Search PubMed⌕ Search

Biomedical subjects

R A Chase

Publications and source records attributed to R A Chase.

At least 37 records · Page 2Linked to original sources
PubMed1981

Disturbances of lactate metabolism in patients with liver damage due to paracetamol overdose.

Six patients with liver damage following paracetamol overdose, one patient with viral hepatitis and six control subjects were infused with sodium L(+) lactate. In controls the results were analysed using a single compartment model while in paracetamol patients a two compartment system was used to derive the fractional rate removal constant and lactate distribution volume. Forearm arterio-venous differences of lactate were also determined in order to assess the role of voluntary muscle in removal of a lactate load. In paracetamol patients with fractional rate removal constant was decreased to less than half the control value (P less than 0.001) while total distribution volume was similar to the two groups. Fasting lactate concentrations were significantly increased in paracetamol patients due to diminished lactate removal since the endogenous production rate of lactate was not significantly different from controls. A greater proportion of the lactate load was removed in voluntary muscle in paracetamol patients (39%) than controls (17%). Since the balance of lactate removal occurs principally in the liver, the decrease in the fractional rate removal constant in patients following paracetamol overdose indicates a severe derangement of hepatic lactate metabolism with a compensatory increase in lactate metabolism in voluntary muscle.

Acetaminophen↗
PubMed1981

The gut hormone profile of fulminant hepatic failure.

Twenty-five patients with fulminant hepatic failure and grade III or IV hepatic encephalopathy were studied. Plasma insulin, glucagon, pancreatic polypeptide and enteroglucagon were significantly raised. Levels of secretin and gastrin were normal, while motilin concentrations were significantly depressed. Vasoactive intestinal polypeptide was increased in six patients and was significantly higher in those patients who were hypotensive or who had marked prolongation of prothrombin time.

Acute Kidney Injury↗
PubMed1980

The treatment of contractures of the hand using self-hypnosis.

The successful treatment of a man with severe posttraumatic contractures of the hand using a combined psychological and physical rehabilitation approach is reported. The contractures had functional and organic components, as did the treatment, which involved teaching the patient self-hypnosis exercises and the use of a splint. The patient obtained virtually complete return of movement after 3 1/2 years of total disability. The importance of identifying and mobilizing rather than challenging the patient's motivation for recovery using a rehabilitation approach is discussed. Hypnosis can facilitate recovery in such psychosomatic disorders in patients with the requisite hypnotic capacity and motivation.

Adult↗
PubMed1980

A dynamic myocutaneous flap for hand reconstruction.

Relocation of functional units by neurovascular pedicle transfer is firmly established in reconstructive hand surgery. Transfer of muscle and overlying skin, the myocutaneous flap, to provide skin cover is equally established. The dynamic myocutaneous flap is an extension of these concepts. Injection studies confirmed that the abductor digiti quinti muscle and its overlying hypothenar skin could be transferred on its neurovascular bundle. This dynamic myocutaneous flap was used to reconstruct both skin cover and functional opposition following resection of an arteriovenous malformation involving the thumb. Other clinical applications would include reconstruction of thenar skin and muscle lost secondary to electrical burns, avulsion, or tumor resection.

Adult↗
PubMed1980

Forearm glucose uptake in cirrhosis and its relationship to glucose tolerance.

1. Oral glucose-tolerance tests (100 g) were carried out in six patients with stable well-compensated cryptogenic cirrhosis and in 12 control subjects. 2. In confirmation of previous studies, patients with cirrhosis had high post-glucose serum insulin levels and were glucose intolerant (mean incremental glucose area 954 +/- 186 compared with 482 +/- 35 mmol 3 h-1 l-1 in controls; P < 0.05). 3. Forearm arteriovenous differences of glucose and forearm blood flow were measured to estimate the proportion of the glucose load metabolized in peripheral tissues. Values in cirrhotic patients and control subjects (5614 +/- 1630 compared with 5344 +/- 672 mumol of glucose min-1 l-1 of forearm in 3 h) were similar despite higher glucose levels and sustained high insulin levels in the cirrhotic patients. 4. Peak lactate concentrations after glucose were of similar magnitude in the two groups (0.66 +/- 0.12 compared with 0.62 +/- 0.75 mmol/l) but in the patients with cirrhosis the peak occurred later and was more sustained. 5. The glucose intolerance of cirrhosis is primarily due to impaired hepatic retention of the glucose load. Insulin resistance in peripheral tissues may also be important since the higher insulin concentrations found in cirrhotic patients failed to enhance peripheral glucose uptake.

Adult↗
PubMed1979

Intracranial pressure in pigs with surgically induced acute liver failure.

Cerebral edema has now been noted to occur frequently in patients dying of fulminant hepatic failure. In the present study, intracranial pressure was monitored in an animal model of acute liver failure. Acute liver failure was induced surgically by hepatic devascularization. Serial monitoring of the electroencephalogram revealed progressive slowing of the frequency with decreasing amplitude. Elevation of the blood ammonia was also observed from baseline values of 64 +/- 12 SE to 744 +/- 97 mumol/liter. Monitoring of the intracranial pressure with a subdural pressure transducer demonstrated a progressive and reproducible rise from 12.8 +/- 2.5 mm Hg immediately after the operation to a mean value of 51.6 +/- 11.8 mm Hg just before death 6--12 hr later. At autopsy, the brains of the test animals were found to be swollen with flattened cortical gyri. In the control animals, intracranial pressure rose slightly but returned toward normal levels (8.0 +/- 2.5 mm Hg) 8 hr after laparotomy and remained normal until their death. There was a statistically significant difference between intracranial pressure levels of the test animals and those of the controls (P less than 0.01). Intravenous methylprednisolone (2.0 g initially followed by 0.5 g every 2 hr) administered immediately before and after hepatic devascularization prevented rises in intracranial pressure but had no effect when given 4 hr after operation. The early and progressive increase in intracranial pressure was an unexpected finding, and an assessment of such a sequence in patients with fulminant hepatic failure is currently in progress.

Animals↗
PubMed1977

Treatment of fulminant hepatic failure by polyacrylonitrile-membrane haemodialysis.

24 patients with fulminant hepatic failure who had deteriorated to grade-IV coma were treated by repeated periods of haemodialysis with a polyacrylonitrile membrane. 9 patients fully recovered consciousness, and 8 (33%) survived to leave hospitals. These results are to be compared with those of conservative management alone (15% survival in 53 cases) and those obtained initially with charcoal haemo-perfusion (38%). Of the 16 treatment failures, cerebral oedema was found at necropsy in 13 (18%). Whether this would have been less of problem if treatment had been started earlier in the course of the illness remains to be determined.

Acrylonitrile↗
PubMed1977

Reexamination/recertification: measurement of professional competence and relation to quality of medical care.

Over the past half decade, there has been an increment in forces moving the profession toward recertification and a decrement in the restraining forces. The whole process will be catalyzed by available funding through grants to implement continuing medical education, development of performance-, and competency-based assessment measures and recertification. Specialty boards serving relatively small numbers of candidates have serious difficulty funding certification, to say nothing of recertification. An adequate mechanism to implement recertification can emerge only from the profession itself, working through the American Board of Medical Specialties and specialty boards. The means to discharge this responsibility should, at the outset, come from public and private sources. Eventually the system may become self-supporting through evaluation and certification fees. The public interest will be best served when there are adequate mechanisms to assess continuing competence of all physicians. As a minimum, there must be a system to guard against incompetence through obsolescence of any of the practicing professionals.

Certification↗
PubMed1977

The role of the false neurotransmitter octopamine in the hypotension of fulminant hepatic failure.

1. An investigation was carried out into the mechanism of unexplained hypotension in patients with fulminant hepatic failure. The cardiac output and peripheral resistance were compared in normotensive and hypotensive patients. In addition, the serum concentration of the false neurotransmitter octopamine and the pressor response to noradrenaline, and to the indirectly acting sympathomimetic agent tyramine, were measured in hypotensive and normotensive patients with fulminant hepatic failure and in healthy subjects. 2. The cardiac output and the peripheral resistance were decreased in the hypotensive patients, and their mean heart rate was slower than in the normotensive patients. Although the serum octopamine concentration was significantly elevated in the patients compared with the control subjects, the highest octopamine concentrations were unexpectedly found in the normotensive patients and a significant positive correlation could be demonstrated between the resting blood pressure and the serum octopamine concentration. The pressor response to tyramine and noradrenaline were similar in the hypotensive patients, the normotensive patients and control subjects. 3. These results suggest that neither increased serum concentrations of the false neurotransmitter octopamine, nor end-organ insensitivity to released noradrenaline are responsible for the hypotension. A more likely explanation is toxic depression of the vasomotor centre. The opening of peripheral arteriovenous shunts, possibly as a result of endotoxaemia, might be an additional factor.

Cardiac Output↗