Spinal cord blood flow following subarachnoid tetracaine

Spinal cord and spinal dural blood flow in the cervical, thoracic and lumbosacral regions were measured in dogs using the radioactive microsphere technique. Measurements were taken before and 20 and 40 minutes after lumbar subarachnoid injection of one of the following: physiologic saline; tetracaine 20 mg or tetracaine 20 mg with epinephrine 200 micrograms. No significant change in spinal cord or spinal dural blood flow occurred following subarachnoid physiologic saline or tetracaine with epinephrine. Dogs receiving subarachnoid tetracaine demonstrated a significant increase in lumbosacral spinal cord, and thoracic and lumbosacral dural blood flow at 20 and 40 minutes following injection. Cervical dural blood flow was significantly increased at 40 minutes after subarachnoid tetracaine. Lumbar subarachnoid tetracaine (20 mg) produces a regional spinal cord and generalized dural hyperemia which is prevented by the addition of epinephrine (200 micrograms).     

Spinal cord blood flow following sub-arachnoid lidocaine

Twelve mongrel dogs were randomized into two equal groups. Cervical, thoracic and lumbosacral spinal cord and spinal dural blood flows were measured using the radioactive microsphere technique. Blood flow determinations were made prior to and 20 and 40 minutes following lumbar subarachnoid injection of: two per cent lidocaine (100 mg) or two per cent lidocaine (100 mg) with 1/25,000 epinephrine (200 micrograms). Dogs receiving subarachnoid lidocaine demonstrated a decrease in mean arterial blood pressure of 23 per cent and 14 per cent (p less than 0.05), while dogs receiving lidocaine with epinephrine had a decrease of 38 and 34 per cent (p less than 0.05) at 20 and 40 minutes respectively. Cardiac index was not significantly changed in either group. Lumbar subarachnoid lidocaine (100 mg) produced a rapid regional dural hyperemia (observed at 20 minutes postinjection) and a delayed regional spinal cord hyperemia (observed at 40 minutes postinjection) which were not observed following the addition of epinephrine (200 micrograms).     

Spinal cord blood flow following subarachnoid lidocaine

Twelve mongrel dogs were randomized into two equal groups. Cervical, thoracic and lumbosacral spinal cord and spinal durai blood flows were measured using the radioactive microsphere technique. Blood flow determinations were made prior to and 20 and 40 minutes following lumbar subarachnoid injection of: (I) two per cent lidocaine (100 mg) or (2) two per cent lidocaine (100 mg) with 1/25,000 epinephrine (200 μg). Dogs receiving subarachnoid lidocaine demonstrated a decrease in mean arterial blood pressure of 23 per cent and 14 per cent (p < 0.05), while dogs receiving lidocaine with epinephrine had a decrease of 38 and 34 per cent (p < 0.05) at 20 and40 minutes respectively. Cardiac index was not significantly changed in either group. Lumbar subarachnoid lidocaine (100 mg) produced a rapid regional durai hyperemia (observed at 20 minutes postinjection) and a delayed regional spinal cord hyperemia (observed at 40 minutes postinjection) which were not observed following the addition of epinephrine (200 μg).     

The effect of subarachnoid epinephrine and phenylephrine on spinal cord blood flow

Eighteen mongrel dogs were divided into three equal groups. Spinal cord and spinal dural blood flow in the cervical, thoracic and lumbosacral regions were measured using the radioactive microsphere technique. Measurements were taken before and 10 and 40 minutes after lumbar subarachnoid injection of one of the following: physiologic saline; epinephrine 200 micrograms or phenylephrine 5 mg. No significant change in spinal cord blood flow occurred in any of the groups, nor was there any difference between the groups. Dogs receiving subarachnoid phenylephrine did demonstrate a significant reduction of thoracic dural blood flow at ten minutes. Dogs receiving intrathecal epinephrine or phenylephrine demonstrated a significant reduction in lumbo-sacral dural blood flow at ten minutes after injection. The reduction in dural blood flow was still evident at 40 minutes in dogs receiving phenylephrine. Subarachnoid epinephrine (200 micrograms) and phenylephrine (5 mg) do not effect spinal cord blood flow but do produce regional dural vasoconstriction.     

The effect of dopamine,atropine, phenylephrine and cardiac pacing on oxygen consumption during fentanyl-nitrous oxide anaesthesia in the dog

In animals deeply anaesthetized with fentanyl and nitrous oxide the artierial blood pressure and heart rate were increased using dopamine, atropine, electrical pacing and phenylephrine in order to study the accompanying change in whole body oxygen consumption. Seven dogs (16–24 kg) were anaesthetized with fentanyl 1 μg · kg^-1 · min^-1. After completing instrumentation a dopamine infusion was started at a rate of 39 μg · kg^-1 · min^-1. After the mean blood pressure reached 18.6 kPa the infusion was reduced to 10 μg · kg^-1 · min^-1 and maintained for 10 minutes. After waiting 45 minutes an infusion of atropine 20 μg · kg^-1 · min^-1 was started and when the heart rate reached 120 b/min the infusion was slowed to 1.25 μg · kg^-1 ’ · min^-1 and maintained for 10 minutes. Twenty-five minutes later the heart rate was increased to 150 beats/min and maintained at that level for 10 minutes using electrical pacing. The pacing was removed and an infusion of phenylephrine 5 μg·kg^-1·min^-1 was started. When the blood pressure reached 21.3 kPa the infusion was reduced to 2.5 μg · kg^-1· min^-1 and maintained for 10 minutes. The results show increases in oxygen consumption of 14 per cent with dopamine, 19 per cent with atropine, 16 per cent with pacing, and 14 per cent with phenylephrine. All changes were significantly different from the control values. The magnitude of change in whole body oxygen consumption was best predicted by either the cardiac output x blood pressure product or by the cardiac output alone.     

Adequacy of caudal analgesia in children after penoscrotal and inguinal surgery using 0.5 or 1.0 ml·kg−1 bupivacaine 0.125%

To determine the optimal volume of bupivacaine 0.125% for postoperative caudal analgesia, we compared the effectiveness of 0.5 ml·kg^?1 and 1 ml·kg^?1 of bupivacaine 0.125% with 1:200,000 epinephrine in 80 children undergoing penoscrotal and inguinal surgery. The adequacy of caudal analgesia and supplemental analgesic requirements did not differ between the two groups at any time during the first 12 hr after surgery. We conclude that 0.5 ml·kg^?1 of bupivacaine 0.125% with 1:200,000 epinephrine is as effective as 1 ml·kg^?1 of the same solution and recommend its use for penoscrotal surgery. The evidence for ss of 0.5 ml·kg^?1 of bupivacaine 0.125% for inguinal owever, is inconclusive because of an insufficient patients studied.     

Resuscitation strategies from bupivacaine-induced cardiac arrest

Objectives: Local anesthetic (LA) intoxication with cardiovascular arrest is a potential fatal complication of regional anesthesia. Lipid resuscitation has been recommended for the treatment of LA‐induced cardiac arrest. Aim of the study was to compare four different rescue regimens using epinephrine and/or lipid emulsion and vasopressin to treat cardiac arrest caused by bupivacaine intoxication. Methods: Twenty‐eight piglets were randomized into four groups (4 × 7), anesthetized with sevoflurane, intubated, and ventilated. Bupivacaine was infused with a syringe driver via central venous catheter at a rate of 1 mg·kg^?1·min^?1 until circulatory arrest. Bupivacaine infusion and sevoflurane were then stopped, chest compression was started, and the pigs were ventilated with 100% oxygen. After 1 min, epinephrine 10 μg·kg^?1 (group 1), Intralipid^® 20% 4 ml·kg^?1 (group 2), epinephrine 10 μg·kg^?1 + Intralipid^® 4 ml·kg^?1 (group 3) or 2 IU vasopressin + Intralipid^® 4 ml·kg^?1 (group 4) were administered. Secondary epinephrine doses were given after 5 min if required. Results: Survival was 71%, 29%, 86%, and 57% in groups 1, 2, 3, and 4. Return of spontaneous circulation was regained only by initial administration of epinephrine alone or in combination with Intralipid^®. Piglets receiving the combination therapy survived without further epinephrine support. In contrast, in groups 2 and 4, return of spontaneous circulation was only achieved after secondary epinephrine rescue. Conclusions: In cardiac arrest caused by bupivacaine intoxication, first‐line rescue with epinephrine and epinephrine + Intralipid^® was more effective with regard to survival than Intralipid^® alone and vasopressin + Intralipid^® in this pig model.     

Impact of propofol on electrocardiographic alterations during intravascular application of bupivacaine--a study in piglets

Background: Intravascular application of a small dose of local anesthetics (LA) with epinephrine as well as larger doses of LA under sevoflurane anesthesia results in increase in T‐wave amplitude in the electrocardiogram (ECG). The aim of this study was to elucidate whether propofol anesthesia affects these ECG alterations or not. Methods: Thirty neonatal pigs were randomized into two groups. Group 1 was anesthetized with sevoflurane, group 2 with sevoflurane plus continuous propofol infusion (10 mg·kg^?1·h^?1). A test dose of 0.2 ml·kg^?1 bupivacaine 0.125% + epinephrine 1 : 200 000 was injected intravenously. Arterial pressure was monitored. ECG was analyzed for changes in T‐wave amplitude (positive if ≥25% baseline) and heart rate. In another setting, bupivacaine 0.125% was intravenous infused at a rate of 4 mg·kg^?1·min^?1. ECG was analyzed for alteration in T‐wave amplitude and heart rate at 1.25, 2.5, and 5 mg·kg^?1 bupivacaine infused. Results: T‐wave elevation after the administration of an epinephrine containing LA test dose was similar between the two groups. Increase in heart rate caused by the test dose were significantly higher in group 2 (P = 0.008). During continuous bupivacaine administration, T‐wave elevation occurred in 40% and 71% (group 1 and 2) at 1.25 mg·kg^?1, in 80% and 100% at 2.5 mg·kg^?1, and in 93% and 86% at 5 mg·kg^?1 bupivacaine infused. Conclusion: Continuous propofol infusion does not suppress the ECG signs of a systemically administered epinephrine containing LA test dose nor does it suppress the ECG signs caused by high doses of intravenous applied bupivacaine.     

Intrathecal clonidine decreases propofol sedation requirements during spinal anesthesia in infants

Background: Propofol is a popular agent for providing procedural sedation in pediatric population during lumbar puncture and spinal anesthesia. Adjuvants like clonidine and fentanyl are administered intrathecally to prolong the duration of spinal anesthesia and to provide postoperative analgesia. We studied the propofol requirement after intrathecal administration of clonidine or fentanyl in infants undergoing lower abdominal surgeries. Methods: Sixty‐five ASA I infants undergoing elective lower abdominal surgery under spinal anesthesia were assigned into four groups in this prospective randomized double‐blinded study. Group B received bupivacaine based on body weight (<5 kg = 0.5 mg·kg⁻¹; 5–10 kg = 0.4 mg·kg⁻¹). Group BC received 1 μg·kg⁻¹ of clonidine with bupivacaine, group BF received 1 μg·kg⁻¹ of fentanyl with bupivacaine, and patients in group BCF received 1 μg·kg⁻¹ each of clonidine and fentanyl with bupivacaine. A bolus of 2–3 mg·kg⁻¹ of propofol bolus was administered for lumbar puncture. Sedation was assessed using a six‐point sedation score (0–5) and a five‐point reactivity score (0–4) which was based on a behavioral score. After achieving a sedation and reactivity score of 3–4, the patients were placed lateral in knee chest position and lumbar puncture performed and test drug administered. Further intraoperative sedation was maintained with an infusion of 25–50 μg·kg⁻¹·min⁻¹ of propofol infusion. Results: The mean ± sd infusion requirement of propofol decreased from 35.5 ± 4.5 in group B to 33.4 ± 5.4 μg·kg⁻¹·min⁻¹ in group BF and further decreased to 16.7 ± 6.2 μg·kg⁻¹·min⁻¹ and 14.8 ± 4.9 μg·kg⁻¹·min⁻¹ in group BC and BCF, respectively. There were no statistically significant differences between BC and BCF groups. The mean sedation and reactivity scores were higher in groups BC and BCF when compared to groups B and BF. Conclusion: Our study show that the requirement of propofol sedation reduces with intrathecal adjuvants. The reduction was significant with the addition of clonidine and clonidine–fentanyl combination as opposed to bupivacaine alone or with fentanyl. There was no significant difference in propofol infusion requirement with the use of bupivacaine alone or with fentanyl.     

Pharmacokinetics of sufentanil in patients undergoing renal transplantation

Renal failure and chronic haemodialysis are often associated with alterations in fluid status and plasma proteins. These changes, in turn, may result in pharmacokinetic alterations in affected patients. The purpose of this study was to investigate the pharmacokinetics of sufentanil in chronic renal failure patients undergoing kidney transplantation. Ten male patients were studied. Following induction of anaesthesia each patient received sufentanil 2.0 ?g· kg^-1 IV with subsequent serial plasma sampling for drug measurement from one to 360 minutes. A biexponential equation provided the best fit of the sufentanil concentration data with mean ± SEM distribution (alpha) and elimination (beta) half-lives of 2.9 ± 1.3 and 176 ±87 minutes, respectively. The mean Vc and Vd beta values were 0.15 ± 0.05 L·kg^-1 and 0.85 ± 0.16 L·kg^-1, respectively; plasma drug clearance was 11.5 ± 3.7 ml· kg^-1 ·min^-1. Mean values for K10, K12 and K21 were0.15 ± 0.06· min^-1, 0.4 ± 0.14 · min^-1 and 0.1 ± 0.04·min^-1, respectively. With the exception of Vd beta, these pharmacokinetic values are similar to those reported in previous studies in general surgical, elderly and burn patients. The Vd beta values observed in this study may have resulted from alterations in drug distribution or elimination following revascularization of the implanted kidneys. Nevertheless, it appears that modification of sufentanil doses is unnecessary in chronic renal failure patients undergoing renal transplantation.     

Inhibition of cerebral metabolic and circulatory responses to nitrous oxide by 6-hydroxydopamine in dogs

Purpose

To determine whether cerebral metabolic and circulatory consequences of N₂O result from activation of the sympathoadrenal system. The effects of pretreatment with intracistemal injection of 6-OHDA, which produces chemical sympathectomy, were studied in dogs.

Method

Seven days before measurement dogs were pretreated with intracisternal injection of either saline vehicle (sham-group) or 100 μg· kg^?1 6-hydroxydopamine (6-OHDA group). Cerebral blood flow (CBF) was measured using an electromagnetic flow-meter probe and cerebral metabolic rate for oxygen (CMRO₂) was calculated as the product of CBF and arterial-sagittal sinus blood oxygen content difference [C(a-v)O₂].

Results

In the sham group, N₂O (60%) increased CMRO₂ from 6.11 ± 0.21 ml· 100 g^?1· min^?1 to 7.10 ± 0.39 ml· 100g^?1· min^?1 and CBF from 63 ± 5 ml· 100 g^?1 · min^?1 to 173 ± 26 ml· 100 g^?1· min^?1. In the 6-OHDA group, CMRO₂ did not change during N₂O exposure, whereas CBF increased from 61 ± 3 ml· 100 g^?1· min^?1 to 135 ±19 ml· 100 g^?1· min^?1 but less then in the sham group. The 6-OHDA group displayed a reduction in cortical noradrenaline (NA) concentration from 263.2 ± 35.6 ng·g^?1 to 102.7 ± 16.5 ng· g^?1. Cortical dopamine (DA) concentration was not affected by 6-OHDA administration.

Conclusion

These results suggest that most of the increase in CMRO₂ and, at least a part of, the increase in CBF during N₂O exposure in the sham-group are related to sympathoadrenal-stimulating effects of N₂O.     

Comparison of epinephrine vs lipid rescue to treat severe local anesthetic toxicity – an experimental study in piglets

Objectives: Local anesthetic (LA) intoxication with severe hemodynamic compromise is a potential catastrophic event. Lipid resuscitation has been recommended for the treatment of LA‐induced cardiac arrest. However, there are no data about effectiveness of Intralipid^® for the treatment of severe cardiovascular compromise prior to cardiac arrest. Aim of this study was to compare effectiveness of epinephrine and Intralipid^® for the treatment of severe hemodynamic compromise owing to bupivacaine intoxication. Methods: Piglets were anesthetized with sevoflurane, intubated, and ventilated. Bupivacaine was infused with a syringe driver via a central venous catheter at a rate of 1 mg·kg^?1·min^?1 until invasively measured mean arterial pressure (MAP) dropped to 50% of the initial value. Bupivacaine infusion was then stopped, and epinephrine 3 μg·kg^?1 (group 1), Intralipid^® 20% 2 ml·kg^?1 (group 2), or Intralipid^® 20% 4 ml·kg^?1 (group 3) was immediately administered. Survival, hemodynamic course, and ET_CO2 were recorded. Results: Twenty‐one piglets (3 × 7), with median age of 26 days (19–43) and weighing 4.9 kg (4.3–5.8), were investigated. All animals in group 1 (100%) but only four of seven (57%) piglets in group 2 and group 3, respectively, survived. Normalization of hemodynamic parameters (HR, MAP) and ET_CO2 was fastest in group 1 with all piglets achieving HR and MAP values at or above baseline within 1 min. Conclusion: For the treatment of severe hemodynamic compromise owing to bupivacaine intoxication in piglets, first‐line rescue with epinephrine was more effective than Intralipid^® with regard to survival as well as normalization of hemodynamic parameters and ET_CO2.     

Studies of fentanyl-supplemented anaesthesia: Effect of naloxone on the circulation and respiration

Ninety-nine unselected patients were given a standardized general anaesthetic with fentanyl 1.5 jag · kg^-1 every 30 minutes and were randomly divided into three equal Groups: Group I patients received naloxone 0.1 mg, Group II naloxone 0.2 mg, and Group III naloxone 0.4 mg, at the end of operation and after the reversal of neuromuscular blockade. After administration of naloxone systolic blood pressure increased by 4, 8 and 7 per cent and mean arterial blood pressure increased by 3, 8 and 8 per cent in Groups I, II and III respectively; heart rate increased by 4, 11 and 8 per cent and rate-pressure product increased by 7, 18 and 15 per cent in Groups I, II and III respectively. Tidal volume increased by 97, 101 and 95 per cent and minute volume increased by 122, 164 and 143 per cent in Groups I, II and III respectively after naloxone. Forty-nine percent of patients had a tidal volume of less than 5 ml · kg^-1 ora minute volume of less than 50 ml · kg^-1 before administration of naloxone; after naloxone three patients in Group I (naloxone 0.1 mg) had a tidal volume of less than 5 ml · kg^-1 and no patient had a respiratory minute volume of less than 50 ml · kg^-1. It is concluded that under the conditions of this study naloxone 0.1 mg is adequate to reverse the respiratory depressant effect of fentanyl in the majority of cases.     

Propranolol pretreatment reduces cardiorespiratory toxicity due to plain,but not epinephrine-containing,intravenous bupivacaine in rats

The purpose of this study was to evaluate the effects of pretreatment with propranolol on the cardio-respiratory toxicity of bupivacaine, either plain or with epinephrine 1:200,000 (5 μg · ml^{? 1}) added. Adult male Sprague Dawley rats, anaesthetized with intraperitoneal pentobarbital, were divided into four groups. Groups I and III were pretreated with iv propranolol 150 μg · kg^{? 1}, and Groups II and IV recei ved iv NS as a placebo. Three minutes later, rats in Groups I and II received plain 0.5% bupivacaine, 4 mg · kg^{? 1}, and Groups III and IV received 4 mg· kg^{? 1} of 0.5% bupivacaine with epinephrine, 5 μg · ml^{? 1} iv. Five of eight rats pretreated with propranolol survived (Group I), compared with uniform fatality with NS pretreatment (Group II) (P < 0.05). Addition of epinephrine to the bupivacaine eliminated the protective effect of propranolol. All rats pretreated with propranolol (Group III) or NS (Group IV) died when given bupivacaine with epinephrine. In conclusion, acute propranolol pretreatment reduced the fatal cardiotoxicity due to iv bupivacaine in male Sprague Dawley rats, but the addition of epinephrine 5 μg · ml^{? 1} to bupivacaine eliminated the protective effect of propranolol.     

Vasodilator therapy after cardiac surgery: a review of the efficacy and toxicity of nitroglycerin and nitroprusside

Eight-five patients who required vasodilator therapy in the postoperative period after cardiac surgery were studied to compare the haemodynamic effects of nitroglycerin and nitroprusside, to evaluate local and systemic toxicity, and to develop long-range dosage recommendations. Ninety-one per cent of the patients received the vasodilators for postoperative hypertension, while nine per cent had low output syndromes. Both drugs significantly decreased blood pressure and central venous pressure, and increased heart rate. Nitroglycerin decreased both right and left ventricular filling pressures more than nitroprusside. No local toxicity or methaemoglobinaemia was found with either drug. Elevated thiocyanate levels were detected in 44 per cent of the nitroprusside group; however, none of the patients developed progressive metabolic acidosis. For prolonged infusions we found that nitroprusside at 1 μg·kg^-1·min^-1 and nitroglycerin at 0.5 μg·kg^-1· min^-1 were without significant toxicity.     

Assessment of immediate post-anaesthetic recovery in young children following intravenous morphine infusions,halothane, and isoflurane

Within 15 minutes of terminating general anaesthesia, progressive recovery of consciousness, spontaneous ventilation and cough, and limb movements were assessed in 60 young children (age range 0-5 years, mean ± SEM; 2.$3 ± 0.34; weight 13.86 ± 0.41 kg). All patients were ASA physical status class I-III, received a standard intravenous induction (atropine 0.02 mg·kg^-1, thiopental sodium 5 mg·kg^-1, diazepam 0.2mg·kg^-1), were intubated with an orotracheat tube following the administration of metocurine, 0.4 mg·kg^-1, and were maintained under general anaesthesia with nitrous oxide and oxygen in a 70:30 mixture administered by a T-piece circuit. They were ventilated mechanically to maintain normal blood- oxygen tension and normocarbia. The patients were assessed in three equal groups according to the anaesthetic supplement they received. Group I received intravenous infusions of morphine sulfate (loading dose 60 μg·kg^-1administered over 5 minutes followed by a continuous intravenous infusion of 2 μg·kg^-1min^-1. Patients in Groups II and HI had 0.5 per cent halothane and 1.0 per cent isoflurane respectively added to the nitrous oxidel oxygen fresh gas mixture rather than morphine sulphate infusions. By the end of the study period, there was no significant difference in the degree of recovery between the morphine and the isoflurane groups but the patients in the halothane group had recovered to a lesser degree. Generally, the patients in the morphine group were awake but not crying, while those in the other two groups were less sedated.     

New regimen for interpleural block in children

A new regimen for postoperative analgesia after thoracic surgery is proposed. Eight children received an interpleural infusion using bupivacaine 0.1% in a regimen from 0.5 ml·kg^?1·h^?1 up to 1 ml·kg^?1·h^?1, for 48 h according to the pain scores. The plasma levels after 24 h and 48 h were measured as well as the pleural level and in two patients the free fraction of plasma bupivacaine and the plasma PPX (a metabolite of bupivacaine) and one patient the orosomucoid (main plasma protein involved in bupivacaine protein binding) were also measured pre and postoperatively. The results shows the safety of such a regimen, for two days of postoperative analgesia.     

Intravenous nitrogly-cerin administration during infrarenal aortic clamping

Twenty-five patients requiring infrarenal abdominal aortic clamping were studied during halothane, nitrous oxide anaesthesia. Aortic clamping caused reductions in cardiac index (CI), stroke volume index (SVI) and left ventricular stroke work index (LVSWI). Systemic vascular resistance (SVR) increased. In seven patients CI was less than 1.8 l·min^-1m^-2. Intravenous administration of nitroglycerin, 1μg·kg^-1min^-1, for 20 minutes, accompanied by volume loading to maintain pulmonary capillary wedge pressure, resulted in a significant improvement in haemodynamic parameters. CI increased 24 per cent as a result of a 14 per cent increase in SVI and an eight per cent increase in heart rate, LVSWI increased 13 per cent and SVR decreased 21 per cent. The plasma nitroglycerin concentration at the time of these measurements was 2.9 ± 1.0ng·ml^-1, Aortic unclamping resulted in a mean maximum decrease of 14 ± 2 torr mean arterial pressure. Epinephrine, norepinephrine and plasma renin activity gradually increased during the period of the anaesthetic.     

Correction of the unfavourable effects of vasopressin by nitroglycerin infusion

Nitroglycerin was administered with vasopressin to prevent adverse effects. Vasopressin 0.25U.70kg^-1 . min^-1 was infused intravenously in four dogs for 40 minutes, when a venous infusion of nitroglycerin 1.2 μ.g.kg^-1 min^-1 was added for 20 minutes. Nitroglycerin 1.2 µg.kg^-1 .min^-1 alone was infused intravenously in another four dogs for 40 minutes. The venous blood pressures (mesenteric and central) and arterial pressures (mesenteric and femoral), the electrocardiogram and arterio-venous difference were recorded. Nitroglycerin was shown to annul the unfavourable effects of vasopressin without altering its efficacy upon portal pressure.     

Respiratory depression after low-dose caudal morphine

Purpose

To report a case of respiratory depression after a small dose of caudal morphine administered to a 15-mo-old child.

Clinical features

A 15 mo, 9.8 kg boy underwent ureteral reimplantation with general endotracheal anaesthesia and 10 ml bupivacaine 0.25% (2.5 mg · kg^?1). Ninety minutes after the bupivacaine, 0.4 mg (1 mg · ml^?1, 0.4 ml, 0.04 mg · kg^?1) preservative-free morphine was injected after negative aspiration. Slighly more than two hours after caudal morphine, the patient became lethargic and developed decreases in oxygen saturation (to 62%) without change in heart rate or respiratory rate. Intravenous naloxone 0.1 mg (0.01 mg · kg^?1) markedly improved his level of consciousness. Racemic epinephrine was administered for treatment of coincident stridor. The patient required 11 hr continuous naloxone infusion (0.001–0.002 mg · kg^?1 · hr^?1) in the intensive care unit. He was discharged on the second postopertive day without further complication.

Conclusion

Respiratory depression can occur in children greater than one year of age, even when small doses of caudal morphine are used. Decreased arterial oxygen saturation and lethargy are important heralds. A normal respiratory rate despite substantial hypoxaemia argues that pulse oximetry (without supplemental oxygen where possible) has a clear advantage over impedance pneumography for electronic monitoring.