52 COBALT CONCENTRATIONS IN URaeMIC MYOCARDIUM
drainage with widely known.
I
a
fine needle
Pædiatric Department, Charing Cross Hospital, London W6 8RF
*Normal values
(in 0.001-0.018) fLglg.
15
men
and 5
women
aged 12-65)
0.012
cannula deserves
to
be
more
RICHARD GRAY HERBERT BARRIE
HYDROPS FETALIS ASSOCIATED WITH SMALL-BOWEL VOLVULUS
(range
common, other with fetalis are increasing hydrops being recognised frequency.’ We describe here a case of non-immunological hydrops fetalis in a patient with an intrauterine small-bowel volvulus. A male baby weighing 2700 g was born at term after a normal pregnancy. Fetal bradycardia was present before delivery, and the Apgar score at 1 min was 2. The baby was oedematous, lethargic, and cyanotic and had a distended abdomen. He was put on artificial ventilation. The heart-rate was 110/min with a gallop rhythm; blood-pressure 60/40 mm Hg; central venous pressure (via umbilical venous line placed above the diaphragm) 20 mm Hg. The abdomen was distended and firm; pupils were mid-position and non-reactive, and the extremities were flaccid, except for intermittent seizure activity. Multiple petechize were present. Haemoglobin 7.1g/dl; hwmatocrit, 21.9%; white blood-cells, 28 600/fl-I, with 3% metamyelocytes, 6%
SIR,-As Rh-isoimmunisation becomes less
causes
These results support our belief that trace elements may be very important in renal failure. In particular, cobalt may be one, or even the prime, astiological agent for ursemic cardio-
myopathy. Information on other trace elements and a discussion of their possible metabolic roles and the hasmodynamic results from patients with progressive renal failure will be presented elsewhere. Department of Medicine, KENNETH PEHRSSON Karolinska Hospital, LARS-ERIC LINS S-104 01, Stockholm, Sweden
DECOMPRESSION OF HYDROCEPHALUS DURING DELIVERY
SIR,-The finding of fetal hydrocephalus in late pregnancy raises obstetric and ethical problems. Crude destructive operations are no longer acceptable, and the perforator and cranioclast are instruments of the past. Although gross hydrocephalus is not compatible with normal survival, it is often important to the parents that the baby dies not during birth, but of natural causes afterwards. The obstetrician has to choose between vaginal delivery and elective section, and an important consideration is the extent to which the size of the head can be reduced safely. A 26-year-old primigravida had a normal pregnancy until 34 weeks when hydrocephalus was diagnosed by ultrasound and X-ray. She went into spontaneous labour at 38 weeks but after a short trial of labour no descent of the fetal head had occurred and a lower-segment cxsarean section was done. The head was delivered with considerable difficulty, necessitating wide skin and uterine incisions. The baby, a girl with gross hydrocephalus and a lumbar meningomyelocele, survived for 6 days. With the parents’ consent, the head was decompressed after death using a 12 gauge ’Medicut’ cannula inserted through the lateral angle of the anterior fontanelle. 1370 ml of fluid was drained and the following changes in head size were noted:
Anteroposterior diameter (cm) Biparietal diameter (cm) Head circumference (cm) The operative delivery in this case would certainly have been easier if drainage had been used, and the baby would probably have survived this relatively atraumatic procedure. A similar technique was described by O’Connor and Gorman in 1942.’ They used a spinal needle to drain the head during vaginal delivery, 1400 ml of fluid being removed in 25 min; the delivery was normal and the baby lived for 2 h. Intraventricular puncture was recommended as the method of choice, especially where the delivery of a live baby is ethically important. Alternative methods using catheters or more traumatic procedures are still advocated. This simple technique of 1. O’Connor, C. T., Gorman, A.
or
J. Am. J. Obstet. Gynec. 1942, 43, 521.
of
myelocytes, 10% bands, 8% polymorphonuclear neutrophil leucocytes, 70% lymphocytes, and 3% monocytes. There were 50 nucleated red blood-cells per 100 white blood-cells. Bloodshowed occasional fragmented erythrocytes, and marked anisocytosis, poikilocytosis, and polychromatophilia. There was no hypochromia. Reticulocyte-count 11-2%; platelets 60 000/jjd; prothrombin-time 21.2 s (control 11 -2); partial thromboplastin-time 116 s (control 41-4); fibrinogen, 130 mg/ml. Blood group 0+ (mother 0+). Direct and indirect Coombs tests negative. Bilirubin less than 0-2 mg/dl. Haemoglobin electrophoresis normal for age. Bone-marrow aspirate showed normoblastic hyperplasia. No fetal erythrocytes were found in maternal blood at 48 h (Kleihauer-Betke technique). An abdominal X-ray at 15 h showed no gas below the level of the stomach. Bacterial and viral cultures of blood, urine, throat, stool and nasopharynx were negative. The rubella titre was 1/20; cytomegalovirus and toxoplasmosis titres negative; herpes-simplex titre 1/8. An exchange transfusion was performed and antibiotic therapy was started. Emergency laparotomy at 27 h of age revealed a mid-gut volvulus with infarcted necrotic bowel and a large amount of blood in the abdominal cavity. The small bowel was resected and reanastomosed end-to-end from the ligament of Treitz to the terminal ileum about 1 -cm from the ileocxcal valve. The infant’s condition deteriorated and he died 34 h after birth. The surgical specimen and necropsy revealed hxmorrhagic necrosis of jejunum and ileum with extravasation of blood obscuring the normal architecture. Generalised oedema is a well-known complication of severe fetal anaemia.I,2 Besides erythroblastosis fetalis, causes of anaemia in the newborn such as transplacental transfusion between monochorionic twins, marrow replacement by neuroblastoma, homozygous a-thalassaemia, chronic infections, and fetomaternal bleeding have been reported to cause hydrops fetalis.’I The haematological data pointed to chronic blood-loss or haemolysis as a cause of the anaemia. The low bilirubin and the absence of blood-group incompatibilities suggested bleeding into the abdominal cavity as the predominant reason for this patient’s anaemia. Disseminated intravascular coagulation smear
1. 2.
Turberville, D. F. and others. Obstet. Gynec. 1973, 43, 567. Lewy, J. E., Moel, D. I. Clin. Perinat. 1975, 2, 117.
53 leads to red-cell fragmentation and hxmolysis. However, anaemia of this severity due to haemolysis of any kind would have produced a much higher bilirubin. Other factors such as decreased oncotic pressure3 (serumalbumin not available) and the loss of plasma volume described in association with bowel obstruction4 may have played important contributory roles in the pathogenesis of the oedema. We thank Dr Rowena
Spencer
and Dr Norman
Woody for
C.E.A. CONCENTRATIONS
(ng/ml) IN PLEURAL EFFUSIONS AND PLASMA
I
I
review-
ing the manuscript. Department of Pediatrics, Tulane University School of Medicine, New Orleans, Louisiana 70112, U.S.A.
JANE F. SEWARD JAIME ZUSMAN
CONCURRENT ASSAYS OF PLASMA AND PLEURAL-EFFUSION LEVELS OF CARCINOEMBRYONIC ANTIGEN IN THE DIAGNOSIS OF PULMONARY DISEASE concentrations of carcinoembryonic have been demonstrated in the plasma of patients with many different types of neoplasia including carcinomas of the colon5and bronchus.6The c.E.A. value seems to vary with the stage of disease and the quantity of tumour or the use of palliative therapy.’ Raised plasma-c.E.A. values are not, however, diagnostic of cancer because they are found in patients with various inflammatory diseases, including those of the lung.When a patient presents with a pleural effusion it is sometimes difficult to determinethe cause, unless malignant cells or bacteria are isolated from the pleural fluid. Biopsy is not always helpful. Several workers have compared plasma with pleural-effusion values for C.E.A. in an attempt to improve the diagnostic accuracy. Some have found raised pleural-fluid C.E.A. concentrates in patients with a variety of cancers and inflammatory lung diseases,9,lo while othersll,12 have found raised C.E.A. values only in patients with cancer. We have measured C.E.A. levels in plasma and pleural fluid to see if their combined estimation would help to separate patients with primary bronchial carcinoma from those with mesothelioma or inflammatory lung disease (empyema and tuberculosis). We measured C.E.A. concurrently in plasma and pleural fluid by double-antibody radioimmunoassay8 (normal plasma-c.E.A.
drainage with widely known.
I
a
fine needle
Pædiatric Department, Charing Cross Hospital, London W6 8RF
*Normal values
(in 0.001-0.018) fLglg.
15
men
and 5
women
aged 12-65)
0.012
cannula deserves
to
be
more
RICHARD GRAY HERBERT BARRIE
HYDROPS FETALIS ASSOCIATED WITH SMALL-BOWEL VOLVULUS
(range
common, other with fetalis are increasing hydrops being recognised frequency.’ We describe here a case of non-immunological hydrops fetalis in a patient with an intrauterine small-bowel volvulus. A male baby weighing 2700 g was born at term after a normal pregnancy. Fetal bradycardia was present before delivery, and the Apgar score at 1 min was 2. The baby was oedematous, lethargic, and cyanotic and had a distended abdomen. He was put on artificial ventilation. The heart-rate was 110/min with a gallop rhythm; blood-pressure 60/40 mm Hg; central venous pressure (via umbilical venous line placed above the diaphragm) 20 mm Hg. The abdomen was distended and firm; pupils were mid-position and non-reactive, and the extremities were flaccid, except for intermittent seizure activity. Multiple petechize were present. Haemoglobin 7.1g/dl; hwmatocrit, 21.9%; white blood-cells, 28 600/fl-I, with 3% metamyelocytes, 6%
SIR,-As Rh-isoimmunisation becomes less
causes
These results support our belief that trace elements may be very important in renal failure. In particular, cobalt may be one, or even the prime, astiological agent for ursemic cardio-
myopathy. Information on other trace elements and a discussion of their possible metabolic roles and the hasmodynamic results from patients with progressive renal failure will be presented elsewhere. Department of Medicine, KENNETH PEHRSSON Karolinska Hospital, LARS-ERIC LINS S-104 01, Stockholm, Sweden
DECOMPRESSION OF HYDROCEPHALUS DURING DELIVERY
SIR,-The finding of fetal hydrocephalus in late pregnancy raises obstetric and ethical problems. Crude destructive operations are no longer acceptable, and the perforator and cranioclast are instruments of the past. Although gross hydrocephalus is not compatible with normal survival, it is often important to the parents that the baby dies not during birth, but of natural causes afterwards. The obstetrician has to choose between vaginal delivery and elective section, and an important consideration is the extent to which the size of the head can be reduced safely. A 26-year-old primigravida had a normal pregnancy until 34 weeks when hydrocephalus was diagnosed by ultrasound and X-ray. She went into spontaneous labour at 38 weeks but after a short trial of labour no descent of the fetal head had occurred and a lower-segment cxsarean section was done. The head was delivered with considerable difficulty, necessitating wide skin and uterine incisions. The baby, a girl with gross hydrocephalus and a lumbar meningomyelocele, survived for 6 days. With the parents’ consent, the head was decompressed after death using a 12 gauge ’Medicut’ cannula inserted through the lateral angle of the anterior fontanelle. 1370 ml of fluid was drained and the following changes in head size were noted:
Anteroposterior diameter (cm) Biparietal diameter (cm) Head circumference (cm) The operative delivery in this case would certainly have been easier if drainage had been used, and the baby would probably have survived this relatively atraumatic procedure. A similar technique was described by O’Connor and Gorman in 1942.’ They used a spinal needle to drain the head during vaginal delivery, 1400 ml of fluid being removed in 25 min; the delivery was normal and the baby lived for 2 h. Intraventricular puncture was recommended as the method of choice, especially where the delivery of a live baby is ethically important. Alternative methods using catheters or more traumatic procedures are still advocated. This simple technique of 1. O’Connor, C. T., Gorman, A.
or
J. Am. J. Obstet. Gynec. 1942, 43, 521.
of
myelocytes, 10% bands, 8% polymorphonuclear neutrophil leucocytes, 70% lymphocytes, and 3% monocytes. There were 50 nucleated red blood-cells per 100 white blood-cells. Bloodshowed occasional fragmented erythrocytes, and marked anisocytosis, poikilocytosis, and polychromatophilia. There was no hypochromia. Reticulocyte-count 11-2%; platelets 60 000/jjd; prothrombin-time 21.2 s (control 11 -2); partial thromboplastin-time 116 s (control 41-4); fibrinogen, 130 mg/ml. Blood group 0+ (mother 0+). Direct and indirect Coombs tests negative. Bilirubin less than 0-2 mg/dl. Haemoglobin electrophoresis normal for age. Bone-marrow aspirate showed normoblastic hyperplasia. No fetal erythrocytes were found in maternal blood at 48 h (Kleihauer-Betke technique). An abdominal X-ray at 15 h showed no gas below the level of the stomach. Bacterial and viral cultures of blood, urine, throat, stool and nasopharynx were negative. The rubella titre was 1/20; cytomegalovirus and toxoplasmosis titres negative; herpes-simplex titre 1/8. An exchange transfusion was performed and antibiotic therapy was started. Emergency laparotomy at 27 h of age revealed a mid-gut volvulus with infarcted necrotic bowel and a large amount of blood in the abdominal cavity. The small bowel was resected and reanastomosed end-to-end from the ligament of Treitz to the terminal ileum about 1 -cm from the ileocxcal valve. The infant’s condition deteriorated and he died 34 h after birth. The surgical specimen and necropsy revealed hxmorrhagic necrosis of jejunum and ileum with extravasation of blood obscuring the normal architecture. Generalised oedema is a well-known complication of severe fetal anaemia.I,2 Besides erythroblastosis fetalis, causes of anaemia in the newborn such as transplacental transfusion between monochorionic twins, marrow replacement by neuroblastoma, homozygous a-thalassaemia, chronic infections, and fetomaternal bleeding have been reported to cause hydrops fetalis.’I The haematological data pointed to chronic blood-loss or haemolysis as a cause of the anaemia. The low bilirubin and the absence of blood-group incompatibilities suggested bleeding into the abdominal cavity as the predominant reason for this patient’s anaemia. Disseminated intravascular coagulation smear
1. 2.
Turberville, D. F. and others. Obstet. Gynec. 1973, 43, 567. Lewy, J. E., Moel, D. I. Clin. Perinat. 1975, 2, 117.
53 leads to red-cell fragmentation and hxmolysis. However, anaemia of this severity due to haemolysis of any kind would have produced a much higher bilirubin. Other factors such as decreased oncotic pressure3 (serumalbumin not available) and the loss of plasma volume described in association with bowel obstruction4 may have played important contributory roles in the pathogenesis of the oedema. We thank Dr Rowena
Spencer
and Dr Norman
Woody for
C.E.A. CONCENTRATIONS
(ng/ml) IN PLEURAL EFFUSIONS AND PLASMA
I
I
review-
ing the manuscript. Department of Pediatrics, Tulane University School of Medicine, New Orleans, Louisiana 70112, U.S.A.
JANE F. SEWARD JAIME ZUSMAN
CONCURRENT ASSAYS OF PLASMA AND PLEURAL-EFFUSION LEVELS OF CARCINOEMBRYONIC ANTIGEN IN THE DIAGNOSIS OF PULMONARY DISEASE concentrations of carcinoembryonic have been demonstrated in the plasma of patients with many different types of neoplasia including carcinomas of the colon5and bronchus.6The c.E.A. value seems to vary with the stage of disease and the quantity of tumour or the use of palliative therapy.’ Raised plasma-c.E.A. values are not, however, diagnostic of cancer because they are found in patients with various inflammatory diseases, including those of the lung.When a patient presents with a pleural effusion it is sometimes difficult to determinethe cause, unless malignant cells or bacteria are isolated from the pleural fluid. Biopsy is not always helpful. Several workers have compared plasma with pleural-effusion values for C.E.A. in an attempt to improve the diagnostic accuracy. Some have found raised pleural-fluid C.E.A. concentrates in patients with a variety of cancers and inflammatory lung diseases,9,lo while othersll,12 have found raised C.E.A. values only in patients with cancer. We have measured C.E.A. levels in plasma and pleural fluid to see if their combined estimation would help to separate patients with primary bronchial carcinoma from those with mesothelioma or inflammatory lung disease (empyema and tuberculosis). We measured C.E.A. concurrently in plasma and pleural fluid by double-antibody radioimmunoassay8 (normal plasma-c.E.A.
