scholarly journals Pressure ulcers in patients with diabetes: a bibliometrics analysis

2021 ◽  
Vol 10 (10) ◽  
pp. 10515-10526
Author(s):  
Junhua Dong ◽  
Lingxia Li ◽  
Min Lu ◽  
Xuejun Cheng ◽  
Yucui Zhai
Author(s):  
Hugo Farne ◽  
Edward Norris-Cervetto ◽  
James Warbrick-Smith

Venous ulcers account for by far the majority (about 70%), with mixed arterial/venous (about 10%) and arterial (about 10%) most of the remainder. Pressure ulcers have become increasingly common because of the increase in elderly, frail, and relatively immobile patients. The other causes are relatively rare with the exception of neuropathic ulcers in patients with diabetes mellitus. Note that many leg ulcers may have a multifactorial aetiology, i.e. they may involve more than one of the pathologies listed in Figure 29.1. The first thing is to ask about the ulcer. You should consider: • Is the ulcer painful? ■ Venous ulcers are caused by venous stasis in the leg and are thus less painful when elevated and drained of blood. However, only about 30% of venous ulcers are painful. ■ Arterial (atherosclerotic) ulcers are caused by ischaemia to the leg and are thus more painful when elevated and drained of blood. Patients often say the ulcers are painful enough to wake them up at night and that they obtain relief by lowering their leg over the side of the bed. ■ Neuropathic ulcers are caused by loss of sensation (which predisposes to constant trauma) and are thus not painful. ■ Pressure ulcers are caused by, as the name suggests, prolonged pressure on the affected site. They tend to be exquisitely tender but not necessarily painful if no pressure is being applied. • How long has the ulcer been there? ■ Venous ulcers are less painful and can therefore present late. They often have a long and recurring history. ■ Arterial ulcers tend to present relatively early because of pain. They often occur secondary to trivial trauma. ■ Neuropathic ulcers are associated with a loss of sensation and thus often present late. ■ Pressure ulcers can develop surprisingly rapidly (e.g. days in immobile patients if they are not turned regularly during their admission, even hours in patients who suffer a long lie following a fall), but can have a more indolent course depending on how much pressure is put on for how long. Thus the time course is not especially helpful. ■ A long history should arouse suspicion of a Marjolin ulcer, which only occurs in long-standing ulcers.


2021 ◽  
Vol 30 (Sup6) ◽  
pp. S12-S21
Author(s):  
Diana G Sami ◽  
Ahmed Abdellatif

Objective: Pressure ulcers (PUs) are a major healthcare problem, commonly associated with older people, patients who are bedbound and patients with diabetes. The impact of PUs can decrease patients' quality of life, and lead to high morbidity and mortality rates. In this study, we aimed to describe a novel PU model that simulates pressure ulcers in humans to provide a research tool for new drug testing. Method: Diabetes was induced using streptozocin in 75 adult Sprague Dawley rats. To create the PU, skin was sandwiched between two magnets, one of them implanted below the panniculus carnosus muscle and the other above the skin. The model was tested on nondiabetic rats and diabetic rats, each with pressure ulcers, compared to nondiabetic rats with excisional wounds. Results: Results showed that the PU model in diabetic (p-value<0.000001) and non-diabetic rats (p-value<0.05) exhibited significantly delayed healing (no healing over 21 days) compared with the excisional wound that was completely healed by day 21. Conclusion: Diabetic rats showed significant changes in intact skin compared with non-diabetic rats, as well as a significant delay in the healing process compared with the non-diabetic group. By effectively impairing the skin contraction otherwise seen in the rats, and thereby delaying healing and making it similar to that seen in hard-to-heal PUs in humans, this model provides an effective tool for wound healing research.


2020 ◽  
Vol 29 (11) ◽  
pp. 632-641
Author(s):  
Diana G Sami ◽  
Ahmed Abdellatif

Objective: Pressure ulcers (PUs) are a major healthcare problem, commonly associated with older people, patients who are bedbound and patients with diabetes. The impact of PUs can decrease patients' quality of life, and lead to high morbidity and mortality rates. In this study, we aimed to describe a novel PU model that simulates pressure ulcers in humans to provide a research tool for new drug testing. Method: Diabetes was induced using streptozocin in 75 adult Sprague Dawley rats. To create the PU, skin was sandwiched between two magnets, one of them implanted below the panniculus carnosus muscle and the other above the skin. The model was tested on nondiabetic rats and diabetic rats, each with pressure ulcers, compared to nondiabetic rats with excisional wounds. Results: Results showed that the PU model in diabetic (p-value<0.000001) and non-diabetic rats (p-value<0.05) exhibited significantly delayed healing (no healing over 21 days) compared with the excisional wound that was completely healed by day 21. Conclusion: Diabetic rats showed significant changes in intact skin compared with non-diabetic rats, as well as a significant delay in the healing process compared with the non-diabetic group. By effectively impairing the skin contraction otherwise seen in the rats, and thereby delaying healing and making it similar to that seen in hard-to-heal PUs in humans, this model provides an effective tool for wound healing research.


Author(s):  
Bruce R. Pachter

Diabetes mellitus is one of the commonest causes of neuropathy. Diabetic neuropathy is a heterogeneous group of neuropathic disorders to which patients with diabetes mellitus are susceptible; more than one kind of neuropathy can frequently occur in the same individual. Abnormalities are also known to occur in nearly every anatomic subdivision of the eye in diabetic patients. Oculomotor palsy appears to be common in diabetes mellitus for their occurrence in isolation to suggest diabetes. Nerves to the external ocular muscles are most commonly affected, particularly the oculomotor or third cranial nerve. The third nerve palsy of diabetes is characteristic, being of sudden onset, accompanied by orbital and retro-orbital pain, often associated with complete involvement of the external ocular muscles innervated by the nerve. While the human and experimental animal literature is replete with studies on the peripheral nerves in diabetes mellitus, there is but a paucity of reported studies dealing with the oculomotor nerves and their associated extraocular muscles (EOMs).


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