Cerebral venous thrombosis as a cause of neonatal seizures

Intracranial venous thrombosis has been described in newborns, but there have been no reports of intractable neonatal seizures due to this condition. We report cortical venous sinus thrombosis in two term neonates who presented with seizures in the first 24 hours of life. The diagnosis was made by cranial computed tomography and was confirmed by cerebral angiography. Both patients improved clinically after the intracranial venous thrombosis resolved. These patients demonstrate that intracranial venous thrombosis should be considered in the differential diagnosis of neonatal seizures.     

Retained pacemaker leads

Increasingly, functionless pacemaker leads are being abandoned in place because they cannot be safely removed. One hundred eighty-nine intact or partially removed pacemaker leads were abandoned in situ in 152 patients between Jan. 1, 1965, and Dec. 31, 1985. The leads, sometimes several leads in a single patient, were deemed uninfected at the time of abandonment in 137 patients and contaminated with Staphylococcus epidermidis in 15 patients. All of the contaminated leads have remained clinically uninfected during follow-up. One clean lead became infected early after implantation and the patient died after an open cardiac operation to remove that lead and an adjacent abandoned lead that was adherent to the subclavian vein. No other patient has had a late complication during follow-up to 256 months (mean 47.6). Properly managed abandonment of an uninfected lead can carry a very low complication rate.     

Studies of the induction and maintenance of long-term graft acceptance by treatment with FK506 in heterotopic cardiac allotransplantation in rats

Immunosuppressive activities of the newly discovered FK506, isolated from Streptomyces tsukubaensis, were examined by using cardiac allotransplantation in the rat, and the mechanisms underlying induction and maintenance of FK506-induced long-term allograft survival were studied. Male rats of WKA (RT1k) and F344 (RT1lvl) strains were used as recipients and donors, respectively, and those of BN (RT1n) strain were used as third-party donors. Treatment with FK506, beginning from the day of allografting for 14, 10, or as few as 4 days, prolonged allograft survival significantly across the major histocompatibility barrier. The minimum doses for prolonging graft survival were 0.1 mg/kg/day by intramuscular treatment and 1.0 mg/kg/day by oral treatment. Treatment with FK506 at a dose of 0.32 mg/kg/day from day 4 until day 10 resulted in all the grafts surviving indefinitely and from days 5 to 10, half the grafts survived indefinitely, suggesting that the agent inhibited ongoing rejection. On the other hand, cyclosporine treatment at a dose of 20 mg/kg/day from day 2 did not prolong graft survival time statistically significantly. Induction of prolonged graft survival was not obtained by pretreatment of the prospective donor or recipient; prolonging effects were observed only when the agent was administered after allografting. Thus, the primary effect of the agent is exerted on responder lymphocytes reacting to the donor antigens in the induction phase of long-term graft acceptance. The mechanisms underlying the maintenance of long-term grafts were analyzed by testing the capacity of lymphocytes or serum of long-term graft-bearing rats to inhibit graft rejection in irradiated grafted hosts. Transfer of 2 x 10(8) lymphocytes from FK506-induced long-term F344 graft-bearing WKA rats resulted in indefinite survival of F344 heart allografts, but it did not prolong survival of third-party BN hearts. Transfer of 2.5 ml serum from long-term graft-bearing rats also prolonged graft survival of F344 hearts, but not BN hearts. These results suggest that donor strain-specific suppressor cells and humoral factor(s) are induced by treatment with FK506 in the presence of allografts, and that they play at least partial roles in the maintenance of long-term allograft acceptance.     

Cardiocirculatory disturbances after surgery of carcinoma of the thoracic esophagus

From 1976 to 1985, 277 cases of carcinoma of the esophagus were resected in the Second Department of Surgery, Tohoku University School of Medicine. Postoperative cardiocirculatory disturbances occurred in 114 cases (41.2%), arrhythmia being the disturbance most frequently observed (86.8%). Low cardiac output syndrome occurred in 8 cases and myocardial infarction occurred in 3 cases. The majority of the cases were treated successfully, but 5 patients died within one month after operation. Causes of death were as follows: myocardial infarction, constrictive pericarditis, cardiac tamponade, non-occlusive mesenteric ischemia and acute cardiac failure. Postoperative arrhythmia occurred mainly up to the third postoperative day. Low cardiac output syndrome occurred just after operation or on the first postoperative day. All cases of myocardial infarction occurred on the first postoperative day. The rate of occurrence of cardiocirculatory disturbances in aged patients (greater than or equal to 70) was significantly higher than other group (less than or equal to 69), (56.7%:38.1%, p less than 0.05). The rate of occurrence of cardiocirculatory disturbances in patients who had a history of hypertension or in patients with abnormal preoperative electrocardiographic findings were relatively higher than those in patients who had no history of hypertension or in patients with no abnormal preoperative electrocardiographic findings. The rate of occurrence of cardiocirculatory disturbances in patients who had undergone total resection of the thoracic esophagus was significantly higher than that in patients who had undergone partial resection of the thoracic esophagus (42.8%:23.8%, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Continuous positive airway pressure in the treatment of postoperative hypoxia

The physiopathology of postoperative hypoxia has been analysed, the cause being identified in the worsening of the V/Q ratio consequent on the reduction in CFR. By increasing CFR, CPAP reduces the superimposition of Tidal Volume and Closing Volume, thus reducing dysventilated zones and thereby improving the V/Q ratio and oxyaemia. With these premises, 18 patients undergoing cholecystectomy were examined; 8 of them were treated in the postoperative period with CPAP at pre-established intervals. The results confirm its effectiveness in terms of PaO2 improvement and the need for constant administration, considering that the benefits are lost when the patient is disconnected from the mask.     

Pressure constant, transurethral resection with the new suprapubic "overflow regulator"

A new suprapubic device that regulates the intravesical pressure automatically during TUR is introduced. This flow controller ensures a constantly low intravesical pressure during TUR. The irrigation fluid constantly flows over into a small open glass jar adjusted to the trocar immediately above the abdominal wall. In this way the pressure is determined by the height of the jar above the bladder, which makes it independent of the irrigation flow. Having constant low pressure conditions between 14 and 18 cm H2O, the bladder wall does not collapse. Thus, the anatomical situation does not change throughout the entire operation, which leads to markedly better overall vision.     

Cytophotometric investigations on atypical epithelial cells of the human seminal vesicle

Normal seminal vesicles were studied histologically in 80, and by Feulgen’s cytophotometric method in 10 autopsied cases (males, 44–82 years of age). In every case large, hyperchromatic nuclei were found. By cytophotometry euploid polyploid atypia was also shown in every case, which is characteristic of benign hormonal dysplasia.     

A clinical and pathological study of diffuse axonal injury

There is increasing evidence from human and experimental studies that the most important factor governing the outcome in head injury is the severity of diffuse axonal injuries. The authors have experienced 18 cases of severe diffuse axonal injury which showed post-traumatic coma for more than 24 hours and CT findings resembling those of shearing injuries of the cerebral white matter such as have been presented by Zimmerman et al. (1978). The consciousness levels on admission were 6 or less on the Glasgow Coma Scale and all cases were shown clinically to have primary brain stem injury. The main type of head trauma resulted from road traffic accidents (83%). Skull fractures were found in only 5 cases (28%). These findings suggested that acceleration/deceleration injury produce in the patients severe diffuse axonal injury. Initial ICP was below 20 mmHg in 11 cases out of 13 (85%). Parenchymal small hemorrhagic lesions of initial CT were basal ganglia (7 cases), corpus callosum (4 cases), pons (4 cases), midbrain (3 cases) and thalamus (2 cases). Extraparenchymal hemorrhagic lesions included intraventricular hemorrhage (6 cases) and subarachnoid hemorrhage (6 cases). Two autopsied cases of severe diffuse axonal injury (acute case and chronic case) showed remarkable congestion and edema in the deep part of the frontal white matter. Microscopic examination revealed marked axonal degeneration including axonal retraction ball in the corpus callosum, in the internal capsule and in the white matter of the brain stem. Glasgow Outcome Scale of the 18 patients at 3 months after the trauma made us concerned that no patients indicated good recovery or even only moderate disability.(ABSTRACT TRUNCATED AT 250 WORDS)     

The hepatotropic properties of nonsteroidal anti-inflammatory agents

The hepatotropic effect of nonsteroidal anti-inflammatory drugs (NSAID) such as indomethacin, voltaren, piroxicam, phenylbutazon, mefenamic acid was studied. It was found that according to their level of the pharmacological protection of the liver against tetrachlormethan these agents may be arranged in the following sequence: mefenamic acid, phenylbutazon, voltaren, piroxicam. The hepatoprotective effect of NSAID correlates with the antioxidant properties and fails to correlate with the antioxidant ones. The hepatotoxic effect of NSAID was determined by their ability to suppress synthesis of prostaglandins.