Clipping vs. coiling in acute aneurysmal subarachnoid haemorrhage: Should the patient's medical condition influence treatment modality?

INTRODUCTION: Acute subarachnoid haemorrhage (SAH) resulting from aneurysmal rupture is a medical condition associated with significant morbidity and mortality. Medical complications resulting from the bleeding itself, along with the patient's underlying medical conditions are known to represent possible prognostic factors in acute SAH. However, their respective significance on the patient's overall clinical outcome following either endovascular coiling (EC) or surgical clipping (SC) remains to be ascertained as well as their potential role in choosing a definitive treatment option. We thus reviewed the evidence concerning the patient's medical condition as a factor in this decision making process. METHODOLOGY: Source data were obtained from a MEDLINE search of the medical literature and by manual review of published randomised trials comparing EC to SC. RESULTS: The last three decades allowed for detection of medical complications with increasing frequency in the context of SAH, as awareness for them has improved. Despite the fact that a patient's extra-neurological condition can be a significant prognostic factor after a SAH, our review demonstrates that medical conditions in general were not taken into consideration in randomized trials comparing EC to SC. Also, we found no analysis comparing the potential role of prior versus post-SAH medical conditions in choosing either therapeutic avenue. CONCLUSION: It is not determined whether it is appropriate for SAH patients to be offered treatment for a ruptured aneurysm based mostly on anatomical criteria or if, within certain subgroups of patients, EC and SC should also be recommended in light of what the patient can tolerate from a medical standpoint. Although we hypothesize that in practice, the patient's medical condition is considered in the decision making process, it remains to be documented. Patient, aneurysm and institution-related factors are all interrelated, as is patient care. Data on all of these factors are thus needed and their analysis by association rather than by dissociation may be the key in answering our question.

Inhaled prostacyclin (PGI2) is an effective addition to the treatment of pulmonary hypertension and hypoxia in the operating room and intensive care unit.

PURPOSE: There is a growing interest in the intraoperative and intensive care use of inhaled epoprostenol (PGI2) for the treatment of pulmonary hypertension (PHT) and hypoxia of cardiac or non-cardiac origin. We report our experience with this form of therapy. METHODS: A retrospective chart review of all patients who received inhaled PGI2 over a one-year period was undertaken. Demographic, hemodynamic, oxygenation status, mode of administration, side effects, duration of hospital stay, and mortality were noted. RESULTS: Thirty-five patients, of which 33 (92%) were in the intensive care unit, received inhaled PGI2. Of the 27 patients whose pulmonary artery pressure (PAP) was monitored, a significant decrease in mean PAP from 34.8 +/- 11.8 mmHg to 32.1 +/- 11.8 mmHg was observed within one hour after the start of therapy (P=0.0017). Selective pulmonary vasodilatation occurred in 77.8% of the patients. Thirty-three patients had arterial blood gases before and after therapy. There was an improvement in the PaO2/FIO2 ratio in 88% of these with a 175% improvement on average. The ratio of PaO2/FIO2 improved from 108 +/- 8 to 138 +/- 105 (P=0.001). Six patients (17%) presented hypotension, two had subsequent pneumothorax, one had bronchospasm and in one patient PGI2 inhalation was stopped because of increasing peak pulmonary pressures from the secondary flow coming from the nebulizer. Mortality of the cohort was 54%. CONCLUSION: Inhaled PGI2 can be useful in the treatment of patients with PHT and severe hypoxia. It can however be associated with systemic side effects.

Acute respiratory distress syndrome: 30 years later.

Acute respiratory distress syndrome (ARDS) was first described about 30 years ago. Modern definitions and statements have recently been proposed to describe ARDS accurately, but none is perfect. Diffuse alveolar damage is the basic pathological pattern most commonly observed in ARDS, and the term includes permeability edema. The alveolar epithelium of the alveolar-capillary barrier is clearly a key component requiring repair, given its multipotent functional activity. Lung inflammation and neutrophil accumulation are essential markers of disease in ARDS, and a wide variety of pro- and anti-inflammatory cytokines have been described in the alveolar fluid and blood of patients. These molecules still have to prove their value as diagnostic or prognostic biomarkers of ARDS. Supportive therapy in ARDS improved in the past decade; mechanical ventilation with lung protective strategies and patient positioning are gaining interest, but the indications for corticosteroids for ARDS are still debated. Nitric oxide may have a place in the treatment of one-third of patients. Novel approaches, such as surfactant replacement and liquid ventilation, may further improve supportive therapy. Innovative interventions may be on the horizon in treatments that help to resolve or modulate common pathways of ARDS, such as inflammation (eg, granulocyte-colony stimulating factor) or epithelial repair (eg, keratinocyte growth factor).

Inhaled nitric oxide in acute respiratory distress syndrome: a pilot randomized controlled study.

This pilot randomized controlled clinical trial of patients with ARDS was implemented to study the impact of inhaled nitric oxide (inhNO) on lung function, morbidity, and mortality. Thirty patients with ARDS were randomly allocated to usual care or usual care plus inhNO. The optimal dose of inhNO was determined to be between 0.5 and 40 parts-per-million daily. All therapeutic interventions were standardized. ARDS resulted mainly from sepsis (25 of the 30). During the first 24 h, the hypoxia score increased greatly in patients treated with inhNO +70.4 mm Hg (+59%) versus +14.2 mm Hg (+9.3%) for the control group (p = 0.02), venous admixture decreased from 25.7 to 15.2% in the inhNO group, and from only 19.4 to 14.9% in the control group (p = 0.05). After the first day of therapy no further beneficial effect of inhNO was detected. Forty percent of the patients treated with inhNO were alive and weaned from mechanical ventilation within 30 d after randomization compared with 33.3% in the control group (p = 0.83). The 30-d mortality rate was similar in the two groups; most deaths (11 of 17) were due to multiple organ dysfunction syndrome. This study shows that inhNO, in this population, may improve gas exchange but does not affect mortality.

Effect of synchronous increase in intrathoracic pressure on cardiac performance during acute endotoxemia.

In the anesthetized closed-chest canine model of Gram-negative endotoxemia (n = 10), we tested the hypothesis that the effect of cardiac cycle-specific intrathoracic pressure pulses delivered by a heart rate-(HR) synchronized high-frequency jet ventilator (sync HFJV) on systolic ventricular performance is dependent on the level of preload. To control for HFJV frequency, hemodynamic responses were also measured at fixed frequency within 15% of HR (async HFJV). Biventricular stroke volumes (SV) were measured by electromagnetic flow probes. Measurements were made before (baseline) and 30 min after infusion of 1 mg/kg Escherichia coli endotoxin (serotype 055:B5) and then after 2 mg/kg propranolol at both low (less than 10 mmHg) left ventricular filling pressure (LVFP) and high (greater than 10 mmHg) LVFP. Ventricular function curves, aortic pressure-flow (P-Q) relationships, and venous return (VR) curves were analyzed. We found that endotoxin did not alter VR curves but shifted the aortic P-Q curves to the left with pressure on the x-axis (P less than 0.05). Volume loading increased SV (P less than 0.01) because of a rightward shift of the VR curve. No specific differences occurred with either sync or async HFJV during endotoxin, presumably because of preserved VR and shifted aortic P-Q. The lack of cardiac cycle-specific effects of ITP appears to be due to the selective endotoxin-induced changes in peripheral vasomotor tone that counterbalance any depressed myocardial contractility.

Augmentation of cardiac function in end-stage heart failure by combined use of dobutamine and amrinone.

A patient with end-stage congestive cardiomyopathy had progressive hemodynamic deterioration while awaiting orthotopic heart transplantation. Attempts to support cardiovascular function by high-dose dobutamine infusions were complicated by life-threatening cardiac arrhythmias. The addition of the noncatecholamine inotropic agent, amrinone, improved ventricular performance, enabling reduction of the dose of dobutamine and resolution of the cardiac arrhythmias. Beta receptor stimulation by dobutamine combined with phosphodiesterase inhibition by amrinone may additively or synergistically augment cardiac function despite severe congestive heart failure and also have an adrenergic "sparing effect."