Metoclopramide-induced raised intracranial pressure after head injury

We report a case of raised intracranial pressure in a head-injured patient following the intravenous administration of metoclopramide. The patient required admission to an intensive care unit after a road traffic accident. A CT scan of the head was consistent with diffuse axonal injury and supportive management included intracranial pressure monitoring. On the third day after admission, intravenous metoclopramide 10mg was administered to aid gastric emptying during nasogastric feeding. Intracranial pressure increased to 39mmHg from a baseline of 15-20mmHg. The same dose of metoclopramide was repeated the next day during transcranial doppler studies with an increase in ICP to 34mmHg and an associated rise in middle cerebral artery systolic blood velocity from 122cms-1 to 150cms-1. This effect of metoclopramide has not been previously reported.     

Clinical observations on the relationship between cerebrospinal fluid pulse pressure and intracranial pressure

Summary A method is described for monitoring the relationship between CSF pulse pressure and ICP in clinical patients. Highly significant linear relationships were found during 65 continuous ICP recordings in 58 patients. The slope value of this relationship showed a positive correlation with the elastance coefficient, a volume-pressure parameter assessed by bolus injection. However, the correlation was too weak to allow for a confident prediction of the elastance coefficient on the basis of CSF pulse pressure in the individual patient. This was attributed to the variable magnitude of the volume change underlying the CSF pulse pressure: the pulsatile variation in cerebral blood volume. This quantity was calculated on the basis of a mathematical model from the slope value and the elastance coefficient and was found to vary between 0.36 and 4.38ml. During plateau waves a disproportionate increase in pulse pressure with the ICP was observed in contrast with a relative decrease in intracranial elastance. This phenomenon was ascribed to an increase in the pulsatile variation in cerebral blood volume. It is concluded that, under certain conditions, the intracranial volume-pressure relationship can be continuously monitored by means of CSF pulse pressure analysis. The findings during plateau waves suggest that the pulse pressure also reflects the state of the cerebral vasomotor tone.     

Effect of cervical hard collar on intracranial pressure after head injury

Background: Patients suffering head trauma are at high risk of having a concomitant cervical spine injury. A rigid cervical collar is usually applied to each patient until spinal stability is confirmed. Hard collars potentially cause venous outflow obstruction and are a nociceptive stimulus, which might elevate intracranial pressure (ICP). This study tested the hypothesis that application of a hard collar is associated with an increase in ICP. Methods: A prospective series of 10 head‐injured patients with a postresuscitation Glasgow coma scale score of nine or less had ICP measurements before and after cervical hard collar application. Results: Nine out of 10 patients had a rise in ICP following application of the collar. The difference in pre‐ and postapplication ICP was statistically significant (P < 0.05). Conclusions: Early assessment of the cervical spine in head‐injured patients is recommended to minimize the risk of intracranial hypertension related to prolonged cervical spine immobilization with a hard collar.     

The management of head injury and intracranial pressure

Severe head injury occurs predominantly in the young population. Although the incidence is decreasing in the United Kingdom, the eventual outcome of these patients has major social and economic implications. Damage to brain tissue during head injury is both primary, due to the initial insult, or secondary, which occurs later. Because little can be done about the primary injury, the intensive care management is targeted at reducing the secondary insults which may cause further brain damage. The prevention of secondary injury involves prompt airway management and treatment of hypoxia and hypotension. Severe head injury often causes raised intracranial pressure (ICP). The management is focused on maintaining cerebral perfusion pressure, which should be maintained above 70 mmHg by adequate fluid replacement or by the judicious use of inotropes. The methods to control ICP include general measures (15° head up position, avoidance of jugular venous obstruction, prevention of hyperthermia and hypercarbia) and neurospecific measures. The neurospecific measures are particularly useful in patients with refractory intracranial hypertension. The patient may need sedation, paralysis, use of barbiturate coma, osmotherapy, moderate cooling, controlled hyperventilation or surgical intervention. This review focuses on the rationale for the use of these interventions, outlining their benefits and their pitfalls.     

High level of extracellular potassium and its correlates after severe head injury: relationship to high intracranial pressure

OBJECT: Disturbed ionic and neurotransmitter homeostasis are now recognized as probably the most important mechanisms contributing to the development of secondary brain swelling after traumatic brain injury (TBI). Evidence obtained in animal models indicates that posttraumatic neuronal excitation by excitatory amino acids leads to an increase in extracellular potassium, probably due to ion channel activation. The purpose of this study was therefore to measure dialysate potassium in severely head injured patients and to correlate these results with measurements of intracranial pressure (ICP), patient outcome, and levels of dialysate glutamate and lactate, and cerebral blood flow (CBF) to determine the role of ischemia in this posttraumatic ion dysfunction. METHODS: Eighty-five patients with severe TBI (Glasgow Coma Scale Score < 8) were treated according to an intensive ICP management-focused protocol. All patients underwent intracerebral microdialyis. Dialysate potassium levels were analyzed using flame photometry, and dialysate glutamate and dialysate lactate levels were measured using high-performance liquid chromatography and an enzyme-linked amperometric method in 72 and 84 patients, respectively. Cerebral blood flow studies (stable xenon computerized tomography scanning) were performed in 59 patients. In approximately 20% of the patients, dialysate potassium values were increased (dialysate potassium > 1.8 mM) for 3 hours or more. A mean amount of dialysate potassium greater than 2 mM throughout the entire monitoring period was associated with ICP above 30 mm Hg and fatal outcome, as were progressively rising levels of dialysate potassium. The presence of dialysate potassium correlated positively with dialysate glutamate (p < 0.0001) and lactate (p < 0.0001) levels. Dialysate potassium was significantly inversely correlated with reduced CBF (p = 0.019). CONCLUSIONS: Dialysate potassium was increased after TBI in 20% of measurements. High levels of dialysate potassium were associated with increased ICP and poor outcome. The simultaneous increase in dialysate potassium, together with dialysate glutamate and lactate, supports the concept that glutamate induces ionic flux and consequently increases ICP, which the authors speculate may be due to astrocytic swelling. Reduced CBF was also significantly correlated with increased levels of dialysate potassium. This may be due to either cell swelling or altered vasoreactivity in cerebral blood vessels caused by higher levels of potassium after trauma. Additional studies in which potassium-sensitive microelectrodes are used are needed to validate these ionic events more clearly.     

Management of head injury. Treatment of abnormal intracranial pressure.

Intracranial hypertension is recognized as a fundamental pathophysiologic process in brain injury. Although the exact pressure level defining intracranial hypertension remains to be firmly established, the majority of evidence available currently suggests that ICP should generally be treated when it exceeds 20 mm Hg. We suggest that lesions in the temporal lobe be treated at 15 mm Hg owing to the special relationship of this region to the brain stem. Along with the individual intracranial pressure reading, however, the course of the pressure over time and the status of the intracranial compliance as reflected in the ICP waveform must be considered when evaluating the intracranial dynamics. There is mounting evidence that patients with intracranial hypertension may comprise a heterogeneous group and that subgroups differ in their optimal treatment strategies. Although we cannot as yet identify such groups, factors such as age, CT diagnosis, responsiveness to hyperventilation, pressure-volume index, and ICP waveform are emerging as important differentiating factors. In particular, young patients with absent perimesencephalic cisterns and a tight brain on CT scan who manifest intracranial hypertension may comprise a group more suitable for treatment with hyperventilation and hypnotics than with osmotic agents. Although this is yet to be firmly established, currently it should be considered when such a patient responds poorly early in the course of conventional therapy for raised ICP. Treatment of intracranial hypertension remains rooted in the conventional therapeutic maneuvers. Maintenance of the basic homeostatic state of the patient is to be supplemented with head elevation, sedation, pharmacologic paralysis, hyperventilation, CSF drainage, and osmotic therapy as indicated. Outside of the special considerations discussed earlier, barbiturates should only be considered in patients with refractory intracranial hypertension without preexisting cardiovascular contraindications. Although several other agents have shown promise, currently the most exciting agent appears to be etomidate, which may prove quite useful. As ICP is better defined and understood, many significant and experimentally approachable questions are recognized. The basic mechanisms of raised ICP are slowly becoming elucidated. Clinical clues with which to subdivide patients with intracranial hypertension are being defined. New agents with efficacy in lowering raised ICP are appearing, and determination of their mechanisms of action may provide insight into the underlying disorder.     

Relationship between hyperventilation and intracranial pressure in patients with severe head injury

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Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow.

Increased brain tissue stiffness following severe traumatic brain injury is an important factor in the development of raised intracranial pressure (ICP). However, the mechanisms involved in brain tissue stiffness are not well understood, particularly the effect of changes in systemic blood pressure. Thus, controversy exists as to the optimum management of blood pressure in severe head injury, and diverging treatment strategies have been proposed. In the present study, the effect of induced alterations in blood pressure on ICP and brain stiffness as indicated by the pressure-volume index (PVI) was studied during 58 tests of autoregulation of cerebral blood flow in 47 comatose head-injured patients. In patients with intact autoregulation mechanisms, lowering the blood pressure caused a steep increase in ICP (from 20 +/- 3 to 30 +/- 2 mm Hg, mean +/- standard error of the mean), while raising blood pressure did not change the ICP. When autoregulation was defective, ICP varied directly with blood pressure. Accordingly, with intact autoregulation, a weak positive correlation between PVI and cerebral perfusion pressure was found; however, with defective autoregulation, the PVI was inversely related to cerebral perfusion pressure. The various blood pressure manipulations did not significantly alter the cerebral metabolic rate of oxygen, irrespective of the status of autoregulation. It is concluded that the changes in ICP can be explained by changes in cerebral blood volume due to cerebral vasoconstriction or dilatation, while the changes in PVI can be largely attributed to alterations in transmural pressure, which may or may not be attenuated by cerebral arteriolar vasoconstriction, depending on the autoregulatory status. The data indicate that a decline in blood pressure should be avoided in head-injured patients, even when baseline blood pressure is high. On the other hand, induced hypertension did not consistently reduce ICP in patients with intact autoregulation and should only be attempted after thorough assessment of the cerebrovascular status and under careful monitoring of its effects.     

Continuous cerebral compliance monitoring in severe head injury: its relationship with intracranial pressure and cerebral perfusion pressure

Summary Background. Cerebral compliance expresses the capability to buffer an intracranial volume increase while avoiding a rise in intracranial pressure (ICP). The autoregulatory response to Cerebral Perfusion Pressure (CPP) variation influences cerebral blood volume which is an important determinant of compliance. The direction of compliance change in relation to CPP variation is still under debate. The aim of the study was to investigate the relationship between CPP and compliance in traumatic brain injured (TBI) patients by a new method for continuous monitoring of intracranial compliance as used in neuro-intensive care (NICU).Method. Three European NICU’s standardised collection of CPP, compliance and ICP data to a joint database. Data were analyzed using an unpaired student t-test and a multi-level statistical model.Results. For each variable 108,263 minutes of data were recorded from 21 TBI patients (19 patients GCS≤8; 90% male; age 10–77 y). The average value for the following parameters were: ICP 15.1±8.9 mmHg, CPP 74.3±14 mmHg and compliance 0.68±0.3 ml/mmHg. ICP was ≥20 mmHg in 20% and CPP<60 mmHg for 10.7% of the time. Compliance was lower (0.51±0.34 ml/mmHg) at ICP≥20 than at ICP<20 mmHg (0.73±0.37 ml/mmHg) (p<0.0001). Compliance was significantly lower at CPP<60 than at CPP≥60 mmHg: 0.56±0.36 and 0.70±0.37 ml/mmHg respectively (p<0.0001). The CPP – compliance relationship was different when ICP was above 20 mmHg compared with below 20 mmHg. At ICP<20 mmHg compliance rose as CPP rose. At ICP≥20 mmHg, the relation curve was convexly shaped. At low CPP, the compliance was between 0.20 and 0.30 ml/mmHg. As the CPP reach 80 mmHg average compliance was 0.55 ml/mmHg., but compliance fell to 0.40 ml/mmHg when CPP was 100 mmHg.Conclusions. Low CPP levels are confirmed to be detrimental for intracranial compliance. Moreover, when ICP was pathological, indicating unstable intracranial equilibrium, a high CPP level was also associated with a low volume-buffering capacity.     

Circadian rhythm of cerebral perfusion pressure and intracranial pressure in head injury

The aim of the study was to determine if Cerebral Perfusion Pressure CPP and Intracranial Pressure ICP, in patients with head injury, has a circadian rhythm. CPP and ICP data of 13 patients were analysed using the Regressive and Iterative Cosinor methods. The Regressive Cosinor method did not detect a strong 24 hour rhythm. Therefore, the Iterative Cosinor method was used to seek rhythms with period not necessarily equal to 24 hours. Studying consecutive patient days by the Iterative cosinor method showed that rhythm is present but the rhythm period was often not 24 hours. A significant rhythm in the range of 20-30 hours was detected in eight patients for CPP 62 and in six patients for ICP 46. To validate the results real and surrogate time series were compared. The clinical implications of rhythmic data analysis are discussed.     

Monitoring of cerebrospinal dynamics using continuous analysis of intracranial pressure and cerebral perfusion pressure in head injury

Summary Cerebrospinal dynamics has been investigated by statistical analysis of results of computerised monitoring of 80 head injured patients admitted to the Intensive Care Unit at Pinderfields General Hospital. One minute average values of intracranial pressure (ICP), systemic arterial pressure (ABP), cerebral perfusion pressure (CPP), amplitude of the fundamental component of the intracranial pressure pulse wave and the short-term moving correlation coefficient between that amplitude and mean ICP (RAP) were recorded. It was found that reduction of CPP down to 40mmHg was more often caused by decrease in ABP than increase in ICP. Further falls in CPP below 40mmHg were caused by substantial increases in ICP above 25 mmHg. The relationship between the ICP pulse wave amplitude and CPP showed a significant gradual increase in amplitude with CPP decreasing from 75 to 30 mmHg. For CPP below 30 mmHg there is a sharp decrease in amplitude followed by a change in the coefficient RAP from positive to negative values. This was interpreted as a sign of critical disturbance in cerebral circulation.     

Early changes of intracranial pressure, perfusion pressure, and blood flow after acute head injury. Part 1: An experimental study of the underlying pathophysiology

The present study examines intracranial pressure (ICP), cerebral perfusion pressure (CPP), and cerebral circulation immediately after experimental head injury in an animal model. The underlying systemic hemodynamic changes were also observed. To produce a standardized head injury, a fluid-percussion device was applied to the dura at the midline of 10 piglets. Seven other nontraumatized animals served as a control group. Hemodynamic parameters as well as ICP and CPP were recorded on-line, one value every 1.4 seconds. Cerebral blood flow (CBF) and cerebral vascular resistance (CVR) were measured three times using a microsphere technique. Immediately after head injury, the traumatized animals showed a sudden increase in ICP, with a maximum of 40 torr at 3 to 5 minutes, while there was a pronounced decrease in CPP from 85 to 40 torr. The CBF in the various brain areas fell from 55 to 22 ml/min/100 gm within 5 minutes after the impact, and CVR increased to 300% of control values within 90 minutes. The findings of this study demonstrated that cerebral circulation is critically jeopardized within a few minutes after trauma. This, in combination with a subsequent increase in CVR, makes the early development of ischemic brain damage very likely. In traumatized patients, treatment prior to hospital admission must therefore be directed at prevention of this fatal course.     

Efficacy of hyperventilation,blood pressure elevation,and metabolic suppression therapy in controlling intracranial pressure after head injury

OBJECT: Hyperventilation therapy, blood pressure augmentation, and metabolic suppression therapy are often used to reduce intracranial pressure (ICP) and improve cerebral perfusion pressure (CPP) in intubated head-injured patients. In this study, as part of routine vasoreactivity testing, these three therapies were assessed in their effectiveness in reducing ICP. METHODS: Thirty-three patients with a mean age of 33 +/- 13 years and a median Glasgow Coma Scale (GCS) score of 7 underwent a total of 70 vasoreactivity testing sessions from postinjury Days 0 to 13. After an initial 133Xe cerebral blood flow (CBF) assessment, transcranial Doppler ultrasonography recordings of the middle cerebral arteries were obtained to assess blood flow velocity changes resulting from transient hyperventilation (57 studies in 27 patients), phenylephrine-induced hypertension (55 studies in 26 patients), and propofol-induced metabolic suppression (43 studies in 21 patients). Changes in ICP, mean arterial blood pressure (MABP), CPP, PaCO2, and jugular venous oxygen saturation (SjvO2) were recorded. With hyperventilation therapy, patients experienced a mean decrease in PaCO2 from 35 +/- 5 to 27 +/- 5 mm Hg and in ICP from 20 +/- 11 to 13 +/- 8 mm Hg (p < 0.001). In no patient who underwent hyperventilation therapy did SjvO2 fall below 55%. With induced hypertension, MABP in patients increased by 14 +/- 5 mm Hg and ICP increased from 16 +/- 9 to 19 +/- 9 mm Hg (p = 0.001). With the aid of metabolic suppression, MABP remained stable and ICP decreased from 20 +/- 10 to 16 +/- 11 mm Hg (p < 0.001). A decrease in ICP of more than 20% below the baseline value was observed in 77.2, 5.5, and 48.8% of hyperventilation, induced-hypertension, and metabolic suppression tests, respectively (p < 0.001 for all comparisons). Predictors of an effective reduction in ICP included a high PaCO2 for hyperventilation, a high study GCS score for induced hypertension, and a high PaCO2 and a high CBF for metabolic suppression. CONCLUSIONS: Of the three modalities tested to reduce ICP, hyperventilation therapy was the most consistently effective, metabolic suppression therapy was variably effective, and induced hypertension was generally ineffective and in some instances significantly raised ICP. The results of this study suggest that hyperventilation may be used more aggressively to control ICP in head-injured patients, provided it is performed in conjunction with monitoring of SjvO2.     

Relationship between intracranial pressure and cortical spreading depression following fluid percussion brain injury in rats

Traumatic brain injury (TBI) is known to be accompanied by an increase in intracranial pressure (ICP) and in some cases, by spontaneous generation of cortical spreading depression (CSD) cycles. However, the role of CSD in the pathophysiology of cerebral contusion is still unknown. A multiparametric monitoring assembly was placed on the right hemisphere of the rat brain to evaluate ICP, DC potential, extracellular K(+), cerebral blood flow (CBF), and electrocorticogram in 27 rats during 5 h. Fluid percussion brain injury (FPBI) with the magnitude of the impact 2.9, 3.3, 4.1, and 5.0 atmospheres was induced to the left parietal cortex in animal groups A, B, C, and D, respectively. A slow increase in ICP was evident, and was pronounced in group C and especially in group D, where four of nine animals died during the monitoring. At the end of the 5 h experiment, the mean ICP levels were 6.75 +/- 2.87, 8.40 +/- 2.70, 12.75 +/- 4.03, 29.56 +/- 9.25, and the mean total number of CSD cycles was 2.00 +/- 1.41, 4.29 +/- 4.23, 11.71 +/- 13.29, and 20.11 +/- 19.26 in groups A, B, C, and D, respectively. The maximal level of intensity of CSD cycle generation after FPBI was obtained in group D, where almost constant activity was maintained until the end of the experiment. A significant coefficient of correlation between ICP level and total number of CSD cycles was found for all ICP measurements (r = 0.47-0.63, p < 0.05, n = 27), however more significant (p < 0.001) was the coefficient during the period of monitoring between 2 and 4 h after FPBI. Our results suggest that numerous repeating CSD cycles are typical phenomena in moderate and especially severe forms of FPBI. The rising number of CSD cycles under condition of an ICP level >/=20 mm Hg may demonstrate, with high probability, the unfavorable development of TBI, caused by growing secondary hypoxic insult.     

The prognostic value of intracranial pressure monitoring after severe head injuries.

ICP monitoring appears not to be essential for the prognosis of head injury patients, but it may be of some clinical value in association with the neurological status and other clinical data. The results of ICP measurement show that a high level in brain pressure and the poor outcome have a better correlation with one another than a lower level of brain pressure and a good recovery.