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Biomedical subjects

M J Rosner

Publications and source records attributed to M J Rosner.

At least 19 recordsLinked to original sources
PubMed1999

Propofol in the treatment of moderate and severe head injury: a randomized, prospective double-blinded pilot trial.

OBJECT: Sedation regimens for head-injured patients are quite variable. The short-acting sedative-anesthetic agent propofol is being increasingly used in such patients, yet little is known regarding its safety and efficacy. In this multicenter double-blind trial, a titratable infusion of 2% propofol accompanied by low-dose morphine for analgesia was compared with a regimen of morphine sulfate in intubated head-injured patients. In both groups, other standard measures of controlling intracranial pressure (ICP) were also used. METHODS: Forty-two patients from 11 centers were evaluated to assess both the safety and efficacy of propofol: 23 patients in the propofol group (mean time of propofol usage 95+/-87 hours) and 19 patients in the morphine group (mean time of morphine usage 70+/-54 hours). There was a higher incidence of poor prognostic indicators in the propofol group than in the morphine group: patient age older than 55 years (30.4% compared with 10.5%, p < 0.05), initial Glasgow Coma Scale scores of 3 to 5 (39.1% compared with 15.8%, p < 0.05), compressed or absent cisterns on initial computerized tomography scanning (78.3% compared with 57.9%, p < 0.05), early hypotension and/or hypoxia (26.1% compared with 10.5%, p = 0.07). During treatment there was a trend toward greater use of vasopressors in the propofol group. However, the mean daily ICP and cerebral perfusion pressure were generally similar between groups and, on therapy Day 3, ICP was lower in the propofol group compared with the morphine group (p < 0.05). Additionally, there was less use of neuromuscular blocking agents, benzodiazepines, pentobarbital, and cerebrospinal fluid drainage in the propofol group (p < 0.05). At 6 months postinjury, a favorable outcome (good recovery or moderate disability) was observed in 52.1% of patients receiving propofol and in 47.4% receiving morphine; the mortality rates were 17.4% and 21.1%, respectively. Patients who received the highest doses of propofol for the longest duration tended to have the best outcomes. There were no significant differences between groups in terms of adverse events. CONCLUSIONS: Despite a higher incidence of poor prognostic indicators in the propofol group, ICP therapy was less intensive, ICP was lower on therapy Day 3, and long-term outcome was similar to that of the morphine group. These results suggest that a propofol-based sedation and an ICP control regimen is a safe, acceptable, and, possibly, desirable alternative to an opiate-based sedation regimen in intubated head-injured patients.

Adult↗
PubMed1996

Posterior left thoracic cardiac sympathectomy by surgical division of the sympathetic chain: an alternative approach to treatment of the long QT syndrome.

Although high thoracic left sympathectomy via an anterior surgical approach is a highly efficacious treatment for refractory ventricular arrhythmias in patients with the long QT syndrome, the degree of sympathetic denervation has been variable, success of the operation is influenced by anatomical differences between patients, and Horner's syndrome may result. We hypothesized that interruption of sympathetic input to the heart could be accomplished using a posterior thoracic approach to this variable and often complex anatomy by division of the sympathetic chain rather than by direct destruction of the stellate and superior thoracic ganglia with the more conventional anterior, supraclavicular approach. In addition, the posterior approach should decrease the risk of Horner's syndrome by avoiding the ocular sympathetic efferent nerves. This posterior approach is described in five patients with the long QT syndrome and recurrent ventricular arrhythmias. After a mean follow-up of 18 +/- 12 months, all are alive without Horner's syndrome.

Adult↗
PubMed1995

Cerebral perfusion pressure: management protocol and clinical results.

Early results using cerebral perfusion pressure (CPP) management techniques in persons with traumatic brain injury indicate that treatment directed at CPP is superior to traditional techniques focused on intracranial pressure (ICP) management. The authors have continued to refine management techniques directed at CPP maintenance. One hundred fifty-eight patients with Glasgow Coma Scale (GCS) scores of 7 or lower were managed using vascular volume expansion, cerebrospinal fluid drainage via ventriculostomy, systemic vasopressors (phenylephrine or norepinephrine), and mannitol to maintain a minimum CPP of at least 70 mm Hg. Detailed outcomes and follow-up data bases were maintained. Barbiturates, hyperventilation, and hypothermia were not used. Cerebral perfusion pressure averaged 83 +/- 14 mm Hg; ICP averaged 27 +/- 12 mm Hg; and mean systemic arterial blood pressure averaged 109 +/- 14 mm Hg. Cerebrospinal fluid drainage averaged 100 +/- 98 cc per day. Intake (6040 +/- 4150 cc per day) was carefully titrated to output (5460 +/- 4000 cc per day); mannitol averaged 188 +/- 247 g per day. Approximately 40% of these patients required vasopressor support. Patients requiring vasopressor support had lower GCS scores than those not requiring vasopressors (4.7 +/- 1.3 vs. 5.4 +/- 1.2, respectively). Patients with vasopressor support required larger amounts of mannitol, and their admission ICP was 28.7 +/- 20.7 versus 17.5 +/- 8.6 mm Hg for the nonvasopressor group. Although the death rate in the former group was higher, the outcome quality of the survivors was the same (Glasgow Outcome Scale scores 4.3 +/- 0.9 vs. 4.5 +/- 0.7). Surgical mass lesion patients had outcomes equal to those of the closed head-injury group. Mortality ranged from 52% of patients with a GCS score of 3 to 12% of those with a GCS score of 7; overall mortality was 29% across GCS categories. Favorable outcomes ranged from 35% of patients with a GCS score of 3 to 75% of those with a GCS score of 7. Only 2% of the patients in the series remained vegatative and if patients survived, the likelihood of their having a favorable recovery was approximately 80%. These results are significantly better than other reported series across GCS categories in comparisons of death rates, survival versus dead or vegetative, or favorable versus nonfavorable outcome classifications (Mantel-Haenszel chi 2, p < 0.001). Better management could have improved outcome in as many as 35% to 50% of the deaths.

Adolescent↗
PubMed1995

Introduction to cerebral perfusion pressure management.

This article offers a broad review of cerebral autoregulation to help understand the principles of cerebral perfusion pressure (CPP) management. Discussed are cerebral autoregulation, Poiseuille's law, mannitol-induced hypertension and CPP, prognosis by CPP, management of CPP, and a summary of physiologic basis for CPP management.

Blood Pressure↗
PubMed1990

Cerebral perfusion pressure management in head injury.

A method of ICP management is presented based upon maintenance of cerebral perfusion pressure ( CPP = SABP - ICP) at 70-88 mm Hg or in some cases greater. To do this, we have employed volume expansion, nursed patients in the flat position, and actively used catecholamine infusions to maintain the SABP side of the CPP equation at levels necessary to obtain the target CPP. CSF drainage and mannitol have freely been used to maintain the ICP portion of the equation. Thirty-four consecutive patients with GCS less than or equal to 7 were admitted to the Neurosurgical Intensive Care Unit (GCS = 5.1 +/- 1.4) and managed with this protocol. CPP was maintained at 84 +/- 11 mm Hg, ICP was 23 +/- 9.8 mm Hg, and SABP averaged 106 +/- 11 mm Hg. CVP was 8.0 +/- 3.7 mm Hg and average fluid intake was approximately 5.4 +/- 3.9 liters/d. Output averaged 5.0 +/- 4.0 liters/d; additionally, albumin (25%) (33 +/- 44 gm/d) and PRBCs were used for vascular expansion and hemoglobin was maintained (11.5 +/- 1.4 gm/dl). Three patients died of uncontrolled ICP (all protocol errors). Four other patients succumbed, none secondary to ICP and all secondary to potentially avoidable complications. Morbidity (GOS = 4.2 +/- 0.87) appeared to be as good or superior to previous methods of therapy. Overall, mortality was 21% and that from uncontrollable ICP was 8%. This approach to the management of intracranial hypertension proved safe, rational, and greatly enhanced the therapeutic options available. It was also consistent with optimal care of other organ systems. The results bring into question many of the standard tenets of neurosurgical ICP management and suggest new avenues of investigation.

Adolescent↗
PubMed1988

Alterations in cerebrospinal fluid uridine, hypoxanthine, and xanthine in head-injured patients.

1. Examination of the cerebrospinal fluid (CSF) of head-injured patients reveals that the concentration of intraventricular xanthine is elevated and that of uridine is decreased relative to those of adult lumbar CSF. 2. No correlations were observed between CSF lactate and CSF hypoxanthine, xanthine, or uridine, suggesting that changes in purine metabolites and the pyrimidine nucleoside do not index similar cellular events as does lactic acid production. 3. Ventricular CSF from hydrocephalic infants had uridine and hypoxanthine concentrations not significantly different from those of normal adult lumbar CSF, but xanthine was significantly elevated. 4. Since uridine has anticonvulsant properties and is a crucial substrate for cerebral metabolism, it may be useful to evaluate this pyrimidine for use in the management of patients with head injury.

Adult↗
PubMed1987

Cerebral perfusion pressure: a hemodynamic mechanism of mannitol and the postmannitol hemogram.

Sixteen patients each received infusions of 1 g of mannitol per kg over 5 to 10 minutes, and serial determinations of intracranial pressure (ICP), systemic arterial blood pressure (SABP), central venous pressure, cerebral perfusion pressure (CPP), hematocrit, hemoglobin, serum Na+, K+, osmolarity, and fluid balance were carried out for 4 hours. Urine output was replaced volume for volume with 5% dextrose in 0.45% NaCl solution. We tested the hypothesis that patients with high (greater than or equal to 70 torr) CPP would respond less well to mannitol by either ICP or CPP criteria than patients with low (less than 70 torr) CPP. The rationale for this hypothesis was based upon the association of low CPP with autoregulatory vasodilatation, whereas high CPP is associated with vasoconstriction. If mannitol should work by a vasoconstriction mechanism, the ICP effects should be most apparent under conditions of low CPP. Those patients with CPP greater than or equal to 70 torr responded relatively poorly to mannitol, with ICP decreasing from 25 +/- 4 to 17 +/- 5 (SE) mm Hg at 45 minutes postinfusion. Patients with CPP less than 70 responded with ICP declining from 35 +/- 5 to 13 +/- 4 mm Hg. The initial SABP was 81 +/- 5 mm Hg in the CPP less than 70 group and immediately rose to 90 +/- 7 at 15 minutes postmannitol. The SABP increase correlated with ICP (r = -0.40, P less than 0.01), but not when CPP greater than or equal to 70. SABP was significantly higher in the latter group (105 +/- 6) and increased to 107 +/- 8 postmannitol. The ICP decrease began immediately with the SABP increase. No mannitol "rebound" occurred in these patients. Measures of acute volume expansion all correlated with ICP (Na+, r = -0.67, P less than 0.001; hematocrit, r = -0.27, P less than 0.01; serum osmolarity, r = 0.32, P less than 0.05) when CPP less than 70 torr. None correlated with ICP when CPP greater than or equal to 70. These data suggest that mannitol infusion is at least partly dependent upon hemodynamic mechanisms that allow vasoconstriction to occur with reduction in cerebral blood volume and that little may be gained by using mannitol when CPP greater than or equal to 70 either by SABP, ICP, or CPP criteria because vasoconstriction is already nearly maximal. This mechanism is not exclusive of other potential mechanisms of action. Mannitol "rebound" may be a function of net dehydration, hemoconcentration, and SABP decline.

Adolescent↗
PubMed1987

Pressure-volume index as a function of cerebral perfusion pressure. Part 1: The effects of cerebral perfusion pressure changes and anesthesia.

The pressure-volume index (PVI) was measured as a function of cerebral perfusion pressure (CPP) in 12 adult cats. Anesthesia was induced with methohexital in six animals and with pentobarbital in six animals; all were maintained on an N2O:O2 (70%:30%) mixture. The CPP was either increased in 10-torr increments using norepinephrine or decreased by a combination of adenosine triphosphate and hemorrhage in subgroups. Three estimations of PVI were made at each level of CPP. The PaCO2, body temperature, and hematocrit were controlled at normal levels throughout. In both groups there was a linear relationship between PVI and CPP with increasing CPP being reflected by a rise in PVI. This relationship was more marked in the methohexital group: PVI = 0.37 ml + 0.0005 mm Hg CPP in the pentobarbital group, and PVI = 0.14 ml + 0.0019 mm Hg CPP in the methohexital group. These results indicate that the PVI is not independent of CPP but is a function of CPP and is profoundly influenced by anesthesia.

Animals↗
PubMed1987

Pressure-volume index as a function of cerebral perfusion pressure. Part 2: The effects of low cerebral perfusion pressure and autoregulation.

The pressure-volume index (PVI) was measured in six adult cats while cerebral perfusion pressure (CPP) was reduced from normal levels to below the autoregulatory range by a continuous infusion of adenosine triphosphate. Anesthesia was induced with methohexital and maintained with an N2O:O2 (70%:30%) mixture. Body temperature, hematocrit, and PaCO2 were held constant throughout each experiment. Cerebral blood flow (CBF) was measured by the hydrogen clearance method. At CPP levels over 50 mm Hg, CBF remained relatively constant despite changes in CPP. Within this range, the PVI varied directly with CPP (PVI = 0.24 ml + 0.0013 mm Hg CPP). Below the autoregulatory range, CBF fell progressively with further decreases in CPP; in this range, PVI was found to increase as CPP fell (PVI = 0.84 ml - 0.0071 mm Hg CPP). These results indicate that the PVI is a complex function of CPP, varying directly with CPP within the autoregulatory range and indirectly with CPP below the autoregulatory range.

Animals↗
PubMed1986

Cerebral perfusion pressure, intracranial pressure, and head elevation.

Previous investigations have suggested that intracranial pressure waves may be induced by reduction of cerebral perfusion pressure (CPP). Since pressure waves were noted to be more common in patients with their head elevated at a standard 20 degrees to 30 degrees, CPP was studied as a function of head position and its effect upon intracranial pressure (ICP). In 18 patients with varying degrees of intracranial hypertension, systemic arterial blood pressure (SABP) was monitored at the level of both the head and the heart. Intracranial pressure and central venous pressure were assessed at every 10 degrees of head elevation from 0 degree to 50 degrees. For every 10 degrees of head elevation, the average ICP decreased by 1 mm Hg associated with a reduction of 2 to 3 mm Hg CPP. The CPP was not beneficially affected by any degree of head elevation. Maximal CPP (73 +/- 3.4 mm Hg (mean +/- standard error of the mean] always occurred with the head in a horizontal position. Cerebrospinal fluid pressure waves occurred in four of the 18 patients studied as a function of reduced CPP caused by head elevation alone. Thus, elevation of the head of the bed was associated with the development of CPP decrements in all cases, and it precipitated pressure waves in some. In 15 of the 18 patients, CPP was maintained by spontaneous 10- to 20-mm Hg increases in SABP, and pressure waves did not occur if CPP was maintained at 70 to 75 mm Hg or above. It is concluded that 0 degree head elevation maximizes CPP and reduces the severity and frequency of pressure-wave occurrence. If the head of the bed is to be elevated, then adequate hydration and avoidance of pharmacological agents that reduce SABP or prevent its rise are required to maximize CPP.

Blood Pressure↗
PubMed1985

Cerebellar infarction: analysis of twenty-one cases.

Review of 3000 cranial computed tomography scans performed in the past 7 years at North Carolina Memorial Hospital revealed 21 patients who showed evidence of cerebellar infarction. The presenting symptoms and signs closely resembled benign labyrinthine disease. Five of the patients presented for seemingly unrelated medical problems and had no history suggestive of recent cerebellar insult. Hypertension and cardiovascular disease were common in these patients, and in the majority of instances, the cerebellar deficits were mild and showed progressive resolution. Angiograms demonstrated numerous, often diffuse abnormalities. Computed tomography scanning is mandatory for patients with sudden onset of labyrinthine or cerebellar signs or symptoms. Cerebral angiography is recommended to detect potentially treatable vascular lesions.

Adult↗
PubMed1985

Recovery from aphasia following extracranial-intracranial bypass surgery: case report.

The Boston Diagnostic Aphasia Exam and brief measures of memory, stereognosis, and limb praxis were administered to an extracranial-intracranial bypass surgery patient with moderately severe transcortical aphasia preoperatively and postoperatively. Significant improvement in language function was documented 2 days following surgery. Three month followup demonstrated continued improvement across all major areas of language function. These improvements were not felt to be attributable to practice effect, the natural remission of aphasic symptomatology or change in general medical status. Our experience with this patient leads us to speculate that patients with multivessel occlusive disease limiting cerebral oxygen supply to the vascular borderzone area may be more likely to benefit from bypass surgery and an increase in cerebral blood flow than some other subgroups of patients with cerebrovascular disorders.

Aged↗