South African Paediatric Surgical Outcomes Study: a 14-day prospective, observational cohort study of paediatric surgical patients.

BACKGROUND: Children comprise a large proportion of the population in sub-Saharan Africa. The burden of paediatric surgical disease exceeds available resources in Africa, potentially increasing morbidity and mortality. There are few prospective paediatric perioperative outcomes studies, especially in low- and middle-income countries (LMICs). METHODS: We conducted a 14-day multicentre, prospective, observational cohort study of paediatric patients (aged <16 yrs) undergoing surgery in 43 government-funded hospitals in South Africa. The primary outcome was the incidence of in-hospital postoperative complications. RESULTS: We recruited 2024 patients at 43 hospitals. The overall incidence of postoperative complications was 9.7% [95% confidence interval (CI): 8.4-11.0]. The most common postoperative complications were infective (7.3%; 95% CI: 6.2-8.4%). In-hospital mortality rate was 1.1% (95% CI: 0.6-1.5), of which nine of the deaths (41%) were in ASA physical status 1 and 2 patients. The preoperative risk factors independently associated with postoperative complications were ASA physcial status, urgency of surgery, severity of surgery, and an infective indication for surgery. CONCLUSIONS: The risk factors, frequency, and type of complications after paediatric surgery differ between LMICs and high-income countries. The in-hospital mortality is 10 times greater than in high-income countries. These findings should be used to develop strategies to improve paediatric surgical outcomes in LMICs, and support the need for larger prospective, observational paediatric surgical outcomes research in LMICs. CLINICAL TRIAL REGISTRATION: NCT03367832.

Postoperative pain management in the paediatric patient

The text provides a brief overview of approaches to and management of pain in children that will be useful for the general practitioner

Plasma volume expansion with Haemaccel does not impair haemostasis during reduction mammaplasty.

OBJECTIVES: An in vivo study under well-controlled conditions was undertaken to determine the effect of Haemaccel, a colloidal plasma volume expander, on normal haemostasis. METHODOLOGY: Twenty patients, who were admitted for reduction mammaplasty, were included in this study. A standardised anaesthesia protocol was followed with all patients. Ten patients received 500 ml Haemaccel and 10 controls received 1,500 ml Ringer's lactate, a crystalloid solution. The solutions were administered intravenously during surgery over a period of 30-40 minutes. Standardised clinical observations and haematological tests were done at the following time intervals: after anaesthesia but before infusion of the plasma substitute, immediately after infusion was completed, and 20, 40 and 60 minutes after infusion. RESULTS: The blood pressure, pulse rate and O2 saturation levels were not influenced by the treatment given. Haemodilution was similar for the two patient groups. The platelet count and plasma levels of fibrinogen decreased in parallel with haemodilution. Thereafter the platelet count gradually increased to pre-infusion counts at 60 minutes. The prothrombin time (PT), activated partial thromboplastin time (aPTT), thrombin time (TT) and platelet aggregation in response to adenosine diphosphate (ADP) and collagen were not affected by the plasma volume expander given. Arachidonic acid-induced aggregation decreased significantly after Ringer's lactate was given but did not change when Haemaccel was given. The bleeding time was prolonged slightly, but not significantly, from 7.4 +/- 1.6 minutes to 8.8 +/- 1.6 minutes with Ringer's lactate and from 6.9 +/- 2.0 to 9.7 +/- 3.7 minutes with Haemaccel. CONCLUSIONS: We could not find any scientific evidence that Haemaccel affects haemostasis; neither does it increase bleeding relative to Ringer's lactate.

Continuous infusions of propofol administered to dogs: effects on ICG and propofol disposition.

We have studied the effects of stepwise increasing infusion rates of propofol 200-500 micrograms kg-1 min-1 on blood concentrations of propofol and the disposition and clearance of a bolus dose of indocyanine green (ICG) 0.5 mg kg-1 in 10 acutely instrumented dogs. Drug concentrations and ICG clearance were measured 30 min after each change of infusion rate and after reverting for 60 min to the basal propofol infusion rate. Increasing infusion rates resulted in significant prolongation of the elimination half-life of ICG and decrease in ICG clearance at the largest infusion rate (500 micrograms kg-1 min-1) compared with the basal rate. Similarly, there were greater than predicted blood concentrations of propofol at the largest infusion rate. When the infusion rate reverted to 200 micrograms kg-1 min-1, and continued for 60 min, there was a significant difference between the initial blood concentration of propofol at this basal infusion rate and this latter value (P < 0.01). These changes reflect the persistent myocardial depression observed during the recovery phase.

Diltiazem and regional left ventricular function during graded coronary constriction and propofol anesthesia in the dog.

Although calcium channel blockers may preserve function in ischemic myocardium, they may also produce myocardial depression and dysfunction in the presence of decreased coronary flow. This study was designed to examine the issue of possible protection afforded by diltiazem against ischemia-induced myocardial dysfunction during propofol anesthesia. In eight anesthetized and ventilated dogs, regional myocardial (ultrasonic crystals in both left anterior descending [LAD] and left circumflex [LC] perfusion areas) and global ventricular function were evaluated during progressively severe degrees of myocardial ischemia (LAD constriction) before and after intravenous diltiazem (150 micrograms/kg). As coronary flow decreased, heart rate increased, and arterial and coronary perfusion pressures, left ventricular dP/dt, and cardiac output decreased. Systemic vascular resistance was unaffected. Diltiazem without coronary constriction increased heart rate, and decreased diastolic arterial pressures, left ventricular (LV) end-diastolic, coronary perfusion pressures, LV dP/dt max, LAD coronary blood flow, stroke volume, and cardiac output. At all levels of coronary constriction following diltiazem, there were decreases in systolic and diastolic arterial pressures, stroke volume, cardiac output, LV dP/dt, and coronary perfusion pressure. Heart rate increased at critical coronary constriction, and then remained constant relative to the prediltiazem state. The regional muscle effects of the reductions in coronary flow in the LAD perfusion territory included decreased systolic shortening and increased postsystolic shortening before and after diltiazem. Diltiazem did not alter the magnitude of the alterations in systolic or postsystolic shortening brought about by coronary constriction. No changes occurred in the LC area.(ABSTRACT TRUNCATED AT 250 WORDS)

Nitrous oxide causes myocardial ischemia when added to propofol in the compromised canine myocardium.

We sought to determine the influence of nitrous oxide on the compromised heart during propofol anesthesia. This study investigated the cardiovascular effects of the combination propofol and nitrous oxide (N2O). Seven beagles were monitored to measure global and regional left ventricular function. Recordings both before and after critical constriction (CC) of the left anterior descending coronary artery (LAD) were performed after propofol, 300 micrograms.kg-1.min-1, and 10 min after exposure to and discontinuation of 67% N2O. Data were analyzed with ANOVA for repeated measures at 95% confidence level. In the absence of CC, N2O caused moderate, reversible hemodynamic depression (LVdP/dtmax, -13.8%; cardiac output, -17.2%; LAD coronary blood flow, -10.9%) and no regional dysfunction. After CC global hemodynamic depression was of similar magnitude (LVdP/dtmax, -19.9%; cardiac output, -9.2%; stroke volume, -9.2%) but did not recover completely. Systolic shortening in the compromised area decreased (-30.3%) and postsystolic shortening developed to represent 20.3% of total shortening. Despite only moderate hemodynamic depression, 67% N2O causes substantial regional dysfunction in compromised myocardium when added to propofol.

Effect of graded infusion rates of propofol on regional and global left ventricular function in the dog.

We have studied the effects of graded infusion rates of propofol (0.2-0.5 mg kg-1 min-1) on left ventricular global and regional function, in eight acutely instrumented dogs. Global function was assessed by measurement of aortic and left ventricular pressure, LV dP/dtmax, aortic blood acceleration and stroke volume. Regional function was assessed by measurement of systolic shortening and the end-systolic pressure-length relationship. The response of the coronary circulation to short periods of occlusion was also assessed. Administration of propofol significantly reduced left ventricular preload, as indicated by reductions in end-diastolic pressure and length; contractility was depressed, the depression being greater in the apex than in the base of the left ventricle. High infusion rates impaired relaxation. Regulation of coronary blood flow was not disrupted. Reductions in preload and contractility contributed to the propofol-induced hypotension. After 60 min, recovery from the greatest infusion rate was incomplete.

Canine end-systolic pressure-length relationships: depressed by diltiazem, invalidated by ischemia.

This study was designed to determine whether the end-systolic pressure-length relationship (ESPLR) reflects changes in regional contractility during the imposition of graded ischemia, and whether it is modified by diltiazem during propofol anesthesia. Seven beagles were anesthetized and instrumented to measure left ventricular pressure and subendocardial segment lengths (sonomicrometry) in the region of the left anterior descending (LAD) and circumflex (LC) arteries. Afterload was increased by the tightening of a snare around the descending thoracic aorta. Pressure-length loops were constructed and the slope of the ESPLR and the x-axis intercept, Lo, were calculated. Graded ischemia of the apical myocardium only was accomplished by the tightening of a micrometer-controlled snare around the LAD to produce Critical Constriction (CC), Ischemia 1 and 2 (I1, I2), and Total Occlusion (TO). In the basal LC region, LAD ischemia had no effect on either the ESPLR slope or Lo. In contrast, the ESPLR slope in the LAD area was decreased by ischemia at I1 (-40%), increased at TO (+69%), and unchanged at CC and I2, and was reduced by diltiazem at CC and I2 (-31% and -36%, respectively). The LAD ESPLR Lo was increased by ischemia by 64% and 61% at I2, and 91% and 122% at TO, before and after diltiazem, respectively. In the LC region, diltiazem decreased systolic shortening and the ESPLR slope. These results indicate that diltiazem has negative inotropic properties in both ischemic and nonischemic areas. Also, Lo is not a constant and must always be redetermined for every intervention. In the absence of ischemia, the ESPLR may be a reliable measure of myocardial contractility.(ABSTRACT TRUNCATED AT 250 WORDS)

Verapamil and nitrous oxide exert only minor effects on the normal myocardium in the presence of fentanyl.

While the association of inhalational anaesthetics and verapamil has been shown to cause myocardial dysfunction, the interactions between fentanyl, verapamil and nitrous oxide on regional function in normal hearts have not been investigated. Seven mongrel dogs were instrumented to measure aortic and left-ventricular pressure, aortic blood flow and apical and basal regional left-ventricular function (sonomicrometry). Haemodynamic values were recorded during anaesthesia with 1% halothane, fentanyl 100 micrograms kg-1 (followed by 1.5 micrograms kg-1 min-1) and then after the addition of verapamil 250 micrograms kg-1 over 30 min (followed by 60 micrograms kg-1 min-1). At each stage 67% nitrous oxide was added and recordings obtained before and during its administration. The addition of verapamil during fentanyl anaesthesia caused a moderate depression of global haemodynamics. Only little dysfunction of the apical region (9.5 +/- 2.4% post-systolic shortening) was noted. The addition of nitrous oxide caused a small amount of additional depression without significant regional dysfunction.

Use of a personal computer for fast acquisition of cardiovascular data over an extended period.

This paper describes data collection during open chest cardiovascular research based on an IBM compatible personal computer. Data from eight analogue data channels are collected at a rate of 500 Hz per channel for a period of more than 40 sec per run. General analysis functions include the integration of the data obtained from any channel as well as an exponential curve fitting routine. Special functions are available for the calculation of cardiac parameters. This includes the automatic determination of end-diastole and end-systole, as well as maximum and minimum values of all curves for both the systolic and diastolic phases of contraction.

Effect of verapamil on canine left ventricular function in the presence of fentanyl when apical blood flow is critically limited.

Instruments were inserted to seven dogs under halothane anaesthesia, to measure global and regional left ventricular function. Anaesthesia was continued with fentanyl (100 micrograms kg-1 bolus, then 1.5 micrograms kg-1 min-1). Critical constriction was applied to the left anterior descending coronary artery. Control recordings were made, followed by bolus administration of verapamil 0.08, 0.16 and 0.32 mg kg-1, with recordings 10 min after each bolus. At the highest dose, verapamil decreased systemic arterial pressure, left ventricular dP/dt, stroke volume and systemic vascular resistance, and increased heart rate significantly. Coronary perfusion pressure decreased and, in the presence of critical constriction, coronary flow per beat decreased significantly. In the region with constriction, systolic shortening of myocardium decreased and post-systolic shortening increased significantly with addition of verapamil. The addition of a high dose of verapamil to fentanyl anaesthesia caused reduction in systolic function and development of early diastolic dysfunction in myocardium with critically limited blood supply.

Regional differences in left ventricular wall motion in the anesthetized dog.

Data regarding left ventricular function suggest that the extent of shortening may differ between regions. This study was undertaken to determine the effects of negative inotropic drugs used during anesthesia on different areas of the left ventricle. Forty mongrel dogs were anesthetized and instrumented for measurement of global and regional function. Regional function in the short axis of the basal and apical territories of the left ventricle was assessed by subendocardial sonomicrometry. Three different interventions were performed: In the first group 67% N2O, replacing 67% N2, was added to opiate anesthesia; in the second group halothane was given by stepwise increases in inspired concentration to 2%; in the third group verapamil (60 micrograms.kg-1.h-1) was infused during isoflurane anesthesia. Apical and basal segmental shortening were compared. During baseline conditions and with agents in concentrations that caused minimal myocardial depression (67% N2O or 1.0% as opposed to 0.5% halothane) differences in systolic shortening between regions were statistically significant. Further myocardial depression affected the apex significantly more than the base: when substantial myocardial depression was induced by halothane (1.5 or 2%) or verapamil, differences in regional function were abolished. Thus, the apical region of the left ventricle is more dynamic and more sensitive to negative inotropic interventions than the basal region. This should be borne in mind when segmental myocardial function is evaluated.