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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.

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.

Nine medical centers collaborated in a prospective randomized study to evaluate prolonged extracorporeal membrane oxygenation (ECMO) as a therapy for severe acute respiratory failure (ARF). Ninety adult patients were selected by common criteria of arterial hypoxemia and treated with either conventional mechanical ventilation (48 patients) or mechanical ventilation supplemented with partial venoarterial bypass (42 patients). Four patients in each group survived. The majority of patients suffered acute bacterial or viral pneumonia (57%). All nine patients with pulmonary embolism and six patients with posttraumatic acute respiratory failure died. The majority of patients died of progressive reduction of transpulmonary gas exchange and decreased compliance due to diffuse pulmonary inflammation, necrosis, and fibrosis. We conclude that ECMO can support respiratory gas exchange but did not increase the probability of long-term survival in patients with severe ARF.

Previous work by the authors has established decreased brain ATP concentration after a combined hypoxic-hypotensive episode. This study was undertaken to determine what changes, if any, occur in brain norepinephrine (NE), dopamine (DA), and serotonin (5HT) concentration in association with hypoxia and hypotension, and to correlate any observed changes with simultaneously measured ATP concentrations. Rats were subjected to a 30-minute period of hypoxia (F102 = 0.075) and hemorrhagic hypotension (MAP = 30 mm Hg) and then resuscitated. Significant increases (P less than .05) in cortical 5HT were observed at a time when ATP concentration was significantly (P less than .005) reduced. Additional experiments were conducted on rats depleted of 5HT by prior treatment with 5,7-dihydroxytryptamine. Equal decreases in ATP concentration were measured, and the cardiovascular response to hypoxic hypotension in 5HT-depleted rats was similar to that in 5HT-intact rats. We conclude that the increased 5HT after hypoxic hypotension does not cause the decreased ATP concentration, nor does 5HT play a major role in cardiovascular homeostasis under the conditions of this experiment.

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.

The clinical management of 47 patients with vascular injuries of the extremities is presented with emphasis on functional results. The method of restoration of vascular continuity or the presence of associated fractures or venous injury had little bearing on either the success of arterial repair or functional result. The most significant factor adversely affecting restoration of extremity function was the presence of associated major proximal nerve injury.

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.

An experimental model was examined in which rats were subjected to 30 minutes of hemorrhagic hypotension and hypoxia. In addition to resuscitation by infusion of blood and saline and increasing the fraction of inspired oxygen (FIO2), the possible beneficial effects of including intravenous epinephrine as part of the resuscitative regimen were studied. Mean arterial pressure, cortical microflow, and brain tissue oxygen tension were increased after epinephrine (P less than 0.05). Cortical ATP concentration was decreased after hypoxic hypotension and failed to improve after epinephrine.

An investigation of the effect of glucagon on liver high energy phosphate concentration during a low flow state is presented. Two groups of dogs were subjected to a 120-minute period of hemorrhagic hypotension followed by reinfusion of shed blood plus additional normal saline to restore the central venous pressure to 10 cm H2O. One group received glucagon intravenously in addition. Despite a significant increase in portal flow and oxygen delivery and a significant increase in liver glucose associated with glucagon administration, there was significant impairment in the ability of the liver to regenerate adenosine triphosphate (ATP). Evidence is presented to show the decreased ATP concentration was not related to hepatic blood flow, but was presumably due to increased catabolism.

We have previously implicated uncoupling of oxidative phosphorylation and the associated decreased concentrations of tissue adenosine triphosphate (ATP) in the liver and brain as major factors contributing to death after hypoxia and hypotension. To determine if intravenously administered ATP-MgCl2 complex would result in increased liver and/or brain concentration of ATP, rats were pretreated with intravenous ATP-MgCl2 prior to exposing them to hypoxic-hypotensive stress. In this preliminary work, pretreatment was selected based on the premise that such an experimental design was most apt to demonstrate an effect if such existed. Baseline cerebral cortical and liver ATP and lactate concentrations were obtained immediately after the intravenous infusion of either saline (control group) or ATP-MgCl2 (treated group). ATP and lactate concentrations were again determined after 30 min hypoxic-hypotension and 20 min after resuscitation. ATP-MgCl2 pretreatment resulted in a modest increase in hepatic ATP concentration when measured after 30 min of hypoxic-hypotension. This increase was not evident 20 min later. No increases in cerebral ATP concentrations were noted at any sample time after ATP-MgCl2 pretreatment.

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.

Rats were "stressed" by a 30-minute period of breathing 7.5% oxygen combined with hemorrhagic hypotension (x arterial pressure = 25 mm Hg), and then "resuscitated" by restoring the inspired oxygen concentration to 30% and reinfusing the blood previously removed to produce hypotension. We have previously noted in initial return of brain adenosine-triphosphate to normal after this "stress" followed by a progressive decline during the post-resuscitation period. In this study, substrate deficiency was investigated as a possible etiology for the decreased adenosine-triphosphate. Glucose and glucose-6-phosphate concentrations in the brain were measured before "stress" and after resuscitation and were found not to change, indicating no deficiency of substrate.

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.

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.