Goal-Directed Therapy for Septic Shock in Neonates and Infants

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M. Piastra
Paediatric ICU and Emergency Department, Institute of Anaesthesia/Intensive Care, Catholic University Medical School, Rome, Italy (t: +39 (0)63 0155203; e: marco_piastra@yahoo.it)

Sepsis is a predominant cause of morbidity and mortality in the newborn and young infant. Although around 50% of paediatric sepsis occurs in the neonatal period, there is a paucity of trials investigating newborn sepsis. Clinical practice guidelines for the management of septic shock in the term newborn (excluding the preterm newborn) have been recently revised [1, 2]. Acute bacterial meningitis or the sepsis/meningitis syndrome occurs in the neonate and young infant, despite the development of highly effective conjugate vaccines and the generalised use of antibiotics. Group B streptococcus (GBS), pneumococcus and E. coli are still responsible for this syndrome in the young infant. Late-onset GBS invasive infections are complicated by meningitis in over 50% of cases [3].

In recent years, more emphasis has been given to goal-directed therapy [4], both in adults and in childhood, as the mortality rate has been reduced by early aggressive fluid resuscitation. Superior vena cava oxygen saturation (scvSatO2) is being increasingly used as an assessment of oxygen delivery and consumption, with low values reflecting increased tissue oxygen extraction due to an inadequate cardiac output, paralleling raised serum lactate.

Case presentation
The patient was a male term newborn infant, born through Caesarean section delivery, with a gestational age of 39 weeks; birth weight 2620 g, and an Apgar score of 4, 6 and 8 at, respectively, 1, 5 and 10 minutes of life. Maternal and family history were unremarkable. The neonate was classified as being small for gestational age, classified under the 10th percentile of the Curve of Intrauterine Growth. After birth, breastfeeding was introduced, with good acceptance, and he was discharged on Day 5 in good clinical condition. On Day 20 of life, the infant’s mother alerted the Pediatric Emergency Room of the Catholic University Medical School, reporting a history of fever (39°C) and respiratory failure. In addition to the fever, the newborn infant presented cyanosis, tachycardia (195/min) and tachypnoea (83/min); he was then placed on oxygen inhalation and material was collected for infection screening (whole blood count, blood culture, urine culture, cerebrospinal fluid (CSF), C-reactive protein and X-ray). The infant’s bodyweight on admission to the Paediatric Intensive Care Unit (PICU) was 2850 g. Intravenous fluids and antibiotics were given (cefotaxime and amikacin), as the first clinical suspicion was late meningitis/sepsis syndrome. Moderate metabolic acidosis was detected (pH 7.28; base excess: –12; lactate: 5 mmol/L) without electrolytic alterations, and blood glucose was 225 mg/dL. The CSF showed 1042 cells/mm3 (21% lymphocytes, 12% monocytes and 62% neutrophils), a protein level of 435 mg/dL, and glucose <10 mg/dL; bacterioscopy showed the presence of numerous Gram-positive rods and polymorphonuclear leukocytes. The whole blood count showed the following: haematocrit, 32%; haemoglobin (Hb), 10.7 g/dL; 4,500/mm3 leukocytes (5% of myelocytes, 5% of metamyelocytes, 22% of rod neutrophils, 13% of segmented neutrophils, 32% of lymphocytes, 8% of monocytes) and platelet count of 68,000/mm3. The C-reactive protein was 149 mg/dL. Coagulation tests revealed: international normalised ratio (INR), 2.5; activated partial thromboplastin time (aPTT), 92 sec; fibrinogen, 105 mg/dL; and D-Dimer test, 2540. The infant became progressively pale and phases of reduced consciousness and apnoea required invasive ventilation. A cuffed 4.0 mm ID tracheal tube was used, while anaesthesia was induced with ketamine-midazolam. Central pulses were only appreciable, and capillary refill was 4 sec. A 22G catheter was placed in the right femoral artery and a 2-lumen 4.5 Fr line was introduced under ultrasound guidance in the right internal jugular vein (IJV). Subsequent to this, respiratory support became quite difficult, despite an increase of FiO2 to 1.0, as well as high inspiratory and end-expiratory pressures. He was shifted to high-frequency oscillatory ventilation (HFOV) with the following initial settings: mean arterial pressure (MAP), 26 cmH2O; amplitude, 55; frequency, 8 Hz, which resulted in respiratory improvement. At HFOV institution, PaO2:FiO2 ratio was 175. Blood and CSF cultures yielded GBS.

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