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.     

Slope of the intracranial pressure waveform after traumatic brain injury

BACKGROUND: The measurement and treatment of ICP within the management of TBI generally focuses on keeping the mean ICP to less than 20 mm Hg. More sophisticated analysis of the intracranial pressure waveform has yielded important relationships, but those methods have not gained widespread use. Prior analysis of the slope of the ICP waveform during inspiration and expiration in patients with hydrocephalus has provided valuable information that has never been applied to patients with TBI. This study used digital methods to examine ICP and the slope of the ICP waveform in relation to the respiratory cycle in subjects with TBI. METHODS: Intracranial pressure was monitored in 6 randomly selected patients admitted with acute TBI. In the first 3 subjects, a single 5-minute recording was analyzed. In 3 subsequent subjects, 4 nonsequential 5-minute epochs were analyzed during periods of varying ICP. The systolic slope of the ICP waveform was compared during inspiration and expiration, and then evaluated in relation to simultaneous mean ICP. RESULTS: The slope of the systolic ICP waveform was significantly greater during inspiration than during expiration (P < .0001 for 5 subjects and P < .03 for 1 subject). Within each subject, the ICP slope was positively correlated with simultaneous ICP (P < .0001 in all 6 cases). CONCLUSION: Greater systolic ICP waveform slope during inspiration has not been described previously after TBI and is consistent with prior observations in subjects with hydrocephalus. The strong correlation between ICP slope and simultaneous mean ICP suggests that increasing ICP slope might indicate loss of intracranial compliance after TBI.     

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.     

An analysis of the relationship between fluid and sodium administration and intracranial pressure after head injury.

Severe head injury is the leading cause of traumatic death. When a severe head injury is combined with hypotension the mortality doubles. The use of asanguineous salt solutions to maintain blood pressure, however, may contribute to cerebral swelling and intracranial hypertension. For this reason, restrictions of fluids (FLD) and sodium (Na) have been advocated. To our knowledge, however, there are no clinical data to support this recommendation. We hypothesized that in adult patients sustaining severe head injuries (Glasgow Coma Scale score less than or equal to 8) with or without associated injuries: (1) FLD balance and total Na administered during the initial 72 hours of hospital admission are positively and significantly correlated with each other, and (2) total FLD, FLD balance, and total Na administration during the initial 72 hours are significantly and positively correlated with changes in ICP and adverse outcome. We retrospectively studied 40 adult trauma patients with severe head injuries. We found a significant correlation between total Na and FLD balance (R2 = 0.54; p less than 0.05). However, we found no significant correlation between total FLD and maximum ICP (R2 = 0.081), ICP score (R2 = 0.01), or outcome (R2 = 0.066), no significant correlation between FLD balance and maximum ICP (R2 = 0.000), ICP score (R2 = 0.000), or outcome (R2 = 0.01), and no significant correlation between total Na and maximum ICP (R2 = 0.000), ICP score (R2 = 0.001), or outcome (R2 = 0.02). We conclude that Na and FLD administration are not independent determinants of ICP during the initial 72 hours after brain injury.     

Changes in intracranial pressure and epidural pulse waveform following cold injury

Summary Using anaesthetized spontaneously breathing cats, intracranial pressure (ICP) was monitored for twenty hours following the insult of cold injury; simultaneous recordings were also made of cerebral blood flow (CBF), epidural pulse waveform (EDP-WF), and systemic arterial pressure (SAP). Results could be divided into two groups depending on whether or not ICP exceeded 30 mmHg. In group one, in which marked increase in ICP including occasional episodes of pressure waves were observed, an initial increase in CBF and the changes in EDP-WF from polyphasic to monotonous at about 20 mmHg were characteristic. On the other hand, in group two, ICP never exceeded 30 mmHg, CBF slightly and continuously decreased and EDP-WF was polyphasic throughout the course. There were no significant differences in trends in SAP, in the extent of spread of oedema and in water content of the white matter between both groups. Therefore, the amount of cerebral blood volume (CBV) due to cerebral vasodilatation was considered to account for the further increase in ICP. Moreover, changes in EDP-WF were regarded as a useful indicator in predicting the trends in ICP since these changes could be observed in a relatively lower pressure range prior to a marked increase in ICP.     

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.     

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.     

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.     

Analysis of intracranial pressure waveform during infusion test

Summary An analysis of intracranial pressure (ICP), based on an examination of the temporary correlation between the changes in amplitude of the pulse wave and the mean ICP level, is presented. The paper contains a discussion of the preliminary results of the method when applied to the analysis of ICP as monitored during infusion tests in a group of 24 children. Infusion of a certain volume of CSF is a good example of an uncompensated volume process, introduced externally into the intracranial space. Results allow an interpretation of the short term correlation coefficient RAP (correlation coefficient between ICP and variations of the amplitude of fundamental component of the pulse wave AMP), as a steady state index. According to this interpretation, the presented analysis enables the observation of a loss of equilibrium during the test. Other phenomena can also be observed, for instance a recovery to equilibrium after the test, nonlinearities of amplitude-pressure relationship, vasomotor reflexes etc.     

Effect of total parenteral nutrition upon intracranial pressure in severe head injury

Animal investigations suggest that administration of hyperosmolar total parenteral nutrition (TPN) solutions may potentiate cerebral edema following head injury. Intravenous nutrition (TPN) is often required after head injury due to intolerance to enteral feeding (EN). This study evaluates the effect of TPN on intracranial pressure (ICP) measurements in severely brain-injured patients. Ninety-six severely brain-injured patients were randomly assigned to receive TPN or EN and were studied from hospital admission until 18 days postinjury. The TPN was started within 48 hours postinjury and the EN was started when tolerated. Peak daily ICP was not significantly different on admission and over time (overall mean +/- standard error of the mean 32.01 +/- 1.62 for TPN versus 32.5 +/- 1.25 for EN). Intracranial pressure was greater than 20 mm Hg in 75% of TPN patients and 73% of EN patients. Conventional therapy failed to control elevated ICP in 36% of TPN patients and 38% of EN patients. Of these patients, subsequent barbiturate therapy failed to control ICP in 56% of TPN patients and 64% of EN patients. Serum osmolality was not significantly different between groups at admission or over the course of the study. The TPN group tended to have higher mean serum glucose levels for the first 13 days postinjury, while the EN group had a higher mean serum glucose content thereafter, but these differences were not statistically significant. This study shows that TPN can be given safely to the severely brain-injured patient without causing serum hyperosmolality or affecting ICP levels or ICP therapy.     

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

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Continuous monitoring of intracranial compliance after severe head injury: relation to data quality, intracranial pressure and brain tissue PO2

The objective of the present study was to test the new continuous intracranial compliance (cICC) device in terms of data quality, relationship to intracranial pressure (ICP) and brain tissue oxygenation (PtiO2). A total of 10 adult patients with severe traumatic brain injury underwent computerized monitoring of arterial blood pressure, ICP, cerebral perfusion pressure, end-tidal CO2, cICC and PtiO2 providing a total of 1726 h of data. (1) The data quality assessed by calculating the 'time of good data quality' (TGDQ, %), i.e. the median duration of artefact-free time as a percentage of total monitoring time reached 98 and 99% for ICP and PtiO2, while cICC measurements were free of artefacts in only 81%. (2) Individual regression analysis showed broad scattered correlation between cICC and ICP ranging from low (r = 0.05) to high (r = 0.52) correlation coefficients. (3) From 225 episodes of increased ICP (ICP > 20 mmHg > 10 min), only 37 were correctly predicted by a preceding decline in cICC to pathological values (< 0.5 ml/mmHg). (4) In all episodes of cerebral hypoxia (PtiO2 < 10 mmHg > 10 min), cICC was not pathologically altered. Based on the present results, we conclude that the current hardware and software version of the cICC monitoring system is unsatisfactory concerning data quality, prediction of increased ICP and revelance of cerebral hypoxic episodes.     

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.     

Indomethacin: its role in the management of intractable intracranial pressure (ICP) after severe head injury

Intracranial hypertension that fails to respond to first linemedical and surgical treatment after head injury is associatedwith a 92% mortality overall.¹ The addition of barbiturateswill result in a good or moderate neurological outcome in 35%of patients,² but those with hyperaemia do significantly worse.However barbiturates may not be a logical choice for those patientswhose intracranial hypertension is secondary to hyperaemia,and may be associated with significant complications. In thesepatients cerebral vasoconstrictors such as indomethacin maybe more appropriate and possibly associated with fewer unwantedeffects. In one study six out of 10 patients who received indomethacinfor intracranial hypertension unresponsive to barbiturates survived.³However it is unclear how many were hyperaemic since jugularvenous saturation (Sj_O2) was not monitored. We report our experiencewith indomethacin in 10 severely head-injured patients. Our protocol aims to maintain a target cerebral perfusion pressure(CPP) and ICP through the application of sedation, diuretics,CSF drainage, mild hypothermia, muscle relaxation and controlof arterial carbon dioxide (Pa_CO2). If the ICP remains elevatedthen Sj_O2 is monitored. The combination of raised ICP and Sj_O2is taken to indicate hyperaemia (absolute or relative). In thesecircumstances the patient is hyperventilated to a Pa_CO2 of 28mmHg and if necessary an intravenous infusion of thiopentonecommenced. We used indomethacin infusions in 10 patients fulfillingthese criteria of hyperaemia. In seven patients the hyperaemiawas confirmed as absolute by demonstrating a raised middle cerebralartery velocity (MCAV) with transcranial Doppler. The mean ageof the patients was 21.2 yr (range 8–55). Indomethacinwas infused for a mean of 3.8 days (1–11) at a rate of3–11 mg h^–1. The effect of indomethacin on mean(SD) ICP, CPP and Sj_O2 is shown in Table 4. At 6-month follow up there were seven survivors (three goodrecovery, three moderate recovery, one severely disabled). Threepatients died with intractable ICP and septic shock. Two ofthese patients had associated renal failure. There were no episodesof gastrointestinal bleeding. Two of the three patients whodied did not have MCAV measured, and therefore indomethacinmay not have been strictly indicated. These results achievedin this subgroup of head injured patients is much better thanthat expected, and matches the outcome achieved in the overallICU head injury population. Indomethacin may have a role inthe management of raised ICP associated with hyperaemia aftersevere head injury. We recommend however that it should onlybe used with monitoring of both Sj_O2 and MCAV.     

High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury

In a five-center study, 73 patients with severe head injury and elevated intracranial pressure (ICP) were randomly assigned to receive either a regimen that included high-dose pentobarbital or one that was otherwise similar but did not include pentobarbital. The results indicated a 2:1 benefit for those treated with the drug with regard to ICP control. When patients were stratified by prerandomization cardiac complications, the advantage increased to 4:1. A multiple logistic model considering treatment and selected baseline variables indicated a significant positive treatment effect of barbiturates, a significant effect of time from injury to randomization, and an interaction of treatment with cardiovascular complications. However, of 925 patients potentially eligible for randomization, only 12% met ICP randomization criteria. The results support the hypothesis that high-dose pentobarbital is an effective adjunctive therapy, but that it is indicated in only a small subset of patients with severe head injury.     

Hypertonic saline lowers raised intracranial pressure in children after head trauma

Eighteen pediatric patients who sustained traumatic brain injury were enrolled in a double-blind, crossover study comparing the effects of 3% saline and 0.9% saline infusions on raised intracranial pressure (ICP). After resuscitation, each patient received a bolus of each saline concentration, and ICP was monitored for 2 h. Initial mean ICP before 0.9% saline infusions equaled 19.3 mm Hg and averaged 20.0 mm Hg during the subsequent 2-h trials (p = 0.32). Baseline mean ICP before 3% saline administration equaled 19.9 mm Hg and averaged 15.8 mm Hg for 2 h postinfusion (p = 0.003). Central venous pressure did not change significantly in either group, nor did measurements of renal function. Serum sodium concentrations increased in all 18 trials of 3% saline. Maximal concentrations of serum sodium occurred 30 min after bolus administration of 3% saline. Three percent saline significantly reduces raised ICP after traumatic brain injury when compared with normal saline. Intravascular dehydration, as measured by central venous pressure, did not occur during the study period.     

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.