Partial preservation of cerebral vascular responsiveness to hypocapnia during isoflurane-induced hypotension in dogs

This study was undertaken to determine whether the cerebral vascular response to hypocapnia is preserved during isoflurane-induced hypotension. In six dogs (group 1) cerebral vascular resistance and cerebral blood flow were determined at normocapnia (PaCO2 40 mm Hg) and at hypocapnia (PaCO2 20 mm Hg) while mean arterial pressure was normal, and then again during isoflurane-induced hypotension to a mean arterial pressure of 50 mm Hg. Hypocapnia increased cerebral vascular resistance and decreased cerebral blood flow during both normotension and isoflurane-induced hypotension. However, the magnitude of these responses was greater when mean arterial pressure was normal. In another six dogs (group 2), CO2 responsiveness was examined during isoflurane-induced hypotension without prior determination of CO2 responsiveness at normal mean arterial pressure and during sodium nitroprusside-induced hypotension to a mean arterial pressure of 50 mm Hg. As in group 1, partial preservation of CO2 responsiveness was observed during isoflurane-induced hypotension; the magnitude of the response in group 2 during isoflurane-induced hypotension was similar to that in group 1. In contrast, in group 2 during sodium nitroprusside-induced hypotension, hypocapnia caused no significant change of cerebral vascular resistance or cerebral blood flow. It is concluded that cerebral vessels respond to changes in PaCO2 differently during isoflurane-induced hypotension than during hypotension with other commonly used hypotensive treatments. Hypocapnia decreases cerebral blood flow during isoflurane-induced hypotension and, therefore, may also decrease cerebral blood volume, brain bulk, and intracranial pressure.     

Acute brain swelling during evacuation of subdural hematoma caused by delayed contralateral extradural hematoma: report of two cases

Two patients experienced severe brain swelling during the evacuation of acute subdural hematomas. Postoperative computed tomographic (CT) scans revealed delayed extradural hematomas on the sides opposite the subdural hematomas. Extradural bleeding occurred in the area of the fractured skull. One patient improved neurologically after evacuation of the extradural hematoma, and the other was not operated because he was moribund. Drilling exploratory burr holes in the fractured area may have been a better strategy than awaiting a postoperative CT scan. The reduction of intracranial pressure after the removal of subdural hematoma was postulated to be the most important factor contributing to the formation of the extradural hematoma.     

Hemodynamic effects of nisoldipine (Bay k 5552), a calcium antagonist, in coronary surgery patients

The hemodynamic effects of the intravenous application of nisoldipine (0.2 microgram/kg bw per minute and 0.1 microgram/kg bw per minute) were studied in 70 patients with coronary artery disease. Measurements were performed before the induction of anesthesia, during anesthesia (prior to the cannulation of the great vessels) and 5 min after the end of extracorporeal circulation (ECC) (with the same preload as before ECC) as well as during ECC. Each group was compared to a group of patients who received a placebo injection. The preoperative and intraoperative application of nisoldipine produced a decrease in the mean arterial pressure and total systemic resistance, whereas the cardiac index and the stroke-volume index increased. Only during preoperative measurement did the heart-rate increase. The central venous pressure, pulmonary artery pressure and pulmonary capillary wedge pressure remained unchanged. There was no change in the dp/dtmax after 0.2 microgram/kg bw per minute of nisoldipine. There was no difference in hemodynamic outcome between the three groups 5 min after the end of ECC. During ECC, nisoldipine did not reduce the vascular resistance, possibly because of the hypothermic conditions. The principal effect of nisoldipine is to increase the cardiac index by decreasing the total systemic resistance without influencing the myocardial contractility.     

Two cases of impending herniation due to multiple traumatic acute subdural hematomas: combination of burr hole evacuation and craniotomy

A contralateral extra-axial hematoma sometimes occurs during an operation on an acute subdural hematoma and may become fatal. Using a combined procedure of burr hole evacuation and craniotomy, we treated 2 cases of multiple traumatic acute subdural hematomas. Our policy for such cases is first to perform a burr hole evacuation for the acute subdural hematoma in the emergency room, while simultaneously preparing the operation room for a possible further operation. Next, we perform computed tomography (CT) of the brain. If the evacuation does not provide enough decompression, we either carry out a craniotomy at the same site, or, we observe the patient without resorting to craniotomy. However, if the patient's condition deteriorates, burr hole evacuation is repeated and/or craniotomy is carried out as soon as possible on the lesion at the already prepared operation room. Both of our patients received craniotomy for another subdural hematoma after the burr hole evacuation. Though his intracranial pressure was well managed during the acute stage, one of the patients died 21 days after the trauma due to an extensive brain infarction caused by vasospasm. The other regained consciousness and was able to walk 5 months after the trauma in spite of cerebral infarction from vasospasm. The possible mechanism of vasospasm in severe head injury is also discussed.     

Early hemodynamic effects of olprinone hydrochloride after coronary artery bypass grafting

Our purpose was to evaluate the hemodynamic effects of olprinone hydrochloride early after coronary artery bypass grafting (CABG). Fifteen patients undergoing CABG were administered a constant infusion of 0.1 μg/kg/min of olprinone and continued for 4 hours. No bolus infusion of olprinone was administered before continuous infusion. Systolic systemic arterial pressure, systolic pulmonary arterial pressure, systemic vascular resistance and pulmonary vascular resistance were significantly decreased. There were no significant changes in heart rate, mean central venous pressure, mean left atrial pressure and left ventricular stroke work index. Cardiac index was significantly increased, but a correlation between cardiac index and mixed venous blood oxygen saturation was not found. Double product was significantly decreased, which described above suggest that olprinone achieved improvement of left cardiac function without more myocardial oxygen consumption. Severe transient hypotension (systolic arterial pressure <80 mmHg) after infusion of olprinone was observed in three patients. Olprinone administered soon after CABG surgery had beneficial effects in terms of improvement of hemodynamic status without more oxygen consumption and reduction of pulmonary vascular resistance. However transient hypotension was a serious clinical problem in patients after open heart surgery, especially in CABG patients who need suitable systolic arterial pressure to keep enough blood perfusion of arterial bypass grafts.     

The cerebral and systemic hemodynamic and metabolic effects of desflurane-induced hypotension in dogs

The cerebral and systemic hemodynamic and metabolic effects of hypotension induced with desflurane were examined in 11 dogs. During a steady-state baseline period under 1 MAC desflurane (7.2%), the following were measured or derived: arterial, pulmonary artery, and pulmonary artery occlusion pressures; arterial, mixed venous, and sagittal sinus blood gases; cardiac index and cerebral blood flow (CBF); whole-body and cerebral O2 consumption; systemic and cerebral vascular resistance; intracranial pressure; and blood glucose and lactate concentrations. After the baseline period, hypotension to a mean arterial pressure (MAP) of 50 mmHg was produced by 15.5% (2.2 MAC), and hypotension to an MAP of 40 mmHg was produced by 17.1% (2.4 MAC) for 1 h. During this hypotensive period all measurements were taken at 5- or 15-min intervals. At the end of the hypotensive period, brain biopsy specimens were taken for measurement of cerebral concentrations of ATP, phosphocreatine, and lactate to determine whether there was any metabolic evidence of cerebral ischemia. Desflurane-induced hypotension produced a significant, 40-50% decrease in cardiac index with a significant change in systemic vascular resistance at the lower blood pressure, but produced little change in heart rate. Even though whole-body O2 consumption did not decrease, adequate peripheral perfusion was maintained with the lower cardiac output, as evidenced by lack of accumulation of blood lactate. Induced hypotension caused a significant, 50 (at MAP = 50 mmHg) to 64% (at MAP = 40 mmHg) decrease in cerebral perfusion pressure, accompanied by a significant, 36 (at MAP = 50 mmHg) to 60% (at MAP = 40 mmHg) decrease in CBF.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intracranial hypotension with subdural hematoma following lumbar puncture: case report

BACKGROUND AND PURPOSE: Lumbar puncture is a common procedure highly contributive to neurological diagnosis. It can also cause serious adverse side effects including subdural hematoma and intracranial hypotension as illustrated by this case report. CASE REPORT: A 38-year-old women presented severe intracranial hypotension after a lumbar puncture. Magnetic resonance imaging was compatible with intracranial hypotension and revealed an acute subdural hematoma with midline deviation. A first blood patch was unsuccessful. Symptom relief was achieved with a second patch. The patient was, then, discharged but developed recurrent headache subsequent to the transformation from acute to chronic subdural hematoma. Surgical drainage was required. The postoperative imaging and physical examination returned to normal and the patient was discharged with no recurrence. CONCLUSION: The serious adverse effects of lumbar puncture is an easy and common medical procedure that must be kept in mind.     

Acute nontraumatic spinal subdural hematomas in three patients.

STUDY DESIGN: The clinical data, magnetic resonance imaging, intraoperative findings, and functional outcome were reviewed for three patients under anticoagulant therapy who experienced acute nontraumatic spinal subdural hematoma. OBJECTIVES: To draw attention to this rare complication of anticoagulant therapy and to assess the magnetic resonance findings and clinical outcome of patients with spinal subdural hematoma after surgical evacuation. SUMMARY OF BACKGROUND DATA: Among intraspinal hematomas, spinal subdural hematomas are by far the least common. Magnetic resonance findings have been demonstrated in only a few cases of spinal subdural hematomas. The timing of the operation and the anatomic location of the hematoma essentially determine the functional outcome. METHODS: Three case reports of spinal subdural hematomas in patients receiving anticoagulant therapy are presented. Particular interest was given to the clinical and magnetic resonance data, the intraoperative findings, and the functional outcome. RESULTS: The three patients each had a complete preoperative neurologic deficit. Sagittal T1- and T2-weighted magnetic resonance images of the spine proved to have high sensitivity for defining the type of bleeding and delineating the craniocaudal extension of the hematoma. Surgical evacuation was performed within 26 hours after the onset of symptoms. Intraoperative findings showed the hematoma to be confined between the dura and the arachnoid in two patients, and to be associated with rupture into the subarachnoid space in one patient. Postoperative recovery was incomplete in two patients, and did not improve in the remaining patient. CONCLUSIONS: Spinal subdural hematoma must be considered in patients under anticoagulant therapy with spontaneous signs of acute spinal cord or cauda equina compression. Magnetic resonance imaging with sagittal T1- and T2-weighted images were adequate and reliable for diagnosis of spinal subdural hematoma. On the basis of previous studies and the authors' intraoperative findings, spinal subdural hematomas could be viewed as spinal dural border hematomas. The level of preoperative neurologic deficit seemed to be critical for recovery despite prompt surgical evacuation.     

Local cerebral blood flow mapping before and after removal of acute subdural hematoma in the rat.

The cause of hemispheric swelling and high intracranial pressure after acute subdural hematoma is unknown, yet this is a major cause of death related to this condition. To investigate whether vascular engorgement is the cause of this form of hemisphere swelling, we have autoradiographically mapped regional cerebral blood flow before and after removal of acute subdural hematoma in a rat model. Hyperemia was patchy and infrequent. The major cause of the significant hemisphere swelling seen after hematoma removal was enlargement of the zone of focal tissue ischemia and edema under the hematoma.     

急性硬膜下血肿清除术后迟发性硬膜下积液的诊治

目的 探讨急性硬膜下血肿清除术后硬膜下积液的原因、早期诊断、手术治疗方法和疗效。方法 对急性硬膜下血肿后硬膜下积液29例进行回顾性分析。结果 痊愈14例，占48．7％；轻残5例，占17．2％；重残4例，占13．8％；植物状态3例，占10．3％，死亡3例，占10．3％。引流效果良好，无一例颅内感染。结论 急性硬膜下血肿清除后可能发生硬膜下积液；术后意识无改善或意识好转后又加重、出现颅内压增高征象、神经系统定位体征、减压区膨隆、瞳孔及生命体征改变应予CT检查可明确诊断：积液区颅骨钻孔或减压区小切口置管引流简便易行，有效满意疗效。     

Hypotension from spinal anesthesia in patients aged greater than 80 years is due to a decrease in systemic vascular resistance

Study ObjectivesTo determine the exact mechanism underlying spinal anesthesia-induced hypotension in the elderly patient.DesignRetrospective case-control study.SettingOperating room (OR) in a general hospital.MeasurementsRecords from 60 consecutive patients over 80 years of age, who underwent hip fracture repair (intramedullary nail or compression hip screw) during spinal anesthesia were studied. After injection of isobaric 0.5% bupivacaine in the L₃-L₄ intervertebral space in the lateral decubitus position, patients were turned supine. Acetate Ringer’s solution (300 mL) was infused over 30 minutes after subarachnoid puncture. A decrease in systolic arterial pressure to less than 100 mmHg was treated with an intravenous injection of 5 mg ephedrine. The hypotension group (n=18) comprised patients who required ephedrine during the 30 minutes after the puncture, and the nonhypotension group (n=42) consisted of patients who maintained stable arterial pressure with crystalloid infusion only.MeasurementsCardiac output (CO) and stroke volume variation (SVV) every 20 seconds using the Vigileo-FloTrac system continuously from arrival in the operating room (OR) to 30 minutes after the subarachnoid puncture were recorded. Serial changes in systemic vascular resistance (SVR), CO, and SVV from baseline after puncture were compared between the two groups.Main ResultsThe decrease in SVR over 20 minutes after the puncture was significantly greater in the hypotension group than the nonhypotension group (P = 0.047). Cardiac output was stable in the two groups. Stroke volume variation in the first 10 minutes after the puncture increased to similar levels in the two groups, then decreased gradually to baseline. No significant differences were noted in circulatory parameters on arrival at the OR.ConclusionsA decrease in SVR, not CO, is the main mechanism of hypotension seen during spinal anesthesia in elderly patients.     

Hemodynamic effects of induced hypotension by ketanserin in anesthetized dogs]

Hemodynamic effects of hypotension induced by ketanserin were investigated in 18 mongrel dogs under 0.87% halothane in oxygen (1 MAC). They were randomly allocated to one of two groups. Group C (n = 9) received no vasodilator therapy and served as a control and group K (n = 9) received 0.1% ketanserin solution. Mean arterial pressure decreased and was maintained at 60 mmHg for 60 minutes in group K. No change was noted in hemodynamic variables measured in group C throughout the experiment. During and after induced hypotension in group K, stroke volume index increased significantly compared with the control value. On the other hand, systemic vascular resistance was significantly reduced, reaching 50% of the control value at the end of the hypotensive period. Left ventricular maximum dp/dt showed a significant reduction during hypotension but then increased gradually to the control value. In addition, heart rate decreased significantly during and after induced hypotension, therefore these vasodilator effects were not accompanied by reflex tachycardia. Cardiac index remained unchanged throughout the experiment. Further, no changes in central venous pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure and pulmonary vascular resistance were observed. In conclusion, the data indicate that ketanserin is a potent systemic vasodilator producing stable hemodynamics. It also reduces systemic vascular resistance without reflex tachycardia and this is a favorable effect of ketanserin.     

Beneficial effects of prostaglandin El on hemodynamic changes during liver transplantation in pigs

Abstract  The vasodilative action of prostaglandin E, (PGE,) on the systemic and pulmonary circulation was investigated in swine models of orthotopic liver transplantation. In the PG -treated group ( n = S), PGE, (0.05 μg/kg per minute) was intravenously infused from the onset of the anhepatic stage to 30 min after revascularization. During the anhepatic stage, PGE, decreased systemic vascular resistance without a corresponding hypotension, so cardiac output was maintained at a higher level. In the control group ( n = 8), pulmonary vascular resistance increased to 3 times the anhepatic value during reperfusion, accompanied by a decline in cardiac output with a 28 % decrease in blood pressure. In the PG -treated group, on the other hand, pulmonary vascular resistance was maintained within the normal range without any associated decrease in cardiac output. The blood pressure decreased slightly by 12 %. In conclusion, in this model, PG increased cardiac output without hypotension during the anhepatic stage and also prevented postreper-fusion pulmonary hypertension and the subsequent systemic hypotension.     

Acute epidural hematoma following evacuation of chronic subdural hematoma with continuous closed system drainage]

The authors report a case of acute epidural hematoma occurring after evacuation of chronic subdural hematoma with continuous closed system drainage. Laboratory data of the patient including bleeding time were within normal limits. The cause of the postoperative intracranial hematoma was the rapid surgical decompression of the initial lesion, and we considered that it could be prevented if chronic subdural hematoma was treated using closed system drainage and slow decompression. But acute epidural hematoma occurred after this operative procedure and it was accelerated by evacuation of the chronic subdural hematoma through the drain. An emergent craniotomy and removal of the hematoma was performed, so the patient was discharged from hospital with satisfactory neurological recovery. A careful check of the evacuated hematoma volume is very important, and CT scanning should be immediately performed if postoperative hematoma is suspected.     

Single burr hole evacuation for traumatic acute subdural hematoma of the posterior fossa in the emergency room

A 57-year-old man and a 55-year-old man presented with acute subdural hematoma of the posterior cranial fossa due to trauma. Both were comatose preoperatively. Emergent single burr hole evacuation in the posterior cranial fossa was performed in the emergency room immediately after computed tomography. Neurological symptoms improved dramatically just after initiating the burr hole evacuation in both patients. A 57-year-old man became alert and could walk unassisted 1 month after surgery. The other could walk with assistance 4 months after surgery, although psychic disturbance resulting from cerebral contusion remained. Single burr hole evacuation in the emergency room is a useful treatment for acute subdural hematoma of the posterior cranial fossa because the procedure can be performed easily and rapidly, thus achieving reduction of intracranial pressure. Progressing neurological deterioration, reversibility of brainstem function by mannitol administration and the sign of brainstem compression and noncommunicating hydrocephalus are good indicators for this treatment.     

Hemodynamic and hormonal responses to the sudden interruption of caval flow: insights from a prospective study of hepatic vascular exclusion during major liver resections

Hepatic vascular exclusion (HVE) combines portal triad clamping and occlusion of the inferior vena cava. Although HVE has been performed for major liver resections during the last 2 decades, little is known about the mechanisms that explain its satisfactory hemodynamic tolerance. Consequently, we performed a comprehensive study of both hemodynamic and hormone responses to HVE. Twenty-two patients who underwent liver resection for secondary tumors developed in noncirrhotic livers were prospectively studied. Heart rate, arterial blood pressure, pulmonary artery pressure, mixed venous saturation, cardiac output, and left ventricular dimensions determined by transesophageal echocardiography were monitored in HVE patients. Blood concentrations of arginine vasopressin (AVP), epinephrine, norepinephrine, dopamine, and atrial natriuretic peptide and plasma renin activity (PRA) were measured before clamping; 5, 15, and 30 min after clamping; and 15 min after unclamping. Hemodynamic response to HVE was characterized by a significant (P < 0.05) decrease in left ventricular dimensions, fractional area change, and pulmonary artery pressure. We also observed a marked decrease in cardiac output (50%) and an increase in heart rate and systemic vascular resistance. After unclamping, there was peripheral vasodilation, assessed by a significant decrease in systemic vascular resistance from the preclamping value to unclamping. An acute and sustained increase in AVP and norepinephrine that returned to baseline after unclamping and the absence of modification in PRA concentrations were noted. The marked decrease in venous return that characterizes HVE is compensated for by an increase in vascular resistance secondary to an important activation of the AVP and sympathetic systems. The PRA system does not play an important role in maintaining arterial blood pressure during HVE. IMPLICATIONS: Hemodynamic and hormonal responses to the acute interruption of caval venous return to the heart were investigated in patients undergoing liver resection with hepatic vascular exclusion. A compensatory role for arginine vasopressin and sympathetic systems that provoked increased vascular resistance was demonstrated.     

High intraoperative blood loss may be a risk factor for postoperative hematoma

The authors studied the incidence of postoperative intracranial hematoma to improve care after intracranial surgery. Five years (1995-1999) of surgical records were analyzed retrospectively. Patients were included if evacuation of an intracranial postoperative hematoma was reported. A control group was randomly selected. Forty-nine patients (0.8%) had postoperative hematomas requiring evacuation. The amount of intraoperative blood loss was significantly larger in the hematoma group (762 +/-735 mL [median 500 mL]) than in the control group (415 +/-403 mL; median 300 mL) (P = 0.004). Clinical deterioration occurred within the first 24 hours in 80%, within 6 hours in 51%, and within 1 hour in 12% of the patients. Those who deteriorated within 24 hours had a faster and more life-threatening deterioration than those who had a hematoma after 24 hours. A decreased level of consciousness was found in 61% and increased focal neurologic signs were found in 33% of the patients. An elevated intracranial pressure was seen significantly more often in the hematoma group (9/10 patients, 90%) than in the control group (1/8 patients, 12.5%) (P = 0.001). In this study, a large amount of intraoperative blood loss and elevated intracranial pressure were warning signs of postoperative hematoma and should alert the clinician to the increased risk. Most hematomas occurred within 24 hours after surgery, and in this time period the deterioration was more severe compared with the hematomas that occurred later.     

Intracoronary shunts reduce transient intraoperative myocardial dysfunction during off-pump coronary operations

BACKGROUND: This study investigated the hemodynamic changes in patients undergoing multiple vessel beating heart coronary revascularization in the presence or absence of an intracoronary shunt. METHODS: Forty patients were randomized to off-pump with a shunt (n = 20) or with the proximal coronary artery occluded by a soft snare (n = 20). Hemodynamic measurements were recorded at base line, during construction, and after completion of each distal anastomosis. RESULTS: Grafting of the left anterior descending coronary artery anastomosis was associated with a significant decrease in stroke volume, cardiac index, and mean arterial pressure, and an increase in pulmonary capillary wedge pressure and systemic vascular resistance in the snare but not in the shunt group. During grafting of the posterior descending coronary artery there was a marked decrease in stroke volume and cardiac index, and an increase in central venous pressure in both groups, and an increase in heart rate, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, and systemic vascular resistance only in the snare group. The most extensive changes were observed during the circumflex coronary artery anastomosis with a reduction in stroke volume, cardiac index, and mean arterial pressure, and an increase in central venous pressure, pulmonary capillary wedge pressure, pulmonary arterial pressure, and systemic vascular resistance in both groups. In all settings, these changes were transient and recovered after the heart was returned to its anatomical position in the shunt group, whereas stroke volume and cardiac index remained reduced, and systemic vascular resistance was elevated in all settings in the snare group. CONCLUSIONS: Stabilization of the left anterior descending coronary artery to perform the anastomosis resulted in temporary hemodynamic changes, which are prevented by the use of an intracoronary shunt. The hemodynamic deterioration during the construction of the posterior descending coronary artery and circumflex coronary artery anastomoses is transient in the shunt group, whereas the snaring technique is associated with an impairment of early functional recovery.     

Dynamics of extravascular pulmonary water and intracranial pressure in patients with ischemic stroke

The objective of the present study was to examine the relationship among extravascular pulmonary water, intracranial and cerebral perfusion pressure, hemodynamic parameters (eg, cardiac index, system vascular resistance index), and brain stem function during acute ischemic stroke. The subjects were 17 comatose patients with ischemic stroke who were admitted to an intensive care unit. The results revealed an elevation in extravascular lung water in the absence of cardiac dysfunction. The absence of correlation between indices of brain vascular resistance and mean arterial pressure confirmed that a disturbance of cerebral blood flow was present. There was a correlation between auditory-evoked potential parameters and extravascular lung water during the study period. The correlation between auditory-evoked potentials and extravascular lung water may imply that ischemic brainstem injury plays a significant role in the development of increased pulmonary capillary permeability and the elevation of extravascular lung water. Brain stem injury is a cause of noncardiogenic lung edema in comatose patients following acute ischemic stroke.     

Beneficial effects of prostaglandin El on hemodynamic changes during liver transplantation in pigs

Abstract The vasodilative action of prostaglandin E, (PGE,) on the systemic and pulmonary circulation was investigated in swine models of orthotopic liver transplantation. In the PG -treated group (n= S), PGE, (0.05 μg/kg per minute) was intravenously infused from the onset of the anhepatic stage to 30 min after revascularization. During the anhepatic stage, PGE, decreased systemic vascular resistance without a corresponding hypotension, so cardiac output was maintained at a higher level. In the control group (n= 8), pulmonary vascular resistance increased to 3 times the anhepatic value during reperfusion, accompanied by a decline in cardiac output with a 28 % decrease in blood pressure. In the PG -treated group, on the other hand, pulmonary vascular resistance was maintained within the normal range without any associated decrease in cardiac output. The blood pressure decreased slightly by 12 %. In conclusion, in this model, PG increased cardiac output without hypotension during the anhepatic stage and also prevented postreper-fusion pulmonary hypertension and the subsequent systemic hypotension.