Many times a person will be admitted into a hospital with one disorder only to be discharged later with a new and more serious hospital acquired illness. These days it is not always what you check into the hospital with that a patient and his family needs to be most wary of but rather, the bevy of collateral medical complications which come from poor nursing care and hygiene that can turn a short visit to the hospital into a slow and painful death. One such nightmare which occurs in hospitals across the country involves the formation of bedsores.
Bedsores, more properly known as pressure ulcers or decubitus ulcers, are lesions caused by many factors such as: unrelieved pressure; friction; humidity; shearing forces; temperature; age; continence and medication; to any part of the body, especially portions over bony or cartilaginous areas such as sacrum, elbows, knees, ankles etc. Although easily prevented and completely treatable if found early, bedsores are often fatal - even under the auspices of medical care - and are one of the leading iatrogenic causes of death reported in developed countries, second only to adverse drug reactions. Prior to the 1950s, treatment was ineffective until Doreen Norton showed that the primary cure and treatment was to remove the pressure by turning the patient every two hours. Patients must be kept clean and dry in order for a bedsore prevention protocol to be effective. Although bedsore prevention is simple due to chronic understaffing and or professional apathy they are commonplace in modern hospitals.
Bedsores are classified in stages. The definitions of the four pressure ulcer stages are revised periodically by the National Pressure Ulcer Advisory Panel (NPUAP) in the United States. Briefly, however, they are as follows:
•Stage I is the most superficial, indicated by non blanchable redness that does not subside after pressure is relieved. This stage is visually similar to reactive hyperemia seen in skin after prolonged application of pressure. Stage I pressure ulcers can be distinguished from reactive hyperemia in two ways: a) reactive hyperemia resolves itself within 3/4 of the time pressure was applied, and b) reactive hyperemia blanches when pressure is applied, whereas a Stage I pressure ulcer does not. The skin may be hotter or cooler than normal, have an odd texture, or perhaps be painful to the patient. Although easy to identify on a light-skinned patient, ulcers on darker-skinned individuals may show up as shades of purple or blue in comparison to lighter skin tones.
•Stage II is damage to the epidermis extending into, but no deeper than, the dermis. In this stage, the ulcer may be referred to as a blister or abrasion.
•Stage III involves the full thickness of the skin and may extend into the subcutaneous tissue layer. This layer has a relatively poor blood supply and can be difficult to heal. At this stage, there may be undermining damage that makes the wound much larger than it may seem on the surface.
Stage IV pressure ulcer
•Stage IV is the deepest, extending into the muscle, tendon or even bone. • Unstageable pressure ulcers are covered with dead cells, or eschar and wound exudate, so the depth cannot be determined. .
Suspected Deep tissue injury: Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue.
Further description: Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal treatment.
With higher stages, healing time is prolonged. While about 75% of Stage II ulcers heal within eight weeks, only 62% of Stage IV pressure ulcers ever heal, and only 52% heal within one year It is important to note that pressure ulcers do not regress in stage as they heal. A pressure ulcer that is becoming shallower with healing is described in terms of its original deepest depth (e.g., healing Stage II pressure ulcer).
Unfortunately, once a bedsore proceeds past stage II the likelihood that the sore will ever heal diminishes substantially with only 62% of all stage IV ulcers ever fully healing. Once a bedsore forms that open area of the body if more susceptible to infections, such as MRSA which is resistant to modern antibiotics. Many times these infections lead to sepsis and death.
Often time's families and patients are lulled into a false sense of security because of the international reputation of the hospital or clinic in question. This is a critical mistake. A bedsore can literally form within hours and once there it can be very difficult to control. People with peripheral vascular disease and diabetes are particularly susceptible to the formation of these ulcers and often have a more difficult time with the healing process. High protein intake is crucial in order to facilitate the healing process. People who are weal and sick tend to eat less. This makes them ideal candidates for the formation and aggressive evolution of these bedsores.
Patients and families should be aware of the bedsore prevention protocols in place when a loved one is admitted to the hospital and should make sure they are being followed. This includes regular baths and timely changing of diapers should the patient be incontinent.
Michael Kosner, Esq. President, The Kosner Firm, Chtd.
