Warm Carolina rinse solution prevents graft failure from storage injury after orthotopic rat liver transplantation with arterialization

An injury to nonparenchymal cells, characterized by loss of viability of sinusoidal endothelial cells and activation of Kupffer cells, occurs after reperfusion of livers stored for transplantation. Recently, a new solution, Carolina rinse solution, was shown to prevent reperfusion injury to endothelial cells in vitro almost completely and to improve graft survival after orthotopic rat liver transplantation (ORLT) without arterialization. ORLT with arterialization permits longer cold storage of donor livers and more closely models human surgery. Therefore, we evaluated the effects of Carolina rinse solution on graft survival after ORLT with arterialization in syngeneic Lewis rats. Just prior to implantation, donor livers stored in University of Wisconsin (UW) solution were rinsed with 30 ml of Ringer's solution, saline, or Carolina rinse solution at 1°–4°C. In livers stored for 15 h and rinsed with Ringer's or saline solution, long-term graft survival was only 8%. Using Carolina rinse solution containing 1 mmol and 200 mol adenosine per liter, graft survival improved to 40% and 80%, respectively. Graft survival did not improve when using Carolina rinse solution with adenosine omitted or Ringer's solution containing 200 mol adenosine per liter. Livers were also rinsed with Carolina rinse solution containing 200 mol adenosine per liter at 28°–30°C rather than at 1°–4°C. With warm Carolina rinse solution, survival improved further to 100%, 80%, and 50% after 15, 18, and 21 h of storage. After 18 h of storage, light and electron microscopy demonstrated marked denudation of the sinusoidal lining and activation of Kupffer cells in grafts rinsed with Ringer's solution. Use of Carolina rinse solution greatly improved endothelial structure but did not reduce Kupffer cell activation. In conclusion, these findings show that Carolina rinse solution substantially improves graft survival after ORLT with arterialization. Adenosine and warm temperature are important factors contributing to efficacy. A mechanism of protection appears to be prevention of reperfusion-induced endothelial cell injury.     

Subdural hygroma after head injury

Summary This is a review of 26 cases of traumatic subdural hygroma (TSH). Special attention was paid to frequency of occurrence, angiographic features, and the relationship between subdural fluid appearance and clinical course, since these have been seldom reported previously. TSH was infrequent among the intracranial mass lesions following head injury. Cerebral angiography was useful in diagnosis. There were occasional postoperative difficulties when the subdural fluid was xanthochromic or blood-tinged.     

Gastric emptying after head injury

Gastric emptying was measured in patients after head injury and compared with that of healthy volunteers using the rate of paracetamol absorption as an indicator of gastric emptying rate. There was a trend towards slower gastric emptying in the head injured patients, but the differences were not statistically significant.     

Papilledema after acute head injury

Low grade papilledema after acute, severe head injury was identified in 15 (3.5%) of 426 patients. Papilledema was recognized immediately after head injury in 1 patient, during the 1st week in 10 patients, and in the 2nd week or after in 4 patients. Initial computed tomographic scans showed evidence of brain injury in 11 of these patients. The intracranial pressure (ICP) was monitored continuously for 3 or more days in 9 patients; it was mildly elevated (20 to 40 mm Hg) in 7 patients and moderately elevated (40 to 60 mm Hg) in 2 patients. Intracranial hypertension was controllable in each patient. A sudden, severe, but transient increase in ICP best explained the immediate development of papilledema and survival of 1 patient. Sustained but mild to moderately elevated ICP accounted for papilledema appearing in the 1st week. Papilledema in the 2nd week or after occurred from impaired cerebrospinal fluid absorption and consequent communicating hydrocephalus or delayed focal or diffuse cerebral swelling. A lesser degree of head injury in patients with posttraumatic papilledema was suggested by a higher Glasgow coma score, milder and controllable elevations in ICP, and the absence of any fatality in this group. The favorable outcome was significant compared to the mortality of the more severely injured patients (chi square-4.327; P less than 0.04). Papilledema did not occur in 6 patients with sustained, severely elevated ICP (greater than 60 mm Hg) for 3 or more days. Each of these patients died. The severity of the trauma apparently accounts for the failure of papilledema to develop, possibly by arresting axoplasmic production and transport in retinal nerve fibers.     

Severe hypophosphatemia after head injury

Hypophosphatemia occurs in a variety of clinical conditions. It develops in parallel with phosphate depletion from body losses or more commonly as a sequel to the redistribution of phosphate from the extracellular to the intracellular compartment. Hypophosphatemia is a multisystem disturbance capable of involving the neurological, immunological, and muscular systems, among others. In this report, we describe five patients with severe head injury who developed marked hypophosphatemia (less than 1 mg/dl) within 24 hours of hospitalization. This fall in serum phosphate coincided with the induction of respiratory alkalosis consequent to mechanical ventilation. In four of the five patients, as acid-base parameters returned to normal, serum phosphate values rose, in all instances reaching values greater than 2.5 mg/dl. Urinary phosphorus excretion, ordinarily negligible after hypophosphatemia induced by hypocapnia, was still present in Cases 1 and 4 (greater than 600 mg/24 hours). This is unexplained by any of the known hormonal or fluid alterations that accompany head injury. These five patients developed severe, yet transient, hypophosphatemia that resolved upon correction of hyperventilation-induced acid-base abnormalities. We discuss the pathophysiology of this entity and the implications for the head trauma patient.     

Brain injury without head injury after multiple trauma

Watershed infarction has previously been described after cerebral trauma, when it is due to raised intracranial pressure or systemic hypotension. A case is reported, so far as is known for the first time, of bilateral watershed infarction following blunt systemic trauma, without injury to the head or neck. The importance of resuscitation in preventing secondary brain injury caused by systemic hypotension is highlighted. The advantages of HMPAO-SPET in detecting cerebral perfusion defects are discussed.     

Fluent aphasia after closed head injury

A case of post-traumatic, contre-coup Wernicke's aphasia resulting from left posterior temporal hemorrhagic contusion localized by angiography and CAT scan is reported. Categorization of aphasia is reviewed, emphasizing that a fluent language disorder can be elusive to laymen and non-neurologically oriented physicians.     

Subjective symptomatology after traumatic head injury

Background: Controversy persists regarding the reasons for persistent subjective complaints after mild traumatic head injury (THI). Statement of purpose: To evaluate the influence of injury severity, psychological factors, and financial contingencies on symptomatology after THI. Methods: Subjective complaints about cognitive, emotional, and somatic symptoms, as assessed by a standardized self-report inventory (Minnesota Multiphasic Personality Inventory-2; MMPI-2) were evaluated in 150 patients with THI. Results: Individuals with mild THI demonstrated paradoxically greater symptomatology on the MMPI-2 than patients with moderate-to-severe THI. Furthermore, specific actuarial criteria for possible symptom magnification (Fake Bad Scale) were met about twice as often in patients with mild THI who were seeking financial compensation for alleged acquired dysfunction than in patients with mild THI without such external contingencies. Conclusion: The evaluation of persistent subjective complaints after THI should consider injury severity in concert with psychological and financial/motivational factors. Great caution should be taken in attributing persistent symptomatology after mild THI to cerebral dysfunction.     

Driving after a severe head injury

The driving activities of 50 head-injury survivors were surveyed 6 months or more post-discharge. Of these, 21 (42%) possessed a valid drivers licence, but only 19 (38%) were actually operating motor vehicles at follow-up. Only measures of spatial/perceptual deficits were found to discriminate between groups of drivers and non-drivers. The recommendations of rehabilitation staff did not appear to have much influence on the final decision whether or not the survivor resumed driving activities. Most of the drivers did not report post-injury accidents or traffic violations, perhaps because several participants were restricting their driving activities. The willingness voluntarily to restrict driving behaviours may offer some head-injury survivors the opportunity to continue to enjoy this important daily living activity under selected circumstances.