Search

Unexplained subdural and retinal haemorrhages in an infant are commonly attributed to 'shaking', the mechanism of which is believed to be traumatic venous rupture. However, the haemorrhagic retinopathy reported as a result of Valsalva manoeuvres and the subdural bleeding that is a rare complication of pertussis together demonstrate that if a sustained rise in intrathoracic pressure is transmitted to cerebral and retinal vessels, it may result in bleeding, similar to that reported in inflicted injury. Such haemorrhages would be expected to occur whenever severe paroxysmal coughing were induced, whatever the cause. This study used a computer modelling approach to investigate feeding accidents as the trigger for bleeding. A dynamic circulatory model of a 3-month-old infant was induced to 'cough', and the response to changes in physiological variables monitored. It showed that coughing causes intracranial pressures to build up exponentially to approach a maximum, proportional to the amount of pressure the musculature of the thorax can produce, as venous return is impeded. They do not have time to become dangerous during individual coughs, as blood quickly returns after the cough is over, reestablishing normal pressures. Paroxysmal coughing, however, does not allow blood to return between coughs, with the result that very high luminal pressures may be generated, sufficient to damage veins. A history of coughing, vomiting or choking is not uncommon in otherwise normal infants with retinal and subdural bleeding. Our findings suggest that paroxysmal coughing could account for such bleeding in some cases.

High pulsatility indices ( PIs) and/or notches on the Doppler flow velocity waveforms of the uterine artery have been interpreted as indications of high placental flow impedance, and are known to be associated with poor fetal outcome. A software model of the uteroplacental blood path and its use to investigate possible interactions within the uteroplacental unit in more detail are described. Increasing transcotyledonary resistance to represent intervillous obstruction raised the cotyledonary core pressure and spiral artery PI. Increased spiral artery flow resistance, representing failed spiral artery invasion, reduced the cotyledonary core pressure and reduced the spiral artery PI. In vivo, such changes in cotyledonary core pressure would modify the transplacental water balance, promoting oligohydramnios for spiral artery invasion failure and polyhydramnios for villous obstruction. Both mechanisms increased the uterine and arcuate PI, but failed to produce a notch. It was found that notch formation depended on terms representing increased compliance (distensibility) of the uterine and/or arcuate artery walls, which have no direct effect on uteroplacental mean flow. The same mechanism steepened and increased uterine artery peak systolic flow, contributing to increased PI. The notch phenomenon seems to be an indicator of abnormal maternal artery wall status, independent of placental obstructive mechanisms, which can mask obstructive PI changes. Computer analysis of the frequency index profile should allow separation. Copyright © 1995 International Society of Ultrasound in Obstetrics and Gynecology

Doppler flow velocity waveforms (FVW) in fetal veins that discharge into the atria show fluctuations related to atrial events. Pulmonary veins are of particular interest because both ends (atrial and collecting venule) are within the intrathoracic pressure environment reducing fetal breathing artifacts. Indices, such as pulsatility index for veins (PIV), have been suggested to classify FVWs and relate them to fetal well being. We wished to examine the relationship between function and FVW in circumstances which cannot ethically be examined in vivo, by studying the mechanisms which produced altered 'flows' in a detailed fetal computer model. We then related these findings to current flow indices.A computer model of the feto-placental unit, responding to changes in organ oxygenation and regional flow is briefly described. In vivo intracardiac pressures and FVWs obtained from other studies were used to extend detail in the model until matching 'pressures' and 'flows' resulted. The effects of flow redistribution in the hypoxic fetus on pulmonary vein 'Doppler' flow velocity waveforms were then studied.Flow reversal in pulmonary veins during atrial contraction indicates hypoxia, but change of shape of the FVW envelope reflects the changes in the pressure waveform of the left atrium. Of the major veins the pulmonary vein Doppler FVW gave the truest representation of atrial pressure response to both intracardiac and systemic vascular status. Although current indices indicate general fetal condition, more specific indices are needed if pulmonary venous flow is to be used as an end-point. A pulmonary vein pressure gradient index is suggested.

The pathophysiology of recurrent cyanotic episodes has been investigated in 51 infants and children. Episodes began at a median age of 7 weeks (range 1 day to 22 months, 39 at less than 4 months). They were characterised by the rapidity of onset and progression of severe hypoxaemia with early loss of consciousness from cerebral hypoxia. The most common precipitating factor was a sudden naturally occurring stimulus from pain, fear, or anger. In uncontrolled trials, cyanotic episodes were reduced in frequency and severity by tetrabenazine (n = 15) and additional inspired oxygen (n = 10). Eight patients died suddenly and unexpectedly (four during cyanotic episodes). Twenty eight patients underwent physiological studies during cyanotic episodes. There was no evidence of seizure activity at the onset and although prolonged absence of inspiratory effort with continued expiratory efforts was common, breathing sometimes continued. Episodes were not caused by upper airway obstruction and sometimes occurred during positive airway pressure ventilation. The rapidity of fall in arterial oxygen pressure and continued breathing suggested a right to left shunt of sudden onset. The results of contrast echocardiography and lung imaging studies confirmed that this was occurring within the lungs. These cyanotic episodes included both intrapulmonary shunting and prolonged expiratory apnoea. They are best explained by interactions between central sympathetic activity, brainstem control of respiration and vasomotor activity, reflexes arising from around and within the respiratory tract, and the matching of ventilation to perfusion in the lungs. They are a cause of sudden unexpected death in infancy and early childhood.

Amniotic pressure was measured in 49 pregnancies with abnormal quantities of amniotic fluid. Among 17 with polyhydramnios, the pressure was always above the normal mean for gestation and exceeded the upper limit of normal in nine. In polyhydramnios, amniotic pressure correlated positively with the depth of the deepest pool (r = 0.65, P = .04) and negatively with fetal PO2 (r = -0.57, P = .03) and pH (r = -0.56, P = .04). Amniotic pressure was raised in all those with a deepest pool of greater than 15 cm, and was normal in all with a deepest pool less than 15 cm. Amniotic pressure fell significantly with drainage of amniotic fluid in those with raised pressure (mean 12.7 mmHg, 95% confidence interval 7.0-18.3; P = .002) but not in those with normal pressure (mean 0.3, 95% confidence interval -3.2 to +3.9; P = .82). Restoration of normal amniotic pressure in one pregnancy was accompanied by marked improvement in fetal acid-base status. Among 24 pregnancies with severe oligohydramnios, amniotic pressure was always below the normal mean, falling below the lower limit of normal in eight; whereas in another eight pregnancies with mild/moderate oligohydramnios, amniotic pressure was scattered evenly within the normal range. Amnioinfusion of 55-500 mL of normal saline in cases of severe oligohydramnios led to a significant rise in pressure (4.7 mmHg, 95% confidence interval 3.5-5.9; P less than .0001). We conclude that amniotic pressure is high in polyhydramnios and low in oligohydramnios. Pressure monitoring may be beneficial during amnioinfusion and therapeutic amniocentesis.

SummaryWomen in late pregnancy were subjected to mild psychological stress by listening, through headphones, to a prerecorded sequence of sounds which included that of a baby crying. Maternal reaction was detected using maternal heart rate and maternal skin resistance. Coincidental changes were observed in fetal heart rate patterns. Fetal heart rate pattern changes similar to those induced by the tape-recorded sounds have been observed during ‘non-stressed’ antepartum monitoring when patients were disturbed by sounds significant to them.

Summary. The assumptions of the Kubicek technique for measurement of cardiac output by detection of changes in the chest wall electrical impedance have been re-examined. The fall in cardiac output in the latter half of pregnancy which Crawforďs group calculated using the Kubicek technique can be almost entirely accounted for by a fall in the term dZ/dT of the Kubicek equation, as pregnancy progress. One key assumption of the Kubicek technique is a constant ejection flow rate equal to the initial flow as the pulmonary valve opens, which is multiplied by the estimated ejection time to obtain stroke volume. Initial flow rate is represented by the term dZ/dT in the Kubicek equation. Although this assumption has been shown to give a reasonable correlation with other techniques for measurement of cardiac output in the non-pregnant state, this may not be so for longitudinal studies in pregnancy because of the changes in lung mechanics and in the circulation which occur in this state. Crawforďs data emphasizes the necessity for validating the Kubicek technique very critically during pregnancy.

Traditionally the majority of abnormal infantile apnoea, including apnoea or prematurity, is considered to be the result of a primary disorder of respiratory control. In this paper we review evidence to suggest that the primary problem lies within the lungs and is best explained by an underlying defect in the function of lung surfactant.

The assumptions of the Kubicek technique for measurement of cardiac output by detection of changes in the chest wall electrical impedance have been re-examined. The fall in cardiac output in the latter half of pregnancy which Crawford's group calculated using the Kubicek technique can be almost entirely accounted for by a fall in the term dZ/dT of the Kubicek equation, as pregnancy progress. One key assumption of the Kubicek technique is a constant ejection flow rate equal to the initial flow as the pulmonary valve opens, which is multiplied by the estimated ejection time to obtain stroke volume. Initial flow rate is represented by the term dZ/dT in the Kubicek equation. Although this assumption has been shown to give a reasonable correlation with other techniques for measurement of cardiac output in the non-pregnant state, this may not be so for longitudinal studies in pregnancy because of the changes in lung mechanics and in the circulation which occur in this state. Crawford's data emphasizes the necessity for validating the Kubicek technique very critically during pregnancy.