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Biomedical subjects

P Feiss

Publications and source records attributed to P Feiss.

At least 91 records · Page 5Linked to original sources
PubMed1983

[Prolonged brachial plexus block with bupivacaine].

A prolonged brachial plexus block with bupivacaine hydrochloride is described. Anaesthesia was induced with 40 ml of a solution made of equal parts of 0.50% bupivacaine hydrochloride and distilled water. Reversal of the motor block began 24 h later. Total recovery was observed 30 h after the onset of anaesthesia. Neurotoxicity of bupivacaine hydrochloride was known to be weak and could not explain the increased length of the block. The dilution of 0.50% bupivacaine hydrochloride resulted in a very low osmolality (141 mosm X kg-1 vs 242 mosm X kg-1 for 0.25% bupivacaine hydrochloride commercial solution). Whether this low osmolality caused nerve lesions was unknown. Postoperative exploration revealed a bilateral slowing down of conduction in the brachial plexus of this 73 year old patient. The importance of this finding could not be assessed.

Aged↗
PubMed1978

[Acute renal insufficiency caused by phenyl-indane-dione. Apropos of 1 case].

One case of Phenindione (PID) adverse reaction is reported. The patient showed a typical picture of immunological reaction to the drug. In spite of severe bacteremia, she recovered. Only 33 cases of PID intolerance are reported in the literature. In all these patients, renal failure occurred. Superinfection is the most frequent cause of death. PID adverse reaction should be evoqued in the presence of signs such a fever, asthenia, anorexia and cutaneous reaction. The PID should be stopped immediatly but renal failure yet develops. During a PID treatment, frequent evaluation of blood azotemia, creatinine and proteinuria should be performed.

Acute Kidney Injury↗
PubMed1976

[Case of giant intra-petrous and intra-cavernous internal carotid aneurysm in a child].

The authors report the case of an eight-year-old girl hospitalised for severe headache with paroxysmal left otalgia, vomiting, aprexia, paralysis of the left 6 th cranial nerve and slight left facial weakness. Left carotid arteriography revealed a very large aneurysm of the internal carotid, involving its entire intra-petrous and intra-cavernous course. Treatment consisted of ligation of the internal carotid in the neck. Postoperative angiographic studies showed complete exclusion of the aneurysm, and it was unecessary to carry out "trapping" by ligation of the supra-cavernous carotid, as had initially been envisaged. The postoperative course was uneventful : immediate disappearance of otalgia, secondary complete recovery of the oculo-motor involvement and facial paresis. The absence of any infections or traumatic past history, together with the young age of the patient, represent arguments in favour of the congenital origin of this intra-petrous carotid aneurysm.

Carotid Artery, Internal↗
PubMed1976

[Desquamative interstitial pneumonia (apropos of one case)].

Suspected to be a syndrome rather than an authentic clinical entity, the "desquamative interstitial pneumonia" (DIP) exhibits typical anatomo-pathological aspects of intra-alveolar proliferation of granular pneumocytes, type II pneumocytes, leaving the alveolar interstitium unaffected. In absence of superinfection, it remains almost free of fibrous or inflammatory manifestations. The association of DIP to 4 other fundamental histological varieties of diseases of the pulmonary interstitium (UIP, BIP, LIP, GIP) is at the origin of Liebow's classification. The clinical individualization of these entities is still questioned.

Adrenal Cortex Hormones↗
PubMed1975

[Pulmonary edemas. Classification and mechanisms].

Water exchanges in the lung under physiological conditions, are still badly known. Starling's classical equation is a too simplified view of the phenomenon. In addition, a certain number of its factors are badly determined. Such is the case with the hydrostatic pressure and the oncotic pressure of the interstitium. In pathological conditions secondary edema is opposed to lesions of the alveolocapillary membrane and hemodynamic edema where the increase in intravascular pressure increases a loss of liquid between the junctions of the endothelial cells. Between these two situations there are edemas, of which the mechanism is still subject to discussion, for example altitude edema, edema in heroin addicts, neurogenic edema.

Humans↗
PubMed1975

[Reduction and anti-inflammatory technics in non-hemodynamic pulmonary edemas].

All hypervolemia or any decrease in plasma oncotic pressure leads to deterioration in lesional pulmonary edema. The aim of albumin infusions is to restore the plasma oncotic pressure and to oppose the passage of water into the extravascular space. This therapy is however debatable owing to the abnormal increase in the permeability of the alveolo-capillary membrane to proteins. Diuretics enable one to lower the volemia and to maintain the pulmonary capillary pressure at its minimum level. However, strict hemodynamic supervision is absolutely necessary. Cortico-steroids have been recommended without serious physiopathological justification. However, they have a preventive action on interstitial edema in endotoxic shock.

Adrenal Cortex Hormones↗