Page 670 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Toxic Gases and Vapors Chapter | 48 635

VetBooks.ir dorsal thalamus, can be expected in animals that survive permanent neurological, neurocognitive, and neuropsychiat-
ricsequelae(Hampson et al., 2001; Weaver, 2004; Hopkins
significant CO poisoning (Kent et al., 2010).
In pigs, the most common clinically observable effects
and Woon, 2006; Tapeantong and Poungvarin, 2009).
are abortion storms, stillbirth, increases in perinatal mor-
tality, and reduced neonatal growth rates (Wood, 1979; Prevention
Dominick and Carson, 1983; Morris et al., 1985a,b).
The best form of prevention is the effective use of CO
Reduced hatching rates may be observed in poultry
monitors and alarms in addition to well-adjusted heating
(Swarbrick, 1989). Critically, human workers in these
equipment and good ventilation.
facilities may also experience symptoms of CO poisoning,
the most common of which are headache, nausea, dizzi-
ness, vomiting, and weakness. Hydrogen Sulfide
Overview, Uses, and Sources of Exposure
Diagnostic Testing
Note that polioencephalomalacia in ruminants due to
Elevated blood COHb is the most definitive form of test- excessive intakes of sulfur (which is converted to hydrogen
ing (Weaver, 2004). The presence of COHb cannot be sulfide by rumen microflora-mediated metabolism) is dis-
determined by normal pulse oximetry because these cussed in other chapters of this textbook. Within the veteri-
instruments cannot discriminate between COHb and oxy- nary context, hydrogen sulfide (H 2 S; “sewer gas,” “swamp
hemoglobin. Specific CO pulse oximeters are necessary. gas,” “sour gas,” and “stink damp”) is most commonly
The presence of fetal Hb may give falsely elevated COHb encountered as a byproduct of the decomposition of sulfur-
levels during the use of CO pulse oximeters. containing organic material, particularly with manure
Electrocardiography is recommended because of the tanks, septic tanks, sludge pits, cesspools or settling ponds,
likely presence of cardiac arrhythmias and myocardial or enclosed spaces containing decomposing feed (Caravati,
damage. Computerized tomography (CT) and magnetic 2004; Chou et al., 2006). H 2 S may also be produced when
resonance imaging of the brain may reveal brain neuro- hydrochloric acid and/or sulfuric acid are used to clean
logical injury (particularly in the globus pallidus and other drains or when wool, hair, and hides are burned. H 2 Sis
basal ganglia and the hippocampus); however, CT images also a byproduct of petroleum refining, tanning, rubber vul-
may be normal in the early stages of poisoning. canizing, coal and gas production, and a number of other
industrial processes. H 2 S is colorless, heavier than air (con-
Postmortem Findings centrates in low-lying areas), flammable, and explosive.
H 2 S is a common and important cause of sudden death
Common gross lesions include cherry red discoloration of
in humans, and carries with it the (somewhat exaggerated)
the subcutaneous tissues, muscle, blood, and viscera.
mantra “one breath means death” (Caravati, 2004). Within
Unlike cases of cyanide poisoning, the cherry red discolor-
the farm context, agitation of solutions containing dis-
ation does not fade relatively quickly over time.
solved H 2 S may greatly increase the level in air (Hooser
Histopathology findings include focal leukoencephalomala-
et al., 2000). This is of great importance in the case of
cia and other lesions that resemble brain ischemic hypoxia,
manure tanks, septic tanks, sludge pits, and settling ponds.
particularly in the basal ganglia (especially the globus pal-
Exposure of confined cattle to H 2 S liberated by agitation
lidus), cerebral cortex, and cerebral white matter.
of a manure pit has resulted in significant mortality. A
common cause of human casualties due to H 2 Spoisoning
Treatment
involves misguided rescue attempts (referred to as the
The immediate treatment priority is the prompt removal “H 2 S lemmings over the cliff phenomenon”).
of the patient from the source of exposure. Rescuers need
to take great care not to become casualties in such cir- Toxic Dose
cumstances. The administration of 100% oxygen may be
Relevant dose thresholds for H 2 S are summarized in
helpful because this reduces the CO t 1 /2 . Hyperbaric oxy-
Table 48.2. A critical point in the dose response is the
gen therapy may offer some additional benefits, but it is
onset of odor fatigue and paralysis of the olfactory nerves
rarely available in veterinary practice (Stoller, 2007).
(Caravati, 2004). At this point, individuals can no longer
readily detect that they are being exposed to H 2 S.
Prognosis Furthermore, the capacity of humans to detect the odor of
In cases of significant poisoning, the prognosis is typically H 2 S is genetically determined, i.e., a proportion of the
poor. Although few data are available from the veterinary human population is unable to detect the odor at all. Odor
literature, human data indicate that a high proportion of sur- detection is not an adequate method of determining
vivors of significant CO poisoning develop long-term or exposure.