Orthopedics

Case Reports 

Stenosing Flexor Tenosynovitis Following a Rattlesnake Bite

Lydia Lee, MD; Jeffrey Yao, MD

  • Orthopedics. 2010;33(7)
  • Posted July 1, 2010

Abstract

Snakebite victims have been described previously in orthopedic literature in regard to complications such as compartment syndrome and carpal tunnel syndrome. We introduce a previously unreported complication of stenosing flexor tenosynovitis in a patient bitten by a rattlesnake. After being bitten in her right forearm, the patient experienced mild systemic symptoms of fever and nausea and was assessed at an outside hospital, where it was determined that she did not suffer from envenomation and therefore did not require antivenin therapy. She presented to our institution 1 week later with signs and symptoms of acute, new-onset right thumb flexor tenosynovitis, with pain and tenderness at the level of the A1 pulley of the thumb, with intermittent triggering. She also presented the following week with ipsilateral carpal tunnel syndrome. The patient reported no such symptoms prior to the snakebite. Given the recent development of these conditions after her snakebite, in addition to her history of endocrine disorders, we believe that our patient suffered from envenomation that led to these complications. Nonoperative measures including splinting and steroid injections were taken, with mixed results, and surgical intervention was necessary. While the proper management of snakebites is controversial, especially in regard to the administration of antivenin, we believe our patient would have benefitted from immediate evaluation and consideration for antivenin.

Adults are most commonly bitten by snakes in the upper extremities.1 Rattlesnake bites are known to have hemotoxic, neurotoxic, and cytotoxic effects.2 Injuries range from mere puncture wounds (resulting from “dry bites”) to other local sequelae such as pain, edema, erythema, ecchymoses, and hemorrhagic blebs, to systemic consequences of envenomation including nausea, weakness, muscle fasciculations, paresthesias, coagulopathy, renal failure, and death.3

Of note to orthopedic surgeons is the development of compartment syndrome secondary to envenomation.4 Controversy surrounds the management of envenomation. Nonoperative measures such as limb elevation and the administration of mannitol and/or antivenin, as well as surgical interventions for impending complications such as compartment syndrome and carpal tunnel syndrome including fasciotomy and carpal tunnel release, have been used with varying degrees of success.

To our knowledge, there have been no previous reports of the development of acute stenosing tenosynovitis following a rattlesnake bite. This article describes a case of stenosing tenosynovitis of the thumb, which developed acutely in a patient 1 week after she was bitten by a rattlesnake.

A 50-year-old, right-hand-dominant woman was referred to orthopedic surgery in the emergency department to rule out suppurative flexor tenosynovitis approximately 1 week after being bitten by a rattlesnake. Her medical history was significant for thyroid cancer (status post thyroidectomy), pancreatic neuroendocrine tumor (status post Whipple procedure), meningioma (status post craniotomy), and Scheuermann’s disease (status post thoracic spine fusion).

One week prior, the patient was bitten by a Southern Pacific rattlesnake on the right volar forearm (Figure 1). The strike penetrated the skin. The patient developed nausea, vomiting, and a fever of 102°F and presented to the local emergency department. Her condition was determined to be “not acute,” and she was assured that she had sustained a “dry bite.” Therefore, neither antivenin nor antibiotics were deemed necessary and were not administered.

Figure 1: Snakebite wounds on the right volar forearm. Figure 2: Healed puncture wounds on the right forearm. The thumb interphalangeal joint is locked in 60° of flexion. Figure 3: The right trigger thumb. Tenderness to palpation is elicited at the A1 pulley and the nodule palpated at the volar metacarpophalangeal joint.

One week after the incident, she presented to our emergency department with increased swelling in her right hand and fingers and a significant increase in pain. The patient also reported an inability to…

Abstract

Snakebite victims have been described previously in orthopedic literature in regard to complications such as compartment syndrome and carpal tunnel syndrome. We introduce a previously unreported complication of stenosing flexor tenosynovitis in a patient bitten by a rattlesnake. After being bitten in her right forearm, the patient experienced mild systemic symptoms of fever and nausea and was assessed at an outside hospital, where it was determined that she did not suffer from envenomation and therefore did not require antivenin therapy. She presented to our institution 1 week later with signs and symptoms of acute, new-onset right thumb flexor tenosynovitis, with pain and tenderness at the level of the A1 pulley of the thumb, with intermittent triggering. She also presented the following week with ipsilateral carpal tunnel syndrome. The patient reported no such symptoms prior to the snakebite. Given the recent development of these conditions after her snakebite, in addition to her history of endocrine disorders, we believe that our patient suffered from envenomation that led to these complications. Nonoperative measures including splinting and steroid injections were taken, with mixed results, and surgical intervention was necessary. While the proper management of snakebites is controversial, especially in regard to the administration of antivenin, we believe our patient would have benefitted from immediate evaluation and consideration for antivenin.

Adults are most commonly bitten by snakes in the upper extremities.1 Rattlesnake bites are known to have hemotoxic, neurotoxic, and cytotoxic effects.2 Injuries range from mere puncture wounds (resulting from “dry bites”) to other local sequelae such as pain, edema, erythema, ecchymoses, and hemorrhagic blebs, to systemic consequences of envenomation including nausea, weakness, muscle fasciculations, paresthesias, coagulopathy, renal failure, and death.3

Of note to orthopedic surgeons is the development of compartment syndrome secondary to envenomation.4 Controversy surrounds the management of envenomation. Nonoperative measures such as limb elevation and the administration of mannitol and/or antivenin, as well as surgical interventions for impending complications such as compartment syndrome and carpal tunnel syndrome including fasciotomy and carpal tunnel release, have been used with varying degrees of success.

To our knowledge, there have been no previous reports of the development of acute stenosing tenosynovitis following a rattlesnake bite. This article describes a case of stenosing tenosynovitis of the thumb, which developed acutely in a patient 1 week after she was bitten by a rattlesnake.

Case Report

A 50-year-old, right-hand-dominant woman was referred to orthopedic surgery in the emergency department to rule out suppurative flexor tenosynovitis approximately 1 week after being bitten by a rattlesnake. Her medical history was significant for thyroid cancer (status post thyroidectomy), pancreatic neuroendocrine tumor (status post Whipple procedure), meningioma (status post craniotomy), and Scheuermann’s disease (status post thoracic spine fusion).

One week prior, the patient was bitten by a Southern Pacific rattlesnake on the right volar forearm (Figure 1). The strike penetrated the skin. The patient developed nausea, vomiting, and a fever of 102°F and presented to the local emergency department. Her condition was determined to be “not acute,” and she was assured that she had sustained a “dry bite.” Therefore, neither antivenin nor antibiotics were deemed necessary and were not administered.

Figure 1: Snakebite wounds on the right volar forearm Figure 2: Healed puncture wounds Figure 3: The right trigger thumb

Figure 1: Snakebite wounds on the right volar forearm. Figure 2: Healed puncture wounds on the right forearm. The thumb interphalangeal joint is locked in 60° of flexion. Figure 3: The right trigger thumb. Tenderness to palpation is elicited at the A1 pulley and the nodule palpated at the volar metacarpophalangeal joint.

One week after the incident, she presented to our emergency department with increased swelling in her right hand and fingers and a significant increase in pain. The patient also reported an inability to flex her right thumb. She was afebrile, and her vital signs were stable. She reported no chest pain, shortness of breath, nausea, vomiting, abdominal pain, lightheadedness, or dizziness. Physical examination revealed minor edema, minimal erythema, and no drainage at the puncture sites, 6 cm proximal to the distal wrist flexion crease on the ulnar volar aspect of the forearm (Figure 1). There was tenderness over the right thumb A1 pulley, as well as mild pain on passive extension. Laboratory studies suggested no infectious, metabolic, or hematologic disorders. Splinting, elevation, intravenous antibiotics for the possibility of bacterial inoculation during the bite, and appropriate pain management were recommended. A steroid injection was held in case it might blunt the patient’s immune response to any infection.

Two weeks later, the patient returned for follow-up with worsening signs of stenosing tenosynovitis, as well as some carpal tunnel syndrome. Her thumb interphalangeal joint was not locked in approximately 60° of flexion (Figures 2, 3). She was unable to extend the thumb interphalangeal joint actively without assistance from her other hand. She also reported numbness and paresthesias in her thumb, index, and long fingers, as well as nocturnal pain. On examination, the patient had 2 well-healed puncture wounds on the anterior right forearm (Figure 2). She had worsening tenderness to palpation at the right thumb A1 pulley, with a palpable nodule at the volar metacarpophalangeal joint. She had a positive Tinel’s sign at the carpal tunnel and positive Phalen’s sign. As her symptoms were mild to moderate, a trial of nonoperative management was warranted. We recommended a corticosteroid injection for her trigger thumb, an electromyogram and nerve conduction velocity test, as well as a cock-up wrist splint for carpal tunnel syndrome.

Four weeks following the injection, the electromyogram and nerve conduction velocity test studies were found to be normal with no evidence of carpal tunnel syndrome. However, the stenosing tenosynovitis had improved only marginally. Surgical release of the A1 pulley of the right thumb was performed without complication and demonstrated inflammatory tenosynovium surrounding the flexor pollicis longus with no evidence of infection. The patient subsequently followed a routine postoperative course without further sequelae.

Discussion

While trigger digits and carpal tunnel syndrome are commonly seen by hand surgeons, trigger digits following a snakebite have not been described previously, and carpal tunnel syndrome in the absence of compartment syndrome secondary to envenomation is uncommon.5

Trigger finger and carpal tunnel syndrome may occur concomitantly in association with rheumatoid arthritis and endocrine disorders (eg, diabetes mellitus and thyroid disorders).6 They may also occur together idiopathically. However, both trigger finger and carpal tunnel syndrome occur gradually, with the majority of symptoms developing over >6 months.7 The temporal relation to and rapid onset of symptoms after the snakebite suggest that the snakebite was the cause, whether direct or indirect, of our patient’s acute trigger thumb and carpal tunnel syndrome. While our patient had a history of total thyroidectomy, recent thyroid function tests were unavailable. Despite taking pancrelipase (pancreatic enzymes) given her history of a Whipple procedure, our patient did not require insulin or any other diabetic medications. As symptoms of carpal tunnel syndrome and compartment syndrome typically arise within hours of the snakebite, we hypothesize that the inflammation following this patient’s snakebite may have added injury to endocrine insult, leading to trigger finger and carpal tunnel syndrome several days after the initial event. This patient may not have sustained a dry bite but suffered from envenomation, as indicated by both her local and systemic symptoms.

Proteolytic enzymes in snake venom lead to cell lysis, edema, and tissue necrosis, and the proximity of the patient’s puncture site to Parona’s space implicates the involvement of not only the carpal tunnel but also the origin of the flexor pollicis longus.8 Similar enzymes such as phospholipases also stimulate the production of inflammatory mediators that cause fever, and neurotoxins in venom can be responsible for nausea and emesis.2 Antivenin could have altered the systemic symptoms of envenomation but not the local symptoms of injury.

Prompt arrival at a medical facility is recommended for the evaluation and treatment of all snakebites. Traditional first aid measures such as incision and suction of the wound, tourniquet, and cryotherapy have not been proven to be of medical benefit and may be detrimental.2,9 The affected extremity should be immobilized and monitored for signs of envenomation, such as moderate to severe pain and gross swelling.2,10 Antivenin should be administered in the presence of features such as rapid extension of swelling, systemic shock, arrhythmia, coagulopathy, paralysis, and acute renal failure. Symptoms suggestive of compartment syndrome (eg, pain out of proportion to the injury, poikilothermia, paralysis, and pulselessness) should be assessed.6 In the unlikely case that fasciotomy is necessary, any hematologic abnormalities should be corrected to prevent severe hemorrhage. Most cases of snakebites, however, may be managed with pain medication and a prophylactic course of antibiotics and tetanus toxoid booster to cover bacterial inoculation.

This case introduces a previously unreported complication following snakebite. Trigger digit as well as carpal tunnel syndrome may arise in the patient with or without endocrine disorders after being bitten by a snake. Administration of antivenin during our patient’s initial hospital assessment may have prevented some of her symptoms. However, the indications for antivenin use are not clearly defined, nor is the application without risk, as patients may experience adverse reactions such as serum sickness and anaphylaxis.2,3 Proper management of snakebites remains debatable, but supportive and nonsurgical measures continue to be the appropriate first line of treatment, although surgical intervention may still be necessary.

References

  1. Shaw BA, Hosalkar HS. Rattlesnake bites in children: antivenin treatment and surgical indications. J Bone Joint Surg Am. 2002; 84(9):1624-1629.
  2. Ahmed SM, Ahmed M, Nadeem A, Mahajan J, Choudhary A, Pal J. Emergency treatment of a snake bite: Pearls from literature. J Emerg Trauma Shock. 2008; 1(2):97-105.
  3. Gold BS, Barish RA, Dart RC. North American snake envenomation: diagnosis, treatment, and management. Emerg Med Clin North Am. 2004; 22(2):423-443.
  4. Hardy DL Sr, Zamudio KR. Compartment syndrome, fasciotomy, and neuropathy after a rattlesnake envenomation: aspects of monitoring and diagnosis. Wilderness Environ Med. 2006; 17(1):36-40.
  5. Gold BS, Barish RA, Dart RC, Silverman RP, Bochicchio GV. Resolution of compartment syndrome after rattlesnake envenomation utilizing non-invasive measures. J Emerg Med. 2003; 24(3):285-288.
  6. Kumar P, Chakrabarti I. Idiopathic carpal tunnel syndrome and trigger finger: is there an association? J Hand Surg Eur Vol. 2009; 34(1):58-59.
  7. Phalen GS. The carpal-tunnel syndrome. Seventeen years’ experience in diagnosis and treatment of six hundred fifty-four hands. J Bone Joint Surg Am. 1966; 48(2):211-228.
  8. Schweitzer G, Lewis JS. Puff adder bite—an unusual cause of bilateral carpal tunnel syndrome. A case report. S Afr Med J. 1981; 60(18):714-715.
  9. Roberts RS, Csencsitz TA, Heard CW Jr. Upper extremity compartment syndromes following pit viper envenomation. Clin Orthop Relat Res. 1985; (193):184-188.
  10. Aggarwal P, Jamshed N. What’s new in emergencies, trauma, and shock? Snake envenomation and organophosphate poisoning in the emergency department. J Emerg Trauma Shock. 2008; 1(2):59-62.

Authors

Dr Lee is from Baylor College of Medicine, Tempe, Arizona; and Dr Yao is from Stanford University Medical Center, Stanford, California.

Drs Lee and Yao have no relevant financial relationships to disclose.

Correspondence should be addressed to: Lydia Lee, MD, 2057 E Myrna Ln, Tempe, AZ 85284 (lydia.c.lee@gmail.com)

doi: 10.3928/01477447-20100526-20

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