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Biomedical subjects

P R Black

Publications and source records attributed to P R Black.

At least 19 recordsLinked to original sources
PubMed2000

The Viladot implant in flatfooted children.

In 1991, Viladot described an implant for the treatment of painless flatfeet in children. This was inserted through a double approach to allow the talus to function while limiting its ability to slide off the calcaneus. The wineglass shaped prosthesis was inserted into the sinus tarsi with a tibialis posterior advancement and soft tissue correction to allow the foot to adopt a neutral position. This is in keeping with other procedures described for the correction of flatfoot. Viladot reported excellent results in 234 feet operated on in such a manner using clinical, radiological and photopodographic parameters. In Sheffield, over three years, 22 implants were inserted for similar painless flatfeet in children. The results were assessed using clinical, radiological and pedobarographic parameters. Viladot was able to demonstrate an improvement in all cases, clinically, radiologically and photopodographically with little or no discomfort and a return to preoperative levels of activity including sport. We found that in all cases, postoperative pain was a major feature which limited activity in all but 2 feet and which reduced the ability to take part in sport and other preoperative pastimes. Unlike Viladot, we were unable to demonstrate consistent improvements radiologically. Pedobarographically, the loading of the first metatarsal head remained unchanged and the centre of pressure was corrected in only 14%.

Adolescent↗
PubMed1997

Acute carpal tunnel syndrome as a complication of oral anticoagulant therapy.

Acute carpal tunnel syndrome is well recognized in patients with haemophilia and conservative management with factor replacement and temporary splinting is recommended. There have, however, been very few reported cases of acute carpal tunnel syndrome as a complication of oral anticoagulant therapy. We describe such a case in a patient on long-term warfarin anticoagulation, drawing attention to particular features of the history and clinical findings. In contrast to previous reports, we recommend prompt decompression under local anaesthesia and continuation of the anticoagulant therapy.

Anticoagulants↗
PubMed1994

Mesenteric defects as a cause of intestinal volvulus without malrotation and as the possible primary etiology of intestinal atresia.

Mesenteric defects can lead to intestinal volvulus even when the midgut is normally rotated. There are two types of mesenteric defects: basilar, in which the entire base of the mesentery is involved, and segmental, in which only an isolated portion of the mesentery is affected. These defects can present at any age, and the clinical symptoms depend on the extent of the disease and the amount of intestine involved in the volvulus. In the newborn, the basilar defects have clinical signs and symptoms similar to those of midgut volvulus secondary to malrotation. Similar to midgut volvulus secondary to malrotation, this is a surgical emergency. In older patients, basilar defects can be misdiagnosed because of the normal placement of the ligament of Treitz and because of failure to consider mesenteric defects as a possible cause. The treatment for basilar mesenteric defects is intestinal fixation. Intestinal volvulus secondary to segmental defects always presents as intestinal obstruction. In the newborn, these lesions may be indistinguishable from intestinal atresia. Older children present with intestinal obstruction of an unknown cause. Resection of the affected intestine is the treatment for segmental mesenteric defects. Intestinal mesenteric abnormalities as a cause of intestinal atresia unifies under one etiology all the lesions observed in intestinal atresia. Although this theory does not rule out other causes of intestinal atresia, intestinal mesenteric defects may be the primary condition under which intestinal atresia occurs.

Child↗
PubMed1993

An association of pulmonary hypoplasia with unilateral agenesis of the diaphragm.

During a period of 5 years, 33 newborns with congenital diaphragmatic hernia were treated. Three groups presenting with respiratory distress in the delivery room were identified. These included 8 newborns with agenesis (group 1) and 4 newborns with nonagenesis (group 2), all of whom died. There were 19 nonagenesis survivors (group 3), giving an overall survival rate of 61%. Two newborns who presented beyond 6 hours of life were excluded. No one specific arterial blood gas value or ventilation parameter obtained preoperatively could predict survival. Postmortem right and left lung weights, lung/body weight ratio, and radial alveolar counts demonstrate that agenesis is a unique subgroup with profound pulmonary hypoplasia and a dismal prognosis.

Diaphragm↗
PubMed1990

Adenosine reversal of in vivo hepatic responsiveness to insulin.

Modulation by adenosine of hepatic responsiveness to insulin was investigated in vivo in 10 healthy mongrel dogs of both sexes by determining net hepatic glucose output (NHGO) in response to insulin during the presence or absence of exogenous adenosine infusion. In addition, two separate series of experiments were performed to study the effect of adenosine (n = 7) or glucagon (n = 5) on NHGO. Basal NHGO, quantitated via the Fick principle, was significantly decreased by insulin infusion (4 U/min; 4.8 +/- 0.6 vs. -1.7 +/- 2.6 mg.kg-1.min-1, P less than 0.05). The addition of an intrahepatic arterial infusion of adenosine (10 mumol/min) during insulin infusion caused glucose output to return to basal levels (insulin, -1.7 +/- 2.6 mg.kg-1.min-1; insulin + adenosine, 3.8 +/- 1.6 mg.kg-1.min-1, P less than 0.05). The addition of intrahepatic arterial saline (control) during insulin infusion had no effect on insulin's action (insulin, -1.0 +/- 1.9 mg.kg-1.min-1; insulin + saline, -1.2 +/- 1.6 mg.kg-1.min-1, P greater than 0.05). Hepatic glucose, lactate, and oxygen deliveries were not affected during either insulin or insulin plus adenosine infusion. Intrahepatic arterial infusion of adenosine alone had no effect on NHGO, whereas intrahepatic arterial infusion of glucagon alone stimulated glucose output approximately fivefold (basal, 2.7 +/- 0.4 mg.kg-1.min-1; glucagon, 15.5 +/- 1.2 mg.kg-1.min-1, P less than 0.01). These results show that adenosine completely reversed the inhibition by insulin of NHGO. These data suggest that adenosine may act as a modulator of insulin action on the liver.

Adenosine↗
PubMed1986

Insulin stimulates branched chain amino acid uptake and diminishes nitrogen flux from skeletal muscle of injured patients.

Resistance to insulin-mediated glucose disposal occurs in uninjured skeletal muscle of trauma patients but the effect of insulin on the accelerated proteolysis of trauma is unknown. We examined the influence of insulin on forearm amino acid and substrate exchange in five normals and four trauma patients using the hyperinsulinemic glucose clamp technique. Forearm substrate and amino acid flux (Q, nM/100 ml tissue/min), the product of blood flow and arterial deep venous concentration difference, was calculated before and during insulin infusion. Total nitrogen release (NQ, nM/100 ml tissue/min) was calculated as the algebraic sum of all nitrogen groups contained in the amino acids released. Among normal subjects, total nitrogen release from the forearm did not change (581 +/- 197 nM/100 ml tissue/min to 1167 +/- 455) during insulin infusion nor did total branched chain amino acid flux (0 +/- 30 nM/100 ml/min to 106 +/- 36). Under conditions of hyperinsulinemia, neither glutamine nor alanine changed in control subjects. In trauma patients, total nitrogen release (3843 +/- 1383 nM/100 ml/min) was inhibited during insulin administration (819 +/- 314, P less than 0.05). Total branched chain amino acid flux went from a net release of 460 +/- 134 nM/100 ml/min to a net uptake of 10 +/- 82 (P less than 0.05). In patients, statistically significant (P less than 0.05) differences were seen in individual amino acids as well. Forearm nitrogen flux was directly related to total branched chain amino acid flux in patients (r2 = 0.89). Additional studies in normals (n = 4) at higher insulin infusion rates confirmed that these effects were unique to injured subjects and not an effect of the insulin dose. Insulin attenuates the accelerated release of skeletal muscle amino acid in trauma patients. This effect may be mediated in part by facilitated branched chain amino acid uptake. The manipulation of both insulin and branched chain amino acid concentrations may provide a method to reduce post-traumatic protein catabolism.

Adult↗
PubMed1986

Pulmonary agenesis (aplasia), esophageal atresia, and tracheoesophageal fistula: a different treatment strategy.

This is a report of a patient with esophageal atresia, distal tracheoesophageal fistula, and right pulmonary agenesis who survived for 10 months. Death was due to progressive respiratory failure following a complicated clinical course. Several lessons were learned. First, the remaining lung is at high risk. Since the number of respiratory units in these infants is already decreased, the loss of more units has a more profound effect than in an otherwise healthy child. Second, while the establishment of esophageal continuity is important, all attempts to perform an esophagoesophagostomy should be abandoned if doing so further jeopardizes the solitary lung. Third, since all of these children have some degree of tracheomalacia, early tracheostomy should be considered. The tracheostomy will not only act as a tracheal stent but will also avoid progressive laryngeal pathology, which would result from long-term endotracheal intubation.

Abnormalities, Multiple↗
PubMed1986

Juxtapancreatic intestinal duplications with pancreatic ductal communication: a cause of pancreatitis and recurrent abdominal pain in childhood.

Pancreatic duplications with ductal communications should be included in the differential diagnosis of any child presenting with recurrent abdominal pain of unknown etiology and should be considered as a possible cause of pancreatitis in childhood. Such duplications most likely arise from nonregressing diverticula of the pancreatic bud during embryologic development. Their clinical presentation is unique from other duplications because of their anatomic association with the pancreatic duct. Pain and weight loss are the major presenting complaints, although many patients have nausea and vomiting. Serum chemistries, in particular the serum amylase, are usually normal and are of little help in the differential diagnosis. Radiographic evaluation has not been particularly helpful in the past. ERCP, ultrasonic examination, and CT scan show great promise, however. Operative intervention should be tailored for the individual patient. The operation performed will depend upon operative findings. Intraoperative pancreatograms or cystograms are very helpful in differentiating these cysts from others at the time of operation. Pathologically, most of the duplications have a thickened muscular coat that usually has some evidence of inflammation. They are usually lined with gastric mucosa. Except in the most severe cases, the pancreas is histologically normal, suggesting that most of the pain experienced by these patients is secondary to inflammation within the duplication. The inflammatory response may completely destroy the mucosal lining and cause fibrosis within the muscular coat of the duplication. In those instances, these lesions cannot be differentiated from pancreatic pseudocyst. This may account for some of the "idiopathic" pseudocysts reported in the literature.

Abdomen↗
PubMed1984

Post-traumatic insulin resistance in uninjured forearm tissue.

Insulin resistance is a hallmark of post-traumatic metabolism. The mechanism and site of this resistance, however, have not been elucidated. To further define the site of this abnormality, glucose uptake across the uninjured forearm was measured in conjunction with hyperinsulinemic glucose clamp studies in 21 normals and 5 patients with multiple trauma. Under these conditions, glucose infused approximates whole body glucose disposal (M, milligrams/kilogram/min). Forearm glucose flux (Q, milligrams/100 ml tissue/min) is the product of blood flow and arterial-deep venous glucose difference (A-DV). In the basal, unperturbed state forearm glucose uptake (Q) was significantly lower in the patients (0.01 +/- 0.04 mg/100 ml/min) than in the normals (0.06 +/- 0.02) and not significantly different from zero. Basal serum insulin in patients (17 +/- 3 microU/ml) was significantly greater than controls (11 +/- 1). During steady-state conditions of euglycemia and hyperinsulinemia, forearm glucose uptake in the patients (0.36 +/- 0.18 mg/100 ml/min was not significantly different from the basal value. At comparable serum insulin levels in controls, forearm glucose uptake was approximately three times that of the injured patients. This is the first in vivo confirmation of the hypothesis that post-traumatic insulin resistance occurs in uninjured forearm tissue, primarily skeletal muscle. Diminished forearm glucose uptake is present in the resting basal state and cannot be overcome by increasing insulin concentrations.

Adult↗
PubMed1984

The pulmonary hemodynamic response to perioperative anesthesia in the treatment of high-risk infants with congenital diaphragmatic hernia.

The continuing high mortality in congenital diaphragmatic hernia led us to study the cardiopulmonary disturbances associated with this lesion. Since these infants infrequently have right-to-left shunting in the operating room, we adopted a treatment protocol of: continuing general anesthesia in the postoperative period using fentanyl and pancuronium; cardiac catheterization postoperatively, including placement of a pulmonary artery line and a pulmonary angiogram; rapid frequency ventilation; moderate fluid restriction; and avoidance of vasodilators until other means of management had clearly failed. Fourteen high-risk infants, presenting within 6 hours of birth, were studied and compared to 17 high-risk infants, who served as historical controls. As revealed by the physiologic data acquired in the catheterization laboratory, high-risk infants divided into "Responder" and "Nonresponder" groups. Seven of 10 "Responders" actually shunted left to right during the catheterization, demonstrating a low pulmonary vascular resistance. Seven of 10 subsequently demonstrated significant right-to-left shunting at the level of the ductus and the foramen ovale, indicating the hyperreactivity of the pulmonary vascular bed. All but one was managed successfully by ventilatory adjustments and deepening of the level of anesthesia. "Nonresponders" had a fixed right-to-left shunt unresponsive to any medical or ventilatory manipulation. All "Nonresponders" died. Pulmonary angiography suggested a smaller diameter of the affected pulmonary artery compared to the main pulmonary artery in the "Nonresponders." This implies true hypoplasia resulting in a vasculature too small to accept a full cardiac output. Survival in the treatment group "Responders" was eight of 10 (80%) v seven of 14 (50%) in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1983

Epinephrine acutely mediates skeletal muscle insulin resistance.

Alterations in carbohydrate metabolism and insulin resistance are major features of the metabolic response to injury. The mediators of these changes are not defined. In this study we investigated the influence of epinephrine on insulin-mediated glucose uptake by peripheral tissue. Forearm blood flow and substrate exchange were determined during insulin clamp studies with and without epinephrine infusion in normal persons. During control studies insulin concentration was raised to 103 +/- 5 microU/ml. Whole body glucose disposal was 9.23 +/- 1.01 mg/kg . min. At a comparable level of hyperinsulinemia (93 +/- 4 microU/ml), epinephrine reduced glucose disposal to 4.54 +/- 0.39 mg/kg . min (P less than 0.01). Forearm glucose uptake was reduced from 0.66 +/- 0.08 to 0.18 +/- 0.13 mg/100 ml . min (P less than 0.05) despite a doubling of forearm blood flow. Epinephrine reduces whole body glucose disposal in part by reducing glucose uptake in peripheral tissue, primarily muscle. Epinephrine-induced skeletal muscle insulin resistance may play a major role in insulin-resistant states and may contribute to accelerated protein catabolism seen following injury.

Adult↗
PubMed1982

Mechanisms of insulin resistance following injury.

To assess the mechanisms of insulin resistance following injury, we examined the relationship between insulin levels and glucose disposal in nine nonseptic, multiple trauma patients (average age 32 years, Injury Severity Score 22) five to 13 days postinjury. Fourteen age-matched normals served as controls. Using a modification of the euglycemic insulin clamp technique, insulin was infused in 35 two-hour studies using at least one of four infusions rates (0.5, 1.0, 2.0 or 5.0 mU/kg min). Basal glucose levels were maintained by a variable infusion of 20% dextrose using bedside glucose monitoring and a servo-control algorithm. The amount of glucose infused reflected glucose disposal (M, mg/kg.min). Tracer doses of (6,6,2D2) glucose were administered in selected subjects to determine endogenous glucose production. At plasma insulin concentrations less than 100 microU/ml, responses in both groups were similar. However, maximal glucose disposal rates were significantly less in the patients than in the controls (9.17 +/- 0.87 mg/kg . min vs. 14.3 +/- 0.78, mean +/- SEM, p less than 0.01). Insulin clearance rates in the patients were almost twice that seen in controls. To further characterize this decrease in insulin responsiveness, we studied six additional patients and 12 controls following the acute elevation of glucose 125 mg/dl above basal (hyperglycemic glucose clamp). In spite of exaggerated endogenous insulin production in the patients (80-200 microU/ml vs. 30--70 in controls), M was significantly lower (6.23 +/- 0.59 vs. 9.46 +/- 0.79, p less than 0.02). In conclusion, this study demonstrated that (1) the maximal rate of glucose disposal is reduced in trauma patients; (2) the metabolic clearance rate of insulin in the injured patients is almost twice normal and; (3) insulin resistance following injury appears to occur in peripheral tissues, probably skeletal muscle, and is consistent with a postreceptor defect.

Adult↗