Acute Severe Head Injury Research Articles

Clinical significance of admission hyperglycemia and factors related to it in patients with acute severe head injury

Patients in the acute stage after a severe head injury often exhibit systemic stress responses. The aim of the present study is to assess in such patients the clinical significance of the change of catecholamines (CA) and of blood glucose. The levels of serum of norepinephrine (NE), epinephrine (E), and dopamine (DA) were measured in 48 adults in the first 7 days after a severe head injury, and in 35 normal adults as a control group. The blood level of glucose at the time of admission was also measured. It was found that: (1) The serum CA level was significantly higher in the injured group than in controls. (2) The serum NE and E levels were higher in patients with lower Glasgow Coma Scores (GCS) and in the group of patients who did not survive. (3) The blood glucose level on admission was related both to the serum NE and E levels within the first 24 hours after head injury (r = 0.574, p < 0.05 and r = 0.410 and p < 0.05, respectively) and also the GCS and Glasgow Outcome Score (GOS) in these patients. (4) Patients with GCS of 3-4, 5-6, and 7-8 had mean glucose levels on admission of 12.805 +/- 3.205 mmol/L (228 +/- 67.23 mg/100 mL), 9.133 +/- 1.228 mmol/L, (160 +/- 12.28 mg/100 mL) and 6.029 +/- 1.228 mmol/L (107.66 +/- 21.9 mg/100 mL), respectively (p < 0.01). (5) Ninety percent of the patients with blood glucose levels of 9.6 mmol/L (171.4 mg/100 mL) at admission died within the first month; in the patients with lower glucose levels the mortality was 15%. These findings suggest that in the acute stage of severe head injury hyperglycemia and elevation of serum levels of CA are common components of the stress response, significant indicators of severity, and significant predictors of outcome.

Biochemical parameters of recovery in acute severe head injury

Levels of urinary catecholamines (noradrenaline, adrenaline, dopamine), plasma acetylcholinesterase, serum serotonin and plasma 3-methoxy-4-hydroxyphenylglycol were recorded in 38 adult subjects during the first 21 days after severe head injury. Levels of acetylcholinesterase, serotonin and 3-methoxy-4-hydroxyphenylglycol differed significantly between survivors and those who died. For survivors, initially abnormal biochemical levels recovered toward the norm as time after injury progressed.

The role of neuroeffector mechanisms in cerebral hyperperfusion syndromes

Cerebral hyperperfusion, a state in which blood flow exceeds the metabolic needs of brain, may complicate a number of neurological and neurosurgical conditions. It may account for the propensity with which hemorrhage, cerebral edema, or seizures follow embolic stroke, carotid endarterectomy, or the excision of large arteriovenous malformations, and for some of the morbidity that accompanies acute severe head injury, prolonged seizures, and acute severe hypertension. Hyperperfusion syndromes have in common acute increases in blood pressure, vasodilatation, breakdown of the blood-brain barrier, and the development of cerebral edema. These common features suggest the possibility that they share the same pathogenic mechanisms. It was believed until recently that reactive hyperemia was caused primarily by the generation of vasoactive metabolites, which induced vasodilatation through relaxation of vascular smooth muscle. However, the authors have recently established that the release of vasoactive neuropeptides from perivascular sensory nerves via axon reflex-like mechanisms has a significant bearing upon a number of hyperperfusion syndromes. In this article, the authors summarize their data and discuss possible therapeutic implications for blockade of these nerves or their constituent neuropeptides.

The management of acute severe head injury.

Immediate phase (minutes) There is an acute increase in systemic arterial pressure (SAP), a smaller increase in intracranial pressure (ICP), apnoea, and an isoelectric EEG. z The SAP increases because of hypothalamic discharge; ICP because autoregulation of cerebral blood flow (CBF) is exceeded, and because there is widespread intracranial vascular spasm. The latter in due to microvascular haemorrhage and reflex vessel responses to shearing forces. After about a minute all these disturbances abate, perhaps in part due to mobilization of endogenous opioids. 3

A decision tree for the treatment of acute severe head injury : Ueda M, Matsumae M, Yamada S, et al. Jpn J Acute Med 1987;11(1):81–89

A decision tree for the treatment of acute severe head injury : Ueda M, Matsumae M, Yamada S, et al. Jpn J Acute Med 1987;11(1):81–89

The alterations of plasma potassium in patients with severe acute head injury: Trouwborst A, Kooijman J. Injury 1984; 15:293–295.

The alterations of plasma potassium in patients with severe acute head injury: Trouwborst A, Kooijman J. Injury 1984; 15:293–295.

The alterations of plasma potassium in patients with severe acute head injury

Twenty patients with a severe head injury were studied; 70 per cent of these were admitted with hypokalaemia accompanied by tachycardia and sometimes arrhythmias. These abnormalities are easily corrected by means of a rapid infusion of supplementary potassium.

Comprehensive monitoring and computerized tomographic follow up in patients with acute severe head injury: coma-outcome correlations.

In 88 patients with acute severe head injury the Glasgow coma scale (GCS), computerized tomography and autonomic monitoring during the first 24 hours were used to characterize different types of post-traumatic brain dysfunction. A subgroup is defined--GCS 8.1--with signs of diffuse brain swelling and autonomic instability which included two cases with dorsal midbrain lesions. These preliminary results suggest that autonomic instability is a valid criterion for identifying patients suffering from diffuse axonal injury.

Auditory function in acute severe head injury

AbstractThere are few clinical neuro‐otologic investigations of acute head injury. We obtained impedance and auditory brain stem response measures for 25 acute head‐injured patients, usually within 76 hours following injury. All patients were comatose at the time of assessment. Impedance abnormalities were found for over three‐fourths of the patients. Generally, they were associated with transient, reversible dysfunction, such as high negative middle ear pressure. The acoustic stapedius reflex, however, was seldom observed, even in patients with apparently normal middle ear function.Auditory brain stem response measures showed evidence of CNS dysfunction in 80% of the patients. Abnormalities ranged from prolonged latency and reduced amplitude of the wave V auditory brain stem response component to total absence of brain stem auditory activity. There was a relationship between auditory brain stem response findings and neurologic outcome at 1 month post assessment. Electrophysiologic auditory measures are clinically valuable in neuro‐otologic diagnosis and neurologic prognosis of acute, severe head injury.

Assessment of brainstem damage by the auditory brainstem response in acute severe head injury.

In 64 cases suffering from severe head injury (Glasgow coma scale: less than seven- the auditory brainstem responses (FARs) recorded at the vertex, which are thought to be volumet conducted far-field potentials reflecting the sequential electrical activities of the auditory afferen) system in the brainstem, were recorded in the neurosurgical intensive care room immediately after admission. The alterations in the responses were compared with the types of primary injury, neurological signs., CT findings and outcome following treatment. Based on the results obtained, it is concluded that the FAR is a useful indicator for predicting the effects of treatment on brainstem damage in patients with severe head injury, and that it provides more reliable information about the function of the brainstem than the neurological signs or CT findings. Moreover, it also offers a diagnostic method for primary brainstem injury. Three cases or primary brainstem injury without lesions in the supratentorial region were diagnosed by means of combined CT and FAR recording.

Reproducibility of regional cerebral blood flow measurements in acute severe head injury.

In order to evaluate the reproducibility of regional cerebral blood flow (rCBF) measurements in pathological brain tissue, serial measurements were carried out in 13 determinations performed in patients who were comatose after severe head injuries within the first 2 weeks after the head trauma. The xenon-133 intra-arterial method was used for the flow measurements, and the flow was studied separately in 16 areas of the brain, producing 197 regional double determinations. The patients were maintained in a steady state during and between the measurements, and only differences of less than 2 mm Hg in the arterial CO2 pressure and less than 5 mm Hg in the perfusion pressure were tolerated. The reproducibility was found to be reasonably good as regards initial slope-flow indices and height/area flow indices and height/area flow values, whereas that of the compartmentally calculated flow parameters was poorer. On dividing the series into severely and moderately pathological areas, it could be shown that the reproducibility of the flor values in the moderately pathological brain areas was acceptable and similar to the results reported by others, whereas the reproducibility in the most severely pathological areas of the brain was rather poor, as regards the flow in the fast compartments. The correlation between the various flow parameters was found to be fairly good.

Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury.

Regional cerebral blood flow (rCBF), cerebral intraventricular pressure (IVP), systemic arterial blood pressure, and cerebral ventricular fluid (CSF) lactate and pH were studied repeatedly in 23 patients during the acute phase of severe brain injury lasting from 3 to 21 days after the trauma. Cerebrovascular autoregulation was tested repeatedly by means of angiotensin infusion in 21 of the patients, and CO2 response in 14 by means of passive hyperventilation. The pressure in the brain ventricles was measured continuously in all patients and kept below 45 mm Hg during the study. If the IVP increased more than 10 mm Hg during the angiotensin infusion (as in one case), the autoregulation test was considered contraindicated and the angiotensin infusion was discontinued. Dissociation between cerebrovascular autoregulation and CO2 response was a common phenomenon. Typically, autoregulation appeared preserved in the most severely injured areas of the cerebral cortex when the patient was deeply comatose, but deteriorated concomitantly with recovery; by the time the patient became alert, the autoregulation was always impaired. The CO2 response was impaired only in patients who were deeply comatose and had attacks of decerebrate rigidity; during recovery the CO2 response became normal. Thus, preserved autoregulation associated with imparied CO2 response indicated very severe brain damage, whereas impaired autoregulation associated with preserved CO2 response suggested moderate or severe brain damage in recovery. These paradoxical observations raise the question whether the preserved autoregulation seen in severely injured brain tissue is a true autoregulation caused by an active vasoconstrictor response to an increase in blood pressure.

Cerebrospinal fluid lactate and pH in patients with acute severe head injury

Cerebral ventricular fluid (CSF) lactate and pH were measured repeatedly in 21 comatose patients with severe head injury during the first three weeks after trauma. In addition, regional cerebral 133Xe blood flow (rCBF) was measured two to four times in each patient at various time intervals, depending on the indications for carotid angiography, and the pressure in the cerebral ventricular system (IVP) was measured continuously. The series was divided into three groups: (1) patients with local cortical cerebral lesions, (2) patients with brain-stem symptoms, and (3) patients with both local cortical lesions and brain-stem symptoms. The results showed that a high CSF lactate level in patients with severe acute brain injury suggested severe and extensive brain lesions and predicted a poor outcome of the injury. In the individual patients, increasing CSF lactate foreboded clinical deterioration, whereas decreasing CSF lactate indicated recovery. The CSF pH was decreased in most patients, but very low pH levels (below 7.20) were seen only in three patients who all had a poor outcome. Correlation was not observed between CSF lactate and rCBF or between CSF pH and rCBF. It is concluded that repeated determination of CSF lactate and pH during the post-traumatic period may be a valuable tool in the assessment of the course and outcome of the brain injury.

Medical management of severe acute head injury.

Medical management of severe acute head injury.

132. Acid-base Balance Disorder in the Cases of Severe Acute Head Injury

132. Acid-base Balance Disorder in the Cases of Severe Acute Head Injury