Elsevier

Legal Medicine

Volume 10, Issue 1, January 2008, Pages 1-5
Legal Medicine

Near-drowning and clinical laboratory changes

https://doi.org/10.1016/j.legalmed.2007.05.007Get rights and content

Abstract

Opposite to clinical laboratory findings in experimental drowning of animals (erythrocytic lysis, hyperkalemia, and final cardial fibrillation) are the observations in drowned humans (increase of pCO2, hypoxic encephalopathy), which leads to a different pathophysiological interpretation of the drowning process. This process, however, is recently discussed again, therefore an additional study seemed to be recommended. In a retrospective study, 31 cases of near-drowning (23 cases: fresh water; 8 cases: brackish water) clinical laboratory data were analysed. While 21 of the cases were fatal with a delay of up to 180 days, 10 individuals survived the accident, four cases with severe neurological deficits. Data of pH, potassium, sodium, chloride, hemoglobin and total protein were collected during the very early post-drowning period. Nearly all cases (96%) revealed a reduction of pH due to hypoxic acidosis, and only two cases (6.5%) exhibited a slight hyperkalemia. The hemoglobin level was normal in most of the cases (83%) and slightly reduced in the others (17%) while the protein level was slightly reduced in most of the fatalities (80%). As a result of our investigation we have to state the lack of hyperkalemia as well as of an increase of the hemoglobin level indicate that there is no distinct intravascular red cell lysis due to influx of water into the vascular compartment. Therefore the death by drowning in humans in most cases is the result of a hypoxic cerebral process. A comparison with animal experiments obviously is not helpful because the drowning process in humans leads to an aspiration of only 2–4 ml water/kg, while in animal experiments more than 10 ml water/kg will be artificially aspirated leading to red cell lysis as well as to electrolyte disturbances and cardial fibrillation.

Introduction

In 1921, Gettler [1] reported a decrease of the serum chloride concentration of blood from the left heart in human drowning victims in fresh water and an increase of the chloride level after drowning in sea water. As a consequence a discussion arouse on the diagnostic value and the fatal sequelae of these phenomena. Meanwhile numerous attempts have been made to confirm Gettler’s findings by comparative determination of the electrolyte concentrations as well as of hemoglobin- and/or protein-values in blood from the right and left side of the heart of drowned human victims, but the results largely have been disappointing [2], [3], [4].

On the other hand, animal experiments gave reproducable evidence on a different – but distinct – biochemical influence of water on the drowning process, especially marked by a fresh water induced red cell lysis, hyperkalemia and cardial fibrillation [5], [6], [7], [8], [9]. Those findings are based on an experimental insufflation of 10–50 ml/kg water in lungs of anesthetized animals which finally leads to a ventricular fibrillation secondary to an increase of serum potassium as a consequence of intravascular erythrocytic lysis [10]. This process was caused by the water flux from pulmonary alveoli into the intravasal compartment.

In humans, however, as little as 1–4 ml/kg water will be aspirated during drowning (about 300 ml/person – see [3], [11]). This event may primary produce alterations in the pulmonary gas exchange and a decrease of pulmonary compliance by 10–40% [12], [13], [14], [15]. Obviously humans rarely aspirate sufficient water quantities to provoke significant electrolyte disturbances [16]. In different studies of electrolyte measurements after survived drowning most of the victims needed no initial electrolyte corrections [17], [18]. Ventricular fibrillation in drowned humans obviously is related to acidosis and hypoxia and not to hemolysis and hyperkalemia, as the aspiration of water initially causes breath holding and laryngospams finally leading to hypoxic injury of the brain. In humans the aspiration of fresh or sea water may produce surfactant destruction, alveolitis, a non-cardiogenic pulmonary edema and a blockage of alveolar-capillary gas exchange. The increased pulmonary shunt may lead to a profound and partly fatal hypoxia [3], [18], [19], [20], [21], [22].

Despite of these general accepted hypotheses, the drowning process in humans is still under discussion. In a recent published leading German textbook on legal medicine [23], the chapter,, Drowning“ sums up the electrolyte disturbances of animal experiments in connection with an explanation of the human drowning process [24]. Therefore an additional proof of the pathophysiologic background seems to be necessary which is based on clinical laboratory findings in victims of near-drowning in a retrospective study answering the question (see also [24]): Do these data give any evidence on an electrolyte imbalance which eventually will influence the dying process by drowning?

Section snippets

Cases

The evaluation was based on 31 victims of near-drowning. The clinical data, the police protocols and the autoptic findings were considered. 21 victims died with delay and 10 cases survived. Male victims predominated (m:f = 20:11). The mean age was 15.5 years as most of the victims have been younger than 16 years. All cases needed cardiopulmonary resuscitation.

The duration time of suspension was unknown in all cases as well as the temperature of the water. The type of water in most cases was fresh

Results

The results are presented in Table 1. As no significant nor systemic differences could be established between immersion by fresh or brackish water we summed up the results of both groups and documented only the different results of surviving and fatal cases.

Discussion

Drowning is a process resulting in primary respiratory impairment from submersion/immersion in a liquid medium [25], [26]. In the beginning of the drowning process the victim voluntary hold his breath followed by an unvoluntary period of laryngospasm [27]. The victim then becomes hyperbaric, hypoxemic, and acidotic which results in a abating of the laryngospasm and active breathing [28]. If the victim is not ventilated soon enough circulatory arrest will ensue as a consequence of multiple organ

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