Mechanism of Battery-Induced Injury
Batteries cause tissue injury through three
interacting mechanisms, although the relative contribution of each remains
somewhat elusive. These mechanisms come into play when a battery is lodged
in the gut, ear, nose or other orifice, rather than free-floating and in
transit. The mechanisms, listed in the likely order of importance, include:
Generation of an external electrolytic current
that hydrolyzes tissue fluids and produces hydroxide at the battery’s
Leakage of battery contents, especially of an
alkaline electrolyte, and
Physical pressure on adjacent tissue.
Several authors have demonstrated that button
battery-induced physical pressure or compression alone does not cause damage
to the esophagus. Tanaka implanted and immobilized control batteries
without battery contents (incapable of generating current or of leaking) in
the esophagus of dogs, but found no damage to the esophageal mucosa or
deeper tissues other than slight depression . Yamashita implanted dummy
batteries without contents and fully discharged batteries in the esophagus
of 3 dogs and found flattening and compression without mucosal discoloration
or erosion after 24 hours .
In vitro tests at pH 1.4, using hydrochloric acid to
simulate the gastric environment, showed evidence of battery leakage as
early as 2 hours after submersion (mean 26.5 hours, range 2-62 hours) with
fully charged mercury cells but no leakage or corrosion when fully charged
zinc air cells or discharged mercuric oxide cells were submerged in the same
solution or in actual gastric fluid (pH 1.12) . Since corrosion
facilitates leakage by dissolving the battery can, and since a current is
required for corrosion to occur, the absence of leakage from charged zinc
air cells would be anticipated since no air was accessible to activate the
cell. Similarly, discharged mercuric oxide cells would not generate an
external current, although the authors failed to clarify whether these were
fully discharged cells or cells discharged only to the level that would
render them nonfunctional in products. The authors also failed to mention
how leakage was determined.
The possibility of battery injury without leakage is
supported by a number of investigations. In 1970, Leeming demonstrated
alkaline dermal burns with pain and the most severe tissue damage at the
negative electrode after applying low voltage DC current, just 3V, to the
investigators hand. Litmus paper turned dark blue indicating a strong
alkaline substance only at the burn site in contact with the negative
electrode . The disparity between the burns at the negative electrode
compared to the positive electrode, and the buildup of alkali at the
negative electrode suggest that the observed burns were not merely thermal.
These findings are explained by the electrolysis of saline solutions (or
tissue fluids), with sodium hydroxide and hydrogen gas generated at the
negative electrode and chlorine gas, oxygen or both appearing at the
Yamashita inspected batteries removed from the nasal
passages of two patients, one after 4 hours and the other after 2 days. Both patients had perforations of the nasal wall. However neither battery
showed evidence that the battery contents had been disgorged. The authors
surgically placed batteries in the upper esophagus of anesthetized dogs,
lightly secured them in place with silk sutures to prevent movement, then
examined the tissue pathology after sacrificing the dogs at intervals up to
72 hours. Tissue damage was evident, and ulceration seen by 4 hours, but
there was no evidence that the batteries had leaked (no loss of potassium
from the cells) until in the esophagus for more than 48 hours (one battery
present for 72 hours leaked) [2,5]. Assuming that the necrotic tissue
resulted from current flow rather than leakage (since there was no leakage
up to 48 hours but there was tissue damage), the authors repeated the
experiment, this time using a doubly-encapsulated battery (can within a
can). Again tissue injury occurred despite the fact that there was no
possibility of battery leakage. Finally, to exclude the role of physical
pressure or compression causing tissue damage, the experiment was repeated
with a completely discharged battery and a dummy battery (of the same shape
and weight but with no alkaline contents); in both cases no tissue damage
occurred. The authors further hypothesize that the damage was caused by the
accumulation of sodium hydroxide at the negative electrode and this
hypothesis was supported by the observation that tissue damage observed
occurred in the section of the esophagus in contact with the negative pole (the term “anode” is used in this paper;
see the note below about confusing
terminology) but not sections in contact with the positive battery pole
[cathode]. Based on the residual capacity of the 1.5 V, 220 mAh batteries
used (59% after 48 hours), the authors estimate a discharge of 90.2 mAh. Since 1 Faraday (26.8 Ah) will generate 1 mol of NaOH, 134.6 mg of sodium
hydroxide would have been generated – an amount sufficient to damage tissue
if focused on one section of tissue rather than diluted and dispersed . We add that this amount of sodium hydroxide is comparable to the total
amount of potassium hydroxide found in a fully charged 1.5 V alkaline button
cell (about 115 mg KOH), thus over time, the button cell is capable of
generating more hydroxide through hydrolysis than it could release through
leakage. The implication of the external current and electrolysis as the
cause of injury suggests that lithium cells, often 3 V instead of 1.5 V,
would be expected to be more dangerous than alkaline cells, even though
lithium cells don’t contain an alkaline electrolyte which could leak. In
addition, zinc-air cells would be expected to cause less damage as in much
of the gut they would have limited access to the oxygen required for
activation. Likewise, discharged cells would be expected to cause less
damage – with the caveat that batteries discharged through use to the point
that they no longer can power a product still contain significant residual
Yoshikawa confirmed these findings by implanting 12
mm diameter lithium cells (3V) and identical but fully discharged control
batteries into the esophagus of rabbits . The animals were sacrificed at
intervals, and the pH of esophageal and tracheal surfaces, residual voltage
and current were measured. Completely discharged batteries (to 0 V and 0 mA)
implanted in the rabbit esophagus caused no histologic changes, corrosion,
or battery leakage after 27 hours, confirming that pressure was not a major
cause of injury. In contrast, the mucosal pH became acidic at the positive
pole and alkaline at the negative pole, with significantly more severe
injury on the alkaline side. A time-dependent decline in residual voltage
and current was also observed, confirming that battery discharge through an
external current had occurred.
Maves confirmed in cats that the orientation of the
battery was an important predictor of injury, and also concluded that the
negative pole was adjacent to the most severe area of the burn. However
since his experiment involved alkaline and mercuric oxide cells (both with
potassium hydroxide electrolyte that could leak), he attributed this finding
to leakage at the weak point: the plastic seal .
These findings have clinical implications,
suggesting that batteries positioned in the upper esophagus with an
anteriorly-facing negative pole are at greater risk of tracheoesophageal
(TE) fistula. Battery orientation is described in only a small number of
reported cases, but where described, TE fistulas occurred when the negative
pole faced the anterior esophageal wall [8,9,10].
ANODE vs. CATHODE –
Beware the Confusing Terminology:
non-rechargeable (primary) button batteries, the negative pole is termed the
anode, the site where the external electrical current flows into the
battery and electrons flow out; similarly, the positive pole is termed the
cathode. However, when these same batteries are immersed in a saline
solution and electrolysis occurs, the negative pole is redefined as the
cathode, or the site of the reduction reaction (gain of electrons).
Similarly, the positive pole of the battery becomes the anode, or the
site of oxidation reactions (loss of electrons). To avoid confusion, the
anode and cathode need to be associated with an electrochemical process. The
terms change when the focus changes from the electrochemical process on the
exterior of the battery (when the cell is immersed in an electrolyte) to the
reaction on the interior of the can during normal cell discharge. During
the exterior electrochemical process, the negative pole is cathodic; however
that same negative can is called the anode when referring to the reaction on
the interior of the can during normal battery discharge. As a result of the
changing terminology, health professionals are urged to refer to the
positive and negative pole of the button cell, since the terms anode and
cathode reverse depending on the context of the discussion.
During electrolysis, the
following reduction reaction (gain of electrons) occurs at the negative
pole, leading to the accumulation of hydrogen gas and hydroxide ions at the
2H2O + 2e-
During electrolysis, the following oxidation
reaction (loss of electrons) occurs at the positive pole, leading to the
accumulation of chlorine gas at the positive pole:
Cl2 + 2e-
In vitro studies of hearing aid batteries
(EP675E, 1.5V, mercuric oxide cells) immersed in a simulated gastric
environment (0.1 N hydrochloric acid) showed significantly less crimp
dissolution when cells were discharged prior to immersion. Likewise, less
crimp dissolution was observed for discharged cells and dummy cells ingested
by dogs . Crimp dissolution serves both as a marker for leakage and for
electrolysis. Leakage is facilitated by dissolution of the side of the
battery can (the crimp), but that dissolution also requires corrosion caused
by an external electrolytic current. Thus crimp dissolution fails to
differentiate between the two injury mechanisms. Clinical data (human
ingestion cases) fail to show a correlation between battery discharge state
and patient outcome, likely because most outcomes are benign. However,
focusing on the subset of large diameter cells, new cells were 3.2 times as
likely to be associated with a moderate, major or fatal outcome compared to
spent cells .
In 1986 Yasui reported studies of alkaline
(manganese dioxide) 1.5 V, 11.6 mm diameter, button batteries implanted in
the stomach or appendix of rats and in vitro investigations of
batteries immersed in pH adjusted solutions . This study provided
definitive experimental confirmation of the role of an external electrolytic
current. Through a series of in vivo and in vitro experiments, these
The speed of electrolytic reactions was faster in acidic pHs
compared to alkaline pHs, however over the range expected clinically, the
differences were not profound. Electrolytic reactions were about 2/3 as
great at a pH of 8 compared to a pH of 2.
Prior to leakage of the alkali from the battery, there was a
reduction in battery voltage, a rise in mucosal pH, and often ulceration or
perforation. These effects occurred both in the acidic (gastric implant)
and alkaline (appendiceal implant) models.
Batteries discharged from 1.5 V to 1.2-1.3 V, the level at
which electronic devices become nonfunctional, also showed continued
discharge, electrolytic reactions, and intestinal perforation or necrosis
when implanted in the rat appendix, demonstrating that even used batteries
pose a danger on ingestion.
In 1998 Tanaka showed histopathological changes
following fixation of the increasingly popular CR 2032 lithium batteries in
the esophagus of dogs. No leakage of battery contents was observed in
batteries removed 15 or 30 minutes after implantation, but necrosis had
extended into the outer muscle layers of the esophagus. Leakage (determined
by a reduction in residual amount of lithium perchlorate in the battery) was
detected in batteries recovered 1 to 5 hours after implantation. However
lithium batteries do not contain alkali and the leaking contents are not
markedly irritating to tissues. Tanaka further demonstrated that sodium
hydroxide is produced much more rapidly with lithium cells (3 V) than with
other button cells (1.5 V) since the amount of alkali produced in tissue is
proportional to the electric current produced, and the same amount of
current is produced more rapidly with the higher voltage lithium cell .
Langkau used EPX 825 1.5 volt batteries constructed
as a cell within a cell (primary cell contained in a second outer cell
package for the purpose of achieving the correct physical battery size
needed for a product). This doubly sealed construction makes rapid leakage
extremely unlikely since only the outer can is exposed to fluid and
susceptible to corrosion. A few drops of 1 N sodium chloride or tap water
were placed on the negative terminal and a strip of pH-indicator paper laid
across the terminal to bridge the insulating seal and provide an
electrolytic path between the positive and negative terminals. A pH of 11
was reached in just 30 seconds with the sodium chloride solution and in 90
seconds with the less conductive tap water. These rapid pH changes suggest
it is extremely unlikely that the change could be caused by leakage from the
double sealed cell .
Rauber confirmed the alkaline pH change without
leakage by extending electrodes from the battery poles and immersing only
the electrodes, not the battery, in a compartmentalized beaker containing
saline. An increase in pH was observed in just 15 minutes in the
compartment with the negative electrode. Manganese dioxide 11.6 mm (A76)
batteries were used in the investigation .
Experiments in rabbits showed significantly lower
resistance (8 K Ohms) for artificial gastric fluid compared to stomach
tissue (100-500 K Ohms), and concluded that most of the electrical current
runs over the mucosal surface rather than through the tissue. A number of
investigators have demonstrated considerable residual voltage (1.3 to 1.5 V)
in button batteries which no longer powered the product .
Whether through leakage of an alkaline electrolyte
or generation of an external current which then produces hydroxide, the
caustic damage to the gastrointestinal mucosa can cause necrosis. While
acid exposures cause a self-limiting coagulative necrosis, strongly alkaline
substances produce a progressive liquefaction necrosis – solubilizing
protein and collagen, saponifying lipids, and dehydrating cells, making
perforation a more likely outcome.
WHY THE ESOPHAGUS?
Most severe complications following battery
ingestions occur in the esophagus. Batteries must become lodged or impacted
for tissue damage to occur. Batteries moving freely in the gut or
surrounded by volumes of fluid do not cause focal tissue damage due to the
failure of enough hydroxide to accumulate at one location to produce focal
damage. The esophagus is especially susceptible to foreign body retention
due to its several anatomic areas of narrowing and weak peristalsis.
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