[A diabetic patient with a fulminant hand infection caused by a domestic rat bite]. / Ernstige handinfectie bij een patiënt met diabetes door een tamme-rattenbeet.

BACKGROUND: Animal bite wounds are common and can cause serious hand infections. Risk factors not only include the oral flora of the animal and the anatomy of the teeth, but also the comorbidities of the bitten patient. CASE DESCRIPTION: In this case report we describe a 46-years old female patient with comorbidities, including diabetes mellitus type 2 and peripheral artery disease, suffering a fulminant hand infection after a domestic rat bite with the newly described bacterium Rodentibacterratti. Despite extensive antibiotic therapy and surgical debridement, a ray amputation was inevitable to maintain adequate hand function. CONCLUSION: Infections after animal bites may be caused by a variety of pathogens. The pathogen Rodentibacterratti has not previously been associated with infections in humans and future research is indicated to assess therapeutic strategies. Patients should be referred to a (plastic) surgeon if there is no clinical improvement within 48 hours of initiating antibiotic treatment.

[A woman with a chronic wound on her index finger]. / Een vrouw met een lang bestaande wond aan haar vinger.

A 79-year-old woman consulted a plastic surgeon, because since 3 years she had a large wound at the base of her left index finger. Histology of a skin biopsy showed cutaneous squamous cell carcinoma. Because of the extension of the defect, amputation of the index finger with a split-skin-graft was performed.

[Maggots in the wound, debridement, disinfection and wound healing]. / Vliegenmaden in de wond: débridement, desinfectie en wondgenezing.

An 87-year-old man had a longstanding untreated large basosquamous carcinoma on his right ear. He was admitted to the emergency department at our hospital. A large portion of the auricle had perished, together with part of the tumour. Surgery was planned but two days before, the patient complained of an irritating loud noise in his ear. We discovered this was caused by maggots in his external acoustic meatus: myiasis. Dozens of maggots were removed. A striking finding was that the smell of the wound had disappeared and that the wound was much cleaner, with a reddish aspect and less necrosis. The surgical procedure was uneventful. Larval therapy has been known for centuries. In recent years it has gained renewed interest as it may enhance wound debridement, wound disinfection, and may promote wound healing.

Effect of HTK on the microcirculation in the rat cremaster muscle during warm ischemia and reperfusion.

Histidine-tryptophan-ketoglutarate (HTK) preserves rat muscle function during cold storage. We examined the effect of HTK perfusion on preservation of microvascular function during 4 h of warm ischemia and subsequent reperfusion (I/R) in the rat cremaster muscle. Leukocyte-endothelium interactions, capillary perfusion, and arteriole diameters were quantified prior to HTK-perfusion and/or ischemia, and at 0, 1, and 2 h after restoration of blood flow. In all groups, the number of rolling leukocytes increased with time, whereas I/R induced a slight increase in leukocyte adhesion. After ischemia, capillary perfusion rapidly recovered to about 50% and returned to near normal (90%) after 2 h. HTK at 22 degrees C did not affect the assessed microcirculation variables, whereas HTK at 4 degrees C reduced leukocyte rolling, but not adhesion. Therefore, microvascular function of HTK-perfused muscles was not better preserved during warm I/R than that of nonperfused muscles. Contrary to other preservation solutions, HTK perfusion in itself was not detrimental to the microcirculation.

Can angiogenesis induced by chronic electrical stimulation enhance latissimus dorsi muscle flap survival for application in cardiomyoplasty?

In cardiomyoplasty, the latissimus dorsi muscle is lifted on its primary neurovascular pedicle and wrapped around a failing heart. After 2 weeks, it is trained for 6 weeks using chronic electrical stimulation, which transforms the latissimus dorsi muscle into a fatigue-resistant muscle that can contract in synchrony with the beating heart without tiring. In over 600 cardiomyoplasty procedures performed clinically to date, the outcomes have varied. Given the data obtained in animal experiments, the authors believe these variable outcomes are attributable to distal latissimus dorsi muscle flap necrosis. The aim of the present study was to investigate whether the chronic electrical stimulation training used to transform the latissimus dorsi muscle into fatigue-resistant muscle could also be used to induce angiogenesis, increase perfusion, and thus protect the latissimus dorsi muscle flap from distal necrosis. After 14 days of chronic electrical stimulation (10 Hz, 330 microsec, 4 to 6 V continuous, 8 hours/day) of the right or left latissimus dorsi muscle (randomly selected) in 11 rats, both latissimus dorsi muscles were lifted on their thoracodorsal pedicles and returned to their anatomical beds. Four days later, the resulting amount of distal flap necrosis was measured. Also, at predetermined time intervals throughout the experiment, muscle surface blood perfusion was measured using scanning laser Doppler flowmetry. Finally, latissimus dorsi muscles were excised in four additional stimulated rats, to measure angiogenesis (capillary-to-fiber ratio), fiber type (oxidative or glycolytic), and fiber size using histologic specimens. The authors found that chronic electrical stimulation (1) significantly (p < 0.05) increased angiogenesis (mean capillary-to-fiber ratio) by 82 percent and blood perfusion by 36 percent; (2) did not reduce the amount of distal flap necrosis compared with nonchronic electrical stimulation controls (29 +/- 5.3 percent versus 26.6 +/- 5.1 percent); (3) completely transformed the normally mixed (oxidative and glycolytic) fiber type distribution into all oxidative fibers; and (4) reduced fiber size in the proximal and middle but not in the distal segments of the flap. Despite the significant increase in angiogenesis and blood perfusion, distal latissimus dorsi muscle flap necrosis did not decrease. This might be because of three reasons: first, the change in muscle metabolism from anaerobic to aerobic may have rendered the muscle fibers more susceptible to ischemia. Second, because of the larger diameter of the distal fibers in normal and stimulated latissimus dorsi muscle, the diffusion distance for oxygen to the center of the distal fibers is increased, making fiber survival more difficult. Third, even though angiogenesis was significantly increased in the flap, cutting all but the single vascular pedicle resulted in the newly formed capillaries not receiving enough blood to provide nourishment to the distal latissimus dorsi muscle. The authors' findings indicate that chronic electrical stimulation as tested in these experiments could not be used to prevent distal latissimus dorsi muscle flap ischemia and necrosis in cardiomyoplasty.