Muscle weakness is an infrequent but significant feature of critical illness in children. Transplant recipients seem to be at particular risk.

Background: The persistent airway neutrophilia observed in chronic lung disease of prematurity (CLD) may reflect inappropriate suppression of neutrophil apoptosis. Methods: 134 bronchoalveolar lavage (BAL) samples were obtained from 32 infants requiring mechanical ventilation for respiratory distress syndrome (RDS): 13 infants (median gestation 26 weeks, range 23 to 28) subsequently developed CLD (CLD group), and 19 infants (gestation 31 weeks, range 25 to 39) recovered fully (RDS group). A further 73 BAL samples were obtained from 20 infants (median age 2 days, range 1 to 402) receiving extracorporeal membrane oxygenation (ECMO) for severe respiratory failure. Results: Neutrophil apoptosis was increased in the RDS group (mean (SEM) neutrophil apoptosis on day 7 BAL: RDS 17.0 (8.6)% v CLD 0.7 (0.2)% (p,0.05)). BAL fluid obtained from RDS but not CLD patients was proapoptotic to neutrophils (apoptosis ratio BAL fluid/saline control: day 1, RDS 9.8 (5.5) v CLD 1.2 (0.1) (p,0.05); day 2, RDS 4.32 (2.8) v CLD 0.5 (0.4) (p,0.05)). There were similar findings in the ECMO group: survivors had proapoptotic BAL fluid compared with non-survivors (apoptosis ratio day 1, survivors 7.9 (2

Primary repair at an early age has excellent short-term outcome. Patients less than 3 months of age have an increased but transient intensive care unit morbidity.

Nephrotoxicity from non-steroidal anti-in ammatory drugs (NSAID) is well recognized. We report a case of severe hypokalaemia and weakness due to renal tubular acidosis in a young woman who was taking 40-60 tablets per day of Nurofen Plus 1 (ibuprofen 200 mg and codeine phosphate 12 ¢ 8 mg). Proprietary brands of ibuprofen are freely available to the public and those containing codeine may be potentially subject to abuse. This case highlights the need to be aware of this potential and of the life-threatening electrolyte and acid-base disturbances that might be encountered with the widespread availability of these types of NSAID. Case reportA 28-year-old woman presented to the emergency department with a 2-day history of severe generalized weakness. She was unable to stand up or hold her neck straight. She said that she had one episode of vomiting on the day before admission and that, 2 weeks earlier, she had bronchitis for which her general practitioner prescribed amoxycillin. She was taking pantoprazole for a duodenal ulcer, diagnosed 7 months earlier. She was also taking over-the-counter analgesics for relapsing knee pains. She had a history of depression and alcohol dependence for which she had previously received psychiatric counselling.On examination, she was afebrile (36¢78C), her pulse rate was 90 per min, regular, and blood pressure 110/60 mmHg. She had severe generalized muscle weakness but no neurological de¢cit. Body mass index was 20¢4 kg/m 2 . The ECG showed prolonged QT intervals and inverted T waves.Blood tests on admission, showed serum potassium 1Í4 mmol/L (3Í6-5Í3), sodium 141 mmol/L (138-146), urea 6Í4 mmol/ L (2Í5-7Í5), creatinine 64 mmol/L (50-130), calcium 2Í54 mmol/ L (2Í2-2Í6) and phosphate 0Í43 mmol/ L (0Í8-1Í4). Further investigations revealed serum bicarbonate 14Í7 mmol/ L (21-28), chloride 112 mmol/ L (96-104) and an anion gap of 15Í7 mmol/L (12-16). Urinary potassium was inappropriately high at 26Í6 mmol/ L and the renal tubular maximum reabsorption of phosphate (TmP/GFR) was low at 0 Í31mmol/ L GFR (0 Í8-1Í4).In view of the hypokalaemia, hyperchloraemia, low serum bicarbonate and normal anion gap, the diagnosis of renal tubular acidosis was made. She was treated with intravenous potassium therapy over the following 4 days (a total of 340 mmol) and her serum potassium rose gradually to 3Í7 mmol/ L and bicarbonate to 23Í9 mmol/ L by day 4; 2 days later, and without any further treatment, her serum potassium was 4Í9 mmol/ L and bicarbonate 26Í5 mmol/ L. The TmP/GFR was normal (1Í4 mmol/ L GFR) and the fractional excretion of bicarbonate was 1%. An ammonium chloride acidi¢cation test was undertaken but was inconclusive because she vomited shortly after ingesting the ammonium chloride.A review of her notes revealed that, 8 months earlier, she was admitted to hospital with an episode of abdominal pain and diarrhoea. Her serum potassium at the time was 2Í4 mmol/ L and had normalized with intravenous and oral potassium. Her hypokalaemia was thought to be due to the diarrhoea and she...

Background: It is likely that the imbalance between the pro- and anti-inflammatory cytokines will determine the outcome in infants with severe respiratory failure receiving extracorporeal membrane oxygenation (ECMO). Aims: We determined if there was an imbalance between pro- and anti-inflammatory cytokines in serial bronchoalveolar lavage (BAL) fluid obtained from survivors and non-survivors of ECMO. Methods: We therefore measured the cellular changes and the molar ratios of pro-inflammatory and anti-inflammatory cytokines in serial BAL fluid obtained from survivors and non-survivors of ECMO. Fifteen infants surviving ECMO (median age 1 day, range 1–120) and 7 who did not (28 days, range 1–402) were studied. Results: In the lungs of survivors, the increased proportion of airway neutrophils at presentation decreased with time and was matched by a parallel increase in percent alveolar macrophages as the infants’ condition improved. The pro- and anti-inflammatory pulmonary cytokine ratios were static in the survivors. In the non-survivors, the ratio of tumour necrosis factor-α (TNF-α) against soluble TNF-receptor 1 (sTNF-R1) and soluble TNF receptor 2 (sTNF-R2) was increased at days 2–3 when compared to the survivors, but the molar ratio interleukin-1β (IL-1β)/soluble IL-1 receptor antagonist (sIL-1RA) was largely undetectable due to undetectable IL-1β. Conclusions: These data suggest that the infants who survive ECMO resolve their pulmonary inflammation and that in non-survivors the ratio of TNF-α against its receptor antagonists is increased and is associated with a poor outcome. Furthermore, this group of infants were unable to produce significant concentrations of IL-1β.