[Coronary artery bypass by mini-thoracotomy: noticeable benefits with clinical experience of the treatment team]. / Pontages coronariens par mini-thoracotomie: bénéfices visibles avec l'expérience croissante de l'équipe traitante.

AIM OF THE STUDY: Minimally invasive coronary artery bypass surgery is fundamentally different as compared to open sternal approach under cardiopulmonary bypass. Modifications of the surgical, anesthesiologic and post-operative techniques are necessary before evaluation of its real benefit. We analyze the potential effect of a learning period on the short term results of this technique. METHODS: From July 1997 to February 1999, 20 patients were operated using this method. We compare the results of the first 10 patients (group 1: 8M/2F, 59.6 +/- 13.8 years) to those of the last 10 patients (group 2: 8M/2F; age = 63.2 +/- 6.1 years). DISCUSSION: Progress between the two groups is striking. Left anterior descending coronary clamping time could be reduced from 28.5 +/- 2.4 min. in group 1 to 22.2 +/- 1.8 min. in group 2 (p < 0.05), and operative time was reduced from 125 +/- 4 min. to 97 +/- 5 min. (p < 0.005). The post-operative atrial fibrillation rate diminished from 4/10 in group 1 to 1/10 in group 2.3/10 patients in group 1 suffered a post-operative pneumonia whereas none in group 2 had pulmonary complication. The stay in the intensive care unit could be reduced from 2.3 +/- 0.3 days to 1.4 +/- 0.2 days (p < 0.05) and the total post-operative stay diminished from 8.5 +/- 0.9 days to 4.7 +/- 0.5 days (p < 0.005). CONCLUSION: There are evidence for a learning period in minimally invasive cardiac surgery. Short term benefits of this technique are then evident as demonstrated by a reduction in the ICU stay and the hospital stay.

Human errors in a multidisciplinary intensive care unit: a 1-year prospective study.

OBJECTIVES: To determine the incidence and identify risk factors of critical incidents in an ICU. DESIGN: Prospective observational study of consecutive patients admitted over 1 year to an ICU. Critical incidents were recorded using predefined criteria. Their causes and consequences were analysed. The causes were classified as technical failure, patient's underlying disease, or human errors (subclassified as planning, execution, or surveillance). The consequences were classified as lethal, leading to sequelae, prolonging the ICU stay, minor, or without consequences. The correlation between critical incidents and specific factors including patient's diagnosis and severity score, use of monitoring and therapeutic modalities was analysed by uni- and multivariate analysis. SETTING: An 11-bed multidisciplinary ICU in a non-university teaching hospital. PATIENTS: 1,024 consecutive patients admitted to the ICU. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: The median length of ICU stay by the 1,024 patients was 1.9 days. Of the 777 critical incidents reported 2% were due to technical failure and 67 % to secondary to underlying disease. There were 241 human errors (31%) in 161 patients, evenly distributed among planning (n = 75), execution (n = 88), and surveillance (n = 78). One error was lethal, two led to sequelae, 26 % prolonged ICU stay, and 57 % were minor and 16 % without consequence. Errors with significant consequences were related mainly to planning. Human errors prolonged ICU stay by 425 patient-days, amounting to 15 % of ICU time. Readmitted patients had more frequent and more severe critical incidents than primarily admitted patients. CONCLUSIONS: Critical incidents add morbidity, workload, and financial burden. A substantial proportion of them are related to human factors with dire consequences. Efforts must focus on timely, appropriate care to avoid planning and execution mishaps at the beginning of the ICU stay; surveillance intensity must be maintained, specially after the fourth day.

[Hyponatremia in neurologic intensive care: cerebral salt wasting syndrome and inappropriate antidiuretic hormone secretion]. / Les hyponatrémies en neuroréanimation: syndrome de perte de sel et sécrétion inappropriée d'hormone antidiurétique.

Hyponatraemia is a frequent complication in neurologically injured patients; it is a secondary cerebral injury. Hyponatraemia leads to consciousness problems, convulsions, worsening of the neurological status and thus the neurological evaluation. Hyponatraemia is secondary to free water retention (inappropriate ADH secretion) or to renal salt loss. The cerebral salt wasting syndrome (CSWS) has been described with head injury, subarachnoid haemorrhage and after several sorts of brain insults. It is characterised by an increased natriuresis and diuresis. Diagnosis is based on hyponatraemia, hypernatriuresis, increased diuresis and hypovolaemia. However, inappropriate ADH secretion and CSWS share several diagnostic criteria. The atrial natriuretic factor and the C-type natriuretic factors play a role in the development of the CSWS. The diagnostic approach and monitoring are based on the assessment of sodium and water losses. Therapy is based on correction of the circulating volume and natraemia. Speed of correction is a matter of debate: slow correction presents the risk of further neurological injury whereas rapid correction presents the risk of central pontine myelinosis.

Fatal fat embolism syndrome: a case report.

Fat embolism syndrome is a dire complication of long bone trauma. It is usually associated with neurological, hematological and respiratory involvement, the latter being the major cause of death. We present a case of severe fat embolism syndrome occurring 3 hours after a long bone injury, leading to permanent vegetative state and death without any respiratory signs. The diagnosis was confirmed by cytology of the bronchoalveolar lavage fluid. Clinical presentation of the puzzling fat embolism syndrome and diagnostic tests in suspected fat embolism syndrome are reviewed.

Pulmonary injury after ski wax inhalation exposure.

A wide variety of irritants can lead to respiratory failure after inhalation injuries. We present a case of adult respiratory distress syndrome after exposure to a fluorocarbon resin (PFF 1020) used as ski wax. The patient sustained a mild but prolonged exposure to this substance, which subsequently led to symptoms of severe respiratory failure over the next 24 hours. Except for hypocalcemia, there were no systemic manifestations and recovery was uneventful. Ski wax is considered to be nontoxic and there are no reported side effects of these products. Injury was related to the heated fluorocarbon particles. This case report of a severe lung inhalation injury points out the increasing risk of environmental hazards associated with the use of synthetic substances.

-The effect of ondansetron on intracranial pressure and cerebral perfusion pressure in neurosurgical patients-. / Effet de l'ondansétron sur la pression intracrânienne et la pression de perfusion cérébrale chez le patient neurochirurgical.

OBJECTIVE: To determine the effect of ondansetron on intracranial pressure (ICP), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP). STUDY DESIGN: Prospective, comparative, randomized double-blind study. PATIENTS: Twenty-six patients undergoing intracranial surgery. METHOD: Induction was obtained with propofol (1-2.5 mg.kg-1), fentanyl (1.5 micrograms.kg-1) and pancuronium (0.1 mg.kg-1), and maintenance was achieved with propofol and fentanyl. Intermittent positive pressure ventilation was used to ensure mild hypocapnia at 35 +/- 2 mmHg. Positioning of the patient was followed by 15 minutes steady-state. Patient received thereafter either 8 mg ondansetron or a placebo intravenously. The ICP was measured using a lumbar malleable spinal needle. CPP was calculated using the formula CCP = MAP-ICP. All variables were measured every minute for 15 minutes. RESULTS: The ICP, MAP and CPP did not differ between the two groups. There were no differences in the highest ICP values in patients receiving either ondansetron or placebo (11 +/- 5 versus 9 +/- 5, mean +/- SD), respectively. CONCLUSION: Intravenous administration of 8 mg ondansetron affects neither cerebral hemodynamics nor ICP.

[Minimally invasive surgery for coronary disease: a new alternative]. / Chirurgie mini-invasive pour la maladie coronarienne: nouvelle alternative.

To avoid the inflammatory syndrome generated by cardiopulmonary bypass, a new surgical technique, minimal invasive direct coronary artery bypass (MIDCAB), has been developed. An anastomosis is performed between the left internal mammary artery (LIMA) and the left anterior descending artery (LAD) on a beating heart, through a limited anterior thoracotomy. We describe our experience with this technique. Ten consecutive patients underwent a MIDCAB procedure. (9 males, age 65.9 +/- 9 years). There were 8 bypasses of the LIMA on the LAD, one bilateral mammary bypass on the LAD and the right coronary artery, and one conversion to a standard sternotomy with CPB for a saphenous vein bypass on the LAD because of injury to the LIMA (2nd case). There was one redo for haemostasis of the mammary artery bed (3rd case). The first 3 patients required postoperative blood transfusion. From the 4th operation onwards, with the introduction of new instrumentation which was better adapted to the narrowness of the surgical field, there were no further surgical complications. During the follow-up (mean 5 months; range 2-9), no patient suffered anginal recurrence. With the improvement of instrumentation, the MIDCAB technique offers satisfactory short- and mid-term results, while avoiding CPB with its adverse effects. Lastly, the cosmetic result is far better than with the conventional procedure.

[Cerebral hemodynamics and intracranial hypertension]. / Hémodynamique cérébrale et hypertensions intracrâniennes.

Various cerebral aggressions, either primary or secondary, can lead to the development of raised intracranial pressure. The presence of an elevated intracranial pressure often results in cerebral ischaemia/hypoxia and, eventually, neuronal death. In face of this cascade of events, several therapeutic approaches have been suggested. Two management concepts for patients with raised intracranial pressure have retained the most attention in recent years: the first suggests a therapeutic increase in cerebral perfusion pressure with the objectives to improve perilesional collateral perfusion and decreased cerebral blood volume, and consequently intracranial pressure in areas where autoregulation is preserved. The second concept supports the diminution in perilesional capillary pressure with the aim of decreasing vasogenic oedema. Although these two concepts are antagonistic and cannot be used simultaneously, they are probably complementary in the sequence of therapeutic events of patients experiencing severe head injury. This article reviews these therapeutic concepts and their clinical applications.

[Hypertonic solutions and intracranial pressure]. / Liquides hypertoniques et pression intracrânienne.

The properties of the endothelium differ between the brain and the remainder of the body. In most non-CNS tissues the size of the junctions between endothelial cells averages 65 A. Proteins do not cross these gaps, while sodium does. In the brain, the junction size is only 7 A, which is too small to allow crossing by sodium. Investigations with changes in osmotic and oncotic pressure have demonstrated that: (1) reducing osmolality results in edema formation in all tissues including normal brain; (2) a decrease in oncotic pressure is only associated with peripheral edema but not in the brain; (3) in case of brain injury, a decrease in osmolality elicits edema in the part of brain which remained normal; (4) similarly, a decrease in oncotic pressure does not cause an increase in brain edema in the injured part of the brain. The determinant factor of water exchange in the brain is mediated through the osmolality and not the oncotic pressure. The use of hypertonic solutions (Ringer lactate or NaCl) for intravascular fluid resuscitation of patients suffering from hypovolemic head trauma has gained popularity. A research survey in regard with this observation can be summarized as follows: NaCl 7.5% (2400 mOsm/l) is becoming the most popular hypertonic solution because of its favorable systemic and cerebral effects. It improves myocardial contractility, precapillary dilatation, and reactive venoconstriction, and it has a plasmatic expansion factor of 3.8. In regard to the brain tissue, it improves the PO2 and the cerebral blood flow (CBF) as a result of decreasing cerebrovascular resistance. Finally, it reduces the cortical water content of intact blood-brain barrier area. The overall consequence is reduction of intracranial pressure (ICP). Although the homeostasis of the cerebral intracellular compartment remains unknown, it is possible that brain cells are able to resist important osmolar overload. NaCl 7.5%/dextran 70.6% is clinically at this moment the most studied hypertonic/hyperoncotic agent in prehospital emergencies. Its effects on cerebral homeostasis are identical to NaCl 7.5%. However, the addition of a colloid agent has the advantage of prolonging the systemic effects without affecting the brain. The plasmatic expansion factor is 4.5, which is slightly superior to NaCl 7.5%. Mannitol improves CBF by maintaining autoregulation as a result of changes in viscosity and reactive cerebrovascular constriction. It generates an osmotic gradient which reduces the cerebral volume and subsequently the ICP. In the presence of a cryogenic cerebral lesion, its reductive effects on brain water are superior to the hypertonic/hyperoncotic solution. Because mannitol has less spectacular systemic responses than the other solutions, it is not indicated for resuscitation following hemorrhagic shock. In conclusion, it is important to note that hypotension and hypoxemia represent the determinant factors of secondary cerebral insults. Therefore, in the presence of patients with head injury and especially hemorrhagic shock, it is essential to ensure a cerebral perfusion pressure (CPP) of > 80 mm Hg. Hypertonic solutions have gained popularity in these clinical situations because of their combined effects on ICP, mean arterial pressure (MAP) and CPP. However, the therapeutic approach to polytraumatized patients with small intravascular volume (4-6 ml/kg) of hypertonic solutions should not be a substitute for the usual volemic resuscitation technique. The clinical indication for these solutions should be limited to the initial resuscitation maneuvers in traumatized patients. Prolonged use of hypertonic solutions for the purpose of intravascular resuscitation would only contribute to increasing the side effects and eventually counteract the initial beneficial advantages.

Effect of clonidine on ICP and on the hemodynamic responses to nociceptive stimuli in patients with brain tumors.

The effect of clonidine on intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), heart rate (HR), and drug requirements was studied in 24 patients scheduled for elective cerebral tumor resection (ICP < or = 20 mm Hg). The patients were randomly assigned to one of two groups: Group P (placebo), 12 patients; Group C (clonidine 3 micrograms/kg 10 min before induction), 12 patients. In all patients, anesthesia was induced with a propofol infusion (500 micrograms/kg/min) combined with fentanyl 2 micrograms/kg, lidocaine 1.5 mg/kg, and vecuronium 0.1 mg/kg. Propofol was also used for maintenance. During the preinduction period, clonidine had no effect on ICP or HR, but in clonidine-treated patients, MAP and CPP decreased significantly in comparison to those of the placebo group. During induction, ICP and HR were stable and similar in both groups. MAP and CPP remained significantly lower in Group C. At intubation and Mayfield clamp application, ICP increased in both groups, with similar values at all times. MAP increased in both groups at intubation, Mayfield clamp application, and incision, staying lower, however, in Group C. CPP followed a pattern similar to that of MAP. Propofol requirements up to the 20th min were lower in Group C than in Group P (2.08 +/- 0.83 vs. 3.3 +/- 0.7 mg/kg, p < 0.05). Finally, throughout the study, eight patients in Group C versus two in Group P had a CPP value < 60 mm Hg for > or = 1 min (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

[Prehospital air ambulance and systemic secondary cerebral damage in severe craniocerebral injuries]. / Médicalisation préhospitalière héliportée et agressions cérébrales secondaires d'origine systémique chez les traumatisés craniocérébraux graves.

Advanced supportive therapy at the site of the accident, associated with direct transfer to a trauma centre increases survival and reduces morbidity rates. Patients with severe head injury, especially those with multiple injuries, often arrive in the emergency department with potentially causes of serious secondary systemic insults to the already injured brain, such as acute anemia (Hematocrit < or = 30%), hypotension (systolic arterial pressure (Pasys) < or = 95 mmHg, 12.7 kPa), hypercapnia (Paco2 > or = 45 mmHg, 6 kPa) and/or hypoxemia (Pao2 < or = 65 mmHg, 8.7 kPa). The incidence of such insults and their impact on mortality were studied in a group of 51 consecutive adults suffering from non penetrating severe head injury (Glasgow score < or = 8, mean age 31 +/- 17 yrs) rescued by a medicalized helicopter. Each patient received medical care on the site of the accident by an anaesthesiologist of a university hospital (UH) complying with an advanced trauma life support protocol including intubation, hyperventilation with FiO2 = 1, restoration of an adequate Pasys and direct transportation to the UH. Mean delay from call to arrival of the rescue team on the site was 15 +/- 5 min. Mean scene time was 32 +/- 10 min in cases not requiring extrication. Nineteen patients (Group I) were admitted without secondary systemic insults to the brain, 13 with isolated head injury, and 6 with multiple injuries, with a low Glasgow Outcome Score (GOS 1-3) of 42% at 3 months. In 32 patients (Group II), despite advanced supportive measures at the scene of the accident and during transportation, one or more secondary systemic insults to the brain were detected upon arrival at the emergency room, one with isolated head injury, 31 with multiple injuries, with a bad GOS of 72% at 3 months. We conclude that: 1) advanced trauma life support prevents from secondary systemic insults in the great majority of isolated severe head injured patients. 2) secondary systemic insults to the already injured brain are frequent in patients with multiple injuries and are difficult to avoid despite rapid aeromedical trauma care, 3) secondary systemic insults to the brain have a catastrophic impact on the outcome of severely head injured patients.

[Treatment of hypovolemia in brain injured patients]. / Traitement de l'hypovolémie chez le traumatisé craniocérébral.

The appropriate administration of intravenous fluids in neurosurgical patients remains an area of disagreement between neurosurgeons and anaesthetists. Fluid restriction has long been advocated by the former and is widely believed to reduce or prevent the formation of cerebral oedema. However, such restriction can lead to hypovolaemia which in turn can result in haemodynamic instability. Thus, brain homeostasis should be aimed for through adequate fluid administration and normal or slightly elevated mean arterial pressure. The properties of the endothelium differ between the brain and the remainder of the body. In most non CNS tissues the size of the junctions between endothelial cells averages 65 A. Proteins do not cross these gaps while sodium does. In the brain, the junction size is only 7 A, which is too small to allow crossing by sodium. Investigations with changes in osmotic and oncotic pressure have demonstrated that: 1) reducing osmolality results in oedema formation in all tissues including normal brain; 2) a decrease in oncotic pressure is only associated with peripheral oedema but not in the brain; 3) in case of brain injury, a decrease in osmolality elicits oedema in the part of brain which remained normal; 4) similarly, a decrease in oncotic pressure does not cause an increase in brain oedema in the injured part of the brain. Thus, a major reduction in oncotic pressure is unimportant for the brain, whereas changes in total osmolality are the dominant driving force at this level. To conclude, in a hypovolaemic patient with severe head injury, the crystalloid of choice is NaCl 0.9% and the colloid of choice is hydroxyethylstarch, both with an osmolality > 300 mosm.kg-1. Ringer-lactate is hypoosmotic (255 mosm.kg-1) and may cause or increase cerebral oedema. Mean arterial pressure should be maintained above 80 mmHg.