RESUSCITATION AND TREATMENT FOLLOWING SUBMERSION

PEDIATRICS ◽  
1966 ◽  
Vol 37 (4) ◽  
pp. 666-668
Author(s):  
Joseph S. Redding

In resuscitation from drowning it must be remembered that when breathing movements are absent no time must be wasted in attempts to drain the lungs. Reoxygenation must be started immediately with exhaled air. Positive pressure ventilation with oxygen should be substituted as soon as possible. It should be continued in victims of sea water submersion until a blood specimen can be examined and any plasma deficiency corrected. In fresh water drowning intermittent positive pressure ventilation combined with closed chest cardiac massage is a preliminary to external electrical defibrillation. Prevention of delayed death depends upon the management of massive hemolysis, hypervolemia, electrolyte imbalances, aspiration pneumonitis, and myocardial failure.

PEDIATRICS ◽  
1966 ◽  
Vol 37 (4) ◽  
pp. 684-698
Author(s):  
Jerome Imburg ◽  
Thomas C. Hartney

Animal studies have shown that fluid enters the body via the lungs in sea-water and fresh-water drowning. In fresh-water drowning in dogs, there is marked and rapid hemodilution with death due to ventricular fibrillation in about 4 minutes. In sea-water drowning in dogs, there is hemoconcentration; the blood water is lost into the sea water in the lungs with bradycardia and death due to asystole in 6 to 8 minutes. Studies of human drowning victims show similar, but less striking, changes in hemodynamics. In human non-fatal submersion the problems are usually those produced by impaired pulmonary function and central nervous system damage due to hypoxia. Hemodilution and ventricular fibrillation have not been documented in human nonfatal submersion. Therapeutic measures may be divided into those of an immediate urgent nature to be employed at the accident scene: expired air resuscitation, which should be started on reaching the unconscious victim in the water, and external cardiac massage, when indicated. Later measures to be instituted in the hospital include: cardiac resuscitation, intermittent positive-pressure breathing, hypothermia, tracheostomy and tracheal tiolet, oxygen therapy, antibiotics, steroids, and intravenous fluids to correct defects in blood elements (hemoglobin, electrolytes, pH). Later, pulmonary function should be studied for impairment due to alveolar damage and fibrosis. Permanent neurologic sequellae may develop.


Author(s):  
Bayane Sabsabi ◽  
Ava Harrison ◽  
Laura Banfield ◽  
Amit Mukerji

Objective The study aimed to systematically review and analyze the impact of nasal intermittent positive pressure ventilation (NIPPV) versus continuous positive airway pressure (CPAP) on apnea of prematurity (AOP) in preterm neonates. Study Design In this systematic review and meta-analysis, experimental studies enrolling preterm infants comparing NIPPV (synchronized, nonsynchronized, and bi-level) and CPAP (all types) were searched in multiple databases and screened for the assessment of AOP. Primary outcome was AOP frequency per hour (as defined by authors of included studies). Results Out of 4,980 articles identified, 18 studies were included with eight studies contributing to the primary outcome. All studies had a high risk of bias, with significant heterogeneity in definition and measurement of AOP. There was no difference in AOPs per hour between NIPPV versus CPAP (weighted mean difference = −0.19; 95% confidence interval [CI]: −0.76 to 0.37; eight studies, 456 patients). However, in a post hoc analysis evaluating the presence of any AOP (over varying time periods), the pooled odds ratio (OR) was lower with NIPPV (OR: 0.46; 95% CI: 0.32–0.67; 10 studies, 872 patients). Conclusion NIPPV was not associated with decrease in AOP frequency, although demonstrated lower odds of developing any AOP. However, definite recommendations cannot be made based on the quality of the published evidence. Key Points


1995 ◽  
Vol 79 (1) ◽  
pp. 176-185 ◽  
Author(s):  
V. Jounieaux ◽  
G. Aubert ◽  
M. Dury ◽  
P. Delguste ◽  
D. O. Rodenstein

We have recently observed obstructive apneas during nasal intermittent positive-pressure ventilation (nIPPV) and suggested that they were due to hypocapnia-induced glottic closure. To confirm this hypothesis, we studied seven healthy subjects and submitted them to nIPPV while their glottis was continuously monitored through a fiber-optic bronchoscope. During wakefulness, we measured breath by breath the widest inspiratory angle formed by the vocal cords at the anterior commissure along with several other indexes. Mechanical ventilation was progressively increased up to 30 l/min. In the absence of diaphragmatic activity, increases in delivered minute ventilation resulted in progressive narrowing of the vocal cords, with an increase in inspiratory resistance and a progressive reduction in the percentage of the delivered tidal volume effectively reaching the lungs. Adding CO2 to the inspired gas led to partial widening of the glottis in two of three subjects. Moreover, activation of the diaphragmatic muscle was always associated with a significant inspiratory abduction of the vocal cords. Sporadically, complete adduction of the vocal cords was directly responsible for obstructive laryngeal apneas and cyclic changes in the glottic aperture resulted in waxing and waning of tidal volume. We conclude that in awake humans passive ventilation with nIPPV results in vocal cord adduction that depends partly on hypocapnia, but our results suggest that other factors may also influence glottic width.


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