from the NSW Sea Kayak Club
Attack of the Killer Ray
by Trevor Gardner
The stingray is ubiquitous in most areas of Australia where sea kayakers lurk.
Stingrays inhabit tropical to temperate water, from open sea to many kilometres upstream in brackish water. There are Whiprays, Giant Stingrays, Butterfly Rays, Eagle Rays, Round Stingrays, Cow-nose Rays, Mantas, Freshwater Stingrays and River Rays.
Stingrays are bottom dwellers, so that their flat body is often submerged in sand and only detectable by an eye or two, a piece of tail or the spiracles (water intakes) showing above the elevated disk or mud. Usually shallow water creatures they have been found in tropical waters at 30 to 60 metres. At up to 2 metres across and 4 metres long, a 2 ton ray is an impressive creature. Manta often jump out of the water and have occasionally damaged fishing boats. Stingrays feed on a variety of shellfish, molluscs, crustaceans and worms. The one or more spines are used for defence.
The stingray is non-aggressive, but is capable of protecting itself. Treading on the dorsal surface by mistake or swimming too close above a ray can result in a reflex upward and forward swing of the tail. The injuries can be either a sword like lacerations or penetrating injuries with the serrated spine. Serious injury can either be from the physical trauma of a vital body part, from the venom of the spine or both. In the USA 1,500 stingray injuries are reported annually.
I regularly see small and medium stingrays in 30 to 60 cm of water in the Port Hacking estuary system south of Sydney. On one occasion I disturbed a 1 metre ray in 60 cm of water by paddling over its back. I have subsequently pondered whether the stingray spine is capable of penetrating the hull of sea kayak. Probably a good selling point for kevlar over fibreglass hulls; ‘This hull is ISO certified stingray resistant’.
The paper below was recently published in the Medical Journal of Australia and has been edited and reproduced with permission of the author. The case history makes an interesting and dramatic read of the most severe consequences of a stingray misadventure. The discussion highlights some of the sequelae associated with a stingray spine injury and is followed by the current management principles of a stingray injury. The literature indicates that disabling sequelae can persist for more than a year due to incomplete initial wound management. Specifically, failure to adequately image the injury (x-ray or ultrasound) and debride the wound of spine and integument remnants.
Reference: Dangerous Marine Creatures – Field Guide for Medical Treatment, Carl Edmonds MD, 1995, Best Publishing Company
SURVIVOR OF STINGRAY INJURY TO THE HEART
MJA 2001; 175: 33-34 - Beatrix Weiss MBBS FRACS & Hugh Wolfenden MBBS FRACS
Injuries to the extremities from stingray barbs are not uncommon along the Australian seaboard. Cardiac injuries from Stingray barbs are rare, even worldwide, and all but one have been fatal. We report a survivor of a cardiac injury caused by a stingray barb. Penetration of a body cavity by a stingray barb requires early surgical referral and management.
Australian coastal waters contain many species of stingrays, and injuries to the extremities caused by the barb or barbs on a stingray’s tail are not uncommon. These wounds are painful, and may develop necrosis and secondary infection. Penetration of a body cavity by a stingray barb may cause major morbidity and even death, particularly with cardiac injury, and requires early surgical referral and management.
CLINICAL RECORD
A 33 year old man was snorkeling at Coogee, a popular Sydney swimming beach, when he was noticed to be in distress. He was rescued by lifeguards, and found to be unconscious, not breathing, and had an increased heart rate (150 beats/min). After a short period of expired air resuscitation performed on the beach, he regained consciousness and said he had been struck by the tail of a stingray. He complained of difficulty breathing and severe, left-sided chest pain where the tail had struck.
When paramedics arrived he was cyanosed, with a systolic blood pressure of 75 mmHg (usually 110 to 140) and sinus tachycardia (heart rate 150 beats/min), but with normal level of consciousness. He was given fluid resuscitation on the way to hospital with no improvement in blood pressure.
On arrival at the emergency department, he remained in cardiogenic shock with a low blood pressure and high heart rate, hypothermia (temperature of 31C), poor peripheral perfusion and central cyanosis. He had a 2 cm laceration over the lower left chest next to the sternum. His Glasgow coma score (level of consciousness; 15 normal, 3 dead) had deteriorated to 10. He was intubated and manually ventilated. Invasive monitoring catheters were inserted and cardiac support commenced with adrenaline.
Echocardiography revealed a cardiac tamponade, fluid trapped in the sac around the heart causing restriction to cardiac function. A needle drainage was performed and 150 ml of blood was aspirated from the pericardial sac. This resulted in prompt restoration of blood pressure to 170/80 mmHg, and reduction in heart rate to 100 beats/min.
Because of the possibility of foreign material in the pericardial space and the known necrotic effects of stingray venom, the patient was transferred to the operating theatre, where the chest was opened the pericardial space and left pleural cavity were explored. A puncture wound that had spontaneously sealed over was found in one of the coronary arteries. There was no injury to the cardiac muscle. No foreign material was found. The area was copiously irrigated to remove all potential venom. Intravenous antibiotics were commenced and continued for five days.
His recovery was uncomplicated. He was discharged home on the sixth day after the operation and was well at the two month follow up.
DISCUSSION
Stingrays are the largest of the venomous fish, and there are many species in the Australian coastal waters. The tail of the stingray carries at least one barb or spine that may be up to 37 cm long. The barbs are cartilaginous and retroserrate, and covered by a film of venom and mucous contained within an integumentary sheath. Two longitudinal ventrolateral grooves contain venom secreting glands. Stingrays usually lie in the sand on the seabed. When disturbed by pressure over the dorsum of the body, the tail is thrust upward and forward, driving the barb in to the victim. Rupture of the integumentary sheath on penetration allows the venom to be released.
The venom contains toxic proteins. The effects of the venom may be local and/or systemic. Local effects include severe pain at the site of injury and tissue necrosis. Systemic effects include nausea, vomiting, salivation, sweating, respiratory depression, muscle fasciculation, convulsions, cramping abdominal pain, cardiac arrhythmia, myocardial ischaemia and, rarely, death. Many of the systemic effects have been documented only in patients with viscus penetration (gut), and not in those with peripheral stingray injuries.
Local venom effects are usually more troublesome in peripheral stab injuries, but if the barb pierces a vital organ or structure mechanical damage may be more dangerous then the venom effects.
Instances of serious, penetrating, non-cardiac injuries include collection of pus within the chest three days after netting a stingray and sustaining a barb injury to the chest; penetration of the liver; multiple bowel perforations; and laceration of a femoral artery, with death by exsanguination. Penetrating cardiac injuries have generally been fatal. In 1938, an adult women died after a stab wound to the heart by a stingray. The autopsy showed that the ventricles had been completely transfixed by the barb. An Australian soldier died in 1945 after a stab wound to the left heart, sustained while swimming in seawater baths near Melbourne, Victoria. The current patient was fortunate to have a sustained an injury to the coronary artery rather than the heart muscle. The bleeding artery immediately washed the venom away, whereas injury to the heart muscle is difficult to debride and carries the risk of delayed necrosis and perforation (seen in a 12 year old boy in Queensland in 1989).
