A Case of Splenic Injury Caused by a Blow from a Dolphin’s Tail Fin

Abstract

To the Editor:

The common bottlenose dolphin, Tursiops truncatus, has a global distribution. The mammal weighs an average of 150 to 200 kg and reaches 2 to 4 m in length.¹ Dolphins are characterized as high-speed swimmers, propelled by a powerful horizontal lunate tail fin consisting of 2 flukes, which play an important role in their swimming.² They can leap in the air or stand out of the water using this tail fin. They are also intelligent creatures and able to learn tricks, perform in shows, or interact with humans after appropriate training.³ We herein report a case of splenic injury induced by a blow from a dolphin’s tail fin.

A 12-y-old boy in a wetsuit was travelling through the water while holding the dorsal fin of a trained bottlenose dolphin in an aquarium. He had no remarkable personal or family medical history and was a tourist from Saitama, located near Tokyo. When he erroneously released the dorsal fin, he sustained a sharp blow to the left flank by the dolphin’s tail fin. He acutely felt severe pain, but he returned to his hotel with his parents. He then experienced a generalized tonic clonic seizure of approximately 10 s in duration at 3 h after the injury. He vomited 5 times within 7 h after the seizure. These symptoms did not recur throughout the night or the following day. However, the flank pain did not improve. His parents called an ambulance, and he was transported to our hospital by a physician-staffed helicopter. Helicopter transportation was arranged owing to the distance needed to travel to arrive at the hospital; ground ambulance would take more than 90 min, versus 15 min by helicopter.

On arrival, his level of alertness was Glasgow Coma Scale score of 14 (E3V5M6) with a blood pressure of 129/70 (normal range: 110–124/70–79) mm Hg, a heart rate of 109 (55–85) beats·min^-1, a respiratory rate of 30 (12–18) breaths·min^-1, and a percutaneous oxygen saturation of 97% on room air. The physical examination findings included only localized rebound tenderness in the right flank without skin lesions, contralateral to the side of the initial injury. The main results of a blood analysis were as follows: white blood cell count, 15,800·μL^-1 (normal 4000–10,700·μL^-1); hemoglobin, 10.5 g·dL^-1 (normal 12.7–15.7 g·dL^-1); platelets, 31.0 × 10⁴ μL^-1 (normal 18–44 × 10⁴ μL^-1); aspartate aminotransferase, 29 IU·L^-1 (normal 15–31 IU·L^-1); alanine aminotransferase, 10 IU·L^-1 (normal 9–32 IU·L^-1); blood urea nitrogen, 21.1 mg·dL^-1 (normal 6.8–19.2 mg·dL^-1); and creatinine, 0.63 mg·dL^-1 (normal 0.39–0.62 mg·dL^-1). An abdominal ultrasound revealed hyperechoic areas at Morrison’s pouch, around the spleen, and at the rectovesical pouch. Enhanced computed tomography showed a grade III splenic laceration, according to the American Association for the Surgery of Trauma splenic injury scale (Table 1),⁴ with no findings of extravasation or pseudoaneurysm (Figure 1), as well as fluid retention of the small intestine in the right abdomen, probably due to the subileus state after splenic injury. He was diagnosed as having an isolated splenic injury with a large amount of hemorrhaging in the intra-abdominal space, and he underwent angiography for embolization. However, the radiologists were unable to insert a catheter into the splenic artery, and the patient was admitted under observational status.

Table 1

Spleen organ injury scale—2018 revision⁴

AAST Grade	Imaging criteria (computed tomography findings)
I	Subcapsular hematoma <10% surface area Parenchymal laceration <1 cm depth Capsular tear
II	Subcapsular hematoma 10–50% surface area; intraparenchymal hematoma <5 cm Parenchymal laceration 1–3 cm
III	Subcapsular hematoma >50% surface area; ruptured subcapsular or intraparenchymal hematoma ≥5 cm Parenchymal laceration >3 cm depth
IV	Any injury in the presence of a splenic vascular injury or active bleeding confined within splenic capsule Parenchymal laceration involving segmental or hilar vessels producing >25% devascularization
V	Any injury in the presence of splenic vascular injury with active bleeding extending beyond the spleen into the peritoneum Shattered spleen

Figure 1

Findings of enhanced computed tomography on arrival. Computed tomography showed a grade of III (see arrow) according to the American Association for the Surgery of Trauma splenic injury scale.

On Day 2, the patient’s hemoglobin level dropped to 8.0 g·dL^-1, and he received a transfusion of 2 units of red blood cells for fatigue. The patient tolerated the transfusion well. On Day 3, his hemoglobin level increased to 9.0 g·dL^-1, and he began to eat and was initiated on an iron agent and acetaminophen. Subsequent contrast-enhanced computed tomography on Days 4 and 7 revealed no significant changes, and the posttransfusion course was uneventful. An electroencephalogram was normal, and he was free from seizures during hospitalization, without the need for an anticonvulsant. The precise mechanism was unclear, but the cause of the convulsions might have been transient hypotension or some cranial damage. After the final computed tomography examination, his bedrest was finished. His hemoglobin level returned to 11.2 g·dL^-1. On Day 12, he was transported to a local hospital in Saitama for evaluation of late-presenting complications after splenic trauma, with a plan to return to school.

The patient in the present case underwent angiography for embolization of the splenic artery even though he had stable vital signs. The American Pediatric Surgical Association guidelines state that embolization should be performed only in patients with evidence of ongoing hemorrhaging.⁵ However, the results of a study comparing prophylactic splenic arterial embolization (pSAE) with surveillance and then embolization only if necessary (SURV) in a randomized clinical trial revealed significantly fewer splenic pseudoaneurysms and a shorter duration of hospitalization for adult patients in the pSAE group than for those in the SURV group.⁶ Accordingly, pSAE was performed in the present case.

Several newspaper articles have reported human injuries induced by dolphins.⁷^-9 Dolphins can injure or kill humans by biting, attacking, hitting with their tails or snouts, or drowning by dragging humans underwater. During the literature review, the authors found a news report involving an encounter between 2 intoxicated tourists and a dolphin. The tourists grabbed the dolphin, rode it like a horse, and even attempted to insert an ice cream stick into its blowhole. The dolphin attacked the tourists. One of the tourists died as a result of internal organ damage sustained during the attack, and the second tourist sustained a broken rib and injuries to the head caused by blows from the animal’s tail fin.⁹ Such potential risks based on historical accounts of human–dolphin interactions are described in a previous paper.¹⁰

The present case was indeed an accident. However, dolphins can be dangerous animals, and caution may be necessary when humans interact with these creatures. There are many regulations protecting dolphins. We could find no regulations, guidelines, or protective measures in place to ensure the safety of humans when interacting with dolphins, suggesting no such measures have yet been established.¹⁰ In addition, there were few medical reports concerning dolphin-related injury. A further analysis with the accumulation of reports concerning dolphin-related injury will be necessary; such findings will function as the basis for establishing relevant regulations.

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