Mga Pahina

BULLYING: THE MAJOR PROBLEM OF THE WORLD


WHAT IS BULLYING?
Bullying is a pattern of aggressive behaviour meant to hurt or cause discomfort to another person. Bullies always have more power than victims. Their power comes from physical size, strength, status, and support within the peer group.
There are three types of bullying:
  1. Physical: a person is harmed or their property damaged
    Some examples are:
    • slapping, hitting, pinching, punching, kicking
    • locking in a confined space
    • unwelcome touching
    • extortion
  2. Verbal: a person’s feelings are hurt through insults and name-calling
    Some examples are:
    • name-calling
    • unwelcome teasing
    • taunting
    • spreading rumours, gossiping
    • racist or homophobic comments
  3. Social: a person is shunned or excluded from groups and events.
    Some examples are:
    • excluding from a group
    • threatening or insulting graffiti
    • threatening notes, letters, emails, telephone calls
    • threatening words, actions or weapons
Bullying may be obvious or hidden. Children who are being bullied...or are bullying others may:
  • complain of being poorly treated
  • change their behaviour (for example, sleeplessness, loss of appetite, angry outbursts, being sick in the morning, become more aggressive towards siblings)
  • be unwilling to leave the house, change their route to school, or skip school
  • come home with torn clothes, unexplained bruises, new clothes or other items, or money not accounted for
  • talk about responding to others in a way that may result in the school taking disciplinary action
  • start doing poorly in school
The terms harassment and intimidation are sometimes used when referring to bullying situations involving junior and senior high students.
Harassment is any behaviour or comment that is hurtful, degrading, humiliating or offensive to another person.
Intimidation is the act of causing fear in order to force or influence someone to do, or not to do, something.
Some examples of harassment and intimidation:
  • name-calling
  • unwelcome teasing
  • locking in a confined space
  • racist or homophobic slurs
  • unwelcome touching
  • threatening notes, letters, e-mails
  • threatening words, actions or weapons
  • taunting
  • excluding from a group
  • spreading rumours
  • threatening or insulting graffiti
  • stalking
  • extortion

SERIOUS MENTAL DISORDER

Finnish researchers have recently discovered that bullying could result in serious mental disorders — mainly an anxietydisorder or antisocial personalitydisorder — among both the bullies and those being bullied.

While victims of bullying were more likely to develop anxiety disorders, the bullies themselves were at higher risk to developantisocial personality disorder. Those who have both been bullies and bullied tended to develop both anxiety and antisocial personality disorders, the researchers found. The study was published in the journal Pediatrics.

Bullying was defined in the study as an aggressive act that can be physical, verbal, or indirect, with an imbalance of power in which the victim cannot defend him or herself. In the study, the bullying behavior also had to be repetitive.

Andre Sourander, the lead researcher, noted that information about the long-term effects of bullying had considerable public health significance that would justify universal or targeted preventive interventions and research directed at school bullying.

The Finnish researchers examined 2,540 boys born in 1981. At the age of 8 years, these boys were asked whether and how often they bullied other children, were targets of bullying, or both. Parents and teachers also answered questions about bullying or victimization. This information was then compared with psychiatric diagnoses in young adulthood, made during medical exams for compulsory military service and army registry at 18 to 23 years of age.

Bullying and victimization are both associated with poor family functioning, parental violence, subsequent conduct and personality disorders, and increased criminality.

Boys in the study who were both bullies and victims were at five-times increased risk for a psychiatric disorder than those who were neither a bully nor a victim.

The study concluded that combined bullying and victimization posed the greatest risk for psychiatric morbidity followed by bullying and victimization.

“Both bullying and victimization during early school years are public health signs that identify boys who are at risk of suffering psychiatric disorders in early adulthood,” the researchers wrote. “The school health and educational system has a central role to play in detecting these boys at risk.”

Researchers recommended increased efforts at targeted mental health screening to identify bullies, victims, and combined bullies and victims.

In a US survey, 17% of children in grades 6 to 10 reported being bullied, 19% being bullies, and 6% being both bullies and victims.

THE CAUSE OF BULLYING


The serial bully
How to spot signs and symptoms of serial bullies, sociopaths and psychopaths
including the sociopathic behaviour of the industrial psychopath and the corporate psychopath

Types of serial bully: The Attention-Seeker, The Wannabe, The Guru and The Sociopath

"All cruelty springs from weakness."

"Most organisations have a serial bully. It never ceases to amaze me how one person's divisive, disordered, dysfunctional behaviour can permeate the entire organisation like a cancer."
Tim Field

"The truth is incontrovertible; malice may attack it, ignorance my deride it, but in the end, there it is."
Winston Churchill

"Lack of knowledge of, or unwillingness to recognise, or outright denial of the existence of the serial bully is the most common reason for an unsatisfactory outcome of a bullying case for both the employee and employer"
Tim Field

I estimate one person in thirty, male or female, is a serial bully. Who does the following profile describe in your life?

The serial bully:

is a convincing, practised liar and when called to account, will make up anything spontaneously to fit their needs at that moment has a Jekyll and Hyde nature - is vile, vicious and vindictive in private, but innocent and charming in front of witnesses; no-one can (or wants to) believe this individual has a vindictive nature - only the current target of the serial bully's aggression sees both sides; whilst the Jekyll side is described as "charming" and convincing enough to deceive personnel, management and a tribunal, the Hyde side is frequently described as "evil"; Hyde is the real person, Jekyll is an act excels at deception and should never be underestimated in their capacity to deceive uses excessive charm and is always plausible and convincing when peers, superiors or others are present (charm can be used to deceive as well as to cover for lack of empathy) is glib, shallow and superficial with plenty of fine words and lots of form - but there's no substance
is possessed of an exceptional verbal facility and will outmanoeuvre most people in verbal interaction, especially at times of conflict is often described as smooth, slippery, slimy, ingratiating, fawning, toadying, obsequious, sycophantic relies on mimicry, repetition and regurgitation to convince others that he or she is both a "normal" human being and a tough dynamic manager, as in extolling the virtues of the latest management fads and pouring forth the accompanying jargon is unusually skilled in being able to anticipate what people want to hear and then saying it plausibly cannot be trusted or relied upon fails to fulfil commitments is emotionally retarded with an arrested level of emotional development; whilst language and intellect may appear to be that of an adult, the bully displays the emotional age of a five-year-old
is emotionally immature and emotionally untrustworthy  exhibits unusual and inappropriate attitudes to sexual matters, sexual behaviour and bodily functions; underneath the charming exterior there are often suspicions or hints of sex discrimination and sexual harassment, perhaps also sexual dysfunction, sexual inadequacy, sexual perversion, sexual violence or sexual abuse in a relationship, is incapable of initiating or sustaining intimacy holds deep prejudices (eg against the opposite gender, people of a different sexual orientation, other cultures and religious beliefs, foreigners, etc - prejudiced people are unvaryingly unimaginative) but goes to great lengths to keep this prejudicial aspect of their personality secret is self-opinionated and displays arrogance, audacity, a superior sense of entitlement and sense of invulnerability and untouchability
has a deep-seated contempt of clients in contrast to his or her professed compassion is a control freak and has a compulsive need to control everyone and everything you say, do, think and believe; for example, will launch an immediate personal attack attempting to restrict what you are permitted to say if you start talking knowledgeably about psychopathic personality or antisocial personality disorder in their presence - but aggressively maintains the right to talk (usually unknowledgeably) about anything they choose; serial bullies despise anyone who enables others to see through their deception and their mask of sanity displays a compulsive need to criticise whilst simultaneously refusing to value, praise and acknowledge others, their achievements, or their existence shows a lack of joined-up thinking with conversation that doesn't flow and arguments that don't hold water flits from topic to topic so that you come away feeling you've never had a proper conversation refuses to be specific and never gives a straight answer is evasive and has a Houdini-like ability to escape accountability undermines and destroys anyone who the bully perceives to be an adversary, a potential threat, or who can see through the bully's mask is adept at creating conflict between those who would otherwise collate incriminating information about them is quick to discredit and neutralise anyone who can talk knowledgeably about antisocial or sociopathic behaviors may pursue a vindictive vendetta against anyone who dares to held them accountable, perhaps using others' resources and contemptuous of the damage caused to other people and organisations in pursuance of the vendetta
is also quick to belittle, undermine, denigrate and discredit anyone who calls, attempts to call, or might call the bully to account gains gratification from denying people what they are entitled to is highly manipulative, especially of people's perceptions and emotions (eg guilt) poisons peoples' minds by manipulating their perceptions when called upon to share or address the needs and concerns of others, responds with impatience, irritability and aggression is arrogant, haughty, high-handed, and a know-all often has an overwhelming, unhealthy and narcissistic attention-seeking need to portray themselves as a wonderful, kind, caring and compassionate person, in contrast to their behaviour and treatment of others; the bully sees nothing wrong with their behavior and chooses to remain oblivious to the discrepancy between how they like to be seen and how they are seen by others

  • is spiritually dead although may loudly profess some religious belief or affiliation
  • is mean-spirited, officious, and often unbelievably petty
  • is mean, stingy, and financially untrustworthy
  • is greedy, selfish, a parasite and an emotional vampire
  • is always a taker and never a giver
  • is convinced of their superiority and has an overbearing belief in their qualities of leadership but cannot distinguish between leadership (maturity, decisiveness, assertiveness, co-operation, trust, integrity) and bullying (immaturity, impulsiveness, aggression, manipulation, distrust, deceitfulness) often fraudulently claims qualifications, experience, titles, entitlements or affiliations which are ambiguous, misleading, or bogus often misses the semantic meaning of language, misinterprets what is said, sometimes wrongly thinking that comments of a satirical, ironic or general negative nature apply to him or herself knows the words but not the song is constantly imposing on others a false reality made up of distortion and fabrication sometimes displays a seemingly limitless demonic energy especially when engaged in attention-seeking activities or evasion of accountability and is often a committeeaholic or apparent workaholic


Responsibility

The serial bully appears to lack insight into his or her behaviour and seems to be oblivious to the crassness and inappropriateness thereof; however, it is more likely that the bully knows what they are doing but elects to switch off the moral and ethical considerations by which normal people are bound. If the bully knows what they are doing, they are responsible for their behaviour and thus liable for its consequences to other people. If the bully doesn't know what they are doing, they should be suspended from duty on the grounds of diminished responsibility and the provisions of the Mental Health Act should apply.

CHRONIC BACK PAIN: CAUSES AND EFFECTS


What are the causes of Back Pains?

Back pain is most commonly felt as soreness, tension or stiffness in the lower back (the area between the bottom of the ribs and the top of the legs) but it can also be felt in the neck, shoulders, buttocks and thighs.
The pain sometimes develops suddenly after lifting something heavy or twisting your back awkwardly, or it can develop gradually as a result of years of poor posture.

Sometimes the pain develops for no apparent reason. Some people just wake up one day with a sore back. Typically, the pain eases when you lie down flat, whereas moving, coughing or sneezing makes it worse.



When to get medical help

Most cases of back pain usually improve without you having to get medical help, but if your condition does not get any better within three days see your GP. You should also see your GP if you suffer regular episodes of back pain for more than six weeks.

There are several warning signs, known as red flag signs, that may indicate that your back pain is caused by a more serious condition that requires immediate medical help. These include:
  • unexplained weight loss
  • a fever of 38ºC (100.4ºF) or above
  • swelling of the back
  • constant back pain that does not ease after lying down
  • pain in your chest or high up in your back
  • pain down your legs and below the knees
  • pain caused by a recent trauma or injury to your back
  • loss of bladder control
  • inability to pass urine
  • loss of bowel control
  • numbness around your genitals, buttocks or back passage
  • pain that is worse at night

Other types of back pain

Pain in the upper back, legs, neck and shoulders can also be felt as back pain but it may be caused by another condition:

  • pain in the lower back that moves down the buttocks into one or both of the legs may be a symptom of sciatica
  • soreness in the lower back, muscle weakness, tight muscles and loss of bladder control may be the result of a slipped disc
  • back pain, buttock pain, swollen joints and tendons and extreme tiredness are common symptoms of ankylosing spondylitis
  • pain in the joints (including the back) when walking and stiffness first thing in the morning are symptoms of arthritis
  • painful stiffness of the shoulder, which makes it very difficult to dress, drive or sleep, may be a sign of frozen shoulder
  • neck pain and stiffness, headaches and lower back pain following an accident are common symptoms of whiplash
Almost everyone has back pain at some point in their lives. According to the National Institutes of Health, back pain is the second most common neurological disorder in the United States -- only headache is more common.

If you have back pain, the first step is to be properly assessed by your primary care provider. Back pain has many causes, from muscle strain to more serious conditions such as a herniated disc, spinal stenosis, spondylosisthesis, osteoporosis, or a tumor, so it's important to find out what is causing the back pain.

1) Acupuncture

A study conducted at Sheffield University in the United Kingdom looked at the long-term symptom reduction and economic benefits of acupuncture for persistent low back pain. An average of 8 acupuncture treatments were given to 159 people, while 80 people received usual care instead.

After one year, people receiving acupuncture had reduced pain and reported a significant reduction in worry about their pain compared to the usual care group. After two years, the acupuncture group was significantly more likely to report that the past year had been pain-free. They were less likely to use medication for pain relief.

How does acupuncture work? According to traditional Chinese medicine, pain results from blocked energy along energy pathways of the body, which are unblocked when acupuncture needles are inserted along these invisible pathways.

A scientific explanation is that acupuncture releases natural pain-relieving opioids, sends signals that calm the sympathetic nervous system, and releases neurochemicals and hormones.

An acupuncture treatment generally costs between $60 and $120. Acupuncture is tax-deductible (it's considered a medical expense) and some insurance plans pay for acupuncture.

If you want to try acupuncture, plan on going one to three times a week for several weeks initially.

2) Capsaicin Cream

Although you may not have heard of capsaicin (pronounced cap-SAY-sin) before, if you've ever eaten a chili pepper and felt your mouth burn, you know exactly what capsaicin does. Capsaicin is the active ingredient in chili peppers.

When it is applied to the skin, capsaicin has been found to deplete substance P--a neurochemical that transmits pain--causing an analgesic effect.

In one double-blind study, 160 people were treated with capsaicin for 3 weeks, while another 160 people used a placebo. After 3 weeks, pain was reduced by 42% in the capsaicin group compared to 31% in the placebo group. Investigators rated capsaicin significantly more effective than placebo.

Capsaicin cream, also called capsicum cream, is available in drug stores, health food stores, and online. A typical dosage is 0.025% capsaicin cream applied four times a day. The most common side effect is a stinging or burning sensation in the area.

If possible, wear disposable gloves (available at drugstores) before applying the cream. Be careful not to touch the eye area or open skin. A tube or jar of capsaicin cream typically costs between $8 and $25.

3) Vitamin D

Chronic muscle pain can be a symptom of vitamin D deficiency. Vitamin D is found in fish with small bones, fortified milk and cereal, and exposure to sunlight.

Risk factors for vitamin D deficiency are:

darker pigmented skin (e.g. Hispanic, African American, Asian) does not convert UV rays efficiently to vitamin D digestive disorders, such as celiac disease use of glucocorticoid medications for conditions such as lung diseases and allergies minimal sun exposure (elderly, institutionalized, homebound, veiled or heavily-clothed individuals) latitude and season - for example, people in Boston do not produce vitamin D from sun exposure between November and February.  A study by the University of Minnesota looked at the prevalence of vitamin D deficiency in 150 people with chronic musculoskeletal pain. Researchers found that 93% of patients had vitamin D deficiency. All people with darker pigmented skin (African American, East African, Hispanic, and Native American origin) had vitamin D deficiency.

Another interesting finding was that the majority of people with severe vitamin D deficiency were under 30 years of age. Season was not a significant factor.

The researchers concluded that all people with persistent, non-specific musculoskeletal pain should be screened for vitamin D deficiency.

4) Music Therapy

Music therapy is a low-cost natural therapy that has been found to reduce the disability, anxiety, and depression associated with chronic pain.

A study evaluated the influence of music therapy in hospitalized patients with chronic back pain. Researchers randomized 65 patients to receive, on alternate months, physical therapy plus 4 music therapy sessions or physical therapy alone.

Music therapy significantly reduced disability, anxiety, and depression. Music had an immediate effect on reducing pain, although the results were not statistically significant.

5) Vitamin B12

Vitamin B12 has been found to relieve low back pain. A double-blind Italian study examined the safety and effectiveness of vitamin B12 for low back pain. People who received vitamin B12 showed a statistically significant reduction in pain and disability. They also used less pain medication than the placebo group.

Besides pain, other symptoms of vitamin B12 deficiency are numbness and tingling, irritability, mild memory impairment, and depression.

Risk factors for vitamin B12 deficiency are :

  • pernicious anemia
  • medications (stomach acid-blocking medications)
  • inadequate intake of meat or dairy products
  • infection (small intestine bacterial overgrowth, parasites)
  • Digestive diseases (stomach removal surgery, celiac disease, Crohn's disease
  • Vitamin B12 muscle injections are the standard treatment for vitamin B12 deficiency. Studies have found vitamin B12 sublingual tablets (placed under the tongue for absorption) and nasal gel are also effective.
6) Magnesium

Magnesium is the fourth most abundant mineral in the body. It's involved in over 300 biochemical reactions in the body.

Magnesium helps maintain normal muscle and nerve function, keeps heart rhythm steady, supports a healthy immune system, and keeps bones strong. Magnesium also helps regulate blood sugar levels, promotes normal blood pressure, and is known to be involved in energy metabolism and protein synthesis.

Symptoms of magnesium deficiency include muscle spasms and pain, premenstrual syndrome, irritability, depression, insulin resistance, high blood pressure, irregular heart rhythms, and heart disease.

A German study found that mineral supplements increased intracellular magnesium levels by 11% and was associated with a reduction in pain symptoms in 76 out of 82 people with chronic low back pain.

7) Willow Bark

The bark of the white willow tree (Salix alba) has pain-relieving properties similar to aspirin. An ingredient in white willow bark, called salicin, is converted in the body to salicylic acid (aspirin is also converted to salicylic acid once in the body). Salicylic acid is believed to be the active compound that relieves pain and inflammtion.

A number of studies have compared white willow to medication or placebo:

A University of Sydney study compared the effects of willow bark extract to refecoxib, a Cox-2 inhibitor pain medication. In the study, 114 patients received a herbal extract containing 240 mg of salicin and 114 received 12.5 mg of refecoxib every day. After four weeks, both groups had a comparable reduction in pain.

A study in the American Journal of Medicine examined 191 patients with an exacerbation of chronic low back pain. They were randomly assigned to receive a willow bark extract with either 120 mg (low-dose) or 240 mg (high-dose) of salicin, or placebo. In the fourth week of treatment, 39% of people receiving the high-dose extract were pain-free, 21% receiving the low-dose were pain-free, and 6% of people receiving the placebo were pain-free. People in the high-dose group improved after the first week. Significantly more people in the placebo group required pain medication.

8) Yoga for Back Pain

Yoga creates balance in the body through various poses that develop flexibility and strength. A study of people with chronic mild low back pain compared Iyengar yoga to back education. After 16 weeks, there was a significant reduction in pain intensity, disability, and reliance on pain medication in the yoga group. Benefits were also seen at three month follow up assessments.

Another study compared yoga, conventional exercise, and a self care book for people with chronic low back pain. Back function in the yoga group was superior to the book and exercise groups at 12 weeks. Although there was no difference in symptoms at 12 weeks, at 26 weeks, the yoga group was superior to the book group.

9) Bowen Therapy

Bowen therapy is a type of gentle bodywork that was developed in Australia by osteopath Tom Bowen (1916-1982). Bowen therapy is more widely used in Australia and Europe, but it has been growing in popularity in North America.

Bowen therapists use a series of specialized "moves" using their fingers and thumbs. The moves typically involve the therapist pulling the skin slack away from the muscle, applying pressure, and then quickly releasing the tension.

These moves are performed on precise areas of muscles where special receptors are located. Nerve impulses are sent to the brain, resulting in muscle relaxation and reduction of pain.

The moves are not continuous - the therapist allows the client to rest for a few minutes between each move. A typical treatment is between 30 to 40 minutes.

10) Breathing Techniques

Breathing techniques that make use of the mind-body connection have been found to reduce pain. These techniques integrate body awareness, breathing, movement, and meditation. What's great about breathing techniques is that you can do them yourself at home at no cost.

One study compared 6-8 weeks (12 sessions) of breath therapy to physical therapy. Patients improved significantly with breath therapy. Changes in standard low back pain measures of pain and disability were comparable to those resulting from high quality, extended physical therapy. Breath therapy was found to be safe. Other benefits of breath therapy were improved coping skills and new insight into the effect of stress on the body.

11) Massage Therapy

When many people have back aches and pain, the first thing they think of is massage. Studies have found that massage may be effective for subacute and chronic pain. It has also been found to reduce anxiety and depression associated with chronic pain. Massage therapy is the most popular therapy for low back pain during pregnancy.

12) Chiropractic

Back pain is one of most common reasons people see a chiropractor. Doctors of chiropractic use chiropractic spinal manipulation to restore joint mobility. They manually apply a controlled force to joints that have become restricted by muscle injury, strain, inflammation, and pain. Manipulation is believed to relieve pain and muscle tightness and encourage healing.

A study published in the Spine Journal examined manipulations compared to simulated manipulations in 102 people with back pain and/or radiating pain. The researchers found that active manipulations were more effective at reducing acute back pain and sciatica with disc protrusion.

13) Alexander Technique

Alexander technique teaches people to improve their posture and eliminate bad habits such as slouching, which can lead to pain, muscle tension, and decreased mobility. This technique was created by Frederick Matthias Alexander (1869-1955), an Australian actor who learned how to correct hoarseness in his voice by improving his posture.

You can learn Alexander technique in private sessions or group classes. A typical session lasts about 45 minutes. During that time, the instructor notes the way you carry yourself and coaches you with verbal instruction and gentle touch.

14) Prolotherapy

Prolotherapy addresses damaged ligaments (bands of connective tissue that help keep bones attached to each other) to relieve chronic musculoskeletal pain.

How does it work? Tendons and ligaments in the back often do not heal completely after injury. Bones of the spine become less stable, which can lead to chronic pain.

Prolotherapy involves the injection of a liquid solution into soft tissues such as ligaments and tendons. This triggers local inflammation and triggers the body's natural healing response which repairs the weakened soft tissues and relieves pain. Unlike drugs, prolotherapy is thought to address the underlying problem. 

After locating the areas that require treatment, the doctor inserts a thin needle with the solution into the area. There is often mild pain, but it can be reduced by using a local anaesthetic. A typical course of treatment is 10 to 25 sessions for back pain. Since it is believed to repair the joint, no other treatment is necessary. 

Preliminary studies have found that back pain, which often involves ligament injury, responds particularly well to prolotherapy. It is the position of the American Association of Orthopaedic Medicine that prolotherapy is a safe and effective therapy for the treatment of selected cases of low back pain and other chronic myofascial pain syndromes. Prolotherapy injections must be administered by a medical doctor (M.D.), osteopath (D.O.) or by a state-licensed naturopathic doctor (N.D.) in certain states.

15) Balneotherapy

Balneotherapy is one of the oldest therapies for pain relief. The term "balneo" comes from the Latin word, balneum, meaning bath. Balneotherapy is a form of hydrotherapy that involves bathing in mineral water or warm water.
A study compared bathing in mineral water to plain tap water in 60 people with low back pain. They found that mineral water containing sulphur was superior in reducing pain and improving mobility compared with tap water.

A systematic review and meta-analysis published in the journal Rheumatology assessed spa therapy and balneotherapy for low back pain. The researchers found that the data suggest beneficial effects compared to control groups. They concluded that the results were encouraging and that large-scale trials were warranted.
Dead Sea salts and other sulphur-containing bath salts can be found in spas, health food stores, and online.

People with heart conditions should not use balneotherapy unless under the supervision of their primary care provider.

BACK PAIN SYMPTOMS AND MANAGEMENT


Why occur back pain at work?

Back Pain & the Workplace
After the common cold, back pain is the leading reason adults under 45 years of age stay home from work, according to the American Academy of Orthopaedic Surgeons. All told, back pain results in about 83 million lost work days each year. It’s one of the most common work-related injuries, especially among those working in physically demanding jobs, and the leading cause of job-related disability and work limitations in those under 45 years of age.

According to experts at the Mayo Clinic, there are four work-related factors that are associated with increased risk of back pain and injury:


Applying too much force to your back by lifting or moving heavy objects
Repetitive tasks, which can lead to muscle fatigue or injury, particularly if they involve stretching to the limit of your range of motion or awkward body positioning
Poor posture, especially if you stay in the same position for an extended period of time; according to experts your body can remain in one position for an average of 20 minutes before you need to adjust
Too much stress at work or at home can result in pain or injury by leading to muscle tension and tightness, which can result in back pain.

Many jobs place stress and strain on the back, making you more prone to getting back pain.

Episodes of acute and chronic back pain are more likely for people working in nursing, construction, factory work and truck driving because of the demands placed on the spine. Nurses, for example, put a great amount of strain on the lower back every time they help transfer patients from bed to bed, lift them from a chair or change positions. Nursing aides, orderlies and attendants had more back injuries and other musculoskeletal disorders than any other occupation in 1999, according to the United States Bureau of Labor Statistics.

Some jobs that increase the risk of back pain include:

Nursing
Construction
Truck driving
Service jobs, including police officers and firefighters
Janitors and cleaners
Factory and farm work
Sedentary office work
Teaching, especially in nursery schools
Even routine office work can worsen back pain, especially if you have bad workplace habits (for example, slouching over your desk, not taking regular breaks, using a chair that doesn’t give enough support) or your workspace isn’t well designed.


You are more likely to experience back pain if your job involves:

Physical labor, particularly heavy lifting and forceful movements; this is true for nurses, factory workers and those in other manual labor jobs
Bending or twisting, especially in awkward postures; for example, early childhood educators who are often reaching down to talk to or pick up a small child
Whole body vibrations; construction workers who use machinery and tools that vibrate their entire body or truck drivers whose vehicle’s vibration can cause back pain
Spending hours on end in the same position; for example, spending your days at a desk typing


Fortunately, there are steps employees and employers can take to help protect their backs and prevent or reduce further injury and pain.

Steps to protect your back at work

If your job is physical in nature, be aware of the way you move your body. When lifting or carrying a load, never bend and lift with your back only. Instead, bend your knees and let your legs do the work. Hold the object close to your body and engage other muscles - especially your core - to lift. Always consider asking for help. If you find that you are on your feet all day at work, make sure you wear supportive footwear.

Look at how your work area is setup. If you work in an office, the best way to protect your back from unnecessary stress is to make your workplace more ergonomically friendly. Ergonomics is the science of making sure that workplace conditions and equipment - such as desks, lighting and uniforms - fit the worker. These principles can help prevent work-related back strains and injury by identifying and controlling the risk factors that might strain workers' bodies.

There are many small changes that can help make a desktop office space more ergonomically friendly, says Karen Jacobs, EdD, OTR/L, CPE, FAOTA, occupational therapist, board certified professional ergonomist and occupational therapy professor at Boston University. She suggests:

Adjusting your computer monitor so that it’s directly in front of you. This will prevent straining the neck and upper back muscles, a common complaint of many computer-users.
Making sure your chair fits your weight and height. Often, chairs are not adjusted appropriately and may not provide enough support.
Using a foot rest. A small foot rest - even a thick phone book - placed under your feet may help support legs and reduce strain on the lower back, especially if your feet don’t comfortably rest on the floor. When you sit in your chair, your feet should rest flat on the floor, and your thighs should be parallel to the floor.
Keeping your elbows close to your body and at a 90 degree angle when typing. Adjustable keyboard trays with extra space for a mouse are best because they reduce excessive and repetitive reaching.
Checking that the lighting in your office has minimal glare. When lighting is poor, workers often have to compensate by putting their bodies in awkward positions, causing back strain.
Making sure you move your body properly at work. For example, while sitting at the computer, instead of twisting to reach something, swivel your chair to avoid unnecessary strain on your back muscles. If you have to slide a heavy object, push rather than pull.
It’s also important to build in time to stretch before, during and after work. Take a few moments to deep breathe during periods of stress.

For people who want a deeper stretch, workplace yoga is increasing in popularity. Dedicating 10-15 minutes per day to workplace yoga not only provides physical benefits including relaxed muscles and improved circulation, but mental renewal as well. Some people may also benefit from progressive muscle relaxation exercises.

Other advice for employees

Talk to your supervisor. Although it might seem daunting to approach your boss, remember that as an employee you have a right to be safe of all known harm at work. If you have chronic back pain or are returning to work after an injury, talk with your employer about your work conditions and limitations. Make sure you both have the same expectations about the work you will be doing and any modifications that are needed to your workspace or tasks.

Plan ahead. When dealing with back pain at work, try to anticipate what might lead to or aggravate back pain. Plan out your moves to prevent problems or flare ups. For example, limit the time you spend carrying and moving heavy objects by knowing exactly where you’re going and the shortest route.

Listen to your body. Pace yourself to avoid feeling overloaded at work and excessive activities while at home. If you feel a flare up of back pain beginning, stop any activities that may aggravate it. Take frequent breaks and rest your back (set a timer as a reminder if you need to). If you’ve worked with a PT, use the stretches or exercises he or she has taught you. Consider creating a comfort kit that is well stocked and easily accessible. You might want to include a heating pad, ice pack, counterirritants, medication, and soothing music. Some people find it helpful to keep an exercise ball at the office to sit on during meetings or when they need a break from their chair. Make sure to drink plenty of water to stay hydrated - dehydration can cause more discomfort.

Advice for employers

Employers have a responsibility under health and safety laws to provide a safe workplace for their employees. Back pain is the sixth most costly condition in the U.S. Together, health care and other indirect costs due to back pain are over $12 billion per year, according to research. In addition, surgery for low back pain is one of the top five claim costs each year. As an employer, take steps to minimize employees’ risk of injury that may cause episodes of back pain.

Communication is key. Talk and listen to employees. Let them know it’s okay to share workplace concerns.

Provide education and training. If employees are among those at higher risk for back pain or injury, it’s important to provide information and training on ways to keep their backs healthy. APF and other organizations have resources that can help.

Adopt a philosophy of health and wellness. Promote this philosophy to employees, and stress the importance of proper exercise and taking small breaks throughout the day. Investigate the benefits of offering health club memberships as an incentive bonus or a means to reduce health insurance premium costs to your employees. Plan health fairs on-site. Encourage group walks before or after work or during lunch hour. It’s a great way to boost morale too.

Invest in proper equipment and technologies to create a safer workplace. If a job requires employees to stand for the majority of the day, invest in anti-fatigue mats to help support their backs. Use ergonomically friendly office equipment for those whose spines may be affected from sitting in the same positions for a long time each day. Make sure conference rooms and other meeting places are also included.

Consider inviting safety representatives or occupational therapists to assess current work conditions and provide ideas to improve health and safety. Occupational therapists can perform job site analysis and make recommendations on improvements. They are able to work with OSHA, employees and employers regarding the workplace and concerns.

As an employer, it is important to identify and reduce employees’ exposure to hazards in the workplace. By training and engaging employees in their own safety, you can reduce the occurrence of workplace injuries, increase employee productivity and morale and lowers workers’ compensation costs.


Making sure a workplace is fit (and safe) for its workers has many benefits including:

Greater productivity
Reduced risk of illness, injury and recurrence
Increased satisfaction among the workers
Be in the know

You may be able to avoid back pain and injuries if you understand what might cause it or trigger a flare up. For more information, check out other articles in APF’s Spotlight on Back Pain.

The information on this website is provided to help users find answers and support. Readers may wish to print the information and discuss it with their doctor. Always consult with health care providers before starting or changing any treatment.

HYPOTHYROIDISM: CAUSES AND TREATMENT

What is Hypothyroidism?


Hypothyroidism

Clinical features
Classic clinical features of hypothyroidism include weight gain, cold intolerance, dry skin, constipation, memory loss, lethargy/slow thought/‘slowing up’, menorrhagia, periorbital/facial oedema, loss of outer two-thirds of eye brows, deafness, chest pain and coma. Rarely seen nowadays as thyroid function tests are easy to perform and detect the disease usually at an earlier stage. Weight gain, dry skin and lethargy are frequently reported, but even in biochemically hypothyroid individuals can only confidently be ascribed to thyroid status if they reverse on treatment.


Biochemical diagnosis

  • TSH with T4 in the normal range is referred to as subclinical hypothyroidism.
  • TSH with 5 T4 is overt hypothyroidism. 5 T4 with TSH in the normal range may be due to pituitary failure (2° hypothyroidism) and if persistent requires pituitary function testing. See Fig. 2.14 for other patterns of thyroid function tests.

Differential diagnosis (causes)

In iodine sufficient countries, the vast majority of spontaneous hypothyroidism is due to autoimmune thyroiditis (Hashimoto’s disease if goitre present, atrophic thyroiditis if goitre absent)—antithyroid antibodies
present in 80–90% of cases. Other common causes are post-thyroidectomy, post-radioiodine therapy and side effects of amiodarone or lithium. Rarer causes include treatment with cytokines (e.g. interferons, GM-CSF, interleukin-2), vast excess iodine intake (iodine drops, water purifying tablets), congenital hypothyroidism (caused by a variety of genetic defects, should be detected by neonatal screening programme), iodine deficiency (urinary iodide excretion <45μg/day, commonest cause worldwide esp.
mountainous areas, S Germany, Greece, Paraguay—‘endemic goitre’), thyroid-blocking substances in the indigenous diet (goitrogens esp. in brassicas and cassava, e.g. in Sheffield, Spain, Bohemia, Kentucky, Virginia, Tasmania—‘endogenous goitre’ without iodine deficiency), Pendred’s syndrome (mild hypothyroidism with sensineural deafness due to Mondini cochlear defect, positive perchlorate discharge test).

Diagnostic catches
4 TSH and 5 T4 always represents hypothyroidism. If the TSH alone is 4 and the T4 is not even slightly low, a heterophile antibody interfering in the TSH assay may be present in the patient’s serum. This is especially
likely if there is no change in TSH level after thyroxine treatment but the T4 level rises (confirming compliance with tablets). For unusual patterns of thyroid function tests. Note that within the first 1–3 months (or longer) after treatment of hyperthyroidism, profound hypothyroidism may develop with a 5 T4 but the TSH may still be suppressed or only mildly raised due to the long period of TSH suppression prior to treatment.

Raised TSH alone with disproportionate symptoms of lethargy may be seen in hypoadrenalism. If suspected treat with steroids first as thyroxine may precipitate an Addisonian crisis.

Transient hypothyroidism
Transient or self-resolving hypothyroidism, often preceded by hyperthyroidism, is seen in viral thyroiditis, after pregnancy (post-partum thyroiditis) and in some individuals with autoimmune thyroiditis (positive
antithyroid antibodies). Treatment temporarily with thyroxine is only required if the patient is very symptomatic. Thyroid function should return to normal within 6 months. Hypothyroidism may also be transient in the first 6 months after radioiodine therapy.

Subclinical hypothyroidism
A raised TSH (<20mU/L) with normal T4/T3 is very common and seen in 5–10% of women and ~2% of males. It is usually due to subclinical autoimmune thyroid disease and is frequently discovered on routine testing. In randomised trials, ~20% of patients obtain psychological benefit from beginning T4 therapy, in many others it is probably truly asymptomatic. If antithyroid antibodies are detectable, the rate of progression to overt hypothyroidism is ~50% at 20 years, but higher than this with higher initial TSH levels. If the TSH alone is raised with negative antibodies (or the TSH is normal with raised antibodies alone), overt hypothyroidism develops in 25% at 20 years. A reasonable approach is a trial of thyroxine for 6 months in symptomatic patients with subclinical hypothyroidism or TSH >10mU/L, and observing the TSH level at 6–12-monthly intervals in asymptomatic patients with TSH <10mU/L.

Hypothyroidism and pregnancy
Overt hypothyroidism is associated with poor obstetric outcomes. Recent evidence suggests that subclinical hypothyroidism is associated with a slight reduction in the baby’s IQ and should be treated. Many authorities
advocate screening for hypothyroidism in all antenatal patients as early as possible in pregnancy. Patients on T4 need to increase their dose by 50 g from the first trimester of pregnancy. Maternal thyroxine can compensate for fetal thyroid failure in utero but congenital hypothyroidism must be detected at birth (screening test) to avoid mental retardation developing.

Where the mother and fetus are both hypothyroid—most commonly due to iodine deficiency—mental retardation can develop in utero (cretinisim). Note that mothers with positive antithyroid antibodies and/or subclinical hypothyroidism have a 50% chance of developing (transient) post-partum thyroiditis.


How is hypothyroidism treated?

With the exception of certain conditions, the treatment of hypothyroidism requires life-long therapy. Before synthetic levothyroxine (T4) was available, desiccated thyroid tablets were used. Desiccated thyroid was obtained from animal thyroid glands, which lacked consistency of potency from batch to batch. Presently, a pure, synthetic T4 is widely available. Therefore, there is no reason to use desiccated thyroid extract.

As described above, the most active thyroid hormone is actually T3. So why do physicians choose to treat patients with the T4 form of thyroid? T3 [liothyronine sodium (Cytomel)] is available and there are certain indications for its use. However, for the majority of patients, a form of T4 [levothyroxine sodium (Levoxyl, Synthroid)] is the preferred treatment. This is a more stable form of thyroid hormone and requires once a day dosing, whereas T3 is much shorter-acting and needs to be taken multiple times a day. In the overwhelming majority of patients, synthetic T4 is readily and steadily converted to T3 naturally in the bloodstream, and this conversion is appropriately regulated by the body's tissues.

The average dose of T4 replacement in adults is approximately 1.6 micrograms per kilogram per day. This translates into approximately 100 to 150 micrograms per day.

Children require larger doses.

In young, healthy patients, the full amount of T4 replacement hormone may be started initially.

In patients with preexisting heart disease, this method of thyroid replacement may aggravate the underlying heart condition in about 20% of cases.

In older patients without known heart disease, starting with a full dose of thyroid replacement may result in uncovering heart disease, resulting in chest pain or a heart attack. For this reason, patients with a history of heart disease or those suspected of being at high risk are started with 25 micrograms or less of replacement hormone, with a gradual increase in the dose at 6 week intervals.
Ideally, synthetic T4 replacement should be taken in the morning, 30 minutes before eating. Other medications containing iron or antacids should be avoided, because they interfere with absorption.

Therapy for hypothyroidism is monitored at approximately six week intervals until stable. During these visits, a blood sample is checked for TSH to determine if the appropriate amount of thyroid replacement is being given. The goal is to maintain the TSH within normal limits. Depending on the lab used, the absolute values may vary, but in general, a normal TSH range is between 0.5 to 5.0uIU/ml. Once stable, the TSH can be checked yearly. Over-treating hypothyroidism with excessive thyroid medication is potentially harmful and can cause problems with heart palpitations and blood pressure control and can also contribute to osteoporosis. Every effort should be made to keep the TSH within the normal range.

AMYOTROPHIC LATERAL SCLEROSIS

What is amyotrophic lateral sclerosis?

Amyotrophic lateral sclerosis (ALS) is the most common degenerative disease of the motor neuron system. ALS was first described in 1869 by the French neurologist Jean-Martin Charcot and hence is also known as Charcot disease; however, it gained popular recognition and its best-known eponym after the baseball player Lou Gehrig announced his diagnosis with the disease in 1939. ALS is also known as motor neurone disease (MND).

Amyotrophic Lateral Sclerosis, also known as Lou Gehrig disease, is an incapacitating disease of unknown cuase that results from degeneration of upper and lower motor neurons or of the cerebral cortex, brain stem, and spinal cord. This causes progressive loss of voluntary muscle contraction and functional capacity, accompanied by other lower motor neuron signs such as atrophy or fasciculations. ALS usually affects men between ages 40 and 70. It is invariably fatal, usually within 2 to 5 years of diagnosis, death usually results from a complication such as respiratory failure, aspiration pneumonia, or cardiopulmonary arrest.



The cause of ALS is unknown, although 5-10% of cases are familial. Some research is showing that ALS may share common biological mechanisms with Alzheimer disease, Parkinson disease, and other neurodegenerative diseases. Collaborative research is increasing.

In its classic form, ALS affects motor neurons at 2 or more levels supplying multiple regions of the body. It affects lower motor neurons that reside in the anterior horn of the spinal cord and in the brain stem; corticospinal upper motor neurons that reside in the precentral gyrus; and, frequently, prefrontal motor neurons that are involved in planning or orchestrating the work of the upper and lower motor neurons.

Loss of lower motor neurons leads to progressive muscle weakness and wasting (atrophy). Loss of corticospinal upper motor neurons may produce stiffness (spasticity), abnormally active reflexes, and pathological reflexes.

Loss of prefrontal neurons may result in special forms of cognitive impairment that include, most commonly, executive dysfunction but may also include an altered awareness of social implications of an individual’s circumstances and, consequently, maladaptive social behaviors. In its fully expressed forms, the prefrontal dysfunction meets established criteria for frontotemporal dementia.

The term classic amyotrophic lateral sclerosis is reserved for the form of disease that involves upper and lower motor neurons. The classic form of sporadic ALS usually starts as dysfunction or weakness in one part of the body and spreads gradually within that part and then to the rest of the body. Ventilatory failure results in death, on average, 3 years after the onset of focal weakness.

If only lower motor neurons are involved, the disease is called progressive muscular atrophy (PMA). Although many patients with PMA have a course indistinguishable from that of classic ALS, others have a course that may be longer.

When only upper motor neurons are involved, the disease is called primary lateral sclerosis (PLS). The course of PLS differs from that of ALS and is usually measured in decades. Rarely, the disease is restricted to bulbar muscles, in which case it is called progressive bulbar palsy (PBP). In most patients who present with initial involvement of bulbar muscles, the disease evolves to classic ALS.

Worldwide, ALS occurs sporadically in 90-95% of cases and with Mendelian patterns of heredity (familial ALS) in 5-10% of cases. Most familial ALS is inherited in an autosomal dominant pattern.

The diagnosis of ALS is primarily clinical. Electrodiagnostic testing contributes to the diagnostic accuracy.

ALS is a fatal disease, with median survival of 3-5 years. Aspiration pneumonia and medical complications of immobility contribute to morbidity in patients with ALS. Although ALS is incurable, there are treatments that can prolong meaningful quality of life; therefore, diagnosis is important to patients and families.

Assessment:
1. Progressive weakness and wasting of muscles of arms, trunk, and legs
2. Muscle fasciculations and spasticity
3. Tachypnea, hypopnea, restlessness, poor sleep, and excessive fatigue caused by hypoxia from respiratory weakness.
4. Cranial nerve dysfunction, particularly gag reflex and swallowing difficulty, as well as nasal and unintelligible speech.


What causes ALS?

The cause of ALS is not known, and scientists do not yet know why ALS strikes some people and not others. An important step toward answering that question came in 1993 when scientists supported by the National Institute of Neurological Disorders and Stroke (NINDS) discovered that mutations in the gene that produces the SOD1 enzyme were associated with some cases of familial ALS. This enzyme is a powerful antioxidant that protects the body from damage caused by free radicals. Free radicals are highly reactive molecules produced by cells during normal metabolism. If not neutralized, free radicals can accumulate and cause random damage to the DNA and proteins within cells. Although it is not yet clear how the SOD1 gene mutation leads to motor neuron degeneration, researchers have theorized that an accumulation of free radicals may result from the faulty functioning of this gene. In support of this, animal studies have shown that motor neuron degeneration and deficits in motor function accompany the presence of the SOD1 mutation.

Studies also have focused on the role of glutamate in motor neuron degeneration. Glutamate is one of the chemical messengers or neurotransmitters in the brain. Scientists have found that, compared to healthy people, ALS patients have higher levels of glutamate in the serum and spinal fluid. Laboratory studies have demonstrated that neurons begin to die off when they are exposed over long periods to excessive amounts of glutamate. Now, scientists are trying to understand what mechanisms lead to a buildup of unneeded glutamate in the spinal fluid and how this imbalance could contribute to the development of ALS.

Autoimmune responses—which occur when the body's immune system attacks normal cells—have been suggested as one possible cause for motor neuron degeneration in ALS. Some scientists theorize that antibodies may directly or indirectly impair the function of motor neurons, interfering with the transmission of signals between the brain and muscles.

In searching for the cause of ALS, researchers have also studied environmental factors such as exposure to toxic or infectious agents. Other research has examined the possible role of dietary deficiency or trauma. However, as of yet, there is insufficient evidence to implicate these factors as causes of ALS.





DIABETES MELLITUS: UNDERSTANDING TYPE 1 AND TYPE 2

WHAT is Diabetes Mellitus?


Diabetes mellitus is a metabolic disorderis characterized by hyperglycemia that results from defective insulin production, secretion, or utilization. The classification of diabetes includes:

In type 1 DM, the pancreas produces little or no endogenous insulin.

In type 2 DM, disease results from a defect in insulin manufacture and release from the beta cells and from insulin resistance in the peripheral tissues. It has a strong genetic component and is commonly associated with obesity. Onset is usually in adulthood; however, cases are increasingly occurring in teenagers and older children.


Glycosuria
Urine testing is a valuable pointer to diabetes mellitus (DM) but is insufficient to establish the diagnosis. Although modern glucose oxidase test strips are free from interference by other reducing substances, glycosuria does not always indicate DM; the converse also pertains. Thus, glycosuria has low sensitivity  and specificity.

Causes of glycosuria
2 DM.
2 Impaired glucose tolerance (IGT).
2 Lowered renal threshold for glucose (esp. pregnancy, children).
2 Casual (random)—usually the first line investigation.
2 Fasting plasma glucose (FPG)—an alternative to a casual reading.
2 75g oral glucose challenge—if necessary.

Neither the confirmation nor exclusion of DM should rest on measurement of longer term indicators of glycaemia such as glycated haemoglobin or fructosamine. Although of high specificity, these tests are not sufficiently standardised nor do they have sufficient sensitivity. False negative results are particularly likely with less marked degrees of hyperglycaemia, especially in subjects with IGT or IFG.

Blood glucose
A blood glucose measurement is the essential investigation in the diagnosis of DM. A glucose-specific assay is required. An appropriate sample must be collected, usually venous plasma (in a tube containing fluoride
oxalate as an inhibitor of glycolysis) and the sample tested without undue delay in an accredited laboratory.

Reagent test strips
Although convenient and readily available, reagent test strips for monitoring of capillary glucose (even when used in conjunction with a calibrated reflectance meter) are unsuitable for diagnosing DM; a confirmatory laboratory measurement must therefore always be performed. In the absence of typical symptoms the diagnosis should be confirmed by a repeat measurement on a separate day; this may be either a
casual or FPG sample.

Confirmation of the diagnosis is especially important in asymptomatic individuals.
An oral glucose tolerance test (OGTT) is rarely required to confirm the diagnosis and should not be regarded as a first line investigation. The OGTT is time consuming, requires trained staff and is less reproducible than FPG.

The diagnostic FPG is lower than the previous National Diabetes Data Group (1979) and WHO (1980, 1985) criteria which specified a diagnostic fasting plasma glucose >7.8mmol/L.
The 1997 criteria introduced the new intermediate category of impaired fasting glucose (IFG) defined as:
2 FPG 6.1–6.9 mmol/L.
False +ve diagnoses may arise if the subject has prepared inadequately. This possibility is more likely following the reduction in the diagnostic threshold for diabetes based on FPG in the 1997 revised criteria.

Impaired glucose tolerance
The diagnosis of IGT can only be made using a 75g oral glucose tolerance test; a random blood glucose measurement will often point to the diagnosis when other results are non-diagnostic.
This category denotes a stage intermediate between normal glucose levels and DM (􀀉OHCM, section 9). By definition, plasma glucose levels are not raised to DM levels so typical osmotic symptoms are absent. Although subjects with IGT are not at direct risk of developing chronic microvascular tissue complications, the incidence of macrovascular complications (i.e. CHD, CVD, PAD) is increased. Presentation with one of these conditions should therefore alert the clinician to the possibility of undiagnosed IGT (or type 2 DM). Note that a proportion of individuals who are diagnosed by an OGTT may revert to normal on re-testing.
Impaired fasting glucose If an OGTT is performed, the 120min glucose concentration must be <7.8mmol/L. This category is also usually asymptomatic. To date, crosssectional studies suggest that IGT and IFG may not be synonymous in terms of pathophysiology and long-term implications.

Oral glucose tolerance test
The OGTT (see table below) continues to be regarded as the most robust means for establishing the diagnosis of diabetes in equivocal cases. The WHO suggests that only when an OGTT cannot be performed should the diagnosis rely on FPG. OGTTs should be carried out under controlled conditions after an overnight fast.

The interpretation of the 75g glucose tolerance test. These results apply to venous plasma. Marked carbohydrate depletion can impair glucose tolerance; the subject should have received adequate nutrition in the days preceding the test.

Effect of intercurrent illness on glycaemia
Patients under the physical stress associated with surgery, trauma, acute MI, acute pulmonary oedema or stroke may have transient 4 of plasma glucose—often settles rapidly without antidiabetic therapy. However, the hormonal stress response in such clinical situations is liable to unmask pre-existing DM or to precipitate DM in predisposed individuals. Blood glucose should be carefully monitored and urine tested for ketones.
Sustained hyperglycaemia, particularly with ketonuria, demands vigorous treatment with insulin in an acutely ill patient.

Oral glucose tolerance test
Anhydrous glucose is dissolved in 250ml water; flavouring with sugar-free lemon and chilling increase palatibility and may reduce nausea. The subjecrt sits quietly throughout the test.

Blood glucose is sampled before (time 0) and at 120min after ingestion of the drink, which should be completed within 5min.

Urinalysis may also be performed every 30min although is only of interest if a significant alteration in renal threshold for glucose is suspected.

Acute myocardial infarction (􀀉OHCM section 5)
Hyperglycaemia at presentation is associated with a higher mortality—even in subjects with previously undiagnosed DM; tight metabolic control using an intravenous insulin-dextrose infusion (followed by subcutaneous insulin) significantly reduced mortality in a recent multicentre Swedish study.

Stroke (􀀉OHCM section 10)
Hyperglycaemia on admission may be associated with a poorer outcome; however, there is no clinical trial evidence to date that intensive control of hyperglycaemia improves prognosis.

Re-testing is usually indicated following resolution of the acute illness—an OGTT at a 4–6-week interval is recommended if glucose levels are equivocal.

Potential diagnostic difficulties of DM
Type 1 DM
This is diagnosed principally on clinical and biochemical features (􀀉OHCM section 12). The presence of serum islet cell antibodies (ICA, in ~30–60% of patients) at diagnosis may confirm the diagnosis.
The proportion of patients testing positive for ICA 5 with increasing duration of type 1 DM. If there is doubt, treat with insulin if indicated on clinical and biochemical criteria; the need for insulin can be considered
at a later date. However, discontinuation of insulin can be disastrous in patients with type 1 DM. The decision to stop insulin should be made only by an experienced diabetologist. iA –ve test for ICA
does not necessarily exclude type 1 DM.

Other humoral markers of autoimmunity, e.g. anti-GAD65 antibodies, anti-insulin antibodies, are generally only available in research laboratories.
Stiff man syndrome: rare condition presenting as a progressive spastic paraparesis with polyglandular endocrine involvement (􀀉p246). Anti- GAD65 antibodies are present; approximately 30% of patients develop insulin-requiring DM.

MODY: a small percentage of young patients with relatively minor hyperglycaemia and no ketonuria, will prove to have relatively uncommon inherited forms of DM, e.g. MODY. Such patients often receive insulin therapy from diagnosis, the assumption being that they have type 1 DM. Prerequisites for the diagnosis include:
– A family history with an autosomal dominant inheritance.
– Diagnosis under the age of 25 years.

In some subtypes of MODY (glucokinase mutations; MODY 2), good glycaemic control may be maintained life-long without insulin or even oral antidiabetic agents. The exception is pregnancy; insulin may be
required temporarily in order to ensure optimal control—oral antidiabetic agents should be avoided. The diagnosis of MODY may be confirmed by molecular genetic testing although presently this is not widely available. Appropriate counselling is required. Seek expert advice through your local hospital diabetes unit.
2 Early-onset type 2 diabetes—In recent years there has been a dramatic increase in the incidence of type 2 diabetes in younger patients (children and adolescents) from non-white ethnic minorities. This may present diagnostic difficulties but some pointers suggest the diagnosis:
– Obesity is usually a prominent feature.
– Serum autoantibody tests for type 1 DM are negative.
– A skin marker of insulin resistance (acanthosis nigricans) may be present.

If in doubt, it is usually safer to treat younger patients with insulin; this is especially true if ketosis is present.

Monitoring diabetic control
Self-testing by diabetic patients
Self-testing of urine and/or capillary blood glucose testing can readily be performed by the majority of patients. Measurements of longer term gly- caemic control are laboratory-based or require specialised techniques generally suitable only for use in a hospital clinic.

Urine testing
Glycosuria: Semiquantitative testing for glucose using reagentimpregnated test strips by patients is of limited value. Urinalysis provides retrospective information over a limited period of time. Other limitations:

The renal threshold for the reabsorption of glucose in the PCT is ~10mmol/L on average but varies between individuals. Subjects with a low threshold will tend to show glycosuria more readily, even with normal glucose tolerance (‘renal glycosuria’). Children are particularly liable to test positive for glucose. The renal threshold is effectively lowered in pregnancy. Conversely, a high threshold, common among the elderly, may give a misleadingly reassuring impression of satisfactory control. Fluid intake and urine concentration may affect glycosuria.

Renal impairment may elevate the threshold for glucose reabsorption. Delayed bladder emptying, e.g. due to diabetic autonomic neuropathy (􀀉OHCM section 9), will reduce the accuracy of the measurements
through dilution.

Hypoglycaemia cannot be detected by urinalysis.
Ketonuria: Semiquantitative test strips for acetocetate (e.g. Ketostix®) are available for patients with type 1 DM. Useful when intercurrent illness leads to disturbance of metabolic control. The presence of ketonuria on dipstick testing in association with hyperglycaemia indicates marked insulin deficiency (absolute, or more commonly, relative). Increased doses of insulin are indicated in such circumstances to avert more severe metabolic decompensation (DKA, see below and 􀀉OHCM section 21). Occasionally, patients with type 2 DM develop ketosis during severe intercurrent illness, e.g. major sepsis. Neither Ketostix® nor Acetest® tablets detect 3-hydroxybutyrate (although acetone is detected by Acetest®). Occasional underestimation of the degree of ketonaemia using these tests is a well-recognized, albeit uncommon caveat of alcoholic ketoacidosis (􀀉OHCM section 9).

Self-testing of blood glucose
Self-testing of capillary blood glucose obtained by fingerprick has become an established method for monitoring glycaemic control. Frequent testing is a prerequisite for safe intensive insulin therapy such as that employed in the DCCT. Enzyme-impregnated dry strip methods are available which can be used in conjunction with meter devices to improve accuracy. Most are based on the glucose oxidase reaction:
Glucose + O2————7Gluconic acid + H2O2
Glucose oxidase
The hydrogen peroxide generated by the reaction reacts with a reduced dye in the test strip producing an oxidised colour proportional to the amount of H2O2 formed. This reflects the amount of glucose that was oxi- dised. In most strips, blood cells are excluded by a layer within the strip.
Thus, the glucose concentration in capillary plasma is measured.

Adequate training and a system of quality control are important; even when trained health professionals use such systems in clinics or hospitals misleading results are possible, particularly in the lower range of blood
glucose results. Where there is doubt, an appropriate sample (in a tube containing the glycolysis inhibitor fluoride oxalate) should be collected immediately for analysis by the clinical chemistry laboratory. However,
acute treatment of hypoglycaemia, where indicated, should not be delayed.

Laboratory assessment of glycaemic control Glycated haemoglobin HbA1c (comprises 60–80% total glycated haemoglobin, HbA1) is formed by the slow, irreversible, post-translational non-enzymatic glycation of the N-terminal valine residue of the chain of haemoglobin. In retina and renal glomerulus this process is implicated in the pathogenesis of the longterm complications of diabetes (􀀉OHCM section 9). The proportion of HbA1c : total haemoglobin (normal non-diabetic reference range approximately 4–6%) provides a useful index of average glycaemia over the preceding 6–8 weeks. The result is disproportionately affected by the blood glucose levels during the final month before the test (~50% of value).

Average HbA1c levels collected over a longer period (i.e. years) provide an estimate of the risk of microvascular complications. Sustained high concentrations identify patients in whom efforts should be made to improve long-term glycaemic control.

In patients with type 1 DM, a landmark randomised, controlled clinical trial (the DCCT) confirmed a causal link between degree of metabolic control and the development and progression of microvascular complications of diabetes (especially retinopathy) and neuropathy. Consensus panels in the USA and Europe have suggested targets for HbA1c of approximately 7–8% for most patients (if circumstances and frequency of hypoglycaemia allow). By contrast, tight glycaemic control may be contraindicated
by advanced complications, e.g. clinical nephropathy with renal impairment. It is recommended that HbA1c should be measured every 6 months in younger patients with type 1 DM. Pregnancy requires
monthly monitoring of HbA1c concentrations (although other measures may be preferable in pregnancy—see below: fructosamine). Blood can be collected by venesection ahead of the clinic visit (in primary care, by the hospital phlebotomy service or even by a nurse in the community if necessary). Alternatives include rapid assays for use in the clinic, or self-collection in advance of a fingerprick sample (in a capillary tube or on filter
paper) which is mailed to the laboratory.

Limitations of HBA1c measurements
Although glycated haemoglobin levels are a reliable indicator of recent average glycaemic control they do not provide information about the daily pattern of blood glucose levels; this supplementary information required
for logical adjustment of insulin doses is derived from home blood glucose monitoring (see below). More recent changes in glycaemia (i.e. within the preceding 4 weeks or so) will influence HbA1c level more than glucose levels 12 or more weeks ago.

Spurious HbA1c levels may arise in states of

  • Blood loss/haemolysis/reduced red cell survival (low HbA1c).
  • Haemoglobinopathy (􀀉OHCM section 16).
  • 4 levels of HbS.
  • 4 levels of HbF (high HbA1c).

Uraemia due to advanced diabetic nephropathy is associated with anaemia and 5 RBC survival thereby falsely lowering HbA1c levels. Fructosamine: refers to protein-ketoamine products resulting from the
glycation of plasma proteins. The fructosamine assay measures glycated plasma proteins (mainly albumin) reflecting average glycaemia over the preceding 2–3 weeks. This is a shorter period than that assessed using
glycated haemoglobin measurements and may be particularly useful when rapid changes in control need to be assessed, e.g. during pregnancy. Levels can be misleading in hypoalbuminaemic states, e.g. nephrotic syndrome (􀀉OHCM section 8). Some fructosamine assays are subject to interference by hyperuricaemia or hyperlipidaemia.

Measurements of fructosamine are less expensive than glycated haemoglobin assays; this may be an important consideration for some laboratory services. The methodology is suitable for automation and
rapid results can be obtained for use within a clinic attendance obviating the requirement for a prior blood test.

Diabetic emergencies: diabetic ketoacidosis, hyperosmolar non-ketotic syndrome & lactic acidosis Diabetic ketoacidosis (DKA) should be considered in any unconscious or hyperventilating patient. The hyperosmolar non-ketotic (HONK) syndrome is characterised by marked hyperglycaemia and dehydration in

the absence of significant ketosis or acidosis. Lactic acidosis (LA) associated with metformin is uncommon. A rapid clinical examination and bedside blood and urine tests should allow the diagnosis to be made
(􀀉OHCM, section 12). Treatment (IV rehydration, insulin, electrolyte replacement) of these metabolic emergencies should be commenced without delay.

Confirm diagnosis by bedside measurement of 2 Capillary blood glucose (glucose-oxidase reagent test strip)>

  • Urinary dipstick for glucose and ketones (e.g. Ketostix®). Note: nitroprusside tests detect acetoacetate, but not 3-hydroxybutyrate. This may be relevant in some circumstances, e.g. alcoholic ketoacidosis. Venous plasma may also be tested for ketones. 
  • Urine for nitrites and leucocytes (UTI).
  • Venous blood for urgent laboratory measurement of Plasma glucose (fluoride-oxalate; itrue ‘euglycaemic’ DKA is rare).
  • U&E (arterial K+ can be measured by some gas analysers). Plasma Na+ may be depressed as a consequence of hyperglycaemia or marked hyperlipidaemia.
  • Plasma creatinine (imay be falsely elevated in some assays by DKA).
  • Plasma lactate (if indicated—can also be measured by some gas analysers).
  • Indicated if acidosis without heavy ketonuria is present. LA is a complication of tissue hypoxia (type A) and is a rare complication of metformin treatment in patients with type 2 DM (type B).


  • Plasma osmolality in HONK—either by freezing point depression or calculated: 2 × [plasma Na+] + [plasma K+] + [plasma glucose] + [plasma urea].
  • FBC (non-specific leucocytosis is common in DKA).
  • Blood cultures (signs of infection, e.g. fever, may be absent in DKA).
  • ABGs (corrected for hypothermia) for:  – Arterial pH, bicarbonate, PCO2 and PO2 (if shock or hypotension). 
  • Repeat laboratory measurement of blood glucose, electrolytes, urea at 2, 4 and 6h and as indicated thereafter. Electrolyte disturbances, renal impairment or oliguria should prompt more frequent (1–2 hourly) measurements of plasma K+. Capillary blood glucose is monitored hourly at the bedside.
Avoidance of hypokalaemia and hypoglycaemia are most important during therapy.
Other investigations, as indicated

  • CXR.
  • Microbial culture of urine, sputum, etc.
  • ECG (acute MI may precipitate metabolic decompensation; note that serum transaminases and CK may be non-specifically elevated in DKA).
  • Sickle cell test.
  • Venous plasma PO4 3– (if there is respiratory depression).

Performance of investigations should not delay initiation of treatment and transfer to a high-dependency or intensive care unit.

A severe metabolic acidosis in the absence of hyperglycaemia (or other obvious cause of acidosis such as renal failure) raises the possibility of Lactic acidosis, Endocrinology & metabolism, Alcoholic ketoacidosis—this occurs in alcoholics following a binge.

Alterations in hepatic redox state may result in a misleading negative or ‘trace’ Ketostix® reaction. A similar caveat may occasionally be encountered when significant LA coexists with DKA. Venous plasma glucose may be normal or 4.

Anion gap (􀀉p432) >15mmol/L. Normally, the anion gap (<10mmol/L) results from plasma proteins, SO4
2–, PO4 3– and lactate ions. When the anion gap is increased, measurement of plasma ketones, lactate, etc. usually confirms the aetiology.

Investigation of hyperlipidaemia
Primary dyslipidaemias are relatively common and contribute to an individual’s risk of developing atheroma (e.g. CHD, CVD). Prominent examples include familial combined hyperlipidaemia (FCHL, ~2–3% of UK
population) and heterozygous familial hypercholesterolaemia (FH, UK incidence  1 in 500). Major hypertriglyceridaemia also predisposes to pancreatitis.

The key features of familial FH, FCHL and diabetic dyslipidaemia are considered later.
Investigations
Although many subtle alterations in plasma lipids have been described, therapeutic decisions rest on measurement of some or all of the following in serum or plasma (plasma being preferred since it can be cooled rapidly):

  • Total cholesterol (may be measured in non-fasting state in first instance since levels are not greatly influenced by meals).
  • Triglycerides (after 12h fast).
  • Low-density lipoprotein (LDL)-cholesterol (calculated using the Friedewald formula when triglycerides are <4.5mmol/L):


HDL-cholesterol (regarded as the ‘cardioprotective’ subfraction—HDL particles are synthesised in the gut and liver and thought to be involved in ‘reverse transport’ of cholesterol from peripheral tissues to the liver where it can be excreted as bile salts.
Notes on sampling in relation to lipoprotein metabolism


  • Triglycerides (triacylglycerols) are measured after a ~12h overnight fast in order to clear diet-derived chylomicrons.
  • Alcohol should be avoided the evening prior to measurement of triglycerides (can exacerbate hypertriglyceridaemia).
  • A weight-maintaining diet is recommended for 2–3 weeks before testing.
  • Lipid measurements should be deferred for 2–3 weeks after minor illness and 2–3 months after major illness, surgery or trauma since cholesterol may be temporarily 5 and triglycerides 4. Following acute myocardial infarction it is generally accepted that plasma cholesterol is reliable if measured within 24h of the onset of symptoms. 
  • The effects of certain drugs on lipids should be considered. 
  • Glycaemic control should be optimised wherever possible before measuring plasma lipids in patients with diabetes.

Important additional considerations are

  • Day-to-day variability—generally, decisions to treat hyperlipidaemia should be based on more than one measurement over a period of 1–2 weeks.
  • Exclusion of secondary hyperlipidaemia—many common conditions, drugs and dietary factors can influence plasma lipids.
  • Family members should also have their plasma lipids measured if a familial hyperlipidaemia is suspected in a proband.

Both cholesterol and triglycerides may be affected to some degree by these factors, but one often predominates. Pre-existing primary hyperlipidaemias may be exacerbated.

Clinical features
E.g. xanthelasma, tendon xanthomas, etc. should always be sought. A detailed family history, drug history and medical history (for diabetes and other cardiovascular risk factors such as hypertension) should always be obtained. Certain endocrine disorders, impaired hepatic or renal function can influence circulating lipid composition and cardiovascular risk. A classification of the major familial dyslipidaemias. Specialist advice should be sought in the management of major or resistant hyperlipidaemias.



Test protocols

Insulin tolerance test (insulin stress test)
Indication: suspected ACTH or GH deficiency.
Contraindications: patients with epilepsy, coronary heart disease (check
ECG).

Children: use no more than 0.1U/kg. Considerable care should be exercised; the test should only be performed in a centre with expertise.

Alternatives: short synacthen test for hypocortisolism; stimulation tests for growth hormone deficiency

Preparation: patient fasting overnight. Bed required (though day case procedure). Patient must be accompanied home and may not drive. OMIT morning hydrocortisone or other steroid hormone replacement if patient is taking this and previous day’s growth hormone. Physician must be present throughout the test. Requires written consent.

Procedure: early morning outpatient test in fasting patient. Indwelling venous cannula and constant medical supervision required throughout.

Cannula is kept patent by running saline infusion with three-way tap for sampling. Discard initial 2–3mL when each sample is taken. Label all samples clearly with time and patient details. Near-patient testing
glucometer required.

1. Take baseline blood for glucose, cortisol and GH. Check IV access working well. Review test with the patient and explain symptoms he/she is likely to experience.
2. Draw up 25mL of 50% dextrose for immediate administration IF REQUIRED.
3. Give soluble (regular) insulin as an intravenous bolus in a dose of 0.15U/kg after an overnight fast. Consider 0.1U/kg (lower dose) if suspected profound hypocortisolism. iThis appears a very small dose,
e.g. typically around 10 units. CHECK DOSE CALCULATION CAREFULLY.
Usually an insulin syringe is used to draw it up and then transfer it to a 2mL syringe containing saline.
4. Take blood at 15min intervals (0, 15, 30, 45, 60min) for glucose, cortisol and GH.
5. Observe for symptoms and signs of hypoglycaemia. First sign is usually profuse sweating. Patient may then be aware of symptoms such as palpitations, hunger, paraesthesiae. This typically occurs 30–45min into
the test. Check near-patient glucose to confirm <3.5mmol/L. Continue to talk to and reassure patient. If patient becomes very drowsy or unrousable then given 25mL of 50% glucose. This does not invalidate
the test as the hypoglycaemic stimulus has already occurred. Continue blood sampling at standard times.
6. If patient has not experienced hypoglycaemia by 45min and nearpatient glucose is >4mmol/L, give a further intravenous bolus of 0.15U/kg or 0.3U/kg if patient known to be very insulin resistant (e.g.
acromegalic). Repeat sampling at 15min intervals for 60min after this second bolus.
7. At end of procedure (usually 60min), give IV 25mL dextrose if patient still has symptoms of hypoglycaemia. 8. Give patient a meal including complex carbohydrate (e.g. sandwiches or lunch) and observe for a minimum of 1h further before accompanied discharge.
Unwanted effects: severe hypoglycaemia with depressed level of consciousness or convulsion requires immediate termination of test with 25mL of 50% dextrose IV. Repeat if necessary and follow with 5 or
10% dextrose infusion. Continue to collect samples for hormone and glucose measurements.
Interpretation: test is only interpretable if adequate hypoglycaemia is achieved (<2.2mmol/L). Normal maximal cortisol response >550nmol/L. Normal GH response >20mU/L. Impaired responses (if
hypoglycaemic stimulus adequate) denote corticotrophin (assuming adrenal glands are normal) or GH deficiency or both. Peak GH response <10mU/L is sufficient to consider GH replacement; peak GH response <5mU/L is severe growth hormone deficiency.

Combined anterior pituitary function testing
Indication: assessment for anterior pituitary hypofunction.
Contraindications: previous reaction to stimulatory hormones.
Alternatives: insulin tolerance testing for GH and adrenal axis; metyrapone test for adrenal axis.
Preparation: test usually performed in morning for basal sampling.
Procedure: IV cannula inserted. Basal blood samples taken for cortisol, oestradiol (3) or testosterone (9), free T4 and IGF-1. Hypothalalmic hormones are given sequentially intravenously each as a bolus over
around 20s: LHRH 100μg, TRH 200μg and ACTH 250μg. Additionally GHRH (1μg/kg body weight) may be given. (Reduce doses in children.)
Samples are drawn at 0, 20, 30, 60 and 120min for LH, FSH, TSH cortisol and prolactin. If GHRH is given, samples are drawn at the same time points for GH.

Interpretation: normal values as follows:
TRH: Suspect secondary hypothyroidism if peak response (at 20min) <20mU/L (Note: low levels also seen in hyperthyroidism—ensure free T4 or total T4 not raised).
ACTH: Peak cortisol response >550nmol/L at 30 or 60min.
LHRH: Peak LH/FSH response 2–5 × basal value.
LH: Peak at 20min, FSH later.
GHRH: Normal GH peak response >15mU/L.

Water deprivation test
Indication: diagnosis of diabetes insipidus (DI) and to distinguish cranial and nephrogenic diabetes insipidus.
Contraindications: none if carefully supervised. For correct interpretation, thyroid and adrenal deficiency should be replaced first.
Interpretation in the presence of diabetes mellitus and uraemia can be difficult.
Alternatives: morning urine osmolality of >600mOsmol excludes significant degrees of DI. No other definitive test for diabetes insipidus.
Patient preparation: usually an outpatient procedure. Correct thyroid and adrenal insufficiency in advance. Renal function and blood glucose should have been checked in advance. Steroid and thyroid hormone replacement should be taken as normal on the day of the test. If the patient is on DDAVP, omit the dose on the evening before the test (or if not possible, halve this dose). Free fluids, but not too excess, up to 0730h on the day of the test. No alcohol on the night before the test or in the morning of the test. Light breakfast but no tea, coffee or smoking on the morning of the test. Empty bladder before attending for the test.

If urine volume is <3L/day (‘mild cases’), ask patient to have no fluids or food from 1800h on the evening before the test (‘prolonged water deprivation test’).
Requirements for test: accurate weighing scales. Supervision for the whole test (up to 8h). DDAVP for injection (2μg). Immediate access to serum electrolyte, plasma and urinary osmolality assays. Access to a
plasma AVP (ADH) assay desirable.

Procedure: 0730h
1. Weigh patient and calculate 97% of body weight.
2. Mark this target on the chart.
3. No food or fluid for next 8h.
4. Insert cannula for repeated blood sampling and flush. 0800h
5. Obtain plasma for Na+ and osmolality and urine for osmolality.
6. Then collect urine hourly for volume and osmolality and plasma every 2h for Na+ and osmolarity.
7. Weigh patient before and after passing water if unobserved.
8. If patient loses 3% body weight, order urgent plasma osmolality and Na+.
9. If plasma osmolality >300mOsmol (Na+ >140mmol/L) stop test, allow patient to drink and give DDAVP
10.If plasma osmolality <300mOsmol, patient may have been fluid overloaded before test and water deprivation can continue.
11.Stop test at 8h (4pm) and take final recordings of urine and plasma.
12.Save an aliquot of plasma for vaspressin levels in case of difficulties in test interpretation.
13.Ideally urine osmolalities will have reached a plateau (<30mOsmol rise between samples).
14.Now give 2μg DDAVP IM (or 20μg intranasally) and collect urine samples only for a further 2h. Allow free fluids at this stage.

Interpretation: normal response: plasma osmolality remains in the range 280–295mmol, urine osmolality rises to >2 × plasma (>600mOsmol). If urine volumes during water deprivation do not reduce and yet the
plasma does not become more concentrated (rising osmolality) and weight does not fall, suspect surreptitious drinking during test.

Diagnostic trial of DDAVP
Indication: distinction of partial diabetes insipidus from primary polydipsia.
Contraindications: cardiac failure. Current diuretic use (test uninterpretable). Note that this test may precipitate severe hyponatraemia in primary polydipsia and should be preformed in an inpatient unit with clinical and biochemical regular review.
Preparation: admission to assessment unit. First line tests for polydipsia/polyuria should have been performed.

Procedure:
1. 24h urine volume, morning urine osmolality, weight, fluid intake (as far as possible), serum osmolality, Na+, urea and creatinine should all be performed daily and the results reviewed the same day.
2. Subjects should have access to fluid ad libitum but should be reminded that they should only drink if they are thirsty.
3. After an initial 24h period of observation, desmopressin (DDAVP) is administered at a dose of 2mg bd SC for 3 days.

Stop test if serum Na+ falls to <130mmol/L.
Interpretation: reduction in urine volume to <2L/day, 4 in urine osmolality to >600mOsmol/L without fall in serum Na+ to <140mmol/L suggests central diabetes insipidus. Reduction in urine volume with no increase in urine osmolality >600mOsmol/L and without a fall in serum Na+ suggests partial nephrogenic diabetes
insipidus. Limited reduction in urine volume, with some increase in urine osmolarity but a fall in serum Na+ suggests primary polydipsia.

Low dose dexamethasone suppression test

Indication: to distinguish hypercortisolism from normality. The dexamethasone suppressed CRH test is believed to have less false positives in cases of alcholic or depressive pseudo-Cushing’s syndrome.
Patient preparation: patients should not be on oral steroids or drugs that increase steroid metabolism.
Overnight dexamethasone suppression test: 1mg dexamethasone is taken PO at midnight. Serum sample for cortisol is taken the following morning between 0800 and 0900h.

Interpretation: serum cortisol should suppress to <140nmol/L (usually <50nmol/L). Values 140–175nmol/L are equivocal and suggest a 2-day test should be performed. 10–15% false +ve rate.

2-day low dose dexamethasone suppression test (preferred): dexamethasone 0.5mg is giv
en PO every 6h for 8 doses (2 days) starting in the early morning. Ideally tablets are taken strictly at 6-hourly intervals (0600, 1200, 1800, 0000h) which may necessitate an inpatient stay. A 24h collection for urine free cortisol is taken on the second day of the test and serum cortisol is measured at 0600h on the 3rd day, 6h after the last dose. IV administration of dexamethasone can be used if there are concerns over absorption or compliance.

Interpretation: serum cortisol 6h after the last dose should be <140nmol/L, usually <50nmol/L. Urinary free cortisol on the second day should be <70nmol/L, normally <30nmol/L. The 2-day test strictly
performed has less false +ves than the overnight test.

Dexamethasone suppressed CRH test: dexamethasone 0.5mg is given PO every 6h for 8 doses (2 days) but starting at midnight and ending at 0600h. Tablets are taken strictly at 6-hourly intervals (0000, 0600,
1200, 1800h) which may necessitate an inpatient stay. Last dose is taken at 0600h and an injection of CRH (100μg IV or 1μg/kg) is given at 0800h. A blood sample for cortisol is taken at 0815h (i.e. 15min later).

Interpretation: serum cortisol level should be <38nmol/L (normal).

High dose dexamethasone suppression test

Indication: to distinguish between patients with Cushing’s disease (ACTH-secreting pituitary tumour) and ectopic ACTH production in patients with established hypercortisolism.

Patient preparation: as low dose test except that the test can be performed immediately following the 2-day low dose test.

Procedure:
1. 2 × 24h urine free cortisol collections are made to calculate the mean basal 24h urine free cortisol.
2. Baseline serum cortisol measurement is also taken before the first dexamethasone dose, ideally at 0600h. If the low dose test is performed first, the baseline values (urine and blood) must be taken prior to the
low dose test (i.e. any doses of dexamethasone).
3. Dexamethasone 2mg is given PO every 6h for 8 doses (2 days) starting in the early morning. Ideally tablets are taken strictly at 6-hourly intervals (0600, 1200, 1800, 0000h) which may necessitate an inpatient stay.
4. A 24h urine collection for urinary free cortisol (final) is taken on day 2 and a blood sample is taken for (final) cortisol 6h after the last dexamethasone dose (0600h on day 3). Creatinine excretion should be
measured and compared between urine samples to confirm true 24h collections.

Interpretation: % suppression of basal cortisol is calculated as: (basal cortisol–final cortisol)/basal cortisol × 100.
The same calculation is made for basal and day 2 urine free cortisol. 50% suppression is suggestive of pituitary-dependent disease. 90% suppression increases the likelihood (strict criteria). Thymic carcinoids
and phaechromocytomas releasing ACTH are source of false positives.

Short synacthen test
Indication: suspected adrenal insufficiency. Will not detect recent-onset
secondary adrenal insufficiency.

Contraindication: asthma/allergy to ACTH—risk of allergic reaction (can be performed with careful medication supervision of patient).
Preparation: patient must not take hydrocortisone on the morning of the test as this will be detected in the cortisol assay. The test can be performed on low dose dexamethasone but the morning dose should
be omitted until after the test. May have some value in patients on higher dose steroid therapy to indicate the degree of suppression of adrenocortical function.
Procedure: 250μg of synthetic ACTH (synacthen) given IM or IV. Blood taken at times 0, 30 and 60min for serum cortisol. A value at any time >550nmol/L makes the diagnosis very unlikely.


Low dose test: the test can be performed with a very low dose of ACTH  (e.g. 1μg). This may detect more subtle degrees of hypoadrenalism but the clinical significance of these findings remains uncertain.

Long (depot) ACTH test
Indication: distinguishing 1° and 2° adrenal failure.
Patient preparation: a short synacthen test should be performed prior to the test to diagnose adrenal failure. If patient is on steroid replacement, change to dexamethasone 0.5mg/day.
Procedure: blood is taken at 0900h for basal cortisol. 1mg of depot synthetic ACTH (synacthen) is then given IM on 2 consecutive days and blood collected 5h after each dose (1400h). A final cortisol sample is
taken at 0900h on the 3rd day.

Interpretation: serum cortisol should rise to >1000nmol/L on the last day and, if adrenal failure previously indicated by a short synacthen test, such a rise indicates secondary adrenal failure (pituitary/hypothalamic
cause inc. suppressive drugs).

Medical Guidebook