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Biomedical subjects

N Snyder

Publications and source records attributed to N Snyder.

At least 19 recordsLinked to original sources

Trigger finger release with hand surface landmark ratios: an anatomic and clinical study.

The purpose of this study was to identify surface landmark ratios to locate the A1 pulley and clarify the controversy of differing anatomic descriptions of the A1, C0, and A2 pulleys. Minimally invasive and percutaneous approaches to A1 pulley release may be facilitated with surface landmark ratios, which identify and predict the proximal and distal margins of the A1 pulley. Two-hundred fifty-sixty fingers were dissected in 64 preserved cadaver hands. Measurements of A1 pulley lengths and pulley margins in relation to surface landmarks were obtained. We found that the distance from the palmar digital crease to the proximal interphalangeal crease (mean, 2.42 +/- 0.03 cm) corresponds to the distance of the proximal edge of the A1 pulley from the palmar digital crease (mean, 2.45 +/- 0.03 cm). The mean absolute difference between these two measured distances in each finger was 0.13 cm, with a 95 percent confidence interval of 0.11 to 0.14 cm. Thus, the distance between the palmar digital crease and the proximal interphalangeal crease can be used to predict the distance between the palmar digital crease and the A1 pulley proximal edge with reasonable accuracy. A1 pulley length averaged 0.98 +/- 0.02 cm for the small finger and 1.17 +/- 0.02 cm for the index, middle, and ring fingers. The length of the A1 pulley was significantly shorter (p < 0.001) for the small finger than for the index, middle, and ring fingers. Additionally, a cruciate (C0) pulley was consistently located between the A1 and A2 pulleys, an average of 0.46 cm proximal to the palmar digital crease, which can serve as guide for concluding the release of the A1 pulley. Clinically, hand surface landmark ratios were used to release 32 trigger fingers with a minimally invasive technique, without a complication during 4- to 30-week follow-up. We conclude that hand surface landmark ratios can serve to locate the proximal A1 pulley edge, thus facilitating complete trigger finger release by either open or minimally invasive techniques. Additionally, our study clarifies the discrepancy of prior smaller reports of the pulley system anatomy regarding the existence of the C0 pulley between the A1 and A2 pulleys. The cruciate fibers of this C0 pulley can serve as the distal boundary for release of trigger finger.

Biophysical Phenomena↗

Bipedicle paraspinous muscle flaps for spinal wound closure: an anatomic and clinical study.

The purpose of this study was to evaluate the vascular anatomy of the paraspinous muscles and review their clinical use as bipedicled flaps in spinal wound closure. Anatomically, through cadaver dissections, lead oxide injections, and radiographic imaging, the blood supply to the paraspinous muscles was determined. Clinically, 29 consecutive patients treated with spinal wounds and exposed bone or hardware were reviewed retrospectively. Of these patients, 19 underwent closure in delayed primary fashion, whereas 10 were referred to plastic surgery for reconstruction because of the complex nature of their wounds. The cadaver study demonstrated the paraspinous muscles to possess a segmental arterial supply through medial and lateral perforators. Division of the medial perforators allowed for medial advancement of the muscles. Lead oxide injection of the lateral perforators demonstrated adequate medial muscle perfusion with ligation of the medial perforators. Ten of the 29 patients (six women, four men, 32 to 62 years of age) were reconstructed with paraspinous (eight), latissimus (one), and trapezius (one) muscle flaps. A higher complication rate was found in wounds closed in delayed primary fashion (13 of 19 patients, 68 percent) than those reconstructed with muscle flaps (2 of 10 patients, 20 percent) (p = 0.021). Follow-up of the muscle flap reconstructed patients averaged 12 months (range, 3 to 27 months). Cadaver muscle injections predicted and clinical cases confirmed that the paraspinous muscles can be raised on lateral perforators and advanced medially to close lumbar spine wounds reliably with fewer complications.

Adult↗

The effect of inducible nitric oxide synthase (iNOS) inhibition on smoke inhalation injury in sheep.

Recent studies on smoke inhalation injury have been focused on nitric oxide (NO) as an essential factor of progressive lung injury. We studied the effects of inducible nitric oxide synthase (iNOS) inhibition on inhalation injury in sheep. Sheep (n = 14) were prepared surgically for chronic study. After recovery period, the sheep received 48 breaths of cotton smoke. The animals were then randomised into two groups: MEG group [30 mg/kg mercaptoethylguanidine (MEG), selective inhibitor of iNOS and peroxynitrite scavenger, was given 1 h after injury and then 8 h for 41 h, n = 7] and control group (0.9% NaCl, n = 7). All animals were ventilated mechanically, and airway blood flow was measured using colored microspheres. In the control group, following significant increase in airway blood flow, deterioration in the PaO2/FiO2 ratio was observed. Whereas in the MEG group, it was not observed. In addition, the MEG group did not show significant increase in pulmonary vascular resistance and intrapulmonary shunt fraction. Lung wet/dry ratios, a marker of pulmonary edema, were significantly lower in the MEG group. At 48 h after injury, lung tissue-conjugated dienes, an index of lung oxidative tissue injury, were significantly lower in the MEG group than in the control group. Our data suggest that 1) iNOS-NO produced in the airway circulation plays a major role on the significant increase in airway blood flow, which may contribute to the spread of injury from injured airway to the lung parenchyma; 2) iNOS-NO induced in the pulmonary circulation contributes to the loss of hypoxic pulmonary vasoconstriction; and 3) iNOS-NO plays an important role on the lung oxidative tissue injury.

Animals↗

Depressed delayed cutaneous hypersensitivity in alcoholic hepatitis.

Delayed cutaneous hypersensitivity was studied in 10 patients with severe alcoholic hepatitis, 9 patients with either inactive alcoholic cirrhosis or alcoholic fatty liver, and 10 agematched controls. The mean response of the alcoholic hepatitis group was significantly less compared to controls for SK-SD (P less than 0.001), mumps (P less than 0.001), trichophyton (P less than 0.025), and Candida albicans (P less than 0.025). Upon clinical recovery, the response of the 6 surviving patients with alcoholic hepatitis was similar to controls for 4 of the 5 antigens tested, and the improvements in response to SK-SD and Candida albicans were significant (P less than 0.02 and P less than 0.05). The mean percentage and absolute numbers of thymus-derived lymphocytes were significantly less in the alcoholic hepatitis group compared with controls. Both the alcoholic hepatitis patients and patients with less advanced alcoholic liver disease had a diminished response to concanavalin A and phytohemagglutinin. This study demonstrates a reversible depression of delayed cutaneous hypersensitivity in alcoholic hepatitis. Several mechanisms may help account for this finding. We recommend that skin tests in patients with alcoholic hepatitis be interpreted with this phenomenon in mind.

Antigens↗

Viral hepatitis in pregnancy with disseminated intravascular coagulation and hypoglycemia.

A case of a 26-year-old woman who presented at 38 weeks of gestation with severe hepatitis B complicated by disseminated intravascular coagulation (DIC) and hypoglycemia is reported. The clinical features of the illness suggested acute fatty liver of pregnancy. Cesarean section was followed by resolution of the coagulopathy and the hypoglycemia. Both mother and infant survived and remain well. The diagnosis of hepatitis B was confirmed by a transiently positive hepatitis B surface antigen and percutaneous liver biopsy. This case emphasizes the difficulty in distinguishing acute viral hepatitis from acute fatty liver of pregnancy. In addition, the predominant features of DIC and hypoglycemia in our case are reported.

Adult↗

Hyperglucagonemia in cirrhosis: altered secretion and sensitivity to glucagon.

Plasma glucagon concentration was elevated 2- to 6-fold in cirrhotic patients with spontaneous portal systemic shunting or surgically induced portacaval anastomosis but was comparable to controls in cirrhotics without portal-systemic shunting. The metabolic clearance rate of glucagon (mol wt 3500) was normal in all of the cirrhotic groups, but the estimated basal systemic delivery rate of glucagon was increased 2- to 6-fold in the hyperglucagonemic patients. The blood glucose response to infusion of glucagon (3 ng per kg per min) was reduced in the cirrhotics with portal-systemic shunting or portacaval anastomosis, and correlated inversely with the delivery rate of endogenous glucagon. Administration of ammonium chloride (3 g) failed to elevate plasma glucagon concentration. It is concluded that hyperglucagonemia in cirrhosis is a consequence of hypersecretion rather than decreased hormonal catabolism. A negative feedback signal may exist between hepatic sensitivity to glucagon and the secretion of this hormone.

Adult↗

Antral gastrin concentration in upper-gastrointestinal disease.

Antral gastrin concentration (AGC) was measured in prepyloric mucosa specimens obtained by forceps biopsy during endoscopic examination of 174 clinic and hospital patients. AGC in 32 patients who had normal endoscopic findings, the control group, varied widely from 2 to 38.6 ng gastrin/mg tissue. The mean AGC of the control patients was 14.2 +/- 1.4 (mean +/- 1 SE) ng gastrin/mg tissue. AGC was similar to control values in 18 patients with duodenal ulcer, 14.7 +/- 2.1; 12 patients with a pyloric channel or antral ulcer, 16.4 +/- 3.5; and 48 patients with miscellaneous diagnoses, 14.3 +/- 1.5. AGC was significantly less than control values in 13 patients with a ulcer in the body or fundus of the stomach, 5.9 +/- 1.5, and 4 patients with the Zollinger-Ellison syndrome, 4.9 +/- 2.4. AGC was significantly greater than in control values in 16 patients with gastritis, 25.8 +/- 4.3;22 patients with esophagitis, 23.2 +/- 3.0; and 9 patients with gastric atrophy and fasting serum hypergastrinemia 44.6 +/- 12.3. In group of 77 of these patients with heterogeneous diagnoses, meal-stimulated 3-hr integrated gastrin output was directly related to AGC (r = 0.47, P less than 0.001). In a group of 106 patients AGC was inversely related to histalogstimulated maximum acid output. The correlation was very weak (r = -0.20) but significant (P less than 0.05).

Atrophy↗

Basal and calcium-stimulated gastroesophageal sphincter pressure in patients with Zollinger-Ellison syndrome.

Basal lower esophageal sphincter (LES) pressure was measured in 6 patients with the Zollinger-Ellison syndrome (ZES) and hypergastrinemia, and in 6 patients with duodenal ulcer and normogastrinemia. Basal LES pressure in ZES patients, 17.0 +/- 3.7 (mean +/- SE) mm Hg was similar to basal LES pressure in duodenal ulcer patients, 18.3 +/- 3.5 mm Hg (P greater than 0.10). LES pressure and serum gastrin concentration were not related in the ZES patients, r = 0.03, or in the duodenal ulcer patients, r = 0.20. Intravenous infusion of calcium gluconate in ZES patients produced a marked rise in serum gastrin concentration, delta = 1580 +/- 1110 pg per ml (P less than 0.001), and a moderate but significant rise in LES pressure, delta = 5.9 +/- 0.9 mm Hg (P less than 0.05). In duodenal ulcer patients calcium infusion produced only slight rises in gastrin concentration, delta = 10 +/- 12 pg per ml, and LES pressure, delta = 2.1 +/- 0.5 mm Hg, which were not significant (P greater than 0.10). This study suggests that basal LES pressure is not regulated by blood gastrin levels in the ZES. We interpret the calcium infusion study to show that the LES pressure in patients with ZES may respond to acute changes in endogenous gastrin levels.

Adult↗

Cruveilhier-Baumgarten disease.

An unusual case of portal hypertension in an asymptomatic 33-year-old man is presented. The findings of splenomgealy, esophageal and gastric varices, a patent umbilical vein with associated venous hum, and three normal liver biopsies qualify him for the diagnosis of Cruveilhier-Baumgarten disease. Possible etiologic explanations of his portal hypertension are discussed.

Adult↗