More than 107 particulate contaminants >2um and many more <2um are infused daily in parenteral
medications to intensive care patients. They may form emboli with aggregated platelets
and damage pulmonary vasculature [1], perhaps contributing to alveolar fibrosis in
very premature babies. We studied this possibility in neonatal pigs.
Nineteen newborn pigs were randomised to either daily 0.2um filtered salineas controls,
or infusions of particles similar to drug contaminants at 10x greater than the patient
equivalent dose/kg given via subcutaneous injection portals with tunnelled central
venous catheters. Four weeks later, autologous platelets were labelled with llllndium
and arterial and Swann Ganz catheters inserted under general anaesthesia. Before particle
or filtered saline infusion and at 5 and 20 minutes later platelet count, lung platelet
uptake, mean arterial pressure (BP), pulmonary vascular resistance, pulmonary shunt
and alveolar-arterial P02 difference were measured.
Initially, there were no significant differences between the groups indicating no
measureable effect from chronic particle dosing over 4 weeks. Within 30 sec of bolus
particle injection BP fell from a mean ( ± sem) of 68.9+2.1mmHg to 61.0±2.1 (p<0.01,
paired t-test) but returned to normal within 5 minutes. This was not seen with controls
or particle injections given over 5 minutes. Platelet counts fell in the particle
group from 660±43 (x109/L) to 584±46 at 20 minutes (p<0.01) but lung platelet accumulation was insignificant.
Transient fall in blood pressure due to contaminating particles can be avoided by
slow injection or 0.2um in-line filters. Particles stimulate a loss of circulating
platelets but with insignificant pulmonary accumulation and no impairment of pulmonary
function after 4 weeks of daily particle injection at considerably higher doses than
patients receive.
1. Chia C, Cattell V. The role of platelets in mesangial localisation: carbon uptake
in thrombocytopaenic rats. BrJ Exp Path 1985; 66: 465-474.
