Heat-damaged red cell scan for intraoperative localization of the accessory spleen.

Destruction of platelets by the reticuloendothelial system in immune thrombocytopenia purpura (ITP) is enhanced by platelet-associated IgG. Relapse after splenectomy may result from IgG produced in the accessory spleen. These structures may be located at any site between Gerota's fascia and the left ovary or testicle as well as adjacent to the spleen. The heat-damaged red cell scan (HDRCS) has been demonstrated to be an accurate method for identifying accessory spleens. HDRCS using semi-in vitro labeling of the patient's red blood cells with technetium 99m pertechnetate delineated accessory splenic tissue as the etiology of post-splenectomy relapse three times in two patients 3 to 9 months postoperatively. A labeled intraabdominal probe and HDRCS were subsequently used by the surgical team for identification and excision of the accessory spleen. Four additional patients underwent splenectomy for ITP between 1989 and 1992; heat-damaged red blood cells were injected after the major splenic tissue was removed. Accessory spleens were identified in two patients. All patients were discharged within 6 days, without perioperative complications. Two patients currently require steroids. The techniques of intraoperative HDRCS allow rapid localization and removal of the accessory spleen at the time of laparotomy. Evidence of growth of accessory splenic tissue postsplenectomy was demonstrated.

Antiserum to endotoxin in hemorrhagic shock.

Antiserum to Escherichia coli J5, a mutant endotoxin (LPS) which contains only core determinants, has proven effective in reducing mortality from endotoxic shock due to a wide variety of gram-negative bacteria. Twenty New Zealand white rabbits with coliforms in the gut were subjected to hemorrhagic shock of 36 mm Hg for 3 hr. Treated rabbits were resuscitated with 15 cc of rabbit J5 antiserum (hemagglutinating antibody titer against J5 lipopolysaccharide of 1:1024), remaining shed blood, and lactated Ringer's to achieve a mean arterial blood pressure (MABP) within 20% of baseline. The control group was similarly resuscitated but received 15 cc normal rabbit serum (titer 1:2). Catheters were removed and rabbits were returned to their cages until death or 5 days of survival. Hemodynamic parameters (heart rate, MABP, cardiac output, and total peripheral resistance) did not differ significantly between groups. However, six treated rabbits survived 5 days (60%) and no control rabbit lived past the third postexperimental day (P less than 0.019). Our data suggest that systemic endotoxemia may contribute to morbidity and mortality in severe hemorrhagic shock.

Improved survival with primary anastomosis in the low birth weight neonate with esophageal atresia and tracheoesophageal fistula.

Management of esophageal atresia with tracheoesophageal fistula (TEF) has evolved over the past 5 years at Children's Hospital and Medical Center, Seattle, in the premature patient weighing less than 2.5 kg. Traditionally, these low birth weight infants underwent gastrostomy and fistula ligation followed by repair after a period of weight gain. However, since 1980, of the 31 neonates weighing 2.5 kg or less with type-C TEF, a primary repair was performed in 22 within the first five days of life. There were no mortalities and only one subclinical anastomotic leak. All anastomoses were done extrapleurally in a single-layer interrupted fashion. Staged repair was elected for nine neonates. Seven had severe respiratory distress requiring mechanical ventilation and two in the staged group expired prior to repair. The survival for the entire group of 31 neonates was 94%. Primary repair may be performed safely in the premature neonate. The presence of severe pulmonary disease is the critical factor that might necessitate a staged repair.

Individualized management of colonic atresia.

Atresia of the colon represents the least common cause of neonatal intestinal obstruction, comprising less than 10 percent of gastrointestinal atresias. Eleven patients underwent surgical repair of colonic atresia during a 5 year period. Five of the patients were premature. Two had associated gastroschisis and other congenital anomalies were present in three patients. Hypaque enema was utilized to diagnose intestinal atresia and laparotomy was then undertaken. Primary repair could be performed in four patients, one with type I and three with type 3 atresias. These four patients did well and were discharged within 13 days after operation. Three deaths occurred in patients with associated anomalies, yielding a mortality rate of 28 percent. Operative therapy of colonic atresia should be individualized, based on the condition of the patient at presentation and the presence of associated birth defects.

Maternal serum alpha-fetoprotein is a marker for fetal anomalies in pediatric surgery.

Maternal serum alpha-fetoprotein (MS-AFP) screening has become part of routine obstetric care. Although elevated MS-AFP was originally associated with neural tube defects (NTD), it is also able to detect several fetal anomalies of interest to a pediatric surgeon, ie, ventral abdominal wall defects, intestinal atresias, and sacrococcygeal teratomas. Previously, decreased MS-AFP had only been associated with fetal trisomies, but not surgically correctable lesions. In the present study, we review our recent experience with both elevated and decreased MS-AFP as a marker to detect fetal anomalies of concern to the pediatric surgeon. Forty-one fetal anomalies were associated with 333 pregnancies referred for follow-up after abnormal MS-AFP screening results from November 1985 through November 1986. One hundred ninety-six were elevated and 139 were decreased. In most cases, evaluation included counseling, repeat MS-AFP, level II ultrasound, and amniocentesis. This revealed elevated MS-AFP to be associated with 32 (16.3%) anomalies (2 NTD, 5 anencephalics, 5 ventral abdominal wall defects, 1 stage IV-S neuroblastoma, 1 renal anomaly, 1 ventriculomegaly, 15 fetal demises, and 2 fetal-maternal bleeds). Decrease in MS-AFP was associated with nine (6.4%) anomalies (2 congenital diaphragmatic hernias, 3 Down's syndrome, 1 Turner's syndrome, 2 duodenal atresias, and 1 choroid plexus cyst). In this study, MS-AFP detected several fetal anomalies known to be associated with abnormal MS-AFP and three anomalies not previously described (congenital diaphragmatic hernia, neuroblastoma, and choroid plexus cyst). Elevated as well as decreased MS-AFP are significant and should be pursued by a full prenatal evaluation.(ABSTRACT TRUNCATED AT 250 WORDS)

Humoral factors in primate endotoxin shock.

Many biologically active substances are released from the cell in endotoxic shock and thought to contribute to morbidity and mortality. Whether or not these substances are independently toxic or require endotoxin as a catalyst is uncertain; 20 mg/kg E. coli endotoxin was infused into seven rhesus (R) macaca monkeys (toxin donor). Seven R macaques received an equivalent volume of normal saline (control donor). Animals were monitored for 12 h and lactated Ringer's was infused to maintain a minimum MABP of 40 mmHg. Donor animals were exsanguinated; plasma was extracted and a Limulus lysate assay (LAL) was utilized to determine the approximate amount of endotoxin present in toxin donor plasma. This volume of endotoxin (0.125 mg/kg) was added to control donor plasma. Plasma was infused into seven toxin receivers and six control receivers. Receiver animals were monitored for 24 h and killed after 3 d. Lungs were evaluated histologically for evidence of acute injury. Five of the seven toxin receivers and no control receivers died within 3 d (P less than .005). Significantly more hemorrhage occurred in toxin receivers (P less than .01). Our data suggest a humoral factor present in the plasma of toxin donor capable of promoting tissue injury and death of recipient animals independent of endotoxin.

Lung abscess: a changing pattern of the disease.

Alcoholic stupor with aspiration has been the most commonly recognized cause of lung abscess. Eighty-nine patients treated for lung abscess in a large community hospital from 1968 through 1982 have been described. Forty-six percent of these patients were 60 to 80 years of age. The most common predisposing factors included pneumonia, immunosuppression steroid therapy, carcinoma at a distant site, alcoholism, and lung cancer. Surgical therapy was employed in 23 patients when there was suspicion of cancer and failure to improve with medical management. Fifty-seven percent of patients were either cured or improved at the time of discharge. Twenty-nine percent died from other causes during hospitalization, and 9 percent died as a direct result of the abscess. Thus, the patients encountered in the community hospital setting tended to be older and had a wide variety of illnesses that precipitated the development of lung abscesses.