The investigators want to evaluate the short duration HBOT can improve glycohemoglobin
(HbA1c) levels, leukocyte count, and serum creatinine levels in patients with DFU (diabetic
foot ulcer) Wagner 3-4.
The Efficacy Of Nalbuphine Versus Fentanyl As Additives To Bupivacaine In Spinal Anaesthesia
For Internal FixationI Of Tibia
Ulcerative colitis (UC) is a chronic inflammatory bowel disease associated with recurrent
mucosal inflammation. Clinically, the disease is characterized by bloody diarrhea, abdominal
pain, and constitutional symptoms such as fever and weight loss. Treatment strategies vary
based on disease activity and target various aspects of the inflammatory cascade. Options
include: anti-inflammatory drugs (mesalamine), immunosuppressive or modulatory medications
(corticosteroids, thiopurines, cyclosporine) and biologic agents (Anti-TNF). Disease severity
can be wide ranging, and nearly 25% of UC patients are hospitalized for acute severe disease.
Of these patients, 30% will undergo colectomy after the acute episode, a quarter of which
will experience post-operative complications. Although there has been great progress in
treatment of UC over the past decade, even with the anti-TNF agent infliximab, the one-year
remission rate for patients not responding to conservative management is barely 20%.
Furthermore, corticosteroids have significant long-term consequences and immune suppressive
drugs such as 6-mercaptopurine, azathioprine and infliximab have been associated with serious
adverse events including life-threatening infections and lymphomas. With growing evidence
that the pathogenesis of UC is multi-factorial and involves a complex interaction of genetic
and environmental factors, newer treatment modalities are being evaluated to target the
mucosal immune response and mucosal inflammatory regulatory system.
Hyperbaric oxygen offers a promising new treatment option since it targets both tissue
hypoxia and inflammation. Recent small scales studies evaluating the impact of hyperbaric
oxygen treatment in acute ulcerative colitis flares demonstrated improved outcomes. The
mechanisms underlying the improvement are not known. In this study, we will treat ulcerative
colitis flares with hyperbaric oxygen and measure changes in both markers of tissue hypoxia
and inflammation. We hypothesize that hyperbaric oxygen will (a) improve outcomes, and (b)
show reductions in markers of both tissue hypoxia and inflammation.
Background and Rationale:
Cerebrovascular disease is always ranked at the top causes of death and most of hospitalized
acute stroke patients have ischemic stroke [1].
Although the mortality rate of acute ischemic stroke is less than that of hemorrhagic stroke
[1], it still results in patient disabilities and complications that often lead to
significant costs to individuals, families, and society.
Traditional treatment for acute ischemic stroke includes thrombolytic therapy by injecting
tissue plasminogen activator (t-PA) within three hours after onset of symptoms [2],
antiplatelets and/or anticoagulant agents administered within the first 48 hours. Clinically,
the narrow time window of thrombolytic therapy and coexisting contraindications limit the use
of t-PA [2]. Thus, searching for an effective supplemental treatment for acute ischemic
stroke is imperative.
Hyperbaric oxygen therapy (HBOT) is valuable in treating acute carbon monoxide poisoning
[3,4], air or gas embolism [5], facilitating wound healing [6] and has been used as an
adjuvant treatment for many neurological disorders that need further study as concussion [7]
, stroke [8,9], cerebral palsy [ 10],traumatic brain injury [ 11], cerebral air embolism
[12], Autism [13] and multiple sclerosis [14].
Indications of hyperbaric oxygen therapy recommended by undersea and hyperbaric medical
society (UHMS) [15] are 1.air or gas embolism [5], 2.carbon monoxide poisoning [3,4],
3.clostridial myositis and myonecrosis [16], 4.crush injury, compartment syndrome and other
acute traumatic ischemias [17], 5.decompression sickness [18], 6.arterial insufficiencies
[19], 7.severe anemia [20], 8.intracranial abscess [21], 9.necrotizing soft tissue infections
[22],10. refractory osteomyelitis [23], 11.delayed radiation injury [24], 12.compromised
grafts and flaps [25], 13.acute thermal burn injury [26] and 14.idiopathic sudden
sensorineural hearing loss [27].
Known mechanisms of HBOT-induced neuroprotection include enhancing neuronal viability via
increased tissue oxygen delivery to the area of diminished blood flow, reducing brain edema,
and improving metabolism after ischemia [28,29]. Furthermore, a recent study performed on a
rat suggested that upregulation of the expression of glial derived neurotrophic factor (GDNF)
and nerve growth factor (NGF) might underlie the effect of HBOT [30].
The effectiveness of use of Hyperbaric oxygen therapy in human ischemic stroke is still
controversial that need further evaluation.