Cerebrospinal fluid acid-base status and lactate and pyruvate concentrations after short (less than 30 minutes) first febrile convulsions in children.

Twenty-nine infants and children with short (less than 30 minutes) first febrile convulsions were studied between 3 and 22 hours after convulsive episodes. Arterial and CSF acid-base variables, lactate and pyruvate concentrations, and lactate/pyruvate ratios were measured. Biochemical signs of cerebral hypoxia were found in only 2 patients, one of whom had short, repeated convulsions. Our findings indicate that hypoxic damage is unlikely to result from a short-duration febrile convulsion.

Cerebrospinal fluid acid-base status and lactate and pyruvate concentrations after convulsions of varied duration and aetiology in children.

Twenty-two infants and children were studied after convulsions of varied cause and duration. Arterial and CSF acid-base variables, lactate and pyruvate concentrations, and lactate/pyruvate ratios were measured between 3 and 18 hours after convulsive episodes. Biochemical signs of cerebral hypoxia were found in 7 patients with prolonged (greater than 30 minutes) or recurrent short convulsions. These signs were absent in patients with single short convulsions. These findings indicate that cerebral hypoxia and possible brain damage is a hazard of prolonged or rapidly recurring short convulsions.

Osmolar relation between cerebrospinal fluid and serum in hyperosmolar hypernatraemic dehydration.

The relation between cerebrospinal fluid (CSF) and serum osmolality was studied in 16 patients with hyperosmolar hypernatraemic dehydration before treatment. After correcting shock and acidosis, 0-45% saline in 2-5 or 5% dextrose was infused in each patient over a 48- to 72-hour period. During rehydration, serum osmolality, electrolyte concentrations, urea nitrogen, and blood pH were measured sequentially. Five patients developed severe neurological abnormalities within 48 hours of addmission (convulsions 2, convulsions with hemiplegia 2, hemiplegia 1). Of these, 3 had residual defects on follow-up at least one year later. This group was indistinguishable from the 11 without significant neurological abnormality, both on clinical grounds before rehydration, and after analysis of admission and subsequent serum biochemical variables. A significant osmolar gap (greater than 4 mmol/kg H2O) between serum and CSF was found in 13 patients. Severe neurological disturbance only occurred when CSF osmolality exceeded that of serum by 7 or more mmol/kg H2O. Discriminant analysis of the paired osmolar data showed that D = -117+1-74 X(CSF osmolality) -1-41 X (serum osmolality), and that severe neurological abnormality was predicted when D was positive.

Fluid and electrolyte metabolism in the newborn infant.

This chapter has sought to gather together the background information on systems controlling homoeostasis of salt and water and their clinical derangement. The temptation to adopt an all-embracing approach to the management of these problems is strong but such an approach is difficult to achieve and indeed dangerous. The circumstances of each sick infant are unique and plans for treatment must be individually tailored and flexible, dependent upon clinical and biochemical progress. Future developments in this field are likely to involve further understanding of renal and hormonal control of fluid and electrolyte and it might be expected that as new methods of management emerge they will be accompanied by their own peculiar risks of inducing secondary homoeostatic disturbances. With regard to infant feeding each advance appears to underline the desirability of breast feeding and support current moves toward provision of low solute feeds for those who are artificially fed. Paediatricians should be vocal in their advocation of breast feeding and ensure that the major principles of salt and water handling are understood by all who work with small infants. An extra scoop of powdered milk can be more of a poison than a food.

Toxic encephalopathy and acute brain-swelling in children.

Problems in the diagnosis and management of children who present with an acute encephalopathic illness are examined. The aetiology, pathogenesis, pathology and clinical features of acute toxic encephalopathies are discussed, together with the differential diagnosis of those encephalopathies which are not induced by toxicity. Guidance is given on measures for the reduction of raised intracranial pressure and the management of defects of homeostasis. It is essential that facilities for intensive monitoring of these children be available during the acute phase of illness in order to reduce the number surviving with sequelae of mental and physical handicap.

Acute respiratory failure in bronchiolitis and pneumonia in infancy. Modes of presentation and treatment.

The modes of presentation and the management of acute respiratory failure in 11 infants with severe lower respiratory tract infections (due to respiratory syncytial virus in eight) are described. Progressive respiratory difficulties leading to exhaustion, peripheral circulatory collapse, recurrent apnoeic attacks, or generalized convulsions were the main clinical presentations resulting in severe ventilatory failure. In nine infants preventilation carbon dioxide tensions exceeded 65 mm Hg. It seems likely that the use of intermittent positive-pressure ventilation in these patients contributed to the low mortality rate, less than 0.5%, from such illnesses during the 15-month study period.