBI) is a major medical and socio-economic problem and is the leading cause of death and disability in young adults (1). In the United States, approximately 60,000 to 75,000 deaths (2-4) and 70,000 to 90,000 disabling injuries occur each year (5-7).

Intracranial hypertension is a common secondary brain insult that may occur in up to 70% of patients with severe TBI (8-10). Several studies have demonstrated a correlation between intracranial hypertension and poor outcome in patients with severe TBI (10-15). For several years, continuous monitoring of intracranial pressure (ICP) and therapies that lower it have been major components and the mainstay of management of patients with severe TBI.

In 2007, the Brain Trauma Foundation (BTF) published the third edition of "Guidelines for the Management of Severe Traumatic Brain Injury" which included "Indications for Intracranial Pressure Monitoring" (16). The BTF recommended that "ICP should be monitored in all salvageable patients with a severe TBI (Glasgow Coma Scale [GCS] score of 3 to 8 after resuscitation) and an abnormal computed tomography (CT) scan". Also, "ICP monitoring is indicated in patients with severe TBI with a normal CT scan if two or more of the following features are noted at admission: age over 40 years, unilateral or bilateral motor posturing, or systolic blood pressure <90 mmHg". These guidelines are based on Class II and III evidence, respectively; however, they have not been validated using either prospectively or retrospectively collected data.

There is contradicting evidence about whether ICP monitoring improves outcome. Several studies demonstrated that ICP monitoring reduces the overall mortality rate of severe TBI (11,17-23). However, other studies have not shown benefits from ICP monitoring (24-26). Moreover, a few studies have demonstrated that ICP monitoring was associated with worsening of survival (27,28). In the Cochrane database, a recent systematic review found no randomised controlled trials that can clarify the role of ICP monitoring in acute coma whether traumatic or non-traumatic (29).

The purpose of this study was to examine the relationship between ICP monitoring and outcomes in patients with severe TBI. We hypothesised that ICP monitoring may not be associated with a reduced mortality in patients with severe TBI.

MATERIALS AND METHODS

Setting

The study was conducted in a 21-bed, tertiary care medical-surgical and trauma intensive care unit (ICU) in an 800-bed teaching hospital in Riyadh, Saudi Arabia. The ICU, which admits more than 1000 patients per year, is run as a closed unit 24 hours a day, seven days a week, by in-house, full-time critical care board-certified intensivists (30). A consultant neurosurgeon is available 24 hours, seven days a week for definitive neurosurgical care. The rehabilitation process of patients with TBI starts in the hospital and is included in the hospital length of stay (LOS).

Study design

This is an observational, retrospective cohort study that was approved by the institutional review board.

Patients

From February 2001 to December 2008, all consecutive adult ([greater than or equal to] 18 years) patients with severe TBI were included in the study. Patients with a diagnosis of brain death upon admission to the ICU were excluded. All patients with severe TBI received a standardised ICU management in a protocol form based on the clinical practice guidelines published by the BTF recommendations. The protocol aimed to prevent secondary brain injuries and consequently cerebral ischemia, and included several items as follows: maintenance of oxygenation (Sp[O.sub.2] [greater than or equal to] 95%, or [P.sub.a][O.sub.2] [greater than or equal to] 80 mmHg) and normoventilation (eucapnia: [P.sub.a]C[O.sub.2] 35 to 40 mmHg) with endotracheal intubation and mechanical ventilation, maintenance of euvolaemia using normal saline to keep central venous pressure at 8 to 12 mmHg, maintenance of cerebral perfusion pressure (CPP) >60 to 70 mmHg if the patient had an ICP monitor or mean arterial pressure >80 to 90 mmHg if no ICP monitor was placed, using appropriate fluid management and administration of vasopressors, treatment of sustained intracranial hypertension (ICP >20 mmHg, for [greater than or equal to]5 minutes), transtentorial herniation or progressive neurological deterioration, with deepening of sedation, treatment of a reversible physiological abnormalities, drainage of cerebrospinal fluid if ICP monitoring was in place, osmotic therapy using mannitol or hypertonic saline solution, acute hyperventilation, hypothermia, or muscle relaxation, as appropriate, maintenance of serum osmolarity >290 mOsm and serum sodium >145 mmol/l, prophylaxis of early post-traumatic seizure using phenytoin for seven days, maintenance of analgesia and sedation using appropriate opioids and sedatives, prevention and treatment of hyperthermia (T >36.5[degrees]C), maintenance of blood sugar between 5 and 10 mmol/l, maintenance of the head of the bed elevated at 30[degrees] (unless contraindicated), nutritional support with early enteral feeding, stress ulcer prophylaxis and thromboembolic prophylaxis as appropriate. This protocol was implemented in February 2001 and was associated with a significant improvement in patients' outcomes as published elsewhere (31). However, the decision for the insertion of an ICP monitor was at the discretion of the consultant neurosurgeon, based on their clinical judgment, with trend towards less use of ICP monitoring over the years due to change of neurosurgeons and individual preferences. The ICP monitor used was solely intraventricular and was kept in place for [less than or equal to] seven days. A daily cerebrospinal fluid sample was sent for study of the diagnosis of meningitis/ventriculitis.

Data collection

The following data was collected by a full-time dedicated data collector: patients' demographics including age and gender; Acute Physiology and Chronic Health Evaluation (APACHE) II (32) score; GCS (33) score; Injury Severity Score (34); associated injuries; admission category (non-operative vs postoperative); and the presence of ICP monitoring. The main exposure in the study was the presence of an ICP monitor. The primary outcome was hospital mortality, and the secondary outcomes were ICU mortality, mechanical ventilation duration, need for tracheostomy and ICU and hospital LOS.

Statistical analysis

The Statistical Analysis Software (SAS, Release 8, SAS Institute Inc., Cary, NC, 1999, USA) was used for statistical analysis. Continuous variables were summarised by providing the mean and standard deviation ([+ or -] SD) and compared using the independent sample Student's t-test. Categorical variables were expressed as absolute and relative frequencies and compared using the chi-square test. To assess the association between ICP monitoring and the different outcomes while controlling for potentially confounding variables (age, APACHE II, GCS, isolated TBI and operative status), we carried out stepwise multivariate logistic regression analyses, where the adjusted odds ratio (aOR), 95% confidence interval (CI) and P value were reported. For the selection purposes of the model, a P value of 0.1 was selected for entry into the model, whereas a P value of 0.2 was selected for staying in the model. Relationship between ICP monitoring and hospital mortality was examined based on the severity of TBI by stratifying the patients according to their admission GCS score (GCS 3 to 4, GCS 5 to 6, and GCS 7 to 8), and by carrying out stepwise multivariate logistic regression analysis controlling for the same variables mentioned above. A P value of [less than or equal to]0.05 was considered statistically significant.

RESULTS

Baseline characteristics

Four hundred and seventy-seven patients were included in the study (ICP monitoring=52, no ICP monitoring=425). There were no group differences in age, gender, APACHE II, GCS, Injury Severity Score or isolated TBI. Also, there was no difference in the presence of associated injuries; including chest, abdomen, ortho/soft tissue, other head/neck, spinal or vascular. However, because in our institution ICP monitoring is routinely performed in the operating room, there were more postoperative patients in the ICP group. The baseline characteristics of both the ICP monitoring group and no ICP monitoring group are summarised in Table 1.

Outcomes

Crude analysis showed that ICP monitoring, compared with no ICP monitoring, was not associated with significant difference in hospital or ICU mortality (21.2 vs 15.3%, P=0.28; 13.5 vs 11.5%, P=0.68, respectively). However, ICP monitoring was associated with a significant increase in mechanical ventilation duration (15.8[+ or -]8.8 vs 10.7 [+ or -] 7.6, P <0.0001), need for tracheostomy (59.6% vs 41.7%, P=0.01), and ICU LOS (17.0 [+ or -] 8.8 vs 11.6 [+ or -] 8.3, P <0.0001), with no significant difference in hospital LOS (86.7 [+ or -] 81.9 vs 78.4 [+ or -] 332.2, P=0.86). Multivariate logistic regression analyses were performed to adjust for potential confounding factors including, age, APACHE II, admission GCS, isolated TBI and postoperative status. After adjustment, ICP monitoring was not associated with a statistically significant difference in hospital or ICU mortality (aOR 1.71, 95% CI 0.79 to 3.70, P=0.17; aOR 1.01, 95% CI 0.41 to 2.45, P=0.99, respectively). ICP monitoring was associated with a significant increase in mechanical ventilation duration (coefficient 5.66, 95% CI 3.45 to 7.88, P <0.0001), need for tracheostomy (OR 2.02, 95% CI 1.02 to 4.03, P=0.04), and ICU LOS (coefficient 5.62, 95% CI 3.27 to 7.98, P <0.0001), with no significant difference in hospital LOS (coefficient 8.32, 95% CI -82.6 to 99.25, P=0.86). Table 2 summarises the crude and adjusted analyses of the association between ICP monitoring and different study outcomes. Hospital mortality, stratified by the admission GCS score and adjusted for the confounding factors, was significantly higher in the group of patients with GCS score 7 to 8 who underwent ICP monitoring as compared to those who did not (aOR=12.89, 95% CI 3.14 to 52.95, P=0.0004). However, there was no significant difference in hospital mortality in the group of patients with GCS score 5 to 6 (aOR 3.74, 95% CI 0.61 to 22.82, P=0.15), or GCS score 3 to 4 (aOR 0.51, 95% CI 0.17 to 1.59, P=0.25) (Table 3).

DISCUSSION

The main findings of our study were that the use of ICP monitoring in patients with severe TBI was not associated with reduced hospital mortality; it was, however, associated with a significant increase in mechanical ventilation duration, need for tracheostomy and ICU LOS, and with a significant increase in hospital mortality in the group of patients with GCS of 7 to 8.

ICP monitoring has become an integral part of the management of patients with severe TBI in many trauma centres in the USA and Europe. Based on physiological principles, the potential benefits of ICP monitoring include earlier detection of intracranial mass lesion, avoidance of indiscriminate use of therapies to control ICP, drainage of cerebrospinal fluid with reduction of ICP and improvement of CPP, and determination of prognosis. Although experts have advocated the use of ICP monitoring, there is considerable variation in the use of ICP monitoring among trauma centres (22,23,25).

Studies of ICP monitoring have yielded contradictory results. Several observational studies have demonstrated that ICP monitoring reduces the overall mortality rate of patients with severe TBI (11,17-23,35,36). In the 1980s, the introduction of routine ICP monitoring was associated with a reduction of the mortality rate to 28 to 36%35 compared to 50% observed in 1977 (36). In a prospective study of 233 patients with severe TBI, Saul et al documented that early aggressive treatment based on ICP monitoring significantly reduces the overall mortality rate of severe head injury (28 vs 46%; P <0.0005) (11). Lane et al retrospectively reviewed the data files from the Ontario Trauma Registry from 1989 to 1995 to examine the relationship between insertion of ICP monitors and outcomes after severe TBI. Of 9001 registered cases of TBI, 541 patients had an ICP monitor inserted. There was wide variation among the institutions in the rate of insertion of ICP monitors in these patients (ranging from 0.4 to over 20%). Multivariate analyses, controlling for multiple confounding factors, indicated that ICP monitoring was associated with significantly improved survival (P <0.015) (23). In a recent, prospective observational study of 50 severe TBI patients, Aarabi et al found that decompressive craniectomy for intracranial hypertension is associated with better outcomes in those patients that have a decrease in ICP (20). Bulger et al, in a retrospective analysis of US nationwide ICUs, found a decreased hospital mortality in patients who were managed in centres that use ICP monitoring routinely, however, with no significant difference in functional outcome (22).

Other studies have not shown beneficial effects from ICP monitoring. In an Austrian prospective, multicentre cohort study, the use of ICP monitoring was not associated with hospital outcome (24). Cremer et al conducted a retrospective cohort study with prospective assessment of outcome, to determine the effect of ICP monitoring on functional outcome. Three hundred and thirty-three severe TBI patients were managed at two different trauma centres (centre A and centre B) that differed in the use of ICP monitoring. One hundred and twenty-two patients were managed in centre A that did not monitor ICP but used empiric ICP-lowering treatment such as sedation and muscle relaxation, mannitol, hyperventilation and ventricular drainage. Two hundred and eleven patients were managed in centre B that used ICP monitoring in 142 (67%) of severe TBI patients and treated ICP significantly more except for hyperventilation and ventricular drainage which was equally used in both centres. There was no difference in in-hospital mortality between centre A and centre B (34 vs 33%, respectively; P=0.87) or in a 12-month favourable functional outcome (following ICP monitoring) (OR=0.95, 95% CI 0.62 to 1.44). Furthermore, ICP/CPP-targeted intensive care resulted in prolonged mechanical ventilation and increased levels of therapy intensity26. Patel et al conducted a retrospective study to document the effect of an ICP/CPP-guided protocol on outcome in acute head injury. They reported an improved functional status, however not a reduced mortality rate, in a post hoc subgroup of the most severe cases only (37).

Moreover, a few studies have demonstrated that ICP monitoring was associated with worsening of survival (27,28,38). Gelpke et al, in a comparison between the outcome distributions of two Dutch series of patients with severe head injuries, reported higher survival rates in centres with a more conservative management regimen compared with more 'aggressive' treatment (38). In a retrospective study, Shafi et al analysed The National Trauma Data Bank (1994 to 2001) of the American College of Surgeons. Inclusion criteria were: age [greater than or equal to] 20 to [less than or equal to] 50 years, blunt TBI and the following BTF criteria for ICP monitoring: GCS <8 and abnormal CT scan. A total of 1646 patients were included in the study. Patients who underwent an ICP monitoring (n=708, 43%) were compared with those who did not (n=938, 57%). There was no difference between the two groups in age, gender, admission GCS, systolic blood pressure or in presence or severity of associated injuries. After adjusting for multiple confounding factors, ICP monitoring was associated a 45% reduction in survival (OR=0.55, 95% CI 0.39 to 0.76, P <0.001), and a significant increase in complications including pneumonia (37 vs 23%, P <0.001), renal failure (2.7 vs 1.1%, P=0.02), and infections (39% vs 24%, P <0.001). Functional outcome, using modified functional independence measure (39) score, was significantly worse in patients who underwent ICP monitoring (functional independence measure 5.9 [+ or -] 0.16 vs 7.9 [+ or -] 0.14, P=0.000) (28).

ICP monitoring has been widely advocated for patients with severe TBI and has been a component of the evidence-based guidelines for the management of severe TBI (16). However, there are no randomised controlled trials that have been performed to establish the usefulness of ICP monitoring or that have demonstrated its effectiveness in improving outcome. Similar to some other studies, in our centre, ICP monitoring was used in only a minority of patients with severe TBI who met the current BTF criteria for monitoring, and when used, it was not associated with reduced mortality (24-26). However, it may be associated with worsening of outcomes including increase in mechanical ventilation duration, need for tracheostomy and ICU LOS (27,28). Moreover, in patients with GCS 7 to 8, ICP monitoring was associated with a significant increase in hospital mortality.

There may be several potential reasons for a worse outcome that we found associated with ICP monitoring. First, although there were no statistical differences in baseline characteristics or in indications for monitoring between the ICP- and no ICP-monitoring groups, it is likely that neurosurgeons chose to insert ICP monitoring in patients who, based on their clinical judgment, were at greater risk for mortality; such decisions would have been a significant unmeasured confounding factor. Second, false reading of high ICP (ICP >20 mmHg) may lead to indiscriminate use of therapies to control ICP that cause more harm than benefit. Third, aggressive ICP-lowering therapies may fail to control ICP in approximately one-fourth of patients (26). Fourth, successful lowering of ICP does not always consequently produce a similar improvement of cerebral physiologic homeostasis. It has been demonstrated that augmenting CPP does not significantly reverse hypoperfusion in pericontusional ischaemic areas (40) and is unpredictably effective in improving ICP, cerebral autoregulation and brain tissue oxygenation (41). Fifth, following a TBI when cerebral autoregulation is disturbed and the blood-brain barrier is disrupted, measures to maintain CPP >50 mmHg to prevent cerebral ischaemia may increase hydrostatic vasogenic oedema and aggravate intracranial hypertension (42). Sixth, interventions designed to decrease ICP and improve CPP may be misused, harmful or associated with complications. Hyperventilation, due to cerebral vasoconstriction, has been shown to decrease cerebral perfusion and cause cerebral ischaemia and has been shown to be associated with worse outcomes (43-45). Hyperosmolar therapy with mannitol, by causing osmotic diuresis, may cause hypovolaemia and result in episodes of arterial hypotension, which have been confirmed to significantly increase mortality in TBI patients (46-49). Aggressive fluid resuscitation, to improve CPP, may result in cardiopulmonary complications and has been reported to be associated with a five-fold increase in the incidence of acute respiratory distress syndrome with a targeted CPP >70 mmHg (50). Consequently, in 2003 the BTF issued an update notice, reducing the recommended treatment threshold for CPP to 60 mmHg (51). Inappropriate use of medications to lower ICP and improve CPP, such as high-dose infusions of propofol and vasopressors, has been reported to be associated with cardiac complications in severe TBI patients (52). Excessive use of sedatives and muscle relaxants to control intracranial hypertension may be associated with an increase in mechanical ventilation duration, incidence of ventilator-associated pneumonia and ICU LOS, all of which may contribute to increased mortality (53-55). Finally, complications related to placement and/or presence of the ICP monitoring such as haemorrhage or infection may have contributed to the increased mortality. The reported incidence of haemorrhagic complications after insertion of an ICP monitors range from 0 to 15% (56-58). The risk of infectious complications increases with increasing duration of catheterisation and with repeated insertions and ranges from 1.7 to 4% for intraparenchymal fibreoptic probes and from 6 to 19% for intraventricular catheters (25,59-62). Therefore, it is possible that the potential beneficial effects of ICP monitoring have been offset by the mechanisms suggested above.

In patients with an admission GCS of 7 to 8, ICP monitoring was associated with a significant increase in hospital mortality, while in patients with an admission GCS of 5 to 6 or 3 to 4, ICP monitoring was not associated with a statistically significant difference in hospital mortality. This suggests that the association between the ICP monitoring and the hospital mortality might be related to the GCS component of the indications for ICP monitoring and not to the ICP monitoring itself and that the current BTF guidelines do not identify patients who may benefit from ICP monitoring.

This study has a number of strengths, including the prospective nature of data collection by a fulltime dedicated data collector and the inclusion of all consecutive patients with severe TBI during the study period. As potential limitations, the study was conducted in a single centre, was retrospective in nature and has potentially unmeasured confounding factors such as CT scan findings. The number of patients who received ICP monitoring is small compared with patients who did not. The use of ICP monitoring was at the discretion of neurosurgeons based on their clinical judgment and the complications associated with ICP monitor placement, such as bleeding or infection, were not collected.

CONCLUSION

In patients with severe TBI, despite adjustment for key severity factors, ICP monitoring was not associated with improved patient outcomes. Moreover, adverse outcomes were suggested especially in patients with an admission GCS of 7 to 8. Although unmeasured factors influencing neurosurgeons' decisions to insert an ICP monitor probably account for some of our findings, a prospective randomised controlled trial of ICP-guided management is required to determine the group of patients with severe TBI who may benefit from ICP monitoring.

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S. HADDAD *, A. S. ALDAWOOD ([dagger]), A. ALFERAYAN ([double dagger]), N. A. RUSSELL ([section]), H. M. TAMIM **, Y. M. ARABI ([dagger][dagger]) Intensive Care Department, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia

* M.D., C.E.S., Section Head, Surgical Intensive Care Unit and Anaesthetist and Intensivist.

([dagger]) M.D., F.R.C.P.C., F.C.C.P., Deputy Chairman.

([double dagger]) M.D., F.A.C.H.A.R.Z.T., Section Head, Department of Neurosurgery.

([section]) M.D., F.R.C.P.(C), Consultant, Department of Neurosurgery.

** M.P.H., Ph.D., Assistant Professor.

([dagger][dagger]) M.D., F.C.C.P., F.C.C.M., Chairman.

Address for correspondence: Dr S. Haddad, Intensive Care Department, MC 1425, King Fahad National Guard Hospital, King Abdulaziz Medical City, PO Box 22490, Riyadh, 11426, Saudi Arabia.

Accepted for publication on June 19, 2011.
Table 1
Baseline characteristics

 ICP No ICP
 monitoring, monitoring,
 n=52 n=425

Age, mean [+ or -] SD, y 28.0 [+ or -] 11.3 29.3 [+ or -] 14.0
Male gender, n (%) 51 (98.1) 406 (95.5)
APACHE II, mean [+ or -] SD 20.6 [+ or -] 5.4 20.0 [+ or -] 5.8
Admission GCS, 4.5 [+ or -] 1.9 5.0 [+ or -] 1.9
mean [+ or -] SD
 GCS 3 to 4 31 (59.6) 200 (47.1)
 GCS 5 to 6 11 (21.2) 100 (23.5)
 GCS 7 to 8 10 (19.2) 125 (29.4)
ISS, mean [+ or -] SD 29.7 [+ or -] 11.8 30.0 [+ or -] 11.2
Isolated TBI, n (%) 15 (28.9) 102 (24)
Postoperative status, 24 (46.2) 82 (19.3)
n (%)
Associated injuries, n (%)
 Chest 23 (44.2) 201 (47.3)
 Abdomen 3 (5.8) 55 (12.9)
 Ortho/soft tissue 18 ( 34.6) 182 (42.8)
 Other head/neck 21 (40.4) 149 (35.1)
 Spinal 15 ( 28.9) 88 (20.7)
 Vascular 1 (1.9) 5 (1.2)

 P

Age, mean [+ or -] SD, y 0.51
Male gender, n (%) 0.39
APACHE II, mean [+ or -] SD 0.44
Admission GCS, 0.08
mean [+ or -] SD
 GCS 3 to 4 0.19
 GCS 5 to 6 0.19
 GCS 7 to 8 0.19
ISS, mean [+ or -] SD 0.83
Isolated TBI, n (%) 0.44
Postoperative status, <0.0001
n (%)
Associated injuries, n (%)
 Chest 0.68
 Abdomen 0.14
 Ortho/soft tissue 0.26
 Other head/neck 0.45
 Spinal 0.18
 Vascular 0.65

ICP=intracranial pressure, APACHE=Acute Physiology
and Chronic Health Evaluation, GCS=Glasgow Coma Scale,
ISS=Injury Severity Score, TBI=traumatic brain injury.

Table 2
Outcomes

ICP=intracranial pressure, OR=odds ratio, CI=confidence interval,
ICU=intensive care unit, LOS=length of stay.

 ICP monitoring, No ICP monitoring,
 n=52 n=425

Hospital mortality, n (%) 11 (21.2) 65 (15.3)
ICU mortality, n (%) 7 (13.5) 49 (11.5)
Tracheostomies, n (%) 31 (59.6) 177 (41.7)
Coefficient
 Mechanical ventilation 15.8 [+ or -] 8.8 10.7 [+ or -] 7.6
 duration, mean
 [+ or -] SD, d
 ICU LOS, mean [+ or -]
 SD, d 17.0 [+ or -] 8.8 11.6 [+ or -] 8.3
 Hospital LOS, mean
 [+ or -] SD, d 86.7 [+ or -] 81.9 78.4 [+ or -] 332.2

 Adjusted 95% CI P
 OR

Hospital mortality, n (%) 1.71 0.79-3.70 0.17
ICU mortality, n (%) 1.01 0.41-2.45 0.99
Tracheostomies, n (%) 2.02 1.02-4.03 0.04
Coefficient
 Mechanical ventilation 5.66 3.45-7.88 <0.0001
 duration, mean
 [+ or -] SD, d
 ICU LOS, mean [+ or -]
 SD, d 5.62 3.27-7.98 <0.0001
 Hospital LOS, mean
 [+ or -] SD, d 8.32 -82.61-99.25 0.86

Table 3
Hospital mortality stratified by the admission GCS

 ICP No ICP Adjusted
 monitoring monitoring OR

GCS 3 to 4, n (%) 4/31 (12.9) 49/200 (24.5) 0.51
GCS 5 to 6, n (%) 2/11 (18.2) 7/100 (7) 3.74
GCS 7 to 8, n (%) 5/10 (50) 9/125 (7.2) 12.89

 95% CI P

GCS 3 to 4, n (%) 0.17-1.59 0.25
GCS 5 to 6, n (%) 0.61-22.82 0.15
GCS 7 to 8, n (%) 3.14-52.95 0.0004

GCS=Glasgow Coma Scale, ICP=intracranial pressure, OR=odds ratio,
CI=confidence interval.
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Author:Haddad, S.; Aldawood, A.S.; Alferayan, A.; Russell, N.A.; Tamim, H.M.; Arabi, Y.M.
Publication:Anaesthesia and Intensive Care
Article Type:Report
Geographic Code:1USA
Date:Nov 1, 2011
Words:6042
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