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At least 919 records · Page 51Linked to original sources
PubMed1978

Lung injury following a 50-metre fall into water.

The pulmonary complications of a 50-metre fall to the water (a form of suicide attempt producing 87% mortality) were studied in 15 survivors. Presenting findings included crackles, haemoptysis, and hypotension. The alveolar-arterial oxygen difference was greater than 150 mmHg (20 kPa) in nine subjects on admission. Ventilatory failure developed in 10 of the patients, including all of those with massive haemoptysis. Radiographic findings included pneumothorax and diffuse pulmonary opacities adjacent to the area of impact. Pneumothorax developed within 12 hours of admission in 10 of 15 subjects but was associated with rib fractures in only four subjects. The clinical course of the condition is consistent with the hypothesis that the traumatic pulmonary tears produced interstitial emphysema, with subsequent development of pneumomediastinum, subcutaneous emphysema, and pneumothorax. Pneumothorax is a common complication of severe lung contusion even in the absence of penetrating pleural injury.

Adult↗
PubMed1983

Gardner-Diamond syndrome.

The case of a patient suffering from Gardner-Diamond syndrome is described. Owing to the uncertain etiology, we suggest that the functional platelet defect found may intervene, maintaining and making the ecchymotic lesions worse.

Adult↗
PubMed1979

Skin petechiae and ecchymoses (vasculitis) due to anticoagulant therapy.

The appearance of petechiae and ecchymoses following anticoagulant and fibrinolytic therapy is an unusual and rare complication. The mechanism of the vasculitis is obscure but may be related to a chemical vasotoxic reaction. During anticoagulant and fibrinolytic therapy, 6 patients developed petechiae and ecchymoses which was accompanied by pain and fever. There were no disturbances of blood clotting factors. In spite of the varied action of the different anticoagulants and fibrinolytic drugs, the clinical course and the histological examination demonstrated a similar identical vasculitis.

Aged↗
PubMed2001

A family with complement factor D deficiency.

A complement factor D deficiency was found in a young woman who had experienced a serious Neisseria meningitidis infection, in a deceased family member with a history of meningitis, and in three relatives without a history of serious infections. The patient and these three relatives showed a normal activity of the classical complement pathway, but a very low activity of the alternative complement pathway and a very low capacity to opsonize Escherichia coli and N. meningitidis (isolated from the patient) for phagocytosis by normal human neutrophils. The alternative pathway-dependent hemolytic activity and the opsonizing capacity of these sera were restored by addition of purified factor D. The family had a high degree of consanguinity, and several other family members exhibited decreased levels of factor D. The gene encoding factor D was found to contain a point mutation that changed the TCG codon for serine 42 into a TAG stop codon. This mutation was found in both alleles of the five completely factor D-deficient family members and in one allele of 21 other members of the same family who had decreased or low-normal factor D levels in their serum. The gene sequence of the signal peptide of human factor D was also identified. Our report is the first, to our knowledge, to document a Factor D gene mutation. The mode of inheritance of factor D deficiency is autosomal recessive, in accordance with the localization of the Factor D gene on chromosome 19. Increased susceptibility for infections in individuals with a partial factor D deficiency is unlikely.

Adult↗