Standardized management of intracranial pressure: a preliminary clinical trial.

OBJECTIVE: To test a standardized protocol for management of intracranial pressure (ICP) after severe head injury (i.e., traumatic brain injury), consistent with published guidelines. METHODS: We compared prospective use of a standardized protocol for ICP management in 12 patients with severe head injuries and retrospective ICP management using preprinted hospital orders in combination with ad hoc physician orders in 12 historical control patients with severe head injuries. With the standardized protocol, flow-chart decision logic diagrams were applied at patient bedside by critical care practitioners, with nursing shift review. RESULTS: ICP and its variation during the first 6 intensive care unit days was less for the standardized protocol- than for the preprinted order-managed group (p <0.001), indicating better process control with the standardized protocol. ICP exceeded 25 mm Hg for less time for the standardized protocol group (182 hours; 15+/-23 hours/patient) than for prescribed order group (429 hours; 36+/-28 hours/patient) (p = 0.03). On average, ICP exceeded 20 mm Hg for 2.3 days for the standardized protocol-managed group and for 4.7 days for the prescribed order-managed group. Cerebral perfusion pressure was significantly greater and its variation less for the standardized protocol- than for the preprinted order-managed group. Fewer interventions were made for ICP management for the standardized protocol- than for the preprinted order-managed patients (601 vs. 876), suggesting more effective nursing time using the standardized protocol. CONCLUSION: ICP management was more consistent, and intracranial hypertension was better controlled, in patients managed according to a standardized, data-driven protocol for escalation and weaning of therapies in response to immediate patient needs. We recommend computerized implementation and a randomized clinical trial to compare the protocol with prescribed orders.

Clinical trial of an ex vivo arterial blood gas monitor.

PURPOSE: The purpose of this study was to test the performance of a patient attached, on demand ex vivo arterial blood gas (ABG) monitor, and to compare the frequency of ABG analysis using the monitor, where the monitor was operated by intensive care unit (ICU) staff on shock trauma and neurosurgical intensive care patients for < or = 6 days, with standard clinical laboratory analysis. MATERIALS AND METHODS: The ABG monitor (SensiCath; Optical Sensors Inc., Minneapolis, MN) incorporates fiber optic pH, PCO2, PO2, and thermistor temperature sensors in a 0.3-mL sensor chamber that attaches in line with the patient's arterial pressure tubing and connects via a fiberoptic cable to a bedside instrument. The monitor and standard clinical laboratory performance were compared following an institutionally approved protocol. Adult ICU patients (n = 30) were studied for whom an arterial cannula was required, the expected ICU stay was > 72 hours, > or = 2 ABG analyses/day were anticipated, and informed consent had been obtained. Paired comparison ABG analyses and quality assurance checks were performed daily. The frequency of ABG analyses in this study, for which monitor values were used for clinical decision making, was compared with the frequency previously reported for the same ICUs, for which the monitor and laboratory results were compared but only the latter were used for clinical decision making. RESULTS: Five hundred ABG analyses, 436 over the first 72 hours, were obtained using the monitor for patient management over 3,248 patient hours (85 +/- 47 hours/patient). Monitor-laboratory comparison ABG analyses (n = 258) indicated stable performance over 6 days: For pH, the range of laboratory measurements was 7.200 to 7.540, accuracy (mean difference between monitor and laboratory measurement) was +0.013, and precision (standard deviation of difference between monitor and laboratory measurements) was +/-0.031. For PCO2, range: 18 to 78.5, accuracy: -0.8, precision: +/-3.4 mm Hg. For PO2, range: 41.0 to 344.0, accuracy: +2.3, precision: +/-12.8 mm Hg. The frequency of ABG analyses obtained using the monitor (ie, 15.0 +/- 11.6 ABGs/patient/72 hours) was significantly greater than that using the clinical laboratory (ie, 8.8 +/- 4.2 ABGs/patient/72 hours) (P = .01). CONCLUSION: The ABG monitor provides performance comparable to standard clinical laboratory analysis for < or = 6 days (< or = 144 hours), consistent with ICU arterial cannula changeout schedules. More frequent ABG analyses are obtained by critical care practitioners using the monitor compared with the clinical laboratory system, suggesting that clinical decision making based on ABG data may be limited by the frequency of ABG analysis.

Effects of injury and therapy on brain parenchyma pO2, pCO2, pH and ICP following severe closed head injury.

Simultaneous monitoring of brain parenchyma pO2, pCO2, and pH (PbO2, PbCO2 and pHb) has been tested in ICU environments using fiber optic sensors incorporated in probes 0.5 mm in diameter. An Institutionally approved protocol was used to test the concept and technology for monitoring PbO2, PbCO2 and pHb, and to observe the effects of injury and therapy interventions on each of the variables monitored, including ICP, the clinical standard. ICP and fiber optic pO2, pCO2 and pH probes were placed in 10 SCHI patients at bedside in the ICU using sterile technique. The probes remained in place for the duration of ICP monitoring, and were functional in the ICU environment for up to 10 days. Trend patterns recurred in this series of SCHI patients: Extreme PbCO2 (high) and pHb (low) are associated with poor perfusion; increasing pbCO2 and decreasing pHb may be early indicators of ICP crisis, i.e. ICP > 20 mm Hg that tends to be unresponsive to therapy, and; pentobarbital "loading" and maintenance is associated with increased pbO2. These preliminary results from monitoring pbO2, pbCO2 and pHb in SCHI patients indicate that fiber optic sensor technology functions and is able to be used in this application. Trend patterns from this data may further indicate practical utility as a more direct monitor of the delicate balance between tissue perfusion and cell metabolism than ICP alone.

Skeletal muscle PO2, PCO2, and pH in hemorrhage, shock, and resuscitation in dogs.

OBJECTIVE: To test fiber-optic PO2, PCO2, and pH sensors placed in skeletal muscle as monitors of hemorrhage, shock, and resuscitation, compared with mean arterial blood pressure, cardiac output, and blood gas variables. DESIGN: Observational study in physiology laboratory, using a canine controlled hemorrhagic shock model. MATERIALS AND METHODS: Mongrel dogs (20-35 kg; n = 10) were monitored with arterial, venous, and pulmonary artery catheters. A probe (0.5 mm in diameter) with fiber-optic PO2, PCO2, and pH sensors was placed percutaneously in the adductor muscle of the right medial thigh. Mean arterial blood pressure of 45 to 50 mm Hg was maintained for 1 hour with controlled hemorrhage, after which shed blood was reinfused. The animals were monitored for 4 hours after reinfusion. MEASUREMENTS AND MAIN RESULTS: Skeletal muscle PO2 (PmO2) decreased from 31+/-9 to 5+/-4 mm Hg during shock and recovered with reinfusion. Skeletal muscle pH (pHm) decreased from 7.24+/-0.10 to 6.94+/-0.12 during shock, to 6.90+/-0.13 with reinfusion, and recovered to near baseline 2 hours after reinfusion. PmCO2 increased from 48+/-14 to 134+/-86 mm Hg during shock, to 138+/-92 mm Hg with a time course inverse to pHm, and recovered to near baseline 30 minutes after reinfusion. On average, skeletal muscle PCO2 (PmCO2) and pHm did not recover to baseline, possibly indicating persistent anaerobic metabolic effects. O2 delivery, mixed venous PO2, mixed venous O2, saturation and PmO2 responded with similar time courses. CONCLUSION: PmO2, PmCO2, and pHm can be monitored simultaneously for several hours with fiber-optic sensors in a single, small probe. PmO2 may provide information comparable to O2 delivery. PmCO2 may reflect adequacy of perfusion. pHm may indicate success of resuscitation. This technology may offer new insight into the extent of injury and refinement of shock resuscitation and monitoring.

Current concepts in treatment of closed head injury.

Standards for management of severe closed head injury should help to establish a foundation for routine care and ongoing research. Studies of cerebral blood flow, oxygenation and metabolism suggest a pattern seen in patients with low c\scores on the Glasgow Coma Scale (GCS), who are known to have poor outcomes. Moderate hypothermia, although improving outcome for patients with GCS of 5-7, has not been beneficial for patients with lower GCS scores.

Preliminary clinical trial of an ex vivo arterial blood gas monitor.

PURPOSE: The purpose of this study was to test the analytical performance of a new ex vivo arterial blood gas (ABG) monitor based on fiberoptic sensor technology (SensiCath; Optical Sensors, Inc., Minneapolis, MN) when operated by critical care practitioners in intensive care environments. MATERIALS AND METHODS: Arterial blood analyses using a new ex vivo ABG monitor and standard clinical laboratory bench top analyzers were compared according to an institutionally approved protocol. The subjects were adult intensive care unit (ICU) patients (n = 20) with an arterial cannula for pressure monitoring, expectation of ICU stay > 72 hours, need for > or = 2 ABG analyses per day, and written informed consent. The clinical setting was two ICUs, a shock trauma ICU, and a neurological ICU in a metropolitan area trauma center. RESULTS: One hundred seventy-five paired ABG analyses were obtained over 1,146 hours of monitor use (52 +/- 20 hours per patient). Comparison of ABG monitor and laboratory analyses of blood samples obtained at the time of measurement by the monitor provided the following results: For pH, the range of laboratory measurements was 7.197-7.512, accuracy (mean difference between the monitor and laboratory measurement) was +0.010, precision (standard deviation of the difference between monitor and laboratory measurements) was +/- 0.027, and the correlation coefficient (r) = 0.913. For PCO2, the range of laboratory measurements was 24.5-61.5 mm Hg, accuracy was +1.4 mm Hg, precision was +/- 3.3 mm Hg, and r = 0.942. For PO2, the range of laboratory measurements was 47.3-163.3 mm Hg, accuracy was +4.0 mm Hg, precision was +/- 7.9 mm Hg, and r = 0.970. No adverse events occurred associated with the monitor. CONCLUSION: A practical ex vivo ABG monitor has been developed that offers accurate data and potential advantages to the critical care practitioner and the critically ill patient over other ABG analysis systems: one 10-minute calibration procedure; 1-minute analysis time; no permanent blood removal from the patient; and a closed arterial monitoring system. Precision performance is comparable to standard laboratory ABG analysis. The ABG monitor offers reliability and ease of use, and the ability of the critical care practitioner (nurse, respiratory therapist, or physician) to obtain accurate ABG analyses as needed at bedside.

Brain parenchyma PO2, PCO2, and pH during and after hypoxic, ischemic brain insult in dogs.

OBJECTIVES: 1) The investigation of fiberoptic PO2, PCO2, and pH sensor technology as a monitor of brain parenchyma during and after brain injury, and 2) the comparison of brain parenchyma PO2, PCO2, and pH with intracranial pressure during and after hypoxic, ischemic brain insult. DESIGN: Prospective, controlled, animal study in an acute experimental preparation. SETTING: Physiology laboratory in a university medical school. SUBJECTS: Fourteen mongrel dogs (20 to 35 kg), anesthetized, room-air ventilated. INTERVENTIONS: Anesthesia was induced with thiopental and maintained after intubation using 1% to 1.5% halothane in room air (FiO2 0.21). Mechanical ventilation was established to maintain end-tidal PCO2 approximately 35 torr (-4.7 kPa). Intravenous, femoral artery, and pulmonary artery catheters were placed. The common carotid arteries were surgically exposed, and ultrasonic blood flow probes were applied. A calibrated intracranial pressure probe was placed through a right-side transcranial bolt, and a calibrated intracranial chemistry probe with optical sensors for PO2, PCO2, and pH was placed through a left-side bolt into brain parenchyma. Brain insult was induced in the experimental group (n = 6) by hypoxia (FiO2 0.1), ischemia (bilateral carotid artery occlusion), and hypotension (mean arterial pressure [MAP] approximately 40 mm Hg produced with isoflurane approximately 4%). After 45 mins, carotid artery occlusion was released, FiO2 was reset to 0.21, and anesthetic was returned to halothane (approximately 1.25%). The control group (n = 5) had the same surgical preparation and sequence of anesthetic agent exposure but no brain insult. MEASUREMENTS AND MAIN RESULTS: Monitored variables included brain parenchyma PO2, PCO2, and pH, which were monitored at 1-min intervals, and intracranial pressure, MAP, arterial hemoglobin oxygen saturation (by pulse oximetry), end-tidal PCO2, and carotid artery blood flow rate, for which data were collected at 15-min intervals for 7 hrs. Arterial and mixed venous blood gas analyses were done at approximately 1-hr intervals. Baseline data agreed closely with other published results: brain parenchyma PO2 of 27 +/- 7 (SD) torr (3.6 +/- 0.9 kPa); brain parenchyma PCO2 of 69 +/- 12 torr (9.2 +/- 1.6 kPa); and brain parenchyma pH of 7.13 +/- 0.09. Postcalibration data were accurate, indicating stability and durability over several hours. In six experiments, during the brain insult, brain parenchyma PO2 decreased to 16 +/- 2 torr (2.1 +/- 0.3 kPa), brain parenchyma PCO2 increased to 105 +/- 44 torr (14 +/- 5.9 kPa) (p < .05), and brain parenchyma pH decreased to 6.75 +/- 0.08 (p < .05). Intracranial pressure (ICP) remained nearly constant (baseline 16 +/- 6 to 14 +/- 5 mm Hg at the end of the brain insult). Cerebral perfusion pressure (CPP = MAP - ICP) decreased (baseline 95 +/- 15 to 28 +/- 8 mm Hg; p < .05). On release of brain insult stresses, ICP increased to 30 +/- 9 mm Hg and CPP increased to 71 +/- 19 mm Hg (p < .05). A biphasic recovery was observed for brain parenchyma pH, which had the slowest recovery of the monitored variables. On average, brain parenchyma pH gradually returned toward baseline, and was no longer significantly different from baseline 3 hrs after release of insult stresses. Brain parenchyma PCO2 continued to decrease rapidly after brain insult and then remained approximately 52 +/- 10 torr (approximately 6.9 +/- 1.3 kPa) (p < .05). Brain parenchyma PO2 increased from a minimum at the end of brain insult to a maximum of 43 +/- 17 torr (5.7 +/- 2.3 kPa) within 1.25 hrs (p < .05), and then gradually decreased to approximately 35 +/- 10 torr (approximately 4.7 +/- 1.3 kPa). Cerebral perfusion pressure gradually decreased as ICP increased 3 to 5 hrs after insult. CONCLUSIONS: Intracranial chemistry probes with optical sensors demonstrated stable, reproducible monitoring of brain parenchyma PO2, PCO2, and pH in dogs for periods lasting > 8 hrs. Significant changes in brain p

Methylmethacrylate and atrioventricular conduction in dogs.

The effect of intravenous methylmethacrylate (MMA) on atrioventricular conduction times was studied in dogs, utilizing His-bundle electrograms. Dogs were anesthetized with halothane or enflurane; then MMA in a dose causing minimal to profound hemodynamic changes was administered and His-bundle electrograms, and arterial, pulmonary artery, and central venous pressures were recorded. This experimental model did not demonstrate a prolongation of atrioventricular conduction intervals which could be implicated as etiologic in MMA-induced dysrhythmias.