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Pulse oximetry is now a widely available technology that provides easy and continuous reliable measurements of oxygen saturation, the percentage of O2 bound to Hb (SpO2). Pulse oximetry has become a standard monitoring not only in intensive care, but also in other clinical settings, although several factors can interfere with a correct reading, as low perfusion conditions, such as low cardiac output, vasoconstriction, hypothermia. We performed a prospective observational study in two groups of twenty-eight patients admitted to the ICU, in which we compared the values ​​obtained (SpO2) with digital and forehead pulse oximetry, with arterial oxygen saturation (SaO2) obtained from blood gas analysis (EGA). Comparison measurements into two distinct groups, though homogeneous might be a limitation of the study, but at the same time provide a representative picture of a polyvalent intensive care unit. The result was that both the values ​​obtained with digital and frontal pulse oximetry are accurate and reliable in comparison to EGA. In situations of hypoxia, the reliability of frontal pulse oximetry appears superior compared to digital oximetry.

This case report has the scope to review the etiology and pathophysiology of pneumomediastinum in severe blunt trauma, with a special interest to its more frequent origin: the Macklin effect. The Macklin effect is a pathophysiologic process characterized by the blunt traumatic alveolar ruptures, air dissection along bronchovascular sheaths, with the formation of blunt pulmonary interstitial emphysema, radiologic marker, until the formation of a pneumomediastinum. Its premature diagnostic acknowledgment is important in the managing of the blunt chest trauma.

The aim of the paper was to describe an unusual case of non lactic metabolic acidosis connected to hypophosphatemia and refractory to infusion of bicarbonate. A 37 year old man was admitted to Intensive Care Unit with a severe metabolic acidosis. On admission the arterial gas analysis showed non lactic metabolic acidosis (pH 7.17; base excess [BE] -20.3; lactic acid 0.8 mMol/L), with hypoxemia and critical hypocapnia. Despite therapy with bicarbonate the acidosis persisted. After 4 hours glucose phosphate was administered, although the phosphoremia was unknown. After phosphate supplementation an improvement of acidosis was observed. Our hypothesis is that in the kidney phosphate depletion caused impaired tubular reabsorption of bicarbonate, which led to a non lactic metabolic acidosis.

Rhabdomyolysis is a disorder characterized by skeletal muscle injury and fatal complications at times. The causes of rhabdomyolysis are usually traumatic and non-traumatic, such as neuroleptic malignant syndrome and rhabdomyolysis associated to septicemia. The cases of 2 schizophrenic patients with rhabdomyolisis during pneumonia infection and neuroleptic therapy are reported. At admission, both patients had important respiratory distress and hyperthermia; the clinical conditions required endotracheal intubation. Blood and urine cultures were always negative, while the bronchial sputum culture was positive. The diagnosis of rhabdomyolysis was confirmed by myoglobinemia dosage and ortholuidine test. Pneumonia infection was treated with antibiotic specific therapy whereas renal failure was treated with adequate hydratation and strained diuresis. The absence of muscle rigidity, the improvement of X-r images and the reduction of corporeal temperature, during antibiotic treatment, excluded neuroleptic malignant syndrome. The impro-vement allowed extubation and discharge of the patients from intensive care unit. In both cases neuroleptic malignant syndrome was excluded, therefore rhabdomyolysis was the consequence of pneumonia infection or of a combination of factors capable to cause an important damage of skeletal muscles.