Kodali Bhavani Shankar

Arterial to end tidal carbon dioxide tension difference during Caesarean section anaesthesia

The relationship between arterial carbon dioxide tension and end tidal carbon dioxide tension was studied in 19 patients during general anaesthesia for Caesarean section. Thirteen patients scheduled for elective abdominal hysterectomy formed a nonpregnant group. There was significant correlation between arterial and end tidal CO2 tensions in both groups. During Caesarean section, this difference was significantly less than in the nonpregnant group.

Regional anesthesia in parturients with low platelet counts

To the Editor: The lowest platelet counts at which one can safely administer neuraxial anesthesia for labour and delivery is controversial. Published studies are few and sample sizes small.1–3 We report our institutional experience with thrombocytopenic parturients, probably the largest group to date. Medical records from 1997 to 2002 of parturients with platelet counts < 100,000·μL–1 during the peripartum period were reviewed for methods of anesthesia/analgesia for delivery, peripartum, and hospital course and incidence of neurological complications; 177 patients were identified. Of these, 170 (96%) received regional anesthesia. Ninety percent of identified patients had platelet counts > 70,000·μL–1; all received regional anesthesia for either vaginal or Cesarean delivery, as did all parturients with platelet counts 70,000·μL–1 to 60,000·μL–1 requesting regional anesthesia. In paturients with platelet counts between 50,000 to 60,000·μL–1, six received regional anesthesia and one was denied. Spinal, instead of epidural, was more often chosen in this group than in those with counts > 60,000·μL–1 (4/6 vs 29/160 P < 0.005, Chi square test), probably because five of seven parturients in this group presented for Cesarean delivery for worsening pre-eclampsia without being in labour and because of a perception among anesthesiologists of the lower risk of epidural hematoma associated with spinal (1:220,000) vs epidural anesthesia (1:150,000).4 Parturients with counts < 50,000·μL–1 received regional anesthesia only after platelet transfusion. In 82%, the platelet count was over 60,000·μL–1 at catheter removal in our study. In some women, platelet count decreased after epidural placement and the catheter was left in place for up to 36 hr until the platelet count showed a steady rise. Five patients had counts < 50,000·μL–1 (two of them, 36 and 38,000·μL–1, respectively) when catheters were removed. The causes of thrombocytopenia were gestational thrombocytopenia, pre-eclampsia, and idiopathic thrombocytopenia. There were no other associated coagulation abnormalities. No neurological complications were documented in any patients reviewed. Our retrospective study by no means proves that it is safe to administer regional anesthesia to parturients with platelet counts < 100,000·μL–1. Using the standard formulae for zero numerators,5 we estimate, with 95% confidence, that the incidence of epidural hematoma in our population is not greater than 1.8%. If our data are combined with other published reports, the expected incidence becomes even lower. Assessment of the incidence of a rare event is difficult in clinical practice. Therefore, in the absence of large, unfeasible studies, it is prudent to evaluate the risk-benefit ratio on a case-by-case basis before administering regional anesthesia to parturients.

Anesthesia outside the operating room for emergency procedures.

Non-anesthetists usually provide sedation and anesthesia outside the operating room for emergency procedures. Techniques vary from no sedation to deep sedation using drugs with a good safety profile and few side effects. Newer methods of airway control may allow volatile agents such as sevoflurane to be used. Anesthetists may need to join sedation teams if they are to maintain control of their specialty.

Intranasal cocaine/adrenaline during halothane anaesthesia.

We find the paper (Anaesthesia 1988; 4 3 3568) interesting particularly because there is yet no controlled scientific study to provide experimental data about the use of halothane anaesthesia during topical application of cocaineladrenaline mixture in clinically useful doses in humans.’ May we be permitted to comment? Firstly, Delilkan e t aLz found that the increases in mean pulse rate and in the mean systolic blood pressure were higher in the group who received nasal application of cocaine/adrenaline mixtures than in the group who received cocaine alone, whereas in the present study there was no significant difference between pulse rate and blood pressure in the two groups. The amount of cocaine used in these two studies is similar, so the use of halothane in Bromley’s study may have prevented the increase of blood pressure and pulse rate after nasal application of cocaine/adrenaline mixtures. Secondly, is this technique of spontaneous ventilation with 2% halothane used by the authors justified especially when their study showed cocaine levels which approached toxic levels in two patients? The commonly used combination of topical adrenaline and cocaine is widely considered to be a potentially dangerous mixture. 5 Experimental animal studies have shown that cocaine potentiates the arrhythmic effects of halothane and adrenaline combinations.6 The increased carbon dioxide levels which may be associated with spontaneous ventilation could further increase the risk of arrhythmias. The bradycardia observed by Bromley e t al. in three patients could be due to the effect of cocaine and 2% halothane. Adrenaline, in the presence of possible hypercarbia could have resulted in ventricular ectopics. Our practice is to use controlled ventilation of the lungs with a Bain system (fresh gas flow 100 ml/kg/minute) in all patients who require intranasal cocaine/adrenaline applications during halothane anaesthesia.’ The arterial carbon dioxide tensions are predictable with the Bain system even in the absence of end-tidal COz monitoring. We studied electrocardiograms during halothane general anaesthesia in 26 patients who had topical applications of 2 ml either 5% cocaine (100 mg) with 1 in 1000 (2 mg) adrenaline or 10% cocaine (200 mg) with 1 in 10 000 (0.2 mg) adrenaline.’ A critical analysis of the ECGs revealed no serious arrhythmias except junctional rhythm in two patients and broad and bifid T-waves in five. The ECG changes described occurred at 15 minutes after nasal application of cocaine/adrenaline and persisted for up to 30 minutes, during which time the plasma concentrations are at their peak.’