No abstract available.
Home Care Services* ; Humans ; Peritoneal Dialysis, Continuous Ambulatory*

No abstract available.
Humans ; Infant, Newborn*

Medial orbital wall fracture was described by Converse and Smith in the first time in 1957. These fractures which comprise more than 30% of all the orbital wall fracture are may easily be overlooked in routine orbital radiology. Accordingly, examination with orbital CT is essential for accurate diagnosis and appropriate treatment. These type of fracture are followed frequently by post-oprative complication such as diplopia and enophthalmos because it is very difficult to approach to orbital medial was in these operations. The mechanism of the orbital wall fractures are abruptly increased hydraulic pressure by sudden impact on orbital rim or soft tissue of orbital region. So patients who show the signs of subcutaneous emphysema, edema on the orbital region or diplopia need to get through examination with orbital CT for accurate diagnosis and immediate reconstruction of the fractured orbital wall. Conventional approaches in the operations of the orbital medial wall fractures are that with bicoronal incision, subciliary incision, transconjunctival incision and infra-orbital rim incision. But, approach with bicoronary incision, needs broader dissection and longer time for operation. Operations with transconjunctival incision and that with subciliary incision have difficulty to approach to fractured sites. Operations with other conventional methods may be also followed by scar problem. The authors performed reduction and reconstruction of the fractured orbital medial wall fractures successfully without any complications and difficulties by intra-eyebrow approach with which they made incision of 2 - 2.5 cm on mid-area of eyebrow to expose fractured medial wall with good operative field.
Cicatrix ; Diagnosis ; Diplopia ; Edema ; Enophthalmos ; Eyebrows ; Humans ; Orbit* ; Subcutaneous Emphysema

BACKGROUND: The purpose of this study was to compare the time course of the bradycardia and hypotensive effects of esmolol. METHODS: Thirty patients who undergoing gynecologic operation were anesthetized with nitrous oxide and enflurane. After the steady state of anesthesia was achieved, esmolol 500microgram/kg for 1 minute followed by 25, 50, or 100microgram/kg/min for 60minuts infused by intravenous catheter. Heart rate, mean arterial pressure, cardiac index, stroke volume, and systemic vascular resistance was measured by 1, 3, 5, 10, 15, 20, 25, 30, 45, and 60 minutes. RESULTS: Heart rate was changed abruptly within 3 to 5 minutes, and decreased rapidly for 15minutes. Mean arteral pressure was decreased rapidly for 30 minutes, but slower than heart rate. Cardiac index was decreased rapidly for 20 minutes and differed significantly on the dose of 25, 50, 100microgram/kg. Stroke volume was decreased for 30 minutes, and systemic vascular resistance was increased rapidly for 10 minutes. It was decided the onset time that was expressed 90% of ultimate response of esmolol effect, and was calculated in each group. The onset time of heart rate of esmolol 25, 50, 100microgram/kg were 8.0 +/- 4.1, 4.8 +/- 2.3, 8.1 +/- 4.4 minutes, the time of mean arterial pressure were 30.0 +/- 7.5, 21.1 +/- 6.2, 19.9 +/- 7.8 minutes, and the time of cardiac index were 25.1 +/- 4.7, 14.8 +/- 5.0, 14.2 +/- 4.6 minutes. Thus heart rate, mean arterial pressure, cardiac index, stroke volume, and systemic vascular resistance responses of administration of esmolol did not occur with equal rapidity. CONCLUSIONS: Thus although esmolol has an ultrashort kinetic half life, only the heart rate effect can be considered to have an ultrashort onset.
Anesthesia ; Arterial Pressure ; Bradycardia ; Catheters ; Enflurane ; Half-Life ; Heart Rate ; Humans ; Nitrous Oxide ; Stroke Volume ; Vascular Resistance

True cysts of the pancreas are rare, and enterogeous (duplication) cysts are extremely rare. We describe a case of enterogenous cyst of the pancreas located in the retroperitoneum, in which homogenous low attenua-tion, multiloculation, internal septation and cyst wall calcification were noted.
Pancreas*

Freys syndrome is characterized by attacks of facial erythema and gustatory sweating occurring in the cutaneous distribution of the auriculotemporal nerve. After sugery, trauma, abscess, or other diseases of the parotid gland, the postganglionic sympathetic and parasympathetic nerve fibers are disrupted. Some misdirected auriculotemporal nerve fibrils join with the distal sympathetic nerves innervating the sweat glands and subcutaneous vessels. We report a case of Freys sindrome in a 6-year old boy without any definite injury to the parotid gland. After considering our case and review of literature of Freys syndrome in children, we conclude that there may be a congenital defect in the auriculotemporal nerve innervation responsible for cases occuring in children.
Abscess ; Child* ; Congenital Abnormalities ; Erythema ; Humans ; Male ; Nerve Fibers ; Parotid Gland ; Sweat Glands ; Sweating, Gustatory

No abstract available.
Gastroenteritis* ; Humans*

No abstract available.
Bipolar Disorder*

Zygomatic arch is a prominent structure among facial bone and this is the major cause of vulnerability from the facial trauma. The fracture of zygomatic arch has been treated by ancillary methods of closed reduction approaching through temporal incision or intraoral incision. But, these methods gas a limitation of reduction force vector and it has a difficulty in maintaining the secure fixation of the reduced unstable fractured bones. All 22 cases of zygomatic fracture were reduced by transcutaneous screw and fixed with external fixation device successfully. There was no post-operative complication, such as non union, malunion, and visible scar. This method also has advantages of less post-operative edema and pain.
Cicatrix ; Edema ; External Fixators ; Facial Bones ; Zygoma* ; Zygomatic Fractures

Rickets is a syndrome, characterized pathophysiologically by a failure of normal mineralization of bone and epiphyseal cartilage and clinically by skeletal deformity in growing children. The five principal causes of rickets are vitamin D deficiency, absorptive defects, renal tubular insufficiency, chronic renal insufficiency and hypophosphatasia. In addition to these causes of rickets a defective reabsorption mechanism of the proximal renal tubule is currently believed to be a factor in the development of hypophosphatemic vitamine D resistant rickets. Simple type of hypophosphatemic vitamine D resistant rickets is the most common of all the cases of rickets due to tubular insufficiency. It has a familiar incidence and is a sex-linked dominant disease. There is hypophos-phatemia and an elevated alkaline phosphatase but usually no glomerular disease or uremia. All the clinical manifestations are those of advanced rickets of the ordinary type and usually begin early. We experienced four cases of hypophosphatemic vitamine D resistant rickets which developed in a family.
Alkaline Phosphatase ; Child ; Congenital Abnormalities ; Growth Plate ; Humans ; Hypophosphatasia ; Incidence ; Kidney Tubules, Proximal ; Miners ; Renal Insufficiency, Chronic ; Rickets ; Uremia ; Vitamin D Deficiency ; Vitamins