Resuscitating neonatal and infant organs and preserving function. GI Tract and Kidneys

Transcription

1 Resuscitating neonatal and infant organs and preserving function GI Tract and Kidneys

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3 Australian and New Zealand Resuscitation Council Joint Guidelines

4 Outline Emphasis on the infant - PICU Kidney Gastrointestinal tract Liver dysfunction Necrotising enterocolitis The Future

5 Brain most important, but the more organs involved the worse the prognosis Good resuscitation, hard, fast, minimise interruptions Primary insult Minimising secondary harm and preserving or replacing function

6 Renal Dysfunction Commonly accompanies asphyxial states Severity usually dependant upon degree of insult Acute diffuse tubular dysfunction Decreased GFR Impaired re-absorption of sodium and water Decreased or absent urine output Loss of renal concentration ability (milder insult)

7 Diagnosis of Renal Dysfunction Acute renal failure diagnosed if the serum creatinine is increased (> mg/dl, micromol/l) May be nonoliguric, oliguric or anuric Exclude prerenal failure with a fluid challenge A catheter should be inserted to exclude lower urinary tract obstruction and measure output An ultrasound should be done to exclude renal anomalies or thrombosis

8 Renal Support Renal failure a jolly nuisance, but doesn t define outcome in PICU PD Continuous Veno Veno Haemofiltration (CVVH, CRRT) ECMO in line filter 2 kg

9 Renal Dopamine Dopamine synthesised in the proximal tubule of the kidney (also renal nerves that contain dopamine) Affects sodium excretion and renal haemodynamics via receptors DA1 and DA2 Dopamine is a natriuretic hormone, increasing NA excretion by diminishing reabsorption

10 Renal Dopamine In low dose (0.5-3 ug/kg/min) dopamine dilates arteries and arterioles in the kidney, resulting in increased blood flow In higher concentrations (>5 ug/kg/min) it induces renal vasoconstriction via alphaadrenergic receptors. The increase in renal perfusion may not be seen in patients with acute tubular necrosis

11 Renal Dopamine Some clinicians use low dose dopamine to improve renal perfusion Efficacy of this not proven Adult literature suggests low dose dopamine is with out benefit in patients with acute renal failure no infant/neonatal studies Lancet 2000 Dec; 356: Bellomo et al. Multicentre (230) placebo-controlled blinded randomised study by ANZICS. No clinical advantage or protection from renal dysfunction

12 Gastrointestinal Dysfunction Hepatic dysfunction Necrotising enterocolitis.

13 Hepatic Dysfunction Ischaemia can interfere with synthetic, excretory and detoxifying functions of the liver Glucose look for and treat hypoglycaemia, may have increased glucose requirement Coagulation look for and treat if clinically appropriate No replacement therapy available

14 Necrotising Enterocolitis NEC much more common in premature infants and has different characteristics in full term infants Ischaemia can cause alterations in intestinal blood flow for up to 3 days (Akinbi et al, J Peds,1994) These changes may lead to ischaemia and subsequent development of NEC, which may have significant long term implications

15 Necrotising Enterocolitis Only 10-15% of all NEC occurs in full term infants The majority of whom have a pre-existing condition or precipitating cause Eg: congenital heart disease, sepsis, seizures, IUGR, pre natal asphyxia, birth asphyxia or post natal asphyxia

16 Prematurity and NEC In preterm infants the risk factors are: Maternal and obstetric factors that predispose the fetus of newborn to asphxia Antepartum, intapartum, or postnatally LBW eg: gm 11.5%, gm 4% Low apgar score Antenatal steroids Need for ventilator support Rx for PDA Enteral feeds

17 Necrotising Enterocolitis: Clinical Presentation Non specific systemic signs Apnoea, temp instability, lethargy Abdominal signs Distension, feed intolerance, vomiting, pr blood Later systemic signs of circulatory collapse

18 Necrotising Enterocolitis: Diagnosis Clinical finding Abdominal distension and tenderness and pr blood Radiology Abnormal gas pattern, pneumatosis intestinalis, free air, air in bilary tract Ultrasound Laboratory Coagulopathy, FBC (low platelet count), positive blood cultures

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20 Necrotising Enterocolitis: Prevention Maintain GI tract perfusion Good CPR Volume and inotropic support After ischaemic event Delay feeds Human milk vs formula High index of suspicion

21 Necrotising Enterocolitis: Treatment Supportive Bowel rest and TPN, Rx CVS and coagulopathy Antibiotic Laboratory and radiographic monitoring Surgical Perforation, dead gut, peritonitis, abdominal compartment syndrome Overall survival 70-80% but long term morbidity can be significant

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23 The Future Both the preterm fetus and the newborn are critically susceptible to functional renal and gut impairment in the first few days of life This is closely related to hypo-perfusion brought about by an increase in renal and mesenteric vascular resistance (and may be in presence of normal BP)

24 The Future This is speculated to be due to a selective increase in sympathetic nerve activity, which needs to be measured in the future This is thought to be actively mediated and that it is likely to play a role in supporting the cardiovascular system after hypoxia (as BP falls when gut perfusion normalised by alpha blockade)

25 The Future These findings are consistent with the fact that many interventions (volume, inotropes) have equivocal effects The future should include focused physiological studies to evaluate when and how (and if) promotion of blood flow should be manipulated to maintain and optimise organ function

26 We are quite some time off this! In the meantime we are left with good resuscitation, followed by supportive care with attention to detail! And ongoing inquisitive minds and research..

27 The End

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