Life- and limb-threatening infections following the use of an external fixator.

External fixation is widely used in orthopaedic and trauma surgery. Infections around pin or wire sites, which are usually localised, non-invasive, and are easily managed, are common. Occasionally, more serious invasive complications such as necrotising fasciitis (NF) and toxic shock syndrome (TSS) may occur. We retrospectively reviewed all patients who underwent external fixation between 1997 and 2012 in our limb lengthening and reconstruction programme. A total of eight patients (seven female and one male) with a mean age of 20 years (5 to 45) in which pin/wire track infections became limb- or life-threatening were identified. Of these, four were due to TSS and four to NF. Their management is described. A satisfactory outcome was obtained with early diagnosis and aggressive medical and surgical treatment. Clinicians caring for patients who have external fixation and in whom infection has developed should be aware of the possibility of these more serious complications. Early diagnosis and aggressive treatment are required in order to obtain a satisfactory outcome.

Phagocytosis of monosize polystyrene-based microspheres having different size and surface properties.

In this study, nondegradable monosize polystyrene (PS) based polymeric microspheres with different size and surface chemistries were prepared by different polymerization techniques. Surfaces of the plain microspheres were further modified biologically by albumin (BSA) or fibronectin (Fn) preadsorption. Phagocytosis of these polymeric microspheres by leukocytes and macrophages were investigated. The phagocytic response of both leukocytes and macrophages decreased by increasing size of the particles. More hydrophilic particles phagocytosed less. Positive charges increased the uptake while negative charges oppositely reduced the uptake. BSA on the surface almost prevented the uptake, while Fn caused opsonization.

Decreased natural killer (NK) cell activity in zinc-deficient rats.

1. In the study, the effect of zinc deficiency, a natural killer (NK), and lipopolysaccharide (LPS) activated NK cell activity were investigated. 2. Rats were fed with zinc-deficient and normal diet for 3 weeks. 3. NK and LPS activated NK cell activity was 7.2 +/- 1.8%/10(6) cells (n = 10) and 9.5 +/- 4.3%/10(6) cells (n = 10), respectively, in the zinc deficient group. In the control group fed with normal diet, NK and LPS activated NK cell activity was 22.2 +/- 3.3%/10(6) cells (n = 10) and 32.5 +/- 3.5%/10(6) cells (n = 10), respectively. 4. Plasma zinc concentration was 131.7 +/- 8.8 micrograms/dl in the zinc-deficient group and 206 +/- 17.7 micrograms/dl in the control group. 5. The results suggest that decreased NK and LPS activated NK cell activity is associated with zinc deficiency.

[Complete traumatic separation of the distal humeral epiphysis in a battered child].

Complete traumatic separation of the distal humeral epiphysis is a rare finding in children, and is usually seen in the battered child. An 11-month-old girl with a complete traumatic separation is described. The family pathology was diagnosed and proper social and legal steps were taken after the only clue, the fracture, was properly interpreted.

Phagocytosis by macrophages in zinc-deficient rats.

Phagocytosis by polymorphonuclear cells has been found to be significantly reduced in zinc-deficient patients and this finding was confirmed in animal experiments. In order to find out whether phagocytosis by macrophages is similarly altered, experiments were conducted in three groups of 18 rats. Control, zinc-deficient and pair-fed rats were given 99mTc nanocolloid intravenously. In ten other experiments (5 experimental and 5 control rats) 99mTc-sulfur colloid was injected intravenously. The biodistribution was determined by a well-type gamma counter and the results were evaluated statistically. The greatest amount of radioactivity was taken up by the liver, followed by the spleen, lung and kidney. In both series of experiments however the zinc-deficient animals appeared to take up a greater amount of the radiotracer (P less than 0.05).

Changes of bile lipid composition induced by methylprednisolone.

Experiments were carried out on three groups of male guinea pigs to study the influence of methylprednisolone on the bile lipid composition. The cholesterol, phospholipid, and bile acids concentrations of the gallbladder bile in the control series were not significantly different from those of Group II, receiving SF for 45 days. In the methylprednisolone group, however, the absolute and relative molar concentrations of cholesterol increased while those of bile acids decreased compared to the former groups. Phospholipids on the other hand revealed only a relative increase. The observations indicate that use of methyl prednisolone for 45 days increases the lithogenicity of the bile in guinea pigs.

Changes of reduced glutathion, glutathion reductase, and glutathione peroxidase after radiation in guinea pigs.

In this series of experiments the protective action of reduced glutathion due to ionizing radiation has been studied. In the experimental group 18 guinea pigs were exposed to successive radiations of 150 rad 3 or 4 days apart. Total dose given amounted to 750 rad which is the LD50 for guinea pigs. Blood samples were taken 30 min after each exposure. The control series were sham radiated but otherwise treated identically. The cells of the removed blood samples were separated by centrifugation and were subjected to the reduced glutathion stability test. GSSGR, GPer, and LDH enzyme activities were also measured of which the latter served as a marked enzyme. It was found that LDH did not show any alteration after radiation. The reduced glutathion stability test showed a consistent but minor reduction (P greater than 0.05), in the experimental group. GSSGR enzyme activity on the other hand was reduced significantly (from 176.48 +/- 11.32 to 41.34 +/- 1.17 IU/ml of packed erythrocytes, P less than 0.001) in the same group. GPer activity showed a consistent but minor elevation during the early phase of the experimental group. It was later increased significantly beginning after 600 rad total radiation on the fourth session (P less than 0.050).

Liver blood flow rate and glucose metabolism in hemorrhagic hypotension and shock.

Liver blood flow was measured in dogs using 133Xe clearance technique under control conditions and during various stages of hypotension and of hemorrhagic shock. Initial liver mean blood flow rate in all dogs combined are 101.9 +/- 11.5 ml/100 gm liver/min and was not significantly altered in the control group. Liver blood flow rate was reduced in the experimental group during hemorrhagic hypotension and shock and was correlated with the severity of the disease. Peripheral vasodilatation was observed in one subgroup of experimental animals while severe vasoconstriction was found in another subgroup. Glucose concentrations in the hepatic vein were significantly above that of arterial and portal venous blood; all experimental animals were hyperglycemic. The outflow of glucose from the liver was increased during shock in ten animals. It was, however, reduced in 17 animals.

Alteration by kallikrein and bradykinin of the conversion of angiotensin I to angiotensin II in the isolated perfused rat lung.

Pure kallikrein and bradykinin, when added to the perfusion medium of the isolated perfused rat lung, produced an equal inhibition in the conversion of angiotensin I to angiotensin II as measured in the venous return superfused over the rabbit aortic strips. Acetylsalicylic acid (ASA) prevented the inhibitory effect of kallikrein and bradykinin. Aprotinin, however, prevented the inhibitory effect of kallikrein without altering that of bradykinin. The recovery brought about by ASA of the bradykinin-produced inhibition of angiotensin I conversion was also prevented by prior addition of prostaglandin E2 (PGE2) into the perfusion medium. Neither kallikrein and bradykinin nor ASA altered the myotropic activity of angiotensin II. 5-Oxo-L-prolyl L-tryptophyl-L-prolyl-L-arginyl-L-prolyl-L-glutaminyl-L-isoleucyl-L-prolyl-L- proline (SQ 20 881), when added to the medium, greatly reduced the responses to angiotensin I but potentiated those of angiotensin II. The possible mechanisms of the inhibitory effects of kallikrein and bradykinin are discussed.

The role of zinc ion in the development of gastric ulcers in rats.

The properties of the gastric mucosal barrier and acid output were investigated in zinc deficient rats. A decline in total acid output, a significant diminution in hydrogen and sodium ion fluxes and an increase in gastric lesions suggest a marked breakdown of the gastric mucosal barrier in zinc deficient rats.

Net insulin secretion and IRI response to 1 mg glucose during OGTT.

Dogs in postabsorbtive state were anesthetized with IV nembutal. Their femoral arteries were catheterized, and the abdomens were entered via a midline incision. A small branch of the pancreatic artery and a corresponding small vein were catheterized. 133Xe was injected through the artery, and the the pancreatic blood flow rate (PBFR) was determined. Net insulin secretion was calculated using the insulin concentration of pancreatic vein-artery difference and pancreatic plasma flow rate (PPFR). After control studies an oral glucose tolerance test (2 g/kg body wt.) was performed. Under control studies the mean value of net insulin secretion was 3,753.2 +/- 699.1 microunits/100 g P/min and the maximum values were 10,610.2 +/- 3,658.7 and 11,108.0 +/- 2,852.6 microunits/100 g P/min at 20 and 60 min after glucose loading, respectively (P less than 0.05). Insulin response per mg of glucose was 83.2 +/- 12.2 microunits under control conditions. Twenty minutes after glucose loading this figure rose to 173.4 +/- 41.7 microunits/mg glucose and at 60 min 207.9 +/- 49.2 microunits/mg glucose.

Pancreatic blood flow in hemorrhagic shock.

Pancretic blood flow rates were determined using a 133Xe washout technique in a total of 40 dogs, 14 of which were used as a control group and the remaining 26 as the experimental group. The initial pancreatic blood flow rates of control group and of the experimerntal group were 85.1 +/- 10.1 ml/100 g/min of pancreas/min and 81.1 +/- 5.4 ml/100 g/min respectively. These values were not significantly different from each other (P > 0.05). In the control group the blood flow was determined 3 times at 30 min intervals. These mean values were 73.0 +/- 9.4, 74.6 +/- 8.7, and 79.4 +/- 10.4 m/100 g/min respectively (P > 0.05). The dogs in the experimental group were bled and the peripheral arterial blood pressure was reduced stepwise to 80, 50, and 30 mm Hg. At each level at 30 min of stabilization period the pancreatic blood flow rates were 49.8 +/- 3.7, 29.3 +/- 2.3 and 20.2 +/- 2.3 ml/100 g/min respectively. These mean values were very significantly reduced compared to those of the control group at 30 min (P < 0.02), at 60 and 90 min (P > 0.001). They were also very significantly different from their own initial values (P < 0.001). The metabolic consequences of this reduction in pancreatic blood flow are discussed.

Hepatic blood flow during rapid intravenous glucose tolerance test.

Twenty-nine dogs anesthetized with Na-pentobarbital were laparatomized and liver blood flow was measured by 133Xe clearance method. Fifteen dogs of the experimental group were subjected to rapid i.v. glucose tolerance test whereas 14 animals of the control group were treated identically except for infusion of glucose. It was found that the arterial and the portal venous blood glucose rose significantly during the glucose tolerance test. Liver blood flow in the experimental group was 123.8 ml/100 g L/min after operative procedures. It reached 171.9 ml/100 g L/min at 10 min after infusion of glucose (P < 0.01). At 20, 30, and 40 min of the test it was 145.4 (P < 0.05), 143.4 (P < 0.01), 135.1 (P < 0.05) mg/100 g L/min, respectively. Liver blood flow did not change significantly during the observation period in the control series. It is concluded that glucose loading may produce some metabolic effects secondary to rising liver blood flow in addition to changes induced by its rising concentration.

The role of endogenous prostaglandins in the renal vascular response to clonidine.

The effect of clonidine has been studied in the isolated perfused rabbit kidney. The drug produced a dose-dependent increase in perfusion pressure and in urine flow both of which could be blocked by phentolamine. Addition of acetylsalicylic acid to the medium caused an increase in perfusion pressure and a decrease in urine volume induced by clonidine. Further addition of prostaglandin E2 to the medium prevented the changes induced by acetylsalicylic acid. These results were taken as evidence that clonidine can increase the biosynthesis of prostaglandins which could act as a modulator system for the effects of the drug in the kidney.

Zinc deficiency and lung converting enzyme activity in rats.

Angiotensin converting enzyme activity was found to be significantly decreased in the isolated perfused lung from zinc-deficient rats when compared with that of controls. Addition of zinc ion to the superfusion medium did not cause a recovery in this decreased activity of the enzyme. It is postulated that zinc deficiency probably produces a structural change in the lung angiotensin converting enzyme.

Hyperinsulinemia in childhood cirrhosis.

Circulating insulin was determined by radioimmunoassay in ten children with cirrhosis of the liver and in 6 age-matched controls. They were found to be elevated in cirrhotics during fasting as well as at 1/2, 1, 1 1/2 and 2 h during the oral glucose tolerance test. These determinations were also carried out in two children with extrahepatic portal hypertension to show the possible role of portal systemic shunts for the elevated serum insulin levels. We believe that the hyperinsulinemia of these patients was related to decreased insulin degradation by the liver as well as to portal-systemic shunting.