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Biomedical subjects

J Watkins

Publications and source records attributed to J Watkins.

At least 91 records · Page 5Linked to original sources
PubMed1989

Fatal haemopathological consequences of general anaesthesia.

A previously healthy 63-yr-old female died following an anaphylactoid response to anaesthesia with thiopentone and suxamethonium. Postmortem findings strongly suggested that disseminated intravascular coagulation played a significant role in her death. The local mechanism behind the reaction is unknown, but the formation of thiopentone-suxamethonium colloid aggregates during induction, may have led to "aggregate anaphylaxis".

Anaphylaxis↗
PubMed1989

Second report from an anaesthetic reactions advisory service.

The continued work of the advisory service is reported; this now amounts to at least 300 enquiries about clinically severe adverse reactions each year. Thiopentone is still the most commonly associated intravenous induction agent with adverse reactions (76%), particularly when it is used with suxamethonium. Local anaesthetics account for between 5 and 10% reports.

Anaphylaxis↗
PubMed1988

Anaphylactoid reaction to vecuronium followed by systemic reaction to skin testing.

An unusual case is presented of a systemic anaphylactoid reaction to tubocurarine and subsequently to vecuronium. Intradermal testing with vecuronium following the latter response was negative at recommended test dose levels but at a higher concentration it initiated a hazardous systemic response. The laboratory investigations and possible mechanisms involved in this unusual case are discussed in detail since they may relate to other patients who experience anaphylactoid responses to anaesthetic drugs and who then undergo intradermal testing.

Adult↗
PubMed1988

Anaphylactoid reaction following the use of etomidate.

A 13-year-old female suffered urticaria and severe bronchospasm sufficient to cause hypoxic cardiac arrest after intravenous induction of anaesthesia. Etomidate was strongly implicated in the reaction. The management and mechanism of the reaction are described and discussed, together with consideration of future anaesthesia in the patient.

Adolescent↗
PubMed1988

Does monotherapy of pulmonary infections in cystic fibrosis lead to early development of resistant strains of Pseudomonas aeruginosa?

We report the development of ceftazidime-resistant strains of Pseudomonas aeruginosa in a small population of cystic fibrosis patients who had ceftazidime monotherapy over a 5-year period as clinically indicated. The background rate of less than 30% of patients with a ceftazidime-resistant strain of P. aeruginosa in their sputum each month is similar to the resistance rate to other anti-pseudomonas antibiotics that have seldom been used here. In practice this resistance has meant that for about 10% of patients each month consideration has to be given to the use of an agent other than ceftazidime.

Ceftazidime↗
PubMed1988

The relevance of immunologic responses to anesthesia and surgery.

Out of some three million general anesthetic (GA) procedures administered in the UK each year some 10,000 patients will suffer clinically a severe immediate hypersensitivity-type (anaphylactoid) response: some will suffer neurological deficit, a few will die. The problems are essentially those intrinsic to all intravenous administration and infrequently drug specific. The problems of local anesthesia (LA) are fewer and reflect accident, local and regional CNS and CVS toxicity effects and, less frequently, systemic response. The relative incidence of severe LA to GA reactions reported nationwide to Sheffield lies between 5% and 10% of the total reports. In the post-operative period the dramatic changes in laboratory parameters of immunity refer largely to the stress response to surgery and probably have little relevance to post-operative infection and wound healing in elective surgery.

Anaphylaxis↗
PubMed1986

Prolonged bleeding time, reduced platelet aggregation, altered PAF-acether sensitivity and increased platelet mass are a trait of asthma and hay fever.

In a case control study 31 asymptomatic patients with asthma and/or hay fever and 31 normal controls had their bleeding time measured using the Simplate II device and venostasis. Mean bleeding time in the atopic group (527 s) was significantly prolonged compared to the controls (393 s) (p less than 0.0005). Platelet aggregation to collagen and ADP (but not to PAF-acether) was significantly depressed in the atopics. Mean circulating platelet mass was significantly greater in atopics than in the controls (p = 0.006). Stepwise multiple regression analysis showed that within the control group bleeding time was best predicted by platelet mass (p = 0.007). No such relationship was found in the atopics. However stepwise multiple regression analysis showed that bleeding time in the atopics (but not in the controls) was best predicted by PAF-acether induced platelet aggregability (p less than 0.05). In neither group was bleeding time related to collagen induced platelet thromboxane B2 production. It is hypothesised that in respiratory atopy the depressed aggregatory function of platelets is not compensated for sufficiently by an increase in platelet mass, leading to prolongation of the bleeding time. This haemostatic imbalance, whose cause remains to be established, appears to constitute a trait of atopy.

Adenosine Diphosphate↗
PubMed1986

Bronchospasm following the use of vecuronium.

A case history is presented which records bronchospasm due to vecuronium. Immunological investigations, including basophil degranulation tests, indicated that the bronchospasm was not caused by direct histamine release and was not IgE mediated. It was of interest that intradermal testing gave a positive wheal response against neuromuscular agents other than those involved in the anaesthetic procedure under investigation. A positive reaction to vecuronium was only obtained when given in a high concentration and accords with the general belief that vecuronium has extremely low potential for histamine release.

Aged↗
PubMed1986

Plasma histamine levels following atracurium.

Plasma histamine levels were determined in 41 patients, 1.5 and 4 minutes after the intravenous administration of 0.6 mg/kg of atracurium. Clinical features of histamine release were sought at the time of blood sampling. Sixteen patients had elevation of plasma histamine 2.6 (SD 1.2) ng/ml 1.5 minutes after the injection of atracurium. Plasma histamine had returned to control levels at 4 minutes. There was a poor correlation between plasma histamine levels and the clinical manifestations observed. We conclude that atracurium has a low plasma histamine release potential and that cutaneous reactions after atracurium do not always indicate that plasma histamine levels are elevated.

Adolescent↗