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Biomedical subjects

I M Ledingham

Publications and source records attributed to I M Ledingham.

At least 19 recordsLinked to original sources
PubMed1979

Dural dimpling in the dog.

Indentation of the dura has been proposed as the cause of subatmospheric pressure in the extradural space, but has never been demonstrated directly in humans. In this study, radiographs have been produced showing dimpling of the dura by a needle tip lying in the extradural space in the dog. Pressure tracings demonstrate that advancement of the needle tip produces a progressive decrease in extradural pressure, and observations made using an image intensifier have confirmed that the pressure changes are proportional to the degree of dural indentation.

Anesthesia, Epidural↗
PubMed1978

Prospective study of the treatment of septic shock.

A study of 113 patients with septic shock admitted to an intensive therapy unit (I.T.U.) during a 3-year period showed that a significant reduction in mortality was achieved after the introduction of a treatment programme which included early intermittent positive-pressure ventilation and aggressive surgery in addition to conventional management with fluids, oxygen, and antibiotics. Vasoactive drugs played an important but not essential role in therapy.

Adult↗
PubMed1978

Movement of the critically ill within hospital.

Critically ill patients can be safely moved within hospital using a mobile intensive care unit (MICU). The MICU allows the critically ill to benefit from specialised investigation and treatment they might otherwise be denied. The MICU in use at the Western Infirmary, Glasgow is described and its merits outline in the light of clinical experience gained over a twelve month period.

Adult↗
PubMed1978

Shock.

Explore the source record for details and available documents.

Blood Vessels↗
PubMed1977

The pulmonary manifestations of septic shock.

Septic shock carries a high mortality. It is manifest haematologically by thromobocytopaenia and other coagulation disturbances. The radiological manifestations are various degrees of pulmonary oedema, usually affecting the lower zones, without evidence of pulmonary hypertension. Radiological signs are always preceded on accompanied by thrombocytopaenia.

Adult↗
PubMed1977

Necrotizing fasciitis.

The author's experience of fourteen patients with necrotizing fasciitis is reviewed. The pathognomonic feature of this condition is an extensive necrosis of subcutaneous tissue caused by a vicious cycle of infection, local ischaemia and reduced host defence mechanisms. The diagnosis can only be confirmed by immediate exploratory incision. The reported mortality of 30-40% reflects the inadaquacy of conservative surgery in the treatment of this serious condition. Mortality can be reduced by early recognition followed by radical excision of the necrotic fascia and overlying skin. The preservation and subsequent use of the excised skin has the advantage of economy in the use of donor areas and reduction in morbidity. Hyperbaric oxygen therapy does not halt the spread of the necrotizing process and is not a substitute for radical surgery.

Bacterial Infections↗
PubMed1977

Effect of angiotensin-converting enzyme inhibitor (SQ 20881) on the plasma concentration of angiotensin I, angiotensin II, and arginine vasopressin in the dog during hemorrhagic shock.

The effect of an angiotensin-converting enzyme inhibitor on the circulating levels of angiotensin I, angiotensin II, and arginine vasopressin was studied in dogs subjected to hypotensive hemorrhagic shock. In dogs subjected to hemorrhage but not given the inhibitor, angiotensin II rose 20-fold (from 69 to 1,343 pg/ml of plasma), whereas in dogs subjected to hemorrhage but pretreated with the inhibitor, angiotensin II rose only 2-fold (from 92 to 171 pg/ml of plasma). In the pretreated dogs angiotensin I rose 30-fold (from 108 to 3,232 pg/ml of plasma). There was no statistically significant difference between the vasopressin levels found in the untreated dogs and the levels found in dogs given the inhibitor (1,016 and 1,095 pg/ml of plasma). Of the 15 dogs in the untreated group, five died before retransfusion was completed (four of cardiac failure and one of cardiac arrhythmia); none of the 10 dogs in the inhibitor-treated group died. These observations suggest that the very high levels of angiotensin II observed following severe hemorrhage do not contribute significantly to the increased secretion of vasopressin and that the inhibitor protects against death, possibly by suppressing the very high blood levels of angiotensin II observed following this type of experimental hemorrhagic shock.

Angiotensin II↗
PubMed1976

Heart failure in experimental refractory shock.

Severe haemorrhagic shock was studied in a series of animal experiments. Reduction in myocardial oxygen and substrate utilisation in association with cardiac failure was demonstrated when the duration of shock was prolonged. The probable aetiological factors included ischaemia and the presence in the blood of certain vasoactive and metabolic depressant substances. It was concluded that the process leading to irreversible shock was multi-factorial in origin but failure appeared to play an important role.

Angiotensin II↗