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Biomedical subjects

N M Dearden

Publications and source records attributed to N M Dearden.

At least 19 recordsLinked to original sources
PubMed1998

Cerebral haemodynamics and embolization during carotid angioplasty in high-risk patients.

BACKGROUND: Patients with symptomatic internal carotid artery (ICA) stenosis greater than 70 per cent in association with a contralateral ICA occlusion may have an increased risk of stroke following carotid endarterectomy. Such patients might benefit from the theoretically shorter ischaemic time offered by carotid angioplasty and stenting. METHODS: Nine patients who underwent carotid angioplasty and stenting were monitored using near-infrared spectroscopy, continuous jugular venous oximetry and transcranial Doppler ultrasonography to detect both haemodynamic ischaemia and embolic events. RESULTS: Significant ischaemia occurred in four of the nine patients once the stenosis had been crossed by the guidewire (spectroscopy and oximetry). Inflation of the angioplasty balloon resulted in a brief period of ischaemia and showers of emboli in all patients (ultrasonography) and this persisted for more than 3 min after balloon deflation in three patients. One patient had a major disabling stroke due to ICA thrombosis. CONCLUSION: Angioplasty and stenting in these high-risk patients may not confer any advantage over conventional surgery in terms of both haemodynamic ischaemia and embolization.

Aged↗
PubMed1996

The differing effects of regional and general anaesthesia on cerebral metabolism during carotid endarterectomy.

OBJECTIVES: To examine the effects of either regional (RA) or general (GA) anaesthesia upon parameters of cerebral metabolism (near infrared spectroscopy, continuous jugular venous oximetry) during carotid endarterectomy. DESIGN: Prospective, non-randomised, observational study. MATERIALS: Sixty-five consecutive patients (33 RA; 32 GA) undergoing carotid endarterectomy. METHODS: (i) Near infrared spectroscopy: measurement of concentrations of cerebral oxyhaemoglobin (HbO2), deoxyhaemoglobin (HHb) and oxidised cytochrome oxidase (caa3). (ii) Continuous jugular venous oximetry: O2 saturation of jugular venous blood (SJvO2). (iii) Stump pressure in internal carotid artery. RESULTS: A reduction in SJvO2 (RA: 13% (95% CI-3 to 29%) GA: 9% (95% CI-2 to 20%), p < 0.08) and a fall in caa3 levels (RA vs. GA: 25/31 vs. 19/31, p = 0.2) was more likely in patients given a RA following application of the carotid clamps. When HbO2 and caa3 did fall however spontaneous recovery occurred more often (RA vs. GA; caa3: 18/25 vs. 5/19, p < 0.005; HbO2: 30/31 vs. 4/28, p < 0.001). CONCLUSIONS: Although GA may offer a degree of cerebral protection by reducing cerebral metabolic rate (lower falls in SJvO2 and caa3) RA preserved cerebral autoregulation as judged by the spontaneous recovery in caa3 and HbO2 levels.

Aged↗
PubMed1995

Effects of changes in mean arterial pressure on SjO2 during cerebral aneurysm surgery.

Twenty-six patients requiring clipping of cerebral aneurysms were anaesthetized with propofol, alfentanil and atracurium infusions and their lungs ventilated mechanically to hypocapnia (3.4-4.5 kPa). SjO2 was measured continuously with an Oximetrix fibreoptic oximetry catheter. Normovolaemia was maintained by observing the response of mean arterial pressure (MAP) and central venous pressure (CVP) to fluid administration. The response of SjO2 to increased MAP was noted and the lactate oxygen index (LOI) calculated at regular intervals. SjO2 measurements indicated a critical MAP of between 80 and 110 mm Hg in nine patients, and one patient had a persistently low SjO2 value despite an MAP of 110 mm Hg. An increase in MAP was associated with an increase in SjO2 in 19 patients (P < 0.001). When the effects of changes in PaCO2 were eliminated, this change was still significant (P = 0.004) (n = 9). Patients with an LOI > 0.08 at any time during the procedure had a worse initial outcome (within the first day) (P < 0.02) than patients who had a normal LOI throughout. Long-term outcome was similar to those with a normal LOI. Increasing MAP did not have a consistent effect on LOI. Jugular bulb cannulation to assess hypoperfusion in conjunction with lactate measurements and calculation of LOI provide useful information on which to base the intra- and postoperative management of patients with subarachnoid haemorrhage.

Blood Pressure↗
PubMed1994

Role of intracranial pressure monitoring in severely head-injured patients without signs of intracranial hypertension on initial computerized tomography.

Previous studies have suggested that only a small proportion (< 15%) of comatose head-injured patients whose initial computerized tomography (CT) scan was normal or did not show a mass lesion, midline shift, or abnormal basal cisterns develop intracranial hypertension. The aim of the present study was to re-examine this finding against a background of more intensive monitoring and data acquisition. Eight severely head-injured patients with a Glasgow Coma Scale score of 8 or less, whose admission CT scan did not show a mass lesion, midline shift, or effaced basal cisterns, underwent minute-to-minute recordings of arterial blood pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) derived from blood pressure minus ICP. Intracranial hypertension (ICP > or = 20 mm Hg lasting longer than 5 minutes) was recorded in seven of the eight patients; in five cases the rise was pronounced in terms of both magnitude (ICP > or = 30 mm Hg) and duration. Reduced CPP (< or = 60 mm Hg lasting longer than 5 minutes) was recorded in five patients. Severely head-injured (comatose) patients whose initial CT scan is normal or does not show a mass lesion, midline shift, or abnormal cisterns nevertheless remain at substantial risk of developing significant secondary cerebral insults due to elevated ICP and reduced CPP. The authors recommend continuous ICP and blood pressure monitoring with derivation of CPP in all comatose head-injured patients.

Adolescent↗
PubMed1994

Measuring the burden of secondary insults in head-injured patients during intensive care.

Primary traumatic brain damage may be compounded by secondary pathophysiological insults that can occur soon after trauma, during transfer to hospital or subsequent treatment of the head-injured patient. The aim of this prospective study was to quantify the burden of a wide range of secondary insults occurring after head injury and to relate these to 12-month outcome. In 124 adult head-injured patients studied during intensive care using a computerized data collection system, < or = 14 clinically indicated physiological variables were measured minute-by-minute. Verified values falling outside threshold limits for > or = 5 min, as defined by the Edinburgh University Secondary Insult Grading scheme, were analysed by insult grade and duration. A greater incidence of secondary insults was detected than previous studies have indicated. Insults were found in 91% of patients and occurred in all severities of head trauma, at all ages, and at every level of Injury Severity Score (ISS). The cumulative durations were much greater than previously recorded although 85% of the total time was at the least severe grade. Short duration insults were common. In 71 patients, in whom 8 insults could be assessed (intracranial pressure, arterial hypo- and hypertension, cerebral perfusion pressure, hypoxemia, pyrexia, brady- and tachycardia), outcome at 12 months was analysed using logistic regression to determine the relative influence of age, admission Glasgow Coma Sumscore, ISS, pupil response on admission, and insult duration on both mortality and morbidity. The most significant predictors of mortality in this patient set were durations of hypotensive (p = .0064), pyrexic (p = .0137), and hypoxemic (p = .0244) insults. When good versus poor outcome was considered, hypotensive insults (p = .0118) and pupil response on admission (p = .0226) were significant.

Adult↗
PubMed1993

Management of intracranial hypertension in head injury: matching treatment with cause.

Raised intracranial pressure (ICP) is common after head injury and strongly associated with mortality and morbidity. Empirical and prophylactic therapy with steroids and barbiturates has proved unsuccessful. Ideally, therapy should be targeted at the predominant cause of the increase in ICP. In head injury these may be (1) an increase in cerebral blood volume best treated by hyperventilation and hypnotic drugs. (2) an increase in brain water content best treated by osmotherapy and (3) increased CSF outflow resistance best treated by CSF drainage. This last cause seldom predominates in head injury. To determine whether it is possible to identify the best therapy in individual head injured patients, we are comparing osmotherapy (mannitol) and hypnotic drugs (thiopentone and gamma-hydroxybutyrate) in selected patients with severe head injury where it is possible to maintain standard conditions of ventilation and stable blood pressure and to measure ICP, CPP, brain electrical activity, PR ratio of the ICP wave form and cerebral AvDO2 before and during each of the two forms of therapy. Effective therapy means that ICP has been reduced to 20 mm Hg with preservation or improvement in CPP. 17 patients have been studied so far and 4 groups identified. Osmotherapy was superior to hypnotic in 5 cases, hypnotic superior to mannitol in 3 cases, both were effective in 5 cases and neither effective in 4 cases. Patients in whom hypnotics were superior tended to be younger, with diffuse rather than focal brain injury, had the highest levels of brain electrical activity prior to treatment and a higher PR ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Damage, Chronic↗
PubMed1993

Transcranial Doppler-sonography in severe head injury.

Ischaemic brain damage is present in over 90% of patients suffering from fatal head injury. Early detection and treatment of ischemia may improve outcome after head trauma. Monitoring of blood flow velocity of the middle cerebral artery by noninvasive transcranial doppler ultrasound provides an alternate means of identifying cerebral ischaemia.

Blood Flow Velocity↗
PubMed1993

Technical considerations in continuous jugular venous oxygen saturation measurement.

Fibreoptic reflection oximetry allows continuous in-vivo estimation of jugular venous oxygen saturation. In combination with pulse oximetry the oxygen extraction ratio SaO2-SjO2/SaO2 can be derived enabling identification of states of global luxury perfusion, normal coupling of global cerebral blood flow with global cerebral metabolism, global cerebral hypoperfusion and global cerebral ischemia. Several technical difficulties may arise affecting the accuracy of SjO2 recordings which must be recognised by the clinician before medical intervention is contemplated.

Artifacts↗
PubMed1993

Multimodality monitoring as a guide to treatment of intracranial hypertension after severe brain injury.

Transcranial doppler measurements of blood flow velocity in the middle cerebral artery were made during treatment of raised intracranial pressure (ICP) in 22 patients with severe brain injury. Twenty patients also had continuous measurement of arterial and jugular bulb venous oxygen saturation (SJO2). The transcranial Doppler parameters studied included both mean flow velocity and pulsatility index (PI). Successful treatment was defined as a reduction of ICP to less than 20 mm Hg with improvement or preservation of cerebral perfusion pressure (CPP) above 60 mm Hg. Successful therapy was associated with a significant rise in SJO2 and reduction of cerebral arteriovenous oxygen content difference (AVDO2) and PI only when the pretreatment CPP was less than 60 mm Hg. An increase in CPP beyond 70 mm Hg did not further improve cerebral oxygen delivery and PI, suggesting that autoregulation became a factor above this CPP threshold. Treatment failure during administration of hypnotic drugs resulted in a reduction in arterial pressure, CPP, SJO2, and mean velocity and in an increase in PI and AVDO2, despite a decrease in ICP. CPP is the most important parameter to monitor during ICP therapy. It should be maintained above 70 mm Hg in patients with severe brain injury.

Adolescent↗
PubMed1992

Progress in the management of head injury.

Three 1-year surveys of head injury management spanning a 9-year period in a single regional centre are presented. There was a reduction in total numbers of head injury admissions after guidelines for admission and referral were implemented. More liberal use of computed tomography resulted in detection of a greater number of intracranial haematomas with the majority detected in non-comatose patients. The early mortality rate in severe head injury fell from 45 per cent to 34 per cent despite referral of large numbers of patients with multiple injuries and a substantial proportion (12 per cent) of patients aged more than 70 years in whom outcome did not improve. Total occupied bednights and bednights occupied per surviving patient with severe head injury fell over the period of study. Care for patients with significant head injury should be based on regional neurosurgical units associated with trauma services.

Aged↗
PubMed1992

Transcranial Doppler waveform differences in hyperemic and nonhyperemic patients after severe head injury.

Although increased cerebral blood flow velocity is readily measured by transcranial doppler ultrasonography (TCD), the causes of the velocity elevation may differ. After severe head injury, increased blood flow velocity can develop both in patients with global hyperemia (suggestive of vasodilation) and in those without hyperemia (suggestive of vasospasm). The present study attempts to determine whether TCD can differentiate these two mechanisms of velocity increase. Fourteen severely brain-injured patients who developed increased middle cerebral artery blood flow velocity (time-averaged mean velocity > 100 cm/s) were studied. Eight cases were nonhyperemic and six were hyperemic as defined by arterial-jugular venous oxygen content differences of more than 4 mL/dL and less than 4 mL/dL, respectively. The TCD waveform of all eight nonhyperemic cases showed a diastolic notch, which was absent in all six hyperemic patients (p = 0.00066). TCD waveform profile appears to provide a noninvasive means of differentiating at the bedside the two causes of increased flow velocity. If associated with raised intracranial pressure, these require different treatment.

Adolescent↗
PubMed1992

Intracranial blood flow velocity after head injury: relationship to severity of injury, time, neurological status and outcome.

Middle cerebral artery (MCA) blood flow velocity was measured daily by transcranial Doppler ultrasonography in 121 patients with severe (50), moderate (16) and minor (55) head injury during their hospital stay, and the results compared with findings in control subjects. Admission MCA velocity was significantly lower after severe 35.8 (31.9-39.7) cm/s, mean (95% confidence limits), moderate 45.5 (40.0-51.0) cm/s and minor 51.7 (47.9-55.5) cm/s head injury when compared with normal controls 60.1 (56.9-63.3) cm/s. Initial mean velocity in severe head injury was significantly lower than in moderate and minor injury. At discharge, MCA velocity in severe injury remained below normal 46.2 (43.2-49.0) cm/s, whereas, in moderate and minor injury flow velocity had returned to normal. Correlation (r = 0.46, p less than 0.01) was found between MCA velocity and Glasgow Coma Score (GCS) on admission but not on discharge. Persistently low flow velocity was found in all 10 patients who died within 72 hours (early deaths). An admission MCA velocity of less than 28 cm/s correctly predicted 80% of the early deaths. Patients who made a good recovery or had only moderate disability at six months showed a significant increase in velocity from admission 36.2 (31.5-41.2) cm/s to discharge 47.8 (43.7-51.9) cm/s in contrast to those who were severely disabled, in whom velocity generally remained low.

Adolescent↗
PubMed1992

The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain injury.

Middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation (SJO2) were measured by transcranial Doppler (TCD) ultrasonography and continuous venous oximetry, respectively, in 41 severely brain-injured patients. The purpose of the study was to examine the relationships between TCD flow velocity, SJO2, and alterations in blood pressure (BP), intracranial pressure (ICP), and cerebral perfusion pressure (CPP). In these patients, CPP was reduced either by rising ICP or by falling BP. Both forms of reduction of CPP resulted in a greater fall in diastolic flow velocity than other flow parameters. As CPP decreased below a critical value of 70 mm Hg, a progressive increase in TCD pulsatility index (PI) was observed (r = -0.942, p less than 0.0001), accompanied by a fall in SJO2 (r = 0.78, p less than 0.0001). At pressures above 70 mm Hg, there was no correlation of either PI or SJO2 with CPP. The relationship between PI and CPP held true in patients with both focal and diffuse pathologies and was the same whether changes in CPP resulted from alterations in ICP or BP. The PI and SJO2 correlated better with CPP than with ICP or BP. Transcranial Doppler ultrasonography can identify states of reduced CPP. Decreases in SJO2 with falling CPP suggested progressive failure of cerebral blood flow to meet metabolic demands. Monitoring of TCD and SJO2 may be used to define the optimum CPP level for management of severely brain-injured patients.

Adolescent↗
PubMed1992

The significance of posttraumatic increase in cerebral blood flow velocity: a transcranial Doppler ultrasound study.

Using transcranial doppler ultrasonography, cerebral blood flow velocity was measured daily from both middle cerebral arteries in 121 patients who had suffered minor (n = 55), moderate (n = 16), or severe (n = 50) brain injury. Serial computed tomographic scans were performed to identify noncontusion-related infarction (NCI). Cerebral perfusion pressure was monitored continuously in 41 patients who had severe head injury; of these, 22 had continuous measurement of arterial and jugular bulb venous oxygen (SJO2) saturation. Abnormally high mean flow velocity (greater than 100 cm/s) was observed in 23 patients (minor injury, n = 3; moderate injury, n = 3; severe injury, n = 17), but was recorded only when cerebral perfusion pressure exceeded 60 mm Hg (P less than 0.0001). Fourteen patients who underwent SJO2 monitoring developed increased mean flow velocity (MFV). In 6, the arterial-jugular venous oxygen content difference (AVDO2) was below 4 ml/dl, indicating global cerebral hyperemia. All had bilateral elevation of MFV, and 6 of the 8 nonhyperemic patients (AVDO2, 4-9 ml/dl) had a unilateral increase of MFV (P = 0.018). Four of the 23 patients with increased MFV developed NCI, as compared with none of the patients without elevated MFV (P = 0.015). All patients with NCI had suffered severe brain injury, had unilateral elevation of MFV in the terriory of the relevant cerebral vessel, and had received therapy to correct reduced cerebral perfusion pressure (P = 0.008). NCI did not occur in any patient with increased MFV that was associated with global hyperemia.

Adolescent↗
PubMed1992

Control of intracranial pressure in patients with severe head injury.

Raised intracranial pressure (ICP) occurs at some time in 50-75% of severely head injured patients. Measurement of ICP alone is not sufficient. Arterial pressure must also be monitored: the important physiological variable is cerebral perfusion pressure. Detailed analysis of the ICP recording yields valuable information on the nature and cause of ICP, with implications for appropriate therapy. Additional measurements of importance include brain electrical activity, arterial and jugular venous oxygen saturation, and blood flow velocity in major intracranial arteries measured by transcranial Doppler sonography. These assessments not only add information about the cause of intracranial hypertension (vascular vs. nonvascular) but also help to regulate therapy, providing early warning that a treatment for reducing the ICP is actually producing global brain ischemia. In the management of raised ICP, all correctable factors must first of all be dealt with, then a choice made between hypnotic drugs and osmotic therapy according to whether the cause of raised ICP is, respectively, vascular or nonvascular.

Blood Volume↗
PubMed1991

Jugular bulb cannulation: description of a cannulation technique and validation of a new continuous monitor.

We have compared in vivo oxygen saturation recordings obtained from the Oximetrix 3 with in vitro measurements using the Instrumentation Laboratories 282 Co-Oximeter. The small mean difference (0.85%) and close limits of agreement (-4% to 6%) are close enough for clinical purposes, provided in vivo calibration is performed after insertion of the fibreoptic catheter and repeated at least every 12 h. Continuous monitoring of jugular bulb oxygen saturation during intensive care of brain injured patients is now possible using fibreoptic technology. This technique may be of value in detecting global ischaemia, and as a predictor and monitor of cerebral perfusion pressure therapy.

Catheterization, Central Venous↗