A Fatal Case of Septic Shock Secondary to Acinetobacter Bacteremia Acquired from a Platelet Transfusion.

BACKGROUND: Transfusion of blood products is a frequent and often necessary lifesaving intervention. While changes to blood bank practices over the past several decades have reduced the infectious complications associated with transfusions, risks still exist. Septic transfusion reactions caused by bacterial contamination of blood products, especially platelets, still occur relatively frequently. Unfortunately, clinical recognition of septic transfusion reactions is difficult due to significant symptom, exam, and laboratory abnormality overlap between different types of transfusion reactions, as well as other conditions. Novel methods have been developed to detect blood product contamination but have yet to be widely implemented in the United States. CASE REPORT: A 67-year-old male with chronic thrombocytopenia was transfused with platelets prior to a planned procedure. Shortly afterwards, he developed fever and hypotension. He was transferred to the intensive care unit where he was treated with aggressive fluid resuscitation and broad-spectrum antibiotics. The patient went on to develop progressively worsening shock and profound disseminated intravascular coagulation. Blood cultures from the patient and the transfused platelets grew an Acinetobacter species. Despite aggressive resuscitative efforts and appropriate antibiotics, the patient died approximately 48 hours following the transfusion reaction. CONCLUSION: We report a fatal case of septic shock associated with Acinetobacter bacteremia caused by platelet transfusion. Our review of the literature revealed only one other documented platelet transfusion associated fatality caused by Acinetobacter species. Novel pathogen reduction and contamination detection methods have been developed but have yet to be widely adopted in the United States.

[Morphological signs of mitochondrial cytopathy in skeletal muscles and micro-vessel walls in a patient with cerebral artery dissection associated with MELAS syndrome].

Skin and muscles biopsy specimens of a patient harboring A3243G mutation in mitochondrial DNA, with dissection of internal carotid and vertebral arteries, associated with MELAS were studied using histochemical and electron-microscopy techniques. Ragged red fibers, regional variability of SDH histochemical reaction, two types of morphologically atypical mitochondria and their aggregation were found in muscle. There was correlation between SDH histochemical staining and number of mitochondria revealed by electron microscopy in muscle tissue. Similar mitochondrial abnormality, their distribution and cell lesions followed by extra-cellular matrix mineralization were found in the blood vessel walls. In line with generalization of cytopathy process caused by gene mutation it can be supposed that changes found in skin and muscle microvessels also exist in large cerebral vessels causing the vessel wall "weakness", predisposing them to dissection.

[Ultrastructural changes of skin arteries in patients with spontaneous cerebral artery dissection].

Spontaneous cerebral artery dissection is a common cause of ischemic stroke in young adults and children. Dissection is often related to arterial wall weakness the cause of which is unknown. An aim of the present paper was to carry out an electron microscopic study of skin arteries and arterioles in patients with ischemic stroke caused by cerebral artery dissection. Skin biopsy samples from 3 patients (2 men and one women, 15, 25 and 43 years of age, respectively) were studied. Electron microscopy revealed changes of endothelial, smooth muscle cells and fibroblasts in the skin microvessels. These changes included the decrease in the number of mitochondria and their alterations (vacuolization, destruction of the cristae, the presence of the needle-shaped crystals and crystal-like inclusions) and swelling of the endoplasmic reticulum. Some of these changes were characteristic of mitochondrial diseases. The changes in the extracellular matrix (thickening of the subendothelial layer and deposition of microcalcificats) were also detected. It is assumed that the mitochondrial cytopathy found in the skin microvessels may be also present in large cerebral arteries. This could underlie dysplastic changes in the cerebral artery wall and predispose to its dissection.

[Mitochondrial arteriopathy as a cause of spontaneous dissection of cerebral arteries].

The vascular wall weakness caused by dysplastic alterations predisposes to the spontaneous dissection of cerebral arteries. The authors hypothesized for the first time that dysplasia might be the result of mitochondrial cytopathy. To test this hypothesis, the muscle biopsy was conducted in 3 male patients, aged 30-38 years, with the spontaneous dissection of the internal carotid (2) and posterior cerebral (1) arteries. Clinically dissections manifested by ischemic stroke (2) or the peripheral paresis of the hypoglossal nerve (1). The morphological study of fresh frozen sections of muscle by modified Gomori trichrome method revealed ragged-red fibers The histochemical study showed the severe decrease of the stain on succinate dehydrogenase and cytochrome-c-oxidase as well as the focal intensive staining of peripheral regions of muscle fibers. The complex of found changes is characteristic for a mitochondrial pathology. No patients had A3243G tRNA gene mutation, the most common mutation for MELAS. The serum lactate level was elevated only in one patient. We suggest that the mitochondrial disorder occurs not only in muscle, but also in cerebral artery wall--mitochondrial arteriopathy, which predisposes to spontaneous cerebral artery dissection.