The scombroid poisoning is due to the ingestion of poorly preserved fish (especially tuna, sardines, and mackerel) out of the cold chain. Under the influence of the proliferation of gram negative bacteria that occurs for heating, the histidine content in the muscle of the fish is converted into histamine, by the action of the enzyme histidine decarboxylase. If the histamine is ingested in large quantities, it causes an anaphylactoid reaction with a variety of symptoms from moderate to severe to life-threating. We will describe two cases that came under our observation after consuming a meal of bluefin tuna. The diagnosis of scombroid syndrome was made on the basis of the anamnestic data and the clinical one. The rapid resolution of the signs and symptoms after treatment with histamines H1-H2 receptor blockers confirmed the suspected diagnosis.

The spider bites are quite frequent and often resolve quickly without leaving outcomes; only some species are capable of causing necrotic and systematic lesions in humans. Among them, we should mention the genus Loxosceles. The venom released from the spider bite of Loxosceles species is composed of proteins, enzymes, and nonenzymatic polypeptides. The phospholipase D family was identified as the active component of the venom. This family of enzymes is responsible for the local and systemic effects observed in loxoscelism. Phospholipases D interact with cell membranes triggering alterations which involve the complement system and activation of neutrophils and they cause the dermonecrotic skin lesions and systemic effects. We describe a fatal case of acute intoxication caused by a spider bite probably belonging to the species Loxosceles. The initial lesion was localized to a finger of a hand. Clinical course was worsening with deep necrotic lesions on limb, shock, hemolysis, acute kidney failure, and disseminated intravascular coagulation. All therapies were ineffective. This is the first fatal case described in Europe.

Traumatic rhabdomyolysis is a clinical and biological syndrome secondary to lysis of striated muscle fibers resulting in extended musculoskeletal damage. An acute muscle damage causes the release of constituent elements of the sarcoplasmic reticulum, such as muscle enzymes, potassium, and myoglobin in plasma circulation; these conditions are at great risk of dangerous systemic complications for life such as hypovolemic shock, hyperkalemia, and acute kidney injury. We describe the case of a patient who suffered a severe musculoskeletal and vascular trauma with elevated creatine kinase values and myoglobinemia treated early with coupled plasma filtration adsorption in order to prevent kidney damage, associated with volume replacement, loop diuretics, and correction of metabolic acidosis.

Drowning is an acute respiratory failure as a result from immersion or submersion of the airways in a liquid medium (predominantly water). Inhalation of water causes severe lung damage due to the destruction of pulmonary surfactant, resulting in decreased lung elasticity, alveolar collapse, alteration of ventilation-perfusion ratio, intrapulmonary blood shunting, hypoxia, acute lung injury, and Acute Respiratory Distress Syndrome (ARDS). Poractant alfa (Curosurf®), a natural surfactant effective in the treatment of newborn respiratory distress, has been used in various forms of ARDS, but in drowning syndromes, experience is still poor. We describe a series of nine clinical cases of drowning, six adults and three children, treated in our Intensive Care Unit (ICU) with endobronchial administration of poractant alfa. After 24 and 48 hours of administration in all cases, there was an improvement in arterial blood gas analysis (ABG) parameters and imaging. All patients were discharged without clinical consequences.