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Biomedical subjects

N M Dearden

Publications and source records attributed to N M Dearden.

16 recordsLinked to original sources
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↗
PubMed1990

Secondary insults during intrahospital transport of head-injured patients.

Secondary pathophysiological insults occurring after injury have been prospectively assessed in 50 head-injured patients who required intrahospital transfer. 35 patients were transported from the intensive care unit (ICU) and 15 from the accident and emergency department. Physiological variables were recorded every minute in the four hours before transfer (ICU group only), during the move, and for four hours afterwards. Pretransfer insults were predictive of further insults during and after transport. There was significant correlation between increased frequency of insults post-transfer (compared with pre-transfer) and high injury severity score. A greater proportion of the patients transported from the emergency department had secondary injuries post-transfer. Adequate resuscitation before moving the patient, especially in patients with multiple injury, is important.

Adolescent↗
PubMed1990

Systems analysis of cerebrovascular pressure transmission: an observational study in head-injured patients.

In an observational study in head-injured patients, cerebrovascular pressure transmission was investigated using a systems analysis approach whereby the blood pressure (BP) waveform was used as a measure of an input stimulus to the cerebrovascular bed (CVB) and the intracranial pressure (ICP) waveform as the response to that stimulus. The transfer function is a measure of how much pressure is transmitted through the CVB at a given frequency and is calculated using Fourier analysis of the pressure waveforms. The transfer function allows quantification of the pressure transmission performance of the CVB, thus providing a basis for comparison between normal and abnormal function. Fifteen hundred samples of ICP and BP waveforms were collected from 30 head-injured patients via microcomputer. Off-line spectral analysis of the waveform database revealed four main classes of transfer function: those with an overall flat transfer function (curve type 1); those with an elevated low-frequency response (curve type 2); those with an elevated high-frequency response (curve type 3); and those exhibiting both an elevated low- and high-frequency response (curve type 4). Curve types 2 and 4 were most often associated with raised ICP (greater than 20 mm Hg), whereas curve types 1 and 3 were most often affiliated with ICP less than 15 mm Hg. Studies of this type may provide insight into the pathophysiology of the CVB and ultimately aid in the prediction and treatment of raised ICP.

Adolescent↗
PubMed1989

Coagulation disorder due to apparent inadvertent heparin administration.

A new competitive binding assay, which measures the concentration of heparin rather than its activity, was used to confirm the presence of a high concentration of heparin in blood samples from a patient which showed unexpected gross prolongation of thrombin time (TT) and activated partial thromboplastin time (APTT). Extrapolation of the heparin concentration enabled estimation of the likely time of administration and the probable dose given. It is possible that an error in dosage may have arisen due to the striking resemblance of vials containing different amounts of heparin marketed by different manufacturers. There is a need for the adoption by manufacturers of a standard coding scheme for vials containing different amounts of heparin (as is adhered to in the case of some drugs, e.g. warfarin), in order to pre-empt this possible source of error.

Adult↗
PubMed1986

Effect of high-dose dexamethasone on outcome from severe head injury.

The conflicting evidence concerning the influence of high-dose steroids on intracranial pressure (ICP) and outcome following severe head injury has led to the institution of the prospective double-blind controlled trial reported here. Severely head-injured patients admitted to intensive care during a 3-year period were randomly allocated to a dexamethasone- or placebo-treated group. Adults in the steroid group received dexamethasone, 50 mg intravenously, as a bolus on admission to the neurosurgical unit, then 100 mg on Days 1, 2, and 3, 50 mg on Day 4, and 25 mg on Day 5 on continuous intravenous infusion. Children received proportionate intravenous dosages calculated on a weight basis. Severity of head injury was assessed from admission Glasgow Coma Scale (GCS) scores and the appearance of the admission computerized tomography scan. Intracranial pressure (ICP) was monitored in all patients from the surface subarachnoid space. Outcome at 6 months was assessed using the Glasgow Outcome Scale. Steroid and placebo groups were similar in terms of admission GCS score, intracranial pathology, incidence of associated injuries, and time interval from injury to admission to intensive care. The ICP generally increased during the first 48 hours of intensive therapy; there was no difference in this trend between the steroid and placebo groups. A poorer outcome was observed in patients with elevated ICP who received steroids. No increase in the incidence of pulmonary, gastrointestinal, or other extracranial complications was seen in the steroid group. The 6-month outcome did not differ between the steroid and placebo groups. No advantage of high-dose dexamethasone on ICP trends or clinical outcome in the treatment of severe head injury has emerged from this study.

Adolescent↗
PubMed1986

Management of raised intracranial pressure after severe head injury.

The mainstay of early management following severe head injury (less than 8 on the Glasgow coma scale [GCS]) remains urgent cardiopulmonary resuscitation, triage, transfer to a neurosurgical centre, emergency CT scanning and appropriate surgical intervention (Rose et al, 1977; Seelig et al, 1981; Langfitt and Gennarelli, 1982; Bricolo and Pasut, 1984). Subsequent therapy usually includes a period of intensive care with or without artificial ventilation (Becker et al, 1977; Bruce et al, 1978; Marshall et al, 1979). Intracranial pressure (ICP) monitoring is employed in many centres during the first post-traumatic week, however conservative or aggressive the management regimen is.

Barbiturates↗
PubMed1985

Ischaemic brain.

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Barbiturates↗
PubMed1985

Comparison of etomidate and althesin in the reduction of increased intracranial pressure after head injury.

The increasing use of shorter-acting hypnotic agents to control intracranial pressure (ICP) following severe head injury has prompted a prospective double-blind controlled trial comparing the efficacy of etomidate and Althesin, given by i.v. infusion. Over the dose ranges used, the two drugs appeared equipotent in decreasing ICP whilst preserving cerebral perfusion pressure. However, in two patients (one in each group) ICP did not respond to hypnotic infusion, a feature noted in other studies to occur in a minority of patients. With the cessation of Althesin manufacture and the discussion about the use of etomidate infusions, it is timely to document the effectiveness of etomidate in decreasing ICP.

Adolescent↗
PubMed1976

Cyto-differentiation and portal vascular development in the mouse adenohypophysis.

Pituitaries of fetal and postnatal (15 days p.c.-28 days p.n.) and adult (male) mice were studied by light and electron microscopy to correlate the developmental pattern of the hypothalamo-hypophysial vascular system with the time of onset of function of the adenohypophysis. The superior and anterior regions of the adenohypophysis become vascularized at 17 days p.c., when portal vessels extend from oral primary plexus to the pars distalis for the first time. Adenohypophysial vascularity and the number of portal vessels steadily increase to reach the adult pattern at 5 days p.n. At 1 day p.n. deep capillary loops appear in the caudal regions of the oral primary plexus; a capillary (tangential) plexus underlies the ependymal lining of the third ventricle by 6 days p.n. Superficial capillary loops were not observed until the third postnatal week. Granulation of secretory cells commences at 16 days p.c., predominantly in the upper and anterior adenohypophysis; at 17 days thyrotropes, gonadotropes and corticotropes are recognizable and by morphological criteria appear actively secretory on days 17-18 p.c., although few appear active at 19 days p.c. and 1 day p.n. Somatotropes are first seen at 18 days p.c., predominantly in the central and lateral regions of the pars distalis. Active secretory cells increase in number over the period 2-10 days p.n., but after 11 days p.n. thyrotropes and corticotropes seem to become progressively less active; fewer gonadotropes are seen after 15 days p.n., and these apparently become progressively less active from day 19. Most somatotropes appear active until 28 days p.n. The observations suggest that hypothalamic control of adenohypophysial function may exist in the mouse from 17 days p.c.

Age Factors↗