Significance of intracranial hypertension in severe head injury

Measurements of intracranial pressure (ICP) were begun within hours of injury in 160 patients with severe brain trauma, and continued in the intensive care unit. Some degree of increased ICP (greater than 10 mm Hg) was present on admission in most cases (82%), and in all but two of the 62 patients with intracranial mass lesions requiring surgical decompression; ICP was over 20 mm Hg on admission in 44% of cases, and over 40 mm Hg in 10%. In patients with mass lesions only very high ICP (greater than 40 mm Hg) on admission was significantly associated with a poor neurological picture and outcome from injury, while in patients with diffuse brain injury any increase in ICP above 10 mm Hg was associated with a poorer neurological status and a worse outcome. Despite intensive measures aimed at prevention of intracranial hypertension, ICP rose over 20 mm Hg during the monitoring period in 64 of the 160 patients (40%). Postoperative increases in ICP over 20 mm Hg (mean) were seen in 52% of the patients who had had intracranial masses evacuated, and could not be controlled by therapy in half of these cases. Even in patients without mass lesions, ICP rose above 20 mm Hg in a third of the cases, despite artificial ventilation and steroid therapy. Of the 48 patients who died, severe intracranial hypertension was the primary cause of death in nearly half and even moderately increased ICP (greater than 20 mm Hg) was associated with higher morbidity in patients with mass lesions and those with diffuse brain injury. Measurement of ICP should be included in management of patients with severe head injury.     

Analysis of heart-rate variability: a noninvasive predictor of death and poor outcome in patients with severe head injury

BACKGROUND: Analysis of heart-rate variability (HRV) is a promising new technique for noninvasive quantification of autonomic function. We measured HRV in patients with severe head injury to assess its potential as a monitoring tool. METHODS: Analysis of HRV was prospectively done on all intensive care unit patients. Concurrent data on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were collected. Registry data were reviewed to identify patients with severe head injury, defined as Head/Neck Abbreviated Injury Scale score > or = 4. Mortality, likelihood of discharge to home, ICP, and CPP were compared between patients with abnormal HRV and those without. RESULTS: Low HRV was associated with increased mortality and decreased rate of discharge to home. Abnormal HRV was associated with episodes of increased ICP and decreased CPP. CONCLUSION: Assessment of HRV is a noninvasive method that can be widely used. Abnormal HRV was associated with poor outcome and altered cerebral perfusion. Monitoring of HRV may improve outcome by allowing earlier detection and treatment of intracranial pathology.     

Severe head trauma. Review of the factors influencing the prognosis

A series of 72 severely head injured patients are reported, 24 (33%) with surgical intracranial hematomas. All patients were intensively cared for under the same therapeutic regime; intracranial pressure (ICP) was monitored and treated if increased. The series mortality was 39%. Uncontrollable increase of ICP (UI-ICP), always fatal, was observed in 18% of patients and in 13 of 28 deaths (46%); the incidence of UI-ICP among deaths was higher in patients less than in those more than 40 years old (55% vs 25%). Patients with UI-ICP were frequently deeply comatose and with arterial hypotension on admission; almost all died in the first days. Patients directly admitted from the scene with well staffed Life Flight Helicopter Emergency Care compared with those directly admitted from the scene with different type of ambulance service (paramedics, police, firemen and private) had a mortality rate significantly less (20% vs 54%) and an incidence of UI-ICP strongly lower both among patients (5% vs 29%) and among deaths (25% vs 54%). Thus in this small series intensive care after admission was not effective to obtain good results if patients had received poor preadmission emergency care. Review of the literature on main clinical predictors of outcome in severe head injury, have made possible some observations. Ischemic and intracranial hypertension brain lesions were generally present in patients killed by head trauma; while diffuse axonal injury, frequently responsible for vegetative, severe disability survival and late deaths, was observed only in 20-30% of postmortem examinations. Old age, poor neurological status and cardiocirculatory and respiratory disturbances prior to and upon admission positively worsened the outcome, while intracranial hematomas had a more variable predictive value. Intracranial hypertension was a definitively ominous predictor only if very high when the risk to be or become uncontrollable seems to be much elevated. UI-ICP, often fatal despite any aggressive therapy, was the single most frequent killer after severe head injury, responsible for about half of all deaths after admission. The different outcome among severe head injury series could be conceivably related to a different frequency of UI-ICP. Besides the severity of head injury and delay and mode of admission, we suggest that preadmission respiratory and cardiocirculatory and the quality of emergency medical system could strongly affect the incidence of uncontrollable increase of ICP in admitted patients and thus the mortality rate and favorable recovery of the series. The advanced preadmission emergency care service with intensive care after admission could significantly explain the better results often observed in severe head injury series.     

Improved outcome after severe head injury with a new therapy based on principles for brain volume regulation and preserved microcirculation

OBJECTIVE: To assess the new "Lund therapy" of posttraumatic brain edema, based on principles for brain-volume regulation and improved microcirculation. DESIGN: A prospective, nonrandomized outcome study over a 5-yr period on severely head-injured patients with increased intracranial pressure, comparing the results with a historical control group with the same selection criteria for patients who were treated according to conventional principles. SETTING: General intensive care unit of a university hospital. PATIENTS: Fifty-three consecutive head-injured patients with a Glasgow Coma Score of <8, and with increased intracranial pressure (>25 mm Hg), despite conventional treatment. INTERVENTIONS: Interstitial fluid resorption was obtained by lowering intracapillary hydrostatic pressure, by preserving normal colloid osmotic pressure, and by maintaining a normovolemic (normal albumin/serum and hemoglobin/serum), not overtransfused patient. Intracapillary pressure was reduced by the combination of precapillary vasoconstriction (low-dose thiopental, dihydroergotamine) and reduction of mean arterial pressure, the latter attained with a beta1-antagonist (metoprolol 0.2 to 0.3 mg/kg/24 hrs iv) and an alpha2-agonist (clonidine 0.4 to 0.8 microg/kg x 4 to 6 iv). Clonidine, in combination with normovolemia, also improves microcirculation by reducing catecholamines in plasma. Intracranial blood volume was reduced by arterial (low-dose thiopental sodium and dihydroergotamine) and large-vein (dihydroergotamine) vasoconstriction. The start dose of dihydroergotamine (maximum 0.9 microg/kg/hr) was successively reduced toward discontinuation within 4 to 5 days. MEASUREMENTS AND MAIN RESULTS: There were 8% of patients who died and the neurologic conditions of 13% remained severely damaged, compared with 47% and 11%, respectively, for the control group. CONCLUSIONS: The low mortality compared with previous outcome studies strongly indicates that this therapy improves outcome for severe head injuries. However, a randomized, controlled study is needed to reach general acceptance of this new therapy.     

Effects of sufentanil on cerebral hemodynamics and intracranial pressure in patients with brain injury

BACKGROUND: The current study investigates the effects of sufentanil on cerebral blood flow velocity and intracranial pressure (ICP) in 30 patients with intracranial hypertension after severe brain trauma (Glasgow coma scale < 6). METHODS: Mechanical ventilation (FIO2 0.25-0.4) was adjusted to maintain arterial carbon dioxide tensions of 28-30 mmHg. Continuous infusion of midazolam (200 micrograms/kg/h intravenous) and fentanyl (2 micrograms/kg/h intravenous) was used for sedation. Mean arterial blood pressure (MAP, mmHg) was adjusted using norepinephrine infusion (1-5 micrograms/min). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a 2-MHz transcranial Doppler sonography system. ICP (mmHg) was measured using an epidural probe. After baseline measurements, a bolus of 3 micrograms/kg sufentanil was injected, and all parameters were continuously recorded for 30 min. The patients were assigned retrospectively to the following groups according to their blood pressure responses to sufentanil: group 1, MAP decrease of less than 10 mmHg, and group 2, MAP decrease of more than 10 mmHg. RESULTS: Heart rate, arterial blood gases, and esophageal temperature did not change over time in all patients. In 18 patients, MAP did not decrease after sufentanil (group 1). In 12 patients, sufentanil decreased MAP > 10 mmHg from baseline despite norepinephrine infusion (group 2). ICP was constant in patients with maintained MAP (group 1) but was significantly increased in patients with decreased MAP. Vmean did not change with sufentanil injection regardless of changes in MAP. CONCLUSIONS: The current data show that sufentanil (3 micrograms/kg intravenous) has no significant effect on middle cerebral artery blood flow velocity and ICP in patients with brain injury, intracranial hypertension, and controlled MAP. However, transient increases in ICP without changes in middle cerebral artery blood flow velocity may occur concomitant with decreases in MAP. This suggests that increases in ICP seen with sufentanil may be due to autoregulatory decreases in cerebral vascular resistance secondary to systemic hypotension.     

Cranioencephalic trauma in adults: clinical and radiologic features

BACKGROUND: To analyse extracranial complications and basic variables in head-injury patients, such as Glasgow coma score (GCS), intracranial pressure (ICP) and cranial computerized tomography (CT), in relation to the outcome of these patients. PATIENTS AND METHODS: 64 consecutive patients (47 males and 17 females) with head injury, admitted from January 1992 to May 1994, were studied in this prospective study. Mean age was 37 +/- 18 years. Overall mortality was 23% (15/64). Student-t and Chi-square tests were used for statistical analysis, and p < 0.05 was considered statistical significant. RESULTS: Overall GCS was 7 +/- 3, survivors presenting GCS of 7.7 +/- 2.9 and non-survivors 4.7 +/- 1.5 (p = 0.04). CT were classified as follows: diffuse injury, 4 patients (7%); focal injury, 32 (53%), and mixed injury 24 (40%). Depending on the presence or absence of mesencephalic cisterns in the CT, GSC was 7.6 +/- 2.8 and 4.3 +/- 1.4, respectively (p = 0.04). Subarachnoid hemorrhage (SAH) was associated to a GCS of 6.3 +/- 2.5 and its absence to 8 +/- 3.3 (p = 0.03). The absence of mesencephalic cisterns and SAH were more frequent in the non-survivors, 72% and 32% (p = 0.01 and 0.04), respectively. ICP was recorded in 42 patients. Regarding to ICP, mortality was: 6.7% with ICP < or = 20 mmHg, 37% with ICP 21-30, 44% with ICP 31-40 and 67% with ICP > 50 mmHg (p = 0.03). Diabetes insipidus, cardiorespiratory arrest, shock, prolonged mechanical ventilation, SDRA and sepsis were the most frequent extracranial complications in non-survivors. CONCLUSIONS: There is an association between the outcome of head-injury patients with the GCS and ICP values. Absence of mesencephalic cisterns and SAH were radiologic signs of poor prognosis. Patients who died had more extracranial complications.     

An attempt at reversibility and increase of the virulence of axenic strains of Entamoeba histolytica

Sequential changes of cerebral autoregulation were studied in 20 cats after recirculation of cerebral ischemia. The cerebral autoregulation was evaluated by autoregulation index (A.I.), calculating % delta cerebral blood flow (CBF)/delta cerebral perfusion pressure (CPP), with changing the mean arterial blood pressure (MABP) within 80-130 mmHg. Duration of ischemic insult was 15 min after disappearance of direct cortical response (DCR). Following recovery of cerebral circulation, MABP, CBF and intracranial pressure (ICP) were observed sequentially for at least 48 hours. In 6 of 20 cats the autoregulation was disturbed early after recirculation, and the ICP was increased, resulting in no cerebral blood flow (early deteriorated group). In the other 14 cats the autoregulation was restored immediately, but in 7 of the 14 cats it was disturbed again after 24 hours following recirculation (delayed deteriorated group), finally the ICP was elevated and the CBF became 0 as same as early deteriorated group. In another 7 cats it was not disturbed until 5 days. The changes in CBF following insult were five patterns. These were classified into type A (Gradual decrease), type B (Transient increase), type C (Constant maintenance), type D (Relatively rapid decrease) and type E (Rapid decrease). The delayed cerebral dysautoregulation occurred in the types except for type A and type E. These results suggested there was close relation between delayed dysautoregulation and delayed neuronal dysfunction that we reported previously. Moreover, we considered the delayed dysautoregulation could be speculated from the value of ICP/CBF immediately after recirculation and the pattern of the changes in CBF during ischemic insult.     

Stroke in the medical intensive-care unit

OBJECTIVE: To analyze the occurrence and outcome of new-onset stroke in critically ill patients admitted to a medical intensive-care unit. MATERIAL AND METHODS: We reviewed the medical records of patients admitted to the medical intensive-care units of two hospitals between 1985 and 1995. In addition, computed tomographic scans or scan reports were assessed. RESULTS: We identified 19 patients with a critical medical illness and a new-onset stroke. Of this study group, ischemic stroke developed in 10 patients, 8 of whom were found to have bihemispheric infarction. A single territory infarct (the middle cerebral artery territory) was noted in two patients. The presumed mechanisms for ischemic stroke were disseminated intravascular coagulation (N = 6), cholesterol embolization (N = 1), discontinuation of warfarin therapy before an invasive procedure (N = 1), septic emboli (N = 1), and cardioversion (N = 1). In nine patients, an intracranial hemorrhage developed. Seven patients had a single lobar hematoma, whereas multiple intracerebral hematomas were found in two patients. Disseminated intravascular coagulation and rupture of a mycotic aneurysm in proven infective endocarditis were the most common mechanisms for hemorrhagic stroke. In all patients with an ischemic stroke, sudden hemiparesis rapidly progressed to coma. In patients with an intracranial hematoma and sudden onset of coma, unilateral fixed pupil was the most common initial manifestation. Of the 19 patients, 17 died and 2 remained severely disabled. CONCLUSION: Coma is a common initial manifestation of stroke in patients with a critical medical illness, and disseminated intravascular coagulation has a major etiologic role. New-onset stroke in the setting of critical medical illness generally is a complication in a terminally ill patient.     

Outcome of resuscitation following unexpected apparent stillbirth

There are few data to inform a decision to resuscitate babies who are unexpectedly stillborn. The outcome for 42 successfully resuscitated stillborn children, of whom 62% survived to be discharged home, is reported. Of the survivors, a poor outcome with severe disability was found in 23% (including one postneonatal death), equivocal outcome was found in 15% (two mild hypertonia; two with mild hemiplegia and no associated other disability) and 62% were free of any impairment at follow up 20 months to 8 years later. In 39 (93%) fetal problems had been identified and the resuscitation team was present at delivery. Poor outcome was associated with late return of heart beat, delayed respirations, neonatal acidaemia and early onset of seizures. Of the unexpected apparent stillbirths successfully resuscitated, 52% died or survived severely disabled, 10% had an equivocal outcome, but 36% survived apparently intact. Therefore, vigorous resuscitation is clearly indicated in these circumstances.     

Decompressive bifrontal craniectomy in the treatment of severe refractory posttraumatic cerebral edema

OBJECTIVE: The management of malignant posttraumatic cerebral edema remains a frustrating endeavor for the neurosurgeon and the intensivist. Mortality and morbidity rates remain high despite refinements in medical and pharmacological means of controlling elevated intracranial pressure; therefore, a comparison of medical management versus decompressive craniectomy in the management of malignant posttraumatic cerebral edema was undertaken. METHODS: At the University of Virginia Health Sciences Center, 35 bifrontal decompressive craniectomies were performed on patients suffering from malignant posttraumatic cerebral edema. A control population was formed of patients whose data was accrued in the Traumatic Coma Data Bank. Patients who had undergone surgery were matched with one to four control patients based on sex, age, preoperative Glasgow Coma Scale scores, and maximum preoperative intracranial pressure (ICP). RESULTS: The overall rate of good recovery and moderate disability for the patients who underwent craniectomies was 37% (13 of 35 patients), whereas the mortality rate was 23% (8 of 35 patients). Pediatric patients had a higher rate of favorable outcome (44%, 8 of 18 patients) than did adult patients. Postoperative ICP was lower than preoperative ICP in patients who underwent decompression (P = 0.0003). Postoperative ICP was lower in patients who underwent surgery than late measurements of ICP in the matched control population. A statistically significant increased rate of favorable outcomes was seen in the patients who underwent surgery compared to the matched control patients (15.4%) (P = 0.014). All patients who exhibited sustained ICP values above 40 torr and those who underwent surgery more than 48 hours after the time of injury did poorly. Evaluation of the 20 patients who did not fit into either of those categories revealed a 60% rate of favorable outcome and a statistical advantage over control patients (P = 0.0001). CONCLUSION: Decompressive bifrontal craniectomy provides a statistical advantage over medical treatment of intractable posttraumatic cerebral hypertension and should be considered in the management of malignant posttraumatic cerebral swelling. If the operation can be accomplished before the ICP value exceeds 40 torr for a sustained period and within 48 hours of the time of injury, the potential to influence outcome is greatest.     

Production of granulocyte-macrophage colony-stimulating factor in a patient with metastatic chest wall large cell carcinoma

Recent reports of cancers that produce colony-stimulating factors (CSF) and which are associated with leukocytosis indicate that most are granulocyte CSF-producing tumors. A 71-year-old man with metastatic chest wall tumors from large cell lung cancer with marked leukocytosis and eosinophilia was reported. His maximal leukocyte count was 48300/microliter with 37.5% eosinophils. Granulocyte-macrophage CSF (GM-CSF) activity detected by enzyme-linked immunosorbent assay (ELISA) in serum was 112 pg/ml (normal range < 2.0 pg/ml), but G-CSF was normal. Immunohistochemical detection of GM-CSF protein on a chest wall tumor sample was positive. Irradiation of the chest wall tumor was performed and the leukocyte count decreased temporally. However, he died of respiratory failure due to progressive tumor growth 56 days after admission. Based on these results it appears that autocrine production of GM-CSF is a possible cause of this leukemoid reaction.     

Use of hypertonic (3%) saline/acetate infusion in the treatment of cerebral edema: Effect on intracranial pressure and lateral displacement of the brain

OBJECTIVE: To determine the effect of continuous hypertonic (3%) saline/acetate infusion on intracranial pressure (ICP) and lateral displacement of the brain in patients with cerebral edema. DESIGN: Retrospective chart review. SETTINGS: Neurocritical care unit of a university hospital. PATIENTS: Twenty-seven consecutive patients with cerebral edema (30 episodes), including patients with head trauma (n = 8), postoperative edema (n = 5), nontraumatic intracranial hemorrhage (n = 8), and cerebral infarction (n = 6). INTERVENTION: Intravenous infusion of 3% saline/acetate to increase serum sodium concentrations to 145 to 155 mmol/L. MEASUREMENTS AND MAIN RESULTS: A reduction in mean ICP within the first 12 hrs correlating with an increase in the serum sodium concentration was observed in patients with head trauma (r2 = .91, p = .03), and postoperative edema (r2 = .82, p = .06), but not in patients with nontraumatic intracranial hemorrhage or cerebral infarction. In patients with head trauma, the beneficial effect of hypertonic saline on ICP was short-lasting, and after 72 hrs of infusion, four patients required intravenous pentobarbital due to poor ICP control. Among the 21 patients who had a repeat computed tomographic scan within 72 hrs of initiating hypertonic saline, lateral displacement of the brain was reduced in patients with head trauma (2.8 +/- 1.4 to 1.1 +/- 0.9 [SEM]) and in patients with postoperative edema (3.1 +/- 1.6 to 1.1 +/- 0.7). This effect was not observed in patients with nontraumatic intracranial bleeding or cerebral infarction. The treatment was terminated in three patients due to the development of pulmonary edema, and was terminated in another three patients due to development of diabetes insipidus. CONCLUSIONS: Hypertonic saline administration as a 3% infusion appears to be a promising therapy for cerebral edema in patients with head trauma or postoperative edema. Further studies are required to determine the optimal duration of benefit and the specific patient population that is most likely to benefit from this treatment.     

Opioids, cerebral circulation and intracranial pressure

The effects of the opioids alfentanil (A), fentanyl (F), and sufentanil (S) on cerebral blood flow (CBF) and intracranial pressure (ICP) have been discussed in several recent publications. The purpose of this review is to describe the results of studies in animals, healthy volunteers, and patients with and without intracranial diseases. Clinical relevance and mechanisms of the reported ICP and CBF increases are analysed. METHODS. Approximately 70 original articles and abstracts were retrieved by a systematic literature search using the key word list at the end of this abstract. The cited studies came from computerised database systems like Silver Platter and DIMDI, the SNACC reference list, and the bibliographies of pertinent articles and books. These studies were classified into three groups: significant increase of ICP and/or CBF; no significant or clinically relevant alterations; and significant decreases of ICP and/or CBF. RESULTS. The numerical relationship was 6:7:3 for A, 7:16:9 for F, and 5:11:8 for S. Increases of previously normal or only slightly elevated ICP were registered in some studies in connection with a decrease in mean arterial pressure (MAP). On the other hand, in patients with brain injury and elevated ICP opioids did not further increase ICP despite MAP decreases. In studies monitoring ICP and/or CBF continuously, transient and moderate increases of questionable clinical relevance became apparent a few minutes after bolus injection of opioids. Alterations of systemic and cerebral haemodynamics observed after bolus application were not registered during continuous infusion of A and S. DISCUSSION AND CONCLUSIONS. The cerebral effects of opioids are dependent on several factors, e.g., age, species, ventilation, anaesthesia before and during measurements, systemic haemodynamics, and underlying diseases. The probable mechanism of ICP increase during decreasing MAP is cerebral vasodilatation due to maintained autoregulation. With increasing severity of the cerebral lesion autoregulation is often disturbed. Therefore, ICP often remains unaltered despite MAP decreases. However, the resulting decrease in cerebral perfusion pressure makes such patients more susceptible to develop ischaemic neurological deficits. Induction of somatic rigidity or (with high doses) convulsions, exceeding the upper limit of autoregulation, histamine release, cerebral vasodilatation, increased cerebral oxygen consumption, or carbon dioxide accumulation during spontaneous breathing were discussed as mechanisms for transient ICP/CBF increases. It is concluded that opioids are often beneficial and not generally contraindicated for patients with cerebral diseases and compromised intracranial compliance. However, since negative side effects cannot be excluded, opioid effects and side effects should be monitored (MAP, ICP, cerebrovenous oxygen saturation, transcranial Doppler sonography) in patients at risk. It has to be stressed that opioids should be administered only to patients with stable haemodynamic situations and preferably in well-titrated, continuous infusions.     

Infratentorial empyema: analysis of 22 cases

OBJECTIVE: Infratentorial empyema is an uncommon form of intracranial suppuration that is usually secondary to neglected otogenic infection. The diagnosis is frequently delayed and often confused with that of meningitis. The associated mortality is distressingly high, yet it has, as a clinical entity, received scant attention in the literature. We present a 13-year experience of this condition. PATIENTS AND METHODS: From a retrospective analysis of 3865 patients with intracranial suppuration during a 13-year period, 22 patients with infratentorial empyema were identified. The inpatient notes for these patients were analyzed with reference to clinical, radiological, bacteriological, operative, and outcome data. RESULTS: Twenty-two patients with infratentorial empyema accounted for 0.6% of admissions caused by intracranial suppuration during the study period. Of these 22 empyemas, 13 were subdural and 9 epidural. Hydrocephalus was present in 17 (77.3%). Except for two epidural empyemas that did not warrant neurosurgical intervention, all patients underwent standard surgical management (wide posterior fossa craniectomy). Nineteen underwent mastoidectomy because the source of infection was otogenic. Concomitant and persistent hydrocephalus was treated aggressively. Five patients died (mortality rate of 22.7%). All fatalities had subdural empyemas, and all three patients with cerebellopontine angle extension of subdural purulent collections died. CONCLUSION: Although rare, infratentorial empyema, especially when subdural, is a lethal disease. Cerebellopontine angle extension of pus was a particularly ominous sign in our experience. Early surgical drainage via wide posterior fossa craniectomy, aggressive treatment of associated hydrocephalus, eradication of the primary source of sepsis, and, finally, intravenous high dosage of appropriate antibiotics form the mainstay of treatment.     

Physiologic stress responses to laparoscopic cholecystectomy. A comparison of the gasless and pneumoperitoneal procedures

BACKGROUND: Differences in the physiological stress response to pneumoperitoneal (PP) and gasless abdominal wall-lifting (AWL) procedures used for laparoscopic cholecystectomy have not been properly evaluated. METHODS: We compared leukocyte count, interleukin-6 (IL-6) levels, arterial blood gases, creatinine clearance, plasma renin activity, cardiothoracic ratio, and clinical outcome in 27 patients without systemic complications who underwent laparoscopic cholecystectomy, including 11 by AWL and 16 by PP. RESULTS: Transient leukocytosis and high IL-6 levels were observed at POD 1 (postoperative day) in both groups, but both values returned to baseline by POD 2. IL-6 levels correlated significantly with operation time (p < 0.01). Changes in blood gases, creatinine clearance, plasma renin activity, and cardiothoracic ratio were not different for the two groups. The clinical outcome was similar for both groups. CONCLUSIONS: Our results indicate that both PP and AWL are appropriate for patients without serious complications.     

Effect of recombinant human granulocyte-macrophage colony-stimulating factor on HIV-related leukopenia: a randomized, controlled clinical study

OBJECTIVE: To assess the effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on white blood cell (WBC) count and on the rate of opportunistic infections in a large and selected population of leukopenic HIV-positive patients compared with non-treated controls. DESIGN: Open-label, randomized, comparative clinical study. SETTING: University hospitals and AIDS centres. PATIENTS AND METHODS: One hundred and twenty-three leukopenic HIV-positive patients received recombinant human GM-CSF (300 microg subcutaneously daily for 1 week, and 150 microg subcutaneously two times weekly for 11 weeks thereafter); the control group comprised 121 non-treated leukopenic HIV-positive patients. A complete blood cell count with differential, platelet count, reticulocyte count, and CD4+ and CD8+ T-cell subset counts were performed in both patient groups at baseline and at weeks 1, 12 and 24. RESULTS: The administration of GM-CSF resulted in a significant increase of WBC count in patients compared with non-treated controls. Total leukocyte count increased by 22% at week 1 and by 65% at week 12 compared with baseline levels; a 20% increase of total leukocyte count was still present at week 24. Increases of neutrophils, eosinophils and monocytes were responsible for the majority of the increase in WBC count. Opportunistic infections occurred in 61.7% of GM-CSF-treated patients and in 72% of the patients of the control group (relative risk, 0.86; 95% confidence interval, 0.72-1.03; P = 0.123). Mild flu-like side-effects were observed in most patients receiving GM-CSF, although they were not sufficiently severe to warrant withdrawal from the study. CONCLUSIONS: GM-CSF was well tolerated and biologically active in leukopenic HIV-positive patients, with a significant, although time-limited, increase of WBC count compared with non-treated patients. The administration of this growth factor should be considered in ameliorating the myelosuppression observed with some cell-cycle-specific antiviral and anti-neoplastic agents.     

Chronic myelomonocytic leukemia with repeated respiratory failure associated with leukocytosis following splenic arterial embolization and splenectomy

A 32-year-old female was admitted due to splenomegaly and leukocytosis in September, 1993. The leukocyte count was 26,900/microliter with 29% monocytes (7,800/microliter). A diagnosis of the chronic phase of chronic myelomonocytic leukemia was made. On November 19, 1993, splenic arterial embolization was performed. After the embolization, the leukocyte count rapidly increased, and acute respiratory failure developed. The respiratory condition was improved by methylprednisolone (m-PRED) pulse therapy. Subsequently, the effectiveness of chemotherapy gradually decreased, and there was an increase in the leukocyte count. Respiratory failure developed again but was successfully treated with m-PRED pulse therapy in addition to aclarubicin. On July 4, 1995, splenectomy was performed. The leukocyte count rapidly increased, and acute respiratory failure again developed. She did not respond to m-PRED pulse therapy, but the respiratory condition was markedly improved by leukoplasmapheresis. The respiratory failure in this patient may be associated with capillary leak syndrome due to neutrophilia. In addition, stasis of increased monocytes in the pulmonary capillaries and their infiltration into the pulmonary parenchyma and alveoli was thought to have occurred.     

Prognostic factors in postraumatic severe diffuse brain injury

It is usually defficult in clinical practice to establish factors affecting final outcome in patients suffering severe diffuse brain injury (SDBI), due to the absence of specific semiology. METHODS: We studied retrospectively 160 consecutive patients with criteria of SDBI. We performed a statistical analysis of epidemiological, clinical and radiological factors, and relationship with final outcome. RESULT: 35% of patients with severe head injury presented SDBI. Sixty percent were 15-35 year old and 73% male. More than 45% of the patients presented GCS 3 or 4. On CT performed during the first 24 h, haemorrhagic lesions appeared in white matter in 35% and subarachnoid haemorrhage was observed in 28%. During the first 24 h., 66% of patients presented values of intracranial pressure (ICP) above 20 mm Hg and a 33% below 20 mm Hg. Twenty percent of the patients had ICP > 20 mm and no response to treatment. According to the Glasgow Outcome Scale (GOS), mortality of more than 50% and 25% of patients with persistent vegetative state or severe disability were observed. CONCLUSIONS: Clinical evaluation, early CT findings, ICP values and their response to medical treatment and clinical complications were found to be related (p < 0.05) to final outcome (GOS).     

Leukocyte count and aggregation during the evolution of cerebral ischemic injury

We evaluated leukocyte aggregation by means of the leukergy test and count in 26 patients with atherothrombotic stroke and in 10 patients with transient ischemic attacks. The evaluation was performed within 24 h from the onset of symptoms and then repeated on day 2, 4, 6 and 8. Data were compared with those of 10 healthy controls. Stroke patients were followed until day 30 when a clinical examination and brain computed tomography were performed to evaluate the extent and outcome of cerebral damage. Both leukocyte aggregation and count were significantly increased in stroke patients with respect to controls. While leukocyte count was not able to differentiate the severity of neurological impairment in stroke patients, leukocyte aggregation was significantly higher in major than in minor stroke patients on days 2 and 4 (p < 0.05). Moreover, while values of leukocyte count recorded at entry remained substantially stable in the following determinations in all groups, leukocyte aggregation showed a significant increase (p < 0.05) on day 4 with respect to all the other determinations in major stroke patients. These findings show that the extent and temporal profile of changes in leukocyte count and aggregation are different in patients with cerebrovascular disease and suggest an involvement of altered leukocyte rheology in the development of cerebral ischemic injury.     

Place of laparoscopic surgery in Crohn''s disease

PURPOSE: We describe our therapeutic strategy and correlate the anatomic results and clinical outcomes in patients who received immediate fibrinolytic therapy for thromboembolic complications occurring during endovascular treatment of an intracerebral aneurysm. METHODS: The medical records and angiographic examinations of 19 patients were reviewed. All endovascular procedures were performed with the patients under general anesthesia and fully heparinized. Thirteen patients received an intravenous bolus injection of aspirin. Thromboemboli occurred during catheterization or insertion of embolic material (Guglielmi detachable coils or mechanical detachable spirals) or in the first hours after the intervention. Clot distribution was within the MCA territory in 14 patients, the ACA in three patients, and the basilar trunk in two patients. A continuous intraarterial injection of urokinase was administered immediately, either superselectively distal to the thrombus or selectively within or closely proximal to the thrombus. In nine cases, chemical lysis was combined with mechanical clot fragmentation. Initial anatomic recanalization as well as clinical outcome at 3 months were evaluated. RESULTS: Ten patients showed complete recanalization and nine patients showed partial recanalization. Fourteen patients had a good clinical recovery. One patient was moderately disabled and two were severely disabled according to their scores on the Glasgow outcome scale. Two patients died, one as a consequence of the preexisting subarachnoid hemorrhage and the other because of a large intracerebral hematoma that developed after fibrinolysis. Of the 14 patients with a good clinical outcome, nine exhibited complete recanalization and five partial recanalization. CONCLUSION: Pharmacological thrombolysis seems to be a safe and efficient therapy that facilitates the natural fibrinolytic process, increasing the rate of recanalization in thromboembolic events. Clot fragmentation and superselective drug infusion appear to improve the rate of recanalization. Complete recanalization increases the chance of a better clinical outcome; however, clinical outcome does not always correspond to recanalization and vice versa.