From the diabetic foot ulcer and beyond: how do foot infections spread in patients with diabetes?

A diabetic foot infection is usually the result of a pre-existing foot ulceration and is the leading cause of lower extremity amputation in patients with diabetes. It is widely accepted that diabetic foot infections may be challenging to treat for several reasons. The devastating effects of hyperglycemia on host defense, ischemia, multi-drug resistant bacteria and spreading of infection through the foot may complicate the course of diabetic foot infections. Understanding the ways in which infections spread through the diabetic foot is a pivotal factor in order to decide the best approach for the patient's treatment. The ways in which infections spread can be explained by the anatomical division of the foot into compartments, the tendons included in the compartments, the initial location of the point of entry of the infection and the type of infection that the patient has. The aim of this paper is to further comment on the existed and proposed anatomical principles of the spread of infection through the foot in patients with diabetes.

Endovascular treatment is a hope for patient with Buerger's disease and foot ulcer: case report.

Scarce information exists regarding the usefulness of the endovascular approach in patients with thromboangiitis obliterans and critical ischemia. A 41-old-man diagnosed with Buerger's disease had rest pain and a severe ulceration on the big toe. He had been scheduled for a big toe amputation. Typical findings of Buerger's disease were found in the angiogram including below-the-knee involvement and corkscrew collateral arteries. Stenoses of the posterior tibial artery were angioplastied and the plantar artery was recanalized and angioplastied. Healing was achieved and the patient remains asymptomatic 21 months after the procedure. The outcome achieved in this case and recent series should encourage doctors dealing with this problem to attempt limb salvage by means of the endovascular approach.

Long-term inhaled nitric oxide plus phosphodiesterase 5 inhibitors for severe pulmonary hypertension.

BACKGROUND: Inhaled nitric oxide (iNO) is a potent pulmonary vasodilator, but therapeutic experience in patients with severe pulmonary hypertension is scarce. METHODS: Eleven patients with severe pulmonary hypertension, 6 due to pulmonary arterial hypertension and 4 due to chronic thromboembolic disease, were selected for iNO therapy. A phosphodiesterase type 5 inhibitor (PDE5i) was added in cases of clinical worsening. In this study we evaluate the clinical effectiveness and safety of long-term treatment with iNO either alone or combined with a PDE5i. RESULTS: After 1 month of iNO administration, improvements were observed in World Health Organization functional class, Borg scale (p = 0.003), brain natriuretic peptide levels (p = 0.002) and 6-minute walk test (p = 0.003). After 6 months of treatment, 7 patients had clinical deterioration that was reversed upon adding a PDE5i. One of these patients died in Month 8 and another underwent pulmonary transplantation in Month 9. The clinical condition of the remaining 9 patients was unchanged after 1 year. A second right catheterization showed improvement in mean pulmonary arterial pressure (66 +/- 15 mm Hg to 56 +/- 18 mm Hg; p = 0.01), pulmonary vascular resistance (1,234 +/- 380 dyn/s/cm(5) to 911 +/- 410 dyn/s/cm(5); p = 0.008) and cardiac index (2.0 +/- 0.4 liters/min/m(2) to 2.5 +/- 0.4 liters/min/m(2); p = 0.04). There was no significant increase in methemoglobin, no worsening of pulmonary function and no sudden withdrawal syndrome. CONCLUSIONS: We suggest that iNO therapy alone or in combination with a PDE5i could be a therapeutic alternative for severe pulmonary hypertension.

Long-term inhaled nitric oxide plus dipyridamole for pulmonary arterial hypertension.

Inhaled nitric oxide (iNO) has been shown to be a potent and selective vasodilator in pulmonary arterial hypertension (PAH). However, the clinical experience in prolonged treatment is limited. We assess the safety and effectiveness of long-term administration of iNO in severe PAH. Two female patients were admitted to our hospital because of severe dyspnea (World Health Organization functional class IV) and hypoxemia. They were diagnosed with PAH (primary and secondary to congenital heart disease) and treated with iNO for 2 years. The delivery system consisted of an NO tank of 800 ppm, a modified gas-pulsing device, and nasal cannulas. On iNO treatment the patients showed remarkable improvement of symptoms, oxygenation and 6-min walk distance. After 16 months the patients began to experience a progressive rebound of symptoms. A phosphodiesterase type 5 inhibitor (dipyridamole) was added to iNO. This intervention proved useful in improving clinical deterioration and hemodynamics. This is the first study reporting 2-year iNO therapy in 2 patients with primary and secondary pulmonary hypertension. The combination of dipyridamole with iNO augments the pulmonary vasodilatation and may be useful in managing PAH.