Hypoalbuminaemia in critically ill children: incidence, prognosis, and influence on the anion gap.

AIMS: Hypoalbuminaemia has significance in adult critical illness as an independent predictor of mortality. In addition, the anion gap is predominantly due to the negative charge of albumin, thus hypoalbuminaemia may lead to its underestimation. We examine this phenomenon in critically ill children, documenting the incidence, early evolution, and prognosis of hypoalbuminaemia (<33 g/l), and quantify its influence on the anion gap. METHODS: Prospective descriptive study of 134 critically ill children in the paediatric intensive care unit (ICU). Paired arterial blood samples were taken at ICU admission and 24 hours later, from which blood gases, electrolytes, and albumin were measured. The anion gap (including potassium) was calculated and then corrected for albumin using Figge's formula. RESULTS: The incidence of admission hypoalbuminaemia was 57%, increasing to 76% at 24 hours. Neither admission hypoalbuminaemia, nor extreme hypoalbuminaemia (<20 g/l) predicted mortality; however, there was an association with increased median ICU stay (4.9 v 3.6 days). After correction for albumin the incidence of a raised anion gap (>18 mEq/l) increased from 28% to 44% in all samples (n = 263); this discrepancy was more pronounced in the 103 samples with metabolic acidosis (38% v 73%). Correction produced an average increase in the anion gap of 2.7 mEq/l (mean bias), with limits of agreement of +/-3.7 mEq/l. CONCLUSION: Admission hypoalbuminaemia is common in critical illness, but is not an independent predictor of mortality. However, failure to correct the anion gap for albumin may underestimate the true anion gap, producing error in the interpretation of acid-base abnormalities. This may have treatment implications.

The value of the chloride: sodium ratio in differentiating the aetiology of metabolic acidosis.

OBJECTIVE: Stewart's physicochemical approach to acid-base balance defines the aetiology of a metabolic acidosis by quantifying anions of tissue acids (TA), which consist of unmeasured anions (UMA) and/or lactate. We hypothesised that an increase in TA during metabolic acidosis would lead to a compensatory fall in the plasma chloride (Cl) relative to sodium (Cl:Na ratio) in order to preserve electro-neutrality. Thus, the Cl:Na ratio could be used as a simple alternative to the anion gap in identifying raised TA. PATIENTS: Two hundred and eighty two consecutive patients who were admitted to our Paediatric Intensive Care were enrolled in the study. INTERVENTIONS: We obtained 540 samples (admission n = 282, 24 h n = 258) for analysis of blood chemistry, lactate and quantification of TA and UMA. Samples were subgrouped into those with metabolic acidosis (standard bicarbonate < 22 mmol/l) either with or without increased UMA (> 3 mEq/l). MEASUREMENTS AND RESULTS: Metabolic acidosis occurred in 46% of samples, of which 52.3% (120/230) had increased UMA. The dominant component of TA was UMA rather than lactate, and these two components did not always rise in tandem. Our hypothesis of relative hypochloraemia was supported by a lower Cl:Na ratio (P < 0.0001) but not a lower absolute Cl (P = 0.5) in the acidotic subgroup with raised UMA, and by the inverse relationship between TA and the Cl:Na ratio. (coefficient of determination (r2) = 0.37, P < 0.0001). The best discriminator for the presence of raised TA was the albumin-corrected anion gap (AGcorr), however, this could not track changes in TA with clinical accuracy. The Cl:Na ratio discriminated reasonably well, a ratio of < 0.75 identified TA (positive predictive value (PPV) 88%) with a likelihood ratio (LR) similar to the AG (7.8 vs7.4). Conversely, a high ratio (> 0.79) excluded TA (PPV 81%, LR 4.5). Base deficit (BD) and lactate performed poorly. CONCLUSION: In metabolic acidosis due to TA, plasma Cl concentration decreases relative to sodium. The Cl:Na ratio is a simple alternative to the AG for detecting TA in this setting.

Chasing the base deficit: hyperchloraemic acidosis following 0.9% saline fluid resuscitation.

Base deficit is a parameter often used to guide further treatment in acidotic children and is taken as a measure of how "sick" they are. Five children with septic shock are presented who had persisting base deficit after large volume resuscitation with 0.9% saline. Stewart's strong ion theory of acid-base balance is able to quantify the causes of metabolic acidosis and is used to show that our patients had a hyperchloraemic metabolic acidosis. We show how the chloride content of the saline loads given to our patients caused this hyperchloraemia. It is concluded that 0.9% saline and other chloride rich fluids may not be ideal resuscitation fluids; if used, clinicians must be aware of their potential to cause a persistent base deficit.

Congenital symmetrical weakness of the upper limbs resembling brachial plexus palsy: a possible sequel of drug toxicity in first trimester of pregnancy?

We report a 14-month-old girl with a symmetrical paralysis from birth, limited to the upper limbs and resembling a severe, complete bilateral brachial plexus palsy. The presence of dimples over the wrists, shoulders and scapulae and abnormal palmar dermatoglyphics suggested an early prenatal onset. Previous reports and the course of the disease in our case suggest this sporadic condition is not progressive. Although no definitive causative factor has been identified in previously reported cases, the affection in our case is possibly related to Debendox (Bendectin) and nitrofurantoin taken in early pregnancy for nausea and renal tract infection, respectively.