External Ventricular Catheter Placement: How to Improve.

This cadaveric study outlines the efficiency, safety and precision of cerebral ventricular catheter placement comparing classical freehand technique using anatomical landmarks, neuronavigation and XperCT-guided assistance.

Cerebral metabolism and intracranial hypertension in high grade aneurysmal subarachnoid haemorrhage patients.

We evaluated the effect of intracranial hypertension on cerebral metabolism in patients with high grade aneurysmal subarachnoid hemorrhage (SAH) using bedside cerebral microdialysis (MD). Thirty-six patients with SAH were studied and classified into two groups (intracranial pressure, ICP > 20 mmHg, n = 25) and (ICP < 20 mmHg, n = 11). ICP was monitored hourly using an intraventricular drainage (n = 36). The MD catheter was placed after aneurysm clipping into the vascular territory of interest and was perfused with Ringer's solution (0.3 microl/min). The MD samples were collected hourly for measurements of glucose, lactate, and glutamate (CMA 600, Sweden). Lactate/pyruvate ratio was also calculated. To calculate group specific differences, the 24 hours median values of the first 7 days after SAH were compared. Differences were considered statistically significant at P < 0.05. Patient groups were comparable for age, severity of SAH, Fisher's grade and duration of MD sampling. In patients with ICP > 20 mmHg from day 1 to 7 after SAH, extracellular concentrations of glucose were significantly lower, while the lactate/ pyruvate ratio was higher compared to SAH patients with normal ICP values. The differences between groups in glutamate levels was only significant on day 1 after SAH due to high inter-individual differences. We concluded that intracranial hypertension in associated with an anaerobic cerebral metabolism indicated cerebral ischemia in high grade SAH patients.

Relation of cerebral energy metabolism and extracellular nitrite and nitrate concentrations in patients after aneurysmal subarachnoid hemorrhage.

In a prospective clinical investigation on neurochemical intensive care monitoring, the authors' aim was to elucidate the temporal profile of nitric oxide metabolite concentrations-that is, nitrite and nitrate (NO(x))--and compounds related to energy-metabolism in the cerebral interstitium of patients after aneurysmal subarachnoid hemorrhage (SAH). During aneurysm surgery, microdialysis probes were implanted in cerebral white matter of the vascular territory most likely affected by vasospasm. Temporal profiles of NO(x) were analyzed in a subset of 10 patients (7 female, 3 male, mean age = 47 +/- 14 years). Microdialysis was performed for 152 +/- 63 hours. Extracellular metabolites (glucose, lactate, pyruvate, glutamate) were recovered from the extracellular fluid of the cerebral parenchyma. NO(x) was measured using a fluorometric assay. After early surgery, SAH patients revealed characteristic decreases of NO(x) from initial values of 46.2 +/- 34.8 micromol/L to 23.5 +/- 9.0 micromol/L on day 7 after SAH (P < 0.05). Decreases in NO(x) were seen regardless of development of delayed ischemia (DIND). Overall NO(x) correlated intraindividually with glucose, lactate, and glutamate (r = 0.58, P < 0.05; r = 0.32, P < 0.05; r = 0.28, P < 0.05; respectively). After SAH, cerebral extracellular concentrations of NO metabolites decrease over time and are associated with concomitant alterations in energy-or damage-related compounds. This could be related to reduced NO availability, potentially leading to an imbalance of vasodilatory and vasoconstrictive factors. On the basis of the current findings, however, subsequent development of DIND cannot be explained by a lack of vasodilatory NO alone.

Role of bedside microdialysis in the diagnosis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

OBJECT: Ischemia due to vasospasm is a feared complication in patients following aneurysmal subarachnoid hemorrhage (SAH). Cerebral online microdialysis monitoring may detect the metabolic changes in the extracellular fluid associated with ischemia. The aims of the present study were to correlate clinical course, microdialysis-recorded data, transcranial Doppler (TCD) ultrasonography findings, and angiographic findings in patients with SAH. METHODS: In 60 patients a microdialysis catheter was inserted into the brain parenchyma that is most likely to be affected by vasospasm directly after aneurysm clipping. Hourly analyses of glucose, pyruvate, lactate, and glutamate levels were performed using a bedside device. Blood-flow velocities were obtained using serial TCD measurements. Cerebral angiography was routinely performed on Day 7 after aneurysm clipping or earlier in cases of clinical deterioration (30 patients). In all patients the results of microdialysis monitoring, TCD ultrasonography, and angiography were correlated. The mean duration of monitoring was 7.3+/-2.5 days. In patients with acute ischemic neurological deficits (18 patients) immediate microdialysis-recorded alterations were observed if the probe was placed close to the malperfused region. In 13 of 15 patients with symptomatic vasospasm (delayed ischemic neurological deficit [DIND]), the microdialysis-recorded values revealed secondary deterioration. In terms of confirming DIND, microdialysis had the highest specificity (0.89, 95% confidence interval [CI] 0.78-1) compared with TCD ultrasonography (0.63, 95% CI 0.46-0.8) and angiography (0.53, 95% CI 0.35-0.7). For microdialysis, the positive likelihood ratio was 7.8, whereas this was significantly lower for TCD ultrasonography (1.7) and angiography (2.1). CONCLUSIONS: Although angiography also demonstrates vessel narrowing in asymptomatic patients, online microdialysis reveals characteristic metabolic changes that occur during vasospasm. Thus, online microdialysis may be used to confirm the diagnosis of vasospasm.

Detection of secondary insults by brain tissue pO2 and bedside microdialysis in severe head injury.

We evaluated bedside cerebral on-line microdialysis for early detection of cerebral hypoxia in patients with traumatic brain injury. 24 severely head injured patients (Glasgow Coma Score < or = 8) were studied. Patients underwent continuous brain tissue PO2 (PtiO2) monitoring using the LICOX (GMS mbH, Germany) microcatheter device. The catheter was placed into the non-lesioned frontal white matter within 32.2 (7-48) hrs post injury. The microdialysis catheter (CMA 100, Sweden) was placed close to the PtiO2 probe via a 2- or 3-way skull screw, connected to a pump and perfused with Ringer solution (0.3 microliter/min). The microdialysis samples were collected hourly and analyzed at the bedside for glucose, lactate, lactate-pyruvate-ratio and glutamate (CMA 600, Sweden). We identified 252 episodes of impending hypoxia (PtiO2 < 15 mm Hg; 11,810 minutes) and 38 episodes of cerebral hypoxia (PtiO2 < 10 mm Hg; 1996 minutes). Before cerebral hypoxia, glucose decreased significantly. Glutamate was unchanged when no hypoxia or impending hypoxia occurred but increased 3-4 fold before a hypoxic episode appeared. We conclude that early metabolic detection of cerebral hypoxia before a critical decrease in brain tissue PtiO2 is seen and possibly allows earlier changes in treatment (e.g. reduction of hyperventilation therapy).

Temporal profiles of extracellular nitric oxide metabolites following aneurysmal subarachnoid hemorrhage.

The temporal profile of nitric oxide metabolite concentrations i.e. nitrite and nitrate (NOx) was investigated in brain parenchyma of patients following aneurysmal subarachnoid hemorrhage (SAH). In a subset of ten patients (7F/3M, age: 47 +/- 14 yrs) included in a prospective clinical trial on neurochemical intensive-care monitoring, microdialysis (MD) probes (CMA70, Sweden) were implanted at time of aneurysm surgery. Samples from patients clipped electively (n = 3) were considered "normal" in regard to SAH patients (n = 7). MD was performed for 162 +/- 63 hrs. NOx was measured off-line using a highly sensitive, fluorometric assay (2-3-diaminonaphtalene, DAN). NOx concentrations determined from electively operated patients averaged 36.7 +/- 9.6 microM (n = 59, pooled data). Regardless of the development of delayed ischemic neurological deficits (DIND), SAH patients showed a specific temporal profile of NOx consisting of an initial peak followed by an exponential decay. In detail, NOx decreased from initial values of 46.2 +/- 34.8 microM to 23.5 +/- 9.0 microM on day 6-7 after SAH (p < 0.05). Following SAH extracellular concentrations of NO metabolites decrease over time. This is in agreement with hypothetical NO scavenging by products of hemolysis. However, subsequent development of DIND cannot be explained by a lack of vasodilatory NO alone.

Mannitol decreases ICP but does not improve brain-tissue pO2 in severely head-injured patients with intracranial hypertension.

Little is known about the effect of post-traumatic mannitol infusion on cerebral metabolism and oxygenation. The purpose of this study was to investigate the effects of mannitol in comatose patients on PtiO2, PtiCO2 and brain tissue pH using Clark-type electrodes implanted into cerebral white matter. In the neurosurgical intensive care unit PtiO2, PtiCO2, brain tissue pH, arterial blood pressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and jugular bulb oxygen saturation (SjvO2) were prospectively studied in eleven patients with severe traumatic brain injury (TBI) during a total of 30 mannitol administrations (125 ml of 20% Mannitol infused over 30 min through a central vein). When the initial ICP before mannitol infusion was below 20 mmHg neither ICP nor any of the other parameters changed significantly during or after mannitol infusion. With a pre-infusion ICP above 20 mmHg a significant effect was seen on ICP (decrease from 23 +/- 1 to 16 +/- 2 mmHg at 60 min) and CPP (increase from 68 +/- 2 to 80 +/- 3 mmHg at 120 min). These effects were not reflected in PtiO2 or SjvO2, which were 29 +/- 4 mmHg and 61 +/- 3%, respectively, at the beginning of mannitol injection and remained unchanged during the observation period. PtiCO2 and brain tissue pH were not affected by mannitol infusion. Future studies should focus on the identification of ICP or CPP thresholds where infusion of mannitol may actually improve O2-supply to the brain.

Influence of hyperventilation on brain tissue-PO2, PCO2, and pH in patients with intracranial hypertension.

A harmful effect of prolonged hyperventilation on outcome has been shown in comatose patients after severe head injury. The purpose of this study was to assess the acute effect of moderate hyperventilation for treatment of intracranial hypertension (ICP < 20 mmHg) on invasively measured brain tissue-PO2 (PtiO2), PCO2 (PtiCO2) and pH (tipH) in severely head injured patients. 15 severely head injured patients (GCS < or = 8) were prospectively studied. Intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP), endtidal CO2 (ETCO2), PtiO2, PtiCO2 and tipH (Paratrend or Licox microsensors) were continuously recorded using multimodal monitoring. Following a baseline period of 15 minutes, patients were hyperventilated for 10 minutes. Arterial blood gas analysis was done before, during and after hyperventilation. At least three hyperventilation maneuvers were performed per patient. For statistical analysis the Friedman test was used. Hyperventilation (paCO2: 32.4 +/- 0.6 to 27.7 +/- 0.5 mmHg) significantly reduced ICP from 25.3 +/- 1.5 to 14.2 +/- 1.9 mmHg (p < 0.01). As a consequence, CPP increased by 9.6 +/- 3.4 mmHg to 76.8 +/- 3.2 mmHg. Brain tissue PCO2 decreased from 37.5 +/- 1.3 to 34.6 +/- 1.2 while tipH increased from 7.13 to 7.16. In all patients, hyperventilation led to a reduction of brain tissue PO2 (PtiO2/Licox: 24.6 +/- 1.4 to 21.9 +/- 1.7 mmHg, n.s.; PtiO2/Paratrend: 35.8 +/- 4.3 to 31.9 +/- 4.0 mmHg, n.s.). In one case hyperventilation even had to be stopped after 7 min because the drop in brain tissue PO2 below 10 mmHg signalized imminent hypoxia. As well known, hyperventilation improves CPP due to a reduction in ICP. However, this does not ameliorate cerebral oxygenation as demonstrated by the decrease in PtiO2. This underlines that hyperventilation should only be used with caution in the treatment of intracranial hypertension.

Cerebral oxygenation in contusioned vs. nonlesioned brain tissue: monitoring of PtiO2 with Licox and Paratrend.

Brain tissue PO2 in severely head injured patients was monitored in parallel with two different PO2-microsensors (Licox and Paratrend). Three different locations of sensor placement were chosen: (1) both catheters into non lesioned tissue (n = 3), (2) both catheters into contusioned tissue (n = 2), and (3) one catheter (Licox) into pericontusional versus one catheter (Paratrend) into non lesioned brain tissue (n = 2). Mean duration of PtiO2-monitoring with both microsensors in parallel was 68.1 hours. Brain tissue PO2 varied when measured in lesioned and nonlesioned tissue. In non lesioned tissue both catheters closely correlated (delta Licox/Paratrend: mean PtiO2 < 5 mm Hg) after 20 hours post insertion. In pericontusional tissue PtiO2 was reduced relative to non lesioned tissue (delta lesioned/non lesioned: mean PtiO2: 10.3 mm Hg). In contusioned brain tissue PtiO2 was always below the "hypoxic threshold" of 10 mm Hg, independent of the type of microsensor used. During a critical reduction in cerebral perfusion pressure (< 60 mm Hg), PtiO2 decreased measured with both microsensors. Elevation of inspired oxygen fraction, normally followed by a rapid increase in tissue PO2, only increased PtiO2 when measured in pericontusional and nonlesioned brain. To recognize critical episodes of hypoxia or ischemia, PtiO2-monitoring of cerebral oxygenation is recommended in nonlesioned brain tissue.

Ibn Sina (Avicenna). Historical note.

Ibn Sina (often known by his last name in Latin, Avicenna; 980-1037 A.D.) was the most famous physician and philosopher of his time. His Canon of Medicine, one of the most famous books in the history of medicine, surveyed the entire medical knowledge available from ancient and Muslim sources and provided his own contributions. In this article the authors present a unique picture of the neurosurgical technique of Ibn Sina and briefly summarize his life and work.

Bedside microdialysis for early detection of cerebral hypoxia in traumatic brain injury.

OBJECT: The authors evaluated the use of bedside cerebral online microdialysis for the detection of impending and present cerebral hypoxia in patients who had sustained traumatic brain injury. METHODS: Thirty-five severely head injured patients (with Glasgow Coma Scale scores < or = 8) were studied. Patients underwent continuous brain tissue PO2 (PtiO2) monitoring. The PtiO2 catheter was placed into the unaffected frontal white matter within 32.2 hours postinjury (range 7-48 hours). The microdialysis catheter was placed close to the PtiO2 probe via a 2- or 3-way skull screw that was connected to a pump and perfused with Ringer's solution at 0.3 microl/minute. The microdialysis samples were collected hourly and analyzed at the bedside for glucose, lactate, lactate-pyruvate ratio, and glutamate. Data were analyzed for identification of episodes of impending (PtiO2 10-15 mm, Hg > 5-minute duration) and present cerebral hypoxia (PtiO2 10 mm Hg, > 5-minute duration). In 62% of the patients hypoxic episodes occurred and were most frequently associated with hyperventilation (p < 0.001). During impending hypoxia, extracellular glutamate concentrations were increased (p = 0.006) whereas energy metabolites remained stable. During cerebral hypoxia, the extracellular glutamate (p < 0.001) and lactate (p = 0.001) concentrations were significantly higher than during normal oxygenation, whereas the lactate-pyruvate ratio was only slightly increased (p = 0.088, not significant). CONCLUSIONS: The authors conclude that a PtiO2 below 10 mm Hg is critical to induce metabolic changes seen during hypoxia/ischemia. Early markers of cerebral hypoxia are increased levels of glutamate and lactate. Regional hypoxia is not always associated with anaerobic cerebral metabolism. In the future, this technology of bedside monitoring may allow optimization of the treatment of severely head injured patients.

Cerebral lactate correlates with early onset pneumonia after aneurysmal SAH.

Pneumonia is a significant medical complication following aneurysmal subarachnoid hemorrhage (aSAH). The aSAH may initiate immune interactions leading to depressed immunofunction, followed by an increased risk of infection. It remains unclear as to whether there is a possible association between cerebral metabolism and infections. Clinical and microdialysis data from aSAH patients prospectively included in the CoOperative Study on Brain Injury Depolarisations protocol Berlin were analyzed. Levels of glucose, lactate, pyruvate, and glutamate were measured hourly using microdialysis in the cerebral extracellular fluid. The occurrence of pneumonia (defined by positive microbiological cultures) and delayed ischemic neurological deficits (DIND) was documented prospectively. Eighteen aSAH patients (52.7 ± 10.7 years), classified according to the World Federation of Neurological Surgeons in low (I-III, n = 9) and high (IV-V, n = 9) grades, were studied. Eight patients (45%) experienced DIND, 10 patients (56%) pneumonia (mean onset day 2.6). Lactate was elevated at day 3 in infected patients (n = 9, median = 6.82 mmol/L) vs. patient without infections (n = 6, median = 2.90 mmol/L, p = 0.036). The optimum cut-off point to predict pneumonia at day 3 was 3.57 mmol/L with a sensitivity of 0.77, and a specificity of 0.66 (area under curve was 0.833 with p = 0.034). Lactate at day 7 was higher in DIND patients compared to no-DIND-patients (p = 0.016). Early elevated lactate correlated with occurrence of bacterial pneumonia, while late elevations with DIND after aSAH. Future investigations may elucidate the relationship between cerebral lactate and markers of immunocompetence and more detailed to identify patients with higher susceptibility for infections.

[Aneurysmal subarachnoid hemorrhage. Significance and complications]. / Aneurysmatische Subarachnoidalblutung. Bedeutung und Komplikationen.

Despite substantial improvement in the management of patients with aneurysmal subarachnoid hemorrhage (SAH), including early aneurysm occlusion by endovascular techniques and surgical procedures, a significant percentage of patients with SAH still experience serious sequelae of neurological or cognitive deficits as a result of primary hemorrhage and/or secondary brain damage. Available neuromonitoring methods for early recognition of ischemia include, among others, measurement of brain tissue O(2) partial pressure, brain metabolism with microdialysis and monitoring of regional blood flow. The triple-H therapy (arterial hypertension, hypervolemia and hemodilution) is the treatment of choice of a symptomatic vasospasm and leads to an enduring recession of ischemic symptoms, if initiated early after the onset of a vasospasm-linked ischemic neurological deficit. Further promising therapy approaches are the administration of highly selective ET(A) receptor antagonists and intracisternal administration of vasodilators in depot form. This review summarizes the major neurological and non-neurological complications following aneurysm occlusion. Possible neuromonitoring techniques to improve diagnosis and therapy for treatment of symptomatic vasospasm as well as extracranial complications are discussed.

Bedside-microdialysis for early detection of vasospasm after subarachnoid hemorrhage. Case report and review of the literature.

Continuous monitoring of cerebral metabolism would be desirable for early detection of vasospasm in SAH patients. Bedside-microdialysis, a new technique for on-line monitoring of cerebral metabolism, may reflect changes seen in cerebral vasospasm diagnosed by transcranial Doppler sonography (TCD). This report represents the first case of combined TCD monitoring and on-line microdialysis from the brain extracellular fluid in a SAH patient. A 48-year-old woman suffered subarachnoid hemorrhage grade IV according to Hunt and Hess. Angiography revealed an aneurysm of the left carotid artery. The aneurysm was clipped 45 hours after bleeding. The microdialysis catheter was inserted after aneurysm clipping into the white matter of the left temporal lobe. Sampling of microdialysates started immediately, analyzing time for glucose, lactate, pyruvate and glutamate was four minutes. Postoperatively, the patient was doing well and microdialysis and TCD parameters remained within normal range. On the third postoperative day a shift to anaerob metabolism (decrease of glucose, increase of lactate and the lactate-pyruvate ratio up to pathological levels) and an increase in glutamate was observed suggesting insufficient cerebral perfusion. The patient progressively deteriorated clinically. Vasospasm was diagnosed by TCD monitoring 36 hours after onset of ischemic changes monitored by microdialysis. After elevation of mean arterial blood pressure, TCD values and metabolic parameters normalized. Interestingly, the pathological changes in on-line microdialysis preceded the typical increase in blood flow velocity by TCD and the clinical deterioration. Our case suggests, that bedside-microdialysis may be useful for early detection of vasospasm and continuous surveillance of treatment and may be a new guide to treat ischemic neurological deficits following SAH.

Metabolic changes during impending and manifest cerebral hypoxia in traumatic brain injury.

The objective was to measure metabolic changes monitored by bedside microdialysis during impending and manifest hypoxia in traumatic brain injury. In 41 patients, a PtiO2-catheter (Licox; 1/min) was placed into non-lesioned frontal white matter together with a microdialysis catheter (CMA, hourly). Data were analysed for identification of episodes of impending (PtiO2 < 10 - 15 mmHg > 5 min) and manifest cerebral hypoxia (PtiO2 < 10 mmHg, > 5 min). In 69% of patients hypoxic episodes occurred, most frequently associated with hyperventilation (p < 0.001). During impending hypoxia, glutamate was increased (p = 0.03), while the energy metabolites remained stable. Manifest hypoxia was reflected by significant increases of glutamate (p = 0.007) and lactate (p = 0.044), but normal lactate-pyruvate ratios. We conclude that hyperventilation had a potential adverse effect on cerebral metabolism and was most frequently associated with cerebral hypoxia. A PtiO2 < 10 mmHg can induce metabolic changes with increase of glutamate and lactate. The presence of anaerobic cerebral metabolism probably depends on duration and severity of the hypoxic episode.

Neuroprotective effect of melatonin on cortical impact injury in the rat.

The pineal hormone melatonin is a highly efficient physiological scavenger of free radicals involved in secondary brain damage. A variety of experimental studies have demonstrated a neuroprotective effect for melatonin, based on its antioxidant activity. The purpose of the present study was to investigate the time-dependency and a possible protective effect of exogenous melatonin in the cortical impact model in rats. The protective effect was quantified determining contusion volume, brain edema and brain water content. 45 anesthetized male Sprague-Dawley rats (250-350 mg) were subjected to cortical impact injury of moderate severity (7 m/s, deformation 2 mm). Melatonin (100 mg/kg bw i.p.), or a vehicle was injected 20 min before trauma, immediately after, and 1 and 2 hours after trauma during daytime and nighttime. Posttraumatic lesion volume using hematoxylin-eosin staining, hemispheric swelling, brain water content, cerebral perfusion pressure and intracranial pressure 24 hours after injury were investigated. Melatonin, given during nighttime, significantly reduced contusion volume corresponding to a mean reduction of contusion volume of 27% (placebo, n = 7: 41.9 +/- 5.2 mm3, melatonin, n = 8: 30.5 +/- 4.2 mm3, p < 0.05). Given during daytime, the reduction in contusion volume was not significant (placebo, n = 8: 42.1 +/- 5.1 mm3, melatonin, n = 8: 35.9 +/- 2.2 mm3, reduction of 15%, p = 0.08, n.s.). Hemispheric swelling was unchanged by melatonin treatment. Mean arterial blood pressure and rectal temperature remained stable before and after the cortical impact injury and injection of melatonin. This study shows that melatonin significantly reduces contusion volume with major effects during night.

Multimodal monitoring in patients with head injury: evaluation of the effects of treatment on cerebral oxygenation.

BACKGROUND: Recently, invasive intensive care unit monitoring of cerebral oxygenation has become feasible. The purpose of this study was to investigate the effects of standard therapeutic interventions used in the treatment of intracranial hypertension on cerebral oxygenation and other physiologic parameters in comatose patients. METHODS: In the neurosurgical intensive care unit, Ptio2, and jugular bulb oxygen saturation (Sjvo2), arterial blood pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) were prospectively studied (0.1 Hz acquisition rate) with a multimodal monitoring system in 21 patients with severe traumatic brain injury during various treatment modalities: dopamine and mannitol infusion, head positioning, and induced arterial hypocapnia. RESULTS: For baseline CPP values below 40 mm Hg, dopamine infusion was more effective in decreasing ICP and improving Ptio2 and Sjvo2 than for initial CPP values above 60 mm Hg. Treatment with mannitol, although improving CPP and lowering ICP, did not affect Ptio2 and Sjvo2. CPP in this group, however, was always above 60 mm Hg. Forced hyperventilation to an end-tidal Pco2 of 21 mm Hg normalized ICP and CPP, but significantly reduced cerebral oxygenation. CONCLUSION: A CPP > 60 mm Hg emerges as the crucial factor guaranteeing sufficient brain oxygenation. Any intervention used to further elevate CPP does not improve cerebral oxygenation, to the contrary, forced hyperventilation even bears the risk of inducing brain ischemia.

Secondary insults in severe head injury--do multiply injured patients do worse?

OBJECTIVES: To study the occurrence of secondary insults and the influence of extracranial injuries on cerebral oxygenation and outcome in patients with closed severe head injury (Glasgow Coma Scale score < or =8). DESIGN: Two-year prospective, clinical study. SETTING: Two intensive care units in a level III trauma center. PATIENTS: We studied 119 patients. Eighty patients had severe head injury and were divided into two categories: "isolated" severe head injury patients (n = 36, Injury Severity Score <30), and severe head injury patients with associated extracranial injuries (n = 44, Injury Severity Score >29). Thirty-nine patients with extracranial injuries and no head injury served as the control group. INTERVENTIONS: After patients were admitted to the intensive care unit, we began continuous multimodal cerebral monitoring of intracranial pressure, mean arterial blood pressure, cerebral perfusion pressure, end-tidal Co2, brain tissue Po2 (Licox), jugular bulb oxyhemoglobin saturation in severe head injury patients, and mean arterial blood pressure in the control group. Targets of management included intracranial pressure <20 mm Hg, cerebral perfusion pressure >60 mm Hg, Paco2 > 30 mm Hg, control of cerebral oxygenation, and delayed surgery for non-life-threatening extracranial lesions. MEASUREMENTS AND MAIN RESULTS: Data were analyzed for critical thresholds. The occurrence of secondary insults (intracranial pressure >20 mm Hg, mean arterial blood pressure <70 mm Hg, cerebral perfusion pressure <60 mm Hg, end-tidal Co2 <30 torr, brain tissue Po2 <10 torr, jugular bulb oxyhemoglobin saturation <50%) was comparable in patients with isolated severe head injury and those with severe head injury with associated extracranial lesions (Abbreviated Injury Scale score < or =5). The duration of intracranial hypertension and arterial hypotension significantly correlated with an unfavorable outcome, independent of the Injury Severity Score. In patients with severe head injury, 1-yr outcome was 29% dead or vegetative, 17% severely disabled, and 54% moderate or good outcome. This was similar to patients with severe head injury and extracranial injuries (31% dead or vegetative, 14% severely disabled, and 56% moderate or good outcome) and was independent of the Injury Severity Score. Patients with no head injury had less secondary insults (mean arterial blood pressure <70 mm Hg, p <.01) and a better outcome compared with both severe head injury groups (p <.044). CONCLUSIONS: In patients with severe head injury who have targeted management including intracranial pressure- and cerebral perfusion pressure-guided therapy and delayed surgery for extracranial lesions, the occurrence of secondary insults in the intensive care unit and long-term neurological outcome were comparable and independent of the presence of extracranial lesions (Abbreviated Injury Severity level < or =5). A severe head injury is still a major contributor predicting an unfavorable outcome in multiply injured patients.