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Inflammation of the appendix is a common cause of acute abdominal pain. The etiology and pathophysiology of appendicitis have been well described. The initiating factor often is obstruction of the appendiceal lumen by inspissated stool, barium, food, parasites, or hyperplastic lymphoid tissue. Two patients have been identified who developed appendicitis temporally related to blunt abdominal trauma, without other clear etiology. Although absolute documentation of trauma as an etiologic factor in these cases is difficult, theoretical mechanisms for the occurrence are discussed. In the setting of right lower quadrant pain following mild to moderate blunt abdominal trauma, acute appendicitis should be considered as a possibility.

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Two hundred eleven patients with adenocarcinoma of the pancreas were reviewed. Seventy had surgically constructed biliary-enteric anastomoses. Forty-two had percutaneous/endoscopic placement of biliary diversion catheters. Surgical biliary diversion was associated with discharge at 7 +/- 2 days postoperatively. Only five patients required subsequent reoperations for anastomotic failure secondary to continued tumor growth. Sixty-one percent of percutaneous/endoscopic catheters were associated with septicemia, and 27% occluded (average life span 36 days). Hospital days averaged 20 days of an average 64-day patient life span. After evaluation of computed tomographic scans and surgical findings, patients' diseases were arbitrarily divided into (A) local, (B) regional, and (C) distant spread. Survival was 417,300, and 53 days, respectively. In view of the morbidity associated with the percutaneous/endoscopic catheter, we recommend that its use be restricted to Group C patients.

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Blunt trauma accounts for 3% to 10% of cervical vessel injuries. Death and severe neurologic impairment have been reported in more than 80% of blunt carotid injuries. In our recent experience, 10 patients sustained 18 blunt cervical arterial injuries: two internal carotid artery (ICA) dissections, three ICA transections with pseudoaneurysm, five ICA thromboses, two vertebral artery dissections, one vertebral artery transection with pseudoaneurysm, one vertebral artery thrombosis, one minimal vertebral artery injury, and three caroticocavernous fistulas. A delay of more than 12 hours in making the diagnosis occurred in seven of the 10 patients. The mental status was initially normal in seven patients. The subsequent development of focal neurologic findings incongruent with CT scanning of the head prompted four-vessel angiography. Treatment was individualized and included supportive management, intravenous heparin, ligation, extracranial-intracranial bypass, and radiologic embolization. We have developed an angiographic classification that may aid management. Early angiography in patients with neurologic findings incongruent with head CT scan or in whom a normal sensorium and hemiparesis are present may permit improved outcomes. We advocate direct operative repair for accessible lesions of recent onset. For surgically inaccessible lesions, those with delayed presentation or in some cases with a fixed neurologic deficit, intravenous heparin can be started and follow-up angiography, head CT scanning, and the patient's clinical status determine further therapy.

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Cats were subjected to a 3.5-atm fluid percussion impact administered to the cerebral cortex. Near-infrared spectrophotometry (NIRS) was used to measure the quantity of oxyhemoglobin and total hemoglobin in the illuminated tissue as well as the cytochrome a, a3 redox state. Corroborative data were obtained by freezing brains with liquid nitrogen and measuring cortical concentrations of ATP, creatine phosphate (CP), and lactate. Immediately postimpact there was a rise in mean arterial pressure with a 38% increase of highly oxygenated blood and a shift toward oxidation in the cytochrome a, a3 redox state. By 4 hours postimpact, cytochrome a, a3 was becoming progressively reduced despite the persistence of hyperemia. This was associated with a significant (p less than 0.01) decrease in ATP and CP concentration. Additional studies in which a 0.5-sec, 100-v electrical seizure was induced before and after fluid percussion demonstrated significant differences in seizure response, indicating a failure of autoregulation.

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Intracranial pressure was increased in cats by infusing 'mock' CSF intracranially, thus decreasing cerebral perfusion and oxygenation. The cats then randomly received either 50% O2 or 50% O2-5% CO2 by inhalation. As monitored by in vivo near-infrared spectroscopy (NIR), no improvement was noted after 50% O2 whereas 50% O2-5% CO2 resulted in increased perfusion, an oxidation of cytochrome a,a3, an increase in oxyhemoglobin, and reduced quantities of de-oxyhemoglobin (p less than 0.01) despite a further increase in intracranial pressure. The authors conclude that: NIR is a useful means of noninvasively and directly assessing brain metabolism and has advantages over simple ICP monitoring; and continued investigations of CO2 as a possible therapeutic modality after head injury appear warranted.

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We studied the effect of nifedipine, a calcium entry blocker, on the recovery of cerebral adenosine triphosphate (ATP), creatine phosphate (CP), and lactate levels following resuscitation from cardiac arrest. Using the cardiac arrest and resuscitation model of de Garavilla, Babbs, and Tacker with an arrest time of eight minutes, 76% of the animals arrested were resuscitated with an average intermittent abdominal compression-CPR time of 3.3 minutes. Rats were assigned randomly to the following groups: nonischemic; eight minutes of arrest without resuscitation; and postresuscitation treatment with either IV normal saline; 3 micrograms/kg nifedipine; 10 micrograms/kg nifedipine; or 30 micrograms/kg nifedipine. Treated animals were sacrificed at either 20 or 120 minutes thereafter. As expected, after eight minutes of cardiac arrest, the levels of ATP and CP dropped to near 0 and rebounded in all resuscitated animals. By 120 minutes after resuscitation, rats given the 10-micrograms/kg dose of nifedipine had levels of ATP equivalent to nonischemic values. Return of CP values to nonischemic levels was seen only at the 3-micrograms/kg dose and was independent of time of measurement. The ATP and CP levels in these nifedipine-treated groups were significantly better when compared to saline-treated controls. There were no treatment-dependent differences in lactate levels. We conclude that clinically appropriate doses of nifedipine had a beneficial effect on the recovery of cerebral high-energy phosphates after cardiac arrest and resuscitation.

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Two experiments were conducted to assess the feasibility of near infrared spectrophotometry (niroscopy) to monitor directly the effects of increased intracranial pressure on brain metabolism. ICP was increased in cats by subarachnoid infusion of a "mock" CSF solution. Cytochrome a,a3 redox state, oxyhemoglobin, deoxyhemoglobin and cerebral blood flow were noninvasively and continuously monitored by niroscopy. The results of both experiments indicated that changes in ICP correlated with a reduction in cytochrome a,a3 redox state (p less than 0.01), a decrease in the quantity of oxyhemoglobin and cerebral flow (p less than 0.01) and an increase in deoxyhemoglobin. The study results suggest that niroscopy has the potential for providing noninvasive and continuous data for assessing brain metabolic activity. The correlations obtained with simultaneous measurements of intracranial pressure make this an attractive method for application to those at risk for increased intracranial pressure.

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Two experiments were conducted to assess the feasibility of near infrared spectrophotometry (niroscopy) to directly monitor the effects of increased intracranial pressure on brain metabolism. Intracranial pressure (ICP) was increased in cats by subarachnoid infusion of a "mock" CSF solution. Cytochrome a,a3 redox state, oxyhemoglobin, deoxyhemoglobin and cerebral blood flow were non-invasively and continuously monitored by niroscopy. The results of both experiments indicated that untreated increases in ICP correlated with a reduction in cytochrome a,a3 redox state (p less than 0.01), a decrease in the quantity of oxyhemoglobin and cerebral blood flow (p less than 0.01), and an increase in deoxyhemoglobin. This study suggests that niroscopy has the potential for providing noninvasively and continuously data assessing brain metabolic activity. The excellent correlations obtained with simultaneous direct measurements of intracranial pressure make this an attractive method for eventual application to humans at risk for increased intracranial pressure. The value of niroscopy is even more evident in Exp. II where it can be seen that knowledge only of ICP would give the physician a false sense of security, whereas direct, non-invasive, continuous assessment of brain perfusion and oxygenation may well prove to be more appropriate parameters to monitor.

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Intracranial pressure was increased in cats by infusion of "mock" cerebrospinal fluid into the cisterna magna. This condition was then treated by hyperventilation. In addition to direct measurement of intracranial pressure, cerebral metabolism was assessed by near infrared spectrophotometric (niroscopic) measurement of cytochrome a,a3 redox state and the quantity of reduced and oxygenated hemoglobin in the illuminated brain. Cerebral perfusion was assessed by injection of Cardio-Green. Increased intracranial pressure resulted in the expected reduction in cytochrome a,a3,a decrease in HbO2, an increase in Hb, and a reduction of blood flow. The vasoconstriction produced by hyperventilation, while reducing intracranial pressure, produced a further reduction in cytochrome a,a3 and HbO2, with no improvement in blood flow. The data illustrate the fallacy of governing therapy solely by intracranial pressure and demonstrate the need for a direct assessment of brain metabolism. The data also demonstrate the strengths and weaknesses of niroscopy as a noninvasive monitor of the brain metabolism if applied to patients at risk for increased intracranial pressure.

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Current clinical methods for assessing fetal oxygenation in labor are indirect and remain somewhat imperfect. Since infrared light passes through the cranium and infrared light absorbance by tissues has been shown in adult animals to vary with oxygenation, monitoring of infrared light absorbance may serve as the basis for a new, more direct technique for the assessment of fetal condition. Described here is the application of infrared reflectance spectrophotometry to a fetal sheep model and the precision of the relationship between fetal arterial or venous PO2 and infrared light absorbance at selected wavelengths. A very strong, linear correlation (r = 0.915) was found between fetal arterial PO2 and intracranial infrared light absorbance according to an algorithm developed for selective monitoring of the state of hemoglobin oxygenation in tissue. With further development, this method holds promise for a more direct, noninvasive assessment of fetal condition in labor than is currently available.

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Treatment of respiratory insufficiency using continuous positive pressure ventilation (CPPV) with positive end-expiratory pressure (PEEP) is often associated with high airway pressures and large tidal volumes resulting in parenchymal damage and an exacerbation of ventilation/perfusion mismatch. High-frequency jet ventilation and high-frequency oscillation purportedly provide adequate ventilation and might preclude these harmful side effects. Few data exist comparing these methods in a model of respiratory insufficiency. Respiratory insufficiency was produced in three groups of six rabbits by 15 pulmonary lavages with saline (35 ml kg-1) to remove surfactant, following which ventilation for the subsequent 5 hr was as follows: group I, CPPV with a frequency of 60 bpm, and a minute volume of 400 ml min-1 kg-1; group II, oscillatory ventilation with a loudspeaker system delivering a tidal volume of 6-8 ml at a frequency of 5 Hz; and group III, jet ventilation with volumes of 6-8 ml at a frequency of 5 Hz. All groups were ventilated with a PEEP of 10 cm H2O and a FiO2 of 1.0. Arterial blood samples were taken every hour. All three methods provided adequate oxygenation without important differences. The arterial pCO2 rose in all three groups owing to the seriousness of the respiratory insufficiency created. This rise was the highest with oscillatory ventilation. Three of the six rabbits deteriorated after 3 hr of jet ventilation and died with elevated pCO2S with pO2S with bloody edema coming out of the trachea. Because of this apparent damaging effect of jet ventilation and because oscillatory ventilation achieved the same gas exchange but at lower airway pressures as compared to jet ventilation and CPPV, it is thought that oscillatory ventilation is superior over both jet ventilation and CPPV for application in respiratory insufficiency.

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Recent reports have demonstrated the efficacy of Fluosol-DA (20%) as a temporary erythrocyte substitute. We investigated two groups of pregnant ewes that underwent exchange transfusion. In group 1, the animals underwent a nearly total isovolemic exchange of Fluosol-DA (20%) for maternal whole blood; in group 2, the red blood cells were removed and the plasma along with Ringer's lactate was replaced isovolumetrically. Although group 1 animals received 100% oxygen and Fluosol-DA (20%), the maternal arterial P02 increased to 350 to 400 torr. However, the maternal blood oxygen content decreased during the exchange, with no change in fetal pH, Pco2, or hematocrit. Maternal blood pressure remained stable and there was a 40% to 50% increase in cardiac output and mean pulmonary arterial pressure. During the exchange, the maternal hematocrit decreased from a mean of 32% to 5.5%; the maternal fluorocrit at the end of the exchange was 9%. Throughout the Fluosol-DA (20%) exchange, the proportion of fetal brain oxyhemoglobin as estimated from infrared transcranial transmittance increased, as did the fetal blood P02 and oxygen content. In group 2, the maternal mean blood pressure decreased, and the hematocrit decreased from a mean of 32% to 8%. Despite an increase in the maternal P02 to 250 torr, the fetal P02 and oxygen content decreased in group 2. This investigation demonstrated that Fluosol-DA (20%) exchange of the mother does not impair delivery of oxygen to the fetus under the conditions of the study.

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Many trauma victims who have hemorrhagic shock are also intoxicated. Ethanol could worsen the severity of shock and decrease the amount of blood loss necessary to reach or maintain the shock state, perhaps by increasing lactic acidosis. We examined the effect of ethanol on lactic acidosis in a group of rats that were intoxicated, then put in a state of hemorrhagic shock (MAP = 40 mm Hg). These animals were compared to a control group that were in a similar state of hemorrhagic shock but not intoxicated. The volumes of blood necessary to reach and maintain the predetermined model state of shock for two hours in each group were also measured. The animals were paralyzed and placed on controlled ventilation. The ethanol produced an expected baseline lactic acidosis, and it took significantly less blood volume loss to keep the intoxicated group in shock. However, during shock there was no significant difference in the state of lactic acidosis. These results suggest that acute ethanol intoxication made the animals more sensitive to hemorrhage. This effect was not mediated by an increase in lactic acidosis in our model.

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Rats were subjected to 30 minutes of hypoxic-hypotension and then allocated to one of four treatment groups. Group I was resuscitated by restoration of FIO2 = 30% and reinfusion of shed blood plus an equal volume of additional saline. Group II received in addition nifedipine, 10 micrograms/kg, and groups III and IV received in addition either verapamil, 0.2 mg/kg or 1 mg/kg, respectively. Significantly (P less than 0.01) higher concentrations of creatine phosphate and ATP were present in the brain after nifedipine and after 1 mg/kg verapamil treatment.

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Considerable controversy exists regarding the optimal method of surgical relief of the pain of chronic pancreatitis. We previously made a retrospective study of 49 patients with chronic pancreatitis who were operated upon only for relief of pain. Those results indicated that patients who had an internal decompression had lower mortality, less morbidity, less postoperative pancreatic insufficiency, and better relief of pain (88% vs 76% improved). Since then, we have prospectively determined the operative treatment based upon the criteria outlined in that previous report. Seventeen patients had 19 operations (12 resections, seven internal drainage procedures). The patients' ages, duration of symptoms, and sex distribution are similar. Eight-five percent of patients with internal decompression had good to excellent relief of pain vs 60% of patients with resection. Pancreatic insufficiency occurred in 70% of patients who had resection and in only 14% of those who had drainage. Forty percent of patients who had resection had mild to severe postoperative morbidity vs 14% of those who had drainage. There was one postoperative death in the resection group. These preliminary results indicate that internal decompression in properly selected patients can provide superior relief of pain, with lower mortality, less morbidity, and less pancreatic insufficiency.

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The beneficial vs deleterious effects of hypothermia superimposed on hypoxia and hypotension have been argued and are clinically important. In this study, cerebral cytochrome a,a3 redox state and the quantity of intracerebral oxygenated hemoglobin (HbO2) were measured continuously and noninvasively in rats subjected to hemorrhagic hypotension (MAP = 30 mm Hg) and hypoxia (F1O2 = 7.5%) utilizing near infrared spectrophotometry. Prior to the experiment the rats were briefly respired on 100% oxygen to establish 100% oxidation of cytochrome a,a3 and hemoglobin, and at the conclusion of the experiment they were respired on 100% nitrogen to establish 100% reduction. Data are reported as percent oxidation within this range at baseline and after 15 and 30 min of hypoxic hypotension. Arterial blood gases were measured. Body temperature as monitored by a rectal probe was altered by placing anesthetized-paralyzed rats inside a circulating water jacket. Three groups of rats were studied: 38, 33, and 22 degrees C. Group III rats had a significantly (P less than 0.01) greater quantity of intracranial HbO2 than group I or II. Since MAP was held constant at 30 mm Hg, we assume this is largely due to the higher (P less than 0.01) arterial PO2 in group III (101.5) compared to group I and II (48.5, 51.3). Both groups II and III had a significantly (P less than 0.01) greater oxidation of cytochrome a,a3 indicating greater oxygen availability for a given metabolic rate. This was associated with improved survival inasmuch as all rats in groups II and III lived, and only one group I rat survived. It can be concluded that, as used in this study, hypothermia is beneficial and deserves further investigation.

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