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Objectives: To evaluate the practical utility of the PiCCO system for monitoring cardiac output and its derived variables during lung resection surgery., Patients and Methods: Patients scheduled for lung resection surgery were enrolled. After anesthesia had been induced, a Pulsiocath catheter was placed in the femoral artery ipsilateral to the thoracotomy. The following parameters were evaluated: ease of placement of the arterial catheter, functioning of the system, and appearance of complications. When the catheter was connected to the PiCCO monitor, cardiac output and derived variables were recorded throughout the procedure., Results: Fifteen patients were enrolled in the study. Placement of the catheter in the femoral artery was easy in 9 cases (60%), difficult in 4 cases (27%), and impossible in 2 cases (13%). The catheter functioned correctly in 7 patients but problems developed in 6 patients (2 cases of a poor-quality pressure curve, 1 case of a discrepancy of more than 20% in comparison with blood pressure, and 3 cases of impossibility of extracting blood samples through the arterial catheter because the patients were in a lateral decubitus position). No complications relating to arterial puncture were observed. Hemodynamic monitoring showed increased cardiac output after surgery., Conclusions: The results suggest that using the PiCCO system during lung resection surgery is of limited utility, given that problems developed in relation to 53% of the catheters. This makes the technique unreliable in the event of its being required.

Purpura fulminans is a serious disease associated with high rates of morbidity and mortality. It usually leads to disseminated intravascular coagulation and septic shock related to reduced levels of protein C. Recombinant protein C (rPC) activator has been used successfully to inhibit this process. Intracranial hemorrhages are the most important, life-threatening adverse effects of treatment with rPC activator. We report 3 cases of patients with meningococcal purpura fulminans who developed septic shock and multiorgan dysfunction. They were treated with the protocol for septic shock, antibiotics and rPC activator from the time of admission, and improvement in hemodynamic dysfunction was observed within hours in all patients. All received platelet replacement transfusions. Subarachnoid bleeding complications occurred in 2 patients. One patient died 5 days after admission and 2 were discharged from the intensive recovery care unit 28 days after admission.

A 69-year-old man with no remarkable medical history was admitted to the intensive care unit in septic shock due to severe community-acquired pneumonia. Twelve hours later he developed electrocardiographic abnormalities with ST elevation in leads II, III, aVF, V5, and V6 in the absence of chest pain and the presence of dyspnea, agitation, and hypertension. Serial measurements of cardiac enzymes were also elevated. Acute coronary syndrome was suspected. A cardiac ultrasound revealed left ventricular dilation with akinesia and systolic dysfunction (ejection fraction, 40%). Emergency catheterization revealed normal coronary arteries, suggesting a probable diagnosis of acute myocarditis. From the fourth day, the patient was progressing favorably. Findings in a follow-up ultrasound were consistent with the onset of dilated myocardiopathy, and angiotensin converting enzyme inhibitors were prescribed. All serology and microbiological studies were negative. Fifteen days after admission the patient was discharged to home after clinical, radiologic and analytic recovery.

A 64-year-old woman came to the emergency room complaining of vomiting and abdominal pain; appendicitis was suspected and surgery ordered. A blood work up showed a significantly low platelet count (39,000/microliter) and 6 units were transfused before surgery. The only observations during surgery were ileitis and Meckel's diverticulum. Thrombocytopenia persisted over the first 48 hours after surgery in spite of another transfusion of platelets, with worsening awareness and acute renal failure. After diagnosis of thrombotic thrombocytopenic purpura (TTP), the patient was admitted to the intensive care unit and treatment with fresh plasma and corticoids was started. Two weeks later, after complex evolution and ten sessions of plasmapheresis, the patient was transferred to the hematology ward. TTP must be considered a medical emergency. Platelet transfusions are contraindicated, as they can cause serious clinical deterioration. A low platelet count before surgery should lead to differential diagnosis to determine the cause, with the aim of judging whether platelet transfusion is warranted or not. In some etiological processes, such as in the case we report, platelet transfusion may be life-threatening; corrective measures must be taken early in the process and such transfusion avoided.

Objectives: a) To study the binding of propofol to proteins in plasma samples from healthy volunteers and in solutions of albumin and alpha 1-acid glycoprotein (AGA); b) to describe the nature of the bond and possible interactions with other substances that are potential displacers: salicylate, phenylbutazone, sulfisoxazole, tolbutamide, sodium valproate, sodium oleate and penbutolol; c) to assess the effect of propofol on the binding of specific markers and possible binding sites in the following proteins: 14C-warfarin, 3H-diazepam, 3H-midazolam, 3H-imidazole, 3H-penbutolol and 3H-morphine., Material and Methods: The free fraction was obtained in all samples by ultrafiltration and measurement of the free concentration of propofol by liquid chromatography and of the markers by scintillation spectrometry., Results: The free fraction of propofol in plasma was 0.98 +/- 0.12% and binding was not saturable. Albumin seems to play an important role (95% bound), whereas the participation of AGA was low (54% bound). Propofol did not affect the binding of any of the markers studied. Nor did the presence of other drugs at therapeutic plasma concentrations affect the binding of propofol., Conclusions: The binding of propofol to plasma proteins seems unlikely to cause drug interactions in clinical practice.