A Pilot Study to Assess the Performance of Phase-Sensitive Breast Tomosynthesis.

Background A new modality, phase-sensitive breast tomosynthesis (PBT), may have similar diagnostic performance to conventional breast tomosynthesis but with a reduced radiation dose. Purpose To perform a pilot study of the performance of a novel PBT system compared with conventional digital breast tomosynthesis (DBT) in patients undergoing additional diagnostic imaging workup for breast lesions. Materials and Methods In a prospective study from June 2020 to March 2021, participants with suspicious breast lesions detected at screening DBT or MRI were recruited for additional PBT imaging before additional diagnostic workup or biopsy. In this pilot study, nine radiologists independently evaluated image quality and assessed the likelihood of lesion malignancy by retrospectively evaluating DBT and PBT images in two separate reading sessions. Image quality was rated subjectively using a Likert scale from 1 to 5. Areas under the receiver operating characteristic curve (AUCs) were used to compare the lesion classification (malignant vs benign) performance of the radiologists. Results Images in 50 patients (mean age, 56 years ± 12 [SD]; 49 women) with 52 evaluable lesions (28 malignant) were assessed. For image appearance and general feature visibility, DBT images had a higher total mean image quality score (3.8) than PBT images (2.9), with P < .002 for each comparison. For classification of lesions as benign or malignant, the AUCs were 0.74 for both PBT and DBT. PBT images were acquired at a 24% mean radiation dose reduction (mean, 1.78 mGy vs 2.34 mGy for DBT; P < .001). Conclusion The phase-sensitive breast tomosynthesis system had a 24% lower mean radiation dose compared with digital breast tomosynthesis, although with lower image quality. Diagnostic performance of the system remains to be determined in larger studies. © RSNA, 2022 Online supplemental material is available for this article. See also the editorial by Gao and Moy in this issue.

A phase sensitive x-ray breast tomosynthesis system: Preliminary patient images with cancer lesions.

Phase-sensitive x-ray imaging continues to attract research for its ability to visualize weakly absorbing details like those often encountered in biology and medicine. We have developed and assembled the first inline-based high-energy phase sensitive breast tomosynthesis (PBT) system, which is currently undergoing patient imaging testing at a clinical site. The PBT system consists of a microfocus polychromatic x-ray source and a direct conversion-based flat panel detector coated with a 1 mm thick amorphous selenium layer allowing a high detective quantum efficiency at high energies. The PBT system scans a compressed breast over 15° with 9 angular projection views. The high-energy scan parameters are carefully selected to ensure similar or lower mean glandular dose levels to the clinical standard of care systems. Phase retrieval and data binning are applied to the phase contrast angular projection views and a filtered back-projection algorithm is used to reconstruct the final images. This article reports the distributions of radiation dose versus thickness of the compressed breasts at 59 and 89 kV and sample PBT images acquired from 3 patients. Preliminary PBT images demonstrate the feasibility of this new imaging modality to acquire breast images at lower radiation dose as compared to the clinical digital breast tomosynthesis system with enhanced lesion characteristics (i.e. lesion spiculation and margins).

Xylitol.

Xylitol is a prevalent sugar substitute found in a wide variety of foods, particularly those labeled as "low carb." It is found in many medicines and dental products both for its antibacterial activity and to increase palatability. Originally, this toxin was recognized as a problem in dogs following sugarless gum ingestions. Xylitol is generally nontoxic to mammals except for dogs. In the dog, xylitol induces marked increases in insulin production and occasionally hepatopathy. The clinical syndrome is manifested with signs consistent with profound hypoglycemia, hypokalemia, hypophosphatemia, and acute hepatic failure. Treatment relies upon administration of intravenous glucose, hepatic support, and general supportive care.

Bromethalin.

Bromethalin is a potent neurotoxin capable of inducing fatal cerebral edema in companion animals. Bromethalin decreases adenosine triphosphate production resulting in cerebral edema. Toxicosis can be seen in cats and dogs with oral exposures as low as 0.3 and 2.5mg/kg, respectively. High doses produce severe muscle tremors, hyperthermia, seizures, and death within a couple hours postingestion. The usual presentation after moderate to low exposure develops over 12-24 hours with progressive ataxia, paresis, and hindlimb paralysis. Central nervous system depression continues to semicoma or coma. Diagnosis is based upon history of exposure, development of progressive appropriate clinical signs and chemical confirmation in tissues. Treatment relies heavily upon early emesis induction and prolonged decontamination with pulse dosing of activated charcoal. There is no specific antidote; attempts to control cerebral edema with diuretics and corticosteroids have met with limited success. Significant supportive care is usually required, often including seizure management, nutritional support, and defense against decubital ulceration. Prognosis is guarded to poor.

Cholecalciferol.

The primary source of exposure to cholecalciferol in dogs and cats is ingestion of rodenticide baits with vitamin D3 as the active ingredient. Other sources of this toxin are human medications and rarely, contaminated pet food. Although the reported lethal dose 50% for cholecalciferol is 88 mg/kg, deaths have been seen with an individual exposure of 2 mc g/kg in dogs. Clinical signs are induced by profound hypercalcemia affecting multiple body systems. Clinical presentations may include anorexia, depression, muscle weakness, vomiting, polyuria, polydipsia, dehydration, abdominal pain, hematemesis, melena, and bradycardia. Tissue mineralization may develop if calcium × phosphorous product is greater than 60. Serum testing for hypercalcemia, hyperphosphatemia, and decreased serum parathyroid hormone are confirmatory. Initial treatment relies upon decontamination with emesis induction followed by administration of pulse-dose activated charcoal designed to interfere with the extensive enterohepatic recirculation of toxin. Medical management is designed to decrease serum calcium levels by use of intravenous fluid diuresis with administration of furosemide and prednisolone. Biphosphate pamidronate is used to inhibit calcium release from the bone. Phosphate binders aid in decreasing phosphate availability to interact with calcium. The prognosis is better if treatment is instituted early before development of hypercalcemia and hyperphosphatemia enables tissue mineralization to progress.

A randomized multicenter trial of Crotalidae polyvalent immune F(ab) antivenom for the treatment of rattlesnake envenomation in dogs.

OBJECTIVE: To determine clinical efficacy of the Crotalidae polyvalent immune F(ab) (ovine) antivenom (OPCA) against progressive crotalid envenomation in the dog as reflected in stabilization or improvement of snakebite severity scores (SSS). Additionally, due to the potential decreased half-life of the F(ab) antibodies in dogs we compared SSS between dogs receiving 2 different dosing regimes. DESIGN: Prospective, clinical trial. SETTING: Five veterinary emergency and critical care facilities. ANIMALS: One hundred and fifteen client-owned Crotalid (rattlesnake) snake bitten dogs in whom worsening of the envenomation syndrome was observed before OPCA treatment. INTERVENTIONS: In a multicenter randomized clinical trial a single dose (1 vial) of OPCA alone was compared with 2 doses (1/2 vial each) administered 6 hours apart. Standard supportive care was provided in all cases. MEASUREMENTS AND MAIN RESULTS: Data were available for 115 patients, 9 of which were fatalities. All patients' clinical condition was documented with a standardized SSS system accounting for each major body system. Each fatality received maximum severity scores of 20. The mean severity score of the 115 patients decreased from 4.19 to 3.29 points and there was no difference between the 2 treatment groups. The mean severity score of the 107 patients without fatalities decreased from 4.16 to 2.15. Antivenin-related acute reactions occurred in 6 dogs (6%), and no serum sickness occurred within the 95 cases contacted at the 2-week posttreatment follow-up. CONCLUSIONS: In the first randomized trial in dogs of antivenin in the United States, OPCA effectively stabilized or terminated venom effects. There were no statistical differences detected between treatment groups within the study time frame.

Toxic exotics.

The purpose of this article is to familiarize the reader with the basic venom components, the pathophysiologic responses of envenomated dogs and cats, and some brief treatment guidelines for envenomations by various exotic "pets." Representative toxic species of reptiles, amphibians, and arthropods are included. The growing trend toward the collection of exotic animals by private owners increases the likelihood that veterinarians will face the challenge of treating an exotic envenomation.

Snake bite: coral snakes.

North American coral snakes are distinctively colored beginning with a black snout and an alternating pattern of black, yellow, and red. They have fixed front fangs and a poorly developed system for venom delivery, requiring a chewing action to inject the venom. The severity of a coral snake bite is related to the volume of venom injected and the size of the victim. The length of the snake correlates positively with the snakes venom yield. Coral snake venom is primarily neurotoxic with little local tissue reaction or pain at the bite site. The net effect of the neurotoxins is a curare like syndrome. In canine victims there have been reports of marked hemolysis with severe anemia and hemoglobinuria. The onset of clinical signs may be delayed for as much as 10 to 18 hours. The victim begins to have alterations in mental status and develops generalized weakness and muscle fasciculations. Progression to paralysis of the limbs and respiratory muscles then follows. The best flied response to coral snake envenomation is rapid transport to a veterinary medical facility capable of 24 hour critical care and assisted ventilation. First aid treatment advocated in Australia for Elapid bites is the immediate use of a compression bandage. The victim should be hospitalized for a minimum of 48 hours for continuous monitoring. The only definitive treatment for coral snake envenomation is the administration of antivenin (M. fulvius). Once clinical signs of coral snake envenomation become manifest they progress with alarming rapidity and are difficult to reverse. If antivenin is not available or if its administration is delayed, supportive care includes respiratory support. Assisted mechanical ventilation can be used but may have to be employed for up to 48 to 72 hours.

Black widow spider envenomation.

Black widow spiders are found throughout the continental United States and north into the southern Canadian provinces. Male black widow spiders are of little medical importance. Female black widow spiders can be 20 times larger than males. The female can be identified by the hourglass pattern, red or orange in color, on the ventral aspect of her shiny, globose black abdomen. Black widow spiders control the amount of venom they inject; an estimated 15% of bites to humans are non-envenomating. Cats are very sensitive to the venom and deaths are common. Dogs have severe clinical signs but are considered more resistant than cats. A single bite is capable of delivering a lethal dose of venom to companion animals. There are several toxic components consisting of five or six biologically active proteins. These include a potent mammalian neurotoxin called alpha-latrotoxin, which induces neurotransmitter release from nerve terminals. Acetylcholine, noradrenalin, dopamine, glutamate, and enkephalin systems are all susceptible to the toxin. Onset of clinical signs usually occurs during the first 8 hours post envenomation. The condition is extremely painful in moderate to severe envenomations. Abdominal rigidity without tenderness is a hallmark sign of Latrodectus envenomation. In cats, paralytic signs may occur early and are particularly marked. Hypertension is a significant threat. First aid is of no value in the treatment. The primary treatment for black widow spider envenomation is the administration of specific antivenin, which provides the most permanent and quickest relief of the envenomation syndrome, usually within 30 minutes of infusion. The prognosis of Latrodectus envenomation is uncertain of several days, and complete recovery may take weeks.

Snake bite: pit vipers.

Pit vipers are the largest group of venomous snakes in the United States and are involved in an estimated 150,000 bites annually of dogs and cats. The severity of any pit viper bite is related to the volume and toxicity of the venom injected as well as the location of the bite, which may influence the rate of venom uptake. The toxicity of rattlesnake venom varies widely. It is possible for pit vipers' venom to be strictly neurotoxic with virtually no local signs of envenomation. Venom consists of 90% water and has a minimum of 10 enzymes and 3 to 12 nonenzymatic proteins and peptides in any individual snake. The onset of clinical signs after envenomation may be delayed for several hours. The presence of fang marks does not indicate that envenomation has occurred, only that a bite has taken place. Systemic clinical manifestations encompass a wide variety of problems including pain, weakness, dizziness, nausea, severe hypotension, and thrombocytopenia. The victim's clotting abnormalities largely depend upon the species of snake involved. Venom induced thrombocytopenia occurs in approximately 30% of envenomations. Many first aid measures have been advocated for pit viper bite victims, none has been shown to prevent morbidity or mortality. Current recommendations for first aid in the field are to keep the victim calm, keep the bite site below heart level if possible, and transport the victim to a veterinary medical facility for primary medical intervention. The patient should be hospitalized and monitored closely for a minimum of 8 hours for the onset of signs of envenomation. The only proven specific therapy against pit viper envenomation is the administration of antivenin. The dosage of antivenin needed is calculated relative to the amount of venom injected, the body mass of the victim, and the bite site. The average dosage in dogs and cats is 1 to 2 vials of antivenin.

Brown spider envenomation.

The venom from spiders of the genus Loxosceles, the most famous being Loxosceles recluse (the most brown recluse spider) can cause serious poisoning. These spiders inhabit the south and south central states from Georgia through Texas and north to southern Wisconsin. They are commonly called violin spiders because of the violin-shaped marking on the dorsum of the cephalothorax. Many dermonecrotic lesions are incorrectly diagnosed as Brown recluse bites, as up to 50% of the diagnoses are in geographic regions of the country which do not have Loxosceles spiders. Sphingomyelinase D is the primary venom dermonecrotic factor. The toxin depletes serum hemolytic complement, prolongs the activated partial thromboplastin time and depletes clotting factors VIII, IX, XI, and XII. The venom induces rapid coagulation and occlusion of small capillaries, causing subsequent tissue necrosis. A classic "bulls eye" lesion develops, an erythematous area inside of which is a pale ischemic region that develops a dark necrotic center as the lesion matures. Healing is slow, and these ulcers may persist for months leaving a deep scar. Systemic signs occur less commonly but can be life threatening. The most prevalent sign is a hemolytic anemia with significant hemoglobinuria. There is no specific antidote. Dapsone a leukocyte inhibitor has been shown to be effective in treating dermal lesions in animal models. Conservative therapy includes several cleanings daily with Burrow's solution and hydrogen peroxide. Systemic signs of Loxosceles envenomation are potentially fatal and should be aggressively addressed. Hospitalization and intravenous fluid therapy may be needed to maintain adequate hydration and to protect renal function.