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The technique described is a simple, cost-effective method of assuring accurate gastric tube placement in critically ill patients.

• Background In the medical intensive care unit at the University of Virginia Health System, capnography is used to detect end-tidal carbon dioxide to protect patients from inadvertent airway cannulation during placement of gastric tubes. • Objectives To compare the method in which capnography is used with a method in which a colorimetric carbon dioxide detector is used and to determine what variables affect accurate placement of gastric tubes. • Methods A prospective convenience sample of 195 gastric tube insertions was studied in 130 adult patients in a medical intensive care unit. Standard insertions of gastric tubes (done with capnography) were simultaneously monitored by using a disposable colorimetric device, with a color change indicating the presence of carbon dioxide. • ResultsInsertion variables included tube type (60% Salem sump tubes, 40% soft-bore feeding tubes), route of insertion (71% oral, 29% nasal), mechanical ventilation (81%), and decreased mental status (72%). Carbon dioxide was successfully detected with the colorimetric indicator (within seconds) in all insertions in which carbon dioxide was detected by capnography. When carbon dioxide was detected (27% of insertions), the tubes were withdrawn and reinserted. Carbon dioxide detection during tube placement was significantly associated with nasal insertions (P = .03) and spontaneously breathing/nonintubated status (P=.01) but not with mental status or tube type. • Conclusions A colorimetric device is as accurate as capnography for detecting carbon dioxide during placement of gastric tubes.

The antigenicity of neuronal cytoskeletal lesions was studied immunohistochemically in adult New Zealand white rabbits after intraventricular (subacute) and intravenous (chronic) administration of a water-soluble aluminium compound, aluminium (Al) maltol. After short-term intraventricular administration, rabbits developed widespread neurofibrillary degeneration (NFD) involving pyramidal neurons of the isocortex and allocortex, projection neurons of the diencephalon, and nerve cells of the brain stem and spinal cord. There was a predilection for motor neuron involvement and for the infratentorial portions of the neuraxis. Perikarya and proximal neurites were especially affected. Bundles of 10 nm filaments were frequently present. Three of the animals treated intravenously for 12 weeks or longer displayed NFD in the oculomotor complex and in the pyramidal neurons of the occipital isocortex. Following either mode of administration, the affected neurons exhibited immunostaining with a panel of monoclonal antibodies (MAbs) against phosphorylated (SMI-31), non-phosphorylated/phosphatase-sensitive (SMI-32), and dephosphorylation-independent (SMI-33) epitopes of high and middle molecular weight neurofilament (NF) protein subunits. They were non-reactive with MAbs to microtubule-associated protein 2 and the class III neuron-associated beta-tubulin isotype. Our findings indicate that intraventricular Al maltol produces similar, but more widespread degeneration of projection-type neurons than the less water-soluble Al compounds as reported by others. The NFD lesions are compared with those of senile dementia of the Alzheimer type (SDAT) and motor neuron disease.

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