noted that no sooner 30 to 35mL of CSF was drained, the cry of the child had improved and stridor disappeared. Over the next few days, the child developed recurrent attacks of stridor, which improved only after CSF tap- ping. As the symptoms reverted suc- cessfully after CSF tapping, the need for intubation or tracheostomy was never felt. Within a week, however, the child showed respiratory and neurolo- gic deterioration and died on the fifth day of admission after cardiac arrest from which she could not be revived. Davis and Ross 5 suggest that vocal cord palsies are caused by high in- tracranial pressure. The probable mechanism is not destruction of brain stem cells but rather stretching, compression, or ischemia of the vagus nerves during their course from the nuclei ambigui to the jugular fora- men, as this would resolve, bringing a return of vocal cord function, as the intracranial pressure decreases through conservative or operative management. 5 Similar mechanisms may have occurred in our case also. Repeated tapping of CSF resolved stridor in our patient. Unlike other cases reported in literature, our patient suffered postmeningitic hydro- cephalus and presented with stridor. We suggest that stridor be recognized as a sign of raised intracranial pressure in neurosurgical patients. The sign may not only be associated with congenital malformations (Arnold-Chiari, myelomeningocele) and central nervous system catastrophes (cerebral trauma, infarct), but also with meningitis resulting in hydro- cephalus. Hemanshu Prabhakar, MD Zulfiqar Ali, MD Girija P. Rath, DM Department of Neuroanaesthesiology All India Institute of Medical Sciences New Delhi, India 110029 REFERENCES 1. Rosin D, Handler SD, Potsic WP, et al. Vocal cord paralysis in children. Laryngoscope. 1990;100:1174–1179. 2. Pollack IF, Pang D, Albright AL, et al. Outcome following hindbrain decompres- sion of symptomatic chiari malfor- mations in children previously treated with myelomeningocele closure and shunts. J Neurosurg. 1992;77:881–888. 3. Holinger PC, Holinger LD, Reichert TJ, et al. Respiratory obstruction and apnea in infants with bilateral abductor vocal cord paralysis, meningomyelocele, hydroce- phalus and Arnold-Chiari malformations. J Pediatr. 1978;92:368–373. 4. Solan K, Glaisyer H. Raised intracranial pressure and stridor. Pediat Anesth. 2006; 16:877–879. 5. Davis L, Ross N. Bilateral vocal cord palsy after ventricular drainage in a child. Anesth Analg. 2001;92:358–361. Prolonged Propofol Infusions in Pregnant Neurosurgical Patients To JNA Readership: There are few descriptions of prolonged propofol use in pregnancy, and we would like to describe our experience of using propofol for prolonged neurosurgery in 2 such patients. AX was a 32-year-old primigra- vida at 26 weeks gestation with neurofibromatosis II and a vestibular schwannoma increasing in size and causing neurologic deterioration. Preinduction blood gases showed a respiratory alkalosis consistent with pregnancy. Anesthesia lasted 18.5 hours, and consisted of remifentanil 0.1 to 0.35 mg/kg/min and propofol TCI (Target Controlled Infusion) 3 to 5 mg/mL for 11 hours; this was changed to sevoflurane (ET 0.8% to 1.3%) for the remaining 7 hours. This action was taken because the base excess decreased from 0.1 to  6.2 mmol/L, pH decreased from 7.5 to 7.37 with bicarbonate decreasing from 24.9 to 19.4 mmol/L; although not in the ‘‘acidotic’’ range, the comparative difference was signifi- cant. Lactate ranged from 1.4 to 3.7 mmol/L and chloride from 103 to 112 mmol/L. 1 BX was a 21-year-old primigra- vida who, at 9 weeks gestation pre- sented with a recurrent vestibular schwannoma. Anesthetic time was 14 hours. The technique used was the same as for AX, with sevoflurane (ET 0.4% to 1.4%) being substituted for propofol after 10 hours due to developing acidosis. In both cases, in view of the deteriorating acid-base status, propo- fol was changed to sevoflurane and, because chloride was also rising, 0.9% saline was changed to Hartmann’s (ringers lactate) solution, reducing the chloride infused from 154 to 111mmol/L. No further increase in acidosis developed after these changes, although it took 24 hours for the base deficits to normalize. In searching for a cause for these patients’ metabolic acidosis, it was important to rule out remediable causes; there was no evidence of renal failure, hypoxemia, impaired hepatic lactate metabolism, sepsis, and CO 2 was normal. Generous fluids were given to eradicate hypo- perfusion as a cause of acidosis. A ‘‘massive’’ blood transfusion can oc- casionally cause a metabolic acidosis but AX only received 4 units very slowly. To explain the base deficit being caused by propofol we would have expected an ‘‘anion gap metabolic acidosis.’’ 2 The anion gap remained within the normal range (8 to 16 mmol/L) at all times. Although the measured parameters go against these being examples of ‘‘propofol infusion’’ syndromes, in future cases we would use a volatile-based techni- que from the outset. Metabolism and distribution of propofol is altered in the gravid patient (explained in part by the increased volume of distribution and differences in protein binding) and it may be of interest to readers that during AX’s anesthetic, with the propofol TCI set at 4.5 mg/mL, serum concentration was measured as 2 mg/mL, and later with the TCI at 1 mg/mL, serum concentra- tion was 0.6 mg/mL. This alteration in metabolism compounds the notor- ious difficulty in correctly estimating the weight that should be entered into the TCI algorithm in such patients. We found the use of the Bispectral index monitor invaluable in these 2 cases. There is little data on the effect of propofol infusions and the fate of the unborn child. We are happy to J Neurosurg Anesthesiol  Volume 19, Number 1, January 2007 Correspondence r 2006 Lippincott Williams & Wilkins 67