W I N E TOXINS AND VENOMOUS AND POISONOUS MARINE ANIMALS
345
itself in the sandy or muddy bottom and may remain motionless until
stepped upon. The pressure of the foot on the dorsum of the fish
provokes him to thrust his tail upward and forward, driving his sting
into the foot or leg of the victim (Fig. 16). As the sting enters the
flesh, the integumentary sheath surrounding the spine is ruptured
and the venom escapes into the victim’s tissues. In the withdrawal
of the spine, the integumentary sheath may be torn free and remain in
the wound.
Unlike the injuries inflicted by many venomous animals, wounds
produced by the stingray may be large and severely lacerated, requiring
extensive debridement and surgical closure. A sting no wider than
5 mm may produce a wound 3.5 cm long and larger stings may produce
wounds 7 inches long. The sting itself is rarely broken off in the wound.
The stinging is followed by the immediate onset of intense pain,
out of proportion to that which might be produced by a similar nonvenomous injury. While the onset of pain is usually limited to the
area of injury, it rapidly spreads, and usually becomes more severe
during the first 30 min following the accident. In most caaes the pain
reaches its greatest intensity in less than 90 min and often persists
(if untreated), though gradually diminishing in severity, for 6-48 h.
For the most part, the symptoms and signs of the poisoning are
localized to the injured area. However, syncope, weakness, nausea
and anxiety are common complaints and may be attributed, in part, to
peripheral vasodilatation (Russell and van Harreveld, 1954, 1956),
and in part to the reflex phenomenon precipitated by the severe pain.
Vomiting, diarrhea, sweating, fasciculations in the muscles of the
affected extremity, generalized cramps, inguinal or axillary pain,
and respiratory distress are less frequently reported. Arrhythmias,
paresthesia, and convulsions may occur. True paralysis is extremely
rare, if it occurs at all. All of the “ paralyses ” seen by the author
following severe stingings were muscle contractures, probably initiated
as flexion reflexes stimulated by the intense pain. These contractures
were relieved with drugs which alleviated pain, and which have no
effect on true paralysis. Deaths are very rare following stingray
injuries (Russell et al., 1958a).
Examination reveals either a puncture or a lacerating wound,
usually the latter, jagged, bleeding freely, and often contaminated
with parts of the stingray’s integumentary sheath. The edges of the
wound may be discolored, though the discoloration is not usually
marked immediately following the injury. However, within 2 h the
discoloration may extend several cm from the wound. Subsequent
necrosis of this area occasionally occurs in untreated cases.
345
itself in the sandy or muddy bottom and may remain motionless until
stepped upon. The pressure of the foot on the dorsum of the fish
provokes him to thrust his tail upward and forward, driving his sting
into the foot or leg of the victim (Fig. 16). As the sting enters the
flesh, the integumentary sheath surrounding the spine is ruptured
and the venom escapes into the victim’s tissues. In the withdrawal
of the spine, the integumentary sheath may be torn free and remain in
the wound.
Unlike the injuries inflicted by many venomous animals, wounds
produced by the stingray may be large and severely lacerated, requiring
extensive debridement and surgical closure. A sting no wider than
5 mm may produce a wound 3.5 cm long and larger stings may produce
wounds 7 inches long. The sting itself is rarely broken off in the wound.
The stinging is followed by the immediate onset of intense pain,
out of proportion to that which might be produced by a similar nonvenomous injury. While the onset of pain is usually limited to the
area of injury, it rapidly spreads, and usually becomes more severe
during the first 30 min following the accident. In most caaes the pain
reaches its greatest intensity in less than 90 min and often persists
(if untreated), though gradually diminishing in severity, for 6-48 h.
For the most part, the symptoms and signs of the poisoning are
localized to the injured area. However, syncope, weakness, nausea
and anxiety are common complaints and may be attributed, in part, to
peripheral vasodilatation (Russell and van Harreveld, 1954, 1956),
and in part to the reflex phenomenon precipitated by the severe pain.
Vomiting, diarrhea, sweating, fasciculations in the muscles of the
affected extremity, generalized cramps, inguinal or axillary pain,
and respiratory distress are less frequently reported. Arrhythmias,
paresthesia, and convulsions may occur. True paralysis is extremely
rare, if it occurs at all. All of the “ paralyses ” seen by the author
following severe stingings were muscle contractures, probably initiated
as flexion reflexes stimulated by the intense pain. These contractures
were relieved with drugs which alleviated pain, and which have no
effect on true paralysis. Deaths are very rare following stingray
injuries (Russell et al., 1958a).
Examination reveals either a puncture or a lacerating wound,
usually the latter, jagged, bleeding freely, and often contaminated
with parts of the stingray’s integumentary sheath. The edges of the
wound may be discolored, though the discoloration is not usually
marked immediately following the injury. However, within 2 h the
discoloration may extend several cm from the wound. Subsequent
necrosis of this area occasionally occurs in untreated cases.