Amputation below knee- how it is done?
Indication for amputation below knee
The indication for amputation includes ischemia, infarction, gangrene, severe trauma and burn. It is follow by malignancy such as osteosacroma or malignant melanoma and severe infection such as gas gangrene ( clostirdium perfringens) and necrotising fascitis and rare cause such as intractable ulcer or painful paralysed limbs.
Anatomy of the amputation
The amputation can be divided into three categories such as below knee amputation that includes two technique such as transtibial amputation that requires Buergess long saphenous posterior flap and Robinson's skew flap technique.
Another form of amputation includes ankle level amputation which is seldom perofrmed due to difficulty attaching prosthesis and midfoot amputation that involve Lisfranc's technique invovlving disarticulation betweeb tarsal and metatarsal bones or Chorpart's disarticulartion of the talonavicular and calcaenocuboid joints.
other form of below knee amputation includes Ray's amputation which requires excision of the toe by division through the metatarsal bone and toe amputation that involves division through the proximal phalanx as cutting through, a joint expose avascular cartilage that does not heal well.
Preparation before and after surgery
Pre operative preparation includes multidisciplinary assessment including surgical, anaesthetics, prosthetics specialist, physiotherapist and psychologist. Assessment of the level of amputation given severity of disease and patient factors such as rehabilitation. Insulin sliding scale if diabetic, appropriate blood tests and crossmatch blood, urinary catheterization if appropriate.
The post operative preparation includes deep vein thrombosis prophylaxis, rehabilitation with early physiotherapy, early walking aids ( pneumatic post -amputation mobility aid), prosthesis fitting.
Assess- skin flaps are marked on the skin prior to incision with a longer posterior flap ( Buergess) or skew anteromedial and posterolateral flaps.The level of tibial transaction is 14cm below knee joint or 10-12cm below tibial tuberosity.
Ligation of muscle and vessels- during skin incision the long saphenous vein is ligated and the muscles of the anterior and peroneal compartment divided by diathermy. Arteries and veins are ligated and following diathermy of accompanying vasa nervorum, the tibial nerve divided clearly under general anaesthetics.
Bone amputation - the fibula is divided by 2cm proximally following stripping of periosteum. The tibia is also stripped and divided with filling of bone ends to a smooth surface.
Closure- the posterior flap includes some gastrocnemius muscle to cover the cut tibia, forming a cylindrical stump. After hemostasis is achieved the skin is closed with interrupted sutures. A suction vacuum drains may be left in situ .
Complication from the surgery
Early complication - pain, deep vein thrombosis, flap ischemic, stump hematoma, neuroma or infection, stump length too long or short, bony spurs and psychological problems.
Late complication - 'phantom limb' pain reduced by strong analgesic, neuroma formation, erosion of bone through skin, ischemic, osteomyelitis and ulceration.
Amputations are most often carried out in those with concomitant severe atherosclerotic disease and there is major risk of other vascular problems with survival only 30% at 5 years .
above knee amputation - how it is done
Indication for amputation above knee
The indication for amputation above knee include includes ischemia ( acute or chronic ischemia), infarction, gangrene or cause by severe burns or trauma. The next indication include malignancy such as certain tumours ( osteosacroma or malignant melanoma). Severe infection such as gas gangrene ( clostridium perfringens) or necrotising fasciitis and rare cause such as intractable ulceration or painful paralysed limbs may also indicates the need for amputation.
Anatomy of the amputation.
Amputation above knee include above knee amputation at the level of 15cm above the tibial plate and through knee amputation that is indicated ( if there has been prior orthopaedic fixation of femur ) but the disadvantages is unpredictable healing of skin flaps and bulbous stump with difficult prosthesis fitting. Gritti -stokes amputation involve femur division at the supracondylar level, leaving a longer stump than above knee amputation and increase instability for the patient while sitting. other variants of above knee amputation includes disarticulation of the hip and hindquarter amputation which are rarely done and mainly performed for severe cases such as infection or malignancy.
Pre operation preparation ideally involve multidisciplinary assessment including surgical, anaesthetic, prosthetic specialist. Assessment of the level of amputation based on severity of the disease and patient factors ( e.g rehabilitation prospects). Insulin sliding scale if diabetic, blood test, cross match blood and urinary catheterization if appropriate.
Post operation involve deep vein thrombosis prophylaxis. Rehabilitation with early physiotherapy, early walking aids ( e.g pneumatic post - amputation mobility aid ) or prosthesis fitting.
Access- Two equal fish mouth - shaped skin flaps are marked on the skin, with their upper ends at the level of femur transaction. This is 15cm above the tibial plateau.
Muscle and vessel ligation- during skin incision, the long saphenous vein is ligated and the muscles of the anterior and posterior thigh compartments divided by diathermy. Vastus lateralis is sutured to the adductors and quadriceps to the hamstrings. Arteries and veins are ligated and nerves divided cleanly under gentle traction.
Bone amputation- the femur is stripped of periosteum and divided with filling of bone ends to create a smooth surface.
Closure- Once haemostatis is achieved, the two myoplastic flaps are brought together and the skin is closed with interrupted sutures. A suction vacuum drain may be left in situ.
Complication of the procedure
Early complication includes pain, deep vein thrombosis, flap ischemia, stump hematoma, neuroma or infection, stump length too long or too short, bony spurs and psychological problems.
late complication includes 'phantom limb' pain ( reduced by strong analgesic post operation ), neuroma formation, erosion of bone through skin, ischemia, osteomyelitis and ulceration. Amputations are most often carried out in those with concomitant severe atherosclerotic disease and there is a major risk of other vascular problems with survival only 30% at 5 years post - amputation.
Gout is an inflammatory arthritis that results from the deposition of urate crystals in or around the joints. Although urate crystal deposition is associated with hyperuricaemia, only one quarter of people with hyperuricaemia progress to develop symptomatic gout (the likelihood is directly related to the duration and degree of hyperuricaemia).
Gout is a disease principally of middle-aged men in developed countries. The prevalence of gout in the USA and UK is 300 per 100 000 and is increasing. Males are affected 10 times more frequently than women. The incidence in women increases after the menopause as oestrogen has a uricosuric effect.
The end product of purine nucleotide breakdown is uric acid. Seventy-five per cent of uric acid is excreted in the kidneys; the rest is lost in the faeces. Uric acid is effectively filtered at the glomerulus, however 90% is subsequently reabsorbed.
Hyperuricaemia is defined as a uric acid level greater than 0.42 mmol/L in men and 0.36 mmol/L in women, and develops as a consequence of under-excretion (80%) of uric acid by the kidney, overproduction (20%) of uric acid, or both. An elevated uric acid level is present in up to 5% of the general population at any one point during adult life and is related to age, sex, body habitus and genetic constitution. Under-excretion of uric acid accounts for by far the majority of patients with hyperuricaemia, however the reason for this is unclear.Up to 20% of affected individuals report a family history of the condition. Lesch-Nyhan syndrome is a rare X-linked genetic disorder resulting from the absence of an enzyme responsible for purine metabolism and is characterized by early-onset gout, spasticity, choreoathetosis, mental retardation and compulsive self mutilation.
Overproduction of uric acid occurs in acquired disorders leading to an excessive rate of cell, and therefore nucleic acid, turnover. These include myeloproliferative and lymphoproliferative disorders, haemolytic anaemias, Paget's disease of bone and psoriasis. Certain medications such as low-dose aspirin, diuretics and ciclosporin alter renal tubular handling of uric acid and can contribute to the development of gout. Diuretics are the main cause of hyperuricaemia but clinical gout is an uncommon association.
Acute attacks of gout occur when monosodium urate crystals are deposited in oversaturated joint tissues. Inflammation occurs as a consequence of ingestion of crystals by polymorphonuclear leukocytes with subsequent release of inflammatory mediators. In a minority of patients gouty tophi develop following multiple episodes of acute gout. Urate crystals in synovial fluid may precipitate de novo or result from rupture of preformed synovial deposits . The histopathology of the gouty tophus reveals a core of monosodium urate crystals surrounded by a chronic foreign body granuloma.
Scope of disease
An acute attack of gouty arthritis may cause significant morbidity as a result of severe pain and subsequent immobility. Tophi may cause joint destruction and neural impingement if the spine is involved.Renal impairment from unchecked hyperuricaemia may occur, however renal failure is a rare complication. Acute uric acid nephropathy is now exceedingly uncommon with hyperhydration and the prophylactic use of allopurinol prior to chemotherapy. Other renal complications include chronic urate nephropathy and uric acid stones.Uric acid calculi may develop in up to 10% of gout sufferers, especially in hotter climates. The stones may be radiolucent (uric acid alone) or radio-opaque (combined with calcium salts). Most commonly they are due to overindulgence of purine-rich foods and dehydration. Gout is also associated with several medical conditions and screening for these should be undertaken .
The most common presentation of gout is podagra, i.e. monoarthritis of the great toe (1st metatarsophalangeal joint). However, any joint may be affected-the more frequently affected areas are the feet, ankles, knees, wrists and fingers, and 1 in 10 attacks affects more than one joint.
The pain of gout is excruciating, likened to a vice being maximally twisted around the affected joint. Even the weight of the bedclothes resting on the joint may be unbearable. Without treatment, the attack settles spontaneously in 2-3 weeks. This may be the first and only manifestation of the disorder. In others, multiple attacks are followed by an intercritical phase where the paroxysms are less severe but prolonged. Subsequently chronic tophaceous gout may develop ( with tophi being deposited in any joint or bone. Most commonly these occur at the elbow (olecranon bursa), tragus of the ear and extensor surfaces of the limbs.A detailed clinical assessment includes assessment of the frequency of attacks, precipitating factors and screening for associated diseases such as hypertension, hyperlipidaemia, ischaemic heart disease and diabetes.Fever may develop during an attack, mimicking sepsis, and appropriate investigations are mandatory to exclude the possibility of septic arthritis.
Precipitants of acute gout include joint injury/trauma excessive physical exercise alcohol diet rich in purine nucleotides starvation Surgery Medications: diuretics, initiation of uricosuric agents or allopurinol . Differential diagnosis of gout include acute arthritis septic arthritis other crystalline arthritis, traumatic arthritis rheumatoid arthritis seronegative spondylarthritis,chronic arthritis nodular rheumatoid arthritis osteoarthritis with Heberden's and Bouchard's nodes and Xanthomatosis
Full blood count, markers of inflammation, A leukocytosis with raised inflammatory markers (CRP, ESR) frequently develops.
Serum uric acid levels. The blood uric acid level may be raised, normal or even low in an acute attack and cannot be relied upon to help diagnostically. The greater the hyperuricaemia, however, the more likely gout is to develop.
Many cases of gout are presumed due to the classic presentation of podagra, however a definitive diagnosis can only be made by demonstrating gouty crystals in joint aspirates. The uric acid crystals are needle-like when viewed under polarized light microscopy and are strongly negatively birefringent (yellow when aligned with the compensator and blue when perpendicular to the polarizer.
As gout is associated with other medical conditions, screening for these is appropriate with blood glucose level, lipid profile and blood pressure estimation.
X-ray of the joints
Radiography is helpful in chronic cases as the changes of gouty arthropathy are characteristic with 'punched-out' erosions having sclerotic margins and overhanging edges
Non-steroidal anti-inflammatory agents
An acute attack of gout is best treated with NSAIDs. Traditionally indometacin (50 mg 4-hourly until the attack resolves) has been the treatment of choice, however any NSAID may be used. A course should last for 1-2 weeks in full therapeutic doses.
If NSAIDs are contraindicated, colchicine is appropriate starting at 0.5 mg 6-hourly followed by dose reduction depending upon response. The use of this medication is limited by its side effect profile. Diarrhoea, which may be explosive, is the most untoward effect; however, this settles upon withdrawal of the drug.
Diet and patient education
Long-term therapy is aimed at reducing hyperuricaemia by decreasing the intake of purine-rich foods . A high fluid intake is recommended for patients who develop uric acid stones. Foods need to be avoided includes beef, liver, kidney, sweetbreads, meat extracts, gravy, seafood ( Crustaceans), vegetables such as peas, beans, spinach, lentils, alfalfa, citrus fruits, tomatoes, beer and beer products.
Other treatments include oral corticosteroids or intramuscular or intra-articular corticosteroid injections.
Preventative treatment with allopurinol is reserved for patients who have multiple attacks of gout (more than3 per year), for those with tophi and those with renal impairment.
Allopurinol inhibits the enzyme xanthine oxidase, the final enzyme required for the production of uric acid, andis extremely effective at preventing attacks. Successful lowering of plasma urate abolishes the risk of gout and tophi will eventually disappear. The aim is to lower the uric acid as far as possible. Allopurinol is not given in the acute setting as it may precipitate or prolong an attack. It is commenced several weeks following an acute episode concurrently with an NSAID or colchicine for 3 months and then continued indefinitely.
Sulfinpyrazone and probenecid act by blocking renal tubular transport of uric acid, allowing the filtered load to be excreted. They are not as effective as allopurinol and do not help in patients with renal failure. They are rarely used these days.
Treatment of underlying condition The treatment of associated and any underlying conditions that would predispose to hyperuricaemia is an important aspect in the management of patients with gout. Obese patients should lose weight, alcohol should be reduced and the need for diuretics be reconsidered.
Etoricoxib, a COX-2 inhibitor, has been found to have comparable efficacy to indometacin in the treatment of acute gouty arthritis and is generally safe and well tolerated
With effective treatment the prognosis is excellent and recurrences are limited. Complications such as urate calculi are rare. The main cause of mortality in patients with gout is associated disease such as hypertension, ischaemic heart disease and diabetes.
What is obesity and how to manage it ?
This article describes the worldwide obesity epidemic, including the definition of obesity, its prevalence and health consequences, and the policies and guidelines available for obesity management.
Obesity has become a worldwide epidemic, estimated to affect approximately 300 million individuals across the globe (Blackburn et al., 2009).Indeed, obesity, which is the clinical term used to describe excess body fat, is now classified as a chronic condition.The most frequently utilised measure of obesity is the objective measure of Body Mass Index (BMI), which is measured by dividing an individual’s weight by the square of their height.In adults, a BMI of 25-29.9kg/m2 is considered overweight whilst a BMI of >30kg/m2 is considered obese.
In the UK, the prevalence of overweight and obesity in adults has been increasing over the past 30-years (DH, 2002; NHS Information Centre, 2009a). Between 1993 and 2008, a total of 37% of individuals aged 16-years and over were overweight and 25% obese (NHS Information Centre, 2009b). A ‘Foresight report’ conducted by Sheffield Hallam University indicates that if obesity continues to rise, as many as 36% of men and 28% of women will be obese by 2015 (Aylott, Brown, Copeland, & Johnson, 2008).This could increase further to 60% in men and 50% in women, respectively, by 2050.This increase has dire consequences for individual health and well-being.In addition, the societal costs of obesity continue to raise concern.The most recent figures show the total cost of obesity in the UK to be £7 billion annually (Aylott, et al., 2008).This is likely to rise to £50 billion by 2050.
Obesity is associated with an increased risk of chronic disease and comorbidity, including diabetes, hypertension, coronary artery disease, stroke, and various cancers (Kopelman, 2007).In particular, diabetes is likely to increase as obesity prevalence increases; 90% of individuals with type 2 diabetes are reported to be overweight or obese.There is a 20-80 times increased risk of developing type 2 diabetes for individuals who are obese compared with non-obese individuals (McPherson et al., 2007).Obesity is also associated with the four most prevalent disabling conditions in the UK, namely arthritis, mental illness, learning disabilities, and back problems (Ellis et al., 2006). The likelihood of having a disability is greater among obese individuals compared to individuals of healthy weight.Indeed, it has been found that individuals who are obese are twice as likely to develop a physical disability.They have an 84% increased risk of developing musculoskeletal conditions such as joint or muscle pain, a 35% increased risk of back problems, and four times the risk of developing arthritis (Ellis et al., 2006).
The key independent predictors of obesity have been found to be older age, smoking status, self-reported unhealthy diet, lack of physical activity, and hypertension (NHS Information Centre, 2009).Income and alcohol consumption have also been found to play a role in obesity.Obesity is thus primarily a condition of lifestyle that is preventable.Indeed, lifestyle interventions are the first course of action in tackling obesity.Despite body weight being influenced by genetic and environmental factors, research shows that an individual’s lifestyle significantly influences whether or not they are able to maintain a healthy weight (Aylott, et al., 2008). The World Health Organisation (WHO) state that “there is convincing evidence that a high intake of energy dense foods promotes weight gain” (p. 101) and that “Energy expenditure through physical activity is an important part of the energy balance equation that determines body weight” (p.16).Indeed, the evidence suggests that an individual needs to manage their ‘energy balance’ to maintain a healthy weight so that energy intake (calories from food) does not exceed energy output (calories burned through physical activity) (NICE, 2006).Lifestyle advice for managing weight includes a high intake of dietary fibre and a total of at least 30-minutes daily moderate intensity physical activity on five or more days of the week (WHO, 2003; DH, 2004).
The National Institute of Clinical Excellence (NICE, 2006) have recommended that pharmacological treatments for obesity are only considered if changes to lifestyle have been unsuccessful. Orlistat or Sibutramine are the two most widely prescribed pharmacological treatments for both weight loss and weight maintenance, although continued lifestyle advice and support alongside the drugs is emphasised (NICE, 2006).As an example, it has been advised that Orlistat is only prescribed to adults with a BMI of >28.0kg/m2 or additional risk factors or to adults with a BMI of >30.0 kg/m2.
When lifestyle interventions and pharmacological treatments fail, bariatric surgery is recommended for reducing the risk of obesity-related comorbidities (Adams et al., 2007; Sjostrom et al., 2007).Indeed, recommendations have been made that the Government should make efforts to increase the availability of bariatric surgery for individuals who are morbidly (CREST, 2005).The two main types of bariatric surgery are restrictive surgeries and malabsorptive surgeries.The former includes gastric banding, a restrictive operation that creates a small neogastric pouch to decrease quantity of food intake.The latter includes gastric bypass, where malabsorptive procedures are carried out to rearrange the small intestine in order to decrease the nutrient absorption efficiency of the intestine.In general, restrictive surgery is considered easier and safer, although is likely to lead to less long-term weight loss (Blackburn & Jones, 2006). Furthermore, mortality and serious medical complications have been reported as a result of surgery (Livingston & Langert, 2006). Individuals who receive bariatric surgery require nutritional supplements and medical monitoring for the rest of their lives, which is why it is usually only provided to individuals with a BMI of >40kg/m2 (Fobi, 2004).
The Government has made obesity a priority for intervention, with particular efforts being made to educate people regarding their lifestyle choices.In particular, the ‘White Paper, Healthy Lives, Healthy People: Our strategy for public health in England’ details plans for how the Government will improve public health and tackle the causes of premature mortality and illness, including obesity (DH, 2010). In addition, clinical guidelines have been developed to facilitate the prevention and management of obesity in both adults and children (NICE, 2006). Nevertheless, the battle against the obesity epidemic will be dependent on whether these policies and guidelines are effectively implemented (Poobalan, Aucott, Ahmed, Cairns, & Smith, 2010).
Alopecia (hair loss) - The reasons behind it
Alopecia ( hair loss)- INTRODUCTION
Alopecia is a term that is used to describe the condition of absence of hair in the region where it normally presents.A term such as anagen hairs indicates the condition where the hair is growing while telogen is a description that the hair is dead or resting.
Telogen effluvium which means diffuse pattern of hair that is loss which results in temporary hair loss without causing any further baldness.
Anagen effluvium means a diffuse pattern of hair that is shedding which wills sooner or later leads to complete baldness
Cicatrial alopecia means a condition where the scalp appears to be smooth with no evidence of any follicular opening on the hair. Famous term include scarring alopecia.
Androgenic alopecia is a pattern of hair loss that affects both sexes and most commonly men at the age of 50 years old as a result of hormone stimulation of the hair root.
Alopecia areata is a condition where the pattern of hair loss is patchy and no evidence of scarring is detected.
Traction alopecia most commonly present due to pulling of the hair which leads to a patchy hair loss and it can also be related to trichotilliomania which is a habit of pulling hair
Tinea capitis is caused by fungal infection that leads to a patchy hair loss or broken hair and may or may not associate with any irritation or inflammation. It can be associated with many children.
Post pregnancy individual may also suffer from alopecia as a result of alteration of the body hormone and physiological factors.
Alopecia (hair loss) –EPIDEMIOLOGY
Alopecia (hair loss) is always associated with age and sex where it is more common in male compare to female and increasingly with age (Androgenic alopecia) as well as children ( tinea capitis ). Statistical facts shows that around 50 % of Caucasian male at 50 years of age will suffer from male pattern of baldness while 37% post menopausal women may also suffer from alopecia.
Alopecia (hair loss) – RISK FACTORS
Among the risk factors for alopecia include positive family history, someone who is pregnant or post pregnancy as well as poor source of nutrition and someone who has to face further physical or mental stress. Genetically it is associated with autosomal dominant condition
Alopecia (hair loss) – CAUSES/ETIOLOGIES
Telogen effluvium or diffuse pattern of hair that is loss which result in temporary hair loss without causing any further baldness is caused by several factors such as malnutrition due to lack of iron and zinc , pregnant women or suffer from thyroid problems hyper ( overactive ) or hypo ( under active ) thyroid, any stress, tension or pressure either mentally or physically , any drugs such as ‘blood thinning medicine’ anti coagulation, vitamin A retinoid, blood pressure medication ( beta blockers),immunosuppressant, biology agent or chemotherapeutic agent ( interferon ) .
Anagen effluvium means a diffuse pattern of hair that is shedding which wills sooner or later leads to complete baldness causes by any x ray treatment, or any medication such as levedopa for Parkinson disease, anti –cancer medication such as chemotherapeutic agent ( bromocriptine)for pituitary tumour or suffers from poison attack such as arsenic , bismuth ,thallium)and finally mycosis fungoides.
Cicatricial alopecia means a condition where the scalp appears to be smooth with no evidence of any follicular opening on the hair. Famous term include scarring alopecia is caused by any defect during birth (congenital defect) or developmental defect. Besides that, leprosy or cutaneous leishmaniasis as well as viral infection such as varicella zoster virus may also contribute. Any physical insults such acid or alkali burns or exposure to high temperature or freezing may also leads to this condition. Other conditions such as connective tissue disorder that include sarcodosis or lupus (discoid lupus) or lichen planus and cancer such as basal cell carcinoma may leads to cicatricial alopecia.
Androgenic alopecia which is a pattern of hair loss that affects both sexes and most commonly men at the age of 50 years old as a result of hormone stimulation of the hair root is caused by hormonal disorder such as adrenal, pituitary as well as ovarian hyperplasia and present of cyst on the ovary ( polycystic ovarian syndrome) , carcinoid syndrome and any chemical , drugs or hormone such as progesterone, testosterone, and steroids.
Alopecia areata is a condition where the pattern of hair loss is patchy and no evidence of scarring is detected not reasonable and concrete cause is detected and mostly due to autoimmune causes or Down syndrome, diabetes or vitilgo. Traction alopecia most commonly present due to pulling of the hair which leads to a patchy hair loss is either caused by tight hand band or habit of pulling hairs.
Tinea capitis or fungal infection which is more common in children is caused by (Trichophyton sp.) and ( Microsporum sp.) fungals.
Any of the difficulties going through individuals who're seeking to successfully take care of acne disorder would be the persistent resources involving untrue stories available on the market in relation to the actual causes of acne.Regardless of the varied logical sources of information on the subject of acne together with treatment of acne that happen to be now available,these types of misguided beliefs continue to persist and are passed by simply word-of-mouth to people unfortunate enough to suffer from the illness.Rather then finding methods along with cures to cure all the problems, troubles are typically compounded. Ill-advised cures centred from such lies can result in less than successful final results and definately will actually do further harm in the case of severe acne.
Considering the particular influencethat these false facts may have on both understanding acne break-out and, the regimes of treatment particularly, it might be advisable to get started on with the help of an instant brief summary of some of more established common misguided beliefs which are available on the market, mixing all of the untruths with the truths.
False fact no 1:Acne is caused by poor hygiene
It doesn’t make a difference exactly how many times, how religiously, individuals wash their own facial skin and other parts suffering with acne; it has certainly no effect on both the states of the acne or pimple or even the formation of new acne. In truth, this sort of thorough routines involving cleaning in addition to rubbing can actually inflame skin and also worsen the acne, definitely not better. Even though you have been acknowledge by your mum or dad, growing up or many others that an acne breakout is without a doubt not induced by very poor hygiene. This approach doesn’t imply that good hygiene isn’t critical. The fact is, fine cleanliness will cut down the issues of an acne breakout if used in conjunction with acne breakouts treatment products and services. Instead of numerous, strong cleansing, it’s highly recommended that you really clean the face double to three times a day together with gentle soap and after that keep it dry with towel.
False fact no 2 : Eating habit may cause acne
Many state that enjoying fried meals can provide you with an acne breakout.The majority of you've heard a lot of these and various very similar claims right before, correct? What they're explaining, essentially, is the fact that the foods you eat can lead to acne. Nevertheless, what they'reclaiming isn’t true. It is actually a fabrication. Detailed medical studies have been performed, trying to find possible correlations concerning one’s eating routine and a probable trigger of bad acne, and no positive finding is found
Nevertheless,everyone is not the same. Many people discover that breakouts usually area whole lot worse after consumingselected foods--and the types of food can vary with everybody. For example, a lot of people could very well see acne outbreaks after consuming delicious chocolate; while other people not have any effect with dark chocolate. Alternatively, some people notice pimples occurring after they drink a lot coffee or caffeine. If there is some sort of meals or drinks that you will find affecting your acne breakouts, next cut back and see if that helps.
False fact no 3: acne is cause by stress
Pressure is not a direct root cause of pimples however it's factual that some kinds of strain causes the human body to make a hormone referred to as cortisol, which can irritate already present acne. Not directly, many prescription medications that individuals choose to use relieve and also control excessive pressure or emotional concerns such as sadness can be associated in the production of zits. The truth is, a number of drugs have acne breakouts stated just as one of the side-effect.
False fact no 4: Acne goes away over time
This can be totally untrue plus zits or acne must have treatment solution in order to be cleared up. Considering the selection of reliable acne treatment products and services you can get you cannot find any cause not to ever check out and find what the best result is. Sometimes, a dermatologist has to be contacted as well as other treatment options are often sought
False fact no 5: Tanning removes away acne
The truth is, this has the opposite result. First it may look like that newest tanned in a tanning or sunbathing considerably improved your personal tone, but in fact the tanned and suntanned may very well have disguised or perhaps covered all of the break-outs. The simple truth is, the sun's rays can certainly make your skin layer dry looking as well as inflamed and this can cause additional acne outbreaks. Consequently, if you decided to tan your skin, just remember to choose a real sun screen lotion that doesn’t contain oils and also other products that may clog up your skin pores and also induce zits, pimple or acne to become more painful.
False fact no 6: Popping acne is Likely To Make Them Go Away Faster
Yet again, even though this would seem to be valid, it is actually yet another myth. In preference to increase the whole process of curing, this process definitely prolongs the outcome just as popping the particular whitehead made the acne bacteria’s living inside the skin to end up being pushed deeper directly into the skin area, enabling more irritation to cultivate, and even at some point will cause further skin damage and scar tissue development.
False fact no 7: Only Young adults get acne pimples.
The truth is that around 25% to 30% of most people today in between the age ranges 25- 44 have got lively acne breakout. Therefore the reality that pimples are only a complication with regards to adolescents is another myth.
After dealing with most of these misguided beliefs, it is very important to pay attention to, these problem as it is easy for people to be misguided by the information they read , listen or heard.
Pulsatile mass above umbilicus- abdominal aortic aneurysm
Abdominal aortic aneurysm is a permanent localised dilation of the abdominal aorta and greater than 3cm. 95% of abdominal aortic aneurysm are due to atherosclerosis.Other aetiologies are inflammatory ( variant of atherosclerosis aneurysm ),...
Abdominal aortic aneurysm
Abdominal aortic aneurysm is a permanent localised dilation of the abdominal aorta and greater than 3cm.
Causes of abdominal aortic aneurysm
95% of abdominal aortic aneurysm are due to atherosclerosis.Other aetiologies are inflammatory ( variant of atherosclerosis aneurysm ), traumatic, infective ( mycotic ), and connective tissue disorder, Marfan's syndrome and Ehler- Danlos type IV.
Risk factors for abdominal aortic aneurysm
Risk factors for abdominal aortic aneurysm includes hypertension, smoking and family history.
Presenting complaints for abdominal aortic aneurysm
The majority of patients are asymptomatic, may be found incidentally.Symptoms may be related to vertebral body erosion, distal embolization, thrombosis and rupture).
In emergency setting the patient may present with epigastric or back pain ranging form vague discomfort to excruciating pain or collapse associated with leakage or rupture. Rarely, present with gastrointestinal bleeding due to erosion into the duodenum or high output cardiac failure due to aortocaval fistula.
Examination finding on abdominal aortic aneurysm
A pulsatile mass is felt above the umbilicus. If leaking or rupture, abdominal and back tenderness with pallor, tachycardia, hypotension and hypovolaemic shock.
Pathology of abdominal aortic aneurysm
Atherosclerosis leads to thinning of the media, loss of smooth muscle cells and elastic fibres with progressive replacement of non contractile ineastic collagen leading to generalized dliation of the vessel.Most commonly involve the infrarenal aorta with iliac involvement in 30% of cases.Risk of rupture is related to diameter. e.g > 5.5 cm risk 10-15% per year, if 7cm risk is > 75%. Patients with rupture surviving until arrival in hospital usually have a leak tamponated within the retroperitoneum .
The investigation requires include blood test such as full blood count, urea and electrolyte studies, clotting studies, cross match blood in acute presentation.
Imaging CT scan or ultrasound useful to confirm the presence and size of the aneurysm
Arteriography or MRA may b necessary to measure involvement of the renal arteries prior to treatment.
Management of abdominal aortic aneurysm
The management includes conservative, radiological and surgical. The conservative management includes followed up with regular ultrasound and treatment for cardiovascular risk factors. This is most commonly done with small asymptomatic aneurysm ( < 5.5 cm )
The radiological treatment includes endovascular treatment by stent placement while the surgical approach includes insertion of tube or bifurcation grafts.
Complication of abdominal aortic aneurysm
From disease includes rupture ( most frequent ) , distal embolization, sudden complete thrombosis, infection ( gram negative organisms or staphylococci ) renal failure, gut ischemic, aortic intestinal fistula , arteriovenous fistula from aneurysm eroding into the inferior vena cava.
From surgery includes haemorrhage, embolism, graft thrombosis and graft infection,
Risk of rupture related to sizes of aneurysm.< 50% of patients with a ruptured abdominal aortic aneurysm reach hospital alive and only about 50% of these survive.( overall 80% mortality) .
Elective surgery however have a mortality of < 5% with a 5 year survival of 72%.
What is varicose vein?
Varicose vein is a vein that have become prominently elongated, dilated and tortuous which is moat commonly affecting the superficial vein of the lower limbs. Thread veins also known as spider veins or reticular veins refer to superficial venous telangiectasia and varicosities.
What cause varicose vein?
The cause of varicose veins can be divided into 2 categories such as primary cause that includes a genetic or developmental weakness in the vein wall resulting in reduction in elasticity, dilation over time and valvular incompetence.
The secondary cause are due to pregnancy, pelvic malignancy, ovarian cyst, ascites, lymphadenopathy, retroperitoneal fibrosis.It is also cause after deep vein thrombosis or any arteriovenous fistula.
What is it is associated with ?
Varicose vein is associated with increasing age, family history and certain race ( caucasian ) and obesity .
How common is it ?
Varicose vein is common with increasing age with prevalence 10%-15% adult men and 20%-25% adult women .
How does it present?
Patient with varicose veins may complain of cosmetic appearance or experience symptom such as aching in the legs, worse towards the end of the day or after standing for long period and also present with swelling, itching, or complication such as bleeding, infection or ulceration
How to detect the condition?
The investigation done for varicose vein include duplex ultrasound to locate the sites of incompetence or reflux. Also to exclude deep vein thrombosis.
How to manage this condition?
The management of this condition includes conservative treatment that includes advice on exercise ( to improve the calf muscle pump) and elevation of the leg at rest . Class II support stockings also can be protective.
In the case of venous telangiectasia and reticular veins microinjection or laser therapy can be applied.
The next step is the surgical approach where the veins are marked with the patient in the standing position prior to operation. Stripping of the long saphenous veins to the knee and avulsion of varicosities via small stab incision is performed. However the short saphenous vein is not stripped , just ligated to avoid potential damage to nearby leg. Post operative, the legs are bandaged and early mobilization encouraged. Subfascial endoscopic perforator surgery is a more recent development involving ligation of incompetent perforating veins using an endoscopic technique.
What is the complication?
Varicose vein has its own complication that include venous pigmentation, eczema, lipodermatosclerosis and venous ulceration.
Treatment with sclerotherapy also has its own complication such as skin staining, local scarring. Treatment with surgery also has its own effect such as hemorrhage, infection, recurrence of varicose vein, loss of sensation and injury to the nerve.
What is the prognosis?
In general the condition is slowly progressive and the recurrence rates post surgery can be up to 40 %