Pneumatosis cystoides intestinalis: imaging findings with colonoscopy correlation.

We report on a case of pneumatosis cystoides intestinalis in a 32-year-old woman affected by coeliac disease with stool cultures positive for salmonella. After plain film of the abdomen, patient underwent computed tomography and magnetic resonance colonography studies that demonstrated numerous, diffuse bubblelike intramural gas collections into the ascending, transverse and descending colonic wall. CT and MR findings were correlated with colonoscopy.

MnDPDP-enhanced MRI vs dual-phase spiral CT in the detection of hepatocellular carcinoma in cirrhosis.

The objectives of this study were twofold: (a) to assess safety and tolerability of the hepatobiliary MR contrast agent MnDPDP; and (b) to investigate the sensitivity of MnDPDP-enhanced MRI, in comparison with dual-phase spiral CT, in the detection of hepatocellular carcinoma (HCC) in cirrhosis. Fifty patients with liver cirrhosis and histologically proven HCC were enrolled in a prospective phase-IIIB clinical trial. All patients underwent evaluation with dual-phase spiral CT and pre-contrast and post-contrast MRI at 1.5 T. The MR examination protocol included spin-echo (SE) and gradient-recalled-echo (GRE) T1-weighted images acquired before and 60-120 min after administration of 0.5 micromol/kg (0.5 ml/kg) MnDPDP (Teslascan, Nycomed Amersham, Oslo, Norway); and fast T2-weighted SE images obtained solely before contrast injection. Gold standard was provided by findings at Lipiodol CT in combination with follow-up spiral CT studies, which were repeated at 4-month intervals over a 10- to 27-month (mean +/- SD 20.1 +/- 5.1 months) follow-up period. No serious adverse event occurred. Eighty tumors ranging 0.8-9.1 cm in diameter (mean +/- SD 3.2 +/- 2.4 cm) were detected by Lipiodol CT or confirmed as cancerous foci by follow-up CT studies. Pre-contrast MRI detected 38 of 80 lesions (48%); MnDPDP-enhanced MRI, 65 of 80 lesions (81%); pre-contrast plus post-contrast MRI, 69 of 80 lesions (86%); and dual-phase spiral CT, 64 of 80 lesions (80%). The difference between unenhanced and MnDPDP-enhanced MRI was statistically significant (p < 0.001). The difference between MRI (pre-contrast plus post-contrast) and dual-phase spiral CT was not statistically significant (p = 0.33). The confidence in the final diagnosis, however, was significantly higher for MRI as compared with spiral CT (p<0.001). MnDPDP is a safe and well-tolerated hepatobiliary MR contrast agent. Magnetic resonance imaging with use of MnDPDP is significantly more sensitive than unenhanced MRI and as good as dual-phase spiral CT for detection of HCC in cirrhosis.

Role of iodine in evolution and carcinogenesis of thyroid, breast and stomach.

The authors have hypothesized that dietary iodine (deficiency or excess) is associated with the development of some gastric and mammary cancers, as it is well-known for thyroid cancer. They report a short review of their own work and of the general literature on this correlation and on the antioxidant function of iodide in stomach, breast and thyroid. Thyroid cells phylogenetically derived from primitive iodide-concentrating gastroenteric cells which, during evolution, migrated and specialized in uptake and storage of iodine, also in order to adapt the organisms from iodine-rich sea to iodine-deficient land. Mammary cells also derived from primitive iodide-concentrating ectoderm. Stomach, breast and thyroid share an important iodide-concentrating ability and an efficient peroxidase activity, which transfers electrons from iodides to the oxygen of hydrogen peroxide and so protects the cells from damage caused by lipid peroxidation. The authors suggest that iodide might have an ancestral antioxidant function in all iodide-concentrating cells from primitive Algae to more recent Vertebrates. In Italy, gastric cancer is more frequent in farmers and in iodine-deficient populations, living in mountainous and hilly areas, than in fishermen. In the last two decades, Italian decrease of gastric cancer seems to be correlated more to the higher dietary consumption of iodine-rich fish rather than to consumption of fruit and vegetables, which indeed has decreased in Italy.

Cerebral blood flow velocity in term infants treated with phototherapy.

The relationship between phototherapy and changes in the cerebral circulation was studied in 50 jaundiced newborn infants. The aim of the study was to determine whether important alterations in cerebral hemodynamic occur under blue light therapy. Blood flow velocity, i.e., the pulsatility index (PI) and the area under the velocity curve (AUVC), was measured in the anterior cerebral arteries (ACA) using a Duplex scan technique. No prominent changes compromise flow in the ACA. PI and AUVC values were similar during and after phototherapy (p greater than 0.5) suggesting effective cerebral autoregulation in term infants undergoing light treatment for hyperbilirubinemia.

Cerebral hemodynamics in low-birth-weight infants treated with phototherapy.

Changes of cerebral blood flow were determined in 20 preterm infants undergoing blue-light phototherapy for hyperbilirubinemia. All were healthy very-low-birth-weight infants (less than 1,500 g) with normal brain sonograms and not under pharmacological treatment at the time of the investigation. Blood flow velocity (pulsatility index and area under velocity curve) was measured by Duplex Scan technique during and after phototherapy. No changes of global cerebral blood flow were observed in the anterior cerebral artery (p less than 0.5). Our results suggest no functional disturbance of cerebral autoregulation in low-birth-weight infants treated with phototherapy.

Differential effects of pancuronium on masseter and adductor pollicis muscles in humans.

The sensitivity of the masseter, one of the muscles of the upper airway, to pancuronium was measured in ten adults undergoing elective surgery and compared with that of the adductor pollicis. During thiopental-nitrous oxide-enflurane (end-tidal concentration less than 0.25%) anesthesia, supramaximal nerve stimulation was applied to the ulnar nerve at the elbow and to the nerve to the masseter, at a point inferior to the zygomatic arch, anterior to the mandibular condyle. Jaw closure was measured by a force transducer system attached to both an oral airway and a metal frame fixed to the operating table 10 cm caudad to the chin. Cumulative dose-response curves for pancuronium (initial dose = 0.02 mg/kg, incremental doses = 0.01 mg/kg) were determined. Control twitch tensions were (mean +/- SEM) 473 +/- 75 g at the masseter and 660 +/- 118 g at the adductor pollicis. The masseter was slightly more sensitive to pancuronium, the ED50 being 0.024 +/- 0.001 mg/kg compared with 0.028 +/- 0.001 mg/kg for the adductor pollicis (P less than 0.05). Corresponding values for the ED90 were 0.038 +/- 0.004 and 0.043 +/- 0.002 mg/kg, respectively (P less than 0.05). The time from injection of the first dose of pancuronium to maximum blockade was 3.2 +/- 0.2 min at the masseter and 3.8 +/- 0.2 min at the adductor pollicis (P less than 0.01). Following incremental doses, this time was 1.8 +/- 0.1 and 2.6 +/- 0.1 min, respectively (P less than 0.01). It is concluded that after injection of pancuronium, neuromuscular blockade is greater at the masseter and occurs sooner than at the adductor pollicis. Jaw relaxation can be achieved with relatively small doses of pancuronium. This suggests that return of adductor pollicis function may not imply complete masseter muscle recovery.

The potency of pancuronium at the adductor pollicis and diaphragm in infants and children.

To measure the potency of pancuronium at the diaphragm and adductor pollicis in infants and children, train-of-four stimulation was applied to the ulnar and phrenic nerves under N2O-halothane anesthesia. The force of contraction of the adductor pollicis was measured and compared with the diaphragmatic electromyogram (EMG). Cumulative dose response curves were determined for pancuronium in 18 patients divided equally into three age groups: 0-1 yr, 1-3 yr, and 3-10 yr. The potency of pancuronium at both muscles decreased with increasing age (P less than 0.05), while the adductor pollicis:diaphragm potency ratio remained constant. The mean doses (+/- SEM) required to depress adductor pollicis first twitch responses by 90% (ED90) were 42 +/- 3.3 micrograms/kg in the 0-1-yr group, 47 +/- 4.2 micrograms/kg in the 1-3-yr group, and 62 +/- 4.1 micrograms/kg in the 3-10-yr group. Corresponding figures for the diaphragm were 70 +/- 4.3 micrograms/kg, 81 +/- 5.1 micrograms/kg, and 101 +/- 4.4 micrograms/kg, respectively. The ED90 ratios (diaphragm ED90/adductor pollicis ED90) in the three age groups were 1.69 +/- .07, 1.75 +/- .14, and 1.64 +/- .09, respectively. These results are consistent with similar rates of maturation of the diaphragm and the adductor pollicis muscles in infancy and childhood. Thus, train-of-four monitoring of the adductor pollicis is likely to overestimate the degree of neuromuscular blockade of the diaphragm in pediatric patients.

Accelerated onset and delayed recovery of d-tubocurarine blockade with pancuronium in infants and children.

The effect of age on the onset and duration of action of a d-tubocurarine (DTC) neuromuscular blockade with and without pancuronium priming in children was examined. Sixty ASA physical status I or II patients in three age ranges (0-1 yr, 1-3 yr and 3-10 yr) were anaesthetized with thiopentone, halothane and nitrous oxide. Each patient received either a single paralyzing dose of DTC 0.4 mg.kg-1, or DTC 0.36 mg.kg-1 preceded three minutes earlier by pancuronium 0.007 mg.kg-1. Evoked force of contraction of the adductor pollicis was measured using train-of-four stimulation applied every 12 sec. Time to 90 per cent first twitch depression after a single dose of DTC increased with increasing age (r = 0.65, p less than 0.01), and was 1.6 min (SEM +/- 0.3) in the 0-1 yr group, 1.9 +/- 0.3 min (1-3 yr), and 5.2 +/- 1.2 min (3-10 yr). Time to ten per cent spontaneous recovery after single dose DTC was shorter in older individuals (r = 0.40, p less than 0.05), being 36.4 +/- 5.1 min in infants 0-1 yr, 30.6 +/- 4.6 min (1-3 yr), and 24.0 +/- 2.7 min (3-10 yr). Priming with pancuronium accelerated the onset significantly in all age groups with 90 per cent T1 depression occurring at 0.7 +/- 0.1 min (0-1 yr), 0.9 +/- 0.1 min (1-3 yr), and 2.1 +/- 0.6 min (3-10 yr). However, priming delayed recovery, especially in infants.(ABSTRACT TRUNCATED AT 250 WORDS)

Neostigmine, pyridostigmine and edrophonium as antagonists of deep pancuronium blockade.

To compare the ability of equipotent doses of neostigmine, pyridostigmine and edrophonium to antagonize intense pancuronium neuromuscular blockade, one hundred and twenty ASA physical status I or II patients scheduled for elective surgery received 0.06 mg.kg-1 pancuronium during a thiopentone nitrous oxide-enflurane anaesthetic. Train-of-four stimulation was applied every 12 s and the force of contraction of the adductor pollicis muscle was recorded. In the first 60 patients, spontaneous recovery was allowed until ten per cent of initial first twitch height. Then neostigmine (0.005, 0.01, 0.02 or 0.05 mg.kg-1), pyridostigmine (0.02, 0.04, 0.1 or 0.2 mg.kg-1), or edrophonium (0.1, 0.2, 0.4 or 1 mg.kg-1) was injected by random allocation. Dose-response relationships were established from the measurement of first twitch height (T1) ten minutes later. From these, neostigmine, 0.04 and 0.08 mg.kg-1 was found to be equipotent to pyridostigmine, 0.2 and 0.38 mg.kg-1, and edrophonium, 0.54 and 1.15 mg.kg-1, respectively. These doses were given by random allocation to the next 60 patients, but at one per cent spontaneous recovery. Neostigmine, 0.04 mg.kg-1, produced a T1 of 73 +/- 4 per cent (mean +/- SEM), and a train-of-four ratio (TOF) of 39 +/- 3 per cent. This was significantly greater than with pyridostigmine, 0.2 mg.kg-1 (T1 = 50 +/- 6 per cent; TOF = 25 +/- 3 per cent), and edrophonium, 0.54 mg.kg-1 (T1 = 54 +/- 3 per cent; TOF = 17 +/- 2 per cent).(ABSTRACT TRUNCATED AT 250 WORDS)

Dose-response curves for edrophonium, neostigmine, and pyridostigmine after pancuronium and d-tubocurarine.

To determine the potencies of neostigmine, pyridostigmine, and edrophonium in reversing pancuronium and d-tubocurarine blockade, dose-response curves were established for first twitch height recovery and train-of-four ratio. One hundred and twenty ASA physical status I or II patients scheduled for elective surgery received either 0.06 mg/kg pancuronium or 0.36 mg/kg d-tubocurarine during a thiopental-nitrous oxide-enflurane anesthetic. Train-of-four stimulation was applied every 12 s, and the force of contraction of the adductor pollicis muscle was recorded. When first twitch height had recovered spontaneously to 10% of its initial value, neostigmine (0.005, 0.01, 0.02 or 0.05 mg/kg), pyridostigmine (0.02, 0.04, 0.1, or 0.2 mg/kg), or edrophonium (0.1, 0.2, 0.4 or 1 mg/kg) was injected by random allocation. Recovery was measured 10 min after the injection of the antagonist. First twitch ED50's were 0.013, 0.085, and 0.17 mg/kg after pancuronium, and 0.017, 0.11, and 0.27 mg/kg after d-tubocurarine, for neostigmine, pyridostigmine, and edrophonium, respectively. The ED50 for pyridostigmine and edrophonium obtained after d-tubocurarine was significantly larger (P less than 0.05) than that after pancuronium. The train-of-four dose-response curves were significantly flatter for edrophonium than for the other two agents, indicating a greater ability of edrophonium to antagonize fade at low doses. It is concluded that the potency of reversal agents may be different for different relaxants, and that potency ratios might depend upon the end-point chosen as full neuromuscular recovery.

Onset of pancuronium and d-tubocurarine blockade with priming.

The synergistic effect of pancuronium bromide (PCB) and d-tubocurarine (DTC) on the onset time of neuromuscular blockade was tested in 108 ASA physical status I and II adults anaesthetized with thiopentone, nitrous oxide and halothane. Either saline or a small (priming) dose (DTC, 0.04 mg X kg-1, or PCB, 0.007 mg X kg-1) was administered 3 min before a paralyzing dose of either DTC or PCB. The total dose of relaxant was equivalent to DTC, 0.4 mg X kg-1, or PCB, 0.07 mg X kg-1. Neuromuscular activity was measured using train-of-four stimulation applied every 12 s. Time to 50 per cent first twitch blockade was 63 +/- 4.6 s (mean +/- SEM) with DTC and 88 +/- 5.2 s with PCB (p less than 0.002). Times to 90 per cent blockade were not different between the two drugs (161 +/- 20 s and 141 +/- 21 s respectively). Priming a DTC blockade with either DTC or PCB or priming a PCB blockade with PCB produced an acceleration of less than 10 s at all levels of blockade. Compared with PCB alone, priming PCB blockade with DTC reduced the time to 50 per cent blockade to 71 +/- 4.5 s (p less than 0.02) and to 90 per cent blockade to 111 +/- 8 s (p less than 0.05). Priming did not affect the duration of action significantly, except in the case of PCB priming of DTC, where duration was increased from 39 +/- 4.4 to 57 +/- 4 min (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Potency of pancuronium at the diaphragm and the adductor pollicis muscle in humans.

The measurement of force of contraction of the adductor pollicis muscle following supramaximal stimulation of the ulnar nerve has become a standard method to assess the effect of neuromuscular blocking drugs. However, the diaphragm is regarded as resistant to these drugs, and considerable residual respiratory power might still be present after total block of adductor pollicis function. To quantify this differential effect, train-of-four stimulation was applied to the ulnar and the phrenic nerves in patients under N2O-halothane anesthesia. The force of contraction of the adductor pollicis muscle was measured with a force-displacement transducer and compared with the diaphragmatic electromyogram (EMG). Pancuronium cumulative dose-response curves for both muscles were determined in 10 ASA Class I adults. The mean dose (+/- SEM) required to depress adductor pollicis and diaphragm responses to first twitch stimulation (ED50) was 29.5 +/- 3.5 micrograms/kg and 59.5 +/- 7.0 micrograms/kg, respectively. Corresponding values for ED90 were 45 +/- 5 micrograms/kg and 95 +/- 11 micrograms/kg, respectively, indicating that the diaphragm required approximately twice as much pancuronium as the adductor pollicis block, the diaphragm was only 24 +/- 4% blocked. It is concluded that the adductor pollicis response might underestimate the degree of diaphragmatic relaxation. On the other hand, the administration of pancuronium in a dose sufficient to produce total paralysis might result in the inability to antagonize neuromuscular block in all muscles.

The potencies of edrophonium and neostigmine as antagonists of pancuronium.

Dose response curves were constructed for edrophonium and neostigmine when used to antagonise pancuronium, 0.07 mg/kg during thiopentone-nitrous oxide-halothane anaesthesia. The antagonist was given when 10% twitch height had been restored and the effect was measured 10 minutes later. Recoveries to 50% and 90% twitch height were achieved with 167 and 828 micrograms/kg of edrophonium, and 10.5 and 51 micrograms/kg of neostigmine. The dose response curves were parallel and neostigmine was 16 times more potent than edrophonium. Combinations of equipotent doses of edrophonium and neostigmine were also administered and produced additive but not synergistic effects. It is concluded that either edrophonium or neostigmine may be used for the reversal of pancuronium neuromuscular blockade, but the combination of the two offers no advantage.

Antagonism of phase II succinylcholine block by neostigmine.

The neuromuscular effect of neostigmine, 1.25 mg/70 kg, was assessed in 40 adult patients 10 min after cessation of a succinylcholine infusion. The patients had received a thiopental-nitrous oxide anesthetic supplemented by halothane or fentanyl during which they were given at least 5 mg/kg succinylcholine over more than 90 min. Train-of-four monitoring was used. Neostigmine accelerated recovery of neuromuscular function in all patients. The degree of recovery was directly related to the train-of-four ratio, and the results in patients who had received halothane were no different from those who had received fentanyl. The findings are compatible with the hypothesis that phase I block depends upon the presence of circulating succinylcholine and decreases as the latter is cleared, whereas phase II block decreases more slowly. Thus succinylcholine block can be antagonized by neostigmine if enough time is allowed for phase I block to disappear and for a pure phase II block to be present.

Accelerated onset of pancuronium with divided doses.

To determine the consequences of administering neuromuscular relaxants in divided doses, pancuronium was given either in a single dose, 0.07 mg X kg-1, or in an initial dose of 0.007 mg X kg-1 followed three minutes later with 0.063 mg X kg-1. When the drug was administered in divided dosage the onset time was reduced, the block was more intense and its duration of action was prolonged. It is suggested that such changes may be advantageous in the provision of rapid intense paralysis.

Vecuronium in renal failure.

Neuromuscular blockade during surgery was provided with vecuronium in 24 adult patients in end-stage renal failure and in 21 normal patients who served as controls. Dose response curves were constructed which showed that the effective doses required to produce 50, 90 and 95 per cent neuromuscular blockade in patients with renal failure were 27.5, 43 and 49 micrograms X kg-1 respectively. These were not significantly different from the doses of 31, 49 and 57 micrograms X kg-1 in the normal patients. Repeated small doses of 0.01 mg X kg-1 had a significantly longer duration of action and were associated with some cumulation in the renal failure group. Recovery from the block occurred rapidly after neostigmine, was no different in renal failure and was not associated with recurarization. It is concluded that, when given to subjects in renal failure, vecuronium offers advantages over established agents such as shorter duration of action and easy reversibility.

Prolonged suxamethonium infusion during nitrous oxide anaesthesia supplemented with halothane or fentanyl.

The neuromuscular blockade produced by a prolonged infusion of suxamethonium was studied using train-of-four stimulation in 40 patients receiving either halothane-nitrous oxide or fentanyl-nitrous oxide anaesthesia. Initially, a depolarizing (phase I) block was observed in all patients followed by phase II block which was associated with tachyphylaxis to suxamethonium; the latter changes occurring more rapidly in the halothane group. Infusions were continued for more than 150 min in 17 patients and there was a late decrease in suxamethonium requirement in those who received halothane, but not fentanyl. Ten minutes after the suxamethonium infusion was stopped, most patients received neostigmine which was followed by rapid recovery of neuromuscular transmission.

Antagonism of pancuronium in renal failure: no recurarization.

Neuromuscular transmission was measured using train-of-four stimulation, during and after anaesthesia, in 20 patients with end-stage renal failure. Neuromuscular blockade was provided with pancuronium in single doses of either 3 or 6 mg per 70 kg, and antagonized at 10% recovery with atropine and neostigmine 2.5 mg per 70 kg. Reversal was followed by progressive recovery of muscle twitch in every patient during the 3 h of the study. Recovery was more rapid after the smaller dose of pancuronium and was inversely correlated with the duration of blockade. It is concluded that, when pancuronium is antagonized with neostigmine in patients with renal failure, neuromuscular transmission recovers without evidence of recurarization. However, when large doses of pancuronium are antagonized with neostigmine 2.5 mg, recovery may be insufficient to ensure normal ventilatory function.