Effects of pneumoperitoneum and reverse Trendelenburg position on cardiopulmonary function in morbidly obese patients receiving laparoscopic gastric banding.

We prospectively evaluated the effects of pneumoperitoneum and reverse Trendelenburg position on cardiopulmonary function in 20 ASA physical status II-III morbidly obese patients (body mass index > 35 kg m(-2)) undergoing laparoscopic gastric banding. After general anaesthesia was induced, patients' lungs were ventilated using intermittent positive pressure ventilation (at measurement times, the following parameters were used: tidal volume 12 mL kg(-1) ideal body weight, respiratory rate of 12 bpm, an inspiratory to expiratory time ratio of 1:2). Haemodynamic variables, blood gas parameters, and lung/chest compliance were recorded: in the supine position, after induction of general anaesthesia (T0, baseline) and induction of pneumoperitoneum (T1); after placing the patient in a 25 degree reverse Trendelenburg position (T2); during the surgical time (T3); before deflating the abdomen (T4); after pneumoperitoneum resolution (T5), and before the end of anaesthesia, with the patient supine (T6). The PaO2, PaO2/FiO2 ratio, and lung/chest compliance decreased during the study. After the pneumoperitoneum had been resolved, lung/chest compliance but not oxygenation parameters returned to baseline values. The arterial to end-tidal CO2 tension difference progressively increased from 0.38+/-0.3 kPa (2.85+/-2.25 mmHg) (T0) to 0.63+/-0.3 kPa (4.73+/-2.25 mmHg) (T6). In morbidly obese patients, undergoing laparoscopic gastric banding, a CO2 pneumoperitoneum markedly affected gas exchange and lung/chest compliance, while positioning the patient in a 25 degree reverse Trendelenburg position had no beneficial effects.

[Retinoic acid syndrome. Severe respiratory insufficiency treated with CPAP]. / Sindrome da acido retinoico: grave insufficienza respiratoria trattata con ventilazione in maschera con CPAP.

Retinoic acid syndrome is a potentially life-threatening complication of therapy for acute promyelocytic leukemia (APL) with all-transretinoic acid (ATRA). The case of a 55-year old male patient admitted to the hospital because of a bleeding diathesis is reported. APL was diagnosed and he underwent treatment with idarubicin and ATRA (GIMEMA protocol); 24 hrs after ATRA treatment he developed retinoic acid syndrome and was admitted to the Intensive Care Unit because of severe respiratory insufficiency (dyspnoea, tachypnea and severe hypoxemia (SpO2 75%). Pulmonary insufficiency was treated non-invasively with CPAP and the patient recovered from pulmonary distress one week later.

[Rhabdomyolysis caused by improper intraoperative positioning. Clinical and medico-legal aspects]. / Rabdomiolisi da malposizionamento intraoperatorio. Aspetti clinici e medicolegali.

The etiology, diagnosis, pathology and treatment of rhabdomyolysis due to intraoperative malpositioning and the medico-legal implications of physicians involved in the surgical treatment and anesthesia of the patient are described. According to the Italian law, the anesthesiologist is the only physician of the surgery-anesthesia team responsible for the patient's positioning. The anesthesiologist must assume primary responsibility for protecting the patient from iatrogenic injuries due to improper positioning, and/or inadequate preventive measures.

7.5% hypertonic saline versus 20% mannitol during elective neurosurgical supratentorial procedures.

This prospective randomized clinical study was designed to compare the effects of equal volumes of 7.5% hypertonic saline solution (HS) or 20% mannitol (M) on brain bulk and lumbar cerebrospinal fluid pressure (CSFP) during elective neurosurgical procedures (aneurysm, arteriovenous malformation, or tumor). After informed consent, 50 American Society of Anesthesiologists physical Status I (ASA I) patients were randomly assigned to M (n = 25) or HS (n = 25) groups. Anesthesia protocol was identical for both, and variables monitored included mean arterial blood pressure (MAP), heart rate (HR), central venous pressure (CVP), CSF pressure (CSFP), arterial blood gases (PaCO2 30-35 mm Hg), serum sodium, potassium, and osmolality, and diuresis. The study period started before hypertonic solution administration (T0) and ended at the opening of the dura mater or 60 min after T0. Data were assessed with repeated measures analysis of variance and Student t test with Bonferroni correction (p < or = 0.05). MAP and CVP were the same in the two groups. After treatment, osmolality increased, and the increase at T15 was higher in HS-treated patients [316.6 +/- 9.3 vs. 304.0 +/- 12.0 (SD) mOsmol/kg; p < 0.001]. Sodium decreased after M and increased after HS. During the study, brain bulk was always considered satisfactory. CSFP was not different between M and HS groups and significantly decreased overtime (p = 0.0056) with no difference between treatments. The results of the present study demonstrate that hypertonic saline is as effective as mannitol in reducing the brain bulk and the CSFP during elective neurosurgical procedures under general anesthesia.

Cerebral ischemia after venous air embolism in the absence of intracardiac defects.

Cerebral air embolism occurred in a patient undergoing posterior fossa surgery performed in the sitting position for acoustic neuroma removal. The patient experienced two episodes of venous air embolism, as evidenced by precordial Doppler, end-tidal carbon dioxide reduction, and oxygen desaturation. In both cases, air was aspirated from the central venous catheter; during the second episode there was arterial hypotension and electrocardiogram changes, and air bubbles were visualized in the cerebellar arteries. The patient did not regain consciousness after surgery and developed early tonic-clonic convulsions and electroencephalogram status epilepticus, which was treated with barbiturate coma. Intracardiac septal defects were not detected by transesophageal echocardiography, and computerized tomography of the brain demonstrated multifocal discrete ischemic areas in the cerebral hemispheres. The patient died 6 days after surgery without having regained consciousness. This case appears to represent the occurrence of transpulmonary passage of venous air embolism.

Peri-operative prophylaxis with phenytoin: dosage and therapeutic plasma levels.

Early postoperative epilepsy is a frequent complication of supratentorial intracranial surgery. The lack of consensus on prophylaxis of early postoperative seizures with phenytoin (PHT) may be due to the different dosages used in several studies, owing to inadequate therapeutic plasma level. The aim of this study was to evaluate which dosage of PHT can maintain the therapeutic range in the early postoperative period. Twenty patients operated on for supratentorial neoplasms were randomly allocated to receive, during the last hour of the surgical procedure, loading doses of either 10 mg/kg (group A, n = 10) or 15 mg/kg (group B, n = 10) of PHT. PHT infusion rate never exceeded 30 mg/min. Six hours after the loading dose, PHT maintenance treatment (250 mg, i.v., every 8 hours) was started in all patients. PHT plasma levels were evaluated from the end of the intra-operative loading infusion up to 24 h. During the first six hours after the loading dose, phenytoin plasma levels fell below the therapeutic range (10-20 mg/l) in 7 out of the 10 patients receiving 10 mg/kg, while in the patients treated with 15 mg/kg, PHT plasma levels were always in the therapeutic range (P < or = 0.0001). PHT maintenance dose was sufficient to keep plasma levels within the therapeutic range in 8 patients in group A, and in all the patients in group B. It is concluded that a loading dose of 15 mg/kg, followed by postoperative treatment, is necessary to guarantee therapeutic plasma levels of phenytoin in the immediate postoperative period, when seizure risk is very high.

Regional cerebral metabolism of glucose in comatose and vegetative state patients.

Regional cerebral metabolism of glucose (rCMRglu) was evaluated in patients who were in a coma and vegetative state to determine the level of brain function during these conditions. rCMRglu was measured in 17 discrete brain regions with (/-) [18F] -fluoro-2-deoxy-D-glucose (FDG) and positrn emission tomography (PET) in 15 patients with ;brain pathology subsequent to cardiorespiratory arrest (CA), head trauma (HT), or brain ischemia (BI) resulting from cerebrovascular accident or brain surgery. Five comatose patients (Coma group, n = 5), and 10 vegetative state patients (VS, patients awake but not aware) were studied. The VA patients were subdivided, according to the length of their VS condition, into a VS group (n = 6, < 3 months if CA or BI patients, or < 12 months if HT patients) and a persistent vegetative state group (PVS, n = 4, > 3 months if CA or BI patients of > 12 months if HT patients.) Ten normal age-matched subjects served as control. Global CMRglu was 6.72 +/- 0.93 (+/-SD) mg/100 g/min in control subjects. It was significantly (p < - 0.001) reduced to 3.70 +/- 61 in coma, to 3.45 +/- in VS, and to 2.33 +/- 0.34 mg/100 g/min in PVS patients. rCMRglu was significantly reduced (p < - 01001) from control values in all the 17 structures surveyed in every patient. In the Coma and VS groups, there was an overlapping of rCMRglu in the majority of the brain structures. (ABSTRACT TRUNCATED AT 250 WORDS)

[Transcranial Doppler for the monitoring of gas embolism in neurosurgical operations in the sitting position]. / Doppler transcranico per il monitoraggio dell'embolia gassosa negli interventi neurochirurgici in posizione seduta.

The risk of venous air embolism is significant in neurosurgical procedures performed in the sitting position. Monitoring for venous air embolism, therefore, is crucial and can be approached from several aspects. The most sensitive generally applicable clinical method for the detection of intracardiac gas is based on an application of the Doppler principle. The Authors describe the technique used to adapt a transcranial Doppler (TC 2-64 B, EME, Germany), and a probe designed to record the Doppler signal from intracranial arteries (Transcran FP 2, EME, Germany), as precordial Doppler in order to monitor venous air embolism in neurosurgical procedures performed in the sitting position.

[Complications during preoperative embolization in intracranial meningioma]. / Complicanza in corso di embolizzazione pre-operatoria di meningioma intracranico.

We report a rare case of meningioma of the parieto-occipital convexity accompanied by hemorrhage in the tumor and in the subdural space that occurred while pre-operative embolization was being applied. The patient, a 48 year old woman, presented sudden headache and, in a few minutes, comatose status and decerebrate rigidity. A quick diagnosis with CT-scan of acute intratumoral and subdural hemorrhage and a rapid intervention on the patient led to complete recovery. The possible reason for the hemorrhage is the sudden change in blood pressure of pathologic small vessels triggered by embolization.

[Postoperative cerebral edema. Physiopathology of the edema and medical therapy]. / Edema cerebrale post-operatorio. Fisiopatologia dell'edema e terapia medica.

Cerebral edema complicates many neurosurgical conditions, such as head injuries, neoplasms and infections, and is the direct result of operative trauma. The recognition and the treatment of brain edema are of great practical importance, particularly in those conditions leading to brain herniations and/or intracranial hypertension. Brain edema can be distinguished into two major categories, based on the integrity of the blood brain-barrier (BBB). With intact BBB edema, the crucial pathogenic event is related to disturbances of cellular metabolism and ionic transport. All the cellular elements of brain may undergo swelling, with a concomitant reduction of the extracellular-fluid space of the brain. Open BBB edema, the most common form of brain edema, is characterized by increased permeability of the brain endothelial cells. Brain edema results from the oncotic forces generated from a serum protein influx into the nervous tissue, and edema fluid accumulates primarily in the extracellular space. The non-operative management of brain edema requires attention to the causes that have induced brain edema. Specific pharmacologic therapy with corticosteroids, hyperosmolar agents and furosemide or acetazolamide depend upon accurate assessment of BBB integrity.