Superior Mesenteric Artery Blood Flow Velocity in Necrotising Enterocolitis
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Archives ofDisease in Childhood 1992; 67: 793-796 793 Arch Dis Child: first published as 10.1136/adc.67.7_Spec_No.793 on 1 July 1992. Downloaded from Superior mesenteric artery blood flow velocity in necrotising enterocolitis S T Kempley, H R Gamsu Abstract alone may be the most important factor in its Doppler measurements of blood flow aetiology.13 14 The fact that necrotising ente- velocity were obtained from the superior rocolitis is rare in the absence of enteral feed- mesenteric artery (SMA), coeliac axis, ing demonstrates the importance of intralumi- and anterior cerebral artery (ACA) of nal factors. Breast milk exerts a protective 19 infants with suspected necrotising effect whereas hyperosmolar feeds,2 or hyper- enterocolitis, which was classified as con- osmolar drugs such as high doses of vitamin firmed (n=9) or unconfirmed (n=8). E,'5 may be risk factors. Infants with confirmed disease were com- In order to examine the hypothesis that pared with controls who were either necrotising enterocolitis is due to intestinal enterally fed or who were receiving intra- ischaemia, Doppler ultrasound has recently venous fluids. been used to study the characteristics of blood SMA velocity was significantly higher flow in the superior mesenteric artery of in the infants with confirmed necrotising infants in high risk groups. We have demon- enterocolitis (36.5 cm/s) than in unfed strated a specific reduction in superior mesen- controls (20.4 cm/s) or infants with teric artery (SMA) blood flow velocity in unconfirmed enterocolitis (19.6 cm/s). infants who are small for gestational age, who Three infants with confirmed disease experienced chronic intrauterine hypoxia16; had data from before the onset of symp- and Coombs et al have shown absent diastolic toms. One had low SMA velocity on the flow and reduced velocity in infants with first day of life, and one showed no patent ductus arteriosus.17 However, none of increase in SMA velocity after enteral the infants in these studies went on to develop feeds were started. necrotising enterocolitis. SMA velocity is increased when infants We therefore set out to measure SMA develop symptoms of necrotising entero- blood flow velocity using Doppler ultrasound colitis, suggesting that total gut ischae- in infants who developed necrotising entero- mia is not present at the time that the colitis. By studying from birth a large number disease is clinically apparent, although it of infants who were at risk we also hoped to http://adc.bmj.com/ may precede the onset of symptoms and have data that preceded the onset of this play a part in the pathogenesis of the dis- condition in a number of infants. In order to order. document the specificity of our findings for the mesenteric circulation, we also measured Epidemiological studies have suggested a velocity in the coeliac axis and anterior cere- bewildering variety of risk factors for necrotis- bral artery (ACA). ing enterocolitis. Identified risk factors on September 24, 2021 by guest. Protected copyright. include birth asphyxia,l-4 chronic intrauterine hypoxia,5 6 apnoea,2 4 7 8 umbilical catheteri- Methods sation,' 4 7 9respiratory distress and ventila- SUBJECTS WITH NECROTISING ENTEROCOLITIS tion,4 7 8 patent ductus arteriosus,3 polycyth- The criteria of the British Association of aemia,8 10 hypoglycaemia,8 and hypothermia.10 Perinatal Medicine (BAPM) were used to It is widely believed that intestinal ischaemia define cases of suspected necrotising entero- is the unifying mechanism that explains the colitis which occurred on our unit over a two ability of these many different factors to injure year period.'8 the neonatal bowel. Risk factors might cause A total of 19 infants were studied. To be ischaemia directly or as a consequence of the classified as a case of suspected necrotising 'diving reflex' when blood flow is diverted enterocolitis an infant must have had at least from the abdominal organs during hypoxia, two of the following features: abdominal dis- Children Nationwide thus preserving cerebral oxygenation. tension, blood in the faeces, a distinct clinical Neonatal Centre However, the concept of necrotising entero- deterioration (hypotonia, lethargy, or apnoea), King's College Hospital School of colitis being predisposed to by gut ischaemia or increased intraluminal gas visible on an Medicine, London is not straightforward. Clustering of cases has abdominal radiography. The characteristics of S T Kempley been used to support the idea of an infective these infants are shown in table 1. H R Gamsu aetiology." Although many agents, including Correspondence to: bacteria and viruses, have been implicated in Confirmed cases Dr S T Kempley, some Frederick Still Ward, outbreaks,'2 other studies have not iden- Nine infants were subsequently confirmed to King's College Hospital, tified infective agents to be consistently asso- have necrotising enterocolitis on the basis of London SE5 9RS. ciated with necrotising enterocolitis.7 It has radiological findings (intramural gas, hepatic Accepted 9 March 1992 also been proposed that mucosal immaturity portal venous gas), surgery or postmortem 794 Kempley, Gamsu Table 1 Characteristics ofthe infants with suspected necrotising enterocolitis pathology other than necrotising enterocolitis: Arch Dis Child: first published as 10.1136/adc.67.7_Spec_No.793 on 1 July 1992. Downloaded from Cases Sex Gestation Birth weight Postnatal Mean blood Last enteral one was found to have an ileal perforation in (weeks) (kg) age pressure feedt (days) (mm Hg) association with a meconium plug, and the Hours % intake other had intestinal infarction from an aortic before thrombus, obstructing the coeliac and mesen- Confirmed cases: teric arteries. (These two constitute the 'other 1 F 24 762 12 29 2 F 26 902 25 51 1 100 abdominal pathology' group.) 3 M 28 1248 6 46 15 100 4 F 28 1436 10 46 85 100 5 F 29 1150 8 19 Suspected, unconfirmed cases 6 F 30 1040* 44 64 30 100 Of the remaining eight infants, six were 7 F 34 1220* 6 24 100 8 F 36 2990 22 63 28 100 found to be septicaemic (case 10, C albicans; 9 M 39 3180 1 8 100 cases 11 and 15, Klebsiella sp, cases 12 and Mean 30 4 1550 15 45-4 SD 4 9 890 13-4 16-6 17, Staphylococcus epidermidis; case 13, entero- Suspected, unconfirmed cases: bacter), one was severely growth retarded and 10 M 23 510 8 28 11 F 24 680 14 60 thought to have meconium plugging, and in 12 F 24 720 26 36 32 100 one the cause of his deterioration was not 13 M 26 920 14 34 14 M 28 1246 6 43 identified. 15 F 29 516** 9 40 50 Mean birth weight was significantly lower in 16 F 32 666** 26 79 100 17 M 32 1180** 12 66 the group with unconfirmed necrotising ente- Mean 27-3 810 14 44-4 rocolitis, with three having a birth weight less SD 3-6 280 7-8 15-2 Cases with other pathology: than the third centile for gestation. 18 M 27 1118 18 44 26 100 19 M 28 1100 12 30 13 43 CONTROLS Infants who were small for gestational age are indicated: * birth weight <1Oth centile for gesta- For each infant with confirmed necrotising tion; ** <3rd centile. See text for further details. t Where no figure given, the infant had no enteral feeds. enterocolitis, control data were selected from Doppler measurements performed on babies enrolled in other studies, who had not suf- findings, in accordance with the BAPM crite- fered from gastrointestinal problems or birth ria. One infant (case 3) was a surviving twin asphyxia. Data from a pool of 80 infants were whose cotwin was a miscarriage some weeks available for matching. Control data were before delivery. Another (case 8) was born matched for postnatal age, the birth weight with a diaphragmatic hernia, which had been and gestation of the infant, and the degree of surgically repaired on the first day of life. intrauterine growth retardation. For each There was a term infant (case 9) whose index case we selected one control who was mother had admitted to abusing a number of receiving enteral feeds, and one who was drugs during pregnancy. Only one infant receiving intravenous fluids only, giving two (case 1) had an umbilical arterial catheter in control groups. The characteristics of the con- place at the time of measurement, and only trol infants are shown in table 2. two had blood cultures positive (case 1, http://adc.bmj.com/ Candida albicans; case 7, Staphylococcus MEASUREMENTS aureus). Measurements of blood flow velocity and pul- satility index were obtained from the SMA, Cases with other abdominal pathology coeliac axis, and ACA as previously Two infants had proved intra-abdominal described.'6 The artery was visualised in real time and range-gating used to sample pulsed wave Doppler signals from the particular ar- on September 24, 2021 by guest. Protected copyright. Table 2 Characteristics the control tery under study. All readings were corrected of infants for the angle of insonation. The measure- Controls Gestation Birth weight Postnatal Mean blood ments were obtained after the onset of symp- (weeks) (g) age pressure (days) (mm Hg) toms during the acute phase of the illness. Controls on intravenous fluids: 1 25 768 7 36 70 * Enterally fed 2 26 910 9 53 S o 3 28 1164 9 - 60 No enteral feeds 4 29 1510 11 57 5 30 1300 9 - E 50 6 30 1026* 7 45 0 7 34 1260** 7 - 8 40 3482 5 60 . 40 9 42 3482 2 - 0 es ° Mean 31-6 1656 7-3 50-2 0 30 SD 6-0 106 2-6 9-7 % Enterally fed < 0S O controls: 20 - Cl) 8 1 25 870 13 * 2 26 966 28 - 10 3 27 942 16 - 8 4 28 1038 7 - 0 ' 5 30 1506 8 - Confirmed Other pathology IV fluids 6 30 946* 8 - Unconfi.rmed Feeds 7 36 1798** 9 - 8 34 1980 14 56 NEC Controls 9 41 3910 1 - Mean 30-8 1500 12 Figure I Bloodflow velocity in the SMA for individual SD 5-3 980 7-6 infants with suspected necrotising enterocolitis (NEC), and Infants who were small for gestational age are indicated: *birth for infants in the control groups, receiving enteralfeeds or weight <Oth centile for gestation; **<3rd centile.