Hyperdynamic therapy for cerebral vasospasm.

The effects of hyperdynamic therapy on patients with cerebral vasospasm following subarachnoid hemorrhage (SAH), under normal blood pressure (BP) and normal blood volume conditions, are reported. Forty-four patients, who underwent surgery for aneurysms in acute stage, received hydroxyethyl starch (500 ml/day) postoperatively to prevent dehydration. Twenty-four of the 44 patients with prominent SAH on the computed tomographic (CT) scan, anticipating to develop cerebral ischemia due to vasospasm, were given dobutamine (DOB). The BP was maintained within the normal range, and the heart rate was kept below 130/min. In the 24 patients treated with DOB, cerebral blood flow (CBF) was measured repeatedly by the 133Xe intravenous injection method. In 8 of these 24 patients, the cardiovascular function was monitored with Swan-Ganz (S-G) catheters. Twelve of the 44 patients (27%) developed delayed neurological deficits associated with cerebral vasospasm. The neurological deficits were reversed by the administration of DOB, at a dose of 8-25 (average 12.4) micrograms/kg/min. In 43 patients, the ischemic lesions associated with vasospasm did not appear on CT scan and the patients were of normal condition at discharge. However, one patient showed multiple low-density lesions on CT scan. This was because of the failure of hyperdynamic therapy due to pulmonary complications. No case of pulmonary edema or heart failure due to volume overload was noted. In the 24 patients with prominent SAH, CBF increased significantly by up to 20% following DOB administration, although the BP stayed in the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)     

Treatment of symptomatic vasospasm with GIK (glucose-insulin-potassium) infusion

GIK (glucose-insulin-potassium) solution has been administered to myocardial infarction patients as a polarizing therapy, but the effects of GIK administration on vasospasm after subarachnoid hemorrhage have never been reported. We used GIK solution to treat 7 cases of symptomatic vasospasm with congestive heart failure due to hypervolemia-hypertensive treatment. The GIK solution, composed of 200cc of 50% glucose solution, 250cc of water, 40 mEq of KCl, and 20 units of actrapid insulin, was administered continuously through a central venous catheter. The GIK therapy improved congestive heart failure following elevation of cardiac output in 7 cases, and simultaneously stabilized the serum glucose level within the range of 88-175 mg/dl. After GIK administration, remarkable improvement in the consciousness level was achieved in all cases, and cerebral infarction due to vasospasm appeared in only one case in spite of severe subarachnoid hemorrhage. It is thought that GIK therapy will be effective in the treatment of symptomatic vasospasm with congestive heart failure through the normalization of hemodynamics, the improvement of hyperglycemia and protection against cerebral ischemia.     

Pulmonary complications of aneurysmal subarachnoid hemorrhage

OBJECTIVE: Pulmonary complications challenge the medical management of patients who have sustained aneurysmal subarachnoid hemorrhage (SAH). We assessed the frequency and types of pulmonary complications after aneurysmal SAH and analyzed the impact of pulmonary complications on patient outcome. METHODS: We reviewed the records of all patients with acute SAH treated at our institution between 1990 and 1997. Three hundred five consecutive patients with an aneurysmal hemorrhage source documented by angiography and treated within 7 days of ictus were analyzed. Outcomes at longest follow-up (mean, 16 mo) were measured by use of the Glasgow Outcome Scale. RESULTS: Pulmonary complications were documented in 66 patients (22%). The pulmonary complications were nosocomial pneumonia in 26 patients (9%), congestive heart failure in 23 (8%), aspiration pneumonia in 17 (6%), neurogenic pulmonary edema in 5 (2%), pulmonary embolus in 2 (<1%), and other pulmonary disorders in 4 (1%); 11 patients had two pulmonary complications. The incidence of symptomatic vasospasm was greater in patients with pulmonary complications (63%) than in patients without pulmonary complications (31%) (P = 0.001), and this association was independent of age and clinical grade at admission (odds ratio, 3.68; P < 0.001). Overall clinical outcomes were worse in patients with pulmonary complications (mean Glasgow Outcome Scale score, 3.3) than in patients without pulmonary complications (mean Glasgow Outcome Scale score, 4.0; P = 0.0001), but pulmonary complications were not an independent predictor of worse outcome when adjusted for age and clinical grade at admission (odds ratio, 1.38; P = 0.315). CONCLUSION: Patients who experience pulmonary complications after aneurysmal SAH have a higher incidence of symptomatic vasospasm than do patients without pulmonary complications. This most likely reflects both the failure to maintain aggressive hypervolemic and hyperdynamic therapy in patients with pulmonary compromise and the possible precipitation of congestive heart failure by hypervolemic therapy in patients with preexisting delayed ischemic neurological deficit. Although patients with pulmonary complications have worse overall clinical outcomes than do patients without pulmonary complications, this is attributable to older age and worse clinical grades at admission.     

Two patients treated with intra-aortic balloon pump counterpulsation after subarachnoid hemorrhage

Intra-aortic balloon pump counterpulsation (IABP) was used to treat two patients with symptomatic vasospasm after subarachnoid hemorrhage. One could not tolerate triple H therapy (hypertensive hypervolemic hemodilution) because of poor cardiac function and another suffered acute myocardial infarction after aneurysm surgery followed by cardiac failure. IABP increased cerebral blood flow and prevented cerebral infarction in the former case but this could not reverse cerebral ischemia in the latter. IABP may be one choice for patients with vasospasm after subarachnoid hemorrhage.     

Postoperative pulmonary bleeding and reperfusion pulmonary edema in an adult patient after repair of tetralogy of Fallot with pulmonary atresia--percutaneous cardiopulmonary support (PCPS) and lung protective ventilatory strategy

After total correction of tetralogy of Fallot, pulmonary atresia and major aorto-pulmonary collateral arteries, a 31-year-old man developed life-threatening pulmonary hypertension and reperfusion pulmonary edema, leading to pulmonary hemorrhage, right heart failure and hypoxia. Because of difficulty in weaning from cardiopulmonary bypass and in controlling hemorrhage from pulmonary arteries, we applied percutaneous cardiopulmonary support (PCPS) for 281 hours with strategy of delayed sternal closure (17 days) and a large quantity of transfusion. We also applied lung protective ventilatory strategy for reperfusion pulmonary edema (high PEEP, limited peak inspiratory pressure and recruitment maneuver). As the result, he was discharged alive without any major complications. We report our postoperative managements, in terms of 1) lung protective ventilatory strategy, 2) surgical control of pulmonary blood flow, and 3) evaluation of the cardiopulmonary function during PCPS for early weaning from PCPS.     

Intra-arterial papaverine-induced seizures: case report and review of the literature

BACKGROUND: Microcatheter-guided intra-arterial (IA) papaverine infusion in conjunction with balloon angioplasty is an available therapy for patients with symptomatic vasospasm after subarachnoid hemorrhage (SAH) that is refractory to hypertensive, hypervolemic therapy. However, side effects and complications have been reported in association with its use. CASE DESCRIPTION: We report on a patient who developed symptomatic vasospasm after subarachnoid hemorrhage due to rupture of a left terminal internal carotid artery (ICA) saccular aneurysm. Seven days after the hemorrhage and 4 days after surgical clipping, the patient developed aphasia and right hemiparesis due to vasospasm, which was refractory to maximal medical treatment with volume and blood pressure elevation. Cerebral angiography identified severe narrowing of distal ICA and proximal middle cerebral artery segments bilaterally. These findings partially resolved after balloon angioplasty. However, after 300 mg of IA papaverine, the patient developed generalized convulsions. This occurred despite therapeutic serum levels of phenytoin. Twenty-four hours later, after brief neurologic improvement, recurrent neurologic deficits prompted repeat papaverine administration. Seizures again occurred after the administration of 240 mg of IA papaverine and prevented administration of the full dose. The patient did not develop further seizures and her neurologic deficits continue to resolve. CONCLUSIONS: IA papaverine-induced seizures are infrequently reported. This potential complication should be considered when papaverine administration is entertained in the treatment of anterior circulation refractory symptomatic vasospasm after SAH.     

Neurogenic stress cardiomyopathy following aneurysmal subarachnoid hemorrhage in a very elderly patient--case report

A 90-year-old woman presented with aneurysmal subarachnoid hemorrhage (SAH) corresponding to Hunt and Hess grade II. Acute congestive heart failure and pulmonary edema developed following uneventful surgical clipping. Serial electrocardiography and echocardiography led to a diagnosis of neurogenic stress cardiomyopathy (NSC), also known as tako-tsubo cardiomyopathy. The outcome was favorable after supportive therapy with respiratory management and diuretic administration. Neurosurgeons treating SAH must take into account the various general treatment strategy options on a case by case basis after prompt recognition of NSC.     

Cardiogenic shock following nasal septoplasty: a case report and review of the literature

PURPOSE: Nasal septoplasty is a surgical procedure offered to patients with chronic snoring secondary to nasal obstruction. We describe a case of cardiogenic shock following the administration of metoprolol to treat hypertension, (likely) induced by systemic absorption of topical epinephrine used during a routine nasal septoplasty. CLINICAL FEATURES: A 29-yr-old male, with no significant medical history, was scheduled for nasal septoplasty for mild nasal obstruction. Following routine anesthetic induction, cotton balls, soaked with epinephrine (1:1000), were applied to the nasal mucosa. The patient became hypertensive with a blood pressure of 207/123 mmHg. Intravenous metoprolol was administered. Severe pulmonary edema ensued, with resulting hypoxic respiratory failure and cardiogenic shock. The patient was transferred to a tertiary care facility for percutaneous cardiopulmonary bypass. After five days of cardiopulmonary bypass support and six weeks of intensive care monitoring, the patient's cardiac status returned to normal limits. CONCLUSION: A hypertensive response, following systemically absorbed topical vasoconstrictors, including both phenylephrine and epinephrine, can be associated with dire consequences when treated with a beta-adrenergic blocking drug and, possibly, calcium channel blockers. To prevent severe complications including; pulmonary edema, cardiogenic shock, cardiac arrest, and, possibly, death, these drug interactions need to be appreciated.     

Coronary vasospasm following subarachnoid hemorrhage as a cause of stunned myocardium. Case report

A patient with subarachnoid hemorrhage was found to have electrocardiographic abnormalities resembling an acute myocardial infarction as well as left ventriculographic findings of cardiac dysfunction. These cardiac abnormalities resolved following surgical clipping of the aneurysm and the patient recovered well from the operation. She died 2 months later from cancer and a postmortem examination at that time revealed no evidence of myocardial necrosis. In this report, the authors discuss coronary vasospasm and reversible postischemic "stunned myocardium," a condition that has not been considered previously in relation to subarachnoid hemorrhage.     

Anesthetic management of a patient with severe subarachnoid hemorrhage and diffuse lung edema

One of the most common problems in emergency anesthesia for cerebral aneurysm surgery is clinically significant ECG abnormalities. We had a 58 year old patient with severe subarachnoid hemorrhage and diffuse lung edema leading to fatal outcome probably due to catecholamine myocardial injury. During the operative intervention with enflurane and oxygen anesthesia, ST elevation on ECG suddenly appeared and heart failure developed in this patient. Intraoperative ECG suggested the development of acute myocardial infarction of the anterior and inferior wall, but echocardiography revealed a discrepant result; the wall motion abnormality was confirmed in the apex only. The serum CPK in this patient increased a little over the normal limit perioperatively. Overall results suggested that a cause of this patient's death was myocardial injury due to the excessive release of catecholamine. Therefore, we urge the need of through cardiac examinations as well as the administration of preventive drugs for catecholamine myocardial injury in the perioperative management of patients with severe subarachnoid hemorrhage.     

A case of ruptured true posterior communicating artery aneurysm with neurogenic pulmonary edema treated early by GDC embolization

A case of ruptured true posterior communicating artery aneurysm with neurogenic pulmonary edema is presented. A 31-year-old male suffered the sudden onset of unconsciousness with respiratory dysfunction and pinkish foamy sputum. Computed tomography demonstrated diffuse subarachnoid hemorrhage and chest roentgenogram disclosed pulmonary edema. An emergency cerebral angiogram under controlled ventilation revealed that an aneurysm had arisen from the right posterior communicating artery itself. Subsequently GDC embolization and lumbar drainage were performed on day 0. The patient showed full recovery from pulmonary edema on day 6. He suffered multiple cerebral infarctions caused by vasospasm but he atlained a full recovery after 7 months. The follow-up angiogram showed complete obliteration of the aneurysm. This case report suggests that endovascular treatment with lumbar drainage is useful for severe aneurysmal SAH complicated with pulmonary edema in the acute stage.     

Ischemic myocardial disorder in acute phase subarachnoid hemorrhage: clinical study of 52 patients

Fifty-two cases of acute phase subarachnoid hemorrhage were studied by brain CT scanning to determine the presence and incidence of ischemic myocardial disorder, the relationship between ischemic change and severity, disease prognosis, and the relationship between acute phase circulatory dynamics and so-called neurogenic pulmonary edema. In all cases, ECGs were carried out and CPK-MB determined. Some of the patients underwent Tl myocardial scintigraphy, echocardiography, cardiac catheterization, as well as circulatory dynamic investigation (by Swan-Ganz catheter) and arterial blood gas analysis. In 31 of the 52 cases (59.6%), 3-day ECG series revealed ischemic changes. These findings were backed up by other cardiac function tests, thus suggesting that myocardial ischemia was present. Results in cases undergoing cardiac catheterization revealed that the myocardial ischemic changes were not due to organic constriction of the coronary artery. Included in those cases in which ECG markedly changed and CPK-MB rose substantially were many patients for whom the prognosis was poor. Evaluation of respiratory function and circulatory dynamics in cases of so-called neurogenic pulmonary edema seemed to indicate decline in cardiac function owing to myocardial ischemic change. This could account for onset of symptoms. These findings support the need for adequate circulatory management in cases of acute subarachnoid hemorrhage with pulmonary edema and/or changes on ECG. In such cases, concurrent catheterization and cerebral angiography (cerebro-cardiac catheterization: CCC) proved effective for evaluating cardiac function and determining whether heart disease was also present.     

Treatment of cerebral vasospasm. Usefulness of Swan-Ganz catheter monitoring of volume expansion

A practical approach to the treatment of neurological deficits associated with cerebral vasospasm by means of volume expansion and hypertension is illustrated by the management of two patients. In each instance, monitoring of cardiac and volume status was performed with a triple-lumen thermodilution Swan-Ganz catheter to determine what mean pulmonary artery wedge pressure would generate the greatest cardiac output. Intravascular volume was expanded with increased fluids, albumin, and blood. Neurological deficits in both patients were reversed completely. Neither patient developed pulmonary hypoxia, congestive heart failure, pulmonary edema, myocardial infarction, or symptoms of intracranial hypertension.     

Normovolaemic induced hypertension therapy for cerebral vasospasm after subarachnoid haemorrhage

Summary We showed that normovolaemic induced hypertension therapy was effective in reducing ischaemic symptoms attributed to cerebral vasospasm in 41 patients after subarachnoid haemorrhage. By inducing hypertension to 25% to 50% above normal systolic arterial blood pressure, we observed that in 17 of 24 cases (71%) neurological deficits improved. In four cases of haemorrhagic infarction, the blood pressure rose to over 50% of systolic arterial pressure, and a low density area was confirmed on computerized tomography (CT) scan prior to vasospasm. Induced hypertension was therefore not considered when a low density area was revealed on CT scan.Restriction of fluid input is usually a factor in producing hypovolaemia after a neurosurgical operation. Intravascular volume expansion has been reported effective in reversing ischaemic deficits. However, according to Poiseuille's equation, increasing blood volume to a state of hypervolaemia can not enhance flow. The cerebral blood flow (CBF) was raised by increasing perfusion pressure, reducing viscosity, or increasing blood vessel diameter. Intravascular volume expansion elevates not only systemic arterial pressure, but also pulmonary artery wedge pressure over 18 mmHg and cardiac index over 2.2. Since pulmonary oedema and congestive heart failure may develop, one should monitor haemodynamic parameters with the Swan-Ganz catheter as a preventive measure.We emphasize that normovolaemic induced hypertension, maintaining haemodynamics subset 1 of the comparable haemodynamic subsets, is effective in raising perfusion pressure of CBF.     

Serious pitfalls which can be encountered in a course of hypertension-hypervolemia therapy for vasospasm]

Hypertension-hypervolemia therapy (HHT) is widely employed for treatment against vasospasm after subarachnoid hemorrhage (SAH). A few investigations have been reported to establish the fact that HHT results in a high incidence of congestive heart failure and pulmonary edema as well as deterioration of brain edema. From the point of view that the cerebral circulation is not independent of the systemic circulation, the authors investigated the effect of HHT on the systemic circulation of patients with SAH. In 72 patients, intracranial pressure (ICP), pulmonary catheter wedge pressure (PCWP), pulmonary arterial pressure (PA), central venous pressure (CVP), arterial pressure (AP), cardiac index (CI), arterial blood gas (ABGS), electrocardiogram (ECG), serum and urine electrolytes were monitored postoperatively. Furthermore, among these patients, the flow (Flow), volume (Volume) and velocity (Velocity) of the cortical vessels were monitored by means of a Laser Doppler in 25 patients. A cisternal or spinal drain was placed in all of the patients. Elevation of PCWP and CVP and Flow were observed when 300ml of 10% glycerol was administered within a period of 30 minutes, whereas administration of the same dose of glycerol over a period of 60 or 120 minutes caused no significant changes on these parameters. Elevation of PCWP and CVP and decrease of CI and Flow, occasionally associated with premature ventricular contraction (PVC), were observed in some patients when 100ml of 25% albumin was administered. However, administration of the same dose of albumin over a period of 120 or 240 minutes did not cause deterioration of the cardiac function. These facts could be explained by Guyton's law in which massive transfusion causes cardiac dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Neurogenic pulmonary edema: treatment with dobutamine

In the case of a patient with complicating subarachnoid hemorrhage, an infusion of dobutamine was followed by a massive diuresis and regression of severe neurogenic pulmonary edema. It is suggested that the reduction in total peripheral vascular resistance and the increase in cardiac contractility accounts for the observed beneficial effect and indicate that dobutamine is a suitable drug for the treatment of neurogenic pulmonary edema.     

Circulatory characteristics of normovolemia and normotension therapy after subarachnoid hemorrhage, focusing on pulmonary edema

Background and purpose

Cardiopulmonary complications are common after subarachnoid hemorrhage (SAH), and include pulmonary edema (PE). The purpose of this study was to investigate circulatory characteristics of normovolemia and normotension therapy after SAH using pulse contour analysis, and to reveal the mechanisms of PE after SAH.

Methods

Pulse contour analysis was performed from day 3 until day 12 after the onset of SAH in 49 patients.

Results

Global end-diastolic volume index (GEDI) was normal, although net water balance was estimated to be negative and central venous pressure (CVP) was low in all patients. Seven patients (14?%) suffered from pulmonary edema. Cardiac function index (CFI) and global ejection fraction (GEF) were lower in patients with pulmonary edema (PE group) than in patients without PE (non-PE group) throughout the study period (CFI, P≤0.0119; GEF, P≤0.0348). The PE group showed higher GEDI from days 7 to 10, and higher extravascular lung water index (ELWI) throughout the entire study period compared to the non-PE group (GEDI, P≤0.0094; ELWI, P≤0.0077).

Conclusions

The appropriate preload was kept despite negative net water balance and low CVP. PE after SAH was biphasic, with cardiogenic PE caused by low cardiac contractility immediately after SAH, and hydrostatic PE caused by low cardiac contractility and hypervolemia on and after day 7 of SAH. Pulse contour analysis was useful to monitor this unique circulatory change and effective for detecting cardiopulmonary complications after SAH.     

Noncardiogenic pulmonary edema after cardiopulmonary bypass: An anaphylactic reaction to fresh frozen plasma

Nine episodes of fulminant noncardiogenic pulmonary edema after cardiopulmonary bypass were observed in eight patients between September 1977 and December 1982. All these catastrophic reactions occurred during administration of fresh frozen plasma 30 minutes to 6 hours after discontinuation of cardiopulmonary bypass. In one patient, two episodes of noncardiogenic pulmonary edema occurred 4 hours apart. In each instance, fresh frozen plasma was being administered. In all patients, pulmonary artery diastolic pressure became elevated during the administration of fresh frozen plasma while left atrial pressure or pulmonary capillary wedge pressure progressively decreased, and cardiac output deteriorated markedly in all but one patient. Corticosteroids, postive end-expiratory pressure, and catecholamines were administered to all patients.All deaths were due to a decrease in cardiac output. Cardiac output did not increase substantially with the use of an intraaortic balloon pump or the administration of catecholamines. The last two patients in the series showed a steady and remarkable improvement in cardiac output when the wedge pressure was increased to a level above 15 mm Hg with the administration of normal saline solution. Our data suggest the following: (1) noncardiogenic pulmonary edema after cardiopulmonary bypass is most probably an anaphylactic reaction to fresh frozen plasma. (2) The syndrome is reversible within hours; in only one patient (who suffered noncardiogenic pulmonary edema twice) did adult respiratory distress syndrome develop. (3) The three deaths were not related to hypoxia but to the deleterious effects of low cardiac output associated with hypovolemia secondary to fluid loss through the lungs and possibly across other capillary beds. Therefore, treatment should include restoration of adequate left-sided filling pressures to achieve satisfactory cardiac output.     

Successful management using airway pressure release ventilation for severe postoperative pulmonary edema

IntroductionPostoperative pulmonary edema is a fatal adverse event after a cardiac surgery. We here report successful management using airway pressure release ventilation (APRV) for severe hypoxia with pulmonary edema after a cardiac surgery.Presentation of caseA 58-year-old man underwent an uneventful mitral valve repair. Immediately afterwards, the patient became agitated and made vigorous inspiratory efforts. His oxygen saturation dropped to 90%. Coarse inspiratory rhonchi were heard on auscultation, and copious, pink, frothy sputum was obtained with suctioning. Initial chest radiograph showed right-sided patchy opacities and interstitial infiltrates. A transthoracic echocardiogram demonstrated normal cardiac function. With worsening respiratory failure on mechanical ventilation, APRV was attempted. His condition and blood gas was subsequently improved. Over the following 3 days, the patient experienced an uneventful postoperative course and was discharged to home on postoperative day 14.DiscussionExtracorponeal membrane oxygenation (ECMO) is the most effective for severe hypoxia with pulmonary edema; however, ECMO is associated with hemorrhage and infectious complications. Alteratively, APRV was required for the successful management for severe hypoxia with pulmonary edema.ConclusionAPRV could be effective for severe hypoxia with pulmonary edema after a cardiac surgery.     

Induced hypertension and hypervolemia for treatment of cerebral vasospasm

The authors discuss a comprehensive management program for patients with cerebral vasospasm following subarachnoid hemorrhage in which therapeutic manipulation and meticulous monitoring of a number of physiologic determinants of cardiac function are employed. Ventricular preload is most significantly affected by hypervolemic therapy, but alternate methods of reversing ischemic neurologic deficits with various inatropic agents are discussed also.