Toxic inoculation associated with a presumptive stingray injury.

INTRODUCTION: Stingray spine injuries are among the most common marine animal injuries in humans. While most resolve with immersion in warm water, a few become infected and require antibiotics. We present a case report of a presumptive stingray injury that evolved to a major slough and which required prolonged healing in a patient with diabetes mellitus. Our literature review was unable to find a similarly reported case. MATERIALS: A co-author was asked to evaluate and manage an ominous-appearing wound on the right foot of a diabetic. The problem developed after the individual had been wading in shallow ocean beach water. The patient's diabetic sensory neuropathy obscured the immediate association of the problem with a stingray injury, but this became the presumptive diagnosis when pain developed and necessitated that he seek medical care. FINDINGS/CLINICAL COURSE: After an initial urgent care visit, increasing pain and worsening appearance of the patient's foot necessitated a visit to our emergency department. The patient was admitted the next day due to symptoms of systemic sepsis. On the fourth hospital day, a large bulla on the lateral side of the right foot was excised. This unroofed a full-thickness slough to the periosteum level of the underlying bones. Not until the 16th hospital day had enough improvement occurred to discharge the patient. Over the next 16 weeks, the wound improved, developed a vascular base and epithelialized. CONCLUSION: With a dearth of literature about stingray injuries in patients with diabetes mellitus reported, our case is unique: The patient's wound course more closely resembled a toxic inoculation than the typical puncture wound-cellulitis presentations associated with stingray injuries.

The Gradient Perfusion Model Part 1: Why and at what sites decompression sickness can occur.

INTRODUCTION: Decompression sickness (DCS) is manifested by the quantity and location of bubbles in body tissues after reduction in ambient pressures. Models have been formulated to explain why bubbles form, but none provide satisfactory explanations as to why the findings of DCS occur as they do. This first of a three-part series explains why and at what sites DCS occurs. MATERIALS AND METHODS: Over a 50-year span and 500 cases of DCS we have managed, it has become apparent that almost all "unexplained" DCS (i.e., cases with no obvious explanation as to how/why they occurred) have physiological explanations. The vagaries of the physiology of tissue perfusion and the physics of gradients as a cause of autochthonous bubble formation were analyzed. FINDINGS: Perfusion is highly variable, with so-called "fast" tissues (i.e., tissues with a rapid rate of saturation) requiring a constant blood supply, "intermediate" tissues requiring a blood supply proportional to needs, and "slow" tissues having minimal perfusion requirements. The 5-liter blood volume in a vascular system with greater than a 20-liter capacity requires careful regulation. Disruptions in the regulation and/or overwhelming gradients explain why DCS occurs. CONCLUSIONS: Our Gradient-Perfusion Model provides an explanation as to why disordering events account for almost all cases of unexplained DCS. We propose that this latter term be discarded and "disordering events" be sought for DCS cases that have no obvious explanations.

The Gradient Perfusion Model Part 2: Substantiation of the GPM with clinical cases.

Introduction: In Part 1 of this three-part series, we provided an explanation as to why and at what sites decompression sickness (DCS) occurs, using the Gradient-Perfusion Model (GPM). In this part, we provide information to substantiate the concept and present clinical cases that were initially labeled as "unexplained DCS," but later disordering events were identified to explain the clinical presentations. Materials and Methods: Among 500 cases of DCS we have managed for over 50 years, a cohort of these patients was initially diagnosed as unexplained DCS. However, some have shown that disordering events are the likely cause of their DCS. Results: By pairing the tissue involved with the patient's dive history, a gradient-perfusion imbalance connection was identified. In all serious (Type 2) presentations of DCS, alterations in perfusion of the fast tissues were able to account for the clinical findings. The consequences demonstrated that the gradients overwhelmed the ability of altered perfusion to offgas/offload the inert gas. Pain-only and peripheral neuropathy presentations involved both intermediate and slowly perfused tissues. Rather than perfusion, gradient limitations were the reasons for the clinical presentations of these patients. Conclusions: The GPM accounts for signs and symptom presentations in DCS. This provides the basis for appropriate treatments and logical recommendations for return to diving. We recommend that the label "unexplained DCS" be discontinued and that the GPM be used to determine the cause. Once the cause is established, "DCS due to disordered decompression" becomes the appropriate term.

The Gradient Perfusion Model Part 3: An extraordinary case of decompression sickness.

INTRODUCTION: Decompression sickness (DCS) has been associated with unusual circumstances such as breath-hold diving, shallow depths, and short bottom times. We report a case of DCS with an extraordinary cause and course. MATERIALS AND METHODS: A 72-year-old healthy Hispanic female was referred to our 24/7 Hyperbaric Medicine Unit for emergency hyperbaric oxygen recompression treatment (HBO2 RCT) after developing lower-extremity paralysis following a hyperbaric air exposure in a homemade hyperbaric chamber. RESULTS: After an uneventful exposure to hyperbaric air at a maximum 72-foot depth (3.2 ATA, 32.3 psig), the patient had the delayed onset of abdominal pain and paraplegia after eating a meal. After HBO2 RCT in accordance with our management algorithm, the patient had a full recovery. CONCLUSIONS: This patient's presentation and course corresponded to what we label as "disordered decompression" and conformed to our Gradient Perfusion Model. With a finite blood volume and the need to perfuse two "intermediate" tissues simultaneously, we postulate that a "steal" syndrome arose to cause the abdominal and paralysis symptoms.