Treatment of hypertension associated with head injury

1983 ◽  
Vol 59 (3) ◽  
pp. 455-460 ◽  
Author(s):  
Claudia S. Robertson ◽  
Guy L. Clifton ◽  
Addison A. Taylor ◽  
Robert G. Grossman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Head Injury ◽  
Cardiac Index ◽  
Injured Patient ◽  
Venous Admixture ◽  
Cardiac Work ◽  
Content Type ◽  
Head Injured ◽  
Consistent Change

✓ Arterial hypertension that occurs after severe head injury is characterized by elevation of systolic blood pressure, tachycardia, increased cardiac output, normal or decreased peripheral vascular resistance, and increased circulating catecholamines. The effects of two drugs used in the management of hypertension, propranolol and hydralazine, on these indices of cardiovascular function were examined in six head-injured patients. Both drugs effectively normalized blood pressure. However, hydralazine increased heart rate by 30%, cardiac index by 49%, left cardiac work by 21%, and pulmonary venous admixture by 53%, and was responsible for an increase in intracranial pressure or decreased compliance in two patients. Hydralazine produced no consistent change in arterial catecholamines. In contrast, propranolol decreased heart rate by 21%, cardiac index by 26%, left cardiac work by 35%, pulmonary venous admixture by 15%, and oxygen consumption by 18%. Propranolol decreased arterial epinephrine levels by 48% and norepinephrine levels by 28%. Propranolol appears to be a useful antihypertensive drug in the hyperdynamic head-injured patient because it normalizes blood pressure and the underlying hemodynamic abnormalities both by its beta-adrenergic blocking action and by decreasing circulating levels of catecholamines.

Cerebral autoregulation following minor head injury

1997 ◽  
Vol 86 (3) ◽  
pp. 425-432 ◽  
Author(s):  
Elisabeth C. Jünger ◽  
David W. Newell ◽  
Gerald A. Grant ◽  
Anthony M. Avellino ◽  
Saadi Ghatan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Head Injury ◽  
Cerebral Autoregulation ◽  
Minor Head Injury ◽  
Lower Blood Pressure ◽  
Content Type ◽  
Lower Blood ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ The purpose of this study was to determine whether patients with minor head injury experience impairments in cerebral autoregulation. Twenty-nine patients with minor head injuries defined by Glasgow Coma Scale (GCS) scores of 13 to 15 underwent testing of dynamic cerebral autoregulation within 48 hours of their injury using continuous transcranial Doppler velocity recordings and blood pressure recordings. Twenty-nine age-matched normal volunteers underwent autoregulation testing in the same manner to establish comparison values. The function of the autoregulatory response was assessed by the cerebral blood flow velocity response to induced rapid brief changes in arterial blood pressure and measured as the autoregulation index (ARI). Eight (28%) of the 29 patients with minor head injury demonstrated poorly functioning or absent cerebral autoregulation versus none of the controls, and this difference was highly significant (p = 0.008). A significant correlation between lower blood pressure and worse autoregulation was found by regression analysis in head-injured patients (r = 0.6, p < 0.001); however, lower blood pressure did not account for the autoregulatory impairment in all patients. Within this group of head-injured patients there was no correlation between ARI and initial GCS or 1-month Glasgow Outcome Scale scores. This study indicates that a significant number of patients with minor head injury may have impaired cerebral autoregulation and may be at increased risk for secondary ischemic neuronal damage.

Enhanced specificity of prognosis in severe head injury

1988 ◽  
Vol 69 (3) ◽  
pp. 381-385 ◽  
Author(s):  
Sung C. Choi ◽  
Raj K. Narayan ◽  
Randy L. Anderson ◽  
John D. Ward
Keyword(s):  
Head Injury ◽  
Severe Head Injury ◽  
Injured Patient ◽  
Pupillary Response ◽  
Prognostic Indicators ◽  
Content Type ◽  
Medical College ◽  
Head Injured ◽  
Actual Outcome ◽  
Probable Outcome

✓ Data from 523 patients admitted to the Medical College of Virginia with severe head injury and known 6-month outcomes were analyzed in order to determine the optimal combination of early-available prognostic factors. Twenty-one prognostic indicators noted in the emergency room at admission were used to predict outcomes into four categories: good, moderately disabled, severely disabled, or vegetative/dead. A combination of the patient's age (in years), the best motor response (graded in the usual six-point scale), and pupillary response (in both eyes) was found to be the most accurate indicator. The model correctly predicted outcome into one of the four outcome categories in 78% of cases (“specifically accurate predictions”). If predictions into an outcome category adjacent to the actual outcome were accepted, this model was accurate in 90% of cases (“grossly accurate predictions”). A set of three simple graphs based on this model can be used for rapid early estimation of probable outcome in a severely head-injured patient at admission.

Stress-induced malignant hyperthermia in a head-injured patient

1988 ◽  
Vol 68 (2) ◽  
pp. 297-299 ◽  
Author(s):  
Tony Feuerman ◽  
George F. Gade ◽  
Robert Reynolds
Keyword(s):  
Head Injury ◽  
Body Temperature ◽  
Malignant Hyperthermia ◽  
Injured Patient ◽  
Drug Induced ◽  
Content Type ◽  
Anesthetic Agents ◽  
Head Injured ◽  
Inhalational Anesthetic ◽  
Fine Print

✓ Susceptibility to malignant hyperthermia is a rare inherited myopathy. Hypermetabolic crises accompanied by a rise in body temperature to as high as 44°C are the hallmark of malignant hyperthermia episodes. These are triggered by inhalational anesthetic agents or depolarizing muscle-relaxant drugs. A similar condition exists in pigs; however, in addition to drug-induced attacks, episodes of malignant hyperthermia occur in these animals as a result of stress. It has been proposed that stress-induced malignant hyperthermia occurs in man. The present paper presents a case of stress-induced malignant hyperthermia in a 21-year-old man in whom the inciting stress was a head injury.

Impairment of helper T-cell function and lymphokineactivated killer cytotoxicity following severe head injury

1991 ◽  
Vol 75 (5) ◽  
pp. 766-773 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Edmund H. Frank ◽  
Claramae H. Miller ◽  
Asim Amin ◽  
Bernardo W. Issel ◽  
...  
Keyword(s):  
T Cell ◽  
Head Injury ◽  
Severe Head Injury ◽  
Cell Cytotoxicity ◽  
Content Type ◽  
Lak Cell ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Infection is a major complication of severe head injury, occurring in 50% to 75% of patients who survive to hospitalization. Previous investigations of immune activity following head injury have demonstrated suppression of helper T-cell activation. In this study, the in vitro production of interferon-gamma (INF-γ), interleukin-1 (IL-1), and interleukin-2 (IL-2) was determined in 25 head-injured patients following incubation of peripheral blood lymphocytes (PBL's) with the lymphocyte mitogen phytohemagglutinin (PHA). In order to elucidate the functional status of cellular cytotoxicity, lymphokine-activated killer (LAK) cell cytotoxicity assays were performed both prior to and following incubation of PBL's with IL-2 in five patients with severe head injury. The production of INF-γ and IL-2 by PHA-stimulated PBL's was maximally depressed within 24 hours of injury (p < 0.001 for INF-γ, p = 0.035 for IL-2) and partially normalized within 21 days of injury. There was no change in the production of IL-1. When comparing the in vitro LAK cell cytotoxicity of PBL's from head-injured patients and normal subjects, there was a significant depression in LAK cell cytotoxicity both prior to (p = 0.010) and following (p < 0.001) incubation of PBL's with IL-2. The results of this study indicate that IL-2 and INF-γ production, normally required for inducing cell-mediated immunity, is suppressed following severe head injury. The failure of IL-2 to enhance LAK cell cytotoxicity suggests that factors other than decreased IL-2 production, such as inhibitory soluble mediators or suppressor lymphocytes, may be responsible for the reduction in cellular immune activity following severe head injury. These findings may have significant implications in designing clinical studies aimed at reducing the incidence of infection following severe head injury.

Role of intracranial pressure monitoring in severely head-injured patients without signs of intracranial hypertension on initial computerized tomography

1994 ◽  
Vol 80 (1) ◽  
pp. 46-50 ◽  
Author(s):  
Michael G. O'Sullivan ◽  
Patrick F. Statham ◽  
Patricia A. Jones ◽  
J. Douglas Miller ◽  
N. Mark Dearden ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ct Scan ◽  
Intracranial Hypertension ◽  
Mass Lesion ◽  
Midline Shift ◽  
Pressure Monitoring ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ 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 ≥ 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 ≥ 30 mm Hg) and duration. Reduced CPP (≤ 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.

High-risk mild head injury

1997 ◽  
Vol 87 (2) ◽  
pp. 234-238 ◽  
Author(s):  
John N. K. Hsiang ◽  
Theresa Yeung ◽  
Ashley L. M. Yu ◽  
Wai S. Poon
Keyword(s):  
Head Injury ◽  
High Risk ◽  
Mild Head Injury ◽  
Radiographic Findings ◽  
Content Type ◽  
Head Injured ◽  
Definition Of ◽  
Gcs Score ◽  
Injured Patients ◽  
Fine Print

✓ The generally accepted definition of mild head injury includes Glasgow Coma Scale (GCS) scores of 13 to 15. However, many studies have shown that there is a heterogeneous pathophysiology among patients with GCS scores in this range. The current definition of mild head injury is misleading because patients classified in this category can have severe sequelae. Therefore, a prospective study of 1360 head-injured patients with GCS scores ranging from 13 to 15 who were admitted to the neurosurgery service during 1994 and 1995 was undertaken to modify the current definition of mild head injury. Data regarding patients' age, sex, GCS score, radiographic findings, neurosurgical intervention, and 6-month outcome were collected and analyzed. The results of this study showed that patients with lower GCS scores tended to have suffered more serious injury. There was a statistically significant trend across GCS scores for percentage of patients with positive acute radiographic findings, percentage receiving neurosurgical interventions, and percentage with poor outcome. The presence of postinjury vomiting did not correlate with findings of acute radiographic abnormalities. Based on the results of this study, the authors divided all head-injured patients with GCS scores ranging from 13 to 15 into mild head injury and high-risk mild head injury groups. Mild head injury is defined as a GCS score of 15 without acute radiographic abnormalities, whereas high-risk mild head injury is defined as GCS scores of 13 or 14, or a GCS score of 15 with acute radiographic abnormalities. This more precise definition of mild head injury is simple to use and may help avoid the confusion caused by the current classification.

The pharmacodynamics of dexmedetomidine in elderly cardiac patients undergoing analgosedation in the ICU

2018 ◽  
Vol 86 (4) ◽  
pp. 265
Author(s):  
Justyna Alicja Ber ◽  
Mirosław Malec ◽  
Agnieszka Bienert ◽  
Małgorzata Nowicka ◽  
Łukasz Żurański ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Single Dose ◽  
Cardiac Index ◽  
Mean Arterial Blood Pressure ◽  
Bispectral Index ◽  
Cardiac Patients ◽  
Health Conditions ◽  
Arterial Blood ◽  
Dexmedetomidine Infusion

Aim. This study aimed to evaluate the pharmacodynamics of dexmedetomidine in elderly cardiac patients.Material and Methods. Twelve patients of 60 years or older and need for analgesia after surgery or as a result of critical health conditions were included into our study. Dexmedetomidine was administered intravenously as a continuous infusion without the initial dose. At the beginning the infusion was started at the rate of 0.7 μg/kg/h and then it was continued in the range of 0.17–1.39 μg/kg/h according to desired level of sedation. Information about heart rate, systolic, diastolic and mean arterial blood pressure, bispectral index and cardiac index were collected a few minutes before, during and in 12 hours after infusion of dexmedetomidine.Results. The hemodynamic data as well as BIS level were collected from 12 patients. The duration of dexmedetomidine infusion was less than 9 hours. For each patient the reduction in blood pressure and heart rate compared to the value before dexmedetomidine infusion was observed. We did not observe bradycardia in any patient. Appropriate sedation level was achieved using only dexmedetomidine and ranged from 60 to 80. In only 2 cases it was necessary to give a single dose of another sedative.Conclusions. To conclude, in the patients’ population involved in the study, which included older cardiac patients dexmedetomidne has been shown as a sedative agent which enabled to achieve desire level of sedation in the recommended ranges without episodes of bradycardia, however hypotension events were noted.

Cell-mediated immunity in severely head-injured patients: the role of suppressor lymphocytes and serum factors

1992 ◽  
Vol 77 (5) ◽  
pp. 694-699 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Claramae H. Miller ◽  
Franklin C. Wagner ◽  
Sally J. DeNardo ◽  
Gerald L. DeNardo ◽  
...  
Keyword(s):  
Head Injury ◽  
Cellular Immunity ◽  
Severe Head Injury ◽  
Normal Subjects ◽  
Lymphocyte Function ◽  
Serum Factors ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Severe head injury results in suppression of cellular immunity associated with defective in vitro functioning of effector lymphocytes, such as helper T cells and cytotoxic T cells. It is not known whether this suppression in effector lymphocyte function is due to intrinsic lymphocyte dysfunction, to suppressor peripheral blood mononuclear cells (PBMC's) such as suppressor lymphocytes or suppressor monocytes, or to serum factors capable of inhibiting effector lymphocyte function. The purpose of this study was to determine whether a subpopulation of PBMC's and/or serum factors) are responsible for this observed suppression in cell-mediated immunity. Cell-mediated immune activity was determined measuring in vitro lymphokine-activated killer (LAK) cytotoxicity following incubation of PBMC's from 15 head-injured patients with those from 15 heterologous normal subjects. The PBMC's were separated into lymphocyte-enriched and monocyte-enriched subpopulations by plastic adherence techniques, and the effect of each population on LAK cytotoxicity was determined. Additionally, the effect on cytotoxicity of serum from the head-injured patients was determined in a dose-response fashion. There was significant depression in LAK cytotoxicity when: 1) PBMC's from normal subjects were incubated with PBMC's from head-injured patients (p < 0.001); 2) lymphocytes (PBMC's depleted of monocytes) from head-injured patients were incubated with PBMC's from normal subjects (p < 0.001); and 3) PBMC's from normal subjects were incubated with serum from head-injured patients (p < 0.001). No suppression in cellular immunity was noted when lymphocytes from normal subjects were incubated with monocytes from head-injured patients. The results indicate that lymphocytes rather than monocytes actively inhibit cellular immunity following severe head injury. The detection of immmunosuppressive serum factors suggests a mechanism by which lymphocytes might be modulated by severe head injury.

Cardiac arrhythmias resulting from experimental head injury

1976 ◽  
Vol 45 (6) ◽  
pp. 609-616 ◽  
Author(s):  
Delbert E. Evans ◽  
William A. Alter ◽  
Stanley A. Shatsky ◽  
E. Neal Gunby
Keyword(s):  
Blood Pressure ◽  
Head Injury ◽  
Cardiac Arrhythmias ◽  
Cardiovascular Events ◽  
Ventricular Arrhythmias ◽  
Adrenergic Blockade ◽  
Content Type ◽  
Arterial Blood ◽  
Before And After ◽  
Fine Print

✓ The cardiovascular events resulting from experimental head injury were studied to determine the incidence of cardiac arrhythmias and to define the autonomic mechanisms responsible for these changes. Electrocardiograms and arterial blood pressure were recorded in anesthetized monkeys before and after the animals were subjected to temporoparietal head impact. Cardiac arrhythmias and hypotension occurred immediately following impact in every animal studied. Various atrioventricular nodal and ventricular arrhythmias were seen. Cholinergic blockade was found to prevent arrhythmias induced by head injury whereas adrenergic blockade was found to be ineffective.

Effect of apolipoprotein E genotype on hematoma volume after trauma

2002 ◽  
Vol 96 (1) ◽  
pp. 90-96 ◽  
Author(s):  
Imran Liaquat ◽  
Laurence T. Dunn ◽  
James A. R. Nicoll ◽  
Graham M. Teasdale ◽  
John D. Norrie
Keyword(s):  
Head Injury ◽  
Ct Scan ◽  
Injury Severity ◽  
Univariate Analysis ◽  
Hematoma Volume ◽  
Patient Age ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. The apolipoprotein E-ϵ4 (APOE-ϵ4) allele is associated with poor outcome after head injury and spontaneous intracerebral hemorrhage (SICH). The aims of this study were to determine if patients in whom one or more APOE-ϵ4 alleles are present are more likely to sustain intracranial mass lesions after head injury and to determine whether there is an isoform-specific effect on the size of the intracranial hematoma. Methods. The authors performed a computerized volumetric analysis of 142 hematomas visible on computerized tomography (CT) scans obtained in 129 patients. The APOE genotype was determined by subjecting buccal smear samples to polymerase chain reaction and restriction enzyme digestion. Allele frequencies were similar in head-injured patients with and without intracranial hematomas (p = 0.36). Univariate analysis revealed that in those patients with one or more APOE-ϵ4 alleles hematoma volume was greater (cube root—transformed values) than that found in patients without the APOE-ϵ4 allele (3.1 cm compared with 2.5 cm, p = 0.0039). The results of univariate analysis also suggested significant effects of patient age, injury severity (mild, moderate, or severe according to admission Glasgow Coma Scale scores) and hematoma location (extraaxial, intraaxial, or both) on hematoma volume. The mechanism of injury (assault, fall, or other) was marginally associated with hematoma volume (p = 0.052). Time from injury to CT scan, hypoxia, and hypotension had no significant effect on hematoma volume. The results of multiple linear regression analysis showed that the presence of an APOE-ϵ4 allele and an extraaxial hematoma location were independent predictors of hematoma volume, after adjusting for patient age, hours between injury and CT scan, injury severity, and injury mechanism. Conclusions. Larger hematomas were found in head-injured patients with one or more APOE-ϵ4 alleles than in patients without the allele. This may contribute to the poorer outcomes observed in these patients.

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