PubMed Health⌕ Search

Biomedical subjects

I R Piper

Publications and source records attributed to I R Piper.

At least 37 records · Page 2Linked to original sources
PubMed1994

Cause, distribution and significance of episodes of reduced cerebral perfusion pressure following head injury.

A group of 74 patients with head injury (54 severe, 17 moderate and 3 minor) had continuous monitoring of both arterial and intracranial pressure with computer-based registration of these pressures, cerebral perfusion pressure and other variables. In 60 patients cerebral perfusion pressure CPP fell below 60 mm Hg for periods of 5 minutes or longer. The distribution over time of these reductions in CPP during up to 12 days of monitoring was studied, and each episode of reduced CPP was attributed to a fall in arterial pressure, an increase in intracranial pressure, or both. Two clusters of reduced CPP were found, one during the first 24 hours of monitoring, when reduced CPP was mainly caused by a reduction in arterial pressure, and the other at 5 or 6 days after injury, when reduced CPP was due mainly to an increase in intracranial pressure. There was a significant correlation between low CPP due to reduced arterial pressure and the Injury Severity Score (p < 0.001), suggesting that resuscitative measures may have been less than optimal in these cases. There was also significant correlation between the duration of low CPP and low arterial pressure and an adverse outcome from injury as assessed at 6, 12 and 24 months after injury (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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

Integrated multimodality monitoring in the neurosurgical intensive care unit.

The selection of variables for continuous monitoring in the neurosurgical intensive care unit is based upon the requirement for constant perfusion and oxygenation of the brain and knowledge of the frequency and prognostic significance of abnormal values. Both arterial and intracranial pressure must be considered in the form of cerebral perfusion pressure. Body temperature and arterial oxygen saturation are essential to monitoring. Measurement of jugular venous oxygen saturation and cerebral blood flow velocity provide information of value in determining the source of raised intracranial pressure, the most appropriate means of treating it, and the safety of therapy.

Adult↗
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

Neuropathological and neurophysiological effects of interstitial white matter autologous and non-autologous protein containing solutions: further evidence for a glioma derived permeability factor.

The feline infusion model of brain edema was used to evaluate the pathophysiological effects of 0.6 ml infusions of autologous serum protein (66%), human serum protein (66%), human glioma cyst fluid and a tissue culture medium (TCM) on the structure and function of the forebrain white matter. These infusions increased local white matter water content by between 10.8 and 12.5 ml/100 g brain and were associated with moderate increases in ICP and CSF outflow resistance and a significant decrease in lumped craniospinal compliance. Cortical somatosensory potentials, motor evoked potentials, EEG and local cerebral blood flow (rCBF) at normocapnia were generally unchanged by the various infusions. All infusates except the 66% autologous serum protein infusion impaired rCBF CO2 reactivity. Histologically all infusates caused marked extracellular edema. The autologous serum protein infusion caused no additional histological changes whereas the glioma cyst infusates caused profound endothelial and astrocytic swelling, focal endothelial necrosis, basement membrane disruption, perivascular microglial reaction and pavementation and perivascular migration of polymorphonuclear leukocytes. Similar but less marked changes were seen after infusion of human serum protein whilst the TCM produced only minimal changes. The intensity and extent of Evans Blue extravasation into the forebrain white matter was greatest with glioma cyst infusates and with all infusions reflected the extent to microvascular changes. These studies show that products derived from gliomas cause additional damage to the blood-brain-barrier than that caused by non-autologous serum proteins. These results add further support for the existence of glioma derived permeability factors (GDPF), but suggest neither serum proteins nor glioma derived compounds in the white matter interstitium significantly influence local electrophysiological function. Some limitations of the infusion edema model when using non-autologous infusions and difficulties quantitating brain dysfunction are emphasised.

Animals↗
PubMed1993

An experimental study of cerebrovascular resistance, pressure transmission, and craniospinal compliance.

To successfully match the treatment to the cause for raised intracranial pressure (ICP) after a severe head injury, it is important to know the underlying mechanism at a given moment for the raised pressure. In particular, it is important to distinguish between active cerebral vasodilation, indicating functional autoregulation, and a passive vascular dilation as the cause for raised ICP. An experimental study was performed in feline models of diffusely raised ICP (n = 6), of active arterial vasodilation caused by arterial hypercarbia (n = 6), and of passive arterial dilation caused by pharmacologically induced arterial hypertension (n = 6) to determine if wave form analysis of ICP can distinguish active from passive arteriolar vasodilation. Pulsatile pressure transmission from the blood pressure pulse to the ICP pulse (cerebrovascular pressure transmission [CVPT]), cerebrovascular resistance, and craniospinal compliance were measured simultaneously at each level of raised ICP, arterial hypercarbia, and arterial hypertension. Arterial hypercarbia, caused by both 5 and 10% inspired CO2 increased low-frequency CVPT, which was followed by an increasingly negative phase shift between the blood pressure and ICP wave form (P < 0.05). Diffusely raised ICP caused by intraventricular infusion of mock cerebrospinal fluid caused increased low-frequency CVPT (P < 0.01) but resulted in no overall change in phase shift, although the sign of the phase shift remained negative. After arterial hypertension, caused by the infusion of angiotensin II, where there was loss of myogenic tone, an increased low-frequency CVPT was accompanied by a positive phase shift (P < 0.01). These data demonstrate it may be possible to distinguish active arteriolar vasodilation from a passive loss of autoregulatory vascular tone through simultaneous measurement of the low-frequency CVPT and phase shift. Analysis of the ICP wave form provides information relevant to the management of raised ICP.

Animals↗
PubMed1992

The role of bradykinin in the etiology of vasogenic brain edema and perilesional brain dysfunction.

The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 microL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 microL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.

Animals↗
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

Cerebral blood flow at constant cerebral perfusion pressure but changing arterial and intracranial pressure: relationship to autoregulation.

Therapeutic agents for reducing raised intracranial pressure (ICP) may do so at the expense of reduced mean arterial pressure (MAP). As a consequence, cerebral perfusion pressure (CPP) = (MAP - ICP) may not improve. It is unknown whether the level of MAP alters cerebral blood flow (CBF) when MAP and ICP change in parallel so that CPP remains constant. This study investigates CBF at a constant CPP but varying levels of MAP and ICP in 12 anaesthetized cats. CBF was studied at three levels of CPP: 60 (n = 4), 50 (n = 4), and 40 mm Hg (n = 4) under conditions of both intact and impaired autoregulation. At CPP levels of 50 and 60 mm Hg, when autoregulation was intact, CBF remained unchanged. With loss of autoregulation, there was a trend for CBF to increase as MAP and ICP were increased in parallel at a CPP of 50 and 60 mm Hg, although the relationship did not achieve statistical significance. Absolute CBF levels were, however, significantly different between the autoregulating and nonautoregulating groups (p <0.001). At a CPP of 40 mm Hg, CBF showed a linear correlation with blood pressure (BP) (r = 0.57, p <0.05). These results demonstrate that when autoregulation is impaired, there is a functional difference between autoregulating and nonautoregulating cerebral vessels despite similar MAP and CPP. These results also show that at a CPP of 40 mm Hg when autoregulation is impaired, CBF depends more on arterial driving pressure than on CPP.

Journal Article↗
PubMed1992

Interstitial white matter brain oedema does not alter the electroencephalogram.

An experimental study was performed to determine the effects of interstitial white mater oedema on the electroencephalogram (EEG). Using both rodent and feline infusion models of focal brain oedema no difference was found between the EEG waveforms recorded epidurally from the infused and control hemispheres. It is concluded that where focal slow-wave EEG abnormalities overlie oedematous brain the EEG abnormalities are not primarily related to the brain oedema but arise from either local biomechanical or other pathophysiological mechanisms.

Animals↗
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

The contribution of arachidonic acid to the aetiology and pathophysiology of focal brain oedema; studies using an infusion oedema model.

Arachidonic acid solution (2 to 15 mg/ml) was infused into the right forebrain white matter of anaesthetised cats over three hours to evaluate its contribution to the genesis and pathophysiology of vasogenic brain oedema. The 0.6 ml infusion increased local white matter water content by a mean of 11.3 ml/100 g tissue but did not increase cortical water content. Histological studies revealed local expansion and trabeculation of the white matter with aggregations of granulocytic neutrophils in the venules and perivenular brain. The adjacent cortical cytoarchitecture was normal. The white matter around the infusion site was stained lightly and over a variable area (15-20 mm2) by intravenously administered Evans Blue dye 2%. Regional cerebral blood flow (rCBF) adjacent to the frontal infusion did not change significantly during the period of infusion and remained similar to rCBF in the contralateral hemisphere. Following the arachidonic acid infusion regional CBF CO2 reactivity was normal and three was no asymmetry of either cortical somatosensory evoked potential (SEP) or motor evoked potential (MEP) waveforms. The increase in brain water content and changes in the ICP and ICP related biodynamics (pressure-volume index, lumped craniospinal compliance and CSF outflow resistance) were similar to those seen following infusion of 0.6 ml saline. These studies suggest that free intraparenchymal arachidonic acid, at concentrations exceeding those occurring in most neuropathological conditions, can increase the normal brain parenchymal capillary permeability but does not disrupt focal cerebrovascular and electrophysiological function. The clinical implications of these findings are discussed.

Animals↗
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

Automated time-averaged analysis of craniospinal compliance (short pulse response).

We have developed an automated method [Short Pulse Response (SPR)] of measuring craniospinal compliance using an electronic square wave pressure generator to produce a small (0.05 ml) and reproducible transient volume increase in the CSF space (pulse duration 100 msec). In experimental models of intracranial hypertension, arterial hypertension, arterial hypotension and arterial hypercarbia in cats, the new method accurately followed physiological changes in compliance when compared to the manual volume-pressure injection method. The VPR overestimated compliance compared to the new SPR method (by 20% to 162%, mean = 77%). The SPR method was less variable between sequential measurements with a coefficient of variation (CV) ranging from 0.6% to 9.6% (mean CV = 2.6%), compared with a CV ranging from 5.6% to 48% (mean CV = 17%) for the VPR method. Repeated compliance measurements by the new method over a 12 hour period, produced no neuropathological evidence of either blood brain barrier breakdown or tissue damage resulting from the repeated volume injections.

Animals↗
PubMed1990

The contribution of secondary mediators to the etiology and pathophysiology of brain oedema: studies using a feline infusion oedema model.

Secondary mediator compounds are postulated to have a role in vasogenic oedematogenesis. They may also cause focal brain dysfunction due to their neuronal, axonal and glial modulating properties. Using the feline model of infusion brain oedema the effects of right frontal intracerebral infusion (200 microliters/hr for 3 hrs) of saline, bradykinin (10(-4) to 10(-6) M), arachidonic acid (10(-2) to 10(-3) M), 20% protein and four human glioma cyst fluids were evaluated. Somatosensory evoked potentials (SSEP), motor evoked potentials (MEPs), rCBF and rCBF CO2 reactivity (Hydrogen clearance). ICP, craniospinal compliance, local brain tissue water content (microgravimety), brain histology and BBB function (Evans Blue 2%) were measured. Brain water content increased locally from 69% to 79%, ICP increased (by mean 14 mmHg) and compliance decreased (mean 70%) and there were the histological features of brain oedema with all infusates. BBB opening occurred with Bradykinin (+), arachidonic acid (++), 20% protein ( ) and glioma cyst fluid (4+). Polymorphic and macrophage infiltrates were seen with all infusions but rCBF and MEPs remained normal. SSEPs changed with high dose bradykinin and some glioma cyst infusates whilst CBF CO2 reactivity was locally impaired by all infusates except saline and arachidonic acid. This study suggests that certain compounds in brain oedema fluid could mediate local brain dysfunction.

Animals↗
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↗